Title: A system of practical medicine. By American authors, Vol. 5 : Diseases of the Nervous System
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A SYSTEM OF PRACTICAL MEDICINE.

BY AMERICAN AUTHORS.



EDITED BY WILLIAM PEPPER, M.D., LL.D.,

PROVOST AND PROFESSOR OF THE THEORY AND PRACTICE OF MEDICINE AND OF
CLINICAL MEDICINE IN THE UNIVERSITY OF PENNSYLVANIA.


ASSISTED BY LOUIS STARR, M.D.,

CLINICAL PROFESSOR OF DISEASES OF CHILDREN IN THE HOSPITAL OF THE
UNIVERSITY OF PENNSYLVANIA.



VOLUME V.

DISEASES OF THE NERVOUS SYSTEM.



PHILADELPHIA:
LEA BROTHERS & CO.
1886.



Entered according to Act of Congress, in the year 1886, by

LEA BROTHERS & CO.,

in the Office of the Librarian of Congress at Washington. All rights
reserved.



WESTCOTT & THOMSON,
_Stereotypers and Electrotypers, Philada._

WILLIAM J. DORNAN,
_Printer, Philada._



VALEDICTORY.


In presenting to the profession the fifth and concluding volume of the
“SYSTEM OF PRACTICAL MEDICINE BY AMERICAN AUTHORS,” the Editor may be
permitted to refer briefly to labors which for years have called forth
his strenuous endeavors. The original prospectus of the work was
issued in 1881. The first volume was published in January, 1885; the
second, in May, 1885; the third, in September, 1885; and the fourth,
in February, 1886. In view of the delays inevitable in large and
complicated literary enterprises, such unusual punctuality reflects
credit alike on the zeal of the contributors and the energy and
resources of the publishers. The duties of the Editor have been
lightened and rendered agreeable by the unvarying courtesy and cordial
co-operation of all connected with him in the undertaking; and he has
been amply rewarded by the realization of his hopes in the favorable
reception accorded to the successive volumes by the profession on both
sides of the Atlantic. The plan of the work has been strictly adhered
to, and the articles promised have been furnished without exception,
although in a very few cases circumstances required a change in the
authorship. Special mention is due to Dr. Louis Starr and to Dr.
Judson Daland for the very valuable assistance they have rendered.

The only alloy to the pleasure which the Editor has had in the
progress of the work has been the removal by death of so many of his
distinguished collaborators: such men as Flint, Van Buren, Armor,
Bemiss, and Elsberg will long be mourned by the profession.

The number of articles is 185, written by 99 authors, covering, with
indexes, about 5600 pages, and throughout its whole extent the
original purpose has been kept constantly in view, that the practical
character of the work should adapt it specially to the needs of the
general practitioner. In conclusion, the Editor feels that it is a
subject of congratulation that through the combination of so many
leading members of the profession it has been rendered possible to
present in this work, for the first time, the entire subject of
practical medicine treated in a manner truly representative of the
American School.

PHILADELPHIA, JUNE, 1886.



CONTENTS OF VOLUME V.


DISEASES OF THE NERVOUS SYSTEM.
                                                                  PAGE
GENERAL SEMEIOLOGY OF DISEASES OF THE NERVOUS SYSTEM; DATA OF
  DIAGNOSIS. By E. C. SEGUIN, M.D. . . . . . . . . . . . . . . .    19

THE LOCALIZATION OF LESIONS IN THE NERVOUS SYSTEM. By E. C.
  SEGUIN, M.D. . . . . . . . . . . . . . . . . . . . . . . . . .    65

MENTAL DISEASES. By CHARLES F. FOLSOM, M.D.  . . . . . . . . . .    99

HYSTERIA. By CHARLES K. MILLS, A.M., M.D.  . . . . . . . . . . .   205

HYSTERO-EPILEPSY. By CHARLES K. MILLS, A.M., M.D.  . . . . . . .   288

CATALEPSY. By CHARLES K. MILLS, A.M., M.D. . . . . . . . . . . .   314

ECSTASY. By CHARLES K. MILLS, A.M., M.D. . . . . . . . . . . . .   339

NEURASTHENIA. By H. C. WOOD, M.D., LL.D. . . . . . . . . . . . .   353

SLEEP, AND ITS DISORDERS. By HENRY M. LYMAN, A.M., M.D.  . . . .   363

ACUTE AFFECTIONS PRODUCED BY EXPOSURE TO HEAT. By H. C.
  WOOD, M.D., LL.D.  . . . . . . . . . . . . . . . . . . . . . .   387

HEADACHE. By WHARTON SINKLER, M.D. . . . . . . . . . . . . . . .   401

VERTIGO. By S. WEIR MITCHELL, M.D. . . . . . . . . . . . . . . .   416

TREMOR. By WHARTON SINKLER, M.D. . . . . . . . . . . . . . . . .   429

PARALYSIS AGITANS. By WHARTON SINKLER, M.D.  . . . . . . . . . .   433

CHOREA. By WHARTON SINKLER, M.D. . . . . . . . . . . . . . . . .   439

ATHETOSIS. By WHARTON SINKLER, M.D.  . . . . . . . . . . . . . .   457

LOCAL CONVULSIVE DISORDERS. By ALLAN MCLANE HAMILTON, M.D. . . .   461

EPILEPSY. By ALLAN MCLANE HAMILTON, M.D. . . . . . . . . . . . .   467

THE NEURAL DISORDERS OF WRITERS AND ARTISANS. By MORRIS J.
  LEWIS, M.D.  . . . . . . . . . . . . . . . . . . . . . . . . .   504

TETANUS. By P. S. CONNER, M.D. . . . . . . . . . . . . . . . . .   544

DISORDERS OF SPEECH. By EDWARD P. DAVIS, A.M., M.D.  . . . . . .   566

ALCOHOLISM. By JAMES C. WILSON, A.M., M.D. . . . . . . . . . . .   573

THE OPIUM HABIT AND KINDRED AFFECTIONS. By JAMES C.
  WILSON, A.M., M.D. . . . . . . . . . . . . . . . . . . . . . .   647

CHRONIC LEAD-POISONING. By JAMES C. WILSON, A.M., M.D. . . . . .   678

PROGRESSIVE UNILATERAL FACIAL ATROPHY. By CHARLES K.
  MILLS, A.M., M.D.  . . . . . . . . . . . . . . . . . . . . . .   693

DISEASES OF THE MEMBRANES OF THE BRAIN AND SPINAL CORD. By
  FRANCIS MINOT, M.D.  . . . . . . . . . . . . . . . . . . . . .   703

TUBERCULAR MENINGITIS. By FRANCIS MINOT, M.D.  . . . . . . . . .   723

CHRONIC HYDROCEPHALUS. By FRANCIS MINOT, M.D.  . . . . . . . . .   740

CONGESTION, INFLAMMATION, AND HEMORRHAGE OF THE MEMBRANES OF THE
  SPINAL CORD. By FRANCIS MINOT, M.D.  . . . . . . . . . . . . .   746

SPINA BIFIDA. By JOHN ASHHURST, JR., M.D.  . . . . . . . . . . .   757

ANÆMIA AND HYPERÆMIA OF THE BRAIN AND SPINAL CORD. By E. C.
  SPITZKA, M.D.  . . . . . . . . . . . . . . . . . . . . . . . .   763

THE CHRONIC INFLAMMATORY AND DEGENERATIVE AFFECTIONS OF THE
  SPINAL CORD. By E. C. SPITZKA, M.D.  . . . . . . . . . . . . .   825

CONCUSSION OF THE BRAIN AND SPINAL CORD. By WILLIAM HUNT, M.D. .   907

INTRACRANIAL HEMORRHAGE AND OCCLUSION OF THE CEREBRAL VESSELS,
  APOPLEXY, SOFTENING OF THE BRAIN, CEREBRAL PARALYSIS. By
  ROBERT T. EDES, M.D. . . . . . . . . . . . . . . . . . . . . .   917

ATROPHY AND HYPERTROPHY OF THE BRAIN. By H. D. SCHMIDT, M.D. . .   993

SYPHILITIC AFFECTIONS OF THE NERVE-CENTRES. By H. C.
  WOOD, M.D., LL.D.  . . . . . . . . . . . . . . . . . . . . . .   999

TUMORS OF THE BRAIN AND ITS ENVELOPES. By CHARLES K.
  MILLS, A.M., M.D., and JAMES HENDRIE LLOYD, A.M., M.D. . . . .  1028

TUMORS OF THE SPINAL CORD AND ITS ENVELOPES. By CHARLES K.
  MILLS, A.M., M.D., and JAMES HENDRIE LLOYD, A.M., M.D. . . . .  1090

INFANTILE SPINAL PARALYSIS. By MARY PUTNAM JACOBI, M.D.  . . . .  1113

DISEASE OF ONE LATERAL HALF OF THE SPINAL CORD. By H. D.
  SCHMIDT, M.D.  . . . . . . . . . . . . . . . . . . . . . . . .  1165

PROGRESSIVE LABIO-GLOSSO-LARYNGEAL PARALYSIS. By H. D.
  SCHMIDT, M.D.  . . . . . . . . . . . . . . . . . . . . . . . .  1169

DISEASES OF THE PERIPHERAL NERVES. By FRANCIS T. MILES, M.D. . .  1177

NEURALGIA. By JAMES J. PUTNAM, M.D.  . . . . . . . . . . . . . .  1211

VASO-MOTOR AND TROPHIC NEUROSES. By M. ALLEN STARR, M.D., PH.D.   1241


INDEX  . . . . . . . . . . . . . . . . . . . . . . . . . . . . .  1277



CONTRIBUTORS TO VOLUME V.


ASHHURST, JOHN, JR., M.D.,
  Professor of Clinical Surgery in the University of Pennsylvania.

CONNER, P. S., M.D.,
  Professor of Anatomy and Clinical Surgery in the Medical College of
  Ohio; Professor of Surgery, Dartmouth Medical College; Surgeon to
  Cincinnati and Good Samaritan Hospitals, Cincinnati.

DAVIS, EDWARD P., A.M., M.D.,
  Lecturer on Physiology, Rush Medical College, Chicago, and lately
  Medical Superintendent of the Presbyterian Hospital, Chicago.

EDES, ROBERT T., M.D.,
  Jackson Professor of Clinical Medicine in Harvard University,
  Boston, Mass.

FOLSOM, CHARLES F., M.D.,
  Visiting Physician for Nervous and Renal Diseases, Boston City
  Hospital; formerly Assistant Professor of Mental Diseases in Harvard
  University, Boston.

HAMILTON, ALLAN MCLANE, M.D.,
  Consulting Physician to the New York City Male and Female Insane
  Asylums; Hudson River State Asylum for the Insane; Consulting
  Neurologist to Hospital for Ruptured and Crippled; Attending
  Physician to Hospital for Nervous Diseases; Member of the New York
  Neurological Society.

HUNT, WILLIAM, M.D.,
  Surgeon to the Pennsylvania Hospital, and to the Philadelphia
  Orthopædic Hospital and Infirmary for Nervous Diseases.

JACOBI, MARY PUTNAM, M.D.,
  Professor of Therapeutics at the Women's Medical College, New York.

LEWIS, MORRIS J., M.D.,
  Physician to the Episcopal Hospital and to the Children's Hospital;
  Assistant Physician to the Orthopædic Hospital and Infirmary for
  Nervous Diseases, Philada.

LLOYD, JAMES HENDRIE, A.M., M.D.,
  Instructor in Electro-Therapeutics in the University of
  Pennsylvania.

LYMAN, HENRY M., A.M., M.D.,
  Professor of Physiology and of Diseases of the Nervous System in
  Rush Medical College, Chicago; Professor of Theory and Practice of
  Medicine in the Woman's Hospital Medical College, Chicago; one of
  the Attending Physicians to the Presbyterian Hospital, Chicago, Ill.

MILES, FRANCIS T., M.D.,
  Professor of Physiology and Clinical Professor of Diseases of the
  Nervous System, University of Maryland, Baltimore.

MILLS, CHARLES K., A.M., M.D.,
  Professor of Diseases of the Mind and Nervous System in the
  Philadelphia Polyclinic and College for Graduates in Medicine;
  Lecturer on Mental Diseases in the University of Pennsylvania;
  Neurologist to the Philadelphia Hospital.

MINOT, FRANCIS, M.D.,
  Hersey Professor of the Theory and Practice of Physic in Harvard
  University; Physician to Massachusetts General Hospital.

MITCHELL, S. WEIR, M.D.,
  Member of the National Academy of Sciences; President of the College
  of Physicians of Philadelphia.

PUTNAM, JAMES J., A.B. (Harv.), M.D. (Harv.),
  Physician to Out-patients at the Massachusetts General Hospital;
  Clinical Instructor at Harvard Medical College.

SCHMIDT, H. D., M.D.,
  Pathologist to the Charity Hospital of New Orleans.

SEGUIN, EDWARD C., M.D.,
  Clinical Professor of Diseases of the Mind and Nervous System in the
  College of Physicians and Surgeons, New York City.

SINKLER, WHARTON, M.D.,
  Physician to the Philadelphia Orthopædic Hospital, and Infirmary for
  Nervous Diseases.

SPITZKA, E. C., M.D.,
  Consulting Neurologist to the North-eastern Dispensary, and
  Physician to the Department for Nervous Diseases of the German
  Poliklinik.

STARR, M. ALLEN, M.D., PH.D.,
  Professor of Diseases of the Mind and Nervous System, New York
  Polyclinic; Attending Physician to Department of Nervous Diseases,
  Demilt Dispensary.

WILSON, JAMES C., A.M., M.D.,
  Physician to the Philadelphia Hospital, and to the Hospital of the
  Jefferson College; President of the Pathological Society of
  Philadelphia.

WOOD, HORATIO C., M.D., LL.D.,
  Clinical Professor of Diseases of the Nervous System and Professor
  of Materia Medica and Therapeutics in the University of
  Pennsylvania; Neurologist to the Philadelphia Hospital; Member of
  the National Academy of Sciences.



ILLUSTRATIONS.


FIGURE                                                            PAGE
 1. DIAGRAM SHOWING THE ARC FOR REFLEX ACTION . . . . . . . . . .   51

 2. DIAGRAM AND TABLE SHOWING THE APPROXIMATE RELATION TO THE
      SPINAL NERVES OF THE VARIOUS SENSORY AND REFLEX FUNCTIONS
      OF THE SPINAL CORD  . . . . . . . . . . . . . . . . . . . .   53

 3. CONTRACTION OF NORMAL ABDUCTOR INDICIS WITH STRONG CURRENT
      (AMIDON)  . . . . . . . . . . . . . . . . . . . . . . . . .   67

 4. CONTRACTION OF PARALYED MUSCLE ON THIRTY-FIRST DAY OF BELL'S
      PALSY OF THE FACE (AMIDON)  . . . . . . . . . . . . . . . .   67

 5. DIAGRAM OF A TRANSVERSE SECTION OF THE SPINAL CORD THROUGH
      THE CERVICAL ENLARGEMENT  . . . . . . . . . . . . . . . . .   69

 6. DIAGRAM OF A TRANSVERSE SECTION OF THE SPINAL CORD THROUGH
      THE LUMBAR ENLARGEMENT  . . . . . . . . . . . . . . . . . .   71

 7. HORIZONTAL SECTION THROUGH THE CENTRE OF THE RIGHT CEREBRAL
      HEMISPHERE  . . . . . . . . . . . . . . . . . . . . . . . .   82

 8. DIAGRAM OF VISUAL PATHS, DESIGNED TO ILLUSTRATE SPECIALLY
      LEFT LATERAL HEMIANOPSIA FROM ANY LESION  . . . . . . . . .   84

 9. LONGITUDINAL (SAGITTAL) SECTION THROUGH THE BRAIN, TO SHOW
      THE DISTRIBUTION OF THE FASCICULI OF THE INTERNAL CAPSULE .   87

10. DIAGRAM OF THE LATERAL ASPECT OF THE CEREBRAL HEMISPHERE  . .   90

11. DIAGRAM OF THE MESAL ASPECT OF THE CEREBRAL HEMISPHERE  . . .   90

12. TOPOGRAPHICAL LINES APPLIED TO THE EXTERNAL CONTOUR OF THE
      HEAD  . . . . . . . . . . . . . . . . . . . . . . . . . . .   93

13. TOPOGRAPHICAL LINES APPLIED TO HENLE'S FIGURE OF THE SKULL  .   95

14. THE SAME TOPOGRAPHICAL LINES APPLIED TO THE LEFT CEREBRAL
      HEMISPHERE IN HENLE'S SKULL . . . . . . . . . . . . . . . .   96

15. SPECIMENS OF HANDWRITING IN TWO CASES OF GENERAL PARALYSIS OF
      THE INSANE  . . . . . . . . . . . . . . . . . . . . . . 184, 185

16. FEET OF A PATIENT WITH ACUTE MYELITIS . . . . . . . . . . . .  266

17. FEET OF A PATIENT WITH HYSTERICAL PARAPLEGIA  . . . . . . . .  266

18. POSITION ASSUMED BY A HYSTERO-EPILEPTIC . . . . . . . . . . .  294

19. POSITION OF CRUCIFIXION ASSUMED BY A HYSTERO-EPILEPTIC (SAME
      CASE AS FIG. 18)  . . . . . . . . . . . . . . . . . . . . .  295

20. POSITION ASSUMED BY A HYSTERO-EPILEPTIC (SAME CASE AS
      FIG. 18)  . . . . . . . . . . . . . . . . . . . . . . . . .  296

21. EXTREME OPISTHOTONOS IN A HYSTERO-EPILEPTIC (SAME CASE AS
      FIG. 18)  . . . . . . . . . . . . . . . . . . . . . . . . .  296

22. PRINCIPAL HYSTEROGENIC ZONES, ANTERIOR SURFACE OF THE BODY
      (AFTER RICHER)  . . . . . . . . . . . . . . . . . . . . . .  298

23. PRINCIPAL HYSTEROGENIC ZONES, POSTERIOR SURFACE OF THE BODY
      (AFTER RICHER)  . . . . . . . . . . . . . . . . . . . . . .  298

24. POSITION ASSUMED BY A HYSTERO-EPILEPTIC . . . . . . . . . . .  302

25. OPISTHOTONOS OF TETANUS . . . . . . . . . . . . . . . . . . .  309

26. CASE OF ATHETOSIS . . . . . . . . . . . . . . . . . . . . . .  459

27. LOWER FACE OF RIGHT HEMISPHERE  . . . . . . . . . . . . . . .  493

28. MOVEMENTS OF WRIST IN TELEGRAPHING  . . . . . . . . . . . . .  509

29. METHOD OF WRITING ADOPTED BY A PATIENT WHO HAS MARKED SPASM
      OF FLEXORS OF FINGERS AND THUMB . . . . . . . . . . . . . .  517

30. TEMPERATURE CHART OF A CASE OF TUBERCULAR MENINGITIS IN A BOY
      EIGHT YEARS OLD . . . . . . . . . . . . . . . . . . . . . .  731

31. TRANS-SECTION OF UPPER LUMBAR CORD OF A PATIENT MODERATELY
      ADVANCED IN TABES DORSALIS  . . . . . . . . . . . . . . . .  845

32. CHANGES IN THE CORD IN A CASE OF DIFFUSE SPINAL SCLEROSIS . .  886

33. CHANGES IN THE CELLS OF THE ANTERIOR HORN IN DIFFUSE SPINAL
      SCLEROSIS (SAME CASE AS FIG. 32)  . . . . . . . . . . . . .  886

34. SECONDARY DEGENERATION OF INTEROLIVARY LAYER  . . . . . . . .  894

35. SECONDARY DEGENERATION OF INTEROLIVARY LAYER, CAUDAL OR
      DESCENDING PORTION  . . . . . . . . . . . . . . . . . . . .  896

36. DECUSSATING DEGENERATION OF INTEROLIVARY LAYER  . . . . . . .  897

37. TEMPERATURE CHART OF A CASE OF CEREBRAL HEMORRHAGE  . . . . .  936

38. TEMPERATURE CHART OF A RAPID CASE OF CEREBRAL HEMORRHAGE  . .  937

39. CHART SHOWING THE EXCESS OF TEMPERATURE IN A CASE OF
      MENINGEAL HEMORRHAGE  . . . . . . . . . . . . . . . . . . .  938

40. CHART SHOWING RISE OF TEMPERATURE BEFORE APOPLECTIC SYMPTOMS
      IN A CASE OF TUMOR OF RIGHT TEMPORAL LOBE . . . . . . . . .  953

41. CHART SHOWING THE DIFFERENCE OF TEMPERATURE BETWEEN THE TWO
      SIDES IN A CASE OF HEMIPLEGIA . . . . . . . . . . . . . . .  961

42. CHART SHOWING THE SAME AS FIG. 41 IN ANOTHER CASE OF
      HEMIPLEGIA  . . . . . . . . . . . . . . . . . . . . . . . .  961

43. FLAT GLIOMA-CELL WITH ITS FIBRILLAR CONNECTIONS (OSLER) . . . 1047

44. HOMOGENEOUS TRANSLUCENT FIBRE-CELL (OSLER)  . . . . . . . . . 1047

45. DIAGRAM OF SPINAL COLUMN, CORD, AND NERVE-EXITS (AFTER
      GOWERS) . . . . . . . . . . . . . . . . . . . . . . . . . . 1102

46. SARCOMA PRESSING CERVICAL CORD (E. LONG FOX)  . . . . . . . . 1102

47. SARCOMA OF LOWER CERVICAL CORD  . . . . . . . . . . . . . . . 1103

48. THE SAME AS FIG. 47 . . . . . . . . . . . . . . . . . . . . . 1103

49. THE SAME AS FIG. 47 . . . . . . . . . . . . . . . . . . . . . 1103

50. THE SAME AS FIG. 47 . . . . . . . . . . . . . . . . . . . . . 1103

51. FIBROMA OF LOWER DORSAL CORD  . . . . . . . . . . . . . . . . 1104

52. TUMOR OF CAUDA EQUINA . . . . . . . . . . . . . . . . . . . . 1104

53. PSAMMOMA OF DORSAL CORD, JUST ABOVE LUMBAR ENLARGEMENT  . . . 1106

54. THE SAME AS FIG. 53 . . . . . . . . . . . . . . . . . . . . . 1106

55. DIAGRAM SHOWING THE MENTAL RELATIONS OF MOTOR AND TROPHIC
      CELLS WITH CEREBRAL AND SPINAL NERVE-FIBRES (AFTER ERB) . . 1146

56. VASO-MOTOR NERVES AND GANGLIA ACCOMPANYING THE ARTERIOLES IN
      A FROG (GIMBERT)  . . . . . . . . . . . . . . . . . . . . . 1242

57. DIAGRAM TO REPRESENT THE MODE OF ACTION OF COUNTER-IRRITANTS
      APPLIED TO THE CHEST (LAUDER-BRUNTON) . . . . . . . . . . . 1249

58. DIAGRAM OF THE ARRANGEMENT AND CONNECTION OF THE MOTOR AND
      TROPHIC CENTRES AND FIBRES IN THE SPINAL CORD AND MOTOR
      NERVE (AFTER ERB) . . . . . . . . . . . . . . . . . . . . . 1270


{17}


DISEASES OF THE NERVOUS SYSTEM.


{19}


GENERAL SEMEIOLOGY OF DISEASES OF THE NERVOUS SYSTEM; DATA OF
DIAGNOSIS.

BY E. C. SEGUIN, M.D.


I. Psychic Symptoms.

ABNORMAL EMOTIONAL STATES.—Emotional manifestations, spontaneous or
provoked from without, are, in the civilized adult, held in check
directly or indirectly by the will, or by so-called strength of
character. Extreme variations are allowed as being within the normal,
from the stupidity of the peasant and the impassability of the hero to
the sensitiveness and almost unrestrained reactions of the child or of
the artist. Each individual must be judged by his own and his racial
and family standards in this respect. It is more particularly when the
dulness or over-active state observed is in contrast with the
subject's habitual demeanor that the condition is called pathological.

Emotional dulness, or the complete absence of any emotional
manifestation, may depend upon (1) diminished sensibility to external
influences; (2) sluggishness of cerebral action, more especially in
the range of sensori-ideal processes, or to general want of
intelligence; (3) absorption of the subject's cerebral powers in some
special object, real or delusive. The first form is illustrated in
various grades of idiocy and backwardness; the second, in fatigue,
prostration, and in conditions of dementia; the third is well
exemplified in cases of insanity where the patient is devoted to one
delusion or dominated by hallucinations (melancholia attonita), in
which case the subject may be told the most painful news, insulted
most grievously, or threatened fearfully without manifesting grief,
anger, or fear. In some instances absolutely no emotional life can be
detected.

Emotional exaltation may be due to (1) increased sensibility to
external influences; (2) to deficient self-control. The first
condition is illustrated in neurasthenic and hysterical subjects and
in forms of mania: slight or almost imperceptible provocations call
forth reaction, a noise causes fear, a look anger or tears, etc.; the
second mechanism is apparent in diseases (dementia paralytica) where
the cerebral hemispheres are extensively diseased and the cerebral
power lessened (more especially is this the case where the right
hemisphere is injured), and in cases of simple debility or asthenia,
as when we see a previously mentally strong man shed tears or start
most easily in convalescence from acute disease.

It may also be stated, in general terms, that the emotions are
manifested in inverse ratio to the subject's mental or volitional
power. {20} Psychologically, the emotions are intimately related, on
the one hand, with sensory functions, and on the other with more
purely mental functions. Anatomically, it is probable that emotions
are generated in basal ganglia of the brain (thalami optici and
ganglion pontis), in close association with the sensory areas of the
cortex cerebri, while the volitional, inhibitory power is derived from
regions of the cortex situated frontad. Clinically, we meet with
abnormal emotional states in a great many diseases of the nervous
system, more especially in hysteria, neurasthenia, and insanity.

DEPRESSION in the psychic sphere manifests itself by the presence of
psychic pain (psychalgia), by slowness of emotive reaction and of
intellection, and by the predominance of fear, grief, and other
negative emotional states. This complex mental state is usually
accompanied by corresponding physical symptoms—general debility,
reduced muscular strength, slowness of visceral functions, and
retarded metamorphosis. The features are relaxed and passive; the
posture sluggish, indifferent, or cataleptoid; the animal appetites
are reduced. It is seldom that the entire economy does not sympathize
with the psychic state. In exceptional cases some emotions are
abnormally active, as in hypochondriasis; or there may be abnormally
active muscular movements, as in melancholia agitata. Usually,
depression is a part (a fundamental part, however) of a more complex
symptom group, as in hypochondriasis, melancholia, hysteria, the
prodromal stage of mania or paralytic dementia, etc.; but sometimes it
constitutes a so-called disease—melancholia sine delirio. Although
depressed subjects often appear indifferent to their surroundings, and
react slowly or not at all, it must not be supposed that their
emotions are not subjectively active. They are often abnormally so,
and psychic hyperæsthesia coexists with psychalgia. No anatomical seat
can be assigned to the processes which constitute this state and the
following; their psychic mechanism is unknown.

EXALTATION, or abnormally great mental activity (including emotions),
so-called psyclampsia, manifests itself by a pleased or happy
subjective state, by increased reaction to external stimuli, by
unusually abundant and rapid ideation, and by a corresponding increase
of somatic activity, as shown by apparent (?) excess of muscular
power, of circulation, of visceral activity, and of the appetites. The
entire being, in certain cases, becomes endowed with additional
capacity and power. In the mental sphere this over-activity easily
passes into incoherence and verbal delirium, while in the physical
sphere it may translate itself into violence. Clinically, exaltation
may show itself as an independent morbid state, known as mania sine
delirio. It more commonly appears, with other symptoms, in the shape
of ordinary mania, of delirium tremens, of dementia paralytica, etc.
Exaltation often follows morbid depression, and these two states
sometimes alternate for years (circular insanity). Exaltation, even
when accompanied by violent muscular action, must not always be
considered an evidence of increased nervous power. On the contrary, it
is often a result of irritable weakness, and as such indicates a tonic
and restorative medication.

ILLUSIONS.—By illusion is meant the result of malinterpretation of an
external impression by disordered sensorial or cerebral apparatuses.
All of the special senses and the common sensory nerves may be the
{21} media of illusions, but they more commonly manifest themselves in
the visual and auditory spheres. A few examples will best illustrate
the exact meaning of the term. An insane person mistakes a casual
visitor for his brother or father: he fancies that a piece of
furniture is a flowering shrub or a threatening animal; another
patient will declare that the food in his mouth tastes of a particular
poison; still another, having pains in the night, solemnly avers that
he has been beaten or cut, etc. A real impression is made upon the
centres for vision, taste, and common sensation, but it is wrongly
interpreted or appreciated. The exact mechanism of illusions escapes
our present means of analysis: the peripheral apparatus or the
perceptive centre may be disordered; probably, in most cases, the
latter. This is borne out by the fact that in many insane the
illusions are in harmony with the delusions present in the mind, and
then they are nearly akin to hallucinations. The word illusion is
sometimes employed as synonymous of delusion, but this is an abuse of
terms to be avoided. Healthy persons are subject to illusions, but the
error is quickly corrected by more careful observation by the same
sense, or by the use of others. The state of intoxication by cannabis
indica (hasheesh) presents numberless illusions of all the senses,
together with hallucinations.

HALLUCINATIONS.—By this term is designated the result of the
projection into the external world, through nerves of common or
special sensations, of formed sensations which arise in a disordered
sense-apparatus or nerve-centre; or, in more popular language, it may
be said to mean the perception of non-existent objects or impressions,
creations of the imagination. Examples: Disease (sclerosis) of the
posterior columns of the spinal cord irritates the roots of the
sensory nerves, the result being pain at the periphery in the parts
connected with the affected segment of the cord. So objective and real
do these peripheral pains seem that if the patient's mind be weakened
he may assert that they are due to his being beaten, stabbed, or
bitten by some one or by an animal. After amputation, the absent
member is long perceived by the subject, often with startling
distinctness, and even after the sensation has passed away it may be
brought back by faradizing the nerve-trunks above the stump. The
patient may hear voices, music, or simple sounds when in reality there
is silence, or he may be surrounded by imaginary images or plagued by
hallucinatory smells and tastes. Hallucinations may also arise in the
distribution of optic nerves.

Besides common hallucinations with their seeming reality and
objectivity, we admit others which are less vivid, which do not
startle or frighten the subject, and which are simply the outward
projections of the patient's own thoughts (delusions). The subject of
persecution by imaginary enemies may see around him the faces of his
pursuers with appropriate expressions, or hears their insulting or
threatening remarks, as outward plastic reproductions of his thoughts;
but the patient himself recognizes the want of actual objectivity and
clearness in these images. These we call, after Baillarger, psychic
hallucinations or pseudo-hallucinations. Similar phenomena are
observed in some sane persons under excitement and betwixt sleep and
waking.

The mechanism of hallucinations is partly understood, and may be
stated as follows: In some few cases a real disorder or defect in the
{22} peripheral sense-organ may give rise to false projections; for
example, a tinnitus may become transformed into a distinct voice, a
scotoma may be the starting-point of false pictures of a man or
animal. The simpler hallucinations of pain, cutaneous, muscular, and
visceral sensations may originate in irritation of the nerve-trunks
(as where the nerves of an arm-stump are faradized and the patient
feels his hand with fingers in motion). But the general or common
genesis of hallucinations is in disordered states of nerve-centres,
those for common sensations and the special centres or cortical areas
in the brain. Thus, a morbid irritation of the cortical visual area or
sphere will give rise to abundant hallucinations of sight; irritation
of the auditory sphere to hallucinations of hearing, as sounds and
voices, etc. It must be borne in mind that, however pathological
hallucinations may be, they arise from the operation of a fundamental
physiological law. In health we constantly refer our sensations or
transfer them into the external world, thus creating for ourselves the
non-Ego. All terminal sensory nerve-endings receive only elementary
impressions or impulses from external agencies, and these are
perceived and conceived as images, formed sounds, etc. in the
appropriate cortical centres; then by the law of reference of
sensations these elaborated, idealized conceptions or pictures are
thrown outward again and contemplated as objective. In this
physiological mechanism lies the kernel of truth which is included in
idealism.

Hallucinations may occur without derangement of mind or impairment of
judgment. Many instances are on record of transient or permanent
hallucinations of various senses in perfectly healthy persons who were
fully aware of the unreal character of what they saw or heard. Being
of sound mind, they were able to make the necessary correction by
reasoning or by the use of other senses. In very many forms of
insanity hallucinations are prominent, though they also occur in
quasi-sane conditions, as in hypochondriasis, hasheesh, belladonna,
and opium intoxication, the stage between sleeping and waking, etc. As
long as the subject is able to correct the false projections by reason
or by the use of other senses he is considered sane.

Hallucinations are sometimes the cause of acts by the insane, some of
them violent and even murderous actions. Hallucinations of sight and
hearing are especially prone to lead to assaults, murders, etc. The
occurrence for any length of time of acoustic hallucinations in
insanity is accounted of bad prognosis.

DELUSIONS are synonymous, in a popular way, with false beliefs. Thus,
we often speak of eccentric opinions, of fanatical or extravagant
creeds, as delusions. In a certain sense probably all mankind cherish
innumerable delusions. In a strictly medical and medico-legal sense,
however, the term is applied only to false beliefs in respect to
clearly-established, indisputable facts. Thus, a man who believes in
Spiritualism or even in metempsychosis, or in the divinity of a
certain personage, is not medically deluded; whereas, one who believes
that a bare court is a flowering garden or that he himself is divine
is deluded. The essential element in the conception of delusion is
belief or conviction on the patient's part; and that is why delusions
mean that the psychic functions are deeply and seriously impaired.
Delusions may be conveniently divided into ideal and sensorial.

{23} (_a_) Ideal delusions are false ideas or concepts arising more or
less spontaneously, or by morbid association in the subject's mind.
For example: he believes that he is a god, that he has millions of
money, that his soul is lost, that he has a thousand children, etc.
Many of the delirious ideas experienced by insane patients are
delusions, and so to a certain extent (subject to temporary
corrections by reasoning and demonstration) are the notions of
hypochondriacs about their health.

(_b_) Sensorial delusions are such as are founded upon illusions and
hallucinations. The moment a subject is convinced of the reality of an
illusion or hallucination, believes in its actuality, he is said to
have a delusion. The change from illusion and hallucination to the
state of sensorial delusion indicates a deeper psychic alteration—a
failure of critical capacity or judgment. Examples: A man imagines the
stump of a tree in front of him to be a human being, but by reasoning,
by closer visual inspection, or by palpation he concludes that it is a
tree, after all; this is a simple illusion. If he persists, in spite
of argument and demonstration, in his assertion that the stump is a
human being, he is said to have a delusion or to be deluded. If a
person sees wholly imaginary flowers or hears imaginary voices, as
long as he is capable of recognizing the falsity or want of actuality
of these images or sounds he has a simple hallucination; if he ceases
to make the necessary correction, and believes the flowers and voices
to really exist, he has sensorial delusions. It should be borne in
mind that sane persons may have hallucinations, and that some insane
have no sensorial delusions; also, that some insane are capable of
correcting, for a time at least or when closely questioned, their
illusions and hallucinations. Apart from these exceptional conditions,
delusions, sensorial and ideal, are most important symptoms of
insanity. We also meet temporary delusions in toxic conditions (from
Indian hemp, alcohol, etc.) and in the delirium of acute general
disease, of low febrile states, starvation, etc. Delusions are
sometimes named in groups, according to the prevailing type of mental
action; then, we have exalted delusions, in which the false notions
and beliefs are rose-colored or extremely exaggerated (as in paralytic
dementia, etc.). Again, we speak of delusions of persecutions, where
the patient fancies himself pursued, maltreated, insulted, or where he
insanely follows up and persecutes others. Such classification is
useful for purposes of clinical and psychical study.

Imperative conceptions or controlling morbid ideas and desires are
ideal delusions presenting certain peculiarities; one of which is that
of growth by accretion and assimilation by a sort of false logic and
grotesque analogical reasoning, until from a mere fancy or notion the
growth invades and governs the entire subjective life of the subject.

VIOLENCE is a complex symptom always deserving of study and
psychological analysis. It may present itself as an increase of a
naturally bad disposition or as a wholly new exhibition of
irritability and temper. Beyond these limits it may assume the shape
of abusive and foul language (not before employed by the subject), or
of physical acts of a destructive or dangerous character. Viewing the
condition from a psychological standpoint, we should endeavor to
distinguish between merely impulsive or animal violence due to
over-activity of the emotional state or to a loss of self-control
(cortical inhibition), and quasi-deliberate acts due either to special
delusions or to delirium. Abnormal irritability, or increase in an
{24} originally bad temper, is met with in hysteria, neurasthenia, and
partial dementia. Masturbators and epileptics frequently exhibit this
condition. In a state less pathological, from mere fatigue or
overwork, irritability may temporarily show itself as a result of
reduced cortical energy; and in such cases rest, a cup of tea or
coffee, alcohol, or even ordinary food, restores good-nature and
equanimity as by magic. In little children bad temper is a frequent
precursor of illness, more especially of cerebral disease. Greater
degrees of violence in speech and acts are met with in hysteria,
neurasthenia, and in many forms of insanity, in the guise of
exaggerations of animal propensities, to make a noise, break objects,
injure persons in an aimless general way. Voluntary or quasi-voluntary
acts of violence are those which are done under the influence of
hallucinations, delusions, or of delirious ideas, usually by insane
patients. The delirium of acute or inflammatory disease or of the
typhous state is rarely active, although pericarditis sometimes gives
rise to very violent delirium, and the mild delirium with picking and
gesticulating of pneumonia, typhoid fever, etc. may sometimes simulate
mania. In general terms, the words and acts of patients represent the
ideas passing through their minds in a rapid confused way, much as in
dreams. Violence done under the influence of clearly-defined
hallucinations and delusions is most dangerous, because it is executed
with apparent deliberation and volition. Thus, a man laboring under
hallucinations of hearing, fancying himself insulted, may turn in the
street and strike or shoot some one near him, the supposed author of
the insult. An epileptic falls in a partial attack or has epileptic
vertigo; as a part of the seizure there is a dream-like scene of
assault, actual or threatened, upon him, and on rising from the
ground, or after the momentary vertigo the patient, acting in
accordance with the demands of the dream-like scene, makes an
onslaught upon those near him or smashes furniture, etc. Seeing such
acts, without knowing their genesis, one is liable to consider them
normally deliberate and malicious. On recovering consciousness (which
may not be for several hours or days) the epileptic patient appears
utterly oblivious of his actions, and is much astonished to learn what
he has done. In many cases of insanity violent acts are done through a
similar psychic mechanism—_i.e._ through the domination of delusions.
Delusions often give rise to what may be termed negative
violence—resistance to personal care, treatment, giving of food, etc.
This is exemplified in acute melancholia, with overpowering fears of
all kinds and terrorizing hallucinations of sight and hearing. The
patients crowd in corners or sit curled up, and resist with all their
might whatever is done for them, even striking and biting the
attendants.

Therapeutically, the question of physical restraint or non-restraint
in the management of violence might be discussed here, but the
question is one which can be much better considered in connection with
the general treatment of insanity, and the reader is consequently
referred for information to the article on that subject.

DELIRIUM is a term which has been so variously applied that a brief
definition of it is wellnigh impossible. Illogical or unreasoning and
incoherent thoughts expressed in words and acts may suffice to give a
general idea of the condition. Extreme applications of the term are,
for example, to say that in a case of extreme dementia the rambling,
disconnected talk is delirium, or that in certain forms of monomania
the {25} expression of the patient's peculiar delusion is delirium. It
seems to us that there should be a certain degree of activity in the
production of morbid ideas, with confusion in their expression, to
justify the use of the term delirium. Again, in some instances the
delirious talking and acting are only the reflex of abundant
hallucinations of various senses which beset the patient. In some
other respects the term delirium is applied in several distinct ways:
first, in a substantive form as a designation for the incoherent words
and acts of a patient. Usually, it is then put in the plural form of
deliria. Thus we have the more or less highly organized, fixed or
changeable deliria of monomania, chronic mania, melancholia, paretic
dementia, etc., and the confused and evanescent deliria of acute
general diseases, intoxications, and many forms of insanity. In short,
we may speak of a sick person's deliria as we would of a normal
person's thoughts; or in still more elementary analysis deliria are
abnormal or insane thoughts and corresponding action. Second, delirium
is used adjectively as designating certain diseases—_e.g._ delirium
tremens, delirium a potu, acute delirium, delirium of acute diseases,
etc. The seat of the psychic processes which go to make delirium is
undoubtedly the cerebral cortex. This view is supported partly by the
clinical consideration that delirium bears a certain relation to the
psychic development of the subject. Thus, we see in children and in
the higher animals rudimentary or fragmentary deliria; in advanced age
the delirium is feeble and wellnigh absent; while in ordinary adults
with well-developed cerebration deliria are abundant and varied. From
pathological anatomy we learn that deliria become simplified and
subside in proportion as the cerebral cortex becomes more and more
damaged by effusions, by pressure effects, or by degenerative changes.
As to the relation between special histological pathological changes,
our knowledge is small and to a certain extent paradoxical. Thus, it
is universally admitted that delirium may be due either to hyperæmia
or to anæmia of the brain. The delirium of alcoholic or cannabis
intoxication may be fairly assumed to be of sthenic or hyperæmic
origin, either by the nervous elements themselves being in an exalted
state of irritability, or because an increase in the circulation of
arterial blood in the brain leads to greater activity of the cellular
elements. Again, delirium appears in conditions of general or cerebral
anæmia, as in starvation, after prolonged fever, after the withdrawal
of customary stimuli, etc. These views are confirmed by the fact that
some deliria cease upon the administration of sedatives and narcotics,
while others are relieved and cured by rest, stimulants, and food. On
the other hand, a large class of deliria, as exhibited in the insane,
escape pathological analysis; for example, the delirious conceptions
of monomania occurring in apparent somatic health and without
well-marked symptoms of cerebral disease. We are much in the dark as
to what the processes may be by which delusional notions grow in the
subjective life and manifest themselves outwardly as deliria. It is
probable that in such cases there is no material lesion (appreciable
to our present means of research), but a morbid dynamic condition,
false reactions, abnormal centripetal and centrifugal associations in
the psychic mechanism, with or without inherited bias. The diagnosis
of delirium as a symptom is usually easy, but it is a task of no small
difficulty to determine its pathological associations in a given case,
and to draw from this study correct therapeutic indications. {26} A
careful review of the antecedent circumstances, of the patient's
actual somatic condition, more especially as regards hæmic states and
vaso-motor action, is indispensable.

LOSS OF CONSCIOUSNESS, COMA.—Suspension of all sensibility, general
and special, with loss of all strictly cerebral (cortical) reflexes,
is met with in many pathological states. Its physiology or mode of
production is unknown, but there are good reasons for believing that
the lesion, vascular or organic, affects chiefly the cortical
substance of the hemispheres. Its clearest manifestation, clinically,
is after depressed fracture of the skull or after concussion of the
brain, without or with abundant meningeal hemorrhage. In the last case
unconsciousness or coma appears as an exaggeration of drowsiness or
stupor; after a fall the patient may be able to walk into the
hospital, but soon becomes drowsy, then stupid, and lastly completely
insensible. In the first case, that of depressed fracture of the
skull, the raising of the depressed bone is often followed immediately
by return of consciousness; the patient seems to wake as from a deep
sleep. In medical practice there are many analogous conditions of
abnormal pressure causing coma, as in meningitis, cerebral abscess,
hemorrhage, embolism of cerebral vessels, etc. Long-continued or fatal
coma may be caused by general morbid states, as uræmia, acetonæmia,
surgical hemorrhage, intoxication by narcotics, alcohol, ether, etc.,
and by asphyxia. Momentary loss of consciousness is induced in the
various forms of epilepsy, lasting from a fraction of a second (so
short as not to interrupt walking) to one or two minutes, followed by
the more prolonged coma of the asphyxial stage. Temporary
unconsciousness is also caused by physical or moral shock, but in many
such cases the heart is primarily at fault, and the condition is
termed syncope. Although in practice it is most important to
distinguish syncope from more strictly cerebral coma, yet it must be
admitted (and such admission is important for therapeutics) that in
both categories of cases anæmia of the brain (cerebral cortex) is the
essential factor or immediate cause of suspension of consciousness.
This view of the pathology of coma is borne out by the fact that the
condition may be produced at will, experimentally or therapeutically,
by compression of both carotid arteries. It may be well to mention
here the pseudo-coma of hysteria. In these cases consciousness is
really present, as shown by responses to violent cutaneous irritations
(faradic brush), by quivering of the closed eyelids and resistance to
attempts to open them, by vascular or muscular movements evoked by
remarks of a flattering or abusive nature made in the patient's
hearing, and by cessation of the condition after complete closure of
the nose and mouth for forty-five seconds or one minute (asphyxia). In
the typically unconscious state, as in cases of fracture of the skull
or of intracranial pressure by exudations, clots, tumors, etc., there
are several objective symptoms to be noted. The pupils are usually
dilated and immovable (exceptions chiefly in narcotic poisoning); the
pulse is reduced in frequency and retarded; it is sometimes full and
bounding, or in other cases feeble and irregular. The breathing is
often slow and irregular; the patient fills out his cheeks and puffs
(smokes the pipe); sometimes the Cheyne-Stokes type of respiration is
observed. In hysterical or hypnotic impairment of consciousness these
important symptoms are absent: the patient seems simply asleep.
Although coma is, strictly speaking, a {27} symptom, it so often
appears as the leading one of a group that it deserves study almost as
a disease. Indeed, there are few more difficult problems for the
physician than the case of a comatose subject without a good history
of the preceding condition, causes, etc. It is impossible here to
consider all the possibilities of this problem in diagnosis;[1] we can
only state the chief and most probable pathological conditions which
may cause coma.

[Footnote 1: An able attempt at the differential diagnosis of comatose
cases, by J. Hughlings-Jackson, will be found in _Reynolds's System of
Medicine_, Am. ed., 1879, vol. i. p. 920.]

(1) The patient may be epileptic. The following signs of a past
convulsive attack should be sought for: a bitten tongue, fleabite-like
ecchymoses on the face, neck, and chest, saliva about the face and
neck, evidences of micturition or of seminal emission in the clothing,
etc. There is usually a small rise of temperature after a single fit,
and consciousness soon returns without assistance, or a second seizure
appears.

(2) The patient may be suffering from surgical cerebral compression or
concussion. Signs of injury about the head or other parts of the body,
oozing of blood or sero-sanguinolent fluid from the ears and nose,
will sometimes clear up the diagnosis. Especially suggestive of
meningeal hemorrhage is a gradually increasing stupor without distinct
hemiplegia.

(3) The coma may be uræmic. In some cases anasarca and slow pulse
point at once to this pathological condition. In all comatose cases
without history the urine should be drawn with a catheter for testing,
and signs of various forms of Bright's disease may be detected. The
ophthalmoscope (easily used in comatose subjects) may yield most
valuable indications by revealing retinitis albuminurica or
neuro-retinitis.

(4) The patient may be under the effects of a clot in the brain or of
acute softening of a considerable part of the organ. Hemiplegia with
conjugate deviation of the eyes and head is usually present, the head
and eyes turning away from the paralyzed side, the patient looking, as
it were, toward the lesion. A latent hemiplegic state may sometimes be
determined by one-sided redness of the buttock, and by a slight
difference of temperature between the two hands (paralyzed side
warmer). The general temperature of the body (measured preferably in
the vagina or rectum) exhibits a marked rise. After cerebral
hemorrhage there is, according to Charcot and Bourneville, a fall
below the normal during the first hour, followed by a steady rise to
106° or 108° F. at death in severe cases. After embolism or
thrombosis, causing softening, the rise of temperature is less in
extent and not as regularly progressive.

(5) The subject may be simply drunk or poisoned by alcohol. In such a
case the patient may usually be roused momentarily by loud speaking,
shaking, or by painful impression; the breath is alcoholic; the
cerebral temperature subnormal or normal. The urine must be tested for
alcohol.[2] It must not be forgotten that on the one hand intoxicated
persons are most prone to falls causing fracture of the skull or
concussion, and on the other hand that the early stage of coma from
meningeal hemorrhage resembles narcosis.

[Footnote 2: Anstie's Test.—A test solution is made by dissolving one
part of bichromate of potassium in three hundred parts by weight of
strong sulphuric acid. The urine is to be added drop by drop to the
solution. If a bright emerald-green color suddenly results from this
manipulation, it signifies that there is a toxic amount of alcohol in
the urine.]

(6) The coma of congestive or malignant malarial fever is to be {28}
distinguished mainly by the absence of physical or paralytic symptoms,
coinciding with a high rectal temperature. The spleen is often
enlarged. Some would add that Bacillus malariæ and pigment might be
found in the splenic blood, withdrawn by a long, fine needle.

(7) Toxic narcosis, from opiates, morphia, chloral, etc., are often
difficult of diagnosis, except that from opiates and morphia, in which
extremely slow respiration and contracted pupils, with lowered
temperature, point at once to the cause.

In studying cases of coma all the above-enumerated symptoms should be
considered as of great negative or positive value: often the diagnosis
is only made by exclusion. The Cheyne-Stokes respiration, pupillary
variations, differences in pulse-rate and volume, are present in such
varied conditions, irrespective of the nature of the lesion, as to
render them of minor value in differential diagnosis.

DOUBLE CONSIOUSNESS is a rare condition, in which the subject appears
to have separate forms or phases of consciousness, one normal, the
other morbid. This occurs in hypnotic and somnambulic states, probably
also in certain cases of insanity and epilepsy. The current of normal
consciousness is suddenly broken; the patient enters into the second
or abnormal state, in which he acts, writes, speaks, moves about with
seeming consciousness; but after a variable time a return to normal
consciousness reveals a break in the continuity of the memory: the
patient has no recollection whatever of what he did or said in the
morbid period. In the hypnotic state subjects may show increased power
of perception, and are strangely susceptible to suggestions or
guidance by the experimenter. In a second attack the patient often
refers back to the first, and does things in continuation or
repetition of what he previously did, apparently taking up the same
line of thought and action. The morbid states, long or short, are
joined together by memory, but are wholly unknown in the normally
conscious states. In other words, the patient leads two (or three,
according to a few observations) separate lives, each one forming a
chain of interrupted conscious states. In epilepsy we observe
remarkable breaks in normal consciousness: the patient goes through
certain acts or walks a distance or commits a crime in a dream-like
state, and suddenly, after the lapse of a few minutes, hours, or days,
becomes normally conscious and has no recollection of what he did with
such apparent system and purpose during the seizure. It might,
perhaps, be as well to classify these phenomena under the head of
amnesia. A case is on record where a man travelled, seeming normal to
fellow-travellers, from Paris to India, and who was immensely
astonished on coming to himself (return to common consciousness) in
Calcutta. Many murders have been committed with apparent design and
with skill by epileptics, who upon awaking from their dream-like state
were inexpressibly horrified to hear of their misdeeds.

AMNESIA, or loss of memory, may vary in degree from the occasional
failure to remember which is allowed as normal, to the absolute
extinction of all mental impressions or pictures. This word and the
expression memory are here used in a restricted sense, reference being
had only to purely intellectual and sensorial acts related to
intellection. If we take the general or biological sense of the term
memory as meaning the retention of all kinds of residua from
centripetal impressions and of motor {29} centrifugal impulses,
including common sensory and visual impressions, special sense
impressions, all unconsciously received impressions, emotional,
intellectual, and motor residua, we should consider amnesia in a
correspondingly general way. This, however proper for a physiological
study, would be far too complex and premature for an introduction to
practical medicine. Recognizing memory, therefore, as a universal
organic attribute—a capacity to retain impressions—we will treat of it
only in the commonly-accepted sense referred to supra.

Failure of memory may be real or apparent. In the latter sense amnesia
is induced by diversion of the attention into a channel different from
that in which the line of inquiry is conducted. A normal example of
this is seen in the state known as preoccupation, where a person
intent upon a certain thought or action forgets who is about him,
where he is, and if asked questions fails to answer or answers
incorrectly. In pathological states, as in acute curable insanity,
apparent loss of memory is often caused by the domination of an
emotion or of delusions. In both cases, if the subject can be roused
or brought to himself, he remembers all that we inquire about and is
amused at his previous false answers or silence. Real amnesia consists
in the actual blotting out of recollections or residua in a partial or
general manner, for a time or permanently. These differences serve as
the basis of a complicated subdivision of amnesia which it is not
necessary to fully reproduce here.

Temporary partial amnesia is a variety which is frequently observed in
normal persons, even the most gifted. A word or fact escapes us, seems
wholly lost for a few minutes, hours, or days; the more we strive to
recall it, the less we succeed; yet later, when not sought for, the
fact or word appears in our consciousness as if spontaneously, but
more probably by some effect of the law of association. Such partial
and momentary forgetfulness may assume proportions which render it
pathological. What is known as transitory aphasia may be classed in
this group. In a few minutes or hours a person without apoplectic,
epileptic, or paralytic phenomena loses all power to express his
thoughts by speaking or writing; there is verbal amnesia and agraphia.
The subject is conscious of his condition and of the wholly futile or
incorrect attempts he makes to communicate with others.

Temporary complete amnesia is almost equivalent to loss of
consciousness, yet not strictly so. For example, after a sharp blow
upon the head a person may perform complicated acts, reply to
questions, and apparently act normally, yet after a variable time he
will declare that he remembers absolutely nothing of the injury and
what he did or said for hours or days afterward. The same phenomenon
is observed in the course of psychoses, neuroses (epilepsy), in some
acute diseases, and in certain states of intoxication.

Permanent partial amnesia occurs in states of dementia, such as senile
dementia, paralytic dementia, and in certain cases of aphasia. Great
gaps exist in the patient's memory; some things are well recalled,
others wholly and for ever effaced. The psychological law governing
the failure of memory in these cases is that the earliest and
strongest impressions survive, while recent and less forcible (_i.e._
less interesting) ones are lost. Substantives or names are especially
liable to obliteration, as are also many of the delicate residua which
lie at the basis of the subject's ethical conceptions and acts.

{30} Permanent complete amnesia is observed at the end of degenerative
cerebral diseases, as organic dementia, whether of the form termed
secondary or that designated as paralytic. Sometimes after acute
general diseases the memory may be a perfect blank for a considerable
length of time, and education has to be repeated. Memory may be so
completely absent that cases are known in which the patient gave a
fresh greeting to the asylum physician every two or three minutes
indefinitely, as if each were a first meeting. Momentary perception
and automatic (reflex) response are there, but no impression is made;
there is no residuum left in the cortical centres. In these cases
amnesia is accompanied by degeneration of the visual, auditory, etc.
cortical areas or centres.

An interesting form of amnesia, not generally recognized as such, is
the loss of acquired skill in muscular movements, such as are
necessary for writing, for using tools, and for doing various delicate
professional movements. Here the motor residua acquired by laborious
education or training are gradually lost without actual paralysis or
ataxia. This variety is exquisitely illustrated by certain cases of
dementia paralytica where long before marked intellectual symptoms
occur there is loss of skill in mechanical arts and in handwriting.

In testing a subject's memory due attention should be paid to the law
of the survival of older and more interesting residua, as well as to
the power of the law of association. Such questions should be asked as
pertain to recent events in the patient's experience, and about
matters which are not closely related logically. A patient who might
tell us nearly all about his early personal experiences, his business
and family relations, incidents of his childhood, etc., would fail to
remember what he had for breakfast, what he did the day before, etc.

The physiological cause of real amnesia is impairment in the vitality
(nutrition) of ganglion-cells in the various cerebral sensory areas or
centres, and of the motor area as well (motor residua). In cases of
transitory amnesia we suppose this to be due to the action of toxic
agents, to anæmia, and impaired molecular or chemical nutrition, as
after acute diseases, in extreme debility, in psychoses, etc. In cases
of terminal permanent dementia, autopsies afford us evidence of
degeneration and disappearance of ganglion-cells: we find granular and
fatty pigmentation, atrophy, calcarous degeneration of these bodies,
thickening and shrinkage of the neuroglia, and degenerative changes in
blood-vessels. Doubtless degeneration or destruction of association
fasciculi of nerve-fibres in the cortex cerebri or in the white
substance plays a considerable part in the production of permanent
amnesia, but we are as yet unable to give a clear demonstration of
this. Theoretically, we may admit an organic loss of memory with the
following conditions of the brain: (1) diseased perceptive (sensory)
centres or motor area with normal association fasciculi; (2) normal
perceptive centres and motor area with degenerate or broken
association fasciculi, connecting these parts with one another and
with the more strictly ideational or expressive (centrifugal) areas
and parts of the brain and spinal cord.

Amnesia—or, more properly speaking, dulness of perception and
feebleness of retention of residua—occurs as a strictly congenital
condition from imperfect cerebral development, or a little later in
life from infantile diseases, constituting one of the aspects of
idiocy.

{31} WORD-DEAFNESS is a special morbid psycho-sensory state in which
the sounds of language lose their significance for the patient. The
sense of hearing is preserved for common sounds, and even music in
certain cases; words are heard, but not understood. A patient of mine
having this symptom used to say, “If I go to a lecture or hear a
sermon, I hear the speaker, but what he says is all Greek to me.” On
the other hand, this gentleman could go to a concert and understand
the musical notes. This condition occurs as a part of the
symptom-group aphasia, or it may show itself independently in the
course of limited cerebral cortical degenerations. The lesion causing
word-deafness is usually found in the left hemisphere, in the first
and second temporal gyri, or it may be in the inferior parietal lobule
and gyrus supra-marginalis, penetrating deeply enough to injure
fasciculi going into the temporal lobe. It would appear, from the
evidence now before us, that the centre for psychic hearing is in the
caudo-dorsal part of the temporal lobe.

WORD-BLINDNESS, or alexia, is another special morbid psycho-sensory
state, in which the visible signs of language lose their significance
for the patient. Usually there is no impairment of sight; the patient
can see the letters and words as objects, but he cannot read them at
all, or must do so letter by letter. Even numerals and pictures of
objects in some cases become unintelligible. In testing for this
condition a possible confusion with verbal amnesia must not be
forgotten. In such a case the patient knows the word or object, but
cannot name it; usually he can, however, inform us by signs or
indirect expressions that he takes proper cognizance of the object.
Alexia is present in a certain proportion of cases of aphasia, and it
may be complicated with lateral hemianopia. The exact seat of the
lesion producing alexia is at present unknown. Theoretically, however,
we must place it in the course of paths from the cortical visual area
(cuneus and adjacent gyri) to the general speech-centre. Psychic
blindness for objects in general (soul-blindness of the Germans) is
now quite conclusively proved to be due to degeneration of both
occipital lobes, more especially their mesal gyri, where the visual
centres are. This psycho-sensory state, with the accompanying cortical
changes, has been demonstrated in cases of dementia paralytica.

APHASIA, or loss of the faculty of language, is so important a symptom
as to deserve elaborate consideration in a separate article of this
volume; and to it the reader is referred. Suffice it here to state
that aphasia may be classified into three forms: (1) Sensory aphasia,
in which there is primary disorder of the psycho-sensory (perceptive
or centripetal) part of the complex central mechanism for speech; (2)
Motor aphasia (including ataxic aphasia), in which the primary lesion
affects the motor (expressive or centrifugal) parts of the mechanism;
(3) Amnesic aphasia, in which loss of memory (effacement of residua)
of words and signs is the prime condition.


II. Sensory Symptoms.

HYPERÆSTHESIA is a condition of exalted excitability in the various
parts of the sensory apparatus: terminal nervous organs, nerve-trunks,
central gray matter. We may admit such a state as existing {32}
independently of consciousness, as where a lesion cuts off
communication between the perceptive cerebral centres and the
periphery, but in practice we consider only conscious hyperæsthesia.
In this state the subject may be able to perceive (feel) slighter
impacts than would affect a normal individual, or he receives an
exaggerated, usually unpleasant, impression from ordinary excitations.
It may also be said that hyperæsthesia exists as a purely subjective
state, psycho-sensory hyperæsthesia, without external mechanical
excitations.

(_a_) Hyperæsthesia of common tactile sensibility in the skin and
mucous membranes is frequent. The least touch is felt with unpleasant
acuteness and causes unusual reactions of a reflex order; frequently,
but not necessarily always, a sensation of pain is produced at the
same time. It has been claimed that in certain cases the points of the
æsthesiometer could be perceived (distinguished as two points) at
smaller distances than the average normal, but I have never been able
to demonstrate this to my satisfaction. The simplest form of tactile
hyperæsthesia is met with in persons of a highly nervous organization,
in those under the influence of strong emotions, in the hypnotic
state, and while intoxicated. The common pathological conditions in
which increased sensibility is found are meningitis (cerebral and
spinal), hydrophobia, tetanus, neuritis, dermatitis, hysteria, and
spinal irritation; also in connection with inflammations and
traumatisms.

(_b_) Hyperalgesia, often coinciding with (_a_), is that condition in
which pain is produced by excitations so slight that they would not
affect a healthy nervous apparatus: it is commonly designated as
tenderness. Acute and dull, superficial and deep tenderness should be
sought for and distinguished, as having different values in diagnosis.
A type of deep tenderness is that found upon pressing steadily upon a
diseased nerve-trunk. Acute superficial hyperalgesia is best studied
in cases of trigeminal neuralgia and spinal irritation. Occasionally,
universal hyperalgesia is met with, usually in hysterical women.

(_c_) Hyperæsthesia to thermal impressions is ordinarily shown with
reference to cold. In cases of neuralgia or neuritis cold is felt
excessively and painfully; in some cases of posterior spinal sclerosis
there is the greatest dread of draughts of cold air, and patients
protect their legs in an extraordinary manner.

(_d_) Hyperæsthesia of the muscular sense.[3] The special sensations
or notions of muscular states and activities which we possess may be
considerably exalted, as shown by greater delicacy and rapidity of
movements, and by the abnormally acute way in which perceptions of
form and dimensions are obtained by the subject without assistance
from other senses. Examples of this condition are met with in hysteria
and hypnotism.

[Footnote 3: This term is employed as clinically sufficient. It is
impossible in this article to enter into a consideration of the
various theories held with reference to the function in question,
whether it be psycho-motor, psycho-sensory, or a true muscular
sensibility. It certainly differs much from the various forms of
common sensibility, and has special paths.]

(_e_) Visceral hyperæsthesia is chiefly shown by abnormal
consciousness of the presence and action of an organ. Visceral pain
usually accompanies this, and is the more prominent symptom.

(_f_) Increased reflex actions (emotional, motor, vaso-motor, and {33}
secretory) rarely fail to accompany hyperæsthesia in its various
forms. In the hypnotic exaltation of muscular sense remarkable psychic
effects may be induced, partly in a reflex way, but perhaps chiefly
through the law of association.

PARÆSTHESIÆ are sensations which arise centrally in nerve-fibres or
nervous centres, and are projected outward and referred to the
periphery or surface by consciousness, in obedience to the general law
of outward projection of sensations in the Ego. They may be produced
by external agencies or arise centrally without demonstrable cause.
Their number and variety are very great, varying somewhat with the
descriptive powers and self-consciousness of the patient, the chief
being pain, formication, numbness, coldness and heat, constriction and
distension, malposition, imaginary movements, etc. etc.

(_a_) Pain, the most distinct and frequent of paræsthesiæ, is by most
authors classed as a hyperæsthesia, yet a careful analysis will show
the difference. Pain and hyperæsthesia often coexist and are
inseparable, yet in a large proportion of cases of nervous diseases
the former sensation occurs independently, sometimes in regions where
absolute anæsthesia exists (anæsthesia dolorosa), and even apparently
in lost parts (neuralgia after amputations). We are consequently
justified in considering most pains as paræsthesiæ. Pain assumes many
forms, some real and typical, others as various as the lively
imagination of nervous patients can make them. Thus we have sharp,
cutting, darting pains in neuralgia, posterior spinal sclerosis, etc.;
aching, throbbing, pounding pains in cephalalgia, inflammatory and
traumatic conditions; boring, crushing, distending, constricting,
burning pains, etc. etc. In some cases the sensation is only
semi-painful, and more akin to paræsthesia (neuritis, parenchymatous
lesions).

(_b_) Numbness, prickling, and formication usually coincide. They may
easily be produced experimentally by pressure upon a nerve-trunk or by
the exhibition of aconitia, so that any one may study these sensations
for himself. By taking one-fiftieth of a grain of Duquesnel's
crystallized aconitia the experimenter will soon find himself the
possessor of intense subjective sensations of prickling, numbness,
vibrations, and cold, lasting several hours. He will be able to
satisfy himself that though the finger-tips feel numb, as if there was
a coating or layer of something interposed between the skin and
objects, he can distinguish tactile perceptions very well. In the more
serious experiment of compression of a nerve-trunk a most interesting
succession of phenomena will be observed: the first effects of
pressure are various paræsthesiæ in the parts supplied by the nerve;
then these sensations (prickling, numbness, swelling, vibration, heat,
and cold) cease; paralysis and anæsthesia occur. If the compression be
now interrupted, after a few moments the paræsthesiæ reappear, more
intensely, as a rule, and as they gradually fade a normal state of
sensibility is re-established. By making such experiments it is easy
to convince one's self that anæsthesia and numbness are different
conditions: indeed, during the stage of recovery from nerve-pressure
distinct hyperæsthesia may be demonstrated. These results throw much
light on the origin and diagnostic value of paræsthesiæ as expressions
of irritation, central or neural, of nervous elements. At the same
time, in practice, we occasionally meet with slight dulness of tactile
sensibility in numb {34} parts. Another point to be remembered is that
while patients usually complain loudly of paræsthesiæ, they are
sometimes wholly unaware of anæsthesia (hysterical analgesia, for
example); therefore sensibility should be tested even if the patient
does not mention sensory disturbances.

Numbness, formication, etc. occur in a vast number of nervous
affections—in cerebral and spinal organic lesions, in neuritis, in
toxic conditions, and in neuroses. The distribution of paræsthesiæ is
a valuable index to the seat of the lesion.

(_c_) Cutaneous itching and prickling may occur independently of any
other skin lesion, constituting true or nervous prurigo. This may be
universal and last for years.

(_d_) Paræsthesiæ of pressure are felt either as expansive or
constrictive. The part appears swollen to consciousness, or it seems
to be tightly compressed. Both these sensations are often felt about
the head in a variety of pathological states, and an absurd and
dangerous fashion has arisen of looking upon a sense of fulness in the
head as indicative of hyperæmia. The sense of constriction may show
itself around one toe, a leg, the trunk, around the neck, etc.; it may
be narrow, like a cord, or broad and extensive, like a stocking or
corset. Sometimes it is localized, and likened to the grasp of a hand
or a spot-pressure. Not infrequently, especially in cases of
paraplegia, the sensation of pressure is combined with subjective
cold, the legs feeling as if tightly encased in ice.

(_e_) Subjective sensations of heat and cold are often of the
strongest kind, and are very distressing. A part whose real objective
temperature is normal may appear to the patient's consciousness as icy
cold or burning hot, even to the degree of apparent contact of fire
(causalgia of Mitchell). We observe such sensations in posterior
spinal sclerosis, myelitis, neuritis, injuries to nerves. In some
functional cases complaint is made of patches of hot or cold skin, not
relieved by cold or heat.

(_f_) Odd sensations, such as rolling or longitudinal motion of
something under the skin, general or local throbbing, coition
movements, are described, especially in functional or hysteroid cases.

(_g_) Sensations of hunger, thirst, dyspnœa, defecation, micturition,
the sexual feeling, may all appear in an abnormal or unprovoked
manner, and are to be classed as visceral paræsthesiæ. An important
paræsthesia of this variety is met with in cases of hypochondriasis
and melancholia; it is a sense of indescribable distress, with
constriction, usually at the epigastrium and about the heart—the
precordialangst of the Germans, or, as we would term it, præcordial
anguish.

(_h_) Paræsthesiæ of the muscular sense occur. The subject has a
feeling as if a part were lying in an unnatural position, or as if it
were being pulled or twisted in various ways, and he is sometimes
obliged to assure himself by the use of sight and by tactile
examination that the sensation is illusory.

(_i_) Hallucinatory paræsthesiæ are those which are so well defined
and strong as to need the aid of other senses and reasoning to
convince the patient of their unreality. A peculiar example of this is
what occurs after amputation of a limb: for days or weeks the lost
member is felt with the utmost distinctness; the absent fingers or
toes may be moved in imagination and their position described.

(_j_) Delusional paræsthesiæ are such in which the patient (usually
{35} insane), no longer correcting his sensations by the use of other
senses and by reasoning, firmly believes in their reality—_i.e._
externality. For example: in such patients visceral sensations give
rise to the belief that there is a foreign body or an animal inside
the patient, or that parts are misplaced or wrenched and beaten. Pains
are thought to be due to blows received or to the bites of animals or
projectiles thrown upon the patient. With perversions of muscular
sense an insane patient may believe that he is flying or floating in
the air.

In hypochondriasis many of the symptoms complained of are nothing but
paræsthesiæ exaggerated by a morbid state of the mind, and sometimes
created (projected) by expectant attention. The hallucinations of the
insane are in great measure phenomena of this group, the projections,
though special and common, never being so strong and definite as to
acquire apparent objectivity.

The auræ of epilepsy are paræsthesiæ. For example: a sensation in the
epigastrium preceding a fit indicates an irritation at the origin of
the vagus nerve and its projection as a subjective sensation at the
distribution of the nerve. An auditory or visual aura similarly
represents a discharge or projection from the acoustic and visual
cortical areas respectively.

In most cases of malingering, and in some cases of so-called railway
spine, the symptoms so loudly complained of belong to the two classes
of hyperæsthesiæ and paræsthesiæ; they are undemonstrable and
non-measurable; only the patient himself can vouch for their reality.
A diagnosis in such cases, without objective symptoms indicating
well-known lesions, should be very reserved.

ANÆSTHESIA, or loss of sensibility, may exist in every degree, from
one so slight as to be hardly demonstrable by delicate tests to the
most absolute loss of all feeling. It manifests itself in various
modes corresponding to the normal physiological varieties of
sensibility; in most cases the loss of feeling involves all of these,
but in others they are separately affected, and we observe the
following types, pure or combined:

(_a_) Tactile Anæsthesia. The capacity to perceive superficial and
gentle impressions upon the skin and mucous membrane, and the ability
to locate and separate such impressions, may be lost, while other
modes of sensibility remain normal.

(_b_) Analgesia is that condition in which painful impressions are not
perceived, though common, caloric, or muscular sensibility may be
normal or nearly so. Pricking, cutting, and bruising are unperceived.
This, the most common variety, is usually met with in hysterical
cases; it occurs at a certain stage of general artificial anæsthesia,
in chronic alcoholism, extreme emotional states, and in hypnotism.
Though a very striking symptom, it is not one of as serious meaning as
loss of tactile or thermic sensibility. Often the patient is unaware
of analgesia until tests reveal its existence.

(_c_) The sensibility of the skin to caloric is usually the last to
disappear in the progress of an organic lesion, so that in certain
cases (injury to nerves or spinal cord, myelitis, etc.) testing by ice
or by a burning object is a sort of last resort. Before deciding in a
given case that there is a complete break in the sensory tract, this
test should be used as well as the application of the most intense
induced electric current delivered upon the dry skin by a wire end.

{36} In some cases of partial anæsthesia (_e.g._ in posterior spinal
sclerosis) cold may be felt as heat and vice versâ, or pinching may be
felt as burning, and be quite persistent.

(_d_) The so-called muscular sense may be greatly impaired or lost
without ordinary anæsthesia. In such a case the subject is no longer
directly and spontaneously aware of the exact position of his limbs,
of passive motions done to them, and he executes voluntary movements
with uncertainty. He is also unable to judge correctly of differences
of weight in objects successively placed in his hand or hung from his
foot. He needs the aid of sight to guide the affected limb and to
judge of its position, etc. The awkwardness and uncertainty in
voluntary movements by impairment of muscular sense must not be
confounded, as is sometimes done, with ataxia, in which the attempted
volitional movement is jerky and oscillatory, owing to the
inharmonious action of antagonistic muscular groups.

(_e_) When a strong induced electrical current is passed through a
muscle by means of wet electrodes applied to the skin, so as to cause
a strong contraction, a special quasi-painful feeling, akin to that of
cramp, is experienced in the contracting muscle, and is clearly
distinguishable from the cutaneous sensation. This, the
electro-muscular sensibility, may be lost independently of other modes
of feeling and without loss of contractile power.

(_f_) Some observers claim that a special mode of sensibility exists
in the skin by which varying degrees of pressure are estimated,
independently of traction upon tendons and muscles (muscular sense),
and that this may be separately impaired or lost.

(_g_) Visceral anæsthesia shows itself in the ordinary way by loss of
that feeble degree of common sensibility which the internal organs
possess, and also by impairment of their special functions, giving
rise to anorexia, hydroadipsia, retention of feces and urine, loss of
sexual feeling (without progenital anæsthesia). Of course, these
symptoms may be due to other conditions, and each case must be
carefully studied. In the insane, visceral anæsthesia gives rise to
delusions of emptiness, destruction of organs, and even, if coinciding
with general cutaneous anæsthesia, to the notion that the body is dead
or absent.

A singular phenomenon often witnessed is retardation in the
transmission of an impression (usually a painful one). Thus, in
testing the sensibility of the skin of the legs in tabetic patients,
it is observed that instead of the normal, almost instantaneous,
appreciation of the impression made by a needle-point, there is a
lapse of two, five, ten, or even sixty seconds between the pricking
and the signal of sensation by the patient. It should always be
determined in such cases whether the retardation is peripheral and
actual, or central and due to psychic conditions (dementia, absorption
in a delusional state). Thus, in a case of profound melancholia we may
observe extreme slowness and dulness of sensory impressions or
complete anæsthesia; but the symptoms would have a very different
significance, diagnostic and prognostic, from the same noted in a
mentally clear patient.

An important result of impairment of sensibility is a reduction or
loss of reflex movements originating from the area or organ which is
anæsthetic. This is shown in anæsthesia of the distribution of the
trigeminus {37} when the reflex protecting movements of the eyelids no
longer take place, in atrophy of the optic nerve when the pupillary
reflex actions are lost. In posterior spinal sclerosis we see several
illustrations of this law: progressive degeneration of nerve-fibres in
the posterior root-zones of the spinal cord, causing loss of patellar
reflex, of vesical, rectal, and sexual reflexes, and in most cases of
cilio-spinal reflexes and of muscular tonus. In these and analogous
conditions one arc of the reflex mechanism is deranged, centripetal
conduction is interfered with, and the reflex motor discharge can no
longer be evoked.

That a similar pathological condition occurs in the cerebral
mechanism, and may serve to explain many psychic symptoms, is very
probable.

On the other hand, a destructive lesion may be so placed in the spinal
cord or brain as to allow centripetal impressions to reach healthy
spinal gray matter in the normal way, but preventing their passage
frontad (upward) to be recognized by consciousness. In such a case we
observe normal, or more commonly exaggerated, reflex action in parts
which are insensible in the ordinary sense of the term. Indeed, in
many cases the disconnected caudal portion of the spinal cord is in a
state of vastly exaggerated reflex activity, as shown by the tetanoid
and convulsive involuntary and reflex movements which take place in
completely paralyzed and anæsthetic limbs (paraplegia from transverse
myelitis). In general terms, it may be stated that when anæsthesia is
due to lesions of peripheral nervous endings, of nerve-trunks, and of
the posterior root system of the spinal cord, reflexes are diminished
or lost.

It is often stated that anæsthesia causes ataxia of movement. This,
from the results of experiments on animals and from clinical study, we
believe to be a gross error. In animals and in man loss of sensibility
gives rise to awkwardness or uncertainty in movement (increased if the
eyes be closed) which is properly to be classed as a special variety
of inco-ordination; but it is not from ataxia, in which irregular,
jerky, oscillating motions occur when a volitional act is attempted,
these movements resulting from want of harmony in the action of
antagonistic muscles which in the normal educated state automatically
act together to produce the desired result. Besides, we occasionally
observe cases of typical spinal ataxia in which no impairment of
sensibility can be observed.

THE TOPOGRAPHICAL DISTRIBUTION of alterations of sensibility requires
careful determination in practice, as from it we obtain most valuable
aid in diagnosis. The following are the principal types observed:

(_a_) Alterations of sensibility in one lateral (vertical) half of the
body and head. We thus have hemihyperæsthesia, hemiparæsthesia, or
hemianæsthesia, and the special senses on one side are frequently
involved. This clearly hemi-distribution indicates that the lesion or
functional disorder is in the cerebral hemisphere of the opposite
side, more especially in the caudal segment of the internal capsule or
in its areas of cortical distribution (occipital, temporal, and
parietal lobes). The distribution of hemianæsthesia, etc. from organic
disease in these parts is identical with that observed in some
functional (hysterical) cases; we can make the diagnosis only by the
help of other data.

If the sensory disorder does not affect the head, but is limited to
one {38} lateral half of the body, it is, if due to organic disease,
quite certainly of spinal origin.

(_b_) Two homonymous extremities or the two lateral halves of the body
may exhibit opposite states of sensibility—anæsthesia on one side and
hyperæsthesia on the other. This rare condition is witnessed in
hysteria and in some forms of injury to the spine (lesion of one
lateral half of the cord at a certain level). In the latter case
paralysis is usually present on the hyperæsthetic side: the symptoms
constituting, with some others, Brown-Séquard's spinal hemiplegia or
hemiparaplegia.

(_c_) Alterations of sensibility in one caudal (horizontal) half of
the body are said to have a paraplegic distribution, and are usually
due to lesions of the spinal cord. The upper level of the symptom may
be at any point between the neck and the toes; and the frontal (upper)
level indicates, due regard being had to the origin and oblique
distribution of the spinal nerves, the highest limit of disease in the
nervous centres. Very often, in organic disease especially, this is
also indicated by the presence of a cincture feeling (paræsthesia) at
the frontal (upper) limit of the anæsthesia, etc.

(_d_) Disorders of sensibility may be limited to one extremity. This
very rarely depends upon cerebral disease, and in such a case the
anæsthesia, etc. is evenly distributed throughout the member, being
most intense at its extremity, and being without sharp, distinct
limits near the trunk. When due to diseases of the spinal cord, the
cerebral (upper) limit of the symptom is usually clearly defined in
accordance with the distribution of sensory nerves from the other
(healthy) parts of the cord: a constriction band often marks the
limit. Sometimes the peripheral anæsthesia, etc. is more or less in
the territory of certain nerve-trunks. When we find the distribution
of the sensory symptoms to coincide exactly in the areas supplied by
the large nerves of the limb, without cincture feeling, it is certain
that the lesions affect one or more of these nerve-trunks or the
plexus above. In not a few cases the symptoms are due to hysterical or
dyscrasic conditions, and the seat of the lesions (dynamic or
molecular lesion) is uncertain. In judging of the distribution of
anæsthesia, etc. in a limb due regard must be paid to variations in
nerve-branching and to collateral nerve-supply.

(_e_) Alterations of sensibility occurring in well-defined areas of
the hand, trunk, or extremities, corresponding to the known
distribution of nerves, almost always indicates disease of the nerve
itself, much more rarely disease in the spinal cord at the origin of
the nerve. The reflexes are then diminished or lost. In judging such
cases Van der Kolk's law of the distribution of the motor and sensory
filaments of nerve-trunks should be remembered: it is, that of the two
sets of fibres in a mixed nerve, the sensory fibres are distributed to
parts which are moved by muscles which receive the motor fibres of the
same nerve. Thus, in nerve lesions the chief sensory symptoms are
always peripheral or distal from the chief motor symptoms.

(_f_) Disorders of sensibility sometimes appear in patches or
irregular areas whose nervous connections are indefinite. Such patches
of anæsthesia, hyperæsthesia, or paræsthesia sometimes indicate foci
of disease in the spinal cord (and brain?); as, for example, the
pains, etc. of posterior spinal sclerosis. These patches may also
occur in consequence of {39} interference with local circulation of
peripheral parts; and we meet with them in such conditions as
hysteria, neurasthenia, alcoholism, etc.

(_g_) Universal hyperæsthesia, paræsthesia, and anæsthesia may be
observed. The last condition, in the insane, is very apt to give rise
to delusions of non-identity and death of the body.

THE SENSORY DISTURBANCES OF THE SPECIAL SENSES are well worth separate
consideration.

(_a_) Optic Apparatus.—Hyperæsthesia of the retina shows itself
directly in photophobia, and indirectly (reflexly) by lachrymation and
involuntary closure of the eyelids. Paræsthesiæ of the optic nerve and
retina show themselves as flashes or projections of white or colored
light in the visual field. These may be irregularly or generally
distributed in the field, or appear as hemiopic (vide infra), or
sector-like forms. Phenomena of this order may be experimentally
produced by pressure on the eyeball or by the application of
electricity over or near the eye. Photopsiæ of most varied sorts, as
flashes, colored scotomata, or quasi forms may immediately precede
epileptic seizures or attacks of migraine, constituting an optic aura.
In some cases this assumes a definite picture form, when it partakes
of the character of an hallucination. Anæsthesia of the optic nerve
and retina varies infinitely in degree, from slight blurring or
veiling of vision (amblyopia) to complete blindness (amaurosis).
Another result is sluggishness or complete immobility of the iris
under the action of light. As regards distribution, optic anæsthesia
may affect the visual fields uniformly and generally, or it may assume
definite geometric forms, or may appear in irregular patches
(scotomata).

The definite geometric defects are classed under the general head of
hemianopsia, by which term is meant that one horizontal or vertical
half of the visual field is obscured. (1) Horizontal hemianopsia is
not bounded by a very sharp or straight boundary-line, and is almost
always due to intraocular disease (retinal lesions, embolism of one
large branch of the retinal artery, injuries, etc.). (2) Vertical
hemianopsia is usually marked by a sharply-defined vertical limit in
the visual field, passing through the point of fixation, or a little
to one side of it more usually, leaving central vision very acute.
(_α_) Temporal hemianopsia, in which the temporal halves of the visual
fields are dark, represents anæsthesia of the nasal halves of the
retinæ, and is usually caused by a lesion of the chiasm of the optic
nerve, so placed at its frontal or caudal edge as to injure the
fasciculi cruciati. This variety is usually bilateral, but a lesion
might be so situated as to affect only one fasciculus cruciatis.
(_β_) Nasal hemianopsia, in which the inner (nasal) halves of the
visual fields are dark, represents anæsthesia of the temporal halves
of the retinæ, and is caused by a lesion injuring one fasciculus
lateralis or both fasciculi. In the former case the nasal hemianopsia
would be unilateral; in the second case, bilateral or symmetrical,
(_γ_) Lateral or homonymous hemianopsia is that condition in which
physiologically similar halves of the visual field are darkened; for
example, the temporal half-field of the left eye and the nasal
half-field of the right. This represents anæsthesia of the nasal half
of the left retina and of the temporal half of the right. The patient
can only see, with one or both eyes, the right half of any object held
directly in front of him. In such cases the lesion is always caudad of
the chiasm, and may consist in interruption of the right optic tract,
{40} of disease of the primary optic centres (corpus geniculatum
laterale and lobus opticus) on the right side, of the caudo-lateral
part of the right thalamus, of the caudal extension of the internal
capsule or optic fasciculus within the right occipital lobe, of the
right superior parietal lobule or gyrus angularis penetrating deep
enough to interrupt the optic fasciculus; or, finally, the lesion may
injure the visual centre itself—viz. the cortex of the right cuneus
and fifth temporal gyrus (of Ecker). Hemianopsia of any type may be
incomplete or only sector-like—_i.e._ involving only a quadrant or
less of one visual field or of both fields. (Vide article on
Localization).

Perception of color may be reduced, confused, or abolished in the
retina, either a diffused general way, throughout the field of vision,
or following the laws of hemiopic distribution. In cases of hysteria,
achromatopsia is not rarely met with, affecting the eye corresponding
to the side on which the skin is analgesic or where paralysis exists.
Hysterical achromatopsia may be transferred from one eye to another by
the application of metals, by hypnotic manipulations, etc.

Hemianopsic phenomena may be functional and transient, as witnessed
just before attacks of migraine or sick headache.

Attempts recently made, from purely theoretical considerations, to
locate centres in the occipital cortex for perception of light, form,
and color separately, are wholly unjustified or at least premature.

Loss of reflex pupillary movements is a symptom of much importance. It
occurs chiefly under these conditions: (1) with paralysis of the iris
due to lesion of the third cerebral nerve; (2) with amaurosis or
anæsthesia of the retina; (3) with posterior spinal sclerosis. The
last condition is distinguished from the others by the fact that while
the reflex iritic movements are lost, the quasi-voluntary movement of
accommodation efforts is preserved. This condition is known as the
Argyll-Robertson pupil.

Diplopia, or double vision, is due to paresis or paralysis of one or
more of the ocular muscles, and as such is to be classed under motor
symptoms.

Megalopsia (apparent enlargement of objects) and micropsia (apparent
reduction in size of objects) are sometimes due to disorder of the
accommodation apparatus within the eye, and to local diseases causing
displacement of the rods and cones of the retina; but they are often,
no doubt, fanciful (in neurasthenia and hysteria). The same remarks
apply to monocular diplopia.

(_b_) Acoustic Apparatus.—We know less of the sensory disturbances in
the organs of hearing. Hyperæsia shows itself by undue (painful)
sensitiveness to sounds, and by the ability to perceive sounds which
are inaudible to normal persons. In meningitis, hydrophobia, the
hypnotic state, etc. this condition is observed. Paræsthesiæ are very
common, appearing as subjective noises or musical tones (tinnitus
aurium) of the most varied kinds (roaring, hissing, blowing, tinkling,
whistling, crashing, bell-sounds, etc.), which seem to the subject to
be in his ear or in his head. In the present state of our knowledge it
is impossible to positively distinguish tinnitus due to local
non-nervous ear disease from that which is strictly neural or cerebral
in origin. Certainly, intense tinnitus may coincide with complete
anæsthesia of the acoustic nerve and a {41} normal state of the middle
ear. Theoretically, we may admit tinnitus (corresponding to photopsia
in the optic apparatus) as due to an irritative lesion of various
parts of the acoustic terminal nervous organ, the acoustic nerve, or
the acoustic centre. An acoustic aura (subjective blowing, hissing,
etc.) may immediately precede an epileptic attack. Subjective noises
may be produced by excitation of the acoustic nerve and terminal
organs by the galvanic currents; these galvanic acoustic reactions are
regular in the normal condition, and are fully stated in works on
electro-therapeutics. Anæsthesia of the acoustic system by peripheral,
neural, or central (?) destructive lesions is frequent, and is
distinguished from other forms of deafness chiefly by the fact that a
sound transmitted through the bones of the cranium (as by a vibrating
tuning-fork held against the upper teeth or above the ear) is not
heard on one or both sides. Although in a few rare cases the attempt
has been made to define nervous deafness for certain sets of notes or
as limitations at either end of the musical scale, yet we are not
prepared to recognize in neurological practice a condition of partial
acoustic anæsthesia corresponding to hemianopsia or achromatopsia. We
believe that this progress will be made, however, thus enabling us to
locate disturbances in parts of the organ of Corti and in the cortical
centre for hearing.

(_c_) Olfactory Apparatus.—Hyperæsthesia of this sense is at present
considered more a personal peculiarity than as a symptom of disease.
Paræsthesiæ show themselves as subjective odors of various sorts, and
when transient may be an olfactory aura preceding epileptic attacks.
In conditions of organic disease subjective odors may coincide with
complete loss of smell. Anæsthesia of the olfactory nervous apparatus
may be due to (1) strictly local disease in the nose, catarrh, etc.;
(2) to anæsthesia of the trigeminus nerve and consequent local
lesions; (3) to a truly nervous lesion affecting the olfactory nerves,
the olfactory bulbs, the olfactory tracts, or, lastly, the cortical
centre for smell (at present unknown in man). The two last morbid
conditions are usually unilateral, and coexist with subjective odors.

(_d_) Gustatory Apparatus.—In this sense hyperæsthesia is clinically
unknown, though as a result of education extreme delicacy of taste, a
relative hyperæsthesia, may be produced. Paræsthesiæ are rare. In two
cases in which we have observed the symptom (one of neurasthenia, the
other of hypochondriacal melancholia) it consisted in a constant and
most distressing sweet taste. The application of the galvanic current
at the base of the brain, under the jaw, on the cheeks, and within the
mouth produces subjective tastes of an acid or metallic nature.
Anæsthesia of the gustatory nerve occurs after section of the lingual
branch of the trigeminus—an operation sometimes done for lingual
neuralgia, in which case the frontal two-thirds of the tongue on one
side loses its property of perceiving taste. As the result of central
disease next to nothing is known of this symptom. It is probable that
sweet and acid tastes are perceived in the mouth and forward part of
the tongue; bitter tastes on its caudal (posterior) third and in the
throat (glosso-pharyngeal nerve). In the insane, paræsthesiæ and
anæsthesia give rise to a great variety of delusions about the state
of the parts, the nature of their food, poison in the food, etc.

As a part of typical complete hemianæsthesia the special senses are
{42} involved. When of hysterical origin the whole retina of one eye
is generally devoid of sensibility, or it does not perceive colors.
When the hemianæsthesia is due to a lesion of the caudal part of the
internal capsule (organic anæsthesia), we should expect to find
lateral hemianopsia, with dark half-fields on the same side as the
cutaneous anæsthesia. We would not be understood as claiming that this
point of distinction is as yet positively determined, but would
advance it suggestively, subject to the result of observations on new
cases.


III. Motory Symptoms.

PARALYSIS, or AKINESIS, is a condition in which loss of voluntary or
involuntary muscular movement occurs through defective innervation.
Such a strict definition is desirable, as excluding cases in which
motion is abolished by local or general morbid states not essentially
nervous, as in acute articular rheumatism, ruptures of muscles or
tendons, fractures, extreme asthenia, etc.

Paresis is a term often employed to designate a paralysis partial in
degree; it does not mean an essential muscular paralysis.

Paralysis varies infinitely in extent and distribution, yet certain
types are recognized as having diagnostic value, and their exact
determination is of great importance in practice.

(_a_) Hemiplegia, or paralysis of many muscular groups in one lateral
half of the body.

(_α_) Common Hemiplegia.—In this, the most frequent form, we find loss
of voluntary motion in many muscles of one side of the face and body.
This condition may or may not be preceded by apoplectic or epileptic
symptoms: it may occur gradually or suddenly. Although it is customary
to say that in hemiplegia a patient is paralyzed on one side, this is
not strictly correct, as careful observation shows that (1) in the
face only the lower facial muscles are distinctly affected; the tongue
itself is rarely paralyzed, but its projecting muscular apparatus is,
so that when protruded it deviates as a whole toward the paralyzed
side; the eye-muscles and masticatory muscles are unaffected; (2) in
the extremities the loss of power is greatest in the hand and foot,
less so in the arm and thigh, very slight in the muscular groups of
the shoulders and hips; (3) the muscles of the neck and trunk, the
respiratory muscles, and in general the muscles of the vegetative life
are practically unaffected. These facts may be summarized by the
statement that in common hemiplegia the greatest paralysis is shown in
those muscular groups whose action is most independent on either side
of the body; or, in other words, in those whose functions are most
highly differentiated and whose innervation is most cortical (from the
motor centres in the cerebral cortex). Those muscular groups, on the
other hand, whose action is usually or necessarily simultaneously
bilateral or associated across the median line—or, in other words,
whose innervation is largely spinal or subcortical—are least
paralyzed; while the purely automatic or reflex muscular apparatuses,
those having a strictly spinal or sympathetic innervation, are not at
all affected.

Common hemiplegia is rarely accompanied by hemianæsthesia.

{43} It must not be forgotten that double hemiplegia may occur, in
which case the symptoms are simply duplicated.

As regards the seat of the lesion in common hemiplegia, it may here be
said, in general terms, that it is in the cerebral hemisphere opposite
to the paralysis (with excessively rare exceptions which are
susceptible of explanation), in its motor cortex, in the subjacent
associated white fasciculi, or in the knee and caudal part of the
internal capsule; the lesion may directly injure those parts or act
upon them by compression.

(_β_) Crossed Hemiplegia (hémiplégia alterne).—In this form there is
paralysis of many muscular groups on one side of the body, while the
facial nerve or some other cranial nerve (or several cranial nerves
together) show loss of innervation on the other side of the median
line. Theoretically, therefore, there may be as many varieties of
crossed hemiplegia as there are cranial nerves, but, practically, we
meet only with a few forms, of which the following are the most
common: (1) motor oculi (N. iii.) on one side, and body and face on
the other; (2) facial nerve (N. vii.) on one side, and body on the
other; (3) trigeminus nerve (N. v.) on one side (anæsthesia of face,
paralysis of masticatory muscles), and body on the other; (4) abducens
(N. vi.), facial (N. vii.), and acoustic (N. viii.) together on one
side, and the body on the other. (5) With symptoms of No. i. we may
have lateral hemianopia, dark half-fields on the same side as
paralyzed extremities.

In crossed hemiplegias anæsthesia is more common; there is a strong
tendency to bilateral extension of the paralysis, and neuro-retinitis
is seldom absent before the close of life.

As regards the location of the lesion in crossed hemiplegias, it may
be stated, in a general way, that it is in the base of the brain on
one side of the median line, so placed as to directly injure one or
more cranial nerves at their origin, and to compress or destroy the
cerebral motor tract (pyramidal tract) above its decussation-point,
and in some cases also the sensory tract in the crura, pons, and
oblongata.[4]

[Footnote 4: For a statement of the exact seat of the lesion causing
various forms of crossed hemiplegia, vide article on the LOCALIZATIONS
OF LESIONS IN THE NERVOUS SYSTEM.]

(_b_) Spinal Hemiplegia.—In this type the face and head are normal,
excepting in some cases the iris; the extremities and trunk are more
or less paralyzed on one side, the loss of power being more evenly
distributed (_i.e._ less distal) than in hemiplegia of cerebral
origin. Often there is also anæsthesia, and this is always on the
other side of the median line, involving more or less of the whole
side. The coincidence of these symptoms below the head indicates
positively that the lesion is in the spinal cord, involving one of its
lateral halves. Where there is no anæsthesia, care must be taken not
to confound the condition with that in which a cerebral lesion causes
paralysis of one arm and leg (combined brachial and crural
monoplegia).

(_c_) Paraplegia.—The loss of voluntary power involves one transverse
half of the body, usually the caudal. When only the lower extremities
are affected, the condition is designated simply a paraplegia; when
all the parts below the head are paralyzed, the term cervical
paraplegia is employed. Frequently, the bladder and rectum are
paralyzed, and in some cases the thoracic muscles also, leaving
inspiration to be performed by the diaphragm alone. Often there is
coextensive anæsthesia.

{44} Hemiparaplegia is a rare variety in which one lower extremity is
paralyzed while the other is anæsthetic.

The location of the lesion in paraplegias is in the spinal cord at
various levels and in various portions of the gray and white columns.
Theoretically, we may now again admit the old proposition that a
paraplegia may be of cerebral origin: in such a case the loss of power
should follow the laws of distal prevalence (vide (_α_)); there should
be no anæsthesia or vesical paralysis, and the lesion ought to be one
involving the paracentral lobules of both hemispheres (meso-vertex at
fissure of Rolando).

(_d_) Monoplegia, or paralysis of one extremity or of one side of the
face, is not rarely observed. It may be caused by central lesions in
the brain or spinal cord, or by an affection of the nerve-trunks of
the part. Cerebral monoplegias are of great importance in diagnosis,
and may be distinguished from others by—(1) loss of power is greatest
in the distal part of the affected member; (2) the precedence or
coincidence of spasm (usually clonic or epileptiform) in the limb; (3)
the absence of marked anæsthesia; (4) the preservation of muscular
nutrition.

(_e_) Localized Paralysis.—The extreme types of this form of paralysis
are paralysis of one external rectus and of one superior oblique.
These muscles are each supplied by one whole nerve, and may therefore
exhibit isolated paralysis. In the rest of the body, however,
localized paralysis shows itself in groups of muscles as innervated by
nerve-trunks or by certain so-called centres in the spinal cord. As
examples of the former variety may be cited common facial paralysis
(Bell's palsy) and paralysis of the extensor muscles of the hand by
injury to the musculo-spinal (radial) nerve, of the foot and leg from
lesions of the sciatic nerve. As examples of the second variety we
have the irregular paralysis of anterior poliomyelitis (infantile
spinal paralysis). In localized paralyses due to lesion of the
nerve-trunks anæsthesia is usually present, whereas it is not common
in the second variety. The determination of the seat of lesion in
neural localized paralysis is much facilitated by bearing in mind Van
der Kolk's law of the distribution of the motor and sensory fibres of
a nerve-trunk.

Pseudo-paralysis—_i.e._ conditions in which voluntary motion is lost
without defect in innervation, as from muscular disease, injuries,
inflammations, etc.—is usually localized or irregularly distributed.

(_f_) The various internal organs, the viscera, supplied with striped
or unstriped muscular fibres, may be paralyzed.

(_g_) The muscular coat of the vascular system beyond the heart may be
paralyzed in extensive or limited areas—the so-called vaso-motor
paralysis. This may assume hemiplegic or monoplegic or localized
forms.

SPASM, or HYPERKINESIS, consists in abnormal and often violent
involuntary muscular contractions, with or without loss of
consciousness.

1. A purely mechanical classification of spasms into tonic and clonic
forms is generally admitted as serviceable for clinical description,
though we have as yet no positive knowledge of their relations to
pathological conditions.

(_a_) Tonic or tetanic spasm is one in which the muscular contraction
is continuous or constant for a measurable length of time. Thus, in
some cases of petit mal there is a momentary stiffness or rigidity of
the entire {45} voluntary muscular apparatus (respiratory muscles
included): the patient sits or stands with staring eyes as if
petrified. In tetanus and local tetanoid seizures the muscles of large
regions or of a part of a limb may remain contracted for many minutes;
in the disease called tetany this condition may endure days and
weeks—in hysteria and in some paralyses dependent upon organic disease
for years or permanently. Prolonged tonic spasms occurring in chronic
diseases are designated as contractures, and the affected parts are
said to be tetanoid or spastic. A tonic spasm of long duration may
show itself in involuntary muscles, as in the arteries, causing
vaso-motor spasm and ischæmia; in the ciliary muscle, causing spasm of
accommodation; in the urethra, œsophagus, etc.

A tonic muscular contraction accompanied by intramuscular pain is
termed cramp.

Under this general head may also be classed the emotional or dramatic
expressive spasms of hysteria and hystero-epilepsy—a condition in
which the emotions or ideas occurring in the patient's mind are
involuntarily translated externally into attitudes or gestures: _e.g._
anger, fear, disgust, amorous and religious feelings, etc.

(_b_) Clonic spasms are those which consist in rapidly intermittent
muscular contractions, local or general. These may be rhythmical in
time or form, as in paralysis agitans, or wholly irregular, as in
chorea. Jerking is a quasi-popular designation of clonic spasms.

Tremor, or trembling, observed in persons during repose in any
attitude, consists in small, wholly involuntary muscular contractions
of sufficient extent to communicate to the parts a visible to-and-fro
movement which is very often rhythmical. In order to distinguish this
from any form of inco-ordination it is necessary that the observed
movement should occur independently of all volitional effort. Thus in
the senile state, in chronic alcoholism, in paralysis agitans, and in
dementia paralytica we observe trembling of the facial and lingual
muscles, of the extremities, and even of the whole body in some cases.
These are usually conditions of permanent or chronic tremor, but the
symptom is sometimes observed as a transient phenomenon, as after
violent muscular effort, after excesses of various sorts, under the
influence of emotions, etc. Occasionally, persons are met with who
have trembled from childhood or early years without actual disease of
the nervous system. It is clinically useful to divide tremor into
varieties, as rhythmical and irregular, fine and coarse, constant and
occasional. These terms define themselves sufficiently, so that no
further statement is necessary, but we would repeat that it is of much
advantage in diagnosis to determine accurately the characteristics of
tremor.

2. A much more useful classification of spasms, and to a certain
extent a physiological one, is into types according to their
distribution in the body, following exactly the classification of
paralyses. There are few topics of more utility for the physician to
study, in our opinion, than that of monoplegias and monospasms, of
hemiplegias and hemispasms in their genesis, mutual relations, and
diagnostic significance.

(_a_) Hemispasm of cerebral origin, tonic or clonic (or both forms
associated), may affect the face and limbs on one side of the body,
with or without paralysis. As in hemiplegia, the morbid phenomena are
greatest in the most distal muscular groups or in those whose
innervation is most {46} cortical. Very often hemispasm precedes,
immediately or remotely, hemiplegia in the same parts. In other cases
the relation is inverse, as when, after a severe hemiplegia, we find
the paralyzed muscles in a state of nearly constant tonic contraction
(secondary contracture), or when hemi-epilepsy follows a cerebral
lesion. In the former case the spasm, clonic or tonic, is designated
as pre-paralytic; in the second case, as post-paralytic. These terms
are useful, because they are associated with laws of diagnosis and
prognosis.

(_b_) Conjugate deviation of the eyeballs and head is an important
symptom of gross cerebral lesions, and may be considered here,
although it is probably due to paralysis. Still, the deviation itself
always strikes the observer as a spasmodic effect. The symptom
consists in a steady turning of the eyes, face, and head toward one or
the other side, and may be best described by likening it to the normal
act of looking at an object which is on one side or a little back of
us. In one form—that due to an irritative lesion of the motor cortex
of one hemisphere—the conjugate deviation forms a part of the
hemiplegic epileptiform convulsions (mixed tonic and clonic) which are
produced: the deviation is away from the lesion. In a second form,
where severe hemiplegia is produced by an acute lesion of the motor
area and the subjacent fasciculi of one hemisphere, whether the
patient be comatose or semi-conscious, the deviation, of paralytic
origin, is away from the paralyzed side of the body and toward the
injured hemisphere: the patient is said to be looking at his lesion.
In a third form, when the lesion is in one side of the base of the
brain (more particularly of the pons), the deviation, again paralytic,
is away from the lesion, as a rule. In some cases conjugate deviation
exists only as a tendency to look to either side. It is always a
valuable symptom in severe cerebral affections, more especially the
apoplectic state.

(_c_) Paraplegic spasm is also shown in tonic and clonic forms.
Partial tonic spasm of this distribution, with paresis of the legs,
causes the gait or attitude known as tetanoid or spastic. The four
extremities may be in this state of mixed paresis and contraction, as
observed in some very young children whose cerebral motor area is
probably undeveloped or ill-developed, or which has been damaged
shortly after birth by meningeal hemorrhage.

(_d_) Monospasm, spasm affecting one side of the face or one
extremity, may be of cerebral, spinal, or neural origin. Very often
monospasm of clonic form serves to indicate with wonderful precision
beginning disease (irritation stage) in limited parts of the cerebrum
(in cortical centres and in the connected fasciculi for the face and
limbs). Cerebral monospasms are sometimes combined so as to almost
constitute hemispasm—_i.e._ brachio-facial or brachio-crural
monospasm. Monospasm may precede or succeed monoplegia.

(_e_) Universal spasms, tonic, clonic, or mixed, occur in numerous
diseased states—in hysteria, epilepsy, chorea, tetanus, toxic
conditions, etc. A universal tonic spasm may last long enough
(tetanus, epilepsy) to kill by apnœa.

(_f_) Localized spasms, not monoplegic, are observed. For example, the
orbicularis palpebrarum may be the seat of clonic spasm, or the
masseters of tonic spasm for long periods of time; the œsophagus or
urethra may be temporarily closed by constriction; chorea may affect a
small muscular {47} group. A rhythmic spasm limited to a single muscle
is termed myoclonus; the use of this term should not lead one to
forget the nervous origin of the spasm. A localized tonic arterial
spasm may be so severe and prolonged as to produce great ischæmia,
even gangrene of the affected part.

(_g_) Fibrillary contractions, non-rhythmic contractions of fasciculi
in muscles, spontaneous or provoked by direct mechanical excitation,
may be considered as hyperkinesis. Subjectively, fibrillary
contractions are felt as a quivering or as if a worm moved under the
skin; objectively, they appear not unlike the rising and falling of a
cord under the cutaneous covering. They unquestionably occur
frequently in muscles which are undergoing degenerative or atrophic
changes (progressive muscular atrophy), but they are also met with in
cases of lead paralysis, neurasthenia, etc.

INCO-ORDINATION, or DYSKINESIS, is the condition in which volitional
movements are not performed with normal precision and steadiness.
Several varieties are recognized.

(_a_) Ataxic tremor is distinguished from common or spasmodic tremor
by the fact that it is developed during the performance of a
volitional act in parts which are quiet when not used. Thus, tremor
appears in speaking, putting out the fingers, using the hands, etc. in
the muscles actively employed, and occasionally also in others at the
same time. This form of tremor is well seen in dementia paralytica,
where in certain cases the patient's muscles are still until we induce
him to make voluntary movements or provoke expression movements. In
cases of disseminated sclerosis the same phenomenon is a
characteristic symptom, a coarse tremulous ataxia or oscillatory
trembling appearing whenever volitional acts are attempted. In
looking, there appears nystagmus, a rhythmic ataxic tremor of some of
the ocular muscles; in speaking, an irregular, jerky, slow, or
syllabic speech is heard; and when the hand is carried to a given
object or pointed the extremity exhibits oscillatory trembling. Common
and ataxic tremors may coincide, as in some cases of dementia
paralytica and in alcoholism.

(_b_) Ataxia is a symptom of the utmost importance, and its strict
definition should be maintained. It is that form of inco-ordination in
which there is want of harmony in the action of the various muscular
groups employed in the voluntary performance of a given act. The
simplest movement of an extremity (and more complicated ones a
fortiori) is made up of simultaneous contractions of flexor and
extensor muscles, often also of adductors and abductors in due
proportion, so as to produce a steady position and movement of the
parts. This is not accomplished by the will acting directly on the
different muscles themselves, but through the medium of a
co-ordinating mechanism which is strictly spinal (including the
intracranial expansion of the cord as far frontad as the third
ventricle), and which is educated or trained from the first days of
life. We will the action and set the co-ordinating mechanism going, so
that the movement is in a certain sense indirectly accomplished. Yet
volition does interfere directly to a certain extent by estimating
through the muscular sense, and by exerting the proper amount of force
required, and by guiding the movement in a general way. The most
striking peculiarity about ataxic movements is the defect in the
harmonious action of the various {48} (antagonistic) muscles employed,
resulting in jerky, oscillatory, but non-rhythmic movements,
constantly made worse by greater tension of the will. In simple tremor
volition may for a few moments stop the movements (as best shown in
paralysis agitans), while in ataxia the more the patient tries to
achieve the act, the greater becomes the disorder. The anatomical
fault is mostly in the spinal co-ordinating mechanism; the
long-established motor and sensori-motor associations are interrupted
or confused, and in some cases besides the muscular sense is
impaired.[5] The idea that ataxia results from faulty centripetal
impressions due to various degrees of anæsthesia is certainly
erroneous and misleading. In the first place, there are cases recorded
in which typical ataxia of the extremities occurred without the
slightest impairment of sensibility; and, secondly, neither in animals
(section of posterior roots of spinal nerves) nor in man does ataxia
appear as a result of anæsthesia. In this condition there is
inco-ordination, to be sure, but not ataxia in the strict meaning of
the term. Ataxia is nearly always a symptom of organic disease of the
spinal cord, more especially posterior spinal sclerosis and
diphtheritic myelitis. It may also occur from disease of the
oblongata, pons, and crura cerebri. In certain cases of lesion in
caudo-lateral part of the thalamus involving the caudal part of the
internal capsule (irritation or partial destruction), we observe
various forms of irregular movements which have been designated by
Weir Mitchell as post-paralytic chorea. We long ago became satisfied
that this term included quite a number of forms of inco-ordination,
some cases showing choreiform and trembling movements, others ataxic
tremor, true ataxia, and athetoid movements (also the true athetosis
of Hammond?). It seems probable that diseases of the cerebellum, by
exerting pressure on or by irritating subjacent parts, may sometimes
cause pure ataxia of the extremities on the side opposite the lesion.
That a strictly localized cortical lesion can give rise to ataxia we
are not now prepared to admit.

[Footnote 5: Ataxia is greatly aggravated by closing the eyes.]

(_c_) Uncertainty in voluntary movements is sufficiently defined by
the term employed and by the absence of ataxia. This is well
illustrated in those rare cases in which the muscular sense is
impaired or lost: in such a case volitional movements, such as placing
the fore finger on an object or fastening a button, are fairly well
done with the aid of sight, but without it the hand and fingers grope
almost or quite hopelessly about the object. It is important to note
that persistent trying to do the act does not aggravate the disorder,
but that, on the other hand, success is often achieved after feeling
about. In certain cases of blindness irregular movements of the
eyeball are observed, due to semi-voluntary efforts to look or to
direct the eyeballs in the direction of a person or object. In states
of cutaneous anæsthesia when the eyes are closed the same disorder
appears in muscular movements. Claude Bernard many years ago showed
that section of the posterior roots of spinal nerves in an animal was
followed, not by ataxia, but by vague inco-ordination and staggering.
In human cases we find that where the sensibility of one hand is lost
or greatly impaired, without paralysis, there is extreme awkwardness
and uncertainty in delicate muscular movements, but no ataxia. The
staggering exhibited by patients having plantar anæsthesia is largely
of this type: they stand fairly well while their eyes are open, but
oscillate or {49} fall when they are closed. This variety of
inco-ordination may result from toxic conditions (alcohol),
peripheral, neural, or central nervous disease. A few cases are on
record which would seem to show that there is a centre for muscular
sense in the cortex of the brain, in a part intermediate between the
caudal sensory area and the central motor one—viz. in the inferior
parietal lobule, supramarginal gyrus (and angular gyrus?). It has also
been shown (by Spitzka and others) that there is a conduction tract
for muscular sense, dorsad of the pyramidal tract in the pons and
oblongata (in the stratum intermedium and interolivary tract), lesions
of which produce inco-ordination (ataxia?) without marked paralysis or
anæsthesia.

(_d_) Titubation, or staggering, is the inability to stand erect or
walk straight because of impaired equilibrium. There is neither tremor
nor ataxia present, and paralysis and anæsthesia are not necessary
factors. It is distinguished from vertigo and dizziness by absence of
subjective sensations of movement. Staggering may show itself in a
general way or in the shape of latero-, retro-, or propulsion (disease
of the internal ear, paralysis agitans). A well-defined variety of
staggering is the wrongly-termed cerebellar ataxia. In this the
patient, having disease of the cerebellum involving its vermis
superior, stands with feet widely separated to increase his base of
support; the body is bent somewhat forward, and the arms and hands are
used as balancing-rods to maintain a sort of equipoise. In walking,
this attitude is exaggerated, and if the feet be bare it will be seen
that the toes are unconsciously clutching the floor for support; there
is no outward jerk of the leg or stamp of the heel as in the ataxic
gait, and closing the eyes does not aggravate the attitude or walk.
Besides, if the extremities be separately tested, it is found that
with closed eyes the patient can perfectly well place his fore-finger
on his nose or one heel on the opposite patella (lying down). The
proper term for the disorder is cerebellar titubation. Yet it must be
remembered that titubation also occurs from disease of the oblongata
and pons, from lesions of the base of the brain in general, and from
alcoholic, etc. intoxication. In many cases titubation occurs in
connection with vertigo or dizziness.

(_e_) Inco-ordination more or less of the ataxic form often affects
the muscles of articulation, phonation, and deglutition, giving to the
symptoms dysarthria, dysphonia, and dysphagia. Dysarthria and
dysphagia are probably often caused by lesions of the insula and
subjacent white substance, as well as by those affecting the
oblongata. There are two recent autopsies which would indicate that
there may be a cerebral cortical centre for phonation laryngeal
movements: in the ventral extremity of the right third frontal gyrus—a
part homologous to the speech centre on the left side of the brain. In
some cases, however, dysphonia and aphonia indicate a lesion of the
laryngeal nerves or of the oblongata (nucleus of NN. x. and xi.).

(_f_) Doubtless the internal muscular organs and the blood-vessels are
frequently the seat of inco-ordinate or quasi-ataxic movements, but
our present knowledge of these conditions amounts to very little.

It may be permissible to consider vertigo under the general head of
inco-ordination, because it usually finds a motor expression, either
actual or subjective. Subjective vertigo consists in a sense of
whirling or horizontal movement which is clearly referred to the brain
by the patient. The {50} sensation is variously expressed: in some the
head seems to whirl around; in others external objects seem to whirl
about the patient horizontally or vertically; in others still there is
a sensation of falling in a given direction or of dropping into a
hole. Dizziness is a minor degree of subjective motion conjoined with
more or less confusion and other paræsthesiæ in the head. Static
vertigo is that form in which there is actual loss of equilibrium, or
falling. It is observed more especially in diseases of the internal
auditory apparatus, and it may be produced artificially by
galvanization of the brain. If the electrodes are placed exactly on
the median line, and the current passed fronto-caudad through the
brain, no loss of equilibrium or vertigo is produced. If, however, the
current is passed transversely through the brain, there is produced at
the moment of the closure and opening of the circuit a distinct
tendency to fall or an actual fall to one side: in closing the current
the fall is always away from the negative pole or cathode. The
greatest amount of disturbance is produced when the electrodes are
placed on the mastoid processes or near them. Whether the disturbance
of equilibrium is caused by a change in electrotonus in the
hemispheres, or by a change in the vascular supply of the hemispheres
(in one anæmia, in the other relative hyperæmia), is uncertain. A
third explanation is equally plausible—viz. that the vertigo is caused
by unequal excitation of the internal acoustic organs and the two
halves of the cerebellum. This view would be supported by the fact
that in animals and man a lesion of the acoustic nerve and of the
processus ad pontem on one side produces strong rotary movements about
the long axis of the body.

ABNORMAL REFLEX MOVEMENTS.—Some reference has already been made to
absence or exaggeration of reflexes in the preceding paragraphs, but
the importance of these symptoms demands that they should be
separately considered.

A reflex action, in its simplest conception, is a movement (muscular,
vascular, or psycho-motor) or a secretion which is the result of the
transformation of a centripetal impression into a centrifugal impulse.
The apparatus required for the accomplishment of the reflex action
consists essentially of a sensitive surface of skin or mucous
membrane, of tendinous or other deep structure, to receive the
impression; a sensory afferent nerve to convey it; a nervous centre of
the simplest structure (one or two ganglion cells) to receive and
transform it; a motor or efferent nerve to transmit the resulting
impulse to a common muscle, to the vascular wall of a vessel or
viscus, or to a gland. These various terminal organs execute their
normal functions in response to the centrifugal impulse, and thus give
external or tangible evidence that the reflex action or reflex is
completed. This mechanism, the reflex arc, is illustrated by the
diagram (Fig. 1), which will also serve for the explanation of many of
the morbid reflex states.

[Illustration: FIG. 1. Diagram illustrating the Arc for Reflex Action.
The centripetal and centrifugal paths, the receptive and terminal
organs of the arc, are shown connected with the spinal centre, which
is a portion of central gray matter containing ganglion cells. The
inhibitory cerebral influence is constantly exerted in health to
moderate reflexes.]

In the healthy animal body many important functions are performed
under the law of reflex action; for example, many organic or secretory
functions, the movements of hollow viscera, vascular movements,
muscular tonus, defensive and expressive muscular movements. In the
process of education many acts which at first must be learned by
oft-repeated efforts, such as walking, playing upon musical
instruments, etc., later become habitual and automatic, and are then
largely executed by reflex {51} action unconsciously, co-ordinated by
the spinal (?) apparatus. Much of our intellectual activity is
governed by the same law operating between the psycho-sensory and the
psycho-motor apparatus.

Reflex actions are only to a moderate extent under the control of
volition—indeed, most of them are subconscious—but a strong
restraining action is unconsciously exerted by the cerebrum (vide Fig.
1) upon the spinal reflex centres. This is the so-called inhibitory
cerebral influence. The existence of such an influence is shown by
experiments upon animals, and by human cases in which, the cerebral
activity being reduced or abolished, we observe a great increase in
the frequency and extent of reflex movements, particularly in the
common muscular apparatus.

Clinically, we distinguish cutaneous or superficial, tendinous or deep
reflexes, according to the seat of the original excitation or
testing-point. Cerebral or psychic reflexes are, however, also to be
borne in mind. These reflexes may be abolished or increased.

(_a_) Diminution and abolition of reflex action are frequent symptoms
of disease of the nervous system. The fault or break may be anywhere
in the reflex arc, so that each case must be analyzed by itself. Let
us consider the phenomena as exhibited by two widely distant and
different apparatuses.

First, in the eye. In case of atrophy of the optic nerve the pupillary
reflex is lost, the reflex action failing because the receptive
surface and efferent nerve are injured. In certain cases of spinal
disease (posterior spinal sclerosis) the same pupillary immobility is
observed (the {52} Argyll-Robertson pupil); and in this case the
lesion either affects indirect efferent spinal fibres destined for the
iris, or it is situated in the centre for the reflex action—viz. the
gray matter of the lobus opticus. There may be loss of pupillary
reflex due to injury of the direct efferent fibres of the arc
(paralysis of the motor oculi, N. iii.). Lastly, the iris itself may
be so diseased as to be incapable of contracting, though it receive
the reflex impulse properly; the lesion is then in the terminal organ
of the arc.

Second, the patellar tendon reflex. In a healthy individual, sitting
at ease with one leg thrown over the other (knee over knee), upon
tapping the ligamentum patellæ of the overhanging or free leg a
contraction of the quadriceps muscle occurs, causing a visible forward
movement of the leg and foot. This is the well-known patellar reflex
or knee-jerk. The arc in this case consists of the ligamentum patellæ
with its included sensory fibres as receptive organs, sensory
(afferent) fibres of the crural nerve, a segment of the lumbar gray
matter of the cord as centre, motor (efferent) fibres of the crural
nerve, supplying the quadriceps extensor femoris, which is the
terminal organ. Theoretically (vide Fig. 1), we can conceive of
numerous abnormal conditions of parts of this arc which would lead to
abolition of the patellar reflex, but in practice the following are
the principal lesions to be thought of: Disease (sclerosis) of the
posterior root-zones of the lumbar enlargement of the cord, as
exhibited in the pre-ataxic stage of tabes; disease of the posterior
roots themselves through meningitis or meningo-myelitis, as in
diphtheritic ataxia; lesion of the nervous centre, as is frequently
observed in cases of infantile poliomyelitis; a lesion of the crural
nerve, involving its efferent or afferent fibres, or both sets of
fibres, would produce the same result, as would also, lastly, a severe
myositis or cancerous infiltration of the quadriceps muscle.

It is therefore evident that there is, or can be, nothing
pathognomonic in the loss of a given reflex: it simply indicates a
break in the reflex arc, the seat and nature of which remain to be
determined in each case. The topographical study of reflexes in
disease is of very great importance, more especially as a help to the
correct location and extent of neural and spinal diseases. To assist
this study, and for use more especially in connection with the ensuing
sections on localization, Gowers's excellent diagram and table are
reproduced in Fig. 2.

[Illustration: FIG. 2. Diagram and Table showing the Approximate
Relation to the Spinal Nerves of the Various Sensory and Reflex
Functions of the Spinal Cord (after Gowers).]

(_b_) Exaggeration of reflex actions. This is due, theoretically, to
any condition which increases the excitability of the reflex arc, but
practically and usually the cause of the increase is more or less
complete removal of the inhibitory supraspinal or cerebral influence.
The reflex arc itself remains structurally sound, but its function is
abnormally active. Thus, we meet with the most exquisite exhibition of
exaggerated reflexes in the paralyzed part after a transverse lesion
of the dorsal part of the cord. The lesion cuts off all communication
between the lumbar enlargement and the brain; no sensations pass to
consciousness, and no volitional influence can be exerted upon the
legs; yet the legs are abnormally active, the least touch on or
pricking of the skin, tapping a tendon, handling a joint, the pressure
of feces in the rectum, etc., produce more or less violent spasmodic
movements of mixed clonic and tonic forms (spinal epilepsy). Increased
knee-jerk, foot-clonus, and epileptoid trepidation are also present.
Other proofs that removal of the inhibitory cerebral influences is the
chief cause of increase of spinal reflexes are given by the {53} {54}
history of various cerebral diseases. Thus, in hemiplegia with
secondary contracture the cutaneous and tendinous reflexes on the
paralyzed side are much exaggerated; in dementia paralytica, as a
rule, the patellar reflex is increased on both sides; and in cerebral
neurasthenia all reflexes are often extremely great.

A variety of increased tendon reflex is known as clonus—a series of
rhythmic clonic muscular contractions set up by stretching the body
and tendon of a muscle. This is best studied at the ankle. By holding
the patient's leg nearly extended upon our left hand, and rather
suddenly forcing back the foot (dorsal flexion) by pressing under the
ball of the foot with our right hand, a series of oscillations or
to-and-fro movements of the ankle-joint are produced for a few moments
(ankle- or foot-clonus). Sometimes the same rhythmic clonic
contractions may be produced in the quadriceps by quickly pulling down
the patella with the leg semi-extended.

In some instances, together with great increase of tendon reflex, we
observe a transfer of the centrifugal impulse to other nerves of the
same extremity, or across the spinal cord to nerves and muscles of the
homologous limb.

Another interesting manifestation of morbid reflex movements is the
defensive tonic spasm of muscles about a diseased joint (of the
hip-muscles in coxitis, of vertebral muscles in Potts' disease). This
constitutes a valuable symptom for the differential diagnosis between
articular and neural diseases in certain cases.

Clinically, increase of reflex action is not as valuable an indication
as its absence, many healthy persons having high reflexes. Still, when
studied comparatively as to topography (comparing the two sides of the
body) and as to variations at different times in a given case, the
symptom is of considerable assistance.


IV. Trophic Symptoms.

Our present knowledge of this great group of symptoms of nervous
disease is in a somewhat chaotic state; and although we possess a
large accumulation of facts of this category, their classification is
incomplete and their explanation is for the most part theoretical and
unsatisfactory. The following subdivisions may be made to include all
the phenomena, and is sufficient for clinical purposes:

1. DEGENERATIVE ATROPHY, as distinguished from the simple atrophy of
insufficient nutrition, of disuse of the parts, and of retarded
growth, includes all those trophic symptoms in which, under the
influence of nervous disease, the solid tissues exhibit histological
and chemical alterations as well as reduction of volume. The principal
factor of this group is—

(_a_) Muscular atrophy due to lesions of some part of the nervous
apparatus (thus excluding directly traumatic or inflammatory atrophy),
as seen in the course of progressive muscular atrophy, of various
forms of poliomyelitis, of lead paralysis, of neuritis, and injuries
of nerves. These muscular atrophies are characterized by reduction in
the size of the affected muscles, by altered electrical reactions, and
by histological {55} changes. Reduction in size may affect one muscle
or a muscular group shortly after paralysis (as in poliomyelitis, lead
paralysis, affections of nerve-trunks), or without evident paralysis
it may involve only small fasciculi of a muscle at a time (as in
progressive muscular atrophy); so that we speak of diffused and
fascicular atrophy, of secondary (post-paralytic) and primary atrophy.
In some cases the wasting proceeds to such a degree that apparently no
muscular tissue remains, and the skin seems to rest directly on the
bones; in others the reduction in bulk is moderate, and is compensated
by increase in the intra- and extra-muscular fat (thus in stout
children the atrophy of severe poliomyelitis may be quite masked to
the eye); in still another category the increase in connective tissue
with fatty accumulation overbalances the muscular wasting, and we have
the pseudo-hypertrophic condition. Alterations in electro-muscular
contractility are most important signs of impaired muscular
innervation and nutrition. They present numerous and somewhat
complicated variations of value for diagnosis and prognosis, but which
cannot here be noticed at length. The general principle underlying
these variations is this: that a muscle deprived of its normal
innervation (centrifugal or motor) soon loses its capacity to respond
to the induced (faradic) current, and reacts in an abnormal way to the
galvanic current. This constitutes the reaction of degeneration of
Erb.[6] The chief abnormality in the galvanic reaction of a paralyzed
and diffusely atrophied muscle is its slow or wave-like contraction,
which on a graphic, or even to the observer's eye, presents a striking
contrast to the sharp, jerking, complete contraction of a healthy
muscle. Besides, the reactions to the two poles become equal, or even
reversed, so that we may obtain in testing by the polar method such
formulas as CaCC = AnCC, or CaCC < AnCC. With reference to the failure
of atrophied muscles to respond to the induced or faradic current,
this qualification must be added: If the poles are applied on the
moistened skin, as usual in testing or treating cases, no reaction
occurs even with most intense currents; but if a needle be made one
pole of the battery and inserted into the affected muscle, slight and
limited contractions may be obtained with a moderate current for many
months. Of this we have repeatedly satisfied ourselves in cases of
poliomyelitis, lead paralysis, and traumatic peripheral paralysis. In
the later stages of diffused paralytic atrophy, after an uncertain
number of years, no reaction can be obtained with either electrical
current. In fascicular non-paralytic muscular atrophy (as in
progressive muscular atrophy) the loss of faradic contractility is
only demonstrable in the affected fasciculi, good contractions being
obtained in adjacent healthy fasciculi of the same muscle. The amount
or extent of contraction varies pari passu with the progress of the
atrophy. The galvanic reactions of this form of muscular atrophy are
not yet well established. Muscles and muscular groups in a condition
of impaired nutrition exhibit at an early period an interesting
condition—viz. that they no longer contract by reflex excitation. Thus
in a case of infantile poliomyelitis with paralysis of the muscles of
the leg, these muscles no longer contract when the sole of the foot is
tickled, and if the thigh-muscles are affected even so slightly as to
appear of normal size and consistence, the patellar reflex is found
wanting. In these and in traumatic cases the {56} reflex act is
prevented by lesion of the centrifugal motor nervous apparatus, and
perhaps also by the associated muscular trophic alterations.

[Footnote 6: Conveniently expressed by the symbol De R.]

Histological changes in atrophied muscles vary somewhat in character
in different diseases, and vary much in degree at different periods of
the atrophy. An early appearance is the presence of proteinaceous and
of fatty granules or molecules in the sarcous substance. Later, the
muscular fibres become reduced in size, lose their striation, and show
inequalities; the interstitial connective tissue becomes active and
increases in amount, at the same time that fat is deposited. The fatty
change in some cases, in others the granular or proteinaceous
transformation, ultimately completely destroys the muscular substance,
so that in the place of a muscle we find abnormal connective and fatty
tissues, blood-vessels, fatty and proteinaceous débris, the whole
presenting a pale yellowish-white aspect. It is in this final stage of
degenerative atrophy that all electrical reactions are lost. In the
pseudo-hypertrophic state the interfibrillary and interfascicular
connective-tissue growth is much more active, and the wasting muscular
fibres are buried in masses of wavy and fatty connective tissue. In
this condition also electrical reactions may be wholly absent.

(_b_) Atrophy due to defective innervation sometimes affects the skin
and bones. In the former, after nerve-injuries more especially, we
observe loss of thickness, glossiness, and perverted circulation and
secretion; the hairs may fall out or grow abnormally; the nails are
slow of growth, thick, rugose, incurvated, and brittle. In other
cases, as in cerebral and spinal paralyses, the skin of the paralyzed
part is abnormally dry, rough, and furfuraceous, and it loses its
elasticity. In some varieties of so-called skin diseases the patches
of altered nutrition (eczema, bullæ, herpes, psoriasis, leucoderma,
scleroderma, etc.) are often, probably, dependent upon nervous
lesions.

In the very rare disease known as progressive facial atrophy the skin,
subcutaneous areolar tissue, and the bones undergo extreme atrophy.
The initial lesion is usually a patch of scleroderma with or without
neuralgic phenomena; the skin is thin, darker and smoother than
normal; it soon adheres to the subjacent bone (maxilla or zygoma),
which itself steadily diminishes in size. Almost the entire half of
the face (including the palate and tongue) may ultimately show the
atrophic changes. We are not yet prepared to state the causal
nerve-lesion in this disease.

The bones are abnormally fragile (fragilitas ossium) in some nervous
diseases, more especially in dementia paralytica and posterior spinal
sclerosis; but whether this condition is due directly to the nervous
disease or is the expression of more general malnutrition is now
undecided.

The complex lesions of joints observed in the course of posterior
spinal sclerosis, the spinal arthropathies of Charcot, probably belong
to this category. The affected joint (knee, shoulder, or ankle) rather
suddenly swells, and the swelling usually invades the rest of the
member or extends to the next distal joint; it is a hard, semi-elastic
swelling unlike common œdema. After its gradual subsidence it is found
that changes have taken place in the articulation itself, and later
distinct evidences of destructive disease, such as erosion of
cartilages, relaxation of ligaments, swelling, are observed. In many
cases extra-articular lesions appear in the shape of osteophitic
formations from the adjacent bones. The hydrarthrosis may persist or
disappear. So complete may be the destruction of {57} the joint
that—for example, in a case of arthropathy of the knee—the leg may be
twisted about in all directions, and even over-extended so as to lie
upon the anterior surface of the thigh. Examination of the joint
post-mortem reveals non-suppurative destruction of all its component
parts, cartilages, ligaments, and epiphyses; the eroded, deformed ends
of the bones rub against one another in a false joint-cavity formed of
the skin, connective tissue, tendons, and remains of ligaments. The
absence of pain and tenderness in the course of arthropathies is a
striking feature—so much so that when, in an adult patient, it is
observed that manipulation or puncture of a diseased joint is
painless, special inquiry should be made for symptoms of posterior
spinal sclerosis.[7]

[Footnote 7: We have known one case in which the diagnosis of tabes
dorsalis was made (and verified after death) in this way, after the
surgeon in charge of the patient had mentioned the fact that
puncturing a swollen diseased knee-joint was painless.]

(_c_) Under the head of degenerative atrophies should be included the
secondary changes which affect certain nerve-tracts within the nervous
system itself. It is impossible in this introduction to treat fully of
this interesting category of trophic changes; the following summary
must suffice: (1) When the cerebral motor cortex or any part of the
associated pyramidal (or motor) tract is destructively injured, there
occurs, in from three to six weeks, a degeneration of the whole tract
caudad of (below) the brain. The myeline becomes granular and
disappears, the cylinder-axes are broken up and vanish, the connective
tissue (neuroglia) increases in amount; the atrophied and degenerated
area appears in a transection rather translucent in contrast to the
pearly white of the normal medullary tissue, and when the preparation
is stained with carmine the patch takes up an abnormal amount of
pigment. This is the so-called descending degeneration, or centrifugal
atrophy of the central nervous system. (2) After total transverse
lesions of the spinal cord, besides the above-described centrifugal
degeneration caudad of the lesion, we observe frontad of (above) it
similar changes in the posterior median columns, and in the direct
cerebellar tracts—centripetal degeneration. At present we have no
knowledge of centripetal (ascending) degenerations in the cerebrum and
in nerve-trunks; and if the results of von Gudden's experimental
method be cited against this statement, it must be replied that its
effects are best seen in newly-born animals, and that its pathology is
yet unknown. (3) Lesions of the anterior gray matter (ventral cornua)
of the spinal cord, and of mixed nerve-trunks produce only centrifugal
or descending degeneration. All the nerve-fibres deriving their
innervation from the injured area in the cord, or in case of nerves
all fibres below the injury, perish—_i.e._ their myeline breaks up and
undergoes granular and fatty degeneration, their cylinder-axes are
segmented and disappear, while at the same time the connective tissue
of the nerve becomes abnormally active and increases. Furthermore, in
cases of this category there are, inevitably, degenerative and
atrophic changes in the attached muscles, and peculiar
electro-muscular reactions (vide supra). All these central and
peripheral nervous degenerations, due to a local lesion, are
conveniently grouped under the name of Wallerian degeneration.

2. ERUPTIONS AND ULCERATIONS.—(_a_) The cutaneous eruption about whose
nervous origin there is the least doubt is that known as herpes or
{58} zona. This manifests itself, with or without paræsthesiæ (pain,
itching, formication, etc.), as vesicles upon deeply-inflamed spots of
skin distributed in the territory of one or more sensory nerves, and
almost always unilaterally. The destructive process in the derma is so
profound as to leave scars which are indelible as a rule. In general
terms it might be stated that herpes may occur in the range of any
sensory nerve distributed to the skin or mucous membranes. The
neuralgia attending its development may be severe, and in some cases
lasts for years after the healing of the eruption. The pathology of
this affection appears to be inflammation of the ganglion of the
posterior root of one or more spinal nerves (including the trigeminus
and glosso-pharyngeal) or of their trunks. Herpes may appear in the
course of spontaneous and traumatic neuritis; and in the last-named
conditions a variety of eruptions have been observed in the area
supplied by affected nerves, such as eczema, bullæ, etc.

(_b_) That ulceration may result directly from a nervous lesion is
shown by the history of herpes, where a destructive process takes
place in the derma under such conditions as to exclude the action of
external agencies. But the same cannot be said of the ordinary
ulcerations and gangrenous lesions observed in a number of nervous
diseases, as the bed-sores of myelitis or of spinal injuries, the
ulceration of the cornea in trigeminal anæsthesia, the digital ulcers
and gangrene of lepra, asphyxia of the extremities, and
nerve-injuries. As regards all these, the proper explanation is, it
seems to us, that the anæsthesia existing as a predisposing cause
(leading to imperfect protection of the part), the ulceration itself,
is directly, actively caused by external agencies. Let me briefly cite
a few instructive experimental and pathological facts bearing on this
question.

It is well known that in animals and man lesions of the trigeminus
nerve sufficient to produce anæsthesia (of its first branch more
especially) are frequently, if not invariably, followed by ulceration
and perforation of the cornea and phthisis bulbi. These were long held
to be true dystropic changes, but about thirty and twenty years ago
Snellen and von Gudden demonstrated independently and by different
methods that these ocular lesions could be entirely prevented by
absolute closure (perfect protection) of the eyelids prior to the
experiment on the trigeminus. Not long afterward Brown-Séquard showed
that the sloughing ulcers which occur about the foot of an animal
whose sciatic nerve has been cut may be entirely prevented by care,
cleanliness, and soft bedding. The conclusion to be drawn from these
observations is that in almost all cases the ulcerations and sloughing
observed in man during the course of a nervous disease sufficient to
produce anæsthesia, such as traumatic neuritis, lepra anæsthetica,
traumatic or simple myelitis transversa, disease of the trigeminal
nerve, etc., are in reality produced by external agencies, injuries to
the cuticle, action of filth, and, we think, the entrance of bacteria,
which are well known to possess extraordinary powers of penetration
into tissues whose protecting epithelial layer is removed. Clinical
observation corroborates this view, for, with strict antiseptic
treatment and under sealed dressings (collodion to ulcerated
finger-tips), these ulcerations heal rapidly and completely, while the
anæsthesia remains unchanged and the nervous lesions may even
progress. At the same {59} time, while we believe the above to be the
pathology of so-called trophic ulcers, we would admit the possibility
of spontaneous neuritic ulceration and gangrene, as shown more
especially in herpes.

3. ALTERED SECRETIONS.—Under the influence of disordered innervation
secretions may be altered in quantity and in quality. Symptoms of this
class may be caused by neural or by central lesions, and the mechanism
of their action may be direct or reflex.

(_a_) After section or lesion by disease of the cervical sympathetic
nerve we observe increased activity of the entire skin in the affected
area of the head and face: there is more perspiration, lachrymation,
and more cerumen is found in the ear. In cases of lesions of a certain
part of the oblongata we find one result to be polyuria. In many cases
of nerve-injuries the sweat-glands and hair-follicles of the parts
supplied by the affected nerve appear to be sometimes abnormally
active, or in other cases inactive. In some rare cases of insanity
profuse salivation and extraordinary growth of hair are striking
symptoms. Lastly, in some functional nervous affections the various
secretions and excretions may be altered to extraordinary extremes
(_e.g._ the polyuria and anuria of hysteria).

(_b_) Qualitative modifications of secretions also occur, as exhibited
in the many variations in the composition of the urine in various
neuritic conditions, the watery urine of hysteria, the phosphatic
urine of neurasthenia. Injuries of a part of the floor of the
oblongata (and very probably other lesions of the nervous system) give
rise to the appearance of sugar, and sometimes of albumen, in the
urine. Under the influence of disease or of an emotion the breast-milk
may become toxic to the nursing child, causing diarrhœa, convulsions,
etc. In some forms of nervous dyspepsia large quantities of acid or of
alkaline fluid may be rapidly poured out into the stomach as a result
of disturbed glandular and vaso-motor action. In a few cases of
neurosis malodorous or perfumed perspiration has been observed.

In a general way it may be stated that, inasmuch as the normal
function of glands is largely, if not exclusively, under direct and
reflex nervous control, their secretions may be quickly altered in
quantity or quality by rapid nervous disease or by functional
disorders. It is probable that much of our future progress in the
semeiology of nervous diseases will be in this direction by the aid of
improved medical chemistry.

4. ASSIMILATION, METAMORPHOSIS OF FOOD, TISSUE-LIFE, and BLOOD-MAKING
are probably under nervous control to a certain extent, but our
knowledge is not now in a state to speak positively and definitely of
alterations in these processes as symptoms of nervous disease.

       *       *       *       *       *

THE PRINCIPLES OF DIAGNOSIS.


Having in the preceding pages surveyed the field of neurological
semeiology in an analytical way, it remains to briefly indicate how
far and in what manner these data can be best utilized for logical
diagnosis in the present state of science. If we may be allowed an
illustration, we {60} would say that the foregoing sections contain a
nearly complete vocabulary of the language of nervous diseases, and
that the following pages express an attempt at formulating its
grammar.

In the first place, it is important to classify the symptoms observed
according to their probable immediate cause in the nervous organs,
whether they are due to irritation or to the destruction of parts. The
extreme value of such a distinction in practice was first emphatically
brought forward by Brown-Séquard in his famous _Lectures on the
Physiology and Pathology of the Central Nervous System_ (Philada.,
1860); and to the observance of this law of genesis of symptoms we
believe that a large part of the subsequent extraordinary progress of
neurological science is due.

The symptoms produced by irritation of nervous organs are usually
hyperkineses or paræsthesiæ in their various forms. The symptoms,
spasm, pain, or numbness, are usually, though by no means always,
intermittent. That paralysis and anæsthesia may occur from irritation,
by an inhibitory process, is not to be denied, yet we must maintain
the extreme rarity of such a mechanism. The phenomena of inhibition
are so prominent in the normal nervous system that a physician who
looks at nervous diseases from the standpoint of the physiologist may
well be excused for seeing morbid inhibitory processes where others do
not.

The symptoms due to destructive lesions—_i.e._ those indicating
destruction of parts of the nervous system—are paralysis,
hyperkinesis, and anæsthesia, of absolutely or relatively constant
presence. Thus, for example, the paralysis of common hemiplegia due to
destruction of the motor part of the internal capsule is constant and
permanent, while the accompanying tonic spasm (late contracture),
which is considered an even more positive sign of serious destructive
injury to the cerebral motor tract, is permanent, but
intermittent—_i.e._ it is absent in profound sleep, and reappears as
soon as the patient awakes.

The association of symptoms of irritation and those of destruction is
frequent but variable. In many cases, as in cerebral tremor and
posterior spinal sclerosis, spasm and paræsthesiæ precede paralysis,
anæsthesia, and ataxia. In other cases (in many at a certain period)
they coexist. In a small group of cases the irritative symptoms follow
those indicating destruction, sometimes occurring years afterward, as
in post-hemiplegic epilepsy and neuralgia due to cicatrices. We would
repeat that very often, more especially in organic nervous affections,
much light is thrown on the diagnosis by careful noting of the
topographic distribution and chronological order of appearance of the
symptoms.

In the second place, it is necessary to group the symptoms of disease
of the nervous system in two great classes—viz. those representing
demonstrable lesions, macro- or microscopic, and those dependent upon
perverted functions or molecular malnutrition of the nervous organs or
elements. The first group is designated as organic diseases; the
second as functional affections. Mental diseases, so called, can also
be classified, according to their symptoms, in either of these groups.

The symptoms of the first group, that of organic nervous diseases, are
characterized by definiteness of distribution, by permanency, by
relative invariability, and by the predominance of objective signs.
Another important characteristic of organic diseases is their
progressive or fatal {61} tendency, either with reference to life in
general or to that of parts or organs. A third peculiarity of these
diseases is that they do not occupy the patient's attention as
strongly or as constantly as neuroses: in other words, the Ego is less
involved.

The symptoms of the second group, that of functional nervous
affections (neuroses and psychoses), are characterized by generality
and indefiniteness of distribution, by relative variability, by easy
removal or spontaneous disappearance, and by the preponderance of
subjective symptoms. The affection may endure for many years or for a
lifetime without fatal result and without special aggravation. The Ego
is very strongly and deeply affected, fear, depression, and constant
dwelling upon the symptoms being prominent features.

These are general statements intended to serve as guides for the
preliminary study of a case. It must be remembered that they are all
liable to exceptions, and that each patient must be separately
considered. It should be borne in mind that what to-day appears as a
functional affection, chiefly indicated by subjective symptoms, may in
a few months present distinct signs of organic changes in the nervous
system. Also, it must be added that in the present state of knowledge
we sometimes are not sure as to the presence or absence of organic
changes even after careful study of a case; as, for example, in some
epilepsies and neuralgias.

Furthermore, allowance must be made for the following sources of
error:

Anatomical variability; as, for example, in the distribution of
peripheral nerves and in the amount of decussation of fibres of the
pyramids;

The coincidence of diseases and multiplicity of lesions;

The toxic effects of drugs taken by the patient previous to our
examination; as, for example, bromism.


I. The Diagnosis of Organic Diseases of the Nervous System.

This should invariably consist, in the observer's mind at least, of
three separate diagnoses, each formed by the application of widely
different sources of knowledge, and each requiring a different logical
process. One diagnosis forms the indispensable preliminary to the
others, and the last one, when correct, demonstrates that the
neurologist is a physician as well as a specialist. A further utility
of this procedure by the method of the threefold diagnosis is, in our
opinion, that it constitutes the sure inductive reasoning to be
employed in the search after the pathology of new diseases, and must
prove of help in the future growth of neurological medicine.

These diagnoses are—

The diagnosis of the symptoms or symptom-group;

The diagnosis of the location of the lesion;

The diagnosis of the nature of the lesion or of the functional
disorder.

1. The diagnosis of the symptom or symptom-group is to be made
by—(_a_) careful inquiry into the manner of appearance, development,
and chronological order of the symptoms as related by the patient or
by his friends, and more especially by (_b_) an exact, and in some
directions {62} minute, determination of the symptoms, obvious or
latent, present in the patient. This valuable method of exact
observation is sometimes, no doubt, carried to a ridiculous extreme,
entailing much loss of time without corresponding results; but in
medical practice, as in all forms of professional work, there enters a
sort of genius, partly innate, but largely developed by cultivation,
which enables the observer to seize at once, apparently by intuition
or in the course of a few minutes of study, the really valuable and
suggestive phenomena; and it is in this line, the line of important
and correlated facts, that observation cannot be too minute and exact.
In following this method technical terms must be correctly used and
definitions rigidly adhered to, as superficial and loose records
nearly always mislead. Sometimes in the course of the examination a
symptom is discovered or a hint is thrown out by the patient which
suggests new lines of inquiry, and occasionally necessitates an entire
rearrangement of the data obtained. Consequently, it is important that
the observer should approach a case tabula rasa, and should, as far as
possible, prevent his being biassed by anticipations of, and immature
guesses at, the third or final diagnosis.

Besides exactness of observation, it is necessary that the physician
should have a thorough knowledge of nervous nosology in order to
complete the first diagnosis: he must be acquainted by book-study and
by personal observation with the numerous types of symptom-groups
which fill up our present classification of diseases, so that he can
at once say, approximately at least, in what category the case before
him belongs.

2. The second diagnosis, that of the location of the lesions, is to be
arrived at by the application of the observer's knowledge of the
anatomy and physiology of the nervous system; and therefore it is here
that special training is of the greatest advantage. The anatomy and
physiology of use in this connection are not the bare sciences as
taught in ordinary text-books, but a higher sort of knowledge,
corrected and extended by the teachings of pathology and pathological
anatomy. The physician must be well versed in the recent revelations
of experimentation and of autopsies bearing upon the architecture and
functions of the central nervous system, and should be able to apply
this knowledge deductively to the case in hand. In this manner the now
abundant material grouped under the term Localization of Cerebral and
Spinal Diseases (vide the next article) can be made of the greatest
utility in every-day practice. The solution of the problem of
localization of the lesion is much simplified if it be first
accurately determined whether the lesion is peripheral, spinal, or
cerebral.

3. The final diagnosis is with respect to the nature of the lesion.
While the second diagnosis may be said to possess the greater
scientific interest, this one must be admitted to possess paramount
practical importance, as from it we derive the indications for
rational treatment and the data of prognosis. The third diagnosis is
to be made by the application of the observer's knowledge of general
pathology and etiology; hence it is in this field that the
best-trained physician succeeds—where the experienced practitioner may
sometimes eclipse the brilliant specialist. The truth of this is
maintained by those who hold, as we do, that it is unwise to embark in
specialism without having had good hospital advantages and extensive
general practice.

{63} In order to arrive at the diagnosis of the nature of the lesion
we must consider the family history, trace out predispositions, study
the various causes of disease to which the patient has been exposed,
and by a thorough examination of the various functions and the
objective condition of the patient ascertain what pathological
processes are active in him. Often the clue to the diagnosis is found
in signs afforded by non-nervous organs, as nervous syphilis by nodes
and cutaneous cicatrices, cerebral hemorrhage by renal disease and
increased arterial tension, cerebral tuberculosis by pulmonary
lesions, etc.

A purely empirical form of knowledge of some utility in proving the
pathological diagnosis is that of the relative frequency of certain
lesions in the two sexes, at different ages, in various professions,
etc.—a statistical knowledge which is to be applied deductively to the
case under study.

Considerable uncertainty sometimes remains even after the most careful
analysis of a case, and often, after stating the first and second
diagnoses quite positively, scientific caution and due regard for
truth compel us to state the third diagnosis in alternative
propositions or as a diagnosis of probability, to be finally settled
by the appearance of new symptoms, or in some rare cases only by a
post-mortem examination.


II. The Diagnosis of Functional Nervous Affections (Neuroses and
Psychoses).

In some diseases of this class—as, for example, epilepsy—it is
desirable to make the triple diagnosis as stated supra, but usually
the two problems to be solved are—What is the symptom-group? and what
is the pathology of the affection? The question of localization is
less important and less easy of solution, as the symptoms are more
usually generalized, often vague, and sometimes purely subjective.

1. The first diagnosis is to be made in the same manner as already
stated, but besides, in many cases, a close psychological analysis is
required to ascertain the emotional and mental state of the patient.
Not only is this indispensable in cases of insanity, but it is often
of great utility in other conditions, as hysteria, hypochondriasis,
and simulation. In the course of this study we are frequently brought
face to face with a most difficult problem—viz. the correct estimation
of the degree of pain experienced by a patient. Is it a
quasi-objective, correctly-portrayed sensation? is it magnified by
abnormal sensitiveness or by true exaggeration? or is it simulated for
a purpose? These questions demand the greatest freedom from prejudice
and most delicate tact for their solution, and occasionally the most
experienced physician is deceived. More especially are caution and
scientific doubt to be exercised when this symptom (pain) stands alone
or nearly so, as in some medico-legal cases and in certain
hypochondriacal states where self-delusion seems to constitute the
only real disease.

2. The diagnosis of the pathological nature of the functional
disturbance (functional lesion) is to be made only by an exhaustive
study of the patient's personal and family history and of his general
condition. The following are the principal lines of inquiry to be
followed:

{64} (_a_) As to hereditary predisposition: direct or indirect
inheritance of neurotic tendencies, of psychic peculiarities, and as
to the presence of the various psychic and physical signs grouped
under the term psychic degeneration.

(_b_) As to personal habits: overwork, masturbation, the abuse of
tobacco, alcohol, or coitus, injudicious diet, abnormal postures,
injurious avocations, etc.

(_c_) As to dyscrasic and hæmic conditions: uræmia, lithæmia, anæmia,
malarial and syphilitic infection, etc.

(_d_) As to the condition of important organs: of the eye in
connection with headaches and vertigo; of the ear in relation to
vertigo and epileptiform attacks; of the heart (and arterial tension)
in various head-symptoms; of the sexual organs in hysteria,
hypochondriasis, epilepsy, etc.

A serious stumbling-block in this last line of inquiry is the
ever-recurring question as to the causal relation between the symptoms
observed. Is the asthenopia the cause of the headache, or does the
neurasthenia, giving rise to the headache, cause the asthenopia? Does
the extremely slow action of the heart in a given case produce the
epileptoid attacks, or are both due to a lesion of the medulla? Does
ovarian hyperæsthesia and neuralgia (with or without organic changes)
cause the hystero-epilepsy, or is the ovaria one of the numerous
peripherally projected sensory symptoms of the hysteric state? Does
the lithæmia, oxaluria, azoturia, or phosphaturia found in a patient
give rise to the nervous symptoms complained of, or are they (the
morbid excretions) the result of defective innervation? The candid
neurologist, looking at his cases from the standpoint of the general
physician rather than from the loophole of narrow specialism, must
admit that these questions vex him daily, and that they are often not
to be resolved in the present state of knowledge except by a
recurrence to the therapeutic test.

For this extremely difficult diagnosis of the pathology of functional
nervous affections we would obtain much immediate assistance if
observers had the courage to publish their cases in continuous series,
instead of giving us successful cases, which often only serve to
mislead. For example, how greatly would the question of the relation
between ovarian symptoms and epilepsy (also hystero-epilepsy) be
advanced if we had the final results of all cases of removal of the
ovaries for these diseases at a period not less than one year after
the operation! And so with the attempts made to cure headaches by the
correction of errors of refraction and weakness of the interni. The
profession has a right to demand a frank and full report of the
experience of those who practice and teach in these directions.


{65}


THE LOCALIZATION OF LESIONS IN THE NERVOUS SYSTEM.

BY E. C. SEGUIN, M.D.


There are two ways in which this important subject may be treated. Of
these, the more interesting and logical would be to systematically
expose the results of anatomical researches and of physiological
experiments which tend to demonstrate the organic independence and the
functions of various parts of the nervous system, and to give a
classified series of results of autopsies bearing on localization.
This would be all the more satisfactory because the questions
involved, although of much importance in practice, are in reality
physiological. The localization of functions being known, the
physician could from the symptoms (_i.e._ perverted or abolished
functions) present make a deductive diagnosis of great exactness. A
treatise on medicine, however, cannot allow the space necessary for
such a treatment of the topic which is best suited for monographic
writing. The other method of exposition, the one we will follow, is
that of summary statement of the association of the symptoms with
definite lesions, with occasional anatomical and physiological
explanations. This will, after all, be a series of diagnostic
propositions stated as concisely and classified as practically as
possible. With this end in view we divide the subject into five parts:

The localization of lesions in the peripheral nervous system
(including the cauda equina);

The localization of lesions in the spinal cord;

The localization of lesions in the medulla oblongata;

The localization of lesions in the encephalon.

Cranio-cerebral topography.


I. Localization of Lesions in the Peripheral Nervous System.

In general terms, it may be said that lesions of peripheral
(cerebro-spinal) nerves give rise to various sensory symptoms in the
area of cutaneous distribution of the affected nerves, and to a
flaccid atrophic paralysis in muscles supplied by the same nerves.
These muscles almost always exhibit the De R. in varying degrees, and
other trophic and vaso-motor symptoms are common. Many of these
symptoms also occur in cerebral and spinal diseases, so that, after
all, the diagnosis of peripheral localization depends largely on a
correct knowledge of the course and {66} distribution of nerves; of
the relative distribution of the sensory and motor filaments of
nerve-trunks; and of the frequent anomalies which occur. The subject
of collateral innervation at the periphery must also receive
attention, as involving a source of error.

Of extreme importance is the law of the relative distribution of motor
and sensory filaments derived from one nerve-trunk. This, Van der
Kolk's law,[1] has hardly received the attention it deserves from
practical neurologists. Briefly stated, it is that of the two sorts of
fibres in a mixed nerve the sensory filaments go to those parts which
are moved by muscles innervated by the motor filaments of the same
nerve. The reader can verify for himself the exactness of this law by
making sketches of an extremity and tracing the motor and sensory
distribution of its various nerves. There are partial and apparent
exceptions to the formula, but this objection applies to almost all
our medical laws. In the cranial system of nerves it is necessary to
consider the trigeminus as the sensory companion of the six anterior
motor nerves; the pneumogastric as the associate of the spinal
accessory (in part).

[Footnote 1: Van der Kolk, _On the Minute Structure and Functions of
the Spinal Cord, etc._, p. 7, New Sydenham Soc. transl., London, 1859;
Hilton, _On Rest and Pain_, p. 101, Am. ed., N. Y., 1879.]

(_a_) Irritative lesions of nerves, as tumors, punctured wounds,
perineuritis, moderate pressure, etc., are indicated by pain,
numbness, and other paræsthesiæ in their cutaneous distribution, and
of spasm or cramp with paresis only, in the associated muscles. Pain
is the most prominent symptom by far, and many cases of so-called
neuralgia belong to this category. As a rule, there is no anæsthesia,
and the electrical reactions of nerves and muscles remain normal, or
at least they do not present De R. In some cases vaso-motor spasm
(coldness, white or bluish appearance of parts) shows itself in the
most peripheral distribution of the nerve. The cutaneous and tendinous
reflexes are variable, but usually preserved.

(_b_) Destructive lesions of nerves, by section, severe pressure, true
neuritis, etc., are characterized by anæsthesia with or without
paræsthesiæ, by motor and vaso-motor paralysis, and by loss of
superficial and deep reflexes. Later, there occurs degenerative
atrophy of the paralyzed muscles with fully-developed De R., and
dystrophic changes in the skin, etc. supplied by the sensory filaments
of the injured nerve. In these anæsthetic parts ulceration is easily
caused by traumatism and want of cleanliness.

The abnormal electrical reactions of the paralyzed muscles are of much
importance for the diagnosis of the amount of injury done to the nerve
and for the purpose of prognosis. They may be summarized as follows,
assuming a case of complete section of a nerve-trunk:

_α_. The Faradic Reactions diminish rapidly in degree in both nerve
and muscles from the third or fourth day, and in the nerve they are,
as a rule, completely lost at the end of from ten to fifteen days. In
the muscles complete loss of faradic reaction is noted only somewhat
later, and is absolute. A return of musculo-faradic contractility is a
most positive sign of recovery of the nerve.

_β_. The Galvanic Reactions.—In the nerve, distal of the lesion, the
result is similar to that stated above—viz. after a few days (from
five to fifteen) all reaction disappears. The anatomical cause of the
complete {67} loss of the faradic and galvanic reactions in the nerve
is its disintegration by the Wallerian degeneration. In the attached
muscles the phenomena are widely different, and present interesting
and complicated variations. In the first place, during a variable
number of days there is increased excitability—_i.e._ the paralyzed
muscles, deprived of innervation, contract to a much weaker current
then do the homologous normal muscles. This is best shown in cases of
peripheral facial paralysis (Bell's palsy) in the second and third
weeks, by placing the electrodes in the median line, one upon the
cervical vertebræ, the other (a small testing interrupting electrode)
on the chin; on closing a very weak current of from four to eight
elements it will be seen that the muscles on the paralyzed side of the
face (the lower muscles) contract distinctly, while those on the
normal side remain quiet. In the course of time, many weeks usually,
the excitability diminishes, and falls below the normal, and in some
cases ultimately disappears. These are known as the quantitative
changes in musculo-galvanic reactions. During the long period
preceding recovery, or without it, various qualitative changes are
also observed in the reaction. The normal general formula of
CaCC > AnCC (with rapid, jerking and full contractions of the muscle)
becomes CaCC = AnCC or CaCC < AnCC. Often, too, distinct opening
contractions occur, usually AnOC. The muscular contractions also tend
to the tonic type or tetanus, expressed as CaDT or AnDT, etc.

The form of the contractions obtained is much altered. Throughout a
practically endless period in some cases, or until regeneration of the
nerve takes place in others, it is observed that musculo-galvanic
contractions are delayed, are slower, less jerking, or assume an
undulating wave-like character, easily passing into tetanus. This
change from the rapid, jerky, and full normal muscular contraction to
one which is slow and wave-like we consider to be the most positive
and reliable evidence of neuro-muscular degeneration and of the
cutting off of the spinal-cord influence. Fig. 4 shows the characters
of a human degenerative myogram contrasted with a normal one, Fig. 3.

[Illustration: FIG. 3. Contraction of Normal Abductor Indicis, CaCC,
with strong current (Amidon[2]).]

[Illustration: FIG. 4. Contraction of Paralyzed Muscle on thirty-first
day of Bell's palsy of the face. CaCC. 20 El. (Amidon). Shows retarded
contraction and slow contraction, with tendency to tetanus.]

[Footnote 2: “The Myography of Nerve-degeneration in Animals and Man,”
_Archives of Medicine_, viii., No. 1, 1882.]

In the period of recovery or regeneration of the nerve the
musculo-galvanic reactions slowly reacquire their normal characters;
the normal suddenness and completeness of the contractions gradually
appear, and faradic excitation causes slight responses. Lastly, the
nerve also begins to exhibit excitability under galvanism and
faradism. These various abnormal electrical reactions, also frequently
observed in diseases of the spinal cord, constitute the so-called
reaction of degeneration, or De R. The subject is one of much
practical importance, and for details the reader is referred to the
treatises on electro-therapeutics of Erb and De Watteville.

Just as we depend upon the De R. to prove interruption of motor
nerve-fibres (or, in other cases, destruction of ganglion cells in the
anterior horns of the cord), so do we rely upon the demonstration of
complete anæsthesia to prove interruption of sensory fibres. In
seeking for the area of anæsthesia several points must be borne in
mind: (1) The normal {68} distribution of the principal nerve-trunks
as taught by ordinary anatomical works; (2) the remarkable anomalies
of distribution which sometimes occur; (3) that many nerves near their
endings exchange filaments in very variable numbers; loops for
collateral innervation, which will supply some sensibility to parts
which, judging by ordinary anatomical rules, should be made anæsthetic
by section of a given nerve-trunk; (4) another consideration is the
degree of anæsthesia. Before pronouncing upon the complete and fatal
division of a nerve-trunk (by injury or by disease), absolute
anæsthesia should be demonstrated in its area of principal and
isolated distribution. Ordinary tests are not, as a rule, sufficient
for this purpose. The best means in our experience consists in the use
of a very strong induction (faradic) current, as follows: The skin of
the suspected region to be thoroughly dried and rubbed with chalk or
powdered starch; one pole, consisting of an ordinary wet electrode, to
be applied just above the part to be tested, and the other pole,
consisting of a single wire, with which different parts of the
anæsthetic area are to be touched. By this means partially insensible
regions, not responding to pricking and burning, may be made to yield
reaction, and the area of absolute anæsthesia be thereby much reduced.
Malingering may also be readily exposed by this test, which presents
another advantage—viz. of not causing local injury or scars as burning
will.

It follows from the preceding statements that in cases of limited
atrophic paralysis with De R. the diagnosis between a central lesion
(destruction of ganglion cells of the anterior horns of the cord) and
a strictly peripheral (or neural) lesion is to be chiefly based upon
two considerations: (1) The distribution of the paralysis, which in
the first case affects muscles which are physiologically grouped or
associated, while in the second case the simple law of anatomical
associations or grouping is observed; (2) by the state of sensibility,
which is normal in disease of the anterior horns of the cord, and is
frequently impaired or abolished in nerve lesions.

Lesions affecting the cauda equina cause all the above-mentioned
symptoms of peripheral lesions in a limited (partial) paraplegic
distribution. If the lesion or injury be in the sacro-coccygeal
region, the symptoms will, as a rule, be found confined to parts below
the knee, occasionally also involving the muscles on the posterior
aspect of the thigh (flexors of the leg). Below the knees we find an
atrophic paralysis with De R., anæsthesia of the foot and part of the
leg, loss of plantar and achillis reflexes, and the sphincter ani will
be paralyzed. The patellar reflex is {69} preserved or exaggerated. In
case the lesion be in the lumbar region, below the first lumbar
vertebræ, the symptoms will be found to extend as high as the groin,
involving also the buttocks and sphincter ani; state of the bladder
variable. All reflexes will be lost in the paralyzed extremities,
except in some cases the cremasteric reflex.

Strange as it may appear, physicians do not always remember that there
is practically no lumbar spinal cord (vide Fig. 2), and that injuries,
etc. of the lumbar vertebræ and dura tend to affect nerves, and not a
nervous centre.


II. Localization of Lesions in the Spinal Cord.

Diseases of the spinal cord are distinguished by the following general
characters, positive and negative:

Positive Characters.—Tendency to primary bilateral or paraplegic
distribution of all the symptoms. In the majority of cases
preservation of electro-muscular excitability, and in one well-defined
group of cases De R. more or less typically developed in the paralyzed
parts. Frequent vesical and rectal paralysis, either of the retaining
or of the ejecting apparatus. Pains and other paræsthesiæ in the
extremities, the pains often possessing the electric or fulgurating
character. Anæsthesia of paraplegic distribution. Sensations of
constriction or cincture about a limb or about the body at various
levels. Occurrence of ataxia without paralysis. Progressive muscular
atrophy without actual paralysis. Easy production of eschars
(bed-sores).

Negative Characters.—Absence of typical hemiplegic or monoplegic
distribution of symptoms. Rarity of head symptoms, as headache,
vertigo, mental disturbance; of lesions of the optic nerve. Absence of
epileptiform convulsions. Absence of such grouping of motor and
sensory symptoms as would exactly correspond to the area of
distribution of one or more large nerve-trunks.

The above symptomatic indications are, of course, of the most general
meaning only, and are liable to exceptions and subject to varying
conditions.

The DIAGNOSIS of the exact localization of lesions in the spinal cord,
considered from the clinical standpoint, is perhaps best arrived at by
following an anatomical and physiological order of subdivision of the
problem into three questions, as follows:

FIRST QUESTION.—BEING GIVEN SYMPTOMS INDICATING DISEASE LIMITED TO ONE
OR MORE SYSTEMS OF THE SPINAL CORD, TO DECIDE WHICH ARE AFFECTED.

Physiology and the results of embryological and pathological
researches justify us in making a general division of the spinal cord,
for purposes of diagnosis, into two great systems, whose limits are
fairly well known—viz. the æsthesodic or sensory system, and the
kinesodic or motor system. The following outline diagram (Fig. 5) of
section through the spinal cord exhibits the ascertained limits of the
two systems.

[Illustration: FIG. 5. Diagram of a Transverse Section of the Spinal
Cord through the Cervical Enlargement: The æsthesodic system is
shaded, the kinesodic system unshaded. Parts of the æsthesodic system:
(1) Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi
cuneati (columns of Burdach, inclusive of posterior root-zones); (4)
fasciculi graciles (columns of Goll or posterior median columns); (5)
ascending cerebellar fasciculi; (6) columns of Clarke. Parts of the
kinesodic system: (7) Anterior roots; (8) anterior columns (inclusive
of anterior root-zones); (9) anterior gray horns; (10) crossed
pyramidal fasciculi; (11) direct pyramidal fasciculi (columns of
Türck); [10 and 11 are the intraspinal prolongation of the cerebral
motor tract]; (12) lateral columns, of ill-defined limits and unknown
functions; P. R., posterior roots; P. S., posterior septum; A. R.,
anterior roots; A. F., anterior fissure.]

A. Lesions of the Æsthesodic System.—Limits of the Æsthesodic
System.—By this term we mean that combinations of ganglion-cells and
nerve-fibres whose functions are locally sensory, and of those fibres
which transmit impressions centripetally (frontad) to the encephalon.
The {70} following are the recognized parts of this system, as
outlined on the diagram: (1) the posterior (dorsal) nerve-roots and
attached ganglia; (2) the posterior gray horn and central gray
substance to an unknown distance ventrad; (3) the fasciculi cuneati
(columns of Burdach), whose lateral parts are more particularly
designated as posterior root-zones; (4) the fasciculi graciles
(columns of Goll) or posterior median columns; (5) the fasciculi ad
cerebellum; (6) the vesicular columns of Clarke (most developed in the
dorsal part of the cord). All of these parts have sensory functions,
or at least transmit impressions centripetally, and they undergo
secondary (Wallerian) degeneration toward the encephalon—_i.e._
frontad of a transverse lesion of the cord.[3]

[Footnote 3: There are some results of physiological experiments and a
few isolated pathological facts which would seem to point to the
existence of other sensory (centripetal) fasciculi in the lateral
columns, but it would be wholly premature to make use of these facts
in a practical consideration of the subject.]

At the present time there is only one lesion of the æsthesodic system
which can be diagnosticated during the patient's life from positive
symptoms.

(_a_) Lesions of the fasciculi cuneati (posterior root-zones, 3). The
symptoms of lesion (usually sclerosis) in this region are wholly
sensory {71} and ataxic. At an early stage acute pains, fulgurating
pains, occur in the extremities; later paræsthesiæ, anæsthesia, and
ataxia. The fulgurating pains caused by the slowly-progressive lesion
of the posterior root-zones are very peculiar, and almost
pathognomonic (vide preceding article for their description). In some
cases paræsthesiæ precede the pains, which inversion of the usual
order must be due to a difference in the starting-point of the
sclerosis within the large fasciculi cuneati. Tendinous reflexes
(especially the patellar) are lost at an early period in the disease,
and by noting the disappearances of the different reflexes we can
trace with some accuracy the longitudinal extension of the sclerosis
(vide Fig. 2). In many cases the pupillary reflex is also abolished,
constituting the Argyll-Robertson pupil.

As negative characters of lesions of the posterior root-zones (and of
the rest of the æsthesodic system) we note absence of paralysis,
contracture, atrophy, and De R.

In the present state of our knowledge of spinal physiology and
pathology we think that a lesion in this location should be recognized
by the physician early and positively—in some cases years before
ataxia and other grosser symptoms make the diagnosis of locomotor
ataxia obvious even to a layman's eye.

(_b_) Lesions of the fasciculi graciles (column of Goll, 4) cannot, we
believe, be recognized directly by positive symptoms. There are a few
cases on record of primary (?) sclerosis of these columns, in which
during life vague sensory symptoms had been noted, but we cannot build
upon such data. Indirectly, however, we can in many cases
diagnosticate degeneration of these fasciculi, reasoning from the data
of pathological anatomy. Thus, for example, in advanced cases of
sclerosis of the fasciculi cuneati (posterior spinal sclerosis) we
know that in the dorsal and cervical regions of the cord the columns
of Goll are in a state of secondary degeneration. After complete
transverse division of the cord by injury, extreme pressure, or focus
of myelitis, etc. the same (centripetal) degeneration exists above the
lesion.

The same remarks apply fairly to our clinical knowledge of the
remaining parts of the æsthesodic system, columns of Clarke (6), and
fasciculi ad cerebellum (5). We know absolutely nothing of lesions of
the posterior horns (2) in their clinical and diagnostic relations.

B. Lesions of the Kinesodic System.—Limits of the Kinesodic System.—In
general this includes the antero-lateral parts of the cord. In a
trans-section of the cord (vide Figs. 5 and 6) the following columns
and fasciculi are recognized, their location and limits being made
known to us by embryology, descriptive and pathological anatomy: (7)
The anterior (ventral) nerve-roots emerging from (8) the true anterior
columns or anterior root-zones; (9) the ventral (anterior) gray horns
with their groups of ganglion cells; (10) the crossed pyramidal
fasciculus, which is the caudal continuation of the cerebral motor
tract of the opposite hemisphere; (11) the direct pyramidal column
(column of Türck), which is the caudal continuation of the cerebral
motor part of the hemisphere on the same side; (12) the antero-lateral
column. Fasciculi 10 and 11 bear an inverse relation to each
other—_i.e._ 11 is larger in proportion as 10 is smaller.

[Illustration: FIG. 6. Diagram of a Transverse Section of the Spinal
Cord through the Lumbar Enlargement: The æsthesodic system is shaded;
the kinesodic system unshaded. Parts of the æsthesodic system: (1)
Posterior nerve-roots; (2) posterior gray horns; (3) fasciculi cuneati
(columns of Burdach, inclusive of posterior root-zones); (4) fasciculi
graciles (columns of Goll, or posterior median columns); (5) ascending
cerebellar fasciculi; (6) columns of Clarke. Parts of the kinesodic
system: (7) Anterior roots; (8) anterior columns (inclusive of
anterior root-zones); (9) anterior gray horns; (10) crossed pyramidal
fasciculi; (11) direct pyramidal fasciculi (columns of Türck) [10 and
11 are the intraspinal prolongation of the cerebral motor tract]; (12)
lateral columns of ill-defined limits and unknown functions; P. R.,
posterior roots; P. S., posterior septum; A. R., anterior roots;
A. F., anterior fissure.]

In a general way it may be stated that lesions of the kinesodic system
are characterized positively by the isolated existence or predominance
of {72} motor symptoms, by impairment of muscular nutrition, and by
De R.; also by contractures. The reflexes are almost never normal,
being either exaggerated or lost. Negative symptoms are—absence of
sensory symptoms, of ataxia, and of vesical or rectal symptoms.

(_a_) Lesions of the anterior gray horns (9) are revealed by most
definite and characteristic symptoms. There occurs a flaccid paralysis
involving more or less extensive groups of muscles in the extremities,
rarely truncal muscles, and never those of organic life. In a few
weeks the paralyzed muscles undergo atrophy, sometimes to an extreme
degree, and various degrees of De R. are present. Cutaneous and
tendinous reflexes are abolished. The bladder and rectum are normal.
Sensory symptoms absent, and if present consist only of mild
paræsthesiæ, which are probably due to postural pressure upon
nerve-trunks or to disturbance of the peripheral circulation. There is
no tendency to the formation of bed-sores, but circulation and
calorification are reduced in the paralyzed members. It should be
remembered that paralysis due to systematic lesion of the anterior
gray horns is never typically paraplegic, with horizontal limit-line
of sensory symptoms, a cincture feeling, and vesical paralysis.

{73} The above symptom-grouping is characteristic of lesion of the
anterior horns en masse; in other words, of poliomyelitis. In that
form of systematic disease of the anterior horns which consists
primarily and chiefly of a degeneration or molecular death of the
ganglion cells there is no true paralysis; the atrophy of muscles is
infinitely slower, and it proceeds in various muscles fasciculus by
fasciculus, the wasting being usually preceded by fibrillary
contractions, and being almost always symmetrically located on the two
sides of the body (affecting analogous or homologous parts). The
electrical reactions are abnormal, in that musculo-faradic reaction is
lost in exact proportion to the wasting; so that in a large muscle one
part may contract normally, while the adjacent fasciculi do not. It is
as yet uncertain whether De R. occur in this disease (progressive
muscular atrophy). Calorification and circulation are much less
impaired than in poliomyelitis; the negative symptoms are much the
same.

It is sometimes difficult to distinguish poliomyelitis from
generalized neuritis. The diagnosis is to be made by the presence in
the latter disease of marked sensory symptoms—neuro-muscular pains,
numbness, slight anæsthesia—and by a grouping of symptoms coinciding
with the distribution of nerve-trunks and branches. No assistance can
be derived from electrical tests, as both diseases yield more or less
typical De R.

(_b_) Lesions of the spinal pyramidal tract (of fasciculi 10 and 11)
are followed by motor symptoms only—viz. paralysis and contracture—or,
in other words, by a spastic paralysis. Sensibility is unaffected; the
bladder, rectum, and truncal muscles are not distinctly paralyzed; the
reflexes are much increased, and ankle-clonus is often present. The
electrical reactions of the paralyzed muscles are normal,
qualitatively at least. The diagnosis of localization may be pushed
still farther by the following considerations:

(1) When the condition of spastic paralysis is unilateral, of
hemiplegic distribution, and follows an attack of cerebral disease of
some sort, we may feel sure that both the crossed and the direct
fasciculi of the pyramidal (10 and 11) belonging to one cerebral motor
tract are degenerated throughout the length of the spinal cord, the
crossed fasciculus on the paralyzed side and the direct on the healthy
side (same side as injured hemisphere). It would thus appear that
lesion of the direct pyramidal fasciculus (11) produces no
symptoms,[4] except, of course, in those rare cases in which it is
larger than its associated crossed fasciculus.

[Footnote 4: Unless it be the increase of reflexes which is so often
observed on the non-paralyzed side in hemiplegics.]

(2) The above symptoms may be bilateral, as observed in children as a
congenital or early-acquired condition. In such cases the four
fasciculi of the motor tract are degenerated or undeveloped, in
correspondence with a symmetrical bilateral lesion of the motor area
of the cerebrum—imperfect development or early destruction.

(3) When the legs alone are the seat of spastic paralysis, with
increased reflexes, spastic or tetanoid gait, without sensory
symptoms, the diagnosis of a primary sclerosis of both lateral columns
(inclusive of 10) of the spinal cord is justified.

(_c_) Lesions of antero-lateral columns of the cord (8 and 12),
primary and independent of lesions of the anterior horns or of the
crossed {74} pyramidal fasciculus, cannot now be diagnosticated during
life. These large masses of fibres include fasciculi whose functions
are probably motor; others (especially in 12) whose functions,
according to recent experiments, may be sensory; and still others
which are associating or commissural.

(_d_) Various combinations of the above lesions occur, and may be
recognized positively during life: (1) Combined sclerosis of the
posterior columns and of the crossed pyramidal fasciculi (3 and 10),
indicated by ataxia with paralysis, absence of patellar reflex,
tendency to contracture, pains, and anæsthesia less marked than in
typical posterior spinal sclerosis. This symptom-group is usually
found in children; it is pre-eminently a family disease, and is known
as Friedreich's disease. Similar cases also occur in adults as a
strictly personal disease. (2) Secondary degeneration of the pyramidal
tract (10 and 11), with more or less localized atrophy of cells in the
anterior horns (9) coexists in two forms: First, in a few cases of
cerebral hemiplegia with contracture, and pathological atrophy of
various muscles on the paralyzed side; second, as a distinctly spinal
bilateral affection, characterized by a spastic or tetanoid state of
the lower extremities, and a mixture of atrophic paralysis (vide
(_a_)), with contracture in the arms and hands. This latter form is
the amyotrophic lateral sclerosis of Charcot.

SECOND QUESTION.—BEING GIVEN SYMPTOMS INDICATING A TOTAL TRANSVERSE
LESION OF THE SPINAL CORD, ONE INVOLVING ITS VARIOUS SYSTEMS AT A
CERTAIN LEVEL, TO DETERMINE THE ELEVATION OR FRONTO-CAUDAL SITUATION
OF THE LESION.

This question is usually easy of solution by the following method:
Since a transverse lesion of the spinal cord gives rise to both motor
and sensory symptoms of horizontal, paraplegic distribution caudad of
the lesion, the first thing to do is to determine accurately the upper
level of the symptom, either the line of anæsthesia or the limit of
paralysis. The former is always much more definite than the latter,
and usually serves as the guide to diagnosis, indicating accurately
the uppermost part of the lesion. In the thorax the levels of sensory
and motor symptoms nearly coincide, but in the extremities the
operation of Van der Kolk's law of distribution of motor and sensory
fibres of nerve-trunks must be borne in mind, although it does not
apply as strictly in this case as in nerve lesions strictly speaking.
Gowers's diagram will prove very serviceable in making a diagnosis of
transverse lesions, and will also prove of use in the study of
vertebral injury and disease, as it indicates with sufficient accuracy
the relation between vertebræ (spinous processes) and segments of the
spinal cord. (Vide Fig. 2.)

The following are the principal transverse localizations of disease
which are usually recognized during life by the above procedure:

(_a_) Lesions of the cauda equina (by tumors, caries, or fracture of
the bones, etc.) produce paralysis, anæsthesia, atrophy of muscles,
with De R., in the range of distribution of the sciatic nerves mainly.
The sphincter ani is paralyzed and relaxed, while the bladder remains
normal as a rule. In all essential respects this paraplegiform, but
not paraplegic, affection resembles that following injury to mixed
nerve-trunks. It is in reality an intra-spinal peripheral paralysis.
The more exact location of the lesion, in the absence of external
physical signs (fracture, etc.), may be {75} approximately determined
by a study of the distribution of the symptoms and their relation to
nerve-supply.

(_b_) Lesions of the lower end of the lumbar enlargement, or conus
medullaris, behind the first lumbar vertebra, will give rise to the
same symptoms as (_a_). The expression, lumbar part of the spinal
cord, should be more carefully used than it is at present in the
discussion of spinal injuries and spinal-cord diseases, disease of the
lumbar enlargement being common enough, but disease of the lumbar part
of the cord very rare. In the discussion of railway cases, more
especially, it is often forgotten that the spinal cord practically
ends behind the first lumbar vertebra.

(_c_) Lesions of the middle and upper parts (segments) of the lumbar
enlargement are evidenced by true paraplegia, without paralysis of the
abdominal muscles. In some cases the quadriceps group, supplied by the
crural nerve, is not paralyzed. The constriction and the limit of
anæsthesia are about the knees, at mid-thigh, or near the groin in
different cases. The paralyzed muscles, as a rule, retain their
irritability and show normal electrical reactions; the cutaneous and
tendinous reflexes are preserved or increased. The sphincter is
usually paralyzed, while the bladder is relatively unaffected.

(_d_) Transverse lesion of the dorsal spinal cord produces the
classical type of paraplegia—_i.e._ paralysis and anæsthesia of all
parts caudad of the lesion. The limit of anæsthesia and the
constriction band are nearly horizontal, and their exact level varies
with the height of the lesion, from the hypogastric region to above
the nipples. Below the level of anæsthesia, which indicates by the
number of the dorsal nerve the upper limit of the cord lesion, there
are complete paralysis, retention of urine, constipation with relaxed
sphincter ani, greatly exaggerated reflexes in the lower extremities,
even to spinal epilepsy; the muscles preserve their volume fairly
well, and their electrical reactions are normal—sensibility in all its
modes is abolished; bed-sores are easily provoked. Retention of urine
is an early symptom in lesion of the middle dorsal region of the
cord—sometimes, in our experience, preceding symptoms in the legs.

(_e_) A transverse lesion of the cord at the level of the last
cervical and first dorsal nerves—_i.e._ in the lower part of the
cervical enlargement—gives rise to typical paraplegia with a sensory
limit-line at or just below the clavicle, but also with some very
peculiar symptoms superadded. These characteristic symptoms are in the
upper extremities, and consist of paralysis and anæsthesia in the
range of distribution of the ulnar nerves. In the arms the anæsthesia
will be found along the lower ulnar aspect of the forearm, the ulnar
part of the hands, the whole of the little fingers, and one half of
the annuli. There will be paralysis (and in some cases atrophy with
De R.) affecting the flexor carpi ulnaris, the hypothenar eminence,
the interossei, and the ulnar half of the thenar group of muscles,
producing in most cases a special deformity of the hand known as
claw-hand or main-en-griffe. Another important symptom of a transverse
lesion in this location is complete paralysis of all the intercostal
and abdominal muscles, rendering respiration diaphragmatic and making
coughing and expectoration impossible. The breathing is abdominal in
type, and asphyxia is constantly impending.

(_f_) A transverse lesion of the upper part of the cervical
enlargement, below the origin of the fourth cervical nerve, gives rise
to symptoms {76} designated as cervical or total paraplegia. The lower
extremities and trunk are as in (_d_) and (_e_), but besides both arms
are completely paralyzed and anæsthetic. The limit of anæsthesia
usually extends along the clavicles to the acromion processes, or a
little below, near the deltoid insertions. All reflexes caudad of this
line are vastly increased, either with tonic or clonic contractions.
In some cases of pressure upon the cervical cord by tumors, caries of
vertebræ, etc. the tetanoid or spastic state of the extremities (the
lower more especially) may precede paralysis for a long time; as the
compression increases paralysis becomes more and more marked, while
the reflexes remain high. This constitutes the clinical group we
described in 1873 as tetanoid pseudo-paraplegia.

(_g_) Transverse lesions of the spinal cord from the decussation of
the pyramids to the fourth cervical nerve are very rare, and usually
of traumatic origin. They produce complete paralysis of the entire
body, and also of the diaphragm (third and fourth cervical nerves),
thus causing death by apnœa in a very short time.

(_h_) In ascending paralysis (Landry) the above symptom-groups,
excepting (_a_), (_b_), are met with at successive stages of the
disease, often by almost daily accession, until finally respiration
ceases.

(_i_) The height of a transverse localized lesion (_e.g._ a
stab-wound) of one lateral half of the spinal cord is to be determined
by the various groupings of symptoms stated in the preceding
paragraphs, the chief guide being the limit-line between the sensitive
and anæsthetic portions of the body, measured vertically. The symptoms
are, however, distributed in a very remarkable manner on either side
of the median line. The paralysis will be found on the same side as
the lesion, often accompanied by hyperæsthesia, vaso-motor paralysis,
and loss of muscular sense, while the anæsthesia is on the other side
of the body. When such a lesion occurs below the first dorsal nerve,
the symptom-group is designated as hemiparaplegia; when the lesion is
higher up, so as to paralyze the arms, the affection is termed spinal
hemiplegia (Brown-Séquard).

Above the decussation of the pyramids total transverse lesions are
practically unknown, so that the second question need not be followed
farther.

By means of the data above given we are also enabled to determine the
length—_i.e._ fronto-caudal extension—of the systematic lesions of the
cord.

The symptoms of transverse lesions of the spinal cord are not
exclusively caudad of the lesion, and some very striking ones are
observable in the head. In lesions of the upper part of the dorsal
cord and of the cervical enlargement (_e_, _f_, _g_) we observe
vaso-motor and pupillary symptoms, due to injury of the spinal origin
of the cervical sympathetic nerve; the pupils are contracted; the
cheeks and ears congested and unnaturally warm; the cutaneous
secretions are increased. In other words, the symptoms about the head,
frontad of the lesion, are the same as those we produce experimentally
in animals by section of the cervical sympathetic or of the lower
cervical cord. In hemi-lesion of the cord, in man as in animals, these
symptoms are unilateral, on the same side as the injury.

Another point to be remembered in the study of transverse lesions of
the spinal cord is that the lesion may involve enough of the anterior
{77} gray horns to give rise to atrophic paralysis with De R. in some
few muscles deriving their motor innervation from the focus of
disease. This is not rarely seen in cervical paraplegia.

THIRD QUESTION.—BEING GIVEN VERY LIMITED MOTOR OR SENSORY SYMPTOMS OF
SPINAL ORIGIN, TO DETERMINE THE EXACT LOCATION OF THE FOCAL LESIONS
CAUSING THEM.

(_a_) In the range of sensory disturbances this question rarely
presents itself for solution. Localized anæsthesia and pain of spinal
origin (except the fulgurating pains of tabes) are rare, and we do not
know the relation of cutaneous areas with the spinal segments as well
as we know the motor innervations. It should be stated here, however,
that the location of a fixed pain and of a zone of anæsthesia is often
of great value in determining what spinal nerve is affected, just
outside of the cord itself, by such directly-acting lesions as
vertebral caries, spinal pachymeningitis, tumors upon the spinal cord,
etc. Among the various symptoms of Pott's disease of the spine, fixed
pains in one side of the trunk, in one thigh, or in the upper
occipital region, etc. is a sign against which the physician should
always be on his guard, as it is a very early and valuable indication
of the existence of an affection which requires special treatment as
soon as a diagnosis can be made.

(_b_) Localized motor symptoms of spinal origin calling for a
diagnosis of the focal lesions causing them are frequent, and are
mostly met with in two affections—viz. progressive muscular atrophy
and poliomyelitis. The problem is now capable in many cases of an
approximately exact solution by the deductive application of our
knowledge of the intimate connection between certain muscles and
muscular groups and limited portions or segments of the spinal cord
(anterior gray horns more especially). This knowledge has been
accumulated and organized from ordinary anatomy, physiological
experiments, and more especially from carefully-made autopsies with
microscopic examination of the cord. We cannot present this subject
better than by reproducing a tabular statement of these results
prepared by M. Allen Starr.[5] Future autopsies may correct this
table, and in making use of it the occurrence of anomalous
nerve-distribution should be remembered:

LOCALIZATION OF FUNCTIONS IN THE VARIOUS SEGMENTS OF THE SPINAL CORD.

  -----------+------------------------+--------------+---------------
   Segment.  |         Muscles.       |  Reflexes.   |   Sensation.
  -----------+------------------------+--------------+---------------
  2d-3d C.   | Sterno-mast. trapezius.| . . . . . .  | Neck and back
             | Scaleni and musc. of   |              |  of head.
             |   neck.                |              |
             | Diaphragm. . . . . . . | Hypochon-    |
             |                        |   drium (?). |
             |                        |              |
  4th C.     | Diaphragm. . . . . . . | Dilatation   | Neck.
             |                        |   of pupil.  |
             | Supra- and             | On irritation| Upper shoulder.
             |   infra-spinatus.      |   of neck.   |
             | Deltoid. . . . . . . . | 4th-7th C.   | Outer arm.
             | Biceps and             |              |
             |   coraco-brach.        |              |
             | Supinator longus.      |              |
             | Rhomboid.              |              |
             |                        |              |
  5th C.     | Deep muscles of        | Scapular.    | Back of should-
             |   shoulder-blade. . .  | 5th C.-1st D.|   er and arm.
{78}         | Deltoid.  . . . . . .  | . . . . . .  | Outer side of
             |                        |              |   arm and
             |                        |              |   forearm.
             | Biceps and             |              | Ant. upper
             |   coraco-brach. . . .  | . . . . . .  |   two-thirds of
             |                        |              |   arm.
             | Supinator longus.      |              |
             | Pectorales.            |              |
             | Serratus magnus.       |              |
             | Triceps.               | Elbow tendon.|
             | Rhomboid, teres minor. | 5th-6th C.   |
             |                        |              |
  6th C.     | Biceps, brach. antic.  | . . . . . .  | Outer side of
             |                        |              |   arm and
             |                        |              |   forearm.
             | Pectorales. . . . . .  | . . . . . .  | Inner and front
             |                        |              |   of forearm.
             | Serratus magnus.       |              |
             | Triceps.               |              |
             | Extensors of wrist and | Wrist        |
             |   fingers.  . . . . .  |   tendons.   |
             | Flexors of wrist. . .  | Wrist        |
             |                        |   tendons.   |
             | Pronators, supinator   | 6th-8th C.   |
             |   brevis. . . . . . .  |              |
             |                        |              |
  7th C.     | Triceps, long head. .  | . . . . . .  | Inner and back
             |                        |              |   of arm and
             |                        |              |   forearm.
             | Extensors of wrist and |              |
             |   fingers.             |              |
             | Flexors of wrist and   | Palmar. . .  | Radial
             |   fingers.  . . . . .  |              |   distribution
             |                        |              |   in the hand.
             | Pronators of wrist. .  | 7th-8th C.   |
             | Subscapular.           |              |
             | Latissimus dorsi.      |              |
             | Teres major.           |              |
             |                        |              |
  8th C.     | Extensors of thumb. .  | . . . . . .  | Forearm and
             | Flexors of wrist and   |              |   hand, median
             |   fingers.             |              |   and ulnar
             | Intrinsic muscles of   |              |   distribution.
             |   hand.                |              |
             |                        |              |
  1st D.     | Extensors of thumb. .  | . . . . . .  | Ulnar
             | Intrinsic muscles of   |              |   distribution
             |   hand.                |              |   to hand,
             | Thenar and hypothenar  |              |   little
             |   eminences.           |              |   finger.
             |                        |              |
  2d-12th D. | Muscles of back and    | Epigastric   | Skin of back
             |   abdomen. . . . . .   |   skin.      |   and abdomen,
             |                        |   4-7 D.     |   and over
             |                        | Abdominal    |   upper gluteal
             |                        |   skin.      |   region.
             |                        |   7-11 D.    |
             | Erector spinæ muscles. | Hypochon-    |
             |                        |   drium (?). |
             |                        |              |
  1st L.     | Ilio-psoas. . . . . .  | Cremasteric. | Skin over groin
             | Sartorius.  . . . . .  | 1st-3d L.    |   and front of
             |                        |              |   scrotum.
             |                        |              |
  2d L.      | Ilio-psoas. . . . . .  | Patellar     | Outer side of
             |                        |   tendon.    |   thigh.
             | Sartorius.  . . . . .  | 2d-4th L.    |
             | Flexors of knee,       | Bladder and  |
             |   Remak (?) . . . . .  |   sexual     |
             |                        |   centres.   |
             |                        | 2d-4th L.    |
             |                        |              |
  3d L.      | Quadriceps femoris. .  | . . . . . .  | Front of thigh.
             | Adductores femoris.    |              |
             |                        |              |
  4th L.     | Adductores femoris. .  | Rectal       | Inner side of
             |                        |   centre.    |   thigh and leg
             | Extensores femoris. .  | 4th L.-2d S. |   to ankle.
             | Tibialis anticus. . .  | Gluteal.     |
             | Peroneus longus.  . .  | 4th-5th L.   |
             | Flexors of knee        |              |
             |   (Ferrier (?)).       |              |
{79}         |                        |              |
  5th L.     | Outward rotators of    | . . . . . .  | Lower part of
             |   thigh.  . . . . . .  |              |   gluteal
             |                        |              |   region.
             | Flexors of knee        | . . . . . .  | Back of thigh.
             |   (Ferrier).           |              |
             | Flexors and extensors  | . . . . . .  | Leg and foot,
             |   of toes.             |              |   outer part.
             | Peronei.               |              |
             | Muscles of calf of leg.|              |
             |                        |              |
  1st S.     | Muscles of calf of leg.| Foot clonus. | Leg and foot,
             | Long flexor of great   | Achillis     |   except inner
             |   toe.  . . . . . . .  |   tendon.    |   part.
             | Intrinsic muscles of   | Plantar.     |
             |   foot. . . . . . . .  |              |
             |                        |              |
  2d S.      | Intrinsic muscles of   | Plantar.     | Perineum, anus.
             |   foot. . . . . . . .  |              |
  -----------+------------------------+--------------+---------------

[Footnote 5: “The Localization of Functions of the Spinal Cord,”
_American Journal Neurology and Psychiatry_, iii., 1884.]

The above table should be studied in connection with Gowers's diagram
of the vertebral column and spinal cord (Fig. 2, p. 53), for the
thorough study of cases of neural and spinal localization. Additional
details of much value with respect to the peripheral nerve
distribution are accessible in the works of Ranney[6] and Ross[7].

[Footnote 6: _The Applied Anatomy of the Nervous System_, N. Y., 1881,
p. 355 _et seq._]

[Footnote 7: _Handbook of Diseases of the Nervous System_, Am. ed.,
Philada., 1885, p. 356 _et seq._]


III. The Localization of Lesions in the Medulla Oblongata.

In general terms, lesions of the oblongata are characterized by the
early appearance and prominence of motor symptoms in the mouth,
throat, and larynx, and by bilaterality of the symptoms. Remote
symptoms consist of disturbances in the cardiac action and in the
functions of some intra-abdominal organs. There may also be more or
less paralysis of all the extremities. These lesions may conveniently
be classified, like those of the cord, into systematic and focal.

A. SYSTEMATIC LESIONS OF THE OBLONGATA.—1. Systematic lesions of the
æsthesodic system of the oblongata are, for purposes of practical
diagnosis, unknown at the present time.

2. Systematic lesions of the kinesodic system of the oblongata, on the
other hand, are often positively recognizable during the patient's
life.

(_a_) The most strictly systematic and most frequent of these lesions
is that of secondary (Wallerian) degeneration of the pyramids, the
prolongation of the cerebral motor tract. This morbid change gives
rise to no distinct bulbar symptoms, and it can only be diagnosticated
inferentially or inclusively by determining the existence of secondary
degeneration of the entire pyramidal tract, from the occurrence of
hemiplegia followed by contracture and increased reflexes. If the
phenomena present be those of double spastic hemiplegia, there is
surely degeneration of both pyramids.

(_b_) A systematic lesion affects the nuclei (origins) of the facial,
hypoglossal, pneumogastric, spinal accessory, and the motor root of
the trigeminus nerves, giving rise to a classical symptom-group. The
symptoms thus produced are exclusively (?) motor and trophic,
consisting of progressively increasing paresis, with atrophy of the
muscles about the lips {80} and cheeks, the intrinsic lingual muscles,
the laryngeal and pharyngeal muscles. Later, the masseters, temporals,
and pterygoids are sometimes involved; and, finally, extremely rapid
action of the heart with pneumonic symptoms indicates the gravest
extension of the morbid process. An early symptom in such cases is
abnormal salivation. These affections, generally designated as
varieties of bulbar paralysis, subacute or chronic, are usually
readily recognized intra vitam, and recent discoveries in morbid
anatomy have enabled us to correctly diagnosticate the seat of the
lesion in its various extensions. The laryngeal paralysis represents
disintegration (atrophy) of ganglion-cells in the bulbar origin of the
spinal accessory nerve; lingual atrophic paralysis indicates the same
lesion in the nuclei of the hypoglossal nerves; the labio-buccal
symptoms are produced by lesion of the facial nerve nucleus (inferior
facial nucleus of older writers); the paralysis of the muscles of
mastication is due to extension of cell-degeneration to the motor
nucleus of the trigeminus in the pons; and the final cardio-pulmonary
symptoms indicate an extension of the lesion into the sensory (?)
origin of the pneumogastric nerves.

It is evident that this systematic lesion of the oblongata is the
equivalent or analogue of the various acute and chronic lesions of the
anterior horns of the spinal cord, described supra, and in practice we
sometimes find these bulbar and spinal lesions associated: progressive
muscular atrophy of the extremities and amyotrophic lateral sclerosis
being complicated with bulbar paralysis.

B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known, occur
mostly in the kinesodic system, but may also involve several fasciculi
and nuclei at one time. The symptoms of such lesions are grouped in
two principal types:

(_a_) Single symptoms, such as atrophy or atrophic paralysis of some
one muscle or muscular group innervated by the hypoglossal, facial, or
spinal accessory nerves. For example, unilateral atrophy of the
tongue, when not due to neural injury, is quite surely the
representative of destruction of one hypoglossal nucleus. It is
possible that some cases of peripheral facial paralysis, so-called, or
Bell's palsy, and cases of paralysis of the sterno-mastoid and
trapezius, are not due to neural lesion, but to primary disease of the
nuclei of the facial and spinal accessory nerves, either as
poliomyelitis or as progressive cell-degeneration and atrophy.

A similar reserve must be used in speaking of the localization of
small lesions in the oblongata, causing diabetes mellitus, polyuria,
albuminuria, and salivation. From experiments upon animals and a few
post-mortem examinations in human cases we know that such lesions may
occur and cause the symptoms, but their recognition during the
patient's life is at the present time next to impossible.

(_b_) The symptoms may be complex and belong to the general class of
crossed paralysis, the mouth, face, tongue, and larynx being paralyzed
(often with anæsthesia of the face) on one side, while the extremities
are paralyzed on the other side. Such a symptom-group would indicate a
large lesion (tumor) in one lateral half of the oblongata, more
especially in its ventral aspect. These localizations will be studied
more in detail farther on, under the general head of Crossed Paralysis
due to Lesions of the Base of the Brain.


{81} IV. Localization of Lesions in the Encephalic Mass.

Under this head, to prevent repetition and to facilitate condensation,
we will consider the various localizations which can now be
diagnosticated in the cerebrum, basis cerebri, and cerebellum.

It would be of the greatest advantage to preface these statements by a
full summary of the anatomical and physiological data on which the
localizations rest, but space is wanting for such an exposition, and
the reader who is not already familiar with these branches of medical
science will have to seek information in other accessible works.[8]

[Footnote 8: Ferrier, _The Functions of the Brain_, Am. ed., N. Y.,
1876; Charcot, _Lectures on Localization in Disease of the Brain_, Am.
ed., N. Y., 1878; Seguin, E. C., “Lectures on the Localization of
Spinal and Cerebral Diseases,” _N. Y. Medical Record_, 1878; Ranney,
_Applied Anatomy of the Nervous System_, N. Y., 1881; Meynert,
_Psychiatry: A Clinical Treatise on Diseases of the Fore-brain_, Part
I., Am. ed., 1885.]

In a general way, encephalic lesions are distinguished by the
following:

Positive Characters.—Tendency to strictly hemiplegic or bilaterally
hemiplegic grouping of symptoms; frequency of contracture or of a
spastic state of the paretic muscles; increase of reflexes in the
affected extremities; spasmodic manifestations in remote muscular
groups, but not in areas of nerve-distribution (forms of Jacksonian
epilepsy); the presence of paralytic and anæsthetic symptoms in the
range of distribution of cranial nerves; frequency of neuro-retinitis
or atrophy of the optic nerves; occurrence of lateral hemianopsia;
production of symptom-groups known as varieties of crossed paralysis;
frequency of head symptoms, as headache, vertigo, apoplectic and
epileptic seizures; mental symptoms of various sorts, dementia, coma,
etc.

Negative Characters.—Absence of truly paraplegiform distribution of
symptoms, even when they are bilateral; of cincture feelings; of pain
or other paræsthesiæ and anæsthesia in the distribution of
nerve-trunks; of muscular atrophy and De R. in paralyzed parts. Rarely
do we observe visceral paralysis and bed-sores.

Pathological localizations in the encephalon may conveniently be
grouped under two heads—viz. systematic and focal lesions.

A. SYSTEMATIC LESIONS OF THE ENCEPHALON.—The recent advances of
embryology, anatomy, physiology, and pathological anatomy have
conclusively established the existence, and fairly well defined the
limits, of a sensory (æsthesodic) and of a motor (kinesodic) tract in
the brain; and certain lesions of these tracts produce such precise
symptom-groups that their diagnosis during the patient's life is often
possible, and that, too, with great exactness.

1. SYSTEMATIC LESIONS OF THE ÆSTHESODIC SYSTEM OF THE ENCEPHALON.—The
limits of this system are as follows: Within the oblongata and pons it
occupies a somewhat uncertain (from a clinical standpoint) location,
its fasciculi and ganglia lying in a general way dorso-laterad of the
motor or kinesodic system. In the crus cerebri the fibres of the
sensory tract are more closely packed together, and constitute a dense
fasciculus of white substance in the lateral part of the crus in its
subcerebral extremity, estimated by Flechsig at about one-fifth of the
entire crus, and thence it enters into the composition of what is
known as the internal capsule. This narrow but all-important mass of
{82} white fibres, as revealed by a horizontal section of the
hemisphere (vide Fig. 7), lies between the nucleus caudatus and the
nucleus lentiformis, and between the latter and the thalamus, thus
assuming a V or elbow shape. Of this, the caudal third of that part of
the capsule behind the bend or angle contains all the sensory paths
for the opposite half of the body, reinforced by paths for the special
senses; it is the carrefour sensitif of French writers. From this
region sensory fasciculi radiate to various parts of the cerebral
cortex—in the parietal, temporal, and occipital gyri—in which
physiological experiments and human cases of disease have shown
sensory areas or centres. Of the fasciculi from special sense-organs
which reinforce the internal capsule, the only one which is well
defined and easily traceable is the fasciculus opticus (fasciculus of
Gratiolet), derived in part directly from the optic tract of the same
side and from the primary optic centres (lobus opticus, corpus
geniculatum laterale, and pulvinar), proceeds, along with fibres of
the internal capsule, dorso-laterad of the posterior cornu of the
lateral ventricle, to the mesal aspect of the occipital lobe. A
fasciculus from the olfactory apparatus doubtless also joins the
internal capsule, but its course is unknown.

The following localization diagnoses are now possible in the
æsthesodic system as above defined:

(_a_) A lesion of the internal capsule, just above the crus cerebri,
involving its bend or knee and caudal segment, with or without injury
to the nucleus lentiformis and thalamus, will give rise to the
following symptoms: Complete typical hemiplegia and total
hemianæsthesia on the opposite side of the body; the anæsthesia
involves the special senses as well as the body. Vision is, however,
unaffected, unless the lesion extend far enough back to involve the
pulvinar and fasciculus opticus, when lateral hemianopsia occurs (dark
half-fields on the side opposite the lesion). When this lesion is in
the left hemisphere, sensory aphasia also occurs.

(_b_) A lesion involving the caudal part of the thalamus and of the
internal capsule. With such a lesion the motor symptoms consist in
transient paralysis, with usually persistent post-paralytic chorea or
ataxia. The sensory symptoms are more marked, and resemble those
produced by lesion (_a_). It may be determined with some degree of
accuracy whether the lesion be in the thalamus border, or in the
internal capsule near to the nucleus lentiformis by the absence in the
latter case of lateral hemianopsia.

The topography of such lesions is illustrated by Fig. 7.

[Illustration: FIG. 7. Horizontal Section through the Centre of the
Right Cerebral Hemisphere: M, median line; _Nc_, nucleus caudatus;
_Nucleus lent._, nucleus lentiformis with its three segments; _To_,
thalamus opticus; _c. i._, internal capsule with its frontal division,
its bend or knee, and its caudal division. 1, mass of fibres destined
for pons and others forming a part of the corona radiata,
non-pyramidal fibres; 2, knee of the internal capsule, containing
fasciculus from cortical centre for the face to the nucleus of facial
nerve (non-pyramidal fibres); 3, fasciculus for the tongue and throat
to nucleus of hypoglossus, etc. (non-pyramidal fibres); 4, fasciculi
from the pre- and postcentral gyri and the paracentral lobule to the
pyramid of the oblongata (the true pyramidal fasciculus, continued in
the cord as fasciculi, 10 and 11 of Figs. 5 and 6); 5, the caudal
third of the internal capsule, containing fasciculi destined to the
sensory cortical centres.]

(_c_) Lesions of cortical areas connected with fasciculi of the
sensory part of the internal capsule (c. i. 5).

(_α_) Lesion of the cortical area or centre for smell cannot at
present be diagnosticated. From the results of experiments upon higher
mammals we would expect such a centre to be in the cortex of the mesal
gyri of the temporal lobe.

(_β_) Lesions of the cortical centre for taste are equally unknown; it
is probably situated in the meso-basal aspect of the temporal lobe.

(_γ_) Lesions of the acoustic centre are somewhat better known, at
least as far as the function of hearing language-sounds (psychic
hearing) is concerned. A number of recently-published cases[9] have
quite positively {83} shown that the existence of word-deafness
indicates a destructive lesion of the dorsal gyri (more particularly
the first and second) of the temporal lobe (the left always?). The
lesion may also be in the inferior parietal lobule and gyrus
supramarginalis, penetrating deeply enough to injure the acoustic
fasciculus on its way from the internal capsule to the centre.

[Footnote 9: R. W. Amidon, “On the Pathological Anatomy of Sensory
Aphasia,” _New York Medical Journal_, xl. 113, 181.]

(_δ_) The centre for visual impressions is now the best known of any
of the sensory cortical areas. The experimental studies and
pathological results of the last few years have indicated that the
occipital lobe was probably the seat of higher, organized vision (for
form and color). More recent autopsies and re-examination[10] of the
subject point to the cuneus and adjacent gray matter as the visual
centre. The anatomical arrangement is, however, peculiar and complex,
in that each cortical visual area receives impressions from one
lateral half of both retinæ, through the fasciculus opticus.

[Footnote 10: E. C. Seguin, “A Contribution to the Pathology of
Hemianopsia of Central Origin (Cortex-hemianopsia),” _Journal of
Nervous and Mental Diseases_, 1886, No. 1.]

Destructive lesion of one visual centre is therefore indicated during
{84} life by the symptom lateral hemianopsia alone (the dark
half-fields on the side opposite the lesion).

The accompanying diagram illustrates the course of the visual paths
from the eyes to the cortical centres, and the mechanism of production
of various forms of hemianopsia:

[Illustration: FIG. 8. Diagram of Visual Paths, designed to illustrate
specially Left Lateral Hemianopsia from any lesion. _L. T. F._, left
temporal half-field; _R. N. F._, right nasal half-field; _O. S._,
oculus sin.; _O. D._, oculus dexter; _N. T._, nasal and temporal
halves of retinæ; _N. O. S._, nervus opticus sin.; _N. O. D._, nervus
opticus dext.; _F. C. S._, fasciculus cruciatus sin.; _F. L. D._,
fasciculus lateralis dext.; _C._, chiasma, or decussation of fasciculi
cruciati; _T. O. D._, tractus opticus dext.; _C. G. L._, corpus
geniculatum laterale; _L. O._, lobi optici (corpus quad.); _P. O. C._,
primary optic centres, including lobus opticus, corp. genic. lat., and
pulvinar of one side; _F. O._, fasciculus opticus (Gratiolet) in the
internal capsule; _C. P._, cornu posterior; _G. A._, region of gyrus
angularis; _L. O. S._, lobus occip. sin.; _L. O. D._, lobus occip.
dext.; _Cu._, cuneus and subjacent gyri, constituting the cortical
visual centre in man. The heavy or shaded lines represent parts
connected with the right halves of both retinæ. The reader may place
the lesion as he pleases.]

{85} The following diagnostic propositions are applicable to cases
presenting the symptom lateral hemianopsia:

“1. Lateral hemianopsia always indicates an intracranial lesion on the
opposite side from the dark half-fields.

“2. Lateral hemianopsia, with pupillary immobility, optic neuritis, or
atrophy, especially if joined with symptoms of basal disease, is due
to lesion of the tractus opticus or of the primary optic centres on
one side.

“3. Lateral hemianopsia, or sector-like defects of the same geometric
order, with hemianæsthesia and choreiform or ataxic movements of
one-half of the body without marked hemiplegia, is probably due to
lesion of the caudo-lateral part of the thalamus or of the caudal
division of the internal capsule (vide Fig. 7).

“4. Lateral hemianopsia, with complete hemiplegia (spastic after a few
weeks) and hemianæsthesia, is probably caused by an extensive lesion
of the internal capsule in its central and caudal part.

“5. Lateral hemianopsia, with typical hemiplegia (spastic after a few
weeks), with aphasia if the right side be paralyzed, and with little
or no anæsthesia, is quite certainly due to an extensive superficial
lesion in the area supplied by the middle cerebral artery; we should
expect to find softening of the speech-centre, of the motor zone and
of the gyri lying at the extremity of the fissure of Sylvius—viz. the
gyrus supramarginalis, inferior parietal lobule, and gyrus angularis.
Embolism or thrombosis of the middle cerebral artery would be the most
likely pathological cause of the softening.

“6. Lateral hemianopsia, with moderate loss of power in one-half of
the body if associated with impairment of muscular sense, but without
ordinary anæsthesia, would probably be due to a lesion of the inferior
parietal lobule and gyrus angularis, with their subjacent white
substance, penetrating deeply enough to sever or compress the optic
fasciculus in its way caudad to the visual centre.

“7. Lateral hemianopsia, without motor or common sensory symptoms;
this symptom alone, is due, we believe from the convincing evidence
afforded by Cases 28, 29, 41, and 45, to lesions of the cuneus only,
or of it and of the gray matter immediately surrounding it on the
mesal surface of the occipital lobe in the hemisphere opposite the
dark half-fields. Most surgical cases of lateral hemianopsia come at
once or after convalescence within this rule, or No. 6.”[11]

[Footnote 11: Seguin, _op. cit._]

The cortical visual area, as above defined, is supplied by one large
vessel—viz. the occipital artery, a branch of the posterior cerebral.
Embolism or thrombosis of the former vessel is to be thought of as the
probable cause of a suddenly-developed lateral hemianopsia without
paralysis or anæsthesia.

(_ε_) The cortical centre for sensory impressions of muscular sense,
so called, is probably located in the inferior parietal lobule. The
diagnosis of a lesion so placed, in a case presenting along with other
sensory or with motor symptoms marked impairments of muscular sense in
the arm and leg of one side, is justified by a few recent cases.[12]
Spitzka {86} believes that he has clinically and pathologically
demonstrated a basal path (fasciculus) for this mode of sensibility in
the pons and oblongata, dorsad of the pyramidal tracts.[13]

[Footnote 12: Westphal, _Charité Annalen_, vii. p. 446, 1882; Stenger,
_Archiv f. Psychiatrie u. Nervenkrankheiten_, xiii. p. 240, Case
viii.; Wernicke u. Hahn, _Virchow's Archiv_, lxxxvii. p. 325; Ball and
Seguin, _Archives of Medicine_, New York, v. p. 136.]

[Footnote 13: Spitzka, “A Contribution to the Morbid Anatomy and
Symptomatology of Pons Lesions,” _American Journal of Neurology and
Psychiatry_, ii. p. 617 (1883).]

(_ζ_) Lesions of the cortical area for common cutaneous sensibility
cannot be positively recognized at the present time. By exclusion of
the better-known centres, and from experimental data, we may
approximately locate it in the gray matter lying ventrad of (below)
the inferior parietal lobule, extending to the base, and possibly the
mesal aspect, of the temporal lobe, and possibly also on the lateral
aspect of the occipital lobe.

2. LESIONS OF THE KINESODIC SYSTEM OF THE ENCEPHALON.—The kinesodic
system is far better understood, anatomically and physiologically,
than the æsthesodic. Its limits, beginning from the junction of the
cord and oblongata, are as follows: The pyramids, containing the
fibres of the direct and crossed pyramidal fasciculi of the cord (Fig.
5, Nos. 10 and 11), form the meso-basal aspect of the oblongata,
appearing on either side of the median line as two large distinct
bundles of white substance which enter the pons under its projecting
transverse fibres. Within the pons each pyramid is divided into quite
a number of fasciculi more or less separated by fibres of other
systems. Again collected, these bundles constitute a considerable part
of the crus cerebri—its basal middle two-fifths. (The outer or
latero-dorsal one-fifth part of the crus belongs to the æsthesodic
system, the middle (intermediate) two-fifths are the pyramidal fibres,
and the remaining two-fifths, meso-basal part, contain some fibres
from the direct cerebral motor tract destined for the hypoglossal and
facial nuclei, and also large bundles probably derived from the
nucleus caudatus and frontal lobes). As the crus enters the cerebrum
and becomes what we know as the internal capsule, the pyramidal fibres
occupy the bend or elbow of the capsule and part of its caudal segment
(vide Fig. 7).

From this level the fibres of the internal capsule again diverge, as
fasciculi whose physiological independence has been well determined,
going dorsad and frontad to certain gyri of the cerebral cortex where
their fibres join ganglion-cells. Three large fasciculi and
corresponding cortical areas are recognized as constituting the
pyramidal tract, strictly speaking: (1) A fasciculus which extends
frontad to the base of the second frontal gyrus where it coalesces
with the precentral, the centre and fasciculus for movements of the
facial muscles of the opposite side; (2) a fasciculus which extends to
the precentral and postcentral gyri, more especially in their middle
part, constituting the centre and fasciculus for movements of the arm
and hand; (3) another fasciculus which goes dorso-mesad, almost
vertically in the brain, to join the ends of the pre- and postcentral
gyri at the top of the hemisphere, and their continuation upon its
mesal aspect known as the paracentral lobule, centre and fasciculus
for movements of the opposite foot and leg. Besides these three great
cortical areas and their connected fasciculi of nerve-fibres, which go
to make up the pyramidal tract, we recognize (4) a cortical centre for
speech movement of the tongue and lips in the base of the left third
frontal gyrus over the fissure of Sylvius (Broca's speech-centre),
with a connected white fasciculus which passes into the elbow of the
internal {87} capsule, and can be traced (by means of secondary
degeneration) into the inner part of the base of the crus and into the
pons, but not to the pyramid. Another probable centre (5), for coarse
lingual movements and for the various movements of deglutition, is in
the folds of the insula, its fasciculus not joining the pyramid.

[Illustration: FIG. 9. Longitudinal (sagittal) Section through the
Brain, to show the distribution of the fasciculi of the internal
capsule. Fasciculi of motor tract in dotted lines, to fronto-parietal
convolutions. Fasciculi of sensory tract in full lines, to
temporo-parieto-occipital convolutions: _N. C._, nucleus caudatus;
_N. L._, nucleus lentiformis; _T.O._, thalamus opticus. 1, level of
crus cerebri; 2, level of pons; 3, level of oblongata. (This diagram
is to be used in conjunction with Fig. 7.)]

The location of two other motor centres—one for the movement of the
eyeballs in or near the gyrus angularis, and one for vocal laryngeal
movements in the base of the right third frontal gyrus (homologous to
the speech-centre in the left hemisphere), is problematical, or at
least not well enough established to be recognized in a practical
treatise.

Recent experimental researches have shown that to electrical
excitation at least the fasciculi for the tongue, face, arm, and leg
yield the same distinct reaction (isolated muscular contractions) as
do their respective centres or cortical areas; perhaps they are more
excitable.

When these cortical areas are destroyed by disease, or when their
connected fasciculi are severed, secondary degeneration takes place
and extends to the end of the respective bundles, even to the lower
extremity of the spinal cord.

Before leaving the subject of the composition of the kinesodic system
it is desirable to add a few words concerning the decussation of the
pyramids or distribution of the pyramidal tract in the spinal cord. As
is well known, this is double, a small part of the pyramidal bundle
remaining on the same side of the median line, the so-called direct
pyramidal fasciculus or column of Türck (Fig. 5, No. 11) forming the
mesal edge of the anterior column of the cord. The larger part of the
pyramid crosses the median line at the decussation, and enters the
opposite lateral half of the cord, in which it is found as the crossed
pyramidal fasciculus (Fig. 5, No. 10) in the posterior part of the
lateral column, rapidly diminishing in size in the dorso-lumbar part
of the cord. The {88} important point to bear in mind for the study of
monoplegias and of hemiplegia is that the amount of decussation is far
from uniform. This variability was first demonstrated by Flechsig.[14]
He found in a series of sixty fœtuses such variations in the relation
of the crossed and direct fasciculi as 100:0 (complete decussation),
92:8, 84:16, 70:30, 52:48 (nearly semi-decussation, producing equal
fasciculi), 35:65, 10:90 (almost non-decussation).

[Footnote 14: _Die Leitungsbahnen im Gehirn und Rückenmark des
Menschen_, Leipzig, 1876.]

It should also be added that quite certainly the cerebellum, nucleus
caudatus, nucleus lentiformis, and nucleus pontis form parts of the
complete kinesodic system, but we are as yet ignorant of their exact
connections and functions.

With respect to the anterior part of the frontal lobe, forward of the
oblique line A B across Figs. 10 and 11, the study of human cases of
destructive injury and disease would indicate that it is not
associated either with the kinesodic or with the æsthesodic systems.

The SYMPTOMS of lesions of the kinesodic system, particularly of the
pyramidal tract, are exclusively motor, consisting of spasm and
paralysis. Contracture of the paralyzed parts follows the paralysis
after a few weeks if the lesion be a destructive one.

Clinically, the following DIAGNOSES of localization of lesions in this
system are now possible:

(_a_) Lesion of the speech-centre (4) and of its associated white
fasciculus is indicated by intermittent or constant aphasia of the
motor form, with or without paralysis of the face and limbs (on right
side usually).

(_b_) Lesion of the facial centre (1) and of its associated fasciculus
is characterized by the occurrence of spasm or paralysis, or of both
in rapid succession, in the facial muscles; their electrical reactions
remaining normal.

(_c_) Lesion of the brachial centre (2) and of its associated
fasciculus is made known by spasm or paralysis, or by both in
succession, in the hand and arm. In many cases (tumor especially) the
first symptom is clonic convulsive movements of two or more fingers,
extending to other parts of the arm. Such brachial monospasm or
monoplegia is usually accompanied or followed by incomplete
hemiplegia.

(_d_) Lesion of the crural centre (3) in the paracentral lobule and of
its associated fasciculus of white substance is indicated by priority
and predominance of convulsive and paralytic phenomena in the foot and
leg: a crural monospasm or monoplegia exists with or without
incomplete hemiplegia.

The positive diagnosis of these separate localizations is most
feasible in cases of tumors or of cranial injury where the initial
lesion is limited in extent and where the morbid process is for a time
localized. As a rule, localized spasm (Jacksonian epilepsy) without
loss of consciousness is the first symptom, followed after a time by
localized paralysis (always in the same muscular groups); and later
still the symptom-group becomes obscured by the supervention of other
symptoms indicating extension of disease to other parts of the
kinesodic system, or even to the æsthesodic system.

(_e_) Lesion of the insula and adjacent white substance laterad of the
nucleus lenticularis (5) may be suspected from the rapid or sudden
development of symptoms imitating those of acute bulbar paralysis, but
{89} without bilateral paresis of the body and anæsthesia. Aphasia is
very apt to coexist with the bulbar symptoms if the lesions involve
the left insula, whose frontal folds are continuous with the
speech-centre.

Common hemiplegia with contracture, but without anæsthesia, represents
a gross lesion of the kinesodic system, involving several cortical
centres or the motor part of the internal capsule:

(1) A widely-spread lesion of the cortex of the brain, softening of
the motor zone (centres 1, 2, 3, 4) from embolism or thrombosis of the
middle cerebral artery.

(2) Hemorrhage from vessels of the nucleus caudatus and nucleus
lentiformis compressing or destroying the motor segment of the
internal capsule at various levels. More rarely there is a form of
softening or gliomatous growth involving the same parts. Any of these
lesions may be so localized as to destroy only one fasciculus of the
capsule, giving rise to monoplegia.

The limits of the so-called sensory and motor centres or cortical
areas, and the possible localization of lesions in them, will be
better understood by the help of the accompanying diagrams (Figs. 10
and 11, p. 90) of the lateral and mesal aspects of the hemisphere.

B. FOCAL LESIONS OF THE ENCEPHALON.—1. FOCAL LESIONS OF THE CEREBRUM,
OF ITS CORTEX AND SUBJACENT WHITE SUBSTANCE, AND BASAL GANGLIA.—(_a_)
Focal lesions of the frontal lobe produce no specific symptoms, and
cannot be directly diagnosticated unless they extend as far caudad as
the base of the second and third frontal gyri. The forward mass of the
frontal lobe, including the orbital lobule (vide Fig. 10), appears to
be inexcitable and insensitive. Even psychic symptoms do not
necessarily appear after the loss of considerable amount of cerebral
substance from this region. The diagnosis of tumors, abscesses, etc.
in this part of the brain must be made by taking into consideration
the seat of pain, the presence of cicatrices or other etiological
indications, the general signs of the cerebral irritation and
compression, but, after all, usually by exclusion. In some cases
unilateral anosmia is produced.

(_b_) Focal lesions of the caudal part of the frontal lobes, of the
insula, the pre- and postcentral gyri, and other parts of the motor
zone are usually easy of diagnosis. The symptoms of such lesions have
already been detailed when speaking of lesions of the kinesodic
system.

(_c_) Focal lesions of the parietal, temporal, and occipital lobes of
the brain have the characteristic semeiology of lesions of the
æsthesodic system, considered supra.

(_d_) Lesions of the so-called basal ganglia, the nucleus caudatus,
nucleus lentiformis, and thalamus, usually give rise to motor and
sensory symptoms indirectly by pressure upon or destruction of the
segments of the internal capsule which lie between these bodies (vide
Figs. 7 and 9). Lesions of the nuclei caudatus and lentiformis are
thus more prone to produce purely motor symptoms, while sensori-motor
and ataxic symptoms result from lesion of the thalamus.

The symptoms indicating lesions strictly limited (in extent and in
effect) to these ganglionic bodies are at present practically unknown.

(_e_) Lesions (tumors, etc.) of the lobi optici (tubercula
quadrigemina) are productive of early neuro-retinitis and blindness,
of convulsions, and of diffused bilateral incomplete paralysis of the
body, without symptoms {90} of disease at the base of the brain (vide
infra). The diagnosis intra vitam remains of great uncertainty,
inasmuch as other lesions in the median line, involving parts adjacent
to the lobi optici, may give rise to the same symptom-group.

[Illustration: FIG. 10.]

[Illustration: FIG. 11.]

2. FOCAL LESIONS OF THE CEREBELLUM.—(_a_) Lesions strictly limited to
one lateral lobe or hemisphere of this organ do not give rise to any
characteristic symptoms—in some cases, indeed, to no symptoms at all.
When the lesion tends basad, irritating and compressing the subjacent
pons and oblongata on one side, incomplete paralysis appears in the
limbs opposite the lesion, the face usually remaining normal.
Occipital {91} headache, attacks of vomiting, opisthotonos, or intense
subjective stiffness of the back of the neck, with neuro-retinitis,
would strengthen the diagnosis. If the lesion extend laterad, so as to
involve the processus ad pontem (lateral peduncle), a tendency to
rotate while lying or to deviate in walking toward the side of the
lesion may be added.

(_b_) Lesions of the middle lobe, or vermis superior in particular,
may be positively recognized during life. Besides the above-mentioned
general symptoms of cerebellar and bulbar irritation and
compression—viz. occipital headache, cervical stiffness, attacks of
vomiting, neuro-retinitis, and atrophy of the optic nerve—there is a
very characteristic, almost pathognomonic, symptom. This is cerebellar
titubation, miscalled cerebellar ataxia. The patient, whose
equilibrium may be perfect while lying or sitting, upon rising and
attempting to walk does so somewhat like an intoxicated person: the
head and body are bent forward; the arms and hands held out and moved
as balancing weights; the feet are widely separated, the toes
clutching the floor or carpet; the body oscillating somewhat over its
base of support. There are not the wide excursions of the entire body,
the zigzagging, of alcoholic intoxication, nor is there any of the
stamping or jerky step of locomotor ataxia. If the patient be tested
lying or sitting, it is found that neither in the hands nor in the
legs is there a trace of ataxia: muscular strength and sensibility are
long preserved, and the patellar reflex is exaggerated.

3. FOCAL LESIONS OF THE BASE OF THE BRAIN, either within the nervous
substance or springing from the dura, and acting by irritation and
pressure upon various parts of the basal aspect of the encephalic
mass.

(_a_) Diffused bilateral lesions of this class situated frontad of the
crura give rise to more or less distinct symptoms, and a diagnosis is
sometimes possible. (1) Lesions in the vicinity of the sella turcica
and optic chiasm produce symptoms in the optic apparatus very early,
and these remain prominent throughout the illness. These symptoms are,
irregular (at least not lateral) hemianopsia, neuro-retinitis followed
by atrophy of the optic nerve, temporary or permanent paralysis of one
or several ocular nerves. If these exist without symptoms of lesion of
other parts of the brain (reasoning by the process of exclusion), we
may strongly suspect the seat of the lesion to be in the region named.
Other symptoms are paroxysmal headache and occasional vomiting,
epileptiform convulsions (never Jacksonian in distribution), partial
hemiplegia, or general muscular weakness. By such data we were
recently led to the correct localization of a tumor. (2) If the lesion
be farther frontad—_i.e._ strictly in the orbital areas of the basis
cerebri—anosmia, uni- or bilateral, usually with hallucinations of
smell, will be an early symptom, along with neuro-retinitis and
obscure motor and sensory symptoms (headache and convulsions more
especially).

(_b_) Lesions situated caudad of the infundibulum. (1) Bilateral
lesions give rise to symptoms which are the symmetrical duplication on
either side of the face and body of those to be next described as
characteristic of—

(2) Unilateral focal lesions of the base of the encephalon from the
crura caudad to the pyramidal decussation.

In a general way, the symptoms of these lesions are designated as
varieties of crossed paralysis.

Clinically, a crossed paralysis is one in which one or several cranial
{92} nerves show symptoms of irritation or destruction on one side of
the median line, while body symptoms are present on the opposite side.

Physiologically and anatomically, a crossed paralysis is one in which
the lesion is so placed as to affect a cranial nerve (or more than
one) at a point caudad (below) of the decussation of the fibres which
connect its nucleus with the cerebral cortex, or at its nucleus of
origin, or so as to injure the nerve-trunk itself; while at the same
time the lesion affects the main fasciculus of the pyramidal tract
frontad (above) of its decussation, in the crus, pons, or oblongata.

In many cases of crossed paralysis, besides common motor and sensory
symptoms, there is apt to be neuro-retinitis with its consequences.

The chief forms or types of crossed paralysis are:

(_α_) Lesions involving the meso-ventral aspect of one crus cerebri.
The direct symptoms of such a lesion are in the range of distribution
of the motor oculi (N. iii.), such as ptosis, mydriasis, external
strabismus, and heteronymous diplopia; the crossed symptoms are more
or less complete paralysis of the lower part of the face and of the
extremities on the opposite side (hemiplegia). This relatively
frequent form of crossed paralysis we designate as the eye-and-body
type.

(_β_) The lesion occupies the latero-ventral part of the crus. This
rare localization would give rise to direct paralysis of the fourth
nerve, indicated by homonymous diplopia in the lower inner field of
vision; to lateral hemianopsia with dark half-fields opposite the
lesion, from injury to the tractus opticus (vide Fig. 8); and to a
mixed motor and sensory disturbance in the opposite side of the face
and body, without anæsthesia of the olfactory and auditory apparatus.
A very large lesion involving almost the entire crus would probably
also cause direct paralysis of N. iii.

(_γ_) Lesion of the basal part of the pons frontad of an imaginary
transverse line passing through the apparent origin of the trigemini
(NN. v.). Symptoms: A common hemiplegia of the lower face and
extremities on the opposite side with neuro-retinitis and other
general signs of basal disease. The abducens nerve (N. vi.) would in
some cases be involved in its course frontad over the pons, giving
rise to internal strabismus and homonymous diplopia on the same side
as the lesion.

(_δ_) A focal lesion in the caudo-ventral part of the pons—_i.e._
caudad of an imaginary transverse line passing through the trigeminus
roots—gives rise to highly characteristic symptoms. These are: Direct
paralysis of the face, not (?) affecting all the muscles, but without
De R., and common hemiplegia of the limbs on the opposite side.

If the lesion be strictly basal—_i.e._ one springing from the
membranes or bone, the trunks of the sixth and seventh (facial) nerves
are directly injured, and the resulting facial paralysis is of the
peripheral form, affecting all the muscles and yielding De R. The body
symptoms on the side opposite the lesion are less marked.

In the first category of cases, those in which the lesion is in the
substance of the pons, the motor fasciculus from the cortex cerebri to
the nucleus of N. vii. is injured caudad of (below) its theoretical
decussation-point on the middle part of the pons, while the pyramidal
tract is involved frontad of (above) its decussation.

This symptom-group is known as face-and-body type, or as crossed
hemiplegia, strictly speaking.

{93} (_ε_) A lesion so placed laterally in or on the pons as to affect
the origin of one trigeminus (N. v.) will cause, besides motor
symptoms in the face and body (types _γ_ or _δ_), special direct
symptoms—viz. anæsthesia in the distribution of the fifth nerve and
paralysis of the masticatory muscles opposite to the body symptoms.
This is the trigeminus and body type.

Lesions may be so placed ventrad or laterad upon or in the oblongata
as to give rise to other types of crossed paralysis: these are easily
assumed in a theoretical manner, but in practice such cases are
extremely rare, present a complicated semeiology, and are usually not
correctly diagnosticated during the patient's life.


V. Cranio-cerebral Topography.

The study of cerebral localizations from a diagnostic and practical
point of view would be incomplete without a brief reference to the
relations existing between the various gyri of the cerebrum and the
external surface of the head, in order to render more accurate the
estimation of the actual location of cerebral injuries and diseases.

The surgical anatomy of the head with reference to its contents has
been developed with remarkable completeness during the past fifteen
years, chiefly by the researches of Broca, Bischoff, Heftler, Turner,
and Féré. Acting upon these data, a number of surgeons have
successfully trephined the skull for the result of injuries, for
abscess, and even for tumors.

The location of many convolutions and fissures of the cerebrum can be
accurately mapped out upon the surface of the skull, or even upon the
head of the living subject, from the projections of certain lines and
measurements from points thus obtained, as well as from some natural
landmarks. For the projection of these lines the head is placed in a
particular position, as can easily be done when we operate upon a bare
skull, but which can also be approximated when we deal with a living
subject either sitting or lying in bed. The skull or the shaven head
should be so placed and held that a line passing from the alveolar
process of the superior maxilla and through the lowest part (condyles)
of the occipital bone shall be truly horizontal. The greatest care
should be used to determine this line—the alveolo-condyloid plane of
Broca—for upon it all other projections and measurements are based.
This position of the head and the alveolo-condyloid plane (line 1-1)
are represented in Fig. 12.

[Illustration: FIG.12. Topographical Lines applied to the External
Contour of the Head.]

From this line (1-1) a vertical line, or one exactly perpendicular to
the first, is drawn through the external auditory meatus. At the top
of head this line—the auriculo-bregmatic line (A A)—indicates the
bregma or true vertex, which important landmark is to be marked with
carmine or aniline upon the scalp. Upon the top of the head an
imaginary horizontal line (4-4), parallel with the alveolo-condyloid
plane, is projected, and upon it we measure backward a distance of
50 mm. (2 inches), and then draw a second vertical line (B B). At the
point where this line reaches the convexity of the head is the
Rolandic point (R), under which, {94} in average heads, lie the upper
or posterior extremity of the fissure of Rolando, the upper ends of
the pre- and postcentral gyri, and within the longitudinal fissure the
paracentral lobe, which together constitute the cortical centre for
the leg of the opposite side. The Rolandic point, thus determined,
should be distinctly marked upon the shaven scalp.

A third horizontal line is next to be drawn from the external angular
process of the frontal bone backward, parallel with Broca's plane.
This line (2-2), which may be termed the fronto-lambdoid because its
posterior extremity usually passes at or near the upper angle of the
lambdoidal suture, serves for the determination of several important
parts. In the first place, the line (2-2) passes at about 5 mm. above
the upper border of the squamous suture, or through it, and under this
line, mostly {95} parallel to it, are the anterior two-thirds of the
fissure of Sylvius. Secondly, at about 5 mm. above and behind the
intersection of lines (A A) and (2-2) is the inferior extremity of the
fissure of Rolando, bounded by the pre- and postcentral gyri. In the
third place, upon this line (2-2), at a distance of 18 or 25 mm.
behind the external angular process, is the folded part of the base of
the third frontal gyrus or Broca's speech-centre (F 3).

[Illustration: FIG. 13. Topographical Lines applied to Henle's Figure
of the Skull. Location of the Rolandic point. Rolandic line,
motor-centres, and the branches of the middle meningeal artery.]

Having exactly determined and marked the situation of the Rolandic
point and of the inferior termination of the fissure of Rolando above
the ear, these two points are to be connected by a line, which is
represented on the diagram by a black bar. This, the Rolandic line, is
the guide for nearly all operations for the relief of spasm or
paralysis of traumatic origin, or of such as may be caused by tumors,
abscesses, etc. It is surrounded by the so-called motor centres for
the face, arm, and leg (?) as demonstrated by experiments upon animals
and by now numerous autopsies in human cases of injury and disease.

Other relations of interest are the apex of the temporal lobe, a
little beneath the line (2-2) and at about 10 to 15 mm. posterior to
the external angular process of the frontal bone; the situation of the
occipito-parietal fissure, almost immediately under the posterior end
of the line (2-2) at its junction with the lines (E E), which indicate
the posterior extremity of the cerebrum; the anterior end of the brain
being marked off by the line (D D).

{96} Furthermore, for certain purposes the limits of the basal or
central ganglia may be estimated as follows: Their superior limit is
indicated by a horizontal line (3-3) drawn at 45 mm. below the vertex,
their anterior limit corresponding to the head of the nucleus caudatus
by the vertical line (C C), and their posterior limit, the hinder end
of the thalamus, by the vertical line (B B).

Upon the median line at the top of the head an allowance of full
15 mm. should be made for the width of the superior longitudinal sinus
separating the hemisphere.

[Illustration: FIG. 14. The same Topographical Lines applied to the
Left Cerebral Hemisphere in Henle's Skull. The motor centres are
approximately indicated by dotted lines. (The leg centre should be
reduced in size as it lies near to and in the longitudinal fissure.)
The Rolandic line is placed a little behind the fissure for the sake
of clearness.]

The location of the middle meningeal artery, which so often furnishes
the blood that compresses the brain after various injuries to the
head, is surgically of great importance. The course of its two
principal branches is approximately indicated upon Fig. 13 by the
branching lines drawn on the anterior inferior angle of the parietal
and the upper part of the squamous portion of the temporal bone. In
the living subject the main trunk of the artery would be found under
the horizontal line (2-2) a little posterior to the speech-centre,
about 30 mm. behind the external angular process, and in front of the
beginning of the fissure of Sylvius.

Upon the shaven head of a patient seated in a chair or lying in bed
the principal landmarks and relations above defined can be mapped out
with sufficient approximation to accuracy by the use of a ruler to
mark {97} the alveolo-condyloid plane, and a cardboard cut so as to
stand astride the head in the auriculo-bregmatic vertical. A light
wooden apparatus can easily be made to indicate these two lines, while
the remaining measurements can be made with a steel tape-measure, and
the points marked with carmine ink or an aniline pencil.

The value of cranio-cerebral topography is obvious for ordinary
surgical purposes, but it may in the future prove of great utility in
the treatment of cerebral diseases (tumors, abscesses, etc.) by
surgical means. A bold and nearly successful attempt at removing a
tumor of the brain has already been made,[15] and doubtless there are
surgeons who will not hesitate to follow the path thus opened up when
physicians give them a diagnosis of localized tumor or abscess in
parts of the cortex cerebri to serve as a basis.

[Footnote 15: Bennett and Godlee, _The Lancet_, 1884, ii. 1090; 1885,
i. p. 891.]

The indications for trephining or raising bone after cranial injuries,
for the relief of symptoms of cerebral irritation, compression, or
disorganization, may be provisionally stated as follows:

(_a_) When aphasia supervenes immediately or within a few days or
weeks after an injury of the anterior portion of the head on the left
side. It is extremely probable that in the first case a clot or bony
spiculum will be found compressing the speech-centre; in the second
case, that an abscess has formed in or near it (Broca's case).

(_b_) When simple hemiplegia or hemiplegia with hemispasm follows an
injury, however slight, in the temporo-parietal region. If the
paralysis or spasm be limited to one side of the face or to one
extremity, the indication to operate is even stronger. Even if in such
cases the injury be not immediately over the motor area, the surgeon
is justified in exploring that region.

(_c_) In conditions of stupor and coma after cranial injuries,
sometimes without external wound, in which meningeal hemorrhage is the
cause of impending death, the discovery of slight hemiplegia should
justify trephining planned according to the topographic rules above
laid down (Weir's case, 1882). In some cases latent hemiplegia may be
discovered by the presence of an erythematous flush on one buttock and
of a slightly increased peripheral temperature (taken between fingers
or toes).

(_d_) In the very rare cases in which paralytic phenomena are found on
the same side as the evident cranial injury, it would be proper to
trephine on the opposite side of the skull in search of fracture or
hemorrhage, the result of contre-coup.

(_e_) In chronic epilepsy after traumatism of the head the indication
for trephining is present, but it is seldom a specific indication
connected with the subject of localization. Lesions of any part of the
skull and dura may be a cause of epileptic attacks, irrespective of
motor centres.

(_f_) In cases of tumor in the motor centres, if there be not symptoms
of tumors in other parts of the brain (multiple tumors) or of
penetration of the tumor to the central parts of the brain, we believe
trephining not only justified, but demanded in the present state of
science.

Some of the contraindications to trephining may be thus stated:

(_a_) Whenever in apparently favorable cases there are signs of injury
to the base of the brain, such as paralysis of cranial nerves, {98}
neuro-retinitis, and Cheyne-Stokes respiration (although the last
symptom may occur from simple compression).

(_b_) When hemispasm or hemiplegia is accompanied by hemianæsthesia,
thus making it probable that the lesion is deeper and farther back.

It should be added, in conclusion, that these indications and
contraindications are formulated from the standpoint of the
neurologist.


{99}


MENTAL DISEASES.

BY CHARLES F. FOLSOM, M.D.


DEFINITIONS OF INSANITY.—The term insanity conveys quite different
meanings to the community, to lawyers, and to physicians. From the
three points of view its definition has been constantly widening for
the past century. A great part of the alleged recent increase in
insanity is due to the fact that its definition is applied to more
people. Our insane asylums are more quiet and orderly, not only
because of the more humane treatment of the inmates, but largely also
because quieter and less insane people are now sent there than
formerly. Doubtless the mistake is sometimes made of going so far, in
zeal for science and philanthropy, as to make the definition of
insanity too broad; and in a refined civilization the nice adjustment
of complicated social relations, or even a fastidious taste, requires
people to be sent to insane asylums who in simpler states of society
would be cared for at home.[1]

[Footnote 1: The physician in general practice is referred to
Clouston's _Clinical Lectures on Mental Diseases_, and to Part 1 of
Spitzka's _Manual of Insanity_. For those who wish to study insanity
thoroughly the literature is rich and its bibliography is readily
available. Of many parts of the subject only an outline, of course,
can be given within the limits of the present paper.]

The popular idea of insanity is of wild, incoherent, or crazy conduct.
If maniacal, the timid or frightened young girl who would not hurt a
fly, and the tottering, harmless old man if confused and partly
demented, are hurried off to the asylum with the use and show of force
suitable for a desperate criminal, while the victim of overwhelming
delusions, because he seems clear, logical, and collected, is
vigorously defended against the physician's imputation of insanity
until he commits an offence against the laws, when he is fortunate if
he is not treated as a criminal. It is often impossible for judges,
juries, counsel, and even medical experts, to wholly divest themselves
of the popular notions of insanity in cases appealing strongly to the
passion or prejudice of the day. Cases involving the question of
responsibility for crime are decided against science and the evidence
because of certain preconceived notions upon insanity which no amount
of skilled opinion can controvert. Jurors, and less often judges, make
up their minds what a sane man would do under given conditions, and of
what an insane man is capable, judging from the facts within their own
experience; and in forming their decisions it is the act itself, and
not the man, diseased or otherwise, in connection with the act, that
chiefly governs them. Often they are right, not seldom wrong. Strange,
apparently purposeless, illogical, inconsistent action is frequently
attributed to the author of it being insane on that subject, whereas
he may be {100} simply acting from strong impulse or emotion, and may
be by no means insane. On the other hand, because a man knows right
from wrong in the abstract, and can ordinarily behave well, the very
characteristic workings of his insane mind are often seized upon as
unquestionable proof of sanity, even when they admit of no other
explanation to the skilled physician than that of insanity. There is
no doubt of the fact that the whipping commonly used in the treatment
of the insane by the monks several centuries ago put an end to much
insane conduct; and in insane asylums now, in spite of the best
efforts of the medical staff to the contrary, a brutal, bullying
patient is sometimes struck by another patient or an attendant in
return for some unusually exasperating and cruel conduct, with the
result of making him behave well in the future. It is with reference
to this class of cases that the crowd oftenest errs in its definition
of insanity. Society claims a voice in the enforcement of the laws for
its own protection, assuming to know who could control themselves from
crime and who not, and naturally wishes the standard of responsibility
to be kept high. Of course its sympathies and prejudices largely
govern its voice in the matter.

With precisely the same degree of insanity and the same power to
control their actions two murderers may be sentenced, one to death for
an act where the motive and method were those of the criminal, and the
other to an insane asylum for killing a person under circumstances
which are not explainable by sane reasons. The Pocasset Adventist who
sacrificed his loved child, as he thought, by the Lord's command,
would probably have been hanged if he had committed a crime similar to
John Brown's, Wilkes Booth's, Orsini's, or Guiteau's. Sometimes the
accused gets the benefit of the doubt, and sometimes society,
according to the view of the merits of the case taken by the judge in
his charge or by the jury in their verdict.

To the lawyer insanity means only a condition of mind with reference
to certain conduct. An insane man is simply non compos mentis.
Insanity is irresponsibility. The whole question to the lawyer is with
regard to a certain act or series of acts. The lawyer's definition is
narrower than that of the physician. In wills and contracts the course
is usually clearer than when there is a question of serious crime, and
even an insane person in an asylum may be a party to a valid contract
or make a will that will hold in law. It is not necessary that a will
or contract be such as would be made by a just man or a reasonable
man, but simply that it fairly represent the wishes and character of
the man making it, uninfluenced by any insane delusion or prejudice
caused by mental impairment; that the will or contract in itself bear
evidence of a correct appreciation of the circumstances and conditions
of the case; and that the mind be able to act independently enough,
with a reasonable knowledge of the duties of the individual and the
just rights of others. An unsound mind, as defined by the physician,
would cover a large portion of the convicts in our workhouses and
prisons to-day if they could be critically examined, but the lawyers
and courts would not find many of them insane. A man is not insane in
law unless his act is traceable to, or its nature has been determined
by, mental disease affecting his free agency; in other words, unless
insanity caused his act either wholly or in great part.

{101} In the partly irresponsible condition of mind often produced by
grave hysteria, so-called nervous prostration, and the general mental
and moral demoralization often seen in seduced and abandoned women, or
after exhausting illness, or following apparent recovery from cerebral
hemorrhages or embolism, blows upon the head, sunstroke, chronic
alcoholism, syphilis, etc., there may be loss of self-control and a
distinct moral perversion or decided change of character without very
evident mental impairment; and the courts recognize a diminished
capacity, as the result of disease, to appreciate and follow what is
right and just and to avoid what is wrong or unjust, and yet not
complete irresponsibility. In this connection the fact should be borne
in mind that a very little mental disease can make bad people
criminals, and may not take others beyond the bounds of propriety. A
criminal may become insane and be still pretty much the same kind of a
criminal as before. Morality, too, is relative, and many criminals,
like children, know almost nothing of abstract truth, justice, or
virtue, because they have never been taught them; and there are many
cases where the perverse or criminal actions of people may be about
equally explainable on the theory of insanity or wickedness. The
criminal, a creature of his surroundings and associations, may often
not be discriminated from the man with mental disease. Indeed, it is
not difficult to take the philanthropic position that all criminals
are insane because they are not in sympathy with the moral conceptions
of their time, or, to use the fashionable expression of the day,
because they are not in harmony with their environment. Such a view of
crime, however, leads to only one of two conclusions—either that
insanity is no sufficient defence for wilful violation of the laws, or
that all criminals should be treated as persons of unsound mind.

The free agency of the individual is affected or modified in many
different ways by the different diseases of the mind, and the question
of responsibility will often be found to be one of the most perplexing
problems with which the physician has to deal. If well-marked forms of
insanity alone were to be investigated, the matter would be
comparatively a simple one; but such is far from always being the
case. The insane man often commits certain crimes precisely as an
ordinary sane criminal would do the same thing. Often the evidence is
contradictory, the testimony as to previous life and character
conflicting, and the disease of so obscure a stage or type that it is
almost impossible to form a clear opinion. The determination of a
man's degree of free agency is no simple affair which can be decided
in all cases by a few or a few dozen interviews. Not seldom the
mystery remains unsolved after the autopsy. Man's free will is not the
property of any substance which can be demonstrated by chemistry,
physiology, or microscopical research, but it is the result of the
combined action of a whole group of functional activities the very
relations of which to each other are as unknown as their method of
action. No stethoscope or ophthalmoscope can reveal its morbid action,
which can only be inferred indirectly from the operations of the mind.

The cases in which the physician is called upon to define insanity as
the term is used by the lawyers are (1) to secure limitation or
control of an individual's actions, usually by a guardianship; (2) to
control him absolutely in an asylum; (3) to estimate his culpability
or criminality, or {102} his capacity to make a will or contract or to
transact business. It is quite important, therefore, that the medical
man should understand that there may be, as regards some particular
person, a wide difference between medical insanity or mental disease
and legal insanity or irresponsibility. He does most wisely when he
confines his testimony to an explanation of the changes caused by
disease in the particular case, and to the effect of such changes upon
the mind, leaving to the judge's charge and the jury's verdict the
questions of guilt and responsibility.

Insanity may be of congenital origin or slowly developed from early
childhood, but usually it indicates a change caused by disease, so
that the person alleged to be insane must, as a rule, be compared with
himself at some previous time, and not with some ideal standard of
mental health which does not exist. Indeed, if we could measure nicely
no two of us could be fairly held to precisely the same degree of
accountability. The knowledge of right and wrong is not a fair
criterion, as many insane men possess that knowledge well enough in
the abstract. The ability to distinguish right from wrong in the
particular act is possessed by some insane persons whose will and
power of self-control have become so limited by disease that they
cannot avoid what they know to be crime. Delusion overpowering the
mind is sufficient evidence of irresponsibility, but all delusions are
by no means so powerful that they cannot be resisted, and many must be
classed as simply false beliefs or mistaken views which could be, and
should be, controlled. In case, therefore, of alleged delusions not
manifestly insane further evidence of insanity is required, and the
way in which a man believes or does anything may be more of an
indication as to the soundness or unsoundness of his mind than what he
believes or does. A crime committed under the influence of maniacal
delirium, acute delirious mania, epileptic furor, uncontrollable
impulse, alcoholic insanity, or hysterical mental disease will usually
explain itself, while a demented insane person is so characteristic an
object that his crime cannot well be mistaken for that of a
responsible agent.

The different conditions of mind grouped under the general terms moral
insanity, affective insanity, and impulsive insanity are still the
bugbear of jurists, and there is a wide difference of opinion as to
the degree of accountability for actions performed under the influence
of moral perversion with only slight intellectual impairment; but the
degree to which the individual deviates from the path of the law may
depend more upon his training and surroundings than upon his
disease—points which must always be considered in establishing a
definition of insanity in obscure cases. Of two persons whose
circumstances in life, in connection with a certain amount of disease,
have produced as nearly as possible identical morbid mental states, it
now and then happens that the necessary surroundings of the one steady
and support him, while the associations and conditions of life throw
the other still more off his balance. The one is able to sustain the
ordinary relations with the world, the other not.

The intelligent study of mental disease by medical men has resulted in
its being detected at so early a stage and in such a mild form that
its proper treatment might almost be called, when successful, the
prevention of insanity. Cerebro-mental disease, though it be only in
its incipient form, implies to the physician the necessity for medical
treatment; but it {103} is another question whether the disease is
sufficient in amount to impair the power of self-control and will so
as to determine irresponsibility. It is not the doctor's province to
punish for crime, but to treat for disease, and he often forgets that
fact. The various medical definitions of insanity in textbooks and on
the witness-stand do not clearly enough state how far the medical and
how far the forensic meaning of the word is implied. What seem to be
wide differences of opinion regarding responsibility for crime, as
given in the courts, are often due to different ways of stating the
question, and nothing more.

Boileau said that all men are insane, the only difference between them
being the varying degrees of skill with which they are able to conceal
the crack; and Montesquieu, that insane asylums are built in order
that the outside world may believe itself sane. In 1832, Haslam, one
of the first experts in mental disease in England at that time,
testified in court that he had never seen a sane man in his whole
life, adding, “I presume the Deity is of sound mind, and He alone.”

It is impossible to give a satisfactory definition of insanity, to
draw any hard and fast line on one side of which we should put all the
sane, and on the other all the insane. It is not possible to divide
insanity from sanity by a single criterion, such as the existence of
delusions, inasmuch as many sane people have very curious delusions;
for instance, Sir William Blackstone's belief in witchcraft, as stated
in his _Commentaries on the Laws of England_; Martin Luther's
assertion that he saw the devil and threw an inkstand at him at a time
when a belief in a personal devil was required by the canons of the
Church of England; Napoleon's faith in his star; the common belief of
the French generals that Joan of Arc's hallucinations were divine
messages. Insane delusions have been defined as false beliefs,
impossible from the nature of things or the circumstances of the case,
according to general belief. One can only judge of each case and each
person by the conditions attending them. A belief consistent with one
person's whole life and character might indicate such a change in
another as to be a mark of insanity.

Hallucinations—“psycho-sensorial disturbances characterized by
sensations perceived when the exercise of the sense has not been
determined by any external excitation”—are characteristic of many
conditions of disturbed health besides insanity; and the same is true
of illusions—erroneous interpretations of sensations actually
perceived. In both cases the existence of insanity is determined by
the fact whether or not the erroneous impressions are corrected by the
judgment. An important point is to consider most carefully every
unnatural, strange, or unexplained action, whether deliberate or from
impulse, particularly in the large class of eccentric, ill-balanced,
or weak-minded persons on the border-line between sanity and insanity.
There are people who at one time seem to belong to the sane and at
another to the insane class. Baillarger states that the essential
element of insanity is loss of free will. Ball of Paris describes an
insane man as one who, in consequence of a profound disturbance of the
intellectual faculties, has lost more or less completely his free will
(liberté morale), and has ceased thereby to be responsible to society
for his actions.

Bucknill describes insanity, in his Sugden prize essay, as “a
condition of the mind in which a false action of conception or
judgment, a {104} defective power of the will, or an uncontrollable
violence of the emotions and instincts has been separately or
conjointly produced by disease.” Maudsley's definition is, “Insanity
is, in fact, disorder of brain producing disorder of mind; or, to
define its nature in greater detail, it is a disorder of the supreme
nerve-centres of the brain—the special organs of mind—producing
derangement of thought, feeling, and action, together or separately,
of such degree or kind as to incapacitate the individual for the
relations of life.... Mind may be defined physiologically as a general
term denoting the sum-total of those functions of the brain which are
known as thought, feeling, and will. By disorder of the mind is meant
disorder of those functions.”

Bucknill considers insanity a disease of the brain affecting the
integrity of the mind. Maudsley calls it a disorder of the mind of
such a degree as to incapacitate one for the ordinary relations of
life, implying that there may be certain deviations from the condition
of sound mind which do not constitute insanity. Tuke's definition is
that “insanity consists in morbid conditions of the brain, the result
of defective formation or altered nutrition of its substance, induced
by local or general morbid processes, and characterized especially by
non-development, obliteration, impairment, or perversion of one or
more of its psychical functions.” Instead of itself being a disease,
insanity, properly speaking, is a symptom of diseases which under
varying manifestations probably affect different functions of the
brain—at least they affect the brain in different ways.

As Krafft-Ebing says, “It is a logical, self-evident proposition that
the organ whose function under normal conditions is to bring about all
mental processes must be the seat of changes when these functions are
disturbed;” and Schüle adds, “The study of disturbances of the mind
involves the changes of the normal mental functions produced by
disease.... Mental diseases are brain diseases, but they are more than
that.” The normal action of the mind is a strange combination of
reason and impulse, varying greatly in different persons, and in the
same person at different times and under varying influences. The
relations of the one to the other, and their influence on action,
often change, under varying conditions and circumstances, in sane
persons, but still more in the insane.

Lord Bramwell once said that insanity is strong but not conclusive
evidence of innocence; and Lord Blackburn has stated that the jury
must decide in each individual case whether the disease of the mind or
the criminal will was the cause of the crime. The position of Sir
James Stephen in his _History of the Criminal Law in England_ best
states the most recent views of irresponsibility—namely, that “no act
is a crime if the person who does it is, at the time when it is done,
prevented either by defective mental power or by any disease affecting
his mind from controlling his own conduct, unless the loss of the
power of control has been produced by his own default.” He says that a
man laboring under such a defect of reason that he does not know that
he is doing what is wrong may be defined as one deprived, by disease
affecting the mind, of the power of passing a rational judgment on the
moral character of the act which he meant to do. There are persons too
insane to make a valid will by virtue of a single delusion, whose
right to vote, under the law prohibiting the insane from voting, would
not be questioned. Another {105} might not be held responsible for
crime, and still make a contract involving the rights of others
besides himself that would hold in law.

Bucknill's recent medico-legal definition of insanity is,
incapacitating weakness or derangement of mind produced by disease;
meaning, in criminal cases, inability of abstaining from the criminal
act, which would be expressed by Lord Bramwell's test, Could he help
it? Bucknill suggests as an amendment to the law of England that no
act is a crime if the person who does it is at the time incapable of
not doing it by reason of idiocy or of disease affecting the mind.

Any definition of insanity would be incomplete without the statement
of Hughlings Jackson's view, that disease only produces negative
mental symptoms answering to dissolution, and that all elaborate
positive mental symptoms (illusions, hallucinations, delusions, and
extravagant conduct) are the outcome of activity of nervous elements
untouched by any pathological process; that they arise during activity
on the lower level of evolution remaining; that the insane man's
illusions, etc. are not caused by disease, but that they are the
outcome of activity of what is left of him (of what disease has
spared), of all there then is of him. His illusions, etc. are his
mind.

THE CLASSIFICATION OF MENTAL DISEASES.—There is no universally
accepted classification of mental diseases, and the same terms even
are used by different writers to convey entirely different meanings.
The classification according to the causes of insanity was suggested
by Morel of Paris, and fully elaborated by Skae of Edinburgh, as
follows: (1) Moral idiocy; (2) intellectual idiocy; (3) moral
imbecility; (4) intellectual imbecility; (5) epileptic insanity; (6)
insanity of masturbation; (7) insanity of pubescence; (8) hysterical
mania; (9) amenorrhœal mania; (10) post-connubial mania; (11)
puerperal mania; (12) mania of pregnancy; (13) mania of lactation;
(14) climacteric mania; (15) ovario- and uteromania; (16) senile
mania; (17) phthisical mania; (18) metastatic mania; (19) traumatic
mania; (20) syphilitic mania; (21) delirium tremens; (22) dipsomania;
(23) mania of alcoholism; (24) post-febrile mania; (25) mania of
oxaluria and phosphaturia; (26) general paralysis; (27) epidemic
mania; (28) idiopathic sthenic mania; (29) idiopathic asthenic mania.

In a large proportion of cases the causes of insanity are so many and
so complex that it is not within human power to say which of a number
has been the most important, or the assigned and classified cause may
be only an accidental complication or the most striking, but by no
means most potent, cause.

The classification, according to the functions interfered with, is
that adopted by Maudsley and by Bucknill. According to Bucknill, we
have

(1) Insanity of the intellect or ideas: Idiocy, imbecility, dementia,
delusional insanity, monomania, mania.

(2) Insanity of the feelings and the moral sentiments: Moral
imbecility, moral insanity, melancholia, religious insanity,
hypochondriacal insanity, nostalgic hypochondriacal insanity,
exaltation regarding religion, pride, vanity, ambition.

(3) Insanity of the propensities, instincts, or desires: Mania,
homicidal mania, suicidal mania, erotomania, dipsomania.

Maudsley's classification, according to the faculties thought to be
affected, {106} is also inconsistent: I. Affective insanity: (1)
Simple mania; (2) simple melancholia; (3) moral insanity. II.
Ideational insanity: (1) General (acute and chronic mania and
melancholia); (2) partial (monomania and melancholia); (3) dementia
(primary and secondary); (4) general paralysis; (5) idiocy and
imbecility.

The classification according to symptoms is most generally adopted,
being used, more or less modified, in Germany, generally in France,
and more commonly than any other in this country and in England. It
has been suggested by different writers in a dozen different forms,
differing only in details. Griesinger's is as follows:

(1) States of mental depression: Hypochondriasis; simple melancholia;
melancholia with stupor; melancholia with destructive tendencies;
melancholia with persistent excitement of the will or impulse (moral
insanity).

(2) States of mental exaltation: Mania; monomania.

(3) States of mental weakness: Chronic mania; dementia; idiocy;
cretinism.

As important complications of insanity he places general paralysis of
the insane and epilepsy, and various disorders of sensation and
movement, such as convulsive gait, general cramps, choreic movements,
hyperæsthesia of the skin, etc.

A classification according to the morbid condition of the brain has
thus far proved unsuccessful. Up to the present time this remains
largely a field of speculation, and even with the immense progress of
the past dozen years it is a subject upon which there is now little
definite to be said. Voisin's system is purely visionary—namely: I.
Idiopathic insanity, due to vascular spasm. II. Insanity dependent on
brain lesions: Congestive insanity; insanity from anæmia; atheromatous
insanity; insanity from brain tumors. III. Insanity from alterations
of the blood: Diathetic insanities; syphilitic insanity.

In basing his nomenclature on the clinical history of the various
forms of insanity, Clouston makes his classification as follows:

(1) States of mental depression (melancholia, psychalgia): (_a_)
Simple melancholia; (_b_) hypochondriacal melancholia; (_c_)
delusional melancholia; (_d_) excited melancholia; (_e_) suicidal and
homicidal melancholia.

(2) States of mental exaltation (mania, psychlampsia): (_a_) Simple
mania (folie raisonnante); (_b_) acute mania; (_c_) delusional mania;
(_d_) chronic mania.

(3) States of regularly alternating depression and exaltation (folie
circulaire, psychorhythm, folie à double forme, circular insanity,
periodic mania, recurrent mania).

(4) States of fixed and limited delusion (monomania, monopsychosis):
(_a_) Monomania of pride and grandeur; (_b_) monomania of unseen
agency; (_c_) monomania of suspicion.

(5) States of mental enfeeblement (dementia, amentia, psychoparesis,
congenital imbecility, idiocy): (_a_) Secondary (ordinary) dementia
(following acute or subacute disease, ending in chronicity); (_b_)
primary enfeeblement (imbecility, idiocy, cretinism), the result of
deficient brain development or of brain disease in very early life;
(_c_) senile dementia; (_d_) organic dementia (the result of organic
brain disease).

(6) States of mental stupor (stupor, psychocoma): (_a_) Melancholic
{107} stupor (melancholia attonita); (_b_) anergic stupor (primary
dementia, dementia attonita); (_c_) secondary stupor (transitory,
after acute mania).

(7) States of defective inhibition (psychokinesia, hyperkinesia,
impulsive insanity, volitional insanity, uncontrollable impulse,
insanity without delusion): (_a_) Homicidal impulse; (_b_) suicidal
impulse; (_c_) epileptiform impulse; (_d_) animal impulse; (_e_)
dipsomania; (_f_) pyromania; (_g_) kleptomania; (_h_) moral insanity.

(8) The insane diathesis (psychoneurosis, neurosis insana, neurosis
spasmodica).

Some of the German mental pathologists have endeavored to combine in
their classification the clinical history with the little that is
known of its morbid anatomy. Meynert has gone so far in this direction
as to have constructed an ideal mental pathology belonging to the
sphere of brilliant speculation rather than exact science. Schüle has
well summarized our knowledge on these points, as follows:

I. States of mental defect or degeneration. (1) States of mental
defect: (_a_) Microcephalism; (_b_) idiocy. (2) States of mental
degeneracy, chiefly as the result or further development of (_a_)
Hereditary insanity, impulsive insanity, moral insanity; (_b_)
insanity from the severe neuroses, epileptic insanity, hysterical
insanity, hypochondriacal insanity; (_c_) periodic and circular
insanity.

II. Insanity in persons of full mental and physical development:

(_A_) The cerebral neuroses causing mental disease, affecting
primarily the mind alone (psychoneuroses): (1) The acute or subacute
typical cerebral neuroses in healthy neurotic persons and with a
vaso-motor origin: (_a_) Primary form, melancholia, melancholia
agitata, simple mania; (_b_) secondary form, chronic mania and
monomania, dementia. (2) The chronic cerebral neuroses giving rise to
mental disease founded on degeneration and of neurotic origin
primarily (delusional insanity): (_a_) Primary monomania of
persecution, with a condition of pure mental depression or with
exaggerated and exalted ideas; (_b_) delusional insanity, strictly
speaking, psycho-convulsive form (maladie du doute), psycho-cataleptic
form (delusional insanity attended with anomalies of sensation).

(_B_) The organic mental diseases affecting the psychic functions
(cerebro-psychoses), differing from (_A_) chiefly in being
deeper-seated: (1) With motor symptoms of excitement (acute mania):
(_a_) Mania furiosa (including mania transitoria); (_b_) mania gravis;
(_c_) acute delirious mania. (2) With motor neuroses and symptoms
resembling catalepsy, tetanus, and anergic stupor, or the various
forms of Spannungsneurosen: (_a_) Melancholia attonita; (_b_)
delusional stupor; (_c_) primary dementia (stupor), acute and chronic.
(3) With progressive paralysis, the typical form of paralytic
dementia.

(_C_) The distinct lesions of the brain, giving rise secondarily to
psychical disturbances. The modified paralyses or cerebral diseases in
which dementia and paralysis are both observed clinically: (_a_)
Meningo-periencephalitis, chronic and subacute; (_b_) pachymeningitis
and hæmatoma; (_c_) diffuse encephalitis with sclerosis, without
mental excitement and with mental excitement; (_d_) diffuse
encephalitis with local softening, apoplexy, capillary aneurisms in
groups or singly, multiple sclerosis; (_e_) diffuse encephalitis
arising from foreign growths in the brain; (_f_) chronic {108}
periencephalitis, with previous tabes dorsalis; tabic paralysis: (_g_)
primary atrophy of the brain, with accompanying spinal tabes, tabic
dementia; (_h_) syphilitic encephalitis, with disturbances of the
mind.

Krafft-Ebing's classification is as follows:

_A_. Mental Diseases of the Normal Brain.—I. Psychoneuroses: 1.
Primary, curable diseases: _a_, Melancholia—_α_, Simple melancholia;
_β_, melancholia with stupor; _b_, Mania—_α_, Maniacal exaltation;
_β_, acute mania; _c_, Stupidity (primary dementia) or curable
dementia; _d_, confusional insanity (Wahnsinn). 2. Secondary,
incurable diseases: _a_, Chronic delusional insanity; _b_, terminal
dementia—_α_, with agitation; _β_, with apathy.

II. Conditions of Mental Degeneration.—_a_, Constitutional affective
insanity (folie raisonnante); _b_, moral insanity; _c_, primary
monomania—_α_, With delusions of persecution; _β_, with delusions of
ambition; _d_, with imperative conceptions; _e_, insanity from
constitutional neuroses—_α_, epileptic; _β_, hysterical; _γ_,
hypochondriacal; _f_, periodic insanity (folie circulaire).

III. Diseases of the Brain with Mental Disturbances
Predominating.—_a_, Paralytic dementia; _b_, cerebral syphilis; _c_,
chronic alcoholism; _d_, senile dementia; _e_, acute delirium.

_B_. Conditions of Arrested Mental Development.—Idiocy and cretinism.

Krafft-Ebing agrees with Schüle in dividing mental diseases into two
classes—those of a degenerative nature arising from the development of
an hereditary or congenital neurotic tendency, or from injury, sexual
or alcoholic excess, etc., and those which occur from what may be
called accidental causes in otherwise healthy persons, in whom mental
disease would not be anticipated, and from which the late Isaac Ray
said that, with sufficient exciting cause, no one has any privilege of
exemption. The essential distinction between them was pointed out by
Moreau and Morel, and is best stated by Krafft-Ebing:

Degenerative insanity is a constitutional disease arising from slight
exciting causes, even physiological conditions (puberty, menstruation,
the puerperal state, climacterium), but for the most part from
pathological conditions, chiefly hereditary predisposition, injury to
the head, acute disease, etc., occurring during development of the
sensitive brain, forming often the last in a series of neuropathic
disorders, such as spinal irritation, hysteria, hypochondria,
epilepsy. The tendency to recovery is slight, and generally there is
only temporary return to the primary condition. Relapses and
progressive development of graver forms of disease are common. There
is progressive hereditary mental degeneration or a strong tendency to
appear in descendants in progressively severer form. All forms of the
psychoneuroses occur, but of severe type and irregular course, with
sudden and rapid changes in the character of the disease, which does
not follow any particular course and cannot be definitely classified,
rarely ending in dementia, and often lasting in some form through
life. The tendency to periodicity is strong. Delusions are chiefly
physio-pathological as direct creations of the diseased brain,
entirely without apparent cause, to the astonishment of the person and
independent of his frame of mind at the time. They appear and
disappear, to be replaced by morbid impulses or mental weakness.
Delusions are strange, mysterious, monstrous, without possible
explanation from the {109} nature of the disease. There is, for the
most part, an inseparable transition from pathological predisposition
to actual disease, with a strange mixture of lucidity and diseased
mental perversion. Acts are often from impulse. There are sudden
outbursts or short attacks; as, for instance, in periodic, hysterical,
and epileptic insanity.

In psychoneuroses developed in persons of previously normal
brain-function heredity is only a latent predisposing cause. The
tendency is to recovery; relapses are infrequent. They are not so
readily transmitted to later generations. The disease follows the
course of some well-defined type. There is not a tendency to
periodicity. Delusions arise chiefly from psychological sources as the
result of diseased mental conditions. They are usually not early
symptoms, and in general they correspond with the prevailing state of
the mind. Delusions correspond with the mental state. The change from
health to disease is well defined.

These are the main features of the two classes of mental disease, but
the line between them is not a hard and fast one, and it is not seldom
impossible to place a particular diseased person definitely in the one
or the other.

The objection to all of the classifications of insanity now in use,
that they have not an accurate scientific basis, and that a diagnosis
must often be delayed or changed as symptoms develop, applies,
although in a less degree, to other diseases than of the mind.

HISTORY.—The history of insanity is probably as old as the human race,
although its rarity among savage nations at the present day, and its
greatest prevalence where there are the widest extremes of wealth and
poverty, indicate that it is essentially a disease of the high
civilizations. It is found even in the lower animals. It is described
in the early writers on medicine from Hippocrates and Plato down. The
ancient Egyptians had temples dedicated to Saturn, where they cared
for the insane with music and dancing. The Greeks and Romans treated
the sick, and probably some of the insane, in rooms adjoining their
temples. The monks of Jerusalem built an asylum for the insane of
their number in the sixth century. There were several asylums in
existence among the Moors in the seventh century, and it is thought
that at the time of their invasion of Spain they introduced them into
Western Europe. The monks, who were the chief depositaries of medical
knowledge in the Middle Ages, treated the insane, as they did to a
less extent each other, by flagellations, until St. Vincent de Paul
and the Knights of Malta proclaimed insanity a disease and treated it
as such. It would be idle to estimate how many were put to the rack,
burned, and otherwise maltreated as possessed of the devil or as
witches—how many were called prophets or saints.

As late as the last quarter of the last century the insane, when not
starving or neglected, were for the most part confined in jails and
poorhouses or kept in chains. In Scotland a farmer reputed to be as
large as Hercules was said to cure them by severity. In England the
practice of exhibiting the inmates of Bethlehem Hospital (Bedlam) to
the populace for a small fee was given up only in 1770. In Paris a few
of the insane were treated in general hospitals, and the asylums were
considered as receptacles for chronic cases, where the attendants,
often convicts serving out their time, were allowed to whip them. Van
Helmont recommended the sudden immersing of the insane into cold water
and keeping them {110} there for several moments—a remedy brought even
to this country. Rush says, as late as 1812, that by the proper
application of mild and terrifying modes of punishment (the strait
waistcoat, the tranquillizer chair, privation of customary pleasant
food, pouring water under the coat-sleeve so that it may descend into
the armpits and down the trunk of the body, the shower-bath continued
for fifteen or twenty minutes, and a resort to the fear of death)
chains will seldom, and the whip never, be required to govern mad
people. The intelligent ideas of the Egyptians, Greeks, and Romans
regarding insanity were degraded first by the Jewish, and then by the
Goth and Vandal, influences in Europe, until, after sixteen centuries
of perverse teaching, the stimulus given to all medical work by John
Hunter and Bichat, and to humanity by John Howard, prepared the way in
France for the philosopher-physician Pinel and his pupil the clinical
observer Esquirol. In Italy, Chiarruggi; in Germany, Langemann; in
England, Tuke; in America, Rush,—began the reform. Up to that time the
metaphysicians had nearly usurped the study of insanity. Hospitals for
the treatment of curable mental disease were built in Germany besides
the asylums for the chronic insane, but still sudden plunges in water,
rapid whirling around, and all sorts of shocks and surprises formed a
part of the treatment, while Heinroth, Pinel's leading pupil in
Germany, thought that all insanity began in vice, that its source was
a conscious neglect of God's will, that its best treatment consisted
in a pious life, and the only means of prevention to be in the
Christian religion. From that time to this, especially since the
metaphysical theory of insanity was abandoned, and more particularly
during the last quarter of this century, during which the theory of
physical disease as the basis of insanity has prevailed, there has
been a great and rapid advance in our knowledge of the pathology and
treatment of the diseases of the mind, so as to place them beyond the
pale of mystery, but on the same footing with other diseases, to be
treated on the general principles of common sense and medical science.

PREVALENCE.—It would be idle to attempt to say what proportion of the
population was insane at any time or in any country of the world until
the most recent years. In Massachusetts in 1820 there were under
custody in the one insane asylum in the State 50 patients, or 9.55 in
each 100,000 of the population. This number had increased to 11.34 to
every 100,000 people in 1830, 61.99 in 1840, 84.97 in 1850, 97.90 in
1855, 122.17 in 1860, 121.24 in 1865, 134.83 in 1870, 138.50 in 1875,
and 177.67 in 1880, in six State, one county, one city, one corporate,
and six private asylums. The number of the insane in asylums had
increased sixty times, and the rate proportionately to the population
had augmented more than eighteen times.

In the United States, even after due allowance for the fact that the
enumeration of the insane was quite complete for the first time in
1880, the following table shows a recent large increase in their
numbers. Of the 91,997 insane reported in 1880, there were 40,942 in
lunatic hospitals, 9302 in almshouses without special departments for
the insane, and 417 in jails. There are no statistics of the insanity
prevalent among the 265,565 Indians living in tribal relations by the
enumeration of 1883.

{111}               CENSUS OF THE UNITED STATES.
                           _Population_.
  -----+------------+------------+-----------+------------+-----------
  Year.|   Total.   |   Native.  |  Foreign. |   White.   | Colored.
  -----+------------+------------+-----------+------------+-----------
  1860 | 31,443,321 | 27,304,624 | 4,138,697 | 26,922,537 | 4,441,830
  1870 | 38,558,371 | 32,991,142 | 5,567,229 | 33,589,377 | 4,880,009
       |            |            |           |            |       [2]
  1880 | 50,155,783 | 43,475,840 | 6,679,943 | 43,402,970 | 6,580,793
       |            |            |           |            |       [3]
       |            |        _Insane_.       |            |
  1860 |     24,042 |     17,399 |     5,784 |     23,276 |       766
  1870 |     37,432 |     26,205 |    11,227 |     35,610 |     1,774
  1880 |     91,997 |     65,651 |    26,346 |     85,840 |     5,998
       |            |            |           |            |
       |            |        _Idiotic_.      |            |
  1860 |     18,930 |     17,685 |     1,125 |     16,952 |     1,978
  1870 |     24,527 |     22,882 |     1,645 |     21,324 |     3,188
  1880 |     76,895 |     72,888 |     4,007 |     67,316 |     9,490
       |            |            |           |            |       [4]
  -----+------------+------------+-----------+------------+-----------

[Footnote 2: Unknown, 55.]

[Footnote 3: Unknown, 148.]

[Footnote 4: Unknown, 1.]

  INSANE AND IDIOTIC POPULATION IN THE UNITED STATES BY THE CENSUS OF
                               1880.[5]

  --------+---------+----------+---------+--------+---------+--------
          |         |          |         | Negro  |         |
   Total. | Native. | Foreign. |  White. |  and   | Native  | Foreign
          |         |          |         | Mixed. | White.  |  White.
  --------+---------+----------+---------+--------+---------+--------
          |         |            Insane.          |         |
   91,997 |  65,651 |   26,346 |  85,840 |  5,998 |  59,600 |  26,240
          |         |          |         |        |         |
          |         |            Idiotic.         |         |
   76,895 |  72,888 |    4,007 |  67,316 |  9,490 |  63,314 |   4,002
          |         |          |         |        |         |
          |         |        Of unsound mind.     |         |
  168,892 | 138,539 |   30,353 | 153,156 | 15,488 | 122,914 |  30,242
          |         |          |         |        |         |
          |         |    Population to 1 insane.  |         |
      545 |     662 |      253 |     505 |  1,097 |     618 |     250
          |         |          |         |        |         |
          |         |    Population to 1 idiotic. |         |
      652 |     596 |    1,666 |     644 |    693 |     581 |   1,642
          |         |          |         |        |         |
          |         Population to 1 of unsound mind.        |
      297 |     314 |      220 |     283 |    425 |     299 |     217
  --------+---------+----------+---------+--------+---------+--------

[Footnote 5: Total population, 50,155,783; native, 43,475,840;
foreign, 6,679,943; white, 43,402,970 (unknown, 148); negro and mixed,
6,580,793; native white, 36,828,640; foreign white, 6,574,330;
civilized Indians, 66,407; Chinese, 105,465. Among the Indians there
were 53 insane, 84 idiotic, 137, or 1 in 485, distributed over 30
States and Territories; among the Chinese, 105 insane, 5 idiotic, 110,
or 1 in 959.]

In England and Wales in 1860, with a population of 19,902,713, there
were known to the lunacy commissioners 38,058 persons of unsound mind,
including the insane, idiots, and imbeciles, or 523 persons to 1 of
unsound mind. In 1870 this number had increased to 1 in 411. It seems
by the census of 1871, however, that there were 39,567 insane and
29,452 idiots and imbeciles, in all 69,019 of unsound mind, or 1 in
330 of the population. In 1880, with a population of 25,708,666, there
were known to the lunacy commissioners 71,191 persons of unsound mind,
or 1 to 362 of the population. The census returns of 1881 are not
available. The most recent statistics in Ireland indicate 1 person of
unsound mind to each 260 of the population by the census, and in
Scotland 1 in 362, according to the returns (not complete) to the
lunacy commission.

In the following list, after the original States, of which Vermont,
Maine, and West Virginia were parts later separated, the others are
given in the order of their having been admitted as States to the
Union, and finally the eight Territories. The States maintaining
slavery up to the time of the civil war are printed in italics. The
large proportion of insane persons in the District of Columbia is due
to the fact that the {112} government hospital contains so many
officers and privates who really belong to the several States; and in
California the insane hospitals have been used to a considerable
extent by the adjoining States and Territories.

By the United States census of 1880 there was 1 person of unsound mind
(insane and idiotic) in the United States to each 297 of the
population; in the _District of Columbia_, 1 in 169; Connecticut, 1 in
245; _Delaware_, 313; _Georgia_, 373; _Maryland_, 294; Massachusetts,
249; New Hampshire, 197; New Jersey, 326; New York, 251; _North
Carolina_, 270; Pennsylvania, 289; Rhode Island, 301; _South
Carolina_, 368; _Virginia_, 290; Vermont, 182; _Kentucky_, 261;
_Tennessee_, 259; Ohio, 232; _Louisiana_, 457, Indiana, 239;
_Mississippi_, 415; Illinois, 330; _Alabama_, 337; Maine, 226;
_Missouri_, 324; _Arkansas_, 371; Michigan, 328; _Florida_, 433;
_Texas_, 414; Iowa, 334; Wisconsin, 305; California, 286; Minnesota,
416; Oregon, 312; Kansas, 478; _West Virginia_, 263; Nevada, 1270;
Nebraska, 561; Colorado, 1104; Arizona, 1263; Dakota, 839; Idaho, 836;
Montana, 529; New Mexico, 434; Utah, 481; Washington, 412; Wyoming,
3464.

The proportion of the enumerated insane in asylums was—District of
Columbia, 90.6 per cent.; Connecticut, 39; Georgia, 36.8; Maryland,
49.1; Massachusetts, 60.1; New Hampshire, 27.1; New Jersey, 67.8; New
York, 57.2; North Carolina, 13.2; Pennsylvania, 36.1; Rhode Island,
57.3; South Carolina, 38.2; Virginia, 45.5; Vermont, 44.7; Kentucky,
50.7; Tennessee, 16; Ohio, 48; Louisiana, 44.9; Indiana, 26;
Mississippi, 33.7; Illinois, 42.7; Alabama, 24.5; Maine, 26.1;
Missouri, 40.7; Michigan, 41.5; Florida, 30; Texas, 22.3; Iowa, 37.8;
Wisconsin, 48.6; California, 80.3; Minnesota, 61.8; Oregon, 65.5;
Kansas, 31.9; West Virginia, 40.1; Nebraska, 38; Colorado, 34.3. In
Arkansas and in Nevada there was no insane asylum in 1880, and in
Delaware the insane were sent to a Pennsylvania asylum or to the
almshouse. In the Territories the provisions for the insane are very
incomplete.

The statistics just given indicate an enormous increase in the numbers
of the insane who become a public charge, and the figures gathered
from all countries prove conclusively that more insane people are
known to be in existence proportionately to the population from decade
to decade. The question naturally arises, Is insanity increasing as
fast as appears at first sight to be the case, or is the increase
apparent rather than real?

In the first place, the definition of insanity has so widened of later
years as to include vastly greater numbers of the population than
hitherto. The nice adjustment of social relations in a high order of
civilization and greater medical skill make insanity easier of
detection. Large numbers of persons now confined would have been
considered far from being fit subjects for insane asylums a half
century ago. Again, it is hardly a generation ago that we began taking
proper care of the insane. Some States have hardly commenced yet, and
even in the oldest parts of our country many of unsound mind are kept
neglected and squalid in town almshouses or county jails. Wherever
humanity has demanded improved accommodations for the insane they have
accumulated enormously, from the simple fact that they are protected
like children, and kept from dying of neglect, suicide, and
exhaustion. In other words, science and humanity have prolonged their
lives of illness, in some cases to as much as tenfold their natural
length if they had been left to themselves, even where nothing can be
done but to prolong their misery. The {113} more intelligent views now
held of insanity as a physical disease rather than a family disgrace
have led people to be less backward in reporting their insane
relatives as such, while the increasing number of insane asylums and
the growing confidence in them have brought many of the insane to
notice who formerly would have been concealed in attics and cellars
and never mentioned.

Whether or not more persons become insane each year in proportion to
the population we have no methods of determining statistically. The
mortality returns in Massachusetts for the last five census years show
that the deaths from insanity, paralysis, apoplexy, softening of the
brain, and unspecified diseases of the brain, including cephalitis,
were 12.06 per 10,000 inhabitants in 1860, 14.39 in 1865, 14.95 in
1870, 16.42 in 1875, and 17 in 1880; which would probably indicate an
increase, even after allowing for a considerable source of error due
to inaccurate diagnoses, imperfect registration, and the influx of a
large foreign population. It is claimed that the table on page 111
indicates a direct importation of insane persons from Europe. It is
certainly a curious fact that the proportion of idiots and of the
insane differs so little in the native population, and that among
foreigners the idiots, who could not easily be sent here without being
detected and sent back, are less than one-sixth of the number of their
insane. But it is also true that the amount of insanity among
strangers in a foreign land would naturally be greater than among
those who are at home.

The prevalence of insanity as compared with other diseases at the
present time may be fairly estimated from the statistics of
Massachusetts for twenty years, where there were 604,677 deaths
reported, including 2145 from suicide, 1995 from insanity, 1838 from
delirium tremens and intemperance. The reported deaths from pulmonary
consumption are fifty times as many as from insanity; from diarrhœal
diseases, thirty times; from pneumonia, twenty times; from diphtheria,
including croup, fifteen times; from scarlet fever, heart disease, and
typhoid fever, each eleven times; from accidents, ten times; from
cancer, five times; from childbirth and measles, each more than twice
as many. The average death-rates reported from insanity per 100,000
inhabitants were 6.24 from 1861-70, and 7.12 from 1871-80, whereas the
increase in the number of admissions to Massachusetts insane asylums
in the twenty years was from 846 to 1610. The total number of insane
people living in the State is less than the number of consumptives
dying each year, and far less than the number of syphilitics.

CAUSATION.—It is clear that only a small proportion of the human race
is liable to become insane, and one can only wonder that so few brains
are overthrown by the multiplicity of causes in modern life which tend
to disturb those “invisible thoroughfares of the mind which are the
first lurking-places of anguish, mania, and crime.” When we come to
investigate the causes of mental disease, we find that they are of two
kinds—remote or predisposing and immediate or exciting. They are also
moral or mental and physical.

Among the predisposing causes heredity includes nearly or quite 75 per
cent. of all cases, and is easily first; in considering which not only
the immediate parents are to be taken into account, but also the
collateral branches, grandparents, uncles, aunts, sisters, brothers,
and cousins, for {114} hereditary insanity often skips one generation,
and even appears, sometimes, first in the child, then later in the
parent. An insane parent may have several children, of whom some may
be exposed to the exciting causes of insanity and become insane,
transmitting their disease, intensified or not, to their children,
while others may avoid the exciting causes of mental disease, escape
insanity, but yet transmit to their children a temperament
predisposing them to disorder of the mind, which becomes the
starting-point for actual mental disease as soon as the exciting
causes are sufficient to develop the taint. If the exciting causes do
not appear, however, in that generation, and wise marriages are made,
the stock returns to the normal healthy standard and the disease
disappears from the family. The same form of disease, too, is
frequently not transmitted from parent to child or grandchild, but the
neuroses, the psychoneuroses, and the cerebro-psychoses, the
degenerative forms and the developed forms, are interchangeable. In
the ancestry of insanity we find not only actual cerebro-mental
disease, but epilepsy, brain disease due to syphilis, habitual
drunkenness, any of the severe neuroses, apoplexy, pulmonary
consumption, a closely-allied disease, and suicide. Very often the
patient's friends think that there is no hereditary predisposition to
mental disease, when the physician trained to study such cases would
discover so strong a taint that he would not expect all of several
children to escape insanity or some of its allied diseases even in a
case where there had not been actual insanity in the family for
several generations. For instance, where one parent is habitually
using alcoholic liquors to such a degree as never to be drunk, and yet
rarely quite himself, with the other a sufferer from one of the severe
neuroses or cerebral diseases, a single child from such a marriage
might stand a fair chance of inheriting and retaining mental health,
but if several children should be born the chances that all would
escape mental disorder are few. Again, if one parent were the victim
of that intense intellectual strain and moral perversion so often seen
in the eager pursuit of position and wealth, and the other, straining
to keep up in the race, died early of pulmonary consumption, if there
had been in the family cases of convulsions, chorea, apoplexy, or
suicide, and if some member were hysterical or, without sufficient
external cause, unreasonable, anxious, irritable, full of baseless
fears, there might have been no insanity in the family, and yet a
tendency to insanity might be transmitted to a considerable proportion
of the offspring. On the other hand, the existence of a number of
cases of insanity in a family may be due to external or accidental
causes, and not indicate any general taint.

It is true that there are families in which insanity occurs where the
allied neuroses do not often appear, and that various diseases of the
nervous system may be frequent in a stock in which insanity is rare or
absent. A person who has recovered from an acute attack of
cerebro-mental disorder, if previously healthy and without hereditary
predisposition to such diseases, may marry and not transmit to
offspring either insanity or any of its allied diseases, while it is
not uncommon for an individual seemingly the least liable to mental
disease of a whole family to become insane, leaving several brothers
and sisters with ill-balanced minds to get through life without
breaking down, the morbid energy in the latter case expending itself
in irregularities of conduct and of mental operations as fast as it is
created, instead of being stored up for {115} occasional outbreaks.
The degree to which insanity may be expected to follow any given
antecedents can only be estimated very approximately, as the laws of
heredity are very little known, and as there is a tendency in nature,
so strong that it is constantly asserting itself, to return to the
healthy type if it has a chance. But, in general, it may be said that
the more individuals of both branches in whom insanity and its allied
diseases are found, just so far may a larger proportion of the
children be expected to suffer. The character of the particular
disease or tendency to disease which is likely to develop from any
given antecedents is still a very obscure matter. But the case is
often clear enough to justify the remark that if childhood has any
rights it has the right to be born healthy.

It must be admitted that geniuses and men of extraordinary talent
appear in families tainted with insanity, and, indeed, that
comparatively few families have had distinguished men among them for
several generations without also showing a considerable number of
insane members. Schopenhauer, “mad Jack Byron's son,” and Johnson—who
said that his inheritance made him mad all his life—are conspicuous
examples of this well-known fact; and it is also observed that
children and grandchildren of men distinguished for their great
intellectual powers are subjects of degenerative mental disorders, or
at least are of less than ordinary mental capacity and moral force.
The sound and the unsound, too, may exist together in the same mind,
each acting in certain ways independently of the other, and
cerebro-mental disease not seldom, occurs in persons of the highest
intellectual attainments. Dean Swift, with his delusion that parts of
his body were made of glass; Bishop Butler, tormented all his life by
his morbid fancies; Chatterton, committing suicide in an attic;
Rousseau, Tasso, Pascal, Comte, Beethoven, Charles Lamb, John Bunyan,
the author of _Rab and His Friends_, Schumann, Shelley, Cowper,
Swedenborg, and the epileptics Julius Cæsar, Mohammed, and
Napoleon,—are only a few of the many illustrations of this law. In the
descending scale from insanity we find also crime, drunkenness, and
all sorts of moral perversions, which may be its antecedents also.
Even a man's self-indulgences may be intensified as mental or moral
degeneration in his children. The degenerative processes may go on
where there is intellectual stagnation in small communities, with the
vices of civilization, as well as in the crowd, producing a large
class of persons for whom doctors have only compassion, considering
them as invalids although treated as responsible by law and society.

It is difficult to estimate the influence of intermarriage as
predisposing to insanity. The history of the early Ptolemies, of
numerous savage or uncivilized races, and of many selected cases in
the enlightened world may be quoted to show that it is often attended
with no evil results; and there are other causes of degeneration in
the royal families and aristocracies of Europe and in the cases of
individuals where intermarriage of relations has resulted in
deterioration of stock. It is, at all events, certain that marriages
may be made so as to intensify morbid tendencies or so as to eliminate
them—to produce a race of clear heads with sober judgment, or a race
part of whom shall be great sufferers from neuralgia or mental pain;
another part ill-balanced or explorers in fields of thought and action
never tried by calmer intellects, perhaps with now and then at {116}
long intervals a genius; a third part morbid and brilliant or stupid
and imbecile; and still a fourth part near enough to the normal
standard of mental health.

Undoubtedly, a great portion of the mental and nervous disorder
commonly attributed to heredity is largely caused or aggravated by
imitation and by vicious training of children. Schopenhauer says that
the normal man is two-thirds will and one-third intellect—in other
words, two-thirds made by education and one-third by inheritance. The
intellect is often trained so as to enfeeble the will as well as to
hinder the development of the physical man. Self-culture may so
degenerate into self-indulgence as to destroy individuality and force;
and mental health, as a rule, depends upon bodily health and the
exercise of self-control.

In the uncivilized and half-civilized races of the world insanity is
rare; in the early civilizations the insane perished from neglect,
were hanged and burned, starved and died in famine and pestilence, and
fell among the foremost in war. Some of the tribes of North American
Indians shoot the insane, considering them possessed of evil spirits,
while their white neighbors keep them in chains and squalor.
Civilization brings better food, clothing, and shelter, and less
danger from war, famine, and pestilence than savage or mediæval times.
In the struggle for existence, however, physical strength no longer
wholly wins the day, but also those faculties that involve great
mental and bodily strain in mines, factories, crowded tenements,
counting-rooms, offices; in the eager, excited over-study for prizes
or rank in overheated, badly-ventilated schools, and, indeed, in every
walk of life. People with marked neuroses, who would have gone to the
wall a couple of centuries ago from want of physical strength, now
support themselves by indoor light work, marry, and reproduce their
kind. Minute division of labor involves monotonous toil and increases
the impairment of the body's resistance to mental and nervous strain,
and abuse of the nerve-stimulants tea, coffee, tobacco, or, worst of
all, alcohol and narcotics, add to the evil. Degeneration due to the
reproduction of poor stock is intensified by intermarriage. Luxury,
idleness, excesses, syphilis, debility, drunkenness, poverty, disease,
and overwork produce vitiated constitutions in which varying types of
insanity appear in various nations and climates, but, so far as is
known at present, not in very different degree under similar
conditions. One of the great problems of the day is whether the many
conditions incompatible with health in our crowded populations can be
overcome so as to prevent the degeneration going on thereby.

In early life chiefly the degenerative or the hereditary type of
insanity occurs, or some modification of it. The prevalent forms
coming next are insanity of puberty and adolescence and the curious
morbid psychological developments of lying, stealing, running away
from home, all sorts of perversity of action and thought—impulse
overpowering reason; often resulting in cure if wisely treated, but
not seldom ending in various forms of so-called moral insanity,
suicide, epilepsy, hysteria, primary insanity, prostitution, and
offences against the laws. It is largely a matter of accident rather
than a result of any established principle whether such boys and girls
are sent to reformatories and prisons or to insane asylums. In the
progressively advancing years of life organic {117} mental disease and
the psychoneuroses are more common, the favorable or unfavorable type
of which depends largely upon the degree of degenerative tendency in
each case.

The exhaustion and the disturbed cerebral circulation arising from
acute and chronic diseases, profound anæmia, or prolonged mental
strain, associated with emotional disturbance from any cause, are
among the antecedents of insanity. By our asylum reports ill-health is
second only to intemperance as an exciting cause of insanity, and
ill-health comes probably more largely from poverty than from any
other direct cause. Diseases and accidents to the mother during
gestation and injuries to the infant's head during parturition may
reasonably be supposed to so affect the fœtal brain as to predispose
to insanity in later life.

Of 18,422 admissions tabulated from reports of Massachusetts asylums,
the prevalence of insanity by ages was approximately as follows:

  ------------------+-------------+-----------------+---------------
                    |             |                 | Admissions per
    Age.            | Number of   | Population by   | 100,000 of
                    | Admissions. | Census of 1875. | Population.
  ------------------+-------------+-----------------+---------------
  15 and under      |       366   |    312,103[6]   |       117
  15 to 20          |     1,380   |    165,936      |       832
  20 to 30          |     5,269   |    310,861      |      1695
  30 to 40          |     4,632   |    240,966      |      1922
  40 to 50          |     3,372   |    182,823      |      1789
  50 to 60          |     1,797   |    126,430      |      1421
  60 to 70          |       976   |     79,186      |      1106
  70 to 80          |       382   |     38,283      |       997
  Over 80           |        58   |     11,167      |       519
  Age not reported  |       190   |     10,302      |
                    +-------------+-----------------+--------------
      Total         |    18,422   |  1,478,057[6]   |      1246
                    +----------------------------------------------
  Total of all ages |      ——     |  1,651,912      |      1115
  -----------------------------------------------------------------

[Footnote 6: Excluding those under five years of age.]

Of the 36,762 persons of unsound mind known to the English lunacy
commission in 1859, there were 31,782 paupers, or 86.45 per cent., as
compared with 4980, or 13.55 per cent., supported by themselves or
their relatives. At the close of 1880, of 73,113 insane, 65,372, or
89.41 per cent., were paupers, and 7741, or 10.59 per cent., were
private patients or self-supporting. The increase in the number of the
latter from 1859 to 1883 was from 2.53 to 2.96 per 10,000 of the
population, or 17 per cent., and of the pauper insane from 16.14 to
25.72, or 59 per cent., while general pauperism had rapidly diminished
from 43.7 to 29.5 per 1000 inhabitants.

Similarly, of 9541 admissions to the State hospitals for the insane in
Massachusetts from 1871 to 1880 inclusive, there were 4166 State
patients, 4050 supported by cities and towns, and 1325 private
patients; in other words, 86 per cent. were supported by public
charity. Of 7963 admissions in the same time in which the nationality
was stated, 4532 were natives and 3431 foreigners, respectively 57 and
43 per cent., whereas by the census of 1875 the natives were 74.64 per
cent. of the population, showing more than twice as great a percentage
among foreigners (chiefly laborers) as among natives. It is quite
clear, therefore, that insanity is more prevalent, or at least
increasing more rapidly, {118} among the lower parts of the social
scale than higher up; but it is impossible to say how many people have
dropped from higher planes of life to lower.

Although women are probably more predisposed to insanity than men, and
men more exposed to its objective causes than women, it is not certain
that more insanity occurs in either sex. It is somewhat more prevalent
in single and widowed and divorced people than in those married. The
period of greatest prevalence is earlier in women than in men.

Insanity prevails not only at a time of life when the strain on mind
and body is great, as is shown by the preceding table, but also in
those places where the effort is most intense. That fact is well shown
in the distribution of insanity over the State in the large and small
towns, being greatest where the concentration of population brings
with it extremes of poverty and wealth, as indicated by the following
table, showing the number of admissions accredited to cities and towns
in the McLean, South Boston, and State hospitals for the insane per
100,000 inhabitants from 1871 to 1880, the difference being
exaggerated by the proximity of the hospitals and greater ease of
commitment in the larger towns:

  -------+------------------+-------------+-----------+--------------
         |                  |             |           |     Insane
  Number |                  | Inhabitants |           |    Patients
    of   |   Population.    |  by Census  |  Insane   |   per 100,000
  Towns. |                  |   of 1875.  | Patients. |  Inhabitants.
  -------+------------------+-------------+-----------+--------------
    341  | The State        |  1,651,912  |   5689    |      344
      1  | Boston           |    341,919  |   1987    |      581
     12  | 20,000 to 50,000 |    405,655  |   1486    |      367
     42  | 5000 to 20,000   |    367,957  |   1193    |      324
    286  | 5000 and under   |    536,381  |   1023    |      190
  -------+------------------+-------------+-----------+--------------

Of 9381 men and 9041 women admitted to our asylums, 7435 were married,
8193 single, and 1620 widowed or divorced. Of the 9381 males, 2215
were laborers, 1357 farmers, 313 clerks, 62 clergymen, 59 physicians,
43 lawyers, 201 students, of whom 114 were in school. Of 4673 females,
52 were school-girls.

The exciting or immediate causes of insanity are usually so complex
that many of the statistics on that point conform to the preconceived
views of the various compilers of them, as it is very easy to pick out
a few from the many; but out of a large number of persons exposed to
the alleged causes of insanity, one can never feel certain how many,
nor indeed what, individuals will become insane.

It is not always easy to say how and when the furrows left in the
brain by the mental and so-called moral causes of insanity have
deepened into actual mental disease. Prolonged emotional and mental
strain or severe mental shock often are directly associated with the
immediate appearance of insanity. In armies, among people separated
from their homes, in prisons, insanity oftener occurs than among the
same people at home. Severe grief, disappointment, great and sudden
joy or success, chagrin, fear, religious or political excitement,
wars, pestilences, domestic or business troubles, poverty, and
misfortune are among the commonly-reported moral causes of insanity,
as are certain occupations involving steady and monotonous toil,
especially if involving mental worry or necessitating unhappy
relations.

{119} Of the physical exciting causes of insanity, intemperance in the
use of alcohol is easily first: luxury and excess in eating, drinking,
and sexual indulgence, especially if associated with overwork or
physical inactivity and mental anxiety, are also dangerous. It is
difficult to estimate the influence of syphilis except when giving
rise to coarse disease of the brain. Masturbation acts as an exciting
cause, chiefly by creating a morbid psychical state and by exalting
the sensibility of the nervous system, but probably not often, even
with the young. Injuries to the brain and nervous system are usually
slow in their operation, unlike the severe mental shock which is at
once followed by insanity. Pain also, if intense, like great loss of
blood, acts slowly by wearing out the powers of resistance, or rapidly
by producing delirium.

A relation between pulmonary consumption and mental disease is
frequently observed—partly, perhaps, due to general anæmia, in part to
circulation of diseased blood in the brain, and partly from tubercular
deposits. Other diseases act directly upon the brain and nervous
system, as leptomeningitis, pachymeningitis, sclerosis, capillary
aneurisms, embolisms, cerebral hemorrhage, tumors, disease of
arteries, syphilis, caries, exostosis, abscess, internal otitis,
sunstroke; still others by disturbances in the cerebral circulation,
as diseases of the heart and kidneys; others by vitiating the blood
circulating in the brain, as in the acute stage of febrile disorders;
others in some general unknown way, as chorea, hysteria, epilepsy,
gout, rheumatism, malaria, pneumonia; and still others during the
period of convalescence or of general exhaustion, which is often
associated with infectious diseases or chronic disease attended with
general anæmia. The more violent and curable psychoses occur at the
height of acute diseases, those of longer duration and of less
favorable result during convalescence. Among other recognized causes
are prolonged and obstinate dyspepsia, the psychological changes, if
morbidly developed or attended with accident, at puberty, during
pregnancy, at childbirth, during the puerperal state or lactation, and
at the climacterium, and rarely various affections of the abdominal
and pelvic organs.

Chronic alcoholism produces disease of the small blood-vessels of the
brain and the consequences of that condition, causing insanity in a
considerable proportion of cases, and almost always some mental
impairment. Insanity occurs under conditions of cerebral hyperæmia and
of cerebral anæmia, although their relation as cause and effect is
very obscure. The habitual use of hasheesh gives rise to a
disagreeable form of dementia, and so does opium, but more rarely. The
effects of poisoning from iodoform, lead, mercury, bromide of
potassium, hydrate of chloral, belladonna, tobacco, when reported as
producing insanity, are usually transitory.

Cases have been reported of two persons being exposed to the same
causes and having similar attacks of insanity (folie à deux), and also
of folie induite or folie communiquée, where several persons have
adopted the delusions of a person of influence among them, one of the
most remarkable instances of which was the case of the seventeen
grammar-school-taught Adventists of Pocasset, who accepted the insane
belief of their leader, Freeman, that, like Abraham, he had been
commanded by the Lord to kill his child, that she was to rise on the
third day after he {120} had killed her, and that he was to become a
great evangelist. So-called epidemic insanity, choreomania, and
demonopathy belong in this class.

From untrained, ill-balanced men and women, whose lives are ill
regulated, the ranks of the insane are largely filled. Insanity is
often the ultimate wreck of a life ill guided, directed chiefly by
caprice and passion and weakened by indulgence. In that case it is,
like much habitual drunkenness, as much a fault as a disease. The
individual will not behave with decency and propriety for so long a
time that, finally, especially after the age when the brain begins to
fail, he cannot.

SYMPTOMATOLOGY AND COURSE.—The distinguishing symptoms of insanity are
mental. In some forms of insanity they are mental only; in others
these symptoms are associated with others, such as also occur in
diseases not necessarily affecting the mind. The earliest mental
symptoms are change of character, increased irritability, less feeling
of accountability, a lower moral tone, moral perversion, diminished
stability, loss of interest, lessened power of concentration and
self-control, impulsive acts, anxiety or the opposite condition of
mind, perverted or exaggerated force of the emotions, restlessness,
apprehension, sleeplessness, impaired will, slight depression or
barely noticeable exhilaration: things and persons seem changed in
some vague, unexplained way. There is an alteration in the way in
which the person is affected by his surroundings.

The next symptoms are more purely intellectual. Delusions are often at
first based upon some fact, and are merged into insane delusions only
as the mind, in becoming weakened, loses power of comparison and
judgment. Often they arise out of the disordered condition of mind.
Hallucinations of any of the special senses, illusions, perverted
ideas, mental confusion, mental hyperæsthesia or anæsthesia, delirium,
stupor, exaltation, depression, impairment or loss of memory,
quickened or dulled conception and perception, increased or diminished
intellectual activity and acumen, distorted association of ideas,
imperative conceptions, all sorts of anomalies of consciousness and
free will, uncontrollable and uncontrolled insane impulses, are
common. The intellectual and moral symptoms appear nearly or quite
together in very acute disease, and they together increase in
intensity, and finally entirely control the individual. Many of the
insane recognize the fact of their insanity. Some of them understand
the nature of their disease quite well, discuss their cases
intelligently, and frequently ask why they, automaton-like, are
impelled by a force which they cannot resist to constantly do things
which their intelligence and better nature condemn. Not a few are
confined in places of safety by their own preference.

The physical symptoms of insanity are perverted sensations of almost
every conceivable kind, resulting in depraved instincts and acts,
psycho-motor excitability, convulsive action, choreic movements,
uncontrollable muscular agitation (springing, shouting, swearing,
dancing, running, destructive tendencies, etc.), elevation or
depression of pulse, respiration, or temperature, loss of appetite,
digestive disturbances, pain, fever, tetanic and cataleptic rigidity,
paralysis, tremor, ataxia, epileptic seizures, convulsions, muscular
contractions, increased or decreased secretions and excretions,
disturbances of general nutrition.

The course of the various mental diseases is to a great extent
chronic, some forms being incurable from the beginning, others curable
to such {121} an extent that of recent cases from one-half to
nine-tenths recover, of whom a considerable proportion remain well to
their death. The duration of the mental diseases is from a few days to
a lifetime, sometimes not even shortening life. The termination is
oftenest in incurable chronicity or dementia, less often in permanent
recovery without recurrence, and still less often in death from the
first attack. Unfortunately, the essentially incurable and the curable
forms of mental disease are classed together in statistics of
insanity. While many types are absolutely fatal or certain to end in
hopeless chronicity or dementia, others tend to recovery. In some
forms relapses and recurrent attacks are to be expected: in others
they seldom occur. In many cases there is no more probability of
transmission to children than in Bright's disease, and no more
likelihood of subsequent attacks than in typhoid fever.

MORBID ANATOMY AND PATHOLOGY.—It is thought by the best observers that
insanity depends upon a functional brain disturbance, or at least upon
a disordered condition which it is beyond our present power to
discover, and that the normal working of the mind depends upon a brain
healthy to such an extent that its millions of functional activities,
in their endless relations to each other, preserve a state of
equilibrium; or, in other words, that the higher centres maintain
their power of control over the lower. It is doubtless true that this
relation depends in general upon a healthy brain, but it is not yet
known to what extent. Disease of the brain or its membranes,
apparently slight, often seems to cause insanity, and often there is
marked disease without insanity. We certainly cannot place all the
pathological conditions found in the brain of a person dying insane in
direct causal relation to his insanity. The anæmia observed by Meynert
in melancholia and the hyperæmia of maniacal excitement, even if
proved to be universal in those conditions, may be only symptoms of
the underlying disease or caused by it. It is certain that there are
indications of as great anæmia or hyperæmia in other states without
insanity.

Insanity in its initial stage does not, as a rule, involve a
recognizable deviation from the normal structure of the brain, and the
patient may die before such pathological changes are so manifest that
we can detect them. But if the disease has been of long standing, in
the majority of cases the brain shows evident marks of disease, and
there may be found no striking indication to the naked eye of
deviation from a healthy condition, when a microscopic examination
reveals signs of advanced cerebral disease. The limited knowledge of
the cerebral structure and function which pathologists possess, and
the consequent difficulty in detecting changes from the healthy state,
indicate that the failure to find them is attributable in not a few
instances to the fault of the investigator rather than to the nature
of the disease. Certain it is that the better acquainted we have
become with the anatomy of the brain and with its functions and
sensible qualities, and the more thorough and painstaking we have been
in our examinations, the rarer it has become to find a case of
insanity where no organic changes are observed after death, although
it is true that we do not understand all the relations between these
changes and the symptoms observed during life.

A large abscess of the brain, a hemorrhage, a tumor, or a wound of the
cortex or other portion of the brain, various degrees of inflammation,
{122} meningitis, are sometimes followed by insanity and sometimes
not; and we do not yet understand the reason for the difference.
Indeed, nearly every pathological condition of the brain known in
insanity—in kind, if not in extent and degree—may be found in diseased
or injured brains where there has been no mental disease in
consequence. There is only one disease, general paralysis of the
insane, in which the morbid appearances discoverable after death with
our present knowledge bear a definite relation to the most constant
manifestations during life. And yet, with pathological changes so
similar that we are not able to detect their essential difference, the
mental symptoms of the first stage of general paralysis may be most
various. Rosenbach has found in the brains of starved dogs and
guinea-pigs as extensive changes as in well-marked primary dementia,
in which the pathological conditions are more extensive than in any
other form of acute insanity.[7] That is to say, when we have
discovered and described all the morbid appearances in the brain of an
insane person we have taken only the first step in accounting for his
insanity.

[Footnote 7: _Centralblatt für Nevr. Psych. und ger. Med._, 1884, p.
33.]

The localization of many of the cerebral functions, the discovery of a
psychomotor tract, and the constant accessions to our knowledge of the
physiology of the brain are throwing much light on the subject. But
all efforts to localize the intellectual and moral functions of the
brain, except generally to agree with the teachings of a century ago
and to place them for the most part in the anterior and antero-lateral
portions of the cortex, have thus far failed of success, the most
careful observers still thinking that local lesions when apparently
causing insanity do so by injuring the action of the brain as a whole,
and not of any particular part.

In some cases of insanity, with never anything like acute disease,
where death occurs from the weakness of old age or some intercurrent
malady, the brain does not present any recognizable difference from
those of sane people whose brains have worn out with their bodies. In
those forms of mental disease where changes are found, the most
important and constant are in the cortex of the brain, especially in
the fore, upper, and middle parts of the periphery, involving usually
also the membranes. In beginning acute mania the condition of the
blood affecting the brain or the pathological changes are probably as
nearly identical with those in the acute stage of pneumonia, certain
forms of typhoid fever, cerebro-spinal meningitis, and other diseases
as the symptoms of the mania are now and then difficult to
differentiate from those of the other diseases just mentioned. In
rheumatism, syphilis, malarial poisoning, and Bright's disease with
mania we find no distinctive pathological conditions to account for
the maniacal symptoms.

If asked whether there is a fixed lesion of the brain or any of its
parts corresponding to given psychological changes, we should be
obliged to say no, except in the case of incurable dementia. If asked
whether there are important morbid changes corresponding with all
cases of insanity, we can only say yes, sooner or later, in the
majority of cases, and that there are certain destructive lesions,
chiefly inflammatory, atrophic, and degenerative, which invariably
mean marked deterioration of the mind. As regards diseases of other
organs than the brain, the insane, like the sane, die of all of them,
and in especially large numbers of pulmonary consumption.

{123} Insanity may, both in its acute and chronic form, be the result
or symptom of simple anomalous excitation or nutrition of the brain or
of inhibition of some of its portions, without any change in its gross
appearance which can be detected by our present methods of research.
In the majority of cases there are found diseased conditions which
become more manifest the longer the duration of the disease, appearing
for the most part in the blood-vessels, pia mater, and cortex of the
brain, but also in the medullary portion, many of which are recognized
only in their late stages. In the functional mental diseases there is
no characteristic lesion of the brain as yet recognizable, even in the
latest stages, more than is to be found in the brains of persons dying
from other causes. When apparently local injuries or diseases cause
insanity, they probably do so through a general disturbance of the
brain or through diffuse disease resulting therefrom and for the most
part affecting both hemispheres. The molecular, chemical, anatomical,
physiological, pathological, or physical changes in the brain which
give rise to insanity, and their relation to the grosser pathological
conditions of the brain, are still not clearly made out.

In terminal dementia, especially in the last stage of paralytic
dementia, nearly every tissue and organ of the body may be found to
have undergone pathological changes, of which by far the greater
portion is secondary to disease of the brain; and it is impossible to
say how much of the brain lesions in these and other conditions of
mental unsoundness is secondary to the disease or an accidental
complication.

DIAGNOSIS.—In the diagnosis of insanity the physician assumes a
responsibility for which he is liable under the common law. It is
important, therefore, to avoid mistakes as far as possible. In the
majority of cases the patient's unsoundness of mind is evident before
he is brought to the doctor, but in not a few the symptoms are
obscure, and they are often rendered more difficult of correct
understanding and appreciation by the deception or reticence of the
patient and by the prejudices of his friends.

First, before seeing the patient it is well to get from his family,
friends, and physician a full knowledge of his natural state, all the
facts known to them relating to strange behavior, delusions, etc., as
they give most useful hints with regard to the method of examination.
Apparent familiarity with an insane person's delusions will often
secure their immediate acknowledgment. In a case of any obscurity or
where there is doubt that other causes than insanity may have produced
the unusual behavior, and particularly if any legal steps are to be
taken regarding guardianship, restriction of liberty, commitment to an
asylum, validity of wills and contracts, capacity to manage property,
marriage, etc., it is imperative that both sides of the question be
fully heard before any positive opinion is given. After the patient's
confidence has been gained in general conversation, during which his
appearance, manner, and mental condition as to intelligence,
coherence, memory, judgment, perception, and capacity may be noted and
compared with his normal standard, he should be examined carefully for
any external evidence of lack of development or of injuries to the
head. As in all other diseases, the condition of every organ of the
body should be noted; a complete diagnosis should be made. The
expression of the face often indicates such excessive excitement,
gloom, stupor, suspicion, or fear as must be due to insanity alone.

{124} Throughout the examination the questions and manner of the
physician should be such as to avoid suggesting unpleasant ideas or
associations to the patient. The matter of suicide should never be
first mentioned by the questioner, and not seldom he does best who
listens most and lets his patient disclose his morbid ideas and
impulses, as he will frequently be led to do, if at all, by the
manifestation of interest and sympathy, and of knowledge of the
symptoms of the disease in hand, on the part of the physician. He
often gets enough for his purpose without getting the whole story,
upon which it sometimes does harm, or at least is not best, that the
patient should dwell. In the diagnosis of mental disease, however, as
well as in estimating responsibility, the fact must be borne in mind
that a controlling delusion may be concealed for months or even years,
and that the symptoms and mental condition of insane people vary so
much at different times that it may be quite possible to get distinct
evidence of unsoundness of mind at one time and not at another. The
power of self-control is also liable to the same variation or
alternation.

If the patient has no reason for simulation, it is commonly best to
tell him the object of the examination. The family history should be
learned from others, as questioning the patient on these points is apt
to put him in a train of thought unfavorable to a hopeful view of his
own case. After full personal questions concerning himself and his
environment, one can usually tell whether there are unreasonable
suspicions, violent impulses, perverted feelings with regard to his
family, delusions, hallucinations, or illusions. A delusion's
existence must often be accepted, however, from the behavior of the
patient and from the statements of those about him. Hallucinations of
hearing must sometimes be inferred from the attitude of listening to
imagined voices; and prolonged observation under circumstances such
that the patient does not know that he is watched will often settle
the question of his insanity when other means have failed. A careful
examination should, of course, be always made for the physical and
rational signs of disease. In the differential diagnosis care must be
used not to mistake for insanity the acute diseases typhoid fever,
meningitis, smallpox before the period of eruption, pneumonia,
cerebro-spinal meningitis, narcotism or delirium from drugs, and
alcoholism—errors which have been made, and which can be avoided by
deferring one's opinion for a sufficient time.

The detection of simulation is more difficult, especially as the
insane sometimes feign insanity for a purpose, or, on the other hand,
accuse themselves of wrong acts which they never committed. In
general, it may be said that sane persons pretending to be insane very
much overdo their part, do not make their symptoms conform to any
recognized type of disease, and have a strong motive for their
deception, as well as for the act for which they wish to be considered
irresponsible. Their insanity first appears after the deed; they are
exhausted by their efforts to seem mad, and appear quite sane if
watched when they think that they are unobserved. A crime performed
without accomplices, with no plan or a silly one for escape, and with
no sane motive, is usually itself evidence of insanity. On the other
hand, people partly demented by chronic insanity often commit crimes
with all the method and motive of the criminal. In not a few cases,
especially when the fact or not of impaired intellect cannot be
decided by comparison with a previous condition, the question of {125}
insanity, or at least of responsibility, will be beyond human wisdom.
A correct diagnosis can, of course, not be made without a familiarity
with the various forms of mental disease; and insanity is now so well
understood that a sufficient examination of an insane person should
develop the clinical history of some known type of disease in nearly
every case.

Little has been said of the physical evidences of insanity, because
there is little to say. Conditions of mental torpor, depression, and
excitement are associated with the physical manifestations which we
would naturally expect in those mental states. Coarse brain disease
with insanity or without may have identical physical signs; paralytic
dementia is the only disease in which corporeal indications really
assist in forming a diagnosis.

A family predisposition to mental disease does not materially affect
the question of fact whether a given individual is insane or not,
except that in a doubtful case it adds to the probability of insanity,
and is thus far a factor of importance as corroborating other
evidences of an unsound mind.

PROGNOSIS.—The prognosis in insanity depends first upon the type of
disease, mania, melancholia, and some forms attended with confusion
and stupor being the most curable; the forms attended with
systematized delusions or with periodicity which is not dependent upon
menstruation, folie circulaire, and moral insanity rarely so, and the
organic brain diseases, congenital insanity, and confirmed primary
delusional insanity (monomania) hopeless. The acute forms are far more
curable than those of a subacute type: 60 per cent. of the cures in
insanity occur in the first half year of treatment, 25 per cent. in
the second half, and 2.5 per cent. in the second year, roughly
speaking. In chronic cases a reported cure is most commonly only a
remission, and after several years of existence insanity is generally
incurable, although rare cases of cure in mania have been reported
after even from six to fourteen years of treatment, and in melancholia
after twelve years. So long as there is no permanent dementia and
there are distinct intervals of mental clearness, no matter how short
or how far apart, there is hope of final recovery in the curable
mental diseases.

People of sound families, with insanity of an acute type arising from
physical causes, often make such speedy and complete recovery as to
justify their subsequent marrying if they wish, while those of
unstable nervous organization recover more slowly and oftener relapse.
Insanity from so-called moral causes, too, is of more unfavorable
outlook than if from the physical causes, if we exclude organic brain
disease. A person with good physical education, excellent mental
training, and self-control is more likely to get well than one with a
vicious bringing up. The ages of maturity and middle years are most
favorable to complete recovery. In women there are more first cures
and more relapses, according to Krafft-Ebing. In general, the
mortality of the insane in asylums is about four times that of the
sane of all ages, or approximately six times that of the sane at the
ages when insanity prevails.

Prolonged stupor, profound incoherence, loss of memory, and moral
debasement are unfavorable symptoms, unless quite acute, of short
duration, or occurring after the rapid subsidence of acute symptoms.
Hallucinations of hearing, and to a less extent of sight, impulses to
violence, and especially systematized delusions, are grave
indications. Paralysis, {126} epilepsy, and convulsions usually mean
chronicity or death. Extensive disease of the heart, kidneys, or
lungs, confirmed dyspepsia, especially of alcoholic origin, and a
previous history of syphilis, seriously affect the prospects of
recovery. If there is actual cause for self-accusation, if the
knowledge of wrong-doing is added to the morbid mental state, the
period of convalescence is apt to be much retarded, or even recovery
is prevented, by the difficulty of establishing a healthy reaction.
Even an irresponsible act is often magnified into so depressing an
influence as to prevent restoration to health, as in the case of those
who have injured or killed members of their family.

Of 9689 persons admitted into the Worcester Insane Asylum[8] during
fifty years ending September, 1881, of whom 1083 had been in other
asylums, 35.49 per cent. were discharged well, 26.61 per cent.
improved, 17.71 per cent. not improved, 0.5 per cent. not insane, and
14.85 per cent. died. Of those discharged, 25.41 per cent. were
readmitted, and of 798 discharged recovered, with regard to whom
inquiries were made, 156 were reported well at the time of replying,
197 as having died sane, 30 committed suicide, 162 relapsed and died,
94 relapsed and were alive, 30 were in hospitals or almshouses insane,
and of 129 no information was got. Out of 798, there were 316, or 39.6
per cent., known to have become insane again or to have committed
suicide. Of 1966 second admissions, 668 recovered; of 607 third, 263;
of 261 fourth, 119; of 132 fifth, 70; of 70 sixth, 42; of 48 seventh,
30; of 37 eighth, 21; of 30 ninth, 19; of 26 tenth, 15; of 23
eleventh, 11; of 18 twelfth, 11; of 15 thirteenth, 10; of 12
fourteenth, 8; of 8 fifteenth, 5; of 4 sixteenth and seventeenth, 3;
of 4 eighteenth, 2; of 2 nineteenth, 1, who was admitted and
discharged well twenty-three times.

[Footnote 8: _Forty-ninth Annual Report_, including tables by John G.
Park, Medical Superintendent.]

Thurnam's statistics, that one-half of the recent cases of insanity
treated in asylums recover, and that of the recovered only two-fifths
remain so, receive constant confirmation. There is a considerable
proportion of the inmates of asylums whose brain-condition is so
unstable that they come in and go out frequently. Their brains are
unstable, too, in the little affairs of life, and many of the
nominally cured remain comfortable only by being shielded from sources
of physical wear and mental worry. It is impossible to get statistics
of the curability of mental diseases properly treated outside of
asylums, but the results would probably be more favorable than those
just quoted, partly from the greater chances of cure in the mild cases
and in those acute cases which can be kept at home, or at least do not
require hospital treatment.

It is difficult to form an opinion as to the probability of subsequent
attacks in those who have recovered from any of the curable forms of
mental disease. The same constitution, of course, remains as that
which predisposed the individual to the first attack, and no one can
look far enough into the future to predict the influences which will
be brought to bear upon any given person for a considerable period of
time. If they are favorable for preserving mental health, the chances
of escaping mental disorder in the future are very much greater than
if the occupation which must be pursued and the life which must be led
predispose to bodily exhaustion, anxiety, and brain-worry. If the
disease first appeared under slight exciting causes, it will not often
be possible to {127} avoid similar conditions again, and some forms of
insanity are characterized by relapses and recurrent attacks.

Of the persons reported recovered from mental disease, a large
proportion fail to recover in the sense of being fully themselves
again. There is left some change of character, no matter how slight,
some moral perversion, irritability, instability, impaired will,
lessened power of self-control, diminished mental capacity—some
lowering of the intellectual or moral standard, some deterioration of
some kind.

TREATMENT.—Not long after Leuret recommended and practised severe
discipline in the treatment of the insane a case was reported at the
Medical Congress in Naples (1845) where douches, setons, blisters,
bleedings, internal medication, shocks, terror, harsh
discipline—nothing succeeded in restoring to sanity a woman become
insane three months after her confinement. There probably are places
where similar methods are practised at the present day, and yet it is
not unreasonable to suppose that the very treatment used is sufficient
to render incurable patients who might otherwise get well. The modern
management of mental disease by rest, diet, baths, fresh air,
occupation, diversion, change of scene, no more medicine than is
absolutely necessary, and the least restraint possible—in a word,
improving the patient's general condition, meeting the indications of
his disease, diverting his mind from its morbid thoughts, or putting
the brain in a splint, so to speak, as each case demands—gives much
better results, the value of which is much diminished by the enormous
increase in the size of our asylums and the great aggregation in them
of diseased persons in all stages of insanity.

In twenty American asylums, the statistics of which have been analyzed
by Pliny Earle in his paper on the _Curability of Insanity_, the
average diminution of reported recoveries for about twenty-five years
has been from 46.08 to 34.26 per cent. annually of cases admitted, and
in the Massachusetts State asylums from 25.95 to 22.25 per cent. of
3371 persons admitted from October, 1879, to October, 1882. The
prospect of treatment of insanity does not, from these figures, look
very hopeful, and it must be conceded that there is in the
proportionate number of reported recoveries a decrease which it is
important should be explained. It is undoubtedly true that a larger
number of the chronic and quiet incurable insane are sent to the
asylums now than formerly, thereby diminishing the curable proportion.
The character of the asylums, too, has changed from being small,
easily-managed institutions to overgrown affairs, crowded with so many
incurables that the duties of the superintendents have become largely
administrative, and the medical treatment of the sick has been driven
to a subordinate position. Medical officers, too, are more cautious in
using the word cured after experience has shown them how many reported
cures are only remissions.

In treating insanity, even more than any other disease, the fact must
be borne in mind that one is treating a diseased person; and indeed it
is often necessary to treat a whole family of persons predisposed to
insanity in giving directions for one actually insane. There probably
has been no time during the last quarter of a century when there was
more uncertainty in the minds of the medical profession regarding the
best treatment for patients suffering from curable mental diseases
than at present. Twenty-five years ago the almost universally-accepted
practice was to send {128} them to an insane asylum with as little
delay as possible, without much regard to the character and duration
of their disease. Twenty years ago, in the medical school the
professor of obstetrics advised sending all well-marked cases of
puerperal insanity early to the hospitals for the insane, and only a
few years later Godding, then superintendent of the asylum at Taunton,
advised that patients with puerperal insanity be kept at home until
every available resource but the asylum had been tried without
success.[9] Meynert lectures to his classes in Vienna that in every
case there is a disadvantage in sending curable insane persons to
asylums, although it is often a necessity to do so. Maudsley thinks
that a large proportion of the curable insane can be treated to best
advantage either at home or in small private asylums or houses; while
Bucknill says that by home treatment more cases would be cured than
with our present methods. The late Isaac Ray summed up his vast
experience in the treatment of the insane by saying that it cannot be
shown that the introduction of insane asylums has added anything to
the curability of insanity, much as they are to be praised from the
humanitarian point of view. According to the statistics of Pliny
Earle—to which the only objection we can make is that they are so
exhaustive and conclusive that we cannot controvert them—the permanent
curability of mental diseases in asylums for the insane is not only
small, but decreasing.

[Footnote 9: _Boston Medical and Surgical Journal_, vol. xci. p. 317.]

Part of the results obtained by Earle may be due to the fact that
curable cases are more treated at home now than formerly, that the
degenerative types of insanity are more common, and that in our
cleaning up and civilizing processes we are not only driving out filth
diseases, but letting in disorders due to greater efforts and more
intense struggles for the kind of existence which modern life demands.
But it is also true that in enlarging our asylums, as we have been
compelled to do, we have lost something in personal care of patients,
and that we have increased the depressing influences of large masses
of sick people to such an extent as to involve serious disadvantages
in their treatment. It is a matter of common observation that some
insane people do well at home, others away from home, and others in
asylums—that some do badly in asylums, and quickly get well if
discharged, and that others, after continually going down at home,
immediately improve upon being sent to an asylum. There seems,
however, to be no fixed rule in individuals, and certainly there is
very far from unanimity of opinion among alienists generally as to the
conditions for home treatment or removal from home or sequestration in
asylums, except, of course, that few men of experience would take the
responsibility of keeping out of asylums persons with alcoholic
insanity or with delusions of persecution, or cases of violence and
delirium, or any insane patients under conditions involving danger to
the community or to individuals, although it is often a matter of
extreme difficulty to decide when restraint becomes necessary or
justifiable.

I have selected from a large number a few cases where I have acted
contrary to the usually accepted views as to indications for removal
from home, and with such success that I am led more and more each year
to rather widen than narrow the lines within which home treatment
seems to me desirable.

Case I.—Mr. ——, age 20, of sound constitution and without {129} marked
hereditary tendency to disease, although several members of his family
are people of very little force. The patient had masturbated in
college, as many boys do, and was compelled to give up his studies
upon his father's failure in business. An attack of slowly-advancing
melancholia developed, for which he was sent to the farm of a relative
in the South without improvement, so that he returned home at the end
of a year in pronounced acute melancholia. He secreted himself in a
marsh not far from home, where he was by accident found bleeding
freely from the radial artery, which he had cut to kill himself. He
had the usual delusions of the disease. He thought the world was all
wrong, that he had committed great crimes—the unpardonable sin—and
that there was nothing but destruction before him and his family. He
was desperately suicidal. The circumstances giving rise to his disease
and the associations of his delusions were entirely connected with his
home and members of his family. His people could not afford to hire a
nurse, but his three brothers and one cousin were only partly
employed, and they agreed to take care of him. The treatment was tonic
and supporting, with plenty of sleep, food and outdoor exercise, with
careful attention to daily details of life, arranging it as to
amusements, occupation, etc. etc. from day to day to suit his
condition, and with absolute watchfulness day and night to prevent
suicide. He remained in the home where his disease arose, and he was
taken care of by the people most actively associated with his
delusions. He made a rapid and perfect recovery, and is now very
successful in his work as a professional man.

Case II.—Miss ——, age 35, a sound, healthy woman, without any known
hereditary predisposition to disease. Without any assignable cause,
except a moderate amount of overwork and steady home-life without
sufficient recreation, she became very ill with acute melancholia,
much mental confusion, very varied delusions that the world was all
wrong, her friends distorted and changed, and herself so great a
sinner that she could not escape everlasting damnation. Her most
constant and distressing delusion was that people were constantly
lying in wait to kill her and her mother and her sisters. When I saw
her she was taking large quantities of hydrate of chloral and bromide
of potassium, which were at once stopped. With plenty of food, fresh
air, exercise, rest, malt, and cod-liver oil she slept well. She was
first put under the care of a professional nurse, who was not liked by
the family, and I then decided to let the mother and sisters assume
full charge. She was watched with unremitting care day and night, and
yet managed to make three attempts at suicide, which of course were
not successful. She made a rapid and most perfect recovery, and is
still perfectly well.

Case III.—A letter-carrier about 25 years old, without known
hereditary tendency to disease, under-fed, over-tired, and worried,
broke down with pronounced mania of the simple type, without marked
delirium or delusions. He was much exhilarated, often excited, rarely
noisy, and, as he had no delusions, he was not dangerous. He was
somewhat troublesome, and I feared that his disease might become more
active, and so I recommended his removal to an asylum, to which his
friends fortunately refused to consent. He became progressively worse,
but still not maniacal or delirious. He had no specific insane
delusions, but he had a generally exalted notion about all the events
of life and his own affairs. His {130} surroundings were not conducive
to quiet, as he lived in the noisy part of the city, and his
associations were those under the influence of which his disease
appeared. But he made a most excellent recovery, and resumed his work
with only a year's interruption.

Case IV.—A healthy young woman, without hereditary predisposition to
insanity, confined with her first child. Her delivery was not attended
with any especial difficulty, and she made rapid progress toward
health and strength until the beginning of the third week, when a
slight change of character was noticed which soon developed into
active mania. She was delirious, profane, obscene, filthy in her
habits, and filled with delusions regarding herself, her family, and
her surroundings. She had a great aversion to her infant, and often
did not know the several members of her household. Hers was as violent
a case of puerperal mania as I have ever seen in an insane asylum. She
was naturally not very strong, however, and people could always be
near enough at hand to prevent her doing any harm to herself or
others. Her infant was kept out of her sight most of the time for five
months, and all of the time for many weeks. The usual treatment was
adopted, an excellent recovery was made in six months, at the end of a
year strength was restored, and the patient remains quite well now.

Case V. was quite similar to the last, except that the disease was
melancholia, and that the patient had tried to kill herself and her
infant before I saw her. She made a complete recovery. Both cases were
taken care of in their own homes, and for the most part by members of
their own families.

I have reported these cases with as little detail as possible to
illustrate the point which I have insisted upon for several years,
that many cases at least of mental disease are to be treated precisely
like typhoid fever or rheumatism or a broken leg, so far as removal
from home is concerned, and that home-associations are no more harmful
in properly-selected cases than in pneumonia or phthisis. I do not
mean, however, that the patient should not be under the most careful
treatment. On the contrary, the little details of medical care are
fully as important as in early Pott's disease or beginning
inflammation of the hip-joint. But it is often difficult to decide
what cases should be best treated at home, what by slow travel or
removal to other places than home, and what in asylums.

The objections to asylum treatment, when it is not absolutely
necessary, are very great. On the other hand, the advantages that
asylums possess for supervision and control are so obvious that they
must continue by far the best means of treating the vast majority of
cases of incurable insanity, and a large proportion of those in which
a cure may be reasonably expected. The exigencies of many cases demand
them. If, however, it can be shown that the aggregation of invalids in
them is unfavorable to the best chances of recovery, and if, as I
think is the case, many of the restraints and restrictions now common
in them are unnecessary—for many of the patients, to say the least—the
deduction is clear that a change must be made in asylum construction
and management to correspond to these views. A common depressing
influence in the treatment of mental disease is the fact that the
patient remembers some member of the family who has had to go to an
insane asylum, and fears the same fate for himself, or after one
commitment and recovery fears that he may {131} have a relapse and be
obliged to enter an asylum again. I am quite sure that a considerable
number of the recovered patients of insane asylums who commit suicide
do so from this dread; which is not altogether unnatural, as the
tendency there is downward, so that the patient, as he in the progress
of his disease more and more loses self-control and power of decent
behavior, is progressively dropped into lower wards, with more
disorderly or demented patients, at a time when all the surrounding
influences should be, on the contrary, of a tendency to lift up. On
the other hand, many who recognize their infirmity wish to be taken
away from old friends and associations, and prefer the seclusion of an
asylum, which is their best home.

The more acute the disease, the more likely it is to be of not long
duration, and, as a rule, the easier it is to treat it without removal
from home, except in cases of great violence. The question whether
home-influences are benefiting or injuring an individual patient must
often be settled by experiment. It is a great comfort to many of the
insane to see their friends, no matter how seldom, at times when they
feel that they need their support and influence; and this is
impossible unless the friends are near at hand. There are cases in
which familiar scenes and faces and voices reassure the patient when
delirium subsides, and during a short interval of comparative mental
clearness their sedative influence is great as compared with the
confusion and worry of trying to understand the new surroundings of a
hospital ward or the sight of strange people and the sound of unknown
voices. The mere fact of delusions being connected with the
home-surroundings and members of the family is not so important as the
character of the delusions; and the influence of the relatives is
often most salutary, even when the patient has most distressing
thoughts concerning them or even when he is too insane to be always
sure of their identity. If the insanity arises in a violent emotional
shock, and home sights and surroundings recall and arouse the mental
pain, as is the rule in such cases, recovery usually depends upon
removal from home. The matter of suicide where there are means of
proper watching does not influence me in my decision, as I think that
the dangers of self-destruction are fully as great in asylums as
outside with sufficient care, whereas the stimulus to the patient to
kill himself from both insane and sane motives is greater the more he
is surrounded with depressing influences. On the other hand, it not
seldom happens that the diversity of sights in the hospital, the
routine, the varied events of the day, the amusements, the walks, the
drives, even the discomforts and annoyances, serve to distract the
patient's mind from his delusions better than the same result can be
accomplished under the pleasant influences at home, while a natural
feeling of self-respect prevents those who have power of self-control
from giving way to their impulses before strangers, especially when
they know that such conduct will take them to a lower ward with less
agreeable associates.

There is no doubt, however, that home-treatment of the insane in the
majority of cases is synonymous with neglect of all those minute
attentions to details that make the difference between recovery and
chronic mental disease. Home-associations often act upon the insane
mind like frequent passive motion to a diseased or fractured hip; the
relatives of the insane patient oftener than not share with him a
common inheritance {132} of an unstable mental organization, and will
not be judicious in their treatment of him, or they cannot be
subjected to the risk of becoming insane themselves in taking care of
an insane brother or parent; and it is seldom that a private house
away from home can be converted into a hospital, as it must be for the
treatment of an insane person. One of the greatest difficulties in the
home-treatment of the insane is during the many months of slow
convalescence, when it is difficult to prevent a too early resumption
of cares or work or methods of life prejudicial to complete
restoration to health; so that in that stage of the disease, if in no
other, removal from the familiar and usual surroundings of the patient
will usually be quite necessary. The small private hospitals, with all
their many and obvious advantages, always have been, and inevitably
must be, chiefly devoted to wealthy patients who wish for a home where
they can have medical supervision, rather than curative institutions
for any large number of persons; and there is not enough going on in
them to sufficiently occupy the attention of certain curable patients
who must be removed from home, although they are well adapted to those
who need quiet and seclusion chiefly. The larger hospitals, with their
large staff of skilled officers and nurses, and with all their
appliances for recreation or rest, amusements or occupation,
discipline or gentle support, must be our chief means for treating the
insane. They are indispensable for a large number of the insane who
are of such unstable mental equilibrium that a little over-exertion or
a trifling deviation from a carefully regulated routine throws them
off their balance; and they must be used, temporarily at least, for
many of the incurable or partially curable insane who need a place and
an opportunity to learn self-control and self-management. Enormous
advances have been made in the construction and management of
hospitals for the insane, more especially in the last fifteen years.
We see it everywhere. But the greatest need, of opportunities to
combine advantages of the asylum treatment with the benefits of
home-comforts, to place sick people where the influences surrounding
them will be healthy, and where there are not so many harmful as well
as useless restrictions upon liberty, and so many morbid associations,
is as yet entirely unfilled in this country. The question of the best,
or even of an improved, organization for our insane asylums is too
wide a subject to be discussed here. That our present system tends to
make the medical staff narrow if they are appointed to their duties
without previous broad training and experience or for political
reasons, is a self-evident proposition; and yet there are manifest
objections to just such a visiting staff as is customary in general
hospitals.

As Maudsley says, squalor in an attic with liberty is better than
being locked up in a palace with luxury. Many of the insane share that
feeling with their sane brothers. To not a few it makes the difference
between recovering their mental health and lapsing into incurable
dementia. Many would voluntarily consent to remain in places less
distasteful to them. If we could separate them into classes, as Mr.
Mould[10] has done in England by buying or hiring ordinary dwellings
one or two miles even from his asylum, we could have separate houses
with open doors or shut, as the case demands, for those who require
them, and reserve the {133} associated halls and large buildings for a
different class. Mr. Mould has not applied his own system to those
cases which need it the most, the curable insane, except to a very
moderate degree.

[Footnote 10: _Presidential Address at the Annual Meeting of the
British Medico-Psychological Society_, October, 1880.]

It is not often that the physician is called, or his advice heeded if
given, in the early stages of mental disease, and the first symptoms
are by no means easy to differentiate from the less harmful results of
mental strain. If there be, however, sufficient loss of equilibrium to
suggest the question of beginning insanity, it is of course better to
take the safer way and recommend removal of all sources of irritation,
and to advise rest, sleep, simple food, attention to the general laws
of health, outdoor life, and change of scene for a sufficient length
of time to restore the mental poise, avoiding narcotics and sedatives
as far as possible, and keeping the patient with a safe adviser or
within easy reach of one. In many cases, especially of young persons,
this may involve a radical change in their choice of a profession and
whole plans of life. If the question of marriage comes up in these
cases before the physician as to preventing further developments of
threatened disorder, it can only be said that what may be well for the
individual is not always best for society. A few years' delay will
usually give time for the question to settle itself.

When insanity has actually appeared the same rules should govern its
management as in other diseases. If, like smallpox and diphtheria, it
is a great source of danger to others, the patient should be put in a
safe place; if, like typhoid fever arising from bad drainage, its cure
depends upon the removal of a given cause, the patient must leave the
infected locality or have the cause displaced; if, like rheumatism in
a damp cellar, it can be treated successfully only under different
conditions, the patient must be removed; and if poverty or other
conditions prevent the best possible treatment, the next best
practicable plan must be followed.

The first question which comes up in the care of the insane is with
regard to removal from home and commitment to an asylum; and here a
great many points must be taken into consideration. It is not always
that a home can be accommodated to the use of an insane member of the
family. There are not many in which there can be proper quiet and
seclusion without depriving the patient of that abundance of fresh air
and outdoor exercise which is so often required in treatment.
Frequently those nearest to him irritate him to the last degree, or he
has some aversion or delusion in regard to them rendering their
presence injurious. If the delusions and impulses of a patient are not
such as to endanger the lives of the household, his violence and
excitement and uneasiness or melancholia may make life simply
intolerable to his relatives, or his exactions may be exhausting to
their strength and his constant presence a means of making still
others insane. His noise may disturb a whole neighborhood. His
vagaries may require control, his indecencies concealment, his
enfeeblement help more than can be sufficiently given outside of a
hospital, his general condition more judicious care than his friends
can command, and his example may have a pernicious effect upon
children growing up with an insane diathesis. In many people a long
time insane much of their vicious conduct is due to habit or to
tendencies which they cannot or will not control without the steady,
kind discipline which cannot be got at home.

A man with delusions by virtue of which he thinks that some one is
{134} plotting to ruin or kill him is apt to commit murder; a mother
who believes that the world is going to ruin and her children to
torture may be expected to put herself and them out of misery; a
demented woman chops off her infant's head because its cries disturb
her; and the maniac's delirium or epileptic's fury drives him into any
horrible act. Such people need to be watched always by some person or
persons fully able to prevent their doing harm, which in many cases
can only be done, with any reasonable degree of liberty to the
patient, in a hospital for the insane. If the danger is obviated by
removal of certain persons—children, for instance—or if watching by
nurses serves the purpose, and there are no Other objections to such a
course, there are cases in which the chances of cure are more if the
patient remains at home whenever the disease pursues an acute course.
Most of the insane, however, have passed the curable stage; the
majority need the moral support and freedom from responsibility or the
regular life and regimen of a hospital; and a large proportion of the
cases following a subacute or chronic course must be removed from
home. The expense attendant upon the safe treatment of mental disease
in a private house is entirely beyond the means of most families, just
as they cannot send their consumptives to Colorado or France, and so
the hospital becomes a necessity. Except in dangerous cases, however,
the hospital should never be hastily decided upon. A little delay does
not diminish the patient's chances of recovery, and may show that the
attack is only transient, whereas removal to a strange place might
aggravate the disease and increase its duration. It is particularly
important not to choose an unfavorable time to commit an insane person
to an asylum, and thereby add to discouraging conditions already
existing an additional source of despair at a time when every
influence should be as elevating and cheering as possible. In most
cases, especially if there is a suicidal or homicidal tendency, it is
best, when removal to an asylum has been decided to be necessary, not
to argue the question with the patient, but to explain why it must be
done, and then do it without delay.

The law provides the methods of commitment to asylums. They are so
different in the different States that they cannot be discussed
here.[11] The one rule holds good everywhere, however—that it is far
better to use force than deception in sending the insane from home to
asylums, and that the cases are very few in treating the insane in or
out of asylums where deception is either justifiable or wise. A second
safe rule is that a person of unsound mind is always a source,
immediate or remote, of more or less danger.

[Footnote 11: An abstract of the various laws may be found in the
appendix to the American edition of Clouston's _Clinical Lectures on
Mental Diseases_.]

Commitment to an asylum means so much that safeguards against improper
action should provide careful examination of the case by competent
physicians, as little restraint as is required by safety, good medical
treatment in the hospital, thorough supervision by experienced persons
on the part of the state, safe-keeping of the dangerous patients, and
easy removal of those who have recovered or who may be sent out to
their own advantage. In too many States confinement in an asylum means
that two physicians, or even one, who may know little or much of
insanity, think it best, and removal depends upon the word of one man,
{135} the superintendent. Once in the asylum, the best practice of the
present day should be followed—namely, to allow free communication and
visits from friends until it is shown that they do harm, to multiply
cheerful and natural influences to the last degree, to furnish rest,
exercise, occupation, or recreation as each case requires, and to
remove all that is morbid and disagreeable so far as that can be done.
A permanent removal from the hospital should be insisted upon as soon
as it is safe to complete the convalescence at home or elsewhere, and
an abundance of fresh air, indoors and out, should be supplied as the
best curative agent from first to last. Arguing, moralizing, cheering
up, rigid restraint, disciplining, sedative drugs simply for quieting
patients, and still more bleeding and blistering, are for the most
part things of the past. Mechanical restraint is all but abolished in
the best hospitals, and is used only so far as it is considered the
best medical treatment. A prison-like appearance of the wards has been
found to be not only quite unnecessary, but harmful.

In many cases of insanity I make the question of removal to a large
hospital one of circumstances and of money. If separation from the
influences under which the disease occurs is necessary, and that
cannot be secured at home, I usually select, as the case demands and
opportunity is afforded, a private house with good nurses, a small
private hospital, or an insane asylum where the general influences are
the healthiest, where the medical treatment is in accordance with the
best modern principles, and where the construction of the hospital is
most nearly adapted to the requirements of the present day.
Accessibility to visits of friends and the family physician where they
help in the cure, and remoteness from them when they do harm, are also
points to be considered. In many cases where the illness is of long
duration a change of scene and association will prove of great
service, even from one hospital to another. The permanent settling
down into the routine of hospitalism is especially to be avoided. Of
course there are cases, or rather conditions, in which a change would
be detrimental to the last degree.

The associations, surroundings, and influences brought to bear upon
the patient—what has been called the moral treatment—are of the first
importance in the treatment of mental disease, and diet and hygiene
come next. Medicines are of use in properly selected cases. The
appetite must often be stimulated, the digestion regulated, and
various painful symptoms must be relieved, so far as possible, without
a resort to internal sedatives and narcotics. Rest and sleep are
essential to recovery, but every effort should be made to obtain them
by judicious regulation of outdoor exercise and of quiet as each case
requires, abundant non-stimulating food frequently given, fresh air,
tonics, baths, and removal of sources of irritation. Stimulants will
sometimes be needed to prevent excessive exhaustion. Seclusion in a
room darkened or not is useful in some conditions of excitement, and
not seldom distressing symptoms are relieved by the simple presence of
another person or by the absence of certain individuals.

Drugs of sufficient strength and in such quantity as to produce quiet
or sleep should be used only when absolutely necessary, and then for
as short a time as possible. Their prolonged use is open to many
manifest objections in all persons, and particularly in those
suffering from mental disorders, inasmuch as with them large doses, if
any, are commonly given, {136} and it is very difficult often, in the
impaired state of mind of the patient, to get indications of symptoms
which contraindicate the use of a particular drug or to learn when it
is producing harmful effects. Tonics are often indicated, but should
be used with discrimination, as some of them, especially those
affecting the cerebral circulation, frequently produce disagreeable
results.

After apparent recovery there should be a long period of
after-treatment, which in most cases will be best met in rest or
travel.

In the various forms of mental disease, through concentration of the
mind on various delusions and by excess or deficiency in mental
activity, the ordinary symptoms of physical disturbance or disease,
independent of the insanity, are so much modified as to be often
overlooked. It goes without saying that intercurrent diseases and
distressing symptoms should be treated on the principles generally
applicable to those conditions, so far as that can be done without
aggravating the insanity. The usual treatment of pneumonia, for
instance, may in an insane person provoke such determined opposition
or so excite or aggravate delusions that, so far as the disease of the
lungs is concerned, it may be better to let it take its chance, with
good general care, including food, warmth, etc.

The conditions of cerebral hyperæmia require cold applications to the
head, the wet pack, prolonged warm baths, a non-stimulating diet, and
quiet. If the condition is acute and of short duration, rest in bed is
useful, provided it can be secured without force. For prolonged mental
excitement from cerebral hyperæmia it will be usually better to
equalize the circulation by that motor activity which is
characteristic of the disease, and to allow free exercise in the open
air, keeping within the limits of exhaustion. My experience has not
justified the use of bleeding, except, possibly, in acute delirium
(mania peracuta). It is difficult to limit the action of blisters, and
they often irritate the patient so much as to do more harm than good.
Persistent refusal of food is usually due to delirium or delusions,
and should be met with a resort to feeding with the stomach-tube
before the point of exhaustion is reached if the tact of a skilled
nurse fails of success. Mechanical restraint increases the cerebral
hyperæmia, and there are few homes or general hospitals where it must
not be used if there is excessive violence or delirium, making the
insane asylum in those cases a necessity. Objectionable as it is,
however, mechanical restraint is less harmful than the continued use
of large doses of sedative drugs, as is so often the practice, in
order to keep patients quiet enough to remain at home.

Ergot, hydrate of chloral, and opiates, which sometimes must be given
by the rectum or stomach-tube, are sometimes advisable for a short
time, but must be used with great caution. Milder sedatives,
especially the bromides, serve a temporary use in the less violent
cases; but less sleep will often serve if secured by quiet, abundant
liquid food, and general measures, and in exhaustion by alcoholic
stimulants.

Menorrhagia is very common in the maniacal states. It usually requires
no special treatment, unless so great as to produce exhaustion.
Amenorrhœa is commonly conservative, and then demands only general
treatment; if it causes evident disturbance of the cerebral
circulation, the ordinary methods, including electricity, massage, and
local use of leeches, should be used.

{137} Galvanism is sometimes useful, applied to the head, in cases of
mental torpor and stupor. That and the faradic current, used with
great care, act as powerful tonics to the general nervous and muscular
system.

Insomnia is often the chief manifestation of the insane taint, in
which case drugs are, for the most part, worse than useless. In all
forms of sleeplessness it is better to try malt, cod-liver oil, beer,
food, massage, baths, exercise, rest, etc. before resorting to
narcotics and sedatives. Camphor, hyoscyamus, cannabis indica, the
valerianates, bromides, codeia are much less objectionable than
chloral, morphine, and opium.

Where masturbation is simply an evidence of loss of self-control, it
is met best by constant watching, and gradually, as the mental state
improves, arranging the daily life so as to develop the feeling of
self-respect. Where it depends upon local paræsthesia, opium and
camphor and cold bathing are indicated.

Constipation is a troublesome symptom, especially in the states of
mental depression. When a full, laxative diet, cod-liver oil, and malt
do not correct it, small doses of laxatives given frequently act
better than the occasional use of purgatives.

There is a class of cases which are best treated by educating the
patients as one would educate a child.

In the general care of the insane it is the duty of the state to see
that they have all the rights of the citizen which are consistent with
their proper and safe treatment, including the benefits of property
and estate. There certainly should be in all countries, as in England,
officers whose duty it is to see that this is done. For a large number
of people with defective or diseased brains, who are now allowed to
wander about committing crimes and serving repeated sentences in
reformatories, houses of correction, and prisons, an enlightened
public policy would find the best, and in the end the cheapest,
treatment to consist in keeping them under supervision and control as
unsound members of society.

The more particular treatment of the insane differs in the various
mental diseases, varying as it necessarily must according to different
conditions. Its prevention is not an easy problem. Many of the
external causes of insanity seem inevitable in our complex
civilization: it would be impossible to widely regulate marriages,
even if we knew how; those people predisposed to insanity are usually
too self-confident and self-willed to receive advice; and moderation
in all things, healthful occupation, temperate habits, good digestion,
and, above all, out-of-door life, seem as much like a sarcasm if
suggested to many of the toilers as a waste of words if recommended to
the idle and luxurious, while the parents who have transmitted to
their children unstable or diseased brains generally impair what
chances they have in life by vicious training.

Where syphilis, drunkenness, and other marked sources of mental
degeneration do not obtain, simple food, plenty of sleep, avoidance of
extremes of heat and cold, plain dressing, baths, good digestion,
out-of-door life, fresh air, careful attention to slight disorders or
injuries of the brain and nervous system, guidance against too much
study and too much excitement or dissipation, development of character
and moral force, intellectual and physical training, avoidance of too
much emotional, sentimental, or even artistic culture, careful
watchfulness during the period of adolescence, occupation without
overwork, healthful recreation, a {138} contented or philosophical
mind, and suitable marriages, would produce the strong wills and
healthy organisms needed to combat the tendencies of modern life. Such
a course would undoubtedly make many a child with an hereditary
predisposition to insanity become a healthy parent of children in whom
the same treatment would soon eliminate the family taint. The
character should be strengthened to learn to overcome difficulties
rather than evade them. There are cases in which such a course can be
adopted, and where the physician's advice may be of untold benefit to
generations.

There are many crises in life when the mind totters and seems ready to
fall, which the physician is more likely to recognize than any other
person. Sometimes the odds are too heavy to fight against, but often
there is a transient mental disturbance in such critical cases, or an
incipient insanity, according as the indications are met with wisdom
and patience or with neglect, indifference, and lack of judgment. The
treatment called for is of the person rather than of the mental state,
and in all forms of mental disease success in treatment depends very
materially upon the personality of the physician, who must adapt
himself also to the personality of the patient.

In about one-fourth of the cases of insanity there is no hereditary
predisposition to the disease, and its prevention can be most
hopefully looked for in attention to the general laws of health, the
observance of which tends to secure immunity from all diseases. In the
remaining cases—three times as many, in round numbers—the most hopeful
course is in abstaining from marriage altogether or in the avoidance
of unwise marriages; and it is an encouraging fact that many people in
the community now take that conscientious view of the matter, although
if they decide what to do without competent advice they are liable to
err in the opposite direction of exaggerating their morbid tendencies,
and so increasing their unhealthy predisposition. There are certain
groups of physical and mental manifestations which the experienced
physician recognizes as signs of tendencies which only await favorable
conditions—a sufficient exciting cause—in the indulgence in drink or
other excesses, in the exclusive search for wealth or fame, in the
absence of healthy occupation, in mental wear and worry, in
over-excitement, in the various conditions of ill-health, to develop
into actual insanity. This physiognomy of temperament suggests to the
observant physician a warning against excess of all kinds, and a
recommendation for that course in life which promises the greatest
likelihood of preserving a quiet mind and a healthy body and of
securing a rational employment. Too much work is less dangerous to
most people than too little.


States of Mental Defect and Degeneration.[12]

[Footnote 12: Compare Moreau's _La Psychologie morbide_ and Morel's
_Traité des Dégénérences physiques, intellectuelles, et morales de
l'Éspèce humaine_.]

MICROCEPHALISM, CRETINISM, INTELLECTUAL IDIOCY, MORAL IDIOCY,
INTELLECTUAL IMBECILITY, MORAL IMBECILITY (under which Westphal,
Spitzka, and others place moral insanity) are really names for
different degrees of similar defects, for the most part hereditary and
{139} congenital or resulting from disease or injury in infancy and
early childhood, as distinguished from dementia, which is the result
of later destructive mental or brain diseases. Idiots and the demented
insane are sometimes so alike in their mental condition that, if young
persons, they can be definitely distinguished one from the other only
by a knowledge of the previous history of the case. Idiocy has its
origin at or before birth or soon after, and terminal dementia seldom
before puberty, commonly after maturity. In the United States census,
where there is a doubt in the matter, the individual is classed as an
idiot if the mental disorder occurred before the age of twelve in
girls and fourteen in boys, and as insane (demented) if above that
age.

The microcephalic brain may be as small as one-fifth the normal size,
due chiefly to intra-uterine conditions for the most part unknown. Of
course that means complete idiocy. The brains of other idiots differ
in size and development. The mental condition in all is similar.
Idiocy with the small or large or asymmetrical brain is classified,
practically rather than scientifically, by Shuttleworth, as follows:

_A_. Congenital or Developmental[13] Cases.—1, Microcephalic, with
small heads: forehead and occiput defective; 2, hydrocephalic; 3,
plagiocephalic, with distorted heads: features in an oblique plane; 4,
scaphocephalic, with keel-like distortion of forehead; 5, scrofulous
cases; 6, Mongol type; 7, cretinoid cases, with stunted bodies:
irregularly expanded heads and enlarged thyroid glands; 8, syphilitic
cases; 9, primary neurotic, with body well developed: signs of
irregular nervous action; 10, sensorial idiocy, with two or more
senses deficient (_e.g._ sight and hearing); 11, mixed cases.

[Footnote 13: Developmental conveniently includes those cases which,
though of intra-uterine origin, become more pronounced as physical
development proceeds.]

_B_. Non-Congenital, Acquired, or Accidental.—1, Traumatic; 2,
post-febrile; 3, hydrocephalic; 4, hypertrophic, with large
square-built heads; 5, eclampsic; 6, epileptic; 7, paralytic; 8,
idiocy by deprivation: loss of two or more senses in infancy (_e.g._
sight and hearing); 9, emotional idiocy, with no bodily deformity:
shrinking, scared expression; 10, toxic idiocy, with no bodily
deformity: malnutrition.[14]

[Footnote 14: “The Physical Features of Idiocy,” _Liverpool
Medico-Chirurgical Journal_, July, 1883.]

From the creature of deformed limbs and ape-like movements, incapable
of articulate speech, even in monosyllables, or systematized ideas,
leading a purely vegetative life, unclean, and with the instincts of a
wild beast, up to moderate mental or moral imbecility, there are
endless varieties of defects and monstrosities in mind, character,
morals, and instincts, differing according to the profoundness of the
disorder of the brain (hydrocephalus, atrophy, sclerosis, inflammation
of the brain substance or membranes, injury from compression, blows,
falls, convulsions, etc.), the extent of the defect in the brain
development, the amount of the degenerative hereditary taint, or, in
the case of cretinism, the importance of the endemic as well as the
congenital influences.

In some of the higher planes of imbecility a considerable degree of
intellectual brightness, or even talent, is often observed, and every
variety of mental and moral perversion or simple reckless brutality.
Training often does a great deal to bring many of these unfortunate
creatures within the bounds of good behavior, but their care oftener
falls within {140} the province of the medical superintendent in an
asylum or the teacher than to the physician in general practice. They
are easily led astray by others, and commit all sorts of motiveless
crimes or with a trivial or disproportionate motive, and with blind
disregard of consequences or inability to comprehend them. In the
gallery, at Washington, of photographs of counterfeiters and of
passers of counterfeit money, the faces of the latter show
conclusively that they belong to the intellectually weak-minded or
imbecile class. Their own amusement, gratification, or impulse is so
far the basis of their conduct that only a minority are harmless if
not more or less constantly watched. Fortunately, a great
portion—unfortunately, not all—of the idiots are sterile, but many of
the mentally and morally weak-minded, with striking congenital defects
which no training can fully remedy, propagate their species
indefinitely for the benefit of our prisons and asylums.

Intellectual idiocy and marked intellectual imbecility are so common
as to constitute 1 in 650 of our population. Less noticeable
intellectual imbecility is quite frequent in the large class of
troublesome and perverse children and youth of both sexes, commonly
called weak-minded.

Moral imbecility, which cannot be corrected by education, is less
common.

Moral idiocy is rare. It consists in such an absence of the moral
sense that it cannot be aroused. It is sometimes associated with
sufficient intellectual powers to make deliberate action and
premeditation quite possible. Such persons are monstrosities, who, for
the safety of the community, must be kept shut up for life like wild
beasts.

The fact should be remembered, from a medico-legal point of view, that
the defective in mind are quite liable to short attacks of simple
mania and mental depression and to epilepsy, both of the obvious type
and of the obscure or masked form, so that their degrees of
responsibility, or rather of irresponsibility, vary from time to time.
As a rule, a good physical organization and a general condition
denoting healthy circulation and nutrition mark the better brains, and
constitute important elements in forming a prognosis in regard to the
possibility of educating imbecile and feeble-minded children up to the
point of reasonably good behavior and ability to at least partly take
care of themselves. The simpler their lives and the more purely
routine or imitative their work, the less their defect is noticed.
Many can wheel a barrow as well as any one.

THE INSANE TEMPERAMENT (Insane Diathesis, Neuro-psychopathische
Constitution) is an exaggeration of the nervous temperament. It is
closely allied to insanity and the neuroses, and at the critical
periods of life is very apt to develop into one of them. It is
congenital or due to early interference with the normal development of
the brain by injury or disease. It shows itself in childhood and
infancy by irregular or disturbed sleep, irritability, apprehension,
strange ideas, great sensitiveness to external impressions, high
temperature, delirium, or convulsions from slight causes, disagreeable
dreams and visions, romancing, intense feeling, periodic headache,
muscular twitchings, capricious appetite, and great intolerance of
stimulants and narcotics. At puberty developmental anomalies are often
observed in girls, and not seldom perverted sexual instincts in both
sexes. During adolescence there are often excessive shyness or
bravado, always introspection and self-consciousness, and sometimes
abeyance or absence of the sexual instinct, which, however, {141} is
frequently of extraordinary intensity. The imitative and imaginative
faculties may be quick. The affections and emotions are strong.
Vehement dislikes are formed, and intense personal attachments result
in extraordinary friendships, which not seldom swing suddenly around
to bitter enmity or indifference. The natural home associations and
feelings easily become disturbed or perverted. The passions are unduly
a force in the character, which is commonly said to lack will-power.
The individual's higher brain-centres are inhibited, and he dashes
about like a ship without a rudder, fairly well if the winds are fair
and the seas calm, but dependent upon the elements for the character
and time of the final wreck. Invention, poetry, music, artistic taste,
philanthropy, intensity, and originality are sometimes of a high order
among these persons, but desultory, half-finished work and
shiftlessness are much more common. With many of them concentrated,
sustained effort is impossible, and attempts to keep them to it result
disastrously. Their common sense, perception of the relations of life,
executive or business faculty, and judgment are seldom well developed.
The memory is now and then phenomenal. In later life there is a ready
reaction to external circumstances, even to the weather, by which the
individual is usually a little exhilarated or somewhat depressed. All
sorts of vaso-motor disturbances are common and create distressing
symptoms. Such people are said to be on the border-line between sanity
and insanity. They are apt to be self-conscious, egoistic, suspicious,
and morbidly conscientious; they easily become victims of insomnia,
neurasthenic, hypochondriacal, neurotic, hysterical, or insane, and
they offend against the proprieties of life or commit crimes with less
cause or provocation than other persons. At the same time that many of
them are among the most gifted and attractive people in their
community, the majority are otherwise, and possess an uncommon
capacity of making fools of themselves, being a nuisance to their
friends and of little use to the world. Many of them get fairly well
through life if their lives are tolerably easy or especially well
regulated; if not, even they seldom escape further disturbance during
the period of growing old. Their mortality-rate, especially from
pulmonary consumption, is high. The prognosis is usually stated as
unfavorable, largely, perhaps, because proper treatment is seldom
pursued. If such children could be placed in the hands of judicious
and experienced physicians from earliest years, much better results
would undoubtedly be got and the downward tendency might be stopped.
In the critical physiological periods of life, and under the influence
of mental worry with physical strain, there is danger of breaking
down. At the senile dissolution some of them lose much of their
lifelong peculiarities, and as the mind fails in force and activity
become more like other people. After the climacteric there may be also
great improvement.

TREATMENT should consist in the general principles of mental hygiene,
especially in training the mind to self-control and to avoid
introspection—in a word, in maintaining health and in having healthy
occupation. The earlier in life it begins, the better. It is well for
such persons, unless of uncommon gifts in some direction, as many are,
to obtain quiet, routine positions in life, and to avoid its wearing
responsibilities as much as possible. The question of marriage is a
difficult one for the physician if he is called upon for advice. Of
course the risk often can be estimated only {142} approximately, even
after knowing both parties, who will heed medical counsel implicitly
if it happens to coincide with their own notions. The further
propagation of the neuro-psychopathic constitution in the world
involves much entirely uncompensated misery, as well as genius,
enthusiasm, and originality, the compensation for which is estimated
by society in one way as regards Burns, Byron, De Quincey, Carlyle,
Goldsmith, John Howard, and Frederick the Great's father, and in
another when considering the inmates of jails and almshouses and the
destroyers of home peace. Maudsley thinks that one such poet as
Shelley justifies the risks of marriage in the insane diathesis, and
Savage considers the neuro-psychopathic constitution a useful element
in society; while Clouston holds that the world would be better off to
lose the few ill-balanced geniuses, the hundreds of impracticable,
unwise talented men and women, and the thousands of people who cannot
get on, shiftless, given to drink, idle, improvident, and unpractical,
to get rid of the insane diathesis, especially if we shall find a
middle course and learn to apply the laws of heredity so as to save
the best and eliminate the unsound. It is to this class probably that
Pinel refers in saying that what he calls moral insanity is largely a
matter of bad education. It is undoubtedly true that judicious
training in very many cases would limit, if not prevent, the further
development of the morbid element and strengthen the healthy side, so
as to prevent actual insanity.

CONSTITUTIONAL AFFECTIVE MENTAL DISEASE is a further development of
the congenital or hereditary predisposition to nervous or mental
disease, with more or less of the marks of the neuro-psychopathic
constitution. It is of two forms, the depressed and the mildly
exhilarated, in neither case amounting to simple melancholia or mild
mania. Sometimes the two forms are seen in a single member or in
different members of one family where mental degeneration has begun.
The frequent association of pulmonary consumption with these cases is
possibly, in part, due to malnutrition in those persons living under
the influence of more or less perpetual gloom, and to exposure and
over-exertion in those who are constantly unnaturally excited,
sleeping too little and driving their alert brains to the extent of
exhaustion. Misanthropists, communists, iconoclasts of all kinds,
enthusiasts and reformers, useful people and worse than useless,
common nuisances, criminals, saints, and heroes, are found among them.
Undoubtedly, in the case of criminals the tyranny of their
organization deprives the intellect of much of the proper inhibitory
power over the passions and evil tendencies, and yet with sufficient
motive they can hold themselves considerably in check.

The PROGNOSIS is not favorable. At the critical periods of life, after
severe diseases or injuries and with undue mental or physical strain,
there is danger of further progress of the disease into more
pronounced types; and this result is often the only way of satisfying
the community that what they called meanness or wickedness was only
disease. The progress of the disease is commonly very slow. It often
seems like simple progressive development of character, except for the
fact, generally overlooked, that it advances often in a different
direction to what would be natural, and is independent of normal
development. The subsidence of habitual severe headache not seldom
marks a sharp advance in the severity of the mental symptoms.

{143} The TREATMENT is hygienic. It must begin early in life, and be
devoted especially to avoidance of mental overwork, to healthy
occupation, to simple habits, and to a wise mental training.

MORAL INSANITY (Insanity of Action, Affective Insanity, l'Insanite
morale, Moralisches Irresein, Folie raisonnante, Folie lucide, Manie
sans délire of Pinel), the general moral mania of Ray, is
distinguished by that writer from partial moral mania (instinctive
mania, manie raisonnante of Pinel, la folie impulsive, impulsive
insanity, emotional insanity, impulsives Irresein), which includes
suicidal insanity, homicidal insanity, dipsomania, pyromania,
kleptomania, erotomania, nymphomania, satyriasis (aidoiomania), animal
impulse, perverted sexual instinct (conträre Sexualempfindung, la
sensation sexuelle contraire), and topophobia, if that disease be
classed among the insanities.

Moral insanity is seldom seen in the insane asylum until the disease
has passed over into pronounced mental enfeeblement or delusional
insanity. Purely moral insanity—“an uncontrollable violence of the
emotions and instincts”—is probably as rare as purely intellectual
insanity. Moral insanity is attended with some mental impairment, just
as moral perversion is part of intellectual insanity. Indeed, I have
heard patients complain as much of the degradation of character in
their insanity as of any symptoms referable directly to the intellect.
The term is not a fortunate one, but, like the expression moral
treatment of the insane, it is in quite general use. It is recognized
by all the authorities on mental disease, whatever may be their
opinions as to the limitations of responsibility in it. It is
especially to it that we can apply the words of the Autocrat of the
Breakfast-Table, that the worst forms of insanity are those to which
the asylum shuts its doors. It is marked by moral perversion, change
of character and action, and so little intellectual impairment as to
be easily overlooked by one not familiar with morbid mental phenomena.

Mild simple mania ending in recovery has been described as moral
insanity even by Pinel and Pritchard, and is so miscalled rather
generally at the present day. Moral deterioration is observed after
fevers or physiological periods of life, following slight and moderate
cerebral hemorrhages or injuries to the back and head, affecting the
brain, mental strain, etc., which, in persons of the
neuro-psychopathic constitution, now and then end in permanent change
of character. A similar but curable mental state is the frequent
beginning of more pronounced insanity, and often remains the sole
evidence of unsoundness of mind even after the patient is thought well
enough to be discharged from the asylum.

Although moral insanity is probably a common cause of young persons of
both sexes being led into lives of licentiousness, wickedness, and
crime, it is to be carefully differentiated from deliberate yielding
to temptation and following lives of vice until a strong enough motive
is offered for doing better or a punishment is made sufficient to be
deterrent.

Moral insanity is essentially a very slowly progressive and incurable
disease, starting in congenital or acquired mental deterioration, and
with its symptoms. It usually ends, after long years of wretchedness
to the individual and misery to his friends, in more general insanity,
slowly advancing dementia, death by intercurrent disease or accident,
or in suicide. It is a most distressing disease in the young, who are
punished {144} by parents and teachers in succession, sent about from
one school to another, boarded with friends or with disciplinarians
until all are wearied out in turn, and all too late conclude that the
case is one for a doctor or perhaps an asylum. At the evolution of the
sexual power and at its decadence, during menstruation, pregnancy,
childbirth, lactation, especially after fevers, blows injuring the
brain, and cerebral disease or disorders of any kind, are the periods
of especial danger, as more general mental disease is then developed
with seemingly trivial exciting causes. The friends observe that the
sufferers do not seem entirely natural. They imagine and suspect a
great deal, rather than possess real delusions. They often say that
their heads are not quite right, and manifest an evidently diminished
capacity for mental work, which tires them or makes them irritable.
Modest girls become indelicate, the truthful lie, the delicate use
profane and obscene language, the mild-mannered destroy furniture and
clothing, the peaceful quarrel, the gentle storm and rave; and yet
there is a standard of virtue and right, often a high one, on which
they theorize, and up to which they often think that they live. They
take strong dislikes to those with whom they are brought in contact,
especially their nearest relatives. They often lose the capacity to do
work, and now and then become spendthrifts or drunkards. As a rule,
there are frequent periods of quiet, amounting to depression, but
rarely reaching the condition of melancholia. Alternation or
periodicity in the symptoms is the rule. After threatening and even
endangering the lives of those nearest to them, insulting and
indelicate conduct in public, perhaps frequent arrests, a dozen times
outwitting those who wish to confine them in asylums, where they
belong, their minds being alert enough to attribute their conduct to
drink or some cause for which they receive slight punishment, and to
argue their own cases so as to convince almost any jury of their
sanity, the rule is that their doubts, imaginations, and suspicions
deepen into active insane delusions, their mental impairment advances
to noticeable dementia, their moral deterioration goes on to such a
degree of depravity that every body wonders why they had not been seen
to be insane long ago, and they are secluded in an asylum or
elsewhere. A not uncommon but unfortunate end is when they kill
themselves before anybody but a few specialists recognize their
irresponsibility. Their recklessness and want of judgment are often
the cause of fatal illnesses and accidents. Clouston reports the case
of a lady who by a series of extraordinary misrepresentations and
clever impostures raised large sums of money on no security whatever,
and spent them as recklessly; imposed on jewellers, so that they
trusted her with goods worth hundreds of pounds; furnished grand
houses at the expense of trusting upholsterers; introduced herself by
open impudence to one great nobleman after another, and then
introduced her dupes, who, on the faith of these distinguished social
connections, at once disgorged money. To one person she was a great
literary character; to another of royal descent; to another she had
immense expectations; to another she was a stern religionist. At last
all this lying, cheating, scheming, and imposture developed into
marked insanity and brain disease, of which she soon died; and it was
seen that all these people had been the dupes of a lunatic whose very
boldness, cunning, and mendacity had been the direct result of her
insanity.

S. K. Towle has reported the case of a man whom he had under {145} his
care at the Soldiers' Home near Milwaukee, Wis., as follows: “He had
been a lieutenant in a volunteer regiment, and I gave him rather more
privileges on that account, but after a time I found that he was more
nearly an example of total depravity than I had ever seen. There was
no truth in him, and he was intelligent enough to make his lies often
seem plausible to me as well as to others. By his writing and talking
and conduct generally he kept the patients and their friends in a
ferment, and gave me more trouble than the whole hospital besides. He
had a small scar about the middle of his forehead, which he said was
due to a slight flesh wound from a glancing ball in battle. While he
was under my care an older brother came to see him, and he told me
that up to the time his brother, my patient, who so tried my patience,
entered the army he was almost a model young man, amiable and
affectionate, the pet of the whole family and intimate friends; ‘But,’
said he, ‘ever since he came back he has been possessed of a devil if
ever any one was.’ After a time, much to my delight, he asked for a
transfer to the Soldiers' Home at Dayton, Ohio, which I got for him
with commendable alacrity; and he went there. His conduct at Dayton
was the same as with me, but after a few months he quite suddenly
died, when an autopsy was made. In sawing open the skull, at the point
of the small scar on his forehead the saw came directly upon the butt
end of a conical bullet, two-thirds of which projected through the
skull, piercing the membranes and into the brain. The internal table
of the skull had been considerably splintered by the ball, the pieces
not being entirely separated, and there was evidence of severe chronic
inflammation all around, and quite a collection of pus in the brain
where the ball projected into it. Here was the devil that had
possessed the poor fellow—that not only took his life, but destroyed
his character, lost him the love and esteem of his friends, and doomed
him for half a dozen years to do things he would most have hated and
despised when he was himself. Dunlap, the assistant surgeon at Dayton,
told me that he found in this man's trunk letters from several—half a
dozen, I think, at least—women in various places, from which it
appeared that he was engaged to be married to each one of them. The
letters were neatly tied up in packages, each one's separately, in
several instances with photographs supposed to be of the writers, and
the date of reception and reply was noted on many of the letters in a
business-like way.”

As Westphal well says[15] of such persons, “They often think correctly
and logically, and show reflection and deliberation to a certain
degree; but there is a certain something lacking, and there are some
general conceptions, general processes of thought and judgment, of
which they are incapable. Their mentality stops short on a certain
plane, especially in matters of judgment where every even uneducated
person easily succeeds. They sometimes act as if they had good
judgment and common sense, of which they are really destitute,
particularly in regard to the proprieties of life and their proper
social relations and duties. Certain of the finer feelings are
absolutely impossible of development in them. Through their various
nets, perverted by their mental defect, the patients often seem
perverse (bösartig), passionate (leidenschaftlich), although of true
sustained passion they are incapable. What seems passion is a sudden
idea or fitful impulse to which they yield at once. Moral insanity is
a defect in the affective {146} sphere, but also an intellectual
defect of a peculiar kind, which is often concealed under the mask of
a perverted moral sense, and which requires time and practice on the
part of the physician for its detection.”

[Footnote 15: _Berl. klin. Wochenchrift_, 1878, No. 15.]

Moral insanity is quite certain to pursue a downward course, although
something can be done by training, general hygiene, simple diet,
mental discipline, avoiding overwork, a judicious choice of the few
occupations of which the moral insane are capable, and a constant
steadying hand to help them try to keep their balance.

IMPULSIVE INSANITY is perhaps more properly called instinctive
monomania, as the morbid impulse is usually shown in only one insane
propensity at a time. Like moral insanity, its manifestations are
commonly periodic, or at least alternating. Under the name of
emotional insanity it furnishes sympathetic juries with an excuse for
finding not guilty of murder women who kill their betrayers and
husbands who shoot a wife's seducer. It is a not uncommon symptom in a
considerable proportion of the persons suffering from the various
forms of insanity. As a separate disease it is quite rare, and
includes those persons whose insanity is manifested, as Marc says, by
what they do rather than by what they say. The insane impulse does not
come from any logical process. It is rarely provoked by or associated
with a criminal motive, except in an analogous way to the production
by excitement of an epileptic attack, to which, indeed, it offers some
points of similarity. There would be reason to doubt the existence of
the disease unless other indications of mental degeneration were
present, especially where there is proof of a criminal motive or where
the criminal act and the prisoner's statements are the sole evidence
of unsoundness of mind. Unconsciousness, even temporary, and loss of
memory, are not symptoms of instinctive monomania. On the contrary,
the mind is quite clear, and resists successfully the insane impulse
so long that the person affected with it has often gained confidence
that he will never yield to it; and he soon learns the fact that,
there being in circumstances external to himself no reason for the
crime suggested to the mind with such force, temptations do not occur
to the act. While the impulse lasts a great variety of distressing
mental symptoms accompany it, so intense that the impulse often cannot
be resisted, and then the terrible brain-tension is relieved. I doubt
whether hallucinations of hearing are found in impulsive insanity, and
incline to think that all the reported cases where crimes of impulse
have been committed in obedience to a voice commanding the individual
to do this or that act of violence are more properly classified under
other forms of mental disease. One kind of instinctive monomania
sometimes disappears to be replaced by another. In developing boys and
girls there is not seldom a pathological mental state during which
lying, stealing, running away from home, etc. are common for several
months or a few years; but this is a curable condition, and does not
by any means necessarily end in instinctive monomania.

Suicidal insanity is probably the most common form of instinctive
monomania. The force, or even presence, of the suicidal impulse is
largely dependent upon the general tone of the system. The suicidal
idea is common; it occurs to the minds of a vast number of sane people
at one time or another under adverse circumstances. Hysterical women
talk a lot of nonsense on the subject. Self-destruction due to {147}
self-depreciation, weariness of life, and general gloom is not
uncommon in the insane temperament. It is also a refuge to proud and
sensitive people who have sacrificed their honor. But this is quite
different from suicidal insanity, in which the impulse is often
strongest at a time when there are the most reasons for living and the
greatest happiness in life if the tormenting demon urging to
self-murder could be excluded. Such people finally kill themselves, in
spite of their best resolutions and efforts to the contrary, if the
various faculties of the mind become more and more involved as the
disease goes on and the power of self-control is progressively
weakened. More general insanity of the degenerative type is sometimes
developed from suicidal insanity.

Homicidal insanity is fortunately still rarer than the last-mentioned
form, although motiveless homicidal ideas occur to husbands and wives
and parents with reference to those dearest to them, under conditions
of prolonged mental strain or exhaustion, during pregnancy and the
puerperal state, and at the climacterium. In suspected crimes the
evidence of homicidal insanity should be clear and should rest upon
the general signs of the degenerative mental state. Homicidal impulses
are common enough among the insane. Just as there are persons who do
not dare to have sharp instruments in their rooms for fear of killing
themselves, so there are others to whose minds axes, knives, and
razors suggest imperative conceptions of plans for killing another. It
is difficult in either case for the physician to satisfy himself at
what point real insanity begins. Seclusion under the morbid influences
of an asylum is very bad treatment for the individual, and symptoms
which seem very serious often disappear by restoring the general
health. In a recent case,[16] where a youth of nineteen was acquitted
of the murder of his mother on the ground of homicidal insanity, he
knew that the act was wrong, realized that he had committed a crime,
and was full of grief for it, as occurs in all such cases. It is the
rule, too, that there is some condition of mental defect or
degeneration out of which the homicidal insanity is developed.

[Footnote 16: _Quarterly Journal of Mental Science_, October, 1883, p.
387.]

Dipsomania, a rare manifestation of impulsive insanity, differs
entirely from the acquired alcohol habit, drunkenness, acute or
chronic alcoholism, delirium tremens, or habitual intoxication, all of
which conditions are also more readily developed in the
neuro-psychopathic constitution than in persons with healthy brains,
and may reach a point constituting insanity. Dipsomania is periodic,
uncontrollable, and associated with other evidences of the insane
diathesis. The prognosis is unfavorable. The treatment is to improve
the general nervous tone and to seclude the patient during his
attacks.

Pyromania and kleptomania are not rare as symptoms of insanity of the
marked forms which are observed in asylums. As manifestations of
impulsive insanity—that is, as constituting a form of insanity—they
are associated with other evidences of mental defect or degeneration.
Burning and stealing alone are not indications of insanity. As such,
they are without sane motive, and directed to objects in burning or
stealing which there is no gain to the person and usually no
gratification except the sense of relief which comes from yielding to
the impulse, and of distressing mental symptoms if the impulse is
resisted.

Nymphomania in the female, satyriasis in the male, and the various
{148} perverse and degrading methods of gratification of the sexual
instinct, may, when joined with other evidences of mental or nervous
disorder, constitute one form of impulsive insanity. Erotomania, an
ideal attachment without erotic feeling, is a more common mental
disease, but the other evidences of insane conduct are quite striking.
The same statement holds true of the many perverted instincts which,
according to circumstances, are or are not manifestations of the
defective brain-inhibition of disease. Animal impulse as a form of
impulsive insanity I had been inclined to doubt until I recently saw
two cases of as extreme mental suffering as I ever witnessed, in two
refined ladies who had suffered also from some cerebral symptoms,
occasional dizziness, and suicidal insanity, but who had no other
symptoms of cerebral disorder than those which are grouped under the
head of insane diathesis, and they not marked. It is not associated
with any erotic feeling or with particular persons. There is more
rapid wasting in flesh and strength and loss of sleep than in the
other forms of impulsive insanity, and, in my experience, greater
dread of yielding to the demon of unrest.

The perverted sexual instinct, with a feeling of repugnance to the
opposite sex, has thus far been observed chiefly in persons who have
been addicted to masturbation. It is marked by a passion for some
individual of the same sex, by other evidences of the neuropathic
condition, and commonly by a grotesque imitation of the habits or
dress of the opposite sex.

The indications for treatment in impulsive insanity are cod-liver oil,
the bromides, simple non-stimulating diet, open-air life, judiciously
regulated exercise, mental occupation so far as is possible, and
removal from suggestive surroundings and associations. The prognosis
is not favorable as to the final result. If the symptoms disappear on
restoration of the general health, other marked indications of
cerebro-mental disorder are pretty certain to appear sooner or later.

HYSTERICAL INSANITY is one of the states of mental degeneration, much
less common among men than among women, arising from the further
development of a neurosis, hysteria, and probably to a great extent
due to bad training. Hysterical symptoms, quite marked, are very
common among young persons and in single women of all ages in simple
mania. They are not uncommon in simple melancholia and in other forms
of mental disease. They add somewhat to the gravity of the prognosis
in these cases. They constitute a group of symptoms which I suppose to
be understood by those authors who speak of hysterical insanity as a
disease in which the cure-rate is high. But hysterical insanity, as
quite distinct from other psychoses, is quite a different matter. It
is characterized by extreme and rapid mobility of the mental
symptoms—amnesia, exhilaration, melancholic depression, theatrical
display, suspicion, distrust, prejudice, a curious combination of
truth and more or less unconscious deception, with periods of mental
clearness and sound judgment which are often of greater degree than is
common in their families; sleeplessness, distressing and grotesque
hallucinations of sight, distortion and perversion of facts rather
than definite delusions, visions, hyperæsthesias, anæsthesias,
paræsthesias, exceeding sensitiveness to light, touch, and sound,
morbid attachments, fanciful beliefs, an unhealthy imagination,
abortive or sensational suicidal manœuvres, occasional outbursts of
violence, a curious combination of unspeakable {149} wretchedness
alternating with joy, generosity, and selfishness—of gifts and graces
on the one hand and exactions on the other. The mental instability is
like a vane veered by every zephyr. The most trifling causes start a
mental whirlwind. There is no disease giving rise to more genuine
suffering or appealing more strongly for the sympathy which, freely
given, only does harm. One such person in the house wears out and
outlives one after another every healthy member of the family who is
unwisely allowed to devote herself with conscientious zeal to the
invalid.

The PROGNOSIS is unfavorable. While the symptoms may be alleviated and
a nominal cure may be effected, a relapse or the development of some
other troublesome form of insanity or neurosis is the rule, to which
the exceptions occur for the most part in women in whom there is also
some serious curable uterine disease or a state of excessive physical
prostration which can be relieved.

The TREATMENT of hysterical insanity demands tact and educating power
which will tax to the utmost the ingenuity of the wisest physician.
Sympathetic friends, and sympathy in general, are useful in
moderation, but they oftener do great harm, because they are
excessive; and the care which does good is that which, while being
kind and firm, tends to develop strength and character. The will and
the imagination are so extraordinarily powerful that their wise
direction and government constitute the most important part of
successful treatment. Diversion, occupation, and the development of
self-control, with careful attention to the general laws of health,
are quite important. The temptation to use drugs is, like the
fascination of being pitied and petted, very great, as alcohol,
chloral, or opium often acts like magic for the time being, and there
is generally a craving for one or all of them. But they are utterly
demoralizing in the end. The habitual use of stimulants and narcotics
in such cases only increases the evil. The fact must be recognized
that the hysterical insane are often least responsible where they seem
most so, and that they must be treated with unending patience,
kindness, gentle firmness, and a wise ignoring of most of the
symptoms. Simple palliative sedatives which cannot do harm must
sometimes be used, but the general rule, the less active treatment the
better, is safest. In the few cases where benefit has been got from
removal of the ovaries, healthy or diseased, the improvement, if it
shall prove to be lasting, will probably be attributable to the great
physiological shock from the operation rather than to any relation of
the ovaries to the disease. Removal from home is usually advisable for
a time at least—often it is necessary; and if residence in an asylum
is not thought to be wise, properly-selected hydropathic
establishments or private asylums are useful. Living in a judicious
physician's home is desirable when a suitable one can be found. In an
asylum a rational letting-alone treatment is found to be the most
successful. If the patient remains at home, hired nurses should be in
charge of the patient, or at least not members of the family. Safe
seclusion will be found necessary for the few who will not otherwise
be prevented from committing crimes and offences of startling
ingenuity or conspicuous publicity.

EPILEPTIC INSANITY arises from a neurosis, epilepsy, which almost
inevitably ends in mental deterioration of greater or less degree,
from scarcely noticeable impairment to complete dementia. The insanity
may {150} be a continuous state; it may be subsequent to the epileptic
attack, or precede it, or take the place of it. Epileptic dementia is
more nearly allied to idiocy than dementia following other mental
diseases, and it is associated with a degree of moral perversion and
brutality which is quite uncommon in other dementia. The insanity
following or preceding the epileptic attack is attended with stupor,
delusions of persecution, confusion, transitory fury, or a condition
quite analogous to somnambulism or cerebral automatism; and the same
may be said of insanity replacing the epileptic attack, except that
the most common condition in it is a violent maniacal fury, with
unconsciousness, and subsequent nearly if not quite complete amnesia.
The forms of mental impairment are progressive in the vast majority of
cases. The other forms are more amenable to the usual treatment of
epilepsy, and sometimes diminish in severity as the disease advances
and the mind becomes weakened. In the fury which takes the place of
the epileptic convulsion there is in nearly every case—I am inclined
to think in all cases—an intellectual aura, a slight change of action,
observable early enough to give warning of the approaching storm,
which can always be mitigated, and often entirely prevented, by
absolute rest in bed and the use of chloral and the bromides.

Although some few epileptics become well without treatment, and a
small number permanently recover under treatment, the PROGNOSIS is
even less favorable for the epileptic insane. The care of insane
epileptics should embrace, in the first place, safety to the community
by secluding those dangerous to it, and, second, the usual hygienic
and medical treatment of epilepsy.

Epileptic vertigo, analogous to petit mal, is a transitory mania,
often associated with passing delusions.

With regard to the responsibility of the epileptic insane—and, indeed,
all epileptics—the facts should be borne in mind that their mental
state is usually one of such instability that a slight irritation of
any kind is apt to induce a full or modified convulsion, and that
under provocation they commit partly volitional crimes, for which they
are not fully responsible.

HYPOCHONDRIACAL INSANITY differs only in degree from hypochondriasis,
described on a subsequent page. It is an incurable manifestation of
one type of the mental degenerations. It is slowly progressive, and
often ends in dementia. It differs from hypochondriacal melancholia in
being an evolution of mental defect or degeneration, and in the fact
that the mental depression, which is usually of a mild, periodic, or
impulsive form, is secondary to the other symptoms, and not, as in
hypochondriacal melancholia, the mental condition out of which the
hypochondriacal symptoms are evolved.

The TREATMENT consists in attention to the general laws of health,
occupation, and a fattening diet. It is seldom successfully managed
without occasional recourse to an asylum at least, and oftenest a
permanent residence in hospitals, occasionally changing, is quite
necessary.

PERIODIC INSANITY, usually mania or melancholia, is marked by attacks
recurring at more or less regular intervals, with a partial but not
complete return to the previous mental health between them. It is one
of the incurable degenerative mental diseases. The seeming recovery is
only apparent, and the mental deterioration is progressive, although
quite slow. The form of insanity is also not seldom a folie
raisonnante (affective {151} or moral insanity) with periods of all
sorts of excesses, destructive tendencies, tramp-life, destructive
acts, drunkenness, stealing, indecent exposure, etc. In the intervals,
which may be short or long, and which sometimes correspond to certain
seasons of the year, the mental condition is still a pathological one,
with the usual signs of mental degeneration, thereby being
differentiated from recurrent insanity, one of the curable
psychoneuroses, in which there is a state of mental health between the
successive attacks, but no sort of regularity or periodicity in the
recurrences. The prognosis is unfavorable, except in so far as a quiet
life in an asylum tends to prolong the intervals between the periodic
outbreaks, as well as to prevent annoyance to the community during
them.

CIRCULAR INSANITY (Alternating insanity, Folie circulaire, Folie à
double forme, Folie à formes alternes, Die cyclische Psychose, Das
circuläre Irresein) consists in a psycho-rhythm or succession, in
uniform order in each particular case, of (1) mental exaltation in all
degrees, from mild exhilaration or even gayness to acute mania, and
(2) mental depression of all conditions, torpor, or anergic stupor.
These two opposite mental conditions are separated in the vast
majority of cases by a shorter or longer interval of the normal mental
state, in which, however, there is soon observed some mental
impairment, however slight, rarely amounting to pronounced dementia
except in old age. Sometimes the three states shade off into each
other, so that it is difficult to say just where one begins and the
other ends; less often the transition is abrupt, sometimes during
sleep. The interval between the two opposite conditions of mind may
succeed either of the other mental stages, but the order once
established is maintained. The duration of the vicious circle varies
in succeeding attacks, sometimes becoming longer, sometimes shorter,
in the progress of the disease. The relative duration of the three
succeeding mental condition also varies, but the type of each remains
identical, or at least changes very gradually. The state of mental
exaltation often resembles moral insanity, with all sorts of immoral
impulses and tendencies, and may then properly be called an insanity
of action. The depression sometimes goes no farther than sluggishness
of will. The tendency of the disease is to shorten life only slightly,
if at all, except from the chance of suicide in the depressed state
and from exhaustion when the excited stage is one of active mania. The
shortest duration of the cycle in my experience has been twenty-four
hours, and the longest reported extends over several years. It
sometimes remains an affective insanity in its whole course, without
delusions and with little more dementia than might happen from simply
a corresponding advance in age without mental disease.

During the period of excitement some supervision or control will
usually be desirable, and removal to some retreat or asylum will often
be necessary. In the depressed stage the indications are to maintain
the general health, to meet the chances of suicide, and if there are
delusions to obviate the risks of danger to other persons. If the
interval of comparative mental health is of considerable duration, the
ordinary occupation of the patient can commonly be followed at that
time for a number of years, rarely for life; but a better result may
be looked for if the patient's circumstances are such that he can give
up active and anxious work for some quiet occupation not involving
great care.

PRIMARY INSANITY (primäre Verrücktheit, primordiale Verrücktheit,
{152} originäre Verrücktheit) is usually a further development of an
hereditary predisposition to mental disease. The term primary
monomania, although used as an equivalent for primäre Verrücktheit,
seems to me too narrow for a disease in which the leading delusion may
change so many times. Primary insanity is sometimes congenital, and
may be developed also by injury or by disease involving the brain
early in life or during the physiological changes at puberty, possibly
by self-abuse, in persons of an unstable mental organization. It often
develops so slowly with the character as to almost seem part of it,
until it reaches such a degree of insane delusion of self-importance
and expansive ideas as to be unmistakable insanity. There are also
delusions of persecution, distrust, and suspicion, erotomania, and
moral perversion, in spite of high claims to superior character, and
indeed in spite of a high standard of life in some particulars.
Perhaps the most striking symptom of primary insanity is the great
variety of imperative conceptions (Zwangsvorstellungen) by virtue of
which the individual is impelled, by a force often irresistible, to
commit various offences against propriety and the laws, even to
murder, as well as to perform countless acts of unwisdom or folly.
There are usually physical indications of chronic or old cerebral
disease, or of defect or degeneration in the incomplete or
asymmetrical development of the brain, which, however, may be no more
than are found in persons who might not be classed as of unsound mind.
Attacks of simple mania (mental excitement) of short duration are
quite common, and there is a progressive impairment of the higher
faculties of the brain—those which come last in a high order of
civilization—although there may be acuteness of memory, perspicacity,
and shrewdness which seem altogether phenomenal as compared with the
other mental qualities. There is no form of mental disease which is
better expressed by the word craziness than primary insanity, no other
in which the victim is more thoroughly in the grasp of his malady, and
yet no other in which he is more likely to be held responsible for the
crazy acts which he may perform, because his inherent mental state,
out of which his generally deluded frame of mind is evolved, gives
rise to delusive ideas of such a character that they are not
universally recognized, even by physicians of experience in mental
disease, as insane delusions, but are considered by some of them as
the prevarications of a criminally-minded person. When these persons
commit crimes, too, they often do so with methods and motives quite
like those of the ordinary criminal.

The PROGNOSIS in primary insanity, after the disease is fully
developed, is in the highest degree unfavorable. It remains to be seen
how much can be done by moral training in childhood and youth to
correct the evil tendency. The education of those who get into the
courts and insane asylums, so far as my knowledge of such cases goes,
has been bad to the last degree, so that, in my opinion, there has
been a fair difference of opinion as to which of them the law should
treat as criminals and which as insane persons.

TREATMENT for the most part requires absolute control of the
individual, which there is usually no one in the family sound enough
to maintain. If begun early, training away from home may accomplish
much. Restraint in some institution is commonly called for, but the
vast majority of the primary insane are allowed to take their chances
in {153} the world, and as many end in jails and prisons or on the
scaffold as in asylums.

The states of mental defect and degeneration, except in the case of
idiocy or marked imbecility, are not associated with such obvious
physical evidences of deviation from a normal mental standard as to
make them pathognomonic. While asymmetry and other cerebral defects
are frequently observed in them, it must be acknowledged with Schüle
that similar and as extensive gross intracranial anomalies are found
in persons who could not be called of unsound mind, and that this
statement holds true even of primary insanity, in which some writers
have laid so much stress upon the value of any indication of imperfect
or asymmetrical cerebral development. Any defect in the brain,
however, is far more common among persons of unsound mind than among
those of sound mind, and therefore in doubtful cases it is of a
certain value as corroborative evidence of mental infirmity or
impairment.

Spitzka places as signs of the insane constitution (1) atypical
asymmetry of the cerebral hemispheres as regards bulk; (2) atypical
asymmetry in the gyral development; (3) persistence of embryonic
features in the gyral arrangement; (4) defective development of the
great interhemispheric commissure; (5) irregular and defective
development of the great ganglia and of the conducting tracts; (6)
anomalies in the development of the minute elements of the brain; (7)
abnormal arrangement of the cerebral vascular channels,—at the same
time acknowledging that there are cases of insanity of inherited
origin in which cerebral defects are not discernible. It is too early
to estimate the value and importance of the finer or qualitative
cerebral defects as giving rise to insanity. Benedikt finds them also
in criminals.

With regard to responsibility before the law, the statutes of no
country provide for any criterion by which accountability is defined
in these cases; medical witnesses differ in opinion as to their
criminality, and the courts are obliged to interpret the law to suit
individual cases.

The states of mental defect and degeneration are not sharply defined.
They run more or less into one another. The fact should also be kept
in mind that isolated symptoms and groups of symptoms belonging to
them are repeatedly found in curable conditions of physical and mental
exhaustion in neurotic persons.

The degenerative mental states are thought to be increasing, to
furnish material for the increase in the otherwise curable insanities,
and to thus include much of that portion of the community which is
most filling up our institutions with incurable cases. It is probably
in the prevention of them, or at least in the proper training and
disposition of children affected with them or predisposed to them,
that the most can be done to stay the increase of insanity. Perhaps at
some time unwise marriages of passion and sentiment will be less
common than now, and the rights of children to a fair start in life
more considered.


Psychoneuroses.

AFFECTIVE MENTAL DISEASE is a folie raisonnante, one of the reasoning
insanities, sometimes called moral insanity, and very like the moral
{154} insanity already described, except in the absence of signs of
mental degeneration and in the fact that it is a curable disorder. It
is an insanity of action, marked by scarcely noticeable mental
impairment. It often is the early stage of more serious mental
disease, and not seldom its symptoms remain, as simply change of
character, after the striking symptoms of extensive mental disorder
have disappeared. It also exists and is cured without the appearance
of more pronounced insanity. At the time of the climacteric it is a
form of mental disorder not uncommon among women, who, however,
usually fail to recognize it as such until they have recovered.
Maudsley includes under this head simple melancholia, simple mania,
and moral alienation, but it will be more convenient for the present
purpose to use the term affective mental disease as indicating a
curable moral alienation or change of character affecting the
intellect chiefly so far as the judgment and sense of propriety only
are concerned, and not dependent upon constitutional defect or
developed degenerative mental state. There is usually slight
exhilaration or depression, which alternates or varies from time to
time.

The PROGNOSIS is favorable.

The TREATMENT is brain-nutrition, with those general measures already
described.

HYPOCHONDRIASIS, as Flint[17] well says, belongs in the list of
disorders of the mind, although the mental alienation is not regarded
as amounting to insanity. The mental state is one of morbid
imagination and apprehension rather than of definite delusion, and it
consists in a belief in the existence, present or to come, of maladies
and diseased conditions for which there is no foundation in fact, in
spite of sufficient proof of their unreality. There is usually, not
always, mental depression. Its causes lie in conditions, usually
obscure, which lower the tone of the general health, including
hereditary weaknesses, or depress the vitality of the brain either by
physical wear or mental worry, and the exhausting influence of
functional disorders or of organic diseases which may not be
discovered before the autopsy. Disappointment, bad habits, want of
proper mental occupation are often at fault.

[Footnote 17: _Practice of Medicine_, p. 854.]

The physical symptoms of hypochondriasis are commonly those associated
with impaired digestion and nutrition—namely, anæmia, dyspepsia,
neurasthenia, constipation, flatulence, headache or a feeling of
discomfort after using the brain, less appetite, slight loss of flesh,
disordered sleep.

The mental indications are more or less melancholy, indisposition to
exertion, irritability, diminished power of self-control, and an
inability to cease except temporarily from interpreting signs, proved
to be trivial, as indicating grave maladies or as forewarnings of
severe disease to come. Sometimes the fixed idea is limited to a
single false conception, but oftener slight changes in physical
symptoms or differing phases of morbid introspection produce a
complete kaleidoscope of pictures of fancied misery. The whole
catalogue of diseases, or a large part of it, may be exhausted, with
the help of some of the many foolish treatises always ready for
hypochondriacs or from reading medical books and talking with
charlatans, who are consulted at rapid intervals, one after another,
both by those who wander from office to office and those who take to
their beds. The most common type of hypochondriasis arises, directly
or indirectly, {155} in some form of unhealthy or false ideas
regarding the sexual function, and in the idea that some imagined or
exaggerated abuse of it has produced or will produce most serious
evils; but there is not an organ of the body which may not be the
basis for the unwholesome thoughts. Not seldom there is simply the
delusion of especial weakness or sensitiveness or delicacy.

Hypochondriasis may be only the early stage of more serious mental
disease. It may be one manifestation of an hereditary neurosis or
psychoneurosis, or it may arise from deterioration of the body's
vitality by organic disease, especially of the abdominal or pelvic
organs or through some incurable weakness or functional disorder. In
either of these cases its cause and duration will be determined by the
clinical history. As an uncomplicated psychoneurosis hypochondria
lasts from a few months to a number of years, with very little change
in its prominent symptoms, resulting in recovery for the most part,
becoming chronic in a moderate proportion of cases, and rarely proving
fatal except by some accidental complication, including suicide.

The PATHOLOGY AND MORBID ANATOMY of the disease are unknown.

The differential DIAGNOSIS consists in the exclusion of other
diseases.

The PROGNOSIS is favorable in uncomplicated cases.

TREATMENT consists in measures to improve the general health,
especially a full diet carefully selected, hydro-therapeutics,
massage, gymnastics, horseback riding, walking, rowing, abundant and
agreeable exercise in the open air, and the management of the
patient's surroundings so as to lighten the mind and relieve from
worry, perhaps by travel, sea-voyages, etc. Argument is commonly worse
than useless, but there should be a decided impression given that the
generally morbid state is due to ill-health. The risk of suicide is so
small that restrictions of liberty directed to its prevention do more
harm than good. It goes without saying that bad habits should be
reformed, narcotics should be avoided, and a healthy occupation should
be encouraged, or, if possible, insisted upon. The difficulties in
treatment are fully as great with the highly-educated superstitious
and credulous people whom we find in the literary and professional
circles as in the ignorant and weak-minded.

MELANCHOLIA (Die Melancholie, Schwermuth, Tiefsinn, Trübsinn,
Lypemanie, Mélaneolie, Aliénation partielle depressive, Monomanie
triste, Phrenalgie, Psychalgia) is one of the functional mental
diseases, in the sense that the pathological condition of the brain
upon which it depends is not yet known, although it is thought to
begin with disturbances in circulation and nutrition, which end, if
not resulting in cure, in atrophic, degenerative, and inflammatory
states, indicating, in the great majority of cases, extensive brain
disease. As a rule, melancholia first appears in a slight change of
character; the patient is said by his friends to be not quite like
himself. After some days or months, as the case may be, the symptoms
develop into settled gloom associated with mental pain—the state known
as

Simple Melancholia (Mélancolie raisonnante), in which the events of
life are correctly observed, but, incorrectly interpreted, are the
source of constant apprehension, self-depreciation, depression, and
despondency. There are no delusions, properly speaking, and yet there
is a disposition to take the dark-side view even of circumstances
which promise {156} favorably, which amounts to a generally deluded
state of mind. Commonly there is increased irritability, now and then
a genuine moral insanity, and occasionally in neuropathic
constitutions the state of mind already described under the head of
Impulsive Insanity, of which the suicidal impulse is the least
infrequent. Sometimes there are no physical indications of disease,
but as a rule there are headache, increased sensibility to light and
noise, sleeplessness, restlessness, impaired appetite and digestion,
gastro-intestinal catarrh, marked loss of flesh, diminished or
abolished sexual desire, and in women usually delayed menstruation or
amenorrhœa. A few persons are able to keep up, in an irregular sort of
way, their customary employment. In the majority of cases it is
impossible to concentrate the mind upon work, mental occupation
fatigues the brain, and the physical strength is too impaired for
steady labor. Suicide is thought of probably in nearly every case, as
it is by many sane people at some time in their lives, but it is very
seldom committed unless there are such disgraceful or distressing acts
performed or suffered by them as would tempt to suicide in sane
people. There is no danger of deliberate homicidal acts in persons of
good character. A criminally disposed person would more readily commit
murder in simple melancholia than if free from that disease.

Simple melancholia may be the initial stage of almost all of the
mental diseases, especially acute mania, paralytic dementia, and the
severer forms of melancholia. It may be differentiated from the first
stage of mania only by waiting until other symptoms appear or not, and
the same is true with regard to distinguishing it from the forms of
melancholia involving danger to life. In the latter case, however,
there is much greater difficulty in diagnosis, inasmuch as insane
delusions may be concealed, and there may be so slight a change in the
patient's behavior when delusions appear in his mind that the closest
observation is needed to guard against them. The simple melancholia
marking the first stage of paralytic dementia is characterized by
noticeable although often slight mental impairment—a distinctly
diminished capacity for work, of which the individual himself is not
seldom conscious, whereas in the disease simple melancholia the mind's
usual power is exerted, provided its attention can be withdrawn from
morbid introspection and concentrated upon any subject, as it commonly
can be for a while.

Melancholia with delusions (acute melancholia) is commonly a further
development of simple melancholia, but sometimes its course is so
rapid that if there is a period of mental depression without delusion
it is overlooked. The earliest and most common delusion is some form
of causeless self-reproach with regard to some matter, whether trivial
or important, or of groundless self-accusation, of impossible sins of
omission or commission, but generally of some vague, undefinable
fault, as having irretrievably offended God or committed the
unpardonable sin, etc. Often this and an unfounded belief in
self-unworthiness are the only delusions present, and in that case
within narrowed limitations the mind acts soundly in other matters.
The feeling of personal fault or sin often expands to a sense of the
justice of punishment, and the consequent delusion that all sorts of
terrible things are to happen—poverty, the poorhouse, or some great
unknown dread, even involving family and friends; and from personal
sin or fault it is only a step to the belief {157} that the world is
all wrong, and to the certainty that everything is going to worse than
ruin. Illusions of sight and hearing may magnify common fires and
locomotive whistles into general conflagrations of the world and
shrieks of tormented persons. Hallucinations of the special senses may
create visions of all sorts of imaginary horrors, sounds of voices
saying every possible dreadful thing, odors most disagreeable, tastes
most vile. Anæsthesia prompts the delusion of death, and hyperæsthesia
of burning, freezing, scalding, etc. Some mysterious force within
them, which they can neither explain nor understand, drives them to
automatic acts of all kinds—to obscenity, profanity, verbigeration,
intonation of sentences, wailing, screaming, destructiveness, etc. In
cases of exceptional severity the mind seems deluded on almost every
subject: the food is poisoned, the atmosphere is deadly, the world
loses all its reality, friends their identity, things their substance.
They are to be burned alive, starved, quartered, suffocated,
smothered, drowned. Every conceivable and inconceivable thing is to
happen. The delusions are nearly always of the illogical or
unsystematized kind, although systematized delusions of persecution
are met, for the most part, in incurable cases. Deliberate plans of
suicide are formed in most cases, and are to be suspected in all.
Homicidal attempts are apt to be made upon persons whom it is desired
to save from impending calamities. Suicidal, and less often homicidal,
impulses occur. Suicide and homicide from deliberation need, to be
successful, (1) the opportunity, (2) lack of power of self-control,
and (3) a strong determination. Sometimes there is the will without
the opportunity, or the opportunity with self-control; and for this
reason persons in danger of killing themselves or others often for
months escape any acts of violence. Not seldom, too, they determine to
kill themselves or family in a particular way, and neglect other
chances so long that they are thought to be not meditating destruction
of self or others. When the determination or impulse to suicide or
homicide is persistent and desperate, no means are too horrible and no
opportunities too hopeless to be attempted. There is no reason for a
special name for these symptoms, but they have been called suicidal
melancholia and homicidal melancholia. No more is there any
justification of the term hypochondriacal melancholia for melancholia
with hypochondriacal symptoms.

In melancholia with delusions there is sooner or later, in the
majority of cases, refusal to eat, from lack of appetite, nausea, or
disgust of food, from disagreeable hallucinations of taste or smell,
from delusions that it is a sin to eat, that the stomach is full, that
the mouth is sealed or the throat obstructed, that the food is not and
cannot be paid for, that eating will do no good, etc., from a wish to
commit suicide by starving, or in the states of stupor
(attonitäts-zustände) from mental torpor or stupidity. Sometimes there
is resistance to the calls to eat, urinate, or defecate by virtue of
resistive melancholia—a condition to resist and oppose everything—or
from delusions that it will destroy the soul, etc. to follow the
natural inclinations. Refusal of food may be under certain conditions
instinctive and conservative. It is the exception for the bodily
functions to be well performed. Usually, there is obstinate
constipation, with headache, coated tongue, greater variation in daily
temperature than is usual in health, accelerated pulse, and rapid
wasting in flesh. The various anomalous sensations observed in
functional diseases of the nervous {158} system are common.
Masturbation is a not infrequent symptom of loss of self-control in
both sexes.

Acute melancholia is sometimes confounded with delusional insanity
with mental depression. In the former the delusions are evolved from
the mental state; in the latter, the mental state from the delusions.
In the former the delusions are for the most part unsystematized: the
patient cannot state why he believes them to be true; in the latter
there is correct reasoning from false premises: the delusions are
logical or systematized and of a depressing character, so that a
belief in them naturally gives rise to sadness.

Before the courts the fact should be kept in mind that persons with
acute melancholia have diminished power of self-control by virtue of
their disease, and so yield more readily to temptation than in health.
They also may have imperative conceptions—ideas so strong that they
cannot, or can with difficulty, resist carrying them out even when
they know them to be wrong; and there may be sudden outbursts of
almost maniacal excitement. They are often able to make wills and
perform contracts, in form and in detail, as well as ever, when they
are so filled with insane delusions as to be on the point of killing
themselves and their families. There is impaired capacity, however, of
recognizing the relations of persons and things to one another, a
distinct moral perversion, and a diminished recognition of obligations
and sense of responsibility. In other words, they are not always fully
themselves on those points in which they seem to be so, and yet
patients in asylums with acute melancholia have been known to give the
best of advice to their business-partners.

Melancholia with stupor (melancholia attonita) appears like complete
dementia or a mindless state, but there are now and then evidences of
intelligence. The mind is filled with overwhelming and terrible
delusions, which paralyze the will and place mental and physical
activity for a while in abeyance. It arises commonly in the course of
the less profound form of melancholia, after some great mental shock,
and there is a condition of marked anæmia of the brain, probably
symptomatic rather than pathognomonic, which if not soon relieved goes
on rapidly to atrophy and degeneration. Except when there are attacks
of frenzy, which may occur at any time, there is little danger of
active violent acts except suicide, desperate refusal of food, and
determined resistance to any care or treatment. There are the usual
indications of physical exhaustion.

In melancholia agitata the mind is clear and active, the opposite of
the condition last described, and the distressing delusions produce
such a degree of motor excitement arising from the mental suffering
that the disease closely simulates acute mania. The mind not only
reacts as readily as in health to distressing ideas, but abandons
itself more fully to their domination through diminished will-power
and lack of self-control. Almost blind acts of desperation and fury
are committed from which the utmost vigilance can hardly save them.

The three severe forms of melancholia just described are
interchangeable in the same person during the course of his illness,
so that the states of frenzy and stupor are more properly called
symptoms than classes of disease.

Melancholia among children is more common than the books state it to
be, although rarely met in the asylums. Magnan has reported a {159}
suicidal case in a child four years old, and it occurs up to the
latest years of life.

The DURATION of simple melancholia is from a few weeks to a dozen
years; of acute melancholia, from a month to two or three years, after
which it is apt to end in chronicity; melancholia stupida (with
stupor) is usually curable, if at all, in the first year, although
relapses are frequent, and in melancholia agitata from a year to three
years is the common limit of the possibility of a cure.

The PROGNOSIS in simple melancholia is favorable. Including cases
treated out of asylums, probably 90 per cent. recover; in acute
melancholia, uncomplicated with other diseases, not far from
two-thirds recover; in melancholia attonita less than half get well;
and in melancholia agitata nominal recovery occurs perhaps in a third
of the cases, although I doubt whether complete restoration to health
is seen often.

In chronic melancholia the process of mental deterioration is slow. As
the mind becomes impaired the delusions lose their activity and the
mind reacts less readily, so that a state of less suffering and
greater calm is reached, and the patients are often useful workers in
asylums for many years, or remain in their own homes a constant source
of anxiety to those who understand their condition. Many of them
commit suicide.

In treatment of melancholia the first indication is to protect society
and the individual against acts of violence. Homicidal acts are not to
be feared in simple melancholia, unless in persons of bad character
and ugly temper, or in those few cases with the symptoms, in addition,
of moral insanity or impulsive insanity. Suicide is so rare that
precautions will not often be needed against it, provided the patient
is so frank or so transparent that the appearance of distinct
delusions may be detected and then guarded against. In cases of long
standing, especially in persons beyond middle age, this is extremely
difficult, and their treatment outside of asylums must always be
attended with risk. In the other forms of melancholia the fact should
be taken for granted that the patient is suicidal, and he may be also
homicidal, so that he should be watched constantly and efficiently,
and never left alone or with weak or helpless persons, no matter how
free from suicidal determination or impulse he may have appeared. The
puerperal mother, especially, is a source of the greatest danger to
her child, even when she seems natural and fond. The degree and kind
of watching varies, according to the severity of the case, from the
constant presence or close proximity of some responsible person, who
may sleep in the same room with the usual home-surroundings, to the
most vigilant and wakeful personal care every moment day and night,
and removal of every source of possible self-injury. In some few cases
this can be well done only in an asylum or in a padded room. Some form
of restraint, either personal or by confining or limiting the
movements of the hands in rare cases of exceptional desperation, will
be found necessary.

Placing the patient in an entirely healthy atmosphere is next in
importance. In the very earliest stage quiet, recreation, change of
scene, and association with a pleasant and judicious companion are
often sufficient to effect a cure. If the disease is pronounced, rest
and removal from sources of irritation are more important until
convalescence, when travel may be tried. The question of removal from
home and commitment to an asylum {160} should be decided upon the
grounds already stated in considering the general treatment of mental
diseases. The degree in which the patient should have exercise,
occupation, and recreation or be let alone will be determined for each
individual case. The fact should be borne in mind that the disease is
a debilitating one, and that it arises in conditions of mental or
physical exhaustion. Massage and a modified rest-cure, without
seclusion, are beneficial in some cases, especially of elderly people.
Baths and the cold pack should be used with discrimination.
Electricity, where it does not give rise or add to delusions, is a
useful tonic, especially in passive cases. There are very few patients
of such desperate frenzy as to require confinement of the hands, and
that should only be done with an attendant close at hand. Whatever is
done, nothing should be attempted which excites delusions unless it be
absolutely necessary. Fresh air, and an abundance of it, are very
important. Experience and careful study of the particular case will be
needed to know how far to press the taking of food. But the necessary
amount should be given by the stomach-tube if ordinary means fail, and
it is better to use it early rather than tire the patient out with
ineffectual attempts with spoons, etc. Whether the nasal or œsophageal
tube be used—of which I prefer the latter—the greatest care should be
taken not to inject food into the lungs, the throat being so devoid of
sensitiveness sometimes that the tube may be passed into the trachea.
Nutrient enemata may be relied upon for a week or two if the patient
is in bed, but no longer.

Tonics are indicated—cod-liver oil with bark, the hypophosphites,
dilute phosphoric acid, malt. Strychnia, iron, and quinine should be
used with caution, as they often cause disagreeable headache with
indisposition to sleep. Fattening food will be found useful in most
cases. The few fat melancholies need nitrogenous food and graduated
exercise. Constipation will be corrected in many cases by a full,
laxative diet, cod-liver oil, malt, or it may be beer. Mineral water
or Sprudel salts are usually indicated. A pill containing aloin,
strychnia, belladonna, mastich, or even colocynth or podophyllin, may
be needed in obstinate constipation.

Medicines to control restlessness and sleeplessness should be avoided
if possible. Hydrate of chloral, opium, bromides, valerian, sometimes
increase the difficulty, and the objections to their prolonged use are
obvious, and yet they must sometimes be used for a time. The bromides,
with cannabis indica, valerianate of zinc, camphor, and hyoscyamus,
may serve an excellent purpose for a time. Opium and its preparations,
where they agree, act like magic in producing mental calm and sleep.
They may relieve constipation and increase the desire for food, but
the danger of the opium habit is so great that their use should be
decided upon only in extreme cases, and the effect should be watched
from dose to dose, each one of which should be given under medical
direction. Wilful masturbation, one of the signs of loss of
self-control which occurs in the best of people, cannot be corrected
by drugs or appliances, but only by constant watching and by placing
the individual where his self-respect, as soon as it can be appealed
to, will keep him from it. If it is uncontrollable and symptomatic,
fresh air and exercise, and, if necessary, bromides or opiates in
moderate doses, with a tonic (not iron), should be used.

{161} MANIA (Manie, Exaltation générale), according to Morel, meant,
in the original Greek, folie or madness, while Esquirol derives it
from the Greek word meaning moon, making the words maniac and lunatic
equivalent. The word mania is still used in this loose way, even by
writers on mental disease, as a synonym of insanity. Its use is
properly restricted to conditions of mental exhilaration or excitement
with motor activity. The morbid anatomy of the disease is not yet made
out, and the indications of hyperæmia observed in the acute stage
after death are no greater than are found in diseases in which mania
is not a symptom. In its final stages atrophic, degenerative, and
inflammatory signs are abundant and well marked.

Simple mania[18] (manie sans délire, manie raisonnante), an exaltation
of the mental faculties similar to the exhilaration produced by too
much wine, with an accelerated flow of ideas, impaired judgment, and
motor activity, without definite delusions, delirium, or incoherence,
has been called an insanity of action, affective insanity, folie
raisonnante, and even moral insanity, from which it differs in being
marked by constant mental elation and exaltation of the physical
functions, and not necessarily by striking moral perversion. It is a
mental erethism, an exaggerated gayety, an uncontrollable
exhilaration, an unbounded joy, an excessive anxiety, a perpetual
anger, unusually good spirits, increased intellectual and physical
energy, with such striking loss of self-control, diminished powers of
reflection, and so decided weakening of the judgment that all sorts of
unwonted errors of commission or omission may be performed. Under its
influence many fortunes have been lost, many reputations have been
ruined, and the happiness of many families has been sacrificed before
the existence of insanity was suspected, except possibly by a very few
persons. Indeed, the wit is usually so sharpened, the flow of ideas
often so clear and rapid, the capacity for brain- and body-work
without fatigue is generally so increased, that not seldom the patient
is remarked upon as being unusually well. The most troublesome
symptoms arise from the tendency to squander property, to drink
alcoholic liquors to excess, and, especially in women, to allow the
exalted sexual desires to get control of the judgment and reason,
thereby bringing about unfortunate marriages or scandalous relations
with the opposite sex. In women there is commonly increased menstrual
flow.

[Footnote 18: Also called by some writers moral insanity, folie
morale, folie des actes, folie or manie instinctive.]

The course of the disease is without material change, and the duration
is from several weeks to a number of years. When it does not
constitute the initial stage of other types of mental disease,
especially severer forms of mania, circular insanity, general
paralysis, or (in the neuropathic constitutions and at the critical
ages) mental degeneration, the termination is in recovery in about 90
per cent. of the cases, although sometimes some moral impairment or
deterioration in character remains for life. The recklessness incident
to the disease leads to unusual risks, now and then to fatal
accidents. Simple mania rarely becomes chronic.

TREATMENT involves the necessity of proper control to prevent
scandals, disasters, and perhaps crimes. The matter of the degree of
seclusion and control should be governed by the general considerations
already mentioned in the general treatment of insanity, bearing in
mind that {162} repression of the motor energy, except to prevent
exhaustion, does harm. The demand for food is enormous; its supply
should be abundant and judiciously chosen with reference to easy
digestion. Frequent prolonged warm baths and cool applications to the
head are indicated, and the usual palliatives for headache,
sleeplessness, constipation, etc. The surroundings should be such as
to favor rest and undisturbed sleep, and to dispel sources of
excitement, whether they arise in certain associations, localities,
occupations, or persons.

Acute mania (Tobsucht) follows an incubative stage of simple
melancholia, often of simple mania, and rarely bursts out without
previous indications of disease. Delusions, unsystematized and
illogical, are abundant; the ideas flow so rapidly that the mechanism
of speech is not adequate to their expression; the motor excitement is
intense. In the most severe forms there is mental confusion, delirium,
incoherence of ideas, and furious muscular action, to the point often
of acts of destructiveness and self-injury. The clothing is torn to
shreds, and no act of violence is too wild not to be attempted without
warning. The skin is hot, the tongue heavily coated, the pulse
accelerated, the temperature elevated, more, probably, than would be
accounted for by the physical activity—from one to two or three
degrees—now and then, in conditions of exhaustion, a little below the
normal. Just as there is liable to be maniacal frenzy in the course of
severe melancholia, so in acute mania outbursts are seen of
desperately suicidal melancholic frenzy. Unless great care is used to
keep up the strength, and often in spite of it, exhaustion rapidly
sets in, under the influence of which the symptoms are very much
aggravated. The amenorrhœa in women in this condition is conservative.

The COURSE AND DURATION of acute mania vary within wide limits, with
an average of not far from six months, with recoveries in about 60 per
cent. of first cases uncomplicated by pneumonia, chronic disease, or a
marked neuropathic state: 5 or 6 per cent. die, chiefly from
pneumonia, phthisis, accidents, or exhaustion, seldom suicide.
Incurable cases drop slowly into dementia or into chronic delusional
insanity, the motor excitement subsiding. The delusional insanity may
be simply a stage in the process toward dementia.

In the DIAGNOSIS of acute mania, unless great care is used, the
physician sometimes finds that he has sent to the asylum a case of
acute, especially infectious disease, in the early stage and with
unusual manifestations of febrile delirium. The indications for
avoiding this unfortunate mistake are care and time in making
diagnoses.

In the TREATMENT of acute mania the matter of foremost importance is
that the physician should be able to sufficiently control his patient
to prevent harm, and that he should have him in such a place as to
give him an abundance of fresh air, unhampered by annoying and
irritating limitations of his free will, restrictions of his liberty,
and repression of his motor excitement. The risks of injury to others
must be reasonably provided against. It goes without saying that few
homes meet these indications: very few people can command a house to
be converted into a virtual hospital, with the care of trained
physicians to direct every little detail of treatment, and proper
nursing. The public asylum, therefore, or the private retreat must
usually be depended upon. In the case {163} of quiet young people,
especially of young women whose illness may be of such a nature as to
justify their marrying after recovery, and in the acute mania
following childbirth, it is well worth the physician's while to make
an effort to keep the patient in a private house when the conditions
are such as to make such a course practicable. To the rest and quiet
which may be had under such circumstances, with all the goings on of
the house regulated to the patient's comfort and convenience, to
prolonged hot baths, a full simple diet, given with the stomach-tube
if necessary, as few medicines as can be got on with, the supervision
of the nurses by some judicious member of the family, and the
gentleness (combined, of course, with proper firmness) of
home-influences, I attach very great importance in properly selected
cases. But I attribute as much to the restful influence of keeping the
patients among familiar scenes, and where some familiar face and voice
can reassure them in their comparatively clear moments, instead of
their being agitated and distressed to know how to account for the
strange people and cell-like room of the insane ward to which they
will awaken from their delirium in the hospital. It is something to
avoid the excitement of commitment and removal to an asylum, with all
that they involve, as well as the sight of demented patients, whose
noise may make sleep impossible just when it is most needed. Acute
mania seems to me to arise much less often than other mental diseases
in definite associations which need to be escaped from for successful
treatment.

The term subacute mania is used by some writers for the milder cases
of acute mania, just as acute delirious mania is a term which is
applied to those violent cases of acute mania in which furious and
prolonged delirium marks the disease, and in which there is a high
death-rate and low proportion of recoveries.

In chronic mania the motor excitement, mental instability, and, sooner
or later, delusions, if not present at the beginning, as is usual,
continue. The progress to dementia is commonly slow, and there are few
cases which it is wise to treat away from an asylum or its
dependencies on account of the possible danger to others from sudden
exacerbations of the disease or through uncontrolled violent impulses.

Although there is no pathological condition distinctive of mania in
its curable stage, conditions indicating hyperæmia are usually found,
whether as a result of the disease or its underlying cause, and
sometimes meningitis. In chronic mania there is in the terminal stages
evidence of atrophic and degenerative changes which do not distinguish
it from other forms of mental disease.

ACUTE DELIRIUM is the typhomania of Bell. Its prevailing mental state
is of mania oftener than of melancholia. It resembles the worst cases
of typhoid fever so closely, and it is so uncommon a form of disease,
that the mistake has often been made of sending typhoid-fever patients
to insane asylums. The mistake is unnecessary, as the clinical
features of typhoid fever are so well marked that with sufficient care
and delay they may be recognized if the physician does not commit the
common error in mania of being too much afraid of his patient to
examine him thoroughly. The tendency to exhaustion in acute delirium
is rarely successfully combated, as the motor excitement is so intense
and the delirium so furious that nourishment to meet the tremendous
demands of the {164} system can seldom be given, and death is the
usual result. Recoveries are rare, but less uncommon in the
melancholic than in the maniacal form.

Little need be said in the way of TREATMENT, except that in so
speedily fatal a disease it is well to keep the patient at home, if he
can be properly cared for there.

TRANSITORY INSANITY is used by Krafft-Ebing[19] (Transitorisches
Irresein) as indicating mental disease differing from other insanity
only in the fact that it is of short duration—namely, from two to six
days. If it is applied to sudden and transient outbursts of mania,
with delirium, loss of power of self-control, and inability to clearly
recollect the circumstances of the attack and what happened during its
continuance, it is a rare disease, occurring for the most part in
epileptics and in persons under the influence of alcohol or addicted
to its habitual use. It is sometimes, under the latter-named
condition, called alcoholic trance. It consists in an automatic state
resembling the epileptic delirium, which may occur also in sleep and
resemble somnambulism. The actions are guided by co-ordinated will
without conscious intelligence, and may consist in crimes and
brutalities and foolishness entirely inconsistent with the character
in health. It seldom lasts more than a few hours. When caused by
alcohol or as a symptom of epilepsy, it may occur without other marked
inciting cause; otherwise it is commonly due to mental shock. Several
cases happened during the mental excitement of the first battle in our
civil war. The most striking case within my own experience was that of
a man who under the strain of prolonged grief and the mental shock of
a great fire destroying a large part of the town in which he lived,
perhaps moderately affected by alcohol, suddenly grasped an axe and
cut off with one blow the head of a beloved child. He was found in the
street without knowing how he had got there or what he had done.

[Footnote 19: _Irrenfreund_, 1883, p. 113.]

One attack is the rule, although several, probably of an epileptic
nature, have been reported. It is an extremely difficult condition to
diagnosticate with certainty, and is therefore often the refuge of
criminals and a resource of criminal lawyers. The most likely honest
mistake liable to be made regarding it is to confound it with an
outburst of passion.

PRIMARY DEMENTIA (Acute dementia, Stuporous insanity, Anergic stupor)
is a disease chiefly of youth and early maturity in persons of
inherited weakness or under the influence of prolonged exhausting
conditions, to which some mental shock usually adds the immediate
cause. Although most of the cases are under the age of twenty-five, it
occurs up to forty-five. Masturbation is so common a symptom in its
course—and it may be one of the debilitating and enervating factors
constituting a predisposing cause—that most of the primary dementia is
classed in some asylums as insanity of masturbation. There may be an
initial stage of a number of days, marked by moderate melancholia or
by maniacal excitement, but there is usually mental torpor advancing
rapidly to pronounced dementia. In rare cases there is marked chorea,
and slight choreic movements are often observed. The course of primary
dementia may be subacute and advance with extreme slowness.

There is no overwhelming delusion paralyzing the mind, so to speak, as
in melancholia attonita (melancholia with stupor). In acute cases the
brain quickly falls into a state of profound anæmia, precisely such as
is {165} found post-mortem in starved dogs, and loses its power to a
greater or less extent of reacting to the stimulus of the senses.
There is little or no sensation of hunger, the sensory nerves are
nearly or quite paralyzed, the bladder and rectum become distended
until urine and feces are voided unconsciously or at least
uncontrolled, and voluntary movements almost cease, although the
muscles are capable of acting if directed: if led or pushed, the
patient walks; if placed in a chair or bed, remains there; and in the
worst cases lies on the floor quite inattentive to all the decencies
of life unless constantly looked after. There is always partial, and
there may be complete, anæsthesia, to such an extent that even the
involuntary muscles do not respond to the ordinary stimuli. There is
rapid loss of flesh, very sluggish circulation, and feeble
heart-action. After recovery the patient speaks of the stage of his
greatest illness as a blank in his memory.

This description of pronounced cases of primary dementia of the most
severe type needs modification as applied to milder cases, which may
exist in all degrees, down to a state of mental impairment of very
moderate extent.

The mental impairment may be progressive and quite incurable, but also
so slight in the beginning, and may make such slow progress, as to
entirely escape detection for several years, and then attract
attention at first by the lowered plane of character and loss of
self-control in little matters of daily life, rather than by the
intellectual deterioration, which by that time has become quite
marked. This subacute form of primary dementia in young people rarely
finds its way into the insane asylum until the second, third, or
fourth year of its course, and then its progress is slowly downward.
It has none of the eccentric or grotesque features of hebephrenia, and
little of its emotional disturbances.

Subacute primary dementia in the later years of maturity, just before
or several years before the climacteric, is of grave import, as it
indicates the development of an hereditary predisposition to insanity
in a form which not only offers no reasonable hope of recovery, but
also is quite certain to manifest a change of character which is even
more difficult to treat and properly control than the intellectual
failure. As it is most likely to arise under circumstances of wear and
worry, its symptoms may be for a long time attributed to
disappointment or bad temper. After the dementia becomes pronounced
its downward course is seldom otherwise than very rapid.

SECONDARY DEMENTIA is a convenient name for the curable dementia which
appears at the subsidence of acute symptoms occasionally in mania, and
rarely in melancholia—that is, just about the beginning of the period
of convalescence. It is also called secondary stupor.

In primary and secondary dementia, resulting in recovery, the progress
of the disease is rarely otherwise than very rapid, and unless a cure
takes place in a few months at the outside, secondary changes occur in
the brain and the tendency is to terminal or incurable dementia. So
many cases are treated outside of asylums that it is difficult to
estimate the cure-rate, but it is probably not less than 60 or 70 per
cent., although it is quite common in the apparent cures for the brain
to remain on a lower intellectual or moral plane than if the disease
had not occurred.

TREATMENT does not involve the necessity of removal from home in {166}
the acute cases, except when that is demanded for convenience of
treatment. There is no melancholia to suggest the possibility of
suicide, and no mental exhilaration or motor excitement to make
restraint necessary. The most important indications are met by
abundant, easily-assimilated food, which must usually, for a time at
least, be given with a spoon or by the stomach-tube; fresh air,
attention to the processes of digestion, relief of the
gastro-intestinal catarrh by the usual remedies, stimulating baths,
tonics, stimulants, and general galvanism. Proper care in emptying the
bladder and rectum and entire cleanliness will suggest themselves.

In mild cases a tonic and stimulating regimen, including sea-bathing
and gymnastics, will often be sufficient.

In the subacute cases young people are easily depressed by the asylum
associations, but there is usually a time in the progress of the
disease when home-discipline is too weak for them, and they must be
sent away; older people have usually complications in their home-life
such as to make a change desirable for the comfort of the household.
Recoveries are extremely exceptional.

In all cases there is little to be gained in keeping up
home-associations for so disturbing, distressing a disease after there
is pronounced dementia.

Medicines, other than tonics, are of little use, except opiates to
control various distressing nervous symptoms, including masturbation,
but they should be used with great caution.

KATATONIA (Katatonie of Kahlbaum; Katatonische Verrücktheit of Schüle)
presents, with more or less regularity of appearance, symptoms of (1)
mild melancholia without the characteristic mental pain; (2) mental
excitation, sometimes ecstatic, with cataleptiform conditions; (3)
confusion and torpor or apathy. There is an underlying well-marked
intellectual impairment, slowly advancing in incurable cases to
pronounced dementia. Delusions, more of the unsystematized than of the
systematized character, but resembling both, constitute a prominent
part of the disease from the beginning. Verbigeration and a curious
sort of pomposity are usually found in more or less pronounced degree.
The delusions are mixed. They are exalted, hypochondriacal,
melancholic, with all sorts of self-accusation, and may be full of
suspicion, fears of poisoning, and ideas of persecution.
Hallucinations of the special senses and illusions are not uncommon.
If the term katatonia is not used, or at least if a special place in
the nosology were not given this disease, it would be difficult to
know whether to class these cases as primary dementia, melancholia
with delusions, delusional insanity, or confusional insanity.

The verbigeration, when it exists, and the expression of delusions are
often associated with a manner on the part of the patient suggesting
disbelief in them, and sometimes the patient smiles or laughs at the
astonishing character of his statements. There is a self-conscious
element at times, suggesting mimicry or hysteria; a certain pathos is
universal; opposition and contradiction, even to refusal to eat, leave
the bed, dress, wash, are quite common; and nurse and physician are
tired out with the monotony of the mental and physical state.
Well-marked catalepsy is not common in my experience, although it
occurs; and in all cases I have seen the mental state and physical
atony suggesting that condition. Little attention has as yet been
given to katatonia in asylums in this country. Judging from my own
experience, it is not a common disease.

{167} Its CAUSES apparently lie in prolonged mental exhaustion and
inattention to bodily health. I have been led to suspect syphilis as
at least a predisposing cause.

The COURSE AND DURATION of katatonia are tedious, and even if there is
apparent recovery from the first attack, the tendency is to relapses
and to slowly-advancing dementia and death from those causes of which
dements in hospitals die, especially phthisis. I have never seen a
complete and permanent recovery.

The MORBID ANATOMY of katatonia suggests a deep-seated neurosis, the
precise nature of which we do not understand. In terminal stages there
are atrophy and degeneration and all that goes with them.

The CLINICAL HISTORY of katatonia is so characteristic that it need be
confused with the other diseases already mentioned as simulating
features of it, and with the early stage of general paralysis, only
through insufficient observation or too hasty diagnosis.

It is difficult to treat katatonia without the conveniences of a
hospital.

PRIMARY CONFUSIONAL INSANITY is a term recently introduced for a form
of mental disease of which the most marked features are moderate fever
rapidly developed, confusion, incoherence, and mild delirium. The
onset of the disease is rapid. In some of the cases which I have seen
the diagnosis was made of typhoid fever, although the clinical marks
of that disease were absent, the general appearance of the patient in
the two diseases being quite similar.

There is no real melancholia or exaltation, no rapid flow of ideas,
and no dementia. Hallucinations of the special senses are common;
there is a consciousness of illness; the delusions are unsystematized,
and the confusion of ideas frequently goes to the point of not being
able to recognize persons and places. The usual signs of fever are
present for a few days, but the temperature rarely exceeds 102° F.,
and soon drops to nearly or quite the normal.

The COURSE of the disease is quite rapid, and if recovery does not
take place in several weeks or a few months, chronic insanity with
delusions or dementia of various degrees may be expected.

The MORBID ANATOMY is not distinctive of this condition in the early
stage, and we cannot yet differentiate it from simple fevers by the
post-mortem. If ending in incurability, the atrophic and degenerative
changes of chronic mental disease are found.

As regards removal from home, the considerations already referred to
should be the guide. It is a good rule to keep the patient at home if
a suitable one for the purpose, and to resort to the asylum in case of
chronicity or troublesome complications.

PRIMARY DELUSIONAL INSANITY (Folie systematisée, Verrücktheit[20])
differs from secondary delusional insanity in the facts that the
disease arises primarily, and not secondarily to other mental
diseases; that there is little or no mental enfeeblement in the early
stage; and that the delusions, although fixed and systematized, are
limited. It has the advantage of allowing the avoidance of the
misleading terms monomanie of the French and monomania of English and
American writers, the narrower forms of which may be included under
the term primary insanity (primäre {168} Verrücktheit), including the
further developments of the neuropathic constitution, especially those
with the physical marks of degeneration described by Sander as
originäre Verrücktheit, and those marked by imperative conceptions and
such delusions of self-importance, suspicion, etc. as seem to some
people evidence of insanity, while by others they are considered as
simply false beliefs not indicating mental disease. Unlike primary
insanity, which is one of the states of mental defect and
degeneration, and incurable, primary delusional insanity may occur in
persons of healthy mental organization, and may end in recovery,[21]
although it is one of the most distinctly hereditary forms of
insanity, generally speaking.

[Footnote 20: Called also by some writers Wahnsinn, although they use
the term for secondary delusional insanity also.]

[Footnote 21: Some writers include both diseases under the term
monomania, and make both incurable degenerative states, which is
contrary to my experience. Clouston also has seen cures in what he
calls monomania (primary delusional insanity) without the neuropathic
taint.]

There are several subdivisions of primary delusional insanity,
according to the character of the delusions: (1) with delusions of
unseen agency, suspicion, and persecution; (2) with delusions of
personal exaltation; (3) with delusions transformed from sensations.

Delusions of unseen agency, suspicion, and persecution appear either
acutely and expand very rapidly in a few weeks, or from a very
insidious beginning so gradually that they may exist for months or
years before they are detected. The general indications of illness
consist in impaired sleep, slight loss of flesh, some reserve or
shyness in relations with other people, and diminished ability to
concentrate the mind in the usual occupations. The mental impairment
at first is very slight, and shows itself (1) in the readiness with
which the absurd delusions are believed and the fixedness of their
hold on the mind, and (2) in the diminished general power of judgment
and self-control in the little matters of daily life, at first so
slight that it is not seen except in matters requiring some effort to
maintain the customary equilibrium. Hallucinations, especially of
hearing, appear. In the progress of the disease the mind loses power
of self-control more and more, the delusions become more fixed,
concealment is no longer possible, and the patient is so annoyed or
angered that he repeatedly seeks relief from the courts
(Querulantenwahnsinn) or commits some act of violence in self-defence.
The common delusions are of marital infidelity, attempts at poisoning,
mesmerism, electricity, influence through telegraphs, telephones,
poisoned air, etc., signs of which are evolved directly from the
consciousness or transformed from common sights and sounds, such as
ringing of bells, striking of clocks, simple ordinary motions, etc.
The delusions in time produce a state of mental depression.

In some cases the primary delusion is of personal exaltation, attended
with persecution and mental depression. The individual thinks himself
some great personage unjustly deprived of his rights.

Delusions of grandeur or of personal exaltation develop in the same
way, usually subacutely from what might seem a foolish fancy rather
than an insane belief. The Napoleons, kings, queens, greatest
financiers, gods, etc. of the insane asylums are those who reason
correctly if one concedes the truth of their false premises, until the
progress of the disease produces such general brain-enfeeblement that
their premises and their {169} reasoning from them are both insane.
The delusions lose their fixedness, and their force too, in the
general lowering of the mind's strength, and complaints and boasts and
acts of anger become fewer, and finally cease.

The COURSE of the disease is nearly always subacute in the beginning
and chronic to the end in the two forms of primary delusional
insanity—that is, with (1) delusions of persecution and mental
depression, and (2) delusions of grandeur. A few cases with acute
development result in recovery, most of which relapse. The course is
for the most part to chronic delusional insanity attended with
moderate dementia.

The MORBID ANATOMY is not known, except that atrophic and degenerative
changes—not distinctive, however—are found in the terminal stages.

The patient is rarely willing to be treated as an ill person, for he
is sure of the correctness of his delusions. If during the first
attack he can be entirely removed from his daily associations by
change of scene and travel, or, if that is not possible, by admission
or commitment to an asylum, before the delusions become fixed and
while it is still safe for him to be at large, there is reasonable
chance of recovery. Second or third attacks very seldom end in
recovery unless they arise from alcoholic excess, when entire
abstinence for a sufficient length of time affords fair hope of a
favorable result, except in cases of long-standing drunkenness.

TREATMENT, when the delusions have become fixed, involves, chiefly,
safety to society or its comfort. The patients rarely commit suicide,
driven to desperation by their delusions of persecution when they are
particularly horrible. The more common tendency is to acts of violence
toward others, so that seclusion in an asylum is usually the only safe
course to pursue for delusions which one week may be directed against
certain persons who can easily be gotten out of the way, the next week
may be directed against others, and so on indefinitely. Delusions of
grandeur may be only a nuisance or annoyance, but may at any time
become sources of danger. The course is, for the most part, to
slowly-advancing dementia. Asylum treatment offers no chances of
recovery in cases not depending upon alcoholic excess, but becomes
necessary for the protection of society.

Transformed delusions (sensorielle Verrücktheit) arise usually in some
anomaly of sensation, which probably directs the delusions already
forming in a mind in the early stage of disease rather than causes the
disease. The causes lie in a deep-seated exhaustion of the nervous
system, especially in the neuropathic constitution and profound
hysteria. Various anomalous sensations give rise to a belief in
delusions as to their being caused by individuals for a purpose, or to
their being an indication of all sorts of impossible and most
extraordinary changes in the part: the chest is of stone, the leg of
brass, the head on fire, the hand ice, and so on indefinitely.
Hallucinations and a cataleptiform state are common. The variety of
delusions which may arise is almost endless, and they may have their
origin in the unhealthy action of any organ in the body: one of the
most troublesome forms, called ovarian insanity by Skae, causes single
women of severely continent lives to imagine all sorts of impossible
marital relations with men whose lives are equally beyond scandal and
above suspicion.

Without proper care the COURSE of the disease is to slowly-advancing
{170} dementia; and this may be expected when there is organic disease
of any important organ of the body.

Before the delusions are fixed, diversion, change of scene, travel
under agreeable circumstances and judiciously regulated, may be of
great benefit. In the later stage of firmly-fixed delusion asylum
treatment offers more chances of success.

In all the forms of primary delusional insanity the whole history of
the case is difficult to get at, and there may be, and usually is, so
strong a tinge of possibility at least, if not of actual probability,
in the delusions, in the early stage of the disease, that a correct
diagnosis cannot be arrived at until the time and opportunity for a
cure have passed.

DOUBTING INSANITY (Folie du doute, Maladie du doute, Grübelsucht) is
classed by Régis[22] as a form of melancholia (mélancolie délirante),
on the ground that it has the three elements of melancholia—namely,
fixed ideas (délire) of a sad nature, general mental depression, and
tendency to suicide. The melancholia is secondary, however, rather
than primary, and doubting insanity belongs more properly under the
head of a psycho-convulsive mental disease closely allied to
delusional insanity, like which it is more commonly a manifestation of
psychoneurotic heredity, appearing for the most part among the
cultivated classes. It consists in an uncontrollable doubt and
indecision, unanswerable by any degree of rational explanation,
regarding the occupations, duties, or events of the day, religion, a
future life, the commonest acts, or the most abstruse problems of
life. Doubting insanity essentially depends upon an anomalous action
of the will, with imperative conceptions and impulses. It is classed
by some writers as a monomania of the degenerative type. Schüle calls
it Verrücktheit sensu strictiori, using the term Verrücktheit also for
the three forms of primary delusional insanity just described.

[Footnote 22: _Manuel pratique de Médecine mentale_.]

Délire du toucher, an insane dread of touching certain objects, and
the morbid fear of defilement, called by Hammond mysophobia (similar
names may be multiplied indefinitely), belong in the same category.

There are mild cases of all these forms of disease, which seem like
simple weakness of character, others requiring for treatment the
conveniences of the retreat for nervous and mental diseases, with a
fair prospect of recovery, and still others tending to chronicity in
which hallucinations, delusions, and dementia appear only as a further
development into another form of insanity. They may, in mild degrees,
be symptoms in the course of other mental diseases, especially
melancholia, like many other manifestations of morbid mental energy,
such as Doctor Johnson's inability to enter a room with his left foot
first or to pass a lamp-post without striking it with his cane, etc.

PRIMARY MENTAL DETERIORATION or PRIMARY BRAIN ATROPHY is a term
suggested for a curable impairment of the mind arising from
brain-exhaustion in persons, usually men, between the ages of from
fifty-five to sixty-five. I have found it in some cases associated
with interstitial nephritis and with degenerative disease of the walls
of the heart, and have suspected atheroma of the cerebral arteries or
possibly endo-arteritis of specific or other origin. It occurs at a
time when atrophy of the brain is naturally taking place. There are
the usual indications of physical wear and such marked deterioration
of the mental powers as to {171} seriously interfere with the capacity
to attend to customary business and every-day duties, and to closely
simulate the early stage of paralytic dementia. There occur also, in a
certain proportion of cases, epileptiform convulsions, slight attacks
of dizziness, petit mal, and always disappearance of sexual power and
desire. There may or may not be headache. The patient recognizes his
condition, his mental depression does not far exceed the physiological
limit, and there is no reasonable risk of suicide, except from reasons
which would impel a sane man to it.

Under the influence of rest, if begun early, tonics, and a strict
regard to the laws of health the symptoms commonly disappear if there
is no organic disease. I have never seen the brain recover its tone to
the extent of making it safe or even possible to resume the previous
kind and amount of work. In a certain proportion of cases there is
striking mental impairment, even dementia, and the primary atrophy of
the brain sometimes makes rapid progress to unconsciousness and death.

It is not possible to say, by the degree of atrophy found post-mortem,
whether there was or was not primary mental deterioration during life.

The TREATMENT consists in entire freedom from care, rest from work,
travel, tonics, etc.

As mental disease is more than a brain disease, and is a disease of
the intellect, each age from infancy up (and each individuality)
impresses its peculiar mark upon it, and there are certain terms in
common use to express insanity associated with certain physiological
processes whose meaning should be explained.

INSANITY OF CHILDHOOD is for the most part only a further development
of a congenital state of mental defect. I have seen, however,
well-marked mania, melancholia, primary dementia, and primary
delusional insanity before the age of puberty. Typical acute mania I
have seen twice in children two years old, apparently arising in
normal brains after severe injuries to the head. This is quite
uncommon, and the number of cases thus far observed is too few to make
me feel sure that my own experience of a favorable result as to
recovery in uncomplicated cases will be generally confirmed. At best,
after a cure there is a more or less decided arrest of brain
development.

HEBEPHRENIA (insanity of pubescence and adolescence) occurs within the
ages of fourteen and twenty-three or thereabouts. Like insanity in
general among persons in early life, it most commonly indicates an
hereditary predisposition to mental or nervous diseases or an
early-developed brain defect or injury, possibly an exalted emotional
state or an increased nervous sensitiveness produced by masturbation.
It is a mild form of primary dementia, modified by the mental changes
going on during adolescence. Indeed, it is simply an exaggeration and
prolongation of the curious psychological development of that period,
too well known to need description, which goes on in the most
insidious way possible through months or years of what seems
silliness, absurd fancies, foolish sentimentality, egotism, impaired
common sense, and diminished judgment and self-control, to a
slowly-advancing dementia, which even then is not always recognized as
disease. The result is an arrest of brain development on various
planes of intellect, and a preservation of the youth's tastes and
sense and intelligence, as modified by the morbid propensities
characterizing an unhealthy development of the change from boyhood or
girlhood and {172} youth to adult life, with the adult's strength—a
curious combination of intellectual brightness, it may be, with lack
of mind. For this characteristic condition Westphal uses the
expressive term Permanenz der Flegeljahre (permanence of the usually
transitory state, which then commonly results in permanent arrest of
brain development on the plane of the mind at a definite age of
adolescence); and yet there may be more than that—mental
deterioration, which in years may lead to pronounced dementia. Cases
of primary dementia occurring within the years of puberty and
adolescence are often classed as hebephrenia and conversely, so that
one term, primary dementia, is thought sufficient by many writers on
insanity.

In the early stage there is sadness, hardly amounting to melancholia,
and it usually constitutes an important symptom to the end, although,
like all the other changes in the mental state, it is superficial to
the extent of at times seeming almost insincere. Masturbation is
common. Occasional outbursts of violence are also common, often with
mental confusion, incoherence, or stupor, and in severe cases there
occur, usually, attacks of temporary fury, with distressing or
agonizing hallucinations of sight and hearing, and delirium, which may
all last for a very short time or for a number of days. In young women
and girls these outbursts may be coincident with menstruation or in
the intervals. The countenance loses somewhat in expression in all
cases, and becomes almost vacant or quite so in those in which the
dementia becomes well marked. A mild form of the disease is quite
common, and consists in an undue intensity or a prolongation of the
curious psychological phenomena commonly observed during adolescence.
It is marked by aimlessness, changeability, self-assertion,
exaggerated self-consciousness, with, perhaps, propensity to lie or
steal or run away from home, and ending without any apparent damage to
the mind, except that the individual is less of a success in life than
he would have been but for his illness.

The course is slow, and although in the majority of cases mental
impairment is arrested before reaching what may be properly called
complete dementia, in well-marked cases the duration of the disease is
long and its results last for life. In many cases progress continues
with extreme slowness to extinction of the mental faculties. Oftener
the individual simply, in a certain sense, fails to reach that stage
of intellectual maturity and strength which he otherwise would have
attained. It is not always easy to draw the line between the
psychological and the pathological changes that take place during the
years of adolescence, and there are many mild cases of hebephrenia in
which various kinds of failure in life are due to this disease rather
than to the faults or vices to which the failure may be attributed.

In TREATMENT irritability, restlessness, absence of a power and sense
of responsibility, and sleepless, excitable nights, are the most
difficult symptoms to combat. The restlessness and irritability often
lead to refusal to be reasonably controlled and to a tendency to
wander away from home with theatrical displays, so as, in the case of
girls particularly, to require restraint, especially if the
excitability should be so great as to amount to outbursts of violence
or should lead to sexual improprieties.

The fact should be borne in mind that there is a diseased brain which
needs nutrition, rest, and discipline, which must be proportioned to
suit each case. Outdoor, simple life, with sea-bathing,
carefully-selected diet, {173} without too much meat, exercise, mental
training limited to the requirements of each patient, are the chief
reliances. Iron, cod-liver oil, and arsenic are useful tonics.
Stimulants, including tea and coffee, should be avoided. Quiet nights
and necessary repose can be secured by bromides, exercise, and opiates
used sparingly, which also control the impulse to masturbation. A
sound education, a healthy experience of the rough and tumble of
youthful life, and the careful avoidance of processes and habits of
indulgence will often prevent the symptoms of disease from growing
into traits of character and habits of life. On the other hand, in
some cases there is a half-conscious struggle between the fine traits
of character and the demoralizing influences of the disease, and a
most pathetic effort to keep the better nature's supremacy over the
lower impulses set free or developed by the destructive tendencies of
a fearful malady.

MENSTRUAL INSANITY differs from other periodic insanity in not being
necessarily a further development of an hereditary or acquired state
of mental degeneration, and in being curable in a fair proportion of
cases.

INSANITY OF GESTATION, PUERPERAL INSANITY, AND INSANITY OF LACTATION
do not call for any further comment than the remark that they
represent causes and conditions rather than types of disease.

CLIMACTERIC INSANITY in women and in men is usually a curable folie
raisonnante—insanity of action or affective insanity, which may
develop into secondary dementia or chronic insanity with delusions. It
does not necessarily include all acute forms of insanity occurring at
the climacterium, but only those slowly developing with the
physiological changes going on.

The course is usually subacute, the duration a couple of years or
more, and the termination in about half the cases is in recovery.
Permanent change of character and further progress to incurable
insanity are perhaps about equally common.

TREATMENT consists in a sedative and fattening diet, simple, healthful
conditions of life. Removal to an asylum or some form of restraint is
needed where the conduct is such as to demand seclusion and control.

SENILE INSANITY arises in suspicions and a generally deluded state of
mind regarding those persons whom there is every reason to
trust—namely, relations and near friends—and as extraordinary
credulousness of designing persons whose interest and character would
naturally suggest being on the guard against them. There is impaired
judgment, as shown by the mismanagement of property and diminished
capacity for business, usually some perversion of the sexual instinct.
The suspicions and credulousness in time amount to insane delusions,
and if life lasts the end is in marked dementia. But there may be no
mental impairment evident to casual observers or to ordinary
acquaintances for many years. The improper relations assumed with the
opposite sex, the neglect or abuse of those nearest by ties of blood,
the squandering of property on strangers, and the omission to provide
properly for the members of the family, are wrongly attributed to a
character become bad rather than to destructive brain disease, where
they belong. Not seldom senile insanity is a moral insanity, and shows
itself by an entire change of character not explainable by other
circumstances than disease, and is then marked by {174} indecent
exposures, loss of the fine sense of the decencies and proprieties of
life, destruction of the discriminating power between right and wrong
acts.

The course of senile insanity is slow, unless there be also some fatal
disease with it, and evident mental impairment may be so late that the
disease may be overlooked for years.

The TREATMENT is abundant nutrition, including wine, removal from
irritating conditions of life, protection of the individual against
himself, and guarding the community against harm or indecencies. Small
doses of morphia daily are often of great benefit, and there is no
real danger of acquiring the opium habit if reasonable discretion is
exercised in its use.

SENILE DEMENTIA is simply an excess of the natural mental weakness of
old age out of proportion to the bodily state, an exaggerated
childishness of senility to the extent of producing irresponsibility.
It is in reality a subacute primary dementia modified by the
peculiarities of old age. Memory fails first, and a condition of
general weakness of mind follows rapidly afterward. Secretiveness,
suspicions, delusions, and hallucinations of the special senses are
almost always present.

It is not uncommon for the early symptoms to consist in an inhibition
of the higher faculties of the mind, so that the lower impulses become
prominent. The sense of right and wrong and the moral perceptions may
become entirely weakened. Acts of indecency, dishonesty, injustice,
depravity may follow impaired judgment, and yet so far precede
strikingly perverted memory and general intelligence as to make the
insanity, which is obvious to an experienced observer, entirely fail
to impress itself upon the minds of the community.

The TREATMENT consists in caring for the comfort of the patient, which
can usually be done at home or at least in a private family, unless
there are persistent impulses requiring the control of an asylum. The
preparations of opium are useful to control extreme restlessness, and
may be given freely, avoiding narcotism. A bland diet of fattening
food is best suited to the wants of the aged. A simplified life often
serves every purpose, especially in the quiet of the country, although
it is best not to remove them from familiar scenes unless as a matter
of necessity.


Complicating Insanities.

Complicating insanities simply add to the usual symptoms of the
special forms of mental disease many of the characteristics of the
particular disease, rheumatism, gout, phthisis, organic diseases of
the heart, etc. Choreic movements depend upon the same pathological
changes as are found in the sane, and certain diseases are attended
with such profound changes in the nutrition of the brain as to give
rise to mental impairment, which amounts to almost extinction of the
mind, such as myxœdema and chronic nephritis. Acute mania occurs in
the last stage of Bright's disease, which may be difficult to
differentiate from uræmia. Mania, melancholia, and delusional insanity
occur in the course of acute febrile diseases or appear during the
period of convalescence; in the latter case the prognosis is much more
unfavorable than in the former. The close {175} alliance between
insanity and pulmonary consumption is a matter of frequent
observation. The two diseases are interchangeable, and they often
coexist. The relation between rheumatism and insanity is less close.


Insanity from Specific Poisons.

Maniacal symptoms have been reported from the use of various drugs,
including iodoform, mercury, etc. Hasheesh dementia is not uncommon in
the East. Acute delirium arises from hydrate of chloral and the
preparations of opium analogous to acute alcoholic mania from
excessive drinking, and chronic impairment from their prolonged use.
Bromide of potassium rarely produces symptoms similar to those of
mania; taken for a long time in even moderate doses, it tends to
mental sluggishness, and in long-continued large quantities given
uninterruptedly there is a danger of well-marked dementia.

All of these conditions may be prolonged beyond the usual action of
the particular drug or give rise to symptoms in excess of those
usually observed. The characteristic indications of the particular
drug, sometimes marked by the combined use of several, will be found
if they are carefully looked for.

The TREATMENT consists in breaking off the bad habit gradually or
abruptly as each case may require, and in otherwise treating the
persisting symptoms in accordance with the general principles already
stated in considering the various mental diseases.

ALCOHOLIC INSANITY includes mental disorder from the use of alcohol in
both the acute and chronic forms.

Acute alcoholic mania may come from a single excess in drinking, which
in some individuals is always attended with maniacal symptoms. It may
constitute the alcoholic trance described under the head of Transitory
Insanity. From long drinking and exhaustion or by withdrawal of the
accustomed stimulant we may have the familiar mania-a-potu or delirium
tremens.

Under the prolonged use of alcohol primary delusional insanity,
melancholia, mania, and dementia occur.

From long-continued drinking of alcohol, even to slight excess, for
many years, it is rare not to find some mental impairment, if only an
“uncontrollable violence of the instincts and emotions,” a sort of
moral insanity.

The PROGNOSIS is more favorable than in most forms of insanity
uncomplicated by the abuse of alcohol, especially in the case of
primary delusional insanity, if the bad habits can be effectually
corrected and if the alcoholic excesses have not been continued long
enough to produce organic changes in the cerebral blood-vessels. In
the latter case the dementia sometimes simulates that of general
paralysis so closely as to be called pseudo-paralytic dementia from
alcohol.

TREATMENT is rarely successful outside of some asylum.

SYPHILITIC INSANITY does not properly include those cases of mania,
melancholia, and delusions of persecution of the ordinary type of
which the exciting cause is found in the train of thought aroused and
kept up by the consciousness of having contracted syphilis, but only
such as {176} depend upon the presence of the syphilitic poison in the
system. There are no diagnostic marks to distinguish it from insanity
not caused by syphilis, except in a certain proportion of cases of
organic syphilitic disease of the brain.

The PROGNOSIS is rendered much less favorable from the fact of the
syphilitic cachexia.

In addition to the usual means of TREATMENT for the several forms of
insanity, the appropriate measures for syphilis should also be tried,
except where there is evidence of diffuse organic disease.


Organic Mental Diseases.

GENERAL PARALYSIS OF THE INSANE is a disease marked by definite
pathological changes in the central nervous system, chiefly in the
cortex of the brain, but which may extend to any part of the
cerebro-spinal tract or to the sympathetic ganglia and cranial and
spinal nerves. Its constant symptoms are—(1) vaso-motor disturbance
ending in vaso-motor paresis; (2) mental impairment, which makes
progress, for the most part unevenly, to complete terminal dementia or
extinction of mind; (3) impaired muscular control, which advances more
or less uniformly to almost entire paresis or nearly total paralysis.
Expansive delusions, the delirium of grandeur, megalomania (which may
change suddenly to micromania), or simply a feeling of elation,
happiness, self-satisfaction, or undue complacency, are found, but
often not until or near the end. The other symptoms vary in individual
cases within a wide range, so as to simulate almost every form of
insanity; and it is quite possible that they include what a more exact
pathology will hereafter recognize as several distinct diseases.

SYNONYMS.—General paralysis is also known as general paresis,
progressive paralysis of the insane, paretic dementia, paralytic
dementia, cirrhosis of the brain, paralysie-générale, folie
paralytique, démence paralytique, periencephalite chronique diffuse,
meningo-myélo-encephalite chronique interstitielle diffuse,
encephalite généralisée, periencephalite chronique diffuse,
encephalite interstitielle diffuse, encephalite avec proliferation
sclereuse interstitielle, Allgemeine Paralyse, progressive Paralyse
der Irren, chronische progressive parenchymatöse Encephalitis der
Rindensubstanz, pericerebritis, periencephalo-meningitis diffusa
chronica, periencephalo-myelitis chronica diffusa, encephalitis
interstitialis corticalis, paralytische Blödsinn, primäre Encephalitis
interstitialis mit Ausgang in Sclerose. Griesinger placed general
paralysis among the complications of insanity. It is popularly known
as softening of the brain (Gehirnerweichung).

HISTORY.—The combination of the two series of symptoms, paralysis and
dementia, was recognized by Haslam, and at the beginning of this
century by French writers, who also knew their fatal import. Esquirol
describes a typical case of general paralysis of the insane under the
head of monomania in his _Maladies mentales_. His pupils, especially
Bayle and Calmeil, have studied and described general paralysis. At
the time of his first visit to England, forty years ago, the late
Luther Bell had never recognized a case, and there can be no doubt of
the fact that it has {177} rapidly increased, particularly in the last
dozen or twenty years, with the rapid increase in the aggregation of
the population.

ETIOLOGY.—So far as heredity is concerned, general paralysis has not
such close relations with mental diseases as insanity in general. It
is estimated to be hereditary, in the sense of being closely related
to other forms of insanity, about one-half as often, and it is nearly
allied to apoplexy and epilepsy. My own experience leads me to the
conclusion that in those cases of general paralysis without a previous
history of syphilis (and the same statement is true in less degree of
persons who have had syphilis) the vast majority occur in families in
which there have been cases of insanity, epilepsy, or apoplexy. It is
rare among people living simple agricultural lives, but is intimately
connected with the faults and vices of civilization—specialized
overwork, involving strain in the office, study, factory, mine, etc.,
especially if to bodily exhaustion and brain wear and worry there be
added hard living and hard drinking, sexual excesses, and syphilis.
The Scotch Highlander rarely has the disease until he comes to
Edinburgh or Glasgow. In Ireland general paralysis is so rare that of
9271 cases of insanity in 1882, only 6 were general paralytics, as
compared with 1151 out of 13,581 in England the same year; during
which, in Scotland, of 238 deaths from insanity, 10 were from general
paralysis; but the Irishman has no special exemption from general
paralysis in American cities or in large English towns and mines and
factories, where he works hard, drinks hard, and lives hard generally.
It is, so far as I am able to learn, unreported thus far among our
negro population until they come to the great centres of population;
it is said to have been unknown among the slaves. Among the English,
Scotch, and Americans it prevails most among those people who are in,
or who have dropped down to, the lower strata of society. Of 2212
private patients in England, 139, or about 6 per cent., were general
paralytics, while 1012, or about 9 per cent., were found among 11,359
pauper patients. French and German writers report it as most common
among the brain-workers. In women of the upper class it exceedingly
seldom occurs. In some of our Western asylums not more than 1 or 2 per
cent., or even less, of the patients are reported as general
paralytics, coming chiefly from farms. In the asylum for the centre of
the manufacturing districts of Massachusetts about 9 per cent. of the
patients are general paralytics. From the iron- and coal-mines of
England from 14 to 17 per cent. of the insane confined in asylums are
general paralytics. It is more common in cold climates than in warm,
other things being equal. From one-sixth to one-tenth of the cases,
varying in different localities, are women.

General paralysis not only is most frequent in the stronger sex, but
it selects the strong individuals in the prime of life, between the
ages of thirty-five and fifty. It is extremely rare under the age of
twenty, although Turnbull has reported an unique case at the age of
twelve;[23] it is not common under thirty or over sixty; I have seen
two cases in men sixty-five years old. It is seldom seen in
individuals who have been weak from childhood, unless as the probable
result of syphilis.

[Footnote 23: _Journal of Mental Science_, October 1881.]

The excesses of the habits of the city and of mining and manufacturing
centres, hard work, high living, late hours, predispose to general
{178} paralysis in strong constitutions at the period of their
greatest activity, especially if the physical strain, the violent
struggle for existence, has begun early in life with insufficient food
and excessive work, and if ordinary paralysis be not uncommon in the
family. Alcoholic and sexual excesses are considered to be
particularly common predisposing causes. Recent investigators find
syphilis to be a part of the antecedent history of from one-half to
three-fourths of the cases, but chiefly in those slowly advancing or
subacute from the beginning. By some writers syphilis is considered to
be in those cases only a diathesis, as is held by Fournier, or a
debilitating antecedent, like chronic malarial poisoning. Others think
that so large a proportion can be accounted for only by some specific
relation between the two diseases. If the fact so often stated is
true, that syphilis is rapidly increasing, perhaps part at least of
the increase in general paralysis can be thus accounted for.

Mental shocks of various kinds, excessive emotional strain with mental
exhaustion, and injuries to the brain, are the commonly reported
exciting causes of general paralysis, but it is not certain that—in
many cases, at least—they do more than hasten the pathological process
and call attention to the symptoms. So far as my observation goes, the
injury to the head, supposed to be the cause of general paralysis,
often has appeared to probably come from an accident due to the
impaired physical strength and to the vaso-motor disturbance in the
brain incident to the early stage of the disease and while it was
still unrecognized. Cases are observed in which no predisposing or
exciting cause is found by the physician. I have seen it following
diphtheria and other debilitating diseases, after long exposure to
malaria, and apparently due simply to prolonged mental strain in
persons otherwise living in moderation under circumstances
exceptionally favorable to health.

SYMPTOMATOLOGY AND COURSE.—As a rule, to which the exceptions are few,
the early symptoms of general paralysis are obscure. Their appearance
and progress are so gradual and insidious that they are usually
overlooked for a period varying from several weeks to a year or more,
sometimes for four or five years, perhaps even longer. There is a
slight change in character, which is frequently attributed to
wilfulness or perverseness arising from some disagreeable
circumstance; to want of a reasonable attention to the little affairs
of daily life; to indifference, temper, carelessness, or recklessness;
to a want of aptitude and receptivity having an ethical rather than
medical significance; to an impaired moral sense. The patient may be
observed to be simply more quiet and heavy; inclined to be depressed
rather than distinctly melancholy; a little heedless; unusually
indifferent, and indisposed to worry over things that formerly would
have disturbed him; drowsy or dropping off to sleep at work or in the
theatre; disturbing the household by his restlessness at night—in and
out of bed, up and down stairs, for trivial and yet not seemingly
insane reasons. He may become easily disturbed by trifles, and yet
careless to more important matters. He begins to overlook, perhaps
rather than forget, recent little things. His power of attention is
diminished, his will weakened, his self-control impaired. He becomes
less careful of the niceties and proprieties of life, less interested
in his family and all that is nearest to him—self-absorbed, egotistic,
indulging in inconsequent stories and remarks. Although the memory is
not {179} distinctly at fault, fresh impressions do not make their
usual imprint on the mind. His moods are unnaturally changeable. A
certain slovenliness in habits or carelessness in dress, an
inattention to customary little courtesies and attentions, slight yet
noticeable, are not uncommon early symptoms of general paralysis.
There is soon observed, often noticeable to the patient, a lack of
endurance, an early sense of fatigue from exertion, a sense of
muscular prostration, physical discomfort, or general pains which may
be attributed to malaria or rheumatism. Commonly, not always, there is
disturbed sleep or restlessness. There may or may not be headache,
slight or severe, transient or persistent. There may be a sense of
pressure or an uncomfortable feeling about the head, especially the
forehead, or it may be the seat of no pain or discomfort whatever.
There may be a slight or severe local or general sensation of distress
or uneasiness in the head after mental effort only. There is often
pain, anæsthesia, hyperæsthesia, paræsthesia affecting any sensitive
nerve, often none at all, or impaired muscular sense.

The average daily temperature is higher in general paralytics than in
health. It is sometimes lower, and the range is greater than the
normal. In the only extremely rapid case which I have seen (two months
in all) it was 97° F., and thereabouts for a number of days, and then
rapidly rose to 103° and 104°, where it remained until near death.
After the congestive, epileptiform, and apoplectiform attacks it rises
from two to seven degrees, and remains high for a considerable time,
while in pure epilepsy it quickly falls. This difference, however, is
not sufficient, as between epilepsy proper and epilepsy as an early
symptom of general paralysis, to establish the differential diagnosis
with certainty in all cases.

The vaso-motor disturbances in the brain are indicated by transient
congestions or local anæmia, dizziness, faintness, temporary outbursts
of anger, excitement, or confusion, and rapid changes in the mental
and emotional state. Convulsive attacks are not common in the early
stage of the disease, except in those cases due to syphilis, but may
occur, and may so resemble hysteria, petit mal, epilepsy, and apoplexy
as to be confidently diagnosticated for those diseases. The emotional
state is of indifference, despondency, gloom, melancholia, elation, a
feeling of self-satisfaction, or mania.

The symptoms thus far are not clear except on minute examination. The
family and most intimate friends of the patient observe that he is
changed, but cannot tell how, and are apt to say that he is not the
same man that he was, that his troubles have been too much for him,
that he does foolish things as never before, etc. Sometimes he
estimates his symptoms correctly, sees the downward change himself,
and is oppressed by it; oftener he is indifferent to it, or still
oftener quite well satisfied with his condition and prospects, or even
mildly elated. He may squander his fortune, ruin his reputation,
become addicted to drink. His sexual appetite, not held back by his
normal power of self-control or exaggerated with a general physical
and intellectual erethism, may lead him into all sorts of
improprieties and immoralities or to exhausting excesses, which are
perhaps more common among the married than among the unmarried; and
yet his disease is not recognized, because the later symptoms of
general paralysis—namely, grand delusions, staggering gait, tremor,
and marked dementia—have not yet appeared.

{180} The pianist loses his skilled touch; the actor fails to learn a
new part; the ready salesman no longer has his great facility of
selling; the singer does not see that his notes have become false and
harsh; the engraver's fine lines are no longer possible to him; the
preacher reads the same hymn three times in his Sunday service; the
man of promptness fails to keep his appointments; the speech seemingly
clear to others becomes indistinct to a deaf wife; the eye trained to
close, exact work loses its capacity of fine distinctions of form or
color; the expert accountant can no longer add up his three columns of
figures at a time; the doctor writes prescriptions showing unwonted
carelessness or impaired judgment to the extent of injuring his
practice; a banker loses his property by foolish ventures; the saving
business-man buys quantities of useless articles; the moral man
becomes licentious or the temperate a drunkard; the respected father
of a family goes to the State prison for running off with a pretty
servant-girl; the lawyer ruins his client's cause; the considerate
husband shows unwonted harshness and violence to his wife; the
industrious worker becomes a tramp or a vagabond; the amiable friend
becomes irritable, disagreeable, perverse, hard to please, easily
excited, cranky. These are some of the facts I have known to occur in
the early stage of general paralysis without giving rise to the
suspicion of cerebral disease, the conduct of the individual generally
not suggesting insanity. In one case the cerebral vaso-motor
disturbance caused marked intoxication from a small amount of wine,
previously taken habitually without showing it, for several weeks
before the most careful examination revealed other indications
suggesting general paralysis. In the upper walks of life, wherever a
nice intellectual adjustment or fine muscular co-ordination is
required in the daily duties, symptoms to put the physician at least
on his guard against general paralysis will rarely be overlooked in
this early stage of the disease if they are sought for with sufficient
care and appreciation of their import. In proportion as the employment
is coarser, and not requiring much mental or muscular exactness, the
symptoms are more difficult of correct apprehension, until we get to
the day-laborers, in whose dull nervous organizations quick reactions
do not occur, and in whose simple labor, requiring little thought and
only muscular co-ordination of a low grade, a partially demented brain
and muscles considerably impaired in strength serve their purpose so
well that an early diagnosis is next to impossible. Routine work, to
which he is long accustomed, is often done well by a general
paralytic, provided it does not require exact mental or muscular
co-ordination, when the disease has so far advanced that any new work
except of the simplest kind could not be performed.

It is seldom that general paralysis, in its early stage, receives
careful enough attention to be recognized or to create a suspicion of
its existence until exhaustion, a long period of sleeplessness,
perhaps a violent shock, a strong emotion, a fall or a blow, a
congestive attack, an epileptiform seizure, an apoplectiform
convulsion, or some unknown cause—probably a vaso-motor disturbance in
the brain—hastens the progress of the disease, and the previously
slight or obscure symptoms (at least some of them) are suddenly so
aggravated as to make them of unmistakable signification. It is usual
in such cases to date the appearance of general paralysis from this
point, and to overlook its previous existence for the weeks, months,
or it may be years, of its prodromal period. It is {181} especially
easy to overlook the period of invasion of general paralysis of the
insane, as the symptoms may, and generally do, have that temporary,
transient, and variable character which is common to diseases or
stages of disease in which vaso-motor disturbances predominate;
inasmuch, also, as the individual character has to be taken so much
into account in estimating the import of particular symptoms, and as
few or many of the leading indications of general paralysis may be
present in a particular individual, while the physician might happen
to make several examinations of his patient at times when the symptoms
did not appear at all. For now and then all symptoms absolutely
disappear in a time which may be short or long. In two cases of
general paralysis in the period of invasion, where the moral
perversion was said by the other members of the family to be a source
of great trouble, I sent both patients to an insane asylum entirely
upon the statements of their wives, without being able myself to see
any evidence of insanity, but where the clinical history of general
paralysis in its early stage was so accurately given that I was sure
there could be no mistake; and a few days' continuous observation in
the hospital showed the diagnosis to be correct.

The dementia, ataxia, and muscular impairment of the prodromal period
of general paralysis of the insane may be masked by the prominence of
almost any of the symptoms of nearly all the mental diseases; and many
of the indications of the prodromal period are symptoms of disease
only as they are departures from ordinary customs and habits, although
in other persons they might be quite the reverse and natural to their
daily life. Much that might be done by a general paralytic with great
care in the early stages may quite resemble the careless work of the
same person in health.

The following case is quite typical of the development of general
paralysis of the insane:

Mr. ——, age 52, married, a clergyman: his mother died of apoplexy; two
of his four brothers are insane. He had the usual illnesses of
childhood in mild form, diphtheria of the worst type in 1869, and in
recent years, according to his belief, malaria, as he had lived in a
malarial region eleven years. As a young man he was of robust frame
and vigorous health, brought up on a farm. He overworked, denied
himself, and overtaxed, in getting his education, a brain not trained
from early years to exacting labor. Eight years ago, for the first
time, and at intervals since then, he has had attacks of mental
confusion, dimness in sight, and indistinct articulation lasting from
a few moments to several minutes. Three years ago, after great
emotional strain, people began to notice that his preaching had lost
in animation and force, and they complained that he had suddenly
become more radical in his views. Great mental worries occurred soon
after. There had been no alcoholic or other excess, except of mental
overwork, and there could be no reasonable possibility of syphilis,
unless we adopt Hebra's dogma, “Jeder Mensch kann syphilitisch
sein”—that the means of innocently acquiring that disease are so
widespread that no one can be said to be free from the danger of it.
Nearly two years ago, in the dark, while feeling tired mentally and
physically, but not ill or dizzy, in alighting from a coach he missed
the step and came to the ground on his feet with great force. He
walked to the house of a friend, and was found by one of the family on
their entry floor {182} groaning, but not unconscious. He could not
stand or talk, vomited incessantly, and complained of a horrible pain
in the back and top of his head. Two days later, and each succeeding
Sunday, he preached, obstinately and unlike him refusing to listen to
advice to keep quiet; but he remained in bed between Sundays for three
weeks, when the striking symptoms disappeared; but he had never felt
entirely well since then—never had the same animation. He was
supplying various pulpits, and found, wherever he had preached before,
that people complained that there was a general lack of vigor in his
preaching. Two years ago he observed that his right leg had less life
in it than was natural, and soon after that both legs seemed
heavy—that it was less easy to run up and down stairs, which his wife
also noticed several months later. He also has had for a year a
strange feeling, a sort of numbness, in his legs. He thought that his
handwriting and speech have continued as good as ever, but has
observed that he has had to change to a stub pen, as he found
difficulty in writing with the old sharper-pointed kind; that his
voice had grown less clear; and that he has rapidly become farsighted.
He has never had any dizziness, pain, ache, or uncomfortable feeling
about his head, except during the attacks already referred to. There
have been no thoracic or abdominal symptoms, no neuralgia or
rheumatism. Appetite and digestion have been faultless. He has lost
about ten pounds in flesh. He has slept soundly, but is often
restless, getting in and out of bed. He says that he was depressed for
lack of employment; that he is not irritable, but that his family
would say that he is not as tractable as he was, not as patient, less
easily satisfied; that his son and wife would say that he is not what
he once was—that his memory is not as clear and vivid as it was. He is
conscious that within the last two years he has had violent,
uncontrollable passionate outbreaks from trivial causes. He preaches
his old sermons, because he thinks they are too good to be lost, and
because he takes pleasure in rewriting them, in doing which he remarks
that the handwriting becomes progressively worse toward the end of
each sermon. He says that he can write still better sermons, but does
not like to make the effort. When he went into the pulpit a week ago
he was told not to announce a second service, but everybody seemed to
him so pleased with his preaching that a week later he gave word that
there would be an evening service, to which, he laughingly said, only
one person came. In standing with his eyes closed and feet together
there was a little unsteadiness. On attempting to turn around or to
stand on one foot with eyes closed there was some, not very great,
ataxia. In these trials the unsteadiness and ataxia soon became very
striking on prolonging the muscular effort a few moments. His hands
had a powerful grasp, each marking 74 with the dynamometer, and on
being stretched to their full extent, with fingers spread, immediately
thereafter the fibrillary tremor could be seen only on close
examination. There was no marked tremor of the muscles of the lips or
face, except in movements which placed them at extreme tension. The
tongue was quite tremulous on being protruded to its full length and
held there. In walking in a rather dark entry the steps seemed to me
shortened and the feet wider apart than in his natural gait, and he
did not raise his feet as much, which he noticed also. In going up
stairs he placed the whole foot, heel and all, on each step to keep
his balance. He turned very deliberately, {183} keeping the feet near
together and not raised from the landing. On coming down he evidently
steadied himself by a muscular effort extending to his head and
shoulders. The knee-jerk was well marked and alike in both legs, but I
could not say that it was exaggerated. There had been no change in the
sexual function.

His general mental state seemed to me to be of a quite superficial
kind of despondency at his prospects, and yet absence of a
corresponding degree of anxiety for the future; of satisfaction with
his ability and worth; of a feeling that his family are unduly anxious
about him; and of a prevailing state of inappreciation of the whole
situation, and of a general state of happiness which was abnormal—an
opinion which his wife afterward corroborated. He was quite emotional,
and easily and rapidly moved to smiles, and from them almost to tears.

In explaining his restlessness at night he stated that he was taking
quinine for his malaria, and that it acted on the liver so as to
increase the flow of urine, which he repeated several times, but
laughingly said, “Of course; how foolish!” when I suggested that he
meant the kidneys. In removing his clothes for a physical examination
I found that he had two starched shirts on—the one in which he went
from home, and that in which he preached, in order not to rumple the
second one. When I asked why he could not take home a soiled shirt in
his valise after having brought a clean one in it, the idea struck him
that he, after all, had done something foolish.

The examination of chest, abdomen, and of the urine was negative. I
could not find anywhere evidence of anæsthesia, hyperæsthesia, or
paræsthesia, general or local. The reaction of the muscles to the
faradic current seemed normal. By ophthalmoscope and otherwise the
eyes showed only the emmetropia already referred to. Hearing was also
normal, as well as the other special senses. In a close examination I
could at first not discover anything about his speech more than an
extreme deliberation in articulation, which might perhaps have been
natural to some scholarly men, but which I afterward learned had been
only of recent origin, and increasing. It was more pronounced after
the patient became a little wearied, and then I found that he could
not articulate a long word with several labials and linguals without
manifest difficulty. I gave him a sheet of paper and asked him to
write from top to bottom. He could not think of anything to write.
When I told him to put down the text of his sermon of the previous
day, he could not possibly remember it; no more could he call to mind
a sentence or a sentiment from it. What he wrote is marked No. 1. His
normal handwriting, No. 2, is of the date of 1881. Nos. 3 and 4 were
copied from an old sermon a few weeks previous to his visit to me, and
are taken respectively from the first page and the next to the last of
the copy. The facts may be observed that the old handwriting is quite
free, with an easy sweep of the pen. In the copy of the sermon the
first page shows that the pen is held stiffly and tightly, and that
the lines are not made with as steady a movement of the hand as in the
old handwriting. The lower lines on the first page are a trifle worse
than the upper, and pretty much like the second and third pages, from
which there is progressive deterioration to the end. The page written
in my office was very carefully done, and, under the circumstances, is
marked by such muscular unsteadiness and evidence of mental {184}
{185} {186} impairment and enfeebled memory as to be almost, if not
quite, of itself pathognomonic of general paralysis.

[Illustration: FIG. 15. Six handwritten examples.]

I purposely made no remark to the patient, and he made no inquiry,
about diagnosis or treatment. He would have missed his train, although
there was a clock in my office, had I not reminded him of the late
hour, whereupon he made all his arrangements with care, good judgment,
and accuracy, and reached his home safely. As he walked briskly down
the even sidewalk I doubt whether any one, even a physician, would
have remarked any unsteadiness or anything abnormal about his gait. If
he had been followed a few blocks, until the idea of catching his
train had ceased to stimulate him, and after he had reached the
crowded thoroughfares of the city, especially as he stepped up and
down curbstones or walked slowly to avoid teams at crossings, a close
examination would undoubtedly have shown the defects in gait already
pointed out.

Mr. ——'s wife had noticed that her husband did not raise his feet as
of old in walking—that he walked as if they were heavy, but under the
influence of coca wine or a decided mental stimulus he walked
apparently as well as ever for a short distance. She had noticed a
slight impairment in memory, an increased fractiousness, a diminished
ability to appreciate things in their proper light, a changeability in
his moods and mental state, a scarcely-observed but noticeable neglect
or oversight of little customary duties, occasional passionate
outbreaks from trifling causes, a disposition to laugh and cry easily;
and that often he did and said unwonted foolish little things, like
attributing increased flow of urine to his liver, wearing two starched
shirts, announcing the Sunday evening service; but she had not
considered any of the symptoms as evidence of disease, especially as
he kept accounts, attended to his preaching, etc., and showed no
manifest indications of a disturbed or impaired mind. She had remarked
a decided change in the character of his handwriting, also an unusual
deliberateness in speech, but no indistinctness or hesitation,
although his voice had become less clear. He had had no delusions,
illusions, hallucinations, or unreasonable ideas. It was for the
weakness in his legs that she asked my advice.

I found that the mental and cerebral symptoms in this case had been
overlooked, and that the weakness in the legs had been attributed to
spinal concussion, for which a favorable prognosis had been given.

I examined the patient after he had been away from home nine days,
preaching two Sundays, and making many new acquaintances in the mean
while, besides having travelled nearly two hundred miles by rail, so
that he was fatigued. After three weeks' complete rest I saw him at
his house. The knee-jerk was increased as compared with the previous
examination. Otherwise the symptoms had so ameliorated that some of
them could be brought out only after a long and patient examination,
and the rest had to be accepted as a matter of history of the case. I
had his photograph taken, and by comparing it with another taken three
years previously his family noticed what was quite obvious in that
light, but what had thus far been overlooked—namely, that the facial
muscles had lost very much in expression.

The specimen of handwriting marked 5 is of a gentleman in whom the
paralytic speech is quite evident after a half hour's talk, but quite
masked in the beginning of a conversation, when rested. It is written
{187} with care, after a long rest, and, as compared with his former
writing when done with equal care, there is seen only a wider
separation of the letters. Its general appearance, on casual
inspection, is better than that of his ordinary writing before his
illness, as that was hurried and careless. But the second or third
page brings out the ataxia distinctly. It shows how well a general
paralytic, under the influence of rest and quiet, may control certain
groups of muscles—how completely the ataxia may be concealed under an
ordinary examination; and yet the symptoms in his case may be clearly
brought out by the method just described. The tongue was quite
tremulous.

The writer of No. 6 was more advanced in general paralysis, but had
been thought not to be ataxic, from the fact that he had been able to
write a single word pretty well. His few lines are quite
characteristic of a general paralytic. Although he was in my office in
Boston, he dated his statement from his home, and wrote the word
Lawrence not badly for a man not in the habit of writing much. Seeing
me for the first time, he addressed me as Friend Folsom, and he signed
his name by his old army title of nearly twenty years before—corporal.

The characteristic writing in advanced general paralysis, irregular,
distorted, full of omissions of letters and words, and finally
illegible, may be seen in the textbooks on insanity.

It very rarely happens that the onset and early progress of general
paralysis are so sudden and rapid that there is no prodromal period or
that it is very short.

The symptoms of well-marked general paralysis include four tolerably
distinct types, as follows: (1) The demented and paralytic; (2) the
hypochondriacal; (3) with melancholia; (4) with exaltation and mania.
There are mixed cases in which some or all of these forms occur. The
period of invasion or prodromal period, be it short or long, has, as a
rule (not always), gone by when the disease has arrived at a point in
its progress to be definitely placed in any or several of these four
types.

The demented form of general paralysis is the most common, and is also
that in which the greatest increase has been noticed during the last
decade, whether from more accurate diagnosis or by reason of an
actually greater proportion, probably to a certain extent due to both
causes. It consists in a very slowly-advancing mental impairment,
making progress side by side with muscular loss of control and power,
which may continue several months or years before their importance is
appreciated, the vaso-motor disturbances not being so marked as in
more acute forms of the disease, and the changes in the mental state
and bodily strength from week to week being so slight as to escape
observation. Attacks of dizziness, petit mal, and epileptiform
seizures are quite common in this type of general paralysis. In one of
my cases a lawyer in the third year of the disease was retained as
counsel in a will case involving over a million dollars, when he fell
repeatedly in the streets, and when his occasional, indeed frequent,
mental lapses were so apparent to his partners that they did not allow
any of his business letters to leave the office without being first
inspected by them. Mental excitement, maniacal symptoms, and delusions
of grandeur rarely occur, except as transient attacks, until the final
stages. The patient commonly realizes that something is the matter
with him until he becomes quite demented, and can often describe his
{188} mental state and general symptoms quite intelligently, although
rarely with a full appreciation of their extent and import. He easily
persuades himself that it is not worth while to take steps for medical
treatment, and keeps on with his work until some distinct failure in
his mental or physical powers, usually a sense of malaise, muscular
pains, a feeling of exhaustion, convinces him and his friends that a
physician should be consulted. Perhaps he goes to some health-resort
or water-cure, or tries rest and recreation in travel, still thinking
his case not an important one, until he seeks medical advice to please
his family or friends. He may say that he is only tired mentally and
physically.

In the hypochondriacal form of general paralysis, vaso-motor
disturbances, flushed or pale face, headache, defective circulation,
and various abnormal sensations referred to the peripheral nerves and
internal organs are associated with a hypochondriacal mental state,
which is also marked by an evident mental impairment, manifested in an
almost childish changeability of complaints. Grand delusions and great
mental and motor excitement do not, as a rule, appear until the later
stages, but the hypochondriacal form is less subacute than the
demented.

In general paralysis with melancholia the sad delusions are apt to be
associated with some form of expansive ideas or to be transformed into
them at some stages of the disease, although the classical delusions
of grandeur are a late symptom.

The maniacal form of general paralysis with the délire de grandeur is
the disease as described by Calmeil. Mental exhilaration and delusions
of personal importance are its conspicuous features. It may develop at
any time in the course of the other three forms just mentioned; its
prodromal period may be such as has been described, usually shorter,
or the symptoms may be of excitement and maniacal from the beginning.
It is the general paralysis of the books until within recent years.

It is doubtful whether these four forms of general paralysis depend
upon any pathological basis which can now be determined, but their
recognition is practically important for an early diagnosis, and they
differ from each other very little in their later and final stages.
They constitute what is known as the descending form of general
paralysis, in the majority of cases of which descending degeneration
of the lateral columns of the spinal cord or posterior spinal
sclerosis, or both, appear, secondary to the brain disease.

In the ascending form of general paralysis there are posterior spinal
sclerosis and the usual symptoms of that condition—which are described
in another article of this work—from one year to a dozen or more years
before there are indications of dementia.

In the first stage of general paralysis, although a distinct loss of
power is an early symptom, it is not so striking in its manifestations
as loss of control. The moral obliquity and the mental lapses seem
entirely out of proportion to the general mental impairment. What
seems moral perversion is often strictly so, but oftener it depends
upon a want of attention or appreciation of the facts in the case,
which can be aroused if there is opportunity for it. There is a clear
inability to use the force that the mind has. The foolish credulity
and readiness to be duped are often only a temporary condition. There
is, at the same time, an inability to co-ordinate the muscles to a
striking degree at a time when there is still {189} only slight
impairment of the muscular strength, or inversely, and the
co-ordinating power may improve up to a certain point, while the
muscular impairment goes on. This ataxia is first noticed in those
muscles requiring the nicest adjustment for their usual work, the
penman's and the pianist's fingers, the proofreader's eyes, the
singer's throat. But it may be for a long time very slight or not
easily detected.

Although this muscular ataxia may be observed, even if not constantly,
in the prodromal period of general paralysis, it is usually well
marked only when the symptoms have become well developed. There is
also a fibrillary tremor of one group of muscles or of one set of
fibres after another when these muscles are exerted, and increasing as
they become wearied, as they soon do, from the exercise. The
handwriting may show no conspicuous fault at the top of the page, and
at the bottom be full of evidences of muscular tremor and
unsteadiness, or a single word may be written without conspicuous
fault, and a few lines serve to show ataxia of the muscles used in
writing. In beginning to read there may be only the most trifling want
of clearness of tone and steadiness of articulation, noticeable only
to the most practised ear, which after a number of minutes becomes a
distinct harshness of voice or evident stumbling over linguals and
labials, or hesitation in speech, which may seem like the utterance of
a person slightly under the influence of wine or with lips cold from
frosty air. The hesitancy of speech is due partly to a slower flow of
ideas than in health, an impaired power of attention to the subject in
hand, a diminished creative power or expression of thoughts, but also
to a distinct ataxia, an inability to promptly co-ordinate the muscles
required to perform the act. The difficulty in reading is partly
mental and in part due to inco-ordination of the muscles governing the
eyes as well as those of articulation.

These muscular defects and mental inefficiencies, when slight, may be
hardly detected after the patient has had a prolonged rest and is
quiet and calm. After some emotional irritation, weariness,
sleeplessness, vaso-motor disturbances, or congestive attacks they
become very pronounced. After several weeks of absolute rest, with the
patient still at rest, it may be impossible for a time to find any
trace of mental defect or muscular deficiency until the patient has
again been put to the strain following some effort. They are very much
increased after epileptiform or apoplectiform attacks, which, however,
are uncommon so early in the case.

In the progress of the disease, as the mental impairment increases,
the reaction of the nervous system to external conditions becomes less
active, the mind weakens, the loss of flesh may be, at least in part,
regained, a great portion of the irritability and active symptoms
disappears, and as the patient grows worse he may seem for a while to
his friends to improve.

The leading symptoms of general paralysis of the insane are—(1)
vaso-motor, (2) mental, (3) physical.

The vaso-motor symptoms consist in a progressive paresis or lessened
power, which in the progress of the disease advances to complete
arterial paralysis—at first a functional disorder of impaired
innervation, and finally organic. They are marked early by rapid
changes in the cerebral circulation, a diminished arterial tension,
with occasional or frequent attacks of vertigo, dizziness, or
faintness, confusion and incoherence that may amount to a transient
dementia, localized and general elevation or {190} depression of the
bodily temperature; frequent attacks of congestion or at long
intervals, with a flushed face or transient cerebral anæmia, may be
marked by sharp emotional disturbances, fits of temper, irritability,
maniacal excitement, loss of self-control, etc., or by epileptiform
and apoplectiform seizures of various degrees of severity, with or
without temporary or transient loss of muscular power, local or of the
monoplegic, hemiplegic, or paraplegic nature, of a much less severe
character than similar attacks later in the disease, due in part also
to organic changes. The circumscribed loss of power of the vessels of
the skin leads to various functional disturbances, and finally to
paralysis, involving bed-sores, etc. Cyanosis, neuroparalytic
hyperæmia of the lungs, bladder, and intestines, cold feet, œdema of
the skin, local sweatings, etc. are final evidences of vaso-motor
paralysis. Throughout the disease, at least nearly to the end, this
vaso-motor paresis and paralysis causes marked variations in the
mental state which are too rapid to be accounted for by organic
changes.

After there is evidence of definite atrophic and degenerative disease
in the brain, as indicated by great mental impairment and muscular
paralysis, the mental and physical symptoms may be subject to great
changes, without any apparent cause but vaso-motor disturbances, and
alternating rapidly from extreme intellectual confusion and absence of
mind to a clear, even if temporary, mental state. Less extreme changes
in the condition of the mind are common.

The mental symptoms, after the disease is pronounced, consist in an
intensification of those already mentioned as characterizing the
prodromal period—in an increase in the loss of power of control over
all mental operations and in the loss of mental power, the two
symptoms making progress side by side. In the form of the disease
attended with maniacal excitement the prodromal period is usually
shorter than in the others, but may last several years. After the
prodromal period has passed the mental impairment increases, so that
the judgment, memory, power of attention and expression grow
progressively worse; and this impairment constitutes the only
characteristic mental state universally present in all stages of
general paralysis of the insane—namely, progressive dementia. The
accidental symptoms may be those belonging to any type of insanity
except logical systematized delusions. They very rarely simulate the
states of mental defect and degeneration.

If there are delusions of persecution, they are marked by a degree of
confusion or incoherence not compatible with logical inference. The
state of melancholia may change rapidly to mania, and the demented
form may at an hour's notice become the excited. Where the symptoms of
mental exaltation and depression alternate, resembling folie
circulaire, the alternation is less regular than in alternating
insanity properly speaking; hallucinations of sight and hearing and of
all the special senses are quite common, although, as a rule, rather
late symptoms, and then confused and often only partially
intelligible. There are also all sorts of illusions and delusions.

The impairment of the sense of right and wrong becomes quite marked;
the patient loses the sense of property and ownership. In no other
disease could the reported case occur of a man, to outward appearance
well, going up to a policeman and asking his assistance in rolling off
a barrel {191} of liquor which belonged to some one else, and which he
meant to appropriate. For this reason what seem to be thefts are very
common, and although by that time there is striking mental impairment,
it may not be obvious to every-day people. Almost every other moral
obliquity occurs, particularly a tendency to drunkenness and every
possible violation of the proprieties and laws regarding property and
the sexual function. It is all done, too, in such a foolish way that
the insanity would be apparent to almost any intelligent person before
whom the facts might be fully and clearly placed. There may be a
curious consciousness in the patient of the fact that something is the
matter with him, and a most extraordinary unconsciousness of what an
inordinate fool he is acting. If he can be made to see what folly he
is committing, perhaps a few moments later he is saying that he was
n-ever b-better in his life. The emotions change most rapidly, and an
adroit examiner will have his patient crying over some trifle one
moment, and another moment laughing over something equally
inconsequent. The prevailing mental state changes as rapidly as the
emotions. Violent anger, outbursts of passion, penitence, amusement do
not succeed each other more rapidly than indifference, melancholy, and
exaltation.

The suicidal idea is common in general paralytics before they become
very demented; the suicidal impulse is rarely strong enough to result
in anything more than futile attempts at self-destruction. Suicide by
deliberation is also rare, for even when it is meditated the weakened,
indecisive mind usually fails to prepare adequate plans for its
successful issue. Homicidal attempts are not to be expected as a rule,
except in the delirium of the states of maniacal excitement or in an
outburst of anger for a fancied wrong or deliberately for some
trifling reason. Even from suicide and homicide a practised physician
or attendant will easily turn the general paralytic who is not
maniacal to some amusing or silly thought. He has become credulous,
simple-minded, and easily moulded to an expert's wishes, so far as his
general conduct is concerned, and yet at any moment he is capable of a
furious mania or a violent storm of passion, which after cerebral
congestive attacks may be long and severe. Sometimes these symptoms
just described may be very pronounced at night and not especially
troublesome during the daytime. I have had patients who were
dangerous, violent, noisy, deluded at night, and entirely quiet by
day, for several months.

The mental state is of progressive impairment. The ideas flow slowly,
and there is slowness or hesitation in speech in giving utterance to
them, even to the degree of amnesic aphasia. Word-blindness occurs,
and word-deafness and the various disturbances of speech associated
with the several forms of aphasia. After the dementia is very marked
there is often a most extraordinary variation in it. The patient may
be confused, incoherent, and to appearance hardly capable of sustained
thought, but soon quite able to perform a business transaction. The
friends say of such patients, “He is crazy to-day,” or “To-day he is
sane;” and this quite independent of the marked increase in the
dementia which occurs from organic changes, epileptiform and
apoplectiform attacks, after which the advance in the mental
impairment is rapid and great. Accompanying dizzy and congestive
attacks there is a temporary dementia which may be over in an hour or
two.

{192} The patient may recall many long-past events fairly well when he
cannot find his way to the dinner-table without blundering, when he
does not know morning from afternoon, and after he is unable to dress
and undress himself without constant remindings or even actual help.
Such paralytics wander off and die of exposure, are picked up by the
police as having lost their way or as not knowing where their home is,
or fall into some fatal danger from which they have not mind enough to
extricate themselves. When the mental impairment has reached this
point the lack of mind shows itself in a lack of facial expression,
which is so characteristic of the disease that with a practised eye it
is recognized as far as the countenance can be distinctly seen; and
from this point the progress is commonly quite rapid to absolute
dementia, entire inability to form or express thoughts, too little
intellect to even attend to the daily natural wants, and a descent to
the lowest possible plane of vegetative life, and then death.

At some time or other in the history of general paralysis delusions of
grandeur, a general feeling of personal expansiveness or extreme
self-satisfaction, may be confidently looked for. In the melancholic
and hypochondriacal forms of the disease, as has already been
mentioned, they are late symptoms; in the demented type they occur
only, for the most part, near the final stage of absolute dementia;
and in the excited form they are usually found from the beginning or
at least developing from a general feeling of bien-être. They may vary
from what would pass as inordinate, silly conceit to a wildness of
delirium which stops hardly short of infinity. The patient is the
greatest financier, the handsomest man, the best runner, can out-box
the champion pugilist, can write the finest sermons. Delusions of this
degree, especially in women, are apt to refer to the reproductive
faculty or to the qualities which please the opposite sex. One man can
make a million dollars a day writing poetry; another is building
cities of solid gold; another owns all the railroads in the country,
is king over all the earth, god over God; another is running
express-trains over his bridge across the Atlantic or has a doctor who
comes to see him in a balloon. There is often a depth of vulgarity and
obscenity about the delusions which is rarely seen in other diseases.
When the grand delusions appear in the melancholic form, they are apt
to be tinged with gloom, as of a queen whose diamonds are withheld
from her, a lover who is kept from his princess bride, etc. In the
hypochondriacal form it may be a crystal liver, a silver stomach, a
brain of solid gold, etc.

Delusions of personal belittlement, called micromania, sometimes
follow or alternate with the megalomania.

Maniacal excitement is a late symptom in the demented,
hypochondriacal, and melancholic forms of general paralysis; and it
rarely occurs in them except in the final months of the disease,
unless as a direct sequence of congestive, epileptiform, or
apoplectiform attacks, and then it lasts usually from a few hours to
several days. These attacks may occur at any time without any warning
whatever, and may be attended with fury or stupor also. As a matter of
fact, they are very rare at an early stage except in the excited form
of general paralysis, of which they are a pretty constant symptom
until marked dementia has appeared, and they may continue to the end.
The fury of these maniacal attacks is of the most furious and maddest
kind, blind, the most utterly regardless of consequences {193} of any
kind of insane excitement, and without the intelligence even of the
acute maniac.

The ability to recognize his own mental state is sometimes retained by
the patient, at certain times at least, to a quite late stage in the
disease, so that he learns to call his visions hallucinations and his
strange fancies delusions. He may even agree that his illusions are
all nonsense, that the disease is in his brain. The so-called lucid
intervals are not uncommon until the final stage of absolute dementia,
when attention, memory, judgment, conception, connection of ideas,
imagination, desires, the exercise of the senses, general sensibility,
after becoming more and more imperfect are at last completely
suspended. The moral sense and finer feelings had gone long before.

Although the story of the mind's decay in general paralysis is a
comparatively short one, from a few weeks to four or five years for
the prodromal period, and then an average of two or three years for
the rest, but varying from a few weeks to a rare extreme of twenty
years, there may be at any stage of the disease, except at the very
end, a more or less complete remission lasting from a few months to
ten years. It is dangerous to say, therefore, that there is any degree
of dementia which may not be temporarily at least, or in some part,
recovered from. Most of the reported cures of general paralysis have
been at last proved to be simply remissions, which may be partial or
so complete as to leave no trace to the most practised observer. It is
not uncommon to see a remission of six months or a year or two, in
which the patient can lead a quiet life; it is seldom that he
undertakes responsibilities without bringing the remission rapidly to
an end. There are a few cases where active business has been resumed
and followed successfully for several years. But there is apt even
then to be some deterioration in character, which may amount to an
actual moral insanity. An arrest in the downward progress, so that the
symptoms remain for a considerable time without essential change, is
not very uncommon, and may occur at any stage of the disease.

The physical symptoms of general paralysis consist in impaired control
over the muscles, diminished power of co-ordinating them, followed at
once by progressive muscular enfeeblement ending in complete
paralysis.

The ataxia first shows itself in the finer muscles—of the eye, of the
fingers, of articulation. There is a little hesitancy or rather
deliberateness of speech, the voice loses its fine quality, the
intonation may be slightly nasal. Instead of contracting smoothly and
evenly as in health, the muscles show a hardly noticeable jerkiness;
an irregular fibrillary tremor is seen when they are exerted to their
utmost and held in a state of extreme tension for several moments. In
attempts to steady the handwriting the patient forms his letters
slowly, makes them larger than usual, or tries to hurry over the
letters, making them smaller. The coarser muscles show ataxic symptoms
much later. It is observed by the patient or his friends that he does
not walk off with his usual rapid gait, and the effort to co-ordinate
his muscles produces an early or unusual fatigue, which may be
associated with general muscular pain. Extreme soreness and pain,
following the course of some one or more of the main nerve-trunks, may
be most persistent and obstinate to treatment, lasting for several
years, limiting the motion of the limb, {194} sometimes beginning a
year or two before other symptoms are observed. Sooner or later,
especially after a little weariness or excitement, there are observed
at times, not constantly, indistinctness or an occasional trip in
enunciating linguals and labials, a tremor in the handwriting, a
slight unsteadiness in the gait. When the tongue is protruded as far
as possible, when the hands and arms are stretched out, when the
muscles of facial expression are exerted, in standing with feet
together with closed eyes, a decided muscular tremor and unsteadiness
are remarked. These muscular symptoms soon become constant, although
they may be so slight as to be well marked only by some unusual test,
such as prolonged use after excitement or fatigue, and the ataxia may
diminish, the gait, speech, or handwriting may improve, while muscular
power is growing progressively less.

In walking the feet are not raised as usual, the steps are shorter,
the legs are kept wider apart; turning about is accomplished in a very
deliberate way, such as to suggest an insecure feeling; movements like
dancing are impossible. Going up and down stairs is difficult; the
whole foot is rested carefully on each step, and the head and
shoulders are held stiffly, so as to maintain the balance. The
muscular movements are generally uneven and tremulous, and yet the
strength may not be so very much impaired, although perhaps available
only for short periods at a time. Even these symptoms may so improve
by a few days' quiet, or even by a night's rest, as to quite throw the
physician off his guard unless a thorough examination is made. The
patient, too, on an even floor or sidewalk may walk so as not to
attract attention, and yet in a new place, over a rough surface, or in
the attempt to perform difficult or rapid movements, exhibit striking
ataxia and feebleness of gait. In starting off with a definite purpose
he may for a short distance walk quite well, as he may do under the
influence of a glass of wine.

From this point the progress is usually rapid. The handwriting becomes
more and more tremulous, unsteady, full of omissions of letters and
words, disjointed, disconnected, and finally illegible; the
articulation more thick, stammering, hesitating, indistinct,
unintelligible; the gait staggering, shuffling, straddling, uncertain,
unsteady, even to causing frequent falls. There may be still a
considerable degree of strength for a single short effort, but the
co-ordination is so imperfect as to make it avail little. The voice,
for instance, may be loud and forcible, but the co-ordination
sufficient for only a short explosive utterance of one syllable, and
then quite an interval before the force can be concentrated for the
next. Progressive muscular paresis becomes finally absolute paralysis.

Remissions in the physical symptoms follow the same general laws as in
the mental symptoms, but are not so complete, and there may be an
arrest in their progress also.

In all stages of the disease, especially the later, there may be
almost any of the symptoms observed which occur in the various
functional and organic diseases of the nervous system. The
hyperæsthesia, local or general, may be most absolute, or the
anæsthesia so complete that acts of self-mutilation ordinarily causing
exquisite pain are performed without apparent suffering. Any motor
ganglia, any nerve, any tissue, may degenerate, giving rise to various
degrees of impairment up to total {195} destruction of function—of the
optic nerve, causing blindness; of the auditory, deafness; of the
olfactory, glosso-pharyngeal, or any of the cranial or spinal nerves.

The pupils may be of normal size. They may be of normal or sluggish
accommodation to light and distance, or there may be dilatation or
contraction of either or both pupils and no response to light or
accommodation. The pinhole pupil is not uncommon. There may be
neuro-retinitis, atrophy of the disc, neuritis, nystagmus, diplopia,
amblyopia, hemianopsia, color-blindness, ptosis, conjugate deviation
of both eyes, or paralysis of any of the ocular muscles. The paralysis
of one of the muscles of the eyeball may be one of the earliest and
most persistent symptoms. The optic neuritis or atrophy may also occur
early, but seldom appears in time to aid in a doubtful diagnosis.

Sugar has in a few cases been found in the urine; albumen is not
uncommon.

The sexual function is commonly exaggerated in the early stages, then
diminished, lost, and finally returns in the stage of absolute loss of
self-respect and self-control, although it may be impaired from the
beginning or not materially changed at first. There may be temporary
or persistent incontinence or retention of urine.

At first there is a marked loss of flesh, then a gain. As the muscles
lose in power they increase in size, with an interstitial
degeneration. The deposit of fat is sometimes enormous. In the final
stage there is emaciation.

The convulsive attacks usually are of the nature of cortical epilepsy,
or at least commonly begin as such. They are associated with and
followed by a considerable rise in temperature—from two to seven
degrees F.—and are immediately succeeded by marked increase in the
severity of the symptoms, both mental and physical, especially if the
attacks follow each other in rapid succession or last for a number of
days. They may be due to hemorrhage, embolism, or effusion, and be
marked by any or all of the usual symptoms and sequences of those
conditions, permanent or transient. General and aural vertigo are not
uncommon.

The muscular tremor before the last stages varies in different
muscles—excessive perhaps in the tongue, moderate in the fingers, and
so on. It may also seem slight as compared with the other symptoms,
or, on the other hand, be enormously exaggerated in certain groups of
muscles out of all proportion to all other indications. At the end
extreme and constant tremulousness accompanies every voluntary
movement.

Spastic paralysis, muscular tension, contractures, rigidity of the
most persistent character seem at times to be under the influence of
the will, although of cortical origin and in a certain sense
automatic, like convulsions.

The knee-jerk is changed in somewhat more than half the cases, a
little oftener exaggerated than abolished; but sometimes the reflexes
are enormously increased all over the body, so that a strong puff of
air in the face even will set the arms and legs going like a
jumping-jack. I have twice seen the patellar reflex abolished in one
leg, and so marked in the other as to seem to me exaggerated.[24] I
have also known it to disappear {196} absolutely in both legs two
weeks after it had been found to be excessively exaggerated. It also
varies under conditions of rest, fatigue, excitement, etc. Intense
pain in the joints occurs, and I have found it where the knee-jerk was
exaggerated, in one case giving rise in a physician to the delusion
that his arms and elbows had been resected. This may disappear in
time. Charcot's joint disease has been observed.

[Footnote 24: There was no evidence, and there had been no history, of
a hemiplegic attack in either case.]

In the final stages the bones are fragile and easily break;
hemorrhages under the periosteum or perichondrium arise from trifling
force or injury, giving rise to hæmatomata, the most common of which
are on parts exposed to pressure, etc., as the ear. The patient is
confined to his bed, fed like a small child, demented, hardly able to
articulate the extravagant delusions which form such a grotesque
contrast to his actual state, until the mind is as incapable of
forming or receiving ideas as of expressing thoughts; and the body is
simply a filthy, helpless mass of humanity, dying of exhaustion or
decay, unless lung gangrene, bed-sores superficial and deep,
necrobiosis, exhausting diarrhœa, pneumonia, pulmonary consumption,
perhaps asphyxia from an epileptic fit or choking, have followed
incontinence of urine and feces to the fatal end, or heart failure or
apoplexy have closed the scene.

PATHOLOGY AND MORBID ANATOMY.[25]—General paralysis of the insane is,
according to Mendel, following Rokitansky's idea, a connective-tissue
disease, affecting the nerve-cells and tissues secondarily, while
Tuczek and Wernicke think that the primary disease is of the
nerve-elements (primäre Atrophie der Nervenelemente)—a diffuse
interstitial cortical encephalitis on the one hand, or a diffuse
parenchymatous cortical encephalitis on the other. There is also, in
well-marked cases, atrophy of the white substance, due, according to
general opinion of pathologists, to primary interstitial encephalitis
ending in sclerosis.

[Footnote 25: For a detailed statement of the post-mortem appearances
in general paralysis compare Spitzka's _Insanity_, pp. 218-243;
_Beiträge zur pathologischen Anatomie und zur Pathologie der Dementia
Paralytica_, von Dr. Franz Tuczek; _Die Progressive Paralyse der
Irren_, von Dr. E. Mendel; _Lehrbuch der Gehirnkrankheiten_, von Dr.
C. Wernicke, iii. pp. 536-541. Westphal's classical work is not
referred to, as his latest views and others of interest are given in a
report of a discussion by the German Association of Alienists in the
_Allgemeine Zeitschrift für Psychiatrie_, iv. 1883, pp. 634-638 and
648-654. In the third number of the _Neurol. Centralblatt_, Mendel
reports an autopsy of a patient diagnosticated to have melancholia,
who died a violent death, where he thought that he found evidence of
the early stage of general paralysis in moderate opacity of the pia
mater, with nodules as large as a pin's head in both parietal regions,
and in slight indications of diffuse interstitial inflammation of the
cortex, the blood-vessels in the frontal convolutions being
extensively filled with white blood-corpuscles.]

In the majority of cases there is pachymeningitis, often extensive and
excessive, with hemorrhages, but which may be no more than is quite
commonly found in persons dying of phthisis or chronic nephritis.
There is also, usually, leptomeningitis, with adhesions to the cortex,
especially of the anterior and antero-lateral portions, so firm that
the arachnoid cannot be removed without tearing off portions of the
brain; but it is sometimes scarcely observed, and may be no more than
is found in persons dying simply of old age. The pia may be in places
thickened, opaque, and without adhesions. Ependymitis is usual.

In the terminal stage of general paralysis there is well-marked
atrophy (with compensatory serous effusion), which is, as a rule, most
marked in the cortex of the brain, but which is of varying degrees in
its different {197} portions. Rarely there is scarcely any atrophy of
the cortex. The central portion of the brain may be of leathery
consistence, but usually shows marked sclerosis, which also may affect
its different portions and the different ganglia very differently. The
changes resulting from inflammatory, degenerative, and atrophic
processes are general and profound.

An opinion is beginning to obtain that general paralysis is primarily
a disease of the small cerebral blood-vessels, functional or
vaso-motor; and Meynert holds that the transition line between that
stage, which he considers curable, and organic disease may be
recognized clinically.

In general paralysis, as in other mental diseases, the nervous
discharge is accompanied by a greater disturbance in the structure of
the gray substance of the brain, a more extensive decompounding of it,
and consequently by a more complete exhaustion of nervous force than
in healthy mental processes. Longer periods of rest and improved
nutrition are therefore necessary to restore healthy function. In
general paralysis, as in all other mental diseases dependent upon
destructive disease of the brain, there is not only decompounding, but
decomposing and disintegrating, of the structure of the brain.

Posterior spinal sclerosis is frequently found. If alone or
predominating over sclerosis of the lateral columns of the cord, the
knee-jerk is abolished if the morbid process has gone far enough. If
descending degeneration of the lateral columns is chiefly found, and
is sufficiently advanced, the knee-jerk is increased. At least one of
these forms of sclerosis exists in the vast majority of cases.

There is also a distinctly syphilitic disease of the smaller cerebral
arteries, together with a diffuse parenchymatous and interstitial
encephalitis of syphilitic origin. At present we have no means of
differentiating it at the autopsy from general paralysis following a
subacute or chronic course, except inferentially from the presence of
other evidences of syphilis. It is not always possible, therefore, to
distinguish between syphilis and a syphilitic diathesis as the chief
factor in diffuse encephalitis.

DIAGNOSIS.—Although a well-marked case of general paralysis is
unmistakable, the diagnosis in the early stages or in obscure cases
may be extremely difficult. The varying degrees in which the various
portions of the cortex, medullary portion, and different ganglia of
the brain may be involved in the morbid process naturally give rise to
a great variety in the symptoms, mental and physical, sensory and
motor, emotional and intellectual, and in the relative preponderance
of one or another in individual cases. The usual symptoms of any form
of mental disease may for a time obscure the dementia which sooner or
later must appear in general paralysis, and which, as has already been
said, is the only mental symptom universally present in all cases.
This mental impairment must also be associated with progressive
muscular loss of power, although the relation of the two symptoms to
each other, the degree to which a given amount of the one leads to a
fair inference of a certain amount of the other, is liable to the
greatest variation, the range of which can only be learned by
observation and experience. There is a certain quality to the
dementia, as already described, which is often sufficient of itself to
establish the diagnosis with a practised physician.

{198} The early mental symptoms may simulate those of cerebral
neurasthenia, in which the patient thinks that there is decided mental
impairment, although there is no progressive dementia. The tremor in
neurasthenia is greater and more universal than in the stage of
general paralysis with which it might be confounded, and the
subjective symptoms are much more prominent.

Muscular malaise and pains throughout the body give rise to the
diagnosis of malaria or rheumatism, in which there may be loss of
power, but no ataxia or dementia.

The sclerosis may be predominating or pronounced in the basal ganglia
and bulbar nuclei, giving occasion for a hasty diagnosis of
labio-glosso-pharyngeal paralysis, until it is found that the clinical
history of that disease is not followed. In the same way, any motor or
sensory ganglia or nerve-roots may be so early implicated in the
degenerative process as to mislead the physician into giving attention
to only the local symptoms.

Once I have known the early convulsions of general paralysis in a very
self-conscious woman mistaken for hysteria, the mental impairment and
physical weakness having been overlooked on account of the prominence
of the convulsive attacks and the hysterical symptoms, which may be a
complication of any form of insanity in young and middle-aged people,
particularly women.

It is not uncommon for the attacks to so thoroughly resemble epilepsy
as to be mistaken for it, the dementia not being observed or being
supposed to be the ordinary mental deterioration generally following
epilepsy. In such cases the progressive dementia, ataxia, and muscular
weakness may advance so slowly as to entirely escape observation for a
long time, and give rise to the confident diagnosis of epilepsy for
five or six years. Epilepsy, however, arising in a vigorous,
middle-aged person without evident cause, should always suggest the
suspicion of syphilis, cerebral tumor, or general paralysis, when
careful scrutiny of all the symptoms will show where it belongs.

Embolisms, hemorrhages, cerebral effusions, more or less diffuse
encephalitis from an injury to the head, sometimes give rise to the
suspicion of general paralysis, until it is found that its
characteristic progressive symptoms do not appear, but chiefly when
the history of the case has not been definitely ascertained, or when
the usual symptoms of those conditions are not well marked.

Chronic endarteritis, arterio-sclerosis, atheroma of the cerebral
arteries may be so diffused as to simulate general paralysis,
especially in drunkards and syphilitics, but the symptoms do not
advance in the manner characteristic of that disease.

Multiple cerebro-spinal sclerosis of the descending form may be
confounded with general paralysis while the symptoms are obscure and
consist in change of character, when, indeed, organic disease can only
be suspected to be present.

Lead has been known to attack the central nervous system in such a way
as to produce an intellectual apathy and muscular weakness somewhat
resembling the early stage of the demented form of general paralysis,
but without its ataxic symptoms and its regular progress. The presence
of lead in the urine, and the marked improvement from the use of {199}
iodide of potassium, tonics, and electricity, are sufficient to
establish the diagnosis.

Chronic and persistent alcoholism is always attended with some mental
impairment, which may so resemble the dementia of general paralysis,
with marked moral perversion, mental exaltation, grand delusions,
muscular tremor, ataxic symptoms, and impaired muscular power, as to
make the diagnosis doubtful for several months, until removal of the
cause (alcohol) in the course of time causes the symptoms to so abate
as to make the real character of the disease evident.

I have once seen chronic interstitial nephritis without its usual
prominent symptoms and with mild uræmic convulsions mistaken for
general paralysis.

A tumor of the brain, if not attended with the common symptom of
vomiting, may be the cause of convulsions and headache resembling
those often seen in general paralysis. Optic neuritis or atrophy is
usual in cerebral tumor, but rare in a stage of general paralysis so
early that the diagnosis might be doubtful.

Hemorrhagic pachymeningitis also now and then simulates an obscure
case of general paralysis in the early stage, but a few weeks at most
settle any doubts in the matter.

Although diffuse cerebral syphilis is more apt to be associated with
distinctly localized symptoms than the demented form of general
paralysis, and although it is characterized by a mental apathy and
physical torpor which follow a more regular course with more definite
symptoms, resulting in a slow decay, yet there may be doubtful cases
in which the differential diagnosis is impossible, and in which
antisyphilitic treatment does not throw any light on the subject.
Syphilitic new growths, endarteritis, and meningitis may so far
improve from the use of mercury or the iodide of potassium as to end
in an apparent cure, but in those cases the symptoms are not so marked
as to make an exact diagnosis always possible. A distinct syphilitic
cachexia is presumptive evidence of syphilitic encephalitis when there
is doubt whether the syphilis is the cause or the diathesis.

Profound melancholia is not so often as varying gloom or moderate
despondency a symptom of general paralysis. When it is such, there are
developed in time the other marks of that disease, and it will only be
necessary to hold the diagnosis in reserve for their appearance. The
melancholia masks the dementia unless it is very carefully sought for,
and the tremor may be as marked in melancholia as in the early stage
of general paralysis, but more universal.

Acute mania is not uncommonly mistaken for general paralysis, when, as
often happens, the delusions are as expansive and the tremor as great
in the mania as in general paralysis; and it may be several months
before the differential diagnosis can be made with certainty. In the
presence of a high degree of maniacal excitement, with great emotional
agitation and muscular tremor, it is difficult to establish the fact
of the existence or not of dementia in doubtful cases until it is well
developed. Acute mania has been known to constitute the prodromal
period of general paralysis for a number of years.

Primary mental deterioration cannot be always differentiated from
general paralysis of the demented type in its early stage. After the
{200} age of sixty the probabilities are in favor of primary mental
deterioration in doubtful cases, but general paralysis occurs—seldom,
to be sure—up to the age of sixty-five.

Early senile dementia may simulate general paralysis of the subacute
form, but has not its clinical history. General paralysis of the
quiet, insidious type and primary mental deterioration have been
called premature senility. The three diseased conditions have certain
points of similarity, and the pathological processes involved in them
do not differ sufficiently to authorize the assumption that they are
not closely related, if not simply variations, due to age and other
causes, in one morbid process.

Finally, the mental impairment caused by the prolonged use of bromide
of potassium and hydrate of chloral has been mistaken for general
paralysis, until a critical examination unmistakably showed the
presence of the well-known symptoms of those drugs.

In examining the patient it is especially important to avoid leading
questions, as in general paralysis and in those conditions which
simulate its early stage the mind is in a condition to readily fall
into the train of thought suggested to it. The fact should be kept in
mind, too, that the symptoms in early general paralysis are so
variable as to be sometimes quite evident, and at other times not to
be got at with certainty at all or only after long and patient
examination; that they sometimes quite disappear under the influence
of complete mental and bodily rest; and that in all stages, until near
the end, such complete remissions may occur as to make the diagnosis,
independent of the history of the case, difficult if not impossible.

A gentleman once committed an offence characteristic of general
paralysis in marrying a pretty servant-girl while temporarily away
from his home. His wife, daughters, and friends saw that the act was
so contrary to his natural character that he was placed in an insane
asylum and kept there several weeks under observation for an opinion
as to his responsibility. He appeared so well in the absolute quiet
and rest that he was declared sane, tried, and sentenced to the State
prison, where he showed his marked mental impairment as soon as he was
set to work. He could not concentrate his mind sufficiently for the
simplest labor, and a couple of years later he was sent to the insane
asylum to die, a complete mental and physical wreck, in the late stage
of general paralysis.

PROGNOSIS.—The very few reported cures in so common a disease as
general paralysis, and the circumstances under which they have been
reported, lead to the suspicion that there was an error in diagnosis
or that the mistake was made of supposing a remission to be a cure, as
has often happened. The course of the disease is more rapid in men
than women, and in young persons than in the older. From the galloping
cases of a couple of months to those slowly advancing, with long
remissions, over twenty years, the average, including the prodromal
period, is probably not far from five (perhaps six) years. Collected
from asylum statistics, it is given as from two to three years. When I
am sure of the diagnosis, I generally say that the patient may die
within twenty-four hours (of paralysis of the heart, from suffocation
by an accident in an epileptic attack, from choking, from cerebral
hemorrhage or effusion, or suddenly with cerebral symptoms of which
the autopsy gives no {201} satisfactory explanation), within a short
time of intercurrent disease, especially diarrhœa or pneumonia, or
that he may live several years, as he probably will, and possibly have
a remission, during which he may lead for a while somewhat the same
kind of life as other people.

Persons presenting symptoms which can in no way be positively
distinguished from those at the beginning of the prodromal period of
general paralysis recover, but not many come under the physician's
care so early. We are not yet in a position to say whether they were
suffering from a mild, transient illness or from what would otherwise
have become serious organic disease.

TREATMENT.—Life may be prolonged in general paralysis, and usually is
prolonged, by the use of such measures as contribute to the patient's
comfort, and which in a general way have already been considered under
the head of treatment of mental disease on a previous page.

In my experience, stimulating tonics, wine, and even coffee, increase
the morbid cerebral energy of the early stage of the disease, but are
sometimes of use later. Cod-liver oil and the hypophosphites do
better, and many of the disagreeable symptoms of the period of loss of
control over the involuntary muscles are relieved by strychnia. Ergot
and the judicious use of the bromides abate the cerebral congestion.
Gastro-intestinal disorders, when not controlled by attention to diet,
require the usual treatment.

Iodide of potassium in the large or small dose, and mercury, I have
never found to benefit those cases of general paralysis with a
previous history of syphilis. On the contrary, they have proved
debilitating and harmful.

When furious excitement is not relieved by prolonged warm baths, with
cool applications to the head if possible, and quiet, chloral is of
use, and sometimes opium and its preparations.

Frequently-repeated violent convulsions, the epileptic state, are
usually at once mitigated by chloral given by the rectum; the
inhalation of nitrite of amyl is reported also to have been of use.

There are few cases in which I find that morphine does not quiet
restlessness, calm delusions, abate distressing hallucinations, and
make the patient generally more comfortable; and I give it freely,
seldom more than twice a day, often almost daily, for two or three
years. In this way it can be used in quite moderate doses. Coca also
relieves symptoms.

Rest and quiet are most important in all stages of the disease. This
can be best accomplished in a quiet private house in the country,
which can be made a virtual hospital, and next in a private asylum.
But such care is beyond the reach of the vast majority of the insane,
to whom the public asylum becomes a necessity. Wherever they are, an
orderly life is best for them, with as little irritating interference
with their ways or control of them as is possible.

If the results of treatment are in the highest degree unsatisfactory,
and consist chiefly in meeting symptoms as they come up, without hope
of permanent recovery, it is not impossible that when we can put the
patient under treatment at the very beginning of his disease, as we
can now do in pulmonary consumption, the prognosis in the former
disease may change as much for the better as it has changed in the
latter.

A general paralytic is at any time liable to congestive or maniacal
{202} attacks of short duration, and so is always, potentially, a
dangerous person. In the prodromal period the risk is small; in all
stages there will, in the majority of cases, be some warning; but in
the developed disease the only safe way is to have some responsible
person near at hand, both to prevent the patient from doing harm to
others and to save him from injuring himself, whether by intent or
through not knowing better than to wander off or fall into all sorts
of accidents. In many conditions several should be readily available,
or else the security of an asylum must be sought.

In the treatment of general paralysis by society the same rule should
obtain as in all forms of insanity—that distinct mental disease is
presumptive proof of irresponsibility, or at least of limited
responsibility; that a diseased mind means lessened intellectual power
throughout and diminished ability to choose the right and avoid the
wrong; that there are changes in circulation or nutrition, or some
unknown condition in the brain, especially in general paralysis, by
virtue of which the mental state and power of self-control vary from
time to time, and as a result of which a person seeming responsible
one day may have been quite irresponsible some previous day.

INSANITY FROM GROSS LESIONS OF THE BRAIN (tumors, new growths of all
kinds, exostoses, spicules or portions of depressed bone, embolisms,
hemorrhages, wounds, injuries, cysticerci, etc.) is attended with the
usual indications of those conditions which may determine diffuse
disorders of the brain, giving rise to any of the symptoms of the
various psycho-neuroses and cerebro-psychoses. The lowered mental and
moral tone after cerebral hemorrhages is a matter of common
observation, and after one an individual is rarely observed to be
fully himself again.

The PROGNOSIS is very unfavorable. Although there are rare cases of
improvement, the tendency is toward profound dementia.

CEREBRAL SYPHILITIC INSANITY comes either under the head of the
insanity last described or belongs to the slowly-advancing dementia
with final paralysis already referred to under the head of Diagnosis
in General Paralysis, and called by some authorities on mental disease
pseudo-paralytic dementia from syphilis.

Antisyphilitic treatment is of value in the first class of cases, and
although most of the recoveries end in relapses and incurability, the
prolonged use of iodide of potassium seems sometimes to effect a
permanent cure. It is claimed that similar treatment is followed by
the same result in the cases of dementia with paresis, but the weight
of authority, and certainly my own experience, are against that
statement.

CHRONIC ALCOHOLIC INSANITY depends upon the vascular and other changes
due to abuse of alcohol so long continued that the pathological
condition has become organic and incurable. It is commonly associated
with delusions of suspicion or persecution. It may be a purely moral
insanity, with gross beliefs rather than distinctly insane delusions,
and it rarely fails to be at least that when the persistent excessive
drinking is kept up until the age of beginning dissolution of the
brain. It then gives rise to all sorts of embarrassing complications
in regard to property, family relations, and wills. Chronic alcoholic
insanity may take the form of mild dementia, by virtue of which the
patient cannot control himself, but can be easily kept within bounds
of reasonable conduct by various degrees of restraint, from the
constant presence of a responsible {203} person to the seclusion of an
asylum. In well-marked cases this dementia is associated with muscular
weakness, tremor, and exhilaration to such an extent as to simulate
general paralysis. It is then called by some—especially French—writers
pseudo-paralytic dementia from alcohol.

The condition is susceptible of improvement by removal of the cause,
alcohol, and by a carefully-regulated life, hydropathic treatment,
etc., but complete recoveries cannot be expected.

SECONDARY DELUSIONAL INSANITY is slowly developed from various mental
diseases, incurable or uncured, where the progress to marked dementia
is slow, by the persistence of delusions in those forms of insanity
characterized by delusions. It is chronic and incurable. In
melancholia and mania the mental depression and the exaltation and
motor excitement disappear to a great extent, and there are left a
slowly-advancing dementia, confusion, and expanding delusions, with
apathy or with agitation, for which the asylum is the only safe place
unless physical weakness makes the patient harmless. It is either a
terminal state in which many forms of insanity end, or a stage through
which they pass to terminal dementia. It depends upon incurable, and
therefore organic, changes in the brain, like all incurable insanity,
although those changes are not yet determined exactly. It might be a
question whether chronic delusional insanity properly belongs under
the head of Organic Mental Diseases, and a similar criticism may be
made regarding terminal dementia. But in this paper no definite
classification of insanity is attempted, because our knowledge of the
subject is still so indefinite, although the several mental diseases
are grouped in a certain order for convenience to the reader and the
writer; and this order of course approximately follows natural lines.

TERMINAL DEMENTIA is the end to which most of the insanity not
resulting in recovery finally comes. The features marking the disease
in its early stages for the most part disappear, leaving all the
functions of the mind impaired in all degrees up to total
extinction—the whole character on a lower plane. It is the disease
which to so great an extent crowds the wards of insane asylums and
almshouses with the (1) agitated or (2) apathetic chronic insane, the
worst of whom are mental and physical wrecks, squatting on floors,
uttering an unintelligible jargon, noisy, filthy, without intelligence
for the simplest natural wants. Their chief function, under the
prevalent methods of construction and management of lunatic hospitals
in most places, is to blight with a certain feeling of hopelessness
many of the curable insane who are obliged to go for rest and quiet to
institutions where the overwhelming majority of the inmates are
manifestly and painfully incurable.

French writers include a great part of chronic delusional insanity
(secondary confusional insanity, Wahnsinn, secundäre Verrücktheit) and
terminal dementia (Blödsinn) under one head, démence; and with much
reason, as it is not always possible to differentiate between the two.

The proper TREATMENT of the incurable, demented insane should provide
not only that they be not at large, where they annoy the strong and
the well, but also that they shall not disturb the insane who are
acutely ill and in need of treatment suited to sick people, and whose
chances of recovery at best are none too favorable. Experiments, now
quite numerous, have shown that the lives and occupations of many of
them may be {204} made not entirely unlike those to which they were
reared, and that nearly all may be suitably provided for without the
expensive hospitals and appliances necessary for the proper treatment
of acute mental disease.

A comparison of countries in which there is and is not a comprehensive
system of State supervision of the insane by a competent board seems
to me to reveal so unquestionably the fact that such a system alone
provides the proper protection for the insane, and the needed variety
and uniformly high standard of excellence in the provisions for their
treatment, that I hope to see the medical profession using its vast
influence upon public opinion to secure it.

If we meet in the wards of our insane asylums hopeless mental and
physical wrecks, if we find there the extremity of human wretchedness,
the supreme control of all that is evil or vile in our nature, the
worst antitypes of all the virtues, so, on the other hand, nowhere
else do we see such struggles for the mastery of the better impulses,
such efforts against such odds to hold back the mind in an unequal
fight. Nowhere else, too, are developed finer sympathy, more beautiful
unselfishness, more generous charity, or more heroic resignation where
no hope in life remains but for death.

The State has taken charge of these most unfortunate people, shutting
up behind the same locked doors and barred windows people of all
social grades, often mingling together in one presence the so-called
criminal insane, insane criminals, idiots, imbeciles, epileptics,
paralytics, the chronic insane, and the demented, with patients
suffering from acute mental disease. Some of them are unconscious of
their condition, many are better off than ever before, but others are
painfully alive to their situation and surroundings, fully aware of
the gravity of their illness, keenly sensitive to the distressing
sights and associations, disturbed by the noises, and discouraged by
the many chances of becoming like the worst incurables around them.
The State cannot evade the responsibility of seeing that their
confinement is made the least rigorous, wretched, and injurious
possible.


{205}


HYSTERIA.

BY CHARLES K. MILLS, M.D.


DEFINITION.—Hysteria is a functional disease of the cerebro-spinal
axis, characterized either by special mental symptoms or by motor,
sensory, vaso-motor, or visceral disorders related in varying degree
to abnormal psychical conditions.

This, like all other definitions of hysteria, is imperfect. No
absolutely satisfactory definition can well be given. It is not
abnormal ideation, although this is so often prominent; it is not
emotional exaltation, although this may be a striking element; it is
not perversion of reflexes and of sensation, although these may be
present. Some would make it a disease of the womb, others an affection
of the ovaries; some regard it as of spinal, others as of cerebral
origin; some hold it to be a disease of the nerves, others claim that
it is a true psychosis; but none of these views can be sustained.

Sir James Paget[1] says of hysterical patients that they are as those
who are color-blind. They say, “I cannot;” it looks like “I will not,”
but it is “I cannot will.” Although, however, much of the nature of
hysteria is made clear in this explanation, hysteria is not simply
paralysis of the will. A true aboulomania or paralysis of the will
occurs in non-hysterical patients, male and female, and of late years
has been studied by alienists.

[Footnote 1: “Clinical Lecture on the Nervous Mimicry of Organic
Diseases,” _Lancet_ for October, November, and December, 1873.]

In many definitions the presence of a spasmodic seizure or paroxysm is
made the central and essential feature; but, although convulsions so
frequently occur, typical hysterical cases pass through the whole
course of the disorder without suffering from spasm of any kind.

In a general neurosis a definition, well considered, should serve the
purpose of controlling and guiding, to a large extent at least, the
discussion of the subject.

The definition given asserts that hysteria is a functional disease. In
the present state of knowledge this is the only ground that can be
taken. It is claimed that in a strict sense no disease can be regarded
as functional; but it is practically necessary to use such terms as
functional in reference to affections in which disordered action
without recognizable permanent alteration of structure is present.
Temporary anatomical changes must sometimes be present in hysteria;
organic disease may be a complication in special cases; post-mortem
appearances may {206} occasionally be found as accidents or
coincidences; it is possible that structural alterations may result
from hysteria; but no pathologist has as yet shown the existence of a
special morbid anatomy underlying as a permanent basis the hysterical
condition.

The mental, motor, sensory, and other phenomena of hysteria cannot be
explained except by regarding the cerebro-spinal nervous system as the
starting-point or active agency in their production.

The term vaso-motor is used in a broad sense to include not only
peripheral vascular disturbances, but also cardiac, respiratory,
secretory, and excretory affections of varying type. Some of these
disorders are also visceral, but under visceral affections are also
included such hysterical phenomena as abdominal phantom tumors,
hysterical tympanites, and the like.

That all hysterical phenomena are related in varying degree to
abnormal psychical conditions may perhaps, at first sight, be regarded
as open to dispute and grave doubt. It is questionable whether in
every case of hysteria the relation of the symptoms to psychical
states could be easily demonstrated. I certainly do not look upon
every hysterical patient as a case of insanity in the technical sense,
but hold that a psychical element is or has been present, even when
the manifestations of the disorder are pre-eminently physical. James
Hendrie Lloyd,[2] in a valuable paper, has ably sustained this
position, one which has been held by others, although seldom, if ever,
so clearly defined as by this writer.

[Footnote 2: “Hysteria: A Study in Psychology,” _Journal of Nervous
and Mental Disease_, vol. x., No. 4, October, 1883.]

The alleged uterine origin of hysteria has been entirely disregarded
in the definition. This has been done intentionally. It is high time
for the medical profession to throw off the thraldom of this ancient
view. The truth is, as asserted by Chambers,[3] that hysteria “has no
more to do with the organs of reproduction than with any other of the
female body; and it is no truer to say that women are hysterical
because they have wombs, than that men are gouty because they have
beards.”

[Footnote 3: _Brit. Med. Journ._, December 21, 1861, 651.]

SYNONYMS.—Hysterics, Vapors. Many Latin and other synonyms have been
used for hysteria: most of these have reference to the supposed
uterine origin of the disease, as, for instance, Uteri adscensus,
Asthma uteri, Vapores uterini, Passio hysterica, Strangulatio uterina
seu Vulvæ. Some French synonyms are Maladie imaginaire, Entranglement,
and Maux ou attaques de nerfs. Other French synonyms besides these
have been used; most of them are translations from the Latin, having
reference also to the uterine hypothesis. In our language it is rare
to have any other single word used as a synonym for hysteria. Sir
James Paget[4] introduced the term neuromimesis, or nervous mimicry,
and suggested that it be substituted for hysteria, and neuromimetic
for hysterical. Neuromimesis is, however, not a true synonym. Many
cases of hysteria are cases of neuromimesis, but they are not all of
this character. Among the desperate attempts which have been made to
originate a new name for hysteria one perhaps worthy of passing notice
is that of Metcalfe Johnson,[5] who proposes to substitute the term
ganglionism, as giving a clue to the pathology of hysteria. His main
idea is that {207} hysteria exhibits a train of symptoms which are
almost always referable to the sympathetic or ganglionic nervous
system. This is another of those half truths which have misled so
many. The term hysteria, from the Greek ὑστερα, the uterus, although
attacked and belabored, has come to stay; it is folly to attempt to
banish it.

[Footnote 4: _Op. cit._]

[Footnote 5: _Med. Times and Gaz._, 1872, ii. 612.]

METHOD OF DISCUSSING THE SUBJECT.—It is hard to decide upon the best
method of discussing the subject of hysteria. One difficulty is that
connected with the question whether certain affections should be
considered as independent disorders or under some subdivisions of the
general topic of hysteria. Certain great phases of hysteria are
represented by hystero-epilepsy, catalepsy, ecstasy, etc.; but it will
best serve practical ends to treat of these in separate articles. They
have distinctive clinical features, and are capable of special
definition and discussion.

HISTORY AND LITERATURE.—To give a complete history of hysteria it
would be necessary to traverse the story of medicine from the time of
Hippocrates to the present. A complete bibliography would require an
immense volume. Volume vi. of the _Index Catalogue of the Library of
the Surgeon-General's Office, United States Army_, which has appeared
during the present year (1885), contains a bibliography of nearly
seventeen double-column pages, most of it in the finest type. The
references are to 318 books and 914 journals. The number of books and
articles cited as having appeared in different languages is as
follows: Latin, 99; Greek, 2; German, 180; British, 177; American,
159; French, 449; Italian, 75; Spanish, 45; Swedish, 12;
miscellaneous, 34. Even this wonderful list probably only represents a
tithe of the works written on this subject. Those desirous of studying
it from a bibliographical point of view can do so by consulting this
great work.

Many as are the names and voluminous as is the literature, certain
names and certain works are pre-eminent—Sydenham, Laycock, and Skey in
England; Tissot, Briquet, Charcot, and Landouzy in France; Stahl,
Frank, Eulenburg, and Jolly in Germany; and in America, Weir Mitchell.
The greatest work on hysteria is the treatise of Briquet.[6]

[Footnote 6: _Traité clinique et thérapeutique de l'Hystérie_, par le
Dr. P. Briquet, 1859.]

Mitchell[7] has organized into a scientific system a valuable method
of treating hysteria, and has given to the world a series of studies
of some types of the affection best or only seen in the United States.

[Footnote 7: _Fat and Blood: An Essay on the Treatment of Certain
Forms of Neurasthenia and Hysteria_, and _Clinical Lecture on Diseases
of the Nervous System, especially in Women_.]

Among other American monographs on hysteria and allied subjects worthy
of note are the contributions of Shaffer on _The Hysterical Element in
Orthopædic Surgery_;[8] Seguin's essay on _Hysterical Symptoms in
Organic Nervous Affections_;[9] Beard's volume on _Nervous
Exhaustion_;[10] the chapters on _Hysterical Insanity, etc._ in
Hammond's text-books;[11] and the papers of G. L. Walton[12] on
_Hystero-epilepsy_. Spitzka, Mann, Hughes, and {208} Kiernan have made
important contributions to the psychical aspects of the subject in
various American medical journals.

[Footnote 8: _The Hysterical Element in Orthopædic Surgery_, by Newlin
M. Shaffer, M.D., New York, 1880.]

[Footnote 9: _Archives of Neurology and Electrology_, for May, 1875,
and _Opera Minora_, p. 180.]

[Footnote 10: _A Practical Treatise on Nervous Exhaustion
(Neurasthenia)_, by George M. Beard, A.M., M.D., New York, 1880.]

[Footnote 11: _A Treatise on Diseases of the Nervous System_, and _A
Treatise on Insanity in its Medical Relations_.]

[Footnote 12: _Brain_, vol. v. p. 458, Jan., 1883; _Journal of Nervous
and Mental Disease_, vol. xi. p. 425, July, 1884.]

During the last five years I have published a number of articles and
lectures on the subject of hysteria and hystero-epilepsy, some of
which have been freely used in the preparation of this and the
succeeding sections.[13] My first paper on hystero-epilepsy, in the
_American Journal of the Medical Sciences_, was written to strongly
direct the attention of the American profession to the subject as
studied in France. It was in large part a translation from the works
of Charcot, Richer, and Bourneville, with, however, notes of some
observed cases.

[Footnote 13: “Hystero-epilepsy,” _American Journal of the Medical
Sciences_, October, 1881.

“Epileptoid Varieties of Hystero-epilepsy,” _Journal of Nervous and
Mental Diseases_, October, 1882.

“Illustrations of Local Hysteria,” _Polyclinic_, vol. i., Nos. 3 and
4, September 15, October 15, 1883.

“Clinical Lecture on the Treatment of Hysterical Paralysis by Rest,
Massage, and Electricity,” _Med. and Surg. Reporter_, vol. 1. p. 168,
February 9, 1884.

“Clinical Lecture on the Differential Diagnosis of Organic from
Hysterical Hemianæsthesia, etc.,” _ibid._ vol. 1. p. 233, 265,
February 23, March 1, 1884.

“Clinical Lecture on Spinal Traumatisms and Pseudo-Traumatisms,”
_Polyclinic_, vol. i. No. 9, March 15, 1884.

“A Case of Nymphomania, with Hystero-epilepsy, etc.,” _Medical Times_,
vol. xv. p. 534, April 18, 1885.

“Hystero-epilepsy in the Male, etc.,” _Medical Times_, vol. xv. p.
648, May 30, 1885.

“Some Forms of Myelitis, their Diagnosis from each Other and from
Hysterical Paraplegia,” _Medical News_, vol. xlvii., Nos. 7 and 8,
August 15 and 22, 1885.

“Clinical Lecture on Acute Mania and Hysterical Mania,” _Medical
Times_, vol. xvi. p. 153, November 28, 1885.]

PATHOLOGY.—Strictly speaking, hysteria cannot be regarded as having a
morbid anatomy. In an often-quoted case of Charcot's,[14] an old
hystero-epileptic woman, affected for ten years with hysterical
contracture of all the limbs, sclerosis of the lateral columns was
found after death. On several occasions this woman experienced
temporary remissions of the contracture, but after a last seizure it
became permanent. This is one of the few reported cases showing
organic lesion; and this was doubtless secondary or a complication. In
a typical case of hystero-epilepsy at the Philadelphia Hospital, a
report of which was made by Dr. J. Guiteras,[15] the patient, a young
woman, died subsequently while in my wards. Autopsy and microscopical
examination revealed an irregularly diffused sclerosis, chiefly
occupying the parieto-occipital region of both cerebral hemispheres.
Undoubtedly, as suggested by Charcot, in some of the grave forms of
hysteria either the brain or spinal cord is the seat of temporary
modification, which in time may give place to permanent material
changes. Old cases of chronic hysteria in all probability may develop
a secondary degeneration of the cerebro-spinal nerve-tracts, or even
degeneration of the nerve-centres themselves may possibly sometimes
occur. Two cases now and for a long time under observation further
indicate the truth of this position. One, which has been reported both
by H. C. Wood[16] and myself,[17] is a case of hysterical rhythmical
chorea in a young woman. Although the hysterical nature of her
original trouble cannot be doubted, she now has contractures of all
the extremities, which seem to have an organic basis. The other
patient is a woman who has {209} reached middle life; she has several
times temporarily recovered from what was diagnosticated as hysterical
paraplegia, in one instance the recovery lasting for months. Now,
after more than four years, she has not recovered from her last
relapse. Contractures, chiefly in the form of flexure, have developed,
and she has every appearance of organic trouble, probably sclerosis or
secondary degeneration of the lateral columns.

[Footnote 14: _Leçons sur les Maladies du Système nerveux_.]

[Footnote 15: _Philadelphia Medical Times_, 1878-79, ix. 224-227.]

[Footnote 16: _Ibid._, vol. xi. p. 321, Feb. 26, 1881.]

[Footnote 17: _Ibid._, vol. xii. p. 97, Nov. 19, 1881.]

Briquet[18] reviews the various hypotheses which have been held as to
the pathological anatomy of hysteria, giving a valuable summary of the
autopsies upon supposed hysterical cases up to the time of the
publication of his treatise in 1859. About the sixteenth century,
Rislau, Diemerbroeck, and Th. Bonet sought to establish a relation
between lesions of the genital organs met with in the bodies of
hysterical women and the affection from which they suffered. About
1620, Ch. Lepois believed that he had established the existence of
certain alterations of the brain in cases of hysteria. Hochstetter and
Willis toward the beginning of the present century arrived at similar
conclusions. That researches into the state of the genital organs have
chiefly occupied those investigating hysteria is shown by the writings
of Pujol, Broussais, Lovyer-Villermay, and, above all, by those of
Piorry, Landouzy, Schutzenberger, and Duchesne-Duparc. Georget,
Brachet, Girard, Gendrin, Bouillaud, Forget, and Lelut, about the
fourth or fifth decades of the present century, made numerous
autopsies on those dying when hysterical phenomena were in full
activity, and concluded that the genital organs of these individuals
revealed nothing in particular. This, in brief, is also the conclusion
of Briquet. Jeanne d'Albret, the mother of Henry IV., who was all her
life subject to hysterical headache, had her brain examined after
death, but absolutely nothing was found. Vesalius made an autopsy with
equally negative results on a woman who died from strangulation in an
hysterical attack. Royer-Collard also found nothing in an old
hysteric. Briquet believed—and I fully accord with this view—that in
some of the cases of Ch. Lepois, Hochstetter, and Willis diseases such
as chronic meningitis were present with the hysteria. He concludes
that anatomy does not show anything positive as to the seat or nature
of hysteria, except the suspicion of a certain degree of congestion in
various parts of the brain.

[Footnote 18: _Op. cit._]

While, however, hysteria may not have a morbid anatomy, it, like every
other disease, has, in a correct sense, a pathology.

The ancients saw only the uterus when regarding hysteria. Hippocrates
described the hysterical paroxysm and its accompanying disorders under
the name of strangulation of the uterus. The ancients generally
supposed that the disease originated in the ascent of the uterus to
the diaphragm and throat. They believed that this accommodating organ
could wander at will throughout the body, doing all manner of
mischief. Hippocrates asserted that it was the origin of six hundred
evils and innumerable calamities.

According to Sydenham,[19] the disorders which are termed “hysterical
in women and hypochondriac in men arise from irregular motions of the
animal spirits, whence they are hurried with violence and too
copiously to a particular part, occasioning convulsions and pain when
they exert {210} their force upon parts of delicate sensation, and
destroying the functions of the respective organs which they enter
into, and of those also whence they came; both being highly injured by
this unequal distribution, which quite perverts the economy of
nature.” Speaking of the strangulation of the womb, or fits of the
mother, he says: “In this case the spirits, being copiously collected
in the lower belly and rushing with violence to the fauces, occasion
convulsions in all the parts through which they pass, puffing up the
belly like a ball.”

[Footnote 19: _The Entire Works of Dr. Thomas Sydenham, newly made
English from the Originals, etc._, by John Swan, M.D., London, 1763,
pp. 416, 417.]

After a time, the idea that the uterus was the exclusive seat of
hysteria was in large measure supplanted by the view that the sexual
organs in general were concerned in the production of hysterical
phenomena. Romberg defined hysteria as a “reflex neurosis caused by
genital irritation.” Woodbury[20] concludes as late as 1876 that only
where the pathological source of hysterical symptoms resides in the
uterus or ovaries, cases may, with some show of propriety, be termed
hysterical; and where the uterus and organs associated with it in
function are not in a morbid condition no symptoms can be correctly
called hysterical.

[Footnote 20: _Medical and Surgical Reporter_, December 2, 1876.]

Bridges,[21] another American writer, in a paper on the pathology of
hysteria, says that hysteria does not occur most frequently in women
with diseased wombs, but in those whose sexual systems, by pampering
and other processes, are abnormally developed and sensitive. He makes
the same point with reference to the male sex. Sometimes, however,
besides the emotional state in the male, there is actual disease of
the sexual organs, caused by abuse or over-indulgence. Uterine disease
and hysteria are sometimes like results of one cause, and not
respectively cause and effect: women are hysterical oftener than men
because the uterine function in woman's physiology plays a more
important part in the production of emotional diseases than any organ
of the male sex.

[Footnote 21: _Chicago Medical Examiner_, 1872, xiii. 193-199.]

The truth would seem simply to be, that, as the uterus and ovaries are
the most important female organs, they are therefore a frequent source
of reflex irritation in hysterical patients.

Seguin[22] adopts with some reservation Brown-Séquard's hypothesis
that cerebral lesions produce the symptoms which point out their
existence, not by destroying organs of the brain, but by setting up
irritations which arrest (inhibit) the functions of other parts of the
encephalon. He says that he finds no difficulty in believing that the
same symptom may exist as well without as with a brain lesion. “In
typical hysteria the functions of parts of the encephalon included in
the right hemisphere, or in physiological relation with it, are
inhibited by a peripheral irritation starting from a diseased or
disordered sexual apparatus or other part; and in case of organic
cerebral disease the same inhibitory action is produced. In both kinds
of cases we may have loss of rational control over the emotions, loss
of voluntary power over one-half of the body, and loss of sensibility
in the same part.”

[Footnote 22: “On Hysterical Symptoms in Organic Nervous Affections,”
_Archives of Electrology and Neurology_, for May, 1875.]

Simply as a matter of passing interest, the attempt of Dupuy[23] to
frame a pathology of hysteria is worthy of attention. According to
him, every {211} local hysterical phenomenon is dependent upon an
abnormal state of either lateral half of the upper part of the pons
varolii. The centres of the pons, he holds, are perhaps merely passive
in the process, only becoming organically implicated when various
forms of permanent contractures and paralyses ensue.

[Footnote 23: _Medical Record_, New York, 1876, ii. 251.]

The pathology of hysteria must be considered with reference to the
explanation of the exact condition of the cerebro-spinal axis during
the existence of certain special grave phenomena of hysteria, such as
hemianæsthesia, hemiplegia, paraplegia, and contractures.

What is the probable state of the nerve-centres and tracts during
these hysterical manifestations? If, for example, in a case of
hysterical hemianæsthesia it is admitted that the brain of the other
side of the body is somehow implicated, although temporarily, what is
the probable condition of this half of the brain? Is the cerebral
change vascular or is it dynamic? If vascular, is the state one of
vaso-motor spasm or one of paresis, or are there alternating
conditions of spasm and paresis? Are true congestions or anaæmias
present? If the condition is dynamic, what is its nature? Is it
molecular? and if molecular in what does it consist? Is it possible to
say absolutely what the pathological condition is in a disorder in
which autopsies are obtained only by accident, and even when obtained
the probabilities are that with fleeting life depart the changes that
are sought to be determined?

Two hypotheses, the vaso-motor and the dynamic, chiefly hold sway. The
vaso-motor, attractive because of its apparent simplicity, has been
well set forth by Walton,[24] who contends that while it may not be
competent to easily explain all hysterical symptoms, it will best
explain some of the major manifestations of hysteria—for example,
hemianæsthesia. Hemianæsthesia, he argues, may appear and disappear
suddenly; it may be transferred from one side of the body to another
in a few seconds; so blood-vessels can dilate as in a blush, or
contract as in the pallor of fear, in an instant. In fainting the
higher cerebral functions are suspended, presumably because of
vaso-motor changes; therefore the sudden loss of function of one-half
of the brain-centres, seen sometimes in hysterical hemiplegia and
hemianæsthesia, may easily be imagined to be the result of an
instantaneous and more or less complete contraction of cortical
blood-vessels on that side. Neurotic patients have a peculiarly
irritable vaso-motor nervous system. He records a case seen in
consultation with H. W. Bradford. The patient had a right-sided
hemianæsthesia, including the special senses, the sight in the left
eye being almost wanting. The fundus of the right eye was normal; the
left showed an extreme contractility of the retinal blood-vessels
under ophthalmoscopic examination; these contracted to one-third their
calibre, and the patient was unable to have the examination continued.
The explanation offered is, that spasm of the blood-vessels on the
surface of the left cerebral hemisphere had caused, by modification of
the cortical cells, a right-sided hemianæsthesia, including the sight,
and by reaching the meninges a left-sided spastic migraine, and by
extending to the fundus of the left eye an intermittent retinal
ischæmia.

[Footnote 24: _Journal of Nervous and Mental Disease_, vol. xi., July,
1884, p. 424 _et seq._]

The vaso-motor hypothesis is held by Rosenthal,[25] who, however,
wrongly {212} gives the spinal cord the preponderating part in the
production of the symptoms. According to this author, the anæsthesia
and analgesia present in hysteria conform to the law as established by
Voigt with regard to the distribution of the cutaneous nerves. The
sensory nerves form at the periphery a sort of mosaic corresponding to
an analogous arrangement in the spinal cord. “It is evident,” he says,
“that the peripheral disorders in hysteria merely represent an exact
reproduction of the central changes, and that the latter are situated,
in great part, in the spinal cord.” He attributes a large part of the
symptoms of hysteria to a congenital or acquired want of resistance of
the vaso-motor nervous system. “Motor hysterical disorders are also
due in the beginning to a simple functional hyperæmia, but in certain
forms the chronic hyperæmia may lead to an inflammatory process which
may terminate (as in Charcot's case) in secondary changes in the
columns of the cord and nerve-roots.” When the brain is involved in
hysteria, he holds that the most serious symptoms must be attributed
to reflex spasms of the cerebral arteries and to the consequent
cerebral anæmia.

[Footnote 25: “A Clinical Treatise on Diseases of the Nervous System,”
by M. Rosenthal, Vienna, translated by L. Putzel, M.D., vol. ii.
_Wood's Library_, New York, 1879.]

The dynamic pathology of hysteria is probably believed in by most
physicians, and yet it is difficult to explain. Thus, Briquet[26] says
that hysteria manifests itself by derangement of the nervous action,
and what is called nervous influence is something like electricity. It
is simply the result of undulations analogous to those which produce
heat and light; in other words, it is a mode of movement. Wilks[27]
compares some of the conditions found in hysteria to a watch not
going; it may be thought to be seriously damaged in its internal
machinery, yet on looking into it there is found a perfect instrument
that only needs winding up. As regards the brain being for a time
functionless, the possibility of this is admitted by all, as in sleep
or after concussion. He mentions the case of a young girl who had been
assaulted, and had complete paralysis of motion and sensation. The
shock had suspended for a time the operations of her brain, and
organic life only remained. We have only to suppose that half of the
brain is in this way affected to account for all the phenomena of
hemianæsthesia.

[Footnote 26: _Op. cit._]

[Footnote 27: _Lectures on Diseases of the Nervous System_, delivered
at Guy's Hospital, by Samuel Wilks, M.D., F. R. S., Philada., 1883.]

According to the dynamic view, the central nervous system is at fault
in some way which cannot be demonstrated to the eye or by any of our
present instruments of research. The changes are supposed to be
molecular or protoplasmic, rather than vaso-motor or vascular.

As innervation and circulation go hand in hand or closely follow each
other, my own view is that both vaso-motor and molecular changes,
temporary in character, probably occur in the central nervous system
in grave hysterical cases.

Whatever the temporary conditions are, it is evident, on the one hand,
that they are not states of simple anæmia or congestion, and, on the
other hand, that they are not inflammations or atrophies. Patients
with hysterical manifestations of the gravest kind as a rule are free
for a time from their harassing and distressing symptoms. This could
not be if these symptoms were due to lesions of an organic nature.
Sudden recoveries also could not be accounted for if the changes were
organic.

{213} Lloyd[28] contends that most hysterical symptoms, if not all,
are due to abnormal states of consciousness. The development of this
idea constitutes his argument for the recognition of the disease as a
true psychosis. In the reflex action, not only of the lower spinal
cord and ganglia of special sensation, but of the highest centres of
the brain, he sees the explanation of many of the characteristics of
hysteria. In other words, he finds that the sphere of the disease is
more especially in the automatic action of the brain and cord.

[Footnote 28: _Op. cit._]

Dercum and Parker[29] have published the results of a series of
experiments on the artificial induction of convulsive seizures which
bear upon this discussion of the pathology of hysteria. The
experiments were performed by subjecting one or a group of muscles to
a constant and precise effort, the attention being at the same time
concentrated on some train of thought. The position most frequently
adopted was the following: The subject being seated, the tips of the
fingers of one or both hands were placed upon the surface of the
table, so as to give merely a faint sense of contact—_i.e._ the
fingers were not allowed to rest upon the table, but were held by a
constant muscular effort barely in contact with it.

[Footnote 29: _Journal of Nervous and Mental Disease_, vol. xi.,
October, 1884, pp. 579-588.]

Tremors commenced in the hands; these became magnified into rapid,
irregular movements which passed from one limb or part to another
until the subject was thrown into strong general convulsions.
Opisthotonos, emprosthotonos, and the most bizarre contortions were
produced in various degrees. No disturbances of sensation were at any
time present. Disturbances of respiration and phonation were often
present in a severe seizure, and the circulatory apparatus was
profoundly affected. A flow of tears, and occasionally profuse
perspiration, were sometimes induced. After severe seizures large
quantities of pale urine were passed. The reflexes were distinctly
exaggerated. No unconsciousness was ever observed, but a progressive
abeyance or paresis of the will. Nitrite of amyl seemed to arrest the
convulsive seizures at once.

In attempting to explain these phenomena Dercum and Parker refer to
the induction of Spencer as to the universality of the rhythm of
motion. Through the whole nervous system of every healthy animal a
constant rhythmical interchange of motion takes place. What might be
called nervous equilibration results. In man the will modifies and
controls the action of the nervous system; it assists in maintaining
nervous equilibrium when it is threatened. The will being withdrawn
from the nervo-muscular apparatus, and this being subjected to strain,
a disturbance takes place. This same explanation may be applied to
some of the convulsive and other phenomena of hysteria.

Comparing and analyzing the various views, it may be concluded with
reference to the pathology of hysteria as follows:

(1) The anatomical changes in hysteria are temporary.

(2) These changes may be at any level of the cerebro-spinal axis, but
most commonly and most extensively cerebral.

(3) They are both dynamic and vascular: the dynamic are of some
undemonstrable molecular character; the vascular are either spastic or
paretic, most frequently the former.

(4) The psychical element enters in that, either, on the one hand,
violent mental stimuli which originate in the cerebral hemispheres are
{214} transmitted to vaso-motor conductors,[30] or, on the other hand,
psychical passivity or torpor permits the undue activity of the lower
nervous levels.

[Footnote 30: Rosenthal.]

ETIOLOGY.—Heredity has much to do with the development of hysteria. It
is not that it is so frequently transmitted directly after its own
kind, but this disorder in one generation generally indicates the
existence of some ancestral nervous, mental, or diathetic affection.

Briquet[31] has shown that of hysterical women who have daughters,
more than half transmit the disease to one or several of these, and,
again, that rather more than half of the daughters of the latter also
become hysterical. Amann, according to Jolly,[32] has stated that in
208 cases of hysteria he proved with certainty an hereditary tendency
165 times—that is, in 76 per cent. This is too big to be true.

[Footnote 31: _Op. cit._]

[Footnote 32: _Ziemssen's Cyclopædia of the Practice of Medicine_,
vol. xiv., American translation.]

Briquet has also made some careful investigations into the subject of
the health of infants born of hysterical mothers. The investigations
were based upon a study of 240 hysterical women, with whom he compared
240 other patients affected with such diseases as fever, phthisis,
cancer, diseases of the heart, liver, and kidneys, but without any
hysterical symptoms. In brief, the result of his investigations was
that children born of hysterical mothers die more frequently and at a
younger age than those who are born of mothers not hysterical.

The relation of hysteria to certain morbid constitutional states has
long been recognized, particularly its connection with the tubercular
diathesis. This has been shown by numerous observers, especially among
the French. The most valuable recent contribution is that of
Grasset,[33] who believes that a direct connection can be traced
between the tubercular diathesis and hysteria. When the relations of
hysteria to the scrofulous and tubercular diathesis are spoken of by
him, it is not meant that hysterical subjects have tubercles in the
lungs, but that these diatheses are found in various generations, and
that among some subjects of the hereditary series the constitutional
states manifest themselves as hysteria. It is not the evidences of
hysteria with pulmonary and other tuberculous conditions that he is
considering, but that hysteria may be, and often is, a manifestation
of the tubercular diathesis. Two cases may present themselves: in one
the neurosis is the only manifestation of the diathesis; in the other,
it is continued in the same subject along with the other diathetic
manifestations. In demonstration of his thesis he concludes with a
series of most interesting cases, which he arranges into two groups.
In the first, hysteria is the only manifestation of the tubercular
diathesis; in the second, are simultaneous pulmonary and hysterical
manifestations. In the first group he has arrayed eight personal
observations and seventeen derived from various authors; in the second
he has two personal and seventeen compiled observations.

[Footnote 33: “The Relation of Hysteria with the Scrofulous and the
Tubercular Diathesis,” by J. Grasset, _Brain_, Jan., April, and July,
1884.]

Personal experience and observation go far to confirm the views of
Grasset, although I recognize fully the strength of the objection of
Brachat and Dubois and others that, phthisis being such a common
complaint, it might be demonstrated by statistics that it was related
to {215} almost any disease. Not only hysteria, but other neuroses or
psychoses, have a close connection with the tubercular diathesis.

Among the insane and idiotic and among epileptics phthisis is of
frequent occurrence. At the Pennsylvania Training School for
Feeble-minded Children the frequency of phthisis among the inmates of
the institution is one of the most striking clinical facts. The insane
of our asylums die of pulmonary troubles oftener almost than of any
other disease. The fact that hysteria is met with in the robust and
vigorous does not invalidate the position taken, for the robust and
vigorous who are not hysterical are not infrequently found in the
descendants of the tuberculous.

Laycock[34] believed that the gouty diathesis was particularly liable
to give rise to the hysterical paroxysm or to irregular forms of
hysteria. Gairdner, quoted by Handfield Jones,[35] supports this view.

[Footnote 34: _A Treatise on the Nervous Diseases of Women_, by Thomas
Laycock, M.D., London, 1840.]

[Footnote 35: _Studies on Functional Nervous Disorders_.]

Gout in England plays a greater part in the production of nervous and
other disorders than in this country, but even here its
instrumentality is too often overlooked. In Philadelphia are many
families, some of them of English origin, in which gout has occurred,
sometimes of the regular type, but oftener of anomalous forms. Among
the most striking examples of hysteria that have fallen under my
observation, some have been in these families. In a few of them
remedies directed to the lithæmic or gouty conditions in connection
with other measures have been efficient. More frequently they have
failed, for while a relation may exist between the neurotic disorder
and the diathesis, it is not the diathesis, but the neurotic disorder,
which we are called upon to treat.

That a certain mental constitution predisposes to hysteria cannot be
doubted. Ribot[36] describes, chiefly from Huchard,[37] the hysterical
constitution. It is a state in which volition is nearly always
lacking. The prominent trait is mobility. The hysterical pass with
increditable rapidity from joy to sadness, from laughter to tears;
they are changeable, freakish, or capricious; they have fits of
sobbing or outbursts of laughter. Ch. Richét compares them to
children, who oftentimes can be made to laugh heartily while their
cheeks are still wet with tears. Sydenham says of them that
inconstancy is their most common trait: their sensibilities are
aroused by the most trivial cause, while profounder emotions scarcely
touch them. They are in a condition of moral ataxy, lacking
equilibrium between the higher and lower faculties.

[Footnote 36: _Diseases of the Will_.]

[Footnote 37: Axenfeld et Huchard, _Traité des Neuroses_, 2d ed.,
1883, pp. 958-971.]

As to sex, it is almost unnecessary to say that hysteria occurs with
greater frequency among females than males; and yet it is all
important to emphasize the fact that it is not exclusively a disease
of the former sex. Some statistics on this subject have been
collected. In Briquet's often-quoted 1000 cases of hysteria, 50 only
occurred in men. I believe, however, that the proportion of hysterical
men to hysterical women is greater than this. Instead of a ratio of 1
to 20, as these statistics would indicate, 1 to 15 would probably be
nearer the truth. Statistics upon this subject are deceptive.

The occurrence of hysteria in the male was little discussed before the
publication of Briquet's great work, but since that time it has
received {216} great attention from the medical profession.
Charcot[38] in some recent lectures at Salpêtrière has called
attention to this subject. From 1875 to 1885 he says that five
doctoral theses have been written on hysteria in men. Batault has
collected 218 and Klein 80 cases. The _Index Catalogue_ contains 102
references to hysteria in the male.

[Footnote 38: _Le Progrès médical_, 1885.]

Hysteria in men may take on almost any form that it shows in women. It
may occur in the strong, although more likely to be seen among the
weak and effeminate. Even strong, vigorous workmen are susceptible, at
times, to hysteria. According to Charcot, the duration of the
affection differs somewhat in the two sexes. In male patients it lasts
a long time and the symptoms are troublesome; in females the contrary
is usually although not always the case. The occurrence of hysteria in
the male sex has probably been overlooked through the tendency to
class symptoms which would be regarded as hysterical in women as
hypochondriacal in men.

One of the most typical half-purposive hysterical attacks that has
ever come under my observation was in a literary man of some
prominence. Hysterical syncope, contracture, hysterical breathing,
hysterical hydrophobia, coccygodynia, hemiparesis, hemianæsthesia, and
blindness are some other forms of hysteria in the male of which there
are clinical records the result of personal observation. A remarkable
case of hysterical motor ataxy was seen in a boy who was for some time
a patient at the Philadelphia Polyclinic. Wilks[39] records several
interesting cases of hysteria in boys. One simulated laryngismus
stridulus, with paroxysmal suffocative attacks and barking. Another
was a case of hysterical maniacal excitement; another was an example
of malleation, or constant movement as in hammering; still others were
instances of extreme hyperæsthesia, of anorexia, and of nervous
dyspnœa. The same author also dwells on the hysterical perversion of
the moral sense found in boys as in girls. He gives some instances
clipped from English newspapers—attempts to poison, murder or attempts
to murder, confessions false and true. Many instances could be added
from our own sensational American sheets.

[Footnote 39: _Op. cit._]

No age is free from a liability to hysteria. Its occurrence, however,
at certain periods of life with great frequency is well known. The
following table has been arranged from tables given by Briquet and
Jolly, and shows that it is of most frequent occurrence between the
ages of fifteen and thirty:

   Age.  Landouzy.  Georget.  Beau.  Briquet.  Scanzoni.  Total.

   0-10       4        1       ...      66        ...       71

  10-15      48        5        6       98         4       161

  15-20     105        7        7      140        13       272

  20-25      80        4        3       71     |
  25-30      40        3       ...      24     |  64       289

  30-35      38       ...      ...       9     |
  35-40      15       ...      ...       9     |  78       149

  40-45       7        1       ...       1     |
  45-50       8       ...       1        3     |  44        65

  50-55       4       ...      ...       3     |
  55-60       4       ...       1        2     |  11        25

  60-80       2       ...      ...      ...        3         5
            355       21       18      426       217      1037

{217} Hysteria in the United States assumes almost every form,
probably because we have here represented almost every race and
nationality, either pure or mixed. While it cannot be clearly shown
that certain races are much more prone to hysteria than others, the
type of this disease is doubtless much influenced by racial and
climatic conditions. Certain phases of the disease prevail in certain
sections more than in others. Mitchell's[40] experience is that the
persistent hystero-epilepsies, and the multiple and severe
contractures which Charcot and others describe, are rare in this
country among all classes, and especially uncommon in the lowest
classes, among which Charcot seems to have found his worst and most
interesting cases. He says that while his own clinic furnishes
numerous cases of neural maladies, and while he has examples of every
type of the milder form of hysteria, it is extremely uncommon to
encounter the more severe and lasting forms of this disease. When
Mitchell's _Lectures_ were first published I was inclined to regard
hystero-epilepsy of the grave type as of rare occurrence, and so
stated in answer to a communication from him. Recently, as the result
of a longer experience, I have become persuaded that some irregular
forms are met with somewhat frequently in various sections of our
country. It remains true, however, that in the Middle and Northern
sections of the United States the graver hysterias of the convulsive
type are not nearly as frequently observed as in the southern
countries of Europe.

[Footnote 40: _Op. cit._]

Dr. Guiteras, formerly physician to the Philadelphia Hospital, and
Lecturer on Physical Diagnosis in the University of Pennsylvania, now
in the United States marine hospital service, has for several years
been on duty, most of the time, in Florida, the West Indies, and the
Gulf of Mexico. In answer to an inquiry made by me, he writes:
“Hysteria prevails with extraordinary frequency amongst the Cubans. It
presents itself in the shape of excito-motory and mental phenomena,
almost to the exclusion of all other manifestations. The motory
anomalies comprise the whole range from mild hysterics to the gravest
hystero-epilepsy. The latter is incomparably more frequent in Key West
than in Philadelphia. The confirmed hystero-epileptics are few, but it
is the rule for well-marked cases of hysteria to present occasionally,
often only once in the course of the disease, hystero-epileptic
seizures which may be of frightful intensity. By mental disorders I do
not mean only the acute attacks of excitement and delirium which
attend upon or take the place of convulsive attacks, but I mean also
to include the chronic form of hysterical insanity, which is generally
some variety of melancholia. These are the peculiarities of hysteria
as seen by myself in the Latin race in the tropics. My experience
teaches me that the Saxon race in the tropics shows the same
peculiarities to a less extent.”

In the region referred to by Guiteras it will be remembered there is a
mixed population composed largely of Spanish, French, and Portuguese.
Climatic and other local influences may have something to do with the
particular form which this disorder assumes in these tropical or
semitropical districts, but race would seem to be the most important
factor. In the section on Hystero-epilepsy I will speak of the
irregular type of this disorder, which has fallen most frequently
under my own observation.

Hysteria in the negro is of somewhat frequent occurrence, and is more
{218} likely to be of the demonstrative or convulsive than of a
paralytic or negative form. Hysterical convulsions, particularly of
the purposive kind, and hysterical mania, are often met with in the
colored population of our large city hospitals and asylums.

The influence which climate exerts, like that of race, is rather on
the type of hysteria than upon the disease itself. Hysteria is found
in every climate, but in warm countries the disorder seems more likely
to be mobile and dramatic than when found in the more temperate or
colder zones.

Season and meteorological conditions have some influence on the
production of hysterical attacks. It is well known that hysteria,
chorea, and other allied nervous disorders are more likely to appear
in the spring than at other seasons. This fact has been shown by
various observers.

Hysteria may occur in any rank of life. It is not, as has been held by
some, a disease of the luxurious classes. The American physician who
has seen much of this disorder—and that means every physician of large
practice—has met with hysterical cases in every walk of life. While
this is true, however, hysteria of certain types is met with more
frequently in certain social positions. Some of the remarks about race
and climate apply also here. It is the type of the disorder, and its
relative frequency among various classes, which are affected by social
position. Young women of the richer classes, who have been coddled and
pampered, whose wants and whose whims have been served without stint
or opposition, often pass into hysterical conditions which do not have
any special determining causative factor, or at least only such as are
comparatively trivial. Occasionally, in them hystero-epilepsy,
catalepsy, and the train of grave hysterical phenomena are observed.
We are more likely, however, to have the minor and indefinite
hysterical symptoms; or, if grave manifestations be present, they are
most usually ataxia, paralysis, contractures, or aphonia, and not
convulsive phenomena. Hysteria in our American cities is especially
prevalent among certain classes of working-people, as among the
operatives in manufacturing establishments. Dividing American society
into the three classes of rich, middle, and poor, hysteria is most
prevalent in the first and the last. It is, however, by no means
absent in the middle class.

The absence of occupation on the one hand, and, on the other, the
necessity of following work for which the individual is unfitted,
particularly irritating lines of work, predispose to the occurrence of
hysteria. It may be caused, therefore, either by no work, overwork, or
irritating work. As to the special occupations, hysteria would seem to
result most commonly in those positions where physical fatigue
combines with undue mental irritation to harass and reduce the nervous
system. In men it occurs often as the result of overwork conjoined
with financial embarrassment. It is met with not infrequently among
teachers, particularly those who are engaged in the straining and
overstraining labor of preparing children for examinations. A good
method of education is the best preventive; a bad method is one of the
most fruitful causes of the affection. The injurious effect of
American school or college life in the production of hysteria is
undoubted, and should be thoroughly appreciated. Our educational
processes act both as predisposing and exciting causes of this
disorder. Both in our private and public educational institutions the
{219} conditions are frequently such as to lead to the production of
hysteria or to confirm and intensify the hysterical temperament. In
our large cities all physicians in considerable practice are called
upon to treat hysterical girls and boys, the former more frequently,
but the latter oftener than is commonly supposed. Hysteria in boys,
indeed, does not always meet with recognition, from the fact that it
is in boys. Cases of hysteria in girls under twelve years of age have
come under my observation somewhat frequently. About or just
succeeding examination-time these cases are largely multiplied. The
hysteria under such circumstances may assume almost any phase;
usually, however, we have not to deal in such patients with convulsive
types of the disease.

Clarke[41] has considered some of these questions in connection
particularly with the physiological processes of menstruation, and its
bearing upon the inability of girls to maintain equally with boys the
stress of such competition.

[Footnote 41: _Sex in Education, etc._, by Edward H. Clarke, M.D.,
Boston, 1873.]

The cramming processes which are resorted to in order to force
children at fixed times from the lower to the higher grades of public
schools, and more especially from grammar to normal or high schools,
is a fruitful source of evil in this direction. It is not always so
much hard study as it is the badly-arranged and too numerous subjects
of study that make the strain. I have spoken of this in another
connection as follows:[42] “Our children are too largely in the hands
of those educationalists to whom Clouston refers,[43] who go on the
theory that there is an unlimited capacity in every individual brain
for education to any extent and in any direction. Children varying in
age and original capacity, in previous preparation, and in
home-surroundings are forced into the same moulds and grooves. The
slow must keep pace with the fleet, the frail with the sturdy, the
children of toil and deprivation with the sons and daughters of wealth
and luxury. A child is always liable to suffer from mental overwork
when the effort is made to force its education beyond its receptive
powers. Education is not individualized enough. The mind of the child
is often confused by a multitude of ill-assorted studies. Recreation
is neglected and unhealthy emulation is too much cultivated. In many
communities admissions to various grades of public schools are
regulated entirely by the averages obtained at examinations, instead
of on the general record of the pupils in connection with proper but
not too severe examinations. In consequence often, after the campaign
of overwork and confusion called an examination, we see children
developing serious disturbances of health or even organic
disease—paroxysmal fever, loss of appetite, headache or neckache,
disturbed sleep, temporary albuminuria, chorea, hysteria, and
hystero-epilepsy.”

[Footnote 42: “Toner Lecture on Mental Overwork and Premature Disease
among Public and Professional Men.” delivered March 19, 1884,
Washington, Smithsonian Inst., January, 1885.]

[Footnote 43: _Clinical Lectures on Mental Diseases_.]

The term students' hysteria has been applied to the neuromimetic
disorders from which medical students frequently suffer during their
attendance upon lectures. Some years since, when engaged in examining
students upon the lectures upon the practice of medicine delivered by
Professor DaCosta, I saw many illustrations of this affection, {220}
some of which were very amusing. In a paper on hysteria which received
the prize at the Physical Society of Guy's Hospital, P. Horrocks[44]
writes that during the fortnight following the death of the late
Napoleon, Sir James Paget was consulted for stone in the bladder by no
less than four gentlemen who had nothing the matter with them. “How
many students,” says Horrocks, “are there, of one year's standing or
more, who have not imagined and really became convinced that they were
suffering from some disease, generally a fatal disease?” In such cases
we have a combination of true psychical influence with overwork and
the unhygienic surroundings for which our medical colleges are
notorious.

[Footnote 44: _Med. and Surg. Reporter_, vol. xxxvii., Nov. 24, 1877.]

It has been my personal experience that comparatively few cases of
hysteria occur among female medical students. Not long since a thesis
was presented at graduation by a woman medical student[45] on the
curative effects of professional training in neurasthenic and
hysterical women. In this she shows that there are certain relations
of mind over body which enable it to modify bodily conditions and ward
off disease when other remedies appear almost powerless. She
illustrates the therapeutic power of mental impressions and
occupations by two cases in which a judicious and careful course of
study acted to cure severe nervous and uterine troubles. One of these
women, who had suffered with neurasthenia and general debility, severe
nervous headaches, and other symptoms, was able during her last year
at college to attend fifteen lectures a week, besides clinics, prepare
for examination on five subjects, and was seldom troubled with even
headache. She afterward was employed in hospital work, and could walk
five miles a day without discomfort. That women medical students know
when and how to take care of themselves during the menstrual period,
and that they can, if they see fit, cease work or lighten their labors
at that time, would partly account for their escaping from nervous
break-down.

[Footnote 45: “The Therapeutic Value of Mental Occupation,” by Hannah
M. Thompson, M.D., _Medical and Surgical Reporter_, November, 1883.]

That any form of irritation in a patient predisposed to hysteria may
act as an exciting cause in this affection has led Laségue to apply
the term peripheral hysteria to certain cases. One of his cases was a
girl fourteen years old, who, having suffered for a few hours with her
eyes because of some sand thrown into one of them by a playmate, awoke
the next morning with a spasm of the eyelid on that side, which
rendered it impossible for her to open that eye; and it remained
closed during four months. He considered that the irritation produced
by the sand was not the immediate cause of the spasm, but that its
long duration was an hysterical phenomenon. The patient afterward
became the subject of hysterical manifestations. In another complete
hysterical aphonia came on after a slight bronchitis. Another, after
an attack of indigestion, refused to touch either food or drink for
twenty-four hours, and later was troubled with regurgitation from
constriction of the pharynx or œsophagus which lasted for some weeks.

Anæmia and chlorosis are frequent exciting causes of hysteria in
children, particularly in girls.

Disorders of menstruation play a prominent part as exciting causes of
{221} special hysterical manifestations. The period of the
establishment of the menstrual function is one that is particularly
fertile in the production of hysteria, much more so than acquired
disorders of menstruation occurring later. Menorrhagia, dysmenorrhœa,
and certain local utero-vaginal disorders may act upon those
predisposed to hysteria as exciting causes. These conditions
themselves are, on the other hand, sometimes caused by nervous,
hysterical states in the individual.

With reference to the very common assertions that continence on the
one hand, and sexual over-indulgence on the other, are the most
prolific causes of hysteria, the true stand to take is that neither of
these positions is philosophically correct; for, as Briquet has shown,
nuns on the one hand and prostitutes on the other are frequent victims
of this protean disorder.

As affirmed by Jolly, sexual over-irritation, particularly that
induced by onanism, more frequently causes hysteria than sexual
abstinence or deprivation.

The occurrence of hysteria and hysterical choreas among pregnant women
has long been recognized. Scanzoni, quoted by Jolly,[46] states that
of 217 patients whom he had treated, 165, or 76 per cent. had been
puerperal, and that of the latter not less than 65 per cent. had borne
children more than three times. Cases of grave hysteria or
hystero-epilepsy have been aggravated by pregnancy and have led to
premature labor.

[Footnote 46: _Op. cit._]

Chrobak attacks the etiological problem of hysteria by referring its
causation to movable kidneys! He observed 19 such patients in Vienna,
16 being in Oppolzer's clinic.[47] Three times no subjective symptoms
accompanied the anomaly; eight times the trouble could be referred
either to the dislocation of the kidneys or to disease of the same;
and eight times the evidence of hysteria was unmistakable. Among the
latter eight cases neither vaginal, uterine, nor ovarian conditions
were recognized. He concludes that there is a direct nervous
connection between the kidneys and the genital organs, and between
both and hysteria.

[Footnote 47: _Medizinische-Chirurgische Rundschan_, quoted by _Boston
Medical and Surgical Journal_, 1870, lxxxiii. 430-432.]

In brief, the truth is that frequent or severe local irritation in any
part of the body in an individual of the hysterical diathesis may act
as the exciting cause of an hysterical paroxysm or of special
hysterical manifestations. Irritation or disease of the uterus or
ovaries may result in hysteria, as may the bite of a dog, a tumor of
the brain, a polypus in the nose, a phymosis, an irritated clitoris, a
gastric ulcer, a stenosis of the larynx, a foreign body in the eye, a
toe-nail ulcer, or a movable kidney.

Whatever tends to exhaust the nervous system will also cause hysteria,
but only in those who have some inherited predisposition to the
disorder. C. Handfield Jones[48] mentions heatstroke and severe
physical labor as such causes. One of the sequelæ of heatstroke
enumerated by Sir R. Martin, and quoted by Jones, is a distressing
hysterical state of the nervous system, with an absence of
self-control in laughing and crying, the paroxysm being followed by
great prostration of nervous power.

[Footnote 48: _Op. cit._]

{222} The effect of imitation in the production of hysteria has been
known in all ages. Most of the epidemics and endemics of nervous
disorders which have from time to time prevailed in various parts of
the world have either been hysterical in character or have had in them
a large element of hysteria. While it is impossible in a practical
work to devote much space to this branch of the subject, a discussion
of hysteria in its etiological relations would be imperfect without
some reference to these outbreaks. In ancient times, in the Middle
Ages, and within comparatively recent periods extraordinary epidemics
have occurred. No country within the range of medical observation has
been entirely free from them. Communities civilized and
semi-civilized, Christian and Mohammedan, Protestant and Catholic,
have had a fair share of the visitations. Some of them constitute
epochs in history, and, as Hecker,[49] their greatest historian, has
remarked, their study affords a deep insight into the work of the
human mind in certain states of society. “They are,” he says, “a
portion of history, and will never return in the way in which they are
recorded; but they expose a vulnerable part of man—the instinct of
imitation—and are therefore very nearly connected with human life in
the aggregate.”

[Footnote 49: _The Epidemics of the Middle Ages_, from the German of
J. F. C. Hecker, M.D., Professor at the Frederick William University
at Berlin, etc., translated by B. G. Babington, M.D., F. R. S., etc.;
3d ed., London, 1859.]

Some authors under hysteria, others under catalepsy, others under
ecstasy, still others under chorea, have discussed these epidemics—a
fact which serves to emphasize the truth that while these affections
have points of difference, they have also an easily-traced bond of
union. They are but variations of the same discordant tune. Briquet in
an admirable manner sketches their history from the age of Pausanias
and Plutarch to the time of Mesmer. Of American writers, James J.
Levick[50] of Philadelphia has furnished one of the most valuable
contributions to this subject.

[Footnote 50: “An Historical Sketch of the Dance of St. Vitus, with
Notices of some Kindred Disorders,” _Med. and Surg. Reporter_, vol.
vii., Dec. 21 and 28, 1861, p. 276, and Jan. 4 and 11, 1862, p. 322.]

In the year 1237 a hundred children or more were suddenly seized with
the dancing mania at Erfurt; another outbreak occurred at Utrecht in
1278.

As early as the year 1374 large assemblages of men and women were seen
at Aix-la-Chapelle affected with a “dancing mania.” They formed
circles and danced for hours in wild delirium. Attacks of
insensibility, of convulsions, and of ecstasy occurred. The disease
spread from Germany to the Netherlands. In a few months it broke out
in Cologne, and about the same time at Metz. “Peasants,” we are told,
“left their ploughs, mechanics their workshops, housewives their
domestic duties, to join the wild revelry, and this rich commercial
city became the scene of the most ruinous disorder.”

The festival of St. John the Baptist was one celebrated in strange
wild ways in these early days. Fanatical rites, often cruel and
senseless, were performed on these occasions. Hecker supposes that the
wild revels of St. John's Day in 1374 may have had something to do
with the outbreak of the frightful dancing mania soon after this
celebration. It at least brought to a crisis a malady which had been
long impending.

{223} The Flagellants afford another illustration of an early
religio-nervous craze. Self-flagellation was indulged in for
generations before the fourteenth century, but it then became
epidemic. A brotherhood of Flagellants was formed; they marched in
processions carrying scourges, with which they violently lashed and
scourged themselves. As late as 1843, Flagellant processions, but
without the whips and scourging, were continued in Lisbon on Good
Friday.

Strasburg was visited by the dancing plague in 1418. Those afflicted
were conducted to the chapel of St. Vitus, where priests attempted to
relieve them by religious ceremonies. The name St. Vitus's dance,
still so common as a synonym for chorea, has come down to us because
of the alleged wonderful doings of this saint in behalf of those
affected during some of the dancing epidemics. Both Hecker and
Madden[51] give interesting details of the personal history of St.
Vitus, who was a Sicilian, born in the time of Diocletian, and even in
childhood is said to have worked great miracles, and was delivered
from many sufferings and torments. He died about the year 303. His
body was moved to Apulia, afterward to St. Denys in France, and still
later to the abbey of Corvey in Saxony. A legend was invented that St.
Vitus, just before he bent his neck to the sword, prayed to God that
he might protect from the dancing mania all those who should solemnize
the day of his commemoration and fast upon its eve.

[Footnote 51: _Phantasmata; or, Illusions and Fanaticisms, etc._, by
R. R. Madden, F. R. S., London, 1857.]

Another strange disorder called tarantismus derived its name from the
fact that it was supposed to be caused by the bite of the tarantula, a
ground-spider common in Apulia, Italy. According to Hecker, the word
tarantula is the same as terrantola, a name given by the Italians to a
poisonous lizard of extraordinary endowments. The fear of the insect
was so general that its bite was much oftener imagined than actually
received. The disorder was probably in existence long before the
fifteenth century, although the first account of it, that of Nicholas
Perotti, refers to its occurrence in this century. Many symptoms
followed the bite or supposed bite: the individuals became melancholy,
stupefied, lost their senses, and, above all, were irresistibly
impelled to dance until exhausted and almost lifeless. It was believed
that the results of the bite could be cured, or at least much
benefited, by dancing to a certain kind of music. Tarantism was at its
height in the seventeenth century. To this day, in some parts of
Italy, dances called tarantellas are performed with intricate figures
to marked time.

Abyssinia was visited by a dancing mania called the tigretier, which,
according to Hecker, resembled the original mania of the St. John
dancers. It exhibited a similar ecstasy. Those affected with it were
cured by dancing to the music of trumpeters, drummers, fifers, etc.

Levick says that the dancing mania of the fifteenth century is still
kept in popular remembrance in some places by an annual festival,
especially at Echtermarch, a small town in Luxembourg, where a jumping
procession occurs annually on Whit Tuesday. In the year 1812, 12,678
dancers were in the procession.

The Anabaptists, a religious sect of the sixteenth century, exhibited
many of the wild and grotesque phenomena of hysteria or
hystero-epilepsy.

{224} The French Calvinists or Camisards, who appeared near the close
of the seventeenth century, were also the subjects of ecstasy and of
peculiar fits of trembling. These trembleurs experienced convulsive
shocks in the head, the shoulders, the legs, and the arms, and were
sometimes thrown violently down.

About 1731 and later great crowds frequented the tomb of Deacon
François de Paris, an advocate of the doctrines of Jansenius. It was
reported that miracles were performed at his tomb: the sick were
brought there, and often were seized with convulsions and pains,
through which they were healed. The subjects of these attacks are
sometimes spoken of as the Jansenist Convulsionnaires. The tomb was in
the cemetery of St. Médard, and hence those who visited the place were
also termed the Convulsionnaires of St. Médard. This disorder
increased, multiplied, and disseminated, lasting with more or less
intensity for fifty-nine years. Great immorality prevailed in the
secret meetings of the believers.

Hecker gives some remarkable instances of the effect of sympathy or
imitation exhibited on a smaller scale than in the epidemics of the
Middle Ages. One is of a series of cases of fits in a Lancashire
factory, the first one brought on by a girl putting a mouse into the
bosom of another. In Charité Hospital in Berlin in 1801 a patient fell
into strong convulsions, and immediately afterward six other patients
were affected in the same way; by degrees eight more were attacked. At
Redruth, England, a man cried out in a chapel, “What shall I do to be
saved?” Others followed his example, and shortly after suffered most
excruciating bodily pain. The occurrence soon became public; hundreds
came, and many of them were affected in the same way. The affection
spread from town to town. Four thousand people were said in a short
time to be affected with this malady, which included convulsions.

Hecker in the edition of his work referred to has also a treatise on
child pilgrimages.[52] These pilgrimages, like the dancing mania,
occurred in the Middle Ages. The greatest was the boy crusade in the
year 1212. The passion to repossess the Holy Land then had its grip on
Catholic Europe. The first impulse to the child pilgrimages was given
by a shepherd-boy, who had revelations and ecstatic seizures, and held
himself to be an ambassador of the Lord. Soon thirty thousand souls
came to partake of his revelations; new child-prophets and
miracle-workers arose; the children of rich and poor flocked together
from all quarters; parents were unable to restrain them, and some even
began to urge them. A host of boys, armed and unarmed, assembled at
Vendôme, and started for Jerusalem with a boy-prophet at their head.
They got to Marseilles, and embarked on seven large ships. Two ships
were wrecked, and not a soul was saved. The other five ships reached
Bougia and Alexandria, and the young crusaders were all sold as slaves
to the Saracens. In Germany child-prophets arose, especially in the
Rhine countries and far eastward. An army of them gathered together,
crossed the Alps, and reached Genoa. They were soon scattered; many
perished; many were retained as servants in foreign lands; some
reached Rome. A second child's pilgrimage occurred twenty-five years
later. It was confined to the city of Erfurt. One thousand children
wandered, dancing {225} and leaping, to Armstadt, and were brought
back in carts. Another child's pilgrimage from Halle, in Suabia, to
Mount St. Michel in Normandy, occurred in 1458.

[Footnote 52: Translated by Robert H. Cooke, M. R. C. S.]

In the convent of Yvertet in the territory of Liège, in 1550, the
inmates were seized with a leaping and jumping malady. The disorder
began with a single individual, and was soon propagated.

Sometimes the convulsive disorders of early days, especially those
occurring in convents, were associated with the strange delusion that
the subjects of them were changed into lower animals. Various names
have been given to disorders of this kind, such as lycanthropia or
wolf madness, zoomania or animal madness, etc. Burton in the _Anatomy
of Melancholy_ gives an interesting summary of these disorders, which
are also discussed by Levick.

In 1760 a religious sect known as the Jumpers prevailed in Great
Britain. They were affected with religious frenzy, and jumped
continuously for hours. Other jumping epidemics have appeared at
different times, both in Great Britain and in this country.

The New England witchcraft episode is of historical interest in
connection with this subject of epidemic hysteria. This excitement
occurred during the latter part of the seventeenth century. Adults and
children were its subjects. The Rev. Cotton Mather records many cases,
some of which illustrate almost every phase of hysteria. Individuals
who were seized with attacks, which would now be regarded as
hysterical or hystero-epileptic, were supposed to have become
possessed through the machinations of others. Those who were supposed
to be possessed were tried, condemned, and executed in great numbers.
Many accused themselves of converse with the devil. The epidemic
spread with such rapidity, and so many were executed, that finally the
good sense of the people came to the rescue.

The nervous epidemics, nearly all religious, which have occurred in
this country have usually been during the pioneer periods, and have
therefore appeared at different eras as one part of the country after
another has been developed. Kentucky, Tennessee, Virginia, and
neighboring States were visited time and again. Even to-day we
occasionally hear of outbreaks of this kind in remote or primitive
localities, whether it be in the far South-west or in the woods of
Maine.

David W. Yandell[53] has published a valuable paper on “Epidemic
Convulsions,” the larger part of the materials of which were collected
by his father for a medical history of Kentucky. From this it would
appear the convulsions were first noticed in the revivals from 1735 to
1742. Many instances are related of fainting, falling, trance,
numbness, outcries, and spasms. The epidemic of Kentucky spread
widely, reappeared for years, and involved a district from Ohio to the
mountains of Tennessee, and even to the old settlements in the
Carolinas. Wonderful displays took place at the camp-meetings. At one
of these, where twenty thousand people were present, sobs, shrieks,
and shouts were heard; sudden spasms seized upon scores and dashed
them to the ground. Preachers went around in ecstasy, singing,
shouting, and shaking hands. Sometimes a little boy or girl would be
seen passionately exhorting the multitude, reminding one of the part
taken by {226} the children in the epidemics of the Middle Ages. A
sense of pins and needles was complained of by many; others felt a
numbness and lost all control of their muscles. Some subjects were
cataleptic; others were overcome with general convulsions.

[Footnote 53: _Brain_, vol. iv., Oct., 1881, p. 339 _et seq._]

The term jerks was properly applied to one of the forms of convulsion.
Sometimes the jerking affected a single limb or part. The Rev. Richard
McNemar has given a graphic description of this jerking exercise in a
_History of the Kentucky Revival_. The head would fly backward and
forward or from side to side; the subject was dashed to the ground, or
would bounce from place to place like a football, or hop around with
head, limbs, and trunk twitching and jolting in every direction.
Curiously, few were hurt. Interesting descriptions of the jerks can be
found in various American autobiographical and historical religious
works. In such books as the _Autobiography of Peter Cartwright_, a
Western Methodist, for instance, striking accounts of some of the
phases of these epidemics are to be found. Lorenzo Dow in his
_Journal_, published in Philadelphia in 1815, has also recorded them.

Hysterical laughter was a grotesque manifestation often witnessed. The
holy laugh began to be a part of religious worship. Dancing, barking,
and otherwise acting like dogs, were still other manifestations. It is
remarkable that, according to Yandell, no instance is recorded in
which permanent insanity resulted from these terrible excitements.

The absurd and extraordinary exhibitions witnessed among the Shakers
belong to the same category, and have been well described by Hammond
and others.

In a _History of the Revival in Ireland in 1859_, by the Rev. William
Gibson, instances of excitement that fairly rivalled those which
occurred in our Western States are given. Cases of ecstasy are
described.

The religious sect known as the Salvation Army, which has in very
recent years excited so much attention, curiosity, and comment both in
America and England, has much in common with the Jumpers, the Jerkers,
and the Convulsionnaires. The frenzied excitement at their meetings,
with their tambourine-playing, dancing, shouting, and improvising are
simply the same phases of religio-hysterical disorder, modified by
differences in the age and environment.

In 1878, in the district of Tolmezo, Italy, an epidemic of hysteria
which recalls the epidemics of the Middle Ages occurred. It has been
described by M. Léon Colin.[54] It was reported to the prefect of
Undine that for three months some forty females living in the commune
of Verzeguis had been attacked by religious mania. “From the report it
appears that the first was in the person of a woman named Marguerite
Vidusson, who had been the subject of simple hysteria for about eight
years. In January, 1878, she began to suffer from convulsive attacks,
accompanied by cries and lamentations. She was regarded as the subject
of demoniacal possession, and on the first Sunday in May was publicly
exorcised. Her affection, however, increased in severity; the attacks
were more frequent and more intense, and were especially provoked by
the sound of the church-bells and by the sight of priests. Seven
months later three other hysterical girls became subject to convulsive
and clamorous attacks. Here, again, an attempt was made to get rid of
the {227} supposed demon. A solemn mass was said in the presence of
the sufferers, but was followed only by a fresh outbreak. At the time
of the visit of the delegates eighteen were suffering, aged from
sixteen to twenty-six years, except three, whose ages were
respectively forty-five, fifty-five, and sixty-three years. Similar
symptoms had also appeared in a young soldier on leave in the
village.” During the attacks the patients talked of the demon which
possessed them, stated the date on which they were seized by it, and
the names of the persons who were possessed before them. Some boasted
of being prophetesses and clairvoyants and of having the gift of
tongues. In all, the sound of church-bells caused attacks, and
religious ceremonies appeared not only to aggravate the disease in the
sufferers, but also to cause its extension to those not previously
attacked. M. Colin points out that the soil is particularly favorable
for the development of an epidemic of this nature. The people of
Verzeguis are backward in education and most superstitious. Functional
nervous diseases are common among them. The inhabitants of the village
are largely cut off from intercourse with the adjacent country in
consequence of comparative inaccessibility and the frequent
interruption of communications by storms and floods. Craniometric
observations on twelve of the inhabitants seemed to show that the
brachycephalic form of skull predominated, and that the development of
the cranium was slightly below the average. The epidemic proved
extremely obstinate.

[Footnote 54: _Annales d'Hygiène_, quoted in _Lancet_, Oct. 16, 1880.]

In Norway and New Caledonia similar hysterical outbreaks have been
observed in recent times.

An endemic of hysteria from imitation occurred in Philadelphia in
1880. Some of the cases fell under my own observation. A brief account
of them is given by Mitchell in his _Lectures_. The outbreak occurred
in a Church Home for Children, to which Dr. S. S. Stryker was
physician. The Home contained ninety-five girls and six boys; all of
them were well nourished and in good condition. The epidemic began by
a girl having slight convulsive twitchings of the extremities, with a
little numbness. Attacks returned daily; respiration became loud and
crowing. She soon had all the phenomena of convulsive hysteria. Many
of her comrades began to imitate her bark. Soon another girl of ten
was attacked with harsh, gasping breathing, with crowing,
speechlessness, clutching at her throat, and the whole series of
phenomena exhibited by the first girl attacked. Nine or ten others
were affected in like manner, and many of the remaining children had
similar symptoms in a slight degree. At first convulsions occurred
irregularly; after a while they appeared every evening; later, both
morning and evening. The presence of visitors would excite them. Many
interesting hysterical phases occurred among the children. One night
some of them took to walking about on their hands and knees; others
described visions. The girls often spoke of being surrounded by wild
beasts, and one child would adopt the fiction which another related in
her hearing. The cases were scattered about in different hospitals,
and made good recoveries in from one to two months.

The Jumpers or Jumping Frenchmen of Maine and Northern New Hampshire
were described by Beard in 1880.[55] They presented nervous phenomena
in some phases allied to hysteria. In June, 1880, Beard {228} visited
Moosehead Lake and experimented with some of them. Whatever order was
given them was at once obeyed. One of the Jumpers, who was sitting in
a chair with a knife in his hand, was told to throw it, and he threw
it quickly so that it struck in a beam opposite; at the same time he
repeated the order to throw it with a cry of alarm. They were tried
with Latin and Greek quotations, and repeated or echoed the sound as
it came to them. They could not help repeating any word or sound that
came from the person that ordered them. Any sudden or unexpected
noise, as the report of a gun, the slamming of a door, etc., would
cause them to exhibit some phenomena. It was dangerous to startle them
where they could injure themselves, or if they had an axe, knife, or
other weapon in their hands. Since the time of Beard's observation
accounts of their doings have now and then found their way into
newspapers. One recent account tells of one of these peculiar people
jumping from a raft into the Penobscot River on an order to jump.

[Footnote 55: _Journal of Nervous and Mental Diseases_, vol. vii.,
1880, p. 487.]

Hammond[56] has described under the name Miryachit an affection which
seems to be essentially the same disorder as that of which the Jumpers
are the victims. He quotes from a report of a journey from the Pacific
Ocean through Asia to Europe by Lieutenant B. H. Buckingham and
Ensigns Geo. C. Foulk and Walter McLean of the United States Navy, an
account of this disease. The party made their first observations on
this affection while on the Ussuri River in Siberia. The captain of
the general staff approached the steward of the boat suddenly, and
without any apparent reason or remark clapped his hand before his
face; instantly the steward clapped his hand in the same manner, put
on an angry look, and passed on. When the captain slapped the
paddle-box suddenly, the steward instantly gave it a similar thump.
Some of the passengers imitated pigs grunting or called out absurd
names, etc.; the poor steward would be compelled to echo them all. The
United States naval officers were informed that the affection was not
uncommon in Siberia, and that it was commonest about Yakutsk, where
the winter cold is extreme. Both sexes were subject to it, but men
much less than women. It was known to Russians by the name of
Miryachit.

[Footnote 56: _New York Med. Journ._, Feb. 16, 1884.]

In both these classes of cases a suggestion of some kind was required,
and then the act took place independently of the will. “There is
another analogous condition known by the Germans as Schlaftrunkenheit,
and to English and American neurologists as somnolentia or
sleep-drunkenness. In this state an individual on being suddenly
awakened commits some incongruous act of violence, ofttimes a murder.
Sometimes this appears to be a dream, but in others no such cause
could be discovered.” Curious instances are mentioned by Hammond of
this disorder.

The phenomena of automatism at command in hypnotized subjects have
much similarity to the phenomena of these affections, and the same
explanation to a certain extent will answer for both.

Paget[57] has ably discussed the subject of neuromimesis in general,
and Mitchell[58] devotes two lectures to its consideration. As already
stated when discussing the synonyms of hysteria, the mistake must not
be made of supposing all cases of hysteria to be instances of
neuromimesis; but, as Mitchell remarks, the hysterical state, however
produced, is a fruitful {229} source of mimicry of disease in its
every form, from the mildest of pains up to the most complete and
carefully-devised frauds. “Its sensitiveness and mobility, its
timidity and emotionalness, its greed of attention, of sympathy, and
of power in all shapes, supply both motive and help, so that while we
must be careful not to see mimicry in every hysteric symptom, we must
in people of this temperament be more than usually watchful for this
form of trouble, and at least reasonably suspicious of every peculiar
or unusual phenomenon.”

[Footnote 57: _Op. cit._]

[Footnote 58: _Op. cit._]

SYMPTOMATOLOGY.—At the outset of the discussion of the symptomatology
of hysteria, hysterical cases should be divided into four classes—viz.
(1) Cases in which the symptoms are involuntary; (2) cases in which
the symptoms are artificially induced and become involuntary; (3)
cases in which the symptoms are acted or simulated, but in which the
patient, because of impaired mental power, is irresistibly impelled to
their performance; (4) cases in which the symptoms are purely acts of
deception which are under the control of the patient.

Keeping in mind these different classes, we will always be able to
link to the phenomena of hysteria the psychical element which is
present in all genuine cases of this disorder. To comprehend the
existence of the psychical element in the first class, in which the
manifestations are absolutely involuntary, may offer difficulties. In
these cases, at a period more or less recent or remote, psychical
stimuli may have acted to produce the hysterical phenomena, and, once
produced, these have been repeated and intensified by habit, and
continue independently both of volition and consciousness. The
experiments of Dercum and Parker show how hysterical symptoms may be
artificially induced and may get beyond the patient's control. The
difference between induced and simulated manifestations must always be
clearly borne in mind. To induce a set of phenomena a certain
mechanism must be set in action, and this, through rational,
explicable processes, leads to certain results. The psychical element
enters here both positively and negatively—positively, in the
determination to produce a certain train of events; negatively, in the
condition of mental concentration or abstraction which is a part of
the procedure. In the third class of cases acting or simulation is
dependent upon the irresistible inclinations of the patient. This may
seem to some an uncertain and even dangerous ground to take. I am
convinced, however, after observing many hysterical cases, that acts
clearly purposive, so far as the particular performance is concerned,
are sometimes the result of a general unstable mental condition. Some
at least of these patients are as irresistibly impelled to swallow
blood and vomit, to scream and gesticulate, etc., as is the monomaniac
to commit arson, to ravish, or to kill. In the fourth class, the cases
of pure, unmitigated, uncontrollable deception, the psychical element
is very evident, although some may question whether such cases should
be ranged under the banner of hysteria, where it is both convenient
and customary to place them.

The symptoms of hysteria may develop in any order or after any
fashion. The graver hysterical phenomena, such as convulsions,
paralysis, and anæsthesia, often seem to come on suddenly, but usually
this suddenness of onset is apparent rather than real. Minor
hysterical symptoms, such as general nervous irritability, pains,
aches, and discomforts, and mental peculiarities, have usually been
present for a long {230} time. These minor evidences of the hysterical
constitution are sometimes the only phenomena ever presented.

Todd[59] has described an expression of countenance which he
designates as the facies hysterica. The characteristics of this
expression are a remarkable depth and prominent fulness, with more or
less thickness, of the upper lip, and a peculiar drooping of the upper
eyelids. It would be absurd to assert that all hysterical patients
presented this cast of countenance, but an appearance which approaches
closely to this description is presented in a fair percentage of
cases. It has seemed to me that male hysterics were more likely to
have this peculiar facies than hysterical females.

[Footnote 59: _Reynolds's System of Medicine_, vol. ii. p. 656.]

The psychical peculiarities or mental disorders of hysteria form a
large and important part of its phenomena. We have to deal not only
with peculiar and diverse psychical manifestations, but to one form of
mental disorder it is clinically convenient and correct to apply the
designation hysterical insanity.

In the mildest cases of ordinary hysteria conditions of mental
irritability and mobility are sometimes the only striking features.
“Patients,” says Jolly,[60] “are timid, easily overcome by any
unexpected occurrence, sentimental, and sensitive. Every trifle annoys
and upsets them; and there is this peculiarity—that a more recent
stimulus may often effect a diversion in an exactly opposite
direction.”

[Footnote 60: _Op. cit._]

As bearing upon the question of the mental state in hysteria, the
confessions obtained by Mitchell from several patients are of great
interest. One patient, who had learned to notice and dwell upon any
little symptom, vomited daily and aroused much sympathy. She took
little or no food. Spasms came on, and she confessed that every new
symptom caused new anxiety, and that somehow she rather liked it all.
She gradually lost all her symptoms except vomiting, and overcame this
by desperate efforts. Another patient confessed to having played a
game upon her doctor for a long time by pretending she took no food.
She would get out of bed at night, but remain there all day; she
filled up a vessel with water to make others believe she passed large
quantities of urine, etc. Another patient, a girl of nineteen, who
came on a litter from a Western State, after a time regained her feet.
In her confession she stated that what she lacked was courage. She
believed that she would have overcome her difficulties if any one had
told her that nothing was the matter. “In looking back over the year
with the light of the present,” she says, “I can only say that I
believe that there was really nothing the matter with me; only it
seemed to me as if there was, and because of these sensations I
carried on a sort of starvation process physical and mental.”

The older and some of the more recent classifications of insanity
recognize hysterical insanity as a distinct form of mental disease.
Morel and Skae, however, in their etiological classifications, and
Hammond, Spitzka, Mann, and Clouston in their recently-published
works, give it a “local habitation and a name.” Krafft-Ebing not only
recognizes hysterical insanity as a distinct form of mental disease,
but, after the German fashion, subdivides it quite minutely, as
follows: First, transitory forms: _a_. with fright; _b_.
hystero-epileptic deliria; _c_. ecstatic visionary forms; {231} _d_.
moria-like conditions. Second, chronic forms: _a_.
hystero-melancholia; _b_. hystero-mania; _c_. degenerative states with
hysterical basis.

Spitzka[61] speaks of chronic hysterical insanity as an
intensification of the hysterical character, to which “a silly
mendacity is frequently added, and develops pari passu with advancing
deterioration.” At the State Hospital for the Insane at Norristown and
at the department for the insane of the Philadelphia Hospital cases of
chronic hysterical insanity have come under my observation. Hammond
under hysterical mania includes several different and somewhat
distinct mental disorders.

[Footnote 61: _Insanity, its Classification, Diagnosis, and
Treatment_, by E. C. Spitzka, M.D., New York, 1883.]

With regard to the occurrence of hysterical manifestations amongst
patients suffering from some well-recognized non-hysterical forms of
insanity, a tour through any large asylum will afford abundant
evidence. Cases of tremor closely simulating cerebro-spinal sclerosis
have been observed frequently among the insane. Paralysis,
contracture, hysterical joints, hysterical neuralgias, convulsions,
and cataleptoid phenomena are among other hysterical manifestations
which have fallen under personal observation among the insane of
various classes.

A remarkable case of hysterical motor paralysis was observed at the
State Hospital for the Insane at Norristown. This patient was an
intelligent single woman about thirty-five years of age, of good
family, well educated; she had been a teacher and writer, and became
insane through family and business troubles. When only eight years of
age she was paralyzed for two years and a half, and had had at times
during her life, before becoming insane, attacks of partial or
complete unconsciousness. Prior to coming under observation she had
been an inmate of an English private asylum. She was sick on shipboard
coming to this country, and on her arrival was in a state of delirium
and insomnia, with attacks of loss of sight. Four months later she
developed mania with suicidal inclinations. Just before the
development of this maniacal condition her lower limbs became
comparatively helpless, and soon after she entirely lost their use. I
found her in this condition, and examination showed no change in
knee-jerk, electrical reactions, nutrition, nor genito-urinary
conditions, which led me to diagnosticate the absence of any organic
spinal trouble. The case was pronounced one of hysterical paralysis,
and it was prophesied that she would eventually completely recover,
probably suddenly. For one year her paralysis remained, her mental
condition varying very greatly during this time—sometimes in a
lethargic state; sometimes with variable delusions and delirium;
occasionally violent and destructive, again peaceable and pleasant;
sometimes requiring strong anodynes and hypnotics. Fourteen months
after her paralytic condition began, one day she suddenly threw away
her crutches and ran up and down the corridor of the hospital. From
that time she walked without difficulty, although her mental condition
did not entirely clear.

I wish to impress the fact that because hysterical manifestations
occur in a case of insanity it should not necessarily be
diagnosticated as one of hysterical insanity. Monomania, melancholia,
mania, paretic dementia, epileptic insanity, and other forms of mental
disorder may at times have an hysterical tinge or hysterical episodes.

{232} The whole question of hysterical insanity is one of great
difficulty. The psychical element is probably at the root of all cases
of hysteria, but this does not justify us, as I have already stated,
in declaring that all cases of hysteria are insane. In practical
professional life we must make practical distinctions. In the matter
before us distinctions are necessary to be made for legal as well as
medical purposes. It might be right and proper to place a case of
hysterical insanity in a hospital or asylum under restraint, but no
one would dare to claim that every case of hysteria should be so
treated.

Hysterical insanity may be conveniently subdivided into an acute and
chronic form.

Acute hysterical insanity or hysterical mania is a disorder usually,
in part at least, purposive, and characterized by great emotional
excitement, which shows itself in violent speech and movement, and
often also in deception, simulation, and dramatic behavior. The
phenomena indicated by this definition may constitute the entire case,
or, in addition, the patient may have, at intervals or in alternation,
various other phases of grave hysteria, such as hystero-epileptic
seizures or attacks of catalepsy, trance, or ecstasy.

In chronic hysterical insanity we have a persisting abnormal mental
condition, which may show itself in many ways, but chiefly as follows:
(1) A form in which occur frequent repetitions, over a series of
years, of the phenomena of acute hysterical insanity, such as
hysterical mania, hystero-epilepsy, catalepsy, etc.; (2) a form in
which sensational deceptions—sometimes undoubtedly self-deceptions—are
practised.

In a case of chronic hysterical insanity you may have both of these
forms commingling in varying degree, as in the following case: G—— is
a seamstress, twenty-one years of age. Although young in years, she is
an old hospital rounder: she has at various times been in almost all
the hospitals of the city. She has been treated for such alleged
serious affections as fractured ribs, hemorrhages from the lungs,
stomach, and vagina, gastric ulcer, epilepsy, apoplexy, paralysis,
anæsthesia of various localities, amenorrhœa, dysmenorrhœa, and fever
with marvellous variations of temperature. She has become the bane and
terror of every one connected with her treatment and care-taking. She
has developed violent attacks of mania, with contortions and
convulsions, on the streets and in churches. Sums of money have been
collected for her at times by those who have become interested in her
as bystanders at the time of an attack or have heard of her case from
others. She has made several pseudo-attempts at suicide. Recently an
empty chloroform-liniment bottle tumbled from her bed at a propitious
moment, she at the same time complaining of pain and symptoms of
poisoning. She has refused to partake of food, and has been discovered
obtaining it surreptitiously. Her large and prolonged experience with
doctors and hospitals has so posted her with reference to the
symptomatology of certain nervous affections that she is able at will
to get up a fair counterfeit of a large variety of grave nervous
disorders.

One of her recent attacks of hysteria was preceded by a series of
hysterical phenomena, such as vomiting, hemorrhage, aphonia,
ovaralgia, headache, and simulation of fever. She began by crying and
moaning, which was kept up for many hours. She fell out of bed,
apparently {233} insensible. Replaced in bed, she passed into a state
closely simulating true acute maniacal delirium. She shrieked, cried,
shouted, and moaned, threw her arms and legs about violently, and
contorted her entire body, snapping and striking at the nurses and
physicians in attendance. At times she would call those about her by
strange names, as if unconscious of the true nature of her
surroundings. Attacks of this kind were kept up for a considerable
period, and after an interval of rest were repeated again and again.

Many of the extraordinary facts which fill the columns of the
sensational newspapers are the results of the vagaries of patients
suffering from the second of the forms of chronic hysterical insanity.
“When,” says Wilks,[62] “you see a paragraph headed ‘Extraordinary
Occurrence,’ and you read how every night loud rapping is heard in
some part of the house, how the rooms are being constantly set on
fire, or how all the sheets in the house are torn by rats, you may be
quite sure that there is a young girl on the premises.” It is
unnecessary to add that said girl is of the hysterical genus.

[Footnote 62: _Op. cit._]

A story comes from an inland town, for instance, of a respectable
family consisting, besides the parents, of three daughters and six
sons, one of whom died of pneumonia. Since his death the family had
been startled by exciting and remarkable events in the house—a clatter
of stones on the kitchen floor, the doors and windows being closed;
shoes suddenly ascending to the ceiling and then falling to the floor,
etc. Search revealed nothing to explain the affair. As throwing light
upon this matter, a visitor, who confessed his inability to explain
the occurrences, nevertheless referred to one of the daughters as
looking like a medium.

Charcot and Bourneville give frequent instances of extraordinary
self-deceptions or delusions among hysterical patients. The story of
an English lady of rank, who reported that she was assaulted by
ruffians who attacked her in her own grounds and attempted to stab
her, the weapons being turned by her corsets, is probably an example
of this tendency. Investigation made by the police force threw grave
doubts upon the story.

Many of the manifestations classed as hysterical by medical writers
are simply downright frauds. The nature of others is doubtful. The
erratic secretion of urine, for example, has frequently engaged the
attention of writers on nervous diseases, and has awakened much
controversy. American hysterics are certainly fastidious about this
matter, as I have not yet met, in a considerable experience, with a
single example of paruria erratica. Charcot[63] refers sarcastically
to an American physician who in 1828 gravely reported the case of a
woman passing half a gallon of urinous fluid through the ear in
twenty-four hours, at the same time spirting out a similar fluid by
the navel. He also alludes to the case of Josephine Roulier, who about
1810 attained great notoriety in France, but was discovered by Boyer
to be a fraud. This patient vomited matter containing urea, and
shortly after came a flow of urine from the navel, the ears, the eyes,
the nipples, and finally an evacuation of fecal matters from the
mouth.

[Footnote 63: _Op. cit._]

Hemorrhages from eyes, ears, nostrils, gums, stomach, bowels, etc.
{234} have often been observed among the hysterical; these cases
sometimes being fraudulent and sometimes genuine. In the Philadelphia
Hospital in 1883 was a patient suffering from grave hysteria, vomiting
of blood being a prominent symptom. Although close watch was kept,
several days elapsed before it was discovered that she used a hair-pin
to abrade the mucous membrane of her nose, swallowed the blood, which
passed into the throat, and then vomited it.

Sir Thomas Watson tells of a young woman who made a hospital surgeon
believe that she had stone in the bladder; and Fagge, of a patient who
had been supposed to have hydatid in the liver, and who produced a
piece of the stomach of a rabbit or some other small animal, which
piece she declared she had vomited. A few hours later she again sent
for her medical man to remove from her vagina another fragment of the
same substance.

A case is reported by Lopez[64] of spiders discharged from the eye of
an hysterical patient. He regarded the case as one of hysterical
monomania. Fragments of a dismembered spider were undoubtedly from
time to time removed from the eye of the patient. Lopez believed that
at first the fragments may have got into the eye accidentally, but
that afterward the patient, under the influence of a morbid condition,
introduced them from day to day. The total number of spiders removed
in fragments was between forty and fifty. Silvy[65] relates a case in
which a large number of pins and needles made their exit from a
patient. Other needle cases are given, and also examples of insects
and larvæ discharged from the human body. In one case worms crawled
out of the nose, ears, and other natural openings; in another worms
were found in active motion under the conjunctiva; in a third a beetle
was discharged from the bladder, and several beetles were vomited by a
boy.

[Footnote 64: _American Journal of Medical Sciences_, Philadelphia,
1843, N. S., 74-81.]

[Footnote 65: _Mémoires de la Société médicale_, Anné 5, p. 181.]

Jolly[66] records in a foot-note a case published in 1858, by I. Ch.
Leitz of Pesth, of a young girl from whose eyes fruit-pips sprang,
from whose ears and navel feces escaped, and from whose anus and
genitals fleshy shreds came away, while worms with black eyes were
vomited. He further tells of a woman from whose genitals
four-and-twenty living and dead frogs passed, some of these, indeed,
with cords of attachment. The birth of the frogs was witnessed and
believed in by several physicians!

[Footnote 66: _Op. cit._]

Hardaway[67] reports a curious case with simulated eruptions. The
woman appeared to be in fear of syphilis contracted by washing the
clothes of a diseased infant. She had blebs irregularly distributed
upon the fingers and arm of the left side; these, the doctor
concluded, had been caused by the application of vitriol. He reports
another case in which a woman had an eruption on her left arm, and the
sores, instead of getting better under treatment, got worse. On one
visit he found needle-scratches on the old sore. Nitric acid,
according to Hardaway, is a favorite substance for the production of
such eruptions. The best diagnostic test is that the blister is
linear, while in pemphigus it is circular, unlike that which would be
produced by a running fluid. Hysterical women have irritated their
breasts with cantharides. Niemeyer[68] mentions a woman at
Krutsenberg's clinic who irritated her arm in such a way that
amputation became {235} necessary, and after that she irritated the
stump until a second amputation had to be performed.

[Footnote 67: _St. Louis Courier of Medicine_, 1884, xi. 352.]

[Footnote 68: _Textbook of Practical Medicine_.]

Nymphomania is a form of mental disorder which sometimes occurs among
the hysterical; or it would perhaps be more correct to say that
nymphomania and grave hysterical affections are sometimes associated
in the same case. It is a condition in which is present extreme
abnormal excitement of the sexual passion—a genesic, organic feeling
rather than an affection associated with the sentiment of love.
Hammond treats of it under the head of acute mania, and considers
cases of nymphomania as special varieties of this disease.
Undoubtedly, this is the correct way of looking at the subject in many
cases. In man the corresponding mental and nervous condition often
leads to the commission of rape and murder. In woman the affection is
most likely to show itself with certain collateral hysterical or
hysteroidal conditions, as spasms, hystero-epilepsy, and catalepsy, or
with screaming, crying, and other violent hysterical outbreaks.
Sometimes there is a tendency to impulsive acts, but this does not
usually go so far as to lead to actual violence.

Nymphomaniacs may be intelligent and educated, and if so they usually
resist their abnormal passions better than the ignorant. A number of
nymphomaniacs have been under treatment at the Philadelphia Hospital.
One case was an epileptic and also hysterical girl. She had true
epileptic seizures, and at other times had attacks of a hysteroidal
character. She would make indecent proposals to almost any one, and
would masturbate and expose herself openly. She also had occasional
maniacal attacks. She died in the insane department of the hospital.

Nymphomania and what alienists call erotomania are sometimes not
differentiated in practice and in books. They are, however, really
different conditions. Erotomania and nymphomania may be associated in
the same case, but it is more likely that erotomania will not be
present in a case of nymphomania. Erotomania may exist as a special
symptom or it may be one of the evidences of monomania. It is found in
both men and women. Patients with this condition may have no sexual
feeling whatever. The individual has some real or imaginary person to
love. It is rather the emotion of love which is affected, not the
sexual appetite. It is shown by watching or following the footsteps of
the individual, by writing letters, and by seeking interviews. In the
history of Guiteau an incident of this kind is mentioned by Beard.[69]
He followed a lady in New York whom he supposed to be the daughter of
a millionaire—followed her, watched her house and carriage, and wrote
letters to her. Out West he showed the same sort of attentions to
another lady. He went to the house, but was kicked out. Many of the
great singers have been followed in this way.

[Footnote 69: _Journal of Nervous and Mental Disease_, vol. ix., No.
1, January, 1882.]

Some time ago I examined a man condemned to be hanged and within
twenty-four hours of his death. He was an erotomaniac, whatever else
he may have been. In the shadow of the gallows he told of a lady in
the town who had visited him and was in love with him, and how all the
women in the neighborhood were in love with him. He had various
pictures of females cut from circus-posters in his cell. Erotomania is
not generally found associated with hysteria.

Convulsions or general spasms are among the most prominent of {236}
hysterical manifestations. Under such names as hysterical fits,
paroxysms, attacks, seizures, etc. they are described by all authors.
Their presence has sometimes been regarded as necessary in order that
the diagnosis of hysteria might be made; but this, as I have already
indicated, is an erroneous view.

Under hysterical attacks various conditions besides general
convulsions are discussed by writers on hysteria; for instance,
syncope, epileptiform convulsions, catalepsy, ecstasy, somnambulism,
coma, lethargy, and delirium. According to the plan adopted in the
present volume, catalepsy, ecstasy, somnambulism, etc. will be
considered in other articles, and therefore my remarks at this point
will be limited to hysterical general convulsions.

These convulsions differ widely as to severity, duration, frequency,
motor excitement, and states of volition and consciousness. Efforts
have been made to classify them. Carter[70] describes three forms as
primary, secondary, and tertiary. In the primary form the attack is
involuntary and the product of violent emotion; in the secondary it is
reproduced by the association of ideas; and in the tertiary it is
deliberately shammed by the patient. Lloyd[71] divides them into
voluntary and involuntary forms, and discusses the subject as follows:
“The voluntary or purposive convulsions are such as emanate from the
conscious mind itself. Here are the simulated or foolish fits into
which women sometimes throw themselves for the purpose of exciting
sympathy or making a scene. I am convinced that a large number of
hysteric fits are of this class: these are the patients who are cured
by the mention of a hot iron to the back or the exhibition of an
emetic. The involuntary forms of convulsion are more important. They
happen in more sensible persons, and some of them are probably akin to
starts, gestures, and other forcible or violent expressions of
passions or states of the mind. A person wrings the hands, beats the
breast, stamps upon the floor in an agony of grief and apprehension,
and if terror is added he trembles violently. It is no great stretch
of the imagination to suppose that great fear, anger, or some kindred
passion, acting upon the sensitive nervous organization of a delicate
woman or child, should throw them into a convulsion. This, in fact, we
know happens. Darwin[72] believes that in certain excited states of
the brain so much nerve-force is liberated that muscular action is
almost inevitable. He instances the lashing of a cat's tail as she
watches her prey and the vibrations of the serpent's tail when
excited; also the case of an Australian native, who, being terrified,
threw his arms wildly over his head for no apparent purpose. The
excito-motor reflexes of the cord may possibly take on true convulsive
activity if released from the control of the will, which, as already
said, is apt to be weak or in abeyance to this disease. Increased
temperature is stated by Rosenthal to be always present in the great
fits of epilepsy and tetanus, but absent in those of hysteria.”

[Footnote 70: _On the Pathology and Treatment of Hysteria_, London,
1853.]

[Footnote 71: _Op. cit._]

[Footnote 72: _Expression of Emotion, etc._]

This subdivision of hysterical convulsions into voluntary and
involuntary, or purposive and non-purposive, is a good practical
arrangement; but the four groups into which I have divided all
hysterical symptoms—namely, the purely involuntary, the induced
involuntary, the impelled, {237} and the purely voluntary—include or
cover these two classes, and allow of explanation of special cases of
convulsion which cannot be regarded as either purely shammed or as
entirely, and from the first, independent of the will.

Absolutely involuntary attacks with unconsciousness constitute what
are commonly called hystero-epileptic seizures, and will be described
under Hystero-epilepsy.

The voluntary, impelled, or induced hysterical fit may be ushered in
in various ways—sometimes with and sometimes without warning,
sometimes with wild laughter or with weeping and sobbing. The
patient's body or some part of it is then usually thrown into violent
commotion or convulsion; the head, trunk, and limbs are tossed in
various directions. Frequently the arms are not in unison with each
other or with the legs. Screaming, shouting, sobbing, and laughing may
occur during the course of the convulsive movement; sometimes,
however, the patient utters not a word, but has a gasping, noisy
breathing. She may talk in a mumbling, incoherent manner even during
the height of the attack. She is tragic in attitude or it may be
pathetic. The face is contorted on the one hand, or it may be
strangely placid on the other. Quivering, spasmodic movements of the
eyelids are often seen; but the eyes are not fixed and turned upward
with dilated pupils, as in epilepsy. The patient does not usually hurt
herself in these purposive attacks. She may or may not appear to be
unconscious. She does not bite her tongue, nor does she foam, as does
the true epileptic, although she may spit and sputter in a way which
looks somewhat like the foaming of epilepsy. She comes out of the fit
often with evident signs of exhaustion and a tendency to sleep, but
does not sink into the deep stupor of the post-paroxysmal epileptic
state. The paroxysm may last a few or many minutes. Large quantities
of colorless urine are usually passed when it is concluded.

Hysterical paralysis, so far as extent and distribution are concerned,
may be of various forms, as (1) hysterical paralysis of the four
extremities; (2) hysterical hemiplegia; (3) hysterical monoplegia; (4)
hysterical alternating paralysis; (5) hysterical paraplegia; (6)
hysterical paralysis of special organs or parts, as of the vocal
cords, the œsophagus and pharynx, the diaphragm, the bowels, and the
bladder. Russell Reynolds[73] has described certain cases closely
allied to, if not identical with, some forms of hysterical paralysis
under the head of paralysis dependent upon idea. These patients have a
fixed belief that they are paralyzed. The only point of separation of
such cases from hysterical paralysis is the absence of other
hysterical manifestations. Perhaps it would be better to regard the
condition either simply as hysterical paralysis or as a true
psychosis—an aboulomania or paralysis of the will. Such cases often
last for many years.

[Footnote 73: _Brit. Med. Journ._, 1869, pp. 378, 483.]

Among the 430 hysterical cases of Briquet, only 120 were attacked with
paralysis. In 370 cases of Landouzy were 40 cases of paralysis.

Briquet reports 6 cases in which paralysis attacked the principal
muscles of the body and of the four extremities; 46 cases of paralysis
of the left side of the body, and 14 of the right; 5 of the upper
limbs only; 7 of the left upper limb, and 2 of the right; 18 of the
left lower limb, {238} and 4 of the right; 2 of the feet and hands
only; 6 of the face; 3 of the larynx; and 2 of the diaphragm. Landouzy
gathered from several authors the following results: General paralysis
in 3 cases; hemiplegia in 14; 8 cases of paralysis of the left side;
in other cases the side affected not indicated; and 9 cases of
paraplegia.

Hysterical paralyses, no matter what the type, may come on in various
ways—suddenly, gradually, from moral causes or emotional excitement,
or from purely physical causes, as over-fatigue. They may have almost
any duration, from hours or days to months or years, or even to a
lifetime. They are frequently accompanied by convulsive or emotional
seizures. They may be of any degree of severity, from the merest
suspicion of paresis to the most profound loss of power. Hysterically
paralyzed muscles retain their electro-contractility. Limbs which have
become atrophied from disuse may show a temporary lessening of
response, but this is quantitative and soon disappears. In rare cases,
owing probably to the condition of the skin, the response to
electricity is not obtained until the current has been applied for
several minutes to the muscles.

Hysterical hemiplegia and monoplegia may simulate almost any type of
organic paralysis. The paralysis is usually in a case of hemiplegia,
confined to the arm and leg, the face being slightly, if at all,
implicated. Hysterical paralysis, limited to the muscles supplied by
the facial nerve, is very rare. According to Rosenthal, it sometimes
coexists with paralysis of the limbs of the same side, and is usually
accompanied by anæsthesia of the skin and special senses. In a few
rare cases, according to Mitchell, the neck is affected.

Several cases of hysterical double ptosis have come under my
observation. The condition is usually one of paresis rather than
paralysis. Cases of unilateral ptosis hysterical in character have
also been reported. Alternating squints are sometimes hysterical, but
they are usually of spasmodic rather than of paralytic origin.

Hysterical hemi-palsy is more frequent on the left than in the right
side. In Mitchell's cases the proportion was four left to one right.
The figures of Briquet have been given. It is usually, but not always,
accompanied by diminished or abolished sensibility, both muscular and
cutaneous. Electro-sensibility especially is markedly lessened in most
cases.

When hemiplegia is of the alternating variety, the arm on one side and
the leg on the other, or, what is rare in paralysis of organic
causation, both upper extremities and one lower, or both lower and one
upper, may be affected. Alternating hemiplegia of the organic type is
usually a paralysis in which one side of the face and the leg and arm
of the opposite side are involved.

Hysterical paraplegia is one of the most important forms of hysterical
paralysis, and is sometimes the most difficult of diagnosis. It occurs
usually, but not exclusively, in women. It comes on, particularly in
young women, between puberty and the climacteric period, commonly
between the twentieth and thirtieth years. Such a patient is found in
bed almost helpless, possibly able to move from side to side, but even
by the strongest efforts seemingly incapable of flexing or extending
the leg or thigh or of performing any general movements of the foot.
The feet are probably in the equino-varus position—extended and {239}
turned inward. Certain negative features are present. The muscles do
not waste to any appreciable extent, as they would in organic
paralysis. Testing the knee-jerk, it is found retained, possibly even
exaggerated. The electrical current causes the muscles to contract
almost as well as under normal conditions; if a difference is present,
it is quantitative and not qualitative in character. Paralysis of the
bowels and bladder is not usually found, although it is but fair to
state that this appears not to be the conclusion arrived at by some
other observers.

Paralysis or paresis of the vocal cords, with resulting aphonia, is a
common hysterical affection. Hysterical aphonia is also due to other
conditions—for instance, to an ataxia or want of co-ordinating power
in the muscles concerned in phonation; or to spasm, real or imaginary,
in the same parts. Hysterical paralysis of the vocal cords is almost
invariably bilateral; viewed with the laryngoscope, the cords are seen
not to come together well, if at all. One may be more active than the
other; but a distinct one-sided paralysis of this region nine times
out of ten indicates that the case is not hysterical.

The following case is of interest, not only because of the aphonia,
but because also of the loss of the power of whispering. The patient,
a young lady of hysterical tendencies, while walking with a friend
stumbled over a loose brick and fell. She got upon her feet, but a
moment or two after either fainted or had a cataleptoid attack.
Several hours later she lost her voice and the power of whispering.
She said that she tried to talk, but could not form the words. This
condition had continued for ten months in spite of treatment by
various physicians. She carried a pencil and a tablet, by means of
which she communicated with her friends. She had also suffered with
pains in the head, spinal hyperæsthesia; and occasional attacks of
spasm. Laryngoscopic examinations showed bilateral paresis of the
vocal muscles, without atrophy. The tongue and lips could be moved
normally. She was assured that she could be cured. Faradic
applications with a laryngeal electrode were made daily; tonics were
given; and the patient was instructed at once to try to pronounce the
letters of the alphabet. In less than a week she was able to whisper
letters, and in a few days later words. In three weeks voice and
speech were restored. Just as this patient was recovering another came
to be treated for loss of voice. She was markedly aphonic, but could
whisper without difficulty. She was told, to encourage her, that she
need not be worried about her loss of voice, as another patient, who
had lost not only her voice, but the ability to whisper, had
recovered. The patient returned next day unable to whisper a syllable.
She made, however, a speedy recovery. Under the name apsithyria, or
inability to whisper, several cases of this kind have been reported by
Cohen.

Hysterical paralyses of the pharynx and of the œsophagus have been
reported, but are certainly of extreme rarity. Hysterical dysphagia is
much more frequently due to spasm or a sensation of constriction.

Paralysis of the diaphragm in hysteria has been described by Duchenne
and Briquet. I have had one case under observation. The abdomen is
drawn inward instead of being pushed outward in the act of inspiration
in organic paralysis of the diaphragm; this condition is simulated,
but not completely or very closely, in the hysterical cases. In some
of the {240} cases of nervous breathing, which will be referred to
hereafter, the symptoms are rather of a spastic than of a paretic
affection of the diaphragm.

Paralysis or paretic states of the stomach and intestines are not
uncommon among the hysterical, and produce tympanites, one of the
oldest symptoms of hysteria. Jolly asserts that this “sometimes
attains such a degree that the patients can be kept afloat in a bath
by means of the balloon-like distension of their bellies”! The loss of
power in the walls of the stomach and bowels is sometimes a primary
and sometimes a secondary condition. The abdominal phantom tumors of
hysterical women sometimes result from these paralytic conditions.
These abdominal tumors are among the most curious of the phenomena of
local hysteria. At one time two such cases were in the women's nervous
wards of the Philadelphia Hospital. Both patients had been hysterical
for years. In the first the tumor occupied the middle portion of the
abdomen, the greater portion of its bulk more to the right of the
median line. It was firm and nearly spherical, and the patient
complained of pain when it was handled. She was etherized, and while
under ether, and during the time that she was vomiting from the
effects of the anæsthetic, the tumor disappeared, never to return. The
other patient had a similar tumor for three days, which disappeared
after the etherization of the first case.

Mitchell[74] has recorded some interesting paretic and other
hysterical disorders of the rectum and defecation. Great weakness, or
even faintness, after each stool he has found not uncommon, and other
more formidable disorders occur. A patient who had been told that her
womb was retroverted and pressing upon her rectum, interfering with
the descent and passage of the feces, was troubled with
hypersensitiveness of the lower bowel. This condition Mitchell
designated as the excitable rectum. Patients in whom it is present
apparently have diarrhœa; certainly they have many movements daily.
Single stools, however, are small, and may be quite natural or they
may seem constipated. The smallest accumulation of fecal matter in the
rectum excites to defecation. One case had small scybalous passages
every half hour. The forms of hysterical paresis or paralysis or
pseudo-paralysis of the rectum observed by Mitchell were due—(1) to a
sensory paralysis of the rectum; (2) to a loss of power in the rectal
muscular walls; (3) a want of co-ordination in the various muscles
used in defecation; (4) to a combination of two or of all of these
factors. In rare cases the extrusive muscles act, but the anal opening
declines to respond.

[Footnote 74: _Op. cit._]

Hysterical locomotor ataxia, or hysterical motor ataxia, is an
affection less common than hysterical palsy, but by no means rare.
Various and diverse affections of motion are classed as hysterical
ataxia by different authors. Mitchell speaks of two forms independent
of those associated with vertigo. The first, that described by Briquet
and Laségue, seems to depend upon a loss of sensation in both skin and
muscles; the second often coexists with paralysis or paresis, and is
an affection in which the patient has or may have full feeling, and is
able to use the limbs more or less freely while lying down. As soon as
she leaves the recumbent position the ataxia is very evident. She
falls first to one side and then to the other. She “seems to be unable
to judge of the extent to which balance is lost, and also to determine
or evolve the amount of {241} power needed to overcome the effect.”
Mitchell believes that this disorder is common in grave hysteria, and
is likely to be confounded with one of the forms of hysterical
alternating spasm, in which first the flexors and then the extensors
contract, the antagonistic muscles not acting in unison, and very
disorderly and eccentric movements being the result. I have reported a
case of hystero-epilepsy[75] in which a spasmodic condition closely
simulated hysterical ataxia. The patient had various grave hysterical
symptoms, with epileptoid attacks. She became unable to walk, or could
only walk a few steps with the greatest difficulty, although she could
stand still quite well. On attempting to step either forward or
backward, her head, hips, shoulders, and trunk would jerk
spasmodically, and she would appear to give way at the knees. No true
paralysis or ataxia seemed to be present, but locomotion was
impossible, apparently because of irregular clonic spasms affecting
various parts of her body.

[Footnote 75: _Journal of Nervous and Mental Disease_, vol. ix., No.
4, October, 1882.]

Mary Putnam Jacobi[76] has reported a case occurring in an Irish woman
aged thirty-five years as one of hysterical locomotor ataxia. It is
questionable whether this case was not rather one of posterior spinal
sclerosis with associated hysterical symptoms. The existence of pain
resembling fulgurating pains, and especially the absence of the
patellar tendon reflex, would incline me to hesitate a long time
before accepting the diagnosis of hysteria, particularly as it is
known that organic locomotor ataxia often has a much-prolonged first
stage, and that wonderful temporary improvements sometimes take place.

[Footnote 76: _Arch. of Medicine_, New York, 1883, ix. 88-93.]

Ataxic symptoms of a mild form are of frequent occurrence in hysteria.
They are shown by slight impairments of gait and difficulty in
performing with ease and precision many simple acts, as in dressing,
writing, eating, etc.

Hughes Bennett and Müller of Gratz call attention to the fact that
young women may exhibit all the signs of primary spastic paralysis,
simulating sclerosis, and yet recover.[77] I have seen several of
these cases of hysterical spasmodic paralysis, and have found the
difficulties in diagnosis very great. These patients walk with a stiff
spastic or pseudo-spastic gait, and as, whether hysterical or not, the
knee-jerk is likely to be pronounced, their puzzling character can be
appreciated.

[Footnote 77: Quoted by Althaus: _On Sclerosis of the Spinal Cord_, by
Julius Althaus, M.D., M. R. C. P., etc., New York, 1885, p. 330.]

In one class of cases, which cannot well be placed anywhere except
under hysteria, a sense or feeling of spasm exists, although none of
the objective evidences of spasmodic tabes can be detected. Comparing
these to those which Russell Reynolds describes as paralysis dependent
upon idea, they might be regarded as cases of spasm dependent upon
idea.

One case of this kind which was diagnosticated as lateral sclerosis by
several physicians recovered after a varying treatment continued for
several years, the remedy which did him the most good being the actual
cautery applied superficially along the spine. The patient described
his condition as one of “spasmodic paralysis of all the muscles of the
body.” If sitting down, he could not at once get up and walk or run,
but would have to use a strong effort of his will, stretching his
limbs several times {242} before getting on his feet. Movements once
started could be continued without much difficulty. When his hands
were closed he would be unable, at times, to open them except by a
very strong effort of the will. If one was opened and the other shut,
he could manipulate the latter with the former. He sometimes
complained of a sensation as of a steam-engine pumping in his back and
shaking his whole body. He would sometimes be in a condition of stupor
or pseudo-stupor, when he had a feeling as if he was under the
influence of some poison. The spasms or jumpings in the back he
thought sometimes caused emissions without erections. He compared the
feeling in his back to that of having a nerve stretched like a piece
of india-rubber. The excitement of mind would then cause the nerve to
contract and throb. This description shows that the symptoms were
purely subjective. Examination of the muscles of the legs and arms did
not reveal, as in true spastic paralysis, conditions of rigidity. The
limbs would sometimes be stiff when first handled, volition
unconsciously acting to keep them in fixed positions; but they would
soon relax. The knee-jerk, although well retained, was not markedly
exaggerated, as in spastic paralysis, nor was ankle clonus present.
The patient did not get progressively worse, but his condition
vacillated, and eventually he recovered. A friend of the patient,
living in the same neighborhood and going to the same church, was
affected with true lateral sclerosis. It is worth considering how far
in an individual of nervous or hysterical temperament observation of
an organic case could have influenced the production of certain
subjective symptoms, simulating spasmodic tabes.

Certain special forms of chorea are particularly liable to occur in
the course of cases of hysteria. The most common type of the chorea of
childhood, if not strictly speaking hysterical, is frequently
associated with a hysteroid state, and is best treated by the same
measures that would be calculated to build up and restore an
hysterical patient. The following conclusions, arrived at by Wood[78]
after a clinical and physiological study of the subject of chorea,
show that certain forms of chorea may be hysterical or imitated by
hysteria:

1st. Choreic movements may be the result of organic brain disease.

2d. Choreic movements exactly simulating those of organic brain
disease may occur without any appreciable disease of the
nerve-centres.

3d. General choreic movements, as well as the bizarre forms of
electric and rhythmical chorea, may occur without any organic disease
of the nervous system.

[Footnote 78: “Chorea: a Study in Clinical Pathology,” by H. C. Wood,
M.D., LL.D., _Therapeutic Gazette_, 3d Series, vol. i., No. 5, May 15,
1885.]

To these propositions may be added a fourth—viz. Choreic movements may
be the result of a peripheral irritation, or, in other words, may be
reflex.

Hysterical rhythmical chorea is a form of chorea in which involuntary
movements are systematized into a certain order, so as to produce in
the parts of the body which are affected determinate movements which
always repeat themselves with the same characters. The movements are
strikingly analogous to the rhythmical movements, as those of
salutation, which often occur in the second period of the
hystero-epileptic attack. Rhythmical chorea should undoubtedly be
arranged among the {243} manifestations of grave hysteria. An account
of an interesting case of this kind is given in a lecture by Wood,
reported by me in the _Philadelphia Medical Times_ for Feb. 26, 1881.

As Charcot has shown, rhythmic chorea is usually of hysterical origin,
although it may exist without any of the phenomena which usually
characterize hysteria. In these cases the movements imitated are
according to a certain plan; thus, they may be certain expressive
movements, as some particular form of dancing or the so-called
saltatory chorea. They may be, again, certain professional or trained
actions, such as movements of hammering, of rowing, or of weaving.
Charcot speaks of a young Polish girl in whom movements of hammering
of the left arm lasted from one to two hours, and occurred many times
in a day for seven years. He has also given an account of another
case, a patient with various grave hysterical manifestations, who
would have a pain and beating sensation in the epigastrium,
accompanied by a feeling of numbness. The right upper extremity would
then begin to move; this would soon be followed by the left, and then
by the lower extremities; then would follow a succession of varied
action, complex in character, but in which rhythm and time and correct
imitation of certain intentional and rational movements could readily
be recognized. The attacks could be artificially induced in this
patient by pulling the right arm or by striking on the patellar
tendons with a hammer. During the whole of the attack the patient was
conscious. In another patient rhythmical agitations of the arm, the
movement of wielding a hammer, were produced in the first stage; then
followed tonic spasms and twisting of the head and arms, suggesting a
partial epilepsy; finally, rhythmical movements of the head to the
right and left took place, the patient at the same time chanting or
wailing.[79]

[Footnote 79: Charcot's lectures in _Le Progrès médical_ for 1885.]

In the following case an hysterical jumping chorea was probably
associated with some real organic condition or was due to malarial
infection. The patient was a middle-aged man. During the war he
received a slight shell wound in the back part of the right thigh, and
from that time suffered more or less with numbness and some weakness
of the right leg. He was of an active nervous temperament. About three
months before coming under observation he had without warning a
peculiar attack which, in his own words, came on as if shocks of
electricity were passed through his head, back, limbs, and other parts
of the body. In this attack, which lasted for fully an hour, he jumped
two or three feet in the air repeatedly; his arms, legs, and even his
head and eyes, shook violently. He was entirely conscious throughout,
but said nothing except to ask for relief. His wife, who was present,
stated that at first he was pale, and afterward, during the attack, he
became almost turgid under the eyes. Attacks appeared to come at
intervals of seven and fourteen days for a time, so that his family
physician surmised that there might be some malarial trouble, and
prescribed for him accordingly. They soon, however, became irregular
in character, and did not occur at periodical intervals. After the
attacks he would lie down and go to sleep; he did not, however, pass
into the condition of stupor that is observed after a grave epileptic
seizure. His sleep seemed to be simply that of an exhausted nervous
system.

{244} Hysterical tremor is of various forms and of frequent
occurrence: a single limb, both upper or both lower extremities, or
the entire body may be affected. In a case of hystero-epilepsy, which
will be reported in the next article, the patient had a marked tremor
of the left arm, forearm, and hand, which was constant, but worse
before her attacks; it remained for many months, and then disappeared
entirely. Caraffi[80] reports the case of an hysterical girl of
eighteen, anæsthetic on the right side and subject to convulsive
attacks, who fell on the right knee and developed an arthritis. At the
Hôpital Beaujon service of Lefort and Blum she presented herself with
the above symptoms, aphonia, and an uncontrollable tremor of the right
lower extremity, and trophic disturbances of the same. Immobilization
of the limb was tried without benefit, and Blum then stretched the
sciatic, with complete relief of the tremor and of the troubles of
sensibility and of nutrition.

[Footnote 80: _L'Encéphale_, June, 1882.]

Hysterical contracture, like hysterical paralysis, may assume a
variety of forms: it may be hemiplegic, monoplegic, paraplegic,
alternating, or local, as of the ocular muscles, the facial or neck
muscles; laryngeal, pharyngeal, or œsophageal; of the fingers or of
the toes.

Richardson[81] records the case of a young lady who saw in India a
religious devotee with his leg flexed upon his body and fastened
there. In a few hours she was found with her leg in a similar
position, and this contracture remained until after she had been taken
to London; then it disappeared as suddenly as it came. Conscious
purpose could not have maintained the leg in such a position for an
hour.

[Footnote 81: _Diseases of Modern Life_.]

Some of the most remarkable cases of hysterical contracture are those
chiefly studied by the French, which originate before or after
convulsive seizures. Among the hystero-epileptics at Salpêtrière,
Richer[82] reports many varieties of contracture: one with
hemianæsthesia and varying pain in the right side had permanent
contracture with tremulousness of the lower extremities; another, with
hemianæsthesia, pain, and frequent attacks of demoniacal delirium and
paresis, had momentary contractures of the upper and lower extremities
on the right side. In two other cases the contractures were of the
hemiplegic form, while three others were paraplegic. In still other
cases the contracture was monoplegic. Besides hemiplegic, monoplegic,
and paraplegic contractures, I have seen illustrations of a number of
local forms—among others, several remarkable cases of hysterical
contractures of the wrist and hand and of the feet and toes, and one
of hysterical torticollis. Hysterical contracture in any of its forms
may occur as an isolated symptom or series of symptoms unconnected
with the grave hysterical attack.

[Footnote 82: _Op. cit._]

Many forms of hysterical local spasms occur. Hysterical strabismus
from spasm of the ocular muscles has been observed. Several cases have
come under observation in which hysterical blepharospasm was present.
In these cases, when the lids are forced open, the eyes disappeared in
an extraordinary manner, usually being drawn downward and toward the
internal canthus. Hysterical facial spasm occurs, and is usually
clonic. One of the most remarkable hysterical local spasmodic
affections which has come under personal observation was reported by
me in a paper on chorea.[83] In this case the right ear twitched and
moved up and down. {245} The movement of the ear was peculiar; it
continued nearly all the time, even when the patient's attention was
not directed toward the part. The act seemed to be partially under the
control of the will, as by a strong effort the left ear could be moved
very slowly in the same up-and-down direction. The nostrils and upper
lip were affected with twitching, and slight choreic movements were
present in the entire right side of the body. The patient's general
condition improved under treatment, but when last seen the local
affection persisted, although it was not so severe.

[Footnote 83: _Philada. Med. Times_, March 27, 1875.]

Spasm of the pharynx, larynx, and œsophagus have been separated by
several authors. In hysterical laughter spasmodic contraction of the
laryngeal muscles occurs. Spasm of the glottis occurs in rare cases,
according to Rosenthal, from the reflex effect of hyperæsthesia of the
laryngeal mucous membrane, from irritation of the recurrent laryngeal
nerve. Death from asphyxia has occurred in consequence of this form of
spasm of the glottis.

Hysterical dysphagia, which is usually spasmodic, is sometimes a
dangerous, and always an annoying, affection. An unmarried lady, forty
years old, with a neurotic family history, a maternal uncle and aunt
having been insane, at intervals since puberty had had various
hysterical manifestations. After a severe winter, during which she had
suffered more or less with rheumatism, she became depressed with
reference to her spiritual condition: she had, in fact, a form of mild
religious melancholia. After this had lasted for weeks she began to
experience difficulty in swallowing. She would rise from the table
suddenly, alarmed and gasping, and exclaiming that she could not
swallow and was choking. She got so bad that she could not take
anything but liquid food, and not nearly enough of this. She believed
that her throat was gradually closing, and of course suspected cancer.
She was assured that if any local obstruction existed it could be
removed with one application of a probang. Cancer was also confidently
excluded, and she was given iron, valerian, and quinine, and in a few
days an instrument was passed down her throat. She as told that she
would have no more difficulty. Tonics and full feeding were continued,
and in less than a week she swallowed without any difficulty.

Of the so-called hysterical asthma or hysterical breathing I have seen
several examples. A curious form of hysterical breathing, at least
partly spasmodic, recently came to the Philadelphia Polyclinic—a young
man twenty-one years of age, who confessed that he had been guilty of
excessive masturbation for five or six years. He had been a moderate
drinker and was the victim of an old hip disease. According to his
story, this abuse had never appeared to have impaired his health until
about one month before applying for treatment, when he began to have
attacks of peculiar breathing. He would have a series of rapid, forced
expirations which lasted for a period of from one to two or three
minutes. He would then stop for a moment; then again the shallow
breathing with forced expirations would ensue. He said that he
breathed in this way because he thought he was going to die, and did
so to keep alive. When he stopped he felt cold. He thought his belly
did not go outward as it should in the act of breathing. During the
time that the symptoms had been present he had had several frightful
attacks of excitement, in one of which he ran breathing in the manner
described to a {246} drug-store from one to two blocks away, jumping,
gesticulating, and calling for remedies. He had an anxious expression
of the face, a look of excitement and worriment. His pulse was 110 and
weak. Respirations during these attacks ranged from 38 to 50.

Coates,[84] speaking of hysterical or nervous breathing, gives the
details of five cases. Four of these had been supposed to be suffering
from phthisis; the fifth was apparently a case of hypertrophy of the
heart. The breathing was quick and shallow. The patients could not be
induced to draw long breaths until the expedient was adopted of having
them count twenty without taking breath. During this the lungs
expanded perfectly, air entering freely into every part. Coughing, and
even blood-spitting of a venous character, were present. They might
perhaps be classed as cases of hysterical or simulated phthisis.

[Footnote 84: _British Medical Journal_, 1884, ii. 13.]

Vaginismus, or spasm of the vagina, may with propriety be regarded as
hysterical in some but not in all cases. Spasmodic contracture of the
sphincters of the bladder and anus is also mentioned by Rosenthal.
Goose-flesh, according to the same author, is a frequent phenomenon in
the hysterical, and is due to spasmodic contraction of the muscular
fibres contained within the skin.

The sensorial affections of hysteria can be classified according
either to character or location. According to the character of the
sensory disturbance a good practical arrangement is into cases of (1)
Anæsthesia; (2) paræsthesia; (3) hyperæsthesia; (4) neuralgias and
localized pains,—although one of these classes may sometimes be
difficult to separate from another, or a doubt may arise as to whether
or not a special symptom should be placed under one or another head.
In hysterical anæsthesia sensation is decreased or abolished; in
paræsthesia it is faulty or perverted; in hyperæsthesia it is
increased over a more or less extensive surface; in neuralgia, pain is
confined to certain nerve-trunks. The localized pains are neuralgic or
mimetic, and are found in special localities, as in joints and in the
breast.

Anæsthesia is one of the most frequent of hysterical phenomena, but is
not, as stated by some authorities, present in all cases of genuine
hysteria.

In 400 hysterical cases Briquet found 240 positive examples of
anæsthesia. In this statement, however, he does not include cases of
insensibility of the conjunctiva of the left eye or those cases in
which anæsthesia lasted but a few hours after an attack. It is safe to
say that anæsthesia of some sort is present in from 60 to 75 per cent.
of all cases of well-marked hysteria. Analgesia, or insensibility to
pain, is present frequently when loss or diminution of sensibility to
touch, pressure, heat and cold, etc., is not observed.

Hysterical anæsthesia, may be of various forms, according to the parts
of the body affected, as general anæsthesia; hemianæsthesia;
anæsthesia of the lower half of the body; anæsthesia of one limb or
one side of the face; anæsthesia of mucous membranes; anæsthesia of
muscles, bones, and joints; anæsthesia of the viscera.

General anæsthesia is extremely rare. No example of it has ever fallen
under my observation, but by Briquet and others a few cases have been
reported.

{247} Hemianæsthesia has in recent years received much attention from
neurologists. In hystero-epilepsy it is the rule to find it present,
but it is also observed in cases without spasms. In hemianæsthesia the
loss of sensation exists in one lateral half of the body. Parts are
insensible to various methods of stimulation—to impressions of touch,
pain, temperature, and weight. Sometimes the mucous membranes of the
side affected are involved. The sight, hearing, taste, and smell are
commonly impaired if not lost.

Much attention has been paid to the study of hemianæsthesia by French
physicians. Charcot[85] has an admirable historical summary and
clinical description of the condition, leaving little for others to
add. Piorry, Macario, Gendrin, Szokalsky, and Briquet are referred to
by him. Briquet found it present in 93 cases out of 400. It is of much
more frequent occurrence on the left side. According to Briquet, 70
cases were affected on the left side to 20 on the right.

[Footnote 85: _Op. cit._]

Next to hemianæsthesia, anæsthesia of the lower half of the body is
most common in hysterical cases. While hemianæsthesia often presents
itself conjoined with hystero-epileptic symptoms, anæsthesia of the
lower half of the body may be present as frequently without as with
convulsive manifestations. Anæsthesia of one limb or of one side of
the face is almost as rare as general anæsthesia, but does occur.

Anæsthesia of mucous membrane is an old observation. It may affect
mucous membranes everywhere—of the nose, pharynx, larynx, vagina,
urethra, the bladder, rectum, etc. Many of the peculiar and apparently
inexplicable hysterical symptoms are due to the presence of this
anæsthesia—such symptoms, for instance, as want of inclination to
evacuate the bowels or the bladder, absence of sexual desire, absence
of sensibility when applications are made to the throat, etc. Loss of
sensibility in muscles, bones, joints, and viscera may be present, but
is of course frequently overlooked from want of minute investigation.
In hemianæsthesia the viscera of the anæsthetic side are sometimes
hyperæsthetic. Thus the ovary, as has been especially shown by
Charcot, may be very painful on pressure when the abdominal wall is
perfectly insensible.

A striking characteristic of hysteroid sensory disorders of the
anæsthetic variety is the suddenness with which they come and go. A
complete transference of anæsthesia from one side of the body to
another may occur in a few seconds, either without special
interference or under the use of metals or electricity.

The term achromatopsia is due to Galezowski. Hysterical achromatopsia
is a condition in which there is a failure to appreciate colors. In
Daltonism, or true color-blindness, one color may be taken for
another; in achromatopsia the notion of color may be completely lost.
These colors are found by the patient to disappear in a regular order,
and return in a reverse order as the patient recovers. Some remarkable
cases of this kind have been reported as occurring among French
hysterics. A few examples of the same affection have been reported in
America. Sometimes the patient has lost perception of one or several
colors. When only one color is lost, it is usually the violet; if two,
the violet and green; then in regular succession follow the colors of
the spectrum.

{248} Hysterical blindness and achromatopsia have been well studied by
Charcot and Richer and others of the French school. Special articles
on hysterical or simulated affections of the eye have also been
published by Schweigger,[86] Harlan,[87] and others.

[Footnote 86: “On Simulated Amaurosis,” by C. Schweigger, Prof. at the
University of Berlin, _New York Medical Journal_, Feb., 1866.]

[Footnote 87: “Simulated Amaurosis,” by George C. Harlan, M.D.,
_American Journal of Medical Sciences_, October, 1873; “Hysterical
Affections of the Eye,” _Transactions of the College of Physicians of
Philadelphia_, 3d Series, vol. ii., 1876.]

In several cases of hystero-epilepsy under my care both amblyopia and
achromatopsia were present. In one of these cases the patient was
unable to read print of any size or to distinguish any colors,
although she could tell that objects were being moved before the eyes.
An ophthalmoscopic examination showed a normal fundus. Each eye was
tested for near vision. It was found that she could read quite well
with the right eye, and not at all with the left. While reading at
about sixteen inches a convex glass of three inches focus was placed
in front of the right eye, but she still continued to read fluently.

C. H. Thomas of Philadelphia has given me the particulars of a case of
a woman about thirty-eight years old, both of whose eyes were, to all
appearances, absolutely blind. The attack came on suddenly, the
apparent cause seeming to be worry over a sick child. Ophthalmoscopic
and other examinations of the eye showed nothing. She had no
perception of light. She could look without winking at a blinding
reflection of a whitewashed fence. In six weeks under a mere tentative
treatment she got absolutely well. S. D. Risley of Philadelphia,[88]
in a discussion at the Philadelphia Neurological Society, held that
the feeble innervation of the hysterical patient was liable to
diminish the range of accommodation and power of convergence,
rendering the comfortable use of the eye impossible; and also that the
feeble or deranged circulation in the hysterical individual might set
up a group of symptoms in the eye presenting many of the
characteristics of serious disease; which, however, were not
simulated, but were, in fact, a relative glaucoma. While there was no
absolute increase of intraocular tension, the normal tension of the
eyeball was sufficient to interrupt the entrance of the feeble
blood-stream into the eyes, and thus was set up the same group of
symptoms as were present in actual increase of tension—viz. inadequate
blood-supply to the retina, contracted field of vision, impaired
central perception, diminished range of accommodation, and inability
to use the eyes, particularly at a near point.

[Footnote 88: _The Polyclinic_, vol. ii., No. 8, Feb. 15, 1885, p.
124.]

Very few observations in cases of hysteria have been made with the
ophthalmoscope, and probably little is to be learned in this way. In
one of Charcot's patients, however, Galezowski saw an infiltration and
capillary reddening of the disc with fusiform dilatations of the
artery.

What might be termed hysterical dilatation of the pupil is sometimes
observed. In the case reported by Harlan, to be hereafter detailed,
the patient, a young girl who had a train of hysterical symptoms,
began to complain of blindness or imperfect vision in the right eye,
the pupil of which was found to be dilated. No proof could be obtained
of the use of any mydriatic. The pupil remained dilated when exposed
to a bright light. The dilatation came and went at intervals, and
finally disappeared under {249} the applications of a wooden magnet.
W. Chester Roy has acquainted me with the facts of the case of a man
who could at will alternately contract and dilate his pupils. This
case would seem to lend color to the idea that the hysterical girl may
have had voluntary control of the pupillary movements. In her case,
however, only one pupil was involved. F. X. Dercum has given me the
particulars of a case of rhythmical dilatation of the irides in a case
of confirmed masturbation with hysterical symptoms.

Hysterical deafness has been observed and studied. Walton,[89] at
Charcot's suggestion, has published the results of the examination at
La Salpêtrière of 13 patients affected with hemianæsthesia with
reference to anæsthesia of hearing. He divides hemianæsthetic patients
into three classes: (1) Those with complete anæsthesia of one side,
the other side remaining normal; (2) those having incomplete
anæsthesia on one side, the other remaining normal; (3) those with
anæsthesia more or less complete on both sides. In the first class
anæsthesia of hearing extended to the deep parts of the ear; the
membrane of the drum could be touched without eliciting any
acknowledgment of sensation and without the least reflex movement. He
also showed that the anæsthesia extended to the middle ear by the fact
that insufflation by Politzer's air-douche produced no sensation in
the ear of the affected side. In this class neither the watch, voice,
nor tuning-fork was heard. In the second class, with incomplete
anæsthesia on one side, the lost sensibility corresponded, as a rule,
with that of the body in general. A common form was analgesia with
thermoanæsthesia and diminution of the tactile sensibility. In the
third class completeness of the anæsthesia is rarely the same on both
sides, a common form being complete hemianæsthesia on one side and
analgesia on the other.

[Footnote 89: _Brain_, January, 1883.]

A noticeable feature in all the cases under consideration was the
uniformity with which the deafness for conveyance by the bone exceeded
that for sounds conveyed by the ear. Walton says: “This is probably
due to the fact that the vibrations conveyed to the ear by the air are
better adapted for the irritation of the peripheral auditory apparatus
than those conveyed by the bone. When, then, the receptive power of
the auditory centres is lessened, as is probably the case in
hysterical patients, the hearing for sounds conveyed by the bones
disappears before that for sounds conveyed by the ear. This
enfeeblement of the auditive centres in hysteria is quite analogous to
that in old age, in which, as is well known, the perception for sounds
conveyed by the bone disappears before that for sounds conveyed by the
air, the former being sometimes completely lost before the age of
sixty.” His principal conclusions are as follows: (1) The sensibility
of the deep parts of the ear, including the tympanum and middle ear,
disappears in hysterical hemianæsthesia with that of other parts of
the body, and in the same degree. (2) The degree of deafness
corresponds with that of the general anæsthesia, being complete when
the latter is complete, and incomplete when the latter is incomplete.
(3) When loss of hearing is incomplete, the deafness for sounds
conveyed by the bone exceeds that for sounds conveyed by air. (4) When
the transfer is made, the hearing, as well as the general sensibility
of the deep parts of the ear, improves on one side (allowance being
made for accidental {250} lesions in the ear itself) in exactly the
same degree in which it disappears on the other.

The following case has been kindly furnished to me by Charles S.
Turnbull, the patient having in the first instance come to
Philadelphia to consult his father, Laurence Turnbull: The patient was
a young lady from New Jersey, eighteen years old. Her general health
was good, although at times she had a pale and anxious look. She had
never had any unusual sickness. Soon after the death of her mother,
for whom she grieved very much, she began to grow deaf, and was for a
time treated by her family physician. When she first came to
Philadelphia she was absolutely deaf, but the most careful examination
failed to discover a cause for the deafness in any affection of the
external or middle ear. A current from ten cells of a galvanic battery
was painful, but elicited no sound. She declared that she could not
hear a musical box held close to the side of her head. In
communicating with her, everything had to be written. A faradic
current was used daily to her ears. Suddenly one morning, after a
powerful current had been applied, her hearing returned, but before
she came back for treatment the next day it had again left. The
electrical treatment was continued: each day the hearing stayed longer
and longer, and finally returned in full force and remained good.

By hysterical paræsthesia is meant that form of perverted sensation
which is not distinctly depressed on the one hand or markedly
increased on the other. Under this head would come such conditions as
numbness, formications, prickling and tingling sensation, the
sensation of a ball in the throat or globus hystericus, etc. These
forms of perverted sensation are quite common among the hysterical.

Hyperæsthesia may present itself in almost any locality, its areas of
distribution corresponding very well to those which have been given
for anæsthesia. Hyperæsthesia of the special senses is of especially
frequent occurrence. Great sensitiveness to sounds and to bright
lights or to particular colors is commonly observed. What might be
termed hysterical tinnitus aurium is met with occasionally.

Perversions of the senses of smell and taste are among the rarer
phenomena in the sensory sphere in hysteria. These may be of three
kinds: the senses may be completely obtunded; they may be hyperacute;
or they may show peculiar perversions. To some individuals of the
hysterical temperament certain smells are almost unendurable, and
these may be odors which to others are particularly pleasant. In like
manner, certain articles of food or drink may be the source of great
discomfort or absolute suffering. It is one of the oldest of
observations that hysterical and morbid cravings for disagreeable or
disgusting substances sometimes exist.

In one group of hysterias the presence of pain is the predominating
feature. Some of the situations in which hysterical pains are most
frequently felt are the head, the pericardial or left inframammary
region, over the stomach and spleen, the left iliac region, the region
of the kidneys, the sacrum, the hip, the spine, the larynx and
pharynx, one or both mammæ, or over the liver and the joints. Of these
locations, omitting the consideration of headache, the most common
seats of hysterical pain are the spine, the breasts and inframammary
region, the left iliac or ovarian region, the sacrum or coccyx, and
the joints.

{251} Charles Fayette Taylor, in a brochure on sensation and pain,[90]
has given a philosophical explanation of such pain, drawing largely
from Carpenter, Bain, Spencer, and others. The pith of the matter is
that many of our sensations are centrally initiated, the memory of
previous objective sensations. “Pain is different from ordinary
sensations, in that it requires an abnormal condition for its
production, and that it cannot be produced without that abnormal
condition. Hence it is impossible to remember pain, because the
apparatus does not exist for causing such a sensation as pain after
the fact or when it is to be remembered. Memory is a repetition, in
the nerve-centre, of energy which was first caused by the sensory
impulse from without. But centrally initiated sensations may be
mistaken, in consciousness, for pains depending wholly on a certain
intensity of excitability in the cerebral mass.”

[Footnote 90: _Sensation and Pain_, by Charles Fayette Taylor, M.D.—a
lecture delivered before the New York Academy of Sciences, March 21,
1881.]

A large percentage of all cases of hysteria complain more or less of
spinal irritation. Spinal periostitis, spinal caries, and perhaps some
cases of spinal meningitis, are organic diseases which may give rise
to tenderness on pressure along the spine; but the majority of cases
of spinal irritation are found among neurasthenic or hysterical
patients. So much has already been written about spinal irritation
that much time need not be spent on the subject, were it not that even
yet many practitioners are inclined to regard cases as organic spinal
trouble because of the presence of great spinal tenderness, whereas
this symptom is almost diagnostic of the absence of real spinal
disease.

Painful diseases of the joints, especially in women, are not
infrequently hysterical or neuromimetic. Many such cases have been
reported. Taylor states, as the results of much carefully-guarded
experience, that hundreds of lame people are walking about perfectly
who do not know that they ought to limp, and that a much larger number
are either limping and walking on crutches, or not walking at all, who
have no affection whatever causing lameness.

Paget—and his experience accords with that of others—makes the hip and
knee, among the joints, the most frequent seats of nervous mimicry as
well as of real disease. According to him, mimicries in other joints
are almost too rare for counting; and yet in my first case of this
kind the pain was located in the shoulder. This case made a lasting
impression. The patient was a young lady of nervous temperament, who
came complaining of severe and continuous pain in the left shoulder.
No history of injury was given. The pain was said to be rheumatic.
Handling the arm and pressure round the joint caused extreme pain. No
heat, no redness, no swelling were discoverable. The patient left me
and went to a magnetic doctor, who entirely dispelled the disorder on
her first visit by gently stroking the arm and shoulder. Another
patient had been accidentally struck in the knee. No swelling, heat,
or other signs of inflammation followed the accident, and did not
afterward appear; but at intervals, for several years, she complained
of severe pain in and around this joint. She would be for days, or it
might be for weeks, without speaking of the pain; and then again she
would complain almost incessantly, and would sometimes limp. These
periods {252} always corresponded with times of mental and physical
depression, and the pain was evidently neuromimetic or hysterical.

The affection which has come down to us from ancient times under the
name of clavus hystericus is an acute boring pain confined to a small
point at the top of the head, and is sometimes described as resembling
the pain which would be produced by driving a nail into the head;
hence the term, from _clavus_, a nail. It may last for hours, days, or
even weeks. Instead of clavus hystericus, hemicrania, occipital
headache, or nape-aches may be present. On the whole, aches and pains
of the head in hysterical cases are more likely to be localized to
some point or area than to be general. Hysterical patients, however,
not infrequently complain of constricting, contracting, or compressing
sensations in the head.

In hysterical women the pulse is apt to be rapid, even sometimes
twenty, thirty, to fifty pulsations to the minute above normal. The
heart in these patients is irritable and prone to beat rapidly. One of
Mitchell's cases is worthy of brief detail: A neurasthenic, hysterical
woman, thirty-eight years old, when lying down had a heart-beat never
less than 130 per minute. Exertion added twenty or thirty pulsations.
Despite this irritability, however, the rhythm was good. Ovarian
pressure and pressure along the spine would suddenly increase the
heart-beats. Her temperature ranged from 95° in the morning to 100° or
101.5° F. in the evening, although she had no pulmonary or visceral
trouble.

The high temperatures which have been observed in many cases of
hysteria have been due to some form of shrewd fraud; but Briand[91]
maintains with Gubler, Rigel, Dieulafoy, and others that the term
hysterical fever is correct, and he describes three forms of the
fever: (1) The slow continued fever of Briquet, characterized
sometimes by simple acceleration of the pulse, without elevation of
temperature; sometimes by a temperature rise, either with or without
phenomena or accompanied by headache, thirst, and other symptoms; (2)
a shorter form, always the result of a more or less active disturbance
of the nervous system by terror, fear, chagrin, and like causes; (3) a
form with intermittent febrile phenomena. Examples of the different
forms are given. Debove[92] supports the view of the entity of the
hysterical fever, citing cases—one a woman twenty-four years old who
had, at intervals, marked fever, the temperature sometimes reaching
102-1/5° to 104° F. Malaria and tuberculosis were excluded. Sulphate
of quinia had no influence upon her attacks, but antipyrine reduced
the temperature and her general condition improved. Debove has
observed the temperature to rise from 1° to 2° F. by mere suggestion
when the patient was in a somnambulistic state.

[Footnote 91: _Gazette hébdomadaire_, quoted in _Med. News_, Dec. 1,
1883.]

[Footnote 92: _Ibid._, quoted in _Med. News_, April 4, 1885.]

On the other hand, it has been claimed that a true hysterical fever
never occurs or is extremely rare. Admitting this view, several
explanations may be given of the rise of temperature observed. It may
be due to intercurrent affections, as typhoid or intermittent fever,
or some local inflammatory disorder. It may be secondary fever, the
result of muscular effort or some similar cause. Lastly, and most
probably, it may be due to ingenious fraud, as to friction of the
bulb, pressure, or tapping {253} with the finger, dipping the
instrument into hot water, connivance with the nurse, etc.
Du Castel[93] has reported a trick of this kind. An hysterical girl,
convalescent from an attack of sore throat, displayed remarkable
alternations of temperature. One day the thermometer reached
163.4° F.! By carefully watching the patient it was found she had
learned the trick of lightly tapping the end of the thermometer, which
caused the mercury to ascend as far as she wished. In the case of
chronic hysterical insanity of which the details have been given the
temperature in the axilla on several occasions reached 102°, 103°, and
even 105° F.

[Footnote 93: _Revue de Thérapeutique méd.-chir._, No. xi., 1884.]

Extreme states of pallor or blushing, sometimes in the extremities and
at others in the face, are mentioned by Mitchell as among the
vaso-motor disturbances of hysteria. Rosenthal gives a most
interesting observation with reference to vaso-motor conditions in
hysteria: the patient, a girl twenty-three years old, had epileptiform
attacks, which were preceded by a subjective sensation of cold and
discoloration of the hands and tips of the fingers. The hands became
very pale, the tips of the fingers and nails of a deep blue; the
patient experienced a disagreeable sensation of cold in the hands, and
their temperature sank more than 3°, while the pulse dropped from 72
to 65 or 66. After the attack the temperature rose 2° higher than the
normal condition; the fingers and nails became very red, and were the
seat of an abundant perspiration; the pulse increased to 84 or 88.
Other interesting symptoms were present.

Mitchell[94] has put on record three cases of hysteria in which was
present unilateral increase in bulk at or near the menstrual period,
and also at other seasons after emotional excitement. He does not give
any opinion as to its nature, but believes that it is not a mere
increase of areolar serum, and that it does not appear to resemble the
vasal paralysis in which the leg throbs and exhibits a rise in
temperature and tint. He is unable also to identify it with any form
of lymph œdema which it resembles, for in this disorder there is more
obvious œdema, and it is also quite permanent. Whatever the cause of
the swelling, he believes that it is under the influence of the
nervous system, and that it varies with the causes which produce
analgesia or spasm. I have seen swelling of this kind in several
cases, and have probably overlooked it in others. In one of my
reported cases of hystero-epilepsy it was a very marked symptom,
coming and going, increasing and diminishing, with other symptoms.

[Footnote 94: _American Journal of the Medical Sciences_, New Series,
vol. lxxxviii., July, 1884, p. 94.]

Buzzard calls attention to the fact that in many cases belonging to
the class of hysteria the epidermis, which has arrived at
extraordinary thickness, apparently from disuse of the limbs, offers
great resistance to the passage of electric currents. Under these
circumstances a more than usual amount of care in thoroughly soaking
and rubbing the skin, as well as in selecting the motor points, is
necessary to avoid fallacies. Absence of reflex from the sole of the
foot, according to the same authority, is a very constant symptom in
hysterical paraplegia.

Some wasting does not negative the idea of hysteria, but this wasting
a not associated with changing the electrical reaction.

Disturbance of the secretion of the urine is among the most frequent
of the minor hysterical troubles, and has often been noted by writers
upon {254} this subject since a very early date. Sydenham[95] says
that of the “symptoms accompanying this disease, the most peculiar and
general one is the making great quantities of urine as clear as
rock-water, which upon diligent inquiry I find to be the
distinguishing sign of those disorders which we call hypochondriac in
men and hysteric in women. And I have sometimes observed in men that
soon after having made urine of an amber color, being suddenly seized
with some disturbance of mind, they made a large quantity of clear
water, with a continued violent stream, and remained indisposed till
the urine came to its former color, when the fit went off.” This
symptom shows itself as strikingly in the hysteria of the present day
as in the age of Sydenham.

[Footnote 95: _Op. cit._]

A complete anuria or ischuria is one of the older observations in
hysteria. Laycock, Charcot, and many others have written at length on
this subject. Finch[96] has published a curious case of complete
anuria. The patient had various hysterical symptoms, including
paroxysms with unconsciousness, contracture, also vomiting.
Micturition and defecation were entirely suspended (?) from Dec. 24,
1877, to Feb. 22d of the following year. During a period of
fifty-eight days paroxysms were frequent; but on using the catheter
the bladder was always found empty. The probability of hysterical
fraud is very great in this case. A few case of hysterical retention
of the urine in men have been reported.

[Footnote 96: _Nice médicale_.]

Increase of the uterine and vaginal secretions is mentioned by Jolly
as sometimes attributable to nervous influences in cases of hysteria.
He mentions the case of a woman suffering from hysterical symptoms at
the change of life whose disposition was decidedly depressed; though
at times lively, particularly erotic. In this case simultaneously with
tympanites appeared a thin, clear fluor albus. Local treatment with
quiet had no decided effect, but it disappeared with the tympanites
when the patient was excited by the visit of a sister who overwhelmed
her with reproaches.

Hysterical vomiting of food sometimes persists for weeks; strangely
enough, the patients usually appear to suffer little in consequence.
Chambers believes that the articles swallowed do not all get into the
stomach. The phenomena of rejection in these cases are similar to
those of an œsophageal stricture; some of the matter swallowed is
really retained, and therefore the patient will not starve as soon as
might be supposed.

Two cases of simulated pregnancy by hysterical women have come under
my observation. Cases are reported also in which hysteria simulated
closely the process of natural labor, as one for instance, by
Hodges.[97] A woman said to be in the fifth month of pregnancy engaged
him to attend her at term. Four months afterward he was sent for, the
patient having severe pains, supposing herself to be in labor. On
examination, however, a tumor present turned out to be the bladder
distended and prolapsed. Sparks[98] reports the case of a young
married woman who had the symptoms of the third stage of labor, the
case being purely hysterical.

[Footnote 97: _Lancet_, 1859, ii. 619.]

[Footnote 98: _Chicago Med. Journ. and Examiner_, 1880.]

Walker[99] reports a group of hysterical symptoms closely simulating
the prodromes of puerperal eclampsia. The patient, a married woman
only {255} eighteen years old, when pregnant six months lifted a tub
of water, rupturing the membranes. In the eighth month, after she had
remained in bed three days, she began to complain of severe headache;
soon she said she was blind; the pupils of the eye were neither
dilated nor contracted, and responded sluggishly to light.
Ophthalmoscopic examination gave negative results, but she did not
flinch from the light of the mirror. Temperature, pulse, and
respiration were about normal. The urine contained no albumen. She
recovered her sight in twelve hours, and had no continuing trouble.

[Footnote 99: _Arch. of Medicine_, New York, 1883, x. 85-88.]

Paget mentions cases of phantom tumor occurring in the calf, thigh,
and breast. These phantoms shift from one place to another, or
disappear when the muscles are relaxed by anæsthetics or otherwise.
The nervous mimicry of aneurisms (of Paget) are what Laycock and
others treat of as pulsations. They are most frequent in the carotid
artery and abdominal aorta. Of imitations of cancer it need only be
said that the average hysterical female suspects every lump in the
breast and elsewhere to be a cancer.

Mitchell mentions certain peculiar symptoms quite common among
hysterical women, but which also occur, but more rarely, among men.
When falling asleep these patients have something like an aura rising
from the feet and going up toward the head. One patient had an aura
which passed upward from his feet, and when it had reached his head he
felt what he described as an explosion. Another had a sensation as
though something was about to happen, but no distinct ascending aura.
If he roused himself in time, he could by turning over release himself
from the sensation and break the chain of morbid events. At the close
of the attack he had a noise in his head—something like the sound of a
bell which had been struck once. Other patients when going to sleep
have constant sounds, faint usually and rarely loud and without a
feeling of terror. Most of the patients were women worn out or tired
out and hysterical.

Sometimes hysterical women awake with numbness and tingling, which
rapidly passes away or yields to a little surface friction. Some
persons who have in a measure recovered from hemiplegia of organic
origin are liable to awake out of sleep with a numbness and lessening
of power on the side once palsied. Palpitation of the heart, vertigo,
and a certain fear of a respiratory character are among the milder
forms of trouble which Mitchell mentions as haunting the sleep of
nervous or hysterical women.

Under hysteria some of the affections, more common among men than
women, known as railway brain, railway spine, etc., may be classified.
These disorders might be termed traumatic hysteria. The amount of
money that has been paid out by corporations, beneficial societies or
individuals because of suits or threatened suits for damages in cases
of railway or other accidents is something almost incredible. At least
two classes of cases, besides those of recognizable gross lesion, are
to be found in the ranks of those claiming such damages. These are
first the bogus cases or malingerers, and secondly cases of nervous
mimicry. An hysterical individual who has been in a railway collision,
or has been the victim of an accident for which somebody else may
possibly be made responsible, may deliberately practise fraud, or he
may {256} consciously or unconsciously imitate or exaggerate real
symptoms of serious import. Sometimes there may be in the same case a
mingling of real and of simulated or of neuromimetic disorders. As
long as a claim of damages in this class of cases exists, great care
should be taken in making a diagnosis. The neuromimetic cases,
however, do occur, particularly in the hysterical and neurasthenic,
without any reference to litigation.

A lady fell off her chair backward. She was not rendered unconscious,
but became nervous, and began to have considerable pain and soreness
in the sacral region and about the right sacro-iliac juncture. She had
no palsy, nor spasm, nor anæsthesia, nor paræsthesia, and had no
difficulty in her bladder, but nevertheless was helpless in bed for
many weeks, supposing herself unable to stand. She recovered promptly,
under treatment with electricity, as soon as a favorable prognosis was
given in a very positive manner.

A man fell on the ice and struck his back, but was able to go on with
his usual occupation, although complaining of his limbs. Two months
afterward, while recovering from typhoid fever, he fell from a chair,
and was unable to raise himself, and found that he had lost control of
his legs and arms. During the attack he was not unconscious. He was
bed-ridden for two months, but did not lose control of his bladder and
bowels. He was put on his feet by a little treatment and much
encouragement.

A woman was badly pushed about while riding in a street-car by the car
being thrown off the track. She miscarried in about six weeks,
flooding a good deal after injury to the time of miscarriage. Later,
spinal symptoms began. She had extensive pain and tenderness at the
lower end of the spine. She sometimes fainted. Examination revealed
general spinal tenderness, much more marked in the sacro-coccygeal
region. She was pale, anæmic, and neurasthenic. She brought suit
against the railway company for damages, which were very properly
awarded, as the miscarriage, hemorrhage, and consequent anæmia were
without doubt the result of an accident for which she was in no wise
responsible. Some organic spinal-cord disease, however, was supposed
to exist, the chief foundation for this view being the extreme spinal
tenderness, which was hysterical.

Finally, some hysterical cases present a succession of local
hysterical phenomena following each other more or less rapidly. One
symptom seems to take possession of the patient for the time being,
but when relieved or cured of this, suddenly a new manifestation
occurs. A new figure appears upon the scene, or perhaps I might better
say a new actor treads the boards. Even in these cases, however, it
would be difficult to say that the phenomena are really simulated.
They are rather induced, and get partly beyond the patient's will.

A remarkable case of this kind is well known at the Philadelphia
Polyclinic and College for Graduates in Medicine. She is sometimes
facetiously spoken of as the “Polyclinic Case,” because she has done
duty at almost every clinical service connected with the institution.
The case has been reported several times: the fullest report is that
given by Harlan.[100] The patient was taken sick in September with
sore throat, and was confined to the house for about two weeks. She
was attended by S. Solis {257} Cohen. There was difficulty in
swallowing, and some regurgitation of food. At the same time she had
weakness of sight in the right eye. Later, huskiness of voice came on,
and soon complete aphonia. Her voice recovered, and she then had what
appeared to be pleuro-pneumonia. During the attack her arms became
partially paralyzed. She complained of numbness down her legs and in
her feet.

[Footnote 100: _Transactions of the Amer. Ophthalmological Soc._, 20th
annual meeting, 1884, 649.]

Before these symptoms had disappeared twitchings of the muscles of the
face set in, most marked on the right side. The face improved, but in
two days she had complete spasmodic torticollis of the left side. One
pole of a magnet was placed in front of the ear, and the other along
the face; and under this treatment in a week the spasm ceased
entirely.

In a short time she complained of various troubles of vision and a
fixed dilatation of the pupil. Homonymous diplopia appeared. Reading
power of the right eye was soon lost. The pupil was slightly dilated,
and reacted imperfectly to light. She had distressing blepharospasm on
the right side and slight twitchings on the left. Two months later a
central scotoma appeared, and eventually her right eye became entirely
blind except to light. The pupil was widely dilated and fixed, and the
spasm became more violent and extended to the face and neck. The sight
was tested by Harlan by placing a weak convex lens in front of the
blind eye, and one too strong to read through in front of the sound
eye, when it was found that she read without any difficulty. The use
of the magnet was continued by Cohen. Blepharospasm and dilatation of
the pupil improved. She, however, had an attack of conjunctivitis in
the left eye, and again got worse in all her eye symptoms. A perfect
imitation of the magnet was made of wood with iron tips. Under this
imitation magnet the pupil recovered its size and twitching of the
face and eyelids ceased.

The next campaign was precipitated by a fall. She claimed that she had
dislocated her elbow-joint; she was treated for dislocation by a
physician, and discharged with an arm stiff at the elbow. A wooden
magnet was applied to the arm, the spasm relaxed, and the dislocation
disappeared.

This ends Harlan's report of the case, and I had thought that this
patient's Iliad of woes was also ended; but I have just been informed
by J. Solis Cohen and his brother that she has again come under their
care. The latter was sent for, and found the patient seemingly choking
to death. The right chest was fixed; there was marked dyspnœa;
respiration 76 per minute; her expectoration was profuse; she had
hyperresonance of the apex, and loud mucous râles were heard. At last
accounts she was again recovering.

This patient's train of symptoms began with what appeared to be
diphtheria. The fact that she had some real regurgitation would seem
to be strong evidence that she had some form of throat paralysis
following diphtheria. She was of neurotic temperament. From the age of
seven until ten years she had had fits of some kind about every four
weeks. Because of her sore throat and subsequent real or seeming
paralytic condition she came to the Polyclinic, where she was an
object of interest and considerable attention, having been talked
about and lectured upon to the classes in attendance. Whether her
first symptoms were or were not hysterical, those which succeeded were
demonstrably of this character. {258} Frequently some real disease is
the starting-point of a train of hysterical disorders.

DURATION AND COURSE.—Hysteria is pre-eminently a chronic disease; in
the majority of cases it lasts at least for years. Its symptoms may be
prolonged in various ways. Sometimes one grave hysterical disorder, as
hysterical paralysis, persists for years. In other cases one set of
symptoms will be supplanted by others, and these by still others, and
so on until the whole round of hysterical phenomena appears in
succession.

Deceptive remissions in hysterical symptoms often mislead the unwary
practitioner. Cures are sometimes claimed where simply a change in the
character of the phenomena has taken place. Without doubt, some cases
of hysteria are curable; equally, without doubt, many cases are not
permanently cured. It is a disease in which it is unsafe to claim a
conquest too soon. In uncomplicated cases of hysteria the disorder
often abates slowly but surely as age advances. As a rule, the
longevity of hysterical patients is not much affected by the disorder.

COMPLICATIONS.—We should not treat a nervous case occurring in a woman
or a man as hysterical simply because it is obscure and mysterious.
Unless, after the most careful examination, we are able by exclusion
or by the presence of certain positive symptoms to arrive at the
diagnosis of hysteria, it is far better to withhold an opinion or to
continue probing for organic disease. I can recall five cases in which
the diagnosis of hysteria was made, and in which death resulted in a
short time. One of these was a case of uræmia with convulsions, two
were cases of acute mania, another proved to be a brain abscess, and
the fifth a brain tumor. Hughes Bennett[101] has reported a case of
cerebral tumor with symptoms simulating hysteria in which the
diagnosis of the true nature of the disease was not made out during
life. The patient was a young lady of sixteen at the time of her
death. Her family history was decidedly neurotic. She was precocious
both mentally and physically, was mischievous and destructive,
sentimental and romantic; she had abnormal sexual passions. She had a
sudden attack of total blindness, with equally sudden recovery of
sight some ten days afterward. Sudden loss of sight occurred a second
time, and deafness with restoration of hearing, loss of power in her
lower limbs, and total blindness, deafness, and paraplegia. Severe
constant headaches were absent, as were also ptosis, diplopia, facial
or lingual paralysis, convulsions with unconsciousness, vomiting,
wasting, and abnormal ophthalmoscopic appearances. She had attacks of
laughing, crying, and throwing herself about. Her appearance and
character were eminently suggestive of hysteria. The patient died, and
on post-mortem examination a tumor about the size and shape of a hen's
egg was found in the medullary substance of the middle lobe of the
right hemisphere.

[Footnote 101: _Brain_, April, 1878.]

The association of hysteria with real and very severe spinal
traumatism partially misled me in the case of a middle-aged man who
had been injured in a runaway accident, and who sustained a fracture
of one of the upper dorsal vertebræ, probably of the spines or
posterior arch. This was followed by paralysis, atrophy of the
muscles, contractures, changed reactions, bladder symptoms, bed-sores,
and anæsthesia. The upper extremities were also affected. Marked
mental changes were present, {259} the man being almost insanely
hysterical. The diagnosis was fracture, followed by compression
myelitis, with descending motor and ascending sensory degeneration. An
unfavorable prognosis was given. He left the hospital and went to
another, and finally went home, where he was treated with a faradic
battery. He gradually improved, and is now on his feet, although not
well. In this case there was organic disease and also much hysteria.

Seguin[102] holds that (1) many hysterical symptoms may occur in
diseases of the spinal cord and brain; (2) in diseases of the spinal
cord these diseases appear merely as a matter of coincidence; (3) in
cases of cerebral disease the hysterical symptoms have a deeper
significance, being in relation to the hemisphere injured. He
collects, as illustrative of the propositions that hysterical symptoms
will present themselves in persons suffering from organic disease of
the nervous system, the following cases of organic spinal disease: One
case of left hemiplegia with paresis of the right limbs, which proved
after death to be extensive central myelitis, with formation of
cavities in the cord; two cases of posterior spinal sclerosis, two of
disseminated sclerosis, and one of sclerosis of the lateral column. In
some of these cases the organic disease was wholly overlooked. Sixteen
cases of organic disease of the brain accompanied by marked hysterical
manifestations are also given: 9 of left hemiplegia; 2 of right
hemiplegia with aphasia; 1 of left alternating with right hemiplegia;
1 of hemichorea with paresis; 1 of double hemiplegia; and 2 of general
paresis. It is remarkable and of interest, in connection with other
unilateral phenomena of hysteria, that emotional symptoms were present
in 14 cases of left hemiplegia and in only 2 of right.

[Footnote 102: _Op. cit._]

Among the important conclusions of this paper are the following: “1.
In typical hysteria the emotional symptoms are the most prominent, and
according to many authors the most characteristic. In all the cases of
cerebral disease related there were undue emotional manifestations or
emotional movements not duly controlled. 2. In typical hysteria many
of the objective phenomena are almost always shown on the left side of
the body, and we may consequently feel sure that in these cases the
right hemisphere is disordered. In nearly all of the above sixteen
cases the right hemisphere was the seat of organic disease, and the
symptoms were on the left side of the body.”

The possibility of the occurrence of hysteria in the course of acute
diseases, particularly fevers, is often overlooked. Its occurrence
sometimes misleads the doctor with reference to prognosis. Such
manifestations are particularly apt to occur in emotional children. A
young girl suffering from a moderately severe attack of follicular
tonsillitis, with high fever, suddenly awoke during the night and
passed into an hysterical convulsion which greatly alarmed her
parents. Her fingers, hands, and arms twitched and worked
convulsively. She had fits of laughing and shouting, and was for a
short time in a state of ecstasy or trance. Once before this she had
had a similar but slighter seizure, during the course of an ephemeral
fever.

Among other complications of hysteria which have been noted by
different observers are apoplexy, disease of the spleen, mania-a-potu,
heart {260} disease, and spinal caries, and among affections alluded
to by competent observers as simulated by hysteria are secondary
syphilis, phthisis, tetanus, strychnia-poisoning, peritonitis, angina
pectoris, and cardiac dyspnœa.

DIAGNOSIS.—Buzzard[103] significantly remarks that you cannot cure a
case of hysteria as long as you have any serious doubt about its
nature; and, on the other hand, if you are able to be quite sure on
this point, and are prepared to act with sufficient energy, there are
few cases that will not yield to treatment. The importance of a
correct diagnosis is a trite topic, but in no affection is it of more
consequence than in hysteria, that disorder which, although itself
curable, may, as has been abundantly shown, imitate the most incurable
and fatal of diseases.

[Footnote 103: _Clinical Lectures on Diseases of the Nervous System_,
by Thomas Buzzard, M.D., Philada., 1882.]

A few remarks with reference to the methods of examining hysterical
patients will be here in place. Success on the part of the physician
will often depend upon his quickness of perception and ability to
seize passing symptoms. It is often extremely difficult to determine
whether hysterical patients are or are not shamming or how far they
are shamming. The shrewdness and watchfulness which such patients
sometimes exercise in resisting the physician's attempts to arrive at
a diagnosis should be borne in mind. A consistent method of procedure,
one which never betrays any lack of confidence, should be adopted.
“Trifles light as air” will sometimes decide, a single expression or a
trivial sign clinching the diagnosis. On the other hand, the most
elaborate and painstaking investigation will be frequently required.

The physician should carefully guard against making a diagnosis
according to preconceived views. On the whole, the general
practitioner is more likely to err on the side of diagnosticating
organic disease where it does not exist; the specialist in too quickly
assigning hysteria where organic disease is present, or in failing to
determine the association of hysteria and organic disease in the same
case.

Special expedients may sometimes be resorted to in the course of an
examination. Not a few hysterical symptoms require for their
continuance that the patient's mind shall be centred on the
manifestations. If, therefore, the attention can, without arousing
suspicions, be directed to something else during the examination, the
disappearance of the particular hysterical symptom may clear away all
obscurity. In a case reported by Seguin,[104] in which staggering was
a prominent symptom, the patient was placed in the middle of the room
and directed to look at the ceiling to see if he could make out
certain fine marks; he stood perfectly well without any unsteadiness.
In the case of a boy eleven years old whose chief symptoms were
hysterical paralysis with contracture of the lower extremities, great
hyperæsthesia of the feet, and a tremor involving both the upper and
lower extremities, and sometimes the head, I directed him, as if to
bring out some point, to hold one arm above his head and at the same
time fix his attention on the foot of the opposite side. The tremor in
the upper extremities, which had been most marked, entirely
disappeared. This experiment was varied, the result being the same.

[Footnote 104: _Op. cit._]

The method adopted in the cases supposed to be phthisis, but which
proved to be hysterical, which has already been alluded to under the
{261} head of hysterical or nervous breathing, is worthy of note. The
patients, it will be recalled, could not be induced to draw a long
breath until the plan was adopted of having them count twenty without
stopping, when the lungs expanded and the diagnosis was clear.

It is important to know whether or not children are of this hysterical
tendency or are likely, sooner or later in life, to develop some forms
of this disorder. In children as well as in adults the hysterical
diathesis will be indicated by that peculiar mobility of the nervous
system, which has been referred to under Etiology. It is chiefly by
psychical manifestations that the determination will be made. These
are often of mild degree and of irregular appearance. Undue
emotionality under slight exciting cause, a tendency to simulation and
to exaggeration of real conditions, inconsistency in likes and
dislikes, and great sensibility to passing impressions, are among
these indications. Children of hysterical diathesis are sometimes,
although by no means always, precocious mentally, but not a few cases
of apparent precocity are rather examples of an effort to attract
attention, which is always present in individuals of this temperament.

It is also important, as urged by Allbutt,[105] to make a distinction
between hysterical patients and neurotic subjects, often incorrectly
classed as hysterical. Many cases of genuine malady and suffering are
contemptuously thrown aside as hysteric. Allbutt regards some of these
neurotic patients as almost the best people in this wicked world.
Although, however, this author's righteous wrath against the too
frequent diagnosis of hysteria, hysterical pain, hysterical spine,
etc. is entirely justifiable, he errs a little on the other side.

[Footnote 105: _On Visceral Neuroses, being the Gulstonian Lectures on
Neuralgia of the Stomach and Allied Disorders_, delivered at Royal
College of Physicians, March, 1884, by T. Clifford Allbutt, M.A., M.D.
Cantab., F. R. S., Philada., 1884.]

Hysteria and neurasthenia are often confounded, and, while both
conditions may exist in the same case, just as certainly one may be
present without the other. The points of differential diagnosis as
given by Beard[106] are sufficient for practical purposes. They are
the following: In neurasthenia convulsions or paroxysms are absent; in
hysteria they are among the most common features. In neurasthenia
globus hystericus and anæsthesia of the epiglottis are absent, ovarian
tenderness is not common, and attacks of anæsthesia are not frequent
and have little permanency; in hysteria globus hystericus, anæsthesia
of the epiglottis, ovarian tenderness, and attacks of general or local
anæsthesia are all marked phenomena. The symptoms of neurasthenia are
moderate, quiet, subdued, passive; those of hysteria are acute,
intense, violent, positive. Neurasthenia may occur in well-balanced
intellectual organizations; hysteria is usually associated with great
emotional activity and unbalanced mental organization. Neurasthenia is
common in males, although more common in females; hysteria is rare in
males. Neurasthenia is always associated with physical debility;
hysteria in the mental or psychical form occurs in those who are in
perfect physical health. Neurasthenia never recovers suddenly, but
always gradually and under the combined influences of hygiene and
objective treatment; hysteria may recover suddenly and under purely
emotional treatment.

[Footnote 106: _Op. cit._]

{262} An affection termed general nervousness has been described by
Mitchell. It does not seem to be strictly a neurasthenia, nor does it
always occur in hysterical individuals. These cases are sometimes
“more or less neurasthenic people, easily tired in brain or body; but
others are merely tremulous, nervous folks, easily agitated,
over-sensitive, emotional, and timid.” It is sometimes an inheritance;
sometimes it results from the misuse of alcohol, tobacco, tea or
coffee. Usually, it is developed slowly; occasionally, however, it
arises in a moment. Thus, Mitchell mentions the case of a healthy girl
who fell suddenly into a state of general nervousness owing to the
fall of a house-wall. General nervousness is to be distinguished from
hysteria, into which it sometimes merges, only by the absence of the
mental perversions and the special motor, sensory, vaso-motor, and
visceral disorders peculiar to the latter.

The differential diagnosis of hysteria and hypochondria, or what is
better termed hypochondriacal melancholia, is often, apparently at
least, somewhat difficult. Formerly, it was somewhat the fashion to
regard hysteria in the male as hypochondria; but this view has nothing
to support it. Hypochondria and hysteria, as neurasthenia and
hysteria, are sometimes united in the same subject; one sometimes
begets the other, but they have certain points of distinction.
Hypochondria more frequently passes into real organic disease than
does hysteria; it is more frequently associated with organic disease
than is hysteria. Hypochondria is in the majority of cases a true
insanity, while hysteria can only be regarded as such in the special
instances which have been discussed. In hypochondria the individual's
thoughts are centred upon some supposed disease until a true
delusional condition is developed; this does not often occur in
hysteria. Hypochondria is seen with as great a frequency in the male
as in the female, while hysteria prevails much more largely in the
female sex. In typical hypochondria more readily than in hysteria the
patient may be led from one set of symptoms to another, the
particulars of which he will detail in obedience to questions that are
put to him, these symptoms not unusually partaking of the absurd and
impossible. In hypochondria are absent those distinctive symptoms
which in nearly all cases of hysteria appear in greater or less
number, such as convulsions, paralysis, contracture, aphonia,
hysterical joints, and the like. In hypochondria is present the
groundless fear of disease without these outward manifestations of
disease. The symptoms of hypochondria, as a rule, but not invariably,
are less likely to change or abate than those of hysteria.

It is often of moment to be able to distinguish between two such
well-marked affections as common acute mania and hysterical mania. In
acute mania the disorder usually comes on gradually; in hysterical
mania the outbreak of excitement is generally sudden, although
prodromic manifestations are sometimes present. This point of
difference is not one to be absolutely depended upon. In acute mania
incoherence and delusions or delusional states are genuine phenomena;
in hysterical mania delusional conditions, often of an hallucinatory
character, may be present, but they are likely to be of a peculiar
character. Frequently, for instance, such patients see, or say that
they see, rats, toads, spiders, and strange beasts. These delusions
have the appearance of being affected in many cases; very often they
are fantastical, and sometimes at least they are spurious or
simulated. In hysterical mania such {263} phenomena as obstinate
mutism, aphonia, pseudo-coma, ecstasy, catalepsy, and trance often
occur, but they are usually absent in the history of cases of acute
mania. In acute mania under the influence of excitement or delusion
the patients may take their own lives: they may starve or kill
themselves violently; in hysterical mania suicide will be threatened
or apparently attempted, but the attempts are not genuine as a rule;
they are rather acts of deception. In acute mania the patients often
become much reduced and emaciated; in hysterical mania in general,
considering the amount of mental and motor excitement through which
the individuals pass, their nutrition remains good. In acute mania
sleeplessness is common, persistent, and depressing; in hysterical
mania usually a fair amount of sleep will be obtained in twenty-four
hours. In many cases of hysterical mania the patients have their worst
attacks early in the morning after a good night's rest. Acute mania
under judicious treatment and management may gradually recover;
sometimes, however, it ends fatally: this is especially likely to
occur if the physician supposes the case to be simply hysterical and
acts accordingly. Hysterical mania seldom has a serious termination
unless through accident or complication.

In order to make the diagnosis of purposive hysterical attacks
watchfulness on the part of the physician will often suffice. Such
patients can frequently be detected slyly watching the physician or
others. Threats or the actual use of harsh measures will sometimes
serve for diagnostic ends, although the greatest care should be
exercised in using such methods in order that injustice be not done.

In uræmia, as in true epilepsy, the convulsion is marked and the
condition of unconsciousness is usually profound. An examination of
the urine for albumen, and the presence of symptoms, such as dropsical
effusion, which point to disorder of the kidneys, will also assist.

Hysterical paralysis in the form of monoplegia or hemiplegia must
sometimes be distinguished from such organic conditions as cerebral
hemorrhage, embolism or thrombosis, tumor, abscess, or meningitis
(cerebral syphilis).

When the question is between hysteria and paralysis from coarse brain
disease, as hemorrhage, embolism, etc., the history is of great
importance. The hysterical case usually has had previous special
hysterical manifestations. The palsy may be the last of several
attacks, the patient having entirely recovered from other attacks. In
an organic case, if previously attacked, the patient has usually made
an incomplete recovery; the history is of a succession of attacks,
each of which leaves the patient worse. In cerebral syphilis it
happens sometimes that coming and going paralyses occur; but the
improvement in these cases is generally directly traceable to specific
treatment. Partial recoveries take place in embolism, thrombosis,
hemorrhage, etc. when the lesion has been of a limited character, but
the improvement is scarcely ever sufficient to enable the patient to
be classed as recovered. The exciting cause of hysterical and organic
cases of paralysis is different. While in hysterical paralysis sudden
fright, anxiety, anger, or great emotion is frequently the exciting
cause, such psychical cause is most commonly not to be traced as the
factor immediately concerned in the production of the organic
paralysis. In the organic paralysis an apoplectic or apoplectiform
attack of a peculiar kind has usually occurred. In cerebral hemorrhage
or embolism the {264} patient suddenly loses consciousness, and
certain peculiar pulse, temperature, and respiration phenomena occur.
The patient usually remains in a state of complete unconsciousness for
a greater or less period. In hysteria the conditions are different. A
state of pseudo-coma may sometimes be present, but the temperature,
pulse, and respiration will not be affected as in the organic case.

Hysterical monoplegia or hemiplegia, as a rule, is not as complete as
that of organic origin, and is nearly always accompanied by some loss
of sensation. The face usually escapes entirely. In organic palsy the
face is generally less severely and less permanently affected than the
limbs, but paresis is commonly present in some degree. Hysterical
palsies are more likely to occur upon the left than upon the right
side. Embolism is well known to occur most frequently in the left
middle cerebral artery, thus giving the palsies upon the right. In
hemorrhage and thrombosis the tendency is perhaps almost equal for the
two sides. Some of these and other points of distinction between
organic and hysterical palsies have been given incidentally under
Symptomatology.

In organic hemiplegia aphasia is more likely to occur than in
hysterical cases; and acute bed-sores and wasting of the limbs, with
contractures, are conditions frequently present as distressing
sequelæ. Such is not the rule in hysterical cases, for while there may
be wasting of the limbs from disuse and hysterical contractures,
bed-sores are seldom present, and the wasting and contractures do not
appear so insidiously, nor progressively advance to painful permanent
conditions, as in the organic cases. Mitchell mentions the fact that
in palsies from nerve wounds feeling is apt to come back first, motion
last; while in the hysterical the gain in the power of motion may go
on to full recovery, while the sense of feeling remains as it was at
the beginning of treatment. This point of course would help only in
cases where both sensory and motor loss are present.

The examination of an hysterically palsied limb, if conducted with
care, may often bring out the suppressed power of the patient.
Practising the duplicated, active Swedish movements on such a limb
will sometimes coax resistance from the patient. As already stated,
electro-contractility is retained in hysterical cases.

The disorders from which it may be necessary to diagnosticate
hysterical paraplegia are spinal congestion, subacute generalized
myelitis of the anterior horns (chronic atrophic spinal paralysis of
Duchenne), diffused myelitis, acute ascending paralysis, spinal
hemorrhage, spinal tumor, posterior spinal sclerosis or locomotor
ataxy, lateral sclerosis or spasmodic tabes, multiple cerebro-spinal
sclerosis, and spinal caries.

In spinal congestion the patients come with a history that after
exposure they have lost the use of their lower limbs, and sometimes of
the upper. Heaviness and pain in the back are complained of, and also
more or less pain from lying on the back. Numbness in the legs and
other disturbances of sensation are also present. The paralysis may be
almost altogether complete. Such patients exhibit evidences of the
involvement of the whole cord, but not a complete destructive
involvement. A colored woman, age unknown, had been in her ordinary
health until Nov. 24, 1884. At this time, while washing, she noticed
swelling of the feet, which soon became painful, and finally
associated with loss of power. She had also a girdling sensation about
the abdomen and pain in the back. She was {265} admitted to the
hospital one week later, at which time there was retention of the
urine and feces. She had some soreness and tenderness of the
epigastrium. She complained of dyspnœa, which was apparently
independent of any pulmonary trouble. It was necessary to use the
catheter for one week, by which time control of the bladder had been
regained. The bowels were regulated by purgatives. She was given large
doses of ergot and bromide and iodide of potassium, and slowly
improved, and after a time was able to get out of bed and walk with
the aid of a chair. An examination at the time showed that the
girdling pain had disappeared. There was distinct loss of sensation.
Testing the farado-contractility, it was found that in the right leg
the flexors only responded to the slowly-interrupted current, while in
the left both flexors and extensors responded to the interrupted
current. In both limbs with the galvanic current the flexors responded
to twenty cells, while the extensors responded to fifty cells. She
gradually improved, and was able to leave after having been in the
hospital three months.

The diagnosis of subacute myelitis of the anterior horns from
hysterical paraplegia is often of vital importance. “A young woman,”
says Bennett,[107] “suddenly or gradually becomes paralyzed in the
lower extremities. This may in a few days, weeks, or months become
complete or may remain partial. There is no loss of sensation, no
muscular rigidity, no cerebral disturbances, nor any general affection
of the bladder or rectum. The patient's general health may be robust
or it may be delicate. She may be of emotional and hysterical
temperament, or, on the contrary, of a calm and well-balanced
disposition. At first there is no muscular wasting, but as the disease
becomes chronic the limbs may or may not diminish in size. The entire
extremity may be affected or only certain groups of muscles. Finally,
the disease may partially or entirely recover, or remain almost
unchanged for years.” This is a fair general picture of either
disease.

[Footnote 107: _Lancet_, vol. ii. p. 842, November, 1882.]

Two facts are often overlooked in this connection: first, that
poliomyelitis is just as liable to occur in the hysterical as in the
other class; and, secondly, that the symptoms of hysterical paraplegia
and poliomyelitis may go hand in hand.

The history is different in the two affections. Frequent attacks of
paralysis in connection with hysterical symptoms are very suggestive,
although not always positive. In poliomyelitis the disease may come on
with diarrhœa and fever; often it comes on with vomiting and pain. The
patellar reflex is retained, often exaggerated, and rarely lost, in
hysteria, while it is usually lost in poliomyelitis. Electro-muscular
contractility is often normal in hysterical paralysis, although it is
sometimes slightly diminished quantitatively to both faradism and
galvanism: the various muscles of one limb respond about equally to
electricity: there are no reactions of degeneration in hysterical
paralysis as in poliomyelitis. In poliomyelitis reactions of
degeneration are one of the most striking features. The cutaneous
plantar reflex is impaired in hysterical paraplegia; bed-sores are
usually absent, as are also acute trophic eschars and the
nail-markings present both in generalized subacute myelitis and
diffused myelitis. True muscular atrophy is also wanting in hysterical
paraplegia, although the limbs may be lean and wasted from the
original {266} thinness of the patient or from disuse. The temperature
of the limbs is usually good. There is no blueness nor redness of the
limbs, nor are the bowels or bladder uncomfortably affected.

Buzzard[108] gives two diagrams (Figs. 16 and 17), which I have
reproduced. They are drawn from photographs. They show two pairs of
feet, which have a certain superficial resemblance. In each the inner
border is drawn up into the position of a not severe varus. They are
the feet of two young women who were in the hospital at the same time.
A (Fig. 16), really a case of acute myelitis, had been treated as a
case of hysteria; and B (Fig. 17), really a case of hysteria, came in
as a paralytic. In these cases the results of examination into the
state of the electrical response and of the patellar-tendon reflex was
sufficient to make a diagnosis clear. In the organic case the
electrical reactions were abnormal and the patellar-tendon reflex was
abolished. These conditions were not present in the hysterical case.

[Illustration: FIG. 16.]

[Illustration: FIG. 17.]

[Footnote 108: _Clin. Lectures on Diseases of the Nervous System_,
London, 1882.]

The diagnosis of hysterical paraplegia from diffused myelitis is
governed practically by the same rules which serve in subacute
myelitis of the anterior horns, with some additional points. In
diffused myelitis, in addition to the motor, trophic, vaso-motor,
electrical, and reflex disorders of myelitis of the anterior horns,
affections of sensibility from involvement of the sensory regions of
the cord will also be present. Anæsthesia and paræsthesia will be
present.

Acute ascending paralysis, the so-called Landry's paralysis,
particularly when it runs a variable course, might be mistaken
sometimes for hysterical paralysis. In one instance I saw a fatal case
of Landry's paralysis which had been supposed to be hysterical until a
few hours before death. In Landry's paralysis, however, the swiftly
ascending character of the disorder is usually so well marked as to
lead easily to the diagnosis. In Landry's paralysis the loss of power
begins first in the legs, but soon becomes more pronounced, and passes
to the arms, and in the worst cases swallowing and respiration become
affected.

Spinal hemorrhage and spinal tumors, giving rise to paralysis, may be
mistaken for hysterical paralysis, partly because of the contractures.
Reactions of degenerations are usually features of this form of
organic paralysis. The contractures of hysterical paralysis can be
promptly {267} relieved by deep, strong pressure along supplying
nerve-trunks; this cannot be accomplished in the organic cases. Severe
localized pains in the limbs, sometimes radiating from the spinal
column, are present in the organic cases. Pain may be complained of by
the hysterical patient, but close examination will show that it is not
of the same character, either as regards severity or duration.

Hysterical locomotor ataxy is usually readily distinguished from
posterior spinal sclerosis, although the phenomena are apparently more
marked and more peculiar than those exhibited as the result of organic
changes. Hysterical ataxic patients often show an extraordinary
inability to balance their movements, this want of co-ordinating power
being observed even in the neck and trunk, as well as the limbs. In
hysterical cases a certain amount of palsy, often of an irregular
type, is more likely to be associated with the ataxia than in the
structural cases. The knee-jerk, so commonly absent in true posterior
spinal sclerosis that its absence has come to be regarded as almost a
pathognomonic symptom of this affection, in hysterical motor ataxy is
present and exaggerated. In hysterical locomotor ataxy other
well-marked symptoms of general hysteria, such as hysterical
convulsions, aphonia, etc., are present.

In the diagnosis of spastic spinal paralysis from hysterical
paraplegia great difficulties will sometimes arise. A complete history
of the case is of the utmost importance in coming to a conclusion. If
the case be hysterical, usually some account of decided hysterical
manifestation, such as aphonia, sudden loss and return of sight,
hysterical seizures, etc., can be had. Althaus holds that a
dynamometer which he has had constructed for measuring the force of
the lower extremities will, at least in a certain number of cases,
enable us to distinguish between the functional and spinal form of
spastic paralysis. In the former, although the patient may be unable
to walk, the dynamometer often exhibits a considerable degree of
muscular power; while in the latter, more especially where the disease
is somewhat advanced, the index of the instrument will only indicate
20° or 30° in place of 140° or 160°, and occasionally will make no
excursion at all.

The diagnosis of multiple cerebro-spinal sclerosis from hysteria
occasionally offers some difficulties. Jolly goes so far as to say
that it can only with certainty be diagnosticated in some cases in its
later stages and by the final issue—cases in which the paralytic
phenomena frequently alter their position, in which paroxysmal
exacerbations and as sudden ameliorations take place, and convulsive
attacks and disturbances of consciousness of a like complicated nature
as in hysteria are met with. Disorders of deglutition and
articulation, also characteristic of multiple cerebro-spinal
sclerosis, are now and again observed in the hysterical. Recently,
through the kindness of J. Solis Cohen, I saw at the German Hospital
in Philadelphia a patient about whom there was for a time some doubt
as to whether the peculiar tremor from which he suffered was
hysterical or sclerotic. At rest and unobserved, he was usually quiet,
but as soon as attention was directed to him the tremor would begin,
at first in the limbs, but soon also in the head and trunk. If while
under observation he attempted any movement with his hands or feet,
the tremor would become violent, and if the effort was persisted in it
would become convulsive in character. The effort to take a glass of
water threw him into {268} such violent spasms as to cause the water
to be splashed in all directions. The fact that this patient was a
quiet, phlegmatic man of middle age, that his troubles had come on
slowly and had progressively increased, that tremor of the head and
trunk was present, that cramps or tonic spasms of the limbs came and
went, indicated the existence of disseminated sclerosis. The knee-jerk
was much exaggerated, taps upon the patellar tendon causing decided
movement; when continued, the leg would be thrown into violent spasm.

Spondylitis, or caries of the vertebræ, is sometimes difficult to
distinguish from hysterical paraplegia or hysterical paraplegia from
it, or both may be present in the same case. Likewise, painful
paraplegia from cancer or sarcoma of the vertebræ may offer some
difficulties. A woman aged forty-four when two years old had a fall,
which was followed by disease of the spine, and has resulted in the
characteristic deformity of Pott's disease. She was apparently well,
able to do ordinary work, until about five years before she came under
observation, when her legs began to feel heavy and numb, and with this
were some pain and slight loss of power. These symptoms increased, and
in three months were followed by a total loss of power in the lower
extremity. She was admitted to the hospital, and for about three years
was unable to move the legs. She went round the wards in a wheeled
chair. The diagnosis was made of spondylitis, curvature, and paralysis
and sensory disorders depending on compression myelitis, and it was
supposed she was beyond the reach of remedies. One day one of the
resident physicians gave her a simple digestant or carminative, soon
after which she got up and walked, and has been walking ever since.
She attributes her cure entirely to this medicine.

What is the lesson to be learned from this case? It is, in the first
place, not to consider a patient doomed until you have made a careful
examination. There can be much incurvation of the spine without
sufficient compression to cause complete paralysis. In this patient
organic disease was associated with an hysterical or neuromimetic
condition. This woman had disease of the vertebræ, the active symptoms
of which had subsided. The vertebral column had assumed a certain
shape, and the cord had adjusted itself to this new position, yet for
a long time she was considered incurable from the fact that the
conjunction of a real and a mimetic disorder was overlooked.

Another patient aged twenty-seven had whooping cough, which lasted six
weeks, and was followed by severe pain in the back. For this she
consulted various physicians, being treated for Pott's disease and
spinal irritation. She, however, continued to grow worse, and every
jar and twist gave severe pain. At this time she had lost much flesh,
had pain in her back and elsewhere, and was subject to numerous and
violent spasms. When first seen by the physician who consulted me she
was complaining of pains in her legs, hips, and left shoulder, which
she considered rheumatic, and with pain in the abdomen. Examination of
the back with the patient on her side showed a slight prominence over
the position of the first or second lumbar vertebra. The spot was
painful on pressure, and had been so ever since the attack of whooping
cough three years before. A tap on the sole of either foot made her
complain of severe pain in the back. The same result followed pressure
on the head. The {269} patient was unable to stand or walk, but
occasionally sat up for a short time, although suffering all the time.
There was no muscular rigidity. The limbs and body were quite thin,
but, so far as could be detected, she had no loss of motor or sensory
power. At times, when the pains were worse, the arms would be flexed
involuntarily, and she stated that once the spine was drawn back and a
little sideways. The pain in the hips was augmented by pressure.
During the application of a plaster bandage she had a sort of fit and
fainted, and the application was suspended. She soon recovered
consciousness, but refused to allow the completion of the dressing. I
diagnosticated the affection as largely hysterical, and a few months
later received word that the patient was on her feet and well.

Kemper[109] relates the case of a lady who eventually died of sarcoma
of the vertebræ, the specimens having been examined by J. H. C. Simes
of Philadelphia and myself. She was supposed at first and for some
time to be a case of hysteria with spinal irritation. In the case of a
distinguished naval officer, who died of malignant vertebral disease
after great suffering a short time since, this same mistake was made
during the early stages of the disease: his case was pronounced to be
one of neurasthenia, hysteria, etc. before its true nature was finally
discovered. The absence of muscular rigidity in the back and
extremities is the strongest point against vertebral disease in these
cases.

[Footnote 109: _Journal of Nervous and Mental Diseases_, vol. xii.,
No. 1, January, 1885.]

In hysterical hemianæsthesia, ovarian hyperæsthesia, hystero-epileptic
seizures, ischuria, and other well-known hysterical symptoms have
usually been observed. The anæsthesia in hysterical cases is most
commonly on the left side of the body, but it may happen to be so
located in an organic case, so that this point is only one of slight
value.

Some older observers, as Briquet, who is quoted and criticised by
Charcot, believed that hemianæsthesia from encephalic lesions differed
from hysterical hemianæsthesia by the fact that in the former case the
skin of the face did not participate in the insensibility, or that
when it existed it never occupied the same side as the insensibility
of the limbs. Recently-reported cases have disproved the accuracy of
this supposed diagnostic mark. In his lectures, delivered ten years
ago, Charcot observed that up to that period anæsthesia of general
sensibility alone appeared to have been observed as a consecutive on
an alteration of the cerebral hemispheres, so that obtunding of the
special senses would remain as a distinctive characteristic of
hysterical hemianæsthesia. He, however, expected that cases of
cerebral organic origin would be reported of complete hemianæsthesia,
with derangements of the special senses, such as is presented in
hysteria. His anticipations have been fulfilled. In the nervous wards
of the Philadelphia Hospital is now a typical case of organic
hemianæsthesia in which the special senses are partially involved.

Paralysis and contractures, if present, are apt to be accompanied in
cases of organic hemianæsthesia, after time has elapsed, by marked
nutritive changes, by wasting of muscle, and even of skin and bone.
This is not the case in hysteria.

The subsequent history of these two conditions is different. The
hysterical patient will often recover and relapse, or under proper
{270} treatment may entirely recover; while all the treatment that can
be given in a case of organic hemianæsthesia will produce no decided
improvement, for there is a lesion in the brain which will remain for
ever. Hemianopsia, so far as I know, has not been observed in
hysterical hemianæsthesia.

In the monograph of Shaffer, with reference to both true and false
knee-joint affections certain conclusions are drawn which I will give
somewhat condensed:

Chronic synovitis produces very few if any subjective symptoms;
hysterical imitation presents a long train of both subjective and
objective symptoms and signs, the former in excess. Chronic ostitis
may be diagnosticated if muscular spasm cannot be overcome by
persistent effort; when the spasm does not vary night nor day; when it
is not affected by the ordinary doses of opium or chloral; when
reaction of the muscles to the faradic current is much reduced; when a
local and uniform rise of temperature over the affected articulation
is present; when purely involuntary neural symptoms, such as muscular
spasm, pain, and a cry of distress, are present. Hysterical knee-joint
is present, according to this author, when the muscular rigidity or
contracture is variable, and can be overcome by mildly persistent
efforts while the patient's mind is diverted, or which yields to
natural sleep, or which wholly disappears under the usual doses of
opium or chloral; when the faradic response is normal; when rise of
temperature is absent or a reduced temperature is present over the
joint; when variable and inconstant, emotional, and semi-voluntary
manifestations are present.

To recognize the neuromimesis of hip disease Shaffer gives the
following points: The limp is variable and suggests fatigue; it is
much better after rest; it almost invariably follows the pain. Pain of
a hyperæsthetic character is usually the first symptom, and it is
found most generally in the immediate region of the joint. “In place
of an apprehensive state in response to the tests applied will be
found a series of symptoms which are erratic and inconstant. A
condition of muscular rigidity often exists, but, unlike a true
muscular spasm, it can in most cases be overcome in the manner before
stated. A very perceptible degree of atrophy may exist—such, however,
as would arise from inertia only. A normal electrical contractility
exists in all the muscles of the thigh.”

In the neuromimesis of chronic spondylitis or hysterical spine the
pain is generally superficial, and is almost always located over or
near the spinous processes; it is sometimes transient, and frequently
changes its location from time to time; a normal degree of mobility of
the spinal column under properly directed manipulation is preserved;
the nocturnal cry and apprehensive expression of Pott's disease are
wanting.

With reference to the hysterical lateral curvature, Shaffer, quoting
Paget, says “ether or chloroform will help. You can straighten the
mimic contracture when the muscles cannot act; you cannot so
straighten a real curvature.”

In the diagnosis of local hysterical affections one point emphasized
by Skey is well worthy of consideration; and that is that local forms
of hysteria are often not seen because they are not looked for. “If,”
says he, “you will so focus your mental vision and endeavor to
distinguish the minute texture of your cases, and look into and not at
them, you will {271} acknowledge the truth of the description, and you
will adopt a sound principle of treatment that meets disease face to
face with a direct instead of an oblique force.” According to Paget,
the means for diagnosis in these cases to be sought—(1) in what may be
regarded as the predisposition, the general condition of the nervous
system, on which, as in a predisposing constitution, the nervous
mimicry of disease is founded; (2) in the events by which, as by
exciting causes, the mimicry may be evoked and localized; (3) in the
local symptoms in each case.

Local symptoms as a means of diagnosis can sometimes be made use of in
general hysteria. A case may present symptoms of either the gravest
form of organic nervous disease or the gravest form of hysteria, and
be for a time in doubt, when suddenly some special local manifestation
appears which cannot be other than hysterical, and which clinches the
diagnosis. In a case with profound anæsthesia, with paraplegia and
marked contractures, with recurring spasms of frightful character, the
sudden appearance of aphonia and apsithyria at once cleared all
remaining doubt. Herbert Page mentions the case of a man who suffered
from marked paraplegia and extreme emotional disturbance after a
railway collision, who, nine months after the accident, had an attack
of aphonia brought on suddenly by hearing of the death of a friend. He
eventually recovered.

To detect hysterical or simulated blindness the methods described by
Harlan are those adopted in my own practice. When the blindness is in
both eyes, optical tests cannot be applied. Harlan suggests
etherization.[110] In a case of deception, conscious or unconscious,
he says, “as the effect of the anæsthetic passed off the patient would
probably recover the power of vision before his consciousness was
sufficiently restored to enable him to resume the deception.”
Hutchinson cured a case of deaf-dumbness by means of etherization. For
simulated monocular blindness Graefe's prism-test may be used: “If a
prism held before the eye in which sight is admitted causes double
vision, or when its axis is held horizontally a corrective squint,
vision with both eyes is rendered certain.” It should be borne in mind
that the failure to produce double images is not positive proof of
monocular blindness, for it is possible that the person may see with
either eye separately, but not enjoy binocular vision, as in a case of
squint, however slight. Instead of using a prism while the patient is
reading with both eyes at an ordinary distance, say of fourteen or
sixteen inches, on some pretext slip a glass of high focus in front of
the eye said to be sound. If the reading is continued without change,
of course the amaurosis is not real. Other tests have been
recommended, but these can usually be made available.

[Footnote 110: _Loc. cit._]

The diagnosis of hysterical, simulated, or mimetic deafness is more
difficult than that of blindness. When the deafness is bilateral, the
difficulty is greater than when unilateral. The method by etherization
just referred to might be tried. Politzer in his work on diseases of
the ear[111] makes the following suggestions: Whether the patient can
be wakened out of sleep by a moderately loud call seems to be the
surest experiment. But, as in total deafness motor reflexes may be
elicited by the concussion of loud sounds, {272} care must be taken
not to go too near the person concerned and not to call too loudly.
The practical objection to this procedure in civil practice would seem
to be that we are not often about when our patients are asleep. In
unilateral deafness L. Müller's method is to use two tubes, through
which words are spoken in both ears at the same time. When unilateral
deafness is really present the patient will only repeat what has been
spoken in the healthy ear, while when there is simulation he becomes
confused, and will repeat the words spoken into the seemingly deaf ear
also. To avoid mistakes in using this method, a low voice must be
employed.

[Footnote 111: _A Textbook of the Diseases of the Ear and Adjacent
Organs_, by Adam Politzer, translated and edited by James Patterson
Cassells, M.D., M. R. C. S. Eng., Philada., 1883.]

Mistakes in diagnosis where hysteria is in question are frequently due
to that association with it of serious organic disease of the nervous
system of which I have already spoken at length under Complications.
This is a fact which has not been overlooked by authors and teachers,
but one on which sufficient stress has not yet been laid, and one
which is not always kept in mind by the practitioner. Bramwell says:
“Cases are every now and again met with in which serious organic
disease (myelitis and poliomyelitis, anterior, acute, for example) is
said to be hysterical. Mistakes of this description are often due to
the fact that serious organic disease is frequently associated with
the general symptoms and signs of hysteria; it is, in fact, essential
to remember that all cases of paraplegia occurring in hysterical
patients are not necessarily functional—_i.e._ hysterical; the
presence of hysteria or a history of hysterical fits is only
corroborative evidence, and the (positive) diagnosis of hysterical
paraplegia should never be given unless the observer has, after the
most careful examination, failed to detect the signs and symptoms of
organic disease.”

PROGNOSIS.—Hysteria may terminate (1) in permanent recovery; (2) in
temporary recovery, with a tendency to relapse or to the establishment
of hysterical symptoms of a different character; (3) in some other
affection, as insanity, phthisis, or possibly sclerosis; (4) in death,
but the death in such cases is usually not the direct result of
hysteria, but of some accident. Death from intercurrent disorders may
take place in hysteria. It is altogether doubtful, however, whether
the affection which has been described as acute fatal hysteria should
be placed in the hysterical category. In the cases reported the
symptom-picture would in almost every instance seem to indicate the
probability of the hysteria having been simply a complication of other
disorders, such as epilepsy, eclampsia, and acute mania.

As a rule, hysterical patients will not starve themselves. They may
refuse to take food in the presence of others, or may say they will
not eat at all; but they will in some cases at the same time get food
on the sly or hire their nurses or attendants to procure it for them.
In treating such cases a little watchfulness will soon enable the
physician to determine what is best to be done. By discovering them in
the act of taking food future deception can sometimes be prevented.
Hysterical patients do sometimes, however, persistently refuse food.
These cases may starve to death if let alone; and it is important that
the physician should promptly resort to some form of forcible feeding
before the nutrition of the patient has reached too low an ebb. I have
seen at least two cases of hysteria or hysterical insanity in which
patients were practically allowed to starve themselves to death, but
an occurrence of {273} this kind is very rare. Feeding by means of a
stomach-tube, or, what is still better, by a nasal tube, as is now so
frequently practised among the insane, should be employed. Nourishment
should be administered systematically in any way possible until the
patient is willing to take food in the ordinary way. In purposive
cases some methods of forcible feeding may prove of decided advantage.
Its unpleasantness will sometimes cause swallowing power to be
regained.

Wunderlich[112] has recorded the case of a servant-girl, aged
nineteen, who, after a succession of epileptiform fits, fell into a
collapse and died in two days. Other cases have been recorded by
Meyer. Fagge also speaks of the more chronic forms of hysteria proving
fatal by marasmus. He refers to two cases reported by Wilks, both of
which were diagnosticated as hysterical, and both of which died. Sir
William Gull describes a complaint which he terms anorexia nervosa vel
hysterica. It is attended with extreme wasting; pulse, respiration,
and temperature are low. The patients were usually between the ages of
sixteen and twenty-three: some died; others recovered under full
feeding and great care. In many of the reported fatal cases careful
inquiry must be made as to this question of hysteria being simply a
complication.

[Footnote 112: Quoted in _The Principles and Practice of Medicine_, by
the late Charles Hilton Fagge, M.D., F. R. C. P., etc., vol. i. 1886,
p. 736.]

Are not hysterical attacks sometimes fatal? With reference to one of
my cases this view was urged by the physician in attendance.
Gowers[113] on this point says: “As a rule to which exceptions are
infinitely rare, hysterical attacks, however severe and alarming in
aspect, are devoid of danger. The attacks of laryngeal spasm present
the greatest apparent risk to life.” He refers to the paroxysms of
dyspnœa presented by a hemiplegic girl as really alarming in
appearance, even to those familiar with them. He refers also to a case
of Raynaud's[114] in which the laryngeal and pharyngeal spasm
coexisted with trismus, and the patient died in a terrible paroxysm of
dyspnœa. The patient presented various other hysterical
manifestations, and a precisely similar attack had occurred previously
and passed away, but she had in the interval become addicted to the
hypodermic injection of morphia, and Raynaud suggested that it might
have been the effect of this on the nerve-centres that caused the
fatal termination. Such cases have been described in France as the
hydrophobic form of hysteria.

[Footnote 113: _Epilepsy and Other Chronic Convulsive Diseases_, by
W. R. Gowers, M.D., London. 1881.]

[Footnote 114: _L'Union médical_, March 15, 1881.]

Patients may die in hysterical as in epileptic attacks from causes not
directly connected with the disease. One of these sources of danger
mentioned by Gowers is the tendency to fall on the face sometimes met
with in the post-epileptic state. He records an example of death from
this cause. He also details a case of running hysteria or
hystero-epilepsy, in which, after a series of fits lasting about four
hours, the child died, possibly from some intercurrent accident.

TREATMENT.—Grasset,[115] speaking of the treatment of hysteria, says
that means of treating the paroxysm, of removing the anæsthesia, of
combating single symptoms, are perhaps to be found in abundance, but
the groundwork of the disease, the neurosis or morbid state, is not
attacked. Here he indicates a new and fruitful path. In his own {274}
summing up, however, he can only say that the hysterical diathesis
offers fundamental grounds for the exhibition of arsenic, silver,
chloride of gold, and mineral waters!

[Footnote 115: _Brain_, January, 1884.]

No doubt can exist that the prophylactic and hygienic treatment of
hysteria is of paramount importance. To education—using the term
education in a broad sense—before and above all, the most important
place must be given. It is sometimes better to remove children from
their home surroundings. Hysterical mothers develop hysterical
children through association and imitation. I can scarcely, however,
agree with Dujardin-Beaumetz that it is always a good plan to place a
girl in a boarding-school far from the city. It depends on the school.
A well-regulated institution may be a great blessing in this
direction; one badly-managed may become a hotbed of hysteria.

Recently I made some investigations into the working of the
public-school system of Philadelphia, particularly with reference to
the question of overwork and sanitation.[116] I had special
opportunities during the investigations to study the influences of
different methods of education, owing to the fact that the
public-school system of Philadelphia is just now in a transition
period. This system is in a state of hopeful confusion—hopeful,
because I believe that out of its present condition will come
eventually a great boon to Philadelphia. At one end of the system, in
the primary and the secondary schools, a graded method of instruction
has been introduced. The grammar and the high schools are working on
an ungraded or differently graded method. I found still prevailing,
particularly in certain of the grammar schools for girls, although not
to the same extent as a few years since, methods of cramming and
stuffing calculated above all to produce hysteria and allied disorders
in those predisposed to them.

[Footnote 116: The results of these investigations were given in a
lecture which was delivered in the Girls' Normal School of
Philadelphia before the Teachers' Institute of Philadelphia, Dec. 11,
1885.]

Education should be so arranged as to develop the brain by a natural
process—not from within outward; not from the centre to the periphery;
not from above downward; but as the nervous system itself develops in
its evolution from a lower to a higher order of animals, from the
simple to the more complex and more elaborate. Any system of education
is wrong, and is calculated to weaken and worry an impressionable
nervous system, which attempts to overturn or change this order of the
progress of a true development of the brain. To develop the nervous
system as it should be developed—slowly, naturally, and evenly—it must
also be fed, rested, and properly exercised.

In those primary schools in which the graded method was best carried
out this process of helping natural development was pursued, and the
result was seen in contented faces, healthy bodies, and cheerful
workers. In future the result will be found in less chorea, hysteria,
and insanity.

To prevent the development of hysteria, parents and physicians should
direct every effort. The family physician who discovers a child to be
neurotic, and who from his knowledge of parents, ancestors, and
collateral relatives knows that a predisposition to hysteria or some
other neurosis is likely to be present, should exercise all the moral
influence which he possesses to have a healthy, robust training
provided. It is not within the {275} scope of an article of this kind
to describe in great detail in what such education should consist.
Reynolds is correct when he says that “self-control should be
developed, the bodily health should be most carefully regarded, and
some motive or purpose should be supplied which may give force,
persistence, unity, and success to the endeavors of the patient.” In
children who have a tendency to the development of hysteria the
inclinations should not always or altogether be regarded in choosing a
method or pursuing a plan of education. It is not always to what such
a child takes that its mind should be constantly directed; but, on the
contrary, it is often well to educate it away from its inclination.
“The worst thing that can be done is that which makes the patient know
and feel that she is thought to be peculiar. Sometimes such treatment
is gratifying to her, and she likes it—it is easy and it seems kind to
give it—but it is radically wrong.”

In providing for the bodily health of hysterical children it should be
seen that exercise should be taken regularly and in the open air, but
over-fatigue should be avoided; that ample and pleasant recreation
should be provided; that study should be systematic and disciplinary,
but at the same time varied and interesting, and subservient to some
useful purpose; that the various functions of secretion, excretion,
menstruation should be regulated.

The importance of sufficient sleep to children who are predisposed to
hysteria or any other form of nervous or mental disorder can scarcely
be over-estimated. The following, according to J. Crichton
Browne,[117] is the average duration of sleep required at different
ages: 4 years of age, 12 hours; 7 years of age, 11 hours; 9 years of
age, 10½ hours; 14 years of age, 10 hours; 17 years of age, 9½ hours;
21 years of age, 9 hours; 28 years of age, 8 hours. To carefully
provide that children shall obtain this amount of sleep will do much
to strengthen the nervous system and subdue or eradicate hysterical
tendencies. Gymnastics, horseback riding, walking, swimming, and
similar exercises all have their advantages in preventing hysterical
tendencies.

[Footnote 117: _Education and the Nervous System_, reprinted from _The
Book of Health_ by permission of Messrs. Cassell & Co., Limited.]

Herz[118] has some instructive and useful recommendations with
reference to the treatment of hysteria in children. It is first and
most important to rehabilitate the weakened organism, and especially
the central nervous system, by various dietetic, hygienic, and
medicinal measures. It is important next to tranquillize physical and
mental excitement. This can sometimes be done by disregard of the
affection, by neglect, or by removal or threatened removal of the
child from its surroundings. Such treatment should of course be
employed with great discretion. Anæmia and chlorosis, often present in
the youthful victims of hysteria, should be thoroughly treated. Care
should be taken to learn whether children of either sex practise
masturbation, which, Jacobi and others insist, frequently plays an
important part in the production of hysteria. Proper measures should
be taken to prevent this practice. The genital organs should receive
examination and treatment if this is deemed at all necessary. On the
other hand, care should be taken not to direct the attention of
children unnecessarily to those organs when they are entirely innocent
{276} of such habits. Painting the vagina twice daily with a 10 per
cent. solution of hydrochlorate cocaine has been found useful in
subduing the hyper-irritation of the sexual organs in girls accustomed
to practise masturbation. Herz, with Henoch, prefers the hydrate of
chloral to all other medicines, although he regards morphine as almost
equally valuable, in the treatment of hysteria in children.
Personally, I prefer the bromides to either morphia or chloral. Small
doses of iron and arsenic continued systematically for a long period
will be found useful. Politzer of Vienna regards the hydrobromate and
bihydrobromate of iron as two valuable preparations in the hysteria of
children, and exhibits them in doses of four to seven grains three to
four times daily.

[Footnote 118: _Wien. Med. Wochen._, No. 46, Nov. 14, 1885.]

Hysteria once developed, it is the moral treatment which often really
cures. The basis of this method of cure is to rouse the will. It is
essential to establish faith in the mind of the patient. She must be
made to feel not only that she can be helped, but that she will be.
Every legitimate means also should be taken to impress the patient
with the idea that her case is fully understood. If malingering or
partial malingering enters into the problem, the patient will then
feel that she has been detected, and will conclude that she had better
get out of her dilemma as gracefully as possible. Where simulation
does not enter faith is an important nerve-stimulant and tonic; it
unchains the will.

Many physicians have extraordinary ideas about hysteria, and because
of these adopt remarkable and sometimes outrageous methods of
treatment. They find a woman with hysterical symptoms, and forthwith
conclude she is nothing but a fraud. They are much inclined to assert
their opinions, not infrequently to the patient herself, and, if not
directly to her, in her hearing to other patients or to friends,
relatives, nurses, or physicians. They threaten, denounce, and
punish—the latter especially in hospitals. In general practice their
course is modified usually by the wholesome restraint which the
financial and other extra-hospital relations of patient and physician
enforce.

Although hysterical patients often do simulate and are guilty of
fraud, it should never be forgotten that some hysterical
manifestations may be for the time being beyond the control of
patients. Even for some of the frauds which are practised the
individuals are scarcely responsible, because of the weakness of their
moral nature and their lack of will-power. Moral treatment in the form
of reckless harshness becomes immoral treatment. The liability to
mistake in diagnosis, and the frequent association of organic disease
with hysterical symptoms, should make the physician careful and
conservative. It is also of the highest importance often that the
doctor should not show his hand. The fact that an occasional cure,
which is usually temporary, is effected by denunciation, and even
cruelty, is not a good argument against the stand taken here.

Harsh measures should only be adopted after due consideration and by a
well-digested method. A good plan sometimes is, after carefully
examining the patient, to place her on some simple, medicinal, and
perhaps electrical treatment, taking care quietly to prophesy a speedy
cure. If this does not work, in a few days other severe or more
positive measures may be used, perhaps blistering or strong electrical
currents. Later, but in rare cases only, after giving the patient a
chance to arouse {277} herself by letting her know what she may
expect, painful electrical currents, the hot iron, the cold bath, or
similar measures may be used. Such treatment, however, should never be
used as a punishment.

The method of cure by neglect can sometimes be resorted to with
advantage. The ever-practical Wilks mentions the case of a
school-teacher with hemianalgesia, hemianæsthesia, and an array of
other hysterical symptoms who had gone through all manner of
treatment, and at the end of seven months was no better. The doctor
simply left her alone. He ordered her no drugs, and regularly passed
by her bed. In three weeks he found her sitting up. She talked a
little and had some feeling in her right side. She was now encouraged,
and made rapid progress to recovery. Neglect had aroused her dormant
powers. It must be said that a treatment of this kind can be carried
out with far more prospects of success in a general hospital than in a
private institution or at the home of a patient. It is a method of
treatment which may fail or succeed according to the tact and
intelligence of the physician.

I cannot overlook here the consideration of the subject of the
so-called faith cure and mind cure. One difference between the faith
cure as claimed and practised by its advocates, and by those who
uphold it from a scientific standpoint, is simply that the latter do
not refer the results obtained to any supernatural or spiritual
agency. I would not advise the establishment of prayer-meetings for
the relief of hysteria, but would suggest that the power of faith be
exercised to its fullest extent in a legitimate way.

A young lady is sick, and for two years is seen by all the leading
doctors in London; a clergyman is asked in and prays over her, and she
gets up and walks. The doctors all join in and say the case was one of
hysteria—that there was nothing the matter with her. Then, says Wilks,
“Why was the girl subjected to local treatment and doses of physic for
years? Why did not the doctors do what the parson did?”

Tuke[119] devotes a chapter to psychotherapeutics, which every
physician who is called upon to treat hysteria should read. He
attempts to reduce the therapeutic use of mental influence to a
practical, working basis. I will formulate from Tuke and my own
experience certain propositions as to the employment of psychological
measures: (1) It is often important and always justifiable to inspire
confidence and hope in hysterical patients by promising cures when it
is possible to achieve cures. (2) A physician may sometimes properly
avail himself of his influence over the emotions of the patient in the
treatment of hysterical patients, but always with great caution and
discretion. (3) Every effort should be made to excite hysterical
patients to exert the will. (4) In some hysterical cases it is
advisable to systematically direct the attention to a particular
region of the body, arousing at the same time the expectation of a
certain result. (5) Combined mental and physical procedures may
sometimes be employed. (6) Hypnotism may be used in a very few cases.

[Footnote 119: _Influence of the Mind upon the Body_.]

The importance of employing mental impression is thoroughly
exemplified, if nothing else is accomplished, by a study of such a
craze as the so-called mind cure. Not a few people of supposed sense
and cultivation have pinned their faith to this latest Boston hobby. A
glance at the published writings of the apostles of the mind cure will
show at once to the {278} critical mind that all in it of value is
dependent upon the effects of mental impression upon certain peculiar
natures, some of them being of a kind which afford us not a few of our
cases of hysteria. W. F. Evans has published several works upon the
subject. From one of these[120] I have sought, but not altogether
successfully, to obtain some ideas as to the basis of the mind-cure
treatment. It is claimed that the object is to construct a theoretical
and practical system of phrenopathy, or mental cure, on the basis of
the idealistic philosophy of Berkeley, Fichte, Schelling, and Hegel.
The fundamental doctrine of those who believe in the mental cure is,
that to think and to exist are one and the same, and that every
disease is a translation into a bodily expression of a fixed idea of
mind. If by any therapeutic device the morbid idea can be removed, the
cure of the malady is assured. When the patient is passive, and
consequently impressible, he is made to fix his thoughts with
expectant attention upon the effect to be produced. The physician
thinks to the same effect, wills it, and believes and imagines that it
is being done; the mental action _to_ the patient, sympathizing with
that of the physician, is precipitated upon the body, and becomes a
silent, transforming, sanitive energy. It must be, says Evans, “a
malady more than ordinarily obstinate that is neither relieved nor
cured by it.”

[Footnote 120: _The Divine Law of Cure_.]

Hysteria cannot be cured by drugs alone, and yet a practitioner of
medicine would find it extremely difficult to manage some cases
without using drugs. Drugs themselves, used properly, may have a moral
or mental as well as a physical influence. Among those which have been
most used from before the days of Sydenham to the present time,
chiefly for their supposed or real antispasmodic virtues, are
galbanum, asafœtida, valerian, castor and musk, opium, and hyoscyamus.
The value of asafœtida, valerian, castor, and musk is chiefly of a
temporary character. If these drugs are used at all, they should be
used in full doses frequently repeated. Sumbul, a drug of the same
class comparatively little used, is with me a favorite. It can be used
in the form of tincture or fluid extract, from twenty minims to half a
drachm of the latter or one to two drachms of the former. It certainly
has in many cases a remarkably calmative effect.

Opium and its preparations, so strongly recommended by some, and
especially the Germans, should not be used except in rare cases.
Occasionally in a case with sleeplessness or great excitement it may
be absolutely indispensable to resort to it in combination with some
other hypnotic or sedative. The danger, however, in other cases of
forming the opium habit should not be overlooked. According to
Dujardin-Beaumetz, it is mainly useful in the asthenic forms of
hysteria.

Of all drugs, the metallic tonics are to be preferred in the
continuous treatment of hysteria. Iron, although not called for in a
large percentage of cases, will sometimes prove of great service in
the weak and anæmic hysterics. Chalybeates are first among the drugs
mentioned by Sydenham. Steel was his favorite. The subcarbonate or
reduced iron, or the tincture of the chloride, is to be preferred to
the more fanciful and elegant preparations with which the drug-market
is now flooded. Dialyzed iron and the mallate of iron, however, are
known to be reliable preparations, and can be resorted to with
advantage. They should be given in large doses. Zinc salts,
particularly the oxide, phosphide, and {279} valerianate; the nitrate
or oxide of silver, the ammonio-sulphate of copper, ferri-ferrocyanide
or Prussian blue,—all have a certain amount of real value in giving
tone to the nervous system in hysterical cases.

To Niemeyer we owe the use of chloride of sodium and gold in the
treatment of hysteria. He refers to the fact that Martini of Biberach
regarded this article as an efficient remedy against the various
diseases of the womb and ovaries. He believed that the improvement
effected upon Martini's patient was probably due to the fact that
this, like other metallic remedies, was an active nervine. He
prescribed the chloride of gold and sodium in the form of a pill in
the dose of one-eighth of a grain. Of these pills he at first ordered
one to be taken an hour after dinner, and another an hour after
supper. Later, he ordered two to be taken at these hours, and
gradually the dose was increased up to eight pills daily. I frequently
use this salt after the method of Niemeyer.

The treatment of hysteria which Mitchell has done so much to make
popular, that by seclusion, rest, massage, and electricity, is of
value in a large number of cases of grave hysteria; but the proper
selection of cases for this treatment is all important. Playfair[121]
says correctly that if this method of treatment is indiscriminately
employed, failure and disappointment are certain to result. The most
satisfactory results are to be had in the thoroughly broken-down and
bed-ridden cases. “The worse the case is,” he says, “the more easy and
certain is the cure; and the only disappointments I have had have been
in dubious, half-and-half cases.”

[Footnote 121: _The Systematic Treatment of Nerve-Prostration and
Hysteria_, by W. S. Playfair, M.D., F. R. C. P., 1883.]

Mitchell[122] gives a succinct, practical description of the process
of massage: “An hour,” he says, “is chosen midway between two meals,
and, the patient lying in bed, the manipulator starts at the feet, and
gently but firmly pinches up the skin, rolling it lightly between his
fingers, and going carefully over the whole foot; then the toes are
bent and moved about in every direction; and next, with the thumbs and
fingers, the little muscles of the foot are kneaded and pinched more
largely, and the interosseous groups worked at with the finger-tips
between the bones. At last the whole tissues of the foot are seized
with both hands and somewhat firmly rolled about. Next, the ankles are
dealt with in the same fashion, all the crevices between the
articulating bones being sought out and kneaded, while the joint is
put in every possible position. The leg is next treated—first by
surface pinching and then by deeper grasping of the areolar tissue,
and last by industrious and deeper pinching of the large muscular
masses, which for this purpose are put in a position of the utmost
relaxation. The grasp of the muscles is momentary, and for the large
muscles of the calf and thigh both hands act, the one contracting as
the other loosens its grip. In treating the firm muscles in front of
the leg the fingers are made to roll the muscles under the cushions of
the finger-tips. At brief intervals the manipulator seizes the limb in
both hands and lightly runs the grasp upward, so as to favor the flow
of venous blood-currents, and then returns to the kneading of the
muscles. The same process is carried on in every part of the body, and
especial care is given to the muscles of the loins and spine, while
usually the face {280} is not touched. The belly is first treated by
pinching the skin, then by deeply grasping and rolling the muscular
walls in the hands, and at last the whole belly is kneaded with the
heel of the hand in a succession of rapid, deep movements, passing
around in the direction of the colon.”

[Footnote 122: “Fat and Blood,” etc.]

Massage should often be combined with the Swedish movement cure. In
the movement cure one object is to call out the suppressed will of the
patient. This is very applicable to cases of hysteria. The cure of
cases of this kind is often delayed by using massage alone, which is
absolutely passive. These movements are sometimes spoken of as active
and passive, or as single and duplicated. Active movements are those
more or less under the control of the individual making or taking part
in them, and they are performed under the advice or direction, and
sometimes with the assistance, of another. They proceed from within;
they are willed. Passive movements come from without; they are
performed on the patient and independently of her will. She is
subjected to pushings and pullings, to flexions and extensions, to
swingings and rotations, which she can neither help nor hinder. The
same movement may be active or passive according to circumstances. A
person's biceps may be exercised through the will, against the will,
or with reference to the will.

A single movement is one in which only a single individual is engaged;
speaking medically, single movements are those executed by the patient
under the direction of the physician or attendant; they are, of
course, active. Duplicated active movements require more than one for
their performance. In these the element of resistance plays an
important part. The operator with carefully-considered exertion
performs a movement which the patient is enjoined to resist, or the
latter undertakes a certain motion or series of motions which the
former, with measured force, resists. Still, tact and experience are
here of great value, in order that both direct effort and resistance
should be carefully regulated and properly modified to suit all the
requirements of the case. By changing the position of the patient or
the manner of operating on her from time to time any muscles or groups
of muscles may be brought into play. It is wonderful with what ease
even some of the smallest muscles can be exercised by an expert
manipulator.

The duplicated active movements are those which should be most
frequently performed or attempted in connection with massage in
hysterical patients. The very substance of this treatment is to call
out that which is wanting in hysteria—will-power. It is a coaxing,
insinuating treatment, and one which will enable the operator to gain
control of the patient in spite of herself. As the patient exerts her
power the operator should yield and allow the part to be moved.

Much of the value of massage and Swedish movements, in hysteria as in
other disorders, is self-evident. Acceleration of circulation,
increase of temperature, direct and reflex stimulation of nervous and
muscular action, the promotion of absorption by pressure,—these and
other results are readily understood. “The mode in which these
gymnastic proceedings exert an influence,” says Erb,[123] “consists,
no doubt, in occasioning frequently-repeated voluntary excitations of
the nerves and muscles, so that the act of conduction to the muscles
is gradually rendered {281} more facile, and ultimately the nutrition
of the nerves and muscles is augmented.”

[Footnote 123: _Ziemssen's Cyclopædia_.]

The objects to be attained by the use of electricity are nearly the
same as from massage and duplicated active movements: in the first
place, to improve the circulation and the condition of the muscles;
and in the second place, to make the patient use the muscles. The
faradic battery should be employed in these cases, and the patient
should be in a relaxed condition, preferably in bed. A method of
electrical treatment introduced some years ago by Beard and Rockwell
is known as general faradization. This is sometimes used in the office
of the physician. In this method the patient is placed in a chair with
his feet on a large plate covered with chamois-skin; the operator then
takes hold of the patient's hand and the other electrode is passed
over the muscles of the neck, back, trunk, and extremities.

When the patient is in bed, as in the regular rest treatment, this
method has to be modified, and then the best treatment is by direct
muscular faradization. Two sponge electrodes are employed. The sponges
are moistened, so that the current may pass through the skin and reach
the muscles. Both electrodes are taken in one hand, the handle of one,
pointing backward, being between the first and second fingers, while
the handle of the other is between the third and fourth fingers. In
this way the distance between the points of application can be readily
altered. The current is then applied to the muscles everywhere,
beginning with those of the feet. Muscles should be relaxed before
passing the current through them. The whole body can be gone over in
this way in the course of half an hour.

The hydropathic treatment of hysteria is one that has much in it to be
commended. Jolly approves the systematic external application of cold
water; Chambers advocates the daily morning use of shower-baths,
holding that the bracing up of the mind to the shock of a cold
shower-bath is a capital exercise for the weak will-power of the
hysterical individual, and some admirable results have been reported
by Charcot in inveterate neurasthenics and hysterics. Hydrotherapeutic
treatment, continued perseveringly for a long time, says Rosenthal,
“diminishes the extreme impressionability of hysterical patients,
strengthens them, and increases their power of resistance to
irritating influences, stimulates the organic functions, combats the
anæmia, calms the abnormal irritability of the peripheral nervous
system, and by diminishing the morbid increase of reflex power
relieves the violence of the spasmodic symptoms. Even chronic forms
which are combined with severe paroxysms of convulsions are
susceptible of recovery under this plan of treatment.”

The hydrotherapeutic treatment may be contrasted with the treatment by
seclusion, rest, massage, and electricity. Undoubtedly, one class of
hysterical patients is greatly benefited by the latter method
systematically carried out; these have already been described. In
other cases, however, this method of treatment is useless; in some of
them it has a tendency to prolong or aggravate the hysterical
disorder, while in the same cases a well-managed hydrotherapeutic
treatment will answer admirably. This is applicable in hysterical
patients who eat and drink well, who, as a rule, preserve a good
appearance, but whose mind and muscles are equally flabby and out of
tone, and need to be stirred up both physically and mentally.

{282} Dujardin-Beaumetz recommends prolonged warm baths of from one to
two hours' duration, and believes that the therapeutic virtues of
these baths are augmented by infusions of valerian.

In order to obtain satisfactory results from hydrotherapy, as well as
from massage, electricity, etc., it is best to remove patients from
their family surroundings. Good sanitariums near our large American
cities where hydrotherapy and other special methods of treatment can
be carried out are sadly needed. Hydrotherapeutic treatment is much
more efficacious when conducted at a well-regulated institution, for
several reasons. Measures troublesome in themselves are here carried
out as a matter of daily routine. Numerous patients permit of the
employment of competent attendants. The change is often of great
benefit. The close personal supervision which hysterical patients are
likely to have in a hydrotherapeutic establishment is also to be taken
into consideration. Better modes of living, proper forms of exercise,
regulated diet, etc. also enter; but still, a fair share of the good
which results can be attributed to the water treatment.

While, however, it is better to remove hysterical patients, for
hydrotherapeutic as well as for other treatment, from their family
surroundings, and to place them in some well-regulated establishment,
it is not by any means impossible to carry out such treatment in
private practice, particularly in a house supplied with a bath-room.
Many of our hydrotherapeutic institutions are in the hands of
charlatans or of individuals who are not practically well fitted for
their work. Not infrequently, however, good results are obtained even
under these circumstances. Much more can be done in this direction
with modest buildings and appliances than is generally supposed. It is
not necessary to have numerous apartments: three or four rooms in a
well-appointed house, if the arrangements for carrying out the
hydrotherapeutic treatment are of a proper kind, will suffice for a
large amount of good work. In almost any house provided with
bath-rooms with hot and cold water some useful hydrotherapy may be
attempted. The spinal douche or pour can be used by placing the
patient in a sitz- or ordinary hip-bath and pouring the water from a
spout or hose held at a certain height, the distance being regulated
according to the patient's condition. Again, the patient sitting in a
tub, water can be poured upon her, beginning at first with a high
temperature and gradually lowering it. The shower-bath may also be
used. An extemporaneous shower-bath can be provided by an ordinary
watering-pot. Whole, three-quarters, or half baths at different
temperatures can be given. One method of carrying out the wet pack is
very simple. A comforter is spread upon the bed; next to this is
placed a woollen blanket, and over the blanket a wet linen sheet, upon
which the patient rests, with the head on a low pillow. The wet sheet,
blanket, and comforter are then wrapped closely about the patient,
bottles of hot water being placed at the feet. The cold drip-sheet
method is another easily used. It consists in placing about the
patient, while sitting up or standing, a sheet wet with cold water,
and then vigorously rubbing her through the sheet.

Baths to the head may be used in some cases; cool head-baths are most
frequently applied. One method of using these baths is to have the
patient lie in such a position that the head projects a little beyond
the {283} edge of the bed and over a basin or receptacle of some kind.
Water of a suitable temperature is then poured gently or squeezed out
of a sponge over the head. For some forms of insomnia or some of the
disorders of sleep in hysteria this treatment is a valuable auxiliary
to other measures.

For the hysterical spine cold compresses may be used along the spine.
On the other hand, hot fomentations may be found of benefit in some
cases. Where hydrotherapeutic measures are employed attention should
be paid to the condition of the circulation, particularly in the
extremities. If the feet or hands are cold, hot applications or
frictions should be used.

For certain of the vaso-motor disorders of hysteria, such as cold or
hot feet, flushings, etc., local hydrotherapeusis will be of service.
In hysterical contractures local stimulation by the douche method or
by the steam bath may be tried. For the excitable rectum cold enemata
in small quantities, so as not to be expelled, will be found to be
very efficacious. For spasmodic attacks, whether purposive or
involuntary, the use of the wet pack or the plunge-bath will sometimes
be found of good service. In neuralgias and other painful local
disorders of hysteria, frictions, fomentations, Turkish or Russian
baths, and the wet pack are often very beneficial.

When hysteria is complicated, as it very often is, with disorders of
the liver and stomach, hydrotherapeutic measures will be of added
efficacy. When it is associated with genito-urinary disorders, even
though the latter are not regarded as the cause of the former, special
beneficial effects, both local and general, can be obtained from
hydrotherapeutic measures. Locally, sitz-baths, hip-baths,
douche-baths, hot and cold injections, and foot-baths may act as
revulsives, astringents, or local tonics, while at the same time they
are measures which tend to strengthen the system as a whole.

Sea-bathing is often of the greatest value, although it is sometimes
difficult to induce hysterical patients, who are willing enough to go
to the seashore, to resort to surf-bathing. Few measures are better
calculated to bring up the tone of the nervous system of an hysterical
or neurasthenic patient than well-directed sea-bathing. Where
sea-bathing cannot be employed sea-water may be used indoors.
Sea-water establishments, where baths at various temperatures may be
had, are now to be found at all the best seaside resorts. In a few
cases the internal use of large quantities of either hot or cold
water, or of the ferruginous mineral waters, may be associated with
the external treatment.

The climatic treatment of hysteria has received little or no
attention; undoubtedly, much could be said in this connection. In a
great country like ours a climate suited to the requirements of almost
every form of disease can be had. The climate of those regions, either
of the seaboard or inland, particularly well suited to cases of lung
trouble, will often be useless, and sometimes harmful, to neurotic
patients. For a certain class of hysterical patients a sojourn at the
seashore, if not too protracted, will prove of great value. On the
whole, for most hysterical patients of the neurasthenic type the best
plan is to go first to the seashore for a few weeks, and then resort
to an inland hilly or mountainous country, but not at too great an
elevation. I have known the climate of some of the high altitudes of
Colorado to be of positive injury by depressing the nervous system.
Resorts like Capon Springs in West Virginia, out of {284} the reach of
steam and worry, with prevailing south-west winds, are desirable
places.

The treatment of hysteria by the method of metallotherapy is worthy of
some consideration. It is a method by no means new. It was known and
practised by the ancients with rings and amulets. Popularized at the
beginning of the present century by certain travelling charlatans, it
was later, for a time, wholly ignored. In recent years it has been
received with considerable attention. One Burq for many years
practised metallotherapy in Paris disregarded or scouted by the
profession, but claiming many remarkable cures. Finally, Charcot was
induced to give him an opportunity of demonstrating the truth or
falsity of his claims at Salpêtrière.[124] Cases of grave hysteria
were submitted to the treatment, and in certain instances with
striking results.

[Footnote 124: _Lancet_, Jan. 19, 1878.]

After having determined by a series of experiments the particular
metal to which the patient is sensitive, bits of metal may be applied
to the surface of the body in various places; this constitutes
external metallotherapy. Or the metal, in the form of powder (as
reduced iron) or an oxide or some other salt, may be administered;
this is internal metallotherapy. That certain definite effects may be
produced by the application of metals to the surface of the body is
unquestionable. Some of the results which have followed their
employment are the removal of anæsthesia and analgesia, relief of
hysterical paralysis, improvement in the circulation, removal of
achromatopsia, relief of contracture.

Many investigations in Germany, England, France, and this country have
demonstrated that the same or similar effects can be produced by the
application of other non-metallic substances, such as discs of wood,
minerals, mustard plasters, etc. Hammond, among others, has shown
this. How the results are obtained is still a matter of dispute. On
the one hand, it is claimed, principally by the French observers, that
the cures are due to the metals themselves, either by virtue of some
intrinsic power or through some electrical currents generated by their
application. On the other hand, it is asserted, particularly by the
English observers, that the phenomena are best explained on the
doctrine of the influence of the mind on the body; in other words, by
the principle of expectant attention. Some at least of the effects are
to be explained on the latter hypothesis, but it is likely that the
monotonous impressions made upon the peripheral sense-organs by
different substances applied locally may act reflexly on the brain.

Seguin[125] reports a case of convulsion and hemianæsthesia in an
adult male cured by metallotherapy; the metal used was gold. Two
ordinary twenty-dollar gold pieces were placed in the patient's hands,
and afterward on his forearm, cheek, and tongue. Nothing else was
suggested or done to him; sensibility returned, and the staggering and
other symptoms disappeared. The patient left the hospital claiming to
be perfectly well. The same author reports several other successful
cases of metallotherapy, all of them reactions to gold. One was a girl
sixteen years old with analgesia.

[Footnote 125: _Arch. of Medicine_, New York, 1882.]

Not a few cases are now on record of the cure of hysterical
contracture and other forms of local hysterical disorders by the
application of a magnet. Charcot and Vigouroux cured one case of
hysterical contracture {285} of the left arm by repeated applications
of the magnet to the right or healthy arm. Debove by prolonged
application of magnets relieved hemianæsthesia and hemiplegias—not
only the hysterical varieties, but also, it is said, when dependent
upon such conditions as alcoholism, plumbism, and even cerebral
lesions. Maggiorani of Rome studied the physiological action of the
magnet and laid down the first rules for its therapeutic use. In the
case of powerful magnets we have more room for believing that an
actual, tangible force is at work in producing the results than in the
case of simple metals.

The question has been sometimes asked whether hypnotism can be used
with success in the treatment of hysteria. Richer reports a few cures
of hysteria through this agency. Braid has put on record between sixty
and seventy cases which he claims to have cured by the same means.
This list undoubtedly includes some hysterical cases—of paralysis,
anæsthesia, aphonia, blindness and deafness, spinal irritation, etc.
Both on theoretical grounds and from experience, however, I believe
that the practice of hypnotization may be productive of harm in some
cases of hysteria, and should be resorted to only in rare cases of
mental or motor excitement.

By some, special measures during the hysterical fit are regarded as
unnecessary. Jolly, for instance, says that we must merely take care
that the patients do not sustain injury in consequence of their
convulsive movements, and that respiration is not impeded by their
clothing. Rothrock[126] reports several cases of hysterical paroxysms
relieved by the application of either snow or ice to the neck. The
applications were made by stroking up and down either side of the neck
along the line of the sterno-cleido-mastoid muscles. He believed that
the most probable explanation of the results obtained was the shock
received from the cold substance, but that supplemental to this there
may have been supplied through the pneumogastric nerve a besoin de
respirer. This measure and the use of the cold spinal douche are both
to be recommended.

[Footnote 126: _Philada. Med. Times_, 1872-73, iii. 67.]

Emetics are sometimes valuable. Miles[127] reports several cases of
severe hysterical seizure in which tobacco was promptly efficient in
controlling the affection. He used the vinum tabaci in doses of one
drachm every half hour or hour until the system was relaxed and nausea
induced, the effects usually being produced after taking three or four
doses. Fifteen grains of sulphate of zinc may be used in adult cases.
James Allen for a case of hysterical coma successfully used a
hypodermic injection of one-tenth of a grain of apomorphia. Recently,
at the Philadelphia Hospital this remedy has been successfully
employed in two cases, one of hysterical coma and the other of
hysterical mania. Inhalations of nitrite of amyl are often of
surprising efficiency. This and other measures referred to under
HYSTERO-EPILEPSY are also applicable in the treatment of any form of
hysterical spasm.

[Footnote 127: _Clinical Med. Reporter_, 1871, iv. 25-27.]

For hysterical convulsions occurring during pregnancy an enema of
asafœtida, camphor, the yolk of an egg, and water, such as has been
recommended by Braun of Vienna, will often be found promptly
efficacious.

Fagge[128] mentions a procedure which he had often seen adopted by
Stocker—namely, pressure upon the arteries and other structures on
each side of the neck.

[Footnote 128: _British Medical Journal_, March 27, 1880.]

{286} For hysterical paralysis faradism and galvanism hold the chief
place. Metallic-brush electricity should be used in the treatment of
anæsthesia.

Whenever, in local hysteria, particularly of the paralytic, ataxic, or
spasmodic form, it is possible to coax or compel an organ or part to
perform its usual function long unperformed or improperly performed,
treatment should be largely directed to this end. Thus, as Mitchell
has shown, in some cases of aphonia, especially in those in which loss
of voice is due to the disassociation of the various organs needed in
phonation, by teaching the patient to speak with a very full chest an
involuntary success in driving air through the larynx may sometimes be
secured. Once compel a patient by firm but gentle means to swallow,
and œsophageal paralysis begins to vanish.

Mitchell makes some interesting remarks upon the treatment of the
peculiar disorders of sleep, which he describes and to which I have
referred. When the symptoms are directly traceable to tobacco, he
believes that strychnia and alcohol are the most available remedies,
but gives a warning against the too liberal use of the latter. A
treatment which was suggested to him by a clever woman who suffered
from these peculiar attacks consists in keeping in mind the need of
breaking the attack by motion and by an effort of the will. As soon as
the attack threatens the patient should resolutely turn over, sit up,
or jump out of bed, and move about, or in some such way overcome the
impending disorder. Drugs are of little direct use. Small doses of
chloral or morphia used until the habit is broken may answer, but
general improvement in health, proper exercise, good food, and natural
sleep are much more efficient.

Fagge says that he has seen more benefit in hysterical contracture
from straightening the affected joints under chloroform, and placing
the limb upon a splint, than from any other plan of treatment.
Hammond[129] (at a meeting of the New York Neurological Society, Nov.
6, 1876) reports a case of supposed hysterical contracture in the form
of wry neck, in which he divided one sterno-cleido-mastoid muscle;
immediately the corresponding muscle of the other side became
affected; he cut this; then contraction of other muscles took place,
which he kept on cutting. The case was given up, and got well
spontaneously about two years later. Huchard[130] entirely relieved an
hysterical contracture of the forearm by the application of an elastic
bandage.

[Footnote 129: _Philadelphia Medical Times_, vol. vii., Nov. 25,
1876.]

[Footnote 130: _Revue de Thérapeutique_, quoted in _Med. Times_, vol.
xiii., June 16, 1883.]

A lady with violent hysterical cough was chloroformed by Risel of
Messeberg[131] for fourteen days at every access of the cough, and
another for eight days. In both the symptoms were conquered. Nitrite
of amyl is useful in similar cases.

[Footnote 131: _Allg. Med. Centralzeitung_, Oct. 9, 1878.]

Graily Hewitt[132] reports a case of hysterical vomiting of ten
months' duration, caused by displacement of the uterus, and cured by
reposition of that organ. The same authority, in a paper read to the
London Congress, advanced the opinion that the exciting cause of
attacks of hysteria and hystero-epilepsy was a distortion of the
uterus produced by a flexion of the organ upon itself, either forward
or backward. He believed the attacks were the result of reflex
irritation. He recited {287} eighteen cases, all of which were
relieved. Flechsig[133] favors the gynæcological treatment of
hysteria, including castration or oöphorectomy. He reports three cases
with good results. His article favors the idea that any morbid
condition of the genital organs present ought to be remedied before
treating the hysterical symptoms. Zeuner,[134] on the other hand,
refers to a number of cases in which gynæcological treatment gave
either entirely negative results or was productive of positive injury
to hysterical patients. He quotes Perreti,[135] physician to an asylum
for the insane, who gives the details of a number of cases in which
gynæcological examinations or treatment were directly productive of
injury. He mentions a case of a female patient who had delusions and
hallucinations of a sexual type in which the physician was the central
figure. He reports cases in which proper constitutional treatment,
without gynæcological interferences, led to a full recovery. Playfair,
also quoted by Zeuner, states that he has often known the condition of
hysterical patients to be aggravated by injudicious gynæcological
interference. Oöphorectomy will be more fully discussed under
HYSTERO-EPILEPSY.

[Footnote 132: _Med. Press and Circ._, June 2, 1880.]

[Footnote 133: _Neurol._, 7 Abt., 1885, Nos. 19, 20.]

[Footnote 134: _Journ. American Med. Ass._, Chicago, 1883, i.
523-525.]

[Footnote 135: _Berliner klinische Wochenschrift_, No. 10.]


{288}


HYSTERO-EPILEPSY.

BY CHARLES K. MILLS, M.D.


DEFINITION.—Hystero-epilepsy is a form of grave hysteria characterized
by involuntary seizures in which the phenomena of hysteria and
epilepsy are commingled, and by the presence in unusual number and
severity, between the paroxysms, of symptoms of profound and extensive
nervous disturbance, such as paralysis, contracture, hemianæsthesia,
hyperæsthesia, and peculiar psychical disorders.

SYNONYMS.—Hystero-epilepsy has long been known under various names, as
Epileptiform hysteria, by Loyer-Villermay and Tissot; as Hysteria with
mixed attacks, by Briquet; as Hysteria major or Grave hysteria, by
Charcot. The term hystero-epilepsy has been used with various
significations, and often without due consideration, and for these
reasons some authorities advise that it should not be used at all.
Gowers,[1] for instance, refers to epileptic hysteria, hysterical
epilepsy, and hystero-epilepsy as hybrid terms which tend rather to
hinder than to advance the study of the nature of these convulsive
attacks and their relations to other forms of hysteria. He holds that
it is a clear advantage to discard them as far as possible, and
suggests the use of the term hysteroid, as proposed by W. W. Roberts,
or that of co-ordinate convulsions, as describing accurately the
character of the attack. These suggested terms do not strike me as
improvements upon those which he wishes the profession to avoid. The
word hysteroid, while good enough in its way, is certainly
objectionable on the ground of indefiniteness. Co-ordinate is
proposed, because the convulsive movements are of a quasi-purposive
appearance; that is, they are so grouped as to resemble phenomena
which may be controlled by the will. This meaning of co-ordinate,
however, as applied to the disorder in question, would not be easily
grasped by the average physician. When it is impossible to name a
disease from the standpoint of its pathological anatomy, the next best
plan is to use a clinical term which in a plain common-sense manner
gives a fair idea of the main phenomena of the affection.
Hystero-epilepsy, if it means anything, means simply a disorder in
which the phenomena of both hysteria and epilepsy are to some degree
exhibited. Certainly, this is what is seen in the cases known as
hystero-epileptic. In forming the compound the hysterical element is,
very properly, expressed first, the disease being a hysteria with
epileptic {289} or epileptoid manifestations, rather than an epilepsy
with hysterical or hysteroid manifestations. A study of the definition
of hystero-epilepsy which has been given will show that it is intended
to restrict the application of the term in the present article to
cases with involuntary or non-purposive attacks, the voluntary or
purposive having been considered in the last article.

[Footnote 1: _Epilepsy and other Chronic Convulsive Diseases: their
Causes, Symptoms, and Treatment_, by W. R. Gowers, M.D., F. R. C. P.,
etc., London, 1881.]

HISTORY.—The greatest impulse to the study of hystero-epilepsy in
recent years has been given by the brilliant labors of Charcot and his
pupils and assistants in his famous service at La Salpêtrière. In his
lectures on diseases of the nervous system[2] (edited by Bourneville),
and in various publications in _Le Progrès médical_ and other
journals, Charcot has reinvestigated hysteria major with great
thoroughness, and has thrown new light upon many points before in
obscurity. He deserves immense credit also for the work which he has
stimulated others to do. Bourneville, well known as the editor of some
of Charcot's most valuable works, has published, alone or with others,
several valuable monographs upon hysteria and epilepsy.[3] The most
valuable work on hystero-epilepsy, however, because the most elaborate
and comprehensive, is the treatise of Richer.[4] Richer was for a time
interne in the Salpêtrière Hospital, and with Regnard pursued his
investigations under the superintendence and direction of Charcot. His
book is a volume of more than seven hundred pages, containing a vast
amount of information and profusely illustrated, in large part by
original sketches by the author. Charcot himself has written for it a
commendatory preface.

[Footnote 2: _Leçons sur les Maladies du Système nerveux_. A portion
of these lectures have been translated by G. Sigerson, M.D., and
published by the New Sydenham Society of London, and reprinted in 1878
and 1879 in _Medical News_.]

[Footnote 3: Bourneville, _Recherches clinique et therapeutique sur
l'Épilepsie et l'Hystérie_, 1876; Bourneville et Voulet, _De la
Contracture hystérique-permanente_, 1872; Bourneville et Regnard,
_Iconographie photographique de la Salpêtrière_. I have made special
use of the second volume of the last of these works.]

[Footnote 4: _Études cliniques sur l'Hystero-épilepsie, ou Grande
Hystérie_, par le Dr. Paul Richer, Paris, 1881.]

No article on hystero-epilepsy can be written without frequent use of
this work of Richer, and also of the numerous contributions of
Charcot. To them we are indebted for new ways of looking at this
disease, as well as for an almost inexhaustible array of facts and
illustrations of the diverse phases of this disorder.

While the curious, grotesque, or outrageous manifestations now known
as hystero-epileptic have been discussed with more or less minuteness
by authors from the time of Sydenham to the present, usually, and more
especially in all countries but France, these manifestations have been
studied as isolated phenomena. Charcot and Richer, however, present a
comprehensive view of hysteria as a disease of a certain typical form,
but often manifesting itself in an imperfect or irregular manner. This
regular type is characterized particularly by a frequently- or
infrequently-recurring grave attack, which is divided into distinct
periods, and these periods into phases.

This regular type of grave hysteria once understood, a place of
advantage is gained from which to study the disease in its imperfect,
irregular, and abortive forms. Whatever its pathology may be, such
striking symptoms as loss of consciousness with spasm, hallucinations,
and {290} illusions show at least temporary disturbance of the
integrity of the cerebrum.

Hystero-epilepsy of imperfectly developed or irregular type is a not
uncommon affection in this country, but the disease in its regular
type is comparatively rare.

VARIETIES.—Hysteria and epilepsy, so far as seizures are concerned,
may show themselves in two ways in the same patient; but I believe
that it is best that the term hystero-epilepsy should be restricted in
its application, as Charcot, Bourneville, and Richer have advised, to
the disorder in which hysterical and epileptic symptoms are commingled
in the same attack—what is spoken of by the French as hystero-epilepsy
with combined crises. The other method of combination is in the
affection known as hystero-epilepsy with separate crises, in which the
same patient is the victim of two distinct diseases, hysteria and
epilepsy, the symptoms of which appear independently of each other.

The fact that hysteria is at times associated with true epilepsy is
often overlooked. A patient who is known to have had pure hysterical
seizures of the grave type has also a genuine paroxysm of epilepsy,
and thus the medical attendant is deceived. I will dismiss the
consideration of hystero-epilepsy with separate crises with a few
paragraphs at this place, devoting the rest of the article to the
disorder with combined crises.

The coexistence of hysteria and epilepsy, with distinct manifestations
of the two neuroses, has been most thoroughly considered by
D'Olier.[5] Beau in 1836, and Esquirol in 1838, first showed this
coexistence. Landouzy in 1846 first made use of the name
hystero-epilepsy with separate crises.

[Footnote 5: Memoir which obtained the Esquirol prize in 1881, by M.
D'Olier, interne of the hospitals of Paris, on “Hystero-Epilepsy with
Distinct Crises, considered in the Two Sexes, and particularly in
Man,” translated and abstracted by E. M. Nelson, M.D., in the
_Alienist and Neurologist_, April, 1882.]

In France the distinct existence of hysteria and epilepsy in the same
individual is not, according to D'Olier, a very exceptional fact. Beau
has reported it 20 times in 276 cases. The different modes of
coexistence have been summed up by Charcot as follows: “1, Hysteria
supervening in a subject already epileptic; 2, epilepsy supervening in
a subject previously hysterical; 3, convulsive hysteria coexisting
with epileptic vertigo; 4, epilepsy developing upon non-convulsive
hysteria (contracture, anæsthesia).”

The following case, now in the Philadelphia Hospital, illustrates the
first of these modes of combination: S——, aged thirty-nine, female, a
Swede, came to this country in 1869. She said that her mother had fits
of some kind. The patient had her first fit when she was four years
old. Her menses did not come on until she was nineteen. With the
appearance of her periods she had fainting-spells off and on for two
years, and in these spells she would fall to the ground. After two
years she improved somewhat, but still would have an occasional
seizure like petit mal. Four years ago she had a severe fit, in which
she bit her tongue. This was a paroxysm of true epilepsy. It was
witnessed by the chief nurse in the hospital, a competent observer.
Since then she has had attacks of some kind every month or oftener.
She rarely had a true epileptic seizure. Often, however, she had
hysterical and {291} hystero-epileptic attacks. These paroxysms have
been witnessed by myself and by the resident physician and nurse.
Rarely they were epileptic, frequently they were hysterical. Mental
excitement will often induce an hysterical spasm.

PATHOLOGY.—Holding that hystero-epilepsy is a form of grave hysteria,
the remarks which have been made in the last article on the probable
nature of severe convulsive attacks will be applicable here. In
hystero-epilepsy with the typical grave attack we have the highest
expression of that disturbance of cerebro-spinal equilibrium which
constitutes the pathology of hysteria.

ETIOLOGY.—It will also be unnecessary to go at length into the
discussion of the predisposing and exciting causes of
hystero-epilepsy. In general, its predisposing causes are those of
hysteria of any form. Certain causes or conditions, however,
predispose to certain types or forms of hysteria. The Latin races are
more inclined to the hystero-epileptic form of hysteria than are the
natives of more temperate or colder climates. Bearing upon this point,
I have already quoted the letter of Guiteras with reference to
hysteria and hystero-epilepsy in Cuba and semi-tropical America. Forms
of religion which cultivate to an extreme degree the emotional or the
sentimental side of human nature tend to produce hystero-epilepsy.

With reference to sex it may be said that hystero-epilepsy prevails to
a greater extent among females than males, even proportionately to a
larger degree than some of the other marked phases of hysteria. It
does, however, occur in men and boys, although rarely. Richer records,
from the practice of Charcot, a case in a lad of twelve years. Several
cases have fallen under my own care.

Ten years since I saw a case of hystero-epilepsy, which in some
respects closely simulated tetanus, in a youth nineteen years old. He
was well until seventeen years of age, when he slightly wrenched his
back. Shortly afterward he felt some pain between the shoulders. From
that time, at irregular intervals, generally of a few days only, he
was subject to attacks of dull pain, which seemed to run up the spine
to the head. About two months after this injury he first had a
spasmodic attack. A spasm would come on while he was quietly sitting
or working. The body assumed the backward-arched position. As his
father described the case, there was always space enough under his
back for a baby to crawl through. Generally, he would have more than
one seizure on a given occasion. He would sometimes have as many as
six or seven in one hour. On coming to, he would stare and mutter and
work his mouth and lips, at the same time pointing around with his
hands and fingers in a wild way. Sometimes he would sleep for several
hours afterward if not disturbed, but his sleep was not of a
stertorous character. He said that he could feel the attacks coming
on; his body felt as if it was stretching, his head going back. He
thought he was not conscious during the whole of the attacks, but
between the spasms he could take medicine when directed. When first
examined he had decided tenderness on pressure over the second, third,
and fourth dorsal vertebræ. Pressure in this region would sometimes
bring on a convulsive paroxysm. When first seen he had been for three
months having seizures every two or three weeks. He was under
observation for several months, during which time he was treated with
faradization to the spine, the hot spinal douche, tonics, and
bromides, and made a complete recovery.

{292} W. Page McIntosh[6] has reported several cases of
hystero-epilepsy in the male, one of which is doubly interesting
because it was in a negro. This patient was twenty-one years old,
stout, and previously in good health. He complained of intense pain in
the stomach, and soon passed into a violent convulsion. To show the
importance of diagnosis in these cases, it is interesting to note that
the doctor first thought of strychnia-poisoning, then of acute
indigestion, next of tetanus. Soon, however, he decided that he had a
case of hysteria. The patient had other convulsions on the day
following the first attack. The seizures were evidently
hystero-epileptic or hysterical. He was not unconscious, and believed
that on a recent previous evening he had been conjured by an old
negress. The spell was to work in three days, which it did. The doctor
counter-spelled him with a hypodermatic syringe, after which he
promptly recovered. McIntosh reports another case in a man forty years
old and the father of six children, who was laboring under strong
mental excitement because of the sufferings of a dangerously ill
child. His whole form was convulsed, and his body underwent a variety
of peculiar contortions. He had had similar attacks before, and had
subsequent recurrences.

[Footnote 6: _Med. News_, vol. xlviii., No. 1, Jan. 2, 1886, pp. 5-8.]

The following case was observed in the Philadelphia Hospital:
W. F. ——, aged twenty-eight years, married, has one child. His
seizures began seven years ago, when he had an attack while playing a
game of pool. At this time he had, according to his account, a sudden
feeling of giddiness or vertigo in which he fell over and had a spasm,
during which he thinks he was unconscious. After the seizure he
suffered from headache, but had no disposition to sleep.

From that time until the present he has been subject to these spells,
though the paroxysms are very irregular in frequency. Sometimes he
will have several attacks in a day; again, he will be free from them
for days, and perhaps for two or three weeks, but never for more than
a month at a time. They have come on him while walking in the street,
and on several occasions he has been taken to different hospitals. He
was admitted to the Philadelphia Hospital four times. On his first
admission he only remained over night; on his second and third he
remained for two or three weeks. On the last admission he remained
four weeks, and had spasms every day and night after admission. He
had, by actual count, from five to six hundred after he went in; and
in one evening, from seven P.M. to midnight, he had no less than
thirty-eight. These seizures, which were witnessed by myself and two
resident physicians, differed but little from each other, although at
times some were more violent than others. They began with a forced
inspiration; then the patient straightened himself out and breathed in
a stertorous or pseudo-stertorous manner. The pulse in that stage
became slow, and at times was as low as 48 per minute. The temperature
was normal or subnormal. The arched position was sometimes taken, but
the opisthotonos was not marked. The paroxysm ceased by an apparent
forced expiration, and the breathing then became normal; the patient
remained in a somewhat dazed condition, which was only momentary.
During the attack the patient said that he was unconscious of his
surroundings. In the interval between the attacks he suffered from
headache and from pain {293} over the region of the stomach. He also
had tenderness on pressure over the lumbar vertebræ. He never bit his
tongue.

Age has some influence in the development of hystero-epilepsy. It is
of most common occurrence at the period of pubescence; it is rare in
old age, but occurs with comparative frequency in middle life; or,
rather, it should be said that middle-aged hystero-epileptics are not
uncommonly met with, individuals who have for many years been subject
to the attacks. In young children, girls or boys, it is certainly
rare.

With reference to the exciting causes of hystero-epilepsy, it will
only be necessary to say that of those which have already been
enumerated in the general discussion of the etiology of hysteria, a
few, such as domestic troubles, abnormal sexual excitement, and
painful menstruation, are likely to induce the paroxysm, but fright,
excitement, anxiety, sudden joy, and other psychical disturbances are
the most frequent of the exciting causes of the seizures. A threat or
a blow has been known to precipitate an attack. The use or abuse of
alcohol is sometimes an exciting cause. Reflex irritation, such as
that from intestinal worms, and digestive disorders sometimes produces
hystero-epileptic attacks in children.

SYMPTOMATOLOGY.—In considering the symptoms of hystero-epilepsy the
subject must be approached from several points of view. In the first
place, the disorder can be divided (1) into the regular or typical
grave attack; and (2) into the irregular attacks. These irregular
seizures can be greatly subdivided, but their discussion will be
confined to those types which have been most observed in this country,
although I do not think that any variety of hystero-epilepsy is
distinctively American; and this is what might be supposed from the
largeness of our country and the different nationalities of which it
is composed.

I have seen but few cases of hystero-epilepsy of the regular type. One
of these was first described at some length in the _American Journal
of Medical Sciences_ for October, 1881. I will here give the case,
with illustrations, somewhat condensed from the accounts as first
published.[7]

[Footnote 7: For the opportunity of studying and treating this case I
was under obligations to Charles S. Turnbull and J. Solis Cohen, the
patient having been for several months under their care at the German
Hospital of Philadelphia. Carefully prepared notes of the case were
furnished to me by H. S. Bissey and H. W. Norton, resident physicians
at the hospital. I was also under great obligations to my friend J. M.
Taylor for a series of sketches of the positions assumed by the
patient at different stages of the attack.]

R——, æt. 21, single, was first admitted to the German Hospital Nov.
13, 1879. Between her ninth and twelfth years she had had several
attacks of chorea. During childhood she was often troubled with
nightmare and unpleasant dreams; she often felt while asleep as if she
were held down by hands. She was frequently beaten about the head and
body. Her menses did not appear until she was nearly eighteen. Before
and at her first menstrual epoch she suffered severe pain and cramp.
During the first year of her menstruation, while at Atlantic City, the
flow appeared in the morning, and she went in bathing the same
afternoon. She stayed in the water two hours, was thoroughly chilled,
and the discharge stopped. Ever since that time she had only
menstruated one day at each period, and the flow had been scanty and
attended with pain. When about eighteen she kept company with a man
for five months, and after having put much confidence in him learned
that he had a wife and two children. This episode caused her much
worriment. She positively {294} denied seduction. She became much
depressed. September 2, 1879, she was seized in a street-car with a
fainting fit. On coming to, she found her left arm was affected with
an unremitting tremor. Seven weeks later she was admitted to the
German Hospital. She had severe spasmodic attacks, and the diagnosis
of hysteria was made. She remained in the hospital about four weeks.
On leaving she again went into service. She was readmitted June 9,
1880, in an unconscious or semi-conscious condition. She had been on a
picnic, and while swinging was taken with an attack of spasm and
unconsciousness. During two hours after admission she had a series of
convulsions. After this she had similar attacks two or three times a
week, or even oftener.

I first saw her about the middle of January, 1881. She had an
hysterical face, but was possessed of considerable intelligence, and
when questioned talked freely about herself. The most prominent
physical symptom that could be discovered was a large tremor,
affecting the left arm, forearm, and hand. This was constant, and had
been present since her admission to the hospital. The left half of her
body was incompletely anæsthetic, the anæsthesia being especially
marked in the left forearm. Ovarian hyperæsthesia could not at this
time be made out. She was, however, hyperæsthetic over the occipital
portion of the scalp and the cervico-dorsal region of the spine.
Pressure or manipulation of these regions would in a few moments bring
on an attack of spasm. The attacks, however, usually occurred without
any apparent exciting cause.

For a period of from six to twelve hours before an attack she usually
felt dull, melancholy, and strange in the head. Frequently she had
noises like escaping steam in her ears, but more in the right ear than
in the left. She complained of cardiac palpitations. She usually had
pain in the small of her back. Her limbs felt weak and tired. Just as
the attack was coming on her eyes became heavy and misty, her head
felt as if it was sinking backward, and if not supported she would
fall in the same direction.

On several occasions I had the opportunity of watching every phase of
the attack or series of attacks, the spasms continuing sometimes from
one to four or five hours. The order of events was not always the
same, and yet a general similarity could usually be seen in the
successive stages of the phenomena. I will try to give an outline of
the different stages and phases as observed on an occasion when the
seizures were severe.

[Illustration: FIG. 18.]

After lying down, the first noticeable manifestation was a twitching
of {295} the eyelids and of the muscles of the forehead and mouth. Her
head was next moved from side to side, and she looked around vaguely.
Respiration became irregular. In a few moments a convulsive tremor
passed down her body and limbs. Her arms were now carried outward
slightly from the body, the hands being partly clenched. The lower
extremities were straightened, the left foot and leg being carried
over the right (Fig. 18). Her limbs were rigid. Her mouth was closed,
the teeth being ground together. Consciousness was lost, and
respiration seemed to stop.

[Illustration: FIG. 19.]

A series of strong convulsive movements next ensued. Her entire body
was tossed up and down and twisted violently from side to side.
Sometimes she assumed a position of opisthotonos. Her whole body was
then again lifted and hurled about by the violence of the movements. A
{296} few seconds later she became quiet but rigid, in the position
shown in Fig. 19, corresponding to the position of crucifixion of the
French writers.

[Illustration: FIG. 20.]

Soon she assumed the position represented by Fig. 20, and the
convulsions were renewed with violence, the patient's limbs and body
being frequently tossed about and the latter sometimes curved upward.
After these movements had continued a brief period the patient became
calm and partially relaxed; but the respite was not long. A series of
still more remarkable movements began, chiefly hurling and lifting of
the body. Eventually, and apparently as a climax to a succession of
efforts directed to this end, she sprang into the position of extreme
opisthotonos represented in Fig. 21. This sketch, by Taylor, is a very
faithful view of her exact position. She remained thus arched upward
for a minute, or even more. A series of springing and vibratory
movements followed, the body frequently arching.

[Illustration: FIG. 21.]

As the spasms left she sat up on her bed, and at first looked around
with a bewildered expression. She turned her head a little to one side
and seemed to gaze fixedly at some object. Her expression was slightly
smiling. When spoken to she looked straight at the one addressing her,
but without appearing to know what was said, and the next moment the
former position and attitude were resumed. After a few minutes she lay
down muttering incoherently, and in about a quarter of an hour fell
asleep.

I have simply described one attack. Sometimes she would have several
in succession, or the spasmodic manifestations would be repeated
several times in a regular or an irregular manner. Strong pressure in
the ovarian regions usually would not cut short the spasms. They could
be stopped, however, by etherization or by active faradization of the
limbs or trunk. She did not always conduct herself in the same manner
in the period which succeeded the spasms. Sometimes, after getting
into the sitting posture, instead of smiling, she would look enraged
and speak a few words. The following expressions were noted on one
occasion: “You know it! Yes, you do! Yes! yes!” Often she was heard to
mutter for hours after the attack. Her lips would sometimes be seen to
be moving without any words being heard. Sooner or later she would
fall into sound sleep which would last several hours.

{297} During the spasms she seemed to be entirely unconscious of her
surroundings. To a looker-on her movements seemed sometimes to have
the appearance of design, but I soon convinced myself that such was
not the case. She was insensitive to painful or other impressions. Her
expression was blank and unchanging. She said that the only thing that
she remembered about the attacks was that she heard a strange,
confused sound; this was most probably just as she was returning to
consciousness.

Numerous remedies were tried without any apparent effect. These
included sodium and potassium bromides, iron, zinc salts, physostigma,
cimicifuga, camphor, ether, etc. A uterine examination was made, but
nothing especially calling for local treatment was found. She was
placed upon equal parts of tincture of valerian and tincture of iron
in half-teaspoonful doses three times daily. Capsules of apiol were
also ordered to be taken three times daily just before and during her
menstrual period. Her menses became more profuse and continued longer.
The attacks began to diminish in frequency, and became less severe. In
March, not having had a seizure for several weeks, she left the
hospital and again went into service. Six months elapsed and she had
no attack. She reports occasionally at my office. She says that she
feels entirely well. The tremor of the left upper extremity entirely
disappeared. She continued to take valerian and iron for four months,
but stopped the apiol after the second or third menstrual period.

With this case before us the phenomena of the disease can be more
readily grasped. I will necessarily make free use of the labors of
Richer in my description of symptoms.

Hystero-epileptic attacks usually, although not always, have distinct
prodromes. These have been more thoroughly studied and reported by
Richer than by any other author. They are classed by him under the
four heads of psychical affections, including hallucinations,
affections of the organic functions, motor affections, and affections
of sensibility. The patient's condition is changing; she is listless,
irritable, melancholy, despairing, slovenly. Sometimes she is noisy,
sometimes mute. At times she is full of wild excitement.
Hallucinations of sight sometimes come on at this period—most commonly
visions of cats, rats, spiders, etc. These visions of animals, as
first pointed out by Charcot, in passing before the patients run from
the left to the right or from the right to the left, according as the
hemianæsthesia is situated on the left or on the right. Hallucinations
of hearing, as of music, threats, demands, whistling, trumpeting,
etc., also occur, chiefly on the hemianæsthetic side. These
hallucinations are worse at night. Sometimes at night the patients are
the victims of imaginary amours. Want of appetite, perverted taste,
nausea and vomiting, flatulence, tympanites, ptyalism, unusual flow of
urine, feelings of oppression, hiccough, laughing, barking, loss of
voice, palpitation of the heart, and flushings are among some of the
many disorders of the organic functions which are sometimes present
during the prodromal period. Loss of muscular power or a species of
ataxia, peculiar limited spasmodic movements, contracture, first of
one limb and then of another, may be observed. Charcot, Bourneville,
Regnard, and Richer, all give admirable illustrations of different
forms of contracture. In one case the right arm and wrist are flexed,
{298} and the hand held at the level of the shoulder with fingers
extended. Anæsthesia—total, unilateral, or local, tactile, of pain,
temperature, etc.—may also occur. Sometimes achromatopsia or
color-blindness shows itself; sometimes deafness in one ear is
present. Tenderness over the ovarian region is often an immediate
precursor. To Charcot we owe the most careful study of these symptoms.

Among the most interesting prodromic affections of sensibility are the
hysterogenic or hystero-epileptogenic zones. These have been well
studied and described by Richer, from whose work Figs. 22 and 23 have
been taken. Brown-Séquard has shown that animals rendered epileptic by
lesions of the spinal cord, medulla oblongata, or nerves are sometimes
attacked with convulsions spontaneously, but it is also possible to
provoke these attacks by exciting a certain region of the skin which
he designates as the epileptogenic zone. This zone, situated on the
same side of the body as the nervous lesion, has its seat about the
angle of the lower jaw, and extends toward the eye and the lateral
region of the neck. The skin of this region is a little less sensitive
than that of the opposite side, but touching it most lightly provokes
epileptic convulsions. The simple act of breathing or blowing on it
brings about the same result.

Something analogous to this epileptogenic zone has been noticed among
hystero-epileptics, and has been pointed out by several writers.
Richer gives the particulars of a number of cases. In one patient the
hyperæsthetic zone was between the two shoulder-blades. Simply
touching this region was sufficient to provoke an attack, and this was
more easily done if near the time of a spontaneous seizure. After the
grave attacks the excitability would seem to be exhausted, and
pressure in the zone indicated would not cause any convulsive
phenomena. A second case presented a similar condition. If touched
over the dorsal spine between the shoulders, she felt a violent pain
in the belly, then a sense of suffocation, which brought on at once
loss of consciousness. In a third patient the hysterogenic zone was
different. It was double. It was necessary to touch two symmetrical
points situated to the outside and a little below the breasts in order
to bring on the hystero-epileptic convulsions. Touching one of these
points did not produce any result. Other cases are given in detail,
but a glance at the two figures (22 and 23) will show some of the
principal hysterogenic zones both for the anterior and posterior
surfaces of the body. A zone of ovarian hyperæsthesia was common to
all the patients. It did not differ essentially from the other
hysterogenic zones. If the ovarian hyperæsthesia existed along with
other hysterogenic points, the excitation of the ovarian region was
always the most efficacious. The hysterogenic zones always occupy the
same place in the same case. They are found on the trunk exclusively;
they are more frequently in front than behind; in front they occupy
lateral positions, and are often double and symmetrical; behind they
are more often single and median; they exist more frequently to the
left than to the right, and the unilateral zones have always been met
with on the left side.

[Illustration: FIG. 22. Principal Hysterogenic Zones, anterior surface
of the body: _a_, _a′_, supramammary zones; _b_, mammary zones; _c_,
_c′_, infra-axillary zones; _d_, _d′_, _e_, inframammary zones; _f_,
_f′_, costal zones; _g_, _g′_, iliac zones; _h_, _h′_, ovarian zones
(after Richer).]

[Illustration: FIG. 23. Principal Hysterogenic Zones, posterior
surface of the body: _a_, superior dorsal zone; _b_, inferior dorsal
zone; _c_, posterior lateral zone (after Richer).]

The hysterogenic zones bear no constant relation to the
hemianæsthesia. It is true that the ovarian pain is most often seated
on the hemianæsthetic side, but sometimes it is present on the
opposite side. They {299} are not at all times equally excitable. They
are more so when the convulsive attack is imminent.

Ovarian pressure gives rise to the spasmodic attacks: the same
pressure arrests them. What is true of ovarian compression is equally
true of all the hysterogenic zones. A light touch brings on the
convulsions, which have scarcely commenced when they can be stopped by
a new excitation of the same point.

As already stated, the attack of hystero-epilepsy, having fully begun,
is divided by Richer into distinct periods. Although these are seldom
seen in perfection, it is necessary to have some clear idea of their
{300} phenomena in order to view the affection comprehensively. They
were seen well developed in the case given. These periods are—(1) The
epileptoid period; (2) the period of contortions and of great
movements; (3) the period of emotional attitudes; (4) the period of
delirium.

In the first or epileptoid period of the hystero-epileptoid attack,
which receives its name from its resemblance to true epilepsy, various
phases always reproduce themselves in the same order. Loss of
consciousness and arrest of respiration, muscular tetanization in
various positions, followed by clonic spasms, and, finally, muscular
resolution, are the successive phenomena of this period, which usually
lasts several minutes. Loss of consciousness is complete during this
period. Muscular {301} tetanization shows itself in movements large
and small, sometimes of the whole body. The trunk may become as stiff
as a bar of iron; the face is sometimes cyanosed, puffed; froth even
appears, which it is well to remember, as this is considered by some
as absolutely diagnostic of epilepsy. Many positions may be assumed.
The important significant features of the tonic phase of period are
muscular tetanization with loss of consciousness and respiratory
spasm. In the clonic phase movements at first rapid and short, later
larger and more general, ensue, and are accompanied by whistling
inspiration, jerking expiration, hiccoughs, noisy deglutition. The
phase of muscular resolution comes on, in which the patient completely
relaxes; sometimes a true stertor occurs. The epileptoid period
usually lasts altogether several minutes, the first two phases usually
occupying about one minute.

In the period of contortions and great movements wonderful attitudes
and contortions are observed in one phase, and in another great
movements. One of the attitudes particularly fashionable with
hystero-epileptics is the arched position, in which the body is curved
backward in the form of an arch so as to rest only on the head and
feet. Sometimes the patient may rest on the belly or side, the
remainder of the body preserving its curved position; the body may
indeed assume almost any strange and seemingly impossible attitude.
The so-called great movements are executed by the entire body or by a
part of the body only; they are of great variety; sometimes they are
movements of salutation; sometimes the semiflexed legs are projected
upward, etc. Often the phase of great movements is marked at its
beginning by a piercing cry; loss of consciousness is not the rule.

The period of emotional attitudes or statuesque positions is the most
dramatic stage of a highly dramatic disease. Hallucinations ravish and
transport the patient: sometimes they are gay, sometimes they are sad.
The dramatic positions assumed are in consonance with the patient's
hallucinations. The patient reproaches, opposes, supplicates, is
angry, is furious; she assumes positions of supplication on her knees,
becomes menacing, and even strikes. In the great works of Bourneville,
of Regnard, and of Richer many cases are related at great length and
with vivid details. Camera and pencil are frequently called in to
assist the pen in presenting scenes which read as if drawn from an
exciting drama or novel. Among the expressions and attitudes which
they have succeeded in photographing are those illustrating emotions
of menace, appeal, amorous supplication, erotism, ecstasy, mockery,
beatitude.

After the period of the emotional attitude consciousness returns, but
only in part, and for a time the patient remains a prey to a delirium
whose character varies. This delirium may be concerned with subjects
the most varied; it may be gay, sad, furious, religious, or obscene.
It is mingled with hallucinations; voices are heard; sometimes are
seen personages who are known; sometimes the scenes are purely
imaginary. During this fourth period the patients will sometimes make
the most astounding statements and accusations. They will wrongfully
charge theft, abuse, etc. upon others; they believe in the reality of
their hallucinations, and, what is more important, they will sometimes
persist in this belief after the attack is over. The third and fourth
periods are sometimes confounded. When the four periods described
succeed each other in {302} order, they constitute a regular and
complete attack of hystero-epilepsy.

By comparing the notes upon the case detailed with the description
given of the typical hystero-epileptic attack, it will be seen that
the different periods, and even the phases, can be made out with but
little difficulty. After a few moments of convulsive movements and
irregular breathing the patient was attacked with muscular
tetanization, arrested respiration, and loss of consciousness. Tonic
convulsions followed, and then immobilization in certain positions.
Next came the clonic spasms and resolution. In the period of
contortions the arched position is one more extreme than any
represented by the illustrations of the French authors, although it is
closely approximated by some of their illustrations. After this
position of opisthotonos had been taken a succession of springing and
lifting movements occurred, probably corresponding to the phase of
great movements. The period of emotional attitudes was very clearly
represented by the position assumed, the expression of countenance,
and sometimes by the words uttered. Even the period of delirium was
imperfectly represented by the mutterings of the patient, which were
sometimes long continued after the attack.

[Illustration: FIG. 24.]

A beautiful illustration of one of the positions assumed by a
hystero-epileptic is shown in Fig. 24 from Allan McLane Hamilton's
treatise on _Nervous Diseases_. The patient, æt. eighteen, represented
in the figure had suffered from hystero-epileptic attacks since the
beginning of the menstrual period. Usually, she had severe but
distinct epileptic seizures, and afterward an hystero-epileptic
paroxysm. The muscles of her back were rigidly contracted in
opisthotonos. Her arms were drawn over her chest, and her forearms
slightly flexed and crossing each other. Her thumbs were bent in and
covered by her other fingers, which were rigidly flexed. Her toes were
also flexed, and her right foot presented the appearance called by
Charcot le pied bot hystérique, or hysterical club-foot.

As has already been stated, hystero-epilepsy of irregular, imperfect,
or abortive type is most commonly observed in this country, or at
least in the Middle States, of which my own knowledge and experience
are greatest. As has been demonstrated by Richer and Charcot, the
irregular type may be of any form, from a paroxysm with a scarcely
detectible convulsive seizure and scarcely recognizable loss of
consciousness up to {303} frightful attacks which from their terrible
nature have been termed demoniacal, and in which occur the wildest
phenomena of movement, frightful contortions and contractions, with
grimaces and cries of fury and rage. Sometimes the movements show a
violence beyond description. These frightful seizures are of extreme
rarity in America. Sometimes attacks of ecstasy or attacks of delirium
are the predominating or almost the only feature. The epileptoid
attack, so far as my experience has gone, is the most prevalent
variety of hystero-epilepsy. Epileptoid attacks are simply the result
of the predominance and modification of the first or epileptoid period
of the typical grave attack. Richer has described several varieties.

I have seen a number of cases of the epileptoid variety or other
irregular forms. These cases have presented a few or many of the
symptoms of grave hysteria, such as anæsthesia, analgesia,
hyperæsthesia, blindness, aphonia, paralysis, contracture, etc., and
have also had attacks of tonic and clonic spasm, with complete or
partial loss of consciousness. The phenomena of the periods of
contortions and great movements, of emotional attitudes, and of
delirium have been, however, altogether or almost entirely absent.
These epileptoid attacks have varied somewhat in different cases.

The following are the notes of three cases observed by me:[8]

[Footnote 8: Published in _Journal of Nervous and Mental Disease_,
vol. ix., No. 4, October, 1882.]

M——, æt. twenty-seven, a widow, admitted to the Philadelphia Hospital
February 4, 1882, was married thirteen years before, when only
fourteen years of age, and remained in comparatively good health for
four years after her marriage, during which time she had three
children, all of whom died in early infancy. Four years after her
marriage, while carriage-riding, she for the first time had a spasm.
According to her story, the seizure was very severe; she lost
consciousness, and passed from one spell into another for an hour or
more. She had a second attack within two weeks, and since has had
others at intervals of from one week to three or four months. Four
years ago she passed into a condition of unconsciousness or lethargy
in which she remained for three days. On coming out of this state she
found that the left half of her body was paralyzed and that she was
speechless. In two weeks she recovered her speech and the paralysis
disappeared. On June 15, 1881, she gave birth to a male child. On the
night of the 16th she became delirious, and on the 17th she again lost
her speech and had a paralytic seizure, the paralysis now affecting
both legs. She recovered her speech in a few days, but the paralysis
remained. Her babe lived, and with her was admitted to the hospital.
He had had seven attacks of spasm at intervals of about a month. The
patient's mother was for a time insane, and had been an inmate of an
insane asylum for some months since her first epileptiform attack.

She was carefully examined on the day of her admission. She was
bright, shrewd, and observant. She gave an account of her case in
detail, and said she was a puzzle to the doctors. Both legs were
entirely helpless; the feet were contractured in abduction and
extension, assuming the position of talipes equino-varus; the legs and
thighs were strongly extended, the latter being drawn together firmly.
The left upper extremity was distinctly weaker than the right, but all
movements were retained. She {304} had no grasping power in the left
hand. She was completely anæsthetic and analgesic below the knees, and
incompletely so over the entire left half of the body. Pain was
elicited on pressure over the left ovary and over the lower dorsal and
lumbo-sacral region of the spine. Both knee-jerks were exaggerated.

I lectured on this patient at my clinic at the hospital, stating that
I believed the case to be one of hystero-epilepsy, and only needed to
see an attack of spasm to confirm the diagnosis. Up to this time she
had not had a seizure since admission. She had, however, been
complaining for several days of peculiar sensations in the head and of
severe headache. She had also been more irritable than usual, and said
that she felt as if something was going to happen to her. The same
afternoon, Dr. Rohrer, the resident physician in charge of the
patient, was sent for, and found her in a semi-conscious state. She
did not seem to know what was going on around her, but was not in a
stupor. Her pulse was 114 to 120; respirations were 20 to 22, regular.
The corneæ responded on being touched. Some twitching movements of the
eyeballs and eyelids were noticed; the thumb and forefinger of the
left hand also moved, as if rubbing something between them.

In a few moments an epileptoid paroxysm ensued. She became unconscious
and rigid. The lower extremities were strongly extended in the
equino-varus position already described. The arms were extended at her
sides, the wrist being partly flexed and rotated outward, the hands
clenched. Her face, at first pale, became deeply congested. Her trunk
became rigid in a position of partial opisthotonos. Brief clonic
spasms followed, then resolution, the whole seizure not lasting more
than from two to three minutes. She lay for a minute or two unmindful
of anything or anybody, and then sat up and looked around wildly. She
dropped back again and began to mumble, as if she wished to speak, but
could not. Paper and pencil were given to her, and she wrote that she
was conscious, but could not speak. Her temperature, taken at this
time, was 99.8° F.

Attacks similar to the one just described occurred at irregular
intervals for two days. On their cessation she was speechless, and the
permanent symptoms already detailed—the anæsthesia, paralysis,
etc.—were deepened. During the attacks but little treatment was
employed; hypodermic injections of morphia and potassium bromide by
the mouth were, however, administered. After the attack the
valerianate of iron by the mouth, faradization of the tongue, and
galvanization of the legs below the knees with weak currents, were
ordered. Her speech returned in a week. For about a month she showed
no other signs of improvement; then she began to mend slowly,
gradually using her limbs more and more. On May 11, 1882, she was
discharged, and walked out of the hospital with her child in her arms,
apparently perfectly well. During the last month of her stay no
treatment was used but mild galvanization every other day.

Mrs. A——, æt. forty-five, was seen by me in consultation. For some
months at her menstrual period she had been out of sorts. At times she
had had hallucinations of sight. For several weeks she had been
troubled more or less with a feeling of numbness and heaviness in the
left arm and leg, particularly in the latter, and also with diffused
pain in the head and {305} a sensation of aching and dragging in the
back of the neck. For three weeks, off and on, she had had diarrhœa,
which had weakened her considerably. She awoke one morning feeling
badly and yawning every few minutes. She passed into a condition of
unconsciousness with attacks of spasm. I did not see her on this the
first day of her severe illness, but obtained from the physician in
attendance some particulars as to the character of her seizures.
Evidently the condition was similar to that presented by the last
case, that described by Richer as the epileptoid status, in which
tonic and clonic spasm and resolution are repeated again and again.
Attack after attack occurred for nine or ten hours, sometimes one
immediately following another, sometimes an interval of several
minutes or of half an hour or more intervening. Respiration was
partially arrested. Tonic spasm predominated; the limbs became rigid
in various positions; sometimes the neck and trunk were strongly bent
backward, producing partial opisthotonos. While the body and limbs
remained tetanized they were thrown into various positions (clonic
phase of an epileptoid attack). Although she answered questions
addressed to her by her physician between the spells, she did not
recognize him until evening, after the spasms had ceased, and then was
not aware that he had been in attendance during the day, although he
had been with her almost constantly. Leeching and dry cupping to the
back of the neck were employed, and potassium bromide and tincture of
valerianate of ammonia were given.

Early on the morning of the next day she had another attack of
unconsciousness and spasm, in which I had the opportunity of seeing
her. The spasm amounted only to a slight general muscular
tetanization. The whole attack lasted probably from half a minute to a
minute. The following day, at about the same hour, another paroxysm
occurred, having a distinct but brief tonic, followed by a clonic,
phase, in which both the head and body were moved. The next day, also
at nearly the same hour, she had an attack of unconsciousness or
perverted consciousness without spasm. She had a similar seizure at
4 P.M. For two days succeeding she had no attacks; then came a spell
of unconsciousness. After this she had one or two slight attacks, at
intervals of a few days, for about two weeks.

Between the attacks the condition of the patient was carefully
investigated. On lifting her head suddenly she had strange sensations
of sinking, and sometimes would partially lose consciousness. She
complained greatly of pain in the head and along the spine. Her mental
condition, so far as ability to talk, reason, etc. was concerned, was
good, but any exertion in this direction easily fatigued her and
rendered her restless. She had at times hallucinations of animals,
which she thought she saw passing before her from left to right. The
left upper and lower extremities showed marked loss of power. The
paralysis of the left leg was quite positive, and a slight tendency to
contracture at the knee was exhibited. She was for two weeks entirely
unable to stand. The knee-jerks were well marked. Left unilateral
sweating was several times observed.

A zone of tenderness was discovered in the occipital region and nape
of the neck, and she had also left ovarian hyperæsthesia. Left
hemianæsthesia was present, head, trunk, and limbs being affected. She
complained of dimness of vision in the left eye, and examination by
the {306} attending physician and myself showed both amblyopia and
achromatopsia, she was unable to read print of any size or to
distinguish any colors with the left eye, although she could tell that
objects were being moved before the eye. A distinguished
ophthalmologist was called in consultation. An ophthalmoscopic
examination showed a normal fundus. Each eye was tested for near
vision. It was found that she could read quite well with the right
eye, and not at all with the left. While reading at about sixteen
inches a convex glass of three inches focus was placed in front of the
right eye, but she still continued to read fluently. A few minutes
later, however, on retesting, she could not read or distinguish colors
with the left eye. Sometimes toward evening her feet would become
slightly œdematous. Examination of the urine showed neither albumen
nor sugar. The heart-sounds were normal.

Owing to the apparent periodicity of the attacks quinine in large
doses was administered, and seemed to act beneficially. In addition,
valerianate of zinc and iron, strychnia, and other nerve-tonics were
used in her subsequent treatment. Applications of faradic electricity,
both with the metallic brush and the moist sponges, were made every
other day. She was persistently and strongly encouraged as to the
certainty of her recovery. Her paralysis, anæsthesia, etc. gradually
disappeared, and in little more than two months she was able to leave
home and go to the country. She has since remained well, but is more
easily fatigued than formerly, and does not feel as strong in the left
side of her body as she did when in perfect health. At her menstrual
period she becomes very nervous.

M——, æt. twenty-three, a well-educated young lady,[9] in the autumn of
1880 had nursed her mother faithfully through a serious illness. She
became anæmic and nervous. Choreic twitchings and occasional slight
spasms were the first symptoms that alarmed her family. The spasms
came on apparently from any over-exertion. Gradually they became a
little more severe in character. Under rest-treatment, with gentle
massage, tonics, and steady feeding, in six weeks she greatly
improved. A few weeks later, however, she again relapsed, and became
worse than she had ever been. The spasms returned with greater force
and frequency. She became unable to walk, or could only walk a few
steps with the greatest difficulty, although she could stand still
quite well. On attempting to step either forward or backward her head,
shoulders, hips, and trunk would jerk spasmodically and she would
appear to give way at the knees. No true paralysis or ataxia seemed to
be present, but locomotion was impossible, apparently because of
irregular clonic spasms affecting various parts of her body.
Eventually she became extremely hypersæsthetic in various regions
(hysterogenic zones), along the spine, beneath the breasts, in the
ovarian area, etc. The slightest pressure or any applications of heat
or cold, electricity, etc. would generally bring on an attack of
spasm.

[Footnote 9: This patient was for a long time under the professional
care of George McClellan of Philadelphia, who has kindly furnished me
with some notes. I shall simply give an outline sketch of the case,
describing particularly her epileptoid attack. For several weeks,
during the absence of McClellan from the city, she was attended by M.
O'Hara, and with him I saw her frequently in consultation.]

While trying to apply galvanism on one occasion she suddenly
complained of nausea, and her expression changed, becoming somewhat
fixed. {307} Her face became flushed, her limbs and body rigid. The
head and body were thrown backward to a moderate extent. Next, the
shoulders were drawn upward, the head appearing to be sunk between
them; the arms were found to be rigidly extended at her sides, the
wrists partly flexed, and the fingers clenched; the legs also were
spasmodically extended, the thighs drawn together, and the feet in the
equino-varus or hysterical club-foot position. Phenomena like those
described above as visceral spasm now were observed. The chest, and
even the abdomen, were lifted up and down rapidly, and the respiration
became quick, irregular, and apparently very difficult. Consciousness
seemed to be impaired, but not absolutely lost. The symptoms just
described took about one minute for their exhibition. Muscular
relaxation now occurred, and an interval of calm, lasting about two
minutes, followed, during which the patient spoke, answering one or
two questions addressed to her. After the brief period of repose,
however, another phase of the attack came on. In this the heaving
movements of the body and what appeared to be intense respiratory
spasms were the chief features. This portion of the attack endured
scarcely a minute; the patient came to quickly, and was able to
converse. In general, her attacks were of a similar character.

The drugs used included bromides, iodides, strychnia, chloride of
sodium and gold, zinc salts, iron, etc. etc.; her condition
vacillating, sometimes better, sometimes worse. She was finally placed
in bed by McClellan, and an extension apparatus was employed, under
which treatment, in a little more than one year from the time she was
first attacked with spasm, she recovered.

       *       *       *       *       *

The permanent or intervallary symptoms of hystero-epilepsy are in the
main the phenomena which have been described when speaking of the
prodromes of this affection. They are, indeed, the whole train of
symptoms—the mental or psychical disorders, the motor, sensory,
reflex, vaso-motor, and isolated phenomena—which have been described
under special heads when considering the general symptomatology of
hysteria. The full-fledged case of hystero-epilepsy is hysteria with a
full array of special permanent hysterical manifestations, and the
great paroxysm superadded. Certain phenomena are, however, more
prominent and of much more frequent occurrence. Among these are
paralysis or paresis, either of the unilateral or paraplegic variety;
hemianæsthesia, including anæsthesia of all the senses; and
contractures, particularly in the lower extremities.

DURATION AND COURSE.—The duration and course of hystero-epilepsy are
very uncertain; most cases last many years. In a few instances the
hystero-epileptic attacks are all from which the patient suffers; even
in the cases of long duration the general health does not appear to
become greatly impaired.

DIAGNOSIS.—To arrive at a correct diagnosis between hystero-epilepsy
and epilepsy is sometimes very difficult. The fact that the patient is
a male does not decide for epilepsy. In making this diagnosis close
attention should be given to—1, The history and the causes of the
disease; 2, the physical and mental condition of the patient; 3, above
all, the phenomena of the spasmodic attacks.

In hystero-epilepsy a careful study of the history of the case will
often {308} elicit a moral cause. The patients rarely injure
themselves seriously by falling, whereas in true epilepsy they often
suffer from severe injuries. The mental and physical health of a
person suffering from hystero-epilepsy differs widely from that of the
true epileptic. In hystero-epilepsy the number of attacks has little
or no apparent influence on the patient's mental or physical
condition. Little or no deterioration of the mind occurs. The memory
is not much impaired. Hystero-epileptics are usually well nourished
and frequently of good physique. This is not the case in true
epilepsy; the number of attacks has a decided effect on the patient's
mental condition. The demented appearance of the old epileptic is well
known, whereas in the hystero-epileptic nothing in physiognomy or
carriage indicates that the patient has been suffering from any
disease. It cannot be said that all epileptics have no mental power,
but some deterioration of the mind usually occurs, and becomes well
marked as the case progresses.

The paroxysms in epilepsy are very well marked, especially if it is
epilepsy of the grave form. They are often ushered in with a scream.
The patient suddenly falls, and at times is severely injured. The
convulsion is generally violent, rapidly alternating from clonic to
tonic spasm, without special phases or periods. Complete and profound
loss of consciousness, with great distortion of face and eyes, is
present. The tongue is frequently bitten. After the attack the patient
passes into a deep stupor. In hystero-epilepsy usually the seizure
does not begin with a scream or sudden fall, the convulsion has
periods and phases, and the tongue is not bitten.

It is said that in hystero-epilepsy there is no loss of consciousness,
but this is not strictly true. This point is the most difficult one
for physicians to clear up in arriving at a diagnosis, as in many
textbooks complete loss of consciousness is laid down as the strongest
evidence of epilepsy. Loss of consciousness does occur in
hystero-epilepsy, particularly in certain varieties. Richer says that
the loss of consciousness is complete during the entire epileptoid
period in a case of the regular type. To decide as to consciousness or
unconsciousness is not as easy as might be supposed. Varying degrees
of consciousness may be present. At times in hystero-epileptic attacks
the patient may respond to some external influences and not to others.
Consciousness is perverted or obtunded often, and it is hard to decide
whether the patient is positively and entirely unconscious of her
surroundings. In epilepsy the loss of consciousness is profound and
easily determined. In regard to the distortion of the face and eyes,
this sign is usually absent in hystero-epilepsy, as in the German
Hospital case, in which the patient had a series of violent seizures
lasting two hours, with marked opisthotonos, yet the facial expression
remained calm and serene throughout.

In hystero-epilepsy the attacks are rarely single; usually they are
repeated, constituting the hystero-epileptic status. They are more
frequently repeated than in epilepsy, although it is of course well
known that there is an epileptic status terrible in character. In a
series of hystero-epileptic attacks usually the seizures come on in
rapid succession, the interval being brief. These series are apt to
last for hours or days. The attacks that compose a series in
hystero-epilepsy vary in duration and in violence. At first they are
of violent character; toward the end {309} the seizures may gain in
extent, but they are likely to lose in intensity.

Charcot and Bourneville make a strong diagnostic point between
hystero-epilepsy and true epilepsy of the fact that in epilepsy there
is a peculiar rise of temperature during the convulsion, even to
104° F., whereas in hystero-epilepsy the temperature is nearly or
quite normal.

Arrest of attacks by ovarian compression in females, and by nerve
compression, nitrite of amyl, and the application of electric
currents, can be brought about in hystero-epilepsy, and not in
epilepsy. A study of the effect of bromides may assist in arriving at
a diagnosis. The action of bromides, drugs which are often used in
both affections, favors the opinion that the two diseases are
distinct. Bromides, according to Charcot and Richer, so effective in
epilepsy, are without effect in hystero-epilepsy. Dujardin-Beaumetz,
however, on the other hand, declares that “who says hysteria says
bromides,” and also that at the present time there is not an
hysterical patient but has taken bromides, the bromide of potassium
being most frequently used. The truth is, that bromides may be useful
for temporary purposes, for certain phases and symptoms of the
disease, but produce no radical permanent improvement in the disease
hystero-epilepsy.

D. Webster Prentiss,[10] in reporting a case, gives some good points
of distinction between real and hysterical tetanus, which is
practically hystero-epilepsy. In his case, which was hysterical, the
attack was ushered in by noise in the ears, deafness, and blindness,
whereas in true tetanus and strychnia-poisoning the senses are
preternaturally acute. There was unconsciousness during the paroxysm,
which does not occur except just before death in the other affections.
The eyes were closed during the spasms; they stare wildly open in the
other diseases. The patient had long, uninterrupted sleep at night; in
true tetanus no such relief comes until convalescence.

[Footnote 10: _American Journal of the Medical Sciences_, 1879.]

[Illustration: FIG. 25.]

The figure is a representation of the opisthotonos of tetanus.[11] It
is the sketch of a soldier, struck with opisthotonos after having been
{310} wounded in the head; and in connection with it I will briefly
call attention to the points of differential diagnosis as given by
Richer, and which have been confirmed by my own observations. In the
opisthotonos of tetanus the contraction of the face and the peculiar
grin are distinguishing points, and are well represented in Bell's
sketch. In the hysterical arched position, while the jaws may be
strongly forced together, the features are most often without
expression. The contracture of the face and the distortion of the
features will be met with more often in the other varieties of
contortion. The curvature of the trunk differs but little in the two
cases, but the abdominal depression observed in the sketch of Bell is
far removed from the tympanitic appearance present in the majority of
hystero-epileptics. In the tetanic cases the patient rests only on the
heels, while in the hysterical cases the knees are slightly flexed,
and the patients are usually supported on the bed by the soles of the
feet.

[Footnote 11: From Sir Charles Bell's _Anatomy and Physiology of
Expression as connected with the Fine Arts_.]

Hystero-epileptics are often suspected of simulation. Richer refers to
many facts which seem to throw out conclusively the idea of
simulation. Among these are the results obtained by æsthesiogenic
agents, the experiments in hypnotism, where many of the results
produced could not be simulated. Some English authors—and among them
notably the physiologist Carpenter—have endeavored to find the
explanation of the results obtained by the æsthesiogenic agents in a
special action of the moral on the physical nature which they
designate expectant attention. While the reality of the action of
expectant attention in certain cases will not be denied, it cannot be
invoked to explain satisfactorily all the phenomena. The patients are
not aware of the results sought; which, indeed, in some cases, are
contrary to the expectations of the observer himself.

PROGNOSIS.—A few cases of hystero-epilepsy get well, either with or
without treatment, in a short time. Some cases, which in addition to
the grave attack have had in the intervals the other striking symptoms
of major hysteria, such as hemianæsthesia and contractures, get well
only after many months or years; some never recover, although, as a
rule, they do not die from anything directly connected with the
disease, but from some accident or more commonly from some
intercurrent disorder. Cases supposed to be cured often relapse. The
patient may be apparently well for months, or even years, when under
some exciting cause the old disorder is again aroused. On the whole,
the prognosis is more serious the longer the case has endured. Family
history and environment have much to do with determining the
prognosis.

TREATMENT.—In considering the treatment of hystero-epilepsy I will, in
the main, confine my attention to a discussion of the methods of
managing and treating the convulsive seizures. With reference to the
numerous special phenomena of this disease, the directions given and
the suggestions made in the general article on Hysteria will be
equally applicable in this connection.

Ruault[12] has recently recommended compression of a superficial
nerve-trunk in order to terminate an attack of hysteria or
hystero-epilepsy. The face being always accessible, he prefers making
pressure on the infraorbital nerves as they emerge from their
foramina, but he has also {311} compressed the ulnar nerve behind the
inner condyle of the humerus. In a brief note to the Philadelphia
Neurological Society, made Feb. 23, 1884, I called attention to the
value of strong nerve-pressure for the relief of hysterical
contracture, and can confirm from several successes Ruault's
recommendation for the employment of the same measure to avert
convulsive attacks.

[Footnote 12: _La France médicale_, vol. lxxxvi., p. 885.]

Thiery[13] of the Saint Pierre Hospital, Brussels, arrests paroxysms
by what he calls torsion of the abdominal walls. He grasps in his
hands the walls of the abdomen and imparts to them a certain kind of
torsion, which he gradually increases. This treatment is practically
the same as the deep ovarian pressure of Charcot. This compression of
the ovary on the side of the seat of the lesion ordinarily will arrest
immediately the convulsions. The patient is extended horizontally, and
the physician plunges the closed fist into the iliac fossa, often
using great force to overcome the muscular resistance. Poiner has
invented an apparatus called a compressor of the ovaries, which can
sometimes be used with advantage.

[Footnote 13: _Medical and Surgical Reporter_, Oct. 7, 1876.]

Nitrate of amyl is undoubtedly of value in averting grave hysterical
attacks—convulsions, trance, ecstasy, pseudo-coma, mania, etc. It is
frequently used with marked success. Its action was studied on a vast
scale at La Salpêtrière. The convulsions usually stop almost
immediately after one, two, or three inhalations. It is to be
preferred to inhalations of chloroform or ether.

Nitro-glycerin can be used in the treatment of the hystero-epileptoid
convulsions. Notes of a very interesting case of hystero-epilepsy in
which this remedy was successfully employed have been furnished me by
David D. Stewart of Philadelphia. The case was one of hystero-epilepsy
with combined crises. Amyl nitrate on several occasions broke the
convulsive attack, but the patient did not completely regain
consciousness. Stewart was called in during an attack, and found that
the patient had been unconscious for an hour and a quarter. He gave
her hypodermically three minims of a 1 per cent. solution of
nitro-glycerin, and another injection after an interval of about eight
minutes. She became conscious within one minute after the second
injection. After this she had two seizures, both of which occurred on
the same day, and yielded with remarkable promptness to a few minims
of nitro-glycerin given by the mouth. She was put on three minims
three times a day of this drug, the dose being gradually increased.
Sufficient time has not elapsed to report as to the effect of the drug
given during the intervals.

Strong faradic currents, applied with metallic electrodes to the soles
of the feet or to the spine, are occasionally efficacious. The
galvanic current to the head has been extensively employed in the
service of Charcot to arrest hysterical and hystero-epileptic attacks
of the grave variety. One electrode is applied to the forehead, the
other to any convenient place upon the body, as the leg, the ovarian
region, or the spine. The current is applied continuously for several
minutes, or voltaic alternations are made. This method has been used
with success in a few instances, but should never be resorted to by a
physician uncertain of his diagnosis or one practically unfamiliar
with the powers and properties of the electrical current.

{312} The question of oöphorectomy for the relief of hystero-epilepsy
is one of increasing importance in these days of major surgery. At the
meeting of the American Neurological Association (June, 1884) G. L.
Walton read a paper[14] in which he concludes that hysteria is
sometimes set up by ovarian irritation, and can be relieved by
removing the offending organ. He cited a single case. Carsten[15]
concludes that it is criminal neglect not to perform Battey's
operation in cases which fail to be benefited by other treatment. In
the discussion which followed the reading of this paper the subject
was well traversed by Spitzka of New York, Putnam of Boston,
Putnam-Jacobi of New York, and others. Spitzka referred to one case of
Israel's of Breslau, in which a patient was cured of hystero-epilepsy
by a sham operation—a superficial incision in the parietes of the
abdomen. Under the title of castration in hysteria the _Lancet_[16]
tells of an hysterical patient who had suffered for years from
obstinate vomiting and severe ovarian pain. She became extremely weak,
and finally consented to spaying as the only hope. The
operation—performed under chloroform with antiseptic precautions—was a
mockery, the skin only being incised; she was, however, perfectly
cured of her hysterical symptoms.

[Footnote 14: “A Contribution to the Study of Hysteria as Bearing on
the Question of Oöphorectomy.”]

[Footnote 15: Quoted by Walton from _American Journal of Obstetrics_,
March, 1883.]

[Footnote 16: Vol. ii. p. 588.]

In two clinical lectures published in the _Philadelphia Medical
Times_[17] I have given the histories of two cases of hystero-epilepsy
in which oöphorectomy was resorted to for hystero-epilepsy. In the
first of these cases, in which clitoridectomy was also performed,
nymphomania, which was a distressing symptom, was benefited, but even
this was not completely cured. The following is the patient's own
statement: “Since the removal of the ovaries I have been able to
control the desire when awake, but at times in my sleep I can feel
something like an orgasm taking place. My experience leads me to say
that my cure (?) is not due to the absence of the ovaries; there is no
diminution of the sexual feeling. There would be as much excitement of
the parts if the clitoris were still there. If my will gave way, I
would be as bad as ever.” Her general mental and nervous condition is
much the same as before the operations. She is still dominated by
morbid ideas, still unable to take up any vocation which demands
persistence, and still the frequent subject of hystero-epileptic
seizures.

[Footnote 17: April 18 and May 30, 1885.]

The second of these cases was a young girl about seventeen years old
who had never menstruated. She had had epileptic or hystero-epileptic
seizures for several years. An operation was performed in which the
ovaries and Fallopian tubes were removed. Twelve days after the
operation, from which she made a good recovery, she had four
convulsive seizures. She had several attacks subsequently, and then
for a considerable period was exempt. She had, however, acute
inflammatory rheumatism, with endocarditis and valvular trouble. About
seven months after the operation she had several severe convulsions
with loss of consciousness, and died about a year after the operation,
having had many severe seizures during the last few weeks of her life.

There is no warrant either in experience or in a study of the subject
for spaying hysterical girls who have never menstruated. In a case
{313} diagnosticated as hysterical rhythmical chorea removal of the
ovaries was advised by a distinguished specialist. The girl's trouble
came on at about the age of thirteen years. She had never menstruated
properly, although on one occasion, after several weeks of electric
treatment, she had a slight show for a few days. It was proposed to
remove the ovaries in this case on some general principle of given
hysterical trouble; the ovaries must go. In this case, as in the last,
it would have been far better to have put in a good pair of ovaries,
or to have developed these rudimentary organs into health and
activity.

With reference to oöphorectomy for hystero-epilepsy or any form of
grave hysteria it may be concluded—1, It is only rarely justifiable;
2, it is not justifiable in the case of girls who have not
menstruated; 3, when disease of the ovaries can be clearly made out by
local objective signs, it is sometimes justifiable; 4, it is
justifiable in some cases with violent nymphomania; 5, the operation
is frequently performed without due consideration, and the statistics
of the operation are peculiarly unreliable.

When we come to consider the treatment of the disease
hystero-epilepsy, the practical importance of the distinction between
this affection and true epilepsy becomes apparent. Cures of
hystero-epilepsy are not rare. The original cases here reported have
all apparently recovered. Grave hysteria is sometimes cured
spontaneously, either by gradual disappearance with the progress of
age, or suddenly because of some violent impression or under the
influence of unknown causes. One of the worst cases in the service of
Charcot has shown a gradual diminution of the hystero-epileptic
manifestations with the advance of age. In another case under the
influence of strong moral impressions the disease disappeared at a
stroke. The affection, however, should not be abandoned to nature, as
treatment is often of value.

The hydrotherapeutic method of treatment has been found of the
greatest service. Hydrotherapy must be methodically employed by
experienced hands. A number of cases cited by Richer were cured at
hydrotherapeutic institutions. Limited success has followed the use of
metallo-therapy. Besides metallic plates, the same results may be
obtained with other physical agents, to which have been given the name
of æsthesiogenic agents. Among these are feeble electric currents,
vibrations of a tuning-fork, static electricity, etc.

Static electricity has a position of undoubted importance in the
treatment of hystero-epilepsy in some of its phases. Those who have
walked in the wards and visited the laboratories of Salpêtrière will
recall the enormous insulated stools to which are brought troops of
hystero-epileptic patients, who, to save time, are given a vigorous
simultaneous charge of electricity. Even this wholesale plan of
treatment is sometimes markedly efficacious. Vigoroux recommends
static electricity as an æsthesiogenic agent, and regards it as the
most valuable of all agents of this character.

Those drugs should be resorted to which have a tonic influence on the
nervous system. Potassium bromide, as has already been indicated, is
not efficacious. More is to be hoped from tonics and antispasmodics,
such as valerian, iron, salts of silver, zinc, copper, sodium, and
gold chlorides, etc. Good hygienic influences, moral, mental, and
physical, are of the utmost importance.


{314}


CATALEPSY.

BY CHARLES K. MILLS, M.D.


DEFINITION.—Catalepsy is a functional nervous disease characterized by
conditions of perverted consciousness, diminished sensibility, and
especially by muscular rigidity or immobility, which is independent of
the will, and in consequence of which the whole body, the limbs, or
the parts affected remain in any position or attitude in which they
may be placed.

Catalepsy sometimes, but not frequently, occurs as an independent
disease; that is, the cataleptic seizure is the only abnormal
phenomena exhibited by the patient. It is sometimes present, although
also rarely, in organic disease of the nervous system. It has been
noted, for instance, as occurring in the course of cases of cerebral
hemorrhage, softening of the brain, abscess, tumor, and tubercular
meningitis. One case is referred to by C. Handfield Jones in which it
seemed to be due to intracranial epithelioma. As commonly seen, it is
a complication, or perhaps, more properly speaking, a form of
hysteria—hystero-catalepsy.

SYNONYMS.—Some of the many synonyms which have been used for catalepsy
are Catochus, Morbus attonitus, Stupor vigilans, Synochus, Eclipsis,
and Hysteria cataleptica. Trance and ecstasy are discussed sometimes
as synonymous with catalepsy, but they will be considered as separate
affections, as they have certain distinctive features. Catalepsy,
trance, ecstasy, hystero-epilepsy, and other severe nervous
disturbances may, however, all appear in the same patient at different
times or at different stages of the same seizure.

With reference to the term catochus (_κατοχη_, from _κατεχω_, I take
possession of), which has been used as synonymous with catalepsy,
Laycock[1] points out what he considers to be the proper use of this
word, differentiating two cataleptic conditions, which he designates
as the tetanic and the paralytic states. Catochus is the tetanic form,
in which the trunk and limbs are rigidly extended and consciousness is
abolished. Catalepsy proper is Laycock's paralytic form, although the
term paralytic, as here applied, is by no means happy. It is the form
characterized by the peculiar and striking symptom known as waxen
flexibility (flexibilitas cerea)—a condition in which the limbs or
parts are passive and are capable of being moulded like wax or lead
pipe. Rosenthal would not consider any case as one of genuine
catalepsy if this waxen flexibility was absent. I do not think that
this rigorous criterion should always be imposed, {315} although it
might perhaps be better to apply the term cataleptoid to all cases
which do not present true wax-like flexibility. The distinction
sometimes made between catalepsia vera, or true catalepsy, and
catalepsia spuria, or false catalepsy, is practically that indicated
between Laycock's two forms. According to Charcot and Richer,[2] the
flexibilitas cerea is not present in the cataleptic state of
hypnotism.

[Footnote 1: _A Treatise on the Nervous Diseases of Women_, by Thomas
Laycock, M.D., London, 1840.]

[Footnote 2: _Journal of Mental and Nervous Diseases_, Jan., 1883.]

HISTORY.—The word catalepsy was used by Greek writers in its
etymological signification of a seizure or surprise. Hippocrates
described catalepsy; Galen, Aëtius, Rondeletius, and Fernelius have
all related cases; Aëtius has left an accurate description of both
catochus and catalepsy. In 1683, Laurence Bellini published a quarto
volume on various subjects, one of which was catalepsy. From time to
time interesting cases of catalepsy have been reported by medical
writers. One of the best is that recorded by John Jebb in 1782, and
quoted by Chambers in _Reynolds's System of Medicine_. The researches
in hypnotism during the present century, and particularly those of
Heidenhain and of Charcot and Richer, have thrown new light on many
cataleptic phenomena.

ETIOLOGY.—In catalepsy, as in hysteria, insanity, and many neuroses,
inheritance frequently plays a predisposing part. Eulenburg places it
in the large group of diseased conditions designated by Griesinger
constitutional neuropathies. The cataleptic of one generation may be
the descendant of the insane, the epileptic, the syphilitic, or the
alcoholized of a former. Catalepsy is particularly likely to occur in
families which have a history of insanity or drunkenness. Of the cases
detailed or alluded to in this paper, more than a majority had a clear
neurotic history. Catalepsy, like hysteria, occurs with some frequency
among the tuberculous.

Age plays some part in the development of catalepsy. It is of most
frequent occurrence between the ages of fifteen and thirty, but has
been observed at all ages. It is of unusual occurrence in very early
childhood, but A. Jacoby,[3] Clinical Professor of the Diseases of
Children in the College of Physicians and Surgeons in New York,
reports a case of well-marked catalepsy in a child three years old.
This patient, a girl, was admitted to the Mt. Sinai Hospital, New
York, in September, 1879. She had whooping cough and some symptoms of
typhoid fever. After she had been in the hospital three weeks choreic
twitchings of the eyes and eyelids, with divergent strabismus, were
observed. Examining her, it was found that she was cataleptic; her
arms and legs would remain in any position in which they were placed;
she would drop the uplifted arms slowly when commanded; sensibility to
contact, pain, and temperature were entirely lost, and the skin and
patellar reflexes were diminished. Her appetite was ravenous, and
urine was passed in large quantities. Other phenomena and details of
cataleptic symptoms, which continued for about a month, are recorded
by Jacoby. The child recovered, but remained weak and anæmic for a
long time.

[Footnote 3: _American Journal of Medical Science_, N. S. lxxxix.,
1885, p. 450.]

Monti[4] records eleven cases of catalepsy met with in children, male
and female in about equal numbers, of from five to fifteen years, the
average age being nine years. Eulenburg speaks of catalepsy at five
{316} years of age, and quotes Schwartz, who noticed in a boy seven
years old, in consequence of rough treatment, first a choreic
condition, which later passed into catalepsy. Lloyd's case, to be
detailed later, also studied by myself at the University Hospital, was
in a boy eight years old. B. L. Hovey[5] of Rochester, New York,
reports an interesting case of catalepsy in a boy eight years old.

[Footnote 4: _Gerhardt's Handb. d. Kinderk._, vol. v., L. P., 186 _et
seq._, quoted by Jacobi.]

[Footnote 5: _The Hospital Gazette_, 1879, vi. p. 19.]

C. E. de Schweinitz of Philadelphia, Ophthalmic Surgeon to the
Children's Hospital and Prosector of Anatomy at the University of
Pennsylvania, has kindly put into my hands the unpublished notes of a
highly interesting case of catalepsy or automatism at command, or of
both, in a child two and a half years old. I will give this case in
full, chiefly in the language of De Schweinitz, because it is, so far
as I know, the youngest case on record. Some of the tests which were
applied in this case are among the most useful which can be resorted
to in determining how far the phenomena presented are genuine or
induced, simulated, or imitated:

The patient was a girl aged two and a half years, who had recently
recovered from an attack of diphtheritic conjunctivitis. During the
period of her convalescence the attending nurse called attention to
the unusual position assumed by the child while sleeping—viz. a
lateral decubitus, the head raised a short distance from the pillow,
and the forearm slightly elevated and stretched out from the body, the
muscles at the same time exhibiting marked tremulousness. A series of
trials readily demonstrated that the child when awake could be placed
in any position compatible with her muscular power, and that she could
thus remain until released. She was placed, for instance, in the
sitting posture, the arm brought at right angles to the body, the
forearm at right angles to the arm, and the hand at right angles to
the forearm, both legs raised from the bed, and the head bent
backward. This position, a most uncomfortable and difficult one to
preserve, would be maintained until the little subject dropped from
sheer exhaustion. Flexion and extension of each separate finger were
easily produced, and the fingers remained until replaced in the
positions in which they had been fixed. At the beginning the child's
mind was sluggish, although she asked for food and made known her
various wants. How far she appreciated surrounding objects could not
be accurately ascertained, inasmuch as the previous disease of her
eyes had left her with a central corneal macula on each side,
rendering her almost sightless in one eye and with but indifferent
object-perception in the other. Voluntary motion was preserved, and
she sat up, turned, and moved whenever she pleased, but most often
when at rest at this stage maintained somewhat of the position before
described which during sleep first attracted attention to this
condition.

In conjunction with Morris Lewis an examination of the cutaneous
sensibility and reflexes was made, which showed diminished sensibility
in the legs and thighs, but not higher up, where the pricks of the
instrument were quickly appreciated. Her knee-jerk was apparently
absent on the right side and present on the left; but this test,
always most unsatisfactory in children, yielded no certain evidence
and constantly gave contradictory results. Scratching the skin of the
soles of the feet, legs, thighs, and abdomen with a pointed instrument
was {317} followed by marked reflex movements. Electro-muscular
contractility was everywhere preserved. The child at this time was
feeble and anæmic, but her appetite was good—not depraved nor
voracious; the tongue was clean, the bowels regular. The urine was of
a light amber color, specific gravity 1020, free from albumen and
sugar.

As the nutrition of the child improved, it was found that the curious
positions could be produced by word of command as well as by
manipulation. In short, within six weeks after the first
manifestations of this disorder, as a usual thing the little patient
ate, slept, and played as a normal child should do, but could at any
time be thrown into this cataleptoid state. Her one dominant idea
apparently was to maintain the position in which she had been placed.
She was often turned into some constrained posture, and all attendants
absented themselves from the room and left her to her own devices; but
no attempt on her part was made to in any way change her attitude. If
at dinner-time a bowl of broth was placed before the patient, she
would begin to eat with great relish, but if the spoon was taken away
and her hands raised over her head, they would so remain, the child
making no effort to return to her meal, although the bowl stood before
her and all watchers again retired from the room. This experiment was
suggested by H. C. Wood, who examined the child with me. To show how
completely her consciousness was occupied with one idea of maintaining
any position in which she had been placed, the following additional
experiments may be quoted: If she was put into a sitting position, as
in the act of supplication, with her hands folded and arms extended,
and then given a sudden push sufficient to overthrow her equilibrium,
the arms would be quickly and intuitively thrown out to protect her
from the impending fall, but, the fall accomplished, they would as
quickly be returned to their former position. If a heated silver spoon
was gradually brought in contact with her extended hand, an expression
of pain would pass the child's face, perhaps a cry escape her, and the
injured member be rapidly withdrawn, but again almost immediately
returned to its original place. It seemed as if the idea of fixity in
a certain position which occupied the child's mind was suddenly
disturbed by another outside impression, but, being dominant, it
quickly drove away the intruder and the former state was restored. At
this time the phenomena noted were somewhat in accord with those
induced by the mesmeric process, inasmuch as the consciousness seemed
largely given up to the one impression operating at that time—_i.e._
the maintenance of certain fixed positions. Unlike this condition,
however, the readiness to receive new impressions, and the complete
abeyance of those senses not operating was wanting, for, as seen
above, the new impression only for a moment disturbed the child's one
idea, to which she quickly returned; nor was there any true absence of
sensibility, as was evidenced by the result from touching her with a
heated spoon.

As time wore on, a new phase of this condition became evident. The
induced manifestations seemed to act the part of some amusement to the
child, and the complete absence of volition which had been an early
characteristic phenomenon was not now so marked a feature. Thus, if,
after the experimenter had for a time moulded and twisted the child
into various shapes, he would suddenly leave the room, the little
subject {318} would cry lustily, as a child does when suddenly
deprived of its playthings, although, curiously enough, no matter how
hard she cried, she would not release herself from the last position
in which she had been left. Often during any series of observations
that were being made it was noted that a faintly-amused look played
about her lips, which speedily gave way to a fit of crying when the
performance stopped. The hand which, when formerly placed in any
position, remained a perfectly motionless and passive object, was now
seen slightly to change its place, move the fingers, or the like—an
observation first made by A. K. Meigs while examining the patient. The
house-physician, Nathan P. Grimm, took great care and interest in
observing the case.

De Schweinitz, in reporting the case, briefly discusses the probable
cause of the phenomena exhibited. He discards the views that either
fear of the experimenter, such as is shown by a trained animal, or the
partial blindness of the child, was responsible for the
manifestations. He believes that a direct relation existed between the
phenomena and the state of the child's nutrition. The more run down
her system was, the more nearly did the nervous phenomena resemble
those of true catalepsy. Evidently, her symptoms were partly
cataleptic and partly phenomena of automatism at command, similar to
those which have been observed in hypnotic experiments, and which will
be alluded to later.

Catalepsy is of more frequency in the female than in the male sex, but
the statistics are not sufficient to give any exact ratio.

The periods of puberty and early menstruation and of pregnancy furnish
the most favorable opportunities for the development of cataleptoid
seizures in predisposed individuals. In 3 of 10 cases observed by
Landouzy catalepsy appeared to be developed in consequence of the
sudden suppression of menstruation; in a fourth it occurred in a young
girl after a dysmenorrhœa with chronic phlegmasia of the genitals.
Masturbation is sometimes mentioned as a cause, particularly in boys.

Reflex irritation undoubtedly often acts as an exciting cause of
catalepsy. Preputial irritation, relieved in part by circumcision, was
present in the case of Lloyd, and has been noted by others. Handfield
Jones mentions a case, recorded by Austen in his work on _General
Paralysis_, in which the cataleptic seizure was, to all appearances,
due to fecal accumulations. The attack disappeared promptly after an
enema had thoroughly operated.

Briquet believed that catalepsy, when it did not follow upon organic
disease, was ordinarily the result of moral causes, such as vivid and
strong emotions—fear, chagrin, indigestion, anger, or profound and
prolonged meditation. He refers to the able and curious thesis of
Favrot,[6] who states that in twenty cases in which the causes of the
malady were indicated it had been always the result of a moral
affection. A magistrate insulted at his tribunal, seized with
indignation, is suddenly taken with catalepsy, etc. According to Puel,
its causes are always depressing moral affections, as chagrin, hatred,
jealousy, and terror at bad treatment. Unrequited love is set down as
a cause, but what has not unrequited love produced? Jones mentions a
case which occurred in a man sixty years old on the sudden death of
his wife.

[Footnote 6: “De la Catalepsie”—Mémoire couronné par l'Académie de
Médecine, _Mémoires de l'Académie de Médecine_, Paris, 1856, t. xx. p.
409, A. 526.]

{319} Cullen believed that catalepsy was always a simulated disease;
he preferred, therefore, to place it as a species of apoplexy.
Temporary catalepsy may, according to Rosenthal, be produced in
hysterical patients by covering their eyes with their hands or a
cloth. Malaria has been charged with the production of catalepsy, and
apparently properly. Traumatism is another of its well-authenticated
causes. Blows upon the head have been particularly recorded as having
an etiological relation to this disorder.

Partial catalepsy has been observed after typhoid fever with severe
cerebral symptoms, and also associated with meningitis and
intermittent fever. Mancini[7] relates a case of cerebral rheumatism
complicated or causing catalepsy. A blacksmith, aged thirty-three, had
nearly recovered from a rheumatic attack when he became melancholic,
complaining also of severe headache. When admitted to the hospital he
was found to be imperfectly nourished. He lay on his back, his face
without expression, speechless, motionless, pupils insensible to the
light, smell impaired, sensation of heat and pain and reflexes absent,
galvanic and faradic contractility increased, the rectum and bladder
paralyzed. He presented the phenomena of waxen flexibility, the trunk
and limbs remaining in whatever position was given them. Considering
the previous attack of articular rheumatism and the sudden appearance
of nervous disorder during the convalescence of this disease, Mancini
believed that the case was probably one of cerebral rheumatism. The
man recovered under diaphoretics and counter-irritation.

[Footnote 7: _Lo Sperimentale_, March, 1878.]

Among the important causes of catalepsy bad nutrition may undoubtedly
be placed. In the case of De Schweinitz the cataleptoid phenomena
rapidly improved, and eventually disappeared as the child's general
health was restored by tonics and good diet. Hovey's case was
insufficiently clad and badly fed. One of Laségue's cases, quoted by
Handfield Jones, died of gradual marasmus, another of pulmonary
phthisis. Attacks of catalepsy have sometimes resulted from a
combination of excitement, fatigue, and want of food. They occur also
in diseases or conditions like phthisis, anæmia, and chlorosis,
affections which practically gives us the same cause—namely, bad
nutrition. In these cases the nervous system, like other parts of the
body, takes part in the general exhaustion.

Rosenthal refers to the production of symptoms of temporary catalepsy
by the administration of narcotics and the inhalation of ether and
chloroform. In a somewhat ancient American medical periodical[8]
Charles D. Meigs of Philadelphia gives an interesting account of a
case of catalepsy produced by opium in a man twenty-seven years of
age. The man had taken laudanum. His arms when in a stuporous
condition remained in any posture in which they happened to be left;
his head was lifted off the pillow, and so remained. “If he were made
of wax,” says Meigs, “he could not more steadily preserve any given
attitude.” The patient recovered under purging, emetics, and bleeding.
Darwin, quoted by Meigs, mentions a case of catalepsy which occurred
after the patient had taken mercury. He recovered in a few weeks.

[Footnote 8: _The North American Medical and Surgical Journal_, vol.
i. p. 74, 1826.]

That imitation is an exciting cause of catalepsy has been shown by the
{320} often-told story of epidemic hysteria, but more especially by
accounts given of certain peculiar endemics of catalepsy. Handfield
Jones[9] gives an account of an endemic which prevailed at
Billinghausen near Wurzburg: “The population consists of peasants who
are well off, but who intermarry very much, and are small and
deformed. The affected individuals constitute half of the number,
males as well as females. They are called there the stiff ones
(starren). A chill is commonly said to be the exciting cause of the
attacks. The patients are suddenly seized by a peculiar sensation in
their limbs, upon which all their muscles become tense, their
countenances deadly pale; they retain the posture which they first
assume; their fingers are bent and quiver slightly, and the eyeballs
in the same way, the visual axis converging; their intellects and
senses are normal, but their speech consists only of broken sounds.
The attack ceases in from one to five minutes, and the body becomes
warm.”

[Footnote 9: _Op. cit._, quoted from _Schmidt's Jahrbuch_.]

SYMPTOMATOLOGY.—The cataleptic seizure, when it is not the result of
some hypnotizing procedure, usually takes place in the following
manner: The patient usually, after some patent exciting cause,
suddenly ceases whatever she may chance to be doing, becoming rigid
and immobile in the last position which she had been in before the
attack ensued. “She remains,” says Rosenthal, “as if petrified by the
head of Medusa.” The features are composed, the eyes usually directed
forward. She is pale; breathing, pulsation, and temperature are
usually somewhat reduced. At first the limbs may be found to offer
some resistance; soon, however, and sometimes from the beginning, they
can be moulded like wax into any possible position, where they will
remain until again changed by external agency.

Attacks of catalepsy, as a rule, come on suddenly, without special
warning; sometimes, however, special phenomena, which may be compared
to epileptic aura, may precede the attack. Thus, Rosenthal speaks of
two cases that were ushered in, and also bowed out, by hiccough. The
attacks may terminate as suddenly as they begin, but sometimes the
patients come out of the state gradually. They are quite likely to
appear dazed and stupid when emerging.

Perverted consciousness is another marked symptom of catalepsy.
According to some authors, the loss of consciousness is absolute, and
upon this symptom they base their diagnosis from two or three other
somewhat similar conditions. As I have already indicated in discussing
the general subject of Hysteria, this question of consciousness or
unconsciousness is not one to be decided in haste. In catalepsy, as in
hystero-epilepsy, the conditions as to consciousness may differ. What
might be termed volitional consciousness is in true catalepsy
certainly in abeyance. Flint[10] divides catalepsy, according to the
condition as to consciousness, into three kinds—namely, complete,
incomplete, and complicated. He, however, regards trance and day-mare
as instances of incomplete catalepsy, in which the intellectual
faculties are not entirely suspended and the senses are not materially
affected, the patient being unable to move or speak, but conscious of
all that is going on around him. He believes that such cases resemble
more closely the cataleptic condition than they do that of ecstasy. In
genuine catalepsy with waxen flexibility, analgesia, etc. there may be
{321} greater or less depths of unconsciousness, but some degree of
unconsciousness or of obtunded consciousness is necessary to the
existence of true catalepsy.

[Footnote 10: _Buffalo Medical Journal_, xiii., 1857-58, p. 141.]

Catalepsy presents well-marked disturbances of sensation, although
these, like the conditions as to consciousness, differ somewhat in
different cases. Anæsthesia in its different forms, and especially
analgesia, are always present in some degree. Experiments without
number have been tried on cataleptic patients, showing their
insensibility to painful impressions: they have been pinched, pricked,
pounded, burned with heated irons, and rubbed down with blocks of ice.
Skoda reports a case in which general sensibility was abolished, but a
lighted paper rotated rapidly before the eyes gave rise to tremors of
the limbs, and strong odors induced slight movement, redness of the
cheeks, lachrymation, acceleration of the pulse, and elevation of the
temperature.

Hyperæsthesia, although rare, has been noted in a few isolated cases
of catalepsy. Puel records a case in which, during the cataleptic
paroxysm, the slightest touch or noise caused the patient to grind the
teeth and cry out. In some cases sensibility to certain special
impressions, as to a strong current of electricity, has been retained,
while all others were abolished. In a case of hystero-catalepsy at the
Philadelphia Hospital, when all other measures had failed an attack
was aborted and evidence of pain produced by the application of a
strong faradic current with metallic electrodes.

A marked change in the state of reflex irritability is another of the
striking symptoms of true catalepsy. Varying conditions as to reflex
irritability have been observed by different authors. So far as I am
aware, few special observations have been made upon the tendon
reflexes in catalepsy. In the case of De Schweinitz the knee-jerk was
apparently absent on one side and present on the other, although the
cataleptic symptoms were not unilateral.

The symptom known as flexibilitas cerea, or wax-like flexibility, to
which I have referred under Synonyms, is, as has been stated, by some
considered pathognomonic of this affection. While I do not hold to
this view, I regard the symptom as the most important phenomenon of
the disease. It is a symptom which from its very nature can be, up to
a certain point, readily shammed, and when considering Diagnosis some
methods of determining its genuineness will be given.

Careful observation as to the pulse, respiration, and temperature are
lacking in the reported cases of catalepsy. According to
Eulenburg,[11] “the respiration is generally of normal frequency,
sometimes rather slow, more frequently of diminished or irregular
intensity, so that lighter and deeper inspirations alternate. The
pulse may also be slower, with slight excursion and diminished tension
of the arteries. The temperature generally remains normal, but in
certain cases is decidedly lowered.” The lowering of temperature, and
particularly the presence of extreme coldness of the surface, with
exceedingly weak pulse and respiration, have doubtless always been
present in the cases—a few, at least, authentic—in which catalepsy has
been supposed to be death.

[Footnote 11: _Op. cit._]


{322} Hypnotic Catalepsy.

The investigations into the subject of hypnotism made in recent years
have given to the profession a series of interesting phenomena which
should be considered, at least briefly, under the symptomatology of
catalepsy. In a general review of the subject of hypnotism[12] by me
many of the facts observed and theories advanced by Braid, Heidenhain,
Charcot, Richer, and others were examined. I will here recall those
observations of Heidenhain[13] and of Charcot and Richer[14] which
relate to the production of a cataleptic or cataleptoid state, and to
the phenomena which take place in this state.

[Footnote 12: _Am. Journ. Med. Science_, Jan., 1882.]

[Footnote 13: _Animal Magnetism: Physiological Observations_, by
Rudolph Heidenhain, Prof. Physiology in the University of Breslau,
London, 1880.]

[Footnote 14: _Etudes cliniques sur l'Hystero-epilepsie, ou Grande
Hystérie_.]

The method of Heidenhain was similar to that employed by Braid. The
latter, however, did not make use of passes. In the first place, the
individual was made to gaze fixedly at a shining faceted glass button
for some six or eight minutes, the visual axes being made to converge
as much as possible. Heidenhain, like Braid, found the most
advantageous direction of the visual axes to be that of upward
convergence. According to Carpenter, in the fixation this upward
convergence is very important; it suffices of itself in blind people
or in the night to produce hypnosis. After the fixation of gaze had
been continued for some six or eight minutes, the operator stroked
over the face, without immediately touching the surface, from the
forehead to the chest, after each pass bringing the hands, which were
warm, around in an arc to the forehead again. He either allowed the
eyelids to be closed or gently closed them. After ten or twelve passes
he asked the person to open his eyes. When this occurred without
hesitation or with only slight difficulty, he again made the person
stare at the glass for some six minutes, and then repeated the passes,
which often brought about the hypnotic state when the simple fixation
did not succeed.

The symptoms of the hypnotic state were in the main those which have
just been described as the symptoms of catalepsy—namely, diminution of
consciousness, insensibility, increased reflex irritability, and
fixity of the body or limbs in any position given.

In the slighter forms of hypnotism the subjects were able to remember
what had occurred during their apparent sleep. In more fully-developed
forms they had no remembrance of what had taken place, but by giving
hints and leading questions of their various actions they were able to
call them to mind. In the most complete forms of hypnotism no
remembrance whatever was retained. It can nevertheless be proved that
even during the most completely developed hypnosis sensory perceptions
take place, but they are no longer converted into conscious ideas, and
consequently are not retained by the memory; and this is undoubtedly
because the hypnotized individuals have lost the power of directing
their attention to their sensations.

A symptom of the hypnotic state in its most complete development was
highly marked insensibility to pain. A pin could be run right into the
hand, and only an indistinct feeling of contact was brought about.
{323} Immediately on awaking the full sense of pain was again present.
The fact that the tactile sense and the sense of pain are distinct was
corroborated.

Increased reflex irritability and tonic spasm of the voluntary muscles
accompanied the hypnotic condition. Stroking the flexible right arm of
a subject, it at once became stiff, since all the muscles were thrown
into a state of reflex spasm. Reflex muscular contraction spread over
the body when certain definite cutaneous surfaces were irritated. With
slight increase of reflex irritability those muscles alone contracted
which lay immediately under the area of the skin which had been
stroked. Stroking the ball of the thumb caused adduction of the thumb.
Stimulating the skin over the sterno-mastoid caused the head to assume
the stiff-neck position. When the irritability was somewhat more
increased, by a continuous irritation of a definite spot of skin
neighboring and even distant groups of muscles could be set into
activity. Heidenhain stroked continuously the ball of the left thumb
of his brother, when the following muscle-groups were successively
affected with spasm: left thumb, left hand, left forearm, left upper
arm and shoulder, right shoulder and arm, right forearm, right hand,
left leg, left thigh, right thigh, right leg, muscles of mastication,
muscles of the neck.

From a study of such phenomena Heidenhain was inclined to consider
that the hypnotic state was nothing more than artificially produced
catalepsy.

The possibility of fixing any part of the body in any given position
constituted an essential factor in the exhibition of Hansen. He made
one of his subjects, for instance, sit before him in a chair, and
adapted the hands to the seat so that his fingers grasped the edges.
After hypnotizing him he stroked along his arms, and his fingers took
convulsive hold of the edges of the seat. Placing himself in front of
the subject, he bent forward; the subject did the same. He then walked
noisily backward, and thereupon the subject followed him through the
hall, carrying his chair with him like a snail its shell.

One of the observations of Richer was on the influence of light on
catalepsy and hysterical lethargy. The patient was placed before a
bright focus of light, as a Drummond or electric light, on which she
was requested to fix her sight. In a short time, usually a few seconds
or several minutes, sometimes instantaneously, she passed into the
cataleptic state. She was as one fascinated—immobile, the wide-open
eye fixed on the light, the conjunctiva injected and humid. Anæsthesia
was complete. If the patient was hemianæsthetic, she became totally
anæsthetic. She did not present contractures. Her limbs preserved the
suppleness of the normal state or nearly this—sometimes being the seat
of a certain stiffness; but they acquired the singular property of
preserving the attitude which one gave them. One interesting
peculiarity was the influence of gesture on physiognomy. The features
reflected the expression of the gesture. A tragic attitude imprinted a
severe air on the physiognomy; the brows contracted. If one brought
the two hands to the mouth, as in the act of sending a kiss, a smile
immediately appeared on the lips. It was an example of what Braid
calls the phenomena of suggestion—of Heidenhain's imitation. The state
of catalepsy endured as long as the agent which produced it—that is,
as long as the light continued to impress the retina.

{324} The characteristics of the two abnormal states—catalepsy and
lethargy—into which hystero-epileptics may be thrown were summarized
by Richer as follows: (1) Cataleptic state: The eyes wide open; total
and absolute anæsthesia; aptitude of the limbs and different parts of
the body to preserve the situation in which they are placed; little or
no muscular rigidity; impossibility of causing muscular contraction by
mechanical excitation. (2) Lethargic state: The eyes wide open or half
closed; persistent trembling of the upper eyelids; convulsion of the
eyeballs; total and absolute anæsthesia; muscular hyperexcitability;
the limbs, in a condition of resolution, do not preserve the situation
given to them, except the provoked contracture impressed upon them.

In the experiments at Salpêtrière the hystero-epileptics were
sometimes plunged into the states of catalepsy and lethargy under the
influence of sonorous vibrations instead of frights.

During the state of provoked hysterical catalepsy it was found that
sight and hearing could be affected by various procedures. The eyes
were fixed, and seemed not to see anything. If, however, an object was
slightly oscillated in the axis of the visual rays at a little
distance from the eyes, soon the gaze of the patient followed these
movements. The eyes, and sometimes even the head, seemed to turn at
the will of the operator. Hallucinations were produced. When the look
was directed upward the expression became laughing; when downward,
sombre. The cataleptic state might now cease completely. The patient
walked, followed the object on which her gaze was fixed, and took
attitudes in relation with the hallucination suggested. Music also
caused her to assume positions related with the various sentiments
suggested to her by the music. Sudden withdrawal of the object from
before the eyes or of the sound from the range of hearing caused a
return of the catalepsy. The cataleptic patient in whom the eye was in
such a state as to perceive the movements of an experimenter placed in
front of her reproduced these movements exactly. At the Philadelphia
Hospital I have repeated most of the experiments of Heidenhain and of
Charcot and Richer.


Unilateral Catalepsy.

Hemi-catalepsy or unilateral catalepsy is sometimes observed, and has
been studied both in hypnotic investigations and as a special nervous
affection. Charcot and Richer found that hemi-catalepsy or lethargy
may be produced on a patient, and that they may both exist
simultaneously in the same subject. When, for instance, a patient was
plunged into the cataleptic state under the influence of a bright
light, shutting with the hand one of the eyes, the patient at once
became lethargic on the same side only; the other side remained
cataleptic. Heidenhain and Gruetzner studied some remarkable
phenomena, which they have recorded under the name of unilateral
hypnosis, in which some surprising sensory disturbances occur. They
also found, among other things, a striking disturbance in the process
of accommodation and in the perception of colors in the eye of the
cataleptic side. In a case of hystero-epilepsy upon which I performed
numerous hypnotic experiments which have been reported[15] {325} the
patient nearly always presented unilateral cataleptic phenomena. These
were present on the left side, the patient being subject to
convulsions which were more marked on the right side, this being also
much wasted.

[Footnote 15: _Philadelphia Med. Times_, Nov. 19, 1881.]

I witnessed some curious unilateral cataleptoid phenomena in the case
of a medical friend, who has made a note of his experience.[16] He
says: “In the course of some experiments on table-tipping, which were
conducted mainly to satisfy the curiosity of persons who had never
seen anything of the kind, I became the subject of a very peculiar and
marked hypnotic influence. The ordinary tricks of tipping, answering
questions, guessing numbers, etc. had been performed with the table,
during the greater part of which I had been one of the circle, when my
right hand began to contract so as to form an arch, and was then
lifted from the table. These movements were not volitional; I was
unable to control them. While my hand was in this position one of the
persons sitting at the table suddenly put his hand on my forehead, and
I sank back in the chair, passing into a conscious but apparently
powerless state, but only for a few moments. Later in the evening the
hypnotic influence in the right hand was still more distinctly
manifested. If allowed to remain a short time on the table, the
fingers began to vibrate vertically and horizontally, the motion
finally extending to the forearm and becoming so violent as to throw
the hand about in a rapid and forcible manner. While thus affected I
found it utterly impossible to sign my name. I would be able to form
the first letter or so, and then most extraordinary gyrations would be
made. In one instance I wrote very slowly, using all the muscular
control at my command, and succeeded in writing the full name, but in
a form wholly different from my ordinary signature.”

[Footnote 16: _Polyclinic_, Sept. 15, 1883.]

My attention was called to these phenomena, and the experiments were
repeated the next week in my presence, with like results. In addition,
I succeeded in forcibly placing the affected arm in various
positions—bent at right angles, the hand resting on the top of the
head, etc.—from which positions he was unable to move it. He seemed to
have lost the connection between volition and the motor impulse. The
experiments were continued for several hours at each sitting, but
owing to the depressed mental state which was produced for a short
time, apparently by them, they have not been repeated.

Occasionally, cases of unilateral catalepsy associated with rotatory
phenomena are met with, especially in hysterical children. In 1882, I
studied in the nervous dispensary of the hospital of the University of
Pennsylvania an interesting case with rotatory and unilateral
cataleptoid symptoms. This case has been reported by James Hendrie
Lloyd.[17] The patient was a boy eight years old. His paternal
grandfather hanged himself. On the mother's side there was a history
of tuberculosis. Two years before coming to the hospital he had had
four attacks of spasms. For two weeks he had been having from twelve
to twenty similar spasms daily; some of these were observed in the
dispensary. “The boy's head was suddenly drawn upward and to the right
to its extreme limits by the action chiefly of the
sterno-cleido-mastoid muscle. The eyes turned also to the extreme
right, with slight convulsive (clonic) action, and became {326} fixed
in that position, with very wide dilatation of the pupils. In a second
or two he began to rotate his whole body to the right, and turned
completely around, perhaps ten or twelve times. On some occasions he
had fallen down, his mother said, toward the end of the spell. If
taken hold of and steadied—which required but little force by the
physician—the rotation could be stopped, though the head and eyes
remained drawn, and the boy's arms could be placed in any desired
position. If now he was once more let loose, his body again rotated,
while his arms were held in true cataleptoid rigidity. The whole
duration of the attack was from one half to one minute. The boy was
intelligent, and said he knew what was taking place about him while he
was in the fit, though he gave no satisfactory evidence of such
knowledge at the time. There was no history of headache or any
disease. His ears were subsequently examined and found normal. He had
taken worm medicine in abundance from the family physician without
results. There were no psychical traits of importance to suggest
foolish or wilful simulation. The only accident had been a fall from a
wagon years previously. As the patient had an adherent prepuce, Wood
advised circumcision, and took pains to explain the operation to the
mother. This evidently made a great impression on the child's mind,
which is worthy of notice in considering the case. The potassium
bromide was continued. At the third visit, which had been appointed
for the operation of circumcision, the mother reported the patient
much better. The boy had been having great fear of the proposed
operation, and now said that he thought he could control the spells. A
psychical element was thus distinctly indicated, and its likeness to
chorea major to some extent increased. It was thought best, however,
instead of circumcision, to break up adhesions and retract the
foreskin, which was done by J. William White. At the fourth visit,
after ten days, a still greater improvement was noted.”

[Footnote 17: _Philada. Med. Times_, vol. xii., June 17, 1882.]

Lloyd in reporting this case discusses the physiology of the
condition, and refers to other cases in medical literature. According
to Brown-Séquard, the great cause of rotation phenomena is a
convulsive contraction in some of the muscles on one side of the body.
Carpenter believes they are due to weakness of the sensori-motor
apparatus of one side. Laycock holds that the cerebellum is involved.
Lloyd likens the case to chorea major. He refers to cases reported by
Radcliffe[18] and J. Andrew Crawford.[19]

[Footnote 18: _Reynolds's System of Medicine_, art. “Chorea.”]

[Footnote 19: _Cycl. of Pract. Medicine_, art. “Chorea.”]

At the Pennsylvania Training School for Feeble-minded Children at
Elwyn is a little patient familiarly spoken of as the Dervish. I have
examined this boy several times, and have frequently watched his
performances. I. N. Kerlin, superintendent of the institution, has
kindly furnished me with some notes of this case. The antecedents of
the patient are unknown. He is about fifteen years of age, is of small
stature and weight, a demi-microcephalic, epileptic, and mute idiot.
His epilepsy, however, supervened only in 1884, and the seizures
continue now at the rate of three or four a month. At all times he is
subject to certain automatic tricks with his hands, putting and
twisting them into various positions. Periodically almost during every
day he gives exhibitions of the habit which has led him to be called
the {327} Dervish. He commences by tattooing his chin with his left
hand; next he delicately and rapidly touches the fingers of his left
hand to the wrist of the right, makes two or three salaams, and then
impulsively gyrates the body from left to right. The right heel is
pivotal, and the force is maintained by touches of the left toe or
heel upon the floor. He will usually take from three to seven turns at
a time, with a salaam or two between every series. Fifteen minutes or
more will be thus consumed before he darts away toward a window, where
he remains a few moments in a dazed state, from which he rouses to
recommence his hand tricks. Perhaps he will select a broad belt of
light in which to display his hand for visual enjoyment. He has a
cataract of the right lens, and possibly partial amaurosis of the left
eye. A supplemental performance sometimes indulged in is to stand at
one fixed point and throw his head and shoulders from side to side,
describing with the former two-thirds of a circle, the occiput being
flexed backward as far as the neck will permit. These movements,
rapidly made, reach three and four hundred under favorable conditions.

Kerlin regards the displays made by this boy to be the pure automatic
phenomena of idiocy which have been developed to an artistic finish,
and out of which the patient gets enjoyment. This enjoyment probably
exists in some anæsthetic or stuporous condition of certain
nerve-centres, something like the sensation of common dizziness. He
does not look upon the case, therefore, as one of genuine catalepsy,
but I have recorded it here in connection with the case just given
because it illustrates a phase of automatism and rotation movements
closely allied to cataleptoid conditions.


Catalepsy and Cataleptoid Phenomena among the Insane.

Catalepsy and cataleptoid or cataleptic phenomena are of comparatively
frequent occurrence among the insane. Niemeyer says[20] that they are
especially common among persons suffering from melancholia.
Kahlbaum[21] has described a form of insanity which he names
katatonia, from the Greek _κατατονος_, stretching down. This disease
is “characterized by alternate periods, supervening with more or less
regularity, of acute mania, melancholia, and epileptoid and
cataleptoid states, with delusions of an exalted character and a
tendency to dramatism.”[22]

[Footnote 20: _Textbook of Practical Medicine_, Felix von Niemeyer,
American trans., 1876, vol. ii. p. 387.]

[Footnote 21: _Klinische Abhandlungen über psychische Krankheiten_, 1
Heft, “Die Katatonie,” Berlin, 1874.]

[Footnote 22: _A Treatise on Insanity in its Medical Relations_, by
William A. Hammond, M.D., New York, 1883, p. 576.]

Kiernan[23] has written a valuable memoir on this affection. He has
collected fifty cases, a few of which he gives in detail. Hammond and
Spitzka discuss the disorder, giving new cases, in their treatises on
insanity.

[Footnote 23: _American Journal of Insanity_, July, 1877, and
_Alienist and Neurologist_, October, 1882.]

Katatonia may begin in various ways, but it usually pursues a certain
cycle. First appears stuporous melancholia, accompanied or followed by
cataleptoid manifestations; then a period of mania with illusions,
hallucinations, and delusions. Melancholia reappears in some form,
with {328} cataleptoid, waxy condition of the muscles, and a
disposition to talk in a pompous or dramatic manner; convulsions or
choreic movements may be present.[24] Sometimes some phase of the
cycle is absent.

[Footnote 24: Hammond.]

In some cases in which the peculiar cycle and special phenomena which
characterize katatonia are not present marked cataleptic or
cataleptoid states may be observed among the insane, either as
episodes or as long-continuing conditions.

As cases illustrating cataleptoid phenomena among the insane have not
yet been published in large number, and are not well understood, I
will record here, under the Symptomatology of Catalepsy, some
illustrative cases which have either fallen under my own observation
or have been supplied to me directly by medical friends.

M. A. Avery, assistant physician to the insane department of the
Philadelphia Hospital, has kindly furnished notes of the following
interesting case:

T——, aged twenty, single, dressmaker. The patient was somewhat below
medium height, slender and emaciated, of nervous temperament,
expression melancholy. The attack of insanity for which she was
admitted was her first. It began four months before admission. No
satisfactory history of the attack could be obtained; she was said to
have been depressed in spirits and to have delusions of poisoning. She
had attempted suicide by throwing herself from the window.

Upon admission, Sept. 20, 1883, she was quiet and gentle in her
manner, but much depressed; she answered questions rationally. No
delusions were detected. Sept. 21st she sat quiet and motionless. Her
eyes were fixed, with marked double, inward squint. She was apparently
insensible to external impressions. This condition lasted about three
hours, when she suddenly sprang up, rushed through the ward, and made
vigorous efforts to escape. On the 22d she lay in bed in a perfectly
passive state, with eyes open and fixed, but the squint had
disappeared. There was a constant slight tremor of the lids. The
conjunctiva was apparently insensible to touch. She seemed to be
unconscious of what was going on around her. Her arms remained raised
in any position in which they were placed. About three o'clock in the
afternoon this condition passed away, and from that time until she
went to bed at eight o'clock she was bright and cheerful and talked in
a rational and intelligent manner. For five days she was quiet and
melancholy, with one spell of a few hours in which she was in a
passive and cataleptic state, as on the 22d.

On the 28th she stood erect with arms extended, whirling rapidly. She
continued this for about half an hour, and then, after a short rest,
began again. She paid no attention to what was said to her, and seemed
unconscious of what took place around her. The next day she remained
in a stupid condition most of the time, but occasionally sprang up and
danced violently or spun round rapidly with arms extended for a few
moments at a time. On the 30th her cataleptic condition was
uninterrupted. She lay motionless, with pulse slow and feeble,
extremities cold; her limbs were easily placed in any desired
position, and remained so for about twenty minutes; then they returned
slowly to a more natural and comfortable position. She continued for
several days in this condition, then aroused and ate heartily. She
seemed brighter and more cheerful, {329} and talked rationally. She
said that she knew all that was said and done when she seemed
unconscious, and that she wanted to speak, but could not. For several
weeks cataleptic symptoms prevailed, with occasional lucid intervals
of a few hours. She eventually settled into a childish, demented
condition.

In the insane department of the Philadelphia Hospital was a
middle-aged man who remained for several years in a stuporous and
cataleptoid state. On several occasions he was before the class in the
clinic-room. He could not be made to speak, but remained perfectly
silent in any condition in which he was placed. His head and trunk
could be bowed forward, sideway, or backward; one foot could be
elevated while he stood; his arms could be placed in grotesque
positions. In whatever attitude he was placed he would remain for a
long time. The only history that could be obtained of this man was
that he had for several months been in a state of melancholia, after
which he was maniacal for three or four months. He escaped from the
hospital, and was brought back in the stuporous and cataleptoid
condition in which he continued. He had been a masturbator.

A Dane, while on a voyage from Copenhagen, fell and broke his leg, for
which he was treated in a hospital. He recovered and became a nurse in
the institution. He fell in love with a female nurse, and was to be
married, but the lady suddenly fell dead. He became melancholic, and
three weeks afterward tried to hang himself. He also had
hystero-epileptic seizures, and was for a long time in a condition of
extreme stupor with cataleptoid phenomena, from which he passed into a
rather excited condition. He had no special delusions, but there was a
tendency to dramatism.

Another case came into the nervous wards of the Philadelphia Hospital.
No history could be obtained from the patient. Whether or not he had
previously suffered from melancholia could not be learned. He would
retain for a long time any position in which he was placed. He also
had hystero-cataleptic spells, and a peculiarity of enunciation with a
tendency to pose. When asked, “How are you to-day?” he would reply, “I
pre-sume-that-I-am-a-bout-the-same—
that-it-is-likely-that-some-thing-has-dis-ap-peared-in-the-mind.” When
asked, “How long have you been sick?” he would begin in the same way:
“I-pre-sume-that-I-will-have-to-say-that-at-a-time-re-mote-ly-dis-
tant;” and then he would branch off into something else.

Wilks[25] speaks of a man whom he saw in the asylum at Morningside who
could be moulded into any position. While in bed on his back his arms
and legs could be arranged in any position, and there they would
remain. He also speaks of a case seen by Savage in Bethlem—a young man
who kept his arms stretched out for two hours, and stood on one leg
for a very long time or until he fell.

[Footnote 25: _Lectures on Diseases of the Nervous System_, delivered
at Guy's Hospital.]

William Barton Hopkins of Philadelphia has given me brief details of a
case observed by him at the Pennsylvania Hospital, which would seem to
have been either one of katatonia or one of cataleptoid attacks
occurring in an inebriate. The patient was an habitual moderate
drinker. For three weeks before he was admitted to the hospital he had
been drinking heavily. His family history showed a tendency to
insanity. He showed {330} great mental anxiety; his face was pale and
had a very troubled aspect. He had no hallucinations. Two days after
admission a sudden outbreak of mania occurred, in which he showed
destructive and dangerous tendencies, and mechanical restraint had to
be employed. Under treatment he became quiet, and was removed by his
friends, having been altogether five days in the hospital. On the day
of his departure, while awaiting some of his friends in the main hall,
he suddenly ran up stairs, and was quickly followed by a nurse, who
found him raising a window with the apparent intention of jumping out.
His face at this time had lost its troubled look, and had rather a
pleased but vacant appearance. While in this condition his limbs were
placed in various positions, and there remained. On another occasion,
while lying on the bed, his limbs and trunk were placed in various
grotesque positions, and there remained. The condition of waxen
flexibility was well marked; many tests were made.

To Wharton Sinkler I am indebted for the unpublished notes of the case
of a woman twenty-seven years of age, who had no family history of
insanity, but whose father was a highly nervous man. She had always
had good health, and was of good physique. Seven years ago she had an
attack of melancholia lasting four or five months; since then she had
no trouble until six months since. At this time she began to be
low-spirited. Then delusions came on—that she was unworthy to live;
that it was wicked for her to eat, because no one else had food; that
those about her were in ill-health. She refused to eat, and would not
talk, and slept badly. When first seen by Sinkler she was stout and
with apparently good nutrition, but was said to have lost flesh. Her
face was expressionless, and she was unwilling to converse, but said
she was quite well, and that her stepmother was ill and needed
treatment. She was undecided in all her movements, and would stand in
one spot until led to a chair, where she would remain if seated.

The patient was placed under the care of two nurses, and for a week
improved daily—ate food, conversed, read aloud, and sewed. At the end
of this time she was left with one nurse, but became obstinate about
eating, and had an altercation with the nurse, in which she became
violent. After this she gradually got into a cataleptoid state. At
first she would stand for a long time in one place, and if seated in a
chair would remain in any position in which she was placed. She began
to have attacks in which she would lie on the floor motionless for
hours. A sharp faradic current was applied to the forearms on one
occasion, and she soon became relaxed. In the attacks the eyes were
closed or rolled upward and fixed on the ceiling. The muscles were
rigid. The arms and legs could be placed in any attitude, and would
there remain. There was no analgesia: she had decided objection to
pin-pricks. For two or three days she was readily aroused from the
cataleptic state by electricity, but it lost its effect, and
etherization was resorted to. The first time a few whiffs of ether
relaxed the rigid limbs. The next day the rigidity continued until
complete etherization was effected. In fact, when the breathing was
loudly stertorous and the conjunctiva insensible to touch, the
rigidity was complete, and it was not until a large amount of ether
had been inhaled that the limbs relaxed. While under the effects of
the ether a vaginal examination was made, and the uterus found normal
in position and size. No evidences {331} of self-abuse were found, nor
had there been any reason for suspecting this. She continued in the
condition described for many days. She was filthy in her habits, and
would not use the commode, although she was made to sit on it for
hours. She would have a stool on the floor or in bed immediately after
rising from the commode. She seemed imbecile, and scarcely spoke, or,
if she did, would say she was dead or was a baby. She would eat
nothing voluntarily: food was put into her mouth, and she would
swallow it, but made no effort to close the lips herself. She was fed
in this way for four or five weeks. If taken up to be dressed, she
would make the procedure as difficult as possible, and when dressed
would not let her clothing remain buttoned, so that her clothes had to
be sewed on her.

After about ten weeks a slight improvement showed itself, first in her
taking food voluntarily, then in speaking. By degrees she became
reasonable, and in about four months from the time she was first seen
was perfectly well. The medication used was very slight, but she was
thoroughly fed, took bromide of sodium and ergot for a time, and
occasionally a dose of paraldehyde to produce sleep. She had two
efficient nurses, who carefully carried out all directions, and who
never yielded a point, but tried to be always as kind as firm. This
case is instructive, not only because of its phenomena, but also
because of the method of feeding and managing the patient and the
result of treatment.

At a meeting of the Philadelphia Neurological Society held February
22, 1886, I exhibited, at the request of Dr. C. P. Henry, of the
Insane Department of the Philadelphia Hospital, a case presenting
cataleptoid symptoms, the phenomena of automatism at command, and of
imitation automatism.

This patient had been recently admitted to the hospital, and no
previous history had been obtained. He was a middle-aged man, not
unintelligent-looking, and in fair physical condition. His condition
and his symptoms had remained practically the same during the short
time that had elapsed since admission. He remained constantly
speechless, almost continually in one position; would not open his
eyes, or at least not widely; would not take food unless forced; and
his countenance presented a placid but not stupid or melancholy
appearance. He had on several occasions assumed dramatic positions,
posing and gesticulating. It had been discovered by Henry that the
patient's limbs would remain where they were placed, and that he would
obey orders automatically. The case had been regarded as probably one
of katatonia, but in the absence of previous history it was not known
whether or not he had passed through the cycle of mania, melancholia,
etc. which constitutes this fully-developed disease. He had had since
admission attacks of some severity, probably, from description,
hystero-epileptic in character.

In exhibiting the patient I first placed his arms and legs and body
and head in various positions, where they remained until he was
commanded to place them in other positions. His mouth was opened, one
eye was opened and the other was shut, and he so remained until
ordered to close his mouth and eyes. In most of these experiments the
acts performed were accompanied by remarks that the patient would do
thus and so as he was directed.

Various experiments to show automatism at command were performed.
{332} I remarked, for instance, that the gentleman was a good
violin-player, when he immediately proceeded to imitate a
violin-player. In a similar way he took a lead-pencil which was handed
to him and performed upon it as if it were a flute. He danced when it
was asserted that he was an excellent dancer; placed his arms in a
sparring position and struck out and countered on telling him that he
was a prize-fighter; went through many of the movements of drilling as
a soldier, such as attention, facing, marking time, and marching. He
was told that he was a preacher and must preach, and immediately began
to gesticulate very energetically, as if delivering an earnest
exhortation. He posed and performed histrionically when told that he
was an actor. He was given a glass of water and told that it was good
wine, but refused to drink it, motioning it away from him. He was then
told that it was very good tea, when he tasted it, evincing signs of
pleasure. During all these performances he could not be induced to
speak; his eyes remained closed, or at least the eyelids drooped so
that they were almost entirely closed. He showed a few phenomena of
imitation, as keeping time and marching to the sound of the feet of
the operator.

In the nervous wards of the Philadelphia Hospital there is now an
interesting case of melancholia with catalepsy and the phenomena of
automatism at command—a man aged twenty-five, white, single, who for
thirteen years had worked in a type-foundry. Three years before coming
to the hospital he had an attack of acute lead-poisoning with
wrist-drop. Two years later he had an attack of mental excitement with
other evidences of insanity. He had hallucinations of sight and
hearing, and thought that he heard voices accusing his sister of
immorality. He at times accused this sister of trying to poison him.
He believed that his fellow-workmen were trying to have him
discharged. This condition lasted for six weeks, when he became gloomy
and stuporous, and would make no effort to do anything for himself.
His friends had to feed him. When first admitted to the nervous wards
he sat in the same position all day long, with his head almost
touching his knees, his arms fully extended by his sides. He would not
help himself in any way. His eyes were always open, and he never
winked. He never slept any during the day, but was perfectly oblivious
to all surroundings. He did not speak or move out of any position in
which he was placed. He could be placed in all sorts of uncomfortable
positions, and would remain in them. After treatment with strong
electrical currents and forced exercise he brightened considerably,
and would walk, after being started, without urging. When treatment
was discontinued, he relapsed into his former state. Frequent
experiments have been performed with this man. Placing his limbs in
any position, they will remain if a command is given to retain them.
He marches, makes movements as if boxing, etc. at command.

The phenomena shown by both of these patients are those which have for
many years been known and described under various names. I well
remember when a boy attending a series of exhibitions given by two
travelling apostles of animal magnetism, in which many similar
phenomena were shown by individuals, selected apparently at haphazard
from a promiscuous audience, these persons having first undergone a
process of magnetizing or mesmerizing. In experiments of Heidenhain of
{333} Breslau upon hypnotized individuals many similar phenomena were
investigated, and described and discussed by this physiologist under
the names of automatism at command and imitation automatism. The
hypnotized subjects, for instance, were made to drink ink, supposing
it to be wine, to eat potatoes for pears, to thrust the hand into
burning lights, etc. They also imitated movements possible for them to
see or to gain knowledge of by means of hearing or in any other way.
They behaved like imitating automatons, who repeated movements linked
with unconscious impressions of sight or hearing or with other sensory
impressions. It was noted in the experiments of Heidenhain that the
subjects improved with repetition. The manifestations of my patients,
although not simulated, improved somewhat by practice. Charcot,
Richer, and their confrères have made similar observations on
hysterical and hypnotized patients, which they discuss under the name
of suggestion. Hammond[26] suggested the term suggignoskism, from a
Greek word which means to agree with another person's mind, as a
proper descriptive designation for these phenomena. In referring to
persons said to be in one of the states of hypnosis, he says that he
does not believe that the terms hypnotism and hypnosis are correct,
as, according to his view, the hypnotic state is not a condition of
artificial somnambulism; the subject, he believes, is in a condition
where the mind is capable of being affected by another person through
words or other means of suggesting anything. In the clinical lecture
during which these opinions were expressed he is reported to have
performed on four hypnotized young men experiments similar to those
which were exhibited by my insane patients. His subjects, however,
were not insane. A bottle was transformed by suggestion into a young
lady; sulphur was transmuted into cologne; one of the subjects was
bent into all sorts of shapes by a magnet; another was first turned
into Col. Ingersoll and then into an orthodox clergyman, etc. In
reading such reports, and in witnessing public exhibitions of the kind
here alluded to, one often cannot help believing that collusion and
simulation enter. Without doubt, this is sometimes the case,
particularly in public exhibitions for a price; but what has been
observed in the mentally afflicted, what has been shown again and
again by honest and capable investigators of hypnotism, prove,
however, not only the possibility, but the certainty, of the
genuineness of these phenomena in some cases.

[Footnote 26: _Med. and Surg. Reporter_, vol. xlv., Dec. 10, 1881.]

Catalepsy and this automatism at command are sometimes confused, or
they may both be present in the same case; indeed, they are probably
merely gradations of the same condition, although it is well to be
able to differentiate them for the purposes of more careful and
accurate investigation. In automatism at command the individual does
what he is directed as long as he remains in this peculiar mental
condition. In experimenting upon him, his arms or legs, his trunk or
head, may be put in various positions, and if commanded to retain them
in these positions he will do so, or he will, at command, put them in
various positions, there to stay until a new order is given. Imitation
automatism occurs also in such cases; patients will imitate what they
see or hear. These cases differ only from those of genuine catalepsy
in that they do not seem to present true waxen flexibility. The
phenomena presented are those {334} which result from control over an
easily-moulded will, rather than phenomena due to the fact that the
will is entirely in abeyance.

PATHOLOGY—Attempts to explain the nature of catalepsy leave one in a
very uncertain and irritable frame of mind. Thus, we are told very
lucidly that most authors are inclined to the opinion that the
cataleptic rigidity is only an increase of the normal tonus of the
voluntary muscles occurring occasionally in the attacks. What appears
to be present in all genuine cases of catalepsy is some absence or
abeyance of volition or some concentration and circumscription of
cerebral activity. The study of the phenomena of catalepsy during
hypnosis throws some light upon the nature of catalepsy. Heidenhain's
theory of hypnotism is that in the state of hypnosis, whether with or
without cataleptic manifestations, we have inhibition of the activity
of the ganglion-cells of the cerebral cortex. Herein is the
explanation of many cataleptic phenomena even in complicated cases. In
hysteria and in catalepsy the patient, dominated by an idea or
depressed in the volitional sphere by emotional or exhausting causes,
no longer uses to their full value the inhibitory centres. When
organic disease complicates catalepsy, it probably acts to inhibit
volition by sending out irritative impulses from the seat of lesion.

DURATION.—Usually, attacks of catalepsy recur over a number of years;
but even when this is the case the seizures are not as frequent, as a
rule, as those of hystero-epileptic paroxysms. Uncomplicated cases of
catalepsy, or those cases which occur in the course of
hystero-epilepsy, usually preserve good general health.

Of the duration of attacks of catalepsy it need only be said that they
may last from a few seconds or minutes to hours, days, weeks, or even
months. The liability to the recurrence of cataleptic attacks may last
for years, and then disappear.

DIAGNOSIS.—In the first place, the functional nervous disorder
described as catalepsy must be separated from catalepsy which occurs
as a symptom in certain organic diseases. It is also necessary to be
able to determine that a patient is or is not a true katatonic.

It must not be forgotten that genuine catalepsy is very rare. Mitchell
at a recent meeting of the Philadelphia Neurological Society said that
in his lifetime he had seen but two cases of genuine catalepsy—one for
but a few moments before the condition passed off. The other was most
extraordinary. Many years ago he saw a young lady from the West, and
was told not to mention a particular subject in her presence or very
serious results would ensue. He did mention this subject, rather with
the desire to see what the result would be. She at once said, “You
will see that I am about to die.” The breath began to fail, and grow
less and less. The heart beat less rapidly, and finally he could not
distinguish the radial pulse, but he could at all times detect the
cardiac pulsation with the ear. There was at last no visible
breathing, although a little was shown by the mirror. She passed into
a condition of true catalepsy, and to his great alarm remained in this
state a number of days, something short of a week. Throughout the
whole of this time she could not take food by the mouth. Things put in
the mouth remained there until she suddenly choked and threw them out.
She apparently swallowed very little. She had to be nourished by
rectal alimentation. She was so remarkably cataleptic that if the
pelvis were raised, so that {335} the head and heels remained in
contact with the bed, she would retain this position of opisthotonos
for some time. He saw her remain supported on the hands and toes, with
feet separated some distance, with the face downward, for upward of
half an hour. She remained as rigid as though made of metal. On one
occasion while she was lying on her back he raised the arm and
disposed of the fingers in various ways. As long as he watched the
fingers they remained in the position in which they had been placed.
At the close of half an hour the hand began to descend by an
excessively slow movement, and finally it suddenly gave way and fell.
Not long after this she began to come out of the condition, and quite
rapidly passed into hysterical convulsions, out of which she came
apparently well. He was not inclined to repeat the experiment.

Catalepsy is to be diagnosticated from epilepsy. It is not likely that
a grave epileptic seizure of the ordinary type will be mistaken by an
observer of even slight experience for a cataleptic attack. It is some
of the aberrant or unusual types of epilepsy that are most closely
allied to or simulate catalepsy. Cataleptic or cataleptoid conditions
undoubtedly occur regularly or irregularly in the course of a case of
epilepsy, but I do believe that it is true, as some observers contend,
that between catalepsy and some types of true epilepsy no real
distinction can be made. Hazard,[27] in commenting on a case reported
by Streets,[28] holds that no difference can be made between the
attacks detailed and those forms of epilepsy described as petit mal.

[Footnote 27: _St. Louis Clin. Rec._, iii. 1876, p. 125.]

[Footnote 28: “Case of Natural Catalepsy,” by Thomas H. Streets. M.D.,
Passed Assistant Surgeon U. S. N., in the _American Journal of Medical
Sciences_ for July, 1876.]

The case was that of a sailor aged forty-two years, of previous good
health. The attacks to be described followed a boiler explosion, by
which he was projected with great force into the water, but from which
he received no contusion nor other appreciable injury. There was no
history of any nervous trouble in his family. It was the patient's
duty to heave the lead. The officer noticed that he was neglecting his
business, and spoke to him in consequence, but he paid no attention to
what was said to him. “He was in the attitude he had assumed in the
act of heaving the lead, the left foot planted in advance, the body
leaning slightly forward, the right arm extended, and the line held in
the left hand. The fingers were partially flexed, and the
sounding-line was paying out through them in this half-closed
condition. The eyes were not set and staring, as is the case in
epilepsy, but they were moving about in a kind of wandering gaze, as
in one lost in thought with the mind away off. The whole duration of
the trance was about five minutes.”

Dickson[29] reports a very striking case, and in commenting on it
holds to the same views. The patient had apparently suffered from some
forms of mania with delusions. She was found at times sitting or
standing with her body and limbs as rigid as if in rigor mortis, and
her face blanched. These spells were preceded by maniacal excitement
and followed by violence. On being questioned about the attacks, she
said that chloroform had been given her. Numerous experiments were
performed {336} with her. Her arms and hands were placed in various
positions, in all of which they remained; but it was necessary to hold
them for a few moments in order to allow the muscles to become set.
She was anæsthetic. After recovering she said that she remembered
being on the bed, but did not know how she came there; also, that she
had been pricked with a pin, and that her fit had been spoken of as
cataleptic. Her mind became more and more affected after each attack,
and she finally became more or less imbecile. From the facts observed
with reference to this case, Dickson thinks that we may fairly
conclude that the mental disturbance in either epilepsy or catalepsy
is identical, and results from the same cause—viz. the anæmia and
consequent malnutrition of the cerebral lobes; while its termination,
dementia, is likely to be the same in either case; also, that
catalepsy, instead of being a special and distinct form of nervous
disorder, is to be considered as a specific form of epilepsy, and to
be regarded as epilepsy, in the same manner as le petit mal is
considered epilepsy, and a result of the same proximate cause; the
difference in the muscular manifestation bearing comparison with any
other specific form of epilepsy, and occurring in consequence of one
or other particular cerebral centre becoming more or less affected.

[Footnote 29: “On the Nature of the Condition known as Catalepsy.” by
J. Thompson Dickson, M.A., M.B. (Cantab., etc.), _British Med.
Journ._, vol. ii., Dec. 25, 1869.]

I do not believe that this ground is well taken. The conditions
present in petit mal are sometimes somewhat similar to, but not
identical with, those of genuine catalepsy. In the first place, the
loss of consciousness, although more complete and more absolute—or
rather, strictly speaking, more profound—than in genuine catalepsy, is
of much briefer duration. The vertigo or vertiginous phenomena which
always accompany genuine petit mal are rarely if ever present in
catalepsy. To say that the mental disturbance in catalepsy and in
epilepsy is identical is to admit an imperfect acquaintanceship with
both disorders. The mental state during the attack of either disorder
it is only possible to study by general inspection or by certain
test-experiments.

Tetanus is not likely, of course, to be mistaken for catalepsy, but
there is a possibility of such an occurrence. The differential
diagnosis already given between hystero-epilepsy and tetanus will,
however, furnish sufficient points of separation between catalepsy and
tetanus.

Catalepsy has been supposed to be apoplexy, or apoplexy catalepsy. The
former mistake is, of course, more likely to be made than the latter.
A careful study of a few points should, however, be sufficient for the
purposes of clear differentiation. The points of distinction given
when discussing the diagnosis of hysterical and organic palsies of
cerebral origin will here apply. In true apoplexy certain peculiar
changes in pulse, respiration, and temperature can always be expected,
and these differ from those noted in catalepsy. The stertorous
breathing, the one-sided helplessness, the usually flushed face, the
conjugate deviation of the eyes and head, the loss of control over
bowels and bladder, are among the phenomena which can be looked for in
most cases of apoplexy, and are not present in catalepsy.

It is hardly probable that a cataleptic will often be supposed to be
drunk, or a man intoxicated to be a cataleptic; but cases are on
record in which doubts have arisen as to whether an individual was
dead drunk or in a cataleptic stupor. The labored breathing, the fumes
of alcohol, the absence of waxen flexibility, the possibility of being
half aroused by {337} strong stimuli, will serve to make the diagnosis
from catalepsy. The stupor, the anæsthesia, the partial loss of
consciousness, the want of resistance shown by the individual deeply
intoxicated, are the reasons why occasionally this mistake may be
made.

Catalepsy is simulated not infrequently by hysterical patients.
Charcot and Richer[30] give certain tests to which they put their
cataleptic subjects with the view of determining as to the reality or
simulation of the cataleptic state. They say that it is not exactly
true that if in a cataleptic subject the arm is extended horizontally
it will maintain its position during a time sufficiently long to
preclude all supposition of simulation. “At the end of from ten to
fifteen minutes the member begins to descend, and at the end of from
twenty to twenty-five minutes at the most it resumes the vertical
position.” These also are the limits of endurance to which a vigorous
man endeavoring to preserve the same position will attain. They have
therefore resorted to certain experimental tests. The extremity of the
extended limb is attached to a tambour which registers the smallest
oscillations of the member, while at the same time a pneumograph
applied to the chest gives the curve of respiratory movements. In the
case of the cataleptic the lever traces a straight and perfectly
regular line. In the case of the simulator the tracings at first
resemble those of the cataleptic, but in a few minutes the straight
line changes into a line sharply broken, characterized by instants of
large oscillations arranged in series. The pneumograph in the case of
the cataleptic shows that the respirations are frequent and
superficial, the end of the tracings resembling the beginning. In the
case of the simulator, in the beginning the respiration is regular and
normal, but later there may be observed irregularity in the rhythm and
amplitude of the respiratory movements—deep and rapid depressions,
indicative of the disturbance of respiration that accompanies the
phenomena of effort. “In short, the cataleptic gives no evidence of
fatigue; the muscles yield, but without effort, and without the
concurrence of the volition. The simulator, on the contrary, committed
to this double test, finds himself captured from two sides at the same
moment.”

[Footnote 30: _Journal of Nervous and Mental Diseases_, vol. x., No.
1, January, 1883.]

Chambers[31] says that no malingerer could successfully feign the
peculiar wax-like yielding resistance of a cataleptic muscle. He
speaks of using an expedient like that of Mark's. Observing that
really cataleptic limbs finally, though slowly, yield to the force of
gravity and fall by their own weight, he attached a heavy body to the
extended hand of a suspected impostor, who by an effort of will bore
it up without moving. The intention of the experiment was explained,
and she confessed her fraud. This rough test, although apparently
different, is in reality similar to that of Charcot and Richer. In
both proof of willed effort is shown.

[Footnote 31: _Reynolds's System of Medicine_, vol. ii., No. 108.]

It must not be forgotten that in catalepsy, as has been already noted
in hysteria, real and simulated phenomena may commingle in the same
case; also, that upon a slight foundation of genuine conditions a
large superstructure of simulated or half-simulated phenomena may be
reared.

PROGNOSIS.—The prognosis of catalepsy is on the whole favorable. It
must be admitted, however, that owing to the presence of neurotic or
neuropathic constitution a tendency to relapse is present. {338}
Hystero-catalepsy tends to recover with about the same frequency as
any of the other forms of grave hysteria. Those cases which can be
traced to some special reflex or infectious cause, as worms, adherent
prepuce, fecal accumulations, scars, malaria, etc., give relatively a
more favorable prognosis. Cases complicated with phthisis, marasmus,
cancer, insanity, etc. are of course relatively unfavorable.

TREATMENT.—The treatment of the cataleptic seizure is not always
satisfactory, a remedy that will succeed in one case failing in
another. Niemeyer says that in case of a cataleptic fit he should not
hesitate to resort to affusion of cold water or to apply a strong
electrical current, and, unless the respiration and pulse should seem
too feeble, to give an emetic. The cold douche to the head or spine
will sometimes be efficacious. In conditions of great rigidity and
coldness of surface Handfield Jones recommends a warm bath, or, still
better, wet packing. Chambers quotes the account of a French patient
who without success was thrown naked into cold water to surprise him,
after having been puked, purged, blistered, leeched, and bled. This
treatment is not to be recommended unless in cases of certain
simulation, and even here it is of doubtful propriety and utility. If
electricity is used, it should be by one who thoroughly understands
the agent. A galvanic current of from fifteen to thirty cells has been
applied to the head with instantaneous success in hystero-epileptic
and hystero-cataleptic seizures. A strong, rapidly-interrupted faradic
current, or a galvanic current to the spine and extremities, sometimes
succeeds and sometimes fails. Rosenthal reports that Calvi succeeded
in relieving cataleptic stiffness in one case by an injection of
tartar emetic into the brachial vein—a procedure, however, not to be
recommended for general use. Inhalations of a few drops of nitrate of
amyl is a remedy that should not be passed by without a trial; it is
of great efficacy in the hysteroidal varieties. Inhalation of ammonia
may also be tried. A hypodermic injection of three minims of a 1 per
cent. solution of nitroglycerin, as recommended for severe
hystero-epileptic seizures, would doubtless be equally efficient in
catalepsy.

Music has been used to control hysterical, hystero-epileptic, and
cataleptic seizures. The French cases reported have all been of the
convulsive types without loss of consciousness and those varieties in
which the special sensibility sometimes persists, as in
hystero-catalepsy, lethargy, and somnambulism. Music has been used as
medicine from the times of Pythagoras to the present, although it can
hardly be claimed to have attained a position of much prominence as a
therapeutic agent.

In one case a vigorous application of fomentations of turpentine to
the abdomen was promptly efficacious in bringing a female patient out
of a cataleptic seizure.

Meigs, whose case of catalepsy produced by opium has been reported
under Etiology, suggests that purgative medicines, used freely in the
treatment of his case, might be advantageously resorted to in any case
of catalepsy.

Powerful tonics, such as quinine, iron, salts of zinc and silver,
should be used in connection with nutrients, such as cod-liver oil,
peptonized beef preparations, milk, and cream, to build up cataleptic
cases in the intervals between the attacks.


{339}


ECSTASY.

BY CHARLES K. MILLS, M.D.


DEFINITION.—Ecstasy is a derangement of the nervous system
characterized by an exalted visionary state, absence of volition,
insensibility to surroundings, a radiant expression, and immobility in
statuesque positions. The term ecstasy is derived from two Greek
words, _ἐκ_ and _στάσις_, which means to be out of one's senses or to
be beside one's self. Commonly, ecstasy and catalepsy, or ecstasy and
hystero-epilepsy, or all three of these disorders, alternate, coexist,
or occur at intervals in the same individual. Occasionally, however,
the ecstatic seizure is the only disorder which attracts attention.
Usually, in ecstasy the concentration of mind and the visionary
appearance have reference to religious or spiritual objects.

SYNONYMS.—Trance is sometimes used as synonymous with ecstasy. While,
however, ecstasy is a trance-like condition, conditions of trance
occur which are not forms of ecstasy. Other synonyms are
Carus-extasis, Catochus, Catalepsia spuria.

HISTORY AND LITERATURE.—Accounts of cases of ecstasy abound in both
ancient and modern medical and religious literature. The epidemics of
the Middle Ages, the days of the New England witchcraft, the revivals
in England and America, have afforded many striking illustrations. Not
a few special cases of ecstasy have become historical. Elizabeth of
Hungary and Joan of Arc were both cataleptics and ecstatics. Saint
Gertrude, Saint Bridget, Saint Theresa, Saint Catharine, and many
other saintly individuals of minor importance have owed their
canonization and their fame to the facility with which they could pass
into states of ecstasy, catalepsy, or hystero-epilepsy.

Gibbon[1] has well described the occurrence of ecstasy in the monks of
the Oriental Church in the following passage: “The fakirs of India and
the monks of the Oriental Church were alike persuaded that in total
abstraction of the faculties of the mind and body the purer spirit may
ascend to the enjoyment and vision of the Deity. The opinions and
practices of the monasteries of Mount Athos will be best represented
in the words of an abbot who flourished in the eleventh century. ‘When
thou art alone in thy cell,’ says the ascetic teacher, ‘shut thy door
and seat thyself in a corner; raise thy mind above all things vain and
transitory; recline thy beard and thy chin on thy breast; turn thine
eyes and thy thoughts toward the middle of thy belly, the region of
the navel; {340} and search the place of the heart, the seat of the
soul. At first all will be dark and comfortless; but if you persevere
day and night you will feel an ineffable joy; and no sooner has the
soul discovered the place of the heart than it is involved in a mystic
and ethereal light.’ This light, the production of a distempered
fancy, the creature of an empty stomach and an empty brain, was adored
by the Quietists as the pure and perfect essence of God himself; and
as long as the folly was confined to Mount Athos the simple solitaries
were not inquisitive how the divine essence could be a material
substance, or how an immaterial substance could be perceived by the
eyes of the body. But in the reign of the younger Andronicus the
monasteries were visited by Barlaam, a Calabrian monk, who was equally
skilled in philosophy and theology, who possessed the languages of the
Greeks and Latins, and whose versatile genius could maintain their
opposite creeds according to the interest of the moment. The
indiscretion of an ascetic revealed to the curious traveller the
secrets of mental prayer, and Barlaam embraced the opportunity of
ridiculing the Quietists, who placed the soul in the navel—of accusing
the monks of Mount Athos of heresy and blasphemy.”

[Footnote 1: _Decline and Fall of the Roman Empire_, by Edward Gibbon,
Esq., in 8 vols., vol. viii. p. 64, London, 1838.]

Some of Swedenborg's supernatural visions were, so far as can be
judged, simply accounts of attacks of ecstasy; and of like character
were the visions of John Engelbrecht as related by Arnold.[2]

[Footnote 2: _Observations_, etc., London, 1806.]

In a very curious American book[3] published in 1815 a history is
given of the wonderful performances of a woman named Rachel Baker, who
was undoubtedly in the habit of passing into conditions of religious
ecstasy, during which were present many of the phenomena which occur
in ecstatics, Catholic or Protestant, religious or otherwise. When
seventeen years old she witnessed the baptism of a young lady, which
impressed her strongly and caused her to become much dejected and
affected about her religious state. She began to have evening reveries
or night talks which soon attracted attention. She united with the
Presbyterian Church. These reveries after a while expanded into
evening exercises which began with prayer, after which she exhorted
and made a closing prayer. She removed from Marcellus to Scipio, New
York, in 1813, and shortly afterward, in the same year, she went to
New York City for medical advice. While there she gave many
opportunities to witness her powers when in what her editors quaintly
call her somnial paroxysms. Her discourses were good illustrations of
what is sometimes termed trance-preaching.

[Footnote 3: _Devotional Somnium; or, A Collection of Prayers and
Exhortations Uttered by Miss Rachel Baker_, by Several Medical
Gentlemen, New York, 1815.]

One of the most interesting parts of this curious book is a
dissertation by Samuel L. Mitchill, M.D., on the function of somnium.
He says there are three states of animal existence—wakefulness, sleep,
and vision or dream. The definition of somnium, which he quotes from
Cicero, is a very fair one to be applied to some of the conditions
which we now speak of under such heads as lethargy, trance, ecstasy,
etc. “By somnium,” he says, “may be understood the performance of
certain mental and bodily actions, which are usually voluntary,
without the direction or government of the will or without the
recollection afterward that such volition existed.” He divides somnium
into symptomatic and {341} idiopathic. The symptomatic somnium occurs
from indigestion, the nightmare, from affusions of water into the
chest, from a feverish state of the body, from debility with fasting,
from fresh and vivid occurrences, etc. The idiopathic somnium is
divided into somnium from abstraction, somnium with partial or
universal lunacy, with walking, with talking, with invention, with
mistaken impressions of sight and of hearing, with singing, with
ability to pray and preach or to address the Supreme Being and human
auditors in an instructive and eloquent manner, without any
recollection of having been so employed, and with utter incompetency
to perform such exercises of devotion and instruction when awake. To
the last of these affections he refers the case of Rachel Baker, whose
devotional somnium he describes.

A number of other curious cases are recorded in this book: that of Job
Cooper, a weaver who flourished in Pennsylvania about the year 1774;
that of the Rev. Dr. Tennent, who came near having a funeral in one of
his states of trance, who has related his own views, apprehensions,
and observations while in a state of suspended animation. He saw hosts
of happy beings; he heard songs and hallelujahs; he felt joy
unutterable and full of glory: he was, in short, in a state of
ecstatic trance. Goldsmith's history of Cyrillo Padovando, a noted
sleep-walker, who was a very moral man while awake, but when
sleep-walking a first-class thief, robber, and plunderer of the dead,
is also given.

One of the most remarkable instances of ecstasy is that of the girl
Bernadette Soubirons, whose wonderful visions led to the establishment
of the now famous shrine of Our Lady of Lourdes in the south of
France. It is related of this young girl by her historian Lasserre[4]
that when about to cross the Gave, a mountain-stream of the Pyrenees,
she suddenly saw in a niche of a rock a female figure of incomparable
splendor, which she described as a real woman with an aureola about
her head and her whole body of surprising brightness. The child
afterward described in detail the vision she had seen. Later, on a
number of occasions at the same spot, she saw the same vision,
described as appearing transfigured. The child believed that she saw
the Immaculate Virgin. The Virgin told her that she wished a church to
be built on the spot. The place has since become a shrine for
Catholics of all nations.

[Footnote 4: _Our Lady of Lourdes_, by Henri Lasserre, translated from
the French, 7th ed., New York, 1875.]

Meredith Clymer[5] has written an elaborate communication on ecstasy.
Ambrose Paré, quoted by Clymer, defines ecstasy as a reverie with
rapture of the mind, as if the soul was parted from the body. Briquet
describes it as a state of cerebral exaltation carried to such a
degree that the attention, concentrated on a single object, produces
the temporary abolishment of the other senses and of voluntary
movements.

[Footnote 5: “Notes on Ecstasy and other Dramatic Disorders of the
Nervous System,” _Journal of Psychological Medicine_, vol. iv., No. 4,
October 1870.]

ETIOLOGY.—Under the predisposing causes of ecstasy may be comprised
almost all of those described under hysteria. The predisposition to
the development of ecstasy will be governed in great measure by
peculiarities of religious education and of domestic and social
environment.

Extreme religious feeling is undoubtedly among the most frequent of
{342} the exciting causes of ecstasy. The accidents and incidents of
love have also had a place. Sexual excitement is sometimes associated
with the production of ecstasy. “In pre-Christian times,” says
Chambers, “when, in default of revelation, men worshipped their
incarnate passions, we have from the pen of Sappho a description of a
purely erotic ecstasy which can never be produced again.” Fear or
fright has been known to throw a predisposed individual into an attack
of ecstasy. Severe threats have occasionally had the same influence.

SYMPTOMATOLOGY.—In considering the symptomatology of ecstasy it will
only be necessary to call attention to the ecstatic attack. The
accompanying phenomena are those of hysteria, hystero-epilepsy, etc.,
already fully described. I cannot do better than quote from Lasserre
the account of one of the ecstatic seizures of Bernadette Soubirons.
Although given in turgid language and from the religious point of
view, the description is a good one of the objective phenomena of
ecstasy:

“A few moments afterward you might have seen her brow light up and
become radiant. The blood, however, did not mantle her visage; on the
contrary, she grew slightly pale, as if Nature somewhat succumbed in
the presence of the apparition which manifested itself to her. All her
features assumed a lofty and still more lofty expression, and entered,
as it were, a superior region, a country of glory, significant of
sentiments and things which are not found below. Her mouth, half open,
was gasping with admiration and seemed to aspire to heaven. Her eyes,
fixed and blissful, contemplated an invisible beauty, which no one
else perceived, but whose presence was felt by all, seen by all, so to
say, by reverberation on the countenance of the child. This poor
little peasant-girl, so ordinary in her habitual state, seemed to have
ceased to belong to this earth.

“It was the Angel of Innocence, leaving the world for a moment behind
and falling in adoration at the moment the eternal gates are opened
and the first view of paradise flashes on the sight.

“All those who have seen Bernadette in this state of ecstasy speak of
the sight as of something entirely unparalleled on earth. The
impression made upon them is as strong now, after the lapse of ten
years, as on the first day.

“What is also remarkable, although her attention was entirely absorbed
by the contemplation of the Virgin full of grace, she was, to a
certain degree, conscious of what was passing around her.

“At a certain moment her taper went out; she stretched out her hand
that the person nearest to her might relight it.

“Some one having wished to touch the wild rose with a stick, she
eagerly made him a sign to desist, and an expression of fear passed
over her countenance. ‘I was afraid,’ she said afterward with
simplicity, ‘that he might have touched the Lady and done her harm.’”

Side by side with this description by the devout Lasserre of the
appearance presented by Bernadette when in a state of ecstasy, I will
quote the often-recorded account which Saint Theresa has given in her
_Memoirs_ of her subjective condition while in a similar state:

“There is a sort of sleep of the faculties of the soul, understanding,
memory, and will, during which one is, as it were, unconscious of
their working. A sort of voluptuousness is experienced, akin to what
might {343} be felt by a dying person happy to expire on the bosom of
God. The mind takes no heed of what is doing; it knows not whether one
is speaking or is silent or weeping; it is a sweet delusion, a
celestial frenzy, in which one is taught true wisdom in a way which
fills us with inconceivable joy. We feel as about to faint or as just
fallen into a swoon; we can hardly breathe; and bodily strength is so
feeble that it requires a great effort to raise even the hands. The
eyes are shut, or if they remain open they see nothing; we could not
read if we would, for, though we know that they are letters, we can
neither tell them apart nor put them together, for the mind does not
act. If any one in this state is spoken to, he does not hear; he tries
in vain to speak, but he is unable to form or utter a single word.
Though all external forces abandon you, those of the soul increase, so
as to enable you the better to possess the glory you are enjoying.”

Occasionally striking illustrations of ecstasy are to be found among
hysterical and hystero-epileptic patients in whom religious faith has
no place. In these cases usually other special phases of grave
hysteria are present. In some of the descriptions given by Charcot and
Richer of hystero-epileptics in the stage of emotional attitudes or
statuesque positions the patients are, for a time at least, in an
ecstatic condition in which the hallucinations may be connected with
sentiments of religion, love, fear, or other emotions. One shows an
attitude of menace or an expression of fear; in another the expression
is of beatitude or saintly happiness: to this expression perhaps
succeeds one of intense joy; to this, one of passion and lubricity.
Throughout all the changing phases of attitude and expression the
patient has the other concomitants of the true ecstatic state, such as
want of volition and insensibility.

DIAGNOSIS.—A cataleptic may also be an ecstatic or the reverse; but
not a few cases are on record in the history of which, on the one
hand, an individual has been subject over a long period to cataleptic
seizures without the recurrence of ecstasy, or, on the other hand, to
fits of ecstasy without a single attack of true catalepsy. Cataleptic
attacks usually occur with more suddenness than ecstasy; the
cataleptic may suddenly become rigid and statuesque—the ecstatic
gradually, although it may be somewhat rapidly, passes step by step
into a visionary state. In catalepsy and ecstasy the expression of the
patient differs. One of the striking features of ecstasy is not simply
the absorbed and abstracted, but also the radiant, expression of
countenance. In catalepsy the expression is more likely to be vacant
or at least negative. In ecstasy waxen flexibility is not present. The
muscles can act in obedience to the will, and the trunk and limbs do
not maintain the positions in which they are placed for any unusual
time. In genuine catalepsy the consciousness is so suspended or
altered that the period of the seizure afterward remains a blank in
the memory of the patient. In ecstasy, however, the visions and
fancies present during the fit can afterward be recalled, and are
frequently recounted by the individual.

DURATION, COURSE, PROGNOSIS.—Nothing need be said as to duration,
course, prognosis, etc. of ecstasy. The remarks made in considering
hysteria, hystero-epilepsy, etc. fully cover these matters.

TREATMENT.—With reference to the treatment of ecstasy little need be
said. It must, in part at least, be directed to rousing and changing
{344} the dormant or dreamy condition of the individual. As it is the
mind or the volitional nature which is chiefly affected, the use of
agents which either directly or reflexly exert a powerful impression
on the cerebral centres is indicated. Thus, in all ages harsh measures
have received more or less applause in the treatment of ecstasy. The
cold douche or shower-bath, the plunge-bath, the hot iron, painful
electric currents, scourging, and beating have all had their
advocates. Flint[6] gives details of a case in which burning with a
heated hammer was employed for three weeks, the patient eventually
recovering, either because of, or in spite of, the treatment. Chambers
believes in the forcible repression of ecstatic and emotional
exhibitions. “In Unst, the most northerly of the Shetland Islands,” he
says, “an epidemic of convulsive fits occurring in sermon-time began
to prevail in several parish churches. At one of these, Northmaven,
the disease was cut short by a rough fellow of a Turk who carried out
a troublesome patient and tossed her into a wet ditch. Nobody else
caught it. From what scandalous scenes Europe might have been saved
had the first dancer on St. John's Eve been tossed into a wet ditch!”

[Footnote 6: _Loc. cit._]


Trance, Lethargy, and Morbid Somnolence.

Trance may be defined as a derangement of the nervous system
characterized by general muscular immobility, complete mental inertia,
and insensibility to surroundings. The condition of a patient in a
state of trance has been frequently, and not inaptly, compared to that
of a hibernating animal. Trance may last for minutes, hours, days,
weeks, or even months. Astonishing stories, some true, others—and
these the greater number—false, frequently find their way into
newspapers. A recent story is that of a hystero-cataleptic young woman
of Nebraska who is reported to have been for seventy days in a state
of trance, during which she was to all appearance lifeless with the
exception of respiration and pulsation. She said that she was
unconscious during the whole time of her protracted trance, but,
although she exerted her utmost power to evince her consciousness, she
could not move a muscle. Such cases like the Welsh fasting girl either
live or seem to live for a long time on little or no food; doubtless
food is often taken secretly.

In an interesting case which, so far as I know, has never been put
upon record in any medical publication, attacks of catalepsy or of
trance, or of both, occurred three times at long intervals during the
life of this individual. The first time was while held in the arms of
his mother preparatory to receiving the baptismal rite: the clergyman
and others observed that the infant changed appearance and suddenly
became rigid. It was feared that he was dying; the ceremonies were
stopped, but in response to efforts after a time he came back to a
normal state. When about sixteen years of age, while at school, he was
accidentally wounded; it was necessary to probe for the ball, and
while this was being done he again passed into a trance-like
condition. Many years later, while in good health, a prosperous and
well-known citizen, he suddenly again fell into an unconscious
condition, and was believed to be dead. So marked were the appearances
of death {345} that after numerous efforts to resuscitate him
preparations were made for his funeral. The knowledge of his previous
attacks, however, induced his friends and relatives to defer his
interment and continue their efforts. He finally revived just as they
were about to give up in despair.

Aëtius, according to Laycock,[7] mentions hysteric death as being very
common in his day, and asserts that real death may supervene without
any of the ordinary symptoms. The eyes preserve their brightness and
the color of the skin remains vivid. Good cites the case of a woman
whose funeral was postponed to ascertain the cause of her death, and
whom the first touch of the scalpel brought to her senses. Authors and
travellers have described wonderful cases of trance which have been
observed in Persia and in India. A Persian youth is recorded to have
possessed the power to restrain his breath for two days; and fakirs in
India are said sometimes to have allowed themselves to be buried alive
for weeks. Doubtless, a little Caucasian light let in upon some of
these stories might dissolve them, as the esoteric Buddhism of Madame
Blavatzsky has been dissipated into thin air by a hard-headed English
investigator. According to Diogenes,[8] Empedocles, a celebrated
disciple of Pythagoras, obtained great fame by curing a female
supposed to be dead, but whom he discovered to be suffering from
hysteria. He termed the affection under which she labored apnoë, and
maintained that a female might live in an apparently lifeless state
for thirty days.

[Footnote 7: _Op. cit._]

[Footnote 8: Quoted by Laycock.]

Landouzy has reported an interesting instance of lethargy produced by
the application of a magnet to a patient suffering from hysteria
major. The attacks of hysterical sleep are often preceded by
convulsive phenomena, and, according to Briquet, are often ushered in
by epileptoid signs, such as whistling inspiration, movements of
deglutition, frothing, and transient rigidity of the limbs. Richer
reports a remarkable case of Plendlers of Vienna, in which a young
girl, after a series of violent hysterical attacks, fell apparently
dead. Preparations were made to bury her, when she was found to be
living, having been in a state of lethargy. Among cases observed in
Salpêtrière the duration of lethargy has been from two to eight days.
Sometimes, in cases of grave hysteria, attacks of lethargy complicated
with general or partial contractures and epileptoid phenomena have
been observed. The presence of neuro-muscular hyperexcitability is of
diagnostic value in determining the nature of such cases; if present,
we have probably to deal with phenomena of hysterical lethargy. This
symptom may, of course, pass unperceived. A woman came under
observation a short time since, being then far gone in pregnancy.
About a month before delivery she had a very marked hysterical
outbreak, in which she so simulated apoplexy as to make it almost
impossible to decide what was the matter with her. She had apparently
lost sensation, her breathing was stertorous, her pulse labored, and
she had divergent strabismus. In the course of half an hour the
symptoms passed off.

In trance, as in ecstasy, the patient may remain motionless and
apparently unconscious of all surroundings; but in the former the
visionary state, the radiant expression, and the statuesque positions
are not necessarily present. In trance, as stated by Wilks, the
patients may lie {346} like an animal hibernating for days together,
without eating or drinking, and apparently insensible to all objects
around them. In ecstasy the mind, under certain limitations, is
active; it is concentrated upon some object of interest, admiration,
or adoration. Conditions of trance, as a rule, last longer than those
of ecstasy.

Beard's[9] theory of trance is that it is “a functional disease of the
nervous system in which the cerebral activity is concentrated in some
limited region of the brain, with suspension of the activity of the
rest of the brain, and consequent loss of volition. Like other
functional nervous diseases, it may be induced either physically or
psychically—that is, by all the influences that act on the nervous
system or on the mind; more frequently the latter, sometimes both
combined.”

[Footnote 9: Quoted by Crothers in _Quarterly Journal of Inebriety_,
January, 1880.]

T. D. Crothers[10] has contributed some papers upon the subject of the
trance state in inebriety. He gives the clinical history of some cases
of inebriety which presented the phenomena of cerebral automatism or
trance. He concludes that loss of memory and consciousness may come on
in inebriety and the patient give little or no evidence of his actual
condition. His conclusions are, that when the trance state is
established beyond doubt the individual is irresponsible for his acts
during this period. The study of the trance state in affections of
such definite origin and positive pathology as inebriety helps to
throw light upon its occurrence and explanation in cases of hysteria.

[Footnote 10: “Cerebral Trance; or, Loss of Consciousness and Memory
in Inebriety,” _Quarterly Journal of Inebriety_, January, 1880; and
_The Trance State in Inebriety: its Medico-Legal Relations; with an
Introduction on the Nature and Character of the Trance State_, by
George M. Beard, M.D., a paper read before the New York Medico-Legal
Society, November 2, 1881, Hartford, Conn., 1882.]

Dana[11] reports about fifty cases of prolonged morbid somnolence.
Nearly all those reported previous to 1878 are cases of what has been
termed trance-like sleep or lethargy. In 1878, Gelineau called
attention to a disease which he termed narcolepsy. Dana has seen five
cases, and reports two others from notes furnished by Putzel of New
York. Some of the cases collected are both interesting and remarkable.
Dana calls attention to the distinction made by Briquet between
prolonged hysteria and lethargy. In lethargy the condition of
unconsciousness is generally more profound, the reflexes are
abolished, and the patient cannot be aroused. A patient may even have
periods of sleep within the lethargy.

[Footnote 11: “Morbid Drowsiness and Somnolence,” _Journ. of Nervous
and Mental Disease_, vol. xi., No. 2, April 18, 1884.]

Dana excludes from his cases of prolonged somnolence those cases of
drowsiness due to ordinary causes, as old age, diseased blood-vessels,
cerebral malnutrition, or inflammation; various toxæmiæ, as malaria,
uræmia, colæmia, and syphilis; dyspepsia, diabetes, obesity,
insolation, cerebral anæmia and hyperæmia, cerebral tumors and cranial
injuries, exhausting diseases, and the sleeping sickness of Africa.

He found that the prolonged somnolence shows itself in very different
ways. Sometimes the patient suffers from simply a great prolongation
of natural sleep; sometimes from a constant, persistent drowsiness,
which he is often obliged to yield to; sometimes from frequent brief
attacks of somnolence, not being drowsy in the intermission; sometimes
from single or repeated prolonged lethargic attacks; finally,
sometimes from {347} periodical attacks of profound somnolence or
lethargy which last for days, weeks, or months.

He says that most cases of functional morbid somnolence are closely
related to the epileptic or hysterical diathesis; but a class of cases
is met with in which no history or evidence of epilepsy or hysteria
can be adduced, and though they may be called epileptoid or hysteroid,
these designations are simply makeshifts; the patients seem to be the
victims of a special morbid hypnosis. Possibly they have a cerebral
hyperæmia or anæmia.

Under the name of morbid somnolence a case has been reported by P. J.
Cremen.[12] The patient was a man fifty-five years old, who was
admitted to the hospital under the care of Cremen. He said he had
recently returned from America, where he had taken a drink which had
affected his head. He went to bed, and the next morning was found in a
deep sleep, from which he could not be aroused. He presented the
appearance of a person in a sound sleep or under the influence of
anæsthetics. All ordinary measures were unavailing to awaken him from
his trance-like condition. He was completely analgesic over the entire
surface of the body. He would not eat or drink when simply directed,
but when the drinking-cup was placed in his hand he drank, and when
bread or meat was given he ate. Subsequently he was seen eating while
in the somnolent state with the eyes closed; but after a time he would
stop, and had to be urged to commence again. Evidently, tactile
sensibility was not lost. The muscular sense appeared to be
diminished. The superficial reflexes were abolished, the knee-jerks
exaggerated; ankle clonus was absent. Smell and taste were obtunded.
Hearing was retained. The state of muscular rigidity during the
somnolence was remarkable. He was placed between two chairs, the tip
of the shoulder resting upon one chair, the heel of the left foot on
the other, and the right leg bent at a right angle to the trunk. A
weight of forty pounds was then supported on the rigid chest without
causing the slightest yielding or movement from the position described
until muscular relaxation took place. He often remained in this state
for four or five days at a time or longer. He could be aroused by a
strong magneto-electric current. In the intervals between the attacks
he was sometimes bright and cheerful, at others gloomy and depressed.
When requested to walk, he would do so in a perfectly straight line,
from which he would not deviate for obstacles. When told to walk
around a table, however, or other obstacle, he would do so. He would
try to do anything that he was told, even to standing on his head. The
somnolent or hypnotic state could be induced at will by closing the
eyelids and pressing the eyeballs for about two minutes. Of the
genuineness of the phenomena Cremen had no doubt; he believed that the
somnolence partook, in some degree, of the nature of that which has
been designated narcolepsy. This case in many respects is similar to
cases of catalepsy and automatism at command. A very similar case has
been reported in the article on Catalepsy.

[Footnote 12: _Brit. Med. Journ._, Dec. 12, 1885.]

Self-concentration in those of robust minds differs rather in degree
than in essence from ecstasy or trance and allied conditions in the
weak and hysterical. “Archimedes,” says Clymer, “engrossed with a
problem in {348} geometry, feels no hunger and is deaf to the tumult
of the soldiers in a captured town; Socrates, occupied with his own
thoughts, stands twenty-four hours immovable in one spot exposed to
the burning rays of the sun.” Goethe, Blake, and others are on record
as having the power to call up images at will. Francis Galton[13] in a
recent work advocates the cultivation of this power of the
reproduction at will of mental imagery. Clarke[14] records many
wonderful instances of pseudopia. In what does the ecstatic differ
from these except in that the mental status of the individual is
different, and that the object of mental concentration is of a special
character, consonant with the person's ideas, training, and
surroundings?

[Footnote 13: _Inquiries into Human Faculty and its Development_,
Francis Galton, F. R. S., New York, 1883.]

[Footnote 14: _Vision, a Study of False Sight_, by Edward H. Clarke,
M.D., Boston, 1878.]

In brown study or reverie, according to Laycock, the eye is fixed by a
muscular action analogous to that of the cataleptic; and not the eye
only, for a limb or the whole body will remain in the same position
for many minutes, the senses themselves being in deep abstraction from
surrounding objects.


Stigmatization.

Stigmatization (from the Greek _στιγμα_, a small puncture) is a
symptom or appearance which usually presents itself in the form of
bloody or blood-like markings on the palms of the hands, the backs of
the feet, and the left side, the positions in which Christ was
lacerated by the nails and the spear at the crucifixion. In some cases
the stigmata are found in scattered points on various parts of the
body, sometimes upon the forehead at the position of the lacerations
produced by the crown of thorns. In various ages it has been claimed
by Catholics that cases of genuine stigmatization have occurred. It is
not, however, a matter of Catholic faith, the claim being simply that
it is a genuine experience which has some supernatural significance.
Hammond[15] has an interesting chapter on the subject of
stigmatization, of which I have made use, and Clymer's[16] article,
already referred to, gives the details of several of the most
interesting historical cases. Space will not permit more than a glance
at this subject. A case of stigmatization is not necessarily one of
hysteria, but the phenomena of simulated, and possibly of genuine,
stigmatization usually occur among the hysterical.

[Footnote 15: _On Certain Conditions of Nervous Derangement_, New
York, 1881.]

[Footnote 16: _Op. cit._]

According to Garres, the first to exhibit stigmatization was Saint
Francis of Assisium, who was born in 1186 and died in 1236. In 1224 he
was marked, and in memory of the event the 17th of September was set
apart as the Feast of the Holy Stigmata by Pope Benedict XI. The story
of this occurrence is of a highly emotional and sensational character.
Christine de Stumbele, born in 1242, a few miles from Cologne, is
another of the famous hystero-cataleptics and ecstatics who were the
victims of numerous stigmata. These were irregular as to position and
to times of appearance. On one occasion, for instance, she had wounds
on each foot from which the blood flowed freely; a little later, on
the same {349} occasion, she was wounded on the knee, and to the
wondering priest who was ministering to her at this time she showed
hot nails of hideous shapes. She was not only a case of ecstasy and
stigmatization, but a filthy creature withal, who covered herself and
others with excrement, which they had the foolishness to believe came
from the hand of the devil. Veronica Giuliani, another ecstatic, who
conversed with Christ and the Virgin Mary, received the stigmata
during one of her prayers, and was canonized in 1839. Imbert-Gourbeyre
gives a list of 145 persons who have received stigmata, besides 8 now
living known to him. He details one American case, that of a young
French Canadian.

Two of the most extraordinary recent cases are those of Palma d'Oria
and Louise Lateau. These have become stock cases in books and
dissertations on the subject under consideration, and therefore the
briefest accounts of them will be all that is required. Palma in 1871
was sixty-six years old, humpbacked, thin, small, and with light
expressive eyes. It is important to note that she had seen Louisa
Lateau in ecstasy. Wonderful accounts are given of her
performances—eating the Host in the presence of the priest; having
visions of the devil with a little horn on his forehead; on another
occasion Jesus Christ himself bringing to her the communion; seeing
the Host flying through the air before entering her mouth. After the
communion, usually when others were not present, the stigmatization
occurred. Bleedings from the forehead or near it, and hemorrhagic
spots on various parts of the body of various shapes, as of hearts and
of the cross, appeared. Examination of the skin subsequently showed it
to be intact, except that she had a hole in the cranium, which Hammond
suggests was of syphilitic origin. Plates are given in the work of the
credulous Imbert-Gourbeyre representing these figures.

In most respects the most celebrated of all cases of stigmatization is
that of Louise Lateau—celebrated because of the investigations which
have been made of her case; because of the amount of literature,
theological, scientific, and medical, which has been devoted to her;
because of the conflict of opinions even among medical observers in
regard to the true explanation of the phenomena she exhibited. Louise
Lateau was a Belgian peasant-girl, born January 30, 1850. Her parents
were poor. She suffered the hardships of her class, and was as badly
nourished and educated as a poor Belgian peasant-girl is likely to be.
During the cholera epidemic of 1866 she nursed kindly and patiently
many of the victims. In 1867 she became weak, pale, and neuralgic, and
sometimes spat blood. On Friday, April 24, 1868, she for the first
time noticed blood immediately below the left breast; the following
Friday it appeared at the same place, and also on the back of the left
foot; later, it oozed from the left side and both feet, from the palms
and backs of the hands, and from the forehead. Some weeks after this
she began to exhibit the phenomena of ecstasy; and subsequently for
months and years, regularly on every Friday, she had a recurrence of
the stigmata and ecstasy, with accompanying phenomena, sometimes
varying a little in detail. Some of the accounts given by Lefevre and
others of her seizures are beautiful descriptions of attacks of
ecstasy. She stated that during her attacks she had a distinct vision
of the whole scene of the crucifixion.

Numerous experiments, some of them cruel in character, were {350}
performed to test the genuineness of her conditions of unconsciousness
and insensibility. Sight, hearing, and touch were tested. The mucous
membrane of the nose was tickled; strong hartshorn was applied to the
nostrils; she was pricked and stabbed with needles, pins, and even
penknives; painful currents of electricity were used. To none of these
did she respond. During her attacks her pulse was thready, ranging
from 120° to 130° and upward; respiration sometimes could be scarcely
detected, and sometimes fell as low as 10; body-heat was also much
diminished. She recollected everything which passed during the attack.
Different from Palma d'Oria, the examination of her skin revealed
certain appearances. Between Saturday and Thursday oval spots and
patches of rosy hue were to be seen on the backs and palms of the
hands and on the backs and soles of the feet. They were very much in
appearance as if the epidermis were thinned or scraped. The marks on
the forehead were not permanent; the chest was only examined during
the ecstasy. Before the bleedings blebs began to rise at the position
of the spots. The bleeding commonly began in the night between
Thursday and Friday. From the forehead of the girl blood sometimes
oozed from minute points, which looked as if they had been made by
microscopic leeches.

As regards the phenomena presented by Louise Lateau, various
hypotheses have been advanced; the chief, however, are the three
following: (1) The theological view—namely, that the stigmata were
genuine miraculous performances, the blood flowing by supernatural
command. (2) The view that the stigmata were genuine pathological
phenomena, vaso-motor in character—that the bleedings were in some way
similar to attacks of purpura hemorrhagica or to hæmidrosis or bloody
sweat. (3) The view that the stigmata were produced by deceit—that in
all probability, in order to excite the sympathy and astonishment
which are so dear to the hysterical mind, the girl in some way caused
the bleedings. The carefully detailed accounts of the phenomena seem
to lend the strongest support to the last view.

A good test was employed for the detection of simulated stigmatization
in the following case,[17] which came under the care of Mr. Henry Lee
at St. George's Hospital, London. An unmarried seamstress aged sixteen
had on the outside of her right leg above the ankle a discolored
patch, from which she said that every month for two years there had
been a discharge of about a tablespoonful of blood. The patch was
covered with minute red spots resembling flea-bites. Fresh red spots
and effusion of blood were seen at succeeding visits. Lee ordered a
sheet of lead to be applied over the bleeding surface, to be secured
by a starched bandage. On the next visit, when the dressings were
removed, a few spots and a little blood were found, but the sheet of
lead was pierced with holes large enough to admit a needle. When asked
how this had happened the girl was silent, and was discharged as a
convicted impostor. In Lefevre's experiment with Louise Lateau he
placed a leather glove upon one hand, tying and sealing it at the
wrists; but it is easily to be seen why this test was not as thorough
as that with the lead.

[Footnote 17: _British Medical Journal_, vol. i., 1871, p. 479.]

Another case of ecstasy with stigmatization is cited by Bourneville
and Hammond from Magnus Huss of Stockholm—a servant-girl twenty-three
years old who was subject to convulsions, and also to {351}
hemorrhages, which usually came on as the result of great emotional
disturbance. In her case examination showed no cicatrices. The
hemorrhages occurred from the scalp, the eyes, the face around the
eyes, the left ear, and the stomach. Her menstruation went on
regularly during the attacks: sometimes she had ecchymoses and
apparent bruises on the left half of the body, the limbs of which were
semi-paralyzed for short periods. The attacks occurred with
convulsions and unconsciousness, which usually lasted about half an
hour, and from which she awakened as if from a long sleep.


Autographic Women.

Certain peculiar phenomena have been described under the head of
femmes autographiques, or the autographic women, and are worthy of
note. Dujardin-Beaumetz[18] in a case of well-marked hysteria with
loss of general sensibility reports that he was able to write or trace
with a needle or pointed instrument on the skin. Within a space thus
traced the skin was elevated in a white patch or plate. After some
five minutes the line would show itself more and more in relief, until
it attained from one and a half to two millimeters in thickness. It
would remain from three to six, and sometimes twelve, hours. He varied
the experiments in many ways, executing upon the skin designs, tables,
and names of from ten to fifteen letters. He detected in the centre of
some of the spaces traced a marked elevation of temperature, sometimes
appreciable to the hand. This woman was known by the name of femme
diche, or the autographic woman.

[Footnote 18: _Bull. et Mém. Société médicale de Hôpital de Paris_,
1880, 12, xvi. 197-202.]

Dujardin-Beaumetz held that the phenomena were vaso-motor. The red
lines traced readily admit of this explanation. The white space in
relief, however, was not so easily explained. He had observed among
hysterical women, under the influence of pressure, irritation, or the
application of magnets, the appearance of patches of urticaria. One of
the common tricks of the Spiritualists is to have the name of a spirit
that has been called up appear upon the bared arm of the medium. Among
friends and private patients, and among the hysterical patients in the
wards of the Philadelphia Hospital, I have successfully performed
experiments similar to those reported by Dujardin-Beaumetz. Such
phenomena are by no means confined to cases of hysteria. One of my
most striking successes in an attempt at skin-writing was in the case
of a male physician of a peculiarly clear and pale complexion. Certain
peculiar conditions of the skin will allow this to be done with
facility. The similarity of this class of phenomena to that of the
stigmata will at once appear evident. Such phenomena occur among the
hysterical with a tendency to vaso-motor deficiency of control.


Fasting Saints and Fasting Girls.

The wonderful saints who starved themselves or lived on sacramental
bread are almost a multitude. Saint Joseph, Saint Catherine of Sienna,
{352} Saint Rose of Lima, Saint Collete, Saint Peter of Alcantara are
of the number. In modern and even in recent times not a few of these
cases have become widely known. Margaret Weiss, about whom a book was
written in 1542, is said to have done without food and drink for three
years. She suffered from pains and contractures. She passed neither
urine nor feces; at least, such are the accounts which have come down
to us.

Sarah Jacob, the Welsh fasting girl, has shared with Louise Lateau
popular and medical notoriety. When about ten years old she suffered
from various hysterical and hystero-epileptic symptoms. The quantity
of food she took gradually dwindled; on October 10, 1867, it was said
that she ceased to take any food whatever, and so continued till the
day of her death, more than two years later. She had many visitors,
pilgrims from far and near, who often left money or gifts. The vicar
of her neighborhood came to believe in her, and an investigation was
suggested. At one investigation, not very rigidly conducted, nothing
was discovered. After a time she was visited by Fowler of London, who
decided that the case was one of hysteria with simulation, probably
associated with the power or habit of long fasting. Trained nurses
were sent from Guy's Hospital to conduct the second watching. Under
the watching the girl died, starved to death. The father was afterward
condemned to imprisonment and hard labor for twelve months, the mother
for six months. In Brooklyn a few years since one Molly Fancher, a
similar case, attracted much attention, and was written about and
commented upon by the press.


{353}


NEURASTHENIA.

BY H. C. WOOD, M.D.


INTRODUCTION.—The term neurasthenia, signifying nervous weakness, and
not rarely paraphrased by nervous exhaustion, indicates by its very
derivation that it denotes not a distinct disease, but a condition of
the body. The relations of the nervous system to the functions of
organic and animal life are so intimate that almost all forms of
exhaustion might well be discussed under the present heading. A
further difficulty in attempting to decide the exact limitations of
this article is to be found in the fact that hysteria, insanity,
chorea, and various other nervous diseases are very closely connected
with nervous exhaustion. Indeed, many of the cases which are
considered by authorities as instances of neurasthenia would be more
appropriately classed with one or other of the especial diseases.
Thus, the nervous fears discussed in such detail by George M. Beard in
his work upon neurasthenia plainly belong with the monomaniacal
insanities, and, although they usually are associated with nervous
depression, may coexist with great physical and mental power.

Further, very many chronic diseases produce neurasthenia. It has not
been many years since general debility was a common inscription upon
records of diagnosis. In very many cases the general debility
afflicted the diagnostic powers or zeal of the physician rather than
the body of the patient, and it is to be feared that neurasthenia not
rarely at present replaces it. Malarial poisoning, chronic Bright's
disease, chronic diarrhœa, lithæmia, and various other affections may
be readily overlooked, and patient and physician satisfied with the
diagnosis of neurasthenia; indeed, in my own experience in a very
considerable proportion of the cases which had been diagnosed as
nervous exhaustion the patient was really suffering from definite
disease.

The folly of attempting to make neurasthenia a distinct affection is
strongly brought out whenever it is attempted to give sharp diagnostic
differences between it and other diseases. As examples may be noted
the flat contradictions which exist in the different diagnostic tables
given in the elaborate work of the late George M. Beard.

It is necessary, therefore, in the outset, to recognize that
neurasthenia is a bodily condition which is very frequently associated
with various chronic disorders, or not rarely coexists with perverted
functional activity of the nervous centres, which perverted
nerve-functions may, however, exist independently of any perceptible
neurasthenia, and are not simply the outcomes of the neurasthenia.
Under these circumstances an apology {354} for devoting an article in
this work to the consideration of neurasthenia may seem necessary to
readers. The justification of the present discussion is to be found in
the facts that neurasthenia often exists without the presence of
definite disease, and that still more frequently it is a bodily
condition which dominates in its therapeutic importance the
manifestations of perverted functions, so that the patient is to be
treated for it rather than for the disease with which it is
associated.

ETIOLOGY.—There are various chronic diseases which may lead directly
to nervous exhaustion. Neurasthenia may, moreover, be the result of
disease which is long past; neglected diarrhœas, bleeding piles, and
other affections with exhausting discharges, when they have been
cured, may leave behind them conditions whose source and nature it is
most important to recognize.

Overwork, excessive mental emotion, need only to be alluded to as
capable of producing a pure neurasthenia. As Samuel Jackson was
accustomed to say, in his lectures at the University of Pennsylvania
thirty years ago, “Whenever the expenditure of nerve-force is greater
than the daily income, physical bankruptcy sooner or later results.”
It is to be remembered that the nerve-capital of persons differs
almost as widely as does their moneyed capital. There are numerous
families many of whose members are neurasthenics from birth—_i.e._ who
are born with less power of creating nervous energy than is necessary
to meet the requirements of the ordinary duties of life. There is
every grade of natural endowment between the most feeble person,
scarcely able to produce more nervous energy than is necessary for
breathing, eating, and drinking, and the organism that is capable of
enduring incessant toil. The development of neurasthenia is therefore
not so much the result of a strain which is absolutely great as of a
strain which is excessive in its relations to the organism which has
to bear it.

SYMPTOMS.—The onset of neurasthenia is always gradual, although at
times the condition appears to develop with great suddenness. Under
these circumstances, however, the explosion has been preceded by a
long train of more or less overlooked phenomena: thus, in a case that
just now occurs to me a gentleman had long suffered from the
premonitory symptoms of neurasthenia, to which he had paid but little
attention until he was one day seized with violent vertigo,
accompanied by such prostration of strength that he had to be taken
home from the street in a carriage. The symptoms vary very much
according to the portion of the nervous system which is especially
affected, and also to some extent according to the etiology of the
attack. Nervous exhaustion may in the beginning affect the whole of
the nervous system, or it may be at first purely local and coexist
with general nervous strength. Many cases of spermatorrhœa are
instances of the local form of neurasthenia, the sexual centres being
primarily affected; but as in these cases, sooner or later, the whole
of the nervous system becomes implicated, so in other forms of the
disorder the exhaustion, at first local, finally, if neglected,
implicates the whole organism. There are not rarely cases of brain
exhaustion in which the symptoms are at first purely local. Almost
always the cause of a local neurasthenia is excessive use of the part;
thus, cerebral asthenia is usually the result of mental overwork,
sexual asthenia of sexual excesses, etc. When to the intellectual
fatigue is added the depressing effects {355} of excessive anxiety or
allied emotions, the symptoms usually from the first are more general.
The exhaustion may affect chiefly a single function of the brain. As
an instance may be cited the case of a postal clerk now under my care,
who has been accustomed to distribute five to eight thousand letters
every day from a general mass into three hundred pigeon-holes
representing as many post-office districts scattered over a large
territory. As soon as the address is read there must be an
instantaneous automatic recognition of the district to which the
letter goes. It is at this place where, in the case now under
consideration, the symptoms manifest themselves. Reading the address
fails to produce immediate recognition of the locality to which the
letter is to be assigned. Asked in what district such a post-office
is, the clerk answers instantly, but seeing the address himself he
hesitates, and sometimes balks so that he can distribute only about
one-third as many letters as when in health. As in most cases of local
nerve exhaustion, in this patient some evidences of general
implication exist, there being decided disturbance of the sexual
organs.

Another form of local neurasthenia which is frequently associated with
brain exhaustion is that of writer's cramp. I have repeatedly seen it
come on as the herald of a general breakdown; but under such
circumstances the symptoms have usually not been those of typical
writer's cramp: there have usually been not so much marked spasms as
loss of power and distress in the arm on attempting to write.

In pure brain exhaustion loss of the disposition to work is usually
the first symptom, the sufferer finding that it constantly requires a
more and more painful effort of the will to perform the allotted task.
The basis of this difficulty is largely loss of the power of fixing
the attention, and this by and by is accompanied with weakness of the
memory. Disturbances of sleep are frequent. Various abnormal
sensations in the head are complained of. In most cases there is not
absolute headache, but a feeling of weight or fulness or an
indescribable distress, usually aggravated by mental effort.

It is true that in some cases of very dangerous brain-tire cerebration
is performed with extraordinary vigor and ease; the power of work is
for the time markedly increased, and even the quality of the product
may be raised; the patient may even glory in a wild intellectual
exaltation, a sense of mental power, with an almost uncontrollable
brain activity. It is probable, however, that these cases are not
instances of pure neurasthenia, but that there is an active congestion
of the cortical gray matter. It is certain that they are very prone to
end in serious organic brain trouble. In some cases of cerebral
asthenia there are disturbances of the special senses, tinnitus
aurium, flashes of light, and even the seeing of visions. Under these
circumstances it is again probable that active congestion of the
affected centres exists.

Severe cerebral neurasthenia may be associated with good spirits, but
usually there is marked depression, and this perversion of function
may finally go on to decided melancholy. The will-power, as all other
functional activities of the brain, is prone to be weakened; morbid
fears may finally develop themselves; and at last that which was at
the beginning a simple brain exhaustion may end in hypochondriasis or
insanity. In my own experience such ending is very rare unless there
have been from the {356} beginning marked symptoms of hypochondriasis
or melancholy; in other words, unless there be the inborn tendency to
distinct mental disorders, cerebral neurasthenia rarely produces them,
but in a person who inherits such tendency the brain exhaustion may
become an exciting cause of insanity.

The symptoms of brain-tire may be very largely existing in the
individual who still has muscular strength and is capable of enduring
much physical labor; but in most cases, sooner or later, the more
general symptoms of neurasthenia manifest themselves.

Amongst the earliest of these symptoms may be disorder of the special
senses. For reasons which are not very evident it is the eye which is
generally affected. Although existing deafness is often greatly
intensified by the coming on of nervous exhaustion, I cannot remember
ever to have seen severe deafness entirely neurasthenic. The nature of
the optical trouble is to be recognized by the fact that vision is at
first good, but fails when the eye is steadily used for a few minutes,
although the organ is physically perfect. This weakness of the eye may
long be the most troublesome manifestation of the disorder.

In some instances, before any loss of muscular strength is marked,
vaso-motor weakness is prominent. Excessive blushing on the slightest
provocation, great flushing of the face after the use of alcohol or
other stomachic irritant, waves of heat passing over the body,
occasional pallors provoked by exertion or apparently causeless, and
cold extremities, are some of the phenomena which mark the lack of
power in the centres that control the blood-vessels. Closely allied to
these disturbances are those of secretion. In my own experience the
most marked of these is a tendency to night-sweats, but in some cases
the hands, and more rarely the palms of the feet, are perpetually
bathed in perspiration, which may be greatly increased by any
emotional disturbance. In some patients there is a very great tendency
to serous diarrhœa, which in its turn of course increases the nervous
exhaustion.

In many neurasthenics the heart as well as the vaso-motor system
sympathizes in the weakness, so that palpitation and shortness of
breath not rarely follow even slight exertion: a more characteristic
symptom is, however, a peculiar dropping of the heart's beat, which is
to the patient at first very alarming, but which is entirely
independent of any lesion of the heart itself. The true nature of this
cardiac intermission is to be recognized by the existence of other
symptoms of neurasthenia, and by the fact that it is not constant, and
that it is very prone to follow eating or gastric irritation of any
kind. Not rarely it is relieved at once by the belching up of wind.
When tobacco has been very freely used the cardiac symptoms of
neurasthenia usually come on very early, and may be very severe. Under
these circumstances it is really a mixture of neurasthenia and
tobacco-poisoning with which we have to deal.

The muscular strength may finally fail almost altogether. It is almost
characteristic that the patient should be capable of much exertion
under excitement, and should suffer from the results of such exercise
not immediately, but after one or two days.

In many cases of neurasthenia atonic dyspepsia exists, but it is
always a question for careful consideration how far a nervous
condition is due to the dyspepsia and how far the dyspepsia is caused
by the nervous condition.

{357} Disturbances of sensation are common in neurasthenia, these
disturbances taking the form in many instances of itchings or
formication or other similar minor ills. Neuralgia is often severe and
its attacks frequent, but I am convinced that something more than
simple nervous exhaustion is responsible for its production. I believe
that there is a neuralgic diathesis or temperament which is often
associated with neurasthenia, but may exist without it, and which
probably has, at least on many occasions, relations to a gouty
ancestry. When such temperament exists the neuralgic attacks are
greatly aggravated by the coming on of neurasthenia. Hyperæsthesia and
anæsthesia mark the line where simple neurasthenia passes into
hysteria. The same also is true of the peculiar tenderness over the
spinal processes of the vertebræ, which is especially frequent in
women, and is the chief symptom of the so-called spinal irritation or
spinal anæmia—an affection which I believe to be a form of
neurasthenia allied to hysteria.

In neurasthenia disturbances of the sexual organs are very common; in
women great pain on menstruation, ovarian irritation, the so-called
irritable uterus of Hodge, are closely connected with a general nerve
weakness. In not a small proportion of the cases of uterine disorders
which are often locally treated I believe the local disease is largely
the expression of the general condition. It is well known that
masturbation and sexual excess in the male may produce an exhaustion
of the nerve-centres especially implicated and also a general nervous
exhaustion. This is the common history of spermatorrhœa. It is no less
true that a general neurasthenia may produce a local weakness of the
sexual centres, with symptoms at least resembling those of
spermatorrhœa—namely, great irritability of the sexual organs, with a
practical impotence due to immediate seminal discharge whenever
coition is attempted. I have certainly seen this condition result from
excessive intellectual labor when there has been no sexual excess, and
at a time when the muscular strength was still good. Such cases may,
perhaps, be distinguished by the fact that unprovoked emissions are
not nearly so apt to occur as in true spermatorrhœa.

TREATMENT.—The natural cure for neurasthenia is rest, and my own
experience coincides with the logical inferences to be drawn from an
etiological consideration of the subject—namely, that medicines are
only of limited value, and unless very judiciously administered may
readily do harm. Disturbing symptoms should be met and tonics may be
used, especially strychnine and arsenic, but all drugs hold a
secondary position in the relief of a pure neurasthenia. In using
remedies the practitioner must be guided by general principles, and I
shall not engage in any detailed consideration of the subject, but
employ the space at my disposal with a discussion of rest.

When nervous exhaustion has been produced by over-use of any one organ
or system of organs, absolute rest of such organ is a primary
necessity. Thus, when there has been sexual excess absolute avoidance
of use of the sexual organs must be enjoined, and in married Americans
it is often essential to insist upon man and wife occupying distinct
apartments[1] or even to separate them by a journey.

[Footnote 1: Because in this country man and wife habitually occupy
one bed. Sexual continence under these circumstances can only be
obtained at the cost of a suppressed sexual excitement worse than
moderate indulgence.]

{358} Again, in cases of brain-tire it is the brain which should be
rested. To rest an overwearied, excited brain is often not an easy
task. In attempting it the effort should be to obtain the following
results: 1st. The removal of all cares, anxieties, and all brain-work,
especially those of such character as have been connected with the
breakdown. 2d. The maintenance of the interest of the patient, so that
the past shall for the time being be forgotten, and the present not
overweighted with irksomeness. 3d. Invigoration of the physical health
of the whole body, and especially of the nervous system. In order to
obtain the first of these measures of relief, isolation of some sort
is essential; for the second mental occupation is usually required;
for the third fresh air, exercise, or some substitute is to be
superadded to abundant food and rest.

The proper method of meeting these indications varies greatly, not
only with the varying physical conditions and idiosyncrasies of
patients, but also with their diverse domestic and pecuniary
relations. To give detailed directions for every case is impossible,
and I shall therefore limit myself first to simple cases of brain-tire
in which the muscular strength is preserved; second, to cases of
profound general neurasthenia.

In brain-tire travel is usually recommended, and travel affords, when
properly directed, separation from old cares and thoughts, a
maintenance of interest by a succession of novel sights and
experiences, and the physical stimulation of fresh air and exercise.
In bad cases general travel is too stimulating, and ocean-voyaging is
much better. Upon the ocean is to be found nothing provocative of
thought, only complete isolation, fresh air, enjoyment if the patient
be fond of the sea, and a sufficient exercise, especially if the
sufferer in any large measure works in the management of a sailing
vessel. Hence prolonged yachting affords in many cases our best method
of relief. The isolation of the North Woods or any other large
primeval wilderness may be complete, the air most fresh, and the
exercise to be had also boundless, but at the same time controllable;
the man may, according to his will, lie in his tent and be fed by his
guide or be unceasingly active. If the life be agreeable to the
sufferer, and sufficient care against undue exposure be exercised, the
camp-cure is most efficient. European travel may serve almost equally
well, provided hard journeying, sight-seeing, and even cities are
avoided. The quiet of Switzerland or the Tyrol may bring restoration
when the bustle of London and Paris might complete the ruin.

To those who cannot travel extensively the seashore, mountains, or
lowlands of the United States are open, and the best way of meeting
the indications in any individual case must be determined by a joint
consultation between doctor and patient.

There are cases of neurasthenia in which the slightest exercise does
harm, and in which even the unconscious effort of company and
conversation is an injury. Between the extremely exhausted and the
slightly brain-tired is every grade of case, and much tact is often
required in properly regulating the treatment of the individual case.

It is only the most severe forms of neurasthenia which require the use
of the so-called rest-cure. For such, however, it is a very valuable
method of treatment. It finds its most brilliant application
undoubtedly in neurasthenic women, but, more or less modified
according to circumstances, it has a wide scope in the treatment of
both sexes. When the bodily condition is {359} developed by prolonged
lactation, nursing, grief, overwork, acute disease, or other temporary
or removable cause, the rest-cure may give permanent relief; and even
when the cause of the neurasthenia is largely inherited feebleness of
constitution, it is a valuable though a more temporary remedy. This
method of treatment has long been used in this city, and was
especially dwelt upon in its general scope by Samuel Jackson, but in
its modern form it has become a very valuable method of treatment,
essentially different in its details from what it was formerly, and
far more potent in its influence. To S. Weir Mitchell is due a great
debt of gratitude, for by him has this improvement been made.

The principles of the rest-cure are absolute rest, forced feeding, and
passive exercise. Absolute rest is often prescribed by the physician
without being sufficiently definite and insisted upon. When it is
desired to apply it most strictly, it should be clearly explained that
the patient is not to be allowed to get out of bed even to pass urine
or feces, not to feed himself or herself, or perform any act of the
toilet whatsoever. The rest also must be for the mind as well as for
the body, and it is essential that the patient be isolated. Separation
from friends should especially be insisted upon in the case of women.
It may be possible to separate a man in his own house completely from
his daily cares, but a woman in her own house is in the midst of her
daily business, and is like a man placed in the corner of his factory.
In obstinately severe cases of neurasthenia complete and absolute
isolation is a sine quâ non, and especially when there is a decidedly
hysterical element is it necessary to separate the patient entirely
from her friends. Under these circumstances there must be a
well-trained nurse who is personally agreeable to the patient. The
confinement would be very irksome to any except the most exhausted
patient were it not for the daily visit of those engaged in the
treatment; to further provide against ennui the nurse should be a good
reader, so that under the definite instructions of the physician she
can occupy a certain portion of the time in reading to the patient.

In order to maintain the functions of the skin the patient should be
well sponged in bed every morning after breakfast. A strong solution
of salt, or, better, sea-brine, is to be preferred to simple water,
and frequently it may be followed by the use of alcohol. In very
feeble cases the alcohol may be employed alone. I have seen very good
effects from momentarily rubbing each portion of the skin with ice
just after the bathing.

The question of feeding is one of great importance, and requires the
utmost care and attention from the physician. The end to be attained
is to feed the patient as much as can be digested, but not to overdo
and derange the digestion. Food should be given at intervals of two or
three hours, and must be both light and nutritious. It should, at
least at first, largely consist of milk, except in those rare cases in
which that fluid does really disagree, and not merely is thought to do
so. The milk should be skimmed or given in the form of koumiss. Beef
and other concentrated meat-essences are valuable as stimulants, and
may be used, especially as the basis of soups. Various farinaceous
articles of food may be added to them, or if an egg be broken into the
concentrated bouillon or beef-essence just as it ceases boiling a
nutritious, and to many persons palatable, dish is obtained. When
constipation exists, oatmeal {360} porridge, Graham bread, fresh or
dried fruits may be allowed if readily digested by the patient. In
order to give an idea of the general plan of the dietary, the
following schedule of the daily life is given. Such a schedule should
always be put into the hands of the nurse, who should be required to
follow it strictly. It must be altered from day to day, so as not to
weary the patient with monotony. It is especially important to
remember that the diet must be carefully studied for each patient, and
be adapted to the individual requirements of the case. Success will in
a great measure depend upon the practical skill and tact of the
physician in this adaptation:

 8 A.M. Rolls or toast; cocoa or weak coffee, or roasted wheat coffee;
          beefsteak tenderloin or mutton chop.

 9 A.M. Bathing.

11 A.M. Oatmeal porridge, with milk, or else a pint of koumiss.

12 M.   Massage.

 2 P.M. Dinner: Bouillon with or without egg; beefsteak; rice; roast
          white potatoes; dessert of bread pudding, blanc mange, or
          similar farinaceous article of diet.

 4 P.M. Electricity.

 5 P.M. Milk toast.

 9 P.M. Half pint of skimmed milk or koumiss.

In many cases the patient at first can take very little food, and it
is very frequently best to begin the treatment with an entirely liquid
diet, giving milk every two hours, or using Liebig's raw-meat soup,
with milk or plain farinaceous food, and only after a time gradually
accustoming the patient to solid food. Not rarely a prolonged
treatment by the so-called milk diet is of avail. The rest-cure is
indeed largely based upon a careful regulation of the food; but a full
discussion of the various dietaries to be used would require a
treatise upon dietetics.

Passive exercise is to be obtained by the use of electricity and
massage, the object being to get the effects of exercise upon the
nutrition and circulation without the expenditure of the patient's
nerve-force. By the use of electricity muscular contractions are
secured which simulate those which are voluntary and more or less
thoroughly replace them. By the general application of the current to
the whole body we probably affect the tone of all of the minute
blood-vessels, and certainly in this or some other way stimulate the
general nutrition, and, as has been shown by S. Weir Mitchell, for the
time being elevate the bodily temperature.

The faradic current is alone used. It is applied in two ways: first,
to the individual muscles; second, to the whole body. The séances
should be daily, the operator beginning at the hand or foot, and
systematically faradizing each muscle of the extremities and trunk.

The slowly-interrupted current is generally preferable, but advantage
is sometimes gained by varying the rapidity of the interruptions. The
general rule is to select that current which produces most muscular
contraction with the least pain. The poles should be applied
successively to the motor points of the muscles, so as to contract
each firmly and thoroughly. This process should occupy from thirty to
forty minutes. The electrodes are then to be replaced by large sponges
well dampened with salt water: one of these should be put at the nape
of the neck and the other against the soles of the feet, and a
rapidly-interrupted current, as {361} strong as the patient can bear,
should be sent through the body for twenty minutes or half an hour. It
is not necessary for the operator to remain during this time. In some
cases the electrical programme may be varied so as to get a local
stimulant action from the general current; thus, when digestion is
enfeebled and the bowels costive for a portion of the time one of the
sponges may be placed upon the epigastric region. In women when there
is great abdominal and pelvic relaxation one pole may be placed high
up in the vagina. I have seen old-standing prolapses cured in this
way. Some electro-therapeutists claim great advantage from
galvanization of the cervic sympathetic ganglia, but I do not myself
believe that they ever succeeded in reaching these ganglia with the
current.

Massage, like electricity, affects greatly the peripheral circulation,
empties the juice-channels, and gives tone to the muscular system. It
must be clearly distinguished from rubbing of the skin. It consists in
manipulations of such of the muscles as are not too deep to be
reached, and of the cellular tissue: in order to lessen as much as may
be the skin friction by these manipulations, it is often well to
anoint the surface with cocoanut or other bland oil. As sold in the
drug-stores, cocoanut oil is very often rancid, and at any time it is
well substituted by the cheaper cottonseed oil. In practising massage
it is essential to remember that the natural course of the venous
blood and the juices of the cellular tissue is toward the centre of
the body; therefore, all general movements should be practised in this
direction.

The manipulations are percussion, rolling, kneading, and spiral. They
consist of movements made with the pulpy ends of the fingers and
thumbs, and spiral movements with the whole hand so folded as to adapt
its palm to the limb. In percussion the strokes should be from the
wrist, and should be quick and short. It is probably not possible,
even by long strong strokes, to affect deep muscles. In the rolling
manipulation the effort is to roll the individual muscles beneath the
pulps of the fingers. This manipulation may be varied by pinching the
muscles, not the skin, and kneading. In each case it is intermittent
pressure upon the muscles which is aimed at. The circular movements
are to be in opposite directions with both hands simultaneously, the
limb being grasped by one hand a little above the other, and a spiral
sweep made up the limb, the ball of the thumb and the palm of the hand
resting upon the patient, and the pulpy parts of the thumb and the
fingers grasping the limb. It is especially such motions as these
which affect the circulation of the flesh-juices.

The length of time the patient is to be kept in bed and treated in the
manner described varies of course with the individual case, but
usually less than four weeks is not sufficient, and rarely are more
than six weeks required. In getting up, the patient should begin by
sitting up one or two hours a day, increasing daily, but not too
rapidly, the time of being out of bed and the amount of exertion made.
The electrical treatment should be gradually intermitted: in many
cases massage twice a week seems to be of service even after the
patient is about. In the going back to ordinary daily life great care
is to be exercised to proportion the amount of exertion to the
newly-obtained strength, so as not to lose what has been gained. In
cases of natural or of long-standing acquired {362} severe
neurasthenia the mode of life must be arranged to correspond with the
small daily product of nervous energy.

In dismissing this subject I desire to caution against a routine
employment of this so-called rest-cure, which might readily degenerate
into a species of quackery; and, again, to call attention to the
widespread value of the principles which underlie it, and the
importance of the physician applying those principles with endless
modifications of detail.


{363}


SLEEP, AND ITS DISORDERS.

BY HENRY M. LYMAN, A.M., M.D.


The regularly-recurring incidence of natural sleep forms one of the
most important subjects of physiological investigation. Occurring
ordinarily at stated intervals connected with the diurnal revolution
of the earth, it may for a time be postponed by an effort of the will,
but an imperious necessity for repose finally overcomes all
opposition, and the most untoward circumstances cannot then prevent
the access of unconsciousness. Thus produced, the relation of cause
and effect between weariness and sleep becomes very apparent. The
refreshing influence of such repose points clearly to the restorative
character of the physical processes that continue despite the
suspension of consciousness; it also renders evident the final cause
of that periodical interruption of activity which the brain
experiences in common with every other living structure.

Careful observation of the manner in which sleep invades the body
indicates that its evolution is not associated with a simultaneous
suspension of every mode of nervous function. The sense of sight is
the first to yield. The eyelids close and the muscles that support the
head give way. The body seeks a recumbent position; quiet and
seclusion are instinctively sought. The purely intellectual faculties
are not yet depressed, and the reflex energies of the spinal cord are
exalted. Soon, however, the other senses fail; hearing persists the
longest of all. Released from the control of external impressions, the
internal senses preserve their functions after a strangely-disordered
fashion, dependent upon the progressive suspension of activity in the
various cerebral organs. First the power of volition ceases; then the
logical association of ideas comes to an end. Presently the reasoning
faculties disappear, and judgment is suspended. We thus become no
longer capable of surprise or astonishment at the vagaries of memory
and imagination, the only mental faculties that remain in action. To
their unrestrained function we owe the presentation in consciousness
of the disorderly picture which we call a dream. During the early
stages of this somnolent state we often remark the fact of dreaming,
and an effort at attention may produce a partial awakening; but
usually the subsidence of cerebral function is progressive and rapid.
The fire of imagination fades; the field of consciousness becomes less
and less vividly illuminated; the entire nervous apparatus yields to
the advancing tide; and, finally, the dominion of sleep is fully
confirmed.

{364} During the act of awaking the order of sequences is reversed.
From the end of the first hour of repose the depth of sleep, at first
rapidly, then more gradually, diminishes.[1] Dreams disturb its quiet,
mental activity increases, the power of volition revives; once more
the individual is awake.

[Footnote 1: Kohlschütter, _Messungen der Festigkeit des Schlafes_,
Dissert., Leipzig, 1862, and _Zeitschr. f. Rat. Med._, 1863.]

Sleep, then, is that condition of physiological repose in which the
molecular movements of the brain are no longer fully and clearly
projected upon the field of consciousness. This condition is normal,
and must, consequently, be differentiated from all pathological states
which produce its counterfeit by the more or less complete abolition
of consciousness. This distinction becomes the more necessary because
the presence of the common factor, unconsciousness, in the result has
frequently led to the mistake of supposing a community of antecedents
in the changes by which the passage from sensibility and consciousness
to insensibility and unconsciousness is effected. It needs no argument
to show that the insensibility of artificial anæsthesia is a very
different thing from the unconscious condition which obtains during
natural sleep. Between the stupor of intoxication and the healthful
restoration of cerebral energy which accompanies genuine sleep there
can be no rational comparison. It is therefore in the phenomena of
syncope that the likeness of sleep has usually been sought. The
well-known fact that a copious hemorrhage can speedily develop a
condition of muscular relaxation, insensibility, and unconsciousness
has led certain observers to the belief that natural sleep is, after
all, only a species of physiological syncope. The antecedent
conditions of syncope are so different from the prodromata of sleep
that it is difficult to see how either state can be properly likened
to the other. The bloodless condition of the brain which occasions
syncope is always the result of pathological or accidental causes, and
is not identical with the comparatively insignificant reduction of
blood-pressure which may be observed in the brain of the healthful
sleeper. It is, moreover, worthy of note that sleep is the normal
condition of the unborn child, despite the fact that the growing brain
receives a richer supply of oxygenated blood than the trunk and the
lower limbs—a state of the circulation quite unlike that of syncope.

Fully impressed by the force of such considerations, certain
physiologists[2] have reasoned from the analogies suggested by the
results of muscular fatigue, and have imagined an hypothesis
accounting for the occurrence of sleep by a supposed loading of the
cerebral tissues with the acid products of their own disassimilation
during wakeful activity. The acid reaction of the brain and of the
nerves after exertion suggested the probability that an excessive
presence of lactic acid and its sodic compounds might be the real
cause of cerebral torpor and sleep. Could the hypothesis be proved,
ordinary sleep would take its place in the anæsthetic category and
sodic lactate should be the very best of hypnotic agents.
Unfortunately for this doctrine, the administration of the lactates
has yielded only the most contradictory and unsatisfactory results.
It, {365} moreover, furnishes no explanation of intra-uterine sleep
nor of the invincible stupefaction produced by cold.

[Footnote 2: Obersteiner, “Zur Theorie des Schlafes,” _Zeitschr. f.
Psych._, xxix.; Preyer, “Ueber die Ursachen des Schlafes,” _Vortrag.
Stuttgart_, bei Enke, 1877; and _Centralbl. f. d. Med. Wiss._, 1875,
S. 577.]

Far more comprehensive is the hypothesis of Pflüger.[3] According to
this view, the cortical tissues of the brain are recruited by the
assimilation of nutrient substances derived from the blood. By this
process oxygen is stored up in chemical combination, forming explosive
compounds whose precise composition is not fully understood. Under the
influence of the various nervous stimulations that reach the brain
these unstable compounds break up into simple forms. The motion thus
liberated by these explosions is, in some way at present utterly
unintelligible to us, projected into the field of consciousness where
the mind dwells, and we are thus brought into conscious relation with
the external world. That the capacity for thus signalling across the
gulf which separates matter from mind is the result of a certain
perfection and complexity of material structure is rendered probable
by the utter failure of the infracortical organs of man to impress the
conscious intelligence by any amount of independent activity. It is
also indicated by the unconscious sleep of the rudimentary fœtal brain
and by the brevity of the intervals of wakefulness which mark the life
of the new-born babe. That this capacity is dependent upon the
mobility of the atoms of the brain is shown by the speedy cessation of
intelligence which follows great reduction of temperature, as in
hibernation or during exposure to severe frost. That its exercise is
largely dependent upon the activity of the senses is proved by the
effects of interference with their function. A recent observation,
recorded by Strümpell,[4] is very significant in this connection: A
young man had lost all power of sensation excepting through the right
eye and the left ear. A bandage over the eye and a plug in the ear
arrested all communication between his brain and the external world.
Thus imprisoned within himself, he gave utterance to an expression of
surprise, and sought in vain, by clapping his hands, to arouse the
sense of hearing. At the end of two or three minutes these efforts
ceased; respiration and pulsation were deepened and retarded, and
removal of the bandage exhibited the patient with his eyes closed in
genuine sleep.

[Footnote 3: “Theorie des Schlafes,” _Arch. f. d. Ges. Physiol._, x.
468.]

[Footnote 4: “Beobachtungen ueber ausgebreitete Anästhesien und deren
Folgen,” _Deutsch. Arch. f. klin. Med._, xxii.]

The dependence of the waking state upon the presence and functional
activity of a sufficient quantity of a peculiarly unstable form of
protoplasm in the brain is an hypothesis which presents no great
difficulty of comprehension. But how may we explain the passage from
the vivacity of that waking state into the inactivity of sleep? I have
elsewhere[5] discussed the manner in which artificial sleep is
produced by impregnation of the brain with anæsthetic substances, and
the same general line of argument may be extended to cover the action
of every stupefying agent with which the blood may become overcharged.
Could the hypothesis of Obersteiner and Preyer be accepted, it would
be an easy matter to explain the advent of sleep when it gradually
supervenes; but we cannot thus explain the rapid and intentional
passage from wide-awakefulness into the profoundest sleep, such as
becomes a matter of habitual experience with sailors and with others
who have formed the habit of going at once {366} to sleep at
regularly-recurring periods of time. Certain writers have endeavored
to account for this fact by imagining a special mechanism at the base
of the brain (choroid plexuses of the fourth ventricle, etc.), by
means of which the current of blood through the brain may be
voluntarily diminished, with a consequent arrest of conscious
activity. But, still adhering to the hypothesis of Pflüger, we shall
find a clearer explanation of the facts by considering the phenomena
connected with the succession of impressions upon the organs of sense.
It has been ascertained[6] that such impressions must persist for a
certain measurable length of time in order to excite conscious
perception. A sound must be prolonged for at least 0.14″, a ray of
light must agitate the retina for 0.188″–0.2″, ordinary contact with
the surface of the body must continue during 0.13″–0.18″, in order to
produce any knowledge of sound and light and common sensation. For the
simplest act of perception 0.02″–0.04″ are necessary. It is therefore
perfectly reasonable to suppose that when the explosive material of
the brain has been sufficiently reduced in quantity and quality by
prolonged cerebral effort, the impression of sense may no longer
suffice to excite in the cortical substance vibrations of sufficient
length, or following each other in sufficiently rapid succession, to
sustain the conscious state. The cortex of the brain may then be
likened to the surface of a body of water into which bubbles of
soluble gas are introduced from below. When the bubbles are large and
succeed each other rapidly, the surface is maintained in a state of
continual effervescence. But if the size of the bubbles be diminished
or if the solvent capacity of the liquid be increased, its surface
will become almost, if not quite, perfectly tranquil. In some such
way, without any great amount of error, may we picture forth the
molecular changes that determine the advent of sleep.

[Footnote 5: _Artificial Anæsthesia and Anæsthetics_, pp. 15-17.]

[Footnote 6: Carpenter's _Physiology_, 8th ed., p. 852.]

Returning now to the subject of the rapid induction of sleep, we find
that it usually occurs among people who lead an active life in the
open air, like children and laborers, and are perhaps compelled to
endure frequent interruptions of their rest. The sailor who is trained
to sleep and to work in rapidly-successive periods of time—four hours
on deck and four hours below—has virtually become transformed by this
habit into a denizen of a planet where the days and the nights are
each but four hours long. His functions become accommodated to this
condition; his nervous organs store up in sleep a supply of protoplasm
sufficient only for an active period of four or five hours, so that
when his watch on deck is ended he is in a state as well qualified for
sleep as that of a laborer on shore at the end of a day of twelve or
fifteen hours. Moreover, the majority of those who manifest the
ability thus to fall asleep are individuals whose waking life is
almost entirely sustained by their external perceptions. So soon,
therefore, as such excitants are shut out by closing the eyes and by
securing shelter against the sounds and impressions of the air,
comparatively little remains for the production of ordinary
consciousness, and sleep readily supervenes, especially if the
excitable matter of the brain has been already depleted by active
exertion.

It is well known that a predisposition to sleep may be very quickly
induced by extraordinary expenditures of force; witness the effect of
the venereal act and the consequences of an epileptic fit. That
analogous {367} predispositions may indeed be very rapidly developed
by modifications of cerebral circulation is shown by the sudden
reduction of cerebral excitability during the act of fainting. But
this does not prove that cerebral anæmia should be elevated to the
rank of the principal cause of natural sleep. In all such cases the
nervous process is the primary factor and the direct cause of change
in the circulation.[7] The character of these changes has been
admirably illustrated by the observations of Mosso.[8] By the aid of
the plethysmograph this experimenter was enabled to compare the state
of the circulation in the human brain, laid bare by erosion of the
cranial bones, with the movement of the blood in other portions of the
body. The occurrence of sleep caused a diminution in the number of
respirations and a fall of six or eight beats in the pulse. The volume
of the brain and its temperature were at the same time slightly
reduced through the diversion of a portion of the blood-current to
other regions of the body. If during sleep a ray of light was allowed
to fall upon the eyelids, or if any organ of sense was moderately
excited without waking the patient, his respiration was at once
accelerated, the heart began to beat more frequently, and the blood
flowed more copiously into the brain. Similar incidents accompanied
the act of dreaming. The renewal of complete consciousness was
followed by an immediate increase in the activity of the intracranial
circulation.

[Footnote 7: W. T. Belfield, “Ueber depressorische Reflexe erzeugt
durch Schleimhautreizung,” _Du-Bois Reymond's Archiv_, 1882, p. 298.]

[Footnote 8: _Ueber den Kreislauf des Blutes im menschlichen Gehirn_,
Leipzig, 1881.]

In all these variations it is worthy of note that the nervous
impression was the primary event. The changes of blood-pressure and
circulation were invariably secondary to the excitement of
nerve-tissue. Sleep, therefore, is the cause, rather than the
consequence, of the so-called cerebral anæmia which obtains in the
substance of the brain during repose. This condition of anæmia is
nothing more than the relatively lower state of circulation which may
be discovered in every organ of the body during periods of inactivity.
Every impression upon the sensory structures of the brain occasions a
corresponding liberation of motion in those structures. The movement
thus initiated arouses the vaso-dilator nerves of the cerebral vessels
and excites the vaso-constrictor nerves of all other portions of the
vascular apparatus. Hence the superior vascularity of the brain so
long as the organs of sense are fresh and receptive; hence the
diminishing vascularity of the brain as its tissues become exhausted
and unexcitable; hence the unequal and variable vascularity of
different departments of the brain as sleep becomes more or less
profound. These modifications of the brain and of its circulation are
well illustrated by the effects of a moderate degree of cold applied
to the cutaneous nerves of the body, as not infrequently happens when
the night air grows cool toward morning. Such moderate refrigeration
of the skin excites its sensitive nerves, which transmit their
irritation to the brain. The excitement of this organ causes
dilatation of its vessels, with increased irritability of the cortex,
vigorous projection into the field of consciousness, and the
consequent occurrence of dreams denoting imperfect slumber or even
complete awakening. The remedy consists in the application of gentle
heat to the surface of the body. By this means the transmission of
peripheral irritation is checked; the brain becomes tranquil; sleep
{368} supervenes. A similar wakefulness is in like manner produced by
unusual heat. The remedy here consists in the employment of measures
calculated to reduce the temperature of the skin to the normal degree.
Sometimes wakefulness is maintained by some less general irritant. The
feet alone may be cold, either because of previous refrigeration or
because of local hyperæmia occurring elsewhere in an anæmic subject.
There, again, equalization of the circulation—that is, the removal of
cerebro-spinal irritation—may be all-sufficient to procure sleep.
Noteworthy also is the tranquillizing effect of foot-baths or of the
wet sheet in many cases of cerebral excitement and wakefulness. In
like manner, that form of sleeplessness which often follows intense
mental activity may generally be obviated by a light supper just
before going to bed. Activity of the stomach is thus substituted for
activity of the brain, and the consequent diversion of blood is
sufficient to reduce the production of excitable matter in the brain
to a point that permits the occurrence of sleep. A morbid exaggeration
of this process is sometimes witnessed in the soperose condition that
accompanies digestion in patients whose blood has been reduced by
hemorrhage or by disease. In such cases the nutrition of the brain
proceeds at so slow and imperfect a rate that any considerable
diversion of blood toward other organs produces a syncopal slumber
which resembles normal sleep only by the fact of unconsciousness. If,
however, food be taken in excessive quantity or of irritable quality,
the consequent indigestion will produce nervous excitement, reaching
perhaps to the brain, and preventing sleep.


Dreams.

The most interesting question regarding sleep concerns the condition
of the mind during repose. We know that while the body is awake the
mind is always active: does this activity entirely cease during the
period of sleep? The phenomena of certain varieties of trance indicate
that the mere semblance of death is not incompatible with great mental
activity. In like manner, the phenomena of dreams serve to prove that
various intellectual processes, such as memory, imagination,
attention, emotion, and even volition, may still be exercised while
every external avenue of special sense is closed by sleep. The result
of the exercise of mental activity under such conditions constitutes a
dream. The fact that observers who have made trial in their own
persons have always found themselves engaged with the details of a
dream when suddenly awakened from deep sleep has been supposed to
afford valuable proof of the proposition that the mind is never wholly
inactive during the deepest sleep. To say nothing of the significance
of certain somnambulic states (double consciousness), in which
intelligence evidently exists for a long period of time without
leaving any subsequent trace in memory, the mere fact that we remember
very few of the events that occupy the mind in dreams cannot be urged
against the doctrine of continuous mental action, for we remember very
few of the images and ideas that have stirred the depths of
consciousness during the waking state. Our recollection of dreams is
exceedingly variable. Sometimes we retain in memory all the events of
a long and complicated vision, but usually, though entranced by the
vivid {369} beauty of the spectacle that unrolls its splendor before
the eye of the mind in sleep, and though the intensity of its seeming
action may be sufficient to awaken the dreamer, who recalls each
incident as he reviews the picture during the first waking moments,
the impression soon fades, and the coming day finds him incapable of
reproducing a single scene from the nocturnal drama.

The space allotted to this article will not admit a full discussion of
the physiology of dreams. A brief reference to the definition of sleep
must suffice to indicate what is signified by the process. Sleep does
not wholly arrest the functions of the brain. A certain amount of
projection into the field of consciousness seems to continue even
during the most perfect repose, and the ideas thus aroused form the
material of our dreams. Our waking hours are occupied with the ideas
and with the associated trains of thought that are presented in
consciousness through the action of our several senses. As a
consequence of the harmonious function of these senses, correcting and
supplementing each other, a continuous process of logical thought is
maintained. But along with the procession of ideas which are
distinctly conceived by the mind, the field of consciousness is also
invaded by a cloud of half-formed perceptions that are too imperfect
and too fleeting to occupy the attention. As in the act of sight,
though the periphery of the visual field is clouded with a whole world
of objects dimly perceived without arresting particular attention, the
centre of that field alone presents a clear image before the brain, so
the eye of the mind perceives clearly only a few of the impressions
which enter the sphere of consciousness. These neglected perceptions,
however, are none the less the result of abiding impressions graven in
the substance of the brain, from which, through the action of memory,
they may at any favorable opportunity re-enter consciousness. It is
well known that a suspension of the functions of any portion of the
nervous apparatus tends to increase the energy of the remaining
organs; consequently, it becomes highly probable that with the arrest
of external perception in sleep the activity of certain portions of
the brain must be considerably exalted, so that the impressions which
they have previously registered may now more clearly reach the seat of
consciousness. The probability of this hypothesis is greatly
strengthened by numerous facts that lie open to observation. During
the first moments that succeed the closing of the eyes mental activity
and the power of attention are not diminished, but are rather
increased. As the controlling influence of the cerebrum is withdrawn
the reflex energy of the spinal cord becomes temporarily exalted.
Witness the paroxysms of cough that sometimes harass a sleeping child
who has scarcely coughed at all during his waking hours. Witness the
voiding of urine in the bed by nervous children during the early hours
of sleep. Witness the phenomena of night-terrors, which always occur
at the time of night when sleep should be most tranquil.

It appears, therefore, that the harmonious activity of all parts of
the nervous system is indispensable to the highest exercise of the
conscious mind. Healthy intellectual life is the perfectly-balanced
outcome of the complex polygon of forces which has its seat within the
brain. But the suppression of certain lines of this polygon does not
suppress life, nor does it necessarily destroy consciousness. It only
occasions a redistribution of force and a proportionate narrowing of
the stream of related {370} ideas. Since the suppression just
mentioned is not an absolute quantity, but a variable factor, the
polygon of forces in the brain and the corresponding succession of
ideas in consciousness must necessarily be in a state of continual
change. Accordingly, our dreams are as variable as the clouds that
drift upon the currents of the air. As on a hot day in summer, when
the steady equatorial draught has ceased to guide the wind, we may
observe all manner of local tides in the masses of vapor which arise
from the earth, so in sleep, when the guiding influence of the senses
is withdrawn from the brain, the ideas that still arise are chiefly
dependent upon its automatic and reflex action for their origin and
association. Undisturbed by impulses from the external world, the
brain seems then more sensitive to impressions that originate within
the body. An overloaded stomach, an enfeebled heart, a turgid sexual
apparatus, or an irritable nervous ganglion may become the source of
irregular and uncompensated movements which may invade the cerebral
cortex, and may there set in motion a whole battery of mechanisms
whose influence upon consciousness would be quite unnoticed were the
external senses in full operation.


Night-Terrors.

The preceding argument will render it easy to comprehend the phenomena
of night-terrors. These are commonly observed in young children of a
highly nervous temperament before the conclusion of their second
dentition. The subjects of the disorder are generally of neurotic
descent. Insanity, hysteria, neurasthenia, epilepsy, chorea, and
nervous dyspepsia are often discovered among their near relatives. Not
infrequently they have been or will become themselves choreic.

The attack is often preceded by symptoms of indigestion, but it may
result simply from the commotion of a brain wearied by the excitement
and effort of the previous day. The little patient starts up out of an
apparently sound sleep crying with alarm, calling for his mother, and
staring wildly with every possible expression of terror. Sometimes he
springs from his couch and runs headlong into a corner or seeks to
hide under the bed, as if escaping from some frightful object. The
eyes are open, tears flow, perspiration covers the skin, there is the
greatest excitement, and the little one, convulsively clinging to its
parent, will not be quieted. Only after fifteen or twenty minutes, as
tranquillity gradually returns, does the child seem to recover the
power of recognizing his friends. Presently, however, he lies down and
falls quickly asleep, waking in the morning without the slightest
recollection of the unpleasant event.

Such paroxysms occur during the early part of the night, one or two
hours after the child has been put to bed, just at the time when,
according to the previously-quoted experiments of Kohlschütter, sleep
is passing from its maximum intensity to a lesser degree of depth.
This, then, is the time when the controlling power of the sensory
apparatus over other portions of the nervous system has already
reached its minimum. The spinal centres and those intracranial ganglia
which do not share in the full measure of this repose are therefore in
a condition of relative {371} exaltation. Disturbances of internal
organs consequently produce inordinate excitement of these waking
portions of the nervous apparatus. The morbid quality of this
excitement is attested both by the history of the patient and by the
fact that it does not arouse the whole brain. The distribution of
motion in the cerebrum is impeded, so that certain portions of the
organ remain asleep while other regions are thrown into a state of
tumultuous uproar. Disconnection of these different organs of the
nervous system, by withdrawing particular portions from the inhibitory
influence of the remaining parts, gives opportunity for violent
explosions of nervous force analogous to the convulsions of a headless
fowl or to the course of an epileptic paroxysm. Now, in sleep, in
somnambulism, in hypnotism, in delirium, in certain stages of
intoxication with alcohol or with narcotics, such ungearing of the
different nervous ganglia is more or less completely effected. In
narcotic and anæsthetic sleep besides the disassociation of ganglia
there is paresis of the nervous molecules; hence the phenomena soon
merge into insensibility and coma. But in natural sleep, in
somnambulism, or in hypnotism there is no toxic paresis; hence the
dissociated portions of the brain and nervous system, if aroused, are
in a physiological condition to dispense great stores of force. Hence
the vividness of certain dreams and the astonishing vigor of
particular nervous functions in somnambulism and hypnotism.


Somnambulism.

The phenomena of night-terrors constitute merely a special form of
somnambulism, a condition of which the mechanism, so far as the
present state of cerebral physiology will permit, has been already
suggested. The affection should not be ranked by itself as a
particular variety of disease, but should rather be considered a
violent perturbation in the cerebral organs of a neurotic subject
during the period of sleep. In ordinary dreaming the muscular
apparatus usually remains passive, even though the dream be a
nightmare or an incubus of the most terrifying character. But when the
desires and the emotions are powerfully addressed by the dream, a
certain amount of muscular movement may ensue, as when a dog barks in
his sleep, or when a child laughs upon his nurse's lap, or when a
weary soldier marches on though overpowered by sleep. One night, when
parched with thirst during a voyage at sea,[9] I saw in sleep a
sparkling fountain, by the side of which appeared a young girl holding
out a cup of cold water. Awakened by the excitement, I found myself
sitting up in bed with my right arm extended in the direction of the
tantalizing vision: my dream had merged itself in action. In like
manner, the victim of night-terrors not only moves his body, but gives
vocal expression of his feeling of apprehension and alarm. In like
manner, projecting his dream into action, a sleep-walker may arise
from his bed; he climbs out of the window and descends to the ground,
executing all manner of complicated and dangerous movements; he walks
long distances, and finally returns to his couch without waking. In
the morning no recollection of the event of the night survives. Again,
the movement {372} may be less locomotive in its character. The
intellectual faculties chiefly may be aroused, and then only such
movements are executed as may be necessary to give expression to the
mental process.

[Footnote 9: A proclivity to dreaming has often been remarked among
the consequences of partial starvation.]

Such, then, are the principal characteristics of somnambulism, a state
in which dreams are supplemented by more or less complete and
appropriate action, ordinarily without subsequent recollection of
either dream or action.

The somnambulistic dream generally occurs during or soon after the
period of deepest sleep, when the influences of the external world are
largely suppressed. Released from the control of its sensory portion,
the remainder of the brain awakes and becomes aroused to a condition
of functional exaltation. No longer distracted by the recollection of
the special senses, the attention is concentrated upon the
hallucinations which constitute the dream. In the simpler forms of
noctambulism only the automatic locomotive apparatus is awakened, and
the sleeper moves in accordance with the impressions derived from
habit aided by exaltation of the muscular sense. But in some of the
more complicated cases a certain amount of special sensibility seems
to exist. The patient is capable of exercising just that amount of
sensation which is necessary to accomplish his purpose, though blind
and deaf and insensible to every other impression. The more complete
the waking of the organs of sense, the closer the resemblance to the
condition of ecstasy in which cerebral exaltation is the prominent
feature. Accordingly, it sometimes happens that the somnambulist can
recall the events of his paroxysm.[10] In such cases the power of
recollection is due to the same conditions that control the
recollection of our ordinary dreams. We remember very imperfectly, if
at all, the dreams that occur during sound sleep, but the visions with
which sleep sometimes commences (hypnagogic hallucinations) and those
that occupy the period of morning slumber are very easily reviewed in
memory, because they are associated with impressions directly derived
from the partially-waking organs of sense. Such dreams are therefore
chiefly recalled through their association with the train of our
waking thoughts. But the dreams of somnambulism and the dreams of
night-terrors, and all other visions during profound sleep, are as
completely as possible cut off from all connection with the mental
activities which arise directly from the action of the senses. By
reason of such isolation the ordinary association of ideas affords no
help to the memory, and the dream remains in the limbo of oblivion.

[Footnote 10: A. Bertrand, _Traité du Somnambulisme_, p. 80.]

Alfred Maury expresses the opinion[11] that the principal cause of
forgetfulness of the events of somnambulism consists in the exhaustion
of the cerebral elements through the intensity of the excitement to
which they are subjected during the paroxysm. Doubtless this in
certain cases may contribute to the loss of memory, but it should be
remembered that the excitement may be relative rather than absolute.
Certain elements wake while others are asleep, and the waking cells
may be aroused to a degree far in excess of what is usual during the
sleep of the brain without attaining to the level of their diurnal
activity. The mind, undisturbed by external impressions, gives its
attention to the activity of these waking organs, and a dream with all
its consequences, somnambulic or otherwise, is the result. In other
words, the plane of consciousness, so to speak, is lowered {373}
during sleep to the level of these molecular vibrations. But when the
whole brain is again awakened after sleep the residual vibrations of
those elements which yielded the physical basis of the dream, and
which, had they occurred during the waking state, might have persisted
with energy sufficient to furnish a groundwork for recollection of the
ideas which they had originally suggested, are no longer sufficiently
energetic to be felt in consciousness. Recollection of mental states
thus generated must necessarily be impossible so long as the mind is
dependent upon the brain as its register of events. Sometimes,
however, the somnambulist, who while awake had forgotten all the
incidents of his somnambulic experience, can remember in a subsequent
paroxysm all that occurred during the preceding attack. Facts of this
kind have been observed in the waking life of certain hysterical
persons,[12] but the apparent interruptions of their personality
attach to the waking state, while in ordinary somnambulism it is only
in sleep that the alternations of memory and forgetfulness occur. A
similar recollection of previous visions is sometimes experienced in
dreams, showing the close relation that subsists between the dreams of
sleep and of somnambulism. The bond of association between these
events thus isolated in time must be sought in a renewal of like
conditions of the brain during the successive periods of somnambulic
exaltation. We must suppose that the molecules which were in a state
of functional excitement during the first paroxysm are again aroused
in like manner after a period of waking quiescence. If, during sleep,
their movements, though of an exalted character, have only just
sufficed to arouse consciousness in the form of a dream, it would not
be probable that during the phase of comparative inactivity which
supervenes when the whole brain is awake their residual motion could
disturb the sphere of consciousness. Hence the time occupied by their
somnambulic vigor must remain a blank in memory during the waking
state. But when the original state of exaltation has been reproduced
by a second period of disorder, if the same molecular movements be in
any way renewed, the conditions of memory are fulfilled; consciousness
is once more aroused as before, and the patient remembers the dream or
the events of the previous attack.

[Footnote 11: _Le Sommeil et les Rêves_, p. 226.]

[Footnote 12: _Annales Medico-psychologiques_, 5e Série, t. xvi. p. 5,
1876.]


Artificial Somnambulism, or Hypnotism.

The phenomena which have now been passed in review are of apparently
spontaneous origin during the ordinary period of sleep. But from the
remotest antiquity it has been known that certain persons may be
thrown into an artificial sleep which closely resembles the condition
of the somnambulist. During the persistence of this state certain
portions of the nervous system become utterly insensible to external
impressions, while other portions acquire an exalted degree of
sensibility. The subject of the experiment can then by special methods
be placed in such relations with other waking individuals that his
surviving sensations, mental processes, and physical actions shall be
no longer regulated by his own volition, but by the will of another.
Such susceptibility is not common to all persons. About 20 per cent.
of the ordinary population is, by some observers, considered capable
of experiencing this condition. {374} Heidenhain,[13] experimenting
upon a class of medical students, found only one in twelve who was
thus susceptible. Charcot, whose field of observation covers the
inmates of the Salpêtrière Hospital, finds the best exemplars of the
hypnotic state among the hystero-epileptic females in that asylum. To
these experimenters we are largely indebted for the most extended
scientific observation of the phenomena of hypnotism, giving precision
and publicity to the knowledge of facts which, though equally well
known within a narrow circle of investigation[14] during the earlier
decades of the present century, have been compelled to await the
development of cerebral physiology before their full significance
could become apparent to the mass of the medical profession.

[Footnote 13: _Animal Magnetism: Physiological Observations_, by
Rudolph Heidenhain.]

[Footnote 14: Braid, _Neuro-hypnology considered in Relation with
Animal Magnetism_, London, 1843.]

The antecedent condition most favorable to the production of the
hypnotic state is a highly unstable constitution of the nervous
system. For this reason the larger number of qualified subjects is
furnished by the female sex, especially by those who possess the
hysterical temperament. Frequent repetition of hypnotic exercises
renders the subject still more susceptible. Heidenhain was at first
inclined to believe that such experiences were not prejudicial to the
health of the subject, but the observation of Harting in the
University of Utrecht, and of Milne-Edwards in Paris,[15] have
demonstrated danger to the health of animals subjected to similar
experiments. It is easy to discover, in the various clinical
narratives published by Charcot and his pupils,[16] evidence that
hysterical patients often manifest considerable exhaustion after
hypnotic exhibitions; consequently, it cannot be admitted that the
practice is devoid of risk to the health of the individual.

[Footnote 15: _Lancet_, July 29, 1882, p. 164.]

[Footnote 16: Paul Richer, _L'hystéro-Epilepsie_, Paris, 1881; _Le
Progrès médical_, 1881-82.]

Numerous methods of inducing the hypnotic state have been employed by
different experimenters. The greater number consist in modifications
of the sensory impulses derived from the periphery of the body. Gentle
pressure upon the closed eyelids; convergence of the axes of the
eyeballs upon some object nearer than the proper focal distance of the
eyes; fatigue of the retina by gazing upon any brilliant or luminous
object; monotonous excitation or sudden surprise of the auditory
nerve; various impressions through gentle friction or pressure upon
different regions of the body,—all these are capable of inducing
hypnotic sleep. An appeal to the imagination, or even the mere attempt
to abnegate the possibility of vigorous thought by confining the
attention to the most trivial of things, sometimes suffices to produce
the desired phenomenon. Thus, Heidenhain put one of his students to
sleep at a distance by merely informing him beforehand that at a
certain hour he would hypnotize him in his absence. The state of
ecstatic meditation into which the monks of Mount Athos plunged
themselves by the practice of omphaloscopy affords an illustration of
the hypnotic effects of concentrated attention.

The duration of hypnotic sleep is exceedingly variable, but if left to
himself the patient usually wakes spontaneously, without recollection
of anything that has happened. If it be desirable to awaken him before
the natural termination of the paroxysm, consciousness can be restored
by almost any sudden and energetic appeal to the senses, such as an
{375} electric shock, a sudden illumination of the eye with vivid
light, or a sharp puff of air upon the face.

According to Charcot,[17] three principal types may be remarked among
the hysterical subjects upon whom he experimented: (1) the cataleptic,
(2) the lethargic, and (3) the somnambulic. Of these, the first may be
developed primarily by any abrupt and powerful impression upon an
organ of sense, as a bright light or a loud noise (gong). Fixing the
eyes upon some object may produce the same result. Dumontpallier, for
example, has reported the case of a young woman[18] who accidentally
hypnotized herself by gazing at her own image in the mirror before
which she was dressing her hair. The cataleptic state may also be
secondarily induced by merely opening the eyes of a patient in whom a
condition of hypnotic lethargy has been previously developed. If only
one eye is thus opened, the corresponding side of the body alone
becomes cataleptic. Closing the eyes causes the disappearance of this
symptom, with complete restoration of the purely lethargic state.
During the cataleptic condition the several tendinous reflexes
disappear, neuro-muscular hyperexcitability ceases; the skin becomes
insensible, but the special senses, particularly those of sight and
hearing, maintain a partial activity. In this state the senses may
become avenues of suggestion for the production of muscular movements,
but if left to themselves the limbs remain motionless.

[Footnote 17: _Le Progrès médical_, Feb. 18, 1882, p. 124.]

[Footnote 18: _Ibid._, March 25, 1882, p. 223.]

The lethargic state may be induced by simply closing the eyes of the
patient or by causing him to fix his gaze upon some definite object.
The paroxysm begins with a deep inspiration causing a peculiar
laryngeal sound, followed by the appearance of a little foam on the
lips. The eyelids are either wholly or partially closed, and are in a
state of continual tremulous motion. The eyeballs are generally turned
upward and inward. The muscles are completely relaxed. The tendinous
reflexes are exaggerated; pressure over a muscle or upon a nerve
arouses a peculiar contraction of synergic muscles and of groups of
muscles which are supplied by the excited nerve-trunk. The facial
muscles, however, do not thus become contractured: they merely
contract during the application of the stimulus. If the lethargic
patient be rendered cataleptic by opening the eyes, these contractions
persist even after awaking, and they can only be dispelled by renewing
the lethargic state before resorting to pressure upon the antagonistic
muscles—a process by which the contractures peculiar to this species
of lethargy may always be annulled. By the approach of a magnet to a
contractured limb the phenomenon may be completely transferred to the
corresponding muscles upon the opposite side of the body. If upon a
limb of a lethargic patient who has been rendered cataleptic by
opening the eyes an Esmarch's band be applied, pressure over the
bloodless muscles excites no contracture until the band is removed. A
contracture is then developed, and it may even be transferred to the
opposite limb by the approach of a magnet. To this phenomenon has been
applied the term latent contracture.

The extraordinary muscular excitability manifested by these hysterical
hypnotics is further illustrated by an observation recorded by
Dumontpallier.[19] If one end of a caoutchouc tube one centimeter in
diameter and {376} five or six meters in length be applied over a
muscle in the leg, and if the other end be in like manner connected
with a watch, every movement of the second hand will be followed by a
slight contraction in the muscle. The same result follows connection
with the wire of a telephone, and if a microphone be introduced into
the circuit the incidence of a ray of artificial light upon the
instrument, or even its glancing reflection from the eye, will arouse
a responsive muscular contraction. Charcot has sometimes observed
muscular contractions upon the opposite side of the body when a mild
galvanic current was applied to the parietal surface of the head.
During the manifestation of muscular hyperexcitability there is
complete analgesia, but the senses of sight and hearing seem to
preserve some degree of activity. The patient, however, does not
manifest any susceptibility to influence by suggestion.

[Footnote 19: _Ibid._, Jan. 14, 1882, p. 25.]

The somnambulic state may be directly induced by fixed attention with
the eyes, by feeble and monotonous excitation of the senses, and by
various other methods of an analogous character. This forms the most
common variety of the hypnotic condition. It may very easily supervene
during either the lethargic or the cataleptic state as a consequence
of pressure or gentle friction upon the top of the head. Thus,
Heidenhain caused muscular paralysis by rubbing the scalp. Unilateral
friction of the same surface produced paralysis of the opposite side
of the body without notable affection of consciousness. The eye and
the eyelids behave as in the lethargic state. The patient seems
asleep, but there is less muscular relaxation than in hypnotic
lethargy. There is no exaggeration of the tendinous reflexes, and
muscular hyperexcitability is absent. But by lightly touching or
breathing upon the surface of a limb its muscles may be thrown into a
condition of rigidity which differs from the contracture of the
lethargic state in the fact that it does not yield to excitation of
the antagonistic muscles, though yielding readily to a sudden
repetition of the same form of excitement by which it was originally
produced. From the immobility of the cataleptic state it also differs
by a greater degree of resistance to passive motion. Though analgesia
may be perfectly developed in this state, there is generally an
exalted condition of certain forms of cutaneous sensibility and of the
muscular sense. Strange perversions of other special senses are
sometimes remarked. Cohn[20] discovered that a patient who was
naturally color-blind “when unilaterally hypnotized was able to
distinguish colors which were otherwise undistinguishable.”
Conversely, when the cataleptic state is induced the eye becomes
incapable of discerning colors. Spasm of accommodation is also
present, and is one of the earliest demonstrable symptoms of the
hypnotic condition.

[Footnote 20: _Brain_, vol. iii. p. 394.]

These remarkable exaggerations and perversions of special sensibility
have been the cause of much scepticism on the one hand regarding the
verity of the phenomena of hypnotism, and of much credulity on the
other, extending even to a belief in the existence of supernatural and
miraculous gifts. But when the fact is once comprehended that in this
capacity for uncommon feats of vision, hearing, touch, etc. we observe
merely the exaggeration of a process which occurs in every act of
attention, the miraculous semblance of the phenomena disappears.
Attention implies an increase of activity in certain portions of the
brain, with {377} diminution of the function in the remainder of the
organ. In the wild excitement of a cavalry charge the soldier feels
not the sabre cut which will fill his consciousness with pain so soon
as his attention is released from the fetters imposed by the more
engrossing events of the combat. So in the somnambulic sleep those
parts of the brain which remain awake perform their functions with a
vigor that is enhanced by a concentration of cerebral energy in
certain restricted portions of an organ that, by reason of its
naturally excessive instability, had been previously fitted for the
liberation of an inordinate amount of molecular motion. Hence the
slightest suggestion of sense may suffice for the most extraordinary
perception. Such persons see through their eyelids and hear at a
surprising distance. The memory of past events, the recollection of
long-forgotten words and thoughts, supplies in this state an abundance
of materials out of which an exalted imagination may construct the
most astonishing scenes. By this method of combination are produced
those remarkable oratorical utterances which by the ignorant have been
so widely attributed to the supervision of guiding spirits from
another world. In this condition the essential characteristics of the
mind of the so-called medium become the real guides of his mental
processes. Hence the infinite variety and contrariety of the
utterances of such declaimers.

Among other consequences of this exalted susceptibility of the waking
portions of the brain may be noticed the effect of suggestions by
others upon the mind of the somnambulist. Numerous examples scattered
through the literature of the subject[21] illustrate the manner in
which the course of our ordinary dreams may be thus directed. The
hypnotic dream is far more easily modified.[22] The simplest
manifestations of such influence are exhibited in movements in
obedience to the command of the hypnotizer. Next in rank are those
more complicated actions that are effected by excitement of the
imitative faculties of the subject. Every suggested movement that can
be in any way perceived by the patient will be at once reproduced.
Various emotions and passions may thus be aroused by simply placing
the sleeper in the appropriately suggestive attitudes. Under the
influence of a pregnant idea intruded upon the mind of the patient the
subsequent association of ideas will suffice for the evolution of a
complicated series of hallucinations, as in the case of a young woman,
who on being directed to put out her tongue immediately began to feel
sensations of uneasiness in her stomach, followed by nausea and
attempts at vomiting, accompanied by the impression of being on
shipboard. In the lowest grades of the hypnotic state consciousness
may remain, and the subsequent recollection of the events of the
paroxysm may be quite persistent. In such cases illusions that were
produced by suggestions from other minds generally survive in memory
and become the causes of serious delusion. Witness the manner in which
susceptible individuals, partially hypnotized in a so-called spiritual
circle, believe in the reality of the illusions which have occupied
their senses during a séance.

[Footnote 21: Carpenter's _Physiology_, 8th ed., p. 765; _Le Sommeil
et les Rêves_, par L.-F. Alfred Maury, 4th ed., p. 153 _et seq._]

[Footnote 22: _Loc. cit._, p. 357.]

A higher degree of insensibility to ordinary impressions is necessary
to the production of the phenomena of passive obedience and of
automatic {378} imitation. It is probable that the degree of sensory
hyperæsthesia which enables certain hypnotic patients to read the
thoughts of others belongs rather to the first than to the last of
these classes. This capacity is usually associated with preservation
of consciousness and memory, and is, essentially, a mere exaggeration
of that power which all possess in greater or less degree. Numerous
well-authenticated examples of a surprising manifestation of this
faculty have been recorded, so that the possibility of its existence
no longer admits of doubt.[23] In all cases it has been remarked that
the hypnotic mediums can only respond correctly to questions for which
the true answer is present in the mind of the questioner. For all
other interrogations the replies are delivered purely under the
influence of random suggestion. In certain of these cases the pathway
of communication lies through actual physical contact, as in ordinary
mind-reading, where the insensible molecular oscillations of the
muscular elements of one individual serve to guide the movements of
another. But more frequently the transmission of ideas is effected
through the eyes. With these organs the table-rapper or the
planchette-writer reads the unspoken words of the questioner in a
manner very like, yet vastly more deliberate than, that by which
deaf-mutes now learn to interpret the movements of the lips of persons
with whom they converse. This fact is well illustrated by the
experience of Maury[24] in an interview with a celebrated
table-rapper, who without the slightest hesitation made known to him
the age, name, and date of death of a brother whom he had lost. She
also gave the same information regarding his father, and related the
names of other persons upon whom he had fixed his attention. But if he
turned away his face or concealed his eyes, so that the woman could no
longer watch their expression, her responses ceased to be of any
value.

[Footnote 23: Luther V. Bell, _Two Dissertations on what are termed
the Spiritual Phenomena_, read at the meetings of the Association of
Medical Superintendents of American Insane Hospitals at Washington and
Boston in 1854 and 1855.]

[Footnote 24: _Le Sommeil et les Rêves_, 4th ed., p. 361.]

In these partial developments of the hypnotic state it is worthy of
note that the phenomena of sleep are so few and so comparatively
insignificant that they are usually overlooked. Hence the veil of
mystery which has so often obscured the interpretation of such cases.
Careful observation, however, will always detect some characteristic
departure from the normal standard—some loss of balance between the
different parts of the nervous system—by means of which the true
relations of each example may be determined.

TREATMENT.—A large proportion of the phenomena of somnambulism and
hypnotism depend rather upon an originally irritable organization than
upon a specially diseased condition of the nervous system. Their
treatment, therefore, frequently resolves itself into the management
of hysteria or of cerebrasthenia. But if the manifestations of
somnambulism develop for the first time in a person advanced in years,
who has previously enjoyed good health and a sound mind, it should be
regarded as an omen of grave import, signifying the imminence of
organic cerebral disease. Though the meaning of such incidents is less
sinister in early life, they reveal an ill-balanced state of the
nervous system and an imperfect process of nutrition in the growing
body. Such children are the {379} frequent victims of night-terrors,
the form of disorder most commonly evolved by their somnambulistic
proclivities. The treatment of night-terrors should therefore be
chiefly directed to the invigoration of the general health of the
patient. Indigestion and malnutrition are among the most prominent
antecedents, and they should constitute the principal objects of
therapeutical attention. Constipation is usually present. This may be
relieved by the use of compound rhubarb powder or any other gently
stimulating laxative. Digestion should be aided with pepsin as soon as
the catarrhal condition of the alimentary canal, so uniformly present,
has been measurably improved. Cod-liver oil or its substitutes should
be administered for a long period of time. If the nocturnal paroxysms
be frequently renewed, it may be well to employ the bromides, either
with or without chloral hydrate; but as a general rule it is better to
rely upon hygienic and restorative treatment, rather than upon any
form of merely hypnotic medication.


INSOMNIA.

The departures from the course of natural sleep which have been thus
considered are not so much the direct consequence of acute disease as
the result of structural deviation from the normal type of the nervous
system. We must now briefly review the strictly pathological
modifications to which sleep is liable.


Lithæmic Insomnia.

Among those who indulge freely in the pleasures of the table a form of
insomnia is not uncommon. Originating at first in mere overloading of
the stomach, and consisting in a direct irritation of the brain
through the medium of the intervening nervous apparatus, sleeplessness
finally becomes a symptom of more serious mischief. The tissues become
charged with nitrogenous waste, and a lithæmic[25] or gouty condition
is established. Such patients are wakeful, or if they sleep their
slumbers are imperfect and unrefreshing.[26] Grinding of the
teeth,[27] noticed by Graves during the sleep of the gouty, is a
symptom indicative of a highly irritable condition of important
ganglia at the base of the brain. These symptoms are sometimes
associated with turgidity of the superficial vessels of the head,
indicating imperfect function of the circulatory organs, with a
tendency to accumulation of the blood in the venous channels of the
body. The sleep of such partially-asphyxiated patients is fitful,
irregular, and akin to stupor. Occurring in the subjects of periodical
gout, these disturbances of sleep become increasingly serious as the
paroxysm is approached, until loss of sleep and the unrefreshing
character of such {380} slumber as may be obtained become important
factors among the causes of failing health.

[Footnote 25: DaCosta, “Nervous Symptoms of Lithæmia,” _Am. Journ.
Med. Sci._, Oct., 1881.]

[Footnote 26: Dyce Duckworth, “Insomnia in Persons of Gouty
Disposition,” _Brain_, July, 1881.]

[Footnote 27: Trousseau, _Clinical Medicine_, Am. ed., vol. iv. p.
362.]

For all such patients a proper recognition of the cause of their
disorder is essential. This must be corrected by measures appropriate
to the treatment of the gouty diathesis. Since the condition of the
cerebral tissues is a state of irritation caused by the presence of
excrementitious substances, such hypnotic remedies must be selected as
will not interfere with the defecation of those tissues. Bromide of
potassium, valerian, scutellaria, hyoscyamus, hops, and cannabis
indica are useful, together with all that class of drugs which quiet
the brain without hindering the process of excretion. Chloral hydrate
often produces an excellent result, but care should be taken to
prevent its habitual use.


Febrile Insomnia.

Closely related with the sleeplessness of lithæmia are the
disturbances of repose which attend the evolution of the various
specific fevers. In many cases the condition varies all the way from
stupor to delirium. Excessive somnolence, such as often ushers in the
fever, is an indication for evacuant treatment. Cerebral excitement
calls for remedies like the bromides and chloral hydrate, which do not
interfere with elimination. If pain, like headache or backache, be a
symptom demanding attention, the addition of morphia in small doses
forms a valuable reinforcement for the hypnotic mixture; but, as a
general rule, opiates should be used with a sparing hand. The various
resources of hydrotherapy are often invaluable when wakefulness
results from the cutaneous irritability of the eruptive fevers. During
the later stages of a protracted illness the occurrence of insomnia
should direct attention to the nutrition of the patient. Wakefulness
is then the symptom of an irritable weakness of the brain, demanding
remedies which delay the process of disassimilation. The failing power
of the heart requires attention, and diffusible nutriment must be
given to convey the elements needful for restoration of the exhausted
brain. These indications are most perfectly answered by the associated
administration of opiates with alcohol, milk, and beef-juice in small
and frequent doses.


Insomnia from Exhaustion.

Cerebral exhaustion is a not uncommon cause of wakefulness in cases
uncomplicated with fever. It is usually the result of chronic
conditions of ill-health and depression, such as are often encountered
as the result of various cachexias or of dyspepsia, with or without
the abuse of alcohol, tea, coffee, or tobacco. Overwork, debilitating
discharges, pregnancy, parturition, mental anxiety, depressing
emotions, chronic heart disease, and incipient insanity are fruitful
causes of the exhaustion which produces this most distressing form of
insomnia. In such cases the cessation of healthy nutrition leads to a
condition of excessive instability in the cerebral tissues. The oxygen
which they receive from the blood is not stored with any degree of
permanence, but tends to pass directly into {381} stable combinations
with the oxidizable elements of the brain. Consciousness is thus
continually aroused. The state of such a patient presents a very close
analogy to the condition of the victim of diabetes whose liver refuses
to retain its glycogen. The inordinate discharge of sugar into the
blood not only exhausts the tissues of the liver, but also excites
other organs—notably the kidneys—to excessive and unwholesome
activity. In somewhat similar fashion, the failure of the brain to
assimilate and to retain oxygen leads to an abnormal intramolecular
oxidation, which excites an excessive and unwholesome activity on the
part of the Ego in another region—namely, in the field of
consciousness. Such wakefulness might justly be termed a psychical
diabetes.

This variety of insomnia has frequently been ascribed to cerebral
anæmia occurring as a part of a general spanæmia. But this universal
impoverishment of the blood, though a sufficient cause of the morbid
instability, the irritable weakness, of the cortical tissues, does not
necessarily imply a comparatively bloodless condition of the brain.
Unequal circulation and local hyperæmia in different organs of the
body are no unusual consequences of the anæmic state. Slight
disturbances suffice to arouse the brain of such a patient. The
vaso-motor apparatus shares in the general irritability, permitting
blood to inundate the cortical substance almost without provocation.
The unstable protoplasm is only imperfectly renovated, usually at the
expense of the other tissues of the body. The weary patient, busying
himself with an unwilling review of the events of the day, tosses long
upon his couch before he can secure the approach of “tired Nature's
sweet restorer, balmy sleep.” When at length he yields, his slumbers
are brief, and the latter part of the night is but a repetition of the
earlier vigil.

Such patients need a very radical course of general treatment. A
complete change of habits should be effected. A long vacation in the
country, or, best of all, a protracted voyage in a sailing vessel, is
desirable. Hot foot-baths, with cold affusion upon the head, and warm
sponge-baths, or even the full bath in tepid water, at bedtime, are of
great service as means of tranquillizing the nervous system. The
indications for medicinal treatment, besides attention to the
predisposing cachexia, are twofold—to calm and to nourish the
enfeebled nervous substance. Opiates calm, but do not nourish—they
hinder the process of nutrition; hence the sufferer wakes unrefreshed
by the sleep which they procure, and is soon in a condition worse than
ever. The same objection lies against the continuous use of the
bromides. But alcohol and its hypnotic derivatives (chloral,
paraldehyde, etc.) not only calm the excitable brain, but they also
furnish to the tissues a certain amount of diffusible nutriment which
suffices to steady the brain until a change of occupation, with rest
and wholesome food, can produce a complete restoration of its normal
stability. To this effect of alcohol must be ascribed its value as an
hypnotic in the wakefulness of old people who cannot sleep without a
preliminary nightcap. A moderate draught of hot toddy in such cases
serves to arouse the feeble heart and to equalize the circulation by
the production of a moderate degree of general vascular dilatation.
The sugar and water afford an easily assimilated food, while the
alcohol benumbs the cortical protoplasm to a degree which favors the
cessation of conscious perception. If administered in excessive doses,
it is not sleep but anæsthetic intoxication {382} which follows. If
this condition be unduly repeated, the phenomena of chronic alcoholism
supervene, with all the horrible forms of insomnia that accompany
cerebral starvation and delirium tremens. Non-alcoholic
nerve-stimulants and tonics, with careful administration of
easily-digested food, are then more than ever needed to overcome the
neurasthenic wakefulness.


Insomnia from Active Cerebral Congestion.

Still another form of sleeplessness is often experienced as a result
of actual inflammation in some portion of the body, either involving
the intracranial contents directly or reacting upon the brain through
the medium of its circulation. In such cases many of the symptoms of
acute inflammation are present. The head aches, the temples throb, the
face and eyes are suffused with blood, the temperature is considerably
increased. The senses become exalted, ideas pursue a tumultuous
course, there may be actual delirium. These disturbances are due to an
active hyperæmia of the brain. The substance of the cortex becomes
hyperexcitable, and the ordinary incitements of sense produce an
exaggerated effect in consciousness. The patient does not sleep, and
he feels no need of sleep, because the nutrition of the brain is
sustained at the expense of the remainder of the wasting body. The
most speedy and effectual relief in such cases is obtained through a
diminution of the current of blood in the brain. Moderate compression
of the carotid arteries has been proposed as theoretically useful.
Sedatives, like aconite, conium, digitalis, veratrum viride,
ipecacuanha, and tartar emetic are useful, either alone if pain be
absent or combined with opiates if the patient is suffering. Dover's
powder or tartar emetic and morphia in small doses was formerly in
general use. If there be a disposition to nausea the substitution of
aconite for antimony is of great value. A combination of morphia,
bromide of potassium, and chloral hydrate often gives excellent
results. Paraldehyde may be preferable to chloral by reason of its
more thoroughly sedative effect. Derivative measures—mercurial
cathartics, cupping, leeching, or even general bleeding—may become
necessary in certain cases. After the acute stage is passed blisters
behind the ears should be employed. In the sleeplessness of acute
mania Newington[28] has used mustard baths with great satisfaction.

[Footnote 28: _Brain_, vol. i. p. 126.]


Coma.

Turning now to the other extreme, we find a class of cases in which
the disorder consists not in wakefulness, but in an excess of sleep.
Excluding those exceptional cases in which healthy individuals, as a
consequence of inordinate physical exertion, have slept for many hours
beyond their ordinary limit, every extraordinary manifestation of
sleep-like unconsciousness must partake of the nature of coma. Between
natural sleep and this condition may be placed the distinction that
the one is always the effect of natural physiological processes, while
the other is always the result of injury, of disease, or of some form
of intoxication. Comatose {383} unconsciousness may be the result of
cerebral compression caused by traumatic impact or by the presence of
inflammatory exudations. Intracranial tumors, embolisms, thrombi,
degeneration of tissue, diseases of the arteries of the brain—in
short, every morbid change of which the liquids and the solids within
the cranium are capable—may become the causes of coma. So also the
blood and lymph, contaminated with the products of internal
disintegration, may benumb the brain with comatose sleep. Again, the
tissues of the brain may be overwhelmed with poisons introduced from
without the body, and thus a condition of coma may result. Few
diseases, therefore, exist without the possibility of coma as one of
their consequences—a coma which, however, must not be confounded with
the genuine sleep which sometimes occupies the larger part of certain
stages of convalescence from acute illness. During such convalescence
there is a reversion to the infantile type of nutrition, with all its
need of prolonged and frequent periods of repose. Like normal sleep,
the comatose condition admits of considerable variation of intensity.
The patient may sometimes be partially roused, as from the coma of
alcoholic intoxication, and he may finally recover complete
consciousness, but very often the reverse is the fact. The coma
deepens into paralysis, and death terminates the scene without the
slightest manifestation of sensibility or intelligence.


Sleeping Dropsy (Maladie du Sommeil).

A singular disorder, characterized by daily paroxysms of somnolence,
tending to become more and more continuous and profound until merged
in fatal coma, is encountered among the negro inhabitants of the
Atlantic coast of tropical Africa. Similar cases have been
occasionally reported in other regions of the world, but it is among
the Africans that they have been principally observed. For our
knowledge of this disease we are chiefly indebted to the writings of
Clark,[29] an English surgeon residing at Sierra Leone, and of
Guérin,[30] a surgeon in the French navy, who enjoyed unusual
opportunities for its study among the laborers recently brought from
Africa to the island of Martinique. According to these observers, the
onset of the malady is gradual, commencing with a slight frontal
headache. Very soon a disposition to sleep after meals is remarked.
This becomes increasingly urgent, and the paroxysms of sleep are
prolonged, until at length the patient becomes continually soperose.
The wakeful intervals are marked by a sluggish state of the
intellectual faculties. The pulse is not accelerated, but remains full
and soft. The veins of the sclerotic become turgid and the eyeball
seems unusually prominent. The temperature does not increase, but
rather tends to diminish its figure. The skin becomes dry and
moderately cool. The tongue continues moist, and is covered with a
white fur. The contents of the bowels and of the bladder are regularly
voided, and the appetite persists with considerable vigor. Finally,
the patient becomes completely comatose and dies quietly. Sometimes,
however, the evolution of the disease is less tranquil. Epileptiform
convulsions, followed by {384} progressively deepening paroxysms of
coma, interrupt its course, until a continuous muscular tremor marks
the closing period. At the same time the pulse grows weaker and more
frequent, until its movements cease in death. Recovery is almost
unknown, though the duration of the disease often varies from three
months to a year or longer. Examination of the body after death has
thus far yielded very negative results: the sinuses and larger vessels
of the brain are engorged with blood, but no evidence of inflammation
is anywhere apparent. The other organs present no pathological
alterations whatever. These observations seem to indicate that the
disease originates in some form of general blood-poisoning rather than
in any local inflammation or degeneration, and Clark has called
attention to an enlargement of the cervical glands as a feature of the
malady. According to G. H. Bachelder,[31] the native physicians cure
the disease by extirpation of the affected glands. He has also
observed an initial lesion in the nasal mucous membrane. If this be
confirmed, the malady will take its place among the forms of coma
produced by septic poisoning.

[Footnote 29: _Transactions of the London Epidemiological Society_,
vol. i. p. 116.]

[Footnote 30: _De la Maladies du Sommeil_, 1869.]

[Footnote 31: _The Medical Record_, July 1, 1882, p. 23.]


Lethargy.

A pathological variety of sleep, in which the repose of the body is
even more complete than in coma. The victim of coma often presents a
countenance suffused with blood; the pulse beats vigorously, and
respiration may become stertorous. But in lethargy the abolition of
bodily movements is almost total. In the milder forms of this disorder
the patient may be partially roused, so as to attempt an answer when
addressed, appearing like a person in very profound sleep; but in the
majority of cases he remains insensible, unconscious, and utterly
irresponsive to ordinary forms of irritation. Respiration and
circulation are reduced to a minimum, even becoming for a time
imperceptible. Uncomplicated with hysteria, the disorder is rapidly
fatal, but according to Rosenthal[32] hysterical lethargy is never
mortal.

[Footnote 32: _Real Encyc. der ges. Heilkunde_, vol. viii. p. 276.]

Many examples of this disorder have been furnished by the records of
apparent death.[33] I am well acquainted with a lady who in early
childhood was laid out for burial at the supposed termination of some
infantile disease. Her mother alone insisted that the child was still
alive. After some time spent in weeping and expostulation, she applied
a blister to the thorax of the babe, who at length began to exhibit
signs of consequent irritation, followed by a complete recovery. Still
more instructive is the case related by Rosenthal[34] of a young woman
twenty-four years of age who in consequence of violent emotional
excitement became unconscious and presented no sign of life, though
tested with a mirror before the mouth and by dropping melted
sealing-wax upon the skin. On raising her eyelids the pupils gave no
response to light; the limbs remained perfectly placid and the radial
arteries were motionless. Careful auscultation, however, detected a
very feeble and intermittent sound in the cardiac region. The thorax
exhibited no movement, but the lateral surfaces of {385} the abdomen
presented a slow and almost imperceptible oscillation. Gentle
faradization of the muscles and nerves of the face and hand aroused
definite muscular contractions. By these observations Rosenthal became
satisfied that, although the patient had remained for thirty-two hours
in this condition, she was only apparently dead. In fact, after
continuing forty-four hours in a state of suspended animation she
awoke spontaneously, made a rapid recovery, and enjoyed as tolerable
health as an excitable nervous temperament would permit.

[Footnote 33: See article “Mort apparente,” _Dic. Encyc. Sci. méd._,
2d Series, vol. ix. p. 598.]

[Footnote 34: _Loc. cit._, p. 272.]


Apparent Death.

Certain authors make a distinction between lethargy and apparent
death. But, leaving out of view the cases of so-called lucid lethargy,
a variety of the trance state, the difference is rather one of degree
than of kind. The movements of respiration and of circulation, though
greatly diminished, are readily observed in ordinary forms of
lethargy, while in apparent death the pulse can no longer be
discovered, and only the faintest sound can be distinguished in the
region of the heart. It therefore becomes imperative to have within
reach a crucial test of the persistence of general vitality. Such a
test, according to Rosenthal, exists in the faradic current. Within
two or three hours after genuine death the muscles cease to be
excitable by the induced current, but in a case of apparent death this
form of electro-muscular contractility never disappears. Every other
test that has been proposed has failed under certain circumstances.
This alone gives uniformly positive indications.


Lucid Lethargy.

In certain cases of apparent death the patient presents the external
phenomena of suspended animation, but the power of conscious
perception does not cease. The senses of sight and hearing remain, and
are perhaps intensified by inhibition of the power of projecting
cerebral volitions into space. The sufferer hears and sees;
perception, memory, reasoning, judgment, emotion, volition, all
persist. The possibility of centrifugal projection from the sphere of
consciousness into the realm of space seems to be the only thing that
is wanting.

The victims of this form of apparent death are usually women, or men
who are characterized by a feminine nervous organization. Great mental
excitement, fatigue, semi-starvation, and exhausting diseases are the
principal proximate causes of the event. The following case, which was
observed by my friend P. S. Hayes of Chicago, illustrates all these
facts: A female physician, about thirty years of age and consumptively
inclined, after a long and wearisome hospital service was attacked
with typhoid fever. After a period of great prostration the hour of
death seemed to have arrived. In the presence of her physician and
surrounded by her relatives she ceased to breathe and the pulse
stopped. Bottles of hot water were applied to the limbs, and other
methods of restoration were employed, but a number of hours elapsed
before these efforts yielded any result. At last she began to breathe
once more; life was resumed and {386} a gradual recovery followed.
During all this time of apparent death consciousness had been
preserved. She seemed to be looking down from above her bed, by the
side of which she could see the physician holding her wrist, and she
felt grief at witnessing the sorrow of her friends. Ordinary sensation
was suspended, for she did not feel the scalding heat of the bottles
that were applied to her limbs. Borne upon the wings of a liberated
imagination, she thought she beheld the celestial city, but might not
enter within its gates. In this exaltation the reasoning faculties
also shared, so that certain philosophical problems which had long
baffled her intellect were now perfectly comprehensible, and the
memory of their interpretation persisted after recovery.

Many similar narratives have been duly authenticated, but the limits
of the present article will not permit a discussion which properly
belongs to an investigation of the phenomena of trance. The important
fact for present consideration is the persistence of conscious life
despite the appearance of death. In this preservation of
consciousness, notwithstanding temporary suspension of certain forms
of sensibility, together with loss of the power of voluntary motion,
may be discovered a relationship between the events of lucid lethargy
and various somnambulic modifications of sleep which have been
previously passed in review.


{387}


ACUTE AFFECTIONS PRODUCED BY EXPOSURE TO HEAT.

BY H. C. WOOD, M.D., LL.D.


There are two distinct diseases—or, more correctly, conditions—of the
human body which are produced by exposure to heat, and which have a
certain similarity in their symptoms, but are very different in their
immediate pathology and require directly opposite methods of
treatment. Although their individuality was pointed out as long ago as
1851 by the late D. F. Condie of this city,[1] yet they have been
frequently confounded by writers upon the subject, and the terms
heat-exhaustion and sunstroke have not rarely been used as strictly
synonymous. In the present article it is proposed to consider them as
separate affections under the respective names of heat-exhaustion and
thermic fever.

[Footnote 1: _Amer. Journ. Med. Sci._, Jan., 1852.]


Heat-Exhaustion.

Any one who has been long exposed to a high temperature under
circumstances requiring physical exertion must have noticed the
feeling of general weakness and relaxation which results. Thus far
reaches our every-day experience, but cases in which acute symptoms
are severe enough to cause alarm occur, although somewhat
infrequently. The attack may come on slowly, but may be as abrupt as
that of true sunstroke, and the severest cases may happen in those who
have been in robust health as well as in the weak and feeble. The mind
is usually clear, the pulse rapid and feeble, the surface cool, the
voice very weak, muscular strength greatly lessened, and the feeling
of exhaustion extreme. If this condition be intensified, syncope may
be developed with its usual symptoms. In all this there is nothing
peculiar and little that is necessary to notice here; but there is a
form of heat-exhaustion in which the heart does not seem to suffer
principally, but in which there is collapse with palsy of the
vaso-motor system, great fall of the bodily temperature, and marked
general nervous symptoms. At the International Exhibition of 1876 a
very powerful man, whilst working in an intensely hot, confined space,
fell down without giving warning, and was brought into the hospital.
He was in a state of restless, delirious unconsciousness, incessantly
muttering to himself, and when shaken and shouted at responding only
by a momentary grunt. The pulse was rapid, fluttering and feeble. The
{388} surface was covered with a very heavy sweat and exceedingly
cold. The muscular relaxation was extreme. The facies was that of
collapse, and the temperature, as taken in the mouth, 95.25° F.

The PATHOLOGY of heat-exhaustion is best discussed in conjunction with
that of thermic fever, and will therefore be for the present
postponed.

The TREATMENT of heat-exhaustion is a very obvious one. The
indications are to stimulate the circulation and warm the body by
external heat with an energy proportionate to the severity of the
attack. In mild cases the exhibition of a whiskey punch or similar
beverage may suffice, but in severer attacks alcohol acts too slowly
and is not capable of filling all the indications. It may re-excite
the flagging heart, but it is probably not a vaso-motor stimulant, and
if given too freely may even increase the vaso-motor depression.
Digitalis is an excellent stimulant of the heart, and probably also of
the vessels. It acts, however, comparatively slowly even when
hypodermically injected, but in severe cases it should always be
employed. The tincture is the most eligible preparation, and when
injected under the skin in doses of fifteen drops causes no local
irritation. Ammonia would be a very valuable remedy did not its use
offer so many difficulties of administration: injected into the
cellular tissue, it causes great pain and usually sloughing, and its
intravenous use is by no means always easy. As a vaso-motor stimulant
atropia is an excellent remedy, and, as it has also a very powerful
influence in arresting the secretion from the skin and in raising the
animal temperature, it should produce very good results in the
peculiar form of collapse under consideration.

When the bodily temperature is below normal the most important measure
of treatment is the use of the hot bath: the water should be from 100°
to 120° F.—_i.e._ as hot as can be borne—and the whole body should be
immersed in it until the mouth temperature becomes normal.


Thermic Fever.

SYNONYMS.—Coup de soleil, Sunstroke, Heat apoplexy, Heat asphyxia,
Heat fever, Sun fever, Thermohæmia, Erethismus tropicus, Insolation.

The immediate cause of thermic fever is always exposure to excessive
heat in some form. As the body can cool itself much more readily in a
dry than in a moist atmosphere, it is able to resist the influence of
a dry, overheated air much better than when there is also moisture. It
is for this reason that sunstroke is so much more infrequent upon the
high table-lands of Abyssinia or in the dry belt of our Texan prairies
than in the lowlands of India or upon our own seacoast. For the same
reason it is especially prone to attack indoor workers in confined,
moist factories, and especially in laundries and sugar-refineries. At
one time it was thought that exposure to the direct rays of the sun
was the chief cause of the disease, but there is now abundant clinical
testimony to the fact that such exposure is in no sense necessary.
Without occupying space in giving detailed references, it suffices, as
an illustration of the fact that the most complete darkness is no
protection, to allude to the epidemic upon the French man-of-war
Duquesne, as recorded by M. Boudin, in which a {389} hundred cases of
sunstroke occurred in a short time, most of them at night when the men
were lying in their bunks. Bonniman[2] says: “By far the greater
number of cases that yearly occur in India are of men who have not
been exposed to the sun. It is not unusual for men to go to bed in
apparent health, and to be seized during the night; and patients in
hospitals who have been confined to bed for days previously are
frequently the subjects of attack.”

[Footnote 2: _Edinburgh Med. Journ._, vol. xiv. p. 1029, 1864.]

Although the immediate cause of the attack is excessive heat, there
are certain conditions which act as predisposing causes by lessening
the power of the system to resist the heat, or, in accordance with the
theory of sunstroke which I believe established, by so weakening the
inhibitory heat-centre that it is readily exhausted. The chief of
these predisposing causes are race, excessive bodily fatigue, and
intemperance. It is true that males are much more frequently affected
than females; thus, in an epidemic occurring in St. Louis, Missouri,
in 1878, there were 115 deaths in males and 39 in females. This is
due, however, not to one sex being predisposed to the attacks, but to
the habitually greater exposure of males than of females to heat. The
much greater frequency of sunstroke in the laboring than in the upper
classes has similar explanation.

Those races which are least accustomed to a tropical climate are most
apt to be attacked; thus, both in this country and in India, Europeans
suffer far more than do the natives. No race is, however, absolutely
exempt. Even the negro and the Hindoo inhabitant of tropical India are
occasionally prostrated.

The general experience in the United States shows that habitual excess
of alcohol very strongly predisposes to attack, but some of those who
have had widest experience in India are inclined to deny this. It has
been especially noted in India that persistent bodily fatigue greatly
weakens the resisting power of the European. As an instance of this
may be cited the case of the Forty-third regiment of the line during
the Sepoy rebellion, as recorded by its surgeon, Barclay. It had made
a most extraordinary march of over eleven hundred miles, chiefly
through the lowlands of India, and at the hottest season of the year.
This march was continuous, with the exception of a few brief halts. No
cases of sunstroke occurred until nine hundred and sixty-nine miles
had been traversed and the men had become thoroughly exhausted and
even markedly emaciated. Shortly after this the regiment rested some
eight days, and then started again, arriving soon in a narrow ravine
in the Bisramgunge Ghat, with precipitous walls nearly a mile in
height. During the day the thermometer in the tents ranged from 115°
to 127°, and on one occasion was noted 105° at midnight. The number of
cases of insolation now became very great, and, although most of them
recovered, 2 officers and 11 men were lost in the four days during
which the regiment remained encamped. The air became cooler as the
command emerged from the hills, yet 7 more fatal cases occurred in
three days.

SYMPTOMS.—Under the name of ardent continued fever, or febris
continuis communis, has been described in India an affection which may
be considered as representing a mild form of thermic fever. In C.
Morehead's clinical work _On the Diseases of India_ the following
account of the symptoms is given: “The attack is generally sudden,
often without {390} much chilliness. The face becomes flushed; there
are giddiness and much headache, intolerance of light and sound. The
heat of skin is great; the pulse frequent, full, and firm. There is
pain of limbs and of loins. The respiration is anxious. There is a
sense of oppression at the epigastrium, with nausea and frequent
vomiting of bilious matters. The bowels are sometimes confined; at
others vitiated discharges take place. The tongue is white, often with
florid edges. The urine is scanty and high-colored. If the excitement
continues unabated, the headache increases, and is often accompanied
with delirium. If symptoms such as these persist for from forty-eight
to sixty hours, then the febrile phenomena may subside, the skin may
become cold, and there will be risk of death from exhaustion and
sudden collapse. In most cases the cerebral disturbance is greater in
degree, and in these death may take place at an earlier period in the
way of coma.”

Until very recently the existence within the United States of this
class of cases has not been recognized. But in a very able article in
the _Therapeutic Gazette_ of March 16, 1885, John Guiteras shows that
the so-called typhoid fever of Key West is the disease described by
Morehead.

In the _Philadelphia Medical Times_, vol. v. p. 664, C. Comegys calls
attention to the cases of entero-colitis which are so abundant in the
young children of our cities during the hot months. The immediate
enormous rise of the mortality-rate among children which always
accompanies a marked rise of temperature during July or August
indicates very strongly that excessive heat is the chief factor in the
production of the disorder. The symptoms may be summed up as high
fever, dry tongue and mouth, rapid pulse and respiration, intense
thirst, vomiting, purging of greenish, watery, fecal or serous matters
with undigested particles of food, and more or less pronounced
evidences of cerebral disturbance, such as insomnia, headache,
contracted pupils, delirium, and finally coma. In some cases the
bodily temperature rises before death to a point comparable with that
it reaches in sunstroke of the adult. As pointed out first by Comegys,
these cases are almost uniformly relieved by cold water used either,
as Comegys himself employs it, in the form of cold affusions practised
until the temperature of the child becomes normal, or, as, according
to my own experience, is preferable, simple cold baths administered
every two to three hours, with just sufficient vigor to produce the
desired effect.

Thermic fever in the adult and in this latitude is usually first seen
by the physician after the stage of insensibility has been reached. In
many cases this condition comes on with great suddenness, but in other
instances there are distinct prodromata, such as inaptitude and
disinclination to exertion, vertigo, headache, confusion of ideas,
great oppression or distress at the præcordia or epigastrium, and
disturbances of the special senses. Swift has noticed a peculiar
chromatopsia, the sufferer seeing everything of a uniform color, in
most cases blue or purple, but in others red, green, or even white,
and W. H. Kesteven[3] has reported a case in which a man, after
exposure to an excessively hot sun, was seized with severe headache,
saw everything red or green, and had for some days a distinctly
impaired color-sense.

[Footnote 3: _Trans. Clin. Soc. of London_, 1882, xv. 101.]

At one period I saw a large number of advanced cases of sunstroke in
{391} the hospital, and the symptoms were quite constant. Total
insensibility was always present, with, in rare instances, delirium of
the talkative form, and still more rarely the capability of being
roused by shaking or shouting. The breathing was always affected,
sometimes rapid, sometimes deep and labored, often stertorous, and not
rarely accompanied by the rattle of mucus in the trachea. The face was
usually suffused, sometimes, with the whole surface, deeply cyanosed.
The conjunctiva was often injected, the pupils various, sometimes
dilated, sometimes nearly normal, sometimes contracted. The skin was
always intensely hot, and generally, but not always, dry; when not dry
it was bathed in a profuse perspiration. The intense burning heat of
the skin, both as felt by the hand and measured by the thermometer,
was one of the most marked features of the cases. The degree of heat
reached during life was, in my cases, mostly 108°-109° F., but it
sometimes reaches 112° F. The pulse was always exceedingly rapid, and
early in the disease often not wanting in force and volume; later it
became irregular, intermittent, and thready. The motor nervous system
was profoundly affected: subsultus tendinum was a very common symptom;
great restlessness was also very often present, and sometimes partial
spasms or even violent general convulsions. The latter were at times
epileptiform, occurring spontaneously, or they were tetanoid and
excited by the slightest irritation. Sometimes the motor system
suffered paralysis, the patient moving neither hand nor foot.

This extreme motor relaxation, which in my observation is rare, seems
to have been very common in the epidemic described by Barclay,[4] as
he states that in a large proportion of the cases, from the
commencement of the attack until its termination in death, the patient
never moved a limb or even an eyelid. Petechiæ and ecchymoses, the
evidences of broken-down blood, were present in some of my cases, and
there was in one or two instances a fetid hemorrhagic exudation from
the nostrils during life. A symptom which has almost escaped the
attention of authors was a peculiar odor, which was most marked in
patients who had involuntary passages, but was very distinct from any
fecal odor. The stools emitted it very strongly, but so did the skin
and breath. It was so distinctive as to render possible the
recognition of a case by the sense of smell alone. The discharges from
the bowels were liquid and very often involuntary. None of my cases
passed urine whilst under observation.

[Footnote 4: _Madras Quarterly Journal_, 1860, 364.]

It is plain that the symptoms of coup de soleil, as usually seen, may
be summed up as those of intense fever, accompanied by profound
nervous disturbance (as manifested by insensibility with or without
delirium, and by motor symptoms, such as convulsions or paralysis), by
arrest of glandular action, and by changes in the blood. In this
ordinary form of sunstroke death takes place by asphyxia or by a slow
consentaneous failure of both respiration and cardiac action. It very
rarely occurs in less than half an hour after the first decided
symptoms, and usually is postponed for a much longer period.

There is a form of coup de soleil in which death results almost at
once, and probably always by cardiac arrest, and to which the name of
the cardiac variety may well be given. It is very rarely, if ever, met
with in civil life, and among soldiers is especially seen during
battle or at other {392} times when great exertion is being made.
These cases will be more fully discussed in a later portion of this
article.

POST-MORTEM CHANGES.—Owing to the excessive heat of the body,
putrefactive changes occur very rapidly after death from sunstroke,
and various described lesions, especially of the heart, have been
undoubtedly the result of post-mortem changes. Later observers have
confirmed my original observation, that if the body be opened directly
after death the left ventricle will be found firmly contracted, though
the right heart and the pulmonary arteries, with their branches, are
gorged with dark fluid blood. In my cases the lungs did not present at
all the appearance of congestion of their minute capillaries, but when
they were cut the blood poured from them abundantly, seemingly from
their larger vessels. Not only do the lungs suffer from venous
congestion, but the whole body also. The blood appears to leave, as it
were, the arterial system and collect in the venous trunks. The
arterial coats are often stained red, apparently by the broken-down
red corpuscles of the blood.

There can be no doubt that the blood suffers in sunstroke very
similarly to what it does in low fevers. Its coagulability is
impaired, but not always destroyed; and it is possible that in the
very rapid cases it may not be decidedly affected. After death it
appears as a dark, often thin, sometimes grumous fluid, whose reaction
is very feebly alkaline, or, as I have seen it, even decidedly acid.
Levick[5] appears to assert that the blood-discs, as seen by him under
the microscope, were shrivelled and crenated, and showed very slight
tendency to adhere in rouleaux. In several of my cases the blood was
carefully examined by the microscope, but nothing abnormal was found.
The extravasations of blood which have been found by K. Köster in
various parts of the nervous system are probably of the nature of
petechiæ, the results of the altered blood-crasis, and not due to any
especial affection of the nerve-centres.

[Footnote 5: _Pennsylvania Hospital Reports_, 1868, 373.]

THEORY OF THE DISEASE.—The theories which have been brought forward as
explanatory of the phenomena of sunstroke are so various that it would
be impossible in the limits of this paper to discuss them. It does
seem, however, proper to give a very brief historical sketch of the
development of our present knowledge of the subject. In 1854, H. S.
Swift[6] said that the disease is “now generally admitted to be merely
exhaustion produced by fatigue,” although he recognized the existence
of an “apoplexy produced by insolation.” The cases which Swift so well
describes as those of heat-exhaustion were true instances of thermic
fever. The physicians of the Pennsylvania Hospital, especially
Gerhard, early called attention to the resemblance of sunstroke to a
fever, but it was not until January, 1859, that their views found
expression in print in the paper published by James J. Levick in the
_American Journal of Medicine_. This observer tabulated the
post-mortem appearances of typhus fever and of sunstroke in contrast,
calling attention also to the similarity of symptoms during life. In
1863, H. C. Wood[7] claimed distinctly that sunstroke is a fever due
to the development of a poison in the blood, and gave to the disease
the name of thermic fever. To R. Cresson Stiles is due the credit of
having first proven[8] the possibility of producing in animals a
sunstroke with symptoms and {393} pathological changes similar to
those which occur in man. He also came to the conclusion that the
symptoms are the results of the direct action of heat, especially upon
the muscular system. He says: “The dilatation of the capillaries is
explicable by the direct effect of the heated blood upon the muscular
fibres of the arteries and the arterioles. The cerebral symptoms and
the full and forcible pulse may also be due to this dilatation.”
George B. Wood, in the sixth edition of his _Practice of Medicine_
(Philadelphia, 1866), wrote an elaborate article upon the disease,
giving it the name of heat fever, and affirming that it “is, I
believe, strictly an idiopathic fever.” He further asserts: “In heat
fever all the organs, the brain, heart, lungs, stomach, kidneys, etc.,
are excessively stimulated by the great heat, and all exhibit disorder
and at length depression of their functions.” The article of George B.
Wood was not based upon experimental researches, but upon a very
philosophic rendering of the clinical phenomena, and was a carrying
out of the ideas which had permeated the medical teaching of the
Pennsylvania Hospital.

[Footnote 6: _New York Med. Journ._, vol. xiii. p. 53.]

[Footnote 7: _Amer. Journ. Med. Sci._, October.]

[Footnote 8: _Boston Med. and Surg. Journ._, June, 1864, p. 349.]

About 1869, Eulenberg and Vohl[9] advanced the theory that death from
sunstroke is the result of the sudden liberation of gases in the
blood; and Weikard affirmed that the death is due to the increase of
the coagulability of the blood and consequent formation of clots in
the vessels, being in this supported by Richardson of London.[10]
Contrasting with these in its being really an important contribution
is the article of Vallin:[11] its chief merit is the conception of the
idea of the local heating of isolated parts of the body, and the
devising of a plan for carrying the idea into effect. The experiments
of Vallin did not themselves prove very much, and led him to the
erroneous conclusion, first, that the death in sunstroke is the result
either of a coagulation of the left ventricle or else of a disturbance
of the innervation of the heart by an action of the heat upon the
nerve-centres in the base of the brain; second, that these two forms
of death correspond to sthenic and asthenic varieties of
insolation—varieties which, I believe, have no proper existence.

[Footnote 9: _Virchow's Archiv_, t. lxii.]

[Footnote 10: _St. Bartholomew's Reports_, vol. vii.]

[Footnote 11: _Archives générales de Médecine_, Fèvrier, 1870.]

The first experiments of Claude Bernard upon the action of external
heat were given in a lecture upon muscular respiration on May 3, 1864,
published in his _Leçons sur les Propriétés des Tissus vivants_
(Paris, 1866). They were merely incidental to another research, and
simply showed that when a warm-blooded animal was exposed to heat it
died, the death being, according to the observations of Bernard, the
result of cadaveric rigidity suddenly attacking the heart. The more
elaborate researches of Claude Bernard upon the effect of exposure of
animals to external heat, so far as I have knowledge, were not
published in detail until after the nature of sunstroke was
determined, although the lectures were delivered in the years 1871 and
1872; they may be found reported in full in his _Leçons sur la Chaleur
animale, sur les Effets de la Chaleur, et sur la Fièvre_ (Paris,
1876).

It is proper also to state here that some of the physicians of India
had previous to this time more or less imperfectly recognized the
relation of sunstroke to fever, but, I believe, none of them
distinctly postulated the theory.

The above historical sketch shows that by many authors the relation
{394} of sunstroke to fever had been more or less dimly perceived, and
that George B. Wood had very clearly stated the true nature of the
affection, in that it was simply the result of the direct action of
heat. Such statement, however, not resting upon proof, had not been
accepted: it was also wanting in detail, and where such details were
attempted the surmises were not always correct. Under these
circumstances my researches, made in 1870 and 1871, and first
published in 1872, led to the complete understanding of the affection.

The space allotted to me in the present volume will not allow of any
detailed account of my experiments, but I shall quote from my summing
up of the results obtained by them. It was shown that sunstroke may be
produced in animals as readily as in man either by natural or
artificial heat; that the symptoms are similar to those seen in man;
that death takes place ordinarily by asphyxia; that after death the
characteristic lesions are alteration of the blood and rigidity of the
heart, with immediate or quickly-appearing post-mortem rigidity of the
general muscular system; that this rigidity of the heart comes on in
most cases after, not before, death, and is a result, not cause, of
death; that post-mortem rigidity is dependent upon coagulation of
myosin, and that the rigidity of the heart is of similar origin,
coagulation of the muscle-plasma occurring almost instantaneously at
115° F., a degree almost attained in sunstroke; that when a muscle has
been in great activity immediately before death, myosin coagulates at
a much lower temperature, and that the cases of sudden cardiac death
occurring in battle among the East Indian English troops were no doubt
due to the coagulation of the heart's myosin; that heating the brain
of a mammal produces sudden insensibility, with or without
convulsions, at a temperature of 108° F., and death when a temperature
of 113° is reached; that this effect of the local application of heat
is not due to induced congestion, but is the result of the direct
action of the heat upon the cerebrum, and that consequently the
nerve-centres are as perniciously affected by high temperature as the
muscles are; that the nerve-trunks bear a temperature of 125° F.
without their conducting power being immediately affected; that whilst
the general symptoms induced by heating the brain of a rabbit are very
different from those of sunstroke, the nervous symptoms are exactly
similar; that the life of the blood is not destroyed by any
temperature reached in sunstroke, the amœboid movements of the white
blood-cells and the absorption power of the red disks not being
injured; that the amount of oxygen of the blood is greatly lessened,
as the result of gradual asphyxia combined with abnormal consumption
of oxygen; that there is no reason for believing that capillary
thrombi are common in sunstroke; that there is no specific poison
developed in the blood; that the deterioration of the vital fluid is
due to the rapid tissue-changes induced by the fever and the more or
less complete arrest of excretion; that such deterioration is
secondary to the nervous symptoms, not primary; that if the heat be
withdrawn before it has produced permanent injury to the nervous
system, blood, or other tissues, the convulsions and unconsciousness
are immediately relieved and the animal recovers.

As a postulate from these facts and deductions, I think it follows
that the nature of sunstroke is that of a fever; or, in other words,
that coup de soleil is a fever, not dependent upon blood-poisoning,
but upon heat.

{395} It is of course possible that the external heat causes the
fever, simply by preventing the body from throwing off the caloric
which it is constantly forming. The extreme suddenness of the onset,
however, indicates that in at least many cases there is a sudden
outburst, as it were, in the production of heat in the body. This
indication becomes more important when it is remembered that in
cerebral rheumatism, so called, there is often an equally sudden
attack of symptoms plainly the result of a sudden production of animal
heat.

In an elaborate research[12] I showed the truth of Setschenow's
theory, that there is in the pons a centre whose function it is to
inhibit the production of animal heat, and that in the medulla a
centre (probably the vaso-motor centre) which regulates the
dissipation of the bodily heat; and that fever is due to disturbance
of these centres, so that more heat is produced than normal, and
proportionately less heat thrown off. Let it be supposed that a man is
placed in such an atmosphere that he is unable to get rid of the heat
which his body is forming. The temperature of his body will slowly
rise, and he may suffer from a gradual thermic fever. If early or late
in this condition the inhibitory heat-centre becomes exhausted by the
effort which it has been making to control the formation of heat, or
becomes paralyzed by the direct action of the excessive temperature
already reached, then suddenly all tissues will begin to form heat
with the utmost rapidity, the bodily temperature will rise with a
bound, and the man drop over with some one of the forms of coup de
soleil.

[Footnote 12: _Fever_, Smithsonian Institute, 188-.]

Under this view of the case the widespread popular belief, that
protecting the back of the head and upper neck from the direct rays of
the sun is useful against sunstroke, gains in significance, because it
is possible that local heating of the parts spoken of may occur and
aid in the production of inhibitory paralysis.

If this theory of thermic fever be correct, heat-exhaustion with
lowered temperature probably represents a sudden vaso-motor
palsy—_i.e._ a condition in which the exhausting effects of the heat
paralyzes not the inhibitory heat-centre, but the vaso-motor centres
in the medulla, since my experiments have shown that vaso-motor palsy
increases enormously the loss of animal heat and diminishes its
production.

In most cases of sunstroke death comes on gradually by arrest of
respiration, such arrest being without doubt due to direct paralysis
of the respiratory centres by the excess of heat. Allusion has already
been made to the cases of sudden death by cardiac arrest, which have
especially been seen in India, almost always during a march or during
a battle. “As an example of it may be cited the account given by a
witness to Parkes, and incorporated in his work on hygiene,[13] of an
occurrence during the first Chinese war. The Ninety-eighth regiment
was marching on a very hot day, and the surgeon who was with the
rear-guard stated to Parkes that the men fell suddenly on their faces
as though struck with lightning, and on his running up and turning
them over many of them were already dead. Maclean, who was present at
this occurrence, confirms the account given by Parkes, but states that
it was at the attack on Chiang-Kiang-Foo. The men were thickly
clothed, with tight accoutrements and tight, rigid stocks, and were
charging up a very steep hill. A great {396} number of them were
stricken down, and fifteen died instantly, falling on their faces and
giving merely a few convulsive gasps.”

[Footnote 13: _Pract. Hygiene_, 2d ed., p. 360.]

It has been shown that excessive exercise so alters the condition of
the myosin of muscle as to cause it to coagulate much more readily
than normal. During battle the amount of muscular effort that is made
is enormous, and hence it is that men are so often found stiffened in
the attitude in which they were struck by the bullet, instantaneous
death being followed by equally instantaneous post-mortem rigidity.
The description that has been given by Parkes and Maclean of the
circumstances in which the sudden deaths just described occurred shows
that the heart-muscles must have been strained to their utmost limit.
The men were making violent exercise going up hill, so that the heart
must have been in exceedingly active exertion, increased by the
impediment to the circulation afforded by the tight accoutrements, and
under these circumstances the victims probably died instantly because
the heart-muscle suddenly set itself from life into the stiffness of
death.

The DIAGNOSIS of thermic fever is usually made with great readiness.
In distinguishing between it and heat-exhaustion the temperature of
the body is the guide. In apoplexy with high temperature it is
possible that a little embarrassment might be experienced, but in
apoplexy the high temperature follows the nervous symptoms after a
distinct interval, but in thermic fever it precedes the
unconsciousness. An apoplexy may develop during a sunstroke, but such
occurrence is rare. T. S——, now under my care, has had frequently
repeated attacks of local convulsions affecting two fingers of the
right hand, and one general epileptic attack whilst under observation.
He dates his illness to a sunstroke on July 7, 1885, and O. D.
Robinson of Georgetown, Delaware, writes me that the attack was
undoubtedly true thermic fever, and that the movements of the fingers
came on whilst the patient was recovering consciousness. It is
probable, therefore, that there was a rupture of a small vessel in the
brain-cortex during the sunstroke. The appearance of local convulsions
or of localized paralysis during a sunstroke would be good ground for
believing that either a clot or a thrombus had formed.

PROPHYLAXIS AND TREATMENT.—The prophylaxis of sunstroke is so evident
in its nature that it may be dismissed in a few words. When exposure
to heat is imperative the bodily health should be maintained by
avoidance of alcoholic, sexual, or other excesses, and, as far as
possible, of great bodily or mental fatigue; the diet should be almost
purely farinaceous, and the glandular apparatus of the bowels,
kidneys, and skin kept in an active state by the use of fruit, water
in abundance, and mild salines if necessary. Many persons have a very
strong prejudice against the drinking of cold water during exposure to
heat; and it is conceivable that large draughts of intensely cold
ice-water may do harm by suddenly chilling the stomach; but when the
water is taken in small quantities at short intervals, by its action
in reducing the general temperature, but especially by its rendering
free perspiration more easy, it must exert a most favorable influence.
The addition of claret or some other local stimulant to the water is
often of great service when there is a tendency to gastric or
intestinal depression.

In the mild cases of continued thermic fever the basis of the
treatment should be the use of the cold bath. The plan adopted by
Guiteras at Key {397} West was to wrap the patient in a dry sheet,
lift him into a tub of water, having the temperature between 80° and
85°, and then rapidly cool this water by means of ice. The time of the
immersion lasted from fifty to fifty-five minutes, it being regulated
by the thermometer in the mouth of the patient. The patient was then
lifted out upon a blanket, the skin partially dried, and the body
covered. Guiteras found great advantage by giving a moderate dose of
whiskey and thirty minims of the tincture of digitalis twenty minutes
before the bath. He states that it is very important to avoid currents
of air blowing upon the patient and to have the bath given in a small
warm room. The result of the bath was invariably a lowering of the
temperature, a reduction of the rate of pulse and respiration, and a
refreshing sleep. After the second bath the course of the temperature
seemed permanently influenced for the better. It was never necessary
to give more than two baths in the twenty-four hours, but in some
cases they had to be used for many days.

In the severe acute form of thermic fever it is essential that the
bodily temperature be reduced at once, and no time should be lost
waiting for a physician. As soon as the patient falls he should be
carried into the shade with the least possible delay, his clothing
removed, and cold affusions over the chest and body be practised. This
must not be done timidly or grudgingly, but most freely. In many cases
the best resort will be the neighboring pump. In the large cities of
the United States during the hot weather hospital ambulances should be
furnished with a medical attendant and with ice and antipyrin, so that
when a sunstroke patient is reached he may be immediately stripped
underneath the cover of the ambulance and remedial measures applied
during his passage to the hospital. I believe many lives are now
sacrificed by the loss of critical moments in the interval between the
finding of the patient and his reaching the hospital ward.

If circumstances favor, instead of the cold affusions, rubbing with
ice may be practised. The patient should be stripped and the whole
body freely rubbed with large masses of ice. When practicable, a still
better plan is to place the patient in the cold bath (50° F.) The
employment of enemata of ice-water, as originally suggested by Parkes,
may sometimes be opportune.

In using these various measures it must always be borne in mind that
the indication is the reduction of temperature: if the means employed
do not accomplish this, they do no good.

Relaxation of the pupil is said to be “the first symptom that shows
the good of the cold affusion;”[14] but as, in my experience, the
pupil frequently has not been contracted, reliance cannot be placed
upon this, and the thermometer in the mouth or the rectum affords the
only proper guide as to the effect of the treatment.

[Footnote 14: Aitken, _Practice of Medicine_, vol. ii. p. 394.]

It must be borne in mind, however, that the cold douche, cold bathing,
etc. are powerful remedies, and are capable, if used too long, of
doing harm. In my experiments upon animals I have seen the
temperature, when reduced by the cold bath after sunstroke, continue
to fall, after the animal had been taken out of the water, until it
was many degrees below normal.

In the cases which have come under my own observation after the use
{398} of the cold bath but little treatment has been required. If,
however, the period of insensibility has lasted too long, there may be
no return to consciousness, even though the bodily temperature be
reduced to the norm. Under such circumstances the case is almost
hopeless, and I know of no treatment other than that of meeting the
symptoms as they arise, excepting that a large blister should, in my
opinion, be applied to the whole of the shaved surface of the scalp.

After the temperature has been reduced, and even after consciousness
has returned, there is sometimes a great tendency to a fresh rise of
temperature, and consequent relapse. This tendency may be met by
wrappings in wet sheets, and, if necessary, by a recourse to the more
powerful measures for reduction of temperature which have been already
cited. It can be to some extent controlled by the use of quinine, ten
grains of which may be given hypodermically. During the heated term of
the summer of 1885 antipyrin has been used both in New York[15] and in
Philadelphia[16] with asserted most excellent results; and the
testimony is so strong that I think it should always be employed as an
aid to, not as a substitute for, the direct extraction of the bodily
heat. It should be given hypodermically, as soon as the patient is
found, in doses of from fifteen to thirty grains.

[Footnote 15: B. F. Westbrook, _New York Med. Journal_, July 25,
1883.]

[Footnote 16: Orville Horwitz, _Trans. College of Physicians of
Philada._, Oct., 1885.]

In cases complicated with repeated severe convulsions, hypodermic
injections of one-quarter of a grain of morphia have been very
frequently given in the Pennsylvania Hospital, with excellent results.
In such patients the use of anæsthetics to facilitate the giving of
cold baths would be very proper, but so long as the temperature is
high nothing should be allowed to substitute the external cold.

Severe headache and other evidences of cerebral inflammation,
manifesting themselves directly after the recovery of consciousness,
should be met by local or even general bleeding, blistering, the use
of arterial sedatives, mercurials, etc.; or, in other words, by the
treatment of cerebral inflammation from other causes adapted to the
exigencies of the individual case.

Formerly, venesection was largely practised in sunstroke, with
occasional excellent effects, but with, on the whole, very bad
results. As free bleeding lowers temperature markedly, it can be
readily understood that in some cases it might bring about a return of
consciousness and yet be a very improper remedy. If in any instance
sthenic apoplectic symptoms persist after the lowering of the bodily
temperature by the bath, venesection should be carefully considered.
There are cases of sunstroke in which the high temperature irritates
the brain or its membranes into an acute congestion or inflammation.
These complications are especially prone to occur when the high
temperature has been allowed to continue for a long time. A case of
this character, in which the autopsy revealed proof of the presence of
an acute meningitis, may be found on p. 121 of my book on _Thermic
Fever_. When, then, the patient has a tendency to excessive headache
and continuous fever, bleeding may become an essential remedy, not for
the cure of thermic fever, but of the cerebral inflammation which has
been produced by that fever. The case of S. Weir Mitchell is in point.
In his early manhood he had a sunstroke, and when {399} consciousness
began to return “the first sensation was that of an intense, agonizing
headache, and the next was the perception of his father—J. K.
Mitchell—and Mütter discussing the possibility of his recovery. As
soon as he could speak, he said, ‘Bleed me.’ His father, coming to the
bed, shook his head, but the son repeated, ‘Bleed me.’ He persisted in
simply repeating this until they thought him delirious; but at last he
mustered strength to say, ‘I am not delirious, but have a frightful
headache: if you don't bleed me I will die.’ By this time his pulse
had become full and bounding, and finally he sat up and was bled. Ten
or fifteen ounces were taken without avail; but as more blood flowed
the headache vanished, to be succeeded by a feeling of most delightful
languor and rest from pain. Between twenty-five and thirty ounces were
taken, and afterward recovery was a very simple matter.”

That Mitchell by the bleeding was saved from meningitis appears almost
certain, but it is most probable that if he had been primarily
immersed in a cold bath no bleeding would have been required.

SEQUELÆ.—Almost all persons who have had a coup de soleil suffer from
after-effects. In the mildest form these are inability to bear
exposure to heat without cerebral distress or pain, with more or less
marked failure of general vigor, dyspeptic symptoms, and other
indications of disturbed innervation. In other cases the symptoms are
more decided. Pain in the head is usually prominent: it may be almost
constant for months, but is always subject to exacerbations. It
sometimes seems to fill the whole cranium, but not rarely is fixed to
one spot; and I have seen it associated with pain in the upper
cervical spine and decided stiffness of the muscles of the neck. With
it may be vertigo, decided failure of memory and of the power of
fixing the attention, with excessive irritability. When the symptoms
approach this point in severity, there is usually marked lowering of
the general health, loss of strength, possibly some emaciation, and
the peculiar invalid look produced by chronic disease.

Epileptic convulsions occasionally follow a sunstroke, but, at least
in my experience, are always associated with more constant evidences
of cerebral disease.

A pathognomonic symptom in the sequelæ of sunstroke is the effect of
heat. The glare and heat of summer are the most trying, but usually
artificial heat is not well borne. It is very common for headache and
severe general distress to be produced by going into a warm room even
in the winter months. Where cerebral symptoms are affirmed to be the
result of a sunstroke, if there be no excessive susceptibility to heat
the alleged sunstroke has almost certainly been an attack of some
other nature; and on several occasions I have been enabled to
determine that a supposed epileptic attack or a fall followed by
unconsciousness from violence was really a sunstroke by noting the
extreme susceptibility to heat. The symptom I believe to be a
diagnostic one.

The lesion in these cases is usually chronic meningitis, though it is
possible that in some instances the gray matter rather than the
membrane of the brain may be affected, and in severe cases the gray
matter is of course more or less compromised. In one case occurring in
the care of S. Weir Mitchell, and in one in my own practice in which
death occurred from extraneous causes, severe chronic meningitis was
found at the autopsy.

{400} The TREATMENT of these cases is that of chronic meningitis, with
the added precautions against exposure to heat. In any severe case
change of habitation to a cool climate during the hot period of the
year is essential: twenty-four hours' exposure may undo all the good
achieved by months of careful treatment.

It is hardly proper here to enter into a detailed discussion of the
remedial measures to be employed in this as in the other forms of
non-specific chronic meningitis. Local bleedings, the use of
counter-irritation, especially by the actual cautery, the internal
administration of mercurials and of iodide of potassium in small
continued doses, with abstinence from brain-work and the regulation of
the habits of life, constitute an array of measures which will no
doubt be fully discussed by the author of the article upon Chronic
Meningitis.

Provided the patient can be entirely controlled, the PROGNOSIS in
these cases is not so bad as at first it appears to be. As an instance
of a remarkable recovery I condense from my notebook the case of T. W.
H——, aged 49, who came under my care with a history that two years
previously he had been seized during a hot day in the summer with a
very violent headache, which continued for five weeks, confining him
to bed, and was associated, as he said, with fever, but no other
symptoms. This attack had been diagnosed by several physicians
variously, but as I found that he was excessively affected by any
exposure to the sun, was always worse in summer, and that in winter
his symptoms were extremely exaggerated even by such heat in a room as
is agreeable to many persons, I concluded that the original attack had
really been one of thermic fever. He had lost about forty pounds in
weight; his memory had become so bad for recent events that he could
not call to mind things which had transpired one or two hours
previously. Sight had failed much, and there was double vision. He
suffered from almost incessant dull headache and excessive general
wretchedness; the optic discs were slightly swollen, and one of the
margins obscured. There was no albuminuria, and the dyspeptic symptoms
were so bad that the man had been treated for months for dyspepsia.
Nine months of treatment sufficed to restore this patient almost to
his original health. The treatment consisted essentially in the
alternate administration of minute doses of calomel and of iodide of
potassium—in the meeting of various minor symptoms as they arose, but
chiefly in the persistent, merciless use of counter-irritation at the
nape of the neck. The actual cautery was applied every one or two
weeks, and antimonial ointment freely used on the burnt surface.


{401}


HEADACHE.

BY WHARTON SINKLER, M.D.


SYNONYMS.—Cephalalgia, Cephalœa.

It is not possible to give in a few pages a complete treatise on
headache, and it is therefore intended merely to describe the most
common types of this malady.

Many forms of headache are symptomatic of some organic cerebral
disease, like tumor of the brain or syphilitic diseases of the skull.
Headache also constantly accompanies fevers of all kinds. A great
number of cases are met with in which no cause for the headache can be
discovered, and in which the pain is the only symptom. In these there
must be some disordered state of the sensory nerves within the
cranium, but just what the nature of the abnormal condition is it is
impossible to decide.

The character of the pain in headaches is various. In some cases there
is a violent general pain over the entire head. In others the pain is
localized in one particular spot, feeling as if a nail were being
driven into the skull. This is called clavus, and is often met with in
hysterical patients.

Patients sometimes describe the head as feeling as if it were
splitting open, or, again, as if it were being compressed. The pain
may involve one side of the head alone, hemicrania, or it may be only
in the back of the head. The top of the head is a frequent seat of
pain, especially in women who have uterine disorders. In short, the
pain may be in any or every portion of the head, or it may move about
from place to place.

In almost all varieties of headache the pain is aggravated by noises
or strong light. Any movements of the patient increase it, and
coughing, sneezing, or straining—as, for instance, at stool—adds to
the suffering. Tapping on the head usually does not increase the pain,
and in some instances alleviates it.

Accompanying the headache is a variety of other symptoms: some of them
are nervous, while others are not. There are often disturbances of
vision, such as bright spots or zigzags before the eyes; and there may
be ringing in the ears; palpitation or slowing of the heart. Nausea
occurs in most varieties of headache, and a feeling of general
prostration or nervous excitability is often experienced both during
and after an attack.

The duration of an attack of headache varies from a few minutes to
{402} days or even months: one occasionally sees a patient who says
she has not known what it is to have been without pain in the head for
years.

The character of the pain may be either a dull aching or it may be
excessively intense, so as to cause temporary aberration of mind. As
to the structures within the cranium in which the pain is located, it
is a mooted question. Some writers believe the dura mater may be the
seat of pain in headaches, while other observers have declared this
membrane to be insensitive. Probably the intracranial branches of the
fifth pair of nerves are the principal site of pain.

We will now consider particularly the different varieties of headache
most commonly met with.

ANÆMIC HEADACHE.—The pain is of a dull kind, often diffused over the
head, but frequently in the vertex or temples. It occurs in weak,
thin-blooded persons, and is relieved by the recumbent position. If
the patient is sitting or walking, the pain becomes worse, and there
is a sense of faintness or dizziness. Women are the most common
sufferers from this form of cephalalgia, and uterine diseases or
disorders of menstruation are connected with it. It is associated with
palpitations of the heart, difficulty of breathing, a tendency to
faint, and general weakness. Anything which exhausts the nervous
system, like over-study or anxiety, loss of rest and sleep, is likely
to bring on an attack.

CONGESTIVE (HYPERÆMIC) HEADACHE.—In this variety of headache, which is
common, the pain seems to affect the whole head and is of a dull,
throbbing character. The recumbent position aggravates it, as does
coughing or straining. During the paroxysm the face is flushed, the
eyes suffused, and the arteries throb violently. Sleep relieves the
pain of a hyperæmic headache for a time, but as soon as the patient
begins to move about, or even to exercise the mind, the pain returns.
Erb[1] speaks of a violent pain in the brow and temple, with a sense
of pressure and fulness in the head, and heat and redness in the face
and ears. This form may come in regular paroxysms. He has seen one
case of this kind in which there was violent pain accompanied by
fainting, and intense redness of the brow and vertex was observed.

[Footnote 1: _Cyclopædia of the Practice of Medicine_ (Ziemssen), vol.
xiv. p. 140.]

THE HEADACHE OF HYSTERIA is usually seen in females, although it may
occur in males. It is sometimes general throughout the head, but is
often located in one spot (clavus), and is very intense. The seat of
clavus hystericus is at the top of the head to one side of the
sagittal suture. The pain is described as boring, gnawing, and
burning. The headache is more severe at the menstrual period, and is
increased by worry or trivial excitement. Nervous and hysterical
subjects complain of headache which never ceases.

TOXIC HEADACHES are the result of the introduction into the system of
various kinds of poisons. The headache following alcoholic excesses is
a well-known instance of this kind. The pain, which is deep-seated and
often intense, is supposed to be in the sensory nerves of the dura
mater. Other forms of chronic poisoning give rise to headache. Lead,
when retained in the system, produces headache, and so do many of the
narcotic drugs. In some persons the administration of iron always
causes pain in the head. The headache following a dose of opium is
familiar to all. The excessive use of tobacco is often followed by
dull headache next {403} day. The intense pain in the head caused by
uræmic poisoning is a well-marked symptom of this condition. Seguin
has lately well described the headache of uræmia.[2]

[Footnote 2: _Archives of Medicine_, vol. iv. p. 102.]

RHEUMATIC HEADACHE is often violent, and the pain seems to be located
in the head-muscles. It occurs in rheumatic subjects. It is brought on
by exposure to cold, and is increased by damp changes in the weather.
In acute rheumatism there are sometimes met with attacks of intense
headache. Headache also is associated with the gouty cachexia, and is
accompanied usually by depression of spirits and sometimes vertigo.

PYREXIAL HEADACHES.—In all of the acute fevers headache is a prominent
initial symptom, and usually continues throughout the course of the
disease. The pain is generally dull and deep-seated, and is probably
congestive in character. The headache of typhoid fever is constant,
and often precedes the fever by many days. Following an attack of
typhoid fever, it is not infrequent to find headache persisting for
months or even for years.

SYPHILITIC HEADACHE is one of the most violent forms of headache. The
pain is diffused or limited to one part of the head, and is associated
with tenderness of the scalp. It becomes most severe at night, but
never entirely intermits. The nocturnal exacerbations, although very
common, do not always occur. The pain is so violent and so constant
that the patient is unable to do any work or to occupy himself in any
way. There is great mental depression, and the patient becomes gloomy
and morose. The pain may be dull and heavy or acute and lancinating;
sometimes it is like a succession of heavy blows on the skull. During
a severe paroxysm of pain the scalp becomes so sensitive that the
lightest touch cannot be borne. The sufferer is unable to sleep, and
presents a worn, haggard appearance. Often he has hallucinations at
night. Syphilitic headache is often a forerunner of some form of
organic cerebral disease. One of the characteristic features of
syphilitic headache is its constancy. It never ceases entirely,
although at times there are paroxysms in which the pain is so intense
as to cause great agony. During the little sleep the patient is able
to get he is moaning or tossing about his bed. Minute doses of
mercury, repeated at short intervals, have been found to afford great
relief in headaches of this kind.

ORGANIC HEADACHE may be described as the headache which accompanies
organic disease of the brain or its membranes. Violent pain, seated in
one spot and constant in character, is one of the most unvarying
symptoms of tumors within the cranium. Brain tumors may exist without
headache, but rarely. The pain may be situated in any part of the
head: sometimes it is occipital and sometimes frontal, and
occasionally it extends over the entire head. It does not always
correspond to the seat of the disease. The pain is constant and
lasting, and, like syphilitic headache, is liable to exacerbations of
excessive violence. These often occur at night. Localized tenderness
of the scalp is often present, and percussing the skull over the seat
of the disease will increase the pain.

Disease of the membranes of the brain, such as meningitis or new
growths in the dura mater, will give rise to persistent headache. So
will {404} caries or any syphilitic affections of the skull. Catarrhal
inflammation of the frontal sinuses causes dull frontal pain. In
inflammatory diseases of the ear there is often headache. In these
latter conditions the cephalalgia is probably reflex.

NEURASTHENIC HEADACHE is more or less allied to the hysterical
headache. It is met with in persons who are run down in their nervous
system by mental worry or overwork—in other words, in persons who are
suffering from neurasthenia. Such patients describe the pain as being
constant and deep-seated—seldom acute, but dull and throbbing. It is
accompanied by a sense of weight and pressure on the vertex, and
sometimes by a feeling of constriction. Mental effort increases the
pain, and the patient usually prefers solitude and quiet on account of
the relief he obtains. The headache of neurasthenia often persists
after other symptoms of the affection have disappeared.

SYMPATHETIC HEADACHE is generally connected with disorders of the
digestive and sexual organs. The headache of ovarian disease is well
known to gynæcologists, and most of us have experienced the pain in
the head associated with gastric disturbances. The headache from
eye-strain may be considered in this connection, and deserves careful
consideration. Many persons have suffered from headaches for years
from this cause without its being suspected. Weir Mitchell brought
prominently to notice the frequency with which headaches may be caused
by defects of vision.[3] The fact had been long known to oculists that
disorders of the refractive apparatus of the eye would give rise to
cerebral discomfort and pain, but it had not before occurred to
physicians to look to defects of the eye to explain headaches whose
cause was obscure. The points made by Mitchell were—1, that many
headaches are caused indirectly by defects of refraction or
accommodation; 2, that in these instances the brain symptom is often
the only prominent symptom of the eye trouble, so that there may be no
ocular pain, but the strain of the eye-muscles is expressed solely in
frontal or occipital headache; 3, that long-continued eye troubles may
be the unsuspected cause of insomnia, vertigo, and nausea; 4, that in
many cases the eye trouble becomes suddenly injurious, owing to
break-down in the general health or to increased sensitiveness of the
brain from mental or moral causes.

[Footnote 3: _Med. and Surg. Reporter_, Aug. 1, 1874, and _Amer.
Journ. of the Med. Sci._, April, 1876.]

Occasionally the form of headache produced by eye-strain is a
migraine, but most commonly there is a steady frontal or occipital
pain, which comes on after undue use of the eyes, which are defective
as to refraction or accommodation. Accompanying the pain are sometimes
nausea and occasionally vertigo. It is not only over-use of astigmatic
eyes in reading or other near work which causes the cerebral
disorders, but the use of the eyes in the ordinary walks of life may
produce pain in a sensitive brain should there be any imperfection in
refraction or accommodation.

HEADACHE FROM SUNSTROKE.—A person who has had an attack of sunstroke
often suffers from headache for years. The attacks are most likely to
occur from exposure to the sun and in summer months, but they are
brought on in some individuals even in winter should they be in the
sun. Sometimes heat-exhaustion or exposure to the influence of the sun
in hot weather, even should there be no actual sunstroke, is {405}
followed for a long time by violent headaches. Persons who have
suffered in this way have to be extremely careful about exposing
themselves to the sun or they will have severe and prostrating pains
in the head. The cephalalgia in these cases is probably from
congestion of the cerebral meninges or some disturbance of the
submeningeal gray matter of the brain. The pain is usually frontal or
on the top of the head. Sometimes it is confined to one side of the
head. Mitchell[4] has seen two cases in which this form of headache
was relieved by ligature of the temporal arteries.

[Footnote 4: _Med. and Surg. Reporter_, July 25, 1874.]

HEADACHE OF CHILDHOOD.—Children often suffer from headaches
unconnected with meningitis or other organic brain trouble. Over-use
of the brain in study is a frequent source of headache, in children
especially, if associated with worry or anxiety. If a child complains
of headache after study, it is always important to examine the eyes
for defects of vision; but while this is often found to be the cause
of the headache, in many cases there will be discovered no errors of
refraction sufficient to account for the pain; and here the only
relief will be to take the child from school and give him plenty of
exercise and fresh air.

Another cause of headaches in children is hypertrophied tonsils, which
prevent the free return of blood from the brain. Children also suffer
from headaches from over-eating or improper food, or from
over-exercise in the sun. Migraine, as will be seen later, is a
disease which often begins in early childhood, and a child may suffer
from frequent attacks of headache of this nature for a long time
before they are understood.

Children who are precocious in any way are apt to be sufferers from
neuralgias and headaches; but sexual precocity especially predisposes
to headaches of the type of migraine. Anstie[5] goes so far as to say
that the existence of a severe neuralgic affection in a young child,
if it be not due to tubercle or to other organic brain disease, is,
primâ facie, ground for suspecting precocious sexual irritation.

[Footnote 5: _Neuralgia and Diseases that Resemble it_, p. 31.]

Hillier[6] observes that anæmic children from seven to ten years of
age frequently suffer from neuralgic headache, and that girls between
eight and twelve have violent headaches accompanied by nausea and
vomiting (migraine).

[Footnote 6: _Diseases of Children_, p. 194.]

HEADACHE FROM DYSPEPSIA.—Persons who have indigestion have more or
less headache, either in paroxysms or as a constant pain. The pain is
either frontal or occipital, and may affect the whole head; but it is
not confined to one side of the head, as in migraine. The pain is
usually dull, and is accompanied by nausea from the beginning of the
attack. The tongue is coated, and has red edges, and there are general
evidences of gastric disturbance, together with a history of some
indiscretion in diet. Sleeping does not always relieve the headache.

       *       *       *       *       *

DIAGNOSIS.—The diagnosis of the different forms of headache may be
made by considering the symptoms. All of the means at our command
should be used to carefully distinguish the variety of headache we
have to deal with. The head should be palpated for tender or swollen
and soft spots, such as are found often in syphilitic headaches.
Sometimes percussion of the head will give us some indications as to
the kind of {406} headache which exists. The eyes should be examined
ophthalmoscopically for changes in the fundus oculi, and the vision
should be tested for errors of refraction should there be any reason
to connect the pain with the use of the eyes. Inquiry into the habits,
occupation, and family history of the patient will aid in arriving at
a correct diagnosis.

TREATMENT.—Having reached a correct diagnosis, the treatment will
naturally be directed to the special form of headache with which we
have to deal. The indications vary more or less with the different
varieties, but in all the same object is in view; that is, the relief
of pain in the paroxysms, and the breaking up of the diseased
condition which leads to the attacks. The means to be used for the
former will be considered in the treatment of Migraine, and are more
or less applicable to the treatment of all forms of headache.

In children, if no ocular cause is present, it will often be necessary
to take them from school and study, and make them take plenty of
exercise in the fresh air.

In all varieties of cephalalgia change of climate and travel exert a
most beneficial influence. The seashore does not always benefit
sufferers from headache, and sometimes the sea air seems to increase
the pain.


Migraine.

SYNONYMS.—Hemicrania, Sick headache.

This form of headache is of great importance, from the frequency with
which it is met in practice. It occurs in paroxysms at longer or
shorter intervals, but the attacks come at periods of tolerable
regularity, and, generally speaking, the intervals are entirely free
from pain. From the name hemicrania it may be inferred that the pain
is confined to one side of the head. This is often the case, but is
not invariably the rule.

Migraine has been known for many years, and the term hemicrania is
used by the old writers. Until recently, however, there has been some
confusion regarding it. Hemicrania often meant trigeminal neuralgia,
and nervous sick headache was generally believed to have its origin in
the stomach or to be the result of biliousness. Of late years the
disease has come to be better understood, and the valuable works of
Liveing, Anstie, and others have given a full literature of the
subject.

Various conditions predispose to migraine, and of these the foremost
are period of life and hereditary influence. Sex also bears a part in
the etiology. The majority of patients who are victims of migraine are
females. Eulenburg[7] states that the proportion is about 5 to 1 in
favor of females. My own experience would lead me to believe that in
this country the preponderance of migraine in females is not so great.
Men are not so likely to consult a physician about headaches, unless
they become very frequent and severe; especially is this true of the
laboring classes, from whom Eulenburg's statistics were mainly taken.
It is true that women are especially prone to neuroses of various
kinds through menstrual disorders and at the time of the climacteric,
but these do not always take the form of migraine.

[Footnote 7: _Ziemssen's Cyclopædia_, vol. xiv. p. 5.]

Age has a decided influence on the production of migraine. Sometimes
{407} the attacks begin in very young children. Eulenburg mentions
cases at four or five years. It is during the period of bodily
development that the first outbreaks of migraine occur, but more
particularly do they set in in both sexes at puberty, a time when
sexual development is active and making a strong impression on the
whole nervous system. Should migraine become established at this time,
it will probably continue to harass the individual until he is
forty-five or fifty years of age. After the development of puberty
migraine is not likely to originate; indeed, Tissot[8] declares that a
person who is not attacked by migraine before his twenty-fifth year
will escape from it for the rest of his life. It certainly is the case
that in later life this affection is much more rare than earlier, as
many of the old cases get well and new ones scarcely ever develop. It
is a common thing to hear a patient who has reached the age of fifty
extolling some new system or remedy as a cure for his headaches, from
which he has suffered all his life, when in reality the attacks have
ceased or become infrequent on account of the natural course of the
disease.

[Footnote 8: Quoted by Eulenburg, _op. cit._]

Hereditation markedly affects the production of migraine. Eulenburg
states that it follows the female line, and is inherited from the
mother only; but this is surely a mistake, as we often see males whose
fathers suffered from migraine. Persons whose ancestors were of a
neurotic type, who suffered from neuralgias, paralysis, hysteria,
insanity, etc., are particularly liable to migraine. Epilepsy is also
likely to be in the family of an individual who has migraine. There
has been observed by many writers the association of migraine and
epilepsy in the same person. Epileptics who are predisposed to the
disease by inheritance are likely to have attacks of it preceding the
outbreak of epilepsy. In families of constitutional nervous tendencies
it is common to see certain members who have hemicrania, while others
have epilepsy or are insane.

Other predisposing causes in migraine are not so marked as those
already mentioned. Station in life exerts but little influence in the
causation of the disease. It is met with as often in the laboring
classes as in the wealthy. Those who use the brain to any extent in
study or business are likely to suffer more often from migraine than
those who lead an outdoor life with much physical exercise. Habitual
loss of sleep and anxiety also predispose to it.

As to the conditions connected with the immediate production of an
attack of migraine, we are in ignorance. It has been thought to depend
upon disorders in the circulation of the blood, but then the question
arises, Whence these disturbances of circulation? Probably those
circulatory disorders which are marked in every case are effect rather
than cause of the attack. Indigestion and biliousness must be admitted
to favor outbreaks of migraine.

SYMPTOMS.—Migraine occurs at intervals of one or two weeks or longer;
often the attacks are not more frequent than every month or even two
or three months. I have seen a number of patients who have attacks of
migraine on Sunday with regularity, and escape during the interval.
Some of these cases ascribed the attacks to sleeping later on this day
than on others, but it is more likely that the attacks were the result
of the culminating effect of a week's hard work. Between the attacks
the patient is usually quite well as far as headache is concerned,
{408} but he may have slight neuralgia in branches of the trigeminal.
The attacks are more or less alike. They are often preceded by
prodromal symptoms for a day or two. The patient may feel languid or
tired for a day before the attack. Sometimes there is unusual hunger
the night before a paroxysm, or there may be violent gastralgia before
each attack. The patient often wakes in the morning after sound sleep
with a pain in the head. Should the attack come on in the day, it may
be preceded by chilliness, yawning, or sneezing and a sense of general
malaise. Ocular symptoms are frequent as a forerunner of an attack.
First muscæ volitantes are seen, then balls of fire or bright zigzags
appear before the eyes, making it impossible for the patient to read.
These symptoms last for a few minutes or a half hour, and then cease,
to be immediately followed by pain. Hemianopsia is a precursory
symptom of rather frequent occurrence. Ross mentions a case in which
the hemianopsia usually lasted about a half hour, and was followed by
severe hemicrania. The ocular symptoms are often very alarming to
patients.

The pain, as a general rule, is at first in the ophthalmic division of
the fifth nerve and its branches. It may begin in the branches of the
occipital nerve or in the parietal region. It comes on gradually, is
dull and boring at first, but becomes more intense and spreads to one
lateral half of the head, more especially the front part. As it
increases in intensity the pain seems to involve the entire head.
Either side of the head may be affected. Eulenburg thinks that the
left side is attacked twice as often as the right. An individual may
have the pain on opposite sides of the head alternately in different
attacks. The pain is described by patients as dull and boring or
intense, and the head feeling as if it would burst. Patients often
make pressure on the head to obtain relief. At times the pain seems to
be of a violent, throbbing kind, keeping time, as it were, with the
pulsation of the arteries. Lying down usually relieves the pain, but
if it is violent the recumbent position seems to favor the afflux of
blood to the head, and thereby increases the pain. The eye of the
affected side becomes bloodshot, and the tears stream from it. The
eyelid droops, and the sight is dim and clouded or may fail entirely.
The least light is unbearable. During the attack the subject is chilly
and intensely depressed, and the feet are very cold. The pulse is at
first slow, small, and compressible.

Painful points (Valleix's points) are not present, but there is
usually tenderness over the supraorbital notch during an attack of
migraine, and after the paroxysm there is a general soreness of the
scalp and forehead. Sometimes there remains a tenderness of the parts
surrounding the affected nerve. This is not in the nerve itself, but
in the adjacent tissues. Anstie[9] says that in his own case, after
repeated attacks of migraine, the bone had become sensibly thickened
in the neighborhood of the supraorbital notch. There is sometimes
hyperæsthesia of the skin in the affected regions of the forehead and
scalp during an attack. As well as hyperæsthesia, there may be an
abnormal acuteness of the sense of touch. Deep pressure over the
superior and middle ganglia of the sympathetic causes pain, according
to Eulenburg. This observer also states that the spinal processes of
the lower cervical and upper dorsal vertebræ are painful on pressure.

[Footnote 9: _Op. cit._, p. 182.]

{409} During the attack of migraine there is complete loss of
appetite, and any food that may be taken remains undigested in the
stomach for hours. As the pain intensifies there comes on a sense of
nausea, there is a profuse flow of saliva, and large quantities of
limpid urine are passed. Finally, when the pain seems to have reached
its maximum, vomiting occurs. Immediately afterward the pain is
greatly increased, but this is the result of the increased amount of
blood in the cranial cavity from straining. Soon after, the patient is
easier, and falls into a sleep, from which he awakes free from
headache. The crisis is not always accompanied by vomiting. In some
instances there is no nausea, but at the acme of the pain there are
two or three profuse diarrhœic stools, after which the pain is
relieved. I have lately seen such a case in a young man of
twenty-three years of age. Sometimes there is only a profuse sweat or
large flow of urine.

During the attack there are disorders of the circulation. The pulse
may be intermittent or irregular, and the extremities are usually
cold. Disorders of cutaneous sensibility are also often present. A
condition of numbness confined to one lateral half of the body is
sometimes experienced during the early part of the paroxysm. This
numbness is noticed even in one half of the tongue.

The German writers have divided migraine into two types, and the
arrangement may be followed in some instances. The first is called
hemicrania spastica or sympathico-tonica. In this form there is
supposed to be vascular spasm and a diminished supply of blood in the
brain. The symptoms are as follows: When the attack has reached its
height the face is pale and sunken; the eye is hollow and the pupil
dilated; the arteries are tense and feel like a cord. The external ear
and the tip of the nose are cold. Eulenburg[10] states that by actual
measurement he has found the temperature in the external auditory
meatus fall 0.4° to 0.6° C. The pain is increased by stooping,
straining, or anything which adds to the blood-supply in the head. At
the end of the attack the face becomes flushed and there is a sense of
heat. The conjunctiva becomes reddened, the eye is suffused, and the
pupil, which had been dilated, contracts. The sense of warmth becomes
general, the pulse is quickened, and the heart palpitates. The crisis
is reached with vomiting and a copious flow of urine or perhaps a
diarrhœic stool. There is sometimes an abundant flow of saliva. One
observer has reported that he has estimated a flow of two pounds of
saliva during an attack.

[Footnote 10: _Op. cit._]

The other variety is termed hemicrania angio-paralytica or
neuro-paralytica. Here we find the opposite condition of things from
that met with in hemicrania spastica. There is marked increase in the
amount of blood in the brain. When the attack is at its height the
face on the affected side is flushed deeply, hot, and turgid. The
conjunctiva is injected, the lachrymal secretion increased, and the
pupil contracted. Sometimes there is slight ptosis. The ear on the
affected side is hot and red. The temperature of the meatus may rise
0.2° to 0.4° C. The temporal artery is swollen, and throbs with
increased force. The carotid beats visibly. There is free
perspiration, which is sometimes unilateral. Compression of the
carotid on the painful side relieves the pain, while pressing on the
opposite carotid makes it worse. The heart beats {410} slowly, the
pulse being sometimes as low as 48 to 56. At the end of the attack the
face becomes paler and the other symptoms subside.

There are many cases in which the vascular conditions present no
peculiarities during the attack, and which cannot be classed with
either of the varieties just described.

In all forms, if the patient can be quiet, he usually falls asleep
after the crisis has been reached, and awakes free from pain, but
feeling haggard and prostrated.

The paroxysm lasts for several hours, generally the greater part of
the day. It may last for several days, with variations of severity.
The attacks are at longer or shorter intervals of time, and in women
they often appear at the menstrual period. The attack may be brought
on by over-mental or bodily exertion, imprudence in eating or
drinking, and exposure to cold draughts of air. It will often begin as
a supraorbital neuralgia from exposure to cold, and go on through all
the phenomena of a regular migraine.

Seizures are often brought on by fatigue, and there are some persons
who invariably have a violent attack of migraine after a journey.
Nursing women are liable to more frequent paroxysms, and I have
recently seen a lady who within a few days after delivery after both
of her confinements suffered from typical attacks of migraine,
although during gestation she had escaped them.

DIAGNOSIS.—Migraine can readily be distinguished from the other forms
of headache by the comparative regularity of the attacks and its
numerous other characteristics. It differs from neuralgia in the pain
being less acute and shooting. The pain of migraine is more dull and
throbbing, and extends more generally over the head. The ocular
phenomena are more or less constant in migraine and do not occur in
neuralgia.

PROGNOSIS.—Migraine is never fatal, and usually becomes less severe
and less frequent as middle life is reached. Some patients continue to
suffer from it during their entire life, and often when the typical
migraine has ceased it is replaced with paroxysms of neuralgia.
Therapeutic and hygienic means are of decided influence in the course
of the disorder, and many patients experience great relief or
temporary immunity from attacks as a result of treatment. Cases of
long standing and those of an hereditary type are most unfavorable as
to relief from treatment or by spontaneous cure.

PATHOLOGY AND MORBID ANATOMY.—Migraine not being a fatal disease, we
know nothing of the changes which exist in the brain; we can only
surmise what are the conditions which exist in the brain during and
before an attack.

It is evident that there is a strong relationship between migraine and
neuralgia of the trigeminal nerve, and if we study the symptoms of the
two conditions, and consider the causes which produce attacks of each,
we cannot but arrive at the conclusion that migraine is a variety of a
neuralgia of the ophthalmic division of the fifth. The late Anstie has
most clearly and forcibly given his reasons for believing this to be
the case, and we cannot but uphold his view.

Migraine is constantly met with in early life as the type of a
neuralgia which in later years loses the special features of a sick
headache and becomes {411} a pure neuralgia. The same forms of trophic
lesions may occur in migraine and in trigeminal neuralgia. Anstie
instances his own case, in which in early life he had distinct attacks
of migraine, with corneal ulceration, orbital periostitis, and
obstruction of the nasal duct, while later in life his attacks were
only neuralgic, without any stomach complications.

Migraine, as already remarked, attacks early life especially at the
time of sexual development, and the same is true of epilepsy. There is
also the same hereditary predisposition to the former as to the
latter. Patients who have migraine belong often to families other
members of which suffer from epilepsy, chorea, and an uncontrollable
tendency to alcoholic excesses. Indeed, occasionally migraine and
epilepsy are interchangeable in the same individual. Many cases of
epilepsy have suffered at some time of their lives from severe
headaches.

Hughlings-Jackson describes the attacks of migraine as arising from a
discharging lesion of the cortex of the brain in the sensory area, or
in that part of it which corresponds to the region of pain in the
head. Genuine epilepsy he holds to be due to a discharging lesion from
the motor area of the cortex. During an attack of migraine the
discharging lesion does not remain confined in the sensory portion of
the cortex, but extends into the medulla oblongata and the
cilio-spinal region of the cord, causing irritation or paralysis of
some of these centres, and causing the vaso-motor and oculo-pupillary
symptoms which are conspicuous during an attack.

In the form of migraine known as hemicrania sympathico-tonica there is
tonic spasm of the vessels of one side of the head. This explains the
pallid face, the lowered temperature, and the sunken eyes. After the
cause of the contraction is removed, then the vessels relax and the
amount of blood-supply greatly increases. Hence the redness of the
conjunctiva, lachrymation, and redness of the ear at the close of an
attack. The vomiting is explained by Eulenburg as being due to
variations in the intracranial blood-pressure. This causes fitful
contractions of the vascular muscles, alternating with partial
relaxation. These conditions must arise in the sympathetic nerve of
the corresponding side.

The dilation of the pupil during an attack depends upon irritation of
the cervical sympathetic ganglia. Other symptoms, such as the largely
increased flow of saliva and the flow of tears or drying of the
Schneiderian mucous membrane, indicate a morbid condition of the
cervical sympathetic. The sensitiveness to pressure in the region of
the upper cervical ganglia and over the spinous processes of the lower
cervical and upper dorsal vertebræ, corresponding to the cilio-spinal
region of the cord, confirms the idea of a morbid state of the
cervical sympathetic.

In hemicrania angio-paralytica there is supposed to be a relaxed
condition of the vessels of one side of the head. Here, instead of an
irritation of the sympathetic, there is a paralytic condition, and we
have the same results as are seen in animals when the cervical
sympathetic is divided. There seem to be good grounds for holding this
view when we consider the flushed face, contracted pupil, retraction
of the eyeball, and occasional ptosis which accompany this form of
headache. Possibly there may be a brief stage of spasm of the vessels
preceding the relaxation which occurs in hemicrania angio-paralytica.

{412} The slowing of the pulse during an attack of migraine is due
probably to cerebral hyperæmia from relaxation of the vessels, or to
the secondary anæmia and irritation of the medulla oblongata. This
irritation of the medulla is also able to explain the other symptoms
of vaso-motor disturbance which occur during an attack of migraine;
for instance, the small and contracted radial artery, the extreme
coldness of the hands and feet, and the suppression of perspiration
over the whole body except perhaps on the affected side of the head.
Following the stage of irritation of the medulla with contraction of
the vessels comes one of exhaustion with relaxation of the vessels.
This latter state may account for the profuse flow of saliva and the
copious secretion of sweat and urine, as well as the increased
secretion of bile and the condition of broncho-tracheal catarrh during
the attack.

We now come to the question of the origin and seat of the pain in
migraine. This question has involved a great deal of thought, and has
been answered in various ways by different writers. E. du Bois-Raymond
thought that the pain was due to tonic spasm of the muscular coats of
the vessels, and that thereby the nerves in the sheaths of the vessels
were pinched, as it were, and so caused pain. Moellendorff was of the
opinion that the pain was due to dilatation of the vessels, and not to
contraction; and this theory might explain the pain in the
angio-paralytic form. There are many cases in which neither of these
views is sufficient, for we have no reason to believe that a condition
of either anæmia or hyperæmia is present.

Romberg believed that the pain was situated in the brain itself, and
Eulenburg holds that the pain must be caused by alterations in the
blood-supply, without regard to their origin, in the vessels of one
side of the head. He thinks that the vessels may contract and dilate
with suddenness, just as is often seen in some neuralgias, and thus
intensely excite the nerves of sensation which accompany the vessels.
The increase of pain upon stooping, straining, or coughing, and the
influence upon it by compression of the carotids, seem to give force
to this view. But are we not here confusing cause with effect? Are not
these variations in the calibre of the vessels due to the irritation
of the sensory and vaso-motor nerves, which are in a state of pain? No
doubt increase in the blood-supply augments the pain, just as it does
in an inflamed part when more blood goes to the part. Let a finger
with felon hang down, or let a gouty foot rest upon the floor, what an
intensity of pain follows!

Anstie very ably advocated the theory of migraine being a variety of
trigeminal neuralgia in the ophthalmic division; and we incline
strongly to his view. An attack of migraine often begins with pain
distinctly located in the supraorbital nerve as the result of exposure
to cold. Frequently it begins in the infraorbital nerve or in the
branches of the inferior maxillary division of the fifth. The pain
then spreads over one side of the head, both outside and inside, and
goes through the recognized symptoms of migraine. In my own case I
have often had an attack begin with sharp pain in the supraorbital
notch in a spot which could be covered by the tip of the finger. The
nerve has seemed swollen, and has been highly sensitive to pressure.
Then have come pain extending over the entire side of the head,
without its limits being distinctly definable, and the accompanying
phenomena of lachrymation, excessive salivation, {413} and copious
flow of urine, winding up with vomiting or ineffectual nausea and
retching.

Anstie brings forward as arguments to support his view the facts that
the attacks of migraine often interchange with neuralgic seizures, and
that a person who has been migraineuse in early life may in later
years lose his hemicranial attacks, and have violent neuralgia in the
ophthalmic division of the fifth nerve.

The true seat of the lesion, if we may so call it, upon which the
exaggeration of pain-sense depends, is probably in the nerve-centre;
that is, in that part of the trigeminal nucleus back to which the
fibres go which are distributed to the painful areas. The pain is no
doubt chiefly intracranial, and in those portions of the cerebral mass
and meninges to which branches of the trigeminal are distributed. All
of the divisions of the trigeminus send branches to the dura mater.
Many nerves are found in the pia mater as plexuses around the vessels,
some of which penetrate into the centre of the brain. Most of these
nerves come from branches of the trigeminus.

TREATMENT.—The treatment of migraine must be directed to the
palliation of the attacks and to their prevention. So little is known
of the direct cause of the disease that it is difficult to lay out any
distinct course to be followed. Many cases, however, which seem to
depend upon a run-down state of the patient are vastly improved by a
course of tonics and building up. I have often seen anæmic and feeble
women whose attacks were frequent become exempt for a long period by
simply taking iron, quinine, and strychnia, and taking an increased
amount of nourishment. The rest-treatment of Weir Mitchell is
particularly applicable to these cases. In persons whose digestion is
bad, and who suffer from constipation, much can be done by relieving
these conditions. Some cases which are due to uterine disturbances are
benefited by treatment directed to the womb. There are many cases,
however, in which no cause is apparent. The patient is well nourished,
his eyes are good, he undergoes no strain mentally, morally, or
physically, and yet the attacks of migraine come with tolerable
regularity. In these persons change of climate sometimes works
marvellously beneficial results. I saw last year a young lady who
suffered from terrific headaches which sometimes lasted for days. No
plan of treatment or regimen seemed to exert the slightest influence
upon the attacks, and yet on going to the far West for the summer she
remained without an attack during the whole time she was there. In
some individuals all forms of treatment may be tried in vain.
Anti-periodics have been tested, but with doubtful benefit. Cannabis
indica is probably the most potent remedy which is at our command. Its
effects are most decided, and many cases of severe hemicrania have
been cured by this means alone. It must be given for a long time, and
in some instances it is necessary to give gradually-increasing doses
up to the physiological effects. The drug must be of good quality,
otherwise we need expect no good from it. Indian hemp is well known to
be variable in strength, and the best form in which to use it is a
fluid extract made by some reliable chemist. Arsenic, phosphorus, and
strychnia do not seem to do as much good as in other neuralgias,
except so far as they build up the general health.

Ergot has been used with success as a curative means, and it probably
{414} acts by contracting the vessels of the medulla oblongata. A
combination of ergotin and extract of cannabis indica may be given
together; and if persisted in for a long time will often be of benefit
in lessening the frequency of the attacks. The prolonged use of one of
the bromides is sometimes found curative.

Anstie has found the careful use of galvanism to the head and
sympathetic of positive advantage in keeping off attacks, and
Eulenburg has had the same experience.

In the treatment of the attack the patient should be freed from all
sources of external irritation. He should lie down in a darkened room,
and all noises should be excluded. If the attack is of the hyperæmic
variety, the patient's head should not be low, as this must favor
increase of blood to the head. In this form the patient is often more
comfortable sitting up or walking about. Occasionally an impending
attack can be warded off by the administration of caffeine, guarana,
or cannabis indica. Purgatives are of but little value in this form of
headache. The local application of menthol or of the oleate of
aconitia to the brow of the affected side will sometimes prevent an
attack. If a person can lie down quietly when he feels an attack
coming on, one or two doses of fifteen grains each of the bromide of
lithium will enable him to sleep, and wake free from pain. I have
found the lithium bromide far more valuable in migraine than any other
of the bromides. An effervescing preparation known as bromo-caffeine
is often efficacious in aborting a paroxysm or in palliating it when
it has got under way.

Quinine, in my experience, seems to be of little use in preventing or
cutting short a paroxysm of migraine, although Ross[11] has found that
a dose of ten or fifteen grains may arrest it. Ergot has been found
useful, and, as it acts by contracting the arterioles, should be given
only in the angio-paralytic form. The fluid extract of ergot may be
administered, but ergotin in pill form is more acceptable to the
stomach.

[Footnote 11: _Diseases of the Nervous System_, vol. ii. p. 558.]

Inhalations of nitrate of amyl have been used with advantage. Berger,
who was the first to employ this remedy, found that a single
inhalation of a few drops relieved the pain at once, and it did not
return that day. It is indicated only in the sympathico-tonica type.
If it is used, two or three drops of the nitrate in a glass pearl may
be crushed in the handkerchief and inhaled. Nitro-glycerin may also be
given in this variety of migraine.

Once the attack has begun fully, we can only attempt to mitigate the
pain. Firm pressure on the head generally gives relief, and encircling
the head firmly with a rubber bandage is often of great comfort.
Compression of the carotids gives temporary but decided ease to the
pain. Strong counter-irritation in the shape of a mustard plaster to
the nape of the neck or a stimulating application, like Granville's
lotion, to the vertex, will afford relief. I have found in some cases
that placing a hot-water bag, as hot as could be borne, against the
back of the head alleviates the pain. In other instances cold affords
more relief, and an ice-bag resting upon the forehead is the most
efficacious way of applying cold. Hot bottles to the feet are an
accessory not to be overlooked.

In the way of medicine we may give the bromide of lithium every hour.
The bromide of nickel has been recommended by DaCosta as {415} having
peculiar advantages. Cannabis indica may be given in doses of a
quarter of a grain of the extract every two hours until relief is
obtained. Anstie believes strongly in chloral, and says that a single
dose of twenty or thirty grains will often induce a sleep from which
the patient wakes free from pain. The same writer advises the
administration of muriate of ammonium, but it is too nauseous a dose
to be given when the stomach is as much disturbed as it usually is in
an attack of migraine.

Croton chloral is preferred by some to the chloral hydrate. Ross, for
example, gives it in doses of five grains every four hours until
relief is obtained.

Galvanism through the head is often of relief, especially at the
beginning of an attack; but this means is not often available, for it
is not easy to have the suitable apparatus for the constant current at
a patient's home when it is needed. Should galvanism be used, one pole
should be placed on each mastoid process, and a weak current passed
through the head for two or three minutes. The sympathetic may be
galvanized by placing one pole over the upper cervical ganglion, just
behind and below the angle of the jaw, while the other pole is held in
the hand or placed upon the sole of the foot. In hemicrania spastica
the positive pole is put over the ganglion, and in the angio-paralytic
type the negative pole is placed in this location.

Should all of the above means fail, we may resort to morphia
hypodermically. Jewell[12] favors the administration of morphia and
atropia, either by the mouth or hypodermically, from the beginning of
an attack until the pain is eased; but I believe that morphia, except
as a last resort, is very undesirable in migraine. Although a small
dose hypodermically will usually promptly bring relief, there are the
unpleasant after-effects of opium felt, and the patient feels more
prostrated and with more disordered digestion than had no morphia been
used. Besides, the morphia habit is liable to be formed, especially in
women, when the drug has once begun to be taken.

[Footnote 12: _Journal of Nervous and Mental Diseases_, 1881.]

It is for this reason that I prefer to use the bromides, and if a
patient is seen at the beginning of a paroxysm, given a fifteen-grain
dose of bromide of lithium, his feet put in hot mustard-water, and he
then goes to bed, he will almost always cut his attack short, and on
waking from sleep will feel refreshed and able to take food.

I am strongly convinced of the importance of arresting or shortening
the paroxysms of migraine, especially in the young, at the beginning
of the disease. By this means the habit of long attacks is prevented,
and their prostrating after-effects are avoided. Should we succeed in
checking the first few attacks, we may by tonics and regimen improve
and fortify the constitution so as to eradicate or modify the
neuralgic tendency.


{416}


VERTIGO.

BY S. WEIR MITCHELL, M.D.


DEFINITION.—The clinical meaning of vertigo has gone, as is common,
far beyond what the term implies. We may define vertigo to be a sense
of defective equilibrium, with or without actual disturbance of
position, and accompanied by varying amounts of subjective feelings of
motion of external objects, of the body itself, or of the contents of
the cranium.

SYMPTOMATOLOGY.—Vertigo consists of attacks which are single or repeat
themselves during a continuous condition lasting for hours or days,
and which I have elsewhere described as the status vertiginosus.[1]

[Footnote 1: _Med. and Surg. Rep._, June, 1877.]

The mildest form of vertigo is that in which the patient has a
sensation of the contents of the head as being in motion. If more
severe, there is disturbed equilibrium, an effort is needed to stand
erect, or there is, as in most vertigo, a fear of falling. The brain
seems to be moving round or upward. This type is found in insanity, in
hysteria, and in the vertigo of mental effort observed in extreme
cerebral exhaustion.

In a second clinical species of vertigo the patient appears to himself
to be in motion, while outside objects maintain for him their places.
This may or may not be accompanied with sensory disturbance or an
approach to mental confusion. It is really a delirium of movement. The
patient feels as if he were rolling or falling or reeling or dropping
through space. Meanwhile, however grave the hallucination, he walks
and stands without the least sign of defect in balancing power. These
cases are very rare, but are sometimes seen as temporary results of
hysteria.

Perhaps it is doubtful whether we should really class this
symptom-group as vertigo.

The more common or typical expression of vertigo is marked in its
fulness by a false sense of the movement of external objects and of
the relations in space of the individual to such objects. The pavement
rolls or seems to be coming up in front of him; the houses stand at
angles; walls, pictures, chairs, and tables reel around him, are still
a moment, and again move; or the bed seems to be aslant or to rock to
and fro. In extreme instances objects are seen as if inverted, and
whenever the vertigo is marked the victim reels or falls, or seeks by
rest supine or by closing his eyes to lessen the terrors of the
attack. In severe examples no such help avails, and for hours or days
the patient may lie clutching at the bed for support or in deadly fear
of a new onset of vertigo, {417} which in some cases is brought on by
the least movement of the head, by taking food, by efforts to think,
or by mechanical vibrations.

In most cases there is some mental confusion, or even brief loss of
consciousness at the close of the attack, and nearly always more or
less nausea or vomiting occurs—symptoms which have frequently misled
observers as to the cause of the vertigo, but which have in most cases
only the significance gastric disturbance has in migraine. As in that
disorder, but more rarely, the emesis may be associated with or
replaced by looseness of the bowels, and is very apt to be followed by
a flow of pale clear urine.

Fits of vertigo are often as distinct clinically as epileptic attacks.
The patient has for a few moments, in an acute form, all of the
phenomena of vertigo, and may then recover promptly, or it may chance
that he has a vertiginous status and a series of fits, or remains for
long periods in a state of chronic disorder of head, with now and then
an acute onset.

Physicians do not often witness these fits: I have been so fortunate
as to see several. I take this description of one from my notes: A
young clergyman, after excessive overwork among the poor, came to
consult me for vertigo. As I talked to him an attack came on. I asked
him to keep as composed as possible and to tell me what he felt. He
said: “It has just begun. The objects in the room are moving from
right to left; I can seem to hold them still for a moment, then they
go on and move faster. If I shut my eyes it is relief, but only for a
time. I feel myself as if I were now going round with them. The chair
rocks, and my brain seems moving too.” At the same time he became very
pale, and slipped from his seat. His pulse was quick and feeble and
rapid, and as he lay on the floor unconscious a profuse sweat broke
out on his face. In a moment he was again himself, but did not recover
so as to walk for a half hour. He then complained of headache, but was
able to walk home. This is a fair example of a fit of vertigo, due, as
it proved, to at least two of the causes of vertigo, which I shall
presently discuss.

A few persons insist that something like a distinct aura precedes the
attacks. In other cases the brain symptoms develop gradually, from a
faint sense of dizziness up to a tumultuous feeling of confusion with
sensory illusions. In a few rare cases there is, as in that above
mentioned, an abrupt onset. Something seems to snap in the head, and
the vertigo follows; or, most rare of all, we have a sensory discharge
felt as light or sound, and followed by the ordinary symptoms.[2]

[Footnote 2: See the author in lectures on _Nerv. Diseases, Disorders
of Sleep_, p. 63, 2d ed.]

DIAGNOSIS.—Vertigo is of course, as a rule, only a complex symptom of
one or more numerous conditions. Acute isolated fits of vertigo are
sometimes puzzling, because epilepsy may be preceded by brief vertigo
and exist without notable spasms. Time may bring to us a frankly
expressive epilepsy to explain former and less distinct fits. But
usually it is the attacks of vertigo which are the causes of doubt. A
man has sudden giddiness, and falls unconscious for a moment. These
attacks persist. How shall we know them as vertigo? how be secure that
they be not some form of the lesser epilepsy? As a rule, if they be
vertigo there will be nausea or emesis, while the intervals between
attacks will offer the usual signs of confusion of head, fear of
losing balance, and all the numerous evidences of disturbed and easily
excitable states of the {418} sensorium—conditions rare in the
interepileptic periods. The effect of bromides may aid the diagnosis,
for, although often of use in vertigo, they have not such power to
inhibit the fits as they possess in epilepsy. Persons long liable to
any form of vertigo can readily cause attacks, or at least vertiginous
feelings, by closing the eyes while standing, by the least rotation,
or by putting a prism on one eye, so that among these tests we may
frequently find the material for a diagnosis, which will of course, in
many instances, be made easy enough by the presence of causes
obviously competent to occasion the one or the other disease.

PROGNOSIS.—In true vertigo, if we exclude the organic causes, and
especially intracranial neoplasms, there is very little to be feared.
Deaths have been seen in Menière's disease, but are most rare. Even in
grave examples of labyrinthine vertigo there is a probability that the
worst which can occur will be deafness, and that vertigo will
gradually cease as the delicate neural tissues become so degenerated
as to cease to respond to irritations.

The DURATION of other forms of vertigo it is less easy to predict.
Ocular vertigoes get well soon after the eye trouble is corrected, and
the like is true of most vertigoes due to peripheral causes. So also
the giddiness which is sometimes seen as a very early symptom in
locomotor ataxia is transient, and will be apt, like the ocular and
bladder troubles which mark the onset, to come and go, and at last to
disappear entirely. It is to be remarked that vertigo at the beginning
of posterior sclerosis is common, and is not due to ocular motor
conditions.

Sometimes in vertigo, as in epilepsy, the removal of a long-existing
cause may not bring about at once a cessation of the abnormal symptoms
its activity awakened, so that it is well, as to the prognosis of
duration, to be somewhat guarded in our statements. Nor is this need
lessened by the fact that vertigo may be an almost lifelong
infliction, without doing any very serious damage to the working
powers of the person so disordered.

ETIOLOGY.—It is generally taken for granted that vertigo has always
for its nearest cause some disorder of cerebral circulation; but while
either active congestion or anæmia of brain may be present with
vertigo, and while extreme states of the one or the other are
certainly competent to produce its milder forms, it does not seem at
all sure that they are essential to its being. Indeed, there is much
reason to believe that vertigo is due in all cases to a disturbance of
central nerve-ganglia, and that the attendant basal condition is but
one incident in the attack.

In vertigo there are the essential phenomena, as disturbed balance,
with a false sense of movement within or without, or of one's self.
Then there are the lesser and unessential phenomena, which vary in
kind and degree, and these are the moral and mental symptoms—terror,
confusion of mind, and sensory illusions; and, last, the nausea and
sickness met with here as in migraine, and the flow of clear, thin
urine.

All of these symptoms should be accounted for in speaking of the
intracranial organs, disorder of which causes vertigo. Ferrier has
especially made it clear that equilibration involves afferent
impressions, co-ordinative centres, and efferent excitations
preservative of balance.

Guiding impressions, which direct the muscles through centres below
the cerebrum, so as to aid in preserving our balance, reach these
centres {419} from the skin and the muscles, so that great loss of
tactility or of the compound impressions called muscular sensations
results in disturbance of equilibrium, but not in true vertigo, which
is clinically this and something more.

A second set of impressions, of use in preserving equilibrial status,
come through the eye, or rather habitually through the eyes, because
the consensual impressions arising out of double vision and the
co-ordinate movements of the two fields of sight have, as is well
known, much to do in this matter. It is hardly needful to dwell on
this point. Certain parts of the ear have, however, the largest share
in maintaining our balance, and it seems likely that the semicircular
canals—the part most concerned—although lying within the petrous part
of the temporal and receiving nerves from the stem which constitutes
the nerve of hearing, may have slight relations or none to the sense
of audition.[3] When the horizontal canals are cut, the head moves
from side to side and the animal turns on his long axis. When the
posterior or lower vertical canals suffer, the head sways back and
forward, and the tendency is to fall or turn over backward. When the
upper erect canals are cut, the head moves back and forward, and the
tendency is to turn or fall forward.

[Footnote 3: I have seen a single case of vertigo, with slight
deafness on both sides, in which the sense of the position of sounds
was absolutely lost.]

In pigeons, injury on one side may get well, but when the canals are
cut on both sides there is permanent loss of balance. In some way,
then, these little organs appear to be needful to the preservation of
equilibrium; and of late some interesting attempts have been made to
explain the mechanism of this function. It probably depends on the
varying pressure relations of the endo-lymph to the nerve-ends which
lie in the membranous canals.

Wm. James of Harvard has shown that total loss of hearing is usually
accompanied by lessened susceptibility to vertiginous impressions, so
that the stone-deaf are not apt to be seasick or giddy from rotation,
owing to their having lost the organ which responds to such
impressions. It would seem also that the entirely deaf have peculiar
difficulty in certain circumstances, as when diving under water, in
recognizing their relations to space.

There is a general tendency to regard the cerebellum as the centre in
which all the many impressions concerned in the preservation of
equilibrium are generally received and made use of for that purpose.
There may be several such centres, and the matter is not as yet clear.
Whatever be the regulative ganglion, it seems clear that it must be in
close relation to the pneumogastric centres, to account by direct
connection or nerve-overflow for the gastric symptoms. But, besides
this, vertigo has clinical relation to moral and mental states not
easy to explain, and in extreme cases gets the brain into such a state
of excitability that mental exertion, emotion, strong light, or loud
sounds share with the least disorder of stomach capacity to cause an
attack.

Vertigo may be due to many forms of blood-poisoning, as at the onset
of fevers, inflammations, the exanthemata—notably in epidemic
influenzas. It may arise in malarial poisoning, sometimes as the
single symptom, as well as in diabetes, albuminuria, lithæmic
conditions, and in all the disorders which induce anæmic states.
Common enough as sign of brain {420} tumor, and especially of growths
in or near the cerebellum, as a result of degenerated vessels, it is
also not very rare in the beginning of some spinal maladies,
especially in posterior sclerosis, and is not always to be then looked
upon as of ocular origin.

Alcohol, hemp, opium, belladonna, gelsemium, anæsthetics, and tobacco
are all, with many others, drugs capable of causing vertigo.

In hot countries heat is a common, and sometimes an unsuspected, cause
of very permanent vertigo.

Lastly, excess in venery, or, in rare cases, every sexual act,
profound moral and emotional perturbations, and in some states of the
system mental exertion, may occasion it, while in hysteria we may have
almost any variety of vertigo well represented. Outside of the brain
grave organic diseases of the heart are apt to produce vertigo,
especially where the walls of the heart are fatty or feeble from any
cause. Suppression of habitual discharges, as of hemorrhoids or
menstrual flow, is certainly competent, but I have more doubt as to
the accepted capacity of rapidly cured cutaneous disease.

The following are some of the more immediate causes of vertigo: They
are disorders of the stomach or of the portal circulation; laryngeal
irritation; irritation of the urethra, as passing a bougie, especially
when the patient is standing up; affections of nerve-trunks; nerve
wounds; sudden freezing of a nerve (Waller and the author); catarrhal
congestion of the nasal sinuses; inflammation and congestion of inner
ear, many irritations of the outer and middle ear; prolonged use of
optically defective eyes; insufficiency of external muscles of the
eye.

It will be needful to treat of some of these causes of vertigo in
turn.

Gastric Vertigo.—Trousseau certainly misled the profession as to the
frequency of this form, but he did little more than represent popular
medical views, and we may now feel sure that a good many so-called
gastric vertigoes are due to lithæmia or to troubles of ear or eye.
There are, I think, three ways in which the gastro-duodenal organs are
related to the production of vertigo. Acute gastric vertigo arises in
some persons inevitably whenever they eat certain articles, and the
limitations are odd enough. Thus, I know a gentleman who cannot eat a
mouthful of ice-cream without terrible vertigo, but otherwise his
digestion is perfect. I know another in whom oysters are productive of
vertigo within ten minutes; and a curious list might be added,
including, to my knowledge, milk, eggs, oysters, crabs, etc. In these
cases digestion is arrested and intense vertigo ensues, and by and by
there is emesis and gradual relief.

In other cases, owing to over-feeding or any of the numerous causes of
acute dyspepsia, an individual has a sudden attack of acid stomach,
and as this gets to its worst he has alarming vertigo. In these cases
the room whirls around or the pavement rocks; the balancing power is
disturbed or lost; the sense of movement in the brain itself is
sometimes felt; there are slight buzzing or humming sounds in one or
both ears; there may be double vision, which comes and goes, while the
power to think is lessened and the terror created is quite
unendurable. At last come the sweat of nausea, emesis, and relief,
with a gradual fading away of all the symptoms.

As a rule, such an attack need cause no uneasiness as to a fatal
result, but, unless the case be handled with skill, it is apt to
repeat itself with {421} or without repetitions of the originating
cause, until what I have called the status vertiginosus is created,
and we have more or less steadily present a slight sense of defective
balance, of confusion of mind, of blurred vision, and, more rarely, of
slight noises in the ears. After two or three grave attacks, attacks
are added for which the patient sees no cause. He lives in a state of
constant terror, and the status vertiginosus attains its highest
development, and may last for unlimited periods, while the brain
becomes endowed with new morbid susceptibilities. To read, to write,
to face sudden sunlight, to see moving bodies or passing crowds, cause
vertigo. Loud sounds disturb the balance; even music will affect it.
Emotions or any decided mental efforts are equally competent to bring
on attacks, while fatigue or sudden changes of posture have to be
alike avoided.

I have sketched an extreme case, but whatever causes grave vertigo is
able to bring on the set of symptoms here described, which are, after
all, more apt to be due to aural than gastric states.

Vertigo as a result of chronic dyspepsia in any of its forms is rare,
and as a rule is less severe than that which grows out of acute
gastric dyspepsia. The sensory symptoms are trifling, and the
confusion of head and the lack of balance less notable, while the
vertigo, which is more or less constant, seems to be most often met
with two to four hours after meal-time, so that it is usually doubtful
as to how much is due to reflected impressions from the digestive
tracts, and how much to the direct influence of imperfect material in
the circulation.

In a third form the gastro-intestinal tract is but indirectly
concerned. In a person who is anæmic, or who is nervous and perhaps
hysterical without being anæmic, but in whom it is impossible to
detect in the stomach or bowels, in the feces or urine, any sign of
defective digestion or of malassimilation, we find that during the act
of digestion there is at some time, and in a few cases constantly,
some transient but not grave vertigo.

This is due simply to the influence exerted on an over-sensitive head
of a normal functional activity, which may act directly as any
peripheral cause would act, or may be due, in the anæmic, with this to
the withdrawing of blood from other parts of the body which occurs in
digestion. It is an illustration of what is too often overlooked, the
capacity of a healthy functional act to disturb morbidly a sensitive
brain.

Aural Vertigo.—Vertigo may be due to a variety of irritative causes
acting on the outer, middle, or inner ear. We shall consider them
separately.

Vertigo from Causes acting on the External Ear.—In animals I have
found that the injection of iced water or a rhigolene jet into the
meatus is at once the cause of convulsive movements in the rabbit, and
that repetitions of this cause at last a permanently vertiginous
state, so that when a rabbit or guinea-pig thus disordered was shut up
in darkness for some hours, sudden sunlight caused it to be for a few
moments vertiginous. It is remarkable that while in birds many parts
of the skin are competent under irritations (Weir Mitchell, Ott,
Brown-Séquard) to give rise to vertiginous phenomena, in mammals only
the skin of the external auditory meatus appears to be thus
responsive. The author was himself the best illustration of this fact.
Some years ago, when by {422} mishap water at about 52° F. was thrown
into his left ear, he fell instantly on his left side, with slight
disturbance of vision, the room seeming to rock in the direction of
the fall—that is, to the left. He arose with some difficulty, his head
swimming, and with a distinct sense of lack of power in the whole left
side, and with, for a half hour at least, an alarming tendency to
stagger to the left.

Thus, injections of cool water in some cases (or in others of water at
any temperature), and in certain persons very hot water, will cause
vertigo. Foreign bodies—hardened wax, aspergillus, ulcers—or any
inflammation may occasion it, while it is curious that usually the
painful abscesses of the ear do not, especially in children, who are,
as a rule, less liable to vertigo than are adults.

The tendency of aurists is, I believe, to explain the phenomena by
either direct influence propagated as sound-waves through the auditory
apparatus to the labyrinth, or by admitting inhibitory impressions
affecting the vaso-motor loops and causing increased pressure in the
semicircular canals. I am disposed to think that the effect may be a
more direct one, and to regard the centres as directly influenced
through the fifth nerve, including vaso-motor phenomena of course—a
question to be, however, easily solved in the laboratory.

In this form of vertigo tinnitus is slight or transient, coming and
going, or if permanent but faintly felt.

Middle-ear vertigo may arise from any inflammation of the part or from
closure of the Eustachian canal. There are then direct mechanical
influences affecting the labyrinth, as well as sensory irritations,
not causing auditory phenomena; whilst also the inner ear is apt soon
to suffer from direct propagation of inflammatory processes. There is
then paroxysmal vertigo, variable hearing,[4] and early tinnitus.

[Footnote 4: Burnett, Sect. Otol., _Int. Med. Cong. Proc._, 1876.]

Inner-ear vertigo seems to be due to irritations, auditory,
mechanical, or inflammatory—whatever disturbs seriously the nerves of
the semicircular canals, since, if we may trust recent research,[5]
the cochlea is not a source of vertiginous impressions. This form of
vertigo was first described with pathological proof by Menière in
1860, and is probably in its variety of degrees the most common of all
the origins of dizziness.

[Footnote 5: Gellé.]

The acute attack is nearly always preceded by more or less deafness,
and in many cases by middle-ear catarrh,[6] with or without tinnitus.
More rarely all the symptoms arise abruptly. There are sudden
tinnitus, deafness, nausea, vertigo. The loss of hearing remains, and
is variable, or, finally, the hearing is lost altogether. The tinnitus
is permanent or varies in amount, but as the deafness grows complete
the vertigo disappears, and although cases of death have been
described, labyrinthine vertigo is, as a rule, prone to get well in
time.

[Footnote 6: Burnett.]

Single attacks are rare. It is apt to repeat itself, and finally to
cause all the distressing cerebral symptoms which characterize the
worst gastric vertigo, and at last to be capable of easy reproduction
by light, heat, over-exertion, and use of the mind or eyes, by
emotion, or by gastric disorder.

Even after the vertigo has ceased to exist the fear of loss of balance
remains, while perhaps for years the sense of confusion during mental
effort continues, and gives to the sufferer a feeling of what a
patient {423} described to me as mental vertigo—some feeling of
confusion, lack of power to concentrate attention, loss of hold on
trains of thought, with now and then a sensation as if the contents of
the cranium moved up or down or swayed to and fro.

The attack in the gravest forms is often abrupt, and, according to
Charcot, is always preceded by a sudden loud noise in the affected
ear. I have, however, notes of many cases in which this was not
present. The patient reels, staggers, or falls, usually forward or to
one side, loss of consciousness being very rare. The sensory
hallucinations are remarkable. If at rest or after his fall he seems
to himself to sway, and tends to pitch or roll over; the bed rocks,
the room and its contents reel. The patient's terror is intense; he
clutches the bed; seeks relief in fixing his eyes on an object, which
in slight attacks is competent to relieve, or else he closes them. The
least motion starts the vertigo afresh. In some cases turning the head
or looking up will bring it back, or the patient may remain for days
or weeks in this condition, with continuous dizziness and frequent
recurrences of severe vertigo, while there is more or less constant
nausea and sometimes vomiting.

There should be no trouble in distinguishing the cases in which
deafness exists, but the nausea is apt to direct attention to the
stomach. Tinnitus is common in vertigo, however arising; and when, as
I am sure does chance, there is for years now and then a slight and
transient deafness with vertigo, or a permanent deafness in one ear,
and therefore not noticed, the inner ear is apt to be overlooked as a
source of trouble.

Vertigo from growths on the auditory nerve before it enters the inner
ear is rare in my experience. It is described as slow in its progress,
the deafness and tinnitus being at first slight, but increasing
steadily, while there is tendency to fall toward the side affected.[7]
In the cases of disease attacking the seventh nerve within the cranium
there is usually so much involvement of other and important
nerve-tissues as makes the disorder of audition and equilibration
comparatively unimportant.

[Footnote 7: Burnett.]

Vertigo from coarse organic lesion of brain, such as a tumor, is
common, and is, indeed, rarely absent in such cases. The cases in
which it is lacking or least remarkable are, I think, to be found in
the anterior and middle cerebral lobes, while it is almost sure to
exist at some time when the tumor is in or near the cerebellum.

Growths or other causes of irritation in the crura of the cerebrum or
cerebellum, or on the pons, are sure to give rise to disturbed
equipoise or to methodical involuntary actions; but these are not
always, though often, accompanied with delusive impressions as to
exterior objects, or with the other symptoms found in typical vertigo.
I recall one remarkable case where a blow on the left side of the
occiput resulted in a tendency to roll to the left which finally
triumphed over volitional control, so that the patient would at times
roll over on the floor until arrested by a wall. After the rotation
had lasted for a minute there was, when it ceased, a false sense of
movement of objects to the left, but at the outset there were no
sensory illusions, and at no time any mental disorder. The patient
recovered, and is now in good health; but it is interesting to learn
that while, during the time of these attacks, he had normal hearing,
he has gradually lost hearing in the left ear and acquired permanent
{424} tinnitus. I have reached the conclusion that there is a group of
functional vertigoes, and that in some of them the trouble lies in the
semicircular canals; that is to say, the lesion is slight or
transient, but in rare cases recurs until a more distinct and
permanent result justifies the original diagnosis.

OCULAR CAUSES OF VERTIGO.—For the most part, the eyes as a source of
vertiginous impressions are neglected in the textbooks; but as the
cause of certain of the slighter vertigoes, and as a fertile agent in
emphasizing or recalling vertigoes due to the stomach or inner ear,
they are well worthy of careful study, nor is it ever wise to neglect
these organs in cases either of headache or of vertigo.

A number of eye conditions cause giddiness or increase it or reproduce
it. Thus, sudden loss of accommodation in one eye or in both may
occasion it, and perhaps the enlarged pupil may have its share, since
even in healthy people, and surely in all habitually vertiginous
patients, sudden exposure to brilliant light gives rise to sense of
instability.

Abrupt change in intraocular pressure is another cause, as in acute
glaucoma or in sudden partial collapse of the eye from discharge of
the aqueous humor.

Permanent vertigo of quite severe character may arise from astigmatic
defects, and from almost any form of disorder affecting steadily the
power of the eye to accommodate itself to distances; but simple myopia
of moderate grades, excessive one-sided myopia, or presbyopia is
unlikely to do so. Oculo-motor troubles, paralytic or spastic, are
very effective causes of vertigo, which is sometimes quite promptly
producible by the wearing of a prism on one eye or by the use of
glasses which over-correct, or if exact are for some reason badly
borne. This latter is apt to be the case, I think, in accurate
corrections of long-standing hypermetropic astigmatisms. There is one
point on which, in this connection, I have again and again insisted:
Optically defective eyes may exist through life without notable brain
disturbance, unless, from over-use with worry, work under pressure,
the strain of prolonged or of brief and intense emotion, or any cause
of ill-health, the centres become sensitive, as they are then apt to
do. When this occurs defective eyes, and in fact many other sources of
irritation, grow at once into competence for mischief, and occasion
vertigo or headache or other cerebral disorders.

Then it is that even slight defects of the eye may cause vertigo,
which if usually slight and transient, coming and going as the eyes
are used or rested, is sometimes severe and incapacitating. I have
over and over seen vertigo with or without occipital pain or distress
in persons whose eyes were supposed to be sufficiently corrected with
glasses, but who found instant relief when a more exact correction was
made; and this is, I think, a matter which has not yet generally
received from oculists the attention it demands.

When vertigo, essential, gastric, or aural, is present, the use of the
normal eye becomes a common source of trouble. Bright lights, things
in irregular motion, reading or writing, and especially rapid changes
in accommodation, as watching the retreat or approach of a moving
object, are prone to cause or increase the dizziness.

Vertigo in old age, if not due to the stomach or defective states of
the portal system, kidneys, or heart, is either caused by atheromatous
vessels {425} or multiple minute aneurismal dilatations of vessels, or
in full-blooded people by some excess of blood or some quality of
blood which is readily changed by an alteration in the diet, of which
I shall presently speak. Whatever be its source, it is in the old a
matter of reasonable anxiety.

Laryngeal Vertigo.—Under this name J. R. Gasquet,[8] and later M.
Charcot, have described a form of vertiginous attack in which
irritation of the larynx and a spasmodic cough invariably precede the
onset. I have never seen such cases, nor do they seem to me entitled
to be called vertigo. The symptoms are these: After bronchitis, gout,
or rheumatism there occurs an irritation of the larynx or trachea, or
of both, which at times is expressed in the form of a tickling cough,
simple or in spasms. With these arises a slight sense of vertigo, or
else in the grave attacks the patient falls insensible, without
convulsion or with no more than one may see at times in fainting. The
face is flushed, even deeply, and the attacks last but a few moments.
The term vertigo seems to have in such a group of symptoms but little
application, nor do these attacks ever bring upon the sufferer the
status vertiginosus.

[Footnote 8: _Practitioner_, Aug., 1878.]

Vertigo in Anæmia and in Neurasthenia and Hysteria.—A passing vertigo
readily caused by abrupt changes of posture, felt even in health, at
times is far more profoundly experienced in grave anæmic states, while
in neurasthenic conditions, with deficiency of globules or defect of
hæmaglobin, it is still more common. In well-pronounced neurasthenic
states, where there is no measurable lack of red corpuscles, but where
hæmaglobin is apt to be deficient, it is a frequent symptom, and is
then either an immediate result of functional central disorder or of
gastric or optical troubles. While the dizziness of neurasthenia is
never profound, certainly never repeats the agony of Menière's
vertigo, it is apt to be but a too constant symptom, and to be, like
the other disqualifying cerebral symptoms of neurasthenia, almost the
last to get well. Usually there is little, often no, tinnitus, no
deafness, no nausea, slight but a pretty constant sense of
unsteadiness, and rarely or but for a few moments any false subjective
visual illusions. This, at least, is the type, but, on the other hand,
in extreme cases and within these limits the brain is liable to be
confused, and the sense of need for difficult controlling volitions
called out by almost any use of the eyes in near vision, owing usually
to oculo-muscular paresis. Even looking at a mirror or at persons
passing by, or the least distinct mental effort, may reproduce it.
There is, too, in most of these cases an extreme sense of mental
confusion, and more often a false sense of movement within the head
than without, while in no other patients is the sexual act so apt to
increase all of the symptoms in question.

Hysteria, as might be expected, offers now and then examples of
vertigo. It does not exclude the presence of true aural, optic, or
gastric dizziness, which is then apt to become the starting-point of a
long train of hysterical disorders. On the other hand, we meet with
hysterical vertigoes which, in a sense, may be said to simulate any of
the more usual types. I have certainly seen hysterical girls with
deafness, tinnitus, and a great development of equilibrial
disturbance, in whom the disease passed away without leaving a trace
behind it, so that in these cases some caution is needed as to
prognosis. They become far more difficult to deal {426} with when they
are found in old women or women in advanced middle life, since it is
then hard to know what share senile changes may have in the production
of the symptoms.

Vertigo from mechanical causes, such as sea-sickness, railway
sickness, swinging, etc., it is hardly worth while to deal with here
at length. The research of Prof. James has made it probable that
disturbances of the labyrinth are responsible for the vertigo of
sea-sickness. Certainly, deaf-mutes seem to have lost the power to be
made vertiginous from rotation, and do not suffer at sea.

It is, however, worth recording here that I have more than once seen
enduring vertiginous status, with occasional grave fits of vertigo,
arise out of very prolonged sea-sickness. In the last example of this
sequence seen by me there was, after a year or more, some deafness.

The elevators in use in our hotels sometimes cause, in those who live
in them all day and control their movements, a cumulative vertigo, and
I have known such persons to be forced on this account to seek other
occupation.

Essential Vertigo.[9]—There can, I think, be no doubt that the centres
may evolve the symptom vertigo from causes which are transient, and
the nature of which sometimes evades our most careful search. We reach
the diagnosis of a state of essential or true central vertigo by
exclusion, but, once developed, this vertigo does not greatly differ
from vertigo of peripheral cause. It is sometimes associated with
states of pallor, at others with flushing, while the disturbance of
balance and the false perceptions as to the place of outside objects
may vary from the least to the most profound disturbance. In some of
these examples the nausea or emesis does not appear at all, and the
patient, escaping acute attacks altogether, may with occasional
aggravation continue to be merely and almost constantly vertiginous.

[Footnote 9: Ramskill and others.]

The TREATMENT of acute attacks of vertigo, however caused, consists,
of course, in rest in bed and in the use of large doses of bromides or
hydrobromic acid, and if the trouble be grave in that of hypodermatic
injection of morphia, and where there is plainly pallor of face in
inhalations of amyl nitrite or in the exhibition internally of
nitro-glycerin and alcoholic stimulants. Sometimes to lie on the floor
in total darkness is helpful when the disorder continues and is
severe. I have known patients liable to be attacked suddenly to carry
a little flask of brandy, and to find that very often an ounce of
brandy, taken at the first sign of trouble, would enable them, by also
lying down, to break the attack; and ether is yet more efficient.
After the severer sense of vertigo has gone they find that stimulus is
comforting, and for a time at least gives strength. I have used amyl
nitrite but twice. In each case it is said to have broken the attack,
but I have had no larger experience with it.

Gastric vertigo demands, in the acute attacks, a treatment directed to
the cause. Antacids may be valuable, or in arrested digestion emetics,
but in all cases these should be followed for some weeks by moderate
doses of bromides, while gouty or lithæmic states should be treated by
the usual means.

Vertigoes from portal disturbances are best treated by aperients, and
a like lessening of animal food, which, in the vertigo of old age or
middle {427} life arising from excess of blood, will also be found
available. The change of cerebral states of passive congestion, which
can be brought about by a pure vegetable or milk-and-vegetable diet is
sometimes quite remarkable; and I know of few things in therapeutics
which are more satisfactory.

The treatment of anæmic or neurasthenic vertigo involves nothing
peculiar. So long as the want of blood lasts, or some one of the
several groups of symptoms loosely classed as neurasthenia exists, so
long will the associated vertigo endure.

Aural vertigoes are easy or difficult to treat, as they arise from
external or middle and internal ear troubles. Irritations in the
external ear are of course to be removed, and catarrh of the middle
ear to be treated by attention to its conditions, whether of blocking
of the Eustachian canals with depression of the membrana tympani or of
accumulations in the middle ear, with the opposite state of fulness.
Aural vertigo, as has been pointed out, may arise from disorders of
any part of the ear, so that it is needful to look for wax, ulcers,
foreign bodies, etc. in the external meatus; for catarrhal states,
closure of the tubes of Eustachius, states of fulness or of vacuum in
the middle ear; and for inflammatory conditions, direct or
transmitted, in the inner ear. Very often vertigoes from irritations
of the outer or middle ear may be relieved with more or less ease, but
labyrinthine vertigo, however acquired, is always troublesome, often
lasting, and if grave gets well only when deafness has become great.

In this form of vertigo, and while acute, morphia is very serviceable,
and is to be used with full doses of bromides. When, as happens, both
cease to be of value, Charcot's plan of the heroic use of quinia salts
I have seen do good; but it is advisable to use with it hydrobromic
acid in full doses. It has been constantly my practice to employ over
the mastoid or on the neck frequent but not deep cauterization. It is
well in these cases to warn some near relative that while remote
relief from the vertigo is probable, it will be bought at the cost of
increasing deafness, and that we can rarely do more than help the
patient to endure his state until time and the slow processes of
pathological change have come to our aid.

Optic vertigo, if essentially that, is rarely discovered without the
help of some one trained to study the defects of vision. Its relief
demands, of course, as a rule, glasses, or in extra-optical
muscle-troubles these or a compensatory operation. When, however, the
vertigo has been grave, it is needful to manage corrections of the
eyes with care and judgment, and sometimes experimentally. The
sensorium, having become over-excitable, does not always bear accurate
correction of the eyes, or this increases the vertigo. Then the
glasses are cast aside and the case progresses. In others—and this is
purely a matter of individual experimentation—nothing will answer
except the most careful and absolute corrections: anything less does
no good.

These remarks apply with equal force in chronic vertigoes, essential,
gastric, or other. Defective eyes, unfelt in health, soon begin to
trouble a head sensitized by chronic dizziness, and optical defects
which are sometimes but trifling become then competent to increase the
growing intracranial disorders, or to assist lithæmia or a troublesome
stomach to create and sustain vertigo.

{428} The Status Vertiginosus.—I have tried to make clear elsewhere
and in this article that in several forms of vertigo the disorder
ceases to owe its onsets to extracentral irritations, and becomes
essential, precisely as happens in some epilepsies, and that we then
are apt to have, with more or less distinct attacks or with no
attacks, long continuance of a group of symptoms which constitute the
status vertiginosus. Its treatment is important, because of its
alarming and disqualifying effects. The attacks are often the least
part of it, while the lack of power to read and write, to go into
crowded streets, to face light, or to exercise, or stand emotions or
the slightest mental strain, surround its management with
embarrassments, and are well fitted to end in melancholia or
hypochondriasis.

In these cases, after the eye has been corrected, the diet should be
regulated with care. In extreme cases it may become desirable to limit
it to milk, fruit, and vegetables where no obvious peculiarities
forbid such a regimen; and I have found it useful to insist also on
some food being used between meals.

I like, also, that these patients rest an hour supine after each meal,
and spend much time out of doors, disregarding their tendency to lie
down. Exercise ought to be taken systematically, and if the vertigo
still forbids it, massage is a good substitute. At first near use of
the eyes is to be avoided, and when the patient resumes their use he
should do this also by system, adding a minute each day until
attainment of the limit of easy use enjoins a pause at that amount of
reading for a time.

Now, as in vertigo, especially labyrinthine, the eyes become doubly
valuable as guiding helps to correct equilibration, I have long found
it useful to train these patients to stand and walk with them closed.
At first this is as difficult, or may be as difficult, as in locomotor
ataxia, but the practice is sure to add steadiness to the postures.
Somewhat later I ask my patient deliberately to make such movements of
the head and such efforts of mind or memory as are apt to cause
vertigo or confusion of head, and to conquer or inhibit these
consequences by a prearranged effort of will; and these means also I
have found useful. Meanwhile, nothing usually in these cases forbids
the use of tonics or of moderate doses of bromides. As I have said,
change of air is very serviceable. It is indeed rare that cases do not
yield to some such combination of means, but very often it will happen
that the fears of the patient are his most grievous foes, and are to
be dealt with after every real symptom has vanished.


{429}


TREMOR.

BY WHARTON SINKLER, M.D.


Tremor is a prominent symptom of many diseases of the nervous system,
and is met with as an effect of certain poisons which have been taken
into the system; so it should not be considered as a disease in
itself. It may, however, occur without being associated with any other
abnormal condition which can be discovered. It is then called tremor
simplex or tremor essentialis. The tremor of old age (tremor senilis)
comes under this head.

Tremor is sometimes hereditary, and may exist from early life. I have
a patient in whom there is a trembling of the hands which has lasted
since childhood. This lady's mother and grandmother both had the same
form of tremor, and one of her own daughters also has it. In this case
the trembling is most marked when voluntary movements are attempted,
but it does not materially interfere with writing, sewing, or any
other act she wishes to accomplish. There is slight tremor when the
hands are at rest.

Tremor simplex is seen in hysteria. In this disease it affects the
hands and the facial muscles as well. It is not uncommon in these
cases to find the tongue tremble excessively when protruded.

Tremor from chronic poisoning is usually from the absorption of lead,
mercury, or some of the narcotic drugs or alcohol. Lead tremor is to
be looked for among persons who are exposed to the action of lead,
such as painters, printers, or manufacturers of white lead.[1] Such
persons generally have had some other symptom of lead-poisoning, such
as colic or paralysis. The tremor, however, may be the only symptom of
saturnine poisoning. Mercurial tremor is not so often seen. It occurs
in looking-glass makers or those who work in quicksilver, and may also
be a result of the medicinal administration of mercury. The tremor
from the excessive use of alcohol or opium is familiar to all.
Tobacco, if used immoderately, also causes trembling in the hands. Tea
or coffee may have the same effect. There are other drugs which, when
taken for a length of time, are liable to cause tremor. Quinine is one
of these.

[Footnote 1: Lead in hair dyes or in cosmetic powders often gives rise
to plumbism by its absorption by the skin.]

Exhausting diseases, like the fevers, or any conditions which enfeeble
the system, cause tremor which occurs in voluntary effect. I saw a
lady some years ago who was greatly weakened by a malignant growth.
She was extremely anxious to sign her name to a legal paper, but,
although the hand was perfectly quiet when at rest, when she attempted
to write {430} the first letter such intense tremor came on that it
was impossible for her to make any mark which was legible.

Tremor follows violent bodily exertion or mental excitement. The
action of cold or the chill of intermittent fever is accompanied with
an extreme degree of trembling, which we all know. Tremor is also a
result of neuritis, but in this case it is associated with other
symptoms.

SYMPTOMS.—Tremor is met with as a fine or a coarse trembling. We may
also find a fibrillar tremor, such as exists in progressive muscular
atrophy. Tremor is divided by some (Van Swieten, Charcot, and others)
into two classes: the first is where the tremor occurs while the part
is at rest; the second is where it comes on during volitional muscular
movements. The former has been termed by Van Swieten tremor coactus,
because he believed that it arose from an irritation which affected
the nervous centres in an intermittent way. The latter he conceived to
depend upon a defect of stimulus, the result of an insufficient amount
of nervous fluid, which causes contraction of the muscles under the
influence of the will. This he called tremor a debilitate.[2]

[Footnote 2: Charcot, _Lectures on Diseases of the Nervous System_.]

In paralysis agitans we have an example of tremor coactus, and in
disseminated sclerosis, where the tremor occurs only as muscular
effect, it belongs to the variety of tremor a debilitate. Those
divisions, however, are of but little importance.

When tremor first begins it is slight in degree and extent, and occurs
generally only on voluntary effort. Later there may be a constant
trembling even when the part is at rest. Beginning usually in the
hands, it may extend to the head and legs. It is seen in the tongue
and facial muscles after the disease has lasted for some time.

In some cases the trembling can be controlled to some extent by a
strong effort of will. The tremor from alcohol or opium is most marked
when the individual has been without the use of the stimulant for a
short time, and the trembling may be temporarily checked by renewing
the dose of alcohol or opium as the case may be.

The muscular trembling from plumbism and mercurial poisoning is more
violent than the other forms of simple tremor, and often resembles the
tremor of paralysis agitans. In toxic tremors there are often
secondary paretic symptoms and indications of other disturbances of
the brain and nervous system.

In simple tremor there is no loss of muscular power, and the
electrical reactions of the affected muscles are not abnormal. The
duration of simple tremor is almost always great. Usually it persists
throughout life, becoming more general and more intense as the subject
of it grows older. The tremor of hysteria is shorter in duration.
Occasionally there are seen cases of simple tremor, which are
apparently the result of some trivial cause in a nervous person, which
last but a short time.

I have seen a case of tremor of the head in a woman of about forty
years, in which the trembling ceased entirely after it had lasted
several weeks. Hammond[3] describes what he calls convulsive tremor.
Under this name he includes cases of non-rhythmical tremor or clonic
convulsions, which are unaccompanied by loss of consciousness, but are
paroxysmal in character. Pritchard in 1822 presented an account of
this affection and {431} related two cases; Hammond mentions six
cases. The affection is characterized by paroxysms of violent and
rapid convulsive movements, which are more or less general and occur
many times a day. The seizures last from a few minutes to several
hours.

[Footnote 3: _Diseases of the Nervous System_, p. 696.]

The PROGNOSIS in convulsive tremor seems to be favorable.

Tremor may be regarded as a form of clonic spasm. It consists of
slight intermittent contractions of individual muscles or groups of
muscles. Fibrillar tremor, such as is seen in progressive muscular
atrophy, depends on contractions and relaxations of the muscular
fibrillæ, and can be seen under the skin, but does not cause any
movements of the limb.

There are no pathological data for explaining what portions of the
nervous system are the seat of disease in simple tremor. In
experiments upon the lower animals it has been found that trembling
occurs in muscles which have been separated from the nerve-centres by
division of the nerve. So too in man: when there has been a wound or
section of a nerve accidentally, there is likely to be tremor in the
muscles which it supplies.

The tremor does not begin at once on section of the nerve, but comes
on after a few days. As the peripheral end of the nerve undergoes
degeneration the tremor increases. It may last months or even years.

In some of the conditions where tremor occurs the influence of the
will is weakened or is entirely absent. This is seen in hysterical
trembling and in the tremor of old age as well as in those cases where
there is general enfeeblement of the body, as in the fevers.

Trembling is connected with disease of the pyramidal tracts, because
in this way the influence of the cerebral centres is withheld from the
muscles. When a muscle is in a condition of tonic spasm, it is the
result of the running together of very rapidly-repeated muscular
contractions. It is like the contraction in a muscle from an
interrupted electrical current. If the interruptions are slow, the
muscular contractions are seen at intervals like a tremor; but if the
interruptions are rapid from frequent vibrations of the hammer of the
instrument, then the contractions in the muscle are fused together, as
it were, and the muscle is in a state of tonic spasm.

It is held by some writers that tremor is caused by the want of
balance between the cerebrum and cerebellum. When, for example, the
control of the cerebrum is enfeebled the action of the cerebellum is
so great as to bring about tremor by its uncontrolled power.

If we accept the first view, we must consider the tremor as a
preliminary stage of paralysis; for the lesion, which at first is
slight and causes only an interruption of the conduction of impulses
from the brain to the muscles, as it becomes more extensive totally
prevents conduction, and paralysis ensues.

Hughlings-Jackson's view, that general convulsions are the result of
discharges from the cortex of the brain, and that the tonic
contractions of tetanus are caused by discharges from the cortex of
the cerebellum, may be applied to the pathology of tremor as well.
When, for instance, in a disease like disseminated sclerosis a
voluntary effort instead of causing a steady muscular contraction
results in irregular spasmodic contractions and relaxations of the
muscle, we may imagine that a series of discharges were taking place
from the cortex of the cerebellum as long as the voluntary efforts
were persisted in. On the other hand, in paralysis agitans {432} it is
more probable that a lack of conducting power in the pyramidal tracts
prevents the influence of the centres being continuously exerted upon
the muscles through their motor nerves.

It is probable that in simple tremor the lesion is situated in the
spinal cord; for in this disease we seldom see any evidences of
cerebral disturbance. There are no paralytic or psychical symptoms,
and no vertigo. In toxic tremors the disease is no doubt located in
the brain, for accompanying the trembling resulting from alcohol,
opium, mercury, and other drugs are mental changes and more or less
muscular enfeeblement.

TREATMENT.—Should the tremor depend upon some cause which can be
discovered, of course the obvious course is to attempt to remove the
source of trouble. The effort is of greater or less success in
different conditions. The tremor from mercurial poisoning sometimes
yields to treatment which is directed to the elimination of the
mercury. The free administration of the iodide of potassium is the
best means to be used, and is often successful. The same means are
available in lead tremor. Of course the patient must be removed during
treatment from the risk of further absorption of the poisonous
substances.

In simple tremor many remedies have been recommended, but the results
of treatment are not encouraging. Baths of various kinds and galvanism
have been used, and many drugs are advised. Hyoscyamus and its
alkaloid, hyoscyamine, have enjoyed a high reputation, and good
results have been reported from their use. I have seen relief, but not
cure, from their administration. Arsenic is a more reliable remedy and
it may be used hypodermically. Eulenburg[4] has used this method with
good results. I have given arsenic per orem with beneficial effects in
cases of simple tremor. In a case to which I have referred above the
tremor was relieved while the patient was taking Fowler's solution,
and on changing to hyoscyamus the trembling got worse. On returning to
the arsenic the symptoms improved, and finally the tremor ceased after
the remedy had been taken for some weeks. Hysterical tremor requires
that the hysteria should be relieved. Franklinic electricity sometimes
controls the tremor in these cases.

[Footnote 4: _Ziemssen's Cyclopædia_, vol. xiv. p. 392.]


{433}


PARALYSIS AGITANS.

BY WHARTON SINKLER, M.D.


SYNONYMS.—Parkinson's disease; Shaking palsy; Trembling palsy; Senile
chorea; Chorea festinans. The first name is due to the fact that the
disease was first fully described by Parkinson in a book published in
England in 1817.

Paralysis agitans is a neurosis, chronic in its forms and
characterized by a tremor which gradually increases in extent and
severity. The tremor is not increased by voluntary muscular movements.
A peculiar manner of walking, known as festination, comes on later in
the disease, and there are also alterations in the attitude of the
head and trunk.

It is a disease which belongs to middle age, being rarely seen before
forty years, although cases are quoted by Charcot as early as twelve
and sixteen years. Constant and prolonged exposure to dampness and
cold seems to bring on the disease, and it is sometimes caused by
sudden emotion, like fear or distress. The following case is an
instance of the latter:

Case I.—Mr. A. M——, æt. fifty-two years, consulted me Oct. 1, 1883. He
is a bookbinder by occupation. His habits have been good. He had a
chancre in 1861, but had no secondary troubles. He was in the army
from 1861 until 1866. In 1866 he went into business for himself, and,
although his business was large, he had no great anxiety or worry. His
general health has been good, and he has had no illness except an
attack of malarial fever about six years ago. In May, 1883, he was
standing by an elevator door on the fourth floor of his place of
business, and, seeing that the elevator was caught by something,
released it. It immediately fell with a crash to the second floor, and
as there were two or three persons on it, Mr. M—— thought they must
have been killed or severely injured. He was greatly excited and
alarmed, and soon after he had assured himself that none of the
occupants of the elevator had been hurt, discovered a trembling of the
right hand. The tremor has continued ever since, and has extended to
the arm and leg.

On examination there is seen a coarse tremor of the right arm and leg
while the limbs are at rest. A voluntary muscular movement stops the
tremor, and it also ceases during sleep. When he makes an effort with
the right hand, as, for instance, in squeezing the dynamometer, the
tremor ceases in the arm, but becomes greatly exaggerated in the right
leg. While occupied in doing anything he does not notice the tremor,
and it stops when he is lying down.

The dynamometer shows, right hand 150°, left hand 120°. After two
years have elapsed the disease has gradually progressed in severity.

{434} SYMPTOMS.—The course of the disease has been divided into three
stages—the period of invasion, the stationary period, and the terminal
period.[1]

[Footnote 1: _Lectures on Diseases of the Nervous System_, by J. M.
Charcot.]

Period of Invasion.—There are several modes of invasion, but the most
frequent by far is slow in its onset. The disease comes on gradually,
first showing itself as a slight tremor in the hand or fingers while
the part is at rest. It is not constant, and ceases as soon as the
patient's attention is called to it. There is sometimes preceding the
tremor rheumatic or muscular pain in the affected arm. The tremor may
first occur in the foot. Should the disease begin in the hand—and this
is most common—the movements are peculiar. They may consist of a fine
rhythmical tremor, or the fingers move in a methodical way over each
other. Charcot speaks of the thumb and forefinger being rubbed
together as if the patient were spinning wool. While this movement of
the thumb and finger is going on the wrist is being flexed by jerks.
During the early stages of the disease the tremor is observed only at
intervals. It comes on intermittently when the patient is not thinking
of it and while the limb is at rest, and ceases as soon as any
voluntary muscular effort is attempted. The act of grasping the hand
or taking up an object is enough to check it for the time. In a
patient now under my care I have often noticed during the early stages
a well-marked tremor of the right hand while it was lying in her lap,
but it would at once cease when I called attention to it. As soon as
the mind of the patient was diverted to some other subject the tremor
would begin again.

As the disease progresses voluntary effort no longer controls the
tremor, or if it does at all it is only for a few seconds, when it
begins again. As the tremor increases in violence it extends to other
parts of the body. At first it may have been confined to the hand; now
it extends to the arm, a little later to the foot and leg on the same
side. Then the other arm will be affected, and finally all of the
limbs will succumb to the tremor.

Charcot speaks of decussated invasion—that is, the disease begins in
the right upper extremity, for example, and next passes to the left
lower extremity. This is a rare form; it is much more frequent to see
the hemiplegic type, which may persist for some time, or the
paraplegic type, when both legs are affected.

There is a progressive form of invasion when the tremor is not the
first symptom. The patient has neuralgic or rheumatic pains in the
limbs, which are afterward affected with tremor. Sometimes there is
some mechanical injury of the limb, which subsequently is the seat of
pain and tremor. The general health of the patient is at the same time
more or less impaired. There is a sense of general weakness and
lassitude; the temper is irritable, and there may be some vertigo. The
features and countenance are characteristic even at the earliest
periods of the disease. There is an absolute absence of expression,
and the features are fixed. The face looks like a mask, and although
the patient may smile or laugh, immediately after the features return
to the original blank expression. Amidon showed two cases of paralysis
agitans to the American Neurological Society in 1883, in which there
was no tremor whatever, but all the other features of the disease were
present.

{435} After a great mental or moral shock the trembling begins
suddenly, abrupt invasion, as in Case I., or the case described by
Charcot, where the wife of a gendarme, seeing her husband's horse
return riderless to the barracks, received a shock of great severity,
which was followed on the same day by tremor. The tremor is at first
confined to one limb. It may even disappear for a time, but gradually
and slowly extends to the other limbs, and takes the same progressive
course.

Period of Stationary Intensity.—After the disease has become fully
developed the tremor is incessant. The intensity is not the same all
the time. It may be augmented by cold, over-excitement, or voluntary
effort, and is lessened by repose and sleep. The trembling ceases
during anæsthesia.

During this time all the characteristic movements are at their height.
The moving of the thumb and finger, already referred to, is present,
and seems like a partly co-ordinated movement. Charcot describes these
movements as being in some cases like the rolling of a pencil or a
paper ball between the thumb and finger, and in others the movements,
he says, are more complicated, and are like what occur in crumbling a
piece of bread.

The handwriting is almost illegible, and every letter shows the
excessive trembling of the hand, most marked in the up strokes of the
pen. All this time the head and neck are unaffected. There is no
nodding or shaking of the head to be observed on the closest
inspection. This is an important fact to bear in mind, for it is a
distinguishing feature between the disease under consideration and
disseminated sclerosis. There is no nystagmus, and the muscles of the
jaw are unaffected by tremor. The tongue, however, while lying on the
floor of the mouth undergoes tremor, and this is increased when the
organ is protruded.

The speech is slow and jerky, and the patient usually speaks in a low
tone of voice. He eats his food without difficulty, but in advanced
cases the saliva sometimes escapes from the mouth during deglutition.
A characteristic symptom of the disease is a rigidity of the muscles
of the extremities, trunk, and of the neck. When the muscular
stiffness first begins the patient complains of cramps followed by a
sense of rigidity. The flexor muscles are first affected. This
stiffness causes peculiarities in the patient's attitudes. The head
and neck are usually bent forward, and seem fixed in that position.
The body is inclined slightly forward in standing. The elbows are held
somewhat away from the chest, the forearms are flexed on the arms, and
the hands are flexed on the forearms. The thumb and forefinger are
extended and brought together as if holding a pencil. The other
fingers are also flexed. The attitude of the hand and the prominence
of the knuckles make it closely resemble the hand of rheumatoid
arthritis. In paralysis agitans, however, there are no bony deposits
in the joints, and no cracking is heard on bending the knuckles.

In the lower extremities there is often intense rigidity. Contractions
occur, and the legs are strongly flexed. The feet often are extended
in the position of equinus. It is this rigidity which causes the
difficulty in walking (Charcot).

The gait of the patient now becomes very striking. He gets up from his
seat slowly and with difficulty; hesitates a moment before starting to
{436} walk; then, once having made a few steps, goes at a rapid pace.
The tendency is to fall forward; in order to preserve his equilibrium
the patient hurries forward as if to catch up with his centre of
gravity. This gait has been called paralysis festinans—festination or
propulsion.

Although propulsion is the usual form the gait assumes, sometimes
there is a tendency to fall or run backward. This tendency is not
always apparent even when it exists. Charcot has a method of showing
its existence which is very successful: when a patient is standing he
pulls her slightly backward by the skirt, and this is sufficient to
start a movement of retropulsion.

Propulsion and retropulsion are not necessarily always present. Many
cases progress to the end without these symptoms.

As the disease advances the muscles become more rigid and the patient
is confined to bed. He is, however, restless from a sense of
prostration and fatigue. He is unable to turn himself, and often calls
to his attendant to change his position. The sufferers from this
disease, although not having actual pain, complain of disagreeable
sensations. There is a constant sense of excessive heat whether the
temperature of the room be high or low. In winter they cannot bear
much bed-clothes at night, and prefer to wear very light clothing.
Associated with this sensation of heat is often profuse perspiration
(Charcot). Notwithstanding all these troublesome sensations the
sensibility of the skin is not changed. Heat and cold are readily
felt, and there is no anæsthesia or analgesia.

Terminal Period.—The duration of paralysis agitans is generally great.
The disease may extend over many years—even as long as thirty years in
some cases. As the tremors and rigidity increase in intensity the
patient becomes obliged to sit all day in a chair or is confined to
bed. Occasionally the tremor becomes less while the rigidity
increases. The nutrition suffers, and the muscles especially become
greatly wasted. Up to a certain point the intellect remains
unaffected, but late in the disease the mind fails. General
prostration of the whole system sets in, bed-sores occur, the urine
and feces are passed unconsciously, and the patient dies of
exhaustion. It is not often that the end comes in this way. It is much
more frequent that some intercurrent disease, like pneumonia, ends the
life of the patient. The disease is undoubtedly a most painful and
trying one to both patient and physician. It lasts for years, and
there is no prospect of relief. Charcot says that he has seen the
terminal period last for three or four years. The following case is a
fair example of the disease:

Case II.—Margaret Hays, aged fifty-four, single, applied for treatment
at the Infirmary for Nervous Diseases, Oct. 9, 1882. She is
housekeeper for her brother, who keeps a restaurant. She has had to be
up late at night, and has had very much washing to do for many years.
The kitchen in which she is most of the time is damp, and opens into a
yard into which she has often to go. About two years ago she thought
that she hurt herself in lifting something, and soon after this, on
putting her hands from hot into cold water, suddenly felt a numbness
in both forearms. One year ago she noticed tremor in both hands and
both legs. The tremor interfered with her work, and has increased. She
also felt as if there were loss of power.

Present Condition.—The face is expressionless and looks as if it were
{437} a mask. She articulates without using her lips to any extent,
and speaks in a low tone, scanning the syllables. The head is held
stiffly, and the attitude of the whole body is peculiar.

The tremor is fine, and is constant while the hands are at rest. On
voluntary effort the tremor ceases. On examination with the
dynamometer, right hand 95°, left hand 80°. She feels weak generally,
and says she cannot use her hands even to button her clothes or to
dress or undress without aid. She performs all movements slowly and
with great deliberation. The patellar reflex is not excessive.

Sensation.—She has lost the sense of numbness she used to have, but
says she cannot feel a needle between the fingers when she attempts to
sew. There is loss of sensation in the finger-ends; the compass points
are not felt at less than three lines.

Her walk is slow and deliberate like all her movements, and there is
no festination. Her eyes were examined, and there was no decided
change in the fundus and vision was about normal. Pupillary reflexes
good.

This patient was under observation for several months, and steadily
grew worse. One peculiar feature was observed, however: it was that at
one time the tremor almost ceased, although all of the other symptoms
were worse.

ETIOLOGY.—As already mentioned, the causes which have been observed
are fright or sudden grief and prolonged exposure to cold and
dampness. A number of cases of the former are mentioned by Charcot,
and a case which I have related above is a good illustration of
paralysis agitans produced by fright. When caused in this way the
disease does not present any peculiar features in its progress or
termination. I have seen many cases in which the disease had been
preceded by more or less exposure to dampness. One of my patients had
worked in a basement room which was damp; another (Case II.) was a
great deal of the time in a kitchen which opened on a wet yard, and
she was constantly going in and out of doors, getting her feet wet
frequently. Sometimes irritation of a peripheral nerve seems to have
been the origin of the trouble. Charcot quotes several cases of this
kind.

Sex does not appear to exert any special influence in the production
of the disease. Some writers assert that it is more common in males
than in females, but Charcot in his large experience at La Salpêtrière
has not found this to be the case.

MORBID ANATOMY.—A number of autopsies have been made in cases of
paralysis agitans without any constant lesion of the nervous system
having been discovered. Charcot refers to three cases in which he made
careful post-mortem examinations in which the results were negative.
Parkinson and Oppolzer each report one case in which was found
induration of the pons, medulla, and cervical portion of the cord.
More recently, however, Charcot and Joffroy have examined cases in
which microscopic examination revealed blocking up of the central
canal of the cord by increase of the epithelium of the ependyma and
pigmentations of the ganglion-cells.

Leyden has reported a case in which the disease was confined to the
right arm, and on post-mortem examination a tumor of the left optic
thalamus was found.[2]

[Footnote 2: Quoted by Hamilton, _Diseases of the Nervous System_, p.
500.]

{438} Dowse and Kesteven found degeneration of the nerve-cells of the
anterior pyramids, changes in the olivary body, nucleus of the ninth
nerve, laminæ and corpus dentatum of the cerebellum and of the
anterior cornua of the spinal cord. Also cortical sclerosis of the
right lateral column of the cord and miliary changes in the white
matter of the corpus striatum and hemispheres.[3]

[Footnote 3: Ross, _Diseases of the Nervous System_, vol. ii. p. 797.]

In this disease, as in chorea, there must be two classes of
cases—those in which there is no lesion to be discovered after death,
and others in which there are changes throughout the brain and spinal
cord more or less widespread. The cases in which the disease comes on
suddenly from some moral shock probably belong to the former class;
while in cases which have come on gradually during senility one would
expect to find organic changes in the nervous system. Ross[4] suggests
that the cause of the tremor is probably a diminution in the
conductivity of the fibres of the pyramidal tract, which prevents
impulses from the cortex reaching the muscles in sufficiently close
proximity to produce a continuous contraction. This, however, does not
explain the cause of the tremor in the cases where it began suddenly
from fright.

[Footnote 4: _Op. cit._, p. 798.]

DIAGNOSIS.—The only diseases with which paralysis agitans may be
confounded are disseminated sclerosis, senile tremor, and chorea in
the aged. From senile tremor it may be distinguished from the fact
that it begins before old age—that the tremor is more excessive and
the gait and facial expression are distinctive. Chorea in old persons
resembles paralysis agitans, but is not progressive, the tremor is not
lessened as a rule by voluntary effort, and the peculiar gait and
expression of the face are wanting.

There are many points of difference between paralysis agitans and
disseminated sclerosis, as can be seen below:

       PARALYSIS AGITANS.        |      DISSEMINATED SCLEROSIS.
                                 |
  Tremor ceases on voluntary     | Tremor induced by muscular effort,
  effort, or is not increased by | and ceases during repose.
  it.                            |
                                 |
  Tremor regular and fine.       | Coarse tremor, becoming more so
                                 | during voluntary effort.
                                 |
  Face expressionless; tremor of | Facial muscles affected; nystagmus
  face rare.                     | frequent.
                                 |
  No tremor of head.             | Tremor of head generally present.
                                 |
  Belongs to advanced age.       | Usually comes on before middle age.
                                 |
  Propulsion (festination) and   | Staggering walk.
  retrogression.                 |

TREATMENT.—The results of treatment are not encouraging. Cases have
been reported in which cures were effected, but it is doubtful if they
were true instances of paralysis agitans. Hyoscyamus and conium have
been given with temporary relief to the tremor. Trousseau recommends
strychnia, but Charcot declares that it aggravated the cases in which
he gave it. Hammond advises the use of galvanism, at the same time
giving strychnia or phosphorus. I have seen one case in which decided
relief was obtained from arsenic hypodermically, and another in which
the patient was benefited for a long time while taking small doses of
strychnia combined with iron and quinine, and at the same time static
electricity was applied.


{439}


CHOREA.

BY WHARTON SINKLER, M.D.


Chorea, or St. Vitus's dance, has been known for years, and the
literature of the subject, especially among the older writers, is as
extensive as that of any other disease.

It has been recognized by a variety of names, some of the most common
being derived from some saint who enjoyed a popular reputation of
power to cure the disease. For example, it has been called St. John's
dance, St. Guy's dance, St. Modestus's dance, and St. Anthony's dance.
Besides these names it has been termed ballismus, paralysis vacillans,
epilepsia saltatoria, and orchestromania.

It will be observed that almost all of the names which have been
applied to the disease relate to a dancing movement. This arises from
the fact that the first notice of the affection dates back to the
fourteenth century, when a kind of religious mania appeared in
Southern Europe in the form of an epidemic. It was characterized by
excessive dancing and gesticulatory movements, and affected large
numbers of people at a time. In 1375 an epidemic which arose was
spoken of as St. John's dance, and in 1418, in another outbreak of the
disorder which occurred at Strasburg, by the order of the authorities
those suffering were conducted in troops to the chapel of St. Vitus in
Zabern, and there masses were said and other religious ceremonies
performed for its cure.

We are informed that St. Vitus removed from Sicily when a boy, at the
time of Diocletian's persecution of the Christians in the year 303,
and suffered martyrdom in Florence in company with Crescentia and his
tutor, Modestus.[1]

[Footnote 1: “Hecker's Epidemics of the Middle Ages,” _Sydenham
Society's Transactions_, contains full details of these outbreaks.]

Von Ziemssen states that as a pandemic disease the dancing mania died
out in the fifteenth century, but that traces have remained on the
Rhine up to the present time.[2]

[Footnote 2: _Cyclopædia of the Practice of Medicine_, vol. xiv. p.
416.]

In our own country there have been many epidemics of the same disorder
on a small scale, and we may regard the Shakers as representing a type
of the dancing mania. Weir Mitchell reports[3] an outbreak which
occurred quite recently In a children's asylum in Philadelphia. Prompt
measures and separation of those affected from the well children
checked the disorder, which at one time threatened to spread through
the entire institution.

[Footnote 3: _Lectures on Nervous Diseases_, p. 69.]

{440} These epidemics were quite different from what we now call
chorea, and the individuals suffering were clearly affected by a
psychical disorder of an hysterical form. In time, however, the name
has come to be applied to a systematic disease characterized by
irregular spasmodic movements of the limbs and other parts of the
body.

The disease has been divided by some writers into chorea magna and
chorea minor. The former, however, as described, is only an aggravated
variety of hysteria, and need not be considered in connection with
this subject.

Although the name chorea does not correctly describe the disease under
consideration, it has been used for so many years that it is more
convenient to retain it.

DEFINITION.—Chorea, as we now understand it, is a spasmodic neurosis,
characterized by constant involuntary and irregular jerkings and
twitchings of muscles or groups of muscles, which, in the majority of
cases, cease during sleep, and are accompanied by more or less
psychical disturbance in most instances.

ETIOLOGY.—Hereditary influence in the production of chorea is more or
less marked. In some cases the connection seems to be remote, but in
many instances it will be found that one of the parents has suffered
from some form of nervous disease or has inherited a nervous
diathesis.

George Huntington of Pomeroy, Ohio,[4] has recorded some remarkable
instances of hereditary chorea. The affection, as he describes it,
differs in many features from chorea as ordinarily met with, but it is
apparently the same disease. It is found in the eastern end of Long
Island, and has been studied in several generations by Huntington, his
father, and grandfather. This part of Long Island is remarkably free
from the usual type of chorea, none of these physicians having ever
met with an example of it. The hereditary chorea is confined to a few
families. It occurs more frequently in males than in females, and
never attacks the patient until after middle life. It comes on
gradually and takes years to develop, but when once established it
yields to no form of treatment. In most cases there is a marked
tendency to insanity and suicide in the later stages of the disease.

[Footnote 4: _Medical and Surgical Reporter_, April 13, 1872.]

Some additional cases of hereditary chorea have been lately recorded
by Peretti in No. 52 of the _Berliner klin. Wochenschrift_, 1885, and
others by Clarence King in the _New York Medical Journal_, vol. i.,
1885. The history of all these cases is strikingly like those of
Huntington, and establishes without question a distinct form of
chorea.

Mrs. N., one of Peretti's cases, had a mental affection with choreic
movements, and there was a history of a similar condition in her
parents and grandparents. Two of Mrs. N.'s four children, Mrs. A. and
Anton N., had chorea in adult life; some of these became insane. Mrs.
A. had five children; three of these became choreic; one had tremors
and one became insane. Anton N. had ten children; of these six had
chorea. In all of Peretti's cases the disease came on after the age of
forty years, and persisted. In several members of the family insanity
was associated with the chorea.

In the families where it occurs the nervous temperament predominates.
It sometimes will be found that neither of the parents of the patient
has {441} had chorea or any other nervous disease, but that an uncle
or an aunt has had St. Vitus's dance in childhood.

Chorea may occur at any period of life, from infancy to extreme old
age. I have reported two cases in patients over eighty years of
age[5]—one at eighty-two and the other at eighty-six—who had
characteristic attacks of St. Vitus's dance. Robert Saundby has
collected twelve cases of chorea in the aged. The two cases just
referred to are included in the number. He considers the affection
very rare in old persons.[6] The following case is an example of
congenital chorea, and I believe this to be very unusual. The
movements of all infants are choreic, so that it is difficult to say
when the chorea begins; still, it seems fair to infer that when a
child has never had any but choreic movements it is a case of
congenital chorea:

Case. I.—Jennie W——, aged nineteen years. Family history is good as
regards nervous diseases. Her mother was frightened by seeing a case
of chorea some time before the child was born. The movements were
observed at birth, and have continued always. The patient was brought
to my clinic at the Infirmary for Nervous Diseases, and her condition
noted as follows: The movements are general and continuous; the arms
and legs are in constant motion, and the mouth is perpetually
grimacing; there is tremor of the tongue when it is protruded;
volitional efforts increase the movements; during sleep they cease
entirely; tendon reflexes are normal; there is no paralysis;
heart-sounds are normal and the general health is good; menstruation
is regular, and the choreic movements were not influenced in any way
at the time of its first appearance.

[Footnote 5: _Journal of Nervous and Mental Diseases_, July, 1881.]

[Footnote 6: _Lancet_, Nov. 24, 1884.]

Chorea occurs most frequently during the period of approaching
puberty. Sée in an examination of 531 cases found 453 between the ages
of six and fifteen years.

I have examined the notes of 282 cases of chorea, most of which are in
the case-books of the Infirmary for Nervous Diseases; the rest are
from my own note-books. Of the 282 cases, 217 were between six and
fifteen years. They were distributed as follows:

  Under 1 year  2 | At  7 years 23 | At 16 years  6
  At 2 years    6 |     8  "    24 |    17  "    10
     3  "       4 |     9  "    31 |    18  "     5
     4  "       7 |    10  "    23 |    19  "     5
     5  "       9 |    11  "    18 |    20  "     1
     6  "      24 |    12  "    25 |    21  "     3
  At 22, 25, 27, 28, 35, 38, 82, and 86 years, each 1 case.

Sex exerts considerable influence on the disease. Sée states that
three-fourths of all the cases observed in the Children's Hospital in
Paris occurred in girls. Of 328 cases which I have examined in
reference to this point, 232 were females and 96 males.

Social condition has little or no effect on the production of chorea,
but it is more common in cities than in the country. Indeed,
everything which increases the excitability of the nervous system
during development adds to the tendency to the disease.

West and Hamilton point to over-study as a cause, and I have
frequently verified their observations. The annual examinations at our
public schools give a number of cases of chorea.

{442} A. McLane Hamilton[7] has recently investigated the frequency of
St. Vitus's dance among school-children in New York, and found that 20
per cent. of the children in the schools were affected with some
variety of the disorder.

[Footnote 7: _American Psychological Journal_, Feb., 1876.]

Rheumatism is certainly a predisposing cause, in my experience, but I
have not found it associated with chorea as frequently as some authors
have. In 279 cases which I examined with regard to this question,
there was a clear history of rheumatism in but 37. Cardiac
complications were much more frequent. In 82 cases there was a cardiac
murmur heard. In some of these the murmur was no doubt anæmic, but in
the majority there had probably been a rheumatic endocarditis. Many
cases in which there is said by the friends of the patient to have
been a previous attack of acute rheumatism, on investigation are found
not to have had articular rheumatism, but merely some muscular or
joint pains which were not inflammatory. Quite recently Joffroy and
Saric have expressed the opinion that the pains in the joints during
an attack of chorea are to be regarded as choreal arthropathies of
nervous origin.

English and French writers have observed the relation between
rheumatism and chorea in a large proportion of cases. Hughes and
Burton Brown[8] found that in 104 cases which they examined as to
rheumatism and affections of the heart, there were but 15 in which
some rheumatic condition had not preceded the attack or a cardiac
murmur did not exist.

[Footnote 8: _Guy's Hospital Reports_, 1856.]

Sée and Roget consider the causal relation between the two diseases so
close as to make their connection almost a pathological law.

On the other hand, Steiner made quite opposite observations in Prague.
He saw among 252 cases of chorea only four which originated during the
course of acute articular rheumatism.[9] This statement does not prove
the absence of a relation between chorea and rheumatism, for Steiner
does not say what proportion of cases occurred after an attack of
rheumatism which had taken place some time previous. Hammond[10]
believes “that the influence of rheumatism upon chorea is not greater
than that of a depressing agent to the organism.”

[Footnote 9: _Ziemssen's Cyclopædia, loc. cit._, p. 427.]

[Footnote 10: _Dis. of the Nervous System_, p. 715.]

Octavius Sturges, physician to the Hospital for Sick Children, Ormond
St., London, says that in two years 219 cases of chorea have been
treated at that institution: 20 per cent. of them were connected with
rheumatism, but he does not believe in the rheumatic origin of the
disease, because 15 per cent. of all children have rheumatism.[11]

[Footnote 11: _Lancet_, Sept. 20, 1884.]

The following cases illustrate the direct sequence of chorea upon
acute rheumatism:

Case II.—Kate S——, æt. 17 years, came under my care in May, 1877, with
an attack of acute rheumatism which lasted for two weeks. She regained
strength slowly, and about June 11th, not more than two weeks after
the subsidence of the rheumatic symptoms, choreic movements were
noticed in the right arm. The movements were constant, and were worse
when she was conscious of being observed. She often dropped things.
The right leg jerked often and gave away under her in walking. Under
the use of liq. arsenici bromidi the patient was entirely well in one
month. A sister had had chorea.

{443} Case III.—Rudolph C——, æt. 5 years, was placed under my care May
12, 1883. He has had scarlatina, and in Dec., 1882, he had an attack
of inflammatory rheumatism, accompanied with slight choreic movements,
from which he recovered in a short time. Three or four weeks before
coming under my charge he had a return of rheumatism from getting his
feet wet, and at the same time choreic trouble began again. He rapidly
became worse, and in a short time was utterly helpless. On examination
he is found unable to sit up or make any voluntary movements. He is
unable to move the legs on account of the intense pain in the knees
and ankles from the rheumatism. These joints are swollen and red. The
right arm is in constant and violent motion, swinging about or
thrashing up and down. The left arm lies motionless, and, although
painless, he seems unable to move it. The fingers are clenched, and
they are continually and rhythmically being pressed against the palm.
He cries if an attempt is made to open the fingers. The facial muscles
are contorted all the time, and there is a peculiar vermicular
movement of the upper lip. He cannot speak a word nor can he protrude
the tongue. He sleeps but little, and during sleep the movements are
occasionally seen. He is very fretful and irritable, but is perfectly
intelligent. The appetite is poor. Bowels regular; urine phosphatic
and contains no albumen. There is a loud but not harsh cardiac murmur
heard at the apex, replacing the first sound of the heart.
Temperature, May 12, evening, 100°; May 13, morning, 100-2/5°. Pulse,
140. He was ordered sodii salicylat., gr. v. q. q. h., and inunctions
of cod-liver oil.

On May 18 the rheumatism was so much better that the salicylate was
stopped and Fowler's solution of arsenic was given instead. The chorea
had also become better. The arsenic was continued in increasing doses,
and the case convalesced steadily. On June 26 he was able to return to
his home in Maryland entirely well.

He remained well until July, 1884, when he had a slight attack of
chorea, which was preceded for about a week by rheumatism. The cardiac
murmur, which was almost absent after recovery from the first attack,
was now heard again, but faintly.

Scarlatina is sometimes the forerunner of an attack of chorea. Other
diseases, whooping cough or measles, may also be the immediate cause
of an attack of chorea, but it is generally in cases where there is a
predisposition to the disease.

The connection between pregnancy and chorea is of great interest.
Barnes[12] has collected 58 cases, and Bodo-Wenzel[13] has added 8
more, making 66 in all. Of 51 of these patients, 31 were primiparæ,
and in the majority of cases the ages were between twenty and
twenty-three years. Four cases which came under my own personal
observation were all young primiparæ, and were between the second and
fourth months of gestation when the disorder began. The affection
usually appears in the first half of pregnancy. It may cease before
the eighth month or may continue to the end of gestation. Sometimes it
persists after delivery. It does not necessarily occur in patients who
have had the disease in childhood, but from the above cases it would
seem that an attack in one pregnancy would tend to its recurrence in
another. Of the 66 cases, 14 {444} had had chorea in previous
pregnancies. Sometimes the chorea appears only at the time of labor.

[Footnote 12: _Obstet. Transactions_, vol. x. p. 147.]

[Footnote 13: _Ziemssen's Cyclopædia, loc. cit._, p. 428.]

The immediate cause of chorea in pregnancy, when a cause can be found,
is most often fright or rheumatism. In two of my own cases the
patients were unmarried. Of the 66 cases of Barnes and Wenzel, fright
is named as a cause in 7, and in 7 more rheumatism and endocarditis
are stated to have preceded the attack.

Climate has been supposed to have a marked influence upon chorea. It
was thought to be less frequent in warm than in cold regions; but
Hirsch denies this, and Weir Mitchell[14] states that it does not
appear to exist to any less extent in the southern than in the
northern portion of this country.

[Footnote 14: _Loc. cit._]

Season, according to Mitchell,[15] largely affects the production of
chorea. He has gone to great pains to collect statistics on the
subject. He shows that the majority of attacks in his cases occurred
in spring. This agrees with Wicke,[16] who found that among 35
relapses, 13 were in spring, 12 in winter, 9 in autumn, and 1 in
winter. On the contrary, Hammond[17] found 54 attacks in the six
months from October to March, and but 28 in the remainder of the year.
Gerhard[18] in a study of 80 cases found that of 68 attacks, 39
occurred in spring, 10 in summer, 7 in autumn, and 12 in winter. In
Mitchell's cases a study was made of 170 attacks. In the spring and
summer months there were 115 attacks against 55 in the winter and
autumn months. This observer does not find that rain or dampness has
any notable effect in causing the disease, but that the influence of
storms is probably great.

[Footnote 15: _Loc. cit._, p. 128.]

[Footnote 16: _Ziemssen, loc. cit._, p. 443.]

[Footnote 17: _American Journ. Med. Sciences_, July, 1876.]

[Footnote 18: _Loc. cit._, p. 715.]

Mitchell has written upon the relation between race and chorea. He
states that in answer to a circular bearing on this question, sent out
by the Smithsonian Institution, he has received a large number of
letters from physicians in our Southern States and the West Indies.
The general testimony was that chorea is rare among negroes.

Among the exciting causes of chorea are fright or mental apprehension
of some kind. Of my 279 cases, 44 were ascribed to fright.

Malaria has been pointed out as influencing the production and course
of chorea. Kinnecut has reported some cases in which the movements
were aggravated with a certain periodicity.

Chorea may also be brought on by reflex irritation from nerve-injury.
In a case which I saw in the practice of John H. Packard several years
ago there was an injury to one of the digital nerves of the thumb from
a splinter, which was the apparent cause of an attack of chorea; a
portion of the nerve was excised, and the chorea ceased in a short
time.

I have lately seen a case in which an attack of chorea came on
apparently in consequence of a severe mash of the finger. The finger
had been crushed by the runner of a sled, and the choreic movements
began before the wound was healed.

Hamilton[19] has found chorea associated with eczema. He saw a case in
which eczema of the calves of the legs and of the scalp developed at
the same time with an attack of chorea. Both got well about the same
time.

[Footnote 19: _Nervous Diseases_, p. 490.]

{445} SYMPTOMS.—An attack of chorea is usually preceded by more or
less failure of the general health and evidences of some mental
disturbance. It is quite common to be told by the parents of a child
suffering from chorea that the little patient had seemed unwell for
some time previous to the attack; that the appetite had failed, and
that the child had looked pale; that he had been irritable or
excitable, and at school the teacher had complained of restlessness or
inattention in the pupil. In a little girl who was brought to me
recently with her second attack of chorea her mother stated that for
several days before the outbreak the child had been in excessive
spirits, and that she had been singing loudly and in a peculiar
manner. The same symptoms had preceded the first attack. Sometimes
nothing is observed until it is found by the parents or teacher that
there are abnormal twitchings and movements of the limbs.

At first there is a general restlessness and fidgetiness. The child
may be punished at school for not keeping still or for dropping
things. Soon irregular movements of groups of muscles are seen. The
shoulder is shrugged or the fingers move spasmodically. At first the
patient is aware of the movements and tries to control them, but
before long the twitching and jerking are constant, and extend to most
of the voluntary muscles of the body. He is then unable to control
them for any length of time.

The sudden jerk of a limb followed by an odd grimace, the quick
protrusion of the tongue, and the rolling of the eyes or snapping of
the lids give a characteristic picture which can hardly be mistaken.

The extent of the movements varies in different cases. In some they
are slight and affect only certain muscles. Often the disorder is
confined to one lateral half of the body. In other cases the movements
involve all the limbs and the trunk, and are so violent and constant
that the patient does not seem to have a moment's rest. The trunk may
be suddenly drawn backward, then the arms are extended or thrown up,
and the legs flexed and tossed about with great quickness. Sometimes
the patient is thrown off the bed or from the chair on which he may be
to the floor.

The speech is often affected. The patient speaks in a thick or jerky
manner, as if the tongue were too large for the mouth, and saliva
usually flows in great quantities. Sometimes in bad cases there are
involuntary utterances made at frequent intervals.

The features undergo contortions continually, and when at rest relapse
into a condition of vacancy which makes the patient look almost
idiotic. The expression of a child with chorea is so peculiar that the
disease may almost be diagnosticated by this.

During sleep the movements usually cease, but generally the patient is
restless while asleep, and in some instances the irregular movements
continue even at this time.

The mental condition commonly shows some change. The child is
irritable and peevish, cries and laughs readily, or is sullen and
morose. Sometimes he is violent to those about him, but this is rare.
Intellectually the patient suffers somewhat. He is not able to study
as before, and the memory may be impaired. Sometimes there is a mild
form of dementia.

{446} During the course of the disease there may be exacerbations, and
sometimes after convalescence has seemed established there are
relapses.

Recovery is gradual, and as the abnormal movements cease the mental
condition improves, and the patient regains his health without any
traces of the disease remaining.

We will now consider some of the symptoms separately. First, as to
disturbances of motion. As before remarked, the disorderly movements
occur soon after the general restlessness is seen. They most commonly
begin in one upper extremity. The hand is thrown into various
positions, the fingers are flexed and extended or separated, and all
of the movements occur with great rapidity. In a day or two the whole
arm is affected, and then the leg of the same side is involved in the
jerkings and twitchings. In many cases the facial muscles are
contorted, the mouth is pursed up or opened wide, and then quickly
twisted into some other shape. If the patient is told to put out his
tongue, it is protruded after a moment's hesitation, and then suddenly
retracted, the jaws coming together with a snap. A smacking sound is
made with the lips quite often, and words are uttered involuntarily.
The movements may remain confined to one side of the body,
constituting what is called hemichorea. This is quite common, and the
right side is rather more frequently involved than the left. There is
so great difference of opinion among authors on this point that it is
probable that one side is affected about as often as the other. Of 252
cases which I have examined, 69 were right and 43 left hemichoreas.
Gerhard[20] found in 80 cases of chorea that 32 were unilateral; of
these 20 were right and 12 were left. Sée, however, found that in 97
of 154 cases the movements were either confined to the left side or
were more marked on that side. He states that in his experience the
proportion between left and right hemichorea is as 37 to 27. Pye-Smith
in 33 cases of unilateral chorea found 15 on the right and 18 on the
left side. Many cases which begin as hemichorea soon become general.

[Footnote 20: _American Journal of Med. Sci._]

The disease reaches its greatest severity in about two weeks, and if
the case is a bad one we find by this time all of the voluntary
muscles are in constant movement. At this time the French name for
chorea, folie musculaire, is most appropriate. Patients are often
unable to walk or to sit up, and sometimes they may be thrown from the
bed by violent spasmodic movements of the trunk. Strange as it seems,
patients rarely complain of fatigue, notwithstanding the violent
muscular exercise. This is probably because each set of movements is
of short duration and is constantly changing its seat.

As a rule, the movements cease completely during sleep or under an
anæsthetic. Sometimes occasional twitchings of muscles are seen in
sleep, and in rare instances we are told by the parents of a child
with chorea that the movements are as active in sleep as in the waking
hours.

The movements of chorea occur either while the limbs are at rest or
under the influence of voluntary effort. This fact has been pointed
out by Mitchell and by Gowers. In some cases the movements are most
marked when the patient is at rest. If a directed effort is made to
use the member for a time, the choreic movements are suspended. For
example, a patient may be able to carry a glass of water to the mouth
without {447} spilling a drop, while a moment before the hand may have
been performing a continual dance. I have often observed that while
the limb to which the whole attention has been directed in performing
some movement has been steadied, the other limbs become violently
agitated.

In another class of cases the movements are comparatively slight when
the part is at rest, but when a motion is attempted the disorder of
the muscles is so much increased that it is almost impossible for the
act to be completed. The patient is told to pick up some small object:
he throws the hand out toward it, and it is jerked away before he can
grasp it. He again puts the hand forward, reaches the object, and the
fingers open and shut and sprawl over the article before it is taken
up. Sometimes it cannot be grasped at all. This has been called
choreic ataxia, but it is only one type of the cases commonly seen.

This brings us to the influence of the will on the movements in
chorea. There are some cases, as mentioned above, in which the
movements may be controlled by the will for a brief period, but they
will sooner or later return. In other cases it is quite impossible for
the patient to check the movements at all, and one frequently sees in
a case of hemichorea the sound hand used to grasp the other, so as to
control the movements. We have referred to this because of Niemeyer's
opinion that corporeal punishment would shorten an attack of chorea.

Chorea is sometimes confined to a single muscle or group of muscles.
When limited in this way it is generally in the head, face, or perhaps
in the shoulder. These cases of localized chorea have been spoken of
by Mitchell as habit chorea.[21] They are often very obstinate in
resisting treatment, and sometimes last during life.

[Footnote 21: _Lectures on Nervous Diseases_, p. 146.]

PARALYSIS.—Not infrequently in chorea there is paralysis to a greater
or less extent. It is generally one-sided, and most often involves the
upper extremity. The limb affected is the one in which the movements
were most violent. The arm may hang entirely powerless or it may be
only enfeebled, and feeling to the patient like a dead weight. The
paralysis always recovers with the chorea or soon after.

POST-PARALYTIC CHOREA.—Under this term Mitchell and Charcot have
described a variety of chorea which is seen in patients after an
attack of hemiplegia. The movements are chiefly on voluntary effort,
and are those of inco-ordination. They come on from one to several
months after an attack of unilateral paralysis, and are sometimes seen
in cases in which almost complete recovery has taken place. Mitchell
has reported[22] a case which was under my care for several years, and
which he saw in consultation with me. This patient had two attacks of
left hemiplegia, the last being fatal. After the first attack there
was great gain of power to use the arm and leg, but the movements were
performed awkwardly and with an irregular jerking movement. A
post-mortem examination revealed a spot of softening the size of a
filbert in the left corpus striatum, which was apparently recent, and
a point of red degeneration in the right crus cerebri. The vessels at
the base of the brain were extensively atheromatous.

[Footnote 22: _American Journal of the Med. Sci._]

Of the electrical condition of the muscles in chorea but little is
known. Rosenthal[23] found increase of faradic contractility in three
cases of hemichorea, and the galvanic test showed a high degree of
excitability, {448} demonstrated by the fact that weak currents gave
contractions at cathodic closure, or even tetanic contractions, and
also contractions were produced at cathodic opening.

[Footnote 23: _Ziemssen's Cyclopædia, loc. cit._, p. 434.]

The affection of speech which is so common in chorea is due to
disordered action of the laryngeal muscles, or it may be from choreic
action of the abdominal muscles. Sometimes it is chiefly from the
awkwardness of the tongue. The usual form of trouble is that the
patient speaks in a staccato manner and the syllables seem as if they
were driven out. When the chorea is in the laryngeal muscles, the tone
and pitch of the voice are altered.

Chorea of the heart is sometimes spoken of, but it has never been
satisfactorily demonstrated that there is any real disorder of cardiac
rhythm in chorea. It is not unusual in chorea to meet with over-action
or palpitation of the heart, but these conditions do not necessarily
depend on the disease.

Valvular murmurs are often met with from the beginning of an attack.
In some instances they are the result of an endocarditis, but
frequently they are functional or anæmic. They are usually heard at
the apex. Sometimes there is a reduplication of the first sound,
giving the idea of a want of synchronism in action of the two sides of
the heart; but this is probably not the result of chorea of the heart.
I recall one patient, a child of seven or eight years, in whom the
reduplication of the first sound was very distinct during an attack of
St. Vitus's dance. She was brought to me at the beginning of a second
attack a year later, and the reduplication of the cardiac sounds was
heard again, so it is likely that it had continued during the
interval, and was probably a congenital condition.

The pupils are commonly dilated in chorea and respond sluggishly to
light.

REFLEXES.—I have examined the condition of the patellar reflex in 50
cases. In 26 of these it was present in normal degree, in 15 it was
diminished, and in 9 it could not be excited. In one patient it was
absent during the height of the choreic movements, but could be
readily produced after the patient had recovered. The condition of the
reflexes has also been examined by Joffroy and Saric,[24] and they
found that of 16 cases of chorea the reflexes were abolished or
diminished in 12.

[Footnote 24: _L'Union médicale_, Sept. 22, 1885.]

SENSIBILITY.—Authors state that disorders of sensation are met with in
chorea, such as localized anæsthesia or a general hyperæsthesia: I
have never met with any such instances. Patients often complain of
pain in the joints or in the limbs, and this may be unaccompanied with
swelling or tenderness on pressure. Tenderness on pressure over the
vertebræ is rare in my experience, although others speak of its being
of frequent occurrence. Mental disorders are generally present, but
only to a slight extent. There is almost always irritability of temper
and peevishness. The most sweet-tempered children become cross and
perverse, laugh immoderately at trifling things, or cry as readily if
they are annoyed. There is generally failure of memory and incapacity
for study or thought. In most cases, however, this exists to so slight
an extent as not to be noticed except on very close observation.
Sometimes there is marked mental disorder amounting almost to
imbecility, and occasionally the mental weakness remains for some time
after the motor disorders have recovered.

{449} The condition of the pulse is generally unchanged, but sometimes
it is abnormally frequent. The temperature, according to Von Ziemssen,
is unchanged.

The nutrition generally suffers. The patient rapidly loses flesh, and
becomes anæmic; the skin grows dry, and the hair gets harsh. The
digestion is apt to be disordered. The tongue is large, pallid, and
coated thickly, and there is sometimes nausea or vomiting. The
appetite is not good. The bowels are often constipated. The urine has
been examined by several observers. Bence Jones found an excess of
urea at the height of the disease. Albumen is not present except
accidentally, but there is usually an excess of phosphates. In several
cases in which we have examined the urine at the Infirmary for Nervous
Diseases we found that the specific gravity was high while the chorea
was at its height, but fell to normal as the patient recovered.

Chorea is spoken of as acute and chronic, but all cases are more or
less chronic. Those cases which last eight or ten weeks may be
considered acute, while those running on for months or years are
properly called chronic.

DURATION.—Considerable difference of opinion exists as to the duration
of chorea. Some writers speak of three or four weeks as an average
attack. Gray and Tuckwell, in a series of cases treated by the
expectant plan,[25] found an average duration of ten weeks.
Occasionally a patient is seen with an attack of chorea which lasts
only a few days. The parents of a little patient whom I saw a few days
ago assured me that her second attack lasted only a week. They are
educated and intelligent persons whose statement can be relied upon.

[Footnote 25: _Lancet_, Nov. 28, 1876.]

The course is not always regular. In some cases the disease gradually
reaches a crisis, remains stationary for a few days, and then by
degrees declines; in others there are exacerbations. The patient will
seem to be almost well, and then become very much worse for a time.
Relapses are not infrequent, and are generally caused by fright or
excitement.

The recurrence of attacks of chorea is well known. A child who has had
the disease one year may have it a second or third year. It is most
likely to recur in the spring. Some cases have as many as five
attacks, but as puberty approaches the attacks are lighter, and
finally cease. Of 282 cases to which I have referred, 198 were first
attacks, 47 had had chorea twice; 23 were in their third attack, 8 in
the fourth, and 3 in the fifth attack.

TERMINATION.—The disease in most instances terminates in complete
cure, but sometimes there is nervousness or want of co-ordination
remaining for a time. Rarely the inco-ordination or a certain
quickness in movement becomes permanent.

Death is a rare termination of chorea except in pregnancy. If it does
occur, it is usually from some complication. In pregnancy the
mortality is great. Of 64 cases collected by Wenzel, 18 died. In
Philadelphia, in seventy-four years from 1807 to 1881, there have been
but 64 deaths from chorea; of these, 38 were under twenty years, and
26 over that age.

Hutchinson reports a fatal case in a boy of twelve years.[26] After
complaining of headache and rheumatic pains for several days, choreic
{450} movements began. They soon became general and very violent. At
the end of two weeks he was admitted to the Pennsylvania Hospital. At
this time the patient was so extremely convulsed that it was
impossible to keep him in bed without tying him. The movements
continued but little abated, and the child died in two days.

[Footnote 26: _Philadelphia Med. Times_, vol. vi. p. 535.]

Another case of unusual interest is reported by Hunt.[27] The patient,
a man of twenty-nine years, had suffered from chorea of the face and
arms for years. In consequence of a fall on the pavement he fractured
the left humerus. The movements were immediately exaggerated, and in
spite of a carefully adjusted splint it was impossible to keep the arm
at rest. The fragments were in a state of constant movement, and the
points of bone threatened to penetrate the skin. The skin was so much
excoriated that it was determined to dispense with the splint and
attempt to keep the limb at rest by the administration of morphia
hypodermically in half-grain doses three times daily. This failed to
keep the arm quiet, and the seat of fracture became greatly inflamed.
No form of appliance or medication succeeded in keeping the arm at
rest, and the patient finally sank and died from exhaustion on the
tenth day after admission to the hospital. The post-mortem examination
revealed no gross lesion of the brain or cord. No microscopic
examination was made of the brain.

[Footnote 27: _Pennsylvania Hospital Reports_, vol. ii.]

MORBID ANATOMY AND PATHOLOGY.—In a disease so seldom fatal as chorea
it is not surprising that there have been but few post-mortem
examinations made. In the earlier autopsies, before the microscope was
extensively used, but little of value was recorded. Sée, who collected
84 cases in which post-mortem examinations were made, reported that in
16 no changes were found in the nervous system. In 32 there were
lesions in the brain and nervous centres, usually softening and
tuberculosis, and in the remainder inflammatory changes in the serous
membranes. In 29 there were evidences of heart disease. Sée considered
that but few cases of death in chorea were caused by inflammatory
diseases of the heart, but that the majority should be referred to
nervous excitement and anæmia.

Ogle[28] in a report of 96 cases of chorea mentions 16 which were
fatal. Post-mortem examinations were made in all of these. Cardiac
lesions were found in 13. In 10 of these deposits were found upon the
valves, and in 3 there was some change in the pericardium. He speaks
of having noted congestion of the nervous centres six times, and
softening of the cord once.

[Footnote 28: _Brit. and For. Med.-Chir. Review_, Jan., 1868.]

In all of 11 autopsies reported by Pye-Smith[29] there were cardiac
lesions found. In every case old or recent deposits were observed upon
the valves. In two instances the heart was hypertrophied, and in one
there was pericarditis. Changes in the nervous system were less often
found by this writer. In 1 case there was hyperæmia of the cord, and
in 3 cerebral hyperæmia.

[Footnote 29: _Guy's Hospital Reports_, 1874.]

Dickinson found in 22 fatal cases of chorea 17 in which the heart was
diseased. “In every instance making up the large tale of cardiac
disease there were recent vegetations on the mitral valve, and often
also elsewhere.”

In the fatal case of Hutchinson referred to above the heart was found
diseased, the aortic valves were incompetent, the leaflets being
swollen {451} and softened, and the aorta was atheromatous above the
sinus of Valsalva.

Of late years a number of careful autopsies have been made in cases of
chorea. The brain and spinal cord have been closely examined, and in
almost every instance some lesion has been found in both of these
organs.

Steiner reported in 1868 the results of post-mortem examinations in 3
fatal cases of chorea. In 1 case he found cerebro-spinal anæmia,
serous effusion into the spinal canal, and proliferation of the
connective tissue in the upper part of the cord; and in another
hyperæmia of the brain and cord.

Elischer,[30] who reports a fatal case in a parturient woman who had
an attack of chorea in her eighth year, two in her sixteenth year, and
another in a previous pregnancy, found at the autopsy hyperæmia and
œdema of the brain and gray substance of the cord. Microscopically,
the brain showed fatty, amyloid, and pigmentary changes in the
nerve-elements and vessels of the large central ganglia, small
secondary extravasations of blood in the connective tissue, and
numerous emboli in the smallest vessels, especially in the cortex. In
the spinal cord there was seen abundant proliferation of nuclei in the
adventitia of the vessels. In the central canal serum was found, and
the surrounding connective tissue was harder than usual.

[Footnote 30: _Cyclopædia of the Practice of Medicine_, Von Ziemssen,
vol. xiv. p. 450.]

Dickinson has contributed an excellent paper on the pathology of
chorea.[31] He relates the particulars of the autopsies in 7 fatal
cases in which he personally made microscopical examination of the
brain and spinal cord. He also adds the results of post-mortem
examinations in 17 other cases at St. George's Hospital and at the
Hospital for Sick Children. In all of the 7 cases in which microscopic
examinations of the brain and cord were made there were found
hyperæmia of both of these structures, in many instances hemorrhages
into the substance of the nervous tissues, dilatation of the smaller
vessels, and in chronic cases sclerotic changes in the course of the
vessels. “The first visible change,” he remarks, “would seem to be the
injection or distension of the arteries, succeeded by extrusion of
their contents, to the irritation and injury of the surrounding
tissue.” The changes seemed to affect both brain and cord in all
cases. The parts of the brain most constantly affected lay between the
base and the floor of the lateral ventricles in the track of the
middle cerebral arteries, the substantia perforata, the corpora
striata, and the beginning of the Sylvian fissures. “Of the cord no
region was exempt, but perhaps the cervical and dorsal regions were
usually more affected than the lumbar. With regard to the vertical or
physiological divisions of the cord, these all, whether white or gray,
shared in the vascular destruction; this condition, however, was
usually most marked in the vessels belonging to or in connection with
the lateral part of the gray matter about the root of each posterior
horn. And it is to be observed that this was also the chosen situation
of the more definite and special changes, whether hemorrhagic (as in
two instances), sclerose, or exudatory. Speaking generally, the chosen
seats of the choreic changes are the parts of the brain which lie
between the beginning of the middle {452} cerebral arteries and the
corpora striata—the parta perforata; and in the cord the central
portion of each lateral mass of gray matter comprising the root of
each posterior horn.”

[Footnote 31: _Medico-Chirurgical Transactions_, vol. xli. p. 1,
1876.]

The embolic theory of chorea has been held by several investigators,
among them Hughlings-Jackson. It is undoubtedly an attractive and
reasonable view, especially when we consider the large proportion of
cases in which there is valvular disease of the heart. Dickinson,
however, does not consider this hypothesis tenable. In none of the
cases in which he made post-mortem examinations did he find evidences
of embolism. “In none of the instances described were decolorized
fibrin, detached clots, or signs of impaction detected, and the
erraticism of embolic accident was wanting: the constancy indeed with
which the changes repeated themselves in certain positions, and the
equality with which they affected both sides of the body, are
conclusive objections to this hypothesis. The corpora striata, for
example, were affected with almost absolute symmetry, notwithstanding
that these bodies receive their blood respectively from the right and
left carotids and different parts of the aortic arch.”

Rheumatism is associated with or precedes chorea in a large proportion
of cases, and this was pointed out by Kirkes in 1850 and again in
1863. This connection between rheumatism and chorea, and the frequent
occurrence of endocarditis in chorea, has led some authors to believe
that the endocarditis is always rheumatic, and that the chorea is the
result of the endocarditis. Dickinson, however, points out that in
cases in which there is a distinct history of the chorea beginning
suddenly from fright there are often well-marked cardiac murmurs
heard. He believes that in all cases of chorea in which there are
cardiac murmurs they are due to endocarditis, and suggests that in
these cases from fright the endocarditis is due to irregularity of
cardiac action. This, of course, is mere hypothesis, and we must bear
in mind that in all cases of chorea there is anæmia, and that the
murmur may be purely functional.

H. C. Wood, in a communication read before the College of Physicians
of Philadelphia,[32] gives his views of the pathology of chorea, based
upon the results of post-mortem examinations made in a number of dogs
who had the disease. He believes the history of chorea to be this:
“Owing to emotional disturbance, sometimes stopping of various vessels
of the brain, or sometimes the presence of organic disease, there is
an altered condition of the ganglionic cells throughout the
nerve-centres. If the cause is removed and the altered condition of
the nerve-cells goes only so far, it remains what we call a functional
disease. If it goes so far that the cells show alteration, we have an
organic disease of the nervous system.”

[Footnote 32: _Philada. Med. News_, May 30, 1885.]

In two dogs which were choreic the movements continued after section
of the cord. This shows that in dogs, at any rate, the movements
originate in the cord. In four instances of canine chorea in which
Wool made autopsies there were found in the cords of three mild grades
of infiltration of leucocytes in the gray matter. In the fourth, in
which the dog had died of the disease, the ganglion-cells were
degenerated, and in some places had disappeared. He concludes,
therefore, that choreic movements may depend upon a diseased condition
of the motor cells of the cord.

{453} Although there are several recorded cases of human chorea in
which lesions of the spinal ganglionic cells have been found, we
cannot believe that this can be a constant lesion in chorea. The
disease is too transient in many cases, and presents too many
variations and anomalies, for the cord to be always the seat of the
diseased condition.

In an interesting paper read by Angel Money before the London Medical
and Chirurgical Society in 1885 he detailed some experiments in which,
by injecting a fluid containing arrowroot, starch-granules, or carmine
into the carotids of animals, he produced movements closely resembling
chorea; and this was found to be associated always with embolism of
the capillaries of the cord. In the discussion which followed
Broadbent and Sturges expressed their disbelief in the embolic origin
of chorea in man. Hughlings-Jackson said that he held the view of the
cerebral origin of chorea, one of his reasons being the frequency with
which the face-muscles are affected in this disease.

The probabilities are that in chorea there is a disordered condition
of the brain and cord more or less general. The lesions are no doubt
slight in mild cases of short duration, but in severe cases of long
standing there occur well-marked changes in portions of both brain and
cord. We cannot do better than to sum up the pathology of chorea in
the words of Dickinson: “A widely-distributed hyperæmia of the nervous
centres, not due to any mechanical mischance, but produced by causes
mainly of two kinds—one a morbid, probably a humoral, influence which
may affect the nervous centres as it affects other organs and tissues;
the other, irritation in some mode, usually mental, but sometimes what
is called reflex, which especially belongs to and disturbs the nervous
system, and affects persons differently according to the inherent
mobility of their nature.”

DIAGNOSIS.—The only diseases for which chorea may be mistaken are
paralysis agitans and disseminated sclerosis. The former occurs only
in adult life, and the tremor is of a regular rhythmical character. In
the latter the tremor occurs only on voluntary effort, and is also
more regular than the movements of chorea. There are forms of
congenital sclerosis seen in children which closely resemble chorea.
Here the duration of the disease and the association of contractures
with it distinguish it from chorea.

Hysterical subjects have a form of chorea which can only be
differentiated from the true disorder by noting the general hysterical
character of the case and the result of treatment, which strongly
influences the will-power of the patient.

PROGNOSIS.—In the great majority of cases this is favorable. If the
disease occurs in childhood and is without complications, recovery
generally takes place spontaneously after a few weeks. Should the
movements be violent and continuous, so as to interfere with sleep and
the taking of food, or should there be any complication, such as acute
rheumatism or cardiac disorder, then the prospect of recovery is not
so good.

The prognosis as to relapses should be given with caution. If in a
child, it is possible that there will be a return of the disease after
a longer or shorter interval. It is not likely to recur until after
several months, usually at about the same season the following year.
As the child grows older the intervals become longer, and it may
safely be {454} asserted that after puberty is passed and bodily
development completed there will be no more returns of the affection.

The cure is usually complete. It must be remembered, however, that for
some time after an apparently complete cure there may be slight
inco-ordination of movements, particularly in the arms and the face.
These are shown in the unnecessary haste in making uncertain motions
or in slight grimaces, or if excited an awkwardness in the use of the
fingers.

Death is a rare termination in uncomplicated cases, especially in
children. The fatal cases are generally when acute rheumatism has been
associated with the chorea or when there has been a fracture or an
injury as a complication.

In Sée's statistics there is a mortality of 5.7 per cent. in 158 cases
in the Children's Hospital. In adults, and more particularly in
pregnant women, death is more common. Wenzel's cases referred to above
gave a mortality of 27.3 per cent.

The cause of death in chorea may be from the intensity of the disease,
and in this case the symptoms are generally violent from the outset,
increase to an extreme extent, and then collapse and coma come on. The
movements may cease when the collapse occurs, but they may continue to
the last, growing gradually less until death.

TREATMENT.—A vast number of remedies have been popular in this disease
from all ages. The medicine which is most generally depended upon at
the present day is arsenic. It is advised by most writers, and in my
own experience is decidedly the most reliable remedy for chorea which
we know. The best way to administer it is in the form of Fowler's
solution, and it should be given in large doses. I have given the
bromide of arsenic, but did not find it superior to Fowler's solution.
The amount of arsenic which can be safely borne by children with
chorea is surprising to those who have not had experience in its
administration. The medicine should be given in gradually increasing
doses until the toxic effects are well marked or until the patient is
convalescing. In a child of six years three drops may be given to
begin with, three times a day. One drop additional should be added to
the dose each day, and the child soon acquires a remarkable tolerance
of the drug. As much as twelve or fifteen drops at a dose is borne by
a child of eight years. If vomiting or much œdema of the face occurs,
the medicine should be stopped for a day or two, and then the original
dose should be taken, to be again increased as before.

Seguin recommends that the patient should begin again with the dose at
which tolerance ceased. For instance, if vomiting occurred after a
dose of nine drops, he stops the medicine for a day, and begins again
with eight drops. I have found that sometimes this causes vomiting
again, and I think it preferable to resume the medicine with a small
dose.

It is often seen that a patient becomes worse during the first few
days that the arsenic is taken, but improvement generally begins after
a week of the arsenical treatment, and is well marked after two weeks.

In obstinate cases it is of marked advantage to give the arsenic
hypodermically. Cases which do not yield to the drug when given by the
mouth often improve at once when it is given hypodermically. Chronic
cases which have resisted all forms of medication sometimes are cured
by {455} hypodermic injections of arsenic. For giving arsenic in this
way it is best to use Fowler's solution, made without the compound
spirit of lavender. It is less likely to cause abscess to form at the
point of puncture.

Other remedies enjoy a reputation in the treatment of chorea. Sulphate
of zinc is relied upon by many, and it is the means which Ross
recommends. It should be given in increasing doses like arsenic, and
very large doses may often be taken without disturbing the stomach.
Trousseau, Hammond, and Hamilton favor strychnia, but I have had no
experience in its use.

Cimicifuga and conium are both often beneficial in their effects. I
have seen the former do good when arsenic had failed. Conium to be
efficacious must be given in large doses. Eserine and hyoscyamine have
both been successfully employed, the former by Bouchut, and the latter
by Oulmont and Laurent. Recently, DaCosta[33] has reported, in a
clinical lecture at the Pennsylvania Hospital, a case of very severe
chorea successfully treated with hyoscyamine. The patient was a boy of
eleven years, and the disorder had followed an attack of acute
rheumatism. He was given 1/100 gr. of hyoscyamine three times a day.

[Footnote 33: _Philada. Med. Times_, Jan. 23, 1886.]

Ziegler[34] has recorded several cases which recovered under the use
of nitrite of amyl. The bromides and chloral are useful adjuncts to
treatment in case of sleeplessness or mental irritability. Cases of
cure by the use of chloral alone have been reported. Bouchut gave a
girl of fourteen and a half years, with chorea and dementia, 45 grains
of chloral a day for twenty-seven days. She slept most of the time,
but improvement was seen on the fifth day, and cure was completed on
the twenty-eighth day of the use of the chloral. Electricity has been
efficient in the hands of many writers. I have found galvanization of
the spine to produce a quieting effect in some cases.

[Footnote 34: _Ibid._, vol. vi. p. 486.]

Iron is always of use in chorea; it may be given during the course of
the disease, and is generally necessary in convalescence. Cod-liver
oil or malt extract should be given in feeble persons.

It is scarcely necessary to mention the other remedies which have been
recommended. DaCosta has used the bromide of iron. H. C. Wood has used
a preparation of skunk cabbage, and there are a great number of other
remedies which have been found of value.

Next to the internal means come external applications. Baths and
frictions are useful in their effect on the general health. The ether
spray to the spine or the application of an ice-bag for ten minutes
once or twice daily is sometimes found to assist the other means. Cold
douches have been advised by some, but they may do harm. The care of
the general health of the patient is of first importance, and his
surroundings should be as quiet as possible.

It is of the greatest value in bad cases to place the patient in bed
and keep him there until the symptoms improve. John Van Bibber of
Baltimore has treated a number of cases of chorea successfully by
keeping them secluded in a darkened room. Such an extreme degree of
isolation is not often necessary, and it might make a child more
nervous.

In children the patient should always be taken from school and kept
from exciting play. Plenty of fresh air and wholesome food should be
{456} insisted upon. Change of air to the mountains or to the seashore
often effects a cure in a short time.

Some cases do not appear to be benefited by any treatment. These are
the hereditary form of chorea and some of the localized choreas. The
latter are often helped or cured by the hypodermic use of arsenic even
in long-standing cases.


{457}


ATHETOSIS.

BY WHARTON SINKLER, M.D.


This disease was first described by Hammond in his work on _Diseases
of the Nervous System_ in 1871, and cases have since been reported by
many observers, among them Clifford Allbutt, Claye Shaw, Eulenburg,
Oulmont, and Gowers. The disease is named by Hammond from the word
_ἀθετος_, without fixed position.[1] The principal features are an
inability to retain the fingers and toes in any position in which they
may be placed, and the continual movements which persist in the
parts—a condition called by Gowers mobile spasm.

[Footnote 1: _Diseases of the Nervous System_, p. 722.]

Athetosis is often connected with impaired mental powers; many of
Shaw's cases were in imbecile children.

The movements of athetosis are not confined to the hand in all cases,
but they are sometimes met with in the foot, and even in the muscles
of the face and back.

The following is Hammond's original case:[2] “J. P. R——, aged
thirty-three, a native of Holland, consulted Hammond Sept. 13, 1869.
His occupation was bookbinding, and he had the reputation, previous to
his present illness, of being a first-class workman. He was of
intemperate habits. In 1860 he had an epileptic paroxysm, and since
that time, to the date of his first visit to me, had a fit about once
in six weeks. In 1865 he had an attack of delirium tremens, and for
six weeks thereafter was unconscious, being more or less delirious
during the whole period. Soon after recovering his intelligence he
noticed a slight sensation of numbness in the whole of the right upper
extremity and in the toes of the same side. At the same time severe
pain appeared in these parts, and complex involuntary movements ensued
in the fingers and toes of the same side.

“At first the movements of the fingers were to some extent under the
control of his will, especially when this was strongly exerted and
assisted by his eyesight, and he could, by placing his hand behind
him, restrain them to a still greater degree. He soon, however, found
that his labor was very much impeded, and he had gradually been
reduced from time to time to work requiring less care than the
finishing, at which he had been very expert.

“The right forearm, from the continual action of the muscles, was much
larger than the other, and the muscles were hard and developed like
those of a gymnast. When told to close his hand he held it out at
arm's length, clasped the wrist with the other hand, and then,
exerting all his power, {458} succeeded, after at least half a minute,
in flexing the fingers, but instantaneously they opened again and
resumed their movements.

“In this patient there was impairment of intellect, his memory was
enfeebled, and his ideas were dull. There was no paralysis of any part
of the body, but there was slight tremor of both upper extremities.
The involuntary movements were of the right arm, and continued during
sleep. Sensation was normal. The spasm of the muscles causes severe
pain in the arm, and keeps him from sleeping at night.” Hammond used
various remedies without relief, and had the patient under his charge
for many years. Finally, he showed the patient to the American
Neurological Society at the annual meeting in 1883, with almost
complete relief to the movements as a result of nerve-stretching.

[Footnote 2: _Ibid._]

Athetosis is found in two forms—the hemiplegic and the bilateral
varieties. In the former there has usually been an attack of
hemiplegia more or less marked, or there has been an epileptic fit or
unconsciousness from alcohol, as in Case I. There is often
hemianæsthesia or some disorder of sensation. In the bilateral type
the movements exist in all of the limbs, and are unaccompanied by
weakness or disorder of sensation. The degree of movement varies in
different cases. In some it is very slight, and can be controlled by
extreme effort on the part of the patient. In other cases the
movements are violent and uncontrollable. The muscles of the affected
limbs become hypertrophied from the constant exercise.

The following case of athetosis has come under my care:

Case II.—W. A——, aged thirteen years, male. He had good health until
1877, when at the age of six years he had diphtheria. The attack was
not severe, and he was up most of the time. About ten days after
apparent convalescence he was suddenly seized with left hemiplegia.
The paralysis was complete, involving the left arm and leg, the left
side of the face, and the muscles of deglutition. There was also
aphonia. In two weeks he began to talk, but indistinctly. In a month
he could move the arm, but the movements were inco-ordinate. At about
the same time he began to walk, but dragged the leg. The arm never
regained power of voluntary motion, but instead there came on a
spasmodic condition of the muscles which fixed the arm in various
positions, and at the same time there were kept up constant but
irregular movements of the hand and fingers. No spasmodic action of
the leg-muscles occurred until a year later. He has never walked well
since the attack of hemiplegia. The positions which the arm has
assumed have varied at different times, but it usually retains one
attitude for several months at a time. Sometimes the arm has been held
in extension; at another time it has been flexed; indeed, the
positions have been numerous. His general health improved and the
speech became perfect.

Condition on examination Aug. 14, 1884: General health good, well
grown for age. The nutrition of the affected side is good, but the
left side of the face is markedly smaller than the right, although
there is no paralysis. The position of the arm attracts immediate
attention. The arm, hand, and fingers are in extreme extension, as
shown in the cut, which is made from a photograph. The arm-muscles are
tense and rigid. The fingers are continually in motion, sometimes
flexed, sometimes extremely extended; then in a few moments they will
be widely separated or distorted in some other way. The favorite {459}
position, however, seems to be with the fingers extended until bent
backward, separated from each other, and the thumb adducted slightly.
The patient is unable to bring the arm down by a voluntary effort, but
when asked to put it by his side he pulls it down with the right hand,
and keeps it down by sitting upon the hand. The muscles of the arm are
hypertrophied, especially those of the upper arm and shoulder. The
circumference of the left arm around the biceps is almost an inch
greater than that of the right. The leg is stiff and the foot is
usually inverted. Here also the position changes at different times.
When he walks the stiffness increases and the foot is dragged. The
speech is clear and distinct, and the intellect perfect. He goes to
school, and is fully equal to or more advanced than boys of his age.
There is no evidence of cardiac disease.

[Illustration: FIG. 26. Case of Athetosis.]

The patient's condition in Oct., 1885, had changed somewhat. The arm
is in a different attitude. It is still extended, but is held down by
the side or away from the body. At times the forearm is strongly
supinated. There are still constant but slowly-changing movements of
the fingers. One plan which the patient has of keeping the arm flexed
is to put the forearm behind the back with the right hand, and it
becomes locked there by the action of the extensors. By a strong
effort of will he can slowly and with great difficulty open and shut
the fingers, and can flex the forearm. The leg is in the same
condition as before.

The resemblance between athetosis and post-paralytic chorea is very
close. Most of the cases of the former disorder which have been
reported have been of the hemiplegic type. In Case I. the disease came
on after an attack of delirium tremens, which was followed by six
weeks of unconsciousness. The first symptom the patient was capable of
noticing was numbness of the right arm and leg. The involuntary
movements came on later. This would look as if there had been some
lesion involving the left hemisphere of the brain. It is stated that
no paralysis existed when the case was examined by Hammond, but there
may have been a slight hemiplegia which had passed away. In another
case reported by the same author the peculiar movements were preceded
by hemiplegia and aphasia.

Oulmont has written a complete essay on athetosis, and has collected
therein all the literature of the subject.[3] He sustains the view of
the close connection between athetosis and post-paralytic chorea, but
he {460} considers that, although nearly allied, a difference does
exist between the two affections. He believes this is most marked in
the bilateral form of athetosis, for here the disorder is usually not
preceded by paralysis, and it is not accompanied by disturbances of
sensation.

[Footnote 3: _Étude clinique sur l'Athétose_, Paris, 1878.]

Gowers[4] has also collected a number of cases, some of which came
under his own observation, and has written a valuable treatise on the
subject.

[Footnote 4: _Medico-Chirurgical Transactions_, 2d Series, vol. xli.]

PATHOLOGY.—The symptoms point to a brain lesion, probably in the gray
matter, and a perverted condition of the nerve-cells which leads to
over-action, either spontaneously or under the influence of a motor
impulse. In most of the cases reported by Claye Shaw there was
imbecility. Charcot found in three post-mortem examinations lesions in
each instance in the posterior portion of the optic thalamus, the most
posterior part of the caudate nucleus, and the most posterior part of
the corona radiata. Gowers has made an autopsy in one case in which
there was post-hemiplegic inco-ordination affecting the arm only,
without the spasmodic fixation of the limb. In the brain was found but
one lesion, and that was a cicatricial induration of the optic
thalamus, extending across its centre beneath its upper surface, and
approaching at its outer part, but not involving, the ascending white
fibres of the crus. No secondary degeneration was found in the cord.

PROGNOSIS.—This is almost always unfavorable. In some cases the
inco-ordination decreases and the spasm becomes less violent, but it
seldom disappears altogether. One of Gowers's cases was benefited by
treatment, and two of those related by Hammond were relieved.

TREATMENT.—Many remedies have been given without marked benefit. In
Gowers's case there is no doubt that the decided improvement which
took place was due to galvanism. The treatment lasted three months,
and a descending galvanic current was used. The positive pole was put
upon the nucha, and the negative on the over-acting muscles and on the
hand and foot. One of Hammond's cases, as related above, was
apparently cured by stretching the median nerve. A prolonged course of
galvanism and some alterative, like mercury or chloride of gold and
sodium, would seem to offer the best prospect of benefit.


{461}


LOCAL CONVULSIVE DISORDERS.

BY ALLAN MCLANE HAMILTON, M.D.


Thomsen's Disease.

SYNONYMS.—Rigidité musculaire avec impuissance de la volonté; Rigidité
et hypertrophie musculaire; Myotomé congenitale.

In the year 1876, Thomsen,[1] the medical officer of Kappeln,
described a curious form of nervous disease which affected several
members of his own family, himself included. It consisted of a
tendency to cramp and limited spasm when a voluntary act was
attempted, and a seeming and sudden loss of power. This condition
disappeared after the performance of the act and its repetition. An
attempt at walking would be attended by spastic rigidity of the flexor
muscles of the lower extremities, by flexion of the thighs and legs at
an angle of 120°, so that the patient often fell forward upon his
knees. An attempt to arise from the chair was attended by the same
difficulty, the person becoming utterly helpless. The arms and legs
were most frequently affected, the trunk-muscles being usually exempt.
In some cases the muscles supplied by cranial nerves were the seat of
spasm, so that the patient could not close his mouth nor shut his
eyes. Westphal, Erb, Peters, Schönfeld, Engel, and others have
reported about eight cases in all, and in addition to the symptoms
above referred to it was found that mental excitement and cold chiefly
precipitated the seizure. The sphincters were never affected, and the
general nervous functions were not impaired. The patients talked
stiffly, and this was probably due to a spasmodic affection of the
lips, tongue, and other articulating organs. The tendinous reflexes
were normal, but irritation of the soles produced a peculiar cramp of
the leg-flexors and bending of the knees. There is a species of
muscular increase which resembles pseudo-hypertrophic paralysis.

[Footnote 1: _Berliner klin. Woch._, Mar. 12, 1883.]

The malady seems to be of an hereditary nature, if we are to judge by
Thomsen's cases. It begins early in life, and does not materially
shorten the same. I have seen one case, a young child, which presented
the main symptoms of, and was first mistaken for, pseudo-hypertrophic
paralysis.

Westphal regards the affection as an “anomaly of muscular tonus;”
others have shed no light upon its pathology.

I believe the condition to be an occasional feature of certain organic
disorders, notably posterior spinal sclerosis, and there is a variety
of paralysis agitans where there is no tremor which presents all the
symptoms. The very rare nature of the malady and its peculiar {462}
expression render diagnosis easy. It possibly may be mistaken for
pseudo-hypertrophic paralysis in young subjects, but in this latter
disease we find electrical change in the muscles, and an absence of
the tendon reflex. An examination of the enlarged muscles will not
reveal fatty increase.


Painless Facial Spasm.

There is a form of spasm of the muscles supplied by the facial nerves
which differs from ordinary tic douloureux by the fact that there is
no pain in the former. The trouble may be one of a very limited
nature, consisting of the involvement of a few fibres, or of limited
groups of muscles, or of all the muscles of the side of the face. I
never have seen a case of double spasm, though such undoubtedly exist.

The nature of the paroxysm is cumulative, and, as a rule, the attack
increases until it reaches an acme of intensity, then quite suddenly
ceases. It often begins by a slight drawing of the corner of the
mouth, the levator anguli oris and other muscles in the neighborhood
being the seat of chronic spasms. This limited spasmodic action is
followed by further facial contractions. The orbicularis palpebrarum
is often the sole seat of the convulsive movement, and this is common
in excessive smokers.

As a rule, the trouble is peripheral and due to some reflex cause,
such as cold, injury, bad teeth, which produces reflected irritation
through the branches of the fifth nerve, or in rare cases it may be
central or due to some bony or other pressure upon the nerve in its
passage through the skull. In a recent case the trouble was of evident
central origin, and I obtained a history of lightning pains in the
lower extremities, some inco-ordination of muscles in both upper and
lower extremities, and some paresis of the facial muscles. In this
case the spasms involved all the muscles of the right side of the
face, and recurred every few minutes. They had first appeared five or
six years before I saw the patient, and had gained in frequency from
two or three daily until within the past four months they occurred, as
I have said, every few minutes. The other symptoms were of
insignificant character compared to the spasms.

Of the large number of cases I have seen, many impressed me as being
the result of a simple bad habit, yet moral or other measures did not
avail much.

It is important to diagnose certain unusual forms of facial spasm from
the petit mal of epilepsy, and careful observation will detect a
transitory loss of consciousness in the latter. It is equally
important to find a cause if any exists, and a careful examination of
the state of the teeth, the integrity of vision, and the possible
existence of aural disease should be made in all cases. In some cases
over-use of the eyes, which may be defective in their power of
accommodation, may precipitate blepharospasm. In other cases the act
of masticating hard substances or taking very hot or cold fluids into
the mouth may give rise to the spasm.

Hyoscyamine in repeated doses of from 1/200 to 1/25 grain of Merck's
crystals does more in the way of relieving the spasms than any other
drug of which I know. If this does no good, gelsemium cautiously used
is often of great service. Local galvanic applications with currents
of great intensity will form a valuable adjuvant. So far, I have never
tried {463} nerve-section or stretching in these cases, but recommend
them as a dernier ressort.


Torticollis.

SYNONYMS.—Wry neck, Rheumatismus colli, Obstipite, Cephaloxia.

Wry neck or torticollis consists essentially of a spasm of the
sterno-cleido-mastoideus, though other muscles are nearly always
involved: the result is a peculiar and striking distortion which is
quite familiar. It consists in the drawing downward and backward of
the head on the affected side, while the chin is pointed forward and
upward to the other. The disease is presented in several forms. It may
be a temporary disorder as the result of a rheumatic condition,
disappearing rapidly, or occurs as an hysterical affection, or it may
be a chronic and intractable nervous disease. We must also consider it
from the standpoint of the form of distorted motility. In some cases
there is simple tonic contraction, which may eventually result in
tense contracture, shrinking, and tendinous hardness; and in others
the attention of the physician is attracted by a species of tremor and
agitation. Unlike the tremor of sclerosis, this is uninfluenced by the
attempts of control upon the part of the patient, but is aggravated by
fatigue and excitement. It rarely happens that both muscles are
affected so that the head is drawn backward. Most of the cases are
single, chronic, and progressive, and, though very slow in the onward
march, are usually beyond the reach of remedies. The patient becomes
greatly annoyed by his infirmity, and seeks every measure to overcome
his unfortunate deformity. He commonly tries to hold his head or chin,
pressing the latter downward, or, holding his cane against his head
upon the dependent side, strives to keep it up. As a result, there is
a sagging or drooping of the affected side of the body, so that one
shoulder is lower than the other.

The disease, as a rule, begins in adult life, yet there are many young
cases.[2] Wilks calls attention to the fact that in these latter there
is apt to be some facial asymmetry on the contracted side. One side of
the head is smaller than the other, and one eye seems to be lower.

[Footnote 2: _Diseases of the Nervous System_, p. 454.]

Most of the cases I have seen have been men, though I have met with
many hysterical examples in young girls. The double torticollis
(Newnham's salaam convulsion) usually affects children, and it is the
rule to find associated strabismus and intellectual disturbance. In
the adult cases there has usually been a history of hereditary
neurotic influence and overwork.

Electrically, we find a susceptibility to both currents, and the
reaction of degeneration may be detected in the affected muscles in
old cases. The opposing muscles are usually the seat of diminished
electrical excitability.

Torticollis may be due to peripheral or deep causes. Cold, reflex
irritation, forced and uncomfortable positions, are to be mentioned
among the former, and intracranial or vertebral disease as examples of
the latter. The pathological explanation lies in a disorder of the
motor fibres of the spinal accessory nerve. Any affection of the
external branch will result in the condition above described.

{464} In young cases the PROGNOSIS is good as a rule, though this is
by no means invariably so, for sometimes the special symptoms are but
forerunners of others of a more grave character. Hysterical
torticollis is often instantly, or at least very readily, cured by
electro-therapeutics and cauterization. A well-established adult case
is almost hopeless and resists all ordinary treatment.

Many forms of TREATMENT have been recommended from time to time, and
such drugs as the bromides, chloroform, conium, and hyoscyamine are
suggested. The latter I believe to be the most serviceable remedy.
Electricity has done good in either form, and vigorous faradization
with the electric brush is earnestly recommended in hysterical,
rheumatic, or functional cases. Some years ago I devised a method
which in a number of cases has been of great service. I allude to the
combined and simultaneous use of the galvanic and induced currents. A
double electrode is applied to the back of the neck. This contains the
anodal pole of the galvanic current and the cathodal of the faradic.
The two other poles are placed—one, the galvanic cathode, over the
origin of the affected muscle, the induced anodal pole over the
weakened muscle which is not in spasm. I suppose in old cases the most
valuable treatment is that of a surgical nature. I have twice seen the
spinal accessory exsected with the result of a complete cure; and I
think this is the only sure measure. H. B. Sands of this city has
performed the operation quite successfully in other instances. Care
should be taken not to operate in cases presenting other symptoms
which suggest the remotest suspicion of organic cerebral disease, and
the existence of unilaterally increased tendinous reflexes or tremor
should be carefully looked for as contraindications.

Braces and apparatus are often worse than useless, increasing not only
the patient's discomfort, but aggravating the malady.


Eclampsia.

(_Εχλαμψις_ and _λαμβω_, “I shine,” brilliancy, flashes of light from
the eyes.—Dunglison.)

DEFINITION.—A term used to express certain irregular convulsive
attacks, as a rule due to eccentric irritation, uræmic poisoning, or
like causes, and chiefly used in connection with the convulsions of
infants.

This term has gradually been dropped in scientific medical literature,
and many authors think it useless, believing the condition to be
usually epileptoid. Nothnagel,[3] who is more liberal than many other
clinicians, says: “What is there now remaining of what was formerly
eclampsia? Are we altogether justified in still retaining the name? We
believe so, and are of the opinion that the title eclampsia should be
reserved as the name of an independent affection, which, it is true,
can at present be defined only by its clinical symptoms. We propose
that the designation eclampsia should be made use of for those cases
of epileptiform spasms which, independent of positive organic
diseases, present themselves as an independent acute malady, and in
which, so far as our present knowledge allows us to judge, the same
processes arise generally in the way of reflex {465} excitements, and
the same mechanism in the establishment of the paroxysms comes into
play, as in the epileptic seizure itself.”

[Footnote 3: _Cyclopædia of the Practice of Med._, Von Ziemssen, Am.
ed., vol. xiv. pp. 301, 302.]

If any distinction at all be made, it should be one founded upon the
fact that epilepsy itself is usually an organic disease, or, more
precisely, a disease which when established is dependent upon some
disorganization, while eclampsia is used to express those seizures of
a purely functional nature.

By far the greater number of eclamptic seizures are found among young
children. There is no uniformity in their expression or return. Any
eccentric irritation is apt to precipitate one or more attacks, and
those forms of irritation dependent upon sensory disturbances of the
mucous membrane are commonly present. The convulsions of teething
belong to this class, as well as those in which gastric disorder plays
a part; and in the first instance the cutting of the large teeth, and
in the latter the presence of indigestion with diarrhœa, are quite
commonly associated with the convulsion.

The high degree of irritability of the nervous system of children
renders them peculiarly susceptible to causes which in after years
would effect little or no disturbance; and this is especially true
before the fifth year. West and Reynolds are of the opinion that
convulsions occur in children as delirium in adults; in other words,
they are the most common expression of neurotic instability.

Infantile convulsions are usually general, and neuro-spasms are not
common, except when they are dependent upon neoplasm, ventricular
dilatation, or local meningitis. It evidently takes very limited
peripheral excitement to precipitate a general convulsion in the
child, and a familiar example is the disturbance which may involve the
peripheral branches of the fifth nerve in difficult dentition.

Eclamptic seizures occur at any time, and may be very slight: a
trifling twitching may be all, or, on the other hand, the attack may
consist of violent opisthotonos. There is great difficulty, of course,
in getting anything from a young child as to its feelings before an
attack, and I hardly think we are authorized in saying that there is
any aura or ascertainable precursor. The history of a previous nervous
state is, however, usually ascertainable, which is expressed by crying
fits, peevishness, and great restlessness. Sometimes there is a
disposition to sleep which almost amounts to stupor. The behavior of a
child is often likened to that which marks the commencement of acute
tubercular meningitis—night-terrors, grinding of the teeth, and
flushing of the face. The first convulsions may be only partial, but
in a short time their character becomes general, and they become
exceedingly violent, and are sometimes fatal. The clinical features of
an eclamptic seizure may in every respect resemble one of epilepsy,
making allowance for the age of our patient.

The stage of pallor is perhaps more extended in the child.

Handfield Jones speaks of a form of eclampsia of hyperæmic causation
in association with certain exanthemata. In children convalescing from
scarlatina he observed the development of attacks which were relieved
by carotid pressure and bleeding in subjects who presented anasarca
and other indications of renal disease.

We are familiar enough with the convulsions of puerperal women, which,
as a rule, though not always, are presented by subjects whose {466}
urine is albuminous. It can sometimes distinctly be traced to what
must be regarded as uterine excitement. Just as chorea is often a
feature of the pregnant state, so may convulsive seizures arise. The
peculiarities of the epilepsy of pregnancy will, however, be elsewhere
considered.

I shall purposely refrain from the consideration of those forms of
symptomatic infantile convulsions which mark the occurrence of
cerebral accidents or grave disease.


{467}


EPILEPSY.

BY ALLAN MCLANE HAMILTON, M.D.


SYNONYMS.—Epilepsia; l'Épilepsie (_Fr._); Fallsücht (_Ger._);
Epilessia (_Ital._); Epilepsin fallendsot (_Scand._); Falling
sickness; Fainting sickness.

DEFINITION.—According to the most recent authorities, an epileptic
attack is nothing more nor less than a discharge of nervous energy
from an overexcited, or what may be called a dynamo-pregnant
nerve-centre, or collection of centres, and the predominance of motor
or sensory phenomena determines the extent and order of the parts
involved. As a rule, an epileptic paroxysm is but a symptomatic
expression of a complex derangement, and it is best to formulate our
nomenclature with the idea, in the first place, of location; in the
second, with reference to the prominence of motor or sensory
expressions; and, finally, with regard to etiology.

HISTORY.—There is probably no nervous disease which has been more
extensively written upon (even in ancient times) than that under
consideration. We find references to it as early as the tenth century,
when it figured in the text of Avicennes. Hippocrates called it _ιερόν
νοσεμα_, or sacred malady, and _πάθοϛ παιδήιον_, or malady of
children, believing that the attacks had their origin always in early
infancy and never later. Plato and Aretæus advanced the theory that
the disease sprang from a thirst for gold, and equally absurd and
unreasonable explanations are found in the writings of the fathers of
medicine. The older French writers were diligent investigators, but
with them prevailed the tendency to explain the origin of the disease
by mysticism, and among many it was supposed to bear some connection
with the coming of St. John. The popular humoral theory of the malady
originated by Mercurialis was afterward opposed by Averrhoes and
Fernel, but even to this day it has devoted adherents. Bouchet and
Causauvieilh maintained that the disease was inflammatory—a view that
was vigorously combated by Bouillaud and Delasiauve. The theory of
Broussais—which was and is the basis of the conclusions of modern
investigators—is that it is dependent upon cerebral irritation. It is
hardly necessary to refer to the many untenable and curious attempts
that have been made to explain the pathology of the malady: suffice it
to say that many of them were as extravagant as that of Vepfer, who
considered the pineal gland to be the locus morbi of the affection—a
conclusion in which Descartes coincided. Marshall Hall was the first
writer to advance the theory of reflex irritation, {468} believing
that gastro-enteric or uterine irritation acted upon the brain. In
later years Schroeder Van der Kolk, Reynolds, and others have written
quite fully upon the part played by the medulla, while recently
numerous French and German writers—among them Bourneville, Meynert,
Sommers, and Tagges—have attached much importance to the discovery of
a sclerosis of parts lying at the floor of the lateral ventricles.

Perhaps our knowledge of epilepsy has received its greatest impetus
from the elaborate and exact researches of Hughlings-Jackson; and his
observations, taken in connection with the recent work of the numerous
students of localization, open up a new field of research, and, as
matters stand, the future study of epilepsy must be fruitful in the
extreme.

DIVISION.—It has been the custom to divide the epilepsies into
epilepsia gravior and epilepsia mitior, the haut mal and petit mal of
the French. These terms are in one way misleading, and only define
differences in degree. The terms general and limited would much more
properly express the forms of attack, and I shall use them as far as
possible in the present article. A general epilepsy is one that
corresponds with haut mal, in which there is an extensive convulsion,
absolute loss of consciousness, and perversion of a widespread
character. Limited epilepsy includes those forms in which there is a
convulsion confined to a small group of muscles, and in which loss of
consciousness plays an unimportant part. Under this latter head
belongs the form known as petit mal and those monospasms which depend
upon a cortical irritative lesion. There are other divisions which
partake of the nature of one or the other, and are unilateral and
dependent upon the destructive discharge of a motor centre. Under this
head may be placed the epilepsie partielle of the French or the
hemi-epilepsy or Jacksonian epilepsy of the English. There are also
irregular or aborted attacks—the so-called masked epilepsy—and lastly
the sensory varieties.

ETIOLOGY.—It cannot be denied that heredity plays the most important
part in the genesis of epilepsy. Nearly one-half of my own cases when
carefully investigated were clearly traceable to some inherited
predisposition. Insanity, epilepsy, and phthisis in ancestral history
stamp their constitutional imprint upon the unfortunate descendant,
and the history of ten cases from my notebook (see Table) will show
the extent of saturation that may exist in paternal or maternal
branches and the evolution of the disease in male and female subjects.
The statistics of other writers, though not showing quite so large a
proportion of cases with hereditary history as my own, are quite
significant. Gowers found that in “1218 cases, 429, or 35 per cent.,
presented evidence of neurotic inheritance.” Echeverria estimated the
proportion of hereditary cases at 28 per cent., while Reynolds fixes
it at 31 per cent. Of 980 cases, the notes of which I have examined,
many of whom have been under my personal care, 435 presented a family
history of insanity, phthisis, epilepsy, cerebral apoplexy, tumor, or
some lesser neurosis. So far as the history of hereditary influence is
known, it appears that females are more apt to present this form of
epilepsy than males, and, according to Gowers's as well as my own
investigations, the transmission comes from the mother's side more
frequently than the other. So far as my own inquiries have gone, I
find insanity more often among the progenitors of the epileptic than
any other nervous disease, and in many cases phthisis. I am {469}
{470} inclined, therefore, to give greater weight to this relationship
than Nothnagel and others. Anstie, Bastian, Savage, and other careful
clinicians have pointed out not only the close connection between
phthisis and epilepsy, but between the former disease and migraine;
and no one who has seen much of epilepsy can fail to be impressed with
the frequent association of migraine with the more serious convulsive
affection of which it is quite often the precursor. Perhaps the fact
that phthisis was found so often—in 230 of my 980 cases—may be due to
the fact that many of the patients were of the lower classes and among
the Irish, who in this country are so frequently phthisical.

  _Heredity in Ten Cases of Idiopathic Epilepsy, with Existing Disease
  or Cause of Death_.

     +------+---------------------------------------------------------
     |      |                   Paternal Ancestry.
     |      +----------+-----------+------------+---------+-----------
     |      |          |  Grand-   |            | Grand-  |
     | Sex. | Father.  |  father.  |  Uncles.   | mother. |  Aunts.
     +------+----------+-----------+------------+---------+-----------
   1 |  F.  | Died     | Suicide;  | Eccentric. |   ...   |   ...
     |      | insane.  | probably  |            |         |
     |      |          | insane.   |            |         |
   2 |  M.  | Alive.   | Cerebral  | Insane.    |   ...   |   ...
     |      |          | hemor-    |            |         |
     |      |          | rhages.   |            |         |
   3 |  F.  | Alive in | Phthisis. |    ...     |   ...   | Phthisis.
     |      | third    |           |            |         |
     |      | stage of |           |            |         |
     |      | post-sp. |           |            |         |
     |      | sclero-  |           |            |         |
     |      | sis.     |           |            |         |
   4 |  M.  | Died of  | Not known.| Phthisis.  |   ...   | Epileptic.
     |      | phthisis.|           |            |         |
   5 |  M.  | Congest- | Cerebral  | Insane.    |   ...   | Migraine.
     |      | ive head-| hemor-    |            |         |
     |      | aches.   | rhage.    |            |         |
   6 |  M.  | Alive.   | Insane.   |    ...     |   ...   | Insane.
   7 |  M.  | A con-   | Died of   |    ...     |   ...   | Insane.
     |      | firmed   | embolism  |            |         |
     |      | drunkard.| and       |            |         |
     |      |          | softening |            |         |
     |      |          | at 76.    |            |         |
   8 |  M.  | Phthisis.| Eccentric.| One        |   ...   |   ...
     |      |          |           | phthisis;  |         |
     |      |          |           | one        |         |
     |      |          |           | cerebral   |         |
     |      |          |           | tumor.     |         |
   9 |  M.  | A dipso- | A genius. | One died   | Cerebral| None.
     |      | maniac   |           | insane.    | hemor-  |
     |      | and      |           |            | rhage.  |
     |      | eccentric|           |            |         |
     |      | person.  |           |            |         |
  10 |  M.  | Most ec- |    ...    |    ...     |   ...   | Migraine.
     |      | centric; |           |            |         |
     |      | a somnam-|           |            |         |
     |      | bulist.  |           |            |         |
     +------+----------+-----------+------------+---------+-----------

     +---------------------------------------------------------------
     |                    Maternal Ancestry.
     +-----------+-------------+------------+-----------+------------
     |           |   Grand-    |            |  Grand-   |
     |  Mother.  |   mother.   |  Uncles.   |  father.  |  Aunts.
     +-----------+-------------+------------+-----------+------------
   1 | Died of   | Eccentric;  | Drunkard.  |    ...    |   ...
     | cerebral  | died of     |            |           |
     | hemor-    | cerebral    |            |           |
     | rhage.    | hemorrhage. |            |           |
   2 | Phthisis. |    ...      | One died   |    ...    | Phthisis.
     |           |             | of         |           |
     |           |             | phthisis.  |           |
   3 | Alive     | Not known.  |    ...     | Cerebral  |   ...
     |           |             |            | embolism. |
   4 | Migraine. | Phthisis.   |    ...     |    ...    |   ...
   5 | Phthisis. |    ...      |    ...     |    ...    | One died of
     |           |             |            |           | phthisis;
     |           |             |            |           | one
     |           |             |            |           | hemiplegic.
   6 | Phthisis. |    ...      | Phthisis.  |    ...    |   ...
   7 | Phthisis. | Died in     |    ...     |    ...    | Phthisis.
     |           | childbirth. |            |           |
   8 | Migraine. |    ...      |    ...     |    ...    |
   9 | Peculiar  | Migraine.   | Peculiar   | Insane,   |   ...
     | and       |             | character. | and       |
     | eccentric.|             |            | committed |
     |           |             |            | suicide.  |
  10 | Epileptic.|    ...      |    ...     |    ...    | Migraine.
     +-----------+-------------+------------+-----------+------------

     +---------------------+----------------------+-------------------
     |      Brothers.      |       Sisters.       |       Remarks.
     +---------------------+----------------------+-------------------
   1 | One a dipsomaniac;  | One epileptic.       | A history of
     | one in good health. |                      | criminal
     |                     |                      | proclivities.
   2 | One brother has     | Two sisters died of  | Peculiar cranium.
     | infantile           | organic disease of   |
     | paralysis.          | the brain; one of    |
     |                     | cerebro-spinal       |
     |                     | sclerosis.           |
   3 | Younger brother     |         ...          |
     | died of tubercular  |                      |
     | meningitis.         |                      |
   4 | No brothers.        | No sisters           |
   5 | No brothers.        | No sisters.          | Peculiar cranium.
   6 | Eight brothers and  | One died of epilepsy,|
     | sisters.            | and cerebral tumor   |
     |                     | was found; one       |
     |                     | paralyzed.           |
   7 |       ...           |         ...          | Criminal
     |                     |                      | proclivities.
   8 | One brother died of |         ...          | Child of this
     | secondary           |                      | parent was
     | tubercular          |                      | choreic.
     | meningitis, the     |                      |
     | other in an asylum. |                      |
   9 | Several brothers    | No sisters.          | Criminal
     | unaffected.         |                      | proclivities.
  10 | No brothers.        | No sisters.          |
     +---------------------+----------------------+-------------------

In many idiopathic cases we find vices of cranial conformation, bodily
asymmetry, and a history of early congenital syphilis. Laségue lays
great stress upon cranial malformation, and goes so far as to say that
all epilepsies not dependent upon some osseous trouble, either
developmental or traumatic, are not epilepsies at all. Such epilepsy,
which owes its origin to cranial asymmetry, rarely develops after the
eighteenth year. The head is most often dolichocephalic or
brachycephalic, and there is facial asymmetry. Laségue concludes that
all the convulsions are identical; that it is not hereditary; that the
attacks are always matutinal. It seems to me that Laségue's
conclusions in regard to the non-existence of epilepsies from other
causes are rather too arbitrary in view of the large amount of
evidence to the contrary. In others, a very few, we find an apparent
history of heredity explained by forceps-pressure during delivery.

So far as age and sex are concerned, and their predisposing influence,
we find that by far the greatest number of cases begin before the
twentieth year. This is the experience of Gowers, of Hammond, and of
many others. Of my own 980 collected cases in which the beginning of
the disease was known, there were—

                    Females. Males. Total.
  Under 10            103      95    198
  Between 10 and 20   171      97    268
     "    20 and 30   145      92    237
     "    30 and 50    81     136    217
  Over 50              11      49     60
                      ---     ---    ---
                      511     469    980

Of 1288 cases collected by nine French authorities, in 486, or over
one-third, the disease began between the tenth and twentieth years. In
Gowers's 1450 cases we find the following showing:

                 Cases.  |                Cases.
  Under 10        422    |  From 40 to 49   31
  From 10 to 19   665    |   "   50 to 59   16
   "   20 to 29   224    |   "   60 to 69    4
   "   30 to 39    87    |   "   70 to 79    1

In 29 per cent. of these cases the disease therefore began before the
tenth year.

As to sex, it appears that females are much more subject to the
disease than males, but this is not true at any age. Epileptics under
ten are more apt to be girls, but the proportion is nearly equal:
between ten and twenty the proportion of females is undeniably
greater. In adult cases we find that pure epilepsy (excluding
hysteria) is much more often a disease of males than females.

{471} In the hereditary form the disease in the great proportion of
cases begins before the twentieth year; and, so far as my experience
goes, this kind of the disease makes its appearance at a very early
age. The part played by particular predisposing influences appears to
be well defined. The children of syphilitic parents develop the
disease at a more advanced age than when alcoholism is found to exist.
In adult males, when the disease develops late in life, it is almost
always possible to find syphilitic or coarse brain diseases, while
among women the history of antecedent migraine or menstrual
derangement is nearly always present, and the convulsions in a very
large number of instances have a hysteroid character.

The exciting CAUSES of the disease are quite numerous. Traumatism is a
frequent and important etiological factor, and the head-injuries may
be recent or remote. It is quite common to find old fractures, with
depressions which have existed for years without any seeming bad
effects, suddenly lighting up convulsions under the influence of some
new excitement. Under such circumstances the depressed bone is quite
apt to give rise to symptoms suggestive of meningeal irritation and
inflammation, so that the diagnosis is comparatively easy. Several
observers have called attention to epilepsy which has been undoubtedly
due to cicatrices not only of the scalp, but elsewhere, and these may
or not be found in association with osseous lesions. The literature of
the subject is replete with curious cases which go to show that
epilepsy may occur from a few days to many years—even twenty—after the
initial head-injury. Unsuspected cortical pressure, the inner table
being alone depressed, is common; in fact, the cases in which the most
serious mischief is done seem to be those where the only external
evidence of violence is the contused scalp. As a consequence of such
injury we may have exostoses developed.

The influence of syphilis in the production of epilepsy is one of very
great importance. Not only has specific epilepsy characteristics of
its own, but its origin may be distinctly traced to syphilitic
infection. Cases dependent upon gross cerebral disease, such as
meningitis or gumma, are excluded from consideration, but it is
conceded by all syphilographers that an epilepsy may mark the second
stage of the disorder, and its pathological dependence is probably a
simple vascular disturbance which cannot be determined after death.
So-called specific epilepsy may be congenital.

Orwin[1] mentions as a cause the influence of prolonged lactation. In
several cases I have seen a metrorrhagia, or a loss of blood from
hemorrhoids has been followed by a readily curable epilepsy.

[Footnote 1: _Prov. Med. and Surg. Journal_, London, 1862, v. 48.]

As eccentric irritating causes may be mentioned intestinal worms, but
I am convinced that it is too often the fashion to ascribe convulsions
in children to intestinal parasites: in very young children, however,
there are frequent examples of the disease in which the attacks are
precipitated by worms. The fits are usually very severe, and are not
regular in their appearance, occurring at night-time more often than
during the day, and, though they usually disappear when the bowels are
cleared of their unpleasant occupants, may recur when once initiated,
even though anthelmintics of the most powerful kind are employed.
Gall-stones are mentioned by Ross as an eccentric cause of the
disease, but I have never witnessed a case of this nature.

{472} Sudden terror, fright of all kinds, morbid example, and other
psychic causes are detailed, and undoubtedly all have more or less
influence. Hysteroid attacks are notably precipitated by these mental
causes, and all forms of the disease are greatly modified by abnormal
exercise of the mind.

A number of writers, among them Baly[2] and Booth,[3] have called
attention to cases of the disease dependent upon carious teeth. I have
seen but one such case, where a wisdom tooth produced so much violent
inflammatory action that middle-ear disease followed, and with it
subsequent extension to the brain took place.

[Footnote 2: _London Med. Gazette_, 1851, xlviii. 534-540.]

[Footnote 3: _Am. Journ. of the Med. Sciences_, 1870, N. S. lix. 278.]

In rare cases the administration of anæsthetics is followed by
epilepsy, and Gowers alludes to a case in which convulsions were due
to the inhalation of nitrous oxide gas.

Concussion of the brain as the result of railroad injury or falls may
give rise to a progressive epilepsy which is usually of serious
character.

Reflex causes play a prominent part in many instances, though I am
inclined to think that their importance has been greatly exaggerated.
This is especially true of so-called uterine epilepsy. It cannot be
doubted that difficult menstruation, ovarian neuralgia, etc. are found
in connection with epilepsy, but whether as a cause or effect it is
not always possible to say. The fact that in some women we find accès
at periods identical with menstruation would point to a very close
relationship. Carstens[4] reports a case due undoubtedly to stenosis
of the cervix; Cohen,[5] an example in which there was a uterine
fibroid; and others have spoken of erosion of the cervix, etc. as
possible explanation of the seizure.

[Footnote 4: _Detroit Lancet_ (8), 1880, N. S. iii. 153.]

[Footnote 5: _Wochenschrift f. d. ges. Heilkunde_, Berlin, 1839, vii.
648, 673.]

The toxic forms of epilepsy hardly need discussion in this article.
Metallic poisoning, which gives rise to a veritable plumbic
encephalopathy, is rather the cause of a symptomatic than generic
epilepsy. Curious cases of epilepsies which have followed the use of
oil of tansy (Mitchell[6]), ergot, absinthe (Magnan[7]), and various
drugs show that occasionally their mode of origin may explain the
convulsive seizure. Alcoholic epilepsy I do not regard as being the
rare affection some authors consider it. In cases of prolonged
saturation, where perhaps there are no other symptoms of chronic
alcoholism, I have found it perhaps associated with the trance state
(cataleptoid) or appearing in the psychic form.

[Footnote 6: _Cincinnati Lancet and Clinic_, 1881, N. S. vi. 479.]

[Footnote 7: _Recherches sur les Centres nerveux_, Paris, 1876.]

In old persons I have found gout to have an undoubted influence in
producing the disease, there being a spasm of the cerebral vessels
which usually betokens a condition of uric-acid saturation. In these
cases the painful symptoms were not decided. Such epilepsies have
quite often preceded serious evidence of arterial degeneration.

Malarial epilepsy is rare: Jacobi[8] reports a case and Payne[9]
another. A young man was brought to me last year who had lived for
many years in a part of Pennsylvania which was exceedingly malarious.
His attacks, which were more or less periodic, were violent, and his
convulsions were {473} general and attended by very great preliminary
rise of temperature and intense congestion of the face and head. The
patient was unusually somnolent, and between the paroxysms frequently
suffered from facial neuralgia. The influences of change of habitation
and quinine determined the correctness of my diagnosis.

[Footnote 8: _Hospital Gazette_, New York, 1879, v. 41-43.]

[Footnote 9: _Indian Ann. Med. Sci._, Calcutta, 1860-61, vii. 597 _et
seq._]

Day[10] and Kerr[11] have both ascribed epilepsies seen by them to
hepatic congestion.

[Footnote 10: _Clin. Histories, etc._, London, 1866, 143-145.]

[Footnote 11: _Med. Times and Gazette_, London, 1871, i. 568.]

The important etiological relation of the exanthemata to epilepsy has
been the subject of much attention. The books are full of cases which
owe their origin not only to scarlet fever and measles, but to
whooping cough, diphtheria, and the various zymotic fevers. In 35
cases tabulated by Gowers[12] (p. 28) no less than 19 were due to
scarlet fever, while the first fit followed measles in 9 cases. So far
as my individual experience goes, I have in 23 cases found epilepsy to
be the result of scarlet fever, and this form of the disease was often
associated with other manifestations of coarse brain trouble.
Cerebro-spinal meningitis was the undoubted cause of epilepsy in 6
cases I examined. It is probable that just as smallpox acts upon the
nervous centres, so does scarlet fever, and I agree with Gowers that
the convulsions that may begin during or just after the fever are not
always due to uræmia. Bright's disease may give rise to an epilepsy,
but this can hardly be regarded as a distinct affection.

[Footnote 12: _Op. cit._]

There are many cases, especially in adults, which grow out of a
prolonged depletion of the brain—a continued cerebral anæmia. Among
these cases are some which depend upon pressure upon the great vessels
of the neck, and some due to debilitating disease of a general
character. Schulz[13] has seen a case which followed compression of
the jugular vein, and enlarged cervical glands have in other cases
acted as mechanical agents. Hammond alludes to the influence of
prolonged general anæmia in the production of epilepsy.

[Footnote 13: _Cor. Bl. Deutsches Gesellsch. f. Psych._, Neuwied,
1855, ii. 35.]

While I do not place much reliance on the claims that have been made
regarding the frequent dependence of the disease upon preputial
irritation, or that it may arise from phymosis or urethral stricture,
it cannot be denied that some cases have originated in difficulties of
the kind, and especially the former. Simmons[14] reports a case of
attachment of the prepuce to the glans in which a cure followed
separation. Disease of the testicles in certain cases plays a part in
its genesis, and Liégey[15] details an epilepsy clearly due to
testicular pressure. Some years ago I saw a case in which the pressure
of an improperly applied truss, I am now convinced, had much to do
with the development of the convulsions. The alleged sexual causes are
many, and some of them are very doubtful. A fanciful continental
writer, Montmeja,[16] believes that sodomy explained the appearance of
the disease in one of his patients.

[Footnote 14: _Am. Journ. Med. Sci._, 1880, N. S. lxxix. 444.]

[Footnote 15: _Gaz. méd. du Strasbourg_, 1856, xvi. 105-107.]

[Footnote 16: _Rev. Photo. des Hôpitaux de Paris_, 1873, v. 229-232.]

The existence of vesical calculi as an exciting cause cannot be
disregarded, and, while rare, the observations of Duncan,[17]
Muscroft,[18] and one {474} or two others have shown that the removal
of a stone was followed by a cure of the epilepsy.

[Footnote 17: _Ed. Med. Journal_, 1868-69, xiv. 140.]

[Footnote 18: _Arch. Sci. and Pract. Med. and Surg._, 1873, 1360.]

Masturbation is a popular etiological factor. I really do not believe,
even in face of the numerous alleged cases that have been recorded,
that the habit of self-abuse often results in genuine epilepsy. So far
as my experience goes, onanism is practised by epileptics as well as
by healthy boys, and when indulged in to excess is due to the
congenital moral deficiency which is so common, especially in
hereditary cases. In rare examples the frequently-repeated act may
give rise to a form of the disease of the nature of petit mal.

Gastric disorders have attracted much attention, especially from
Paget, who speaks of a gastric epilepsy and reports cases. While I do
not believe in the sole etiological influence of digestive
derangement, I have too often witnessed examples in which disorders of
this kind markedly influenced the precipitation of attacks and the
duration of the disorder.

Occasional cases of peripheral origin have been from time to time
presented, and go to support in some measure the pathological views of
Brown-Séquard. Among observers who have brought forward cases besides
those referred to on a previous page are Lande,[19] who reported a
case of epilepsy dependent upon injury of the right median nerve, and
Short,[20] in whose case a neuroma explained the cause of the
convulsions. Billroth,[21] Garnier,[22] Brown-Séquard,[23] and
Raymond[24] have brought forward cases where injury of the sciatic
nerve was the origin of the trouble, and in more than one instance a
cure was effected by excision. It seems strange that a bone
dislocation should have anything to do with the genesis of epilepsy,
yet in one case reported a severe dislocation at the shoulder-joint
explained the appearance of the attacks, and reduction was speedily
followed by cure.

[Footnote 19: _Mém. et Bull. Soc. de Méd. et Chir. de Bordeaux_, 1878,
i. 56-65.]

[Footnote 20: _Med. Essays and Observation Soc._, Edin., 1737, iv.
416.]

[Footnote 21: _Archiv f. klin. Chir._, Berlin, 1872, xiii. 379-395.]

[Footnote 22: _Union médicale de Paris_, 1872, 3d S., xiii. 656-658.]

[Footnote 23: _New York Medical Record_, 1872, vii. 472.]

[Footnote 24: _Rev. méd. de Limoges_, 1869-72, iii. 102-105.]

I have seen several cases where disease of the internal ear or injury
of the temporal bone gave rise to the most obstinate and violent
epilepsies. Westmoreland[25] and others report such cases, but more
often the epilepsy is only symptomatic of pachymeningitis or abscess.
Some years ago I presented[26] a case of genuine epilepsy in which the
seizure was produced at will by irritating the meatus auditorius. By
simply blowing into the ear the same effect would be produced. Since
then Blake and others have related examples. Quite lately a writer in
_Brain_ has collected other cases of this species of auditory
epilepsy. A year or so since I examined a patient in whom not only
hemi-epilepsy, but other unilateral symptoms, followed erosion of a
large part of the mastoid and petrous portion of the temporal bone as
the result of a bullet wound.

[Footnote 25: _Atlanta Med. and Surg. Journal_, 1876-77, xiv.
717-719.]

[Footnote 26: _New York Medical Record_, 1878, xiii. 107-109.]

The influence of climate and varying barometric pressure has been
considered by Delasiauve. His conclusion was that the attacks were
much more common during the season of the year when the prevailing
winds were from the north-west, north, or south-west.

{475} PRODROMATA.—There are various minor disturbances of sensation
and motion which may not amount to the dignity of an epileptic attack.
These may be so fugacious as to escape the attention of the persons in
whose company the patient may happen to be, or he himself may be
unaware of any disordered state of feeling. They may precede a severe
paroxysm, when they are known as warnings or auræ. The term aura was
originally applied to the familiar premonitory sensation which is so
often likened by the subject to the blowing of wind over the skin,
from whence it receives its name, but it has come to be applied to all
primary indications of a fit. Such auræ may be sensory or motor—in the
preponderance of cases the former, for motor precursors are quite
rare, and when they occur are most likely to be but one stage, though
a slight one, of the convulsion itself. There is no general rule about
the occurrence of an aura, but, so far as my experience goes, there is
great constancy in the character of the warning in each particular
case. The sensory disturbance may vary from a vague feeling of
confusion to a well-marked sensation. In many instances the patient
speaks of an indescribable mental disturbance, which may precede the
attack and last anywhere from a few minutes to several hours. This
confusional state or psychical aura is most protean in its expression.
It may simply be a heavy feeling, a feeling of tension, a sleepy
feeling; a restlessness which is manifested by the patient changing
his position frequently or wandering forth into the streets; an
irritability of temper which often lasts twenty-four hours or more,
and during the display of which he rebukes those who may be solicitous
about him, or wantonly destroys articles of furniture, or vents his
spleen upon inoffensive persons. I have had epileptic children under
my charge who were wont to bite their little brothers and sisters or
their nurses. A feeling of terror sometimes precedes the attack, and
very often there is a sense of impending danger which has no basis
whatever, and with it is associated a depth of depression which is
very painful. In other cases the patient manifests a strange
exhilaration, which may precede the occurrence of the attack for a
period of from one or two hours to two or three days; and this is made
manifest by great loquacity and a lively play of spirits. It is not
rare to find errors in the speech as indications of an approaching
attack. A minor degree of aphasia, slowness of speech, or anarthria
betrays occasionally the preparatory state which is the precursor of a
severe convulsion. By far the most common warnings, however, consist
of disorders of the special senses, and generally these are visual.
From an inspection of my notes I find that the patients saw colored
lights, rings of fire, bright objects, dark spots, luminous clouds, a
flood of light, sparks, stars, bright balls, lights which approached
them, lights which receded, fireworks, and all became dark. While many
were unable to define the color perceived, I found among those who
were positive that red was the color most frequently seen, while blue
came next; and this is a conclusion which I believe is accepted by
Jackson and others who have analyzed their cases.

Hemiopia and diplopia in rare cases precede the major attacks, and are
sometimes associated with distal pain and anæsthesia and with
supraorbital pain as well.[27] Among these ocular warnings we find
constriction of the visual field to be often present, especially in
cases where there is a {476} history of migraine. Vague disorders of
hearing, which may even amount to the dignity of hallucination, are
complained of by some persons. There may be simply roaring in the ears
or a sound of bells, and in one instance my patient declared that he
heard whisperings at the time of the seizure. Some patients smell
smoke or other foul odors, and in exceptional instances the odor of
some particular flower or of some aromatic substance, such as camphor,
turpentine, or tar, is perceived by the epileptic; and these are
probably psychical.[28] Sometimes there is a feeling of great
suffocation, constriction of the chest or of the throat, palpitation,
or vertigo.

[Footnote 27: See Sensory Epilepsy.]

[Footnote 28: For curious examples of this kind consult Sir Charles
Bell's _Nervous System of the Human Body_.]

There are disorders of cutaneous sensation of great diversity of
character, but those auræ which are of the most constant occurrence
are the epigastric, which consist of a vague sensation starting below
the sternum and ascending, its arrival at the throat being coincident
with the commencement of the fit, and the patient very often likens
its culmination to the violent grasp of a strong hand. So, too, we
find crawling sensations starting in the extremities and running up to
the trunk. These have been compared to the contact of insects in
motion or to the blowing of wind over the surface. There may be
tingling in one or two fingers or the whole hand, and such sensations
may be unilateral or bilateral. It is quite common for the sensory
warning to begin in the hand and foot of one side and to run up to the
knee and elbow. Sometimes the tongue becomes hyperæsthetic, and I have
frequently found that the gums became exquisitely tender just before
the attack. According to Gowers, 17 per cent. of his cases began with
unilateral peripheral auræ, but I think this is too small a
proportion, for, so far as I have observed, at least 30 per cent. of
all my cases in which any auræ at all could be ascertained presented
the history of a one-sided warning, beginning most often in the right
hand. Gowers says that in three-fourths of his cases in which the
attack began in the hand consciousness was lost before the seizure
extended beyond the arm, while in the others it extended much farther
before the actual fit was precipitated. In Gowers's cases he rarely
found that unilateral auræ were associated with other warnings; and
his experience, which is like my own, goes to prove that unilateral
sensory auræ and one-sided initial motor expressions go together, and
very often indicate gross organic disease. In some cases there may be
for several days a decided unilateral or general muscular weakness or
recurring chronic spasms which may be frequently repeated. In aborted
or irregular attacks there are also peculiar motor symptoms, to which
reference will be made later on.

In two or three patients I have found that the attack was immediately
preceded by a profuse discharge of saliva, and in one case the patient
had frequently bleeding from the nose. Several authors have called
attention to certain local vaso-motor disturbances which are expressed
by limited patches of cutaneous hyperæmia or anæmia, so that the
fingers—or, in fact, the whole hand—may either be swollen and of a
dusky-red color, or, contrariwise, there may be blanching and an
apparent diminution in size.

Sometimes the patient immediately before the attack makes more or less
automatic movements, pressing his hands to his head, clasping his
breast, {477} or clutching at some imaginary object, and after this he
loses consciousness and falls to the ground. In some irregular cases
the patient runs aimlessly for some distance or describes a circle,
and after a variable time, which rarely exceeds a minute or two, the
actual fit begins. Here are two examples:

Case I.—Boy aged fifteen, has been subject to somnambulism; attacks
began two years ago. He frequently when sitting at table rises
suddenly, and runs either around the room or out into the street if
possible. In thirty seconds or so he falls to the ground in a
convulsion. Always falls backward in opisthotonos.

Case II.—Man aged thirty-four. Attacks always begin by stage of
violent temper. While unconscious he runs about office, striking all
who try to restrain him; finally falls to the floor. Convulsions, when
they occur, are always severe. Sometimes running attack is the sole
feature.

This disposition to run is no less remarkable than another queer
prodroma I have seen in several patients, who began to take off their
clothing when first seized, no matter where they were or under what
circumstances. This is not, as has been suggested, the remains of a
half-formed idea that they must seek their beds because of their
impending trouble, but it is a much less complex mental act, and the
several patients I have seen were fully unconscious when they did
this, and were in places where there was no bed within reach. Equally
curious mental precursors of the attack have come to my notice, and
these I will detail subsequently.

SYMPTOMATOLOGY.—The Light Attack.—The epileptic attack may, as I have
said, be scarcely perceptible to those about the patient, or may
consist simply of a momentary loss of consciousness and very feeble
convulsive movements. Reynolds has described two forms: (1) That
without evident spasm; (2) that with evident spasm. Such seizures are
always fugacious, and consist merely in some transient loss of
consciousness and very little or no convulsive movement. The tonic
spasms prevail, if any, and the disorder of motility may often consist
simply in the arrest of some act in the performance of which the
patient is engaged. While playing the piano the patient's hands may
for a moment remain suspended over the keys he is about to strike; if
eating, the hand which holds the fork may be arrested between the
plate and his mouth. The attack consists sometimes in the rolling
upward of the eyeballs, or when crossing the room the patient may
stop, remaining quiet for an instant. Temporary unconsciousness, shown
by cessation of conversation, by change of color, and absence of
intelligent expression, accompanies the other trouble. In a
well-marked attack of petit mal the patient may move his lips
convulsively, and remain otherwise quiet, but bereft of consciousness,
for one or two minutes.

The patient sometimes loses himself and loses the thread of the
conversation, repeating what he has just said or showing his want of
appreciation of what his companion has said. To this light grade
belongs the case reported by Jackson of the individual who blew his
nose upon a piece of paper and gave the conductor £2 10_s._ instead of
twopence halfpenny.

The Major Attack.—An attack of epilepsy of the familiar severe form
may or not follow an aura. The first intimation to the bystander may
be a noise made by the patient, which is either a loud, startling,
wild cry, or a gurgling groan due to compression of the thorax and the
{478} forcible escape of wind through the vocal cords. There are three
stages of the attack: (1) The stage of tonic convulsion; (2) the stage
of clonic convulsion; (3) the reactionary stage.

The first stage of the attack is symptomatized by tonic spasms, which
may be local or general, usually the latter. It is very often
unrecognized, for its duration may be so short that it is lost in the
stage of clonic spasms, which is much more protracted. There is
usually unilateral seizure, the muscles of the face being primarily
involved, then those of the hand and upper extremity, and then those
of the lower extremity; and finally there is a general involvement, so
that the patient may be in a position of opisthotonos. In some cases
there is strong tonic contraction to one side, or pleurosthotonos. The
notes of a case which illustrates the beginning and development of
convulsion with reference to the parts involved, which I observed
carefully, are the following:

Bindewald: Epileptic attack observed at hospital for paralyzed and
epileptic, Sunday, Mar. 12, 1882:

1. Long, shrill cry which attracted my attention. It probably lasted
five seconds. At same time patient threw up arms and became
unconscious, and fell to floor. Nurses ran to him and placed him upon
bed.

2. Tonic convulsions began by fine twitchings at right corner of
mouth. These became gross, and were separated by succeeding long
intervals. Eyes directed to left side, face pale.

3. In twenty seconds twitching began in right hand and arm, which were
rigidly flexed (five seconds); then leg and foot of right side became
agitated, the face meanwhile changing in color successively from
red-gray to purple; lips purple, ears livid and purple, edges white;
eyes still turned to the left, pupils dilated, eyes widely open;
breathing stertorous and irregular.

4. General convulsions of right side.

5. Head suddenly twisted to left side; position of eyes the same. Chin
drawn down, movements moderated; still livid. A fit of coughing and
expectoration of much frothy mucus. Left side, with exception of head,
not implicated. Whole attack lasted about one minute and thirty-five
seconds. Deep sleep afterward, lasting forty-five minutes.

This attack was one of many in a confirmed epileptic, and is a fair
example of those commonly met with, though not as general as we
sometimes find. In most cases the attack appears to be very much
longer than it usually is, and the phenomena noted above, which seemed
to occupy a considerable space of time, really lasted but little more
than a minute and a half. Axenfeld and Beau fix the average period of
the attack as follows: “Duration of the complete attack, which Beau
divides into four phases: first stage, tetanic stage, five to thirty
seconds; second stage, clonic convulsions, from one to two minutes;
third stage, stage of stupor, three to eight minutes; fourth stage,
return of sensibility and intelligence. It is not complete until the
end of from ten to thirty minutes.”

To be more explicit, the manifestation of an ordinary epileptic attack
of the more severe kind is very much like this: Usually without any
warning to those about the patient he utters a shrill, peculiar cry of
a character never to be forgotten if once heard, and then, perhaps
throwing up his hands, he falls to the ground rigid and contorted. His
body may {479} be arched laterally or antero-posteriorly, his legs are
thrown out, his forearms flexed, and his fists doubled, the thumbs
being beneath the other fingers. His face may be for a moment flushed,
but the color recedes, and it assumes a dusky-bluish tint, the lips
being ashy-gray. The eyes are usually open, and the balls are rolled
up and the pupils widely dilated. The breathing may for a moment be
suspended, but it soon quickens, and becomes labored and noisy, and
the pulse grows hard and full. The tonic contractions are succeeded in
a very short time by more or less violent clonic contractions, which
increase in violence and rapidity; the jaws work and the lips are
covered with foam, which is blown in and out by the rapid inspirations
and expirations. It may be tinged with blood in the severe attack if
the tongue is bitten, which is by no means an uncommon accident. The
teeth are sometimes firmly set and the jaws locked. The head is
usually drawn to one side in the first stage, but afterward may be
rolled from side to side. The movements are now more or less general,
and occasionally the agitation is so great that the patient throws
himself from the bed on which he may be lying. The face grows more
pale, or rather more livid, and toward the end of this stage there may
be a puffiness and congestion such as are seen in partially
asphyxiated individuals, for this alteration in color is due to
dyspnœa and consequent imperfect oxidation. The patient may defecate
or pass his urine unconsciously, and sometimes we find seminal
emission. The movements, after a period varying from ten seconds to a
minute or two, become less violent, and he may talk in a silly manner,
as a person does who is recovering from profound ether
unconsciousness; or deeply sigh, and he is restless. The pulse is now
much weaker and more rapid, and may be irregular. The color returns to
the face, the patient closes his eyes, and the body is covered with
profuse perspiration. The fingers are unlocked and every evidence of
spasmodic movement disappears. He falls asleep, and remains so for
several hours, awaking with a confused feeling, headache, and no
remembrance of the attack, and is only reminded that something has
happened by his wounded tongue or lips, the bruises he has received,
or by the information of friends. He looks jaded and tired, and is
indisposed to exert himself for several days if the attack has been at
all severe. The transition from the attack to the normal state is not
always the same. Some patients do not sleep at all, but after being
dazed go about their occupation. This is even true occasionally of the
severe form of disease.

The usual termination of the attack is, however, by sleep preceded by
a period of confusion. The patient, after coming out of the clonic
stage, mutters incoherently. He is apt to pass large quantities of
wind from his bowels, or vomits. This is attended by a subsidence of
the spasmodic movements, and perhaps by oscillation of the eyeballs.
The pulse loses its rapid, hard character, and the reaction brings
with it diminished frequency of respiration and the evidence of
exhaustion.

Special Symptoms.—The eyes are, as a rule, open, and, there being
spasmodic movement of the ocular muscles, we find that the balls are
either rolled up or directed away from the side in which the spasms
begin. This is especially true in those epilepsies due to cortical
disease, and the same law of conjugate deviation laid down by
Bourneville may be remembered.

{480} The pupils are dilated pretty much throughout the fit, though
they may vary, and a transient contraction may occur at the
commencement of the first stage. During the clonic stage, especially
toward the end, they not infrequently undergo a species of
oscillation. The interparoxysmal state is revealed by a very great
mobility of the pupil, which has been observed by Gray and others.
Gray is disposed to consider it a diagnostic indication of value, but
so far I have found it only in two-thirds of my cases. Dilatation of
the pupil I believe to be a very constant feature of epilepsy.

The ophthalmoscope reveals in certain cases an abnormal increase in
the circulation at the fundus, in others a very decided emptiness of
the retinal vessels. Jackson is disposed to consider that certain
visual auræ depend upon spasm of the arterioles in this location.
Loring, whose opportunities for research have been very great, is not
disposed to attach much importance to the ophthalmoscopic appearances,
at least during the periods between the fits.

The pulse of the epileptic between the paroxysms is small and
irritable. Voisin has found the following changes: “Two or three
seconds before the attack it becomes rapid, sharp, and the
sphygmographic curves are higher, rounded, and nearer together. When
the attack begins we see five or six little undulations in the course
of the ascending line, and the curves are higher and more accentuated.
Several minutes after the attack there is dicrotism, and the line of
descent is very sharp, the angle with the ascending being quite acute.
This form of pulse lasts an hour or half hour after the attack. There
is in some cases great irregularity, with paroxysms of cardiac pain
resembling angina pectoris. There is occasionally epistaxis or more
marked hemorrhages.” Parrot speaks of hemorrhages from the eyes and
ears, and occasionally the cerebral congestion is so great as to
result in cerebral hemorrhage in old subjects.

The temperature is usually lowered before the attack, but the surface
temperature is increased during or after the second stage.

Cutaneous sensibility is often very much disturbed. Spots of
hyperæsthesia and anæsthesia are sometimes left after the attack. The
scalp is not infrequently exceedingly tender. The sensory troubles
have been alluded to as prodromata of the ordinary motor attack. Some
attacks of the sensory variety in which psychical excitement plays a
part are characterized by unilateral and persistent formications.

A consequence of some epileptic paroxysms is the appearance of
petechiæ, chiefly upon the face, neck, and upper extremities. The skin
of old epileptics is harsh, cold, and rough, and the face is apt to be
studded with spots of acne even when the patient is not taking the
bromides. The hair is stiff and dry, and the ears and tip of the nose
are apt to be the seats of a passive and old hyperæmia.

The urine of epileptics is apt to contain evidence of muscular waste,
and an increase in the amount of earthy phosphates as well. Zapolsky
found, however, that immediately after the attack there was diminution
in the quantity of the phosphates. The occurrence of glycosuria has
been noted by numerous clinicians. De Renzi[29] has published an
interesting article. I have seen no less than six well-marked cases
within two years in which constant glycosuria was a feature of the
disease, but in two of {481} the patients well-marked symptoms of
disease of the pons were present. After the paroxysm it is by no means
uncommon to find the urine loaded with albumen. Otto, Mabille,
Saundby, Bazin, and other writers speak of a transitory albuminuria.
Kleudgen,[30] however, does not attach much importance to this
feature, believing that the albumen is often due to semen.

[Footnote 29: _Gior. internaz. d. Sc. Med._, Napoli, 1880, ii.
357-359.]

[Footnote 30: _Archiv für Psychiatrie, etc._, 1880, xi. 478-506.]

The tendinous reflexes are frequently abolished during the attack, but
not always so, and in several cases in which I was enabled to make a
test during the convulsion I found that the patellar reflex was very
active, and in one case elsewhere reported it was transferred. The
skin reflexes are ordinarily exaggerated.

Tongue-biting is, I think, a more common feature of the nocturnal than
the other attacks. It is rare in infantile epilepsy, and is always a
bad feature. The wound is sometimes very serious, and cases are
mentioned where the tongue has been severed. An occasional sequel of
the attack is a urinary difficulty and vesical tenderness. It is
sometimes connected with great urethral irritability and spasmodic
stricture, which prevents the introduction of a sound or catheter.
Romberg speaks of the supervention of asthma and dysphagia.

THE IMMEDIATE AND REMOTE EFFECTS OF THE EPILEPTIC PAROXYSM.—As a
result of violence we often find wounds and bruises, quite rarely
fractures, but more often dislocations. Cases have been communicated
to me where as a result simply of the great muscular force the humerus
has been dislocated at its superior articulation. Muscular pain of
great severity, and sometimes of great persistency, follows unusually
severe fits, and rupture of muscular substance is not uncommon. An
epiolecranon bruise in one of my cases produced a severe neuritis
which was very intractable. In old cases, according to Axenfeld, there
may be great muscular hypertrophy, the sterno-mastoidii attaining the
size of the biceps, and in other cases there is fatty degeneration. He
also calls attention to defects that may be due to frequent exercise
of violence upon bones through repeated exaggerated muscular
contraction. Paralysis of nerves which supply convulsed members is
mentioned.

The psychical effects are various. For several days following the
attack there may be simply confusion of ideas, irresolution, or
drowsiness, which subsides in a short time. In not a few cases I have
regarded the attack as beneficial in the sense of an explosion of
relief when perverted mental states had preceded it. In such persons
the discharging lesion was followed by a very conspicuous restoration
of the mental equilibrium.

Occasionally the attacks are terminated by great violence or screaming
or the commission of purposeless acts.

Post-epileptic aphasia has been described by Winslow, Moreau, and
others, and among my own cases of the sensory variety of this disorder
I have met with speech disturbance. The aphasia is of short duration,
and consists either in a total incapacity for verbal expression or a
transposition. It is not rare for it to be associated with the
commission of a number of quasi-automatic actions.

Unilateral epilepsies are quite apt to leave behind them a species of
paresis which may last even for several days. The loss of power is
confined to the convulsed members, and may be accompanied by tingling.
{482} In the greater number of instances, however, there is some
central organic change, and the epilepsy is purely symptomatic.

Deafness, amaurosis, and other pareses of the organs of special sense
are rare sequelæ of the epileptic state.

The remote effects of the grave disease are not so decided as when the
patient has been the subject of petit mal. Slight repeated losses of
consciousness are apt to be followed by mental decay. The ultimate
result is mental enfeeblement, a progressive and very great loss of
memory, which advances to such an extent that a veritable dementia
ensues. With this there is usually a very decided perversion of the
emotions and affections, so that a good-natured, amiable child may in
a few years become everything that is bad and trying, and the acts of
mischief are almost inconceivable. Theft, incendiarism, and various
moral perversions are common in some chronic epileptics. The dementia,
it is true, is tardy in its establishment, but it comes eventually if
the individual lives long enough.

In some individuals there is a very early tendency to the development
of mania; there is a certain periodicity about the explosions, and
when established the excitement either precedes the attack by a few
days or occurs shortly afterward. The violence is characteristically
acute, and such insanity very often makes itself known in homicidal
acts rather than in those of a suicidal character. Hypochondriasis is
quite likely to follow continued epilepsy.

It is the rule for epilepsy to undergo decided modifications in the
beginning of its course. The first attack may be simply eclamptic,
without any peculiarities or definite character, and with recurrence
there is a tendency to regularity and constancy in expression.
Infantile convulsions, that may occur at any time after inconsiderable
exciting causes, may eventually be confined to the early morning or
night. So-called fainting attacks may precede petit mal, and headache
may be the precursor of ill-defined seizures. So, too, the relation of
grave and light attacks may vary. In the beginning there may be
nothing but attacks of petit mal, while later these may be
supplemented by severe fits, and even disappear entirely. So far as my
own cases go, I find that nearly two-thirds of the entire number
happen at night or in the early morning, while the others may occur in
the day or at any other time, or by day and night. Besides the terms
nocturnal and diurnal, we may use the word matutinal in relation to
the time of attack. So far as the number of attacks is concerned, we
find great irregularity. It is not always possible to count them, or
even to recognize them, for the examples are numerous where nocturnal
attacks have been undetected for years, and have finally been followed
by fits during the daytime. I have cases who have seizures but once or
twice a year, and others who have ten to forty or fifty daily. In some
cases there may be eight or ten attacks of petit mal daily, and but
two or three grave attacks during the week.

The statistics of Delasiauve and Leuret go to show that of 296 cases
of epilepsy, the cases of general epilepsy were most common—that is to
say, the attacks which occur both by day and night.

  Attacks occurring occasionally by day . . . . . . .  26
     "       "      habitually by day . . . . . . . .  30
     "       "      only at night . . . . . . . . . .   9
     "       "      habitually at night . . . . . . .   8    {483}
     "       "      equally by day or night . . . . .  87
     "       "      in larger proportion by day . . .  70
     "       "      "    "        "      by night . .  44

Delasiauve, Herpin, and others make delicate distinctions between the
attacks, and the former grades the seizures beginning at accesses, and
successively advancing to vertiges, accès intermédiares, and attaques
or accès compléts.[31] In fact, these are but varying degrees of
violence of the discharge, after all. We thus have light discharges
and severe discharges at different times, or, as the habit is
established, only the light or only the severe, the manifestation
depending probably upon the number of discharging cells and the
importance of the exciting cause.

[Footnote 31: _Traité de l'Épilepsie, etc._, Paris, 1845, p. 55 _et
seq._]

When the attacks occur in alarming frequency, as they sometimes do,
the condition is known as the status epilepticus. Leuret had a patient
who had eighty in two hours, and Delasiauve reports the case of a
young man fifteen years old who had twenty-five hundred in one month.
They may be so numerous as to be apparently continuous. The patient
remains in a state of coma (the status epilepticus), with very high
temperature. If he be not restored, he sinks into a deeper coma, and
all the signs of collapse manifest themselves. Bed-sores form, œdema
of the lungs ensues, and the patient dies. Happily, this condition of
affairs is rare.

Delasiauve calls attention to the fact that the first two or three
attacks that usher in this state do not usually attract much
attention, but the succeeding ones are so violent as to immediately
suggest violent consequences. In one of my cases the attacks, when
they had once become numerous, were readily excited by the least
jarring, noise, or handling, just as we find in strychnine-poisoning
or tetanus.

Irregular Forms.—There are occasional cases of psychical or masked
epilepsy, the study of which is intensely interesting. Such forms are
characterized by perverted consciousness and a low degree of
volitional direction which may vary from automatism to the undoubted
exercise of complex functions of the mind, though badly co-ordinated.
Mesnet's soldier, when subject to a paroxysm and apparently
unconscious, would perform a number of suggested acts in a rhythmical
manner and with no subsequent knowledge of the previous event: when
started off by the word of command to march, he would blindly go on,
marking time when he met with an obstruction until stopped, or when a
paper and tobacco were placed in his hands he would proceed to roll an
unlimited number of cigarettes.

Two cases of a more complex exercise of certain intellectual powers,
while others were dormant, came under my observation some time ago.
One of them was a young man of twenty-three, who had had irregular
epileptic seizures for some years. He went to bed one evening as
usual, arose, and breakfasted with his family without creating any
suspicion that he was at all unwell. He then went down to his place of
business, and after his arrival was sent to a distant part of the city
for some tool. On his return down town he stopped at a tobacconist's
and became involved in a quarrel with one of the persons in the shop.
A policeman was called, who, more intelligent than many of his class,
immediately detected something queer about the man, arrested him, and
afterward took him to Bellevue Hospital. There he remained three days,
and suddenly {484} returned to consciousness and a knowledge of his
surroundings, but was entirely ignorant of his unfortunate experience.
It is unnecessary to say his habits were perfectly good and he was not
drunk at the time of the quarrel or arrest. His last recollection was
that of going to bed the night before the day of his arrest.

Another case of unusual interest which came under my care,
illustrating a phase of sensory epilepsy, is worthy of reproduction:

C. O——, aged twenty-two, is a reporter attached to one of the New York
afternoon papers, who received a severe injury of the head when but
three years old. He fell from the second story of an unfinished
building to the cellar, striking the upper and back part of his head
upon a beam. He was rendered unconscious, and remained so for a day or
more. He recovered from the immediate bad effect, but has suffered
from severe general headaches, which recur every week or so, with an
increase in the amount of urine excreted. About six months ago he
began to have epileptic convulsions of a violent character almost
every day, and sometimes more often. These were precipitated by
excitement, and he had a great many when worried about his wife at the
time of her delivery. Upon one occasion he fell down stairs and
injured himself quite severely. The attacks were, as a rule, preceded
by an epigastric aura of long duration, and occasionally by a visual
aura, and, according to the testimony of his associates, he became
strange and queer. When in such a dazed condition he would restlessly
wander about his office, and suddenly, without any cry, become
convulsed. After the attack he slept soundly. The bromides of sodium
and ammonium and digitalis did little or no good, but the bromide of
nickel appeared to have some influence. During the past month he has
had only two or three attacks, but these have been of a quite
irregular character. He told me that there were times when he felt
like doing himself an injury, and that he had impulses to kill some
one else. His companions said he was irritable, pugnacious, and easily
thwarted, and his brother-in-law stated that upon several occasions he
had queer turns, when he would raise his hand to strike some member of
the family—that he subsequently knew nothing of his conduct, and when
it was detailed to him he appeared greatly astonished.

Mr. O—— came to my office in company with a friend at ten o'clock in
the morning of December 27, 1883. He had had one of his attacks at the
newspaper office, of rather more severe character than usual, at eight
o'clock, with a psychical aura, during the existence of which he was
very morose and sullen. Upon recovery he was speechless, though he
could communicate by signs. Upon his arrival at my office his manner
was composed and he appeared somewhat dazed. His pupils were dilated,
but contracted readily to light. I asked him one or more questions
regarding his inability to speak, which he perfectly understood, and
when I gave him a pencil and a piece of paper he replied without
difficulty in writing. When told to make a great effort to speak he
did so, and I thought I detected the word ‘To-day,’ but he could not
repeat it, though he tried and expressed great annoyance. He was
unable to utter any sound except a sort of groan, which could not in
any way be taken as an element of speech. I examined his larynx, but
found nothing which could explain his impaired phonation, and I sent
him to Dr. Asch, who found absolutely no abnormal appearances to
account for the speech {485} difficulty. The patient could not
phonate, and though he made attempts to enunciate the vowel-sounds,
and the vocal cords were approximated, he made no orderly sound. Asch
found a slight laryngitis of no importance.

The patient went home, and remained speechless all day, and was seen
by my associate, G. de Forrest Smith, in the evening. What occurred
during and after that gentleman's visit is contained in his notes: “I
was called to see patient about 8.15 P.M. He was lying upon the bed,
but had not slept; recognized me and motioned that he could not speak,
and I found that he could only say one or two words, and this with the
greatest effort, and so all my questions were put so that he could
answer them by nodding or shaking his head. He knew that he had had an
attack in the morning, that he had seen Hamilton and Asch, and
recalled various incidents of the day, answering intelligently my
questions in regard to them. He indicated by motions that his
inability to speak was due to a lump in his throat. When asked if he
had any trouble to think of the word he wanted, he shook his head, but
shortly afterward hesitated in an answer, and when asked if this was
due to his inability to think of the word, said ‘Yes.’ Was asked if he
had any loss of power in either side, and he motioned to his right arm
and leg, and said that he felt a numbness and pricking on that side.
On his grasping my hands with his, the right was perceptibly weaker.

“At one time he seemed confused as to which was his right or left
side, and put up both hands, and after looking at first one and then
the other in a puzzled manner, at last decided correctly, then smiled
apparently at his confusion.

“All this time he had been half lying on the bed. He now intimated
that he was tired, put his head down on the pillow and began to belch
up wind, and as he appeared about to vomit I called for a basin; but
this was only the beginning of an attack; the muscles of the neck and
right side assumed a state of tonic spasm, the extensors
predominating, so that the head was turned a little to the left and
forcibly thrust back into the pillow, and the right arm and leg were
firmly extended. He remained in this position about one minute; then,
taking two or three full inspirations, put his hand to his throat and
said plainly, ‘Something has fallen from there.’ On being asked
‘What?’ he replied, ‘A bone has fallen from my throat.’ I told him it
was well that the bone had fallen, as now he could speak. ‘Why,’ said
he, ‘I have had no difficulty in talking.’ On being asked why he had
seen Asch, he said ‘Who is Dr. Asch? I never saw any such person.’
Further questioning showed that all the occurrences of the day (except
those which had taken place immediately before the first attack) were
an absolute blank, and he thought it still morning. He asked the time,
and I told him half-past eight o'clock in the evening. At this he
seemed much surprised and said, ‘Why, I went to work this morning; how
did I come here?’ I then explained to him that he had been ill. After
further conversation he said he felt sleepy, and, after resting a few
minutes, he arose, put on his slippers, and came out into the room. He
walked with difficulty, because of the loss of power in the right
side, which he said felt numb and sore, as if it had been pounded,
also a sensation of pins and needles. After the attack his mind was
perfectly clear, and he could talk as well as ever, and all that had
happened before the attack in the morning he could remember {486}
perfectly well, but the interval between the two was a complete blank.
His inability to speak seemed due, not to lack of knowledge of what he
wanted to say, but rather to want of power to form the words, although
there was no paralysis of the vocal muscles. When he did manage to say
a word, it was invariably the correct one, but it was always done with
the greatest effort. The day after the attacks he remained at home;
the next day he went to work, but his head felt heavy and confused.
Two days after he complained of a pressure on the left side and back
part of the head; otherwise he was all right. At this visit he said
that after I had left him on the night of the attacks he intently
thought, striving to recall the incidents of the day, and after a time
concluded he could remember being at Thirty-third street, but did not
know how he got there. He thought he could recall going to see Asch,
but would not know him if he should see him. I then asked him how
questions were answered by him on that day; he answered he did not
know, as he had not thought of that; then, after a few moments'
reflection, said he must have written the answers. He was then shown
some of the answers he had written, which he recognized, and by an
effort of memory could recall some of the incidents of writing them.
He was still unable to remember anything that occurred after his
arrival home previous to the last convulsion.”

January 27, 1885: This patient subsequently suffered from several
attacks in which the psychical element predominated. His head
presented a remarkable deformity, there being a prominence posteriorly
which might be compared to a caput succedaneum, only it was entirely
osseous. The upper margin was separated from the anterior parts by a
deep sulcus.

Under such circumstances we find very often that acts of great
violence are committed by such epileptics for which they are entirely
irresponsible. Two or three cases of the kind occur to me now. One of
them was a boy who always bit every one and everything—his family, the
domestic animals, and inanimate objects; another, a most dignified and
lady-like woman, who violently struck different members of her family;
and within the past week a woman was brought to me who hurled a
kerosene lamp at a perfect stranger with whom she was quietly talking
before the seizure was precipitated. Numerous instances are related
where individuals while in the masked epileptic state have wandered
for long distances and committed a variety of purposeless acts, and
undoubtedly many of the mysterious disappearances are of this order.

SENSORY EPILEPSY.—Some years ago Hammond referred to certain peculiar
epileptic attacks in which sensory manifestations were very
pronounced. To this condition he gave the name thalamic epilepsy,
believing the condition to be one of the optic thalamus. Among the
large number of unclassified and irregular cases reported by various
authors there are many so much resembling each other that I think they
should be relegated to a special place.[32] The notable examples of
Sommers, Bergmann, Tagges, Guislain, and others belong to this
category.

[Footnote 32: I shortly afterward, believing the term a misnomer,
invented that in use: “On Cortical Sensory Discharging Lesions or
Sensory Epilepsy,” _New York Med. Journal and Obstetrical Review_,
June, 1882; also see “A Contribution to the Study of Several Unusual
Forms of Sensory Epilepsy which are probably Dependent upon Lesions of
the Occipital Cortex,” _New York Med. Record_, April 4, 1885.]

{487} The features of this form of epilepsy are (1) the expression of
some hallucination (prodromal stage), or hemiopia; (2) supraorbital
neuralgia; (3) aphasia, formication; (4) slight loss of consciousness,
and little if any motor disturbance.

I may present two illustrative cases:

A few months ago I was consulted by a medical gentleman in regard to a
patient who had for years presented a curious train of nervous
symptoms, which afterward assumed a form leading me to think she might
have sensory epilepsy. She would, in the presence of the gentleman who
consulted me, who was a personal friend of the patient and a medical
man, stop short in the midst of an animated conversation, look fixedly
ahead, appearing momentarily lost, remaining abstracted for a short
period, possibly a minute, and on recovering herself go on, finishing
the sentence she had commenced before the seizure. At this time she
constantly had hallucinations of a visual character, when she saw
animals, birds, figures of men and women, who approached her, as well
as a variety of other objects. A common hallucination, which had been
repeated quite frequently, consisted in visions in which green leaves
and white rabbits and other objects familiar to her in childhood
figured extensively. Upon one occasion, while sitting in the
drawing-room, opposite a door which communicated with the hall, she
suddenly called her companion's attention to the hand of a man which
she saw clasping the baluster rail. The hand was seemingly
disconnected from the arm. She was somewhat agitated, and it was
nearly half a minute before the vision was dismissed. Sometimes she
would call attention to the hallucinations before the attack, but more
often she became transfixed, apparently lost, and then recovering she
described her visions minutely. She has apparently been able to
foresee the attacks and ward them off by a strong voluntary effort. So
far as can be learned, there is no hysterical element in the case, but
her seizures are more frequent at the time of menstruation. In a
private note it is stated that “the family history of the patient is
very good, and she has always seemed remarkably healthy and robust,
and has shown more than usual intellectual ability. She has appeared
to persons generally to be of a contented, happy disposition.... At
night, when she closed her eyes, she suffered from these
hallucinations, especially after a day of fatigue. Her pupils are
usually dilated, but her color undergoes no change during the
seizure.”

The second case is one of a more complex type:

J. B——, a bright boy aged sixteen, was sent to me by F. H. Bosworth in
April, 1883. He comes of nervous stock, his mother being subject to
epilepsy, and his father is an eccentric man who manifests his mental
peculiarities chiefly in a morbid restlessness and irascibility. There
is a brother who is healthy. The attention of the parents was first
called to the boy's condition by his recital of a sudden attack which
occurred during the summer of 1882. While rowing upon a river he
suddenly and completely lost the visual use of the right eye, so that
in looking at a number of ducks swimming near his boat he failed to
perceive those upon one side of the flock. This condition lasted for
twenty minutes, and after a brief and severe pain over the right eye
he became unconscious, the unconsciousness being preceded by a
tingling and numbness of the hand, forearm, arm, and left side of the
tongue. He has {488} subsequently had eight or ten of these attacks,
of which the following is an example: Usually without any bad
feelings, physical or mental, he, while engaged in any duty or at any
time, suffers a sudden unilateral blindness. This is never gradual,
and not like the form of amblyopia in which the visual field is
gradually reduced. There is some hemichromatopsia. It would seem as if
the retinal anæsthesia was unequal, for while usually the loss is
complete and universal, it sometimes happens that there is only a
limited loss. Upon one occasion, while reading, he suddenly lost the
printed matter of the right lower half of the page below a diagonal
line extending from the right upper corner to the left lower corner.
There is never diplopia. This deprivation lasts anywhere from ten to
twenty minutes; meanwhile, a distal anæsthesia, coming very gradually,
involves at first the fingers of the opposite hand, and successively
extends to the forearm, arm, and other parts, as I have already
mentioned. There seems to be analgesia as well as anæsthesia, for a
pin may be run into the muscles without producing pain, and upon one
occasion the gum was freely pricked without any discomfort to the
patient. It invariably happened that the cutaneous sensory trouble
occurred upon the side opposite to the hemianopsia and neuralgia, and
in the greater number of instances the left side was that affected.
The third stage of the attack consists in migrainous headache of a
very severe kind, and which sometimes lasts for an hour or more. There
is a subjective feeling as if the eye was pushed forward. This
disappears with nausea and relaxation. More often he loses
consciousness when the anæsthesia reaches its limit, which seems to be
the extension of the anæsthesia to the gums. Occasionally there are
slight convulsive movements upon the anæsthetic side. While the
attacks involve the left side of the body as a rule, it happens that
when there is primary left hemianopsia and right-sided anæsthesia the
boy becomes very much confused in speech, and sometimes is paraphasic,
the trouble being but transitory. He is sometimes unable to speak at
all, though perfectly conscious and in possession of his faculties. No
pupillary disturbance has been noticed at any time. Upon two occasions
there was a swelling of gums and tongue, which was not only
subjective, but perceived by the mother. Occasionally he sees
prismatic colors and rays before the blindness, but this has been only
once or twice. During his early life he had attacks of slight numbness
of the hands and feet which were not thought much of, and he had
headache as well. He has been a somnambulist.

MORBID ANATOMY AND PATHOLOGY.—The literature of the experimental
physiology of epilepsy is enriched by the observations of a variety of
careful students, among them Sir Astley Cooper, Kussmaul and Tenner,
Brown-Séquard, Nothnagel, Schroeder Van der Kolk, Pitres,
Hughlings-Jackson, and the followers of the localization school, as
well as many others more or less distinguished.

The experiments of many of the early writers were directed for the
purpose of ascertaining the relations of circulatory variations to
convulsive seizures, and the most notable were those of Burrows and
Kussmaul and Tenner. These latter produced compression of the carotid
arteries, and instituted cerebral anæmia by free and exhausting
hemorrhages. As a consequence, the emptying of the cerebral vessels
was followed by a loss of consciousness and by epileptiform
convulsions, and it was {489} necessary to produce the same result to
compress all the great afferent vessels of the brain. The experience
of surgeons generally is, that ligation of the common carotid upon one
side of the neck is sometimes very apt to produce an alarming anæmia,
with occasional convulsions, and sometimes fatal consequences.

The experiments of Hall, Landois, Hermann, and others, as well as
those of the writers just mentioned, show that carotid compression
results in capilliary anæmia and venous hyperæmia, and that with
cessation of this pressure there is a sudden congestion of all
vessels. The susceptibility of the brain is greatest at its posterior
part and between the optic thalami and the cord. When the bulb was
subjected to sudden changes in its nutrition—such, for instance, as
followed the experiments of Hermann, who ligated simultaneously the
superior and inferior venæ cavæ of a rabbit—there were not only
convulsions, but various cardiac and other disturbances which were
undoubtedly due to central impairment of function. Kussmaul and Tenner
conducted their experiments with watch-glasses luted into the
cranium—a procedure which, however, at best, is unreliable.

Brown-Séquard some years ago in part established an important
pathological truth, the theory of epileptic zones, and demonstrated in
certain animals that bruising and injury of the great nerve-trunks,
especially the great sciatic, would give rise to epilepsy, and that
irritation of certain tracts would precipitate the paroxysms. He
further announced that the progeny of animals in whom epilepsy had
been thus induced very frequently inherited the epilepsy of the
parent. By some it was held that such epilepsies were purely
peripheral, and Brown-Séquard even believed in spinal epilepsy. His
spinal epilepsic theory has, for the most part, been explained by the
anatomical researches of Hitzig and the doctrine of interrupted spinal
inhibition. In fact, many of the spinal epilepsies are examples of
exaggerated reflexes.

The epileptiginous zone theory, which, while it induced many to
believe that the disease might have its origin outside of the brain,
gave rise to the false assumption that attacks with distal auræ were
primarily non-cerebral, has been discarded, and most observers have
arrived at the conclusion that even in these cases the first explosion
is due to some cerebral cell-discharge.

Hughlings-Jackson's grand work has revolutionized the views held prior
to his first published writings, about twelve years ago. He believes
that any part of the gray matter may, through over-excitability, give
rise to convulsive attacks.

The production of convulsions by cortical irritation is now an old
story.

The experiment of Pitres and Frank[33] bears upon the sensorial
function of the cortex in showing that, when the cortex is irritated,
epileptiform convulsions follow, but if the exposed surface be
subjected to the ether spray the same irritation will only produce
definite movements, but no convulsions.

[Footnote 33: _Gazette des Hôpitaux_, No. 38, 1883.]

The investigations of Van der Kolk especially, and his followers,
certainly give the medulla an important place as the locus morbi of
the malady; and it must be assumed, bearing in mind the existence of
the vaso-motor centres of Dieters and the presentation of symptoms
indicative {490} of disturbance at the floor of the fourth ventricle,
that the most important pathological changes must be looked for in
this part of the brain.

Jackson's cortical explanation is, however, fully in consonance with
the medullary theory. If we study the different stages of the attack,
we shall find that there is probably a suspension of cortical
inhibition—that a derangement of the cortical cells or discharge may
cause a resulting disturbance in the bulb. On the other hand, a reflex
irritation through the pneumogastric or from some distal part brings
about the same disturbance of equilibrium. There is anæmia due to
irritation of the vaso-motor centre, an inhibition of the great
ganglion-cells, and a disturbance of function of the important cranial
nerves. The primary anæmia and unconsciousness are accounted for by
this primary irritation of sympathetic filaments and vascular
constriction; the secondary hyperæmia is explained by the experiments
of Kussmaul, which demonstrated the succeeding congestion; or by
irritation of the spinal accessory and contraction of the muscles of
the neck and compression of the large veins. The pupillary, ocular,
respiratory, and other symptoms indicate the disturbance of the
nerve-nuclei in the bulb. The respiratory difficulty and the
interrupted decarbonization of the blood undoubtedly account for the
secondary unconsciousness.

Van der Kolk[34] in localizing the lesion in the medulla found
capillary dilatations in the neighborhood of the hypoglossal nuclei in
tongue-biters. In epileptic patients who were in the habit of biting
their tongues during the fit the vessels were wider than in those who
did not bite the tongue, on an average in the course of the
hypoglossus by 0.096; in the corpus olivare, which certainly here
plays an important part, by 0.098 mm.; and in the raphé by 0.055. In
those who did not bite the tongue, on the contrary, the vessels in the
path of the vagus were 0.111 wider than in those in the first, Table
A.[35]

[Footnote 34: “On the Minute Structure and Functions of the Spinal
Cord,” by J. L. C. Schroeder Van der Kolk, _New Syd. Soc. Trans._]

[Footnote 35:                   TABLE.
  --------------------+-----------+-----------+-----------+----------
  Different           | Hypo-     | Corpus    |           |
  Epileptics.         | glossus.  | olivare.  |  Raphé.   |  Vagus.
  --------------------+-----------+-----------+-----------+----------
  Table A—tongue      |  0.306    |  0.315    |  0.315    |  0.237
           biters     |           |           |           |
  Table B—non biters  |  0.210    |  0.217    |  0.217    |  0.348
                      +-----------+-----------+-----------+----------
    Difference        | +0.096 A. | +0.098 A. | +0.055 A. | +0.111 B.
  --------------------+-----------+-----------+-----------+----------]

Nothnagel[36] is of the opinion that the anæmia of the brain is not
the cause of the convulsions, but that the “excitation of the
vaso-motor centre and that of the centre for the muscles are
co-ordinate—that both go on side by side, and are independent of each
other.”

[Footnote 36: _Ziemssen's Encyclopædia_, vol. xiv. p. 268.]

He by this theory explains the occurrence of those forms of petit mal
in which there is loss of consciousness without convulsions, and, on
the other hand, twitchings before the coma.

The best argument in favor of this hypothesis is in Jacksonian
epilepsy, when monospasms exist oftentimes with a succeeding
extension.

In those cases which are the outgrowth of migraine the pathological
condition is probably an exaggerated tendency to angio-spasm, the
original impaired vascular tonus in the beginning giving rise simply
to pain and lesser troubles, while after repeated changes of calibre
not only {491} nutritive alterations ensue, but hyperexcitability of
the bulbar convulsion centres as well.

The labors of those who have endeavored to connect epilepsy with
cerebral-tissue alterations have been attended by nothing very
definite or positive, so far as pathological explanation is concerned.
The post-mortem appearances have varied widely, and the only
conclusion to be reached is that which shows that almost any morbid
gross alteration of the cerebral mass may be symptomatized by
convulsions, but such a production of paroxysmal trouble is much more
likely to be the case, and in a more definite manner, when the
cortical motor-centres are subject to destructive disease or
irritative pressure. This is even not always the case, for numerous
cases of injury of the paracentral lobe have been recorded with no
showing of resulting convulsions. The long list of autopsies which I
will not here consider show that an epilepsy may owe its origin to the
pressure of a spicula of bone, or to the pressure exercised by
depressed fragments of the same—to tumors or adventitious products,
meningitis, cortical encephalitis, vascular degeneration, ventricular
œdema, contusio-cerebri, and many other morbid processes which result
in rapid or tardy degeneration. Of course, in such cases the genesis
of the disease depends not so much upon the nature of the lesion as
the location. The fruitful collections of cases of Ogle and Jackson
are full of examples of limited growth or disease involving the
cerebral cortex, while numerous cases collated by other writers show
disease of the bulb or various peripheral parts which have been
closely connected with the growth and behavior of the affection.

Several able pathologists have independently and repeatedly found that
sclerotic degeneration of the hippocampal folds often existed.
Delasiauve and Lébert first observed this lesion, but many modern
authorities—among them Meynert, Nothnagel, and Charcot—who have also
found this appearance, regard the change as of purely secondary, and
consequently unimportant, character.

Tamburini[37] reports a case of hemiplegic epilepsy with induration of
the left optic thalamus and the left cornu ammonis, in which aphasia
existed. Pfleger[38] and Henkes have also found the sole lesion to be
induration of the cornu ammonis. Of Pfleger's[39] 43 autopsies,
atrophy and sclerosis of the cornu ammonis were found twenty-five
times, and it was noted that the extent of the morbid change bore
relation to the violence and frequency of the seizures.

[Footnote 37: _Sallanzani_, Modena, 1879, viii. 550-557.]

[Footnote 38: _Allg. Zeitschrift f. Psychiatrie, etc._, Berlin, 1879,
xxxvi. 359-365.]

[Footnote 39: _Ibid._, lxxvi., and _Arch. de Neurologie_, No. 2, 1880,
p. 299.]

In many examples, especially where the disease has been found to be
unilateral and associated with more or less hemiatrophy, the autopsy
disclosed a corresponding hemiatrophy of the brain. Many such cases
are reported. I have frequently found epilepsy in association with
cerebral hypertrophy, and as a symptom of cerebral tuberculosis it has
long been recognized, and numerous cases are reported in which for a
long time the paroxysms were the only manifestations of the condition.
In one of these cases, reported by Luys,[40] the bulb was found
involved by tuberculous matter.

[Footnote 40: _Archives gén. de Méd._, 1869, ii. 641 _et seq._]

{492} Convulsions have very frequently been noted in association with
imperfect cerebral development, and Echeverria laid great stress upon
the hyperplastic increase in volume of certain parts of the brain.

Marie Bra[41] has thus summed up her conclusions relating to the
morbid anatomy of epilepsy:

“1. The mean weight of the brains of epileptics is less than the
physiological mean.

“2. The cerebellum is greater than the physiological mean.

“3. There frequently exists an asymmetry between the lobes (not
peculiar to epilepsy). The increase of weight is sometimes found on
the right and sometimes on the left side. Equality is the exception.

“4. In no form of mental disease (excepting perhaps general paresis,
which is accompanied also by epileptiform crises) have we met with so
marked and constant a variation between the weights of the hemispheres
as exists in epilepsy.”

[Footnote 41: Referred to by Axenfeld.]

Drasche, Green, Greenhow, Löbel, and others have detailed cases in
which tuberculous deposits were undoubtedly the causes of the disease.

Kussmaul and Tenner, Hoffman, and others have held that a stenosis of
the superior part of the vertebral canal may explain, through pressure
upon the cord, the genesis of the attack, and Kroon found asymmetry of
the medulla oblongata.

The microscopical changes that have been found in brains where no
gross lesion was apparent are by no means distinctive. I have myself
examined the brains of many epileptics with discouraging results. The
varying granular cell-degeneration, capillary dilatation, and
exudative changes are common enough. In several cases of cortical
epilepsy I found more or less advanced degeneration of the great cells
in limited regions.

By far the most important and exact changes are those observed in the
cases of sensory epilepsy. I have elsewhere collected some continental
cases. In brief, areas of occipital softening or degeneration have
been discovered in those cases with hallucination, sensory
expressions, and hemiopia. In one case attended by hallucination of
smell the autopsy disclosed the following:

M. M——, was a stout Irish woman about forty years of age. She had
suffered from a light form of epilepsy dating from the tenth year, and
resulting, as she stated, from a fall, when she struck her head and
was unconscious thereafter for some hours. No scar was visible,
however. No satisfactory history could be obtained regarding her early
life and the first paroxysms. In the beginning these were rather
frequent, and she had as many as four or five a month. They afterward
diminished in number and severity, and for many years she had but
three or four in the course of the year. They were not very severe,
and she was enabled to pursue her work as a housemaid, but did not
keep her places for any great length of time. She rarely bit her
tongue, but usually frothed at the mouth and became livid and
convulsed for a short time. There was no history of one-sided spasms.
As I have stated, I could gain no accurate account of the previous
attacks, except that she nearly always had an aura of a peculiar
character, which was a prominent feature of the seizure and very
pronounced. She suddenly perceived a disagreeable odor, sometimes of
smoke, sometimes of a fetid character, and {493} quite uncomplicated
by other sensory warnings; and afterward became unconscious, and
remained so for two or three minutes. She was invariably able to
describe her sensations when she recovered, which she always did when
I asked her, comparing her warning to the smell of burning rags, to
the smell from a match, and, as she expressed it, it sometimes rose up
in her head and choked her. She was under my observation for one or
two years, but eventually developed phthisis, and died, her attacks
occurring from time to time until her death.

Besides well-marked tuberculous lesions in the lungs, there was little
of interest so far as the visceral examination was concerned. The
brain was removed and its peculiarities were carefully observed. A
great quantity of fluid was found, especially at the dependent
portions of the membranes and in the ventricles, while the dura was
thickened and pearly in spots. There was a condition that might be
likened to a low grade of hemorrhagic pachymeningitis, and at the base
of the brain old plastic changes were found, there being adhesions,
especially in the region of the middle lobes, but more particularly on
the right side and near the median line. The brain as a whole was
small, and weighed forty-one ounces and a fraction. The sulci were
deep and gaping, and the convolutions were distinct. There was no
atrophy of the fore-brain convolutions, and no other pathological
appearance was presented except that found in the meninges, but at the
lower part of the temporo-sphenoidal lobe of the right side an
appearance was found of an exceedingly interesting nature. At this
point a decided shrinkage of tissue was discovered, with depression
and adhesion of the pia, the induration involving the uncinate gyrus
and parts of the adjacent convolutions, as represented in the drawing.
No induration or softening of the great motor tracts was observed, and
the optic thalamus and parts adjacent were uninvolved, as was the
cord. An attempted microscopic examination, undertaken some months
subsequently, was unsatisfactory, because of the bad condition of the
brain, the preserving fluid having been improperly made. The olfactory
nerves were not involved. The third frontal convolution was examined,
but no disease was found there. Consequently, it is to be inferred
that no lesion of the external root of the olfactory nerve existed.

[Illustration: FIG. 27. Lower Face of Right Hemisphere.]

DIAGNOSIS.—Having spoken of epilepsy as in most instances a
symptomatic disorder, it would be proper to confine this section to
the differentiation of the simpler and more classical form of the
idiopathic disorder from certain purely eclamptic attacks or those due
to cerebral tumor or {494} coarse degeneration. The epileptic attack
itself is to be considered from its time of happening, its duration,
the element of unconsciousness, its associations, and the antecedent
history of the individual. It may be confounded with the similar
phenomenon dependent upon cardiac weakness, uræmic poisoning, toxic or
alcoholic saturation, etc.

Of course, when we find recurring seizures with a certain amount of
what Carter-Gray calls quasi-periodicity, preferring perhaps the
night, the early morning, or only the daytime, we are almost sure of
epilepsy. This supposition is strengthened by the association with
attacks of petit mal. The duration of an attack, which may be from a
few seconds to several minutes, is also a guide, for in certain toxic
and other paroxysms the rule is for a succession of attacks to occur.

The question of consciousness is one that has drawn forth a great deal
of discussion, especially with reference to medico-legal cases. I
think the majority of clinicians are agreed that loss of consciousness
is an absolute belonging of epilepsy, yet there are cases in which the
lapse is scarcely perceptible. It is a dangerous precedent to
establish, for the convulsive symptoms in such cases are taken from
the epileptoid category. It is quite true that there are many
hemi-epilepsies in which the intellectual condition is one that may
easily be mistaken. I have seen numerous cases in which an apparent
conservation of consciousness remained throughout a slight monospasm,
but I do not feel at all sure of this; and in cases of aborted or
masked epilepsy there is a dual mental state which would readily
deceive the lay observer. The case of Mrs. S—— is an example of this
kind. After the obvious subsidence of the dramatic and conspicuous
feature of the fit she remained for hours and days in a state of
undoubted transposition, performing acts which required something more
than a high degree of automatism—going to the table, talking about
certain subjects which were suggested, with apparent ease, but not
connecting them intelligently with her surroundings, as she would
before and after the epileptoid state. After a time she apparently
resumed her normal state, but was entirely unconscious of the
happenings of her previous hours or days, not even recollecting her
simplest actions. Julian Hawthorne's hero in _Archibald Malmaison_,
though not drawn by a physician's pen, suggests the state of which I
speak, and it has the merit of being based upon one of the elder
Forbes Winslow's interesting cases.

When we find paroxysmal attacks occurring in individuals with atypical
heads, thick swollen lips, scarred tongues, and irregular teeth, we
may strongly suspect the patient to be epileptic. To these we may add
the appearance of the eyes, the fishy, lack-lustre expression which
betokens old epilepsy. The hands are clammy and the skin mud-colored;
the hair is dry and coarse; and the body often has a death-like odor.

In children, certain mental peculiarities are to be inquired into.
Unnatural brightness or dulness—what may be called the clumsy
organization—is often present, and the muscular use is often
imperfect. We find that there is often but little nicety in walking,
in using the hands, in speaking, or after learning to write there is
an incapacity, with ever so much teaching, to develop a character or
style. Such children can never become ambidextrous. These little
points may seem trifling, but to the physician who carefully studies
his cases they may prove of great help. The history of the nights may
often lead to the discovery perhaps of a {495} long-existing nocturnal
epilepsy. Incontinence of urine, blood upon the pillow, nightmares,
morning headache, and petechiæ betoken unsuspected night attacks; and
Le Grand du Saulk mentions the case of a young Englishman who
committed a purposeless crime and was discovered to be epileptic, the
diagnosis being confirmed by an antecedent history of nocturnal
seizures, and subsequent watching resulted in the discovery of many
night attacks.

As to special conditions with which the epilepsy may be confounded, I
may refer to cardiac weakness. It not rarely happens that simple
fainting attacks are confounded with those of an epileptic nature.
Such is the case more often in heat-prostration, when some rigidity
attends the loss of consciousness. The duration of such a state, the
condition of the pulse and color, however, will easily clear up any
doubts upon the part of the observer. The existence of a cause should
also be considered, and the fact that usually the epileptic paroxysm
is sudden, while a feeling of depression and feebleness precedes the
fainting attack, should be remembered. I may present in tabular form
the points of difference:

              EPILEPSY.              |            SYNCOPE.
                                     |
  Loss of consciousness sudden.      | Loss of consciousness follows
                                     | feeling of faintness.
                                     |
  Period of complete unconsciousness | Unconscious throughout, no
  usually short.                     | convulsions.
                                     |
  The existence of auræ of a         | The existence of preliminary
  well-defined type.                 | vague prostration, nausea, and
                                     | irregular heart action.
                                     |
  Often involuntary discharge from   | Quite rare or never.
  bowels and bladder.                |
                                     |
  Patient usually falls into heavy   | After slight weakness patient
  sleep or is indifferent after      | is anxious and worried, and
  convulsion.                        | quickly seeks relief.

The difficulty of diagnosis, however, is only in cases of petit mal.

There are light forms of auditory vertigo that may resemble
vertiginous epilepsy. In the former there is never loss of
consciousness, and the patient refers to the rotary character of the
vertigo. A history of antecedent attacks, tinnitus, aural disease, and
a certain constancy which is not a feature of petit mal, may be
mentioned.

There are cases, however, which are puzzling, and come under the head
of auditory epilepsy rather than auditory vertigo; and in these there
is a multiplicity of expressions, the auditory symptoms predominating.

Of uræmic convulsions it is hardly necessary to speak. There is a
previous history of renal disease which the microscope and less
delicate tests will reveal, and clinically there is antecedent
headache, some stupidity, and not unrarely thickness of speech and
somnolence. There are some cases, however, which are obscure. I have
known patients with chronic renal disease—such as waxy kidney, for
instance—to develop a species of epilepsy, the paroxysms recurring
from time to time and behaving very much as the idiopathic disease
would; and their occurrence would mark some imprudence in diet or
exposure, and their disappearance an improvement in the patient's
general condition. The attacks were not classical, inasmuch as there
seemed to be but one stage of violent clonic convulsion, preceded by
intellectual dulness, and followed by a semi-comatose condition which
was far mere profound than the somnolent {496} stage of epilepsy. The
movements were not accompanied by a great degree of opisthotonos or
pleurosthotonos.

Alcoholic and absinthic epilepsies are usually preceded and followed
by symptoms indicative of profound saturation.

The consideration of hysterical epilepsy may be found elsewhere, but
it may do to briefly refer to some cases which do not present the
phenomenon first described by Charcot and Bourneville. The ordinary
hysterical attack is never attended by loss of consciousness, by any
of the pupillary changes so constant in epilepsy, by the mobility of
the pupil between the attacks which is present in a large number of
true epileptic individuals. There are never the succeeding changes of
color, and the seizures are commonly produced or attended by some
emotional disturbance, or are associated with ovarian disturbance.

Epilepsy is occasionally simulated by malingerers, and sometimes the
skill of the subject is so great as to even deceive the practised eye.
Prisoners, soldiers, and litigants may counterfeit an epilepsy, and go
through with great personal suffering to accomplish their purpose.
“Clegg, the dummy-chucker,” whose remarkable case has figured in the
medical journals, upon one occasion threw himself from an iron
platform to the stone floor of the jail, nearly twenty feet below, to
convince a suspicious physician of his honesty. The simulator rarely
bears close watching. The dilatation and contraction of the pupil
cannot be simulated, nor can the corneal or pupillary insensibility.
The fraud cannot voluntarily change his color, as is the case in true
epilepsy, and as a rule the thumbs of the impostor are never flexed,
as they should be. Suggestions for a purpose are readily heard, and
sometimes adopted, by the apparently unconscious man. Gottardi[42]
lays great stress upon the use of the ophthalmoscope as a means of
detecting simulated epilepsy. He calls attention to the frequency of
retinal changes with facial asymmetry and other evidences that suggest
cerebral disease or non-development. Gottardi has found that the pulse
in true epilepsy is always lower after an attack, but it soon reaches
its normal standard.

[Footnote 42: Abstract in _Journal of N. and M. Dis._, Oct., 1881, p.
843.]

The differentiation of idiopathic epilepsy from that due to syphilis
is possible when we consider the element of pain. Besides the tibial
pains of syphilis, the epilepsy thus produced is often preceded by
intense frontal headache, while that of ordinary epilepsy follows the
attack. The syphilitic epilepsy is not attended by so great or
continued a loss of consciousness as the non-specific form, and the
movements are apt to be most violent on one side or the other. The
association of the attacks with various bodily signs, such as nodes,
old scars, alopecia, erosions, etc., and in connection with possible
cranial nerve-paralyses, will throw light upon its true character. The
paralyses referred to seem most frequently to involve the motor
ocularis, abducens, and patheticus. Syphilitic epilepsy, too, is quite
irregular in its time of manifestation, and is not unrarely followed
by aphasia; but the interparoxysmal mental state is one of extreme
dulness, memory being blunted and there being a peculiar hebetude.

PROGNOSIS.—Within the past quarter of a century the ideas of the
medical profession regarding the curability of epilepsy have certainly
undergone a change. The statistics of Bennett and others show that
since the introduction of the bromic salts the proportion of cures has
{497} been decidedly increased. Nevertheless, the disease is a most
discouraging and troublesome one to manage, and especially is this the
case when it assumes the form of petit mal. The rapid recurrence of
light attacks is, as has already been said, very apt to lead not only
to mental enfeeblement, but is very often followed by very severe
paroxysms.

Epilepsy of a more or less constant form, in which the seizures
resemble each other, is far more incurable than that of variable type;
for example, we find that unilateral seizures are much more apt to be
associated with established cortical disease than when they are
general and simply explosive manifestations. It has been held that a
tendency to permanency is marked by a diminution in the extent of the
interval. This is by no means true. I have had cases under observation
for ten or twelve years in which attacks separated by intervals of six
months or one year marked the course of the disease, in which frequent
initial attacks were present. These cases I regard as very bad so far
as prognosis is concerned. I much prefer a history of irregular and
comparatively disorderly attacks. In female subjects the menstrual
influence is not always a bad factor. When we are enabled to remove
some production of an exciting cause in connection with the catamenia
the prognosis is more hopeful; but an opinion must be expressed with
great caution, especially in those cases beginning at an early age and
not after the establishment of the menses. Traumatic cases are not
always bad, but those in which the element of heredity plays a part
most certainly are, Herpin and Gowers to the contrary; and though
these cases for a time do well under treatment, its good effects are
not constant. Individuals with misshapen heads, whose deformity
suggests premature sutural ossification, are not susceptible to the
influence of treatment, and all other osseous changes, such as
exostosis, plaques in the dura, and bony growths, whose existence can
only be guessed at or inferred from suggestive appearances elsewhere,
give rise to a variety of epilepsy which is beyond the reach of drugs.
With symptomatic epilepsies the case is sometimes different, for while
the seizures which arise from the irritation of a cerebral tumor are
almost as hopeless as the form I have just mentioned, we know from
experience that the epilepsy of syphilis and other allied diseases,
and those of toxic origin, with the exception sometimes of those
occasionally due to alcohol or lead, are curable. The meningeal
thickening of alcoholic origin or the encephalopathy of lead may be
the pathological bases of very intractable paroxysms.

So far as age is concerned, it may be stated that many eclamptic
seizures of young children which are due to well-recognized irritable
causes are promptly cured if there be no hydrops ventriculi or
preossification of the coronal sutures, and if the epileptic habit is
not established. The epilepsies of six or eight years' standing are
not encouraging from a therapeutic point of view, and those of
advanced life developing in aged persons are equally unfavorable.

The treatment of epilepsy due to heat-stroke is by no means
satisfactory, and, though the attacks are often separated by long
periods, they are apt to recur in spite of drugs.

Gowers has prepared several valuable tables which show the influence
of age upon recovery. He says: “The following table shows that age has
a distinct influence on prognosis. The percentage of the unimproved
{498} cases to the whole is 30 (43:143::30:100). The percentage of the
cases commencing at each age arrested and unimproved is stated, and
between brackets is indicated the excess of the arrested or unimproved
cases at each period of life over the proportion for the whole 30 and
70 per cent. respectively:

               --------Cases.--------   ------Percentage.-------
               Unimproved.  Arrested.   Unimproved.  Arrested.
  Under 10         14          29       32.5 (+2.5)     67.5
  From 10-19       23          45       34   (+4)       66
  20 and over       6          26       19              81 (+11)
                   --          --       --              --
                   43         100       30              70

Thus, the proportion of the cases commencing under twenty in which
arrest was obtained is considerably less than the proportion of cases
commencing over twenty, the difference amounting to about 13 per cent.
The period of the first twenty years of life at which the disease
commences has little influence, but the prognosis is little better in
the cases which commence under ten than in those which commence
between ten and twenty: arrest is more frequently obtained. The cases
which commence in women at the second climacteric period are also
obstinate, although not sufficiently numerous to be separately given.”

He also finds, from an analysis of the same cases, the fact noted by
others, that the prognosis is favorable in inverse proportion to the
duration of the disease.

Attacks which chiefly occur in the daytime are much more amenable to
treatment than the nocturnal seizures, and especially is this the case
in the tongue-biting form. Sudden blows upon the head or falls have
been known in isolated cases to effect an amelioration in the
patient's disease, but these examples are rare.

The existence of an aura is much better than if none existed.

Death from the attack itself is rare, yet in the large pauper
institution with which I was connected for many years I have known of
several cases. More often the death results from asphyxia resulting
from a bolus of food which chokes the patient or from a fall in some
dangerous place—into the fire or elsewhere. Accidental death from
drowning is more common than any other form.

The status epileptica into which patients sometimes pass who have had
many convulsions is occasionally a fatal termination of the malady,
and is always a serious feature.

The influence of different epochs in life is worthy of consideration:
of menstruation, of marriage, of pregnancy, and of the menopause there
is much to be said. I have sufficiently spoken of the establishment of
the menstrual flow, and I would only add another word of caution
against giving a too favorable prognosis except in those cases of very
recent origin. Marriage appears to have very little to do with
changing the attacks, unless they be of an hysteroid character. I have
never known epilepsy to influence the course of a pregnancy in any
unfavorable way, and I think this has been the observation of others.
Gowers refers to cases in which the attacks ceased during the time the
mother was carrying the child.

The occasional bad influence of the pregnant state has been
illustrated {499} by a case reported by Terrillon.[43] This example
was a woman who had been the victim of epilepsy of hereditary origin
since her seventh year. At the commencement of menstruation her
attacks became periodic, and recurred every two months, and she had
several two or three days before the flow. Two pregnancies followed
several years afterward. During the periods they were increased in
number and severity, and occurred several times daily. She had more
attacks at this period than in all the time after delivery.

[Footnote 43: _Annales de Gynécologie_, June, 1881, p. 401.]

I have found that the relief of uterine flexion or the establishment
of menstruation has exercised a decidedly modifying influence for the
better in several cases.

Sometimes the disease is interrupted by the menopause, but very often
in my experience it has changed in type and been followed by mental
degeneration.

The prognosis of the epileptoid mental state is serious in the
extreme, and even when in early life the attacks are aborted or
changed to perversion of the intellect or emotions existing as a
complication, the hope of cure dwindles almost to nothing.

The spontaneous cure of epilepsy is rare. Its course, however, is more
often interrupted by some intercurrent disease. Of 33 cases observed
by Delasiauve in which there was some complicating disease, such as
erysipelas, pneumonia, pleurisy, acute articular rheumatism, burns and
contusions, scarlatina, erythema, or the condition of pregnancy, it
was found that in 25 cases there was a decided improvement (une
heureuse influence), and in 8 only was there no modification of the
attacks. Axenfeld is disposed to believe that acute and febrile
disorders more decidedly influence the course of epilepsy than those
of a chronic nature. The influence of either may be small or may
diminish the number of attacks without curing the disease.

TREATMENT.—The treatment of epilepsy depends so much upon the form of
the disease that no arbitrary rule can be laid down upon general
principles, and we must bear in mind the necessity for removing the
exciting causes if possible, the preservation of the balance of
cerebral blood-pressure and cell-equilibrium, and the nutrition of the
cerebral mass. It may be our purpose to remove various toxæmic or
cachectic states as well. As a minor division of treatment we must
consider the abortion of the attack when auræ are detected. It has
been the custom, I think among too many, to manage the disease in an
empirical manner, depending upon some routine course of treatment,
such as the indiscriminate use of the bromides, for example. I am
convinced that the intractable character of the disease has come to be
greatly exaggerated through failures attendant upon the wholesale use
of the bromic salts, without regard to the indication in each
particular case. It behooves us first to select a reliable bromide,
and then to give it with relation to the time of the fit, its
severity, and the condition of the individual. The importance of this
has impressed me very often. An equally divided daily dose will not do
a patient who has matutinal attacks the same good as will a large dose
at night, and in certain anæmic individuals the bromides very often
increase the attack. Then, too, the cases in which seizures of petit
mal predominate are not benefited to the extent that those are in
which {500} the repetition of severe attacks is the feature. The
bromide should always be well diluted and given when the stomach is
empty or nearly so. The bromide of sodium is, to my mind, the most
serviceable salt, and when given alone or combined with the bromide of
ammonium is better than the potassic salt or the various others. It
should be carefully kept in solution or in waxed-paper powders in a
tight preserve-jar. As to its method of administration, I much prefer
the use of a solution which shall combine other adjuvants which I will
presently mention, and separate powders as well, which may be used to
reinforce the dose. The latter are to be employed by the patient in
the event of an unlooked-for series of attacks, and are to be used to
the point of producing mild bromism at the time. In certain cases it
is all-important to take into consideration the condition of the
heart. In some cases where there is manifest and continued cerebral
congestion, with full vessels and hard pulse, I have found that the
combination with chloral or aconite was desirable. In other cases
where the heart's action was irregular and weak my experience with
digitalis and nitro-glycerin or with strychnine was most happy. In
those cases that passed large quantities of clear urine of low
specific gravity the action of nitro-glycerin and digitalis has been
most prompt, and the same has been true of epilepsies of migrainous
origin.

There have been various methods of using the bromide suggested which
are more or less practical. The writers of a few years ago suggested
the prompt production of bromism—a state in which the patient should
be kept for a long time. This I strongly disapprove of, not only
because the mental and physical depression is a very disagreeable and
sometimes permanent condition, but because I have found that the
attacks are often increased after a time, though at first they may
have been suppressed. Others believe in giving the bromides at
intervals, with periods when no medicine at all is administered.

For my own part, I am in favor of the establishment of a mild bromism
which does not extend beyond a slight anæsthesia of the fauces or the
appearance of slight acne. If I find it necessary to increase the
dose, I give cod-liver oil, iron, and bark or some of the many
preparations of the hypophosphites for a time; and they do not
diminish the specific effects of the drug to any great extent. In the
event of a series of attacks I direct the patient to take an extra
dose at such time as will anticipate the seizure.

This treatment should be kept up for at least two or three years after
the attacks have disappeared, and it may be even necessary to continue
a bromide course in a small way for an unlimited period.

If there be an hysterical element, or if ovarian excitement is
supposed to have anything to do with the attacks, the combination of
cannabis indica is strongly recommended. This suggestion holds good in
the cases where migraine is associated with the epilepsy, or the
latter is an outgrowth of the former.

Next to the bromides of potassium and sodium I have been very
successful with the nickel bromide. I find that it is retained with
little trouble, producing no gastric derangement if taken after
eating. A syrup prepared by most of the good pharmacists is preferable
to any other method of administering the salt. Quite recently
Leaman[44] has reported {501} two cases of severe epilepsy which were
greatly benefited. His conclusion is that it does most good in the
form of the disease when the attacks are separated by long intervals.

[Footnote 44: _Med. News_, Apr. 18, 1885.]

The bromate of potassium, which has been used by Weir Mitchell[45] and
Hinsdale, may be worthy of a trial. It should never be given, however,
in larger doses than five or ten grains thrice daily. These
investigators found that thirty grains slowed the heart very
considerably, and forty grains produced watery discharges from the
bowels and drowsiness. In their hands, notwithstanding these
disagreeable effects, it controlled the seizures. The hydrobromate of
conia is a comparatively new remedy which has been recommended. My own
experience does not support that of Wolfenden.[46] Severe cases were
treated by him with benefit. The dose he recommends is half a grain,
and not more than four and a half grains are to be given in
twenty-four hours. Headache and dizziness attended its use.

[Footnote 45: _Med. News_, Dec. 27, 1884, p. 718.]

[Footnote 46: _Practitioner_, June, 1884.]

Erlenmeyer[47] is an advocate of the mixed treatment, and his best
results have been obtained by combining the bromides of potassium,
sodium, and ammonium in the proportion of 1:1:½. He thinks much
greater permanency of effect follows such a combination. A curious
result witnessed by this author is the fact that the acne produced by
one salt given alone is apt to disappear when the combination is
administered.

[Footnote 47: _Centralblatt für Nervenheilkunde, Psychiatrie, etc._,
No. 18, 1884.]

A solution of hydrobromic acid, prepared after Fothergill and Wade's
formula, is recommended by H. C. Wood of Philadelphia,[48] who
presented the record of its use in twelve cases of obstinate epilepsy.
It seems that in his hands large doses acted much better than when the
bromides were given alone. He recommends ounce iij per diem. My own
experience, which I detailed some years ago, was to the effect that it
possessed no virtues whatever in ordinary doses. The solution is so
difficult to take, and so disagreeable in every way, that many
patients prefer almost any other treatment. It cannot be doubted that
some cases of epilepsy are benefited by a change of treatment, no
matter what, and possibly Wood's cases belong to this class.

[Footnote 48: _Med. News_, Feb. 23, 1884.]

Belladonna and ergot are remedies that have had many advocates,
Trousseau being the most pronounced champion of the former. Their use
in the lighter attacks is attended sometimes by the most happy
results, but they cannot be said to have any permanent effect. The
first is advantageous because of its power to diminish reflex
excitement, and in those undeveloped infantile convulsions which are
often grouped under the head of eclampsia its virtues are decided.
Belladonna or its alkaloid may be given in combination with the
bromides. Ergot or ergotin, in spite of its undeservedly bad
reputation, may be given in large doses, one to two drachms of the
tincture thrice daily, or five grains of the aqueous extract in the
course of the day. Of chloral there is not much to be said. At one
time it was thought to possess great virtues, especially in
combination with the bromides, but subsequent experience has taught me
that its use has many drawbacks, and only in exceptional cases is it
to be recommended—viz. in those in which there is a disposition to
excitement—either as a substitute for the attack or as a sequel.

{502} The use of the iodide of potassium in combination with the
bromides is of great service in symptomatic epilepsies or those of
syphilitic origin. The iodide should be pushed, so that the patient
may take three or four drachms daily, and its injurious gastric action
and unpleasant taste may be done away with by administering it in
large quantities of milk or some mild alkaline water, such as Vichy.
Among the other remedies used and advocated by various writers are
hyoscyamine, the salts of zinc, chloral, the ammonio-sulphate of
copper, picrotoxin, strychnine, curare,—all of which have little or no
effect in permanently changing the course of the disease. Cerebral
galvanism, if properly employed, is certainly worthy of a trial as an
adjuvant.

As abortants we may resort to diffusible stimulants—ammonia, alcohol,
or some carminative. If the aura be perceived, a drachm of the
aromatic spirits of ammonia or a glass of sherry will often prevent
subsequent developments, and the inhalation of ten or fifteen drops of
nitrite of amyl will avert the attack. Nitrite of amyl may be
conveniently used in the form of pearls, which may be first crushed in
the handkerchief. The nitrite of soda, which has been recommended as a
substitute, is an unstable and dangerous drug, and is not to be
recommended.

I called attention some years ago to the virtues of nitro-glycerin as
an abortant in epilepsy. It may be given in alcoholic solution or
tablets from 1/50-1/25 of a grain at a dose, to be perhaps repeated.
Great care should be taken to procure a reliable preparation.

When a sensory aura proceeds from a particular locality in preference,
the application of some local form of irritant is strongly
recommended. A blister or light touch of the button of the actual
cautery will do, and if the point of origin be one of the extremities
a circular blister or cautery-line, after the method recommended by
Buzzard, will be serviceable in the treatment of the case.

Buzzard has observed the fact, in several of his patients who
complained of a sensory aura in the biceps, that when an encircling
blister was applied just above this spot the attacks were aborted. In
more than one of his cases of partial epilepsy the extraordinary
result of a transfer of the convulsion to the other extremity is
noted. He found that the circle should be complete, for a blister
which half encircled the arm did no good. I have used the same
treatment in cases of writer's cramp with marked benefit.

Brown-Séquard has pointed out the good effects of forcible and painful
extension of one finger or toe if the aura is of sufficient duration
to enable the individual to resort to this procedure.

The condition known as the status epilepticus is best treated by amyl
nitrite, which can be administered frequently. Repeated doses of
nitro-glycerin, so that its full effects are produced, do more good
than chloroform or any of the well-known anæsthetics.

Of setons I have very little to say. At best, they are a barbarous and
painful mode of treatment, and, although cures have been effected, I
have never been much encouraged by their so-called influence.

Certain intractable cases are helped by surgical procedure, and
trephining has sometimes resulted in a cure. I know of one brilliant
result obtained by Leo of this city in an old epileptic, in which the
use of the instrument over the occipital region resulted in a complete
removal of {503} the disease. It is especially recommended in cases in
which the form of the attacks bears some relation to the probable
disturbance of the cortical motor-centres; and even in such cases
there must be constancy in the method of expression of the convulsion.
So often do we find meningeal thickening of an extensive district that
it is manifest that trephining would do little or no good. The
statistics of the operation are unsatisfactory, for in the large mass
of testimony there is great want of exactness as to the pathological
suggestions of the attack, and a great deal about the method of
procedure and recovery from the operation itself, and very little
about the phenomena of the disease.

The diet of the epileptic should be of the most simple kind.
Merson,[49] whose carefully-prepared paper is full of valuable
statistics, is strongly in favor of vegetable diet, and his results
are encouraging. I am convinced that many children never would have
become hysterical or epileptic but for injudicious indulgence in
animal food. Whenever possible, I confine my patient to a diet of
fish, poultry, and fresh vegetables, with fruit. As an exciting cause
the overloading of the stomach has so often precipitated attacks as to
lead Paget and others to invent the term gastric epilepsy for this
form of the disease. The greatest care must be paid not only to diet,
but to the general habits of the patient—over-exercise, especially
after eating, the avoidance of hot places and high altitudes. A
residence by the seashore is preferable to mountainous places; and
excitement, over-study, and all agencies favoring cerebral congestion
are to be avoided.

[Footnote 49: _West Riding Reports_, vol. v. p. 1.]


{504}


THE NEURAL DISORDERS OF WRITERS AND ARTISANS.

BY MORRIS J. LEWIS, M.D.


DEFINITION.—These neural disorders consist of a certain train of
nervous symptoms, such as spasm, paralysis, pain, tremor, vaso-motor
disturbances, etc., either alone or in more or less complicated
combinations, which follow certain muscular acts and are occasionally
accompanied by a marked condition of general nervousness; they occur
in many of the occupations of every-day life that require for their
performance a constant muscular strain combined with more or less
delicate movements of co-ordination continued for long periods at a
time.

SYNONYMS.—Among the terms used to designate the various forms of the
affections produced in the manner just stated may be mentioned the
following:

Special Terms.—Writers' cramp, Scriveners' palsy, Steel-pen palsy,
Chorea scriptorum, Paralysis notariorum, Graphospasmus, Mogigraphia,
Crampe des écrivains, Nevrose des écrivains, Schreibekrampf, Le mal
télégraphique, Crampe télégraphique, Klavierkrampf, Pianists' cramp,
Tailors' cramp, Loss of grip, etc.

General Terms.—Professional dyscinesiæ, Professional impotence,
Anapeiratic paralysis, Nevrose co-ordinatrice des professions,
Functional spasm, Fatigue diseases, Professional hyperkineses, etc.

None of these terms are satisfactory, and, in fact, it is difficult to
fine one that will include the various symptoms arising from the
habitual use of a muscle or group of muscles, in the same way for long
periods at a time, in the different occupations known to give rise to
these neuroses, without including diseases belonging to entirely
different classes.

It is with some hesitation that I suggest the term copodyscinesia
(_κόπος_, toil, weariness, fatigue; and _δυσκινησια—δυς_, faulty,
difficult, hard, and _κινησις_, motion, movement) as signifying
difficult or faulty motion due to constant repetition of the same act.

HISTORY.—Some of these neuroses have been recognized for years; this
is particularly true of writers' cramp, the earliest notice of which I
have been able to discover is in a small work by Ramazini,[1] printed
in 1746.

[Footnote 1: Bern. Ramazini, _Treatise on the Diseases of Tradesmen,
etc._, translated by Dr. James, London, 1746.]

Most of the articles upon this subject have been written during the
last fifteen or twenty years.

{505} ETIOLOGY.—Many of our every-day actions, which we perform almost
automatically, are the result of months and even years of practice;
this is well exemplified in the act of writing. At first each letter
is made by a separate and deliberate act of volition, and considerable
thought has to be expended upon its formation; but little by little
the preponderance of the volitional element decreases, until at last
we write with but little consciousness of each separate movement, and
the act becomes almost an automatic one, the sentence being conceived
and the hand committing it to paper with but little thought of the
intermediate muscular acts. In a somewhat analogous manner do we learn
to walk, each movement being laborious and requiring much thought for
its execution: in addition to this, we must regulate the amount of the
movement and keep in abeyance all associated muscular action.

This last is spoken of by Hasse[2] as an important factor in the
etiology of these affections. When, however, any one of the various
muscles whose integrity is necessary for the automatic performance of
any act becomes affected, let the lesion be in the muscle itself or
anywhere in the nerve-substance between it and its centre, or in that
centre itself in such a way as to hinder its free response to the
nervous stimulus, then the will has to be especially directed to the
act in order to counteract the effect of the disability, and some
other muscle or group of muscles must be substituted in the place of
the one incapacitated. That which was previously performed easily and
without fatigue now becomes difficult and exhausting.

[Footnote 2: _Handbuch der speciellen Pathologie u. Therapie_,
“Krankheiten des Nervensystems,” 1te A., Bd. iv., 1869.]

It will be in place here to consider in detail the action of the
muscles concerned in performing one or two of the acts most prolific
of the affections under consideration.

The first of these that will be examined is the act of writing.

Generally speaking, the methods of writing may be divided into two:
1st, where the fingers do all the stroke movements, the arm remaining
quiescent except for the lateral movement; 2d, where the pen is held
steadily by the fingers and the letters formed by the movement of the
whole arm. In the latter the muscles of the hand and forearm are used
almost entirely for pen-prehension and poising, although there is
generally a slight finger movement for the long strokes; the forearm
is allowed to rest upon the bellies of the flexor muscles as a sort of
movable fulcrum, the pectorales, teres major, and latissimus dorsi,
together with the biceps and triceps, being mainly employed in forming
the letters.

This last method of writing is the one mostly taught in the public
schools at the present day; and as a large number of muscles are
brought into play, and as there is a more even division of the work,
it is claimed that fatigue is not so soon complained of as in the
first or older method.

The act of writing is primarily divisible, according to Poore,[3] into
three acts: 1st, the act of prehension; 2d, the act of moving the pen;
3d, the poising of the forearm and hand. The muscles concerned in the
act of prehension are—the first two dorsal interossei, the opponens,
abductor, and flexor brevis pollicis, and, to some extent, the flexor
longus pollicis and the extensors of the thumb. The adductor should
also be included in this enumeration.

[Footnote 3: G. V. Poore, _Electricity in Medicine and Surgery_,
London, 1876.]

{506} The muscles employed in the movement of the pen differ somewhat
according to the method of writing. In the finger movement Poore
enumerates the following muscles as the ones used, viz.: flexor longus
pollicis, extensor secundi internodii pollicis, flexor profundis
digitorum, extensor communis digitorum, and also, to a lesser degree,
the interossei.

In the second method of writing these muscles are comparatively quiet,
except in making the letters which extend far above or below the line,
while the muscles previously mentioned when describing this method are
the ones called into play. The poising of the arm and hand is mainly
accomplished by the supinator longus, supinator brevis, and possibly
by the extensors of the thumb.

From a study of what has been written it will be seen that there are
two classes of muscular actions concerned: 1st, the steady contraction
of the muscles that poise the hand and hold the pen; and 2d, the
intermittent contractions of the muscles concerned in moving the pen:
both of these classes are equally important in the etiology of
writers' cramp.

Chronic fatigue of the muscles is undoubtedly, in some cases, a
precursor, if not a cause, of copodyscinesia, and, according to
Poore,[4] is occasionally the expression of hyperæmia or mild
inflammation of a motor nerve. Acute local fatigue has symptoms which
are well known to us all after having taken violent exercise, cramp
and pain being the two most prominent ones.

[Footnote 4: “Writers' Cramp and Impaired Writing-Power,”
_Medico-Chirurgical Transactions_, vol. lxi.]

Any student who has dissected much has experienced the intense feeling
of fatigue in the muscles required to hold the dissecting forceps,
particularly when the spring is a little too strong. Much the same
thing is noticed when one who has not been accustomed to write much is
for some cause compelled to do so; he will probably notice that in a
few hours he is exerting a greater amount of muscular force in
pen-prehension than usual, and may even find that he is producing a
disagreeable feeling in the distal phalanges by the pressure he is
using; he will also probably be aware of a burning sensation between
the shoulder-blades.

These symptoms are in all probability dependent upon, or are at least
coincident with, a hyperæmia of the nerves and spinal cord, and, if
persisted in for a long time without proper intervals of rest must
sooner or later interfere with the healthy condition of the spinal
cord, as well as of the nerves and muscles of the hand and arm.

Poore, while considering the symptoms of fatigue as in large part
peripheral in origin, readily admits that they must generally be
accompanied by central changes.

The manner of writing and of holding the pen is of considerable
influence in the causation of this trouble. Practically, the fluent
writer is more apt to contract this affection than he who writes
badly, for the latter seldom obtains a position where steady copying
is to be done; theoretically the reverse is true if the amount of work
in the two cases is the same.

When the pen-holder is allowed to drop below the head of the first
metacarpal bone the movements of the fingers are restricted; the
middle and fore finger upon one side of the holder and the thumb on
the other act upon the principle of the toggle-joint, so well known in
mechanics, and, {507} as the pen-holder is drawn backward to make a
stroke, bind the distal phalanges tightly against the holder: this in
a short time causes fatigue and awkwardness in writing; but if the
holder is made to cross the proximal extremity of the first phalanx of
the fore finger the toggle-joint movement is destroyed.

These remarks apply of necessity more strongly to the finger movements
than to the conjoined finger-and-arm movement.

Writing with a pencil is not as liable to bring on fatigue and nervous
trouble as pen-writing, this being mainly owing to the fact that with
the former no particular angle is required to be maintained between
the point and the paper; there is therefore less effort at poising, as
the pencil may be rotated at pleasure, while with the pen one angle
has to be maintained. The same remarks should apply to the fluid
pencils (stylographic and Mackinnon pens) now so universally used; in
fact, they have been considered by Putnam[5] as much easier to write
with than the pencil, as less weight need be applied upon the tip in
order to write.

[Footnote 5: J. J. Putnam, M.D., “A New Adjuvant in the Treatment of
Writers' Palsy,” _Boston Med. and Surg. Journ._, vol. ci. p. 320,
1879.]

The idea that these troubles of writers were due to using steel pens,
as once thought, is manifestly without foundation, as the affection
was recognized before the time of the introduction of steel pens,
which was from 1800 to 1820.

Fine sharp pens are, however, more productive of evil than composition
pens or those with a broad soft nib, as they do not move as easily
over the paper, and therefore introduce a difficulty, although a
slight one, in the act of writing. The theory that the chemical action
between the ink and the metallic pens, and the friction of the pen on
the paper, generate sufficient electricity to affect the fingers
through the medium of the metallic portion of the pen-holder is too
preposterous to mention, except to show what curious reasons are given
in attempting to explain obscure and difficult subjects.

The next occupation which very frequently gives rise to these
affections is telegraphy.

The invention of the Morse telegraph in 1844, and its general
introduction, both here and abroad, a few years later, has proved a
most fertile source of copodyscinesia, although but little has been
written on this form of neurosis, Onimus,[6] Robinson,[7] and
Fulton[8] being among the few to describe it, although several later
writers mention its existence.

[Footnote 6: “Le Mal télégraphique ou Crampe télégraphique,” _Compte
Rend. Soc. de Biol._, 1878, 6, S. V. 92-96; also “Crampe des Employés
au Télégraph,” _Gaz. méd. de Paris_, 1875, p. 175.]

[Footnote 7: Edmund Robinson, M.D., “Cases of Telegraphists' Cramp” (4
cases), _British Med. Journ._, Nov. 4, 1882.]

[Footnote 8: Thomas Weymss Fulton, “Telegraphists' Cramp,” _Edinburgh
Clin. and Path. Journ._, Feb. 2, 1884.]

Telegraph operators, particularly those employed in large cities,
whose time is nearly all taken up with their work, are more exposed to
the causes of copodyscinesia than those following other trades. They
are not only exposed to the danger of contracting the affection by
using the telegraph-key in transmitting messages, but when not so
employed are receiving messages by sound and writing them down,
frequently at the rate of thirty to forty, or even more, words per
minute. Thirty words a minute is good telegraphy: this would require,
on the average, nearly 600 {508} separate contractions. This would be
36,000 contractions per hour, while to write the same sentences would
require about 10,000 less.

The operators employed by the Associated Press, although comparatively
few in number, two hundred probably including all in the United
States, write for hours at a time, using a stylus and manifold
writing-books, making as many as twelve copies at one writing; this
obliges them to grasp the stylus very firmly and to press with
considerable force, making the act of writing much more difficult.

In addition to the work mentioned above, those who have large numbers
of messages to transmit become so expert that to save time they make a
record concerning the last message sent with the left hand, while they
are telegraphing the next one with the right hand. A complicated act
of co-ordination is thus being performed with each hand, the
difficulty of which may be appreciated by any one if he but try to
perform it.

An editorial in the _London Lancet_[9] states that “telegraphers'
cramp will, we have little doubt, take its stand among the
last-mentioned curiosities” (milkers' cramp, hammer palsy, etc.), and
“that the telegraph clerk usually enjoys repeated intervals of
complete rest, and runs consequently hardly any risk.”

[Footnote 9: 1875, vol. i. p. 585.]

Hammond[10] likewise states that telegraphers' cramp is rare in the
United States, but a slight investigation proves these two statements
to be, unfortunately, very far from the truth. According to recent
statistics,[11] the Western Union Telegraph Company employs nearly
twenty thousand operators, who transmit annually over thirty-five
million messages, and as investigation seems to prove that a very
large number, if not the majority, sooner or later show some symptoms
of copodyscinesia, it becomes evident that this neurosis is far from
rare, although hitherto almost entirely overlooked by the medical
profession.

[Footnote 10: Wm. A. Hammond, M.D., _Dis. Nervous System_, 6th ed.,
New York, p. 789.]

[Footnote 11: J. B. Abernethy, _Commercial and Railway Telegraphy_,
Cleveland, Ohio, 1883, 2d ed.]

Operators are very loath to confess that they are suffering from loss
of grip, as they have termed it, for then they are considered as less
efficient than formerly, and may be asked to resign in favor of one
not affected, or be lowered in their salary—a point of great moment,
as telegraphy is their means of support. This accounts for the
apparent small number of the cases.

In telegraphing, the knob of the key, a circular disc of hard rubber
more than one inch in diameter, and placed about one and a half inches
above the level of the table, is grasped, as a rule, between the thumb
and middle finger, with the tip of the index finger resting on top,
the position being quite analogous to the method of pen-prehension,
the strain, although much less, falling on the same muscles, but as
all lateral movements of the key are impossible, the muscles employed
in poising are not brought into play as in writing. The arm is either
allowed to rest upon the table, upon the flexor mass of muscles of the
forearm near the elbow as a kind of movable fulcrum, or is held with
the forearm parallel to the table and a short distance above it.

The movements of telegraphing are made by the alternate action of the
triceps, which depresses the wrist by extending the forearm, assisted
by the flexor carpi radialis, flexor carpi ulnaris, flexor sublimis,
and flexor {509} profundus digitorum on the one hand, and the biceps
and supinator longus, which elevate the wrist by flexing the forearm,
assisted by the extensor carpi radialis longior, extensor carpi
radialis brevior, extensor carpi ulnaris, and extensor communis
digitorum on the other.

The movement of the key-knob, being about the one-twenty-fifth of an
inch, is so slight that it may be entirely ignored, so that with the
fingers upon the key and the forearm resting upon the table near the
elbow the motion must be a downward and upward one of the wrist; when,
however, the arm is held above the table and parallel to it, the
motion is more extended, the shoulder-muscles being used to support
the arm.

The wrist is held in a supple manner, and not rigidly, the momentum of
the downward movement being used to close the circuit; this, as before
stated, is made mainly by the triceps, and is checked by the flexors
and supinator longus.

The extensors of the wrist and fingers have a double duty to perform,
for, besides assisting in recovering from the downward stroke, they
have to support the hand during the whole act of telegraphing, in
order to prevent the weight from resting on the key, which would
prevent quickness in making and breaking the circuit.

On long circuits, particularly in wet weather, when much electricity
escapes from the line, the movements have to be made with much more
decision than usual in order to make the signals intelligible at the
distant station.

The accompanying diagram shows well the movement of the wrist as above
described, the hand and wrist moving into the position of the dotted
lines when the downward stroke is made.

[Illustration: FIG. 28.]

Our hand is essentially a prehensile organ, and as such causes us to
educate the flexors the most; the extensors, being mainly used to
relax the grasp of the fingers, are weaker, and the constant strain
spoken of above, being thrown upon them, explains the fact that in
telegraph operating these are the muscles most frequently attacked by
cramp. (See Symptomatology.)

The following figures are of interest as proving the great
superiority, in point of strength, of the flexor over the extensor
muscles of the wrist and fingers. The measurements were made by the
dynamometer of V. Burq, great care being taken to apply the instrument
upon corresponding points of the palmar and dorsal surfaces of the
hand. The grasp of the average man, which includes all the flexor
muscles of the fingers and thumb, equals 125 pounds, while the power
of the flexors of the wrist, exclusive of the fingers, equals 40
pounds. In marked contradistinction {510} to this the extensors of the
wrist register 35 pounds, and the extensors of the fingers only 7. The
total power of all the flexors is therefore 165 pounds, and that of
the extensors 42 pounds, nearly four times less (3.92). In women the
ratio is the same, although the number of pounds registered is about
half.

From the foregoing enumeration of the muscles used in writing and
telegraphing it may be seen that the brunt of the work does not fall
on the same muscles in the two acts, so that operators are seen
utterly unable to telegraph more than a few words intelligibly who can
still write a fluent hand. The two forms of neuroses often coincide in
the same subject, as all telegraphers are of necessity scriveners; in
fact, the majority suffer from both forms, and as a rule the most
difficulty is experienced in telegraphing, and not in writing,
although the reverse is frequently seen. But rarely does one see an
operator who, unaffected as far as telegraphing is concerned, has
difficulty in writing on account of this curious neurosis.

Of the muscles enumerated in the foregoing discussion, six are
supplied, either wholly or in part, by the ulnar nerve—namely, the
first two interossei, adductor pollicis, flexor brevis pollicis (inner
half), flexor carpi ulnaris, and flexor profundus digitorum (inner
part); and seven by the median nerve wholly or in part—namely, the
opponens and abductor pollicis, flexor brevis pollicis (outer half),
flexor longus pollicis, flexor profundus digitorum (outer part),
flexor carpi radialis, and flexor sublimis digitorum.

The remaining important muscles are supplied by the musculo-spiral and
its branches, except the biceps, which is supplied by the
musculo-cutaneous.

The ulnar nerve supplies fifteen of the muscles of the hand; many of
these are not prominently brought forward in writing, but are more or
less used in keeping the hand in the required position.

Poore, after a careful study of 32 cases of undoubted writers' cramp,
found the muscles affected in the following proportions:

  Interossei             (supplied by the ulnar nerve)      18 times.
  Extensors of the thumb (    "    "   "  musculo-spiral)   10   "
  Flexor brevis pollicis (    "    "   "  median and ulnar)  7   "
  Abductor         "     (    "    "   "  median)            7   "
  Flexor longus    "     (    "    "   "    "   )            4   "
  Adductor         "     (    "    "   "  ulnar)             3   "
  Opponens         "     (    "    "   "  median)            2   "
  All the muscles of the forearm, more or less,              2   "

—showing that the muscles supplied by the ulnar nerve were affected
more often than those supplied by the others.

The musculo-spiral and its branches supply the extensors of the thumb,
fingers, and wrist, besides the two supinators; and by referring to
the muscles most called into action in the act of telegraphing it will
be seen that the majority are supplied by this nerve and by the
median, which supplies the majority of the flexors. This statement
explains to a great extent the fact that telegraph operators may be
unable to telegraph and yet be able to write, as the muscles most
important in the two acts have not the same nerve-supply.

The integrity of these nerves is therefore of the first importance in
all {511} cases requiring the use of the fingers and forearm, and many
cases of copodyscinesia undoubtedly have a subacute inflammation of
these nerves, or at least a congestion of the same, as their
foundation, the neuritis or congestion being overlooked, owing to its
mild type.

S. Weir Mitchell[12] states that subacute neuritis is often incapable
of distinct clinical discrimination when of a mild type and when there
is an absence of traumatic cause. Mills[13] states that “a lesion of
the sensitive fibres profoundly affecting this power of conducting
impressions may not cause pain, and that pain is not a necessary
symptom of inflammation of a mixed nerve: this is an important fact,
as I think too much stress is often laid on pain as a symptom of
neuritis, leading to error in diagnosis and treatment.”

[Footnote 12: _Injuries of Nerves, and their Consequences_, by S. Weir
Mitchell, M.D., Philada., 1872.]

[Footnote 13: F. T. Mills, M.D., “On Two Cases of Neuritis of the
Ulnar Nerve,” _Maryland Med. Journ._, vol. viii. p. 193, 1881.]

Other Forms of Copodyscinesia.—In violin-playing the bow is held
steadily between the fingers and thumb for long periods at a time, and
the left arm is forcibly held in supination in order to bring the
fingers upon the strings—actions well calculated to cause trouble if
persisted in, not taking into account the rapid movements of the
fingers which are necessitated in playing and the movements of the arm
in bowing. The violinist is therefore liable to suffer in both arms,
but in a different manner in each, as different muscles are used in
bowing and in fingering.

The other musical instruments necessitating great education in the
movements of the fingers and wrist are also liable to cause these
neuroses, but this is not true of those wind instruments which require
education of the movements of the lips and tongue. Piano-playing is a
frequent cause of these troubles, which have been known to appear
quite suddenly during the practising of some difficult piece.

In fact, all occupations which require a muscle or a group of muscles
to be kept in a constant more or less firm contraction, together with
fine movements of co-ordination in themselves and in the neighboring
muscles, may be expected to furnish cases of this class of disease;
the muscles affected necessarily varying with the work done, mere
routine work being more liable to cause trouble than that which is new
and original, as in the latter case time has to be taken to elaborate
it, thus giving temporary rest to the muscles.

Besides the forms already mentioned these neuroses have been known to
effect compositors, engravers; seamstresses, tailors, from using the
needle or scissors; cobblers; bricklayers, from using the trowel;
artificial-flower makers; weavers; milkers; painters; dentists;
ballet-dancers, from standing on their toes; blacksmiths and those
using the hammer; carpenters, from using the saw and screw-driver;
electrical-instrument makers, from winding coils; turners;
watchmakers; fencing-masters; cigar-makers; makers of photographers'
gelatin plates; knitters and those using the crochet-needle;
billiard-players; counters of money; dressers of hides; pedestrians;
and a few others.

Writers, telegraph operators, and musicians are those which by far are
the most frequently affected, the others being almost curiosities.
Among the latter may be mentioned the case, recently coming under my
notice, of pain in the right forefinger and arm, with cramp in the
former, upon {512} any prolonged attempt to read with this finger the
raised letters of the alphabet of the blind. The patient was a blind
woman depending for her living upon crocheting, which occupation was
also seriously interfered with by this trouble.

After inquiring, in factories, etc., I find that the disease is by no
means a recognized one among the workmen. Among telegraphers, however,
it is so well known that they have called it the loss of grip, while
in France it is known among them as le mal télégraphique.

Gardner,[14] after a careful investigation, finds no proof that
physical disease originates in, or is even aggravated by, the use of
the sewing-machine, and he has “never even heard of a case of cramp.”
He comes to this conclusion after having visited many large factories
where sewing-machines are used and worked by foot-power; his remarks
apply to those machines where the feet are worked together, and not
alternately, which last has been known, according to Down,[15] to
cause serious troubles, of an entirely different kind, however, from
the one under consideration, and with which this subject has nothing
in common.

[Footnote 14: A. K. Gardner, M.D., “Hygiene of the Sewing-Machine,”
_Am. Med. Times_, Dec 15-29, 1860.]

[Footnote 15: “Hygiene of the Sewing-Machine,” _London Lancet_, 1866,
vol. ii. p. 447.]

PREDISPOSING CAUSES.—Tobacco and Alcohol.—Both of these articles exert
a powerful effect upon the nervous system, tobacco particularly being
a factor in the causation of many cases of neurasthenia. The first
effect of tobacco and alcohol in small doses on the brain and spinal
cord is, according to Boehm and Von Boeck,[16] that of an excitant;
subsequently it acts as a depressant. Eulenburg[17] mentions tremor as
of very frequent occurrence, and states that he has frequently noticed
it in young cigar-makers who smoke to excess.

[Footnote 16: _Ziemssen's Cyclopædia_, Amer. ed., vol. xvii.]

[Footnote 17: _Ibid._, vol. xiv.]

Cigarettes are more injurious than other forms of tobacco used in
smoking, as the smoke is nearly always inhaled, a greater effect being
thus produced by a given amount of the drug. Besides this, cigarettes
contain a large amount of other substances deleterious in their
effects. Trembling of the fingers and hand is frequently seen in those
smoking cigarettes freely.

The majority of the cases of copodyscinesia that are in the habit of
using either of these articles acknowledge that their use increases
their disability; in very exceptional cases the moderate use of
tobacco appears to soothe and quiet, and thus relieve some of the
symptoms.

Age.—Copodyscinesia is a disease of early adult life; it is rare in
old age. In 39 out of 43 cases of telegraphers' cramp coming under my
notice the age of the patient at the outset of the disorder could be
accurately determined. The average was 23.94 years. The average age of
all cases of the various forms of copodyscinesia seen by me up to the
present time (1886) is 25.96 years.

Sex.—The influence of sex as a predisposing cause of these affections
has not been studied with sufficient care, although a few authors
allude to it.

Onimus[18] states that women are more frequently affected than men
with telegraphers' cramp. Erb[19] states that writers' spasm is met
with more {513} frequently in men, much more rarely in women, and that
pianoforte-players' spasm occurs more frequently in women, and
particularly in neuropathic persons who belong to nervous families.
Hasse[20] and Romberg[21] consider that writers' cramp especially
occurs in men, women being affected very rarely. Of the 75 cases of
impaired writing-power reported by Poore,[22] only 17 were women,
while of the 31 cases of undoubted writers' cramp included in the 75,
all were men.

[Footnote 18: _Loc. cit._]

[Footnote 19: “Writers' Cramp and Allied Affections,” _Ziemssen's
Cycl._, Amer. ed., vol. xi.]

[Footnote 20: _Loc. cit._]

[Footnote 21: _Nervous Diseases_, vol. i. p. 320.]

[Footnote 22: _Loc. cit._]

It may be seen that the male sex has been employed far more frequently
than the female in most of the occupations previously mentioned, so
that a larger percentage of men would naturally be affected; but now
that women are being employed more generally a larger number of the
female sex may be expected to suffer in this way.

Whether sex, per se, has much influence as a predisposing cause is
difficult to say, as statistics are wanting, but it is probable that
with the same amount of work given to each sex a large proportion
would be found among women.

Women are being employed to a considerable extent in telegraphy, and
although I have been able to collect but 4 cases of this form of
copodyscinesia affecting women out of a total of 43, I have reason to
believe it is quite common among them, my mode of collecting
statistics (soliciting replies to printed questions) being much more
likely to give a larger percentage of answers from men.

Hereditary Influence and Nervous Temperament.—Both of these factors
seem to play an important rôle as predisposing causes to these
affections. Cases are on record where several members of the same
family were the subjects of writers' cramp. The statement made by Erb
(vide supra), that neuropathic persons and those who belong to nervous
families are more subject to these affections than others, seems to me
to be true, at least to a great extent, for a careful inquiry into the
history of cases coming under my knowledge has quite often elicited
the statement that migraine, functional spasm, epilepsy, hay fever,
neuralgia, writers' cramp, telegraphers' cramp, or general
neurasthenia has existed either in the immediate family or in the
patients themselves. Hasse[23] is also of the same opinion.

[Footnote 23: _Loc. cit._]

Whittaker[24] states that many of the cases coming under his notice,
if not the majority, occurred in individuals of irritable nervous
temperament, subject themselves to, or the descendants of parents
afflicted with, migraine, chorea, epilepsy, paralysis, or some form or
other of neurosis, but that a certain contingent of the minority of
cases occurred independently of any neurosis or any abuse of alcohol
or sexual excess.

[Footnote 24: _Cincinnati Lancet and Clinic_, N. S., vol. iv. p. 496,
1880.]

Fritz,[25] after studying 25 cases of writers' cramp, found 7 who
either stuttered, squinted, or had choreoid movements or œsophageal
spasm at the same time; but it is probable that a few of these cases
at least were due to some central lesion (post-paralytic chorea?).

[Footnote 25: “Ueber Reflexionsfingerkrampf,” _Oesterr. Jahrb._, März
u. April, 1844, quoted by Hasse, _loc. cit._]

Beard[26] holds an opinion directly the reverse of the vast majority
of the authorities upon this subject, and states that this disease
occurs mostly in {514} those who are of strong—frequently of very
strong—constitution, and that it is quite rare in the nervous and
delicate; and when it does occur in those who are nervous it is easier
relieved and cured than when it occurs in the strong.

[Footnote 26: G. M. Beard, M.D., _loc. cit._]

That in the majority of the cases there is an emotional factor is
evident to every one who has seen a considerable number, the knowledge
that some one is looking on and will notice the disability being
almost sure to aggravate the symptoms. This is frequently noticed
among telegraph operators, and is well exemplified in the following
answer made by a female operator: “If I am working with a disagreeable
or fault-finding operator, who I know will make unpleasant remarks
about my sending, and break me (break the circuit) on certain
difficult letters, it is almost impossible to make those letters
correctly with either hand.” Again she says, “If I come to the
difficult letters without thinking about them, I can make them much
easier than if I look ahead in the message and see them; for instance,
some time after I had ceased using my right hand on account of the
cramp, an outside occurrence made me very angry; just then a message
was placed on my desk, and with my mind fully occupied with my
grievance I sent the message with my right hand very easily and
quickly.”

Wasting Diseases.—These favor the production of these affections in
those predisposed to them by occupation or otherwise, by the constant
drain upon the system. Numbness of the fingers and stiffness are
occasional symptoms of renal disease, and would naturally aggravate
any difficulty of writing and so-forth that the patient might have.
Mitchell[27] reports two cases of writers' cramp dependent upon or
coincident with albuminuria, which were treated in vain until the
condition of the kidneys was discovered: under appropriate treatment
for this condition one recovered entirely from the cramp and the other
improved greatly.

[Footnote 27: S. Weir Mitchell, M.D., “Nervous Accidents in
Albuminuria,” _Philada. Med. Times_, Aug. 1, 1874, p. 691.]

Traumatism, etc.—Injuries, etc. occasionally act as predisposing
causes; thus cases are on record where the starting-point seemed to
have been an ingrowing thumb-nail, and others where it was the
pressure of large sleeve-buttons upon the ulnar nerve; and tight
sleeves seem to have been the starting-point of inflammatory troubles
ending in writers' cramp. An inflammation of the periosteum of the
external condyle (node) and a painful ulcer upon the forearm are
reported by Runge[28] as giving rise to symptoms closely allied to
this affection. Seeligmüller[29] mentions a case where the symptoms
came on after an insignificant grazing bullet-wound of the knuckle of
one of the fingers.

[Footnote 28: “Zür Genese u. Behandlung des Schreibekrampfes,” _Berl.
klin. Wochensch._, x. 21, 1873.]

[Footnote 29: Adolph Seeligmüller, “Lehrbuch der Krankheiten der
Peripheren Nerven, etc.,” _Wreden's Sammlung, Kurzer Med. Lehrb._,
Band v. p. 29.]

SYMPTOMATOLOGY.—Owing to the fact that various causes give rise to
these affections, and that the different groups of muscles implicated
differ with the varying occupations of those suffering, no one
stereotyped set of symptoms can be described as applicable to each
case, and no one symptom can be looked upon as diagnostic.

The symptoms most frequently seen may be classified under five
heads—viz.: I. Cramp or spasm; II. Paresis or paralysis; III. Tremor;
IV. {515} Pain or some modification of normal sensation; V. Vaso-motor
and trophic disturbances.

These may, and generally do, exist in various combinations, and they
may be accompanied by other symptoms of nervousness; they are not of
necessity confined to the hand or arm, but may become more or less
general. At first they are usually only seen after long continuance of
the occupation which produced them, but later any attempt to perform
this act will cause their appearance, although it may not be noticed
in any other of the daily avocations.

In some of the rarer cases the neurosis makes its appearance suddenly
after a prolonged siege of work. It has been generally stated that
writers' cramp, for instance, only manifests itself on attempting to
write, but this is due to the fact that there is no other occupation
which exactly needs the same co-ordination of the muscles, for others
can be substituted in the place of those affected. This is
particularly seen in the early history of the cases, but when it has
become pronounced in character any analogous movement, such as holding
a spoon or fork or paint-brush, will be sufficient to produce it.
Difficulty in buttoning the clothes with the fore finger and thumb is
frequently noticed.

I. Cramp or Spasm (Spastic Form).—The first form of this disease to be
considered is that in which cramp or spasm is present. This is one of
the most frequent symptoms, and when present usually attracts the most
attention. In most of the articles written upon these affections great
importance has been given to this symptom, which, however, may be
absent during the whole history of the case, but when it does appear
it usually indicates an advanced stage. The term writers' cramp is an
evidence of the widespread opinion of the importance of this symptom.

The cases that present themselves to the physician have usually been
affected for some time, and where cramp is present an earlier
examination would probably have resulted in the discovery of
premonitory signs before the appearance of the spasm or cramp; and in
fact it may be stated that this symptom is always preceded, or at
least accompanied, by one or two more. The muscular contraction may be
so slight as to amount to a mere occasional awkwardness, in writers'
cramp an abnormal grasp of the pen-holder being all that is noticed;
or it may be so severe as to cause a tonic contraction of the muscles
affected, which may continue for some time after the exciting cause
has been removed, as in the cases reported by Poore[30] and S. Weir
Mitchell.[31]

[Footnote 30: _Electricity in Medicine and Surgery_, London, 1876, p.
209.]

[Footnote 31: “Functional Spasm,” _Amer. Journ. Med. Sciences_, Oct.,
1876, pp. 322, 323.]

As might be supposed, these spasms affect most usually the upper
extremities, although they may affect the lower, as is occasionally
seen in workers on the lathe and in pedestrians. Other muscles than
those necessary to perform the act that has become difficult may also
be seized with spasm coinstantaneous with the spasm of the affected
part; thus the left arm may be the seat of associated movements while
the right is being used: these are, however, most frequently seen in
the affected arm when the other is being used to relieve it; they may
also be noticed in the legs, although much more rarely.

Gallard[32] reports a case of a street-pavior who had associated spasm
of {516} both sterno-cleido-mastoid muscles, which came on only when
using the instrument to settle the stones. Dally[33] reports a case of
a woman who had spasm of the left sterno-cleido-mastoid muscle at the
time the right hand was seized with cramp in writing. More rarely all
the muscles on one side of the body may be affected. Reynolds[34]
reports such a case.

[Footnote 32: “Crampe des Écrivains,” _Progrès médical_, v., 1877, p.
505.]

[Footnote 33: “Traitement des Spasms professionnels,” _Journ. de
Thérapeutique_, No. 3, 10 Fèvrier, 1882.]

[Footnote 34: _System of Medicine_, “Writers' Cramp,” vol. ii. p.
287.]

In the spastic form of the disease an early investigation usually
shows a rigidity or spasm of one or more of the fingers, coming on
when an attempt is made to perform the act which originated the
trouble, and occasionally only on performing that act; but this
statement, so strongly insisted upon by some authors as a diagnostic
symptom, does not universally obtain.

The contraction may affect either the extensors or the flexors; in the
former case—in writing, for instance—the pen can with difficulty be
kept upon the paper, and the stroke movement is interfered with; if
the spasm is of the flexors, which is of the most common occurrence,
it usually affects the fore finger and thumb; the pen is then forced
downward, and upon attempting to make the upward movement catches in
the paper; besides, there may be with this a flexion and adduction of
the thumb, which causes the pen-holder or pencil to be twisted from
the grasp, occasionally with sufficient force to throw it to some
distance. The other fingers may be similarly affected. The supinator
longus is quite a common seat of spasm, the pen being thereby drawn
from the paper by a partial supination of the forearm.

Sometimes the character of the spasm cannot be described, the hand
seeming to run away with the pen.

The patient who feels these spasms or contractions coming on soon
changes the manner of holding the pen-holder, so as to relieve the
affected muscles and to use those which are but slightly or not at all
affected. Many grotesque manners of writing may thus be encountered.
One sometimes employed by those seriously affected is to grasp the
holder in the closed hand, holding it nearly at a right angle to the
forearm, all movements being made with the whole arm, thus relieving
the finger-muscles. The diagram on p. 457 shows the method of writing
adopted by a patient who has a marked spasm of the flexors of the
fingers and thumb, preventing his writing in the ordinary manner; he
is also the subject of telegraphers' cramp.

These means, however, give but temporary relief, as, sooner or later,
if writing is persisted in, the muscles of the arm and shoulder become
implicated.

In telegraphers the extensors of the wrist are frequently affected, so
that the operator is unable on account of the spasm to depress the key
of the instrument with sufficient force to close the circuit, the
signals being made, so to speak, in the air, or else a dot (.) is made
in place of a dash (—). The extensor spasm seems to be the most
frequent form of the cramp among telegraphers, many of them saying
that they are unable to keep their fingers upon the key-knob. It will
generally be found that the characters that are the most difficult to
make are those which are composed entirely of dots, such as _h_
(....), _p_ (.....), _6_ (......), or those {517} ending with dots,
such as _b_ (—...), _d_ (—..), _8_ (—....). Some of the spaced
characters are also difficult to make, such as _z_ (... .), _&_
(. ...), _y_ (.. ..).

[Illustration: FIG. 29.]

Occasionally one finger will become rigidly extended during
telegraphing, and any attempt to prevent this will bring on great
discomfort and greater disability. When, more rarely, it is the
flexors which are affected, the key is depressed with undue force at
the wrong time, and a dash is made where a dot was intended, or an
extra dot or so introduced, or the proper spacing of the characters
prevented, thus rendering the message unintelligible.

The telegraph operators who experience the most difficulty in
transmitting usually have a cramp of the extensors, and those having
the most difficulty in receiving (writing) usually have a cramp of the
flexors, although the reverse is occasionally seen.

In some cases of the spastic form of copodyscinesia the contraction
almost becomes tetany; thus there may be a contraction of the flexors
of the wrist, which comes on whenever any attempt is made to use the
hand, although the fingers may be entirely unaffected, or there may be
a more or less constant contraction, greatly exaggerated on any
attempt at motion.

Lock-spasm, as described by Mitchell,[35] is a rare form of this
affection: in this the fingers or hand become locked, so to speak, in
a strong contraction, even stronger than the patient could ordinarily
produce by an effort of will; this lasts for a considerable time, and
after its disappearance the customary work may be resumed.
Duchenne[36] likewise reports some curious cases of functional spasm
analogous to the foregoing.

[Footnote 35: _Loc. cit._]

[Footnote 36: Duchenne (de Boulogne), “Note sur le Spasm functionnel,
etc.,” _Bull. de Thérap._, 1860, pp. 146-150.]

{518} II. Paresis or Paralysis (Paretic Form).—More or less weakness
of some of the muscles of the hand or arm is frequently seen in cases
of copodyscinesia; this is, however, less common than the spastic
form, and, like the latter, is preceded or accompanied by other
symptoms. This form occasionally follows the spastic, or it is seen in
those cases where the cause of the trouble has been a preceding
neuritis, or it may be due to professional muscular atrophy as
described by Onimus,[37] where, contrary to the ordinary rule,
excessive use of a muscle or set of muscles produces, instead of
hypertrophy, a condition of considerable atrophy, usually of the
larger muscles first, which is preceded for some time by pain and
cramp in the affected parts, with fibrillary twitchings; this is
amendable rather rapidly under appropriate treatment, and thus differs
from progressive muscular atrophy, with which it is apt to be
confounded.

[Footnote 37: E. Onimus, “On Professional Muscular Atrophy,” _Lond.
Lancet_, Jan. 22, 1876.]

Some of the cases of this group may be confounded with those of the
former, as there may be an apparent cramp or spasm of the unopposed
healthy muscles. Zuradelli[38] considers this condition to be the one
ordinarily found in this disease.

[Footnote 38: Crisanto Zuradelli, _Gaz. Med. Ital. Lomb._, Nos. 36-42,
1857; also _Ann. Universali_, 1864.]

A paretic condition of one muscle may coincide with a spastic
condition of another not its opponent, the paralyzed muscle being the
one first affected.

When a patient with paresis or paralysis as the most prominent symptom
attempts to write, an intense feeling of fatigue usually appears, and
the writing becomes difficult or impossible—not from a too ready
response and spasm, but from an inability of the muscles to obey the
will; the pen-holder is held in a feeble manner, and sometimes falls
from the grasp. There may be a sense of utter weakness and
powerlessness, the arm feeling as if glued to the table.

Duchenne[39] calls attention to this form of trouble, which he styles
paralysie functionelle, and states that it is much less common than
functional spasm.

[Footnote 39: _Loc. cit._]

New methods of holding the pen are as constant in this form as in the
spastic, as it is as necessary in one as in the other to avoid as much
as possible the use of the affected muscles. A carpet-weaver, seen by
myself, was obliged to tie the knots in the warp on the distal
extremity of the second phalanx of the thumb, as the extensor secundi
internodii pollicis was partially paralyzed, so that he was unable to
keep the distal phalanx extended. This condition came on when he was a
compositor, and compelled him to change his trade. A condition of
spasm had preceded the paralysis.

The first dorsal interosseus muscle is frequently the seat of paresis;
this is readily discovered by measuring the power which the patient
has of lateral movement of the index finger and comparing it with that
of the sound hand.

III. Tremor (Tremulous Form).—Trembling or unsteadiness of the fingers
is occasionally seen, usually most marked in the fore finger when the
hand is at rest with the fingers slightly separated. In some cases
this may be sufficient to cause unsteadiness in work, prolonged work
and over-fatigue being most apt to produce it; as previously
mentioned, this is one of the premonitory symptoms of professional
muscular atrophy. {519} An oscillatory trembling, due to implication
of the supinators and pronator, is described by Cazenave,[40] which
interfered greatly with the act of writing. Tremor is of itself rarely
complained of by those affected with copodyscinesia, unless it becomes
sufficiently marked to cause interference with work.

[Footnote 40: “Observations de Tremblements oscillatoires de la Main
Droite,” _Gaz. méd. de Paris_, 1872, pp. 212-215.]

A peculiar form of nystagmus occasionally seen in miners may be
considered as belonging to this category. According to Nieden of
Bochum[41] it is caused by eye-strain in the defective illumination of
the mines, and consists not of a spasm, but of a defective
innervation, like the tremor of old persons. C. B. Taylor[42] of
Nottingham and Simeon Snell[43] also speak of this as a fatigue
disease.

[Footnote 41: “The Pathogenesis and Etiology of Nystagmus of Miners,”
_Am. Journ. Med. Sci._, Oct., 1881.]

[Footnote 42: Quoted by Poore, _loc. cit._]

[Footnote 43: “Miners' Nystagmus,” _Brit. Med. Journ._, vol. ii.,
1884, p. 121.]

IV. Pain, or Some Modification of Normal Sensation.—Every case of
copodyscinesia, without exception, has at one period or another of the
disease some modification of normal sensation in the hand or arm.
Usually the very first symptom that attracts the patient's attention
is a sense of fatigue or tire in the hand or arm, which at first
appears only after a considerable amount of work; if rest is taken
now, the part regains its normal condition, but if the work is
continued the sensation increases, and the amount of labor necessary
to cause the disability gradually grows less and less until any
attempt suffices to produce it. A painful sensation or a sense of heat
may be experienced in the shoulders or in the cervical or upper dorsal
spine at the time the foregoing symptoms are felt.

These symptoms are due to chronic fatigue in many instances, this
being an important factor in the causation of these troubles. An
expression frequently used by those affected is that the hand or arm
becomes lame; this sense of tire may be slight or may be of an intense
aching character, almost unendurable.

Should spasm supervene, then there will be a sense of tension and pain
in the rigid bellies of the muscles. When a subacute neuritis is
present, as frequently occurs, all the symptoms common to that
condition appear—viz. pain over the various nerve-trunks and at the
points of emergence of their branches, either spontaneous or only
solicited on pressure; areas of hyperæsthesia or anæsthesia; a sense
of itching or tingling or pricking in the arm or hand; or a sense of
numbness, causing the part to fall asleep.

As previously mentioned under Etiology, pain may be absent in some
cases of subacute neuritis. Occasionally, the distal phalanx of the
fore finger or thumb becomes exquisitely sensitive to pressure, and
there may be a burning or stinging pain under the nail, severe enough
to make the patient think local suppuration is about to take place.

Sensory disturbances in the region of the hand supplied by the radial
nerve are quite common, less so in the region supplied by the median,
and least of all in the ulnar distribution. This last having never
been seen by Poore, although, as pointed out by him, the muscles
supplied by the nerve are those most frequently implicated in this
disease when it affects scriveners, his explanation is that the deep
motor branches are {520} widely separated from the sensory branches of
the nerve, while this is not true of the radial.

One case of impaired sensation affecting the ulnar distribution, and
consisting of slight numbness of the palmar surfaces of the ring and
little fingers, has come under my observation. The patient was a young
woman affected with pianists' cramp, having as its foundation a
subacute neuritis of the musculo-spiral and ulnar nerves; the trouble
had lasted five years.

A curious form of pain, as of a bar thrust diagonally through the
hand, has been complained of; again, the arm, hand, or fingers may be
the seat of a subjective sensation of weight, so that one arm will
feel very much heavier than its fellow, or the hand may feel as heavy
as lead. A soreness and sense of tightness, as of a band around the
wrist, a throbbing and pulsation, or a tense feeling as if the skin
would burst when the hand was closed, have been noticed occasionally.

V. Vaso-motor and Trophic Disturbances.—Among the rarer symptoms seen
are vaso-motor and nutritional changes; these never occur alone, but
are accompanied by cramp and fatigue or by some evidence of
nerve-lesion.

When a patient with this symptom attempts to perform the task which
produces the disability, in addition to the fatigue, spasm, or pain
the veins on the back of the hand and fingers will be seen to slowly
enlarge; this may gradually increase until it extends over the whole
arm, the parts becoming more or less turgid with blood, the
temperature at the same time being somewhat increased. A marked
sensation of throbbing accompanies these symptoms.

Other parts more distant may become affected, the face becoming
flushed, palpitation of the heart and profuse perspiration, either
local or more or less general, ensuing, followed by exhaustion.

When there is a marked hyperæsthesia of the distal phalanges of the
fingers, there may be a glossy appearance of the skin, or the parts
may appear inflamed and as if about to suppurate, or there may be
chilblains. A rare symptom is change in the character of the nails,
which become brittle and crack off like shell, either spontaneously or
when an attempt is made to cut them.

GENERAL SYMPTOMS.—Besides the various symptoms above enumerated, there
may be others more general in character, such as intense headache and
great general nervousness, the emotional character being generally
well marked, as is shown by the disability being greatly increased
when the patient knows some one is watching and criticising. There may
be also vertigo and sleeplessness. When there is an associated spasm
of the analogous muscles of the other arm and hand, although there is
no apparent trouble in the arm which is being used, it shows that the
hitherto almost automatic act is losing some of its automatism: this,
although rare, is an important premonitory symptom.

A rare symptom, which, as far as my knowledge allows me to say, is
confined to telegraph operators, is an inability to mentally grasp the
proper number of dots and dashes composing certain Morse characters:
this usually coincides with the difficulty experienced in making those
characters after they have been thought of, and also makes it
difficult for them to recognize them by sound even when properly made
by another {521} person. The characters composed entirely of dots seem
to cause the most trouble in this way.

Electrical Reactions.—In those cases where spasm of one or more
muscles is a more or less marked symptom electrical examination shows,
both to the faradic and galvanic current, a quantitative increase in
the reaction, both in the nerves and muscles; with the galvanic
current the cathodal closing contraction is more marked than the
anodal closing contraction, as in health (KaSZ > AnSZ); only this
formula is most marked in the affected arm. When paresis is present
there will be a quantitative decrease in the reaction, the formula
still being KaSZ > AnSZ. In the same arm some muscles may show a
quantitative increase and others a quantitative decrease. Where there
is a neuritis present the electrical examination will show a
quantitative increase, but where the disease has advanced to
degeneration of the nerve the reaction of degeneration will be found,
and the formula will be AnSZ > KaSZ; there is, therefore, a
qualitative change, but this must be looked upon as rather uncommon in
this class of diseases.

Poore[44] is of the opinion that increased irritability shows an
early, and decreased irritability a late, stage of the same condition.
According to his tables, but very few of his 75 cases of impaired
writing-power showed this quantitative increase, while every case
showing the least evidence of cramp that has come under my observation
has shown it in one or more muscles; in a few cases the antagonistic
muscles showed a decrease. Increased sensitiveness to both currents is
sometimes noticed.

[Footnote 44: “Writers' Cramp and Impaired Writing-power,” by C. V.
Poore, M.D., _Medico-Chirurgical Trans._, vol. lxi, 1878.]

COURSE.—The course of the disability is slow and, unless appropriate
treatment is instituted, progressive, although at times there are
periods during which the symptoms ameliorate without assignable cause,
thus giving rise to false hopes. The usual history is that group after
group of muscles becomes implicated as these are in turn used to
relieve those first affected, the left arm, should this be used,
becoming disabled in the same manner as the right, and the unfortunate
sufferer is then compelled to give up his calling or else to lessen
very materially the amount of his labor.

DURATION.—As might be inferred from what has been written, those who
have suffered for years with this affection may expect it to continue
for the remainder of their days; but the later investigations upon
this subject give rise to much hope that in future the duration of
this troublesome complaint will be materially shortened when the
disease is recognized early and treatment instituted at the very first
symptom.

DIFFERENTIAL DIAGNOSIS.—Although many of the cases of copodyscinesia
are diagnosed with comparative ease, there are others which require
much study, as there are several disorders which are apt to mislead by
the similarity of symptoms.

Any affection of the finger-joints or of the muscles of the hand or
arm, or any disease of the nerves or of the spinal cord, from which
these nerves arise, or of the corresponding part of the brain, will
necessarily interfere more or less with the finer movements of the
hand, and yet all these, manifestly, cannot be considered cases of
this affection.

Where the symptoms are undoubtedly caused by over-use of a part, by
the constant repetition of the same muscular act, although the lesions
{522} may vary considerably in the different cases, they may be
classed with propriety under the above head; but there is a second
class which cannot be so considered, in which there has been a central
lesion which has arisen entirely independently of the occupation which
has become difficult to perform, and which disability is only one of
the many symptoms that have arisen on account of the aforesaid lesion:
these are the cases that it is important to differentiate from cases
of true copodyscinesia.

When a patient is suffering from a difficulty in performing a fine act
of co-ordination where previously there had been no trouble, much
information as to the cause may be gained by examining critically the
method in which that act is attempted to be carried out; thus, if the
patient has a difficulty in writing, his method of holding the pen and
his style of writing may throw some light upon the diagnosis; if he
holds his pen too firmly or if the down strokes are too heavy, or the
writing gradually grows smaller and smaller toward the end of the
line, there is a spasm of the flexor muscles; if, on the contrary, the
down strokes are imperfectly made or the thumb rises upon the holder,
or one finger shows a tendency to straighten itself, the extensors are
at fault. Each muscle should then be examined. By asking the patient
to make the different movements possible with the fingers and hand of
the affected side, and comparing them with those of the sound side, a
feebleness of one or more muscles may be detected. The offending
muscle may also be detected by electrical examination—by its reacting
more or less strongly than its fellow on the other side to the faradic
current or showing a quantitative change to the galvanic current.

By stripping the patient to the waist, or at least the arms, and
making a careful examination, atrophy or local lesions may be detected
that will aid in clearing up the diagnosis.

In telegraphers the mode of manipulating the key should be noted if
possible, and the faults made in the different Morse characters
studied; this will show as much in this form of the trouble as the
mode of writing does in scriveners' palsy.

The condition described by Mitchell[45] as post-paralytic chorea may
easily be mistaken for these affections, especially where the cerebral
lesion was coincident with much manual work (as writing or
telegraphing), and was so slight in extent that the paralysis was
transient and overlooked, the choreoid movements appearing later, and
affecting, as they may do, only the hand. Of this condition Mitchell
states “that it may exist in all degrees, with partial loss of power
and with full normal strength—that it may consist in mere awkwardness,
or exist to the degree of causing involuntary choreoid movements of
the parts.”

[Footnote 45: “Post-paralytic Chorea,” by S. Weir Mitchell, _Am.
Journ. Med. Sci._, Oct., 1874.]

The diagnosis can, in most cases, be satisfactorily arrived at by
careful consideration of the history of the case, the mode of onset,
the presence of some other signs of cerebral lesion, and the
examination of the heart and of the urine.

Some cases of paresis of the arm or hand from lesions of slight extent
affecting the arm-centres in the brain (minute emboli, disease of the
finer vessels, etc.) might possibly be mistaken for the paretic form
of copodyscinesia. Two cases[46] will illustrate this point:

{523} Case I.—Mr. G.——, æt. 58, dentist. A great writer, although
writing was always a difficult task and soon fatigued him. One day,
after excessive writing the day previous, he awoke with a loss of
power to write from an inability to properly co-ordinate his muscles;
his hand was not unsteady, motion was apparently unimpaired, and his
power good, but after laboring for ten or fifteen minutes he would
drop the pen. He was treated for writers' paralysis, and gradually
improved. One year later he was seized with aphasia and entire loss of
power in the right arm and leg. His further history is that of right
hemiplegia, and not interesting in this connection.

Case II.—Mr. W——, civil engineer, æt. 54. Until July, 1881, he
considered himself a healthy man, although very excitable; he was then
engaged in calculating and writing almost steadily for one week, which
exhausted him exceedingly; following this, he was engaged in an
abstruse calculation lasting another week, and at the end of this
period he awoke to find himself powerless to extend or flex his wrist,
and, to use his expression, his thumb would gravitate into his palm.
The movements of the shoulder and arm were comparatively unimpaired,
and with the exception of occasional dimness of vision of the right
eye there was no other symptom noticed. In one week he considered
himself well again. In July, one year later, after again passing
through a period of exceedingly hard work, he awoke to find that he
had lost sensation on the right side and had some difficulty in
articulating (muscular). Although thus warned, he worked steadily for
twelve hours the next day, in consequence of which he completely broke
down. After this he would occasionally write down a wrong word or put
down a wrong figure in calculating, etc. One month later he had a
transient attack of loss of power in right leg and other signs of
partial right hemiplegia, which was in all probability due to an
embolus, as there was a marked aortic systolic murmur.

[Footnote 46: From S. Weir Mitchell's notebooks.]

The point brought forward by Axenfield[47] that the paralysis in brain
lesions manifests itself equally in all movements of the fingers,
while in writers' cramp, etc. there is integrity of all movements
except those necessary for the special act, cannot be accepted as
diagnostic.

[Footnote 47: _Des Névroses_, par le Docteur Axenfield, Paris, 1864,
p. 389.]

Progressive muscular atrophy, as previously mentioned, bears a close
resemblance to professional muscular atrophy (Onimus), which may be
considered one of the forms of copodyscinesia. The resemblance,
together with the few points of difference, may be best seen in the
form of a table, thus:

   PROGRESSIVE MUSCULAR ATROPHY.   | PROFESSIONAL MUSCULAR ATROPHY.
                                   |
  1. Heredity in 24.63 per cent.   | 1. Heredity not marked.
  (Roberts).                       |
                                   |
  2. Affects adult males           | 2. Affects adult males
  principally.                     | principally.
                                   |
  3. Frequently follows exhausting | 3. Always follows exhausting
  muscular activity.               | muscular activity.
                                   |
  4. Atrophy a cardinal symptom.   | 4. Atrophy a cardinal symptom.
                                   |
  5. When it affects the upper     | 5. The muscles first affected are
  extremities, the interossei and  | generally the largest ones,
  the thenar and hypothenar        | particularly those in the
  eminences are the first          | neighborhood of the
  affected. (Eulenburg says in his | shoulder-joint. The muscles of
  experience the first dorsal      | the hand may be affected first.
  interosseus is always first      |
  attacked, and the others later.) |
                                   |
  6. Fibrillary twitchings         | 6. Fibrillary twitchings
  frequent.                        | frequent.
                                   |                             {524}
  7. Premonitory pains rare.       | 7. Pains and cramps at the onset
                                   | in the affected parts a
                                   | distinctive sign.
                                   |
  8. Diminution of electrical      | 8. (?).
  reactions to both faradism and   |
  galvanism. Reaction of           |
  degeneration occasionally a late |
  symptom.                         |
                                   |
  9. Prognosis generally           | 9. Rapid amendment under rest and
  unfavorable: as regards perfect  | the use of constant and
  restoration of muscles, almost   | continuous electric currents.
  hopeless.                        |

The ordinary course of symptoms in this disease is not always followed
out, and occasionally the resemblance of the initiatory symptoms to
one of the forms of copodyscinesia is great; the following is a case
in point:

W. F. G——, æt. 34, clerk, at one time an excessive smoker and a steady
writer. In the autumn of 1883 he noticed a numbness on the ulnar side
of the tip of the right index finger and on the radial side of the
middle third of the right middle finger, at about the points touched
by the pen-holder, which he held between these two fingers; this was
soon accompanied by a hyperæsthesia to light touches, and the two
together seriously interfered with pen-prehension; he then changed the
pen to the left hand, and soon noticed a numbness on corresponding
points on the left fingers. Any sudden extension of the right arm
would cause a thrill to shoot down into the fingers. Weakness of the
right opponens pollicis was present at the same time. These symptoms
caused the first physician consulted to make a diagnosis of writers'
palsy, but the later manifestations of the disease, six weeks
subsequently, soon showed its true character: these were marked
atrophy of the external portion of the thenar eminence (opponens
pollicis) and weakness and partial atrophy, and finally total loss of
power, of the anterior group of muscles of right leg (tibialis
anticus, extensor proprius pollicis, and extensor longus digitorum);
numbness and hyperæsthesia, as in the hand, appeared over instep.
Fibrillary twitchings were absent. The affected muscles did not
respond to the faradic current, while to the galvanic current there
was a quantitative lessening, the reaction still being normal in
kind—viz. KaSZ > AnSZ.

Paralysis agitans and multiple sclerosis both interfere with writing
on account of the tremor of the muscles; the latter disease markedly
so, as voluntary effort increases the trembling.

According to Sigerson,[48] the flexors are the least affected in the
former disease, and the extensors most so, especially the interossei,
which are the earliest involved; the down strokes of the writing will
therefore be made with comparative firmness, while the up strokes will
show the tremor.[49]

[Footnote 48: _Lectures on the Diseases of the Nervous System_, by J.
M. Charcot, trans. Philada., 1879, foot-note by Sigerson, p. 113.]

[Footnote 49: _Ibid._, p. 112.]

The writing in multiple sclerosis is much more wavy and irregular,
although the same tendency to firmness in the down strokes may still
be seen.[50]

[Footnote 50: _Ibid._, foot-note by Bourneville, pp. 153, 154.]

Both these diseases, when well pronounced, should occasion no trouble
in diagnosis, but there are cases where the symptoms are not typical,
and where the sclerotic change is slight in amount and principally
limited to the arm-centres in the cord, or at least to the anterior
columns, the symptoms being confined to the finer movements of
co-ordination of the hand and arm, and necessarily interfering with
such occupations as writing {525} much more than with those which only
necessitate coarser movements. The following cases illustrate this
point:

Case I.—J. S——, æt. 67, male. Two relatives had paralysis agitans (?).
Previous health good; present trouble began nine years ago. Tremor
first noticed in writing, and only then, but later any voluntary
effort of right arm was accompanied by a fine tremor, which became
particularly noticeable when the arm was semiflexed. This is now equal
in both arms. When patient writes slowly and with great attention to
each movement, he can write fairly for a short time; but if he
attempts to write quickly, there is a marked tremor which renders the
letters sometimes almost illegible. The up strokes show the most
tremor. There is no festination, no change in voice, no loss of power
over the sphincters, and no loss of reflexes; the reaction to the
galvanic current is normal.

Case II.—W. H——, æt. 58, male. For fifty years the patient has been a
hard writer, first as an editor and later as a cashier. In 1882 he
noticed difficulty in raising arm to put away papers in pigeon-holes
above his head; this movement caused pain in shoulder and arm. Shortly
after this he found that his hand became tremulous when he attempted
to write, and later any voluntary effort was sufficient to cause the
tremor. There has been no cramp. The grip of both hands is good, nor
is there any wasting of the muscles. Standing with eyes closed causes
no swaying, although there are occasional vertiginous attacks. While
walking he has noticed that the right arm does not swing with its
usual freedom. No ataxic pains are present. Reflexes of right arm and
shoulder are very much exaggerated; there are no changes in nutrition
or sensation. Galvanic reaction normal and alike in both arms. The
urine is non-albuminous.

The following case is in all probability one of diffused sclerotic
changes in the right lateral half of the cord, where the disease has
apparently ceased advancing:

Case III.—T. L——, æt. 45. In 1880, three years ago, patient noticed
occasional formication in various parts of the right face, hand, and
leg, which ceased after he suspended the use of tea and coffee; soon
after this he noticed that his writing began to lack ease and that the
letters became crowded toward the end of the line; later, a fine
tremor appeared in the fingers of the right hand; crampy sensations
then appeared in the hamstring muscles of right leg, chiefly while
sitting with the knee bent at right angles; writing with the right
hand was sufficient to cause, or at least aggravate, this. In 1882 the
right arm lost its automatic swing during walking, although holding
the left arm still would enable the right arm to swing automatically.
Lately the symptoms have ceased advancing, and some seem to improve.
His present condition is an inability to write with right hand without
paying great attention and making each letter separately, and a
trembling of fingers during excitement of any kind. Coarse movements
of co-ordination can, as a rule, be well performed; there is no
increase of reflexes, nor are they absent; there is no ataxic gait,
and there are no trophic changes. Galvanic reaction is normal, and
alike on both sides. There is no history of hereditary disease or of
venereal taint.

In this connection it is proper to mention tremor mercurialis and
{526} tremor saturninus, which might possibly lead to mistake should
proper attention not be paid to the history and to the symptoms.
Paul[51] reports a case of the former affection, and gives a specimen
of the handwriting of the patient.

[Footnote 51: C. Paul, _Bull. et Mém. de la Soc. de Thérap._, Paris,
1881, xiii. pp. 129-131.]

Traumatisms, etc. of the various nerves of the arm usually interfere
with the proper play of the muscles supplied by them, and although
certain of the milder forms of inflammation or of congestion, as
previously mentioned, are sometimes present in cases of
copodyscinesia, it is manifestly improper to include all cases of
impairment of hand-and-arm movement from nerve-injury under this head.

Palsy from pressure, as from sleeping with the head resting upon the
arm or with the arm hanging over the back of a chair, is a frequent
cause of paresis or paralysis of the muscles supplied by the
musculo-spiral.

Tumors pressing upon the nerves in any part of their course, or
neuromata, may be mentioned among the more ordinary affections that
possibly might mislead.

Tenosynovitis which is described by Hopkins[52] as a congestion of the
tendinous sheaths in the forearm, with insufficient lubrication of the
same, causing pain and interfering with motion, might be mistaken for
the disease in question, especially as it occurs in many of the same
occupations which furnish cases of copodyscinesia.

[Footnote 52: Wm. Barton Hopkins, “Tenosynovitis,” _Med. News_,
Philada., July 15, 1882.]

The exciting cause of tenosynovitis is “usually the resumption of work
to which the individual is thoroughly accustomed after a shorter or
longer interval when he is out of practice,” and not the monotonous
repetition of the same act. The differential diagnosis should occasion
no difficulty, as there is soreness amounting to positive pain upon
motion or pressure along the course of the affected tendons, and the
peculiar creaking which is communicated to the finger on palpation.

PATHOLOGY AND MORBID ANATOMY.—Unfortunately for correct determination
of the pathological conditions underlying these neuroses, there have
been no reported examinations of the spinal cord and nerves in
subjects affected with copodyscinesia dying from intercurrent
diseases, although it is probable that no macroscopic lesion would be
discovered.

Solly[53] reports the post-mortem appearance in a case of impaired
writing-power in which he found a granular disintegration of the
cervical portion of the cord; but this case, from his description, was
evidently one in which the impairment of power was merely one of the
numerous symptoms dependent upon disease of the cervical cord from
degenerative changes, and not a true case of writers' cramp. If such a
condition underlaid these neuroses, the cures occasionally reported
and the relief frequently felt after the use of the galvanic current
could not be explained.

[Footnote 53: _London Lancet_, vol i. p. 113.]

In default, then, of positive information upon this point, conclusions
must be drawn from a study of the symptoms, the course, and the
behavior of these diseases under treatment. An affection of such
protean aspect is not likely to have one settled pathological
condition underlying it.

Many affections considered hitherto purely functional have under our
{527} more advanced knowledge been found to have as a basis a positive
organic change.

On the subject of fatigue, Poore[54] concisely states that the
symptoms “are referable to the muscles, but we must always bear in
mind that muscles and motor-nerve are one and indivisible, and that
recent experiments have given great probability to the idea that every
muscle is connected with a definite spot in the brain; when,
therefore, we speak of a sense of fatigue, we must necessarily be in
doubt, notwithstanding the fact that the symptoms are referred to the
muscles, whether brain, nerve, or muscle, one or all of them, be
really at fault.”

[Footnote 54: “On Fatigue,” _London Lancet_, vol. i., 1875, p. 163.]

There is a certain limit to which exercise of a given group of muscles
may be carried without producing fatigue and local congestion, or
perhaps even inflammatory results; this varies greatly in different
individuals, but if it is continually and uninterruptedly overstepped,
and insufficient time given for rest and recuperation, the centres in
the spinal cord which regulate the action of the various muscles
implicated become overstimulated, and the result is an undue amount of
nervous energy induced by the peripheral excitation, or there is a
distortion of the central impulses in passing through these centres: a
perturbation of the co-ordinating power ensues and inco-ordination is
the result. Under rest and appropriate treatment these symptoms may
pass away, but if the part is continuously used it is highly probable
that nutritive changes will be produced in that part of the spinal
cord from which the nerves supplying the overtaxed muscles proceed.

In some cases of hemiplegia there is produced during gaping and
sneezing an automatic movement of the paralyzed arm; this was noticed
as early as 1834 by Marshall Hall,[55] and in 1872, Onimus[56] noticed
that movements of the hand and fingers of the non-paralyzed arm
produced similar movements in the paralyzed side.

[Footnote 55: Quoted by Charcot, _Diseases of Spinal Cord_, transl. by
Comyges, Cincinnati, 1881, p. 110.]

[Footnote 56: _Ibid._]

Erb[57] states that these movements in certain spinal troubles are
partly owing to the establishment of conditions of irritation in the
neighborhood of the lesion.

[Footnote 57: _Ziemssen's Cyclopædia_, Amer. ed., vol. xi. p. 409.]

Hitzig[58] states that in certain pathological conditions where the
ganglionic elements (in the cord) are superexcitable, the least
disturbance produced on one side, and which determines there a
voluntary movement, may be communicated to the other side, and
provoke, according to the case, either movements similar to a
voluntary one or a spasmodic movement which is really a contraction;
and also in certain cases relations of the same nature may be
established among cellular groups quite distant from each other; and
we can comprehend that in these cases the voluntary movements executed
by the sound side may be re-echoed in that which is diseased.

[Footnote 58: Quoted by Charcot, _loc. cit._, p. 124.]

This apparent digression bears an important relation to the pathology
of copodyscinesia, and lends force to the view that the associated
movements which occur in the well arm, or in the affected arm when the
sound side is used, or even in the face and legs, and which are quite
often seen in these affections, are due to the fact that there is a
central change.

Mitchell,[59] in speaking of functional spasms, states that it will be
found {528} in all these cases that when an ordinary functional motor
act gives rise to spasms elsewhere, these occur in muscles which have
physiological, and therefore anatomical, relations to the muscles
which by their normal use give rise to the morbid activities. He
considers that there is a hypersensitizing of the sensory centre which
takes record of the activities of the affected muscles.

[Footnote 59: “Functional Spasms,” _Amer. J. Med. Sciences_, Oct.,
1876.]

The fact that the left hand becomes implicated in some cases where it
is used to relieve the right should be mentioned in this connection as
lending weight to this hypothesis, especially as in a few cases of
telegraphers' cramp the left hand has been found implicated in the
very first attempt to use it in telegraphing.

Poore[60] considers this transfer as no evidence that the change is
central, and is one of the few who consider the pathological
conditions as purely peripheral in character. Hamilton[61] and De
Watteville[62] also consider the peripheral hypothesis the correct
one.

[Footnote 60: _Loc. cit._]

[Footnote 61: _Nervous Diseases_, Philada., 1881.]

[Footnote 62: “The Cure of Writers' Cramp,” _Brit. Med. Journ._, 1885,
vol. i. pp. 323-325.]

Fritz[63] (and after him Poincaré[64]) considers the disease a
reflected neurosis, due to a perversion of the muscular sense. Onimus
and Legros[65] incline to the same opinion.

[Footnote 63: _Oesterr. Jahrb._, März u. April, 1844.]

[Footnote 64: _Le Système nerveux-péripherique_, Paris, 1876.]

[Footnote 65: _Traité d'Electricite médicale_, Paris, 1872, p. 327.]

The older theory that the disease is solely central in its pathology
is advocated by Duchenne,[66] Solly,[67] Reynolds,[68] Althaus,[69]
Wood,[70] Vance,[71] Erb,[72] Dally,[73] Axenfield,[74] Whittaker,[75]
Waller,[76] Gowers,[77] Hammond,[78] Romberg,[79] Cederschjöld,[80]
Robins,[81] Ross,[82] and some others. Roth[83] considers that there
are two entirely separate classes, the central and the peripheral or
local.

[Footnote 66: _De l'Électrisation localisée_, 3d ed., pp. 1021 _et
seq._]

[Footnote 67: _London Lancet_, Jan. 28, 1865.]

[Footnote 68: _System of Medicine_.]

[Footnote 69: Julius Althaus, _London Mirror_, vol. vii., Aug. 1,
1870; also, pamphlet, _Scriveners' Palsy_, London, 1870.]

[Footnote 70: _Practice of Medicine_.]

[Footnote 71: Reuben A. Vance, _Bost. Med. and Surg. Journal_, vol.
lxxxviii. p. 261.]

[Footnote 72: _Ziemssen's Cyclopædia_, vol. xi. p. 355.]

[Footnote 73: _Journal de Thérapeutique_, Paris, 10 Fév., 1882.]

[Footnote 74: _Des Névroses_, Paris, 1864.]

[Footnote 75: _Cincinnati Lancet and Clinic_, 1880, N. S., vol. iv. p.
496.]

[Footnote 76: Aug. Waller, _Practitioner_, 1880, vol. ii. p. 101.]

[Footnote 77: W. R. Gowers, _Med. Times and Gaz._, 1877, vol. ii. p.
536.]

[Footnote 78: _Treatise on Dis. of Nervous System_, 6th ed., New York,
1876.]

[Footnote 79: _Manual of Nervous Dis. in Man_, Sydenham Society, vol.
i.]

[Footnote 80: _Gustaf. Upsala läkarefören_, förhandl. xv., 3 och. 4,
S. 165, 1880, review in _Schmidt's Jahrb._, Bd. clxxxvii., 1880, p.
239.]

[Footnote 81: “Writers' Cramp,” _Amer. Journ. Med. Sci._, April, 1885,
pp. 452-462.]

[Footnote 82: _A Treatise on Diseases of the Nervous System_, London,
1881, vol. i. pp. 464-469.]

[Footnote 83: _The Treatment of Writers' Cramp_, by Roth, London,
1885.]

The later theory, that the disease is at first peripheral, but that by
abuse may become central (spinal), is advocated by Beard,[84]
Liebman,[85] Bartholow,[86] Frazer,[87] and a few others. The latter
theory, and not the idea that it is a disease of the co-ordinating
centres in the brain or of the spinal centres only, best explains, in
my opinion, the various symptoms encountered.

[Footnote 84: _New York Med. Record_, 1879, p. 244.]

[Footnote 85: _Maryland Med. Journ._, June, 1880-81, vol. vii.]

[Footnote 86: _Medical Electricity_.]

[Footnote 87: _Glasgow Med. Journ._, 1881, vol. xv. p. 169.]

{529} Many others have written upon this subject, but upon the
probable pathology they have been silent.

The experiments recently made by Dercum and Parker[88] on the
artificial induction of convulsive seizures are of considerable
interest, and certainly tend to throw light on the point in question.
These convulsions were produced by subjecting a group of muscles to a
constant and precise effort, the attention being at the time
concentrated upon some train of thought. The position most frequently
adopted was to cause the arms to be held so that the tips of the
fingers barely touched the surface of the table before which the
subject was seated, the fingers not being allowed to rest upon the
table, but maintained by a constant muscular effort barely in contact
with it. After this position was maintained for a variable length of
time tremors commenced in the hands; a little later these tremors
became rapidly magnified into rapid movements of great extent
sometimes to and fro, sometimes irregular; if the experiment was
carried still farther, the muscles of the arms, shoulders, back,
buttocks, and legs become successively affected, and the subject was
frequently thrown violently to the ground in a strong general
convulsion, the consciousness being always retained.[89] The more
frequently these experiments were performed, the more readily the
seizures were brought on, and, other things being equal, with
successively increasing intensity. One subject thus experimented upon
became so susceptible that the jar of a passing wagon sufficed to
induce a partial seizure. These experiments throw a new light upon the
associated movements previously mentioned, and show how easily the
phenomena noticed in one part may pass to another having physiological
relationship with it. It is highly probable that some nutritional
change in the cord would follow the too frequent repetition of these
experiments.

[Footnote 88: “The Artificial Induction of Convulsive Seizures,”
Dercum-Parker, _The Polyclinic_, Philada. 1884, vol. ii. pp. 95-97.]

[Footnote 89: These experiments were subsequently repeated before the
Philadelphia Neurological Society in 1885.]

Peripheral pathological conditions undoubtedly exist in many cases of
copodyscinesia; these may be so slight that they can scarcely be
demonstrated, or, on the other hand, they may be marked, and even
present a well-marked inflammation of one or more of the nerves of the
arm, as evidenced by pain on motion, tenderness on pressure, and
sensory and nutritive disturbances in the areas which they supply.

There are some cases where the disability is pronounced, and yet the
most careful examination fails to reveal peripheral changes of
sufficient gravity to account for the severity of the symptoms; these,
in my opinion, are best explained by supposing a hyperexcitability of
the spinal centres, as previously expressed.

The electrical reaction in many cases tends to prove an irritable
condition of the spinal centres. In most of the cases of the spastic
group there will be found a quantitative increase in the reaction of
both nerve and muscle to the galvanic current. Gowers[90] states that
he has found such an increase in diseases regarded as functional, as
paralysis agitans and chorea, and considers it an interesting proof of
the molecular changes which underlie or result from functional
maladies. He previously {530} remarks[91] that such a condition of
exalted irritability is to be ascribed to a corresponding change in
the nutrition of the nerve-cells of the spinal cord, secondary to the
irritative influence which caused it.

[Footnote 90: _Dis. of Spinal Cord_, 2d ed., Philada., 1881, p. 40.]

[Footnote 91: _Med. Times and Gaz._, London, vol. ii., 1877, p. 536.]

Erb[92] also considers that quantitative increase in the electrical
reaction points to central lesion. Buzzard[93] quotes several authors
upon tetany—which some cases of copodyscinesia closely resemble—who
state that the electrical reactions are increased quantitatively in
that affection, and considers, himself, that the change is due to
central lesion.

[Footnote 92: _Loc. cit._]

[Footnote 93: Thomas Buzzard, _Dis. of the Nervous System_, London,
1882.]

It must be borne in mind, however, that in those cases of congestion
of the nerves, or neuritis, previously mentioned a quantitative
increase may be found, indicating a hypersensitiveness of the
peripheral nerve, and not necessarily of the spinal centres.

Poore[94] states: “Thus we see that alterations of irritability” (he
especially alludes to depressions) “accompany many conditions, both
central and peripheral,” and “there is no necessity for assuming that
central change exists in every case of altered irritability, and we
have no warrant for such an assumption in the absence of independent
evidence of central change.”

[Footnote 94: “Impaired Writing-power,” _loc. cit._]

Exactly what the alteration in the condition of the spinal cord is
which probably occurs in many of these cases it is impossible to
state, but the view that it is a nutritive change of the upper dorsal
and lower cervical portion of the spinal cord (that is, when the arm
is the part affected, as it is in all but the rarer cases) is quite
attractive, the condition being secondary to a peripheral irritation
in many cases.

Althaus[95] considers that there is a “constriction of the small
arteries, dilatation of the veins, and slight serous effusions
compressing the nervous matter in the cervical spinal cord.”

[Footnote 95: _Loc. cit._]

Pain in the cervical and dorsal spine during work may be mentioned
here as an evidence that some of the symptoms are due to central
alterations.

Those few cases that exhibit great difficulty in performing one set of
movements that requires a certain combination of muscles, but are able
to use those same muscles in combination with others with ease, are
difficult of explanation by the peripheral theory of the disease
alone; but less difficulty is encountered if a superexcitability of
the spinal centres is supposed to exist, for here we can imagine that
when all the centres so affected are called into use, and only then,
there will be an undue amount of nervous energy transmitted to the
periphery, and disordered movement be the result.

The explanation offered by those who believe in the peripheral theory
is, that the affected muscle is always imperfect in its action, but
that this imperfection is masked in other combinations by the action
of the healthy muscles, so that it is no longer noticeable.

PROGNOSIS.—The prognosis in these affections varies with the
conditions found and with the previous duration of the disease.

A favorable prognosis may generally be given where the case is an
acute one, and where the disability can be proved to be due to some
one of the peripheral conditions previously mentioned. When the
condition is in the forming stage, when fatigue, stiffness, tremor,
tingling, aching, {531} sense of heat, coldness, or powerlessness are
the only symptoms which exist, the disease is quite amenable to
treatment and a good prognosis may be given; but, unfortunately,
patients are loath to believe that these trivial symptoms, which do
not prevent their work, are precursors of any serious trouble, and
therefore pay but little attention, if any, to them, so that the
physician is seldom consulted during this period.

When positive cramp has made its appearance, it is an evidence of a
more advanced stage of the malady, and the prognosis becomes less
hopeful, although still the symptoms may be greatly ameliorated, or a
complete cure even be effected.

When the cramp has existed for years and is present in many of the
finer acts of co-ordination, the case becomes almost hopeless as far
as cure is concerned; and even though the part is rested, so far as
the disabling occupation is concerned, for months or even years, it
will be found to return upon resumption of the old work. Roth[96]
considers those cases due to central changes totally incurable.

[Footnote 96: _Loc. cit._]

When a congestion of the nerves or a well-defined neuritis is
discovered to be the cause of the trouble, the probability of a
favorable termination is rather more hopeful.

Paralysis is to be looked upon as an unfavorable symptom, pointing as
a rule to a late stage of the disease.

It may be stated with positiveness that when the premonitory symptoms
are neglected and constant work persevered in, the case will go on
from bad to worse: periods of amelioration, it is true, may occur, but
cramp usually supervenes, and the affection becomes gradually
progressive as group after group of muscles becomes implicated, until
the part becomes useless for all delicate work.

The probability of the left hand escaping, should it be used to
relieve or replace the right, is slight; and for two reasons: 1st. The
same predisposition which favored the trouble in the right arm still
exists; and, 2d. The proximity of the spinal centres for the two arms
is such that the morbid process may easily be conveyed from one to the
other, as was shown while considering associated movements.

Poore disbelieves in the possibility of such a transfer, and with
Gowers is of the opinion that the liability of the left hand to suffer
has been overestimated.

In my experience, as regards telegraph operators, the majority who use
the left arm soon notice symptoms of the disability in it. Of 43 cases
of this form of copodyscinesia which have come under my observation,
in 21 the left arm was implicated; in 12 there was no such
implication, although the arm was used; of the remaining 10, 8 had
never tried to telegraph or write with the left arm; 1 had only one
arm, the left; and 1 was doubtful. Throwing out of consideration the
last 10, 21 out of the 33 had this symptom, equivalent to 63.63 per
cent.

PROPHYLAXIS.—The only prophylactic measures are the observance of the
most easy and least fatiguing method of performing the act which it is
feared will bring on the trouble, and the avoidance of overwork.

Tobacco and alcohol generally act injuriously, and therefore should be
avoided as much as possible by those who are predisposed by occupation
or otherwise to these disorders.

{532} In writing it is advisable to avoid an awkward manner of holding
the pen-holder, which should be of good size; large, moderately soft
pens and paper of good quality should be used.

It is also important that the table or desk upon which the writing is
done should be of a convenient height, with plenty of room for the
arrangement of the paper; otherwise an awkward manner is inevitable.

As regards the position of the paper, R. Berlin[97] (Stuttgart) states
substantially as follows: In writing the head is almost invariably
held so that the line passing through the two eyes, if projected upon
the paper, shall cross at right angles the oblique line of the
writing: when the paper is placed to the right and parallel to the
edge of the table, as generally directed by teachers, the tendency is
to twist the spine and incline the head to the right in order to
conform to this rule, and a cramped position is the result; but by
placing the paper in an oblique position directly in front of the
writer—_i.e._ turned toward the left—this cramped position is avoided,
and the least fatigue, both to the muscles of the spine and arm,
produced. Tight sleeves or anything that might possibly impede the
free play of the muscles or cause pressure upon the nerves should be
discarded.

[Footnote 97: “Physiology of Handwriting,” _Von Graefe's Archiv_,
xxviii. p. 259, review in _Ophth. Review_, London, vol. i. No. 14,
Dec., 1882, and Jan. 1, 1883.]

It is now almost universally conceded that the conjoint movement in
writing—that is, the arm movement for all the small letters, and the
finger movement only to assist in making the long ones—is least likely
to produce fatigue.

It has been stated, and quite generally believed, that the slighter
degrees of scriveners' palsy are relieved by avoiding contact with the
metallic portion of the pen-holder,[98] and one of the methods taken
to avoid this contact, especially among telegraph operators, is to
slip a piece of rubber tubing over the pen-holder; this certainly does
relieve the fatigue slightly, but the cause is not the avoidance of
contact with metal or the insulation, etc., but simply that the holder
is thus made larger and softer for the fingers, and thus takes the
place of a cork pen-holder, which for some time has been in use for
this purpose.

[Footnote 98: W. Bathurst Woodman, St. Andrews Grad. Ass., 1872-73.]

Holding the pen-holder or pencil between the different fingers is
another prophylactic measure, and relieves fatigue considerably; for
instance, when it is placed between the index and middle fingers there
is much less effort at pen-prehension, and the fingers may be
temporarily rested without any effort to hold the pen-holder, as the
friction between the fingers keeps it in position. This method is
frequently adopted by stenographers.

The stylographic and Mackinnon pens, although they destroy much of the
originality in handwriting, are easier to write with than a pen, as
less pressure is needed and no particular angle is required to be
maintained between the point and the paper.

The type-writer is one of the newer inventions destined to come into
extended use for the purpose of relieving the fatigue of writing,
which it does to a marked degree, besides having other merits; and
although one of these is said to be the immunity of its users from
writers' cramp, {533} I venture to assert that cases of this class of
trouble will ensue from its over-use, exactly as they do in
piano-playing.[99]

[Footnote 99: To print this article by this machine would require
nearly one hundred and fifty thousand separate flexions of the
fingers.]

Thurber's kaligraph, which was invented before the type-writer, has
never come into general use: it works upon the principle of a
pentagraph, and all finger movements are done away with and the arm
movement used exclusively, the motions of writing being much coarser
than ordinary. This instrument is not as well adapted for prophylaxis
in these troubles as it is for use in some deformities of the hand
hindering pen-prehension, as rheumatoid arthritis, contractions after
burns, etc.

In regard to the means to be taken to avoid the occurrence of
telegraphers' cramp, but little can be said, except that if any of the
premonitory symptoms of the neurosis should occur (fatigue, pain,
tingling, numbness, flushing, associated movements, etc.) after
performing the amount of work which previously caused no discomfort,
it should be taken as a warning that the operator is attempting more
work than can be done without detriment, and that a curtailment of the
work is absolutely necessary if he or she wishes to avoid the disease.

Onimus[100] has said that if further investigation proves that the
operators upon the Morse instrument are more liable to suffer than
those using other systems, it should be the duty of those in authority
to abolish that system and adopt some other: he suggests for this
object the Hughes, which is a printing instrument. That the operators
upon the Morse are more liable to suffer than any others is
self-evident after a very slight inquiry, and because of the very
general introduction of that machine. This instrument is far more
practical, takes up less room, and is less likely to get out of order,
than any other yet invented, and no other, it is probable, will be
introduced so generally. The telephone has not diminished the amount
of work for the telegraph operator, but has given rise to a new
industry. In all of the systems the instruments are manipulated at
least in part by the fingers, so that all are liable to cause this
disease.

[Footnote 100: _Loc. cit._]

The telegraph key should be placed some distance from the edge of the
table, so that the forearm may have sufficient support, resting upon
the bellies of the flexor group of muscles, and thus relieve the
shoulder-muscles, which otherwise would have to support the weight of
the arm. Some operators prefer to hold the arm raised from the table,
but this method is more liable to cause fatigue.

Several keys have been invented for the purpose of lessening the
amount of force needed to manipulate them, and to avoid the jarring
caused by the metallic contact; and, although everything that lessens
the amount of labor should be adopted, the movements of telegraphing
must remain the same no matter which key is used.

Tapping upon the key or attempting to operate by flexing the fingers
while the wrist is held still should be avoided.

It is needless to enumerate the other forms of copodyscinesia, as the
same general principles apply to the prophylaxis of all.

TREATMENT.—Rest.—It is an assured fact that as long as the patient
continues without curtailment the amount of work he was performing
{534} when the symptoms of this trouble appeared, treatment will be
negative in its results. Rest in itself is powerless to cure, except
in the very earliest stages of the disease, for many sufferers have
found, to their dismay, that after having given the arm complete rest,
as far as the disabling occupation was concerned, for months at a
time, the symptoms reappear upon returning to the accustomed work.

During treatment rest is essential, but this need not of necessity be
complete; a curtailment of the work will often be all that is needed
in the lighter cases. This may be effected by using the unaffected arm
for a part of the work at least, but great care must be exercised lest
the symptoms appear on this side also, as the left arm, from want of
use, is wanting in strength and dexterity, and is more liable to be
overtaxed by an amount of work that could be performed without fatigue
by the right; for should this happen the end sought for is defeated,
and the condition of the patient rendered far worse than before.

In writers' cramp the type-writer, as mentioned under Prophylaxis, is
an important adjuvant in the treatment; unfortunately, it is not
applicable to much of the work done by clerks.

The other means described in the last section are also useful in the
treatment as affording temporary rest to the affected muscles.
Hamilton[101] has seen occasional benefit from forced rest by
fastening the hand upon a splint.

[Footnote 101: _Loc. cit._]

In telegraphing, besides using the left arm, the key may be grasped in
a different manner, or if the operator has been holding his arm raised
from the table, let him rest it upon the latter, or vice versâ.

These remarks only apply to those who are compelled to continue
moderate work during treatment.

Electricity.—The majority of the later writers unite in considering
electricity as one of the most important agents in the treatment of
these affections: the form and the manner in which it is applied are,
however, all important.

The faradic or secondary current has often been tried in undoubted
cases of copodyscinesia, and in the majority has failed. It may be of
great service in the paralytic group, where the affected muscle shows
signs of atrophy and of being temporarily deprived of nerve-influence;
it may be also of service in those apparent cases of the spastic group
due to contracture of the unopposed muscles, but in the vast majority,
where there is a true spasm of the affected muscles or a tendency in
that direction, as evinced by rigidity more or less pronounced during
work, or even where there is only a quantitative increase to either
current (faradic or galvanic), the application of this form of
electricity is contraindicated, as the muscular contraction is already
excessive, and should this extra stimulus be applied the muscle may be
exhausted, for we know how readily this effect may be produced by a
too strong or a too lengthy application in a perfectly healthy
subject.

It is hardly necessary to mention that the manner of applying
electricity so often followed by individuals—viz. holding the
electrodes in the palms of the hands—is unscientific and productive of
no good. The proper method of application in the suitable cases is to
place one electrode of the secondary coil (preferably the negative, so
called) over {535} the muscle that is weakened or over its
nerve-point, and the other in some indifferent position, using a
current that is just strong enough to cause a fair contraction, and
employing a slow interrupter, which breaks the current from one to
four times a second. The application should be short, five to ten good
contractions of each muscle being sufficient.

Buzzard[102] has used this current with success in two cases of
impaired writing-power, one of these depending upon a local paralysis.
Zuradelli,[103] Meyer,[104] and Haupt[105] have also seen good results
by this method. Duchenne[106] states that he has “not even seen one
success obtained by those who have praised this method of treatment.”
The majority of the later writers coincide with this last opinion as
regards the spastic form at least.

[Footnote 102: “Two Cases of Impaired Writing-power,” _Practitioner_,
Aug., 1872.]

[Footnote 103: Quoted by Erb and Poore, _loc. cit._]

[Footnote 104: _Ibid._, _loc. cit._]

[Footnote 105: _Der Schreibekrampf mit Rücksicht auf Path. u.
Therap._, Wiesbaden, 1860, review in _Schmidt's Jahrbucher_, Bd. cxv.
3, 136, 1862.]

[Footnote 106: _Loc. cit._]

The galvanic current has of late been considered one of the most
important agents in the treatment of these affections, but there is
considerable variance among authorities as to how it should be
applied. The most efficacious method is the descending current (anode
on the spine and the cathode at the periphery), as this has been found
to be more soothing in its effects than the reverse. The anode should
be placed upon the spine over the cervical cord, and the cathode in
the hand of the affected side or over the affected muscles or nerves.

A stabile current—_i.e._ where the poles are not moved about—is to be
preferred to a labile current—_i.e._ where the poles are moved
constantly—as this is more stimulating than the former; but if a
current of proper strength is used, one that can be plainly felt when
the circuit is made and broken only, the importance of the stabile
over the labile does not obtain.

The treatment should not be prolonged for more than fifteen or twenty
minutes, and may be repeated three times a week or every other day.

Onimus and Legros[107] recommend this mode of treatment, but from a
different pathological standpoint, as they consider the neurosis to be
an excitability of the sensitive nerves of the muscles, and employ the
descending current to allay this.

[Footnote 107: _Loc. cit._]

All sudden shocks or reversals of the current should be avoided in the
treatment, although this may be necessary in using the galvanic
current for diagnosis.

As the seat of the trouble in many cases is probably in the cervical
cord, it is well that special treatment should be applied to this
part, and for this purpose Althaus[108] recommends that the anode be
placed, as previously mentioned, over the cervical cord, and the
cathode in the depression between the angle of the lower jaw and the
sterno-cleido-mastoid muscle, which position corresponds to the
superior cervical ganglion of the sympathetic. The current should be
allowed to flow from three to five minutes at a time; it should be a
mild one, and not be broken or increased or diminished suddenly, as
vertigo may be produced. Both sides should be treated should the left
hand be suffering also. A reversal of this method—_i.e._ cathode to
spine—does little if any good, according to the same author.

[Footnote 108: _Loc. cit._]

{536} Poore[109] employs the descending stabile current of a strength
just short of producing muscular contraction when the current is
broken, but at the same time he employs rhythmical movements of the
muscles supplied by the nerve upon which the cathode is placed during
the flow of the current.

[Footnote 109: _Loc. cit._]

A novel mode of applying the galvanic current in scriveners' palsy has
been recommended by Imlach.[110] He has an electric desk so
constructed that when the patient makes the movements of writing the
extensors and flexors are alternately galvanized, the muscles being
thus assisted in their movements. While this might be of service in
some cases, it is entirely too complicated for practical use. He
reports one case benefited by its use.

[Footnote 110: Francis Imlach, “Automatic and Other Medical
Electricity,” _Practitioner_, vol. ii. p. 270, 1879.]

Franklinic or Static Electricity.—This form of electricity is now
being much used, especially abroad, in the treatment of nervous
affections, but does not appear to have been employed in the different
copodyscinesiæ, as but few reports of such treatment have found their
way into current literature. Romain Vigouroux[111] states that he has
cured one case by statical electricity. Another case is reported by
Arthuis[112] as rapidly cured by this treatment after many other
means, carried on during a period of five years, had failed; but his
brochure contains too many reports of cures of hitherto incurable
diseases to be relied upon.

[Footnote 111: _Le Progrès médical_, Jan. 21, 1882.]

[Footnote 112: A. Arthuis, _Traitement des Maladies nerveuses, etc._,
Paris, 1880, 3me ed.]

Gymnastics and Massage.—As those suffering from copodyscinesia are
generally compelled by their vocation to be more or less sedentary,
exercise in the open air is indicated, inasmuch as it tends to
counteract the evil effects of their mode of life; but the use of
dumb-bells or Indian clubs, riding, rowing, and similar exercises do
not ward off the neuroses in question or diminish them when they are
present.

Such is not the case when rhythmical exercises and systematic massage
of all the affected muscles are employed, as marked benefit has
followed this method of treatment. The method employed by J. Wolff, a
teacher of penmanship at Frankfort-on-the-Main, which consists of a
peculiar combination of exercise and massage, appears to have been
wonderfully successful, judging from his own statements and editorial
testimonials of such eminent men as Bamberger, Bardenleben, Benedikt,
Billroth, Charcot, Erb, Esmarch, Hertz, Stein, Stellwag, Vigouroux,
Von Nussbaum, Wagner, and De Watteville. The method is described by
Romain Vigouroux[113] and Th. Schott,[114] the latter claiming
priority for himself and his brother, who employed this method as
early as 1878 or 1879. Wolff,[115] however, states that he had
successfully treated this disease by his method as early as 1875.
Theodor Stein,[116] having had personal experience in Wolff's
treatment, also describes and extols it: 277 cases of muscular spasms
of the {537} upper extremities were treated; of these, 157 were cured,
22 improved, while 98 remained unimproved; these comprised cases of
writers', pianists', telegraphers', and knitters' cramp.

[Footnote 113: _Le Progrès médical_, 1882, No. 13.]

[Footnote 114: “Zur Behandlung des Schreibe- und Klavierkrampfes,”
_Deutsche Medizinal Zeitung_, 2 März, 1882, No. 9, Berlin; also “Du
Traitement de la Crampe des Écrivains, reclamation de Priorité,
Details de Procedes, par le Dr. Th. Schott,” _Le Progrès médical_, 1re
Avril, 1882.]

[Footnote 115: “Treatment of Writers' Cramp and Allied Muscular
Affections by Massage and Gymnastics,” _N. Y. Med. Record_, Feb. 23,
1884, pp. 204, 205.]

[Footnote 116: “Die Behandlung des Schreibekrampfes,” _Berliner
klinische Wochenschrift_, No. 34, 1882, pp. 527-529.]

It must be borne in mind that Wolff, not being a physician, can refuse
to treat a case if he thinks it incurable; and in fact he does so, as
he has personally stated to the writer, so that his statistics
probably show a larger percentage of cures than otherwise would be the
case.

His method may be described as follows: It consists of a combined
employment of gymnastics and massage; the gymnastics are of two kinds:
1st, active, in which the patient moves the fingers, hands, forearms,
and arms in all the directions possible, each muscle being made to
contract from six to twelve times with considerable force, and with a
pause after each movement, the whole exercise not exceeding thirty
minutes and repeated two or three times daily; 2d, passive, in which
the same movements are made as in the former, except that each one is
arrested by another person in a steady and regular manner; this may be
repeated as often as the active exercise. Massage is practised daily
for about twenty minutes, beginning at the periphery; percussion of
the muscles is considered an essential part of the massage. Combined
with this are peculiar lessons in pen-prehension and writing.

The rationale of this treatment is not easy, but any method which even
relieves these neuroses should be hailed with pleasure, as they
heretofore have been considered almost incurable.

The method employed by Poore, as mentioned under Electricity, of
rhythmical exercise of the muscles during the application of the
galvanic current, is worthy of further trial, as it combines the two
forms of treatment hitherto found most successful.

Internal and External Medication.—Generally speaking, drugs are of
comparatively little value in the treatment of these affections. This
statement does not apply to those cases where the symptoms are
produced by some constitutional disorder, or where there is some other
well-recognized affection present which does not stand in relation to
these neuroses as cause and effect.

In any case where an accompanying disorder can be discovered which is
sufficient in itself to depress the health, the treatment applicable
to that affection should be instituted, in the hope, however unlikely
it is to be fulfilled, that with returning health there will be a
decrease of the copodyscinesia. In the majority of cases no
constitutional disease can be detected, and it is in these that
internal medication has particularly failed.

The following are some of the remedies that have been employed:
Cod-liver oil, iron, quinine, strychnia, arsenic, ergot, iodoform,
iodide and bromide of potassium, nitrate of silver, phosphorus,
physostigma, gelsemium, conium, and some others.

Hypodermic Medication.—Atropia hypodermically, as first suggested by
Mitchell, Morehouse, and Keen[117] in the treatment of spasmodic
affections following nerve-injury, has been used with good effect in
those cases where there is a tendency to tonic contraction; it should
be thrown into the body of the muscle. Vance[118] speaks very
favorably of one-sixtieth {538} of a grain of atropia used in this
manner three times a week. Morphia, duboisia, and arsenic in the form
of Fowler's solution have been used hypodermically with but little
effect. Rossander[119] reports a cure in one month of a case of two
years' duration by the hypodermic use of strychnia. Onimus and
Legros[120] used curare in one case without effect.

[Footnote 117: _Gunshot Wounds and Other Injuries to Nerves_,
Philada., 1864.]

[Footnote 118: Reuben A. Vance, M.D., “Writers' Cramp or Scriveners'
Palsy,” _Brit. Med. and Surg. Journal_, vol. lxxxvii. pp. 261-285.]

[Footnote 119: J. C. Rossander, _Irish Hosp. Gazette_, Oct. 1, 1873.]

[Footnote 120: _Loc. cit._]

Local Applications.—The apparent benefit following the local
application of lotions, etc. to the arms in some cases appears to be
as much due to the generous kneading and frictions that accompany them
as to the lotions themselves. Onimus and Legros, believing the lesion
to be an excitability of the sensitive nerves at the periphery,
employed opiated embrocations, but report amelioration in one case
only.

When there are symptoms of congestion of the nerves or of neuritis,
then the proper treatment will be the application of flying blisters,
or the actual cautery very superficially applied to the points of
tenderness from time to time, so as to keep up a continual
counter-irritation. This treatment may be alternated with the
application of the galvanic current (descending, stabile, as
previously mentioned) or combined with it. As these conditions are
often found in nervous women, care should be taken lest this treatment
be too vigorously carried out.

Considerable relief has been reported from the use of alternate hot
and cold douches to the affected part—a procedure which is well known
to do good in some cases of undoubted spinal disease; the application
peripherally applied altering in some way, by the impression conveyed
to the centres, the nutrition of the spinal cord.

Tenotomy.—Tenotomy has been but little practised for the cure of these
affections. Stromeyer[121] cut the short flexors of the thumb in a
case of writers' cramp without any benefit, but in a second case,
where he cut the long flexor of the thumb, the result was a cure.
Langenbeck[122] quotes Dieffenbach as having performed the operation
twice without success, and states that there has been but one
observation of complete success, and that was the one of Stromeyer.
Aug. Tuppert[123] has also performed this operation, and Haupt[124]
advises it as a last resource.

[Footnote 121: “Crampe des Écrivains,” _Arch. gén. de Méd._, t. xiii.,
1842, 3d Series, p. 97.]

[Footnote 122: _Ibid._, t. xiv., 1842, 3d Series.]

[Footnote 123: Quoted by Poore, _loc. cit._]

[Footnote 124: “Der Schreibekrampf,” rev. in _Schmidt's Jahrbuch_, Bd.
cxv., p. 136, 1862.]

Very few would be willing to repeat the experiment in a true case of
copodyscinesia after the failures above enumerated, for the temporary
rest given the muscle does not prove of any more service than rest
without tenotomy, which has failed in all the more advanced cases,
which are the only ones where tenotomy would be thought of.

Nerve-Stretching.—It is curious that no cases have been reported (at
least I have not been able to discover them) of nerve-stretching for
aggravated cases of copodyscinesia, as the operation has been
performed in several cases of local spasm of the upper extremity
following injuries to the nerves.

Von Nussbaum[125] alone mentions the operation, and states that it has
been of no avail, but gives no references; he previously[126]
stretched the ulnar nerve at the elbow and the whole of the brachial
plexus for spasm {539} of the left pectoral region and of the whole
arm, following a blow upon the nape of the neck; the patient made a
good recovery.

[Footnote 125: _Aerztliches Intelligenzblatt_, Munich, Sept. 26, 1882,
No. 39, p. 35.]

[Footnote 126: _London Lancet_, vol. ii., 1872, p. 783.]

This operation, according to an editorial in the _American Journal of
Neurology_,[127] has been performed seven times for spastic affections
of the arm with the following results: 2 cures (1 doubtful), 3 great
improvement, and 2 slight relief.

[Footnote 127: _Am. Journ. of Neurology and Psychiatry_, 1882.]

This procedure would seem to be indicated in those cases of
copodyscinesia where spasms are present which have a tendency to
become tonic in their character, where other means of treatment have
failed. One such case has fallen under the writer's notice, which, on
account of its singularity and the rarity of the operation, seems
worthy of record. The patient is a physician in large practice, and
his account, fortunately, is more exact than it otherwise would be:

—— ——, æt. 36. Paternal uncle had a somewhat similar trouble in right
arm, father died of paralysis agitans, and one brother has writers'
cramp. From nine to twelve years of age he was considered an expert
penman, and was employed almost constantly, during school-hours,
writing copies for the scholars. At the age of eleven he began to feel
a sense of tire in right forearm and hand when writing; soon after
this the flexors of right wrist and hand began to contract
involuntarily and become rigid only when writing. He remembers being
able to play marbles well for two years after the onset of the first
symptoms. The trouble gradually increased until every motion of the
forearm became involved. At the age of nineteen he became a
bookkeeper, using his left hand, but at the end of one year this
became affected also. Since then both arms have been growing gradually
worse, and at one time exhaustion would bring on pain at the third
dorsal vertebra. At the age of thirty a period of sleeplessness and
involuntary contractions of all the muscles of the body came on,
accompanied by difficulty in articulation from muscular
inco-ordination. After persistent use of the cold douche to spine
these symptoms ameliorated, but the general muscular twitching
sometimes occurs yet, and overwork brings on spasm of the extensors of
the feet. The condition of his arms in December, 1882, was as follows:
At rest the right forearm is pronated, the wrist completely flexed and
bent toward the ulnar side, the thumb is slightly adducted, and the
fingers, although slightly flexed, are comparatively free, enabling
him to use the scalpel with dexterity. This contraction can be
overcome by forcibly extending the fingers and wrist and supinating
forearm, but if the arm be now placed in supination the following
curious series of contractions occur, occupying from one to two
minutes from their commencement to their completion: gradually the
little finger partially flexes, then the ring, middle, and fore finger
follow in succession; the wrist then slowly begins to flex and to turn
toward the ulnar side, and finally the arm pronates, in which position
it will remain unless disturbed. The contraction is accompanied by a
tense feeling in the muscles, but is painless. The left arm behaves in
a somewhat similar manner, and if this is placed in supination a
gradual pronation of the arm begins; then follows the flexion of the
fingers, commencing with the little finger and ending with the thumb;
the wrist also flexes, but not as much as the right, although the
flexion of the fingers is more marked. There is no pain on pressure
over {540} muscles or nerves. The extensor muscles of both arms,
although weaker than normal, are not paralyzed, those of the right
responding more readily to both faradic and galvanic currents than do
the left. There is no reaction of degeneration. The flexors respond
too readily, the right showing the greatest quantitative increase.

In 1879, while abroad, his condition being essentially as above
described, he consulted Spence of Edinburgh, who as an experiment
stretched the left ulnar nerve at the elbow; immediately after the
operation the muscles were paralyzed and the arm remained quiet; in
twenty-four hours the nerve became intensely painful, and remained so,
day and night, for three weeks; this gradually subsided, and ceased
with the healing of the wound two weeks later. Forty-eight hours after
the operation the spasm of the muscles returned, and in a short time
became as bad as ever, proving the operation to have been a failure.

An interesting point to decide in this case is whether the symptoms
point to an abnormal condition of the nerve-centres, first manifesting
itself in difficulty of writing, or whether the constant writing
induced a superexcitability (for want of a better term) of the spinal
cord in a patient markedly predisposed to nervous troubles. This last
hypothesis I believe to be the correct one.

It might be considered at first sight that the symptoms presented by
this patient were due to a paralytic condition of the extensors, and
not a spasm of the flexors, or at least that the latter was secondary
to the former. While the extensors are somewhat weaker than normal
from want of use, a careful study of the mode of onset of this
affection and the symptoms presented later prove this idea to be
erroneous.

In regard to the operation and its results, it seems that a fairer
test of the efficacy of nerve-stretching in this case would have been
made if the median and not the ulnar nerve had been stretched, as the
latter only supplies in the forearm the flexor carpi ulnaris and the
inner part of the flexor profundus digitorum, while the former
supplies the two pronators and the remainder of the flexor muscles.

Of the mode of action of this operation we are still much in the dark,
but it would seem to be indicated in any case where the contractions
are very marked and tonic in their nature—not, however, until other
means have failed to relieve.

In the ordinary forms of copodyscinesia, it is needless to say, the
operation would be unjustifiable.

Mechanical Appliances.—Most of the prothetic appliances have been
devised for the relief of writers' cramp, the other forms of
copodyscinesia having received little if any attention in this
direction. The relief obtained by their use is usually but temporary,
especially if the patient attempts to perform his usual amount of
work, which is generally the case.

These instruments are of undoubted benefit when used judiciously in
conjunction with other treatment, as by them temporary rest may be
obtained, or in some cases the weakened antagonists of cramped muscles
may be exercised and strengthened. They all, without exception,
operate by throwing the work upon another set of muscles, and failure
is almost sure to follow their use if they alone are trusted in, as
the new set of muscles sooner or later becomes implicated in the same
way that the left hand is apt to do if the whole amount of work is
thrown upon it.

{541} To accurately describe these instruments is out of place in this
article: those wishing to study this branch of the subject more fully
are referred to the article by Debout,[128] where drawings and
descriptions of the most important appliances are given.

[Footnote 128: “Sur les Appareils prothetiques, etc.,” _Bull. de
Thérap._, 1860, pp. 327-377.]

Their mode of action may be considered under the following heads:

I. Advantage is taken of muscles as yet unaffected, which are made to
act as splints (so to speak) to those affected, greater stability
being thus given and cramp controlled when present.

Under this head may be mentioned the simple plan of placing a rubber
band around the wrist, wearing a tight-fitting glove, or applying
Esmarch's rubber bandage with moderate firmness to the forearm. Large
cork pen-holders, by distributing the points of resistance over a
larger surface, are thus much easier to hold than small, hard
pen-holders.

Two of the instruments devised by Cazenave—one, consisting of two
rings joined together in the same plane (to which the pen-holder is
attached), and through which the index and middle fingers are thrust
as far as the distal joints; and another consisting of two rings of
hard rubber, one above the other, sufficiently large to receive the
thumb, fore and middle fingers, which are thus held rigidly in the
writing position—act in this manner, and are used when the cramp
affects the thumb or fore finger.

II. The cramp of one set of muscles is made use of to hold the
instrument, the patient writing entirely with the arm movement.

The simple plan of grasping the pen-holder in the closed hand, as
previously described, or of thrusting a short pen-holder into a small
apple or potato, which is grasped in the closed hand, occasionally
affords relief and acts in this way. The instruments of Mathieu,
Velpeau, Charrière, and one by Cazenave are based upon this principle.
The first consists of two rings rigidly joined together about one inch
apart, one above the other, through which the fore finger is thrust,
and of a semicircle against which the tip of the thumb is pressed; the
pen-holder is attached to a bar adjoining the semicircle and rings.
Velpeau's apparatus consists of an oval ball of hard rubber carrying
at one extremity the pen-holder at an angle of 45°; the ball is
grasped in the closed hand, and the pen-holder allowed to pass between
the fore and middle fingers. Charrière's instrument is a modification
of the last, having in addition to the ball a number of rings and
rests for the fixation of the fingers. The latter has also devised an
instrument consisting of a large oval ball of hard rubber; this is
grasped in the outstretched palm, which it fills, and is allowed to
glide over the paper; the pen-holder is attached to one side.
Cazenave's instrument is simply a large pen-holder with rest and rings
to fix the fingers.

III. The instrument prevents the spasm of the muscles used in poising
the hand from interfering with those used in forming the letters.

One of the instruments devised by Cazenave acts in this way: it
consists of a small board, moving upon rollers, upon which the hand is
placed; lateral pads prevent the oscillations of the arm due to
spasmodic action of the supinators. The pen-holder is held in the
ordinary manner.

IV. The antagonistic muscles to those affected by cramp are made to
hold the instrument, while the cramped muscles are left entirely free.

{542} But one instrument acts in this manner—viz. the bracelet
invented by Von Nussbaum,[129] which consists of an oval band of hard
rubber to which the pen-holder is attached. The bracelet is held by
placing the thumb and the first three fingers within it and strongly
extending them.

[Footnote 129: _Aerztliches Intelligenzblatt_, Munich, 1883, No. 39.]

The inventor claims great success by its use alone, as the weakened
muscles are exercised and strengthened and the cramped muscles given
absolute rest.

Résumé of Treatment.—In the complicated cases of copodyscinesia rest
of the affected parts, as far as the disabling occupation is
concerned, must be insisted upon: this should be conjoined with the
use of the galvanic descending stabile current, combined with
rhythmical exercise of the affected muscles and of their antagonists,
and massage. Where there is evidence of a peripheral local congestion
or inflammation, this must be attended to; for instance, if there is
congestion of the nerves, or neuritis, flying blisters or the actual
cautery should be applied over the painful spots, followed by the
galvanic current. Where there is paralysis of one or more muscles,
with evidence of interference of nerve-supply, the faradic current may
be used with advantage.

Evidences of constitutional disease should lead to the employment of
the treatment suitable for those affections.

            RÉSUMÉ OF 43 CASES OF TELEGRAPHERS' CRAMP.

  Age at time of onset:
    Under 20 years . . . . . . . . . . . . . . . . . .   7
    Between 20 and 30  . . . . . . . . . . . . . . . .  25
       "    30 and 40  . . . . . . . . . . . . . . . .   7
    Doubtful . . . . . . . . . . . . . . . . . . . . .   4--43

  Average age  . . . . . . . . . . . . . . . . .  23.94 years.
     "     "  of males . . . . . . . . . . . . .  24.22   "
     "     "  of females . . . . . . . . . . . .  20.66   "

  Average length of time before the disease appeared after the
      commencement of telegraphing was—
    In males . . . . . . . . . . . . . . . . . .   7.27 years.
    "  females . . . . . . . . . . . . . . . . .   4      "
    The shortest period being  . . . . . . . . .   6   months.
    The longest    "      "    . . . . . . . . .  20    years.

  Left arm implicated in . . . . . . . . . . . . . . .  21
  (Not counting case with amputation of right arm) . .   1
  Never used left arm  . . . . . . . . . . . . . . . .   8
  Left arm not affected, although used . . . . . . . .  12
  Doubtful . . . . . . . . . . . . . . . . . . . . . .   1--43

  Percentage with left arm implicated  . . . . . . . .  63.63

  No. of cases with difficulty in telegraphing only  .   9
       "      "      "      "     writing       "    .   0
       "      "      "      "     telegraphing most  .  22
       "      "      "      "     writing       "    .  11
       "      "      "      "     both alike . . . . .   1--43

  Use of tobacco or alcohol:
    No   effect                 in  . . . . . . . . .   14
    Bad    "                    "   . . . . . . . . .   16
    Good   "    (in moderation) "   . . . . . . . . .    3
    Don't use either  . . . . . . . . . . . . . . . .   10--43   {543}

  Flushings in arm or face during work in . . . . . .   22
  Brittleness of nails                  " . . . . . .    5
  Emotional factor present              " . . . . . .   29
  Sympathetic movements in other parts  " . . . . . .    9
  Pain in back during work              " . . . . . .   18
  Trouble in performance of other acts  " . . . . . .   19
  Pain on pressure over nerve or muscle " . . . . . .   13

  Cramp of flexor group of muscles:
    In writing only . . . . . . . . . . . . . . . .  0
     "    "    most . . . . . . . . . . . . . . . .  3
     " telegraphing only  . . . . . . . . . . . . .  1
     "      "       most  . . . . . . . . . . . . .  5-- 9
  Cramp of extensor group of muscles:
    In writing only . . . . . . . . . . . . . . . .  0
     "    "    most . . . . . . . . . . . . . . . .  0
     " telegraphing only  . . . . . . . . . . . . .  4
     "      "       most  . . . . . . . . . . . . .  7--11
  Doubtful as to character of cramp . . . . . . . . . . 11
  No cramp  . . . . . . . . . . . . . . . . . . . . . . 12--43

  Manner of telegraphing:
    Arm resting on table  . . . . . . . . . . . . . . . 22
     "  raised from  "    . . . . . . . . . . . . . . . 12
    Alternating one with the other  . . . . . . . . . .  7
    Doubtful  . . . . . . . . . . . . . . . . . . . . .  2--43

  Manner of writing:
    Arm movement  . . . . . . . . . . . . . . . . . . . 13
    Finger movement . . . . . . . . . . . . . . . . . .  6
    Combination of the two  . . . . . . . . . . . . . . 24--43


{544}


TETANUS.

BY P. S. CONNER, M.D.


Tetanus (_τεινω_, to stretch) is a morbid condition characterized by
tonic contraction of the voluntary muscles, local or general, with
clonic exacerbations, occurring usually in connection with a wound.
Cases of it may be classified according to cause (traumatic or
idiopathic); to age (of the new-born and of those older); to severity
(grave and mild); or to course (acute and chronic), this latter
classification being the one of greatest value.

Though known from the earliest times, it is in the civil practice of
temperate regions of comparatively rare occurrence, and even in
military surgery has in recent periods only exceptionally attacked any
considerable proportion of the wounded.

Occurring in individuals of all ages, the great majority of the
subjects of it are children and young adults. Women seem to be
decidedly less liable to it than men. That this is due to sexual
peculiarity may well be doubted, since the traumatic cases are by far
the most numerous, and females are much less often wounded than males.
The traumatisms of childbed are occasionally followed by it (puerperal
tetanus).

That race has a predisposing influence would appear to be well
established; the darker the color, the greater the proportion of
tetanics. Negroes are especially likely to be attacked with either the
traumatic or idiopathic form.

Atmospheric and climatic conditions, beyond question, act powerfully
in, if not producing at least favoring, the development of tetanus.
Places and seasons in which there is great difference between the
midday and the midnight temperature, the winds are strong, and the air
is moist, are those in which the disease is most prevalent; and it is
because of these conditions that the late spring and early autumn are
the periods of the year when cases are most often seen.[1]

[Footnote 1: In his account of the Austrian campaign of 1809, Larrey
wrote: “The wounded who were most exposed to the cold, damp air of the
chilly spring nights, after having been subjected to the quite
considerable heat of the day, were almost all attacked with tetanus,
which prevailed only at the time when the Reaumur thermometer varied
almost constantly between the day and the night by the half of its
rise and fall; so that we would have it in the day at 19°, 20°, 21°,
and 23° above zero (75°-84° F.), while the mercury would fall to 13°,
12°, 10°, 9°, and 8° during the night (50°-61° F.). I had noticed the
same thing in Egypt.”]

Cold has, from the time of Hippocrates, been regarded as a great
predisposing if not exciting cause, and the non-traumatic cases have
been classed together as those a frigore. It is not, however, the
exposure to simply a low temperature that is followed by the disease,
but to cold combined with dampness, and quickly succeeding to a
temperature decidedly {545} higher, as in the cool nights coming on
after hot days in tropical regions, or in the spring and fall seasons
of temperate latitudes, or in the cold air blowing over or cold water
dashed upon a wound or the heated skin. That such cold, thus
operating, does most usually precede the attack of tetanus is
unquestionable; and it has by many been held that without it no
traumatism will be followed by the disease. Observers generally are
agreed, with Sir Thomas Watson, that “there is good reason for
thinking that in many instances one of these causes (wound and cold)
alone would fail to produce it, while both together call it forth.”

In the low lands of hot countries (as the East and West Indies) the
disease is very frequently met with, at times prevailing almost
epidemically; and, on the other hand, it is rare in dry elevated
regions and in high northern latitudes, as in Russia, where during a
long military and civil experience Pirogoff met with but eight cases.
Trismus nascentium would seem to be an exception to the general rule
of the non-prevalence of tetanus in places far north, since, _e.g._,
it has been at different periods very common in the Hebrides and the
small islands off the southern coast of Iceland. But these localities,
from their peculiar position, are not extremely cold, and their
climate is damp and variable; so that, even if the lockjaw of infants
be accepted as a variety of true tetanus, the geographical exception
indicated is but an apparent one.

Traumatic cases are greatly more numerous than idiopathic, and no
class of wounds is free from the possibility of the supervention of
tetanus. Incised wounds are much less likely to be thus complicated
than either of the other varieties, though operation-wounds of all
sorts, minor and major, have been followed by this affection. So
frequently has it been associated with comparatively trivial injuries
that it has become a common belief that the slighter the traumatism
the greater the danger of tetanus. That this is not true the records
of military surgery abundantly show. Wounds of the lower extremity are
much graver in this respect than those of the upper. Injuries of the
hand and feet, especially roughly punctured wounds of the palmar and
plantar fasciæ (as, _e.g._, those made by rusty nails), have long been
regarded as peculiarly liable to develop the disease, and accidents of
this nature always give rise to the fear of lockjaw. Though there can
be no question but that more than one-half of the cases of tetanus in
civil life are associated with wounds of these localities, yet the
number of such injuries is so much greater than of those of other
parts of the body that the special liability of the subjects of them
to become tetanic may well be questioned. In this connection it is a
significant fact that during our late war of perhaps 12,000 or 13,000
wounds of the hand, only 37 were followed by tetanus, and of 16,000 of
the foot, but 57. A few years ago numerous cases of tetanus were
observed in our larger cities complicating hand-wounds produced by the
toy pistol—injuries that were often associated with considerable
laceration of the soft parts, and generally with lodgment of the wad.

Not even the complete cicatrization of a wound altogether protects
against the occurrence of the disease, the exciting cause of which,
under such circumstances, is probably to be found in retained foreign
bodies or pent-up fluids.

ETIOLOGY.—Almost universally regarded as an affection of the central
nervous system, inducing a heightened state of the reflex
irritability, {546} though some have maintained that the reflex
excitability of the medulla and the cord is actually lessened, how
such affection is produced is unknown; and it is an unsettled question
whether it is through the medium of the nerves or the vessels, whether
by ascending inflammation, by reflected irritation, or by the presence
of a septic element or a special micro-organism in the blood.

That the disease is due to ascending neuritis finds support in the
congested and inflamed state of the nerves leading up from the place
of injury (affecting them in whole or in part, it may be in but a few
of their fibres), and in the inflammatory changes discoverable in the
cord and its vessels. But time and again thorough and careful
investigation by experienced observers has altogether failed to detect
any alterations in the nerves or pathological changes in the cord,
other than those that might properly be attributed to the spasms, the
temperature, or the drugs administered. The symptoms of acute neuritis
and myelitis (pain, paralyses, and later trophic changes) are not
those which are present in cases of tetanus. The evidences of
inflammation of the cord are most apparent, not in that portion of it
into which the nerves from the wounded part enter, but, as shown by
Michaud, so far as the cellular changes in the gray matter are
concerned, always in the lumbar region, no matter where the wound may
be located.

The much more generally accepted theory of reflex neurosis is based
upon the association of the disease with “all forms of
nerve-irritation, mechanical, thermal, chemical, and pathological;”
upon the direct relation existing between the likelihood of its
occurrence and the degree of sensibility of the wounded nerve;[2] in
the, at times, very short interval between the receipt of the injury
and the commencement of the tetanic symptoms; in the local spasms
unquestionably developed by nerve-pressure and injury; in the primary
affection of muscles at a distance from the damaged part; in the
already-referred-to absence of the structural lesions of inflammation;
and in the relief at times afforded by the removal of irritating
foreign bodies, the temporary cutting off of the nerve-connection with
the central organs, or the amputation of the injured limb. But that
something more than irritation of peripheral nerves is necessary to
the production of tetanus would seem to be proved by the frequency of
such irritation and the rarity of the disease; by the not infrequent
prolonged yet harmless lodgment of foreign bodies, even sharp and
angular ones, against or in nerves of high sensibility;[3] by the
primary affection of the muscles about the jaws, and not those in the
neighborhood of the wound; by the almost universal failure to produce
the affection experimentally, either by mechanical injuries or by
electrical excitations; by certain well-attested instances of its
repeated outbreak in connection with a definite locality, a single
ship of a squadron, a particular ward in a hospital, or even bed in a
ward; by the usual absence of that pain which is the ordinary effect
of nerve-irritation; and by the small measure of success which has
attended operations, even when early performed, {547} permitting the
taking away of foreign bodies pressing upon or resting in a nerve,
interrupting the connection with the cord, or altogether removing the
wound and its surroundings. Even in the idiopathic cases—many of
which, it would at first sight appear, can be due only to reflected
irritation—another explanation of the mode of their production may, as
we will see, be offered.

[Footnote 2: According to Gubler, the danger is greatest in wounds of
parts containing numerous Pacinian corpuscles.]

[Footnote 3: Heller has reported a case in which a piece of lead was
lodged in the sheath of the sciatic nerve. Though chronic neuritis
resulted, the wound healed perfectly. Two years later, after exposure
while drilling, the man was seized with tetanus and died of it.]

The so-called humoral theory would find the exciting cause of the
disease in a special morbific agent developed in the secretions of the
unbroken skin or the damaged tissues of the wound, or introduced from
without and carried by the blood-stream to the medulla and the cord,
there to produce such cell-changes as give rise to the tetanic
movements. It finds support in the unsatisfactory character of the
neural theories; in the strong analogy in many respects of the
symptoms of the disease to the increased irritability and muscular
contractions of hydrophobia and strychnia-poisoning, or those produced
by experimental injections of certain vegetable alkaloids; in the
recent discoveries in physiological fluids, as urine and saliva, of
chemical compounds,[4] and in decomposing organic matter of ptomaïnes
capable of tetanizing animals when injected into them; in the
rapidly-enlarging number of diseases known to be, or with good reason
believed to be, consequent upon the presence of peculiar microbes; in
the more easy explanation by it than upon other theories of the
ordinary irregularity and infrequency of its occurrence, its
occasional restriction within narrow limits, and its almost endemic
prevalence in certain buildings and even beds; in the extreme gravity
of acute cases and the protracted convalescence of those who recover
from the subacute and chronic forms; in the very frequent failure of
all varieties of operative treatment; and in the success of
therapeutic measures just in proportion to their power to quiet and
sustain the patient during the period of apparent elimination of a
poison or development and death of an organism.

[Footnote 4: Paschkie in some recent experiments found that the
sulphocyanide of sodium applied in small quantities caused a tetanic
state more lasting than that caused by strychnia.]

This theory is as yet unsupported by any positive facts. Neither
septic element nor peculiar microbe has been discovered.[5] Failure
has attended all efforts to produce the disease in animals by
injecting into them the blood of tetanics. There is no testimony
worthy of acceptance of the direct transmission of the disease to
those, either healthy or wounded, coming in contact with the tetanic
patient; nor can much weight be attached to such reports as that of
Betoli of individuals being attacked with it who had eaten the flesh
of an animal dead of it.

[Footnote 5: Curtiss of Chicago thought that he had found a special
organism, but further investigation showed that it was present in the
blood of healthy members of the family and in the water of a
neighboring pond.]

The ordinary absence of fever has been thought to prove the
incorrectness of this theory, but increased body-heat is not a symptom
of rabies or strychnia-poisoning, of the tetanic state following the
injection of ptomaïnes, or of cholera—a disease very probably
dependent upon the presence and action of a bacillus. Martin de Pedro,
regarding the affection as rheumatic in character, located it in the
muscles themselves, there being produced, through poisoning of the
venous blood, a muscular asphyxia.

{548} MORBID ANATOMY.—The pathological conditions observed upon
autopsy in the wound, the nerves, the central organs, and the muscles,
have been so various and inconstant that post-mortem examinations have
afforded little or no definite information respecting the morbid
anatomy of the disease. Many of the reported lesions have
unquestionably been dependent upon cadaveric changes or defective
preparation for microscopic study. The wound itself has been found on
the one hand healthy and in due course of cicatrization,[6] on the
other showing complete arrest of the reparative process (“the sores
are dry in tetanus,” wrote Aretæus),[7] or even gangrenous, with
pus-collections, larger or smaller, in its immediate vicinity, usually
in connection with retained foreign bodies.

[Footnote 6: Of one of Hennen's cases it is reported that “the life of
the patient and the perfect healing of the wound were terminated on
the same day.”]

[Footnote 7: Morrison seventy years ago wrote: “Wounds from which
there is a copious discharge of bland pus are seldom or never followed
by this disease;” and as a rule this is true.]

The nerves in and about the injured area have often been found
reddened and swollen, their neuroglia thickened and indurated, and
blood extravasated at various points. At times, even when to the naked
eye healthy, microscopic examination has shown one or a few of the
constituent bundles inflamed. But repeatedly the most thorough search
has failed to find any departure from the normal state, and the same
appearances of congestion and inflammation are not seldom observed
when there has been no tetanic complication. In an interesting case
reported by Michaud the sciatic in the uninjured limb presented the
same neuritic lesions as that of the wounded side.

In the cord and the medulla vascular congestion has been the condition
most generally seen, associated not infrequently with hemorrhages and
serous effusions—a condition occasionally absent, and when present
due, it is probable, in great measure, perhaps wholly, to the muscular
spasms, or consequent in part upon post-mortem gravitation of the
fluids. Increase in the amount of the connective tissue of the white
columns of the cord (thought by Rokitansky to be the essential lesion
of the disease); disseminated patches of granular and fluid
disintegration (to which Lockhart Clarke called attention in 1864);
atrophy of the cells, especially those of the posterior gray
commissure; nuclear proliferation; changes in the color, form, and
chemical reaction of the ganglion-cells; dilatation and aneurismal
swellings of the vessels, with development of granulation-masses in
their walls; and changes in the sympathetic ganglia,—such have been
the reported lesions. But each and every one has at times been
absent—at times been discovered in the bodies of those dead of other
diseases. Some of the changes have without doubt been produced after
death; some perhaps have been but errors of observation.

The muscles have been found healthy in appearance and constitution;
discolored, softened, and the seat of blood-extravasations large and
small; undergoing the vitreous degeneration; and ruptured, the
laceration affecting a few fibres or the entire thickness of one or
more muscles, as the rectus abdominis, the muscles of the neck, those
in the vertebral gutter, and even the heart. The rigor mortis appears
at once or very soon, thus confirming Brown-Séquard's observation,
that cadaveric rigidity is “quick in coming on and quick in passing
off in direct proportion to the amount {549} of long-continued violent
action which preceded death.” The visceral congestions that have been
observed cannot be regarded as in any way peculiar, but as due simply
to the muscular spasms and the mode of dying.

It is probably by chemical and microscopical examinations of the
blood, and, much more, the solids and fluids of the damaged part or
the secretions of the skin in the non-traumatic cases, that the cause
of this obscure affection is to be discovered, and not from study of
the nerves, the cord, and the brain; which study up to the present
time has only shown that “tetanus has no morbid anatomy, except
perhaps its traumatic cause and the asphyxial congestions resulting
from it.”

SYMPTOMS.—Following the receipt of a wound, tetanus may be developed
quickly or only after many days, cases of more or less credibility
being on record of immediate appearance, and of an elapsed interval of
one, two, three, even seven months (in a case occurring during our
late war). Doubt, however, may very properly be entertained as to the
true tetanic character of some at least of these very long-delayed
cases, or of their dependence upon the previous traumatism. The very
common belief that after the lapse of three weeks no fear of the
disease need be entertained is unquestionably an erroneous one, but
the danger certainly is slight when the wounded person has escaped for
twenty-two entire days. In by far the larger proportion of cases the
outbreak occurs between the fifth and fifteenth days after injury—in
about two-thirds, according to Yandell's, or about four-fifths,
according to Joseph Jones's and Otis's statistics.

Not infrequently for a day or two before any distinct evidences of the
disease are manifested there is prodromal malaise, associated at
times, but by no means constantly, with unusual sensitiveness, or even
positive pain, in the wound and slight muscular twitching in its
vicinity. In the larger number of cases the first symptoms noticed are
stiffness about the jaw, more or less difficulty in opening the mouth,
and perhaps slight interference with deglutition, the patient feeling
as if he had taken cold; such symptoms often appearing early in the
morning after waking from the night's sleep. With more or less
rapidity well-marked trismus comes on, the jaws being locked, the
corners of the mouth retracted, and the lips either firmly closed or
separated so as to uncover the teeth, producing the peculiar grin long
known as the risus sardonicus.

In rare cases it is the depressors, and not the elevators, of the
lower jaw that are in a state of contraction, the mouth consequently
being kept wide open. The forehead is wrinkled, the eyes staring, the
nose pinched, and not seldom there is the facial expression of old
age. The voice is altered and swallowing is difficult. Occasionally
the spasms of the muscles of deglutition are so intense as to be the
principal tetanic symptom, such dysphagic or hydrophobic (Rose)
tetanus very generally proving fatal. In a few cases, after wounds of
the face and head, these violent spasms have been found associated
with facial paralysis, almost always, if not always, on the injured
side; such paralysis having been present in at least one case (Bond's)
in which throat-spasm was wanting, the wound being in the
temporo-parietal region. Often there is early felt in greater or less
intensity pain, as from pressure, in the epigastrium, piercing through
to the back—a symptom by some regarded as pathognomonic, and due
without doubt to contraction of the diaphragm.

{550} From the region of the jaw the disease passes on to successively
attack the muscles of the neck, the back, the abdomen, the chest, the
lower, and, last of all, the upper, extremities, those of the forearm
long after those of the arms. The muscles of the fingers, of the
tongue, and those of the eyeball are very late if at all affected, the
tongue probably never being tonically contracted. The anterior
abdominal wall is broadened, depressed, and hard. In the
fully-developed acute cases the whole body is rigid, remaining
perfectly straight (orthotonos), arched backward (opisthotonos),
forward (emprosthotonos), or laterally (pleurosthotonos), according as
the muscular tension is balanced or greater on one side than another.
The action of the extensors being usually the more powerful, backward
bending (opisthotonos) to a greater or less extent is the ordinary
condition; but only in rare and extreme cases is the contraction such
as to curve the body like a bow and keep it supported upon the occiput
and heels. Frequently the bending is not specially noticeable except
in the neck. Emprosthotonos is rare, and pleurosthotonos has been so
seldom observed that its very existence has been denied. Occasionally,
in well-marked cases of opisthotonos, there is some associated lateral
arching, due rather to voluntary efforts on the part of the patient
(for the purpose of obtaining relief) than to tetanic contraction.
Larrey's opinion that the location of the wound (behind, in front, or
on the side) determined the direction of the curving has been proved
to be incorrect. Except in a small proportion of cases to the
persistent tonic spasm[8] there is added convulsive seizures of the
affected muscles, developed upon any, even the slightest, peripheral
excitation of the reflex irritability, as by a movement, a touch, a
draft of air, a bright light, a sudden noise, an attempt at
swallowing, etc. The frequency of these clonic exacerbations and their
intensity vary much, being severer and coming on closer together in
the grave acute cases and in the later stages of those terminating
fatally. They may occur only once in several hours or four, five, or
more times in a single hour, each spasm lasting from but a few seconds
to a minute or two. During its continuance the suffering is intense,
both from the pain of the contraction and the experienced sense of
suffocation. Between the paroxysms there is usually but little pain,
the sensation being rather one of tension or pressure. Occasionally
cessation of spasms and complete relaxation of all muscular
contraction suddenly take place six, eight, or twelve hours before
death, the patient quickly passing into a state of collapse.

[Footnote 8: This is not, in reality, a state of uninterrupted spasm,
but one of very numerous, quickly-repeated muscular contractions, as
many even as six hundred and sixty per minute (Richelot).]

Throughout the whole course of the disease the mind remains clear,[9]
except in the later stages of a few cases; and then the existing
delirium or coma is often, it is probable, an effect of the treatment
that has been employed. Except in the more chronic cases the patient
is generally unable to sleep, and even when fortunate enough to do so
the tonic spasm may not relax. In other than the mildest attacks there
is usually noticed a marked increase, local or general, of the
perspiration; such sweating {551} being a much more prominent symptom
of the disease as met with in tropical than in temperate regions.

[Footnote 9: “The brain alone in this general invasion has appeared to
us to constantly preserve the integrity of its functions down to the
very last moment of existence, so that the unfortunate subject of this
disease is, as it were, an eye-witness of his own death” (Larrey).]

The pulse, which is normal in the earlier stages, may later be but
little increased in frequency (except during the exacerbations, when,
small and compressible, its beats may run up to 140, 160, or even 180
per minute), or it may become progressively feebler and more rapid as
the case advances toward the fatal termination. The irregularity often
noticed during the convulsive seizures is doubtless owing to the
muscular contractions so compressing the vessels as to hinder the
passage of the blood through them. That the heart itself is not
tetanically contracted would seem to be proved by its regular quiet
action during anæsthesia.

The body-heat varies greatly in different cases, the temperature being
oftentimes normal, or even subnormal, until toward the very last. Not
infrequently, even in severe and fatal cases, it is not increased more
than two or three degrees, and quite rarely, except just before death,
does it rise much above 103° F. Exceptionally, very high temperatures
have been observed; I have myself seen one of 108° F. an hour before
death. Prévost had a patient whose axillary temperature was 110¾° F.
Lehmann reports a heat of 111.9° F. just before death, and in one of
Wunderlich's cases the temperature (that three hours earlier was
103.5° F.) fifteen minutes before death was 110.1° F., and at death
112.5° F., with a further post-mortem rise of more than a degree
(113⅔° F.)—a phenomenon that has been observed in a number of cases.
This increased temperature of tetanus is not of inflammatory origin
(except as a part of it, at times, may be due to intercurrent
affections, especially a broncho-pneumonia), but depends doubtless
upon a combination of causes, among them the violent muscular spasms,
and, more particularly, the disturbance of the regulating heat-centre
or centres from the alterations of their blood-supply in quantity and
quality.

The bowels are usually constipated, because of the little food taken,
the profuse sweating, the tonic spasms of the abdominal muscles, and
the contraction of the external sphincter and the levator ani, the
muscular coat of the bowel, like all the other involuntary muscles,
remaining unaffected.

Micturition, generally infrequent because of scanty secretion, may or
may not be disturbed. In many cases it is true, as written by Aretæus,
“the urine is retained so as to induce strong dysuria, or passes
spontaneously from contraction of the bladder,” though it is the
external muscles, and not the bladder itself, the contraction of which
produces the retention or the discharge; which latter is of rare
occurrence.

DIAGNOSIS.—When fully developed, with all its characteristic symptoms
present, tetanus cannot, or at least ought not to, be mistaken for
anything else; yet a study of reported cases will show that errors of
diagnosis have been made, and because of such errors various methods
of treatment have been given undue credit as curative measures.
Wound-spasms, clonic in character, of different degrees of severity,
beginning in and confined to the muscles of the injured part or limb
(even of the lower segment of the upper extremity), have not seldom
been regarded as tetanic, which they certainly are not; and recovery
having taken place, it has been attributed to the adopted treatment,
operative or therapeutic. The comparatively few cases in which,
primarily located in the vicinity {552} of the wound, these traumatic
spasms have become generalized in strict accordance with Pflüger's
laws, or, much more rarely, passing over the intervening parts of the
body, have seized upon the muscles of the jaw and neck, may perhaps,
for want of accurate knowledge of the essential nature of tetanus, be
regarded as a variety of the disease; but it is much to be regretted
that observers and reporters have not clearly separated them from the
cases of true tetanus (or the commonly met-with variety of tetanus) in
which the first or first important symptoms are always in connection
with the muscles whose nerves take origin in the medulla oblongata, no
matter where the wound may be located or whether there is any wound at
all. Not a few of the idiopathic cases may justly be regarded as of
tetany, that “little tetanus” in which the spasms always proceed from
the periphery toward the centre; are especially likely to affect the
forearms and the fingers, forming in their contractions the
obstetrical hand; are followed by periods of complete relaxation; can
be brought on by compression of the main artery or nerve of the limb,
or by light tapping of the affected area; may cause a rigid state of
the trunkal muscles or even well-marked opisthotonos; are associated
with impairment or paralysis of sensation; may last for a few minutes
or for hours; and sooner or later spontaneously cease, a fatal
termination of the affection being exceedingly rare.

Hysterical spasms may strongly simulate those of tetanus, and such
attacks have without doubt been wrongly diagnosticated, the cases
going to swell the number of those successfully treated by one remedy
or another. They ought, however, to be readily recognized if due
consideration be had of the age and character of the patients, the
history of the attack, and the order and nature of the symptoms
themselves, especially their frequent limitation to one member
(preferably a leg), the absence of consciousness during the attacks,
the long and uninterrupted rest at night, their more or less often and
prolonged complete intermissions.

Cerebro-spinal meningitis, because of the developed stiffness of the
neck and retraction of the head, the orthotonos, or even well-marked
opisthotonos, the epigastric pressure-pain, the occasional trismus,
and rigidity with reflex convulsive movements of the muscles of the
extremities, may, and doubtless has been, mistaken for tetanus; but
its generally epidemic prevalence, the headache, the cutaneous
hyperæsthesia, the temperature, and the other well-known symptoms of
the disease ought to suffice for its ready determination.

Strychnia-poisoning has many symptoms in common with tetanus, but
there is an absence of the wound which is generally associated with
the latter affection, a much more rapid development of severe
convulsions, and a quickly-appearing opisthotonos. The spasms from the
commencement affect the extremities, producing early contractions of
the muscles of the hands and feet, and only later those of the jaw.
Complete intermissions of greater or less length usually occur, and
either death or marked amelioration of pain and spasm follows in a
comparatively short time.

Hydrophobia, the dysphagic symptoms of which are like those at times
observed in tetanus, has its peculiar wound of origin and protracted
period of incubation, its absence of trismus or general tonic muscular
contractions, its usual dread of water and inability to swallow
fluids, its attendant restlessness, and its frequently-observed
delirium, the entire {553} aggregation of symptoms being
characteristic of itself and nothing else except the simulating
nervous affections occasionally developed in individuals bitten by
rabid or supposed rabid animals.

PROGNOSIS.—As declared by Hippocrates, “the spasm that comes on after
the receipt of a wound is a frequent cause of death.” Violent acute
cases, developing early, are excessively dangerous; and there is much
truth in Poland's declaration that “there is scarcely a
well-authenticated instance of recovery on record.” Taking all the
traumatic cases together as met with in military and civil hospitals,
the death-rate may safely be placed at not less than 80 per cent. Of
1332 cases reported from the wars of the last thirty years, and
occurring in six large hospitals during the last twenty years, 1060
proved fatal—_i.e._ 79.6 per cent.[10]

[Footnote 10: Crimean war, 23—21, 91 per cent.; Confederate army,
(Sorrel), 66—60, 91 per cent.; U. S. army, 505—451, 89.3 per cent.;
Italian war (Demme and Chenu), 176—162, 91 per cent.; Franco-German
war (Poncet), 316—181, 57.28 per cent. (omitting Richter's 224 cases
with only 107 deaths, the mortality of the remaining 92 cases (74) was
80 per cent.); St. Thomas's Hospital, 43—24, 55.8 per cent.; St.
George's Hospital, 30—21, 70 per cent.; St. Bartholomew's Hospital,
63—47, 74.6 per cent.; Guy's Hospital, 60—51, 85 per cent.;
Pennsylvania Hospital, 26—20, 76.9 per cent.; Boston City Hospital,
24—22, 91.6 per cent. The mortality-rate at Guy's (85 per cent.) is
almost the same as that given by Poland for the period from 1825 to
1858 (86.1 per cent.).]

As met with in private practice, under favorable hygienic
surroundings, a decidedly larger percentage of recoveries probably
takes place—how much larger cannot be even approximately determined,
since, as a rule, only those cases which get well are reported, but
few patients come under the care of any single observer, and the
chances of error in diagnosis are much greater than in a large general
hospital. The mortality rate of the idiopathic cases is very much
lower (not exceeding perhaps 25 or 30 per cent.), localized trismus
being “never mortal, though it may last for a number of weeks”
(Poncet). That recovery should take place much more frequently in
cases of this variety than in those associated with wounds might be
anticipated, since, as a rule, they are more chronic in their course;
the attacks are less frequent; if generalized, the spasms do not
involve all the muscles at once, but by progressive seizures and
relaxations; and they less often and less severely affect the muscles
of respiration. The earlier the disease shows itself after the receipt
of a wound (other things being equal), the stronger the likelihood of
a fatal termination; and, for obvious reasons, the more powerful, more
general, and more quickly repeated the spasms, the greater is the
danger. The larger part of the deaths occur within the first week, a
majority by the fifth day; all experience tends to show that there was
much truth in the Hippocratic observation, that “such persons as are
seized with tetanus die within four days, or if they pass these they
recover.” From the end of the first week on, the chances of recovery
rapidly increase day by day, and after the second week there is but
little danger of a fatal termination, though death may take place
(from exhaustion usually) after the lapse of several weeks, six or
more.[11] I have myself seen it occur on the thirty-seventh day.

[Footnote 11: Of the 358 cases reported in the _Medical and Surgical
History of the War of the Rebellion_, the duration of which was known,
64.8 per cent. died within five, and 83.5 per cent. within ten days.
Of 327 cases reported by Poland and Hulke, 56 per cent. died within
the earlier, and 83.5 per cent. the later, period. Of Richter's cases,
76.6 per cent. died within five days. Of 170 cases tabulated by
Yandell, 53 per cent. died within the first four days, and 77 per
cent. within nine days.]

{554} Recovery is usually slow. Even in the non-traumatic cases the
period of convalescence very seldom is less than two months, and, as
has been truly said, “it is a very mild case that the patient is well
of in thirty days.” More or less stiffness of the muscles usually
continues for many weeks; in one case (Currie's) “his features
retained the indelible impression of the disease;” and Copland reports
having seen a man who had had tetanus nine years before, whose jaws
were still permanently locked. Relapses may easily be brought on by
exposure or slight imprudences, and such secondary attacks not
infrequently prove fatal. The earlier and more severely dysphagic
symptoms are manifested, the more grave the prognosis; and the sooner
disturbances of respiration are shown, the speedier the death, since
spasm of the respiratory muscles, in the words of Aretæus, “readily
frees the patient from life.” Generally stated, “the more powerful the
contractions, the greater the irritation and the danger;” and the
longer the delay of involvement of the respiratory muscles, the more
favorable the prognosis. The occurrence of strabismus is of grave
import (Wunderlich), as might be expected, since only in very severe
cases or in the later hours are the deep muscles of the eye affected
by spasm. The manifestation of delirium (which is rare, and sometimes,
if not generally, due to over-medication) indicates with almost
absolute certainty a speedy death.

The pulse-rate and temperature, especially the latter, afford
prognostic indications of value.

A rapid pulse is an unfavorable symptom; and if at the same time it is
feeble and irregular, the probabilities of an early death are very
great.[12] Though, as has already been stated, the temperature often
varies but slightly from the normal, even in acute and rapidly fatal
cases, yet when the thermometer does not indicate a body-heat of over
100° F. the prognosis is unquestionably more favorable than when it is
two or more degrees higher; and there is certainly much truth in the
opinion (Arloing and Tripier) that as long as the rectal temperature
is not above 100-2/5° F. (38° C.) the prognosis is favorable; whereas
when it rises the prognosis at once becomes much more grave, few
patients recovering in whom it reaches 103° F. Oscillations of
temperature are of no prognostic value, good or bad.

[Footnote 12: Few at the present time share Parry's belief, that “if
in an adult the pulse by the fourth or fifth day does not reach 100 or
perhaps 110 beats in a minute the patient almost always recovers,” and
“if, on the other hand, the pulse on the first day is 120 or more in a
minute, few instances will be found in which he will not die.”]

Death usually occurs suddenly, from spasm of the external respiratory
muscles or of those of the larynx, but it may be consequent upon a
slow strangulation, upon exhaustion (as it frequently is in the
chronic cases), or even upon heart rupture, as in a patient of
Dujardin-Beaumetz.

How far the age of the patient affects the prognosis cannot be very
definitely stated. The prevalent opinion (entertained as long ago as
the time of Aretæus), that the disease is less dangerous in the middle
part of life than as either extreme is approached, is probably an
erroneous one. Yandell, from the analysis of the cases he had
collected, found that the mortality was greatest in children under
ten, and least in individuals between ten and twenty years old. Kane's
statistics would place the time of greatest danger in the early adult
period, from the age of twenty to that of thirty-five or forty.

{555} In traumatic cases the location of the wound does not seem to
materially influence the death-rate. As occurring during our late war,
those associated with injuries of the upper extremity were the least,
and of the head, face, and neck the most, fatal, but the difference in
the mortality rates was but 8.4 per cent. (86.8:95.2 per cent.). It
has long been believed that wounds of parts supplied by the cranial
nerves are not only less often followed by tetanus than those of other
regions, but that the disease when present is of a less fatal
character. Of the 10 cases of the peculiar head-tetanus already
referred to, collected by Bernhardt, 6 died (60 per cent.).

TREATMENT.—For the relief of tetanus agents of most diverse action and
power have been employed, intended to control inflammation, allay
nervous irritability, arrest spasm, and sustain the general strength;
and operations have been performed with the view to destroy
nerve-conduction, remove external irritants, change the character of
the associated wound, or take away the originally damaged part. Much
of the confusion and uncertainty that have prevailed respecting the
therapeutic treatment has doubtless arisen from the want of distinct
separation of the idiopathic from the traumatic cases, because of
incorrect diagnosis, or through an unwarranted assumption of the
general applicability of a method of medication found advantageous in
individual cases of perhaps rheumatic, malarial, or meningeal disease.

Regarding the affection as inflammatory, the older surgeons treated it
antiphlogistically, and until within comparatively recent times
bloodletting and mercury were largely employed. General and local
bleedings, resorted to as far back as the time of Hippocrates, were
not seldom made in excessive amounts,[13] the patient occasionally
surviving both the disease and the treatment. The mercurials were
pushed until profuse ptyalism was produced—a condition which could but
add to the distress (because of the great difficulty experienced in
clearing the throat and mouth), and likely to induce and increase the
severity of the convulsive seizures. Combined with opium, calomel was
formerly held in high repute, and numerous recoveries have been
attributed to such treatment—recoveries, however, almost always of
cases of chronic character and no great severity. Should the mycotic
origin of the disease ever be demonstrated, there will be good reason,
in its well-known destructive action upon minute organisms, for the
administration of the mild or corrosive chloride of mercury. Cold
baths and affusions have sometimes caused entire relaxation of the
spasms, leaving the patient as supple as a glove, and not seldom have
been followed by muscular ruptures or sudden death.[14] The local
application of ice to the spine has been credited with many cures,
particularly of cases of the non-traumatic variety, and benefit has
seemed to follow the employment of ether or rhigoline spray. Hot
baths, water {556} or air, general or local, have been largely used
from the time of Paré down, and the induced free perspiration has in
some instances seemed to have been of service, as have the medicinal
agents acting as sudorifics, of which jaborandi has of late been the
one ordinarily employed. “To relieve the contractions and provoke
sweating are the two principal bases of treatment,” wrote Martin de
Pedro. But it should not be forgotten that in many of the more severe
and rapidly-fatal attacks profuse sweating is characteristic of the
disease.

[Footnote 13: In a case of Lisfranc's, in twenty-six days venesection
was made nineteen times, and seven hundred and seventy-two leeches
were applied.]

[Footnote 14: An interesting and frequently-mentioned case is reported
by Sir James McGrigor. A soldier having tetanus (unusually severe) was
“during the first part of the day drenched with rain, the thermometer
standing at 52°, but after ascending one of the highest mountains in
Galicia the snow was knee-deep and the thermometer below 30°. The
patient was exposed to this inclement weather from six o'clock in the
morning till ten at night, when he arrived half starved to death, but
perfectly free from every symptom of tetanus.”]

All violent depleting measures should be abstained from, since in the
acute attacks they can do no good, and in the more chronic ones can
only increase the general debility; and it is from exhaustion that the
subjects of these latter usually die.

To lessen the reflex irritability, to quiet the muscular spasms, and
support the patient are the prime indications; to fulfil which every
agent in the materia medica that has, or has been supposed to have,
any sedative action upon the nervous system has been employed, as well
as remedies directly controlling muscular movements. Of the greater
number of such it may be truly said, “They have the same value, and
the best of them is good for nothing” (Giraldes).

At the present time the medicinal agents that are deserving of
consideration are tobacco, the anæsthetics, curare, conium, cannabis
indica, calabar, opium, chloral, and the bromides.

Tobacco, that in virtue of its depressant action so powerfully relaxes
the muscles, was until the introduction of the anæsthetics largely
employed and regarded with much favor, but of late years has rarely
been used, inhalations of chloroform or ether securing more rapid and
complete relaxation, with far less danger to the patient. Nicotine, in
doses of from a fraction of a minim to a full minim (6/10 gr.) by the
mouth, or two by the rectum (Houghton), has been given instead of the
tobacco infusions with equally good effects, and of course the same
dangers of producing fatal collapse.

The anæsthetics, chloroform and ether, have been frequently
administered, but although muscular relaxation and sleep have been
thereby secured, the natural progress of the disease toward a fatal
termination has not been materially affected: death has at times been
directly and suddenly produced, and not infrequently, though the
inhalations have lessened suffering, they have seemed to hasten the
end.

Curare, which “powerfully impairs and destroys the conductivity of
motor nerves,” and of which, consequently, much was hoped at one time,
has proved to be of but little value.[15] In order that benefit may
follow its administration the agent must be given in large doses and
until a decided impression is made upon the innervation of the muscles
of respiration, great danger meanwhile existing of producing asphyxia,
for the relief of which artificial respiration must be instituted.
McArdle of Dublin, in reporting recently a successful case of the
acute variety in which gr. ⅔ was given every fifth hour, suggested the
combination of curare and pilocarpine, “in the hope that the cardiac
and respiratory trouble produced by the former might be prevented by
the latter.” Uncertain in composition, cumulative in action,
“dangerous, difficult to manage, {557} and variable in its effects,”
curare is not, so far as has as yet been determined, an agent to be
recommended in the treatment of tetanus.

[Footnote 15: Of Demme's 22 cases, 14 died (63.6 per cent.); of
Busch's 11 cases, 6 died (54.5 per cent.); and in 51 cases collected
by Knecht the mortality-rate was 49 per cent.]

Conium, the action of which is much akin to that of curare, and which
primarily is upon the terminal portions of the motor nerves, has been
occasionally employed—successfully in two cases by Christopher Johnson
of Baltimore, who gave it hypodermically in doses of from 1/6 to 2
minims every one, two, or three hours. In two other cases under the
care of the same surgeon death took place, but the remedy seemed to
have acted beneficially in relieving the spasms and relaxing the tonic
rigidity.

Calabar bean—which produces a paralyzing action on the spinal cord,
abolishing its reflex functions, and later “diminishes and destroys
the conductivity of the motor nerves”—though apparently of service in
certain cases (almost all of them, however, in young subjects and of
chronic character), has proved to be of little or no more value than
other less dangerous agents. It was first clinically employed by Vella
in the Italian war of 1859. Of the 39 cases in Yandell's table, 39 per
cent. recovered; of the 60 in Knecht's, 45 per cent.; and of the 60
collected by H. C. Wood, 55 per cent. It may be administered by the
mouth, the rectum, or subcutaneously in doses (of the extract) of from
⅓ gr. to 2 grs. every quarter hour, half hour, hour, or two hours
(Ringer gave 4 grs. in an hour),[16] according to the violence of the
symptoms, being stopped when there is produced “vomiting, diarrhœa, or
a rapid small pulse and clammy sweat.” Yet its beneficial action in
severe cases is only manifested when it has been “pushed to the extent
of rendering the patient collapsed, the temperature of his body
falling perhaps to 94° or 95° F., the pulse being hardly perceptible
at the wrist” (Macnamara); under which circumstances there is about as
great risk of death from the treatment as from the disease itself.
Always, fever is a contraindication to its employment.

[Footnote 16: E. Watson gave to a patient in the course of forty-three
days the equivalent of 1026 grs. of the solid extract, a tincture of
the powdered bean being largely employed.]

Cannabis indica, originally used by the East Indian surgeons, and
believed by them to have a powerful influence in controlling the
tetanic spasms, has proved much less efficacious in cases occurring in
Europe and this country, perhaps because of the unreliable character
of the extract used; though of 42 cases of the traumatic variety
treated in the Chadnie Hospital at Calcutta in five years (1865-69),
62 per cent., and of 39 idiopathic cases 40 per cent., died, and of
Chuckerbutty's 13 cases in India, 6 (_i.e._ 46 per cent.) died. Of the
25 cases in Yandell's table, the mortality-rate was 36 per cent. If
given, it should be in doses of from ½ to 2, or even 4, grs. of the
extract, or minim 15 to drachm j of the tincture, every two or three
hours. Having a strong hypnotic action, it is to this probably that
the beneficial effects of its administration are due, rather than to
its secondary influence upon sensation and muscular movements.

Of all the sedatives and narcotics, opium has been longest and most
often used, and in so far as it relieves pain and causes sleep it is
of service. Like the other agents, it must be administered in large
doses, reference being had to the effect produced and not to the
number of grains given. The difficulty of swallowing even the liquid
preparations has of late years made the hypodermic injections of
morphia the favorite mode of administering the drug. Demarquay has
advised that the solution (1 part to 50 of water) should be thrown
deeply into the substance {558} of the affected muscles, as near as
possible to the place of entrance of their supplying nerves; the
result being to especially relieve the trismus and allow of the taking
of food. Fayrer in India found opium-smoking of advantage. The
mortality-rate of the 185 cases tabulated by Yandell treated with
opium was 43 per cent., but, as is true of the other drugs that have
been referred to, it is chiefly if not wholly in the mild and chronic
cases that the beneficial effects have been observed.

So far as has yet been determined, chloral is our most valuable drug
in the treatment of tetanus, as it is in that of the allied condition
of strychnia-poisoning—not because of any direct antidotal action, but
by reason of its producing sleep, lessening the reflex irritability of
the spinal cord, and diminishing the violence and frequency of the
muscular spasms, thus enabling the patient to keep alive until the
morbid state can spontaneously disappear. Given usually by the mouth
or the rectum, it has been administered hypodermically (as much as 5
grs. at a time by Salter) or, as proposed by Oré, thrown directly into
a vein. If it is true, as has been claimed, that its beneficial effect
is due entirely to the sleep secured (not infrequently after waking up
the spasms return with increased violence), the drug should be
administered in doses sufficiently large and repeated to maintain a
continuous slumber. Verneuil (whose therapeutic formula has three
terms, rest, warmth, sleep) has found that while with certain patients
a drachm a day is enough, to others four times as much must be given,
and directs that the chloralic coma be continued for about twenty
days. Further experience may show that small doses may suffice to
secure the needed quiet—as, _e.g._, the 40 grs. at bedtime, with, if
necessary, 30 grs. more at midday, recommended by Macnamara. Such
small doses are far safer than the enormous ones that have at times
been employed,[17] since chloral can exert a powerful toxic influence
upon the circulatory and respiratory centres, death being almost
always due to arrest of respiration, though in tetanic cases it may be
the effect of slight spasm upon a heart the enfeebled state of which
is indicated by a very rapid and thready pulse. The intravenous
injections expose the patient further to the risk of the formation of
clots and plugging of the pulmonary artery, several instances of which
accident have already been reported, though this method of treatment
has but seldom been employed. The death-rate of those treated by
chloral alone was 41 per cent. in the 134 cases analyzed by Knecht,
and 41.3 per cent. of the 228 tabulated by Kane.

[Footnote 17: Beck is reported to have given 420 grs. in three and a
half hours, and Carruthers 1140 grs. in six days; both patients
recovered—Beck's after a continuous sleep of thirty hours. In one case
the chloral sleep was maintained without interruption for eight days,
from 250 to 300 grains a day being given; and in another, which also
recovered, over 3000 grs. were taken in the course of thirty-eight
days.]

Of late years use has been made, either alone or in combination with
opium or chloral, of the bromides, especially that of potassium, which
in full dose unquestionably diminishes reflex irritability, lessens
the sensibility of the peripheral nerves, and moderates excessive
body-heat. Under its influence mild cases of tetanus have recovered
and more severe ones been somewhat relieved, and it has the decided
advantage over the other drugs that have been noticed of not being a
direct cause of death even when given in large dose—as much in some
instances as six, seven, or nearly eight drachms a day. Knecht found
that of 10 {559} cases treated with chloral and the bromide, 9 got
well; and Kane, of 21 to whom such a combination was given, only 5
died (23.8 per cent.); but the number of cases is too small to make
conclusions deduced therefrom of any special value. Voisin reports a
case (in which it should be noted the spasms began in parts near the
wound, and that on the fourteenth day after the receipt of the gunshot
injury of the right thigh) that had for eleven days been treated
without effect with chloral in large quantity, which at the end of
that time was put upon drachm ij doses of the bromide, with three
hypodermics a day of about ½ gr. of morphia each: in three days
decided improvement had taken place, and in four days more the patient
was well.

The sedative and sustaining action of alcohol has many times been
taken advantage of in the treatment of this affection. The
administration of wines or spirits in large amounts has certainly been
found of much service, though it will seldom or never be necessary to
give wine, as Rush advised, “in quarts, and even gallons, daily.” 80
per cent. of recoveries appear to have taken place in the 33 cases
that Yandell found to have been treated with stimulants; but, on the
other hand, of Poland's 15 cases treated with wine, 75 per cent. died:
here, again, the numbers are too few to make any deduced conclusions
of much value.

As tetanus (or at least tetanoid spasm) has at times been observed as
a consequence of malarial poisoning, and successfully treated with
quinine, this remedy has occasionally been employed in cases not
dependent upon paludism, but very generally to no purpose.

Fowler's solution of arsenic in doses of from 5 to 20 minims every
two, three, or four hours has been believed by certain of our American
surgeons (Hodgen, Prewitt, Byrd) to be of service.

Because of the supposed origin of the disease in peripheral
nerve-inflammation or irritation, operative procedures have many times
been adopted to interrupt the conduction or remove the part.

Amputation, which was so highly commended by Larrey, is now recognized
as of no service in the severer and more acute cases, and as
unnecessary mutilations in the chronic ones; and if performed in those
of intermediate severity, when recovery takes place it will generally
be difficult or impossible to determine of how much benefit the
operation really was, and in some at least of the fatal cases the
result can fairly be attributed to the amputation itself. When the
disease is associated with an extensive lesion of an extremity, there
can be no objection to the removal of the damaged part (if performed
early), except that it may by the added shock still further weaken the
patient and render him less able to hold out against the tetanus. In
cases of severe spasms limited to the muscles of the injured limb (and
such are frequently said to be of tetanus) amputation is often
strongly indicated, and not seldom is the only treatment that will
afford relief. During our late war “amputation was resorted to in 29
instances after incipient tetanic symptoms; 10 of the cases resulted
favorably, and in several instances it is noted that the symptoms
ceased after the operation.”[18] Of Yandell's 17 cases, 60 per cent.
recovered.

[Footnote 18: _Medical and Surgical History of the War of the
Rebellion_.

As there is here, apparently, recovery in 34.5 per cent. of the
gunshot cases treated by amputation (nearly one-fifth of all the
non-fatal cases reported)—a very gratifying degree of success, and one
that might properly encourage the resorting to this method of
treatment—somewhat careful analysis may well be made of the 7 cases
the histories of which are given. In 2, shell wounds of the foot,
operated upon by the same surgeon, the disease appeared while the men
were still upon the field. Of one of them it is stated that “there was
but little hemorrhage, but the shock was excessive and tetanic
symptoms were present;” and of the other, that “the peculiarities in
the case were that symptoms of tetanus were quite marked, with great
exhaustion.” There are certainly good reasons for believing that these
two cases were not of tetanus, but of simple convulsive movements from
shock and anæmia. Of the remaining 5 cases, the symptoms manifested
themselves on the fourteenth, nineteenth, twenty-first, thirty-fifth,
and fifty-fourth day after the receipt of the wound. One of the
patients (in whom the disease was longest delayed), having a much
inflamed and suppurating compound fracture of the bones of the
forearm, “was suddenly seized with a chill followed by threatening
tetanus,” and amputation was made the following day. In another
(thirty-fifth day case) the “arm became much swollen and symptoms of
tetanus ensued, including stiffening of the jaws, great pain and
restlessness, and irritable pulse;” two days later the limb was
removed, and “all symptoms of tetanus disappeared after the
operation.” In another (twenty-first day) the man when admitted into
hospital, one month after the date of the injury, stated that “he was
first taken with trismus about a week before.” “As he was certainly
getting worse every day,” the forearm was removed forty days after the
receipt of the wound and nearly three weeks after the commencement of
the tetanic symptoms. Other remedies employed after the operation
(brandy, chloroform, and blisters to the spine) doing no good, drachm
ss doses of the tr. cannabis indica were given every two hours, “under
which the patient slowly improved.” In another case (nineteen days)
the symptoms were those of tetanus; the amputation was made on the
following day; twenty-four hours later “rigidity of the muscles had
partly disappeared, and improvement continued until the patient was
entirely relieved.” In the remaining case (fourteen days) the first
symptoms of tetanus “were relieved by active purgatives, calomel, etc.
Three days later the symptoms returned,” and on the next day “tetanus
supervened in its usual form.” Five days afterward “the leg was
amputated at the middle third, after which the tetanus subsided and
the patient made a rapid and good recovery.”

In all of these five cases the disease appeared so long after the
receipt of the wound that the chances were that if it was tetanus
recovery would take place without regard to the treatment adopted; and
of two some doubt may properly be entertained as to their real nature,
there being present in both much inflammation—in one an initial chill,
and in the other restlessness, great pain, and an irritable pulse. If
the unpublished histories of the other three cases are similar to
those given, these reported ten successful amputations can affect but
little, or not at all, the previously entertained opinion of the real
value of this method of treatment—that it is destructive to part,
dangerous to life, and only very exceptionally, if ever, curative of
the disease.]

{560} Nerve-section, first made by Hicks in 1797, and
nerve-stretching, first performed by Vogt in 1867—reason for which can
be found only in the neuritis (or, much more strongly, the
reflex-neurosis) theory of the disease—has not been followed by relief
in any unusually large proportion of cases,[19] and should be
practised only when the affected nerve is clearly indicated, when
there is much pain in the wound, or when a distinct aura proceeds
therefrom. In determining what nerve shall be divided or stretched
regard may with advantage be had to Wood's symptom—to wit, the
development of pain when pressure is made upon the nerve-trunk,
branches from which terminate in the wound.

[Footnote 19: Of section, 21 cases, 10 deaths—_i.e._ 47 per cent.
(Poncet); of stretching, 46 cases, 36 deaths—_i.e._ 78.2 per cent.
(Harte).]

Arloing and Tripier strongly advised total neurotomy (_i.e._ division
of all the nerves going to the damaged part), and that high up—an
operation that must be followed by extensive paralysis; not, however,
permanent, they claim; in six months, at the latest, the power of
motion being regained. This period is altogether too limited, as has
been proved more than once. Fayrer reports having seen a case in which
the hand was permanently crippled. It is to be noted that in most of
these nerve-operation cases that terminate in recovery the tetanic
spasms in the other parts of the body do not cease at once, but often
quite slowly, and in the {561} larger number of them internal
medication of some kind is steadily employed. The removal of foreign
bodies from the wound, the freeing of nerves from constricting
ligatures, the division of the parts around containing nerve-fibres,
and cauterization of the unhealed surface—each has at times proved
beneficial, and the first two should always be early resorted to if
the necessity therefor exists, no matter what views may be entertained
respecting the nature and cause of the disease.

Tracheotomy, first proposed by Physick and later advised by Marshall
Hall, has rarely proved of service, since the dyspnœa generally
depends upon causes other than spasm of the laryngeal muscles.
Verneuil, however, has recently stated that he has saved several lives
by this operation.

Careful analysis of reported cases clearly indicates that neither in
drug nor operation has a cure for tetanus as yet been found. Almost
without exception “in the fully-developed cases all remedial measures
fail, and the cases run on unchecked to a fatal termination;” and with
the subjects of such acute attacks the physician, in the words of
Aretæus, “can merely sympathize.” If not quickly overpowered by the
violence of the seizure, and if he can be sufficiently supported, the
patient may recover; and if there is late appearance, slow
development, and infrequent and limited spasms, he probably will do
so, whatever may be the treatment adopted.

“The first indication,” wrote John Hunter, “should be to strengthen
the system;” and in the fulfilment of this indication food is of prime
importance:[20] “many patients perish from too much medication and too
little feeding” (Agnew). Stimulants and hypnotics indirectly yet
powerfully sustain the strength, and the removal of sensory irritants,
as light and noise, by lessening the frequency of the spasms
contributes to the production of the desired result, since in the
convulsed muscles themselves there are developed substances that cause
contraction. “Quiet and warmth are indispensable.” Fecal accumulations
can but irritate, and therefore an early action through enema or mild
drug should, if possible, be secured. As has been happily said by
Labbé, “one must treat the tetanics, not tetanus.”

[Footnote 20: If necessary, fluids may be administered by means of a
tube passed through the nose, or given by the rectum.]

If little can be done to cure, much can be done to prevent. The
influence of predisposing causes (anxiety, care, excesses, paludism)
is to be counteracted as far as may be; the hygienic surroundings of
the wounded are to be rendered as favorable as possible; especially is
proper ventilation to be secured, and exposure to cold and rain
avoided. Whether or not one believes with Rose that the disease
depends not on the kind of wound, but on its treatment (“the earlier
it is treated in the most careful manner the less frequently do we
have tetanus”), there can be no question as to the great advantage to
be derived from the thorough cleansing of the wound, the removal of
irritating foreign bodies, the securing of free drainage, and the
lessening of the amount of inflamed and dying tissue. The marked
diminution in the number of cases observed in the last thirty years,
as compared with that of a century or three-quarters of a century ago,
is the direct result, we may well believe, of improved treatment of
wounds and the wounded. The greater danger of slight injuries very
possibly lies in their liability to be neglected or mistreated, {562}
and the special gravity of punctured wounds of the hand and foot in
the anatomical obstacles presented to the ready outflow of blood,
serum, or pus. In the exceedingly fatal toy-pistol wounds is it not in
the decomposing débris of the lacerated tissues, or in the retained
wad saturated with the secretions, that the danger lies of the
development of tetanus, and not in nerve-irritation or any peculiar
character of the injury? Certainly in the only case I have myself
seen, in which the disease was not developed, the damaged hand was
kept under hot water from the time it was hurt until healing was
complete, and free drainage was from the first maintained.

Tetanus is reported to have appeared notwithstanding the associated
injury was antiseptically dressed; but in modern wound-treatment, with
its cleanliness, its protection of the damaged part, its infrequent
manipulations, and its power to diminish inflammation and prevent
decomposition, lies, we may well believe, the means of reducing to a
minimum the danger of occurrence of those spasms that, once developed,
are of “exceedingly painful nature, very swift to prove fatal, but not
easy to be removed” (Aretæus).


Puerperal Tetanus.

As met with after abortion or labor at term, tetanus presents no
special peculiarities in course, treatment, or termination. Of very
rare occurrence in temperate regions, it is often met with in hot
countries in women of the darker-colored races. Grief, anxiety,
overwork, and profuse hemorrhage predispose to it, as do obstetrical
operations and the retention of pieces of the placenta. Unlike the
ordinary puerperal affections, it is more common in the country and in
private practice than in cities and hospitals. Rather elderly women
are more often attacked than are those younger. First and second
pregnancies are the more dangerous if completed; later ones if
abortion occurs. Abortion in the earlier months, especially in the
third, is most likely to be followed by the disease (Garrigues).
Ordinarily manifesting itself within ten days after labor, it has been
known to occur after an interval of a month.

Hysteria, eclampsia, and especially tetany, may be mistaken for it.
The latter affection, which generally attacks young women, may occur
at any time during pregnancy or lactation—tetanus only within a
comparatively few days after delivery.

Its TREATMENT is the same as that of ordinary tetanus, care being
taken to remove from the uterus as speedily as possible any contained
foreign body. Antiseptic irrigations may prove of service, though it
is doubtful if their employment can accomplish much after the
commencement of the spasms. Aveling has thought that transfusion might
perhaps be of benefit.

The occurrence of intracranial congestions, hemorrhages, and venous
thrombosis[21] will, almost of necessity, render any medication of no
value.

[Footnote 21: Such as were found upon autopsy in the case reported by
Macdonald, and believed by him to be the essential lesions of the
disease.]

Under all circumstances the PROGNOSIS is exceedingly grave. The {563}
mortality-rate of the cases after abortion collected by Garrigues was
92 per cent. (25—23), and of those after labor 84.37 per cent.
(32—27).[22]

[Footnote 22: As indicating the extreme gravity of tetanus occurring
in connection with a wound of the genital tract, it may be noticed
that of 17 cases after ovariotomy collected by Parvin, 16 died, 94.1
per cent., and of 24 cases tabulated by Olshausen, 23 died, 95.83 per
cent.]


Tetanus Neonatorum.

From the earliest times it has been known that newly-born children are
occasionally the subjects of trismus and generalized spasms, and that
those thus affected usually die.

More common among the darker races[23] and in warm countries (though
some of the southern races and tribes are almost or altogether free
from it), it has been for years together endemic in places far north
(_e.g._ the islands of Heimacy and St. Kilda), and a veritable scourge
in certain lying-in hospitals (_e.g._ Dublin, Stockholm, St.
Petersburg). Occasionally it has prevailed epidemically.

[Footnote 23: Wallace, however, found that in the Medical College
Hospital at Calcutta the disease occurred proportionably more
frequently in the children of European than of native mothers, though
the actual number of cases among the latter was very much the
greater.]

Attacking usually the children of the poor, others have not been
altogether exempt from it, though unquestionably “it is most often
seen where the mothers of the children are very young or very poor or
very worthless” (Mosely). Rarely appearing before the third day, it as
rarely occurs after the twelfth, generally manifesting itself within
the first week.

Its cause has been thought to be navel-string injuries; inflammation
of the umbilical arteries or vein; reflected irritation from the skin,
the bowels, or the external genitals; uræmic encephalopathy; cold and
dampness; defective ventilation; and indirect pressure upon the
cerebellum and the medulla.

The supposed causative umbilical lesions have time and again been
found in young infants presenting none of the symptoms of the disease;
and the same is true of the vessel inflammations[24] and of the reflex
irritations. Atmospheric and climatic states and the hygienic
condition of the child and its surroundings, however much they may
contribute to the development of the affection, cannot be regarded as
directly producing it; though experience has shown (as in the lying-in
hospitals before referred to) that by securing proper care of the
children, by improving the ventilation, and by preventing
overcrowding, its prevalence may be very greatly diminished.

[Footnote 24: Mildner of Prague reports that in 46 fatal cases of
inflammation of the umbilical vein, convulsions occurred in but 5, and
in these the spasms were not like those of tetanus.]

Forty years ago Marion Sims believed that he had discovered the
exciting cause in “pressure exerted on the medulla oblongata and its
nerves, the result most generally of an inward displacement of the
occipital bone,” occasionally, though rarely, of the parietal. That
intracranial pressure may give rise to tetanic symptoms is beyond
question, seizures identical with those of tetanus having been
observed in connection with tumors of the cerebellum (Hughlings
Jackson), as also trismus, confined even to one side (Wernicke).

{564} In some cases without doubt the occipital depression is
secondary, the result of intracranial shrinkage; and even if primary,
there may be no lockjaw.[25]

[Footnote 25: H. G. Lyttle of New York recently reported the case of a
child two months old whose occipital bone was depressed and overlapped
by the parietals, in which there had been no trismus, though the child
had slight convulsive movements of the hands and rolling of the eyes.]

Parrot regarded the disease as a form of eclampsia, the uræmic
encephalopathy manifesting itself as one or other of the three
varieties recognized (by Cederschjöld) a half century ago—viz.
trismus, tetanus, and ordinary eclampsia. The articular rigidity,
especially noticeable in the temporo-maxillary joint, he held to be
largely independent of the convulsive tonicity of the muscles, and due
in no small measure to induration of the overlying soft parts, such
hardening being the result of that loss of fluid which, as it affects
the body in general, produces the rapid and extreme emaciation which
is so characteristic of the disease.[26]

[Footnote 26: Parrot adds: “In the new-born in a state of health great
difficulty is experienced in separating the jaws, the muscles that
bring them together having, relatively, considerable power, and the
infants making quite an active resistance when one attempts to
separate them. It follows that when a pathological state exaggerates
this tendency it may be thought that we have to do with a veritable
trismus.”]

Though there is at times a prodromal period of restlessness and
fretfulness, usually the disease is first indicated by an inability to
nurse, the nipple being eagerly seized upon, but quickly dropped—an
action that may be regarded as almost pathognomonic. Swallowing,
difficult from the first, soon becomes impossible. The lower jaw in
the earlier hours in many cases is dropped, but nearly always
well-marked trismus is more or less quickly developed, at first
intermittent, but later persistent. Opisthotonos in some degree is
almost certain to be present, and in a large proportion of cases the
tetanic convulsions become generalized, clonic exacerbations occurring
as often as every half hour or hour, and capable of being induced at
any time by pressure upon the abdomen (Morrison), or indeed by any
external irritation, noise, touch, draft of air, etc.

All observers have noticed the peculiar cry, or rather whine, of the
little patient. The bowels have in some cases been constipated, in
others diarrhœa has been present. The temperature is generally
decidedly elevated, and has been known to reach 111.2° F. Usually in
from twelve to twenty-four or thirty-six hours collapse occurs, and
the child speedily dies; though the fatal result may be deferred for a
number of days or suddenly produced at any moment by spasm of the
respiratory muscles.

Upon autopsy there has generally been found hyperæmia of the brain and
cord with extravasations (commonly perithecal) in the spinal canal,
occasionally in the meninges of the brain and in the ventricles. Very
probably, as in true tetanus, these vascular conditions are the
effect, and not the cause, of the spasms; and sometimes, doubtless,
they are hypostatic.

As usually observed and commonly treated, the PROGNOSIS is very bad.
Whether occurring in India or in Iceland, in the Rotunda Hospital in
Dublin or in the Foundling Hospital in St. Petersburg, in the negro
cabins of our Southern States or in New York or Washington, the
subjects of it almost always die, generally in from six to forty-eight
hours.[27] It has been very exceptional to have 20 per cent.[28] of
{565} recoveries, or even 15;[29] and the non-fatal cases have almost
invariably been those in which the disease appeared late and in mild
form.

[Footnote 27: 80 per cent. of the cases collected by Hartigan
(207—165).]

[Footnote 28: 8 out of 40 cases tabulated by Smith; 8 out of 42 in the
Stockholm Lying-in Hospital in 1834. It is very probable that these
latter were cases of infantile meningitis.]

[Footnote 29: 5 out of 34 cases reported by Wallace from the Medical
College Hospital of Calcutta.]

When treated by manipulation and position, as recommended by Marion
Sims, the chances of recovery seem to be very much greater. Even in
the acute cases under the care of Sims, of Wilhite, and of Hartigan,
death occurred only in those seen late, after extravasations had taken
place.

The Sims's method consists simply in releasing the overlapped
occipital bone by manipulation (or, if that fails, by an operation),
and then placing the child so that the head shall rest flat upon its
side, the face looking directly toward the horizon. The success
attending this postural treatment has been so remarkable that the
practitioner cannot be justified in failing to determine the relative
positions of the occipital and parietal bones and to keep the head
resting upon its side.

Of the medicinal agents that have been administered (the same as those
employed in ordinary tetanus), calabar and chloral have of late years
been the favorites, chloral to-day standing highest in professional
estimation. Calabar is best given hypodermically in doses of from 1/12
to 1/6 gr. of eserine; chloral, either by the mouth (½ to 1½ or 2
grs.) or preferably by the rectum (2 to 4 grs.), either drug being
pushed until relaxation takes place and sleep is secured, or toxic
symptoms become so grave as to compel suspension of the treatment.
Though favorable results have rarely followed such medication,[30] and
(with but few exceptions) only in late-developed and mild cases that
very possibly would have gotten well of themselves; yet as recovery
from an acute attack has occasionally been reported, at least the
chloral treatment should be instituted in every case not found to be
promptly relieved by change of position of the head.

[Footnote 30: Monti, however, reported 11 recoveries out of 16 cases
treated with calabar (68.75 per cent.), 3 out of 5 in his own
practice; and Widerhofer was credited in 1871 with 6 recoveries in the
10 or 12 cases that he treated with chloral.]

Whatever views may be entertained as to cause or nature, it is to
measures that will prevent development that we must chiefly look for
relief from this lockjaw of infants, that even in our own country
annually carries off a great number of children—25,000, as estimated
by Hartigan. If mechanically produced, its occurrence should be
rendered impossible by having the child's head from the time of birth
properly placed, and at regular intervals changed in position. If
defective hygiene, personal and social, is the one common and constant
condition wherever the disease prevails, then due regard should be had
to dressing the umbilical (and perhaps the preputial) wound; to
bathing, clothing, and keeping quiet[31] the child; to thoroughly
airing,[32] warming, and disinfecting the lying-in room; and to
overcoming, as far as may be possible, the evil influences of
unfavorable atmospheric and climatic conditions.

[Footnote 31: In these new-born children, though the reflex
irritability is less than in those older, the response to irritation
is very much greater, because of the lessened inhibitory power at this
age (Soltmann).]

[Footnote 32: By increasing the air-supply and lessening the number of
beds the mortality at the Rotunda was in seven years reduced from
about 1 in 7 to about 1 in 19 of the children born.]


{566}


DISORDERS OF SPEECH.

BY EDWARD P. DAVIS, A.M., M.D.


Development of Speech.

The study of speech, a complex function, enlisting at once the
activities of mind and body, invites the physician to enter alike the
domains of the psychologist and physiologist.

Distinguishing man from beast, articulate expression has its
foundation in purely mental phenomena; its successful accomplishment
requires the reflex mechanism common to man and beast.

Let us consider as concisely as possible the physiology of speech.

DEVELOPMENT OF SPEECH IN THE INDIVIDUAL.—The earliest observation has
noted in the common name of the new-born child its speechless
condition; it is the infant, or not-speaking being. Born with a
nervous system in a highly unstable condition, the babe is a most
favorable recipient of the many impressions which stream upon it from
all sides. With sight and hearing undeveloped, the field of early
infantile impressions is limited to hunger, need of sleep, and
cutaneous impressions. Speech under such conditions is inarticulate,
an animal cry, unconscious and without intelligence. But with the
growth of the cerebrum the child's environment suggests to the
embryonic intelligence its primal impression. The parental relation is
dimly apprehended, and designations of the father and mother are
uttered in scarcely articulate sounds.

Sight and hearing open extensive fields of sensation, and with their
development begin the primal, physical impressions from which proceed
the emotions. The acoustic and optic centres of perception become
established, and the mental formation of symbols and signs, an
imitative process, marks the stage of childish cerebration, beyond
which the savage often does not proceed. The symbolic function is the
basis of language and of pictorial representation; as man requires the
trade medium of the symbol for the interchange of his ideas, so his
legal tender appears with the first emergence of mental enterprise.
The hieroglyphic and the onomatopoetic word are as old as humanity.

The co-ordinating mechanism of speech is of equal development. With
the growth of the child the varied impressions of education, of
surroundings, of heredity, all are influencing speech. With mental
growth, stimulated by these numerous impressions, comes the gradual
mental habit of forming ideas after certain models—of trading, so to
speak, in the coin of the country, of making and using a vocabulary.
Intuition, {567} induction, and deduction are established, the general
nervous function of memory develops, observations are made, and mind
and body, master and instrument, enter upon full activity.

PHYSIOLOGY OF NORMAL SPEECH IN THE ADULT.—Let us consider normal
speech in the adult. From a purely mental aspect speech is not
included in the nervous reflexes. The conception before the individual
may arise without sight or sound, it may be the object of the mental
processes only; but if it is to be communicated, or transferred from
the subjective to the objective, it calls into play the denotative
faculty or facultas signatrix.

As we are cognizant through the senses of phenomena only, so we
communicate only phenomena, or more particularly symbols; the spoken
or written word, the gesture, are necessary to make ideas tangible to
another mind. The symbolic faculty, then, is the mental faculty most
concerned in speech.

Cerebral localization has not included this faculty in its areas; it
is assigned to the anterior cortex, which as yet is the indiscriminate
site of the formation of ideas. The idea conceived, the symbol formed,
the motor area whose integrity is essential, is found in the region
commonly known as Broca's convolution, the posterior third of the left
third frontal convolution. This region is especially connected with
the corona radiata coming from the corpus striatum, with the corpus
striatum and the anterior portion of the internal capsule: like the
anterior, or motor, cornua of the spinal cord, it possesses giant, or
branching, nerve-cells; its anatomy would assign to it a motor
function. Its blood-supply is derived through the inferior frontal
branch of the Sylvian vessel, whose occlusion in a case cited by
Charcot was followed by complete aphasia.

Ferrier distinguishes just adjacent to this centre the motor centres
for the tongue and mouth and upper extremities, showing an anatomical
association of the processes of articulate and written speech.

But purely motor impulses comprise only a portion of the phenomena of
speech. The external world must be brought into relation with the
mind, and this is done through the perceptions. We may say that
perceptions are apprehended sensations, and this apprehension demands
a localized field of cerebral activity, as well as the motor energies.
It seems natural enough that experiment should have located (Ferrier)
perceptive, visual, and acoustic centres in the posterior cortical
areas and temporo-sphenoidal lobes—that the motor and perceptive areas
should be contiguous and sharing a common blood-supply.

The perceptive visual centre is found to occupy the occipital lobes,
while the acoustic centre occupies the whole length of the first
temporo-sphenoidal convolution.

As motor impulses found a path to the motor ganglia, and finally to
the cord, so the course of sensory perceptive impressions can be
traced back through the posterior internal capsule and through the
optic thalami to the sensory columns of the medulla and cord.

Intuitive and sense perception, even when reinforced with motor power,
cannot result in articulation. The mechanism of speech requires a
co-ordinating centre, and this basal phonic centre of Kussmaul is
located in the medulla near the origin of the hypoglossal and facial
nerves. From the medulla proceed the nerves supplying the machinery of
{568} phonation, the superior laryngeal nerve to the mucous membrane
of the larynx and to the crico-thyroid muscle, the most important
muscle of phonation. The remaining laryngeal muscles are supplied by
the recurrent laryngeal; the motor processes of articulation are
guided by the hypoglossal, facial, and fibres of the
glosso-pharyngeal.

The larynx is a reed, with the addition of numerous resonance-cavities
producing abundant overtones. It may be considered as a box composed
of two segments, the lower of which has vertical motion upon the joint
at the posterior junction of the superior and inferior segments. By
this motion the tongue of the reed (vocal cords, stretching
antero-posteriorly from lower segment to junction with upper segment)
is tightened or relaxed, the vibratory blast of air coming through the
trachea from the lungs. The superior aperture of the tube is guarded
by the epiglottis and false vocal cords. As auxiliaries are the
pharyngeal, oral, and nasal cavities, with the associated bony
cavities of the skull, the soft palate acting as a movable partition
or switch, the hard palate as a sounding-board or resonance-surface.
The reed is applicable to the production of musical sounds; the
tongue, lips, and teeth are required for the checks in those sounds,
constituting the consonants or division utterances.

The curious phenomenon of the falsetto voice is thought by Helmholtz
to be produced by the attenuation of the true cords and the vibration
of their thinned edges.

DEVELOPMENT OF LANGUAGE.—The study of language demonstrates its origin
to have been largely in exclamations and imitative sounds, from which
our vowels can easily have arisen. The growth of all synthetic
language illustrates the aggregation of accessory sounds about the
primitive root-sound, while the common tendency to the insertion of
consonants shows their addition to the primitive vowels. That the long
vowels should have undergone countless modifications from the physical
peculiarities and environment of those speaking them is but natural,
for the number of vowels remaining in actual use in any language is
not large. Consonants serve to make more clear by their separation of
vowel-sounds the meaning to be conveyed; their development resulted
from vowel changes, and their number is small.

The written characters of language represent only the usage of the
majority. Individual speech and pronunciation vary as greatly as do
languages themselves, and it is evident that the speech of any
individual is as truly peculiar as his physical conformation.

To recapitulate, we find ideas, the material of speech, formed in the
cerebral cortex. Speech-volition becomes motor impulse at Broca's
convolution; such impulse passes along the internal capsule to the
corpus striatum, where it is co-ordinated probably in the formation of
syllables, thence to the medulla, whence the mechanism of the larynx
receives its co-ordinated stimulation.


Disorders of Speech.

The classification of the disorders of speech should depend on the
anatomical site of the lesions by which they are occasioned. Broadly
{569} speaking, speech disorders resolve themselves into those of the
formative apparatus for ideas and symbols and those of the purely
co-ordinating and conducting mechanism. Abbreviating the schedule of
Potter, we may say that the disorders of speech may be included in
three classes—alalia, or lack of speech; paralalia, defective speech,
the stammering of most observers; and dyslalia, difficult speech or
stuttering.

The anatomy of the blood-supply of the speech-centres affords some
explanation of alalia. The Sylvian artery will be remembered as the
feeder of the speech-centres—an artery often the source of hemorrhage,
as Charcot suggests, from the angle at which it leaves the carotid.
Ducrot explains the frequency of left-sided softening and hemorrhage
from the manner of origin of the left carotid, its axis being more
nearly that of the ascending aorta and furnishing a ready channel for
cardiac clots. In regard to the relative frequency of peripheral and
central hemorrhage, Andral and Durand-Fardel cite 119 cases, of which
but 17 were in the anterior or posterior lobes. It is admitted that
cerebral lesions are largely those of the circulatory system, and the
fact that such lesions result in the suspension of the activity of
restricted areas is due to the circumstance that the cerebral arteries
are terminal vessels giving off no anastomosing branches and supplying
restricted areas only. With blood-supply so arranged it is not
difficult to understand how the different portions of the motor
centres may be separately involved, and thus the motor functions of
speech may become singly at fault.

Inability to remember words and inability to form the motor impulses
necessary for speech or writing are the common forms of alalia or
aphasia, the former being known as amnesic, the latter as ataxic,
alalia. In addition, we may cite the failure of cerebral power
occurring in general softening, in microcephalic brains, and the
curious instances of voluntary silence from some strong belief or
prejudice. Instances of the gradual resumption of cerebral function
after its loss are not wanting; and, occurring where subsequent
post-mortem examinations reveal a limited area of destruction of
brain-tissue, they afford examples of the vicarious performance of
cerebral functions by contiguous areas.

The phenomena of amnesic alalia are commonly seen in cases of recovery
from cerebral hemorrhage, cerebral injury, and severe febrile
affections. Numerous cases are recorded where the memory of things
themselves remained, but the faculty of denoting them had been
destroyed.

Kussmaul distinguishes here two conditions: 1st, where the word is
entirely effaced from memory, 2d, where it still remains, but its
association with that which it represents is suppressed. Cases of the
second class are the most frequent, the fundamental part which the
association of ideas plays in mental activity and the extent to which
memory is dependent on association explaining this fact. A marked
example of the failure of the denotative faculty lies in the cases of
forgetfulness of one's own name, as described by Crichton in the case
of an ambassador at the Russian court, who was obliged to say to his
companion, when visitors asked his name, “For Heaven's sake, tell me
what I call myself!” Piorry mentions the case of an aged priest who
after right-sided paralysis lost entirely the use of substantives;
wishing to ask for his hat, the word _hat_ failed him utterly, and he
was obliged to express himself in the remaining parts of speech: “Give
me that which I place upon the {570} ——;” but the word _head_,
denoting the object most commonly in relation with the _hat_, was
wanting also. When either hat or head was mentioned he spoke the word
without difficulty.

Instances of failure in linguistic faculty are not uncommon. Witness a
case, reported by Proust, of an Italian who after long residence in
France, though understanding his native tongue, could speak only in
French. Cases in which after acute disease one language is gone
entirely while several others are retained are not wanting. A striking
case of amnesic alalia was that of Lordat, a French physician, who
thus described his malady: “I find myself deprived of the value of all
words. If any words remain to me, they become useless, because I can
no longer remember the manner in which I must co-ordinate them to
express my thoughts. I am conscious that I recognize all ideas, but my
memory does not suggest a word. In losing the memory of the meaning of
spoken words I have lost that of their visible signs.”

Fortunately, these cases are among the more tractable of cerebral
disorders. Bristowe has reported a case wherein elementary instruction
in speech-formation was tried with marked success. The patient, aged
thirty-six, after a violent cerebral disturbance without traumatism
became paraplegic, speechless, and deaf. Gradual recovery ensued
until, seven months after his first illness, he was admitted into St.
Thomas's Hospital in the following condition: Numbness and paresis in
left leg, less in left arm; special senses healthy; no incontinence;
some pain about head and neck; complete loss of speech. It was found
that the patient was very intelligent, wrote legibly, could make all
kinds of voluntary movements with lips, tongue, and teeth, and was
capable of vocal intonation; articulation alone was lacking.

The law of the evolution of language designates as primitive forms of
word-signs those words affirming qualities, while those denoting
relative positions are of secondary formation (Whitney.) Remembering,
also, the fact that amnesia in general “is a regression from the new
to the old, from the complex to the simple, from the voluntary to the
automatic, from the least organized to the best organized,”[1] we are
able to understand the cause of amnesic alalia, and also the steps of
the process of recovery, in which the inverse order is observed.

[Footnote 1: Ribot, _Diseases of Memory_.]

Amnesic alalia can hardly be regarded as susceptible of treatment
other than as a general neurasthenia. Though we may develop memory by
cultivating the association of ideas and by repetition, yet, regarding
it as a general function of the nervous system, it is evident that
recovery from its disorders is conditioned by the general vigor of the
nervous centres. A partial recovery usually occurs in such cases;
complete recovery is more infrequent.

Ataxic alalia, the failure of the motor powers of speech, occurs in
all forms of general paralysis, most typically in bulbar paralysis.
This disease is fully described in the standard works on neurology.
Ataxic alalia will also occur in disseminated sclerosis, posterior
spinal sclerosis, dementia paralytica, and cretinism. It forms in
general disorders an instructive symptom, and is to be distinguished
by a tremulous utterance and by facial spasm from the hesitation of
the stammerer and from the convulsive utterance of the stutterer.

{571} Paralalia embraces all abnormalities of speech, from trivial
mannerisms to difficulties in the utterance of certain letters,
including those painful defects which depend upon physical
malformations.

The free discussion of paralalia would cover the domain of elocution;
the physician is called upon to advise in those cases only where
either a physical malformation is evident or the difficulty
experienced by the patient in enunciating certain letters has led to a
suspicion of the existence of malformation. The former cases lie in
the province of the surgeon; the latter come within the scope of those
elocutionists, speech-trainers, and instructors who hope to cure
stammering and stuttering.

Discrimination between stammering and stuttering will give the
physician a basis for judgment from which he can reasonably offer
encouragement in many cases and avoid the creation of false hopes in
others. As a cardinal point of difference, it will be remarked that in
the case of the stutterer the muscles of phonation are thrown into a
state of spasm when speech is attempted, while in the stammerer their
movements are merely lacking in proper co-ordination. It may also be
observed that the respiration of the stammerer is marked by irregular
contractions of the diaphragm, which render the expiratory blast of
air irregular in its delivery. In the stutterer the spasm is
pronouncedly laryngeal and facial. The nervous embarrassment of the
stutterer is proverbial, and is increased by excitement, while a
moderate degree of excitement, stimulating respiration, greatly
improves the speech of the stammerer.

Whispering, a difficult respiratory act, exaggerates the stammerer's
fault, but the spasm of the stutterer is often relaxed by the
diminished pressure of whispered breath.

As articulation is effected by the larynx and the oral organs, the
stutterer makes his spasmodic articulation particularly noticeable,
while the stammerer finds little difficulty in the utterance of words.
_R_, _L_, _S_, and other letters whose enunciation demands the
continued expiratory blast, are imperfectly uttered by the stammerer,
while these letters when joined to a long vowel-sound occasion little
or no difficulty for the stutterer.

TREATMENT.—It follows that if stammering is recognized as
inco-ordinate enunciation, owing largely to irregular action of the
diaphragm, any training of the respiratory muscles which will ensure a
regular delivery of the expiratory air will improve this defect. It
follows, then, that the treatment of stammering resolves itself into
careful attention to general hygiene, associated with such persistent
respiratory and vocal gymnastics as shall effectually develop
regularity, depth, and co-ordination of action on the part of all the
muscles concerned in the act of respiration. Drugs will be of service
only as aids to the correction of errors in the essential
physiological functions. In the child the powers of imitation may be
enlisted to effect a cure, and the familiar fact that the habits of
childhood are easily formed would indicate this as the best time for
treatment.

Childhood once passed, however, the steadiness of purpose of the adult
is requisite to break up a confirmed habit, and active treatment
should be deferred until after adolescence. Most important in all
cases are judicious moral influences exerted by those about the
patient, the ridicule so often visited upon the unfortunate stammerer
being most harmful in its consequences. The many tricks and devices so
often employed in these {572} cases are of use simply by varying the
monotony of vocal drill; they may be employed or abandoned as the
judgment of the physician may dictate.

Regarding the prognosis in these cases, it follows that with a fairly
developed and healthful nervous system, reinforced by proper mental
and physical hygiene, the stammerer's case is far from hopeless in the
hands of a patient and intelligent physician.

An unfavorable prognosis would be demanded by hereditary defects and
vices of the nervous system, by the lack of general nervous vitality,
by enfeeblement of the will and the mental tone of the individual, by
advanced age, and by irremediable hygienic conditions. Under favorable
conditions recovery should be the rule.

DYSLALIA OR STUTTERING.—Recalling to mind the points of difference
between stuttering and stammering, it becomes evident that while the
prospect of success in the treatment of the stammerer is often
favorable, the case of the stutterer presents such difficulties as
render it too frequently hopeless.

We may liken the confirmed stutterer to those rare cases of chorea
which defy treatment, and to those cases of hereditary deterioration
of the nervous system where the most patient and painstaking care
fails to overcome the defect. The laryngeal and facial spasms depend
upon no malformation for their exciting cause; hence surgery fails to
remedy the defect. Drugs which are given with hope of invigorating the
nervous system have only a general tonic influence, while the motor
depressants and antispasmodics find but partial success. We must again
rely upon hygiene, and also upon those aids to enunciation which come
from rhythmical associated movements, such as stamping with the foot,
beating time with the hand, the employment of a sing-song tone, or
other modes of specially rhythmic enunciation. The sing-song mode of
utterance is a familiar resource with parents in attempting to aid a
stuttering child, and the measured forms of articulation offer the
only vocal drill that possesses any permanent value. It is especially
essential in the stutterer's case that the patient be protected from
ridicule and from all disturbing emotions: the burden of difficult
speech is sufficient to greatly depress the nervous system without the
added suffering of emotional distress. It is evident that childhood,
characterized as it is by especial instability of the nervous system,
is the period when we can hope for the best results from care and
training; the long-formed habits of the adult are rarely broken.

We have thus traced the disorders of speech to their origin as
symptoms of grave central lesions of the nervous system, as results of
heredity or of a general neurasthenic condition; very rarely are they
dependent upon malformations of the organs of speech.

The treatment of such malformations, when they occur, is largely
unsatisfactory and is seldom curative.

The thorough treatment of those speech disorders that are not
susceptible of surgical aid would embrace such mental and physical
hygiene and training as should ensure the formation of a thoroughly
conceived vocabulary and its co-ordinated expression by words either
spoken or written. The study of expression in its highest forms would
necessarily conduct the investigator far into the realm of the
plastic, harmonic, and literary arts.


{573}


ALCOHOLISM.

BY JAMES C. WILSON, M.D.


DEFINITION.—Alcoholism is the term used to designate collectively the
morbid phenomena caused by the abuse of alcohol.

SYNONYMS.—Alcoholismus, Ebrietas, Ebriositas, Temulentia, Drunkenness,
Delirium potatorium, Mania potatorium, Delirium tremens, Chronic
alcoholic intoxication, Dipsomania; _Ger._ Trunkenheit, Trunksucht;
_Fr._ Ivresse, Ivrognerie.

These terms are in common use to describe such conditions and
outbreaks in alcoholic individuals as amount to veritable morbid
states or attacks of sickness, but they are not interchangeable, nor
are they all sufficiently comprehensive to constitute true synonyms.
They are names applied to various conditions due to acute or chronic
alcohol-poisoning properly and distinctively comprehended under the
general term alcoholism.

CLASSIFICATION.—It was formerly the custom to restrict this term to
affections of the general nervous system induced by continued excesses
in the use of alcoholic drinks.[1] But the nervous system bears the
brunt of the attack and suffers beyond all others alike in transient
and in continued excesses. The artificial restriction of the term to
the cases caused by continued excesses was therefore illogical in
itself, and has been productive of much needless difficulty in the
treatment of the subject and in the classification of the cases. The
use of the term chronic alcoholism to denote an established condition,
and of acute alcoholism to describe outbreaks of various kinds which
occur in individuals subject to that condition, has also proved a
source of embarrassment to the student. Not less vague has been the
employment of such terms as delirium tremens, mania-a-potu, and the
like, which are unsatisfactory in themselves, and tend to exalt
symptoms at the expense of the morbid condition of which they are only
in part the manifestation. I am of the opinion—which is at variance
with established usage—that the systematic discussion of alcoholism
requires that all forms of sickness, including drunkenness, due to
that poison must receive due consideration, and that the term acute
alcoholism, hitherto used in a sense at once too comprehensive and too
variable, should be reserved for those cases in which the sudden
energetic action of the poison is the occasion of like sudden and
intense manifestations of its effects. Furthermore, the uncertainty
and lack of precision in the use of the terms acute and chronic
alcoholism are due to errors of theory formerly almost universal in
medical {574} writings and popular belief concerning the disease. The
chief source of these errors was the recognition only of the more
acute nervous affections caused by alcoholic excess—delirium tremens,
maniacal excitement, and terrifying hallucinations—and the belief that
these conditions occurred only after a temporary abstinence in the
course of habitual or prolonged indulgence. It has now long been known
that abstinence from drink by no means necessarily precedes the
outbreak of mania or delirium, and modern researches have established
the existence of a chronic alcoholic intoxication of long duration
extending over a period of months or years, in which such outbreaks
merely exhibit the full development of symptoms that have already been
occasionally and partially recognizable.

[Footnote 1: Anstie, _Reynolds's System of Medicine_, vol. ii., 1868.]

The following arrangement of the topics will facilitate the discussion
of the subject in the present article, and serve, I trust, a useful
purpose for the classification of cases in accordance with existing
knowledge:[2]

I. Acute Alcoholism: Drunkenness, Debauch.
  A. Ordinary or Typical Form.
  B. Irregular Forms.
    1. Maniacal;
    2. Convulsive;
    3. In persons of unsound mind.
  C. Acute Poisoning by Alcohol: Lethal doses.

II. Chronic Alcoholism.
  A. Visceral Derangements.
    1. Local disorders:
      _a_. Of the digestive system;
      _b_. Of the liver;
      _c_. Of the respiratory system;
      _d_. Of the circulatory system;
      _e_. Genito-urinary system.
    2. Disorders of special structures:
      _a_. Of the locomotor apparatus;
      _b_. Of the skin.
    3. General disorders:
      _a_. The blood;
      _b_. Obesity;
      _c_. Cachexia.
  B. Derangements of the Nervous System: Cerebro-spinal Disorders.
    1. Cerebral disorders.
    2. Spinal disorders.
    3. Disorders of the peripheral nerves.
    4. Disorders of the special senses.
  C. Psychical Derangements.
    1. The moral sense.
    2. The will.
    3. The intellect.
    4. Alcoholic delirium in general.
    5. Delirium tremens.
    6. Alcoholic insanity:
      _a_. Melancholia;
      _b_. Mania;
      _c_. Chronic delirium;
      _d_. Dementia;
      _e_. Paretic dementia.

III. Hereditary Alcoholism.

IV. Dipsomania.

[Footnote 2: This classification is in part based upon that of Lentz,
_De l'Alcoholism et de ses Diverses manifestations, etc._, Bruxelles,
1884—a prize essay.]

HISTORY.—The history of the abuse of alcohol would be the history of
society from the most remote period until the present time, not only
among civilized but among barbarous races of men, for the abuse of
narcotics, of which alcohol is at once the most important and the most
widely used, forms a dark background to the broad picture of healthful
human progress. In truth, the most sketchy account of our knowledge of
the effects of alcoholic excess, as manifested in the individual and
in society at large, interesting as it might prove to the general
reader, would be out of place in this article. To be of real {575}
value it would necessarily embody a record of experiences so vague,
facts so indeterminate, opinions so at variance, and citations so
numerous, that they would require for their mere presentation a volume
rather than an article. The object of the writer in the following
pages shall be, therefore, to present the subject in its present
aspect, without reference, beyond that which is absolutely necessary,
to considerations of mere historical interest. This being the case, he
considers further apology for the lack of laborious historical studies
unnecessary.

ETIOLOGY.—_A_. Predisposing Influences.—We are at this point
confronted with a series of problems the complex nature and grave
importance of which appeal with peculiar urgency to all thoughtful
physicians. Their discussion, however, involving as it does unsettled
questions of great moment in social science, is beyond the scope of
the present article. A few practical points only can occupy our
attention.

The influences which predispose to alcoholism arise from unfavorable
moral, social, and personal conditions.

Among the unfavorable moral conditions may be mentioned a want of
wholesome public sentiment on the subject in communities. This arises
too often, but by no means exclusively, from poverty and its attendant
evils ignorance and vice. Rum is at once the refuge and the snare of
want, destitution, and sorrow. To the vacant and untrained mind it
brings boons not otherwise to be had—excitement and oblivion. That
both are brief and bought at a ruinous cost exerts little restraining
influence. Of equal if not greater importance are the influences which
spring from ill-regulated and demoralizing domestic relations, and the
absence of motive and the contentment which properly belong to the
family as an organization. Everywhere also do we find in example a
potent influence. In the individual, in addition to hereditary
propensities, the evil results of a lax, over-indulgent, or vicious
early training, as shown in a want of power of application, of moral
rectitude, in self-indulgence, craving for excitement, and a weak
will, powerfully predispose to the temptations of alcoholic excess.

Among social conditions which must be regarded as predisposing
influences occupation takes the first rank. The occupations which
render those pursuing them especially liable to alcoholism may be
divided into two classes—those in which the temptation to drink is
constantly present, and those in which the character of the work
begets a desire for stimulation, while the opportunities for the
gratification of the desire are but little restricted.

To the first of these groups belong all classes of workmen in
distilleries, breweries, and bottling establishments; keepers and
clerks of hotels, public houses, and restaurants; the barmen and
waiters in the same trades; the salesmen who travel for dealers in
wines and spirits. To this group must also be referred the
professional politician of the lowest order. These occupations have
furnished by far the larger number of cases that have come under my
care, both in hospital and in private practice.

To the second class belong occupations involving great exposure to the
inclemency of the weather. We frequently find cabmen, expressmen,
coal-heavers, hucksters, and street-laborers habitually addicted to
excesses in alcohol. The stringent regulations of corporations exert a
powerful {576} protective influence in the case of men employed on
railways, ferry- and other steamboat service, and in and about dépôts
and stations. Exhausting toil under unfavorable circumstances as
regards heat and confinement predisposes to drink, as in the case of
foundrymen, workers in rolling-mills, stokers, and the like. The
men-cooks who work in hotels and restaurants are especially liable to
alcoholism. Monotony of occupation, as in the cases of cobblers,
tailors, bakers, printers, etc., especially when associated with
close, ill-ventilated workrooms and long hours of toil, exerts a
strong predisposing influence. Persons following sedentary occupations
suffer from excesses sooner than those whose active outdoor life
favors elimination. To the monotony of their occupations may be
ascribed in part, at least, the disposition of soldiers, ranchmen,
sailors, etc. to occasional excesses as opportunities occur.
Irregularity of work, especially when much small money is handled, as
happens with butchers, marketmen, and hucksters, also often leads to
intemperance.

The lack of occupation exerts a baleful influence. Men-about-town, the
frequenters of clubs, dawdlers, and quidnuncs often fall victims to a
fate from which occupation and the necessity to work would have saved
them. In this connection it may be permitted to call attention to the
custom of treating as enormously augmenting the dangers to which such
persons are habitually exposed in the matter of alcoholic excesses.
The occasional moderate use of alcohol in the form of wine with food
and as a source of social pleasure is not fraught with the moral or
physical evils attributed to it by many earnest and sincere persons.
It is, on the contrary, probable that the well-regulated and temperate
use of sound wines under proper circumstances and with food is, in a
majority of individuals, attended with benefit. Those who suffer from
the effects of excesses do not usually reach them by this route, nor
would they be saved by any amount of abstinence on the part of
temperate and reasonable members of society.

When we turn our attention to the unfavorable personal conditions
which predispose to alcoholism, we at once enter upon the familiar
field of work of the practical physician. Numerous influences having
their origin in the individual himself, some occasional, others
constant, all urgent, demand our careful consideration. Some of the
conditions out of which these predisposing influences spring are
tangible and easy of recognition; others are elusive and uncertain. To
point them out is, unfortunately, not to remedy them. As a rule, they
have wrought their evil effects long before the individual has cause
to regard himself in the light of a patient.

First in importance is heredity. A peculiar inherited constitution of
the nervous system is as influential in leading to alcoholic excess
and in aggravating its disastrous effects as any other cause
whatsoever. A considerable proportion of individuals who suffer from
alcoholism are found upon inquiry to come of parents who have been
addicted to drink. A still greater number belong to families in which
nervous disorders, and in particular neuralgia, epilepsy, and
insanity, have prevailed. Others, again, are the offspring of
criminals. It can no longer be doubted that particular causes of
nervous degeneration in one or both parents may lead to the hereditary
transmission of a feeble nervous organization, which, on the one hand,
renders its possessor peculiarly liable to neuroses {577} of every
kind, and, on the other hand, an easy prey to the temptation to seek
refuge from mental and physical suffering in occasional or habitual
narcotic indulgence. Thus, as Anstie pointed out, “the nervous
enfeeblement produced in an ancestor by great excesses in drink is
reproduced in his various descendants, with the effect of producing
insanity in one, epilepsy in another, neuralgia in a third, alcoholic
excesses in a fourth, and so on.” When it is possible to obtain fairly
complete family histories, covering two or three generations, in grave
nervous cases, facts of this kind are elicited with surprising
frequency. The part which heredity plays in many of the more
inveterate and hopeless cases of alcoholism is wholly out of
proportion to the obvious and easily recognizable part played by
momentary temptation. To the failure to recognize the real agency at
work in such cases must be ascribed the disappointment of too many
sanguine and unsuccessful social reformers.

Various forms of disease exert a predisposing influence to alcoholic
excesses. In the first place, bodily weakness and inability to cope
with the daily tasks imposed by necessity impel great numbers of
persons of feeble constitution, especially among the laboring classes,
to the abuse of alcohol.

In the second place, many conditions of chronic disease attended by
suffering are susceptible of great temporary relief from the taking of
alcohol. Especially is this the case in the neuralgias, in phthisis,
in dysmenorrhœa and other sexual disorders of women, in the faintness
and depression of too-prolonged lactation, in the pains and anxieties
of syphilis, and in the malaise of chronic malaria. When the patient
has learned that alcohol is capable of affording relief from
suffering, it is but a short step through ignorance or recklessness to
habitual excess.

The administration of alcohol during convalescence from attacks of
illness is not unattended by the danger of subsequent abuse. It is
well for the physician to inform himself of the hereditary tendencies
and previous habits of the patient before assuming the responsibility
of continuing alcohol beyond the period of acute illness under these
circumstances; and it is a rule never to be disregarded that the
stimulant ordered by the physician is to be regulated by him in
amount, and discontinued when the patient passes out of his care.

Irregularities of the sexual functions in both sexes, and especially
sexual excesses, strongly predispose to alcoholism. The custom of
administering to young women suffering from painful menstruation
warming draughts containing gin, brandy, or other alcoholic
preparations in excessive amounts is a fertile cause of secret
tippling.

The abuse of tobacco, to the depressing effects of which alcohol is a
prompt and efficient antidote, must be ranked as an important
predisposing influence.

Depressing mental influences of all kinds tend strongly to drinking
habits. This is true of persons in all classes of society.

Habit constitutes an influence the importance of which can scarcely be
over-estimated. Much of the drinking done by active business-men has
no other cause than this. Alcohol, like opium and other narcotics,
exerts its most pernicious influence through the periodical craving on
the part of the nervous system for the renewal of the stimulating
effects which it causes, while it progressively shortens the period
and diminishes the {578} effect by its deteriorating action upon the
nutrition of the peripheral and central nervous tissues.

_B_. The Exciting Cause.—Alcohol, or ethyl hydrate, is the product of
the fermentation of solutions which contain glucose or a substance
capable of transformation into glucose. Other alcohols, as propyl,
butyl, and amyl alcohol, etc., are also formed in small quantity in
the fermentation of saccharine liquids. Ethyl alcohol is the type of
the series, and forms the normal spirituous ingredient of ordinary
alcoholic beverages. The others when present, except in minute
quantities, constitute impurities. Their toxic effects are much more
pronounced than those of ethyl alcohol.

Alcohol is a colorless mobile liquid having an agreeable spirituous
odor and a pungent, caustic taste, becoming fainter upon dilution. It
mixes with water and ether in all proportions.

Alcoholic beverages form three principal groups: 1, spirits, or
distilled liquors; 2, wines, or fermented liquors; and 3, malt
liquors.

1. The various spirituous liquors, as whiskey, gin, rum, brandy, etc.,
contain, in addition to the ethyl alcohol and water common to them
all, varying minute proportions of ethereal and oily substances to
which each owes its peculiar taste and odor. These substances are
œnanthic, acetic, and valerianic ethers, products of the reaction
between the corresponding acids and alcohol, and various essential
oils. Traces of the other alcohols are also present. Amyl alcohol, the
so-called fusel oil, is present in new and coarse spirit, but
especially in that derived from potatoes, in considerable amounts. It
is to this ingredient that potato spirit owes its peculiarly
deleterious properties. Richardson[3] experimentally produced with
amyl alcohol phenomena analogous to delirium tremens in man. Spirits
also frequently contain sugar, caramel, and coloring matters derived
from the cask, to which certain products of the still also owe in part
their flavor. These liquors are of varying strength, and contain from
45 to 70 per cent. of absolute alcohol by volume.[4]

[Footnote 3: _On Alcohol_, Lond., 1875.]

[Footnote 4: Vide Baer, _Der Alcoholismus_, Berlin, 1878.]

Liqueurs (anise, kümmel, curaçoa, Benedictine, etc.) are the products
of the distillation of alcohol with various aromatic herbs, sweetened,
or of its admixture with ethereal oils and sugar. These compounds
contain a very high percentage of alcohol. Two of them, absinthe and
kirsch, by reason of their peculiarly dangerous properties deserve
especial mention.

Absinthe is an alcoholic distillate of anise, coriander, etc. with the
leaves and flowers of the _Artemisia absinthium_, which yields a
greenish essence. This liqueur contains from 60 to 72 per cent. of
alcohol, and exerts a specific pernicious effect upon the nervous
system, largely due to the aromatic principles which it contains.[5]
Kirsch, which owes its {579} peculiar flavor to the oil of bitter
almonds and hydrocyanic acid which it contains in varying and often
relatively large proportions, is still more dangerous. The toxic
effects produced by these liqueurs are of a very complex kind, and
scarcely fall within the scope of this article.

[Footnote 5: As early as 1851, Champouillon (referred to by Husemann,
_Handbuch der Toxicologie_) called attention to the fact that the
French soldiers in Algiers, in consequence of excessive indulgence in
absinthe, suffered especially from mania and meningitis. Decaisne (_La
Temperance_, 1873, Étude médicale sur les buveurs d'absinthe) found
absinthe in equal doses and of the same alcohol concentration to act
much more powerfully than ordinary spirits, intoxication being more
rapidly induced and the phenomena of chronic alcoholism earlier
established. Pupier (_Gazette hébdom._, 1872) found in those addicted
to the use of absinthe marked tendency to emaciation and to cirrhosis
of the liver; and Magnan (_Archives de Physiol._, 1872) asserts that
the chronic alcoholism due to this agent is characterized by the
frequency and severity of the epileptic seizures which accompany it.
There is reason to believe that the consumption of absinthe in the
cities of the United States is increasing.]

2. Wines are the product of the fermentation of the juice of the
grape. Their chemical composition is extremely complex. They owe their
general characteristics to constituents developed during fermentation,
but their special peculiarities are due to the quality of the grape
from which they are produced, the soil and climate in which it is
grown, and the method of treatment at the various stages of the
wine-making process. So sensitive are the influences that affect the
quality of wine that, as is well known, the products of neighboring
vineyards in the same region, and of different vintages from the same
ground in successive years, very often show wide differences of
flavor, delicacy, and strength.

The most important constituent of wine is alcohol. To this agent it
owes its stimulating and agreeable effects in small, its narcotic
effects in large, amounts. The proportion of alcohol, according to
Parkes, Bowditch, Payen, and other investigators, varies from 5 to 20
per cent. by volume, and in some wines even exceeds the latter amount.
The process of fermentation, however, yields, at the most, not more
than 15 to 17 per cent. of alcohol, and wines that contain any excess
of this proportion have been artificially fortified.

Further constituents of wine are sugar, present in widely varying
amounts, and always as a mixture of glucose and levulose—inverted
sugar; traces of gummy matter, vegetable albumen, coloring matters,
free tartaric and malic acid, and various tartrates, chiefly potassium
acid tartrate, or cream of tartar. In some wines there are found also
traces of fatty matters. Tannin is likewise found. Small quantities of
aldehyde and acetic acid are due to the oxidation of alcohol. The
acetic acid thus formed further reacts upon the alcohol, forming
acetic ether. To the presence of traces of compound ethers, acetic,
œnanthic, etc., wines owe their bouquet. Carbon dioxide, produced in
the process of fermentation, is retained to some extent in all wines,
and is artificially developed in large quantities in champagnes and
other sparkling wines.

Much of the stuff sold as wine, even at high prices, in all parts of
the world, is simply an artificial admixture of alcohol, sugar,
ethereal essences, and water. The wines rich in alcohol are especially
liable to imitation.

Wine is the least harmful of alcoholic drinks. In moderate amounts and
at proper times its influence upon the organism is favorable. In
addition to its transient stimulating properties, it exerts a salutary
and lasting influence upon the nutrition of the body. Only after
prolonged and extreme abuse, such as is sometimes seen in wine-growing
countries, does it lead to alcoholism.

3. Malt liquors—beer, ale, porter, stout, etc.—are fermented beverages
made from a wort of germinated barley, and usually rendered slightly
aromatic by hops. This process is known as brewing. Malt liquors, of
which beer may be taken as the type, contain from 3.75 to 8 per cent.
by volume of alcohol, free carbon dioxide, variable quantities of
saccharine matters, dextrin, nitrogenized matters, extractive, bitter
and coloring matters, essential oil, and various salts. Much
importance has {580} been ascribed to the quantity of malt extractive
in beer: it has even been seriously spoken of as fluid bread. But,
granting the nutritive value of the malt extractives, it is, as
compared with the nutritive value of the grain from which they are
derived, so small that beer must be regarded as a food of the most
expensive kind.

Sound beer is wholesome and nutritious, and serves a useful purpose in
the every-day life of a considerable part of the earth's population.
But it is wholesome only in moderate amounts. Its excessive
consumption results in progressive deterioration of mind and body.
Undue accumulation of fat, diminished excretion of urea and carbon
dioxide, are followed by disturbances of nutrition. Incomplete
oxidation of the products of tissue-waste leads to the abnormal
formation of oxalates, urates, etc., to gout, derangements of the
liver, and gall-stones. In long-continued excesses in beer one of the
effects of the lupulin is to enfeeble the powers of the reproductive
organs. The inordinate consumption of beer induces intellectual
dulness and bodily inactivity, and lessens the powers of resistance to
disease. The dangers of acute and chronic alcoholism are obvious. Five
glasses of beer of 5 per cent. alcohol strength contain as much
alcohol as half a beer-glassful of spirits of 50 per cent.

The moderate consumption of beer in communities is to some extent a
safeguard against alcoholism. To secure this end, however, the beer
must be sound and of light quality. The stronger beers, and especially
those which are fortified with coarse spirits, besides the direct
dangers attending their use, tend rapidly to the formation of
spirit-drinking habits.

The action of alcohol varies according to its degree of concentration,
the quantity ingested, and its occasional or habitual use. On the one
hand, when well diluted, taken in small amount and occasionally only,
it may be without permanent effect upon any function or structure of
the body; on the other hand, its frequent administration in large
doses and but little diluted is, sooner or later, surely followed by
widespread tissue-changes of the most serious kind.

The Physiological Action of Alcohol.—Alcohol is very rapidly taken up
by absorbent surfaces. According to Doziel,[6] it has been detected in
the venous and arterial blood and in the lymph of the thoracic duct a
minute and a half after its ingestion. It is very slightly if at all
absorbed by the unbroken skin. Denuded surfaces and extensive wounds
permit its absorption, as in the case of surgical dressings, and
instances of intoxication from this cause have been recorded. It is
also freely absorbed in the form of vapor by the pulmonary mucous
surfaces. Some surfaces, as the pleura and peritoneum, absorb it, as
has been demonstrated by the effects following its injection into
those cavities. Its constitutional effects are also rapidly developed
after hypodermic injection. Under ordinary circumstances, however, it
is by the way of the absorbents and veins of the gastric mucous
membrane that alcohol finds its way into the blood. It is probable
that the greater part of the alcohol taken into the stomach undergoes
absorption from that organ, and that very little of it reaches the
upper bowel. Alcohol is readily absorbed by the rectal mucous
membrane. Having entered the blood, {581} it reaches all the organs of
the body, and has been recovered by distillation not only from the
blood itself, but also from the brain, lungs, liver, spleen, kidneys,
and various secretions.[7]

[Footnote 6: _Pflüger's Archiv für Physiologie_, Band viii., 1874.]

[Footnote 7: Strauch, _De demonstratione Spiritus Vini in corpus
ingesti_, Dorpati, 1862.]

Lentz and other observers believe that certain organs have a special
affinity for alcohol. The author named and Schulinus place the brain
first in this respect, and in the next rank the muscles, lungs, and
kidneys. But Lallemand and Perrin regard the liver and the brain as
having an equal affinity for alcohol. The opinion of Baer, who rejects
the view that alcohol has an especial predilection for particular
organs, is more in accordance with known physiological law. This
observer holds that alcohol, having found its way into the blood,
circulates uniformly throughout the whole organism, and explains the
greater amount recoverable from certain organs as due to the fact that
these organs contain more blood than others.

The elimination of alcohol is at first rapid, afterward very gradual.
It begins shortly after ingestion, and in the course of two or three
hours one quarter, and perhaps much more, of the amount passes from
the organism. Nevertheless, after the ingestion of large amounts
traces of alcohol were discovered on the fifth day in the urine by
Parkes and Wollowicz, although the elimination by the lungs had
entirely ceased.

Elimination takes place for the most part by way of the kidneys, the
lungs, and the skin; alcohol has been recovered also from the bile,
saliva, and the milk.

Whatever may be the affinity of certain organs for alcohol, whatever
the channels by which it is eliminated, the general belief is that
some portion of it undergoes chemical decomposition within the body.
The steps of this process and its ultimate results are as yet unknown;
nor, indeed, are the proportional amounts decomposed and eliminated
established. Some observers regard the amount eliminated as less than
that decomposed. Others suppose that the amount consumed within the
body is relatively very small as compared with that disposed of by
elimination. It is, however, established that the sojourn of alcohol
in the body, unlike that of many other toxic substances, is transient,
and that in the course of from twenty-four to forty-eight hours after
the ingestion of a moderate amount there remain only traces of this
substance.

The local action of alcohol upon organic tissues depends upon its
volatility, its avidity for water, its power to precipitate albuminous
substances from solution and to dissolve fats, and, finally, upon its
antiseptic properties.

Applied externally and permitted to evaporate, it produces a fall of
temperature and the sensation of cold; if evaporation be prevented, a
sensation of warmth is experienced, the skin reddens, and, if the
action be prolonged, desquamation results. The sensation produced when
diluted alcohol is applied to mucous surfaces is burning and stinging;
when concentrated, it may excite inflammation.

Dilute alcohol has been much employed as a surgical dressing for
wounds and ulcerated surfaces. Its value for this purpose depends on
its stimulating properties, by virtue of which it exerts a favorable
influence upon granulating surfaces; and on its antiseptic qualities,
which are, however, much inferior to those of salicylic and carbolic
acids among organic substances and to the chlorides among the
inorganic salts.

{582} The direct action of alcohol upon the mucosa of the digestive
system depends upon the quantity ingested and degree of concentration.
In moderate amounts and diluted to the extent of 50 per cent. or more,
it produces a sensation of warmth in the tissues over which it passes.
This sensation is due in part to the impression upon the
nerve-endings, and in part to reflex hyperæmia, which is at once
excited. In individuals unaccustomed to its use reflex contractions of
the constrictor muscles of the pharynx, with gagging, are sometimes
provoked. The secretion of saliva and of the gastric juice is
increased, diluted alcohol being, in respect to its physiological
effect in stimulating the buccal and gastric mucous glands, inferior
to no other agent. This action is due as much to reflex as to local
action, as has been shown experimentally by the application of a few
drops of alcohol to the tongue of a dog with gastric fistula,
increased secretion of gastric juice immediately resulting.

It is in consequence of this action that moderate doses of diluted
alcohol exert a favorable influence upon the appetite and digestion.
Increased amounts of food are well borne; fats especially are more
tolerable and better digested; and a more energetic peristalsis favors
the absorption of the food solutions. In those habituated to the use
of alcohol these effects do not always follow; and if the amount be
increased or the repetition become frequent, some part of the alcohol
undergoes in the stomach, with the food, acid fermentation, and acid
eructations or vomitings occur. With these phenomena is associated
gastro-hepatic catarrh with its characteristic symptoms—loss of
appetite, feeble digestion, diarrhœa alternating with constipation,
sallowness, mental depression, and headache. In still greater amounts
and little diluted, alcohol is capable of exciting acute gastritis or
congestion and catarrhal inflammation of the liver.

When we come to study the action of alcohol upon the circulatory
system, we find that in small doses it has little or no influence
either upon the action of the heart or the condition of the vessels.
In augmented amounts it increases the action of the heart both in
force and frequency, and the arterial blood-pressure. After large
doses these effects quickly pass away, and the circulation becomes
depressed. The heart's action grows feebler, often slower, the pulse
weaker; blood-pressure sinks and arterial tension is diminished. Its
physiological action is that of a direct stimulant to the heart and
the pneumogastric nerve; its toxic action, that of a depressant. Upon
the vaso-motor system the action is from the first that of a
depressant. Dilatation of capillary vessels and increased afflux of
blood manifest themselves in the flushed face, brilliant eyes, and
warmth of surface which are familiar phenomena. Frequent repetition
tends to permanently impair the activity of the peripheral
circulation. Hence the visible vascular twigs and rubicund nose that
characterize the physiognomy of the habitual drinker.

This congestion no less affects the internal organs, setting up, by
interference with their functions, chronic derangements of nutritive
processes on the one hand, and on the other the liability to acute
local diseases and complications.

The reactions which take place between the blood and alcohol remain,
notwithstanding the energy devoted to their investigation, among the
unsolved problems of physiological chemistry. It were a profitless
task to here review the researches into this subject or to set forth
their {583} conflicting results. It may be stated that conclusions
based upon the reactions between blood drawn from the vessels and
tested with alcohol in the laboratory are wholly inapplicable to the
inquiry. While it is generally conceded that some part of the alcohol
ingested undergoes decomposition within the organism, what the steps
of the process are and what the products are have not yet been
demonstrated. Rossbach and Nothnagel[8] state that it has not yet been
possible to detect in the organism the products of the oxidation of
alcohol—namely, aldehyde, acetic acid, and oxalic acid; nevertheless,
acetic acid formed in the economy by the general combustion of alcohol
may form acetates, which, undergoing decomposition, are transformed
into carbonates and water, and are eliminated as such in the urine.[9]
This view is also held by Parkes.[10]

[Footnote 8: Cited by Peeters, _L'Alcool, physiologie, pathologie,
médecine légale_, 1885.]

[Footnote 9: Henri Toffier found in the brain of a man who died of
acute poisoning by alcohol not only alcohol, but also aldehyde:
_Considerations sur l'empoisonment aiqu par Alcohol_, Paris, 1880.]

[Footnote 10: _Journal of Practical Hygiene_, 4th ed., Lond., 1873.]

According to Peeters, the action of alcohol upon the blood may be
summed up as follows: That portion of the ingested alcohol which
undergoes decomposition takes from the blood some part of its oxygen
for this purpose, with the result of a diminished amount of oxygen and
an increase of carbon dioxide, the blood thus being made to resemble
venous blood. A part of the oxygen destined for the oxidation of waste
products being thus diverted, these substances are not completely
transformed. In this respect also blood charged with alcohol resembles
venous blood. Alcohol even when diluted is capable of retarding the
combustion of oxidizable organic substances, and there is no reason to
doubt that this agent has in the blood the same chemical properties
that it elsewhere possesses.

The exhalation of some part of the alcohol circulating in the blood by
the way of the pulmonary mucous membrane interferes with the
elimination of carbon dioxide, with the result that the latter agent
further tends to accumulate in the blood.[11]

[Footnote 11: David Brodie, _Medical Temperance Journal_, October,
1880.]

Alcohol must act, to some degree at least, directly upon the water of
the blood and upon its albuminoid principles. The products of the
reactions normally taking place within the corpuscles pass with
greater difficulty into serum containing alcohol as the current of
osmosis tends rather from the serum to the corpuscles. It is in accord
with this fact that the corpuscles of alcoholized animals have been
found relatively large.

The blood of individuals who have died in a state of alcoholic
intoxication has been frequently found to contain an unusual amount of
fatty matter in a fine state of subdivision.

Upon the respiration the influence of alcohol is twofold: it modifies
the respiratory movements and the results of the respiratory
processes. After moderate doses the movements are accelerated without
disturbances of rhythm; after large doses the respiratory acts become
embarrassed, feeble, irregular, finally wholly diaphragmatic.

Alcohol modifies the results of respiration in a constant manner and
in all doses. This modification consists in a decrease in the amount
of oxygen absorbed and carbon dioxide exhaled. This effect is usually
more marked when alcohol is taken fasting than during digestion.

{584} The influence of alcohol upon the renal secretion is that of a
diuretic, but the fact must not be overlooked that this tendency is
much increased by the large amount of water which alcoholic drinks
necessarily contain. But that alcohol acts as a diuretic, even in
small doses and altogether independently of the water with which it is
taken, does not admit of doubt. The changes in the urine are
qualitative as well as quantitative. The amount of urea, uric acid,
and other solids is always notably diminished. The diminution of the
amount of phosphoric acid is even greater than that of the
nitrogenized substances, especially during the period of excitation.

The diuretic effect of alcohol is dependent upon its direct action on
the parenchyma of the kidneys, the qualitative changes in the urine
upon its influence on nutrition.

Upon the temperature of the body alcohol has a marked effect. The
sensation of warmth experienced after moderate doses is chiefly
subjective, and is accompanied by a very slight actual rise in
temperature, amounting to some fraction of a degree Fahrenheit, and of
but short duration. This rise is followed by a rapid fall, amounting
to a degree or more below the norm. This effect is manifested within
the course of an hour after the administration, and is of
comparatively brief duration, being largely influenced by the
condition of the individual at the time as regards mental or physical
exercise, digestion, and the like. It is in part due to the increased
loss of heat from the surface of the body, favored by more active
cutaneous circulation, but chiefly to the action of alcohol in
retarding oxidation and the activity of nutritive changes. Toxic doses
are followed by marked fall of temperature. The influence of alcohol
upon the temperature is more pronounced in febrile conditions than in
health.

The influence of physiological doses of alcohol upon the nervous
system is, among all its effects, the most marked and the most
difficult to describe with exactitude. It is usual to regard this
agent as a stimulant and to separate the period of its direct effects
into two stages—that of excitement and that of depression. John Hunter
defined stimuli as agents which increase some natural action or
tendency, in contradistinction to irritants, which produce actions
altogether abnormal. Anstie[12] sought to restrict the use of the term
stimulant to agents which by their direct action tend to rectify some
deficient or too redundant natural action or tendency. Without
entering upon the discussion of the doctrine of stimulation, I may say
that the views of Anstie have served a useful purpose in making clear
some vexed questions. In accordance with these views, the
physiological action of alcohol is followed neither by excitement nor
by depression, and when its administration is followed by these
conditions, its action is not truly physiological, but narcotic or
toxic.

[Footnote 12: _Stimulants and Narcotics_, Lond., 1864.]

The effects of this agent upon the nervous system vary within very
wide limits according to innumerable conditions which relate to the
temperament, health, habits, occupation of the individual, season,
climate, social circumstances, and the quantity, kind of alcoholic
drink, and its mode of administration. Its first action in moderate
doses and under circumstances free from complications is to increase
the functional {585} activity of the brain: the ideas flow more
easily, the senses are more acute, speech is fluent, and movement
active. These effects accompany the increase in the heart's action,
the slight rise in temperature already described, and increased
activity of the organism in general. They appear to be in part due to
the direct action of the substance upon the cerebrum, and in part to
increased activity of the circulation. The effect upon the nervous
system has been compared by Nothnagel to the effect, in a higher
sphere, of strong moral impulses. Without otherwise modifying existing
traits of character, such impulses call them into action, and lead to
the accomplishment of deeds quite impossible under ordinary
circumstances. To a man worn out by some prolonged task which from
sheer fatigue he despairs of finishing, let there be announced some
joyful news; he at once feels refreshed, applies himself with renewed
energy to his work, and perhaps finishes it with ease. In kind at
least this is the effect also of alcohol.

But the limits of the physiological effects are easily transcended,
and the manifestations then become those of its toxic influence,
between the slightest grades of which and drunkenness the difference
is one rather of degree than of kind. These effects must therefore be
described under the heading Acute Alcoholism.

Passing to the influence of alcohol upon nutrition, we recognize two
modes of action. Of these the first is direct and in part local, and
results from the stimulation of the glandular apparatus of the mucous
membrane of the mouth and stomach, from increased activity of the
circulation, and from direct stimulation of the pneumogastric nerve.
Hence increased secretion of the digestive juices, augmented appetite,
more active peristalsis, and improved digestion, to which, indeed, the
direct action of alcohol upon the cerebrum doubtless contributes. It
is to these effects that the favorable influences of this agent in the
extremes of life, when it is so well borne and so useful, must be
largely attributed.

The second mode of action is indirect and general. It has been shown
that alcohol diminishes the amount of carbon dioxide expired and of
oxygen inspired, that it diminishes the quantity of urea excreted, and
that it lowers the temperature of the body. It follows that normal
oxidation goes on more slowly—that there is diminished tissue-change.
Alcohol supports the body, not by nourishing it as a food, but by
curtailing waste; it favors nutrition, not by augmenting the receipts,
but by cutting down the expenses of the organism. But nutrition and
waste are in health correlated and complementary. They are, in fact,
essential and associated processes of life, of which one is not more
necessary than the other to the maintenance of health. In various
pathological states the arrest of waste is a cardinal indication, and
for this purpose alcohol holds the first place. But in health this
action itself is pathological, and the beginning of evil. The fat
accumulation of the drunkard is due in part to the sugar and starchy
matter taken in malt liquors, but much more to this control of waste,
as is shown by the fact that spirit-drinkers who have sufficient food
also often become fat. Alcoholic excesses tend not only to fat
accumulation, but also to fatty degeneration of the tissues. The
opinion that alcohol in any dose or under any circumstances is a food
in the ordinary acceptation of the term is no {586} longer tenable.
Chauffard has well said: “Not only is alcohol not an aliment; it is
the very reverse. Not only does it not contribute to the nutrition of
the body; it opposes it and destroys it little by little.”[13]

[Footnote 13: This opinion is at variance with the views generally
entertained by English and American writers upon materia medica. T.
Lauder Brunton (_Textbook of Pharmacology, Therapeutics, and Materia
Medica_, Am. ed., 1885) regards “all the evidence as pointing to the
fact that alcohol is a food, and in certain circumstances, such as
febrile conditions, may be a very useful food; but in health, when
other kinds of food are abundant, it is unnecessary, and, as it
interferes with oxidation, it is an inconvenient form of food.”]


THE PATHOLOGICAL ACTION OF ALCOHOL.


I. Acute Alcoholism.

In accordance with the classification laid down at the beginning of
this article, the term acute alcoholism is here used to denote the
various forms of primary alcoholic intoxication in contradistinction
to the conditions which are brought about by the gradual but
long-continued action of the poison, and to the violent and sometimes
abrupt outbreaks which are secondary to these conditions. From this
point of view, which is at variance with the established usage of
writers upon alcoholism, but which is here adopted in the hope that it
will tend to simplify the treatment of a subject at present in much
confusion, acute alcoholism includes all forms of drunkenness, from
mere transient derangement of the normal functions of life, scarcely
amounting to tipsiness, to profound intoxication. It includes also
poisoning by lethal doses. Chronic alcoholism may be the outcome of
frequent repetitions of acute alcoholism at short intervals, or it may
result from the constant abuse of alcohol in doses so small that the
evidences of its poisonous effects are at no time actively manifested.
I hope to be able to show that the seemingly acute outbreaks, the
symptoms of which chiefly relate to the nervous system, that occur
after the condition of chronic alcoholism is fully established, are
commonly preceded for a longer or shorter period by imperfectly
developed symptoms of an analogous character, and that these outbreaks
differ in essential particulars from acute alcoholism in all its
forms.

That persons suffering from some degree of chronic alcoholism may, and
as a matter of common occurrence do, after excessive doses suffer from
acute alcoholism—in other words, get drunk—is too obvious to demand
more than passing consideration at this point; but it is scarcely
necessary to point out to those who are familiar with the life-history
of such individuals that the time comes when no degree of excess will
produce the ordinary manifestations of transient intoxication. It is
then that phenomena of another and more serious kind are apt to occur.
The difference is that between the reactions of normal or as yet
quasi-normal tissues and alcohol on the one hand, and on the other the
manifestations induced by the supersaturation of tissues previously
alcoholized to the point of an acquired tolerance. This tolerance of
the nervous system is in a high degree a pathological condition, and
is therefore in an equally high degree {587} unstable and liable to be
overthrown by accidents of various kinds as well as by extraordinary
excess in alcohol.

The variety of forms and admixtures in which alcohol is taken is so
great, and the susceptibility of individuals to its action so
different, that it would be a hopeless task to attempt to describe the
manifold phases of acute alcoholism. Unfortunately, most of them are
too familiar. The following description embraces the more important
phenomena, and is intended to serve as a type:

_A_. THE ORDINARY OR TYPICAL FORM.—The physiological effects of
alcohol in moderate doses are followed by no reaction, but they are
evanescent. When, however, the dose is repeated at short intervals and
the effect is sustained, the condition by its continuance becomes
pathological, and the subject enters upon the prodromic period of
acute alcoholism. From this condition to that in which the poison
manifests its distinctly toxic effects the transition is a speedy one.
The face becomes flushed, the eyes brilliant; the heart's action
increases in force and frequency; muscular force seems augmented;
there is excitation of the mental processes; intelligence seems more
active; ideas flow readily; preoccupation ceases; anxieties are
forgotten. The future is full of hope, the past has lost its sorrows,
its regrets. The powers of expression are brought into fullest play;
conversation becomes animated, brilliant, often sparkling and keen.
Reason is thrown aside, the judgment relaxed; vanity, pride, rashness,
assert themselves. Emotions, sentiments, habitually repressed, are
manifested without reserve, often with emphasis and insistance. Hence
the proverb, In vino veritas.

Then speech degenerates into loquacity; improper confidences are made,
indiscretions committed; the bent of disposition is made clear; he who
is by nature sad grows sombre, melancholy; he who is irritable becomes
cross and quarrelsome; the generous man grows lavish, and a
good-natured fellow is everybody's friend. But this intensification of
normal characteristics is by no means invariable. Not seldom do we see
the timid man become in his cups violent and aggressive, the refined
coarse, and the gay melancholy. The sensation of increase in muscular
force manifests itself in unusual activity. Gesticulation is frequent,
energetic, and apt; there are bodily restlessness and desire to move
about. Shouts of laughter, bursts of song, are followed by a
disposition to easily-provoked quarrels. At this stage there are
evidences of some degree of cerebral congestion. The temples throb,
the heart is full, and dizziness is felt. The skin is moist, the mouth
pasty, thirst is experienced, and there is frequent desire to pass
water. There yet remains some degree of self-control. The phenomena
which characterize this condition are more or less transient, and if
alcohol be now discontinued they speedily cease, commonly in sleep,
sometimes without it, and are followed by sensations of weariness and
fatigue, with headache, gastric disturbances, and temporary loss of
appetite.

If, however, the influence of alcohol be pushed beyond this point, the
manifestations of mere exaltation of function give place to grave
perversion of the processes of life. A gradually increasing vertigo is
associated with obscured intelligence, dulled imagination, blunted and
confuted perception, disjointed ideation, and incoherent speech. The
recollection grows indistinct, the will purposeless. Now the baser
{588} passions are aroused; evil impulses and illusions of all kinds
sway the drunken man. All control of conversation and action is lost.
Reason is replaced by delirium, and he becomes a maniac, dangerous
alike to himself and to others, liable upon some sudden impulse to
commit the most atrocious crimes.

The countenance betrays the profound disturbance of the intellectual
and moral nature: its expression is changed, its lines are blurred;
the flush deepens, the veins are distended, the arteries pulsate
visibly, the gaze is staring, the pupils contracted. The respiration,
at first quickened, becomes irregular. The heart's action is rapid and
bounding, and sometimes there is palpitation. Somnolence soon deepens
into an invincible desire to sleep. At this point great muscular
relaxation not infrequently occurs in connection with vomiting,
profuse sweating, and dilatation of the pupils.

Muscular movements are irregular and uncertain, the gait vacillating
and staggering; the movements of the superior extremities, wanting in
precision, become trembling and awkward. At the same time speech
becomes embarrassed. Articulation is difficult and imperfectly
executed. At length standing becomes impossible; the drunkard,
profoundly poisoned, sinks helplessly to the ground, and not
infrequently the control of the sphincters is lost. The development of
this condition is accompanied by a gradual perversion of general and
special sensibility. Dull headache, ringing in the ears, phosphenes,
and other disturbances of vision, hallucinations of taste and smell,
are followed by abrogation of the special senses. Loss of cutaneous
sensibility, beginning at the extremities, invades the whole body, and
finally the subject sinks into more or less profound coma, from which
it is no longer possible to arouse him. Muscular resolution is
complete, sensation is lost; the face is now bloated, deeply flushed,
sometimes livid, sometimes ashy pale; the pupils are dilated; the
temperature below normal; the respiration stertorous and accompanied
by abundant mucous râles. The pulse is feeble, fluttering, the surface
covered with sweat, and involuntary evacuations take place.

VARIETIES.—Three varieties of acute alcoholism are recognized by
Lentz—the expansive, the depressive, and the stupid. The first is
characterized by gayety, self-satisfaction, and content. The drunkard,
smiling and happy, is satisfied with the present and full of hope for
the future. The second variety is characterized by sadness and
melancholy. The drunkard becomes sombre and taciturn; if he talk at
all, it is to bewail his misfortunes and to recount his mishaps. In
the third variety the period of excitement is wanting and the drunkard
passes rapidly into a condition of stupor.

Great as are the modifications of the course of acute alcoholism under
different circumstances and in different individuals, it is evident,
upon close investigation, that its phenomena—and especially those
which relate to the nervous system—manifest themselves in a
progressive series more or less constant in the majority of persons.
This series includes three well-characterized periods: 1. The stage of
functional exaltation of the nervous system; 2. The stage of
functional perversion; 3. The stage of depression.

We may, then, recognize the degrees of acute alcoholism corresponding
{589} to these stages.[14] Of these, the first scarcely goes beyond
the stage of excitement already described, and if the dose have been
moderate or its repetitions not too long continued, the symptoms
gradually subside, leaving perhaps no sequels beyond slight headache,
tinnitus aurium, some degree of muscular relaxation, and mental
depression.

[Footnote 14: These stages correspond to the three degrees of
alcoholic intoxication recognized and described by German writers as
Rausch, Betrunkenheit, and Besoffenheit. To these may be added the
prodromic period, designated as Weinwarme Zustand. These three degrees
are known to the French as l'ivresse légère, l'ivresse grave, and
l'ivresse suraiguë.]

The second degree is characterized by partial abolition of
intelligence, of general and special sensation, and of motor power.
Hence incoherent speech, extravagant actions, blunted perceptions,
hallucinations and delusions, inco-ordination of movements, a reeling
gait, and not rarely vomiting and involuntary discharges of urine and
feces. This degree of acute alcoholism usually ends in deep sleep with
abundant perspiration, to which succeed great lassitude and
depression, accompanied by much gastro-intestinal derangement, of
which the symptoms are inability to take food, coated tongue, viscid
mouth, foul breath, repeated vomiting, and occasionally diarrhœa.
These sequels are less serious in those individuals accustomed to
excesses than in others.

In the third degree the subject falls by gradual stages or abruptly
into more or less profound coma. The abolition of intelligence,
sensation, and motion is complete. The face is now swollen, livid, or
pale, the pupils dilated, the respiration stertorous, the pulse
feeble, often slow, sometimes imperceptible, the surface cool and
often bathed in sweat. The man is dead drunk. The symptoms are now of
the gravest kind. It is no uncommon occurrence for this condition to
end in death.

Well characterized as these three degrees of alcoholic intoxication
are, they are not, when occurring successively in the same individual,
separated by abrupt lines of demarcation. On the contrary, the
evolution of the symptoms is from the beginning to the close a gradual
and progressive one.

While the scope of this article precludes extended discussion of the
symptoms of acute alcoholism—which, indeed, present an almost endless
variety in their intensity and combination—yet it seems necessary to
the elucidation of the subject to point out some of the more prominent
modifications due to variations in the conditions under which alcohol
acts upon the organism.

First among these are differences in the nature and composition of the
drink. Here we have to do not only with the well-known differences in
alcoholic beverages, as spirits, wines, and malt liquors, and their
quality and grades, but also with differences in the chemical nature
of the alcohols themselves which enter into their composition. The
principal of these alcohols are—

  Methyl alcohol, CH_{3}OH.
  Ethyl alcohol,  C_{2}H_{5}OH.
  Propyl alcohol, C_{3}H_{7}OH.
  Butyl alcohol,  C_{4}H_{9}OH.
  Amyl alcohol,   C_{5}H_{11}OH.

Richardson was the first to call attention to the differences in the
physiological and pathological action of the members of this series.
Other {590} observers, among whom may be named Dujardin-Beaumetz and
Andigie,[15] and Rabuteau,[16] have also investigated the subject. The
researches of these observers have established the fact that the
effects of the different alcohols in depressing the temperature of the
body and in paralyzing sensation and motion are exactly the same, but
that their narcotic influence upon the nervous system increases, dose
for dose, in proportion to the amount of carbon which they contain.
Ethyl alcohol is, with the exception of methyl alcohol or wood-spirit,
the least rich in carbon and the least dangerous to health.[17] The
increased consumption of alcohol, both as a beverage and in the arts,
the demand for cheap, coarse spirits producing their primary narcotic
effects with promptness, and the cupidity of manufacturers, have led
to the almost universal adulteration of the liquors of commerce with
the more dangerous alcohols.[18] So extensive has this substitution of
the high-carbon alcohols for ethyl or ordinary spirit of wine become
that it has been suggested that alcoholism should be divided into
ethylism, amylism, propylism, and butylism—not so much for clinical
reasons as to direct attention to the composition of alcoholic drinks
and to their deleterious properties.[19]

[Footnote 15: _Recherches expérimentales sur la Puissance toxique des
Alcools_, Paris, 1879.]

[Footnote 16: “Contributions à l'Étude des Effets physiologiques et
therapeutiques d'Alcool,” _Compt. rend. Société de Biologie_,
1870-71.]

[Footnote 17: “Methylic alcohol is the safest of the series of bodies
to which it belongs” (B. W. Richardson, _Lectures on Alcohol_).]

[Footnote 18: M. Girard, chief of the municipal laboratory in Paris,
has recently called attention to the enormous diminution in the
production of alcohol by the natural method—that is to say, by the
distillation of wine. The falling off he ascribes to the ravages of
the phylloxera. This loss is made up by the substitution of spirits
obtained by the distillation of various fermented grains, potatoes,
beets, molasses, etc. To give some idea of the extent to which the
alcohols of industry at present replace the alcohols of wine, he cites
the following figures: From 1840 to 1850 the mean annual production of
alcohol in France was 891,500 hectoliters, of which the alcohols of
wine amounted to 715,000 hectoliters. In 1883 the product reached
1,997,280 hectoliters, of which alcohols obtained by the distillation
of wine amounted to only 14,678 hectoliters.]

[Footnote 19: Peeters, _L'Alcool_, 1885.]

The effects of propyl, butyl, and amyl alcohols upon the nervous
system are not only more marked than those of ethyl alcohol, but they
are more rapid. The stage of excitement is speedily induced, and its
manifestations are intense. Hence the preference often manifested by
drunkards for cheap, coarse spirits. On the other hand, the stage of
depression quickly follows, and is itself of relatively shorter
duration than that induced by ethyl alcohol, probably for the reason
that the amount required to bring it about is smaller. Muscular
resolution soon becomes general and complete; insensibility speedily
succeeds; the fall of temperature is rapid; vomiting, occasionally
absent in the intoxication produced by ethyl alcohol, is the rule, and
is frequently repeated. Muscular tremor—and especially is this true of
amyl alcohol—comes on earlier, is more general and more marked, and
lasts longer than that which occurs in consequence of excess in ethyl
alcohol. Richardson states that the complex alcohols are more slowly
eliminated than ethyl alcohol, but the French observers are of a
different opinion.

But these differences in action are probably rather differences in
degree than in kind. Peeters says: “Ethyl alcohol is less dangerous
than the more complex members of the series. It is less irritating,
less charged with carbon, its specific gravity is less, its fumes are
less dense and escape {591} more readily from the economy; its action
ought to be less profound, less prolonged, than that of butyl, propyl,
and amyl alcohol, but it is of the same nature. It is not
qualitatively but quantitatively different. I suspect that the effects
of liquors containing ethyl alcohol are, as a rule, less decidedly
injurious, by reason of the more favorable surroundings of those who
can afford to use them.”

The three principal groups of the alcoholic drinks of commerce
produce, independently of the properties of the different kinds of
alcohol which they contain, forms of acute alcoholism which differ in
important respects.

The intoxication induced by the exclusive use of malt liquors is dull
and heavy, slow in coming on, and of long duration. The stage of
excitement is relatively brief, not often characterized by gayety,
often brutal; drowsiness soon supervenes and deepens slowly into
unconsciousness. The after-effects are disagreeable and prolonged. The
enormous quantity of fluid and the large amount of malt extractives
cause gastro-hepatic derangements of a more or less distressing kind.
To the hops must be ascribed the prolonged dulness which is so
characteristic of the after-effects of beers and ales. The influence
of the various substances used in the adulteration of beers without
doubt modifies the symptoms of the alcoholism which these beverages
cause when impure. These substances consist of glucose, various
vegetable bitters, and salt—articles not necessarily hurtful in small
amounts, but capable of exerting deleterious action when taken in
excess and in connection with the normal ingredients of beer.

The intoxication produced by pure wines is, as a rule, characterized
by a bodily and mental activity strongly in contrast with the
drunkenness produced by malt liquors. The drunkard is usually gay and
vivacious—at all events, lightly merry or not hopelessly despondent.
His mood is variable, changing from grave to gay. The first stage is
prolonged, and the manifestations of the later stages less grave, nor
are the sequels apt to be so severe. The action is that of ethyl
alcohol and certain ethereal substances, the latter being present,
however, only in minute amounts. The rapidity of the effects depends
upon the proportion of alcohol which the wine contains, which varies
from about 7 per cent. in the clarets to 15, to 18, or even to 20 per
cent. in port and madeira. The sparkling wines, moselle and champagne,
produce more transient effects than the still wines—a fact probably to
be explained by their greater and more prompt diuretic action.

The foregoing remarks apply only to pure wines. The intoxication which
follows the use of artificial compounds sold in all parts of the world
as wines betrays in its course and symptoms the high percentage and
toxic characters of the mixed alcohols which form their essential
ingredients.

The intoxication which follows excesses in the various spirits of
commerce presents no special characters. Its symptoms are determined
to a considerable extent by the relative purity—that is, freedom from
admixture with the various complex alcohols—of the liquor by which it
has been produced. Potato spirit causes drunkenness which is profound,
overwhelming, and preceded by a brief period only of excitement.

Even more important than the kind of liquor is its quantity. Here,
{592} however, it is impossible to formulate precise statements. A few
glasses of wine will produce effects in some persons more decided than
much strong spirits in others. Those conditions which favor the
absorption of alcohol hasten the production and augment the intensity
of alcoholism; and the contrary is true. Thus, alcohol taken while
fasting does much more harm than the same amount taken with a meal.
Intense excitement, anger, mortification, or other violent emotion is
said by Lentz to increase the effects of alcohol. Sudden transition
from a warm to a cold atmosphere intensifies the action. That this
effect of cold is due to suppression of perspiration, and the
consequent interference with one of the elements of elimination, is
much less likely than that it is due to the further depressing
influence of cold upon the nervous system, already depressed by the
alcohol imbibed. Occupation has in an indirect way much to do with the
facility with which alcohol is borne. Hard work, requiring great and
continuous muscular effort, especially in the open air, diminishes the
liability to acute alcoholism, while sedentary occupations and
confinement strongly predispose to it. These well-recognized facts are
to be accounted for by the influence of different occupations and
modes of life upon the elimination of the poison. Persons who are
debilitated by chronic disease or are convalescent from acute
maladies, and the otherwise feeble and anæmic, are peculiarly
obnoxious to the action of alcohol. Previous custom and hereditary
peculiarities of organization exert an influence upon the liability of
individuals to acute alcoholism, and upon its nature when induced.

Persons of an impressible nervous organization are peculiarly prone to
the evil effects of drink. With such persons slight excess is often
followed by serious consequences; the intellectual disturbance is
early developed and out of proportion to the derangements of motility
and sensation. The effects of alcohol are manifested more promptly and
more intensely in children and women than in men or in the aged.
Drunkenness is induced more rapidly and with smaller quantities of
alcohol in summer than in winter, in warm than in cold countries.

_B_. IRREGULAR FORMS OF ACUTE ALCOHOLISM.[20]—1. _The Maniacal
Form_.—The outbreak is usually sudden, sometimes occurring after the
ingestion of comparatively small quantities of alcohol; at others
after excesses which in a certain proportion of the cases have already
ceased. The transition from a condition apparently normal, or marked
at most by mental concentration, restlessness, and some degree of
irritability, to furious mania is sometimes almost instantaneous, and
the subsidence of the latter no less swift. More commonly there are
prodromic symptoms, among which are general malaise, præcordial
distress, palpitations, flushing of the face, vertigo, tinnitus
aurium, phosphenes, and dull, throbbing headache. The attack is
characterized by maniacal excitement, usually of a furious kind. The
restlessness is, however, far from being aimless and purposeless. On
the contrary, impelled by the wildest passions, transported with rage,
the patient seeks the destruction of life and property, and wreaks his
fury alike upon animate and inanimate objects. So great is his
strength for the time being that several strong men may be scarcely
able to restrain him. He pours forth a torrent of commingled threats
and curses, in which may be heard unintelligible, and often {593}
inarticulate, sounds. He is beside himself, yet, so far as can be
learned, there are neither hallucinations nor delusions by which his
fury can be explained. In this respect the condition is wholly unlike
that form of alcoholic mania in which the actions are explained by the
imaginary surroundings and circumstances of the patient. In the
maniacal form of acute alcoholism the most trifling incident, a word,
a look, are sufficient to produce a tempest of rage that may end in
scenes of violence. Nevertheless, the patient yet retains for a time
some notion of his surroundings. At length, however, he falls into a
state of complete unconsciousness, and the delirium is like that of
fever, of the delusions of which no recollection afterward remains.
This form of acute alcoholism is almost invariably associated with the
symptoms of a high degree of cerebral hyperæmia. The hands are hot,
the eyes injected, the pupils dilated or contracted, the expression
eager. There are abundant secretion of saliva, frequent and irregular
respiration, a rapid pulse—often exceeding 100—throbbing arteries,
distended veins, and a hot skin, often bathed with sweat. The urine is
scanty and constipation usual. There is, as a rule, increased
sensibility to light and sound. The attack is liable to come to a
tragic close in murder or suicide.

[Footnote 20: Ivresses anormales ou pathologiques of the French
writers.]

The termination of the paroxysm is as abrupt as its onset. Some
abatement of its violence is quickly followed by signs of mental and
bodily exhaustion; this deepens into profound sleep, which often lasts
from twelve to twenty-four hours, and from which the patient awakes
clear, tranquil, and as if nothing had happened, or dimly recollecting
the occurrences that have passed as a hideous dream. In a small
proportion of the cases the sleep deepens into coma which ends in
death.

2. _The Convulsive Form_.—The analogy to the form just described is
very close. Here, however, the morbid manifestations directly relate
to the muscular system. The attack is commonly sudden, often abrupt.
When prodromes occur, they are such as have been described as
preceding the maniacal form—mental irritability, headache, præcordial
distress, etc. The attack is thus described by Lentz: “The phenomena
consist not in ordinary convulsions, but in convulsiform movements of
remarkable disorder, only to be compared with the extraordinary
convulsive movements of grave hysteria. We have happened to see
several cases during the attack. These patients threw themselves to
the ground, giving themselves up to the most irregular and disorderly
contortions, rolling from side to side, throwing the body into the
air, striking out with the legs and arms, kicking at random, biting at
persons and things—now knocking the head against the floor, again
rising for a moment, only to fall back and commence again the same
contortions. Their movements are energetic and violent. There are
madmen whom it is dangerous to approach by reason of the violence of
their movements, but they are certainly much less dangerous than those
suffering from the maniacal form of acute alcoholism, for their morbid
motility has no tendency to take the shape of co-ordinated actions. It
is movement wasted in pure loss. Their muscular energy is excessive;
it is difficult to restrain them. To resume: the peculiarity of these
movements is this, that they are not intentional, but that they are
rather purely convulsiform, automatic.

“Another phenomenon of this form, one of its characteristic symptoms,
is the state of intellectual enfeeblement which accompanies it. The
loss {594} of consciousness is complete, and were it not for the
movement produced by the convulsions the patient would be plunged into
a condition of profound coma. He has not the least knowledge of
himself; not even delirium denotes intellectual activity; only an
occasional harsh cry or inarticulate sound indicates the existence of
mind.”

The other symptoms differ but little from the maniacal form. The
duration of the attack varies from a few hours to half a day; its
termination is usually abrupt, the patient falling into a condition of
extreme exhaustion with stupor, or into a deep and prolonged sleep,
from which he awakens without the slightest recollection of the attack
through which he has passed.[21]

[Footnote 21: Consult also _Dict. des Sciences méd._, t. xxvi.]

3. _Acute Alcoholism, in Persons of Unsound Mind_.—The insane,
imbeciles, epileptics, and persons suffering from nervous diseases
are, as a rule, abnormally susceptible to the action of alcohol, and
present more or less striking peculiarities in the symptoms which it
causes. Brief notice of certain of these peculiarities is in
accordance with the scope and plan of this article.

In general paralysis propensity to alcoholic excesses is not rarely an
early symptom. The subject is very susceptible to the action of
alcohol, and under its influence rapidly passes into a state of
intense excitement, characterized by incoherence, delirium, excessive
restlessness, and unwillingness to seek repose until exhaustion is
complete. It is under the influence of this easily-provoked alcoholic
excitement that the vagabondage, quarrels, thefts, robberies,
incendiarisms, and other grave crimes observed during the first stage
of this form of insanity are often committed.

Imbeciles and idiots are likewise quickly, and often intensely,
excited by alcohol. They are then apt to be quarrelsome, perverse, and
ungovernable, defiant of authority, and capable of shocking crimes,
often evincing latent vicious tendencies previously wholly
unsuspected.

Epileptics are easily affected by alcohol, and usually violent in the
stage of excitement; not rarely this period terminates in a true
epileptic seizure.

The drunkenness of the dipsomaniac is characterized by a prolonged,
uninterrupted stage of excitement without the stage of depression.
Such individuals are capable of consuming in their periodical excesses
large amounts of drink without the evolution of the ordinary
successive phenomena of acute alcoholism.

Persons of unsound mind are, as a rule, so susceptible to the
influence of alcohol, and suffer so promptly and intensely from its
primary effects, that they are rarely able or permitted to consume a
sufficient quantity to bring about a comatose state.

The irregular forms of acute alcoholism are only to be explained by
the inherited or acquired constitutional peculiarities of individuals.
To attempt to explain them in any case by the quality of the alcohol
by which they are induced meets with the difficulty indicated in the
fact that they are isolated and comparatively rare, even where the
coarser spirits are habitually consumed. They occur in individuals who
habitually commit excesses, but they cannot be viewed as
manifestations of chronic alcoholism, for the reason that they also
occasionally occur in those who are {595} not habitual drinkers, and
even in persons who have not for a long time previously tasted strong
drink. Furthermore, as has been pointed out, they are not only
occasionally, but indeed even as a rule, induced by relatively small
amounts of alcohol. They are then the manifestations of idiosyncrasy.
One of the striking peculiarities of this peculiar bodily organization
is this very susceptibility to the action of alcohol in doses smaller
than are taken with impunity by ordinary individuals. It is also
characterized by a special tendency to delirium in febrile states, to
hallucinations, to disturbances from trifling changes in climate,
food, or manner of life, to irritability of the nervous system, and in
particular of the vaso-motor system, and by a tendency to convulsions.
With these tendencies is associated an unstable mental and moral
character. Such persons are liable to headaches, vertigo, and
epistaxis—signs of cerebral hyperæmia, which is easily induced—and
their family histories indicate strong hereditary tendencies to
neurotic disorders, and not rarely addiction to alcohol on the part of
one or several ancestors.

But this idiosyncrasy is by no means always an inherited one. It is
acquired as one of the results of profound disturbance of the nervous
system, such as is produced by moral causes, by temporary or recurrent
insanity, by wounds and injuries of the head, by the infectious
diseases, especially syphilis, enteric and typhus fever, and
small-pox, and by inflammations of the meninges.

What may be the precise mode of action of alcohol in the production of
its acute effects yet remains a matter of conjecture. It cannot be
doubted that its primary and direct action is upon the nervous system,
and that the circulation is secondarily but rapidly implicated. But it
is quite impossible to say, in the present state of knowledge, what
this action is. It has been suggested that certain chemical
modifications of alcohol in the blood, or of the blood itself in the
presence of alcohol, cause these phenomena; that aldehyde is the
active agent in their production; that the chemical changes by which
alcohol is transformed into aldehydes, acetic acid, and finally into
carbon dioxide, deprive the blood of the oxygen necessary for the
proper performance of the functions of the nervous system.
Unfortunately for these views, neither the presence of aldehydes in
the blood in acute alcoholism, nor these transformations themselves,
have yet been demonstrated, and a high degree of deoxygenation of the
blood is frequently observed in asphyxia, the inhalation of nitrous
oxide, etc., without the train of symptoms characteristic of the
condition now under consideration.

It is more than probable that varying conditions of the cerebral
circulation, secondary in themselves, have much to do in the causation
of certain symptoms. The experimental investigations of Bernard and
others have established the fact that during the period of excitement
there is actual congestion of the meninges. This condition is
transient, and reproduced after each repetition of the dose. After a
time, or if the dose at first be excessive, the congestion is
succeeded by anæmia.

PATHOLOGICAL ANATOMY.—Upon the examination of the bodies of persons
who have died by accident while drunk or in consequence of drunkenness
itself, deep congestion of the cerebral meninges, and especially of
the pia, has been almost constantly observed. In the pia effusions of
blood are occasionally encountered. The condition of the cerebral
{596} substance is not always the same. It is in a majority of the
cases more or less deeply congested, yet it presents in other
instances no appreciable departure from the normal state, and in a
smaller number still there is actual anæmia.

The sinuses and choroid plexuses are distended with dark blood; the
cerebro-spinal fluid is increased, and often tinged with blood; the
ventricles are distended with fluid, which not rarely has an alcoholic
odor. Occasionally the ventricles contain blood, and hemorrhage into
the substance of the brain has been observed.

The condition of the elementary nervous tissues after death from acute
alcoholism is not yet known.

The lungs are deeply congested, with small extravasations of blood
into their substance, and often œdematous. Congestion of the liver,
spleen, and kidneys in varying degrees of intensity is also seen. The
pancreas is usually deeply injected, occasionally the seat of large
extravasations of blood. The mucous membrane of the stomach is
invariably deeply injected when the alcohol has been introduced into
the organism in the ordinary manner. The observation of Caspar that
post-mortem decomposition takes place with diminished rapidity has
been denied by Lancereaux and others.

Other post-mortem conditions appear to be neither constant nor
characteristic. The stomach usually contains partially digested food
and alcohol. Lallemand, Perrin, and Du Roy observed, both during life
and after death, in the blood of animals subjected to experiments,
great numbers of minute glistening points, which upon microscopic
examination proved to be fat-globules. The same condition has been
observed in man, not only when death has taken place owing to acute
alcoholism, but also when it has occurred during the digestion of a
hearty meal without alcohol. The blood itself is often fluid and
dark-colored; the heart sometimes empty, sometimes containing a few
soft clots. Tardieu[22] states that in sudden death during drunkenness
pulmonary apoplexy and meningeal apoplexy, if not constant lesions,
are at least extremely frequent, and almost characteristic. Baer, on
the other hand, denies the occurrence of specific or characteristic
lesions.

[Footnote 22: “Observationes médicales sur l'Etát d'Ivresse,” _Annales
d'Hygiene publique et de Médecine légale_, tome xl.]

_C_. ACUTE POISONING BY ALCOHOL IN LETHAL DOSES.—The symptoms are much
modified when overwhelming doses of strong alcohol are introduced into
the organism at once or in the course of a short time. Here alcohol
produces death as an acute poison. The cases may be arranged in two
groups:

1. _Corrosive Poisoning_.—These cases are very rare. They are caused
only by undiluted alcohol, and depend upon the action of this agent in
coagulating albumen and disorganizing the tissues with which it comes
in contact by its affinity for the water which they contain. Absolute
alcohol is a powerful corrosive poison. It produces intense
phlegmonous inflammation of the œsophagus and stomach, with erosion of
the mucous membrane, accompanied by vomiting, diarrhœa with bloody
stools, prostration, and stupor. Death occurs by heart-failure. Among
the direct effects of large doses somewhat less concentrated are acute
and subacute gastritis with characteristic symptoms.

{597} Percy[23] injected by means of an œsophageal tube 90 grammes of
absolute alcohol into the stomach of a dog. Death followed in the
course of eight hours in consequence of violent gastro-intestinal
inflammation with ulceration. Dujardin-Beaumetz and Andigie found the
gastric and intestinal mucous membrane of dogs poisoned by alcohol,
red, deeply injected, and “presenting at certain points a black
coloration due to effused blood.” This fact they regard as worthy of
note, because in their experiments the toxic agent was introduced, not
by the mouth, but hypodermically, and they explain it by the
supposition—which appears to me warrantable—that it is due to
elimination by the mucous glands. Hence the congestion, softening, and
hemorrhage.[24] These observers also found that the symptoms were more
acute and the lesions more marked when poisoning was caused by propyl,
butyl, or amyl alcohol than when it was produced by ethyl alcohol.

[Footnote 23: _An Experimental Inquiry concerning the Presence of
Alcohol in the Ventricles of the Brain after Poisoning by that Liquid,
together with Experiments illustrative of the Physiological Effects of
Alcohol_, London, 1839.]

[Footnote 24: Chatin and Gublier have emphasized the fact that certain
poisons introduced by intravenous injection or by absorption through
the respiratory tract are eliminated by the intestines, with the
production of the same local symptoms as when administered by the
mouth (_Bulletin de l'Académie de Médecine_, Séance du 6 Novembre,
1877).]

2. _Acute Narcotic Poisoning_.—Much more common are the cases in which
death is rapidly produced by excessive doses of ordinary diluted
alcohol taken at once or rapidly repeated. This happens under various
circumstances, as when a drunkard avails himself of some favorable
opportunity to gratify to the full a bestial appetite, or upon a wager
drinks a number of glasses of spirits in quick succession or a given
quantity down, or when a man already drunk is plied by his companions
for pure deviltry. Suicide by this means is, in the ordinary sense of
the term, rare, and murder still more so. The latter crime has, as a
rule, been committed upon infants and children. Blyth[25] estimates
the fatal dose of absolute alcohol, diluted in the form of ordinary
whiskey, gin, etc., at from one to two fluidounces for any child below
the age of ten or twelve years, and at from two and a half to five
ounces for an adult. In the instance recorded by Maschka[26] two
children, aged respectively nine and eight years, took partly by
persuasion, afterward by force, about one-eighth of a pint of spirits
of 67 per cent. strength—about 1.7 ounces of absolute alcohol. Both
vomited somewhat, then lay down. Stertorous breathing at once came on,
and they quickly died. Taylor relates a case in which a quantity of
brandy representing about two fluidounces of absolute alcohol produced
death in a child seven years old.

[Footnote 25: _Poisons, their Effects and Detection_, Am. ed., New
York, 1885.]

[Footnote 26: Cited by Blyth.]

The symptoms are uniformly the same. The period of excitement is
transient or absent altogether; occasionally the patient falls at once
to the ground while in the act of drinking or immediately thereafter;
complete coma, interrupted by shuddering convulsions, may terminate in
the course of a short time in death. If the fatal issue be delayed,
there are vomiting and involuntary discharges; the respiration becomes
slow, embarrassed, stertorous; the heart's action is feeble and
irregular, the pulse almost or wholly imperceptible; the temperature
rapidly falls several degrees: 90° F. has been observed. The pupils
are dilated; insensibility and muscular resolution are complete. The
face is bloated, cyanotic; the {598} surface bathed in a clammy sweat;
the mucous membrane of the mouth often swollen and blanched. Vomiting
is usual, but not constant, and there is occasionally thin mucous
diarrhœa, the stools being mixed with blood. If the patient survives
any considerable length of time, acute superficial gangrene of the
parts most exposed to pressure is liable to take place. Recovery is
rare; its possibility is, however, increased in proportion as the
subject is of vigorous constitution, previous sound health, beyond the
period of childhood, not yet approaching that of physiological
decadence, and as treatment is early instituted and carried out with
judgment.

The diagnosis is difficult, almost impossible, in the absence of
witnesses: it is rendered still more obscure by the fact that this, as
other forms of alcoholic coma, may be complicated by cerebral or
meningeal hemorrhage and by cerebral congestion, in themselves
fatal—lesions the onset of which may have been the cause of mental
aberration leading to the commission of impulsive alcoholic excesses.

The prognosis, in the highest degree unfavorable in all cases, is
rendered yet more so by the occurrence of intense cerebral and
pulmonary congestions.

The lesions found post-mortem are those of acute alcoholism, already
described. As this form of alcoholic poisoning frequently occurs in
the subjects of chronic alcoholism, the lesions of that condition are
often encountered, and must be distinguished from those due to the
lethal dose. Nor must we overlook the fact that in the action of
alcohol just described we have to do with a process differing from
ordinary acute alcoholism in degree rather than in kind—a
consideration which tends to simplify our notions of the pathology of
alcoholism in general.


II. Chronic Alcoholism.

The prolonged abuse of alcohol brings about a series of changes which
affect alike the organism at large and its various structures. The
changes thus brought to pass are of the most varied kind, and depend
upon individual differences too manifold and complex for enumeration
and classification. Among the more important of these individual
peculiarities are those which relate to temperament, constitution,
hereditary predisposition, occupation, social position, personal
habits, tendency to or already-existing disease of particular organs
and systems, and the like. The degree of the pathological change is
determined by the strength and quantity of alcohol consumed and the
duration of habitual excess. The human body is capable of adapting
itself to the habitual consumption of large quantities of alcohol,
just as to other directly acting agents of an injurious nature, such
as foul air, bad drinking-water, and unwholesome food, or even to the
action of substances dangerous to life, as opium or arsenic, and yet
presenting for a considerable time the appearance at least of health.
Degeneration of the tissues of the body and disorders of its functions
are nevertheless surely produced. These alterations are not the less
dangerous to health and life because they are insidious and remain for
a time latent. Furthermore, like the habit of which they are begotten,
they are progressive, and sooner or later declare themselves in open
disease.

{599} The condition, whether latent or manifest, that is produced by
prolonged habitual alcoholic excess is designated chronic
alcoholism.[27]

[Footnote 27: The writer, although fully aware of its imperfections,
regards the above definition of the term as more in accordance with
the present state of our knowledge of the subject, and therefore more
useful, than any other that he has been able to find. It is scarcely
necessary to repeat here that the restriction of the term chronic
alcoholism to accidental or occasional manifestations of a permanent
state is misleading and unscientific. The same criticism is applicable
to the attempt that has been made to establish this condition as a
substantive disease, chronic, progressive, and characterized
anatomically by inflammatory, sclerotic, and steatogenous processes.]

The symptoms of this condition, when fully established, differ within
wide ranges in kind and degree. They are the manifestations of
derangements of the viscera, of the nervous system, and of the mind.
Varying among themselves according as the stress of the pathological
action has fallen upon one organ or another, forming combinations at
once curious and inexplicable, developing quietly, without event,
almost imperceptibly at one time, breaking into the most furious
paroxysms at another, they present for our study perhaps the most
complex of chronic morbid conditions. The chronic alcoholism which is
latent is not, therefore, always without symptoms. They are, however,
often slight and escape observation, or when manifest they are not
infrequently ascribed to other causes; or, again, their etiological
relations being concealed or overlooked, they are exceedingly obscure
and puzzling. This is especially the case in the chronic alcoholism
produced by the secret tippling of otherwise respectable persons, and
especially women.

To facilitate description, we shall consider the derangements of the
viscera, the nervous system, and the mind in regular order, according
to the scheme on p. 574. But the reader will observe that whatever may
be the prominence of particular symptoms or groups of symptoms in any
given case, all parts of the organism are involved, and that there is
no such thing as chronic alcoholism restricted to any particular
viscus or group of viscera, to the nervous system, or to the mind.

_A_. VISCERAL DERANGEMENTS.—There is nothing specific in the lesions
of chronic alcoholism. The chronic hyperæmia, steatosis, and sclerosis
induced by alcoholic excesses differ in no respect from those
conditions brought about by other causes. That which is specific is
the evolution of a series of morbid changes in the different
structures of the body under the influence of a common and
continuously acting cause. The digestive system is affected, as a
rule, long before the vascular or the nervous system.

1. _Local Disorders_.—_a_. Disorders of the Digestive System.—The
Mouth and Throat.—The action of insufficiently diluted alcohol upon
the mucous tissues is that of an irritant. The habitual repetition of
this action causes subacute or chronic catarrhal inflammation. The
condition of the tongue varies with that of the stomach. The mouth in
acute alcoholism is apt to be pasty and foul, the tongue slightly
swollen and coated with a more or less thick yellow fur; there is
often also an increase of saliva; in chronic alcoholism the tongue is
usually small, sometimes red, sometimes pale, often smooth from
atrophy of the papillæ, not rarely deeply fissured. In a word, the
condition of this organ is that seen in the various forms of subacute
or chronic gastritis. The salivary secretion is often notably
diminished, the sense of taste impaired. Relaxation of the throat and
{600} uvula and granular pharyngitis are common. Those who, whilst
leading a sedentary life, are inclined to the pleasures of the table
and a free indulgence in spirituous liquors often suffer from these
affections. Mackenzie[28] states that the worst cases of chronic
catarrh of the throat generally arise from the habitual abuse of the
stronger forms of alcohol. The associated influence of tobacco in the
causation of this group of affections is not to be disregarded.

[Footnote 28: _Diseases of the Pharynx, Larynx, and Trachea_, 1880.]

Lancereaux encountered ulceration of the œsophagus, and Bergeret a
case of narrowing of that organ, in chronic alcoholism.[29]

[Footnote 29: Peeters regards it as probable that the
connective-tissue hyperplasia and resulting stenosis seen in the
stomach as a result of the action of alcohol may also occur in the
œsophagus.]

The Stomach.—In addition to functional dyspepsia, which is scarcely
ever absent in chronic alcoholism, all forms of gastritis, from simple
erythematous inflammation of the mucous membrane to sclerosis and
suppurative inflammation of the stomach, are encountered. Armor[30]
assigns to the habit of spirit-drinking, especially to the habit of
taking alcohol undiluted on an empty stomach, a high place among the
causes of indigestion. He regards this habit as a prominent factor in
the production of chronic gastric catarrh—a condition very frequently
present in indigestion. This observer also regards the excessive use
of alcohol as the most frequent among the direct exciting causes of
gastric inflammation in this country, exclusive of acid or corrosive
poisons. Next to errors in diet as a cause of chronic gastritis he
places the immoderate use of alcohol, especially by persons whose
general health and digestive powers are below a healthy standard. The
primary lesions are vascular dilatation and hyperæmia. The mucous
membrane is discolored, red or bluish, in scattered patches of varying
size, with occasional ecchymoses of a bluish hue or spots of
pigmentation. These patches occupy more commonly the region of the
cardia and the lesser curvature. Vascular injection is conspicuous;
the veins are dilated, tortuous; the mucous glands hypertrophied; the
surface covered with thick, ropy, acid-smelling mucus. After a time
permanent changes in the mucous membrane are set up. It undergoes
atrophy or softening; or, again, it becomes hardened, thickened, and
contracted, its rugæ more prominent, its surface mammilated—sclerosis.
Grayish-brown pigmentation, the remains of former
blood-extravasations, is seen at many points. Minute retention-cysts
are formed in consequence of the occlusion of the ducts of certain
glands. The submucous connective tissue and the muscular coat
occasionally undergo, in consequence of prolonged gastritis, local
hypertrophy.

[Footnote 30: See this _System of Medicine_, Vol. II. pp. 446, 464,
470.]

Acute suppurative inflammation of the stomach, with purulent
infiltration of, or the formation of abscesses in, the submucous
tissue, has been met with in drunkards. It is extremely rare, and
results from the violent irritant action of large doses of strong
alcohol in subjects debilitated by previous excesses.

Gastric ulcer is much more common. The abuse of alcohol is regarded as
an indirect cause of this lesion by the majority of writers. In the
present state of knowledge alcohol as usually taken can scarcely be
regarded as a direct cause of ulceration. Nevertheless, gastric ulcer
is relatively {601} common in alcoholic subjects. Leudet[31] found
gastric ulcer in 8 of 26 necropsies of drunkards. Baer and Lentz also
regard the abuse of alcohol as a very common cause of ulceration. The
ulcers are usually superficial, occupy by preference the neighborhood
of the cardia and the lesser curvature, and are apt to be multiple. In
these respects they differ from simple gastric ulcer. The latter
lesion is also probably as frequent, if indeed not more frequent, in
individuals dying of chronic alcoholism than in others.

[Footnote 31: _Clinique médicale de l'Hôtel Dieu à Rouen_, 1874.]

The view formerly entertained that alcohol was an important cause of
cancer of the stomach has been shown by Kubik, Magnus, Huss, Engel,
and others to be untenable. Carcinoma ventriculi is rarely associated
with chronic alcoholism.

The dimensions of the stomach are rarely normal. Dilatation is usually
present in the early stages, and in beer-drinkers throughout; in the
advanced course of alcoholism due to spirit-drinking the organ
undergoes, in consequence of changes secondary to prolonged
inflammation, more or less contraction, which is in many cases
irregular.

Dyspeptic symptoms are common: the appetite is variable, irregular,
and at length wholly lost. There is especially distaste for food in
the morning. This, together with the disordered state of the
secretions of the mouth and a feeling of nervous depression on rising,
leads to the disastrous habit of taking spirits early in the day.
Gastric digestion is performed with difficulty; it is accompanied by
sensations of distension and weight, by flatulence and acid
eructations. Heartburn is a common symptom. The drunkard is not rarely
tormented by an uneasy craving or sense of emptiness in the region of
the stomach, which he temporarily allays by nips and pick-me-ups and
morsels of highly-seasoned foods at odd times, with the result of
still further damage to his digestion and the complete loss of
appetite for wholesome food at regular hours. In the course of time
the characteristic morning sickness of drunkards is established. On
arising there is nausea, accompanied by vomiting—sometimes without
effort or pain, at others attended by distressing retching and
gagging. The matter vomited consists usually of viscid mucus, at first
transparent, then flaky, and at length, if the efforts be violent, of
a green or yellow color from the admixture of bile. These symptoms
ordinarily do not recur until the following day. In other cases
vomiting is more frequent, recurring at irregular periods during the
day, and not uncommonly an hour or two after the ingestion of food.
When gastric ulcer is present, portions of the vomited matter are
often dark and grumous like coffee-grounds or the settlings of
beef-tea, and are found upon microscopic examination to contain
blood-corpuscles. Actual hæmatemesis may also occur under these
circumstances, and be repeated from time to time. The quantity of
blood thrown up is frequently small; at times, however, it is
excessive, and occasionally so great as to cause death.

Common as are the evidences of gastric disturbance in chronic
alcoholism, they are far from being constant, and it is worthy of note
that in proportion to the number of the cases serious gastric
affections are, except in the later stages, relatively infrequent.

The Intestines.—Lesions of the small intestine due to alcoholism are
{602} extremely rare. Even when simple or ulcerative inflammation of
the stomach is localized at, or extends to, the pylorus, it rarely
passes any great distance into the gut. The large intestine is, on the
contrary, frequently the seat of chronic inflammatory processes. Here
we find vascular engorgement, patches of pigmentation, localized
thickening of the mucous and submucous tissues, enlargement of the
solitary glands, and an excessive secretion of viscid mucus. The
tendency to permanent vascular dilatation, which is a characteristic
result of alcoholic habits, constitutes a powerful predisposing
influence in the causation of hemorrhoids, which are common. Alcohol
acts directly upon the hemorrhoidal plexus of veins, and indirectly by
causing permanent congestions of more or less intensity in the greater
number of the abdominal viscera. When a prolonged course of excesses
in alcohol has led to chronic congestion with hypertrophy, cirrhosis,
or other structural change in the liver which is capable of causing
permanent mechanical obstruction of the portal circulation,
hemorrhoids constitute a very common affection in the group of morbid
entities secondary to these conditions.

The symptoms of intestinal derangement are in the beginning, as a
rule, slight and occasional. They consist of uneasy sensations or
colicky pains in the abdomen, a feeling of fulness with or without
tympany, and constipation alternating with diarrhœa: in a word, they
are the symptoms of acute or subacute intestinal indigestion
terminating in an attack of intestinal catarrh. Attacks of this kind
repeat themselves in a considerable proportion of the cases with
variable but increasing frequency, until at length the conditions of
which they are the expression become permanent, and the patient
suffers, among other distressing symptoms hereafter to be described,
from chronic diarrhœa. The stools are now of the most variable
character—occasionally bilious, sometimes containing small dark
scybalous masses, rarely formed, but usually containing more or less
abnormal mucus, too much fluid, and traces of blood. Indeed, at this
stage several causes—among which I may mention visceral congestions,
local inflammation of the intestinal mucous membrane, dilatation of
the hemorrhoidal veins, and structural changes in the liver—conspire
to determine blood toward the interior of the intestinal tube. Traces
of blood in the stools are therefore frequent, and actual hemorrhage
and the appearance of the dark, tarry, and altered blood formerly
described under the term melæna are by no means rare. Colliquative
diarrhœa and dysenteric attacks also occur, and at length an intense
enteritis with uncontrollable diarrhœa may end the life of the
patient. The conditions just described lead to rapid emaciation, and
contribute when present to the establishment of the cachexia so marked
in many cases of chronic alcoholism.

The Glands.—The salivary glands were found by Lancereaux[32] to have
undergone softening, with granulo-fatty changes in their epithelium.
If such changes are among the usual effects of alcohol, they are
doubtless productive of alterations in the saliva, which explain, in
part at least, the dryness of the mouth so frequent among drunkards.

[Footnote 32: _Dictionnaire de Médecine_, art. “Alcoholism.”]

The pancreas is, as the result of interstitial inflammation, the seat
of similar changes. It is sometimes enlarged and softened, sometimes
atrophied, shrivelled, or cirrhotic. In the latter condition its
consistence is {603} firm, its surface uneven, its color deep yellow,
brown, or pale. Hyperplasia of the interacinous connective tissue,
with subsequent contraction and atrophy and destruction of the
glandular tissue, characterizes the more chronic forms of
pancreatitis, and the organ is frequently the seat of scattered minute
blood-extravasations. I have already alluded to the enlargement of the
solitary glands which constitutes a feature of the condition of the
large intestine. The solitary glands and Peyer's patches of the small
intestine are rarely altered.

_b_. Disorders of the Liver.—Next in order to the stomach, the liver
is more directly exposed to the action of alcohol than any other
viscus. For this reason lesions of the liver are frequent and grave.
It is worthy of note, however, that in a small proportion of cases of
chronic alcoholism terminating fatally, with widespread evidences of
the destructive action of alcohol upon the other organs of the body,
the liver has been found, both in its macroscopic and microscopic
appearances, wholly normal. Absorbed by the gastric vessels, alcohol
passes directly, by way of the portal vein, into the parenchyma of the
liver, there giving rise to various disturbances, the nature of which
is determined by the tendencies of the individual on the one hand, and
on the other hand by the character of the alcohol consumed. The danger
of hepatic disease is in direct proportion to the amount and the
concentration of the alcohol habitually taken. The steady drinkers of
spirits of whatever kind, whether gin, brandy, whiskey, or rum,
present the largest proportion of diseases of the liver. These
affections are far less common among beer-drinkers, and infrequent
among wine-drinkers in wine-growing countries. In this connection it
is to be borne in mind that the presence of food in the stomach
retards to some degree the absorption of the alcohol ingested, and to
a certain extent constitutes a means of dilution.

Hepatic disorders due to alcohol may be arranged in two groups: first,
congestion and inflammation; second, fatty infiltration or steatosis;
and the inflammatory process may affect chiefly the interstitial
connective tissue on the one hand, giving rise to sclerosis, or on the
other the glandular substance, constituting a true parenchymatous
inflammation.

Congestion.—Congestion of the liver is an early lesion. It is brought
about by the direct irritant action of the alcohol itself in part, and
in part by the extension of inflammation from the stomach by
continuous mucous tracts. Its development is insidious. Anatomically,
the condition is characterized by vascular dilatation, moderate
tumefaction, slight increase in the consistence of the organ; the
surface is of a deeper red than normal; on section the color is more
intense and the oozing more abundant. At a later period we have, as
the result of chronic congestion, the cyanotic liver; the color is
brownish or violet, mottled, and on section the surface is granular
and the lobules distinct. The organ may now be somewhat diminished in
size, but it lacks the firmness of sclerosis and the hobnail
appearance due to the contraction of the interlobular connective
tissue in that condition.

The symptoms of congestion of the liver are the familiar symptoms of
gastro-hepatic catarrh, varying from the transient disturbance known
as biliousness to serious sickness, characterized by acute
gastro-intestinal phenomena, with vomiting, headache, and other
derangements of the nervous system—constipation, succeeded by diarrhœa
and by more or less {604} distinct jaundice. The graver forms of
hepatic congestion are characterized by intense nausea, frequent
vomiting, pain and soreness in the epigastrium and right hypogastrium,
the physical signs of augmentation of the volume of the liver, and
well-marked yellow discoloration of the conjunctivæ and skin. These
attacks are usually afebrile: the pulse is slow; there is considerable
nervous and mental depression, a tendency to vertigo, and occasional
syncope. The urine is scanty and high-colored, and presents the
reactions of bile-pigment. Muscular tremor, especially marked in the
extremities and tongue, is often present, but is to be attributed
rather to the direct action of alcohol upon the nervous system than to
the condition of the liver.

Hepatitis.—There are two principal forms of inflammation of the liver
induced by alcohol—parenchymatous hepatitis and interstitial hepatitis
or sclerosis.

Several varieties of parenchymatous hepatitis have been described. The
anatomical discrimination of these varieties is attended with less
difficulty than their clinical diagnosis. One of the more serious is
diffused parenchymatous hepatitis or acute yellow atrophy. Alcoholic
excesses appear to constitute a predisposing influence to this grave
disorder (Lentz). In several cases prolonged and repeated excesses
have preceded its development. It is a true parenchymatous
inflammation, in which the glandular elements of the organ undergo
disintegration. The liver is diminished in volume in all its
diameters. It is of a uniform yellow color; its tissue is soft and
friable; upon section the hepatic cells are found to be replaced by a
granular detritus mingled with globules of coloring matter and a
greasy, grayish-yellow liquid exudation.

The symptoms of this affection are those of an acute parenchymatous
hepatitis of the gravest kind. In the early stages there is intense
jaundice, gastro-intestinal disturbance, and fever, followed by speedy
evidences of profound toxæmia. The patient rapidly falls into the
so-called typhoid state, with a tendency to coma. The prognosis is, in
the greater number or cases, a fatal one. So close is the resemblance
between acute yellow atrophy of the liver and the phenomena of acute
phosphorus-poisoning that by many observers these two conditions are
held to be identical.[33]

[Footnote 33: Consult this _System of Medicine_, Vol. II., article
“Acute Yellow Atrophy of the Liver.”]

There is little doubt that the view now generally held, that acute
yellow atrophy is due to the action of some unknown toxic principle,
is correct. Alcoholic excess must therefore be regarded merely in the
light of a predisposing influence. Acute yellow atrophy of the liver
is an exceedingly rare disease.

Suppurative Hepatitis.—Abscess of the liver is in temperate climates
infrequent as the direct result of alcoholic excess. It is frequently
ascribed, however, to improper alcoholic indulgence, especially when
combined with the eating of large quantities of improper food, in
tropical and subtropical climates. A form of hepatitis has been
described by Leudet under the head of chronic interstitial hepatitis
with atrophy. The symptoms are for the most part not very well marked,
and consist chiefly in general malnutrition, which may in fact be
dependent upon the associated gastric disturbance. Chronic jaundice is
usually present.

Interstitial Hepatitis.—Cirrhosis of the liver is in a large
proportion of cases directly attributable to alcoholic excess. In this
view the greater {605} number of observers coincide. But that alcohol
is not the sole cause of chronic interstitial hepatitis has been
abundantly established. As long ago as 1868, Anstie[34] wrote as
follows: “Considering the enormous quantities of spirituous liquors
which are drunk by many of the patients who apply for relief from the
consequences of chronic alcoholism, it would be natural for the reader
who holds the usual opinion as to the origin of cirrhosis of the liver
to expect that serious symptoms produced by the latter disorder must
often complicate cases of the former. The case is, however, far
otherwise in my own experience. Of the immense number of patients in
whom the nervous disorder has been clearly identified, I have only
seen thirteen cases in which the symptoms of cirrhotic disease called
for any special treatment, although a certain degree of cirrhosis was
doubtless present in many of the others; and I cannot avoid the
conclusion that some very powerful element over and above the
influence of alcoholic excess is needed to produce the severe type of
that disease.” Formad[35] states as the result of his investigations
as coroner's physician of the city of Philadelphia that cirrhosis of
the liver is much less common in alcoholic subjects than has been
generally thought. My own experience during eleven years as attending
physician at the Philadelphia Hospital leads me to endorse this
opinion.

[Footnote 34: _A System of Medicine_, Reynolds, vol. ii. p. 74.]

[Footnote 35: _Proceedings of the Pathological Society of
Philadelphia_, Dec., 1885.]

The anatomical lesions of chronic interstitial hepatitis consist
essentially in hyperplasia and hypertrophy of the connective tissue of
the organ. The progress of the affection is insidious and gradual;
some degree of enlargement, due in part to congestion and in part to
interstitial exudation, is followed by gradual diminution, with
retraction of the new connective tissue. When the connective-tissue
new formation is excessive, and retraction fails to take place, the
organ remains permanently enlarged (hypertrophic cirrhosis). During
the first period the volume of the organ is increased, its consistence
is more firm, and its surface is slightly granular. The second period
is characterized by induration, with diminution of the volume of the
organ and alteration of its form. The surface is uneven, deeply
granular, and usually of a mottled yellow color. The tissue is firm,
creaking under the knife. The connective tissue is enormously
increased, the glandular elements being proportionately atrophied.

The contracting connective tissue exercises at the same time a
compressing influence upon the hepatic cells and upon the vascular
supply throughout the organ; the radicals of the portal vein and the
branches of the hepatic artery are alike compressed, and in part
obliterated. The same is true of the bile-ducts. The functional
activity of the liver, at first diminished, is finally, to a
considerable extent, arrested. In consequence of these physical
alterations in the structure of the organ, the symptoms, which are at
first insignificant, become progressively more grave, until at length
they constitute complications of the most serious kind.

It can be no longer asserted that the interstitial hepatitis produced
by alcohol presents specific characters. It nevertheless differs in
many respects from that form due to valvular lesions of the heart, in
which there are induration, usually augmentation in the volume of the
organ, {606} and persistent congestion. Congestion, in truth, is the
chief characteristic of the latter form, in which the surface is
smooth and glistening, of a deep brown or violet hue, and on section
yellowish or brown—a condition which has been well described under the
term cyanotic liver.

Sclerotic changes due to alcohol usually affect the organ throughout.
In this respect alcoholic cirrhosis differs from that form due to
syphilis in which the lesions are irregularly distributed.

The functional disturbances due to cirrhosis are, in the beginning,
obscure in themselves and masked by the concomitant gastric
derangement. Later, ascites constitutes the chief as well as the most
constant symptom. It is rarely altogether absent. Emaciation is also a
prominent symptom. No affection, not even diabetes or phthisis,
produces loss of flesh so rapid, so marked, and so significant as
cirrhosis of the liver in chronic alcoholism. Not only do the adipose
tissues waste, but the muscles themselves undergo rapid atrophy. This
fact is not surprising when we consider that the lesions of the liver
give rise to grave interference with every function of that organ. In
addition to the more common gastric symptoms, there is constipation,
not rarely alternating, without assignable cause, with serous and
sometimes bloody diarrhœa. Epigastric distress, epistaxis, and
hemorrhages from other mucous surfaces are common, and are due in part
to the disturbance of the general circulation, and in part to
alterations in the character of the blood itself. The physical signs
indicate in the early stages increase, and afterward diminution, in
the volume of the liver. Enlargement of the superficial abdominal
veins is a characteristic sign. Cirrhosis of the liver is a grave
affection, the course of which, at first slow, afterward more rapid,
almost invariably leads to a fatal termination.

Fatty Degeneration of the Liver.—Steatosis of the liver is of
extremely common occurrence in the advanced stages of alcoholism. The
anatomical changes consist in accumulation of fat-globules in the
liver-cells. French writers distinguish two varieties of hepatic
steatosis: first, that in which the cellular elements undergo no
change beyond that of an accumulation of fat-globules within their
substance; and second, that in which the liver-cells undergo an actual
disintegration, in the course of which fat-granules are formed, and
which is, as a matter of fact, a true fatty degeneration. The first of
these conditions is not incompatible with the functional integrity of
the organ, and is in many instances unattended by symptoms, being
discovered only upon examination after death. Its occurrence is to be
explained by the imperfect oxidation of waste products due to the
constant presence of alcohol in the blood, and by the habitual excess
of fat in the latter fluid. When fatty infiltration is of moderate
amount there are no changes in the volume or the contour of the organ,
and the condition is recognized only on microscopical examination. At
a later stage the organ becomes enlarged, particularly in its
antero-posterior diameter. The surface is now smooth and glistening,
its color yellow or reddish-yellow; upon section it is anæmic, of a
yellowish color, with patches of a reddish hue, and its consistence is
diminished. The indentation caused by pressure of the finger persists.
Under the microscope the hepatic cells are enlarged, rounded, packed
with fat-globules of varying size. In some of the cells these globules
coalesce and form more or less extensive drops of fat. The bile which
is {607} secreted in this condition presents in most instances the
normal characteristics.

Disorders of digestion do not occur in consequence of the fatty change
in the liver until the lesion has reached an advanced stage;
nevertheless, they constitute the earliest symptoms of this condition.
Imperfect digestion, accompanied with flatulence, distension of the
belly, epigastric tenderness, with light-colored stools, and
constipation alternating with diarrhœa, are common symptoms. There is
no pain properly referable to the region of the liver. Whilst icterus
does not occur, there is, nevertheless, a peculiar earthy pallor of
the complexion and persistent greasiness of the skin—conditions,
however, which are not in themselves sufficiently marked to possess,
in the absence of other signs, clinical value.

The second form of fatty degeneration, in which the liver-cells
undergo actual and destructive metamorphosis, accompanied by the
production of fat, is of a much more serious character. It appears to
constitute the stadium ultimum of various forms of interstitial
hepatitis, and is manifested by symptoms of the gravest character, in
many particulars much like those met with in acute yellow
atrophy—namely, visceral congestions, hemorrhages from mucous
surfaces, serous effusions, profound and rapidly developing anæmia,
nervous depression, and coma.

Biliary Catarrh.—The biliary ducts are usually the seat of catarrhal
inflammation, due less perhaps to the direct irritant action of the
alcohol than to the extension of the inflammation of the gastric
mucous membrane in the form of gastro-duodenal catarrh. Gall-stones
are not common in alcoholism.

The spleen is, as a rule, enlarged, soft, and friable; occasionally it
is small and shrivelled. No characteristic changes in its contour and
structure have been recorded.

The great omentum and mesentery are loaded with fat, very often to an
extreme degree. This condition is more marked in the chronic
alcoholism of beer-drinkers than in that of spirit-drinkers. Not
infrequently there are found evidences of chronic peritonitis, which
has been attributed by Lancereaux, in the absence of other assignable
cause, to the effect of alcohol itself. The symptoms of this condition
are usually obscure, consisting of diffused dull pain, augmented upon
pressure, diarrhœa, digestive troubles, and abdominal distension,
sometimes voluminous, often irregular.

_c_. Disorders of the Respiratory System.—The Larynx.—Catarrhal
inflammation of the mucous membrane of the air-passages is common in
drunkards. Some degree of subacute or chronic laryngitis is an early
symptom of chronic alcoholism. It may result from repeated attacks of
acute alcoholism, or it may be among the first signs of excesses that
are continuous, without at any one time being extreme. In the
production of this local trouble the direct action of alcohol is
reinforced by the foul and smoke-laden air of the apartments in which
tipplers spend much of their time and by heedless exposure to the
vicissitudes of the weather. The anatomical changes are those of
chronic laryngitis in general, hyperæmia of the mucous membrane with
minute ecchymoses, local destruction of epithelium with superficial
ulcerations or granulating surfaces. The mucus is often thick, opaque,
and adherent.

{608} These lesions are accompanied by more or less decided impairment
of function. The voice is hoarse and husky; there is fatiguing
laryngeal cough, usually harsh and grating in character, and attended
by scanty muco-purulent expectoration. This cough is often paroxysmal;
especially is it apt to be so on rising, and it then provokes the
vomiting previously described.

The Bronchi.—After a time similar anatomical changes are brought to
pass in the bronchial tubes. Subacute bronchitis is little by little
transformed into the chronic form, characterized by hyperæmia and
thickening of the mucous membrane, extending to the finer twigs, with
submucous infiltration and implication of the connective-tissue
framework of the lung. The exudation, tough and adherent or fluid and
copious, occasions more or less frequent cough, and interferes with
the function of respiration. Hence it is common to encounter in the
subjects of chronic alcoholism bronchiectasis, pseudo-hypertrophic
emphysema, easily excited or permanent dyspnœa, asthmatic seizures,
and some degree of cyanosis. These local affections, interfering with
the circulation of the blood and its proper aëration, react
unfavorably upon the nutrition of the organism at large, and largely
contribute to the production of the ultimate dyscrasia.

The Lungs.—Pulmonary congestion and œdema are of common occurrence.
Favored by the action of alcohol upon the vaso-motor system, they are
readily excited by the careless habits and frequent exposures of the
subject. The lesions occupy by preference the lower and posterior
parts of the lungs, and consist in relaxation of the parenchyma, with
vascular dilatation and serous infiltration. The vesicles are capable
of distension, but contain little air. The tissue is friable, deep-red
or brownish in color, and floats upon water. The symptoms of this
condition are sometimes obscure: usually they consist in a sensation
of constriction of the thorax, more or less dyspnœa, mucous
expectoration, sometimes streaked with blood, and lividity of the
countenance and finger-tips. The chief physical signs are impaired
percussion resonance and mucous, subcrepitant, and occasionally a few
scattered crepitant râles.

Pulmonary Apoplexy.—When the congestion is extreme, blood may escape
into the parenchyma of the lung with laceration of its substance. This
lesion is more frequent in intense acute alcoholism than in the
chronic form.

Pneumonia.—Habitual alcohol-drinkers are far more liable to pneumonia
than others. It has even been asserted that alcohol is of itself
capable of acting as an efficient exciting cause. Whilst it is
indisputable that the action of this agent upon the pulmonary
blood-vessels and in favoring pulmonary congestion constitutes a
powerful predisposing influence, it cannot be admitted, regard being
had to the fact that it is largely eliminated by the lungs, that
alcohol can, in the absence of a specific cause, ever produce a
specific acute febrile disease, such as croupous pneumonia. The
pneumonia of alcoholic subjects, like that of aged persons and that
occurring in the convalescence from acute diseases, is apt to be
latent. The exudation is often of limited extent; the symptoms are
insidious, and the striking clinical features of the ordinary frank
form of the affection are not rarely absent altogether. It is no
infrequent occurrence that pneumonia is overlooked in the delirium
tremens which it has induced.

The anatomical changes are those of the ordinary form. The prognosis
{609} is always grave. When recovery occurs resolution is often
tedious and prolonged.

Catarrhal pneumonia is also common. It is marked by its usual
phenomena.

The most striking fact in the pneumonia of alcoholic individuals is
the contrast between the local and the constitutional symptoms. The
former are in the greater number of the cases insignificant and easily
overlooked. Even the physical signs, when sought for, are often
obscure and indeterminate: relative dulness, enfeebled or absent
vesicular murmur, faint scattered crepitation masked by mucous râles,
and a bronchial respiratory sound scarcely appreciable, are all that
can be detected upon physical examination. In strong contrast to this
almost negative picture is that of the constitutional disturbance,
which is commonly of the gravest kind. The prostration is extreme;
there is delirium with tremor, restlessness, sleeplessness, mental
agitation, profuse sweating, feeble action of the heart,
gastro-intestinal irritation, with vomiting and often complete
inability to retain food. The temperature-curve lacks the characters
of pneumonia of the ordinary form. Not seldom is febrile movement
absent altogether.

The view that alcohol, independently of and in the absence of other
lesions, occasionally produces changes in the lungs analogous to the
chronic interstitial inflammatory processes of cirrhosis of the
liver—_i.e._ fibroid phthisis—is not borne out by clinical or
pathological investigation, and appears to be wholly without
foundation in fact.

Pulmonary Phthisis.—The question whether or not chronic alcoholism
exerts any influence in the production and evolution of pulmonary
phthisis has been the subject of no little fruitless controversy.
There are medical men of experience who do not hesitate to affirm that
the abundant use of alcohol constitutes in certain cases an actual
prophylaxis, while there are others who insist with equal positiveness
that alcoholic excesses favor the development of this affection.
Whatever may be the influence of alcohol in depressing the forces of
the body and in the production of serious lesions of pulmonary
structures, and thus predisposing the subject to phthisis, it can be
asserted with confidence that it does not directly cause any form of
phthisis whatever. The alcoholic phthisis of Lancereaux, Richardson,
Drysdale, and others cannot be now regarded as a distinct, independent
affection. The process of exclusion by which alcohol was made to seem
the real cause of the disease in 36 of 2000 of the cases examined by
Richardson was not sufficiently rigid to meet the requirements of our
present knowledge. There is reason to believe that by its favorable
influence upon the appetite and digestion, its power to reduce
temperature, its retarding influence upon tissue-waste, alcohol in
moderate quantities is of great use in the management of this
affection. That phthisical subjects occasionally seem to derive
benefit from, and to lengthen their lives by, excesses in alcohol is
capable of explanation—first, by the fact that an extraordinary
tolerance for alcohol is natural to or acquired by certain
individuals; and, second, by the favorable influence of alcohol upon
ulcerative and suppurative processes, and in determining
connective-tissue new formation—a process by which certain
inflammatory products, including tubercle, are capable of being
rendered inert. The foregoing remarks are applicable to all forms of
pulmonary phthisis.

{610} The Pleuræ.—The pleura is sometimes the seat of patches of
fibrinous exudation of varying extent and thickness, which are,
according to Lentz, the expression of the formative action which
constitutes one of the modalities of alcoholism, and which are of the
same nature as the fibrinous exudations which occur in the peritoneum
and the dura mater. These false membranes cause pleural adhesions, and
occasionally contain within their meshes a turbid serous fluid.

_d_. Disorders of the Circulatory System.—The Heart.—This organ is
usually implicated to a greater or less extent in the course of
chronic alcoholism. Lesions of the muscular substance are more common
than those of the valvular apparatus.

Hypertrophy is common. It affects usually both sides of the heart—the
left, however, more than the right—and is associated with some degree
of dilatation. The part played by alcohol in the production of cardiac
hypertrophy is a dual one: first, that of constantly-repeated direct
stimulation of the heart; second, that of the indirect stimulation to
over-action caused by the necessity to overcome the obstacles which
the lesions of the viscera interpose to the circulation of the blood
in the later periods of the disease. Nor are the lesions of the
blood-vessels themselves, hereafter to be described, without influence
in inducing hypertrophy. Bollinger and Schmidbauer have shown that the
habitual consumption of beer in excessive quantities leads to cardiac
hypertrophy of characteristic form. Both sides of the heart
participate in the overgrowth: there is enormous increase in the
volume of the primitive muscular elements, with enlargement of the
nuclei. Whether or not actual numerical increase in the muscular
fibres takes place cannot be determined. This form of enlargement of
the heart occurs in the absence of lesions of the valves, disturbances
of the pulmonary circulation, arterial sclerosis, atheroma, or
granular kidneys. Some few of these cases of so-called idiopathic
hypertrophy are perhaps due to prolonged excessive bodily effort and
bodily strain. But the greater number are only to be explained by
habitual excesses in beer-drinking, as shown by carefully worked-out
personal histories of the patients. Neither fatty degeneration nor
myocarditis enters into the pathological process under consideration.
The hypertrophy is due to the direct action of the alcohol consumed,
to the enormous amount of fluid introduced into the body, and to the
easily-assimilated nutritive constituents of the beer itself.
Furthermore, such habits are often associated with great bodily
activity and a relatively luxurious manner of life. The greater number
of alcoholic subjects who suffer from this form of hypertrophy perish
after brief illness with symptoms of heart-failure. At the necropsy
are discovered moderate dropsy, congestion and brown induration of the
lungs, congestion of the liver, spleen, kidneys, and other organs,
bronchitis and moderate serous effusions or general anasarca. Death is
probably due to paralysis of the cardiac nerves and ganglia. This form
of hypertrophy is of course much more common among men than among
women. It is much less common in this country than in Germany, but is
occasionally met with among brewers' employés.

Fibroid Degeneration.—This condition has been ascribed to a number of
causes, among which long-continued excess in alcohol is unquestionably
an important one. Bramwell holds the opinion that in a certain {611}
proportion of cases of this description, in which fibroid degeneration
of the heart is connected with similar changes in the kidneys
(sclerosis), the lesions of both organs are due to alcoholism.
Alcoholic fibrosis differs in no respect from that due to other
causes. The condition may escape recognition by the unaided eye if it
be disseminated throughout the muscle and the change consist in
thickening of the perimysia around undivided fibres. The heart is
larger than normal, perhaps a little paler, and its consistency a
little more firm. When, as is more commonly the case, the fibroid
change is localized, and masses of new tissue are developed in and
around the muscular fibres, the heart assumes a flecked or streaked
appearance, due to the contrast between the yellowish-white fibroid
tissue and the brownish-red muscular structure. The microscope shows
excessive development of fibrous tissue, with atrophy of muscular
fibres. The effect is to weaken the force of the heart's action, and
to weaken the walls of the cavities at the affected parts in such a
manner as to cause local bulgings or cardiac aneurisms.

The symptoms and physical signs of fibroid degeneration of the heart
are very obscure and indefinite, and the diagnosis is always attended
with difficulty, and in many cases is impossible. Jubel-Renoy,
however, regards the diagnosis as having already attained some
clinical exactitude, and regards as important the association of the
following diagnostic data: first, feebleness of the systole and the
pulse, with augmentation of the frequency without irregularity;
second, moderate enlargement, varying within considerable limits; and
third, absence of murmurs in the greater number of the cases. Death is
apt to occur suddenly. Welch, upon investigation of the clinical
histories of cases in which fibroid degeneration of the heart was
found after death, concluded that they might be clinically grouped as
follows: first, cases in which there is no symptom of heart disease;
second, cases of sudden death without previous heart symptoms; third,
sudden death preceded by one or more attacks of angina pectoris;
fourth, after cardiac insufficiency of a few days' standing; and
fifth, in cases of old heart disease.

Fatty Heart.—Under the term fatty heart two distinct pathological
conditions are comprised. Of these the first is fatty infiltration,
which consists in an excessive development of the normal
subpericardial fat, with a deposition of fat-cells in considerable
number between the muscular fibres of the myocardium. This condition
occurs chiefly in individuals suffering from general obesity, and is
particularly apt to occur in alcoholic obesity. Large masses of fat
fill the grooves and furrows of the organ, the surface of which is
covered with a thick layer of yellowish fat. The right heart is first
and most affected, but in advanced cases the whole heart may be
encased in a thick fatty layer. When the fat-cells infiltrate the
intermuscular spaces, they exert pressure which may produce atrophy
and degeneration of the muscular elements. This condition may exist to
a certain extent without symptoms, but it is, however, apt to be
manifested by a certain amount of cardiac dyspnœa and inability to
endure excessive strain or acute illness. In cases in which the fatty
infiltration attains a high grade, inducing by mechanical pressure
degenerative changes in the muscular substance of the heart, there are
signs of embarrassment of the circulation. The precise diagnosis is
usually difficult, often impossible.

{612} The second form of fatty heart is known as fatty degeneration,
and consists in changes in the muscular fibres by which the albuminoid
constituents are broken up and replaced by microscopic particles of
fat. After a time the transverse striæ disappear, and the functional
activity of those muscular fibres which are affected is completely
lost. All conditions which interfere with the supply of oxygen to the
muscular tissue or which seriously derange its nutrition are capable
of producing fatty degeneration. Among these are alcoholic excesses.
The color of the heart is paler than normal, usually fawn or pale
buff. It has been described as the faded-leaf color. The consistence
is softer than normal, the wall of the heart in many instances being
readily broken down by the pressure of the finger. The left ventricle
is the part most likely to be affected, the papillary muscles being
often profoundly altered. Next in order the right ventricle is
involved, then the left auricle, and finally the right auricle. When
this form of degeneration is due to disease of the coronary arteries,
the lesion is usually localized, sometimes limited to the distribution
of the branch of the artery which is affected.

Upon microscopical examination the affected muscular fibres are found
to contain minute molecules of fat, often of a uniform size, sometimes
arranged in rows, but commonly distributed irregularly throughout the
substance of the fibre. The transverse striæ are indistinct, and
sometimes wholly absent. The functional activity of the affected
fibres is seriously interfered with or wholly lost, and as a result
the force of the circulation is greatly weakened. These two forms of
fatty change are occasionally associated. Among the more common
symptoms are shortness of breath upon exertion, with dry hacking
cough. In advanced cases the dyspnœa may become constant. The fatal
issue is sometimes preceded by the Cheyne-Stokes respiration. Other
symptoms are due to cerebral anæmia. The memory is impaired, the
patient becomes wayward and irritable, and is apt to become faint upon
suddenly changing from the recumbent to the erect posture, and in most
instances is incapable of concentrated mental effort or active bodily
exertion.

The Blood-vessels.—Capillary dilatation is one of the earliest and
most persistent effects of alcohol. The visceral congestions which
constitute so important a factor in the pathology of alcoholism are in
part the result of the paralyzing action of alcohol on the vaso-motor
system, and in part of the degenerative changes in the unstriped
muscular fibres of the arterial walls.

Atheroma.—Alcoholic excesses play an important part in the etiology of
atheromatous degeneration of the arterial walls, not so much by the
direct action of the alcohol itself, as by its indirect action in
increasing the tension in the main trunks, and in leading to an
irregular life in which excitement, sudden and severe exertion,
exposure to cold, and depressing influences of all kinds play a part.

Valvular lesions of the heart do not occur as a direct result of the
action of alcohol.

_e_. Disorders of the Genito-urinary Apparatus.—The Kidneys.—Alcohol,
as has been shown above, is a diuretic. In large doses it produces
renal congestion. Ollivier[36] observed acute transient albuminuria
resulting from the influence of excessive doses of alcohol.

[Footnote 36: _Essai sur les Albuminuries produites par l'Elimination
des Substances toxiques_, Paris, 1863.]

{613} Much difference of opinion exists as to the part played by
alcohol in the causation of the various forms of Bright's disease. It
was at one time thought that a large proportion of the cases were due
to the abuse of this substance. Bright held this view, and Christison
attributed from three-fourths to four-fifths of all cases of granular
degeneration of the kidneys to the abuse of spirits. The latter
considered that not alone in notorious drunkards was this result
likely to occur, but even in those accustomed to the moderate daily
consumption of spirits with only occasional excesses. This opinion for
a long time largely prevailed among English writers. Of late years,
however, in consequence partly of the teachings of Anstie and
Dickinson, partly of more precise methods of reasoning, the direct
causative relation between chronic alcoholism and disease of the
kidneys has come to be questioned. Nevertheless, many teachers of
authority adhere to the former view. It is, however, more than
probable that the action of alcohol is not of itself capable of
producing these effects in the absence of other causes, among which
are insufficient or improper diet, irregular living, damp
dwelling-places, occupations necessitating great or prolonged exposure
to cold and wet or such exposure from accidental causes—circumstances
to which those who, especially among the poorer classes, are addicted
to drink are peculiarly liable. Nor must we overlook the influence of
exposure to paludal poison, of lead, and of heredity in the causation
of diseases of the kidneys. While alcohol cannot be regarded as the
direct exciting cause of acute or chronic nephritis, chronic
alcoholism acts as an influence predisposing to the development of
these affections in persons otherwise liable to them.

Congestion of the Kidneys.—The general action of alcohol in inducing
visceral hyperæmia is aided by its special diuretic action in causing
chronic congestion (cyanotic kidney). The kidney is of a dark
violet-red hue, slightly enlarged, especially in its transverse
diameter, of a consistence firmer than normal, and bleeds freely upon
section.

Acute parenchymatous nephritis is of rare occurrence in chronic
alcoholism. Of chronic parenchymatous nephritis Bartels[37] writes: “I
may say that alcoholic excesses, to which the disease is by many
attributed, cannot be charged with being the cause of it. None of the
cases treated by me occurred in drunkards, and in no instance have I
encountered the large white kidney at the autopsies of notorious
drinkers, of which I have made a not inconsiderable number during my
many years' active hospital service.” The same author in discussing
the etiology of chronic interstitial nephritis (contracted kidney)
enters a protest against the view which is widespread in England that
the abuse of spirituous liquors favors the development of the genuine
contracted kidney. He says: “In the first place, among all the
patients whom I have treated, three only were brandy-drinkers to any
notorious excess, while by far the greater number who were affected
with this complaint had lived remarkably abstemious lives. In the
second place, throughout my twenty-five years of active service as a
hospital physician I have had the most abundant opportunity of
watching the consequences of intemperance, both at the bedside and
upon the post-mortem table; yet these three cases have hitherto been
the only ones in which I have found atrophied {614} kidneys in the
bodies of habitual drunkards.” Baer also testifies to the infrequency
of contracted kidneys among drunkards.

[Footnote 37: _Ziemssen's Cyclopædia of Medicine_.]

Fürstner detected by very exact testing a trace of albumen in the
urine of almost all cases of delirium tremens examined. Its presence
was, however, transient, and appeared to be not associated with
structural changes in the kidneys.[38]

[Footnote 38: _Berliner klin. Wochenschrift_, 1876, No. 28.]

Fatty infiltration and fatty degeneration of the kidneys occur in
chronic alcoholism, the former as part of the general fat
accumulation, the latter as a result of the general nutritive
disturbances.

Amyloid degeneration is rare, and can in no case be ascribed to the
direct action of alcohol.

Griesinger saw excessive diabetes insipidus follow a prolonged and
severe attack of acute alcoholism in a man twenty-eight years old, and
terminate fatally in the course of four months. Ebstein attributes the
polyuria of acute alcoholism to lesions of the brain.

Glycosuria is rare among drunkards.

The Bladder.—Catarrh of the bladder is not rare in chronic alcoholism,
especially in that form originating from excesses in malt liquors.
This condition, however, scarcely occurs with sufficient frequency to
be regarded as in any sense a symptom of alcoholism.

The Genital Organs.—The subjects of alcoholism are especially prone to
sexual disorders of all kinds—a fact to be explained by the influence
of alcohol on the imagination, and especially upon the sexual
appetite, its debasing effect on the moral sense and upon the
judgment, and the indifference to the consequences of exposure which
it begets. In the later stages of chronic alcoholism sexual power is
apt to be greatly enfeebled or wholly lost. This condition, which is
usually attended also by loss of sexual desire, is to be attributed to
the action of alcohol upon the nervous system rather than upon the
sexual organs themselves. It has nevertheless been established that
long-continued alcoholic excesses are apt to be followed by atrophy of
the testicles. Lancereaux has described a condition of these organs
resembling in all respects senile atrophy. On the other hand, Huss
attributed the impotence of alcoholic subjects to loss of nervous
tone. In the female, alcoholism produces disturbances of menstruation
and premature menopause. Alcoholic excesses are said also to produce a
liability to abortion, and Lancereaux has observed atrophy of the
ovaries in alcoholic subjects.

2. _Disorders of Special Structures_.—_a_. Disorders of the Locomotive
Apparatus.—The muscles at large, like the heart, are liable to fatty
infiltration and degeneration. Fatty infiltration, frequent at some
period in the course of the affection, is apt to be widespread. The
muscles are paler than normal, softer in consistence, and streaked
with fat. True fatty degeneration is less frequent, and apt to be
localized. Here the muscular fibres lose their striation, and present
within the myolemma minute fatty deposits in the form of granules.
This change is accompanied by atrophy. The symptoms consist in
feebleness and difficulty in movement and in locomotion.

Changes in the bones, notably enlargement of and increase in the
contents of the medullary canal in the long bones, and arthropathies
of various kinds, have been observed in alcoholic subjects.

{615} _b_. Disorders of the Skin.—Alcohol is a sudorific, and is
largely eliminated by the skin. This effect is purely physiological;
therefore the moderate and occasional use of alcohol exerts an
influence rather favorable than otherwise upon the tegumentary
structures, but in repeated excesses it gives rise to more or less
cutaneous irritation. The skin, partly for this reason, and partly
because it shares in the general disturbance of nutrition, becomes
dry, harsh, and scaly; after a time the face, and especially the nose
and neighboring parts, assumes in many instances a violaceous hue, the
minute superficial cutaneous veins are enlarged, and acne is common.
The resulting appearance is almost characteristic of the habits of the
individual. Alcoholic subjects frequently suffer from pruritis,
urticaria, and eczema. In certain cases the skin, instead of being dry
and harsh, is soft and unctuous, and in others, especially in the more
advanced cases, it becomes slightly yellow or earthy in hue. Owing in
part to changes in the nutrition, and in part to vascular dilatation,
the skin of the extremities is not rarely mottled and cyanotic. In
certain forms of alcoholism of the nervous system, and particularly in
alcoholic paralysis, in which we have to do with multiple peripheral
neuritis, the skin of the affected parts, especially that overlying
the atrophied muscles, becomes, in consequence of trophic changes,
dusky in color and hard, smooth, and glossy. It has been stated that
chronic alcoholism is a cause of pellagra, and numerous observations
have been advanced in support of this view (Hardy). The excessive
rarity of this condition in countries in which the abuse of alcohol is
most common renders it probable that the occasional association of
these affections is accidental rather than causal. Chronic alcoholism
predisposes to gangrene of the skin and to bed-sores; slight wounds
readily inflame and are slow to heal; alcoholic subjects are
especially predisposed to erysipelas, while the enfeeblement of the
circulation and the lowered tone in the later stages of chronic
alcoholism often result in œdema of the inferior extremities.

3. _General Disorders_.—In addition to the various local disorders
thus far described, the prolonged excessive indulgence in alcohol
leads to profound disturbances of the processes of nutrition, which
are manifested in alterations in the blood, in excessive accumulation
of fat, and in a well-marked cachexia.

_a_. The Blood.—The alterations in the blood, although sufficiently
manifest in disorders of nutrition, have not yet been studied with
satisfactory results. In chronic alcoholism the proportion of water is
increased, while that of fibrin is diminished. After death the blood
remains fluid. The red globules are diminished in number. The blood
also contains free fat, to which it owes its pale, opalescent, and
sometimes almost milky hue. The presence of fat has been demonstrated
after the injection of alcohol into the veins of animals.

_b_. Obesity.—Fat-infiltration and fat-accumulation must be regarded
as among the most characteristic disturbances produced by alcohol. Fat
is abundantly stored up in the subcutaneous tissues. The anterior
abdominal wall is especially liable to its accumulation. The heart,
kidneys, omentum, and mesenteries are also not infrequently the seat
of abnormally large accumulations of fat. Fat also collects in the
muscles and in the intermuscular planes, but to a less extent. Obesity
is not, however, so frequent in the advanced stages of alcoholism as
it is while the subject {616} has not yet lost the appearance of
health, and in a large proportion of the individuals it does not
manifest itself at all. It appears to depend largely upon the
character of the drink, and is especially frequent among those
addicted to excesses in beer. It is less common among wine-drinkers,
and relatively infrequent and of moderate degree in those who confine
themselves to spirits. A sedentary life, and perhaps also an
hereditary tendency, exerts an important influence upon the
development of obesity in alcoholism.

_c_. Alcoholic Cachexia.—The action of alcohol in excessive amounts
upon the nutrition of the body at large, and in particular upon the
nutrition of the nervous system, is radically unfavorable. This
unfavorable influence manifests itself from the beginning, while the
subject yet presents the appearance of health, and long before the
occurrence of either the symptoms or physical signs of organic
disease. The powers of resistance to unfavorable influences of all
kinds are diminished; the ability to endure hardships, privations, and
fatigue is lessened; sickness and injuries are badly borne;
complications are frequent and grave; and convalescence is apt to be
tardy and insecure. It is among the more striking peculiarities of the
alcoholic subject that blood-losses are badly borne and slowly
repaired. It is this want of tone, often latent for a long time under
ordinary circumstances, which unfits those addicted to alcohol for
Arctic and exploring expeditions and for military and scientific
enterprises involving prolonged hardship and exposure. In the course
of time disorders of the digestion, of hæmatosis, of circulation,
increase the difficulty and render it more apparent. The fat now
rapidly diminishes; anæmia develops; the complexion becomes dull,
earthy, or slightly jaundiced, the tissues flabby. Then follow
diarrhœa, hemorrhages from mucous surfaces, serous effusions, visceral
congestions of high degree, hypostasis, œdema, and progressive
deterioration of all the powers alike of the body and the mind until
the dyscrasia is complete.

The subjects of chronic alcoholism are especially prone to affections
of the respiratory tract and to the infectious diseases. They furnish,
as a rule, the earliest victims in epidemics. They not rarely die of
pneumonia. They develop troublesome delirium in simple maladies, and
in all acute affections the prognosis is unfavorable as compared with
that in persons of sober habits. As Clouston well says, “The whole
organism suffers sanative and mental lowering, alteration of functions
and of energizing.”

_B_. DERANGEMENTS OF THE NERVOUS SYSTEM: CEREBRO-SPINAL DISORDERS.—The
disorders of the central nervous system in chronic alcoholism are even
more numerous and more important than those already described. Many
transient and permanent disturbances of function occur without
anatomical lesions recognizable by existing methods of examination;
many others are associated with readily-discoverable changes of
structure. These changes are encountered in the blood-vessels, the
meninges, the substance of the cerebro-spinal axis, and in the
peripheral nerves. Much as they differ in appearance and in their
clinical manifestations, they may all be referred to three processes:
(_a_) congestion and inflammation; (_b_) sclerosis; and (_c_)
stentosis.

1. _Cerebral Disorders_.—The Cranium.—The bones of the skull are often
thicker and more dense than normal. This change implicates the {617}
diploë and the outer and inner tables. The last is then deeply
channelled for the blood-vessels and deeply indented for the
Pacchionian bodies, which are commonly hypertrophied.

The Vessels.—Disturbances of the cerebral circulation are among the
earliest and most important symptoms. Due primarily to the increased
action of the heart and vaso-motor dilatation of the blood-vessels
excited by repeated large amounts of alcohol, and secondarily to
permanent enlargement of the vessels in consequence of fatty or
atheromatous degeneration of their walls, some degree of active or
passive congestion is almost always present. It is probable also that
in consequence of irregular and complex disturbances of the
circulation secondary localized ischæmia occurs. Lentz states that
anæmia is more common in the cerebral substance than in the membranes.

The capillaries are usually much altered—sometimes uniformly dilated
to a considerable extent, sometimes forming capillary aneurisms. They
are more sinuous than normal, their walls show evidences of fatty
degeneration, and they sometimes contain minute thrombi. Extravasated
blood, in the form of circumscribed collections, of diffuse layers, or
finally of capillary hemorrhages, also occurs. These collections are
sometimes free, sometimes encysted.

The Meninges.—The dura mater is congested; occasionally it shows more
or less extensive areas of inflammation with exudation of lymph.
Purulent exudation in the absence of traumatism is rare. The lymph may
be deposited in the form of patches of varying extent, or it may form
more or less extensive false membranes. These accumulations are of
variable, often considerable, thickness, and constitute the condition
described as pachymeningitis hæmorrhagica interna, or, from the large
amount of blood which they contain, hæmatoma of the cerebral meninges.
They occupy the convexity of the brain, and are developed upon the
inner surface of the dura; they are usually nearly symmetrical in
outline, but of different thickness upon the two sides. They consist
of superimposed layers of lymph, between which, or within the
substance of which, are more or less extensive blood-extravasations,
either fluid, coagulated, or undergoing resorption. More frequently
the exudation consists of mere shreds of lymph within the cavity of
the arachnoid.

The arachnoid is almost invariably altered. Upon the convex surface of
the hemispheres, especially along the median fissure, it is thickened
and opaque. This condition may be uniform or distributed in patches,
and is apt to follow the line of the blood-vessels.

The pia mater is congested, often œdematous, not rarely the seat of
blood-effusions of greater or less extent.

The cerebro-spinal fluid is usually more abundant than normal, of a
deeper color, cloudy, sometimes tinged with the coloring matter of the
blood.

The Brain.—The intimate lesions of the substance of the brain are not
yet known. The volume of the encephalon, as a rule, undergoes no
change. Occasionally it appears to be swollen, and protrudes with some
degree of force through the incision first made in the membranes. More
commonly, the brain is throughout or in certain parts atrophied or
shrivelled, its convolutions flattened, its surface retracted. This is
sometimes the result of the pressure of collections of hemorrhagic or
inflammatory products.

{618} The consistence of the cerebral mass is sometimes increased; it
becomes harder, more resistant to pressure, and preserves its form
when removed from the cranium better than the normal brain. This
condition may be present throughout the brain or it may be localized.
In the latter case it is usually due to patches of sclerosis.
Softening in more or less extensive areas may occur in the advanced
stages of the more severe forms of chronic alcoholism. It is found
chiefly in the gray substance, where the vessels are more numerous,
especially in the cortex and central ganglia. In this as in other
affections cerebral softening is the result of obstruction of the
circulation in consequence of atheroma, thrombosis, or other change in
the arteries. It varies from simple diminution in consistency to
diffluence.

The nervous substance of the brain doubtless undergoes changes
proportionate to the degree and duration of its exposure to an
alcohol-charged blood. What these changes are has not yet been fully
determined. The nerve-cells of the cortex have been found rounded and
contracted, so that instead of being surrounded by a small lymph-space
they seem to be lying in large cavities, and so granular that the
nucleus can hardly be made out. Slight increase in the number of the
small round cells in the cortex and in the adjoining parts of the
white matter has also been observed (Hun). These changes are not,
however, constant. Not only has the microscopical morbid anatomy of
the lesions of nerve-substance peculiar to chronic alcoholism not yet
been worked out, but even macroscopic changes adequate to account for
symptoms that were during life serious, persistent, and apparently
referable to well-defined lesions, are sometimes absent altogether.

It is important to distinguish the disorders due to the direct action
of alcohol, which are often functional or dependent upon lesions too
subtle for recognition, from those which are secondary and dependent
for the most part upon coarser changes of structure.

In consequence of hyperæmia of the brain and its membranes there not
infrequently occur a sense of confusion or dulness, increasing to
headache, which may become almost unbearable, mental disturbances of
the most varied character, disorders of movement and sensation, and
disorders of the special senses.

Cerebral hemorrhage, to which the subjects of chronic alcoholism are,
in consequence of the vascular lesions already described, peculiarly
prone, manifests itself by the usual primary and secondary phenomena.
Meningeal hemorrhage, save in the form of hæmatoma, is rare except in
the advanced stages of paretic dementia.

The blood in alcoholic dyscrasia undergoes changes which favor its
transudation through the walls of the vessels; hence a tendency to
œdema and to accumulations in serous sacs. This tendency implicates
the structures of the nervous system in common with the organism at
large. The ventricles of the brain become distended with fluid, and
the brain-substance itself and the meninges not rarely become
œdematous in the last stage of chronic alcoholism, in consequence of
grave disturbances of the circulation or as complications of
affections of the lungs, heart, or kidneys. These conditions are
attended by mental obscuration, somnolence alternating with
sleeplessness, delirium, maniacal paroxysms, impairment {619} of
muscular power, of general and special sensibility, impaired reflexes,
inability to speak, deepening stupor, and death.

2. _Spinal Disorders_.—Lesions of the spinal cord or its membranes
have been rarely discovered. When present they have been invariably
associated with similar or corresponding lesions of the brain or its
envelopes. Leyden[39] states that not only do the cerebral meninges
present inflammatory changes in chronic alcoholism, but the meninges
of the cord are sometimes found in an analogous condition; that
pachymeningitis hæmorrhagica interna spinalis has also been observed,
as well as other forms of spinal meningitis, with thickening and
discoloration of the pia and dura; and that œdema of the pia has been
especially noted. While anatomical lesions of the cord are less
frequent than lesions of the brain, nutritive and functional
disturbances, as manifested in the general symptomatology, are quite
as common in one as in the other.

[Footnote 39: _Klinik des Rückenmarkskrankheiten_.]

3. _Disorders of the Peripheral Nerves_.—Magnus Huss found no change
in the peripheral nerves in five cases in which they were carefully
examined. Lancereaux discovered degenerative changes in the peripheral
filaments in alcoholic paralysis. Leudet found hypertrophy of the
neurilemma and alterations in the cubital nerve in an individual
suffering from chronic alcoholism in whom this nerve was paralyzed.
Dejerine[40] observed in two fatal cases of alcoholic paralysis
neuritis of peripheral nerves with integrity of the nerve-roots, the
spinal ganglia, and the cord. In one of Dreschfeld's cases of
alcoholic paralysis,[41] in which the cord was found perfectly normal,
the “sciatic appeared thin and grayish, and was surrounded by a great
deal of adipose tissue. Vertical sections showed, when treated with
perosmic acid and stained afterward with picro-carmine, a moniliform
appearance of the nerve-tubes, due to breaking up of the myelin; the
nuclei were increased, and there was also some interstitial
cell-infiltration. Transverse sections showed in some few places an
increase in the diameter of the axis-cylinder, and again the
interstitial infiltration.”

[Footnote 40: _Archives de Physiologie nerv. et patholog._, No. 2,
1884.]

[Footnote 41: _Brain_, Jan., 1886.]

Disorders of General Sensibility.—Disorders of general sensibility are
among the earliest of the nervous phenomena of chronic alcoholism.
They occur in the following order: hyperæsthesia, dysæsthesia, and
anæsthesia. Disturbances of sensibility manifest themselves, quite
independently of hallucinations, as sensations of malaise, of
discomfort, of chilliness, of cramps, or of abnormal warmth or cold.
Sometimes they amount merely to momentary discomfort, at other times
to extreme pain. They are usually limited, often to the feet and legs,
sometimes to the hands and arms; again, they are experienced in the
trunk, and especially in the back. They are most common during the
evening; less frequently they are induced by the warmth of the bed;
and, again, they are experienced on rising. They are apt to be
associated with occipital or frontal headache.

Among the most frequent nervous phenomena of chronic alcoholism are
disturbances of sleep. Sleep is light, uneasy, and disturbed,
difficult to obtain, troubled with dreams, and unrefreshing. More or
less complete insomnia is by no means rare. It is more apt to occur,
however, after acute exacerbations of alcoholism than in the ordinary
chronic condition.

{620} Hyperæsthesia manifests itself as an increased sensibility to
pain, to mere contact, to temperature, and in an exaggeration of the
muscular sense. Two general forms may be distinguished—the superficial
and deep. The former usually manifests itself by an exaggerated
sensibility of the skin, especially along the course of the
superficial nerves and at their points of emergence from the deeper
structures. The latter consists in a more or less intense sensation of
pain, often diffuse, sometimes almost unbearable, and associated with
a sensation of heat or cold, which is most commonly experienced in the
lower extremities. It is often referred by the patient to the deeper
muscles or to the bones and joints, and is increased by movement or
pressure.

Anæsthesia is a much more common occurrence. It is usually developed
during the later period of chronic alcoholism, and may implicate the
skin, the mucous tissues, or the deeper structures. It presents all
degrees from mere impairment to absolute loss of sensation. In the
latter case, contact, pain, temperature, and electrical stimulation
equally fail to excite sensation. In the deep anæsthesia of alcoholism
pressure and electro-muscular sensibility are alike impaired. The
muscular sense is also enfeebled or abolished. The regions which are
the seat of anæsthesia are, as a rule, of a lower temperature than
those in which sensation is normal. The anæsthesia may extend to the
conjunctiva, and even to the cornea and to the mucous membrane of the
mouth and throat. It has also been observed in the mucous membrane of
the genitalia and at the verge of the anus.

Disorders of Motion.—Disorders of motion consist of tremor, subsultus,
spasm, convulsions, muscular paresis, and palsies. Tremor is a very
frequent phenomenon in chronic alcoholism. It consists generally of a
series of rapid rhythmical movements. Sometimes the extent of the
movement is increased and their rhythm irregular. They are then
choreiform. The tremor may be continuous; much more frequently it only
appears in the morning. The subject has then some difficulty in
dressing himself, particularly in buttoning his clothing, in shaving
himself, and in raising a cup to his lips. This symptom commonly
ceases after the ingestion of a certain quantity of alcohol, only to
return on the following morning or after a considerable period of
abstinence. Voluntary movements intensify the tremor. It most commonly
affects the upper extremities, next in frequency the muscles of the
face, and finally the lower extremities. In rare cases it affects the
muscles of the whole body. Alcoholic tremor affecting the hands and
arms renders the subject awkward and interferes with his ability to
work; affecting the lower extremities, it gives rise to an
embarrassing, irregular gait; affecting the lips and tongue, it
produces hesitation of speech or stammering, and when it is of a high
degree articulation may be so imperfect that conversation is
impossible; affecting the muscles of the eyes, it gives rise to
nystagmus. Tremor is not infrequently associated with subsultus
tendinum, spasmodic contractions, and cramps. These phenomena are
usually localized, and affect by preference the muscles of the face
and those of the lower extremities.

Loss of muscular power, which may pass, little by little, into
complete palsy, also occurs. It is, however, neither constant nor
proportionate to the gravity of the case in other respects. Whilst, as
a rule, it is developed insidiously, it occasionally shows itself with
suddenness. In the latter {621} case it is usually preceded by some
acute complication, and may disappear as quickly as it came. At first
it is a mere feebleness, which, beginning in the fingers, extends to
the hands and arms. It may after a time manifest itself in the feet.
More or less muscular paresis is invariably associated with the tremor
above described.

Alcoholic Paralysis.—The earliest account of alcoholic paralysis is
that of James Jackson,[42] who designated the disease, from its most
prominent symptom, arthrodynia. He attributes it to ardent spirits,
and chiefly observed it among women. “This arthrodynia comes on
gradually. It commences with pain in the lower limbs, and especially
in the feet, and afterward extends to the hands and arms. The hands
may be affected first in some instances, but in all cases in the
advanced stage of the disease the pain is more severe in the feet and
hands than in the upper limbs. The pain is excruciating, and varies in
degree at different times. It is accompanied by a distressing feeling
of numbness. After the disease has continued a short time there take
place some contraction of the fingers and toes and inability to use
these parts freely. At length the hands and feet become nearly
useless. The flexor muscles manifest, as in other diseases, greater
power than the extensors, and the whole body diminishes in size,
unless it be the abdomen; but the face does not exhibit the appearance
of emaciation common to many visceral diseases. The diminution is
especially observable in the feet and hands. At some time the skin of
these parts acquires a peculiar appearance. The same appearance is
noticed in a slighter degree in the skin of other parts. This
appearance consists in great smoothness and shining, with a sort of
fineness of the skin. The integument looks as if tight and stretched,
without rugæ or wrinkles—somewhat as when adjacent parts are swollen.
The skin is not discolored. In this disease there is not any effusion
under the skin, and the character which it assumes arises from some
change in the organ itself.”

[Footnote 42: _New England Journal of Medicine and Surgery_, vol. xi.,
1822, “On a Peculiar Disease resulting from the Use of Ardent
Spirits.”]

Since Jackson's day, Huss, Lancereaux, Leudet, and others have
described various forms of paralysis due to alcohol. Wilks[43] under
the term alcoholic paraplegia described a form of alcoholic paralysis
of which he had seen numerous cases, especially in women addicted to
alcoholic excesses. The symptoms are severe pain in the limbs,
especially the lower ones, with wasting, numbness, anæsthesia, only
slight power of movement or total inability to stand. The symptoms are
not unlike those of ataxia. Wilks regarded the disease as due to
degeneration of the cord and thickening of the membranes. Several of
the cases terminated in recovery in a comparatively short time after
the abrupt and complete withdrawal of alcohol. Since that time a
number of cases have been reported by various observers.[44]

[Footnote 43: _Lancet_, 1872, vol. i. p. 320.]

[Footnote 44: See, in particular, Hun, _American Journal of the
Medical Sciences_, April, 1885, “Alcoholic Paralysis.” This paper
contains a valuable résumé of the reported cases up to that time.
Consult also Dreschfeld, _Brain_, July, 1884, and January, 1886.]

Hun concludes that alcoholic paralysis may be regarded as a special
form of disease with the following symptoms: “Neuralgic pains and
paræsthesiæ of the legs, gradually extending to the upper extremities,
and accompanied at first by hyperæsthesia, later by anæsthesia, and
{622} in severe cases by retardation of the conduction of pain. Along
with these symptoms appears muscular weakness, which steadily
increases to an extreme degree of paralysis, and is accompanied by
rapid atrophy and great sensibility of the muscles to pressure and to
passive motion. Both the sensory and motor disturbances are
symmetrically distributed. The paralysis attacks especially the
extensor muscles. In addition to these motor and sensory symptoms,
there is also a decided degree of ataxia. The tendon reflexes are
abolished, and vaso-motor symptoms, as œdema, congestion, etc., are
usually present. Symptoms of mental disturbance are always present in
the form of loss of memory or transient delirium.”

Lesions of the cord are absent, but degenerative processes in the
peripheral nerves have been discovered in a number of cases. The
symptoms are those of multiple neuritis, and the essential lesions
consist in degenerative changes in the peripheral nerve-fibres. The
associated mental derangement, tremor, and ataxia have been ascribed
to changes in the cerebral cortex.

Dreschfeld has divided the cases, according to the more prominent
symptoms, into two clinical groups—alcoholic ataxia and alcoholic
paralysis.

The ataxic form represents a milder type. The symptoms are lancinating
and shooting pains in the lower extremities, sometimes in the upper,
with areas of anæsthesia and retarded sensibility. The muscles are
painful upon pressure, and atrophy may be moderate or absent
altogether. Inco-ordination is marked. The tendon reflexes are absent.
Shooting pains down the legs to the toes of a paroxysmal character,
and followed by a sense of numbness, also occur. Eye symptoms are
wanting.

The paralytic form is usually associated with atrophy, affecting
chiefly the extensors of the fingers and toes. The paralysis and
atrophy in some cases come on acutely, in others more slowly. When the
patients come under observation they are usually unable to stand or
walk, and it is therefore not easy to make out whether or not the
paralytic stage has been preceded by a stage of ataxia. As the sensory
phenomena in these cases are the same as in the first group, it is
probable that pseudo-ataxic symptoms have preceded the slowly oncoming
paralysis. Paralysis and atrophy of the extensors of the fingers and
toes, with paresis of the other muscles, are associated with the
sensory phenomena above described. Tendon reflexes are absent; the
superficial reflexes are much diminished. Recovery takes place in a
considerable proportion of the cases upon the withdrawal of alcohol.
The atrophy and paralysis pass away altogether, the tendon reflexes
are restored, and the disturbances of sensation disappear. In the
greater number of these cases persistent delusions are present.

Lancereaux[45] describes alcoholic paralysis as symmetrical, affecting
either the upper or lower extremities and gradually extending toward
the trunk. The lower extremities are invariably more affected than the
upper, and the extensor than the flexor muscles. There is diminished
reaction to electricity, and anæsthesia is present. The brain and
spinal cord are normal, but the peripheral nerves show extensive
degenerative changes.

[Footnote 45: _Gazette des Hôpitaux_, No. 46, 1883.]

4. _Disorders of the Special Senses_.—_a_. The Sight.—Disorders of
vision {623} are among the most frequent and the earliest symptoms of
chronic alcoholism. Phosphenes, scintillations, sensations of
dazzling, muscæ volitantes, and streams of light are often complained
of. These phenomena may be constant or transient. Diplopia and other
visual disturbances of the most irregular and annoying character also
occur. Sometimes there is dyschromatopsia; the colors are confounded:
red appears brown or black, and green appears gray, etc. In the more
advanced stages amblyopia may occur. The acuity of vision rapidly
diminishes, sometimes to the point that the patient with difficulty
distinguishes the largest print. Objects appear as seen through a fog,
and their outlines are distinguished only after repeated and close
effort. Again, blindness almost absolute occurs for the course of some
minutes—passes away rapidly, only to return again at intervals. Not
infrequently the sight is better in the morning and evening than
during the day. Achromatopsia, characterized by enfeeblement, and not
infrequently by the momentary loss of the power to recognize colors,
and particularly the secondary tints, also occurs. Cases of Daltonism
occasionally seem to depend, to some extent at least, upon alcoholic
disturbances of vision. Impairment of the power to distinguish colors
must not, however, be confounded with the difficulty experienced by
many alcoholic subjects in recognizing different colors successively
presented to the eye with some degree of rapidity. Such individuals
are able to distinguish colors when sufficient time is permitted them.
Their difficulty depends upon tardiness of perception, such as is
often experienced by neurasthenic subjects in recognizing faces in a
crowd, rather than upon any failure in the power of recognizing
colors. As a rule, the disorders of vision are not permanent, at least
in the beginning. Later, they are of longer duration, and alcoholic
amblyopia occasionally degenerates into irremediable amaurosis.
Ophthalmoscopic examination reveals at first no appreciable lesion,
and the disturbance of circulation, venous stasis, and peri-papillary
infiltration thus observed appear to be inadequate to explain the
visual disturbance. Atrophy of the optic nerve occasionally occurs as
a direct result of alcoholism. Nystagmus has been frequently observed.
The state of the pupils is variable and without constant relation to
the acuity of vision. The pupils are not infrequently uniformly
dilated, contracting slowly under the influence of light. More rarely
they are permanently contracted; occasionally they are unequal. These
modifications are often without demonstrable relation to anatomical
lesions.[46]

[Footnote 46: Vide this _System of Medicine_, Vol. IV. p. 803.]

_b_. The Hearing.—The disturbances of hearing encountered in chronic
alcoholism are in many respects analogous to those of sight. Patients
complain of curious subjective sensations, which are described as
humming or whistling sounds, the ringing of bells, music, or the
murmur of a crowd. At times the sense of hearing is so exquisite that
the least noise causes pain. On the other hand, hearing may be greatly
impaired, diminishing by degrees until it becomes in some cases,
without recognizable lesion, almost or completely lost.

_c_. The Taste.—As a rule, the sense of taste is impaired in chronic
alcoholism; occasionally it is wholly lost.

_d_. The Smell.—The sense of smell is in most cases to some extent,
and in many cases greatly, impaired, the most powerful odors being
scarcely perceived by old topers.

{624} Alcoholic Epilepsy.—Alcohol, and especially that combination of
alcohol with oil of wormwood and aromatics known as absinthe, is
capable of producing convulsive seizures resembling epilepsy. Certain
forms of alcoholic convulsions can scarcely be distinguished from
ordinary epilepsy. Acute alcoholism may be an exciting cause of the
convulsive seizures in an epileptic. Alcoholic epilepsy is, however,
peculiar to chronic alcoholism, and particularly in individuals in
whom there is an hereditary tendency to nervous disorders. Once
established, alcoholic epilepsy may continue even after the alcoholic
habit has been discontinued. The attack is usually followed by marked
mental disturbances. These vary from profound dulness to stupor or
mania; they last from some hours to several days, and present the
characters of similar conditions following non-alcoholic epileptic
paroxysms.

_C_. PSYCHICAL DERANGEMENTS.—Yet more important than the visceral and
nervous lesions of chronic alcoholism are the indications which it
affords of a progressive debasing influence upon the mind. The moral
sense, the will, and the intellect are involved successively in a
process of deterioration, which, manifesting itself only in part and
by little at first, becomes after a time general and plain to all the
world, and ends at length in ruin more complete and more hopeless than
that of the body. Indeed, it not infrequently happens that while the
general health appears to be good and the nervous system, save in
transient disturbances of function, presents no evidence of the toxic
action of alcohol upon its tissues, serious psychical disorders are
established. The alcoholic subject develops propensities, otherwise
latent, that tend to refer him to the criminal or the insane classes
of society. The psychical debasement, of which these propensities are
the outcome, is, like the alcohol habit itself, progressive. This fact
cannot be too strongly insisted upon. Like the loss of vascular tone,
the sclerosis, the steatosis which alcohol induces in the body, this
mental deterioration is cumulative and destructive. It is to its
psychical manifestations that alcoholism owes its chief importance,
not only as a study in pathology, but also as a problem of the gravest
moment in social science.

1. _The Moral Sense_.—Deterioration of the sense of moral obligation
is among the earlier of the mental phenomena of alcoholism. The moral
sense is perverted and enfeebled. Sentiments of honor, of dignity, of
reputation, and of decency are no longer cherished or regarded. The
amenities of social life and the proprieties of personal conduct are
disregarded or set at naught. He who was punctilious, considerate, and
thoughtful becomes negligent, selfish, and indifferent to sentiments
of honor and emulation; he gives himself up to indulgences formerly
considered unworthy; his reputation and that of his family are no
longer matters of concern to him; respect for public opinion is
replaced by cynicism. Little by little the conception of duty, of
justice, of honor are lost to him, or if he regards them at all it is
rather as subjects for idle and purposeless discussion than as motives
to regulate his life. These changes are gradual and progressive, their
evolution being largely influenced by the hereditary traits and
previous moral culture of the individual. The deterioration of the
sense of right, and the coincident exaltation of those passions which
are normally under its control, lead to the commission of the crimes
peculiar to the early period of alcoholism. {625} Indifference is
another characteristic of this period—indifference not incompatible
with a selfishness of the most intense kind. The sense of obligation
to the family is forgotten, and the responsibility of providing for
and caring for others is unfelt. If the drunkard's own wants, and
especially his craving for drink, are gratified, the necessities of
those formerly dear fail to move him. The affections are not only
enfeebled, but they are also perverted; not rarely they are replaced
by aversion, disdain, and hatred. The individual who has been calm,
reasonable, and patient becomes excitable, perverse, and intolerable
of contradiction or opposition. Prone to acts of sudden violence, he
becomes gloomy, taciturn, and preoccupied. He is disturbed by fixed
tormenting ideas or by vague pursuing terrors. He thus becomes
self-conscious, irritable, fault-finding, and easily provoked to
passion. The character, after a time, undergoes still more decided
change: alternations of indifference and irritability characterize his
varying moods. After a time the joys and the sorrows of life alike
fail to provoke real feeling. At length the confirmed sot manifests
moral traits that are simply infantile; he laughs without motive, he
weeps without cause.

2. _The Will_.—At the same time the will undergoes an enfeeblement
even more marked. Except in paroxysms of transient excitement it is
feeble and uncertain. The subject of chronic alcoholism scarcely knows
his own mind under ordinary circumstances. Aware of his duties and his
obligations, he is unable to discharge them. Especially does he lack
the power to say No. Vacillation, indecision, and dependence upon
others become characteristic traits. This loss of moral energy,
combined with the loss of physical power brought about by continued
and repeated excesses, begets at once a distaste for the ordinary
occupations of life and an inability to perform them.

3. _The Intellect_.—Loss of intellectual power comes last. In some
cases it shows itself only after the most prolonged excesses, when the
body itself is becoming thoroughly broken down. Exceptionally, fitful
intellectual power is curiously sustained to the last. The first
evidence of intellectual failure consists in diminution of vivacity
and readiness. The intellectual state is marked by apathy, obtuseness,
and indifference; mental processes are performed slowly and with
difficulty. This is perhaps one of the causes of the mental indolence
characteristic of alcoholism. After a time the drunkard becomes timid,
loses confidence in himself, and is unwilling to engage in enterprises
demanding mental effort. Some tardiness of appreciation then shows
itself; conversation becomes difficult; ideas are not spontaneous, but
must be sought for; replies are not made with the usual promptness; it
is difficult to arouse and fix the attention. The sense of
self-respect is now lost, and it is almost impossible to make the
subject comprehend his degradation. The intellectual deterioration
becomes more and more marked. The memory fails little by little and
becomes treacherous. Names and dates are recalled with difficulty. The
conversation is interrupted by an inability to choose the proper words
with precision, hence hesitancy, interruptions, and various forms of
circumlocution. The power of argument and of reasoning is now much
impaired, the judgment is uncertain, the association of ideas is
inexact, and at length the intellectual degradation attains a degree
that unfits the subject for the ordinary relations of life.

{626} The above-described derangements of the viscera, of the nervous
system, and of the mind are the morbid phenomena induced by
long-continued excesses in alcohol. Whether merely functional or
dependent upon recognizable anatomical lesions, they indicate
pathological changes in the organism which are radical, and which
under the influence of the continuously acting cause are progressive.
Taken together, they constitute the condition known as chronic
alcoholism. In view of the familiar experiences of every-day life, it
is hardly necessary to repeat that these derangements are manifested
in all degrees of intensity and in the most variable and complex
combinations. The specific nature of chronic alcoholism is, in truth,
due not to the derangements themselves, the greater number of which
are such as we may encounter in morbid states not occasioned by
alcoholic excesses, but to the combinations in which they occur in
consequence of the action of the specific cause upon the organism as a
whole. The prominence of particular symptoms or groups of symptoms in
any given case is to be accounted for largely, if not wholly, by
individual peculiarities.

Chronic alcoholism, however latent it may be, however sedulously
concealed, warps the life of the individual in all its relations. In
its advanced degrees it amounts to mental and physical dyscrasia.
Between these extremes is every grade of incapacity and degradation.
It is beyond the scope of this article to discuss the moral, social,
or medico-legal bearings of this condition. Its purely medical
relations are sufficiently obvious from what has gone before. It has
been the writer's aim to make clear the existence and nature of the
continuing condition.

It remains to describe certain other psychical disturbances which
occur in chronic alcoholism, and which require separate consideration
for the reason that they are accidental rather than essential, many
cases running their course without their manifestation.

4. _Alcoholic Delirium in General_.—True alcoholic delirium,
presenting the traits about to be described, is never the result of
the direct primary action of alcohol upon the nervous system.
Transient excesses produce acute alcoholism, drunkenness, which,
varied as its manifestations are, differs essentially from that
peculiar delirium which occurs only in individuals in whom the nervous
system has undergone those nutritive changes that are brought about by
prolonged alcoholic saturation.

The most striking peculiarity of this delirium relates to the
hallucinations which attend it. These are almost invariably visual;
occasionally they are also auditory. Their objects, whether men,
animals, or things are in constant and unceasing motion, appearing and
disappearing, coming and going, and changing from place to place with
extreme rapidity. In this respect they differ from the hallucinations
of other forms of delirium, of which the objects are fixed and more or
less permanent. As a result of this peculiarity, the objects of
alcoholic delirium are almost invariably multitudinous, as swarms of
vermin, herds of animals, multitudes of demons, and the like.

A second peculiarity is the restlessness of the delirium. The patient
is invariably uneasy, apprehensive, always on the alert, declaring
that some calamity threatens him or that some evil is about to befall
him. In consequence of these apprehensions even momentary repose is
wanting. If he lies down for a moment, it is only to rise again and
peer under the bed {627} or into the corners, turning his head from
side to side in search of some realization of the fears that torment
him. This sense of apprehension impels the patient to hurry ever
onward from place to place in search of the repose which he nowhere
finds. It is increased to positive terror by the ever-varying and
constantly-renewed hallucinations which torment him, and from which he
seeks to escape, no matter how great the obstacles to be overcome.

A third peculiarity of alcoholic delirium is insomnia. This condition
is of the must marked and stubborn character, even continuing for
several days in succession.

5. _Delirium Tremens_.—This is the characteristic form of alcoholic
delirium, and, as is indicated by the name, is invariably accompanied
by tremor. It must be looked upon as an episode or epiphenomenon of
chronic alcoholism. It is rare that even prolonged temporary excesses
in persons ordinarily sober are followed by delirium tremens. Such
excesses in the subjects of chronic alcoholism are, however, perhaps
the most common cause of this condition. Orgies, especially when
associated with venereal excesses, very frequently terminate in
delirium tremens. Occasionally also, but much less frequently than was
formerly supposed, the abrupt discontinuance of alcohol is followed by
the outbreak. Other exciting causes are violent emotions, as anger or
fright; hardships, such as prolonged hunger, over-exertion, or
watching; acute maladies, as pneumonia, dysentery, erysipelas, the
exanthemata, or rheumatism; finally, serious traumatisms, with or
without great loss of blood. Delirium tremens usually occurs in those
addicted to the abuse of spirits, less frequently in beer-drinkers,
and comparatively rarely in those whose excesses have been restricted
to wine. The attack does not, as a rule, begin abruptly; its prodromes
usually consist in an exaggeration of the previously existing symptoms
of chronic alcoholism. The patient complains of malaise, restlessness;
he becomes depressed, morose, anxious without cause, apprehensive of
some calamity, or he is more impatient and choleric than before. The
ability to apply himself to his ordinary occupations is lost. He
complains of vertigo, ringing in the ears; sleep is disturbed, or
there is already insomnia. At the same time the stomach is deranged,
appetite is lost, the tongue is covered with a thick yellowish-white
fur, and there is constipation or diarrhœa. The period of prodromes
may last from a few days to a week.

The outbreak is characterized by delirium, without, at least in the
greater number of cases, absolute loss of consciousness. That is to
say, it is possible by addressing the patient with energy or by
strongly arousing his attention to interrupt the delirium and for a
moment recall the patient to himself. In the graver cases, however,
loss of consciousness appears to be complete. The subjective
impression of the delirium, as recollected at the termination of the
attack, is that of a sense of overwhelming confusion and inability to
recollect or co-ordinate the ideas that were crowding upon the brain.
The hallucinations, as has already been indicated, relate almost
exclusively to the organ of sight, more rarely to the hearing; also,
and exceptionally, to the other organs of sense. They are almost
always either terrifying or repugnant. The objects of the
hallucinations of the sight have already been described. They consist
of animals, serpents, and monsters, which crowd into the apartment,
coming {628} usually toward the patient, disappearing in the walls, in
the floor, under the bed, or among the bed-clothing. These visions are
usually aggressive, threatening the patient, throwing themselves upon
him, striking him, or tearing at his vitals. They are sometimes
replaced by phantoms, spectres of the most horrible character,
skeletons, death's-heads, or by flames which surround the patient and
threaten to consume him. Sometimes the hallucinations relate to the
daily occupation of the patient, and he pursues his tasks with a
feverish and distressing anxiety. These hallucinations are almost
invariably of the most fleeting, incoherent, and variable kind.

Auditory hallucinations occur usually in individuals of marked
neurotic tendencies. They are apt to be more coherent than the
hallucinations of vision, and are often of the nature of those which
occur in the delirium of persecution. Sometimes they consist of cries,
of chiding, of menacing voices, of the repetitions of obscene words
and suggestions; sometimes they are cries of horror or the roars of
animals, sometimes explosions or the discharge of firearms; or, again,
they are terrifying threats. Hallucinations of taste and smell are
much more rare, and occur in the subacute forms of delirium tremens.
The patient complains of annoying odors or disagreeable tastes, either
constantly present or upon the taking of food or drink. Disturbances
of general sensibility show themselves in hallucinations in regard to
sensations of pricking, burning, or tearing of the surface of the
body, or of animals or vermin crawling over the patient.
Hallucinations relating to the sexual instinct are far from rare. The
hallucinations of every form are apt to be more frequent and more
troublesome during the night than during the day.

Restlessness, fear, and anxiety are characteristic phenomena of
delirium tremens. The patient is not only terrified by the imaginary
objects which surround him, but often in their temporary absence he
experiences an equal degree of fear for which he can assign no cause.
It is to this condition of apprehension that is due the desire to
escape from his present surroundings which is so characteristic of the
delirium in question. Under its influence the patient occasionally
commits acts of violence of the most serious kind. Sometimes the
delirium is more quiet: the patient converses with individuals whom he
supposes to surround him; he busies himself with his familiar
occupations, giving orders, directing work, dictating letters, and
arranging his affairs. At other times the delirium takes the form of
apprehension of poisoning, and food and medicine are alike stubbornly
refused.

The countenance, as a rule, is animated, the eyes brilliant and
injected, the look fixed or peering, but always eager, or the
expression may be haggard and agitated. The physiognomy, although
largely influenced by the character of the delirium, may be said to be
in most cases characteristic.

Sensation is usually impaired; especially is this true of sensibility
to pain.

Tremor, although occasionally slight, may be said to be never wholly
absent. Sometimes it affects the muscles of all parts of the body;
more commonly it is limited to the hands, arms, tongue, and lips; less
frequently it manifests itself in the lower extremities. Slight tremor
may be increased by causing the patient to hold his hands extended
with the {629} fingers separated. The movements of the hands consist
of rapid rhythmical oscillations of nearly equal extent and duration.
The tongue is protruded with a rapid jerking movement, and withdrawn
with equal suddenness. It shows fibrillar trembling. The trembling is
increased by voluntary movement, and is ordinarily associated with
some loss of motor power. The gait is often hesitating and awkward;
movements of the upper extremities are executed with difficulty, and
speech is irregular and interrupted. The motor disturbances are
occasionally associated with choreiform movements or actual epileptic
convulsions.

Insomnia is a constant condition. It usually persists throughout the
attack, and occasionally proves troublesome for several weeks after
convalescence is in other respects complete.

In the absence of pulmonary complications the respiration is not
disturbed, save as a result of the restlessness and physical effort
which sometimes quicken it. The same statement is true of the pulse.
The action of the heart is usually enfeebled, and the first sound
weak. The temperature is normal. The skin is frequently bathed in
copious perspiration. There is complete loss of appetite, and in most
cases inability to retain food. Thirst is constant, often tormenting.
The tongue is sometimes moist, and coated with thick white or yellow
fur; sometimes hard and dry, sometimes red. The urine is scanty,
dark-colored, and sedimentary. It occasionally shows traces of
albumen. Constipation is the rule.

The duration of delirium tremens is from three to seven, or even ten
or twelve, days. The course of the attack is paroxysmal or remittent.
The symptoms usually undergo some improvement during the day, only to
become more urgent at night. The periods of remission are occasionally
marked by transient slumber; the recovery by prolonged and deep sleep.
But this is by no means the rule. Several varieties of delirium
tremens have been described by writers upon the subject. These are—the
grave form, characterized by violence of the motor disturbances,
aggravated delirium, and gravity of the general condition; the febrile
form, in which after the third or fourth day the temperature, without
pulmonary or other discernible complications, suddenly rises to 104°
F. or beyond that point, with great aggravation of the general
symptoms; the adynamic form, marked by failing heart-power, feeble or
imperceptible pulse, profuse sweats, collapse, stupor, which deepens
into coma and ends in death; and finally, the subacute form. Here the
patient is quiet, but restless. The delirium scarcely passes beyond
the limits of occasional wandering, and relates chiefly to matters
connected with the daily interests and occupations of the patient.
Tremor is more or less marked, and sleeplessness is stubborn.

The termination of delirium tremens is in—1, recovery; 2, in death; 3,
in the chronic form; and 4, in other forms of insanity.

1. Recovery.—Except in the grave forms recovery may be said to be the
rule. Occasionally ushered in by a prolonged, almost critical, sleep,
more frequently it takes place by gradual improvement. In the latter
case the remissions are more and more prolonged, and attended by
increasing repose alike of body and of mind, and by tendency to sleep.
The hallucinations become feebler and less tormenting, at length
recurring only in the evening or at night, and especially as the
patient is about {630} falling asleep. The anxiety and restlessness
grow less urgent, consciousness becomes more secure, the trembling
diminishes, and recovery is slowly established. The tremor is apt to
persist some days into convalescence.

2. Death.—This mode of termination is not very common in the ordinary
forms of delirium tremens. In the grave forms it is usual, sometimes
occurring suddenly, sometimes gradually from intensification of the
symptoms and failure of nervous power; or it may occur in consequence
of pulmonary, cerebral, or renal complications; finally, the fatal
termination is often due to the acute disease or the traumatism by
which the delirium tremens has been excited, and of which it is, in
fact, a complication.

3. Chronic Delirium Tremens.—This mode of termination, described by
Lentz, is rare. The acute phenomena subside; the restlessness and the
mental agitation diminish. Insomnia gives place to sleep, which is
light and disturbed by dreams and nightmare; most of the
hallucinations lose their activity and frequency, and finally
disappear. The changing delirium settles into a fixed delirium of
persecution; the tremor, while it becomes fainter, persists, and the
condition is permanent.

4. Other Forms of Insanity.—This mode of termination has been studied
especially by Magnan, who has classified the cases of delirium tremens
into three different groups, according to their tendency to recover or
to the development of mental alienation. The first group includes
those cases which run a favorable course and terminate in complete
convalescence; the second group, those cases in which the
convalescence is prolonged and characterized by repeated relapses; the
third group is composed of cases which likewise show a strong tendency
to relapse, but in which the delirium continues after the other active
symptoms have subsided. This form shows itself most frequently among
the subjects of hereditary alcoholism. After repeated attacks the
delirium becomes chronic. Morbid mental phenomena replace or accompany
symptoms more directly referable to organic disturbances of the
nervous system. Tremor gradually diminishes and disappears, the
gastric symptoms subside, insomnia passes away, even hallucinations
disappear, or at all events become infrequent; but the delirium which
developed coincidently with these symptoms continues, and finally
becomes chronic, losing to a great extent its original characteristics
and constituting a form of insanity. Finally, dementia constitutes an
occasional mode of termination in delirium tremens. It does not often
develop immediately, although cases of this kind have been recorded.
More commonly, the alcoholic subject, losing little by little his
mental activity after each attack of delirium tremens, subsides by
degrees into absolute and irremediable dementia. Paretic dementia may
also develop after prolonged alcoholic excesses characterized by
repeated attacks of delirium tremens.

The anatomical lesions after death from delirium tremens shed no light
on the pathogenesis of the condition. Meningeal congestion, œdema of
the pia mater and of the cortical substance of the brain, scattered
minute extravasations of blood, and some augmentation of the
cerebro-spinal fluid have been observed. In the greater number of
cases no lesions whatever beyond those characteristic of chronic
alcoholism have been discovered.

{631} 6. _Alcoholic Insanity_.—Among the psychical derangements, it
remains to notice briefly the more prominent forms of insanity which
develop in the course of chronic alcoholism, in consequence either of
hereditary or of acquired morbid mental tendencies. These are—_a_,
melancholia; _b_, mania; _c_, chronic delirium; _d_, dementia; _e_,
paretic dementia.

Alcohol is the most common of all the causes of insanity. Clouston[47]
estimates that from 15 to 20 per cent. of the cases of mental disease
may be put down to alcohol as a cause, wholly or in part. Those forms
of insanity in the production of which alcohol is merely an occasional
cause are not, however, properly included in the group of alcoholic
insanities. Still less are we to include in this group cases of
symptomatic dipsomania; that is to say, cases of insanity in which
morbid impulse to drink constitutes a prominent symptom of the
prodromic or fully-developed periods of various forms of mental
disorder.

[Footnote 47: _Clinical Lectures on Mental Diseases_, Am. ed., 1884.]

Alcoholic insanity manifests itself as an outcome of chronic
alcoholism, just as epileptic and hysterical insanity show themselves
as the outcomes of epilepsy and hysteria. This group properly includes
various forms of mania-a-potu, especially the maniacal form of acute
alcoholism, delirium tremens, and other transitory psychoses which
occur in acute and chronic alcoholism.

In truth, the mental derangements of ordinary drunkenness constitute
in many cases a form of transient insanity. These forms, have,
however, already been considered at sufficient length. Dipsomania, for
reasons already stated, cannot be regarded, either in its symptomatic
form or in its essential form, as belonging to the group of alcoholic
insanities.

_a_. Melancholia.—Melancholia is the most frequent form of true
alcoholic insanity. It may begin abruptly or gradually, with changes
of character, vague disquietude, great irritability, and disturbances
of sleep amounting in many cases to insomnia. Hallucinations of
hearing are characteristic. In this respect the morbid mental
condition in question is in strong contrast with delirium tremens, in
which the hallucinations are principally visual. The hallucinations of
hearing usually consist of accusing or threatening voices. These
voices inform the patient that he is to be poisoned, assassinated,
murdered, or that outrages of all kinds are to be committed upon him;
they accuse him of murder, of robbery, of rape, and of other shameful
crimes. Præcordial distress is also apt to be present. In consequence
of these hallucinations of hearing the patient falls into a profound
melancholia, often characterized by suicidal impulses which are
sometimes the direct outcome of hallucination, at other times blind
and unreasoning. There is apt to be cephalalgia and insomnia.
Trembling is not usually a marked symptom. Local anæsthesia and
hyperæsthesia, if they occur, are transient. The ordinary duration of
this form of alcoholic melancholia is much longer than that of
delirium tremens, sometimes extending throughout several months. The
termination usually is in recovery, less frequently in chronic
delirium.

_b_. Mania.—This form of alcoholic insanity is characterized by
various hallucinations which present peculiar characters. Thus, the
hallucinations of vision commonly relate to supernatural apparitions,
attended with luminous phenomena of various kinds. These visions may
be {632} occasional or they may be frequently repeated, or the
hallucinations may consist of images of emperors, kings, princes, and
potentates, or of military chieftains, in the midst of whom the
patient passes his existence. Or, again, the hallucinations may be
made up of historical scenes, pageants, the movements of armies,
battles, and the coronations of kings, or they may be landscapes
pleasant to the eye—snow-clad mountains, valleys filled with flowers,
magnificent forests, and the like. These phantasmagoria are by no
means fixed; on the contrary, they are of the most shifting character.

Auditory hallucinations are even more frequent, and quite as
changeable. They bear a more or less well-defined relationship to the
hallucinations of vision. They consist not rarely of promises of
money, honors, titles, and the like. Sometimes they are voices from
heaven, even the voice of God himself, commanding the patients to
perform definite acts and promising in return equally definite
blessings.

Hallucinations of general sensibility occur much less frequently. When
present, they consist of various painful sensations, giving rise to
the delusions of blows, stabs, bites of animals, electrical
discharges, etc. In consequence of these hallucinations the delusions
are often of a grandiose character. Patients believe themselves to be
God, the pope, or some great potentate, or enormously rich, etc.

The somatic condition depends upon the degree of chronic alcoholism
existing at the time of the manifestation of the mania. There are
usually marked tremor, hesitation and uncertainty of speech, stubborn
sleeplessness. Acute mania may show itself abruptly, attaining its
full development in the course of a few days, or the development may
be gradual. The prognosis in alcoholic mania is unfavorable;
recoveries are rare. The fatal termination is sometimes the result of
the maniacal condition itself, and sometimes the result of visceral
complications. This form of insanity occasionally terminates in
chronic delirium.

_c_. Chronic Delirium.—This form of alcoholic insanity is one of the
terminations of acute alcoholic melancholia and of acute alcoholic
mania. It is also one of the results of repeated attacks of delirium
tremens. Finally, it may develop independently of these affections.

Developing independently, chronic delirium is usually of rapid
invasion, and is characterized by the prodromes common to the various
forms of alcoholic insanity—irritability, headache, vertigo, insomnia,
etc. Hallucinations of hearing are very common, and relate principally
to the sexual life of the patient. Voices taunt him with the fact that
he is maimed or impotent; he hears persons whispering that he is about
to be castrated or that he is the subject of loathsome venereal
diseases, or they declare that he is known to be addicted to vile
crimes and bestiality. Hallucinations of sight are much less common;
those of the other special senses occasionally occur. The delirium
takes the form of delusion of persecution. The patient believes
himself the object of plots and conspiracies; his enemies are seeking
to ruin his good name, to tarnish his reputation, to poison him. They
put filth in his food or charge him with electricity; they steal away
his vital force or his sexual power; they taunt him; they mock him;
they beat him and rob him.

A delusion so frequent as to be almost characteristic of chronic {633}
alcoholic delirium relates to marital infidelity.[48] The patients
cherish unjust and often absurd suspicions of the virtue of their
wives. These delusions arise independently of hallucinations either of
sight or hearing, and are of the greatest importance, because they
supply logical motives for the most appalling and brutal crimes.

[Footnote 48: “The combination of a delusion of mutilation of the
sexual organs with the delusion that the patient's food is poisoned,
and that his wife is unfaithful to him, may be considered to as nearly
demonstrate the existence of alcoholic insanity as any one group of
symptoms in mental pathology can prove anything” (Spitzka, _Insanity_,
N. Y., 1883).]

Alcoholic delirium differs in the transitory and incoherent character
of its delusions from ordinary chronic delirium, in which the
delusions are much more apt to be fixed and permanent.

_d_. Dementia.—This is a common terminal condition of alcoholism. It
may develop, without the intervention of other forms of mental
disease, in the course of chronic alcoholism as a mere intensification
of the intellectual and moral degradation of that condition. This is
especially liable to occur in hereditary alcoholism. Dementia also
closes the scene in a considerable proportion of cases characterized
by repeated attacks of delirium tremens. It likewise constitutes the
terminal condition in other forms of alcoholic insanity.

The symptoms are sometimes so slight as to escape ordinary
observation. More commonly they are fully developed. As compared with
ordinary dementia, they present but little that is characteristic.
Alcoholic dements are perhaps more filthy and more difficult to
manage, duller and more mischievous, than others. Their somatic
disorders are more marked. In them hyperæsthesias are replaced by
anæsthesias; sleep is apt to be irregular and disturbed; the
hallucinations characteristic of the antecedent alcoholic psychosis
now and then reappear. Slowly-developing failure of intellect,
forgetfulness, stupor, end in more or less complete loss of mental
power. Nevertheless, a small proportion of the milder cases are
capable of arrest under treatment.

_e_. Paretic Dementia.—Alcoholism is an important etiological factor
in the production of this condition. The intellectual disorders and
motor disturbances which characterize it, varied as they are, are
associated with cerebral lesions, and especially with lesions of the
cortex equally varied—lesions which are common in chronic alcoholism.
These lesions vary from meningeal congestion and inflammation to
profound inflammatory and degenerative alterations in the cerebral
substance.

Paretic dementia may develop after long-continued excesses without
previous appreciable mental or cerebral symptoms. In such cases it
presents no specific indications of its alcoholic origin. The
difficulty of determining the influence of alcohol in its causation is
increased by the fact that alcoholic excesses—symptomatic
dipsomania—are frequent in the prodromic and early stages of this form
of mental disease. Paretic dementia may also develop after repeated
attacks of delirium tremens. Here the early attacks end in recovery
apparently complete; later, the convalescence is unsatisfactory and
prolonged, leaving some indications of intellectual enfeeblement,
which, after renewed attacks, increases, and is accompanied by
delusions of grandeur, embarrassment of speech, unequal dilatation of
the pupils, and general paresis. The prognosis is practically
hopeless.


{634} III. Hereditary Alcoholism.

This term has been used in a somewhat vague manner to designate the
morbid tendencies and pathological conditions directly transmitted by
alcoholic subjects to their offspring. Chronic alcoholism on the part
of one or both parents may be followed by morbid manifestations in the
child. The hereditary transmission of the effects of alcoholism has
been recognized from remote antiquity. Aristotle believed that a woman
given to drunkenness would bear children with the same tendency.
Plutarch affirms that the children of drunkards will abandon
themselves to the same vice. Hippocrates speaks of the distressing
effects of drunkenness upon the product of conception. Bacon states
that many idiots and imbeciles are born of drunken parents. In more
recent times the fact has been generally recognized that many maladies
caused by the abuse of alcohol are liable to be transmitted to
succeeding generations, and that alcoholism may in this way, in the
course of two or three generations, lead to the complete extinction of
families. Alcoholism on the part of the parents certainly exerts an
unfavorable influence upon the health of their children, who are
especially disposed to cerebral congestion, hypochondriasis,
intellectual feebleness, and insanity. Two forms of hereditary
alcoholism have been recognized: First, that in which the disease or
defect of the parent is transmitted to the offspring; and second, that
in which the disease or defect is not directly transmitted to the
offspring, but a morbid tendency which manifests itself in diseases or
defects of a different kind.[49]

[Footnote 49: 1. Heredite de similitude, Alcoolisme hereditaire
homotype; 2. Heredite de transformation, Alcoolisme hereditaire
heterotype.]

1. The appetite for strong drink is frequently transmitted from
parents to the children, just as other traits of the mind or body.
Sometimes it develops early, sometimes late in life; as a rule,
however, this hereditary propensity shows itself at an early age, and
is apt to be intensified at the time of puberty and the menopause.
Objections have been urged against the theory of hereditary
alcoholism. Among these the strongest is perhaps that the taste for
drink in the offspring of alcoholic subjects is the result rather of
opportunity and example than of heredity. The frequency with which
alcoholic tendencies develop themselves in children reared and
educated away from their parents, and the number of cases in which
these tendencies show themselves only at an advanced period of life,
long after the influence of example in childhood has ceased,
sufficiently disprove this assumption. The hereditary influence does
not, however, invariably manifest itself in the desire for drink. On
the contrary, not rarely it consists in feebleness of nervous
constitution, characterized by irritability, want of mental repose, or
a restless or vicious disposition which demands constant excitement.
Hence such individuals, although intellectually well developed, are
often scarcely more than moral imbeciles, in whom the passion for
drink may be replaced by the opium habit, addiction to gaming and to
other vices, and whose career is shaped largely by an inordinate and
insatiable craving for excitement of all kinds. Hereditary alcoholism
follows the laws of heredity in general. The tendency may be
transmitted directly from one generation to another, {635} or may skip
one or more generations, taking in the intermediate periods some
different form.

2. The second variety is that in which the symptoms of chronic
alcoholism are manifested in the offspring in the absence of the
direct action of alcohol; that is to say, not the taste for alcohol,
but the results of the gratification of that taste are transmitted,
just as epileptic or hysterical patients may transmit to their
offspring epilepsy or hysteria; thus it is not rare to encounter in
the descendants of alcoholic parents perverted sensation, both general
and special, hyperæsthesia, anæsthesia, flying neuralgias which do not
always follow the course of particular nerves, but frequently affect
in a general way the head or the members or manifest themselves as
visceral neuralgias. These persons are much troubled with headache
from slight causes and with migraine. Nor are disturbances of vision
rare, nor vertigo. Insomnia is also frequent in such individuals, and
augments the other symptoms. Digestive troubles also frequently occur,
notwithstanding a regular and perfectly temperate life. Such persons
are often subject to hallucinations of sight and hearing, and are
liable to have delirium in trifling illnesses.

The second form of hereditary alcoholism manifests itself in a wholly
different manner. The descendants, without a special appetite for
strong drink, and in the absence of the special morbid manifestations
above described, are singularly liable to mental and nervous diseases
of various kinds. Among these convulsions and epilepsy are especially
frequent; hysteria and various forms of insanity also occur. In this
group of cases we find every degree of arrest of intellectual
development, from mere feeble-mindedness to complete idiocy. As
manifestations of the influence of alcoholism upon the offspring may
be cited certain moral peculiarities otherwise inexplicable, such as
are seen in children who at a very tender age show themselves
vindictive, passionate, and cruel, to whom the sufferings of others
afford pleasure, who torment their companions and torture their pets,
and show precocious vicious tendencies of all kinds. Later in life
these persons become lazy, intolerant of discipline, vagabonds,
unstable of character, without the power of application and without
moral sense. Given to drink, defiant of law, they constitute the great
body of tramps, paupers, and criminals. The children of alcoholic
subjects are often feeble and puny, pale, badly nourished, and
curiously subject to morbid influences.


IV. Dipsomania.

Dipsomania, which has also been described under the term oinomania, is
rather a form of insanity than of alcoholic disease. The
characteristic symptoms are, however, in the greater number of
instances, due to indulgence in alcohol. The subjects of this
affection usually belong to families in which insanity, and especially
this particular form of insanity, is hereditary.

There are two forms of dipsomania—the essential and the symptomatic.
Of these, the latter is the more frequent. Its consideration requires
in this connection very few words. It manifests itself by an
irresistible desire on the part of many insane people for alcohol. It
occurs both in {636} the prodromic and in the fully-established
periods of insanity. It is especially common in various forms of mania
and in the prodromic periods of general paralysis. The dominating
influence in essential dipsomania is heredity. Occasional causes may
bring on particular attacks, but their influence is secondary.
Dipsomania cannot be looked upon as a distinct recurrent affection in
an otherwise healthy person. At some period in their lives, and often
long before the occurrence of characteristic paroxysms, dipsomaniacs
show peculiarities indicating defects of mental organization. Certain
symptoms of dipsomania are often mistaken for its cause. Thus,
dyspepsia is more frequently an effect than a cause of the alcoholic
excesses. The despondency, irritability, restlessness, hysterical
manifestations, and insomnia which precede the attack are not the
cause of it: they are its earliest symptoms.

The affection usually begins insidiously and is progressive. As a
rule, although not always, it begins in early adult life. The
manifestations of this disease are essentially intermittent and
paroxysmal, but the impulse to drink must be regarded as a symptom
which may be replaced by other irresistible desires of an impulsive
kind, such as lead to the commission and repetition of various crimes,
as the gratification of other depraved appetites, robbery, or even
homicide. The paroxysms are at first of short duration, and are
followed by return to the previous regular and decent manner of life.
They become, however, by degrees, more violent and more prolonged. At
first lasting for a few days or a week, by and by they extend to
periods of a month or six weeks, the attack wearing itself out, and
recurring with a periodicity sometimes variable and sometimes
constant. In the intervals of these attacks for a considerable time
the patients very often lead sober, chaste, and useful lives. At
length, however, evidences of permanent mental trouble are manifested,
and the case settles into confirmed insanity. The attack is usually
preceded by evidences of mental derangement; the patient becomes
restless and irritable; sleep is irregular and unrefreshing; he
complains of general malaise, and is anxious, troubled by vague
apprehensions. He presently abandons his usual occupations and gives
himself up to disordered impulses, among which alcoholic excesses are
the most frequent and the most easily gratified. Sometimes the patient
passes his time at taverns drinking with all comers; at others he
shuts himself up in a chamber and gratifies his desire for drink to
the most extreme degree alone. Dipsomaniacs not rarely leave their
homes and associates without warning or explanation, and pass the
period of the paroxysm among associates of the most disreputable
character. The desire for drink is gratified at all costs, and not
infrequently they return to their friends without money and without
sufficient clothing, most of it having been sold or pawned in order to
purchase drink. The paroxysm is succeeded by a period of more or less
marked mental depression, during which the patient not rarely
voluntarily seeks admission to some asylum.

The true nature of dipsomania is frequently overlooked. As a symptom
of hereditary insanity it is in striking contrast with the habitual
propensity to drink which occurs in the ordinary alcoholic subject.
The latter seeks occasions to drink. He renews his excesses not
intermittently, but habitually. If in consequence of disgrace or
misfortune or under strong moral suasion he is for a time abstemious,
it is only to renew and to {637} continue his indulgence upon the
first favorable occasion. On the contrary, the true dipsomaniac
recognizes his malady and struggles against it. Even more: for a time
he shows much skill in concealing it. He avoids occasions to drink,
and, reproaching himself for his mad and unreasonable desire, seeks by
every means to overcome his impulse to it. The ordinary drunkard may
become insane because he drinks; the dipsomaniac drinks because he is
insane.[50]

[Footnote 50: Magnan, _Le Progrès médical_, 1884.]

Dipsomaniacs are apt to manifest precocious or retarded intellectual
development. They are from infancy or childhood especially prone to
convulsive or other paroxysmal nervous phenomena. They are often
choreic, often hysterical. This association with instability of the
nervous system is related to the fact that dipsomania is more common
in women than in men.

       *       *       *       *       *

DIAGNOSIS.—1. Acute Alcoholism.—The diagnosis of the ordinary form of
acute alcoholism, with the exception of alcoholic coma, requires no
consideration. The diagnosis of alcoholic coma from profound coma due
to other conditions is, in the absence of the previous history of the
case, always attended with difficulty, and is in certain cases quite
impossible. It is therefore of great practical importance to obtain
the history where it is possible to do so. The odor of alcohol upon
the breath is of less positive diagnostic value than would at first
thought appear. In the first place, sympathetic bystanders may have
poured alcoholic drinks down the throat of one found unconscious, or,
in the second place, individuals who have taken a certain amount of
drink may be, and not unfrequently are, seized with apoplexy in
consequence of the excitement thereby induced. The more common
conditions with which alcoholic coma is confounded are apoplexy from
cerebral hemorrhage and narcotic poisoning, especially
opium-poisoning. To these may also be added uræmic coma and, under
exceptional circumstances, sunstroke. In all these cases the
circumstances under which the individual has been found are of
diagnostic importance.

In alcoholic coma the pupils are more commonly dilated than
contracted, the heart's action feeble, the respiration shallow, the
muscular relaxation symmetrical, and the temperature low. There is a
strong odor of alcohol upon the breath.

In apoplexy from cerebral hemorrhage the condition of the pupils will
depend upon the location of the clot. They may be moderately dilated,
firmly contracted, or unequal. The enfeeblement of the heart's action
is, as a rule, less marked than in profound alcoholic coma. The pulse
may be small or full and slow or irregular. It is usually slow and
full. The respiration is often, although not invariably, slow and
stertorous. Not uncommonly, the eyes and also the head deviate from
the paralyzed side. If the coma be not absolute, the muscular
relaxation is unilateral. The temperature is at first slightly below
the normal, but less, as a rule, than in alcoholic coma; after several
hours it rises to or above the normal.

In complete opium narcosis the insensibility is profound; the heart's
action is slow or rapid, but feeble; the respirations slow and shallow
or quiet or stertorous; the face at first flushed, afterward pallid
and cyanosed; the pupils minutely contracted or dilated as death
approaches; {638} and the muscular relaxation complete, with abolition
of reflex movements. In cases of doubt it is important to use the
stomach-pump.

Uræmic coma is apt to be preceded by or alternate with convulsions.
The pupils are more commonly slightly contracted than dilated, but are
without diagnostic significance. The temperature is not elevated; it
may even be low. The face may be pallid, pasty, and puffy, and there
may be general anasarca if the nephritis be parenchymatous. On the
other hand, in interstitial nephritis there is hypertrophy of the
heart, without evidence of valvular disease, and some degree of
puffiness of the lower extremities. In doubtful cases the urine should
be drawn by a catheter and subjected to chemical and microscopical
examination.[51] Diabetic coma occurs suddenly without convulsions.
This condition may be suspected when the emaciation is extreme or upon
the recognition of sugar in the urine.

[Footnote 51: The following is the method recommended by Green
(_Medical Chemistry_, Philadelphia, 1880) for the detection of alcohol
in the urine: If its reaction be acid, the urine is exactly
neutralized by potassium acid carbonate. It is then distilled on a
water-bath in a flask or retort connected with a condensing apparatus.
When about one-sixth of the liquid has passed over the distillate
will, if alcohol be present, present the following characteristics:
first, the peculiar alcoholic odor; second, a specific gravity lower
than water; third, upon being mixed with dilute sulphuric acid and
treated with a few drops of potassium bichromate solution the liquid
becomes green, owing to the separation of chromic oxide; the odor of
aldehyde may at the same time be observed. This reaction is not
characteristic, but may serve to confirm other tests. Fourth, if
dilute alcohol be shaken with an excess of solid and dry potassium
carbonate in a test-tube, the greater part of the water will be
appropriated by the potassium carbonate, and two layers of liquid will
be formed. The alcohol constitutes the upper layer, and if
sufficiently concentrated will burn upon the application of a flame.
Finally, a small trace of alcohol may be separated from the urine
without difficulty after the ingestion of alcoholic liquids by means
of a good fractionating apparatus. Less than 1 per cent. of alcohol
cannot be detected.]

Sunstroke is characterized by dyspnœa, gasping respiration,
jactitation, and intense heat of the skin. The pulse varies. It may be
full and labored or feeble and frequent. The face is usually flushed.
The pupils, at first contracted, are afterward dilated. The coma is
apt to be interrupted by transient local or general convulsions.

It is impossible to lay down any rules by which the maniacal form of
acute alcoholism may be at once diagnosticated from acute mania from
other causes. For the characteristics of the convulsive form of acute
alcoholism and those forms which occur in persons of unsound mind the
reader is referred to the descriptions of those conditions. The
diagnosis of acute poisoning by alcohol in lethal doses can only be
established during life by investigation of the history of the case.

II. Chronic Alcoholism.—The lesions of chronic alcoholism, as has
already been pointed out, are not in themselves peculiar to that
condition. Many of them occur with more or less frequency in morbid
states not induced by alcohol. It is their association and progressive
character which gives to chronic alcoholism its individuality. The
occasional prominence of certain symptoms or groups of symptoms may
thus in particular cases lead to some confusion of diagnosis,
especially where the history is unknown or the habits of the
individual are concealed. In the greater number of cases, however, the
association of symptoms is such as to render the diagnosis, even in
the absence of a direct history, a comparatively easy one.

Chronic alcoholism is a condition rather than a disease—a condition
{639} characterized by varying lesions of the viscera and nervous
system, by profound disturbances of nutrition, and by grave mental and
moral derangements. This fact being recognized, the cardinal error of
diagnosis to be guarded against is that of overlooking the condition
upon which the disease itself with which we have to do depends or is
associated. Congestion, inflammation, sclerosis, and steatosis affect
the various organs of the body and produce their characteristic
symptoms. Profound and lasting disturbances of nutrition demand our
attention. Psychical derangements of all grades, from mere moodiness
to confirmed and hopeless insanity, take place. These affections must
be diagnosticated for themselves here as elsewhere in clinical
medicine. The recognition of the underlying condition can, however,
alone supply the key to their true pathology.

Delirium tremens is occasionally diagnosticated with difficulty from
some forms of insanity not caused by drink. Here transitory and fixed
delusions, not mere terrors and hallucinations, are of importance, not
less than the absence of the varied and complex associations of
symptoms which are characteristic of alcoholism. The delirium of the
acute infectious diseases may be mistaken for delirium tremens.
Pneumonia, typhoid fever, and the exanthemata occasionally begin with
delirium resembling in some respects delirium tremens. Here the
history of the case, the pyrexia, and the general condition of the
patient are sufficient to establish the diagnosis if the danger of
error be borne in mind.

III. Hereditary Alcoholism.—The diagnosis of this condition can only
be established by careful investigation of the family history and
systematic study of the stages of progression by which the morbid
condition presented by the patient has been reached.

IV. Dipsomania.—The diagnostic points are the hereditary transmission
of this or other forms of insanity—the mental instability of the
patient in early life and in the intervals of the paroxysms, the
intermittent or cyclical recurrence of the attack, the morbid impulses
of a different kind associated with the impulse to drink, and the
struggle of the patient against his recurring impulses to
uncontrollable excesses.

PROGNOSIS.—The prognosis in acute alcoholism of the ordinary form is
favorable, so far as the immediate attack is in question. The
prognosis in rapidly-developing, overwhelming coma from enormous doses
of alcohol is in the highest degree unfavorable. Acute coma from
moderate doses usually passes off in the course of some hours. It
occasionally, however, terminates in fatal pneumonia.

The prognosis in delirium tremens of the ordinary form is favorable.
It becomes, however, more and more grave with each recurring attack.
Delirium tremens in patients suffering from advanced disease of the
heart, lungs, liver, or kidneys, or complicated by acute diseases of
these organs, is apt to prove fatal.

The prognosis of chronic alcoholism is gloomy. If the lesions be not
advanced, permanent discontinuance of alcoholic habits may be followed
by restoration of health, but, unfortunately, the discontinuance is
too often merely temporary, the habit being too strong to be
permanently broken off.

The prognosis in hereditary alcoholism is unfavorable, both as regards
the alcoholic habit and as regards the development of serious diseases
of {640} the nervous system under adverse circumstances, even in the
absence of the direct action of alcohol.

The prognosis in dipsomania is unfavorable. The paroxysm may recur
many times without apparent serious result; the patient in the course
of some days or weeks recovers, abandons his evil courses, and resumes
his usual occupations. After a time, however, the insanity of which
the dipsomania is the recurring manifestation declares itself as a
more or less permanent state. The outbreaks become more frequent and
more prolonged, the mental condition in the intervals progressively
more morbid, until the patient lapses by degrees into confirmed
insanity.

The prognosis in all forms of alcoholism, both acute and chronic, is
rendered in a high degree uncertain by the psychical disorders which
characterize so many of its phases. In consequence of some of these
conditions the patient loses at once his appreciation of bodily
dangers and his power to avoid them; by reason of others, to escape
imaginary evils he plunges into real ones; and finally some of them
are of such a nature that they impel him to the blind and unreasoning
commission of the most grievous crimes, including suicide and
homicide.[52]

[Footnote 52: “I believe that more suicides and combined suicides and
homicides result in this country from alcoholism in its early stages
than from any other cause whatsoever” (T. S. Clouston, _Clinical
Lectures on Mental Diseases_, Am. ed., 1884).]

TREATMENT.—The prophylaxis of alcoholism has regard to communities at
large and to individuals. The prevention of the evils of excess by the
control of the sale of drink constitutes one of the more important
objects of state medicine. At the same time, the traffic in alcohol is
curiously evasive of legal enactments. The difficulties attending the
enforcement of sumptuary laws are well known. Restrictive laws
concerning the making and sale of alcoholic drinks, while partaking of
the nature of sumptuary laws are of more comprehensive character,
being obnoxious to powerful commercial interests and to the sense of
personal liberty of large numbers of persons of all classes. As a
result of organized opposition and individual violation they are to a
great extent inoperative as regards the prevention of alcoholism.

Aside from the question of revenue from taxation, the practical
influence of law is in this matter somewhat limited, being confined
chiefly to the prevention of the sale of liquors to minors and persons
already intoxicated, and to ineffectual attempts in certain countries
to regulate the quality of the drink sold. The penalties for personal
drunkenness which does not lead to overt acts are, as a rule, wholly
inadequate to restrain it. The best results upon anything like an
extended scale have been obtained by the co-operative action of
philanthropic individuals in endeavoring to influence the moral tone,
especially among workingmen, to diminish temptations, and to provide
for leisure hours, in the absence of drink, reasonable amusements and
occupation to occupy the time ordinarily spent in taverns and similar
places.

The decrease in the consumption of alcoholic drinks in the United
States within recent years is doubtless due in part to increasing
popular knowledge concerning the dangers of alcoholic excess and to
the growth of a more wholesome public sentiment. It is, however, in
part also due to poor wages among workingmen.

As regards the individual, prophylaxis against alcoholism consists
{641} either in total abstinence from, or in the most guarded
indulgence in, alcoholic beverages. It is unfortunate that individuals
whose moral and physical organization is such as renders them most
liable to suffer from the consequences of alcohol are by that very
fact most prone to its temptations, and hence contribute largely to
the subjects of alcoholism. These individuals are found among the
ignorant, the very poor, and especially among neurotic subjects of all
classes of society. Due consideration of this fact cannot fail to
establish the responsibility of those fortunately not belonging to
these classes, in two respects: first, that of example; and second,
that of personal restraint from the standpoint of heredity. The
influence of heredity among races addicted to alcohol has not yet
attracted the attention it deserves. It is probable that much of the
tolerance for alcohol exhibited by individuals, families, or even
nations, is to be accounted for by heredity. Still more probable is it
that most of the evils and crimes that befall alcohol-drinking
communities and individuals are due directly or indirectly to the
abuse of this agent. No argument against the indulgence in narcotics
can be more potent than that derived from a consideration of the laws
of heredity.

I. The Treatment of Acute Alcoholism.—The medical treatment of mere
drunkenness requires no consideration. The rapid elimination of
alcohol, and the transient nature of its pathological effects in
excesses which are not repeated or prolonged, explain the spontaneous
recovery, which is usually sufficiently prompt and permanent. The
physical suffering and mental distress following unaccustomed excesses
are of salutary influence. Under certain circumstances a powerful
effort of the will is sufficient to control, at all events for a time,
the more moderate effects of alcohol. A similar result follows the use
of cold douches, the Turkish bath, and full doses of certain
preparations of ammonium, particularly the officinal solution of the
acetate of ammonium. In alcoholic stupor of an acute kind the patient
may be left to himself, care being taken that the clothing is loosened
and that the position is such as to prevent local paralysis from the
nerve-pressure. Alcoholic coma, if of moderate intensity, may be
managed in the same way. Profound alcoholic coma requires, however,
more energetic measures. Frictions, artificial warmth, stimulating
enemata, as of turpentine or of hot salt and water, an ounce to the
pint, hypodermic injections of strychnia or atrophia in minute doses
and occasionally repeated, inhalations of ammonia, and occasional cold
affusions, followed by brisk frictions with warm flannel and faradism
of the respiratory muscles, may be needed to tide over the threatened
fatal collapse. The stomach should be at once washed out with hot
coffee.

In the convulsive form of acute alcoholism chloral in twenty-grain
doses, repeated at intervals until sixty grains have been given,
usually serves to arrest, or at all events to moderate, the paroxysm.
It may be administered by the mouth or in double doses by the rectum.
If chloral be inadmissible by reason of weakness of the circulation,
paraldehyde may be substituted in doses of from half a drachm to one
drachm, repeated at intervals of from one to two hours until quietude
is produced. Where the convulsive paroxysms are of great violence it
may be necessary to control them by the cautious administration of
ether by inhalation.

The mania of acute alcoholism calls for energetic management. To {642}
avert injury to the patient himself or to those about him he must be
confined, if practicable, in a suitable apartment in a hospital; if
not, in his own house and carefully watched. Here, as a rule,
paraldehyde, chloral, or large doses of the bromides constitute our
most efficient means of medication.

In all forms of acute alcoholism it is a rule admitting of no
exception to at once withhold alcohol in every form and all doses. If,
under exceptional circumstances, great nervous depression or flagging
circulation seems to call for the use of alcohol in small amounts, it
is far better to substitute other drugs. The frequently repeated
administration of hot beef-tea or rich broths in small doses, with
capsicum and the use of the various preparations of ammonia, or small
doses of opium with or without quinia and digitalis, proves useful in
proportion to the skill and discrimination with which they are
selected and repeated. It is a good plan to commence the treatment
with an active purge.

In the acute collapse following excessive doses—lethal doses—the
stomach is to be immediately emptied by the tube or pump and washed
out with warm coffee. In the absence of the stomach-tube emesis may be
provoked by the use of mustard or sulphate of zinc or by hypodermic
injection of apomorphia. The patient must be placed in the recumbent
posture and surrounded with hot blankets. The cold douche may be
occasionally applied to the head and face, and the muscles of
respiration may be excited to action by faradism. Artificial
respiration and friction of the extremities may also be required.
Inhalations of ammonia may be used. The flagging heart may be
stimulated by occasionally tapping the præcordia with a hot
spoon—Corrgan's hammer. Hypodermic injections of digitalis may also be
employed. Overwhelming doses of alcohol, leading promptly to collapse,
usually prove fatal despite all treatment.

II. The Treatment of Chronic Alcoholism.—Whatever may be the
prominence of particular symptoms or groups of symptoms, whether they
indicate derangement of the viscera, of the nervous system, or of the
mind, whatever their combination, the fundamental therapeutic
indication in chronic alcoholism is the withdrawal of the poison. The
condition is directly due to the continuous action of a single toxic
principle: its relief when practicable, its cure when possible, are
only to be obtained by the discontinuance of that poison. This is a
matter of great, often of insurmountable, difficulty. The obstacles
are always rather moral than physical. Occasional or constant
temptation, the iron force of habit, the malaise, the faintness, the
craving of the nervous system, and, worse than all, the enfeebled
intellectual and moral tone of the confirmed drunkard, stand in the
way. Even after success seems to have been attained, and the patient,
rejoicing in improved physical health and in the regained
companionship and consideration of his family and friends, feels that
he is safe, it too often happens that in an unguarded moment he yields
to temptation and relapses into his old habits. A patient of the
writer, after seven years' abstinence from drink, again became its
victim in consequence of the incautious suggestion of a young medical
man, met at a summer hotel, to take brandy for some transient
disorder, and died after eight months of uncontrollable excesses. It
is necessary to guard the patient against the temptation to drink. To
secure this he may he sent as a voluntary patient for a length of time
to a suitable institution, {643} or, still better, he may place
himself under the care of a conscientious, clear-headed country doctor
in a sparsely-settled region, preferably in the mountains or at the
seaside. The malaise, depression, insomnia, and other nervous symptoms
when of moderate degree are best treated by abundance of nutritious
and easily-assimilable food, taken often and in moderate amounts. To
this end gastro-intestinal disturbances may be practically
disregarded, except in so far as they regulate the selection of a
highly nutritious diet. As a matter of fact, in the early periods of
chronic alcoholism, while visceral lesions of a grave character are
yet absent, appetite and digestion alike improve in the majority of
cases upon the withdrawal of alcohol, provided a sufficiently abundant
and easily assimilable dietary is insisted upon. Grave visceral
lesions characterize a more advanced alcoholic cachexia and
necessarily complicate the treatment. Nevertheless, even here the
indication is the withdrawal of the poison. The nervous symptoms
require special medication. The whole group of tonics, from simple
bitters to quinia and strychnia, is here available. It is impossible
to lay down rules for the treatment of particular cases except in the
most general manner. In the absence of conditions calling for special
treatment, such as gastritis, hepatic or pulmonary congestion, fatty
heart, etc., good results follow the frequent administration of small
doses of quinia and strychnia; thus, the patient may take one grain of
quinia six or eight times a day, or a little gelatin-coated pill
containing 1/200-1/100 of a grain of strychnia every hour during the
waking day, amounting in all to one-twentieth, one-tenth, or one-fifth
of a grain in the course of twenty-four hours. This treatment is often
followed by the relief of tremor, the quieting of nervous
irritability, and the production of good general results. The malaise,
the general depression, and especially the sinking feeling at the pit
of the stomach so often complained of by patients, are best relieved
by food. Fluid extract of coca is also useful in these conditions. The
value of cocaine in the management of the nervous symptoms of chronic
alcoholism, and in particular as a temporary substitute for alcohol,
is doubtful. The writer, having used it in a number of cases by the
mouth and hypodermically in doses of ¼-1 grain, has had variable
results. In some cases it temporarily relieved the craving and
concomitant symptoms; in others it failed wholly: in one instance
one-fourth of a grain was followed by great nervous depression. It is
desirable not to inform the patient of the nature of the remedy,
especially if its use be followed by good results, lest the cocaine
itself supplant alcohol as an habitual narcotic. Cold or tepid
sponging, the occasional hot bath at bedtime, and the Turkish bath are
useful adjuvants to the treatment. As a rule, opium is
contraindicated. Sleep often follows the administration of a cupful of
hot broth or milk at bedtime. Lupulin is here useful, and the writer
has come to regard an ethereal extract of lupulin in doses of from one
to three grains as a valuable and harmless hypnotic. If necessary,
hypnotic doses of chloral or paraldehyde may be used, but care is
required in their administration, and their early discontinuance is
advisable. If anæmia be profound, chalybeate tonics do good, and among
the preparations of iron pills of the dried sulphate with carbonate of
potassium (Blaud's pills) are especially useful.

The obesity of drunkards, as a rule, diminishes on the withdrawal of
alcohol. Under circumstances of partial or complete abstinence from
{644} drink measures to reduce the weight of such patients are wholly
inadmissible.

In conditions characterized by failure of mental power, in beginning
dementia or threatened insanity, the syrup of the hypophosphites, the
compound syrup of the phosphates, or cod-liver oil should be
administered. These remedies are likewise useful in various forms of
alcoholic paralysis, as are also faradism and galvanism employed
secundum artem. The various forms of alcoholic insanity require
special treatment, only to be had in institutions designed for the
care of patients suffering from mental diseases in general.

Whilst it is desirable in the treatment of all forms of chronic
alcoholism to secure the permanent discontinuance of the alcoholic
habit, the skill, judgment, and experience of the physician must
determine the degree of rapidity with which this, when practicable, is
to be done. The number of cases in which alcohol can be discontinued
at once and finally is limited; those in which it can be wholly given
up in the course of a few days constitute the largest proportion of
the cases; finally, in a small number of cases alcohol can only be
withdrawn cautiously and by degrees.[53] Whilst it is in most cases
essential to remove the patient from his customary surroundings and
companionships, it is in the highest degree important to provide for
him mental occupation and amusement. To this end a wholesome open-air
life, with sufficient daily exercise to induce fatigue, is highly
desirable, as indeed is the companionship of interested and judicious
friends.

[Footnote 53: It must be borne in mind that in chronic alcoholism
acute maladies of all kinds, including traumatism, both accidental and
surgical, act as exciting causes of delirium tremens. The part played
by the abrupt diminution or withdrawal of alcohol under such
circumstances is often an important one. It is the opinion of the
writer that a certain amount of alcohol should be administered for a
time at least in the accidental injuries and acute sicknesses of
alcoholic subjects, and that the reduction should be gradually made.]

The Treatment of Delirium Tremens.—The patient should be confined in a
large, well-aired apartment, without furniture except his bed, and
when practicable he should have a constant attendant. The favorable
influence of a skilful nurse in tranquillizing these patients is very
great. The custom of strapping them to the bed by the wrists and
ankles is to be deprecated. If the case be a mild one, and especially
during convalescence, open-air exercise in the sunshine with an
attendant is of benefit; care must, however, be taken to guard against
the danger of escape.

Under no circumstances should visitors be permitted to see the
patient. In young persons the treatment may be preceded by an active
saline or mercurial purge. In elderly persons, those suffering from
cachectic conditions, or in cases characterized by marked debility and
feeble circulation—conditions frequent in persons who have had
repeated attacks—it is not desirable to purge. Alcohol should be
either wholly withdrawn or more or less rapidly diminished. It must be
replaced by abundant food in the form of concentrated broths or
meat-extracts. In cases of vomiting these must be given hot and in
small doses frequently repeated. Bitter infusions may also be given,
or milk or equal parts of milk and Vichy water. If there be thirst,
the effervescent waters may be given freely. Patients often drink with
satisfaction and apparent benefit hop tea, which may be made simply
with water or with equal parts of water and porter.

{645} The medicinal treatment will depend to a large extent upon the
peculiarities of the case. In mild cases a combination of the watery
extract of opium in small doses, not exceeding a quarter of a grain,
with quinia and digitalis, repeated every four or six hours, is often
useful. Although the view once entertained that the graver symptoms
were the result of prolonged sleeplessness is no longer tenable, the
induction of sleep, or at all events of mental and physical repose, is
among the more important therapeutical indications. For this purpose
hypnotic doses of opium are not only not desirable, but are even, in
the majority of instances, attended with danger. The sleep which
follows repeated and increasing doses of opium in delirium tremens has
too often terminated in coma deepening into death. As calmatives,
extract of cannabis indica, hyoscyamus, or the fluid extract of
piscidia are useful. As hypnotics, the bromides, chloral, and
paraldehyde yield, in the order here given, the best results. The
bromides are better in large single doses than in small doses often
repeated, better in combination than singly. Chloral, either by the
mouth or by the rectum, in doses of from twenty to forty grains, is
often followed by beneficial sleep. It is contraindicated where the
heart's action is much enfeebled. Paraldehyde, in doses of half a
drachm to one drachm, repeated at intervals of two or three hours
until sleep is induced, is still more efficient. This drug may be
administered without the fear of its exerting a depressing influence
upon the heart. The depression characteristic of grave delirium
tremens may be combated by repeated small doses of champagne or by
carbonate of ammonium in five- or ten-grain doses; the vomiting, by
withholding food and medication by the mouth, and giving them for some
hours wholly by the rectum or hypodermically. Excessive restlessness
is sometimes favorably influenced by cold affusion, followed by brisk
friction and warm blankets with continuous artificial heat. The cold
pack has proved useful.

Digitalis may be employed, ex indicatione symptomatica, but the
enormous doses of tincture of digitalis used by the late Jones of
Jersey and others are here mentioned only to be condemned.

To sum up, the chief indications for treatment are complete isolation,
the withdrawal of alcohol, abundant, readily assimilable, nutritious
food, and control of the reflex excitability of the nervous system.

III. Hereditary Alcoholism.—The treatment of the vicious propensities
of the descendants of alcoholic parents does not fall directly within
the province of the physician. It is among the most difficult problems
of education. The recognition of the cause of evil traits manifested
in childhood and youth may do something to avert dangers commonly
unsuspected. All things considered, the outlook is not hopeful. The
recognition, on the part of the physician, of the influence of
hereditary alcoholism in cases of arrested development, feeble
organization, or declared disease of the nervous system will perhaps
do less to aid his treatment in many cases than to reconcile him to
its want of full success. The cry of warning is to those who are
eating sour grapes that the teeth of their children will be set on
edge.

IV. Dipsomania.—The general indications for the treatment of
dipsomania are two: first, the management of the paroxysm; second, the
control of the general condition itself.

First, then, during the paroxysm the patient must be saved, in so far
{646} as is possible, from the danger of injuring himself or others
and from squandering his property. If the excesses are of such a
degree as to render it practicable, the same treatment must be carried
out as in cases of acute alcoholic mania and delirium tremens—namely,
confinement in a suitable apartment under the care of an experienced
nurse and the control of the doctor. Unfortunately, this plan is not
always practicable in the early days of the outbreak. Here tonics,
coca, and repeated small doses of quinia and strychnia are of
advantage. Courses of arsenic at the conclusion of, and in the
intervals between, the paroxysms are of use, on account of the
excellent influence they exert on the general nutrition. These may be
advantageously alternated with iron, cod-liver oil, and the compound
syrup of the phosphates or of the hypophosphites. Hydrotherapy may
also be used with advantage, and the influences of a well-regulated
hydropathic establishment are much more favorable than those of
institutions specially devoted to the treatment of alcoholic subjects.
In the latter the moral atmosphere is apt to be bad; the patients
support each other, and too often conspire to obtain in secret that
which is denied them openly, or, if the discipline be too strict for
this, they sympathize with each other in their restraint, react
unfavorably upon each other in the matter of shame and loss of
self-respect, and plot together to secure their liberty.

Few dipsomaniacs in the earlier periods are proper subjects for
treatment in hospitals for the insane. If cerebral excitement or
sleeplessness persist after the paroxysms, chloral, paraldehyde, or
the bromides in large doses may be used to secure sleep. Various
combinations of the bromides are often of use where the single salts
fail. It must not be forgotten that during the paroxysm there is great
danger lest the patient do himself or others harm. When there are
indications of an impending attack, and during the period of
depression following the attacks, benefit is derived from the daily
use of bitter infusions. As a matter of fact, however, the management
of these cases is among the most unsatisfactory of medical
undertakings. The difficulty is increased by the latent character of
the mental disorder in the intervals between the attacks. Even when
such patients voluntarily enter hospitals for the insane, they cannot
be retained there sufficiently long to derive any permanent benefit.
What we want is, in the words of Clouston, “an island where whiskey is
unknown; guardianship, combined with authority, firmness,
attractiveness, and high, bracing moral tone; work in the open air, a
simple natural life, a return to mother Earth and to Nature, a diet of
fruits, vegetables, bread, milk, eggs, and fish, no opportunity for
one case to corrupt another, and suitable punishments and deprivations
for offences against the rules of life laid down. All these continued
for several years in each case, and the legal power to send patients
to this Utopia for as long a period as medical authority determines,
with or without their consent.”


{647}


THE OPIUM HABIT AND KINDRED AFFECTIONS.

BY JAMES C. WILSON, M.D.


Next in order to alcohol, opium and morphine are habitually abused to
a greater extent than any other narcotic. Chloral is used in the same
way by a large number of individuals. Paraldehyde, cannabis indica,
ether, chloroform, and cocaine are also used to a less extent. The
scope of this article does not include the consideration of acute
poisoning by these drugs.

The habit of taking narcotics, whether medicinally or as a mere matter
of indulgence, is apt speedily to become confirmed. The physiological
dose more or less rapidly loses its power to affect the nervous system
in the ordinary way. Tolerance increases with increasing doses, and in
a comparatively short space of time poisonous doses are taken with
impunity as far as immediate danger to life is concerned. The toxic
effects of the poison are shown in characteristic perversion of the
functions of the nervous system and of the mind. A condition is
established in which the ordinary functions of life are properly
performed only under the influence of the habitual narcotic, and in
which its absence results in languor, depression, and derangement of
bodily and mental processes. The habit, once established, thus makes
for itself a constantly recurring plea for its continuance. Especially
is this true of opium and morphia.


Opium and Morphine.

Opium-eating is chiefly practised in Asia Minor, Persia, and India. It
is also prevalent in Turkey. It has been practised in India from very
ancient times. The prevalence of this habit in the East is probably
largely due to the restrictions placed upon the use of alcoholic
beverages among the Mohammedans, and to some extent also to the long
religious fasts observed by the Buddhists, Hindoos, and Moslems,
during which opium is often used to allay the pangs of hunger. The
prevalence of the opium habit in India is shown by the fact that the
license fees for a single year amounted to nearly five hundred
thousand pounds sterling. It is stated that in Samarang, a town of
1,254,000 inhabitants, the average quantity of opium consumed monthly
is 7980 pounds. The town of Japava, with 671,000 inhabitants, consumed
in fifteen days 5389 pounds {648} of opium. In 1850, 576,000 pounds of
opium were imported into Java, besides an unknown quantity
smuggled.[1]

[Footnote 1: _Archiv für Pharmazie_, 1873, cited by Von Beck,
_Ziemssen's Cyclopædia_, vol. xvii.]

The habit is not confined to Oriental countries, but is also practised
in various forms in the West. It is by no means rare on the continent
of Europe. In certain districts of England, especially in Lincolnshire
and Norfolk, more opium is consumed than in all the rest of the United
Kingdom. Shearer[2] states that the increase in the practice of
opium-eating among the workpeople of Manchester is such that on
Saturday afternoons the druggists' counters are strewed with pills of
opium of one, two, and three grains, in preparation for the known
demand of the evening. The immediate occasion is said to be the
lowness of wages, opium being used as a cheap substitute for alcohol
or as a food substitute, or with the view of removing the effects of
disease and depression. According to the same observer, laudanum is
more or less in use as a narcotic stimulant in the cotton-spinning
towns, where female labor is in requisition and is well paid. Children
are accustomed to it from their earliest infancy. Their parents drug
them with daily potions of Godfrey's cordial, Dalby's carminative,
soothing syrup, and laudanum itself, during the long hours of their
absence from home. While the habit of opium-eating cannot be said to
be generally prevalent in any part of the United States, instances of
it are frequently encountered in all classes of society, and
particularly among people of means and refinement. The preparations
employed in this country are crude opium, tincture of opium or
laudanum, camphorated tincture of opium or paregoric, McMunn's elixir,
Dover's powder, and the salts of morphia. All of these preparations
are used by the mouth; opium is very frequently, especially among
women of the better classes of society, habitually taken in the form
of suppositories; finally, the acetate and sulphate of morphine are
used by means of the hypodermic syringe. While it will be necessary to
point out some differences in the effects of these drugs due to the
preparation used or to the method in which it is employed, the
distinction between the opium habit and the morphine habit, in itself
an artificial one, will not be regarded in the course of the present
article.

[Footnote 2: _Opium-smoking and Opium-eating, their Treatment and
Cure_, by George Shearer, M.D., F. R. S.]

Opium-smoking is chiefly practised by the inhabitants of China and of
the islands of the Indian Archipelago. It has been imported into those
countries where Chinese labor is largely employed. The Chinese have
transmitted it, to an extent which is fortunately very limited, to the
inhabitants of certain of our cities. Opium-smoking is habitually
practised in this country only among the more debased orders of
society.

SYNONYMS.—Opiophagia, Morphiopathy, Morphinism, Morphinomania,
Morphiomania, Morpheomania, are terms occasionally employed to
designate the opium or morphia habit.[3] Landowski, Levinstein, Jouet,
and others use the term morphinism to denote the condition of the
body; morphinomania, the condition of the mind in chronic
morphine-poisoning. This distinction may be misleading. In effect, the
pathological condition is complex, including derangements both somatic
and psychical.

[Footnote 3: The word morphiomania, used by writers, is contrary to
all etymological rule (Zambaco, _De la Morphéomania_, Paris, 1883).]

{649} ETIOLOGY.—_A_. Predisposing Influences.—Pain holds the chief
place among the influences which predispose to the formation of the
opium habit. By far the greater number of cases have taken origin
either in acute sickness, in which opium administered for the relief
of pain has been prolonged into convalescence until the habit has
become confirmed, or in chronic sicknesses, in which recurring pain
has called for constantly repeated and steadily increasing doses of
opiates. In view of the frequency and prominence of pain as a symptom
of disease, and the ease and efficiency with which opium and its
preparations control it, the remote dangers attending the guarded
therapeutic use of these preparations are indeed slight. Were this not
so, the number of the victims of the opium habit would be lamentably
greater than it is. In a considerable proportion of cases of painful
illness the relief afforded by opiates is attended by at least some
degree of malaise, nausea, vomiting, and vertigo—symptoms which render
the speedy discontinuance of the remedy scarcely less desirable than
the control of the pain for which it was administered. Occasionally
these symptoms are so distressing as to render opium wholly
inadmissible. In other instances each successive dose is attended by
an aggravation of the distress. More commonly, especially in acute
illnesses, decreasing pain may be controlled by diminishing doses,
thus rendering practicable entire discontinuance of the drug before
those modifications of the nervous system, and especially before that
tolerance for large doses, which constitutes the beginning of the
opium habit, are established. For these reasons the use of opiates in
acute sickness, if properly regulated, is attended with but little
danger. Far different is it, however, in chronic painful illnesses.
Here to procure relief by opium is too often to pave the way not only
to an aggravation of the existing evils, but also to others which are
often of a more serious kind. Opium is at once an anodyne and a
stimulant. The temptations to its use are of a most seductive
character. To the overworked and underfed mill-operator it is a snare
more tempting than alcohol, and less expensive. It allays the pangs of
hunger, it increases the power of endurance, it brings forgetfulness
and sleep. If there be myalgia or rheumatism or neuralgia, and
especially the dispiriting visceral neuralgias so common and so often
unrecognized among the poorer classes of workpeople, opium affords
temporary relief. The medical man suffering from some painful
affection, the worst symptoms of which are relieved by the hypodermic
injection of morphine, falls an easy prey to the temptation to
continue it—a danger increased by the fact that he is too often
obliged to resume his work before convalescence is complete. Indeed,
the self-administered daily doses of physicians sometimes reach almost
incredible amounts. To women of the higher classes, ennuyée and
tormented with neuralgias or the vague pains of hysteria and
hypochondriasis, opium brings tranquillity and self-forgetfulness.

Of 100 cases collected by Jouet,[4] the habit followed the therapeutic
use of morphine in 32 cases of ataxia, 24 of sciatica and other
neuralgias, 8 of asthma, 2 of dyspepsia, 4 of hypochondriasis, 2 of
madness, 9 of painful tumors, 2 of prostatic inflammation, 7 of
nervous conditions (not specified), 1 of peritonitis, 2 of
periostitis, 1 of gastro-enteralgia, 4 of pleuritic pains, 1 of
contracture, and 1 case of hæmoptysis.

[Footnote 4: _Étude sur le Morphinism chemique_, Thèse de Paris,
1883.]

The responsibility of the physician to his patient becomes apparent
{650} when we reflect that with very few exceptions the opium habit is
the direct outcome of the use of the drug as a medicine.

The decade of life at which the opium habit is most common is between
thirty and forty. But it may be developed at any age. Even infants are
not rarely made the subjects of chronic opium narcotism by the use of
soothing syrups and other poisonous nostrums.

Sex in itself exerts very little influence as a predisposing cause.
Owing to collateral circumstances, the number of women addicted to
opium is greater than the number of men. Kane[5] states that females
more frequently fall victims to these drugs than males, in the
proportion of three to one, and attributes this excess to the fact
that women more often than men are afflicted with diseases of a
nervous character in which narcotic remedies are used for long
periods. This observer suggests as an additional explanation the
occasional preference on the part of women for opium as a stimulant in
place of alcohol, its effects being less noticeable and degrading. On
the other hand, Levinstein observed in 110 cases 82 men and 28 women.
He does not, however, regard the conclusion that the use is more
common among men as warranted by these figures. The habit resulted in
these 110 cases from the following causes: In 20 men and 6 women after
acute affections; in 46 men and 17 women after chronic affections,
these diseases being in each instance accompanied by great pain. One
man began to use morphine as an antiaphrodisiac. Either to produce
mental excitement simply or to cause forgetfulness of the ordinary
cares of daily life, 15 men and 5 women indulged to an uncontrollable
extent.

[Footnote 5: _Drugs that Enslave_, Philadelphia, 1881. I refer with
pleasure to the early labors of this observer. His later publications
tell their own story.]

Occupation has in some respects much to do in favoring the development
of the opium habit. Familiarity with the use of drugs exerts a
powerful influence. Of Levinstein's 110 cases, 47 occurred in persons
belonging to the medical profession or dependent upon it; thus, 32
physicians, 8 wives of physicians, 1 son of a physician, 4 nurses, 1
midwife, and 1 student of medicine.

A predisposing influence of more importance than would at first sight
appear is found in sensational popular writings upon the subject. As
Kane has well said, “At the time in which De Quincey, Coleridge, and
Southey lived the people and the profession knew little of the opium
habit save among foreign nations. The habitués were few in number, and
consequently when De Quincey's article appeared it created a most
decided impression upon the popular mind—an impression not yet
effaced, and one which bore with it an incalculable amount of harm.
Men and women who had never heard of such a thing, stimulated by
curiosity, their minds filled with the vivid pictures of a state of
dreamy bliss and feeling of full content with the world and all about,
tried the experiment, and gradually wound themselves in the silken
meshes of the fascinating net, which only too soon proved too strong
to admit of breaking.” There can be no question that a percentage of
cases of the opium habit, small though it be, is even in our day to be
attributed to this cause.

Somewhat analogous in its etiological importance is the influence of
example upon persons of idle and luxurious habits. Nowhere in Western
countries, with the exception of the opium-smoking dens of the {651}
Chinese and their depraved associates, are there public places of
resort devoted to the practice of the opium and morphine habits, as
there are in Turkey and the East. According to Jouet—whose statements
are corroborated by occasional statements in French newspapers—the
habitual injection of morphine is to-day, in France at least, almost a
matter of fashion. Landowski states that friendship is occasionally
pushed to the extent of the exchange of pretty syringes in silver
cases as presents, and that a patient received upon his birthday a
hypodermic syringe as a present from his sister. Zambaco, whose
observations were made at Constantinople, states that among the
Moslems the opium habitués prefer the crude drug, either alone or
associated with certain aromatic substances, such as ambergris,
canella, or saffron, which are used for their aphrodisiac effect.
These mixtures are prepared openly in the family, and carried upon the
person in the form of pills in rich boxes of gold and enamel among the
better classes. This observer further says that the ladies of the
better classes carry jewelled cases containing hypodermic syringes and
artistic flaçons for the seductive solution, and that they avail
themselves of favorable opportunities to take an injection of morphine
even when together.

In addition to the predisposing influences already mentioned, it has
been customary to regard insanity as a cause of the opium habit.
Laehr[6] and Fidler[7] have gone so far as to class the morphine habit
among the psychoses. This view appears to be no longer tenable. The
opium habit must be classed with the taste for alcohol, gambling,
avarice, and lust as among human passions. That nervous subjects,
invalids, and individuals wanting in moral and physical tone are
specially prone to it is obvious. It constitutes in these cases,
however, an expression of the morbid constitution rather than a
substantive affection in itself. In the same manner, the opium habit
in insane persons must be looked upon as an epiphenomenon of the
morbid mental condition.

[Footnote 6: _Allgemeine Zeitschrift für Psychiatrie_, 1872.]

[Footnote 7: _Jahresb. der Gesellschaft für Natur und Heilkunde_,
Dresden, 1876.]

Levinstein has with reason insisted upon the essential difference
between the disturbances resulting from chronic poisoning by alcohol,
lead, arsenic, etc., and that produced by morphine. In the former
group the mental conditions are expressions of physical and chemical
alterations of the central nervous system, which, once established,
persist for an indefinite period, whereas in morphinomania the
troubles of the nervous system are chiefly functional and of a
transitory character. He regards the nervous disorders developed from
the prolonged use of morphine as the result simply of depression of
the nervous system, and the extreme suffering experienced on the
withdrawal of the regular dose to which the subject has been
accustomed as a trouble of innervation rather than as a psychical
derangement. This physical suffering and the mental depression which
accompanies it have their analogues in the angina occasionally seen in
paroxysmal affections of the heart, the blood-vessels, and the
respiratory organs. Certain it is that individuals addicted to opium
and morphine excesses in a high degree not only frequently retain full
possession of their intellect, but occasionally achieve and maintain
great distinction in professional and scientific life. Furthermore,
subjects of the opium habit, notwithstanding the gravest mental
disturbance manifested during the {652} continuance or upon the
cessation of the habit, usually exhibit when cured no further
indication of mental disorder.

_B_. The Exciting Cause.—In addition to the usual constituents of
vegetable substances, mucilage, albumen, proteids, fat, volatile
substances, and salts of ammonium, calcium, and magnesium, opium
contains a number of alkaloids, two neutral substances, and meconic
acid. Some of the alkaloids are probably derivatives from morphia. The
three most important alkaloids are morphine, codeine, and thebaine.
The neutral substances are meconin and meconiasin. Morphinæ
hydrochloras, acetas, and sulphas, codeina, and apomorphinæ
hydrochloras are officinal in the United States Pharmacopœia. Opium
and its alkaloids act principally on the central nervous system, and
in mammals on the brain. The functions of the nervous system, as
Brunton has pointed out, are abolished in the order of their
development, the highest centres being the first affected. In man the
action of opium is chiefly manifested upon the brain. With small doses
a stage of excitement, attended by increased activity of the
circulation, augmented nervous energy, and under favorable
circumstances an agreeable languor, followed by quiet sleep,
constitute the effects of the drug; with larger doses, of from one to
two grains, the transient stage of excitement is followed by deep
sleep, the awakening from which is marked by headache, nausea, and
evidences of gastro-intestinal catarrh; with still larger doses, of
three grains or more, deep sleep is produced, which speedily passes
into coma. The drug has an especial action on the vaso-motor system,
which is manifested in its power to diminish congestion and relieve
inflammation. With the exception of the urine and the sweat, the
secretions of the body are diminished by opium. The action of the drug
upon the intestines varies with the dose. In moderate doses it
diminishes peristalsis and causes constipation; in very small doses it
increases peristalsis; in large doses peristaltic action ceases.
Morphine is eliminated unchanged by the kidneys. It is eliminated also
by the gastro-intestinal mucous membrane, having been found in the
stomach after hypodermic injection. The action of opium and its
derivatives, as that of other narcotics, is much influenced by habit.
In those accustomed to the drug large (and sometimes enormous)
quantities are required to induce the characteristic manifestations.
Not rarely these manifestations are much retarded. The enormous amount
of two pints of tincture of opium has been taken in the course of a
day; a female patient afterward successfully treated by the writer
took habitually for a long period of time from ten to twelve grains of
morphine per diem, hypodermically. Diedriech[8] assumes that a portion
of the morphine introduced into the organism is converted into
oxydimorphine or other analogous substances which have the property of
counteracting to some extent the toxic effects of the morphine.

[Footnote 8: _Ueber oxydimorphine_, Inaug. Diss., Göttingen, 1883.]

Levinstein concludes as a result of experiments upon animals that
morphine, besides its influence upon the nervous system, exerts an
especial action upon two sets of organs: first, upon the digestive
tube; and second, upon the sudoriferous glands. Taken by the mouth, it
irritated the gastric mucous membrane. Whether taken by the mouth or
hypodermically, it diminishes the secretion of gastric juice and the
peristaltic movements of the intestine. These disturbances serve to
explain not {653} only certain of the phenomena of the opium habit
itself, but even more fully some of the symptoms manifested upon its
discontinuance. The nausea, vomiting, and constipation occurring
during the continuance of the habit must be looked upon as a result of
the derangement of function of the gastro-intestinal glandular
apparatus and the chronic catarrh which accompanies it. The abrupt
discontinuance of the drug is followed by the sudden return of
functional activity, hence salivation, persistent vomiting, anorexia,
and diarrhœa.

The effects of habitual excesses in opium and morphine upon the
nervous system are in essential particulars the same. Upon the
functions of the digestive system and upon nutrition they differ to a
considerable extent. Opium, as a rule, soon produces gastro-intestinal
derangements of a marked kind. These derangements consist in loss of
appetite, enfeebled digestion, nausea, vomiting, and constipation
alternating with occasional diarrhœa. The anorexia is usually
persistent and of a high degree, and has much to do with the
development of the wasting which is so common and so marked. The
occasional excessive appetite for food manifested by opium-eaters is
of brief duration. Its gratification aggravates the functional
disturbances, provokes gastro-intestinal catarrh, and thus tends to
increase the general malnutrition. On the other hand, morphine is much
better borne. At the present time almost all morphine habitués use the
hypodermic syringe, and, notwithstanding the elimination of the drug
in part by the gastric mucous membrane, thus escape in part its evil
effects upon the organs of digestion, and remain for a long time,
often despite enormous excesses, free from the nutritive disturbances
which are almost characteristic of the habitual abuse of crude opium.

SYMPTOMATOLOGY.—The symptoms of the confirmed opium habit may be
divided into two principal groups: first, the symptoms of chronic
opium- or morphine-poisoning; and second, the symptoms due to the
withdrawal of the drug.

I. Symptoms of Chronic Poisoning.—A considerable percentage of the
individuals addicted to the opium habit preserve for a longer or
shorter period of time the appearance of health; indeed, it is
possible for very large doses of opium to be occasionally taken by
certain individuals without appreciable impairment of the functions
either of the body or the mind. These cases must, however, be looked
upon as exceptional. It is estimated that from one-fourth to
three-tenths of the entire population of China are addicted to the
habit of opium-smoking. The statements of travellers concerning the
effect of this habit are somewhat conflicting. When practised within
bounds it appears to resemble in its effects the moderate use of
alcoholic stimulants, increasing the ability to endure fatigue and
diminishing for a time the necessity for food. In moderation it
appears to have little injurious effect upon the general health. On
the other hand, in the greater number of individuals the confirmed
opium habit causes in a variable period of time symptoms of the most
decided character; the appetite and general nutrition fail; emaciation
is often rapid, commonly marked, and sometimes extreme. There are
thirst and anorexia; a little later the patient begins to suffer from
nausea with occasional vomiting. At this time a loathing for food
alternates with boulimia. These occasional excesses in food are
followed by epigastric {654} distress, heartburn, and great mental
depression. The skin becomes relaxed, inelastic, and dull.
Exceptionally, especially in women who use morphine hypodermically,
embonpoint is preserved and the skin retains its normal tension and
appearance. The countenance is pale, muddy, and sometimes slightly
cyanotic. There is increased tendency to perspiration. Acne and
urticaria are common. Herpes zoster is encountered with considerable
frequency among opium subjects. In cases in which morphine is
administered by means of the hypodermic syringe the resulting lesions
of the skin are of importance. If the habit be concealed or denied,
they are of diagnostic value. Not rarely they constitute serious
affections in themselves. They are of all grades, from mere
inflammatory points to coarse infiltration and ulceration. The wounds
are frequently so thick set over the greater part of a limb as to
present the appearance of a continuous eruption. In other cases
scattered points of ulceration occur or extensive surfaces are
occupied by a series of ulcerations varying in size from a split pea
to an inch or more in diameter. Purulent inflammation of the
subcutaneous tissues, with burrowing, also occurs. Numerous scars bear
witness to the duration and extent of the habit. These lesions are
usually due to unclean needles and impure solutions; in certain cases
they are to be explained by the peculiarities of the individual as
regards the tendency to inflammation of the integumentary structures;
finally, instances are related in which immunity from skin lesions has
existed in spite of rusty needles and carelessly kept solutions.

The expression of the countenance is sometimes dull, much more
frequently furtive and timid. The repetition of the dose renders it
eager and bright. The pupils are commonly contracted, sometimes
enlarged, and occasionally unequal. Diminished power of accommodation
is common, and diplopia has been occasionally observed.

The action of the heart is often irregular and weak. Disturbances of
the vaso-motor system give rise to flushing of the face, irregular
sensations of heat over the body, and sweating. It is probable that
the albuminuria hereafter to be described is due to disturbance of the
circulation in the kidneys. The pulse is variable; it is sometimes
tense and full, sometimes small and thready, often irregular. The
volume, tension, and rhythm of the pulse depend largely upon the state
of the vaso-motor and general nervous systems. They vary according to
the periods of stimulation, following doses or the periods of
depression characterizing the intervals between the doses.
Palpitations occasionally occur. Respiration is, as a rule, normal.
Transient dyspnœa sometimes occurs after doses a little larger than
usual. Subacute bronchitis is common. The urine is often diminished in
quantity. Its specific gravity varies within extreme limits, being
influenced rather by collateral circumstances than by the dose of
opium or morphine consumed. In grave cases albuminuria occurs. Casts
of various kinds are also encountered. As Levinstein[9] has pointed
out, these changes in the urine are often transitory, disappearing
upon the suppression of the opium habit.

[Footnote 9: _La Morphiomanie_, 2d ed., Paris, 1880.]

In confirmed cases uric acid is increased and urea diminished. The
chlorides are also diminished in amount. Vesical irritation is
likewise common. It is apt to be accompanied by neuralgia of the
urethra and {655} of the rectum. Strangury and retention of urine also
occur in old cases. These complications are often followed by vesical
catarrh.

Derangements of the central nervous system are constant and serious.
The disorders which originally led to the use of opiates are in many
instances intensified. The temper is capricious, fanciful, and
discontented. There are giddiness, headache, and vertigo. Disturbed
sleep, irregular flying neuralgic pains, and hyperæsthesia also occur.
Spinal tenderness is occasionally encountered, with characteristic
painful spots. Reflex excitability is augmented, but in aggravated
cases the tendon reflexes are often impaired. Itching is common and
troublesome. It may be local or general. Trembling of the hands and of
the tongue also occurs. This tremor resembles in all particulars the
tremor of chronic alcoholism, and, as many individuals addicted to the
opium habit also abuse alcohol, it is not always easy to say to which
of these poisons the symptom in question is to be referred: it may be
due to their combined action. Disturbances of speech are not very
uncommon. Sleeplessness is troublesome, but absolute insomnia is rare.
The sleep which is obtained is late, irregular, and unrefreshing. In
several cases that have occurred under the observation of the writer
there has been habitual inability to sleep during the night, the
patients wandering about, occupying themselves in attempts to read or
write until toward morning, and then, under the influence of repeated
doses, falling into a more or less profound slumber, which has often
been prolonged till after midday. The effects of the dose upon the
mind are in the early periods of the habit agreeable exhilaration,
increased activity of imagination, and stimulation of the powers of
conversation. These effects are sometimes manifested for a long
period, and in many instances the most brilliant conversation, and
among professional men and public speakers the ablest efforts, have
followed the taking of large doses of opiates, and been followed in
turn by periods of the most profound physical and mental depression.
In the absence of the necessity for intellectual effort, and in
individuals incapable of it, the mental condition produced by the dose
is one of profound revery, largely influenced by the mental
organization of the subject. This state is described, and in many
particulars much exaggerated, in the writings of De Quincey,
Coleridge, and others.

The voluptuous play of the imagination ascribed to the action of the
drug by Orientals is for the most part absent among opium-takers in
this country. If present at all, it occurs only to a limited degree.
The corresponding fact is also worthy of note—namely, so long as the
habit is continued the depression between the doses is less profound
than that described as occurring in the East. One of the mental
peculiarities of individuals addicted to the opium habit is
secretiveness concerning their vice. Not infrequently, the real cause
of the grave derangements of health thus produced is wholly
unsuspected by the family or friends of the patient. When the habit is
suspected or admitted, the amount and frequency of the dose are rarely
fully known, patients almost invariably deceiving their friends in
regard to the particulars of their indulgence. Individuals above
reproach in other matters, and previously of unquestioned veracity,
lie without any hesitation in this matter. A patient under my care who
had secreted in her room a quantity of morphine when about to undergo
treatment, denied either having taken or then having {656} in her
possession any opium or morphine whatever, using the expression, “I
call God to witness that I neither now have, nor have had since I
began the treatment, any preparation of opium or morphine whatever.”
Within ten minutes sixty quarter-grain pills of morphine were
discovered secreted under the bolster. This patient was a devout,
refined, and, in regard to other matters, a trustworthy person.

The functions of the reproductive organs both in the male and in the
female are seriously deranged. In the male sex enfeeblement of the
sexual function is manifested in all degrees, even to complete loss of
sexual desire and sexual power. In certain individuals opium and
morphine in moderate doses produce some increase of sexual desire and
power, which is, however, speedily lost on the continuance of the
habit. Some doubt exists whether this is of psychical or physical
origin—a question at once difficult to decide by reason of the
reticence of opium-habitués upon this subject, and unimportant in
itself. Levinstein makes the interesting statement that in no cases
coming under his observation did the wives of morphomaniacs who had
injected as high as fifteen grains of morphine a day reach the full
term of pregnancy for two years prior to the treatment,
notwithstanding the fact that they were still young, that they had
borne children before their husbands had become addicted to morphine,
and that they had not, up to the time of the formation of the habit by
their husbands, suffered from premature accouchements.

Among women the morphine habit invariably produces derangement of the
menstrual function. Menstrual irregularity, both as regards time and
amount, is succeeded after a time by amenorrhœa. Vicarious hemorrhages
do not occur. Complete amenorrhœa is sometimes established abruptly,
and married women not infrequently suspect for this reason that they
have conceived. In several cases of this kind under the observation of
the writer the absence of enlargement of the breasts, of alteration of
the areola, and of softening of the os after several months, indicated
the improbability of these fears, notwithstanding the irregular
appetite, the morning vomiting, the occasional palpitations and
faintness, the hysterical condition, and the mental peculiarities of
the individuals—phenomena unquestionably due to the action of the
morphine itself. The amenorrhœa of the morphine habit is associated
with sterility—a fact that renders probable the supposition that it is
dependent upon absence of ovulation. Women addicted to the opium habit
are capable of conceiving so long as menstruation persists, those
only, however, going to full term who use very moderate quantities. In
women using large doses abortion invariably occurs. The functional
integrity of the reproductive system is re-established upon the
permanent cessation of the habit. Women who are cured may again
menstruate regularly and may again bear children. Morphine in women,
as in men, is said to increase, when first habitually taken, the
capacity for sexual pleasure.

Levinstein and others have described certain febrile conditions
observed in individuals addicted to morphine. First, a form of
intermittent fever closely resembling malarial fever. This fever of
intermittent type occurs in individuals neither living in malarious
regions nor previously exposed to malaria. In addition to periodicity,
it presents other points of resemblance to malarial intermittent. The
earlier paroxysms cease after the {657} administration of quinine.
They are favorably influenced by change of residence, and recur with
intensity after over-exertion, exposure, and upon the occurrence of
acute maladies. The favorable influence of quinine is only transient;
the febrile paroxysms recur after a time, notwithstanding the
continued use of the medicament. This fever disappears without special
treatment upon the discontinuance of the habit. It is more frequently
of the tertian than of the quotidian type. Its paroxysms are marked by
the symptoms of paludal intermittent. Neuralgias of various kinds,
especially supraorbital, intercostal, and præcordial neuralgias, are
apt to occur. The temperature during the paroxysm ranges from 102.5°
to 104°. The area of splenic dulness is increased. More or less mental
and physical depression follows the paroxysm, continuing in most cases
through the period of apyrexia. These observations require further
confirmation. Secondly, confirmed opium-habitués are peculiarly liable
to transient febrile disturbances from slight causes. Finally,
ephemeral fever, ushered in by chills or rigors and accompanied by
headache, vertigo, thirst, malaise, restlessness, and even mild
delirium, and terminating with profuse perspiration, occasionally
occurs immediately after the injection of large doses of morphine.

The course of the opium habit, when once established, is,
notwithstanding its occasional transient interruptions, gradual and
progressive. Certain individuals endure enormous doses of opium or
morphine for years without serious symptoms. In others moderate doses
give rise in the course of a few months to anorexia, disturbances of
nutrition, neuralgias, fitful and difficult sleep, and serious mental
derangement. These symptoms are usually controlled by increasing doses
and diminution of the intervals. Finally, however, the drug fails to
produce either excitement or repose, and enormous doses are taken with
but insignificant relief. This is the period of grave derangement of
the mental and physical functions and of nutrition amounting to a true
dyscrasia. The phenomena are analogous to those produced by the
withdrawal of the dose. They are the symptoms of inanition, which in
the absence of well-directed and energetic treatment speedily
terminates in death.

II. Symptoms Due to the Withdrawal of the Drug.—Opium-habitués,
differing as they do among themselves in the manifestations of the
effects of the drug so long as it is freely taken, all alike develop
characteristic symptoms upon its speedy or gradual withdrawal. The
apparent immunity exceptionally observed now comes to an abrupt
termination. The nervous system, whether it has been accustomed for
months merely or for years to the influence of opiates, is upon their
withdrawal forthwith thrown into derangement of the most serious and
widespread kind. In the course of a few hours after the last dose the
steadying influence of the drug disappears. General malaise is
associated with progressive restlessness; the ability to perform the
ordinary duties of life gives way to profound depression and
indifference; præcordial distress, accompanied by cough, is followed
by insomnia, hallucinations, and sometimes by mania. The habitual
pallor of the face is replaced by deep flushing or cyanosis. The
heart's action becomes excited and irregular, then feeble; the pulse,
at first tense, becomes slow, thready, and irregular. Colliquative
sweats appear. Attacks of yawning and sneezing are followed by
convulsive twitching and trembling of the hands. Speech becomes
hesitating, drawling, and {658} stuttering. Troubles of the
accommodation and even diplopia occur, often accompanied by excessive
lachrymation. Transient and varying differences in the pupils are very
frequent. Retinal hyperæsthesia may occur. In the amblyopia
occasionally observed in subjects of the opium habit the
ophthalmoscope reveals persistent anæmia of the retina. These
phenomena are associated with a sense of perfect prostration which
obliges the patient to take himself to his bed. Pain in the back and
limbs, followed by neuralgias, now occurs. Complete anorexia, with
easily-provoked or even causeless vomiting and persistent nausea and
diarrhœa difficult to control, adds to the gravity of the condition.
The abrupt discontinuance of the drug is followed in many individuals
by mental phenomena of a marked character: hallucinations, illusions,
and delirium continue for several days. The hallucinations relate to
all of the senses, but especially to those of sight and hearing. The
sense of smell is also occasionally affected, that of taste rarely.
Syncopal attacks occur. These are usually transient; occasionally,
however, profound syncope calls for the active interference of the
physician. Epileptiform seizures also take place. Women who have
previously suffered from hystero-epilepsy are prone to the recurrence
of severe paroxysms. Trembling of the limbs, and especially of the
lower extremities, rhythmical in time and often violent, must be
ranked among the more characteristic phenomena produced by the
abstinence from the drug. Sweating, although by no means constant, is
among the earlier and more persistent phenomena. Urticaria occurs.
Dyspnœa is common. Sometimes it is provoked by exertion; sometimes
paroxysmal shortness of breath occurs spontaneously. Irritable cough
is frequent. It is in many cases unattended by râles. Pre-existing
bronchitis is of course accompanied by its characteristic signs and
symptoms. Præcordial distress, with palpitation and a sense of
oppression, is common. During the earlier days of abstinence the
evidences of cardiac failure are marked. Enfeeblement of the first
sound, irregularity of the heart's action, and intermission are
common. The pulse phenomena correspond to the heart's action. Thirst
is a very frequent symptom. It is often out of proportion to the loss
of fluid by perspiration and diarrhœa. The urine does not contain
sugar. Salivation is rare and of moderate degree. Nausea is
persistent. Œsophageal spasm, provoked by every effort to swallow,
occasionally occurs and constitutes a distressing symptom. Many
patients also complain of spasmodic contraction of the anus. Neuralgia
of the testicles also occurs. The cure of the opium habit is followed
by rehabilitation of the sexual power in the male and by menstrual
regularity and fecundity in the female. Levinstein has observed sexual
hyperæsthesia during the first weeks of abstinence in both sexes.
Albuminuria occurs in a large proportion of the cases. The albumen
shows itself, as a rule, from the third to the sixth day after the
discontinuance of the morphine, and disappears in the course of a very
few days. It is usually of slight amount.

The behavior of patients undergoing the suffering attendant upon the
abrupt, or even the gradual, withdrawal of the drug is variable. It
depends upon the mental and physical organization of the different
individuals and upon their ability to endure pain. Some rest quietly
in bed, enduring with fortitude suffering from which there is no
escape; others, silent, uncomplaining, and apathetic, present the
{659} appearance of utter despair; a few, more fortunate than their
fellows, lapse into a condition of almost continuous drowsiness. In
the greater number of cases, however, these states of repose are but
momentary or absent altogether. Restlessness is continuous, and very
often intense; the patients are with difficulty kept in bed; if left
to themselves they move frantically about the room, moaning, bewailing
their condition, and begging the attendants for that which alone is
capable of relieving their distress. This condition gradually
subsides, giving way to a state of the most profound exhaustion. The
exhaustion due to the reaction of the nervous system deprived of the
stimulus of the drug is, on the one hand, favored by pre-existent
derangement of the nutritive processes, and on the other increased by
the pain, wakefulness, diarrhœa, and vomiting which accompany it. The
appearance of the patient is now most pitiable; the countenance is
blanched and pinched, the body occasionally drenched with sweat; the
heart's action is feeble, and the pulse thready and irregular. This
condition of collapse is usually of short duration, disappearing in
favorable cases under the influence of appropriate nourishment
administered in small quantities and with regularity. Where, however,
the gastric irritability is unmanageable, an increasing tendency to
collapse may threaten life. In rare cases suddenly-developed fatal
collapse has occurred at a later period in the treatment, even after
the patient has become able to take and retain food. The restlessness
does not, however, always subside in this manner. In a considerable
proportion of cases it increases. Hallucinations and delusions occur,
and a condition of delirium tremens, scarcely differing from the
delirium tremens of chronic alcoholism, is established. Tremor is a
constant phenomenon of this condition. Sometimes the gravest symptoms
of the suppression of the drug are developed with great rapidity.
Jouet relates a case of a patient at the Salpêtrière who during a
temporary absence from the hospital forgot her syringe and solution;
her return being delayed from some cause, she, notwithstanding her
struggles against the symptoms caused by the want of her habitual
dose, suddenly fell in the street, her countenance haggard and
anxious, her hands shrivelled, and her whole body bathed in drenching
sweat. She immediately became maniacal, and demolished the glass and
lamps of the coupé in which she was taken to the hospital. No sooner
had she received her ordinary hypodermic dose than she recovered her
usual quietude. This patient was neither hysterical nor had she
previously suffered from nervous paroxysms. She was, however,
accustomed to administer to herself at four o'clock every day a large
hypodermic dose of morphine, and it was at a few minutes past four
that the above-described seizure occurred.

DIAGNOSIS.—The diagnosis of the opium habit is in many cases attended
with considerable difficulty. Many habitués, it is true, do not
hesitate to admit the real cause of their symptoms; others, while
seeking to conceal it, do so in such an indifferent manner that
detection is not difficult; but the greater number for a long time
sedulously conceal their passion, not only from their friends, but
also from the physician whom they consult voluntarily or at the
solicitation of those interested in them. If inquiries be made upon
the subject, they deny the habit altogether, often with vehement
protestations. If forced to admit it, they are very apt to misstate
the amount employed or the frequency of the repetition of the dose. As
a rule—to which there are, however, not infrequent {660}
exceptions—emaciation is marked, appetite is diminished and variable,
the pulse is small, the circulation feeble, the respiration shallow
and occasionally interrupted by long-drawn sighs, the pupils are as a
rule contracted, constipation is present, often alternating with
diarrhœa. When to these conditions, for which no cause can be found
upon careful examination, there are added marked change in
disposition, periods of unaccountable dulness and apathy alternating
with unusual vivacity and brightness, especially when insomnia
alternates with periods of prolonged and heavy sleep, the abuse of
morphia may be suspected. If the hypodermic syringe be used the wounds
made by the needle confirm the diagnosis. These punctures are usually
found in groups upon the thighs, legs, arms, and abdomen. Close
inquiry into the habits of the patient, who either goes himself or
sends at short intervals for unusual quantities of opium or morphia to
some neighboring apothecary, is sometimes necessary to confirm the
diagnosis. Finally, the presence of morphine in the urine[10] renders
the diagnosis positive, notwithstanding the most vehement assertions
of the patient as regards his innocence of the habit and the extreme
cunning with which it is concealed.

[Footnote 10: “According to Bouchardat, morphine, when taken in the
free state or under the form of opium, speedily appears in the urine,
and may be detected by the liquid yielding a reddish-brown precipitate
with a solution of iodine in iodide of potassium. Since, however, as
we have already seen, this reagent also produces similar precipitates
with most of the other alkalies and with certain other organic
substances, this reaction in itself could by no means be regarded as
direct proof of the presence of the alkaloid. Moreover, we find that
the reagent not unfrequently throws down a precipitate from what may
be regarded as normal urine, while, on the other hand, it sometimes
fails to produce a precipitate even when comparatively large
quantities of the alkaloid have been purposely added to the liquid”
(Wormley, _Micro-chemistry of Poisons_).

The presence of meconic acid or morphine in the urine can only be
positively determined by elaborate chemical analysis. In cases of
doubt the urine should be submitted to a competent analyst. To make
sure that opium or its derivatives are not being taken, the feces must
also be examined.]

PROGNOSIS.—The prognosis is favorable as regards the discontinuance of
the habit for a time, doubtful as regards a permanent cure. Relapses
are apt to occur. They are more common in men than in women, in the
aged than in middle life, and in persons of feeble physical and mental
organization than in those who are possessed of bodily and mental
vigor. Relapses also occur more frequently in those individuals
addicted to alcohol, and in those who are habitually subjected to
temptation by reason of their avocation, such as doctors, nurses, and
apothecaries, than in others. The danger of relapse is greater where
the habit has been formed in consequence of chronic painful affections
than where it has been rapidly developed in the course of acute
illnesses. Of 82 men treated by Levinstein, relapses occurred in 61;
of 28 women, in 10; of 38 physicians, in 26. The danger of relapse
diminishes with the lapse of time; nevertheless, a single dose of
morphine or a hypodermic injection may, after an abstinence of months,
precipitate a relapse. Indeed, the return of the habit is in the
majority of instances caused by the thoughtlessness of medical men in
prescribing in these cases opiates for maladies which are often in
themselves insignificant.


Chloral Hydrate.

The prediction made by B. W. Richardson, within two years of
Liebreich's announcement of the medicinal properties of chloral, that
its {661} abuse would become widespread, has been abundantly
fulfilled. The consumption of this substance as a narcotic has reached
an extent in certain classes of society which raises it, after alcohol
and opium, to the third place among such agents.

SYNONYMS.—The Chloral habit, Chloralism.

ETIOLOGY.—_A_. Predisposing Influences.—Age exerts but little
predisposing influence. Cases occur almost exclusively in adults, and
the greater proportion of these are in middle life. The abuse of
chloral is relatively somewhat more common among males than among
females. Individuals addicted to this habit usually belong to the
refined and educated classes of society; the fascinations of chloral
remain thus far unknown to the great mass of the people. Professional
men and those engaged in literary work form a very considerable
proportion of the cases. Chloral is occasionally used by hospital
nurses, and very frequently by prostitutes. Chronic alcoholism is an
important predisposing element in the formation of the chloral habit;
in fact, morbid conditions attended by insomnia from whatever cause
tend to the formation of this habit.

_B_. The Exciting Cause.—Chloral is a powerful hypnotic, usually
without unpleasant after-effects. In full doses it is a depressant to
the nerve-centres at the base of the brain and to the spinal cord. It
enfeebles the action of the heart, depresses respiration, and lessens
reflex activity. It has no action on the secretions except that of the
kidneys, which it frequently augments.

The habit has in some few instances been developed in consequence of
the indulgence in a morbid desire to experience the effects of the
drug. In a majority of instances it is due to the continuance of the
medicine indefinitely after the sickness in which it was originally
prescribed has ceased. I have known apothecaries to renew
prescriptions of chloral often enough to supply a daily dose of from
forty to sixty grains for years—in one instance for more than four
years.

The dose taken by victims of the chloral habit varies greatly. Thirty
or forty grains daily is a moderate amount. Not rarely this quantity
is repeated twice or oftener within the space of twenty-four hours.
The tolerance after a time exhibited by the organism for enormous
doses of alcohol and opium is not established, as a rule, in regard to
chloral. The victim of the latter after a little time discovers the
average dose required to produce narcotic effects, and, while he may
vary it within limits, he is liable to acute toxic effects if it be
greatly exceeded. Death from such excesses is not uncommon.

SYMPTOMATOLOGY.—I. Symptoms Due to Habitual Excesses.—The habitual use
of chloral, notwithstanding its ruinous consequences in a certain
proportion of the cases, is less dangerous than that of opium or
morphine. Many individuals take chloral in considerable doses for
years without obvious ill effect. The craving for it is much less
intense than that for opium or morphine, and is readily satisfied by
other drugs. In point of fact, persons addicted to chloral very
frequently exchange it for other narcotics. For these reasons the
chloral habit is more easily cured.

Derangements of the digestive system are common, but by no means
constant. They are (1) primary, and due to the direct irritant action
of the drug upon the mucous tissues of the month and stomach; and (2)
secondary, due to its effects upon the nervous system and the
circulation. {662} Irritation of the mucous membranes is very common.
This not rarely amounts to gastro-duodenal catarrh with its
characteristic symptoms. Jaundice is common, sometimes intense. A
sense of fulness with pain and tenderness in the hepatic region is
frequent. Constipation, with clay-colored stools, is the rule. It
occasionally alternates with diarrhœa. The tongue is often coated and
the breath foul. On the other hand, in a fair proportion of the cases
the digestive organs are not affected. Chloral has been said to
occasionally exert even a favorable influence upon appetite and
digestion when taken before meals. The recent observations of Fiumi
and Favrat[11] in a man suffering from a gastric fistula and insomnia
have shown that chloral hydrate in twenty- or forty-grain doses,
administered before or at the beginning of a meal, retarded digestion
by increasing the secretion of mucus in the stomach. The acidity of
the gastric juice is diminished temporarily. The secretion of pepsin
is not changed. Taken two hours after meals, doses not exceeding forty
grains caused no derangement of gastric digestion.

[Footnote 11: _Archives Ital. de Bioloqie_, vol. vi. No. 3.]

Persons not habituated to chloral usually experience a sense of
constriction upon swallowing it, and a disagreeable after-taste.

The circulation is much affected. Chloral weakens, and finally
paralyzes, the vaso-motor centre, and thus dilates the vessels; it at
the same time weakens the action of the heart. Its habitual use is
attended by flushing of the face, congestion of the eyes, and fulness
of the head. The heart's action is weak, intermittent, irregular;
palpitation occurs; the pulse is full and compressible or small and
weak. It is usually slow.

The blood undergoes changes corresponding to the general disturbances
of nutrition. What the special changes in its composition may be is
not known. Many of the cases, even after the prolonged use of the drug
in considerable doses, show few evidences of malnutrition or of
anæmia. In the greater number, however, wasting is marked, and the
physical signs and rational symptoms of profound anæmia are present.
Deterioration in the composition of the blood is further indicated by
petechiæ, hemorrhage from mucous surfaces, sponginess of the gums, and
serous effusions.

The respiration is not permanently affected, save in grave cases. It
is then slow, irregular, and shallow. Dyspnœa is common and easily
provoked. It is usually accompanied by cough and abundant frothy
expectoration. These symptoms vanish upon the discontinuance of the
drug. In a fatal case of chloral-poisoning seen by the writer, in
which the daily use of the narcotic in non-poisonous amounts had been
for a long time varied at intervals of five or six weeks by doses
sufficient to induce prolonged coma, death was preceded by
Cheyne-Stokes respiration. This patient was a retired dentist, and
kept the solution of chloral in a large unlabelled bottle. The actual
doses taken were not ascertained.

The muscular system shares in the general malnutrition. The muscles
become flabby and wasted. Persons addicted to chloral are very
frequently of nervous organization and sedentary habits, and hence of
poor muscular development prior to the use of the drug.

The kidneys show no constant derangement. In a certain proportion of
the cases chloral acts as a diuretic, largely increasing the urinary
excretion. Albumen is present in a certain proportion of the graver
{663} cases, when it is apt to be associated with anæmia, serous
effusions, and a tendency to hemorrhages from mucous tracts. The
occurrence of casts and the persistence of albuminuria after the
discontinuance of chloral suggest an antecedent or coincidently
developed nephritis. The reducing substance present in the urine after
small doses of chloral is uro-chloralic acid (Mering and Musulus). It
gives the reaction of sugar with the copper and bismuth tests, but is
levogyrate. Glycosuria is occasionally encountered.

Vesical and urethral irritation occurs in a small proportion of the
cases. When these symptoms vanish upon the discontinuance of the drug
and recur upon its resumption, it may be fairly assumed that they are
due to its action. A great number of morbid phenomena relating to the
genito-urinary tract and to the urine, that have been ascribed to the
action of chloral in those addicted to its use, are due to associated
conditions rather than to the drug itself.

It has been claimed upon evidence that does not appear to the writer
adequate that chloral sometimes acts upon the sexual system as an
aphrodisiac, sometimes as the reverse. More or less complete
impairment of sexual power and appetite is the rule in individuals
addicted to great excesses in narcotics of all kinds. Menstruation is
not arrested by chloral as by morphine, nor does it necessarily cause
sterility in the female.

The skin undergoes nutritive disturbances of a marked kind. As a
result of individual peculiarity, single doses or medicinal doses
continued for brief periods of time have occasionally caused
erythematous, urticarious, papular, vesicular, and pustular eruptions.
Of these, the first named is of most frequent occurrence. The habitual
abuse of chloral causes in many individuals chronic congestion of the
face, neck, and ears. This redness is often very striking. It is
increased by the use of alcohol. Erythematous patches upon the chest,
in the neighborhood of the larger articulations, and upon the backs of
the hands and feet, also occasionally occur. They are often associated
with urticaria. General eruptions resembling measles, scarlatina, and
even mild variola, are said to have been observed after large doses of
chloral. Purpura is by no means rare in old cases, and falling of the
hair and atrophy and loss of the nails occur.

The nervous system bears the blunt of the disturbance, and the more
significant symptoms relate directly to it.

The hypnotic effect is usually preserved. Hence the chloral habitué is
dull, apathetic, somnolent, disposed to neglect his ordinary duties
and affairs. He passes much of his time in a state of dreamy lethargy
or in deep and prolonged sleep, from which he awakes unrefreshed and
in pain. In one of my cases, however, even larger doses than usual at
length failed to induce more than fitful slumber, and the insomnia
which led to the formation of the habit finally reasserted itself,
reinforced by the unutterable miseries of chloralism.

Headache is a frequent symptom. It is usually general, sometimes
frontal, often referred to the top of the head. It is commonly severe,
not rarely agonizing, and is described as a pressure, weight, or a
constricting band. It is associated with injection of the eyes,
flushing of the face, confusion of thought, inability to converse
intelligently or to articulate distinctly, and other evidences of
cerebral congestion. Vertigo is common.

{664} Sensory disturbances are frequently present. They consist in
local areas of hyperæsthesia, more frequently of anæsthesia, numbness
of the hands and fingers or of the feet, formication of the surface of
the body and limbs, and burning or neuralgic pains in the face, chest,
and extremities. The pains in the limbs are almost characteristic.
They are acute and persistent, neuralgic in character, but not
localized to particular nerve-tracts. They are more common in the legs
than in the arms, and occupy by preference the calves of the legs and
the flexor muscles between the elbows and the wrists. They do not
implicate the joints, are not aggravated to any grave extent by
movement, and are often temporarily relieved by gentle frictions. The
pains of chloralism have been described as like encircling bands above
the wrists and ankles.

Sensations of chilliness alternating with flashes of heat are
experienced. The temperature is, in the absence of complications,
normal. Excessive doses are followed by a reduction of one or more
degrees Fahrenheit, lasting several hours.

Among the motor disturbances are the following:

Tremor.—This symptom is not common. It is neither so pronounced nor so
distinctly rhythmical as that of alcoholism or the opium habit. It is
increased upon voluntary effort. It affects chiefly the hands and arms
and the tongue.

Palsy.—Loss of power in the lower extremities has been observed in a
number of instances. It varies in degree from paresis to complete
paraplegia. Its occurrence may be gradual or sudden. It passes away
upon the discontinuance of the habit. In many respects this condition
resembles alcoholic paraplegia.

Impairment of Co-ordinating Power.—Ataxic phenomena are sometimes
present. The patient has difficulty in walking in the dark, cannot
stand with his eyes closed, has trouble in buttoning his clothes, and
the like.

Impairment or Abolition of the Knee-jerk.—In a man aged fifty, who had
taken thirty to sixty grains of chloral hydrate at night for eighteen
months, the writer observed complete loss of the knee-jerk, which,
however, reappeared in the course of a few weeks after the
discontinuance of the drug.

In rare cases epileptiform seizures have occurred.

Chloral produces in certain individuals, even as the result of a
single dose, congestion and irritation of the conjunctiva. Apart from
this idiosyncrasy, its habitual use not infrequently causes
conjunctivitis. This affection is occasionally of a severe grade and
accompanied by œdema of the eyelids and great photophobia. Retinal
congestion has been noted by several observers. Amblyopia,
disappearing upon the cessation of the habit, has also been observed.

Psychical Derangements.—The mental and moral perversion caused by
immoderate chloral-taking shows itself rapidly. The transient
stimulating effects of the dose of opium or morphine in those
accustomed to these drugs are seen not at all or to a very slight
extent in chloralism. Hence the mental state is characterized by
dulness, apathy, confusion, and uncertainty. These conditions
alternate with periods of irritability and peevishness. The physical
sufferings of the chloral-taker in the daily intervals of abstinence
are greater than those of the {665} morphine-taker; his mental
depression less. The one is tormented by the agony of pain, the other
by the anguish of craving. To the former repetition of the dose brings
stupor and sleep, to the latter exhilaration and activity. In certain
respects, however, the effects of these drugs upon the mind are
similar. They alike produce intellectual enfeeblement, inability to
concentrate the mind, habitual timidity, and impairment of memory. In
the worse cases of chloralism hallucinations, delusions, and delirium
occur. Acute mania may occur, and dementia constitutes a terminal
state.

II. Symptoms Due to Abstinence from Chloral.—The symptoms occasioned
by the abrupt discontinuance of even large habitual doses of chloral
are not, as a rule, severe. In this respect the difference between
this drug and opium and its derivatives is very marked. The
chloral-taker not infrequently substitutes some other narcotic, as
alcohol or opium, for his usual doses without discomfort, and in many
instances voluntarily abstains from the drug, without replacing it by
others for periods of weeks or months.

The more important of the symptoms induced by sudden discontinuance
relate to the nervous system. Insomnia is usual. It is not always
readily controlled, and constitutes one of the principal difficulties
in the management of these cases. Headache is rarely absent; it is in
many cases accompanied by vertigo. Occipital neuralgia frequently
occurs, and is often severe. Neuralgias of the fifth pair also occur.
Darting pains in the limbs are usual, and the fixed aching pains
already described as peculiar to habitual chloral excess are present,
and often persist for a long time after the withdrawal of the drug.

Irregular flushes of heat, nervousness, restlessness, inability to fix
the attention, formication, burning sensations in various regions of
the surface of the body, are unimportant but annoying symptoms.

In a considerable proportion of the cases delirium occurs. It is
commonly associated with tremor, great prostration, complete insomnia,
sweating, inability to take food, and vomiting, and resembles in every
particular the delirium tremens of alcoholic subjects. In the absence
of this condition gastric derangements are not of a grave kind. The
nausea, vomiting, epigastric pain, and diarrhœa which are induced by
the discontinuance of opium are absent, or if present at all only to a
slight degree. As a matter of fact, the functions of the digestive
system are in a very short time much more perfectly performed than
before. Hemorrhage from the stomach, bowel, or urinary tract may also
occur.

The conjunctivitis and cutaneous eruptions usually disappear with
promptness as soon as the influence of the habitual chloral excesses
passes away.

DIAGNOSIS.—The diagnosis of the chloral habit is attended with much
less difficulty than that of the morphine habit. In the first place,
there is general and often serious derangement of health without
adequate discoverable cause. The appetite is poor and capricious, the
digestion imperfect and slowly performed; jaundice of variable
intensity, often slight, sometimes severe, occurs in many cases; the
bowels are not, as a rule, constipated. Dyspnœa upon slight exertion
is, in the absence of pulmonary, cardiac, or renal cause, of
diagnostic importance. The circulation is, as a rule, feeble.
Disorders of the skin, persistent or easily provoked conjunctivitis,
puffiness about the eyelids, and a tendency to hemorrhage {666} from
mucous surfaces also occur. When with these symptoms, irregularly
grouped as they are, we find a tendency to recurring attacks of
cerebral congestion, persistent or frequently recurring headaches, and
the characteristic pains in the legs, the abuse of chloral must be
suspected. This suspicion becomes the more probable if there be a
history of protracted painful illness or of prolonged insomnia in the
past. The adroitness of these patients in concealing their vice, and
the astonishing persistency with which they deny it, are remarkable.
In the absence of the characteristic association of pains,
conjunctivitis, and affections of the skin the diagnosis is attended
with considerable difficulty. It becomes probable from the association
of chronic ill-health, not otherwise explicable, with perversion of
the moral nature, enfeeblement of the will and of the intellectual
forces. It is rendered positive, notwithstanding the denials of the
patient, by the discovery of the drug or the prescription by means of
which it is procured.

PROGNOSIS.—If the confirmed chloral habitué be left to himself, the
prognosis, after excessive doses or the stage of periodical debauches
has been reached, is highly unfavorable. The condition of mind and
body alike is abject. There is danger of sudden death from cerebral
congestion or heart-failure—a mode of termination by no means rare.

On the other hand, the prognosis under treatment may be said to be
favorable. The habit is much more readily broken up, and the danger of
relapse is far less, than in cases of confirmed opium or morphine
addiction. Nevertheless, the underlying vice of organization which
impels so many individuals to the abuse of narcotics precludes a
permanent cure in a certain proportion of the cases of chloralism.
Sooner or later relapse occurs—if not relapse to chloral, relapse to
opium, morphine, or alcohol, or into that wretched condition in which
any narcotic capable of producing excitement and stupor is taken in
excess as occasion permits.


Paraldehyde.

The use of this hypnotic is not unattended with danger. In a single
case afterward under the observation of the writer paraldehyde was
used in large and increasing doses for the sake of its narcotic
properties. The patient, a young married woman whose family history
was bad, her mother having died insane, contracted the chloral habit
after an acute illness. After some months a cure was effected without
great difficulty. She relapsed into chloralism after a second sickness
which was attended with distressing insomnia. The habit was again
broken up. In consequence of over-exertion in social life during a
winter of unusual gayety insomnia recurred. For the relief of this
condition paraldehyde was prescribed with success. Notwithstanding its
disagreeable and persistent ethereal odor, and the precautions taken
by the physician, this lady managed to secure paraldehyde at first in
small quantities, afterward in half-pound bottles from a wholesale
druggist, and took it in enormous amounts, with the result of
producing aggravated nervous and psychical disturbances corresponding
to those produced by chloral, but without the disturbances of
nutrition attendant upon the abuse of the latter drug. The patient
remained well nourished, retained her appetite and digestion, and was
free {667} from disorders of the skin and the intense neuralgia which
had been present during both periods of chloral abuse. She suffered,
however, from a persistent binding headache, disturbances of
accommodation, phosphenes, and brow-pains. Under the influence of
moderate doses she was enabled to take part in social life with some
of her old interest and vivacity. The brief intervals of abstinence
which occasionally occurred were characterized by distressing
indifference to her friends and surroundings and by apathy and
depression. At frequently-recurring intervals the indulgence in
excessive doses, constituting actual paraldehyde-debauches, was
followed at first by maniacal excitement of some hours' duration,
later by profound comatose sleep lasting from one to three days. Upon
the complete withdrawal of the drug this patient manifested the
symptoms produced by complete abstinence in the confirmed morphine
habit—yawning, anorexia, epigastric pains, vomiting, diarrhœa,
absolute sleeplessness, extending over several days, heart-failure,
collapse, colliquative sweating, and finally well-characterized
delirium tremens. At the end of a week, under the influence of
repeated small doses of codeine, sleep was secured, and within a month
convalescence was complete. This person now continues free from
addiction to any narcotic, in good health, and able to sleep fairly
well, after the lapse of several months since the complete
discontinuance of paraldehyde.


Cannabis Indica, Ether, Chloroform, and Cocaine.

These drugs are habitually used as narcotic stimulants by a limited
number of individuals. Cannabis indica, or Indian hemp, the hashhish
of the Arabians, is said to be largely used in India and Egypt. It is
occasionally taken by medical students and other youths of an
experimental turn of mind, but no case of habitual hashhish addiction
has come under the observation of the writer.

The use of ether as a narcotic stimulant is occasionally observed
among druggists, nurses, and other hospital attendants, but does not
give rise to clinical phenomena sufficiently marked or distinctive to
demand extended consideration in this article. The same remark may be
made of chloroform, which is also used in the same way to a
considerable extent among women suffering from neuralgia and other
painful or distressing affections of the nervous system. The fact that
individuals are every now and then found dead in bed with an empty
chloroform-bottle by their side serves to indicate the extreme danger
attending the vicious use of this substance.

Cocaine, within the short time that has elapsed since its introduction
into therapeutics, has unquestionably been largely abused, both within
the ranks of the profession and among the people. Highly sensational
accounts of the disastrous effects resulting from its habitual use in
excessive doses have appeared in the newspapers and in certain of the
medical journals. No case of this kind has fallen under the
observation of the writer, and it would appear premature to formulate
definite conclusions concerning the effects of cocaine upon the data
thus far available.


{668} Treatment.

The treatment of the opium habit and kindred affections is a subject
which derives its importance from the following facts: First, the
gravity of the disease, as regards the functions both of the body and
of the mind; second, the enormous suffering and misfortune, alike on
the part of the patient himself and on the part of those interested in
him, which these affections entail; third, the fact that they are not
self-limited, and therefore cannot be treated with indifference or
upon the expectant plan, but are, on the other hand, progressive and
gradually destructive of all that makes life worth living, and at last
of life itself; and finally, because they are capable at the hands of
skilful and experienced physicians of a cure which in a considerable
proportion of the cases may be made permanent.

The treatment of these affections naturally arranges itself under two
headings: (_a_) the prophylactic, (_b_) the curative treatment.

_a_. Prophylaxis.—It is impossible to overrate the importance of a
true conception of the duty of practitioners of medicine in regard to
the prophylaxis of the opium habit and associated affections. In
communities constituted as are those in which the physicians practise
into whose hands this volume is likely to fall, a large—I may say an
enormous—proportion of the cases of habitual vicious narcotism is due
to the amiable weakness or thoughtlessness of medical men. A majority
of the cases occur either in chronic painful affections attended or
not by insomnia, or as a result of acute illness in which narcotics
have been employed to relieve pain or induce sleep. The chronic
affections constitute two classes: First, those manifestly incurable,
as visceral and external cancer, certain cases of advanced phthisis,
confirmed saccharine diabetes, and tabes dorsalis. In such cases the
use of morphine in large and often-repeated doses, although attended
with evils and likely to shorten life, amounts to a positive boon. It
is neither practicable, nor would it be desirable, to interfere with
it. To this class may be added those cases of grave valvular or
degenerative disease of the heart where the patient has become
addicted to the habitual use of narcotics. Here, notwithstanding the
evils resulting from these habits, among which the likelihood of
shortening the period of life must unquestionably be counted, the
dangers of the withdrawal of the drug are so great that it must be
looked upon as neither desirable nor feasible. Attention must, at this
point, be called to the fact that great caution is required in the
management of pregnant women addicted to narcotics. Incautious
attempts to withdraw the habitual drug are almost certain to be
followed by speedy loss of the fœtus; and it is to my mind
questionable whether anything more than the most guarded reduction of
the daily dose should be attempted while the pregnancy continues.

The second class of chronic cases includes individuals suffering from
diseases which are remediable or capable of decided or prolonged
amelioration. Among these affections are painful diseases curable by
surgical procedures, such as certain obstinate and intractable
localized neuralgias, painful neuromas, irritable cicatrices, pelvic
and abdominal tumors, and surgical affections of the joints and
extremities. Here, either before or after radical surgical treatment,
an effort to relieve the patient from the bondage of habitual
narcotism should be made. For reasons that are {669} obvious, measures
having this end in view should be instituted by preference
subsequently to surgical treatment. To this class also belong certain
painful affections occupying the border-region between surgery and
medicine. These are floating kidney, renal and hepatic abscess,
calculous pyelitis, cystitis, impacted gall-stones, and thoracic and
abdominal aneurism. In these cases the possibility of a cure renders
it in the highest degree desirable that the opium habit should be
stopped. Whether this attempt should be made while the patient is
under treatment for the original affection, or deferred until relief
has been obtained, is a question to be decided by the circumstances of
the particular case under consideration. Finally, we encounter a large
group of chronic painful affections coming properly under the care of
the physician in which the opium habit is frequently developed. This
group includes curable neuralgias of superficial nerves, as the
trigeminal, occipital, brachial, intercostal, crural, and sciatic, and
visceral neuralgias, as the pain of angina, gastralgia, enteralgia,
and the pelvic and reflex neuralgias of women. Here also are to be
mentioned the pains of neurasthenia, hypochondriasis, and hysteria. In
this group of affections the original disease constitutes no obstacle
to the attempt to break up the habit to which it has given rise.

The practice of using narcotics, especially the preparations of opium,
in large and increasing doses for the relief of frequently-recurring
pains, especially in neurotic individuals, is a dangerous one. When
necessary at all, the use of these drugs should be guarded with every
possible precaution. In the first place, in so far as is practicable,
the patient should be kept in ignorance of the character of the
anodyne used and of the dose. In the second place, the physician
should personally supervise and control, in so far as is possible, the
use of such drugs and the frequency of their administration, taking
care that the minimum amount capable of producing the desired effect
is employed. In the third place, the occasional alternation of anodyne
medicaments is desirable. Fourthly, an effort—which, unfortunately, is
too often likely to be unsuccessful—should be made to prevent repeated
renewals of the prescription without the direct sanction, or indeed
without the written order, of the physician himself. Finally, the
danger of yielding to the temptation to allow a merely palliative
treatment to assume too great importance in the management of painful
affections must be sedulously shunned. Too often these precautions are
neglected, and the patient, betrayed by a dangerous knowledge of the
drug and the dose by which he may relieve not only physical pain, but
also mental depression, and tempted by the facility with which the
coveted narcotic may be obtained, falls an easy victim to habitual
excesses. The lowered moral tone of convalescence from severe illness
and of habitual invalidism increases these dangers. Yet more
reprehensible than the neglect of many physicians in these matters is
the folly of the few who do not hesitate to fully inform the patient
in regard to the medicines given to relieve pain or induce sleep, and
to place in his hands designedly the means of procuring them without
restriction for an indefinite period of time. Almost criminal is the
course of those who entrust to the patient himself or to those in
attendance upon him the hypodermic syringe. No trouble or
inconvenience on the part of the physician, no reasonable expense in
procuring continuous medical attendance on the part of the patient for
the sake of relief from pain, can ever offset, save in cases of the
final stages {670} of hopelessly incurable painful affections, the
dangers which attend self-administered hypodermic injections.

The uniform and efficient regulation of the sale of narcotic drugs by
law would constitute an important prophylaxis against habitual
narcotism. Unfortunately, the existing laws relating to this subject
are a dead letter. They are neither adequate to control the evil nor
is their enforcement practicable. Nostrums containing narcotics, and
particularly opium and morphine, in proportions that occasionally
produce fatal results are freely dispensed at the shops to all comers.
Prescriptions calling for large amounts of opium, morphine, codeia,
chloral, cannabis indica, etc. are dispensed to the same individuals
at short intervals over the counters of apothecaries for months or
years after the illness in which they were originally prescribed is
over. Yet more, occasional cases come to light which serve to indicate
the appalling frequency with which opium, its tincture, morphine, and
solutions of chloral are directly sold to unauthorized individuals. If
the evil thus accomplished were better understood, the paltry profit
realized from such nefarious trading would rarely tempt men to the
commission of the crime which these practices constitute.

Finally, the dissemination of a wholesome knowledge of the methods by
which the opium habit and kindred affections are induced, of the
serious character of these affections, and of the dangers attendant
upon an ignorant and careless employment of narcotics, would
constitute an important measure of prophylaxis. I am fully aware of
the evils resulting from the publication of sensational writings
relating to this subject. Notwithstanding these dangers, I am
convinced that a reasonable and temperate presentation of the facts in
the popular works upon hygiene used in schools and in the family would
exercise a wholesome influence in restraining or curing the tendency
to the practice of these vices.

Where these habits have resulted in consequence of the medicinal abuse
of narcotics in acute cases from which the patient has long recovered,
a determined effort to break them up should at once be instituted.

_b_. The Curative Treatment.—The responsibility assumed by the
physician in attempting to cure patients suffering from the confirmed
abuse of narcotics is often a serious one. Much judgment must be
exercised in the selection of cases. The responsibility of the
physician, beginning as it does with the judicious selection of the
cases, does not cease with the active management of the patient until
the habit has been completely broken up, but involves for a
considerable period of time such continued personal influence and
supervision as is needed to avert relapse. It is needless to say that
such supervision and influence must, after a more or less extended
period, in nearly every case come to an end, but the important fact is
to be borne in mind that the danger of relapse becomes less and less
with the progress of time; therefore, the more extended the period
during which the personal control of the physician may act as a
safeguard to his patient the better.

The question as to whether the cure should be attempted in the
patient's own home or away from it does not appear to the writer to
admit of discussion. Some trustworthy observers[12] have reported
successful cases not only {671} of the home-treatment of
opium-addiction, but even under circumstances in which the patients
have been permitted to go at large. Many physicians do not hesitate to
undertake the treatment with certain precautions at the home of the
patient. On the other hand, those whose experience in the management
of these cases is most extended look upon attempts of this kind as
likely to be unsuccessful in the great majority of the cases of the
opium or morphine habit. In cases of chloralism and the abuse of less
formidable narcotics, as cannabis indica, paraldehyde, etc., the
home-treatment, if judiciously carried out, usually succeeds, but the
cases in which the home-treatment proves successful in curing the
confirmed addiction to opium or morphine must be looked upon as
exceptional. The reasons for this are obvious. They relate to a
variety of circumstances which tend to weaken the mutual relations of
control and dependence between the physician and his patient. The
doubts, criticisms, remonstrances, even the active interference, of
the patient's friends tend to weaken the authority of the physician
and to hamper him in the management of the case; the discipline of the
sick-room is maintained with greater difficulty; the absolute
seclusion of the attendant with his patient is a practical
impossibility. Affectionate but foolish friends come with sympathy at
once disturbing and dangerous. Some devoted and trusty servant
cunningly conveys from time to time new supplies of the coveted drug,
or, if these accidents be averted, the very consciousness of the
separation which amounts to a few feet of hall-way only is in itself a
source of distress to the patient and his friends alike. Furthermore,
the period of convalescence following the treatment is attended with
the greatest danger of relapse—a danger which is much increased by the
facility of procuring narcotics enjoyed by the patient in his own home
as contrasted with the difficulties attending it away from home under
the care of a watchful attendant. The desirability of undertaking the
treatment away from the patient's home can therefore scarcely be
questioned. That this plan is more expensive, and that it involves a
radical derangement of the ordinary relations of the patient's life,
are apparent rather than real objections to it. The very expense of
the cure within the limits of the patient's ability to pay, and the
mortification and annoyance of temporary absence from usual
occupations and seclusion from friends, are in themselves hardships
that enhance the value of the cure when achieved, and constitute, to a
certain extent, safeguards against relapse. Whether the treatment can
be more advantageously carried out in a private asylum designed for
the reception of several such cases, or in a private boarding-house,
or at the home of the physician himself, is a question to be
determined by circumstances. The writer is of the opinion that with
well-trained and experienced attendants, well-lighted, airy rooms in
the upper part of a private house are to be preferred on account of
the seclusion thus secured.

[Footnote 12: See, for example, Waugh, “A Confirmed Case of
Opium-addiction treated Successfully at the Patient's Home, with
Remarks upon the Treatment, etc.,” _Philadelphia Medical Times_, vol.
xvi., March 20, 1886.]

In general, two methods are recognized: (_a_) that of the abrupt
suppression of the drug, and (_b_) that of the gradual diminution of
the dose. Both of these methods demand the isolation of the patient,
and to some extent at least the substitution of other narcotics. The
isolation of the patient under the care of skilled and experienced
attendants may be secured in a suitable private boarding-house, in the
home of a physician, or in a private room of a well-appointed general
or special hospital. Favorable opportunities are also afforded in
private institutions devoted {672} to this purpose. The apartment
occupied by the patient should be so arranged as to guard against
attempts at suicide, and the furniture should be of the simplest
character. The heating and lighting arrangements must be such as to
render any accidental injury to the patient during paroxysms of sudden
maniacal excitement quite impossible. From the beginning of the
treatment the patient must under no circumstances be left alone. Two
attendants are required, one for the day and one for the night. They
should be not only skilful and experienced, but also patient and firm;
and, as a considerable proportion of the patients are persons of
education and refinement, intelligence and good manners are desirable
on the part of those who must be for a length of time not only the
nurses, but also the companions, of the sufferer. It is desirable that
the separation of the patient from his family and friends should be
made as complete as possible. During the continuance of the active
treatment no one should be admitted to the patient except his
physician and regular attendants. Communication with his friends by
letter should be interdicted. The enforcement of this rule must be
insisted upon. So soon as the acute symptoms caused by the withdrawal
of the drug subside and convalescence is fairly established, brief
visits from judicious members of the family in the presence of the
nurse may be permitted. At the earliest possible moment open-air
exercise by walking or driving must be insisted upon, and change of
scene, such as may be secured by short journeys or by visits to the
seashore, is useful. These outings require the constant presence of a
conscientious attendant.

The Treatment of the Opium and Morphine Habit.—_a_. The Abrupt
Discontinuance of the Drug: the Method of Levinstein.—This method is
thus described by the observer whose name it bears: Directly upon
admission the patient is given a warm bath, during which time careful
examination of his effects is made by a responsible person for the
purpose of securing the morphine which the patients, notwithstanding
their assertions to the contrary, frequently bring with them. These
measures of precaution are by no means unnecessary. An officer had
saturated his cigarettes and cigars with a solution containing opium,
and smoked for twenty-four hours almost without interruption. Another
officer had slipped morphine between the soles of new slippers. Other
individuals concealed immediately after their arrival morphine in
powder in the upholstery of the sofa, upon the canopy and in the
ventilators of the windows. Other patients enclosed morphine in
envelopes of thin paper, which were placed between the leaves of their
books, stitched it in the folds and lining of their garments, etc.

The first symptoms of the withdrawal of the drug show themselves in
delicate individuals at the end of three or four hours, and in robust
persons about fifteen hours, after the last dose. These symptoms
consist of malaise, restlessness, a sense of muscular tension, chilly
sensations, and the like, but do not demand treatment. As soon as
shivering commences the patient must be put to bed—a measure to which,
as a rule, he readily assents on account of the sense of muscular
fatigue now experienced. For the relief of the headache, which is
rarely absent, applications of cold water or of ice or ether-douches
to the forehead may be employed. For the distressing gastralgia
compresses moistened with chloroform may be applied to the
epigastrium. The colic, which is often distressing, {673} may be
treated by sinapisms or hot compresses. The nausea and vomiting and
epigastric distress, which are apt to continue for several days, may
be treated by a solution of bicarbonate of sodium with tincture of nux
vomica and essence of mint. If the vomiting be excessive, recurring
twenty or thirty times in the course of twenty-four hours, small doses
of morphine by the mouth must be given. If by reason of the continued
vomiting and inability to retain nourishment dangerous exhaustion
develops, nutritive enemata must be administered. The diarrhœa
requires little treatment during the early days. If, however, it be
excessive and persists beyond the third or fourth day, large enemata
of warm water of a temperature of 98° F., repeated two or three times
during the day, are attended by excellent results. The insomnia, which
constitutes a most distressing symptom, defies every kind of treatment
during the first three or four days. During this time prolonged baths
are not well borne, and even when they are employed they scarcely
produce more than half an hour or an hour of sleep. Chloral is also,
under these circumstances, inadmissible, whether administered by the
stomach or by the rectum. It does not induce sleep, and its employment
is very often followed by a high degree of excitement. After the
fourth day it is well borne by many persons, and manifests its usual
hypnotic property. Warm baths of five minutes, followed by cold
affusions, exert an excellent influence upon the general debility and
mental depression of the first days. The objections of patients to
these baths cease after they have experienced the excellent results
which follow their use. During the bath stimulants, such as champagne,
port, and hot bouillon, may be given. Care must be paid to the
alimentation from the very beginning of the treatment. During the
first days liquid nourishment should be given, and abundance of wine
and other alcoholic beverages according to the previous habits of the
patient. Some nourishment is to be given every hour or every two
hours. Many patients experience an intense craving for alcoholic
drinks; others, on the other hand, are unable to take them. To the
former wine, beer, etc. may be given freely during the first three or
four days; to the latter a restricted milk diet may be given, one to
two quarts in the course of twenty-four hours. Such is the method of
Levinstein, to which he adds, however, important modifications for
those—and their number is large—who are unable to bear the abrupt
withdrawal of the drug.

This method is attended in all cases by indescribable sufferings, and
in many by serious dangers. Among the last, collapse and delirium
tremens demand special consideration. The collapse which occurs in a
certain proportion of the cases requires prompt and energetic
treatment. The pulse becomes feeble, small, gradually or suddenly
diminishes in frequency; the countenance is pale; the previous
agitation gives place to an ominous calm; there is a tendency to
syncope, accompanied by persistent somnolence and slowing of the
respiration. Inhalations of ammonia and the administration of aromatic
spirits of ammonia, champagne, brandy, or hot coffee, with frictions
of the surface and cold applications to the head, may occasionally
produce reaction. As a rule, however, it is necessary to administer a
hypodermic injection of morphine. This condition of collapse, once
having shown itself, is apt to recur upon the same or the following
day. The treatment of the delirium tremens {674} consists in
isolation, the administration of abundant nourishment, the use of the
bromides, chloral, or paraldehyde, with alcoholic stimulants. As this
complication is unattended by danger to life, and usually disappears
in the course of a few days, the administration of morphine is not
required.

The modifications of this method suggested by Levinstein for those who
are unable to bear the abrupt suppression of the drug are as follows:
The patient is isolated and guarded; for two or three days his
habitual dose is administered, this duty being performed by the
physician himself. The drug is then abruptly discontinued. At the end
of twenty-four hours the phenomena of abstinence are manifested; the
pulse loses its regularity, distressing diarrhœa and vomiting occur,
etc. These symptoms are controlled by the injection of morphine, the
dose being much smaller than that to which the patient has been
accustomed. By this means the sufferings of the patient are
ameliorated, and the dangers attendant upon the rapid suppression of
the drug are averted. At the end of twenty-four hours it becomes
necessary to again administer the drug, but in diminished dose. After
a time it is discontinued altogether.

_b_. The Gradual Diminution of the Dose.—This method is now generally
employed. It consists in isolation of the patient with proper
attendants and the progressive diminution of the dose. The drug should
always be administered by the physician himself. The rapidity with
which it is suppressed will be determined by the circumstances of the
individual case. The time occupied should not exceed ten days. In the
majority of cases it will be much shorter than this. If the
administration of morphine to correct urgent symptoms be at all
required after this time, it will be at most on one or two occasions
at intervals of twenty-four or forty-eight hours. When the process of
reducing the dose is too greatly prolonged, the sufferings of the
patient are unnecessarily aggravated. As the diminution progresses the
relief produced by each dose is followed by distressing reaction. The
anticipation of smaller doses from time to time or from day to day is
a matter of great distress to patients. After a while their courage
and endurance fail them, and they seek by every possible means to
secure at least one good dose of the coveted drug.

The symptoms produced by the suppression of the drug speedily show
themselves, increasing in intensity as the dose diminishes. Temporary
amelioration is, however, produced by each of the successively
diminishing doses of the drug. Whatever may have been the method
followed by the patient, the hypodermic injection of morphine is to be
preferred in the treatment. The disturbances of the digestive system
which speedily appear require but little special medication. The
danger of inanition which attends the complete loss of appetite, the
inability to take ordinary food, and the frequent often uncontrollable
vomiting, are best met by the systematic administration of easily
assimilable liquid diet, consisting of lime-water and milk, milk and
Vichy water, pancreatized milk, koumiss, concentrated broths, the
expressed juice of fresh partly-cooked beef, and the various
commercial foods used in the artificial feeding of infants. Vomiting
rarely occurs immediately after the ingestion of articles of this
kind. If it takes place in the course of an hour, some degree of
digestion and absorption will have taken place. Should, however, all
food be rejected by the stomach, efforts at rectal {675} alimentation
must be attempted. Efforts to control the vomiting by medicines other
than the administration of opium or morphine in some way are not
usually attended by success. The diarrhœa is usually frequent, the
stools being liquid, sometimes small, often copious, and amounting in
number from eight or ten to thirty or more in the course of
twenty-four hours. They are not usually attended by pain. Some relief
to this symptom follows the administration for a time of large doses
of bismuth subnitrate (grs. xx to xxx) every second, third, or fourth
hour. The sinking feeling at the pit of the stomach and the epigastric
pain are to some extent alleviated by external applications. Hot
fomentations or compresses containing a few drops of chloroform or
turpentine are also useful.

The derangement of the respiratory system, which consists usually in a
certain amount of bronchitis with more or less cough and some dyspnœa
aggravated by exertion and movement, does not usually require special
treatment.

Disturbances of the circulation constitute a very important group of
symptoms, and require close watching always, active interference
frequently. For the relief of the phenomena due to flagging action of
the heart the recumbent posture, external warmth, friction of the
extremities, the application of turpentine stupes or mustard to the
præcordial and epigastric regions, the inhalation of ammonia or the
administration of preparations of ammonia, and sometimes digitalis,
which may be given either by the mouth or hypodermically, will be
required. Alcohol, however, will prove in the greater number of cases
a most useful remedy—in many an indispensable one. It may be given in
the form of milk-punch, hot toddy, or of port, champagne, etc.,
according to the requirements of the case. Failure of the circulation
may, notwithstanding every effort to control it, reach such a degree
as to jeopardize the patient's life. Under such circumstances the
treatment must be interrupted by the immediate administration of small
but efficient doses of morphine, which, if necessary, must be
repeated. As diarrhœa increases the quantity of urine excreted rapidly
diminishes. It may not exceed eight or ten fluidounces in the course
of twenty-four hours. After the third or fourth day of the treatment
the urine in a considerable proportion of cases contains albumen and
occasionally casts. The oliguresia is largely due to the excessive
loss of fluid by the bowel, and does not require treatment. Nor,
indeed, is active treatment demanded by the albuminuria, which usually
spontaneously subsides in the course of a few days, although it
sometimes persists for some weeks or months. Persistent albuminuria
requires appropriate treatment.

The nervous symptoms, which constitute a most important group, are
favorably influenced by methodical alimentation and the free use of
alcoholics. Care must be taken to reduce the amount of alcohol
administered as convalescence progresses. With the re-establishment of
the normal functions of the body, the disappearance of insomnia, and
improved nutrition, alcohol may in the majority of cases be rapidly
diminished or wholly withdrawn. This course, favored by the regular
life which the patient should be obliged to lead on becoming
convalescent, and the feeling of general bienaise which is gradually
developed as the cure progresses, is rendered especially important by
the fact that a considerable proportion of opium-habitués are
individuals of unstable nervous organization, which in itself
constitutes a powerful predisposing influence to alcoholism.

{676} It seems hardly necessary to describe in detail the treatment
demanded for the relief of the varied disturbances of the nervous
system. The use of coca in the form of a good preparation of the wine
or fluid extract in appropriate doses, to which may be added tincture
of cannabis indica, exerts a favorable influence. The administration
of cocaine by the mouth and hypodermically has in some instances
seemed to me to be followed by favorable results. It is not, however,
to be adopted as a routine practice, by reason of its occasional
depressing effect and the possible danger of replacing the opium habit
by a craving for cocaine. Lupulin, and in particular an ethereal
extract of lupulin, exerts a favorable but not very powerful influence
in tranquillizing the nervous system. With the view of controlling to
some extent the insomnia, the hypodermic injections should, during the
early part of the treatment, be so timed that the period of sleep or
drowsiness which they produce should occur during the night. As soon
as the number of injections is reduced to one daily, that one should
be administered at the latest convenient hour before midnight. For
twenty-four or forty-eight hours after the final discontinuance of
morphine but little effect may be expected from ordinary doses of
other sleep-inducing drugs. Chloral in single large doses (grs. xx to
xxx), either alone or associated with a corresponding large dose (grs.
xl to lx) of one of the bromides, administered on the second or third
night after total suppression, is very often followed by prolonged,
tranquil, and refreshing sleep. Caution must be observed, however, in
administering chloral so long as the indications of feeble circulation
persist. Paraldehyde, although less certain, is a less dangerous
hypnotic under such circumstances. Massage, hot baths, and the cold
pack are all useful adjuvants to the treatment. The sweating when
copious and distressing is favorably influenced by sponging with hot
alcohol.

The abject mental state of the patient calls for much firmness,
gentleness, and tact on the part of the physician and attendants.
Every effort should be made to inspire courage and hope. Neither the
importance of the symptoms nor the intensity of the sufferings of the
patient should be underrated; nevertheless, the ordeal is a limited
one. In the majority of instances, to get rid of the opium means to
get well, because opium, unlike alcohol, does not leave permanent
structural lesions of any organ. The expectation of a radical cure
must therefore be confidently presented to the patient as a
consolation in his sufferings.

With the return of convalescence sexual power is restored and
menstruation is re-established. Insomnia and muscular weakness usually
persist into the convalescence for some weeks, and only gradually
yield to careful regulation of the daily life of the patient, with
abundant nutritious food, open-air exercise, and change of scene. The
insomnia of this period constitutes a serious symptom, for the reason
that it constantly subjects the patient to the temptation to return to
the use of hypnotics. In the course of time, however, the normal
physical and mental condition is regained, and the patient may be
permitted to return to his former pursuits and associations.

The Treatment of the Chloral Habit.—That which has been said in the
foregoing pages concerning the prophylaxis against the opium habit
applies with equal force to chloral and other narcotics. The curative
treatment of habitual addiction to chloral is attended neither by the
{677} difficulties nor the dangers which are encountered in the
management of the opium habit. The symptoms attending the
discontinuance of chloral are less severe and less persistent; in
fact, individuals accustomed to the taking of large doses of chloral
not infrequently voluntarily discontinue its use for considerable
periods of time. As a rule, the treatment may be carried out at home,
the patient, however, being isolated and cared for by a watchful
attendant. The drug should be stopped at once. For the first few days
alcoholic stimulants should be freely given. Systematic feeding,
pepsin, full doses of quinine, followed after a time by strychnia,
and, as soon as the condition of the digestive system will permit of
it, by iron, fulfil the general indications. Cod-liver oil and malt
extracts may be given with advantage. Cardiac failure, collapse, and
delirium tremens are to be treated in the same manner as similar
complications occurring in the treatment of the opium habit. Vomiting
is much less likely to occur, and when present is less persistent and
less difficult of management. Diarrhœa does not usually prove
troublesome, the bowels, on the contrary, being constipated. The
latter condition yields to mild laxatives or to simple enemata.
Hemorrhages from the various mucous tracts may be controlled by fluid
extract of ergot, the hypodermic injection of solution of ergotin,
minute doses of wine of ipecac, or fluid extract of hamamelis. The
conjunctivitis which is occasionally present usually subsides
spontaneously upon the discontinuance of chloral. It may be treated by
instillations of a 2 per cent. solution of cocaine and mild borax
lotions (grs. v to fluidounce j). The after-treatment must be
carefully carried out. Relapses are less frequent than after the opium
habit.

The Treatment of Habitual Addiction to Paraldehyde, Cannabis indica,
Ether, Chloroform, etc. must be based upon the general principles
indicated in the foregoing pages. Cases of the habitual abuse of these
drugs are comparatively infrequent on the one hand, and on the other
do not often present the serious and progressive symptoms produced by
excesses in opium and chloral; hence they come but rarely under the
care of the physician, except in those unhappy individuals in whom the
propensity to vicious narcotism is such that any drug capable of
producing excitement and oblivion is made the means of gratification,
and all are used by turns as the opportunity occurs.


{678}


CHRONIC LEAD-POISONING.

BY JAMES C. WILSON, M.D.


DEFINITION.—The term chronic lead-poisoning is used to designate the
morbid phenomena induced by the gradual accumulation of lead in the
organism.

SYNONYMS.—Plumbism, Saturnism, Morbus plumbeus, Molybdosis,
Molybdonosus, Intoxication saturnine, Bleivergiftung.

CLASSIFICATION.—Chronic lead-poisoning manifests itself in serious
disorders of nutrition which are widespread and implicate all the
tissues of the body; but for the reason that its more striking and
characteristic symptoms relate to the nervous system, it has been
classed among disorders of that system as a toxic neurosis.

Acute poisoning by lead is an entirely different affection. It depends
upon the power of the salts of lead to coagulate albumen. Its symptoms
are those of acute corrosive gastritis; derangements of the nervous
system are secondary. It does not fall within the scope of the present
article.

HISTORY.—Chronic lead-poisoning must have existed from the infancy of
the arts in which the metal is employed. It does not, however, appear
to have been recognized until after the time of Hippocrates. Celsus
was aware of the danger attending the administration of lead.
Nicander, Dioscorides, Aretæus, and Paul of Ægina recognized lead
colic and the paralysis resulting from its long-continued introduction
into the stomach. Among Arabian physicians, Rhazes and Avicenna
accurately describe the effects of the preparations of lead. No
considerable addition to the knowledge of the subject was made until
the seventeenth century. In 1616 was printed at Poitou the famous work
of Citois, _De novo et populari apud Pictones dolore Colico bilioso
Diatriba_. The epidemic colic described by this author was caused,
although he little suspected it, by the common use of wine which had
been treated by lead to remove its acidity. This practice, which is of
very ancient date, and is described in the writings of Cato, Pliny,
and Columella, was at one period very general in Europe, and had been
forbidden by imperial ordinances as early as 1437.[1] It remained for
Stockhausen, in a treatise published at Goslar in 1656, and entitled
_De Lythargyrii Fumo, noxio, morbifico ejusque metallico frequentiori
morbo vulgo dicto Hutten-Katze_, to demonstrate that Poitou colic was
produced by lead in particles in {679} emanations, and for Wepfer in
1671 to first clearly point out the fact that the epidemic colic so
often described was usually caused by lead in wine. During the
eighteenth century the epidemic colic attracted much attention among
medical men, and its etiology was made clear. Henkel called the
affection founder's colic, and showed how it was produced in those
engaged in casting lead; Huxham, in his work on _Fevers_ (1745),
described the disease as it prevailed in Devonshire, and several
English observers conclusively proved that the epidemics of colic
frequently appearing in certain districts were caused by the presence
of lead in cider, and that it was due to the action of the apple-juice
upon lead used in the construction of the presses and implements
employed in the manufacture of that popular beverage.

[Footnote 1: Vide Tanquerel des Planches, _Lead Diseases_, translation
by S. L. Dana, M.D., LL.D., Lowell, 1848.]

During the current century the closer study of the etiological
relations of disease has revealed many unsuspected sources of
lead-poisoning in the arts, and of lead contamination, both accidental
and intentional, in articles of food, drink, and luxury. Hence the
literature of the subject has assumed very extensive proportions. The
French physicians have devoted much attention to this subject. The
great work of Tanquerel des Planches, to which reference has already
been made, remains to this day the most complete and comprehensive
authority. Quite recently valuable additions to existing knowledge
have appeared in some of the Paris theses.[2]

[Footnote 2: Vide Capelle, _De l'Intoxication saturnine_, Paris, 1883;
Séguin, Ch., _De l'Albuminurie transitoire des Saturnins_, Paris,
1883; Goudot, _Étude sur la Goutte saturnine_, Paris, 1883; Verdugo,
_Contribution à l'Étude de la Goutte saturnine_, Paris, 1883; and
Coutard, _La Colique du Poitou considérée comme Intoxication
saturnine_, Paris, 1884.]

ETIOLOGY.—_A_. Predisposing Influences.—Individuals exposed to lead
and its compounds are not all equally prone to its effects. The degree
of liability is to some extent dependent upon individual
susceptibility, and to a much greater extent upon circumstances which
are determined by the season, climate, age, sex, diet, and mode of
life of different persons. It will be convenient to consider the
predispositions which arise from occupation under the head of the
Exciting Cause.

Variations in the degree of susceptibility to chronic lead-poisoning
appear to be explicable in a majority of the cases solely upon the
theory of idiosyncrasy. While a large proportion of the cases are in
well-developed, strong, and previously healthy adults, individuals of
feeble constitutions do not escape. Those occupations which involve
the greatest exposure to the danger of contracting this affection at
the same time demand the powers of a robust frame. Habitual
recognition of these dangers, such as begets the habitual exercise of
reasonable precautions against them, diminishes to some degree the
liability of a few workmen.

Season.—Due allowance being made for the difference in the number of
workmen employed in manufactures which involve exposure to lead, and
especially in the making of white lead, at different seasons of the
year, it has been found that attacks of lead colic and of lead palsy
are more common in warm than in cold weather. Heat predisposes to the
attack, either by favoring the dissemination of the lead compounds or
by facilitating their absorption by various channels, especially by
the skin, which is more freely exposed in summer, and at the same time
more or less bathed in sweat in which the dust of lead salts may be
dissolved.

{680} Climate.—In the absence of definite statistics upon the subject,
it appears probable that the dangers of chronic lead-poisoning would
be greater in warm than in cold climates. The clinical features of the
affection are alike in all parts of the globe.

Age.—The majority of individuals attacked are adults. Nevertheless,
children employed in occupations involving exposure to lead are
attacked with great frequency—so much so that it may be concluded that
their liability is in fact greater than that of adults.

Sex exerts a decided influence, women being, under nearly similar
circumstances, less frequently attacked than the men employed in the
same factories—a fact to be explained only by their greater
willingness to exercise the recognized precautions.

Diet does not constitute a predisposing influence. It is nevertheless
probable that a deficient diet favors the development of the
affection. Excesses in food, and especially excesses in drink,
predispose to lead colic.

The mode of life is important. Those who lead sober, regular, and,
above all, cleanly lives are less liable to the affection than the
intemperate, irregular, and careless. Particularly are the dangers in
factories increased by neglect of ventilation. Persons suffering from
affections of the digestive tract are not, among lead-workers, more
prone to lead colic than their comrades who are free from such
diseases.

_B_. The Exciting Cause.—Metallic lead is probably inert, but, owing
to the ease and rapidity with which it oxidizes and forms salts, lead
in any form, if introduced into the body continuously for a length of
time, produces characteristic toxic effects. The oxides, acetates, and
carbonate of lead, being soluble in the gastric juice, act more
surely.[3] But the sulphate, the least soluble of the lead compounds,
may also have this effect (Gasserow).

[Footnote 3: Naunyn, _Ziemssen's Encyclopædia_, vol. xvii.]

The channels by which lead is introduced into the body are the
alimentary canal, the respiratory tract, and the cutaneous surface.
Hence the modes of introduction are of almost endless variety. The
conveyance of lead into the stomach constitutes the most common as
well as the most important means of access to the organism. This may
be in the form of medicine, as the acetate, the unduly prolonged use
of which, even in moderate doses, sometimes produces chronic
poisoning. Articles of diet are not infrequently contaminated by lead
derived from different sources, of which the most common is the lead
glaze of earthenware vessels, which is soluble in acid fluids.
According to Naunyn, beer drawn through lead pipes may cause chronic
lead-poisoning, which has also been frequently ascribed to the use of
shot in cleaning bottles used for wine and malt liquors.
Drinking-water is occasionally contaminated with lead derived from
pipes made of this metal and cisterns painted with lead colors. Pure
water, freed from gases, does not act upon lead when the air is
excluded. In the presence of air, however, an oxide of lead is formed
which is partially soluble in water. If nitrates, nitrites, and
chlorides, such as constitute ingredients of sewage, are also present,
they form soluble compounds with lead and increase the proportion of
lead salts soluble in the water. For this reason water contaminated by
sewage is rendered decidedly more dangerous if carried in leaden
pipes. On the {681} other hand, the purer the water the greater the
danger. Hence rain-water and pure spring-water cannot safely be stored
in cisterns painted with lead colors nor conveyed in leaden pipes, nor
can lead covers be used for cisterns, because of the condensation of
the vapor of water, which drops back, holding lead salts in solution.
The sulphates, phosphates, and carbonates usually found in
river-waters form insoluble lead compounds, which, being deposited
upon the interior of the pipes, act as protectives and prevent further
chemical changes.

Still more common is the accidental conveyance of lead dust and lead
compounds to the mouth in consequence of their adhering to the hands
or settling from the atmosphere upon articles of food and drink, in
the case of workmen engaged in the various arts in which lead is
freely used. As a rule, to which the exceptions are rare, the more
severe cases of chronic lead-poisoning occur only among workers in
lead, as miners, those employed in white-lead factories, painters,
typesetters, plumbers, and lapidaries.

Potters engaged in the glazing of common pottery and tiles, workmen in
file-factories, workers on colored papers and in enamels, especially
in glass enamels, brushmakers for the reason that the bristles are
sometimes colored by lead preparations, and those engaged in sewing
coarse goods because the thread is sometimes treated with a
preparation of lead in order to add to its weight, are likewise liable
to chronic lead-poisoning. The introduction of lead into the body
through the respiratory tract is a subject of the greatest importance
in the trades. Inadequate ventilation of working-rooms, living or
sleeping in apartments connected with or contiguous to factories in
which lead is largely used, and particularly in lead-factories, is
attended with serious dangers, as is also the habit of eating food in
such apartments or drinking water that has been standing in them. The
possibility of lead-poisoning by way of the respiratory tract has been
questioned. In view of existing knowledge as to the readiness with
which carbon in minute states of subdivision finds its way into the
connective lymph-channels of the lung, there can be no doubt that the
habitual respiration of an atmosphere loaded with the dust of lead or
its preparations in a minute state of subdivision may give rise to
chronic lead-poisoning. At the same time, the experiments of Hassel[4]
render it probable that less absorption takes place directly by means
of the pulmonary mucous membrane than by way of the mucous membrane of
the mouth and throat. It must be borne in mind that none of the
preparations of lead are volatile. This affection is also occasionally
observed in clowns and others upon the stage or elsewhere, who
habitually use cosmetics containing lead. The use of cheap tinfoil,
into the composition of which lead enters largely, as a wrapper for
tobacco and snuff is said to occasionally produce chronic
lead-poisoning. It is stated by Naunyn that mattresses filled with
horse-hair died black by lead compounds have occasioned this
affection. The same authority states that a proof-reader was poisoned
by reading printed proof for many years. Chronic lead-poisoning is
pre-eminently a disease of the industrial arts. The means of obviating
or diminishing the dangers of those exposed by their occupation to the
preparations of lead will be considered under the head of Prophylaxis.
{682} The quantity of lead absorbed is of less importance than is its
continuous introduction. As stated in the definition, the phenomena of
chronic lead-poisoning are those brought about by the gradual
accumulation of lead in the system, the amount absorbed into the blood
in any given cases being comparatively small, even where large
quantities are ingested. Hence prolonged exposure to small amounts of
lead is attended with greater danger than a comparatively brief
exposure to larger quantities. It is stated that the members of the
household of Louis Philippe at Claremont manifested the symptoms of
chronic lead-poisoning after the lapse of seven months in consequence
of drinking water which contained a mere trace of lead. On the other
hand, several grains of acetate of lead may often be administered
medicinally to patients for a week at a time without inducing the
phenomena of this affection, although, in view of the idiosyncrasy of
many individuals, the exhibition of lead preparations for prolonged
periods is not advisable.

[Footnote 4: _The Inhalation Treatment of the Diseases of the Organs
of Respiration, including Consumption_, London, 1885.]

According to Heubel,[5] the blood and internal organs contain but very
small amounts of lead—.02 per cent. in the maximum. It is probable,
therefore, that the more insoluble of the lead compounds may yield a
sufficient amount of absorbable lead to produce the characteristic
constitutional effects.

[Footnote 5: _Pathogenese und Symptome der Chronic Bleivergiftung_,
Berlin, 1871.]

So long as the urine remains free from albumen, it serves for the
elimination of a mere trace of lead. In albuminous urine the amount is
larger. Lead is found in the bile and feces in small quantities.

SYMPTOMATOLOGY.—The general description of chronic lead-poisoning must
include a great number of symptoms that do not always occur in regular
order or sequence. According to the prominence of certain of these
symptoms in particular cases the specific effects of lead may be
grouped under the following five heads: (1) disturbances of nutrition;
(2) the colic; (3) the arthralgia; (4) the paralysis; and (5) lead
encephalopathy.

1. Disturbances of Nutrition—After the long-continued introduction of
lead into the system the signs of impaired nutrition manifest
themselves in almost all cases. The appearance of the patient is
changed; he becomes thin, anæmic, and of a somewhat peculiar yellowish
complexion. This hue of the skin, to which the term icterus saturninus
has been applied, is not due to the deposition of bile-pigments. The
wasting of the tissues of the body seems to implicate the muscular to
a much greater extent than the adipose tissues. In the majority of
cases a dark or bluish-black line is observed at the border of the
gums. This line is more strongly marked in the upper than in the lower
jaw. It is, as a rule, more plainly developed in persons of careless
habits, whose teeth are the seat of deposits of tartar, but the teeth
in such individuals are often discolored and appear to be elongated in
consequence of the retraction of the edge of the gums. This bluish or
violet-black gingival line is due to the deposit of particles of
sulphide of lead in the substance of the gum, in consequence of the
reaction between the sulphuretted hydrogen formed by the decomposition
of particles of food and the lead particles present in the mouth.
According to Tanquerel, this color may extend over the greater part of
the gum or even to the mucous membrane of other portions of the mouth.
If due care be exercised, there is little danger {683} of confounding
the lead-line with the livid border of the gums frequently seen in
people whose teeth are in bad condition. The occasional absence of
this line in otherwise well-characterized cases of chronic
lead-poisoning is to be noted. It does not occur when the teeth have
been lost, and is slight if they are kept clean.

Patients complain of habitual dryness of the mouth and of an insipid,
mildly astringent, sweetish, or faintly metallic taste; the tongue is
coated, the breath fetid. There are nausea and occasional vomiting.
Constipation is common. The patient is now liable to attacks of lead
colic, joint trouble, and the specific palsy, or to cerebral
disturbances of grave character. Of these affections, colic is the
most frequent; the joint affection is next in order; the paralysis far
less common, and the cerebral disturbances comparatively rare.
Continued exposure results after a time in an intensification of the
malnutrition, either with repeated attacks of colic or the other
specific disturbances, or occasionally in their absence, although at
length the positive lead dyscrasia is established, characterized by
obstinate dyspepsia, constipation, and intensification of the curious
earthy or yellowish color of the skin, which is succeeded by the
pallor of profound anæmia. Loss of muscular power with transient œdema
now shows itself. The patient becomes apathetic, irritable, and
morose. As the condition of cachexia deepens muscular tremor
occasionally shows itself. After a prolonged period of profound
ill-health the patient succumbs to some complication, among the more
frequent of which are tuberculosis, pneumonia, and chronic
interstitial nephritis. Gout is a very common complication of chronic
lead-poisoning.

2. Lead Colic; Colica saturnina; Colique de plomb; Bleikolik.—This
affection is also known as painter's colic, Devonshire colic, colica
pictonum, the last term being derived from Poitou. It occasionally
develops abruptly without previous symptoms. In the majority of cases,
however, the earlier disturbances of nutrition before pointed out
precede the attacks, often by a period of weeks or months. An
increased tendency to constipation with transient recurrent abdominal
pains, occurring sometimes immediately after food, more frequently at
irregular intervals, often characterizes the prodromic period. There
is, moreover, an intensification of the other symptoms of chronic
lead-poisoning. The appetite is decidedly impaired, so also are the
powers of digestion; the foul condition of the mouth becomes more
annoying, and the peculiar taste alluded to more persistent and more
marked. Constipation occasionally alternates with diarrhœa. The
colicky pains which constitute the attack are of variable intensity,
but usually severe. They are of the nature of true colic. Pressure
over the seat of pain almost invariably gives relief, particularly in
severe attacks. During the remission pressure is grateful to the
patient. The position of the pain varies. Its most common seat is in
the region of the umbilicus. It may occupy the epigastric and
hypochondriac regions or the lower part of the abdomen, extending from
side to side above the level of the pubic bone. These colics are of
some minutes' duration, recurring after short intervals, which are
characterized by a certain amount of continuous cramp. Tenesmus is
frequent. It may be accompanied by strangury or retention of urine,
with pain in the course of the ureters, the spermatic cord, or in the
penis. Shooting pains in the breast also occur. The abdomen {684} is
retracted, and scaphoid to such an extent in some instances that the
prominence caused by the bodies of the vertebræ is apparent in the
median line of the abdomen. It occasionally happens, however, that
retraction does not occur, the belly, on the other hand, remaining
prominent. As a rule, to which there are few exceptions, the bowels
are constipated. This condition is often stubborn. In rare cases,
however, the colic is accompanied by diarrhœa. Nausea is of common
occurrence. Vomiting is sometimes violent and distressing, being
ushered in by repeated attacks of retching. The vomited matters are
usually discolored by bile, and icterus of slight degree usually
occurs. The pulse is invariably diminished in frequency, sometimes as
low as 40 or even 30, per minute. It is at the same time full and
tense. The pulse-frequency is occasionally variable within
comparatively brief periods of time. Respiration is increased in
frequency during the attack. The urine is small in quantity and of
high specific gravity, and frequently contains small amounts of
albumen. It is sometimes entirely suppressed. Fever is absent, and the
slight increase of temperature occasionally observed is attributable
to the restlessness of the patient. The intellectual condition usually
remains clear, but in violent cases it is characterized by excitement.
The paroxysms of pain are more severe in the latter part of the day
and during the night. The course of the attack is irregular. Relapses,
which may occur in the course of some days or even weeks, are
frequent. The duration of the attack does not, as a rule, exceed a
week, but the illness is often protracted by repeated relapses, and in
continued exposure to the cause the tendency to colic may become
chronic. The termination of the attack is in most instances as abrupt
as its onset, and with the cessation of the colic the associated
symptoms, such as retraction of the abdomen, constipation, vomiting,
and diminished frequency of the pulse, rapidly subside. Lead colic is
not unfrequently associated with the other affections of chronic
lead-poisoning. The prognosis is favorable, the mortality being about
2 per cent.

3. The Arthralgia; Arthralgia saturnina.—The tissues entering into the
formation of the joints and the muscular masses contiguous to them are
frequently the seat of intense paroxysmal pains, which appear more or
less suddenly, either with or without prodromes, and run a course
similar to that of lead colic, exhibiting violent exacerbations and
occasional more or less complete remissions. These pains are
accompanied by painful contractions of the muscles. They are somewhat
relieved by pressure and friction and aggravated by exercise and
exposure to cold. Swelling and redness over the affected joints,
ligaments, and tendons are absent. These pains do not follow the
course and distribution of the nerve-trunks, and lack the tender
pressure-points of true neuralgias. They are more common in the lower
extremities, the knee being especially apt to be affected. When they
affect the upper extremity the elbow and shoulder suffer more
frequently than the other joints. The flexor muscles are much more
frequently attacked than the extensors. The muscles of the back,
especially the great masses of long muscles in the lumbar region,
whose function is to sustain the equilibrium of the body, are
frequently implicated. The intercostal muscles and the muscles of the
neck are also frequently affected. The small joints and the muscles of
the hands and feet as a rule escape. The pain is tearing and burning
in {685} character, and very often severe. It is occasionally
associated with tremor. The derangement of the alimentary canal,
especially constipation, which is so characteristic of lead colic, is
often absent. Fever does not occur.

A careful study of these cases establishes the fact that in a
considerable proportion of them the morbid condition is myalgic.
Whether it be due to simple muscular malnutrition or to some specific
action of lead upon the muscle-substance is not determined. The
analogy between these muscular pains and lead colic renders it
probable that in a large majority of the cases the latter view is
correct. These pains are frequently associated with the attack of lead
colic; sometimes, however, they precede the colic, while at other
times they follow it. After a series of remissions and exacerbations
the pain often ceases as suddenly as it began. As in other lead
affections, relapses are frequent. The prognosis is favorable.

The English physicians, and especially Garrod,[6] Todd,[7] and Bence
Jones,[8] have insisted upon the frequency of gout in chronic
lead-poisoning. Murchison,[9] Wilks,[10] and others regard this
association as causative. This view has not found general acceptance
in France. Lancereaux[11] in particular, after a comparative study of
the lesions of the kidney and of the joints in saturnine cachexia and
the corresponding lesion of gout, concludes that the gouty kidney and
the kidney of lead-poisoning have the same appearance, and are simply
varieties of interstitial nephritis, and that the articular and
arterial lesions in both affections are identical. So-called saturnine
gout differs in no respect, either in its clinical or anatomical
characters, from ordinary gout. It would therefore appear superfluous
to describe saturnine gout. At the same time, it must be insisted upon
that chronic lead-poisoning exercises an important influence in the
production of gout—a causal relation due to the fact that lead
diminishes the excretion of uric acid.

[Footnote 6: _Medico-Chirurg. Transactions_, 1854, vol. lvi.]

[Footnote 7: _Clinical Lectures_, London, 1856.]

[Footnote 8: _Transactions of the Pathological Society, London_,
1856.]

[Footnote 9: _Lancet_, 1868.]

[Footnote 10: _British Medical Journal_, 1875.]

[Footnote 11: “Nephritis et Arthrites saturnines: coincidence de ces
Affections paralleles avec la Nephrite et l'Arthrite goutteuse,”
_Arch. gén. de méd._, Decembre, 1881.]

4. Lead Palsy; Lead Paralysis; Paralysie Saturnine; Bleilähmung.—This
condition is fourth among the affections due to chronic
lead-poisoning, both in frequency and in the order of succession.
Nevertheless, like each of the others, it may be the first in the
order of appearance after disturbances of nutrition which are in some
rare cases of very slight degree. As a rule, however, the paralysis
has been preceded by colic or by joint affection, or by both.
Tanquerel[12] found that in 88 cases of lead palsy 25 had been
preceded by an attack of colic, 15 by two attacks, 3 by ten attacks, 1
by fifteen attacks, and that in single cases as many as twenty, and
even thirty, attacks of lead colic had occurred before the appearance
of paralysis.

[Footnote 12: _Loc. cit._]

The length of time over which habitual exposure to lead without the
development of palsy may extend was found by the same observer to vary
from eight days to ten, twenty, or even twenty-five years. One
individual first suffered from paralysis after fifty-two years of
exposure.

Without dwelling upon the sources of error in statistics of this kind,
{686} it must be conceded that they establish in a general way the
extraordinary differences in the susceptibility of individuals. There
are persons who every time they are attacked with colic, of whatever
degree of severity, suffer also from paralysis. Others, on the
contrary, suffer from repeated attacks of violent colic without the
development of paralysis.

Lead palsy is an affection of adult life. Of 102 cases, 2 only
occurred in individuals below twenty years of age.

Like the other specific lead affections except the encephalopathy,
palsy is more common in the summer than at any other season.

Those who have once suffered are very liable to successive attacks.
Tanquerel and Maréchal have observed many returns of paralysis,
presenting the characters of the original attack, many years after the
patient had withdrawn from exposure to lead.

Perverted sensations of the parts about to be affected, such as
coldness, numbness, and hyperæsthenia, may precede the attack.
Impairment of motor-power, manifested by feebleness, stiffness, or
awkwardness and tremor, also appears in the prodromic period. This
trembling consists in slight agitation of the muscles, rather than in
well-marked rhythmical contractions. These precursors may indeed
constitute the attack, which occasionally, and especially under
treatment, terminates at this point. The prodromic symptoms are less
severe during the day, while the patient is at work; at night they are
aggravated. After some days they end in the characteristic paralysis.
Colic is a common precursor. After the attack some stiffness of the
muscles is experienced, which terminates by rapid loss of power or
abruptly in actual palsy. Occasionally encephalopathy precedes the
paralysis. It is rare that prodromes are wholly absent.

In the great majority of the cases the upper extremities and the
extensor muscles are first attacked. If the paralysis be slight other
muscles may escape. The characteristic form of lead paralysis consists
in loss of power in the extensors of the hands and fingers, especially
of the extensor communis, without implication of the supinator longus.
The muscles affected are in the region of distribution of the
musculo-spinal nerve. The deformity is known as wrist-drop. Next in
order, the triceps and deltoid are most frequently attacked. The lower
extremities commonly escape for a considerable time. When attacked,
the extensor muscles of the feet and toes are the first to suffer.

Paralysis of the dorsal muscles occurs in rare instances. It gives
rise to a peculiar stooping, uncertain, and tottering gait. Paralysis
of the intercostal and laryngeal muscles was observed by Tanquerel.
Paralysis of the muscles of the face or of those of the eye has never
been observed in consequence of lead-poisoning. The loss of power
never corresponds strictly to the distribution of the branches of a
single nerve-track.

The paralysis, as a rule, affects both sides, and frequently the
corresponding muscles of the two extremities. Sometimes, however, the
affected muscles of the two sides are not the same, and it
occasionally happens that the affection is limited to one side. In
very rare cases, the arm and leg on the same side being paralyzed, the
affection resembles hemiplegia.

Local paralysis may be limited to the extensor muscle of a single
finger {687} or may involve all the muscles of a limb. There may be
slight impairment of power in the flexor muscles. The enfeeblement of
certain flexor muscles, especially of those of the fingers, may,
Naunyn suggests, be only apparent, the position of the hands being in
pure extensor paralysis unfavorable to the exercise of the flexors and
limiting their function.

Sensation is not, as a rule, affected in lead paralysis. Pains in the
paralyzed muscles, in neighboring muscular masses, and in the
structures about the joints often precede the attack of paralysis.
Anæsthesia of the skin is rare. When present, it is usually of slight
degree, and corresponds to the region of the paralysis. Deep
anæsthesia has also been observed.

Atrophy of the paralyzed muscles is constant and rapid. It frequently
reaches a high degree, causing characteristic deformities, which are
rendered more marked by the fact that the adjacent non-paralyzed
muscles preserve to a great extent their original state of nutrition.
As the neuro-muscular lesion progresses other deformities arise, in
consequence of derangements of the balance of force between opposing
muscles and from other causes. Among these deformities are partial or
complete dislocations of the more movable joints, as the shoulder and
phalanges, with the formation of tumors, which, when they occupy the
dorsum of the hand, might be carelessly mistaken for the nodosities of
gout. It is to be noted that the latter are occasionally present as
complications.

There is rapid diminution, and finally complete loss, of the reaction
to the faradic current. With the galvanic current the reaction of
degeneration is usually well marked. The reaction of degeneration may
be demonstrated in the extensors of the limbs in lead-poisoning before
wrist-drop has occurred.

The course of lead palsy is very variable. In a few cases it is
progressive. When local emaciation or atrophy arrives at the last
degree of marasmus, the skin seems glued to the bones, to such an
extent are the paralyzed parts wasted; the muscles especially are so
thinned that the contour of the bones is easily distinguished. If the
paralysis attack the whole of the limb, then this organ, abandoned to
its own weight, stretches the ligaments and permits the head of the
bone to leave its cavity. In other rare instances the paralysis
remains stationary for long periods of time, only to grow worse after
each new attack of lead disease. Much more frequently lead paralysis
disappears spontaneously or under treatment in the course of some days
or weeks. The convalescence is gradual, and usually rapid, when the
gravity of the lesion is considered; occasionally it is complete in
the lapse of a few days.

The prognosis depends upon the degree of lead cachexia present, the
possibility of withdrawing the patient from the exposure, and finally
upon the degree and extent of the paralysis and of the atrophy. It is
rendered unfavorable by the necessity of the prolonged exposure of the
patient to lead, by a high degree of disturbance of the general
nutrition of the patient; and by the fact of his having presented for
a considerable period the evidences of lead disease, with occasional
attacks of colic or arthralgia; by the complete loss of power and
electrical reactions in the affected muscles; and, finally, by
absolute wasting of the muscular masses. The prognosis is less
favorable in relapses than in the primary attack.

{688} Progressive muscular atrophy has been frequently observed in
patients suffering from lead disease (Naunyn).

5. The Encephalopathy; Encephalopathia Saturnina.—This term was
suggested by Tanquerel to designate collectively the various morbid
cerebral phenomena produced by chronic lead-poisoning. It embraces,
therefore, those affections due to the action of lead upon the central
nervous system, and occasionally described as lead insanity, delirium,
convulsions, epilepsy, coma, etc. It is, of all the disorders produced
by lead, the most rare. Tanquerel met with seventy cases only. It
occurs only in those individuals who are exposed to large quantities
of lead, and in such a manner as to favor the absorption of the metal
and its compounds by the digestive and respiratory tract. Hence
house-painters and the workers in lead-factories supply the greater
number of cases. The time of exposure elapsing before the
manifestations of the special morbid action of the poison upon the
nervous system show themselves varies from a few days to many years.
In a large proportion of the cases the time has been less than one
year.

Women are much less liable than men—a fact clearly due to the nature
of their occupations even when involving exposure to lead.

The majority of the cases have occurred between the ages of twenty and
fifty. Alcoholic habits, insufficient and unwholesome diet,
privations, exposure, and an irregular life especially predispose
those working in lead to the affection. Lead encephalopathy has
developed with nearly equal frequency in warm and in cold weather.
Relapses are frequent.

Among the prodromes are headache, vertigo, agitated and interrupted
sleep marred by distressing dreams, and troublesome insomnia;
derangements of the special senses, dimness of vision, alterations of
the pupils, tinnitus aurium; dysphagia and a sense of constriction of
the pharynx have also preceded the attack of cerebral disorder. It is
usually preceded likewise, and often by a considerable lapse of time,
by the other lead affections above described—namely, colic,
arthralgia, and palsy. Psychical derangements—stupor, apathy, or
excitement—also precede the attack. In a small number of cases lead
encephalopathy has occurred abruptly without prodromes.

The symptomatology is exceedingly variable and irregular. Three forms,
the delirious, the comatose, and the convulsive, have been described.
These conditions may succeed each other in the same attack. The
delirium is variable in kind. It is apt to be at first tranquil; after
some time it becomes paroxysmal and furious. It is broken by intervals
of somnolence. At length true sleep supervenes, and the patient awakes
restored almost completely to his reason.

Coma may develop suddenly, even instantaneously. In a very few cases
the comatose form has developed itself alone during the course of
chronic lead-poisoning. As a rule, however, it is preceded by delirium
or convulsions.

The convulsive form is the most common. The convulsions may be
partial, involving the face or the one side of it, a single limb, or
one side of the body. They may be general, without loss of
consciousness. These incomplete attacks are apt to be followed, after
a period of dulness or unconsciousness, by acute eclampsia.
Epileptiform attacks may now follow each other in rapid succession,
ending in more or {689} less profound coma. The attacks are sometimes
separated by intervals of uneasiness, restlessness, or delirium. These
attacks continue several days. If they are very violent and frequent
death may rapidly supervene. In favorable cases consciousness is
gradually restored, or the patient may awaken suddenly from his
drowsiness after some hours or a day.

These attacks are not preceded by an aura.

Amaurosis is among the more important of the symptoms produced by the
action of lead upon the nervous system. It is usually accompanied by
dilatation of the pupils. The amaurosis gradually disappears as the
other symptoms subside, and with the improvement in sight the pupils
contract. Recovery is frequently complete. Occasionally vision does
not return with the improved general condition. Norris[13] saw, in two
cases of lead-poisoning due to the use of white lead as a cosmetic,
marked choking of the discs in connection with severe cerebral
symptoms. The terminal condition, when recovery does not take place,
is that of nerve-atrophy.

[Footnote 13: See this _System of Medicine_, Vol. IV.]

Albuminuria is common in this as in other lead affections. It may be
of moderate amount and due to the rapid breaking-down of the
blood-corpuscles which marks the exacerbation of the general
condition. Albuminuria may be a direct consequence of the eclampsia.
Finally, it may be due to coexisting nephritis.

The prognosis is in a high degree unfavorable.

MORBID ANATOMY AND PATHOLOGY.—There are no well-characterized
anatomical lesions in chronic lead-poisoning. Lead has been found in
almost every organ and tissue in the body. It exists in combination
with the albumen of the tissues. The changes in the nervous system
that have thus far been described are neither constant nor
characteristic. The same is true of the lesions of the intestines. The
paralyzed muscles are found to have undergone atrophy, with loss of
the striæ and increase of connective tissue. The nerve-trunks are also
the seat of atrophic degeneration.

The mode of action of lead is not yet determined. The view of Henle,
that lead acts chiefly upon the unstriped muscular fibre, was at one
time generally accepted, and served to explain many of the
characteristic phenomena of the disease. On the other hand, there is
much in the clinical history to support the opinion of Heubel, that
its primary action is upon the nervous system. Whether the peripheral
degeneration by which the paralysis is to be explained is primary or
secondary to central degeneration in the anterior cornua of the gray
matter of the spinal cord, is yet in dispute. Some of the forms of
encephalopathy are doubtless due to the nephritis which is found in
many cases of chronic lead disease, and are, in fact, symptoms of
uræmia. In the great majority of the cases this is not the case. The
morbid condition must be explained by the direct toxic action of lead
upon the central nervous system. No theory adequate to account for all
the cerebral manifestations has yet been suggested. Naunyn has pointed
out the resemblance between the nervous and psychical derangements in
lead encephalopathy and those which characterize chronic alcoholism,
and suggests that lead, like alcohol, produces these effects not as a
direct poison, but indirectly in consequence of abnormal nutrition of
the whole system, brought about {690} by the continued circulation of
a foreign poisonous material in the blood.

Chronic Lead-Poisoning in Animals.—Animals exposed to lead under
conditions favorable to the development of the lead affections in man
suffer in like manner. Instances of this kind are of frequent
occurrence in and about large lead-factories. The drinking of water
containing lead also gives rise to these affections in animals.
Horses, dogs, cats, and fowls have frequently suffered from lead
colic. Horses used in lead-factories suffer from a form of laryngeal
obstruction due to lead paralysis of the muscles of the larynx. Relief
has followed tracheotomy and the introduction of a canula, and removal
to an atmosphere free from lead has resulted in recovery. Cats who
spend some time in red-lead workshops frequently are paralyzed. Even
the rats in lead-factories become paralytic (Tanquerel).

DIAGNOSIS.—The diagnosis of the affections due to chronic
lead-poisoning is, as a rule, unattended with difficulty. The
malnutrition, anæmia, poor digestion, foul mouth, stubborn
constipation, and the gingival line, considered in connection with the
history of prolonged or habitual exposure to lead, would warrant the
assumption that the relation between this poison and the symptoms is a
causal one. When there is added colic, arthropathies, and paralysis,
or the cerebral states having the characters above described, the
assumption becomes a certainty. The absence of any one of the ordinary
phenomena, such as the blue line or constipation, would still leave
the clinical picture sufficiently full to justify the diagnosis. The
reaction of degeneration, which is usually marked in saturnine
wrist-drop, with the escape of the supinators, distinguishes it from
pressure paralysis of the musculo-spiral.

TREATMENT.—_A_. Prophylaxis.—Free ventilation and scrupulous
cleanliness constitute, in general terms, the most efficient
safeguards for those whose occupations involve prolonged exposure to
lead. Workmen employed in lead-factories and those otherwise exposed
to lead should be compelled to wash their hands and change their outer
clothing before eating; they should also bathe regularly every day on
leaving work; under no circumstances should they be suffered to eat or
sleep in or near the workshops. As all kinds of work in the
manufacturing of lead preparations are not attended with equal risk,
the workers should from time to time be transferred from one
department to another or from in-door to out-door work. In order to
prevent the constant rising of dust, the floors are to be kept
constantly sprinkled or covered with moist sawdust. It is unnecessary
to go into further details in regard to the hygiene of the subject. It
is probable that towels and sponges worn over the mouth, or other
forms of respirators, because of the inconvenience which they occasion
and the false sense of security which attends their use, are of less
value than has been generally supposed.

It appears scarcely needful to here insist upon the avoidance of
cosmetics and hair-dyes containing lead, or upon the exercise of
reasonable prudence in the matter of the manufacture, sale, and use of
articles of food or drink which are liable either by accident or
design to become adulterated with lead compounds.

The use of sulphuric-acid lemonade is a measure of prophylaxis of less
real value than was at one time supposed, seeing that the sulphate of
lead {691} is in itself capable of producing the disease. Occasional
doses of magnesia sulphate are of use where a tendency to constipation
exists. Workmen who begins to show signs of chronic lead-poisoning
should without delay abandon their work and seek some occupation free
from its peculiar dangers.

The precautions against the use of water contaminated with lead have
been pointed out under the heading Etiology.

_B_. Curative Treatment.—When the disease shows itself, no matter in
what form, the primary indication is the discontinuance of exposure to
lead. Chronic cases of malnutrition, constipation, functional nervous
disorder, will occasionally be found upon careful search to depend
upon long exposure to lead in some unsuspected way. The cause being
removed, such cases often promptly recover.

Measures aimed first at the separation of the lead from the tissues,
and then at its elimination from the body, constitute a rational
treatment. Sulphur baths and the internal administration of sulphur
may be employed with a view of converting the lead eliminated by the
skin and mucous membranes into an insoluble sulphide, and thus
preventing its resorption. Repeated laxative doses of castor oil will
remove unabsorbed lead from the intestinal canal. The plan of
treatment at present in general favor consists in the combined use of
potassium iodide and magnesium sulphate. From five to twenty grains of
the iodide are to be given in not less than six or eight fluidounces
of water three times daily, the stomach being empty: two hours after
each dose one or two drachms of the magnesium sulphate are to be
taken; after this dose an ordinary meal.

This treatment is designed to dissolve the lead deposited in the
tissues, and cause its elimination by the mucus of the alimentary
canal in part, and to a slight extent also by the urine. The magnesium
sulphate tends to remove such lead as finds its way into the
alimentary canal thence with all possible rapidity. These measures,
together with the removal of the patient from further exposure, exert
of themselves a favorable influence upon the malnutrition and anæmia.
Quinine, strychnine, iron, cod-liver oil may be advantageously
administered as the toxic effects of the lead pass away.

The colic demands the administration of opium or its derivatives to
relieve the pain, which is commonly excruciating. For this purpose the
hypodermic injection of morphia is our most efficient remedy. Alum in
doses of twenty to thirty grains every four or six hours is useful in
lead colic.

For the relief of the local paralytic affections local as well as
general treatment is necessary. Massage is of great use, especially
when combined with passive movements. Galvanism, one large electrode
being applied to the cervical vertebræ, the other to the extensor
surface of the affected limbs, is followed by excellent results.
Labile currents of fifteen or twenty cells should be thus applied, the
poles being changed several times at each sitting. As the nutrition of
the muscles improves faradic currents may be occasionally substituted.
Persevering treatment is necessary to obtain the best results.

For the present relief of the arthralgia gentle frictions with or
without anodyne liniments must be employed. The hypodermic use of
morphine {692} may become necessary in cases in which the pain is
urgent. It is, however, here as elsewhere, to be if possible avoided.
The tendency to recurrent joint-pains rapidly disappears as the poison
is eliminated from the organism.

For the relief of the severe cerebral symptoms which are described
under the term Encephalopathy special treatment is of little avail.
All observers agree in recommending an expectant plan. The measures of
treatment directed against the general condition, as above described,
must be steadily continued. The influence of chronic lead-poisoning
upon pregnancy is very deleterious. Constantine Paul[14] and others
have shown that the early death of the fœtus very constantly occurs.
The prompt removal of women who have become pregnant, from all
exposure to lead, and energetic medicinal treatment, are needed to
obviate the danger of abortion.

[Footnote 14: _Arch. gén. de Méd._, vol. xv., 1860.]


{693}


PROGRESSIVE UNILATERAL FACIAL ATROPHY.

BY CHARLES K. MILLS, A.M., M.D.


DEFINITION.—Progressive unilateral facial atrophy is a disease
characterized by progressive wasting of the skin, connective tissue,
fat, bone, and more rarely muscles of one side of the face.

SYNONYMS.—Progressive facial hemiatrophy, Neurotic atrophy of the face
(Virchow), Facial trophoneurosis (Romberg), Prosopodismorphia
(Bergson), Atrophy of the connective tissue of the face or Laminar
aplasia (Lande).

HISTORY AND LITERATURE.—This disease has been known to the medical
profession since 1825, when, according to Eulenburg, it was first
described by Parry. The _Index Catalogue_ contains references to
thirty books and articles on the subject in various languages.
Eulenburg gives a bibliography which contains thirteen references not
given in the _Index Catalogue_. One personal case, which will be
detailed later, has fallen under observation. In all, I have collected
from fifty to sixty cases. The number of reported cases is slowly
increasing; nevertheless, the disease must still be regarded as rare.
Carswell,[1] according to Lasègue,[2] first arranged scientifically
the various lesions which might arise in consequence of a retardation
and arrest, or even inverted action, in nutrition, and at the same
time that he assigned their causes pointed out the several forms of
atrophy. Aran[3] has written a contribution on the subject, furnishing
valuable material for classifying atrophies. Romberg called general
attention to the disease in his clinical researches, published in
1846. He described the disease under the name of a new form of atrophy
of the face, and took the position that it was a primary
trophoneurosis. Of contributions by American writers, a paper by
Bannister[4] is the most complete and valuable. This not only contains
two fully and carefully reported cases, but also a thorough discussion
of special symptoms and the pathology of the disease. The chapter of
Eulenburg[5] contains an excellent sketch of the disease, and is
especially valuable for the discussion of the various theories as to
its nature.

[Footnote 1: _Illustrations of the Elementary Forms of Disease_,
1836.]

[Footnote 2: _Archives générales de Médecine_, May, 1852, p. 71.]

[Footnote 3: _Ibid._, Sept. and Oct., 1850.]

[Footnote 4: _Journal of Nervous and Mental Disease_, vol. iii., No.
4, Oct., 1876, p. 539.]

[Footnote 5: _Ziemssen's Cyclopædia of the Practice of Medicine_, vol.
xiv., 1877.]

ETIOLOGY.—The disease is of much more frequent occurrence among
females than males. Out of 25 cases which I have been able to
classify, {694} 9 were in men and 16 in women. It is an affection of
comparatively early life. The following were the ages of 25 patients:
under ten years, 7; from ten to twenty years, 11; from twenty to
thirty years, 6; over thirty years, 1.

Graefe[6] reports a case due to syphilis, in which there was also
paralysis of the left oculo-motor externus and trigeminus. In one of
Bannister's cases the patient had suffered repeatedly from slight
frost-bites. Among the causes which seem to be thoroughly established
traumatism holds the first place. The affection could be traced to
injury in a fair number of the published cases. A case is reported by
Maragliano[7] of a child who had a fall in which she struck the left
half of her face, and in consequence of which a circumscribed swelling
appeared near the external angle of the left eye and remained for a
few days. Shortly after this the left half of the face began to grow
smaller than the right. Schuchardt[8] speaks of a fall on the head
which left a cicatrix on the right parietal bone below the coronary
suture, the injury being followed by facial atrophy. Panas[9] reports
a case in which the wasting of the face followed a fracture of the
lower jaw. In one of two cases reported by Bannister,[10] a man, aged
forty-two, is stated to have been thrown from a stage-coach, falling
on his head, and not losing consciousness, but receiving a scalp wound
over the coronal suture. Subsequent to this time he had cerebral
symptoms, physical and mental, and unilateral facial atrophy
developed.

[Footnote 6: Quoted by Rosenthal.]

[Footnote 7: _Note di Clinica Medica_, Genoa, 1881, translated by
Joseph Workman, M.D.—_Alienist and Neurologist_, vol. ii. No. 2,
April, 1881, p. 146.]

[Footnote 8: Quoted by Eulenburg.]

[Footnote 9: _Bull. Soc. de Chir. de Par._, 1869, 1870, 2d S. ex.,
198, and _Gaz. des Hôpitaux_, 1869.]

[Footnote 10: _Journ. Nerv. and Ment. Dis._, Chicago, 1876, iii. pp.
539-560.]

SYMPTOMATOLOGY.—Before discussing the symptomatology I will give brief
notes of the following case, which has not been before reported, and
which was observed by me while in charge of the Nervous Dispensary of
the Hospital of the University of Pennsylvania several years since.

C——, aged seventeen, white, a mill-operative, had a good family
history. Three years before coming under observation a white spot
appeared in the skin over the right malar prominence, and since that
time this side of the face had gradually atrophied. When this patient
was first examined the skin had a mottled appearance. Close
examination showed that the skin, connective tissue, and bone were
decidedly wasted, and there seemed also to be some loss of substance
in the muscles of the right side of the face. The mouth, however,
could be closed properly, the lips showing no puckering or drawing to
one side. The right half arches of the palate were atrophied. The
uvula was drawn slightly but positively to the left. Careful
examination of the membrane of the drum of the right ear showed it to
be atrophied. An ophthalmoscopic examination of both eyes was made,
but no changes were discovered. No changes were noted in the hair of
the patient on the affected side. He was able to perform all movements
with the facial muscles, but the creases and contours of the face in
repose and in motion were less marked on the right side than on the
left. The skin of the right side of the face seemed to be bound
closely to the bone. The muscles on the same side responded well to
{695} the faradic and galvanic current. The patient had at times a
peculiar sensation of stinging in the atrophied half of the face. He
was treated with electricity, local massage, and tonics, and did not
improve, but did not get worse while under observation, a period of
several months.

At the Hospital of the University of Pennsylvania I also observed one
well-marked case of unilateral atrophy of the tongue without atrophy
of the face, of which, unfortunately, I have not preserved the notes.
The patient was a middle-aged man with a syphilitic history. The
atrophy in the reported cases has occurred much more frequently upon
the left than upon the right side of the face.

Changes in the skin are among the most constant and striking
phenomena. By some dermatologists the disease is regarded as a form of
morphœa, the keloid of Addison. Morphœa as described by Duhring[11]
occurs in the form of patches, rounded, ovoid, or irregular in
outline, small or large, tough or leathery, smooth or shiny, and may
also manifest itself in the form of atrophic pit-like depressions in
the skin. The skin alterations differ somewhat in character;
frequently one of the first signs of the disease is the appearance of
a white spot on the cheek. This was the first noticeable phenomenon
observed in the above case. After a time this spot or patch may change
in color, becoming of a yellowish or brownish hue. A number of spots
appearing and undergoing change, the skin after a time assumes a
mottled appearance. In some of the reported cases a yellowish, or
yellowish-gray, or brownish appearance is recorded as having been
present. In these the observations were probably made after the
affection had existed for some time, and in them the white spots or
patches were probably at first present. In one of Romberg's cases,
first recorded when the patient was nine and a half years of age, he
noted the deposit of a yellowish-gray pigment which began at the
median line and extended to the angle of the jaw across the lower half
of the face and neck, divided here and there by portions of healthy
skin. Discoloration, varying in intensity, also existed in irregular
patches on the upper part of the face and on the forehead. The
discolored tissues were glossy and greasy-looking. The skin adhering
to the bone often gives the patient an aged appearance. Pruritus has
been several times observed.

[Footnote 11: _Medical News_, vol. xlv. No. 4, July 26, 1884, p. 85.]

Changes take place in the hair. Sometimes it simply changes color; at
other times it falls out or ceases to grow. The beard or hair of the
head will thus be gray or white upon one side, or in one or two
locations of one side and not of the other; or the hair may be absent
or simply thinned out. Peculiar limitations in the extent to which the
hair is affected are sometimes observed. In one of Romberg's cases,
for example, complete absence of the eyelashes from the inner angle of
the eye to the middle of the lids was noted; the hair was very thin,
and in some parts altogether wanting, and the left eyebrow was almost
entirely devoid of hair. The changes which take place in the color of
the hair in some severe cases of chronic trigeminal neuralgia will be
recalled in this connection. I have known of several instances in
which a few locks of hair were turned gray or white on the neuralgic
side. Anstie, author of the work on Neuralgia, was a sufferer from
supraorbital neuralgia, and the eyebrow of the same side contained a
white tuft. Facts of this kind {696} serve to corroborate and
emphasize the view that unilateral facial atrophy is a
tropho-neurosis.

Anidrosis, or absence of perspiration, on the atrophied side of the
face is a nearly constant phenomenon. In one of Bannister's cases, a
printer, attention was first called to the patient by the fact that in
working a hand printing-press in the hot weather he perspired only on
the right side of his face. The left side remained perfectly dry, no
matter how warm the temperature or hard the labor. This hemidrosis, or
unilateral sweating, was confined only to the right side of the
forehead, the right cheek, side of the nose, and lip. On the chin it
encroached a little on the left. Under the chin and in the throat
there was a little excess of perspiration on the right side; on other
portions of the body no difference was noted. Nicati[12] considers a
combination of symptoms, several of which were present in a recorded
case—namely, lowered temperature, stoppage of perspiration, and
wasting of the side of the face—as indicating a paralysis of the
sympathetic nerve in what he calls its second or more advanced stage.
In true facial hemiatrophy, however, other phenomena of such paralysis
are wanting. Brunner[13] gives a case in which perspiration, tears,
mucous secretions, and temperature were all diminished on the affected
side, and in which were also present exophthalmos and dilatation of
the pupil. The cervical sympathetic in this case was irritated by a
tumor. I agree with Bannister, however, that while we cannot exclude
the possibility of the participation of the sympathetic in hemiatrophy
of the face, the evidence is not sufficiently positive. Mechanical
interference with the sweat-glands by pressure or otherwise has been
suggested. The true view to take would seem to be that the
perspiratory disorder is due to the same central or peripheral
neurotic affection which gives rise primarily to the atrophy.
Eulenburg says that the secretion of the sebaceous follicles is in
most cases diminished or stopped on the atrophied side, while the
sweat-glands often act in a normal manner; but his experience does not
seem to correspond with that of the majority of other observers.

[Footnote 12: _Sur Paralysie du Nerf sympathetique-cervical_,
Lausanne, 1873, quoted by Bannister.]

[Footnote 13: _St. Petersburger Med. Zeitschr._, ii., 1871, quoted by
Bannister.]

Seguin, Dreschfeld, and others have found no notable differences in
surface temperature between the two sides of the face. In one of
Bannister's cases the temperature was tested in both ears, and a
difference of six-tenths of a degree Fahrenheit in favor of the ear of
the unatrophied side was found, that of the left ear being 97.6°, and
that of the right 98.2°. This examination was repeated on another
occasion with nearly the same result.

Weakness of pulsation in the carotid of the affected side has been
observed. Sometimes the power to blush is lost on the affected side,
but this may return. In one instance the cheek, having been reddened
by electrical stimulation, so remained for an hour or more.

Paræsthesiæ, such as pain, numbness, and stinging sensations, are not
uncommon. A diminution of the general tactile sensibility of the skin
of the affected side has been observed by Tanturri[14] and by
Vulpian,[15] and perhaps by others, but anæsthesia is not commonly
present.

[Footnote 14: _Il Morgagni_, 1872, quoted by Bannister.]

[Footnote 15: _L'Appareil vaso-moteur_, ii. p. 430.]

Eulenburg and Guttmann found atrophy of the muscles supplied by the
motor branch of the fifth nerve—namely, the masseter and temporal.
{697} The changes which take place in the muscles of the affected side
are, so far as can be judged, not of the character of fatty
degeneration. Probably a general and uniform shrinkage of calibre of
muscular fibres and bundles occurs. Certainly, this would seem to be
true of the muscles supplied by the portio dura. The muscles on the
atrophied side respond to both the faradic and galvanic currents,
reactions of degeneration not being present. The absence of the
reactions of degeneration in the facial muscles shows that normal
muscular fibres remain. In one reported case the facial muscles seemed
at first to react more readily than in normal conditions. The muscles
of the upper lip sometimes appear to have wasted, preventing full
closure of the mouth on this side. Fibrillary twitchings have been
observed only very rarely. Voluntary control over the muscles of the
affected side is not impaired.

In one of Bannister's cases the first upper molar of the left side
sometimes ached, and the gum and bone were so wasted as to expose its
roots for a considerable distance. Falling out of the teeth has been
observed in a few other cases.

Atrophy of the tongue is associated with the facial wasting in a
certain percentage of cases, and the uvula and soft palate are also
sometimes wasted. On the other hand, atrophy of the tongue has been
observed as an isolated phenomena.

Atrophy of the bones of the face is frequently present, and has been
determined by careful measurements. It will show to a greater or
lesser extent according to the age of the patient. When the disease
arises after the bony development has been fully acquired, there will
be little external evidence of osseous involvement; when it begins
during the time of active growth of the bone, as it does not
infrequently, the arrest in the skeleton will be very apparent. Thus
in a number of cases beginning in early childhood bone atrophy has
been a very marked feature.

Eulenburg says that the functions of taste, smell, hearing, and seeing
are not interfered with in any of the reported cases; but Bannister
reports impairment of the sense of taste in both of his cases. In one
the whole left half of the tongue was involved, in the other only the
left posterior third. In the first of these, in which the whole left
half of the tongue was involved, both the glosso-pharyngeal and the
chorda tympani nerves were affected. According to Bannister, the
significance of this observation is that either the glosso-pharyngeal
and fifth nerves are both involved, or that the taste-fibres for the
base as well as tip of the tongue are derived from the last-named
nerve. In this case, however, which was due to a severe injury, the
headache, mental confusion, loss of hearing, etc. more probably
indicated a widespread intracranial lesion, affecting to some degree
the nucleus of the glosso-pharyngeal. In the other case, which was
apparently a typical one of unilateral facial atrophy in its early
stage, no history of traumatism was present, and the sense of taste,
which was carefully tested several times, was seriously impaired over
the left posterior third of the tongue.

Bannister discusses the probable cause of impairment of taste in each
case, as follows: “The atrophy seemed to involve the region supplied
by the second division of the fifth nerve as much as, or more than,
the other divisions; and on this is situated the spheno-palatine
ganglion which gives off the Vidian nerve, the upper division of
which, the superior {698} superficial petrosal nerve, is supposed by
Schiff to contain the taste-fibres, which return from the lingual
nerve through the chorda tympani. The usual theory of this disease is
that it depends upon an affection of the trophic fibres contained in
the fifth nerve or one or more of its divisions. Accepting this
theory, Baerwinkel,[16] noticing a case of unilateral atrophy of the
face affecting only the second division of the fifth, and, as he held,
indicating trouble with the spheno-palatine ganglion, its trophic
centre, mentions the fact that there was no impairment of taste in the
anterior portions of the tongue as rather against the hypothesis of
Schiff as to the course of the taste-fibres. At the same time he gives
two other observations of lesions of the trifacial and the seventh
nerve that favor it. In our patient I should have expected a priori to
have found the taste affected in the anterior portion of the tongue,
if anywhere, but the reverse was the fact. It is difficult to suppose
an accidental lesion of the glosso-pharyngeal coexisting with the one
of the trigeminus that produces the atrophy when there are no more
signs of nervous disorder than there were in this case. On the other
hand, the taste-fibres of the glosso-pharyngeal are not generally
supposed to have such connections with the fifth nerve as to be
involved in its disease, while those of the chorda tympani, of the
connections of which with the trigeminus there is much more
physiological evidence, escape. The observation is a contradictory
one, and I cannot at present explain it.”

[Footnote 16: _Deutsch. Archiv f. klin. Med._, xvii. 1, 1875.]

So far as I know, ophthalmoscopic changes have never been noted. In a
few cases enophthalmos, or sinking in of the eye, doubtless due to the
disappearance of orbital fat as the disease advances, has been
recorded.

Defects of hearing, and even partial deafness, have been reported in a
very limited number of cases, making it questionable whether this
symptom is a coincidence or a complication. In the case reported by me
careful examination of the membrane of the tympanum by W. Ziegler of
the ear department of the Hospital of the University of Pennsylvania
showed atrophy of this membrane.

Eulenburg speaks of one case in which the external atrophy had reached
as far as the larynx, and in which the pronunciation of the letter _r_
was somewhat impeded. Beverly Robinson,[17] reports a case accompanied
with slight paralysis of the adductors of the vocal cords. The
laryngeal paralysis in this case improved under treatment, which led
Robinson to believe that the relation between the two affections might
have been only one of coincidence.

[Footnote 17: _Am. Journ. Med. Sci._, October, 1878, p. 437.]

Flascher[18] has described a unique case of bilateral facial atrophy
occurring in a woman twenty-three years old. When an infant she fell
and injured her forehead, and soon afterward had an attack of measles
without eruption. Shortly afterward the atrophy appeared. Tactile
sensibility was diminished and the secretion of sweat absent. The
masseter, temporal, and facial muscles and bones were atrophied.
External strabismus of the left eye was present; the pupil of this eye
was dilated, irregular, and non-reactile; sight was diminished, the
optic disc atrophied. This case would appear to differ somewhat from
true facial hemiatrophy. It was probably a peripheral nerve affection
following measles.

[Footnote 18: _Berliner klin. Wochenschr._, 1880, No. 31.]

{699} Mitchell[19] has reported a case of absence of adipose matter in
the upper half of the body. I had an opportunity of examining this
patient, who was exhibited at a meeting of the Philadelphia
Neurological Society, and noticed that both sides of the face
presented a striking similarity to the affected side in cases of
unilateral atrophy. The muscles were apparently not affected. Mitchell
suggests the possibility of separate centres capable of restraining
deposits of adipose tissue.

[Footnote 19: _Am. Journ. Med. Sci._, July, 1885.]

DURATION AND TERMINATION.—The disease pursues a slow but generally
progressive course. In a few instances, after having attained a
certain development, it seems to have remained stationary for many
years. Nothing could better illustrate the slow progress or stationary
character of this affection than the study which Virchow made in 1880
of a patient whose case had been described by Romberg more than twenty
years before. After comparing the patient's present condition with
that described in notes taken twenty-one years before, Virchow was not
able to convince himself that any material alteration had occurred in
the atrophic parts; in fact, he regarded the disease as having long
ago become stationary. Cases reported by Tanturri, Baerwinkel, and
others bear out the same view as to the stationary character of the
affection in some cases.

COMPLICATIONS.—In a case of Virchow's, in addition to the facial
atrophy the patient presented atrophy which, commencing in the
distribution of some of the dorsal cutaneous nerves of the scapular
region, affected the musculo-spiral nerve from its origin downward,
most markedly in the forearm and head. Mendel[20] describes a case of
facial hemiatrophy occurring in a monomaniac, the diagnosis being
complicated by the somatic signs of degeneracy—congenital facial and
bodily asymmetry. The patient was twenty-eight years old, and the
disease could be traced back to the seventh year. In several reported
cases the disease has followed or has been associated with epileptic
seizures. Buzzard[21] has published a case in which the affection came
on in a girl aged thirteen in the course of a second attack of chorea.
In another it followed typhoid fever. In a case reported by Parry[22]
left hemiplegia with temporary disturbance of intelligence preceded
the disease by about two years. In another, observed by Axman and
Hueter, the patient, a man aged thirty-two, had suffered from
irregular contractures of the left masticator muscle, which commenced
in the seventh year. These spasms were associated with an increased
delicacy of sensation in the region of the left trigeminus. Neuralgia
is sometimes a complication. In a case reported by Holland,[23] the
patient for several years suffered from paroxysms of fronto-temporal
neuralgia.

[Footnote 20: _Neurologisches Centralblatt_, June 15, 1883, quoted in
_Journal of Nervous and Mental Disease_, 1883, x. p. 571.]

[Footnote 21: _Transactions of the Clinical Society of London_, vol.
v., 1872, p. 146.]

[Footnote 22: Eulenburg.]

[Footnote 23: _American Practitioner_, vol. xxxi. No. 182, Feb., 1885,
p. 72.]

PATHOLOGY.—Up to the present time, so far as I have been able to
learn, not a single autopsy in a case of typical progressive
unilateral facial atrophy has been made. Conclusions as to pathology
can therefore only be drawn from an analysis and study of symptoms and
from comparisons with other degenerative affections. Most authorities
hold that it is neurotic in origin. {700} Lande, however, regarded it
as having its origin in the connective tissue, affecting the nutrition
of the other tissues by interfering with the circulation.

Different views have been held by those who have believed in its
neurotic origin. Moore regarded it as a form of progressive muscular
atrophy attacking the muscles supplied by the portio dura, but what
has already been shown with reference to the symptomatology is
sufficient to show that this is an erroneous hypothesis. The muscles
supplied by the facial nerve may diminish in volume, but they do not
undergo a true degeneration.

Brunner attributed the affection to continued irritation of the
cervical sympathetic by some continuing lesion. Irritation of such a
lesion, according to him, causes vascular spasms, diminishes
blood-supply, and thus leads to the gradual development of the
atrophy. This view, to say the least, has not been made out.

Virchow holds that the affection is peripheral, and not central. He
believes, however, that a primary process being once set up in the
nerve-trunks, owing to inflammations of the surrounding tissues it may
then extend upward to the spinal and basal ganglia. The disease,
according to this view, has some analogy to herpes zoster. The manner
in which nerve-districts are unequally attacked is similar to what is
observed in the various forms of lepra and in morphœa. The doctrine of
a tropho-neurosis is the one that is best upheld by clinical facts. In
the first place, various arguments can be adduced to show that the
disease is neurotic in origin. It is limited to one side of the face
and to special nerve-distributions. Affections of sensibility in the
domain of the trigeminal nerve are frequently present. In the case
given under Symptomatology, although anæsthesia was absent, the
patient complained of peculiar paræsthesia in the form of stinging
sensation. Either trophic centres or trophic fibres, which have the
same connection and course as the trigeminal, are affected by a
degenerative process. Whether nuclei, ganglia, or peripheral fibres
are primarily affected has not yet been satisfactorily determined.

The case of Romberg, observed by Virchow twenty years after, was
considered by the latter to entirely overthrow the vaso-motor theory,
owing to the condition of the blood-vessels. While the surrounding
tissues from the skin inward were wasted and shrunken, the veins and
arteries of the parts appeared absolutely unchanged, the larger even
projecting above the surface of the skin. Under stimulation the vessel
dilated as in a normal individual, appearing to take no part in the
atrophy.

DIAGNOSIS.—The chief affections from which progressive unilateral
facial atrophy are to be diagnosticated are congenital asymmetry of
the face and head, facial paralysis, progressive muscular atrophy, and
hypertrophy of the opposite side of the face.

Congenital asymmetry of the face is observed in institutions for the
idiotic and feeble-minded. Such asymmetry, however, is usually
associated with corresponding defects of other parts of the body, as
of the head and limbs. In the nervous wards of the Philadelphia
Hospital is now, for instance, a patient the entire right half of
whose body is very decidedly wasted, the case being one of epileptic
idiocy with paralytic and choreic manifestations which point to
atrophy of the opposite half {701} of the cerebrum. At the
Pennsylvania Training-School for Feeble-minded Children want of
development of one-half of the head is often observed, but in these
and in other congenital cases the special changes in nutrition, in the
skin, in the color and growth of the hair, and in sensation, are
absent. In some cases of congenital asymmetry of the head atrophy of
the face or limbs, if present, will be upon the opposite side of the
body; and this is what might be expected, as arrested development of
the cranial vault will probably correspond with arrested development
of the cerebrum of the same side and bodily defects of the opposite
side.

Eulenburg, Maragliano, and others refer to an acquired want of
symmetry of the face sometimes observed in cases of wry neck or
scoliosis with deviation of the spinal column. Eulenburg especially
speaks of the so-called habitual scoliosis, where a curve in the
dorsal region in one direction has a compensatory cervical curve, the
side of the face which corresponds to the dorsal curve being often
smaller than the other. This asymmetry is supposed to result from
compression of the vessels and nerve-roots in the concavity of the
cervical curve. Here, again, the absence of special nutritional
changes will assist in the diagnosis. A study of the spinal curvature
will also be of value. Indeed, only the most careless observation
would allow this mistake in diagnosis to be made.

Facial paralysis—Bell's palsy of the usual type—would not be likely,
except by a careless observer, to be confounded with the disease under
consideration. When the muscles in the facial distribution are
involved, it is only in a very slowly progressive deterioration, which
may be due to mechanical causes, as compression by the contracting
skin. Moore,[24] as already stated, was wrong in speaking of the
morbid changes as entirely confined to the portio dura of the left
side. It is the fat, the connective tissue, and the skin which are
first and chiefly affected. In unilateral facial atrophy no true
paralysis of the facial muscles is present; consequently, the forehead
can be wrinkled, the eye closed, the mouth drawn up or down, or
sideways, etc.; in short, all the movements of the face are possible.
The opposite of this, it goes without saying, is present in general
facial paralysis. The drawing of the face to the side opposite the
paralysis in Bell's palsy is not here observed; the mouth is sometimes
drawn upward slightly on the atrophied side. In facial paralysis of
any severity reactions of degeneration are present. In unilateral
facial atrophy, as in progressive muscular atrophy, the muscles
respond both to faradism and galvanism. As minor aids in making the
diagnosis, the absence of loss of taste in one-half of the tip of the
tongue, and of deflection of the tongue and uvula, are in favor of
facial atrophy.

[Footnote 24: _Dublin Journal of Medical Science_, vol. xiv., August
and Nov., 1852, p. 245.]

It is possible that a case of progressive muscular atrophy might begin
in almost any muscle or group of muscles in the body. In progressive
muscular atrophy, however, the appearance of the skin is different; it
is not mottled; it is not thin, as can be demonstrated by manipulation
of it; it can be raised by the fingers; it is soft and flaccid. In
progressive muscular atrophy also first one muscle and then another,
just as likely as not at some distance from each other, are attacked
by the wasting process; in unilateral facial atrophy the affection
spreads uniformly and regularly {702} over one-half of the face.
According to Duchenne of Boulogne, when progressive muscular atrophy
first appears in the face the orbicularis oris is the muscle most
likely to be attacked, causing the lips to appear enlarged and
pendent, and giving a stupid look to the patient. In unilateral facial
atrophy this appearance is not present. Progressive muscular atrophy
commonly begins at a later age than unilateral facial atrophy.

Hypertrophy of the opposite side of the face is suggested by Eulenburg
as a possible source of mistake; but a little study, however, will
suffice to exclude this affection.

The following points are given by Eulenburg with reference to vitiligo
and porrigo decalvans: “In vitiligo we find the same white
decoloration of the skin, the cicatricial feel, the turning gray and
falling out of the hair, but not the loss of volume, which is the
special characteristic of this disease. In porrigo decalvans
inflammatory symptoms and œdema of the skin come first; the disease
first appears in regular circular spots; the hairs fall out without
previous loss of color; and finally, the disease is contagious, and
fungi can be demonstrated (microsporon Audouini).”

PROGNOSIS.—The prognosis as to recovery is bad, but, as already shown,
the disease may long remain stationary.

TREATMENT.—No well-authenticated case of cure under any method of
treatment has yet been reported. Electricity, either in the form of
galvanism or faradism, has been resorted to in a majority of cases. In
most of these temporary benefit has been produced by the employment of
these agencies. Baerensprung reports two cases as having been greatly
benefited by faradism. In Moore's case it also produced temporary
improvement. Carefully administered massage should be tried. With
reference to friction or massage, however, it is well, as advised by
Eulenburg, to be cautious, as excoriations are easily produced.
Measures directed to building up the nervous centres are
indicated—such medicinal agents, for instance, as the salts of silver,
gold, zinc, and copper, arsenical preparations, strychnia, and iron.


{703}


DISEASES OF THE MEMBRANES OF THE BRAIN AND SPINAL CORD.

BY FRANCIS MINOT, M.D.


The membranes or envelopes of the brain and cord were formerly
reckoned as three in number: the dura mater, lying next to the inner
surface of the bones of the cranium and spinal column, forming an
internal periosteum; the pia mater, which is in immediate contact with
the brain and cord; and the arachnoid, which was described as a
distinct membrane loosely attached to the pia mater, but more firmly
united to the dura, and constituting a closed sac or serous cavity
called the cavity of the arachnoid. This view is now abandoned by most
anatomists, who regard the external arachnoid as simply a pavement
epithelium covering the internal surface of the dura, and the visceral
arachnoid as constituting the external layer of the pia. The term
cavity of the arachnoid has, however, been generally retained for the
sake of convenience; and it gives rise to no obscurity if we remember
that by it we simply mean the space between the dura and the pia.

The diseases of the membranes which I shall consider are—congestion
and inflammation of the dura, including hæmatoma; congestion and
simple and tubercular inflammation of the pia; and meningeal apoplexy.

The membranes of the brain and those of the cord may be separately
diseased, or both may be affected at the same time. Simultaneous
inflammation of the cerebral and spinal meninges is apt to occur
epidemically, and is supposed to be zymotic in its origin. This is
described in another article. (See EPIDEMIC CEREBRO-SPINAL MENINGITIS,
Vol. I. p. 795.)


Inflammation of the Dura Mater of the Brain.

SYNONYM.—Pachymeningitis. Either surface of the dura may be inflamed
separately, and in many cases the symptoms are sufficiently definite
to render it possible to diagnosticate the situation of the disease in
this respect during life, especially when taken in connection with the
causes. For this reason it is usual to speak of external and internal
pachymeningitis. A peculiar form of the latter is accompanied by the
effusion of blood upon the arachnoidal surface, which sometimes forms
a tumor called hæmatoma. Congestion is also sometimes included in the
diseases of the dura mater, but is rarely alluded to by writers on
pathology or clinical medicine.


{704} Congestion of the Dura Mater.

Except as the first stage of inflammation, congestion of the dura can
hardly exist unless in connection with the same condition of the pia
or of the brain. Its causes are either local, such as thrombosis of
the sinuses, syphilitic or other growths in the membranes; or remote,
the principal being obstructions to the general circulation, including
valvular disease of the heart, emphysema and other affections of the
lungs, renal disease, compression of the superior cava or jugulars by
aneurism and other tumors, delayed or suppressed menstruation, etc.
The symptoms cannot be distinguished from those of congestion of the
pia or of the brain—namely, headache, a sensation of throbbing,
pressure, or weight in the head, somnolence, etc. The absence of fever
would serve to distinguish the affection from an inflammatory
condition of the membranes or brain.


Inflammation of the External Surface of the Dura.

SYNONYM.—External pachymeningitis.

ETIOLOGY.—The most frequent causes of external pachymeningitis are
injuries to the cranial bones from violence, caries and necrosis of
the same, and concussion from blows on the head. Next in order of
frequency, if not even more common, comes the propagation of
inflammation from disease of the inner ear and of the mastoid cells.
It is only of late years that this important subject has been brought
prominently forward and the danger of ear diseases in this respect
fully pointed out. The channels of communication, as indicated by Von
Tröltsch[1] in his valuable article on diseases of the ear, are along
the arteries and veins which pass from the skin of the meatus and the
mucous periosteal lining of the middle ear to the contiguous bone,
while the capillaries of the petrous bone are in direct connection
with the dura mater, so that the vessels of the latter are in
communication with the soft parts of the external and middle ear. The
vessels of the ear and the membranes of the brain are also directly
connected through the diploëtic veins of the temporal bone, which
discharge into the sinuses of the dura, as well as through the venæ
emissariæ, which, arising from the sinuses, pass through the bone and
discharge their contents into the external veins of the head. Von
Tröltsch also points out that the extension of an inflammatory process
may occur along the sheath of the facial nerve, the canal of which
(canalis Fallopii) is a branch of the internal auditory canal and is
lined by the dura mater. The latter is separated from the mucosa of
the tympanum only by a thin, transparent, and often defective plate of
bone. Inflammation may also be transmitted from the scalp by means of
the vessels which pass through the bones of the skull. In this way
erysipelas and other diseases of the integument sometimes give rise to
external pachymeningitis.

[Footnote 1: “Die Krankheiten des Gehörorganes,” von Anton von
Tröltsch, in _Gerhardt's Handb. der Kinderkrankheiten_, Tübingen,
1879, 5 B., ii. Abt., p. 150; also English translation of the same, by
J. O. Green, M.D., New York, 1882, p. 107.]

SYMPTOMS.—There are no known symptoms which are characteristic of
inflammation of the external surface of the dura. In cases of death
{705} from other diseases an autopsy may show traces of previous
inflammation, such as thickening of the membrane and its firm adhesion
to the cranial bones, which were not manifested during life by other
symptoms than those which accompany meningeal disease in general; and
in some instances none at all were known to have occurred. At a
variable time after the receipt of an injury to the head the patient
may complain of headache, followed by a chill, with high fever,
vomiting, vertigo, delirium, unconsciousness, convulsions, etc.,
arising from compression by the products of inflammation. The same
phenomena may follow the transmission of inflammation to the dura from
caries or other disease of the bones, or from otitis medea purulenta.
These symptoms usually continue without interruption, though there is
sometimes more or less complete remission of the pain, and the patient
may recover his consciousness for a time, thus giving rise to
fallacious hopes. In a large proportion of cases the disease extends
to the inner surface of the membrane and to the pia, without any
noticeable change in his condition other than coma. In chronic
external pachymeningitis the principal symptom is pain in the head,
which may persist for weeks or months without other manifestations
except drowsiness. Sometimes, on the contrary, there is obstinate
vigilance. Mental symptoms, such as loss of memory, hallucinations,
dementia, or mania, are sometimes noticed, ending, as in the acute
form, in coma.

PATHOLOGICAL ANATOMY.—In chronic cases often nothing is found but
thickening of the membrane, which generally becomes firmly united to
the inner surface of the cranium. Indeed, these appearances are not
unfrequently observed, to a limited extent, when there has been no
history of disease to account for them. In other chronic cases the
connective tissue of the membrane is found to be in part ossified, and
the osteophytes of the cranium sometimes found in pregnant women and
in patients with rheumatic cachexia are supposed to be due to a
chronic inflammatory process of the dura. The first changes observed
in acute external pachymeningitis are increased vascularization, shown
by red lines corresponding to the blood-vessels, with punctiform
extravasations, swelling, and softening of the tissue. Later, there is
thickening of the membrane from new formation of connective tissue,
and exudation of lymph, and sometimes of pus, which latter may
accumulate between the dura and the cranial bones, or in traumatic
cases may escape through openings in the skull. The dura and the pia
become united in most cases of acute inflammation. The lateral sinuses
frequently contain thrombi, which, when ante-mortem, are firm in
structure, reddish-brown in color, often closely adherent to the walls
of the vessel, and may extend to other veins, sometimes reaching as
far as the jugulars. When purulent inflammation of a sinus occurs, its
walls are thickened, softened, and discolored, and the inner surface
is roughened. The thrombus becomes more or less purulent or sanious,
disintegrates, and the infecting particles are carried into the
circulation, giving rise to embolism and disseminated abscesses of the
lungs, kidneys, liver, or spleen. Other lesions, such as injury or
caries of the cranial bones and purulent inflammation of the middle
ear and of the mastoid cells, are frequently found in conjunction with
pachymeningitis, to which they have given rise. When the disease of
the dura extends to the pia, the adjacent portion of the brain is
often found implicated in the {706} inflammation. In traumatic cases
the dura may be detached from the bone and lacerated to a greater or
less extent.

DIAGNOSIS.—The existence of external pachymeningitis may be suspected
from cerebral symptoms following traumatic injury of the skull,
erysipelas, or suppurative otitis medea, but apart from the etiology
it would not be possible to distinguish it from internal inflammation
of the membrane, or even from leptomeningitis.

PROGNOSIS.—In cases of suspected external pachymeningitis the
prognosis will depend upon the evidence of effusion of pus or blood
between the dura and the skull, and the possibility of their removal.
A large proportion of cases are fatal, especially those arising from
caries of the cranial bones and from the propagation of disease from
the middle ear, the mastoid process, or the external surface of the
skull, the inflammation extending through the membrane to the
arachnoid surface of the dura, and also to the pia mater. This would
be shown by a high temperature, rapid pulse, pain, and delirium,
followed by coma and perhaps convulsions. The frequency with which
external pachymeningitis occurs in connection with diseases of the ear
should put the physician on his guard in cases of otorrhœa or pain in
the ear, that he may warn the patient or his friends of the
possibility of danger, and may employ an appropriate treatment.

TREATMENT.—In all cases of injury to the skull or of severe concussion
the possibility of subsequent external meningitis should be borne in
mind. The patient should be confined to the bed and be carefully
secluded from excitement. Cold applications should be made to the
head, the diet should be simple and somewhat restricted, and the
bowels kept free without active purging. If there be evidence or
suspicion of the presence of pus or of blood between the dura and the
skull, means should be taken to evacuate the effusion. In case of
inflammatory symptoms leeches should be applied behind the ears, and a
stimulating liniment or croton oil rubbed on the scalp. There is no
specific treatment. Pain and sleeplessness must be relieved by opiates
and sedatives, and the strength must be sustained by nourishing diet
and stimulants.


Internal Pachymeningitis.

Internal pachymeningitis is of two kinds: 1st, simple inflammation,
which may be accompanied by purulent exudation and by a corresponding
affection of the pia mater: 2d, hemorrhagic inflammation or hæmatoma
of the dura mater. Simple inflammation of the internal or lower
surface of the dura, without the coexistence of external
pachymeningitis is rarely found in the adult. The morbid appearances
differ but little from that of the external form, and the causes and
the diagnosis are also similar. In children, however, it is not
uncommon, according to Steffen.[2] The pus may discharge itself
spontaneously through the fontanels or the sutures, or caries of the
cranial bones may open a passage for its exit. It has also been
evacuated artificially when the symptoms have indicated its presence.
In other cases more or less extensive firm adhesions {707} between the
dura and pia mater have shown the previous existence of inflammation,
but it would be difficult to say in which membrane it began. In some
instances no symptoms are observed during life; in others the
coexistence of inflammation of the pia, effusion into the ventricles,
etc. prevent an exact diagnosis.

[Footnote 2: “Die Krankheiten des Gehirns in Kindesalter,” von Dr. A.
Steffen, in _Gerhardt's Handb._, 5 B., i. Abt., 2te Hälfte, p. 380.]

The TREATMENT does not differ from that of inflammation of the
external layer of the pia.


Hæmatoma of the Dura Mater.

SYNONYM.—Hemorrhagic pachymeningitis.

DEFINITION.—A chronic inflammation of the dura mater, resulting in the
formation upon its inner surface of successive layers of false
membrane, into and between which there is usually an effusion of
blood, the whole sometimes forming a large solid mass between the dura
and the cavity of the arachnoid.

ETIOLOGY.—Hemorrhagic pachymeningitis never occurs in healthy persons
except from traumatic causes. It is most frequently observed in
advanced life, and especially in the male sex. In a large number of
cases the blood is in an unhealthy condition, and hence the disease is
seen in alcoholism, in scurvy, in acute articular rheumatism, and in
the acute febrile affections, as typhoid fever, pleuro-pneumonia, and
pernicious anæmia, of which last, according to Huguenin,[3] it
complicates one-third of the cases. It is frequent among the chronic
insane. It is occasionally met with in young children, but with them
its causes are mostly unknown; according to Steffen,[4] they may
consist in alterations of the blood resulting from insufficient
nourishment or from the infectious diseases, and from abnormal
blood-pressure, as in whooping cough, asthma, etc., as well as from
blows on the head.

[Footnote 3: G. Huguenin, “Acute and Chronic Inflammations of the
Brain,” in _Ziemssen's Encylop._, Am. translation, New York, 1877,
vol. xii. p. 401 _et seq._]

[Footnote 4: _Op. cit._, p. 386.]

SYMPTOMS.—Many cases of hemorrhagic pachymeningitis complicating other
cerebral diseases can be distinguished by no special symptom from the
original malady. Thus, in cases of chronic insanity its existence may
not be suspected during the lifetime of the patient. Steffen quotes[5]
the case, reported by Moses, of a child seven months old who died of
catarrhal pneumonia, and who exhibited no symptom which could suggest
any disease of the brain or its membranes. The autopsy revealed a
pachymeningitic cyst extending over the anterior half of the right
hemisphere. When symptoms are present they vary in different cases
according to the acuteness of the inflammatory process, the amount and
situation of the effusion, and the participation of the pia mater and
brain in the disease. In the beginning they are usually indefinite,
headache being the most common and often the only complaint. This may
continue for weeks without any other indication of disease, but it is
frequently accompanied by tinnitus aurium, vertigo, muscular weakness,
and contraction of the pupils. Wakefulness and restlessness at night
and slight twitching of the facial muscles or of the limbs sometimes
occur. There may be no change in the condition of the patient for a
{708} considerable length of time (weeks or months), or he may improve
to some extent, owing to the absorption of the serous portion of the
effusion or to the tolerance of the foreign body acquired by the
brain. Sooner or later a fresh hemorrhage is followed by a recurrence,
and usually an aggravation, of all the symptoms. Sometimes the patient
becomes comatose, and dies speedily with apoplectic symptoms, but this
is not common at an early period. The extravasation of blood generally
takes place in small quantities at a time, without giving rise to
unconsciousness or paralysis. After a period of uncertain duration,
when the tumor has attained considerable dimensions a condition of
somnolence may take place, the patient sometimes sleeping twenty-four
hours or longer at a time. Distinct paralysis rarely occurs, though
hemiplegia is sometimes seen, and the paralysis has been observed on
the same side with the lesion. When symptoms of compression appear the
pupils become dilated. Toward the end of life the patient is usually
in a state of profound coma, the pulse is slow and irregular, and the
sphincters are relaxed.

[Footnote 5: _Op. cit._, p. 394.]

The distinctive features of internal pachymeningitis, therefore, so
far as they are at present known, are those which would depend upon a
primary cerebral irritation, followed by those of compression of the
brain—persistent, often severe, headache, with contracted pupils, and
occasionally motor and sensory disturbances; afterward, coma, dilated
pupils, and involuntary discharges from the bowels and bladder.

The DURATION of the disease is exceedingly variable, extending from a
few days to more than a year. According to a table made from carefully
observed cases by Huguenin, 74 per cent. of patients die within thirty
days; 18 per cent. live from one to six months; 4 per cent. live from
six months to one year; and 4 per cent. live over one year.

PATHOLOGY.—A difference of opinion has existed among pathologists
concerning the true nature of hemorrhagic effusions of the inner
surface of the dura mater, especially as to whether the membrane in
which they are enclosed is formed by a deposit of fibrin from the
effused blood itself, or whether the disease consists essentially in
an inflammation of the dura, followed by a pseudo-membranous deposit
into which blood is afterward extravasated. The latter explanation,
offered by Virchow, has been generally accepted, but Huguenin, whose
opportunities for observing the disease were unusually good, believes
that the first stage of hæmatoma is not the formation of connective
tissue, but simply an extravasation of blood.

The disease begins with hyperæmia of the dura mater in the area of
distribution of the middle meningeal artery, followed by the formation
upon its inner surface of an extremely delicate membrane in small
patches of a yellowish color and studded with innumerable bloody
points. If the membrane be carefully raised, it is found to be
connected with the dura by very delicate blood-vessels, and to contain
an immense number of very wide and thin-walled vessels, much larger
than ordinary capillaries.[6] At a later stage we find the membranes
to be made up of several distinct layers, of which the innermost
exhibits the character of the primary deposit, being thin and
abundantly supplied with blood-vessels, while those of older formation
have become successively thicker and are {709} composed of tough,
lustrous fibres of connective tissue almost as dense as that of the
dura mater itself. The delicate structure of the false membranes and
of the vessels which they contain leads almost inevitably to the
effusion of blood, which increases in quantity with the thickness of
the whole growth, so that in an advanced stage it is not uncommon to
find large pools of blood, partly clotted and partly fluid,
constituting what is called hæmatoma of the dura mater. The small
bloody points are within the substance of the false membrane; the
extravasations are interstitial, the largest being always found
between the youngest membrane and the older layers. In some cases
serous transudations also occur between the false membranes. In still
rarer instances no blood or serum is found between or beneath the
layers. Occasionally small quantities of blood escape by leakage
through the delicate membrane into the cavity of the arachnoid.

[Footnote 6: See Rindfleisch's _Manual of Pathological Histology_, New
Sydenham Soc.'s translation, 1873, vol. ii. p. 302.]

The usual situation of internal pachymeningitis is the vault of the
cranium, near the median line, the upper or external layer of the
tumor being in relation with the dura mater, to which it is adherent,
and the lower or internal with the arachnoid and pia mater. If the
effusion be extensive, it spreads downward over the frontal and
occipital lobes of the brain, and laterally toward the fissure of
Sylvius. In the majority of cases the disease occupies both sides of
the median line symmetrically, but it may be limited to one side only.
According to Huguenin, 56 per cent. of the cases embrace the surfaces
of both hemispheres; 44 per cent., that of one only. Hæmatoma very
rarely occupies the base of the cranium. The thickness and consistency
of the deposit vary in different cases, depending upon the number of
successive exudations, and hence are most marked in cases of the
longest duration.

Hemorrhagic pachymeningitis is occasionally met with in young
children, but much more rarely than in adults. The disease is usually
more acute than in older persons, but the anatomical appearances are
essentially the same.[7]

[Footnote 7: For an able description of the lesions of hemorrhagic
pachymeningitis in children see the third edition of Rilliet and
Barthez's _Maladies des Enfants_, by Barthez and Sanné, Paris, 1884,
vol. i. p. 152.]

PROGNOSIS.—The great majority of cases end fatally. A few instances of
recovery are reported in which the diagnosis seems justified by the
symptoms. Moreover, it is not very rare to find, on post-mortem
examination of those who have died of other diseases, evidence of the
former existence of hemorrhagic pachymeningitis. According to Steffen,
while the prognosis of simple pachymeningitis in children is
frequently good, owing to the favorable conditions for the exit of pus
through the open fontanels and sutures, in hemorrhagic pachymeningitis
recovery is rare.

DIAGNOSIS.—In a disease whose symptoms are so vague the diagnosis must
of necessity be difficult and often impossible. The chief elements for
the formation of the diagnosis are the slow and interrupted progress
of the affection, persistent headache, tendency to prolonged slumber,
and final coma; the absence of paralysis of the cranial nerves, of
vomiting, and of general convulsions; the age of the patient, the
coexistence of alcoholism, chronic insanity, or acute rheumatism, and
traumatism. The diseases for which hæmatoma would be most likely
mistaken are acute inflammation of the meninges, apoplexy from
cerebral hemorrhage, tumor in the substance of the brain, and
necrobiosis from thrombus or embolus. {710} The absence of symptoms
characteristic of these affections might lead to a probable diagnosis
by exclusion, but in many cases the existence of the disease cannot be
determined with certainty. In children it is most likely to be
confounded with tubercular meningitis, from which it may be
distinguished by the fact that it is most common under the age of two
years, the other being rare before that period, and that the
characteristic symptoms of tubercular meningitis (prodromic period,
vomiting, irregularity of pulse, etc.) are wanting. But the tubercular
disease in young infants may closely resemble hæmatoma, a profound
coma replacing all other symptoms. Here the existence of tuberculous
disease in the parents or other near relatives would point strongly to
tubercular meningitis, while the absence of such antecedents would
suggest hæmatoma.

TREATMENT.—If the disease be a complication of alcoholism, anæmia,
scurvy, rheumatism, etc., the treatment appropriate to those
affections should be employed, along with remedies addressed to the
local disease. For the early symptoms of irritation, perfect rest in
bed, cold to the head, bromide of potassium internally, sinapisms to
the back of the neck, together with simple and nutritious diet, are
the most efficient means. The bowels must be regulated, but purging is
not necessary. The abstraction of blood from the head by leeches to
the temples or behind the ears, or by cupping, is recommended by most
authorities, especially if there be much heat of the head. Mercury may
be tried, care being taken not to salivate the patient. It is obvious
that this treatment, in order to be of any avail, must be instituted
at the earliest stage of the disease. After the probable formation of
the hæmatoma an effort should be made to promote its absorption, which
sometimes actually takes place, as is proved by the autopsies of
patients who, having previously suffered from this affection, have
died from other causes. The iodide of potassium or the iodide of
sodium should be employed perseveringly for this purpose, in the dose
of from ten to thirty grains three times daily. The bromide should
also be continued if necessary. The acne which sometimes accompanies
the continued use of these remedies may be prevented or cured by the
use of three to five drops of the liquor potassæ arsenitis, given once
or twice daily after meals. Counter-irritation to the scalp by means
of stimulating liniments or croton oil, and small blisters to the
temples, are likely to do good. In alcoholic subjects the amount of
wine or spirit taken should be regulated by allowing enough to support
the strength, without too suddenly withdrawing the accustomed
stimulant. In the stage of coma the treatment must be purely
expectant. The state of the bladder must be regularly examined, and
the catheter employed when necessary. Liquid nourishment should be
carefully given as long as the patient is able to swallow.


Cerebral Meningeal Hemorrhage.

SYNONYM.—Meningeal apoplexy of the brain. Hemorrhage of or upon the
membranes of the brain is closely connected with intracerebral
hemorrhage. Both arise from similar causes, and the former may result
directly from the latter. It is for convenience of arrangement that
the two subjects are treated separately in this work.

{711} ETIOLOGY.—The causes of meningeal apoplexy are predisposing and
immediate. The most important predisposing cause consists in disease
of the cerebral vessels, especially the arteries, which favors the
formation of so-called miliary aneurisms, as demonstrated by Charcot
and Bouchard in the case of cerebral apoplexy. Disease of the vessels
in its turn arises from various conditions, among which alcoholism in
adults holds a prominent place from its tendency to favor a fatty
degeneration of the vascular walls. In subjects of purpura or
hæmophilia (the so-called bleeders), in whom, from an inherent
weakness of the capillary vessels or a deficiency of the fibrin of the
blood, or both combined, there is a tendency to extravasation of the
blood in various parts, hemorrhage into the arachnoid cavity may
occur.[8] A new-born child under my observation had bleeding at the
navel and ecchymoses in various parts of the body. Suddenly it became
comatose, and it died with signs of cerebral compression. There was no
autopsy, but it seems probable that hemorrhage into the cavity of the
arachnoid had taken place. A sister of the patient had also had
spontaneous hemorrhage from the navel and from other parts shortly
after birth, but recovered. Chronic general arthritis and gout also
probably predispose to the affection, as well as old age, which is
accompanied by atrophy of all the tissues. The disease is most
frequently met with in the two extremes of life; according to
Durand-Fardel,[9] in adults the largest number of cases occurs between
the ages of seventy and eighty years.

[Footnote 8: A case of this kind is cited in the article “Pathologie
des Méninges” in _Nouv. Dict. de Méd. et de Chirurg. pratiques_,
Paris, 1876, vol. xxii. p. 101.]

[Footnote 9: _Traité clinique et pratique des Maladies des
Vieillards_, par M. Durand-Fardel, Paris, 1854, p. 283.]

The exciting causes comprise injuries to the head, both with and
without fracture; strong muscular effort, as in lifting, straining at
stool or in labor; powerful action of the heart in cases of
hypertrophy. An interesting case is reported[10] by S. G. Webber of
Boston, in which the effusion was evidently caused by vomiting; a clot
of blood covered the greater part of the posterior two-thirds of the
right hemisphere. Sometimes meningeal hemorrhage may arise from the
bursting of an intracerebral apoplexy into the arachnoid cavity, as in
a remarkable case occurring in the practice of Morris Longstreth of
Philadelphia, of bilateral effusion.[11] Outside the dura,
corresponding with the left middle cerebral lobe, was a considerable
amount of blood connected with a fracture of the skull, and on the
right side a large quantity of blood in the cavity of the arachnoid,
originating in the middle lobe, which was torn up. The patient had
fallen in the street; he was stupid, there was no paralysis, active
delirium came on, followed by coma and death in twenty-four hours.
Here was cerebral apoplexy bursting into the cavity of the arachnoid
on the right side, and causing the fall, which was the occasion of the
fracture and hemorrhage on the left side.

[Footnote 10: _Boston Med. and Surg. Journal_, Jan. 17, 1884.]

[Footnote 11: _Ibid._, Dec. 28, 1882.]

In young children, especially in the new-born, meningeal hemorrhage
may follow difficult and instrumental labor, either from injury to the
skull or from delay in the establishment of respiration, as in breech
presentation, though it sometimes occurs in cases in which the labor
has been normal. In a case of breech presentation under my care in
1873 {712} the child, a female weighing nine pounds, did not cry or
breathe for some minutes after birth, although delivery had not been
much delayed. Soon afterward it was noticed that it did not move the
right arm, although it moved the hand and the fingers. In the course
of twenty-four hours, during which time it cried much more than usual,
it became comatose, and remained so until its death, three days after
birth. The whole surface was livid, and the child had two or three
short convulsions. At the autopsy a clot about the size of a grape was
found in the pia mater on the upper surface of the cerebellum, in the
immediate vicinity of the pons Varolii. The brain was so soft that the
amount of injury received by the cerebellum could not be exactly
ascertained, but it was probable that the clot extended into the
fourth ventricle.

Thrombus of the sinuses of the dura mater, and less frequently of the
cerebral arteries, is the origin, in a considerable number of cases,
of meningeal hemorrhage in children, in consequence of pressure upon
the delicate vessels of the membranes caused by the obstructed
circulation. Bouchut[12] reports an observation of hemorrhage produced
in this way.

[Footnote 12: E. Bouchut, _Clinique de l'Hôpital des Enfants
maladies_, Paris, 1884, p. 263. See, also, Steffen, _op. cit._, p.
352.]

SYMPTOMS.—In some cases the attack is preceded by indications of
congestion, such as headache, vertigo, staggering, confusion of ideas,
noises in the ears, feeling of weight in the head, delirium, stupor.
At the time of the attack the patient frequently complains of severe
pain in the head, just as in cerebral hemorrhage, and then falls to
the ground with complete loss of consciousness. Sometimes the symptoms
come on gradually. Hemiplegia occurs in a notable proportion of cases.
Convulsions may occur at any time after the attack. In Webber's case,
already referred to, the first symptom was sharp pain in the head and
neck; this was followed by very severe headache and pain on motion of
the head. Intelligence gradually diminished; on the sixth day there
was almost no consciousness, and the patient died in about eight days.
She had occasional spasms, in which both eyes were turned toward the
left in extreme conjugate deviation, and the left side of the face was
distorted. The spasms were followed by suspension of respiration for
nearly a minute, cyanosis, and paralysis of the left hand and leg.
Both the nature of the lesion and its seat were correctly
diagnosticated during the patient's lifetime.

As a rule, the condition of unconsciousness continues up to the time
of death, but in some cases there are intermissions during which the
patient responds to questions more or less promptly. Death takes place
at a period varying between a few hours and several days.
Durand-Fardel[13] reports a case in which the patient lived a month
from the first attack, with preservation of the intellect and of
motion. An inmate of the Home for Aged Women in Boston, eighty-eight
years old, previously in good health, complained of severe pain in the
head one morning before rising. She took her breakfast in bed, and
immediately afterward vomited copiously. From that moment she became
insensible, and remained so until her death, seven days and three
hours afterward. During this time there was no stertor. No decided
paralysis could be discovered, but there was some rigidity of the left
arm. At the autopsy an effusion of {713} blood was found in the
arachnoid cavity extending from below upward on each side to a level
with the top of the ear. There was a large amount of blood at the base
of the brain, and both lateral ventricles were distended with bloody
serum. The vessels were generally in an atheromatous condition. There
was no laceration of the brain. The source of the hemorrhage could not
be ascertained. In such a case the condition of the patient in respect
to power of movement often cannot be ascertained with certainty, in
consequence of the abolition of consciousness. Complete muscular
resolution is most common when the effusion is bilateral, but when the
hemorrhage is limited to one side more or less paralysis of the
opposite limbs may exist. Should the blood make its way into the
spinal canal, it might give rise to special symptoms, but this is not
probable in view of the large amount of the cerebral effusion under
the circumstances, which would produce complete insensibility or
speedily cause death by pressure on the medulla.

[Footnote 13: _Op. cit._, p. 202.]

The temperature of the body immediately after a copious cerebral or
meningeal hemorrhage falls below the normal point, and remains so for
several hours, after which it rises, its degree varying according to
circumstances. In fatal cases the elevation is extreme, and remains so
until death. If the patient recover, it gradually returns to the
normal standard.

Vomiting is a frequent symptom at the beginning of the attack, just as
in intracerebral hemorrhage, owing probably to compression of the
pneumogastric by the effusion at the base of the brain. In Webber's
case the vomiting was evidently the cause of the hemorrhage, and not
its consequence, since it had been a frequent symptom for several days
before the attack, and was probably due to the presence of a calculus
in the pelvis of the right kidney, which was found at the autopsy, and
there was no blood at the base of the brain.

PATHOLOGICAL ANATOMY.—The chief points of interest in the morbid
anatomy relate to the seat and source of the effusion, the amount and
condition of the blood, the state of the vessels and that of the
brain, including the ventricles. In respect to the seat, the
hemorrhage may occupy the space between the cranial bones and the dura
mater; it may be found on the lower surface of the latter, in the
arachnoid cavity, or in the meshes of the pia mater, the so-called
subarachnoid space. Blood found upon the outer surface of the dura,
between that membrane and the bones, is almost always the result of
traumatic causes, such as blows or other injuries, with or without
fracture, or of caries of the skull. If below the dura, but between
that and the so-called parietal layer of the arachnoid, the lesion
comes under the title of pachymeningitis interna, already described as
an inflammatory disease of the dura with hemorrhagic effusion. The
arachnoid cavity and meshes of the pia are by far the most common
situations in which the blood is found in meningeal hemorrhage. The
origin of the effusion is either the rupture of a capillary aneurism
of one of the arterioles of the membrane or of one of the vessels
themselves in consequence of atheromatous or other degenerations of
its walls. On account of the minute size of the vessels it is seldom
possible to discover the exact point at which the rupture took place.
In rare instances the source of the hemorrhage is within the brain,
the blood being forced through the cerebral tissue, either into the
meshes of the pia {714} or upon the surface of that membrane. The
amount of hemorrhage varies according to conditions which are mostly
unknown, but is probably dependent upon the size of the ruptured
vessel and the conditions under which the accident occurs, such as
muscular effort, cardiac action, etc. In some cases it is so small as
to give rise to no definite symptoms, as is evident from post-mortem
examinations of those who have died from other causes. In these cases
there may be either a single effusion or several. The amount is
largest when the arachnoid cavity is the seat of the extravasation.
The blood, which may be either liquid or more or less coagulated,
according to the time which has elapsed since the hemorrhage, is
usually found upon the convexity of the hemispheres, most frequently
on one side only, and oftenest on the left. But if the rupture have
taken place at the base, it often ascends on each side, as in a case
mentioned above. Where a large vessel has given way, its contents may
cover a great part of the surface of the brain. The coagulum is found
in a thin layer, which at the end of a few days is covered with a
transparent envelope, evidently composed of a deposit or separation of
fibrin. Should the patient survive long enough, this membrane may
become organized, receiving vessels from the adjacent pia, and in turn
become the seat of new hemorrhages, exactly as in the hæmatoma of
internal pachymeningitis. In cases in which absorption of most of the
fluid part of the effusion takes place, the membrane remains more or
less dense and vascular, and usually contains a small quantity of
recently-effused blood within its meshes. Small cysts, containing
transparent or reddish-brown serum, are also occasionally observed
enclosed between the layers of the membrane. In very young children,
whose fontanels are not yet ossified, these cysts sometimes attain to
a large size, containing several pints of fluid, which is more or less
limpid from absorption of the coloring matter of the blood,
constituting the so-called dropsy of the arachnoid.[14] The
convolutions of the brain are more or less flattened according to the
amount of the effusion, and the cortical substance is correspondingly
anæmic from pressure. The blood may make its way, if extravasated in
large quantities, into the ventricles, over the medulla, into the
spinal arachnoid cavity, or even into the central canal of the spinal
cord. The arteries of the brain, especially at the base, are
frequently in a state of atheromatous degeneration, and thrombi often
occupy the sinuses of the dura mater.

[Footnote 14: Charles West, M.D., _Lectures on the Diseases of
Childhood and Infancy_, 6th ed., London, 1874, p. 62. These large
cysts are much more frequently (perhaps solely) found in cases of
hemorrhagic pachymeningitis. (See Barthez and Sanné, _op. cit._, vol.
i. p. 157.)]

DIAGNOSIS.—The distinction between meningeal hemorrhage and cerebral
apoplexy is always difficult, and in the majority of cases impossible.
Sudden pain in the head, vomiting, and lowering of the bodily
temperature (the thermometer should be placed in the rectum), followed
by loss of consciousness, are strongly suggestive of hemorrhage within
the cranium, either cerebral or meningeal. If these symptoms are
followed by coma and resolution without obvious paralysis, the
diagnosis would be almost impossible between intra- and extra-cerebral
extravasation. If the loss of consciousness be not complete, so that
the presence or absence of paralysis can be ascertained, we can
sometimes distinguish the situation of the hemorrhage. Right-sided
hemiplegia, with paralysis of the face or tongue, or with aphasia, is
most probably owing to hemorrhage or {715} embolism somewhere in the
left motor tract, and hence within the brain. If the absence of
paralysis can be certainly ascertained, the probabilities are in favor
of meningeal apoplexy. Convulsions affecting the face or limbs of one
side would point to irritation of the cortical centres of those parts,
and so far to extravasation on the surface of the brain (on the
opposite side), as in Webber's case. Where the amount of hemorrhage is
small it furnishes no diagnostic indications. In the case of new-born
children the presumption is in favor of meningeal effusion.

PROGNOSIS.—If the effusion be considerable in amount, as indicated by
prolonged coma with resolution, the issue is almost inevitably fatal,
though life is occasionally prolonged for a surprising length of time.
Slight hemorrhages are doubtless recovered from, but there are no
means for their certain diagnosis.

TREATMENT.—The treatment, which is essentially the same as that for
cerebral congestion, has for its object the arrest of the hemorrhage,
and, if that can be effected, the absorption of the effused blood. In
view of the former, the patient's head should be elevated and kept
cool by the application of ice. Unless the bowels have previously been
freely moved, saline laxatives, followed by enemata if necessary, must
be given. The state of the bladder must be carefully attended to.
Liquid nourishment alone, in moderate quantities at regular intervals,
is permissible, with stimulants if there be signs of exhaustion. For
the absorption of the effusion mild counter-irritation to the scalp
and the administration of the iodide of potassium may be employed.


Congestion of the Cerebral Pia Mater.

The pia mater consists of two layers, separated by a loose connective
tissue. The outer layer, being that which was formerly called the
visceral layer of the arachnoid, is stretched smoothly over the
convolutions of the brain without dipping into the sulci; the inner
layer is closely connected with the surface of the brain, whose
inequalities it follows. The two layers are more firmly united
together over the convolutions than between them; in the latter
situation the connection is loose, and the space which separates the
surfaces is called the meshes of the pia. The membrane extends into
the ventricles, investing the ependyma and the choroid plexuses, and
over the medulla oblongata and spinal cord. In the normal condition it
is loosely attached to the brain, from which it can be stripped off
without loss of substance. The meshes of the pia, together with the
ventricles, constitute a series of cavities connected with each other,
containing a variable amount of cerebro-spinal fluid, and they
communicate with the lymph-spaces surrounding the blood-vessels.
Pressure within the cranial cavity, from congestion of the vessels or
from the products of inflammation, is thus relieved in a measure by
displacement of the cerebro-spinal fluid, which is driven out through
the perivascular lymph-spaces.

Congestion or hyperæmia of the pia mater probably never occurs
independently of that of the external surface of the brain, on account
of the intimate vascular connection of the two. In the adult it can
only exist to a limited extent, on account of the unyielding nature of
the cranial {716} walls and of the limited compensatory action of the
cerebro-spinal fluid. In young children the incomplete ossification of
the skull and the delicate structure of the vessels are more favorable
to congestion.

ETIOLOGY.—The causes of hyperæmia of the pia mater are in the main the
same as those of congestion of the dura.

SYMPTOMS.—Since congestion of the pia always coexists with that of the
corresponding part of the external portion of the brain, it is
impossible to separate the symptoms belonging to each. They are
therefore usually included under the head of Cerebral Congestion, to
which article the reader is referred.

PATHOLOGICAL ANATOMY.—Arterial hyperæmia of the pia is seldom
discovered after death, the elasticity of the vessels causing
transudation of the fluid part of the blood through their walls.
Venous congestion of the pia is more frequently noticed, usually in
connection with that of the dura, the sinuses with their accompanying
veins being distended with blood, and in cases of long standing often
containing thrombi. Simple hyperæmia of the pia being rarely or never
fatal of itself, these appearances are usually accompanied by those of
inflammation of the membrane or of the cortical layer of the brain
(effusion of lymph or pus), or by hemorrhage.

TREATMENT.—In a case of suspected congestion of the pia the treatment
would be the same as that of cerebral congestion.


Inflammation of the Cerebral Pia Mater.

SYNONYMS.—Meningitis, Leptomeningitis, Acute non-tubercular
hydrocephalus.

Meningitis (by which is generally understood inflammation of the pia)
appears under an acute, a chronic, and an epidemic form. The latter,
being a zymotic disease, is described in a separate article, to which
the reader is referred.

ETIOLOGY.—Meningitis occurs both as a primitive disease and as
secondary to other affections. The former is rare, the latter is more
frequent. The causes of idiopathic meningitis are for the most part
unknown. Exposure to the sun's rays and excessive indulgence in
alcoholic liquors are thought to excite it in some instances. It has
been known to follow blows and falls on the head which have produced
no injury to the skull. It is rather more commonly observed in early
manhood than at other periods of life. Secondary meningitis may follow
injury or disease of the cranial bones or of the dura, and of the
brain. A frequent cause is extension of disease of the ear to the
membranes and substance of the brain. The reader is referred to the
article on MEDICAL OTOLOGY for information concerning the symptoms of
that formidable complication. Certain diseases are known to be
occasionally complicated with meningitis—acute articular rheumatism;
erysipelas of the scalp and of the face; Bright's disease, especially
the chronic interstitial form; peritonitis; ulcerative endocarditis;
pyæmia; the eruptive fevers; the puerperal state; and syphilis.
Meningitis following or complicating acute rheumatism is generally
supposed to be not uncommon, but the number of cases in which the
existence of inflammation of the meninges has been {717} proved by
autopsy is small. Fuller,[15] along with three cases in which
dissection showed suppurative inflammation of the pia, cites several
others in which no cerebral disease was found after death, although
the symptoms gave every indication of it. True meningitis is rare in
chronic Bright's disease, the symptoms resembling it being caused, in
the majority of cases, by uræmia. Meningitis complicating pneumonia is
also rare, although cerebral symptoms are common enough in that
disease, especially in young children with inflammation of the upper
lobes. C. Neuwerk[16] reports seventeen cases of purulent meningitis
complicating acute pneumonia. It was more frequent in men, especially
in alcoholic subjects, than in women. The meningitis was generally
total. The lungs were in a state of gray or yellow hepatization.

[Footnote 15: H. W. Fuller, M.D., _On Rheumatism, Rheumatic Gout, and
Sciatica_, 3d ed., Philada., 1864, p. 271. See also E. Leudet,
_Clinique médicale de l'Hôtel Dieu de Rouen_, Paris, 1874, p. 133.]

[Footnote 16: _Deutsches Archiv für klin. Med._, xxix., 1881, p. 1;
and _Schmidt's Jahrbücher_, Band cxcviii., 1883, Nov. 5.]

SYMPTOMS.—The symptoms of acute leptomeningitis vary much in the
course of the disease. This is readily explained by the complex
character of the functions of the parts involved in the inflammation.
It may be assumed that the cortical layer of the brain is implicated
in every case unless of the most transient and limited kind; the
substance of the brain, cerebellum, and medulla are subjected to
pressure from the afflux of blood, from the effused lymph and pus, and
from the accumulation of serum in the ventricles; the cranial nerves
are exposed to pressure from the deposit of lymph, which may give rise
to irritation or to suspension of function or both; parts at a
distance from the seat of lesion may be functionally disordered by
reflex action through communicating filaments. Finally, the general
system suffers from the effects of the high fever upon the blood and
the nutrition.

It is customary to speak of a stage of excitement followed by one of
depression as characteristic of the course of the disease; but
although active symptoms generally prevail in the early period, to be
succeeded later by coma and paralysis, this disposition is by no means
uniform. Sometimes sopor and paralysis constitute almost the only
symptoms throughout the disease—this is especially noticed in
infants—or active delirium and convulsions may persist until the fatal
termination. More frequently the two conditions alternate several
times with each other. A prodromic period of short duration, a few
hours or a day or two, is sometimes observed in primitive meningitis,
the patients complaining of headache, vertigo, vomiting, restlessness,
or lassitude. Infants are irritable or drowsy, with heat of the head,
quick pulse, and occasional vomiting. In secondary meningitis this
period is usually masked by the symptoms of the primitive disease. In
the majority of cases the beginning of acute meningitis is abrupt.
Rigor is sometimes the first symptom observed, and in children is
usually represented by a convulsion. More commonly, however, the
disease is ushered in by severe headache, which is often referred to
the forehead. The head is hot, the face is flushed, the eyes are
brilliant, the pupils are contracted, the pulse is quick and hard, the
temperature high (104° F. or upward). The patient is wakeful,
restless, and irritable, sensitive to light and to sound. The skin is
hyperæsthetic, {718} especially that of the legs. There may be
wandering or even active delirium. Vomiting is not unfrequent. There
is thirst, but no desire for food. The urine is scanty and
high-colored, the bowels constipated. These symptoms gradually
increase in intensity, especially the pain in the head and the
delirium, and in many cases they are followed by convulsions, at first
in the form of twitchings of the facial muscles or of the limbs,
grinding the teeth, etc., which give place to tonic contractions of
the limbs or of the trunk, often confined at first to one or both
members of the same side, but afterward becoming general; the flexors
of the forearms and of the legs are most usually affected. The upper
dorsal muscles may become contracted, so that the head is drawn
backward, and more rarely trismus occurs.

A diminution in the rapidity of the pulse, which may fall to the
normal rate, or even below that, notwithstanding the persistence of
the high temperature, indicates the beginning of the stage of
depression. This change is sometimes sudden, though more often gradual
in its approach. The activity of the delirium subsides, giving place
to a somnolence which may seem to the inexperienced observer a
favorable indication, but which soon deepens into coma. The face
becomes pale, the features are sunken. Only an occasional grimace or a
movement of the hand to the head shows that the patient is to some
extent conscious of suffering. This condition may alternate with the
previous one from time to time, the comatose state being interrupted
by noisy delirium and tonic or clonic convulsions, or even a partial
return of consciousness, giving rise to fallacious hopes on the part
of the friends, and sometimes deceiving the physician himself into a
belief that a favorable issue is at hand. Before long, however, the
symptoms of brain-compression become permanent. The rigidity of the
limbs gives place to complete resolution. The patient lies absolutely
unconscious, with dilated pupils. The pulse becomes again rapid in
consequence of compression of the medulla, and thread-like and
irregular; for the same reason the respirations increase to 40, 50, or
60 in the minute. The sphincters are relaxed, and the patient dies
without any recurrence of the active symptoms. In rare cases recovery
takes place, although almost never after the symptoms of compression
have continued without interruption for any considerable length of
time. Moreover, it is seldom that recovery takes place in the adult
without leaving some traces of permanent damage, such as general
debility, paralysis of one or more limbs, deafness, mental weakness,
epilepsy, etc. Many cases of general paralysis of the insane and other
forms of so-called mental disease are the result of meningitis.

DURATION.—In the adult usually the disease lasts about a week or ten
days; exceptionally, it may last two or three weeks.

COURSE.—In young children the course of meningitis differs somewhat
from that which is observed in adults, though the symptoms are
essentially the same. It is more sudden in its onset and shorter in
its duration. The prodromal stage may be brief or hardly noticeable;
but in older children restlessness, sensitiveness to light and sound,
wakefulness, slight twitchings of the features or of the limbs, a
half-open condition of the eyelids during sleep, occasional vomiting,
etc., are more commonly noticed. Convulsions are more common than in
the adult, and sometimes constitute the chief symptom. They may be
confined to a single extremity, but in {719} general they shift from
one limb to another. The muscles of the eyeball are usually
implicated, causing strabismus. Retraction of the head is rarely
absent, especially in young infants. These convulsions are almost
always tonic, but occasionally they alternate with clonic ones.
Distension and increased pulsation of the anterior fontanel is always
observed in infants a few months old affected with this disease. When
meningitis is secondary to some other disease, the first symptom
noticed in children is apt to be vomiting, with delirium. According to
Steffen, pneumonia is the disease most frequently complicated with
meningitis in children. As in tubercular meningitis, the most
prominent symptom may be mere sopor, sometimes with intervals of
intelligence. Simple meningitis in children is generally a rapid
disease, proving fatal in most cases within a week, and sometimes even
in a few hours. Exceptionally, it may last much longer. A case
occurring in a girl six years old, the duration of which was
fifty-five days, is reported by J. Bokai, Jr.;[17] the diagnosis was
substantiated by autopsy. Another case, which recovered after seven
weeks, is mentioned by Henoch.[18]

[Footnote 17: _Jahrb. f. Kinderkrankheiten_, N. F., xviii. 1, p. 105;
and _Schmidt's Jahrb._, 1882, No. 6, p. 269.]

[Footnote 18: Eduard Henoch, _Vorlesungen über Kinderkrankheiten_,
Berlin, 1881, p. 277.]

PATHOLOGICAL ANATOMY.—The lesions, which are rarely general, may
occupy a greater or less extent of the membrane. They are usually
disposed symmetrically with regard to the two hemispheres, or occupy
corresponding regions of the base. The vessels are in the beginning of
the disease distended, the finest ramifications being injected, giving
a red color to the membrane, which varies in different places from
crimson to light pink. The perivascular spaces of the larger vessels
are filled with a grayish or yellowish fluid composed of extravasated
liquor sanguinis and white blood-corpuscles. The meshes between the
two layers of the pia are soon infiltrated with pus, and the thickened
membrane can be stripped off from the surface of the brain, which is,
however, adherent to it in places and is torn in the process.
Sometimes a thin layer of pus, which can be scraped off with the
knife, is found upon the surface of the pia. The extent of the lesion
varies much in different cases. It may be confined to a limited region
of the hemispheres, or it may spread to the fissure of Sylvius, where
two surfaces become adherent. Sometimes the concrete pus and fibrin
are deposited in thick masses upon the base of the brain, often
completely surrounding the cranial nerves, and even the medulla. The
inflammation may extend to the lateral ventricles, which become filled
with a turbid fluid containing pus-cells, and sometimes wholly
purulent. The choroid plexuses are often covered with flecks of pus.
When the distension of the ventricles is very great, the gyri of the
brain are more or less flattened by compression against the cranium,
and the outer layer of the cerebral substance is bloodless and
œdematous. The cerebral sinuses are distended with blood, and
frequently contain thrombi due to an early stage of the inflammatory
process, besides recent coagula.

DIAGNOSIS.—The diagnosis of acute meningitis is often difficult, and
sometimes impossible, especially in the early stages, when the line
between congestion and inflammation cannot be drawn, and in
complicated cases. The typical symptoms are sudden and acute pain in
the head, with {720} sensitiveness to light and sound, contracted
pupils, rapid pulse, and vomiting, followed by delirium, convulsions,
and coma. If these symptoms were observed in an individual previously
in good health, they would be strongly suggestive of the disease, and
yet many of them are often present in the beginning of pneumonia,
erysipelas, typhoid, typhus, and other eruptive fevers, uræmia, and
poisoning from narcotic substances. Hence it is important to eliminate
these sources of error before coming to a conclusion, and a neglect of
this precaution is a not infrequent source of error in the diagnosis.
A careful examination of the urine will generally enable us to exclude
uræmia. The presence or absence of the eruptive fevers can usually be
determined by the attendant circumstances, and yet cases of
scarlatina, typhoid fever, variola, etc., beginning with active
cerebral symptoms, are sometimes hastily pronounced to be meningitis
by inexperienced observers. In poisoning by narcotics the history will
often aid us in the diagnosis; moreover, except in the case of opium,
the pupils are dilated instead of being contracted. In traumatic
cases, with fracture of the cranial bones, it is always difficult, and
often impossible, to distinguish between the symptoms of meningitis
and those due to other lesions. In concussion without fracture we must
be guided in our diagnosis by the same rules as in idiopathic cases.
The distinction between extreme congestion of the pia mater and
meningitis must be based chiefly upon the duration of the symptoms.
The former is usually brief in its course; the latter lasts one or two
weeks, and in cases which recover is often followed by after-effects
which are more or less permanent in their duration, such as paralysis
or rigidity of the limbs, mental defects, etc. Rapid recovery from the
acute symptoms would be strongly suspicious of congestion, and
doubtless in many such cases the treatment has been credited with a
success to which it was not entitled. The diagnosis from tubercular
meningitis will be reserved for the article on that disease.

PROGNOSIS.—Acute meningitis is fatal in the majority of cases, though
recovery is possible. A gradual diminution of the severity of the
symptoms, especially in respect to temperature, pulse, pain in the
head, and other cerebral phenomena, would afford encouragement, but we
must not trust too much to the brief appearances of amendment so often
observed.

TREATMENT.—The indications for treatment are threefold: 1st, to
prevent or arrest the inflammation; 2d, to modify its violence and
shorten its duration when arrest is no longer possible; and 3d, to
place the patient in the best condition to withstand the violence of
the disease and to recover from its effects. It is only by prompt
action that we can hope to attain the first object, that of preventing
the passage of hyperæmia into inflammation. The patient should be
placed in a cool and well-ventilated apartment of good size, from
which a bright light is excluded. His head, moderately raised, should
be kept cool by means of pounded ice enclosed in a rubber bag or a
bladder. One or more leeches, according to his age, should be applied
behind the ears, or blood may be drawn from the temples or back of the
neck by means of cupping. The bleeding should be encouraged by
poultices if necessary, but with young children the abstraction of
blood should be done with caution. An active purge should be given,
such as ten grains each of calomel and jalap, followed by castor oil
or infusion of senna; for {721} children, from three to six grains,
according to age, followed by oil, would be sufficient. The medicine
should be repeated in a few hours if there be no effect.
Counter-irritation by means of blisters is recommended by most
authorities as a valuable aid in the first stage of the disease.
Unless the application be very extensive, it is not likely to be of
any avail, and extensive blistering would hardly fail to greatly
reduce the strength of the patient, and also is likely to irritate the
kidneys. There are no medicines which can be relied upon to arrest the
inflammatory process. Nevertheless, the tincture of aconite-root, in
the dose of from one to three drops, according to the age of the
patient, every two hours, might be given early, with the view of
fulfilling the second indication by its sedative property. The bromide
of potassium or of sodium, combined with small doses of chloral
hydrate or of sulphate of morphia, will also calm the excitement and
pain, and diminish convulsions. The success which sometimes follows
the employment of ergot in the epidemic cerebro-spinal meningitis
warrants its trial. Bartholow recommends the wet sheet two or three
times a day if the temperature is high. Steffen advises four grains of
sulphate of quinine with one grain of salicylate of soda, from two to
four times daily, for young children, and in double these doses for
older ones. The alimentation of the patient should be carefully
attended to during this stage. Nourishing liquid food, such as milk,
gruel, broth, eggs, with stimulants if indicated, should be given at
proper intervals, care being taken not to overload the stomach, as is
frequently done. When the patient can no longer swallow the food must
be given by the rectum. During the stage of compression it is useless,
in the present state of our knowledge, to expect any benefit from the
further administration of drugs, and the treatment then consists
mainly in giving small quantities of food at regular intervals, and in
such external applications as the bodily temperature may require. The
bladder must be relieved by the catheter when necessary. Simple
enemata are generally sufficient to prevent constipation.


Chronic Cerebral Meningitis.

Chronic inflammation of the pia mater rarely follows the acute form,
but is generally secondary to other conditions, such as inflammation
and tumors of the dura, tumors and abscess of the brain, disease of
the vessels of the brain, suppurative otitis, and to constitutional
diseases, especially alcoholism, syphilis, and pulmonary tuberculosis.
It is one of the most common lesions found after death from general
paralysis of the insane. As a distinct affection, unconnected with
constitutional disease, it is extremely rare, though less so,
according to Flint,[19] than the acute form. He cites a case in which
the symptoms were intermittent. The patient, fifteen years old, died
after a month's illness. The autopsy showed cerebral hyperæmia, lymph
at the base of the brain, and distension of the ventricles with
transparent fluid. There were no tubercles. In most cases in which the
results of chronic meningitis are found after death the cortical
substance of the brain is involved in the disease; hence {722} the
difficulty in defining its symptoms, which are usually extremely
vague, and not always distinctive of cerebral disease. The principal
are pain in the head, vertigo, vomiting, impairment of the memory,
mental apathy, drowsiness, and muscular weakness. The anatomical
changes are thickening and opacity of the membrane by the deposit of
lymph upon its surface and into the connective tissue, adhesions to
the dura and to the cortical substances of the brain, together with
hyperæmia of the latter. These appearances are usually distributed in
irregular patches of greater or less extent.

[Footnote 19: Austin Flint, M.D., _Principles and Practice of
Medicine_, 5th ed., Philada., 1881, p. 701.]

The DIAGNOSIS of chronic meningitis is often obscure or impossible.
Long-continued pain in the head, accompanied by vertigo, impairment of
memory, drowsiness, mental apathy, etc., without paralysis, would be
suggestive of it, especially if there were occasional intermissions of
the symptoms. The probability would be greatly increased if the
patient had a syphilitic or alcoholic history. The diagnosis should
exclude tumor of the brain, chronic pachymeningitis, and chronic
hydrocephalus, but as these diseases are often complicated with
chronic meningitis, the distinction might be very difficult. As
already stated, chronic meningitis is almost a constant lesion in
general paralysis, as well as in other forms of chronic insanity, but
there are no special symptoms by which its presence can be ascertained
during life.

TREATMENT.—Our aim should be to relieve pain, diminish congestion, and
favor absorption. Counter-irritation to the head and nucha by means of
small blisters or croton oil should be employed with moderation.
Bromide of potassium, or, if necessary, small doses of morphia, may be
given if the pain be severe. Should there be symptoms of cerebral
congestion, such as acute delirium, flushing, and heat of head, an
ice-bag should be applied to the head and leeches behind the ears, or
blood may be drawn from the temples or nucha by cupping. As an
absorbent the iodide of potassium is much recommended, but it is not
likely to be effectual, except in syphilitic cases. The bowels should
be kept free, but without active purging. The general health of the
patient should be promoted by suitable diet and regimen, by relief
from excitement and fatigue, or by change of scene and of climate. For
the treatment of chronic meningitis complicating syphilis, alcoholism,
and tuberculosis, the reader is referred to the articles treating of
those diseases.


{723}


TUBERCULAR MENINGITIS.

BY FRANCIS MINOT, M.D.


DEFINITION.—Inflammation of the pia mater of the brain, with effusion
of lymph and pus, caused by the deposit of miliary tubercles upon its
surface or into its substance.

SYNONYMS.—Scrofulous meningitis, Granular meningitis, Basilar
meningitis, Acute hydrocephalus, Dropsy of the brain.

HISTORY.[1]—It is only within a comparatively recent time that
tubercular meningitis has been distinguished from other cerebral
diseases. Up to the eighteenth century the term hydrocephalus was
employed not only for the dropsical diseases of the head, including
internal and external hydrocephalus, but also for meningeal
inflammations, both simple and tubercular, and for congestion of the
brain and of the membranes; the accumulation of water in the
ventricles or between the membranes being looked upon as the disease,
and not as one of its consequences. The term was even applied to
external tumors, as cephalæmatoma and caput succedaneum. We owe the
first accurate account of the symptomatology of acute hydrocephalus,
or ventricular dropsy, to Robert Whytt of Edinburgh, whose remarkable
monograph, entitled _Observations on the Dropsy of the Brain_, first
published in 1768, after his death, was founded upon the study of 20
cases with 10 autopsies. No addition of importance has been made by
later observers to his graphic description of the disease or to his
rules for its diagnosis. Whytt, however, had no clear notion of its
pathogeny, and it was not till 1815 that Gölis pointed out that acute
ventricular dropsy was a secondary condition depending upon previous
inflammation of the membranes or vessels of the brain.

[Footnote 1: See W. Hughes Willshire's valuable paper, entitled
“Historic Data on Scrofulous Meningitis,” in _Brit. and For.
Med.-Chir. Review_, Oct., 1854.]

In 1827, Guersant remarked that the inflammation of the meninges
constituting acute hydrocephalus presented such peculiarities as led
him to denominate it granular meningitis. He did not, however, connect
the granular deposit with tubercle. This was left for Papavoine to
effect, who in 1830 published two cases of tuberculous arachnitis, in
one of which effusion into the ventricles, or hydrocephalus, existed.
The meningeal granulations or tubercles were described with care, and
their coincidence with tuberculous deposit elsewhere was remarked
upon, as also the apparent occurrence of the former previous to the
inflammatory action in the meninges, and in one case the existence of
the tuberculous granules without the sequence of inflammation. The
important pathological element of acute hydrocephalus thus clearly
pointed out by Papavoine {724} now became apparent to observers, and
obtained almost universal assent. The attention of the profession in
this country was first called to it by W. W. Gerhard of Philadelphia
in 1833, in an admirable paper published in the _American Journal of
the Medical Sciences_,[2] containing the reports of thirty-two cases
with autopsies. In every case but two tubercles were found in other
organs besides the meninges. In one of these two, gangrenous cavities
were found in the lungs without tubercles, though perfectly
characterized miliary tubercles existed in the membranes; in the other
case the lungs were not examined with care, Gerhard not being present
at the autopsy.

[Footnote 2: Vols. xiii. and xiv., 1833-34.]

Finally, the distinction between tubercular and simple meningitis was
pointed out by Guersant in 1839, and clearly established by Barthez
and Rilliet in 1843 in their systematic work on the diseases of
children; and it was further elucidated by Rilliet in 1847.

ETIOLOGY.—The causes of tubercular meningitis are predisposing and
exciting. Among the former are hereditary tendency to tuberculosis and
to the so-called scrofulous diathesis; the previous existence of
tubercle in any part of the body, especially in the lungs; and the
presence of caseous degeneration in the bronchial, the mesenteric, and
other glands, or in the parenchyma of various organs, as the lung, the
testicle, the liver, the spleen, etc. The dependence of miliary
tuberculosis of the pia upon previously-existing caseous or other
inflammatory deposits in some part of the body is acknowledged by most
modern pathologists. Seitz[3] states that out of 130 cases, with
autopsies, of adults, upon which his work is based, such deposits were
found in 93.5 per cent. General constitutional weakness, either
congenital or resulting from grave disease or from overwork, from
insufficient or unwholesome food, and from bad hygienic surroundings,
also favors the deposit of tubercle in the meninges. Sometimes two or
more predisposing causes exist at once. Thus, a child born of
tuberculous parents may be fed with artificial diet instead of being
nursed, or may live in a house whose sanitary condition is bad. Hence
the disease is common among the poor, although by no means rare in the
higher classes of society. In some cases it is difficult or impossible
to assign any predisposing cause. A single child out of a numerous
family may be stricken with the disease, while the rest of the
children, as well as the parents and other ascendants, are healthy.
For instance, while writing this article I had under observation a
little boy six years old whose parents are living and healthy, with no
pulmonary disease in the family of either. The only other child, an
older brother, is healthy. While apparently in perfect health the
child was attacked with tubercular meningitis, and died in seventeen
days with all the characteristic symptoms of the disease. At the
autopsy there was found much injection of the cerebral pia everywhere,
a large effusion of lymph at the base of the brain and extending down
the medulla, abundance of miliary tubercles in the pia and
accompanying the vessels in the lateral regions of the hemispheres,
lateral ventricles distended with nearly clear fluid, ependyma smooth,
choroid plexuses covered with granulations, convolutions of brain much
flattened. Careful investigation, however, will usually {725} enable
us to detect some lurking primary cause, either in the family
predisposition or in the history of the patient himself.

[Footnote 3: _Die Meningitis Tuberculosa der Erwachsenen_, von Dr.
Johannes Seitz, Berlin, 1874, p. 317.]

Season appears to have but little influence on the production of the
disease. The largest number of cases is observed during winter and
spring, owing doubtless to the influence of the temperature and
weather, and to the exclusion from fresh air, in favoring the
development of tubercle and the scrofulous diathesis. Males, both
children and adults, are somewhat more frequently attacked than
females.

In regard to the exciting causes it may be said that where a
disposition to the deposit of tubercle exists, anything which tends to
lower the vitality of the individual is likely to hasten the event. In
infants with hereditary tendency to tubercle, an improper diet is
especially liable to develop meningeal tubercle. In older children,
besides unwholesome or insufficient food and unfavorable hygienic
surroundings, the acute diseases common to that period of life, such
as the eruptive fevers, intestinal disorders, whooping cough, etc.,
often act as immediate causes. Sometimes the development of the
disease may be traced to over-stimulation of the nervous system by
excessive study, often aided by imperfect ventilation or overheating
of the school-room. Caries of the temporal bone from disease of the
middle ear may act as an immediate cause of tubercular meningitis,
although simple meningitis is of course a more frequent result of that
condition. The disease has been known to follow injuries of the head
from blows or falls. In a larger number of cases the exciting cause is
not discoverable, especially when the meningeal affection is simply an
extension of the disease from some other part of the body, as the
lungs, the bronchial or mesenteric glands, etc. This is often the
case, both in adults and in children, when tubercular meningitis
complicates pulmonary consumption.

SYMPTOMS.—The disease is most frequently observed in children between
the ages of two and seven years. It is much less common in adults, who
are generally attacked between the ages of twenty and thirty years. In
the majority of cases the invasion of the malady is preceded by a
prodromic stage, usually occupying from a few days to several weeks,
though sometimes extending over a considerably longer period. This
stage probably represents the process of deposit of miliary tubercles
in the pia mater before their presence has given rise to much
structural change in the tissue. The characteristic symptoms of the
prodromic stage consist chiefly in an alteration of the character and
disposition of the patient, varying in extent in different cases. In
general, it may be said that he becomes sad, taciturn, apathetic,
irritable, indisposed to play, often sitting apart from his
companions, gazing in a strange way into vacancy. There is diminution
or loss of appetite and some emaciation. He is restless at night, is
disturbed by nightmare, or grinds his teeth. The digestion is
deranged. Usually there is constipation, but occasionally diarrhœa, or
these conditions may alternate with each other. Squinting and
twitching of the facial muscles are sometimes noticed. Headache may
occur early in this stage, but it is usually observed later, and it
then forms a prominent symptom. Vomiting is also frequent, usually not
preceded by nausea, sometimes provoked by sudden movement, as in
sitting up in bed, and is apt to occur when the stomach contains
little or no food. These symptoms vary much in degree, and they are
often so slight {726} that they pass unnoticed by the parents or
friends. Occasionally the patient, if a child, will manifest a strange
perversity or an unusual disobedience, for which he is perhaps
punished under the belief that his misconduct is intentional. In older
children and in adults delirium, especially at night, sometimes
followed by delusions which may be more or less permanent, is frequent
at this stage. The above symptoms often remit from time to time, and
during the interval the patient may seem to have recovered his health.
The prodromic symptoms are rarely altogether wanting in children,
although they may have escaped notice from lack of opportunity of
observation on the part of the physician. On the other hand, as
Steffen[4] justly observes, the most characteristic symptoms may be
present, and lead even an experienced observer to a confident
diagnosis of tubercular meningitis during the early stage of a case of
typhoid fever or of cerebral congestion without tuberculosis.

[Footnote 4: “Meningitis Tuberculosa,” by A. Steffen, in _Gerhardt's
Handb. der Kinderkrankheiten_, 5 B., 1ste Abth., 2te Hälfte, p. 465.]

For convenience of description it is customary to divide the disease
proper, after the prodromal period, into three stages—viz. of
irritation, compression, and collapse. In some cases it is not
difficult to observe these divisions, but it must be borne in mind
that in others the symptoms do not follow any regular sequence, so
that no division is possible. In infants profound slumber may be the
only morbid manifestation throughout the entire disease. Steffen
records such a case, and I have seen two similar ones.

First Stage: The interval between the prodromic period and the first
stage is usually so gradual that no distinction between the two can be
detected. In other cases the disease is ushered in suddenly by some
striking symptom, such as an attack of general convulsions, with
dilated pupils and loss of consciousness. This is not often repeated,
though partial twitchings of the limbs or of the muscles of the face
may follow at intervals. In young children a comatose condition, with
unequal pupils, is apt to take the place of these symptoms. The
principal phenomena of the first stage are headache, sensitiveness to
light and sound, vomiting, and fever. The latter varies much in
intensity from time to time, but is not usually high, the temperature
seldom rising above 103° F., and usually, but not always, higher at
night than in the morning; but there is no characteristic curve. The
pulse varies in rate, but is usually slow and irregular or
intermittent. The respiration is irregular, with frequent sighing. The
tongue is dryish and covered with a thin white coat. The bowels are
costive. Delirium is frequent at night, and the sleep is disturbed,
the patient tossing about and muttering or crying out. The eyes are
half open during sleep. These symptoms become more marked from day to
day. The pain in the head is more frequent and severe; the patient
presses the hands to the forehead or rests the head against some
support if sitting up. During sleep he occasionally utters a loud,
sharp cry, without waking. There is increasing apathy, and some
intolerance of light, shown by an inclination to turn toward the wall
of the room or to lie with the face buried in the pillow. The appetite
is lost, the constipation becomes more obstinate, the slowness and
irregularity of the pulse persist. With the rapid emaciation the belly
sinks in, so that the spinal column can be easily felt. Soon the child
falls into a state of almost {727} continual somnolence, from which,
however, he can be awakened in full consciousness, and will answer
correctly, generally relapsing again immediately into slumber. His
restlessness diminishes or ceases altogether, and he lies continuously
on the back with the head boring into the pillow. He becomes more
passive under the physician's examination, in strong contrast to his
previous irritability. At the end of a week or more from the beginning
of this stage symptoms of irritation of some of the cerebral nerves
begin to show themselves, in consequence of pressure from the
increasing exudation at the base of the brain and into the ventricles.
Strabismus (usually convergent), twitching of the facial muscles and
grimaces, grinding of the teeth, or chewing movements of the mouth are
noticed. The somnolence deepens into sopor, from which it becomes more
and more difficult to arouse the patient, who gradually becomes
completely insensible.

Notwithstanding the alarming and often hopeless condition which this
assemblage of symptoms indicates, intervals of temporary amendment not
unfrequently take place. The child may awake from his lethargy,
recognize those about him, converse rationally, take his food with
relish, and exhibit such symptoms of general improvement that the
parents and friends are led to indulge in fallacious hopes, and
sometimes the physician himself ventures to doubt the accuracy of his
diagnosis. Such hopes are of short duration; the unfavorable symptoms
always return after a brief interval. The duration of the first stage
may be reckoned at about one week.

Second Stage: This period is not separated from the preceding one by
any distinct change in symptoms. The patient lies in a state of
complete insensibility, from which he can no longer be aroused by any
appeal. The face is pale or of an earthen tint, the eyes are half
closed. If the anterior fontanel be still open, the integument
covering it is distended by the pressure beneath. Often one knee is
flexed, the opposite leg extended; one hand applied to the genitals,
the other to the head. Sometimes one leg or arm is alternately flexed
and extended. The head is apt to be retracted and bores into the
pillow. The pupils are dilated, though often unequal and insensible to
light: the sclerotica are injected; a gummy exudation from the
Meibomian glands forms on the edges of the lids. The patient sighs
deeply from time to time, and occasionally utters a loud, piercing
cry. Paralysis, and sometimes rigidity of one or more of the
extremities, are often observed, and occasionally there is an attack
of general convulsions. The pulse continues to be slow and irregular,
the emaciation progresses rapidly, and the abdomen is deeply
excavated. The discharges from the bladder and rectum are involuntary.
The average duration of the second stage is one week.

Third Stage: No special symptoms mark the passage of the second stage
into the third, which is characterized by coma, with complete
resolution of the limbs. The constipation frequently gives place to
moderate diarrhœa. The distended fontanel subsides, and often sinks
below the margin of the cranial bones. A striking feature of this
stage is a great increase in the rate of the pulse, the heart being
released from the inhibitory influence of the par vagum in consequence
of the complete paralysis of the latter from pressure. The pulse
varies in rapidity from 120 to 160 or more in the minute. For the same
reason the respiration also {728} increases in frequency, though not
to the same degree. The eyelids are widely open; the pupils are
dilated and generally motionless, even when exposed to a bright light.
The eyes are rolled upward, so that only the lower half of the iris is
visible; the sclerotica is injected from exposure to the air and dust.
Convulsions may occur from time to time. Death terminates the painful
scene, usually in from twenty-four to forty-eight hours, but sometimes
the child lives on for days, unconscious, of course, of suffering,
though the afflicted parents and friends can with difficulty be
brought to believe it.

Certain points in the symptomatology of tubercular meningitis demand
especial consideration.

I have already observed that the division of the disease into definite
stages is purely arbitrary, and is employed here merely for
convenience of description; in fact, few cases pursue the typical
course. A period of active symptoms and another of depression can
often be observed, but these frequently alternate. Stupor and
paralysis may characterize the early stage, and symptoms of
irritation, with restlessness, screaming, and convulsions, predominate
toward the end. Certain characteristic symptoms may be wholly or in
part wanting, such as vomiting, constipation, or stupor.

The temperature shows no changes which are characteristic of the
disease. Throughout its whole course it varies from time to time,
without uniformity, except that it usually rises somewhat toward
night. It seldom exceeds 102° or 103° F., unless shortly before death,
when it may rise to 104° F., or even higher, and may continue to rise
for a short time after death.

During the premonitory stage the pulse offers no unusual
characteristics. Its frequency is often increased, as is usual in any
indisposition during the period of childhood, but it preserves its
regularity. Toward the close of this period, and especially during the
first stage of the disease proper, a remarkable change takes place. It
becomes slow and irregular, the rate often diminishing below that in
health. The irregularity varies in character; sometimes the pulse
intermits, either at regular or irregular intervals. An inequality in
the strength of different pulsations is also observed. These
peculiarities of the circulation are due to the irritation of the
medulla and the roots of the par vagum, by which the inhibitory
function of that nerve upon the action of the heart is augmented.
During the last period, on the other hand, the increasing pressure on
the vagus paralyzes its function, and the heart, freed from its
control, takes on an increased action, the pulse rising to 120 beats,
and often many more, in the minute. Robert Whytt, in his interesting
memoir,[5] dates the beginning of the second stage from the time that
the pulse, being quick but regular, becomes slow and irregular; the
change again to the normal frequency, or beyond it, marking the
commencement of the third stage.

[Footnote 5: “An Account of the Symptoms in the Dropsy of the
Ventricles of the Brain,” in the _Works_ of Robert Whytt, M.D.,
published by his son, Edinb., 1768, p. 729.]

In the early stage the respiration presents nothing abnormal, but when
the pulse becomes slow and irregular the breathing is similarly
affected. Sighing is very common in the prodromal period and first
stage. Toward the end of the second stage the increasing paralysis
{729} of the respiratory centre gives rise to the phenomena known as
the Cheyne-Stokes respiration, consisting of a succession of
respiratory acts diminishing in force until there is a complete
suspension of the breathing, lasting from a quarter to three-quarters
of a minute, when the series begins again with a full inspiration. In
general, the variations in the rate of the respiration follow those of
the pulse, though the correspondence is not always exact.

In the early stage of the disease the pupils are usually contracted
and unequal. They are sluggish, but still respond to the stimulus of
light. At a later period they become gradually dilated, and react even
more slowly to light or not at all, the two eyes often differing in
this respect. Ophthalmoscopic examination frequently shows the
appearance of choked disc and commencing neuro-retinitis. In rare
cases tubercles are seen scattered over the fundus of the eye. They
are about the size of a small pin's head, of a yellowish color, and of
sharply-defined contour. Neuro-retinitis and choked disc are not, of
course, pathognomonic of tubercular meningitis, and choroidal
tubercles are so rarely seen as to be of little avail in diagnosis. In
fact, they are less frequent in this disease than in general
tuberculosis without meningitis. In twenty-six cases of tubercular
meningitis examined by Garlick at the London Hospital for Sick
Children they were found only once.[6] The effect upon the conjunctiva
of the unclosed lids has been already described.

[Footnote 6: W. R. Gowers, M.D., _Manual and Atlas of Medical
Ophthalmoscopy_, Philada., 1882, p. 148. See, also, Seitz, _op. cit._,
p. 347; Steffen, _op. cit._, pp. 452 and 472; and “Tubercle of the
Choroid,” _Med. Times and Gazette_, Oct. 21, 1882, p. 498.]

The tongue is somewhat coated soon after the beginning of the disease,
and the breath is offensive. The appetite is lost, and there is
decided emaciation in many cases during the prodromic period. The
thirst is usually moderate. Vomiting is one of the most constant
symptoms during the first period, and its occurrence on an empty
stomach is characteristic of tubercular meningitis. It is not usually
preceded by nausea, and often takes place without effort, by mere
regurgitation, the rejected fluid consisting chiefly of bile mixed
with mucus. Although constipation is the most common condition in the
early stage, and is often rebellious to treatment, yet in some cases
diarrhœa is observed, which may mislead the physician in respect to
the diagnosis. From the beginning of the second stage, and sometimes
earlier, the discharges from the bowels and the bladder are
involuntary.

DURATION.—The duration of tubercular meningitis, apart from the
prodromic period, which often can hardly be determined, averages from
two weeks to two weeks and a half. In exceptional cases death may take
place in a few days or a week, and occasionally a patient may linger
for several weeks,[7] the difference being apparently due to the
rapidity of the tubercular deposit and of the resulting inflammation
and exudation. The patient usually takes to his bed at the beginning
of the first stage, but he may be up during a part of the day until
the beginning of the second. In rare instances the child will be
about, and even out of doors, until a few days before death.

[Footnote 7: Such a case is reported by Michael Collins in the London
_Lancet_, March 8, 1884.]

PATHOLOGICAL ANATOMY.—The essential lesion of tubercular {730}
meningitis consists in a deposit of miliary tubercles in the pia mater
of the brain, giving rise to inflammation of that membrane and
exudation of serum and pus. In the early stage both surfaces of the
pia are reddened and more or less thickened, and present an opaline
appearance, while between them—that is, in the meshes of the pia—we
find a colorless and transparent fluid which is effused in greater or
smaller amount, resembling jelly when viewed through the arachnoid.
These conditions are sometimes observable on the convexity of the
hemispheres, but are much more abundant on the lateral surfaces, and
especially at the base. More distinct evidence of inflammation is
shown by the presence of a yellowish or greenish-yellow creamy deposit
on the surface of the pia, consisting chiefly of pus, which is also
much more abundant at the base than elsewhere, especially about the
optic commissure, infundibulum, pons Varolii, and the anterior surface
of the medulla. The cranial nerves may be deeply imbedded in the
deposit, which often extends into the fissure of Sylvius, gluing
together the adjacent surfaces of the lobes, and accompanies the
vessels, forming narrow streaks along the sides of the brain up to the
convexity.

The miliary tubercles or granulations consist of semi-transparent
bodies, grayish or whitish in color, varying in size from that of the
head of the smallest pin, indeed almost invisible to the naked eye, to
that of a millet-seed (whence their name). Larger masses are
frequently seen, formed by the aggregation of smaller granulations.
The tubercles are usually found on the inner surface of the pia,
always in the immediate neighborhood of the blood-vessels, which they
accompany in their ramifications, and are also scattered, in greater
or less numbers, throughout the purulent exudation from the surface of
the pia. They are most abundant at the base of the brain, ascending
the sides along the course of the vessels. Sometimes, though rarely,
they are more abundant on the convexity. The total number varies; it
is usually very large, but sometimes only a limited number exists,
even in well-marked cases, and along with intense inflammation of the
pia. The granulations are found in different degrees of
development—sometimes all of them similar in color, size, and
consistency, at others in various stages of fatty degeneration. The
distribution may be symmetrical in the two hemispheres or irregular.
Under the microscope (after suitable preparation of the part) the
bacillus tuberculosus in considerable numbers may be found in the pia,
in places adjacent to the arterioles.[8]

[Footnote 8: See a case reported by Y. Dawson in the London _Lancet_,
April 12, 1884, in which tubercles were visible only by the microscope
with numerous bacilli.]

The ventricles of the brain are usually distended with a clear or
opalescent, rarely bloody, fluid, the amount of which generally
corresponds to the intensity and extent of the meningeal inflammation,
although sometimes it is not above the normal quantity. The two
lateral ventricles are affected in an equal degree; the third and
fourth ventricles are more rarely implicated. According to
Huguenin,[9] it is doubtful whether acute inflammation of the ependyma
takes place in tubercular meningitis. Steffen also[10] says that the
ependyma is not inflamed, and that it is not the seat of the deposit
of tubercles. This latter statement is denied by other authorities,
and Huguenin is inclined to believe that they may exist {731} in that
membrane. In the following case, under my care, abundant granulations
were found on the surface of the ependyma:

[Footnote 9: G. Huguenin, _op. cit._, p. 499.]

[Footnote 10: _Op. cit._, p. 449.]

Olaf M—— (male), æt. 8 years, born in Denmark, entered Massachusetts
General Hospital Sept. 13, 1881. Maternal grandmother died of
consumption; paternal grandfather lived to the age of ninety-five
years. One brother had some disease of hip. Patient was the child of
poor parents and lived in an unhealthy suburb of Boston. During the
two preceding winters he had a bad cough. He was apparently well till
four weeks before his entrance, when he complained of bellyache, and
became listless, but he was out of doors ten days before he came to
the hospital. It was noticed that he was sensitive to sound. No
vomiting, no diarrhœa, no epistaxis, no cry; some cough. He had been
somnolent, and was observed to swing his arm over his head while
asleep. June 14, when first seen by me, he was lying on his back,
unconscious, eyes half closed, pupils dilated, jaw firmly closed, much
emaciated, belly retracted, left leg occasionally flexed and extended.
No priapism. The optic discs were reddened. June 15, there is some
intelligence, he answers questions; keeps one hand on the genitals.
June 16, pupils contracted, does not swallow. June 18, left eye
divergent, conjunctiva injected, whole surface livid, cries out
occasionally. Died at midnight.

[Illustration: FIG. 30. Temperature chart of a case of tubercular
meningitis in a boy eight years old.]

Autopsy.—General lividity of surface, much emaciation. Much fine
arborescent injection on outer surface of dura mater. Numerous
Pacchionian bodies. Yellow matter beneath arachnoid along course of
vessels on each side of anterior lobes. Abundant fine granulations
along course of vessels on each anterior lobe, on upper margins of
median fissure, along fissure of Sylvius, and on choroid plexuses.
Very little lymph at base of brain. Six or eight ounces of serum from
lateral ventricles, and abundant fine transparent granules over
ependyma of both. Numerous opaque granulations in pia mater of medulla
oblongata. Surface of right pleura universally adherent. Mucous
membrane of bronchia much injected; a considerable amount of pus
flowed from each primary bronchus. No tubercles in lungs nor in
peritoneum. No ulcerations in intestines. No other lesions.

The choroid plexuses are generally involved in the inflammatory
process, and are sometimes covered with yellow purulent exudations. As
in the above case, large numbers of tubercles may be found in them,
notwithstanding the opinion of Huguenin that their number is always
small.

The substance of the brain in the vicinity of the tubercular deposit
is generally found in a more or less œdematous condition, owing to the
obstruction of the circulation resulting from compression of the
vessels {732} by the tubercles and effused lymph. Softening, sometimes
even to diffluence, not unfrequently occurs in the neighborhood of the
deposit, probably from ischæmia (necrobiosis). If there be any
considerable amount of exudation in the ventricles, the convolutions
are flattened by compression against the cranial bones.

The above-described lesions are not confined to the brain, but may
extend to the cerebellum, the pons, the medulla, and the spinal cord.
If examinations of the latter were more frequent in autopsies of this
disease, we should doubtless find, as has been done in some instances,
that the membranes often show the characteristic alterations of
tubercular meningitis, and even the presence of granulations in the
cord itself. The lesions may extend throughout the cord, and are
especially noticed in the dorsal region and in the vicinity of the
cauda equina. Their presence explains some of the symptoms evidently
due to spinal origin, such as retraction of the head with rigidity of
the neck and of the trunk, contractions of the limbs, tetanic spasms,
priapism, paralysis of the bladder and rectum, etc., which are common
in simple spinal meningitis.

The deposit of miliary tubercles in the pia mater, with little or no
accompanying meningitis, is met with in rare instances. The tubercles
are few in number, but vary in dimensions, being sometimes united
together in masses of considerable size, which are frequently
encysted. Beyond thickening and opacity of the membrane, their
presence seems to excite but little inflammatory reaction, but they
are generally accompanied by ventricular effusion which by its
pressure gives rise to characteristic symptoms.

The principal lesions found in other organs of the body consist of
tubercle in various stages of development, caseous matter, diseases of
the bones, etc. Miliary granulations are chiefly seen in the lungs,
peritoneum, intestinal mucous membrane, pleura, spleen, liver, and
kidneys. The bronchial and mesenteric glands often contain caseous
masses, some of which are broken down and suppurating. The testicles
sometimes present the same appearances. In adults, the most frequent
lesion which is found external to the brain is pulmonary tuberculosis
in a more or less advanced stage. Tubercles are also sometimes present
in the eye. Angel Money[11] states that out of 44 examinations made at
the Hospital for Sick Children, London, the meninges were the seat of
gray granulations in 42. The choroid (one or both) showed tubercles 14
times (right 3, left 5, both 6), and 11 times there were undoubted
evidences of optic neuritis. Twice the choroid was affected with
tubercle when the meninges were free; in one of these instances there
was a mass of crude tubercle in the cerebellum; in the other, although
there were tubercles in the belly and chest, there were none in the
head. So that 12 times in 42 cases of tubercles in the meninges there
were tubercles in the choroid—_i.e._ about 31 per cent.

[Footnote 11: “On the Frequent Association of Choroidal and Meningeal
Tubercle,” _Lancet_, Nov. 10, 1883.]

DIAGNOSIS.—In many cases tubercular meningitis offers but little
difficulty in the diagnosis. Although the symptoms, taken singly, are
not pathognomonic, yet their combination and succession, together with
their relation to the age, previous health, and antecedents of the
patient, are usually sufficient to lead us to a correct opinion. The
prodromic period {733} of altered disposition (irritability of temper
or apathetic indifference), headache, constipation, vomiting, and
emaciation, followed by irregularity and slowness of the pulse,
sighing respiration, sluggishness and irregularity of the pupils; the
progress from somnolence to unconsciousness and coma; the sudden
lamentable cry; the convulsions and paralysis; the return of rapid
pulse and respiration in the last stage,—are characteristic of no
other disease. Our chief embarrassment arises during the insidious
approach of the malady, before its distinctive features are visible or
when some important symptom is absent. Its real nature is then apt to
be overlooked, and, in fact, in some cases it is impossible to decide
whether the symptoms are indicative of commencing cerebral disease,
or, on the other hand, are owing to typhoid fever, to a simple
gastro-intestinal irritation from error in diet, to worms in the
alimentary canal, to overwork in school, or to some other cause. Under
these circumstances the physician should decline giving a positive
opinion until more definite signs make their appearance. It must be
remembered that very important symptoms may be absent in cases which
are otherwise well marked. In all doubtful cases the family history
should, if possible, be obtained, especially whether one or both
parents or other near relatives have been consumptive or have shown
symptoms of scrofula or tuberculosis in any form, and whether the
patient himself has signs of pulmonary tuberculosis, of enlarged or
suppurating glands, or obstinate skin eruptions. The presence or
history of those conditions would add greatly to the probability of
tubercular meningitis.

The diseases for which tubercular meningitis is most liable to be
mistaken are acute simple meningitis, typhoid fever, acute
gastro-intestinal affections, eclampsia of infants and children, worms
in the intestines or stomach, the hydrencephaloid disease of Marshall
Hall, and cerebro-spinal meningitis.

Acute meningitis is distinguished from the tubercular disease by its
sudden invasion without prodromatous stage, by the acuteness and
intensity of the symptoms, the severity of the headache, the activity
of the delirium, the greater elevation of the temperature, and by its
brief duration, which rarely exceeds one week. In those exceptional
cases of tubercular meningitis in which the prodromal period is absent
or not observed and the course is unusually rapid, it would be perhaps
impossible to distinguish between the two diseases. A family history
of tubercle, or the discovery of the granulations in the choroid by
ophthalmoscopic examination, might save us from error under such
circumstances. The great rarity of idiopathic simple meningitis should
be remembered. Meningitis from disease of the ear sometimes resembles
the tubercular affection, but the history of the attack, usually
beginning with local pain and otorrhœa, will in most cases prevent any
confusion between the two forms of disease.

The early period of typhoid often bears considerable resemblance to
that of tubercular meningitis. Headache, languor, restlessness, and
mild delirium are common to both. Typhoid can be distinguished by the
coated tongue, the diarrhœa, the enlargement of the spleen, the
tympanites, abdominal tenderness and gurgling, the eruption, and,
above all, by the characteristic temperature-curve, which, if
accurately observed, is conclusive. The course of typhoid fever is
comparatively {734} uniform, while that of tubercular meningitis is
often extremely irregular. It should not be forgotten that the two
diseases may coexist.

The presence of worms in the alimentary canal may cause symptoms
somewhat like those of tubercular meningitis, and the symptoms of the
latter disease are occasionally erroneously attributed to those
parasites. The administration of an anthelmintic, which should never
be omitted in doubtful cases, will clear up all uncertainty.

Cerebro-spinal meningitis is usually an epidemic, and therefore not
likely to be confounded with the tubercular disease. In sporadic cases
it can be recognized by its sudden onset and acute character, by the
eruption, and by the prominence of the spinal symptoms.

The so-called hydrencephaloid disease of Marshall Hall is a condition
of exhaustion and marasmus belonging to infancy, caused by
insufficient or unsuitable nourishment, by diarrhœa, and by the
injudicious depletive treatment so much in vogue in former times, when
the affection was much more common than at present. Some of its
symptoms, such as sighing respiration, stupor, pallor, and dilated
pupils, bear a certain resemblance to those of tubercular meningitis,
though it would be more easily confounded with chronic hydrocephalus.
The absence of constipation, headache, convulsions, and vomiting, and
the favorable results of suitable nourishment and stimulants, serve to
distinguish it from cerebral disease.

Eclampsia, or sudden convulsion, is common in infants and young
children, and, since the occurrence of a fit may be the first or the
most striking symptom in tubercular meningitis, it is important to
ascertain its origin. In the majority of cases convulsions in children
arise from some peripheral irritation, such as difficult dentition,
worms in the alimentary canal, constipation, fright, etc., acting
through the reflex function of the spinal cord, which is unusually
sensitive in the early period of life. The absence of previous
symptoms, and the discovery of the source of the irritation, with the
favorable effect of its removal by appropriate treatment, will in most
cases suffice to eliminate structural disease of the brain. In others
we must withhold a positive opinion for a reasonable time in order to
ascertain whether more definite symptoms follow. Convulsions also
occasionally form the initial symptom of the eruptive fevers,
especially scarlatina. Here the absence of prodromal symptoms, and the
speedy appearance of those belonging to the exanthematous affection,
will remove all sources of doubt. Convulsions, with or without coma,
occurring in the early stage of acute renal inflammations, may
simulate the symptoms of tubercular meningitis. An examination of the
urine will show the true nature of the disease.

In addition to the above diseases there are some cerebral affections
of uncertain pathology which resemble tubercular meningitis, but which
are not generally fatal. As Gee justly remarks,[12] “Every
practitioner from time to time will come across an acute febrile
disease accompanied by symptoms which seem to point unmistakably to
some affection of the brain, there being every reason to exclude the
notion of suppressed exanthemata or analogous disorders. After one or
several weeks of coma, delirium, severe headache, or whatever may have
been the prominent symptom, the patient recovers, and we are left
quite unable to say what has been the {735} matter with him. To go
more into detail, I could not do otherwise than narrate a series of
cases which would differ from each other in most important points, and
have nothing in common excepting pyrexia and brain symptoms. There is,
generally, something wanting which makes us suspect that we have not
to do with tubercular meningitis. Brain fever is as good a name as any
whereby to designate these different anomalies; cerebral congestion,
which is more commonly used, involves an explanation which is probably
often wrong, and certainly never proved to be right.” No doubt such
cases are occasionally cited as examples of recovery from tubercular
meningitis.

[Footnote 12: “Tubercular Meningitis,” by Samuel Jones Gee, M.D., in
_Reynolds's System of Medicine_, Philada., 1879, vol. i. p. 832.]

PROGNOSIS.—Although there are on record undoubted instances of
recovery from tubercular meningitis, yet their number is so small that
practically the prognosis is fatal. It is safe to say that in almost
all the reported cases of recovery the diagnosis was erroneous.[13]
Even should the patient survive the attack, he is usually left with
paralyzed limbs and impaired mental faculties, and dies not long
afterward from a recurrence of the disease or from tuberculosis of the
lungs or other organs.

[Footnote 13: Hahn, “Recherches sur la Méningite tuberculeuse et sur
le Traitement de cette Maladie” (_Arch. gén. de méd._, 4^e Série,
vols. xx. and xxi.), claims to have cured 7 cases, but of 5 of them
there is no evidence that they were examples of tubercular meningitis
at all. The subject of the curability of tubercular meningitis is ably
treated by Cadet de Gassicourt (_Traité clinique des Maladies de
l'Enfance_, vol. iii., Paris, 1884, p. 553 _et seq._). His conclusion
is that most of the alleged cures are cases of meningitis of limited
extent, arising from the presence of tubercular tumors, syphilitic
gummata, cerebral scleroses, and neoplasms of various kinds.]

TREATMENT.—In view of the fatality of the disease, and of its frequent
occurrence in childhood, the prophylactic treatment is of great
importance. Every effort should be made to protect children whose
parents or other near relatives are tuberculous or scrofulous, and who
are themselves delicate, puny, or affected with any constitutional
disorder, from tubercular meningitis, by placing them in the best
possible hygienic conditions. Pure air, suitable clothing, wholesome
and sufficient food, and plenty of out-of-door exercise are
indispensable. Sedentary amusements and occupations should be
sparingly allowed. Especial pains should be taken to prevent fatigue
by much study, and school-hours should be of short duration. The
hygiene of the school-room is of paramount importance, and if its
ventilation, temperature, and light are not satisfactory, the child
should not be permitted to enter it. The bed-chamber should be well
ventilated night and day. A sponge-bath, cold or tepid according to
the season or to the effect on the patient, should be given daily,
followed by friction with a towel. The bowels must be kept regular by
appropriate diet if possible, or by simple laxatives, such as magnesia
or rhubarb. For delicate, pale children some preparation of iron will
be useful. The choice must be left to the practitioner, but one of the
best in such cases is the tartrate of iron and potassium, of which
from two to six grains, according to the age, may be given three times
daily after meals. Cod-liver oil is invaluable for scrofulous patients
or where there is a lack of nutrition. A teaspoonful, given after
meals, is a sufficient dose, and it is usually taken without
difficulty by children, or if there be much repugnance to it some one
of the various emulsions may be tried in proportionate dose. Along
with this, iodide of iron will in many cases be found useful or as a
substitute for the oil when the latter cannot {736} be borne. It is
best given in the form of the officinal syrup, in the dose of from
five to twenty drops. Change of air is useful in stimulating the
nutritive functions, and a visit to the seashore or mountains during
warm weather will often be followed by general improvement.

Since it is not possible to arrest the disease when once begun, the
efforts of the physician must be directed toward relieving the
sufferings of the patient as far as possible. In the early period the
restlessness at night and inability to sleep will call for sedatives,
such as the bromide of sodium or of potassium, in the dose of ten or
fifteen grains at bedtime or oftener. This should be well diluted with
water, sweetened if necessary. The addition of five to twenty drops of
the tincture of hyoscyamus increases the effect. Sometimes chloral
hydrate, either alone or combined with the bromide when the latter
fails, will procure quiet sleep. From five to ten grains may be given
at a dose, according to the age. Compresses wet with spirit and water
or an ice-cap may be applied to the head if there be much pain in that
region, or it may be necessary to give opium in some of its forms by
the mouth, such as the tincture or fluid extract, in doses of from one
to five drops. Constipation is best overcome by means of calomel in
three- to five-grain doses, to which may be added, when necessary, an
equal amount of jalap powder, or an enema of soapsuds may be
administered. Active purging should be avoided. Liquid nourishment,
such as milk, gruel of oatmeal, farina, or barley, beef-tea, broths,
etc., must be given in moderate quantities at intervals of a few hours
so long as the patient is able to swallow. Occasional sponging of the
whole surface with warm or cool water, and scrupulous attention to
cleanliness after defecation, especially when control of the
sphincters is lost, will add to his comfort. He should occupy a large
and well-ventilated chamber, from which all persons whose presence is
not necessary for his care and comfort should be excluded. He should
be protected from noise and from bright light, and should lie on a bed
of moderate width for convenience of tending.

There is no specific treatment at present known which is likely to be
of any benefit in this disease, any more than in tuberculosis of other
organs than the brain. Common experience has shown that mercury, which
formerly had so high a reputation in the treatment of cerebral
diseases of early life, not only fails completely, but adds to the
sufferings of the patient when pushed to salivation. The iodide of
potassium is recommended by almost all writers, but, so far as I know,
there is no proof that it possesses any virtue in meningeal
tuberculosis. It has the high authority of Charles West,[14] however,
who thinks the remedy is more encouraging than any other, and who
mentions one instance in which recovery took place under its
employment. He recommends that two grains be given every four hours to
a child three years old, the bowels being kept free. Most authorities
recommend much higher doses, such as ten or fifteen grains, three or
four times daily.

[Footnote 14: _Op. cit._, p. 102.]

Counter-irritation to the head or back of the neck was formerly much
employed, but is now generally abandoned, as giving rise to much
discomfort without obvious beneficial effect. In the cases reported by
Hahn, already alluded to under the head of Prognosis, recovery is
attributed to the energetic application of tartar-emetic ointment to
the scalp, {737} producing extensive ulceration, which in one of them
lasted more than ten months before cicatrization took place. A careful
examination of the reports of these cases satisfies me that but two
out of the seven were really examples of tubercular meningitis. How
far the recovery in the successful cases is to be attributed to the
treatment is very doubtful. Small blisters applied to the vertex or
back of the neck are alluded to favorably by West, but he quotes no
observations in which they were followed by benefit.


Tubercular Meningitis in the Adult.

Tubercular meningitis may occur at any age, but after the period of
childhood it is most frequent between the ages of sixteen and thirty
years. About 75 per cent. of the patients are males, and 25 per cent.
females.[15] The disease does not differ essentially in its course and
symptoms from that in children. A family history of tuberculosis is
common, or the patient may be already suffering from phthisis,
scrofulous glands, cheesy deposits in various organs, caries of the
bone, syphilis, or other constitutional affections. According to
Seitz, in 93.5 per cent. out of 130 cases with autopsies chronic
inflammatory conditions or caseous deposits were found in various
organs of the body. Many cases are examples of acute tuberculosis in
which the brunt of the disease has fallen upon the brain rather than
the other organs.

[Footnote 15: Seitz, _op. cit._, p. 9.]

When cerebral symptoms supervene upon acute disease, such as typhoid
fever, pericarditis, acute rheumatism, pneumonia, the exanthemata,
etc., the diagnosis between tubercular and simple meningitis is
important, because the latter is not necessarily fatal, while the
former is almost never recovered from. If the patient were previously
healthy and presumably free from tubercular disease, the chances would
be in favor of the simple form. A rapid course of the disease would
also speak for acute meningitis, and recovery would almost certainly
preclude tubercular meningitis. In some cases the diagnosis is
difficult or impossible in the beginning.

In cases beginning without acute antecedents—in adults as in
children—there is no pathognomonic symptom, but the combination and
succession of the phenomena are usually sufficient for the diagnosis.
Headache, depression or irritability of temper, delirium, half-closed
eyes, ptosis of one lid, squinting, inequality and sluggishness of the
pupils, moderate fever, sunken belly, vomiting, constipation, slow and
irregular pulse, sopor gradually deepening to coma, with occasional
convulsions or paralysis of the limbs, followed in the course of two
or three weeks by death, especially if occurring in a patient who has
already presented signs of tuberculosis in other organs, point almost
unmistakably to tubercular meningitis. Some of the symptoms may not be
strongly pronounced, one or two may be absent, but the general picture
will suggest no other disease. According to Seitz, tubercle of the
choroid is rare in tubercular meningitis of the adult. It is usually
associated with tuberculosis of other organs, the pia being free. The
subjoined cases are illustrations of the disease in adolescence and
adult life:

Case I.—A lad sixteen years old, always somewhat delicate, with a
{738} cough and morning expectoration of some months' standing,
exerted himself immoderately in gymnastic exercise on the afternoon of
Sept. 24, 1875. That night he was awakened by cough and hæmoptysis.
Signs of consolidation were found at the apices of both lungs. In
three months there were swelling, induration, and suppuration of one
testicle. Some months later, pain in the right arm, stiffness of the
shoulder-joint, and an abscess communicating with the joint, from
which small spicula of bone were discharged. He was about, and even
attended school, for more than a year from the time of the attack of
hæmoptysis. About Jan. 1, 1877, he began to complain of severe pain in
the forehead, with nausea (but no vomiting) and constipation. Jan.
27th he took to his bed, complaining chiefly of pain in the forehead
and eyes. Feb. 1st he was drowsy, irritable, and delirious. Feb. 3d
incontinence of urine and constant delirium. Up to this time the pulse
had not been above 76 in the minute, and on this day it was 64. The
next day, Feb. 4th, he was wholly unconscious; pulse 96, pupils
dilated. Feb. 5th, left hand in constant motion; pulse 112. From this
time the pulse steadily increased in frequency. Feb. 6th he swallowed
food, notwithstanding his stupor. Feb. 7th he answered questions;
there was oscillation of the eyeballs, and epistaxis from constant
picking of the nose. He died Feb. 9th, the pulse being 144 and the
respirations 60 in the minute for several hours previous. The
temperature never rose above 101.7° F. There was never any vomiting.
The duration of the case was thirteen days, in addition to the
prodromic period of twenty-seven days.—Autopsy by R. H. Fitz: The pia
of the base of the brain from the medulla to the optic thalamus
contained a large number of gray miliary tubercles, old and recent,
and the same condition was found in the surfaces of the fissure of
Sylvius. Ventricles distended with fluid, ependyma thick and
translucent. A moderate-sized cavity in the apex of the left lung,
with cheesy contents. Both lungs contained an abundance of hard, gray,
miliary tubercles. Left kidney contained a wedge-shaped, cheesy mass
of the size of a walnut, with numerous tubercles. Left testicle
contained a cheesy mass of the size of a walnut; both epididymes were
cheesy. The mucous membrane of the bladder contained tubercles near
the neck. The vesiculæ seminales contained softened cheesy masses with
openings into the urethra. There was a fistulous opening into the
right shoulder-joint.

Case II.—Emeline K. L——, 32 years old, single, nurse, had become much
exhausted by taking care of a difficult case, and entered
Massachusetts General Hospital March 6, 1883, complaining since four
days of a little cough, slight expectoration, and chilliness, but no
rigor. She seemed hysterical. There was complaint of severe pain in
the head, chest, and abdomen. A slight systolic murmur was found at
the apex of the heart, and a few moist râles at the base of the chest
on both sides behind. The urine was normal. Temperature, 103° F. Three
weeks after entrance she began to be delirious, especially at night.
April 13th, five weeks and three days after entrance, she was
semi-conscious, but would put out her tongue and open her eyes when
requested to do so; the abdomen was distended, the pupils were dilated
and unequal; there was twitching of the muscles of the right side of
the face. Careful examination only disclosed occasional fine râle at
the base of right chest. {739} She died April 16th, having been
completely unconscious for twenty-four hours. There was no vomiting
throughout the case. The temperature was very irregular, ranging
between 100° and 103° F., and once as high as 104° F.; it was usually
one or two degrees higher at night than in the morning. Pulse,
generally from 100 to 110; it rose steadily during the last few days
to 160 at the time of death.—Autopsy: Pia mater of brain œdematous,
slightly opaque; its lower surface, especially at the base of the
brain, showed numerous minute gray tubercles; enlarged cheesy glands
at the base of the neck; small, opaque, gray tubercles scattered
rather sparsely throughout both lungs. There was also miliary
tuberculosis of the liver, spleen, and kidneys.


{740}


CHRONIC HYDROCEPHALUS.

BY FRANCIS MINOT, M.D.


SYNONYMS.—Dropsy of the brain, Dropsy of the head.

DEFINITION.—A gradual accumulation of serous fluid in the brain,
occupying either the ventricles or the cavity of the arachnoid, or
both, occurring chiefly in infants or very young children.

The term hydrocephalus, which was applied by the older writers to
accumulations of serous fluid both within and also without the
cranium, termed distinctively internal and external hydrocephalus, is
now restricted to dropsical effusions either between the meninges or
within the ventricular cavities. These may be acute or chronic, and
they arise from the same conditions which are followed by the effusion
of serum in other parts of the body; that is to say, from an
alteration in the serous membrane lining a cavity, from an obstruction
in the capillary circulation with increased tension in the larger
vessels, from an altered condition of the blood, etc.

Chronic hydrocephalus is almost entirely confined to young children,
and is probably due to an arrested development of the brain, as shown
by its being usually congenital, by the dwarfed intellectual condition
of the patient, and by its frequent association with spina bifida. The
pathogeny of the disease is, however, still obscure. Whether the
abnormal accumulation of serous fluid is to be ascribed to a chronic
alteration of the ventricular walls or of the choroid plexuses, allied
to inflammation, such as occurs in the pleura, for example, causing an
increased secretion, or to a closure of the communication between the
ventricles and the spinal cavity, as suggested by the late John
Hilton, resulting in dropsy by retention, or to some other cause, is
not yet determined. Hilton says:[1] “In almost every case of internal
hydrocephalus which I have examined after death I found that this
cerebro-spinal opening [between the fourth ventricle and the spinal
canal] was so completely closed that no cerebro-spinal fluid could
escape from the interior of the brain; and, as the fluid was being
constantly secreted, it necessarily accumulated there, and the
occlusion formed, to my mind, the essential pathological element of
internal hydrocephalus.” Sieveking, commenting upon Hilton's theory,
says:[2] “While giving these facts due weight, it must be pointed out
that we are yet far from understanding either how the fluid is poured
into the cerebral cavities or how it is removed, and that we do not
positively know that the spinal canal has any better means of getting
rid of an excess of {741} fluid than the cerebral cavities have.” An
arrest of the growth of the brain is supposed by some pathologists to
account for ventricular as well as arachnoidal dropsy by the creation
of a vacuum in the cavity of the cranium, which is filled by exudation
of the more fluid portion of the blood from the vessels or of lymph
from the lymphatics.

[Footnote 1: John Hilton, _Lectures on Rest and Pain, etc._, 2d ed.,
New York, 1879, p. 22.]

[Footnote 2: Jones and Sieveking's _Pathological Anatomy_, 2d ed.,
London, 1875, p. 248.]

ETIOLOGY.—That chronic hydrocephalus in young children is in a large
proportion of cases an hereditary disease is shown by the fact that it
is frequently congenital, that more than one child in a family is
occasionally affected by it, and that while one child is hydrocephalic
others may be idiotic. A scrofulous taint in the family history is
noticeable in many cases, the evil effect of which is frequently
enhanced by unfavorable sanitary conditions of life, especially by
residence in dark, damp, ill-ventilated, and badly-drained apartments
and by insufficient or unwholesome food. Hence the disease is more
frequently met with among the poor than in the well-to-do classes of
society. There is a difference of opinion as to whether it ever arises
in consequence of external violence, such as a blow on the head, or of
some strong impression, like fright or grief, acting on the mother of
the child during pregnancy. The probability is that such causes would
not be efficient except in cases where a predisposition to
hydrocephalus had already existed. West[3] mentions the case of a
healthy child five months old who fell out of the arms of her nurse,
and was taken with a fit the same day. She apparently recovered, but
when a year old had frequent returns of convulsions. At the age of
fifteen months the head began to enlarge, and it continued to increase
in size until she was three years old, when she was attacked by
measles, and died in a few days with convulsions and coma. The
symptoms, both bodily and mental, were typical of hydrocephalus, and
the diagnosis was fully confirmed by the autopsy.

[Footnote 3: _Op. cit._, p. 127.]

The causes of chronic hydrocephalus in older subjects and in adults
are, in addition to the above mentioned, chiefly mechanical. Any
lesion which hinders the exit of venous blood from the cranium may be
followed by dropsy of the arachnoid cavity or ventricles. The
principal ones are tumors of the brain or its membranes, the effusion
of lymph in the neighborhood of veins, thrombosis of the cerebral
sinuses, compression of numerous small vessels by tubercular
granulations, obstructions outside the cranium, including tumors of
the neck, aneurisms, obstructive disease of the heart, emphysema and
cirrhosis of the lungs, besides diseases giving rise to general
dropsy, as the different forms of nephritis, marasmus, the various
cachexiæ, etc.

SYMPTOMS.—When the disease is already somewhat advanced before birth,
the head is often abnormally large, the cranial bones are separated,
the fontanels are distended and fluctuating, and it occasionally
happens that delivery of the distended head can only be effected after
the fluid has been evacuated by puncture. Even when there is no
abnormal increase in the size of the head, indications of cerebral
disturbance are sometimes apparent from birth, such as strabismus or
convulsions recurring with more or less frequency, along with signs of
failure of the general health. In the course of some weeks, or, it may
be, months, the attention of the parents is attracted to the
prominence of the child's forehead, strongly contrasting with the
comparatively diminutive size of {742} the face. Soon an enlargement
of the fontanels is perceived, the sutures between the cranial bones
become broader, and the head assumes a globular shape from the
pressure of the contained fluid. The separation of the bones at the
vertex of the skull causes the os frontis to protrude forward, the
parietals backward and outward, and the occipital backward and
downward. The orbital plates of the frontal bone yield to the pressure
of the fluid behind them, and from a horizontal position tend to
assume a vertical one, protruding the eyeballs, which have a peculiar
downward direction. The sclerotica is visible above the iris, and the
latter is partially covered by the lower eyelid. The enlargement of
the head is progressive, though not uniformly so, there being pauses
of weeks or months during which it is arrested. If it be considerable,
the cranial bones are usually thinned, so that the skull becomes
translucent when opposite a bright light. When there is a wide
separation of the bones there is an unusual development of ossa
triquetra in the sutures.

In cases in which the ossification of the cranium is considerably
advanced before the beginning of the disease, the enlargement of the
head is apt to be correspondingly less. If all the sutures are
consolidated, there may be no increase in size, and this is especially
true of the mechanical dropsy of adult life. The dropsical effusion,
which is then moderate in amount, finds room through compression of
the brain-substance, and part of it escapes into the spinal canal.

The size of the hydrocephalic head varies considerably. Where there
has been an early arrest of the disease it may be but slightly above
the normal. On the other hand, the dimensions are sometimes enormous.
In the Warren Museum of Harvard University is a cranium which measures
27½ inches in its greatest circumference, and 20½ inches from one
auditory foramen to the other over the top of the head. Its internal
capacity is 257 cubic inches. The patient, who died at the age of
three years, was never able to sit up and support the head, or even to
turn it from the left side, on which she continually lay; she never
spoke, and seemed to have no intelligence. The skull of the celebrated
James Cardinal measured 32¼ inches in its largest circumference.[4]
Even more remarkable instances are on record. The dimensions of the
fontanels, particularly the anterior, usually correspond with those of
the skull in general. During any strong muscular effort on the part of
the patient the membrane covering them is seen to be bulged out by
pressure from the fluid beneath. The enlargement is not always
uniform; it may be in part or wholly confined to one side, owing to
consolidation of the sutures of the opposite side, or because only one
of the lateral ventricles is affected. The scalp is traversed by
numerous distended veins. The hair is very scanty. The head has a
soft, fluctuating feel, and the walls sometimes seem to crackle
beneath the fingers, like parchment.

[Footnote 4: _Reports of Medical Cases, etc._, by Richard Bright,
M.D., London, 1831, vol. i. p. 431.]

In cases of moderate severity there may be few or no symptoms of
active cerebral disturbance, such as convulsions or paralysis, but the
child does not learn to talk, to walk, or to control the sphincters
even at the age of three or four years, and the signs of imperfect
mental development are evident. He is apt to be irritable or
mischievous, and even when not actually idiotic is very backward in
evincing signs of intelligence. There are, however, not a few
exceptions to this, and some {743} children with large hydrocephalic
heads are intelligent and amiable. The cranium of a girl who died at
the age of sixteen years is preserved in the Warren Museum. It
measures 24¼ inches in circumference and 17¼ inches from one auditory
meatus to the other over the vertex, and the bone is in no place more
than one-eighth of an inch in thickness. The child was an inmate of a
house of industry, where she was instructed in the usual branches of
knowledge taught in our common schools, until at length, such was her
capacity, she was entrusted with the teaching of the other pauper
children, and she had an excellent character for intelligence and
moral worth. She died of phthisis. On post-mortem examination “the
brain was found floating, as it were, in a large collection of water.”
As in other chronic diseases, there are often pauses, from time to
time, of variable duration, in which there is some improvement in the
condition of the patient, as well as a temporary arrest in the
enlargement of the head. The growth of the child in stature is often
retarded, and when life is prolonged the individual is more or less
dwarfed. In some cases there is a considerable increase in the amount
of adipose tissue, and the appetite is often voracious. L. Fürst
reports[5] the case of a hydrocephalic girl, sixteen years old, whose
height (or, rather, length, for she was unable to stand) was 81
centimeters (nearly 32 inches), corresponding to the stature of a
child between three and four years old. The periphery of the head
measured 51-1/5 centimeters (20¼ inches). The anterior fontanel was
still open. The age was verified by reference to the registry of birth
at the police-office.

[Footnote 5: “Exquisite Wachsthumshemmung bei Hydrocephalus
chronicus,” von Dr. Livius Fürst, _Virchow's Archiv_, June, 1884.]

The symptoms of cerebral disturbance in chronic hydrocephalus are much
less striking than one would expect, doubtless because the increase of
pressure upon the brain is so gradual. Actual paralysis, especially of
the limbs, is rare, but convulsions are not infrequent, as is the
spasmodic constriction of the glottis known as laryngismus stridulus
or spasmodic croup. A general state of uneasiness and restlessness is
common. Vision is often impaired and sometimes wholly lost. Strabismus
is frequently present, or there may be an involuntary rolling movement
of the eyeballs. The pupils are often dilated and insensible to light.
In consequence of the increased weight of the head, the child is
unable to support it, and in most cases is compelled to keep the bed.
Vomiting is common. The digestive functions are disturbed.
Constipation is an almost constant symptom, and the sphincters are
relaxed in the advanced stages of the disease. Although in some cases,
as already stated, the child may grow fat, the reverse of this is the
rule; there is usually progressive emaciation, especially of the lower
extremities.

The duration of the disease varies much in different cases. The
earlier the characteristic symptoms manifest themselves the more rapid
is its course. Most children born hydrocephalic survive but a few days
or weeks. In cases which are more slow in their development the
patient may live some years, and in rare instances attain adult life.
But his feeble vitality usually makes him an easy prey to the ordinary
complaints of childhood, and a large proportion of cases succumb to
inflammation of the lungs or of other organs, to diarrhœa, whooping
cough, or the eruptive diseases. Most of those who escape these
intercurrent maladies {744} perish from defective nutrition, the
result of malassimilation of food, or else are cut off by acute
cerebral inflammation, with convulsions, etc.

PATHOLOGICAL ANATOMY.—It is rarely that a large amount of serum is
found in the cavity of the arachnoid unless a free communication has
been established between it and the ventricles by the destruction of
cerebral tissue. In the pia the quantity may be more abundant than
normal, filling the subarachnoid spaces, separating the convolutions
from each other, and occasionally forming little sac-like elevations
on the surface of the membrane; but it should be borne in mind that a
certain amount of serous infiltration of the tissue of the pia is by
no means rare in cases of death from various diseases, owing to the
obstruction to the circulation during the last hours of life, and
should not be considered pathological unless it exceed the usual
limits. The amount of effusion into the ventricles varies between very
wide limits, from some ounces to two or three pints. It may be
transparent, or turbid from particles of cerebral tissue or epithelial
or pus-cells, and is occasionally slightly tinged with blood. Its
specific gravity is nearly identical with that of water, and it
contains a trace of albumen. The effusion usually occupies the two
lateral and the middle ventricles. Less frequently the dropsy is
unilateral, in consequence, apparently, of an obliteration of the
foramen of Monro. The tissues composing the walls of the ventricles
are compressed and hardened. The ependyma of the walls and of the
plexus is thickened and roughened by the formation of minute
elevations, which the microscope shows to be composed of proliferated
and sclerosed connective tissue. The brain in cases of large effusion
is reduced to a membranous sac, flattened, with hardly any trace of
its original structure at first sight apparent. In the case of James
Cardinal, before alluded to, Bright says, “The brain lay at its base
[of the skull] with its hemispheres opened outward like the leaves of
a book.” Closer inspection shows that all the parts are present,
although atrophied by pressure. The convolutions are flattened and the
brain-substance is pale and softened. The cranial nerves are often
softened and flattened.

In the dropsy of the head in adults which is the result of mechanical
pressure or of cachexia the appearances are widely different. The
effusion may occupy the cavity of the arachnoid, and even the space
between the dura and the skull, as well as the ventricles. The amount
of fluid is much less than in the chronic hydrocephalus of children.
The ventricular walls present no signs of inflammatory changes.

DIAGNOSIS.—Chronic hydrocephalus is usually recognized without
difficulty. The chief points of diagnostic importance are the
progressive enlargement of the head, the separation of the cranial
bones, with their peculiar change of position, as already described,
and the evident signs of arrested intellectual development. If the
head be but little enlarged, the case might be mistaken for that of
chronic hypertrophy of the brain, but this is a very rare disease, and
is not accompanied with defective mental development.

PROGNOSIS.—The elements of prognosis include the size of the head at
birth, its rate of enlargement, the general condition of the child,
both physically and intellectually, his hereditary antecedents, and
the hygienic influences to which he may be subjected. A large
proportion of children born hydrocephalic live but a short time; a few
survive one or more {745} years. The number of those who reach adult
life is extremely small. The favorable indications are a tardy
appearance of the dropsy and its slow progress, without marked
evidence of defective mental and bodily development.

TREATMENT.—The treatment of chronic hydrocephalus is general and
local, the first being the most important, although in many cases it
is difficult to enforce it, from lack of intelligence and of means on
the part of those in charge of the patient. Proper ventilation, good
drainage, and cleanliness are essential. The child should be bathed
daily, and should be protected against changes in temperature by
suitable clothing. If his strength allow, he should be taken into the
open air daily in fine weather. A wet-nurse should be provided for
infants whose mothers are unable to suckle them. Older patients should
take milk, cream, animal broths, farinaceous substances, etc., with
wine or brandy. Tonics, especially cod-liver oil, hypophosphite of
lime, and some preparation of iron or of the iodide of iron, are
important, the choice being determined by the effect apparently
produced. The internal and external employment of mercurial
preparations, once in vogue, is now almost entirely abandoned by the
best authorities. The evacuation of the fluid by puncture, followed by
compression of the head by bandaging, has been occasionally resorted
to, and in a few instances with success, but the cases in which it is
indicated are rare. Thomas Young Thompson[6] reports a case in which
puncture was followed by recovery. The child, fourteen days old, fell,
apparently without ill effects, but three weeks afterward a
protuberance appeared on the crown of the head which continued to
enlarge, and the signs of chronic hydrocephalus were unmistakable. In
three months the circumference over the parietal eminences measured 20
inches, and a year afterward 24½ inches. In spite of energetic
internal and external treatment the enlargement continued to progress,
until the head was punctured, and about three hundred grammes of a
clear, transparent fluid, free from albumen, were evacuated. Five
weeks later a second puncture was made, and sixty grammes of a milky
fluid withdrawn. The child recovered, and two years later was in good
health, the head not being disproportioned to the rest of the body.
West considers the cases in which the effusion is apparently
external—that is, confined to the arachnoid cavity, rather than
ventricular, and in which there are no indications of active cerebral
disease—to be the most favorable for the operation. The proper
situation for the puncture is the coronal suture, about an inch or an
inch and a half from the anterior fontanel. A few ounces of fluid only
should be withdrawn at a time, and compression should be carefully
applied both during the escape of the fluid and afterward.

[Footnote 6: _Med.-Chir. Transactions_, vol. xlvii., 1864.]


{746}


CONGESTION, INFLAMMATION, AND HEMORRHAGE OF THE MEMBRANES OF THE
SPINAL CORD.

BY FRANCIS MINOT, M.D.


Congestion of the Spinal Membranes.

The blood-vessels of the spinal membranes communicate freely with the
general circulation, and there is less opportunity for their
obstruction than in the case of the meninges of the brain. Hyperæmia
of the dura and pia mater is therefore seldom met with, except in
connection with disease of the cord; and, indeed, but little is known
on the subject, which is only alluded to as possible by authorities of
the present day, although the affection was formerly supposed to be a
common one, giving rise to various symptoms, such as numbness and
formication of the extremities, muscular weakness, and even
paraplegia—symptoms which are now known to be caused by structural
diseases of the cord only. As Erb[1] remarks, “It is hardly possible
that any considerable hyperæmia of the meninges should exist without a
similar condition existing in the cord also, as the vascular supply of
both is the same.”

[Footnote 1: “Krankheiten des Rückenmarks,” von Wilhelm Erb, in
_Ziemssen's Handbuch_, Leipzig, 1876; Am. trans., vol. xiii. p. 99.]

ETIOLOGY.—Hyperæmia of the spinal membranes is found after death from
convulsions, especially in cases of tetanus, hydrophobia, eclampsia,
strangulation, poisoning from narcotics, etc., in which the effect is
evidently due to asphyxia. An interesting case of extensive hyperæmia
of the spinal membranes, as well as of those of the brain,
complicating mania, is reported by M. R. G. Fronmüller.[2] A girl of
eighteen years, previously well, being accused of theft, fell into a
state of melancholia, passing into mania, with frequent convulsions,
screaming, etc. There was no spinal tenderness. The urine contained no
albumen. The temperature was never elevated. No opisthotonos. The
sphincters became relaxed, and she died at the end of about three
weeks. The dura was found to be normal, but the pia mater of the
brain, cerebellum, medulla oblongata, and cord was strongly injected.
The brain and cord were normal; no ventricular effusion. Here the
meningeal hyperæmia was doubtless caused by asphyxia resulting from
the convulsions.

[Footnote 2: See _Schmidt's Jahrbücher_, 1883, No. 7.]

Congestion of the spinal membranes has been attributed to sudden
suppression of the menstrual flow or of hemorrhoidal bleeding, and to
portal obstruction, but the evidence of this is very meagre. Exposure
{747} to cold and wet, as from sleeping on the damp ground, is an
alleged and plausible cause.

The SYMPTOMS attributed to hyperæmia of the spinal membranes are pain
in the back extending to the legs, with numbness and tingling of the
toes, sensation of weight in the limbs, muscular weakness, appearing
suddenly without fever and usually of transient duration. There is no
evidence that it gives rise to paralysis. Considering that temporary
congestion of the membranes must occasionally happen from convulsions,
as in epilepsy, etc., it is remarkable that no symptoms attributable
to it have been observed under these circumstances.[3]

[Footnote 3: See _Epilepsy and other Chronic Convulsive Diseases,
etc._, by W. R. Gowers, M.D., London, 1881, p. 106.]

MORBID ANATOMY.—We must be careful not to mistake post-mortem staining
of the tissues from imbibition of the coloring matter of the blood—the
result of decomposition aided by the position of the body—for true
congestion. The latter is recognized by fine vascular arborization
covering the surface of the dura or pia, often accompanied with small
punctate hemorrhages. More extensive extravasations in the connective
tissue, surrounding and between the membranes, are sometimes found.
The spinal fluid is usually increased in amount, and often tinged with
red. On account of the free vascular connection between the membranes
and the cord the latter almost always partakes of the congestion.

DIAGNOSIS.—From what has been said it follows that simple hyperæmia of
the spinal membranes can hardly be distinguished from that of the
cord. (See the article on DISEASES OF THE SUBSTANCE OF THE BRAIN AND
SPINAL CORD.) When the symptoms are unaccompanied by fever, are of
very moderate severity, and of short duration, we may perhaps infer
that the lesion is confined to the membranes.

The TREATMENT is the same as that for congestion of the spinal cord.


Acute Inflammation of the Spinal Dura Mater.

SYNONYM.—Acute spinal pachymeningitis.

Acute inflammation of the spinal dura mater is chiefly confined to the
outer surface of the membrane (peripachymeningitis), and is almost
always consecutive to either injury or disease of the vertebræ
(fracture, dislocation, caries), to wounds penetrating the spinal
cavity, or to suppurative disease in neighboring organs or tissues,
which makes its way into the peridural space through the
intervertebral openings. The symptoms are complex—in part caused by
the original disease, and in part by the pressure of the products of
inflammation exercised upon the nerve-roots, and even upon the cord
itself. Pain in the back, corresponding to the seat of the disease, is
rarely absent, and all movements of the trunk are extremely painful.
When the exudation is sufficient to compress the nerve-roots, the pain
will extend to the trunk and the limbs, and other signs of irritation,
such as a feeling of constriction by a tight girdle, and tingling,
numbness, and cutaneous hyperæsthesia in the limbs, will be observed,
varying in situation according to the seat of the lesion. In some
cases the compression of the cord may be sufficient to cause
paraplegia. General symptoms will vary according to the complications
of the {748} case. Severe injury or extensive disease of the vertebræ
will be accompanied with high fever; but if the external inflammation
be moderate and the meningeal complication be limited in extent, the
fever may be subacute.

MORBID ANATOMY.—The connective tissue between the dura and the bone is
the seat of inflammatory exudation, usually purulent, of greater or
less extent, and more abundant in the posterior than the anterior part
of the spinal cavity, owing to the position of the patient. A more or
less abundant exudation, either of pus or of dry caseous matter, is
found upon the outer surface of the dura or infiltrating the
connective tissue between it and the bony walls. The dura is
thickened, and sometimes the exudation is seen upon its inner walls,
but the pia is seldom involved in the inflammation. The cord may be
compressed or flattened when the amount of exudation is large, and may
in consequence show signs of inflammation in its vicinity. The spinal
nerves likewise are sometimes compressed, atrophied, softened, and
inflamed. The disease rarely occupies the cervical region, on account
of the close union of the dura with the bones of that part; hence
there is an absence of pain in the neck and of retraction of the head.

DIAGNOSIS.—The diagnosis is founded on the presence of general
symptoms of spinal disease—pain in the back, but not extending to the
neck, increased by movements of the trunk; cutaneous hyperæsthesia,
tingling, or numbness in various parts of the surface of the body;
paresis or paralysis of the lower extremities in severe cases; along
with a history of vertebral disease or injury or of suppurative
disease in the neighborhood of the spine. The history of the case will
generally be sufficient to exclude myelitis, tetanus, or muscular pain
(rheumatism, lumbago). From acute leptomeningitis the diagnosis must
also be made by the history, but it should be borne in mind that the
pia may be involved at the same time with the dura.

PROGNOSIS.—In complicated cases the prognosis is grave if the spinal
symptoms are well marked and severe, especially when there is evidence
of much pressure on the cord (paraplegia). If the signs of spinal
irritation were moderate, the danger would depend upon the nature and
extent of the external lesion.

TREATMENT.—This would be addressed mainly to the primitive disease.
For the spinal symptoms the treatment would not differ materially from
that of inflammation of the spinal pia mater.


Chronic Spinal Pachymeningitis.

This affection generally coexists with chronic inflammation of the
pia. Like the acute inflammation of the dura, it is seen in connection
with disease or injury of the vertebræ, and it may also arise from
tumors of the membrane (chiefly syphilitic) and from myelitis. It is
frequent among the chronic insane, and in them is sometimes associated
with hemorrhagic effusions analogous to the hæmatoma of the cerebral
dura mater. Chronic inflammation of the spinal dura is of unfrequent
occurrence, and but little is known of its history and pathology. In a
case reported by Wilks[4] the membrane was thickened to nearly its
whole {749} extent, and in the cervical region presented numerous bony
plates. The pia was also thickened at this part and adhered closely to
the dura. The symptoms, which seemed chiefly due to disease of the
cord from compression, were retraction of the lower limbs and violent
jerking from excessive reflex action.

[Footnote 4: _Transactions of the Pathological Society of London_,
vol. vii., 1856.]

A special form of the disease, occupying chiefly the cervical region,
was first described by Charcot.[5] The membrane is thickened by a
deposit of successive layers of fibrin, compressing the cord, which is
flattened from before backward and inflamed. The nerve-roots are also
more or less compressed. The course of the disease may be divided into
two stages: First, that of irritation of the spinal nerves, with pain
in the back part of the neck, extending to the head and along the
upper limbs. The pain is permanent, but liable to exacerbations, and
is accompanied with stiffness of the neck and a feeling of numbness
and tingling, with muscular weakness of the arms. Sometimes the skin
of the arms is the seat of trophic changes, as shown by the presence
of bullæ or pemphigus. The second period is that of extension of the
disease to the cord. The pain ceases, and is followed by paralysis or
muscular atrophy, especially in the domain of the ulnar and median
nerves, resulting in extension of the hand on the forearm, with
flexion of the fingers toward the palm, giving rise to a claw-like
appearance (main en griffe). In some cases an upward extension of the
disease implicates the root of the radial nerve, and the hand then
assumes a prone position from paralysis of the extensor muscles. The
lower portion of the cord may also become involved, with similar
results in the lower extremities. Although the disease is generally
progressive, it is not always so, and Charcot cites one case in which
great improvement took place in the course of some years, though not
apparently in consequence of any special treatment.

[Footnote 5: _Leçons sur les Mal. du Syst. nerv._, par J. M. Charcot,
Paris, 1875, vol. ii. p. 246. See, also, _Maladies du Syst. nerv._,
par A. Vulpian, Paris, 1879, p. 127; and _Clinique méd. de l'Hôpital
de la Charité_, by the same.]


Acute Spinal Meningitis.

SYNONYM.—Leptomeningitis spinalis acuta.

By the term spinal meningitis is usually meant inflammation of both
the arachnoid and the pia, the two being, as already stated, in
reality one membrane. In connection with meningitis of the brain it
constitutes a distinct disease which is usually epidemic, and probably
zymotic in its origin. (See EPIDEMIC CEREBRO-SPINAL MENINGITIS.)
Sporadic spinal meningitis is a rare disease. It may be acute or
chronic.

ETIOLOGY.—Among the causes of acute spinal meningitis are injuries to
the vertebral column, such as fracture and dislocation from falls,
blows, etc.; wounds by stabbing or shooting; violent bodily effort, as
in lifting heavy weights, etc. Other causes are local exposure to wet
and cold, as from sleeping on the wet ground or standing long in water
while at work. Like cerebral meningitis, it may complicate
constitutional diseases, as rheumatism, pyæmia, etc., but less
frequently than the former. Syphilitic inflammation of the spinal
membranes is, however, not unfrequently met with, but chiefly of the
chronic form. (See the article on SYPHILIS {750} OF THE BRAIN AND
SPINAL CORD.) In tubercular meningitis of the brain the pia mater of
the cord is often implicated in the disease. Acute spinal meningitis
is most frequently met with in young persons, and is more common in
men than in women.

SYMPTOMS.—The onset of the disease is generally sudden, and it is
rarely preceded by the usual inflammatory symptoms of chilly
sensations, restlessness, headache, etc. A sharp rigor is the first
indication of disease in most cases. This is followed by fever, with
high temperature and a quick, full, hard pulse. Pain in the back
follows, either confined to a limited region or extending throughout
the whole extent of the spine, soon becoming acute, and aggravated by
any movement of the trunk or even of the limbs. There is usually but
little tenderness on pressure upon the spinous processes, and often
none at all. The pain extends around the body and throughout the
limbs. In the course of a few hours muscular contraction in the region
of the back, and also of the limbs, is observed. When the disease is
situated in the cervical region, the head is drawn backward, and
cannot be moved without severe pain. If it occupies a considerable
extent of the spine, the dorsal muscles become rigidly contracted and
the body is arched forward (opisthotonos), as in tetanus, so that the
patient may even rest upon his occiput and sacrum. Owing to the
implication of the muscles of respiration, more or less dyspnœa is
common, and may even cause death by asphyxia. There is no paralysis of
the limbs, unless there be complication of myelitis, but the patient
abstains as far as possible from any movement from dread of pain.
Reflex irritability is exaggerated. Retention of urine and
constipation are common, probably for the same reason. Hyperæsthesia
of the surface of the body in limited areas is sometimes noticed,
owing to the irritation of the posterior spinal roots. Provided the
extent of the inflammation be comparatively limited, recovery is
possible, though rare, at this stage of the disease.

When the course of the disease is unfavorable, symptoms of paralysis
appear, from compression of the cord by the products of inflammation.
The hyperæsthesia of the skin gives place to insensibility; the
muscles lose their reflex function and their reaction to electricity;
the bladder and rectum become paralyzed. The invasion of the medulla
by the disease, which is announced by paralysis of the muscles of the
œsophagus and of the tongue, is a fatal complication. The pulse and
the respiration become rapid and irregular from compression of the
vagus, the temperature rises to 106° or 108° F., and death ensues
through asphyxia or failure of the heart.

The course of acute spinal meningitis is rapid. It sometimes
terminates fatally within two or three days, and the average duration
of fatal cases is about a week, but exceptionally the disease may last
for several weeks or even months. Even then complete recovery may take
place, though permanent effects are usually left behind, such as
paresis or paralysis of the lower extremities, muscular contractions,
muscular atrophy, etc., from injury to the nerve-roots or the cord.

The mind is generally clear in the early stage; afterward there may be
delirium, especially along with cerebral complication.

MORBID ANATOMY.—It is rarely that the pia mater is the only tissue
involved in the inflammation. Frequently the inner surface of the dura
{751} is the seat of a fine injection, with delicate false membranes,
and the cord itself—at least its exterior portions—probably always
participates more or less in the congestion. The pia is reddened and
thickened, the surface showing small bloody extravasations, and the
space between its two layers is the seat of a fibro-purulent deposit.
The spinal fluid is turbid and flocculent. The seat and extent of the
morbid appearances vary in different cases; they are always more
abundant in the posterior than the anterior part of the cord, and may
be confined to a limited space or extend throughout its whole length.
It is remarkable that the region of the medulla oblongata is generally
free or only slightly affected; but since bulbar symptoms are often
prominent in grave cases, Leyden[6] accounts for it by supposing that
the exudation is washed away by the constant movement of the
cerebro-spinal fluid. If the cord be involved in the inflammation, it
is softened and injected, the nerve-sheaths are destroyed, and the
axis-cylinders swollen in places. The nerve-roots show hyperæmia,
infiltration of the interstitial tissue with round cells, and
destruction of the nerve-sheaths.

[Footnote 6: _Klinik der Rückenmarks-krankheiten_, von E. Leyden,
Berlin, 1874, vol. i. p. 407.]

DIAGNOSIS.—Spinal meningitis is easily recognized in most cases by its
sudden onset and the severity of its symptoms. The distinguishing
symptoms are sudden and acute pain in the back, extending around the
body and into the limbs, which is increased by every movement of the
trunk, rigidity of the back, hyperæsthesia of the skin, retraction of
the head, with difficulty of breathing and of swallowing. The diseases
from which it must be distinguished are muscular rheumatism (so
called), tetanus, and myelitis. In rheumatism of the dorsal muscles
the pain is confined to the back, does not extend to the limbs, and is
only excited by movement. The fever is moderate or absent; there are
no symptoms of spinal complication, such as cutaneous hyperæsthesia,
retraction of the head, paresis of the limbs, etc.; and the result is
uniformly favorable. Tetanus is almost always due to some well-marked
traumatic cause; the muscles of the jaw are usually first implicated
(trismus); and the attacks of general muscular spasm are easily
excited by peripheral irritation. Myelitis can be distinguished by the
absence of pain in the limbs and by paraplegia, but it must be borne
in mind that myelitis and spinal meningitis may coexist.

PROGNOSIS.—Acute spinal meningitis is always a grave disease, hence a
guarded opinion should be given even in apparently favorable cases.
General mildness of the symptoms, with no indication of extension to
the medulla oblongata, would afford ground for encouragement. The
unfavorable symptoms are those showing compression or inflammation of
the cord, such as paresis, paralysis, twitching of the limbs, muscular
contractions, cutaneous anæsthesia, etc. The extension of the disease
to the medulla, as shown by difficulty of swallowing, speaking, or
breathing, is almost necessarily fatal.

TREATMENT.—During the first stage of the disease an effort should be
made to reduce the hyperæmia of the membranes by the local abstraction
of blood. This is best effected by cupping along each side of the
spine and by the application of leeches to the anus; the bleeding
should be promoted by poultices. Free purging is likely to be of
service, and is best obtained by means of ten grains each of calomel
and jalap (for an {752} adult), followed by saline laxatives.
Counter-irritation to the back may be induced by the application of
blisters or by painting the skin with a strong tincture of iodine (one
or two drachms of iodine to an ounce of sulphuric ether). After the
effusion of lymph and pus, as shown by symptoms of compression of the
nerve-roots and cord, absorbents should be tried, of which the iodide
of potassium, in doses of five to ten grains, four times daily, is
most likely to be of benefit. Pain must be relieved by opium or
morphia and chloral hydrate. The latter, either alone or combined with
hyoscyamus and bromide of potassium, will be useful to allay spasmodic
twitching, opisthotonos, or muscular contraction. The patient should
be enjoined to lie on each side alternately, or on the face if
possible, in order to equalize the hyperæmia of the membranes and
cord. Liquid nourishment must be freely administered, such as milk,
broths, gruel, etc., together with wine and other stimulants in case
of exhaustion and threatening of collapse. During convalescence the
patient should be carefully protected against cold and fatigue, and
the strength must be supported by quinine and iron with suitable diet.


Chronic Spinal Meningitis.

SYNONYMS.—Chronic inflammation of the pia mater of the spinal cord,
Chronic spinal leptomeningitis.

Chronic spinal meningitis may follow the acute form, or it may arise
from chronic disease of the vertebræ or of the cord, especially
myelitis and sclerosis. It is most apt to accompany sclerosis of the
posterior columns, and it is often difficult to say in any particular
case whether the meningeal affection preceded or followed that of the
cord. Probably some cases of chronic myelitis, especially of the
disseminated form, owe their origin to chronic meningitis.[7] It has
been thought to follow blows on the back, and also to arise from
general concussion without traumatism, and has been considered as a
frequent result of accidents from railroad collisions, etc. This view
has been disputed by Herbert W. Page,[8] who says: “Of the exceeding
rarity of spinal meningitis as an immediate result of localized injury
to the vertebral column we are well assured.... And we know of no one
case, either in our own experience or in the experience of others, in
which meningeal inflammation has been indisputably caused by injury to
some part of the body remote from the vertebral column.” Chronic
alcoholism and syphilis, especially the latter, predispose to the
disease. In many cases no adequate cause can be assigned.

[Footnote 7: Leyden, _op. cit._, vol. i. p. 442.]

[Footnote 8: _Injuries of the Spine and Spinal Cord, without Apparent
Mechanical Lesion and Nervous Shock, in their Medico-legal Aspects_,
London, 1883, p. 128.]

SYMPTOMS.—Gowers[9] remarks that a large number of symptoms formerly
assigned to chronic spinal meningitis have nothing to do with that
pathological state, but are now known to be owing to alterations
within the cord which are frequently associated with it. The symptoms
which are really due to the meningeal inflammation—namely, those {753}
arising from interference with the nerve-roots in their passage
through the thickened membranes—do not differ essentially from those
of chronic pachymeningitis of the spine; the principal are pain in the
back, especially on movement, extending to the trunk and limbs,
hyperæsthesia of the skin in various regions within the domain of the
irritated sensory roots, with diminution or loss of the knee-jerk, and
areas of anæsthesia due to their more complete compression. The
compression of the motor roots gives rise to symptoms which are
similar to those of disease of the anterior cornua, consisting chiefly
of muscular wasting, with impairment of motion in corresponding
regions, without fever.

[Footnote 9: _The Diagnosis and Diseases of the Spinal Cord_, by W. R.
Gowers, M.D., 2d ed., Philada., 1881, p. 73.]

The anatomical appearances, which are most pronounced in the posterior
aspect of the cord, and diminish from below upward, are often of
considerable extent. The membrane is thickened, opaque, and often
adherent to the cord. On the inner surface are seen numerous small
bodies composed of proliferating connective tissue.[10] These,
according to Vulpian, are chiefly found in the lower dorsal and lumbar
region and on the cauda equina. The dura is very frequently involved
in the inflammation; it is thickened, and its inner surface is
adherent to the pia, often showing numerous miliary bodies similar to
those found in the pia.

[Footnote 10: Leyden, _op. cit._, vol. i. p. 144; A. Vulpian, _Mal. du
Syst. nerv._, Paris, 1879, p. 126.]

DIAGNOSIS.—Chronic spinal meningitis so rarely exists apart from
disease of the dura or of the cord that its separate diagnosis must be
mainly a matter of conjecture. Leyden justly says we must usually be
content to diagnosticate chronic meningitis without attempting any
further distinction, except in cases which originate in disease of the
vertebræ or of their neighborhood, and afterward penetrate into the
spinal canal, and which would probably give rise to pachymeningitis.
The diseases with which chronic meningitis of the spine is most likely
to be confounded are posterior sclerosis (locomotor ataxia) and
chronic degeneration of the anterior cornua (progressive muscular
atrophy).[11] From the former it is distinguished by the absence of
ataxia; from the latter, by the irregular distribution of the
symptoms; and from both, by the existence of limited areas of
anæsthesia and of extensive spinal pain. It must be remembered that
inflammation of the cord complicating that of the meninges, or
pressure upon the cord by the thickened membranes may give rise to
mixed symptoms. The latter is especially observed in syphilitic cases.

[Footnote 11: Gowers, _op. cit._, p. 74.]

PROGNOSIS.—Simple chronic spinal meningitis is rarely if ever fatal.
How far it is capable of amelioration or of cure is not, in the
present state of our knowledge, known. When complicated with disease
of the cord the prognosis will depend upon that of the latter.
Syphilitic chronic meningitis is to a certain extent amenable to
appropriate medication.

TREATMENT.—The treatment should have for its object (1st) to relieve
pain; (2d) to arrest the progress of the inflammation, and especially
to prevent it from extending to the cord; (3d) to promote the
absorption of the exudation. For the first object the internal or
hypodermic employment of morphia should be combined with external
applications, such as fomentations, liniments, ice, etc.
Counter-irritation by means of dry cupping, blisters, iodine, etc.,
with leeches, shampooing, and douches of hot water, may be of some use
in retarding the progress of the {754} inflammation, and should be
aided by the administration of mercurials and the preparations of
iodine. The biniodide of mercury would be useful for this purpose in
the dose of one-sixteenth to one-eighth of a grain three times daily,
its effect being carefully watched in order to prevent salivation. The
same means will also aid in favoring the absorption of lymph. In
syphilitic cases an appropriate specific treatment is indicated.


Spinal Meningeal Hemorrhage.

SYNONYMS.—Spinal meningeal apoplexy, Hæmatorrhachis.

Spinal meningeal hemorrhage may take place between the dura mater and
the walls of the vertebral canal, or between the dura and the pia
mater—_i.e._ into the arachnoid space.

ETIOLOGY.—Penetrating wounds, injuries to the vertebræ, fractures and
dislocations, and violent blows are apt to give rise to more or less
hemorrhage into the spinal canal. Violent convulsions, as in tetanus,
epilepsy, uræmic eclampsia, hydrophobia, may be followed by meningeal
hemorrhage, owing to the disturbance of the circulation from asphyxia;
and excessive muscular effort, as in lifting heavy weights, etc., has
been said to cause it. In cerebral meningeal hemorrhage and in
effusion into the substance of the brain the blood sometimes escapes
into the spinal canal. An aneurism of the aorta has been known to
communicate with the canal; such a case was reported by Laennec.[12]
In certain diseases with hemorrhagic tendency, as purpura and scurvy,
spinal extravasation is occasionally observed.[13]

[Footnote 12: _Traité d'Auscultation médiate_, 4th ed., Paris, 1837,
vol. iii. p. 443.]

[Footnote 13: A case of scorbutic spinal hemorrhage is reported in the
_British Med. Journal_, Nov. 19, 1881.]

SYMPTOMS.—These vary according to the conditions under which the
hemorrhage is produced and to the amount of bleeding. In traumatic
cases the signs of hemorrhage are often completely overshadowed by
those of the injury of the vertebræ, the membranes, or the cord, and
are undistinguishable. When a large amount of blood is suddenly
introduced into the spinal canal, it usually gives rise, by pressure
on the cord, to paraplegia, which, however, is sometimes of only short
duration. Thus in Laennec's case the bursting of an aneurism into the
spinal cavity was signalized by a sudden paraplegia, but in half an
hour the power of movement returned, though sensation did not. The
patient died in a few hours from hemorrhage into the left pleural
cavity. The amount of blood in the spinal cavity is not stated, and,
in fact, it would appear that the spine was not opened. When the
amount of blood is smaller the symptoms indicate irritation of the
spinal nerves and of the cord. Pain in the back is always present,
extending into the limbs, and is sometimes severe. Its seat
corresponds to that of the effusion. There may be a feeling of
tingling and numbness in the lower extremities, with anæsthesia or
hyperæsthesia of the skin and more or less paresis. A feeling of
constriction around the waist or the chest is sometimes complained of.
In slight effusions the symptoms may be limited to numbness and
formication of the extremities, with slight paresis. There is rarely
fever in the early stages, unless the amount of blood is {755}
sufficient to give rise to inflammatory conditions of the cord or
membranes. If the extravasation be moderate it is generally absorbed,
with relief to the symptoms, although slight numbness and paresis of
the extremities may continue for a long time.

PATHOLOGICAL ANATOMY.—In hemorrhage outside the dura the loose
cellular tissue between the membrane and the bony canal contains more
or less coagulated blood according to the circumstances of the case,
especially in the posterior region of the canal and covering the
nerve-roots. The dura is reddened by imbibition of the coloring matter
of the blood. When the amount of the effusion is large, as in
traumatic and aneurismal cases, or where cerebral hemorrhage has
extended into the spine, the cord may be compressed by it. Hemorrhage
into the arachnoid sac, except in cases of violence, etc., is usually
of limited amount, sometimes only in the form of drops of blood upon
the surface of the dura or pia. When more abundant it may surround the
cord more or less completely, but in most cases it is limited in
longitudinal extent, being confined to the space of one or two
vertebræ. The cord may be more or less compressed, reddened, and
softened. In all cases the spinal fluid is discolored and reddened in
proportion to the amount of the hemorrhage.

DIAGNOSIS.—When the complications are such that symptoms attributable
to hemorrhage are not observed, the diagnosis of spinal hemorrhage is
impossible. This may happen in the case of wounds and injuries of the
vertebræ and of the passage into the spinal canal of blood from an
apoplectic effusion of the brain. In the convulsions of tetanus,
epilepsy, etc. the amount of the hemorrhage is rarely sufficient to
give rise to distinctive symptoms. In idiopathic and uncomplicated
cases the chief diagnostic marks are suddenness of the attack; pain in
the back, usually at the lowest part; disturbances of sensation in the
extremities (anæsthesia, formication, etc.); paresis or paralysis of
the legs; the absence of cerebral or spinal inflammatory symptoms;
and, in many cases, the favorable course of the disease. Sometimes an
ostensible cause, such as scurvy, purpura, suppressed menstruation, or
hemorrhoidal flux, will aid in the diagnosis. The disease for which
spinal hemorrhage is most likely to be mistaken is acute myelitis, but
this is not sudden in its onset, is accompanied with fever, and gives
rise to paralysis both of motion and sensation, and to loss of control
over the sphincters, to bed-sores, etc. Hemorrhage of the cord would
be accompanied by paraplegia and loss of sensation in the lower
extremities and slight tendency to spasmodic manifestations; it is
fatal in the majority of cases, or else is followed by permanent
paralysis. Hysteria might be confounded with spinal hemorrhage, but
the history of the case and the transient duration of the symptoms
would clear up all obscurity.

PROGNOSIS.—In traumatic cases the hemorrhage is usually only one
element in the gravity of the situation, which depends chiefly upon
the character and extent of the original injury. In idiopathic and
uncomplicated cases the prognosis, which must always be doubtful, will
vary according to the severity of the symptoms as corresponding to the
amount of the effusion. The danger is greatest during the first few
days; if there should then be diminution of the more important
symptoms, an encouraging opinion may be given. The immediate effects
may, however, be {756} less grave than the remote, such as bed-sores,
cystitis, etc. Except in the very mildest cases the patient is likely
to be confined to bed for several weeks. In more severe ones the
convalescence may be very protracted, and permanent lameness, etc. may
result.

TREATMENT.—In the early stage absolute rest in bed, with cold
applications to the back and moderate purging, should be employed.
Large doses of ergot are recommended, but there is little evidence of
benefit from this medicine. In traumatic cases no rules for treatment
of the hemorrhage can be laid down. If the extravasation evidently
depends upon a constitutional diathesis, as in purpura, scurvy, etc.,
the remedies appropriate for these diseases should be employed,
especially tonics and astringents, such as the tincture of the
chloride of iron, in doses of from fifteen to thirty drops three times
daily, quinine, and the vegetable acids. Should there be evidence of
blood-pressure from suppressed discharge, as in amenorrhœa, arrested
hemorrhoidal flow, etc., leeches should be applied to the anus, and
blood may be taken from the region of the spine by cupping. In the
later stages an attempt may be made to aid the absorption of the
effused blood by the administration of the iodide of potassium or the
protiodide of mercury, and by the application of blisters or strong
tincture of iodine to each side of the spine. Pain must be relieved
and sleep obtained, when necessary, by means of opium, chloral
hydrate, or other anodynes. Electricity, rubbing, bathing, etc. will
be useful for combating the paralytic symptoms which may remain after
the disease itself is relieved.


{757}


SPINA BIFIDA.

BY JOHN ASHHURST, JR., M.D.


DEFINITION.—By the term spina bifida is meant a congenital
malformation of the vertebral column, consisting in the absence of a
part—commonly the spinous processes and laminæ—of one or more of the
vertebræ, and thus permitting a protrusion of the spinal meninges,
which, with their contents, form a tumor of variable size and shape,
usually in the lumbo-sacral region.

SYNONYMS, ETC.—Of the various names which have been proposed for this
affection, most are objectionable, as not expressing with sufficient
definiteness what is meant. Thus, hydrorachis (the term generally
employed by French writers), hydrorachitis, spinal hydrocele, etc.,
convey merely the notion of an accumulation of fluid within the spinal
canal, and are as applicable to simple serous effusions in that part,
whether occurring as a complication of hydrocephalus or as the result
of injury, as to the special affection under consideration. Again,
myelochysis—pouring out or protrusion of the spinal marrow—would imply
that the cord itself was necessarily involved in the tumor, which is
certainly not always the case. The terms schistorachis (cleft spine)
and atelorachidia (defective spine—a name suggested by Béclard) would
be preferable, and are really more accurate than the name spina
bifida, since, as a matter of fact, the spinous processes are, as a
rule, not bifid, but totally deficient. The latter term, however, has
the advantage of being more familiar, and may be retained simply as a
matter of convenience. It is said by Itard to have been first employed
by the Arabian physicians.

HISTORY.—Spina bifida does not appear to have been known to the
ancients, the earliest recorded observations of the affection being
found in the writings of Bauhinus (1560-1624), of Tulpius (1593-1674),
of Bonetus (1620-89), and of Ruysch (1638-1731). Good accounts of the
affection may be found in the _Dictionnaire des Sciences médicales_
(tome xxii., Paris, 1818), and particularly in Holmes's _Surgical
Treatment of the Diseases of Infancy and Childhood_ (2d ed., London,
1869), in Follin and Duplay's _Traité de Pathologie externe_ (tome
iii.), and in Treves's article on “Malformations and Injuries of the
Spine” in the _International Encyclopædia of Surgery_ (vol. iv., New
York, 1884).

ETIOLOGY.—There are two conditions essential to the formation of a
spina bifida: (1) an arrest of development, or at least a defective
closure, of the vertebral arches; and (2) a dropsical condition either
of the central canal of the spinal cord or of the subarachnoid spaces;
but which {758} of these is the antecedent condition it is, as justly
remarked by Erb, impossible to decide. Spina bifida often occurs as a
complication of hydrocephalus, and is itself often complicated with an
atrophic and deformed condition of the lower extremities—a
circumstance which led Tulpius to suggest that the malformation was
caused by a malposition of the fœtus in utero, an explanation which it
seems hardly necessary to waste time in considering. Salzmann observed
spina bifida in two children born of the same mother, and Camper
noticed it in twins.

SYMPTOMATOLOGY.—Spina bifida forms a tumor—or, more rarely, several
tumors—in the region of the vertebral column, usually discovered at
birth, but occasionally not noticed until a later period. Thus,
Lancisi mentions a case in which the tumor first made its appearance
in a hydrocephalic child at the age of five years, and J. L. Apin one
in which the patient reached the age of twenty before any swelling was
manifested. If these records are accepted as authentic, the only
satisfactory explanation is that of Itard—viz. that the bony
deficiency existed from the time of birth, and that the dropsical
protrusion did not occur until afterward: this seems to me more
reasonable than the suggestion of the younger Andral, that the
vertebræ underwent a process of secondary softening and absorption.
The part most frequently affected is the lumbar region, but cases are
not wanting of the occurrence of spina bifida in the cervical, dorsal,
and sacral regions, and even, in at least one case (Genga's), in the
coccyx. The tumor almost invariably occupies the median line, and
projects directly backward: in at least four cases, however, recorded
by Bryant, Emmet, and Thomas, the tumor protruded anteriorly from
deficiency of the vertebral bodies.

The size of a spina bifida varies from that of a walnut to that of a
child's head, or even larger: in some rare instances, such as those
recorded by Lezelius and Richard, the whole spinal column has been
cleft, and the tumor has extended from nucha to sacrum; but cases of
this kind seldom come under the surgeon's observation, as children
with such extensive deformity usually perish shortly after birth. The
shape of the swelling is rounded, or more often oval; it is commonly
sessile, but occasionally pedunculated; and it is sometimes lobulated,
the lobules being separated by more or less distinct sulci. The skin
covering the tumor is in some cases normal, with more or less fat in
the subcutaneous connective tissue, but more often thin, tightly
stretched, red, shining, and occasionally ulcerated; more rarely it is
thickened and leathery, as in a case referred to by Sir Prescott
Hewett. Sometimes a navel-like depression is found at some part of the
surface, corresponding, as pointed out by Follin and Duplay, and by
Erb, to the place of attachment, on the interior of the sac, of the
terminal extremity of the spinal cord. The cutaneous investment is
sometimes altogether wanting, the spinal dura mater itself forming the
external covering of the tumor. It is in these cases especially that
ulceration and rupture are apt to occur.

Spinæ bifidæ are usually soft and fluctuating, and occasionally
partially reducible; their tension and elasticity are increased when
the child is in the upright position or during the acts of expiration
and crying, and are diminished during inspiration or when the child is
laid upon its face. When the part is relaxed a bony prominence can be
felt on either side, and the aperture in the vertebral column can be
more or less distinctly {759} outlined. The swelling is apt to be
painful on pressure. If the tumor is of moderate size and covered with
healthy skin, there are usually no constitutional symptoms, and, even
where ulceration and rupture occur, the opening may heal and a
spontaneous cure may possibly ensue. More often, as the tumor
increases in bulk—or at any time if pressure be made upon it—various
nervous symptoms are observed: drowsiness, muscular twitchings,
convulsions, and often paraplegia and paralysis of the sphincters.
Rupture is usually followed by the development of spinal meningitis,
or may prove directly the cause of death by the loss of cerebro-spinal
fluid which it causes; in other instances, however, if the rupture be
a small one, healing may occur (as already mentioned) or a fistulous
opening may persist; in rare cases the fluid may escape by a process
of transudation without rupture, as in an example recorded by Laborie.

As may be inferred from what has already been said, the course of
spina bifida is usually rapid and toward a fatal termination. In some
instances, however, as in cases observed by Holmes, and more recently
by Lithgow, spontaneous recovery has followed the obliteration of the
channel which unites the sac with the cavity of the spinal membranes;
and in other instances, without a cure having been effected, life has
been prolonged for very many years. Thus, Behrend reports a case in
which a patient with spina bifida lived to the age of fifty, and
Holmes refers to another in which death resulted from an independent
disease at the age of forty-three. But a still more remarkable case
was recorded by Callender, the patient in this instance having reached
the age of seventy-four.

PATHOLOGY AND MORBID ANATOMY.—The most important points for
consideration in respect to the anatomy of spina bifida are the
relations which the spinal cord and spinal nerves bear to the sac, and
the nature of the contained fluid. It is ordinarily said that the
spinal cord itself commonly enters the sac of a spina bifida—the
report of the London Clinical Society's committee gives the proportion
of cases in which it does so at 63 per cent.—and Holmes figures a
specimen from the museum of St. George's Hospital, London, in which
this condition is obviously present; on the other hand, Mayo-Robson in
eight operations only once found the cord implicated; and the late
John B. S. Jackson of Boston—whose name will be recognized as one of
high authority in regard to all questions of morbid anatomy—once
assured me that he had made very many dissections of spinæ bifidæ, and
that he had invariably found that the cord stopped short of the sac,
and that only the nerves entered the latter: this, as negative
evidence, cannot of course contravene such positive evidence as that
of the specimen referred to by Holmes, but it would seem to show that
the condition was a less common one than is generally supposed, and
that in at least a fair proportion of cases the cord itself did not
form part of the sac contents. This remark applies especially to those
cases in which the fluid is accumulated in the subarachnoid space, and
in which, as pointed out by Sir P. Hewett, the cauda equina or spinal
nerves are pushed by the vis a tergo into the sac; but when the
dropsical effusion occupies the central canal of the cord, this is apt
to be flattened and spread out like a thin lining to the sac, just as
the brain is spread over the inner wall of the skull in cases of
internal hydrocephalus; and, on the other hand, when the accumulated
fluid fills the cavity of the arachnoid the cord is apt to be pushed
forward, and the {760} sac may be entirely devoid of all
nerve-structures. Such, too, according to Giraldès, is the case in
spina bifida of the cervico-dorsal region.

The committee of the London Clinical Society classify cases of spina
bifida in three divisions: (1) Those in which the membranes only
protrude (spinal meningocele); (2) those in which the protrusion
involves both the cord and membranes (meningo-myelocele); and (3)
those in which the central canal of the cord itself forms the cavity
of the sac (syringo-myelocele). The last variety is the rarest, as the
second is the most common. In meningo-myeloceles the spinal cord with
its central canal is continued within the median, vertical portion of
the sac, and at this part there is no covering of true skin; the
nerve-roots which traverse the sac arise from this intramural portion
of the central nervous system.

Humphry of Cambridge, England, makes a somewhat similar classification
of spinæ bifidæ, recognizing as the most common variety the
hydrorachis externa anterior, in which the fluid occupies the
subarachnoid space in front of the spinal cord, and in which “the cord
and the nerves are stretched backwards and outwards upon the sac, and
are there confluent, together with the arachnoid, pia mater, and dura
mater, or their representatives, in the thin membrane which forms the
hindmost part of the wall of the sac;” rarer forms are the
hydro-meningocele, or hydrorachis externa posterior, in which the
fluid accumulates behind the cord, which does not enter the sac, and
the hydro-myelocele or hydrorachis interna, in which the fluid
occupies the central spinal canal.

The theory which, according to the Clinical Society's committee, best
explains the pathological anatomy of spina bifida is that which
assumes a primary defect of development of the mesoblast from which
the structures closing in the vertebral furrow are developed.

The fluid of spina bifida appears to be identical in character with
the cerebro-spinal fluid. Bostock found that it was very slightly
clouded by the application of heat, and that it contained, in 100
parts, 97.8 of water, 1.0 of chloride of sodium, 0.5 of albumen, 0.5
of mucus, 0.2 of gelatin, and some traces of lime. Five specimens more
recently analyzed by Hoppe-Seyler gave an average of 98.8 parts water,
0.15 parts proteids, and 1.06 extractives and salts. Turner found a
reaction somewhat similar to that of grape-sugar, as had been
previously found by Bussy and Deschamps in cerebro-spinal fluid
itself, but in two specimens analyzed by Noad for Holmes it was at
least very doubtful whether sugar was actually present. “The first
specimen was found to be completely neutral; its specific gravity was
1.0077; it contained phosphates, but no reaction could be obtained
resembling that of sugar. The second specimen ... did give a reaction
with copper like that of sugar, but no trace of fermentation could be
obtained.” Three analyses, however, made by Halliburton for the London
Clinical Society's committee showed uniformly a decided trace of
sugar, with a diminution in the quantity of proteids, which appeared
to consist entirely of globulin.

In some cases the sac of a spina bifida contains, besides
nerve-structures and cerebro-spinal fluid, both fibrous and fatty
tissues.

DIAGNOSIS.—Ordinary fatty tumors have been mistaken for spinæ bifidæ,
but such an error could only be committed through carelessness: more
difficult is the diagnosis from certain forms of congenital cyst,
occupying the median line of the back, and still more difficult the
{761} diagnosis from the several affections known as false spina
bifida. In the former case the distinction might be made by noting the
irreducibility, constant shape, and unchanging tenseness of the cyst,
and perhaps, as suggested by T. Smith, by tracing the line of spinous
processes beneath it; some information, too, might perhaps be gained
by chemical examination of the fluid obtained by puncture. Under the
name of false spina bifida Holmes includes three distinct conditions:
these are—(1) a true spina bifida, in which the connection with the
spinal membranes has in some way been obliterated, the sac then
communicating with the vertebral canal, but not with the theca; (2) a
congenital, cystic, or fatty tumor, taking its origin within the
vertebral canal, and projecting through an opening caused by a gap in
the laminæ; and (3) a tumor containing fœtal remains, and properly
regarded as an example of included fœtation. In any of these cases a
positive diagnosis might be impossible, and the probable nature of the
tumor could only be inferred by noting the absence of one or more of
the characteristic symptoms of true spina bifida.

PROGNOSIS.—The prognosis of spina bifida is without question
unfavorable; at the same time the affection is by no means to be
considered, as it was formerly, one of an invariably fatal character,
for, apart from the fact already mentioned that several cases are on
record in which patients with untreated spina bifida have reached
adult life, and even old age, the modern method of treatment has
proved so much more successful than those formerly employed that in
favorable cases surgical interference affords at least a reasonable
prospect of recovery. The circumstances which especially furnish
grounds for an unfavorable prognosis are the rapid growth of the
tumor, the thinning or ulceration of its coverings, and the occurrence
of nervous symptoms, and particularly of paralysis or convulsions.

TREATMENT.—This may be either palliative or radical. If the tumor be
not increasing materially in size, the surgeon may properly content
himself with palliative measures—applying equable support and perhaps
slight pressure by the use of a well-padded cap of gutta-percha or
leather, an air-pad, or, as advised by Treves, a simple pad of cotton
smeared with vaseline, and a bandage; if the tumor be small and
covered with healthy integument, painting its surface with collodion
may be of service through the contractile property of that substance.
Radical measures are only indicated when the child, otherwise healthy,
seems to have his life threatened by the rapid growth of the tumor,
causing risk of ulceration and rupture, or giving rise to convulsions
or paralysis. The principal modes of treatment to be considered under
this heading are—(1) simple tapping or paracentesis; (2) injection of
iodine; (3) ligation of the neck of the sac; and (4) excision.

(1) Paracentesis, a simple evacuation of the fluid contents of the
sac, is the only operation ordinarily justifiable in cases attended by
paralysis or other grave nervous manifestations. The puncture should
be made in the lower part of the sac and at a distance from the median
line (in the course of which the nerve-structures are particularly
distributed), and only a small quantity of fluid—a few drachms or at
most one or two ounces—should be removed at a time, the instrument
being at once withdrawn if convulsions follow, and the wound being
instantly closed with lint dipped in compound tincture of benzoin.
Either an aspirator-tube or a {762} small trocar may be used, and the
operation may be repeated if necessary, pressure being maintained
during the intervals. Paracentesis has occasionally though not often
proved curative.

(2) Injection of Iodine.—This mode of treatment was introduced about
the same time by Velpeau and by Brainard of Chicago. The latter
surgeon's method consists in injecting, after only partially emptying
the tumor, a solution of iodine with iodide of potassium (iodine, 5
grs.; iodide of potassium, 15 grs.; water, 1 fl. oz.), allowing it to
flow out again, washing out the sac with water, and finally
reinjecting a portion of the cerebro-spinal fluid originally
evacuated; and the former's, in completely evacuating the tumor, and
then injecting a mixture of iodine and iodide of potassium, each one
part to ten parts of water. Each of these plans has met with a fair
measure of success;[1] but the modification introduced by James Morton
of Glasgow is a great improvement, and affords what is actually the
most successful mode yet devised for dealing with spina bifida. Morton
employs a solution of iodine in glycerin (iodine, 10 grs.; iodide of
potassium, 30 grs.; glycerin, 1 fl. oz.), which has the advantage of
being less diffusible than the aqueous solution, and therefore less
liable to enter the spinal canal. The tumor is about half emptied, and
a small quantity—from fluid drachm ss to fluid drachm iij of the
solution—is then slowly injected, and allowed to remain. The operation
is repeated after a few days if necessary. Of 50 cases known to Morton
as having been treated in this way up to May, 1885, 41 were regarded
as successful; but of 71 cases collected by the London Clinical
Society's committee, only 39 had been benefited by the operation.

[Footnote 1: In a case recently recorded by Woltering, however, iodine
injection was followed by death within half an hour.]

The introduction of iodine into the sac of a spina bifida is,
according to Morton, only justifiable in cases unattended by
paralysis; under opposite circumstances I should be disposed to try a
plan recently employed with success by Noble Smith in a case of
meningocele—viz. injecting the iodo-glycerin solution into the
coverings of the sac, and as close to it as possible without
perforating it.

(3) and (4). Ligation and excision have each occasionally effected a
cure, but more often have but helped to precipitate a fatal issue. A
successful case of ligation followed by excision has been recently
recorded by Löbker. The elastic ligature, applied around the neck of
the sac (if this be pedunculated), has been employed by Laroyenne,
Ball, Colognese, Baldossare, Mouchet, and other surgeons, and of 6
cases collected by Mouchet, 3 ended in recovery. Another success has
been recently recorded by Turretta. The écraseur has been used, but
its employment cannot be recommended. Compression by clamps is advised
by Schatz of Rostock. Ligation is best adapted to cases occurring in
the cervical and dorsal regions, in which, as pointed out by Giraldès,
nerve-elements are less likely to be involved. Excision, supplemented
by transplantation of a strip of periosteum from a rabbit, has been
successfully resorted to by Mayo-Robson and by R. T. Hayes of
Rochester, N. Y.; and simple excision, with suture in separate lines
of the sac and integuments, by Mayo-Robson, Atkinson, and Jessop. The
Clinical Society's committee in all refers to 23 cases treated by
excision, 16 of which are said to have been successful.


{763}


ANÆMIA AND HYPERÆMIA OF THE BRAIN AND SPINAL CORD.

BY E. C. SPITZKA, M.D.


Cerebral Hyperæmia.

Up to within a few years it was a favorite mode of explaining the
results of the administration of certain narcotic and stimulant drugs,
and certain of the active symptoms of mental derangement, to attribute
them to an increased blood-supply of the nerve-centres. This view
seemed to harmonize so thoroughly with the physiological dictum that
functional activity depends on the supply of oxygenated blood that the
first attempts at questioning it were treated as heresies. To-day,
however, few authorities can be found to adhere unreservedly to this
once-popular and easy explanation. The drift of physiological and
medical opinion is in the direction of regarding some subtle molecular
and dynamic state of the nerve-elements as the essential factor in
intoxications as well as in maniacal and other forms of insane
excitement: if they be complicated by active or passive congestions,
this is probably a secondary occurrence of modifying but not of
intrinsic determining power. While this change in our views is the
natural result of progress in experimental pharmacology and pathology,
it does not justify the extreme assertion that there is no disorder of
the brain functions deserving the name of congestion and hyperæmia.
This assertion seems to have been provoked by the careless manner in
which these terms have been employed to designate conditions which are
in reality the most different in nature that can be well conceived. No
one familiar with the extent to which the term “congestion of the base
of the brain” has been abused in this country will marvel that the
reaction provoked by it has overstepped the boundaries of cautious
criticism. That there are physiological hyperæmias of the brain is now
universally admitted; the most recent experimental observations,
indeed, conform most closely to the claims of the older investigators.
It naturally follows that pathological hyperæmias are both possible
and probable, and even if the observations in the dead-house do not
strongly sustain the existence of pathological hyperæmias and
congestions independently of gross disease, clinical analysis and the
gratifying results of appropriate treatment justify us in retaining
these designations in our nomenclature with the limitation here
implied.

One great difficulty in determining the precise nature of the
disorders which the physician is called upon to treat on the theory of
hyperæmia lies in the number of factors which may contribute to or
modify its {764} development. If, for example, the action of the heart
be increased through hypertrophy, the result to the cerebral
circulation will obviously be different in a plethoric and in an
anæmic person; it will be also very much different in the event of the
stimulation of the centres which contract the calibre of the cerebral
blood-vessels from what it would be if there were a state of vascular
relaxation. Should the cardiac hypertrophy be associated with renal
disease, other disturbing elements may be introduced, such as
arterio-fibrosis, or the presence in the blood of certain toxic
substances having direct effects of their own on the nerve-elements.
The picture may be still more complicated by variations in the
intracranial pressure. It is impossible to prove, either by direct or
indirect evidence, that there is such a pathological state as a simple
cerebral hyperæmia; indeed, there is one fact which militates strongly
against, if it be not fatal to, such an assumption. Were a
physiological hyperæmia to become intensified to a pathological
degree, we should have corresponding clinical phenomena. In other
words, the culmination of the morbid process should be preceded by an
exaggerated physiological excitation similar to that observed with
intoxications. But this is rarely the case, and we accordingly find
that the more cautious writers, like Nothnagel,[1] do not commit
themselves to the view that the results of mental overstrain[2] are to
be classed as simple cerebral hyperæmia. Similar restrictions are to
be made regarding the established congestive states, such as those
following sunstroke. It has been usually supposed that insolation
directly produces cerebral hyperæmia, even to the degree of
engorgement, and that the after symptoms in persons who recover are
due to the non-return of the meningeal and cerebral blood-vessels to
their normal calibre, and to other more remote results of vascular
stasis. The latter half of this proposition is in part correct; the
former is contradicted by numerous pathological observations. Thus,
Arndt,[3] who had the opportunity of studying over one hundred cases
occurring in the course of a forced march of a division of infantry
from Berlin to Pankow, many of which terminated fatally, found almost
uniformly a pale brain, with peculiar color-changes, denoting rather
structural than circulatory trouble.[4] The {765} whole list of causes
of what is commonly designated cerebral hyperæmia, congestion, and
engorgement may be gone through with and similar modifying statements
be found to apply to them. The nearest approach to an ideal cerebral
congestion is that found with acute alcoholic intoxication. This is at
first accompanied by cerebral hyperæmia, which, with the comatose
climax, becomes an engorgement; accordingly, many of the results of
acute alcoholic intoxication are attributed to the circulatory
condition alone. The congestive troubles due to alcoholism which come
to the special ken of the physician, however, are those found with the
chronic form, and here a more complex pathological condition is found
to underlie it; the organization of the brain is altered, the vascular
channels more or less diseased, and the vaso-motor mechanism
continuously deranged. This disorder, as well as the apoplectiform
states attributed to vascular stasis, and the active and passive
hyperæmias associated with tumors, meningitic and other gross diseases
of the brain, as well as with the status epilepticus, are usually
included in the discussion of cerebral congestion, and serve to swell
up the chapters devoted to it. They will be found discussed in more
appropriate situations in this volume. In this place it is proposed to
consider only those congestive states which present themselves to the
physician, independently of conditions which, if associated,
preponderate in clinical and therapeutic importance.[5]

[Footnote 1: _Ziemssen's Cyclopædia_, “Nervous System,” i. p. 39, 2d
German ed.]

[Footnote 2: It has repeatedly happened during the past decade that
young persons competing for admission to higher institutions of
learning in New York City through the channel of a competitive
examination died with symptoms of cerebral irritation; the death
certificates in several such cases assigned meningitis or cerebral
congestion as the cause of death, and attributed the disorder to
mental overstrain. It is not so much the intellectual effort that has
proved hurtful to the pupils as the emotional excitement attending on
all competitive work, the dread of failure, the fear of humiliation,
and anxiety developed by the evident futility of the cramming process.
Some years ago I recorded the results of some inquiries on this head
in the following words: “The mental-hygiene sensationalists, who
periodically enlighten the public through the columns of the press
whenever an opportune moment for a crusade against our schools and
colleges seems to have arrived, are evidently unaware of the existence
of such a disease as delirium grave, and ignorant of the fact that the
disorder which they attribute to excessive study is in truth due to a
generally vitiated mental and physical state, perhaps inherited from a
feeble ancestry. Our school system is responsible for a good deal of
mischief, but not for meningitis” (_Insanity, its Classification,
Diagnosis, and Treatment_). Since then I had an opportunity of
obtaining an excellent description of such a case which had been
attributed to the combined effects of malaria and educational
overstrain, presenting opisthotonos, fulminating onset, and an
eruption!]

[Footnote 3: _Virchow's Archiv_, lxiv.]

[Footnote 4: The observations of Gärntner (_Medicinische Jahrbucher_,
1884, 1) harmonize with this. He found that radiant heat contracts the
blood-vessels of the frog's mesentery.]

[Footnote 5: The same applies to conditions which are discussed under
this head in textbooks, although they have either only a medico-legal
bearing or are inconstant factors, such as the injection of the brain
in death from strangulation. I need but instance the vascular
condition of brains of criminals executed by hanging. In the case of
one where the strangulation had been slow I found an engorgement of
all the vessels and arachnoidal as well as endymal hemorrhages; in a
second, where the criminal had been carried half fainting to the drop,
and death ensued quickly and without signs of distress, the brain was
decidedly anæmic.

It has been also considered best to omit treating of the collateral
hyperæmia of the brain sometimes found with erysipelas of the face and
scalp. This I regard as essentially of the same nature as the
metastatic meningitis of erysipelas, if it be not in reality a first
stage of the latter.]

ETIOLOGY.—An individual predisposition to cerebral congestion was one
of the unquestioned facts of the older medical writers. It undoubtedly
exists, and to-day we attribute it to inherited vascular conditions
either affecting the calibre and coats of the blood-vessels or the
vigor of the vaso-motor apparatus. I have remarked the transmission of
that weakness of the latter which underlies the congestive phenomena
of later life much more frequently in the female than in the male sex.

It has been claimed that external refrigeration produces hyperæmia of
the brain, as of other internal organs, and that this accounts for the
greater frequency of the disorder in cold weather. Niemeyer indeed
speaks of persons who, suffering from this condition, appear and act
in such a way as to convince the laity that they are intoxicated; and
Andral, Falret, and Hammond note the occurrence of a much larger
number of cases in the winter than in the summer months. I apprehend
that the condition described by Niemeyer must be extremely uncommon,
both from individual experience and the rarity of its mention as an
independently observed fact. With regard to the alleged greater
frequency of the disorder in winter, it must be remembered that all
the three observers cited include in their computation a number of
cases in which congestion was a collateral feature; they did not limit
themselves to the disorder as {766} spoken of here. Certainly, the
physician will see few if any persons who consult him because of the
hyperæmia-producing effects of a cold day.

The suppression of habitual discharges, of the hemorrhoidal flux, and
the cessation of menstruation are associated in many instances with
the more formidable grades of cerebral hyperæmia. Many phenomena of
so-called climacteric insanity depend on congestive states. The sudden
closure of an old ulcer or the removal of hemorrhoids in advanced life
has in some well-established instances provoked alarming seizures not
unlike those noted with paretic dementia. The chain of proof
establishing the direct influence of physiological and pathological
discharges on the vascular controlling apparatus of the brain is most
complete. Not alone cumulative clinical observation, but the
occasional happy result of therapeutical procedure based on this
supposed interdependence, support it. Thus, the congestive cerebral
state is recovered from when the menstrual or hemorrhoidal flow is
re-established, or an issue is formed in the nape of the neck, or an
old ulcer is allowed to reopen.[6]

[Footnote 6: The treatment of paretic dementia, particularly of the
congestive type, is also based on this relation. The irritating
antimonial ointment and issues in the nape of the neck, etc. have been
lauded by older observers, and in two of my own cases had the best
results—in one, indeed, with established restitutio ad integrum of now
nearly two years' duration. I am inclined to suppose that its
abandonment is due to an improper selection of cases; in the ordinary
premature senility and syphilitic types such treatment is altogether
ineffective. It is applicable to but a minority of cases at best, and
to them only at an early period. It is probably to a similar form of
congestion that Bouchut refers when (“Les Nèvroses congestives de
l'Encéphale,” _Gazette des Hôpitaux_, 1869) he speaks of a cerebral
hyperæmia developing under the mask of a meningitis—an expression that
may be allowed if understood in the same sense as the comparison
between hydrocephaloid and hydrocephalus.]

The origin of most cases that are brought to the physician's attention
is more or less complicated. A business-man, lawyer, or student
suffering from worry incident to his profession, living so irregularly
as to provoke gastric disturbances, becomes afflicted with insomnia,
and in addition is also constipated. Straining at stool, he finds a
dull, heavy sensation affecting the upper part of his head; attempting
to resume his work, this is aggravated, and after a series of
temporary remissions the condition to be later described becomes
continuous. In such a case the insomnia, usually due to neural
irritability, if not aggravated by an existing dyspepsia, leads to
such a one, and a circulus vitiosus familiar to all physicians is
established. Each of the factors concerned involves strain of the
cerebral vaso-motor apparatus, but none more so than the insomnia. It
is not so much the intensity of the strain as its long duration and
the exhaustion of the centre which in sleep is supposed to be at
comparative rest. This rest is not obtained, and, in conformity to the
laws of neural exhaustion, that centre becomes morbidly irritable.
Now, gastric irritation is competent to produce a reflex influence on
even the healthy cerebral organ; to do so it must be a severe one; but
with the class of persons alluded to the slightest indiscretion in
food or drink is sufficient to set up reflex vertigo or headache. The
current theory regarding these symptoms is that they are due to
stimulation of the vaso-constrictors and ensuing cerebral anæmia; but
the subjects before us will usually be found to flush up instead of
becoming pale, as in simple vertigo a stomacho læso, or if there be
initial paleness, there is a {767} secondary flush, as if the tired
arterial muscle had become exhausted by the effort at obeying the
reflex stimulus. In addition, a profuse perspiration sometimes breaks
out on the upper part of the body.

The influence of traumatic causes and insolation in producing a
tendency to repeated and severe cerebral congestion is recognized,
particularly among alienists. It is supposed that an abnormal
irritability of the vaso-motor apparatus is provoked by these causes.
Abundant evidences are sometimes found in the brains of such persons
of an altered state of nutrition of the brain and its membranes, and
which point in the direction of congestion.

In the conditions thus far alluded to it can be fairly assumed that
the determination of blood to the cerebral blood-vessels is more or
less active. Passive congestion due to impeded return circulation is
of secondary interest, as the primary disease, be it a pertussis or a
laryngeal, cardiac, pulmonary, or surgical condition, will constitute
the main object of recognition and management. Certain
quasi-physiological acts, as coughing, hurried breathing, holding the
breath while straining at stool, and placing the head in a dependent
position while acting in the direction of passive hyperæmia, are to be
considered in connection with the active forms of congestion which
they may momentarily aggravate.

MORBID ANATOMY.—Owing to the non-fatality of the commoner forms of
cerebral hyperæmia, no pathological observations of them are at our
disposal, nor can we assume from analogy that the appearances would be
well marked if they could be made. What little knowledge we have is
derived from a study of more serious conditions of which cerebral
hyperæmia is an initial, collateral, or episodial feature.

In pronounced cerebral hyperæmia the entire brain is, as it were,
tumefied, so that the dura appears tensely stretched over its surface
and the gyri are flattened; both the meningeal vessels proper and
those of the pia are injected. According as the hyperæmia is active or
passive the color of this injection varies, being of a brighter red in
the former, of a purple or bluish color in the latter case. The purest
instances of active cerebral hyperæmia which I have seen were found in
patients dying in the apoplectiform phases of paretic dementia
(progressive paralysis of the insane). Here the cortex on section
exhibited a beautiful rosy tint, which was distributed in darker and
lighter strata in correspondence with the distributional areas of the
short and the long cortical arteries; there were numerous puncta
vasculosa both in the cortex and in the white substance, and in some
instances the arachnoid or the ventricular fluid was tinged with
blood, albeit no vascular rupture could be discovered. The red
blood-corpuscles undoubtedly escape by diapedesis from the surface as
well as the endymal vessels; the same thing occurs in the
intracerebral blood-vessels, whose adventitial spaces are often
crowded with accumulations of red blood-discs, while groups or single
ones are found scattered in the surrounding parenchyma, and even in
the periganglionic spaces. Occasionally accumulations of pigment found
near the vascular channels remain to attest the former existence of
other hyperæmias, and indeed slight accumulations of this kind are
found in the brains of most persons who have reached adult life. These
are to be regarded as remnants of the physiological hyperæmias to
which all active individuals are subject. It is only when the
accumulations become considerable and numerous, as in the chronic
insane, or are associated with those changes in the blood-vessels
{768} which are discussed in the articles on thrombotic and
hemorrhagic cerebral disease, that they can be regarded as indications
of a pathological condition.

Acute simple meningitis is ushered in by cerebral hyperæmia of the
active form. This is not alone demonstrated by the early symptoms of
this disease, but also by the fact, which I have observed in two
cases, that where this form of meningitis originates on one side, as
from extension of the middle-ear trouble, the opposite cerebral
hemisphere exhibited intense congestion of the ideal type.

In that serious form of mental disease known variously as grave or
acute delirium and typhomania (Luther Bell) a form of cerebral
hyperæmia is observed which in its intensity approximates inflammatory
congestion. The surface of the brain appears marbled and mottled;
blood seems to exude from the gyri after the pia is removed; the
cortical lamination is invisible, owing to the hyperæmic discoloration
of the gray substance; and the parenchymatous elements themselves
appear to be in a state of cloudy swelling. In one case I have
observed transudation of a hyaline proteinaceous substance and an
exudation of fibrin around the larger arterioles. In some cases of
typhus fever a less intense but similar congestive hyperæmia is found.
The hyperæmias of paretic dementia, of acute delirium, and of typhus
fever agree in this one feature: that all districts of the brain, from
the cortex and white substance of the cerebral hemispheres to the
medulla oblongata, are involved nearly to the same degree. In the
hyperæmia of simple meningitis of the convexity it is chiefly confined
to the pia mater and the most superficial cortical strata.

Congestion of the brain from stagnation of the venous return
circulation should not be confounded with active hyperæmia. With this
condition, which may be due to thrombosis of the sinuses, morbid
growths near the jugular foramen or in the neck around the internal
jugular veins, or, finally, to certain cardiac and pulmonary
disorders, there is rather a lesser than a greater amount of blood
sent to the brain; and it is not infrequently found that while the
surface of the brain appears congested, owing to the prominence of the
cerebral veins, the deeper parts are quite anæmic; and if the
injection be general, it will be found that the blood, whether in
arteries or veins, has the venous character. An excellent example of
this form of congestion is afforded by persons dying in the status
epilepticus. In their brains the venous channels stand out, filled to
their extreme capacity with blood almost black in color; and in
prepared sections, particularly such as are taken from the pons and
medulla oblongata, a beautiful natural injection of the vessels is
found. But that rosy color which is so characteristic of active
hyperæmia is absent, the tissues appearing purplish, bluish, or
chocolate-colored.

SYMPTOMATOLOGY.—There are few symptoms attributable to the nervous
system which have not been enumerated among the characteristics or the
occasional manifestations of cerebral hyperæmia. Thus, Hammond not
only follows Andral in enumerating apoplectic, convulsive, comatose,
and maniacal symptoms as acute manifestations of active cerebral
congestion, but assures us that aphasia may occur under the same
circumstances. In the course of his work on the subject, “an absolute
want of power to get correct ideas of even simple matters,” confusion
of ideas, weakening of the judgment, vacillation of purpose,
diminished logical power, {769} illusions and hallucinations of every
sense, delusions, morbid apprehension of impending evil, imperative,
suicidal, and other impulses, suspicion, hypochondriasis, furious
delirium, and the use of profane and obscene language, are enumerated
among the characteristic or prominent symptoms of various forms and
cases of cerebral hyperæmia.[7] Not one but several of the recognized
forms of insanity have yielded a fair quota of their symptoms to this
long array. Among somatic signs he in like manner names neuralgic
pains, numbness, spasms, paralysis, false impotence, hyperæmia of the
tympanum, choked disc, abolition or perversion of the sense of smell,
taste, and sight, fibrillary or fascicular twitches, various states of
the urinary excretions, diplopia, and monoplegias. It is here equally
evident that the initial symptoms of a considerable number of organic
and clearly defined affections have been included. It is on account of
the confusion engendered by this wide interpretation of the meaning of
the term congestion of the brain that I have determined to limit the
term as previously indicated, and to consider only the active form
here.

[Footnote 7: _A Treatise on the Diseases of the Nervous System_, 7th
ed., pp. 1-53. The natural inference following a perusal of this
chapter, as well as the monographs to which their author refers, is
that he has gathered together all states in which cerebral hyperæmia
was an associated factor, as well as those in which he appears to
assume its existence on theoretical grounds, and designated them as
cerebral congestion. In some instances he uses the terms hypochondria
and cerebral hyperæmia interchangeably (p. 50, _loc. cit._).]

A feeling of head-pressure, associated with a more or less severe dull
pain, aggravated by mental exertion, by stooping down, by straining at
stool, or when out of breath, and accompanied by a subjective sense of
mental dulness, is the most constant feature of the ordinary cases.
There is usually a vertiginous sensation, and an irritability of the
eye and ear not unlike that described in the article on Cerebral
Anæmia. Sleep is at first disturbed by vivid and sometimes frightful
dreams; later, it becomes interrupted, and ultimately complete
insomnia may develop. The action of the heart is accelerated and
exaggerated in some cases; in that event increased pulsation of the
carotids, flushing of the face, injection of the conjunctiva, and a
subjective sense of heat in the head and face are experienced.
Hammond, in accord with Hasse and Krishaber, believes that febrile
symptoms may develop under these circumstances; most authorities,
however, deny this for the uncomplicated form. I have never found an
objective rise of the general temperature.

Such a condition as that described is usually slowly produced, several
weeks, or even months, being occupied in its development. At first the
unpleasant symptoms occur only at certain hours of the day, with
temporary exacerbations and remissions. It may be arrested with
comparative ease at any time; if neglected, the mental faculties
become affected, not in the grave sense in which Hammond and the older
authors describe it, so as to carry the patient into actual dementia
or delusional insanity, but rather in the way of diminished
working-power. It is more difficult to fix attention, to recollect
words, names, and figures, or to keep up a protracted mental effort,
than in health, but the formal judgment does not suffer. I have known
patients to be in this condition for many months, and several for more
than one year, without any grave deterioration. It is true that in the
prodromal periods of some forms of insanity, such as acute mania,
there is a condition very similar to that of these patients; {770} and
this has led to regarding mania as a possible phase of cerebral
hyperæmia. But the very fact that, typically, mania is preceded by
such a stage—which is always of brief duration—that maniacal
excitement is a constant and unavoidable consequence upon it, while,
as far as known, the condition here described may last for years
without leading to a true psychosis, should prevent one regarding the
two conditions as identical, however similar they may be for the time
being.

In sufferers from cerebral hyperæmia who pass into the chronic state
of this disorder the disturbance of sleep and of the digestive organs
becomes very prominent, and continually reinforces the acting causes
of the disorder. In a large number of cases the head-sensations become
more or less localized; that is, while the general feeling of pressure
or dull ache may continue, a special area, which can be covered by the
palm of one hand, either in the middle part or to one side—usually the
left—of that part of the vertex, is the seat of a more severe pain,
complained of as a hot pressure. The patients frequently claim that
the temperature is higher at this spot, and, contrary to what might be
anticipated on a priori grounds, the statement will be confirmed, not
alone by the coarse method of using the hand, but by the surface
thermometer. The locality where this occasional rise of temperature
and the more common sense of pressure are experienced corresponds to
that part of the longitudinal sinus where the largest cerebral veins
enter. It is a noteworthy fact that nearly all the important
admunctories of this sinus empty into it within the short space of two
inches at this point.

Not all sufferers from cerebral hyperæmia give a history of a gradual
development of their symptoms. A few date their trouble from some
single intellectual, physical, or emotional strain. In one case,
complicated by marked evidences of cerebro-spinal exhaustion, the
patient, a lady, had during an illness of her husband, being deserted
by her servants, and the water-supply having been cut off, carried all
the water required for the invalid and domestic as well as sanitary
purposes up three flights of stairs for two unusually hot days in
July. In two others, strikingly similar in many details of their
cases, both being cornet-players, both attributing their illness to an
extra call upon their instrument, it was brought on in the older
patient within a few hours after playing on a hot day at the State
Camp at Peekskill, and in the second at Narragansett Pier as he left
the sultry concert-room and became exposed to a draught. In both these
cases, as in a large number since examined, some stomach trouble could
be positively determined to have antedated these symptoms. I mention
this because it is only in such cases that I have found the nausea or
vomiting which some writers regard as an occasional occurrence of, and
due to, the lighter form of cerebral hyperæmia.

There are no ophthalmoscopic evidences of cerebral hyperæmia of this
form. I have never found the optic disc presenting variations in tint
beyond those found within normal limits, except in a case of saturnine
encephalopathy with predominant signs of cerebral congestion. I
believe that the statement of Hammond[8] as to the existence of choked
disc in cerebral hyperæmia is generally regarded as due to the
interpretation of organic diseases as congestive states. It is not
confirmed by authorities.

[Footnote 8: _Loc. cit._, p. 41, lines 29-36.]

I have never found the tympanic membrane hyperæmic independently {771}
of ear disease, even when tinnitus was marked. It is claimed to exist
by Hammond, and he adduces as analogous the observation of Roosa that
quinine produces an injection around the handle of the malleus.[9]

[Footnote 9: It certainly is not necessary to look to the injection of
the tympanum as an explanation for the tinnitus of cerebral hyperæmia,
based on such an analogy. The tinnitus of cinchonism is more central
in location, being producible in persons who have pathological or no
tympanic membranes, just as the tinnitus of cerebral hyperæmia occurs
indifferently under like circumstances.]

The congestive states which follow traumatism and insolation are
properly considered in connection with the traumatic neuroses and
certain forms of insanity. But there are some milder cases in which
the symptoms remain within such compass as is comprised in this
section. The patient, after a fall or a blow on the head, suffers from
insomnia, has a sensation of fulness and ache in the head, complains
of a pulsating feeling in the occipital region and an inability to
concentrate his thoughts on subjects which previously were parts of
his routine. Under appropriate treatment recovery ensues, but there
remains behind an intolerance of alcoholic beverages, and at times the
patient experiences momentary fits of abstraction, which may be
regarded as mild analogies of the more serious episodes of the
full-blown traumatic neurosis. Thus, he may be walking along the
street and suddenly lose his train of thought for an instant, to
regain it on observing that he has inadvertently made a misstep. Or in
the midst of an address a previously fluent orator in attempting to
find a certain by-law in the rules of a society is unable to recollect
which he was in search of, and is compelled to take his seat with a
rambling apology. But for the fact that similar sequelæ are noted in
cerebral hyperæmia from other causes, it would be questionable whether
it be proper to attribute them to the congestive element engendered by
the traumatic influence. They are usually noted when the hyperæmic
phenomena proper have become latent or disappear, and, with other
symptoms customarily treated of as mere results of circulatory
trouble, may be regarded as signs of neural exhaustion or inadequacy
rather than of insufficient ensanguination.

A more serious form of cerebral hyperæmia occurs in females in
conjunction with the climacteric period, and in both sexes in
consequences of the suppression of any habitual discharge in advanced,
and exceptionally in middle and juvenile, life. The advent of the
symptoms is rapid, a few hours or days sufficing for the development
of the attack. The face is flushed, the carotids throb violently, the
general cutaneous surface is congested, and the patient is
incoherently talkative. The one side, usually the right, is heavy and
tremulous, the fingers are devoid of their usual skill, and the speech
is more or less thick. The sleep is disturbed or replaced by a
stuporous condition, whose similitude to an apoplectiform seizure is
sometimes heightened by stertorous breathing. After one or several
days the patient emerges from this condition by degrees or suddenly
with complete restitutio ad integrum. But the attack may recur, and
ultimately it is noted in the event of repeated attacks that the
return to the normal state is slower and less complete: the disorder
then undergoes a transition into the congestive type of paretic
dementia described in another portion of this volume.

DIFFERENTIAL DIAGNOSIS.—In some of its clinical aspects cerebral
hyperæmia closely resembles cerebral anæmia. This is not surprising
{772} when we bear in mind that both constitute nutritive disturbances
of the same organ, and that, notwithstanding the apparent difference
in the surface injection of an anæmic and a hyperæmic brain, the state
of affairs in the ultimate capillary districts may be much more alike
than might be anticipated on theoretical grounds. In congestion we
have wider vessels, and perhaps, though not necessarily, a better
quality of blood; but at the same time the intracranial pressure may
be such that the venous emunctories can labor but slowly: the result
will be that although there is more blood in the brain, the lessened
rate of flow places the nerve-elements under nearly the same nutritive
disadvantage that they are placed under with the narrower and vitiated
but more rapid blood-column of ordinary anæmia.[10] It is particularly
the symptoms dependent on those nerve-centres and tracts which are, so
to speak, dynamically sensitive, which resemble each other so much
that an intrinsic difference—both being placed side by side—is not
always determinable. This is true of the aural and optic symptoms.
Tinnitus, photophobia, scotomata, and blurring or darkening of the
visual field occur in both, and in about the same varieties. In my
experience the acuteness of hearing is more apt to be interfered with
by the subjective sounds with hyperæmic than with anæmic tinnitus. The
scotomata of hyperæmia are more distinct and coarser than those of
anæmia; darkening of the visual field is more apt to occur with sudden
rising in anæmia, while in hyperæmia it is provoked by coughing,
straining at stool, or other cause operating directly or indirectly on
the return circulation. It may be stated, as a general rule, that if
any of these symptoms are aggravated on lying down or stooping, they
are due to hyperæmia; while if the same procedures are resorted to in
anæmia, amelioration ensues. But in many chronic cases these symptoms
seem to continue as indications of a permanently altered activity of
the nerve-elements themselves; that is, as a sort of pathological
habit. In that case the position test may not be decisive. In one
respect there is a decided difference between the anæmic and hyperæmic
forms; there is never amaurosis in the latter, while it is approached,
and occasionally fully developed, in the former. Much more importance
attaches to the differentiation of tinnitus due to nutritive brain
disorders and that due to aural disease. As a rule, the tinnitus from
cerebral hyperæmia is symmetrical; if unilateral, it is of short
duration. The procedure of Valsalva[11] aggravates the tinnitus of
hyperæmia, and relieves that which is due to the commoner forms of ear
disease; the former is aggravated and the latter relieved by noise.

[Footnote 10: It is also admitted that the blood stagnating in the
larger veins and accumulating in the arteries, the limits of
compressibility of the other cerebral contents being passed, the
capillaries will suffer, so that with injected and turgescent
arterioles and venules there may be capillary anæmia.]

[Footnote 11: I would caution against Politzer's method in cases of
ear disease coexisting with cerebral congestion. In a patient now
under my treatment each session at the aurist's was followed by a
distinct exacerbation of the cerebral symptoms.]

In the table on p. 773 I have attempted to formulate the principal
differential relations of the protracted forms of cerebral anæmia and
hyperæmia.

There are a number of so-called functional nervous states which, aside
from the fact that they are unwarrantably confounded with cerebral
congestion, do not require mention in a differential relation. Such
are the {773} masturbatory neurosis, certain hysterical states, and
the asthenia resulting from nervous shock and overwork. These states
have found a provisional resting-place under the comprehensive and
non-committing title of neurasthenia or nervous exhaustion—a term
which includes conditions fully recognized by Robert Whytt and
Isenflamm in the last century.

  --------------------+----------------------+------------------------
  Symptomatic State.  | In Cerebral Anæmia.  | In Cerebral Hyperæmia.
  --------------------+----------------------+------------------------
  Pupils.             | Usually dilated and  | Usually small or
                      | mobile.              | medium.
  --------------------+----------------------+------------------------
  Respiration.        | Often interrupted by | Normal.
                      | sighing or by a deep |
                      | breath, even when at |
                      | rest.                |
  --------------------+----------------------+------------------------
  Headache.           | Either sharp and     | If localized,
                      | agonizing, and then  | accompanied by a
                      | in a limited area,   | subjective and
                      | or a general dull    | objective (always?)
                      | ache, intensified in | feeling of heat; if
                      | the temples and over | general, is compared to
                      | or behind the eyes.  | a bursting or steady
                      |                      | pressure.
  --------------------+----------------------+------------------------
  Activity.           | There is lassitude.  | There is indisposition
                      |                      | to exertion, yet
                      |                      | patient is restless.
  --------------------+----------------------+------------------------
  Temperament.        | Lethargic, with      | Choleric, with
                      | exceptions.          | exceptions.
  --------------------+----------------------+------------------------
  Intellect.          | Inability to exert.  | Rather confusion than
                      |                      | inability of.
  --------------------+----------------------+------------------------
  Sleep.              | Insomnia, interrupted| Insomnia, with great
                      | by trance-like       | restlessness,
                      | conditions, in which | variegated by
                      | the patient is       | unpleasant and confused
                      | comparatively        | dreams.
                      | comfortable. Dreams  |
                      | often pleasant.      |
  --------------------+----------------------+------------------------
  Influence of        | Aggravates all the   | Either without
  upright position    | symptoms.            | influence or
  of body.            |                      | beneficial.
  --------------------+----------------------+------------------------
  Influence of        | Amelioration.        | Aggravation.
  recumbent position  |                      |
  of body and         |                      |
  dependent position  |                      |
  of head.            |                      |
  --------------------+----------------------+------------------------
  Influence of acts   | If any, a sharp      | Aggravated.
  involving deep      | headache may ensue,  |
  inspiration, such   | but the other        |
  as blowing,         | symptoms are not     |
  straining at stool, | aggravated.          |
  sneezing, etc.      |                      |
  --------------------+----------------------+------------------------

TREATMENT.—Ergot of rye with its preparations may be regarded as the
cardinal drug in cerebral hyperæmia. There are few drugs in the domain
of neurological therapeutics which are so directly antithetical to the
pathological state as this one. There is scarcely a case of cerebral
hyperæmia that is brought to the physician's attention but may be
regarded as being in part due to an over-distension of the cerebral
vascular tubes. This is directly overcome by ergot, and the quantity
which such patients will sometimes bear without showing signs of
ergotism is something remarkable, in notable contrast with the
subjects of cerebral anæmia, who are usually very sensitive to it.
About three grains of Bonjean's ergotin may be regarded as a safe
trial-dose for an adult, and unless a distinct effect is produced
within two or three days this dose may be raised to six grains twice
or three times within twenty-four hours. It is not advisable to
combine strychnia with the ergotin, as is often done; the effect of
that alkaloid is to increase the psychical and sensorial irritability
of the patient. Chloral hydrate or bromide, or both in combination, is
as useful an adjuvant here as it would be hurtful in cerebral anæmia.

It is not usually necessary to employ special hypnotics in cerebral
congestion. The same drug whose beneficial effect is so potently
marked during the daytime that tinnitus, cerebral pressure, and
subjective drowsiness will disappear before it, if not as rapidly,
more enduringly, than the symptoms of cerebral anæmia disappear before
nitrate of amyl, will also overcome the insomnia in the majority of
cases. Where it fails, warm pediluvia or sitz-baths will prove more
efficient than the majority of hypnotics. Their use, at all events,
involves no hurtful effect on a—possible already—disordered stomach,
and their certainty of action is {774} much more even. Their
temperature should be about 40-42° Centigrade, and the immersion
continue from fifteen to twenty-five minutes.[12]

[Footnote 12: A number of experiments, the most recent of which were
by Musso and Bergesio (_Rivista sperimentale di Freniatria e di
Medicina legale_, 1885, xi. p. 124), have shown that in such baths the
cerebral pulsations become less excursive and that the volume of the
brain decreases. The same applies to general warm baths.]

In those cases where the subject sensations accompanying hyperæmia,
active or passive, are intensified in the posterior segment of the
head or the nuchal region, leeches at the mastoid process, or cupping,
wet or dry according to the severity of the symptoms, will often give
immediate relief. Burning with the actual cautery, or, what is
equivalent and a much neater application, the heated glass rod, has an
equally happy effect in that class of cases where throbbing and pain
are intensified low down. It should be done as near the spot indicated
by the patient's complaints as possible.[13]

[Footnote 13: In a case of gliomatous hypertrophy of the pons
oblongata transition marked by the development of numerous tortuous
and enlarged blood-vessels the episodes of the disease were found to
be of the congestive type, and yielded to no other treatment than that
with the cautery.]

The diet of patients who are suffering from or subject to cerebral
hyperæmia should not be stimulating nor difficult of digestion. It is
much more important to avoid distension or overstrain of the stomach
than to reduce the nutritive value of the food in the majority of
cases, for true plethora is much less common than is supposed. The
bowels should be so regulated that the patient have at least one, and
that an easy, movement a day. The saline cathartics, particularly the
Carlsbad salt, are to be used to effect this if necessary. The
clothing around the neck should be free and not compress the parts.

In those severe forms of cerebral congestion attending the climacteric
period, or occurring in consequence of the suppression of discharges,
and similar causes, the symptoms are often so alarming as to render
energetic measures, such as bleeding, immediately necessary. This may
be affected by applying leeches to the nose, the temples, or by
bleeding at the arm. If due to the suppression of hemorrhoidal
discharges or menstruation, the leeches should be applied to the anus
and hot sitz-baths taken. In the milder forms a pill composed of
aloes, podophyllin, and ox-gall, recommended by Schroeder van der
Kolk, will be found effective.


Cerebral Anæmia.

The oft-confirmed observation of Treviranus, that the brain is paler
in the sleeping than in the waking state, supplemented as it has been
by more elaborate observations, which show that the difference between
the intracranial blood-amounts, as estimated in these opposite states,
is equivalent to one-twenty-fourth part of the total blood-amount of
the body, has been made the basis of much dazzling theory and
premature speculation. Hyperæmia of the central nervous apparatus or
of certain of its provinces becomes regarded as synonymous with
over-activity, and anæmia, general or provincial, as the expression of
the opposite functional state. Elaborate directions may be found, even
in recent treatises on the subject, how to diagnose, not alone
hyperæmia and anæmia of the brain {775} and spinal cord, but also of
special lobes of the former and particular columns of the latter.
These directions are in most instances based on assumptions which are
not supported by direct or tangible evidence, and the consequence is
that they have failed to stand the tests of experience, where this
gauge is applicable, and necessarily failed to advance in any way
either our theoretical or practical knowledge of those states of the
brain mechanism which are due to alterations in its nutrition.

Much of the unsatisfactory state of our knowledge on this head is due
to the grouping together of the physiological anæmia of sleep and the
pathological anæmia with which the physician has to deal. The anæmia
of the brain in a sleeping person is probably a secondary factor; it
ensues after the person falls asleep, the first step in the latter
process being probably an altered dynamic state of the brain which
lessens the requirements of that organ for blood. This can be readily
demonstrated in the case of infants whose anterior fontanelle has not
yet closed. In deep sleep the fontanelle is deeply sunken in, but this
sinking in does not occur simultaneously with the child's falling
asleep, but shortly thereafter. On the other hand, the fontanelle does
not rise simultaneously with the child's awakening, unless it cry,
which adds a disturbing factor. There are a number of other facts
which show that while a comparison between the sleeping state and
cerebral anæmia may be made for the purposes of theoretical
discussion, yet there are many important points in which they are at
variance. To illustrate this I need but refer to the fact that in deep
sleep the pupils are in a state of immobility and pinhole
contraction,[14] while in chronic cerebral anæmia of young persons a
dilated and mobile pupil is the commoner condition. In
acutely-produced cerebral anæmia an initial contraction has been
noted, but it is not then persistent.

[Footnote 14: Inability to counterfeit this feature is one of the most
reliable tests of simulation, and served to convince me that in the
well-known case of a colored cadet, who was tried by a court-martial
on charges involving simulation, the latter was proven. There are
persons who can voluntarily contract the pupils, but as they are
compelled to innervate all the muscles supplied by the third pair, in
so doing they are compelled to converge the optic axes—an act which
does not take place in sleep.]

One of the main reasons of our imperfect knowledge of the nutritive
disorders of the brain is the unsatisfactory state of their
post-mortem evidence. Little has been learned in this field, except in
those extreme cases where the suddenness and intensity of the
circulatory catastrophe were sufficient to prove fatal. Even where all
observations made during life justify us in supposing that the amount
of blood sent to the brain is small, that the velocity of its current
is reduced, and its quantity poor, the autopsy may reveal conditions
apparently conflicting with the supposition based on ante-mortem
observations. This is amply illustrated by the experience of alienists
who have studied the relation between nutritive states of the brain
and certain forms of insanity. It is generally held that in so far as
the antithetical forms of mental disorder known as anæmia and
melancholia can be connected with nutritive disorders, the former is
indicative of hyperæmia and the latter of anæmia. A number of facts
can be adduced in support of this view, particularly as regards the
latter condition. It is found, however, in some examinations made of
the brains of patients dying melancholic that the brain is apparently
hyperæmic; the length of time elapsing before an autopsy is made, the
form of somatic disease with which the patient dies, the position of
the {776} body after death,—all these may play a part in the
production of cerebral injections which do not correctly indicate the
condition of the brain as it existed prior to the moribund period, and
when the symptoms of supposed anæmia or hyperæmia could be
satisfactorily differentiated.

ETIOLOGY.—The best studied form of cerebral anæmia is that ensuing
after extensive hemorrhages or from compression and ligature of either
of the common carotid arteries.[15] In the latter case symptoms are
produced which are in harmony with the doctrine of localization, and
permit us to form a conception of the mode in which a diminution of
the cerebral blood-supply influences the functions of the brain. The
chief symptoms are noted on the side of the body opposite to that on
which the common carotid artery is tied. Thus if the left artery be
tied, there is at first felt a tingling or pricking feeling on the
right half of the body; this is followed by a warm, sometimes a cold,
and ultimately by a numb, feeling. This sensory disturbance may become
of what might be called the capsular type—that is, a complete
hemianæsthesia; but at first it is distinctly like that which is found
with cortical and subcortical disease, being limited to the muscular
sense and the intelligent contact-perceptions of objects, the
æsthesiometer showing but little or no impairment of the cutaneous
space-sense. With the loss of muscular sense the movements become
heavy, and later true paresis may appear with perhaps total
anæsthesia. Aphasia is sometimes noted in such cases, and, in
obedience to the predominant location of the speech-faculty in the
left side of the brain, is rarely if ever found[16] when the right
common carotid artery is the one ligated.

[Footnote 15: As the conditions of the cerebral circulation resulting
from surgical and other rare causes are not apt to be brought to the
physician's attention separately from conditions of more immediate
importance, their symptoms are discussed in the etiological portion of
this section in order to avoid complicating the semeiological picture
of cerebral anæmia of every-day experience. For similar reasons the
anomalies of the cerebral circulation of an embolic and thrombotic
nature, and those associated with eclampsia and epilepsy, are not
mentioned in this connection, as their full discussion properly
belongs to other portions of this work.]

[Footnote 16: I am unaware of the record of any case where aphasia
occurred with ligature of the right common carotid artery. There is a
singular observation by Hagen-Torn of permanent paralysis of the right
hypoglossal nerve after such an operation, but the report to which I
have access does not state whether this may not have been due to some
peripheral involvement of that nerve.]

In this series of symptomatic sequelæ it is seen that the functional
manifestations of the highest centres are the first to be involved,
and this establishes that of all parts of the cerebrum the cortex and
subcortical tracts are the more vulnerable to the influence of a
deficient blood-supply.[17] As we shall see, it is precisely to the
insufficient nutrition of these parts that the more important symptoms
of the cerebral anæmia of ordinary practice are attributable.

[Footnote 17: To this there is an apparent exception: when blindness
occurs in consequence of ligature of one carotid artery, it is
monocular and limited to the side of the ligation. The visual
disturbance of cortical and subcortical disease is bilateral, being of
the character known as hemianopsic. The blindness due to tying of the
carotid is, however, not due to cerebral, but to retinal, anæmia, and
its monocular character does not therefore invalidate the observation
in the text. Litten and Hirschberg (_Berliner klinische Wochenshrift_,
1885, No. 20) found complete bilateral amaurosis in a chlorotic girl
of fifteen, and on ophthalmoscopic examination the peripheral origin
of the blindness was conclusively proven by the existence of an
exquisite choked disc. Both the morbid ophthalmoscopic appearance and
the amaurosis disappeared under tonic regimen. It is well to recollect
that choked disc may occur in chlorosis, and thus be perhaps
erroneously attributed to a coexisting hysteria, as was done in some
cases at least by Rosenthal in his textbook.]

{777} With bilateral ligature[18] of the primary carotids—and this
applies in the main to cerebral anæmia from profuse hemorrhages or
sudden changes in the blood-pressure, such as occur in enteric
affections, ruptures of aneurisms, in obstetric practice, and after
brusque tapping for ascites—the same phenomena noted with unilateral
compression are observed on both sides of the body, and usually in
slighter intensity. In addition, there is a profound and
characteristic disturbance of respiration; a cold sweat breaks out;
the senses of sight and hearing become greatly impaired or perverted;
the mind becomes clouded, consciousness blurred; complete syncope may
ensue, and pass to a fatal termination. In other cases vertigo
preponderates or vomiting, and finally convulsions appear. It would
seem that the respiratory centre exceeds even the cortex in
susceptibility to the evil influence of anæmia. It differs from them
in two features: firstly, it appears to require bilateral involvement
of the brain for its production; secondly, although the respiratory
disturbance precedes that of the higher cerebral functions, it does
not become as intense, for at a time when the intellectual functions
are abolished, as in anæmic coma and syncope, the respiratory
function, however disturbed, is in most cases sufficiently well
carried on to bear the organism safely through the crisis. The
disturbance is marked by the following characters: The respiration is
at first deep and sighing, perhaps frequent; it later becomes slow,
and is associated with a subjective sense of oppression; the patient
feels as if he could not fill his lungs properly; there is an
unsatisfied sensation, as if a deeper breath should be taken, and
when, in obedience to this subjective need, a full deep breath is
taken, the patient feels as if he had stopped short of completing the
act, and remains as unsatisfied as before.[19] Yawning and moaning are
often accompaniments of this symptom.[20] As we shall see, these signs
are often among the chief sources of complaint in the less grave forms
of anæmia of every-day experience. In the serious condition before us
the Cheyne-Stokes phenomena may follow.

[Footnote 18: I exclude the observations of Flemming, Hammond, and
Corning on carotid compression by external pressure, owing to the
difficulty of determining whether or no, and what, other important
structures are compressed at the same time.]

[Footnote 19: The occurrence of this functional respiratory trouble is
a feature of toxic as well as of anæmic irritation of the respiratory
centre; it is accordingly found in cases of profound alcoholic
poisoning.]

[Footnote 20: It is somewhat difficult to understand why in cases of
anæmia induced in both carotid districts the symptoms of anæmia should
be marked in the functions of that part of the brain-axis which
through the basilar trunk derives its blood from the vertebral
arteries. Here the blood-current must necessarily be increased. That
the disturbance of breathing, the yawning, and the sighing belong to
the group of irritative symptoms due to anæmia is in harmony with the
general physiological law which is illustrated in the initial
contraction of the pupil, which is found in experimental cerebral
anæmia. Observations on anæmia of the brain-axis are too few, and, so
far as noted, have been so rapidly fatal that it is not possible to
derive from them any facts bearing on the physiological reactions of
the respiratory centre to high-graded anæmia. One of the curiosities
of medicine appertaining to this subject is the observation recorded
in _Virchow's Archiv_, lxix. p. 93, of the case of a man who had
fractured the base of the skull in its posterior fossa, and, the
basilar artery becoming caught and pinched in the crack, death
occurred rapidly with all the signs of cerebral anæmia, verified by
the post-mortem appearances.]

Anæmia of the brain may develop at any period of life, not excluding
the intra-uterine period. Kundrat and Binswanger regard the deformity
of the brain known as porencephaly as the result of an anæmic
(non-embolic) necrosis of brain-substance, developed either in the
fœtal or the {778} infantile period. The occasional symmetry of the
deformity is in favor of this view. That there are other conditions of
cerebral malnutrition,[21] masking themselves in defective development
and imperfect isolation of the conducting tracts, and that the
consequent differing rate of maturation of these tracts has some
relation to the absence or presence of a predisposition to chorea and
other disturbances of nervous equilibrium so common at this period of
life, I regard as at least probable. But it is at the period of
puberty that we encounter the most important discrepancies between the
requirements of brain-nutrition and the furnished blood-supply. The
disposition to uncomplicated cerebral anæmia is greatest at this
period of life and in the female sex. Beneke[22] has shown that as the
human being grows the arteries, which in children are very large in
proportion to the length of the body, get to be relatively smaller and
smaller toward the period of puberty—that after this period they widen
to again attain a large circumference at old age. There is thus added
to the other and more obscure factors which may determine general
anæmia at puberty a diminished calibre of the arteries in both sexes.
To some extent the disadvantageous influence of (relatively) narrow
vascular channels may be overcome by increased cardiac action, and the
almost sudden increase in size of the heart about this period is
probably the result of the demand made upon its compensatory power.
But, as we learn from the same observer that the female heart remains
relatively as well as absolutely smaller than that of the male, we can
understand why the female should be less able to overcome the
pubescent disposition to cerebral (and general) anæmia than the male.
Menstruation, which in a certain proportion of girls scarcely
maintains the semblance of a physiological process, acting rather as a
drain than a functional discharge, is added to the anæmia-producing
factors. It is among those who marry in the ensuing condition, who
bring forth child after child in rapid succession, perhaps, in
addition, flooding considerably at each confinement, that we find the
classical symptoms of chronic cerebral anæmia developed.

[Footnote 21: I have found in three children under fourteen months of
age, who died with symptoms not unlike those of slowly-developed
tubercular meningitis, including convulsions, strabismus, temperature
disturbance (slight), and terminal coma, without nuchal contracture or
pupillary anomalies, a remarkably anæmic brain. The sulci gaped; there
were few or no puncta vasculosa; the cortex extremely pale, and the
white substance almost bluish-white. On attempting to harden the brain
of the youngest of these children, using every precaution and a
sufficient number of sets of hardening fluids, including the chromic
salts and alcohol, I found that small cavities formed in the cortex,
varying from the scarcely visible to two-thirds of a millimeter in
diameter. Their existence were demonstrable the day after the death
and almost immediate autopsy performed in this case. There had been no
antecedent disease in any one of these cases; the children had been
lethargic, inactive, and the oldest had made no attempt to walk or
talk. There was no morphological or quantitative defect in cerebral or
cranial development, and microscopic examination showed that the
cavities were not perivascular. In all these cases the patients
belonged to the tenement-house population.]

[Footnote 22: An excellent abstract of Beneke's original monograph, by
N. A. P. Bowditch, will be found in volume i. _Transactions of the
Massachusetts Medico-Legal Society_.]

In the male sex the period of adolescence has not the same profound
influence in producing cerebral anæmia that it has in females. To some
extent, however, habitual self-abuse and early sexual excess of the
former produce results similar to those occurring in consequence of
perverted physiological processes in the latter. Many of the symptoms
presented by the inveterate masturbator are probably due to cerebral
anæmia; there {779} are, however, in his case and in that of the early
libertine certain vaso-motor complications frequently present which
render the clinical picture a mixed one.[23] In addition, abuse of the
sexual apparatus has a direct—probably dynamic and
impalpable—exhausting effect on the central nervous apparatus.

[Footnote 23: Kiernan of Chicago has described peculiar trophic
disturbances—dermato-neuroses, color-changes of the hair, etc.—in a
case of masturbatory mental trouble associated with marked anæmia. The
patient whenever he flushed up heard a noise as of a pistol snapped
near the mastoid region. In the case of a young man of eighteen
who—the pampered son of wealthy parents—became his own master at
fifteen, and had at that age indulged in sexual orgies which were
continued to an almost incredible extent, it was found that he
gradually lost his memory, and on one occasion had a violent
epileptiform attack. During his convalescence from the stuporous state
which followed it was noted that the patient was quite bright in the
morning, but that after he had been up a while he relapsed into a
state of apathy, with amnesia, which, decreasing in intensity from
week to week, was eventually only noted toward evening, and finally
disappeared, the case terminating in complete recovery.]

In the vast majority of cases anæmia of the brain is but a part of
general anæmia, and all conditions which tend to impoverish the
character of the blood and to reduce the rapidity of movement and
fulness of the cerebral blood-column are apt to be associated with
signs of cerebral malnutrition. As early an observer as Addison
noticed the wandering of the mind in pernicious anæmia, in which
disorder anæmia and wasting of the brain have been found post-mortem.
In two cases of extreme chlorosis I heard the sound known as the
cephalic soufflé with great distinctness;[24] this sound, when the
other morbid conditions that may lead to it can be excluded, indicates
a high degree of anæmia. Both patients were somnolent and subject to
fainting-spells. In leucocythæmia a rambling delirium is not
infrequently noted toward the close of the patient's life, and the
habitual sadness and depression of many leukæmic patients is due, as
are also certain phases of melancholia, to cerebral malnutrition. In
some stages of most, and in all stages of some, forms of renal disease
the conditions of cerebral anæmia are present; and it is reasonable to
attribute to it some share in the production of the head symptoms of
Bright's disease; but here, as in cases of cardiac disease, symptoms
due to other influences—uræmia in the former, and insufficient
oxygenation of the blood in the latter instance—obscure or conceal
those due to the anæmia strictly speaking.

[Footnote 24: When an anæmic murmur at the base of the heart coexists
with the cephalic soufflé, the latter may be regarded as an evidence
of anæmia; but where the former is absent—that is, when the cephalic
soufflé is an isolated, independent symptom—there is reason to suspect
the existence of a tumor or some other cause of compression of the
carotid artery at or after its entry into the cranium. In one of the
cases referred to in the text, pressing on one or the other carotid
produced numbness and tingling in the opposite arm, leg, and cheek.
Similar observations were made by Tripier (_Revue de Médecine_, March,
1881), who strenuously maintains the existence of the cephalic soufflé
in the adult, against Henry Roger, and in consonance with the
observations of Fisher and Whitney. In the last-mentioned case of mine
the sound could be heard a distance from the head.]

All exhausting diseases, many febrile affections, notably typhoid,
starvation from any cause, and exhausting discharges, may produce
cerebral anæmia. Under the latter head belong the diarrhœal affections
of childhood, which not infrequently lead to an aggravated form of
anæmia of the brain known as hydrocephaloid. In addition to the
provoking causes of cerebral anæmia there are certain accessory ones:
prominent among these is the upright position and sudden rising. The
reason of this influence is self-evident, as is also the fact that it
is most apt to manifest {780} itself in cases of cardiac enfeeblement.
Many a convalescent from an exhausting fever or other disease has on
rising from bed fainted; some have fallen dead from cerebral anæmia
already existing, but fatally intensified by this sudden change of
position. A number of cases are on record by Abercrombie, Forbes
Winslow, J. G. Kiernan, and others where persons manifested the
symptoms of cerebral anæmia only when in the upright position and even
in lying on one side or the other; these are, however, far rarer than
is claimed by some later writers.

The purest form of acute cerebral anæmia, aside from that produced by
surgical interference with the cerebral circulation or extensive
hemorrhages, is that induced by mental influences, such as fright, a
disagreeable odor, or a disgusting or harrowing spectacle. Some
persons, not suffering from general anæmia or any diseased condition
thus far mentioned, on experiencing the emotional influences named
will be observed to turn pale, to breathe heavily, and either sink
into a chair or fall on the floor partly or entirely unconscious. They
are then suffering from a spasm of the cerebral arteries resulting in
acute and high-graded cerebral anæmia or syncope. This condition is
marked by some of the symptoms previously mentioned as occurring with
bilateral ligature of the carotids: thus, the feeling of oppression on
the chest, vertigo, heaviness of the limbs, nausea, and vomiting are
characteristic; a cold sweat breaks out on the forehead; the visual
field becomes darkened; and hearing is rendered difficult by the
tinnitus.[25] The pulse is small and of low tension, but regular.

[Footnote 25: Most authors claim that the sense of hearing is blunted,
as that of vision is. This is so in some, but certainly not in a large
number of other cases. I have now under observation a girl whose
physical conformation—her neck is very long and her shoulders
tapering—and extreme susceptibility combine to favor the occurrence of
syncope. She faints in my office whenever an examination is made, even
though it be entirely verbal; and after recovering frequently lies
down to answer by deputy, as experience has shown her that she is less
likely to faint in this position. I have repeatedly satisfied myself
from her subsequent statements that she heard what was said, while she
appeared to be quite unconscious and “saw everything black or through
a cloud.” It is not improbable that the impressions which most writers
on the subject convey were derived from the experience of novices in
fainting; these, in the alarm and anxiety of their condition, and
confused by the tinnitus, might well fail to hear what the bystanders
said, particularly as on many such occasions the fainting person is
apt to be surrounded by a confused Babel of tongues. While the
auditory nerve is as sensitive to the irritative influence of anæmia
as any, and there is a case of a boy on record (Abercrombie) who could
only hear well when lying down, and was deaf when he stood up, yet the
conclusions of other authorities who have studied the subject would
lead one to think that there are individual differences in this
respect. How often does not the dying person, after feeling for the
hands of a relative whom he cannot see, converse with him
responsively! And how much need is there not of the humane physician
to remember that the sense of hearing is the last intellectual sense
to die, lest he speak unguardedly at the bedside!]

As a rule, the subjects of simple syncope recover, the horizontal
position, which is assumed perforce in most cases, carrying with it
the chief remedial influence—namely, the facilitating of the access of
a fuller blood-supply to the brain. While, as stated, the tendency to
syncope may exist in healthy non-anæmic individuals, it is far more
common with those who suffer either from chronic cerebral anæmia or
from many of its predisposing conditions. The arterial spasm which
causes syncope is an exaggeration of what occurs within physiological
limits[26] in all persons {781} when subjected to emotional or violent
external impressions of any kind.

[Footnote 26: It has been experimentally determined by Istomanow (_St.
Petersburg Dissertation_, 1885) in persons whose brain-surface had
become partially accessible to observation through traumatic causes
that pain, warmth, pleasant smells, and sweet tastes cause a
contraction of the cerebral vessels and a sinking in of the
brain-surface, while tickling, unpleasant odors, bitter and sour
tastes, produce the reverse condition; that is, bulging of the
brain-surface and increased injection of the vessels. Istomanow's
results are verified by other observations, particularly by the fact
that with the latter class of impressions there is an increase in the
general blood-pressure, with sinking of the surface-temperature, and,
as measured by Mosso's method, decrease in the volume of the
extremities. While there is a general correspondence between these
observations and clinical experience, there are a few unexplained
discrepancies.]

MORBID ANATOMY.—In those severe cases of cerebral anæmia which
terminate fatally the entire brain appears bloodless. Since the color
of this organ under ordinary circumstances is in great part due to the
vascular injection, it appears very different when this admixture is
lessened or removed. Then the gray substance, instead of presenting a
reddish-gray tint, is of a pale buff color in infants, and a pale gray
in adults who have died of acute or intense cerebral anæmia. The white
substance exhibits few or no puncta vasculosa, and there is no
indication of the faint rosy tinge which even the white substance has
in the normal brain. All these appearances can be imitated in the
brain of an animal that is bled to death; they are also met with in
those who have died of inanition, particularly in cases of melancholia
attonita, the subjects of which had long refused food. Most writers
state that the ventricular and subarachnoid fluids are increased in
amount,[27] and that the sulci appear wider in anæmic than in normal
brains. That these fluids must be increased to compensate for the
diminished blood-amount is evident. But it is not unlikely that
exaggerated estimates of the increase have been made; and for this
reason: Since the meninges and choroid plexuses are comparatively
bloodless, the cerebro-spinal fluids are more likely to present
themselves free from that admixture of blood which renders the
obtaining and measuring of their quantity so difficult under ordinary
circumstances. The gaping of the sulci has not been verified by me
either in animals that had been bled to death or in cases of cerebral
anæmia in rapidly-fatal atonic and phthisical melancholia. In
protracted cases of this nature I frequently found gaping of the
sulci: here, from the nature of the cases, the patients dying either
from self-starvation, imperfect assimilation, or wasting diseases, the
occurrence of a certain amount of atrophy of the brain-substance
proper could not be excluded.[28]

[Footnote 27: Hammond, on the other hand (_Diseases of the Nervous
System_, p. 77), has the ventricles generally empty.]

[Footnote 28: Up to within a very short time ago it would have
appeared heretical to claim that any considerable amount of
brain-wasting could ensue from starvation alone, as the oft-cited
experiments of Chossat seemed to show that mammals, birds, reptiles,
and amphibians lose in body-weight while being starved, but that the
brain-weight is not disturbed to any appreciable extent. Six years ago
I examined the brain of a tortoise (_Cestudo Virginica_) which had
starved fully a year through ignorance of the keeper of an aquarium.
The atrophy of the brain was so marked that it had undergone
demonstrable changes of contour. Since then Rosenbach (_Archiv für
Psychiatrie_, xvi. p. 276) has demonstrated that brain-wasting and
other changes do occur in starved rabbits.]

With protracted fevers accompanied by inanition—and this applies
particularly to the later period of typhoid fever—a condition of
cerebral anæmia is found which is of the greatest interest to the
clinician. The brain as a whole is bloodless; there may or may not be
apparently hyperæmic districts, but the injection is altogether on the
surface; the consistency of the brain is considerably diminished, and
this organ is often {782} distinctly œdematous. In exceptional cases
the œdema is so great that softening results, the white substance
becoming fluidified at the cortical limit near the base of the sulci
and at the ventricular walls. This is due perhaps as much to
post-mortem maceration as to pre-mortem œdema, but that the latter
condition exists is shown by the condition of the brain as a whole.
The loss of memory, the difficulty of correlating the past and
present, the rambling, incoherent conversation, and anenergic stupor
observed in the decline of typhoid and other exhausting fevers,
especially in older subjects, may be properly attributed to the
injurious effects of post-febrile anæmia and anæmic œdema of the
brain. Aside from fevers, œdema is apt to be associated with anæmia
where venous stagnation is a complicating feature; consequently, it is
not uncommon with certain uncompensated valvular lesions, emphysema,
and other chronic pulmonic troubles.

Positive observations of tissue-changes from simple cerebral anæmia
have not been recorded. Even in extreme cases the essential nervous
structures, the ganglionic bodies, the nerve-fibres, their sheaths,
and the neuroglia, appear healthy. The adventitial and pericellular
spaces are sometimes enlarged, and variations in the number and
distribution of the free nuclei of the neuroglia and the border bodies
of the periadventitial districts have been observed by me, but not
with such constancy as to justify more than this mere mention. In his
researches on starvation Rosenbach found the brain œdematous and the
ventricles dilated; there were also microscopical changes which
indicated a profound disturbance of nutrition; the large cells of the
anterior spinal horn and cerebellum had lost their transparency, being
in a condition resembling cloudy swelling. The neuroglia appeared to
be in a similar condition as that of nerve-cells. Singular as it may
appear on first sight, the capillaries were found crowded with
blood-corpuscles, and there were many evidences of diapedesis of such.
This may indicate a passive accumulation due to deficient cardiac and
vascular contractility. The changes, as a whole, were not unlike those
found in myelitis,[29] except in so far as no actual inflammatory
signs were present.

[Footnote 29: Several distinguished neurologists, notably Westphal,
who were present when Rosenbach presented his conclusions, were unable
to recognize so profound a deviation from the normal structural
conditions as he claimed (_Archiv für Psychiatrie_, xvi. p. 279).]

SYMPTOMS.—The clinical phenomena of acute cerebral anæmia have been in
the main related in connection with the etiology of this disorder. We
shall now proceed to detail those which occur with cases more likely
to engage the attention of the practitioner either on account of their
gravity or protracted duration.

Uncomplicated Chronic Cerebral Anæmia of Adolescents and Adults.—This
condition is one of the common manifestations of general anæmia. Most
anæmic persons are languid, drowsy, suffer from insomnia, tinnitus
aurium, and other signs of imperfect cerebral irrigation. In some
these troubles become alarmingly prominent and may approach the
confines of mental derangement. This is particularly apt to occur with
women who have borne and nursed a large number of children. In
addition to the typical signs of cerebral anæmia, they exhibit
depression, may suffer from hallucinations, and even become afflicted
with lachrymose or suicidal melancholia (insanity of lactation of the
somato-etiological school). {783} Depression of the mental functions
is the most constant symptom of cerebral anæmia, and the one which
most frequently directs the physician's attention to its existence;
its subjects appear mentally blunted, the apperceptive powers are
diminished, and it is difficult for the patient to interest himself in
anything, or when interested to keep up a mental effort—that is, his
attention—any length of time. In more severe grades of the trouble the
patients become somnolent in the daytime. Contrary to what those who
regard sleep as essentially due to cerebral anæmia might expect, sleep
is disturbed, and the patient is wakeful or suffers from vivid and
frightful dreams, or even deliria. Others pass a quiet night, but are
rather in a trance-like condition than a healthy sleep. Lethargic as
the cerebral anæmic person is on the whole, and unable as he feels
himself to exert his will-power (aboulia), yet he is often irritable,
perverse, and petulant in consequence of that morbid excitability
which is a universal attribute of the overworked or imperfectly
nourished nerve-element. The younger the patient the more likely is
the condition apt to impress one as a stupor, while with older
patients irritability is more prominent. In the former the obtuseness
is often rapidly overcome when the patient assumes the horizontal
position.

It was supposed by Abercrombie that an acute exacerbation of cerebral
anæmia of this form in weakly and aged individuals might terminate in
death. This condition corresponded to the so-called serous apoplexy of
the old writers. With increasing accuracy in our autopsies this
condition is more and more rarely recorded, although the possibility
of its occurrence as a pathological rarity cannot be denied. As a
rule, the chronic form of cerebral anæmia when it terminates fatally,
which is exceptional, is marked by a deepening coma and gradual
extinction of the vital processes, the Cheyne-Stokes phenomenon
preceding this.

Patients suffering from chronic cerebral anæmia are afflicted with
morbid irritability of the optic and auditory nerves. Loud sounds and
bright lights are very annoying to them. Roaring, buzzing, and beating
sounds in the ear are common, and scintillations, muscæ volitantes,
and temporary darkening of the visual field—particularly noticed when
the head is suddenly raised—are complained of in all cases. It is
often found that the tinnitus disappears and the hearing power
improves on assuming the horizontal position.

Headache of greater or less severity is found in the majority of
cases: it is more severe in the rapidly-developed forms, and I have
found it to be complained of in agonizing intensity by women who had
risen from childbed and who had flooded considerably. As a rule, the
headache, whether severe or mild, is symmetrical and verticalar, in
some cases associated with an ache subjectively appearing as if it
extended to the back of the orbit. It is remarkable for its constancy,
and its exacerbations are often complicated with vertigo and nausea,
so that it is not infrequently interpreted as a reflex evidence of
gastric disorder. A stitch-like feeling, located in both temples, is
often associated with it.

Occasionally sufferers from chronic cerebral anæmia experience
seizures, or rather exacerbations, of their disorder which approach in
character, while not equalling in degree, an attack of syncope.
Whether in bed or in a chair, they then feel as if their limbs were of
lead; they deem that they cannot stir hand or foot; the other symptoms
related are {784} aggravated; they yawn and breathe deeply, but hear
all that is said by those near them, and do not lose consciousness.
They express themselves as feeling as if everything around them were
about to pass away. One of my patients would frequently find that if
this condition overtook her while lying on one side, that side would
remain numb for some time and be the seat of a tingling sensation
which disappeared on the parts being rubbed. The same was noticed when
she awoke in the morning in a similar position. To what extent these
features were due to the general anæmia is doubtful. As previously
stated, true syncope occurs in chronic cerebral anæmia, but much less
frequently in those subjects of this disorder who have reached middle
life than in adolescents.

The radial pulse in cerebral anæmia does not necessarily show the
anæmic character; not infrequently the general blood-pressure is
increased at the onset of the acute form, and if long continued this
may be followed by a decrease of the same. The pulse-character may
therefore vary greatly in frequency, resistance, and fulness. In
protracted cases it is soft, easily compressible, and rapid.

It is not uncommon to find indications of a slight unilateral
preponderance of the signs of cerebral anæmia. In one case which
terminated in recovery, and was otherwise pure, vertigo was not
produced on turning from the left to the right, but it was produced to
a distressing degree on turning in the opposite direction; in a
second, equally typical, there was for a long time a subjective
sensation of falling over toward the right side.

There appears to be much less constancy in the relationship of the
deficient blood-supply to the severity of the symptoms than is usually
supposed. Much depends upon the time of life at which the disorder
develops: a brain that has acquired stability through education and
exercise is less vulnerable to the influence of general anæmia than
one that has not. The nerve-centres appear, to some extent at least,
to regulate their own blood-supply; and whether it be through a change
in the blood-current rapidity or some other factor neutralizing the
evil effects of the intrinsically inferior quality of the blood, we
must attribute to the self-regulating nutrition power of the brain the
not uncommon phenomena of an active mind in an anæmic body. And where
the general anæmia reaches so high a degree as to involve the brain,
under such circumstances we find that irritability to sensory
impressions and fretfulness are more prominent than the lethargy and
indifference which characterize the juvenile chlorotic form. Although
this distinction is less marked between these two classes in regard to
acutely-produced anæmia, yet it is observable even there. If in a
youth or girl while undergoing phlebotomy cerebral anæmia were to
reach such a degree as to cause subjective sounds, they would either
approach or fall into a faint; but Leuret, the distinguished cerebral
anatomist, while being subjected to the same procedure, hearing a
hissing sound, did not lose consciousness, but complained that some
one must have upset a bottle of acid on a marble table in the same
room, as he supposed he was hearing the sound of effervescence thus
produced.

Much, too, appears to depend on dynamic and other thus far
undiscovered intrinsic conditions of the brain-tissue itself,
irrespective of the mere amount and rapidity of the blood-current. If
the subject be exposed to wasting diseases, to blood-poisons, or to
vicissitudes of temperature and {785} to physical exhaustion in
addition to the causes producing cerebral malnutrition, deliria of a
cortical nature are more apt to characterize the case than in simple
anæmia. These are known as the deliria of inanition, and present
themselves under two forms. The first has been frequently observed in
sailors, travellers, and others who have undergone starvation in
exposed situations, and is tinctured by the psychical influences
incident to such a condition. Just as the Greeley survivors at Cape
Sabine, when reduced to their miserable rations of seal-skin
boot-leather and shrimps, entertained each other with the enumeration
of imaginary culinary luxuries, so others who have suffered in the
same way declaim about gorgeous banquets in the midst of a howling
wilderness, or, as occurred to a miner who lost his way in Idaho a few
winters ago, experienced hallucinatory visions of houses, kitchen
utensils, and persons with baskets of provisions. In others the terror
of the situation leads to the development of rambling and incoherent
delusions of persecution.

The second form, regarded as a variety of starvation delirium, is
found in the post-febrile periods of typhoid and other exhausting
fevers. In aged persons it may even develop shortly after the onset of
the disease. It is usually unsystematized, of a depressive cast, and
may be associated with a condition resembling melancholia agitata. In
a small proportion of cases insanity of the ordinary types, but more
commonly of the special kinds comprised in the group of post-febrile
insanity, develops from the anæmic fever delirium as its
starting-point.

The spurious hydrocephalus (hydrocephaloid, hydrencephaloid) of
Marshall Hall and Abercrombie, referred to in the section on Etiology,
is an important condition for the diagnostician to recognize. A child
suffering from this disorder presents many symptoms which are
customarily regarded as characteristic of tubercular meningitis or of
chronic hydrocephalus; thus the pupils are narrow—sometimes
unequal;[30] there is strabismus, and there may be even nuchal
opisthotonos, while the somnolent state in which the little patient
usually lies may deepen into a true coma, in which the pupils are
dilated, do not react to light, nor do the eyelids close when the
cornea is touched. Ominous as this state appears, it may be completely
recovered from under stimulating and restorative treatment. On inquiry
it is found that the symptoms above mentioned were preceded by cholera
infantum or some other exhausting complaint, such as a dysentery or
diarrhœa, and that the somnolent condition in which infants are often
found toward the close of such complaints passed gradually into the
more serious condition described.[31] The infants thus affected do
not, however, sleep as healthy children do, but moan and cry, while
apparently unconscious of their surroundings. The surface of the body
is cool and pale; the pulse and respiration are normal, except in the
comatose period, but the former is easily compressible. The chief
points distinguishing hydrocephaloid from true hydrocephalus and other
diseases associated with similar symptoms are the following: 1st,
There is no rise of temperature; 2d, the pupils are equal; 3d, the
fontanelle is sunken in; 4th, the pulse and respiration, with the
exception stated, are natural; 5th, there is an {786} antecedent
history of an exhausting abdominal disorder; 6th, also a facial
appearance characteristic of the latter.

[Footnote 30: This is not admitted by most writers, but does occur
exceptionally.]

[Footnote 31: It should not be forgotten, however, that very similar
symptoms occur after cholera infantum, with a much graver pathological
condition—namely, marantic thrombosis of the sinuses.]

One of the gravest and rarest forms of cerebral anæmia is one which
occurs as a result of extreme general anæmia in very young infants. In
a remarkable case which I have had an opportunity of studying, the
abolition of certain cerebral functions reached such a degree that the
opinion of a number of physicians was in favor of tubercular
meningitis.[32] There was at the time of my examination complete
extremity hemiplegia, and there had been conjugated deviation,
restlessness in sleep, and dulness in the waking hours: all these
symptoms except the hemiplegia disappeared whenever a more assimilable
and nutritious food was used than the one previously employed. On one
occasion there were evidences of disturbed vaso-motor innervation; on
several, convulsive movements. This history, associated with ordinary
evidences of general anæmia, covered a period of eighteen months,
without the slightest abnormality of temperature being noted or
discoverable during that period. The mucous surfaces of this child
were almost colorless, certainly without any indication of the normal
tinge; the mother had nursed it, and her milk had been found to
possess scarcely any nutritive value. The case terminated fatally at
the age of twenty months.

[Footnote 32: It was stated by an experienced practitioner that death
occurred with unmistakable symptoms of tubercular meningitis.
Certainly, the absence of temperature disturbance at the time of the
hemiplegic and other exacerbations, as well as other important
features for a period exceeding a year, shows that whatever favorable
soil the earlier condition may have furnished for the secondary
development of such or other gross structural disease, tubercular
meningitis did not exist at the time; while the absence of pupillary
and optic-nerve symptoms, as well as the rapid changes from day to day
or week to week under dietetic treatment, militate against the
assumption of any other organic affection incident to childhood.]

Partial Cerebral Anæmia.—Most writers on cerebral anæmia discuss a
number of varieties of partial cerebral anæmia as distinguished from
the acute and chronic general forms. Some of the conditions thus
described properly appertain to the angio-spastic form of hemicrania,
others to epilepsy, and the majority to circulatory disturbances
dependent on arterial disease. Aside from the partial cerebral anæmia
resulting from surgical causes, I am acquainted with but one evidence
of limited cerebral anæmia which can be regarded as independent of the
neuroses or of organic disease, and that is the scintillating scotoma.
This symptom, in the only case in which I observed it, occurred in a
medical student, accompanied by pallor and nausea in consequence of
the disgust produced in him by the combined odors of a dissecting-room
and of a neighboring varnish-factory. The totally blind area of the
visual field was strictly hemianopsic in distribution and bounded by a
colored zone scintillating, to use the sufferer's words, like an
aurora borealis. The attack, probably protracted by his great alarm at
being blind in one-half of the visual field, lasted three hours. As
the cause in this case was a psychical impression and accompanied by
the ordinary signs of that fainting which is not an uncommon
occurrence in the dissecting-room; as, furthermore, the individual in
question never had a headache except in connection with febrile
affections, and then in the lightest form, and is neither neurotic
himself nor has a neurotic ancestry or relatives,—I regard it as the
result of a simple arterial spasm intensified in the visual field of
{787} one hemisphere, analogous to the more general spasm of ordinary
syncope.[33]

[Footnote 33: It may be remembered that Wollaston had scintillating
scotomata, and that after his death a small focus of softening was
found in the one visual field. Ordinarily, this disturbance is
associated with hemicrania.]

DIAGNOSIS.—There is so little difficulty in recognizing the nature of
those cases of acute cerebral anæmia which depend on recognizable
anæmia-producing causes that it is unnecessary to point out their
special diagnostic features. With regard to chronic cerebral anæmia,
and its differentiation from other circulatory brain disorders, I
refer to the last article. In this place it will be necessary only to
point to some of the symptoms which, individually considered, are
found in other disorders, and may therefore be misinterpreted. The
chief of these is vertigo, which, as already stated, being associated
with nausea, and even vomiting, is not infrequently confounded with
stomachic vertigo, while the opposite error is also, though less
frequently, fallen into. The chief differential points are—that
stomachic vertigo is relieved by vomiting, and anæmic vertigo is not;
that the former is rather episodical, the latter more continuous; that
in the free intervals of the former, while there may be some dulness,
there is not the lethargy found with anæmia; that the headache with
the former is either over the eyes or occipital, and most intense
after the passage of a vertiginous seizure, while anæmic headache is
verticalar or general, and not subject to marked momentary changes. It
is unnecessary to indicate here the positive evidences of gastric
disorder which are always discoverable in persons suffering from
stomachic vertigo; but it is also to be borne in mind that such
disorder is frequently associated with the conditions underlying
general and cerebral anæmia, particularly in the prodromal period of
some pulmonary troubles.

There are a number of organic affections of the brain which are in
their early periods associated with symptoms which are in a
superficial way like those of cerebral anæmia. As a rule, focal or
other pathognomonic signs are present which render the exclusion of a
purely nutritive disorder easy; but with some tumors, as is generally
admitted, these signs may be absent. It is not difficult to understand
why a tumor not destructive to important brain-centres, nor growing
sufficiently rapid to produce brain-pressure, yet rapidly enough to
compress the blood-channels, may produce symptoms like those of simple
cerebral anæmia. It is claimed that with such a tumor the symptoms are
aggravated on the patient's lying down, while in simple anæmia they
are ameliorated.[34] The latter proposition holds good as a general
rule; as to the former, I have some doubts. Not even the
ophthalmoscope, although of unquestionable value in ascertaining the
nature of so many organic conditions of the brain and its appendages,
can be absolutely relied on in this field. Until quite recently, optic
neuritis, if associated with cerebral symptoms, was regarded as
satisfactory proof that the latter depended on organic disease; but
within the year it has been shown by Juler[35] that it may occur in
simple {788} cerebral anæmia, and both the latter and the associated
condition of the optic nerve be recovered from.

[Footnote 34: The increased flow of blood to the brain in anæmia is
not always momentarily remedial: if, for example, the patient stoop
down, he flushes more easily than a normal person, and suffers more
than the latter. The same is observed with regard to stimulants.]

[Footnote 35: _British Medical Journal_, Jan. 30, 1886. In the case
reported suppression of the catamenia is spoken of, as well as the
fact that treatment was directed to the menstrual disturbance. It is
not evident from the brief report at my disposal whether the
suspension of the menstrual flow was symptomatic of general anæmia or
of a local disturbance. Optic neuritis has been recorded as having
been present in a large number of cases with no other assignable cause
than a uterine disorder. As previously stated, Hirschberg and Litten
found choked disc under like circumstances.]

The claim of Hammond and Vance that ordinary anæmia of the brain may
be recognized through the ophthalmoscope is almost unanimously
disputed by experienced ophthalmoscopists, nor is it unreservedly
endorsed by any authority of weight among neurologists. That there may
be color-differences to indicate anæmia is, however, not impossible;
and the fact that a concentric limitation of the visual field
sometimes occurs should not be forgotten. It is distinguished from
that found with organic diseases by its variability through the day
and in different positions of the body.

TREATMENT.—Chronic as well as acute cerebral anæmia, dependent on
general anæmia, usually requires no other medicinal treatment than
that rendered necessary by the general anæmic state of which it is a
part. This has been discussed at length in the third volume of this
work: it remains to speak of certain special precautions and
procedures rendered necessary by the nervous symptoms predominating in
such cases. As the insufficiently nourished brain is not capable of
exertion, mental as well as physical rest is naturally indicated. And
this not only for the reason that it is necessary to avoid functional
exhaustion, but also because the anæmic brain when overstrained
furnishes a favorable soil for the development of morbid fears,
imperative impulses, and imperative conceptions. This fact does not
seem to have been noticed by most writers. The mind of the anæmic
person is as peculiarly sensitive to psychical influences as the
anæmic visual and auditory centres are to light and sound; and in a
considerable proportion of cases of this kind the origin of the morbid
idea has been traced to the period of convalescence from exhausting
diseases. The prominent position which masturbation occupies among the
causes of cerebral anæmia perhaps explains its frequent etiological
relationship to imperative conceptions and impulsive insanity.

Although the radical and rational treatment of cerebral anæmia is
covered by the treatment of the general anæmia, there are certain
special symptoms which call for palliative measures. Most of these,
such as the vertigo, the optic and aural phenomena, improve, as
stated, on assuming the horizontal position. The headache if very
intense will yield to one of three drugs: nitrite of amyl, cannabis
indica, or morphine. I am not able to furnish other than approximative
indications for the use of remedies differing so widely in their
physiological action. Where the cerebral anæmia and facial pallor are
disproportionately great in relation to the general anæmia, and we
have reason to suppose the existence of irritative spasm of the
cerebral blood-vessels—a condition with which the cephalalgia is often
of great severity—nitrite of amyl acts as wonderfully as it does in
the analogous condition of syncope.[36] Where palpitations are
complained of, and exist to such a degree as to produce or aggravate
existing insomnia, small doses of morphine will act very well, due
{789} precautions being taken to reduce the disturbance of the
visceral functions to a minimum, and to prevent the formation of a
drug habit by keeping the patient in ignorance of the nature of the
remedy. When trance-like conditions and melancholic depression are in
the foreground, cannabis indica with or without morphia will have the
best temporary effect: it is often directly remedial to the
cephalalgia. Chloral and the bromides are positively contraindicated,
and untold harm is done by their routine administration in nervous
headache and insomnia, irrespective of their origin. Nor are
hypnotics, aside from those previously mentioned, to be recommended;
the disadvantages of their administration are not counterbalanced by
the advantages.[37] Frequently, in constitutional syphilis, insomnia
resembling and probably identical with the insomnia of cerebral anæmia
will call for special treatment. In such cases the iodides, if then
being administered, should be suspended, and if the luetic
manifestations urgently require active measures, they should be
restricted to the use of mercury in small and frequent dosage, while
the vegetable alteratives may be administered if the state of the
stomach permit.

[Footnote 36: There are disturbances in the early phases of cerebral
syphilis, whose exact pathological character is not yet ascertained,
which so closely resemble the condition here described that without a
knowledge of the syphilitic history, and misled by the frequently
coexisting general anæmia, it is regarded as simple cerebral anæmia.
Under such circumstances, as also with the cerebral anæmia of old age,
amyl nitrite should not be employed.]

[Footnote 37: Urethran and paraldehyde have failed in my hands with
anæmic persons.]

Among the measures applicable to the treatment of general anæmia there
are three which require special consideration when the cerebral
symptoms are in the foreground: these are alcoholic stimulants, the
cold pack, and massage. It is a remarkable and characteristic feature
of cerebral anæmia that alcoholic stimulants, although indicated, are
not well borne[38]—at least not in such quantities as healthy persons
can and do take without any appreciable effect. I therefore order
them—usually in the shape of Hungarian extract wines,[39] South Side
madeira, or California angelica—to be given at first in such small
quantities as cannot affect the cerebral circulation unpleasantly, and
then gradually have the quantity increased as tolerated. In fact, both
with regard to the solid nourishment and the stimulating or nourishing
fluids and restorative drugs the division-of-labor principle is well
worth following. The cerebral anæmic is not in a position to take much
exercise, his somatic functions are more or less stagnant, and bulky
meals are therefore not well borne. Small quantities of food,
pleasingly varied in character and frequently administered, will
accomplish the purpose of the physician much better.

[Footnote 38: Hammond, who classes many disorders under the head of
cerebral anæmia which the majority of neurologists regard as of a
different character, has offered a very happy explanation. He says,
“Now, it must be recollected that the brains of anæmic persons are in
very much the same condition as the eyes of those who have for a long
time been shut out from their natural stimulus, light. When the full
blaze of day is allowed to fall upon them retinal pain is produced,
the pupils are contracted, and the lids close involuntarily. The light
must be admitted in a diffused form, and gradually, till the eye
becomes accustomed to the excitation. So it is with the use of alcohol
in some cases of cerebral anæmia. The quantity must be small at first
and administered in a highly diluted form, though it may be frequently
repeated.”]

[Footnote 39: Such as Meneszer Aszu; there is no genuine tokay wine
imported to this country, as far as I am able to learn.]

The cold pack, strongly recommended by some in general anæmia, is not,
in my opinion, beneficial in cases where the nervous phenomena are in
the foreground, particularly in elderly persons. Gentle massage, on
the other hand, has the happiest effects in this very class of cases.

Of late years my attention has been repeatedly directed to cerebral
anæmia of peculiar localization due to malarial poisoning. It has been
{790} noted by others that temporary aphasia and other evidences of
spasm of the cortical arteries may occur as equivalents or sequelæ of
a malarial attack. I have seen an analogous case in which hemianopsia
and hemianæsthesia occurred under like circumstances, and were
recovered from. Whether more permanent lesions, in the way of
pigmentary embolism or progressing vascular disease, causing
thrombotic or other forms of softening, may develop after such focal
symptoms is a matter of conjecture, but I have observed two fatal
cases in which the premonitory symptoms resembled those of one which
recovered, and in which these were preceded by signs of a more general
cerebral anæmia, and in one case had been mistaken for the
uncomplicated form of that disorder. Where a type is observable in the
exacerbation of the vertigo, headache, tinnitus, and lethargy of
cerebral anæmia, particularly if numbness, tingling, or other signs of
cortical malnutrition are noted in focal distribution, a careful
search for evidences of malarial poisoning should be made; and if such
be discovered the most energetic antimalarial treatment instituted. It
is in such cases that arsenic is of special benefit.

The treatment of syncope properly belongs to this article. Where the
signs of returning animation do not immediately follow the assumption
of the recumbent position, the nitrite of amyl, ammonia, or small
quantities of ether should be exhibited for inhalation. The action of
the former is peculiarly rapid and gratifying, though the patient on
recovery may suffer from fulness and pain in the head as after-effects
of its administration. The customary giving of stimulants by the mouth
is to be deprecated. Even when the patient is sufficiently conscious
to be able to swallow, he is usually nauseated, and, as he is
extremely susceptible to strong odors or tastes in his then condition,
this nausea is aggravated by them. By far the greater number of
fainting persons recover spontaneously or have their recovery
accelerated by such simple measures as cold affusion, which, by
causing a reflex inspiration, excites the circulatory forces to a more
normal action. Rarely will the electric brush be necessary, but in all
cases where surgical operations of such a nature as to render the
development of a grave form of cerebral anæmia a possibility are to be
performed, a powerful battery and clysters of hot vinegar, as well as
the apparatus for transfusion, should be provided, so as to be within
reach at a moment's notice.


Inflammation of the Brain.

Before the introduction of accurate methods of examining the diseased
brain the term inflammatory softening was used in a much wider sense
than it is to-day. Most of the disorders ascribed to inflammatory
irritation by writers of the period of Andral and Rush are to-day
recognized as regressive, and in great part passive, results of
necrotic destruction through embolic or thrombic closure of afferent
blood-channels. Two forms of inflammation are universally recognized.
One manifests itself in slow vascular and connective-tissue changes
and in an indurating inflammation. There are two varieties of it: the
first of these, which is associated with furibund vaso-motor
explosions and regressive metamorphosis of the functional
brain-elements, is known from its typical {791} association with grave
motor and mental enfeeblement as paretic dementia or dementia
paralytica. The second, which is focal in the distribution of the
affected brain-areas, is known as sclerosis. The former is treated of
in a separate article; the latter is considered in connection with the
spinal affections which either resemble it in histological character
or complicate its course. The second form of cerebral inflammation is
marked by the formation of the ordinary fluid products of acute
inflammation in other organs of the body; this is the suppurative
form, usually spoken of as abscess of the brain.

In addition to these two generally recognized inflammatory affections
there are a number of rare diseases which are regarded by excellent
authority as also of that character. The vaguely-used term acute
encephalitis has been recently reapplied with distinct limitations to
an acute affection of children by Strümpell. This disease is usually
of acute onset, infants under the sixth year of age being suddenly,
and in the midst of apparently previous good health sometimes,
attacked by fever, vomiting, and convulsions.[40] Occasionally coma
follows, which may last for several days, perhaps interrupted from
time to time by recurring convulsions or delirium. The convalescence
from this condition is rapid, and in some cases is complete; in others
paralysis remains behind in the hemiplegic form. The paralysis is
usually greater in the arm than in the leg; in extreme cases it
involves the corresponding side of the face, and, as the paralyzed
parts are arrested or perverted in growth, considerable deformity,
even extending to asymmetry of the skull, may ensue. The deformity is
aggravated by contractures. Usually there is some atrophy of the
muscles, but in one case I found actual hypertrophy[41] of some
groups, probably in association with the hemiathetoid movements.

[Footnote 40: As in my case of infantile encephalitis followed by
athetoid symptoms (_Journal of Nervous and Mental Diseases_).]

[Footnote 41: This was followed by atrophy. There are never any
qualitative electrical changes.]

The sequelæ of acute infantile encephalitis present us with the most
interesting forms of post-paralytic disturbances of muscular
equilibrium. Hemichorea and hemiathetosis, as well as peculiar
associated movements and hemicontracture, are found in their highest
development with this class of cases. Occasionally epileptiform
symptoms are noted,[42] and in others true epilepsy is developed. It
is under such circumstances that imbecility is apt to be a companion
symptom or result; and this imbecility is prominently noted in the
moral sphere.

[Footnote 42: Which in one case of my own disappeared spontaneously.]

The grave set of symptoms briefly detailed here are attributed by
Strümpell[43] to an acute encephalitis, analogous, in his opinion, to
the acute poliomyelitis of children. Its frequent occurrence after
measles and scarlatina, as well as the fact that Ross[44] in a
carefully-studied case arrived at the opinion that the disease was an
embolo-necrotic result of endocarditis, would lead to the conclusion
that it is a focal affection, probably due to the transportation of
infectious elements to the brain through the blood-vessels. Its
occurrence in children in the midst of apparent health[45] {792} is
consistent with the fact that rheumatism and an attendant slight
endocarditis frequently pass unrecognized in infancy. It is supposed
that a diffuse form of inflammatory non-suppurative softening exists
by some of the Germans, but the proof advanced in favor of this view
is not conclusive.

[Footnote 43: As a surmise, for up to his writing no reliable
autopsies had been made.]

[Footnote 44: _Brain_, October, 1883.]

[Footnote 45: McNutt (_American Journal of Medical Sciences_, January,
1885) cites Strümpell as attributing the theory of an inflammatory
affection, which is analogous to poliomyelitis in its suddenness and
nature, to Benedict, and refers to p. 349 of Strümpell's textbook
under the erroneous date of 1864. This work was published in 1883-84,
and the theory is advanced by Strümpell as his own. It is only a
synonym, hemiplegia spastica infantile, that is attributed to
Benedict.]

A number of rare forms of interstitial encephalitis have been
described. In one, elaborately studied by Danillo, an inflammatory
hypertrophy of the cortex, involving the parenchyma as well as the
connective and vascular structures, was found in a limited area of the
motor province of the right hemisphere. There had been crossed
epileptiform convulsions during life.[46]

[Footnote 46: _Bulletin de la Société de Biologie_, 1883, p. 238.]

There is some question among pathologists as to the recognition of
Virchow's encephalitis of the new-born. Certainly a part of Virchow's
material was derived from the imperfect study of a condition of
infantile brain-development which, as Jastrowitz showed, is
physiological, and on which Flechsig based his important researches of
tract-development. More recent studies, however, demonstrate that
there is a form of miliary encephalitis in new-born children due to
septic causes, such as, for example, suppuration of the umbilical
cord. The demonstration by Zenker of the occurrence of metastatic
parasitic emboli in cases of aphthous stomatitis, and by Letzerich of
a diphtheritic micrococcus invasion in the brain of his own child,
show that the subject of early infantile encephalitis merits renewed
consideration.[47]

[Footnote 47: The attempt of Jacusiel to revive Virchow's encephalitis
of the new-born (_Berliner klinische Wochenschrift_, 1883, No. 7)
under the title of interstitial encephalitis does not seem to have met
with encouragement, for, besides Jastrowitz, Henoch and Hirschberg
opposed this view in the discussion.]

Strictly speaking, the reactive changes which occur in the
brain-substance bordering on tumors, hemorrhagic and softened foci,
belong to the domain of encephalitis; but as they are considered in
conjunction with the graver lesions to which they are secondary both
in occurrence and importance, it is not necessary to more than refer
to them here.


Abscess of the Brain.

As indicated in the last article, there formerly existed much
confusion in the minds of pathologists regarding the terms softening
and abscess of the brain. As long as softening was regarded as an
inflammation, so long was abscess of the brain regarded as a
suppurative form of softening. Aside from the fact that there is some
resemblance in mechanical consistency between a spot of ordinary
softening and one of inflammatory softening, there is no essential
similarity of the two conditions. True softening is to-day regarded as
the result of a death of brain-tissue produced by interference with
the blood-supply; it is therefore a passive process. Inflammatory
softening, of which abscess is a form, is due to an irritant, usually
of an infectious nature. It is to the results of such irritation that
the term suppurative encephalitis should be limited.

MORBID ANATOMY.—In all well-established inflammatory brain {793}
troubles the active part is taken by the blood-vessels and connective
tissue; the ganglionic elements undergo secondary, usually regressive
or necrotic, changes. The brain, considered as a parenchymatous organ,
is not disposed to react readily in the way of suppurative
inflammation unless some septic elements are added to the inflammatory
irritant. Foreign bodies, such as knitting-needles, bullets, and
slate-pencils, have been found encapsulated in this organ or
projecting into it from the surrounding bony shell without
encapsulation and without any evidences of inflammatory change. As a
rule, a foreign body which enters the brain under aseptic conditions
will, if the subject survive sufficiently long, be found to have made
its way to the deepest part of the brain, in obedience to the law of
gravity, and through an area of so-called inflammatory red softening
which appears to precede it and facilitate the movement downward. This
form of softening derives its color from the colored elements of the
blood, which either escape from the vessels in consequence of the
direct action of the traumatic agent; secondly, in consequence of
vascular rupture from the reduced resistance of the perivascular
tissue in consequence of inflammatory œdema and infiltration; or,
thirdly, in obedience to the general laws governing simple
inflammation.

A cerebral abscess may present itself to the pathological anatomist in
one of three phases—the formative, the crude, and the encapsulated. In
the first it is not dissimilar to a focus of yellow softening, being,
like the latter, a diffuse softened area varying from almost
microscopical dimensions to the size of a walnut, and of a distinctly
yellow tinge. Microscopic examination, however, shows a profound
difference. In pure yellow softening there are no pus-cells; in the
suppurative encephalitic foci they are very numerous, and congregated
around the vessels and in the parenchyma in groups. The crude abscess
is the form usually found in cases rapidly running to a fatal
termination. Here there is an irregular cavity in the brain, usually
the white central substance of the cerebrum or cerebellum, formed by
its eroded and pulpy tissue; it is filled with yellow, greenish, and
more rarely brownish pus. In the most furibund cases broken-down
brain-detritus may be found in the shape of whitish or reddish
flocculi, but in slowly-formed abscesses the contents are free from
such admixture, and thus the third phase is produced, known as the
encapsulated abscess. The cavity of the abscess becomes more regular,
usually spheroid or ovoid; the pus is less fluid, more tenacious, and
slightly transparent; and the walls are formed by a
pseudo-membrane[48] which is contributed by the sclerosing
brain-substance, which merges gradually into the outlying normal
tissue. I have seen one acute cerebral abscess from ear disease which
might be appropriately designated as hemorrhagic; the contents were
almost chocolate-colored; on closer inspection it was found that they
were true pus, mingled with a large number of red blood-discs and some
small flocculi of softened brain-substance. This hemorrhagic admixture
was not due to the erosion of any {794} large vessel, for the abscess
had ruptured into the lateral ventricle at that part where it was most
purely purulent. In a case of tubercular meningitis, Mollenhauer in my
laboratory found an abscess in the white axis of the precentral gyrus,
with a distinct purulent infiltration following the line of one of the
long cortical vessels. The abscess was not encapsulated, the
surrounding white substance exhibited an injected halo, and the
consistency of the contents was that of mucoid material.

[Footnote 48: There is considerable dispute as to the real nature of
the tissue encapsulating cerebral abscesses. It is known, through the
careful observations of R. Meyer, Goll, Lebert, Schott, and Huguenin,
that the capsule may form in from seven to ten weeks in the majority
of cases, about eight weeks being the presumable time, and that at
first the so-called capsule of Lallemand does not deserve the name,
being a mucoid lining of the wall. At about the fiftieth day,
according to Huguenin, this lining becomes a delicate membrane
composed of young cells and a layer of spindle-shaped connective
elements.]

In cases where the symptoms accompanying the abscess during life had
been very severe it is not rare to find intense vascular injection of
the parts near the abscess, and it is not unlikely that the reddish or
chocolate color of the contents of some acutely developed abscesses is
due to blood admixture derived from the rupture of vessels in this
congested vicinity. Sometimes the entire segment of the brain in which
the abscess is situated, or the whole brain, is congested or
œdematous. In a few cases meningitis with lymphoid and purulent
exudation has been found to accompany abscesses that had not ruptured.
It is impossible to say whether in this case there was any relation
between the focal and the meningeal inflammation, as both may have
been due to a common primary cause.[49] In such cases, usually
secondary to ear disease, thrombosis of the lateral sinus may be found
on the same side. Where rupture of an abscess occurs, if the patient
have survived this accident long enough—for it is usually fatal in a
few minutes or hours—meningitis will be found in its most malignant
form. A rupture into the lateral and other ventricles has been noted
in a few cases.[50]

[Footnote 49: Otitis media purulenta in the two cases of this kind I
examined.]

[Footnote 50: In one, observed together with E. G. Messemer, intense
injection of the endymal lining, with capillary extravasations,
demonstrated the irritant properties of the discharged contents.]

Some rare forms of abscess have been related in the various journals
and archives which have less interest as objects of clinical study
than as curiosities of medical literature. Thus, Chiari[51] found the
cavity of a cerebral abscess filled with air, a communication with the
nose having become established by its rupture and discharge.

[Footnote 51: _Zeitschrift für Heilkunde_, 1884, v. p. 383. In this
remarkable rase the abscess, situated in the frontal lobe, had
perforated in two directions—one outward into the ethmoidal cells, the
other inward into the ventricles, so that the ventricles had also
become filled with air. This event precipitated a fatal apoplectiform
seizure.]

The contents of a cerebral abscess usually develop a peculiarly fetid
odor. It has been claimed that this odor is particularly marked in
cases where the abscess was due to some necrotic process in the
neighborhood of the brain-cavity. The only special odor developed by
cerebral abscesses, as a rule, is identical with that of putrid
brain-substance, and it must therefore depend upon the presence of
brain-detritus in the contents of the abscess or upon the rapid
post-mortem decomposition of the neighboring brain-substance.

In two cases of miliary abscess which, as far as an imperfect
examination showed, depended on an invasion of micro-organisms, an
odor was noticed by me which was of so specific a character that on
cutting open the second brain it instantly suggested that of the first
case, examined six years previous, although up to that moment I had
not yet determined the nature of the lesion.[52]

[Footnote 52: Owing to the lack of proper methods of demonstrating
micro-organisms, the first case whose clinical history was known was
imperfectly studied; of the second case, accidentally found in a brain
obtained for anatomical purposes, the examination is not yet
completed.]

{795} That form of abscess which, from its situation in or immediately
beneath the surface, has latterly aroused so much interest from its
important relations to localizations is usually metastatic, and
directly connected with disease of the overlying structures, notably
the cranial walls. In this case the membranes are nearly always
involved. The dura shows a necrotic perforation resembling that found
with internal perforation of a mastoid or tympanic abscess. The pia is
thickened and covered with a tough fibro-purulent exudation;
occasionally the dura and leptomeninges are fused into a continuous
mass of the consistency of leather through the agglutinating
exudation. The abscess is usually found open, and it is not yet
determined whether it begins as a surface erosion, and, bursting
through the cortex, spreads rapidly on reaching the white substance,
or not. The white substance is much more vulnerable to the assault of
suppurative inflammation than the gray, and not infrequently the
superficial part of the cortex may appear in its normal contiguity
with the pia, but undermined by the cavity of the abscess, which has
destroyed the subcortical tissue. Possibly the infecting agent, as in
some cases of ear disease, makes its way to the brain-tissue through
the vascular connections, which, however sparse at the convexity of
the brain, still exist.

CLINICAL HISTORY.—The symptoms of a cerebral abscess depend on its
location, size, and rapidity of formation. There are certain parts of
the brain, particularly near the apex of the temporal lobe and in the
centre of the cerebellar hemisphere, where a moderately large abscess
may produce no special symptoms leading us to suspect its presence.
There are other localities where the suppurative focus[53] indicates
its presence, and nearly its precise location and extent, by the
irritative focal symptoms which mark its development and by the
elimination of important functions which follows its maturation. It is
also in accordance with the general law governing the influence of new
formations on the cerebral functions that an acutely produced abscess
will mark its presence by more pronounced symptoms than one of slow,
insidious development. Indeed, there are found abscesses in the brain,
even of fair dimensions, that are called latent because their
existence could not have been suspected from any indication during
life, while many others of equal size are latent at some time in their
history.

[Footnote 53: Practically, our knowledge of localization of functions
in the human brain begins with the observation by Hitzig of a
traumatic abscess in a wounded French prisoner at Nancy named Joseph
Masseau. The year of the publication of this interesting case
constitutes an epoch in advancing biological knowledge, which will be
remembered when even the mighty historical events in which Hitzig's
patient played the part of an insignificant unit shall have become
obsolete. This, the first case in the human subject where a reliable
observation was made was an unusually pure one; the abscess involved
the facial-hypoglossal cortical field (_Archiv für Psychiatrie_, iii.
p. 231).]

An acute cerebral abscess is ushered in by severe, deep, and dull
headache, which is rarely piercing, but often of a pulsating
character. The pain is sometimes localized, but the subjective
localization does not correspond to the actual site of the morbid
focus.[54] It is often accompanied {796} by vertigo or by a tendency
to dig the head into the pillow or to grind it against the wall. With
this there is more or less delirium, usually of the same character as
that which accompanies acute simple meningitis. As the delirium
increases the slight rise in temperature which often occurs in the
beginning undergoes an increase; finally coma develops, and the
patient dies either in this state or in violent convulsions. The case
may run its course in this way in a few days, but usually one to three
weeks intervene between the initial symptoms and death.

[Footnote 54: Although Ross seems to be of a contrary opinion, it is
the exception for the pain to correspond in location to the abscess.]

Between the rapid and violent course of acute cerebral abscess
detailed, and the insidious course of those which as latent abscesses
may exist for many years without producing any noticeable symptoms
whatever, there is every connecting link as to suddenness and slowness
of onset, severity and mildness of symptoms, and rapidity and slowness
of development and progress. It is the encapsulated abscesses which
are properly spoken of as chronic, and which may even constitute an
exception to the almost uniform fatality of the suppurative affections
of the brain. Thus, the symptoms marking their development may
correspond to those of an acute abscess, but coma does not supervene,
temporary recovery ensues, and the patient leaves the hospital or
returns to his vocation. But all this time he appears cachectic, and
there will be found, on accurate observation, pathological variations
of the temperature and pulse. The appetite is poor; the bowels are
usually constipated; there are frequent chilly sensations and
horripilations, and a general malaise. This condition slowly passes
away in the few cases which recover; in others relapses occur, usually
of progressing severity, and terminate life. The period during which
the symptoms of the abscess are latent may be regarded as
corresponding to the latent period which sometimes intervenes between
an injury and the development of the symptoms of acute abscess, and
which, according to Lebert, may comprise several weeks or months. In
other words, the morbid process may be regarded all this time as
progressing under the mask of a remission. It is this latent period
which it is of the highest importance for the diagnostician to
recognize. There is usually headache, which is continuous and does not
change in character, though it may be aggravated in paroxysms. Usually
the temperature rises with these paroxysms, and if they continue
increasing in severity they may culminate in epileptic convulsions.

Many of the symptoms of cerebral abscess—prominently those attending
the rapidly-developed forms and the exacerbations of the chronic
form—are due to cerebral compression. It is the pulse and pupils,
above all, that are influenced by this factor.

In an affection having so many different modes of origin as cerebral
abscess, and occupying such a wide range of possible relations to the
cerebral mechanism, it is natural that there should exist many
different clinical types. So far as the question of the diagnosis of
localized cerebral abscesses is concerned, I would refer to the
article dealing with cerebral localization, in order to avoid
repetition. With regard to the etiological types, they will be
discussed with the respective causal factors.

ETIOLOGY.—Abscess of the brain is so frequently found to be due to
metastatic or other infectious causes that it is to be regarded as
highly improbable that it is ever of idiopathic occurrence. The most
frequent {797} associated conditions are—suppurative inflammation in
neighboring structures, such as the tympanic cavity, the mastoid
cells, the nasal cavity, or inflammation or injury of any part of the
cranium and scalp. The connection of these structures with the brain
through lymphatic and vascular channels is so intimate that the
transmission of a pyogenic inflammatory process from the former to the
latter is not difficult to understand. But disease of far distant
organs, such as gangrene of the lung, and general affections, such as
typhoid fever, occasionally figure among the causes of cerebral
abscess, particularly of the miliary variety.

Among the commonest causes of cerebral abscesses are those which the
surgeon encounters. The injury may be apparently slight and limited to
the soft parts, or the bone may be merely grazed. Gunshot wounds are
particularly apt to be followed by a cerebral abscess; and it has been
noted that those which granulate feebly, whose base is formed by a
grayish, dirty, and fetid material, are most apt to lead to this
ominous complication. The symptoms do not usually develop immediately,
and after the surgeon is led to indulge in the hope that danger is
past, proper reaction sets in, healthy granulations develop—nay, the
wound may close and be undergoing cicatrization—then the patient
complains of feeling faint or drowsy, and with or without this
premonition he has convulsive movements of one side, sometimes
involving both extremities and the corresponding side of the face.
Consciousness is usually preserved, but the spells recur, and the
patient is noted to be absent-minded during and after the convulsive
seizure. On some later day he is noticed to become pale, as in the
initial stage of a true epileptic seizure; total abolition of
consciousness follows, and the clonic spasms, affecting the same limbs
and muscles involved in the first seizures, now recur with redoubled
violence. After such an attack more or less paresis is observed in the
muscles previously convulsed. A number of such seizures may occur, or
a fatal issue terminate any one of them. Not infrequently the field of
the involved muscles increases with each fit. Thus the thumb or a few
fingers may be the first to show clonic spasm; in the next fits, the
entire arm; in succeeding ones, the leg and face may follow suit. In
such a case the periphery first to be convulsed is the first to become
paralyzed, thus showing that where the disease began as an irritative
lesion the cortex is now destroyed, and that around the destructive
focus as a centre the zone of irritation is spreading excentrically,
first to irritate and then to destroy seriatim the functions of the
various cortical fields in their order. According to the teachings
laid down in the article on Localization, the order of invasion and
extension, as well as the nature, of the focal symptoms will vary.
Finally, the attacks become more severe and of longer duration; the
patient does not recover in the intervals, but complains of nausea,
pain, confusion, and head-pressure. He is noted to be dull, his
temperature is slightly raised (100° F.), and the speech may be
affected. Several attacks may occur in a day, each leaving the patient
more and more crippled as to motility and mind. He is delirious and
drowsy at intervals; his temperature may rise after an attack from one
to four degrees, usually remaining near 103°-104° F. in the evening;
and, coma developing, death occurs, the convulsion or paralytic
phenomena continuing at intervals during the moribund period, and the
temperature and pulse sometimes running up rapidly toward the last. On
examining {798} the parts, it is found that the bone is necrotic at
the point of injury, usually only in its outer table, but sometimes in
its entire thickness. In exceptional cases the normal continuity of
the entire table is not interrupted to all appearances, and a small
eroded spot on the inner table is found bathed in pus, or a detached
necrotic fragment may be found in the latter. Corresponding to the
purulent focus on the inner table the dura mater is detached,
discolored, and perforated in one or more places with irregular rents
or holes which have a greenish or blackish border. An abscess is found
in that part of the brain which corresponds to this opening. There is
no question that it was caused by direct infection from the necrotic
spot.

Cases have been noted,[55] apparently of idiopathic origin, in which a
sudden paralysis of a few fingers was the first symptom produced by
the development of a cerebral abscess. In a few days such a paralysis
extends to the other fingers and to the forearm. Occasionally no
convulsive phenomena are noted, or choreic movements indicate, in
their place, that the cortical field is irritated. Such cases usually
run a rapidly fatal course.

[Footnote 55: Arthur E. W. Fox, _Brain_, July, 1885.]

The most frequent cause of cerebral abscess in civil practice is
suppurative inflammation of the middle ear. It may be safely asserted
that the person suffering from this affection is at no time free from
the danger of a cerebral abscess, a purulent meningitis, or a
phlebitic thrombosis of the sinuses. Cases are on record where the
aural trouble had become chronic, and even quiescent, for a period of
thirty years, and at that late date led to abscess with a fatal
termination. Of 6 cases of this character in my experience, 4 of which
were verified by anatomical examination, not one but had occurred at
least four years after the commencement of the ear trouble, and 1
happened in a man aged fifty-four who had contracted the latter
affection in childhood. In 2 there was in addition diffuse purulent
meningitis, limited on the convexity to the side where the abscess was
situated.[56] In 4 the abscess was in the temporal lobe, 1 of them
having in addition an abscess in the cerebellar hemisphere of the same
side; in a fifth the abscess was in the deep white substance of the
cerebral hemisphere, opening into the lateral ventricle, and in the
sixth it was in one cerebellar hemisphere alone.

[Footnote 56: One of these was seen during life by J. R. Pooley; the
other was a paretic dement at the New York City Pauper Asylum.]

The course of this class of abscesses is usually obscure: focal
symptoms are not commonly present, and the constitutional and local
symptoms usually appear as a gradual outgrowth from the aural
troubles. Thus there is at first usually little fever, vertigo, and
chilliness, but considerable tinnitus, and sometimes pain in the ear.
Occasionally local signs of a septic metastasis of the otitis, such as
œdema over the mastoid or painful tumefaction of the cervical glands,
are visible. The pain previously referred to the region of the ear now
becomes general; commonly—even where the abscess is in the temporal
lobe—it becomes progressively aggravated in the frontal and sometimes
in the nuchal region, and under an increase of the febrile phenomena
death may exceptionally occur without further complication. Even large
abscesses in one half of the cerebellum occur without producing
Ménière's symptom—a fact {799} which leads to the suspicion that the
purulent deposit must have been of slow and gradual development. In
one case distinct symptoms indicating an affection of the subcortical
auditory tract were observed. As a rule, this class of abscesses are
accompanied toward the close by active general symptoms—convulsions,
coma, narrowing and impaired light-reaction of the pupils. Delirium,
when a prominent symptom from the beginning, indicates the probable
association of meningitis with the abscess.[57] Occasionally severe
pain, rigor, high temperature, and paralysis may be absent even with
rapidly-developed abscess from otitis.[58]

[Footnote 57: The same is probably true of oculo-motor paralysis,
which Ross (_loc. cit._, vol. ii. p. 735) refers to uncomplicated
abscess.]

[Footnote 58: This was the case with an abscess containing five ounces
of pus recorded by C. S. Kilham at the Sheffield Medical Society
(_British Medical Journal_, February 13, 1886). As illustrating what
was stated about the non-correspondence of the pain and the location
of the abscess, it may be stated that notwithstanding this large
abscess was in the temporal lobe, what pain was present was in the
forehead.]

Ulcerative endocarditis, infectious osteomyelitis, pulmonary gangrene,
general pyæmia, and, as is claimed by a few authors, typhoid fever,
are often accompanied by multiple abscesses in the brain-substance.
Usually the foci are small, as may be readily inferred from the fact
that they are of embolic origin, the emboli being usually so small as
to lodge in very small vessels, and that the fatality of the primary
disease is so great as to cut short life before the abscess can reach
larger dimensions. For the same reasons the symptoms they produce are
rarely distinctive. In chronic lung affections accompanied by
putrescence in bronchiectatic or other cavities cerebral abscesses are
not uncommon occurrences. Under these circumstances, although we must
assume an embolic origin, the abscess is rarely multiple, and the
symptoms are as marked as in the ordinary varieties. Thus a patient
suffering from chronic phthisis, with or without prodromal malaise or
somnolence, experiences formications and pain in his right leg; he
then notices a slight halt in walking; twitches appear in the affected
extremity; it becomes distinctly paretic. The arm then becomes
affected in like manner; the pupils become unequal; a severe chill
occurs, followed by delirium, convulsions, coma, and death.

DIAGNOSIS.—There is little difficulty in recognizing the existence of
a cerebral abscess in which well-marked focal and constitutional
symptoms coincide, or where a distinct abscess-producing cause, such
as an ear trouble, a head injury, or a putrid bronchiectasis,
coexists.[59] But there are a number of cases, varying from the latent
form to forms with obscure general symptoms, whose recognition is
impossible or at best a matter of conjecture. Such cases may be
readily confounded with certain tumors. The existence of febrile
symptoms, although not excluding tumor, as some tumors are accompanied
by such, is greatly in favor of abscess. On the other hand, choked
disc, which is rare with abscess and found only with the very largest,
is in favor of tumor.

[Footnote 59: Yet a leading and careful authority was misled into
making the diagnosis of abscess in a case of ear disease complicated
by a cerebral tumor.]

PROGNOSIS AND TREATMENT.—The majority of cerebral abscesses must, from
the nature of the case, be regarded as not influenceable by medicinal
measures or surgical treatment. The miliary and other abscesses due to
general septic causes or to mycotic invasion, being in the nature of
{800} the case but features of intrinsically dangerous or fatal
primary diseases, do not call for special measures. It is different
with those due to local trouble about the head and to surgical causes.
Remarkable advances have been made in the operative treatment of
cerebral abscesses, chiefly owing to the increasing accuracy of the
localization of the affected areas through the disturbance of their
function, and to the perfection of surgical methods. A number of cases
by Gussenbauer, Wernicke, and others have shown that some abscesses
may be accurately located during life by the focal symptoms produced
by their presence. Wernicke's observation of a large abscess in the
occipital lobe showed two facts. First, it permitted the study of the
effect of large abscesses on the cerebral movements, as it was found
after trephining that the pulsation movement of the brain was lost and
the dura tensely bulging, thus indicating a high degree of cerebral
pressure. Secondly, the operation showed that an abscess can be
emptied of its contents, under moderate aseptic precautions, without
provoking contiguous inflammatory reaction or infecting the meninges.
Notwithstanding these favorable local conditions, the patient died.
Gussenbauer[60] was more fortunate. He surmised from the fluctuation
of some symptoms and the predominance of others that his patient had
an abscess in the frontal lobe. The suspicion was verified: an abscess
of the size of an apple was found, opened, and emptied of its
contents. The patient recovered without any immediate untoward
symptom.[61]

[Footnote 60: _Prager medizinische Wochenschrift_, 1885, Nos. 1, 2,
and 3.]

[Footnote 61: Epileptic and focal spasms subsequently developed, which
shows that a new inflammatory or other destructive process may have
set in in the vicinity of the emptied sac.]

The uncertainties of localization in some districts of the brain are
so great that a number of attempts to repeat the explorations and
aspiration of Wernicke and Gussenbauer have failed. In one case
recently operated on in New York City the aspirating-needle was run
into the brain-substance in several different directions without
striking the pus. It is a question under such circumstances whether
the chances of an abscess becoming latent, minimal though they be in
cases with pronounced signs, are not to be preferred to those which an
uncertain operation can give. The superficial encephalitic foci offer
far better opportunities for surgical triumphs. Here not only the
symptoms are much more constant, and point more unerringly to the site
of the morbid spot, but there are often other signs, such as the
evidences of impaction of a foreign body, local tenderness on
percussion, or bone disease, which aid in determining the proper spot
for the application of the trephine. Several operations where
traumatic encephalitis existed with or without leptomeningitis of the
convexity, followed by complete recovery, were performed by
Macewen.[62]

[Footnote 62: _The Lancet_, 1885, vol. i. p. 881.]

The medicinal treatment of abscess of the brain is limited to
derivative methods, whose aim is the relief of pressure—an aim whose
fulfilment is more frequently illusory than otherwise.

Benefit has been claimed from the energetic use of mercury, chiefly in
the form of calomel, by older writers; and recently Handfield Jones
has endorsed its administration, attributing to it a remission in a
case in which it was employed. It must be remembered, however, that
remissions occur spontaneously in this disease, and that the purgative
action of calomel may act well for the time being in an affection so
apt to be {801} associated with hyperæmia and increased cerebral
pressure as is an abscess of the brain.[63] In the nature of the case,
even this latter momentarily beneficial effect is at the best
temporary.

[Footnote 63: _Brain_, October, 1884, p. 398.]

The prophylaxis of cerebral abscess can be carried out only in cases
due to cranial and aural affections. The importance of treating all
scalp and cranial injuries under aseptic[64] precautions is recognized
by all surgeons. It is generally admitted that the trephining of a
bone suspected to be the site of an ostitic or necrotic process
involves fewer risks than the allowing it to remain. Similar
principles govern the treatment of the inflammatory involvement of the
mastoid cells often complicating otitis media. If trephined at all,
these should be trephined at the earliest moment. It was a belief
among the older aurists that the sudden cessation of an aural
discharge was of evil augury, and that cerebral complications were
more apt to follow under such circumstances than when the ear
discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have
opposed the exclusive application of the old dogma. In so far as the
older ear-surgeons regarded a profuse aural discharge as an
encouraging sign, in this respect they were of course wrong. But their
observation of the frequent concurrence of cerebral sequelæ with
suppression of discharge is, I think, borne out by a large number of
cases. It does not apply, however, to the suppression of discharge by
the rational employment of aseptic injections.

[Footnote 64: This term is used in its widest sense here.]


Spinal Hyperæmia.

The spinal cord is found to vary considerably in color in different
individuals. To some extent this difference is influenced by the
position occupied by the body after death, but not as markedly as in
the case of the brain. Thus it will be paler in a body which has been
kept in the prone than in one which has been kept in the supine
position.[65] It is usually found more injected in persons who have
died of febrile affection than in those who have died of exhausting
diseases; notably is this the case with typhus fever and with subjects
who die with congestive malarial chill. But the most intense
congestion, where the gray substance instead of having the normal rosy
hue appears like a blood-soaked sponge, and the white substance
instead of the tint to which it owes its name has a pink shade, is
found in subjects dying in convulsive disorders complicated by
asphyxia, such as epileptic status, tetanus, and certain toxic
disorders.

[Footnote 65: I have not seen it noticed anywhere, but it is a fact
readily demonstrable in any autopsy made in a well-preserved body that
when a short segment of cord is observed at the moment of section the
section surface appears pale; but if it be again examined after a few
moments, it will show a reddish tinge, marked as a faint injection
would be; this tinge distinctly deepens under the eye. I have observed
this in specimens which were not held in the hand, so that the
influence of pressure can be excluded. Nor do I believe that the
elasticity of the tissues is such as to account for the phenomenon.]

In attempting to apply the fact that varying degrees of vascular
injection are found on post-mortem examinations of the spinal cord to
the elucidation of certain clinical phenomena, we encounter the same
difficulties and sources of error that confronted us in the study of
nutritive {802} brain disorders. The majority of writers have
therefore contented themselves with making a careful clinical study of
the mostly subjective signs of disorders which, once designated as
spinal anæmia and hyperæmia, are now classified under the
non-committal titles of spinal irritation and exhaustion
(neurasthenia), as in this volume. A number of these disorders, like
the so-called anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet,
Baimer, and Brandis, would to-day be considered as hysterical or
reflex; and a few of the instances cited by their contemporaries as
cases of spinal hyperæmia have been since demonstrated to resemble the
initial phases of organic diseases of the cord.

The causes of active spinal hyperæmia are either direct, as when the
spinal centres are overtasked by muscular strain either through
over-exertion or through toxic convulsions, surprised by violent
shocks, such as concussion accidents, or collateral, as when a
physiological discharge (menstruation) or a pathological one
(hemorrhoidal flux) is suddenly checked. A few cases are reported
where carbonic-oxide-gas poisoning provoked spinal hyperæmia. But,
like the alleged cases of spinal hyperæmia after continued and
exanthematic fevers, they were probably cases of incipient or
established myelitis. Hammond claims that surface chilling exerts the
same congesting influence on the cord which he claims for the brain;
but no definite observations have been made in this direction.

Passive spinal hyperæmia has been attributed to obstructive cardiac
and chronic pulmonary affections. In such cases, as with most causes
acting on the circulation of blood in the nerve-centres, the
coexisting cerebral congestion usually masks the spinal. It is a
question how far the intense hyperæmia of the cord found in some cases
of tetanus, strychnia-poisoning, and the condition called
hydrophobia[66] is primary and an indication of neural
hyperexcitability, and how far it is secondary to the asphyxia
attending the last phases of these convulsive states. The weight of
opinion is in favor of an acceptation of the latter as the chief or
only factor.

[Footnote 66: In a case of hydrophobia clinically as well marked as
has been recorded, which I had the privilege of examining through the
courtesy of Kretschmar, both brain and cord were found remarkably
anæmic.]

Over-exertion and sexual excesses are frequently followed by a
sensation of fulness and tension in the sacral and lumbar regions,
which may be relieved by lying prone, while it is aggravated while
lying supine.[67] From the location of this pain it is evident that it
is not due to congestion of the cord or its membranes, but to fulness
of the vertebral and spinal veins of the lower segment of the
vertebral column. A similar sensation, which may be relieved by the
same change in position or by a hemorrhoidal flux, is complained of by
patients suffering from portal obstruction. The veritable symptoms of
hyperæmia manifest themselves in the parts which receive their nervous
supply from the affected districts. The reflexes are usually more
active; paræsthesias of different kinds, such as formication,
tingling, and creeping sensations, are common; and {803} there is more
or less motor weakness, the limbs feeling heavy and sometimes being
the seat of an acute pain. As a rule, these symptoms are limited to
the lower half of the body.

[Footnote 67: Although this fact has been questioned, I have no doubt
whatever that it is true, from a large number of observations. In many
subjects suffering from the results of excessive venery or
masturbation, an intolerable, sometimes pulsating, feeling in the
lumbo-sacral region is only relieved by raising the lower end of the
trunk with the back up. This condition is influenced by a change of
residence to a district having a different level above the sea, and
consequently a different barometric condition.]

There is very little question when these symptoms exist for any length
of time, and become aggravated, that more subtle nutritive changes
than are covered by the single term hyperæmia become responsible for
them. In a pure hyperæmia the position-test of Brown-Séquard, which
shows relief when the patient is upright or prone and aggravation when
he is supine, particularly if the gravitation of blood to the cord be
facilitated by raising the head and extremities, ought to yield
constant results. But in some cases, particularly those of
long-standing, the very opposite is noted: the patient's symptoms are
aggravated by standing or sitting up, and relieved by lying down. Here
there is probably exhaustion or malnutrition of the nerve-elements,
rendering them abnormally sensitive to exertion. This view is
supported by the fact that molecular disturbances, such as those which
probably accompany simple concussion, predispose the patient to the
development of the symptoms of spinal hyperæmia, and aggravate them if
established previous to such accident.

Hammond,[68] who in his chapter on Spinal Congestion and Anæmia
follows rather the older authors, such as Ollivier, than the newer and
either more cautious or more sceptical writers on the subject,
describes the symptoms of congestion as comprising belt sensations,
paraplegia, erections of the penis, muscular twitches, loss of
expulsive power, and incontinence of the bladder, paralysis of the
abdominal muscles, paralysis of the anal sphincter, loss or abolition
of reflex excitability, diminution of electro-muscular contractility,
and occasionally hyperæsthesia and shooting pains. It is not doubtful
for a moment that if such a case were to occur in hospital experience
it would be regarded as one of organic disease, and not incipient, but
well-established organic disease of the cord. Those making the
diagnosis would have their opinion strengthened if, as Hammond states,
the process took place with great rapidity and had a tendency to
extend itself and eventually involve the whole cord, or if, as
Brown-Séquard is by him cited as stating, bed-sores occurred in
addition. Although Hammond describes certain anatomical changes, such
as increased development of blood-vessels and distension and injection
of them, I am unable to find any cases recorded as spinal congestion
during life, and carefully examined with a due regard to sources of
error after death, in which such changes were found. It is true that
after strychnine- and cocaine-poisoning an intense hyperæmia[69] of
the cord is found. In mammals it is of a far more pronounced character
than in reptiles, and usually more marked in proportion to the
existing asphyxia. That the characteristic toxic effects of these
drugs is not to be sought for in their direct or indirect congesting
influence is shown by the fact that exsanguinated frogs can be made to
undergo strychnine tetanus when their blood is replaced by a saline
solution according to the method of Salkowski. Little support,
therefore, could be derived from a pretended analogy between toxic and
{804} pathological hyperæmias, even if the phenomena of both were
similar; which is not the case.

[Footnote 68: _Diseases of the Nervous System_, 7th ed., p. 392.]

[Footnote 69: It is true that in animals which are so organized that
the congestion cannot be attributed to asphyxia, as I showed (_Hammond
Prize Essay of the American Neurological Association_, 1878) in some
experiments on strychnine, arterial congestion and small foci of
hemorrhage were found in the upper cervical cord of frogs who had been
kept in continuous strychnine tetanus for over seventy days.]

The introduction of subaqueous caissons for workmen engaged in the
building of bridges, in which those employed labor under abnormal
atmospheric pressure, has led to the development of a
previously-unknown cerebro-spinal affection known as the caisson
disease, and in which, it is generally supposed, either congestion or
hemorrhage of the spinal cord occurs in consequence of sudden changes
of vascular pressure resulting from sudden diminution of the
barometric pressure. Clinically, this affection has been studied in
England, France, and above all in America in connection with the
building of the East River Bridge and the one over the Mississippi at
St. Louis.[70] Experiments by Hoppe-Seyler, Bert, and I. Rosenthal
have shown that a sudden diminution of pressure leads to hemorrhages
in various tissues, and, according to the two first-named, a
development of gas occurs in the vascular and other fluids of the
body. A number of peculiar symptoms which do not specially interest us
here occur in conjunction with the so-called caisson disease: these
are—pain in the ear, with or without otitis sicca; peculiar pains in
the joints, which occur on leaving the caisson, and are probably due
to hyperæmia of the joint-surfaces and sudden increase of the
intra-articular fluid; and retardation of the pulse-rate. In some
cases cerebral hyperæmia is added, the patients tottering about as if
drunk. The spinal symptoms consist of a paraplegiform affection. The
paralysis is usually sudden; in some cases the patient a few minutes
after stepping from the air-chamber falls down perfectly helpless as
far as the lower half of the body is concerned. The expulsive power of
the bladder is usually weakened, and there is anæsthesia to all forms
of sensation in the affected limbs, as well as diminished
electro-cutaneous sensibility. The patient often complains of a
strange feeling, as if the lower half of his body were a foreign
substance. With this the electro-muscular reactions are normal. In the
majority of cases these symptoms disappear entirely in from three to
ten days, but occasionally they remain longer; imperfect recovery of
motion and sensation occurs, or, as happened in a few cases, one of
which was carefully examined during life by Lehwess and after death by
Leyden, death occurs as in myelitis. In the only case where an autopsy
and careful microscopical examination were made under these
circumstances[71] peculiar fissures were found in the substance of the
spinal cord, surrounded by areas of reactive myelitis and filled with
granule-cells. The absence of any pigmentary relics of a hemorrhage
induced Leyden to assume that the lacunæ were not of hemorrhagic
origin. He inclines to the view that they were due to the escape of
gas from the blood-plasma, and consequent multilocular inflation of
the tissue. If his observation be confirmed, it constitutes a strong
objection to the hyperæmia theory of the caisson disease. There is
neither permanent hyperæmia nor congestive or hemorrhagic myelitis
developed, as far as the limited material thus far studied permits a
conclusion.

[Footnote 70: Clark, _St. Louis Med. and Surg. Journ._, cited from
Hammond, _loc. cit._]

[Footnote 71: E. Leyden, _Archiv für Psychiatrie_, ix. p. 316.]

Pure spinal hyperæmia rarely presents itself for treatment. The form
due to over-exertion is recovered from by rest in a very short time;
that due to suppressed discharges, by the re-establishment of the
latter or by {805} the application of leeches to the lumbo-sacral and
iliac region. Ergotin is recommended by Hammond in very large doses.
It is a question whether this drug may not exert a bad effect in
protracted cases where its use has to be continued for a long
time.[72] In using it, it is well to bear in mind that imperfect
nutrition of nerve-elements is perfectly compatible with an increased
blood-amount.

[Footnote 72: A young physician, who for a long period took ergotin in
twelve-grain doses for the relief of symptoms regarded as congestive,
acquired a tolerance of the drug such as I have not seen recorded
anywhere, and in addition presents some obscure signs of cerebellar
disease and initial optic-nerve atrophy.]

Strychnia has been given with benefit in the caisson disease—another
evidence, as this drug is theoretically contraindicated in true
hyperæmia, that this disease is not, as Hammond and the majority of
authors with him regard it, essentially a congestive affection. The
treatment of those numerous cases in which signs of venous fulness
accompany spinal exhaustion and irritation is detailed in the articles
dealing with those affections.


Spinal Anæmia.

Anæmia of the cord-substance proper, like hyperæmia, is practically
inseparable from the corresponding condition of the membranes. The
influence of a reduced blood-amount on the functional activity of the
spinal cord is more susceptible of exact demonstration than the
corresponding nutritive disturbance of the brain. As the functions of
this segment of the nervous axis are far simpler than those of the
higher organ, there is more unanimity among observers as to the
interpretation of their disordered states. In Stenon's experiment, and
the more elaborate modifications made by those who have followed his
method, it is found that interference with the supply of arterial
blood to the spinal cord is followed by abolition of the function of
the gray matter; if the supply be still further diminished, the
functions of the white tracts become eliminated; next the peripheral
nerves, and ultimately the muscles themselves, lose their normal
excitability. On the re-establishment of the circulation these various
parts regain their functional capacity in the inverse order of its
suspension—the muscles first, next the nerves, then the white
substance, and last the gray substance of the cord. The initial
symptoms of some cases of myelitis from refrigeration correspond more
nearly to such a result of artificial anæmia of the cord than they do
to anything that is customarily regarded as hyperæmia.[73]

[Footnote 73: I have seen distinct pallor of the spinal meninges on
dipping the posterior extremities of a dog, whose cord had been
exposed, into water. It is to be remarked, however, that other
observers, notably Hammond, have either obtained different results or
interpreted the consequences of refrigeration differently.]

No one has gone farther than Hammond in erecting a theoretical
anatomical framework which elaborately provides for the accommodation
of various symptoms of spinal anæmia. He describes anæmia of the
posterior columns, and sharply discriminates between it and anæmia of
the antero-lateral columns. It is a question whether the conducting
tracts of these columns are seriously affected in their functions by
anæmia as long as the centres of innervation are well nourished.
Undoubtedly, it is the gray substance of the cord which is most
vulnerable to the influence of {806} disturbed circulation and
nutrition, as Stenon's experiment has shown; and a glance at the
distribution of the blood-vessels will show that a partial anæmia or
hyperæmia, limited to special cornua in any considerable length of the
cord, is an exceedingly improbable occurrence. With regard to isolated
anæmia of the white columns, it is to be admitted that the posterior
are most vulnerable to malnutrition. But it is doubtful whether this
vulnerability is so great as to allow of an exclusively posterior
anæmia, or whether a protracted anæmia of this kind could exist for
years as a purely symptomatic—or, as some designate it,
functional—disorder.

Hammond candidly states that in specifically locating the lesions in
these affections he is aware that post-mortem examinations are wanting
to support them, and admits that what he calls anæmia of special parts
of the cord is the spinal irritation of most authors, and in part the
reflex paraplegia of others.

The most clearly-established form of cerebral anæmia is the one which
is indicated by the ischæmic paraplegia of Jaccoud and the paraplegia
following profuse hemorrhages. The former is produced by all causes
which, by obstructing the flow of arterial blood in the abdominal or
thoracic aorta, cut off the proper blood-supply to the cord, which the
latter receives through the intercostal and upper lumbar arteries.
Aneurism, compression by tumors, and embolism of the aorta produce
this result. The consequence is paraplegia corresponding in all
features of its development to the phenomena observed in Stenon's
experiment. These features, already detailed, suffice to show that it
is not the anæmia of the peripheral nerves and muscles that is chiefly
responsible for the paraplegia, but the insufficient irrigation of the
gray and white substance of the cord itself. The same is true of the
paraplegia following hemorrhage which has been noted after uterine,
renal, and enteric hemorrhages. Both affections are exceedingly rare.

The influence of general anæmia on the functions of the spinal cord is
not susceptible of accurate study. The cerebral enlargement of the
nervous axis is so much more unfavorably situated than the cord that
it suffers first and most when general anæmia is present. The
consequence is that the signs of cerebral anæmia mask those of spinal
anæmia. It is supposed, however, by many authorities that the effect
of anæmia on the cord may be regarded as an auxiliary factor in the
production of hysterical and neurasthenic symptoms.

How far the spinal cord is liable to suffer from arterial spasm is as
yet a matter of conjecture. It is supposable that just as a powerful
psychical impression provokes a sudden spasm of the cerebral arteries,
so a peripheral irritation may provoke a spasm of the spinal arteries.
In this way the reflex paralyses, motor and vaso-motor, are explained
by many writers.

The subject of reflex palsy has been so much confused by improper
cataloguing—if it can be so called—that some of the best authorities
have become sceptical as to its occurrence. Among the chief sources of
error has been the attributing to irritation of the genital organs
various convulsive, psychical, and paralytic disorders. Adherence of
the prepuce and its excessive length were charged with being
responsible for idiocy, imbecility, epilepsy, and every form of
paraplegia and panplegia. It was further claimed that instances of
complete cure of each of these {807} affections had followed the
removal of the exuberant or adherent prepuce. I cannot find a single
instance recorded where such a cure was effected in any of our large
medical centres, so as to prove convincing to critical colleagues. On
the contrary, L. C. Gray[74] has shown that various surgical
procedures have been needlessly resorted to on this erroneous theory
in cases of organic diseases of the spinal cord. I have seen two
unfortunate children suffering from the worst forms of anterior
poliomyelitis, one afflicted with pseudo-hypertrophic paralysis, and
several hydrocephalous and microcephalous idiots, whose prepuces had
been sacrificed to the theory alluded to—it is needless to add without
any result, good or bad.

[Footnote 74: _Reflex Irritation from Genital Irritation_. In this
paper written communications from all or nearly all neurologists in
the United States—certainly including all those of national fame and
large experience—are cited, in which they testify to never having seen
a case of this character cured by operations on the penis (_Annals of
Anatomy and Surgery_, Jan. and Feb., 1882.)]

The possibility of a reflex paralysis occurring from genital
irritation in the male cannot be denied; among the lower animals a
ligature around the spermatic cords sometimes produces paraparesis,
and paraplegia is a common complication of renal and vesical troubles
in others. But analogous observations in man are rare, and becoming
rarer with our increasing acumen in diagnosis. In females peculiar
reflex disturbances are found associated with uterine and ovarian
derangements. In one case of retroflexion, with possible dislocation
of the ovary, referred to me by H. J. Boldt, there is a remarkable
vaso-motor paralysis of the right arm during each menstrual period:
this member becomes greatly enlarged, of a purplish-blue color, and
cold. Equally remarkable are the reflex disturbances resulting from
the presence of worms in the intestinal canal. Every form of spinal
and cerebral paralysis, even aphasia, has been observed in connection
with helminthiasis. Such disorders yield as rapidly as they are
developed to the exhibition of vermifuges.

Special interest has been aroused by the discovery laid down in the
joint treatise of J. W. Mitchell, Morehouse, and Keen of reflex
paralysis following injuries, observed in the War of the Rebellion.
The cases cited by them appear singular on first sight. The paralysis
is often observed in parts of the body which are not only remote from
the seat of injury, but have no direct connection, physiologically or
otherwise, with it. The hand may be injured and the opposite leg
paralyzed.

Since Mitchell, Morehouse, and Keen first announced the existence of
this peculiar form of reflex paralysis a careful search has been made
by military surgeons engaged in other campaigns for like results.
Notably was this done in the Franco-Prussian War. A number of
confirmatory instances have been collected, some of which rival in
singularity those related by the discoverers of the affection. In one
case a unilateral paralysis agitans followed a punctured wound of the
opposite shoulder, and in another reflex aphasia followed a gunshot
wound of the lumbar region.[75] A discrimination is to be made between
such cases where the paralysis, anæsthesia, or neuralgia is an
immediate result of the injury, and those where they follow after
weeks or months. In the latter instance we have not true reflex
disorders to deal with, an ascending {808} neuritis having been found
in the few cases which could be carefully followed up.[76]

[Footnote 75: _Sanitäts Bericht über die deutschen Heere im Krieg
gegen Frankreich_, 1870-71, vol. vii.—abstracted in _Neurologisches
Centralblatt_, 1886, p. 207.]

[Footnote 76: In a case of Mollenhauer's, vesical paralysis and
paresis of the right leg occurred six years ago (1880) in a veteran of
our civil war who had a gunshot wound of the right hand, with signs,
which are still present, of occasional exacerbation of brachial
neuritis. Prodromal signs of paresis were noticed at intervals since
his return from the campaign. The bladder trouble and paresis are now
apparently stationary. Such a case can be accounted for only on the
assumption of an organic cord-change secondary to a neuritis.]

The theory that the reflex paralysis from utero-ovarian, intestinal,
and surgical affections, when acutely produced, is due to central
anæmia, is as acceptable as any other would be in the absence of
decisive observations.

Spinal anæmia will but rarely present itself as a subject for special
and separate treatment. When not associated with an intrinsically
grave condition, such as aortic obstruction, dysentery, fatal
hemorrhage, or typhoid fever, it is an exceedingly benign affection,
rapidly yielding to tonic and restorative measures combined with rest.


Embolism, Thrombosis, Hemorrhage, and Abscess of the Spinal Cord.

Although the spinal cord is a segment of the same central organ as the
brain, nourished in a similar way, and subject to the same
physiological and pathological laws, lesions of the vascular
apparatus, which play so important a part in brain pathology, play a
comparatively insignificant one in that of the spinal cord. Embolic,
thrombic, and primary hemorrhagic lesions of the cord are so rare that
their possible existence has even been denied. A primary thrombosis of
the cord has not yet been satisfactorily demonstrated to occur
independently of syphilitic lesions; and when it occurs the ensuing
tissue-changes, as described by Heubner, Julliard, and Greiff, are
usually in the background as compared to the gummatous, sclerotic, or
meningitic changes which coexist. The clinical as well as the
anatomical picture is accordingly either one of a myelitis or
meningitis, as the cases of Charcot-Gombault, Heubner, McDowell,
Wilks, Wagner, Zambaco, Homolle, Winge, Moxon, Schultze, Westphal,
Julliard, and Greiff show. (See Myelitis and Spinal Meningitis.)

With regard to the occurrence of hemorrhage into the substance of the
spinal cord (hæmato-myelia), it is so rare an occurrence that I can
recall but a single case in which I entertained the diagnosis of this
lesion; and in that very case I am unable to declare that it was not a
hemorrhagic myelitis. Aneurismal changes of the spinal arteries are
comparatively of rare occurrence, and as other predisposing causes to
primary vascular rupture are rare in the cord, the probability of its
occurrence is very much diminished. Hebold,[77] in a young girl who
had developed severe cerebro-spinal symptoms during a period of nine
months following an erysipelatous disorder, found the upper dorsal
cord, on section, dotted with numerous reddish and round points. These
points corresponded to {809} aneurismal dilatations of the vessels. As
there were other inflammatory and vascular lesions in the same
subject, the author referred their causation to a general
constitutional vice, the result either of the phlegmonous or of a
tuberculous disorder.

[Footnote 77: _Archiv für Psychiatrie_, xvi. 3. Rupture of miliary and
other aneurisms in the meninges has been reported by Astley Cooper,
Traube, and others. It is remarkable that such cases are more and more
rarely recorded from year to year in inverse ratio to the accuracy of
our spinal autopsies. I have never found a miliary aneurism below the
uppermost cervical level of the cord. On the other hand, I have found
extensive spinal hemorrhage in cases where the vessels of the cord
proper were fairly healthy.]

It is claimed that suppression of the menses, over-exertion, lifting
heavy weights, and concussion are causes of spinal hemorrhage. The
same causes are also mentioned for acute hemorrhagic myelitis; and it
is a question whether the supposed hemorrhage is an initial lesion or
secondary to congestive or anæmic softening.[78]

[Footnote 78: I have never found vascular ruptures, although carefully
searching for them, in the spinal cord of persons dying instantly
after falls from a great height, or, as in one case which I was
fortunately able to secure the cord of, where the subject had been
violently thrown down. Where hemorrhages have been found under these
circumstances they were, as far as I am able to learn from the cases
recorded, meningeal.]

The symptoms attributed to spinal hemorrhage are the same, taking the
same locality of the cord, as those of a very rapidly-developed
transverse myelitis. It is unnecessary to enumerate these here in
anticipation of the next section. They are described as being much
more sudden. This suddenness is the only diagnostic aid on which we
can rely.[79] The fate of the patient is said by Erb to be decided
within a few days. If he survive the immediate consequences of the
hemorrhage, he is apt to recover, as to life, altogether, with such
permanent atrophies, paralyses, and anæsthesias as are entailed by the
destruction of the tracts and gray substance involved in the
hemorrhage. The treatment recommended for this condition consists of
rest, either in the lateral or prone position, local depletion and
derivation to the intestinal canal, as well as the internal use of
ergotin. The local application of ice, which is also advised, is
probably based on illusory views.[80] After the immediate danger is
past the case is to be treated as one of myelitis—a very safe
recommendation in view of the probability that it was a case of
myelitis from the beginning.

[Footnote 79: And even this sign is unavailable as a distinguishing
feature in supposed hemorrhage from concussion, as sudden paraplegias
of motion and sensation are found in some cases of railway spine, and,
although a number of cases terminating fatally have been examined,
there was not always hemorrhage even in the meninges.]

[Footnote 80: Until authorities shall have agreed as to what effect
the exposure of the bodily periphery to certain temperatures has on
the circulation of the cord, it would be premature to make any special
recommendations as to the temperature at which they should be kept. I
am inclined to believe that while, as is universally accepted, a
general cooling of the bodily surface tends to increase vascular
fulness in the cord, as in all other internal organs, a partial
cooling, as of the feet, produces local anæmia at the level of origin
of the nerves supplying the cooled part. Certainly, the bilateral
neural effects of unilateral cooling are in favor of this view.]

The descriptions given of the hemorrhagic foci as observed after death
strengthen the view that they were in the majority of cases of
myelitic origin. Usually, they are stated to extend up and down the
cord in the direction of least resistance—that is, in the gray
substance—resembling an ordinary apoplectic clot. But in their
neighborhood there was usually considerable softening, and, to judge
by the descriptions given, this softening differed in no wise from
that which is the characteristic feature of acute myelitis;[81] and
often the transition from a peripheral zone of white {810} softening,
through an intermediate zone of red softening, to a central compact
clot, is so gradual as to leave it unquestionable that the softening
pre-existed, and that a vessel had broken down in the midst of the
myelitic detritus. Many ancient foci of myelitis betray the
hemorrhagic complication of their initial period by the presence of
pigmented residue of the absorbed clot.

[Footnote 81: In the latest treatise on nervous diseases published in
our language (Ross, _loc. cit._, vol. ii. p. 325) the insufficient
foundation on which a whole chapter has been built up is illustrated
by the admission that the usual evidence of acute central myelitis may
be observed far beyond the limits of the hemorrhagic infiltration. If
a large area of softening in the brain were found to contain a central
or peripheral clot of blood, and histologically resembling a typical
embolic or thrombic softening, no one would be in doubt as to which of
the two was the primary lesion.]

Embolisms and embolic softenings of that part of the spinal cord which
is supplied by the small spinal vessels are so rarely observed in the
dead-house that our knowledge of their possible occurrence and
character is almost entirely the result of experimental observations
or based on analogy. The situation of these vessels, the angle at
which their supply-tubes are given off from the aorta, all act as
protectors of the cord against what is one of the chief dangers to
which the brain is exposed. No definite symptoms have been attributed
to the few doubtful cases of simple embolic occlusion of the spinal
arteries found accidentally in human subjects. Even those emboli
which, when once let loose in the circulation, are found distributed
in nearly every organ of the body, those derived from ulcerative
endocarditis and those due to the invasion of micrococci, are
comparatively rare in the cord. Leyden found multiple capillary emboli
in the spinal cord from the former cause. Small grayish white foci in
a similar distribution were found to be due to an invasion of
cocco-bacteria from a decubitus by Rovigli.[82] In this latter case an
increase of pain and muscular spasm in the history of the case of
sclerosis which was thus complicated was attributed to the parasitic
affection.

[Footnote 82: _Rivista sperimentale di Freniatria_, 1884, x. p. 227.]

Just as simple and infectious embolic lesions are frequent in the
brain and rare in the cord, so purulent inflammation or abscess is an
exceptional occurrence in spinal as compared with cerebral pathology,
and probably for the same reasons.


Simple Acute Myelitis.

SYNONYMS.—Spontane (primäre) acute Rückenmarkserweichung, Softening of
the spinal cord, Ramollissement blanc de la moelle, Myélite aiguë.

As Leyden, whose treatise[83] may be regarded as the foundation of our
knowledge on this subject, correctly avers, it is to Abercrombie and
Ollivier that we owe the determination of the existence of that acute
structural disease of the spinal cord, now termed myelitis, as an
affection independent of meningeal changes. The anatomical
descriptions given by these older writers may be accepted at the
present day as models of accurate observation by the naked eye. Their
statement that in acute myelitis the substance of the spinal cord is
softened and changed into a puriform, yellowish, diffluent mass; that
while the disorganization is sometimes more marked in the posterior,
at others in the anterior, and occasionally in the lateral half, it is
most pronounced in the axis of the cord, because the central gray
substance is the favorite starting-point {811} of the morbid
process,—requires no modification to-day. Considerable doubt existed
in the minds of the contemporaries of Ollivier and Abercrombie as to
whether this change was the result of a true inflammation; and one of
the clearest thinkers of the day, Recamier,[84] regarded myelitic
softening as a lesion peculiar to the nervous apparatus, and different
from ordinary inflammation. I believe that the most profound
investigators of the present day have not been able to rid themselves
of a similar doubt. The discovery of Gluge's so-called inflammatory
corpuscles, which was regarded as settling the question, only served
to confuse the student by the confidence with which it was urged that
they were infallible criteria of the inflammatory process. Under the
non-committal designation of granule-cells these bodies still flourish
in the annals of cerebro-spinal pathology. As we shall see, a number
of products of real disease, of artifice, and of cadaverous change
have passed and do pass muster under this name. The first substantial
progress in our knowledge of the minute processes underlying
inflammation of the spinal cord was made by Frommann and Mannkopf, but
it applied altogether to the chronic inflammatory or cirrhotic
affections of the cord. The difference between acute and chronic
myelitis is greater than is the difference between acute and chronic
inflammation in any other organ; and it must be admitted that if
Recamier is to be regarded as having erred in asserting that acute
myelitis is not a true inflammation, he is justified in so far as he
asserted many features of the process to be altogether peculiar to the
organ affected. Leyden himself attempted to throw light on the subject
by provoking myelitis experimentally in dogs. He injected Fowler's
solution into the spinal cords of three dogs, and in each instance
produced changes which he interpreted as comparable to the myelitis of
human pathology. But the inflammation thus provoked was not of the
cord-substance alone; it also involved the membranes, and the
inflammatory foci were in several instances purulent. Now, pus
never[85] forms in ordinary myelitis. An abscess of the cord never
occurs where a septic agency can be excluded. In six dogs whose spinal
cords I wounded in the dorsal and lumbar regions by aseptic methods,
and who survived from two to seven days, I never found purulent or
indeed any active inflammatory process, as that term is ordinarily
understood, but exactly such passive and necrotic or reactive changes
as occur in the acute myelitis of human pathology.

[Footnote 83: _Klinik der Rückenmarkskrankheiten_, ii. p. 115.]

[Footnote 84: Cited by Leyden.]

[Footnote 85: In the textbooks and encylopædias, without an exception,
the statement that pus may be a product of myelitis is made. This is
true of traumatic cases and of such depending on septic and zymotic
causes alone. I am unable to find a single carefully observed case of
the occurrence of pus in simple myelitis in the literature.]

Owing to the advance of clinical and anatomical knowledge made within
the past fifteen years many forms of spinal disease classed with the
inflammations have been recognized as distinct pathological entities,
no longer to be confounded with simple acute myelitis, ordinarily so
called. Special forms of acute spinal paralysis, notably acute
poliomyelitis anterior of children and the corresponding chronic
affection among adults, have become separated in this way, and are
accordingly treated of in separate parts of this volume.[86]

[Footnote 86: For other and practical reasons the traumatic and
compression forms of myelitis are also assigned a separate place.]

{812} Some dispute exists as to the propriety of making a distinction
between acute and chronic myelitis, since an acute myelitis, if the
initial attack be recovered from with life, presents a similar
condition clinically as chronic myelitis; and this quiescent or
slowly-progressing condition may extend over many years. The term
acute with reference to inflammation of the spinal cord refers only to
the active period of the disease. Just as an embolic softening of the
brain is an acute affection, but may be followed by a chronic
paralysis or aphasia, so the acute myelitic process may be followed by
a chronic paraplegia. It is improper to call the latter a chronic
myelitis. It is merely a protracted symptomatic sequel of the acute
process. The latter is distinguished from chronic myelitis both
clinically (by the rapidity of its onset) and anatomically (by the
early dissolution of nerve-elements in the focus of disease). Limited
in this sense, acute myelitis, excluding the special clinical forms
already adverted to, is rather a rare disease.

MORBID ANATOMY.—The most recognizable change noted in an acute
myelitic focus is one of consistency: the spinal substance is
softened. In some cases the softening is so slight that the observer
may doubt whether he has a pathological or cadaveric softening to deal
with, the dorsal cord, which is most apt to be the site of an acute
transverse myelitis, being precisely the part which is most apt to
show the latter change even in fairly well-preserved bodies. In
extreme cases the softening may be so intense that the cord-substance,
completely fluidified, runs out of the meningeal sac, leaving the
latter a collapsed membranous cylinder to mark the place where the
cord once was. Where the cord-substance is sufficiently firm to permit
of sections being made through it, the normal outline of the gray and
white substance is found obliterated, either presenting the appearance
as if the gray and white matter had been stirred up together or of a
more uniform color-change. The color may be either white, reddish,
yellowish, or chocolate-like. It depends upon the participation of the
blood-vessels in the change. If there be much hyperæmia, there will be
developed what is known as red softening; if there be much
extravasation and commingling of blood with the diffluent cord-tissue,
a chocolate color will mark the diseased area; and similarly one and
the same focus may present different tints in different parts
according to the age and intensity of the process and the more or less
advanced retrogressive metamorphosis of the extravasated fluid. As
already stated, the purulent form of softening or abscess does not
occur in ordinary myelitis.

There is considerable variation in the extent of the affected areas of
acute myelitis. In the typical and severe transverse form the whole
thickness of the cord may be disorganized, and the disorganization may
extend in the length of the cord, so as to involve the level of exit
of from two to five pairs of nerves. In less furibund cases the area
of absolute softening is confined to the gray substance and its
immediate neighborhood, the submeningeal white substance being but
slightly affected or escaping. Sometimes several foci of intense
softening are scattered through a short length of the cord and
connected by less severely involved areas of softening or œdema.
Leyden distinguishes three types of distribution—the transverse, the
longitudinal, and the disseminated insular or multiple form. He
includes under the {813} longitudinal type the so-called central
softening of Albert, but undoubtedly many cases of syringo-myelia have
passed under this designation. The submeningeal form of softening
which, with Ollivier, he states to occur in association with spinal
meningitis, must be a very rare affection, as it is difficult to find
a well-established case recorded. The longitudinal form shows the same
predilection for the gray substance which the acute myelitic process
generally does, but I have seen a finely demarcated fascicular
myelitis limited to the lateral column in a paretic negro. In this
case the pyramid tract and the contiguous area in front of it were so
intensely softened that for a length of twelve centimeters a hollow
canal ran through the cord in the place previously occupied by the
diseased substance. In recent cases of myelitis the diseased area is
usually found surrounded by a transition zone in which, the morbid
change gradually becoming less intense, the consistency is firmer, and
which merges into that of the normal cord. In cases where death occurs
after a few weeks a more abrupt demarcation is usually found; this is
due to the reactive changes occurring in the neighborhood. The
connective tissue becomes firmer, and thus the softening centre
becomes surrounded by a sclerosing capsule. Ultimately, the centre
undergoes complete disintegration and absorption, and a cavity is left
behind filled with a clear fluid; in short, a cyst surrounded by a
firm capsule represents the residua of disease. In cases where the
softening at the centre of the focus does not proceed so rapidly nor
reach so high a degree as to result in liquefaction, the less
vulnerable elements, the blood-vessels and supporting tissues, survive
the death of the ganglionic and conducting substance; the connective
elements hypertrophy, and thus a firm sclerotic patch is formed,
indicating the location of the previously softened field.

It seems to be generally admitted, with Hayem, that the blood found
exuded in the hemorrhagic form of myelitis does not necessarily
indicate an active determination, but is rather, like some forms of
so-called red softening of the brain, the result of capillary rupture
or necrosis in the midst of the disintegrated tissue, now rendered
incapable of supporting the vessels. The existence of a purely white
form of myelitic softening shows that a textural change is the primary
occurrence, and that the participation of hyperæmia or congestion is
not an essential feature of myelitis. The assumption of an initial
inflammatory congestion is made rather on theoretical grounds than on
the basis of observation. It is simply incredible that, as Ross[87]
claims, white softening should be a third stage, preceded by red and
yellow softening as a first and a second stage! How the extravasated
blood, which pathologists generally allow to leave long-lasting
traces, manages to disappear, and how blood-vessels in the midst of
necrotic or œdematous surroundings suddenly acquire such contractile
energy as to produce a total emptying of their contents while the
perishable nerve-elements remain behind, are problems which should be
solved before attempting to assign to a condition which is often found
to be a primary phase of myelitis the position of a late and
regressive stage. Erb admits that red softening, to which he also
assigns the position of a first stage, is very rarely seen, only
traumatic and rapidly fatal cases of central myelitis offering
opportunities of examining it. None of the {814} various forms of
exudation claimed to occur at this period under the names of vitreous,
colloid, or hyaline deposit have been confirmed in any recently
well-studied case.[88] The great mass of authorities, however, still
agree in regarding the minute changes of the initial stage of myelitis
to correspond to those of ordinary inflammation. The vessels are
described as injected, the adventitial spaces as crowded with the
formed elements of the blood, and the vascular walls and the neuroglia
infiltrated with granule-cells and fatty granular matter. By some,
inflammatory changes of the neuroglia are described, but I am unable
to find a single case in which these were determined in early fatal
cases. As far as our observation goes, the hypertrophy of the
neuroglia is a later occurrence.

[Footnote 87: _A Treatise on Diseases of the Nervous System_, 1882,
vol. ii. p. 280. The author states no authority, nor does he advance
his own observations in support of this statement.]

[Footnote 88: Baumgarten's case of hyaline exudation, _Archiv der
Heilkunde_, vol. xvii. 276, was an infectious myelitis and associated
with anthrax.]

As to the nervous elements themselves, they are always found affected.
The nerve-cells appear inflated, their processes fragile, sometimes
suddenly swollen in their course, at others very thin and brittle.
Multiplication of the nuclei of the large multipolar cells has been
described. It must be an unusual occurrence, as it has been confirmed
by but a few of the numerous observers who have examined into this
question. The protoplasm of the nervous elements loses its normal
striation and fine molecular granulation; it becomes either coarsely
granular or hyaline. The axis-cylinders, both in their intracinereal
and their intramyelinic course, show changes similar to those of the
cell-processes in the gray matter. Particularly frequent are swellings
in their course, the diameter of the cylinder being so much increased
as to almost equal that of the myelin tube. This increase in diameter
is regarded as an inflammatory swelling by some, as secondary to
disturbed nutrition by others; it precedes disintegration: the
substance becomes granular, fragile, and in the end dissolves. In the
mean time the myelin loses its continuity, irregular segments of it
fusing into round and oval masses.[89]

[Footnote 89: Many of the bodies represented as granule and colloidal
cells are in reality round spheres of myelin, whose resemblance to a
nucleated cell is sometimes heightened by their occasional inclusion
of a fragment of an axis-cylinder which has not yet lost its power of
imbibing carmine and other dyes. Where softening has proceeded
farthest, there the spherical and other forms of myelin are found
crowding the field, and mingled with them are blood-corpuscles,
fragments of blood-pigment, granular detritus, and bodies known as
fatty granular cells. A number of bodies of very different origin have
received this name, some of them, like the fragments of myelin alluded
to, not even meriting the name of cells. Others, however, are
veritable formed histological elements, either leucocytes or cellular
ingredients of the neuroglia, which, having fed on the products of
myelin disintegration, have become enlarged and coarsely granular. The
longer the duration of the process the more numerous are these bodies,
showing that they are not the coarse and essential factor of the
inflammation, but an accompaniment, subserving some conservative
process, inasmuch as they either remove effete material or contribute
to the permanent organization of the cicatricial or atrophic tissue.]

The period now reached by the morbid process may be regarded as a sort
of interregnum. The necrotic tissues have not yet disappeared on the
one hand, the products of inflammation have not yet organized
themselves on the other. It is in this period that the ganglionic
elements are described as undergoing certain changes in outline and in
appearance. Above all, one change has interested observers, which,
consisting in the development of what appear to be spherical vacuoles
in the interior of the cell, is termed vacuolization. I can compare it
to nothing so nearly as to {815} the appearance which is produced by
the formation of gas-bubbles in a putrefying albumen or other
semifluid substance.

This vacuolization of ganglion-cells is now regarded as a cadaveric
change. It is not agreed, as yet, whether its occurrence in myelitis
is so frequent as to suggest its ante-mortem occurrence as a veritable
feature of the disease. I have been struck by this change in the
neighborhood of wounds artificially produced in dogs, even in the
fresh specimen. It must be remembered, however, that under these
circumstances, the nutrition of the cell being destroyed and exposure
to the macerating effect of the cerebro-spinal and pathologically
exuded fluids occurring, a cadaveric change may take place intra
vitam.

The influence of phosphorus and alkaloid as well as metallic poisons
on the cord has been experimentally studied by a number of observers.
Unfortunately, Popow, Tschisch, and Danillo—who described as
characteristic a resulting change in the staining reaction of the
cells, the development of vacuoli in them, and an atrophy of their
processes—had not made a sufficient number of examinations of normal
cords under like methods of preparation to recognize which of these
deviations is without the physiological confines. Kreyssig[90]
demonstrated the existence of all these conditions in the cords of
perfectly healthy animals preserved in chromic acid;[91] and Schultze
confirms him, and expresses a surprise, which must be shared by all
reflecting investigators, that poisons of so widely different a
character should have an identical effect on the cord-substance, as is
claimed by the writers named.

[Footnote 90: _Virchow's Archiv_, cii.]

[Footnote 91: He attributes the remarkable difference in staining of
nerve-cells of the same ganglionic group and in the same section to
the sudden transferral of the hardened specimens to strong alcohol,
which seems to be the custom in some German laboratories. He claims
that uniformity in staining is effected if the specimen be transferred
from the chromic preparation to weak alcohol, then to stronger, and
thus by gradual increase of the strength to strong spirit. Possibly,
instead of approximating the real structural indications by this
method, Kreyssig may obliterate them. In specimens which alcohol is
not permitted to touch before staining is completed, very deeply and
very lightly stained cells will be found almost side by side. The
shorter the hardening process, the more perfect the staining method,
the more likely are these differences to be found. It is reasonable to
assume that the difference in dye-absorbing power indicates slight
differences in the cell-protoplasm, marking the nutritive state of the
latter and occurring within physiological limits.]

If life be prolonged and the conservative processes assert themselves,
the disintegrated material disappears, and as the white color of the
greater area of the cord was due to the myelin, and the latter has now
become destroyed within the diseased area, the latter presents a
grayish color. This phase is often termed gray softening. The
consistency is, however, much firmer than in the previous stage.
Trabeculæ of connective tissue form, enclosing in their meshes a large
number of neuroglia-nuclei and sometimes spaces filled with fluid.
According as condensation and retraction or rarefication preponderate
the process will terminate either in the formation of a sclerotic
focus or of a cyst. Occasionally an irregular spongy tissue containing
several small cysts results.

Charcot claims that a restitution of anatomical continuity, and
therefore of physiological potentiality, may occur in a myelitic
cicatrix. But the experiments of Kahler[92] and Homén[93] prove that
when a nerve-tract {816} is once destroyed within the spinal cord all
hope of restoring that tract in structure, and thus to restore its
functions, is at an end. Unlike the fibres of the peripheral nerves,
those of the spinal cord and brain do not seem capable of
regeneration.[94] If a restoration of function is to occur at all, it
must occur through other channels than those destroyed—in other words,
by vicarious action.

[Footnote 92: _Prager medizinische Wochenschrift_, 1884, No. 31.]

[Footnote 93: _Contribution expérimentale à la Pathologie et à
l'Anatomie pathologique de la moelle épinière_, Helsingfors, 1885,
abstracted in _Centralblatt für die medizinisches Wochenschriften_,
1886, No. 16.]

[Footnote 94: According to the first observer, this is probably due to
structural differences. The extramedullary fibres have a sheath and
annular constrictions which are absent in the intramedullary.]

In a large number of cases myelitis is a limited affection; that is,
its ravages remain confined to the area originally involved. But
occasionally the morbid process involves the next segments above or
below, extending with specially great rapidity through the anterior
gray horns. Exceptionally, the entire cord may thus become the site of
a generalized myelitis. There is one segment of the cord which may be
regarded as possessing an acquired vulnerability when a myelitic focus
is in its neighborhood, and that is the lower end. It seems that while
the results of a transverse myelitis in the middle dorsal cord may
remain stationary for ten or more years, those of a transverse
myelitis at the upper lumbar level do not; on the contrary, the entire
cord below the lesion appears to be doomed to undergo the same
degeneration by contiguity. This is the only occurrence which seems to
deserve the name of a descending myelitis: an ascending extension is
more frequently noted in other parts of the cord, but the frequency of
both the so-called ascending and descending types has been unduly
magnified by the inclusion of the secondary degenerations, which are
constant sequelæ of all complete destructive transverse lesions of the
cord, but which are rather passive phenomena, and probably influence
the clinical progress of the case but little, except under such
conditions as are potent in that chronic form of myelitis which
underlies tabes dorsalis.

CLINICAL HISTORY.—The symptoms of acute myelitis usually correspond to
those of any more or less completely transverse lesion of the cord,
and accordingly vary with the altitude of the upper level of the
lesion. In a general way, they may be stated as consisting of—

First, paralysis of movement in the parts supplied from the nerves
given off below the level of the lesion. The reason for this can be
easily recognized in those cases where the pyramid tract, which
conveys voluntary impulses centrifugally, is interrupted by the
softening.

Second, paralysis of sensation in the parts supplied by the same
nerves. This is equally explained by the pathological interruption of
the centripetal impressions normally conveyed brainward.

Third, alterations in the nutrition of the parts supplied by the
nerves arising in the affected level.

Fourth, abolition of those reflexes which are translated in the level
of the lesion.

Speaking crudely, then, the symptoms of a transverse myelitis fall
into two natural groups. The one which includes the first and second
categories enumerated are symptoms due to interruption of cerebral
functions; the other, which comprises the last two categories, being
due to abolition or perversion of spinal functions. There is a third
group comprising certain constitutional symptoms.

{817} Aside from those variations due to the distribution, extent, and
intensity of the lesion there are others which depend on the rapidity
of its invasion. There are three types in this respect—the
apoplectiform, the ordinary acute, and the subacute. The term
apoplectiform has been used in two different senses, one being
clinical, and referring to the rapidity of onset of the symptoms; the
other anatomical, and referring to the nature of the lesion. It is,
however, doubtful if a distinction in the latter sense is practically
valuable. The presence of a blood-clot in a myelitic focus is itself
secondary to the softening, and the intensity and rapidity of the
process must have shown itself in the development of the latter.[95]
The term ought, therefore, to be used in a clinical sense only.

[Footnote 95: I am able to recall but a single case in which, even
clinically speaking, a primary hemorrhage into the cord-substance was
plausible. In this instance a sudden arrest of menstruation had
occurred nearly simultaneously with a combined strain and exposure in
a young girl.]

The constitutional symptoms of acute myelitis—which, however, are
often absent—are its most distinctive features in one sense. Disorders
of motion and sensation and perversions of nutrition are signs common
to all destructive affections of the cord, whether of a traumatic,
neoplastic, or a chronic inflammatory character. But fever, headache,
and delirium,[96] associated with gastric and visceral disturbances of
acute development, are not found to be initial and intrinsic symptoms
with them as with acute myelitis. In their absence the mode of onset
is characteristic. A high degree of paralysis, motor or sensory, is
developed with a rapidity unequalled in any chronic affection of the
cord. Sometimes there is a prodromal period in which formication,
numbness, and disorders of movement are observed in the same part of
the body which are destined to become paralyzed at a later stage of
the malady. Within a few hours, days, or at most weeks, complete
paraplegia may become developed. The prodromal symptoms may include
any form of disturbed sensation. Lancinating pains, tingling, a
feeling of the limbs falling asleep, peculiar and indescribable
sensations attending the acts of micturition and defecation or of
placing the feet violently on the ground, are common. Occasionally
they are found in one limb only, although motor and sensory paralysis
may ultimately occupy the symmetrical member as completely as the one
first involved. In some cases it has been noted that the patient is
unable to lie down, or, if lying, to occupy the dorsal recumbent
position. This feature has been utilized to support the theory of an
initial congestion, which is supposed to be relieved or aggravated
according as the cord is kept elevated or depressed.

[Footnote 96: These symptoms are to be regarded as actual parts of the
myelitic symptoms only when they accompany the prodromal or initial
periods. The later complications, uræmia and septicæmia, the latter
arising from pyelitis, cystitis, or decubitus, often lead to
constitutional disturbance which is not due to the myelitis as such.]

In most cases of transverse myelitis, when the anterior cornua are
destructively involved, we possess in the electrical tests valuable
and unerring means of determining the altitude and extent of the
lesion. Whenever we find the atrophy of a paralyzed muscle accompanied
by qualitative electrical changes in myelitis, we must conclude that
the cell-group from which that muscle receives its nerve-supply is
destructively involved.[97] These changes are particularly well
demonstrable when the {818} cervical or lumbar enlargements are
affected. They are not as readily ascertainable in the case of a
transverse myelitis in the upper dorsal region, on account of the
situation of the muscles supplied by the upper dorsal nerves, and the
consequent difficulty of application of the necessary tests.

[Footnote 97: The proposition, originally, I believe, made by myself,
that there are distinct cell-groups in the spinal cord which are
constant with certain animal species, and correspond in relative
development to ventral, dorsal, and appendicular muscular groups
(“Architecture and Mechanism of the Brain,” _Journal of Nervous and
Mental Diseases_, April, 1880), appears to be confirmed in a general
way by the researches and cases of Edinger, Kahler-Pick,
Dejerine-Major, Genzmer, Von Monakow, Sahli, Prévost-David, F.
Schultze, Remak, and Parrot-Joffroy; for the knowledge of the first
and last of which I am indebted to the review of the subject by Starr
(“Localization of the Functions of the Spinal Cord,” _American Journal
of Neurology and Psychiatry_, August, 1883).]

The disturbance of the deep reflexes with very few exceptions affects
the same peripheries as are represented in the destroyed and impaired
gray nuclei. Thus, if the lower part of the lumbar enlargement be
affected, the reflexes of the Achilles tendon and the gluteal muscles
will disappear; if the upper lumbar enlargement, the knee-jerk
disappears.[98] Disease of the lower part of the cervical enlargement
is in like manner associated with absence of the wrist-tendon
reflexes, while the disappearance of the elbow-tendon reflex suggests
a higher involvement at the levels of the fifth and sixth cervical
nerve-roots.

[Footnote 98: The disappearance of the knee-jerk and similar reflexes
was originally supposed to be a phenomenon exclusively pertaining to
spinal disease and to a destructive lesion anywhere in the track of
the centripetal and centrifugal nerves connected with that segment of
the cord in which the reflex is supposed to be translated. But aside
from a number of physiological observations[99] which prove that
cerebral conditions may influence the intensity of the jerk, there are
pathological ones which show that it may be permanently abolished in
disease of the pons and cerebellum, and temporarily abolished or
diminished immediately after capsular and ventricular hemorrhage. The
associated symptoms in the former case, and the history of the onset
and total hemiplegia in the latter, serve to distinguish them from
destructive spinal lesions should the occasion for discriminating
between them ever arise; which is not likely.

[Footnote 99: S. Weir Mitchell and M. J. Lewis found that voluntary
effort increases the jerk at first, but if continued diminishes its
excursiveness (_The Medical News_, 1886, Feb. 13th and 20th).]

In complete transverse acute myelitis of the cervical region high
fever is a constant symptom. In unilateral myelitis of this region
flushing of the face and unilateral sweating are produced, together
with iridoplegia, sometimes preceded by dilatation, owing to initial
irritation and succeeding paralysis of the sympathetic branches
originating at this level of the cord.

Just as the disturbed reflexes and the belt sensations enable us to
distinguish at what levels of the cord the myelitis is situated, so
the distribution of the motor and sensory paralysis affords
corroborative evidence of such location and additional proof of its
extent and intensity.

Transverse myelitis at and above the level of origin of the phrenic
nerve is almost immediately fatal, through its interference with the
innervations required in respiration. In the upper part of the
cervical enlargement it produces complete paraplegia of motion and
sensation in the trunk and all four extremities. In the lowest part of
the cervical enlargement it produces paralysis of the same parts, but
the serratus magnus and scapular muscles escape. The nuclei of origin
of the muscles moving the upper extremity are situated so that those
which are farthest removed from the axis of the body when the arms are
extended are situated lowest in the cord. The sensory paralysis is
distributed in harmony with the motor paralysis; that is, when there
is paralysis of motion in the hand {819} and forearm the anæsthesia or
subjective numbness is also in the hand and forearm. The same
correspondence is not found in affections of the lumbar enlargement,
for anæsthesia of the gluteal region accompanies paralysis of the
crural muscles when the lesion is low down at the level of the lower
lumbar and upper sacral nerves. The distribution of the anæsthesia, in
other words, is not by segments of the limb, but by surfaces. The
gluteal, posterior femoral, gastrocnemial, and outer pedal surfaces
are affected together with the muscles moving the foot, while the
thigh and inner side of the leg and foot become anæsthetic, with
lesion of the upper part of the lumbar enlargement accompanying
paralysis of the quadriceps and deep muscles. It is not difficult to
understand this discrepancy when we bear in mind the different plan of
distribution followed by the brachial plexus as compared with the
lumbar and sacral plexuses. It is not, in my experience, found that
the anæsthesia affects that surface which covers the part moved by the
paralyzed muscle; which is characteristic of associated paralysis and
anæsthesia from cortical disease.

One of the most dreaded occurrences in acute myelitis is the malignant
bed-sore. The ordinary decubitus which results from the protracted
sojourn of the patient in bed, coupled with the prominence of his
trochanters and sacrum resulting from general or atrophic emaciation,
is also common, but is comparatively benign and easy to prevent or to
manage when established. The malignant bed-sore, on the other hand, is
a spontaneous occurrence, due to the same obscure but undeniable
trophic influences exerted for good by the normal and for evil by the
diseased nerve-centres, which play so large a part in the
symptomatology of tabes dorsalis. It cannot be avoided; it is not due
to pressure alone, or, as some have claimed, to the macerating
influence of the dribbling and decomposing urine. The development of
this lesion is exceedingly rapid, and it may be regarded as a sort of
local gangrene. The skin shows a livid color; vesicles appear, then
burst; the part becomes denuded; and within a few days a deep ulcer
with a dark border and base appears, discharging a sanious fluid. The
subsequent history is that of a rapid extension and destruction of the
neighboring tissues, even down to the bone, and if situated over the
sacrum opening into the spinal canal through the necrotic arches of
the sacral vertebra, thus leading either to general septicæmia or to
putrid infection of the spinal meningeal sac. Occasionally, gangrenous
spots coexist on other parts of the body, notably the lower
extremities, where neither pressure nor maceration can be accused of
playing a part, proving that the process is primarily due to the
spinal affection.

Acute central myelitis, as described by Dujardin-Beaumetz, Hayem,
Hallopeau, and Erb, usually runs its course very rapidly. Indeed, all
of these observers speak of it as the most violent and quickly fatal
variety of spinal inflammation. I have, however, seen one case with T.
A. McBride at the Presbyterian Hospital in which all the
characteristic symptoms of acute central myelitis were markedly
developed and present in their characteristic groupings, and yet the
patient had been suffering from progressing symptoms of myelitis for
one year and a half before that time.[100] {820} Usually, complete
anæsthesia and paralysis of the lower half of the body occur in this
form. But the most characteristic feature is a rapidly progressive
atrophy not only of the paralyzed muscles, but also of some which are
still partially under the dominion of the will. With this there is
extreme vesical and rectal trouble, the sphincters being paralyzed. As
a rule, the deep and superficial reflexes are destroyed—they are
always diminished—and trophic disturbances of a malignant type, such
as acute decubitus, joint-changes, and œdema, are common. The
paraplegia is characterized by the flaccid condition of the limbs; the
contractures and spastic symptoms found with other forms of myelitis
are entirely absent, and qualitative electrical changes, beginning
with disappearance of farado-muscular contractility, are found in the
atrophying muscles. There are marked constitutional symptoms with this
form; the tendency to an ascent of the process and successive
involvement of one segment after another of the gray matter is great,
and a fatal issue, as far as known, is inevitable.

[Footnote 100: At the time the patient had undergone such a profound
change in appearance that I failed to remember him, and it was only by
accident I learned that I had seen him in private consultation with
his family attendent, F. A. McGuire, a year previous. On the latter
occasion I had made the diagnosis of subacute myelitis chiefly limited
to the posterior columns; there were ataxia, both static and
locomotor, slight incontinence, belt sensation, and ocular symptoms,
with abolition of the deep reflexes in the lower limbs.]

DIAGNOSIS.—The principles governing the determination of the affected
region of the cord in acute myelitis are exactly the same as those
detailed in the later sections on Chronic Myelitis or Sclerosis, the
acuteness of the onset, and the relapses which sometimes occur, and
the predominance of irritative spasms—which, however, is an inconstant
criterion—serving to distinguish between the acute and chronic form of
spinal inflammation. In the present state of our knowledge it is
impossible to always differentiate between acute central myelitis and
syringo-myelus—a condition in which the formation of a periendymal
neoplasm, and its subsequent breaking down in the axis of the cord,
lead to the formation of a tubular cavity.[101] The neoplasm in this
instance is classified among the gliomatous new formations. The
symptoms depend, exactly as do those of myelitis, on the distribution
of the destructive lesion. In some cases the posterior cornua and
columns are chiefly involved, and extreme anæsthesia is found; in
others the anterior columns are affected, and the symptoms of a
poliomyelitis or an imperfect transverse myelitis may be
imitated.[102]

[Footnote 101: This cavity, unlike that of hydro-myelus, is not a
dilatation of the central canal, but, lying to one side of it, is
excavated in the cord-substance.]

[Footnote 102: Repeated fractures have been noted in cases marked by
profound analgesia. It is believed that they are not always due to
trophic changes, but may be the result of muscular action, exaggerated
on account of the patient's inability to gauge his efforts. Still, in
the majority of cases the presence of positive trophic disturbances of
the skin seems to indicate the probability of some textural change
facilitating the fracture.]

As a rule, the sensory disturbance in syringo-myelus is out of
proportion to the muscular atrophy developed; that is, it involves a
far more extensive province. It is usually of a peculiar character:
some forms of sensation are involved but slightly, or even escape, and
others may be nearly destroyed. Commonly, it is the pain and
temperature-sense which suffer most, while the cutaneous space and
pressure, as well as the muscular sense, are not materially disturbed.
These peculiarities are not commonly found in cases of myelitis, and
when present, and particularly when the paralytic or sensory
affections involve all four extremities {821} alike, they suggest the
existence of syringo-myelus. As yet we are unable to make more than a
probable diagnosis between the two diseases.

DURATION AND PROGNOSIS.—The duration of the disease varies. Cases of
the apoplectiform variety are mentioned, in which the process reached
its height in a few minutes, or where the patient, having retired in
good health the night before, awoke finding himself paralyzed in the
lower half of his body. Death may terminate such a case in a few days
or weeks. In another class of cases, complicated by serious
involvement of the bladder, the fatal termination is often
precipitated by putrid cystitis, pyelitis, or uræmic poisoning, and
even in cases which have passed the dangers of the early period in
safety these ominous complications may develop with the usual result
many years after the beginning of the illness. In a number of cases
the first period, that in which the morbid process becomes developed,
is followed by one of comparative quiescence, in which the paralyses
of sensation and motion then established remain stationary for months
and years. A number of authors, Erb, Leyden, Strümpell, and Ross,
speak of such a case as one in which chronic myelitis has followed an
acute myelitis. It seems improper to use the terms acute or chronic in
this way. As it is generally understood that the term acute applies to
myelitis in which disintegration of the nerve-elements predominates
over interstitial proliferation, and in which the secondary sclerosis
is rather like the cicatrix of an acute inflammation and necrosis, it
should not be confounded at any period, no matter how similar the
clinical signs may be, with a process which is essentially an
interstitial one from the start. If chronic amaurosis results from an
acute glaucoma, we do not change the latter designation to chronic
glaucoma.

In cases where the symptoms at the acme indicate rather an involvement
of the peripheral than the central paths of the cord, and in which an
incomplete motor and sensory paralysis develops, the patients often
regain a considerable amount of motor power and sensation, so that
they may reach a good age, suffering at most from a paresis of some
one muscle or muscular group, occasional bladder trouble, and pains.
It has been laid down as a rule that where paraplegia and other signs
remain stationary for years, there is no hope of even partial
recovery. The following remarkable and well-attested case proves that
this rule is not without exceptions:

Isidor K——, æt. forty-four years, worker in tobacco. After
over-exertion in the fall of the year 1879 he had numbness, tingling,
dorsal pain, and paresis rapidly developed, which induced him to
consult the physicians at the clinic of the University of the City of
New York. After some slight improvement a relapse occurred, and
several others followed, usually provoked by over-exertion, till he
became completely paraplegic. He was, according to his account,
several times exhibited to a medical class by William A. Hammond, and
remembers that this authority spoke of a possible ascent of the
affection and ensuing involvement of the arms. His bladder was at no
time seriously disturbed. For four years and three months he was
totally paraplegic; his lower extremities were without life; and for
the greater part of the time he could not move his toes. The limbs
were cold and pale, but underwent little atrophy. The only exercise
obtained during this time was in a roller carriage. His sexual power
was abolished throughout the whole {822} four years and over. Nothing
can be learned as to his reflexes in this period.[103] The paralysis
of sensation was as complete as that of motion, and the lower limbs
never perspired. The arms remained free. There was a dorsal belt
sensation.

[Footnote 103: Hammond has no notes of the case, having discontinued
the clinic, and Ludwig Weiss, the physician in charge, saw him only
occasionally in behalf of a benefit society.]

On July 23, 1884, shortly before mid-day, while lying on the bed, in
which he had lain a helpless cripple for over four years, except when
lifted into the roller carriage, he felt a sudden rush of warmth.
Surprised at this first sensation he had felt for years in limbs which
had been quasi-foreign appendages, he raised up the bed-clothes and
saw that they changed color. There was some tingling for about three
minutes, and a perspiration broke out in the affected members. With
this he found he could move his feet: half alarmed, half exulting, he
sent for his physician, L. Weiss, who found that the patient could
stand and walk with considerable freedom. I was then consulted, and
found the patient presenting a picture of incomplete transverse
myelitis. He could walk, turn about, stand with closed eyes with
slight swaying, and his knee-phenomenon was of short excursiveness,
but exceedingly spasmodic, and this symmetrically so. He was carefully
watched, and against the advice of his physician engaged in peddling
cigars, and subsequently took a position as attendant at the pauper
asylum on Ward's Island. Here he was on his feet fully twelve hours a
day, and his motion, which had continued improving until it was to all
practical intents and purposes normal, aside from a slight stiffness,
again became impaired, and a joint trouble in the metacarpo-phalangeal
articulation of the right little toe, which had troubled him a week
after his partial recovery, recurred.[104] On January 15th of the
present year I again examined him. His knee-phenomenon was greatly
exaggerated, cutaneous sensations scarcely impaired, gait paraparetic,
but he could walk great distances, and claimed to suffer less from the
exertion than from the tenderness accompanying the joint trouble
referred to. There had, therefore, occurred, without any assignable
cause—for the patient was not under treatment for a year or more
before the event—an almost instantaneous restoration of sensation,
locomotion, and sexual power; all of which faculties, notwithstanding
the infraction of every medical direction given, remained established
for two years, with prospects of so continuing a longer period.

[Footnote 104: This was a trophic joint trouble.]

TREATMENT.—Most of the therapeutic propositions relating to the
treatment of the acute myelitic process are based on the theory that
it is of a congestive character or associated with congestion.
Accordingly, the internal administration of such drugs as ergotin,
which diminish the calibre of the blood-vessels, and local measures,
such as depletion, wet cupping, and counter-irritation, intended to
act in the same way by derivation, are unanimously recommended by
authorities. The suggestion of Hammond, that the patient occupy a
ventral or lateral, and not the dorsal, position, is based on, and
entirely consistent with, this same view. It is difficult to say what
effect is attributable to these measures. Remarkable spontaneous
changes—retrogressions as well as advances of the morbid process—occur
equally under expectant as under active treatment. I have never seen
any improvement in the active phase of simple myelitis which {823} I
felt confident I could attribute to any special remedy employed with a
view of acting directly on the morbid process. Indeed, improvement has
been claimed by Jewell as a result of the use of strychnia—a drug
which under the very dogmas governing the orthodox treatment of the
disease might be expected to do positive damage.[105]

[Footnote 105: Jewell gives very large doses of this alkaloid. L. C.
Gray, in a discussion held before the American Neurological
Association, cited numerous observations directly conflicting with
those of Jewell. I cannot, in view of a recent observation in a
typical case of acute anterior poliomyelitis, in which by accident the
toxic effects of strychnia were obtained, consider this dispute as at
all settled. In direct connection with the toxic symptoms the
abolished patellar jerk returned in an exaggerated form; motion also
returned, and rapid improvement ensued.]

In relapses of acute myelitis which had been brought on by chilling of
the feet I have obtained good results by derivation to the lower
extremities, and on many grounds think that the morbid process in the
cord, if it can be affected at all, can be affected by treating the
periphery where the symptoms are noted more readily than by applying
the cautery or bleeding over the proven site of the disease. Exposure
of the dorsal region to cold has not yet been noted as a cause of
acute myelitis, whereas such exposure of the lower extremities is a
frequent one. This seems to show that the spinal cord is more
vulnerable to influences affecting its nervous distribution than to
those which are topographically nearer. If this is true as regards
morbid influences, it may be urged that it is plausible as regards
remedial influences if these are to drive out the disease tendency by
the same door it entered.

Rest is imperative during the active progress of the disease. It may
be stated as a canon that the earlier the patient takes to his bed,
and the more thoroughly he obeys the injunction to attempt no motion
of the affected members, the better, cæteris paribus, will the result
obtained be. Countless cases are on record where a relapse was
directly traceable to a walk undertaken prematurely or carried farther
than was wise. As convalescence or partial restitution advances,
gradually increasing exercise is to be attempted, not waiting for the
danger-signal of a tired feeling to discontinue it; for that feeling,
developed, means positive harm already done. It is therefore necessary
to allow the returning function to be utilized only within small
limits at first, and extending them slowly.

In all cases of severe myelitis where the formation of bed-sores is to
be apprehended the water-bed should be employed. Owing to the low
temperature which the rubber sac constituting it has, it is necessary
to cover it with some well-warmed and non-conducting material and to
have the room well warmed. If bed-sores are already formed, they are
to be treated according to ordinary surgical principles. Antiseptic
means should be in the foreground in the case of the malignant
bed-sore. It is to be remembered that the latter is a gangrenous
process, and, in so far as the formation of a line of demarcation
between the necrotic and the conserved tissue is concerned, the
ordinary expectant rules of surgery govern the case: the water-bath
appears to yield the best results. Ordinary bed-sores yield readily to
mechanical protection and stimulating ointments or the balsam of Peru.
Iodoform is recommended, but it produces granulations of an indolent
character as compared with those obtained through the use of resinous
ointments.

The warm bath is probably the most useful measure in acute myelitis.
{824} In cases due to exposure I do not believe it can be applied too
soon. Its temperature should, in the beginning at least, not be higher
than about 88° F., and the duration about seven minutes. The continued
administration will depend on the immediate effect on the patient, and
the sittings can be ultimately prolonged to half an hour or even
longer. It should be administered once daily, and, when the patient is
not disturbed by the manipulation connected with its use, even
oftener. Cold baths are recommended by the Germans, but it seems
rather in the passive period of the disease than during its active
phase.

The management of the bladder trouble is one of the most critical
points in the treatment of most cases. The results of retention of
urine are more frequently the cause of a fatal issue than any other
single complication. Where there is complete retention continuous
catheterization is to be employed, as recommended by Strümpell.[106]
In other cases the bladder should be emptied thrice in the twenty-four
hours. The catheter is to be thoroughly disinfected, and if the
slightest sign of cystitis is noted the bladder should be washed out
with astringent and disinfectant solutions. The continuous irrigation
with a solution of corrosive sublimate, 1:2000, appears to give the
best results.

[Footnote 106: A. Nelaton's catheter is introduced into the bladder,
and kept in place by strips of adhesive plaster fixed to the inner
aspect of the thighs. A perforated condom fixed to the catheter, and
then fastened to the inguinal region, is in my opinion a better
measure, especially in patients who have some motor power left. The
catheter is connected with a rubber tube, which should run on a
decline in order to effect complete drainage.]

If there be a syphilitic taint present—and more particularly is this
true of cases where no other cause can be assigned—large doses of
iodide of potassium[107] should be administered, and mercurial
ointment energetically applied, even to the point of salivation.

[Footnote 107: Here, if anywhere, the so-called heroic doses are
applicable.]

I am unable to say anything with regard to the local use of
electricity in the active period of the disease. Ascending currents
are recommended by Erb, weak currents of about five minutes' duration
being employed over the part supposed to be affected. In order to
secure sufficiently deep deflection of the current large electrodes
are applied. The use of galvanism and faradism on the affected
periphery, the former being preferred where atrophic, the latter where
anæsthetic conditions preponderate, is to be instituted early and
continued through the duration of the disease. The rules stated in the
section devoted to electro-therapeutics are to be followed. In cases
where the bladder or rectum are paralytic, these organs should have
galvanism applied to them by means of electrodes shaped like catheters
or sounds.

After the acute phase of myelitis is passed, the secondary period is
to be managed according to the principles laid down in the section on
the Treatment of the Sclerotic Processes.


{825}


THE CHRONIC INFLAMMATORY AND DEGENERATIVE AFFECTIONS OF THE SPINAL
CORD.

BY E. C. SPITZKA, M.D.


The intimate dovetailing of parenchymatous and connective substance in
the spinal cord renders the determination of the precise origin of a
morbid process often difficult if not impossible. Whatever the mode of
origin, the typical termination of inflammatory and degenerative
spinal disorders is sclerosis—a condition in which the essential
nervous elements suffer diminution or destruction, while the
connective substance is either absolutely or relatively in
preponderance. The clinical result is nearly the same in all cases,
and with few exceptions depends less upon the histological character
than on the topographical distribution of the lesion. It is for this
reason that we shall follow rather the topographical than the morbid
histological principle in classification.

The chronic disorders of the spinal cord here considered have as a
common character the slow and progressive displacement of the normal
conducting nerve-tubes by a grayish, reddish, or otherwise discolored
tissue, which is firmer in texture than normal nerve-substance. Minute
examination shows that it is above all the myelin of the nerve-tubes
that is wasted or destroyed, while the axis-cylinders may share in
this dissolution, or, as in one form of sclerosis, they may persist
and even continue in their conducting function. This increased
consistency is found to be due to the increase of connective-tissue
trabeculæ and of the neuroglia. In some cases this increase is active
and absolute, like the increase in certain phases of hepatic
cirrhosis; in others it is rather relative and passive, being merely a
condensation of the connective framework after the intervening
elements have wasted away, just as the texture of a compressed sponge
is more compact than that of an expanded one.

Crudely, the affections of the cord characterized by this change may
be divided into two great groups—the regular and the irregular. The
former are characterized by their limitation to special nerve-tracts.
Thus, in primary lateral sclerosis we find a special tract in the
posterior part of the lateral columns occupied by the lesion. A number
of spinal diseases with well-defined symptoms are due to active morbid
processes which similarly follow the normal distribution of the great
nerve-tracts of the cord, with the same, almost mathematical,
regularity with which the medullary white develops in the fœtal and
infantile cord. In another class of cases we find that the same tracts
are involved in like manner—not in the way {826} of primary disease,
but through the interruption of the physiological continuity of the
nerve-tract by some other disease, to which the sclerosis is therefore
secondary. These are the so-called secondary degenerations.

The irregular affections of the cord comprise cases in which the
sclerotic foci are either disseminated through the cerebro-spinal axis
in numerous foci, or diffusely involve a greater or lesser length and
thickness of the medullary cylinder, or, finally, extend in the
transverse plane completely or nearly so across the section area of
the cord at a definite level.

As the symptoms of the regular affections of the cord are by far the
most readily recognizable, and a preliminary knowledge of them will
facilitate the better understanding of the irregular forms, we shall
consider the former first. They may be subdivided into two groups. The
largest, longest known, and best studied consists of acquired, the
other, containing less numerous cases and varieties, and rendered
familiar to the profession only within the last decade, comprises the
spinal disorders due to defective development of the cerebro-spinal
and spinal-fibro systems.


Tabes Dorsalis.

SYNONYMS.—Locomotor ataxia and ataxy, Posterior spinal sclerosis;
Graue degeneration der Hinterstränge (Leyden), Rückenmarksdarre
(popular), Rückenmarksschwindsucht; Tabes dorsualis (Romberg); Ataxie
locomotrice progressive (Duchenne).

HISTORY.—Undoubtedly, this disease must have been observed by the
ancient masters of medicine, but their descriptions group together so
many symptoms of other organic as well as functional diseases of the
cord that it is impossible to obtain a clear idea as to what special
form they had in view when they spoke of tabes dorsualis. This term
was adopted by the German writers of the last and the earlier part of
this century as designating all wasting affections of the cord; and it
was not till Romberg in 1853 and Duchenne in 1858 differentiated the
characteristic clinical signs, and Cruveilhier and Todd (1847)
determined the distribution of the lesion in the posterior columns,
that the medical profession began to recognize the distinctness of
this the most common form of organic spinal ailment.

At this time, when tabes dorsalis became recognized as a clinical
entity depending on sclerotic degeneration of the posterior segment of
the cord, the inco-ordination or ataxia manifested in the peculiar
gait of the patient was regarded as the most characteristic,
essential, and constant symptom of the disease. It was regarded as an
axiom in physiology that the posterior segment of the cord was
subservient to centripetal and sensory conduction, and nothing
appeared to follow more naturally than the conclusion that the patient
exhibited inco-ordination because, his sensory conduction being
interrupted or destroyed, he had lost the necessary gauge for judging
of the required extent and force of a given movement. Since then both
spinal physiology and pathology have undergone a profound revolution.
So far are we to-day from regarding anterior and motor or posterior
and sensory as convertible terms that we locate the {827} most
important centrifugal tract of the cord behind the plane which divides
it into anterior and posterior halves, while the most recently
differentiated centripetal tract is represented by Gowers as lying in
front of it. It has been determined, through Türck, Bouchard, and
Flechsig and his pupils, that the posterior white columns of the cord
contain several systems of fibres, whose functions—where
determinable—are of an exceedingly complex nature. The elaborate
investigations of Charcot, Schultze, and Strümpell, made during the
past decade, have shown that the distribution of the diseased field in
the posterior segment is not uniform, but is most intense in special
areas. These were found to be affected with a remarkable constancy and
regularity. Almost coeval with this discovery came the recognition of
symptoms found in the earliest phases of the disorder by Westphal,
which, attributable as they were found to be to the involvement of the
special reflex mechanisms of the cord, enable us to demonstrate the
existence and extent of the disease at periods which previously were
not within the ken of the clinician. The reproach which Leyden was
justified in making, that most tabic patients pass through the
pre-ataxic phase of their disorder under the diagnosis of rheumatism
or some similar affection, can now no longer be made. Our ability to
recognize the advent of this disease has reached such a degree of
refinement that the question arises whether we are always justified in
alarming a patient who has a prospect of remaining free from
invalidating complications for many years with the announcement of a
disease which, above all other spinal affections, is looked upon with
dread as equally hopeless, insidious, and distressing.

CLINICAL HISTORY.—The development of tabes dorsalis is typically slow
and its precise commencement usually not determinable. In some cases
this or that one of the characteristic symptoms of the disease
preponderates from the beginning, and continues throughout the illness
as a prominent feature; in others distinct stages can be recognized,
each marked by one or several symptoms which were absent or slight in
the other stages. In some cases the progress of the affection is
marked by episodes which are absent or rare in other cases. As a rule,
however, it may be stated that tabes is a progressive affection,
marked by pronounced temporary changes for better or worse, which are
often developed with astonishing rapidity, and subside as quickly,
terminating fatally unless its progress be arrested by treatment or
interrupted by some other fatal affection. The latter is by far the
more frequent termination in the well-to-do class of sufferers.

For purposes of convenience we may consider the symptoms of the
earlier period of the illness as pre-ataxic, and those of the later as
the ataxic. It is to be remembered, however, that in the strictest
sense of the term there is usually some disturbance of co-ordination
even in the early period, while the symptoms of the pre-ataxic period
continue over the ataxic period, and may even become aggravated with
it. Often the patient does not himself suspect a spinal, or indeed any
nervous, disorder, and consults the physician either on account of
rheumatic pains, double sciatic neuralgia, bladder disturbance,
diminished sexual power, amaurosis, diplopia, or even gastric
symptoms, which on closer examination are revealed to be evidences of
tabes. The determination of the initial symptoms is retrospective as a
rule.

{828} Of the subjective signs, one of the commonest, if indeed it be
ever entirely absent, is a tired feeling, particularly noted in the
knees and ankles. This sensation is compared to ordinary muscle-tire,
but is provoked by slight exertion, and not as easily remedied by
rest. Often a numb feeling is associated with it, although no
objective diminution of cutaneous sensation be determinable. This
combined feeling of tire and numbness, described as a going-to-sleep
feeling in the ankle, has indeed been claimed by one observer[1] to be
pathognomonic of early tabes. Next in frequency, and almost as
universal, are peculiar pains: these are manifold in character and
distribution, but so distinctive as to alone suggest the existence of
the disease from the manner in which the patient describes them. One
variety, the lightning-like, is compared to a sudden twinge of great
intensity shooting through the limb. The sciatic and anterior crural
branches are the lines usually followed by this pain, but there are
cases where perineal and abdominal regions are affected. Often the
pain is so severe that the patient cries out or the limb is violently
contracted under its influence. It differs from rheumatic pain in the
fact that it is distinctly paroxysmal and that the intermissions are
complete; that it is not greatly aggravated by motion nor relieved by
rest, while the rheumatic pain is; that tabic pain is usually
relieved, and rheumatic pain aggravated, by pressure, while
hyperæsthesia is present with the former, and either absent or barely
indicated with the latter. The lightning-like pains are sometimes
combined with another form, which is even more distinctive in
character. This form does not affect the distribution of special
nerves, but is found limited to a small area which the patient is able
to localize definitely: it may not exceed a centimeter or two in
diameter, and within this area the pain is excruciating. It is either
of a burning character or compared to the firm pressure of a vise or
heavy weight, or to the tearing, boring, and jumping of a violent
toothache.

[Footnote 1: Canfield, _Lancet_, 1885, vol. ii. p. 110.]

While some patients escape these pains almost entirely,[2] others are
tormented with them at intervals for years, their intensity usually
diminishing when the ataxic period is reached. There is little
question among those who have watched patients in this condition that
their pains are probably the most agonizing which the human frame is
ever compelled to endure. That some of the greatest sufferers survive
their martyrdom appears almost miraculous to themselves. Thus, in one
case the patient, who had experienced initial symptoms for a year,
woke up at night with a fulminating pain in the heels which recurred
with the intensity of a hot spear-thrust and the rapidity of a flash
every seven minutes; then it jumped to other spots, none of which
seemed larger than a pin's head, till the patient, driven to the verge
of despair and utterly beside himself with agony, was in one continued
convulsion of pain, and repeatedly—against his conviction—felt for the
heated needles that were piercing him. In another case the patient,
with the pathetic picturesqueness of invalid misery, compared his
fulminating pains to strokes of lightning, {829} “but not,” he added,
“as they used to appear, like lightning out of a clear sky, but with
the background of a general electrical storm flashing and playing
through the limbs.”

[Footnote 2: I have at present under observation two intelligent
patients (one of whom had been hypochondriacally observant of himself
for years) who experienced not a single pain, as far as they could
remember, and who have developed none while under observation. Seguin
mentioned a case at a meeting of the Neurological Society with a
record of but a single paroxysm of the fulgurating variety. Bramwell
(_Brit. Med. Journ._, Jan. 2, 1886) relates another in which the pains
were entirely absent.]

Either while the pains are first noticed or somewhat later other signs
of disturbed sensation are noted. Certain parts of the extremities
feel numb or are the site of perverted feelings. The soles of the
feet, the extremities of the toes, the region about the knee-pan, and
the peroneal distribution, and, more rarely, the perineum and gluteal
region, are the localities usually affected.[3] In a considerable
percentage of cases the numbness and tingling are noted in the little
finger and the ulnar side of the ring finger; that is, in the digital
distribution of the ulnar nerve. The early appearance of this symptom
indicates an early involvement of the cord at a high level. Some
parallelism is usually observable between the distribution of the
lightning-like pains when present and the anæsthesia and paræsthesia
if they follow them. With these signs there is almost invariably found
a form of illusive sensation known as the belt sensation. The patient
feels as if a tight band were drawn around his body or as if a
pressure were exerted on it at a definite point. This sensation is
found in various situations, according as the level of the diseased
part of the cord be a low or high one. Thus, when the lower limbs are
exclusively affected or nearly so the belt will be in the hypogastric
or umbilical region; if the upper limbs be much involved, in the
thoracic region; and if occipital pain, anæsthesia of the trigeminus,
and laryngeal crises are present, it may even be in the neck.
Correspondingly, it is found in the history of one and the same
patient: if there be a marked ascent—that is, a successive involvement
of higher levels in the cord—the belt will move up with the
progressing disease. This occurrence, however, is less frequently
witnessed than described. In the majority of cases of tabes
disturbances of the bladder function occur very early in the disease.
Hammond indeed claims that in the shape of incontinence it may be the
only prodromal symptom for a long period.[4]

[Footnote 3: In the exceptional cases where the initial sensory
disturbance is marked in the perineal and scrotal region I have found
that the antecedent fulminating pains had been attributed to the
penis, rectum, and anal region; and in one case the subjective sense
of a large body being forcibly pressed through the rectum was a marked
early sign.]

[Footnote 4: _New England Medical Monthly_, 1883.]

I have under observation a patient who has been compelled to use the
catheter daily for years, who has gradual disappearance of the
knee-jerk and reflex iridoplegia, but who has presented no other
evidence of tabes during the year and a half he has been watched.
Among the exact signs of tabes, reflex iridoplegia and abolition of
the knee-jerk are probably the earliest to appear. It may be assumed
with safety that in ninety-nine out of a hundred cases both the
inability of the pupil to respond to light and the absence of the
knee-jerk will be found long before ataxia is developed. Cases are
recorded where no other positive signs were found, and no other signs
of the disease developed for a number of years,[5] and others where
disappearance of the knee-jerk was the very first indication.

[Footnote 5: Westphal, also Tuczek, _Archiv für Psychiatrie_, xiii. p.
144.]

The opinion of observers as to the frequency of double vision as an
early symptom of tabes is far from being unanimous. The majority of
writers speak of it as rare, but it is probable that this usually
transient symptom is forgotten by the patient, or because of its
apparent triviality {830} escapes notice. The patient while looking at
an object sees a double image of the latter. This may last for a few
seconds, minutes, or hours, and rarely for a day or week.[6] A
distinct history of this symptom was given by 58 out of 81 patients in
whom I recorded the oculo-motor signs. By far the most important of
the exact prodromal signs of tabes are two symptoms—one involving a
special faculty of co-ordination, the other the reflex movements of
the pupil. One or both of these must be present to justify the
diagnosis of incipient tabes.[7] The disturbance of co-ordination
consists in an inability of the patient to stand steadily when his
eyes are closed. The majority of healthy persons when tested in this
way may show a little swaying in the beginning, but eventually they
stand as steadily as they do with open eyes, and there is no
subjective feeling of uncertainty as to falling. But the tabic patient
exhibits oscillations, and makes efforts to overcome them which,
instead of neutralizing, usually aggravate them and betray the great
disturbance of his equilibrium. It is not as if he swayed merely
because he is uncertain of his upright position, but as if some
perverted force were active in throwing him out of it. It is found to
be a pronounced feature even in cases where the patient with open eyes
is able to walk nearly as well as normal persons, and experiences no
trouble in performing intricate evolutions, such as dancing, walking a
line, or even walking in the dark—faculties which the patient is
destined to lose as his disease progresses.[8]

[Footnote 6: It has been asserted that the severer and more persistent
diplopias are found with tabes dependent on syphilis.]

[Footnote 7: Not even the absence of the knee-jerk ranks as high as
these two signs. Aside from the fact that this is a negative symptom,
it is not even a constant feature in advanced tabes.]

[Footnote 8: It does not seem as if the disturbance of static
equilibrium were due merely to the removal of the guide afforded by
the eyes, for it is noted not alone in patients who are able to carry
out the average amount of locomotion in the dark, but also in those
who have complete amaurosis. Leyden (_loc. cit._, p. 334) and Westphal
(_Archiv für Psychiatrie_, xv. p. 733) describe such cases. The act of
shutting the eyes alone, whether through a psychical or some occult
automatic influence, seems to be the main factor.]

In most cases of early tabes it is found that the pupil does not
respond to light; it may be contracted or dilated, but it does not
become wider in the dark nor narrower under the influence of light. At
the same time, it does contract under the influence of the
accommodative as well as the converging efforts controlled by the
third pair, and in these respects acts like the normal pupil. It is
paralyzed only in one sense—namely, in regard to the reflex to light;
just as the muscles which extend the leg upon the thigh may be as
powerful as in health, but fail to contract in response to the reflex
stimulus applied when the ligamentum patellæ is struck. For this
reason it is termed reflex iridoplegia.[9] It is, when once
established, the most permanent and unvarying evidence of the disease,
and is of great differential diagnostic value, because it is found in
comparatively few other conditions.

[Footnote 9: It is also known as the Argyll-Robertson pupil. Most of
the important symptoms of tabes are known by the names of their
discoverers and interpreters. Thus, the swaying with the eyes closed
is the Romberg or Brach-Romberg symptom; the absence of the
knee-phenomenon, Westphal's or the Westphal-Erb symptom; and the
arthropathies are collectively spoken of as Charcot's joint disease.]

In a number of cases ptosis of one or both eyelids is noted at an
early stage of the disease. It is usually temporary, and coincides as
to time with the diplopia, if present.

Patients presenting some or all of the subjective and objective {831}
manifestations of tabes mentioned may continue in a condition of
otherwise comparative health, enabling them to attend to their
vocation for from one to twenty years, and it is not improbable that
the pre-ataxic period may extend over nearly a lifetime. In a less
fortunate minority of cases some of the most distressing evidences
usually marking the last stages of the disease are found developed at
the onset. Thus, cases are known where optic nerve-atrophy preceded
the true tabic period by ten or more years; others in which trophic
disturbances, manifested in spontaneous fractures of bones[10] or
violent gastric crises, or even mental disturbance, inaugurated tabes
dorsalis, instead of closing or accompanying the last chapter of its
history, which is the rule.

[Footnote 10: Berger, _Deutsche medizinische Wochenschrift_, 1885, 1
and 2.]

The disturbance of co-ordination above spoken of as manifested in the
inability of the patient to stand well with his eyes closed is the
first step in the development of the characteristic ataxia which marks
the full-blown affection. The patient finds that he tires more and
more on slight exertion—not because his muscles are weak, but because
he has to make more voluntary effort than a person in health. He finds
that he stumbles easily—is unable to ascend and descend at the
curbstone or to walk over an irregular surface with ease. Going down
stairs is peculiarly irksome. “I would rather,” aptly said one
patient, “troubled as I am in walking, go a mile in the street than
walk up three flights of stairs; but I would rather go up six flights
of stairs than walk down one.” Soon the patient notices that walking
in the dark becomes more a feat of relative skill than the easy,
almost automatic, act it was in health. His vocation, if it was one
involving the use of the feet, becomes irksome, difficult, and finally
impossible, and in a number of cases the upper extremities are also
involved.[11] Delicate motions, such as those required in needlework,
in writing, and by watchmakers, musicians, opticians, and lapidaries,
are clumsily performed; even coarser movements, such as buttoning the
clothes and carrying a glass filled with water to the mouth, are
performed in an uncertain and clumsy manner. Meanwhile, the
disturbance of motion in the lower limbs progresses. Difficult as it
formerly was for the patient to stand on one foot or with both feet
together while the eyes were closed, he is now unable to do either
with the eyes open. He straddles in his walk, or, in order to overcome
the element of uncertainty involved in moving the knee-joint, keeps
this joint fixed and walks with short, stiff steps. If ordered to halt
suddenly while thus walking, the patient sways violently, and makes
movements with his hands or arms to recover his balance, in some cases
staggering and even falling down. He shows a similar unsteadiness when
told to rise suddenly from a chair or to mount one, and it becomes
impossible for him to walk backward. Later on, it will be found that
his feet interfere in walking. He has lost the power of gauging the
extent and power of his motions to such a degree that he may actually
trip himself up. To neutralize in some way this element of uncertainty
of his steps, the patient is compelled to exaggerate all his
ambulatory movements, and there results that peculiar gait which was
the first symptom directing attention to the {832} disease to which it
is due. The feet are thrown outward, and violently strike the ground;
the heel touches the latter first, and the patient appears as if he
were punishing the ground and stamping along instead of walking. The
reason for his adopting these tactics are twofold. In the first place,
he has a subjective sense of walking in a yielding substance, as if on
a feather bed, air-bladders, cushions, or innumerable layers of
carpet, and he therefore makes efforts to touch firm bottom. In the
second place, his motor inco-ordination, in so far as it is not the
result of anæsthesias, is greatest in those segments of his limbs
which are farthest removed from the trunk, and which, enjoying the
greatest freedom of combined motion, are also most readily disturbed.
His uncertainty is therefore greater in the toes than in the ankle,
greater in the ankle than in the knee, and greater in the knee than in
the thigh: he prefers to touch the ground with the heel to touching it
with the toes, and to move his limb in the hip than in the knee-joint.
As the patient advances in life even this limited and clumsy form of
locomotion becomes impossible: he takes to his bed, and it is found
that he loses all sense of the position of his lower and occasionally
of his upper limbs. He is unable to tell which limb overlies the other
when his leg is crossed—unable to bring one limb in parallel position
with another without the aid of his eyes. If told to touch one knee or
ankle with the toes of the other side, his limb oscillates around
uncertainly, and makes repeated unskilful dashes at the wrong point,
and ultimately all but the very coarsest muscular co-ordination
appears to be lost, even when the supplementary aid of the eyes is
invoked.

[Footnote 11: Cases in which the upper extremities are intensely
involved in the beginning are uncommon, and those in which they are
more intensely involved than the lower, or exclusively involved, may
be regarded as pathological curiosities.]

Together with this gradual impairment and abolition of co-ordination,
which has given the name of locomotor ataxia to the disease, but not
always in that strict parallelism with it on which Leyden[12] based
his theory of inco-ordination, the sensory functions proper become
perverted and impaired. Usually the determinable anæsthesias are
preceded by subjectively perverted sensations, such as the numbness
already referred to, or even by hyperæsthesia. Usually, all categories
of cutaneous sensation, whether special or pathic, are impaired in
advanced tabes; the points of the æsthesiometer are not readily
differentiated; the patient is unable to correctly designate the
locality which is touched or pinched; the pain-sense is occasionally
so much blunted that a needle may be run through the calf of the leg
without producing pain, and in some cases without being appreciated in
any form. Even if the pain-sense be preserved, it will be found that
its appreciation by the patient is delayed as to time. Not
infrequently bizarre misinterpretations are made of the impressions
acting on the skin. One of these, the feeling as if the patient were
standing on carpet, cushions, or furs, whereas he may be standing on
stone flagging, has already been mentioned as a factor in the
disturbed locomotion of the patient. In the later period, numerous
perversions of this kind are noted: to one of these, already mentioned
by Leyden, Obersteiner has called renewed attention. It consists in a
confusion of sides; the patient when pricked or touched on one foot or
leg correctly indicates the spot touched, but attributes it to the
wrong side.[13]

[Footnote 12: _Klinik der Rückenmarkskrankheiten_, Band ii.]

[Footnote 13: Allochiria is the term applied by Obersteiner. Hammond
has offered an explanation, which, as it is based on the assumption of
altogether hypothetical nerve-tracts, and not in any sense accords
with positively established facts, is more properly a subject for
consideration in a theoretical treatise.]

{833} While it may be affirmed, as a general proposition, that the
tendency of the tabic process is to abolish sensation below the level
of the disease, there are noteworthy exceptions, not only in
individual cases, but with regard to certain kinds of sensation; nor
do the different kinds of sensation always suffer together. Thus, the
pain-sense may be blunted and the contact-sense preserved, or, more
commonly, the latter blunted and the former exaggerated, so that the
unfortunate patient, in addition to being debarred of the useful
varieties of sensation, those of pressure and space, has the painful
ones exaggerated, as a hyperalgesia. According to Donath,[14] the
temperature-sense is usually blunted in tabes, and a greater degree of
heat or cold can be borne without discomfort than in health; but in
about two-sevenths of the cases studied there was increased
sensitiveness to heat, and in one-seventh to cold. One of the
commonest manifestations is delayed conduction. This interesting
phenomenon has been especially observed in that phase of the disease
where tactile perception is beginning to be blunted. If the patient be
pricked with a pin, he feels the contact of the latter at the proper
moment as a tactile perception, and then after a distinct interval,
varying from one to four seconds, his limb is suddenly drawn up and
his face contorted under the influence of an exaggerated pain. This
fact furnishes one of the chief grounds for the assumption that there
are distinct channels for the transmission of pain and tactile
perception in the cord, and that they may be involved separately or
with different intensity in the disease under consideration. In some
advanced cases it is found that not only the transmission of
pain-appreciation is delayed, but that there are after-sensations
recurring at nearly regular intervals of several seconds, and
accurately imitating the first pain-impression.

[Footnote 14: _Archiv für Psychiatrie_, xv. p. 707.]

To what extent the muscular sense is affected in tabes at various
stages of the disorder is somewhat in doubt. Strümpell[15] by
implication, and other writers directly, attribute the inco-ordination
observed on closing the eyes to the loss of the muscular sense. As
this symptom is also observed in patients who when they lie on their
backs are able to execute intricate movements notwithstanding the
exclusion of the visual sense, and as their uncertainty in an early
stage is not always with regard to the position of their limbs nor the
innervation of individual or grouped muscles, it seems inadmissible to
refer the Romberg symptom[16] to the loss of muscular sense alone.

[Footnote 15: _Lehrbuch der Speciellen Pathologie und Therapie_, p.
193, vol. ii.]

[Footnote 16: It should be designated as static ataxia, in distinction
from locomotor or motor ataxia, which is manifested in unskilled
movements.]

The important part played by eye symptoms in the early stages of tabes
has been already referred to. Reflex iridoplegia is one of these early
and persisting features; it is sometimes complicated with mydriasis,
and occasionally with paralysis of accommodation of one eye. In the
majority of my cases there was spinal myosis, often of maximum
intensity; in a large number there was in addition irregularity of the
outline of the pupil; and where there was mydriasis I found it to be
quite symmetrical, in this respect differing from the experience of
Müller[17] and Schmeichler.[18]

[Footnote 17: _Centralblatt für die Gesammte Therapie_.]

[Footnote 18: _Loc. cit._]

{834} Atrophy of the optic nerve is a common and sometimes, as stated,
the initial symptom of tabes. It is rarely found in its incipient
phase in advanced stages. The patient who escapes involvement of the
optic nerve in the pre-ataxic stage is very apt to escape it
altogether. It is more frequently found either to precede the
pre-ataxic period by months and even years, or to develop during this
period, leading to complete atrophy in the ataxic period, and
sometimes before. Erb calculates that 12 per cent. of tabic patients
have optic-nerve atrophy; he probably includes only such cases in
which the atrophy was marked or led to amblyopia. Including the lesser
degrees of atrophy, it is found in a larger number of patients.
Schmeichler claims as high as 40 per cent.[19] If we regard those
cases in which there is noted progressing limitation of the
color-field of the retina as beginning optic-nerve atrophy, the
majority of tabic patients may be said to have some grade of this
disorder. The ophthalmoscopic changes are quite distinctive: at first
there is noted a discoloration of the papilla and apparent diminution
of the number of arterial vessels; the veins then become dilated; and
finally the papilla becomes atrophied, the vessels usually undergoing
a narrowing after their previous dilatation. In the first stages of
this process visual power is not gravely impaired, but as soon as
shrinkage has set in visual power sinks rapidly to a minimum,
decreasing till only quantitative light-perception remains. This
limited function usually remains throughout, but in a few cases
complete amaurosis ensues. As the field of vision becomes diminished,
the concentric extinction of quantitative perception is preceded by
concentric extinction of color-perception, the color-field for green
being the first to suffer; red follows, and blue remains last.

[Footnote 19: _Archives of Ophthalmology and Otology_, 1883.]

In a large number of cases the only symptoms attributable to a
disturbance of the cerebral functions are those connected with the
motor relations of the eyeball and pupil, and the function and
appearance of the optic nerve. The special senses other than those of
sight and touch are rarely affected. Sometimes there is obstinate
tinnitus, exceptionaly followed by deafness, attributed to atrophy of
the auditory nerve. The development of symptoms resembling those named
after Ménière is not referable with certainty to a disturbance of the
same nerve.

The sexual functions become involved in all cases of tabes sooner or
later. In the majority of cases there is a slow, gradual extinction of
virile power; in a large minority this extinction is preceded by
irritative phenomena on the part of the genital apparatus. Some
patients display increased sexual desire and corresponding performing
powers, but mostly they suffer from erections of long duration which
may be painful, and loss of the normal sensations attending the sexual
orgasm. There is no constant relationship between the intensity of the
general affection and the diminution of sexual power. It is retained
to a limited degree by patients who are barely able to walk, and it
may be entirely destroyed in those who have but entered the initial
period.

The bladder disturbance,[20] which in some forms is usually found
among the initial symptoms, is always a marked feature in the ataxic
period. {835} Usually, there is a frequent desire for micturition,
with more or less after-dribbling; sometimes there is retention,
alternating with involuntary discharge; complete incontinence may
close the scene through the channel of an ensuing cystitis and
pyelitis. With the incontinence of urine there is usually found
obstinate constipation, which may be varied by occasional spells of
incontinence of feces. The crises of tabes often complicate these
visceral symptoms.

[Footnote 20: Contrary to what might be anticipated from the
topographical nearness of the vesical and genital centres in the cord,
the disturbances of bladder function and virile power do not go hand
in hand.]

The reflex disturbances are among the most continuous evidences of the
disease. Of two of these, the disappearance of the patellar jerk or
knee-phenomenon and the inability of the pupil to react to light, we
have already spoken when discussing the initial period. Practically,
it may be claimed that both are always found in typical tabes. It has
been claimed that the patellar jerk may be exaggerated, or even that
its disappearance is preceded by exaggeration. As this disappearance
usually occurs extremely early in the pre-ataxic period, it is
difficult to follow the deductions of those who claim to have watched
an alleged earlier phase of exaggeration. It is more than probable
that cases of combined sclerosis, in which the lateral columns were
affected together with or earlier than the anterior, have been
mistaken for typical tabes. Here, it is true, the jerk is first
exaggerated through the disease of the lateral column, and later
abolished as the lesion in the posterior reflex arch progresses and
becomes absolute.

Other tendinous reflexes[21] suffer with the knee-jerk in the
peripheries corresponding to and below the involved level of the cord.
The cutaneous reflexes are usually abolished, but may be retained in
advanced stages of the disease. The same is true of the cremaster
reflex.

[Footnote 21: Whether the tendon phenomena are true reflexes or not is
a question still agitating physiologists. Opinion inclines in favor of
their reflex nature, and, pathologically considered, it is difficult
to regard them in any other light.]

Opinion is divided as to the electrical reactions in tabes dorsalis.
That qualitative changes never occur in uncomplicated cases all
authorities are agreed, but while Strümpell and other modern writers
claim there is no change of any kind, a number of careful
investigators have found an increased irritability in the initial
period, particularly marked in the peroneal group of muscles (Erb). In
my own experience this is frequently the case, where lightning-like
pains are the only subjectively distressing symptoms complained of.

While the symptoms thus far considered as marking the origin and
progress of tabes dorsalis are more or less constant, and although
some of them show remarkable remissions and exacerbations, yet may in
their entity be regarded as a continuous condition slowly and surely
increasing in severity, there are others which constitute episodes of
the disease, appearing only to disappear after a brief duration
varying from a few hours to a few days: they have been termed the
crises of tabes dorsalis. These crises consist in disturbances of the
functions of one or several viscera, and are undoubtedly due to an
error in innervation provoked by the progressing affection of the
spinal marrow and oblongata. The most frequent and important are the
gastric crises. In the midst of apparent somatic health, without any
assignable cause, the patient is seized with a terrible distress in
the epigastric region, accompanied by pain which may rival in severity
the fulgurating pains of another phase {836} of the disease, and by
uncontrollable vomiting. Usually, these symptoms are accompanied by
disturbances of some other of the organs under the influence of the
pneumogastric and sympathetic nerves. The heart is agitated by violent
palpitations, a cold sweat breaks out, and a vertigo may accompany it,
which, but for the fact that it is not relieved by the vomiting and
from its other associations, might mislead the physician into
regarding it as a reflex symptom. In other cases the symptoms of
disturbed cardiac innervation or those of respiration are in the
foreground, constituting respectively the cardiac and bronchial
crises. Laryngeal crises are marked by a tickling and strangling
sensation in the throat, and in their severer form, which is
associated with spasm of the glottis, a crowing cough is added.[22]
Enteric crises, which sometimes coexist with gastric crises, at others
follow them, and occasionally occur independently, consist in sudden
diarrhœal movements, with or without pain, and may continue for
several days. Renal or nephritic crises are described[23] as
resembling an attack of renal colic. The sudden disturbances of
bladder function have been described as vesical crises, and recent
French observers have observed so-called _crises clitoridiennes_ in
female tabic patients which were characterized by voluptuous
sensations. All of these symptoms have these in common: that they last
but a short time, that their disappearance is as rapid as their
advent, and that they depend for their distribution on the attitude of
the disease in the cord. The vesical crises are more apt to occur
early than late in the disease and where the belt sensation is in the
hypogastric region. The gastric and enteric crises are usually found
when the belt is in the epigastric level, and the bronchial, cardiac,
and laryngeal crises when it is in the thorax and neck. Some
connection has been observed between the occurrence of the
lightning-like pains and these crises. Thus, a sudden cessation of the
former is sometimes the forerunner of the latter. It is also found
that one variety of these crises disappears to give way to another:
this is particularly noticed with the bronchial crises, which often
cease suddenly, to be followed by vomiting.

[Footnote 22: Krause, in a paper read before the Society of
Neurologists at Berlin (_Neurologisches Centralblatt_, 1885, p. 543),
found either laryngeal crises or other laryngeal symptoms, such as
demonstrable ataxia of movement of the vocal cords, in 13 out of 38
cases. This proportion would be far too high for tabes in general; his
cases were probably advanced ones. He established the interesting fact
that the laryngeal crisis may sometimes be provoked by pressure with a
probe on the superior laryngeal nerve at its laryngeal entry-point.
Jastrowitz claims to have determined the existence of actual paralysis
of the vocal cords with the crises, but Krause concludes from the
experimental inductibility of the crisis that it cannot be due to a
posticus paralysis. In a discussion on the subject Remak affirms that
a unilateral paralysis of the crico-arytenoideus posticus may be an
early or the earliest symptom of tabes. It seems, however, that in all
cases where he determined such paralysis there had been disturbances
of function of other cranial nerves in unusual severity at about the
same time.]

[Footnote 23: They must be extremely rare: they have not occurred in a
single one of my 81 private cases, nor do I recall one in clinic or
dispensary experience.]

There is some analogy between the exceptionally-occurring mental
disturbance of tabic patients and the crises. Like them, it resembles
a disturbance of innervation, in this instance the centres regulating
the cerebral circulation appearing to be at fault. It also seems as if
in cases of this character the direction of the mental disturbance
were determined in some sense by the emotional relations of the
oblongata, for the insane outbreak usually consists in a brief but
extreme outburst either of a {837} depressed and melancholiac or an
expansive maniacal or delirious outburst. It is a very rare
occurrence, and usually limited to the latest stages. Much more common
is the development of paretic dementia, but this is to be regarded
rather as a complication than an integral feature of tabes. Most tabic
patients retain their mental equilibrium to the last moment; some
develop truly heroic resignation to their terrible sufferings and
gloomy prospects; and a few, becoming irritable, petulant, and
abnormally selfish, show the effect of invalidism manifested equally
with other chronic diseases.

In addition to the visceral crises there are other disturbances of
innervation of a nutritive or trophic character which are
characteristic of tabes. There is scarcely one of the eruptions or
other changes which are attributable to central nervous disease which
may not occur at some one or other period of this disease. Thus,
herpetic eruptions may occur independently or in conjunction with
lancinating pains, in one case even corresponding to the area of the
belt sensation. Discoloration of the skin or hair, the latter turning
gray or white in circular[24] or in irregular patches, spontaneous
falling of the nails, spontaneous hemorrhages in the matrix of the
nail, ichthyosis,[25] purpura, diffuse œdemas, localized perspiration
sometimes associated with sudamina and accompanied by ecchymoses,
muscular atrophies, bullæ, and pemphigus-like eruptions, have been
noted by various observers. As yet, they are to be regarded rather as
clinical curiosities than as constant features, as diagnostic
criteria, or as presenting special indications for treatment. The
trophic disturbances affecting the bones and joints and a peculiar
ulcerative process known as the perforating ulcer of the foot are
better studied, and, ranking among the most formidable and striking
manifestations of tabes, merit special consideration. The tabic joint
affection, first described by Charcot as a trophic manifestation of
tabes, is usually located in the hip or knee, but almost any joint,
including the temporo-maxillary articulation, may be its seat. The
earlier or lighter forms consist in serous exudations with or without
active local manifestations resembling those of synovitis; but the
commoner and graver form consists in actual deformity of the articular
surfaces, such as enlargement or atrophy, sometimes supplemented by
the formation of osteophytes. In addition, spontaneous dislocations
occur in a manner which is often quite surprising.[26] As a type of
such an occurrence the following may serve: A tabic patient presented
a synovial swelling of the left knee of truly enormous dimensions; as
soon as this became reduced a distinct crepitus was elicited, and both
the femoral and tibial articular surfaces found enlarged. The whole
process occupied only a few days; the lateral ligaments were then
found so relaxed that the leg could be freely moved in every
direction.

[Footnote 24: Rossolymmo, _Archiv für Psychiatrie_, xv. p. 727. I have
never observed this symptom as beautifully developed as in a case of
spinal irritation, in which the possibility of the existence of any
organic disease could be positively excluded. Bulkley has observed
albinism.]

[Footnote 25: In three cases by Ballet et Dutil, _Progrès médicale_,
May 19, 1882.]

[Footnote 26: Boyer (_Revue de Médecine_, 1884, p. 487) records a case
where the hip became luxated spontaneously as an early symptom.]

The connection between the morbid process in the spinal cord and these
remarkable arthropathies is as yet unexplained; and as Charcot's
original {838} proposition, that they can be always referred to
lesions in the anterior horns of the gray matter, has not been
sustained, some of the German clinicians, notably Strümpell, are
inclined to attribute them, in part at least, to ordinary results and
accidents due to the anæsthesia and its disturbing effect on voluntary
and automatic joint protection. A controversy arose which was
participated in by the Clinical Society of London,[27] and evoked
opinions from nearly all the eminent neurologists of Europe. The
result of this thorough discussion has been to establish the joint
affection as a true tabic symptom due to the same morbid process which
underlies the less enigmatical symptoms of the disease. One of the
best reasons for regarding these joint lesions as of trophic origin is
the fact that they are associated with textural bone-changes by which
they become either unduly soft or brittle, and therefore exposed to
apparently spontaneous fracture. Cases of fracture of almost every
long and some of the short bones are recorded, among the most
remarkable being one by Dutil,[28] where fracture of the radius
occurred without adequate cause in the initial period of tabes; and
one by Krönig,[29] in which the patient, who had been tabic for eight
years, broke a lumbar vertebra while catching himself in the act of
falling down stairs.

[Footnote 27: The question was formally raised by Morrant Baker at the
December meeting in 1884, and the discussion participated in by
Charcot himself. Among the opponents of Charcot's theory were Jonathan
Hutchinson and Moxon, the latter of whom administered a sound and
well-merited criticism regarding some of the premature, if not
sensational, announcements of the distinguished French neurologist. He
compared the joint lesions of tabes to decubitus: just as the latter
can be avoided by a proper protection of the exposed parts, so the
former would not occur if the joints could be kept in a, surgically
speaking, normal state. Moxon seems to have forgotten, in suggesting
this comparison, that there is a form of decubitus which will occur
independently of the greatest care and in spite of every measure taken
to arrest it, and which can be attributed only to an obscure but
active perversion of nervous nutritive control. Barwell, Paget,
Herbert Page, Broadbent, and McNamara agreed that the joint lesions
are not of surgical or rheumatic origin, but essentially signs of the
nervous affection. Although Barwell's claim, that the rheumatic and
tabic joint diseases are essentially different, because the former is
hyperplastic and the latter is atrophic, is not borne out by all cases
of tabic joint disease, some of which are certainly hyperplastic, yet
the other reasons advanced for regarding these affections as distinct,
and considering the joint affection of Charcot as a trophic disorder,
far outweighed those advanced by the opponents of this view. In fact,
the only ground the latter had to stand on was the fact that Charcot's
asserted anatomical foundation was found to be chimerical.]

[Footnote 28: _Gazette médicale de Paris_, 1885, No. 25.]

[Footnote 29: _Zeitschrift für klinische Medizin_, 1884, vii., Suppl.
H.]

Another reason for considering the arthropathies as of central origin
is their chronological association with other signs whose trophic
origin cannot be disputed, such as unilateral sweats and œdemas and
visceral crises. They are also found to correspond in many cases to
the lancinating pains both in location and time.

The feet of an advanced tabic patient usually appear deformed; the
extremities of the bones, particularly at the metacarpo-phalangeal
articulation, are thickened, and the axis of the foot as a whole is
bent. It is a question how far this deformity may be due to persistent
faulty innervation of the muscles going to the foot and to ensuing
mechanical influences. A most pronounced deformity found in a few
cases has been designated by Féré as the tabic foot.[30] It consists
in the thickening of the tissues on the inner side of the foot,
obliterating its arch in such a manner that in standing the plantar
surface is everywhere in contact with the floor. {839} With this the
tarso-metatarsal and the metacarpo-phalangeal joints of the great toes
appear greatly swollen.

[Footnote 30: Pied tabétique—_Revue de Médecine_, 1884, p. 473.]

There is less dispute concerning the nature of the so-called
perforating ulcer of the foot. This lesion occurs only in cases where
the central or peripheral nervous apparatus is diseased; thus, it may
occur with neuritis, and it is therefore unanimously regarded as due
to morbid nervous influences. In tabes it may follow an exacerbation
of the fulminating pains. It consists in a swelling of the tissues of
the foot; the skin becomes firm and thickened; deep sinuous ulcers are
then developed, showing but slight if any tendency to granulate, and
which extend down to the bone, the latter usually remaining
unaffected.[31] In a few cases more remarkable accidents due to
disturbed nutrition have been noted. Thus, J. Hoffmann records a
subcutaneous rupture of the Achilles tendon, and in another case the
spontaneous discharge of all the teeth of the upper jaw within about a
week's time.[32]

[Footnote 31: Like most of the manifestations of advanced tabes, the
perforating ulcer may occur exceptionally as a pre-ataxic symptom.
Thus, Suckling (_British Medical Journal_, 1885, April 4, p. 693)
mentions its preceding the development of tabes proper by one year.]

[Footnote 32: _Berliner klinische Wochenschrift_, 1885, No. 12. In
this unique case the loosening and falling out of the teeth preceded
the tabes by a year. Demange, who observed the same phenomenon in two
cases, found that the ascending root of the fifth pair was involved.
The only analogous observation in my experience relates, like the
bleaching of the hair in circular patches, to a case of spinal
irritation: here the gums and alveolar borders underwent atrophy,
exposing the roots of the teeth to beyond the normal alveolar border:
first the right upper row, then the right lower row, and finally the
teeth on the left side in the same order, showed this condition; only
the most posterior fell out.]

COURSE.—Tabes dorsalis is to be regarded as an extremely chronic
affection. Its development, as previously stated, is insidious,[33]
and the symptoms demonstrating the advent of the disease may be so
slight for many years that the patient does not regard himself as ill
or as likely to become so. In this condition he may remain for ten or
more years; and there are cases recorded where the exact signs of the
incipient stage were well marked, and yet no ascertainable progress
was made in a period of such long duration that the inference
naturally follows of a much longer prospective period in which the
patient would not have become ataxic. There may be distinguished two
forms of invasion: the more frequent is marked by the development of
the terebrating, fulgurating, and fulminating pains, to which, sooner
or later, the abolition of the pupillary and certain other deep
reflexes is added. In the vast majority of cases they are found absent
when the physician's attention is directed to the question of the
existence of spinal disease. In about one-fifth of the cases pain is
at no time a prominent feature of the disease, and may be, as is
established by the cases cited, entirely absent. In these patients the
first symptoms noted are muscle-tire on slight exertion. Usually, the
evidences of disturbed sensation and innervation begin in one
extremity or preponderate in it, but symmetry is soon established. The
same is noticed in the extension of the morbid process: when the ulnar
distribution is involved—which is the first danger-signal on the part
of the cervical enlargement of the cord—usually one side is first
involved, but the other soon follows, and becomes affected in equal or
nearly equal degree. In the {840} overwhelming majority of cases the
disease manifests itself in the lower extremities first, remaining
limited to them for a long period, and if extending to the upper
extremities doing so in much slighter intensity than in the lower.
Gull, Leyden, and others have observed cases where the arms were first
and chiefly involved; but this is extremely rare. Cases of a
simultaneous involvement of the upper and lower extremities are more
frequently noted. The symptoms detailed above are developed in varying
order in different patients, and the line has been already indicated
which separates the progressive from the episodial features of the
disease. Even in the ataxic period the patients may remain in a
comparatively stationary period for many months and years.[34] The
general bodily nutrition is usually good, and the muscular strength,
as such, rarely affected to any noteworthy extent until the extreme
phase of the disease is reached. Even the formidable-appearing crises
and trophic disturbances, though occasionally fatal, are not always
so. The direct danger from the disease proper, so far as life is
concerned, is in the possible development of cystitis and pyelitis, of
the malignant bed-sore, and of delirium and coma, the latter of which
is occasionally found to be due to cerebral hemorrhage—a lesion which
some writers regard as possibly due to some impalpable influence of
the spinal disease on the cerebral circulation.[35]

[Footnote 33: Cases of acute locomotor ataxia have been described. In
no instance are they pure or typical, and the last case of the kind
published in America, beginning, as it is evident from the account,
with signs of general myelitis, illustrates the impropriety of
utilizing one or a few symptoms as determining nomenclature.]

[Footnote 34: Thirteen patients are now under my observation, or I
have been able to obtain reliable medical information concerning their
condition, who have been in the ataxic period since the date of my
first examination, varying from a year to seven years ago. Not one of
these patients is materially much worse than at that time. Two only
died, both being bedridden at the time they came under observation. Of
the first group, three have shown more or less lasting improvement in
respect to special symptoms, as will be detailed in connection with
the treatment.]

[Footnote 35: In a case of sudden death, with an asthma-like seizure,
of a tabic patient under the charge of T. A. McBride, I found an
intense injection of one (the right) vagus nucleus, the color of the
ala cinerea and of the nucleus on section being almost black.]

MORBID ANATOMY AND PHYSIOLOGY.—Our knowledge of the structural disease
underlying the symptoms which comprise the clinical picture of tabes
dorsalis is perhaps the clearest in the domain of spinal pathology.
Not alone the commencement of the morbid process and every stage of
its subsequent encroachment on the spinal cord, but also its relations
to special symptoms, have been demonstrated in numerous cases by some
of the most careful German and French investigators.

In advanced cases of tabes the disease of the spinal cord is so
evident that it was noted even by earlier observers, the region of the
cord lying between the posterior nerve-roots being altered in color,
consistency, and dimensions. It is gray instead of white, hard instead
of soft, and considerably shrunken. The gray discoloration of the
surface appears to be complete in the lumbar and lower dorsal region;
it is less intense in the upper dorsal and cervical part of the cord;
and often shows a division into three streaks, of which one, in the
middle line, occupies both columns of Goll, while on either side
another extends in the inner side of the posterior root-entry. The
posterior roots themselves are frequently atrophied, and exhibit a
firmer consistency and darker color than in health. On making
cross-sections of the spinal cord it is found that the gray
discoloration extends inward, involving more or less of the posterior
columns in well-defined areas. Microscopic examination shows that the
myelin of the nerve-tubes is either destroyed or atrophied, and the
axis-cylinder is found to be affected in the same way, usually
presenting alterations in its {841} refraction and diameter where it
is not entirely destroyed. In the maximum foci of disease the
conducting elements of the cord are nearly destroyed, and their place
is occupied by a firm connective substance made up of wavy bundles,
enclosing here and there a few atrophied axis-cylinders with wasted
myelin-sheaths. The blood-vessels participate in the morbid process,
at least as far as the larger vessels are concerned: these are
sclerotic, their lumen appears contracted, the adventitial sheath is
hypertrophied and occupied by a nucleated, fibrillar connective
substance. The capillaries are sometimes normal, or participate in the
morbid process to the extent of a thickening of the extra-endothelial
sheaths which is either hyaline or fibrillary, and may show
inflammatory cell-proliferation. It is evident that the increase of
connective tissue in the posterior columns is not merely a relative
one, due to the condensation of the normal neuroglia after the
disappearance of the normal nerve-tubes, but is the result of actual
proliferation. Opinion is somewhat divided as to whether this is to be
considered as an inflammatory interstitial proliferation or as a more
passive development of tissue compensating for the destroyed
conducting elements. My own observations incline me to the belief that
in syphilitic tabes the morbid process is essentially interstitial,
while in non-syphilitic tabes it is parenchymatous, the disease
beginning in the nerve-tubes proper. Perhaps the controversies between
pathologists as eminent as Schultze, Tuczek, Rumpf, Zacher,
Kahler-Pick, Rosenstein, and Adamkiewicz—who are rather evenly divided
into opposing camps, one maintaining the parenchymatous, the other the
interstitial, origin of the disease—may be solved when we learn to
distinguish between the non-syphilitic and syphilitic cases, which is
clinically, as yet, impossible. The difficulty of deciding what is a
parenchymatous and what is an interstitial disease of the cord is
considerably enhanced by the fact that the neuroglia, which by some at
least is regarded as an interstitial connective tissue, is derived,
like the nerve-substance proper, from the upper or neuro-epidermic
germ-layer of the embryo, and not from the mesoblast, which furnishes
all other connective substances in the body.

It is regarded as well established that the sclerosis of the areas of
the spinal cord which are affected is preceded by a stage of granular
degeneration.[36] This is supported by the facts that the sclerotic
areas are surrounded by a zone in which sclerosis has not yet
developed, but which is in a state of granular degeneration, and that
in more advanced tabes this belt is also found sclerosed. In paretic
dementia, a disease whose complicating cord affection closely
resembles that of locomotor ataxia, a granular degeneration of the
posterior columns is very common in earlier periods, while in later
periods a sclerotic tissue is found in the same locality.

[Footnote 36: Westphal, _Archiv für Psychiatrie_, ix. p. 725.]

I regard these observations as opposed to the assumption of Strümpell
that tabes is a system-disease of the cord in the sense in which he
employs that term. In his fascinating and suggestive thesis on the
systemic affections he cites the observations of Tuczek made on the
posterior sclerosis ensuing from ergotism as confirming his view that
special systems of nerve-fibres are separately vulnerable to special
morbid influences. The remarkable correspondence between the
topographical distribution of the lesion of ergotin tabes described by
Tuczek and the characteristic areas {842} of sclerosis found in the
column of Burdach in ordinary tabes, seems to justify a very different
conclusion. Ergot exerts its morbid influence through a disturbance of
nutrition. Just as it produces gangrene by constriction of the
nutritive vessels of the fingers and of whole extremities, so it
produces interference with nutrition of those nerve-elements in the
cord which are most liable to suffer from general arterial
constriction. These are presumably those portions which are supplied
by the longest and narrowest arterial stems—a condition obtaining in
precisely those parts of the cord which are affected both in ergotin
tabes and in ordinary tabes.

It has also been supposed that the morbid process began in the
posterior roots and crept in with these, thence extending upward.[37]
This view is opposed by the fact that there is no constant
relationship between the root lesion and the cord lesion; the
sclerosis of the root-zones within the columns of Burdach I found to
be absolute in at least one case where the outer nerve-roots were not
distinctly affected.[38]

[Footnote 37: Takacs is the most recent defender of this view.]

[Footnote 38: The root lesion may, like that of the column of Goll,
according to a minority of the interpreters, be a secondary process,
for in ergotin tabes (Tuczek) both are usually intact.]

In typical tabes the sclerotic process begins in a special triangular
field of the posterior column in the lumbar enlargement of the cord.
The innermost of the posterior rootlets run through this field, which
has been designated by the French school as the posterior root-zones,
and the rootlets become exposed to all the vicissitudes which the
conducting tracts are destined to undergo in consequence. Throughout
the remainder of the cord it is the involvement of the root-zone which
indicates the advance of the affection upward. At a time when the
lesion is comparatively slight in the cervical level, manifesting
itself by a slight grayish or reddish streak to the naked eye, a
faint, pale discoloration in chromic-acid specimens, a deeper stain in
carminized, and a pallor in sections stained by Weigert's method, the
affected part in the lumbar region has undergone great shrinkage;
scarcely a single myelin-tube is preserved to receive Weigert's stain
within the affected area; the latter involves nearly the entire field
between the cornua, and absorbs carmine deeply, so that it is
difficult to differentiate the gray and white substance in carminized
sections. A small part of the posterior column which most closely
adjoins the posterior (gray) commissure remains free in all cases; so
also does a small laurel-leaf-shaped field bisected by the posterior
median septum. Examination with higher magnifying powers, aided by the
modern improved methods of preservation and staining, reveals that the
gray substance of the posterior segment of the cord is usually more or
less diseased. In advanced cases the gelatinous as well as the spongy
part of the posterior gray horn, and even the posterior gray
commissure, undergo such considerable atrophy that they may occupy but
half the normal area. In some cases the columns of Clarke appear to be
involved quite early in the disease.[39]

[Footnote 39: Leyden discovered the degeneration in the fibres which
in part make up these columns and correctly traced its origin to the
posterior rootlets. Lissaner and Zacher (_Archiv für Psychiatrie_, xv.
p. 437) confirmed him, the latter finding, as Leyden was the first to
discriminate, that the cells may escape while the fibres are
materially diminished. Krause claims that the columns of Clarke are
constantly affected, but not necessarily in their entire length, the
higher levels appearing quite normal at a time when the lower are
severely involved (_Neurologisches Centralblatt_, 1884, p. 50).]

{843} The triangular field in the lumbar part of the posterior column,
which is one of the typical starting-points of the affection, contains
those ascending nerve-bundles which in their cephalic course
emancipate themselves from the column of Burdach and constitute the
slender columns of Goll. The result is that the degenerative process
creeps up these columns at the same time that it ascends in the
root-zones and deep portions of Burdach's columns. Some authorities
regard this as a mere extension by contiguity;[40] others incline to
consider it a secondary degeneration. It may extend to the medulla
oblongata, becoming lost in the level where the nucleus of the column
of Goll terminates, and is accompanied, at least in those advanced
cases in which the upper extremities are involved, by a comma-shaped
area of degeneration in the adjoining part of the column of Burdach,
which similarly extends into the oblongata and terminates slightly
more cephalad. In typical advanced tabes, therefore, the cross-section
of the cord exhibits a characteristic distribution of the sclerosis in
each level. As this distribution is associated with certain constant
symptoms, it is permissible to attempt bringing certain features of
the lesion in relation with special features of the disease symptoms.
The posterior gray horns and the posterior white columns, together
with other fibre-systems connected with them, are much more
complicated in structural and physiological relations than the
corresponding anterior structures. The relations of the anterior
rootlets to the gray substance, and those of the motor ganglionic
elements to their controlling tracts, are comparatively simple; those
of the posterior roots are very intricate. They run up, in great part,
at an angle to the longitudinal tracts; a few pass in directly, and
still fewer dip to a lower level. The result is that a section of the
cord made in the longitudinal direction through the root-zones, so as
to pass from the root-entry to the anterior commissure, shows the
column and root-fibres to be woven into each other like a plait.
Trabeculæ of connective tissue, dragged in as it were with the
posterior roots, fill up the interstices of this labyrinth. They are
particularly dense in the lowest part of the lumbar enlargement of the
cord, constituting the so-called posterior processi reticulares. It is
reasonable to suppose that the overlapping of ascending and descending
root-fibres, associated with the presence of an extra amount of
connective tissue, imbedded as this fibre-maze is in that part of the
cord which is most distant from its lymphatic emunctories, affords a
favorable soil for slow inflammatory trouble. This is the primary
field of tabic sclerosis, and in it the disease may remain most
intense for years, extending but slowly and with diminishing intensity
upward, hand over hand, as it were, on the natural ladder which the
intertwined fasciculi and their matrix constitute. The longitudinal
tracts which lie in and near the root-zones belong to the so-called
short fibre systems, uniting the segments of higher and lower levels
of {844} the cord with each other. As the sclerotic process ascends it
involves the caudal ends of these systems: they consequently undergo
secondary degeneration, and, shrinking in their turn, affect the
caudal part of the next system above in the same manner. The morbid
process in the column of Burdach may therefore be considered as a
combination of inflammatory and degenerative changes, the inflammatory
products causing a series of short ascending degenerations, and the
vulnerable path thus established being followed by a cirrhotic
condition in which the connective and vascular structures participate
actively. With regard to the reasons for regarding the degeneration of
the column of Goll and that of the comma-shaped field near it as a
secondary process due to the cutting off of its apparent nerve-supply
at the caudal end, and of the posterior nerve-roots or their
provisional terminations, they may be stated in this way: When the
lesion of the primary field is limited to the lower lumbar or sacral
part of the cord, the degeneration of the column of Goll is limited to
its postero-internal part; when the upper lumbar and lower dorsal cord
is involved, the entire tract is affected; and when the cervical
portion is diseased, the supplementary comma-shaped area degenerates.
In other words, the projection tract of the sciatic nerve, as far as
it is represented in Goll's column, suffers in the first, that of the
crural nerves in the second, and that of the brachial nerves in the
third instance. In all advanced cases of tabes the affection of the
column of Goll is in direct proportion to the altitude of the lesion
in the primary field. Symptomatically, it bears an equally constant
relation to the ataxia.[41] No case is on record in which these
columns were totally degenerated without some motor inco-ordination of
the lower extremity having been observed during life; and no case is
recorded in which brachial ataxia had been a marked and persistent
feature in which the comma-shaped area—area of the column of
Burdach—was healthy.

[Footnote 40: It is held by them that the histological character of
the change of the columns of Goll is not different from that in the
column of Burdach. Zacher (_Archiv für Psychiatrie_, xv. p. 435) urges
that it does not resemble true secondary degeneration, beginning in
the vessels and connective substance instead of the nerve-fibres.
Schultze (_ibid._, xiv. p. 386), on the other hand, recognizes a
primary involvement of the nerve-fibres in both of the areas of
fascicular degeneration in tabes. The observation of intact
axis-cylinders by Babinski in the sclerotic fields is in conflict with
the latter's claim, and the various differences of observation and
interpretation seem to be reconcilable only on the assumption that
there are two different modes of origin, both leading to nearly the
same results and occasionally combined in one and the same case.]

[Footnote 41: Krause's case and others show that the ataxia of
movement is not influenced by lesion of the column of Clarke; but we
are not informed as to the static equilibrium of the patients in whose
cords these columns were found intensely affected.]

It is scarcely necessary to seriously consider the suggestion of
Strümpell, that the lesion of the column of Goll is in relation with
the bladder disturbance.[42] Cases are on record by Wolff and others
where this lesion was intense and there was little or no bladder
disturbance.[43]

[Footnote 42: _Archiv für Psychiatrie_, xii.]

[Footnote 43: The column of Goll is not present in those mammals
which, like the porpoise, have no developed hind limbs, but these
animals have urinary bladders.]

If the disease of the column of Goll were a primary systemic affection
independent of the disease of the root-field, it would be difficult to
understand why it, as well as the likelihood of finding a
corresponding degeneration of the direct cerebellar tract, increases
with the extent to which this field is involved. This occurrence
becomes quite clear when we remember that both the direct cerebellar
tract and that of Goll, being centripetal, are under the trophic
dominion of the posterior nerve-roots. The opinion is not distinctly
expressed, but implied in some writings, that the column of Goll
degenerates because of a general transverse cord lesion at a low
level; this is not the case in the tabic cord. There is a difference
in appearance between that part of the primary field which corresponds
to the column of Goll in the lumbar cord and the surrounding sclerosis
in early cases: it is more intensely degenerated, more {845}
homogeneous in appearance, and more evenly stained. The other part of
the triangular field presents a more trabecular appearance. In the
specimen represented in the accompanying figure this is easily
recognized: the darker field corresponds exactly with the ascending
degeneration, which follows compression of the cauda equina,[44] and
is the sciatic equivalent of the column of Goll.

[Illustration: FIG. 31. Trans-section of Upper Lumbar Cord of a
Patient moderately advanced in Tabes: _f_, ventral or anterior
fissure; _g_, caput gelatinosum; _r r′_, entry and deep course of the
posterior rootlets; _d_, degenerated field, including the origin of
the tracts which in higher levels form the columns of Goll; _n_, field
near the posterior commissure which remains free from degeneration,
both in the lumbar and cervical cord; _s_, sharply marked leaf-shaped
field, bisected by posterior septum, which, as claimed by Strümpell
and shown in this case, remains free from disease; _z_, zone of nearly
normal consistency around it; _a_, diseased field, suspected to be
related to the analgesia, not usually affected in early tabes; _v_,
fibres running up and down in front of the gelatinous substance; *,
region where the tabic process sometimes begins.]

[Footnote 44: I have also found that this field corresponds to the
column of Goll in its myelinic development: the lumbar part of this
column—designated as such by Flechsig—is an entirely different tract,
which enjoys a remarkable immunity from disease in tabes.

As illustrating the bearing of the lesion of the column of Goll on the
motor ataxia I may refer to two cases which happen to be related side
by side by Strümpell (_Archiv für Psychiatrie_, xii. p. 737, Cases 1
and 2). As far as the lumbar segment of the cord is concerned, the
distribution of the lesion is similar; but in the one presenting
marked motor ataxia the triangular field was slightly diseased, and
there was no upward extension of the lesion in the column of Goll. In
the other, with marked ataxia, the triangular field was intensely
diseased, and ascending degeneration (?) occurred in the sciatic
fields of the latter.

In support of the view that the comma-shaped area in Burdach's columns
is homologous with the fibres of the column of Goll, it is to be
advanced that degeneration of this field bears the same relation to
symptoms in the distribution of the ulnar nerve that degeneration of
the column of Goll bears to sciatic and crural symptoms. Where the
initial pains and subsequent tactile and locomotor disturbance were
severe, this field was found affected, and most so in the side where
the symptoms had been most intense (Friedreich-Schultze's cured cases,
_Archiv für Psychiatrie_, xii. p. 234). This area has no direct
connection with the root-fields. Secondly, in a primary system disease
of the column of Goll, associated with degeneration of the nucleus of
the column of Goll, described by Scoli, an irregular encroachment of
the column of Burdach was noted. Third, the innermost fibres of the
column of Burdach (those belting the nucleus in the oblongata) have
the same relation to the interolivary layer which the column of Goll
has through its provisional nucleus of termination.

While the evidence of high lesion of the cerebral continuation of the
column of Goll, and, what I regard as its homologue, the comma-shaped
area of Burdach, together with the constant association of marked
degeneration of these columns with motor ataxia, is strong positive
proof of its relation to this symptom, there is equally strong
evidence negativing its relation to any other of the prominent
symptoms of tabes dorsalis. Thus Babesin (_Virchow's Archiv_, lxxvi.
p. 74) found degeneration of the posterior columns limited to the
column of Goll, and the patellar reflex was not destroyed; the
root-fields at the upper lumbar levels were intact. That the columns
of Goll have been found profoundly affected without bladder
disturbance has been stated previously, and constitutes a stronger
argument against Strümpell's view than the frequent observation of
bladder trouble in spinal diseases, along with which these columns may
be entirely free.]

Among the various constituents of the posterior columns which appear
{846} to present a relative immunity to the disease, aside from the
area near the posterior commissure and the laurel-leaf-shaped area of
the posterior septum, Strümpell noted one which is situated at the
periphery of the cord, bordering on the entry-line of the posterior
roots and the inner contour of the posterior roots. In the few cases
where it was found destroyed there was, what is a comparatively rare
thing in moderately severe tabes, complete analgesia. It is not,
however, certain that there is a necessary connection between the
pathological and clinical fact here. The nerve-roots themselves are
involved within the diseased area of the root-zones. The lesion is one
of a kind which, affecting a nerve-trunk, would produce first
irritation of, then impediment to, and ultimately destruction of, its
function. The clinical parallel to this is the occurrence of the
lightning-like pains in the earlier phases of the disease, which are
followed by delayed pain-conduction, and finally by loss of sensation.
Of the rootlets or fibres subservient to the various sensory and
reflex functions mediated by the posterior roots, those which convey
the centripetal impression normally evoking the patellar jerk appear
to be the most vulnerable, or, because of their limited number, the
earliest to be destroyed or compressed, with the result of total
functional paralysis.[45]

[Footnote 45: It is now conceded that, as Westphal claimed, the
patellar jerk is always abolished when the upper lumbar level of the
root-zones (bandelettes externes of Charcot) is involved. Tshirijew
has shown that the translation of the knee-jerk reflex occurs in a
single segment of the rabbit's cord at the homologous level. In
transverse sections a distinct fascicle may be seen coursing from the
innermost root-fibres toward the antero-intermediate cell-group of the
anterior horn; it furnishes a pictorial substratum, if not anatomical
proof, for the patho-physiological observation, and harmonizes with
the fact that it is the innermost rootlets which usually suffer first.
Perhaps the delicacy of this tract accounts for the frequent
disappearance of the jerk in old people as a result of senile
sclerosis.]

With regard to the interpretation of the various tactile sensory
disturbances of tabes and the delayed pain-sense conduction little
positive advance has been made. That the lesion of the root-zones and
gray substance is responsible for them seems to be the general
conclusion of French and German observers. Recent researches have
shown that disease of the peripheral nerves (multiple neuritis) may
produce sensory phenomena which it had previously been customary to
regard as pathognomonic of disturbance of their intraspinal
terminations and continuations. At the same time, we are confounded by
the observation of Erb, that even retardation of conduction of the
pain-sense, which the dictum of Schiff taught us to regard as a sign
of disturbed function of the spinal gray matter, is also produced by
peripheral neuritis.

Immediately adjoining the gelatinous apex of the posterior horn there
is a column of vertical fibres which bear a relation to it resembling
that {847} of the ascending root of the fifth pair in the oblongata to
the tuber cinereum of Rolando. Sclerosis of this column, as well as of
the ascending root in question (Demange), has been found in tabes, and
usually in association with pronounced trophic disturbances. In a
number of cases (Oppenheim, Eisenlohr, and others) where spasmodic
laryngeal crises had been a marked feature during life, lesion of the
floor of the fourth ventricle, or atrophy of the pneumogastric nerve,
or even of its nucleus, was found. In one case with marked gastric
crises I found sclerotic changes of the arteries in the ala cinerea.

With regard to the involvement of the peripheral nerves proper, aside
from the optic, opinion is somewhat divided. The discovery of multiple
neuritis, and the recognition of the fact that it had been erroneously
confounded with tabes, led Dejerine to claim that tabes might be of
peripheral origin. He even proposed to account for the oculo-motor
trouble on the basis of an affection of the oculo-motor nerves. This
explanation has been repudiated by Westphal and sound authorities
generally. That the peripheral nerves are occasionally involved in
tabes was already known to Friedreich in 1863,[46] and later Westphal
found the cutaneous branches in an advanced tabic patient to present
similar changes to those discovered by Friedreich: these findings are
confirmed by his Japanese pupil, Sakaky. The nerve-tubes are
atrophied, the axis-cylinder being often preserved, and the
interneural connective substance is proliferated. But there is no
constant relation between these changes and the symptoms of the
disease; in one of Sakaky's cases the nerves of an extremity which had
been the seat of severe sensory symptoms were entirely normal. The
findings in the peripheral nerves of tabic subjects lose much of their
value in view of their recent discovery in marantic persons[47]
advanced in life, but who had no nervous disease whatever.

[Footnote 46: _Virchow's Archiv_, vol. xxvi. pp. 399-452.]

[Footnote 47: Krause, _Neurologisches Centralblatt_, 1885, p. 53.]

It has been attempted to bring the tabic process in relation to a
supposed primary meningitis. Tabes is a rather common nervous
affection, and primary spinal meningitis is one of the very rarest.
The leptomeninges are found considerably thickened in one out of ten
tabic cords, and those who defend the meningitic origin of the disease
base their theory on this inconstant finding, and allege that in the
cases where it is absent the meningitis has disappeared while the cord
lesion progressed. It is a fatal objection to this view that the part
of the posterior columns immediately adjoining the pia is often quite
free from disease. A meningitic affection, either as an etiological or
a complicating factor, can be admitted in those cases only where there
is a marginal sclerosis.

The changes in the optic nerve resemble those of the white columns of
the cord in their naked-eye and minute character as well as in the
controversial nature of the various interpretations made. When
affected, the nerve is found to be firmer than normal, and discolored;
later it becomes quite gray, and may eventually shrink to two-thirds,
and even less, of its normal diameter. It is generally believed that,
as in the cord, the myelin undergoes wasting before the axis-cylinder
disappears, and that the latter may survive a long time, thus
explaining why the patient may retain his visual power for a
considerable period after the ophthalmoscope determines the existence
of atrophy. No satisfactory explanation {848} has as yet been offered
for the optic-nerve affection of tabes. There is no direct continuity
of the spinal and optic sclerosis. Two theoretical possibilities
suggest themselves. The first is that the lesion of the cord exerts a
remote effect upon the physiological, and through this the structural,
condition of the optic nerve. That such an influence may be exerted is
shown by cases of transverse myelitis low down in the cord, which,
according to Erb and Seguin, were complicated by double optic-nerve
atrophy. The second theory is that the involved part of the cord and
the optic nerve present a similar vulnerability to the same morbid
influences. This is illustrated in some cases of chronic alcoholic and
nicotine poisoning, in ergotism, and in the spinal affections due to
hereditary influences and developmental defects.

To discuss the nature of the disturbing influence which is responsible
for the most characteristic evidence of the disease, the ataxia, would
be equivalent to reviewing almost every mooted question in spinal
physiology. It is to be borne in mind that ataxia is a collective term
designating any inco-ordination of movement which is independent of
motor paralysis. It may be due to abolition or impairment of tactile
perception; it may be due to loss of the muscular sense; it may be due
to hampered motor co-ordination; and, finally, it may be due to a
disturbance of the space-sense. In my opinion it is only in
exceptional cases that any one of these factors can be positively
excluded. Occasionally, one has been noted when the ataxia was grave
but the tactile sense was unimpaired, or where the muscular sense was
perfect but ataxia was well developed. The difficulty with most such
records is that no discrimination is made as to the kind of ataxia
present. That loss of skill which the patient shows when he shuts his
eyes and attempts to perform certain movements without their aid is
undoubtedly due to diminished sensation, either tactile or muscular,
and usually both. The inability to stand with the eyes closed is
probably a cerebellar phenomenon, and in this respect we are on the
way to return to Duchenne's opinion. It is true that the cerebellar
organ is healthy in most tabic subjects, but its centripetal informer,
the direct cerebellar tract, is either itself involved or affected in
its origin in the columns of Clarke. But, besides the static ataxia
and that motor ataxia which can be neutralized by the use of the eye,
there is another disturbance, which, as Erb and his followers hold,
cannot be accounted for on the strength of any sensory disturbance. It
consists in an interference with the proper succession and rhythm of
movement. It seems as if that automatic mechanism by which the
individual or grouped muscular contractions engaged in locomotion
follow each other with the smoothness of the action of
perfectly-fitting cog-wheels were disturbed; the correct
after-movement is hesitated over or skipped, or even takes place at
the wrong moment, neutralizing some other step in the co-ordination
required. The tendency of physiologists and pathologists is to
attribute this form of ataxia to the disease of the intrinsic
co-ordinating apparatus of the cord itself. The experiments of
Tarchanoff on a headless duck, and the determination of the existence
of cursorial co-ordinating tracts uniting the brachial and lumbar
nuclei in mammals, as well as the observations made on automatic
co-ordinate movement in decapitated criminals, demonstrate the
existence in the cord of such an apparatus. The combination of the
ganglionic centres which underlies this co-ordination {849} is
affected by the so-called short tracts of the cord,[48] and it is
precisely a portion of these which are involved in the lesion of the
column of Burdach. A number of arguments have been advanced against
regarding the lesion of this column, or indeed any of the lesions of
the posterior column, as explaining the ataxia-producing effect of
tabes. Westphal has interposed some potent objections. He holds that
lesion of these columns will be found more frequently when
examinations shall no longer be limited to those cases where disease
is suspected because ataxia was observed during life. He found
extensive disease of the posterior columns in sufferers from paretic
dementia who did not exhibit the characteristic ataxic gait of tabes.
I believe this objection can be met by the very cases cited by
Westphal in its support. Where the spinal disorder preceded the
cerebral—that is, where paretic dementia occurred as a complication of
tabes dorsalis—true locomotor and static ataxia had been present
before the insanity exploded. On the other hand, where the spinal
disease followed the cerebral, typical ataxia did not ensue. This
would seem to indicate that the destruction of cortical control is
inimical to the development of typical tabes. Leyden has made a
suggestion in the same direction when he attributes the lesser
manifestness of locomotor ataxia in tabic females to their inferior
cerebral organization.[49] A more convincing proof of the correctness
of this conclusion is furnished by the fact that if the pathological
process, after destroying the posterior columns and producing ataxia,
invades the voluntary motor tract, the ataxic symptom becomes less
palpable.[50] This antagonism between lateral-column and
posterior-column lesion is frequently exemplified in the combined
forms of sclerosis. It would seem, then, that where the brain is
healthy and the controlling voluntary tracts are unimpaired, the
ataxia is aggravated, supporting the beautiful theory of Adamkiewicz,
which assumes that the locomotor ataxia is due to a disturbance of the
balance normally existing between the psycho-motor centres and those
controlling the muscular tone as well as those mediating reflex
excitability.[51]

[Footnote 48: Intersegmental tracts.]

[Footnote 49: In one out of three female eases I found the active
disturbance of gait as severe as in males, but Leyden's observation is
supported by all who have seen a sufficiently large number of female
cases.]

[Footnote 50: Not because of paresis altogether, for it diminishes
materially out of proportion to the paresis.]

[Footnote 51: _Archiv für Psychiatrie_, x. p. 545. There is another
observation which bears in this direction: James of Boston observed
that absolute deaf-mutes in a large percentage of cases are
insusceptible to vertigo or to the allied phenomenon of sea-sickness.
Certainly, the auditory nerve is a space-sense nerve; its
physiological elimination is, however, accompanied by an immunity
against a symptom which may be an evidence of disturbed space-sense
transmission. In like manner, the destruction of the central
perceptive and voluntary centres in the paretic dement inhibits the
legitimate results of posterior spinal sclerosis.

The degeneration of the crossed-pyramid tracts in typical tabes seem
to be strictly an atrophy from disuse, perhaps facilitated by the
general malnutrition of the cord. It is limited to that part supplying
the most or solely affected extremities. Thus, where the lower
extremities are alone grossly involved it is totally degenerated in
the lumbar area, and only in its outer parts in higher levels. As if
to fortify this comparison by analogous observations from every great
segment of the nervous axis, a similar inhibiting influence of pyramid
lesion on co-ordinating disturbance (muscular sense) is noted in
secondary degeneration of the interolivary layer; when uncomplicated
with pyramid lesion (Meyer and my own case,) ataxia is present; when
so complicated (Schrader, Homén) it is not observed, even if
determinable.]

{850} Lissauer[52] has recently determined the existence of a
degeneration of certain fine nerve-fibres, apparently derived from the
outermost of the radicles into which the posterior nerve-roots divide
on entry. They are situated on that border of the apex of the
posterior horn which is in contact with the lateral column, and were
found degenerated in all cases except such as were in the initial
period. No symptomatic relation has been claimed for this lesion.

[Footnote 52: _Neurologisches Centralblatt_, 1885, No. 11.]

One of the most important questions which have grown out of the
pathological studies of tabes is the relationship between the lesions
and the not infrequently observed restoration of functions which had
been more or less seriously impaired in an earlier period of the
disease. Even those symptoms which ordinarily comprise the continuous
and essential clinical background of tabes may exhibit remarkable
changes in this direction. I have two well-established
observations—one of tabes of eight years' standing, the other of more
recent date—in which that symptom which, once established, is the most
constant, the reflex iridoplegia, disappeared, to reappear in two
months in one case where it had been associated with myosis, and to
reappear in eight months in the other, repeating this oscillation the
following year. I have now under observation a tabic patient in the
sixth year of his illness who two years ago had a return of both
knee-phenomena to a nearly normal extent, to lose them in two months,
and to regain the reflex on the left side four months ago, retaining
it up to the present. These three cases were of syphilitic subjects.
In a fourth advanced non-syphilitic tabic patient, whose ataxia had
reached a maximal degree, I found a return of both knee-phenomena for
three days after its absence had been established by medical examiners
for over a year, and had probably been a feature for a much longer
period. Hammond the younger and Eulenburg have reported similar cases.
Nothing is more surprising to those unfamiliar with the progress of
this disease than to find gross ataxia or the electrical pains and
anæsthesia to disappear or nearly so; and the alleged success of more
than one remedial measure is based on the fallacious attributing to
the remedy what was really due to the natural remittence of the
disease-process or of its manifestations. The financial success of
quacks and the temporary but rapidly evanescent popularity of static
electricity, Wilsonia belts, and like contrivances are owing to the
hopefulness inspired in the credulous patient by the mere coincidence
of spontaneous improvement and the administration of a new remedy,
supplemented, it may be, by the influence of mind on body in his
sanguine condition. It is to be assumed that the influences which are
at work in provoking the trophic and visceral episodes of tabes are of
an impalpable character, and that all theorizing regarding the reason
of their preponderance in one and their absence in another case are as
premature as would be any speculation regarding their rapid
development and subsidence in the history of one and the same case.
But we have better grounds for explaining the remissions of the ataxia
and anæsthesia.

It is only in the most advanced stages of tabes that the destruction
of the axis-cylinder becomes absolute or nearly so. Contrary to the
opinion of Leyden,[53] who held that the tabic sclerosis differs from
disseminated sclerosis in the fact that the axis-cylinder does not
survive the myelin {851} disappearance, it is now generally admitted
that a certain number of exposed or practically denuded axis-cylinders
may be preserved in the sclerotic fields.[54] It is on the theory that
these delicate channels may be oppressed at one time, perhaps by
inflammatory or congestive pressure, and relieved at another by its
subsidence, that we may assume them to be the channels through which
the now limited, now liberated, functions are mediated. It is also
reasonable to suppose that vicarious action may supplement the
impaired function, and to some extent overcome the disturbing factors.
This is illustrated by the controlling influence of the visual
function—yea, even of the unconscious and ineffectual co-operation of
completely amaurotic eyes—in neutralizing both locomotor and static
ataxia. One patient who was well advanced in the initial period of
tabes, and who had been encouraged to consider the medical opinion to
that effect as the result of an exaggerated refinement of diagnosis,
made repeated tests of the Romberg symptom in his own case, and
deluded himself into the belief that the physician was mistaken
because he succeeded in practically overcoming it with an effort that
too plainly told its own story; but still he overcame it. Certain
peripheral influences have the power of stimulating the dormant
activity of potentially vicarious tracts, and perhaps also the blunted
activity of those whose function is impaired. The outside temperature,
certain barometric conditions, all may exert an influence in this
direction for good or evil.

[Footnote 53: _Op. cit._, p. 328, vol. ii.]

[Footnote 54: Babinski (_Neurologisches Centralblatt_, 1885, p. 324)
notes this feature, and, consistently with the findings of most modern
observers, discovers much more resemblance to disseminated sclerosis
than to the systemic sclerosis with which Strümpell and Westphal (in
part) incline to classify tabes. Similar objections to the
system-disease theory are advanced by Zacher (_Archiv für
Psychiatrie_, xv. p. 340). I may not pass over in silence the fact
that Babinski considers his observations to militate also against
regarding any phase of the tabic sclerosis as a secondary process. But
while it may fairly be asked that a sclerosis to be regarded as
systemic must be shown to be total, this is not necessary for a
secondary process, unless the primary involvement be total also; and
that is not the case in tabes.]

ETIOLOGY.—Authorities are now agreed that no single cause can be
regarded as the sole responsible factor in all cases of tabes, and
that a number of etiological influences are combined in the
provocation of this disease in most instances. When the
distinctiveness of the affection was first recognized it was customary
to attribute it to sexual excesses, and the unfortunate sufferer had
frequently to bear the implied reproach of having brought his misery
on himself, in addition to the hopeless prospect which those who
followed Romberg and other authorities of the day held out to him.[55]

[Footnote 55: This opinion survives in a large portion of the German
laity and in French novels. About the time that the poet Heine was
dying from an organic spinal affection two other prominent literary
characters of Paris were affected with tabes. It so happened that all
three were popularly regarded as libidinous, and one of their leading
contemporaries, whose name escapes me, took occasion to issue a
manifesto addressed to the jeunesse dorée which closed with the
apostrophe, “Gardons à nos moelles.”]

Heredity plays a very slight part in the etiology of tabes. Writers of
ten and fifteen years ago attributed a greater importance to it than
is now done. But this was due to the incorporation with tabes of the
so-called family form of locomotor ataxia—a disease which is now
regarded as a distinct affection.[56]

[Footnote 56: There is but one record of direct heredity (the father
and son being affected nearly at the same time), to my knowledge. It
was observed at the Berlin Hospital by Remak (_Berliner klinische
Wochenschrift_, 1885, No. 7). Both father and son were syphilitic.]

{852} More importance may be attached to individual predisposition,
but thus far no distinct formulation of this factor has been attempted
except by Schmeichler,[57] who offers the suggestion that there are
persons with a predisposition to the development of connective-tissue
proliferation in various organs of the body, and that in them tabes
and other sclerotic affections are consequently more frequent than in
others. This suggestion appears plausible, but it is unconfirmed by
positive observations.

[Footnote 57: _Op. cit._]

Sex appears on a superficial view to be one of the most important
elements. It is generally admitted that at most one female becomes
tabic for every ten males who do so. Of 81 cases in private practice,
I observed but 3 females. Rockwell, Seguin, Birdsall, and Putnam give
similar figures. This comparative immunity is probably due to the fact
that the female is less exposed to over-exertion, to surface chilling
of the feet, to the injurious consequences of sexual excess, and to
syphilis[58] than the male. As a rule, the affection in females is
more insidiously developed, progresses more slowly, is less marked by
crises and trophic disturbances, and not accompanied by as severe
pains and profound disturbance of co-ordination as is the
corresponding affection in males.

[Footnote 58: Whether the shorter vitality of the syphilitic female as
compared with that of the male is a factor in diminishing the
accumulation of chronic tertiary sequelæ in that sex, or whether it be
the lesser vulnerability of the inferior nervous system, I am unable
to decide from the facts at my disposal. In private and clinical
experience I have been struck by the fact that women affected with
syphilis in the same way and under similar circumstances with tabic
syphilitic males develop symptoms of functional disorder of the brain
and cord, such as spinal and cerebro-spinal irritation. My cases
referred to had in no instance any indication of a syphilitic
condition or history, and a distinct and different cause was found in
all three.]

The most important element in creating an acquired predisposition to
tabes is undoubtedly the existence of constitutional syphilis. Some
difference of opinion still exists regarding the proportion of
syphilitic tabic patients, chiefly due to the neglect of Erb—when he
first announced the prevailing view, and which is generally attributed
to him—to differentiate between cases of demonstrated constitutional
syphilis and the so-called spurious or soft chancre. But although
there occurred a reaction against his view which went to as great an
extreme in the opposite direction, the careful and critically
registered statistics accumulated in the mean time strengthen the view
that there are more syphilitic subjects among the tabic than among any
class of sufferers from other nervous affections.[59] Reumont, a
physician at Aix-la-Chapelle, to which place syphilitic patients in
general resort in large numbers, found that of 3400 cases of syphilis,
290 had nervous affections, 40 being afflicted with tabes.
Bernhardt[60] took occasion to examine a group of hospital patients
who were free from tabes, and found that not fully 16 per cent. were
syphilitic, while of 125 tabic patients, over 46 per cent. were
determined to have had positive syphilitic manifestations. Several of
those observers who have paid attention to the question of the
syphilitic origin of tabes have admitted that the more searching their
inquiry the larger the proportion of detected syphilitic antecedent
histories. Thus, Rumpf's earlier table shows 66, and his later 80, per
cent. of such antecedents. This latter figure exactly corresponds to
the percentage of syphilis in my private {853} cases. At a discussion
held by members of the American Neurological Association in 1884,
Webber gave 54, Putnam 49, Rockwell 40, Birdsall 43,[61] and Seguin 22
per cent.[62] as the proportion in their experiences.

[Footnote 59: Excepting always those having the distinctive and
undisputed syphilitic character.]

[Footnote 60: _Archiv für Psychiatrie_, xv. p. 862.]

[Footnote 61: Derived from over five hundred cases which had presented
themselves at the clinic of the College of Physicians and Surgeons.]

[Footnote 62: In the _Archives of Medicine_ he tabulates 54 (private)
cases as follows:

  Chancre alone . . . . . . . . . . . . . . . . .  23
  Chancre followed by secondary symptoms  . . . .  16
        Total of those with history of chancre  .  39
  No history of chancre in  . . . . . . . . . . .  15
        Total . . . . . . . . . . . . . . . . . .  54]

Of European writers, aside from those already mentioned, Berger claims
43 per cent., and Bernhardt, in commenting on the increasing
percentage obtained by accurate investigation, reports an additional
series of 7 new cases in private practice, all of which were
syphilitic. Fournier, Voigt, Œhnhausen, and George Fisher estimate the
syphilitic tabic patients at respectively 93, 81, and 72 per cent. of
the whole number. The almost monotonous recurrence of a clear
syphilitic history in my more recent records is such that in private
practice I have come to regard a non-syphilitic tabic patient as the
exception. Among the poorer classes the percentage of discoverable
syphilitic antecedents is undoubtedly much less. The direct exciting
causes of tabes, exposure and over-exertion, are more common with them
and more severe in their operation.

The proof of a relationship between syphilis and tabes dorsalis does
not rest on statistical evidence alone. A number of observations show
that the syphilitic virus is competent to produce individual symptoms
which demonstrate its profound influence on the very centres and
tracts which are affected in tabes. Thus, Finger[63] showed that
obliteration of the knee-jerk is a frequent symptom of the secondary
fever of syphilis, and that the relation is so intimate between cause
and effect that after the return of the reflex, if there be a relapse
of the fever, the obliteration of the knee-jerk is repeated. Both the
permanent loss of the knee-jerk (Remak) and the peculiar pupillary
symptoms of tabes are sometimes found in syphilitic subjects who have
no other sign of nervous disorder; and Rieger and Foster[64] regard
the syphilitic ocular disturbances, even when they exist
independently, as due, like those of tabes, to the spinal, and not to
a primarily cerebral, disturbance. Another argument in favor of the
syphilitic origin of tabes is derived from the occasional remedial
influence of antisyphilitic treatment. The force of this argument is
somewhat impaired by the fact that the same measures occasionally
appear to be beneficial in tabes where syphilis can be excluded.
Still, the results of the mixed treatment in a few cases of undoubted
syphilitic origin are sometimes unmistakable and brilliant.[65] As
some cases, even of long {854} standing, yield to such measures, while
others, apparently of lesser gravity and briefer duration, fail to
respond to them, the question as to whether syphilis is a direct cause
or merely a predisposing factor may be answered in this way: That in
the former class it must have been more or less directly instrumental
in provoking the disease, while in the latter class it is to be
regarded as a remote and predisposing factor, to which other causes,
not reached by antisyphilitic treatment, became added. The claim of
Erb, that “tabes dorsalis is probably a syphilitic disease whose
outbreak is determined by certain accessory provocations,” is not
subscribed to unreservedly by a single writer of eminence.

[Footnote 63: “Ueber eine constante nervöse Störung bei florider
Syphilis der Secundärperiode,” _Vierteljahrschrift für Dermatologie
und Syphilis_, viii., 1882.]

[Footnote 64: “Auge und Rückenmark,” _Graefe's Archiv für
Ophthalmologie_, Bd. xxvii. iii.]

[Footnote 65: In one case already referred to a return of both
knee-phenomena and complete disappearance of locomotor and static
ataxia were effected after a duration of four years. The treatment was
neglected and the knee-jerks disappeared, and one has now returned
under the resumed treatment, but accompanied by lightning-like pains.
At a meeting of the Société médicale des Hôpitaux, held November 10,
1882, Desplats reported a case in which even better results were
obtained. Reumont (_Syphilis und Tabes nach eigenen Erfahrungen_,
Aachen, 1881) reports 2 out of 36 carefully observed syphilitic cases
cured, and 13 as improved under antisyphilitic treatment.]

The question has been raised whether the influence of syphilis is
sufficiently great to justify a clinical demarcation between
syphilitic and non-syphilitic cases. A number of observers, including
Reumont, Leonard Weber, and Fournier, incline to the belief that there
are more atypical forms of tabes in the syphilitic group. Others,
including Rumpf, Krause, and Berger, are unable to confirm this, but
the former admits, what seems to be a general impression among
neurologists, that an early preponderance of ptosis, diplopia, and
pupillary symptoms is more common with syphilitic than with
non-syphilitic tabes. Fournier[66] believes that syphilitic patients
show more mental involvement in the pre-ataxic period; but it is
evident that he has based this belief on a study of impure forms. The
advent of tabes in syphilitic cases does not in this respect differ
from the rule. The most protracted and severe diplopia I have yet
encountered in a tabic patient is one, now under observation, in the
initial period of the disease, syphilis being positively excluded as
an etiological factor.

[Footnote 66: _L'Éncephale_, 1884, No. 6.]

It seems to be a prevalent opinion that the cases of syphilis in which
tabes is developed include a large proportion of instances in which
the secondary manifestations were slight and unlike that florid
syphilis with well-marked cutaneous and visceral lesions which is more
apt to be followed by transitory or severe vascular affections of the
cord and brain.

Excesses in alcohol, tobacco, and abuse of the sexual function are
among the factors which frequently aggravate the tendency to tabes,
and one or more of them will usually be found associated with the
constitutional factor in syphilitic tabes. Both alcohol and nicotine
have a deleterious effect on nervous nutrition and on the spinal
functions, as is illustrated in the effect of the former in producing
general neuritis, and of both in provoking optic-nerve atrophy and
general paralysis of the insane, not to speak of the pupillary states
which often follow their abuse, and the undeniable existence of a true
alcoholic ataxia. Sexual excesses were, as stated, at one time
regarded as the chief cause: the reaction that set in against this
belief went to the extreme of questioning its influence altogether. It
is to-day regarded as an important aggravating cause in a large number
of cases, and this irrespective of whether it be the result of a
satyriacal irritation of the initial period or a precedent factor. In
a large number of my patients (18 out of 23 in whom this subject was
inquired into) the habit of withdrawing had been indulged in,[67] and,
as the patients admitted, with distinct deleterious effects, such as
fulness and throbbing in the lumbo-sacral region, tremor {855} and
rigidity, with tingling or numbness, in the limbs, blurred vision, and
sometimes severe occipital headache; in one case lightning-like pains
in the region of the anus ensued.[68]

[Footnote 67: Coitus reservatus, the real crime of the Onan of
Scripture.]

[Footnote 68: Leyden states that coitus in the upright position has
been accused of producing tabes, without mentioning his authority. I
have no observation on this subject touching tabes, but am prepared to
credit its bad effect from the account of a masturbator, who during
the orgasm produced while standing felt a distinct shock, like that
from a battery, shooting from the lumbar region into his lower limbs,
and causing him to fall as if knocked down. He consulted me in great
alarm—was scarcely able to walk from motor weakness, and had no
knee-phenomenon; in a few weeks it returned, and no further morbid
sign appeared. Masturbators of the worst type occasionally manifest
ataxia, and in three cases I have been able to establish the return of
the knee-jerk, together with other improvements in the spinal
exhaustion of these subjects. The loss and diminution of the patellar
jerk, and the frequently associated urinary incontinence, as well as
certain of the peripheral pains found in masturbators, certainly prove
that undue repetition of the sexual act (be it natural or artificial)
is competent to affect the cord in a way that cannot but be injurious
in case of a predisposition to tabes, if not without the latter.]

Of single causes, none exerts so direct and indisputable an influence
on the production of tabes as the action of cold and wet upon the
lower segment of the body. It is usually the case that such exposure
is frequently repeated and combined with over-exertion before the
disease is produced, but it is occasionally possible to trace the very
first symptom of the disease directly to a single exposure. A soldier
who stands up to his knees in a rifle-pit half full of water finds his
limbs numb or tingling; develops slight motor weakness, then
lightning-like pains, and ultimately a typical tabes. In the case of a
peddler who presented an advanced form of the disease, the first
symptoms had developed after a single wetting of his feet: while
walking along one of our watering-places with his wares the swell of a
steamer inundated the beach. He had been subject to perspiring feet
before that, and the perspiration remained checked from that time
on.[69] The influence of surface chilling was remarkably manifest in
all three of my female cases. In one of them it was due to frequent
wetting of the feet; in the second, a midwife, the first symptoms
began immediately after standing on a cold hearthstone while preparing
some article needed in a lying-in case. In the third case, a lady who
contracted and safely passed through a scarlatina in her twenty-eighth
year was taken out driving while desquamation was going on. She became
thoroughly chilled, experienced numbness in the fingers and toes, and
from that day on developed a slowly progressing tabes involving all
extremities alike.[70]

[Footnote 69: Checking of habitual perspiration by violent measures is
mentioned by the German textbook writers as a frequent cause, but
occurs quite rarely in the modern tables.]

[Footnote 70: In view of the absence of spinal—or, in fact, any
nervous—symptoms prior to the exposure referred to, it does not seem
necessary to insist that this was not an instance of a true
post-scarlatinal tabes; and possibly the case thus designated by
Tuczek (_Archiv für Psychiatrie_, xiii. p. 147) may have been really
due to chilling of the delicate body-surface after desquamation or
during that process. The typical form of myelitis and sclerosis after
exanthematous fevers is rather of the disseminated type.]

Spinal concussion has been mentioned by a number of authorities as a
possible cause for tabes, as for other forms of sclerotic spinal
disease. In 1 of 81 cases in my own observation the development of the
disorder could be distinctly traced to a railway injury; in 2 a sudden
aggravation was as distinctly referable to a similar cause.[71] To
what extent railroad {856} travelling, with its attendant continual
jarring of the body, may predispose to the development of tabes or of
other spinal diseases is as yet a matter of mere conjecture. That
railroad travelling exerts a bad influence in some cases of the
established disease is evident; but in others the patients rather like
the motion, and claim to feel benefited by it.

[Footnote 71: A fall from a chair, striking on the back of the latter,
while endeavoring to keep a row of books from coming down in one case,
and the shock of the Ashtabula disaster in the other. The latter
patient, the same one who is referred to as describing the
electric-storm sensation in an earlier part of this article, had his
foot amputated in consequence of that disaster; but, like one of the
characters in _Jacob Faithful_, who felt his toes when the weather
changed, though he left both legs at Aboukir, he felt the terrific
pains of the disease in the absent foot as distinctly as in the other.
Dumenil and Petit (_Archives de Névrologie_, ix. Nos. 25 and 26)
relate cases in which a spinal concussion was the only ascertainable
cause.]

A number of toxic agents have been charged with producing tabes: thus,
Bourdon maintains this of absinthe; Oppenheim attributes one case to
poisoning by illuminating gas, the exposure to its influence being
immediately followed by a gastric crisis, and this by a regulation
tabes.[72] It is supposed that most of the poisons acting on the cord
in this or a similar way, such as arsenic, cyanogen,[73] barium, and
chloral,[74] do not produce a spinal lesion directly, but through the
medium of a secondary cachexia. Of no agent is the effect in producing
tabes so well studied as ergot of rye. It had long been known that
ergot-poisoning provoked certain co-ordinating, motor, and sensory
disturbances, but it was left for Tuczek[75] to show that this
vegetable parasite produces a lesion of the spinal cord which in its
character and distribution apes typical posterior sclerosis so closely
as to justify the designation of a tabes ergotica. Possibly, pellagra,
which is sometimes manifested in a similar way,[76] may yet be shown
to have a like influence.

[Footnote 72: _Archiv für Psychiatrie_, xv. p. 861.]

[Footnote 73: Bunge, _Archiv für experimentelle Pathologie_, xii.]

[Footnote 74: _Transactions of the Clinical Society of London_, xiii.
p. 117, 1880.]

[Footnote 75: _Archiv für Psychiatrie_, xiii. p. 148.]

[Footnote 76: Bouchard, “Étude d'Anatomie pathologique sur un Cas de
Péllagrie,” _Gaz. méd. de Paris_, 1864, No. 39.]

Among the occasional and exceptional causes of tabes, Leyden and Jolly
mention the puerperal state; Bouchut, diphtheria; and several
instances are recorded in which psychical shock was responsible for
the outbreak of the disease. In a small number of cases I found that
mental worry and anxiety coincided with the period of presumable
origin of the disease.

Age seems to have no special determining influence. It is true that
most sufferers from this disease are men in the prime of life or in
the period following it. But it is precisely at these periods that the
exposure to the recognized causes of tabes is greatest. It seems as if
there were very little liability to the development of tabes after the
fiftieth and before the twenty-fifth year; still, some cases of
infantile tabes have been recorded.[77]

[Footnote 77: Excluding the so-called family form of locomotor ataxia:
6 rather imperfectly described cases are cited by Remak (_loc. cit._),
and 3 additional ones related by himself. Of the latter, 2 had
hereditary syphilis, and of 1 the father was both syphilitic and
tabic.]

In the majority of cases tabes is due to a combination of a number of
the above-mentioned factors. The majority of tabic patients in the
middle and wealthy classes have had syphilis, and of these, in turn,
the majority have been guilty of sexual excesses or perverted sexual
acts, while excesses in tobacco and of alcohol are often superadded.
Among {857} the poorer patients we find syphilis less frequently a
factor, but still present, according to various estimates, in from 20
to 60 per cent. of the cases. Excesses in tobacco play a lesser, and
excesses in alcohol a larger, part in the supplemental etiology than
in the other class, while exposure to wet and cold and over-exertion
are noted in the majority; indeed, in a fair proportion they are the
only assignable causes.

DIAGNOSIS.—The recognition of advanced tabes dorsalis is one of the
easiest problems of neurological differentiation. The single symptom
which has given one of its names to the disease—locomotor ataxia—is so
manifest in the gait that even the sufferers from the affection learn
to recognize the disease in their fellow-sufferers by the peculiar
walk.[78]

[Footnote 78: At present I have six tabic patients under treatment,
who are acquainted with each other, and who have made each other's
acquaintance in the singular way of addressing one another on the
strength of mutual suffering at Saratoga, at the Hot Springs of
Arkansas, and in New York City.]

Although there are other chronic affections of the cord which manifest
ataxia, such as myelitis predominating in the posterior columns,
disseminated sclerosis in a similar distribution, and some partially
recovered cases of acute myelitis, the gait is not exactly like that
of tabes. The uncertainty may be as great, but the peculiarly stamping
and throwing motions are rarely present in these affections. The
clinical picture presented by the ataxic patient, aside from his gait,
is equally characteristic in advanced cases. Absence of the knee-jerk
and other deep reflexes, the bladder paralysis, sensory disturbance,
delayed pain-conduction, trophic disturbances, and reflex iridoplegia
are found in the same combination in no other chronic disorder of the
cord. It is supposable that an imperfect transverse myelitis in the
lumbar part of the cord might produce the reflex, ataxic, sensory,
sexual, and vesical symptoms of ataxia, but the brachial symptoms
found in typical tabes as well as gastric crises would be absent. The
pupillary symptoms would also fail to be developed, in all
probability. It is to be remembered that only fascicular cord
affections can produce a clinical picture exactly like that of tabes
in more than one important respect. In analyzing the individual
symptoms of the early stage the more important differential features
can be most practically surveyed.

The discovery of no single symptom of tabes dorsalis marks so
important an epoch in its study as Westphal's observation that the
knee-phenomenon is usually destroyed in it. Had this symptom not been
detected, so Tuczek admits, ergotin tabes would have eluded
recognition.[79] It was claimed by a majority of neurologists at first
that this jerk is always abolished in tabes, but it is now recognized
that there are exceptions, as is shown by cases of Hirt,[80] Westphal,
and others, not to mention some well-established cases of its return
during the progress of the disease.

[Footnote 79: It is not to be wondered that, like most new
discoveries, that of the pathological changes of the patellar reflex
should have been made the basis of premature generalizations. The
attempt of Shaw (_Archives of Medicine_) to establish a relation
between disturbances of the speech-faculty and an increased knee-jerk
has not met with any encouragement or confirmation, and has been
rebutted by Bettencourt, Rodrigues (_L'Éncephale_, 1885, 2), and
others.]

[Footnote 80: _Berliner klinische Wochenschrift_, 1886, 10.]

The knee-phenomenon is supposed to be a constant attribute of
physiological man. It is difficult to elicit it in children, and
frequently impossible to obtain it in young infants. It also
disappears in old age, {858} without having any special signification,
except that this occurrence seems to be in direct relation to senile
involution. In 2403 boys between the ages of six and thirteen years,
Pelizæus[81] found it absent in one only. It is customarily elicited
by having the patient while sitting in a chair throw one leg over the
other; hereupon the ligamentum patellæ is struck a short, quick blow.
Under physiological circumstances the leg is jerked outward
involuntarily after an interval of about one-fifth of a second—one
that is scarcely appreciated by the eye. But if it be found absent by
this mode of examination, the case is not to be regarded as one of
absence of the jerk without further ado. The patient is made to sit on
a table, his legs dangling down and his body leaning back, while he
clenches his fists. By this means the jerk will often be produced
where it appears to be impossible to evolve it by the ordinary means.
It is also well to try different parts of the ligament, and when
comparing both sides to strike on the corresponding spot and in the
same direction. Many subjects who appear to be irresponsive will
respond very well when a point on the outer edge near the tibial
insertion is percussed. The elbow reflex, which has the same
signification for the upper extremity that the knee-jerk has for the
lower, is elicited in the same manner.

[Footnote 81: _Archiv für Psychiatrie_, xv. p. 206.]

The absence of the knee-jerk is usually regarded as a suspicious
circumstance in persons of middle life; and where it can be
demonstrated that it has been present years previously and
subsequently disappeared, it is looked upon as of grave import. I,
however, published three years ago an authentic case of disappearance
of the knee-jerk in a physician now in active practice in New York
City who to this day enjoys excellent health and has developed no
other sign of spinal disease. The knee-jerk is also abolished in a
number of conditions not belonging to the domain of strictly spinal
diseases, such as diphtheria, diabetes, secondary syphilis, and severe
cases of intermittent fever. Of these, diabetes alone can be possibly
confounded with tabes dorsalis. The difficulty of differentiating
early tabes and diabetes is enhanced by the fact that on the one hand
there are often ataxic symptoms with diabetes, while on the other both
glycosuria and diabetes insipidus may complicate tabes. Senator,
Frerichs, Rosenstein, Leval-Piquechef, Charcot, Raymond, Demange,
Féré, Bernard, and T. A. McBride all recognize the occasional presence
of the ataxic gait, paræsthesia, belt sensation, and even fulgurating
pains, besides the abolition of the jerk, in diabetes mellitus.[82] In
pure cases of diabetes, however, I am not aware that spinal myosis or
the reflex paralytic pupil has been found.

[Footnote 82: I have now under observation a case of myelitis with
predominating sclerosis of the posterior columns of five years'
standing in a merchant who has been under antidiabetic treatment for
eleven years.]

Abolition of the knee-jerk is found in all organic diseases of the
spinal cord which destroy any part of the neural arch at the upper
lumbar level, where the translation of the reflex occurs, whether it
be in the posterior root-zones or in the gray matter of the origin of
the crural nerves. Thus, acute or chronic myelitis, disseminated
sclerotic foci of this level, may cause obliteration of the reflex at
any time of the disease; so may acute or chronic anterior
poliomyelitis, neoplasms, and amyotrophic lateral sclerosis of the
anterior cornua type if the destruction of the anterior cornua {859}
be complete enough. It is also found abolished with all diseases of
the peripheral nerves—traumatic and neuritic—which produce absolute
motor paralysis of such nerves.

Among the sources of error possibly incurred in examining for this
important symptom the presence of rheumatism is one. There is
sometimes a tetanic rigidity of the joints which prevents the reflex
from becoming manifest. It is also sometimes found to be absent
immediately after severe epileptic attacks, according to Moeli.[83]

[Footnote 83: In three examinations after severe attacks of epilepsy I
found it normal.]

The condition of the pupil is perhaps a more constant sign of early
tabes than the loss of the knee-jerk; at least it has been found well
marked in cases where the jerk had not yet disappeared. It may be
regarded as a rule in neuro-pathology that wherever reflex iridoplegia
is at any time accompanied by other oculo-motor disturbance, it is
either of spinal origin or in exceptional cases due to disease of the
pons varolii. The peculiar character of the pupillary disturbance of
tabes furnishes us with a criterion for distinguishing it from one
affection which in common with it exhibits loss of the
knee-jerk—diphtheria. In diphtheria there is also a reflex disturbance
of the pupil, but it is the reverse of that of early tabes. In the
latter reaction to light is lost, but the accommodative contraction
power is retained; in diphtheria accommodative contraction power is
lost, but reaction to light is retained.

The bladder disturbance has already been described. It is found as a
marked symptom so prominently in no other systemic affection of the
cord, and in few of the non-systemic forms, of sclerosis. In none of
these is it associated with absence of the patellar jerk, reflex
iridoplegia, and fulminating pains, as in tabes, except there be also
some motor paresis. It is the combination of any two of the important
initial symptoms of tabes without paralysis or atrophy that is
regarded as indicative of the disease by most authorities. Thus the
swaying in closing the eyes, if associated with the Argyll-Robertson
pupil, is considered as sufficient to justify the diagnosis of
incipient tabes, even if the knee-jerk be present and fulminating
pains and bladder trouble absent. Undoubtedly, the tabic symptoms must
begin somewhere. But at what point it is justifiable to give a man the
alarming information that he is tabic is a question. I have a number
of neurasthenic subjects now under treatment who have had reflex
iridoplegia for years; in one the knee-jerk is slowly becoming
extinguished; in two it has been becoming more marked after becoming
less; in all the three mentioned there is slight swaying in closing
the eyes and some difficulty in expelling the last drops of urine
while micturating. I do not believe that such a condition justifies a
positive opinion, although the surmise that they are on the road to
developing tabes may turn out correct for all these and for some of
those who have merely reflex iridoplegia.

Incipient tabes cannot be readily confounded with any other chronic
disease of the spinal cord. Some of the cases produced by sudden
refrigeration resemble a beginning myelitis. But the absence of true
paralysis seems to distinguish it from the latter. In all the cases of
so-called acute locomotor ataxia of myelitic origin that I can find a
record of, paralytic symptoms were marked, if not throughout the
disease, at least in the initial period.

{860} Other forms of sclerosis occasionally limited to the posterior
columns imitate the symptoms of tabes. It is unusual, however, for
such sclerosis to be distributed through so great an extent of the
posterior columns as to produce symptoms consistent with tabes in both
the upper and lower extremities. And even where this condition is
complied with, the typical progress so characteristic of tabes is not
adhered to. As previously stated, the progress is weakened by
variations in certain symptoms. Such variations are found in other
forms of sclerosis, but they are not as great, trophic disturbances
not so common, and visceral crises not so violent, as a rule.

The discovery of ataxic phenomena as a symptom of peripheral neuritis
has added another to the long list of pseudo-tabic affections. Indeed,
Dejerine, who greatly advanced our knowledge of this affection,
undertook on the strength of his discovery to place tabes among the
peripheral affections complicated by secondary affection of the cord.
In a large number of cases of peripheral neuritis, particularly the
alcoholic form described by Fischer, the static ataxia, belt
sensation, bladder trouble, and reflex iridoplegia are absent. In
tabes the severe pains, if influenced by deep pressure at all, are
affected favorably, but in peripheral neuritis pressure on the
affected nerve-trunk greatly aggravates the trouble.

In addition, those severe forms of neuritis that lead to ataxia,
abolition of deep and other reflexes, are accompanied by qualitative
electrical changes and atrophic paralysis—features not found in tabes.
Sometimes a disseminated neuritis will become so generalized as to
cause diplopia and other evidences of ocular paralysis through the
affection of the peripheral nerves, but, so far as my observations
extend, not with the characteristic pupillary phenomena of tabes.

Cerebellar disease, alcoholic and hysterical neuroses, sometimes
produce ataxia, and this may be associated with one or more of the
other characteristic symptoms of tabes. Cerebellar ataxia is usually
very different from that of tabes, as far as the locomotor element is
concerned. In tabes it is the movements the patient makes which cause
him to stagger; in cerebellar disease those movements made to prevent
staggering are usually co-ordinated. The gait properly called
cerebellar is therefore very different from that of tabes. There is,
however, static ataxia in both cerebellar and posterior-column
disease. In addition, the knee-jerk may be abolished in the former,
heightening the resemblance: the history of the case is, however,
decisive where these latter symptoms might lead to doubt. Bladder
trouble in cerebellar disease is not an early feature, nor are
paræsthesias and delayed pain-conduction intrinsic features, of
cerebellar disease. Their presence is in favor of tabes.

Alcoholic ataxia is very rapid in its course, while tabic ataxia is
exceedingly slow. In addition, the former is accompanied by atrophic
paralyses as early features; if such occur in tabes, they occur late
in the disease, and are not marked by degenerative electrical
reactions as alcoholic ataxia is. This disorder is usually, too,
accompanied by fever, which is an exceptional, and certainly never an
intrinsic, feature in tabes. Discontinuing the alcoholic poison is
usually followed by rapid amelioration of the ataxia. Hysterical
ataxia exceptionally apes the ataxia of tabes; the presence of other
hysterical phenomena, the rapid and bizarre change of the symptoms,
are distinguishing features. There are cases of hysterical {861}
ataxia accompanied by concentric limitation of the field of
vision.[84] The outline of the limitation is strikingly like that
accompanying atrophy, but repeated examination shows a variation of a
kind not found in the latter. The blind field advances in one
direction to recede in another on one day, and reoccupies the latter
and recedes from the former on the next.

[Footnote 84: Landesberg, _Journal of Nervous and Mental Diseases_,
vol. xiii. 2.]

Ataxia after most acute diseases, such as scarlatina and typhoid, is
not usually accompanied by loss of the knee-jerk, and never by reflex
iridoplegia. The ataxia after diphtheria is complicated by the former,
but, as already stated, the very opposite state of the pupil serves to
distinguish it.

The hereditary form of tabes is frequently confounded to this day with
true tabes dorsalis. The family history and age of the patient are
collateral evidences of the nature of the case. In the hereditary form
the sphincters, optic nerves, and the eye-muscles are not affected; in
the acquired form the first and last are always involved; and this
involvement occurs so early in the disease as to constitute a valuable
discriminating feature. Although the locomotor ataxia is very similar
in the two affections, static ataxia, the symptom manifested on
closing the eyes, is not found in the hereditary form, while it is
found more constantly than even the locomotor ataxia in the acquired
form.

The electrical reactions in tabes are either normal or quantitatively
slightly increased. This serves to distinguish it from all spinal
affections accompanied by marked paralysis. In the later stages, when
some atrophy results, there may be a quantitative decrease, but these
are without qualitative changes. A change may occur in those
exceptional cases where the anterior gray horns become involved, but
we then have to deal with a true complication; and complications can
be recognized only in their development and by the application of the
diagnostic criteria characterizing the complicating disorder when of
an independent occurrence.[85]

[Footnote 85: It is not impossible that many of the symptoms described
as occurring in advanced tabes are due to independent focal disease.
In the case of a female aged seventy years mentioned by Hirt
(_Berliner klinische Wochenschrift_, 1885, No. 26), who developed
hemiatrophy of the tongue, probably from a hemorrhage in the brain
isthmus, there was no tabes, although this symptom when found with
tabes is supposed to be part of the tabic symptom-group.]

The TREATMENT of tabes dorsalis will be considered at the end of this
article, together with that of the sclerotic processes generally. The
duration and prospects of the disorder have been considered with the
clinical history. In the vast majority of cases the course of the
illness is progressive. A few cases have been reported, but in the
only instance where an autopsy was made to test the matter it was
found that the sclerosis had not been removed. It may be therefore
stated that an arrest of the disease is possible, but that restitution
of the nerve-elements, once destroyed, is impossible.


Spastic Spinal Paralysis.

SYNONYMS.—Primary lateral sclerosis. Tetanoid pseudo-paraplegia,
(Seguin), Tabes dorsal spasmodique. This symptom-group was first {862}
recognized by the American neurologist Seguin[86] thirteen years ago;
two years later Erb[87] described it under the title at the head of
this section, and about the same time Charcot[88] attributed the
well-marked clinical signs thus discovered on both sides of the
Atlantic to a primary sclerosis of the lateral columns of the cord in
that portion which is known as the crossed-pyramid tract, and whose
isolated disease had been known to Türck,[89] but not clearly brought
into relation with what is now regarded as one of the most remarkable
and recognizable of spinal symptom-groups. Our earlier knowledge of
the disease has been much confused through the discovery by
Charcot[90] of the same lesion to which spastic paralysis is
attributed by him, in a female who had been suffering from permanent
contractures of all extremities, and which he persisted in regarding
as hysterical. The only solution of the difficulty is to accept one of
two alternatives—either believing that the sclerosis was in this case
primary, in which case contracture cannot be regarded as hysterical,
or that it was secondary to protracted disuse of the limbs, in which
case it proves nothing. An additional source of confusion has been the
discovery of an analogous affection, now regarded as clinically and
pathologically distinct, known as amyotrophic lateral sclerosis, and
of a corresponding affection of the lateral columns in a large number
of cases of paretic dementia.

[Footnote 86: E. C. Seguin, “Description of a Peculiar Paraplegiform
Affection (tetanoid pseudo-paraplegia),” _Archives of Scientific and
Practical Medicine_, February, 1873. Erb's statement (_Ziemssen's
Cyclopædia_, vol. xi. 2, p. 628) that Seguin's description includes
symptoms which do not properly appertain here can no longer be
sustained, in view of the similar and identical symptoms which have
been since attributed to the same affection and to amyotrophic lateral
sclerosis by later writers. There seems to be no question that the
priority of recognition of the clinical form belongs to this side of
the Atlantic.

That Seguin's title was not as badly chosen as Erb implies in his
first reference to it may be inferred from the fact that Strümpell,
without any reference to Seguin, and evidently independently of him,
uses the following language ten years later: “As also in these cases,
the movements are not immaterially influenced by the ever-occurring
spasms, a motor disturbance may be simulated which we feel inclined to
term spastic pseudo-paralysis, or, more correctly, pseudo-paresis”
(_Pathologie und Therapie_).]

[Footnote 87: “Ueber einem wenig bekannten spinalen Symptomencomplex,”
_Berliner klinische Wochenschrift_, 1875, No. 26.]

[Footnote 88: “Sclérose primitive de la partie postérieure des cordons
antero-lateraux,” _Gazette médicale de Paris_, 1874, pp. 38, 39.]

[Footnote 89: “Ueber primäre degeneration einzelner
Rückenmarkstränge,” _Sitzungsberichte der Kaiserlichen Akademie der
Wissenschaften zu Wien, Mathematisch-Naturwissenschäftliche Klasse_,
Band xxi. Jahrgang 1856, p. 112.]

[Footnote 90: _Gazette hébdomadaire_, 1865, 7.]

CLINICAL HISTORY.—Spastic paralysis manifests itself chiefly in three
symptoms: first and most noticeable, a condition of rigidity of the
limbs; second, an increase of all the muscular reflexes; and third, a
true motor paresis. It manifests itself in the adolescent or middle
period of life, usually without any noticeable cause, beginning in the
lower extremities, and, if progressive, involving the muscles of the
trunk and arms. The invasion of the disease is first marked by an
increase in the excursiveness of the muscular phenomena, such as the
knee-jerk and the ankle-clonus. But while this reflex irritability is
originally only manifested when the diagnostician applies his special
tests, it soon becomes so great that the most trivial influence
suffices to bring about exaggerated muscular reaction. The mere
tension of a tendon in walking, the weight of the limb, the slightest
change in position, suffice to produce reflex muscular tension. The
muscles feel firm and stiff to the touch, as if permanently
contracted, {863} and the lower limbs, as a result of the combined
contraction of special muscular groups, assume a characteristic
position—namely, an extension contracture of the leg on the thigh and
a flexion of the foot on the leg. In advanced cases the contracture is
so extreme that it is almost or actually impossible to flex the leg
and to extend (dorsiflect) the feet. This is particularly noticeable
when it is attempted to overcome the strained position suddenly, while
gradual traction will often succeed in relaxing the contracture. The
latter procedure succeeds because sudden traction of the tendons and
the reflex contraction thereby provoked are avoided by it. Gowers
compares this symptom to the mechanism of a clasp-knife. When the leg
is slowly extended it yields to the manipulator's influence, but as
soon as it reaches full extension it remains like the blade of the
knife fixed by a spring.

Although some degree of muscular weakness is experienced in the
beginning of the affection—often more marked in one leg than the
other—it is insufficient to account for the grave and characteristic
disturbance of locomotion. This is due rather to the stiffness of the
limb resulting from the morbid muscular spasm. As the limbs are rigid,
the steps are short; the leg not being flexed, and consequently not
being lifted from the ground, the gait consists in an awkward
shuffle.[91] The feet are in continuous contact with the ground, and
it is observed that there is a tendency to walk on tiptoe, owing to
the contracture of the gastrocnemius, in this respect resembling the
pes-equinus position. In some cases it has been observed that the
reflex excitability was so great that the mere need of urinating
brought on a sudden tonic spasm, and there have been noted others in
which the very first spasmodic phenomena occurring in the history of
the case appeared while the patient emptied his bladder.[92]

[Footnote 91: It was Theodore Simon, I believe, who first suggested
the registration of peculiarities in gait by using sand on the floor
or compelling the patient to walk over large sheets of paper with
black-leaded shoes. Among the varieties of gait noted in paretic
dementia by him he accurately describes that of spastic paralysis
(_Die Gehirnerweichung der Irren_, Hamburg, 1871).]

[Footnote 92: Westphal, _Archiv für Psychiatrie_, xv. p. 224; _ibid._,
p. 229.]

When the upper extremities are involved, the same initial muscular
weakness and exaggerated reflex excitability are noted, but the
contracture at the elbow, unlike that at the knee, is usually in the
flexed position.

If from any cause the spastic phenomena happen to be in the background
temporarily, so as to admit testing the voluntary muscular power, it
is always found to be grossly impaired.[93]

[Footnote 93: This statement is made by Westphal, but as he considers
the only pure cases of pure primary lateral sclerosis to be those
associated with paretic dementia, and it is in the latter form alone
that there are marked exacerbations and remissions in the spastic
symptoms, it probably does not apply to uncomplicated spastic
paralysis.]

As the disease progresses locomotion becomes impossible; the advancing
rigidity of the trunk-muscles renders sitting impossible, and the
patients become bedridden. But even in this advanced stage no sensory
or vegetative disturbances were noted. The cutaneous reflexes
sometimes appear exaggerated, but this is not an evidence of sensory
hyperexcitability, but of the increased ease with which the motor
response is elicited—a feature which is also illustrated by the spasm
resulting from fulness of the bladder or even from the mere act of
micturition. Ataxia has never been noted in pure cases, and the
uncertainty in gait sometimes {864} noted at the onset of the disease
is secondary to the motor weakness and the interference with free
mobility by the, as it were, frozen state of the muscles. Occasionally
the paresis becomes a veritable paralysis, but this occurrence is
limited to one or several muscular groups. Cases are related in which
the spastic symptoms occurred on one side, involving one arm and leg
for years before involving the other. It is not improbable that these
were cases of some obscure cerebral affection. Other exceptional cases
in which the spastic phenomena appeared first in the arms are better
authenticated.

The early occurrence of ankle-clonus in this disease heralds the
appearance of apparently spontaneous clonus when the toes are put on
the ground, and later on of cramps of the gastrocnemius or other
muscles, which produce an exacerbation of the existing stiffness.
Occasionally sudden spasms occur while the patient is at rest, and
which resemble the sudden shocks which healthy persons occasionally
experience when about to fall asleep.

The electrical reactions show little that can be called
characteristic, and there is little unanimity among observers on this
point. The majority agree that there is a slight quantitative decrease
of both faradic and galvanic excitability in parallelism with the
degree of paresis. In the pure form of the disease there are no other
symptoms than those mentioned. Should evidences of involvement of the
gray substance of the cord or the cranial nerves be added, it is a
certain indication that we have to do with the similar but far from
identical affection, amyotrophic lateral sclerosis.

The course of the disease is extremely slow and its development
insidious. It is considered incurable, and although a few cases have
been described as terminating in recovery, the most recent and
reliable annals fail to make mention of any cure in a well-established
case of spastic paralysis. The disease is not in itself fatal, death
usually occurring from intercurrent affections.

ETIOLOGY.—Our knowledge of the causes of this disease is practically
nil. It has been, like tabes dorsalis, attributed to a family
tendency. Excessive sexual indulgence, over-exertion, and syphilis
have been recorded as possible causes in the few cases in which an
etiological assignment could be attempted. Tuczek surmises that the
spastic phenomena of lathyrism, a constitutional disease analogous to
pellagra and ergotism which is observed in those who live on bread
prepared from a legumen grown in Italy (lathyrus bean), and which
manifests itself in spastic symptoms, may be due to an affection of
the pyramid tract, just as tabes ergotica is due to an affection of
the posterior columns. One case of spastic paralysis of a severe
nature, associated with scanning speech, in consequence of a
lightning-stroke, is reported by Demme.[94] I have been able to assign
a cause in but two cases of spastic paralysis. Both were in Quakers;
in both there had been a history of almost incredible sexual excesses.
The disease in both involved the muscles of the jaw and face. An
autopsy in the one case revealed no lesion whatever.[95]

[Footnote 94: “Bericht über die Thätigkeit des Jennerischen
Kinderspitals,” _Wiener medizinischer Blätter_, 1884, No. 23.]

[Footnote 95: The contracture in the lower extremities, differing from
the rule, was a flexion contracture.]

{865} MORBID ANATOMY AND PHYSIOLOGY.—Although Charcot's announcement
that spastic paralysis is due to sclerosis of the crossed-pyramid
tract was made with great positiveness, the more careful authorities
have not committed themselves to his view without reservation. Their
reserved position is the result of some observations which certainly
show that there is no constancy between the distribution of the lesion
and the distribution of the spastic paralysis;[96] while, on the other
hand, characteristic spastic symptoms have been noted with purely
cerebral lesions.[97] Morgan and Dreschfeld[98] publish cases in which
the lesion was stated to be characteristic, but as the cell-groups in
the anterior horn were found by them to have been more or less
affected, it is evident they had cases of amyotrophic lateral
sclerosis to deal with. In view of similar revelations in a large
number of the cases that had been considered as spastic paralyses
during life, and in which similar findings were found after death,
Westphal,[99] one of the most critical students of the subject,
concludes that thus far an anatomical basis has not been demonstrated
with any constancy for the cases of spastic paralysis uncomplicated
with paretic dementia. With this disease a sclerosis of the lateral
column, apparently independent of the cerebral affection, is often
found. It has no continuity, as a rule, with the cerebral lesion, and
it may be limited to special districts of the cord. It is not usually
intense enough to produce material destruction of the tract itself,
and for this reason, probably, we do not find any other symptoms than
a paretic weakness and an increase of the patellar and other muscular
phenomena developed in the majority of paretics. In some, however, the
characteristic spastic gait and muscular rigidity do develop. Westphal
conjectures that if paretic dements lived as long as the sufferers
from uncomplicated spastic paralysis, they would ultimately show the
typical symptoms.[100] Numerous observations, however, show that the
presence and intensity of the spastic symptoms in paretic dementia are
not related to the presence and intensity of lateral-column lesion.
Thus, Zacher[101] failed to find such lesion in a case where the
spastic symptoms had been well marked. It must be remembered, in
drawing conclusions regarding the pathogeny of simple spastic
paralysis from the lateral-cord affection and associated symptoms of
paretic dementia, that the possibility of the lesion of the pyramid
tract in this affection being secondary to disuse[102] cannot be
excluded. On the other hand, the symptoms of most paretic dements
presenting lateral-column {866} lesion differ in some respects from
those of a pure spastic paralytic. There is a precedent clumsiness and
helplessness of movement; the patient stumbles and trips more than is
the case with the pure spastic gait; he wavers after suddenly turning
around, and there is considerable tremor with intended movement. There
is also more exacerbation and remission of these symptoms than is the
case with true spastic paralysis, and it is observed that the
exacerbations usually follow apoplectiform and epileptiform attacks,
thus showing that the cerebral condition, after all, may be the
determining factor.

[Footnote 96: Fischer and Schultze (_Archiv für Psychiatrie_, xi. 3)
report an impure case in which, with exquisite spastic symptoms in the
neck and arms, the degeneration of the pyramid tract was limited to
the dorsal part of the cord.]

[Footnote 97: Schulz (_Deutsches Archiv für klinische Medizin_, Band
xxiii.) and Strümpell (_Archiv für Psychiatrie_, x.).]

[Footnote 98: _Journal of Anatomy and Physiology_, xv. p. 510.]

[Footnote 99: _Archiv für Psychiatrie_, xv. p. 246.]

[Footnote 100: Another feature which antagonizes the development of
spastic phenomena in paretic dementia is the lesion of the posterior
columns which often ensues. In proportion as this is developed it
neutralizes the exaggerated knee-jerk, stiffness, and spastic gait.]

[Footnote 101: _Archiv für Psychiatrie_, xiii. p. 155.]

[Footnote 102: It has been claimed against this view that if this were
so the degeneration of the pyramid tract should be accompanied by
degeneration of the cells in the anterior horn. This claim assumes
that the cells and the pyramid tract are directly continuous, but the
most modern researches, those of Von Monakow, confirming an older
observation of Homén's, show that a system of small cells in the
lateral reticular processes is interpolated; which I can confirm. It
is certainly compatible with an atrophy from disuse of the voluntary
tract that the cells themselves, presiding over reflex and nutritive
functions not necessarily disturbed in paretic dementia, should remain
nearly intact.]

There is another respect in which the two conditions differ. Spastic
paralysis is usually an ascending affection, the lower extremities
being involved first, the trunk next, and the upper extremities last.
But in paretic dementia the spastic phenomena develop in both upper
and lower extremities simultaneously, and there are universal tremors,
probably of irritative origin. The lower extremities are not commonly
in the extension contracture of spastic paralysis, but in the same
flexed position as the arms, the adductors usually preceding the
flexors in becoming rigid. If it be added to this that the
lateral-column lesion in paretic dementia appears to answer all the
requirements which could be made of the lesion on theoretical grounds
were the case one of pure spastic paralysis—that is, that its area
decreases upward—the inconsistency of the observed anatomical and
clinical facts becomes strongly evident. Thus far, the attributing of
spastic paralysis to a primary lesion of the pyramid tract rests in a
few contested cases, on a number of doubtful analogies, and on the
undoubted fact that sclerosis of this tract in the event of a myelitis
is followed by pronounced spastic symptoms in all those muscles which
derive their voluntary innervation from the part of the tract which
lies below the level of the lesion.

The situation of this tract, which was not discovered by Türck and
Flechsig, as is usually supposed, but accurately known to Burdach[103]
in 1819, may be roughly stated as follows: It lies in the dorsal half
of the lateral column, making up the bulk and core of this part of the
column. It is separated from the pia mater by the direct cerebellar
tract, and from the posterior gray horn by a narrow zone of fibres
differentiated by Lissauer (see Tabes). It is connected with the
lateral reticular processes, and in its cephalo-caudal course becomes
gradually attenuated, giving off its fibres to these processes, thus
to be exhausted in the lower part of the lumbar enlargement of the
cord, where it approaches, if it does not actually reach, the surface.
The fibres controlling the voluntary motions of the lower limbs, and
which have a longer course to run before they reach the brain than
those which mediate the voluntary control of the arms, are situated
nearest the lateral boundary of the cord. Where the spastic phenomena
are mainly marked in the lower limbs the sclerotic process has been
found most marked in the corresponding area.

[Footnote 103: _Vom Bau und Leben des Gehirns_. This gifted author
says that the crossed-pyramid tract lies in the lateral column of the
cord, behind a line corresponding to the attachment of the ligamenta
denticulata and removed from the surface.]

The progress of this affection has not been materially modified in any
case by treatment. The same measures employed in sclerotic processes
generally, particularly galvanism and warm baths, are recommended. It
{867} is difficult to understand what good effect ergotin, which is
mentioned by a number of the German writers, can have in a disease of
this nature.


Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis, so named by Charcot[104] and Joffroy,
who first described it, consists in a disease affecting both the
conducting tracts and nuclear centres of the motor system of the
spinal cord and medulla oblongata, manifesting itself in a combination
of atrophic and irritative phenomena on the part of the muscles. The
relations between the symptoms and lesions of this disease rival in
constancy and preciseness those noted in typical tabes dorsalis. As
the variations in the mode of invasion and distribution of the lesion
account for the widely-differing clinical types of the disease, and
the advanced state of our anatomical and physiological knowledge of
the cord enables us to interpret the reason of this difference, we
shall invert the usual order and discuss the morbid anatomy first.

[Footnote 104: In 1869 and 1874 (_Leçons sur les Maladies de la
Système nerveux_) Charcot termed this, and one other form of disease
associated with muscular atrophy, amyotrophic, to distinguish them
from the myopathic forms. He considers amyotrophic lateral sclerosis
as deuteropathic, the nuclear atrophy being secondary to the lesion of
the white substance, and the progressive muscular atrophy of the type
described by Duchenne and Aran as a protopathic form of the
amyotrophies. Among the true myopathies he enumerates
pseudo-hypertrophic paralysis, Erb's juvenile form, Duchenne's
infantile form, certain mixed forms, and, without justification,
Leyden's hereditary forms (report by Marie et Guivron, _Progrès
médicale_, 1885, No. 10).]

MORBID ANATOMY.—In advanced cases of amyotrophic lateral sclerosis
there is found marked sclerotic degeneration of both the crossed and
the uncrossed pyramid tracts; atrophy of the cells of the anterior
horns; atrophy of some of the nuclei of the motor and mixed cranial
nerve, particularly the hypoglossal and spinal accessory; atrophy of
the anterior roots of the spinal and the roots of certain motor
cranial nerves; and, finally, atrophy of the voluntary muscles. The
greater part of the tract through which the voluntary impulse travels
after leaving the voluntary motor-fields of the cortex is therefore
continuously involved; and it would seem that there are cases
(Kahler-Pick's) where the entire motor system is affected, the morbid
process demarcating the course taken by the motor impulse through the
cerebro-spinal fibre-labyrinth from the cortical motor-field down to
the muscles.

The morbid process in the muscles consists of a narrowing of the
fibres, which subsequently lose their transverse striation and undergo
a granular disintegration. Sometimes a muscle disappears entirely;
usually the connective-tissue elements, including the interstitial
cellular and adipose tissue, undergo proliferation, so as to mask the
wasting of the muscles to some extent.

The morbid process in the nervous system is also a simple degenerative
process. The nerve-fibres and cells atrophy first, and the
connective-tissue proliferation which marks the sclerotic change of
the diseased area is a secondary process. There is still considerable
dispute among authorities as to which segment of the motor-conduits
the degeneration begins in. But from the great difference found in the
individual cases which {868} have become the subject of
patho-anatomical studies there can be little doubt that there is no
uniformity in this respect. In some cases the lesion is far advanced
in the lateral columns, while the anterior horn is but slightly
involved; in others the reverse is found. Sometimes the nuclei of the
motor cranial nerves are the chief foci of disease; at others they are
the least affected parts of the motor apparatus. As we shall see,
there are differences in the clinical picture corresponding to the
variations of the anatomical findings.

CLINICAL HISTORY.—In typical cases the first symptom is a tired
feeling in one arm or leg, usually the former; in dextral persons the
right arm, the one which is subject to the severest strain, is most
frequently the first to be affected. With the increase in this tired
feeling there develops actual loss of power; the muscles become
wasted, and the other arm becomes involved. Often it is observed that
the right leg suffers with the corresponding arm, but as a rule the
lower extremities do not become involved to any marked degree within
the first six months of the illness. It is then noted that a gait not
unlike that of spastic paralysis is noted, but with more loss of motor
power and less stiffness. There is, however, this noteworthy
difference between the affection of the lower and that of the upper
extremities: that atrophy and loss of power are more marked in the
latter, and spastic phenomena in the former. The knee-jerk and other
deep reflexes are greatly increased, and ankle-clonus is usually very
well marked. As with spastic paralysis, there are no visceral or
sensory disturbances. Unlike that affection, there are qualitative
changes in the electrical reaction of the muscles[105] in amyotrophic
lateral sclerosis. The degeneration reaction is found in the atrophied
divisions, and particularly in such groups as those of the thenar and
hypothenar eminence, which undergo complete atrophy at a comparatively
early period of the disease.

[Footnote 105: Moeli, Strümpell, Pick, and Mierzejewski describe cases
in which only quantitative changes were found. They were such in which
spastic phenomena preponderated at the time of the examination.]

Soon after the spastic and atrophic involvements of the lower
extremities, symptoms indicating the involvement of the cranial
nerve-nuclei are developed, usually after the disease has lasted a
year or so. Deglutition becomes difficult and speech indistinct, the
general picture of a glosso-labio-laryngeal paralysis being imitated.
The patient cannot pucker his lips, his lingual muscles undergo
atrophy, and fibrillary and fascicular twitches are noted in the
tongue and lips. But just as the atrophic affection of the muscles of
the arms and legs differs from that of progressive muscular atrophy in
the fact that the deep reflexes are exaggerated with amyotrophic
sclerosis, so in the bulbar symptoms of the latter it is found, unlike
the typical form of bulbar paralysis, that the jaw reflex is
increased.

The duration of the disease may be stated at about three years, death
usually occurring in consequence of the involvement of the cranial
nerves. There are cases recorded where the disease was almost
simultaneously developed in all four extremities and the tongue,
reaching a high degree within a year (Mierzejewski). It is generally
agreed that the reason contractures do not develop in typical cases of
this kind, although the lateral column is sclerosed and spastic
phenomena occur early in the disease, is the destruction of the
cell-groups in the anterior horn. The reflex arch {869} through which
a reflex contracture would be mediated is broken, or rather weakened,
in that part of its course which passes through these cells, and
therefore a contracture is as efficiently antagonized as it would be
if the posterior roots were divided. Still, in some cases a frozen
attitude of the lower extremities is very well marked (Vierordt,
Zacher). To reconcile these conflicting observations it has been
suggested that it may be regarded as a question of speed between the
progress of the pyramid-tract and the anterior-horn lesions. If the
former be much in advance of the latter, spastic phenomena will
preponderate and contractures be possible, to disappear with the
subsequent anterior-horn lesion. But if the latter precede and
preponderate, the spastic phenomena will be in the background and
contractures impossible. Indeed, Zacher[106] suggests that there may
be an ascending form in which the lesion of the pyramid tract is
secondary to the nuclear atrophy, corresponding to the typical class
of cases on which Charcot based his first description of the disease,
and a descending form in which the pyramid tract is first affected and
the nuclear cell-groups follow. Vierordt[107] and Kahler[108] express
similar opinions. The latter goes so far as to suggest that
progressive muscular atrophy, progressive glosso-labio-laryngeal
paralysis, and amyotrophic lateral sclerosis are really due to one and
the same kind of degenerative process, merely differing in location.
There is certainly, as he claims, a remarkably complete chain of
cases, beginning with such (1) in which spastic paralysis
preponderates, passing thence to (2) those in which some muscular
atrophy preponderates, then (3) those in which muscular atrophy is in
the foreground and the spastic phenomena are slight, and ending with
(4) the pure atrophies. A similar transition may be established on the
regional principle between pure glosso-labio-laryngeal paralysis and
amyotrophic lateral sclerosis, for there are cases of this affection
in which the oblongata symptoms preponderate throughout, and the focus
of the disease is formed there, just enough lesion being demonstrable
in the pyramid tract and the spinal gray matter to prove the family
relationship of what clinically appears as a spastic bulbar
paralysis.[109]

[Footnote 106: _Archiv für Psychiatrie_, xv. p. 416.]

[Footnote 107: _Ibid._, xiv. p. 397.]

[Footnote 108: _Zeitschrift für Heilkunde_, 1884, p. 109.]

[Footnote 109: Such a case is described by Freund in _Deutsches Archiv
für klinische Medizin_, xxxvii. p. 405.]

PROGNOSIS.—As far as the typical cases of this disease have been
studied, a fatal termination seems to be invariable. Seeligmüller
reports a few cases in which the progress appeared to become arrested,
but it is not clear that these were not in reality cases of some
juvenile form of muscular atrophy. Not only is the affection in adults
fatal, but it is so in a short period of time as compared with other
spinal disorders, and particularly with the related disorder spastic
paralysis. Few patients survive the third year of their illness; a
number do not live to that length.


The Combined Forms of Sclerosis.

A number of cases of chronic sclerotic disease of the cord have been
discovered and analyzed during the past decade, which, while they show
the regularity of distribution noted in posterior and lateral
scleroses, {870} differ from them in involving at once more than one
column of the spinal cord. Usually, it is the posterior column and the
posterior part of the lateral column which are affected. The symptoms
constitute a combination of those of tabes dorsalis and of spastic
paralysis. But this combination does not represent a mere addition of
symptoms; where the tendency of the two diseases conflicts, they
neutralize each other. Thus the tendency of lateral sclerosis
uncomplicated by posterior sclerosis is to increase the patellar jerk;
when posterior sclerosis complicates it, the jerk is annihilated. The
degeneration of the lateral column and the ensuing motor paresis in
like manner neutralize the ataxic character of the gait by limiting
its excursiveness.

The upper extremities are usually involved equally with the lower. In
the cases of Kahler-Pick considerable atrophy of the muscles
developed; in those of Prévost and Westphal this was not very
noticeable. In a few cases, where the posterior sclerosis did not
involve the lumbar part of the cord, spastic symptoms were noted in
the lower extremity. In the only case of combined sclerosis now under
my observation this peculiarity, noticed by Prévost, is well marked.
In one of Westphal's cases there was evident mimic ataxia. The few
cases of this affection observed show so many variations that it would
be at present premature to attempt sketching a common clinical type.
The majority of the subjects were affected between the twenty-fifth
and forty-fifth years.

ETIOLOGY.—Little is known of the causes of this disease. Usually
beginning insidiously, no special mode of origin can be determined.
Surface chilling has been assigned in a case by Erlitzky and Rybalkin,
and others are reported to have begun during pregnancy. One of
Westphal's cases developed in a lithographer who had been subject to
epileptoid fits.

DIAGNOSIS.—As yet we have no reliable criteria for distinguishing
between a combined sclerosis and certain forms of diffused sclerosis
during life. Ballet and Minor[110] found such a sclerosis diffusely
involving the posterior and lateral columns of the cord in a case
where they were justified from the symptoms in expecting a combined
fascicular sclerosis of these columns, and after a careful study of
all similar cases collated by them in consequence of this experience,
they came to the conclusion that a number of affections of different
origin, but eventually involving both columns, may impose on the
observer as combined fascicular sclerosis during life. Diffuse
meningo-myelitis is one of these affections, and is far from uncommon,
while true system or combined sclerosis is apparently a very rare
disease.

[Footnote 110: _Archives de Névrologie_, vii. p. 44.]


The Family Form of Tabes Dorsalis.

SYNONYMS.—Friedreich's disease, the Family form of locomotor ataxia,
Hereditary ataxia, Hereditary tabes.

Friedreich discovered a peculiar form of co-ordinating disturbance in
a number of children of the same family, which he brought into
relation with a lesion of the posterior columns, and which has been
since found by him and by subsequent observers to occur in other
cases, always {871} affecting several members of the same family, as
in the first case observed by him. The clinical and pathological
features, though resembling those of the tabes dorsalis of adults in
many respects, are distinct in others, and for this reason it is
generally assigned a separate place in classification.

ETIOLOGY.—The disorder is usually manifested in juvenile life, the age
of the affected subjects varying from the seventh to the twenty-fifth
year. The male sex preponderates in the statistics of the affection.
Some neuropathic vice can always be found in the patient's immediate
ancestry, and the limitation of the disease to families burdened by
such a diathesis is exemplified in the fact that the ninety individual
cases thus far accurately studied occurred in thirty-six
families.[111] The disease type of the ancestors of the patients is
usually different from that of the latter. Alcoholism in the father is
one of the commonest forms, but convulsions, hysteria, and insanity
are also frequent features of the family history. In a few cases tabes
dorsalis, properly so called, was present in the father. In others
there was consanguinity of the father and mother. In Musso's group the
parents had been brother and sister, and their mother had been a
melancholic dement. Three other grandchildren and six grandchildren by
the incestuous marriage developed the family form of tabes. In this
family the frequent experience of hereditary transmission was
verified—that the neurotic taint skipped the intermediate generations.

[Footnote 111: Raffaele Vizzioli, _Giornale di Neuropatologia_, 1885.]

CLINICAL HISTORY.—Usually the first symptom is ataxia of the lower
extremities; occasionally this is preceded by severe frontal headache
or by vague rheumatoid pains. The inco-ordination is very similar to
that of true tabes dorsalis, but swaying on closing the eyes is not
noticed early in the disease, as in the latter affection. The arms
soon become involved in the ataxia, but cutaneous sensibility and the
muscular sense remain either intact or nearly so—a fact utilized with
some success by Erb in polemicizing against the theory of Leyden that
the ataxia of tabes is due to imperfect sensation. Later in the
disease, usually after a few years, a peculiar speech-disturbance is
noticed, which resembles the scanning of disseminated sclerosis. It
depends on ataxia of the tongue and lips. This is usually associated
with nystagmus. About this time the patient develops a different set
of motor symptoms from those characterizing the onset of the disease;
contractures, paralysis, and atrophy are found in the affected
extremities; sometimes the patients cannot ascend a stair, owing to
their inability to lift the feet high enough. Pes equino-varus,
deformity of other joints and of the vertebral column, have been
observed[112] to result from the associated effects of paralysis and
contracture. At this stage some sensory disturbance may be developed,
formication having been observed toward the close of the history in a
number of cases. But the distribution of this disturbance is usually
different from that of tabes dorsalis, being more intense in the trunk
than in the extremities or evenly marked in the entire periphery.

[Footnote 112: H. E. Smith, _Boston Medical and Surgical Journal_,
1885, vol. cxiii. p. 361.]

COURSE AND PROGNOSIS.—The progress of this disease is slow. It has not
yet been known to be arrested by any therapeutical procedure. Death
rarely occurs directly from the disease by exhaustion; more commonly
life is cut short by some intercurrent affection. Unless this occurs
{872} the patients may survive the commencement of the illness from
eight to forty and more years.

MORBID ANATOMY.—The sclerosis which is found to be the constant lesion
underlying this disease corresponds in every character to a combined
sclerosis of the pyramid tracts and the posterior columns. Usually,
the crossed-pyramid tract is degenerated in its spinal course, and the
uncrossed in the cervical and dorsal part, which, in many subjects at
least, is its whole extent. The cerebral part of the pyramid tract is
not affected. The nerve-fibres found normally in the gray substance
are materially reduced, probably in dependence upon the atrophy of the
great nerve-tracts.

The lesion of the posterior columns resembles that of true tabes very
closely, particularly in the lumbar part of the cord. It is, however,
not probable that it commences in precisely the same distribution, and
if cases dying early in the disease be autopsied it will be
interesting to see whether the initial sclerosis occupies identical
fields—a contingency which is unlikely, owing to the profound
difference in the initial symptoms of true tabes and the family form.
It is claimed by Schultze that in addition to the pyramid and
posterior tracts the cerebellar tract—or, rather, a large part of the
periphery of the lateral column—may be sclerosed in this disease. In
this way, since the direct pyramid tract in the anterior, the greater
part of the border of the lateral, and the entire posterior column are
degenerated, the sclerosis resembles a marginal ring[113] in shape.

[Footnote 113: _Archiv für Psychiatrie_, xiv. p. 384.]

Anatomically, the sclerosis of the family form of tabes resembles that
form of combined sclerosis in which the lateral and posterior columns
are together affected. It is probably due to a defective development
of these tracts, rendering them liable to premature decrepitude or
increasing their vulnerability. The latter alternative is exemplified
in those cases where some acute disease of childhood, such as
scarlatina or measles, acted as an exciting cause.

DIAGNOSIS.—There are two affections some of whose leading symptoms are
so closely imitated by those of this disease that they may be
confounded with it on first sight. These are tabes dorsalis—of which
the family form is still regarded a variety, as the name indicates—and
disseminated sclerosis. In the gait the former, in the nystagmus and
scanning speech the latter, disorder is approximated. The distinction
from true tabes has already been dilated on. (See Tabes.) The fact
that relatives—usually the sisters and brothers—of the patient are
affected in the same way in their youth speaks in favor of the family
form. The deep reflexes are not abolished early, as in tabes, nor are
anæsthesias or paræsthesias early symptoms, as in the latter. The
speech-disturbance and nystagmus, which in most cases develop later in
the family form, serve to distinguish it from true tabes in the
advanced stage. It is at this period that the disease may resemble a
disseminated sclerosis. The hereditary or family character does not
aid us in making a discrimination here, as there is also a family form
of the latter disease. But the absence of intention tremor, which we
would assume to be present in a case of disseminated sclerosis of the
cerebral type, and of optic-nerve atrophy serves to distinguish the
two. Musso claims that the speech-disturbance is also different in
character. There certainly is more lingual ataxia in the {873} family
form of tabes, and less of typical scanning, but I am doubtful about
our ability to differentiate these characters in all cases. The
following table includes the main points of difference, clinically
considered, between the acquired and the family form of tabes:

                       |    Tabes Dorsalis.    |   The Family Form.
  ---------------------+-----------------------+---------------------
  Prodromata.          | Marked and constant.  | Absent or slight.
                       |                       |
  Static ataxia        | Early and constant.   | Absent.
    (Romberg symptom). |                       |
                       |                       |
  Involvement of upper | Usually late.         | Early.
    extremities.       |                       |
                       |                       |
  Ataxia of tongue,    | Absent or             | Always developed.
    eyes, and          |   unnoticeable.       |
    trunk-muscles.     |                       |
                       |                       |
  Paresis.             | Rare.                 | Characteristic.
                       |                       |
  Anæsthesia.          | Present in some form. | Absent or slight.
                       |                       |
  Paræsthesia.         | Constant.             | Rare.
                       |                       |
  Sexual desire.       | Becomes extinguished. | Remains unaffected.
                       |                       |
  Deep reflexes.       | Abolition usually     | Abolition in course
                       |   initial.            |   of disease.[114]
                       |                       |
  Sphincters.          | Involvement is        | Involvement late, if
                       |   characteristic and  |   at all.
                       |   early.              |
  ---------------------+-----------------------+---------------------

[Footnote 114: There are conflicting observations on this point.]


Disseminated Sclerosis.

SYNONYMS.—Multiple cerebro-spinal sclerosis (also spinal and cerebral
form), Insular cerebro-spinal sclerosis, Focal sclerosis, Multilocular
sclerosis; Herd-sklerose (Ger.); Sclerose en plaques disseminées,
Sclerose en plaques generalisées (French).

The occurrence of disseminated patches of gray degeneration in the
nervous axis was observed by Cruveilhier and Türck, but they regarded
the affection rather from the anatomical than the clinical standpoint,
and it was left for Frerichs to recognize its important position among
the chronic affections of the brain and spinal cord. The earlier
German investigators who followed him were cautious in generalization,
and it was not until Vulpian, Charcot, and their followers announced
the discovery of infallible diagnostic criteria that disseminated
sclerosis received that attention at the hands of the profession which
it merits. But the more thorough researches made during the last two
decades have shown that this announcement was premature. The best
authorities recognize the existence of a large number of cases in
which the supposed pathognomonic signs of disseminated sclerosis are
absent, notwithstanding the existence of characteristic lesions, and
thus the more cautious earlier investigators are justified in the
reserve they had maintained.

It is in perfect harmony with the irregular location of the disease
and the lack of any constant rule governing the distribution of the
sclerotic foci that there is no constant clinical picture by which its
existence can be accurately determined in all cases. The diagnosis of
tabes dorsalis, of spastic paralysis, of amyotrophic lateral
sclerosis, and of transverse myelitis rests on exact and constant
signs, but that of disseminated sclerosis does not. The dictum of
Charcot, that there is always intention tremor and nystagmus in
disseminated sclerosis, has long been overthrown. Well-determined
cases are on record by De Fleury and Westphal, and a number have been
observed by myself, where there was no {874} tremor or no increased
tremor with intended movement, and no nystagmus, nor any other of the
pathognomonic symptoms so considered by Charcot and his followers.

The morbid process of disseminated sclerosis consists in the
development of patches of sclerosed tissue, scattered apparently
without any regularity or rule through the brain and spinal cord. They
are the results of insidious inflammatory changes. The symptoms
marking their presence may include nearly every known focal and
general symptom studied by neurologists, varying with the number,
size, and distribution of the foci. Usually there is some disturbance
of motility, both ataxic and paretic; in the majority there is tremor,
which in a large proportion of cases is of a distinctive character,
and disturbance of the functions of the cranial nerves, amblyopia,
color-blindness, mental enfeeblement; and, above all, apoplectiform
seizures are frequent.

Some writers discriminate between cases in which the lesions are
limited to, or most intense in, the spinal cord, and those in which
the brain is chiefly or exclusively involved, and hence they speak of
a spinal, a cerebral, and a cerebro-spinal form. This discrimination
is not sufficiently supported by clinical evidence to be of any
practical value. Each case is to be studied by itself during life and
after death, and to be regarded as one of a series in which the lesion
may be concentrated in any one segment of the cerebro-spinal axis. It
seems that when the sclerotic foci are limited to or chiefly located
in the spinal cord, the clinical signs are less pronounced than where
the brain is seriously involved; those cases in which the symptoms are
latent, or so vague that they cannot be distinguished from spinal
irritation or spinal exhaustion, have been found to be of the spinal
type. The cases of this character thus far observed are not
sufficiently numerous to justify the creation of special
subdivisions.[115]

[Footnote 115: According as the formation of the sclerotic foci
preponderates in a given segment of the nervous axis, the early signs
of the disease may consist in disturbances of the cerebral or the
spinal functions, and we may speak accordingly of a cerebral or spinal
invasion type. But the principle of classification adopted by several
recent writers, which would rank the spinal type among the spinal
diseases, the cerebral type among the cerebral diseases, and which is
compelled to erect a third category for the reception of the
cerebro-spinal type under the name of cerebro-spinal diseases, is a
bad one. Modern pathology recognizes the existence of affections which
involve whole fibre-systems, which are intracerebral in one and
intraspinal in other parts of their course, such as tabes and
amyotrophic sclerosis, which would therefore have to rank among the
cerebro-spinal, and not among the spinal affections, with which the
authors referred to classify them.]

CLINICAL HISTORY.—Prodromal.—Disseminated sclerosis is usually
inaugurated by a long initial period in which the symptoms are not
characteristic, and in which, unless there be decisive pupillary or
optic-nerve symptoms present, the nature of the disease is not
recognized. The patients feel weak and tired; walking is difficult,
and an element of unsteadiness suggests the development of a tabic
disorder. In other cases ankle-clonus is found and tremor of the foot
on extension (dorsiflexion); it is discovered that the unsteadiness is
due to weakness or to rigidity of the muscles, and thus the impression
of a developing spastic paralysis may be created. But symptoms on the
part of the cranial nerves soon show that the case is one of
disseminated sclerosis. Sometimes a marked belt sensation is
developed, and other forms of paræsthesia are not uncommon; nay, the
symptoms of spastic paralysis and tabes {875} dorsalis may be mingled.
Diplopia of the same transitory character as in tabes usually
accompanies the gradually-developing speech trouble. The reflex and
mechanical excitability of the muscles is increased in all cases where
the lateral column is extensively involved and the gray substance of
the cord is—as it usually is in the main—intact. In some cases a
slight tap on the knee when held in the position required to
demonstrate the knee-jerk produces oscillatory movements of the limb;
as the patient endeavors to suppress these they become more violent,
extend to the trunk and head, and may eventually involve the opposite
side. In those cases which show the cerebral-invasion type headache,
vertigo, and speech disturbance, temporary darkening of the visual
field, and loss of memory are the earliest symptoms directing
attention to the existence of serious disease.

Whether the spinal or the cerebral symptoms preponderate, they
continue increasing slowly and with temporary variations, which are
particularly marked in the cerebral-invasion type. As a rule, the
sensory disturbances are not pronounced at this time, but later, after
the initial symptoms have existed for a few years, they become
intense, and often extremely distressing. Those most complained of by
the patient are neuralgic, lancinating, and other pains. The
lancinating pains are, as a rule, not as severe as those of tabes
dorsalis, but they are apt to be associated with a dull heavy pain
which is located in a whole extremity, referred to the deep
structures, and very persistent. This diffuse pain sometimes occupies
all of the lower half of the body. As in tabes, the pain may be
regarded the forerunner of anæsthesia, which rarely, however, reaches
a high degree or an extensive distribution. Its distribution, like
that of the other peripheral symptoms of disseminated sclerosis, is
commonly irregular. Like the motor disturbance, which at this period
consists in a combination of paretic and spastic—occasionally of
ataxic—symptoms, it is most marked in the lower extremities.

In the majority of cases there is a peculiar tremor, which usually
presents the character to which Charcot directed attention—namely,
that it increases when the patient attempts to carry out a voluntary
movement, and disappears, or at least diminishes, when the muscles of
the part in question are at rest. This is the important symptom known
as the tremor on intended movement or intention tremor. One of the
time-honored means of testing it is to order the patient to take a
glass of water and pass it to his mouth. While he reaches out for it
some oscillatory unsteadiness is observed, but on grasping, this is
increased, and on raising the glass the oscillations increase till he
spills the water; if he succeeds in carrying it to his mouth, there is
a clattering against the teeth, and but for the steadying aid of his
mouth he would throw it aside by the violence of the disturbing
movements. In incipient cases this intention tremor is best shown with
delicate movements, and the more distinctly the more slowly they are
performed. It has been suggested that the peculiar character of the
lesion of disseminated sclerosis has some relation to the intention
tremor. It is a remarkable feature of the morbid process that it
leaves the axis-cylinder comparatively intact, beyond any other form
of myelitis or encephalitis. The myelin, however, is destroyed, and
the consequence is that the naked axis-cylinders lie in a newly-formed
connective tissue, which has not the same faculty the myelin has of
{876} isolating the nervous impulses conducted through the
axis-cylinders. The result is, that when a nervous impulse, such as a
voluntary movement, travels through a sclerotic focus, it may become
deflected to neighboring fibres going to another muscle or muscular
bundle than the one intended to be innervated. An unintended motion
results; the patient makes a stronger effort, intended for the right
channel, but again it slips off, to use a coarse simile, and thus a
number of erroneous messages are transmitted, and an equal number of
disturbing motions respond to these messages.

Whether this histological explanation be correct or not, the tremor is
probably due to the lesion of the peduncular tracts of the brain. At
least, this is rendered plausible for the tremor on intended movement,
which indicates an interference with the transmission of voluntary
impulses. Whether, as Pasternatzky[116] claims, the extreme muscular
oscillation seen in advanced cases is due to irritation of the
cortical motor fields, it is impossible to decide. No strong evidence
can be adduced in favor of his view. A few cases have been described
(Schüle, Jolly, and Greiff); and, in my opinion, such are far more
numerous than is usually supposed, where the tremor did not have the
so-called characteristic feature of ceasing in conditions of rest,
claimed by Charcot, but continued as in paralysis agitans.[117] A
collection of cases by Erb, Ordenstein, and Greiff shows clearly that
with a typical dissemination of sclerotic foci in the cord the tremor
on intended movement may be entirely absent, while no case is known
where the crus and pons were involved to a similar extent in which it
was absent. So it seems that a cerebral lesion is necessary to produce
this symptom in its characteristic form.

[Footnote 116: _Jahrbücher für Psychiatrie_, iii. 3, 1882.]

[Footnote 117: For several years I had been puzzled by the fact that
Charcot's formula failed to correspond to the clinical picture in the
majority of cases, and I registered such cases as incipient multiple
sclerosis or as a connecting group between paralysis agitans and that
disease.]

In advanced cases of disseminated sclerosis the intention tremor
becomes generalized; previously noticed, perhaps, only in one arm, it
now affects all the limbs and the muscles which maintain the trunk and
head in static equilibrium. The result is, that even when the patient
is at rest sitting in a chair, his body, and particularly his head,
are agitated by a violent and coarse tremor, which is increased on
rising and walking, as well as on attempting to use the hands.
Delicate mechanical occupations become impossible, and the handwriting
shows a characteristic change, the forward strokes of the letters and
the curvilinear back strokes, as well as the dots and crosses,
registering the tremor of the hand in their peculiar irregularity.

The speech is usually rough and broken, and sometimes enunciation is
impeded in a peculiar way, the patient appearing to scan his words.
Krause[118] has found relaxation of the vocal cords in a remarkable
degree to underlie the change in phonation. The scanning of speech
appears to be due to impeded innervation of the lips and tongue. When
the patient is told to protrude his tongue, he does so either in
spasmodic instalments of movement or with a sudden jerk after delay.
The same delay and apparent halting are noticed in the mimic
expressions that are observed {877} in speech. The features sometimes
express an emotion opposite to the one experienced by the
patient.[119]

[Footnote 118: _Neurologisches Centralblatt_, 1885.]

[Footnote 119: This symptom is found where there are other reasons for
suspecting the existence of large foci in the pons. I have observed it
in one case of tumor of this region, and one of a focal disease of
undetermined anatomical nature in the same location, in a remarkable
form. In the former case the patient not only exhibited the facial
contortions of hearty laughter when she felt as if about to break out
in tears, and broke out in tears when she felt amused, with perverse
regularity, but both emotional manifestations occurred simultaneously.
The other case is still under observation. There was complete
anarthria in the first, and nearly complete anarthria in the second
case—a fact not unrelated to the inferred site of the lesion, and
which may be associated with the fact that where the perverse mimic
expression occurs in disseminated sclerosis the speech-disturbance
often has an anarthric character.]

Whether diplopia occur as an early symptom or not, nystagmic
oscillation of the eyeballs is commonly found in the developed
affection. This nystagmus is usually universal, noted in associated
movements in every direction, and aggravated by excitement, by
constrained positions, and by any act of innervation of the
eye-muscles. It may be looked upon as an intention tremor of the
latter, and attributed to sclerotic foci in the cerebral axis,
particularly in the tegmental part of the pons varolii.

The deep reflexes are in some cases but slightly affected. Where
spastic phenomena preponderate, they are exaggerated, and where the
posterior root-zones are involved in the lesion, they may be, as in
tabes dorsalis, diminished or absent. The nutrition of the muscles is
not impaired in the early stages, and indeed most functions which
depend for their proper performance on the intact condition of the
gray substance, such as the power of retaining the urine, micturition,
and the functions of the rectum, are properly performed at this
period. The cutaneous reflexes are not markedly abnormal in the
majority of cases. They sometimes become diminished in the last
stages.

In cases regarded as disseminated scleroses and similar disorders
approximating the combined form of sclerosis, Westphal[120] noticed a
paradoxical muscular phenomenon which is the reverse in action of the
tendon reflexes. It is best observed in the tibialis anticus: if the
foot be extended (dorsiflected)—in other words, if the origin and
insertion of this muscle be approximated—the muscle contracts firmly,
keeping the foot in the enforced position, as if frozen into that
attitude. The same occasionally occurs if the patient voluntarily
extends his foot. Westphal observed the same phenomenon in the disease
described by him in which the symptoms of disseminated sclerosis are
present, but the corresponding lesion is not visible.[121]

[Footnote 120: _Archiv für Psychiatrie_, x. p. 243.]

[Footnote 121: _Ibid._, xiv. p. 132. It is a noteworthy fact that this
sign has been observed by its discoverer also in paralysis agitans.]

In a number of cases the mind becomes involved. Simple dementia is the
commoner condition, and some indication of passive mental enfeeblement
is found sooner or later in the history of the disease in the majority
of cases. In addition, there may be a morbid emotional condition,
usually in the direction of depression. I have been struck by the
frequent association of a melancholic state with large foci in the
oblongata. When it is borne in mind that the patient exhibits tremor
and speech-disturbance in addition to his mental trouble, it will be
understood that with some modifications of the typical signs the case
may simulate one of paretic dementia; and there are cases in which it
is exceedingly difficult to decide {878} whether they belong to an
aberrant type of disseminated sclerosis or to the sclerotic type of
paretic dementia. There are some which constitute veritable
connecting-links between the two affections.[122]

[Footnote 122: Zacher, _Archiv für Psychiatrie_, xiii. p. 168; the
writer, _Journal of Nervous and Mental Diseases_, April, 1877, and
_Insanity, its Classification, Diagnosis, and Treatment_, p. 240.]

Like tabes dorsalis, the progress of disseminated sclerosis is often
marked by episodes. Some of these differ in no way from the visceral
crises of posterior-column sclerosis; every form of these symptoms
found with that affection may occur in the present one, while episodes
involving the cerebral functions are much more common. The latter
manifest themselves as apoplectiform or epileptiform seizures. They
are preceded by headache and vertigo, or, if these be continuously
present, by an aggravation of them; then unconsciousness develops,
either accompanied by convulsions or not, and the face is flushed, the
pulse full and frequent, and the temperature raised. Consciousness
returns in a few hours or a day, the attack rarely lasting more than
two days, and it is found that the patient is hemiplegic. But, unlike
the hemiplegia found after vascular rupture, embolism, or structural
cortical disease, it is rapidly recovered from.

In a case of Gnauck's an attack of scotoma scintillans, associated
with a noise of thunder in the right ear and pricking pains on the
right side of the face, preceded anæsthesia and the formation of a
small defect of the visual field.

There is a close resemblance between these apoplectiform and
epileptiform seizures and those of paretic dementia, not alone in
clinical character, but also in the surprisingly complete and rapid
recovery from the more serious symptoms. But just as in paretic
dementia, especially in its advanced stage, each seizure leaves the
patient somewhat more impaired in mind and body than he was before, so
it is in disseminated sclerosis; each attack marks a step forward in
the invasion of the morbid state.

Eye-trouble is much less frequently a premonitory sign of disseminated
sclerosis than of tabes. A few such cases are on record. Magnan
observed the development of the characteristic symptoms of
disseminated sclerosis fourteen years after an amaurosis which
followed typhoid; and Gnauck reports another in which first a right
ptosis, and then a right amblyopia, preceded the ordinary symptoms. In
exceptional cases this premonitory eye-trouble may, like that of
tabes, rapidly lead to extreme amblyopia or even amaurosis. The visual
disturbances are remarkable for their rapid changes. They appear
within a short period, attain their maximum rapidly, and may
occasionally retrograde as quickly. They develop under two forms—the
central and the peripheral scotoma, or, rather, limitation of the
visual or color field. The former, like the amblyopia of alcoholic and
nicotine intoxication, consists in an inability to differentiate
between red and green in the centre of the visual field. It never, in
my experience, proceeds as far as the toxic amblyopias; that is, to
the complete extinction of vision.[123] The peripheral limitation of
vision may be for both quantitative and qualitative light-perception,
but it is not, as a rule,[124] concentric as in tabes, but
sector-like.

[Footnote 123: Gnauck says that the central color-blindness may become
total, and the red-green blindness extend to the periphery.]

[Footnote 124: Concentric limitation of ten to thirty degrees has been
noted for color-perception.]

{879} The atrophy of the optic nerve in disseminated sclerosis is
typically partial, in the majority of cases manifesting itself as a
sharply-marked discoloration of the temporal half of the papilla. In
others the nasal half of the papilla also becomes discolored, but so
much less intensely that the difference between the earlier involved
and later involved portions is quite easy. It is doubtful whether the
subjective visual disturbance is always an indication of the extent to
which the optic nerve is involved. There are good reasons for
believing those amblyopias and limitations of the field of vision
which show marked remissions and exacerbations to be due to some
dynamic central condition involving the visual centres and tracts.
Thus it has been observed that almost total amaurosis occurred after
an apoplectiform attack, to disappear later on. Occasionally the
amblyopia is bilateral and the optic-nerve lesion unilateral. The
frequency of this affection is stated by Gnauck[125] as follows: In
one half the cases there is diminished vision, and in half this half
optic-nerve atrophy with limitation of the visual field. It is only in
exceptional cases that an optic neuritis can be determined to have
preceded the atrophy.

[Footnote 125: Of 50 cases, 22 had no visual trouble, 8 showed simple
diminution of perception, 5 added limitation, and 15 changes of the
optic disc, a case of total atrophy and amaurosis being included in
the latter.]

The pupils are perfectly normal in some cases; in others myosis of the
spinal type is observed; and this I found to be nearly constant in all
advanced cases. Irregularity in outline and inequality exist in a
small proportion, and reflex iridoplegia is found in about 10 per
cent. of the cases.

Thus far, the symptoms which occur either in a majority or in a large
percentage of cases have been enumerated. The typical course of
disseminated sclerosis may be stated as consisting in their gradual
development and intensification, covering a period of from four to
twenty or more years. There are a number of cases in which so many of
the symptoms regarded as typical are either absent or where some given
symptom-group preponderates over the others to such an extent that
they require special mention.

It is not difficult to understand that disseminated sclerosis may ape
other forms of spinal disease. Its symptoms depend on the location of
the sclerotic foci. If these are situated chiefly in the
crossed-pyramid tract, spastic phenomena will predominate, and the
case may resemble a spastic paralysis.[126] If they be distributed in
both the posterior and lateral columns, the symptoms will resemble
those of a combined form of sclerosis in which the tabic and spastic
signs are associated, as far as they do not, in the nature of the
case, neutralize each other. This was well shown in a case of De
Fleury's. Not infrequently an unusually large focus involves the
entire transverse section of the cord, and the case becomes
complicated by the symptoms of a transverse myelitis. In such a case,
described by Rovigli,[127] a large transverse focus in the cord had
led to ascending secondary degeneration in the column of Goll and
descending degeneration of the crossed pyramid tract. In a large
series, instances of which are related by Kilian,[128] Siemens,[129]
Schultze,[130] Zacher,[131] and Greiff,[132] {880} the disseminated
foci were complicated by a diffuse lesion distributed like that of a
diffuse or fascicular myelitis; and there seems to exist every
connecting-link between ordinary chronic myelitis, strictly so called,
and disseminated sclerosis.

[Footnote 126: Gnauck, _Neurologisches Centralblatt_, 1884, p. 315.]

[Footnote 127: _Rivista sperimentale di Freniatria e di Medicina
leqale_, x. p. 227.]

[Footnote 128: _Archiv für Psychiatrie_, vii. p. 28. He designates
this form sclerosis continua multiplex.]

[Footnote 129: _Ibid._, x. p. 135.]

[Footnote 130: _Ibid._, xi. p. 216.]

[Footnote 131: _Ibid._, xiii. p. 168.]

[Footnote 132: _Ibid._, xiv. p. 287.]

Not only does disseminated sclerosis occasionally imitate or
approximate the regular (fascicular) affections of the cord, as well
as diffuse cerebro-spinal affections, but it may appear under the mask
of a nuclear oblongata paralysis.[133] And cases are on record where,
in addition to the disseminated sclerosis, there occurred sclerotic
atrophy of an entire hemisphere or of its capsular tracts, thus
leading to a hemiplegic resemblance of the motor paralysis. In my
experience the cases presenting the type of a nuclear oblongata
paralysis run a more rapidly fatal course than others. The shortest
history in my series, one of four years, was of such a case. A number
of instances are on record by careful observers—and are probably much
more numerous than is commonly suspected—where no decisive evidence of
spinal or cerebral disease could be detected during life, and yet
disseminated foci of sclerosis existed in the nerve-centres. In such
cases the symptoms may be in the direction of simple nervous
prostration, more commonly of spinal irritation. I have now under
observation a case which for years had been regarded as one of spinal
irritation, and which made that impression on me until I discovered
the existence of optic-nerve atrophy, which was the only indication
that the symptoms depended on gross structural disease.[134]

[Footnote 133: It is customary to speak of symptoms referable to the
oblongata as bulbar. The designation bulbus rachidicus is now
obsolete, and just as we speak of a capsular hemiplegia, a pons
paralysis, or a spinal hemiplegia, so we should say an oblongata
paralysis, discriminating between the nuclear, the neural, and the
tract affections by means of a prefix.]

[Footnote 134: At present the symptoms of disseminated sclerosis are
unmistakable. Cases are mentioned by Strümpell and others in which
they remained indecisive throughout.]

Among the anomalous forms of disseminated sclerosis there is one which
is characterized by the preponderance of paraplegia and contractures
in a combination which is usually found in spinal diseases of a
different type. The coexistence of dementia, however, usually enables
the observer to determine that the lesion is both cerebral and spinal,
although those signs which might enable him to decide the disseminated
focal character may be absent.

MORBID ANATOMY.—In advanced cases of disseminated sclerosis the lesion
is visible to the naked eye on the surface of the brain and spinal
cord. Grayish maculas, sometimes elevated, more rarely a little
sunken, and occasionally showing a buff or reddish tinge, are seen on
the surface of the spinal cord, the oblongata, pons, and crura. On
making sections across the region of the spots, it is found that the
color-change is not superficial, but extends inward, involving large
parts of the transverse area of the cord or the cerebral axis; and
patches lying more deeply in their substance are revealed whose
existence could not have been suspected from a mere surface
inspection. Exceptionally, patches are found involving the entire
transverse section of the spinal cord in a length of a half to two
inches. And, similarly, in the brain nearly the entire area of the
pons or one of the crura or an entire division of the internal capsule
may be occupied by a sclerotic focus. Otherwise, they may vary from
almost microscopic dimensions to the size of a chestnut or even
larger. {881} Bourneville[135] has described cases in which the
nerve-centres appeared normal to the naked eye, while the microscope
revealed the existence of sclerotic foci. It is, however, unlikely
that the fresh brain- and cord-tissue, when the site of disseminated
sclerosis, will appear perfectly healthy to the naked eye under fairly
good illumination. Much less intense lesions than those of
disseminated sclerosis reveal their presence by changes in color and
consistency.

[Footnote 135: _Mouvement medicale_, 1869, No. 27.]

On examining the diseased spots more narrowly, they are found to be
slightly diaphanous. Usually, they are rounded or elliptical, but they
are often drawn out, as it were, in the most irregular shapes, and not
infrequently appear to be the result of a confluence of originally
remote and separate foci. In the cord they are sometimes wedge-shaped,
extending inward from the periphery. To the touch they appear
firm—sometimes not much more so than the normal tissue, contrasting
with it as hard-boiled white of egg would contrast with soft-boiled;
in advanced cases they become of almost leathery consistency, and
there are instances recorded where they actually creaked under the
knife. A clear fluid usually runs from their cut surface, and the
latter does not jut up on section like normal nerve-tissue.

The distribution of the diseased areas follows no known law. They may
be numerous and of large size in one segment of the nervous axis, and
small, few in numbers, or even absent, in others. In some altitudes of
the cord the lateral, in others the posterior, in still others the
anterior, columns are chiefly involved. The cerebrum usually contains
a larger number of foci irregularly scattered in the centrum ovale of
Vieussens, the internal capsule and its surrounding ganglia, as well
as in the corpus callosum. Throughout the nervous axis it seems that
the lesion chiefly affects the white substances, and even the roots of
the peripheral nerves, both cranial and spinal, are occasionally found
to contain small foci, gray, firm in consistency, and as distinctly
outlined as those of the central organs.

The morbid process consists in an atrophy and gradual disappearance of
the myelin, which is preceded, if not caused, by an increase of the
enveloping interstitial substance. This change is of the same
character as that found in chronic myelitis. The septa and trabeculæ
of connective tissue become thicker, formless connective substance and
fibrillar tissue, which seems to arise in, if not in part from, it,
constituting the new formation. The neuroglia-nuclei are increased,
enlarged, and develop into spider-shaped cells, whose long processes
contribute (according to some authors exclusively) to the newly-formed
fibrillar network.

While the myelin undergoes wasting, the axis-cylinders remain intact
for a long period, and even in intensely sclerosed regions they may be
found in nearly their normal number, but naked and in direct contact
with the pathological fibrillæ. Some of them become hypertrophied,
increasing to twice, thrice, and, according to Leyden, even more, of
their normal diameter. This change seems to inaugurate the last phase
of the process: the axis-cylinders, becoming sclerosed and brittle,
ultimately disappear, and no trace, or at best but doubtful traces, of
the normal nerve-tissue are left behind. The blood-vessels, following
the rule of {882} the sclerotic process, take part in it. Their walls
become thickened, richly nucleated, and the lumen becomes narrowed in
consequence. In the smaller vessels complete obliteration of the lumen
is sometimes observed.

The gray substance is not involved as frequently as the white, but it
opposes no barrier to the extension of the morbid process when once
established in its neighborhood. The nerve-cells show the same
resistance which the axis-cylinder does; that is, they retain their
outline and fibre-connections a long time in the midst of the diseased
area. But eventually they become discolored, undergo hyaline or
granular disintegration, their processes shrink, and finally they
disappear.

Ribbert and Zacher consider the sclerosis of tabes and the
disseminated affection to be much more similar than Leyden and Charcot
supposed. They locate the starting-point of the morbid process in the
vascular and connective tissues; and Greiff, in harmony with this
view, finds that the foci occur most frequently in those parts of the
cord where the connective-tissue trabeculæ are most numerous, as in
the posterior columns and at the junction of the anterior and lateral
columns.

Although the morbid foci appear to the naked eye to be uniform, and to
be sharply demarcated in the normal tissue, closer examination shows
that the areas of maximum lesion are surrounded by a narrow transition
zone by which the lesion seems to mark its eccentric progress, and
occasionally a focus of intense disease lies in a diffused area of
slight changes, resembling those of diffuse myelitis. Sometimes the
cord appears to be almost continuously involved by a lesion of
moderate intensity, and a few disseminated foci in the brain alone
prove that the case belongs to this form of sclerosis.

A few years ago Greiff described what he considered a new lesion in
multiple sclerosis, under the name of disseminated vitreous
degeneration of the cerebral cortex.[136] I have been familiar with
this lesion since 1876: it can be produced at will in perfectly
healthy brains, and consists in a precipitation of leucine crystals
extracted from the brain-substance by the action of alcohol. His
accompanying figure[137] represents this artificial lesion very
accurately; and Greiff, if he fails to recognize that his vitreous
degeneration is a spurious lesion, at least identifies it with the
miliary sclerosis of Bucknill and Tuke and the spheres of Schüle,
which are now generally recognized to be the results of post-mortem
manipulations and not actual lesions.[138]

[Footnote 136: _Archiv für Psychiatrie_, xiv. p. 286.]

[Footnote 137: _Ibid._, xiv., Plate ii. Fig. 5.]

[Footnote 138: Attention was first called to the artificial nature of
these bodies by the writer in the _Journal of Nervous and Mental
Diseases_, October, 1877, and a more accurate description was given in
the _Chicago Medical Review_ of 1880, and in a demonstration before
the New York Neurological Society in 1883. In commenting on the latter
a German critic stated that the facts related had been long known in
Germany (_Neurologisches Centralblatt_, 1883, p. 283). On inquiring of
the critic what publication contained any reference to this discovery,
he frankly stated that he knew of none, but had had in mind what he
considered a tradition of the laboratory. It was in the same year that
Greiff worked at the Heidelberg laboratory under the eminent
supervision of Fürstner, and it was a few years previous that Schüle,
one of the collaborators of _Ziemssen's Cyclopædia_, had made the same
mistake. So it seems that the tradition is in some danger of expiring,
and that it would do no harm to accept the caution, even though it
travel across the Atlantic in the reverse of the usual direction. It
has been amply confirmed by Savage and Plaxton (_Journal of Mental
Science_, October, 1882, and April, 1883).]

In judging as to the nature and intensity of the inflammatory process
{883} which leads to the development of the sclerotic foci, it must be
remembered that we are acquainted thus far only with the terminal
period of the disease, when, as is to be presumed, the active
inflammatory changes have gone by or are in the background. It is very
probable that the newly-formed tissue is more nucleated in early
periods than is found in the cases which constitute the material of
pathological laboratories. In a case of protracted nervous exhaustion
accompanied by spinal irritation in an alcoholic subject who was
murdered, and whose brain and cord I had an opportunity of examining,
I found, both in the cord and brain, districts in which the white
substance showed a slight grayish discoloration and increased
consistency. Minute examination failed to show any qualitative change
in the conducting elements, but the interstitial tissue was
hypertrophied, richly nucleated, and showed Frommann's cells in
abundance.

ETIOLOGY.—Heredity has been observed in a number of cases by Duchenne,
Erb, and Frerichs. The latter two had each an opportunity of recording
this inheritance in several members—sisters or brothers—of the same
family. In these cases the transmitted affection developed in adult
life. Dreschfeld, however, cites a case where two brothers developed
its symptoms in a marked degree in infancy. As an associated feature
it is found with some cases of congenital defect. Thus Pollak[139]
discovered disseminated sclerosis in an infant which had a defective
corpus callosum and exhibited the characteristic signs of the focal
affection side by side with the imbecility due to imperfect cerebral
development. As a rule, the disease is developed after the twentieth
year. But cases have been related (De Fleury) where the patient
developed the disease and died with an apoplectiform onset in earlier
life. One of the youngest on record is described by Hödemacker.[140]
The subject developed the disease at the seventh year, and died with
it at the fourteenth, having shown the characteristic symptoms,
besides more muscular atrophy than is common. The sclerosis in this
case belonged to the type which has been referred to as a
connecting-link between diffuse and disseminated sclerosis.
Pelizæus[141] reports five cases developing in the same family in
early life, corresponding somewhat in their relation to multiple
sclerosis of advanced life, as the family forms of tabes and spastic
paralysis correspond to the typical adult forms of those diseases. All
the cases were of males, and the ancestral taint had been present in
male members of the family, passing through the females to their
progeny without breaking out in the mothers. Each branch of this
family appeared to develop its own peculiar type of the disorder.

[Footnote 139: _Deutsches Archiv für klinische Medizin_, Bd. xxiv. p.
404.]

[Footnote 140: _Ibid._, vol. xxiii. p. 442.]

[Footnote 141: _Archiv für Psychiatrie_, xvi. p. 698.]

CAUSES.—Disseminated sclerosis may develop as a sequel of an acute
myelitis. An excellent observation of Singer,[142] in which a
unilateral optic-nerve atrophy of central origin occurred after
recovery from an acute inflammation of the cord, proves that sclerotic
foci may develop secondarily to an acute process. Westphal believes
that obstruction to the circulation, both of blood and lymph, in the
cord may act as a predisposing factor in the production of multiple
sclerosis. He rests this opinion on a case where the cord had been
compressed by a tumor, and {884} sclerotic foci of probably later date
were found in the neighboring segments of the cord.

[Footnote 142: _Prager medizinisch Wochenschrift_, 1885, No. 8.]

The myelitic affection discovered by the same observer[143] to be an
occasional sequel of typhus, smallpox, diphtheria, measles, and
erysipelas is a true disseminated sclerosis. The foci are usually very
small and very numerous. A focal sclerosis of the posterior columns of
the disseminated type has been found by Brigidi-Bandi in a case of
pellagra which presented ataxic symptoms.[144]

[Footnote 143: _Archiv für Psychiatrie_, iii. p. 376, iv.; Oertel,
_Deutsches Archiv für klinische Medizin_, viii.; Damaschino, _Gazette
médicale de Paris_, 1871, p. 505. In one case now under observation a
typical disseminated sclerosis developed in a robust young man of
thirty after typhoid fever.]

[Footnote 144: _Lo sperimentale_, December, 1879.]

Among the exciting causes, prolonged exposure to wet and cold are
acknowledged to occupy an important position. The frequent combination
of these factors with over-exertion and depressing emotions among the
poorer classes probably account for its great frequency among them. In
some cases excessive grief has been the only discoverable etiological
factor: in three of my own cases this was so prominent and connected a
feature that I could not doubt its influence, if not as a primary at
least as an exciting cause.[145] Fright has been distinctly connected
with the outbreak of the disease in a number of cases.[146] There is
considerable unanimity among observers regarding the effects of shock
and injury in producing disseminated sclerosis, usually of that
anomalous type which approximates the diffuse or fascicular form.
Railway spine is undoubtedly the mask of a disseminated inflammatory
trouble in a number of cases; the only authority of weight who opposes
this view is Charcot, and his opposition is abundantly neutralized by
a number of carefully-studied American and European cases.

[Footnote 145: The coincidences among these three cases were
remarkable. All three were Germans, all three musicians, two had lost
an only son. In all, the emotional manifestations were pronounced from
the initial to the advanced period of the disease.]

[Footnote 146: A Bohemian cigar-maker was startled by the sudden
firing of a pistol-shot in a dark hallway, and on arriving at the
factory, and not fully recovered from the first fright, he was again
startled by the sudden descent of an elevator and the fall of a heavy
case from it close to where he stood. From the latter moment he
trembled, and his tremor continued increasing till the last stage of
his illness was reached. This was my shortest duration, four years,
and of nuclear oblongata paralysis type.]

Hysterical and other obscure neuroses have been claimed to act as
predisposing causes. But, inasmuch as it is well established that
sclerosis is not a legitimate sequel of even the most aggravated forms
of true hysteria,[147] and, on the other hand, that disseminated
sclerosis, particularly in the early stages, may progress under the
mask of spinal irritative or other neuroses, it is reasonable to
suppose that cause and effect have been confounded by those who
advanced this view. According to Charcot, the female sex shows a
greater disposition to the disease than the male. Erb, who bases his
remarks on the surprisingly small number of nine cases, is inclined to
account for Charcot's statement on the ground that it was at a
hospital for females that Charcot made his observations. On comparing
the figures of numerous observers, it will be found that in the
experience of one the females, and of the other the males,
preponderate. {885} In my own experience the males far exceed the
females both in private and in dispensary practice. Of 22 cases with
accessible records, only 7 were females.

[Footnote 147: Charcot's observation of lateral sclerosis in
hysterical contracture, although made so long ago, has not been
confirmed, and the most careful examinations in equally severe and
protracted cases have proven altogether negative.]

Syphilis has also been assigned as a cause. The connection is not as
clear as in tabes. In the few cases where there appears to be a direct
causal relation the lesion is not typical. There are sclerotic foci,
but in addition there is a general lesion, particularly of the
posterior columns of the cord, such as is found with paretic dementia.
And it has been noted that periendymal and subendymal sclerosis is
more frequent with the cases of alleged syphilitic origin than with
those of the typical form.

DIFFERENTIAL DIAGNOSIS.—In view of what has been already stated
regarding the numerous clinical types found in disseminated sclerosis,
it is easily understood why the diagnosis of this disease is becoming
more and more uncertain: every new set of researches removes some one
or several of the old and cherished landmarks; and it may be safely
asserted that only a minority of the cases show that symptom-group
which was formerly claimed as characteristic of all. The discovery of
a series of cases by Westphal,[148] in which the typical symptom-group
of Charcot was present, but no sclerosis deserving the name found
after death, as well as the interesting experience of Seguin, who
found well-marked disseminated sclerosis in a case regarded as
hysterical intra vitam, illustrates the increasing uncertainly of our
advancing knowledge. It was believed within a few years that the
presence of cranial nerve-symptoms was a positive factor in
determining a given case to be one of disseminated sclerosis, but in
the very cases described by Westphal such symptoms were present
notwithstanding the lesion was absent. Up to this time, however, no
case has been discovered in which, optic-nerve atrophy being present
in addition to the so-called characteristic symptoms of intention
tremor, nystagmus, and scanning in speech, disseminated foci of
sclerosis were not found at the autopsy. This sign may be therefore
regarded as of the highest determining value when present; but as it
is absent in the majority of cases, its absence cannot be regarded as
decisive. The presence of pupillary symptoms also increases the
certainty of the diagnosis when added to the ordinary and general
symptoms of the disorder related above.

[Footnote 148: _Archiv für Psychiatrie_, xiv. p. 128.]

Although the difference between the tremor of typical disseminated
sclerosis and that of paralysis agitans is pathognomonic, yet the
existence of a group of cases of disseminated sclerosis, as well as of
one of cases of paralysis agitans without tremor, renders an exact
discrimination in all cases impossible. It is a question, as yet,
whether the form of paralysis agitans without tremor described by
Charcot, and which is marked by pains in the extremities, rigidity,
clumsiness, and slowness of movement, general motor weakness, a frozen
countenance, impeded speech, and mental enfeeblement, is not in
reality a diffuse or disseminated sclerosis.

The diagnosis of this disease, while readily made in a large number of
cases on the strength of the characteristic symptoms detailed, may be
regarded as impossible in a minority which some good authorities
incline to regard as a large one.


{886} Diffuse Sclerosis.

SYNONYMS.—Chronic myelitis, Diffuse myelitis, Simple or Diffuse spinal
sclerosis, Chronic transverse myelitis, Sclerosis stricte sic dicta
(Leyden, in part), Gray degeneration.

The various forms of sclerosis thus far considered were at one time
considered as varieties of chronic myelitis, and under different
names, founded on leading symptoms, were considered to be merely
local, and perhaps accidental, variations of one and the same morbid
process. More accurate clinical and pathological analysis has
separated from the general family of the scleroses one clearly
demarcated form after another. Tabes dorsalis, disseminated sclerosis,
amyotrophic lateral sclerosis, and the combined forms of sclerosis
have been successively isolated. Still, a large number of cases are
left which cannot be classified either with the regular affections of
the cord, limited to special systems of fibres, or with the
disseminated form last considered. They agree with the latter in that
they are not uniform; they differ from it in that they are not
multilocular. Not a few modern authors have neglected making any
provisions for these cases, while others treat of them in conjunction
with acute myelitis, of which disease it is sometimes regarded as a
sequel. The term diffuse sclerosis is here applied to those forms of
chronic myelitis which follow no special rule in their location, and
to such as are atypical and do not correspond in their symptomatology
or anatomy to the more regular forms of sclerosis. In regional
distribution the foci of diffuse sclerosis imitate those of acute
myelitis: they may be transverse, fascicular, or irregular.

MORBID ANATOMY.—In typical cases the lesion of diffuse sclerosis
constitutes a connecting-link between that of the disseminated form
and posterior sclerosis. Its naked-eye characters are the same. There
is usually more rapid destruction of the axis-cylinders, more
inflammatory vascularization, proliferation of the neuroglia-nuclei,
and pigmentary and hyaline degeneration of the nerve-cells, than in
the disseminated form.

Syphilitic inflammation of the cord extends along the lymphatic
channels, including the adventitial spaces, and leads to a diffuse
fibrous interstitial sclerosis. In one case in which I suspected
syphilis, though a fellow-observer failed to detect it after a rigid
search, I found a peculiar form of what would probably be best
designated as vesicular degeneration, according to Leyden, though
associated with a veritable sclerosis. The lymph-space in the
posterior septum showed ectasis; the blood-vessels were sclerotic, and
each was the centre of the mingled sclerotic and rarefying change. It
appears that while the interstitial tissue hypertrophied, the myelin
of adjoining nerve-tubes was pressed together till the intervening
tissue underwent pressure atrophy. The result was, the myelin-tubes
consolidated, some axis-cylinders perished, others atrophied, a few
remained, and, the myelin undergoing liquefaction, long tubular
cavities resulted, running parallel with the axis of the cord, and
exposed as round cavities on cross-section (Fig. 32). The changes in
the cells of the anterior horn in the same cord (Fig. 33) illustrate
one of the common forms of disease to which they are subjected in the
course of sclerotic disease.

[Illustration: FIG. 32.]

[Illustration: FIG. 33.]

The so-called myelitis without softening, or hyperplastic myelitis of
{887} Dujardin-Beaumetz, which is ranked by Leyden and Erb among the
acute processes, properly belongs here. It is characterized by a
proliferation of the interstitial substance, both of its cellular and
fibrillar elements. The nerve-elements proper play no part, or at best
a very slight or secondary one. In the sense that this affection
occurs after acute diseases and develops in a brief period it may be
called an acute myelitis, but both in its histological products and
its clinical features it approximates the sclerotic or chronic
inflammatory affections of the cord. As far as the clinical features
are concerned, this is particularly well shown in the disseminated
myelitis found by Westphal after acute diseases, such as the
exanthematous and continued fevers.

{888} CLINICAL HISTORY.—Impairment of motion is the most constant
early feature of chronic myelitis; in the transverse form it may be as
absolute as in the severest forms of acute myelitis; as a rule,
however, it is rather a paresis than a paralysis. The patient is
usually able to walk, manifesting the paraparetic gait: he moves along
slowly, does not lift his feet, drags them along, makes short steps;
in short, acts as if his limbs were heavily weighted. This difficulty
of locomotion is preceded and accompanied by a tired feeling before
other sensory symptoms are developed. Rigidity of the muscles, like
that found in disseminated sclerosis, is a common accompaniment, and
may even preponderate over the paresis to such an extent as to modify
the patient's walk, rendering it spastic in character. In such cases
the muscles feel hard to the touch, and the same exaggerated reflex
excitability may be present as was described to be characteristic of
spastic paralysis.

If, while the leg is slightly flexed on the thigh, the foot be
extended,[149] so as to render the Achilles tendon and the muscles
connected with it tense, and the hand while grasping the foot suddenly
presses the latter to still further extension, a quick contraction
occurs, which, if the pressure be renewed and kept up, recurs again
and again, the succession of the involuntary movements resembling a
clonic spasm. This action is termed the ankle-clonus or
foot-phenomenon. Gowers has amplified this test of exaggerated reflex
excitability by adding what he calls the front-tap contraction. The
foot being held in the same way as stated above, the examiner strikes
the muscles on the front of the leg; the calf-muscles contract and
cause a brief extension movement of the foot. It is believed that the
foot-clonus and the front-tap contraction are always pathological, but
a few observers, notably Gnauck, leave it an open question whether it
may not occur in neurotic subjects who have no organic disease. Gowers
considers the foot-clonus found in hysterical women as spurious, and
states that it differs from the true form in that it is not constant,
being broken by voluntary contractions, and does not begin as soon as
the observer applies pressure. But I have seen the form of clonus
which Gowers regards as hysterical in cases of diffuse sclerosis. With
regard to the front-tap contraction, its discoverer[150] admits that
it may be obtained in persons in whom there is no reason to suspect
organic disease. It is significant only when unequal on the two sides.

[Footnote 149: By extension the approximation of the dorsal surface to
the tibial aspect of the leg—what some German writers call dorsal
flexion—is meant.]

[Footnote 150: Gowers, _The Diagnosis of the Diseases of the Spinal
Cord_, 3d ed., p. 33.]

In severe cases contractures are developed in the affected muscular
groups, being, as a rule, preceded by the rigidity, increased reflex
excitability, and the thereon dependent phenomena above detailed.
These contractures may be like those of spastic paralysis, but usually
the adductors show the chief involvement, and sometimes the leg
becomes flexed on the thigh and the thigh on the abdomen in such firm
contraction that the patient, albeit his gross motor power is not
sufficiently impaired, is unable to move about, and is confined to his
bed, his heel firmly drawn up against his buttock. It is stated by
Leyden that the contracted muscles occasionally become
hypertrophied—an occurrence I have not been able to verify. As a rule,
some muscular groups are atrophied, though {889} the limbs as a whole,
particularly in those patients who are able to walk about, are fairly
well nourished.

Pain in the back is a frequent accompaniment of diffuse sclerosis. It
is not pronounced, but constant.

The drift of opinion to-day is to regard pain in the spinal region as
not pathognomonic of organic spinal affections. It is true that pain
is a frequent concomitant of neuroses, and that it is more intense and
characteristic in vertebral and meningeal disease; but in denying a
significance to pain in the back as an evidence of diffuse disease of
the cord itself, I think many modern observers have gone to an
extreme. It is particularly in diffuse sclerosis that a dull heavy
sensation is experienced in the lumbo-sacral region; and in a number
of my cases of slowly ascending myelitis and of tabes dorsalis the
involvement of the arms was accompanied by an extension of the same
pain, in one case associated with intolerable itching, to the
interscapular region. It cannot be maintained that the pain
corresponds in situation to the sclerotic area. It is probably, like
the pain in the extremities, a symptom of irradiation, and corresponds
in distribution to that of the spinal rami of the nerves arising in
the affected level.

As the posterior columns are usually involved in transverse myelitis,
the same lancinating and terebrating pains may occur as in tabes
dorsalis. As a rule, they are not as severe, and a dull, heavy
feeling, comparable to a tired or a burning sensation, is more common.
A belt sensation, like that of tabes, and as in tabes corresponding to
the altitude of the lesion, is a much more constant symptom than acute
pains.

Cutaneous sensibility is not usually impaired to anything like the
extent found in advanced tabes. It is marked in proportion to the
severity of the motor paralysis; where mobility is greatly impaired,
profound anæsthesia and paræsthesia will be found; where it is not
much disturbed, subjective numbness, slight hyperæsthesia, or tingling
and formication may be the only symptoms indicating sensory
disturbance; and there are cases where even these may be wanting.

The visceral functions are not usually disturbed. In intense
transverse sclerosis of the upper dorsal region I observed gastric
crises, and in a second, whose lesion is of slight intensity, but
probably diffused over a considerable length of the cerebro-spinal
axis, there is at present pathological glycosuria. The bladder
commonly shows slight impairment of expulsive as well as retaining
power, the patients micturating frequently and passing the last drops
of urine with difficulty. Constipation is the rule. The sexual powers
are usually diminished, though rarely abolished. As with sclerotic
processes generally, the sexual functions of the female, both
menstrual and reproductive, are rarely disturbed.

It is not necessary to recapitulate here the symptoms which mark
diffuse sclerosis at different altitudes of the cord. With this
modification, that they are less intense, not apt to be associated
with much atrophic degeneration, nor, as a rule, quite as abruptly
demarcated in regional distribution, what was said for acute myelitis
may be transferred to this form of chronic myelitis. The progress of
diffuse sclerosis is slow, its development insidious, and the history
of the case may extend over as long a period as that of diffuse
sclerosis. Sooner or later, higher levels of the cord are involved in
those cases where the primary focus was low down. {890} In this way
the course of the disease may appear very rapid at one time, to become
almost stationary at others. Of three deaths which occurred from the
disease in my experience, one, in which there were distinct signs of
involvement of the oblongata,[151] occurred from sudden paralysis of
respiration; a second from a cardiac complication, which, in view of
some recent revelations concerning the influence of the tabic process
on the organic condition of the valves of the heart, I should be
inclined to regard as not unconnected with the sclerosis; and in a
third, from bed-sores of the ordinary surgical variety. The malignant
bed-sore is not of frequent occurrence in this disease.

[Footnote 151: On one occasion the patient had momentary anarthria,
followed a day later by two successive periods of anarthria, lasting
respectively about twenty seconds and one minute, one of which was
accompanied by diplopia of equally brief duration.]

PROGNOSIS.—The disease may, as in the instances cited, lead to a fatal
termination, directly or indirectly, in from three to twenty years.
The average duration of life is from six to fifteen years, being
greater in cases where the sclerotic process is of slight intensity,
even though it be of considerable extent, than where it is of maximum
or destructive severity in one area, albeit limited. I am able to say,
as in the case of tabes dorsalis, that a fair number of patients
suffering from this disease whom I have observed for from two to six
years have not made any material progress in an unfavorable sense in
that time. One cure[152] occurred in this series, of a patient
manifesting extreme contractures, atrophies, bladder trouble, and
ataxiform paresis, where the cause was plainly syphilis, and the
histological character of the lesion is somewhat a matter of
conjecture in consequence. Diffuse sclerosis of non-syphilitic
origin—and this may apply also to established sclerosis in syphilitic
subjects—is probably as unamenable to remedial treatment as any other
sclerotic affection.

[Footnote 152: The patient went, under direction of Leonard Weber and
R. H. Saunders, to Aix-la-Chapelle, where this happy result was
obtained after mixed treatment had practically failed.]

The same rules of DIAGNOSIS applicable to transverse myelitis of acute
onset apply, level for level, to the diagnosis of transverse myelitis
of insidious development, the history of the case often furnishing the
only distinguishing point between the acute and the chronic form.

The main difference between the diffuse sclerosis and acute myelitis,
clinically considered, consists in the gradual development of symptoms
in the former as contrasted with their rapid development in the latter
disease. Acute myelitis is established within a few hours, days, or at
most, in the subacute forms, a few weeks; chronic myelitis requires
months and years to become a clearly-manifested disorder. It is the
essential correspondence of the symptoms of both conditions,
intrinsically considered, which renders it impossible to distinguish
clinically and in the absence of a history of the case between some
cases of acute myelitis in the secondary period and the processes
which are primarily of a sclerotic character.

It is unusual to find the degeneration reaction in myelitis of slow
and gradual development. Sometimes there is diminished reaction to
both the faradic and galvanic currents, or the so-called middle form
of degeneration reaction is obtained from atrophied muscles, the nerve
presenting normal or nearly normal irritability, and the muscle
increased galvanic irritability and inversion of the formula.

{891} Among the less reliable or accessible points of differentiation
between the residua of acute myelitis and the chronic form is the
history of the onset and the age of the patient at the time of the
onset. Myelitis in young subjects is more likely to be of the acute
kind; in older persons it is more apt to be chronic.

In the diagnosis of diffuse sclerosis the question of differentiation
from neuroses not based on ascertainable structural disease, such as
are called functional, will be most frequently raised. In
differentiating between organic and functional spinal disorders all
known exact signs of organic disease must be excluded before the case
can be considered as appertaining to the latter group. Symptoms of
hysteria, nervous exhaustion, and spinal irritation frequently coexist
with diffuse sclerosis as well as with the disseminated form; and this
is not surprising, for, instead, as seemed at one time to be believed,
of the neurotic taint granting comparative immunity against organic
disease, it is the reverse, and it is not at all uncommon to find a
strongly-marked neurotic diathesis in the family history of sufferers
from diffuse sclerosis. That ordinary hysteria, epilepsy, and what is
vaguely called nervousness are common features in the ancestral record
of the hereditary forms of spinal disease has already been stated in
considering those affections.

One of the commoner forms of the grave phase of hysteria is
paraplegia.[153] Often muscular atrophy—which ensues from
disuse—exaggeration of the deep reflexes, and retention of urine are
added to the paraplegia and heighten the resemblance to an organic
affection. Its development, though sometimes sudden, often occupies
weeks or months, and may be preceded, exactly as in chronic myelitis,
by weakness in the legs, and not infrequently by combined ataxia and
weakness. It is much more difficult to discriminate here than is
generally held or than is enunciated in textbooks. The sufferer from
hysterical paraplegia does not always give other indications of the
hysterical neurosis, and even if she did show a globus and tenderness
at certain points, it is a question whether it could be called a
scientific diagnosis which determined the case to be one of functional
trouble on these signs alone. More than one error has been committed
in this respect. In chronic myelitis retention of urine is less common
than incontinence, which is the reverse of hysterical paraplegia.
Pupillary symptoms do not occur with the latter affection. If there be
sensory anæsthesias, they are bizarre in character or distribution,
and do not usually harmonize with the distribution of the paralysis.
In most cases moral influences can be exerted so as to increase the
power of movement far beyond what would be possible in an organic
disease; and while an electrical examination will not always yield
positive results in chronic myelitis, yet no case of chronic myelitis
with complete or nearly complete paraplegia but will show at least
quantitative changes of such extent as to prove beyond doubt that the
case is of an organic character.

[Footnote 153: I have observed for two years a stationary brachial
diplegia, of undoubted hysterical origin, although the patient had
never shown any ordinary hysterical manifestations, and had had no
other hysterical symptom than chromatopsia, and that only for a short
period. From its long duration, constancy, and the resulting atrophy
of disuse it had been regarded as a case of peculiarly limited chronic
myelitis.]

There is one point in which spinal and cerebral disease involving the
motor tract differs in the majority of cases, which may be utilized in
{892} distinguishing obscure affections of the former from those of
the latter kind. In cerebral paralysis of any standing the superficial
reflexes, such as the cremaster and abdominal reflexes, are usually
diminished or abolished, while the deep or tendon reflexes are
exaggerated. In spastic conditions due to spinal disease—say sclerosis
of any kind affecting the lateral column and leaving the motor nuclei
of the anterior cornua unaffected—the deep reflexes are similarly
increased, but the cremaster reflex is increased also.[154] This
feature of the superficial reflexes is significant in the case of
cerebral disease only when unilateral.

[Footnote 154: Attention has been called, I believe, by Westphal, to
the fact that the cremaster reflex may not be demonstrable when reflex
excitability is at its highest, because the cremaster muscle is
already in extreme spastic contraction.]

The initial period of diffuse sclerosis is sometimes confounded with
rheumatism—an error less pardonable than in the case of tabes,
inasmuch as in diffuse sclerosis the pains are not usually
premonitory, but associated with motor paresis. It is erroneous to
regard a pain as rheumatic because it is aggravated or relieved by
changes in the weather. There are many subjects of myelitis who regard
themselves as veritable barometers, and with more justice than most
rheumatic patients.

In some cases of chronic alcoholism there are motor weakness and a
gait much like that of diffuse sclerosis.[155] It is to be remembered
that the solar tickling reflex is very often abolished in alcoholic
subjects, and profound diminution of the normal cutaneous sensibility
of the leg and feet usually coexist. But unless there is peripheral
neuritis—which is an exceptional and, when present, well-marked
affection—the absence of profound nutritive changes of the muscle, the
presence of the alcoholic tremor, the absence of sphincter and bladder
trouble, and the great variation of the symptoms from week to week,
and even from day to day, serve to distinguish the alcoholic spinal
neurosis from myelitis.

[Footnote 155: Wilks' alcoholic paraplegia.]


The Secondary Scleroses.

In studying the lesions underlying the symptoms of organic spinal
disease, the occurrence of fascicular scleroses, secondary to such
disease and due to the destructive involvement of nerve-tracts, was
repeatedly noted. Türck may be regarded as the discoverer of these
degenerations, and the reliability of this old observer may be
inferred from the fact that one bundle of fibres liable to individual
degeneration still goes by his name, and that, as far as he was able
to discriminate between the various paths which secondary
degenerations follow through the cerebro-spinal fibre-labyrinth, his
statements have not been materially modified by more recent
investigators, such as Bouchard, Vulpian, and Westphal.

The discovery by Meynert that the great cerebro-spinal tracts attain
the white color which they owe to the development of myelin around
their component axis-cylinders with advancing maturity, and that the
tracts of noblest, and therefore most intelligent, function were the
last to show this sign of maturity, was greatly extended by Flechsig,
who found that each tract receives its myelin at a definite period of
intra-uterine life, the lowest or the nerve-roots first; then the
short or intersegmental or—as {893} the physiologist may call them—the
automatic tracts; then the long or controlling tracts; and last, the
associating tracts of the cerebral hemispheres which mediate the
complex relations underlying mental action. It was this discovery
which gave a new impulse to the study of the secondary affections of
the cord and brain. The accuracy with which secondary degeneration
follows the lines marked out by the normal course of the tract is as
great, diminishing when the tract diminishes, changing its position or
direction and decussating where the latter changes its direction or
position or decussates, that it constitutes not alone an interesting
subject for pathological study, but has become one of the most
reliable guides of the cerebral anatomist. It is of great importance
to the pathologist to be able to differentiate between the primary
disease and its secondary results, and, as the controversy concerning
the so-called system diseases shows, even the most studious observers
are uncertain in this direction in many cases.

MORBID ANATOMY.—Secondary degeneration manifests itself by a
discoloration of the affected nerve-tract, which accurately
corresponds in area to the normal area of that tract. The more recent
the degeneration the less pronounced is this change. In advanced cases
the color may be a dark gray, in moderately old ones a reddish or
yellowish gray, and in those of very recent origin no change may be
visible to the naked eye. It is claimed, however, that even here a
loss of translucency of the white substance, giving it a sort of
cheese-like opacity, may be detected. On hardening the specimen
containing the degenerated tract in Müller's fluid or a simple
bichromate salt solution, the affected area, instead of appearing dark
on section in contrast with the gray substance—which in such
preparations appears yellowish or a light brown—contrasts with the
former by its lighter tinge. This contrast is observable even in cases
where the naked eye was unable to detect the change in the fresh
specimen. It can be sometimes found as early as the tenth day after
the primary lesion, and is apparently simultaneously developed in the
whole length of the nerve-tract affected.

The minute changes characterizing secondary degeneration begin in the
essential conducting elements, the axis-cylinder, which exhibits a
finely granular or molecular disintegration, and disappear. According
to Homén, it shows an initial swelling and a failure to stain properly
before this. The myelin then follows suit: it becomes fragile, forms
variously-shaped globules, and also disappears, and together with this
a nuclear proliferation is noticed in the interstitial substance;
fatty granule-cells are observed in large numbers, and manifest a
tendency to accumulate in the perivascular districts. These cells are
not permanent; their gradual diminution is accompanied by a
proliferation of the interstitial tissue, which ultimately appears as
a pure connective substance composed of fine fibrillæ arranged in
undulating bundles. The entire process may be not inaptly compared to
an hypertrophy of the interstitial substance resulting from
overfeeding of its cellular elements by the morbid pabulum furnished
through the disintegration of the nervous substance proper.

The disappearance of the nerve-tubes, and the formation of a new
tissue in their place, which, like all tissues of the same character,
undergoes shrinkage, leads to considerable deformity in the shape of
the part which is the site of secondary degeneration. This is seen in
the {894} accompanying figure, where in an old-standing secondary
degeneration of one interolivary layer the corresponding half of the
medulla is greatly reduced in diameter as compared with the other side
(Fig. 34), and the entire raphé is distorted. When one side of the
cord is the site of such a change a similar asymmetry results.

[Illustration: FIG. 34. Secondary Degeneration of Interolivary Layer:
_D Ds D_, degenerated area; _r_, the distorted raphé.]

According as the original lesion is incompletely or completely
destructive, a larger or fewer number of axis-cylinders may be found
preserved in the sclerotic tissue. It is not yet determined whether in
some instances these fibres may not represent an admixture from
another source than are comprised in the mainly affected tract.

Secondary degenerations are classified as ascending and descending. An
ascending degeneration is one which is found situated brainward of the
primary lesion; a descending one is found caudad of the lesion. It was
once maintained that the direction of the secondary degeneration was
constant for each individual tract. This seems to be true for a few.
Some tracts, particularly in the brain, degenerate on both sides of
the lesion, as I showed with regard to the interolivary layer.

The best studied form of secondary degeneration is that of the
voluntary motor conduit known as the pyramid tract. Beginning in the
so-called motor area of each cerebral hemisphere, the Rolandic loop
passes into the anterior part of the posterior half of the internal
capsule, to be thence continued through the crus, pons, and the
pyramids of the oblongata to the decussation or crossing-point of the
pyramids. Here the greater part of the tract crosses into the opposite
lateral column, occupying the position described in the section on
Spastic Paralysis. A smaller part remains on the same side of the
continuous interpyramidal and ventro-spinal fissure, constituting the
direct fasciculus of Türck.

The crossed-pyramid tract diminishes as it passes caudad in the cord,
giving off its fibres to the lateral reticular processes of the cord,
{895} whence—whether interrupted by cells (Von Monakow) or not—they
probably reach the great cells in the gray substance from which the
anterior rootlets spring. The direct fasciculus probably terminates in
a similar way, and perhaps makes good, as it were, its failure to
participate in the gross decussation at the level of the foramen
magnum by decussating in detail along its entire length. It is usually
exhausted before the lumbar cord is reached, whereas the crossed tract
in the lateral column continues down as low as the origin of the
sacral nerves. A destructive lesion anywhere in the course of the
pyramid tract, whether it be in the motor area of the cortex, in the
loop of Rolando, in the internal capsule, the pons, or the cord
itself, will provoke descending degeneration; that is, sclerosis of so
much of the tract as lies below the lesion. Thus such degeneration is
found with porencephalic defect of the motor area. I found it in a
paretic dement who had extensive cortical destruction following a
submeningeal hemorrhage. It has been observed after focal lesion of
the pons (Homén, Schrader), and after transverse lesions of the cord,
either myelitic, traumatic, or as the result of compression by
vertebral disease. As a rule, the cells in the anterior horn are not
involved, and some observers question whether this ever occurs. I have
never found such involvement, although in its gross dimensions the
anterior horn as a whole appears atrophied. This atrophy I have been
able to account for satisfactorily by the disappearance of many of the
fibres which run into the gray substance from the reticular processes.

While the distribution of degeneration in the cord is rather uniform,
varying only in harmony with the ascertained individual variations in
the relative preponderance of the crossed and uncrossed parts of the
pyramid tract, there is much more variation in the cerebral
distribution of the degeneration according to the extent of the
original lesion. Thus, if the entire capsule be destroyed, the greater
part of the crus is involved. If only the posterior division in its
anterior part be destroyed, the degeneration is in the crus, limited
to that part which runs a subpial course on the crural demi-cylinder,
occupying from a fifth to a third of its surface-area. Still more
limited degenerations are described, but as yet are too few in number
to base other than tentative conclusions on them. Among these is one
occupying a thin strip on the inner side of the crus, which
degenerates after lesions near the genu of the capsule, and probably
represents the tract which governs the cranial nerve-nuclei. An
excellent observation by Von Mannkopf shows that the course of the
motor fasciculus is subject to some individual variation even within
the capsule.

A number of forms of secondary degeneration are described, involving
intracerebral tracts, such as those connecting the cerebrum and
cerebellum. The degeneration of the visual tract, from the optic nerve
to the occipital lobe, observed by Richter and Von Monakow, with some
conflict of opinion between these observers, is often as perfectly
demonstrative of the course of the optic fasciculi as degeneration of
the pyramid tract is demonstrative of the course of the voluntary
innervation of the muscles moving the limbs.

The secondary degenerations following lesion of the pons varolii are
acquiring special interest in view of their relation to special
nerve-tracts of the spinal cord of hitherto unknown function. The
purest instance {896} of an isolated degeneration of other than the
pyramid tract is the case illustrated in the accompanying diagrams. It
involved the interolivary layer, was both ascending and descending,
being traced above into the subthalamic region, and below decussating
into the opposite side of the oblongata, to terminate in the nuclei of
the columns of Burdach and Goll. The leading symptom manifested by the
patient was a hemiplegia of the muscular sense.[156]

[Footnote 156: Besides my case, others have been recorded by Homén,
Meyer (Strassburg), and Schrader, which are impure. In the former and
latter degeneration of the pyramid tract, in the second degeneration
of the olivary fasciculus, coexisted. It is not generally known that
Westphal, in one of the first volumes of the _Archives_ now edited by
him, found an ascending degeneration of the same tract for a short
distance.]

[Illustration: FIG. 35. Secondary Degeneration of Interolivary Layer,
Caudal or Descending Portion: A, in caudal half of pons; B, cephalic
end of oblongata; C, middle of oblongata; D, at level of so-called
upper pyramidal or interolivary decussation; E, at level of true
pyramidal decussation. The atrophy in this level has entirely crossed
the middle line; in D it is seen in the act of crossing.]

Ascending degeneration is found in a very distinct form after
compression of the cauda equina. It is limited to the posterior
columns, occupying nearly the entire area of the latter in the lumbar
cord, particularly the triangular field of Burdach's column mentioned
in the article on Tabes. In the dorsal and cervical cord it is limited
to the columns of Goll, and terminates in the clava of the oblongata
at the nuclei of those columns.

Higher lesions produce the same ascending degeneration of the column
of Goll, and in addition involve other, probably centripetal, tracts
which happen to be injured at their origin or in their course. For
example, a transverse lesion of the dorsal cord would produce
ascending degeneration for its whole length of the column of Goll and
of the direct cerebellar tract. In addition, it would, in obedience to
the law previously stated, produce descending degeneration of the
pyramid tract. This combination is almost a typical sequence of
compression myelitis of the cord, as {897} well as of ordinary
transverse sclerosis. Recently, Gowers[157] has described a secondary
degeneration in such a case of transverse lesion not previously
noticed. It is found in cases showing gross disturbance of cutaneous
sensibility, and occupies a narrow belt encircling the anterior
quarter of the circumference of the crossed-pyramid tract. It is
continuous, in my opinion, with a tract which in the upper cervical
cord is situated in a corresponding situation, and which degenerated a
short distance caudad in a case of secondary degeneration of the
olivary fasciculus described by Meyer, and in which similar sensory
symptoms were noted.

[Footnote 157: _Diseases of the Spinal Cord_, and _Neurologisches
Centralblatt_, 1886.]

[Illustration: FIG. 36. Decussating Degeneration of Interolivary
Layer: _Dr_, _Darc_, the crossing degenerated fasciculi; _Arc_, the
undegenerated fasciculi, after emerging from the partly sclerosed
raphé.]

CLINICAL HISTORY.—Secondary degenerations are passive results of other
more active processes, and few clinical signs are attributable to
them. The most important of these is the contracture which is found in
old hemiplegias, and attributed, like the secondary exaggeration of
deep reflexes in such, to the descending degeneration of the pyramid
tract. Bouchard believed that it was the retraction of the sclerotic
strand which acted as an irritant on the neighboring fibres. The
development of spastic symptoms in amyotrophic lateral sclerosis and
in focal lesions of the crossed-pyramid tract is in favor of this
view. On the other hand, the occurrence of flaccid hemiplegia, and its
conservation for years after the most extensive lesions, is against
it, as it is in these very cases that the secondary degeneration is
most intense. That the retraction of a {898} longitudinal strand
exercises any serious effect on neighboring and parallel fasciculi is
questionable, as the process is slow. There is, however, one situation
where such influence is very likely to occur—the decussations of the
oblongata. In the case already referred to, the retracting sclerosing
bundles undoubtedly must have exercised a damaging effect on their
fellows of the opposite side, which, interdigitating with them, were
compelled to pass through the sclerosing tissue. It has occurred to me
that the slight sclerosis which is sometimes observed in the
crossed-pyramid tract of the same side of a cerebral lesion, even
where that lesion is strictly unilateral, is due to a similar
influence. I think it can be shown that such sclerosis cannot be
traced to the primary lesion; it begins at the decussation, and it is
more than probable that the firm constriction to which the healthy
fibres are subjected in crossing through their shrinking fellows of
the opposite side is not alone the cause of the symmetrical yet
slighter lesion, but also accounts for the observation by Pitrés and
Charcot of a slight motor weakness observed on the same side as the
hemiplegia, producing lesion in ordinary cases of capsular
hemorrhage.[158]

[Footnote 158: Some of the French observers claim that this occurs
only in the early period, but a careful study of the matter by R.
Friedländer shows that the weakness of the side not usually regarded
as involved is found in the later periods, and well marked then
(_Neurologisches Centralblatt_, June 1, 1886).]

The PROGNOSIS and TREATMENT of secondary degenerations are practically
involved in the primary lesion which gave rise to them. The
contractures attributed to secondary sclerosis of the motor tracts is
to be treated on the principles mentioned in the following section.


The Treatment of Spinal Sclerosis.

As the histological character of the different forms of sclerosis is
similar—at least in the terminal period—the causes producing them
identical even in name, and the indications furnished by leading
symptoms analogous if not identical, the treatment of these various
disorders is naturally based on the same leading principles. There are
two objects to be aimed at in dealing with these chronic disorders:
The first is the cure or arrest of the morbid process itself; the
second is the amelioration of distressing and disabling symptoms.

It is generally recognized that a perfect cure of a sclerosis is a
consummation never to be realized by any plan of treatment now at our
disposal. The experiments of Kahler and others have shown that spinal
tissue, once destroyed, is not regenerated. The post-mortem
examination of cases of tabes which were considered as cured during
life (Schultze) has shown that the sclerosis had not been removed; the
process had merely become quiescent, and the apparent recovery had
been due to the vicarization of other nerve-elements than those
destroyed for the latter.

But if attempts at the regeneration of destroyed fibres and cells are
to be regarded as futile, the arrest of the destructive process is to
be considered as an object which offers better chances of realization,
and which is worth attempting for other than merely conservative
reasons. In a number of the forms of sclerosis described, notably in
tabes and the disseminated form, it is remarked that the
axis-cylinders lying within the {899} morbid district are in part
intact and in part but slightly affected. Here and there groups of
nerve-tubes may be found which retain even their myelin. While subject
to the vicissitudes inseparable from their position in the midst of
active pathological changes, these channels of nerve-force, though
anatomically patent, may have their function perverted or destroyed,
just as a nerve outside of the cord may be paralyzed by pressure or
anæmia though its structure be intact. Should the active phase of the
sclerotic process be arrested, these intact or nearly intact fibres
will resume their function, and thus an apparent improvement will be
effected. The spontaneous ameliorations in the course of tabes
dorsalis and the less marked ones of diffuse sclerosis, coupled with
temporarily improved sensation in the former and improved motion in
the latter disease, show that retrogressions of this character are
possible and do occur. How is the physician to imitate the action of
nature? how to intensify it so as to secure the permanent improvement
which nature unaided does not grant? The first factor to be considered
is the removal of the cause of the disease. A number of cases are due
to exposure to wet and cold and to over-exertion. Such exposure and
over-exertion, if not already rendered impossible by the disease, is
to be discontinued. A large number of cases of tabes—according to many
authors, a majority—a considerable number of cases of diffuse
sclerosis, and not a few of other forms, are connected with the
syphilitic dyscrasia. Here, at the very outset, we have a definite
indication for treatment, and while we may be disappointed in the
results of such treatment in a large proportion of cases, yet enough
of well-assured and substantial success has been and is obtained to
render it almost a matter of duty for the physician to try
antisyphilitic measures in every such instance.

The mixed treatment in chronic spinal disorders should be followed out
for long periods and faithfully. Most tabic and other sclerotic
subjects affected with constitutional syphilis are in what is called
the tertiary period of that disease, when iodide of potassium is less
useful than mercury. I have never gained anything by pushing either
drug to the extreme point in advanced cases, and it should be borne in
mind that mercurialization carried too far may itself prove directly
injurious to the nerve-centres.[159] In cases where gastric crises,
gross ataxia, muscular atrophy, and bladder disturbance have been of
long duration this treatment is rarely successful.[160] But in the
initial and early periods of tabes and in diffuse sclerosis of slight
intensity the effect is sometimes gratifying, and of such a nature
that it cannot be attributed to a coincidence with spontaneous
remissions of the disease. In one case both knee-jerks and the
pupillary reflexes returned, to disappear on premature discontinuance
of the treatment; and on resumption one knee-jerk again returned, and
has remained demonstrable now over half a year. In a second case the
fulminating pains and the bladder disturbance disappeared, a slight
indication of the pupillary reflex developed, and the patient has
remained stationary with this gain for a period of three {900}
years.[161] In a third case, one of established ataxia, with which
luetic osseous lesions occurred, the pupillary reflex has returned
twice, disappearing after the first reappearance. In one case of
combined sclerosis in which no syphilitic antecedents could be found
the paresis of the arms has disappeared, and the ataxic paresis of the
lower extremities has improved to such an extent that the patient can
stand with his eyes closed and his feet together, and on one leg with
the eyes open—feats which a year ago he was unable to perform. None of
the changes in symptoms taking place in these cases occur
spontaneously in sclerotic spinal disorders, and they must be
attributed to the treatment. Such treatment is best carried out in
conjunction with warm bathing. The Hot Springs of Arkansas, those at
Las Vegas, New Mexico, and the baths of Aix-la-Chapelle in Europe
enjoy a special reputation in this field. The springs of Arkansas, as
regards the intrinsic character of the water, possess advantages which
are probably not excelled by any European baths, but the therapeutical
management[162] is far from that ideal point of development attained,
for example, at Aix-la-Chapelle.

[Footnote 159: Mendel thus found in his experiments made on dogs,
developing cerebral disease from rotation with the head directed
toward the axis of rotation, that dogs who had previously received
subcutaneous injections of corrosive sublimate showed an increased
vulnerability to the action of the rotary apparatus.]

[Footnote 160: A remarkable exception is related in the section on
Chronic Myelitis.]

[Footnote 161: There was concentric limitation of all color-fields,
and only central perception of green; to-day, if anything, the
color-fields of this patient are a little greater than in the
physiological average. The case was undoubtedly one of initial tabes.]

[Footnote 162: Mercurial ointment is used by the hundredweight, to
quote the expression of a patient, and in certain establishments the
sufferers from the common taint plaster each other from head to foot,
as with mud, with this panacea for most of those ills which flock to
the springs. Still, there seems to be no doubt that enormous
quantities of mercury are borne well by those who use the baths, and
who under other circumstances are susceptible to its most undesirable
effects.]

Optic-nerve atrophy, according to the best authorities, constitutes a
contraindication to the use of mercury in any form. It may be laid
down as a general rule that the more rapidly the symptoms indicating a
sclerotic process are developed, and the more recent its advent, the
more energetically should the treatment be pushed. Mercurial
inunctions and the so-called heroic doses of iodide are to be
employed. But in cases progressing slowly and of long antecedent
history what may be called a dilute plan is more apt to yield good
results. Small doses of mercury,[163] given steadily for years, and
iodide of potassium, administered in well-tolerated doses for periods
of ten days, alternating with corresponding periods of intermission,
have, in my opinion, delayed or arrested the progress of tabes and
other forms of sclerosis for the long periods referred to in the
preceding sections.[164] Although the antisyphilitic measures adopted
in sclerosis of syphilitic origin are the most important, and the
prognosis of no such case can be regarded as hopeless as to recovery
or duration until they have been tried, other procedures, detailed
under the head of Peripheral Treatment, should not be neglected. While
some very severe cases improve rapidly on antisyphilitic treatment,
other much less severe and more recent cases, in which the same cause
is assigned with equal reason, are not affected by it in the slightest
visible degree. The reason for this difference is unknown, but it
necessitates the bearing in mind that by {901} limiting the treatment
to the etiological indication valuable time may be wasted in which the
symptomatic indications could be profitably followed.

[Footnote 163: The tablet triturates of biniodide of mercury or
corrosive sublimate furnished by Fraser & Co. of New York I have found
peculiarly useful; one one-hundredth or more of a grain may be thus
administered every two to four hours.]

[Footnote 164: I am now employing the same treatment in some cases
showing no syphilitic history. If any medicinal measures can act upon
connective-tissue proliferation, it is these very ones.]

In cases of sclerosis due to other causes than syphilis a number of
medicinal agents have been recommended as calculated to affect the
central disease directly. Ergot is recommended in sclerotic troubles,
particularly tabes, by a large number of writers. It is admitted that
this substance can produce tabes itself, so that its administration in
the large doses recommended by some is not without its possible
dangers. I have seen a patient well advanced in the disease who had
received the drug for three weeks consecutively in such
quantities[165] that on estimates made I came to the conclusion that
he had received more than some of the persons in whom Tuczek
discovered the development of ergotin tabes. Favorable results are
reported ensuing after its use in the early stages, particularly where
signs of irritation preponderated, such as lightning-like pains,
hyperæsthesia, and frequent erections; and it has been suggested that
the beneficial action is due to an effect on the blood-vessels, which
are supposed to be congested in the beginning of the disease. Proof of
such congestion has not been furnished: the vessels are usually
sclerosed and their lumen narrowed. In view of the undeniable danger
which attends the administration of ergot in tabes, it may be properly
insisted that its indications be more precisely formulated than has
yet been done. It is commonly noticed in the natural progress of tabes
that the lightning-like pains disappear, usually about the time the
anæsthesia becomes greater. The anatomical parallel is supposed to be
the destruction of the nerve-tubes whose previous irritation caused
these pains. If, as is claimed—and it seems to be
substantiated—ergotin does produce amelioration of the lightning-like
pains, it would prove a damaging revelation which showed that it did
so in imitation of the natural process; that is, by increasing the
sclerosis.

[Footnote 165: An expert ophthalmoscopist found that the retinal
vessels, which were somewhat dilated in this patient, were not
influenced by the treatment.]

The first drug to which an influence was assigned upon the sclerotic
processes, and which has maintained its reputation longest, is nitrate
of silver.[166] Its claim to being regarded as a remedy may be best
characterized by the fact that an author who is far from being
prejudiced against it, and who recognizes the claims of Wunderlich,
its advocate, speaks of it as a valuable placebo.[167] I have never
obtained any effects from this drug in the scleroses, or from the
chloride of gold, which has been also recommended for these
affections, nor have I seen any in cases where either or both had been
faithfully tried by others for years. The same is to be said of the
chloride of barium, which has been warmly extolled on the basis of a
very limited trial in disseminated and diffuse sclerosis.

[Footnote 166: One of the first patients on whom Wunderlich tried this
drug died while I studied at Leipzig. He had extensive argyria and
sclerosis of the posterior columns.]

[Footnote 167: Leyden, _op. cit._, vol. ii. p. 359.]

The direct application of the galvanic current to the spine is
recommended, more particularly by Erb and Neftel.[168] I am unable to
state {902} anything regarding currents derived from as many as twenty
of Siemens cells and applied in the ascending direction, as the latter
recommends beyond an experience which occurred in the practice of a
colleague, who, alarmed by the event to be related, referred the
patient subjected to this treatment to me. The patient suffered from
tabes dorsalis, the symptoms being limited to the lower extremities,
the ulnar distribution, and the pupils. The belt was in the lower
thoracic region; the ataxia and lightning-like pains were not great.
After a single application of an ascending current from twenty-two
cells, continued for ten minutes, the patient suddenly felt a severe
dull pain in the occiput and terrible lancinating pains in the
distribution of the occipital nerves. With this there occurred
scintillation before the eyes, and at the subsequent examination I
found that the belt sensation had moved into the neck. The coincidence
was so close, and sudden changes in the distributional area of tabic
symptoms are otherwise so uncommon, that I attributed the observed
change to the treatment.

[Footnote 168: In describing a case in which this measure not only
ameliorated lancinating pains and vesical symptoms, but also, applied
to the head, relieved the diplopia—usually a spontaneous occurrence,
according to both American and European writers—this writer takes
occasion to state that in the year 1869 tabes dorsalis was practically
unknown to American physicians (_Archiv für Psychiatrie_, xii. p.
619). Duchenne described progressive locomotor ataxia in that and the
preceding year; the necessity of referring to the unfamiliarity of
American physicians with a disease not at the time recognized on
either side of the Atlantic is hence not apparent. Leyden (_op. cit._,
vol. ii. p. 325) candidly admits that the German medical profession
was at first averse to recognizing Duchenne's limitation: this
reproach cannot be laid at the door of American physicians, as I can
distinctly recollect the demonstration of several well-marked cases
exhibiting the characteristic symptoms then known, in the year 1870.
The disease obtained recognition in American textbooks and journals as
early as in those of any other land.]

Erb does not recommend such powerful applications. But the most
sanguine electro-therapeutist must admit that the action of galvanic
currents on the spinal cord is an exceedingly uncertain one. It is
questionable whether weak ones deflect sufficient current-loops to
reach the cord and to exert any material effect. As to currents
powerful enough to produce an effect, it is not known, except in the
loosest and most empirical way, what that effect is. The procedure
followed by Erb is to use large electrodes, the cathodal one being a
little smaller than the anodal, the former being placed stabile, over
the upper cervical sympathetic ganglion of one side, the latter
labile, on the opposite side of the vertebral spines, moving gradually
downward, the session not exceeding three minutes. This is repeated
daily or every alternate day.[169] It would prove a strong proof that
this treatment really affected the morbid process in a remedial
direction if any of the exact signs of the disease were to be modified
by it, be it ever so slightly. If, after galvanization of the cervical
cord and the sympathetic nerve, the initial myosis of tabes were
temporarily lessened or the reflex contraction to light restored for
ever so short a time, a brighter future would dawn for
electro-therapeutics than seems now to be in store for it.[170]

[Footnote 169: Why, if the procedure be really remedial or efficiently
palliative and devoid of evil consequences, it is not recommended to
be repeated oftener I am at a loss to explain or understand. There are
some factors involved in practical electro-therapeutic which it is
scarcely possible to discuss without encroaching on delicate ground.]

[Footnote 170: In healthy persons the extent of the knee-jerk is
increased by the spinal ascending galvanic current, and possibly this
observation may lead to the establishment of a rational basis for its
use in cases where the reflex is abolished or diminished.]

Peripheral Treatment.—A number of therapeutical applications are made
to the periphery where the symptoms of the sclerotic process are
localized. The rationale of such applications is based on the
assumption that peripheral conditions are capable of modifying the
nutrition and functions of the cord. This is proven not alone by a
host of observations made {903} on the normal cord, but is also
disastrously illustrated in the part played by surface chilling in the
etiology of many acute and chronic diseases of the cord.
Notwithstanding this latter, a large and influential body of German
neurologists recommend cold baths and cold spinal douches in these
affections. I have seen such excellent results from the use of warm
baths that I am compelled to plead, in defence of my ignorance of the
effect of cold ones, that I have never dared to use them. In numerous
cases the beneficial effect of a warm bath is almost instantaneous.
Warmth in any shape, whether atmospheric or in the shape of baths, is
usually agreeable to patients suffering from the various forms of
sclerosis. Cold, on the other hand, is disagreeable, aggravates the
symptoms, and in many cases at least hastens the progress of the
disease. A winter spent in the latitude of New York or Boston means so
much ground lost by the patient, and a sojourn during the colder
months in Southern California, New Mexico, Florida, or the West Indies
enables the patient to avoid this loss. As regards the choice of
climate and baths for sclerotic patients, I should be inclined to
roughly formulate the indications as being identical with those of
chronic rheumatism. The reaction against the use of warm baths in
Germany, where they once were popular,[171] is due to the employment
of too high temperatures. Hot baths, in the strict sense of the term,
including the various forms of vapor-bath, act badly. They increase
instead of calming the irritative symptoms, as moderately warm baths
do, and they entail too sudden a change in the bodily state. That, for
the present, it is advisable not to adopt unreservedly either the
extreme plan once in vogue or the equally extreme one which
constitutes the reaction against it, is shown by the observations of
Richter of Dalldorf, who records some discouraging results obtained by
the use of cold baths in cases of tabes dorsalis. It is but necessary
to refer to the fact that the lancinating pains of the latter disease,
the rigidity of diffuse myelitis, and the spasms of lateral sclerosis
are usually most severe in cold weather, and that the diseases
mentioned appear to be rare in warm countries, to show the need of
caution in using a therapeutical measure so similar in its action,
even if it be but momentary and followed by a reaction, to those which
provoke or aggravate the original disease. Eulenburg has seen five
recoveries in tabes, and under such different plans of treatment that
the latter is not credited by him with the good result. Three were
treated with warm baths, one with cold baths, and one with nitrate of
silver. It is seen here that the warm baths were used with good
results more frequently than the cold.

[Footnote 171: The mud-baths of Cudowa in Gallicia had a very high
reputation.]

One of the most singular delusions of modern
therapeusis—nerve-stretching—has, following the prediction made by
several on both sides of the Atlantic, become obsolete. Introduced by
Langenbuch, a surgeon, and attacking the disease at the sciatic
nerve—a point where, as well-versed students knew, it was not
located—the operation was looked upon with distrust from the
beginning. The enthusiasm with which it was taken up by surgeons and
by the interested portion of the laity—ever hopeful as tabic patients
are of new drugs and methods of treatment—has led to a large number of
trials, now numbering several hundred, and from which the useful
lesson can be gathered that the good ripens slowly. Nerve-stretching
in an organic disease of the spinal cord may take its {904} place
among the needless vivisections; it has not influenced the progress of
a single case in any essential feature. On the contrary, it has more
than once been directly responsible for acute myelitis, spinal
hemorrhage,[172] and pyæmia. In a number of cases reported by
Langenbuch,[173] Benedict, Erlenmeyer, Schweminger, Debove, and W. J.
Morton, the ataxia of the patient has been reported as relieved; in
one case, exhibited by the latter operator before the American
Neurological Association, this appeared quite evident, but not because
the disease proper had been influenced, but for the same reason that
prevents the development of marked ataxia in combined sclerosis. Just
as the lateral-column lesion inhibits the ataxia which is due to the
posterior-column lesion, so the motor paresis produced by stretching
the sciatic nerves neutralizes the manifest features of the ataxic
gait. As soon as the paresis is recovered from, the ataxia returns in
its original form, unless, happily, one of the common spontaneous
changes for the better occur. As a therapeutic procedure
nerve-stretching is to-day properly limited to affections of the
peripheral nerves.

[Footnote 172: Zacher, _Archiv für Psychiatrie_, xv. p. 430.]

[Footnote 173: Westphal showed after the autopsy of Langenbuch's first
successful case that there had been no spinal lesion whatever.]

One of the most useful peripheral remedies in the sclerotic processes
is the faradic wire brush. It is both an anodyne and remedial for
anæsthesia. A number of the tabic patients to whom I referred as not
having deteriorated within long periods are provided with a portable
faradic battery, and apply the brush to the spots affected by
terebrating pains the moment these commence, obtaining instantaneous
relief. As has been shown by Rumpf,[174] the cutaneous space-sense
becomes more delicate in healthy and improved in tabic patients under
its continued use. And while the inco-ordination of tabes is in part
independent of the disturbance of cutaneous sensibility, yet if the
latter can be refined the ataxic disturbance may be mitigated—a result
occasionally obtained through the methodical use of the wire brush.

[Footnote 174: Report of a discussion, _Neurologisches Centralblatt_,
1885, p. 526.]

It is frequently found that sufferers from tabes dorsalis and other
forms of sclerosis accompanied by ataxia walk much better in their
stocking feet and in slippers than they do in the conventional street
shoe or boot. The reason for this is obvious. The patient's gait is
impaired by the disease, and, whether the ataxia be a pure
co-ordinatory trouble or no, subjective uncertainty regarding contact
with the ground which is experienced by most ataxic patients is an
aggravating factor. Our modern foot-clothing, with its inflexible
soles and raised heels, handicaps the patient as it were, depriving
him of the use of what little tactile sensibility may be left
him.[175] The use of low-heeled shoes with thin and flexible soles is
therefore advantageous.

[Footnote 175: The question whether tabes dorsalis is a disease of
civilization has not been raised in any treatise I am acquainted with.
Myelitis, both acute and chronic, occurs, however, rarely in the lower
animals, as do also central dilatation of the cord and congenital
defects of the latter. Posterior sclerosis I can find no record of in
veterinary pathology. The influence of the repression of normal aids
to locomotion by the foot-gear of civilized life as a possible
predisposing factor in the etiology of ataxic troubles is a legitimate
subject of inquiry. The lateness of the infant of civilized parents in
acquiring the art of skilled locomotion may be in part, as
philosophers claim, a penalty of exuberant development of the higher
and inhibitive centres. But what part has the artificial obliteration
of solar sensibility and pedal flexibility played in this inherited
feature? What is its influence in establishing a pathological
vulnerability?]

{905} The tremors of sclerotic affections, particularly those
accompanying the disseminated forms, are from their distressing
character prominent objects of special treatment. The bromides have
been given with alleged good effect which I am unable to confirm.
Curare has caused the tremor to disappear for two days in one of
Erlenmeyer's patients. I have seen good results from the descending
galvanic current applied in long sittings to the head and neck,
sliding in to the point of tolerance, and sliding out before
discontinuing. The mydriatics, atropine, and particularly hyoscyamin,
often remove tremor radically for the time being; unfortunately, it is
necessary to give them in almost toxic doses to obtain this effect.
Recently, Feris recommended veratrum in doses of half a milligram
repeated every four to five hours. It acted very well in every case in
which I tried it, but, as it became necessary to increase the dose,
the same objection was encountered as in the case of hyoscyamin. All
these measures should be used as emergency remedies only; they cannot,
in the nature of the case, prove curative, while their continued use
produces a physiological indifference to their effect, and to that
extent decreases their value as the case progresses.

MANAGEMENT OF SPECIAL SYMPTOMS AND COMPLICATIONS.—Among the most
distressing features of many sclerotic affections is pain, which is
usually associated with sleeplessness. The fulminating variety may be
often relieved by the use of the actual cautery applied over the
affected level of the cord and along the course of the nerve involved.
But in the majority of cases morphine will have to be resorted to. Erb
cautions against the use of this anodyne in cases where there is much
reflex irritability of the cord, as morphine is said to increase this
irritability when administered in small doses, and to reduce it again
only when larger ones are administered. It is the latter alone which
are serviceable with pain, and I have not yet seen any bad effects in
the direction apprehended by Erb from such doses as it is necessary to
give. That the physician administering it should be always on guard
against the possible formation of a drug habit it is unnecessary to
add. But it is also unnecessary to add what alternative he shall adopt
when his choice lies between the lesser evil of the opium or morphine
habit and the terrible martyrdom which some patients would be
compelled to submit to if not allowed to indulge in it.[176] The evil
effect of opium and its preparations on the visceral functions is to
be neutralized, as far as possible, by the administration of laxatives
and bitter tonics.

[Footnote 176: Few sufferers from spinal disease use anodynes
habitually; opium and its preparations are not fascinating to the
majority of persons. On the other hand, there are two cases of tabes
dorsalis now under my observation in which the patients have been
compelled to use hypodermic injections of Magendie's solution for two
and three years without any materially bad effect.]

The deep-seated diffuse pains, such as are found in disseminated and
diffuse sclerosis, are not as markedly relieved by opium as the
terebrating and lightning-like variety. Frequently spastic or other
signs of increased reflex excitability are associated with them; and
as both are favorably influenced by the bromides, the latter are
doubly indicated in such conditions.

With pains of a rheumatic character static electricity has been
recommended. It undoubtedly relieves such pains, as skilfully-applied
{906} galvanism would. Its chief effects, it seemed to me from a six
months' trial with it, are on the imagination and hopes of the
patient.[177]

[Footnote 177: A large apparatus of the new and improved make was at
my disposal at the nervous department of the Metropolitan Throat
Hospital. It was very popular with sufferers from rheumatism, who had
been allowed to accumulate in the class before I took charge, and with
a paretic dement who suffered with the rheumatoid pains often found
with diseases such as his.]

The bromides and camphor[178] are recommended for the obstinate
priapism found in some cases of early tabes and transverse myelitis. I
have seen better results from warm hip-baths and general baths in this
condition than from any drug. As a general rule, the exercise of the
sexual function, where not already forbidden by the results of the
disease, should be limited as much as possible. The frequency of
normal seminal emissions in a given case is a guide to the amount of
indulgence in this direction which may be permitted. Where there is
the slightest indication of irritative or destructive lesions in the
upper lumbar cord sexual acts should be entirely prohibited, for under
these circumstances no greater injury could be done the weakened
centres than to permit them. This is particularly noticed in those
cases of tabes dorsalis which are marked by satyriasis in the early
period.

[Footnote 178: Particularly the monobromate of camphor.]

The treatment of the bladder trouble and of bed-sores is carried out
in the manner described in the section on Acute Myelitis. For
bed-sores Hammond recommends the application of a stabile galvanic
element consisting of a plate of silver and one of zinc, the two being
united by a wire isolated in the usual way. The silver plate is laid
on the bed-sore; the zinc plate, covered by a piece of moistened
cloth, is laid on the unbroken skin somewhere in the neighborhood. The
result is a weak current under whose stimulant effect the healing
process takes place very rapidly. I have seen excellent results that
had been obtained by this means in indolent ulcers of the leg. It does
not, however, seem to have been tested with the malignant variety of
bed-sore.

With regard to the management of muscular atrophies by electricity,
massage, and strychnia, the same rules are to be followed which are
laid down in the section on the Myopathic Atrophies. It is only to be
specially remarked that few authorities encourage the administration
of strychnia in sclerotic affections, and fewer still in such large
doses as could be of any benefit in a wasting process.

Faradization of the affected eye-muscles is often useful in diplopia.
The current may be applied by means of a cup-shaped eye-electrode, or,
better, by using a finger as an electrode.

The moral management of sufferers from sclerotic spinal affections is
very important. The popular notion about spinal disease generally is
such that the announcement made to a patient that he is suffering from
any form of it is as alarming as would be the discovery of a tumor in
his brain or a cancer in his stomach, and exerts a depressing effect.
This it should be sought to avoid. A large number of sufferers from
sclerosis live longer and suffer less than a portion of those
afflicted with rheumatic and gouty affections; and the physician is
justified in obtaining the desirable effect which a hopeful or
resigned state of the mind undoubtedly has on the body, by laying
great stress on this undeniable fact.


{907}


CONCUSSION OF THE BRAIN AND SPINAL CORD.

BY WILLIAM HUNT, M.D.


The writer was asked to contribute a short article upon Concussion of
the Brain and Spinal Cord for this work, as these injuries are apt at
first to come under the notice, if not charge, of the general
practitioner. The article will therefore not be an exhaustive one, and
there will be little but the details of personal experience and less
quoting of authorities. Much has been written recently upon the
subject both in volume and in pamphlet.

Diverse views of equally competent judges of the matter have been put
forth, and the brains and spinal cords of the partisans appear to have
received as severe a shaking up as the real recipients of the lesions,
if absolute lesions there be.

This, in fact, is the point of controversy, for there are those who
seem to deny that there can be a jarring or shaking of the
cerebro-spinal mass sufficient to cause positive symptoms without
producing positive lesions, whilst others are as firm in their
convictions that pronounced symptoms may follow a mere disturbing
ripple of the nervous elements. How is the question to be settled? The
slightly shocked or injured recover rapidly, whilst some who only
appear to be as slightly injured or shocked at first, go on to death,
during the progress to which event there is no doubt as to the
existence of lesion and no difficulty in finding it at the autopsy.
Hence, say the lesionists, the first ones had it, but got well, whilst
the non-lesionists affirm that it never existed in them.

The logician would think that these differences in opinion were only
differences in degree about the same thing, but, nevertheless, the
question is one for serious discussion, and is of much greater
importance than would appear to be the case to the average layman.

This importance lies in the medico-legal aspects of the suits arising
out of the alleged injuries and their consequences. Judges, lawyers,
and doctors know them well. In doubtful cases authorities of equal
eminence are quoted, and the results of trials are equally as doubtful
as to whether justice or injustice has been done. These remarks, as
will be seen, are especially applicable to injuries of the spine, but
they also may have place in the consideration of consequences arising
from concussion of the brain.


{908} Concussion of the Brain.

Whatever doubts there may be as to concussion of the spine, there are
none, I believe, who deny the appropriateness of the expression as to
the brain, it being, by its anatomical relations, so much more exposed
to shock than the spine.

We understand that pure concussion, uncomplicated with fracture,
refers to a condition caused by external violence, direct or indirect,
which communicates a jar or shock to the cerebral mass, and which
expresses itself by certain well-defined symptoms. The nervous system
and the circulation are most manifestly involved, but in a pure case
it may be said that all of the symptoms arise from central nervous
disturbance. Even could it be shown that they were dependent on
temporary congestions, these congestions, I think it will be admitted,
would be due to vaso-motor derangements.

The anatomical appearances after early death from concussion of the
brain are often insufficient for us to comprehend the fatal result,
for we know that the organ will bear, both from disease and other
kinds of injury, vastly greater inroads upon its structure and
surroundings without causing death. Often there is mere localized
cerebral congestion, with no ruptures of vessels; then there are
slight extravasations shown as points or dots of blood in the
nerve-matter; and, again, there is what is called the bruised brain.
Sometimes there is nothing abnormal whatever to be found. Most of
these cases, under modern criticism, have been justly shut out from
the record as having no value; for it has been shown that the
post-mortem examinations of them have been very imperfect, the brain
only having been inspected, whereas the chest, the abdomen, or the
spine might readily have revealed the cause of death.

It is fair, however, to assume that there must be a capacity for
serious results in the vibratory jar, as the discoverable lesions in
many well-examined cases have been in themselves insufficient to kill.
The rapidity of recovery of those who get well also bears weight on
this point.

Of nineteen cases of recovery from concussion of the brain of which I
have record, the average stay in hospital was eight days. The range of
stay was from one to twenty-five days. Many of these were at first
profoundly shocked, some of them apparently hopelessly so when we
compared their symptoms with those who died. As they recovered,
however, in so short a time, there surely could not have been any
gross lesion to account for their symptoms. What else, then, can
account for them than vibratory jar? and if this can produce such
severe results within the line of recovery, why cannot the degree of
it be so extended as to involve, for example, the respiratory centres,
and so kill without leaving perceptible sign?

The SYMPTOMS of concussion of the brain range from a mere daze or
stunning to those of deep unconsciousness. There is no paralysis of
the extremities in pure cases. Often the patient is very restless, and
throws his limbs about in all directions. When these are quiet there
is response to irritation and electricity. Loud speaking to him may
elicit some attention, but the answers are mostly incoherent. There is
pallor, often extreme, coldness of surface, and sweating. Vomiting is
usual, and may come on immediately or later, and it continues as long
{909} as there is anything to discharge; sometimes there is retching.
In favorable cases the cessation of vomiting is accompanied by a slow
return to consciousness, which may be preceded by delirium. This
return is never sudden, and the method of it serves to distinguish the
case from that of some forms of epilepsy. The pulse is generally
frequent and feeble, often irregular; in extreme cases it may be slow
and feeble, very rarely, if ever, strong or bounding. After reaction
it becomes more natural, and if recovery follows it will not show much
variation. The temperature is depressed at first. In one
characteristic case it was 98° on the first day, reached 101° on the
third day, and receded to 98½° on the eighth day, when the brain
symptoms disappeared.

There may be retention of urine and sluggishness of the bowels, but in
bad cases coincident with the vomiting there is sometimes involuntary
discharge both of feces and urine. The respiration is irregular,
sometimes almost ceasing, and then returning with great rapidity.

Much has been said and written about the condition of the pupils in
concussion of the brain. I have made this matter a subject of
observation, and am convinced that the state of the pupils is of no
diagnostic value whatever as to determining the existence of
concussion or compression. Their state is of great value in telling us
that the functions of certain brain-centres are partially or wholly
impaired. The progress of the case will tell us whether the impairment
is due to clot or effusion, congestion or jar.

It is wrong, therefore, to say that the pupils are one way in
compression and another in concussion. It is right to say that in
either case they are sluggish or wholly irresponsive to light. In one
person they may be dilated, in another contracted, and in the same
person the eyes may present marked contrasts.

In the light of modern physiology this is what might be expected. The
condition of the pupils is dependent on that part of their
nerve-connections which is involved in the injury, and also upon the
method of that involvement. Clinical experience, I think, amply
sustains this view.

The reaction from what may be called pure concussion is generally
slow. The patient is apt to be dazed for some time, although the pulse
and temperature may be normal. When there is a rebound with fever, and
florid complexion, and suddenly or gradually another but deeper
unconsciousness supervenes, it is almost certain that positive lesion
took place at the time of injury, and that the reaction has brought
with it great congestion if not extravasation.

Now, really, compression to be followed by inflammation is the
condition demanding attention.

DIAGNOSIS.—The history of the case and the symptoms as detailed will
enable us to reach a conclusion in most cases as to the existence of
concussion of the brain. There are some conditions, however, from
which it is to be carefully distinguished. These are simple fracture,
with or without depression, compression from any cause, drunkenness,
and epilepsy.

There may be such profound shock with fracture that at first
concussion symptoms mask those of the lesion, or even keep them for a
time completely in abeyance. The head bruises are often very deceptive
to the touch in the search for fracture.

{910} I am in the habit of directing students to feel their own
scalps, in order that they may appreciate the fact that the touch
gives no sensation whatever of the natural thickness of the cranial
covering. It seems as though something like a piece of thin parchment
only intervenes between the fingers and the bone. The fact is, the
scalp varies from an eighth to a quarter of an inch thick, differing
in different places, and where muscles, as the temporal, for example,
are beneath it, the bone is much deeper. The importance of this
observation lies in the fact that a pulpefied bruised mass of scalp
will cause the edges of its healthy surrounding part to feel almost
precisely like bone around the borders of a depressed fracture. The
accompanying general symptoms will mostly not be in accord with this
condition, but in some cases the deception is so complete that it is
very difficult to persuade those not familiar with the fact that a
fracture does not exist, and to induce them to refrain from rash
proceedings.

One case I can call to mind where the opinion of the attending
physician was only changed by the ultimate favorable result, which
left no sign of permanent injury of any kind. These cases are
particularly apt to occur with children.

I remember also another source of deception. A boy was severely
injured by a blow upon the forehead. Concussion was marked. There was
a lacerated wound reaching to the edge of the orbit; fractured bone
could be felt, and at first sight what appeared to be brain-matter was
oozing from the wound. A hasty unfavorable prognosis was given to the
parents. On closer examination it was found that the fracture was of
the external wall of the frontal sinus, and the supposed brain-matter
was the delicate fat-lobules of the orbit. The patient recovered
rapidly.

There is a marked distinction between the ordinary symptoms of
concussion and those of compression, whether from depressed fracture
or effusion, as of blood in apoplexy. Here there are flushed, often
swollen, countenance, stertorous breathing, slow and it may be strong
pulse, deep or absolute insensibility, and fixed pupils. The injury,
if there is one, is mostly palpable and explanatory. If it is
concealed, the other symptoms point to the true nature of the case.

The diagnosis from drunkenness is not always easy, although deep
intoxication is more apt to be accompanied with compression than with
concussion signs. Drunkards often have bruises on their heads caused
by falls, and some of them are pale and sick after debauch. The smell
of liquor is not always reliable, for it is so common after accident
for friends to administer stimulants before the patient is seen by a
medical man that he might be easily misled into too hasty a judgment.
The general appearance of the old stager is well known, but in cases
where there is the least doubt the patient, whether in hospital or in
private, should be kept a sufficient time under observation for the
effects of drink to pass off. Then it will be seen whether this has
masked a more serious condition. Too hasty conclusions in this matter
have led to most unpleasant occurrences. These are well known in
police administration and to hospital men.

The convulsions of the epileptic, the foaming mouth, and the quick
return to partial or complete consciousness will generally serve to
distinguish the case from one of concussion, but at times there are
those who {911} require also to be kept under observation for some
hours, and even a day or more, in order to come to a correct
conclusion.

The PROGNOSIS in concussion is generally favorable, but if complete
unconsciousness is present it is doubtful as to the individual so long
as this lasts, for, as before intimated, the cases which recover may
present as marked symptoms at first as those which prove fatal.

Recovery is mostly complete, but not suddenly so. The after-effects in
any case may prove serious.

There is, however, an unwarranted tendency to attribute any defect in
character, and even criminal lapses, to a blow upon the head,
especially should the history or marks of one be discovered as having
occurred at any time, no matter how long, previous to the inquiry.

The blow may be the cause of subsequent epilepsy, chronic
inflammations, and insanity or imbecility. These cases have, however,
an almost continuous history of trouble from the date of the injury,
the manifestations varying in severity from time to time as
pathological changes go on or as exciting causes develop them.

TREATMENT.—Absolute simple rest in bed is all that is necessary in
mild cases of concussion. The patient should be well watched for any
symptoms which might supervene and show that the injury was more
severe than at first supposed. On the other hand, serious symptoms may
be present without indicating any great gravity in the case. Children,
for example, often have convulsions from the slightest cause. I have
attended them when these set in immediately after the injury, but in a
day or two there was entire recovery.

The more serious cases equally require rest, but also something more.
To bring about reaction from shock, sinapisms to the extremities, to
the nape of the neck, and over the stomach should be used. Hot-water
bags should be placed along the sides of the body and limbs. Alcoholic
stimulants must be sparingly used, if at all: they are rarely
necessary. The stomach will often reject them unless in minute doses.
If too much is absorbed, unpleasant consequences to the brain may
follow. In extreme cases hypodermic injections of brandy or ether may
be administered. Ammonia, camphor, and other diffusible stimulants may
be useful, either externally or internally.

If the reaction is regular, with gradual restoration to consciousness
and no noticeable rise in temperature, nothing further is required but
a continuance of the rest and the use of cooling drinks and spare
diet. The bowels and bladder must be attended to; the catheter may
have to be used.

Restlessness, with or without delirium, is not unusual, but it
generally subsides under full doses of bromide of potassium.

When reaction is followed by high fever, and especially when there is
with it a passing on into secondary unconsciousness independent of
true sleep, we have almost surely internal compression from
congestion, effusion of serum, or hemorrhage to deal with. Now, blood
may be taken generally or locally with great benefit. Cups, both dry
and wet, to the temples and back of the neck are very useful. Leeching
also is an efficient method of depletion. Ice in bags or towels, or
cold water, should be applied to the head. Hot water, say about 120°
to 130°, to the head is often of great service and very soothing.

{912} The choice between cold and hot water is to be determined by the
effects produced. Sometimes surprisingly good results come from
alternating their use. Hot mustard foot-baths may be given in bed
while the patient is kept lying on his back with the limbs flexed.

The result only in these severe cases will determine whether the
symptoms were due to great congestion or to extravasation, possibly
with brain lesion. Complete recovery takes place in the first
condition. In the latter a fatal termination is much more probable,
and if there is recovery it is apt to be only partial, and the patient
may be the victim of nervous troubles more or less pronounced
throughout a long life.


Concussion of the Spine.

John G. Johnson of New York is authority for the statement that
English railways paid in five years two million two hundred thousand
pounds, or eleven million of dollars, as damages awarded by juries in
cases of concussion of the spine. The statement appears almost
incredible, but the facts are ample to sustain it.

It also illustrates the powerful influence of one great authority
(Erichsen) better than anything I know of in the history of the
medical profession. After this celebrated surgeon's lectures and work
on concussion of the spine, etc. were published, dating back to 1866,
the great body of medical men received them as the standard and guide
in all such cases. They were a godsend to plaintiffs and prosecuting
attorneys, and the defendant had a poor chance with juries when the
possible miseries of any one who claimed compensation for injury to
the spine was pathetically pictured to them.

That the defendants have suffered injustice in a great number of cases
I think there can be no doubt. Is it any wonder, therefore, that a
reaction has occurred of late, and that the views formerly held by
professional men have been subjected to sharp criticism founded upon a
much more scientific and practical knowledge of the subject at issue?

As in all reactions, extreme views have been reached by certain
observers, and there are those who seem to hold that concussion of the
spine cannot occur. By spine here is meant the spinal cord or marrow.

It has been well remarked, I think by Page, that we do not speak of
concussion of the skull. We always say concussion of the brain. The
use of the term spine has given rise to much confusion, but the
professional man will understand what is meant when so-called
concussion of the spine is under discussion.

The advocates of the rarity or even impossibility of the injury call
attention with much force to the anatomical facts. First, to the
immense strength, pliability, and cushioning of the bony and
ligamentous encasement or column; then to the ample calibre of the
canal in which the nervous cord is suspended, and to the pliant
structures intervening between its inner walls and the cord itself.
From without inward, in the canal, we have fat, watery connective
tissue, and the plexus of spinal vessels; then comes the dura mater,
loosely investing the cord and unattached to the bone, not forming
here, as in the skull, the internal periosteum. Within the dura mater
is the arachnoid, its visceral layer {913} separated by a wide
interval from the viscus or cord, which interval contains the
cerebro-spinal fluid; then the pia mater or vascular membrane, which
closely invests the cord.

Besides these structures there is the ligamentum denticulatum passing
from the dense pia mater to the parietes of the canal and supporting
the cord and roots of the nerves in the most efficient way—pliable
enough to yield and break the force of vibrations, and strong enough
to sustain.

Thus we see that the cord is much more securely protected from the
effects of external violence than the brain, and we can understand
that there is reason for the doubt of the sceptics as to the frequency
of the injury described as concussion of the spine.

Clinical observation is, I think, of far greater value in determining
questions of the kind than any theory, however strongly supported by
anatomical facts. Does transient concussion of the spine occur as
transient concussion of the brain occurs? Page, if I understand him,
says not. In his work on _Injuries of the Spine and Spinal Cord_
(London, 1883), in criticising a well-known case as to the claim of
persistent paraplegia without discoverable lesion, he says: “We
italicize the word persistent, for simple concussion of the brain may
give rise to a transient unconsciousness, and, if the analogy holds
good, concussion of the spine should per se produce a transient
paraplegia. _We know of no case, nor can we discover the history of
any case, where this has happened._”

I italicise the last sentence. In 1881 a boy came under my care who
was shot in the back three inches to the right of the third or fourth
dorsal vertebra. He at once had characteristic symptoms in the legs of
being wounded in the spine in such a way as to affect the cord
somehow. There was partial paraplegia, with pains in both limbs. Under
rest these symptoms soon disappeared. In a few days I made a deep
incision and removed some clothing and fragments of bone, and then
from the depths of the spinal gutter I took a large conical ball which
was resting against the bony bridge of a vertebra. The boy recovered
rapidly. I saw him some months afterward perfectly well.

Surely, this was a case of spinal shock or concussion with transient
paraplegia, and the cause of it could have been nothing else than the
impact of the ball against the column, producing vibratory jar
sufficient to affect the cord. The immediate symptoms and the rapid
and complete recovery are, in my opinion, inconsistent with any theory
of congestion or pronounced lesion of the medulla.

Here is another case of transient paraplegia also occurring in 1881,
and, to my mind, still more significant: A man fell from a height of
about twenty feet and landed directly on his feet. He was immediately
paraplegic. On examination no injury to the spinal column could be
detected, but there was fracture of both calcanea. The spinal symptoms
were thoroughly marked. Besides the paralysis of the limbs there was
loss of control of the bladder and bowels, and the other accessories
in such cases. But all went on to recovery. Pari passu with the
fractures the spinal symptoms improved. It is not necessary here to
give further details, but simply to state that in four months, the
time required being chiefly due to the fractures, the patient was
discharged able to walk and well in every other respect.

If this is not a case of transient paraplegia owing to spinal shock or
{914} concussion, I am willing to admit that I do not know the
requirements of the critics when they ask for such cases. I think that
it is no matter how the blow or shock to the column is received,
whether direct or indirect, so that it is shown that the medulla is
influenced within the line of recovery, without having suffered fairly
presumable lesion.

President Garfield surely suffered from transient spinal shock
produced immediately by impact of the bullet upon the column. The
symptoms soon passed off, and at the post-mortem the cord was healthy
in every respect. The differences between his case and the others I
have mentioned were those of degree only, his concussion not being
severe enough to cause paraplegia.

Spinal concussion or shock from railway collisions does not differ
from forms of the same injury received in other ways. It is absurd,
therefore, to give a peculiar pathological history to so-called
railway spine. That the injury occurs, I have no doubt; that the
medulla is seriously affected in the vast majority of cases, I have
very great doubt.

I cannot now, after thirty years of hospital and private practice,
call to mind a single case of concussion of the spine arising from
other accidents than on railways which has had the terrible
after-history that is so often attributed to them; and I have seen in
that time many cases of spinal injuries of all kinds.

There is another fact of personal experience. I have examined many
cases of claimed irreparable or serious injury to the spine in
private, both for plaintiff and defendant, in impending suits, but I
cannot remember a single application of a patient for admission to the
hospital to be treated for the after-effects of concussion of the
spine, the original injury having been received in a railway
collision.

As all sorts of people ride on railways, it is strange that the
numerous recipients of concussions of the spine are pecuniarily
independent of hospitals. One old fraud I do remember who fell from a
street-car and claimed lasting injury to the upper part of the spine
and the head, and adequate compensation for it in court. I was not
called as a witness at the trial, and the plaintiff recovered very
heavy damages. These were afterward reduced to a much smaller amount
when it was discovered what I knew about the case.

Other structures of the spine besides the medulla are much more
subjected to injury than it is, and their consequences often mislead
both patient and doctor, especially the former.

The ligaments and muscles are exposed to contusions, strains,
ruptures, and twists which are wrongly attributed to concussion. From
these injuries and from so-called concussions the patient recovers
rapidly or slowly according to their extent. If damages are looked for
from a corporation, he is in a state of what may be called expectant
pecuniosity, and shows no amendment until the question is settled.
Otherwise, he gets well, as those do who are injured but have no
expectations.

There is a striking want of confirmation by post-mortem examination of
the terrible effects which are said to follow concussion of the spine.

In fact, the records of such examinations are so few, notwithstanding
the immense number of those who have claimed to have the injury that
the sceptics are somewhat justified in attributing the few cases which
have shown great pathological changes in the cord and its membranes to
the {915} coincidence of disease, as myelitis or syphilis, or to much
graver injuries than concussion.

I have reported a case in full in the _Medical News and Abstract_
(Philada., Nov., 1881) which illustrates how coincidence might easily
play its part in a supposed concussion. This feature of it is not
alluded to in that paper. A gentleman began to complain of pain
posteriorly at the root of the neck. Paralytic symptoms gradually
developed. It is unnecessary to repeat the details here, but the
history was a most dreadful one, and precisely that of the few serious
ones described in the works on concussion. Within a year the patient
died. The autopsy revealed a meningitis and softening and destruction
of the cord to the extent of two and a half inches of its brachial
enlargement. There was no other disease. Now, this patient frequently
travelled on railways, and if he had been subjected to the slightest
accidental shock it would have been received on all sides as the cause
of the disease. There was, however, no such history, nor was anything
ever known to account for the fact that a man in otherwise perfect
health should have two and a half inches of his spinal cord as it were
spontaneously destroyed.

I will state in passing that this case did not confirm the views of
Johnson and others as to there not being any severe pain on pressure
in myelitis. It showed also that clinical observation is not always in
accord with plausible anatomical facts or reasoning.

Thus, Johnson says: “It is a mistake to suppose that meningitis or
myelitis is accompanied by pain on pressure: the spinal cord is
surrounded by a bony wall thicker than the bones of the skull, and you
might as well press on the head to see if the brain is diseased.”

Now, in this case the pain was simply atrocious and greatly increased
by pressure. To relieve both it and the disease the actual cautery was
applied on both sides of the spinous processes; and some estimate may
be made of the sufferings of the patient, who would not take ether,
when he exclaimed as the hot irons were burning through his tissues,
“Oh, that is better than the pain.”

To sum up, then, I think I have shown that concussion of the spinal
cord proper occurs. I also believe it may occur in a railway collision
just as it occurred in the man who fell twenty feet. Why should not a
traveller sitting in a peculiar position—with his feet, for example,
firmly against a partition or wall of the car—suffer it in a
collision.

On the other hand, the great majority of those who after accidents
claim injury to the spinal cord as the cause of their disabilities are
wholly mistaken. The question is of great importance, for upon it
depends the testimony as to whether the patient has sustained
temporary or permanent injury.

Each case must be studied on its own merits. There is no class of
injuries so full of opportunity for the exaggerator or malingerer. The
history of many of them is by no means complimentary to human honesty.
Those interested can study the special works on the subject: space is
not given to detail them in this paper.

The SYMPTOMS and PROGNOSIS of concussion of the spine may be almost
inferred from what has been written above. There are tinglings, pain,
and sometimes cramps in the limbs; there may be partial or complete
paraplegia which is transient in character. Complete paraplegia is
{916} very rare, and when it exists it almost always indicates a more
serious injury than concussion. The case I have cited is an
exceptional one.

The bladder is almost always affected; there is either suppression or
incontinence. The bowels are sluggish for a time. The pulse is mostly
quickened; the temperature does not vary much from the normal.
Priapism, which is so frequently present in wounds involving the
spinal column and cord, is not present in concussion.

I have in the _Medical News_ (Nov., 1881) given my reasons for
believing this symptom to be due to a coincident impression or
laceration of the sympathetic nerve when there is a fracture or other
injury of the vertebra. This view I have been able to sustain by a
case reported in the _Medical News_ (Philada., Feb. 25, 1882).

The PROGNOSIS of concussion of the spine is generally favorable. The
recovery is slow in pronounced cases. Where such terrible consequences
follow as are described in some of the cases which have been caused by
railway collision, there is reason to believe that the original injury
was either too severe to come under the head of concussion, or that
some coincident deterioration was present at the time of the accident.

The DIAGNOSIS from fractures and dislocations is mostly easy. In these
cases the local and general symptoms are nearly always so definite as
to give no trouble in coming to a conclusion as to their nature. In
obscure cases time will develop the truth.

In the TREATMENT of concussion of the spine the great remedy is rest.
Under this alone the slight cases will rapidly recover. The more
severe ones will require other aids, such as cupping, both wet and
dry, to the spine over and about the chief seat of complaint.
Sinapisms, blisters, and iodine are useful in the order named. Opium
will be borne much better for the relief of pain and restlessness than
in like injuries of the head. The natural functions must be looked
after. Both the catheter and enemata may be required. Great care must
be taken to provide against chafing of the skin and bed-sores. For
this I know of nothing better than repeated sponging with alcohol, and
drying the surface at once by a good rubbing. The points of pressure
should be frequently changed by shifting the patient.

As soon as the acute symptoms pass away the patient should be
encouraged to rise and use moderate exertion. This, if well borne,
should be increased day by day, for it will be soon found whether the
efforts are injurious or not. All the requirements are present in
these cases to produce chronic hysterical invalids, both male and
female. It is therefore incumbent upon the medical attendant to
protect his patient from discouraging surroundings of any kind. It is
also his duty to so act that while he will be careful to work no
injustice, he will at the same time be on the watch for malingering,
for this will often be practised, especially by those who are among
the expectants already mentioned in this article.


{917}


INTRACRANIAL HEMORRHAGE AND OCCLUSION OF THE CEREBRAL VESSELS,
APOPLEXY, SOFTENING OF THE BRAIN, CEREBRAL PARALYSIS.

BY ROBERT T. EDES, M.D.


The various subjects embraced in this article are so closely united to
each other, both in a clinical and in a pathological point of view,
that they must be considered to a certain extent in common. It is of
course more systematic to group them entirely according to the obvious
and final lesion, as hemorrhage, thrombosis, or embolism; but when it
is considered how very closely the symptoms of one affection may
counterfeit those of another—so closely, in fact, that a diagnosis
with absolute certainty is not only difficult, but often
impossible—and also that similar conditions of the vessels may give
rise either to rupture or occlusion, so that not infrequently two sets
of lesions may be found in the same brain, and, finally, that the
basis of prognosis and of the later treatment is not unlike in
different lesions,—we are surely justified in bringing them, at least
in the beginning, under a common head.

Intracranial hemorrhage, and especially cerebral hemorrhage, is the
lesion which more frequently than any other gives rise to the group of
symptoms known as apoplexy, and from this fact has arisen the frequent
incorrect application of the word apoplexy, in a pathological as well
as a clinical sense, to indicate an extravasation of blood, as in the
so-called pulmonary apoplexy, where the anatomical lesion, being an
extensive effusion of blood into the tissues of the lung, bears an
apparent resemblance to the state of the brain often found in apoplexy
primarily and properly so called, the symptoms, however, being
entirely different. This error receives additional support from the
fact that in some injuries to the brain, especially to the base,
pulmonary hemorrhage may secondarily take place. Apoplexy, however, is
not always the result of hemorrhage, but occurs with many cases of
embolism and of thrombosis, and is sometimes, so far as we can tell,
dependent upon neither of these conditions, recovery in one set of
cases taking place so rapidly as to preclude the supposition of a
considerable organic lesion, and in others, which are fatal, nothing
being found beyond an excess of serum or of vascularity, and sometimes
not even that. The first of these conditions has been called simple
apoplexy, but with our present knowledge its simplicity seems to
border closely on ignorance, or at any rate is not of a character
{918} to satisfy the inquiring mind. It is therefore better to retain
the term apoplexy strictly as a convenient term for a certain set of
symptoms, but, whenever possible to substitute for it an anatomical
description of the lesion found post-mortem or diagnosticated with
reasonable probability during life.

The practitioner may very properly, and without laying himself open to
criticism of his diagnostic accuracy, return the cause of death in a
case of sudden death, or where his opportunity for observation has
been limited, or where no post-mortem examination has been held, as
being apoplexy; but in others, where the symptoms were decisive or a
post-mortem has disclosed the exact lesion, the condition of the
cranial contents should be stated. It is also a not uncommon
mistake—or rather piece of carelessness—to speak of small hemorrhages
in the brain as small apoplexies. A small extravasation may give rise
to slight symptoms or next to none, but a real apoplexy can hardly be
small, although it may be short.

The root from which the word apoplexy is derived seems to have been
used by the classic writers in something like its present clinical
signification (_Απορληκτος_, seized with (apoplexy or)
stupor—Aristophanes; mad—Demosthenes; _Αποπλησσομαι_, to be struck
with amazement—Sophocles). Morbus attonitus, another of its names,
expresses a somewhat similar idea.

Morgagni was familiar with cerebral hemorrhage, and Bonetus in the
_Sepulchretum_ gives several cases. The allusions of Galen and
Hippocrates supposed to refer to this lesion are not unequivocal,
although the Father of medicine could hardly have helped being
familiar with the symptoms of so striking a form of disease.

Cerebral softening has been recognized since the early part of the
present century, and in some of the cases thirty years ago an
efficient cause, in the form of arterial disease, assigned to it; but
the complete theory of its causation forms a part of the general
doctrine of embolism and thrombosis which was so largely developed and
systematized by Virchow. Andral and Durand-Fardel had apparently no
idea of the exact mechanism of its origin, the latter supposing it to
depend upon inflammation, while Todd mentions a case where softening
giving rise to paralysis depended upon a dissecting aneurism of the
carotid. He seems to have generalized so far as to say that white
softening is atrophic, but the precise way in which this localized
atrophy was usually brought about evidently escaped him. According to
him, the suddenness of the attack was owing to a gradual
disorganization of the brain-substance with few or no symptoms, and
then a sudden rupture of diseased fibres by some accidental cause or
by their having reached the extreme limit of cohesion.

Intracranial hemorrhage may be situated outside of the dura mater,
separating this membrane from the bones of the skull and producing
more or less compression of the brain. It is usually the result of a
blow, but not necessarily of a fracture of the skull. When a fracture
is present, blood may pass through it from the interior and give rise
to an external extravasation in addition to that which is likely to be
the direct result of the blow upon the skin and subjacent soft parts.
The middle meningeal artery is a frequent source of this hemorrhage.
Hemorrhage in this position will naturally give rise to symptoms of
compression, and, if the fact of the blow be not known or the fracture
manifest, may be mistaken for some of the deeper-seated forms.

{919} Blood may be effused upon the surface of the brain in the
so-called cavity of the arachnoid—that is, outside of the pia mater—or
in the meshes of this membrane, following its course along the sulci.
This also is not infrequently the result of violence either with or
without fracture of the bone. Its source is likely to be found in the
veins which empty into the longitudinal sinus from the surface of the
brain. Rupture of a lateral sinus from a not very severe blow has been
the source of large and fatal hemorrhage.[1] Blows upon the head, with
or without fracture of the cranial bones, are likely to cause rupture
of the cerebral substance with hemorrhage, and this may find its way
to the outside and cover more or less of the surface. Such injuries to
the brain, it is important to note, do not necessarily correspond
immediately to the place of the blow or to the external ecchymoses.
Meningeal hemorrhage in this region may, however, be observed when no
injury has been received, or at least when there is neither history
nor external traces of any.

[Footnote 1: _Cincinnati Clinic_, p. 135, 1874.]

The conditions under which it occurs may not vary greatly from those
of the more ordinary intracerebral effusion. In two instances under
the observation of the writer the source of hemorrhage has been a
vessel of small, but not the smallest, calibre (artery), situated near
the fissure of Sylvius, in the lower parietal or temporo-occipital
lobe. In children meningeal hemorrhage is, with only a few exceptions,
the usual lesion of apoplexy. The blood is usually dark and coagulated
in recent cases. Blood found under the membranes where no fracture has
taken place is, however, more likely to have been derived from the
brain-substance and to form part of a cerebral hemorrhage.

Hemorrhagic pachymeningitis, indicated by a layer of fibrin included
between the dura on the one hand and a false membrane on the other, is
met with in connection with meningeal and cerebral hemorrhages. It is
supposed to depend on a small and thin hemorrhage upon the surface of
the brain, which forms, by its irritant action, a false membrane about
itself. It is found usually over the vertex.

Hemorrhage into the ventricles is nearly always the consequence of a
hemorrhage in the brain-substance breaking through, although it may in
rare cases originate in the vessels of the choroid plexus, velum
interpositum, or meninges. Its source, however, is sometimes so near
the surface as to cause but little laceration of the cerebral tissue.
The blood breaking into any one of the ventricles may be found in one
or all of them (except the fifth), and form quite an accurate cast of
their shape.

The most common form of intracranial hemorrhage, however, which most
nearly concerns us here, and which is generally meant when sanguineous
apoplexy is spoken of, has its principal seat in the brain itself,
which is, of course, more or less lacerated. Such hemorrhages may vary
greatly in size, from a mere red point (punctate or capillary), of
which many may be present at once, to one of many ounces, filling a
large cavity of nearly the length of one hemisphere, and pushing the
torn and compressed brain-substance before it in every direction. The
amount of laceration produced of course varies greatly; sometimes it
seems as if nothing more than a pushing aside of fibres without
rupture had taken place, while at others large masses of tissue are
torn away and mixed up with the blood into a pulp.

{920} In a recent hemorrhage the clot itself, speaking of those of a
size above the capillary, is usually homogeneous, the brain-substance
surrounding it ragged, œdematous, yellowish or red, and frequently
containing many minute secondary hemorrhages. The rest of the brain is
frequently found anæmic from pressure, the convolutions flattened, the
surface dry, and the section exhibiting a diminished quantity of
blood. In older cases, however, and probably also in some where
atrophy, senile or otherwise, has preceded the hemorrhage, this
condition is not found, and we may have the convolutions shrunken and
the meshes of the pia containing an excess of serum.

If death does not take place speedily, the clot undergoes degenerative
changes. Its color becomes somewhat lighter, chocolate color,
reddish-yellow, or yellowish-red. A portion is absorbed, and after a
time the cerebral substance in the neighborhood forms about it a wall
of some density, so that finally nothing is left but a cyst with fluid
or semifluid contents, and often remains of connective tissue.
Sometimes the absorption of a clot of moderate size is so complete
that only a firm mass of a reddish or yellowish-brown color marks the
seat of an old hemorrhage. The brain-substance in the neighborhood may
be more or less atrophied, and a distinct depression may be noted over
the position. The microscope shows in a fresh hemorrhage only
broken-down nerve-tissue and blood and vessels more or less
degenerated. In an older one the blood-corpuscles have disappeared,
but masses of pigment of a dark yellow or a brownish-red remain to
show the former presence of blood. This pigment occurs in the form of
rounded granules or of small rhombic crystals, and has received the
name of hæmatoidin. The light-yellow masses often found along the
course of the cerebral vessels are not evidence of hemorrhage, but of
congestion merely. The so-called inflammation or granulation
corpuscles, which are simply the fattily degenerated cells of the
organ in which they are found, and which usually possess no
distinctive form, being simply round masses of fat-drops, are often
met with in the brain in hemorrhage or softening. It is sometimes
perfectly evident, however, from their form, triangular or pyramidal,
that they are degenerated nerve-cells. The blood-vessels, those just
above the size of capillaries, are usually in a condition of fatty
degeneration, masses of dark granules occupying more or less densely
the line of their walls. A mere deposit of fatty granules inside the
perivascular sheath, but outside of and not involving the walls of the
arteries, may present the appearance of a degeneration of the walls
themselves. This condition may be a consequence of any lesion
involving degeneration of brain-tissue, and in no way a cause.

The intermediate stages of transformation in a hemorrhage are less
frequently found than the recent or old ones, since the patient, if he
does not die within a few days, is likely to live for some weeks or
months.

The changes taking place in the clot itself within the first few days
are not very marked, but the walls of the cavity may become softer and
more deeply colored, at first red and afterward yellow. Blood-crystals
have been detected on the seventeenth day (Virchow). The following
descriptions have been given of clots of different ages: Eleven
days—reddish-yellow softening clot, with brain-tissue stained for half
an inch in depth, and brain rather hard in vicinity. Eighteen
days—cavity with its {921} edges anteriorly and superiorly sharply
defined, with the edges posteriorly ragged and yellowish, filled with
a tolerably firm brick-red mass adherent to surrounding brain, and
showing in the centre a softened clot about the size of a pea.
Twenty-eight to thirty-five days—soft, brownish, and semifluid.
Forty-one days—spot of softening filled with brownish material. One
hundred days—somewhat darker, and a little more distinctly marked from
surrounding tissues; by microscope granular corpuscles, groups of
fatty granules along the swollen vessels, granules of pigment.
Eighty-three years—old hemorrhagic focus in right optic thalamus,
color yellowish, and areolar structure.

The thirtieth day is given as about the time at which the walls of the
cyst become more firm and distinct. The following statement is
prepared from a considerable number of cases given by Durand-Fardel:
From four to six weeks, the clot is dark-colored, from black to ochrey
or reddish-yellow. It varies in firmness. The capsule is tolerably
firm. From two to four months, it seems to be generally softer,
pultaceous, grumous, or the clot still remaining swimming in serum; in
some cases lighter in color. In six months it has lost more in color,
and the cavity may be smaller. In a year there is still considerable
color left. In a few cases after some years the blood has been found
in the form of a dried mass, not changed or darker in color.

Hemorrhages of several months' standing may be indicated either by a
brownish-red patch somewhat firmer in texture than the surrounding
brain-substance, or by a cavity with firm walls, which often has
strings and septa of connective tissue running across it, so as to
convert it into a kind of spongy mass filled with brownish fluid.

The most important changes which are found in most if not all cases of
ordinary hemorrhages (_i.e._ such as do not depend upon violence or
cachexia) are those of the blood-vessels. They are not, however,
visible in the ordinary inspection of the brain at an autopsy, but
require to be carefully sought for, either with the microscope or a
somewhat tedious process of washing. For this reason there are no
trustworthy statistics of large numbers to determine in how large a
proportion of all the cases alterations in the blood-vessels are to be
found, and in what form. There can be but little doubt, however, that
those cases in which no form of arterial disease is present (if, with
the reservation just noted as to violence or cachexia, such exist) are
to be looked upon as rare exceptions.

The presence of miliary aneurisms in the brain had been noted in some
cases, and even in cerebral hemorrhage, without the great importance
of the observation having been perceived; but the extended and careful
observations of Charcot and Bouchard first showed how extremely common
their presence is, while in many instances they were found actually
ruptured. These aneurisms are present in the largest numbers in the
regions of the brain where hemorrhage is most frequent, and at the age
when death from apoplexy is most likely to occur. They have been found
at the age of twenty, but very rarely at early ages, while after forty
they are not uncommon. It is of course not always that they have gone
on to rupture, but may occasionally be found where no hemorrhages have
taken place. It is not going far, however, to infer that in such cases
the hemorrhage was not very distant.

These aneurisms are dependent upon a periarteritis which is diffused
{922} more or less widely over the cerebral arteries, but not over
those of the rest of the body. The larger arteries get a thin and
shining appearance, compared by Charcot and Bouchard to the skin of an
onion, while the smaller ones present besides distinct aneurisms,
bulgings and irregularities of outline. This condition may be—and, as
would be at once suggested from the age at which both lesions are met
with, is—very likely to be associated with atheroma, but it is not the
same thing, since the development of the aneurisms depends upon a
periarteritis, and that of atheroma upon an endarteritis. It may be
remarked, also, that atheroma usually does not affect the very small
arteries which bear the aneurisms and give rise to the hemorrhage.

These aneurisms are visible to the naked eye, being from two-tenths to
one millimeter, or a little more, in diameter, while the artery to
which they are attached can be seen by the naked eye or with a lens
magnifying two or three diameters. They may be strung along a small
artery like beads or be found in groups like a bunch of grapes.
Charcot and Bouchard found them in every case of cerebral hemorrhage
which they examined, and, although the possibility of other sources
was admitted, concluded that in by far the greater number of cases,
excluding those dependent upon traumatism or hemorrhagic diseases, the
blood effused in the brain has its origin in one of these aneurisms.
The presence of these aneurisms has been abundantly established by
other observers, and the fact that they are not usually demonstrated
proves nothing except the amount of care and time necessary to find
them. One does, however, find occasionally noted that they were sought
for and not found. The statements of Charcot and Bouchard relate, so
far as their own observations are concerned, and as they themselves
remark, chiefly to aged persons, but in their first series of 66 cases
there is found 1 of twenty and 1 of forty years of age. The patient of
twenty was a semi-imbecile and a drunkard. Extensive cerebral
hemorrhage, with atheroma, in the circle of Willis has been found in
an apparently healthy and well-nourished boy of fifteen.[2]

[Footnote 2: Baker, _Annals of Anat. and Surg. Soc. Brooklyn_, 1879,
p. 40.]

Larger aneurisms, often multiple, are not very infrequent upon the
arteries at the base of the brain. They may before their rupture give
rise to symptoms of pressure like any other tumor, and may also be the
source of hemorrhage, which is usually meningeal. They are not
infrequently symmetrical, and a place of election is one of the early
bifurcations of the middle cerebral.

Coats[3] states that aneurism of the larger arteries is the most
frequent source of hemorrhage in persons under fifty. They may be due
to embolism, producing, when the occlusion is not complete, mechanical
injury to the walls of the vessels by the constant hammering upon them
of the embolus under the impulse of the blood. If this etiology is a
common one, it accounts for the frequent situation of these aneurisms
in the middle cerebral arteries.

[Footnote 3: _Glasgow Med. Journ._, 1882, xvii. 109.]

Small vessels in a condition of fatty degeneration are often found in
the neighborhood of a cerebral hemorrhage. In some cases, undoubtedly,
the degeneration is a consequence of the injury to which the cerebral
substance has been subjected, but they have also been found too soon
{923} after the hemorrhage for this explanation to hold; and in cases
where no aneurisms are present the older supposition, that hemorrhage
results from this kind of degeneration, seems to have a certain
foundation, even if only in a minimum of cases.

In several cases of cerebral hemorrhage in purpura, where the general
character of the disease was shown by hemorrhages in other organs,
fatty degeneration of the cerebral vessels has been found, together
with extensive steatosis of the liver, kidneys, muscles, and heart.[4]
In a cerebral hemorrhage found in the brain of a girl of eleven the
walls of the vessels were dotted with fat-globules and dark granules,
and several of them studded with round and oval nuclei closely
resembling the nuclei (small cells?) commonly found in tubercle. There
was no trace of tubercle in any part of the body.[5]

[Footnote 4: _Gazette hébdomadaire_, May 12, 1876, p. 288.]

[Footnote 5: _Trans. Path. Soc._, Cayley.]

There is no possible means of determining in which way any given
bleeding has arisen, except a very minute search, and this may fail to
show the actual point of rupture. It seems highly probable, from the
connection of some cases of hemorrhage with valvular disease of the
heart, that embolism may give rise to effusions of blood, especially
capillary and multiple ones. In such cases the emboli may be deposited
in arteries far too small to be obvious in the ordinary process of
dissection. (See Capillary Embolism.)

Hemorrhage arises in some rare cases from the backing up of blood in
the veins when they are obstructed by thrombosis. A case has been
described where meningeal and ventricular hemorrhage resulted from a
rupture of the straight sinus at its juncture with the torcular
Herophili.[6]

[Footnote 6: Mullar, _Lancet_, 1849, i. 607.]

In many diseases like purpura, idiopathic anæmia, and leucocythæmia
many hemorrhages may take place in the brain as well as elsewhere
throughout the body. Their importance under these circumstances is
usually not great.

The usual localities of cerebral hemorrhage are stated with much
minuteness in the following table from Durand-Fardel, which, although
not very recent (1854), is not the less accurate on that account. No
subsequent statistics have essentially altered its most important
conclusions. In 139 cases the hemorrhage was situated in the
hemispheres 119 times; in the protuberance (pons), 21; in the
cerebellum, 13; total, 153.

I have placed beside these a small number of cases from the records of
the Boston City Hospital and my own practice, and, to avoid the
multiplication of headings, have entered some multiple hemorrhages
under two or more heads, so that from the whole number of cases (46)
there are 81 entries:

                                                    Durand-
                                                    Fardel.  B. C. H.
  Corpus striatum and optic thalamus, together  . .  22        4
  Corpus striatum . . . . . . . . . . . . . . . . .  13       10
  Optic thalamus  . . . . . . . . . . . . . . . . .   5        3
  Corpus striatum, optic thalamus, and middle lobe    2        1
  Corpus striatum, optic thalamus, and a
    considerable portion, not well defined, of the
    hemisphere  . . . . . . . . . . . . . . . . . .  12        2
  Corpus striatum, optic thalamus, with posterior
    lobe  . . . . . . . . . . . . . . . . . . . . .   1
  Corpus striatum and middle lobe . . . . . . . . .   3        3
  Corpus striatum, with a considerable portion of
    hemisphere  . . . . . . . . . . . . . . . . . .   5        1
  Corpus striatum, with an extended portion of base
    of ventricle  . . . . . . . . . . . . . . . . .   1
  Optic thalamus with middle lobe . . . . . . . . .   2        1 {924}
  Optic thalamus with posterior lobe  . . . . . . .   1
  Middle (parietal) lobe  . . . . . . . . . . . . .  19        1
  Sphenoidal horn of middle lobe (temporal) . . . .   2        4
  Anterior (frontal) lobe . . . . . . . . . . . . .  11        3
  Posterior (occipital) lobe  . . . . . . . . . . .  11        5
  A not well-determined extent of one hemisphere  .   4        3
  The superficies of the convolutions (once with
    corpus callosum)  . . . . . . . . . . . . . . .   3        1
  Insula  . . . . . . . . . . . . . . . . . . . . .   —        2
  Cortex (not further defined)  . . . . . . . . . .   —        1
  Small multiple  . . . . . . . . . . . . . . . . .   —        3
  Meninges (secondarily)  . . . . . . . . . . . . .  31        6
  Ventricles  . . . . . . . . . . . . . . . . . . .  66        8
  In the cerebellum, right lobe . . . . . . . . . .   6 |
     "       "       left lobe  . . . . . . . . . .   5 |      4
     "       "       middle lobe  . . . . . . . . .   2 |
  In the protuberance (pons)  . . . . . . . . . . .  13        4
  Protuberance and brain  . . . . . . . . . . . . .   8
  Protuberance, crus cerebri, crus cerebelli,
    external capsule, fourth ventricle  . . . . . .   —        1

It would not have been very difficult to increase these figures from
the large number of recorded cases, but there is nothing in later
statistics to invalidate the statement that the corpus striatum,
including both its nuclei, but especially the nucleus lentiformis, the
optic thalamus, and the white substance in their neighborhood, are the
portions of the brain by far the most frequently affected by
hemorrhage, and especially by hemorrhages of considerable size.

There is no essential difference in the frequency of hemorrhage on the
two sides. It may occur on both sides at once. Hughlings-Jackson says
that he saw a patient who escaped with life from the effects of a clot
which had paralyzed both sides of the face as well as all four limbs.
Charcot and Bouchard give the following localities as containing in
decreasing frequency the miliary aneurisms: optic thalami, corpora
striata, the convolutions, the protuberance, the cerebellum, the
centrum ovale, the middle peduncles of the cerebellum, the cerebral
peduncles, and the bulb. The close correspondence of this list with
the table of Durand-Fardel is in itself a strong argument in favor of
the importance of the miliary aneurisms as the principal factors in
determining cerebral hemorrhage.

The arteries supplying the nucleus lenticularis and external capsule
are small branches arising chiefly from the middle cerebral a short
distance from its origin, with some assistance from the anterior and
posterior cerebral. One of the larger of them runs along the outer
side of the nucleus lenticularis where it is covered by the external
capsule—a disposition which may have something to do with the
occurrence of the larger hemorrhages so likely to take place just
outside this nucleus and into the substance of the hemispheres.

The arteries of the optic thalamus arise from the posterior
communicating or the posterior cerebral. Why these two groups should
furnish, as they do, so large a part of cerebral hemorrhages it is
impossible to state, unless it be that from their origin so near to
the larger trunks before their division they are exposed to more
pressure, and hence a greater tendency to form aneurisms. The
functional activity of these regions is another possible reason. The
largest hemorrhages also seem to spring from these sources, and if a
table of large effusions were compiled {925} it would probably show a
greater predilection for this locality than even the general one given
above, which includes those of all sizes.[7]

[Footnote 7: A very careful study of the form and size of foci of
bleeding arising from the various nutrient arteries of the brain will
be found in the well-known elaborate papers of Duret (_Archives de
Physiologie_, 1874).]

Before proceeding to a minute account of the symptoms accompanying
cerebral hemorrhage, a consideration of the relation between extensive
lesions and the most fully-developed clinical phenomena will be of
value—in other words, the pathology of hemorrhagic or sanguineous
apoplexy. This will naturally demand a reference to the cases where
the same symptoms are present with a different lesion.

The most marked symptom, one which is essential to the definition of
apoplexy, is the sudden, or more frequently rapid, loss of
consciousness, and next, in a great proportion of cases, a unilateral
paralysis or paresis. The latter, in many cases, finds a sufficient
explanation in the rupture of fibres connecting the motor centres in
the brain with the spinal cord; but this does not cover all cases, for
it is well known that we may have paralysis without any laceration. In
fact, in many cases paralysis may disappear so rapidly as to put aside
at once any such explanation. Sufficient pressure upon contracting
fibres is entirely competent to arrest their conductivity, and this
pressure may be diffused over a considerably wider area than that
where total destruction of tissue has taken place. Meningeal
hemorrhage, where, of course, no laceration takes place, may be
attended by a well-marked hemiplegia when the effusion is wholly or
chiefly on one side.

The writer recalls a case of a man, of whose history little or nothing
was known, found unconscious with a very distinct difference in the
amount of motion to be provoked by irritation of the two sides. The
diagnosis naturally inclined to the more common causes of hemiplegia,
but the autopsy showed a purulent meningitis of the vertex, with a
layer of pus considerably thicker on the side opposed to the
paralysis.

A very similar statement may be made in regard to the symptom of
unconsciousness, which seldom occurs more rapidly and completely than
in cases of meningeal hemorrhage (not from injury), where, of course,
there is no question of laceration.

F. Pagenstecher[8] succeeded in producing phenomena closely allied to
apoplexy by injecting at a known pressure, between the skull and dura
mater in dogs, masses of melted wax and tallow. In the first group of
cases the result was somnolence, great depression of the psychical
capacity, and general muscular weakness. The second group showed,
besides the condition of sopor, unilateral paralysis; and the third
contained cases in a part of which death followed in a few hours after
the setting in of coma, and in another part partial recovery took
place after scooping out the waxy mass. The symptoms in these cases
are referred to the pressure upon the vessels; and it is stated that
in order to destroy life the pressure had to be equal to that of the
blood. Convulsions were present in some cases where the pressure was
not steady. The temperature showed a notable peculiarity in that,
after the initial fall, in which it resembles the course in human
apoplexy, it kept on falling in the fatal cases, instead of rapidly
rising, as in man. After injection into the brain of animals {926} of
sufficient quantities of water to produce great tension of the
occipito-atlantoid membrane, Duret[9] found the respiration to cease
and the heart to be slowed. On tearing the membrane so as to allow the
water to escape, respiration began again, and the animals gradually
recovered consciousness. Similar effects could, however, be produced
by blows on the head.

[Footnote 8: _Centralblatt f. d. Med. Wiss._, 1871, p. 706.]

[Footnote 9: _Centralblatt f. d. Med. Wiss._, 1878, p. 454.]

Several cases are reported by P. R. Hoy[10] where pressure upon the
brain produced an arrest of function, which was resumed when the
pressure was removed. In the first of these a piece of bone had been
removed, but the dura was intact. If the patient were asked a question
and the finger immediately pressed upon the dura, no answer was made,
but as soon as the finger was removed the reply came. In two other
cases, which are not without their parallels, the patients resumed
after trephining the mental attitude in which they had been surprised
by the injury—in one case hours, and in the other years, before.

[Footnote 10: _Journ. Nerv. and Ment. Dis._, vol. iv. p. 288.]

The natural generalization to be made from these cases and experiments
is, that pressure upon the brain-tissue suspends, for the time, its
function; but when we find exactly the same symptoms arising from
either sudden or gradual occlusion of the vessels where we can hardly
imagine increased pressure to exist, except perhaps over a very small
area of collateral hyperæmia, we must go a step farther for a common
factor; and it seems possible to find one which will not only explain
the several conditions spoken of, but also others which closely
resemble them. Simple anæmia will cover the cases of hemorrhage and
embolism, but certainly not narcotic poisoning and certain other
conditions where characteristic apoplectic symptoms exist without
discoverable lesion. If, however, we say that a deprivation of a
considerable portion of gray matter of its due supply of arterialized
and healthy blood suspends for a time its functional activity, we can
explain the similarity of results arising from very different causes.

In a case of cerebral hemorrhage of considerable size the pressure is
distributed over a space much exceeding the area of the clot itself,
and renders a large part of at least one hemisphere anæmic. If the
blood finds its way into the ventricles, the conditions are most
favorable for compressing nearly the whole brain. The anæmic
appearance of the cerebral surface is often remarked at autopsies.

When an embolus lodges in an artery and produces complete occlusion,
the portion of brain supplied thereby becomes at once entirely anæmic,
since the arteries on the surface have so slight anastomoses that they
are entirely unable to supply the deficiency, except to a slight
extent around the edges of the vascular territory involved. The
anæmia, however, does not extend beyond the territory originally
affected, and consequently we may have extensive paralysis from
embolism without a marked apoplectic attack. In extreme congestion of
the brain the reverse may seem to be the case.

In reality, the hindrance to the proper functions is nearly the same,
since blood which is not duly renovated and contains the products of
metamorphosis of tissue in excess is worth as little for healthy
nutrition as no blood at all. There is no reason to suppose that blood
in {927} circulation, no matter in how great quantity, gives rise to
unconsciousness. It may cause over-action or disordered action, as in
mania, but not arrest of action.

The narcotic poisons also deprive the nerve-tissue of its healthy
food; whether by interference with oxygenation and depuration, or by a
direct action of the substance itself on the nerve-cells, it is not
easy to say. The fact that the completeness and duration of the
unconsciousness are not in proportion to the paralysis or anæsthesia
shows that they are to some extent independent of each other; and,
although it is possible to locate with some precision the lesion which
abolishes motor power and conscious sensation, yet we cannot say how
much or what part of the brain must be deprived of its function in
order to produce that cutting off of all conscious relation with the
external world and reduction of a feeling, thinking, remembering, and
acting organism to the level of a mere automatic breathing-machine,
which we designate as loss of consciousness.

In fact, in the present state of our knowledge as to what
consciousness is, any speculation as to its seat would be a waste of
time, and we must content ourselves with recognizing that experience
seems to show that a large part, rather than any particular part of
the brain, must be involved, not necessarily in the primary lesion,
but in the resulting pressure or anæmia.

Another theory of unconsciousness is simply that it is due to
shock—that the sudden irruption of blood acts like a blow, as it were,
and abolishes for a time the function of the nervous structure. This
is substituting something indefinite for something comparatively
definite; and it is certainly not true that the more sudden the shock
the more complete the unconsciousness. It may come on after the
paralysis is apparent, and in fact is more commonly gradual than
sudden in its onset. The classical instantaneous shock is the rare
exception. In the celebrated case where a tamping-iron was driven
completely through a man's skull and brain, he himself was able to
give a clear description of the accident to the surgeon who first
attended him. Several other instances of severe and sudden injury to
the brain without loss of consciousness have been recorded.

ETIOLOGY.—As regards the greater number of cases and the most common
pathology, the existence of so specific and peculiar lesion as
aneurism enables us to distinguish between predisposing and exciting
causes, or, in other words, the conditions which lead to the localized
periarteritis with its resulting aneurisms and those which cause their
rupture. Unfortunately, the aneurisms are not usually looked for, and
in the collection of statistics we are obliged to group together cases
the pathology of which is not always the same, and which are usually
collected under the name of apoplexy.

Age, however, is well known, both on clinical and anatomical grounds,
to be the most important factor. Among the predisposing causes of
apoplexy, all statistics, both of recent and older date, agree in
assigning the period of life beyond forty-five or fifty as that in
which the liability to apoplexy is greatly increased. There is no age,
however, below this, even to infancy, in which true cerebral
hemorrhage may not occur, although the intracranial hemorrhage of
children is more usually {928} meningeal. It is probable, however,
that in many of these the rupture of the vessel does not depend upon a
previous aneurism, but on other lesions. The youngest case in which
aneurisms were found by Charcot and Bouchard was twenty.

If we speak of cerebral hemorrhage in general, without reference to
the presence of aneurisms, as we unfortunately are obliged to do in
the great majority of cases, we may often go much below this point. In
youth and childhood, however, it is possible, and often almost proved,
that other conditions must have been of greater importance in
determining the hemorrhage than aneurism.

In our own small series we find cases of eighteen, twenty-three,
twenty-five, twenty-six, twenty-seven years of age, and quite a number
from thirty to forty-five. A little further examination shows many of
them not to have been of the ordinary kind; thus the patient of
eighteen had valvular disease of the heart and advanced parenchymatous
nephritis; the one of twenty was, so far as could be seen, typical,
but no search was made for aneurisms; that of twenty-five had many
small hemorrhages and was a marked case of idiopathic anæmia; that of
twenty-six had valvular disease of the heart, an embolus in the middle
cerebral artery, which was not in the immediate neighborhood of any
hemorrhage, several old hemorrhages, and hemorrhagic infarction in
other organs. The case aged twenty-seven had a very large clot in one
hemisphere and advanced interstitial nephritis.

Cayley[11] describes the case of a girl of eleven with a large cavity
in the left middle cerebral lobe, where nothing was discovered
abnormal upon the left middle cerebral artery, but when the cerebral
matter was washed away with a stream of water, the walls of the
vessels were found to be dotted with oil-globules, and in several
places studded with round and oval nuclei. This was before miliary
aneurisms were known, but the process of preparation was exactly
suited to bring them to light had they been present, and they could
hardly have escaped observation and mention. Other cases of boys have
been reported where the hemorrhage was of the typical kind.

[Footnote 11: _Trans. Path. Soc._, vol. xx.]

Meigs and Pepper speak of nine cases of hemorrhage into the substance
of the brain in children, but give none of their own. Of the two cases
mentioned by West as coming within his own observation, in one the
source of the blood was in the cerebral veins obstructed by the
formation of clots in the longitudinal sinus.

C. W. Dulles[12] describes a case occurring in his own practice in a
child of six months, where a considerable amount of blood was found in
the lateral, third, and fourth ventricles. Nothing is said of
aneurisms in particular, but the brain was carefully examined without
the source of the hemorrhage being found, although it seemed to be in
some of the vessels of the velum interpositum. Dulles mentions further
a case reported in the books of the Philadelphia Hospital by Joseph
Berens, where in the brain of a child ten days old there were found,
besides a large meningeal hemorrhage, many points of subarachnoid
extravasation, a clot filling all the ventricles, and a clot the size
of a pea in the anterior portion of both corpora striata. In addition
to these there were scattered points of hemorrhage throughout the
brain-substance.

[Footnote 12: _Philada. Med. Times_, vol. vi. p. 507.]

{929} Cerebellar hemorrhage seems to show a certain preference for
younger ages than the more usual forms. In a list of 25 cases from
various sources I find the ages given thirty-two, twenty, nineteen,
sixteen, thirteen and a half, eight. In the seven cases detailed by
Hillairet there were two aged fifteen and twenty-six respectively.

These exceptions, however, do not invalidate the rule that cerebral
hemorrhage of the ordinary type is pre-eminently a disease of later
middle or advanced life.

The male sex is more liable than the female. Durand-Fardel gives 54
cases of men, 37 of women (old persons); our own list, 31 men, 15
women. Falret, cited by Rochoux and Durand-Fardel, gives 1670 cases of
apoplexy among men and 627 among women. This, however, is only a rough
approximation as regards cerebral hemorrhage, as it undoubtedly
includes many cases not dependent upon this lesion. The same remark
applies to Lidell's statement that there died in New York during three
years, of apoplexy, 598 males and 440 females. This moderate
predominance is ascribable to greater muscular effort, and probably
also to the greater prevalence of alcoholic intoxication. Greenhow, in
a Parliamentary report,[13] states that in England and Wales the
number of deaths from apoplexy in 100,000 of population is 46 males to
44 females. From paralysis the figures are 42 and 44, so that the
total from the diseases registered under these two heads is alike for
the two sexes—viz. 88 to 88. In London alone the discrepancy is a
little greater on the male side—108 to 101; but in certain districts
of England the excess is on the other side. Race is of little
influence. High altitudes (7000 feet) favor the prevalence of apoplexy
in the population,[14] as in Peru and Mexico. Warm climates are
somewhat, but less markedly, opposed to it.

[Footnote 13: _Results of Inquiries into Different Proportions of
Deaths, etc._]

[Footnote 14: Hirsch, _Handbuch der Hist. Geoqr. Pathologie_, vol.
ii.]

Heredity seems to play an important part in the same sense as in
tuberculosis; that is, in the establishment of a tendency, which of
course means, anatomically speaking, periarteritis. Many deaths from
cerebral hemorrhage may sometimes be found among the members of a
single family. Dieulafoy has been able to trace this disposition
through several generations. Among several instances, Mme. G—— died in
three hours of paraplegia with loss of consciousness. Her mother had
hemiplegia at the age of fifty-two, and two uncles and an aunt were
also paralyzed at ages not stated. A commercial traveller, aged
thirty-nine, was in the hospital with left hemiplegia, second attack;
his mother, aged sixty-six, had an attack a few weeks before, and his
grandmother died at seventy-five of fulminating apoplexy. A woman aged
forty-six was hemiplegic for two months. Her mother, her maternal
aunt, and uncle are all hemiplegic, and her son had a left hemiplegia
at the age of seventeen. According to the cases of Dieulafoy, it is
especially through the female side that the hemorrhagic disease is
transmitted. Of course, the tendency may remain, and usually does so,
latent until the age at which in the average of cases it becomes
manifest by an apoplectic or paralytic attack; but the last two series
given above show that it may develop at an earlier period of life in
the younger than in the older generation.

Alcohol is universally stated by authorities to be one of the most
potent factors in different races in establishing the hemorrhagic
tendency: {930} but it is not easy to get exact facts on this point,
as so large a share of hospital patients are more or less alcoholic,
and in private practice observations of this kind accumulate so slowly
as not to be readily available. The greater frequency of this
affection among the male sex may point in this direction. Two of the
usual effects produced by the long-continued use of alcoholic drinks
in excess probably combine to produce this result: first, the
degeneration of tissues and tendency to low forms of inflammation of
the tissues in general and arteries in particular; and secondly, the
repeated dilatations of vessels under its paralyzing influence on the
vaso-motor nerves, resulting in chronic congestion. This preparatory
influence is distinct from the effect an occasional debauch may have
in precipitating the attack.

Another highly important cause of cerebral hemorrhage is Bright's
disease of the kidneys, in the form known as chronic interstitial
nephritis, contracted, granular, cirrhotic, or atrophied kidney; or,
as it would be perhaps more correct to say, cerebral hemorrhage is one
of the results of the arterial lesion which almost invariably
accompanies interstitial nephritis. As to the supposed or possible
identity or relation of the arterio-capillary fibrosis of Gull and
Sutton with the periarteritis of Charcot and Bouchard, the writer does
not feel competent to express an opinion.

The connection between cerebral hemorrhage and hypertrophy of the
heart was noticed and commented on long before it was known that the
great majority of cases of hypertrophy, where no lesion of valves or
of the aorta was present, were really cases of Bright's disease. The
influence which might be exerted by the high arterial tension in the
rupture of an aneurism is obvious enough theoretically, but it is far
from certain that the effect of the renal disease, or rather the
common cause of renal and cerebral disease, is not a more subtile one
than this, and prepares the way for, as well as hastens along, the
impending catastrophe.

This result, however, is not an extremely common one. Among 43 fatal
cases of interstitial nephritis, well-marked cerebral hemorrhage was
found in 4; in another, cysts and brownish indurations of small size
were found which might have been partly the results of embolism. This
patient had had a distinct paralytic attack. In a fifth the symptoms
pointed unequivocally to a large rapid hemorrhage, although it was not
demonstrated by an autopsy.

Looking at it from the other side, it was found that (in another
series) of 48 cases of cerebral hemorrhage with autopsy, contracted
kidneys were present in 17; and the writer is of the opinion, although
he has not at his command a sufficient number of facts to make such an
opinion conclusive, that if a series of cases were taken of persons
under forty or fifty, excluding those where a hemorrhagic disease or a
valvular disease of the heart might be present, the proportion of
interstitial nephritis to cerebral hemorrhage would be greatly
increased; and especially so if large hemorrhages into the great
ganglia or the interior of the cerebral lobes were alone considered.

The so-called apoplectic constitution should be mentioned here; that
is, the stout, thick-set build with short neck and florid complexion.
The popular notions as to the peculiar dangers of this condition seem
to have arisen rather from suppositions as to what might be supposed
to take place, from inferring a similar state of things to exist in
the brain to {931} what exists in the countenance, than from any
observation as to what has actually occurred. Cerebral hemorrhage may
take place with any sort of complexion or any figure, and there is no
sufficient evidence that persons of the physique above described are
specially liable to it. Many recent writers distinctly deny any such
connection.

Intellectual pursuits have been considered a disposing cause—a theory
which it would be difficult to substantiate. It is not, of course, the
quality of the work, but its relation to the capacity of the
individual brain, which makes any amount of thought a special strain.
The cases of Dieulafoy, in which the hereditary tendency was so
strongly marked, were mostly hospital cases, among which class the
so-called intellectual occupations do not specially preponderate. A
life of constant cerebral excitement, like that of a speculator or
stockbroker, certainly seems more likely to give rise to overstrain of
the vessels than the more quiet and regular, but certainly more
intellectual, labor of the professional or literary man.

Thackrah[15] speaks of affections of the head as frequent among
professional men, but does not advert to cerebral hemorrhage in
particular. He evidently considers a want of sufficient exercise in
the open air a far more potent factor than mental excitement.

[Footnote 15: _Health and Longevity_, p. 183.]

It is very difficult to get statistics which bear upon the influence
of mental labor on the brain, since the recorded occupation of an
individual furnishes but a very rough estimate of the amount of
thought evolved from his brain, and a very much less accurate one of
what is probably of far greater importance—the amount of friction and
anxiety with which it is done.

Hemorrhagic diseases may, for the sake of completeness, be once more
mentioned as among the predisposing causes.

The exciting causes of cerebral hemorrhage are those which give rise
to rupture of the fragile walls either of the aneurisms or fattily
degenerated arterioles. They are to be found chiefly among such
conditions as increase the pressure in the cerebral vessels, chiefly,
though not wholly, from the arterial side. The connection of an attack
of apoplexy with hypertrophy of the heart means, as has already been
shown, in a great many cases, their mutual dependence upon arterial
disease, as in chronic interstitial nephritis, but it seems probable
also that an unusually powerful action of such a heart might be the
immediate cause of the rupture. An excited action of the heart,
connected with a dilatation of the cerebral vessels, naturally
increases the strain on the weak portions, and we have thus the
explanation of those instances where sudden or great excitement brings
on the attack.

Apoplexy is less frequent in summer than in the other seasons, and it
is especially remarked that sudden changes of temperature are likely
to be accompanied by an unusual number of cases. Changes in the
arterial tension consequent upon the varying amount of blood
circulating in the skin are the probable connecting link.

Obstruction to the venous outflow, either alone or in conjunction with
the preceding condition, has undoubtedly a marked effect. In addition
to the cases of hemorrhage from veins obstructed by thrombi, already
mentioned, instances of this method of production are to be found in
{932} the effects of severe muscular effort, as in lifting, in
straining at stool, or, as has occasionally happened, in coitu. It has
been objected to the congestion theory of apoplexy that even in severe
paroxysms of whooping cough, where the face becomes cyanosed and
congested, nothing like unconsciousness or paralysis occurs; but cases
have been reported where aphasia and cerebral hemorrhage into the
optic thalamus and cortex have accompanied whooping cough. Violent
convulsions may be the cause of cerebral hemorrhage, as in puerperal
eclampsia.

Obstruction to the circulation in the neck by tight clothing may be a
means of increasing the back pressure from the veins. It is said that
deaths from apoplexy have been unusually frequent among soldiers who
have been obliged to wear tight stocks for the sake of imparting what
was supposed to be a more military bearing. Probably some of the
hemorrhages found with valvular disease of the heart are to be
explained by venous congestion, although others are due to embolism.

Blows and shocks to the head, not producing fractures, are occasional
causes of cerebral and ventricular as well as of meningeal hemorrhage.
Important medico-legal questions are likely to arise where both
bruises externally and internal hemorrhage are found. It is important
to recollect that ecchymoses of the pericranium[16] have been found in
cases of apoplexy where no violence has been used. These may occur
with occlusion of the cerebral vessels, as well as with hemorrhage,
and are most likely to be situated on the paralyzed side, being
sometimes distinctly limited at the median line. They have been
supposed to be due to the general tendency of the blood toward the
head, and to be of the same pathological origin as the cerebral lesion
they accompany; but the fact that they may not be associated with
hemorrhage proves that this explanation is inadequate. Another
explanation attributes their causation to vaso-motor paralysis,
together with some unknown factor present in only a certain number of
cases. They may be compared to the subconjunctival hemorrhages seen
after violent convulsions.

[Footnote 16: Lepine, _Archives de Physiologie_, tome ii., 1869, p.
667.]

Cerebral hemorrhage depending upon a blow is likely to be accompanied
by meningeal bleeding; to be situated at some point of the cortex, and
not in the regions more frequently affected; and to consist of the
effusion of no great amount of blood, mixed with cerebral substance.
There are also very often more than one. All the circumstances should
be carefully weighed when, as not infrequently happens, there is doubt
as to whether a blow was the cause of a hemorrhage, or whether a
person found insensible, with a bruise upon his head, may have fallen
down suddenly from an apoplectic attack. In the following case it
would be difficult to be sure of the sequence: A negro man aged fifty
fell backward from the first step of a ladder. He got up and went to
work again, but soon became unconscious. He became partially conscious
again in the accident-room of the hospital, but died in a few hours.
There was no sign of injury to the head, but there was a rupture of an
aneurism (not miliary) of the left middle cerebral artery, and
hemorrhage into the meninges and all the ventricles. If the first fall
had occurred in a scuffle, and the autopsy had been made in such way
as not to disclose the aneurism, it might have been considered a case
of homicide.

{933} Alcohol, besides not infrequently counterfeiting apoplexy, and
besides acting as one of the predisposing causes, is occasionally an
exciting cause. The dilatation of cerebral vessels, perhaps present as
an habitual condition, is added to by the effect of the temporary
narcotism and produces the rupture. In many cases these factors have
their activity much increased by heavy sleep, very likely in a
constrained posture, causing pressure on the veins of the neck and
consequent venous congestion, which is in its turn intensified by the
confined air of a station-house or the cold of the weather. The man
who has possibly a vessel ready to burst in his brain should have,
even if demonstrably drunk, the advantage at least of good air and an
unconstrained position.

Other poisons, less frequently taken, may perhaps have a similar
influence. In one case under the observation of the writer a number of
small hemorrhages were found in various parts of the brain of a man
who was found in his room some forty-eight hours after taking a
quantity of opium, and having had, of course, no treatment during that
time. He was aroused in the hospital without great difficulty, but
died after a day or two with his brain in the condition above
described, and bronchitis with inhalation pneumonia. There had been no
paralysis, and the hemorrhages were probably not the immediate cause
of death.

Durand-Fardel gives a table of supposed causes in 21 cases of persons
over fifty: 8 of these were connected with either habitual use of
liquor or a debauch; 9 had an attack immediately after a meal.

After naming all these causes, it must be said that in many cases it
is impossible to find any reason for the occurrence of the hemorrhage
at the particular moment it comes. A person may go to bed in apparent
health, and be found some hours afterward unconscious and comatose, or
unable to stir hand or foot on one side, or to speak. Gendrin, as
quoted by Aitken, states that of 176 cases, 97 were attacked during
sleep. The attack may come on when the patient is making no special
muscular effort and under no special excitement. It is simply the
gradual progress of the lesion, which has reached its limit.

SYMPTOMATOLOGY.—If we take as a point of departure the fully-developed
attack, such as most frequently is found with a large and rapid
hemorrhage into the cerebral hemispheres, pons, or cerebellum, the
symptoms are those usually spoken of as an apoplectic attack, shock,
or stroke, or, as the Germans say, Hemorrhagische Insult. Trousseau
quotes as a satisfactory definition the words of Boerhaave: “Apoplexia
dicitur adesse, quando repente actio quinque sensuum externorum, tum
internorum, omnesque motus voluntarii abolentur, superstite pulsu
plerumque forti, et respiratione difficili, magna, stertente, una cum
imagine profundi perpetuique somni.”

Loss of consciousness, abolition of voluntary motion and sensation,
and usually stertor, the appearance of the patient being that of one
in deep sleep, are found in the extreme cases. In others the loss of
consciousness and sensation are not complete; the patient can be
aroused enough to utter a grunt or raise a hand to his face in order
to brush away a fly or the hand of the physician who is trying to
raise his eyelids, or can make a grimace to show that he is hurt, the
face returning to its indifferent expression as soon as the cause of
irritation is removed. Although the grade of action, both sensitive
and motor, seems to be a little above the {934} purely reflex, it is
but very slightly so, and probably is not sufficient to remain an
instant in the memory.

The rapidity with which this condition comes on varies widely, from a
very few minutes, or even seconds, to some hours. It may even diminish
for a time and return. The cases in which unconsciousness is most
rapidly produced are apt to be meningeal and ventricular, and
presumably depend upon the rupture of vessels of considerable size,
although the location among the deeper ganglia, where the conductors
of a large number of nervous impulses are gathered into a small space,
will, of course, make the presence of a smaller clot more widely felt.
Even in these, however, the onset is not absolutely instantaneous, and
the very sudden attack is rather among the exceptions. Trousseau
denies having seen, during fifteen years of hospital and consulting
practice, a single case in which a patient was suddenly attacked as if
knocked down with a hammer, and that since he had been giving lectures
at the Hotel Dieu he had seen but two men and one woman in whom
cerebral hemorrhage presented itself from the beginning with
apoplectiform phenomena. In each of these the hemorrhage had taken
place largely into the ventricles.

Lidell gives the following case: A colored woman, aged forty-nine, was
engaged in rinsing clothes, and while in a stooping posture suddenly
fell down upon her left side as if she had been struck down by a
powerful blow. She was picked up insensible, and died in ten or
fifteen minutes. The hemorrhage was chiefly meningeal, and especially
abundant about her pons and medulla oblongata. The fourth ventricle
was full of blood, and there were clots in the lateral ventricles.

A woman, aged about forty, had been hanging out clothes in an August
sun. She was observed to run out of the house screaming, and fell to
the ground unconscious. This was at 1 P.M., and she died at 3.30 P.M.
Her temperature just after death was 107.2°. The neighborhood of the
posterior surface of the pons Varolii was occupied by a
broken-down-looking mass, appearing like an aggregation of small
apoplexies (hemorrhages), involving and breaking down the middle crura
of the cerebellum. There was no fatty degeneration nor any miliary
aneurism. (I do not know upon how thorough an examination this last
statement rests.)

In a large number of cases it is difficult to say, in the absence of
any observation, intelligent or otherwise, exactly how rapid the onset
of the symptoms may have been, but in those which occur where the
patient is watched or is in the company of observant persons it is
almost invariable to meet with symptoms less than unconsciousness
which denote the actual beginning of the hemorrhage. From the nature
of the lesion it can rarely give rise to symptoms which justify the
epithet of fulminating in the sense of struck with a thunderbolt. The
unconsciousness, so far as can be known, does not depend on the injury
of any one special small point of the brain in which consciousness
resides, but upon the compression of a considerable portion, which
must necessarily take place gradually, but with a rapidity
proportioned to the size of the current which issues from the ruptured
vessel and the ease with which pressure can diffuse itself over a
large area. It is undoubtedly the greater facility offered to such
diffusion by the communication of the hemorrhage with the so-called
cavity of the arachnoid and the ventricles which gives to {935} these
forms a peculiar severity. The difference between a hemorrhage
spreading through all the ventricles or over a large surface of the
brain, and one which is limited to a focus in the substance of one
hemisphere, being restrained by more or less firm tissue, may be
illustrated by the gain in power in the hydraulic press from the
transfer of the stream of water from a small cylinder to a larger one.

Vomiting is a symptom of some importance in diagnosis, being not very
common in cerebral hemorrhage, but very frequent in cerebellar.

Whether of sudden, rapid, or slow development, the apoplectic attack
is, in its main features, described in the aphorism of Boerhaave given
above. The muscular relaxation of the face imparts to it an
expressionless, mask-like character; the limbs lie motionless by the
side, unless they can be excited to some slight movement by some
painful irritation or are agitated by convulsions, or in a condition
of rigid spasm; the face may be pale or flushed; the cheeks flap
nervelessly—le malade fume la pipe.

Swallowing, in the deepest coma, is not attempted. The fluid poured
into the mouth remains, and distributes itself according to the laws
of gravity without exciting reflex movements of the pharynx. When the
depression is less profound, it may excite coughing or be swallowed.
An attempt to swallow when the spoon touches the lips indicates a
considerably higher degree of nervous activity. Respiration may be
slow, but when the case is to terminate fatally rises with the pulse
and temperature. It is often stertorous and difficult, the obstruction
consisting partly in the gravitation backward of the soft palate and
tongue, and partly in the accumulation of fluids in the pharynx. Hence
stertor is in some cases only an accidental phenomenon, depending upon
the position of the patient on the back, and can be relieved by
turning him on his side and wiping out the mouth as far back as can be
reached. Cheyne-Stokes respiration occurs in severe cases, though not
confined to necessarily fatal ones.

The general temperature in cerebral hemorrhage has been studied enough
to make it of considerable value, especially in prognosis. In a case
which extends over a sufficiently long time several stages can be
distinguished which in shorter ones may be wanting. An initial period
of depression is described by Bourneville[17] as occurring immediately
after an attack, in which the temperature falls a degree or two below
the normal, and, according to his view, continues depressed if death
takes place rapidly. He gives the case of a man who died very shortly
after an attack (his second one), where the temperature, taken in the
rectum at the moment of death, was 35.8°. In cases which survive
longer this initial fall passes either into a stage where it
oscillates within the neighborhood of the normal or immediately begins
to rise; the latter occurrence indicates an impending fatal
termination (unless, of course, something else can be found to account
for it). In the former condition we find patients whose life may be
indefinitely prolonged for days or weeks, when, if a fatal termination
is to result, the thermometer again indicates a rise.

[Footnote 17: _Études cliniques et thermométriques sur les Maladies du
Système nerveux_, 1872.]

The initial fall of temperature is not so likely to be observed except
in institutions like the Salpêtrière, where large numbers of old
persons are collected and under close medical surveillance; and,
indeed, it {936} {937} may be doubted, even from Bourneville's own
table, whether the rule is one without exceptions. At any rate, the
rise is a more important phenomenon than the fall. When the rise of
temperature is interrupted by a fall, and then continues again, it is
due, according to the author already quoted, to a renewal of the
hemorrhage.

These changes of temperature may be noted with various locations of
the lesion, but it seems probable that further study might make them
useful in diagnosis as well as prognosis. Hale White reports the case
of a boy aged six and a half years, who was found unconscious with
right hemiplegia, and who afterward had many and various paralyses
with hyperpyrexia, the highest temperature being 107°. He lived long
enough for secondary degeneration to extend down the crura and into
the anterior cornua. A small soft patch a quarter of an inch in
diameter existed at the anterior part of each corpus striatum.[18]

[Footnote 18: _Guy's Hosp. Rep._, 1882.]

[Illustration: FIG. 37.]

The chart W. H. (Fig. 37) is from a man aged fifty who fell in the
street while returning from work at noon, and whose axillary
temperature was taken at 5 P.M. and every two hours thereafter until
death. The hemiplegia was not very marked, but the hemorrhage was
extensive, involving the pons and left crus cerebri, the external
capsule, left crus cerebelli, and medulla, bursting through into the
fourth ventricle.

[Illustration: FIG. 38.]

The chart M. M. (Fig. 38), as taken from Bourneville, represents the
course of the temperature in a rapid case: each perpendicular line
denotes an hour.

The difference in the temperature of the two sides has been variously
stated, and probably depends on a number of factors besides the length
of time that has elapsed since the first attack. There is probably,
however, a tendency to excess of heat on the paralyzed side soon after
the attack, owing to vaso-motor paralysis; and this difference will be
more marked in the hands than in the axillæ. After a length of time
which may be from days to months the temperature becomes equalized, or
more frequently the relation is reversed, the paralyzed side being
colder as atrophy takes place. Lepine[19] gives a case where the
axillary temperatures of the two sides continued the same within a
small fraction of a degree for three days, and then separated very
slowly, until at death the {938} paralyzed side was six-tenths of a
degree (Cent.) hotter than the other, in both being inferior to the
rectal (107° Cent.).[20]

[Footnote 19: _Mémoires de Société de Biol._, 1867.]

[Footnote 20: The chart in the original, and as reproduced by
Bourneville, is wrongly lettered. The text says that the left side was
the hotter.]

[Illustration: FIG. 39.]

The chart C. M. (Fig. 39) shows the excess of temperature in a case of
meningeal hemorrhage. The dotted line is from the paralyzed side. The
first observation was made two and a half hours after the attack.

A very interesting case is reported by Johnson[21] of crossed
hemiplegia, where the temperature was about a degree higher on the
paralyzed side of the body, and, corresponding to this, the
sphygmograph showed a great diminution of tension; the lesion is
supposed to have been a hemorrhage in the pons. Johnson, in commenting
on the statement of Lorain that in all cases of hemiplegia the pulse
is more full on the paralyzed side, says that it is incorrect for
ordinary cases of hemorrhage into the corpus striatum, though true in
his own case.

[Footnote 21: _Brit. Med. Journ._, Jan. 6, 1877.]

The most marked differences of temperature have been observed where
the lesion has been in the neighborhood of the pons, crus cerebri, or
medulla oblongata. In a case reported by Allbutt there was a
difference of 1.6°; the radial pulse was softer and fuller on the
paralyzed side, and the cheek upon that side was flushed.[22] The
pulmonary hemorrhages which have been noticed by Brown-Séquard and
others in animals after cerebral lesions, and the extravasation,
congestion, subpleural ecchymoses noted by Ollivier[23] in cerebral
apoplexy, are probably to be referred to vaso-motor disturbances.

[Footnote 22: _Med. Times and Gaz._, Dec. 4, 1869.]

[Footnote 23: _Archives générales_, 1873, 167.]

Much more attention has been paid to the pulse than to the
temperature, but it is less easy to lay down definite rules in regard
to it. It may vary in either direction. When the case is approaching a
fatal termination the pulse is apt to accompany the temperature in a
general way in its rise, though not necessarily following exactly, as
is seen in the chart in Fig. 38.

The throbbing or bounding of the arteries often described may indicate
increased activity of heart, but means at the same time vaso-motor
relaxation. The urine and feces are often passed involuntarily.

In some rare cases symptoms closely resembling those produced in
animals by section of the sympathetic have been seen. These are false
ptosis, narrowing of the palpebral opening and sinking of the globe of
the eye {939} into the orbit, diminution in the size of the pupil,
higher temperature on the paralyzed side of the face and the
corresponding ear, abnormal secretion of the eye, nose, and mouth on
the same side.[24] They are supposed to indicate a paralysis of the
sympathetic.

[Footnote 24: Nothnagel, quoted by Grasset.]

The condition of general relaxation may be so profound as to cover up
everything else, but in many cases true paralytic symptoms may be
discovered or provoked, which even at an early period give us
information as to the locality and nature of the lesion.

A greater degree of muscular relaxation may be manifest on one side of
the face than the other; the forehead may be a little smoother on one
side, the corner of the mouth drooping, the downward line from the ala
of the nose flattened, and the cheek flapping. There may be a little
greater resistance to passive motion of the limbs on one side; one
hand on being raised may drop helplessly back to the bed, while the
other is laid slowly down; the right hand when pinched lies motionless
and without power to escape the pain until the left comes to its
assistance. Irregularity of the pupils, if present, is an important
sign, but its absence signifies nothing.

One of the most significant signs is the conjugate deviation of the
eyes, both eyes and the head being turned strongly to one side or the
other. When the lesion is above the pons and is irritative, as in the
early stage of hemorrhage, the deviation is toward the side of the
body affected and away from the lesion; when paralysis is established,
away from the paralysis and toward the lesion. Below the pons the rule
is reversed. The spastic stage of conjugate deviation may coincide
with stiffness (early rigidity) of the paralyzed limbs. This deviation
must not be mistaken for an accidental position of the head. The
patient should be addressed from the side away from which he is
looking. Sometimes the eyes can be brought to the median line, and not
beyond. An attempt to turn the head forcibly beyond the median line
occasionally causes pain. The value of this symptom in diagnosis has
been denied, but a part at least of the apparent contradictions have
arisen from the neglect to notice whether it were of a paralytic or
spastic character.

As the condition of unconsciousness gradually passes off, the face
regaining, at least in part, its natural and more intelligent
expression, the eyes trying to follow the movements of surrounding
persons, an attempt being made, perhaps only by an unintelligible
sound or by a nod, to answer questions, the tongue being protruded, or
at least an attempt toward it made, and some motions being made with
the limbs,—the exact extent and intensity of the paralysis become more
apparent. Conjugate deviation, if it have existed, may disappear
before the other symptoms, or, if it has been of the rigid form
depending on an irritative lesion, it may become paralytic, and is
then in the opposite direction. The patient is then usually found to
be in a condition of hemiplegia, and at this point the history of
hemorrhagic apoplexy becomes identical with that of paralysis from
hemorrhage where no truly apoplectic condition has been present.

Lidell states that in more than one-third of all cases of cerebral
hemorrhage hemiplegia is developed without loss of consciousness or
coma. In some, the paralysis precedes unconsciousness, which then
slowly supervenes.

{940} Hemiplegia (_ἥμι_, half, _πληγη_ blow) is a paralysis or paresis
of a part of the voluntary muscles of one side of the body, and a few,
in some cases, on the other, and is undoubtedly to be referred to a
lesion interrupting the nervous communication between the cortical
centres of motion and the nuclei of the motor nerves, cerebral and
spinal; the conductors passing through the corpora striata, the
internal capsule, the peduncles, and crossing in great part to the
other side above or at the lower border of the medulla oblongata, and
passing down the crossed pyramidal tracts of the cord, to be finally
connected with the anterior gray columns of the cord. The portion
which does not decussate passes down the inner border of the anterior
columns under the name of columns of Türck. The amount of decussation
which takes place varies somewhat, and the suggestion has been made,
in order to explain certain cases of paralysis occurring on the same
side with the lesion, that possibly in some rare cases there may be no
decussation. It has never been shown, however, that this condition,
highly exceptional if even it ever occurs, is present in such cases.

It may be said in a general way, although exceptions to the rule can
be found, that it is those muscles trained to separate, specialized,
or non-associated movements which are chiefly affected, while those
which are habitually associated in function with those of the other
side are less or not at all so. It would not, however, be in the least
correct to say that specialized or educated movements of any set of
muscles are alone paralyzed, since the fingers, which are trained to
the most independent movements, are often just as incapable of making
the slightest movement of simple flexion as of writing or sewing.

We have in ordinary hemiplegia more or less paralysis of the upper
facial, the patient not being able to close his eye or to wink quite
so well as on the paralyzed side. The forehead may be smoother on the
paralyzed side. This condition is usually slight and of short
duration, but varies in different cases. Paralysis of the lower facial
angle of the mouth and cheek is usually better marked, but not
absolute. The corner of the mouth droops, perhaps permits the saliva
to escape; the naso-labial fold is less deep, and the glabella
deviated away from the paralyzed side. The cheek flaps with
respiration. The difference between this facial paralysis connected
with hemiplegia and that dependent upon a lesion of the trunk or
distribution of the nerve (Bell's), as in caries of the temporal bone
or the so-called rheumatic paralysis, is very striking, the latter
being so much more complete, and, by affecting the orbicularis
palpebrarum so as to prevent closure of the eye, giving a very
peculiar expression to the countenance. This distinction between the
two portions of the facial seems to make an exception to the rule
stated above, since in most persons the movements of the corner of the
mouth and of the cheek are quite as closely bilaterally associated as
those of the eyelids.

Paralyses of the third, fourth, and sixth pairs upon one side of the
body are comparatively rare in hemiplegia, and when present are
usually referable to localized lesions in the pons. They are to be
looked upon as something superadded to the ordinary hemiplegia. These
nerves, however, are affected in the peculiar way already spoken of as
conjugate deviation, which phenomenon would seem to denote that
muscles accomplishing combined movements in either lateral direction
of both eyes, {941} rather than all the muscles of each, are
innervated from opposite sides—_i.e._ that the right rectus externus
and the left rectus internus are innervated from the left motor
centres, and vice versâ. Exactly the same remark will apply to the
muscles of the neck which cause the rotation of the head seen together
with the deviation of the eyes. The muscles controlling deviation to
one side, although situated upon both sides of the median line, are
apparently innervated from the side of the brain toward which the head
is turned in paralysis.

The tongue is usually protruded with its point toward the paralyzed
side; and this is simply for the reason that it is pushed out instead
of pulled, and the stronger muscle thrusts the tongue away from it.
The motor portion of the fifth is, according to Broadbent, affected to
a certain extent, the bite upon the paralyzed side being less strong.

The hand and the foot are the parts most frequently and most
completely affected, but one or the other may be partially or wholly
spared, though the latter is rare. The muscles of the limbs nearer the
trunk may be less affected, so that the patient may make shoulder or
pelvis movements when asked to move hand or foot. In severe cases even
the scapular movements may be paralyzed. The muscles of the trunk are
but slightly affected, though Broadbent states that a difference in
the abdominal muscles on the two sides may be perceived as the patient
rises from a chair. The respiratory movements are alike on the two
sides. A woman in the hospital service of the writer had a quite
complete left hemiplegia at about the seventh month of pregnancy.
There was some return of motion at the time of her confinement. None
of the attendants could perceive any difference in the action of the
abdominal muscles of the two sides, although, of course, the usual
bracing of the hand and foot upon the left side was wanting. The pains
were, however, generally inefficient, and she was delivered by
turning. Muscular weakness often exists, and in some cases the
non-paralyzed side shows a diminution of power.

The sphincters of the bladder and rectum frequently, and in severe
cases almost invariably, lose their activity for a time. It is
possible, however, that in some cases of alleged inability to retain
urine and feces the defect is really mental, and akin to the dirty
habits of the demented. The involuntary muscles probably take no part
in hemiplegia, with the very important exception of the muscular coats
of the arteries, which apparently share to a certain extent, and
sometimes the iris.

Speech may be attempted, and the words be correct, so far as they can
be understood, though the patient is apt to confine his remarks to the
shortest possible answering of questions. It is, however, thick and
indistinct, since the muscles of the tongue and lips are but
imperfectly under the control of the will. This condition may be
connected with paralysis of either side, and is to be sharply
distinguished from aphasia or mental inability to select the proper
word or to determine the necessary movements for its pronunciation.
Aphasia is almost invariably connected with paralysis of the right
side, and will be minutely spoken of hereafter. There is, of course,
nothing to prevent the coexistence of the two conditions, but aphasia
cannot well be shown to exist until we have reason to suppose, first,
that the patient has ideas to express, and secondly, that the
paralysis of the muscles of the lips and tongue has more or less
completely disappeared. The patient may indistinctly mumble a word
which, {942} however, can be understood to be appropriate to the
occasion (defective articulation, glosso-labial paralysis), or, on the
other hand, pronounce with distinctness an entire wrong word or a
number of sounds without meaning (aphasia).

Sensibility—that is, ordinary cutaneous sensation—and, so far as we
can judge, the special senses, are not greatly affected after the deep
coma has passed off, but exceptions to this rule will be noted later.

Having described this most typical but not most common form of
cerebral hemorrhage—that is, the form in which both lesion and
symptoms are most distinct and can be most clearly connected—we have a
point of departure for conditions less clearly marked and less easily
explained.

It is probable that cerebral hemorrhage is much less likely than
cerebral embolism to take place without any disturbance of
consciousness or abnormal sensations; but there can also be little
doubt that a certain amount of paralysis is often accompanied by no
other symptoms, and post-mortem appearances often show the remains of
small hemorrhages which have passed unnoticed or are lightly
estimated. It is highly probable that small hemorrhages may give rise
to symptoms which pass for only a little accidental vertigo or a
slight feeling of faintness, until a later and more serious attack
gives a more definite explanation.

On the other hand, we have a set of cases in which all the symptoms of
cerebral hemorrhage may be present without the lesion. Many of these
are of course due to embolism, which will be considered later; but
besides this condition, recognized as softening for many years, we
find described under the head of simple, congestive, serous, and
nervous apoplexy cases where sudden or rapid loss of consciousness
occurs with general muscular relaxation, which, when fatal, show
nothing beyond changes in the circulation—_i.e._ in the amount of
blood in the cerebral vessels or of serum in the meshes of the pia or
at the base of the brain.

Besides these, there are cases of temporary unconsciousness with
complete recovery—the coup de sang of the French, or rush of blood to
the head, which are attributed to congestion of the brain—a theory
difficult to prove or disprove, but not in itself unreasonable.
Trousseau, without denying the possibility, or even probability, of
such a condition, says that which has been called apoplectiform
cerebral congestion is in the greater number of cases an epileptic or
eclamptic accident, sometimes a syncope. Simple epileptic vertigoes,
vertigoes connected with a bad condition of the stomach or diseases of
the ear, are wrongly considered as congestions of the brain. He speaks
of various conditions, such as violent attacks of whooping cough, the
expulsive efforts of women in labor, the congested faces of laborers
under heavy burdens, to show that cerebral congestion does not give
rise to an apoplectiform attack; and it is undoubtedly true that, as a
rule, no long-continued attack is the result; but it must be within
the personal experience of almost every one that decided cerebral
disturbance is produced for a few moments by such efforts, as, for
instance, blowing a fire with the head down. Besides this, a laborer
under a heavy load is presumably healthy and accustomed to his work,
so that his arteries may be supposed capable of maintaining a due
balance between arterial and venous blood in the brain; and, again,
although the ordinary efforts of women in labor do not cause
unconsciousness, puerperal {943} convulsions, involving a longer
period of violent muscular action, may do so, and even give rise to
hemiplegia.

Whatever name we may adopt for the temporary cases which recover,
there are others, and fatal ones, which are not explained by any
change in nomenclature. Epilepsy may, it is true, occur under such
circumstances that no convulsion is observed, but, on the other hand,
convulsions may accompany not only an attack of unconsciousness, but
actual cerebral hemorrhage.

Cases of sudden death with no discoverable lesion furnish abundant
opportunity and temptation for conjecture, and it is well known that
too much dependence must not be placed upon the post-mortem
appearances as to the amount of blood in the brain before death, and
probably just as little upon the amount of serum, except as indicating
a condition of atrophy.

Syncope, either from over-stimulation of the pneumogastric or from
simple failure of the heart, may be put forward to explain some cases
of sudden death, but seems to have no advantage as a universal theory
over the older one, which meets with so little favor. Lidell gives no
less than seventeen cases which he classifies as congestive or serous
apoplexy. They are not all equally conclusive, and were almost all of
alcoholics. In some of these there were absolutely no appearances
which could account for death. The two most characteristic of
congestive apoplexy were, first, a young negress who experienced a
violent fit of passion, became unconscious, with stertorous breathing,
and died, having had some tonic spasms. The brain contained a large
amount of blood in the vessels, but no effusion. Second, a
semi-intoxicated woman, aged thirty, became very angry, fell
insensible, and expired almost immediately. The brain contained an
excess of blood, with no effusion. In both these cases the patients
were subject to fits under the influence of strong excitement, but in
both the author took pains to inquire into and negative the
probability of epilepsy of the ordinary kind; and a change of name
does not go far toward clearing up the pathology.

Lidell's case (XXII.) was that of a man accustomed to alcohol, thin
and pale, who had an apoplectic fit with coma and hemiplegia. He
regained consciousness on the second day, and the hemiplegia
disappeared in a fortnight. This rapid and complete recovery,
exceptional to be sure, cannot be regarded as proof of the absence of
hemorrhage or embolism. In fact, the latter is highly probable. It is
possible that the clot may have been partially dislodged, so as to
allow some blood to pass by it, or that an exceptionally favorable
anastomosis allowed a better collateral circulation than usual to be
established.

The following case occurred in the service of the writer: An elderly
negress, who had extensive anasarca and signs of enfeebled action of
the heart without any valvular lesion being detected, after washing
her face was heard to groan, and found speechless and unable to
swallow, with complete right hemiplegia. There was a slight
improvement in a few hours, but she died two days later. The autopsy
disclosed some hypertrophy and dilatation of the heart without
valvular lesion. A careful search failed to discover any change in the
brain or obstruction in its vessels, although there was chronic
endarteritis.

The relations between epilepsy, apoplexy, and syncope are interesting
{944} and important, but are certainly far from clear. Little is
gained by shifting obscure cases from one category to the other. If
sudden deaths be synonymous with apoplexy, we shall certainly have to
admit that apoplexy does not always demand for its cause cerebral
changes sufficiently marked to be recognizable after death. If, on the
other hand, we refer them to heart disease, we shall have to admit
that a heart without valvular disease or extensive changes in its
muscular substance may cease to beat under influences as yet not well
understood.

Since the paralysis arising from hemorrhage resembles so closely in
its progress that dependent upon occlusion of the cerebral vessels, a
further description will be deferred until the latter lesion has been
described; but this remark does not apply to the premonitory and
initiative symptoms, which may be of great importance, and which are
not always the same with the two or three sets of lesions. There are
many of them, but, unfortunately, no one among them taken alone can be
considered of high significance, unless we except what are sometimes
called premonitory attacks, which are in all probability frequently
genuine hemorrhages of so slight extent that they produce no
unconsciousness, and but slight paralysis easily overlooked. A little
indistinctness of speech or a forgetfulness of words, a droop of one
angle of the mouth, or heaviness in the movement of a foot or hand,
lasting but a few moments, may be real but slight attacks, which may
be followed either by a much more severe one, by others of the same
kind, or by nothing at all for a long time. They are sufficient to
awaken apprehension, and to show in what direction danger lies, but
they give little information as to the time of any future attack.

Retinal hemorrhage is admitted by all modern authors to be connected
with disease of the vascular system, and hence also with renal
inflammation and cerebral lesions. The writer is greatly indebted to
Hasket Derby for the following facts: Out of 21 patients who had
retinal hemorrhage, and of whose subsequent career he had information,
9 had some sort of apoplectic or paralytic attack; 1 had had such an
attack before she was examined; 3 died of heart disease, 1 suddenly,
the cause being variously assigned to heart disease or apoplexy; and 6
were alive when heard from, one of these, a man of forty-eight, being
alive and well fourteen years after.

Bull[25] describes four cases of his own where retinal hemorrhage was
followed by cerebral hemorrhage, demonstrated or supposed in three,
while in the fourth other symptoms rendered a similar termination by
no means improbable. He quotes others of a similar character. The
total number of cases which were kept under observation for some years
is, unfortunately, not given. In a case under the observation of the
writer a female patient, aged fifty-seven, who had irregularity of the
pulse with some cardiac hypertrophy, was found to have a retinal
hemorrhage two and a half years before an attack of hemiplegia. The
hemorrhage was not accompanied by the white spots which often
accompany retinitis albuminuria.

[Footnote 25: _Am. Journ. Med. Sci._, July, 1879.]

In a case reported by Amidon[26] retinal and cerebral hemorrhages seem
to have been nearly simultaneous a few hours before death. There was
diffuse neuro-retinitis and old hemorrhages besides the recent one.

[Footnote 26: _N. Y. Med. Rec._, 1878, xiv. 13.]

{945} The highly interesting observation has been made by
Lionville[27] that when miliary aneurisms are present in the brain,
they may often be found in the retina also. In one case where they
were very numerous in the cerebrum, cerebellum, pons, and meninges,
aneurismal dilatations were found also in the pericardium, mesentery,
cervical region, and carotids (the latter not being more minutely
described). There was very general atheroma and numerous points of
arteritis. The retinal aneurisms varied in size from those requiring a
power of ten or twenty diameters to be examined up to the size of a
pin's head or a millet-seed. He thinks they might have been recognized
by the ophthalmoscope.

[Footnote 27: _Comptes Rendus de l'Acad. des Sci._, 1870.]

The hemorrhages accompanying idiopathic anæmia and other diseases with
a similar tendency are not to be taken into this account. Hemorrhage
accompanying optic neuritis is likely to be due to some disease of the
brain other than the one under consideration.

Mental disturbances of various kinds have been considered as
significant, and Forbes Winslow gives a great many instances of
different forms, but they are to be looked upon rather as indicating
chronic cerebral changes which may result in various conditions, of
which hemorrhage may be one, than as furnishing any definite
indication of what is to be expected. Loss of memory should be
regarded in this way. Some acute or temporary conditions of depression
may affect the nutrition of the brain in such a way, without having
anything to do with hemorrhage actual or anticipated.

Aberrations of the special senses are often observed, such as noises
in the ears more or less definite, the sight of colors (red), or being
unable to see more than a portion of an object. The fact to which
these testify is probably a localized disturbance of the circulation
which may not precede rupture of the vessels.

Distinct hallucinations of hearing, followed by those of smell and
succeeding irritability, sleeplessness, were observed by Savage[28] in
a case which terminated soon after in apoplexy.

[Footnote 28: _Journ. Ment. Sci._, 1883, xxix. 90.]

There are few symptoms which are more likely to excite alarm and
apprehension of a stroke of paralysis than vertigo or attacks of
dizziness, but it is too common under a great variety of circumstances
to have much value, and is, as a matter of fact, rarely a distant
precursor of intracranial hemorrhage, although it frequently appears
among the almost initiatory symptoms, especially when the lesion is in
the cerebellum, so that, if continuous, it is not likely to mean that
anything worse is coming. It has been said to be strongly significant
if occurring without the digestive derangements or circulatory
disturbances likely to cause it, and be unconnected with disease of
the ear. Unfortunately for diagnosis, but fortunately for the
patients, the so-called vertigo a stomacho læso, may arise in cases
where the stomach trouble is very difficult or impossible to detect,
and it often continues for weeks or months after the most careful
regulation of the diet, and yet is followed by no cerebral lesion.
Although a vertigo for which every other cause can be excluded
certainly justifies a suspicion of cerebral trouble, the tendency to
exaggerate its prognostic importance should not be encouraged by the
physician, as it may exist a long time, and disappear without another
sign of the catastrophe which has been keeping the patient in dread.

{946} Among the more significant and immediate symptoms are to be
reckoned paræsthesiæ of the side about to be paralyzed, such as
numbness or tickling. Headache of great severity is often, but not
invariably, present. It has nothing characteristic about it, except
that it may be different from those the patient has been in the habit
of having, or may be of unusual severity, so that the patient says it
is going to kill him. Such a headache in a person in whom there is
good reason, from age, interstitial nephritis, or other symptoms, to
suspect the existence of vascular lesions is likely to be an immediate
precursor of a hemorrhage. Persistent early waking with a slight
headache, which passes off soon after rising, is said by Thompson[29]
to be a somewhat frequent premonition. Vomiting is hardly a
premonitory, but may be an initial, symptom, especially in hemorrhage
of the cerebellum.

[Footnote 29: _N. Y. Med. Record_, 1878, ii. p. 381.]

Reference is had in these statements chiefly to the ordinary form of
cerebral hemorrhage. Of course if, during a leucocythæmia or purpura,
large hemorrhages occur elsewhere, it may be taken as a hint that
possibly the same thing may take place in the brain.

These signs of arterial disease must be considered as of the highest
importance among the (possibly remoter) premonitory signs, not only of
cerebral hemorrhage, but of the other lesions treated in this article.
Atheroma and calcification of the tangible arteries place the
existence of peri-endarteritis among the not remote possibilities.
High arterial tension has already been spoken of in connection with
etiology, and its presence should be sought for. An irregular and
enfeebled cutaneous circulation has been spoken of as an indication of
value.

OCCLUSION OF THE CEREBRAL ARTERIES may take place from several causes
other than those which concern us here, as from the pressure of tumors
or endarteritis, usually syphilitic. Thrombosis and embolism are
grouped together from their great anatomical resemblance and their
frequent coexistence, but the symptoms produced, although ultimately
the same, are often different enough to make it necessary to bear in
mind the fact that there is a distinction—that is, that embolism is
rapid and thrombosis is slow.

A cerebral artery may be occluded from the presence of a plug of
fibrin more or less intermixed with the other elements of the blood.
This plug may have been formed in situ, and is then somewhat firmly
attached to the walls of the vessel, and partly decolorized at its
oldest portion, while on each side of it, but especially on the side
away from the heart, it is prolonged by a looser and darker clot of
more recent origin. This is a thrombus.

When the plug has been transported from elsewhere it is embolus.[30]
It may consist of various substances, as described in the article on
General Pathology, but is usually of fibrin which has formed a
thrombus or vegetation elsewhere, and, having been broken off, is
carried by the blood until it comes to a place too narrow for it to
pass, or where it lodges at the bifurcation of a vessel. The piece of
fibrin thus lodged has a strong {947} tendency to cause a still
further deposition—that is, a secondary thrombus—which may progress
until it comes to a place where the blood-current is too strong for
the process to go on any farther. It may in such cases not be obvious
at the first glance whether the whole process is thrombosis or whether
it started from an embolus.

[Footnote 30: The Greek word _εμβολος_ (_εν_, in, and _βαλλω_, to
throw) signifies the beak or rostrum of a ship of war. _Εμβολον_
signifies wedge or stopper, and would certainly seem the appropriate
form to be adopted for anatomical purposes. As uniformity of
nomenclature, however, seems more to be desired than etymological
accuracy, the writer has conformed in this article to the general
usage.]

It is probable that a thrombus forming at one point in a cerebral
vessel may break to pieces and its fragments be carried farther along,
forming a number of small emboli. (See Capillary Embolism.) Embolism
or thrombosis may take place anywhere in the brain or body generally,
but has certain points of preference. Of these, the most usual in the
brain is in the neighborhood where the internal carotid divides into
the anterior and middle cerebral, or in either of these arteries,
especially the middle, beyond this point. The plug may be situated in
the carotid just before this point, or even as low down as its origin
from the common trunk. Emboli lodge in this region, somewhat more
often upon the left side. The brain is said to be third in the order
of frequency with which the different organs are affected by embolism,
the kidneys and spleen preceding it. It has been found that small
emboli experimentally introduced into the carotids are found in much
larger numbers in the middle cerebral than elsewhere. It is the
largest branch, and most nearly in the direct line of the carotid.
Position undoubtedly influences the point at which an embolus lodges,
as it probably moves slowly along the vessels and along their lower
side. It has been remarked that, on account of this course of the
embolus, it is doubtful whether it can get into the carotid when the
patient is standing, but it certainly can do so when he is sitting up;
which, so far as the direction of the carotids is concerned, is the
same thing. The frequency with which a hemiplegia is observed when a
patient awakes in the morning may perhaps be accounted for by the
position favoring the passage of an embolus into the carotid, which
otherwise would reach organs more remote.

The vertebrals and basilar are not infrequently affected.

The sources whence cerebral emboli may spring are various, but cannot
be found outside a certain range. They may, in the first place, be
torn off from vegetations upon either the mitral or aortic valves; and
this source is probably the most common. The appendix of the left
auricle may furnish a plug from the thrombi formed among its
trabeculæ, or the aorta from an aneurism or from parietal thrombi
formed, upon spots roughened by atheroma. The pulmonary veins are
occasionally the source of the embolus, though this is not very
common.

It is rather doubtful whether an embolus can find its way from the
systemic veins through the lungs to the brain, but it is possible that
small emboli may do so, and increase in size from the addition of
fresh fibrin when floating in the blood-current. The occurrence of
pyæmic abscesses in the brain would suggest the possibility of this,
though it is, on the other hand, possible that the brain abscesses are
secondary to older ones in the lungs. In some cases, however, a
careful examination does not disclose the source of the embolus.

In the blood-current the embolus may give rise to no symptoms
whatever, and even after its arrival in the cerebral circulation it
may lodge in such a way as not entirely to obstruct the current. In
most instances, however, it does not stop until it plugs the vessel
completely and arrests {948} the current of blood beyond it for a
moment. Whether it shall completely deprive the portion of brain to
which it is distributed depends upon its situation as regards
anastomoses and upon the formation of secondary thrombus. Hence the
knowledge of the distribution of the arteries supplying the brain—that
is, the two carotids and two vertebrals—is of more importance in
reference to embolism and thrombosis than to cerebral hemorrhage,
where the effusion takes place from quite small branches.

The anterior portion of the brain, including the anterior and
posterior central convolutions and the first temporal, are supplied
with blood by the two terminal branches of the internal carotid, the
anterior and middle cerebral, the ganglia underlying these portions of
the cortex being supplied, as already stated, by small branches
arising near the origin of these two trunks, and principally the
second. The anterior cerebrals of the two sides are connected by the
anterior communicating, which is a short and usually wide vessel.
Sometimes one anterior cerebral branches in the longitudinal fissure,
and supplies a part of both sides. Hence in plugging of one internal
carotid which does not reach its bifurcation a collateral supply may
be received from the other side. If, however, an embolus or thrombus
has penetrated beyond the origin of the middle cerebral, this vessel
can no longer receive a supply from the anterior.

The posterior communicating arteries are two small vessels which
connect on each side the posterior cerebrals and either the carotid,
just as it gives off its two chief cerebral branches, or else the
middle cerebral close to its origin. These arteries may be of quite
unequal size, that upon the right usually being the larger, and
sometimes so large as to give the appearance of being the principal
origin of the posterior cerebral. When this happens the part of the
posterior cerebral which arises from the basilar may be reduced to a
minute arteriole, and the basilar, almost entire, goes to supply the
left side of the brain. This condition of the posterior communicating
may exist to some extent on both sides in the same brain. It is
probable that in many cases these arteries are too small to be of
great value in re-establishing the circulation in the anterior portion
of the brain when it is suddenly interrupted by an embolus.

When the large trunks leave the circle of Willis to be distributed
upon the surface of the brain, after giving off from the first
centimeter or two of their course the nutrient arteries for the
deep-seated ganglia, they break up into several branches which ramify
upon the surface, but, as Duret has shown, undergo very few
anastomoses. Instead of forming, as was once supposed, a richly
inosculating network, small branches penetrate into the
brain-substance perpendicularly from the superficial vessels, but
these do not communicate freely with each other by vessels larger than
capillaries.

From these anatomical conditions it happens that when a vascular
territory is deprived of its normal supply by an embolus, it cannot be
supplied with blood from surrounding districts. A certain limited
amount of collateral supply is possible through the capillaries and
the rare anastomoses, but it is only around the edges, and the centre
of the territory becomes destitute of circulating blood. Thus an
embolus does not in the brain produce, as it does in other organs with
more abundant collateral supply, a large hemorrhagic infarction.

{949} Small hemorrhages may, however, take place around the edges of
the softening, and when a number of small emboli are present, so as to
afford a number of overlapping areas with their borders of congestion,
a red softening may be the result. When the emboli are very small, and
at the same time not numerous enough to occlude all the ultimate
ramifications of a trunk, the vascular compensation may be rapidly
completed.

The change produced in the cerebral substance from cutting off its
supply of blood is known as anæmic necrosis, and includes what has
been known as white softening, with probably some yellow, and possibly
a little red softening, the latter in case where simple softening has
been complicated by hemorrhage.

When the circulation ceases the substance that should have been
nourished loses its firmness and acquires a custard-like consistency.
The gray and white substances are no longer so distinct in appearance,
the latter losing its milky-white color, the whole surface of a
section becoming of a dirty yellowish-white, somewhat shining, and
looking as if it contained more moisture than normal. When a
considerable portion of the interior of the hemisphere is thus
affected, the brain outside, with its membranes, bags down, looks
swollen, and feels to the fingers as if there were present a sacful of
fluid. The boundaries of such an area of softening are marked off from
the healthy substance with some distinctness, though less than that of
a hemorrhage. There may be some hemorrhage around the edges or into
the cavity, so that the presence of a little blood-pigment is no proof
that the original lesion was not softening from occlusion. In the
further progress the contents of the cavity become more fluid, and
finally a somewhat distinct cyst is formed, not unlike that from a
hemorrhage, with an internal areolar structure from the remains of
connective tissue, and contents of a slightly yellowish or brownish
color, or often of a chalky white. These cysts have little to
distinguish them, when old, from similar ones left by hemorrhage,
except the much greater amount of pigment in the latter. The smaller
spots of softening may after a time lose their fluidity, and remain as
yellowish patches as firm as, or firmer than, the surrounding brain.
The region of the brain involved becomes atrophied, the convolutions
shrink, and the membranes become filled with serous fluid, to
compensate for the sinking of the surface.

The microscope shows gradually increasing fatty degeneration,
disorganization of the nervous tissue, and degeneration of its
elements. The pyramidal cells are sometimes distinctly recognizable by
their form, and show gradual transition into the indeterminate round
granulation-corpuscles. The vessels exhibit fatty degeneration of
their coats, as well as accumulation of fatty granules between the
vessel and the lymphatic sheath. The clot which blocks the artery
becomes adherent to its walls, and the vessel with its contents forms
a round solid cord.

In a few instances the thrombi have become perforated through the
centre, so that a channel is formed for a renewal of the circulation.
There is no reason to suppose that this takes place soon enough to be
of any advantage in restoring the nutrition of the necrosed portions
of brain.

The region involved in softening depends upon the artery which is
plugged and the location of the obstructing body. The place of
election seems to be the carotid near its separation into its large
branches, or these {950} branches after the separation, especially the
middle cerebral, this being peculiarly liable because it is the
largest branch and is the continuation in a direct line of the
carotid. It is more frequent upon the left side. Cases have been
observed where the whole of one hemisphere was softened from
obstruction of the carotid at its bifurcation; which may be accounted
for, as Charcot suggests, by an unusual distribution of the arteries,
as described above, the posterior cerebral as well as the other two
being derived almost entirely from the carotid. In a case recently
observed by the writer the whole right cerebral hemisphere, with the
exception of the tip of the frontal and tip of the occipital lobes,
was softened to the consistency of custard, a thrombus extending from
the bifurcation of the common carotid into all the ramifications of
the middle cerebral. The most common form, however, is where more or
less of the brain around the fissure of Rolando and fissure of
Sylvius, with or without the underlying ganglia, is softened. This
happens from a lodgment of the embolus in the middle cerebral. If the
obstruction be close to the origin of the artery, the corpus striatum
suffers, from the mouths of its small nutrient arteries arising in
this part of its course being stopped, while if it have passed along a
little farther, these remain open, and the cortex, to which the larger
branches are distributed, alone is softened.

The anterior cerebral is not infrequently affected, either alone or
with the middle, and in these arteries as well as the posterior the
embolus, if of small size originally, may penetrate so far as to give
rise only to quite a limited anæmia. The basilar is an artery not very
rarely occluded, though more commonly by thrombus than embolus. This
occlusion may be so limited as to affect only the nutrient arteries of
the pons and cause a very limited softening, the parts before and
behind it being supplied by the unobstructed portion or by collateral
circulation from the carotids. Occlusion of the cerebellar arteries
and softening of the cerebellum are among the rarer forms. The
vertebrals themselves are sometimes plugged. A thrombosis has been
observed in the only inferior cerebellar artery which existed, causing
softening in both lobes. There was atheroma of the heart and arteries,
and a thick calcareous plate in that which was occluded.[31]

[Footnote 31: _Progrès méd._, 1876, 373.]

In a general way, it may be said, with many exceptions on both sides,
that thrombosis and embolism tend to affect the cortex, and hemorrhage
the central ganglia.

What has just been written applies to the simple mechanical action of
emboli. If, however, they have a septic origin, as notably in cases of
ulcerative endocarditis, the region in which they lodge becomes,
instead of a simple spot of necrosis, a septic focus or abscess, with
its results of compression or irritation. In such a case there are
likely to be abscesses of similar origin in other organs, and the
cerebral lesion is only a part of the general pyæmic condition.

ETIOLOGY.—So far as the lodgment of an embolus in an artery is
concerned, it can hardly be said that there is any etiology, for the
detachment of the plug from its place of origin is purely a matter of
accident, and may take place at any time. As to its origin in the form
of fibrinous deposit on the valves of the heart or a roughened spot on
the aorta, we must refer to the article on General Pathology. The most
important {951} condition for embolism is disease of the valves of the
heart, rheumatic or otherwise. Next comes arterial disease, producing
roughening of the inner coat and subsequent deposition of fibrin. So
far as we can tell, the causes leading to endarteritis or atheroma are
essentially the same as those which produce the periarteritis
described in connection with cerebral hemorrhage, and we may therefore
put down old age, alcohol, and strain as among the causes of cerebral
embolism. Injuries of the lungs leading to thrombosis of the veins may
be considered as possible sources for the formation of an embolus, and
we might suppose that phthisis and pneumonia would furnish plugs which
would lodge in the brain, though as a matter of fact they seldom do
so.

Experience shows that embolism, unlike hemorrhage, is not specially a
disease of advanced life, but is distributed over different periods,
with preference for old age less marked than with hemorrhage. Andral
gives the ages of patients with softening—which, however, includes
thrombosis as well as embolism—as follows: the average would
undoubtedly be displaced in the direction of youth if thrombosis could
be taken out of the list:

  -----------------+-------------------+------------------------
        Andral:    |       Andral:     | Cases (with autopsies)
  Beginning of     | Death with        | of embolism,
  softening in 27  | softening in 153  | thrombosis, and
  cases.           | cases.            | softening—25 cases.
  -----------------+-------------------+------------------------
    17-20      4   |   15-20      10   |   20-30         4
       27      2   |   20-30      18   |   30-40         3
    30-37      2   |   30-40      11   |   40-50         3
    43-45      2   |   40-50      19   |   50-60         1
    53-59      4   |   50-60      27   |   60-70         5
    63-69      7   |   60-70      34   |   70-80         2
    76-78      6   |   70-80      30   |   Young         1
                   |   80-89       4   |   Middle-aged   1
                   |                   |   Old           5
  -----------------+-------------------+------------------------

In the etiology of cerebral arterial thrombus there seem to be two
factors of prime importance, although there are cases which seem to
demand a third, and Charcot[32] suggests the possibility of some hæmic
dyscrasia favoring the formation of a thrombus, and relates a case of
thrombosis of the middle cerebral, with three others of the same
process in other arteries, occurring in patients with uterine cancer,
where all the usual sources of emboli were explored with negative
results. The first of the two is disease of the cerebral arteries, not
necessarily extensive, but sufficient to form a starting-point on the
inner wall for the deposit of fibrin. In this respect the etiology of
thrombosis may be various. Syphilitic endarteritis, for instance, may
very easily give rise to this lesion, but it is likely to be
accompanied by others, and has a symptomatology more or less peculiar
to itself. It is not, of course, to be included with the form we are
considering.

[Footnote 32: _Comptes Rendus Soc. de Biol._, 1865, p. 24.]

The second factor—one which is perhaps capable of giving rise to
coagulation of the blood or deposit of fibrin without any arterial
disease—is weakness of the heart, connected or not with anæmia. The
causes of this condition may be manifold, and are likely to lead to
many other consequences than cerebral thrombosis. A thrombus may form
upon a very small basis of atheroma. Several of these points are
illustrated in the {952} following case: A lady, aged about
sixty-five, had had for many months vague symptoms of want of
strength, fatigue, want of appetite, and so on, with complaints of
distress and fulness in the abdomen, for which no special cause could
be found. On one occasion she was unusually long in dressing, and her
expression was noticed to be changed and her voice altered for a few
moments. The pulse was habitually 60 or less, and at times irregular,
but nothing abnormal could be detected in the sounds or position of
the heart. Fatty degeneration was suspected. One morning, after going
to bed in her usual health, she was found on the floor of her room
unconscious and with left hemiplegia. She lived about thirty-six
hours. The autopsy showed nothing abnormal in the abdomen except a
considerable accumulation of fat; and in the thorax the heart appeared
normal, and was not fatty. There was very little atheroma. In the end
of the internal carotid artery was a thrombus, of which the lower and
firmest part was connected with a very small spot of roughening just
at the point where the artery comes through the base of the skull. It
extended just beyond the origin of the middle cerebral artery, which
was of course occluded. The corresponding region of the brain was
converted into a vast mass of softened tissue.

The SYMPTOMS of the lodgment of an embolus in the brain may closely
resemble, or even be precisely the same as, those of hemorrhage.
Unless, however, an embolus makes a pause on its journey, giving rise
to a partial obstruction before there is a complete one, or unless the
obstruction is not absolute until after the formation of a secondary
thrombus, the attack may be absolutely sudden.

A thrombus, however, is slower in its formation, and may produce
gradually increasing anæmia of the region of brain supplied before it
is absolutely complete, with a gradually increasing paralysis and loss
of consciousness slowly approaching. Thus we may have the early
symptoms in the form of headache, vertigo, heaviness, and drowsiness,
peculiar sensations in the limbs about to be paralyzed or in the head,
delirium of various kinds, or hysterical manifestations. Prévost and
Cotard[33] lay special stress upon the importance of severe vertigo
(étourdissement) as a prodrome or warning of softening, especially in
the aged. It is dependent upon anæmia of the brain, and this, in its
turn, upon atheroma of the arteries, and sometimes at least upon
feebleness of the circulation, both of these being conditions likely
to cause the deposit of a thrombus. As, however, the thrombus does not
necessarily result from these conditions, and as the vertigo may arise
from other sources, as stated under the head of Cerebral Hemorrhage,
it is to be looked upon with special suspicion chiefly in those cases
where other symptoms might lead in the same direction, and when other
causes can be excluded.

[Footnote 33: _Mémoires de la Soc. de Biol._, 1865, p. 171.]

The same authors also speak of less defined symptoms, like delirium
and stupor, occurring among the inhabitants of the Salpêtrière (old
women), with intervals of comparative health, as being premonitory.

It is possible, however, for the symptoms of thrombus to be developed
rapidly when, as in the case last described, the thrombus begins to
form in a place which does not entirely interrupt the current, but
afterward reached the mouth of a large vessel, which it closes.

The loss of consciousness, coma, and all the phenomena of the {953}
apoplectic attack, with the possible exception of early rigidity, may
be as fully developed from occlusion of the cerebral vessels as from
their rupture; but it must be said that it is more common to meet with
them in cases of large hemorrhage than with either embolism or
thrombosis.

The general functions are even less disturbed than with a hemorrhage
producing an equal extent of paralysis. The temperature follows nearly
the same course as in hemorrhage, except that the initial fall, if
present—which is not always the case—is said to be less than with
cerebral hemorrhage. To this succeeds a rapid rise, which, even in
cases which are to terminate fatally, gives place to a fall to the
neighborhood of normal, and another rise before death. These are the
statements of Bourneville. The rise is said not to be so high as with
hemorrhage.

The annexed chart is from a man (W. I. W.) who was in the hospital
with ill-defined nervous symptoms, and was suddenly attacked with
convulsions, vomiting, and unconsciousness. He had a small tumor at
the point of the right temporal lobe, and softening of the left corpus
striatum. The apoplectic symptoms occurred on the 15th—that is, as
will be seen by the chart, one day after the temperature began to
rise. The pulse and respiration show no characteristic changes.

[Illustration: FIG. 40.]

It is much more common for the embolus or thrombus to give rise to a
set of symptoms less severe than a fully-developed apoplectic fit.
During such a fit—or, more clearly, as it is passing off—we find more
or less marked paralytic symptoms, but these are quite as frequently
present without the loss of consciousness. The patient states that he
waked up and found one side of his body helpless, or that he was
reading the paper when it fell from his hand, and upon trying to walk
found that he could not do so. Loss of speech may be an initial
symptom. It has been spoken of as premonitory, but it is probable that
it is in reality only the beginning, which, in some cases may go no
farther, but is usually succeeded by more extensive paralysis, which
makes its meaning unmistakable. These symptoms may be hours or even
days in developing, with occlusion as well as with hemorrhage. Very
slight attacks may occur which hardly excite attention, and lesions
are found after death in many cases to which there is nothing in the
history to correspond.

Improvement may begin very rapidly in some cases where the lesion is
small, a sufficient amount of collateral circulation being developed
to {954} prevent the structure from being disorganized. In others a
specially favorable anastomosis may preserve even a larger area, but
in others still it is not easy to account on entirely anatomical
grounds for the amount of improvement which takes place.

From this point onward the history of hemorrhagic and of embolic and
thrombotic paralysis is essentially the same, and the description of
the principal phenomena and progress of hemiplegia will apply to all.

SYMPTOMS AND PROGRESS OF HEMIPLEGIA DEPENDING ON CEREBRAL HEMORRHAGE
OR OCCLUSION OF THE CEREBRAL VESSELS.—The cerebral cortex represents
the centres for many of the higher nervous functions, spread out in
such a way that they may be more or less separately affected, while
the corpora striata and internal capsules are the regions where the
various conductors are crowded together, so that embolism, when
affecting small vessels and limited areas of the cortex, more
frequently gives rise to narrowly-defined groups of symptoms than
hemorrhage, which, taking place oftener in the central ganglia, is
able to cut off the communication from large masses of cerebral tissue
at once. This is a general remark, tending to explain why aphasia, for
instance, is often spoken of as especially a symptom of embolism,
while it is in reality common to all the lesions that affect the
proper locality.

The motor paralysis, more or less complete, which has been described
under the head of Hemorrhage continues indefinitely. It may disappear
rapidly, so that motion begins to return in a day or two, and goes on
to complete recovery in a short time. On the other hand, it may be
months before the flexion of a finger or a toe gives the slightest
token of the will resuming its control. The face often recovers its
symmetry before the limbs are fully restored, but the leg may be used
in locomotion before the complete recovery from paralysis, since the
tone of the muscles is sufficient to keep the knee straight enough for
support, as if the leg were all in one piece, while it is swung around
at each step by the pelvic muscles. We may meet with all degrees of
recovery—from that which is absolutely complete and comparatively
rare, through the case where a little want of play upon one side of
the face, a little thickness of speech, a feeble or awkward grasp of
the hand, betrays what has happened, or that of the man so often seen
in the streets with a mournful or stolid face, the arm in a sling or
dangling straight down by the side, and swinging one leg awkwardly
around, to the helpless paralytic lifted in and out of his chair or
lying almost motionless in bed, and living only to be fed and be kept
clean.

Involuntary movements may take place in limbs entirely incapable of
voluntary ones, and may occur under conditions of excitement or with
other involuntary movements, such as gaping. On the other hand, the
patient often moves the well hand while making utterly ineffectual
attempts on the paralyzed side. Involuntary twitching of the feet may
be annoying. Reflex movements, especially of the feet, are often
exaggerated, and in fact the twitching just spoken of is often excited
by some trifling, perhaps unperceived, irritation. A touch with the
point of a penknife upon the sole of the foot may call out a movement
which the patient is utterly incapable of executing by the force of
the will, and the appearance of volition is often increased by the
grimace or exclamation of pain or annoyance.

{955} Epileptiform attacks may be a sequence of hemiplegia, occurring
at irregular intervals, and not of great severity. Sometimes the
patient seems depressed or less talkative for a day or two previously,
and relieved after the fit has occurred, as in true epilepsy.

Comparatively little attention has been given to the condition of
sensation in hemiplegia. In the more complete apoplectic stupor it is
apparently abolished, like nearly all the functions above those of
respiration and circulation, but it often happens when the patient is
unable or unwilling to make any voluntary response to the voice, and
lies apparently perfectly indifferent, that any moderate irritation
like a pinch will bring out evidence of sensation. It is often stated
that in hemiplegia the sensation is not at all affected; and this is
probably true of many cases, but a more attentive examination will
often disclose a decided diminution on the affected side. Broadbent,
who has tested with pricking, touch, the compasses, and hot
substances, says that it is frequently diminished, and often greatly
so, and not only in the limbs, but in the face, chest, and abdomen.
Tripier[34] says that a lesion of the larger part of the
fronto-parietal region determines at the same time a paralysis of
motion and a diminution of sensibility; and one may conclude that this
region holds under its dependence sensitive as well as motor phenomena
intimately connected with each other. The zone called motor, of which
the limits are difficult to fix, may with more reason be called
sensori-motor.

[Footnote 34: _Revue mensuelle de Méd. et Chir._, 1880, p. 18.]

Anæsthesia probably in most instances disappears more rapidly than
motor paralysis, which accounts for its being frequently overlooked.
The more common location of lesions causing motor paralysis—_i.e._ the
corpus striatum and the motor portion of the cortex—is one not likely,
unless extensive, to concern sensation; but there are cases where a
very complete hemianæsthesia, including the special senses, may be
found; and when, in such cases, the motor paralysis is slight, a
picture is presented almost identical with that of hysterical
hemianæsthesia with great diminution or abolition of the special
senses, hearing, taste, smell, with concentric diminution of the field
of vision and of the color-field, or complete color-blindness on the
affected side.

A man aged thirty-five while at work suddenly felt a prickling
sensation upon his left side, and became unconscious. The bystanders
say he was convulsed. On returning to consciousness after three hours
he had lost his speech, which, however, was rapidly recovered, and his
left side was not so strong as his right, though there was no distinct
history of paralysis. Two or three days afterward it was noticed that
sensation was much diminished upon the left side, two sharp points of
the æsthesiometer being felt as one at two inches on the forearm and
three-quarters of an inch on the tongue. He could feel the touch of a
spoon, but could not tell whether it was cold or hot. Odors were not
recognized upon the left side of the nose, except faintly ammonia and
chloroform, and a watch was heard on that side only when in contact
with the ear. The field of vision was much diminished and
color-blindness was almost complete. A few days later the field of
vision had increased, and there was color-sense, the field of
perception for the different colors being arranged almost exactly as
laid down by Charcot, vision for red being largest, but not so {956}
large as for simple perception of objects; those for blue, green, and
yellow nearly the same and smaller; and that for violet limited to a
small space in the centre of the field.

Less regular forms of anæsthesia may be met with, as well as
hyperæsthesia. These are said to be especially connected with various
lesions of the pons.[35] A case is recorded[36] of complete
hemianæsthesia in a man, coming on like a blow. There was no loss of
motor power; the face was symmetrical, sight and hearing unimpaired.
Taste was lost and smell doubtful. There was aortic and mitral
disease. Hughlings-Jackson speaks of a man who experienced a severe
apoplectiform attack which it was thought would be fatal in a few
hours. He recovered, however, with almost complete loss of hearing.

[Footnote 35: Conty, _Centralblatt f. d. Med. Wiss._, 1878, 571.]

[Footnote 36: _Med. Times and Gaz._, 1871, i. 246.]

Neuralgic pains of long continuance are not infrequent accompaniments
of hemiplegia, and may be lasting even after nearly complete recovery
from the paralysis. A peculiar restlessness, a constant desire for
change of position, has been referred to derangement of the
muscle-sense. It is sometimes very distressing, and causes much
annoyance to attendants as well as to the sufferer, as the patient is
no sooner placed in one position, no matter how comfortable, than he
desires to change it.

The mental condition seldom fails to suffer more or less in cases of
hemiplegia, but the limits are very wide between a slight emotional
excitability on the one hand and almost dementia on the other. This
is, of course, applicable to cases where the lesion is a single or
limited one, and not where a hemorrhage or thrombus is merely a part
of a general vascular degenerative change with chronic meningitis or
atrophy of the brain, where the mental decay can hardly be called the
result of any single lesion. In cases of aphasia the mental condition
is harder to make out, from the peculiar inability to communicate
ideas if present. It is very safe to say, however, that many such
patients possess much greater intelligence than would appear to a
casual observer, and yet the apathy with which they often bear the
deprivation of speech and consequent isolation speaks more strongly in
favor of some blunting of the perceptions than of Christian
resignation. A patient whose general appearance is that of tolerable
comfort is likely to cry when attention is called to the helpless
condition of the hand. It is probable that memory suffers in such
cases, if not the reasoning faculties.

Trousseau cites the case of Lordat, who became aphasic, and after
recovery described his own case. The learned professor claims to have
been in full possession of his faculties, and to have arranged a
lecture with the divisions and subdivisions of the subject, and all
this without the thought of a single word passing through his mind.
Trousseau ventures to doubt the possibility of carrying on complicated
mental processes without words, and thinks Lordat may have
overestimated the precision of his mental processes. It appears in
confirmation of this view that after his attack he always read his
lectures, whereas before he had been distinguished as an extempore
speaker.

McCready, in an excellent article in the _New York Journal of
Medicine_ (September, 1857), discusses this subject at length, and
details a number of cases where it was evident that paralytics and
aphasics (who, however, {957} he did not know by that name, nor the
special lesion connected with their condition) possessed not only
ordinary intelligence, but excellent business judgment and ability. He
says that the confusion of mind and difficulty in pursuing a train of
thought of which apoplectics are apt to complain is, to a great
extent, the mere result of diminished nervous energy—that they
comprehend well and judge correctly. It is fair to say that while the
mind is almost certainly impaired, it is not necessarily in exact
proportion to the severity of other symptoms, aphasia included. The
memory, either special or general, is most apt to be impaired.

The testamentary capacity of a person who has had an apoplectic fit or
who is paralyzed at the time of making a will may be called in
question. The only general remark to be made is that these facts alone
are not sufficient to prove incapacity; neither should the presence of
aphasia or agraphia do so without further evidence of want of
comprehension of the meaning of language used by others; so that if,
for instance, a person were seized with hemiplegia and aphasia between
the drawing up of a will and its signature, it should not be
invalidated unless there be further evidence to show that the testator
was incapable of understanding it when read over to him. In cases of
word-blindness, a patient, like one described by Magnan, may be able
to draw up a will with full comprehension of what he is doing, and yet
be unable to read it understandingly. Inability to signify
intelligibly assent or dissent would, of course, entirely disqualify
one from signing a will.

It is seldom that a paralytic attack fails to leave its mark, though
perhaps slight, for years, if not for the remainder of life. An
extreme ease of shedding tears is a very common symptom, and sometimes
laughter comes on very slight provocation.

Among the most interesting groups of phenomena connected with
hemiplegia, and sometimes the sole representative of this
condition—that is, existing alone without any motor paralysis—is that
embracing the means of communicating with the outer world by means of
language spoken or written. Corresponding to, and usually but not
always connected with, right motor paralysis we have the inability to
use words in speaking, known as aphasia, aphemia, alalia, and others.
The first of these names is the one most frequently used. Agraphia is
the inability to use words in writing.

On the receptive side we have the inability to understand language as
presented to the eye (word- or psychic blindness) or to the ear
(word- or psychic deafness). A case of the former condition has
already been spoken of. One still more singular was reported by Mdlle.
Skwortzoff,[37] where the patient, not being blind, could not
understand letters presented to the eye, but could read with the
fingers and understand raised letters like those used by the blind. In
a case of the latter kind a man whose ears were normal, and who could
distinguish different sounds, answered questions, but entirely at
random, though he could read and understand what was written. All
these defects are manifestly connected with a peculiar loss of memory,
and hence the word amnesia is used sometimes to cover part of the
group, and amnesic as an adjective to qualify aphasia.

[Footnote 37: _Comptes Rendus de la Société de Biologie_, 1883, p.
319.]

It should, of course, be understood that the muscles are not
paralyzed, so that glottis, lips, tongue, and fingers are capable of
making the {958} necessary movements to produce words, and, on the
other hand, that the senses of sight and hearing are intact. Aphasia
was confounded by some of the older writers with paralysis of these
organs, and the whole grouped together under the name of alalia. Even
now the distinction is not always clearly observed.

The act of speaking, according to Kussmaul,[38] consists in three
stages or processes: the preparation in the intelligence and feelings
of the matter to be uttered; the diction, or the formation of the
words internally, together with their syntax; the articulation, or
formation of words outwardly, irrespective of their connection with
one another in the matter spoken. Defects in the first condition have
already been spoken of. In the entire absence of mind, as in the
deepest apoplexy, aphasia can hardly be said to exist, and it is only
later that it becomes manifest. If the second stage is defective,
amnesic aphasia exists, and if the third, ataxic. In the great
majority of cases of aphasia the loss of memory is the most important
factor; and as this exists whatever be the mode in which it is desired
to express the idea, amnesic aphasia is accompanied by agraphia. In
those cases, however, in which the patient retains a few words, they
are not always the same for speech and writing. Occasionally an
instance is found where a person can write perfectly well and
possesses complete intelligence, but is unable to speak a word. This
is pure ataxic aphasia, and is certainly rare. An ataxic agraphia is
less easy to detect, since the aphasic patient is likely to be
paralyzed upon the right side, and thus unable to write, even if he
remembers the words, until educated upon the left side.

[Footnote 38: _Ziemssen's Cyclopædia_.]

There are many degrees and kinds of amnesic aphasia, and, in fact,
every case is a study by itself. The slightest might be called
physiological; at any rate, it is sufficiently common among people
supposed to be well, and consists in the failure to recollect in time
for use the name, most frequently of a person, but sometimes of a
thing, which is really well known, is recognized at once if suggested,
and perhaps returns spontaneously at a later period. Another person
may forget only some words which are not recalled at any time, or
parts of words. A man appeared among the out-patients at St.
Bartholomew's Hospital who had his name written on a piece of paper,
because he could not say it, but could carry on a long conversation.
There were a few other words he could not say. The more complete cases
have no vocabulary at all, or only a few words or syllables applied to
all purposes, and perhaps an exclamation or two. In these cases the
patient may know perfectly well that he is not expressing his ideas,
and he may recognize perfectly well the word when it is told to him or
reject a wrong one. If he be, as happens in nearly all cases, unable
to pronounce the word after he has recognized it as the one he wished
for, there is a combination of ataxic and amnesic aphasia. Incorrect
or deficient words may be corrected or supplemented by gestures or
intonation. “Yes” may do duty without confusion for “yes” or “no,”
according to the tone.

Oaths may be retained, and sometimes an exclamation may be uttered
with perfect propriety of application which cannot be repeated
deliberately a moment afterward. This emotional use of words may be
considered akin to the movement executed by paralyzed limbs under the
{959} stimulus of a movement taking place elsewhere, and may lead to
an erroneous prognosis of recovery. This curious fact, that more or
less automatic expressions are possible when deliberately-willed
pronunciation is not, is a probable explanation for the observation
which has occasionally been made that an aphasic patient is able to
sing words which he cannot speak.

Paraphasia is the use of the wrong words, or of phrases which carry an
entirely different meaning from that intended, as when Trousseau's
patient receives a guest with politeness and invites her to be seated
with the words “cochon, animal, fichue bête,” or an old paralytic,
when a lady declines to drive with him, answers with great suavity,
“It don't make any damnation to me whether you go or not.”

Word-blindness is more common than word-deafness, and is a frequent
accompaniment of aphasia. Rostan, the well-known author of the work on
softening of the brain, experienced an attack of aphasia lasting a few
hours. The symptom which first attracted his attention was the
inability to understand the book, by no means abstruse, which he was
reading. He was, however, able carefully to observe his own symptoms,
and made signs to be bled, which operation was followed by relief.

Gouty aphasia has been described in a man aged thirty-seven who on
several occasions became aphasic, with recovery in a short time. This
condition was connected with localized paralysis, and once with entire
right hemiplegia. Afterward it was accompanied by convulsions. In the
intervals the patient was in fair health.[39] It is difficult to
imagine the lesion in this case. The reporter speaks of “sudden
blocking by a gouty thrombus,” but nothing is known of any thrombus
which can disappear so rapidly. Ball[40] describes twelve attacks of
aphasia occurring within nine months, and accompanied by slight
paresis and convulsive movements in the right hand. The patient
suffered habitually from migraine. He supposes the cause to have been
a temporary anæmia.

[Footnote 39: _Brit. Med. Journ._, Aug. 28, 1880.]

[Footnote 40: _L'Encephale_, 1883, 2.]

Aphasia may be entirely unconnected with motor paralysis, and is then
likely to be of shorter duration, though just as complete. Most of
these cases probably do not depend upon a lesion of the same kind as
when aphasia is only one of several severe symptoms. It shows how
delicate a function of the brain memory for words may be, and is
possibly the result of a temporary malnutrition or a change in the
vascular supply. It has been observed in various conditions of
debility and after acute disease. Rostan was diabetic. It has been
seen after chloroform narcosis, after santonin (5 cgr.), after fright,
and is said to be one of the ordinary symptoms after the bite of
venomous serpents. Aphasia and paraphasia may be met with in thorough
bromization, and, naturally enough, may be part of the symptomatology
of general paralysis. In other cases, even when it is the principal
symptom, it depends upon an organic lesion, and is not infrequently
the precursor of a more fully-developed attack. The diagnosis is of
great importance, and other traces of paralysis should be carefully
sought for. This symptom is far more common with occlusion of the
vessels than with hemorrhage, though not unknown with the latter.[41]

[Footnote 41: _Lancet_, Oct. 11, 1884, p. 655.]

By far the most common situation of the softening or hemorrhage which
gives rise to aphasia is in the third left frontal convolution {960}
(convolution of Broca) or the white substance immediately underlying
it. The island of Reil may be involved in some cases where but little
damage is done to the third frontal.

In a respectable minority of cases aphasia may be associated with left
hemiplegia. A case where a tumor in the third right frontal
convolution was found in a case of aphasia is reported by
Habershon.[42] It is not stated whether the patient was left-handed.
Some of these cases constitute those exceptions which prove the rule,
inasmuch as the patient is left-handed, and Hughlings-Jackson has
shown that the relationship of aphasia to the side which is
congenitally pre-eminent, and which is in the vast majority of human
beings the right side, is not destroyed by a partial education of the
other side to such acts as writing or using a knife.

[Footnote 42: _Med. Times and Gaz._, 1881, i.]

A lesion in the pons may give rise to aphasia or something closely
resembling it, but it is probable that a careful distinction of true
aphasia, both amnesic and aphasic, from paralysis or inco-ordination
of the muscles of speech, would reduce the number of these cases, and
bring the symptom into closer relations with the usual cortical
lesions.

A case of congenital aphasia with right hemiplegia has been
described.[43] When six years old the boy was well developed, though
less so on the paralyzed side; intelligent; heard well, but could say
only a few words, and those badly. Whatever the lesion, which is
thought by the author to have been in the speech-centre, but which may
not improbably have been in the pons, it is interesting, as showing
that the development of the speech-centre is certainly not
accomplished by education.

[Footnote 43: _Centralblatt f. d. Med. Wiss._, 1873, p. 299.]

Post-paralytic chorea is an affection the nature of which is indicated
by its name. As the hemiplegia disappears, irregular movements are
developed in the paralyzed limbs, sometimes closely resembling
ordinary chorea, and at others consisting of irregular movements, as
closing and spreading of the fingers, with curious and bizarre
stiffenings, extensions, and contractions, sometimes known as
athetosis, or in others still a tremor resembling paralysis agitans.
These usually cease during sleep. It is very apt to be associated with
hemianæsthesia more or less complete, though this may be represented
by only a certain amount of numbness. A hemiathetosis has been
observed to be gradually developed from a post-hemiplegic hemichorea
of the more ordinary form.[44]

[Footnote 44: _Archiv für Psychiatrie_, xii. 516.]

This affection is not a common one, and Weir Mitchell states that it
is common in inverse proportion to the age. He thinks it possible that
some of the congenital choreas may be the result of, or at least
closely connected with, intra-uterine cerebral paralysis. It remains
for years or for life. In the absence of history such a case might
present difficulties of diagnosis from the more usual hemichorea,
which is not infrequently accompanied by considerable weakness of the
affected side.

The temperature in the early days of both hemorrhage and embolism has
been described. At a later period of the hemiplegia it remains in the
neighborhood of normal. The temperature of the affected side is often
higher than that of the sound one for an indefinite period, but in
many cases sinks below if atrophy takes place. The time at which the
change occurs is extremely variable. Out of ten cases reported by
Folet,[45] in two of them for three years and one year after the
attack the paralyzed {961} side was eight-tenths and six-tenths of a
degree respectively the warmer. In three others, of twenty months,
four and six years, it was the same on both sides, and in the
remaining five the paralyzed limb was a little the cooler. In the last
eight there was more or less atrophy.

[Footnote 45: _Gaz. hébd._, 1867.]

The coincidence of rise of temperature with vascular relaxation has
already been noted under the head of Cerebral Hemorrhage. It is not
difficult to explain why a vascular paralysis in a comparatively
well-nourished limb, especially when the heart is vigorous, may, by
allowing a larger amount of warm blood to circulate, raise the
temperature, when the same paralysis with atrophied muscles, weak
heart, and impaired general health, merely furnishes a larger
reservoir in which the slowly-moving blood may be cooled. The
accompanying charts represent the difference of temperature between
the two sides in two cases of hemiplegia, the first, O. G. T. (Fig.
41), from embolism, and the second, J. B. (Fig. 42), from hemorrhage,
the observation being made within two or three weeks of the attack.
The dotted line is from the paralyzed side. A subjective feeling of
coldness is not uncommon in paralyzed limbs.

[Illustration: FIG. 41.]

[Illustration: FIG. 42.]

The modifications undergone by the urine in a case of cerebral
hemorrhage are increase of quantity amounting to polyuria, the urine
becoming limpid and afterward returning to the usual color; a
diminution in the quantity of urea coinciding with the fall of
temperature, and afterward a return to the normal or even above it.
When this augmentation is considerable, it constitutes at the same
time with a marked elevation of temperature an unfavorable prognostic
sign.[46] In a case under the observation of the writer, probably of
thrombosis, the acid urine has been {962} remarkable for the amount of
mucus contained in it, so that it pours from one vessel to another
like white of egg. There is a small amount of pus, but no vesical
irritation whatever.

[Footnote 46: Ollivier, _Archives de Physiol._, 1876.]

Since the trophic centres for the muscles are situated in the spinal
cord, cerebral hemiplegia, which does not cut off their connection,
does not produce the rapid wasting seen in some cases of spinal
paralysis, unless descending degeneration involves the anterior gray
columns. The limbs preserve their fulness for a time, although the
muscular masses become flabby and slowly atrophy for want of use. This
atrophy, however, seldom becomes extreme. The skin of the hands
becomes dry, the folds at the knuckles disappear, and the hand loses
its expression, looking more like a stuffed glove. The change,
however, is not much greater than may be seen in a hand kept for a
long time in a bandage. The growth of the nails is retarded, as may be
seen by staining them with nitric acid.

If there is any tendency to œdema, as when nephritis is complicated
with hemiplegia, the swelling is likely to be much greater upon the
paralyzed side. In the adult, of course, there can be no question of
the growth of limbs, but when a child becomes hemiplegic from cerebral
disease, the limbs grow more slowly and remain smaller, as in a case
of ordinary infantile palsy or anterior poliomyelitis.

Much importance has been attached to the fact that large sloughs form
with great rapidity upon the nates of the paralyzed side, and Charcot
says that this tendency is greater than can be accounted for in any
mechanical way. He therefore thinks that a direct trophic influence of
the brain upon nutrition is shown. At the very most, however, that can
only be a contributory cause, and the freedom of other portions from a
similar condition—and that, too, in regions farther removed from the
centres of circulation—makes it highly improbable that anything more
is necessary to account for it than the less sensitiveness of that
side to irritation from urine, roughnesses in the bed, or pressure,
and hence neglect. The writer, among a very considerable number of
hemiplegias, fatal and otherwise, does not remember to have seen a
well-marked case of the kind. Scrupulous cleanliness and changing the
position sufficiently often make the preference for the paralyzed side
a very slight one.

Arthropathies, consisting in a vegetating, and sometimes an exudative,
synovitis, and accompanied by swelling, redness, and pain, are
sometimes observed, especially in the upper extremity. They do not
appear until fifteen days or a month after the attack.

The most significant change which occurs in the course of a hemiplegia
is the development of increased reflexes and rigidity and contracture.
After some weeks or months, during which the aspect of the case has
not essentially changed, the limbs remaining in the same condition, it
will be found on examination that the patellar reflex has become quite
energetic, and ankle clonus developed upon the paralyzed side; the arm
reflexes from the triceps, biceps, and supinator longus are much
exaggerated. This has the same meaning as when similar phenomena are
found with spinal disease, and signifies descending degeneration of
the postero-lateral columns of the spinal cord, the crossed peduncular
tracts. This degeneration may sometimes be traced completely down from
the situation of the lesion in the cortical motor centres through the
basal ganglia, crura, decussation, and cord. The fuller development of
this condition is the {963} contracture or rigidity, which was at one
time referred to secondary changes taking place in the neighborhood of
the original lesion, as well as to a purely reflex action having no
relation to the degeneration of the cord.

The arms are usually flexed at the elbow, the wrists on the arm, and
the fingers in the hand. Sometimes, however, the arm is straight. The
leg, which is not always affected to the same extent, is generally in
extension, though the toes are likely to be flexed. Attempts to move
the limbs are resisted strongly, and in such a way as to show the
reflex nature of the phenomenon. If an attempt be made to open the
fingers of a contractured hand slowly and carefully, it can be often
accomplished and the hand held open with but little pressure, but if
it is twitched the fingers resist like a spring. The violent attempt
to overcome rigidity is often painful.

In some rare cases rapid atrophy of the muscles of one limb may take
place. This has been found to coincide with extension of degenerative
changes in the cord to the anterior gray columns.

Late rigidity is an unfortunately clear symptom. There is little if
any hope of complete recovery of the use of the limb after it has made
its appearance, though it does not prevent walking. After
long-continued contracture the activity of the muscles diminishes, but
the increase of connective tissue and changes in the joints hold the
limb in its fixed position, and the contracture is a more passive one.
The electrical reactions of the muscles and their nerves in cerebral
hemiplegia are not materially altered, but the neuro-muscular
irritability may be somewhat increased for a time by the irritating
influence of the cerebral lesion.

In most cases of flaccid cerebral hemiplegia the electrical
irritability is somewhat decreased, though retaining the normal
character with both currents. Since the muscles and their nerves
retain their connection with the spinal nuclei which are their trophic
centres, and these nuclei are uninjured, their nutrition does not
undergo the changes which affect electric excitability.

When descending degeneration takes place there may be found,
coinciding with increased reflex activity and contracture, increased
sensitiveness to the electric currents. If the degeneration extend to
the anterior columns, as happens in rare cases, the muscles waste
rapidly and exhibit the reactions of anterior poliomyelitis—_i.e._
degenerative.

What has just been said applies to the muscles paralyzed by a central
lesion. If, however, with or without a complete hemiplegia, a limited
lesion, as in the pons, affects the nucleus of a nerve, the peripheral
distribution of that nerve is cut off from its nutritive centre, and
it undergoes the usual changes which lead to the reaction of
degeneration, so that, in some unusual forms of paralysis, the two
kinds of reaction, normal and degenerative, may be present in
different sets of muscles.

DIAGNOSIS.—The apoplectiform attack due to hemorrhage or occlusion of
the cerebral arteries is to be distinguished from narcotic poisoning,
specially by opium or alcohol, or by coal gas; epilepsy with its
succeeding coma; uræmia (so called) or cerebral symptoms connected
with renal disease; comatose form of pernicious intermittent; diabetic
coma; sunstroke; hysteria, and various other forms of intracranial
disease, especially meningitis; concussion and compression of the
brain, which often {964} involve hemorrhage; the apoplectiform attacks
of intracranial syphilis and of general paralysis, as well as the
congestive attacks (coup de sang, rush of blood to the head).

The first of these distinctions is, in a practical point of view,
among the most important and often the most difficult, so that
distinguished authorities insist not only on the difficulty, but
impossibility, of making a positive diagnosis in every case. The
physician who is most familiar with all the different conditions which
may cause coma is least likely to jump at a conclusion.

Persons are constantly being picked up in the street partially or
wholly unconscious, or found alone in a room without history and away
from friends. The physician must then form his opinion from the
present condition, which without a history may be very obscure, though
with one it might present no difficulty. An empty laudanum- or
whiskey-bottle may be of assistance, the former of much, but the
latter of less. The smell of the breath may give a hint, but even if
the smell of alcohol be detected, considering the widespread belief in
its virtues as a panacea, it may be as well the result of amateur
therapeutic attempts as an indication of the cause of the attack.
Neither does it follow that because a man has been or is drunk he has
no organic disease in his brain. Alcohol should simply make us more
careful to examine for possible injuries. In regard to both these
poisons—and in fact in the diagnosis of these conditions generally—the
first thing to be sought for, after assuring one's self that the
patient can breathe and is likely to do so for a few minutes, is some
evidence of hemiplegia. This is not so easy as it might appear at
first sight, since the general muscular relaxation may be so complete
as to cover up local manifestations. The face, however, may show
inequality in its lines or one cheek flap more loosely than the other.
The patient is not likely to undertake voluntary movements at the
request of the physician, but he may make semi-voluntary ones if
annoyed by the examination. The flaccidity of the arms may vary.
Irregularity of the pupils is a piece of evidence to be received with
some caution, as it may be habitual or the result of disease in the
eye. Conjugate deviation of the eyes and head is a form of paralysis,
or sometimes of unilateral spasm, which when present is of great
significance. In opium-poisoning—and to a less extent in alcoholic
coma—the pupils are much contracted, while they are not always so in
apoplexy. Respiration is usually much more rapid in apoplexy than in
opium-poisoning, and this, in the absence of distinct signs of
hemiplegia, would be one of the most important means of distinction.
The pulse is more nearly normal in frequency, while that of opium is
either slow and hard or more often frequent and feeble.

After the time for the initial depression has passed, rapidly-rising
temperature is very strong evidence in favor of apoplexy. If the
patient be only partially unconscious and able to protest against
being handled, to make some short answers, or even be inclined to be
combative, this is not to be taken as evidence of alcohol. Hemiplegia
may then be noticed. This condition of excitement may be observed in
the early stage of an apoplectic attack before it deepens into coma.
Unfortunately, when the lesion is situated in certain portions of the
brain, as in the extremities of either the frontal or occipital lobes,
there may be no paralysis, but then also there is less likelihood of
the extreme symptoms we are supposing {965} to be present. In the
cerebellum, however, the symptoms may be very severe without
hemiplegia, and the diagnosis correspondingly difficult. Vomiting, not
caused by the presence of large quantities of food or liquor, and
persisting after the stomach is once emptied, would be of some value
in this case, but it would often be necessary to wait for a diagnosis.
Cerebellar hemorrhage is, however, a very rare accident, and
cerebellar embolism sufficiently large to cause apoplectiform symptoms
still more so. A limited lesion in the pons may cause
gradually-increasing stupor without distinct paralysis.

Chloroform, especially if swallowed, and chloral might possibly give
rise to difficulties in the way of diagnosis, and would have to be
distinguished on the same general principles as alcohol and opium.

The poisonous gases arising from burning coal, consisting chiefly of
carbonic oxide and dioxide, or illuminating gas, consisting of
carburetted hydrogen with a little carbonic oxide, cause
unconsciousness, coma, and sometimes convulsions and vomiting. In case
of a person found unconscious in bed the possibility of poisoning by
one of these should not be lost sight of, nor, on the contrary,
assumed to be a cause without investigation. A case has been reported
where, after acute poisoning by coal gas, there occurred, presumably
as the result of local anæmia, alternate paralysis, convulsions, and
aphasia.[47] The new water-gas process is said to furnish a product
considerably richer in the poisonous carbonic oxide than that now most
in use.

[Footnote 47: _Boston Med. and Surg. Journal_, Nov. 26, 1885.]

The stupor succeeding an epileptic convulsion resembles apoplexy, and
the fact that cerebral hemorrhage may be accompanied by some
convulsions increases the possible similarity, but it requires only a
short time for epilepsy to make itself manifest, either by a renewal
of the convulsions or a rapid recovery without paralysis. According to
Trousseau, however, many attacks of so-called congestion of the brain
are really epilepsy. Puerperal eclampsia comes under the same head,
but when convulsions are violent they may give rise to actual
hemorrhage. Unilateral epileptiform convulsions are likely to be
dependent on organic disease of the brain, usually not of the kind at
present under consideration, but more frequently of a tumor.

Among the cerebral symptoms connected with renal disease, and not
involving organic change in the brain, may be found unconsciousness,
deep coma, and convulsions. It is obvious that the presence of a few
hyaline casts and a little albumen will not decide the matter, since
these may be present from many causes, and especially the changes in
the circulation accompanying apoplexy. Neither will the most
indubitable evidence of Bright's disease, such as dropsy, hypertrophy
of the heart, rigid arteries, with fatty and waxy casts in the urine,
do so, for, as we have already seen, not only is there nothing in the
presence of nephritis to exclude apoplexy, but the very form, the
interstitial, which, from the supervention of coma not preceded by
other very severe symptoms, most nearly counterfeits apoplexy, is also
the most likely to give rise to actual cerebral hemorrhage. The
extreme and frequent cephalalgia which is so distressing a symptom in
cases where there is no cerebral lesion may also be the precursors of
hemorrhage.

If we have a history, the gradual onset of the symptoms, deepening
{966} unconsciousness without any paralytic or unilateral symptoms,
especially if accompanied by a diminution in the amount of urine or
contained urea or a marked change in the character of the casts,
renders it probable that we are dealing with so-called uræmia alone.
In the absence of history hemiplegia must be the chief dependence, but
it would not be difficult to imagine a case of embolism of the basilar
artery with softening of the pons which would defy a positive
diagnosis.

Pernicious intermittent fever appears in a so-called comatose form,
which, if it were to be accompanied, as in a case related by Bemiss in
the second volume of this work, by paralysis of one arm, might present
difficulties of diagnosis. If it were known that the attack had been
only of short duration, the elevation of temperature would, as in the
case of sunstroke, decide in favor of the fever, but if it had lasted
some hours, this symptom would be of no value, as the temperature may
rise to an equal height in apoplexy.

Diabetic coma is a much less common affection than apoplexy. The
peculiar odor (aceton) of the breath, if present—which is not always
the case—might be diagnostic. The peculiar long and deep respirations
would awaken suspicion which would be confirmed by an examination of
the urine.

Sunstroke, with its sudden onset, complete unconsciousness, and
rapidly rising temperature, may present a very close resemblance for a
while to apoplexy, and in fact has been known as heat apoplexy. Age,
temperature, and surroundings would give strong probabilities one way
or the other, and if the temperature of the patient were at first
below the normal and did not rise for an hour or two, it would
certainly not be sunstroke and would be apoplexy, while if the
temperature were very high a few minutes after the patient had been
observed to cease work or become unconscious, the evidence in favor of
sunstroke would be equally strong.

It might appear that hysteria need hardly enter into our
consideration, and could hardly be mistaken for apoplexy, but most
experienced physicians could relate instances where serious organic
disease has been made light of under the name of hysteria, and many
inexperienced ones could tell of the opposite and safer mistake. An
occasional case of deep coma presents itself where, although the age
and sex of the patient awaken strong suspicion, we cannot at once be
sure that no organic lesion is present; and if, in addition, the
patient should be affected with hemiplegia—a combination which,
although rare, is by no means beyond the limits attainable by this
perplexing disease—an immediate positive diagnosis would be difficult.
Absence of facial paralysis, which might be made manifest by some
irritation like pinching or an attempt to raise the eyelids, would be
of much value under these circumstances. The hysterical physiognomy
might be well enough marked to be almost conclusive by itself. The
urine and feces are not likely to be passed involuntarily in hysteria,
as they are in apoplexy.

Injuries to the head should be carefully looked for in any case with
unknown history. Actual fracture, which perhaps leads to no depression
of bone, may give rise to hemorrhage, probably meningeal, which will
cause the usual symptoms, and a shock which is not accompanied by
fracture may cause considerable laceration of the brain with
consequent hemorrhage. In the latter case, however, unless the brain
be already {967} predisposed by arterial disease, the laceration and
hemorrhage will not be extreme and the symptoms will be those of
concussion. The diagnosis can hardly be said to be between hemorrhage
and concussion, but whether the hemorrhage be the result of
concussion—a question which can hardly be answered without the history
and observation of the further progress. Cuts and bruises may result
from a fall caused by the shock, and pericranial ecchymoses may result
from cerebral hemorrhage through the vaso-motor system without the
intervention of accident.

Rapid meningitis of the vertex, with predominance of the effusion upon
one side, may closely simulate compression from hemorrhage. At the
base, by the time it has become severe enough to cause
unconsciousness, it is likely to have affected the ocular muscles, and
perhaps given rise to other paralyses less regular in their
distribution than the ordinary hemiplegia. Ophthalmoscopic examination
would be of value in these cases if—which is not very likely to
happen—there is no history. The temperature in meningitis is more
likely to be irregular and less rapidly and uniformly rising than in a
severe hemorrhage or occlusion. In many cases emaciation, dry tongue,
and constipation with sunken abdomen will testify to a previous
illness, while after a few hours' observation the progress of the case
will make the diagnosis more clear.

In differentiating cerebral hemorrhage or ordinary embolism from the
apoplectiform attacks met with in syphilitic intracranial disease, it
is rather a question of etiology than of diagnosis in the narrower
sense, since unconsciousness and hemiplegia coming on with syphilis
are often dependent upon a condition of the vessels closely resembling
that which gives rise to the ordinary forms; that is, we are dealing
in either case with an endarteritis which has furnished the basis for
the deposit of a thrombus, and the question is, Of what nature is the
endarteritis? It is obvious that this is only to be answered by a
knowledge of the history, not necessarily of a primary or secondary
lesion, but of previous disease. The syphilitic taint may often be
suspected from the irregularity of the paralysis, the cranial nerves,
for instance—especially the ocular—being much more frequently affected
in syphilitic than in ordinary hemiplegia. After partial recovery or
amendment the characteristics of irregularity and changeableness will
be more strongly marked.

The pathology of hemiplegia and apoplectiform attacks, often
transitory, in the course of general paralysis is not certain, but it
is probable that they are due to sudden congestions of regions of some
extent already in a condition of chronic periencephalitis or to
cerebral œdema. The question of the existence of the previous disease
can only be settled after the return of the patient to consciousness.
Usually, these attacks are not of the severest kind, and are not
necessarily attended with loss of consciousness, which, when it
occurs, is usually not of long duration. An apoplectiform attack
occurring in a young or middle-aged person who has neither cardiac nor
renal disease, rapidly recovered from or changing its character,
should awaken strong suspicions of either general paralysis or
syphilis, or both.

The characteristic of the so-called congestion of the brain, or coup
de sang, is a close resemblance to ordinary apoplexy, but without
hemiplegia and usually with a rapid and complete recovery. A diagnosis
from apoplexy cannot be made at once, except so far as hemiplegia can
be shown to be either distinctly present or absent.

{968} As has already been stated, the doctrine of the dependence of
real apoplectiform attacks upon cerebral congestion alone has been
vigorously combated by distinguished clinicians; and certainly the
diagnosis of congestive (and the same may be stated even more strongly
of so-called serous) apoplexy should never be made until after the
rigorous exclusion of every other possibility.

After the severer apoplectic symptoms have passed off, and in cases
where they have never been present, the diagnosis, so far as most of
the conditions mentioned above is concerned, is divested of many of
its difficulties when we are dealing with cases of well-marked
hemiplegia. The chief points left are the distinctions from the
apoplectiform attacks of general paralysis, cerebral syphilis, and
cerebral tumor, which are to be made as already pointed out.

Slighter and more localized paralyses, such as may occur with limited
lesion of the pons or where a hemorrhage having a large focus in the
substance has escaped under the membranes and presses on some cranial
nerve, would present more difficulties. Paralyses which are very
limited, and at the same time complete, are not likely to arise from
hemorrhage or embolism, though it is possible that they may do so, but
the diagnosis is to be considered rather under the head of local
palsies than of cerebral disease. General rules cannot be laid down
for slighter cases, and each case must be diagnosticated for itself.
In many of them the electrical diagnosis would be of great value and
often decisive.

Hysteria remains, as always, ready to counterfeit anything, but the
following case shows that the error is not always on that side: F.
S——, a young woman, was brought to the hospital, apparently conscious
and understanding what was going on, but unable or unwilling to speak
or to protrude her tongue. There was no history except that she had
probably been in the same condition for thirty-six hours. There was
paralysis of the right side, including the face, and marked anæsthesia
of the same side, quite distinctly limited at the median line;
temperature 97.8°, pulse 60, respiration 20. The next day she seemed
perfectly conscious, but did not speak. The faradic brush to her face
caused loud outcries, and the facial paralysis was diminished. This
condition remained nearly the same, the patient appearing half
conscious, but passing urine in bed. Four days later there was marked
diminution of sensation and motion on the left (previously sound)
side, as well as the right. The note two days later was, “Shuts and
opens her eyes when told, and moves eyeballs in every direction, but
there is apparently no voluntary motion except slight of the head.
Incontinence of urine and feces.” A week later the temperature rose to
100.4°, pulse 140, and she died. The autopsy showed red adherent
thrombus in the left carotid, extending into the cerebrals, with
extensive anæmic necrosis of the cortex and a part of the corpus
striatum. On the right there was a grayish thrombus and softening of
the cortex, while the great ganglia were not affected.

A woman of thirty-two had repeated attacks of loss of consciousness
and somnolence lasting several hours, but leaving her apparently well.
The case was considered hysteria, but the patient died in a similar
attack. Degeneration of the cerebral arteries and hemorrhage were
found.[48]

[Footnote 48: Christian, _Centralblatt f. d. Med. Wiss._, 1873, 864.]

Post-paralytic chorea might present difficulties of diagnosis from
{969} hysteria or malingering, though the difficulty is quite as
likely to be on the other side.

The diagnosis, however, is not complete until the lesion is located
with some precision and its nature determined, although it must be
confessed that when we have got as far as this the diagnosis in most
cases is of more interest to the physician than to anybody else,
except to a slight extent for prognosis, so that the event may be
anticipated by a few hours. As to the localization of the lesion,
recent experiments and observations, involving not only lesions of the
kind we are here discussing, but tumors and injuries as well, permit
this to be done with a reasonable degree of certainty. The general
article on Cerebral Localization may be referred to by the reader for
the minuter points, but certain groups of symptoms may be indicated
here which are available to some extent before the complete return of
the patient to consciousness.

In the vast majority of cases the lesion is situated upon the side of
the brain opposite to the paralysis, except in some instances of
cerebellar lesion, while in the peculiar form known as alternate
paralysis due to lesion of the pons it is on the opposite side to the
paralysis of the limbs and on the same side with the facial. It should
be distinctly stated, however, that there are exceptions which are
inexplicable on the present basis of cerebral anatomy. It is well
known that only a part of the motor tracts cross to the other side of
the cord at the decussation, and also that the proportion between the
fibres which do and those which do not cross is a variable one. It has
been suggested, in some cases of the kind mentioned, that all the
motor fibres, instead of only a minority, as is usual, pass down on
the same side of the cord as their origin. This has not been
demonstrated. The number of such cases are so small that it need not
be taken into account in diagnosis, and if the practitioner should
make a mistake on this basis, he will have the recompense of knowing
that he has assisted in a very rare case, in which it was next to
impossible for him to be right. This condition is said to be found
more frequently when the brain lesion and paralysis are on the right
side.

Severe pain in the head, followed by gradually but rapidly deepening
coma and paralysis of one side, becoming more and more complete,
probably means a hemorrhage into or just outside of the great ganglia
and involving a large extent of one of the hemispheres.

If there have been moderate loss of power or complete paralysis
lasting some hours, with, afterward, sudden loss of consciousness and
general muscular relaxation, with sudden fall, soon followed by rapid
rise, of temperature, it is very probable that a hemorrhage has broken
through into the ventricles or beneath the membranes, and is still
going on.

Rapidly-deepening unconsciousness, with general muscular relaxation
and gradual manifestations of more paralysis on one side than the
other, may come from meningeal hemorrhage.

Very sudden and complete hemiplegia without prodromata, with deep
unconsciousness coming on rapidly or suddenly, but a little after the
paralysis, is likely to denote the occlusion of the middle (and
perhaps anterior cerebral) artery of the opposite side at a point
sufficiently low down to produce extensive anæmia of the motor centres
along the fissure of Rolando as well as the underlying great ganglia.

{970} Aphasia with hemiplegia, often without the slightest disturbance
of consciousness, is in a considerable proportion of cases connected
with a lesion of the third left frontal convolution, and in a somewhat
larger proportion with the frontal lobes in general and the island of
Reil. This lesion is in a great majority of cases occlusion of the
artery. Difficulty of speech, connected with difficulty of swallowing
and associated with a certain amount of amnesic aphasia, has been
found with lesions of the pons. As aphasia, however, may occur without
any fatal lesions at all, it is not certain in all these cases that
the obvious lesion of the pons is a direct cause of all the symptoms.

Word-blindness is associated, according to a case reported by
Skworzoff and a few others,[49] with a lesion of the angular gyrus,
pli courbe (P_{2} of Ecker), and word-deafness with a lesion of the
first temporal (T_{1}). These localizations agree with those
experimentally determined.

[Footnote 49: West, _Brit. Med. Journ._, June 20, 1885.]

Conjugate deviation is of importance as a localizing symptom, chiefly
because it may be manifest when other signs of hemiplegia are
difficult to elicit. I do not find it mentioned in twenty-seven cases
of cerebellar hemorrhage not included in the table of Hillairet, but
it is not infrequent with lesions of the pons; and when the lesion is
in the lower third, it is in the opposite direction to that described
as usual with lesions of the hemispheres.

Hemianæsthesia involving the organs of special sense, unilateral
amblyopia, and color-blindness is supposed to be connected with a
lesion of the posterior third of the internal capsule, or the thalamus
in its immediate vicinity, sometimes also with a lesion of the pons.
Bilateral hemiopia—blindness of the corresponding sides of both
eyes—is apt to be connected with a lesion of the occipital lobe of the
opposite side. Rendu and Gombault remark that hemianæsthesia of the
limbs and face may be met with in certain lesions of the cerebral
peduncles, but in this case the higher special senses (sight, smell)
remain unaltered. Hemichorea points to the same localization as the
more complete hemianæsthesia.

Alternate hemiplegia is due to a lesion of the pons upon the side of
the facial paralysis, and opposed to the paralysis of the limbs and in
the posterior or lower half. Care should be taken not to confound this
with the accidental addition of a facial paralysis to a hemiplegia of
the other side.

Irregular ocular paralyses are very likely to be due to lesion of the
same region. In some of these forms an investigation of the electrical
condition with reference to the presence of the degeneration reaction
may be of great assistance.

With extensive lesions profound coma and relaxation without distinct
hemiplegia are likely to be due to injury of the pons. A thrombus of
the basilar artery may lead not only to rapid, but even to sudden,
death. A phthisical patient died suddenly while eating his supper, and
a thrombosis of the basilar artery, with softening of the pons, was
found. Of course the lesion must have been of older date.[50]
Bright[51] thought that when symptoms pointing to disease of the
intracranial vessels were present the diagnosis was confirmed, and the
location of the lesion in the vertebral arteries rendered highly
probable, by a persistent occipital {971} pain. In the upper part of
one side of the pons the hemiplegia is not alternate, but of the
ordinary form.

[Footnote 50: _Bull. de Société anatomique_, 1875.]

[Footnote 51: _Guy's Hospital Reports_, 1836.]

Any extensive lesion of the medulla must cause death so rapidly as
almost to defy diagnosis, but such rarely occurs. The very rapid
termination of certain cases of hemorrhage into the pons and
cerebellum is due to the escape of blood into the fourth ventricle and
consequent compression of the medulla.

Lesions of the lower and inner part of the crus are indicated by
paralysis of the third nerve of the same, and hemiplegia of the
opposite side of the body.

Obstinate vomiting, severe occipital headache, and vertigo, with or
without a distinct paralysis, render a cerebellar hemorrhage probable,
though no one of these symptoms is necessarily present or
pathognomonic. Vomiting is very much more common with cerebellar
hemorrhage than with cerebral. Ocular symptoms, like nystagmus and
strabismus, accompany cerebellar lesions.

A difference in the temperature of the paralyzed and non-paralyzed
sides, when amounting to one and a half to two degrees and lasting for
a long time, is thought by Bastian to indicate a lesion of the optic
thalamus.

The severe and rapid sloughing of the nates sometimes seen in
rapidly-fatal cases is stated by Joffroy to be most frequently
connected with a lesion of the occipital lobes.[52]

[Footnote 52: _Arch. gén._, Jan., 1876.]

It is plain, from what has been said about the symptoms of the
different kinds of lesion, that a distinction may be often very
difficult, and at times impossible; and in this connection all
observers are agreed, the apoplectiform shock, the hemiplegia, and the
slighter attacks being common to two or three lesions. The diagnosis
can be made, if at all, only by the consideration of more or less
secondary symptoms and the careful weighing of the various
probabilities against each other. Most of the statements of
differences of symptoms are only relatively true.

A glance at the nature of the pathological processes involved may
serve to systematize our observations.

Hemorrhage is a sudden accident, with a severity increasing as the
amount of effusion increases. It has been prepared for by arterial
disease, but this disease is one which may have no previous symptoms.
It is at first an irritative lesion.

Embolism is a sudden attack which may be as severe at first as even a
few minutes afterward. It is also prepared for by disease of other
organs, which may or may not have symptoms according to the origin of
the embolus. As embolism affects especially those regions where the
motor centres are spread out, while hemorrhage attacks more frequently
the conductors in their locality of concentration, the paralyses
arising from the former affection may be more narrowly limited.

Thrombosis is a gradual affection, which may, however, manifest itself
suddenly, from the obstruction reaching a certain point and suddenly
cutting off the supply of blood. This also depends on previous disease
which has more or less definite symptoms.

The severity of the attack is not conclusive, though the completely
developed apoplectic attack is more frequent with hemorrhage. Rapidly
{972} increasing severity, especially if there have been prodromata,
is in favor of hemorrhage. Convulsions, early rigidity, and conjugate
deviation of the eyes of the spastic form, especially if afterward
becoming paralytic, are strongly in favor of hemorrhage, and the
latter possibly conclusive. Hughlings-Jackson states that he cannot
call to mind a single case of hemiplegia from clot in a young person
in which there were not convulsions.

Sudden paralysis without cerebral prodromata, unconsciousness, or pain
can hardly be anything else than embolism; but, unfortunately for
diagnosis, the initial paralysis from the embolus may be slight, and
afterward added to by the secondary thrombus, so as to put on the
appearance of more gradual approach.

Aphasia, and especially aphasia associated with but little or no
paralysis, is very much more frequent with embolism than with
hemorrhage.

The temperature, if we could always have it recorded from the very
beginning, might be of value, as the initial depression is said to be
less with embolism than with hemorrhage, but Bourneville,[53] who lays
down this rule, gives so many cases where no great depression occurred
with hemorrhage that it cannot be considered decisive. Besides this,
we are not likely to get the information at the time it is of the most
value.

[Footnote 53: _Op. cit._]

Etiological information may have a very practical bearing on this part
of the diagnosis. Age gives a slight amount of predominance to the
chances of hemorrhage, and youth a considerably greater one to the
chances of embolism. Interstitial nephritis with hypertrophy of the
heart, after the exclusion of uræmia, gives a strong probability in
favor of hemorrhage. Valvular disease of the heart, especially a more
or less recent endocarditis, is strongly in favor of embolism. A
feeble action of the heart, slow and irregular pulse, are more likely
to be connected with thrombosis.

Atheroma and calcification, as detected by examination of the visible
and tangible arteries like the radial and temporal, is a condition
either connected with the periarteritis aneurysmatica which gives rise
to hemorrhage, or one which furnishes a suitable spot for the
deposition of a thrombus; hence it can be considered conclusive in
neither direction.

Arcus senilis, even of the fatty variety, can only show some
probability of arterial degeneration.

Retinal hemorrhage, if present, favors the presence of a similar
cerebral lesion, but nothing can be argued from its absence.
Landesberg[54] has reported a case in which embolism of the central
artery of the retina, easily diagnosticated by the ophthalmoscope,
preceded by a few days a similar accident in the middle cerebral; and
Gowers[55] another in which the two arteries were occluded
simultaneously.

[Footnote 54: _Archiv für Ophthalmologie_, xv. p. 214.]

[Footnote 55: _Lancet_, Dec. 4, 1875.]

If a sudden paralysis arises in connection with a septic process, we
may diagnosticate an embolus with a good deal of confidence; but it is
not unusual to meet with small abscesses of septic origin which have
given rise to no special symptoms whatever, or only to such as are
covered up by the more general constitutional ones.

PROGNOSIS.—The prognosis quoad vitam of cases of apoplexy still in the
unconscious state is based upon the general severity of the symptoms
{973} as indicated by general muscular relaxation, or, at a later
period, the extent of the paralysis, the amount of affection of the
heart and respiration, and especially the progress during the first
few hours. Too much weight should not be placed upon a very slight
improvement at first, since this often takes place in cases soon to
prove fatal.

Stertorous respiration with perfect tolerance of mucus in the throat,
absolute loss of the reflexes, and immobility of the pupils signifies
profound depression of the organic nervous centres, and is
consequently of unfavorable augury.

The temperature is a valuable guide. In proportion as it moves
steadily and rapidly upward is the prospect of an early fatal result.
A person may die during the initial fall of temperature, but in such a
case there would hardly be need of a prognosis.

In general, the prognosis from hemorrhage, supposing the symptoms to
increase in severity for an hour or two, is worse than that from
occlusion.

Age, aside from the fact that it makes hemorrhage more probable than
occlusion, is not of great importance in prognosis, certainly not out
of proportion to the general impairment of vigor in advanced years.

A renewal of the hemorrhage within a few hours cannot be predicted. It
may be indicated by another fall of the temperature, which, if it have
been previously on the rise, renders, of course, the prognosis more
unfavorable.

After recovery, more or less complete, from the apoplectic condition
the prognosis is favorable, for a time at least, except so far as one
attack may be looked upon as the forerunner of another. After the
temperature has reached a sort of standstill in the neighborhood of
normal, its subsequent rise will furnish among the earliest
indications of an approaching fatal termination.

Urinary trouble, retention, incontinence, or, much more, cystitis, is
to be looked upon as a complication which materially increases the
gravity of the situation. Bed-sores or abrasions may be placed in the
same class, except that the early and extensive sloughing of the nates
described by Charcot is of almost absolutely fatal significance.

After some days or weeks the progress of the paralysis either toward
better or worse may be exceedingly slow, and as time goes on the
danger to be apprehended from the latter becomes less and less.

When paralysis takes place in young persons and the primary attack is
recovered from, it is doubtful if the chances of a long life are
materially diminished. A case has already been referred to in this
article where the consequences of a cerebral hemorrhage occurring in
infancy were found in a woman of eighty-three in the form of atrophied
limbs and an old pigmentary deposit in the brain.

Hemorrhage into the cerebellum would appear, from statistics, to be
exceedingly fatal, but it is certain from old lesions occasionally
found that it is not absolutely so, and its apparent severity is
partly caused by the fact that it is very seldom diagnosticated except
at the autopsy.

The prognosis quoad restitutionem ad integrum cannot be made to
advantage at an early period. After the immediate danger to life has
passed it is safe to say, if pressed for an answer, that it is highly
probable that some recovery from paralysis may take place, but that it
is {974} highly improbable that it will be absolutely complete, and
just how far improvement may go it is impossible to predict with
accuracy at first. Time must be given, in the first place, for
pressure to subside, compressed nerve-fibres to be restored, and for
such collateral circulation as is possible to be established. How
recovery takes place beyond this it is not easy to say. It is hardly
supposable that any considerable portion of nerve-structure is
renewed. A certain amount of substitution, by which one part of the
brain takes up the functions of another part, is among the most
plausible suppositions; but how this is accomplished it is hardly
worth while in the present condition of cerebral physiology to
speculate.

Practically, it may be said that physicians are apt to consider a
paralysis absolute at too early a period, while the patient and his
friends continue to hope for a complete restoration after it is
evident that no really useful increase of power is to be looked for.
Weeks, and even months, may elapse before any return of motion can be
perceived in cases which are really susceptible of considerable
improvement, and a year most certainly does not cover the limit of the
time during which it may go on.

The most unfavorable symptom, one which probably precludes all hope of
useful recovery in the limbs affected, is contracture, heralded for a
time by increase of the deep reflexes, indicating degeneration of the
motor tract in the white substance of the cord. Until this begins,
certainly for many weeks, the patient may be fairly encouraged that
some improvement is possible, though after a few weeks the chances
diminish as time goes on. In the rare cases where the muscles undergo
rapid wasting the prognosis is, if possible, worse still. The
localization of the lesion after the early symptoms are passed does
not greatly influence the prognosis.

A rapid recovery taking place in either hand or foot, and especially
of the hand first, without corresponding improvement in the other
limb, is of unfavorable import for the latter, and, in general, the
prognosis is not exactly the same for both limbs involved. In the rare
cases of hemiplegia from acute brain disease occurring in children the
nutritive disturbances in the form of arrest of growth should be taken
into the account in prognosis, since the result may be nearly or quite
the same as is found after infantile paralysis from disease of the
cord.

In regard to the slighter forms of paralysis, it may be said that the
less extensive the original paralysis is, and the sooner improvement
begins, the better is the chance of complete recovery.

TREATMENT, INCLUDING PROPHYLAXIS.—Cerebral Hemorrhage.—As the
condition upon which the usual form of cerebral hemorrhage depends is
so frequently aneurism, and probably nearly always some arterial
disease, the prophylaxis must evidently consist in such a mode of life
as will least tend to this degeneration, or at least put it off as
long as possible. This, of course, means the avoidance of all the
special causes described under the head of Etiology. It is a disease
of old age, but in a pathological sense old age begins in different
persons after a different number of years. Fortunately for rules of
hygiene, there is little that is contradictory in those to be given
for most chronic and degenerative diseases. Abstinence from alcohol,
as an agent tending at once to paralysis and dilatation of the
vessels, is one of the most important rules and insisted upon by
nearly all writers. The avoidance of over-eating, and especially of
{975} nitrogenous food as tending to lithæmia—a generally recognized
cause of arterial degeneration—is perhaps the next. Over-eating is of
course to be understood as a relative term, and to be estimated with
reference to the habits of exercise of each person. Practically, it
will be decided by its effects; that is, if careful thought be given
to the matter and the statements of the gourmand as to his immunity
from all risk of trouble are not accepted as of scientific value. On
the other hand, insufficient food, producing anæmia, may be a factor
in arterial degeneration. Keeping one's self free from anxiety, and
getting through the world with as little experience of its roughnesses
as possible, might be, properly enough, added in a purely theoretical
point of view if any one ever asked a physician's advice in youth as
to avoidance of the diseases of age, or if any one could or would
profit by this advice if it were given.

Intellectual pursuits have been credited with a special tendency to
apoplexy, but there is no good reason to suppose that healthy exercise
of the mind is otherwise than beneficial to its organ. Hurry,
over-anxiety, and mental tension are undoubtedly potent factors in
general breakdown, but do not necessarily lead to this form. They are
certainly not to be found by preference in those persons who lead an
intellectual life.

Syphilis, one of the most important of the causes of organic cerebral
disease, and that too in the form of thrombosis, is not specially
concerned in the etiology of the forms here under consideration.

If symptoms have occurred that justify the apprehension of apoplexy or
paralysis, such as frequent headaches in an elderly person, hemiopia,
temporary aphasia, or slight and temporary paralyses, or if one have
reached a time of life at which the risk of cerebral hemorrhage
becomes considerable, a stricter attention to the rules laid down
above, and even to some to which but little heed would be given in
health, is not out of place. A certain amount of limitation of diet,
moderate and regular but not violent exercise, clothing suitable to
the season, and especially warm enough in winter, and, most of all,
rest if the patient be doing wearing and anxious work, should be
enjoined. Finally, it should be said that the real prophylaxis of
cerebral hemorrhage is to be begun in early life.

Among the exciting causes to be avoided are those which obstruct the
flow of blood from the head, like tight clothing around the neck.
Increase of the arterial pressure by severe or prolonged muscular
effort, as in lifting or straining at stool, is to be avoided, as well
as violent fits of passion. The condition of the bowels should be
regulated by mild laxatives.

When the apoplectic attack has actually occurred, treatment, though
apparently urgently demanded, is really of little avail. If a patient
is about to die in an hour or two from rapidly increasing pressure,
nothing within the reach of medical science can stop him.

There is one danger, however, easily avoided, but probably often
overlooked. A patient may die from suffocation. The stertor is often a
result of the paralysis of the tongue and palate and of the amount of
fluids collecting in the pharynx from the almost invariable position
of the patient on his back; that is, if he have been seen by some one
who wished to do something for him, but did not know what.
Insensibility and paralysis combine to favor this accumulation, which
obstructs the respiration, and which may find its way to the lungs,
together with brandy and milk, and set up an inhalation-pneumonia. The
simple and obvious thing {976} to do is to place the patient
sufficiently on his side, with the face somewhat downward, for the
tongue and palate and secretions to fall forward, instead of backward
into the pharynx. Swabbing out the pharynx may be of some use, but
cannot be so thorough. An easy position and proper ventilation should
be secured in all cases of unconsciousness, even at the risk of
treating a drunkard with undue consideration. Police-stations should
be provided with rooms where these conditions can be secured, and the
necessity avoided of placing persons picked up in the streets in the
narrow, close, and perhaps distant cells provided for malefactors. The
writer recalls the cases of two young men—one who had been drinking
some time before, and the second roaring drunk—who were locked up in a
suburban station-house in the evening, and found the next morning—one
dying and the other dead.

Artificial respiration may be used to prolong life in some cases until
the nervous centres have sufficiently recovered their functions to
carry on the process without assistance. The condition of the bladder
should be ascertained, and the urine drawn if necessary, though it is
more frequently passed involuntarily.

Although it is manifestly impossible to remove the clot from the
interior of the brain, it may appear that the further flow of blood
may be stopped and the amount of damage done limited. For this purpose
two remedies are proposed—namely, bleeding and purgatives. Both of
these act to diminish arterial pressure, which is forcing the blood
out of the rupture. Though the treatment seems reasonable, it would
not be difficult to imagine a condition where sudden and premature
diminution of pressure in the brain, which of course exists outside of
the arteries as well as inside, would tend to set going again the flow
which has ceased from the very force of the pressure it itself exerts,
very much as if a tampon were prematurely removed from a bleeding
cavity elsewhere. As the conditions are somewhat complicated, and at
the same time only remotely to be estimated, it is safer to be guided
by experience in the use of these remedies than by abstract reasoning.
In some of the cases of temporary aphasia, as notably that of Rostan
narrated by Trousseau, bleeding seems to have given immediate relief.
Trousseau, however, is no advocate of that method of treatment. Most
modern authors speak of venesection as to be used in cases where the
pulse is strong and full and the face red, but not to be thought of in
the opposite class. When a case presents the appearances of plethora
and an attack has come on suddenly, the loss of a few ounces of blood
can certainly do no harm. Other forms of bleeding, such as cups and
leeches, are not rapid enough to be of great value, though a large
number of leeches about the head might be useful. Some French writers
recommend leeches to the anus as revulsives. Cathartics may be more
freely used, although they should be given cautiously when there is
any tendency to cardiac depression. It can be clearly shown that a
brisk purgative lowers the arterial tension decidedly. In case of
cerebral tumor or injury with occasional so-called congestive attacks,
the relief afforded by cathartics is very great, and, although the
conditions are not exactly parallel, it is fair to assume a similar
action in the congestion accompanying cerebral hemorrhage. From one to
three drops of croton oil may be placed far back on the tongue or it
may be diluted with a neutral oil. Ail enema may be desirable for the
unloading of the bowels, {977} but has a much less marked effect on
the tension of the cerebral circulation.

In most cases of apoplectiform cerebral hemorrhage, and probably in
all of simple paralysis, no very active treatment is called for.
Measures directed to the prevention of another hemorrhage, and to
allay any irritation that may supervene during the changes taking
place about the clot and the formation of its capsule, are of the
simplest, and consist in keeping the head high and cool, the clothing
sufficient for warmth, and offering no obstruction to respiration or
circulation, laxatives sufficient to keep the bowels in good order,
and a diet not highly nitrogenous, but sufficient and digestible.

That which will tax most severely, however, the care and patience of
attendants is the scrupulous and minute attention to cleanliness and
pressure over the bony prominences which is necessary when a patient
is helpless and unable to control the discharges from the rectum and
bladder. Frequent change of clothing, bathing, change of position, and
avoidance of wrinkles and roughnesses in the bed may be successful in
keeping the patient free from bed-sores. Bathing with alcohol hardens
the skin and makes it less susceptible to pressure.

Surgical interference may perhaps be of value in cases where the
portion of the clot outside the brain can be clearly demonstrated; and
this would apply with special force where the hemorrhage arises from
injury.

Trephining and removal of the clot has been done in a few cases of
meningeal hemorrhage, though with indifferent success (3 cases—2
deaths, 1 unknown.)[56] An intracerebral clot is obviously a step
beyond, though possibly in some cases not absolutely without, the
reach of the surgeon.

[Footnote 56: _Med. Press and Circular_, Oct. 14, 1885.]

Treatment of Cerebral Embolism.—The prophylaxis is in the avoidance of
such conditions as give rise to the formation of detachable
vegetations or clots. Unfortunately, these are numerous, not
completely known, and not always avoidable. Arterial disease is to be
looked upon as of some importance, but cardiac valvular lesions of
much greater, and the causes of these, like rheumatism, scarlet fever,
and the puerperal condition, are not always to be escaped. The
presence of a detachable piece of fibrin in the pulmonary veins,
heart, or aorta being granted, nobody can possibly say what will
prevent its being loosened and lodging in one of the cerebral
arteries; so that, practically, the prophylaxis of embolism consists
in the judicious treatment of acute rheumatism and the other
conditions just mentioned. The treatment of the first attack must
consist solely in the relief of respiration, bladder, and bowels, if
they have not taken care of themselves. Stimulants may be of use for a
short time, but there cannot be any call for even the slight amount of
depletion suggested for some cases of hemorrhage. Bed-sores are to be
looked out for, just as in hemorrhage, and the subsequent treatment
conducted on the same principles. As regards the primary lesion, we
can do nothing about it either in the way of removal of the embolus or
restoration of the necrosed brain-tissue.

Treatment of Cerebral Thrombosis.—There being two factors in this
affection, both of which are to a certain extent under control,
something may be done toward diminishing the risk of its occurrence.
Arterial disease and its prophylaxis have already been spoken of. The
other {978} condition which is necessary to the production of
thrombosis—namely, an enfeebled circulation—is to some extent under
the control of general hygienic rules: a nutritious, not too highly
nitrogenous, diet, and especially sufficient exercise and the
avoidance of completely sedentary habits. If there is a crasis which
predisposes to the formation of coagula in the vessels, it is not
known that there is any special treatment, medical or otherwise, which
can prevent it. The attack is to be treated exactly on the principles
already laid down. Bleeding is about the last thing to be thought of.
Stimulants, though they cannot dislodge the clot, may be of use for a
time to sustain the heart under the shock. The secretions and the
condition of the skin are to be looked out for.

After a few weeks of waiting the patient and his friends not
unnaturally feel as if something ought to be done to hasten recovery,
and certain measures may be taken, in addition to careful hygiene,
which have this object in view. It is very doubtful, however, whether
anything really shortens the time necessary for such repair as is
possible or diminishes the amount of damage which is to be permanent.
As has already been said, improvement may go on slowly for months. In
the first place, it is sometimes considered desirable to practise
shampooing and massage of the affected muscles in order to keep them
in as good a condition of nutrition as possible. This, as well as the
regular use of the faradic battery if it be not begun too early, will
prevent a certain moderate amount of atrophy, but could not have any
influence in those rare cases where rapid wasting depends upon
secondary degeneration of the anterior gray columns. It may be
doubted, however, whether it is necessary to pay much attention to the
condition of the muscles, as they do not ordinarily atrophy to the
extent of becoming unsusceptible to the nervous stimulus from the
brain so soon as it shall be transmitted to them. Faradism, like many
other agencies, such as magnets, metals, pieces of wood, and so forth,
is said to produce a transfer of sensibility in cases of
hemianæsthesia.

There is no sufficient reason to suppose that any drug is of any value
in the restoration of the nervous structure. Iodide of potassium may
possibly prove to have some effect as a sorbefacient. Very favorable
results have been claimed for ammonia salts in the restoration of aged
persons to a nearly complete use of paralyzed limbs. Phosphorus has
been spoken of as assisting in repair, but the writer is not aware
upon how wide a basis of facts. Silver and gold have been said to
counteract the sclerosing myelitis. Strychnia is certainly useless,
and probably worse. It may make the paralyzed limbs twitch, but this
does just as little good as the involuntary spasmodic movements, which
have never been considered desirable, except as awakening in the
patient false notions of immediate recovery, and which are frequently
a very annoying symptom. The galvanic current has been applied with a
view to a sorbefacient or restorative action directly to the brain, or
rather to the pericranium.

Something can be done for the comfort of such patients: the rubbing
and kneading of the paralyzed limbs, if they do not hasten the
recovery of motion, relieve many of the painful and unpleasant
feelings. Since we do not know how far one part of the brain may
supplement another, attempts at motion after it has once appeared to
ever so slight a degree should not be abandoned by the patient. He
should walk {979} with crutches frequently as soon as he can, though
not to the point of fatigue.

There is one faculty which seems capable of re-education to some
extent: that is of speech in cases of ataxic aphasia, and even in
others the attempt should be made to teach the patient the names of
things. A very interesting case has been reported by Bristowe[57] of a
man who came under his observation after an attack which may have been
anterior poliomyelitis with extensive paralysis, able to write well
and intelligently, but unable to say anything. By gradual education,
first in the sound and formation of letters and afterward of words, he
reacquired the use of language. It is obvious that in this case there
could have been no loss of memory for the words themselves, but simply
the loss of the knowledge of how to produce them. When his speech
returned he spoke with his original American accent.

[Footnote 57: _Clin. Soc. Trans._, iii. p. 92.]

In short, the therapeutics of hemiplegia from arterial disease in the
brain is good nursing and attention to symptoms, with a moderate
amount of care of the paralyzed muscles.


Capillary Embolism.

It may be remarked, in the first place, that the lesions known by this
name are not necessarily strictly capillary, but are situated in the
very small arteries. The microscope marks the transition from the
larger to these smaller embolisms.

More is known about very small embolisms experimentally than
clinically, since they have been produced by the injection of small
seeds and insoluble particles of various kinds. Embolisms arising from
natural causes and deposited in the minutest arteries may have very
similar origin to the larger ones already described, but there are
also other conditions which give rise to particles which pass through
larger arteries without any disturbance, and are arrested in smaller
ones. The softening of thrombi is undoubtedly one source. The same
thrombus which, if detached en masse, would block the carotid artery,
may, if broken up into a number of minute fragments of fibrin and fat,
pass into the ultimate distribution of the cerebrals. The same thing
may of course happen if the thrombus have already undergone one
transportation.

Cases of localized softening are seen where no cause has been found,
except perhaps a thrombus in the heart, which has discharged its
softened and puriform contents; and it is probable that the connecting
links exist in the form of embolisms so minute as to escape ordinary
observation.

The consequences of capillary emboli if they block every minute
ramification of an arterial branch must be essentially the same as if
the branch itself were stopped; but if only a part are thus affected,
the resulting anæmia is not so complete, since the zones of capillary
congestion surrounding the part the supply of which is cut off may be
sufficient entirely to cover it and make more or less complete
compensation. The experimental emboli, in the form of tobacco-seed and
other insoluble substances, which have been traced into the brain in
considerable numbers, {980} often give rise to no distinct lesions in
the cases where the immediate effects are recovered from.

Among the other sources, ulcerative endocarditis may be mentioned as
of special importance, not from the size but the character of detached
emboli, which will give rise, not to simple anæmia, nor, on the other
hand, to merely negative results, but to septic changes at the place
of lodgment.

Aside from these conditions, which are almost the same on a small
scale as we find with the large emboli, we have several peculiar
substances formed in the body and floating in the blood which lodge in
the capillaries of the brain. These are pigment, fat, lime salts, and
white corpuscles. Every one of these, however, is much better known
anatomically than clinically.

Pigment scales, flakes, granules, or cells containing them, are formed
in the course of severe malarial fever, and deposits consisting of
this pigment are found in the spleen, liver, kidneys, heart, lungs,
and lymphatic glands, as well as the brain and spinal cord. The brain,
when a deposit of pigment has taken place, is of a slaty-grayish or
chocolate color, which is marked only in the cortical substance, the
white being unaffected. The pigment is found in the capillaries, and,
according to Frerichs, fibrinous coagula are often associated.
Punctiform hemorrhages in the brain have been seen, as well as
meningeal hemorrhages, in connection with this degeneration.

The point at which these masses are formed is still a matter of
theory. If the liver, as has been supposed, is one of the places of
formation, or if they originate in the blood, it is of course easy to
see how they reach the brain. If in the spleen, they must pass through
the wide portal capillaries before they are arrested in the narrower
ones of the brain.

It is by no means certain, however, that pigment reaches the brain in
the form of emboli. It is quite as probable that it is found in many
organs which undergo repeated congestions from the local destruction
of blood-corpuscles and changes in their pigment. The very general
deposition seems to point to a process of this kind rather than to a
local origin and a distribution through the blood. The punctiform
extravasations which may be found with deposits of pigment are also
found without it.

Minute particles of fat have been found in cerebral capillaries, but
are much less common here than in the lungs. They may be derived from
the decomposition of a thrombus, as described above, or they may come
from a fractured bone, when, of course, only particles fine enough to
pass through the pulmonary capillaries can reach the brain. This form
of embolism has an interest in connection with diabetic coma.

Collections of white corpuscles in considerable number have been
observed to form an embolus. These cannot be considered to differ very
widely in character from the ordinary fibrinous embolus, which
contains white corpuscles. It is, however, not certain that such
emboli are deposited during life.

Calcareous masses formed from the decomposition of bone have been seen
in cerebral arteries.

About the symptomatology of such emboli little is known. An array
{981} of minute emboli from the breaking up of a thrombus in the left
auricle, carotid, or even aorta, might possibly so block up large
numbers of arterial twigs as to give rise to the ordinary symptoms of
embolism; but considering the possibility of the re-establishment of
circulation, provided a certain proportion of the minutest vessels
escape, complete anæmia of a large tract produced in this way must be
rare. It is possible that some of the slighter and more transitory
attacks of hemiplegia or of more or less vague cerebral symptoms may
be referred to a lesion of this kind, the first action of a large
number of emboli being to cause an anæmia, which is compensated for
much more rapidly and thoroughly than would be the case if a single
considerable vessel were obliterated.

Various attempts have been made to connect definite and peculiar
diseases with capillary embolisms. Chorea in particular has been said
to depend upon a lesion of this kind, but, although cases have been
observed where the symptoms and lesion coexisted, yet they are very
far from being the rule, or even from constituting a respectable
minority of cases. The lesion of chorea in the great majority of cases
is not known, although attention has been directed to this theory long
enough to have established its truth.

The same may be said of the relationship between pernicious attacks of
intermittent and pigment embolism. There is occasional coexistence,
but far from invariable. Cerebral symptoms of the same kind and
severity occur without as with the pigment deposit. If pigment
embolism is the cause of coma, delirium, etc. in pernicious fever, it
is difficult to see why such cases can recover so rapidly, and why no
symptoms referable to a localized cerebral lesion are observed after
the primary unconsciousness.

Even less proof can be adduced as to any connection between leukæmic
embolisms and the cerebral symptoms occurring toward the end of severe
acute disease.

Calcareous embolism is a pathological curiosity.

DIAGNOSIS.—In the case of multiple capillary embolism it would be
impossible, if it were complete, to distinguish it from a blocking of
the main branch.

Cerebral symptoms arising in the course of ulcerative endocarditis
might be referred, with a high degree of probability, to an embolus,
but if they were distinct enough to be referred to a localized lesion,
the probability of a single embolus would be much greater than that of
a multitude of capillary ones occluding the same vascular territory.
The diagnosis of pigment embolism might be a probable, or at any rate
a possible, one if in a long-continued case of paludal fever, where
the liver and spleen were enlarged and the skin had the slaty hue
marking the deposit of pigment, there were decisive cerebral symptoms.
It could not, however, be a positive one.

Fatty embolism might be suspected in a case of diabetic coma, though
even if the condition were found it would not establish the relation
of causation.

PROGNOSIS AND TREATMENT can hardly have a definite basis in the
absence of all ground for a satisfactory diagnosis, but do not differ
essentially from those of the larger occlusions.


{982} Thrombosis of the Cerebral Veins and Sinuses.

It has for centuries been known that coagulation of the blood might
take place in the sinuses in a way different from the ordinary
post-mortem clots, but this was looked upon rather as an anatomical
curiosity than as a fact of practical importance and clinical
significance, and it is chiefly among observers of the present century
that we find a growing knowledge of the conditions under which it
occurs and the symptoms to which it gives rise.

Thrombi in the cerebral sinuses are not essentially different from
those formed elsewhere, and the reader is referred to the account
given in the article on General Pathology for a history of their
formation, growth, appearances, and transformations. For our purposes
it is sufficient to recall that they may be white, red, or striated,
either partly or wholly obstructing, and that they may become
degenerated and partly or wholly washed away. The most important
distinction of all, however, is that into two classes, of which the
first consists of those which are simply depositions of fibrin in a
comparatively healthy vessel, and the second of those which are
dependent on a phlebitis.

In order that a thrombus may form it is necessary that there should
be, in the first place, a special condition of the walls of the
veins—not necessarily, however, inflammation, though this is one of
the most frequent and probably the most active form; second, a
slackening of the blood-current; and, third, perhaps a peculiar state
of the blood, though this latter is not certain. A thrombus tends
strongly to grow, and when already formed furnishes a most favorable
point for the deposition of more fibrin.

The cerebral veins furnish a very suitable place for the coagulation
of the blood for several reasons: they are roomy in proportion to the
amount of blood they carry; they are tortuous and abundantly
anastomosing, so that the current of blood is almost reversed at some
points, and can easily stagnate; the veins of the diploë are held open
by their bony walls, and the sinuses by their stiff membranous ones,
so that they cannot collapse and thus limit the extension of a
thrombus once formed.

The sinuses most frequently affected, though none are free from the
liability, are the cavernous, superior longitudinal, and lateral.

The results of thrombosis of the sinuses and veins are not equivalent
to those of a similar process in the arteries, and they may be said in
a general way to be more diffused, as might be expected from the much
greater freedom of anastomosis. Limited softening is rarely a
consequence of occlusion even of a considerable number of veins, but
it has been observed. A large area of softening of one hemisphere, not
involving the temporal and occipital lobes, has been seen with
thrombosis of the parietal veins[58] (the internal capsule and ganglia
were not affected).

[Footnote 58: _Gaz. des Hôp._, 1880, 1066.]

Passive congestion in the brain, as elsewhere, although apparently
entirely incompatible with the normal function, seems to be able to
sustain a low form of structural integrity.

Bleeding may take place from the congested veins behind the
obstruction, constituting a distinct form of cerebral hemorrhage which
does not depend upon an arteritis, although if miliary aneurisms were
present the {983} occurrence of thrombosis would undoubtedly tend to
their rupture. The writer, however, is not aware of such a coincidence
having been actually observed. Hemorrhages are usually diffuse,
composed of or accompanied by a number of small effusions, and
situated on or near the surface of the brain or distinctly meningeal.
Punctiform hemorrhages are exceedingly common.

Phlebitis of the cerebral veins is very likely to run into meningitis,
and the two affections are often so closely united that it is
difficult to say which was the first. Œdema is a consequence of venous
obstruction in the brain as well as elsewhere, and is seen also around
some of the peripheral veins connected with the sinuses.

ETIOLOGY.—Venous thrombosis in the brain depends chiefly on three sets
of causes, though it must be admitted that there are a few cases where
the origin cannot be distinctly traced and where no previous disease
has existed. In the marantic form, occurring chiefly in the very old
and in children, as well as in cases of wasting and depressing
diseases in adults, a simple thrombosis without inflammation takes
place. Two conditions, and sometimes three, are combined here to
produce the result—feebleness of the blood-current from a
corresponding state of the heart, diseased endothelium of the vessels
from defective nutrition, and possibly, where profuse watery
discharges have been going on for some time, an increased tendency to
coagulation from the inspissation of the blood.

Rilliet and Barthez and Von Dusch[59] give the following tables of
ages at which this form of thrombosis has been observed. The
observations of the former were made in a children's hospital, and
hence do not affect the question of its frequency in later life.
Perhaps the rules of admission may account for the absence of cases
under one year of age, of which Von Dusch collected several:

                          Rilliet and Barthez.   Von Dusch.
  Under 1 year . . . . . . . . .  ...                5
  2 years  . . . . . . . . . . .   2                 1
  4   "    . . . . . . . . . . .   4                 1
  5   "    . . . . . . . . . . .   1                 1
  6   "    . . . . . . . . . . .   1
  7   "    . . . . . . . . . . .   1
  9   "    . . . . . . . . . . .   2
  10  "    . . . . . . . . . . .   1
  11  "    . . . . . . . . . . .   1
  12  "    . . . . . . . . . . .  ...                1
  14  "    . . . . . . . . . . .  ...                1
  Adults (20, 23, unknown) . . .  ...                3
  53 years . . . . . . . . . . .  ...                1
  Aged women . . . . . . . . . .  ...                2

[Footnote 59: Sydenham Society's translation.]

The special diseases in which thrombosis is most likely to be met with
are given by Bouchut as follows. The same remark is to be made about
these as about those of Rilliet and Barthez. The table is given as
convulsions from thrombosis of sinuses:[60]

  Chronic enteritis . . . . . . . . .  5
  Measles and catarrhal pneumonia . .  2
  Chronic pneumonia . . . . . . . . .  5
  Phthisis  . . . . . . . . . . . . .  8
  Anasarca without albuminuria  . . .  1
  Chronic albuminuria   . . . . . . .  2
  Whooping cough and pneumonia  . . .  7
  Scrofula, tubercle of bones, etc. .  1
  Gangrene of mouth . . . . . . . . .  1
  Diphtheritis  . . . . . . . . . . .  2

Von Dusch gives a number of cases of the same kind, as do many
subsequent writers, but without tabulation. Virchow[61] reports a case
of congenital variola with thrombosis of the sinuses of the dura
mater, the superior and inferior cava, and vessels of the cord.

[Footnote 60: _Gazette des Hôpitaux_, 1879.]

[Footnote 61: _Arch._, 1859, 367.]

{984} It is probable that simple anæmia may, here as elsewhere, either
alone or with other debilitating influences, lead to thrombosis. Von
Dusch remarks that quickly operating and debilitating influences lead
to thrombosis, and gives as an instance a case where a puerperal
peritonitis, for the cure (?) of which repeated copious abstractions
of blood were made during nine days, was supposed to be the cause. The
puerperal condition seems to have a tendency in this direction in a
way not always to be explained by the ordinary rules of the
transmission of emboli or of phlebitis. Although in those reported by
Ducrest[62] phlebitis of the pelvic veins existed or was suspected, in
the first of these five cases the lesion may have been, so far as the
description goes, arterial instead of venous thrombosis; and in the
second it is possible that the succession of events was uterine
phlebitis (with the addition of a large sacral slough), lobular
pneumonia surrounded and traversed by veins which were affected with
phlebitis, emboli in the arteries of the cortex, and consequent venous
thrombosis. In the third, fourth, and fifth the connection between the
uterine phlebitis and the inflammation of the cerebral veins (in two
cases meningitis) cannot easily be made out, except by the rather
vague assumption of a general tendency to phlebitis, which was shown
in one by a similar condition in the vein of the arm where the patient
was bled. Empyema has been followed by hemiplegia, cerebral softening,
and thrombosis of the lateral sinus. The venous thrombosis in such a
case may be secondary.

[Footnote 62: _Archives générales_, 1847, p. 1.]

Marantic thromboses are more likely to occur upon one side, and that
the side upon which the patient habitually lies.

The second class of cases embraces those where a simple obstruction,
partial or complete, of the current of the blood gives the
starting-point for a thrombus in the veins. Such an obstruction may be
formed by an embolus, but in the veins this cannot be considered an
important factor, although a portion of a thrombus may be detached and
become lodged in a narrower vessel or branch farther along. In this
way the propagation of thrombosis for a short distance toward the
heart may be accounted for.

A tumor or inflammatory exudation may press upon a vein or intrude
into it, but most cases of obstruction-thrombosis are traumatic in
origin. Thromboses arising in connection with tubercular meningitis
may be looked upon as having both an obstructive and marantic cause.
In many wounds of the vertex, gunshot and other, the walls of the
superior longitudinal sinus are pressed upon by pieces of bone, and
sometimes spiculæ have directly penetrated it. This class of injuries
is also likely to cause phlebitis without any actual penetration or
compression of the sinus, simply as a result of the inflammation of
tissues in the neighborhood. The thrombi formed in these cases are not
necessarily completely occluding. Where direct injury to the sinus or
in its immediate neighborhood gives rise to phlebitis and consequent
thrombosis, we have a condition closely resembling that of the third
class, where disease of an inflammatory character in the tissues of
the skull, neck, or face sets up a phlebitis and thrombosis which are
transmitted to the intracranial veins and sinuses.

The most frequent source of this third form of inflammatory thrombosis
{985} is the chronic inflammation of the middle ear with the mastoid
cells. The inflammation may be propagated through a carious or
necrosed portion of the temporal bone to the petrosal and lateral
sinuses, or may, without disease of the bone, be carried by the small
veins which open into the sinuses from the petrous and mastoid portion
of the temporal in this region. Abscesses in the neck may set up a
phlebitis extending up the jugular to the lateral sinuses, to which a
meningitis may possibly be added.

Carbuncles about the root of the nose, face, and so far down as the
upper lip are very prone to give rise to thrombosis propagated through
the ophthalmic vein to the cavernous sinus; and it is probably this
risk which gives to carbuncles in this situation their well-known
peculiar gravity. The divide or watershed between the regions which
drain backward through the cranium and those which are connected with
the facial vein below is apparently situated about the level of the
mouth, so that a carbuncle of the lower lip is much less dangerous.
Billroth, however, gives a case where a carbuncle in this situation
was followed rapidly by cerebral symptoms and death, and where a
thrombo-phlebitis was not improbable. He mentions another case where a
carbuncle upon the side of the head set up an inflammation which
travelled along a vein into the cellular tissue of the orbit, and
thence through the optic foramen and superior orbital fissure into the
skull.

Erysipelas of the scalp apparently causes phlebitis in some cases, and
even eczema in the same situation seems to have done so. When the
erysipelas is situated about the upper part of the face, the path of
transmission is through the ophthalmic vein; but when upon the vertex,
it may be propagated through the small veins that penetrate the bone.
This result is certainly a rare one in facial erysipelas of the
ordinary and superficial kind, which is a notoriously benign disease
for one of such apparent severity. It may, however, be more frequent
than ordinarily supposed, since cerebral symptoms occasionally appear
at a date too late to be accounted for by the fever and too slight to
be referred to extensive interference with the cerebral circulation;
the lesion to account for which, as they do not cause death, can be
only inferred, though it is not unreasonable to suppose it to be a
limited thrombosis.

Dowse[63] describes the case of a robust man who fell on the back of
his head, but walked home. After a few days he had a severe headache,
chill, and total loss of vision. His temperature rose; he had
erysipelas and partial coma, but no convulsions. There was thickening
of the scalp, but no fracture of the skull and no adhesions of the
membranes. The superior longitudinal lateral sinuses were free from
thrombi, though there was a roughness about the latter, as if there
had been a fibrinous deposit. The cavernous sinuses were almost
completely occluded with adherent fibroid masses, and there was
hemorrhage in the anterior lobe. There was some degeneration of the
brain-structure, but no disease of the arteries.

[Footnote 63: _Trans. Clin. Soc._, 1876.]

Ulcerations in the nasal passages and ozæna have proved
starting-points for thrombosis.[64]

[Footnote 64: _Med. Times and Gaz._, 1878, i. 614.]

Thrombosis of the jugular veins and corresponding cavernous sinus,
with paralytic symptoms, has been observed in the horse.

{986} The symptoms produced by venous thrombosis, as might be supposed
from their varying location and extent, and also from the fact of
their being almost invariably connected with other diseases having
marked and severe symptoms of their own, are not always easy to pick
out from among many others, but they are sometimes very well marked
and characteristic. A distinction must obviously be made between the
symptoms of simple thrombosis depending on interruption of the
cerebral circulation and those of phlebitis, which give rise in
addition to febrile phenomena common to phlebitis in any of the large
veins.

The symptoms which indicate venous obstruction, without reference to
its inflammatory or non-inflammatory character, are of two kinds:
first, those dependent upon the disturbance of the functions of the
brain; and, secondly, those which depend upon congestion and
compression of other structures.

According to the locality and completeness of the obstruction we meet
with brain symptoms.

In the marantic thrombosis of children these may be very vague, and
consist either in restlessness, followed by somnolence and coma, or,
most especially, in convulsions. The convulsions may be partial and
involve the face only; they may affect one side only, or, what is more
usually the case, be general. There is almost always strabismus. There
may be conjugate deviation. This latter phenomenon is said by Bouchut
to be of no value in children, as it may take place in either
direction, from or toward the lesion, but possibly the distinction
between the spastic and paralytic forms was not duly observed by him.
The condition of the fontanelles is spoken of as yielding and
depressed, with the edges of the bones overlapping. They may, however,
become again tense in the course of the disease from exudation or
hemorrhage taking place. Paralysis is not so marked as in adults, but
may be present.

In adults delirium takes the place of convulsions, due to a
disturbance of circulation over a considerable area, rather than to a
total suppression in a more limited one. Paralyses are not
infrequently met with, either in the form of a hemiplegia or more
localized. Hemorrhage will naturally be followed by its usual
consequences, according to its location. Headache, often very severe,
is among the early symptoms.

It is evident that none of these symptoms can be considered highly
characteristic. They can only furnish a certain amount of probability
in cases where the general course of the disease has made it likely
that thrombosis may take place.

There is another set, however, which, when present, offer the
strongest kind of confirmation: these are due to the pressure from the
veins themselves.

Œdema about the points at which the intracranial circulation is
connected with that of the face and neck may give rise to protrusion
of the eyeball, conjunctival ecchymoses, swelling of the upper lip,
and even of the upper part of the face, which sometimes becomes
slightly cyanosed from the congestion. Epistaxis has been noted. Œdema
may be noticed about the mastoid process when the thrombosis is
situated in the lateral sinuses, but it would be important in many
cases to distinguish this from inflammatory œdema directly due to
disease of the bone.

Œdema of the optic disc, as shown by obscuration of its outlines, with
large and pale vessels, has been observed by Bouchut.

{987} Veins closely connected with those within the cranium may be
thrombosed, and felt as hard cords by the finger. This may occur in
the facial veins about the orbit, in those around the mastoid, or in
the jugulars. On the other hand, if one cavernous sinus is filled with
a coagulum which does not go down into the jugular, this vein will
naturally be empty or receive only a small amount of blood from other
veins.

When the cavernous sinuses are affected, we are likely to have a set
of phenomena due to the pressure of the clot upon the nerves which
pass through it—_i.e._ the third and fourth, part of the fifth and
sixth—with filaments of the sympathetic accompanying the carotid
artery. Hence dilatation of the pupil, strabismus, or ptosis, and
other ocular paralyses may be the symptoms observed.

It is possible that a headache upon the side of the affected sinus may
be due to vascular dilatation from paralysis of the sympathetic, or to
a direct pressure upon the first branch of the fifth pair.

DIAGNOSIS.—The diagnosis of venous thrombosis may be almost entirely a
conjectural one in those cases where the cerebral symptoms are vague
or mixed with others peculiar to the causative disease. Where wasting
disease has existed, the patient is much emaciated, and profuse
discharges have diminished the fluidity of the blood, the rapid
supervention of coma with slight spasms or general convulsions will
render it highly probably that thrombosis is taking place. Unilateral
symptoms would greatly increase this probability, and if any
accessible veins about the head, neck, or face could be definitely
distinguished as filled with firm coagula, the diagnosis would
approach certainty.

In cases of this kind the only condition likely to put on the
appearance of thrombosis is the simple inanition or so-called
hydro-encephaloid disease, which comes on in exactly the same sort of
cases. Localized phenomena must be the chief point of difference.
Fortunately, the distinction is practically not an important one.

In wounds of the vertex affecting the longitudinal sinus the question
likely to arise where cerebral symptoms supervene is that of
thrombosis or abscess. Here the more definite localization is likely
to be upon the side of the abscess, although, as is well known, this
may remain latent or nearly so for a considerable time, and in general
is much more chronic in its course than thrombosis.

The swelling of the external veins, epistaxis, œdema of the lid,
protrusion of the eyeball, with œdema of the optic papilla, with only
moderate fever, would favor the diagnosis of thrombosis, while optic
neuritis, if present, with chills, would render the abscess more
probable. Unless the wound were sufficiently severe to fracture a
piece of bone into the sinus, or unless the subsequent inflammation
were of an unhealthy character, the abscess in a person of middle age
and previous good health may be considered the more probable of the
two. In the case of Dowse, already mentioned, the diagnosis between
abscess and thrombus must have been very difficult, and, as it seems
to the writer, would have been more likely to rest upon abscess or
meningitis than upon the condition afterward found to exist.

Where inflammatory diseases exist which are known to lead to
thrombosis with phlebitis, the practitioner, if on the lookout, can
often make a diagnosis with a high degree of probability in its favor.
The cerebral {988} symptoms with the venous swelling, collateral
inflammatory œdema in the more immediate neighborhood of the lesion,
and slight œdema and congestion at more distant points, and a febrile
movement indicating a distinct inflammatory exacerbation, will point
very strongly to thrombo-phlebitis.

An absolute distinction between such a condition of the veins and a
meningitis arising under exactly the same circumstances may not always
be possible, and is the less important since the two affections are
likely to coexist and form a part of the same disease.

The localization of the thrombus is to be determined partly by the
paralytic symptoms, if such exist, but principally by the situation of
the secondary œdema and from the lesion which forms the
starting-point. It has been said that the jugular vein of the side on
which thrombosis exists is less full; and this point might be of value
when the lateral sinus is affected.

PROGNOSIS.—From the character of the lesion itself, as well as from
the diseases with which thrombosis is usually connected, it will
readily be seen that the prognosis is in general a highly unfavorable
one; but it is possibly regarded as too inevitably so, for the reason
that a positive diagnosis may be in slighter cases a matter of
considerable uncertainty, so that the practitioner, even if attempting
to make an accurate anatomical explanation of obscure cerebral
symptoms, is as likely to think that he has been mistaken as that his
patient has recovered from so serious a disease.

Cases, however, have been reported where the diagnosis seems as clear
as it can be made without an autopsy, and recovery has taken place.

A case is reported by Voorman[65] of a child aged six months who had
diarrhœa and vomiting, much prostration, sunken fontanelles,
overlapping cranial bones, trembling of the tongue, slight spasm of
the right arm and leg, head drawn back, and strabismus. The head
afterward increased in size, the temporal vein was swollen and hard,
with œdema of the skin in its neighborhood. There was gradual
improvement and recovery, though when the patient was four and a half
years old its mental development corresponded to that of a child two
years younger.

[Footnote 65: _Centralb. f. d. Med. Wis._, 1883.]

In another, by Kolb,[66] a child of seventeen, well nourished, had a
purulent discharge from the right ear. Besides headache, delirium,
hyperæsthesia, convulsions, and then sleepiness and loss of
consciousness, the following symptoms pointed toward thrombosis of the
sinuses: Chills, inflammatory swelling over the right mastoid, with
fulness of a cutaneous vein passing over it; a purely œdematous
swelling in the neighborhood of the internal jugular or temporal
fossa, forehead, and both upper eyelids, with exophthalmos on the
right side; photophobia, blepharospasm, and cloudy vision; nose-bleed.
There was no elevation of temperature, and recovery took place.

[Footnote 66: _Berl. klin. Woch._, Nov. 13, 1876.]

A case of thrombo-phlebitis following otitis and terminating in
recovery is reported at length by Wreden.[67]

[Footnote 67: _Archives of Ophth. and Otol._, 1874, lii.
(translation).]

The PROGNOSIS in any particular case can be based only on the severity
of the symptoms and on the character of the preceding disease.

TREATMENT.—The prophylaxis of this affection evidently consists in
{989} the proper treatment of the diseases upon which it depends, and
might therefore be made to embrace nearly the whole range of tonic,
roborant, antiphlogistic, and antiseptic measures, to say nothing of
surgery and obstetrics. The proper nourishment of infants and
children, the cutting short, when possible, of their acute diseases,
or preventing their debilitating effects, will reduce marantic
thrombosis to a minimum. At a later period of life the proper surgical
management of carbuncle, abscess in the neck, and of the puerperal
condition will tend to avoid this risk.

The most important point of all, however, is undoubtedly the careful
treatment of otitis media and early attention to inflammation in the
mastoid cells, with incision or trephining as may be necessary.

After a thrombus has formed there is little to be done toward its
removal.

It has been claimed[68] that the preparations of ammonia are capable
of diminishing considerably the coagulability of the blood when it is
morbidly augmented. Though this cannot be considered proved, yet since
the tendency of these salts is also to quicken the blood-current, a
trial in a case where other indications are wanting is, to say the
least, justifiable.

[Footnote 68: Lidell, _Am. Journ. Med. Sci._, July, 1874, p. 101.]

In a case reported by O'Hara,[69] where the symptoms pointed very
strongly toward thrombosis of the cavernous sinuses, recovery took
place under mercurials, iodide of potassium, and purgatives. The
reporter was inclined to consider the cause of trouble specific.

[Footnote 69: _N. Y. Med. Record_, vol. xvii. p. 617.]

Considering the fact that cases with such marked and decisive symptoms
as those last recorded have recovered, it is certainly the duty of the
physician to prolong the life of his patient to the utmost, that
absorption and condensation may go on as long as possible and
collateral circulation be developed. Probably most physicians can
recall cases of obscure cerebral disease going on to recovery contrary
to all expectation, in which thrombosis furnishes an explanation quite
as plausible as any other.


Softening of the Brain

is a name which it is yet too early to omit altogether from a
systematic work, although in treating of it we have more to do with
nomenclature and classification than with pathological anatomy. The
phrase may be said to have both an anatomical and a clinical
signification, which do not coincide at all points. Clinically and
among the laity it is used to express various symptoms and groups of
symptoms more or less referable to the brain, some of them connected
with one and some with another lesion, and many purely functional—if
the word may be used—or at any rate unconnected with any known or
definite lesion.

Vertigo, dull headache, sleeplessness, or, on the other hand,
drowsiness, failure of memory, failure of power of concentration, of
steady application, mental depression, fatigue, and even slight
aphasia or actual slight hemiplegia, may any of them be considered
symptoms or forerunners of softening of the brain. As nearly as
anything, the popular notion of this affection corresponds to general
paralysis of the insane or senile dementia, or even mere exhaustion.
Many of these symptoms may, of course, be connected with the real
softening described as the result of embolism or {990} thrombosis, but
it is hardly necessary to say that a symptomatology based on these
elements alone is either too vague or else too much like that of
diseases already described to be considered useful as a separate
clinical grouping.

On the anatomical side softening of the brain has had a definite
meaning, and for many years a part of its pathology has been well
known. A general softening of the whole brain, such as seems to be the
condition supposed when the phrase is used, does not and cannot exist,
since a vascular lesion sufficient to cause anæmic necrosis of the
whole brain must cause death long before softening would have time to
take place. Nearly all the works and reports on softening have been
based upon cases such as are now referred to definite lesions of the
blood-vessels; and a good idea of the change in nomenclature and
pathological views may be obtained by noticing the dates given in the
extensive literature of the subject in the _Index Catalogue_ of the
Surgeon-General's library, which are nearly all previous to 1860 or
1865.

Localized softening has already been described under the heads of
hemorrhage, embolism, and thrombosis, venous and arterial. Whether it
may occur from diseases of the cerebral vessels without actual
occlusion is not certain, but, remembering the difficulty of detecting
thrombi in minute vessels, and also the fact that it is not a great
many years that occlusions have been systematically sought for at
autopsies, it is better for the present to assume, in cases where
softening is found in the usual form and the usual situations for the
results of thrombosis and embolism, that one of these accidents is the
cause, even if the actual point of occlusion is not found.

Softening may take place secondarily from tumors in the brain, and the
name is also sometimes applied to a local encephalitis, which is an
early stage of abscess. When, however, these various forms of disease
are removed from the general heading of softening and referred to
their proper pathological classes, there is a residuum in which the
softening seems to be the primary affection, so far as the brain is
concerned, though depending on other constitutional conditions.

In new-born infants softening of the brain, besides the rare cases in
which it may be dependent on the same conditions which may cause it in
the adult, is observed in two forms, as described by Parrot:[70] _A_.
White softening in multiple foci, dependent upon fatty degeneration,
of which it constitutes the last stage, is found almost exclusively in
the centres of the hemispheres. _B_. Red softening, which affects the
same region, but more extensively, and is accompanied by hemorrhage
into the lymphatic sheaths with rupture.

[Footnote 70: _Arch. de Phys._, 1873, p. 302.]

These two forms may exist with each other, and with other intracranial
lesions, such as thrombi of the sinuses and exudation under the
arachnoid and around the veins.

Parrot compares this form of softening to that occurring in the other
extreme of life, dependent on vascular lesions; but although he
supposes the method of production to be unlike in the two cases, it is
by no means so certain, either from his conclusions or his cases, that
it is always so. In some of his cases the vessels are said not to be
abnormal, but in others old thrombi are distinctly mentioned. As
secondary consequences may {991} be observed intracranial dropsy, with
perhaps hydrocephalic cranium and degeneration of the pons, bulb, and
medulla.

Two cases of red softening of the cerebellum have been reported.[71]
In one of them the pia was adherent, in the other thickened and
covered with exudation. The microscopic details are not given nor the
state of vessels mentioned. They are probably not strictly analogous
to those described by Parrot.

[Footnote 71: _Jahrbuch. f. Kinderheilkunde_, 1877.]

The occurrence of granular corpuscles in the brain of the new-born is
described by Virchow, and it is thought by him to be pathological and
of an irritative character (encephalitis congenita). It is somewhat
doubtful if this process is characterized by any distinct symptoms.

The ETIOLOGY is impaired nutrition, deficient or improper feeding, and
depressing diseases, frequently tubercle.

The SYMPTOMS and DIGNOSIS of this form of softening are even more
obscure than those of venous thrombosis in the same class of cases.
Vague cerebral symptoms arising in an infant poorly nourished and
suffering from acute disease may be due to this condition, but a
positive diagnosis is out of the question. In the two cases of
softening of the cerebellum just mentioned, in one, aged five, there
was dilatation of the pupil, difficulty of hearing, and vertigo; in
the other, aged six, vertigo, inclination to vomit, and clonic spasm
of the left facial muscles. Parrot says that in the greater number of
patients the encephalopathic troubles observed during life cannot be
referred to it (softening), and in no case can it be diagnosticated.

Under these circumstances it is obvious that remarks upon the
PROGNOSIS and TREATMENT must be purely works of the imagination.


Atheroma of the Cerebral Arteries

has already been spoken of as one of the most important factors in
thrombosis, and perhaps of considerable consequence in embolism and
hemorrhage. Its symptoms, when one of these accidents has taken place,
are hardly to be separately considered; and if atheroma have produced
complete occlusion, even without the assistance of a clot, the
symptoms could not be distinguished from those of an ordinary
thrombosis, and would follow the same course.

In some cases, however, the thickening of the artery may interfere
with, without completely interrupting, the circulation in the part to
which it is distributed, and the degree of the interference may vary
from time to time. If, then, in a person whose age and general
physical condition, as shown by the state of the tangible arteries,
arcus senilis, complexion, and so forth, render the existence of
atheromatous arteries in the brain probable, cerebral symptoms of an
ill-defined character arise, it is very probable that they are the
result of irregularities in the circulation dependent on atheroma.

This state of things is to be distinguished from the more clearly
marked conditions which have already been described, partly by the
incompleteness of the attack, and partly by its changes in severity
and character from time to time—a paralysis undergoing alternations of
{992} improvement and the reverse from day to day, delirium appearing
and disappearing in correspondence with the general health, the vigor
of the heart, and the state of the digestive organs.

The diagnosis between these incomplete anæmias and an almost precisely
similar result of syphilitic endarteritis is to be made chiefly by the
history and age. In middle-aged persons general paralysis might
present a not very different set of phenomena. A tolerably distinct,
but not severe, hemiplegia in an old person, subsiding in a few hours
under the influence of a cathartic, and perhaps returning more than
once, may often be due to a local and temporary anæmia from atheroma,
as well as to slight hemorrhage or a not completely occluding
thrombus.

On the other hand, extensive atheroma may exist without serious
impairment of the cerebral functions, provided it be evenly
distributed and do not interfere with the passage of blood in any one
vessel.

The prophylaxis of atheroma has already been considered. We do not
know of any drug that can change the nature or extent of the processes
going on in the arterial walls, but if any influence can be exerted it
is through dietetic and hygienic means.

The consequences of rigidity of the arterial walls, as productive of
resistance to the passage of blood, can be warded off to some extent
by promoting the vigor of the heart. Treatment should therefore be
directed to the improvement of the nutrition of the body in general
and the heart in particular. Heart tonics and laxatives are the
classes of medicaments most likely to be useful. Perhaps it is to its
effect in increasing the force of the heart contractions, like
digitalis, that coffee owes its reputation as a preservative from
apoplexy.


{993}


ATROPHY AND HYPERTROPHY OF THE BRAIN.

BY H. D. SCHMIDT, M.D.


ATROPHY OF THE BRAIN.

INTRODUCTION AND DEFINITION.—Atrophy of the brain may originate during
intra-uterine life or by defective development during the early
periods of childhood, or it may occur during adult life, when the
organ is fully developed. The atrophy is characterized by a diminution
of the normal bulk of the brain-substance, in consequence of which the
latter does not entirely fill the cavity of the cranium, but leaves a
greater or less space to be occupied by a serous fluid. Generally, the
atrophy affects, in a symmetrical or asymmetrical manner, larger or
smaller portions of the brain; an atrophy symmetrically affecting all
parts of the brain has never been observed, even in microcephalia.
Nevertheless, when the atrophy affects both hemispheres of the
cerebrum, it is generally called total, whilst it is designated
partial when it is limited to only one hemisphere or to other
individual parts of the brain, such as the cerebellum, the large
cerebral ganglia, etc.

For the sake of convenience we shall treat the atrophy of the brain
occurring during childhood, when the organ is still developing,
separately from that of the fully-developed brain of the adult.


1. Atrophy of the Brain during Childhood.

When congenital or originating during infancy the atrophy is either
primarily due to certain pathological processes taking place in the
substance of the brain, or secondary, being due to lesions of the
skull, such as premature ossification of the sutures. Total atrophy of
the brain at this period of life leads to an early death, while
children affected with partial atrophy may continue to live, though
almost always in a state of idiocy. The forms mostly observed in
children are unilateral or bilateral atrophy of the cerebrum, partial
or almost entire absence of the cerebellum, imperfect development of
the large cerebral ganglia, and slight partial atrophy of the medulla
oblongata. The large commissures as well as the crura cerebri are very
seldom found atrophied.

The most frequent and, from a practical point of view, the most
important of these forms is the unilateral atrophy of the cerebrum,
for the reason that in a mild form it is to a certain degree
consistent with the {994} mental and physical development of the
child. It is mostly found on the left side. In some cases the atrophy
extends evenly throughout the hemisphere, while in others it affects
more or less one or the other lobe. The loss in the bulk of the
hemisphere may amount to only a slight diminution, or to as much as to
one-half of the normal size. Its thickness above the ventricle may be
reduced to a few millimeters; in some cases even the membranes of the
brain may lie in contact with the ependyma. The ventricle of the
atrophied hemisphere is almost always enlarged. The convolutions of
the cerebrum are very narrow, sometimes quite indistinct. One or both
of the corpora striata also are generally found atrophied. In many
cases even the atrophy extends to one of the crura cerebri and to the
pyramid of the same side, and to the anterior and lateral columns of
the spinal cord on the opposite side. Frequently, one or the other
lateral half of the cerebellum also is found affected. The condition
of the substance of the cerebrum is nearly the same as in the senile
atrophy of the brain to be described hereafter. The skull is mostly
thickened on the side of the atrophy, and frequently asymmetrical.

SYMPTOMS.—In most cases the mental capacity is below the normal
standard, and frequently borders on or represents a state of idiocy.
The temperament of the patient is generally irritable and very
excitable. The most prominent symptom is an incomplete paralysis on
the side opposite to the atrophied hemisphere, which is the more
pronounced the more the corpus striatum, thalamus opticus, and crus
cerebri are involved. Frequently, there are contractures of the flexor
and pronator muscles of both extremities, particularly of the upper;
the muscles of the trunk remain free; sometimes one or the other half
of the face is also paralyzed. Epileptic convulsions also are
frequently present. Blindness and deafness, with a defective sense of
smell and a blunted sensibility of the paralyzed limbs, as well as
neuralgia of the latter, and headache, have also been observed.

CAUSES.—Besides the causes already mentioned, atrophy of the brain
occurring in children after birth may be induced by injuries of the
head, inflammation of the enveloping membranes, of the ependyma, or of
the substance of the brain itself.

TREATMENT.—Atrophy of the brain in children is perhaps, in the
majority of cases, incurable; it is therefore only in the milder cases
that the patient may be benefited by treatment. Electricity and
gymnastic exercises have been recommended. At any rate, it must be
pursued in a very systematic manner, and based upon the principles
established and practised by the late E. Seguin of New York in his
Physiological School for Weak-minded Children, consisting in improving
the mind, first by training the child to the use of his limbs by means
of light mechanical work, etc.


2. Atrophy of the Fully-developed Brain.

In the brain of the adult the atrophy may be partial or total,
symmetrical or asymmetrical, in the same sense as before used in
connection with the atrophy of the brain of children. It may, further,
be stationary, {995} when the atrophying process remains limited to
the part where it originated; or, progressive, when it extends to
other parts of the brain. Generally, partial, asymmetrical, and
stationary atrophy is due to certain accidental pathological
processes, producing a destruction or loss of portions of the
substance of the brain, such as apoplexy, softening, etc., by which
the nutrition of the neighboring parts becomes disturbed. Total,
symmetrical, and progressive atrophy, on the other hand, actually
depends upon certain constitutional disturbances of the nutritive
process in general, such as chronic alcoholic intoxication, etc.

CAUSES.—As already mentioned, the causes of atrophy of the brain in
the adult may be direct or indirect. The former are generally
represented by certain pathological processes which directly affect
the substance of the brain, as, for instance, apoplectic hemorrhagic
effusions into the brain-substance, thrombosis or embolism of the
cerebral arteries, encephalitis, chronic serous effusions into the
ventricles, inflammation and œdema of the pia mater, etc. To the
latter or indirect causes, which affect the organ by disturbing or
lowering the nutrition of its substance, belong the retrogressive
processes of old age or of insanity; the introduction into the system
of certain noxious substances, such as lead or alcohol; furthermore,
certain wasting diseases, such as phthisis, Bright's disease, etc.

PATHOLOGICAL ANATOMY.—The cerebrum particularly is found diminished in
volume. While the convolutions are thinner than normal, their
intervening sulci are broader. The white substance presents a
dirty-white color, and is abnormally dense and tough, especially near
the ventricles. The latter are enlarged and filled with serum; their
ependyma is thickened and frequently covered with granulations. The
cortical layer appears of a dirty, rusty-brown or yellow color, is
pale, soft, or hard, and frequently is found to adhere to the pia
mater. In very pronounced cases the white substance is almost as tough
as leather, and contracts upon section, especially in the
convolutions; its cut surface is rendered concave. Sometimes the
surface of the convolutions, after the removal of the pia mater,
appears finely shrivelled. The dura mater is often found thickened and
adhering to the skull. The space created in the cavity of the cranium
by the atrophy of the brain is filled by serous effusions into the
tissue of the pia mater, the subarachnoidal space, arachnoid sac, and
ventricles.

The histological changes associated with atrophy of the brain differ
in the different forms. In cases of partial atrophy caused by
hemorrhages, etc. the destructive process generally embraces all the
tissues at first, while the secondary degenerations particularly
affect the nervous elements. In total atrophy the pathological process
appears to commence in the connective tissue, and to involve the
nervous elements subsequently; though in a number of cases, especially
of senile atrophy, the nervous elements appear to be primarily
affected. The blood-vessels also undergo certain changes, giving rise
to the contraction of the brain-substance.

SYMPTOMS.—In partial atrophy of the brain the primary symptoms
resemble those which characterize the particular destructive process
to which the atrophy is due. The most prominent are the symptoms of
motor disturbance, which are always semilateral and correspond to the
extent and seat of the lesion; frequently they remain stationary. The
{996} sensibility of the paralyzed parts is but slightly diminished,
and the mind generally undisturbed. But when the effects of the
original lesion extend, in the form of a secondary degeneration of the
nervous elements, to neighboring parts, or even to the other
hemisphere, the cerebral functions may become secondarily disturbed.

In senile atrophy of the brain, which represents the most simple form
of total atrophy of this organ, the first symptoms frequently appear
toward the end of some intercurrent disease. They consist in a very
slow and gradually increasing derangement of the cerebral functions,
associated with a general loss of innervation, manifesting itself by
talkative wanderings of the mind, restless sleep, hallucinations,
foolish activity, attacks of tremor senilis, etc. The intellectual
functions diminish and the memory is lost. The physical forces also
gradually sink, the tremor senilis increases, and the patient, no more
able to walk, becomes confined to bed. Finally, a relaxation of the
sphincters takes place, and death is produced by the disturbance of
the automatic functions of deglutition and respiration.

Total atrophy of the brain, when due to an extensive meningitis or to
a general disturbance of the nutrition, as is met with in drunkards,
may finally lead to a condition known as general paralysis of the
insane. This disease, however, will be found treated elsewhere in this
work.

TREATMENT.—There is no special treatment for atrophy of the brain; all
that can be done is to palliate and combat the symptoms as they arise.


HYPERTROPHY OF THE BRAIN.

INTRODUCTION.—Notwithstanding the numerous measurings and weighings of
human brains made in the course of time by different investigators, no
absolute standard measure or weight has as yet been established by
which we can accurately determine a pathological increase or decrease
in the size and weight of this organ. The want of such a standard is
principally due to the difference generally existing in the dimensions
and weights of even a certain number of brains taken from individuals
belonging to the same race or nation. The same difficulties are met
with in the attempt at establishing a rule by which to measure the
mental capacity of a certain brain, for the question has as yet not
been solved whether this capacity depends upon the quantity or quality
of the brain-substance. In speaking of hypertrophy of the brain,
therefore, we must keep in mind that a large brain must not be
considered hypertrophied unless there exists a disproportion between
its size and that of the cavity from which it was removed; in other
words, when its growth or hypertrophy meets a resistance at the inner
walls of the cranial cavity. According to Virchow, a further
distinction must be made between the increase (hyperplasia) of the
nervous elements themselves and that of the supporting connective
tissue, the neuroglia. To the latter condition particularly
corresponds the peculiar doughy consistence of the white substance of
hypertrophied brains.

{997} ETIOLOGY.—Hypertrophy of the brain is sometimes congenital, and
then associated with dwarfishness and a defective development of the
cranium. Generally, however, it is an extra-uterine affection,
originating mostly during infancy and childhood, though it is also met
with at the age of puberty, and even in adult life. The male sex is
more predisposed to the affection than the female. When hypertrophy of
the brain occurs during infancy, it is almost always associated with
an excessive development of the lymphatic glands, with a defective
involution of the thymus gland, and with rachitis, but generally
without cachexia. No special exciting cause can be assigned to the
affection during youth or adult age, though it has been stated that
during these periods of life the disease may supervene upon tubercle
or carcinoma of the brain. Repeated active or passive congestion
(Rokitanski, Andral), as well as the introduction of lead into the
system, has also been supposed to incite the disease.

PATHOLOGICAL ANATOMY.—Directly after the removal of the vault of the
cranium, and on cutting through the dura mater, the brain, as if
liberated from pressure, is observed to swell out to such a degree as
to render the replacement of the removed skull-cap impossible. The
enveloping membranes are found closely adapted to one another and to
the brain; they are very thin, bloodless, and dry, and their vessels
are empty and pressed flat. The hemispheres of the cerebrum are large,
and their convolutions, mutually pressing against one another, are
flattened at their surfaces, so that the intervening sulci are hardly
recognizable. After the removal of the brain from the skull the
abnormal dimensions of the cerebrum present a remarkable contrast to
the normal size of the cerebellum, pons, and medulla oblongata, which
also appear flat and broad from pressure. When a horizontal section is
made through the hemispheres of the cerebrum and a little above the
corpus callosum, the centrum ovale appears unusually large. The
cavities of the ventricles are very narrow, their walls touching one
another. There is no serum in the pia mater or in the ventricles. The
substance of the brain is pale, bloodless, and dry. The white
substance, upon which the hypertrophy particularly depends, is of a
doughy consistence, comparable to the boiled white of an egg or
cheese, whilst the gray substance is so pale as to be hardly
distinguishable from the former.

The condition of the skull is, according to Rokitanski,[1] as follows:
In cases in which the hypertrophy of the brain has advanced to a high
degree, and in which the sutures of the skull are united, the bones of
the cranium are found thinner and their inner table roughened by
absorption. This is especially the case in the bones which form the
vault of the cranium. The holes or other deficiencies found at the
base of the cranium in the plates of the frontal, ethmoid, and
sphenoid bones are not entirely due to the absorbing process, but
rather to the thinness of these bones. In infants the cavity of the
cranium enlarges in proportion to the hypertrophy of its contents; the
head then resembles in form so much that of hydrocephalus that it may
lead to errors in diagnosis. In some cases in which the disease
rapidly develops to a high degree there is observed on the infant's
skull a loosening and separation of the sutures of the cranial vault,
with red coloration and suffusion of their cartilages.

[Footnote 1: _Lehrbuch der Pathologischen Anatomie_, 3d ed., 1855,
vol. ii. p. 431.]

{998} SYMPTOMS.—There is a gradually increasing muscular weakness,
manifesting itself especially in the lower extremities, and giving
rise to an unsteady, stumbling gait and frequent falling, caused
perhaps by the excessive weight of the head, and also an inability of
securely grasping objects. Besides these disturbances of motion,
epileptic spasms appear, at first light in degree and at long
intervals, but becoming later on in the course of the disease more
frequent and severe. Continuous or intermittent attacks of headache
almost always accompany the disease, and, furthermore, vertigo,
tinnitus aurium, photophobia, and dimness of sight with dilatation of
the pupil; general sensation also becomes blunted, but without ever
amounting to anæsthesia. In a number of cases there is no disturbance
of the psychical functions, though in others symptoms of mental
excitement amounting even to delirium have been observed. Most
frequently the intelligence sinks from the beginning of the disease,
to end in complete idiocy. The pulse also has been observed to fall
considerably during the last stage.

The COURSE of the disease is, according to Andral and Hasse,[2] almost
always chronic, and if an acute development of the affection has been
spoken of, it may be supposed that the latter has commenced a
considerable time previous to the manifestation of the symptoms during
the last stage. Andral divides the disease into two stages, of which
the first is chronic and frequently latent, whilst the other is more
acute and leads to a rapid fatal termination. In most cases death is
caused by such intercurrent affections as give rise to irritation and
hyperæmia of the brain, and thus increase the already abnormal
pressure upon this organ.

[Footnote 2: “Krankheiten des Nervensystems,” 2d ed., 1869, in
_Handbuch der Speciellen Pathologie und Therapie_, edited by R.
Virchow, vol. iv. 1st div., p. 578.]

DIAGNOSIS, PROGNOSIS, AND TREATMENT.—It has already been mentioned
that errors in diagnosis may very easily be committed on account of
the great resemblance in the form of the head in cases of hypertrophy
of the brain and of hydrocephalus, though it has been stated that in
the former affection convulsions, in the form of epileptic spasms,
predominate, to be followed during the last stage by symptoms of
depression; whilst in hydrocephalus the symptoms of depression
manifest themselves from the beginning of the disease, and, moreover,
the rachitic deformities are more prominently shown in the form of a
chicken-breast. A positive diagnosis can only be made by the autopsy.

There are no remarks to be made on the prognosis and treatment of
hypertrophy of the brain.


{999}


SYPHILITIC AFFECTIONS OF THE NERVE-CENTRES.

BY H. C. WOOD, M.D., LL.D.


Introduction.

Syphilitic affections of the nerve-centres are best studied by
separating those of the spinal cord from those of the cerebrum, and in
the present article this natural division of the subject is adopted.
Further, cerebral syphilis in its most characteristic or gummatous
form usually attacks the brain-membranes, or perhaps in some cases the
perivascular sheaths of the vessels, and only secondarily affects the
tissue of the brain itself. The question of the occurrence of specific
disease of the brain-cortex is so important that it shall have a
separate discussion. It is perfectly well proven that with or without
other brain lesion the vessels of the brain may undergo an
atheromatous degeneration as the direct result of a syphilitic
dyscrasia; but such disease links itself on the one hand with the
subject of syphilitic disease of the general vascular system, and on
the other hand with cerebral apoplexies, softenings, and other
degenerations. Moreover, the space here allotted to brain syphilis is
very insufficient. I, therefore, shall not enter upon the further
discussion of syphilitic degeneration of the brain-vessels. The
etiology of brain and spinal syphilis is best discussed under one
heading.

       *       *       *       *       *

GENERAL ETIOLOGY.—We do not know why in any individual case syphilis
selects one portion of the nervous centres rather than another for
attack; indeed, it is only rarely that any exciting cause can be
discovered.

It is not unnatural to expect that any agency which is capable of
exciting an inflammation of a nerve-centre may, when present in a
syphilitic person, provoke a specific disease of such centre. Thus,
thermic fever is a very common cause of chronic meningitis, and in the
_Journ. de Méd. et Chir._ (Paris, 1879, p. 191) a case is reported in
which cerebral syphilis followed a sunstroke; I have myself seen one
similar instance, and in Roberts's case of precocious cerebral
syphilis (see p. 804) the first convulsion came whilst the man was
fishing on a very hot day, and may have been precipitated by the
exposure.

Blows and other traumatisms would be expected to figure largely as
exciting causes of nervous syphilis, but they, in fact, are only
rarely present. I have seen one or two cases of specific brain disease
attributed to violence by the patient, and several cases of possibly
specific spinal {1000} disease—one in which a poliomyelitis followed a
fall on the ice; one in which, after a fall from a cart and marked
spinal concussion, a local myelitis developed;[1] and one of a general
myelitis following an injury by a horse. The only records of such
cases are those of Broadbent[2] and those collected by Heubner.[3]

[Footnote 1: _Univers. Hosp. Dispen. Service-Book_, x., 1875, p. 58.]

[Footnote 2: _Lond. Lancet_, 1876, ii. p. 741.]

[Footnote 3: _Ziemssen's Encyclopædia_, xii. 301.]

Various authorities attach much influence to over-study and other
forms of cerebral strain in exciting brain syphilis. Engelstedt is
stated to have reported cases having such etiological relations, and
Fournier[4] affirms that he has especially seen the disease in
professional men and other persons habitually exercising their brains
to excess. Neither in private nor public practice have I met with an
instance where over-brainwork could be considered a distinct
etiological factor, whilst I have seen some hundreds of cases from
amongst the laboring classes, in whom the intellectual faculties are
chiefly dormant.

[Footnote 4: _La Syphilis du Cerveau_.]

The drift of the evidence in medical literature is so pronounced, and
so in accord with my own experience, that I believe it may be
positively affirmed that in the vast majority of cases of nervous
syphilis no exciting cause can be found.

Inherited syphilis seems to be less prone than the acquired diathesis
to attack the nervous system, but is certainly capable of so acting.
As early as 1779, Joseph Glenck[5] reported a case of a girl, six
years old, cured by a mercurial course of an epilepsy of three years'
standing and of other manifestations of hereditary syphilis. Graefe
found gummatous tumors in the cerebrum of a child nearly two years
old.[6] O. Huebner[7] details the occurrence of pachymeningitis
hæmorrhagica in a syphilitic infant under a year old. Hans Chiari[8]
reports a case in which very pronounced syphilitic degeneration of the
brain-vessels was found in a child fourteen months old. Both Barlow[9]
and T. S. Dowse[10] report cases of nerve syphilis in male infants of
fifteen months. For other similar cases the reader is referred to an
article by J. Parrott,[11] and to a paper by M. E. Troisier.[12]

[Footnote 5: _Doctrina de Morbis Venereis_, Vienna.]

[Footnote 6: _Arch. f. Ophthalm._, Bd. i. Erst Abth.]

[Footnote 7: _Virchow's Archiv_, Bd. lxxxiv. 269.]

[Footnote 8: _Wien. Med. Wochenschrift_, xxxi. 1881, 17.]

[Footnote 9: _Lond. Patholog. Soc. Trans._, 1877.]

[Footnote 10: _The Brain and its Diseases_, vol. i. p. 76.]

[Footnote 11: _Archiv. de Physiologie_, 1871-72, p. 319; also to his
“Leçons sur le Syphilis hered.,” _Progrès méd._, 1877 and 1878.]

[Footnote 12: _Arch. de Tocologie_, x. 411.]

Recorded cases prove decisively that even after puberty specific
nervous affections may primarily attack the unfortunate offspring.
Thus, Nettleship reports[13] the development of a cerebral gumma in a
girl of ten years, and J. A.. Ormerod[14] of a tumor of the median
nerve (probably gummatous) in a woman of twenty-three, both the
subjects of inherited syphilis. Thomas S. Dowse[15] details a case of
cerebral gumma at the age of ten years, and Samuel Wilks[16] one of
epilepsy, from inherited taint, in a boy of fourteen. J.
Hughlings-Jackson reports[17] paraplegia with epilepsy in a boy of
eight, hemiplegia in a girl of eighteen, and hemiplegia in a woman of
twenty-two;[18] the nervous affection in each case being associated
with or dependent upon inherited syphilis. E. Mendel reports[19] a
case of a child {1001} who had inherited syphilis, and developed in
her fifteenth year a maniacal attack with hallucinations. I have seen
cerebral syphilis occur at twenty-one years of age as the first
evident outbreak of the inherited disorder.

[Footnote 13: _Trans. Lond. Path. Soc._, xxxii. 13.]

[Footnote 14: _Ibid._, p. 14.]

[Footnote 15: _Loc. cit._, p. 71.]

[Footnote 16: _Lectures on Dis. of Nerv. Syst._, Philada., 1878, p.
333.]

[Footnote 17: _Journ. Ment. and Nerv. Diseases_, 1875, p. 516.]

[Footnote 18: _Brit. Med. Journal_, May 18, 1872.]

[Footnote 19: _Archiv f. Psychiatrie_, Bd. i. 313.]

When a nervous affection develops first at a comparatively late
period, and no very apparent evidences of the inherited taint are
present, there is great danger of the case being misunderstood;
indeed, in some instances an immediate diagnosis may be scarcely
possible. It is probable that in most of the reported recoveries from
alleged tubercular meningitis the disease has been syphilitic.

Some time since I saw, in an orphan of fourteen, a chronic basal
meningitis, and in the absence of any history and of any evidences of
syphilis gave the fatal prognosis of tubercular disease; but, to my
astonishment, under the long-continued and free use of iodide of
potassium complete recovery occurred. Another child, reported by a
very good practitioner as cured of tubercular meningitis, and
afterward for a long time under my own care, I believe suffered from
hereditary syphilis. Cases of this character have also been reported
by F. Dreyfous.[20]

[Footnote 20: _Revue mensuelle des Malad. des Enfants_, 1883, i. 497;
see also _Gaz. hébdom. Sci. méd. de Montpellier_, 1883, v. 89.]

It is of course very important to diagnose between a tubercular
meningitis and one due to hereditary syphilis. Without a history
certainty is not possible, but a general indefiniteness of symptoms
and slowness of progression should arouse suspicion, especially if the
absence of the pulse-retardation indicated that the vault rather than
the base of the cranium was involved.

The relation of inherited syphilis to various nervous affections not
distinctly specific cannot yet be determined. Arrested development,
and the consequent epilepsy, idiocy,[21] early brain sclerosis, are
probably sometimes due to the inheritance; and the cases collected by
E. Mendel[22] show that chronic hydrocephalus is frequently of
specific origin.[23]

[Footnote 21: See _Brain_, vol. vii. 409.]

[Footnote 22: _Archiv f. Psychiatrie_, Bd. i. 309.]

[Footnote 23: See, also, _Virchow's Archiv_, Bd. xxxviii. p. 129.]

Another very important question connected with the etiology of these
disorders is as to the time of their development. Nervous diseases
following acquired syphilitic infection certainly belong to the
advanced stages of the disorder. Huebner reports[24] a case in which
thirty years elapsed between the contraction of the chancre and the
nervous explosion. I have seen a similar period of thirty years.
Fournier reports intervals of twenty-five years, and thinks from the
third to the tenth year is the period of maximum frequency of nervous
accidents.

[Footnote 24: _Ziemssen's Encyclopædia_, xii. 298, New York ed.]

The fact that nervous syphilis may occur many years after the
cessation of all apparent evidences of the diathesis is of great
practical importance, especially as the nervous system is more prone
to be attacked when the secondaries have been very light than when the
earlier manifestations have been severe. I have repeatedly seen
nervous syphilis in persons whose secondaries have been so slight as
to have been entirely overlooked or forgotten, and who honestly
asserted that they never had had syphilis, although they acknowledged
to gonorrhœa or to repeated exposure, and confessed that their
asserted exemption was due to good fortune rather than to chastity.

{1002} The following citations prove that this experience is not
peculiar. Dowse[25] says: “Often have I had patients totally ignorant
of having at any time acquired or experienced the signs or symptoms of
syphilis in its primary and secondary stages, yet the sequelæ have
been made manifest in many ways, particularly in many of the obscure
diseases of the nervous system.” Buzzard[26] reports a case of nervous
syphilis where the patient was unconscious of the previous existence
of a chancre or of any secondaries. Rinecker also calls attention[27]
to the frequency of nervous syphilis in persons who afford no distinct
history of secondary symptoms.

[Footnote 25: _The Brain and its Diseases_, London, 1879, vol. i. p.
7.]

[Footnote 26: _Syphilitic Nervous Affections_, London, 1874, p. 80.]

[Footnote 27: _Archiv f. Psychiatrie_, vii. p. 241.]

Although syphilis is prone to attack the nervous system many years
after infection, it would be a fatal mistake to suppose that nervous
disease may not rapidly follow the chancre. What is the minimum
possible intermediate period we do not know, but it is certainly very
brief, as is shown by the following cases of this so-called precocious
nervous syphilis. Alfrik Ljunggrén of Stockholm reports[28] the case
of H. R——, who had a rapidly-healed chancre in March, followed in May
of the same year by a severe headache, mental confusion, and
giddiness. Early in July H. R—— had an epileptic attack, but was
finally cured by active antisyphilitic treatment. Although the history
is not explicit, the nervous symptoms appear to have preceded the
development of distinct secondaries other than rheumatic pains.

[Footnote 28: _Archiv f. Dermatol. u. Syphilis_, 1870, ii. p. 155.]

Davaine is said[29] to have seen paralysis of the portio dura “a month
after the first symptoms of constitutional syphilis.” E. Leyden[30]
found advanced specific degeneration of the cerebral arteries in a man
who had contracted syphilis one year previously. R. W. Taylor details
a case in which epilepsy occurred five months after the infection.[31]
In the case of M. X——, reported by Ad. Schwarz,[32] headache came on
the fortieth day after the appearance of the primary sore, and a
hemiplegia upon the forty-sixth day. S. L——[33] had a paralytic stroke
without prodromes six months after the chancre. A. P. L——[34] had an
apoplectic attack seven months after the chancre; A. S——, one five
months after her chancre. In a case which recently occurred in the
practice of A. Sydney Roberts of this city the chancre appeared after
a period of incubation of twenty-six days, and two months and eight
days subsequent to this came the first fit; eight days after the first
the second convulsion occurred, with a distinct aura, which preceded
by some minutes the unconsciousness. An interesting observation in
this connection is that of Ern. Gaucher[35] of a spinal syphilis
occurring six months after the appearance of a chancre.

[Footnote 29: Buzzard, _Syphilitic Nervous Affections_, London, 1874.]

[Footnote 30: _Zeitschrift f. klin. Med._, Bd. v. 165.]

[Footnote 31: _Journ. Nervous and Mental Dis._, 1876, p. 38.]

[Footnote 32: _De l'Hémiplegia syphilitique Prêcoce_, Inaug. Diss.,
Paris, 1880.]

[Footnote 33: _Ibid._]

[Footnote 34: _Ibid._]

[Footnote 35: _Revue de Méd._, 1882, ii. 678.]

This citation of cases might be much extended, but is sufficient to
show that nervous syphilis occurs not very rarely within six months
after infection, and may be present in two months.


{1003} Gummatous Brain Syphilis.

CLINICAL HISTORY.—Brain syphilis of the type now under consideration
may declare itself with great suddenness. An apoplectic attack, a
convulsive paroxysm, a violent mania, or a paralytic stroke may be the
first detected evidence of the disease. In most of these cases the
coming storm ought to have been foreseen, and to a greater or less
degree averted. The onset of cerebral syphilis is, however, generally
more gradual, the symptoms coming on slowly and successively. Proper
treatment, instituted at an early stage, is usually successful, so
that a careful study of these prodromes is most important. They are
generally such as denote cerebral disturbance, and, although they
should excite suspicion, are not diagnostic, except as occurring in
connection with a specific history or under suspicious circumstances.

Headache, slight failure of memory, unwonted slowness of speech,
general lassitude, and especially lack of willingness to mental
exertion, sleeplessness or excessive somnolence, attacks of momentary
giddiness, vertiginous feelings when straining at stool, yelling or in
any way disturbing the cerebral circulation, alteration of
disposition,—any of these, and, a fortiori, several of them, occurring
in a syphilitic subject, should be the immediate signal of alarm, and
lead to the examination of the optic discs, for in some cases the
eye-ground will be found altered even during the prodromic stage. Of
course if choked disc be found the diagnosis becomes practically
fixed, but the absence of choked disc is no proof that the patient is
free from cerebral syphilis. In regard to the individual prodromic
symptoms, my own experience does not lend especial importance to any
one of them, although, perhaps, headache is the most common. There is
one symptom which may occur during the prodromic stage of cerebral
syphilis, but is more frequent at a later stage—a symptom which is not
absolutely characteristic of the disease, but which, when it occurs in
a person who is not hysterical, should give rise to the strongest
suspicion. I refer to the occurrence of repeated, partial, passing
palsies. A momentary weakness of one arm, a slight drawing of the face
disappearing in a few hours, a temporary dragging of the toe, a
partial aphasia which appears and disappears, a squint which to-morrow
leaves no trace, may be due to a non-specific brain tumor, to miliary
cerebral aneurisms, or to some other non-specific affection; but in
the great majority of cases where such phenomena occur repeatedly the
patient is suffering from syphilis or hysteria.

The first type or variety of the fully-formed syphilitic meningeal
disease to which attention is here directed is that of an acute
meningitis. I am much inclined to doubt whether an acute syphilitic
meningitis can ever develop as a primary lesion—whether it must not
always be preceded by a chronic meningitis or by the formation of a
gummatous tumor; but it is very certain that acute meningitis may
develop when there have been no apparent symptoms, and may therefore
seem to be abrupt in its onset. Some years ago I saw, in consultation,
a man who in the midst of apparent health was attacked by violent
meningeal convulsions, with distinct evidences of acute meningitis. He
was apparently saved from death by very heroic venesection, but after
his return to consciousness developed very rapidly a partial specific
hemiplegia, showing that a latent gumma had {1004} probably preceded
the acute attack. On the other hand, an acute attack is liable at any
time to supervene upon a chronic syphilitic meningitis. At the
University Hospital dispensary I once diagnosed chronic cerebral
syphilis in a patient who the next day was seized with violent
delirium, with convulsions and typical evidences of acute meningitis,
and died four or five days afterward. At the autopsy an acute
meningitis was found to have been engrafted on a chronic specific
lesion of a similar character. In the case reported by Gamel,[36] in
which intense headache, fever, and delirium came on abruptly in an old
syphilitic subject and ended in general palsy and death, the symptoms
were found to depend upon an acute meningitis secondary to a large
gumma.

[Footnote 36: _Tumeurs gommeuses du Cerveau_, Inaug. Diss.,
Montpellier, 1875.]

In this connection may well be cited the observation of Molinier[37]
in which violent delirium, convulsions, and coma occurred suddenly. A
very curious case is reported by D. A. Zambaco[38] in which attacks
simulating acute meningitis occurring in a man with a cerebral
gummatous tumor appear to have been malarial. In such a case the
diagnosis of a malarial paroxysm could only be made out by the
presence of the cold stage, the transient nature of the attack, its
going off with a sweat, its periodical recurrence, and the therapeutic
effect on it of quinine.

[Footnote 37: _Revue méd. de Toulouse_, xiv. 1880, 341.]

[Footnote 38: _Des Affections nerveuses-syphilitiques_, Paris, 1862,
p. 485.]

In the cases of chronic brain syphilis which have come under my
observation, most usually after a greater or less continuance of
prodromes such as have been mentioned, epileptic attacks have occurred
with a hemiplegia, or a monoplegia, which is almost invariably
incomplete and usually progressive; very frequently diplopia is
manifested before the epilepsy, and on careful examination is found to
be due to weakness of some of the ocular muscles. Not rarely
oculo-motor palsy is an early and pronounced symptom, and a marked
paralytic squint is very common. Along with the development of these
symptoms there is almost always distinct failure of the general health
and progressive intellectual deterioration, as shown by loss of
memory, failure of the power to fix the attention, mental
bewilderment, and perhaps aphasia. If the case convalesce under
treatment, the amelioration is gradual, the patient travelling slowly
up the road he has come down. If the case end fatally, it is usually
by a gradual sinking into complete paralysis, or the patient is
carried off by an acute inflammatory exacerbation, or, as in two of my
cases, amelioration may be rapidly occurring and a very violent
epileptic fit produce a sudden fatal asphyxia. Death from
brain-softening around the tumor is not infrequent, but a fatal
apoplectic hemorrhage is rare.

The clinical varieties of cerebral meningeal syphilis are so
polymorphic and kaleidoscopic that it is almost impossible to reduce
them to order for descriptive purposes. Fournier separates them into
the cephalic, congestive, epileptic, aphasic, mental, and paralytic,
but scarcely facilitates description by so doing. Heubner makes the
following types:

“1. Psychical disturbances, with epilepsy, incomplete paralysis
(seldom of the cranial nerves), and a final comatose condition,
usually of short duration.

“2. Genuine apoplectic attacks with succeeding hemiplegia, in
connection with peculiar somnolent conditions, occurring in
often-repeated {1005} episodes; frequently phenomena of unilateral
irritation, and generally at the same time paralyses of the cerebral
nerves.

“3. Course of the cerebral disease similar to paralytica dementia.”

In regard to these types, the latter seems to me clear and well
defined, but contains those cases which I shall discuss under the head
of Cortical Disease.

Meningeal syphilis as seen in this country does not conform rigidly
with the other asserted types, although there is this much of
agreement, that when the epilepsy is pronounced the basal cranial
nerves are not usually paralyzed, the reason of this being that
epilepsy is especially produced when the gummatous change is in the
ventricles or on the upper cortex. In basal affections the epileptoid
spells, if they occur at all, are usually of the form of petit mal;
but this rule is general, not absolute. The apoplectic somnolent form
of cerebral syphilis, for some reason, is rare in this city, and it
seems necessary to add to those of Heubner's a fourth type to which a
large proportion of our cases conform. This type I would characterize
as follows:

4. Psychical disturbance without complete epileptic convulsions,
associated with palsy of the basal nerves and often with partial
hemiplegia.

The most satisfactory way of approaching this subject is, however, to
study the important symptoms in severalty, rather than to attempt to
group them into recognizable varieties of the disease; and this method
I shall here adopt.

Headache is the most constant and usually the earliest symptom of
meningeal syphilis; but it may be absent, especially when the lesion
is located in the reflexions of the meninges which dip into the
ventricles, or when the basal gumma is small and not surrounded with
much inflammation. The length of time it may continue without the
development of other distinct symptoms is remarkable. In one case[39]
at the University Dispensary the patient affirmed that he had had it
for four years before other causes of complaint appeared. It sometimes
disappears when other manifestations develop. It varies almost
indefinitely in its type, but is, except in very rare cases, at least
so far paroxysmal as to be subject to pronounced exacerbations. In
most instances it is entirely paroxysmal; and a curious circumstance
is, that very often these paroxysms may occur only at long intervals:
such distant paroxysms are usually very severe, and are often
accompanied by dizziness, sick stomach, partial unconsciousness, or
even by more marked congestive symptoms. The pain may seem to fill the
whole cranium, may be located in a cerebral region, or fixed in a very
limited spot. Heubner asserts that when this headache can be localized
it is generally made distinctly worse by pressure at certain points,
but my own experience is hardly in accord with this. Any such soreness
plainly cannot directly depend upon the cerebral lesion, but must be a
reflex phenomenon or due to a neuritis. According to my own
experience, localized soreness indicates an affection of the bone or
of its periosteum. In many cases, especially when the headache is
persistent, there are distinct nocturnal exacerbations.

[Footnote 39: _Book Y._, p. 88, 1879.]

It will be seen that there is nothing absolutely characteristic in the
headache of cerebral syphilis; but excessive persistency, apparent
causelessness, and a tendency to nocturnal exacerbation should in any
{1006} cephalalgia excite suspicion of a specific origin—a suspicion
which is always to be increased by the occurrence of slight spells of
giddiness or by delirious mental wandering accompanying the paroxysms
of pain. When an acute inflammatory attack supervenes upon a specific
meningeal disease it is usually ushered in by a headache of
intolerable severity.

When the headache in any case is habitually very constant and severe,
the disease is probably in the dura mater or periosteum; and this
probability is much increased if the pain be local and augmented by
firm, hard pressure upon the skull over the seat of the pain.

Disorders of Sleep.—There are two antagonistic disorders of sleep,
either of which may occur in cerebral syphilis, but which have only
been present in a small proportion of the cases that I have seen.
Insomnia is more apt to be troublesome in the prodromic than in the
later stages, and is only of significance when combined with other
more characteristic symptoms. A peculiar somnolence is of much more
determinate import. It is not pathognomonic of cerebral syphilis, yet
of all the single phenomena of this disease it is the most
characteristic. Its absence is of no import in the theory of an
individual case.

As I have seen it, it occurs in two forms: In the one variety the
patient sits all day long or lies in bed in a state of semi-stupor,
indifferent to everything, but capable of being aroused, answering
questions slowly, imperfectly, and without complaint, but in an
instant dropping off again into his quietude. In the other variety the
sufferer may still be able to work, but often falls asleep while at
his tasks, and especially toward evening has an irresistible desire to
slumber, which leads him to pass, it may be, half of his time in
sleep. This state of partial sleep may precede that of the more
continuous stupor, or may pass off when an attack of hemiplegia seems
to divert the symptoms. The mental phenomena in the more severe cases
of somnolency are peculiar. The patient can be aroused—indeed in many
instances he exists in a state of torpor rather than of sleep; when
stirred up he thinks with extreme slowness, and may appear to have a
form of aphasia; yet at intervals he may be endowed with a peculiar
automatic activity, especially at night. Getting out of bed; wandering
aimlessly and seemingly without knowledge of where he is, and unable
to find his own bed; passing his excretions in a corner of the room or
in other similar place, not because he is unable to control his
bladder and bowels, but because he believes that he is in a proper
place for such act,—he seems a restless nocturnal automaton rather
than a man. In some cases the somnolent patient lies in a perpetual
stupor.

An important fact in connection with the somnolence is that it may
develop suddenly without marked premonition. Thus in a case reported
by J. A. Ormerod[40] a man who had been in good health, save only for
headache, awoke one morning in a semi-delirious condition, and for
three days slept steadily, only arousing for meals; after this there
was impairment of memory and mental faculties, but no more marked
symptoms.

[Footnote 40: _Brain_, vol. v. 260.]

Apathy and indifference are the characteristics of the somnolent
state, yet the patient will sometimes show excessive irritability when
aroused, and will at other periods complain bitterly of pain in his
head, or will groan as though suffering severely in the midst of his
stupor—at a time, {1007} too, when he is not able to recognize the
seat of the pain. I have seen a man with a vacant, apathetic face,
almost complete aphasia, persistent heaviness and stupor, arouse
himself when the stir in the ward told him that the attending
physician was present, and come forward in a dazed, highly pathetic
manner, by signs and broken utterances begging for something to
relieve his head. Heubner speaks of cases in which the irritability
was such that the patient fought vigorously when aroused; this I have
not seen.

This somnolent condition may last many weeks. T. Buzzard[41] details
the case of a man who after a specific hemiplegia lay silent and
somnolent for a month, and yet finally recovered so completely as to
win a rowing-match on the Thames. I have seen a fair degree of
recovery after a somnolence of four months' duration.

[Footnote 41: _Clinical Lectures on Dis. Nerv. Syst._, London, 1882.]

In its excessive development syphilitic stupor puts on the symptoms of
advanced brain-softening, to which it is indeed often due. Of the two
cases with fatal result of which I have notes, one at the autopsy was
found to have symmetrical purulent breaking down of the anterior
cerebral lobes; the other, softening of the right frontal and temporal
lobes, due to the pressure of a gummatous tumor, and ending in a fatal
apoplexy.

This close connection with cerebral softening explains the clinical
fact that apoplectic hemorrhage is very apt to end the life in these
cases of somnolent syphilis. But a prolonged deep stupor in persons
suffering from cerebral syphilis does not prove the existence of
extensive brain-softening, and is not incompatible with subsequent
complete recovery. As an element of prognosis it is of serious but not
of fatal import.

Paralysis.—When it is remembered that a syphilitic exudation may
appear at almost any position in the brain, that spots of encephalic
softening are a not rare result of the infection, that syphilitic
disease is a common cause of cerebral hemorrhage, it is plain that a
specific palsy may be of any conceivable variety, and affect either
the sensory, motor, or intellectual sphere. The mode of onset is as
various as the character of the palsy. The attack may be
instantaneous, sudden, or gradual. The gradual development of the
syphilitic gumma would lead us, a priori, to expect an equally gradual
development of the palsy; but experience shows that in a large
proportion of the cases the paralysis appears suddenly, with or
without the occurrence of an apoplectic or epileptic fit. Under these
circumstances it will be usually noted that the resulting palsy is
incomplete; in rare instances it may be at its worst when the patient
awakes from the apoplectic seizure, but usually it progressively
increases for a few hours, and then becomes stationary. These sudden
partial palsies probably result from an intense congestion around the
seat of disease or from stoppage of the circulation in the same
locality; whatever their mechanism may be, it is important to
distinguish them from palsies which are due to hemorrhage. I believe
this can usually be done by noting the degree of paralysis.

A suddenly-developed, complete hemiplegia or other paralysis may be
considered as in all probability either hemorrhagic or produced by a
thrombus so large that the results will be disorganization of the
brain-substance, and a future no more hopeful than that of a clot. On
the {1008} other hand, an incomplete palsy may be rationally believed
to be due to pressure or other removable cause; and this belief is
much strengthened by a gradual development. The bearing of these facts
upon prognosis it is scarcely necessary to point out.

Although the gummata may develop at almost any point, they especially
affect the base of the brain, and are prone to involve the nerves
which issue from it. Morbid exudations, not tubercular or syphilitic,
are rare in this region. Hence a rapidly but not abruptly appearing
strabismus, ptosis, dilated pupil, or any paralytic eye symptom in the
adult is usually of syphilitic nature. Syphilitic facial palsy is not
so frequent, whilst paralysis of the nerve from rheumatic and other
inflammation within its bony canal is very common. Paralysis of the
facial nerve may therefore be specific, but existing alone is of no
diagnostic value. Since syphilitic palsies about the head are in most
instances due to pressure upon the nerve-trunks, the electrical
reactions of degeneration are present in the affected muscles.

There is one peculiarity about specific palsies which has already been
alluded to as frequently present—namely, a temporary, transient,
fugitive, varying character and seat. Thus an arm may be weak to-day,
strong to-morrow, and the next day feeble again, or the recovered arm
may retain its power and a leg fail in its stead. These transient
palsies are much more apt to involve large than small brain
territories. The explanation of their largeness, fugitiveness, and
incompleteness is that they are not directly due to clots or other
structural changes, but to congestions of the brain-tissues in the
neighborhood of gummatous exudations. Squint due to direct pressure on
a nerve will remain when the accompanying monoplegia due to congestion
disappears.

Motor palsies are more frequent than sensory affections in syphilis,
but hemianæsthesia, localized anæsthetic tracts, indeed any form of
sensory paralysis, may occur. Numbness, formications, all varieties of
paræsthesia, are frequently felt in the face, body, or extremities.
Violent peripheral neuralgic pains are rare, and generally when
present denote neuritis. Huguenin, however, reports[42] a severe
trigeminal anæsthesia dolorosa, which was found, after death from
intercurrent disease, to have depended upon a small gumma pressing
upon the Gasserian ganglion. A somewhat similar case has also been
reported by Allen McLane Hamilton.[43]

[Footnote 42: _Schwiez. Corr. Blät._, 1875.]

[Footnote 43: _Alienist and Neurologist_, iv. 58.]

The special senses are liable to suffer from the invasion of their
territories by cerebral syphilis, and the resulting palsies follow
courses and have clinical histories parallel to those of the motor
sphere. The onset may be sudden or gradual, the result temporary or
permanent. Charles Mauriac[44] reports a case in which the patient was
frequently seized with sudden attacks of severe frontal pain and
complete blindness lasting from a quarter to half an hour; at other
times the same patient had spells of aphasia lasting only for one or
two minutes. I have seen two cases of nearly complete deafness
developing in a few hours in cerebral syphilis, and disappearing
abruptly after some days. Like other syphilitic palsies, therefore,
paralyses of special senses may come on suddenly or gradually, and may
occur paroxysmally.

[Footnote 44: _Loc. cit._, p. 31.]

Among the palsies of cerebral syphilis must be ranked aphasia. An
{1009} examination of recorded cases shows that syphilitic aphasia is
subject to vagaries and laws similar to those connected with other
specific cerebral palsies. It is usually a symptom of advanced
disease, but may certainly develop as one of the first evidences of
cerebral syphilis. Coming on after an apoplectic or epileptic fit, it
may be complete or incomplete: owing to the smallness of the centre
involved and the ease with which its function is held in abeyance, a
total loss of word-thought is not so decisive as to the existence of
cerebral hemorrhage as is a total motor palsy. Like hemiplegia or
monoplegia, specific aphasia is sometimes transitory and paroxysmal.
Buzzard[45] records several such cases. Mauriac[46] details a very
curious case in which a patient, after long suffering from headache,
was seized by sudden loss of power in the right hand and fingers,
lasting about ten minutes only, but recurring many times a day. After
this had continued some time the paroxysms became more completely
paralytic, and were accompanyed by loss of the power of finding words,
the height of the crises in the palsy and aphasia being simultaneously
reached. For a whole month these attacks occurred five or six times a
day, without other symptoms except headache, and then the patient
became persistently paralytic and aphasic, but finally recovered. To
describe the different forms of specific aphasia and their mechanism
of production would be to enter upon a discussion of aphasia itself—a
discussion out of place here. Suffice it to say that every conceivable
form of the disorder may be induced by syphilis.

[Footnote 45: _Loc. cit._, p. 81.]

[Footnote 46: _Aphasie et Hemiplégia droite Syphilit._, Paris, 1877.]

Owing to the centres of speech being situated in the cortical portion
of the brain, aphasia in cerebral syphilis is very frequently
associated with epilepsy. Of course right-sided palsy and aphasia are
united in syphilitic as in other disorders. If, however, the
statistics given by Tanowsky[47] be reliable, syphilitic aphasia is
associated with left-sided hemiplegia in a most extraordinarily large
proportion. Thus in 53 cases collected by Tanowsky, 18 times was there
right-sided hemiplegia, and 14 times left-sided hemiplegia, the other
cases being not at all hemiplegic. Judging from the autopsy on a case
reported in Mauriac's brochure, this concurrence of left-sided
paralysis and aphasia depends partly upon the great frequency of
multiple brain lesions in syphilis, and partly upon the habitual
involvement of large territories of the gray matter secondarily to
diseased membrane. An important practical deduction is that the
conjoint existence of left hemiplegia and aphasia is almost diagnostic
of cerebral syphilis.

[Footnote 47: _L'Aphasie syphilitique_.]

Probably amongst the palsies may be considered the disturbances of the
renal functions, which are only rarely met with in cerebral syphilis,
and which are probably usually dependent upon the specific exudation
pressing upon the vaso-motor centres in the medulla. Fournier speaks
of having notes of six cases in which polyuria with its accompaniment,
polydipsia, was present, and details a case in which the specific
growth was found in the floor of the fourth ventricle. Cases have been
reported of true saccharine diabetes due to cerebral syphilis,[48] and
I can add to these an observation of my own. The symptoms, which
occurred in a {1010} man of middle age, with a distinct specific
history, were headache, nearly complete hemiplegia, and mental
failure, associated with the passage of comparatively small quantities
of a urine so highly saccharine as to be really a syrup. Under the
influence of the iodide of potassium the sugar in a few weeks
disappeared from the urine.

[Footnote 48: Consult Servantié, _Des Rapports du Diabète et de la
Syphilis_, Paris, Thèse, 1876; also, case reported by L. Putzel, _New
York Med. Record_, xxv. 450.]

Epilepsy.—Epileptic attacks are a very common symptom of meningeal
syphilis, and are of great diagnostic value. The occurrence in an
adult of an epileptic attack or of an apoplectic fit, or of a
hemiplegia after a history of intense and protracted headache, should
always excite grave suspicion.

Before I had read Fournier's work on _Nervous Syphilis_ I taught that
an epilepsy appearing after thirty years of age was very rarely, if
ever, essential epilepsy, and unless alcoholism, uræmic poison, or
other adequate cause could be found was in nine cases out of ten
specific; and I therefore quote with satisfaction Fournier's words:
“L'épilepsie vraie, ne fait jamais son premier dêbut à l'âge adulte, à
l'âge mûr. Si un homme adulte, au dessus de 30, 35, à 40 ans, vient, à
être pris pour la première fois d'une crise épileptique, et cela dans
la cours d'une bonne santé apparente, il y a, je vous le répète, hui
ou neuf chances sur dix pour que cette épilepsie soit d'origine
syphilitique.”

Syphilitic epilepsy may occur either in the form of petit mal or of
haut mal, and in either case may take on the exact characters and
sequence of phenomena which belong to the so-called idiopathic or
essential epilepsy. The momentary loss of consciousness of petit mal
will usually, however, be found to be associated with attacks in
which, although voluntary power is suspended, memory recalls what has
happened during the paroxysm—attacks, therefore, which simulate those
of hysteria, and which may lead to an error of diagnosis.

Even in the fully-developed type of the convulsions the aura is only
rarely present. Its absence is not, however, of diagnostic value,
because it is frequently not present in essential epilepsy, and it may
be pronounced in the specific disease. It is said that when in an
individual case the aura has once appeared the same type or form of
approach of the convulsion is thereafter rigidly adhered to. The aura
is sometimes bizarre: a severe pain in the foot, a localized cramp, a
peculiar sensation, indescribable and unreal in its feeling, may be
the first warning of the attack. An aura may affect a special sense.
Thus, I have at present a patient whose attacks begin with blindness.

In many, perhaps most, cases of specific convulsions, instead of a
paroxysm of essential epilepsy being closely simulated, the movements
are in the onset, or more rarely throughout the paroxysm, unilateral;
indeed, they may be confined to one extremity. This restriction of
movement has been held to be almost characteristic of syphilitic
epilepsy, but it is not so. Whatever diagnostic significance such
restriction of the convulsion has is simply to indicate that the fit
is due to a cortical organic lesion of some kind. Tumors, scleroses,
and other organic lesions of the brain-cortex are as prone to cause
unilateral or monoplegic epilepsy when they are not specific as when
they are due to syphilis.

Sometimes an epilepsy dependent upon a specific lesion implicating the
brain-cortex may be replaced by a spasm which is more or less local
and is not attended with any loss of consciousness. Thus, in a case
now {1011} convalescent in the University Hospital, a man aged about
thirty-five offered a history of repeated epileptic convulsions, but
at the time of his entrance into the hospital, instead of epileptic
attacks, there was a painless tic. The spasms, which were clonic and
occurred very many times a day, sometimes every five minutes, were
very violent, and mostly confined to the left facial nerve
distribution. The trigeminus was never affected, but in the severer
paroxysms the left hypoglossal and spinal accessory nerves were
profoundly implicated in all of their branches. Once, fatal asphyxia
from recurrent laryngeal spasm of the glottis was apparently averted
only by the free inhalation of the nitrite of amyl. The sole other
symptom was headache, but the specific history was clear and the
effect of antisyphilitic remedies rapid and pronounced.

It is very plain that such attacks as those just detailed are closely
allied to epilepsy; indeed, there are cases of cerebral syphilis in
which widespread general spasms occur similar to those of a Jacksonian
epilepsy, except that consciousness is not lost, because the nervous
discharge does not overwhelm the centres which are connected with
consciousness.[49] On the other hand, these epileptoid spasmodic cases
link themselves to those in which the local brain affection manifests
itself in contractions or persistent irregular clonic spasms.
Contractures may exist and may simulate those of descending
degeneration,[50] but in my own experience are very rare.[51]

[Footnote 49: Case, _Canada Med. and Surg. Journ._, xi. 487.]

[Footnote 50: Case, _Centralbl. Nerv. Heilk._, 1883, p. 1.]

[Footnote 51: A case of syphilitic athetosis may be found in _Lancet_,
1883, ii. 989.]

The clonic spasms of cerebral syphilis may assume a distinctly choreic
type, or may in their severity simulate those of hysteria, throwing
the body about violently.[52] It is, to my mind, misleading, and
therefore improper, to call such cases syphilitic chorea, as there is
no reason for believing that they have a direct relation with ordinary
chorea. They are the expression of an organic irritation of the
brain-cortex, and are sometimes followed by paralysis of the affected
member; in other words, the disease, progressing inward from the
brain-membrane, first irritates, and then so invades a cortical centre
as to destroy its functional power.[53]

[Footnote 52: See Allison, _Amer. Med. Journ._, 1877, 74.]

[Footnote 53: Case, _Chicago Med. Journ. and Exam._, xlvi. 21.]

Psychical Symptoms.—As already stated, apathy, somnolence, loss of
memory, and general mental failure are the most frequent and
characteristic mental symptoms of meningeal syphilis; but, as will be
shown in the next chapter, syphilis is able to produce almost any form
of insanity, and therefore mania, melancholia, erotic mania, delirium
of grandeur, etc. etc. may develop along with the ordinary
manifestation of cerebral syphilis, or may come on during an attack
which has hitherto produced only the usual symptoms. Without
attempting any exhaustive citation of cases, the following may be
alluded to.

A. Erlenmeyer reports[54] a case in which an attack of violent
headache and vomiting was followed by paralysis of the right arm and
paresis of the left leg, with some mental depression; a little later
the patient suddenly became very cheerful, and shortly afterward
manifested very distinctly delirium of grandeur with failure of
memory. Batty Tuke reports[55] a case in which, with aphasia, muscular
wasting, strabismus, {1012} and various palsies, there were delusions
and hallucinations. In the same journal[56] S. D. Williams reports a
case in which there were paroxysmal violent attacks of frontal
headache. The woman was very dirty in her habits, only ate when fed,
and existed in a state of hypochondriacal melancholy. Leiderdorf
details a case with headache, partial hemiplegia, great psychical
disturbance, irritability, change of character, marked delirium of
grandeur, epileptic attacks, and finally dementia, eventually cured by
iodide of potassium.[57] Several cases illustrating different forms of
insanity are reported by N. Manssurow.[58]

[Footnote 54: _Die luëtischen Psychosen_.]

[Footnote 55: _Journ. Ment. Sci._, Jan., 1874, p. 560.]

[Footnote 56: April, 1869.]

[Footnote 57: _Medicin Jahrbucher_, xx. 1864, p. 114.]

[Footnote 58: _Die Tertiäre Syphilis_, Wien, 1877.]

That the attacks of syphilitic insanity, like the palsies of syphilis,
may at times be temporary and fugitive, is shown by a curious case
reported by H. Hayes Newington,[59] in which, along with headache,
failure of memory, and ptosis in a syphilitic person, there was a
brief paroxysm of noisy insanity.

[Footnote 59: _Journ. Ment. Sci._, London, xix. 555.]

DIAGNOSIS.—In a diagnosis of cerebral syphilis a correct history of
the antecedents of the patients is of vital importance. Since very few
of the first manifestations of the disorder are absolutely
characteristic, whilst almost any conceivable cerebral symptoms may
arise from syphilitic disease, treatment should be at once instituted
on the appearance of any disturbance of the cerebral functions in an
infected person.

Very frequently the history of the case is defective, and not rarely
actually misleading. Patients often appear to have no suspicion of the
nature of their complaint, and will deny the possibility of syphilis,
although they confess to habitual unchastity. My own inquiries have
been so often misleading in their results that I attach but little
weight to the statements of the patient, and in private practice avoid
asking questions which might recall unpleasant memories, depending
upon the symptoms themselves for the diagnosis.

The general grounds of diagnosis have been sufficiently mapped out in
the last section, but some reiteration may be allowable. After the
exclusion of other non-specific disease, headache occurring with any
form of ocular palsy or with a history of attack of partial monoplegia
or hemiplegia, vertigo, petit mal, epileptoid convulsions, or
disturbances of consciousness, or attacks of unilateral or localized
spasms, should lead to the practical therapeutic test. Ocular palsies,
epileptic forms of attacks occurring after thirty years of age, morbid
somnolence, even when existing alone, are sufficient to put the
practitioner upon his guard. It is sometimes of vital importance that
the nature of the cephalalgia shall be recognized before the coming on
of more serious symptoms; any apparent causelessness, severity, and
persistency should arouse suspicion, to be much increased by a
tendency to nocturnal exacerbations or by the occurrence of mental
disturbance or of giddiness at the crises of the paroxysms. Not rarely
there are very early in these cases curious, almost indefinable,
disturbances of cerebral functions, which may be easily overlooked,
such as temporary and partial failures of memory, word-stumbling,
fleeting feelings of numbness or weakness, alterations of disposition.
In the absence of hysteria an indefinite and apparently disconnected
series of nerve accidents is of very urgent import. To use the words
of Hughlings-Jackson, “A random association or a random succession of
{1013} nervous symptoms is very strong warrant for a diagnosis of a
syphilitic disease of the nervous system.” Cerebral syphilis occurring
in an hysterical subject may be readily overlooked until fatal
mischief is done. When any paralysis occurs a study of the reflexes
may sometimes lead to a correct diagnosis. Thus in a hemiplegia the
reflex on the affected side in cerebral syphilis is very frequently
exaggerated, whilst in hysteria the reflexes are usually alike on both
sides. When both motion and sensation are disturbed in an organic
hemiplegia, the anæsthesia and motor paralysis occur on the same side
of the body, whilst in hysteria they are usually on opposite sides.

In all cases of doubtful diagnosis the so-called therapeutic test
should be employed, and if sixty grains of iodide of potassium per day
fail to produce iodism, for all practical purposes the person may be
considered to be a syphilitic. No less an authority than Seguin has
denied the validity of this, but I believe, myself, that some of his
reported cases were suffering from unsuspected syphilis. I do not deny
that there are rare individuals who, although untainted, can resist
the action of iodide, but in ten years' practice in large hospitals,
embracing probably some thousands of cases, I have not met with more
than one or two instances which I believed to be of such character. Of
course in making these statements I leave out of sight persons who
have by long custom become accustomed to the use of the iodide, for
although in most cases such use begets increase of susceptibility, the
contrary sometimes occurs. Of course the physician who should publicly
assert that a patient who did not respond to the iodide had syphilis
would be a great fool, but in my opinion the physician who did not act
upon such a basis would be even more culpable.

PROGNOSIS.—Cerebral meningeal syphilis varies so greatly and so
unexpectedly in its course that it is very difficult to establish
rules for predicting the future in any given case. The general laws of
prognosis in brain disease hold to some extent, but may always be
favorably modified, and patients apparently at the point of death will
frequently recover under treatment. The prognosis is not, however, as
absolutely favorable as is sometimes believed, and especially should
patients be warned of the probable recurrence of the affection even
when the symptoms have entirely disappeared. The only safety after the
restoration of health consists in an immediate re-treatment upon the
recurrence of the slightest symptom. The occurrence of a complete,
sudden hemiplegia or monoplegia is sufficient to render probable the
existence of a clot, which must be subject to the same laws as though
not secondary to a specific lesion. If a rapid decided rise of
temperature occur in an apoplectic or epileptic attack, the prognosis
becomes very grave. An epileptic paroxysm very rarely ends fatally,
although it has done so in two of my cases.

The prognosis in gummatous cerebral syphilis should always be
guardedly favorable. In the great majority of cases a more or less
incomplete recovery occurs under appropriate treatment, and I have
seen repeatedly patients who were unconscious, with urinary and fecal
incontinence, and apparently dying, recover. Nevertheless, so long as
there is any particle of gummatous inflammation in the membrane the
patient is liable to sudden congestions of the brain, which may prove
rapidly fatal, or he may die in a brief epileptic fit. On the one hand
there is an {1014} element of uncertainty in the most favorable case,
and on the other so long as there is life a positively hopeless
prognosis is not justifiable.

PATHOLOGY.—Gummatous inflammation of the brain probably always has its
starting-point in the brain-membranes, although it may be situated
within the brain: thus, I have seen the gummatous tumors spring from
the velum interpositum in the lateral ventricle. The disease most
usually attacks the base of the brain, and is especially found in the
neighborhood of the pons Varolii and the optic tract. It may, however,
locate itself upon the vault of the cranium, and in my experience has
seemed to prefer the anterior or motor regions. The mass may be well
defined and roundish, but more usually it is spread out, irregular in
shape, and more or less confluent with the substance of the brain
beneath it. It varies in size from a line to several inches in length,
and when small is prone to be multiple. The only lesion which it
resembles in gross appearance is tubercle, from which it sometimes
cannot be certainly distinguished without microscopic examination.

The large gummata have not rarely two distinct zones, the inner one of
which is drier, somewhat yellowish in color, opaque, and resembles the
region of caseous degeneration in the tubercle. The outer zone is more
pinkish and more vascular, and is semi-translucent.

On microscopic examination the most characteristic structures are
small cells, such as are found in gummatous tumors in other portions
of the body. These cells are most abundant in the inner zone, which,
indeed, may be entirely composed of them. In the centre of the tumor
they are more or less granular and atrophied; in some cases the
caseous degeneration has progressed so far that the centre of the
gumma consists of minute acicular crystals of fat. In the external or
peripheral zone of the tumor the mass may pass imperceptibly into the
normal nerve tissue, and under these circumstances it is that it
contains the spider-shaped cells or stellate bodies described by
Jastrowitch, and especially commented upon by Charcot and Gombault and
by Coyne. These are large cells containing an exaggerated nucleus and
a granular protoplasm, which continues into multiple, branching,
rigid, refracting prolongations, which prolongations are scarcely
stained by carmine. Alongside of these cells other largish cells are
often found without prolongations, but furnished with oval nuclei and
granular protoplasm. Amongst these cells will be seen the true
gummatous cells, as well as the more or less altered neuroglia and
nerve-elements. In the perivascular lymphatic sheaths in the outer
part of the gumma is usually a great abundance of small cells. The
spider-shaped cells are probably hypertrophied normal cells of the
neuroglia, and have been considered by Charcot and Gombault as
characteristic of syphilitic gummata of the brain. In a solitary
gumma, however, of considerable size from the neighborhood of the
cerebellum, studied by Coyne and Peltier, there were no stellated
cells. Coyne considers that their presence is due to their previous
existence in the normal state of the regions affected by the gumma.
Exactly what becomes of syphilitic gumma of the brain in cases of
recovery it is difficult to determine. It is certain that they become
softened and disappear more or less completely, and it is probable
that the cicatrices or the small peripheral cysts which are not rarely
found in the surfaces of the brain are sometimes remnants of gummatous
tumors. In a number of cases collected by Gros and {1015} Lancereaux
there were small areas of softened tissue or small calcareous and
caseous masses or cerebral lacunæ corresponding to the cicatrices of
softening or imperfect cysts, coincident with evidences of syphilis
elsewhere. V. Cornil also states that he has found small areas of
softening with well-established syphilitic lesions of the dura mater
and cranium, but believes that the lacunæ or cysts depend rather upon
chronic syphilitic lesions of cerebral arteries than upon gummatous
inflammation.

When a gummatous tumor comes in contact with an artery, the latter is
usually compressed and its walls undergo degeneration. The specific
arteritis may pass beyond the limit of the syphilome and extend along
the arterial wall. Not rarely there is under these circumstances a
thrombus, and if the artery be a large one secondary softening of its
distributive brain-area occurs.

TREATMENT.—The treatment of cerebral syphilis is best studied under
two heads: First, the treatment of the accidents which occur in the
course of the disease; second, the general treatment of the disease
itself.

It must be remembered that in the great majority of cases in which
death occurs in properly-treated cerebral syphilis the fatal result is
produced by an exacerbation—or, as I have termed it, an accident—of
the disease. Under these circumstances the treatment should be that
which is adapted to the relief of the same acute affection when
dependent upon other than specific cause. In a large proportion of
cases the acute outbreak takes the form either of a meningitis or else
of a brain congestion. In either instance when the symptoms are severe
free bleeding should be at once resorted to. The amount of blood taken
is of course to be proportionate to the severity of the symptoms and
the strength of the patient. I have seen life saved by the abstraction
of about a quart of blood, whilst in other cases a few ounces suffice.
Care must be, of course, taken not to mistake a simple epileptic fit
for a severe cerebral attack; but when this fit has been preceded by
severe headache and is accompanied by stupor, with marked disturbance
of the respiration, measures for immediate relief are usually
required; and if the convulsions be perpetually repeated or if there
be violent delirious excitement, the symptoms may be considered as
very urgent. In taking blood the orifice should be large, so as to
favor a rapid flow, and the bleeding be continued until a distinct
impression is made upon the pulse. In some cases which I have seen in
which the action of the heart continued to be violent after as much
blood as was deemed prudent had been taken, good results were obtained
by the hypodermic injection of three drops of the tincture of
aconite-root every half hour until the reduction of the pulse and the
free sweating indicated that the system was coming under the influence
of the cardiac sedative.

Of course, I do not mean to encourage the improper or too free use of
the lancet in these cases, but in the few fatal cases which I have
seen I have almost invariably regretted that blood had not been taken
at once very freely at the beginning of the acute attack. In most of
these cases the symptoms had progressed too far for good to be
achieved before I reached the patient. After venesection, or in feeble
cases as a substitute for it, the usual measures of relief in cerebral
congestion should be instituted. I shall not occupy space with a
discussion of these {1016} measures, as they are in no way different
from those to be employed in cases not syphilitic.

The most important part of the treatment of cerebral syphilis itself
is antisyphilitic, and the practitioner is at once forced to select
between the iodide of potassium and the mercurial preparations. In
such choice it must be remembered that even a very small amount of
syphilitic deposit in the brain may at any time cause a sudden
congestion or other acute attack, and is therefore a very dangerous
lesion. I have seen a cerebral syphilis which was manifested only by
an epileptic attack occurring once in many months, and in which after
death the affected membrane was found to be not larger than a quarter
of a dollar, and the deposit not more than an eighth of an inch in
thickness, suddenly produce a rapidly fatal congestion; and I have
known a case fast progressing toward recovery suddenly ended by the
too long continuance of the arrest of respiration during an epileptic
fit. I have, myself, no doubt of the superiority of the mercurials
over the iodide of potassium as a means of producing absorption of
gummatous exudates; and as these exudates in the brain are so very
dangerous, a mercurial course should in the majority of cases of
cerebral syphilis be instituted so soon as the patient comes under the
practitioner's care. When, however, there is a history of a recent
prolonged free use of the mercurial, or when there is marked specific
cachexia, the iodide should be chosen. Cachexia is, however, a
distinctly rare condition in cerebral syphilis, the disease usually
developing in those who have long had apparent immunity from the
constitutional disorder. In my opinion the best preparation of the
mercurial for internal use is calomel. It should be given in small
doses, one-quarter of one grain every two hours, guarded with opium
and astringents, so as to prevent as far as possible disturbance of
the bowels, and should be continued until soreness of the teeth,
sponginess of the gums, or other evidences of commencing ptyalism are
induced. After this the dose of the mercurial should be so reduced as
simply to maintain the slight impression which has been created, and
the patient should be kept under the mercurial influence for some
weeks.

A very effective method of using the mercury is by inunction, and
where the surroundings of the patient are suitable the mercurial
ointment may be substituted for the calomel. It should be applied
regularly, according to the method laid down in my treatise on
therapeutics. I have sometimes gained advantage by practising the
mercurial unction and at the same time giving large doses of iodide of
potassium internally.

After a mercurial course the iodide of potassium should always be
exhibited freely, the object being not only to overcome the natural
disease, but also to bring about the complete elimination of the
mercury from the system. There is no use in giving the iodide in small
doses; at least a drachm and a half should be administered in the
twenty-four hours, and my own custom has been to increase this to
three drachms unless evidences of iodism are produced. The compound
syrup of sarsaparilla covers the disagreeable taste of the iodide of
potassium better than any other substance of which I have knowledge.
Moreover, I am well convinced that there is some truth in the old
belief that the so-called “Woods” are of value in the treatment of
chronic syphilis. {1017} I have seen cases in which both the iodide of
potassium and the mercurials had failed to bring about the desired
relief, but in which the same alteratives, when given along with the
“Woods,” rapidly produced favorable results. The old-fashioned
Zittmann's decoction, made according to the formula of the United
States Dispensatory, may be occasionally used with very excellent
effect. But I have gradually come into the habit of substituting a
mixture of the compound fluid extract and the compound syrup of
sarsaparilla in equal proportions. The syrup itself is too feeble to
have any influence upon the system, but is here employed on account of
its flavor. A favorite method of administration is to furnish the
patient with two bottles—one containing a watery solution of the
iodide of potassium of such strength that two drops represent one
grain of the drug, and the other the sarsaparilla mixture above
mentioned. From one to two drachms of the solution of the iodide may
be administered in a tablespoonful of the sarsaparilla well diluted
after meals. When the patient has been previously mercurialized, or
there is any doubt as to the propriety of using mercurials, corrosive
sublimate in small doses may be added to the solution of the iodide,
so that one-tenth to one-fifteenth of a grain shall be given in each
dose. I have never seen especial advantage obtained by the use of the
iodides of mercury. They are no doubt effective, but are not superior
to the simpler forms of the drug.


Syphilitic Disease of the Brain-Cortex.

The psychical symptoms which are produced by syphilis are often very
pronounced in cases in which the paralysis, headache, epilepsy, and
other palpable manifestations show the presence of gross brain
lesions. In the study of syphilitic disease of the brain-membranes
sufficient has been said in regard to these psychical disturbances,
but the problem which now offers itself for solution is as to the
existence or non-existence of syphilitic insanity—_i.e._ of an
insanity produced by specific contagion without the obvious presence
of gummatous disease of the brain-membranes. Very few alienists
recognize the existence of a distinct affection entitled to be called
syphilitic insanity, and there are some who deny that insanity is ever
directly caused by syphilis. It is certain that insanity often occurs
in the syphilitic, but syphilis is abundantly joined with alcoholism,
poverty, mental distress, physical ruin, and various depressing
emotions and conditions which are well known to be active exciting
causes of mental disorder. It may well be that syphilis is in such way
an indirect cause of an insanity which under the circumstances could
not be properly styled syphilitic.

If there be disease of the brain-cortex produced directly by syphilis,
of course such disease must give rise to mental disorders; and if the
lesion be so situated as to affect the psychic and avoid the motor
regions of the brain, it will produce mental disorder without
paralysis—_i.e._ an insanity; again, if such brain disease be
widespread, involving the whole cortex, it will cause a progressive
mental disorder, accompanied by gradual loss of power in all parts of
the body, and ending in dementia with general paralysis; or, in other
words, it will produce an affection {1018} more or less closely
resembling the so-called general paralysis of the insane, or dementia
paralytica.

As a man having syphilis may have a disease which is not directly due
to the syphilis, when a syphilitic person has any disorder there is
only one positive way of determining during life how far said disorder
is specific—namely, by studying its amenability to antisyphilitic
treatment. In approaching the question whether a lesion found after
death is specific or not, of course such a therapeutic test as that
just given is inapplicable. We can only study as to the coexistence of
the lesion in consideration with other lesions known to be specific.
Such coexistence of course does not absolutely prove the specific
nature of a nutritive change, but renders such nature exceedingly
probable.

What has just been said foreshadows the method in which the subject in
hand is to be here examined, and the present article naturally divides
itself into two sections—the first considering the coexistence of
anatomical alterations occurring in the cerebral substance with
syphilitic affections of the brain-membranes or blood-vessels, the
second being a clinical study of syphilitic insanity.

In looking over the literature of the subject I have found the
following cases in which a cerebral sclerotic affection coincided with
a gummatous disease of the membrane. Gros and Lancereaux[60] report a
case having a clear syphilitic history in which the dura mater was
adherent to the skull. The pia mater was not adherent. Beneath, upon
the vault of the brain, was a gelatinous exudation. The upper cerebral
substance was indurated, and pronounced by Robin after microscopic
examination to be sclerosed. At the base of the brain there were
atheromatous arteries and spots of marked softening.

[Footnote 60: _Affec. Nerv. Syphilis_, 1861, p. 245.]

Jos. J. Brown[61] reports a case in which the symptoms were
melancholia, excessive irritability, violent outbursts of temper, very
positive delusions, disordered gait, ending in dementia. At the
autopsy, which was very exhaustive, extensive syphilitic disease of
the vessels of the brain and spinal cord was found. The pia mater was
not adherent to the brain. The convolutions, particularly of the
frontal and parietal lobes, were atrophied, with very wide sulci
filled with bloody serum. The neuroglia of these convolutions was much
increased, and “appeared to be more molecular than normal, the cells
were degenerated, and in many places had disappeared, their places
being only occupied by some granules.” These changes were most marked
in the frontal convolutions.

[Footnote 61: _Journ. Ment. Sci._, July, 1875, p. 271.]

H. Schule reports[62] a very carefully and meritoriously studied case.
The symptoms during life exactly simulated those of dementia
paralytica. The affection commenced with an entire change in the
disposition of the patient; from being taciturn, quiet, and very
parsimonious, he became very excited, restless, and desiring
continuously to buy in the shops. Then failure of memory, marked sense
of well-being, carelessness and indifference for the future, developed
consentaneously with failure of the power of walking, trembling of the
hands, inequality of the pupils, and hesitating speech. There was next
a period of melancholy, which was in time followed by continuous
failure of mental and motor powers, and {1019} very pronounced
delirium of grandeur, ending in complete dementia. Death finally
occurred from universal palsy, with progressive increase of the motor
symptoms. At the autopsy characteristic syphilitic lesions were found
in the skull, dura mater, larynx, liver, intestines, and testicles.
The brain presented the macroscopic and microscopic characters of
sclerosis and atrophy; the neuroglia was much increased, full of
numerous nuclei, the ganglion-cells destroyed. The vessels were very
much diseased, some reduced to cords; their walls were greatly
thickened, and full of long spindle-shaped cells, sometimes also
containing fatty granules.

[Footnote 62: _Allgem. Zeitschrift f. Psychiatrie_, xxviii. 171, 172.]

C. E. Stedman and Robt. T. Edes report[63] a case in which the
symptoms were failure of health, ptosis, trigeminal palsy with pain
(anæsthesia dolorosa), finally mental failure with gradual loss of
power of motion and sensation. At the autopsy the following conditions
were noted: apex of the temporal lobe adherent to dura mater and
softened; exuded lymph in neighborhood of optic chiasm; sclerosis of
right Gasserian ganglion, as shown in a marked increase of the
neuroglia; degeneration of the basal arteries of the brain.

[Footnote 63: _American Journ. Med. Sciences_, lxix. 433.]

These cases are sufficient to demonstrate that sclerosis of the
brain-substance not only may coexist with a brain lesion which is
certainly specific in its character, but may also present the
appearance of having developed pari passu with that lesion and from
the same cause.

It has already been stated in this article that cerebral meningeal
syphilis may coexist with various forms of insanity, and cases have
been cited in proof thereof. It is of course very probable that in
some of such cases there has been that double lesion of membrane and
gray brain matter which has just been demonstrated by report of
autopsies; but if we find that there is a syphilitic insanity, which
exists without evidences of meningeal syphilis, and is capable of
being cured by antispecific treatment, such insanity must be
considered as representing the disease of the gray matter of the
brain. Medical literature is so gigantic that it is impossible to
exhaust it, but the following list of cases is amply sufficient to
prove the point at issue—namely, that there is a syphilitic insanity
which exists without obvious meningeal disease, and is capable of
being cured by antisyphilitic treatment:

  ----+-----------------------+--------------------+------------------
  No. | Reporter and Journal. |     Symptoms.      |Results.—Remarks.
  ----+-----------------------+--------------------+------------------
   1  | Luis Streisand        | Epilepsy, delirium | Rapid cure with
      | _Die Lues als Ursache | of exaltation,     | mercury.
      | der Dementia_, Inaug. | alteration of      |
      | Diss., Berlin, 1878.  | speech, headache,  |
      |                       | failure of memory. |
  ----+-----------------------+--------------------+------------------
   2  | _Ibid._               | Delusions,         | Cure with
      |                       | delirium, general  | mercury.
      |                       | mania, great       |
      |                       | muscular weakness. |
  ----+-----------------------+--------------------+------------------
   3  | Müller of Leutkirch   | Symptoms resembling| Cure by iodide of
      | _Journ. of Mental     | general paralysis, | potassium.
      | Dis._, 1873-74, 561.  | and diagnosis of   |
      |                       | such made until a  |
      |                       | sternal node was   |
      |                       | discovered.        |
  ----+-----------------------+--------------------+------------------
   4  | Esmarch and W. Jersen | Sleeplessness,     | Cure by mercury.
      | _Allgem. Zeitschrift  | great excitement,  |
      | f. Psychiatrie_.      | restlessness,      |
      |                       | great activity,    |
      |                       | incoherence, and   |
      |                       | violence.          |
  ----+-----------------------+--------------------+------------------
   5  | Leidesdorf            | Complete mania;    | Complete cure by
      | _Medizin.             | played with his    | iodide of
      | Jahrbucher_, xx.,     | excrement, and     | potassium.
      | 1864, 1.              | entirely           |
      |                       | irrational.        |
  ----+-----------------------+--------------------+------------------
   6  | Beauregard            | Symptoms resembling| Cure by iodide of
      | _Gaz. hébdom. de Sci. | those of general   | potassium.
      | méd. de Bordeaux_,    | paralysis.         |
      | 1880, p. 64.          |                    |
  ----+-----------------------+--------------------+------------------
   7  | M. Rendu              | Loss of memory,    | Mercurial
      | _Ibid._               | headache,          | treatment, cure.
      |                       | irregularity of    |
      |                       | pupils, ambitious  |
      |                       | delirium, periods  |
      |                       | of excitement,     |
      |                       | others of          |
      |                       | depression,        |
      |                       | embarrassment of   |
      |                       | speech, access of  |
      |                       | furious delirium,  |
      |                       | ending in stupor.  | {1020}
  ----+-----------------------+--------------------+------------------
   8  | M. Rendu              | Hypochondria,      | Mercurial
      | _Gaz. hébdom. de Sci. | irregularity of    | treatment, cure.
      | méd. de Bordeaux_,    | pupils, headache,  |
      | 1880, p. 64.          | failure of memory, |
      |                       | melancholy, stupor.|
  ----+-----------------------+--------------------+------------------
   9  | Albrecht Erlenmeyer   | Melancholia with   | Iodide of
      | _Die Luëtischen       | hypochondriasis,   | potassium, cure.
      | Psychosen_, Neuwied,  | sleeplessness,     |
      | 1877.                 | fear of men, and   |
      |                       | belief they were   |
      |                       | all leagued        |
      |                       | against him.       |
  ----+-----------------------+--------------------+------------------
   10 | _Ibid._               | Religious          | Iodide of
      |                       | melancholia, with  | potassium, cure.
      |                       | two attempts at    |
      |                       | suicide, ending in |
      |                       | mania.             |
  ----+-----------------------+--------------------+------------------
   11 | _Ibid._               | At times very      | Iodide of
      |                       | violent, yelling,  | potassium, cure.
      |                       | shrieking,         |
      |                       | destroying         |
      |                       | everything she     |
      |                       | could get hands    |
      |                       | on, at times       |
      |                       | erotomania; no     |
      |                       | distinct history   |
      |                       | of infection, but  |
      |                       | her habits known   |
      |                       | to be bad, and had |
      |                       | bone ozæna and     |
      |                       | other physical     |
      |                       | syphilitic signs.  |
  ----+-----------------------+--------------------+------------------
   12 | _Ibid._               | Epileptic attack   | Cured by
      |                       | followed by a long | mercurial
      |                       | soporose condition,| inunction.
      |                       | ending in mental   |
      |                       | confusion, he not  |
      |                       | knowing his nearest|
      |                       | friends, etc.;     |
      |                       | almost dementia.   |
  ----+-----------------------+--------------------+------------------
   13 | _Ibid._               | Great fear of      | Cured by
      |                       | gensd'armes, etc., | mercurial
      |                       | mania, with        | inunctions with
      |                       | hallucinations,    | iodide
      |                       | loud crying,       | internally;
      |                       | yelling, etc.,     | subsequently
      |                       | then convulsion,   | return of
      |                       | followed by great  | convulsions,
      |                       | difficulty of      | followed by
      |                       | speech.            | hemiplegia and
      |                       |                    | death.
  ----+-----------------------+--------------------+------------------
   14 | _Ibid._               | Great unnatural    | Iodide of
      |                       | vivacity and       | potassium, cure.
      |                       | loquacity, wanted  | Attended to
      |                       | to buy everything, | business, and
      |                       | bragged of enormous| seems as well as
      |                       | gains at play,     | before. Relapsed.
      |                       | etc.; some trouble | (See Symptoms.)
      |                       | of speech.         |
      |                       |                    |
      | _Ibid._               | Fifteen months     | Failure of
      | Relapse of Case 14.   | after discharge    | various
      |                       | from asylum        | anti-specific
      |                       | relapse; symptoms  | treatment.
      |                       | developing very    |
      |                       | rapidly, delirium  |
      |                       | of grandeur of the |
      |                       | most aggravated    |
      |                       | type, with marked  |
      |                       | progressive        |
      |                       | dementia, failure  |
      |                       | of power of speech,|
      |                       | and finally of     |
      |                       | locomotion.        |
  ----+-----------------------+--------------------+------------------
   15 | A. Erlenmeyer         | Failure of mental  | Iodide of
      | _Die Luëtischen_,     | powers, inequality | potassium in
      | etc.                  | of pupils,         | ascending doses
      |                       | trembling of lip   | failed. Recovery
      |                       | when speaking,     | under mercurial
      |                       | uncertainty of     | inunctions.
      |                       | gait, almost       |
      |                       | entire loss of     |
      |                       | memory, once       |
      |                       | temporary ptosis   |
      |                       | and strabismus.    |
  ----+-----------------------+--------------------+------------------
   16 | _Ibid._               | Failure of mental  | Iodide of
      |                       | powers, pronounced | potassium,
      |                       | delirium of        | corrosive-
      |                       | grandeur,          | sublimate
      |                       | hallucinations of  | injections. Cure.
      |                       | hearing, failure of|
      |                       | memory, strabismus |
      |                       | and ptosis coming  |
      |                       | on late.           |
  ----+-----------------------+--------------------+------------------
   17 | _Ibid._               | Failure of memory  | Cure with use of
      |                       | and mental powers, | iodide and
      |                       | slight ideas of    | mercurial
      |                       | grandeur,          | inunctions.
      |                       | disturbance of     |
      |                       | sensibility and    |
      |                       | motility, aphasia  |
      |                       | coming on late.    |
  ----+-----------------------+--------------------+------------------
   18 | _Ibid._               | Melancholy, great  | Iodide of
      |                       | excitability,      | potassium failed;
      |                       | ideas of grandeur; | mercurial course
      |                       | after a long time  | improved; joint
      |                       | sudden ptosis and  | use cured
      |                       | strabismus.        | patient.
  ----+-----------------------+--------------------+------------------
   19 | _Ibid._               | Various cerebral   |
      |                       | nerve palsies,     |
      |                       | great relief by    |
      |                       | use of mercurial   |
      |                       | inunctions, then   |
      |                       | development of     |
      |                       | great excitement,  |
      |                       | delirium of        |
      |                       | grandeur, failure  |
      |                       | of memory and      |
      |                       | mental powers, and |
      |                       | finally death from |
      |                       | apoplexy; no       |
      |                       | autopsy.           |
  ----+-----------------------+--------------------+------------------
   20 | J. B. Chapin          | Melancholia with   | Iodide of
      | _Amer. Journ.         | attempted suicide, | potassium, cure.
      | Insanity_, vol. xv.   | epilepsy, headache,|
      | p. 249.               | somnolent spells.  |
  ----+-----------------------+--------------------+------------------
   21 | _Ibid._               | Acute mania, noisy,| Iodide of
      |                       | very destructive;  | potassium, cure.
      |                       | syphilitic disease |
      |                       | of tibia.          |
  ----+-----------------------+--------------------+------------------
   22 | Snel                  | Maniacal           | Cured by specific
      |                       | excitement.        | treatment.
  ----+-----------------------+--------------------+------------------
   23 | Wm. Smith             | Apathetic          | Rapidly cured by
      | _Brit. Med. Journ._,  | melancholy,        | conjoint use of
      | July, 1868, p. 30.    | indelicate,        | iodide and
      |                       | speaking only in   | mercurials. The
      |                       | monosyllables, and | symptoms first
      |                       | much of the time   | developed 3
      |                       | not at all, sullen | months after
      |                       | and menacing.      | chancre.
  ----+-----------------------+--------------------+------------------

A study of the brief analyses of the symptoms just given shows that
syphilitic disease of the brain may cause any form of mania, but that
the symptoms, however various they may be at first, end almost always
in dementia unless relieved.

Of all the forms of insanity, general paralysis is most closely and
frequently simulated by specific brain disease. The exact relation of
the diathesis to true, incurable, general paralysis it is very
difficult to {1021} determine. It seems well established that amongst
persons suffering from this disorder the proportion of syphilitics is
not only much larger than normal, but also much larger than in other
forms of insanity. Thus, E. Mendel[64] found that in 146 cases of
general paralysis, 109, or 75 per cent., had a distinct history of
syphilis, whilst in 101 cases of various other forms of primary
insanity only 18 per cent. had specific antecedents. H. Obersteiner
has 1000 cases of mental disease,[65] 175 cases of dementia
paralytica; of these, 21.6 per cent. had syphilis; moreover, of all
the syphilitic patients 51.4 per cent. had dementia paralytica.

[Footnote 64: _Progres. Paral. der Irren_, Berlin, 1880.]

[Footnote 65: _Monatshefte f. prakt. Dermat._, Dec., 1882.]

Various opinions might be cited as to the nature of this relation
between the two disorders, but for want of space the curious reader is
referred to the work just quoted and to the thesis of C. Chauvet[66]
for an epitome of the most important recorded opinions.

[Footnote 66: _Influence de la Syph. sur les Malad. du Syst. nerveux_,
Paris, 1880.]

Those who suffer from syphilis are exposed in much greater proportion
than are other persons to the ill effects of intemperance, sexual
excesses, poverty, mental agony, and other well-established causes of
general paralysis. It may be that in this is sufficient explanation of
the frequency of general paralysis in syphilitics, but I incline to
the belief that syphilis has some direct effect in producing the
disease. However this may be, I think we must recognize as established
the opinion of Voisin,[67] that there is a syphilitic periencephalitis
which presents symptoms closely resembling those of general paralysis.
Such cases are examples of the pseudo-paralysie générale of
Fournier.[68]

[Footnote 67: _Paralysie générale des Alienés_, 1879.]

[Footnote 68: _La Syphilis du Cerveau_, Paris, 1879.]

The question as to the diagnosis of these cases from the true
incurable paresis is of course very important, and has been considered
at great length by Voisin,[69] Fournier,[70] and Mickle.[71]

[Footnote 69: _Loc. cit._]

[Footnote 70: _Loc. cit._]

[Footnote 71: _Brit. and For. Med.-Chir. Review_, 1877.]

The points which have been relied upon as diagnostic of syphilitic
pseudo-general paralysis are—

The occurrence of headache, worse at night and present amongst the
prodromes; an early persistent insomnia or somnolence; early
epileptiform attacks; the exaltation being less marked, less
persistent, and perhaps less associated with general maniacal
restlessness and excitement; the articulation being paralytic rather
than paretic; the absence of tremulousness, especially of the upper
lip (Fournier); the effect of antispecific remedies.

When the conditions in any case correspond with the characters just
paragraphed, or when any of the distinguishing characteristics of
brain syphilis, as previously given, are present, the probability is
that the disorder is specific and remediable. But the absence of these
marks of specific disease is not proof that the patient is not
suffering from syphilis. Headache may be absent in cerebral syphilis,
as also may insomnia and somnolence. Epileptiform attacks are not
always present in the pseudo-paralysis, and may be present in the
genuine affection; a review of the cases previously tabulated shows
that in several of them the megalomania was most pronounced; and a
case with very pronounced delirium of grandeur, in which the autopsy
revealed unquestionably specific brain lesions, may be found in
Chauvet's _Thesis_, p. 31.

{1022} I have myself seen symptoms of general paralysis occurring in
persons with a specific history in which of these so-called diagnostic
differences the therapeutic test was the only one that revealed the
true nature of the disorder. In these cases a primary, immediate
diagnosis was simply impossible.

Case 14 of the table is exceedingly interesting, because it seems to
represent as successively occurring in one individual both pseudo and
true general paralysis. The symptoms of general paralysis in a
syphilitic subject disappeared under the use of mercury, to return
some months afterward with increased violence and with a new obstinacy
that resisted with complete success antisyphilitic treatment. Such a
case is some evidence that syphilis has the power to produce true
general paralysis.

In conclusion, I may state that it must be considered as at present
proven that syphilis may produce a disorder whose symptoms and lesions
do not differ from those of general paralysis; that true general
paralysis is very frequent in the syphilitic; that the only constant
difference between the two diseases is as to curability; that the
curable sclerosis may change into or be followed by the incurable form
of the disease. Whether under these circumstances it is philosophic to
consider the so-called pseudo-general paralysis and general paralysis
as essentially distinct affections, each physician can well judge for
himself.


Spinal Syphilis.

The subject of spinal syphilis is at present a difficult and
unsatisfactory one. The recorded cases with well-observed autopsies
are comparatively few, and when recovery occurs much uncertainty must
rest upon the nature of the lesion. More than this, there is scarcely
any chronic degeneration of the spinal cord which has not been
attributed to syphilis, and my own experience as well as the records
of medical literature lead to the very positive conclusion that all
the various spinal scleroses are much more frequent in infected than
in non-infected persons. Whether this is due to a direct or indirect
influence of the disease is uncertain, but I shall not here discuss
the relation of these chronic inflammations of the cord to syphilis.

It seems necessary to briefly consider at this place acute and
subacute myelitis in their relations to syphilis. That these
affections are not rare in syphilitics is certain. In the _Revue de
Médecine_ (Jan., 1884) Dejerine records the case of a person suffering
from chronic syphilis in whom there were fulgurant pains with
increasing weakness of the legs, and subsequently, after very severe
exposure to the weather, a sudden development of complete paraplegia
followed by trophic troubles, and death in twenty-eight days. At the
autopsy there was found a central myelitis with pronounced lesion of
the ganglionic cells, inflammatory changes of the pia mater,
capillaries, and neuroglia, extreme alteration of the nerve-roots, and
secondary degeneration of the columns of Goll and the lateral columns.
In a second case recorded by Dejerine there appears to have been no
exposure or apparent immediate exciting cause. The symptoms and
lesions were similar to those just spoken of, but death occurred in
eight days.

Whether such attacks as these occurring in syphilitic subjects are
produced directly by the syphilis or not is at present doubtful. The
same is {1023} true of subacute myelitis, of which I have reported two
rather peculiar fatal cases in syphilitic subjects. The general
symptoms of this affection are progressive loss of power with grossly
exaggerated reflexes, severe twitchings and jerkings of the legs,
rigidity, usually more or less marked pain, and other sensory
disturbances in the legs, and finally partial anæsthesia and complete
paraplegia, paralysis of bladder, bed-sores, and death from
exhaustion. At the autopsy the most important change in the cord has
been the presence of great numbers of round neuroglia-cells in both
gray and white matter. One of my cases died of a rapidly developed
central myelitis supervening upon the subacute disease, and affording
lesions similar to those described by Dejerine in addition to the
changes of the subacute affection.

In another class of spinal cases occurring in syphilitics the symptoms
resemble those of the so-called acute ascending paralysis (Landry's
paralysis). The fourth variety of syphilitic diseases of the spinal
cord of Huebner[72] includes these cases. According to Huebner, they
are without anatomical lesions, but in the majority of the recorded
cases no proper microscopic study of the cord has been made. Huebner
states, however, that Kussmaul failed in one case after such study to
detect lesion. As some of these cases may really have been instances
of peripheral neuritis, it is essential that in the future the
peripheral nerves as well as the spinal cord be carefully studied. I
have seen one case which might be placed in this category. The first
symptom was some numbness in the legs, with a small deep sharp-cut
ulcer on the plantar surface of the great toe; directly after this
loss of motion and sensation in the legs and thighs, rapidly becoming
almost complete and spreading quickly to the trunk and arms, so that
in one week the patient was a flaccid, helpless mass, and the
breathing so interfered with that he was believed to be dying. After
almost losing the power of swallowing this patient began to get
better, and finally so regained power of his hands and feet that he
was able to partially dress himself and walk a distance of ten or
twelve feet, when he was suddenly seized with a pleural effusion and
died. During the first week of his disease his temperature was 100° F.
At the autopsy the spinal membranes were found to be normal. But in
the cord there were very distinct lesions found; the neuroglia seemed
everywhere more granular than normal; the ganglionic cells were not
distinctly diseased; the white matter in various places was much
changed, the tissue appearing abnormally dense and opaque where most
affected; the nerve-tubules appeared to gradually lose their myeline,
and in places were reduced to simple axis-cylinders. Finally, the
axis-cylinders became smaller and smaller until in the most altered
portions of the cord they disappeared. As the autopsy was obtained
with great difficulty, it was not possible to get the peripheral
nerves for study.

[Footnote 72: _Ziemssen's Encyclopædia_, vol. xii.]

In regard to these very acute cases, it seems to me uncertain whether
the disease should be attributed to the syphilis. In my own case
twenty years had elapsed since the chancre, alcohol was habitually
used in great excess, and the attack was apparently precipitated by
great exposure. On the other hand, the man bore well enormous doses of
iodide of potassium, and lowly progressed under them.

Finally, there is a class of disease of the spinal cord in which the
{1024} lesion is undoubtedly the direct outcome of a syphilitic
diathesis. In these cases the exudation commences primarily in the
membranes of the cord, and may extend into the cord itself. In this
class I would include the first two varieties of syphilitic spinal
disease of Huebner. The number of recorded autopsies is not great; the
only cases with which I am acquainted are those referred to in the
note at the bottom of this page.[73]

[Footnote 73: Winge (_Dublin Med. Press_, 2d Series, vol. ix., 1863);
Moxon (_Dublin Quarterly Journ._, li., 1870); Charcot and Gombault
(_Archiv. d. Physiologie_, tome v., 143, 1873); Schultze (_Archiv.
Psychiat._, xii. 567); Thos. Buzzard (_Diseases of Nervous System_,
1882, p. 407); Julliard (_Étude Crit. sur les Localis. Spinal de la
Syphilis_, 1879); Westphal (_Arch. Psychi._, vol. xi.); Greif (_Arch.
Psychiat._, xii. 579); Homolle (_Progrès méd._, 1876).]

The lesions in these cases are entirely similar to those of brain
syphilis. The disease very rarely or never begins in the interior of
the cord. I know of no recorded case: Wagner's case, in which a yellow
nodule was found within the cervical marrow, was probably not one of
syphilis. If a gummatous inflammation does occur inside of the cord,
it probably starts from the ependyma. The gummatous exudate may occur
in the form of small multiple formations or of an extensive
meningitis, with an infiltration of the membranes and their spaces
with gummatous material. The membranes are usually agglutinated with
one another and with the surface and with the cord. The exudation is
usually made up of roundish cells, and in several cases spindle-shaped
cells have been noticed, as have also the peculiar Deitres corpuscles
already described as they occur in brain syphilis. The changes in the
cord itself vary somewhat. In Winge's case the white matter seems to
have undergone a rapid myelitis from pressure. It was of a grayish
color, with numerous fine granular masses, corpora amylacea,
pigment-masses, and fatty globules, the nerve-fibres being broken up.
In other cases the change has been a sclerosis. The vessels of the
cord have been noticed by various observers in the different stages of
the degeneration seen in syphilis of the brain. They are often greatly
dilated, their walls thickened, and, together with the lymph-spaces,
infiltrated with small cells. Minute hemorrhages have been found.

The so-called syphilitic callus, as described by Heubner, is probably
the remnant of a true gummatous inflammation. It consists of a
circumscribed induration one to several lines in thickness,
originating apparently from the dura mater, and causing sometimes
adherence with the vertebræ, in others with the membranes of the
spinal cord. In a case described by Virchow of this character the
lesion was cervical, and the symptoms were stiffness in the nape of
the neck, pains in the neck and arms, and finally paralysis in both
arms. A second case is elaborately described by Heubner in his article
in _Ziemssen's Encyclopædia_.

SYMPTOMS.—As the lesion of gummatous spinal syphilis affects primarily
membranes of the cord, in the beginning of the attack the symptoms
chiefly arise from the implication of the nerve-roots. Of course these
symptoms vary with the seat of the lesion, for it must be remembered
that the meningeal irritation is at first usually localized in a small
region. As in a majority of cases this lesion affects a posterior
portion of the cord, and as the posterior nerve-roots seem especially
sensitive to irritations of this character, pain is usually a very
marked and {1025} precocious symptom of spinal syphilis. The seat of
the pain varies with the seat of the lesion. At first the pain is
slight, but in most cases it soon becomes severe. It is sometimes
situated at a fixed spot on the spinal column, where, according to
Heubner, it may be increased on pressure. I have seen two or three
such cases, but have and still do believe that under these
circumstances the patient was suffering not simply from a spinal
syphilis, but also from an implication of the vertebral periosteum or
of the vertebræ themselves. In one of my cases this diagnosis was
confirmed at the autopsy. When the lesion is purely meningeal there is
probably no marked local tenderness. The severe pains usually felt in
the extremities or in the trunk are often fulgurant; sometimes they
are described as resembling the thrust of a knife, and not rarely they
closely resemble the pains of locomotor ataxia. In some instances the
pains are comparatively slight and are aching in character.
Paræsthesiæ are not rare phenomena: such are formications, tingling in
the extremities, numbness and feeling as though the limb were asleep,
intense sense of coldness on the surface, sensation of water running
over the limb. Early in the disorder there is sometimes very marked
hyperæsthesia, but later, even though the pain persists, blunting of
sensibility is marked, and there may be a complete anæsthesia. This
anæsthesia is sometimes localized in certain parts of the limb. Thus,
in a case reported by Alfred Mathieu,[74] although there was complete
anæsthesia of the outer side of the left leg and foot, the inner side
retained its normal sensibility. In some cases there is the abdominal
cincture of ordinary myelitis. The records show that even in these
early stages there may be diplopia, amblyopia, or other disorder of
vision, and the pupil may be distinctly affected. In these cases it is
probably the upper portion of the cord which is affected.

[Footnote 74: _Ann. de Dermatol. et Syph._, vol. iii., 1882.]

Disturbances of motility in the majority of cases do not develop until
some time after sensation has been affected, but may come on very
early. Usually, the first symptoms are those of irritation, such as
rigidity of the neck, back, and limbs or even of isolated groups of
muscles. Tremors have been described as frequently present. These may
be convulsive, and are often plainly reflex in their origin; indeed, I
am inclined to believe that they are always reflex tremblings, and
never true tremors. Heubner describes a case in which a paralyzed limb
was thrown into violent tremblings whenever passive motion was
attempted. The patella-reflex is usually grossly exaggerated, although
it may be lost in the later stages of the disorder. Not rarely there
is the condition which has received the misnomer of spinal epilepsy.
This exaggeration of the reflexes may be limited to one leg, when it
is almost pathognomonic. In some cases severe cramps are excited by
movement. Usually there is no tenderness. These symptoms of the
meningitic stage may continue for weeks or months without there being
pronounced paralysis, although locomotion is not rarely interfered
with by the stiffness of the legs. Finally, if the case progresses the
patient notices a weakness in one or both legs, or (if the disease be
situated high up in the spinal cord) in one arm, which rapidly
increases until there is almost complete loss of power. This rapid
increase of palsy following long-continued disturbance of sensation is
almost pathognomonic. In most cases one side of the body is more
{1026} affected than the other. The sphincters are prone to be
implicated, and in advanced stages of the disease there is usually
complete loss of control over the bladder and rectum. The patient may
live for months without very distinct change of this condition, or
bed-sores and other trophic disturbances may rapidly develop and death
ensue in a short time. I have seen under these circumstances marked
elevation of temperature, rapid feeble pulse, mental weakness, and the
general symptoms of septicæmia last for many weeks. Ammoniacal
cystitis is of course prone to be developed during this stage. When
motility fails, sensibility is usually blunted, although the pains may
even increase. Heubner affirms that an incompleteness of the
anæsthesia is characteristic of the disorder.

The typical course of spinal syphilis, such as has been described, may
be variously departed from. Sometimes the power of co-ordination is
early affected, and the symptoms may resemble those of locomotor
ataxia. I doubt, however, whether under any circumstances there is a
loss of the patella-reflex in the early stages of the gummatous
disease of the spinal cord. In other cases the paralytic symptoms may
be very prominent from the beginning: thus, in the case of R. P——,
aged 27, which I believed to be gummatous disease of the spinal cord,
the first disorder was a feeling of malaise lasting for about a week,
followed by the sudden, rapidly-developed paralysis of the bladder,
loss of power in the legs, and to a less extent in the arms, the only
pain being a dull, steady ache in the arms. The bowels were
obstinately costive. Double vision was soon very pronounced. When I
first saw the patient, about three weeks after this, there was decided
impairment of sensibility in the legs, but not in the arms; marked
muscular weakness of both legs and arms; no loss of co-ordinating
power; dropping of the right eyelid, with double vision; and only some
slight aching pains in the arms. By the use of large doses of iodide
of potassium and other appropriate measures a good recovery was
secured.

A case illustrating the occasional difficulty of diagnosing spinal
syphilis is reported by C. Eisenlohr.[75] The first symptom was
obstinate constipation, with very great discomfort after defecation;
then appeared incontinence of urine with weakness of the legs:
finally, a sudden complete palsy of the right leg occurred, with
marked anæsthesia in both legs, partial loss of power in left leg,
violent boring abdominal pains, and distress in the bladder. In the
last stages there were severe neuralgic pains in both legs, with
complete loss of sensation, bed-sores, atrophy of the leg-muscles,
with reactions of degeneration, and death from exhaustion. At the
autopsy an advanced meningitis was found which had apparently
commenced in the regions of the cauda equina, and given rise to
complete degeneration of the nerves. The only alteration of the cord
was an ascending degeneration of the posterior columns.

[Footnote 75: _Neurolog. Centralb._, 1884, p. 73.]

Again, owing to the diseased condition of the vessels, a spinal
syphilis may be suddenly interrupted by an apoplectic accident.

In a patient of my own, who was believed to be suffering from
gummatous spinal meningitis, there was an abrupt development of
violent tearing pains, loss of power and sensibility, and all the
other symptoms which are characteristic of meningeal spinal
hemorrhage. A. Weber {1027} reports a case in which, after doubtful
premonitory symptoms, such as vertigo, loss of power on the right
side, pressure on the top of the head, and tinnitus aurium, there was
a sudden development of convulsions, and death. At the autopsy a
syphilome of the right vertebral artery was found with a recent
thrombosis of the basilar artery.[76]

[Footnote 76: _American Journ. of Neur. and Psychiat._, vol. ii.]


{1028}


TUMORS OF THE BRAIN AND ITS ENVELOPES.

BY CHARLES K. MILLS, A.M., M.D., AND JAMES HENDRIE LLOYD A.M., M.D.


DEFINITION.—Under the head of Tumors of the Brain and its Envelopes
will be considered all forms of growths occurring within the skull,
whether these involve the cranium itself, the membranes of the brain,
the brain-substance, or several of these parts conjointly. A large
majority of these growths spring from the brain-membranes.[1]

[Footnote 1: To this article will be appended a table of one hundred
cases of brain tumor. Our researches included the investigation of
many more cases, four to five hundred in all. Such a table, indeed,
could be indefinitely extended. Our object, however, has been not so
much to present a large number of cases, and these in great detail,
but rather in the most condensed manner to give a definite number,
carefully selected, from which to draw conclusions. The cases have not
been chosen with the view of upholding any peculiar or preconceived
views as to pathology, diagnosis, localization, etc., but because of
the carefulness with which they have been recorded. They have been
selected also, as will be seen, with the view of determining by
clinico-pathological data the possibility of localizing such growths
during life. Many of our general conclusions as to pathology,
symptomatology, and diagnosis have been drawn from this table.]

With the exception of such merely substitutional terms as cerebral or
intracranial growths, neoplasms, or adventitious products, we have no
general synonyms for brain tumors.

The literature of the subject of brain tumors is second only to that
of such subjects as syphilis and hysteria. Vol. ii. of the _Index
Catalogue of the Library of the Surgeon-General's Office, U. S. A._,
contains no less than 632 references to this subject: number of books,
43; articles, 589. The books and papers occur in different languages,
as follows: British, 142; French, 174; German, 133; American, 91;
Italian, 30; Latin, 15; Swedish, 14; miscellaneous, 33.

ETIOLOGY.—Under predisposing or constitutional causes are first to be
classed such special inheritances as tuberculosis or carcinoma and
tendencies to vascular degeneration. The occurrence of syphilis of
course predisposes its victims to cerebral or membranous growths, as
it does to other so-called tertiary forms of this disorder.

Hereditary predisposition only enters in so far as the individual
inherits a general tendency to the development of such affections as
cancer and tubercle. Hereditary tendency to a brain tumor per se does
not exist, but the individual who is of the tuberculous or cancerous
diathesis under special causes may develop an intracranial growth. As
to the comparative frequency with which diathetic tumors originate, a
reference to the tabular statement which will be given under {1029}
Pathology will be sufficient. Gliomata are very common, but with them
vie in frequency sarcomatous, tubercular, and gummatous growths. Any
table, unless it includes a very large number of cases—at least a
thousand or more—would be misleading as to the proportionate frequency
of these different forms of intracranial constitutional diseases; but
it is safe to say that syphilitic, tuberculous, and carcinomatous or
sarcomatous tumors are of comparatively frequent occurrence.

Tumors of the brain occur oftener among men than women. This fact is
dependent largely upon the difference between the habits and
occupations of the two sexes. Men, in the first place, are much more
addicted to alcoholic, venereal, and other abuses which give rise to
special degenerations or constitutional infection; and secondly, they
are more exposed to traumatisms. In 100 cases the tumors occurred
among males in 58 cases, among females in 40 cases, and sex was not
recorded in 2 cases.

Statistics show that intracranial growths are more likely to occur
between puberty and middle age. Although gliomata may be found at any
age, brain tumors in children are more likely to be of this character.
This is what might be expected from the nature of these growths.
Histologically, gliomata are most closely allied to the embryonal
stage of the connective tissue, and, according to Cohnheim, tumors
generally are the result of a surplusage of embryonal tissue—tissue
which has remained over after the requirements of normal development
have been met. Of 16 gliomata, 3 occurred in patients under ten years,
2 between the ages of ten and twenty, and 4 between twenty and thirty.

One hundred cases gave the following results as to age:

  Under 10 years  . . . .  10 cases.
  From 10 to 20 years . .  12   "
   "   20 to 30   "   . .  18   "
   "   30 to 40   "   . .  24   "
   "   40 to 50   "   . .  12   "
   "   50 to 60   "   . .  13   "
   "   60 to 70   "   . .   3   "
  Over 70 years . . . . .   1   "
  Not recorded  . . . . .   7   "
                          ----------
                          100 cases.

It is now generally admitted that injuries play a most important part
as exciting causes of brain tumors. Frequently in our experience an
apparently direct relation has existed between a head injury and the
origin of the neoplasm. In 6 out of 12 cases reported by one of us,[2]
a history of traumatism was present, although in 5 of these a history
of syphilis was also present. The great frequency with which injuries
of all kinds occur must of course not be overlooked in this
connection. It is said by those who oppose the idea of the direct
causal relations of injury that almost every one could trace such
disease to falls or blows which few escape. In some of the cases of
brain tumor, however, the history of injury bears a direct relation in
time to the initial symptoms of the tumor. Certain tumors, as the
fibromata, osteomata, angiomata, would appear to be of more frequent
occurrence as the direct result of traumatism. The part played by
injuries in the production of carcinomata and sarcomata, whether in
the brain or elsewhere, has not {1030} infrequently been the subject
of dispute. We have no doubt that, a constitutional predisposition
existing, an injury frequently leads directly to the development of
some form of malignant growth. In not a few of the syphilitic cases
the history would appear to show that an injury to the skull had
localized the constitutional poison.

[Footnote 2: _Archives of Medicine_, vol. viii. No. 1, August, 1882.]

Echinococci and cysticerci are found within the cranium, and sometimes
give rise to tumors, but the statement of Obernier can hardly be
regarded as true, that they play an important part in the production
of cerebral tumors. Our table shows only two cases of this kind.

SYMPTOMATOLOGY.—The symptoms of intracranial tumors from the
standpoint of the course or progress of the affection can be divided
into an early or beginning, a middle or developed, and a late or
terminal stage.

Headache, vertigo, and vomiting are early symptoms, varying in
severity from slight to very serious manifestations, and slight and
changing mental phenomena are present. Eye symptoms, such as slight
diminution or blurring of vision, may or may not show themselves; the
ophthalmoscope may reveal the earliest appearances of choked disc or
neuro-retinitis.

In the second or middle stage, the period of the fully-developed
disease, we have an intensification and greatly increased constancy of
all the general symptoms, with some additional manifestations. Mental
disorder increases; headache becomes more violent, and sometimes more
localized; amblyopia tends to advance to complete blindness, with
marked swelling of the papilla, or special disorders of vision, such
as hemianopsia, occur; palsies, ataxia, convulsions, contractures,
rigidity of limbs, altered reflexes, local spasms, anæsthesia,
hyperæsthesia, paræsthesiæ, neuralgias, appear according to the extent
and location of the growth. Certain special phenomena, according
largely to the seat of the tumor, may also appear, such as disorders
of hearing, taste, or smell, polyuria, diabetes, albuminuria,
polyphagia, or dysphagia.

In the third or terminal stage paralysis, anæsthesia, convulsions,
etc. become more profound; mentality sometimes decreases to nearly
complete imbecility, although in many cases a fair amount of mental
power is preserved almost to dissolution. Involvement of the bowels
and bladder becomes a distressing symptom, involuntary evacuations
adding to the torments of the patient. Bed-sores, acquired or trophic,
appear; the patient's limbs are painfully contractured; great
emaciation is usually present. With agonized head, often blind or
deaf, with torturing pains in anæsthetic, paralyzed, and wasted limbs,
covered with painful sores, filthy involuntarily, imbecile or
demented, death comes as a thrice-happy relief.

Cases have been reported in which intracranial tumors of considerable
size were discovered on autopsy, and had evidently been present for
years without their presence having been discovered or even suspected;
but these are extremely rare. In general terms, however, it may be
said that every case of brain tumor must give rise to symptoms. These
symptoms may be few or many, slight or severe, brief or protracted,
constant or paroxysmal, according to circumstances. Our experience and
study of the literature of the subject lead us to the conclusion that
the pathological character of the growth would have some influence as
to the severity and prominence of symptoms. Gliomata—which are {1031}
sometimes hard to distinguish from the brain-substance, particularly
the soft gliomata, producing comparatively little pressure—when
located in certain so-called latent areas of the brain might escape
detection during life; so might also very small tumors of any kind
situated deeply in the substance of the brain.

The position taken by Obernier, that individuality has much to do with
the activity of symptoms of brain tumor, has some strength. He refers
particularly to the psychical response to the irritation caused by
brain tumors, which differs very much in different individuals. The
fact, which has been pointed out in the article on Hysteria, that
hysterical symptoms are often present in cases of brain tumor as well
as in other forms of organic disease, is also sometimes the cause of
mistake by the diagnostician. The cases of Hughes Bennett and Eskridge
will be referred to in this connection under Diagnosis.

When the subject of local diagnosis is considered farther on, those
regions which are most active and those which hold an intermediate
position in the production of particular and distinctive symptoms will
be more particularly discussed.

       *       *       *       *       *

The possibility of the existence of multiple tumors should never be
overlooked. These are of comparatively frequent occurrence, and
sometimes give rise to a puzzling symptomatology. In our search
through the literature of the subject for cases we met with many
examples of multiple tumors. In preparing our table multiple tumors
were usually omitted. They give sometimes symptoms and signs so
conflicting as to make a local diagnosis impossible, and even to
confuse the expert as to general diagnosis. In other cases, however,
one growth of larger size or in an active region takes command of the
situation, and leads clearly to its diagnosis in spite of other less
significant tumors. This was shown, for example, in one of our cases
(Case 14). From the symptoms not only was the presence of the larger
tumor diagnosticated, but its exact location was indicated during
life. Post-mortem examination, however, showed a smaller tumor at the
inferior angle of the right lobe of the cerebellum, and also some
basal meningitis with effusion which had not been suspected. The first
tumor was one of the ascending frontal convolution, extending into the
fissure of Rolando. Its presence and location had been diagnosticated
by the right brachial monoplegia and paresis of the leg, which later
increased to paralysis of the limb, with right facial paresis, ptosis,
partial anæsthesia of right side of face, and slight clonic spasms of
the right arm. At the present time, when the question of operating for
the removal of brain tumors is so prominently before the profession,
and is now generally regarded as justifiable for growths in this one
location, the cortical motor area, the possibility of the coexistence
of another tumor should be carefully weighed. In this case, owing to
the clear diagnostic indications, the question of operation was
considered at the time of consultation, but fortunately—in large part
because the patient was almost in extremis—it was decided not to
operate. The operation would have been futile, the autopsy showing
that the probable immediate cause of death was the basilar effusion
which accompanied the cerebellar growth.

In another case reported by one of us[3] three gummata were found in
{1032} three different locations: one in the prefrontal region,
another in the retro-central fissure, and a third in the supramarginal
convolution. The general symptoms of brain tumor were present in this
case, but no localization was possible.

[Footnote 3: _Arch. Med._, viii. No. 1, August, 1882.]

The following are other illustrations of multiple tumors and of tumors
with other lesions out of a large number which we have collected:

M. 44.—Several severe falls on the head. Recent chancre with secondary
symptoms. Six months before death headache which grew worse; most
severe in right supraorbital region, and also obstinate vomiting,
vertigo, hiccough, insomnia. Some loss of power on both sides. Slow in
answering and indisposed to talk. Choked discs. Involuntary
evacuations. Some improvement under treatment, and then relapse.
Complete blindness. Polyuria. Specific gravity of urine as low as 1003
and 1005. Appetite at times ravenous. During last few weeks of illness
head inclined to the right side, probably from spasm. Intense thirst
throughout the illness.

(1) Large sarcoma in the white substance of the right parietal and
frontal lobes, involving ascending parietal convolutions. (2)
Softening and abscess of the right temporo-sphenoidal lobe and
posterior base of the right anterior lobe. Softened mass size of a
hickory-nut in the upper portion of the right ascending frontal
convolution. (3) Small cystic tumors of the choroid plexuses.[4]

[Footnote 4: J. T. Eskridge, _Trans. of Philada. Path. Society_, for
1878-79, vol. ix. p. 119.]

M. 5.—Convulsions, beginning either in right foot or in right face;
not unconscious during fits. Right-sided hemiplegia. Double optic
neuritis, followed by atrophy. Gradual increase in size of head, with
gaping sutures. Later, rigidity of right arm and leg. Shortly before
death the following symptoms suddenly set in: headache, convulsions of
right side with unconsciousness and retraction of head, rigidity of
right arm, and tremor of right leg. Later, both arms flexed, with
constant tremors of left arm, spreading over whole body. Right
sterno-cleido-mastoid was stiff; almost opisthotonos.

(1) Enormous tubercular tumor of left cerebral hemisphere, extending
from depth of Sylvian fissure and eroding skull. Corpus striatum soft
and diffluent. Weight, over eleven ounces. (2) Tumor, double size of
pea, in lower part of middle lobe of cerebellum.[5] This case was
especially interesting for the onset of the cerebellar symptoms late
in the case, caused probably by a late appearance of the cerebellar
tumor.

[Footnote 5: Hughlings-Jackson, _Med. Times and Gaz._, London, 1872-73
(2), p. 34.]

M. 2.—Screaming fits. Vomiting. Paralysis of left side of face,
including corrugator and orbicularis palpebrarum. Winking in both eyes
suspended. Paralysis of external rectus muscle. Agitation and
contractures of right arm and leg. Later, unsteady movement of head
and right arm and jerking of right leg.

(1) Small glioma in left hemisphere of cerebellum, and (2) a similar
tumor projecting from left lateral half of floor of fourth ventricle
at common nucleus of the abducens and facial nerves.[6]

[Footnote 6: W. H. Broadbent, _Proc. Clin. Soc. Lond._, v. 66-68.]

F. 45.—Epileptiform attacks for fourteen years. Vertigo, occipital
headache, disordered vision, intolerance of light, sleeplessness,
excitability, constipation, with paræsthesia of left side. Retraction
of head, {1033} vomiting. Very late, convulsive movements of right eye
and right side of mouth; then general clonic spasms, coma, and death.
No paralysis. For twenty-six years there had been an induration of one
breast, which toward end of life had a somewhat scirrhous appearance.

(1) Glioma in right hemisphere of cerebellum 1¾ inches in diameter.
(2) Glioma in centre of middle lobe of left hemisphere of the cerebrum
¾ inch in diameter. Surrounding nervous tissue softened and broken
down.[7]

[Footnote 7: William L. Bradley, _Tr. Conn. Med. Soc._, 1880, p. 39.]

M. 65.—Sudden attack of spasm of left arm, with paresis and coldness
and numbness. Headache and staggering. Wandering in mind. Not
unconscious. Twitching in eye. Two days later violent convulsion in
entire left half of body, with vomiting; not unconscious. After
convulsion left hemiplegia, with left deviation of tongue. Head and
eyes turned to right; vertigo. Partial anæsthesia of left face, body,
and limbs. Paræsthesia; painful nervous shocks through affected limbs.
Sounds in back of head. Later, mind cleared up and many symptoms
ameliorated. Very late, convulsion and coma. Cheyne-Stokes
respiration, involuntary evacuations. Duration, seven weeks.

(1) Tumor in ascending parietal convolution at junction of upper and
middle thirds. (2) Large tumor occupied entire occipital lobe, but did
not present on surface, reaching to convexity of descending cornu of
lateral ventricle.[8]

[Footnote 8: W. H. Broadbent, _Tr. Clin. Soc. Lond._, v. 233-236.]

       *       *       *       *       *

Headache is the most frequent and positive symptom of brain tumor. It
is rarely absent; in most cases it has peculiar characteristics. Its
usual type might be described as continuous pain, sometimes of
persistent severity, but generally with exacerbations or paroxysms of
great violence. No suffering can surpass that which some of the
victims of intracranial neoplasms are compelled for months or years to
endure. It is only equalled by the torture produced by malignant
growths in the vertebral axis, the throat, or the bones of the pelvis.
The pain is not, however, always of this character. In a comparatively
few cases it is described by the patient as dull or moderate, or he
simply complains of distressing sensations of weight, pressure, or
constriction. Usually in these cases, however, the pain increases and
becomes less and less endurable. In 100 cases the headache is
described as agonizing, violent, severe, or torturing 20 times; as
moderate or dull, 26 times. It is simply mentioned 20 times, but here
presumably it was of the ordinary severe type. Thus in 66 cases, or 66
per cent., headache of some type was recorded. No mention was made of
headache at all in 29 cases, in some of which, however, it was
doubtless present. In only 5 cases was it stated not to have been
present: 3 out of these 5 were said to be gliomata, and of the other
2, one was probably gliomatous, and the other a cyst in the
brain-substance. Tumors of this kind, which exert comparatively little
pressure and which are not connected with the membranes, are probably
those which are least likely to cause pain. In several instances the
patients complained spontaneously of the pain being greatest in the
region of the head nearest the seat of growth. With reference to
cerebellar tumors, it somewhat generally supposed that occipital pain
is usually present. It {1034} sometimes is and sometimes is not. In 15
cases of tumor of the cerebellum and of the fourth ventricle the pain
was described as occipital twice, as fronto-occipital three times, and
as cervico-occipital once. Callender has noticed that cortical lesions
are more frequently accompanied by localized pains than lesions of
deeper parts.[9] Some of our cases would seem to bear out this view,
although the data are not numerous or complete.

[Footnote 9: _St. Bartholomew's Hospital Reports_, 1869, and Ferrier's
_Localization of Cerebral Disease_, p. 99.]

In a few cases percussion of the head elicited or intensified pain in
the region corresponding to the location of the tumors. We believe
that percussion of the skull may afford valuable aid in localizing
encephalic tumors, particularly when they are meningeal or cortical.
Ferrier[10] holds that percussion often elicits pain over the cranial
region beneath which a lesion is localized, and Alex. Robertson of
Glasgow[11] has also directed attention to the value of percussion of
the skull in the localization of disease on the surface of the brain.

[Footnote 10: _Brain_, January, 1879.]

[Footnote 11: _Abstr. Internat. Med. Congress_, 1881, p. 85, and
_Journal of Nervous and Mental Disease_, April, 1882.]

Vomiting is of frequent occurrence, although it does not usually come
on as early or remain as persistently as headache. It is more likely
to be paroxysmal, with longer or shorter intervals of relief. It
frequently occurs at the time of the exacerbations of the headache,
and between the paroxysms of vomiting, nausea, slight or great, is
often present. It probably occurs in about 50 per cent. of all cases
of brain tumor. It is recorded as having been present in 34 out of 100
cases. It was comparatively infrequent in antero-frontal growths,
occurring only twice out of 10 cases.

A case reported by one of us (Case 70) was a remarkable example of
persistent cerebral vomiting. For four weeks before her death the
patient vomited almost incessantly. The tumor in this case involved
the middle cerebellar peduncle and the adjacent region of the right
cerebellar hemisphere, and had grazed and superficially softened the
floor of the fourth ventricle.

We incline to agree with Ferrier[12] that the majority of cases of
cerebral vomiting can be ascribed to irradiation of irritation by the
nerves of the cerebral membranes or to the physical effects of acute
pain. The nuclei of the trigeminus and of the vagus are in close
anatomical relationship in the medulla oblongata. Irritative
impressions conveyed from the cerebral membranes, and particularly
from the dura mater, to the trigeminal nuclei in the medulla are
transferred to the vagus and give rise to vomiting. In tumors of the
cerebellum the vomiting may be brought about through the affection of
the centres of equilibration and the concurrent vertiginous sensations
(Ferrier), or it may be due to direct irritation by contiguity of the
floor of the fourth ventricle. In general, the tumors situated
farthest forward in the brain appeared to be the least likely to give
rise to vomiting.

[Footnote 12: _Brain_, July, 1879.]

Vertigo was noted in 31 out of 100 cases. Under this general
designation dizziness, giddiness, reeling, insecurity in the erect
posture, etc. have been included. The vertigo can be explained in
several ways {1035} besides by the view which refers it to an
affection of centres of equilibration in the cerebellum. Like headache
and vomiting, it seems sometimes to be the outcome of pure irritation
of the cerebral membranes. Alterations in the intracranial circulation
produced by the growth of the tumor is another probable cause.
Experiments have demonstrated the existence of a communication between
the arachnoid cavity and the labyrinth, and consequently the increased
intracranial tension present may result in pressure on the
labyrinthine fibres of the auditory nerve, and thus occasion vertigo.

The importance of ophthalmoscopic examinations in suspected cases of
brain tumor can scarcely be overestimated. They will often serve to
clinch the diagnosis in favor of tumor. Of the 100 tabulated cases,
choked discs were recorded in 8; optic neuritis or neuro-retinitis in
18. These results serve to show the importance of the examination of
the eyes. It will be seen that with Allbutt, Norris, and others we
make a distinction between choked disc, papillitis, congestion
papilla, or ischæmia of the discs, and descending or interstitial
neuritis. The differences between these two varieties of inflammation
of the interocular ends of the optic nerve are well presented by
Norris in a previous volume of this work,[13] which will make it
unnecessary for us to describe the conditions present in these cases.
An examination of the tabulated cases will show that true choked discs
were present in tumors situated in all portions of the encephalon.
They were not infrequently present in tumors of the convexity.
Descending neuritis would seem most likely to occur when the tumors
are so situated that inflammation set up by them can readily extend by
anatomical continuity along the membranes to the optic nerves. The
lymph-space theory best accounts for the occurrence of choked discs in
cases of tumor situated remotely from the base. In choked disc the
appearance is one of intense swelling and engorgement of the optic
papilla. In descending neuritis, as described by Graefe and Norris,
there is rather a dull-red suffusion of the disc. Some of the cases
reported as neuritis may have been choked discs, and the reverse, as
physicians often do not make any distinction.

[Footnote 13: Vol. IV. p. 771 _et seq._]

Several practical matters should be borne in mind in connection with
this subject of the condition of the eye-ground. In the first place,
sight is not always impaired in cases of even somewhat advanced
choking of the disc, so that when other symptoms and indications lead
to the suspicion of a brain tumor, unexpected confirmation may be
obtained by ophthalmoscopic examination. Some remarkable cases of this
kind have been reported, and doubtless have been observed by all
ophthalmologists and neurologists of large practice. In some cases of
growths of large dimensions also careful ophthalmoscopic examination
has shown neither choked disc nor neuro-retinitis to be present. In
two of Seguin's cases, for instance (Cases 28 and 29), these
appearances were absent. In one he reports no neuro-retinitis, but
only some fulness of the veins. In the other, a large sarcoma of the
centrum ovale, ophthalmoscopic changes were absent. The absence of
disturbance of vision, therefore, should not lead the physician to
overlook making a thorough ophthalmoscopic examination; nor should the
absence of ophthalmoscopic appearances lead him to make up his mind
that serious intracranial disease was not present. {1036} The presence
of double choked discs is in the highest degree significant of a brain
tumor.

Observations on the temperature of the head have been made in a few
cases of tumor of the brain. Full accounts of such observations in two
cases (1 and 3 of Table) have been published by one of us.[14] It is
not within the scope of the present paper to review the general
subject of cranial or cerebral thermometry. We will simply, in
passing, recall the labors of E. Seguin,[15] Broca,[16] Gray,[17]
Lombard,[18] Maragliano and Seppilli,[19] and Amidon.[20]

[Footnote 14: _Philadelphia Medical Times_, Jan. 18, 1879, and _New
York Medical Record_, Aug. 9, 1879.]

[Footnote 15: _Medical Thermometry and Human Temperature_, by E.
Seguin, M.D., New York, 1876.]

[Footnote 16: _Progrès médical_, 1877.]

[Footnote 17: _New York Medical Journal_, Aug., 1878.]

[Footnote 18: _Experimental Researches on the Temperature of the
Head_, London, 1881.]

[Footnote 19: Quoted in _Archives of Medicine_, 1879.]

[Footnote 20: _Archives of Medicine_, April, 1880.]

L. C. Gray[21] has recorded some observations in cerebral thermometry
in one case of tumor of the brain. The tumor, a soft jelly-like mass
the size of a hazelnut, was found between the horizontal branch of the
Sylvian fissure and the first temporal fissure, while the whole of the
right occipital lobe was converted into a colloid, extremely vascular
mass, which gave way under examination, this degeneration also
extending anteriorly to the tumor as far as the fissure of Sylvius.
Microscopical examination showed it to be a typical glioma.

[Footnote 21: _N. Y. Medical Journal_, August, 1878.]

The temperatures at different stations were as follows:

                Left.    Right.
  Frontal . . . 96.75°   98.33°
  Parietal  . . 95°      99.75°
  Occipital . . 96.75°  100.50°

The average of the left side was 96.16°; of the right, 99.52°; of the
whole head, 97.84°.

In a case of frontal tumor (Case 1 of Table) the average temperatures
of the different stations taken were as follows:

  Middle frontal station . .  96.5°
    "    occipital  "    . .  95.5°
  Right frontal     "    . .  95°
  Left     "        "    . .  94.7°
  Right parietal    "    . .  94.7°
  Left     "        "    . .  94.4°

In another case, reported in full by one of us[22] (Case 94), a gumma
involved the basal termination of the corpus callosum, the peduncles
of the corpus callosum, the lamina cinerea, and anterior perforated
spaces; and the average temperatures at the different stations were as
follows:

  Right frontal station . . . . . . .  97.1°
  Left     "       "    . . . . . . .  97.4°
  Right parietal   "    . . . . . . .  97.6°
  Left     "       "    . . . . . . .  94°
  Right occipital  "    . . . . . . .  97°
  Left     "       "    . . . . . . .  94.5°
  Right anterior vertical station . .  97°
  Left     "        "        "    . .  94°
  Right posterior   "        "    . .  96.6°
  Left     "        "        "    . .  94.3°

[Footnote 22: _New York Medical Record_, Aug. 9, 1879.]

{1037} In a gumma in the cortical motor zone of the right side the
head-temperatures, taken once, were found to be for the right parietal
region, 97.2°; for the left, 96°. In another tumor of the right motor
zone the right frontal region gave a temperature of 98°; the left, of
96°. In a tumor of the left occipito-parietal region the temperatures
were for the right parietal region, 98°; for the left, 97.8°. Although
the temperature of the head was only taken once in each of these three
cases, the observations were carefully made with tested thermometers.

J. T. Eskridge, in a case of a tumor of the cerebellum with monocular
hemianopia (Case 76), made the following temperature observations:

  Axillary . . . . . . . . . . .  R. 98.6°; L. 98.6°
  Head:
    Anterior frontal station . .  R. 98.4°; L. 98.4°
    Posterior   "       "    . .  R. 98.5°; L. 98.6°
    Superior    "       "    . .  R. 98.4°; L. 98.4°
    Parietal    "       "    . .  R. 99.2°; L. 98.6°
    Rolandic    "       "    . .  R. 98.8°; L. 99.1°
    Occipital   "       "    . .  R. 99.4°; L. 99.1°
    Posterior central   "    . .     99°.
    Anterior     "      "    . .     99°.

The normal average temperatures, as determined by Gray, were as
follows:

  Left frontal station . . . . . . . . . . . .  94.36°
  Right   "       "    . . . . . . . . . . . .  93.71°
  Left parietal   "    . . . . . . . . . . . .  94.44°
  Right   "       "    . . . . . . . . . . . .  93.59°
  Left occipital  "    . . . . . . . . . . . .  92.66°
  Right    "      "    . . . . . . . . . . . .  91.94°
  Left side of the head  . . . . . . . . . . .  93.83°
  Right     "       "    . . . . . . . . . . .  92.92°
  The whole head, exclusive of the vertex  . .  93.51°
  Motor region of the vertex . . . . . . . . .  91.67°
  The whole head, inclusive of the vertex  . .  92.66°

We conclude that in brain tumors the average temperature of the whole
head is elevated several degrees above the normal, and that the
elevation of temperature is usually greatest at the station nearest
the seat of the growth.

Mental disturbance of some description was present in about one-third
of all the cases studied. Doubtless they were not recorded in a large
number of cases. Obernier says: “If the psychical qualities of a
patient suffering from cerebral tumor be analyzed, and a careful
comparison made of the former with the existing mental condition,
certain symptoms of mental disturbance will be discovered in most
cases where the tumor is a growing one.” The disturbances may be in
any sphere of the mind—in intellection, volition, emotion, or
perception. Mental slowness and uncertainty, inability to fix the
attention, impossibility of continuous mental action, apathy, or
stupidity, with hesitation or slowness of speech, were strikingly
exhibited in cases of tumor of the antero-frontal region. In Case 1
the patient's mental condition was studied with great care, and in the
detailed report of the case[23] the following facts were noted: The
psychical manifestations were among the most important features of the
case. Although comparatively uneducated, he had been when {1038} in
health intelligent and energetic. He had never during his illness had
the gay humor or delirium of grandeur seen in the general paralysis of
the insane. His condition, on the whole, was one of intellectual
slowness and uncertainty. He seemed to have great difficulty in
receiving mental impressions and in directing the movements of his
body. His faculty of attention was, in great measure, destroyed. It
could only be fixed, and then but partially, by distinctly and
vehemently repeating a question or command. He could hear, but it was
necessary to make a tremendous external impression on his sense of
hearing in order to call out a mental response. He sometimes appeared
to me like a man dazed by a great catastrophe which he could not
understand. He was not aphasic, although he manifested certain
striking peculiarities of speech, or, rather, of the manner of
speaking. What he said, either spontaneously or in answer to
questions, was spoken clearly and distinctly and in a firm, loud
voice. His sentences were short, but complete; neither words nor
syllables were omitted; and he made no mistakes in articulation,
enunciation, or pronunciation. In answering he did not seem to be able
to retain for any length of time a hold upon the same idea or to
follow a particular train of thought. He did not wander from one
subject to another, but he would suddenly stop speaking, as if unable
to go farther. Often on being questioned he would try to reply, and
after a sentence or two would sob and burst into tears like a
violently hysterical woman. He would at times have what might be
termed volcanic outbursts of speech. When all was perfectly quiet in
the ward he would suddenly explode with a sentence or two, and then
again subside into stillness. Exclamations of this kind might be
repeated at intervals of a few minutes for hours together, or they
might recur only at intervals of hours. Sometimes what he said would
be connected with some past events of which he seemed to have a vague
recollection; often it would be a demand for something to eat or
drink; and often, again, it would be a paroxysm of profanity.

[Footnote 23: _Philadelphia Medical Times_, Jan. 18, 1879.]

Impairment of will is not uncommon in antero-frontal and other
cerebral tumors, and failure of memory, depression of spirits, and
even acute mania, occur. Many of the patients are emotional,
excitable, and irritable; they often sob and cry, apparently from the
great pain. In some cases, however, emotional conditions are present
which seem to be dependent on some special localization of the tumor.
Hallucinations were noted in two of our tabulated cases. In one case,
a tumor of the motor zone, the patient had delusions that some one was
about to take him away. There were also illusions of fear or
persecution. In another the patient had visual hallucinations.

Speech-defects of various kinds occur in connection with intracranial
growths. Ladame, quoted by Rosenthal, has cited forty-five cases of
disturbances of speech in which the tumor occupied the most varied
regions of the brain. Peculiar disorders of speech from special
localizations will be treated of under Local Diagnosis.

Local spasms, which go under various names, as cramps, twitchings,
epileptoid attacks, athetosis or athetoid movements, are common
symptoms, particularly of growths which involve the cortical motor
area. They are of great diagnostic value. They are commonly, although
not invariably, accompanied by paresis, which is usually most marked
in the {1039} part most affected by the spasm. These local spasms,
beginning in one extremity, in a finger or toe it may be, often spread
toward the centre, until they involve to a greater or less extent the
whole limb, the side of the face, or one-half of the body. Sometimes
instead of this they recur with the same definite movements over a
long period. They are the expression of irritation of cerebral centres
or tracts connected with the muscles or groups of muscles affected by
the abnormal movement. They should always lead the physician to
carefully consider the great probability of a lesion in some way
involving the motor area.

Tumors of the cerebellum, pons, and medulla oblongata sometimes give
rise to general convulsions which closely simulate attacks of grave
epilepsy. These convulsions or general spasms are among the most
important symptoms of intracranial neoplasms. More than paralysis,
they may be regarded as general symptoms, as they are more likely to
occur from tumors situated in different and distant regions of the
brain than paralysis. They are by no means confined to cases in which
the lesion is situated in the so-called motor area of the brain or in
the cerebellum or pons-medulla region. Both physiological and
pathological experiments have shown that convulsions violent in
character, but having certain special characteristics, may originate
from severe irritation of the dura mater. According to Duret,[24]
irritation of the sensory nerves of the dura mater cause reflex spasms
or contractures of the muscles of organic life. These spasms or
contractures may occur in the face, eyeballs, neck, trunk, or limbs,
and sometimes on one side and sometimes on the other. They tend to
diffuse and invade neighboring groups of muscles. “They have never the
localization, the measured and purposed character, of the contractions
which belong to the lesions of the cortex. They frequently become
transformed into permanent contractures.” The application of these
facts and conclusions to brain tumors is evident. As neoplasms are so
frequently connected, either directly with the dura mater or with the
fused membranes, it is evident that the convulsive attacks from which
the patient suffers may occur from tumors located anywhere within the
cavity of the skull.

[Footnote 24: _Sur les Traumatismes cérébraux_, par H. Duret, chapter
iii., summarized in _Brain_. vol. i., 1878, p. 47.]

General convulsions, as well as local or unilateral spasms, are
present in many tumors of the motor cortex; but if their method of
origin and their progress are closely watched they will usually be
seen to begin with local twitchings.

A glance at the table will show examples of convulsion in almost every
region of the brain.

Contractures—conditions of tonic spasm which continue more or less
persistently—may be either early or late symptoms. They may occur in
one or several limbs, in the face, or rarely in the neck. They are
probably due in some cases to persistent irritation of the dura mater,
in others to comparatively slight but continuous irritation of motor
centres, and in still others to advanced degeneration of the motor
tracts.

Choreas and choreic movements are not frequent, unless some of the
forms of local spasm are regarded as local choreas. In one of
Petrina's cases, a glioma involving the substance of both frontal
lobes, choreic movements of the right arm were present, and in this
same case tremor {1040} in both arms was also a symptom. Tremor
simulating that of paralysis agitans or multiple cerebral sclerosis is
occasionally observed, and sometimes a tremor which is nervous or
hysteroidal in character is one of the results of the great suffering
of the patient.

Paralysis or paresis is of course one of the most frequent evidences
of the existence of an intracranial tumor. The palsies of cerebral
tumors are chiefly unilateral, but the loss of power may be in one or
both limbs, in one side of the face, or in the entire one-half of the
body, according to location and extent. Tumors of the cortical motor
zone usually begin their paralytic manifestations with paresis of one
member or one side of the face, which goes on, as the growth increases
in size, to more or less complete hemiplegia.

The paralysis which results from brain tumor is due either to pressure
or to absolute destruction of tissue. In the latter case the
destruction is brought about not only by the simple displacement of
brain-substance, but also through the obliteration of blood-vessels
and the consequent softening.

Peculiar forms of paralysis occur as the result of neoplasm growing in
special locations, as will be more clearly shown under Local
Diagnosis. Thus we have the alternating paralyses from tumors of the
crus cerebri or of the lower part of the pons, and paraplegia, or
perhaps what might be better called double hemiplegia, from multiple
tumors which affect both sides of the brain. In rare cases paralysis
of all four extremities has resulted from a growth in the middle line
of the base of the brain. Some form of paralysis is recorded to have
been present in 20 cases out of 100.

Apoplectiform attacks sometimes take place suddenly during the
progress of cases of brain tumor. A patient who has been suffering for
months with the general symptoms of tumor, and who may or may not have
had some paresis of the limbs or face, has an attack of
unconsciousness, from which he arouses after a time, and is then found
to be almost completely hemiplegic. After such attacks, in some cases,
the symptoms of brain-irritation, particularly the headache and
vomiting, subside or greatly improve. Such attacks may be explained in
several ways—from the occurrence of congestion with œdema, of
intercurrent hemorrhage, or of softening from obliteration of
blood-vessels by the advancing growth; and the temporary subsidence or
more permanent disappearance of the headache and other symptoms is
probably, in some cases at least, owing to the diminution of tension
because of the breakdown of tissue in the neighborhood of the growth.
Sometimes the seizures which occur during the progress of the case are
both epileptiform and apoplectiform in character.

Sometimes in cases of intracranial tumor there are present in the
cranial nerve-trunks and the muscles supplied by them the changes
known as the reactions of degeneration. These changes are
characteristic of the peripheral palsies, and indeed sharply
distinguish them from paralyses of central origin. The exception to
this rule in cases of intracranial growths is, of course, only
apparent and not real, because these palsies, when caused by the
pressure of a tumor on a nerve-trunk, even within the cavity of the
skull, and not upon their proper centres or intracerebral tracts, are
as much peripheral as though the injury was caused by compression of
these {1041} nerve-trunks outside of the skull. These reactions of
degeneration are briefly as follows: The nerve-trunk gradually,
sometimes rapidly, loses its response to both the galvanic and faradic
currents. The muscle loses its response to faradism coincidently with
the nerve-trunk, but to galvanism it is apt to exhibit first increased
excitability, then gradually lessening excitability: and with this
lessening response it puts on the so-called qualitative changes. These
consist of the serial alterations—_i.e._ the negative pole, instead of
exciting the more active reaction at closure, gives a less response
than the positive pole at closure, and also calls forth a response at
opening which may be greater than the opening contraction of the
positive pole, which may be abolished. In health the positive pole
causes often an active response, and the negative pole none, or almost
none, at opening. Finally, occur modal alterations in the affected
muscles, which consist of a slow, lazy contraction instead of a quick,
lively one as in health, and a tendency in the muscle to remain
contracted (tetany) while the current is passing. The many
modifications—or, better, the partial exhibitions of these changes and
the conditions underlying them—are to be sought in detail in special
treatises. It is sufficient to say that they have been reported in a
number of cases of brain tumor, and that the nerves in whose
distributions they would be especially seen are the motor oculi, or
third, the abducens, or sixth, and the facial, or seventh. It is
doubtful if a very exact electrical examination could be made of many
muscles supplied by these nerves, except in the case of the facial,
and possibly the elevator of the upper eyelid. It is in the case of
the seventh nerve that the recorded observations have been made. It
will be noticed, by reference to the table, that the third, sixth, and
seventh nerves are frequently involved in tumors of the crus and
pons-medulla region, and that the paralysis is usually on the side of
the lesion. These are the cases which would exhibit the reactions of
degeneration. It has been said that in ordinary hemiplegia, and also
in paralyses from tumors of the brain high in the motor region, the
affected side exhibits simply a qualitative increase to electrical
excitation; and this may be explained by the increased excitability to
all stimuli of the lower or spinal-cord centres when cut off from the
brain. The statement, however, which has been made, that in tumors of
the cerebellum the sound side exhibits a quantitative decrease, sounds
like a paradox, and requires further tests before being accepted as a
fact in electro-diagnosis.

Ataxia has been observed in cases of brain tumor situated in various
locations. The symptom described as ataxia, staggering, or staggering
backward, is more particularly observed in cases of tumor of the
cerebellum, pons, and corpora quadrigemina.

Changes in the state of the reflexes are somewhat frequent. Usually
the skin and tendon reflexes will be increased on the side opposite
the lesion, although some striking exceptions, probably due to the
positions of the growth, occur.

Atrophy of the limbs is sometimes present, but usually in brain tumor,
as the lesions are above the nutritive connection of the nerve, true
atrophies do not occur.

True neuralgias are frequent, particularly in the distribution of the
trigeminal. Trigeminal neuritis also undoubtedly occurs in lesions
{1042} involving this nerve at its origin, in its course, or in the
Gasserian ganglion.

Anæsthesia, either in the form of local or hemianæsthesia, was
observed in about 20 per cent. of the cases. It is rarely present as
an isolated symptom, but frequently accompanies unilateral paresis. In
a partial or variable form it most frequently is seen in connection
with tumors of the Rolandic region. It is a marked symptom in
postero-parietal growths and those involving the posterior part of the
internal capsule. It may take the form of loss of sensation to pain,
touch, pressure, temperature, etc.

Hyperæsthesia occurs so commonly as to be almost regarded as a general
symptom of brain tumor. Sometimes it is confined to the head;
sometimes it is generally diffused; more frequently it is present in
the limb or limbs affected with the paralysis. With hyperæsthesia the
patients often complain of spontaneous pain in the limbs.

Diplopia or double vision is a somewhat frequent symptom, occurring
most commonly, of course, when the ocular nerves are involved directly
or indirectly by the tumor; hence tumors of the floor of the skull, of
the crus cerebri, of the pons, or of the cerebellum are most likely to
give rise to this symptom. A close study of the character of diplopia
and of other symptoms which go with it will usually enable a local
diagnosis to be made. Diplopia, however, does sometimes occur in
tumors situated remotely from the base, either because of pressure,
because of general nervous weakness, or possibly because of
involvement of cortical oculo-motor centres.

Ptosis is another symptom, generally unilateral, and most frequently
present in connection with strabismus, diplopia, and dilatation of the
pupil from involvement of the third nerve. Dilatation of the pupil and
contraction of the pupil may be present as general symptoms of tumors.
The latter is most probably due to meningeal irritation.

Hemianopsia is another ocular symptom sometimes present in cases of
brain tumor, as it may also be in other forms of encephalic lesion. It
was present in 5 of 100 cases. Norris[25] gives a full description,
brought well up to the present time, of this symptom, and a discussion
of the lesions upon which it depends. Seguin[26] also discusses this
subject. Starr[27] has collected a large number of cases of lesion
causing this symptom, some of which have been reproduced in our table.
We will not go into any details as to the character of this symptom,
referring the reader to the sources indicated. In the first case given
in our table (Case 10) the hemianopsia was produced by a tumor in
front of, and impinging upon, the optic chiasm; in the other four
cases (Cases 40, 41, 42, and 43) the tumor was situated in the
occipital lobe, and was surrounded by an area of destroyed tissue.
Hemianopsia is not, strictly speaking, a symptom of brain tumor, but
is likely to be present in cases occurring in certain regions of the
brain. Starr's conclusions with reference to lateral homonymous
hemianopsia when it is not produced by a lesion of one optic tract are
that it may result from a lesion situated either (1) in the pulvinar
of one optic thalamus; (2) in the posterior part of one interior
capsule or its radiation backward toward the occipital lobe; (3) in
the medullary portion of the occipital lobe; or {1043} (4) in the
cortex of one occipital lobe. The conclusions of Seguin are only
different in so far as they more closely limit the position of the
lesion.

[Footnote 25: Vol. IV.]

[Footnote 26: Pp. 84, 85 of present Volume.]

[Footnote 27: _Amer. Journ. Med. Sci._, N. S., vol. lxxxvii., January,
1884, p. 65.]

Phosphenes, or subjective sensations of light, occur in various
forms—simply flashes or sheets of light, scintillations, balls of
fire, etc. They are not very common as isolated phenomena, and
probably are dependent in most cases upon irritation of the nerve and
retina in some of the stages of neuro-retinitis. Even visual
hallucinations are occasionally present, as in one of Bennett's cases
of tumor of the Rolandic region.

Conjugate deviation of the eyes, with rotation of the head, a symptom
of the early stages of apoplectic attacks, is also sometimes observed
in brain tumor. The patient is found with both eyes turned to one side
and slightly upward, as if looking over one or the other shoulder, the
head and neck being usually rotated in the same direction. Sometimes
the deviation is slight, sometimes it is marked. Frequently the
muscles of the neck on one side are rigid. The eyes are commonly
motionless, but occasionally exhibit oscillations. This sign, well
known to neurologists, usually disappears in cases of apoplexy in a
few hours or days, although it occasionally persists for a long time.
It will be more fully considered under Local Diagnosis.

Diminution or loss of hearing, tinnitus, and hyperæsthesia of hearing
are all occasionally observed. The most decided disturbances of this
sense are those which are found in connection with tumors of the base
or of the cerebellum in such a position as to involve the auditory
nerve or auditory tracts. Tinnitus, acoustic hyperæsthesia, with
complete or partial deafness, accompanying facial paralysis, with or
without paresis of the limbs of the opposite side, indicate clearly a
tumor of the base so situated as to involve the superficial origin or
intracranial course of the auditory and facial nerves.

The sense of smell is affected, of course, when the olfactory bulbs
are involved in the growth, either directly or by pressure, as in
certain tumors of the antero-frontal region (Cases 4 and 8).
Disturbances in the power of consciously perceiving odors, or abnormal
perceptions of odors or hallucinations of smell, are sometimes present
in cerebral tumors involving certain convolutions. The lower
postero-parietal region or the temporo-sphenoidal region of the base
would seem, from the few reported cases, to be implicated when this
sense is centrally affected. Smell was lost or impaired in two cases
of tumors of the postero-parietal region, in one limited to the
supramarginal convolutions. In a case reported by Allan McLane
Hamilton (Case 47), an induration of the lower part of the right
temporo-sphenoidal lobe involving the uncinate gyrus, the patient,
preceding light epileptic attacks, always had an olfactory aura of a
peculiar character—a disagreeable odor, sometimes of smoke and
sometimes of a fetid character. In this case the olfactory nerves were
examined and found to be healthy.

Taste may be involved in several ways. In the first place, subjective
sensations of taste, particularly the so-called metallic taste, may be
present when the growths involve the cranial nerves in such a way as
to cause irritation to be conveyed to the nucleus of the hypoglossal.
When it is remembered that a mild galvanic current applied to the nape
of the neck or face will often cause this metallic taste, it can be
seen {1044} that the irritation of a tumor situated at almost any
point of the base might lead to abnormal taste-phenomena. Neoplasms
involving the trunk of the portio dura may of course cause diminution
or loss of taste on the anterior extremity of the tongue by the
involvement of the chorda tympani nerve. In the very few cases in
which the hypoglossal trunk may be involved disturbances of taste
posteriorly may occur. In two cases (Cases 33 and 36) some possible
indications as to the cortical areas of taste are given. One was a
tumor so situated as to cause pressure on the orbital, and possibly
anterior, portion of the temporo-sphenoidal lobe; the other was a
lesion closely localized to the supramarginal lobule.

Trophic disturbances of decided character are sometimes present in
cases of brain tumor. Their presence, character, and extent depend
upon the position of the tumor and the cranial nerves involved.
Trophic disorders of the eye have been noted in cases of tumor of the
antero-frontal region, and also of various positions at the base,
especially those so situated as to involve the trigeminal nerve. In a
fibroma of the superior antero-frontal region (Case 1) conjunctivitis
and corneitis of the left eye, with anæsthesia of the conjunctiva,
were present, and were very marked symptoms. This patient, who was
under the care of one of us at the Philadelphia Hospital, was examined
by O. E. Shakespeare, ophthalmologist to the hospital. At his first
examination the bulbar conjunctivæ were slightly injected and the
cornea clear. The sensibility of the cornea was possibly a little
lowered. Ten days later, at a second examination, the central corneal
epithelium of the left eye was found to be hazy and the whole bulbar
conjuntivæ much congested. “This condition soon developed into a
severe superficial corneitis, which was mainly limited to a central
area of an extent about equal to three-fourths of the diameter of the
cornea, which threatened to slough, a narrow peripheral ring of the
cornea being comparative unaffected. At the same time the engorgement
of the bulbar conjunctiva increased. The sclera, the iris, and the
deeper parts were apparently not involved in the inflammatory
process.”

Disturbances of respiration were observed in a number of cases in
various stages. Cheyne-Stokes breathing was usually a late symptom. In
a case of tubercular meningitis with a tubercular granulation
springing from the left side of the fourth ventricle (Case 82) it was
present. Extraordinary slowing of respiration occurred in a tumor of
the right middle cerebellar peduncle and cerebellar hemisphere which
caused irritation and softening of the floor of the fourth ventricle.
The respirations ran as low as four and five per minute two weeks
before death.

Persistent epistaxis and a tendency to hemorrhage from the mucous
membranes were interesting vaso-motor phenomena in a case situated in
the upper left quarter of the pons (Case 84). Profuse perspiration,
more marked on one side, was observed in a case of tumor in front of
the optic chiasm. Polyphagia was observed in two cases, one a growth
of the cerebellum and the other on the floor of the skull. Polyuria
was a very marked symptom in Case 95, a tumor at the base of the brain
at a spot corresponding to the sella turcica, and diabetes was present
in a case of frontal tumor. Albuminuria was recorded twice—once in the
same case in which diabetes was present, and again in a case of {1045}
multiple tumor of the supramarginal convolution of one side and the
angular gyrus of the other. Somnolence was occasionally observed.

Constipation or torpor of the bowels occurs somewhat frequently in the
early stages of the brain tumor, giving place in the terminal periods
to involuntary evacuations. The conditions of the bladder are
practically the same. It is either not involved or suffers from torpor
or paresis of the muscular walls early in the disorder, and later, and
especially very late, incontinence from paralysis of the sphincter
results.

DURATION, COURSE, AND TERMINATION.—The duration of cases of
intracranial tumor is very uncertain. In many of the reported cases no
definite information is given as to the exact length of time from the
initial symptoms until the fatal termination. The few cases in which
the time was recorded showed a duration of from three months to as
many years.

In a few cases, even in some which are not syphilitic in character, a
remission of all the symptoms and what appears to be an approximate
cure sometimes take place, the general symptoms, such as headache,
vertigo, vomiting, spasms, etc., disappearing for a time. Even the
condition of the eyes and the paralysis in rare instances make marked
improvement. In these cases, in all probability, the progress of the
growth of the tumor is arrested either by the remedies employed or
spontaneously, and the acute or subacute phenomena of congestion,
œdema, etc. around the tumor subside. These patients may remain for a
long period or until cut off by some other disease without any change
for the worse; but the sword constantly hangs above their heads, and
any excitement, traumatism, the abuse of alcohol or other narcotics,
an attack of fever, or some other special exciting cause, may again
light up the intracranial disorder, to then progress more or less
rapidly to a fatal termination.

This fatal termination may occur in various ways. Sometimes a sudden
apoplectic attack occurs. This may be an intercurrent hemorrhagic
apoplexy, although our personal experience would not lead us to
believe this mode of termination is common. In a few cases the
enormous irritation of the cerebral growth suddenly or gradually
inhibits the heart's action through the impression made on the
pneumogastric. Apoplectic attacks which may or may not terminate
fatally sometimes are the result of a sudden giving way of necrosed
brain-tissue, the necrosis having resulted from the obliteration of
numerous blood-vessels by the advancing growth. Blood-poisoning
occasionally takes place from abscesses in proximity to the tumor. In
some cases the patients slowly but surely emaciate, or are exhausted
and worn out by the agonizing pain and incessant vomiting which they
are called upon to endure. Occasionally a more or less diffused and
violent meningitis hastens the fatal issue.

COMPLICATIONS AND SEQUELÆ.—Tumors of the brain may be complicated with
other affections due to the same cause. Thus, for example, in a case
of gumma other evidences of syphilis may be present in the form of
nodes, eruptions, etc. A sarcoma or carcinoma of the brain may be
associated with similar disease in other organs. Such affections as
cystitis, pyelitis, keratitis, etc., which have been discussed under
Symptomatology, are secondary complications of cases of tumor. As
{1046} intracranial tumors almost invariably terminate fatally,
strictly speaking we have no sequelæ.

PATHOLOGY.—We present in tabular form the various classes of tumors
found in the one hundred cases of brain tumor in the table appended to
this article:

  Carcinoma . . . .  7  |  Glio-sarcoma . .  1
  Cholesteotoma . .  1  |  Gumma  . . . . . 13
  Cyst  . . . . . .  2  |  Lipoma . . . . .  1
  Echinococcus  . .  2  |  Myxo-sarcoma . .  1
  Enchondroma . . .  1  |  Myxo-glioma  . .  2
  Endothelioma  . .  1  |  Osteoma  . . . .  2
  Fibro-glioma  . .  2  |  Sarcoma  . . . . 15
  Fibroma . . . . .  4  |  Tubercle . . . . 13
  Glioma  . . . . . 16  |  Unclassified . . 16

The histology of tumors of the brain does not in the main differ from
that of the same growths as found in other parts of the body, so that
a detailed description of their structures, even though founded upon
original research, could not offer many novel facts in a field which
has been so thoroughly cultivated. Such a description would probably
repeat facts which have already been presented in other parts of this
work, and which are better and more appropriately put forth in special
treatises devoted to the science of pathology. It is proper, however,
for the sake of convenience and thoroughness, to make brief mention of
the structure of brain tumors, and especially to dwell upon certain
features of these morbid growths which may be considered
characteristic of their encephalic location, and hence have not only
pathological but also clinical interest. It is hardly worth while to
refer to speculations which aim to elucidate the very foundations of
the science, except that in a few of these theories we gain an
additional insight into both the structure and conduct of some very
characteristic brain tumors.

Cohnheim's theory was that tumors are formed from foci of embryonal
tissue which had been non-utilized or left over in the intra-uterine
development of the body. Many have not accepted this idea, but have
rather considered that in tumors we witness a reversion of tissue to
lower or embryonic types.[28] Whether we accept either or neither of
these propositions, the idea sought to be conveyed is that in all
these morbid structures we have a tissue of low or degraded character,
springing in most instances from a connective or non-differentiated
tissue. This fact is brought out very clearly in many of these
intracranial growths. Virchow[29] has said that tumors originate in
the cells of the connective tissue, although his law has been
condemned as not of sufficient breadth, since it seems to ignore the
epithelial and myomatous tumors. Dermoid cysts, of which an example is
given in the table of spinal tumors,[30] are said to illustrate the
embryonic function revived—_i.e._ the tendency of lower tissues to
spontaneously differentiate into higher and more complex ones.

[Footnote 28: Article “Pathology” in _Brit. Encyc._, by C. Creighton.]

[Footnote 29: Quoted by Cornil and Ranvier.]

[Footnote 30: Page 1107.]

The gliomata are among the most common and characteristic tumors of
the cerebro-spinal axis, to which system and its prolongation into the
retina they are confined. They invariably spring from the neuroglia or
connective tissue of the nerve-centres, and reproduce this tissue in
an embryonal state. They greatly resemble the brain-substance to
naked-eye inspection, but have, histologically, several varieties of
structure. {1047} These variations depend upon the relations of the
cell-elements to the fibres or felted matrix of the neoplasm. In the
hard variety the well-packed fibrous tissue preponderates over the
cell-elements, and we have a tumor resembling not a little the
fibromata (Obernier). The second variety, or soft gliomata, show a
marked increase of cells of varied shapes and sizes, with a rich
vascular supply which allies these growths to the sarcomata. The
elements of gliomata sometimes assume a mucoid character, which allies
them, again, to the myxomata.

[Illustration: FIG. 43. Flat Glioma-cell with its Fibrillar
Connections (Osler).]

[Illustration: FIG. 44. (1) Homogeneous translucent fibre-cell; (2)
cells like unipolar ganglion-cells; (3) giant cell (Osler).]

W. Osler has recently described[31] to the Philadelphia Neurological
Society the structure of certain of these tumors, from which we
abstract the following facts: One point referred to is that gliomata
sometimes contain larger cells and coarser fibres than are usually
shown. The structures are (1) The “spinnen” or spider-cells
(characteristic of glioma), which present variations in size; (2)
large spindle-shaped cells with single large nuclei (some of the
largest cells met with in tumors); (3) cells like the ganglion-cells
of nerve-centres, with large nuclei and one or more processes: some
are balloon-shaped with single processes; they are larger than the
spider-cells; (4) translucent band-like fibres, tapering at each end,
without nucleus or granular protoplasm, regarded as a vitreous or
hyaline transformation of the large spindle-cells. Klebs (quoted by
Osler) holds that the ganglion-like cells are derived from the
nerve-cells of the gray matter, “and that in the development of this
variety all elements of the nerve-tissue participate.” Osler examined
the advancing region of {1048} the tumor, and was not able to satisfy
himself that the nerve-cells were in process of proliferation. He
thinks they are connective-tissue elements. He has seen but two out of
five cerebral gliomata which were of small-celled type.

[Footnote 31: “Structure of Certain Gliomas,” _Philada. Med. News_,
Feb. 20, 1886.]

The gliomata are subject to fatty degeneration, which usually occurs
in the central (older) portions of the mass. The more vascular forms
are also peculiarly liable to hemorrhage, which is probably caused in
some instances by this process of retrograde metamorphosis. These
hemorrhages resemble apoplexies, not only in their clinical features,
but also on gross examination. Great care is therefore often necessary
at the autopsy to distinguish such a hemorrhage, occurring as it does
in a brain-like neoplasm, from one caused by the rupture of a diseased
artery. The hypertrophy of the pineal gland, sometimes noted, is
caused by the formation of gliomatous tissue. Under the microscope it
is necessary carefully to distinguish some forms of inflammatory new
formations from the gliomata. We have recently seen, by the courtesy
of E. N. Brush of the Pennsylvania Hospital for the Insane,
photographs of microscopic sections from the ependyma of the lateral
ventricles in a case of general paresis, which showed the structure of
this degenerated tissue to be a compound of fibres and cells of marked
resemblance to gliomatous tissue.[32]

[Footnote 32: These micro-photographs were prepared in the laboratory
of the State Lunatic Asylum, Utica, New York, by Theodore Deecke.]

Sarcomata of the brain are common, as our table shows. In them the
cell-elements predominate, both in the large- and small-celled
variety. They are malignant and grow rapidly. The form known as
alveolar sarcoma, which has a distinct stroma, is to be distinguished
from the cancers; which has probably not always been done.

Tubercle, according to Ross, is the most common of all forms of brain
tumor. Our table shows 13 cases out of 100, the gliomata and sarcomata
being in larger number. Its favorite seat is in the cortex of both the
cerebrum and cerebellum: some observations appear to show that it is
more common in the cerebellum and mid-brain region than in the
fore-brain, and in children than in adults; some of which points
distinguish it from the gummata, which are more common in adults and
occur anywhere. Tubercle is another form of development from the
connective tissues, usually dependent upon a constitutional taint or
predisposition: in it the cell-elements have generally undergone a
degeneration into an amorphous cheesy mass. It is apt to be multiple
and accompanied by a similar deposit in other organs of the body.

True neuromata are probably very rare growths, and it is likely that
some tumors which have been described as such are really
connective-tissue tumors of a gliomatous nature, in which some of the
cell-elements have been mistaken for the ganglion-cells. Obernier[33]
says that these tumors are small and grow from the gray matter on the
surface, also on the ventricular surfaces. They are also found in the
white matter. He says they are only found in persons having some
congenital or acquired aberration; by which is probably meant some
other well-marked neurosis or psychosis. The one hundred tabulated
cases afforded no examples of neuromata.

[Footnote 33: _Op. cit._]

Myxomata are not, histologically, to be distinguished from the {1049}
gliomatous tissues by anything but the peculiar mucoid changes which
their structures have undergone. They are more rare in the brain, as
our tables show, than in the spinal cord.

Lipomata are very rare in the brain, according to most observers. The
table shows but one example. These tumors, as their name signifies,
are made of fat-bearing tissues—another of the connective-tissue
class.

The angiomata, somewhat rarely found within the skull, are noted for
their abnormal development of the vascular tissues: they are composed
mainly of blood-vessels and the connective tissue, which supports them
in closely-packed masses. They also present cavernous enlargements.
They are of especial interest in cerebral pathology, because the
lesion known as pachymeningitis hæmorrhagica, often found in dementia
paralytica, is considered by some to be angiomatous; although by far
the most generally accepted view of this latter condition is that it
is due to arterial degeneration, and in part is an inflammatory
exudate.

Syphilitic tumors, or gummata, are, like tubercle, a special
development with degeneration from the connective tissue, due to a
constitutional taint. This new growth is sometimes single, sometimes
multiple. The corpuscles of the neuroglia are the apparent points of
origin of the tumor, the substance of which is the firm, peculiarly
gummy, and non-juicy material from which the name is derived. It would
be impossible in our allowed space to trace this neoplasm through the
successive stages of its development. It has especial clinical
interest, inasmuch as it and its damage are probably amenable to
specific treatment when it has not progressed to too great a
destruction of brain-tissue.

The true cancers, or epithelial neoplasms, are not a common form of
tumor of either the brain or spinal cord. They present, as in other
parts of the body, a stroma forming alveolar spaces in which are
contained the nests of epithelial cells. These tumors thus present
characteristic differences in their histology from the
connective-tissue or mesoblastic groups, but clinically no very
special interest attaches to them. Their location, the rapidity of
their growth, and their fatal import are points which they share with
most other new growths of the cranial cavity.

The cholesteotomata, or pearl cancers, consist of hardened epithelial
cells which have undergone a sort of fatty degeneration.

The psammomata are loosely described as tumors containing sand-like
bodies, which bodies are normal about the pineal gland. These
sand-like bodies are found in tumors of some histological diversity,
and do not appear to have much identity of their own. They occur in
sarcomata and carcinomata, and are probably not to be distinguished
from mere calcareous infiltration and degeneration. They are most
common in sarcomata, as this is one of the most common of cerebral
tumors.

True osteomata—_i.e._ tumors with the structure of true bone—are
probably rare in the brain, although more common on the inner table of
the cranium; but the deposition of calcareous salts has been recorded
in a variety of conditions. F. X. Dercum, in a recent paper read
before the Philadelphia Pathological Society,[34] has recorded the
autopsy of a paretic dement in which case calcareous deposits were
scattered throughout both hemispheres and the cerebellum. He believes
that “the areas in {1050} which the concretions were found were
probably foci of encephalitis of greater intensity than elsewhere. In
these foci inflammatory changes in the walls of the vessels became
pronounced; besides which the vessels increased enormously in size and
number; so marked is this increase that these foci could, with perfect
propriety, be called angiomata.” This is followed by proliferation of
the neuroglia, compression and destruction of nerve-tissue, and
deposit of the calcareous salts especially about and upon the coats of
the vessels. This case illustrates in the simplest manner the
formation of both vascular and sand tumors.

[Footnote 34: _The Medical News_, April 24, 1886, p. 460.]

Pacchionian bodies are very common in the brain, and are really small
fibromata. They may form true tumors (Cornil and Ranvier) capable of
wearing away the bones of the cranium. In fact, even when small they
may have corresponding indentations in the skull. They are not to be
mistaken for tubercle. Clouston[35] has described excrescences from
the white matter of the brain, growing through the convolutions,
projecting through the dura mater, and indenting the inner table of
the skull; which new growths he calls hernia of the brain through the
dura. We have not seen such a condition described elsewhere, and think
that we have here probably Pacchionian bodies growing from the pia
mater. They were found in a case of tumor of the cerebellum.

[Footnote 35: _Journ. Ment. Sci._, xviii. p. 153.]

A cystic formation, constituting a veritable tumor, not unfrequently
occurs in the pituitary body and mounts into the third and lateral
ventricles. Echinococci and hydatids also occur, and have the same
natural history as these parasitic offspring have when found in other
parts of the human body.

Obernier refers to an enchondrosis of the basilar process. Our table
presents one case of enchondroma.

Some of the gross appearances found on autopsies of tumors of the
brain are worthy of note. Often an area of congestion or inflammation,
especially of the membranes, is seen about the new growth, and the
brain-substance in its immediate vicinity is much more frequently
softened. The cerebro-spinal fluid is increased, and, especially when
direct pressure has been exerted upon the veins of Galen, are found
distended lateral ventricles. When a tumor does not approach the
surface, but has attained some size, the hemisphere in which it is
located often has a bulging appearance, crowding over upon its
neighbor, and the convolutions are flattened by the pressure. The
cranial nerve-trunks are occasionally involved in or stretched by the
tumor, and also occasionally the bones of the vault or base of the
cranium are extensively eroded. This happens especially in cancer and
osteo-sarcoma.

A few remarks should be made about the methods of making post-mortem
examinations and the gross appearances and conditions likely to be
found in brain-tumor cases. As not a few intracranial tumors are
connected with the bone or with the dura mater, the latter being
adherent to the skull-cap in some positions because of inflammation
arising from the seat of the growth, especial care should be taken in
removing the calvarium. Examination of the external surface of the
dura mater will sometimes reveal the presence of a growth beneath or
incorporated with this membrane. The dura mater should not be roughly
dragged from the surface of the brain, but should be carefully removed
by a {1051} process of partial dissection. During this process a
meningeal growth will sometimes be found growing apparently from the
fused membrane. In such cases it is usually better to so proceed as
not to entirely separate the outer membrane from the growth. Indeed,
this cannot be done sometimes without injury directly to the specimen,
and especially to its cerebral surroundings. The dura mater having
been removed, a marked opacity, sometimes a dirty-brown hue shading
off into a lighter color, will indicate to the eye the probable
presence of a tumor beneath and growing from the pia mater of the
cortex. In such a case, and even when no such appearance is present,
but a tumor is suspected, the fingers passed carefully over the
cerebral surface will feel a hard, and it may be nodulated, mass at
some position. A growth, having been located in this way, should not
be roughly handled or at once examined by section. An effort should be
made to accurately localize it, not only with reference to lobes, but
also with reference to convolutions and fissures, and even special
portions of these. This is best done, after a thorough examination has
been made of the pia mater, by carefully stripping the pia mater from
the brain, beginning at points some distance from the growth and
gradually approaching it, and leaving the pia mater for a short
distance around the growth connected with it. The location having been
fixed and other portions of the brain having been examined, if it is
not possible or desirable to retain the entire brain as a specimen, a
block should be removed embracing a considerable portion of healthy
brain-tissue on all sides of the tumor. In order to study the gross
internal appearance of the tumor, it is a good plan to make a clean
section through the middle of the tumor. From each side of this cut
fragments can be taken for microscopical examination without deranging
appreciably the size and appearance of the tumor.

When the tumor is not meningeal or cortical, or not situated at the
base or floor of the skull, its presence may be revealed, when it is
in centrum ovale and of considerable size, by either hardness or
fluctuation of the hemisphere in which it is located, this fluctuation
not being due to the tumor itself so much as to the breakdown of
tissue around it. Large sections in known positions with reference to
convolutions and ganglia should be made when examined for tumors
deeply situated. If possible, sections close to and just before and
behind the growth should be made, so as to assist in the accurate
localization.

Small tumors are not infrequently overlooked by careless observers,
and even growths of considerable size have escaped discovery by one
examiner to be found by another. Tumors in certain special localities,
as between the temporo-occipital lobe and the superior surface of the
cerebellum in the great longitudinal fissure, or small growths in the
substance of the cerebellum or deep in the Sylvian fissure, are more
likely than others to be passed by, although this, of course, is not
likely to occur when the examination is made by a competent or careful
physician.

DIAGNOSIS.—The diagnosis of the existence of an intracranial tumor, as
a rule, is not difficult. It can be made with greater certainty than
that of almost any other serious encephalic disease.

It is sometimes important to decide as to the nature of an
intracranial neoplasm, particularly whether or not it is syphilitic.
Little is to be gained by following the plan adopted by some
physicians, of treating all cases as if they were due to syphilis, on
the principle that these {1052} are the only forms of tumor which can
be reached by treatment. The pitiable condition of such patients is
sometimes thus made worse. In every case careful and persistent
efforts should be made to obtain an authentic previous history from
the patient. Whenever possible the physician should search directly
for the physical evidences of the former existence of syphilis—for
cicatrices on the genitals and elsewhere, for nodes and depressions,
for post-cervical and other swellings, etc. A history of previous
disease of the throat and of pains in bones and nerves, of
epileptiform attacks, of headache, and eye symptoms which have
disappeared under treatment, should be sought out. It is not well to
give too much credence to the stories of patients, who are not always
willing to admit their past lapses from virtue; but, on the other
hand, the plan of suspecting everybody who presents advanced cerebral
symptoms is often a grievous wrong. Not infrequently external cranial
nodes are present in cases of intracranial syphilis.

Carcinomata and sarcomata, particularly the former, are comparatively
rapid in their progress. They sometimes involve the bones of the
skull, even to the extent of perforation.

The existence of an inherited tendency and of tuberculosis in other
organs, with the special phenomena of general tuberculosis, assists in
the diagnosis of tubercular tumors.

The frequent occurrence of gliomata in early life, and the
comparatively frequent absence of severe irritative symptoms, with the
well-preserved general nutrition of the patient, speak for these
growths.

Cerebral abscess is, on the whole, more difficult to diagnosticate
from intracranial tumor than any other affection. Abscess, however,
more frequently than tumor, can be traced directly to a traumatism. It
is often associated with disease of the internal ear. Obernier speaks
of the headache of cerebral abscess as slight, but this does not
correspond with usual experience. Headache, on the whole, may be
oftener absent or less agonizing in abscess than in tumor, but it is
frequently present, and sometimes of great severity. Its greater
mildness in a few cases is to be explained by the fact that abscess
does not produce so much pressure within the intracranial cavity, and
does not so frequently cause irritation of the branches of the
trigeminus in the dura. Undoubtedly, the symptoms of abscess often
remain for a long time comparatively latent, with then a sudden
outburst of violent symptoms. The course of brain tumor is more
uniformly and steadily progressive, and febrile phenomena, the results
of pyæmia, are of more frequent occurrence in abscess than in tumor.

In old cases of tumor it is sometimes necessary to differentiate
between it and the results of various forms of apoplexy, such as
hemorrhage, thrombosis, and embolism. Cerebral hemorrhage, embolism,
or thrombosis leaves a condition of paralysis, sometimes with, but
usually without, accompanying spasm or convulsion, which simulates
closely the paralysis and other permanent conditions of cases of tumor
occurring in the same cerebral locality. In these cases, in the first
place, the history of the disease will throw considerable light upon
the diagnosis. In both hemorrhage and embolism the history is usually
one of a sudden attack without special premonitory symptoms.
Hemorrhage gives usually a precedent history of diseased kidneys,
hypertrophied heart, or {1053} atheromatous blood-vessels, and occurs
generally in advanced life; embolism, a history of rheumatism and
valvular disease of the heart, occurring at any period of life, early
or late. In brain tumor the previous history is usually one of
traumatism, of constitutional infection, or of a special predisposing
diathesis. Blows and falls upon the head are common antecedents, or a
history of syphilis, tuberculosis, scrofula, or cancer is present.
Tumor, like embolism and unlike hemorrhage, may occur at any time of
life. While slight or dull headache, with more or less vertigo, may be
present in cases of hemorrhage and thrombosis, the severe and often
agonizing headache, with vomiting and serious vertiginous attacks,
which precedes the paralytic or other phenomena of tumor, is a much
more conclusive symptom in the latter cases than in the former. Choked
discs and optic neuritis are much more likely to occur in tumor than
in the other affections.

Brain tumor must sometimes be diagnosticated from the head symptoms of
some form of Bright's disease. A case not long since presented itself
to one of us with a history of having suffered at frequent intervals
for two years with headache of gradually increasing severity. Dimness
of vision and slight temporary œdema of the feet, circumscribed and
painful swellings along the lymphatics of the thighs and legs, with
some mental irritability, were other marked symptoms. The patient had
been attended by several physicians of prominence, one of whom had
diagnosticated tumor of the brain. The violent, apparently agonizing
headache, with the diminution of vision, and the absence of marked
symptoms indicating other organic disease, made the diagnosis of a
growth in some non-excitable region of the cerebrum most probable.
Examination of the urine showed no albumen. Careful examination of the
eye-ground with the ophthalmoscope, however, revealed the appearances
of retinitis albuminurica. Under a treatment directed to the relief of
chronic nephritis the patient's headache and other symptoms improved.

It must not be forgotten just here, however, that, on the one hand,
ophthalmoscopic appearances very similar to those of albuminuric
retinitis are sometimes present in rare cases of brain tumor, and also
in other constitutional disorders, such as leukæmia; and, on the other
hand, that, as stated by Norris,[36] exceptional forms of albuminuric
retinitis have been reported where the only change seen in the fundus
oculi was pronounced choking of the disc.

[Footnote 36: _Op. cit._]

Intracranial tumors must be diagnosticated from meningitis in its
various forms. In children tubercular meningitis sometimes closely
simulates brain tumor. Tumors of the brain are comparatively rare in
children, but, as has already been shown, gliomata and other tumors do
sometimes occur in early life. The course of tubercular meningitis,
whether in children or in adults, differs from that of brain tumor. It
is more irregular in its method of advance, or if it shows the
regularity which is sometimes present, and which has led authors to
subdivide it into three more or less completely separable stages, the
symptoms of these stages do not correspond with any closeness to those
of the initial, middle, and terminal periods of brain tumor, as
already given. Headache is usually present in both affections,
although the absence of headache in some cases of gliomata in children
must be here borne in {1054} mind. When headache is present in
tubercular meningitis, it is less likely to be localized, and, on the
whole, it is not so severe as the terrible torture of the neoplasm.
Irregular but very decided febrile phenomena are more likely to be
present in meningitis than in tumor. Like brain tumor, tubercular
meningitis of the convexity may give psychical disturbances, palsies,
local spasms, general convulsions, sensory disturbances, peculiar
disorders of the special senses, etc.; but these symptoms in the
former usually come on more irregularly and are accompanied less
frequently with paroxysmal exacerbations of headache, vomiting,
vertigo, etc. Tubercular meningitis of the base can be more readily
distinguished from cases of tumor by the fact that one cranial nerve
after another is likely to become involved in the diffusing
inflammatory process. Tubercular meningitis is of shorter duration
than the majority of cases of brain tumor, and in it delirium and
mental confusion come on more frequently and earlier. A history and
physical evidences of more or less generalized tuberculosis favor the
diagnosis of tubercular meningitis. In both affections the
ophthalmoscope may reveal choked disc or descending neuritis. It will
be seen that the differentiation between the affections is not always
very clear, although in some cases the decision may be quickly reached
from a study of the points here suggested.

Some of the forms of chronic hydrocephalus are difficult to
distinguish from tumors, especially gliomata. In hydrocephalus, when
not the result of, or not accompanied by, tubercular meningitis, the
disease advances more slowly and with less irritative symptoms than in
cases of tumor. Headache, vertigo, vomiting, and the other symptoms of
meningeal irritation are not so frequently present, although the
ophthalmoscopic appearances are often the same.

Rosenthal speaks of the necessity of diagnosticating brain tumor from
the chronic cerebral softening of Durand-Fardel, from acquired
cerebral atrophy, and the cerebral hypertrophy of children. An
elementary knowledge of the general symptomatology of intracranial
tumors will, however, be sufficient to prevent mistakes of
differentiation in these cases. Neither of these affections presents
the violent paroxysmal symptoms, the affections of the special senses,
or the severe motor and sensory phenomena of intracranial growths.

Acute mania and paretic dementia are sometimes confounded with
intracranial growths. A case of brain tumor is more likely to be
regarded as one of acute mania than the reverse. In some comparatively
rare instances in the course of their sufferings the cases of tumor
become maniacal, but even a superficial study of general
symptomatology in such a case will be sufficient to clear up the
doubt.

Paretic dements are occasionally supposed to be cases of brain tumor,
because of the epileptiform attacks and isolated pareses which occur
as the disorder progresses. It is only necessary to refer to this
matter, as the mistake would not be likely to be made by one having
any familiarity with dementia paralytica.

L. J. Lautenbach, in a recent communication to the Philadelphia
Neurological Society, which embodied a large number of ophthalmoscopic
examinations of the insane at the State Insane Hospital, Norristown,
Pennsylvania, and the Insane Department of the Philadelphia Hospital,
and also the results of the investigations of the fundus of the eye in
{1055} cases of insanity by other observers, showed that about 16 per
cent. of cases of acute mania presented well-defined papillitis—a
condition which he described as one of swelling and suffusion of the
disc, corresponding to cases reported as choked disc, descending
neuritis, and severe congestion of the optic nerve. No reports of
post-mortem examinations were made of these cases, but they did not
present the clinical history of meningitis or brain tumor. It
therefore follows that the existence of papillitis in a case of acute
mania does not necessarily point to a gross lesion, such as tumor or
meningitis.

In the early stage of posterior spinal sclerosis some of the symptoms
of the initial or middle stage of intracranial growths in certain
positions are likely to be present; more particularly, such eye
symptoms as diplopia from deficiency or paresis of the ocular muscles
and disorders of the bladder may mislead. In posterior spinal
sclerosis, however, some at least of the pathognomonic symptoms of
locomotor ataxia, such as lancinating pains, absent knee-jerk, or
Argyle-Robertson pupil, will almost invariably be present. Those
tumors of the cerebellum, pons, tubercular quadrigemina, etc. which
give rise to ataxic manifestations are usually readily discriminated
from posterior spinal sclerosis by the headache, vomiting, and other
general symptoms of brain tumor, which rarely occur in ataxia. It is
far more difficult to separate non-irritative lesions of certain
cerebellar and adjoining regions from the spinal disorder.

Strange to say, one of the most frequent mistakes of diagnosis is that
which arises from confounding brain tumor with grave hysteria. In
several of our tabulated cases the patients at different periods of
the disease and by various physicians had been set down as suffering
from hysteria. One of Hughes-Bennett's cases (Case 30), a wayward,
hysterical girl of neurotic family, had had her case diagnosticated as
hysteria by one of the highest medical authorities of Europe, and yet
after death a tumor the size of a hen's egg was found in the cerebrum.
In a case reported by Eskridge (Case 76) hysterical excitement and
special hysterical manifestations were of frequent occurrence, and
misled her physicians for a time. Eskridge remarks, in the detailed
report of this case, that to such a degree was the emotional faculty
manifest that had no ocular lesion been present there would have been
great danger of mistaking the case for one of pure hysteria; and,
indeed, a careful physician of many years' experience, not knowing the
condition of the eyes, pronounced the woman's condition to be
pregnancy complicated by hysteria. A close study of such objective
phenomena as choked discs and paralysis will usually be of the most
value.

Even malaria has been confounded in diagnosis with brain tumor.
Holt[37] reports a case which presented the history of a fever, at
first periodical, with marked splenic enlargement, great muscular
soreness, and incomplete paralysis, which was diagnosticated to be
chronic malarial poison. The patient for a time improved under
quinine, but eventually grew worse, and on an autopsy a glioma-sarcoma
was found on the inferior surface of the cerebellum. Several years
since a physician about fifty years of age was brought to one of us
for consultation, and in his case a similar mistake had been made. The
case was a clear one of {1056} tumor, probably cerebellar, with
headache, neuritis, vertigo, and other general symptoms, which pointed
to an organic lesion. This patient, who came from a malarial district
in the West, had doctored himself, and had been treated by others with
enormous doses of quinine and arsenic.

[Footnote 37: _Med. Record_, March 1, 1883.]

LOCAL DIAGNOSIS.—Niemeyer would hardly say to-day that the brilliant
diagnoses where the precise location of a tumor is fully confirmed by
autopsy are not usually due to the acumen of the observer, but are
cases of lucky diagnosis. It can be asserted with confidence that the
exact situation of a tumor can be indicated during life in at least
two or three locations. Great caution should be exercised, as insisted
upon by Nothnagel,[38] in the localization of tumors of the brain,
because, among other reasons, of the frequent polypus-like extension
of such tumors.

[Footnote 38: _Wien. Med. Bl._, 1, 1882.]

The subject of local diagnosis can be approached in several ways,
according to the method of subdividing the brain into regions. Thus,
Rosenthal discusses, in the first place, tumors of the convexity of
the brain, but as this is a very general term, covering portions of
several lobes, we can see no advantage in making such a subdivision.

A few general remarks might be made in the first place, however, with
regard to the general symptoms presented by surface or cortical
growths as compared with those which are produced by deep-seated
neoplasms. The direct or indirect involvement of the membranes in
nearly all cortical tumors makes the symptoms of irritation referable
to these envelopes very numerous and important.

The various centres so called, motor, sensory, and of the special
senses, which have their highest differentiation in the cerebral
cortex, are each and all represented by well-defined tracts of white
matter in the centrum ovale and capsules which connect these centres
with the lower brain, the spinal cord, and the periphery of the
organism. It therefore follows that symptoms produced by localized
lesions of the cortex will be reproduced in other cases by those of
the tracts which go to or come from these centres. We may thus have a
monoplegia or a hemiplegia, a partial anæsthesia or a hemianæsthesia,
a hemianopsia, a word-blindness or word-deafness, a loss of power to
perceive odors or to appreciate gustatory sensations, from a
peculiarly limited tumor or other lesions of either the gray centres
of the cortex or of the white matter of the central area of the brain;
but these specialized symptoms are more likely to arise from cortical
lesions in the case of intracranial neoplasms, because of the much
greater frequency with which these adventitious products arise from
membranes and therefore involve the cortex.

Peculiar symptoms arise in the case of lesions of the centrum ovale
from the fact that it contains not only projection-fibres which more
or less directly connect cerebral centres with the outer world; but
also a system of commissural fibres which unite corresponding regions
of the two cerebral hemispheres by way of the corpus callosum and
commissures, and a system of association-fibres which connect
different convolutions together, in special cases even those which are
situated remotely from each other, but are associated in function.

It is evident, therefore, as asserted by Starr,[39] that a peculiar
set of additional symptoms will be referable to the destruction or
irritation of these commissural and association fibres. For example,
failure to {1057} perform easily corresponding bilateral motions in
face, hands, or feet would indicate some obstruction to conduction in
the commissural fibres joining the motor convolutions. “Integrity of
both occipital lobes, and simultaneous, connected, and harmonious
action in both, are necessary to the perfect perception of the whole
of any object when the eyes are fixed upon one point of that object.”
Starr gives the following examples of the methods of detecting a
lesion of such fibres: “In the case of the fibres associating the
auditory with the motor speech-area the symptoms to be elicited seem
to be very simple. Can the patient talk correctly? Can he repeat at
once a word spoken to him? These are the questions which any one will
ask who examines a case of aphasia. But this is not all. The patient
must be further questioned. Can he read understandingly to himself,
and tell what he has read? This will test the occipito-temporal tract.
Can he read aloud? This will test the occipito-temporo-frontal tract.
Can he write what he sees? This will test his occipito-central tract.
Can he write what he hears? This will test the temporo-central tract.
Can he write what he says, speaking to himself in a whisper? This will
test his fronto-central tract. Can he name an odor or a color? Brill
has recorded[40] a case of lesion of the cuneus associated with
color-blindness to green, and he states that the patient had
difficulty in naming various colors on account of the presence of a
slight degree of amnesic aphasia.... Can the patient write the name of
an odor? Can he tell how a surface feels—smooth, or warm, or heavy?
Such questions as these will suggest themselves at once to any one who
studies the association of ideas subjectively.

“Take as an example a lesion in the centrum ovale of the
occipito-temporal region. Such a lesion will produce hemianopsia,
because it involves the visual tract of the projection system. It may
also produce a peculiar mental condition known as word-blindness, in
which the patient is no longer able to associate a word or letter seen
with its corresponding sound or with the motion necessary to write it.
Charcot has reported a case of this kind.... The man, who was a very
intelligent merchant, was suddenly seized with right hemianopsia while
playing billiards, and was surprised to find that he saw but one-half
of the ball and of the table. Soon after he had occasion to write a
letter, and after writing it was surprised to find that he could not
read what he had just written. He found, however, that on tracing
individual letters with the pen or fingers he became conscious of the
letters—a few letters (_r_, _s_, _t_, _x_, _y_, _z_), however, being
an exception to this rule. When a book was given him to read he would
trace out the forms of the letters with some rapidity, and thus manage
to make out the words. If his hands were put behind him and he was
asked to read, he would still be observed to put his fingers in motion
and trace the letters in the air. Speech was in no way interfered
with, but reading aloud was only accomplished, like reading to
himself, by the aid of muscular sense. Here, then, was an example of a
lesion which had separated entirely the tract associating sight with
speech—viz. the occipito-temporal tract—but had left intact the tract
associating sight with muscular sense—viz. the occipito-central
tract.”

[Footnote 39: _Med. Record_, vol. xxix. No. 7, Feb. 13, 1886.]

[Footnote 40: _Amer. Journ. of Neurology_, Feb., 1883.]

Our tabulated cases, although collected for the purpose of studying
inductively the phenomena of intracranial tumors from all points of
view, {1058} have been arranged to indicate, so far as is possible,
the special symptoms which are produced by growths in special
localities. Thus we have made thirteen subdivisions:

I. Superior antero-frontal region (5 cases).—The lateral and median
aspects of the hemisphere from the anterior tip backward to the
posterior thirds of the first three frontal convolutions, the region
roughly bounded by the coronal suture.

II. Inferior antero-frontal or orbital region (5 cases).—From the
anterior tip of hemisphere at the base backward to the optic chiasm
and Sylvian fissures.

III. Rolandic region or motor cortex (15 cases).—From antero-frontal
region backward nearly to mid-parietal lobe, including posterior
thirds of superior middle and inferior frontal convolutions, ascending
frontal and ascending parietal convolutions, and anterior extremities
of superior and inferior parietal convolutions—lateral and median
aspects.

IV. Centrum ovale, fronto-parietal region (5 cases).

V. Postero-parietal region (5 cases).—From Rolandic region to
parieto-occipital fissure, including posterior two-thirds of the
superior and inferior parietal convolutions and the præcuneus.

VI. Occipital region (9 cases).—Occipital lobe—cortex and centrum
ovale.

VII. Temporo-sphenoidal region (4 cases).—Temporo-sphenoidal lobe.

VIII. Basal ganglia and adjoining regions (19 cases).—Caudate nucleus,
lenticular nucleus, optic thalamus, internal capsule, corpora
quadrigemina, and ventricles except the fourth.

IX. Cerebellum (9 cases).

X. Floor of fourth ventricle (6 cases).—(Directly or indirectly
involved.)

XI. Pons varolii and medulla oblongata (8 cases).

XII. Crura cerebri (3 cases).

XIII. Middle region of base of brain and floor of skull (7 cases).—In
the main, from optic chiasm backward to pons, in the middle basilar
region, in some instances extending beyond this area in special
directions.

Tumors of the antero-frontal regions can be diagnosticated with
considerable certainty, partly by a study of the actual symptoms
observed and partly by a process of exclusion. Headache of the usual
type, vertigo, choked discs, inflammatory and trophic affections of
the eyes, widely varying body-temperature, and high head-temperature
are among the most positive manifestations. Mental slowness and
uncertainty seem to be greater in these cases than in others. Mental
disturbance of a peculiar character unquestionably occurs in cases of
tumor, as of other lesions, in this region. This disturbance is
exhibited chiefly in some peculiarity of character, showing want of
control or want of attention. The speech-defects present in a number
of cases were rather due to the change in mental condition than to any
involvement of speech-centres. Under Symptomatology has been given in
some detail a study of the psychical condition in one case of
antero-frontal tumor. The absence of true paralysis and of anæsthesia
is characteristic. Nystagmus and spasm in the muscles of the neck and
forearm were present in one instance, but usually marked spasm is not
to be expected. Vomiting is less frequent than in tumors situated
farther back. Facial and other forms of paresis occasionally are
present, but are not marked, and are probably due to involvement
{1059} by pressure or destruction of surrounding tissue of neighboring
motor areas. Hemianopsia, such as was observed in Case 10, showed
involvement of the orbital region. Tumors of the inferior
antero-frontal lobe give the same positive and negative
characteristics as those of the superior frontal region, with the
involvement in addition of smell and certain special ocular symptoms,
such as hemianopsia.

Tumors of the motor zone of the cerebral cortex, the region
surrounding and extending for some distance on each side of the
fissure of Rolando, can be diagnosticated with great positiveness: 15
of the 100 cases are examples of tumors of this region, and in many of
these the diagnosis of the location of the growth was accurately made
during life. Localized spasm in peripheral muscles; localized
peripheral paralysis; neuro-retinitis or choked discs; headache; pain
elicited or increased by percussion of the head near the seat of the
tumor; and elevated temperature of the head, particularly in the
region corresponding to the position of the growth,—are the prominent
indications. The spasmodic symptoms usually precede the paralysis in
these cases. The spasm is often local, and generally begins in the
same part in different attacks—in the fingers or toes or face of one
side.

A study of cases of tumor localized to the cortical motor area will
show that in almost any case a local twitching convulsion preceded the
development of paresis or paralysis. Hughlings-Jackson[41] reports a
case of sarcoma, a hard osseous mass on the right side of the head, of
eighteen years' standing, subjacent to which was a tumor the size of a
small orange growing from the dura mater. The patient was a woman aged
forty-nine, whose symptoms were very severe headache and double optic
neuritis, with paresis in left leg, followed by slighter paresis in
left arm and left face. A very slow, gradual hemiplegia came on by
pressure on the cortex without any fit. Jackson says this is the only
case which he has seen in which the hemiplegia has not followed a
convulsion where the lesion has been on the surface. In all very
slowly oncoming hemiplegias which he has seen, except this one, the
tumor was in the motor tract.

[Footnote 41: _Medical Times and Gazette_, London, 1874, vol. i. 152.]

As the white matter of the centrum ovale and capsules represents
simply tracts connecting cerebral centres with lower levels of the
nervous system, with each other, or with the opposite hemisphere,
lesions of this portion of the cerebrum will closely resemble those
cortical lesions to which the tracts are related. We have already
referred to the peculiar symptoms referable to involvement of
commissural and association fibres. Tumors of the centrum ovale of the
fronto-parietal region, of which five examples are reported in the
table, vary in symptomatology according to their exact location. Those
situated in the white matter in close proximity to the ascending
convolutions give symptoms closely resembling those which result from
lesions of the adjoining cortical motor centres. In the cases of
Osler, Seguin, and Pick (Cases 26, 27, 28, 29) spastic symptoms in the
limbs of one side of the body, with or without loss of consciousness,
were marked symptoms. In two of these cases some paresis preceded the
occurrence of the spasms. They did not, however, fully bear out the
idea of Jackson that the hemiparesis or hemiplegia in tumors of the
motor tract comes on slowly before the appearance of spasm.

{1060} Tumors of the postero-parietal region present some
characteristic peculiarities. In several cases tumors were located in
this region, and in several others the white matter of the parietal
lobe was softened as the result of the obliteration of blood-vessels
by the tumors. In general terms, we might say that hemianæsthesia,
partial or complete, and impairment of sight and hearing on the side
opposite to the lesions, seemed to be the most constant peculiarities.

Tumors and other lesions of the occipital lobes have in the last few
years received extended attention, and, where possible, exact study,
because of the opportunities which they furnish for corroborating the
work of the experimental physiologists. It is unfortunate that the
records of older cases do not furnish the exact detail which would
render these tumors among the most important and interesting to be met
with in the brain: some cases have, however, been observed with great
care, and a few such are included in the table. To understand the
special significance of the symptoms of such tumors, it will be well
briefly to state some of the well-established facts about the function
of the occipital cortex. The investigations of Gratiolet and Wernicke
especially have proved that this surface of the brain is in direct
connection with the fibres (1) which are continued upward from the
posterior or sensory columns of the cord through the posterior portion
of the internal capsule, and (2) with the expansion of the optic
nerve, or the tract which passes, according to Wernicke, from the
thalamus to the occipital lobe. There is but a partial decussation of
the optic nerves at the chiasm, so that each half of the brain
receives fibres from both eyes. This arrangement is best stated by
Munk (quoted by Starr) as follows: “Each occipital lobe is in
functional relation with both eyes in such a manner that corresponding
halves of both retinal areas are projected upon the cortex of the lobe
of the like-named side; _e.g._ destruction of the left lobe produces
loss of function of the left halves of both retinæ.” This, of course,
causes the right halves of both fields of vision to appear black. This
condition is known as lateral homonymous hemianopsia, and was
exhibited in several of the tabulated cases (Cases 40, 41, 42, and
43). It is probable that the dimness of the right eye recorded in Case
38 was really right lateral hemianopsia, as patients mistake this
condition for blindness of that eye alone which is on the side upon
which the visual fields are blank. It follows that this condition of
the eyes will be caused by a destructive unilateral lesion at any
point upon the optic tract behind the chiasm; and its exact nature and
location are to be inferred from other corroborating symptoms. Among
these corroborating symptoms, as will be inferred from the other
functions of the occipital cortex, is especially to be considered
partial hemiplegia and partial hemianæsthesia. This was observed in
Cases 38, 40. These most characteristic localizing symptoms of
occipital tumor have usually others, which, if not of such special
importance, yet help to form a special complexus. Among these diffused
headache is referred to by some writers as characteristic, but it
seems to us that a localized headache, with pain on percussion over
the affected region, is the only kind in this as in other regions
which could have special diagnostic importance. Affections of hearing
are recorded by some. It is not at all uncommon to have an incomplete
hemiplegia and local paralysis. In Case 41 complete hemiplegia with
facial paralysis is recorded. Local palsies, ocular and facial, {1061}
are recorded in Cases 36, 37, 38, and 39. It is doubtless by
transmitted pressure, or by extension of the tumor, or the softening
caused by it, toward the motor fibres, that these more or less
incomplete paralyses are caused. The general symptoms, such as
vertigo, vomiting, and convulsions, are frequently present with tumors
of the occipital lobes. We are at a loss to know upon what data of
theory or experience Rosenthal bases his statement that psychic
disorders are more common in occipital tumors than in those of the
anterior and middle lobes, unless he refers simply to the hebetude and
late coma which seem to come generally in these cases.

Tumors of the temporo-sphenoidal region, so far as we have been able
to study them, present few characteristic features. Physiology seems
to point to the upper temporal convolutions as the cerebral centres
for hearing; thus, according to Starr,[42] “disturbances of hearing,
either actual deafness in one ear or hallucinations of sound on one
side (voices, music, etc.), may indicate disease in the first temporal
convolution of the opposite side. Failure to recognize or remember
spoken language is characteristic of disease in the first temporal
convolution of the left side in right-handed persons, and of the right
side in left-handed persons. Failure to recognize written or printed
language has accompanied the disease of the angular gyrus at the
junction of the temporal and occipital regions of the left side in
three foreign and one American case.” In two of our four cases of
tumor in the temporo-sphenoidal region disturbances of hearing were
noted, but in none was the sense studied with sufficient care to throw
any light upon the actual character of the disorder. The case of Allan
McLane Hamilton (Case 47), already referred to under Symptomatology,
was interesting because of the presence of a peculiar aura connected
with the sense of smell. Stupidity, want of energy, drowsiness, and
general mental failure were marked in tumors of this region.

[Footnote 42: _American Med. Sci._, N. S. vol. lxxxviii., July, 1884.]

Tumors of the motor ganglia of the brain are seldom strictly localized
to one or the other of these bodies. Growths occurring in this region
usually involve one or more of the ganglia and adjacent tracts, and
can only be localized by a process of careful exclusion, assisted
perhaps by a few special symptoms. Paralysis or paresis on the side
opposite to the lesion usually occurs in cases of tumor of either the
caudate nucleus or lenticular nucleus; but whether this symptom is due
to the destruction of the ganglia themselves, or to destruction of or
pressure upon the adjoining capsule, has not yet been clearly
determined. In a case of long-standing osteoma of the left corpus
striatum (Case 49) the patient exhibited the appearance of an atrophic
hemiplegia: his arm and leg, which had been contractured since
childhood, were atrophied and shortened, marked bone-changes having
occurred. Another case showed only paresis of the face of the opposite
side. Clonic spasms were present in two cases, in one being chiefly
confined to the upper extremities of the face. In this case paralysis
was absent. Disturbances of intellect and speech have been observed in
tumors of this region. According to Rosenthal, aphasic disturbances of
speech must be due to lesions of those fibres which enter the
lenticular nucleus from the cortex of the island of Reil.

Tumors of the optic thalamus usually cause anæsthesia or other {1062}
disturbances of sensation in the extremities of the opposite side.
They sometimes show third-nerve palsies of the same side in
association with hemiplegia on the opposite side, these symptoms being
probably due to pressure owing to the proximity of the neighboring
cerebral crus. Speech and gait in such tumors are also often affected.

Tumors of the corpora quadrigemina give rise to disturbances of sight
and special ocular symptoms, such as difficulty in the lateral
movement of the eyes. Spasms were usually present. Automatic
repetition of words was observed in one case, nystagmus in another,
and diminished sexual inclinations in a third. In other cases peculiar
ataxic movements or a tendency to move backward were noted; other
symptoms, such as spasm, vomiting, headache, were general phenomena of
intracranial tumors; still others, such as hemiplegia, hemiparesis, or
anæsthesia, were probably simply due to the position of the growth in
the neighborhood of motor ganglia and tracts.

Tumors of the cerebellum have some special symptoms, which also derive
importance from their characteristic grouping. The symptoms which
depend upon the lesion in the organ must be distinguished from those
which are caused by pressure upon adjacent parts, although these
latter symptoms are very important as corroborative evidence of the
location. Among the special symptoms is occipital headache (often not
present), especially when the pain is increased by percussion about
the occiput or by pressure upon the upper part of the neck. In these
cases weakness of the gait (Case 75) and other motor phenomena, which
are usually described as inco-ordination, are of comparatively
frequent occurrence. They are not so much true inco-ordination as
tremor of the limbs, rotation (which is usually only partial), and the
so-called movements of manége. These movements were present in
one-third of the cases collected by Leven and Oliver (quoted by
Rosenthal). Staggering gait is also present, and may be dependent upon
the vertigo, which is apt to be unusually intense in this kind of
intracranial tumor (Cases 69 and 71). The symptoms caused by pressure
of cerebellar tumors upon adjacent organs are of importance, because
in conjunction with the special symptoms they acquire unusual
significance. Sight and hearing are the two special senses apt to be
affected, because of pressure upon the geniculate bodies and upon the
auditory nerve or its nucleus. Descending optic neuritis, progressing
to total blindness, and varied forms of oculo-motor paralysis may be
present. Strabismus convergens has been said to be a symptom, caused
by the paralysis of the sixth nerve. A hemiplegia and hemianæsthesia
result sometimes from pressure upon the tracts in the pons or medulla.
Continued pressure upon the medulla may eventually, toward the
termination of the case, according to Rosenthal, cause disorders of
the pulse and of respiration and deglutition. This author gives
absence of psychical symptoms as negative evidence which counts for
tumors of the cerebellum, but our table shows several instances (Cases
70, 71, 74, and 76) in which were present hebetude, incoherence, or
hysteroidal symptoms. It is probable, however, that such symptoms are
not as common and distinct as in tumors of the cerebrum.

Certain symptoms—or, better, groups of symptoms—characterize tumors of
the pons varolii, and serve to render the local diagnosis
comparatively certain. These depend upon the fact that the pons
combines in itself, or {1063} has on its immediate borders,
nerve-tracts, both motor and sensory, in great complexity, from or to
almost every special or general region of the body. Among these
symptoms may especially be mentioned alternating and crossed
hemiplegia, paralysis of eye-muscles (strabismus), paresis of tongue,
dysphagia, anæsthesia (sometimes of the crossed type), and painful
affections of the trigeminus. Vaso-motor disturbances have also been
noted. In one case persistent and uncontrollable epistaxis hastened
the fatal termination of the case.

Conjugate deviation of the eyes, with rotation of the head, as stated
under Symptomatology, is a condition often present in tumors of the
pons varolii as well as in the early stages of apoplectic attacks. A
paper[43] has been published by one of us on a case of tumor of the
pons, and from it we will give some discussion of this subject.

[Footnote 43: _Journal of Nervous and Mental Disease_, July, 1881;
Case 84 of Table.]

Vulpian was probably the first to study thoroughly conjugate
deviation. The sign, when associated with disease of the pons, was
supposed by him and by others to be connected in some way with the
rotatory manifestations exhibited by animals after certain injuries to
the pons. Transverse section across the longitudinal fibres of the
anterior portions of the pons produces, according to Schiff, deviation
of the anterior limbs (as in section of a cerebral peduncle), with
extreme flexion of the body in a horizontal plane toward the opposite
side, and very imperfect movements of the posterior limbs on the other
side. Rotation in a very small circle develops in consequence of this
paralysis.[44] The movements of partial rotation are caused, according
to Schiff, by a partial lesion of the most posterior of the transverse
fibres of the pons, which is followed in animals by rotation of the
cervical vertebræ (with the lateral part of the head directed
downward, the snout directed obliquely upward and to the side).

[Footnote 44: Rosenthal's _Diseases of the Nervous System_, vol. i. p.
125.]

This deviation, both of head and eyes, occurs, however, not only from
lesions of the pons and cerebellar peduncles, but also from disease or
injury of various parts of the cerebrum—of the cortex, centrum ovale,
ganglia, capsules, and cerebral peduncles. It is always a matter of
interest, and sometimes of importance, with reference especially to
prognosis, to determine what is the probable seat of lesion as
indicated by the deviation and rotation.

Lockhart Clarke, Prevost, Brown-Séquard, and Bastian, among others,
have devoted considerable attention to this subject. To Prevost we owe
an interesting memoir. Bastian, in his work on _Paralysis from Brain
Disease_, summarizes the subject up to the date of publication (1875).
Ferrier, Priestly Smith, and Hughlings-Jackson have investigated the
relations which cortical lesions bear to the deviation of the eyes and
head.

It has been pointed out by several of the observers alluded to that
when the lesion is of the cerebrum the deviation is usually toward the
side of the brain affected, and therefore away from the side of the
body which is paralyzed. In a case of ordinary left hemiplegia it is
toward the right; in one of right hemiplegia, toward the left. In
several cases of limited disease of the pons, however, it has been
observed that the deviation has been away from the side of the lesion.
In our case (Case 84) the conjugate deviation was to the right, while
the tumor was entirely {1064} to the left of the median line, thus
carrying out what appears to be the usual rule with reference to
lesions of the pons.

During the life of the patient it was a question whether the case was
not one of oculo-motor monoplegia or monospasm from lesion of cortical
centres. It is probable, as Hughlings-Jackson believes, that ocular
and indeed all other movements are in some way represented in the
cerebral convolutions. In the _British Medical Journal_ for June 2,
1877, Jackson discusses the subject of disorders of ocular movements
from disease of nerve-centres. The right corpus striatum is damaged,
left hemiplegia results, and the eyes and head often turn to the right
for some hours or days. The healthy nervous arrangement for this
lateral movement has been likened by Foville to the arrangement of
reins for driving two horses. What occurs in lateral deviation is
analogous to dropping one rein; the other pulls the heads of both
horses to one side. The lateral deviation shows, according to Jackson,
that after the nerve-fibres of the ocular nerve-trunks have entered
the central nervous system they are probably redistributed into
several centres. The nerve-fibres of the ocular muscles are rearranged
in each cerebral hemisphere in complete ways for particular movements
of both eyeballs. There is no such thing as paralysis of the muscles
supplied by the third nerve or sixth nerve from disease above the crus
cerebri, but the movement for turning the two eyes is represented
still higher than the corpus striatum.

It would seem a plausible theory that we have in this conjugate
deviation of the eyes and head a distinct motor analogue to the
hemianopsia which results from certain lesions high in the optic
tracts. The fact that we never have a distinct oculo-motor monoplegia
from high lesions, but always a lateral deviation of both eyes in the
same direction, suggests that only a partial decussation of the fibres
of the motor nerves of the eyes occurs, and that each hemisphere does
not control the whole motor apparatus of the opposite eye, but half of
this apparatus in each eye.

Alternating hemiplegia, or paralysis of one side of the body followed
by a paralysis of the other side, is observed in tumors of the pons,
and is readily accounted for by the close proximity of the motor
tracts, a lesion which affects one tract first being very likely,
sooner or later, to involve, partially at least, the other, as in Case
84. Cross-paralysis of the face and body may be seen, and like crossed
anæsthesia (seen also in Case 84) depends upon the fact that both
motor and sensory fibres to the limbs do not decussate at the same
level as these fibres to the face. Trigeminal neuralgia, from
involvement of the nerve by pressure or otherwise, is recorded in this
characteristic group of symptoms. The association of the general with
the local paralytic symptoms in the manner stated, the involvement of
sensory functions, and the deviation of the eyes and head serve to
distinguish tumors of the pons from cortical or high cerebral local
lesions. Cases 81, 84, 89, and 90 illustrate these facts in various
ways. Case 82, involving the floor of the fourth ventricle, appears to
be an exception, as the deviation is toward the side of the lesion.

The special localizing symptoms which indicate a tumor of the crus
cerebri are paralysis of the oculo-motor nerve upon the same side as
the tumor, and especially the tendency of this paralysis to pass to
{1065} the other side later in the case; disturbance of the
innervation of the bladder; and involvement of the vaso-motor
functions. In considering these symptoms in detail it becomes very
evident why we have the alternating paralysis of the two oculo-motor
nerves. As this trunk arises from the crus, it is in direct risk of
injury by the neoplasm, and the extension of the new growth even
slightly must later in the case involve its fellow. Therefore a
ptosis, followed by a similar symptom on the other side, or other
third-nerve symptoms passing from one side to the other, with other
characteristic and corroborating symptoms, furnish strong evidence of
this lesion, as in Case 93. Rosenthal refers especially to involvement
of the bladder, as difficulty of micturition, but the three cases in
the table do not present such a symptom. He says that experiments
prove that irritation of the peduncle is followed by contraction of
the bladder, and that it has been shown that lesions of the crus
abolish the influence of the will upon micturition. As this occurs at
all levels of the cord, its occurrence with lesions of the crus is not
to be considered a very distinctive symptom. The involvement of the
vaso-motor functions is one of much interest. Its occurrence is not
recorded in the cases of tumors of the crus included in the table, but
in Case 94 of twin tumors in front of the optic chiasm it is recorded
that profuse perspiration occurred. We believe that the centres for
the vaso-motors are not well determined: they seem to be affected by
various lesions, especially about the base of the brain. Among other
corroborating symptoms may be mentioned rotatory movements and
deviation of the head: these rotatory movements are probably caused by
the action of the sound side not antagonized by the muscles of the
paralyzed side. Lateral deviation of the head is referred to by some.
Partial or complete hemiplegia, with facial paralysis on the side
opposite to the lesion, may occur; whereas the oculo-motor palsy is
seen on the same side as the lesion. Diminution of sensibility happens
on the opposite side, or occasionally pain in the legs, as recorded in
Case 92. It is of interest to note, with Rosenthal, that the reactions
of degeneration are not likely to appear in the facial muscles in this
lesion, as it occurs above the nucleus of that nerve, and thus causes
a true centric paralysis. The absence of psychic symptoms is usually
to be noted.

Tumors anywhere in the middle portion of the base of the brain and
floor of the skull, the region of the origin of the various cranial
nerves, can of course be diagnosticated with comparative ease by a
study of the various forms of paralysis and spasms in the distribution
of these nerves, in connection with other special and general
symptoms. Varieties of alternate hemiplegia are to be looked for, and
also isolated or associated palsies of the oculo-motor, pathetic,
facial, trigeminal, and other cranial nerves. In studying these
palsies it must be borne in mind that although the lesions producing
them are intracranial, the paralyses themselves are peripheral.

In most cases apparent exceptions to the ordinary rules as to
localization are capable of easy explanation; thus, for instance, in a
case of tumor of the occipital lobe (Case 44) numbness and pain were
present in the right arm, although the tumor was situated in the right
hemisphere. The tumor was of considerable size, and may have affected
by pressure the adjoining sensory tracts.

{1066} Hughlings-Jackson[45] reports a case of tubercular tumor, half
the size of a filbert, in the pons under the floor of the fourth
ventricle, in the upper third of the left side. A much smaller nodule
was found in the right half of the pons. This patient, a man
thirty-three years old, had inconstant headache, a gradual incomplete
hemiplegia of the right side, with also paresis of the left masseter
and right lower face. Sensation was diminished in the right arm, leg,
and trunk. The optic discs were normal; the left pupil was smaller
than the right. There was lateral deviation of the eyes to the right.
Diplopia was present in some positions, and one image was always above
the other. Aphasic symptoms were also present. Especial interest
attaches to the fact that the facial paralysis in this case was on the
same side as the hemiplegia, opposite that of the lesion; whereas
usually in lesions of the pons facial paralysis is on the side
opposite the hemiplegia. This is explained by the fact that the tracts
of the facial nerve decussate in the pons below its upper third, and
therefore in this case the lesion caught the nerve-tracts above their
decussation.

[Footnote 45: _Med. Times and Gazette_, London, 1874, p. 6.]

PROGNOSIS.—The prognosis in intracranial tumors is of course usually
in the highest degree unfavorable. The early recognition of the
existence of a tumor syphilitic in origin will enable a comparatively
favorable prognosis to be made. It is far from correct, however, to
suppose that all or a majority of the cases of known syphilitic origin
are likely to have a favorable termination. Amidon[46] puts this
matter very correctly as follows: “Has a destructive lesion occurred?
and if so, where is it located, and what is its extent? Indications of
a destructive lesion should lead one to a cautious prognosis as
regards perfect recovery, while the prognosis for life and a moderate
amount of health may be good. A gummy intracranial or spinal growth,
giving rise to alarming symptoms, may vanish as by magic upon prompt
treatment. The symptoms of these frank, specific growths are, as a
general thing, characteristic and widely different from those of the
more insidious destructive lesions.

“An intracranial gumma often heralds itself by sharp, localized
headache, gradually deepening paralysis, aphasia, epilepsy, and optic
neuritis, while destructive lesions are more apt to have diffuse, dull
headache, stationary or lessening paralysis or aphasia, rarely
epilepsy or optic neuritis. Intraspinal gummata give rise to a painful
paraplegia, while an inflammatory or destructive change gives rise to
various and atypical sensory and motor manifestations.

“As to the pathology of these cases, I can say but little, as such
discussion opens the whole subject of the pathology of syphilis. This
I will say, that, so far as can be told without autopsies, no
permanent pathological condition was present in these cases which
might not have been brought about by other etiological factors which
were often present. The periencephalitis might be caused by alcohol,
mental strain, or excesses; the arterial occlusion might be due to
previous disease not specific.”

[Footnote 46: _Medical News_, vol. xlviii. No. 3, Jan. 16, 1886, p.
64.]

TREATMENT.—The surgical treatment of tumors of the brain has recently
received a great stimulus from the report of a case which {1067}
occurred in the practice of A. Hughes-Bennett of London, and which was
operated on by Rickman J. Godlee. The case has been included in the
table (Case 24), where the symptoms and details of treatment may be
read. This case has served to bring into sharp outline many of the
difficulties and dangers of such an operation on the one hand, and the
few possible and exceptional advantages of it on the other. It must be
apparent, in the present state of knowledge and with the additional
light of this interesting case, that success must largely depend upon
the following conditions: The tumor must be exceptionally
localized—_i.e._ not very large—and non-multiple; it must be cortical,
or at least not very deep-seated; it is also quite essential that it
be in the motor zone, in order to admit of accurate diagnosis. It
would seriously impair the usefulness of the operation and the
prognosis if the case were of long standing with much necrosis of
brain-tissue, or if the growth were malignant and recurring. The
secondary complications, as inflammation and sepsis, are of course
possible in all surgical cases, and may be guarded against, as well in
cerebral as in other surgery. If such a criticism narrows the field
for the operation into almost hopeless limits, it may be reflected
that one or two successful cases are better than a hundred
experimental failures; that cases do occur in which the tumor is just
so localized, single, and superficial; that the urgency of distressing
symptoms, as pain and convulsions, urge the operation for palliation
as well as cure; and that these cases, without relief, are necessarily
fatal, and hence justify large risks.

By exclusion and a careful study of the symptoms we believe it may
become possible hereafter in some cases to localize in two other
accessible regions brain tumors with sufficient accuracy for purposes
of operation: these are the antero-frontal region and the
postero-parietal region.

The case of Bennett and Godlee was a most successful test of
diagnosis, and as a surgical endeavor might have been more successful,
as the operator himself suggests, if more careful antiseptic
precautions had been used. In the discussion of this case before the
Royal Medical and Chirurgical Society[47] it was stated by
Hughlings-Jackson that three indications were of special importance
for this diagnosis: (1) local persisting paralysis; (2) epileptiform
convulsions, those beginning locally; (3) double optic neuritis, which
is diagnostic of tumor as distinguished from a sclerotic patch. It is
probable that permanent palsy would be left after a successful
operation in which the cortical tissue were destroyed, but as this is
compatible with life and comfort, it is not likely that, as an
alternative, it would be rejected by the patient. McEwen's case, also
given in the table (Case 25), is not as accurately reported[48] as
Bennett's, but was partially successful. At the opening over the
Rolandic region false membrane was removed, and an incision made which
let out grumous red-colored fluid: this was followed by a decrease in
the paralysis and improvement in other brain symptoms. It is difficult
to understand why the opening was made in the occipital region. The
necessity for antiseptic measures is to be especially considered in
cerebral surgery. In a recent operation for a case of traumatic
epilepsy, under the care of Mills and White, in the Philadelphia
Hospital, in which quite extensive injury was done to the membranes in
removing fragments of bone, rigid {1068} antisepsis was employed; and
it is not too much to assume that the risks of the operation were much
diminished by it and its success ensured in an old and crowded
hospital building.

[Footnote 47: _Brit. Med. Journ._, May 16, 1885, p. 988.]

[Footnote 48: _Glasg. Med. Journ._, xxi., 1884, p. 142.]

In the medication of tumors of the brain we can unfortunately do but
little more than treat the symptoms and ameliorate the various
conditions as they arise. There is no specific for these growths,
unless the syphilomata be an exception; and experience shows that
specific treatment is usually disappointing even when applied to a
syphilitic brain tumor. The dietetic and hygienic rules laid down by
some are only such as are invariably recommended as routine practice
in all kinds of disease; and it almost seems a mockery to offer them
to a patient with an intracranial tumor with the same gravity and
detail as we suggest them in a curable fever or a hopeful surgical
case. It is possible that local depletion and revulsives, by
controlling irritation and hyperæmia, may be beneficial, though we
should hesitate to add to the sorrows of the patient the action of
tartarized antimony, even, with Obernier, in special cases. Hot or
cold effusions and the ether spray are worthy of mention. Local
applications of the galvanic current might be tried for its catalytic
action, but the observations are too few and the theory too
inapplicable to allow us to attach much importance to the suggestion.
The use of electricity to the limbs for paralytic symptoms certainly
does not promise much in the case of an obstinate neoplasm in the
brain.

Morphia and bromide of potassium are the two drugs which offer the
most promise in these fatal cases. They can often control the most
urgent and frightful symptoms. The headache, the obstinate vomiting,
the epileptic seizures, are all more or less amenable to one or other
of these remedies or a combination of them. Although the vomiting is
of centric origin, it is possible that remedies addressed to the
stomach might occasionally afford relief, just as we apply medicines
to that viscus in reflex irritation, in pregnancy, and in debilitating
diseases. The remedies which suggest themselves are the salts of
bismuth and cerium, the more stimulating wines, as champagne, in small
frequent doses, and cracked ice.

While morphia and bromide of potassium are, on the whole, the most
useful remedies for the relief of pain and irritating symptoms of
brain tumor, other remedies can often be used with great advantage as
adjuvants. Ergot in the form of the solid or fluid extract has a
beneficial influence in relieving the congestive symptoms. Cannabis
indica in the form of the fluid extract in doses of five to ten
minims, or the tincture in doses of fifteen to thirty minims, may be
advantageously combined with morphia and a bromide, or sometimes may
be tried alone. Hyoscyamus, either the fluid extract or tincture, in
somewhat larger doses may also be tried. The great severity of the
headache and the imperative demand, however, will usually compel the
physician to fall back at last upon morphia in large dose by the mouth
or hypodermically.

Leeches to the temples or behind the ears or to the mucous membrane of
the nose, either wet or dry cupping to the back of the neck, and
bladders or compresses of ice, or very hot water, may be used to the
head.

The various serious complications which so often accompany
intracranial tumors should be most carefully managed. Among the most
important of these are such affections as the conjunctivitis and
trophic {1069} corneitis, with anæsthesia, present in a few cases,
usually when the trigeminal is directly or indirectly involved.
Cystitis and pyelitis must be appropriately treated, and patients must
be carefully watched in order to prevent injurious consequences of
over-distension of the bladder or enormous fecal accumulations.

            TABLE OF ONE HUNDRED CASES OF BRAIN TUMOR.

_Superior Antero-frontal Region._

1. Sex and Age: M. 35.

Clinical History: Syphilis and traumatism.

Headache; vertigo; mental slowness; loss of attention; hysterical.
Nystagmus. Tonic spasm of neck and forearm. Movements weak and
uncertain. Explosive speech. Gradual blindness; choked discs.
Conjunctivitis and corneitis of left eye. Anæsthesia of conjunctiva.
Polyphagia. Constipation alternating with involuntary evacuations and
urination. Temperature 97°-101°. Head-temperature above normal;
highest at frontal station; average, 96.5.

Pathology and Location: Fibroma.

Anterior superior half of second frontal and anterior superior and
inner half of first frontal; anterior segment of gyrus fornicatus, and
anterior half inch of corp. callosum.

Remarks: C. K. Mills, _Philada. Med. Times_, Jan. 18, 1879 and _Arch.
of Med._, vol. viii. No. 1, Aug., 1882.

2. Sex and Age: M. 50.

Clinical History: Headache, dizziness, and slight right facial
paralysis. Dimness of vision. Day before death had an attack of
unconsciousness, from which he emerged in half an hour. In two hours
had another attack; became comatose; Cheyne-Stokes respiration;
temperature 102.3°; pulse 150. Reflexes completely abolished.

Pathology and Location: Fibroma.

One and a half inches in diameter in the left antero-frontal lobe,
located so as to involve the middle portions of the first and second
frontal convolutions and white substance beneath them almost to the
orbital surfaces. White matter softened posterior to tumor. Adherent
to pia mater.

Remarks: C. K. Mills. Not before published.

3. Sex and Age: M. 16.

Clinical History: Frontal headache, vertigo, staggering gait toward
right. Later, paresis of sphincter of bladder. Some muscles of right
face paretic. Some weakness of mind: emotional. Choreic movements of
right arm, increased with mental excitement. No deafness, loss of
taste, or of tactile or heat sense. Slight traces of sugar. Blurring
of papilla and hyperæmia of retina. Later, vomiting. Urine sp. gr.
1031. Irritability of mind, with erotic conduct. Reduction of
pulse—54. Progressive emaciation and mental failure. Tremor in both
arms, and in right arm automatic movement. Boil on left hand. Scaphoid
abdomen. Later, temperature below normal; also pulse and respiration.
Right facial paralysis unchanged. Still later, contracture of both
elbows. Pupils react tardily. Apathetic. Very late, small quantity
albumen, no sugar.

Pathology and Location: Glioma.

Frontal convolutions flattened; brain-substance doughy; cortex
gray-red; medullary substance reddish-white. Corpus callosum arched
upward; lateral ventricles enlarged in posterior horns. Tumor in
medullary substance of both frontal lobes, springing from septum and
radiating toward parietal lobes, almost filling both anterior lobes,
and also adhering to walls (apparently) of ventricles. At base
extended backward full extent of frontal lobe.

Remarks: Petrina. _Vierteljahrschr. f. die Prakt. Heilk._, 1 Bd.,
1877, p. 126.

4. Sex and Age: M. 36.

Clinical History: History of injury to the head. Frontal and occipital
headache. Vomiting and giddiness. Memory much affected. Double
internal strabismus with unequal pupils. Double optic neuritis.
Hearing unaffected; sense of smell lost. Lies on back. Stumbles on
trying to walk. Answers questions with difficulty; speech slow and
hesitating. Pain in head, apparently increased by percussion to right
frontal region.

Pathology and Location: Endothelioma.

In right frontal lobe anterior portion. Three inches in diameter.
Surrounded by soft diffluent cerebral tissue. Right frontal bone had
on its internal surface a much greater concavity than the left, and at
its upper and outer part was rough, deeper in color, and thin. Dura
mater adherent.

Remarks: Philipson, _Medical Times and Gazette_, vol. ii., for 1882,
Sept. 16, 1882, p. 355.

{1070} 5. Sex and Age: F. 32.

Clinical History: History of chancre with secondary and tertiary
lesions of syphilis. Frontal node. Constant headache. Epileptiform
convulsions. Marked exophthalmus, with impairment of sight in both
eyes. Improved under iodide of potassium. Grew worse again. Dimness of
vision; pain in head constant, and worse at night. Ophthalmoscope
revealed neuro-retinitis with commencing atrophy of optic nerves.

Pathology and Location: Gumma.

From dura mater into the brain-substance at the anterior portion of
the anterior lobe of the left hemisphere. Brain-substance softened
around tumor. Left ventricle dilated, and filled with fluid.

Remarks: H. Knapp, _Arch. of Ophthalmology and Otology_, vol. iv. p.
245.

_Inferior Antero-frontal or Orbital Region._

6. Sex and Age: M. 27.

Clinical History: Loss of sight, increasing to total blindness.
Gradually increasing loss of hearing, of smell, and of taste, in order
named. No anæsthesia. No paralysis mentioned.

Pathology and Location: Fibro-sarcoma.

Involving inferior portion of right anterior lobe. The first and
second pair of nerves were involved, but no other nerves.

Remarks: L. Howe, _Buffalo Med. and Surg. Journ._, xxi. p. 299.

7. Sex and Age: F. 33.

Clinical History: Paralysis and wasting of right leg since childhood.
Sudden severe general convulsions with loss of consciousness, followed
by paresis of right upper extremity. No facial or ocular paralysis.
Special and general sensibility normal. Recurrent convulsions, both
tonic and clonic. Severe frontal headache; continued paresis of right
arm. Apathetic. Right face partially paretic, and right oculo-motor
weakened.

Pathology and Location: Cholesteatoma.

Growing from pia mater at the base between both frontal lobes,
extending to anterior margin of corpus callosum and to optic chiasm.

Remarks: Petrina, _op. cit._, p. 126.

8. Sex and Age: F. 20.

Clinical History: Vomiting. Loss of sight and hearing; inability to
speak. Somnolence. Pupils widely dilated. Later, all special senses
involved. Tongue protrudes to right. Pulse irregular. Right face
anæsthetic. Neuro-retinitis in both eyes, worse in right; left eye
retained some vision. Hearing and taste perfect; smell impaired. No
paralysis. Pain constant over eyes. No convulsions.

Pathology and Location: Under left anterior lobe and extending from
falx cerebri, to which it was adherent, over the cribriform plate of
the ethmoid, involving left olfactory nerve, backward and diagonally
across the sella turcica to right petrous bone, where the end of it
pressed on fifth nerve of right side at its point of exit. Pressed
upon optic chiasm.

Remarks: E. Williams, _Med. Record_, 1868, pp. 29-31.

9. Sex and Age: M. 49.

Clinical History: Vertigo. Always excessively stupid, allowing himself
to be made a fool of. Violent bleeding from the mouth and nose ten
years before death, followed by nasal discharge. Frontal headache,
especially on left side. Failure of sight. Small tumor in inner upper
angle of left orbit, which dislocates left eye outward; right eye also
deviated outward without any apparent mechanical reason. Pupils
dilated and sluggish. Sight much diminished. Mouth slightly drawn to
one side. Speech slow, but not hesitating. Gave replies to questions
slowly, and did not usually keep to the point, but clothed his answers
in general remarks. A certain amount of self-esteem pervaded his
conversation. Continuous headache. Very late, had convulsions which
began on the left side and extended to the right.

Pathology and Location: Tumor the size of a large walnut to the right
of the middle line, external to the dura mater at a point
corresponding to position of right olfactory bulb. Vitreous table of
the frontal bone and crista galli of the ethmoid completely destroyed.
On the inner side of dura mater another tumor fills the right anterior
fossa and a large portion of the left.

Remarks: Obernier, _Virch. Arch._, vol. xxxvi. p. 155, and _Ziemssen's
Cycl. Pract. of Medicine_, Am. ed., vol. xii. p. 268.

10. Sex and Age: M. —.

Clinical History: Diminution of vision. At first much reduced, without
any ophthalmoscopic changes. Slight headache; loss of appetite;
restless sleep; rapid pulse. Vision sank rapidly until completely
extinguished. Remained thus for nineteen days; then sight began to
return, first in the right eye, and then in the left. Increased, so
that an examination of the eccentric fields could be undertaken; this
showed absence of the external halves of the fields of {1071}
vision—hemianopsia. “The transition of the existing portions of the
fields of vision to the lost portions was effected by a region which,
by a low light, should be reckoned to the latter, so that then the
boundary-line of the defect fell somewhat to the outside of the
fixation-point running in the right eye in a vertical direction, and
in the left diagonally from the inside and above downward and outward.
Within the next four weeks the central vision increased in the right
to V = 1/2, and in the left to V = 1/20, while the defect in the
eccentric vision continued in the way described.”

Patient died of symptoms of acute meningitis.

Pathology and Location: Sarcomata.

Two tumors: one about the size of a pigeon's egg between the optic
trunks in front of the chiasm, surrounded by the optic nerve in a
forked manner, the nerve-fibres being parted by it. A second tumor
situated beneath the pons, raising the dura mater. It had probably
originated in cavernous sinus.

Remarks: Saemisch, _Klin. Monatsblätter_, 1865, p. 51, quoted by
Obernier, _Ziemssen's Cycl. of the Pract. of Medicine_, Am. tr., vol.
xii. p. 269.

_Rolandic Region—Motor Cortex._

11. Sex and Age: F. 38.

Clinical History: History of syphilis. Blows on the head. Headache,
with agonizing paroxysms. Top and right side of head sensitive to
percussion and headache severest in these regions. Vomiting; vertigo.
Great mental irritability. Severe left-sided spasms, beginning with
twitchings in left toes and foot. Partial paralysis of right leg and
arm, most marked in leg. Hyperæsthesia. Impaired sight. Choked discs.
Head-temperature taken once: right parietal region, 97.2° F.; left
parietal region, 96° F.

Pathology and Location: Gumma.

Attached to the fused membranes of the right convexity. Involved the
upper fourth of the ascending frontal and a smaller segment of the
ascending parietal convolution, crossing Rolandic fissure at its upper
extremity. A good example of strictly cortical lesion.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, August, 1882.

12. Sex and Age: F. 30.

Clinical History: No history of causation. Headache continuous,
sometimes agonizing. Percussion of head caused most pain in right
parietal region. Vomiting when headache was most severe. Vertigo. Mind
clear, but acted slowly: emotional. Spasm, beginning with twitching of
fingers of left hand: most severe on left side, and especially in left
arm. Upper as well as lower fibres of left facial nerve partially
paralyzed; nearly complete paralysis of left arm; slight paralysis of
left leg. Bowels and bladder partially paralyzed. Impaired sensibility
in limbs of left side. Left patellar reflex diminished. Sight very
imperfect. Choked discs. Hearing defective in right ear.

Pathology and Location: Carcinoma.

The tumor involved the middle portion of the ascending parietal
convolution and the upper part of the inferior parietal lobule,
pushing aside the interparietal fissure. The anterior extremity of the
tumor was about one-fifth of an inch back of the centre of the fissure
of Rolando. On the inner side of the tumor the white matter of the
brain was broken down. Adherent to the pia mater; the pia and dura
mater were united by strong adhesions.

Remarks: C. K. Mills, reported at the meeting of the American
Neurological Association, June, 1881, _Arch. Med._, vol. viii. No. 1,
Aug., 1882.

13. Sex and Age: M. 31.

Clinical History: Evidences of tuberculosis. Headache continuous, with
severe exacerbations; most severe at vertex. Vertigo. Some
irritability and emotionality; hallucination that some one was going
to come and take him away. Spasm confined to left arm. Partial
paralysis of left arm and leg, and, late in his illness, of left side
of face. Left hemianæsthesia, at first partial, but later complete and
persistent. Sight impaired; right pupil dilated and left contracted
before death. No ophthalmoscopic examination. Hearing defective in
left ear; tinnitus aurium. Head-temperature taken once: right frontal
region, 98° F.; left frontal region, 96.3° F. Cheyne-Stokes breathing
on day of death.

Pathology and Location: Tubercular tumor.

Dura and pia mater adherent over the tumor, which involved the
posterior extremities of first and second frontal and upper thirds of
both ascending convolutions of right hemisphere. Interior of
hemisphere broken down; the parts destroyed included white matter of
the parietal lobe, the posterior third of lenticular nucleus, and the
adjacent portion of internal capsule. Miliary tubercles in pia mater
around and near the tumor.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, Aug., 1882.

{1072} 14. Sex and Age: M. 19.

Clinical History: First symptom, headache; then vertigo. Sudden right
brachial monoplegia; possibly some paresis of leg. Recovered use of
arm; went to work; was kicked by a mule, and became worse. Headache
and right-sided paresis returned. Increasing stupor; paralysis of
right arm complete; of leg almost; right facial paresis; ptosis of
right side. Partial anæsthesia on right side of face; pain on right
side. Slight clonic spasms of right arm. Paralysis of bowels and
bladder in last week. Tendency to Cheyne-Stokes respiration. No
vomiting. Eyes not examined.

Pathology and Location: Gumma.

A large tumor in the ascending frontal convolution, at junction of
middle and upper thirds: one-third of mass on convexity of
convolution, the remainder in fissure of Rolando. Smaller tumor at
inferior angle of right lobe of cerebellum. Some basal meningitis with
effusion.

Remarks: C. K. Mills, _Med. and Surg. Rep._, vol. li., Aug. 2, 1884,
p. 119.

15. Sex and Age: M. 56.

Clinical History: Sickness began with an epileptiform seizure lasting
about ten minutes; flexing movements of right arm. Next day dragged
his right leg slightly. Partial convulsions, without loss of
consciousness, followed, and became very frequent. Two months before
death convulsions ceased, but absolute paralysis of the arm and
paresis of the leg remained. One month later complete palsy of right
half of face occurred. Mind became impaired. Complete aphasia.
Right-sided anæsthesia. Reflexes of right foot less marked than those
of the left. Rectal temperature, 100.4° F. At times deviation of the
head and eyes to the left. Left frontal and temporal regions tender to
pressure. Very late nystagmus. No headache.

Pathology and Location: Glioma.

In the left ascending frontal convolution, occupying the upper third
of this convolution. The tumor extended backward to the fissure of
Rolando, and in front was bounded by a vertical line which would meet
the upper extremity of the vertical frontal fissure. The inferior
boundary was distant about one and three-quarter inches from the
longitudinal fissure. Surrounding convolutions flattened and widened.

Remarks: Samt, _Arch. gén. de Méd._, Jan., 1876, from _Berlin. klin.
Wochenschr._, Nos. 40, 87.

16. Sex and Age: M. 49.

Clinical History: Irritability and loss of memory. Paresis, passing to
paralysis, of left arm; paresis of left leg. Slight left-sided
paralysis of tongue. No facial paralysis; no optic neuritis.
Ankle-clonus and exaggerated knee-jerk on left side. No wasting of
muscles or abnormal electrical reactions. Toward end paroxysmal
twitchings of left side, including side of face, with left-sided
paresis of face. Hebetude. Visual hallucinations. Complete left
hemiplegia. Paralysis of sphincter. Vomiting. Strong contraction of
pupils. Duration about two months.

Pathology and Location: Glioma.

Involving the middle portion of the right ascending frontal
convolution and posterior end of middle frontal convolution, extending
as a spheroidal mass downward to roof of lateral ventricle.

Remarks: A. Hughes Bennett, _Brain_, vol. v., 1882, p. 550.

17. Sex and Age: M. 30.

Clinical History: Convulsions for twelve years prior to death.
Character of fit: first, cramping of right big toe, then twitching of
calf-muscles and drawing up of leg and knee. Most of the fits stop
here, without loss of consciousness. In some fits the arm is convulsed
after the leg, beginning in fingers, and consciousness is lost.
Paralysis of right leg. Slight convulsive action of left leg.
Sensation of right leg unimpaired. Temporary aphasia at beginning of
attack; on one occasion the aphasia was present without fit. The right
arm probably paretic after each seizure. No facial palsy. Has as many
as thirty fits daily. Marked cessation of seizures at one time. Three
days before death became hemiplegic, with exaggerated deep reflexes on
paralyzed side; also ankle-clonus. During later years fit sometimes
began in hand. No optic neuritis while under observation.

Pathology and Location: Glioma.

Left hemisphere, including posterior half of superior frontal
convolution and upper half of ascending frontal convolution, except
the extreme end. The superficial area was defined by fissure of
Rolando posteriorly, superior frontal fissure externally, and
longitudinal fissure internally. Anteriorly, the tumor gradually
merged into normal brain. In the longitudinal fissure the growth
extended to calloso-marginal fissure.

Remarks: J. Hughlings-Jackson, _Brain_, vol. v., 1882, p. 364.

18. Sex and Age: F. 58.

Clinical History: General headache, most marked in the occipital
region, and always worse at night. Sore, stiff feeling in neck; at
times nausea and vomiting. Trembling {1073} of left hand; later,
paresis. Two sorts of movements of left arm—one, a fine tremor; the
other, attacks of jerking. Paresis of left arm increasing, with some
contracture; slight paresis of left leg. Sight failing; later,
semi-stupor; pupils small and fixed, the right larger. Right internal
rectus weak. Left lower face paretic. Strong contractures of left arm
and hand. Good knee-jerk. Choked discs. Some days bright, others
almost moribund. Case advanced to complete paralysis of left arm and
leg; involuntary evacuations; divergent strabismus and ptosis;
indistinct speech; delirium and coma.

Pathology and Location: Alveolar carcinoma.

An ovoid tumor in the upper part of the ascending frontal convolution
and in its subjacent white matter. It extended well across the fissure
of Rolando.

Remarks: E. C. Seguin, _Opera Minora_, p. 495, and _Journal of Nervous
and Mental Disease_, vol. viii. No. 3, July, 1881.

19. Sex and Age: M. 50.

Clinical History: History of syphilis and severe fall on the head.
Vertigo. Prickling sensation in left foot, extending to thigh, finally
to arm and head, followed by unconsciousness and convulsion. Stupor
after convulsion. After this, convulsive attacks at intervals.
Eighteen months before death an apoplectic attack, in which was
unconscious for several hours. Spasmodic attacks, preceded by a
peculiar twisting of the fingers of the left hand. Paresis of the
right hand and arm. Some diminution of sensation, not well made out.
Slight want of use of the left leg.

Pathology and Location: Gumma.

One-third of an inch in thickness at the middle of the ascending
frontal convolution. Membranes fused; tumor adherent to them. Œdema of
the brain. Gumma in the lungs.

Remarks: H. C. Wood, “Proceedings of the Philada. Neurological
Society,” _Medical News_, vol. xlviii. No. 9, Feb. 27, 1886, p. 248.

20. Sex and Age: M. 59.

Clinical History: Gradual loss of speech—aphasia. Gradual paralysis of
right side. No headache prior to this. No anæsthesia. Taste, smell,
hearing, and sight intact. Apathetic face. Middle branch of facial
nerve paralyzed, especially the muscles of the right corner of the
mouth. Wrinkles of forehead less strongly marked. Right upper and
right lower extremity in strong contracture. Leg swollen. Increasing
torpor of bladder. Normal electrical reactions, except speedier and
increased reaction of the right facial nerve. Reactions of
convulsibility in the right arm with ten to twenty cells. Very late,
unconsciousness and paralysis of bowels and bladder.

Pathology and Location: Myxo-glioma.

In front of the left ascending frontal convolution, bounded below by
the Sylvian fissure and the upper convolution of the island of Reil;
seems to immediately enter into the structure of the island. Left
optic thalamus and corpus striatum moist, but completely separated
from the tumor. Convolutions flattened.

Remarks: Petrina, _op. cit._

21. Sex and Age: M. 35.

Clinical History: Had epileptic fits for two years before his death.
Occasionally the spasms began in the left half of the face and
extended to the arm and leg, but did not become general. After such
attacks sensation was lost in the left arm, and the arm was paretic
for some hours. Toward the close of life the paresis became permanent,
and extended from the arm to the leg, and sensibility was somewhat
impaired in these limbs. The temperature was 2.5° F. higher over the
right parietal eminence than over the left.

Pathology and Location: Gumma.

Arising from the membranes, two inches in diameter, but very thin,
involved the gray matter of the posterior extremities of the first and
second frontal convolutions, the upper and middle thirds of the
ascending frontal convolution, and the adjacent border of the
ascending parietal convolution of right hemisphere.

Remarks: F. H. Martin, _Chicago Med. Journ. and Exam._, vol. xlvi. 21.

22. Sex and Age: F. 57.

Clinical History: After excitement lost consciousness. Paresis and
heaviness of the right upper extremity. Aphasia; used words
inaccurately; short of words and enunciation impaired. Second attack
of loss of consciousness. Twitching in right half of body and face.
Paralysis of right upper extremity. Severe pains in right arm and leg.
Another attack of loss of consciousness, with spasms of right half of
body. Right lower extremity and right lower face paretic. Slight
trismus; right masseter contracted. Dull headache. Organs of sense not
affected. Understands all that is said to her, although aphasic.
{1074} Sensibility good. Right-sided pneumonia; œdema of lung.

Pathology and Location: Fibro-glioma.

Tumor size of fist occupied the whole of the lower and middle portion
of the parietal lobe, imbedded in both ascending convolutions.
Ascending frontal convolution pushed aside; the annectant gyrus and
island of Reil compressed and flattened. Fissure of Sylvius arched
over by tumor. White substance also pushed toward the corpus striatum.
Meninges congested. Left parietal bone somewhat excavated.

Remarks: Petrina, _op. cit._

23. Sex and Age: F. 39.

Clinical History: Began to suffer with epilepsy two weeks after a blow
on the left parietal region. The fits were preceded by formication in
the right hand and tongue, and began with spasm in the right hand,
which was weak for some hours afterward. A permanent right facial
paresis developed one month after the blow, and two months later the
tongue, arm, and hand were also paretic on the right side. Disturbance
of vision due to choked discs had developed, and temporary attacks of
aphasia occurred after the frequent convulsions. She sank into a
condition of stupor and aphasia four months after the first symptoms.
The skull was then trephined at the seat of the old injury in hopes of
evacuating a chronic abscess, but no pus was found. One week after
this she died.

Pathology and Location: Gumma.

A gumma one inch in diameter was found on the surface of the left
hemisphere, at the junction of the middle and lower thirds of the
ascending parietal convolution, and involving also the convolution
posterior to this. The membranes were adherent to the gumma.

Remarks: H. B. Sands, _Med. News_, April 28, 1883.

24. Sex and Age: M. 25.

Clinical History: Four years previous to death had received a blow on
the left side of the head. A year later, twitching in the tongue and
the left side of the face. Twitching of the left arm. Twitching
increased. Paroxysmal spasm and general convulsions, with loss of
consciousness. Paresis, and then slowly-developed paralysis, of the
forearm and hand. Some paresis of left leg. Double optic neuritis.
Violent headache.

This patient was in charge of Hughes-Bennett at the Hospital for
Epilepsy and Paralysis, London. He diagnosticated brain tumor, and
suggested its removal. Rickman Godlee trephined over suspected region,
and removed a glioma of the size of a walnut. The operation was
performed November 25th. The patient did well until December 16th,
when he was seized with a rigor, followed by fever, sickness, and pain
in the head. A hernia cerebri of large dimensions supervening, he died
December 23d.

Pathology and Location: Glioma.

Meningitis was found at the lower border of the wound, spreading
downward toward the base of the brain.

Remarks: Hughes-Bennett and Rickman Godlee, _British Medical Journal_,
Nov. 29, 1885.

25. Sex and Age: F. —.

Clinical History: Syphilitic history. Tingling sensation and numbness
of the left arm and leg, which increased until it ended within six
weeks from its commencement in complete motor paralysis, with a
deficiency in the perception of touch. Left side of the face also
slightly paretic. Mental confusion and loss of memory.

Pathology and Location: After antisyphilitic treatment and
counter-irritation, trephining was performed over the middle of the
ascending parietal and frontal convolutions. Internal table of the
disc removed was found softened and thicker than usual, having on its
internal surface projections or roughnesses. A second opening was made
over the occipital region, and a similar thickening was found.
Opposite first opening the dura mater pale and thickened. It was
elevated, and a false membrane of yellow color was removed. An
incision was made in the direction of the {1075} paracentral lobule,
when a gush of grumous, red-colored fluid escaped.

Day after the operation much better; on third day moved her toes;
within a week lifted her leg; fingers moved within a week. Mind
greatly changed for the better.

Remarks: Macewen, “Proceedings of Path. and Clin. Soc. of Glasgow,”
_Glasgow Med. Journ._, vol. xxi., 1884, p. 142.

_Centrum Ovale—Fronto-parietal Region._

26. Sex and Age: F. 16.

Clinical History: Fell when sixteen months old from the table on her
head. Left hand, five months later, noticed at times to be stiff and
firmly closed. Three months later the leg became similarly affected,
and two months later general paroxysms. Many seizures for periods of
weeks or months, then intervals of freedom. Spasm began by contraction
of the left hand: she would lie down and jerk for a half minute or
minute, laughing or talking all through it, never losing
consciousness. In about six years left leg became paretic. Seizures
became much worse and more frequent; unconscious for six weeks, and
fifty to eighty spasms in twenty-four hours. Ten months without spasms
until a week before death, when they returned with great violence.
Spasms always began in the left hand; appeared to extend to the leg
first, and then to the face. Intellect clear.

Pathology and Location: Fibro-glioma.

In the white matter, but touching upon the gray at several spots at
the position of the upper end of the ascending frontal convolution of
the right hemisphere. The tumor occupied largely the anterior portion
of the paracentral lobule.

Remarks: Osler, _Medical News_, vol. xliii., Jan. 19, 1884, in
“Proceedings of Medico-Chirurgical Society of Montreal;” also, _Am.
Journ. Med. Sci._, N. S. vol. lxxxix., Jan., 1883, p. 31.

27. Sex and Age: M. —.

Clinical History: Severe fall, followed by insensibility. Paralysis of
the left side followed injury, but improved. Three years later,
epileptic convulsions: sudden fall, general spasm, biting tongue.
These attacks replaced by partial or localized epilepsy without loss
of consciousness: tonico-clonic spasm of muscles of left side of face
and neck and of left upper extremity, especially of the thumb and
index finger. Left pupil a trifle larger than right; left cheek
paretic, left arm and forearm absolutely paralyzed; left leg weak.
Marked tactile anæsthesia on left side. Ophthalmoscope showed fulness
of veins, but no neuro-retinitis. Late, some opisthotonos. Deafness in
right ear; axillary temperature, 36.4° C. Pain in right arm and leg
and in posterior part of head on right side. Conjugate deviation of
head and eyes from palsied side. No neuro-retinitis. Localized and
general convulsions recurred from time to time.

Pathology and Location: Sarcoma.

Larger than a hen's egg in white substance of right hemisphere,
occupying the whole thickness of the hemisphere above the opto-striate
bodies. Exerted much pressure upon these bodies, on convolutions near,
and even upon the inner surface of the left hemisphere. Adherent to
the dura mater. Right half of the brain much enlarged, and lateral
ventricle and septum lucidum forced over to the left. Two depressions
on the top of the skull; dura mater depressed and adherent to
convolutions. Some pachymeningitis.

Remarks: E. C. Seguin, _Opera Minora_, p. 215; reprinted from the
_Transactions of the Amer. Neurol. Ass._, vol. ii., 1877.

28. Sex and Age: M. 34.

Clinical History: Attacks of right-sided epilepsy every four or six
weeks; later, every week or oftener. Spasms wholly restricted to the
right arm or leg; the slightest attacks only momentary shocks on the
right side of the body. No spasm in the face. Only very rarely lost
consciousness. Never frothed at the mouth, bit his tongue, or
micturated in the attacks. In intervals had good use of his right hand
and leg up to a late period. Paresis of right limbs came on with
indefinite numbness of right leg. Diffused headache, mostly frontal.
No facial palsy; no anæsthesia. Knee-jerk absent on left side and
strong on right. {1076} Later, complete paralysis of right arm and
leg, with œdema. Violent headaches, more to the left of the median
line at the vertex; photophobia, nausea, and vomiting. No
neuro-retinitis. Still later, paresis, and then paralysis of right
face. Atrophy; contractures; bed-sores; semi-coma; profuse sweating;
high temperature; conjugate deviation of the eyes to the right; head
straight.

Pathology and Location: Sarcoma.

In centrum ovale, underneath the left cortical motor area, and
completely undermining it, was a large cavity which contained a large
amount of coffee-red serum, and also a tumor lying on its inner side
near the paracentral lobule. The tumor was connected behind with the
falx cerebri in the region of the paracentral lobule.

Remarks: E. C. Seguin, _Opera Minora_, p. 499, and _Journ. of Nerv.
and Mental Dis._, July, 1881.

29. Sex and Age: M. 22.

Clinical History: First symptom was a fit, which was followed by a
rigor. After this fit paresis of right arm and leg, with inability to
articulate properly. Could not raise the affected arm, but could grip
objects weakly. Paralysis of right side of face and tongue. Was quite
rational. No loss of sensation. Later, violent headache, followed by
vomiting. Slight amelioration of many symptoms, soon followed by
second attack of violent headache, which could not be localized;
complete right hemiplegia and aphasia. Later, dysphagia. Death rather
sudden.

Patient had had amputation of thigh about six months before for
sarcomatous enchondroma of head of the tibia. Had also had chancre
four years before.

Pathology and Location: Enchondroma.

In left hemisphere, between anterior part of corpus striatum and
“surface of frontal lobe.” The cortex over tumor and the outer and
anterior portion of corpus striatum were softened and broken down.

Remarks: T. P. Pick, _St. George Hosp. Rep._, vol. ix. p. 663.

30. Sex and Age: F. 16.

Clinical History: Patient was a wayward, hysterical girl of neurotic
family, precocious, and with abnormal sexual instincts and
indulgences. Had a sudden attack of total blindness, then sudden
recovery; sudden blindness again, and deafness; then restoration of
hearing; loss of power in lower limbs, ending with total blindness,
deafness, and paraplegia. Had dilated pupils and some hyperæsthesia;
also marked hysteroidal attacks, becoming at last maniacal.

Negatively, no constant headache or affection of ocular, facial, or
lingual muscles, no convulsions or vomiting; no abnormal
ophthalmoscopic appearances (except slight choked disc).

The case had been diagnosticated by many doctors and one of the “first
authorities in Europe” to be hysteria.

Pathology and Location: Tumor in right hemisphere, size of hen's egg,
translucent, and nodulated, soft, highly vascular, with small
extravasations of blood on its surface, occupied medullary substance
of middle lobe superior to lateral ventricle causing bulging of roof
of ventricle.

Remarks: A. Hughes-Bennett, _Brain_, 1878, vol. i. p. 114.

_Postero-parietal Region._

31. Sex and Age: M. 25.

Clinical History: Kicked on the head. Headache, nearly continuous,
with violent paroxysms. Vomiting at intervals, most when headache was
most violent. Vertigo. Mental confusion; sometimes maniacal. Left
convergent strabismus. Partial right hemianæsthesia. Patellar reflexes
slightly exaggerated; slight ankle-clonus on the right side. Blind in
both eyes; sight of right eye lost first. Choked discs, and eventually
optic atrophy. Hearing defective in right ear. Constipation.
Head-temperatures taken once; right parietal region, 98° F.; left
parietal, 97.8° F.

Pathology and Location: Fibroma.

Adherent to membranes, and involving the left postero-parietal and
occipital region to within half an inch of longitudinal fissure. The
brain-tissue around softened and broken down, the parts disintegrated
being chiefly the white matter of the postero-parietal and occipital
lobes.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, August, 1882.

32. Sex and Age: M. 49.

Clinical History: Dropping of left hand at intervals, with power
regained in about an hour. Brief attacks of loss of speech, and
numbness in lips and tongue on both sides. Numbness in tips of his
fingers and the left hand. Slight paroxysms of general rigidity.
Severe frontal headache. No vomiting. Loss of sight, gradually
increasing to total blindness. Involuntary micturition. Increasing
hebetude. Slow but probably correct intellection. Left upper
extremity, toward last, paretic. Was able to stand, but could scarcely
walk. Hearing and taste preserved. {1077} Some doubt as to smell.
Later, imbecile. After a severe fit of general convulsions he died.
Duration, about four months.

Pathology and Location: Carcinoma.

It occupied nearly exactly the site of the right “poster-parietal
lobule” (superior parietal). It was clear of the ascending parietal
convolution in front, and behind did not quite touch the external
parieto-occipital fissure; below it extended just short of the
intraparietal fissure, and on inner face of hemisphere reached for
half an inch into quadrilateral lobe. Below tumor toward ventricle
brain-substance softened.

Remarks: James Russell, _Brit. Med. Journ._, 1876, ii. p. 709.

33. Sex and Age: F. 36.

Clinical History: Right-sided temporal and orbital neuralgia.
Anæsthesia of left arm. Epileptic attacks. Slighter attacks of spasm,
without unconsciousness, in left face, left arm, and hand. Paresis of
left arm. Blindness. Optic neuritis. Pupils dilated and immobile.
Later, loss of smell and taste. Mental depression.

Pathology and Location: Gummata.

In right supramarginal lobule two tumors size of pea, lying
superficially.

Remarks: Broadbent, _Lancet_, Jan., Feb., 1874, quoted by Bernhardt,
p. 68.

_Beitrage zur Symptomatologie und Diagnostik der Herngeschwülste_, von
Dr. M. Bernhardt, Berlin, 1881.

34. Sex and Age: ——

Clinical History: Left hemiplegia with some anæsthesia. Deafness
developed in the left ear, with a total inability to localize the
origin of sounds.

Pathology and Location: Tumor size of an apple in middle of ascending
parietal convolution and backward. Around the tumor white softening,
which extended forward as far as the fissure of Rolando, and backward
throughout the right parietal lobe, and beneath almost into the
central ganglia.

Remarks: Strümpell, _Neurolog. Centralb._, Aug. 15, 1882.

35. Sex and Age: M. 54.

Clinical History: Middle finger of the right hand began to jerk
violently, also some of the flexor tendons. Twenty minutes after this
he had a fit, in which he became unconscious and beat himself
violently on the chest with the right arm. Had three of these fits.
Aphasic after this for two weeks. Had high fever at the time of the
seizures; was rubbed all over the body with ice. The fingers became
paretic, not the forearm or arm. Arm became numb at times, especially
after exertion. With dynamometer, left hand, 75; right hand, 55.
Headache, which ceased after some months. Right optic disc abnormally
red, but not choked; left disc normal. Had a convulsive attack in the
Philadelphia Hospital, in which the four fingers of the right hand
rapidly vibrated, contracting and extending without pain; no loss of
consciousness or other disturbance. The tongue was also affected, so
that speech was impossible. Later, the patient had a general
convulsion, preceded by a drawing sensation in the face; convulsive
movements began in right hand. Tongue bitten. Attack preceded by
severe headache. Had another attack without loss of consciousness or
convulsion, preceded by a sensation as of a knife cutting through the
flesh, which travelled up from the left hand to the shoulder, and then
to the head. Increasing loss of sensation in the fingers of the right
hand. Increasing difficulty of speech, with spells of melancholia and
crying. Right side of face markedly paralyzed. Right arm almost
entirely paralyzed and much swollen. Speech much affected; difficulty
in swallowing. Paralysis involves the right leg.

Pathology and Location: Gliomata.

A small tumor occupies the lower end of the left supramarginal
convolution, just where it joins the foot of the ascending parietal
convolution. The latter convolution was not involved in the tumor, but
was distinctly pressed upon in its lower third. The ascending frontal
convolution was entirely healthy.

In right hemisphere a similar gliomatous growth in the foot of the
angular convolution where it runs into the middle temporo-sphenoidal
convolution, involving also the upper part of this convolution, and to
a slight extent the deepest portions of the superior
temporo-sphenoidal convolution.

Remarks: H. C. Wood. Not before published.

{1078} _Occipital Region._

Occipital lobe—cortex and centrum ovale.

36. Sex and Age: M. 57.

Clinical History: Headache. Vertigo. Paresis of left side. Left facial
paralysis, especially middle branch. Vomiting. Right pupil dilated.
Tongue not involved. Uvula directed to left. Left velum palati
relaxed. Taste, smell, sight, and hearing normal; sensibility of whole
body normal. Reaction of degeneration on left side of face. Left side
of body shows reaction of convulsibility. Slight quantity of albumen.
Paresis declined with exception of facial nerve. Apathetic. Œdema of
lung.

Pathology and Location: Glioma.

In middle of right occipital lobe; lobe softened. Right lateral
ventricle narrowed and left dilated. Right posterior horn and right
thalamus opticus compressed.

Remarks: Petrina, _op. cit._

37. Sex and Age: M. 27.

Clinical History: Dysphagia, most marked with liquids, caused by
paresis of pharynx, more marked on left. Left hemiparesis for three
years. Headache (frontal and temporal), which is of a boring, tearing
character. Failure of memory. Speech guttural and monotonous. Puriform
expectoration. Later, feeble voice, hiccough, yawning, somnolence.

Pathology and Location: Fibroma.

On posterior face of left petrous bone and inferior occipital fossa,
extending behind occipital foramen and to right of cerebellar falx. A
prolongation involving the pneumogastric and glosso-pharyngeal, and
spinal accessory. Also cerebellar abscess.

Remarks: Cruveilhier, _Bull. de la Soc. Anat._, 1855, xxx. 475-479.

38. Sex and Age: F. 20.

Clinical History: Headache. Dimness in right eye, then in left;
finally, blindness in both. Convulsions. External strabismus; right
pupil dilated, left contracted. Coma, alternating with consciousness.
Vertigo. Optic discs congested, presenting small hemorrhages;
exophthalmus. Paresis of right arm and leg; partial anæsthesiæ on same
side. Earache. Vomiting, not frequent. Coma and death.

Duration, about three months.

Pathology and Location: Sarcoma?

Occupied all the posterior part of right hemisphere of cerebrum,
pressing upon and indenting opposite hemisphere and right half of the
cerebellum.

Remarks: S. O. Habershon, _Guy's Hosp. Rep._, 3d S., xx. 330-334.

39. Sex and Age: M. 18.

Clinical History: Periodical headaches. Pains in the neck and
vertebral column. Points of exit of trigeminal nerve sensitive.
Staggering gait. Diplopia. Confused sounds in right ear. Tetanoid
contractions of neck.

Pathology and Location: Echinococcus.

In right occipital lobe.

Remarks: Visconti, _Annal. Univer._, Oct., 1869, quoted by Bernhardt,
p. 98.

40. Sex and Age: F. 21.

Clinical History: Right hemianopsia. Central vision good. Other
symptoms: headache, dysarthria, anæsthesia of the right half of the
face. No paralysis, no mental symptoms. Choked discs.

Duration seven months.

Pathology and Location: Cystic glioma.

In the left occipital lobe; had reached and destroyed the cortex of
the lobe at its apex, and had extended inward, nearly reaching the
inferior cornu of the lateral ventricle. The entire inner half of the
occipital lobe was thus destroyed.

Remarks: Jany, _Knapp's Archiv f. Augenheilk._, vol. xi. p. 190,
quoted by Starr, _Am. Journ. Med. Sci._, N. S., lxxxvii., Jan., 1884,
p. 72.

41. Sex and Age: M. 42.

Clinical History: Right hemianopsia. Central vision good. Other
symptoms: aphasia, right complete hemiplegia, with facial paralysis.

Pathology and Location: In left occipital lobe, surrounded by a zone
of softening, reaching inward to and involving the pulvinar of the
left optic thalamus. Optic tracts normal.

Remarks: Hirschberg, _Deut. Zeitsch. f. Prakt. Med._, 1878, No. 4,
quoted by M. Allen Starr, _Am. Journ. Med. Sci._, N. S., lxxxvii.,
Jan., 1884, p. 69.

42. Sex and Age: M. 42.

Clinical History: Right hemianopsia, not quite reaching the point of
fixation. Central vision good in both eyes. Ophthalmoscopic
examination negative. Other symptoms: vertigo, loss of memory,
aphasia, and partial agraphia, with temporary right hemiplegia.

Pathology and Location: Gelatinous sarcoma.

In the left occipital lobe, involving all three of its convolutions,
as well as the præcuncus. Softening extended inward through the white
substance to the posterior cornu of the lateral ventricle. Thalamus
and optic tracts normal.

Remarks: Jastrowitz, _Arch. f. Augenheilk._, 1877, p. 254, quoted by
Starr, _Am. Journ. Med. Sci._, N. S., lxxxvii., Jan., 1884, p. 71.

{1079} 43. Sex and Age: M. 40.

Clinical History: For seven years epileptic seizure, beginning with
spasm of left leg and going on to general convulsions; motions more
violent on left side. An aura consisting of a darkness, coming
gradually over the field of vision from the left side, always preceded
the attack. During the intervals left-sided headache was the chief
symptom. It seems probable that a temporary left hemianopsia preceded
the attack.

Pathology and Location: Cyst filled with serum.

In white matter of the right occipital lobe, surrounded by a zone of
softening which did not involve either the cortex or the wall of the
lateral ventricle.

Remarks: Traube, _Gesammt Beitrage zu Pathologie_, ii. 1083, quoted by
Starr, _Am. Journ. Med. Sci._, N. S., vol. lxxxvii., Jan., 1884, p.
73.

44. Sex and Age: M. 52.

Clinical History: Headache. Numbness down right arm. Later, paroxysms
of headache lasting twenty to forty minutes, generally preceded by
pain and numbness in right hand and arm, ascending to head, and so
intense as to produce profuse perspiration. Delirium (lasting two
days) during these attacks. No paralysis or previous fit, nor
vomiting. Few hours before death had convulsions.

The pain and numbness were in right arm, although tumor was in right
hemisphere.

Pathology and Location: Malignant tumor.

Size of pullet's egg at inferior portion of posterior lobe on right
side in substance of cerebrum, approaching within a few lines of
surface.

Remarks: J. C. Langmore, _Trans. Path. Soc. Lond._, iii. pp. 246-248.

_Temporo-sphenoidal Region._

Temporo-sphenoidal lobe.

45. Sex and Age: M. 33.

Clinical History: History of syphilis. Blows on the head. Headache,
continuous, usually dull, occasionally severe. Occasional vomiting.
Stupidity, want of energy, drowsiness. One general convulsion a few
hours before death. Partial anæsthesia on the right side.
Hyperæsthesia of left side. Sight impaired. No ophthalmoscopic
examination. Hearing defective in right ear. Constipation.

Pathology and Location: Gumma.

One and a quarter inches in diameter, attached to adherent membranes,
and involved the middle portions of the first and second temporal
convolutions of left hemisphere. A layer of brain-substance both
anterior and posterior to the tumor was softened. The tumor grazed the
ascending parietal and inferior parietal convolutions. A large foyer
of greenish-yellow pus was found to the inner side of the tumor.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, August, 1882.

46. Sex and Age: M. 42.

Clinical History: At first an attack of vertigo which lasted over
twenty-four hours: some unconsciousness for a time. Continued
headache; loss of memory; giddiness and vomiting, the latter occurring
without connection with the state of the stomach as to food. Partial
bilateral deafness, which the patient stated was of long duration. No
paralysis, but right hand a little weaker than left. Distinct mental
failure during last two weeks of life; incoherence and faulty memory.

Pathology and Location: Epithelioma.

Ovoid tumor about one and a half inches in diameter in the central
portion of the temporo-occipital region. Hippocampal convolution
grazed. Some surrounding softening and meningitis. One corner of tumor
had produced a small spot of softening in the cerebellum.

Remarks: H. C. Wood, “Trans. of Path. Soc. of Philada.,” 1880, _Med.
Times_, vol. xi., Jan. 29, 1881.

47. Sex and Age: F. 40.

Clinical History: Suffered from a light form of epilepsy dating from
tenth year, which resulted, it was believed, from a fall. Rarely bit
her tongue, but usually frothed at the mouth. No history of one-sided
spasms. Always had an aura of a peculiar character. She suddenly
perceived a disagreeable odor, sometimes of smoke, sometimes of a
fetid character, and quite uncomplicated by other sensory warning.
Developed phthisis, her attacks occurring from time to time until her
death.

Pathology and Location: At lower part of right temporo-sphenoidal lobe
a shrinking and induration involving the uncinate gyrus and parts of
the adjacent convolution. The olfactory nerves were not involved. A
form of low-grade hemorrhagic pachymeningitis present.

Remarks: Allan McLane Hamilton, _New York Med. Journ. and Obstet.
Review_, vol. xxxv., June, 1882, p. 575.

{1080} 48. Sex and Age: F. 39.

Clinical History: Attacks of convulsion seven weeks before her death.
In two weeks mind affected; drowsy and stupid; condition of dementia.
Passed into a state of semi-consciousness. No eye symptoms. No
paralysis. Percussion on left side of head painful.

Pathology and Location: Sarcoma.

Occupied the posterior part of the fourth and fifth temporal
convolutions, and the third convolution was atrophied. Did not involve
the lateral ventricle. Under surface flattened and resting partly upon
the left lobe of the cerebellum.

Remarks: W. H. Draper, _New York Hosp. Histories_, N. S. vol. x. p.
445, quoted by M. Allen Starr, _Am. Journ. Med. Sci._, N. S. vol.
lxxxvii., April, 1884, p. 383.

_Basal Ganglia and Adjoining Regions._

49. Sex and Age: M. 59.

Clinical History: Contractures of right arm and leg since childhood.
Death from accident. The arm was atrophied and shortened, flexed at
elbow and wrist; disappearance of some cartilages at wrist and wasting
of joint-surface of radius. Femur flexed at hip; knee-joint flexed;
ankle-joint in position of equinus. Other bone-changes. Right leg
shortened.

Pathology and Location: Osteoma.

Tumor in left corpus striatum on “surface of anterior thick half,”
projecting outward into white substance of brain, and inward into
anterior portion of optic thalamus.

Remarks: A. Bidder, _Arch. f. Path. Anat. und Physiologie, und f.
Klinische Med._ Virchow, 1882, p. 91.

50. Sex and Age: M. 30.

Clinical History: Right frontal and occipital headache. Vertigo.
Paræsthesia of the toes, particularly the right. Face drawn to the
right. Left face paretic. Right eye smaller than left. Weakness and
fatigue of limbs. Convulsions. Vomiting. Slow pulse.

Pathology and Location: Myxo-sarcoma.

In right corpus striatum protruding into right lateral ventricle and
cortex.

Remarks: Schüppel, _Arch. d. Heilk._, p. 357, 1867.

51. Sex and Age: M. 34.

Clinical History: Walked a mile to an infirmary, and in less than one
hour went into a series of severe epileptic attacks, which continued
for four hours. The spasms were clonic, and chiefly in upper
extremities, with violent contortions of face; the latter most marked
on left side and in zygomatici. Between the fits there was deep coma,
especially three hours before death, when, after another violent fit,
he died, seven hours after first seizure. No paralysis, and report
says nothing about any previous fits.

Pathology and Location: Myxomatous glioma.

It exactly occupied the place of right nucleus caudatus, extending
outward as far as white fibres, but not involving them. Brain-tissue
in proximity normal.

Remarks: Dowson, _Med. S. and Gaz._, London, 1878, p. 333.

52. Sex and Age: ——

Clinical History: Partial anæsthesia of right half of trunk. Hyperæmia
of retina, and capillary hyperæmia of left optic disc. Left pupil
dilated; left ptosis; left diverging strabismus. Paralysis of right
side and extremities. Paralysis of muscles around right corner of
mouth. Incontinence of feces and urine. Redness of face. Variations in
temperature.

Pathology and Location: Tubercle.

In left optic thalamus. Partial destruction of left peduncle of
cerebrum.

Remarks: Fleischmann, _Wien. med. Wochenschrift_, 6, 7, 8, 9, 1871,
quoted by Petrina.

53. Sex and Age: F. 44.

Clinical History: Severe headache on left side. Sensibility lessened
in left extremities, at same time frequent pain. Intelligence
diminished. Speech retarded. Strabismus of left eye. Amblyopia. Left
pupil alternately dilated and contracted. Left lagophthalmos.
Chattering of the teeth. Twitchings on the left paralyzed half of the
face. Tongue and uvula tending toward the left.

Pathology and Location: Sarcoma.

Right optic thalamus. Corpora quadrigemina compressed.

Remarks: Friedreich, quoted by Petrina, _op. cit._

54. Sex and Age: F. 38.

Clinical History: Headache. Creeping sensations in right arm and leg.
Right facial paresis. Paresis of left extremities. Convulsions.
Dimness and confusion of sight. Diplopia. Hardness of hearing. Failure
of memory. Difficulty in speaking and swallowing. Improvement under
iodide of potassium.

Pathology and Location: Glioma.

Left optic thalamus.

Remarks: Bruzelius and Blix, 1870, quoted by Bernhardt, 153.

55. Sex and Age: F. 14.

Clinical History: Headache, vertigo. Epileptic attack. Right
hemiplegia. No anæsthesia. Slight dilatation of pupils.

Pathology and Location: Sarcoma.

In left optic thalamus. The right optic thalamus also affected.
Corpora quadrigemina enlarged and pushed backward.

Remarks: Rusconi, _Gaz. Med. Ital._, 1874, No. 11.

{1081} 56. Sex and Age: M. 30.

Clinical History: Headache. Left ptosis; fixation of left eyeball.
Drowsiness. Retarded speech. Gait unsteady. Paresis of right hand and
foot. Emaciation; incontinence of urine.

Pathology and Location: Serous tumor.

Large as a nut, in posterior half of right optic thalamus.

Remarks: Troschel, _Med. das ver. für Heilk. in Preussen_, xliii.,
1839, quoted by Petrina.

57. Sex and Age: F. 36.

Clinical History: Imbecile. Speech inarticulate. Pupils contracted.
Spasms in arms, but light in limbs.

Pathology and Location: Cancer.

Left optic thalamus and corpus striatum without definite boundary,
extending into brain-mass.

Remarks: Brenner, quoted by Petrina, _op. cit._

58. Sex and Age: F. 33.

Clinical History: Headache and vomiting for three weeks: for one week
had been maniacal. Convulsions. Apoplectiform attack, marked by
unconsciousness, general muscular flaccidity, and stertorous
breathing. Paralysis of left face; twitching of right face.

Pathology and Location: Glioma.

Between left optic thalamus and hippocampus minor, extending from the
ventricle to the under surface of the brain. Corpus striatum and optic
thalamus unaffected. Hemorrhage on under surface.

Remarks: Owen, _St. George's Hosp. Rep._, ix., 1877-78, p. 150.

59. Sex and Age: M. 45.

Clinical History: Vertigo, headache, and tinnitus. Five years before
attack had fallen and struck the back of his head. Much exposed to the
sun. One day in August a general feeling of numbness came over him.
This was followed by vertigo, etc., as above. Staggered and stumbled
in walking as if intoxicated. Unable to maintain his balance in the
dark or with his eyes closed. Some numbness in legs and arms, but no
actual loss of sensibility. No neuro-retinitis; no paralysis. When
erect had a constantly increasing tendency to stagger backward.
Divergent squint and diplopia appeared. Potassium, iodide blisters,
and seton were used. Noises and headaches disappeared. During last two
or three weeks some difficulty in swallowing. Involuntary evacuations.
Occasional hallucinations.

Pathology and Location: Glio-sarcoma.

Tumor size of walnut in third ventricle, moulded to the interior.
Extending to base of brain just above corpora albicantia, and forward
as far as anterior commissure. A caudate prolongation completely
blocked up the Sylvian aqueduct. Owing to this obstruction, a large
quantity of serum had been imprisoned, enormously distending the
fourth and lateral ventricle. The growth invaded left optic thalamus.
Superior surface of cerebellum softened from median line to middle of
right hemisphere.

Remarks: F. Woodbury, _Am. Journ. of the Med. Sci._, N. S. lxxvi.,
July 1, 1878.

60. Sex and Age: M. 15.

Clinical History: Epileptic from childhood: had had no fits for last
three years. Had tremors and was dull. Short-sighted, and had a habit
of absurdly frequent winking. Nothing else wrong with eyes. Suddenly,
after a mental disturbance, had intermitting pulse. Cold surface,
dulness, head and face swollen and flushed. Then tonic spasms, loss of
consciousness, involuntary micturition. General tremors, dilated
pupils, stupor. Next diffused dusky-red flush of both cheeks, also
over back of hands and forearms. Temperature depressed to 92° in
axilla. Automatic repetition of words. Taste and smell normal. He
recognized himself in looking-glass on the day he died.

Pathology and Location: Sarcoma.

In third ventricle, lying between corpora striata and optic thalami of
opposite sides. It completely enveloped optic commissure, and
partially involved track of optic nerves issuing from front. The sole
organic connection of tumor was with the commissure. The tuber
cinereum was distinct from its tissue.

Remarks: Russell, _Med. Times and Gaz._, 1873 (1), p. 522.

61. Sex and Age: M. 19.

Clinical History: Periodical headaches. Unsteady gait. Left
hemiparesis. Peculiar swelling of face. Delirium. Convulsions and
sudden death. Bad-smelling discharge of the nose.

Pathology and Location: Echinococcus.

In left lateral ventricle; the whole of the ventricle a sac.

Remarks: Yates, _Med. Times and Gazette_, Aug., 1870.

62. Sex and Age: M. 14.

Clinical History: Convulsions; vomiting; internal strabismus of right
eye; gradually increasing paresis of left leg and arm. Reeling toward
left side. Occipital headache. Pain and numbness in left arm. {1082}
Lateral movements of eyes lost; paralysis of accommodation; nystagmus.
Oscillation of left hand. Left leg ataxic. Patellar reflex
exaggerated, and ankle-clonus present on left side. Superficial
reflexes increased on right side. Partial anæsthesia on left side.
Sight good; double optic neuritis. Left-sided hearing impaired. Taste
and smell normal. Toward end, increasing torpor; left hemiplegia,
except slight power retained in face, with anæsthesia and analgesia.
Tonic fits. Right pupil dilated, and external strabismus in right eye.
Slow respiration. Ankle-clonus and increased knee-jerk in right.

Pathology and Location: Glioma.

Involved right anterior tubercle of corpora quadrigemina; also right
optic thalamus, posterior part of internal capsule, and tegmentum of
crus cerebri. The enlarged optic thalamus pressed back upon right
anterior portion of cerebellum and middle peduncle, and exerted some
transmitted pressure upon medulla oblongata.

Remarks: David Ferrier, _Brain_, vol. v. p. 123.

63. Sex and Age: F. 29.

Clinical History: Cervico-occipital headache. Vertigo. Convulsions.
Right facial paresis. Tendency to fall backward. Uncertain gait. Optic
neuritis. Double amblyopia. Difficulty in moving both eyes toward the
left. Diminished intelligence. Vomiting.

Pathology and Location: Glioma.

In corpora quadrigemina. Cerebellum not involved. Tumor lay upward and
outward from the left cerebellar crus ad pontem.

Remarks: Annuske, _Von Graefe's Arch._, 1873, Bd. xix., quoted by
Bernhardt, 167.

64. Sex and Age: M. 21.

Clinical History: Right temporo-frontal headache. Vertigo. Pains in
right leg. No anæsthesia. Right leg paretic. Tinnitus. Atrophy of the
right optic nerve. Abnormal somnolence. Sexual inclination diminished.
Vomiting. Blindness, first of the right and then of the left. Right
divergent strabismus. Pupils dilated.

Pathology and Location: Lipoma.

Tumor compressed corpora quadrigemina and geniculate bodies.

Remarks: Hirtz, _Bull. de Société Anat._, Mars and April, 1875, quoted
by Bernhardt, 168.

65. Sex and Age: F. 3.

Clinical History: Right hemiparesis. Right-sided tremor. Contraction
of the right elbow. Late, loss of sight in left eye. Ptosis,
dilatation of the left pupil. Stupidity. Peculiar movements when
seated from right backward to the left.

Pathology and Location: Tubercle.

At site of corpora quadrigemina, springing into the third ventricle.
Left cerebral peduncle compressed.

Remarks: Pilz, _Jahrbuch. für Kinderkrankh._, iii., 1870, 2, 133,
quoted by Bernhardt, 168.

66. Sex and Age: M. 25.

Clinical History: Cervico-cephalic pains. Vertigo. Uncertain gait. No
paralysis. Tension of muscles of neck. Optic neuritis. Double
amaurosis. Tinnitus. Diminution of hearing. Intelligence clear until
within fourteen days of death. Insensibility, delirium, coma. Small
irregular pulse.

Pathology and Location: Glioma.

Tumor displaced corpora quadrigemina and pineal gland. Projected into
the third ventricle through aqueduct of Sylvius and into fourth
ventricle.

Remarks: Duffin, _Lancet_, June 17, 1876.

67. Sex and Age: M. 7.

Clinical History: Occipital pains. Staggering gait toward right and
backward. Hydrocephalic cries. Tendency of head forward. Alternating
diverging strabismus. Double optic neuritis. Sudden death in paroxysm
of pain. Paresis of bladder. Vomiting.

Pathology and Location: Tumor took the place of posterior part of
corpora quadrigemina and velum. Cyst in the midst of the cerebellum,
reaching the fourth ventricle.

Remarks: Kohts, _Virch. Arch._, Bd. lxvii., 1876, quoted by Bernhardt,
168.

_Cerebellum._

68. Sex and Age: M. 1.

Clinical History: Frontal headache. Slight control over arms and legs.
Stiff neck. Dilated pupils. Sopor. Vomiting. Duration, one year.

Pathology and Location: Glioma.

Size of an orange in the middle of cerebellum. Chronic hydrocephalus.

Remarks: H. Green, _Trans. Path. Soc._, vol. xx., 1870.

69. Sex and Age: F. 21.

Clinical History: Fall from a swing upon the head, followed by loss of
consciousness for a few minutes. Occasional headache during eleven
years, always located at the occipital region. Eight months before
death severe paroxysmal headaches, increased to one every five or six
days, and lasting three to four days. Great hyperæsthesia of the head.
Choked discs in both eyes. Complete blindness. Slight paresis of left
side of body; twitching of muscles of left side of face. Staggering
gait; sometimes complained of a momentary swinging or rotary
sensation. Intellect clear. During last few days of life loss of power
of deglutition, and also of taste, smell, and hearing.

Pathology and Location: Tubercle.

In left and middle lobe of cerebellum, involving the pia mater. Over
the tumefaction leptomeningitis.

Remarks: H. F. Formad, _Tr. of Philada. Path. Soc._, 1879-81, vol. x.
p. 178.

{1083} 70. Sex and Age: F. 27.

Clinical History: History of syphilis. Headache, with paroxysmal
exacerbations. Vomiting, frequently recurring; for four weeks before
death vomited almost incessantly. Vertigo; impossible to sit or stand
because of vertigo late in illness. Slowness of mind and hebetude.
General muscular weakness. Right partial hemiplegia and
hemianæsthesia. Trigeminal neuralgia. No ophthalmoscopic examination,
but sight impaired. Marked slowness of respiration; respirations ran
down as low as four and five per minute two weeks before death.

Pathology and Location: A nodulated mass involved the right middle
cerebellar peduncle and the adjacent region of the right cerebellar
hemisphere. The right upper half of the floor of the fourth ventricle
superficially softened. A small area of softening was also found
involving the under outer surface of the left optic thalamus, the
breadth of the internal capsule, and a small segment of the lenticular
nucleus.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, August, 1882.

71. Sex and Age: F. 13.

Clinical History: Tubercular history. Headache, with severe paroxysms;
most marked in frontal and occipital regions. Vomiting; vertigo;
attacks of reeling and falling. Mental dulness. Weakness of limbs, but
no distinct paralysis. Hyperæsthesia; severe pains in limbs. Gradually
went blind, first in left eye, and then in right. Descending neuritis
determined nearly a year before death; marked optic atrophy observed a
month before death. Constipation.

Pathology and Location: Tubercle.

A large nodulated mass occupied the lower two-thirds of the right
cerebellar hemisphere; one small nodule extended across the posterior
extremity of the superior vermiform process, destroying altogether
about one-third to one-half of a cubic inch of its substance. Internal
hydrocephalus.

Remarks: C. K. Mills, _Arch. Med._, vol. viii. No. 1, Aug., 1882.

72. Sex and Age: F. 20.

Clinical History: Headache. Occasional vomiting, but only upon a full
stomach and at the beginning of a paroxysm of headache. No impairment
of intellect; no paralysis; no convulsion; no inco-ordination. During
last few days, when in paroxysms of headache, her face would be drawn
toward left side, accompanied by a rigid drawing backward of the head,
by pain in left shoulder and arm, and by a marked diminution of
sensation in the same shoulder and arm. Head-pain excruciating, at
first involving the whole cranium, afterward only the forehead and
temples, but finally only the back of the head and nape of the neck.
Died of sheer exhaustion. Symptoms and physical signs of phthisis.

Pathology and Location: Tubercle.

In right lobe of cerebellum. Tubercular disease of both lungs with
pleuritic adhesion. Fatty liver.

Remarks: L. S. Clark for A. S. Gerhardt, _Tr. of Philada. Path. Soc._,
1878-79, vol. ix. p. 144.

73. Sex and Age: M. 45.

Clinical History: Occipital headache. Movements weak; gait staggering.
Inability to fix eyes; sight retained. Pupils unequal. Partial
deafness in both ears. Vomiting. Sopor. Sudden death. History of fall
upon head at twenty years of age, since which time much headache.

Pathology and Location: Tumor size of nut, compressing cerebellum and
pons, situated between pons, middle peduncle of cerebellum, the
cerebellum, and brain. Corpora quadrigemina atrophied.

Remarks: Luys, _Gaz. des Hôp._, 1867, 105, quoted by Bernhardt, p.
225.

74. Sex and Age: F. 52.

Clinical History: Violent and continuous headache. Gradual loss of
sight. Very irritable. Psychic pain and complaints. Incoherence of
ideas. In three to four years some anæsthesia of left leg; the left
hand became rebellious to the will. Paralysis progressed; symptoms
increased very slowly. Intense coryza, with running from the nose,
accompanied with a feeling as if a strange body filled up this cavity.
Great appetite. Had an attack of unconsciousness, preceded by violent
pains and creepings in the left hand, and presenting the following
conditions: Dorsal decubitus; flushed face; head strongly retracted;
{1084} frowning; respiration difficult, but not stertorous; pupils
large and insensible to light; the left eye widely opened, the right
shut; very marked contraction in the orbicular muscle; stringy mucus
in large quantities from right nostril; the left commissure of the lip
strongly carried downward and backward. Tongue white, not deviated.
Limbs of the right side not anæsthetic or paralyzed; the hand strongly
shut. On the left arm painful pricking; the elbow flexed at a right
angle, hand completely paralyzed. Motion diminished in left leg;
sensibility not altered; intelligence obtuse, but the patient responds
to questions. Nausea; hiccough. Finally, diaphragmatic breathing;
asphyxia by strangulation.

Pathology and Location: Tumor size of hen's egg lodged between the
superior surface of the cerebellum and cerebrum.

Remarks: M. Boullet, _Gaz. méd. de Par._, 1834, 2d S., vol. ii. p.
264.

75. Sex and Age: F. 64.

Clinical History: History of a fall down stairs. Headache. Frequent
vomiting. Stupor, and when admitted to the hospital three weeks before
death could not give any account of herself or of her complaint.
Semi-comatose. No definite paralysis. She could move both arms and
legs, but could not stand. Involuntary evacuations. No deviations of
the eyes; apparently saw well. Pupils equal and moderately contracted;
right disc a little redder than the left, but no swelling of the disc.
Died in a convulsion, the right side being most affected.

Pathology and Location: Tumor size of a greengage plum, sprang from
the dura mater just under the tentorium cerebelli on the left side. It
had caused the deep depression of the left lobe of the cerebellum.
Also a small clot, partly decolorized, just outside the right corpus
striatum.

Remarks: B. Bramwell, quoted in _Med. and Surg. Rep._, vol. xxxiv.,
Mar. 11, 1876.

76. Sex and Age: F. 32.

Clinical History: Headache first. Then pain in right eye and numbness
in right arm and leg; vision poor in right eye, with improvement. The
left soon similarly affected, without improvement. Vomiting (patient
was pregnant); vertigo. Ataxia marked. Patellar reflexes diminished.
Tongue protruded to left. Right pupil dilated. Taste abolished on
right side. The left field of vision showed hemianopia of the temporal
side. Both eyes showed optic neuritis. Later, shooting pains in legs
and left arm. Mind clear, but hysteroidal excitement frequent.
Surface-temperature of head elevated. Toward end mental aberration,
then unconsciousness. Died during labor.

Pathology and Location: Sarcoma.

A nodular tumor, size large horse-chestnut, on upper surface of right
lateral hemisphere of cerebellum.

Remarks: J. T. Eskridge, M.D., _Journ. of Nerv. and Ment. Dis._, vol.
xii. No. 1, Jan., 1885.

_Floor of Fourth Ventricle._

Directly or indirectly involved.

77. Sex and Age: F. —.

Clinical History: Vertigo only on standing. Sensibility normal.
Walking and standing impossible. Ataxia of legs. No paralysis. Facial
and trigeminus intact. Dysphagia. Double amaurosis. Eyeballs fixed,
directed forward. Symmetrically dilated pupils. Hearing, smell, and
taste normal. Consciousness clear.

Pathology and Location: Tumor of whole anterior part of vermiform
process of the cerebellum, lying on floor of fourth ventricle. Corpora
quadrigemina compressed to thinness of paper.

Remarks: Curschmann, _Berlin. klin. Wochenschrift_, 1877, p. 237,
quoted by Bernhardt, 227.

78. Sex and Age: M. 6½.

Clinical History: Fell from a bench, striking the occiput. Headache
for a day or two afterward. Slight irregularity in gait. For weeks
restlessness, headache, and motor ataxia the chief symptoms. In three
months speech became indistinct. “He screamed his words.” Defective
memory. Apparent exophthalmus; ataxic movements of the head, and a
look of profound stupidity; epistaxis; bulbar conjunctiva anæsthetic;
left pupil dilated; vomiting. Ophthalmoscopic examination showed
congestion of right optic nerve and left descending neuritis, going on
to progressive atrophy.

Pathology and Location: Glioma.

Anterior portion of the fourth ventricle occupied by a rounded
swelling of the pons; from under surface of the pons enlargement about
equal on both sides. The anterior pyramids at entrance of pons seemed
abnormally elevated, with the point of entrance also deeper than
normal. Corpora quadrigemina much smaller than usual, and seemed
pushed upward and flattened.

Remarks: V. P. Gibney, _Am. Journ. of the Med. Sci._, N. S. vol. lxx.,
July, 1875, p. 142.

{1085} 79. Sex and Age: M. 11.

Clinical History: Fronto-occipital headache. Vertigo. Staggering gait.
Falls often, and to right. No paralysis. Diminution of sight.
Irregularity of movements of eyes. Right strabismus (?). Vomiting.

Pathology and Location: Tubercle.

Size of hazelnut, in middle of vermiform process, above fourth
ventricle. Some softening of surrounding tissue.

Remarks: Capozzi, quoted by Bernhardt, p. 224.

80. Sex and Age: M. 25.

Clinical History: Fronto-occipital headache. No anæsthesia. No
paralysis; staggering gait. Loss of consciousness, with trembling of
upper extremities. Vertigo. Falls to right. Double optic neuritis;
amaurosis; nystagmus. Dementia; moroseness. Vomiting. Sudden death.

Pathology and Location: Between the amygdalæ of cerebellum; in front
of cerebellum, bulging into fourth ventricle, merging with floor of
fourth ventricle. Medulla oblongata pushed forward to right.

Remarks: Annusk, _V. Graefe's Arch._, Bd. xix., 1873, quoted by
Bernhardt, 223.

81. Sex and Age: M. 58.

Clinical History: Headache, vertigo, diplopia; vomiting. Left facial
paralysis. Ptosis of both eyes, worse in left. Contracture of left
masseter. Speech nasal. Sense of pharyngeal obstruction. Both eyes
diverted to right; on looking toward left the right eye turns to
middle line, and left eye does not follow. Pupils contracted, left
more than right. Anæsthesia of right face. Left ear slightly deaf.
Smell and taste normal. Head movable, with deviation. Trunk and
extremities not anæsthetic or paralytic. Later, smell of left side
diminished. Reactions of degeneration in left face.

Pathology and Location: Floor of fourth ventricle to left of median
line, involving motor root of fifth and nuclei of sixth, seventh,
eighth, and ninth nerves on that side.

Remarks: C. Wernicke, _Arch. für Psychiatrie und Nervenkrankh._, vii.
Bd. 5, iii. Heft., 1877, p. 513.

82. Sex and Age: F. 6½.

Clinical History: Symptoms of tubercular meningitis with a few
irregular symptoms; conjugate deviation of the eyes to the left and
upward. Cheyne-Stokes breathing.

Pathology and Location: Tubercular granulation about the size of a
large pea springing from the left side of the fourth ventricle, just
inside the posterior pyramid, midway between the cerebellar peduncle
and calamus scriptorius; touched the under surface of the middle lobe
of cerebellum. Head hydrocephalic. Miliary tubercles along Sylvian
fissure, and a few elsewhere.

Remarks: Morris J. Lewis, _Trans. of Phil. Path. Soc._, 1879-81, vol.
x. p. 172.

_Pons Varolii and Medulla Oblongata._

83. Sex and Age: F. 8.

Clinical History: Right external strabismus, with contraction of the
right corner of the mouth; contraction disappeared, but squint
remained. Persistent cough, with stringy mucous expectoration.
Staggering. Left hemiparesis, with left partial hemianæsthesia. Severe
constipation. Bowels opened only about once in five days. Water passed
voluntarily once every two days. Difficulty of articulation. Squint
had almost disappeared, but later returned for a few days, and then
disappeared entirely. Became unable to walk, or even to sit,
unsupported. Also became unable to speak, but produced strange
inarticulate sounds. Difficulty in swallowing. A marked feature in
this case was the absence of headache. The only pain suffered was the
pain of dull character referred to the left ear, but which lasted only
two days.

Pathology and Location: Occupied the lower half of the pons and the
upper half of the medulla oblongata, bulging most at the lower border
of the pons at the right side, and extending a little lower and higher
at the right side than on the left. Floor of fourth ventricle bulged
slightly, and appeared to be expanded in all directions, so that the
median fissure was pushed decidedly to the left. Incision revealed the
tumor to be a large cyst filled with bloody fluid and detritus. The
lower part of the ventricular floor not involved.

Remarks: C. K. Mills, not before published.

84. Sex and Age: M. 32.

Clinical History: Thrown from a horse and kicked on the head. History
of syphilis; headache, severe at first, always came on at night;
became less severe later. Vertigo. {1086} Defective memory; apathy.
Right hemiparesis; helplessness of all the limbs before death; partial
ptosis of the right side. Sensation diminished in the left side of the
face and in the right limbs. Pupils small before death. Descending
optic neuritis. Conjugate deviations of the eyes and rotation of the
head to the right. Persistent epistaxis; tendency to hemorrhage from
mucous membranes. Constipation.

Pathology and Location: Gumma and fibroma.

(1) Gumma, half an inch in diameter, distinctly limited to the left
upper quarter of the pons. (2) Fibroma, no larger than a pea, between
the dura and pia mater, causing a slight depression in the first
temporal convolution about the junction of its middle and posterior
thirds, and halfway between the parallel fissure and the horizontal
branch of the Sylvian fissure. Microscopical examination of the optic
nerves showed a descending neuritis of subacute character.

Remarks: C. K. Mills, reported at the meeting of the Amer. Neurol.
Assoc., June, 1881, and published in the _Journ. of Nerv. and Mental
Dis._, July, 1881; and _Arch. Med._, vol. viii. No. 1, Aug., 1882.

85. Sex and Age: M. 35.

Clinical History: History of syphilis. Wounded in head by glancing
bullet. Headache of great severity at intervals. Vomiting at time of
headache. Vertigo. Failure of memory and depressed spirits.
Epileptiform attacks. In the spasms lifted up the right side of his
body and worked over toward the left. Occasional cramps in stomach and
legs. Temporal and orbital neuralgias. Descending neuritis, and
eventual atrophy of both optic nerves. Constipation. Died at the close
of a series of convulsions, death being preceded by general paralysis.

Pathology and Location: Gumma.

A rounded mass, quarter of an inch in diameter, attached to the pia
mater, just to the left of the centre of the anterior surface of the
pons. The entire anterior central portion of the pons was softer and
more doughy than usual. At the junction of the pons with the medulla
oblongata was a recent hemorrhage, which had spread downward to about
the middle of the latter.

Remarks: C. K. Mills, _Brain_, Jan., 1880, and _Arch. Med._, vol.
viii. No. 1, Aug., 1882.

86. Sex and Age: M. 5.

Clinical History: At first left internal squint and nightly paroxysms
of excessively silly laughter. Slight paralysis of right arm, with
rigidity. Paresis of right leg, increasing to paralysis, with
rigidity. During sleep arm and leg became relaxed. Difficulty in
swallowing. Paralysis of left orbicularis palpebrarum and left
external rectus muscles. Sensibility not impaired. Electro-muscular
contractility present in all the paralyzed muscles (?). Speech lost,
apparently from difficulty in articulation. Intelligence preserved
till near the close. Sight, smell, and taste good. Later, suffered
from intense headaches and frequent attacks of palpitation of the
heart, with flushing of face and injection of left conjunctiva, and
with increased rigidity of right arm and leg. Death from paralysis of
the pneumogastric.

Pathology and Location: Glioma.

Gliomatous transformation of the pons, but no distinct separable
neoplasm. Had encroached somewhat on cerebellum, particularly in
region of left pneumogastric lobule.

Remarks: W. Pepper, _Trans. Phila. Path. Soc._, 1878-79, vol. ix. p.
136.

87. Sex and Age: M. 2.

Clinical History: Dysphagia; paresis of left arm and ptosis of left
eye, which improved, followed by same symptoms on right side. “Legs
affected.” Head very large. Dribbling. Paralysis of articulation.
Contraction of orbicular muscle, causing ptosis (?). Clonic spasm of
right side of mouth, and rhythmical jactitation of right arm on
attempted movement. Unable to stand or sit. Optic discs normal.
Evacuations involuntary. Left side of face paralyzed. Tonic spasms of
right sterno-mastoid. Later, left arm jerked like right, and rigid
contractions of legs. Retraction of head and occasional spasm of left
sterno-mastoid. Impossible to gauge sensation.

Pathology and Location: Tubercle.

Tumor of left side of lower part of pons and central and posterior
part of upper half of medulla. Cerebral fluid increased. Medulla
oblongata was twice the normal size.

Remarks: J. M. Hobson, M.D., _Brain_, vol. iv. p. 531.

88. Sex and Age: M. 12.

Clinical History: Slight paresis of right side (arm and leg). He spoke
thickly and swallowed badly. Slight headache. Was depressed. Delirious
at night. Slight paresis of left face. {1087} Irregularity of pulse.
Choked discs. Later, paralysis of sixth nerve. Sudden death, probably
in a fit.

Pathology and Location: Glioma.

Membranes of base congested. Tumor, which appeared to occupy the whole
left half of pons varolii. No trace of fifth nerve on left side.

Remarks: Hughlings-Jackson, _Med. Times and Gaz._, Lond., 1874, i.
151.

89. Sex and Age: F. 60.

Clinical History: Headache frontal, severe and almost constant.
Paresis of right arm and leg. Painful spasm of right arm. Paresis
gradually extended to left half of body. Persistent pain in right arm,
with tremor; later, same symptom, less marked, in left arm, simulating
paralysis agitans. Atheromatous arteries. Melancholic; talks to
herself; very hard of hearing. Head directed constantly to right.
Tremor increased on voluntary motion. Atrophy of muscles of arms.
Flexors of legs contractured. Electro-muscular contractility reduced,
especially on right side. Later, pain on touch in right arm. Febrile
intermitting symptoms, simulating malaria. Still later, distinct
contracture of neck. Conjunctivitis of left eye, with corneal dulness,
followed by kerato-iritis, with ulceration of cornea. Dysphagia;
swelling of submaxillary glands. Œdema of lungs.

Pathology and Location: Sarcoma.

Tumor of left side of pons and left cerebellar crus, extending toward
transverse sinus.

Remarks: Petrina, _op. cit._

90. Sex and Age: M. 54.

Clinical History: Severe continuous headache. Eyes constantly turned
to the right. No diplopia. Eyes, moved together, could not turn beyond
the median line of the left, though the right eye alone could be
turned for some distance to the left beyond the median line. Pupils
equal and mobile. No paralysis or loss of sensation. Some dizziness
and stagger in walking. Died of pneumonia.

After the autopsy the position of the head was regarded not as
compensatory for the position of the eyes, but as due to a severing of
fibres joining the rotatory muscles of the head with their reflex
centres.

Pathology and Location: In the pons at a level one centimeter below
the apparent origin of the fifth nerve on the left side. It was so
situated in front of the eminentia teres that it involved the course
of the fibres of the left abducens, and by a little prolongation
across the raphé toward the right side interrupted the fibres of
communication between the centres for the sixth and third nerves. It
did not involve the common nucleus of the sixth and seventh. It
interrupted the posterior-interior longitudinal bundle and the
adjacent part of the raphé. No other lesion was found. The tumor was
the size of a small nut.

Remarks: Quioc, _Lyon Méd._, 1881, July, Nos. 19 and 20, quoted by M.
Allen Starr, _Journ. of Nerv. and Mental Dis._, vol. xi., July, 1884,
p. 377.

_Crura Cerebri._

91. Sex and Age: M. 25.

Clinical History: No headache. Staggering some days before death.
Apoplectic seizure, with right-sided hemiplegia. Ptosis of left side
(some days before death). Loss of consciousness for three or four
days. No vomiting.

Pathology and Location: Glioma.

In left crus cerebri, including also portion of right.

Remarks: Sutton, _Brit. Med. Journ._, Feb., 1870, quoted by Bernhardt,
p. 163.

92. Sex and Age: M. 9.

Clinical History: Awkwardness in using right hand; soon almost
complete paralysis in the right arm. Headache; nausea; vomiting;
double vision, followed by strabismus, due to paralysis of the left
abducens. Occasional twitchings in right hand, but no convulsions.
Paralysis extended to the right leg; staggering gait. Ataxia and
rigidity in the fingers of the paralyzed hand. Pain in the legs. Optic
neuritis.

Pathology and Location: Sarcoma.

Pressing upon the left crus cerebri and the pons.

Remarks: E. C. Seguin, _Journ. of Nerv. and Ment. Dis._, Jan, 1882.

93. Sex and Age: M. 3.

Clinical History: Headache; unnatural drowsiness. Ptosis of right eye,
with very marked divergent strabismus and fully-dilated pupil; similar
paralysis in left eye, not quite so {1088} marked. Paresis of left
leg. Very late, unconsciousness, constant motion of tongue and lips,
and clonic spasms of left arm and leg. Twitching of right face.
Convulsions, death. Duration, about one year.

Pathology and Location: Tubercle.

Size of a walnut in right crus, almost destroying the crus just at its
junction with pons; making pressure on left crus. Third pair of nerves
diminished in size and softened. Recent inflammatory changes at base.
Increased cerebral fluid.

Remarks: S. Browne, _Dublin Q. J. Med. Sci._, 1849, vii. 496-499.

_Middle Region of Base of Brain and Floor of Skull._

94. Sex and Age: F. 35.

Clinical History: History of syphilis. Headache severe, at first with
long intermissions; later, continuous, and often agonizing. Vomiting
with paroxysmal headache, coming on late in illness. Vertigo, usually
with headache. Excitable and irritable. Slight twitching of mouth,
hands, and forearms. Left hemiplegia; upper as well as lower fibres of
facial nerve paralyzed. Left internal strabismus.
Electro-contractility diminished. Difficulty in enunciation.
Sensibility diminished in left leg. Later, hyperæsthesia and great
pain in paralyzed limbs. Conjunctivitis and necrosis of cornea of left
eye; conjunctiva and cornea insensitive. Sight impaired. Descending
optic neuritis. Hearing impaired on left side. Smell defective.
Profuse perspiration, more marked on right side than on left.
Constipation. Temperature, taken in right and left axilla for eleven
weeks before death, gave the following averages: Right axilla, 99.1°,
M.; 100°, E. Left axilla, 99.4°, M.; 101.4°, E. On some days
remarkable falls in temperature to 96°, 95°, and even 94° and 93°.
Average head-temperatures above the normal: for stations on right side
of head averaging about 97°; on left side, about 94.3° F.

Pathology and Location: Gumma.

A twin-tumor, each mass about two-thirds of an inch in diameter, in
front of the optic chiasm. The growths involved the basal termination
of the corpus callosum, the peduncles of the corpus callosum, the
lamina cinerea, and anterior perforated spaces. They also probably
encroached upon the roots of the olfactory nerves, the optic nerves
and commissure, and the anterior portions of the circle of Willis,
which seemed to have been broken in front. The base of the brain, from
the posterior line of the tumor backward to the pons, was markedly
softened. Microscopical sections of optic nerves showed the
appearances peculiar to descending neuritis in a somewhat advanced
stage.

Remarks: C. K. Mills, _Philadelphia Medical Times_, March 23, 1879, in
“Proceedings of the Pathological Society of Philadelphia;” also, _New
York Medical Record_, Aug. 9, 1879, and _Arch. Med._, vol. viii. No.
1, Aug., 1882.

95. Sex and Age: F. 21.

Clinical History: Suffered for three years from excessive thirst and
polyuria, with occasional vague pains in the head. A constant relation
existed between the amount of fluid imbibed and of urine passed.
Specific gravity of urine, 1002. No albumen nor sugar. Eight liters of
urine passed in the twenty-four hours on an average. Slight headache
and dimness of vision shortly before death; no other nervous symptoms.
No ophthalmoscopic examination was made.

Pathology and Location: Sarcoma.

About the size of a chestnut at the base of the brain, at a spot
corresponding to the sella turcica. It had caused complete
degeneration of the optic chiasm, and had encroached considerably on
the circle of Willis.

Remarks: F. Fazio, _Il Morgagni_, quoted in _Med. and Surg. Rep._,
vol. xlii., May 8, 1880, p. 415.

96. Sex and Age: F. 73.

Clinical History: Suffered for several years from post-nasal catarrh,
with enlargement of tonsils and granular pharyngitis. Fulness in right
side of throat; muco-sanguinolent discharge from post-nasal space;
bulging of soft palate. Severe pain through the right side of the
head. Deafness of right ear and dimness of right eye. Mental failure.
Paresis of levator palpebræ superioris and orbicularis; complete
paralysis of external rectus; possibly slight paresis of the muscles
supplied by the third nerve of the right side. Diminished sensibility
of right half of face and cornea, and conjunctiva of right eye. Cornea
opaque; conjunctival catarrh; vision almost nothing; ophthalmoscopic
examination could not be made. Left {1089} eye showed some diminution
in acuity of vision, with concentric narrowing of visual field;
pigmentation.

Pathology and Location: Lobulated epithelioma.

Involved the cribriform plate of the ethmoid bone, the whole of the
body of the sphenoid, and the anterior part of the basilar process of
the occipital bone. These were softened to the consistency of cheese.
Membranes and cerebral substance firmly adherent to the base of the
skull at the inner portion of the bottom of the right cerebral fossa.
Blood-clot in one of the large arteries of the optic papilla.
Sclerosed blood-vessels. Atrophy of optic nerve and retina.

Remarks: W. Pepper, _Trans. of Philada. Path. Soc._ for 1878-79, vol.
ix. p. 138.

97. Sex and Age: F. 25.

Clinical History: Headache (for six years), with vomiting. For three
years had dimness of vision. For a year had blindness. Exophthalmus,
with dilated pupils and fixation of eyeballs. Painful spasm of right
face occasionally. Occasional paresis of left arm and leg, with pain.
Severe vertical headache. Anosmia. Involuntary discharge of urine and
feces. Convulsions. Stupor. No local paralysis of face or extremities.
Death happened unexpectedly.

Pathology and Location: Cancer.

Tumor apparently springing from pituitary body, passing through
infundibulum into right lateral ventricle. Tumor was “almost the shape
and size of goose-egg.” It occupied anterior half of ventricle, and
flattened out thalamus and corpus striatum. By pressure it had
flattened the olfactory and optic nerves. The growth extended into the
sphenoidal fissure, causing absorption of bone.

Remarks: Habershon, _Med. Times and Gaz._, 1864 (2), pp. 463, 464.

98. Sex and Age: M. 44.

Clinical History: No symptoms during life indicating any brain
disease. The patient had died of phthisis.

Pathology and Location: Osteoma.

Consisting of true bone with Haversian canals, occupying position of
infundibulum and corpora albicantia, which were totally absent. Not
connected at all with dura mater. The pituitary body was apparently
healthy.

Remarks: Bristowe, _Tr. Path. Soc. Lond._, vi. 25.

99. Sex and Age: F. —.

Clinical History: Intense supraorbital neuralgia. Paralysis of the
parts supplied by the third, fourth, fifth, sixth, seventh, and eighth
nerves of the left side. The muscles moving the tongue not affected.
No interference with respiration or the action of the heart; no choked
discs. External tumors on each side of the neck, with a protuberance
of the left eye.

Pathology and Location: Involved the petrous portion of the temporal
bone, with a portion of the sphenoid bone of the left side, size of
walnut.

Remarks: James H. Hutchinson, _Philada. Med. Times_, vol. xiii., Sept.
22, 1883.

100. Sex and Age: F. 66.

Clinical History: One-sided convulsions; first left leg, next left
arm. Slow, syllabic speech, not aphasic. Abnormal, prolonged
somnolence, followed by voracious appetite. Later, incontinence of
urine. Apathetic. Muscles of left half of body, especially arm and
leg, contractured. Pupils contracted. No facial paralysis. Slight
ptosis upon right side. Conjugate deviation of eyes to right; fixed
and immovable. Head drawn to right and backward. Extremities cyanotic
and cold. Accentuated aortic sound; abdominal tympanitis. Taste,
smell, hearing doubtful. Sensibility retained. Electric irritability
rapidly exhausted; reflexes diminished. Unable to stand; constant
tendency to turn to right. No albumen or sugar. All symptoms
intensified; exhaustion; temperature below normal; death.

Pathology and Location: Sarcoma.

Growing from right half of fossa of body of sphenoid bone, and
extending outward and backward along petrous bone, only closely
adherent at basilar portion of sphenoid. Slight depression of middle
peduncle of cerebellum near entrance to pons. Basilar artery pushed to
left. Vessels thick and rigid. Gyrus fornicatus of right side,
temporal aspect, compressed. Right peduncle of cerebrum compressed.
Brain-substance dense; numerous serous cysts in brain and ganglia.

Remarks: Petrina, _op. cit._


{1090}


TUMORS OF THE SPINAL CORD AND ITS ENVELOPES.

BY CHARLES K. MILLS, A.M., M.D., AND JAMES HENDRIE LLOYD, A.M., M.D.


DEFINITION.—Under Spinal Tumors will be included the growths or
adventitious products which arise in the substance of the spinal cord
or spring from its envelopes, membranous or bony, in such manner as to
directly or by pressure involve the spinal cord. Tumors strictly
confined to the cord are extremely rare. First in order of frequency
are the new growths which develop from the spinal membranes, either
the dura mater or pia mater, most frequently the former. Tumors
originating in the bony spine, like those of the substance of the
cord, are comparatively rare.[1]

[Footnote 1: A “Table of Fifty Cases of Spinal Tumor” (which will be
frequently referred to) is appended to this article.]

ETIOLOGY.—Under the predisposing causes of spinal as of intracranial
growths are such diatheses or constitutional affections as cancer,
tuberculosis, and syphilis. Under Pathology a table will be given from
which it appears that of 50 tabulated cases, 3 were cancerous, 5
syphilitic, and 4 tubercular.

Traumatisms, such as a fall from a height, a blow on the back, a
wrench or twist of the spine, or a sudden concussion as in a railway
accident, sometimes serve as exciting causes of spinal tumors. Even
when a diathetic or infectious predisposition exists, the patient
might frequently escape from the special intraspinal localization of
the disease were it not for the accidental infliction of direct injury
to the axis. When no special predisposition is present, an injury is
more likely to produce an osteoma, fibroma, or sarcoma than some of
the other forms which will be mentioned, such as a glioma, myxoma,
neuroma, or psammoma.

Spinal tumors are said by most authors to occur much more frequently
in the male than in the female sex. Our tabulated cases, however, gave
22 cases among males, 21 among females, and 7 in which the sex was not
given.

Fifty cases of spinal tumor gave the following result as to age:

  Under 10 years . . . . .  4 cases.
  From 10 to 20 years  . .  3   "
   "   20 to 30   "    . .  7   "
   "   30 to 40   "    . . 12   "
   "   40 to 50   "    . . 10   "
   "   50 to 60   "    . .  6   "
   "   60 to 70   "    . .  1   "
  Age not given  . . . . .  7   "
                           -------
                           50 cases.

{1091} SYMPTOMATOLOGY.—Can tumors of the spinal membrane be separated
by a study of symptoms from intramedullary tumors? While this may be
theoretically possible, in practice it will be found difficult, and of
little value even when it can be done. The spinal canal is of such
narrow calibre that a growth of any size either in the membranes or
the cord itself will soon directly or indirectly involve both. On this
subject Erb[2] speaks as follows: “The attempt has thus far been made
in vain to secure, from amongst the individual symptoms, at least a
few fixed points on which to base the diagnosis of intramedullary
tumors. The following have been claimed as such: A somewhat long
antecedent history of active local manifestations of irritation,
belt-like pains, eccentric pains, definite paræsthesiæ, local
paralysis, as in meningeal tumors; early and well-marked atrophy,
which points to a larger involvement of the gray substance; striking
fluctuations in the course of the disease, spontaneous improvement,
and equally spontaneous growing worse again (Schueppel); and, finally,
Schueppel has also tried to connect the occurrence of scoliosis
(curvature of the spinal column to the side on which the tumor is
situated) with the presence of a tumor. In this he is doubtless wrong,
as this manifestation merely depends on unilateral paralysis of the
muscles of the back, which may depend on all sorts of causes.”

[Footnote 2: _Ziemssen's Cycl. Prac. Med._, Am. trans., p. 754.]

In the discussion of symptomatology and diagnosis which follows
therefore no effort will be made to separate the phenomena of
meningeal and intramedullary growth. In most cases the symptoms
indicate involvement early of the membranes, and later compression of
the cord.

The symptomatology will differ according to the stage of the
affection. The symptoms can be arranged into those of a first or
early, a middle, and a late stage. As a rule, but not invariably, the
symptoms of the early stage are those of beginning irritation—such
sensory phenomena, for instance, as pain in the parts supplied by
certain nerves in the neck, arms, hands, abdomen, legs, or feet. This
pain is sometimes associated at an early period with more or less
stiffness, which later may become well-marked contracture. Pain in the
back is occasionally an early symptom. Paræsthesiæ, as numbness,
formication, constriction or girdle sensations, coldness or heat or
alternations of hot and cold feelings, are sometimes early symptoms,
but occur in a more positive manner in the middle stages of the
progress of the spinal growth. Hyperæsthesia is more likely to be
pronounced in the middle stage of the disease. A slight paresis, which
may vary a little from day to day for a time, slight twitchings or
spasms, usually localized to certain muscles or groups of muscles, are
also present, in some cases as an incipient manifestation. The
presence of these motor symptoms will depend largely upon the location
of the incipient growth with reference to the columns of the cord.

One general point of differentiation between intramedullary and
membranous tumors is the fact that irritative phenomena, such as pain
in the back and along nerve-tracts, spasmodic twitchings, etc., are
not likely to appear as early in the intramedullary cases as in the
meningeal or mixed forms.

In the middle period of the progress of a spinal tumor the irritative
phenomena, such as pain, paræsthesiæ, hyperæsthesia, twitchings,
cramps, stiffness, and paresis, will be found to persist and increase,
and in {1092} addition other manifestations will appear, chiefly those
of compression of the cord. Anæsthesia frequently develops, and, when
the posterior segment of the cord is the one chiefly implicated, soon
becomes profound; it is, however, often variable in distribution for a
time, and sometimes shows peculiar areas. One leg or one arm may be
partially involved, or both lower or both upper extremities, or
certain portions of any one of the limbs. Anæsthesia dolorosa—that is,
absence of sensation to objective tests, although the patient suffers
pain or distress in the affected part—is common. Hyperæsthesia, best
observed in this middle period, is sometimes cutaneous, but in other
cases follows certain nerve-trunks, probably indicating a neuritis
descending from the seat of the spinal growth. In this and in the last
stage the paresis advances to more or less complete paralysis, which
is also variable in distribution according to the localization of the
growth. Contractures and rigidity come on and changes in the reflexes
now become important symptoms. These may be increase of knee-jerk with
ankle-clonus, or diminished or abolished knee-jerk, according to the
position and the extent of the lesion.

The late symptoms of spinal tumors, especially of those which are
slowly developed, are—usually profound anæsthesia and paralysis of the
limbs, with rigidity and contractures, atrophy, marked changes in the
spinal reflexes, bed-sores, paralysis of bowels or bladders or their
sphincters, impotence, œdema, dyspnœa, vomiting, cardiac palpitation,
cystitis, and pyelitis, and, when the lesion is near the medulla
oblongata, dysphagia and certain intracranial symptoms, as amblyopia,
diplopia, deafness, contracted pupils, affections of speech, etc.

The size of the growth and the rapidity of its development will of
course influence the character and the time of appearance of certain
symptoms. According to the position of the growth, either as to its
level in the spinal axis or as to its relative position to the various
longitudinal segments of the spinal cord, the symptoms will also
differ at special stages. These differences will appear as
symptomatology and diagnosis are now further considered.

Pain in the back occurs, but is not as frequent a symptom as eccentric
pain. Unlike headache in intracranial tumors, it is not a constant
symptom. The headache of brain tumors is due in part at least to the
conditions of tension which are produced by the growth interfering
with the balance of pressure within the skull. Headache is also, as
has been pointed out in the article on Brain Tumors, frequently due to
the irritation of the membranes; but in this case the one great nerve
through which pain expresses itself is the trigeminal, which has its
distribution both within the skull and outside of it to all parts of
the head. In spinal tumors the pains are more likely to be eccentric,
because of the limited character of the lesion and the almost
exclusively peripheral distribution of the nerves. Twisting the trunk
or jarring the spinal column by blows on the head will sometimes cause
pain along the spine, most frequently when the bone is involved. It
sometimes cannot be elicited.

Leyden[3] pointed out the fact that the movement of the spinal column
is often difficult and painful in a certain direction, because this
motion brings a greater pressure upon the tumor.

[Footnote 3: Quoted by Erb.]

{1093} Pain on percussion over the spinal column might be expected
from the character of the affection, but has not been frequently
reported. Like spinal hypersensitiveness and inflexibility with
muscular rigidity, it is much more to be expected in those cases in
which the vertebral bones and cartilages are implicated.

Constriction or girdle sensations are of comparatively frequently
occurrence. When the cervical cord is involved, choking sensations or
a sense of constriction about the neck are common. Tumors located in
the lower cervical and dorsal region give girdle sensations most
frequently in the chest or abdomen. So far as the assistance afforded
by such sensations toward localizing the exact level of the growth is
concerned, however, it must not be forgotten that curious and
unexpected conditions sometimes occur. Thus, in one case (Case 16) a
myxoma at the level of the sixth and seventh cervical vertebræ caused
constriction sense about the legs and abdomen, and in another (Case
44), a glioma of the filum terminale, constriction of the chest.

The paralytic phenomena of spinal tumors have certain peculiarities
which are not exhibited by any other spinal or by cerebral affections.
A glance at the clinical history of a number of cases shows that many
of them began with paresis of a single limb or part of a limb, in
addition to the irritative phenomena. This paresis deepens after a
time into complete paralysis, or before this occurs one or more of the
other extremities become paretic. The progress toward bilateral
paralysis may be comparatively rapid. The appearance and progress of
the paresis or paralysis vary somewhat according to the level of the
cord at which the tumor is located. In tumors of the cervical cord the
paresis usually, but by no means invariably, first attacks the upper
extremity. The fact that the arms are first the seat of irritative
phenomena and paresis is in a case of spinal tumor indicative of a
cervical location or a location in the upper dorsal region; but, on
the other hand, not a few cases are recorded in which in tumors in
these locations the loss of power first exhibited itself in one or
both of the lower extremities. These cases are to be explained by the
manner in which the descending motor tracts are affected directly or
by pressure. In mid-dorsal tumors and those below this level the
paresis shows itself first in the legs, and generally becomes before
long a complete paraplegia.

To Brown-Séquard, more than to any other observer, we owe our accurate
practical knowledge of unilateral lesions of the spinal cord, both in
the cervical and other regions. When the lesion is localized in one
lateral half of the cord and is situated in the cervical region, we
have the affection known as spinal hemiplegia. The main symptoms of
this affection are motor paralysis of the arm and leg on the side of
the lesion and anæsthesia of the opposite limbs. Sensory fibres
decussate in the cord soon after entering it, while the motor tracts
cross at the anterior pyramids of the medulla oblongata; in which
physiological facts we have a simple explanation of the peculiar motor
and sensory phenomena presented by such a case. When the lesion is
below the cervical portion of the cord, instead of spinal hemiplegia
we have the affection known as spinal hemiparaplegia, in which the
paralysis and hyperæsthesia in one lower extremity stand out in strong
contrast to the anæsthesia and retained muscular power in the other.
With a lesion so strictly localized as a spinal {1094} tumor it might
be expected that these crossed phenomena would present themselves in
some cases. They are recorded, more or less distinctly, in Cases 4,
16, and 38, and it is probable that they would have been more
frequently observed if they had been anticipated and looked for
carefully.

Ataxia does not seem to have been a frequent symptom in reported
cases. It has probably been sometimes overlooked or confounded with
paresis. In a case of myxoma of the dura mater in the left dorsal
region ataxia of both leg and arms was present; but in this case,
however, the dura mater of the brain contained fluid and lymph. In the
light of the commonly accepted views as to the physiology of the
spinal cord regarding the posterior columns, as related in function
both to co-ordination and sensation, ataxic manifestations might be
frequently expected. Owing, however, to the narrowness of the spinal
canal, compression of the entire cord takes place so early as to make
paretic symptoms displace those of ataxia.

Atrophy which varies in distribution according to the extent of the
destructive involvement of the cord is frequently present. In a few
instances the atrophy will be of certain muscles or muscular groups.
When true atrophy is present the anterior horn will be involved
directly or indirectly, and accompanying changes in the electrical
reactions will also be found.

The electrical condition of the atrophy of the paralyzed parts will
vary with the extent of the trouble produced by the tumor. In a case
of tumor of the cervical enlargement, for instance, producing more or
less paralysis both of the upper and lower extremities, reactions of
degeneration will be present only in the muscles supplied by the
nerves which spring directly from the seat of lesion.

Spontaneous twitchings or spasms due to irritation of motor-centres or
tracts are comparatively frequent. More or less permanent contracture
in a limb or part is of frequent occurrence, particularly after the
growth has advanced. Forms of torticollis or retraction of the head,
strong flexures of the arms or legs, and, late in the history of many
cases, complete and extremely painful drawing up of the limbs upon the
body, may occur. Persistent subsultus was observed in one case, a
glio-myxoma involving the gray columns from the medulla oblongata to
the cauda equina. Fibrillary twitching is rare, and in our tabulated
cases was observed only in one instance, a glioma of the filum
terminale. General convulsions with unconsciousness are exceedingly
uncommon. In one case, however, a round-celled sarcoma at the level of
the seventh, eighth, ninth, and tenth cervical vertebræ, the patient
is recorded as having died in a fit. Nystagmus was observed once, but
probably had no significance so far as the spinal affection was
concerned, as the cerebral dura mater exhibited evidences of
inflammation.

The condition of the reflexes, both cutaneous and tendinous, is often
peculiar and almost diagnostic, but varies greatly according to the
position and extent of the lesion. Increase of reflex action is
sometimes a marked symptom. The slightest irritation of the soles of
the feet, the calves of the legs, palms of the hands, or other special
regions will often produce decided contractions, and sometimes that
symptom which has been designated by Brown-Séquard as spinal epilepsy,
in which both lower extremities are thrown into violent clonic spasms,
which may last {1095} for many seconds or even minutes. In tumors of
the dorsal region causing marked compression and preventing cerebral
inhibition, clonus and knee-jerk are also markedly exaggerated. The
so-called diplegic contractions—that is, contractions in one extremity
from irritation of the other—are observed, especially when a
transverse area of the cord, large or small, is involved in an
irritative or inflammatory process. They probably result from the
abnormal facility of transmitting impressions which has been acquired
by the cord. When the cervical or the lumbar enlargement of the cord
is completely compressed or destroyed by a tumor, reflex activity is
diminished or abolished in the region supplied by nerves originating
at the seat of lesion.

Alterations in the body-temperatures have been frequently noted in
lesions of the spinal cord, such as fractures of the vertebræ and
inflammatory changes in the cord and its membranes. Some of the
observations are almost incredible, as that of J. W. Teale,[4] who
records an axillary temperature of 122° F. The subject has been
somewhat obscured by physiological speculations. Thus, it has been
asserted that paralysis of motor centres and strands causes an
increase of temperature, while paralysis of sensory tracts produces a
diminution. The accepted clinical facts apparently are as follows:
after crushing the cervical cord a uniform rise in temperature occurs
if peripheral cooling is prevented. This rise is caused by a paralysis
of the vaso-motor nerves, which permits a paralysis of the vessels and
floods the parts with blood. This assumes, of course, that mere
increase of blood in a part means increase of heat. After a variable
period this increase is followed by a decrease which is permanent.
Hutchinson records[5] a case of fracture of the cervical spine at the
fifth vertebra in which the patient's body felt almost as cold as a
corpse and the rectal temperature was only 95° F. In Cases 4 and 16
the affected parts are recorded as cold, just as in atrophic and other
lesions of the cord. The tabulated cases do not show many exact
thermometric observations, but in Case 8 the average temperature for
two weeks before death is given as slightly below normal, while Case 7
shows a sudden rise on the day preceding death. It is probable that
the permanent decrease following crushing and compressing lesions
would also be found in cases of spinal tumors. The following exact
observations, made by one of us[6] upon a case of injury to the
cervical cord, are directly illustrative of this subject. The case was
of several months' standing. The patient could walk imperfectly, and
the right arm was more paretic than the left. The observations were
made at 10 o'clock A.M. on six successive days:

                     Right Axilla.  Left Axilla.
  First observation . .  98.2°         97.3°
  Second     "      . .  99.8°         98.2°
  Third      "      . .  96.4°         96.2°
  Fourth     "      . .  95.6°         96.4°
  Fifth      "      . .  97.2°         96.8°
  Sixth      "      . .  95.2°         93.8°

It will be seen that the temperatures range higher in this series on
the more paretic side; but this did not hold in a series taken a few
weeks {1096} later. The fact is to be noted that all these
temperatures, with one exception, are below the normal.

[Footnote 4: _Lancet_, March 6, 1875.]

[Footnote 5: _Ibid._, August, 1875.]

[Footnote 6: _Hospital Gazette_, Nov. 7, 1879.]

Cystitis, pyelitis, and pyelo-nephritis are usually secondary
symptoms, due to retention of urine, distension of the bladder, etc.
in consequence of paralysis of this viscus. Bed-sores result in two
ways: in the first place, they may be due to emaciation and immobility
and the uncleanliness which it is almost impossible to prevent; or, in
the second, trophic eschars may arise because of the involvement of
nutritive regions of the cord. The so-called sacro-ischiatic eschars
are of this character. Febrile phenomena, such as chills, increased
temperature, increased respiratory action, are frequently secondary
phenomena due to bed-sores, cystitis, continued pain, exhaustion, or
septic infection.

Priapism was recorded in two of the fifty cases, both tumors of the
cervical cord. Impotence was only recorded once, a dorsal myxoma. It
is probable that both priapism and impotence, particularly the latter,
were present, but overlooked in other reports.

Headache was present in three of fifty cases. One of these was a
fibro-sarcoma at the level of the fourth cervical nerve; the other two
were low down in the spinal axis, one in the lumbar enlargement, and
the third, strange to say, in the filum terminale. Vertigo is a rare
symptom in the spinal tumors. In one case in which the growth was
located at the position of the third cervical vertebra its presence
was recorded.

Out of five cases in which vomiting was present, two were in the
cervical regions, one in the dorsal, one in the lumbar, one in the
filum terminale.

Tumors involving the upper cervical and bulbar region of course will
give rise to special symptoms indicating more or less involvement of
cranial nerves.

Unfortunately, very few ophthalmoscopic observations have been made in
cases of spinal tumor. Optic neuritis has been found in a few
cervico-dorsal cases, and in other cases located in the same region no
ophthalmoscopic alterations have been discoverable.

Mental disturbances were only especially recorded in four of the fifty
cases. Such symptoms were certainly not of frequent occurrence, except
those emotional manifestations which were due to the great suffering
which the unfortunate patient was called upon to endure. These
emotional disturbances, as in all forms of painful disease, varied
according to the mental stamina of the patient. In one case the mental
symptoms, in association with other phenomena and a probability of
dog-bite, led to the suspicion of hydrophobia.

In one case (31) an interesting observation was made of an anal
sphincter reflex, with frequent stools. The tumor in this case is
reported at the level of the tenth dorsal vertebra, which would be at
the level of the eleventh dorsal segment. The tumor was tubercular,
and therefore probably meningeal, so that the irritation to the anal
centre, which is in the lumbo-sacral segment, may have been caused by
extension of inflammation along the meninges.

PATHOLOGY.—We present in tabulated form the various kinds of tumors as
found in the fifty cases which have been collected: {1097}

  Aneurism . . . . . . . . . 1  |  Myxoma . . . . . . . . 2
  Cancer (?) . . . . . . . . 2  |  Neuroma  . . . . . . . 1
  Carcinoma  . . . . . . . . 1  |  Organized blood-clot . 1
  Cysticercus and hydatids . 3  |  Osteoma  . . . . . . . 1
  Cyst (Dermoid?). . . . . . 1  |  Phlegmon . . . . . . . 1
  Fibroma  . . . . . . . . . 5  |  Psammoma . . . . . . . 2
  Glioma . . . . . . . . . . 5  |  Sarcoma  . . . . . . . 7
  Gumma  . . . . . . . . . . 5  |  Tubercle . . . . . . . 4
  Myo-lipoma . . . . . . . . 2  |  Unclassified . . . . . 6

It will be observed that the predominance in this list is decidedly in
favor of the sarcomata and structures which are likely to be
associated with or to graduate into them, such as the gliomata,
myxomata, and the psammoma. In one instance the resemblance (Case 15)
to psammoma is referred to by the reporter. The comparatively large
number of unclassified, and the two cases referred to vaguely as
cancer, would probably, on more exact report, have added several more
to the group of the sarcomata. The table shows that next in frequency
come the fibromata and gummata, while the carcinomata have but a
single representative in the group. Tubercular tumors occurred with
comparative frequency, no less than 8 per cent. being recorded.
Although the exact origin of only somewhat more than one-half (29) of
all the tumors is given, it is stated of this fraction that 17 sprang
from the membranes, while of the remainder 8 were located in the cord
itself and 4 in the vertebræ. Of the 3 oases of parasitic invasion, it
is recorded of one (Case 43) that a hydatid cyst was also found in the
liver; and it is probable that in any given case the spinal cord would
not be the only part to suffer. Cobbold's work refers to one case of
hydatid of the spinal cord. Erb refers to 13 cases, all but 2 external
to the dura mater. In Case 43 of the table pains in the back and hip,
simulating rheumatism, were present early.

The dimensions of the spinal tumors of whatever character are never
very great, for the reason that they have but little space in which to
enlarge, and that their presence soon causes such grave changes as to
be incompatible with life. They rarely exceed an inch in their longest
diameter, and not unfrequently are smaller than this. There is usually
about them a more or less marked meningitis and an area of vascular
fulness. Œdema of the membranes is sometimes noted. The substance of
the cord beneath is compressed, atrophied, or softened, and this
softening sometimes extends for a considerable distance both above and
below the neoplasm. These changes were reported in Case 8, in which
there was the addition of an abscess. Secondary degenerations would
probably be found in all cases, unless very recent; and these changes,
following the Wallerian law, would ascend the posterior and descend
the lateral columns. Such degenerations are reported in some of the
cases. The spinal nerves are sometimes compressed and atrophied. Old
or recent hemorrhages are found, as in Case 18. Among the changes
which occur, probably at a late stage, are the formation of cysts,
either large or small, either in the substance of the cord or
consisting simply of a dilatation of the central canal of the cord.
This condition is known as syringo-myelia, and is of exclusive
pathological interest. In Case 1 is recorded, apparently, a
well-marked dilatation of the central canal (hydromyelus), and
cyst-formation is recorded with gliomata, sarcomata, and gummata in
other cases. Caries of the vertebræ is recorded in a number of cases,
and occurred both in cases of gumma (Case 8) and carcinoma (Case 14).
These cases were, however, exceptions to the general rule that the
bony envelope of the cord does not furnish external {1098} evidence of
the location of the tumor. It is worthy of note that the one instance
of phlegmon or inflammatory exudate (Case 20) also presented
infiltration of the tissues of the throat and mediastinal space. A
case of organized blood-clot (Case 39) has been included in the list,
although, properly, a spinal hemorrhage, because it became and acted
as a tumor. The location of the single case of aneurism (Case 48) is
not given. The symptoms were those of tumor in the dorsal spine.

As sequelæ of tumors of the cord may be mentioned especially
bed-sores, which sometimes commit frightful ravages, as in a case (37)
in which the spinal canal was laid open. The bronzing of the skin and
diseased condition of the suprarenal capsules, as recorded in Case 41,
were mere coincidences, and not probably at all connected in
pathological sequence with the spinal lesion. Cystitis, pyelitis, and
pyonephritis are not uncommon in cases of tumor of the cord, just as
they are observed in other compressing and destructive lesions of that
organ. In those cases in which the tumor is the result of a general
taint, as in gummy and tubercular growths, the evidence of this taint
is not usually wanting in other organs; thus in Case 37, of tubercle
of the cord, tubercles were also found in the lungs, bowels, and
uterus. In gummata of the cord it would not be likely to escape
careful inquiry that the patient's history or his body presented
evidence of the disease.

In a case (47) of congenital sacral neuroma amyilinicum the infant was
also hydrocephalic and had a bifid spine—conditions of faulty
development with which the patient cannot long survive.

In one case of psammoma (Case 5) a resemblance to endothelioma is
noted, while in another (Case 15), already referred to, a sarcoma is
said to have resembled a psammoma.

Vascular changes are usually notable. In addition to the congestion
already spoken of, it is recorded in one case (No. 14) that the right
vertebral artery was obliterated. This was a carcinoma which had
partly destroyed one vertebra.

Virchow's case (No. 50) of a stillborn child with a large tumor of the
size of the head of a child of two years, and containing bone, has
some analogies in three cases, referred to by that author, in which
both hair and bone were found.

In several cases a brown or yellow exudate (plastic lymph?) is
mentioned as extending along the cord far beyond the immediate
neighborhood of the tumor.

The histology of tumors of the whole cerebro-spinal axis will be found
described in the article on Tumors of the Brain.

DIAGNOSIS.—The diagnosis of tumors of the spinal cord presents itself
naturally under two heads—the differential, or general, and the local
diagnosis. The conclusions reached in this paper are based on a
careful study of the cases appended, two of which were personal
observations, and the remainder were collected from American, English,
French, and German literature. It cannot be denied that much obscurity
rests upon the diagnosis of tumors of the spinal cord, and that the
doubts expressed by Erb and other writers have much to support them.
It is hoped that the systematized study presented in this table will
do something to dispel this obscurity.

(1) General Diagnosis.—The differential diagnosis has regard first to
{1099} certain general phenomena which are broadly indicative of a
spinal disorder as distinct from a cerebral or peripheral one. Thus,
mental symptoms are absent, or if present are an accompaniment of
tumors high up in the spinal axis, are the results of suffering, or
appear very late in the disease because of progressive weakness.
Briefly stated, the phenomena which point with comparative certainty
to the existence of spinal tumors are symptoms of meningeal irritation
gradually increasing, and symptoms of slow compression of the cord.
These have been sketched at the beginning of Symptomatology. As to
duration, the data in the cases studied were somewhat meagre. The
usual duration is from six months to three years.

The differential diagnosis of spinal tumors will be considered in
reference to the following affections: congestion, hemorrhage,
meningitis (simple and specific), caries, traumatisms, sclerosis,
aneurisms, neuritis, metallic and infectious disorders, and hysteria.
Spinal tumors, it will be recalled, are from constitutional or special
causes, as syphilis, cancer, and tuberculosis. The onset is gradual
and irregular. The duration is comparatively long. The progress is by
irregular advances toward a fatal termination. The symptoms are
inclined to be at first unilateral or local; later, bilateral. Special
symptoms, as paralysis, spasm, sensory and visceral disorders, occur
irregularly as to time. Decubitus and trophic changes are common late
in the history. Reactions of degeneration are often present. Gowers
refers to the fact that two morbid processes often occur, one
consecutive upon the other, as a secondary degeneration or a
hemorrhage, after the establishment of the morbid growth, with
characteristic increase of symptoms.

In spinal congestion a constitutional cause is not likely to be
present. The onset is usually sudden and after exposure. The duration
is shorter than in tumors, and is from a few days to four months. The
disease is stationary for a while; then retrogression of symptoms
toward recovery occurs. The symptoms are more uniformly bilateral, and
motor and other symptoms develop about the same time. Decubitus is
rare. Reactions of degeneration are rare (?). It is desirable that
cases of so-called spinal congestion should be differentiated from the
forms of peripheral neuritis above referred to, the most
characteristic symptom of which appears to be tenderness of
nerve-trunks.

In spinal hemorrhage there is no special history, or a history and
signs of cardiac and vascular degeneration may be present. The onset
is quite sudden and the progress of the case regular. The first
symptoms persist, and secondary degenerations follow, and differ
according to the extent and location of the lesion, but are most
likely to be uniformly bilateral.

In meningitis the symptoms of localized compression are absent. The
girdle symptom is absent. The affection is sometimes curable, and
especially so if it has been of syphilitic origin. The reactions of
degeneration are not marked.

In caries of the spinal vertebræ deformity is rarely absent,
especially if the case has continued a few months. Rigidity of the
muscles of the back is an important symptom, which, however, is
occasionally found with tumor. Jarring of the spinal column by tapping
upon the head or jumping from a chair or stool is more likely to
elicit pain in caries than {1100} in tumors. Strumous symptoms and
evidence of tubercles in the lungs or other organs are often present.

In traumatisms usually a history of the injury can be obtained. The
symptoms are those of caries, myelitis, meningitis, or of combinations
of these, according to the character of the case.

In sclerosis the symptoms are usually those of progressive systemic
affections, with absence of compression symptoms. The duration is
longer. The progress is gradual and more regular.

Aneurisms are only to be distinguished when extra-spinal, causing
erosion and compression.

In neuritis there is the soreness of the nerve-trunk already referred
to, while compression symptoms and visceral disorders are absent. The
motor and sensory symptoms are confined to the area of distribution of
the affected nerve. It is amenable to treatment. In advanced stages
the reactions of degeneration are marked. In the form of general
peripheral neuritis, the existence of which, as a distinct disease, is
being at present claimed, the characteristic symptoms are as yet not
sufficiently determined or the pathology demonstrated by post-mortem
research to admit of much discussion.

In metallic and infectious disorders a history of definite causation
is present. Metallic disorders may present special distinctive signs,
such as lead-line, wrist-drop, etc.

In hysteria a precedent characteristic history is usual. The onset is
often sudden and an emotional element is present. The symptoms are
bilateral and protean. Trophic changes are absent. No reactions of
degeneration are present.

(2) Local Diagnosis.—It may be said of spinal tumors in a modified
sense, as it can be said of brain tumors, that they are not good
pathological experiments for illustrating the functions of the exact
areas which they occupy. The spinal canal has such narrow limits, the
tumor itself soon attains such a relatively large size and causes such
wide vascular engorgement, and the different tracts and systems of the
cord are so closely packed together, that the tumor does not often
invade only one functional area and escape another. Hence the regional
diagnosis presents special and greater difficulties than the diagnosis
of the level of the cord at which the tumor presents itself. A tumor
which destroys the trophic centres for the arm in the anterior cornua
might exert sufficient backward pressure to paralyze the motor tracts
running to the leg; or a cervical tumor, as in Case 5, might produce
symptoms which are almost wholly observed in the legs. It will be
seen, however, by reference to the table, that in Case 3, reported by
Wilks, we have a tumor whose exact anatomical seat could have been
predicted, and which seems to have reproduced almost the upper-arm
paralysis of Remak. When we compare these two cases, in which the
pathological conditions are so similar, it will be observed that the
paralyzed arm is much wasted, which indicates a lesion of its trophic
centre, whereas the affected legs in the other case are irritated by
pressure and by isolation, but are not wasted, because their trophic
centres are far below the point of lesion. The invasion of the trophic
centres, and the accompanying wasting of particular groups of muscles,
especially when this occurs early in the case, with the consequent
reactions of degeneration in these muscles, would furnish very
valuable indications {1101} both as to the region and the level of the
cord involved (Case 29). Unfortunately, the exact observations are
wanting in most of the cases as reported.

M. Allen Starr, in a recent paper,[7] has devoted much labor to the
elucidation of the functions of different segments and regions of the
cord. He demonstrates the existence of groups of cells in the gray
matter, especially in the anterior horns, each of which he believes
constitutes a physiological unit. He affirms that these cell-groups
preside over certain associated movements or combinations of certain
muscles, and, quoting from Spitzka, says that “the nearer a muscle is
to the ventral aspect of an animal the nearer will its nucleus be to
the median line of the cord; and the nearer the muscle is to the
dorsal aspect of the animal the nearer will its nucleus be to the
lateral cornua of the cord. Flexor nuclei are therefore in internal,
extensor nuclei in external and posterior, cell-groups.” The only
light that such a theory throws upon the subject of diagnosis is by
affording a possible explanation of the fact that spastic flexion is
much more common than spastic extension, and may be due to the fact
that the cell-groups for flexion lie deeper and are more protected
than those for extension; and the additional fact above referred to,
that a paralysis of associated muscles or groups of muscles, with
degeneration, as in the types of Remak, would indicate with great
clearness the destruction of the cell-group which presides over them.
Starr, in his article, also tabulates the various reflexes and their
seats in the cord. As this subject is of much importance in any exact
study of spinal-cord diseases, we will state here some of the facts as
given in that article: The neck-pupil reflex (dilatation of the pupil
on irritation of the neck) has its seat from the fourth to the seventh
cervical segment; the elbow-tendon reflex in the fifth and sixth
cervical; the wrist tendons from the sixth to the eighth cervical; the
palmar in the seventh and eighth cervical; the epigastric and
abdominal skin reflexes in the fourth to the eleventh dorsal segments;
the cremasteric reflex in the first to the third lumbar; the patellar
tendon in the second to the fourth lumbar, and bladder and sexual
centres in same; the rectal centre in the fourth lumbar to the third
sacral; the foot-clonus and Achilles-tendon reflex in the first
sacral. A destructive lesion, such as a tumor, at any one of these
points would cause abolition of that particular reflex, and this would
probably occur early in the case. Our table of cases does not present
any such observation, whereas exaggerated reflexes, such as occur from
a compressing lesion above the seat of the excited centre, are
recorded in abundance. Many of these deductions are of course only
possible early in the history of the case, as at a late stage the
secondary degenerations have caused too widespread havoc to admit of
any exact localization. The distinction must also be sought for
between a destructive lesion and the symptoms of irritation which it
may project to distant parts. Fürstner's cases of syringo-myelia,[8]
in which were marked vaso-motor changes, such as pallor, flushings,
copious sweat, and trophic disorders in the integument and its
appendages, seem to show that a lesion in the gray matter just
posterior and external to the central canal is necessary for such
phenomena. Similar vaso-motor changes may be observed in some of the
tabulated cases, as in No. 4, in {1102} which there were islands of
heat and cold in the leg, with a hydromyelia in the cord. Sensory
symptoms are very common in cases of spinal tumor, but they furnish
indications rather of the exact level of the lesion than of its
region.

[Footnote 7: “Localization of the Functions of Spinal Cord,” _Am.
Journ. Neur. and Psych._, 2-3, p. 443.]

[Footnote 8: Quoted by Starr.]

[Illustration: FIG. 45. Diagram of Spinal Column, Cord, and
Nerve-exits (after Gowers).]

[Illustration: FIG. 46. Sarcoma compressing Cervical Cord, Case 17 of
Table (E. Long Fox).]

Before considering briefly the indications which point to the various
levels of the cord as a possible seat of spinal tumor, it will be
necessary also to make plain a few anatomical facts. It must be borne
in mind, first, that the nerve-origins in the cord are never at the
same level as their exits from the spinal canal, or, in other words,
that the spinal segments do not correspond with the bodies of the same
numerical vertebræ, and that there is, in fact, one more cervical
segment than there are cervical vertebræ. The tendency is for the
nerve-trunks to run downward before passing out of the canal, so that
in every instance, without exception, from the medulla oblongata to
the filum terminale the segments of the cord are above the
corresponding vertebral body. This discrepancy increases as we descend
the cord; whereas it is approximately correct to say of the cervical
and dorsal regions that every segment is opposite the vertebral body
which is numerically just above it, this difference becomes much
greater in the lumbar and sacral regions. The cord itself terminates
in the lumbar enlargement which ends opposite the interval between
{1103} the first and second lumbar vertebræ. All the remainder of the
canal is occupied by the descending trunks of the lumbar, sacral, and
coccygeal nerves as they pass to their respective foramina,
constituting the cauda equina. It must be recalled, however, that the
vertebral bodies, lying very deep, cannot serve as guides, but that we
are dependent upon the spinous processes as landmarks in diagnosis.
These again differ in their levels from their respective vertebral
bodies, as they are deflected at somewhat different angles at
different regions of the spine. Gowers has illustrated these facts by
a very graphic wood-cut[9] (Fig. 45), from which the general rule may
be drawn that each vertebral spine is about opposite the spinal
segment which is numerically two places below it; thus the eighth
dorsal spine is opposite the tenth dorsal segment, etc. The
indications afforded by this exact anatomical knowledge have reference
largely to the existence of pain on pressure and to any deformity of
the bony structures. The cases as reported do not indicate that this
method of research has been utilized, and it may possibly be of only
theoretical importance; but it has been considered worthy of reference
as an indication in diagnosis.

[Footnote 9: _Diagnosis of Diseases of Spinal Cord_, p. 6.]

[Illustration: FIG. 47.]

[Illustration: FIG. 48.]

[Illustration: FIG. 49.]

[Illustration: FIG. 50. Sarcoma of Lower Cervical Cord, Case 13 of
Table (Adamkiewicz).]

It will be seen by reference to the table that usually certain general
features in the symptomatology indicate the seat of the lesion. Thus
in tumors of the cervical region pain and stiffness of the neck occur,
while the first appearances of paresis and sensory disturbances are
usually observed in the arms and about the chest. The centres for the
forearm and hand lie in the lower portion of the cervical enlargement;
that for the upper arm, including the supinator longus, in the upper
portion. Mental symptoms are more marked, and in Case 4 several of the
cranial nerves were implicated. In the lower cervical and upper dorsal
region there are symptoms of dyspnœa, fixation of the chest (Nos. 20,
22, 24), and cough. The girdle symptom is an important indication at
any level, {1104} as it is due to irritation of the nerves at the
lowest level of healthy cord just above the transverse lesion. It has
already been discussed under Symptomatology. In many of the dorsal
cases (Nos. 32, 37, 38, 39, and 45) the symptoms are almost entirely
confined to the legs and lower trunk, the arms escaping entirely. The
condition of the bladder is usually given in the table as one of
paralysis; this does not indicate whether automatic evacuation existed
at the beginning of the case; which condition would indicate that the
centre for micturition was below the lesion, and intact. It is
probable that later in these cases the bladder is actually paralyzed
by destruction of its centre in the cord, and this even when the tumor
has been situated some distance above.

[Illustration: FIG. 51. Fibroma of Lower Dorsal Cord, Case 32 of Table
(W. Cayley).]

[Illustration: FIG. 52. Tumor of Cauda Equina, Case 45 of Table (W. W.
Fisher).]

With reference to tumors of the cauda equina, Erb[10] says that they
have in every respect a great resemblance to those which are situated
higher and affect the cord proper. “They are hard to distinguish from
the latter, but may be in many cases perhaps, if it is borne in mind
that tumors of the cauda produce exclusively nerve-root symptoms, and
that the signs of compression of the cord, of secondary myelitis, etc.
are absent. The higher the tumor, the nearer it approaches the lumbar
{1105} portion of the cord, the harder will it be to draw the
distinction. In respect to tumors seated lower the following points
may be attended to: the seat of the pains (which in such cases often
attain enormous violence) is strictly localized in certain
nerve-districts; all nerves leaving the spinal canal above the tumor
are free; thus in myxo-sarcoma telangiectodes of the cauda I observed
the pain strictly limited to the district of the sciatica, while the
crural and the dorsal nerves were perfectly free; constant violent
pain in the sacrum. If palsy occurs the reflex actions necessarily
cease at once. Spasms are seldom observed, more frequently
contractures. Atrophy of the muscles occurs rather frequently. The
palsy and anæsthesia by their localization often give us the
opportunity of fixing the upper limit of the lesion. Increase of the
reflex acts and marked tendinous reflexions do not occur. Paraplegia,
palsy of the bladder, bed-sores, etc. may develop exactly as in tumors
occupying a higher seat, {1106} but the symptoms of paralysis do not
seem to belong necessarily to the disease, as is shown in my case
(just mentioned), which terminated fatally before paralysis or
anæsthesia occurred.”

[Footnote 10: _Op. cit._]

[Illustration: FIG. 53.]

[Illustration: FIG. 54. Psammoma of Dorsal Cord, 38 of Table (after
Charcot).]

PROGNOSIS.—The prognosis of spinal tumors is generally very
unfavorable. Syphilitic cases are of course the most hopeful, but even
in these cases it is only when they are recognized early that much can
be expected. A gumma that has grown to any dimensions will have so
compressed the cord that even when the tumor is melted away by
specific treatment its effects will remain.

DURATION AND TERMINATION.—Most cases of spinal tumor last from about
six months to three years. Occasionally death may result, as from a
rapidly-developing sarcoma, in less than six months, and somewhat more
frequently in slowly-developing tumors, or in those which are held
more or less in abeyance by treatment the sufferings of the patient
are prolonged to four or five years or more. Hemorrhages into or
around the growths sometimes take place, and are the cause of death,
or more frequently of a sudden aggravation and multiplication of
severe symptoms. Death sometimes takes place from the complete
exhaustion which results from the disease and its accompanying
secondary disorders, such as bed-sores, pyelitis, etc. Occasionally
death results from intercurrent diseases, such as pneumonia,
infectious fevers, etc., whose violence the weakened patient cannot
well withstand. Sometimes the symptoms of a rapidly-ascending
paralysis appear, probably due to an ascending myelitis or
meningo-myelitis.

COMPLICATIONS AND SEQUELÆ.—Spinal tumors are sometimes complicated
with other similar growths in the brain or the evidences of the same
constitutional infection in other parts of the body. In one case of
cysticercus of the cord sclerosis of the posterior columns was also
present.

TREATMENT.—The treatment of spinal tumors can be compressed into very
small compass. In cases with syphilitic history, or when such history
is suspected, although not admitted, antisyphilitic remedies should be
applied with great vigor. It should be borne in mind, however, that
even in syphilitic cases after destruction of the cord by compression
or softening specific remedies will be of no avail. In tubercular
cases and in those in which the system is much run down tonics and
nutritives are indicated. Bramwell[11] advises an operation in any
case in which the symptoms are urgent, in which the diagnosis clearly
indicates the presence of a tumor, when there is no evidence of
malignant disease, when the exact position of the growth can be
determined, and when a vigorous antisyphilitic treatment has failed to
produce beneficial results. As some meningitis, meningo-myelitis, or
myelitis is usually present in cases of spinal tumor, treatment for
the complication will assist in relieving the torments of the patient.
Anodynes, particularly opium and its preparations, should be used
freely in the later stages of the affection. Bromides and chloral are
of little value except in association with opiates. Operation offers
even less hope than in brain tumor, but in very rare cases should be
taken into consideration.

[Footnote 11: _Diseases of the Spinal Cord_, Edinburgh, 1884.]

{1107} TABLE OF FIFTY CASES OF SPINAL TUMOR.

1. Sex and Age: M. 33.

Clinical History: Paresis of forearms, left worse. Paraplegia, then
paralysis of all limbs; paralysis of intercostals. Contractures of
hands, then of feet. Pain and stiffness of neck on motion. Wasting of
interossei. Diplegic contractions of legs. Only partial paralysis of
sphincters. Sensation perfect. Bed-sores. Duration, thirteen months.

Path. Anat. and Location: Glioma; syringo-myelus. Dilated lymphatics.

Entire length of cord, and involving medulla oblongata. Upper four
inches of cord greatly enlarged.

Remarks: T. Whipham, _Trans. Path. Soc. London_, 1881, xxxii. 8-12.

2. Sex and Age: F. —.

Clinical History: Constricting pains about abdomen. Paresis of legs.
Persistent subsultus. Temporary improvement after labor. General
paralysis. Scoliosis.

Path. Anat. and Location: Glio-myxoma.

In gray columns from medulla oblongata to cauda equina.

Remarks: Schueppel, _Arch. d. Heilk._, viii. Bd., 1867 (quoted by
Rosenthal).

3. Sex and Age: M. 15.

Clinical History: Paresis of left arm. Pain back of neck. Later,
paralysis of left arm, and wasting of arm, shoulder, and neck muscles.
Slight paresis of right arm. Prolonged vomiting. Constriction of neck;
dysphagia; paralysis of chest.

Path. Anat. and Location: Gelatinous tumor left side of cord, and
involving in some parts the gray matter.

From medulla to sixth cervical vertebra.

Remarks: S. Wilks, _Lectures on Dis. of Nervous System_, p. 266.

4. Sex and Age: M. 18.

Clinical History: Paresis of left leg, increasing; some atrophy.
Weakness in left arm. Later, numbness in both legs. Contracture of
fingers. Some mental confusion. Left hand and leg livid and cold.
Hyperæsthesia of left leg; anæsthesia of right leg, perineum, penis,
scrotum, rectum, and inguinal region, and of left arm. Right arm
normal. Islands of heat and cold in leg, and of cold in arms. Left
ankle clonus. Left pupil contracted. Vomiting. Dysphagia.
Occipito-cervical pain and contracture of cervical muscles. Leg
contractures and tremor. Later, hyperæsthesia disappeared.
Incontinence of urine. Patellar and skin reflexes increased. Facial
spasm. Amblyopia, optic neuritis, diplopia, deafness, paralysis of
left abducens; pupils contracted. Sacral bed-sores. Thick speech.

Path. Anat. and Location: Round-celled sarcoma or glio-sarcoma,
growing from ependyma of central canal, causing hydromyelia,
softening, and secondary degeneration. Dura mater thickened. Brown
exudate in cord and base of brain.

From medulla oblongata to dorsal cord.

Remarks: Schultze (F.), _Arch. f. Psychiat._, Berlin, 1878, viii.
367-393, 1 pl.

5. Sex and Age: F. 48.

Clinical History: Pain in abdomen and down legs, worse on left side.
Tonic spasm in flexors and adductors of thighs. No anæsthesia. Two
months before death paralysis of sphincters. Great emaciation.

Path. Anat. and Location: Tumor (psammoma), growing from dura mater on
right side in cervical region.

Upper part of cervical region.

Remarks: J. Hutchinson, Jr., _Tr. Path. Soc. Lond._, 1881-82, xxxiii.
23, 24.

6. Sex and Age: ——

Clinical History: Pain in arms. Contracture of fingers of right, then
left side. Numbness in right foot, then upward, then left foot. Girdle
feeling. Priapism and dysuria. Complete anæsthesia, later, up to third
rib, with paralysis of legs and paresis of fingers. Respiration
diaphragmatic. Legs very jerky. Later, arms paralyzed.

Path. Anat. and Location: Sarcoma of left post. aspect of cord;
adjacent cord compressed and soft. Belt of yellow substance enveloped
cord to cauda equina.

Between cervical bulb and second cervical vertebra.

Remarks: E. Long Fox, _Bris. Med.-Chir. Journ._, 1883, i. 100-106, 2
pl.

7. Sex and Age: F. 31.

Clinical History: Pain, stiffness in neck; pain radiating, aggravated
by jarring. Sudden paralysis of both arms; next day paralysis of legs,
incomplete. Partial anæsthesia. Marked skin reflexes in legs. Patellar
reflexes retained, weaker on right than left. Dyspnœa. Profuse
perspiration. Cardiac irregularity. Day before death temperature in
right axilla 100°; left, 102.2°.

Path. Anat. and Location: Gumma of dura mater two inches long, with
intercurrent hemorrhage; flattening and softening of cord, with
secondary sclerosis.

From first to fifth cervical vertebra.

Remarks: Charles K. Mills, _Philada. Med. Times_, Nov. 8, 1879, p. 58.

8. Sex and Age: M. 34.

Clinical History: Pain in back of neck, with stiffness and
torticollis. Paresis of arms; later, of legs. Anæsthesia of arms, then
of legs; also paræsthesia of legs. Late symptoms: shortening and great
rigidity of neck, with choking sensation (girdle sensation at neck).
Dimness of vision. Atrophy of arms and less of legs. Complete
paralysis of arms, almost complete of legs. Electro-contractility
preserved. Violent skin reflexes in legs. Involuntary evacuations and
incomplete priapism. Severe pains in knees and ankles. No acute
bed-sores. {1108} Paroxysms of dyspnœa. Average temp. for two weeks
before death, M. 97.9°, E. 98.3°.

Path. Anat. and Location: Gumma of dura mater; caries, probably
syphilitic, of vertebræ. Abscess. Total (almost) transverse sclerosis
of cord. Secondary degeneration. Some softening above and below tumor.
Cervical nerves compressed and atrophied.

From second to fifth cervical vertebra; most in front.

Remarks: Charles K. Mills, _Philada. Med. Times_, Nov. 8, 1879, p. 58.

9. Sex and Age: M. 43.

Clinical History: Pain between shoulders. Numbness in right hand and
arm, with weakness and swelling. Numbness in left arm, which spread
over chest and abdomen. Unable at first to lie down. Felt as though
encased in armor. Pain in back of neck. Tongue protruded to right.
Exaggerated reflexes in legs. Right arm and leg weaker than left.
Vertigo. Dysphagia. Sense of constriction about neck. Breathing
impaired.

Path. Anat. and Location: At third cervical vertebra, to right of
front of cord. Destruction of opposite vertebra.

Remarks: E. H. Clark, _Bost. Med. and Surg. Journal_, 1859-60, lxi.
209-212.

10. Sex and Age: ——

Clinical History: No record of symptoms especially referable to the
cysticercus. Symptoms of tabes dorsalis.

Path. Anat. and Location: Cysticercus in substance of cord. Lesions of
tabes dorsalis.

On level with third cervical nerve.

Remarks: Geo. L. Walton, _ibid._, vol. cv. p. 511.

11. Sex and Age: M. 25.

Clinical History: Pain in back of neck; stiffness. Numbness of left
hand. Gradual loss of power of left arm. Jerking of arm. Paresis of
left leg. Constriction of upper chest. Right limbs involved, and
eventual complete paralysis of trunk and extremities. Severe headache.
Last three days absolute anæsthesia of arms and legs. No
ophthalmoscopic changes. Constipation and dysuria.

Path. Anat. and Location: Fibro-sarcoma at level of fourth cervical
nerves. Cord compressed.

Remarks: H. A. Lediard, _Tr. Path. Soc. Lond._, 1881-82, xxxiii.
25-27.

12. Sex and Age: F. 25.

Clinical History: Œdema of ankles; pain in legs; afterward numbness,
formication, and stiffness of legs. Painful contractures in upper
extremities. Slight left scoliosis. Abdominal pains. Paresis of arms.
Fingers flexed. Fever. Respiration became involved, and bowels and
bladder paralyzed. Mind clear. Died in attack of suffocation.
Duration, two years and three months.

Path. Anat. and Location: Fibroma, size hazelnut, under pia mater.

Between fourth and fifth cervical vertebræ.

Remarks: Bernhuber, _Deutsch. Klin._, Berlin, 1853, v. 406.

13. Sex and Age: M. 16.

Clinical History: Restlessness. Cramps in pharynx on swallowing.
Excitability. Delirium. Hallucination. Pain in the neck. On touching
neck general cramps. Grimaces. Salivation. In three days complete
paraplegia. No fever. Sudden change. Pulse 120. Pupils alternating.
Blepharospasm. Irregular respiration. Pulmonary œdema. Suspicion of
hydrophobia, because patient had been with hydrophobic dog; when
offered coffee had symptoms simulating rabies.

Path. Anat. and Location: Sarcoma.

Extending from fifth to seventh cervical nerve on antero-lateral face
of cord, compressing left half and penetrating into right half, so
that anterior longitudinal fissure described arc of circle around it.

Remarks: Adamkiewicz, _Arch. de Neurol._, Paris, 1882, iv. 323-336, 1
pl.

14. Sex and Age: F.

Clinical History: Paresis and partial anæsthesia in all limbs for many
months, most marked on left side. Brain and special senses unaffected.
Had a tumor at bottom of right side of neck. Extensive bed-sore.

Path. Anat. and Location: Carcinoma.

Tumor caused partial absorption of sixth cervical vertebra. Cord
compressed and twisted. Right lateral aspect especially affected. Cord
atrophied.

At level of sixth cervical vertebra.

Remarks: J. W. Ogle, _Tr. Path. Soc. Lond._, 1885, 6, vii. 40, 41.

15. Sex and Age: F. 34.

Clinical History: Pain in right foot, and paresis increasing to
paraplegia. Paresis of arms. Contractures of legs. Hyperæsthesia in
both legs up to crest of ilia. Later, great pain; paralysis of
sphincters. Bed-sores.

Path. Anat. and Location: Sarcoma, growing from dura mater; nerves
passing through and over tumor. Cord congested and pushed to one side.
Thin, but not softened. Growth resembled psammoma.

Between sixth and seventh cervical nerves of left side.

Remarks: T. Whipham, _Tr. Path. Soc. Lond._, 1873, xxiv. 15-19.

{1109} 16. Sex and Age: M. 57.

Clinical History: Pain in right arm. Numbness in hand, and paresis.
Paresis and coldness of left leg. Some anæsthesia and wasting of right
leg. Later, paraplegia. Diminished reflexes. Contractures.
Constriction sense about legs and abdomen. Triceps, deltoid, and
serratus magnus of right side paralyzed. Incontinence of urine,
difficult defecation, decubitus, fever. Abdominal muscles paralyzed.
Later, other muscles of arms paralyzed. Complete anæsthesia of legs.
Dyspnœa, œdema of lungs.

Path. Anat. and Location: Myxoma from arachnoid. Cord compressed and
softened on right postero-lateral side. Secondary degeneration. Some
œdema of brain.

At sixth and seventh cervical vertebra on postero-lateral surface of
cord.

Remarks: Pel (P. K.), _Berlin. Klin. Wochensch._, 1876, xiii. 461-463.

17. Sex and Age: F. 35.

Clinical History: First, pain in right arm, weakness in right hand.
Then paralysis almost complete in arms, and impaired sensation. In
legs paralysis complete, sensation impaired. Alternate incontinence
and dysuria. Ankle clonus and increased knee-jerks and plantar reflex.
Tapping biceps causes reflex in little and ring fingers. No atrophy or
bed-sores. Cold on one side, hot on other. Pain and little swelling
over sixth cervical vertebra. No eye symptoms. Brain clear. Inability
to turn head. Before death respiratory paralysis and bed-sores.
Duration, fifteen months.

Path. Anat. and Location: Spindle-cell sarcoma, springing from
arachnoid and destroying cord by pressure, except posterior columns.
Cord below tumor soft.

At sixth cervical vertebra.

Remarks: E. Long Fox, _Bris. Med.-Chir. Journ._, 1883, i. 100-106, 2
pl.

18. Sex and Age: M. 50.

Clinical History: Paresis in right arm. Stiffness in neck and back.
Paralysis of all extremities gradually developed.

Path. Anat. and Location: Glioma in right half of cord. Old
hemorrhages in adjacent parts and in medulla oblongata. A more recent
hemorrhage in dorsal cord.

In lower cervical region.

Remarks: Schueppel, _Arch. d. Heilk._, viii. Bd., 1867 (quoted by
Rosenthal).

19. Sex and Age: ——

Clinical History: Coldness, numbness, violent pains, first in left
arm, later in both legs. Paralysis of all limbs and muscles of trunk.
Atrophy. Reactions of degeneration. Violent leg reflexes.

Path. Anat. and Location: Tubercle, large as hazelnut. Consecutive
myelitis of adjacent parts and left anterior horn.

In lower cervical region.

Remarks: Chvostek, _Med. Press_, 33-39, 1873 (quoted by Rosenthal).

20. Sex and Age: M. 45.

Clinical History: Interscapular pain. Chest-pressure and dyspnœa.
Paræsthesia and pain in legs. Spastic paralysis. Difficulty in stools;
bloody urine and dysuria. Œdema of legs. Bed-sores. Kypho-scoliosis.
Pain on pressure over spine. Paralysis of left leg, paresis of right,
some anæsthesia of both. Broncho-pneumonia, fever.

Path. Anat. and Location: Phlegmon of dura mater, compressing cord.
Some infiltration of tissues of throat and mediastinal space.

From seventh cervical to second dorsal vertebra.

Remarks: Mankopff (E.), _Berl. Klin. Wochensch._, 1864, i. 33-46, 58,
65, 78.

21. Sex and Age: M. 22.

Clinical History: Pain in back and side of neck and in limbs. Marked
pain in sternal region on coughing. Pressure and jarring cause pain.
Rapid loss of power in both arms. Feeble and slow movements of thighs,
legs, and feet. Right deltoid and flexors of fingers much wasted. No
paralysis of face. Knee-jerks exaggerated. Later, complete paralysis,
including bladder and rectum.

Path. Anat. and Location: Tumor of membrane. Cord beneath compressed
and degenerated.

Lower cervical and upper dorsal region.

Remarks: H. C. Wood, “Proceedings of Philadelphia Neurological
Society,” _Medical News_, vol. xlviii. No. 9, Feb. 27, 1886.

22. Sex and Age: F. 50.

Clinical History: Pain in neck, shoulders, and chest. Stiffness of
neck, back, and arms. Chest fixed; breathing diaphragmatic. No
paralysis or altered sensation.

Path. Anat. and Location: Secondary cancer of vertebræ.

Cervical region.

Remarks: Gull, by Wilks, in _Lect. on Dis. of Nerv. System_.

23. Sex and Age: F. 40.

Clinical History: Severe pain in back. At height complete paralysis in
legs, some paresis in arms. Variable anæsthesia. Girdle sensation and
mammary pain. Lively and distressing reflexes. Contractures in legs.
Bed-sores and paralysis of sphincter of bladder. Toward close rigors
(pyæmia?).

Path. Anat. and Location: Fibro-cyst on right side, between cord and
dura, and between anterior and posterior nerves.

Top of dorsal region.

Remarks: Risdon Bennett, _Tr. Path. Soc. Lond._, 1855-56, vii. 41-45.

24. Sex and Age: M. 30.

Clinical History: Cough, dyspnœa, wasting, simulating phthisis. Pain
in back of neck and shoulders. Pain in joints; paresis of legs and
bladder. Pain in chest. Paresis of arms. Later, increased paralysis,
bed-sores, sweating.

Path. Anat. and Location: Tumor, size of hazelnut, inner anterior
surface of dura mater. Flattening and softening of cord.

Top of dorsal region.

Remarks: Gull, in _Guy's Hosp. Rep._, (quoted by Wilks in _Lectures on
Dis. Nerv. Syst._, p. 264).

{1110} 25. Sex and Age: F. 43.

Clinical History: Pain in shoulders, chest, and sides. Contractures of
legs; heels to nates. No anæsthesia. Later, retention of urine and
bed-sores. Incessant pain in back and abdomen.

Path. Anat. and Location: Fibro-nucleated tumor from inner surface of
dura mater.

Opposite third dorsal vertebra.

Remarks: Gull, by Wilks, _ibid_.

26. Sex and Age: F. 43.

Clinical History: Pain in chest and shoulder, then in legs. Paresis of
legs. Contractures and jerking of legs. Spasm of abdominal muscles. No
anæsthesia. Paresis of bladder and rectum. Wasting and bed-sores.
Finally, paresis increased, but never complete paralysis. Duration,
nine months.

Path. Anat. and Location: Fibro-nucleated tumor, size of a bean, from
dura mater. Cord compressed backward, and softened.

Opposite third dorsal vertebra.

Remarks: Wilks, _Trans. Path. Soc. Lond._, 1855-56, vii. 37-40.

27. Sex and Age: M. 24.

Clinical History: Paraplegia. Depressed reflexes; girdle symptom.
Partial anæsthesia. Dysuria. Vomiting. Pulse weak and intermittent.
Partial recovery from paralysis, and anæsthesia in left leg, and
reflexes in right foot regained. Later, complete paraplegia,
anæsthesia, and bed-sores. Duration, five months.

Path. Anat. and Location: Probable gumma.

Middle dorsal region.

Remarks: B. G. McDowell, M.D., _Dubl. Q. J. Med. Sci._, 1861, xxxii.
299-303.

28. Sex and Age: F. 44.

Clinical History: Paresis in legs. Spine hypersensitive and
inflexible; least attempt at bending causes great cervico-brachial
pain. Paræsthesia; sense of falling out of abdominal viscera through
abdominal walls. Pains in extremities increasing, and involving right
shoulder, intercostals on both sides, and lumbar region. Paralysis of
right arm (first); complete paralysis of leg. Excessive spinal
tenderness. Loss of sensation (partial) in legs, body, and right arm.
Later, dyspnœa, then dysuria, then complete inability to empty bowels
or bladder. Great tympanites. Girdle sense above umbilicus, and
finally complete paralysis and anæsthesia below this band. Sense of
twisting of legs and feet, so that latter seemed close to face. Œdema.
Later, paresis of left arm. One small bed-sore.

Path. Anat. and Location: Alveolar sarcoma.

Eighth and ninth dorsal vertebræ.

Remarks: G. W. H. Kemper, _Journ. Nerv. and Ment. Dis._, xii. No. 1,
Jan., 1885.

29. Sex and Age: F. 42.

Clinical History: Projection of seventh, eighth, ninth, tenth, and
eleventh dorsal vertebræ. Numbness below ankles, and early girdle
sensation. Peronei and anterior tibial muscles first involved; then
all leg-muscles, then sphincters, then arms. Died in a fit.

Path. Anat. and Location: Round-celled sarcoma. The anterior columns
soft opposite tumor. Bodies of seventh, eighth, ninth, and tenth
vertebræ soft.

Opposite seventh, eighth, ninth, and tenth dorsal vertebræ.

Remarks: E. Long Fox, _Brit. Med. Journ._, 1871, p. 566.

30. Sex and Age: F. —.

Clinical History: Ill-defined hemiplegia; later, paraplegia, with
contractures and rigidity.

Path. Anat. and Location: Gumma and syringo-myelus. Small cavities in
anterior cornua.

At ninth dorsal vertebra anterior aspect.

Remarks: Taylor, _Lancet_, 1883, p. 685.

31. Sex and Age: M. 7.

Clinical History: Paraplegia, except adductors and rotators of thigh.
Reflex contractures; most intense from irritation of penis and
scrotum. Rigidity of legs. Complete anæsthesia of lower half of body.
Later, anuria, incontinence of feces. Anal sphincter reflex; figured
stools. Cystitis. Pain on percussion in dorsal region. Pain in back.
Complete paraplegia. Very late, brain symptoms. Duration, nine months.

Path. Anat. and Location: Tubercle (?).

Cord soft for two inches.

Tenth dorsal vertebra.

Remarks: Geoghegan, _Dublin Med. Press_, 1848, xix. 148-151.

32. Sex and Age: F. 46.

Clinical History: Fixed pain in left iliac region. Paresis in left
leg, increasing to paraplegia. Formication. Girdle sensation.
Incomplete, increasing to complete, anæsthesia of legs. Spontaneous
twitchings. Bladder and sphincter ani paralyzed. Bed-sores. Duration,
one year.

Path. Anat. and Location: Fibroma (?) from inner surface of dura. Cord
hollowed out and softened.

Interval between tenth and eleventh dorsal vertebræ.

Remarks: William Cayley, _Tr. Path. Soc. Lond._, 1864-65, vol. xvi.
21-23.

33. Sex and Age: M. 30.

Clinical History: Hyperæsthesia; later, anæsthesia in legs; then
complete paraplegia.

Path. Anat. and Location: Tubercle size of pea. Adjacent myelitis. In
lower dorsal region.

Remarks: Chvostek, _Med. Presse_, 33-39, 1873 (quoted by Rosenthal).

{1111} 34. Sex and Age: M. 31.

Clinical History: Ataxia; stiffness of legs and cramps in abdomen and
legs. Slight nystagmus. Difficulty in forming words. Ataxia of arms.
Slight wasting of legs, especially of left. Lumbar pains; abdominal
cramps. Dysuria. Impotence. Later, increased spastic state of legs.
Mind depressed and emotional; attempts at suicide. Anuria. Bed-sores.
Urine albuminous. Duration, one year.

Path. Anat. and Location: Myxoma of dura mater 3 inches long. Dura
mater of brain contained fluid and lymph.

Dorsal region, left side.

Remarks: Shearman, _Lond. Lancet_, vol. ii. 1877, p. 161.

35. Sex and Age: F. 50.

Clinical History: Pains in limbs (thought to be rheumatic). Paresis in
legs. Hyperæsthesia in right leg; burning pains alternating with sense
or coldness.

Path. Anat. and Location: Cancer of vertebræ (sarcoma?).

Dorsal region.

Remarks: Gull, by Wilks, _Dis. Nerv. Syst._

36. Sex and Age: F. 35.

Clinical History: Paresis of left leg; soon of right leg. Pain in back
and left side. Tonic spasms of legs. Darting pains in knees. Partial
anæsthesia. Exalted plantar reflexes. Dysuria. Later, complete
paraplegia and anæsthesia; violent reflexes; severe pain in back.
Bed-sores. Duration, seven and a half years.

Path. Anat. and Location: Tumor, osseous or fibrous, three-fourths of
an inch long, growing from dura mater. Cord flattened, and softened
below tumor.

Lower part of dorsal cord.

Remarks: H. Ewen, _Tr. Path. Soc. Lond._, 1848-50, i. 179.

37. Sex and Age: F. 28.

Clinical History: Weakness in legs. Aching and shooting pains in legs.
Numbness and formication. Slight spasm in legs. “Felt as if ground was
some distance below feet.” Œdema of ankles. Later, numbness extended
to abdomen. Paralysis of bladder. Hyperæsthesia in right leg.
Obstinate constipation. Bed-sores. Some paralysis of respiratory
muscles. Duration, fourteen months.

Path. Anat. and Location: Tubercle the size of cherry, which had
almost obliterated cord. Tubercles in lungs, bowels, and uterus.
Bed-sore had opened spinal canal.

Lower part of dorsal cord.

Remarks: S. O. Habershon, M.D., _Guy's Hosp. Rep._, London, 1872, 3d
S., xvii. 428-436.

38. Sex and Age: M. 63.

Clinical History: Progressive paresis of left leg for five years.
Right leg then paretic. Paralysis then in left leg. Rigidity on
extension of right leg. Paroxysms of clonic spasms in right leg. Joint
pains, sciatic pains. In left leg, hyperæsthesia, in right leg,
anæsthesia. Plantar reflex retained; other reflexes exaggerated.
Diplegic contractions in right leg from irritation in left. Late
symptoms: purulent urine, with retention; chest and lumbar pains like
bone pain; extension changed to flexion; swelling of legs and
ecchymosis; sacral and other eschars.

Path. Anat. and Location: Psammoma adherent to dura mater. Cord
softened. Ascending degeneration in posterior columns, and descending
degeneration of lateral columns.

In dorsal region just above lumbar enlargement, anterior left side.

Remarks: Charcot, _Arch. de Physiol._, Paris, 1869, ii. 291-296.

39. Sex and Age: M. 20.

Clinical History: Paralysis of lower extremities; tremor; exaggerated
reflexes, hyperæsthesia of trunk; bed-sores. Œdema of feet. Fever. Pus
in urine.

Path. Anat. and Location: Organized blood-clot exterior to dura mater.
Cord compressed and softened.

Opposite lower dorsal and upper lumbar.

Remarks: C. B. Nancrede, _Am. Journ. Med. Sci._, O. S., lxi. 156.

40. Sex and Age: F. 38.

Clinical History: Pain around abdomen, in back, and legs. Paraplegia.
Anæsthesia and tingling of feet and legs. Paralysis of bladder.

Path. Anat. and Location: Hydatid cysts of vertebræ (?) and spin.
canal.

Lower part of spinal canal (probably lumbar region).

Remarks: S. Wilks, _Dis. Nerv. Syst._, p. 265.

41. Sex and Age: F. 23.

Clinical History: Bronzing of skin for two years; then headache,
giddiness, fever. Choreic movements in left arm, then in leg, then
general. Bronzing increased. Vomiting after meals. Duration, two years
and two months.

Path. Anat. and Location: Tumor, consisting of granular matter, with a
few nerve-fibres and cells, springing from centre of cord backward to
posterior fissure. Cord slightly widened. Suprarenal capsules large
and nodulated.

Lumbar enlargement.

Remarks: W. H. Broadbent, _Trans. Path. Soc. Lond._, 1861-62, viii.
246.

42. Sex and Age: 10 ms.

Clinical History: Twitching and convulsive movements of right leg.
After removal of exterior tumor the movements ceased. Child died of
peritonitis.

Path. Anat. and Location: Tumor outside of sacrum, and also protruding
through sacral opening. Reported to have been behind and pressing upon
cord (?). Fatty growth within membranes.

Remarks: Arthur Johnson, _ibid._, 1856-57, viii. 28, 29.

{1112} 43. Sex and Age: F. 54.

Clinical History: Paresis, first of left arm and leg; then paralysis
of these and of right arm and leg. Pain in back and hips early; then,
suddenly, darting pains and incontinence of urine. Paræsthesia of left
arm and leg; no anæsthesia. Coma.

Path. Anat. and Location: Hydatid cyst. Cyst also in liver. Fluid
beneath membranes of cord and brain.

At first and second left sacral foramen, opposite last lumbar and
upper three sacral vertebræ.

Remarks: H. S. Wood, _Australian Med. Journ._, 1879, N. S. i. 222.

44. Sex and Age: M. 46.

Clinical History: Fibrillary twitching. Increased patellar reflexes.
Paræsthesia and hyperæsthesia in legs, disappearing. Constriction of
chest (?). Headache. Dysuria for two years. Straining at stool.
Indigestion. Bloody vomiting. Cardiac palpitation; intracardial
murmurs; slow pulse. Swollen inguinal glands. Variations in
temperature. Bed-sores.

Path. Anat. and Location: Glioma.

At filum terminale, upper part.

Remarks: Lachman, _Arch. f. Psychiat._, Berl., 1882, xiii. 50-62, 1
pl.

45. Sex and Age: M. 38.

Clinical History: Pain in legs. Œdema. After two years could not lie
down: rested on hands and knees. Paralyzed in legs; pain in seat.
Anæsthesia in legs, not complete in right. Paræsthesia in left.
Dysuria and constipation. Before death had incontinence with
hæmaturia, and was able to lie down.

Path. Anat. and Location: A lobulated tumor from pia mater at lower
end of spinal canal, surrounded by nerves of cauda equina. Structure
not made out.

At cauda equina.

Remarks: W. W. Fisher, _Tr. Prov. M. and S. Ass._, 1882, x. 203-208.

46. Sex and Age: ——

Clinical History: This case had symptoms of posterior spinal
sclerosis, which possibly had no relation to growth, according to
reporter.

Path. Anat. and Location: Myo-lipoma attached to conus medullaris.
Crescentic, clasping cord from anterior to posterior fissure.
Nerve-roots of cauda equina imbedded in it. Contained striated
muscular fibres.

Remarks: W. R. Gowers, _Tr. Path. Soc. Lond._, 1875-76, xxvii. 19-22.

47. Sex and Age: Und. 1 yr.

Clinical History: Spina bifida (?); hydrocephalus; convulsions, bloody
stools; partial paraplegia. (Above symptoms came on after closing of
sacral opening by surgical operation.)

Path. Anat. and Location: Congenital sacral neuroma amyilinicum.

Remarks: W. F. Jenks, M.D., _Trans. Path. Soc. Philada._ (1871-73),
1874, iv. 190-192.

48. Sex and Age: M. 30.

Clinical History: Pain in back; abdominal girdle sensation. Pain in
legs; paraplegia; nearly complete anæsthesia; paralysis of bladder;
bed-sores.

Path. Anat. and Location: Aneurism, eroding vert. and compressing
cord. Location not given.

Remarks: Wilks, _Dis. Nerv. Syst._

49. Sex and Age: M. 54.

Clinical History: Paralysis of both legs, of sphincter ani, and of
bladder; urine alkaline, with pus and blood. Partial anæsthesia.
Pyonephritis.

Path. Anat. and Location: Gumma from inner layer of dura mater and
involving pia mater. Location not given.

Remarks: Delafield, _N. Y. Med. Rec._, 1875, x. 131.

50. Sex and Age: Stillborn.

Clinical History: ——

Path. Anat. and Location: Tumor, size of head of child two years old,
projected between legs from spinal column. Nerves of cauda equina over
anterior part. Some bone in tumor (dermoid cyst?).

Remarks: Virchow, _Monatschr. f. Geburtsk._, Berl., 1857, ix. 259-262.


{1113}


INFANTILE SPINAL PARALYSIS.

BY MARY P. JACOBI, M.D.


SYNONYMS.—Essential paralysis of childhood (Rilliet and Barthez);
Myogenic paralysis (Bouchut); Acute fatty atrophic paralysis
(Duchenne); Atrophic paralysis (Ferrier); Acute anterior poliomyelitis
(Kussmaul, Erb, Seguin); Regressive paralysis (Barlow); Tephromyelitis
(Charcot).

DEFINITION.—Of all the titles which have been given to the disease it
is our purpose to describe, two alone may be considered
irreproachable. In the present state of our knowledge it is
unnecessary to argue that this disease is not essential—_i.e._
destitute of characteristic anatomical lesions. Neither can the theory
of its myogenic origin be maintained; nor even is fatty degeneration
invariably present in the paralyzed muscles. Finally, the disease
cannot longer be regarded as peculiar to childhood,[1] since cases in
adults have been in these last years quite numerously reported[2]—four
with autopsies demonstrating the identity of the lesion. But there are
two definitions in our list of synonyms which embrace between them the
most striking characteristics of the disease, yet contain no error of
fact. Atrophic paralysis describes at once the two most salient
symptoms; acute anterior poliomyelitis defines at once the seat and
nature {1114} of the lesion, classes it with the systematic
diseases[3] of the spinal cord, and notes the peculiarity in the mode
of invasion by which it is so remarkably distinguished from nearly all
the organic diseases of this centre.

[Footnote 1: W. H. Barlow, _On Regressive Paralysis_, 1828. See
_Brain_, April, 1879.]

[Footnote 2: In Dec., 1873, I quoted 14 cases of adult spinal
paralysis, as follows: Duchenne, 4 cases; Charcot and Petitfils, 3;
Moritz Meyer, 2; Bernhardt (_Archiv Psych._, 1873), 1; Cumming
(_Dublin Quart. Journ._, 1869), 1; Lucas Championnière (by Hallopeau,
_Archives gén._, 1861), autopsy, 1; Gombault (_Archives de Psych._,
1873), 1; personal, 1.

In 1874, Seguin published a summary of all the foregoing cases except
the last, and added 6 personal observations, also 3 from Duchenne and
1 from Hammond. In the enlarged edition of his essay in 1877, Séguin
increased the list to 45—by new personal cases, 3; cases related by
Frey (_Berlin. Wochens._, 1874), 4; cases by Erb (_Arch. f. Psych. u.
Nervenkrank._, v.), 4; case by Cornil and Lépine (_Gaz. méd._, 1875),
autopsy, 1; case by Soulier (_Lyon méd._, 1875), 1; case by D. H.
Lincoln (_Boston Med. and Surg. Journ._, 1875), 1; case by Lemoine
(_Lyon méd._, 1875), 1; case by George M. Beard, 1; case by Leyden
(_Klinik Ruckenmarks Krankheiten_) Bd. iv. 1; case by Hammond (6th ed.
_Treatise_), 4; case by Courty (_Gaz. méd._, 1876), 1; case by
Dejerine (_Arch. de Phys._, 1876), 1.

To these may be added—case by Goltdammer (_Berl. klin. Wochen._,
1876), 1; case by Webber (_Trans. Amer. Neurol. Ass._ for 1875, vol.
i.), autopsy, 1; case by Klose (_Diss. Breslau_, 1876), 1; case by
Schultze (_Virchow's Archiv_, Bd. lxviii.; also Bd. lxxiii.), autopsy,
1; case by Bernhardt (_Archiv für Psych._, Bd. ix., 1879); case by
Sinkler (_Amer. Journ. Med. Sci._, Oct., 1878), 5; case by Althaus
(_ibid._, April, 1878), 2; case by Ross (_Dis. Nerv. Syst._, vol. ii.
p. 139), 1—total, 57 cases.

Morton (_St. Bartholomew's Hospital Reports_).

Others have doubtless been published since this date, but, as they do
not immediately concern our subject, need no further citation.]

[Footnote 3: Vulpian, _Leçons sur les Myelitis_, 1880.]

SUMMARY OF CLINICAL HISTORY.—The clinical features of an acute attack
of infantile paralysis are well known. The children affected are
usually between eighteen months and four years of age (Henoch). The
attack is more likely to occur in summer than in winter, as Sinkler[4]
found that 47 out of 57 cases began between May and September, and
Barlow noted 27 out of 53 in July and August.[5]

[Footnote 4: _Amer. Journ. Med. Sci._, April, 1875.]

[Footnote 5: _Loc. cit._, p. 75. Among Sinkler's 57 cases, only 6
furnish autopsies, thus:

Case by Cornil and Lepine and case by Webber (quoted and accepted by
Erb in _Ziemssen's Handbuch_, Bd. xi.); case by Gombault (rejected by
Erb and Westphal); case by Schultze; cases by Dejerine and Lucas
Championnière (quoted by Hallopeau).

The influence of heat is perhaps shown in the case related by
Dyce-Duckworth in the _Lancet_ of 1877: a child two and a half years,
after exposure to great heat on a steamboat-landing, became paralyzed
in all four limbs, but the paralysis was subsequently confined to the
lower extremities. Coincidently, the patient became delirious;
suffered from anæsthesia and temporary paralysis of the sphincters.
The paralyzed muscles wasted rapidly and lost faradic contractility.
Treatment by faradization was begun in a month from the date of the
attack, and recovery was complete three months later.]

The onset of the paralysis is either really sudden, occurring in the
daytime, while the child is under competent observation, or apparently
sudden, being discovered in the morning after a quiet night, the child
having gone to bed in health (West); or is preceded by some hours or
days of fever or of nervous symptoms, especially convulsions, or both.
The paralysis is almost always at its maximum of extent and intensity
when first discovered, and from this maximum begins, within a few
hours or days, to retrocede. The improvement may, however, be delayed
much longer. A variable number of muscles remain permanently
paralyzed, and in these, within a week (thirty-six hours, according to
some observers), faradic contractility is first diminished, then
abolished; galvanic reaction is exaggerated, ultimately is
characterized by the degeneration signs (entartungs reaction). The
temperature of the paralyzed limbs falls; the muscles waste; the
atrophy may rapidly become extreme. The paralysis and loss of faradic
contractility are complete, however, while the atrophy is only
incipient and progressing. The absence of lesions of sensibility, of
visceral disturbance, of trophic lesions of the skin, or of sphincter
paralysis is as characteristic of the disease as are the positive
symptoms above enumerated.

In the third or chronic stage the paralyzed limbs often become
contracted and deformed. At other times, and with more complete
paralysis, the growth of the bones is arrested, the muscles remain
flaccid, the entire limb shrivels, and dangles so loosely from its
articulations that it may be dislocated by slight effort (membre de
Polichinelle). The general health of the patient remains remarkably
good, the intelligence clear, the disposition lively. The duration of
life seems to be in nowise shortened by the paralysis. Thus,
suddenness of development, intimate association of trophic, motor, and
electrical disturbance, absence of cerebral or sensory lesion,
peculiar localization and grouping of the permanent paralyses,—such
are the salient characteristics of this remarkable disease.

SYMPTOMS IN DETAIL.—Three well-defined stages exist—the initial, the
paralytic, and the chronic.

{1115} Initial Stage.—Seeligmüller[6] signalizes three principal
varieties in this stage. The first is characterized by fever; the
second by nervous symptoms, principally convulsions, sometimes
delirium or coma; in the third no symptoms either precede or accompany
the local disease—“la paralysie est toute la maladie.”[7]

[Footnote 6: _Gerhardt's Handbuch der Kinderkrankheiten_, 1880
(separat Abdruck).]

[Footnote 7: Rilliet et Barthez, _Traité des Maladies des Enfants_,
ii. p. 551.]

Mode of Invasion.—I have elsewhere[8] described eight different modes
of invasion: absolutely sudden, coming on in the daytime; morning
paralysis (West), discovered after a quiet night, preceded by fever or
by vomiting alone (?), or by another typical disease, especially one
of the exanthemata, or, finally, by a traumatism, generally slight. An
interval of time almost always elapses between the occurrence of the
traumatism and the development of the paralysis—a fact which already
indicates that a definitely-evolved morbid process must intervene
between the two occurrences. An exception is related by Duchenne
fils;[9] and some apparent exceptions, in which recovery occurred
rapidly, seem to belong to the temporary paralysis of Kennedy,[10]
more recently described again by Frey.[11]

[Footnote 8: _Am. Journ. Obstet._, May, 1874.]

[Footnote 9: _Archives gén._, 1864. A father pulled his child from a
table by the right arm, and set it rather roughly on the ground.
Immediate pain, almost immediate paralysis of arm, which persisted,
and was followed by atrophy of its muscles.]

[Footnote 10: _Dublin Quarterly_, 1850.]

[Footnote 11: _Berlin. klin. Wochens._, 1874. Frey considers these
cases to be identical in nature with, though differing in severity
from, anterior poliomyelitis.]

PRODROMATA.—There is rarely any lengthened period of prodromata.
Seeligmüller has noticed in some cases an indisposition on the part of
the child to stand or walk during several weeks before the occurrence
of the paralysis. He does not say whether such children were
rachitical. In marked contrast with cases of cerebral paralysis is the
habitual absence of generalized nervous symptoms. Thus in only 1 case
of Seeligmüller's (total of 75) did the child suffer, and that during
six months preceding the paralysis, from intermittent muscular
contractions, and also from attacks of laryngismus stridulus.

The fever is usually of moderate severity (Seeligmüller), but
sometimes extremely high (Erb)[12]—as much as 41° C. (Henoch),[13] or
104° F. (Barlow).[14] Duchenne fils observed 7 cases alleged to be
entirely without fever, and Laborde counts 10 cases out of 50 as
apyretic.[15]

[Footnote 12: _Ziemssen's Handbuch_, Bd. xi. Abh. 12.]

[Footnote 13: _Vorlesung. über Kinderkrank._, 2d Aufl., 1881.
Seeligmüller (_Jahrb. für Kinderheilk._, 1878, p. 345) quotes another
case from Henoch's clinic where the fever lasted thirty-six hours, the
temperature on the first evening being 39.2°, the following morning
39.0°, the second evening 39.5°; the second morning, at which date the
paralysis was discovered, it was normal. The author states this to be
the only case known to him in which thermometric measurements were
taken.]

[Footnote 14: _Loc. cit._]

[Footnote 15: _De la Paralysie de l'Enfance_.]

The duration of the fever usually varies from a single night to
forty-eight hours; much more rarely does it last six, eight, twelve,
or fourteen days, or even, but quite exceptionally, three or four
weeks. According to Duchenne, its intensity and duration increase with
the age of the child, perhaps indicating greater resistance on the
part of the nerve-tissues which are the seat of the morbid process of
which it is symptomatic. Rarely does it last after the paralysis has
once occurred, {1116} but ceases then with an abruptness which recalls
the defervescence of pneumonia when the exudation process is once
completed.[16]

[Footnote 16: See p. 1144 for pathogenic inferences to be drawn from
this fact. Seguin (_New York Med. Record_, Jan. 15, 1874) seems to
throw some doubt on the existence of apyretic cases; but, as
Seeligmüller remarks, there is too much testimony to this possibility
to render it really doubtful.]

There is no proportion between the intensity of the fever and the
extent of the subsequent paralysis; nor is there any marked contrast
between the fever in children and that in adults in those rare cases
in which the disease, instead of being subacute, is sudden as in
children.

Erb considers the fever to be purely symptomatic of an inflammatory
process in the spinal cord.[17] But Vogt regards it rather as an
essential factor in the development of a spinal lesion, and thus
explains the occurrence of this in the course of febrile diseases
which at the outset have no special relation to the cord.

[Footnote 17: _Loc. cit._, p. 279.]

Convulsions, usually accompanied by fever, were observed in 11 of
Seeligmüller's cases out of 67; Duchenne had 13 out of 70; Heine, 9
out of 86;[18] thus a total of 33 cases of convulsions in 223 cases of
infantile paralysis—nearly 15 per cent. The paralysis may set in after
a single brief convulsion, or this may be repeated several times at
variable intervals before the paralysis is definitely declared
(Ross).[19] The convulsive movements are apt to be particularly
intense in the limbs destined to become paralyzed (Vogt).

[Footnote 18: _Die Spinale Kinderlahmung_.]

[Footnote 19: _Loc. cit._, p. 107. The author is quoting Laborde.]

The convulsion may be very slight—an isolated spasm of a limb or even
a single group of muscles. Whether, on the other hand, it can ever be
so intense that the child succumbs to it before the development of
paralysis, is a question which could only be decided by repeatedly
examining the cord in the cases of convulsion which have terminated
fatally. In a case of Seeligmüller's the child was affected for eight
days preceding the paralysis by tremblings generalized through all his
muscles.

The convulsion is usually followed by a soporous or even comatose
condition, or this may replace the convulsion. Delirium may take the
place of either.

Special interest attaches to those cases where the paralysis develops
in the course of an acute specific disease; for then becomes most
plausible the suggestion of Vogt, that a fever excited by some cause
remote from the spinal cord may itself become a cause of lesion in
this centre. In Roger's first and most celebrated case, paraplegia
developed suddenly during the course of a fatal scarlatina in a child
already suffering from paralysis of the left deltoid of two months'
standing.[20] The scarlatina was hemorrhagic, and, as will be shown
farther on, the autopsy showed traces of a hemorrhagic extravasation
in the cord. Thus a double influence was presumably exerted by the
scarlatina, while, moreover, the previous and recent occurrence of a
deltoid paralysis indicated a morbid predisposition in the spinal
cord. Of Seeligmüller's 75 cases, 1 occurred during scarlet fever, 1
with measles, 1 in the course of an erysipelas, and 1 of pneumonia.

[Footnote 20: _Gaz. méd._, 1871.]

Apyretic diseases, especially of the gastro-intestinal tract
(Brown-Séquard), also seem to have an influence on the development of
infantile paralysis. Two of my own cases occurred during an attack of
{1117} cholera infantum; another in a child who had been for several
weeks in bed with a purulent conjunctivitis. Study of these varied
antecedents is of interest in connection with the obscure question of
the etiology of infantile paralysis. In this latter connection we will
refer to them again.

Vomiting, or even the entire symptom-complex of gastric fever, not
infrequently ushers in the paralysis. Fever is then usually present,
but I have recorded one case of vomiting where, according to the
mother's assurance, no fever at all existed.

At the moment that the symptoms of the invasion subside, and the child
seems to enter upon convalescence, the terrifying discovery is made
that an arm or a leg or all four limbs, or even they and the muscles
of the trunk, are paralyzed.

In the severest form the child lies motionless, unable to stir hand or
foot, or even a finger or toe. Yet, singularly enough, this extensive
paralysis is sometimes overlooked, especially in very young children,
as the immobility of the patient is attributed merely to weakness
caused by previous illness. General paralysis, during at least the
first few hours of the paralytic stage, is probably more common than
appears from our present statistics. Not only, as has just been noted,
may this condition be overlooked, but it may exist during the hours of
sleep which precede the cases of morning paralysis. Seguin[21] speaks
as if the paralysis were at first always generalized, but this
statement seems to me somewhat exaggerated. Referring merely to the
statements of the parents, a considerable number of paralyses would be
found limited from the beginning. Heine's third table of partial
paralysis is entirely composed of cases so limited. In 16 out of the
19 cases of hemiplegia (monoplegia) the original limitation of the
paralysis is also specified; similarly with 7 out of the 20 cases of
paraplegia contained in the first table.

[Footnote 21: _Loc. cit._]

Paralysis of one or both lower extremities is often first detected
when the child gets out of bed and attempts to walk; or in children
too young to walk the flaccid immobility of the limb attracts
attention as soon as they are again carried on the mother's arm.
Paralysis of the upper extremities is discovered early in proportion
to the liveliness recovered by the child, leading him to occupy
himself with his toys as usual. In unilateral paralysis of the trunk
the child will fall over to one side when placed in the sitting
position; in bilateral paralysis it cannot be made to sit up at all.

From lack of competent observation during the initial stage it is
really not quite certain whether any degree of paresis precedes the
paralysis; but from the testimony at present accumulated the paralysis
is nearly always complete when first observed. This is in striking
contrast with adult spinal paralysis. In some few cases the paralysis
has been observed to creep on slowly, and not reach its maximum for
several days (Ross). Laborde relates a case where recovery from a
first attack of paralysis was followed by two relapses in the same
limbs at intervals, each ushered in by fever. After the second relapse
the paralysis remained permanent.

Significance of Original Extent of Paralysis.—The question of the
{1118} original distribution of the paralysis is of special interest
in connection with that of the original distribution of the morbid
process in the spinal cord. The real effect of the latter cannot be
adequately measured by the permanent paralyses; for, as will be seen,
it is not unusual to find traces of an extensively diffused process in
the cord in cases of quite partial paralysis.

It is interesting to notice that certain muscles are always exempt
from paralysis. With the exception of a single case of paralysis of
one temporal muscle, cited by Seguin,[22] the muscles of the head,
eyeballs, ears, larynx, and pharynx are always exempt, as are also the
diaphragm and intercostals. The arrest of the spinal lesion below the
medulla explains the immunity of muscles supplied by the vagus and
spinal accessory nerves. But since the cervical plexus is often
involved, the constant escape of the diaphragm, innervated by the
phrenic nerve which comes from this plexus, is remarkable. Still more
so the immunity of the intercostal muscles, whose nerves arise in the
dorsal region—a position of the cord frequently affected. This fact
tends to confirm Ross's hypothesis, that the nuclei of the intercostal
nerves lie in the vesicular columns of Clarke—columns confined to the
dorsal region of the cord, and which are invariably found intact at
autopsies of atrophic paralysis.

[Footnote 22: _Loc. cit._]

The immunity of these respiratory nerves explains the absence of the
dyspnœa which is so marked in Landry's ascending paralysis. In the
adult case described by Schultze and Erb[23] dyspnœa was present for a
short time. The disease terminated fatally twenty months from the time
of invasion. In this case traces of myelitis were found extending
through the dorsal region of the cord, and including not only the
anterior nerves, but, to a less degree, the columns of Clarke.

[Footnote 23: _Arch. Virch._, Bd. lxviii.]

The facial nerve (itself a respiratory nerve) shares the immunity of
the phrenic and intercostals. In the cases in which facial paralysis
has been noted the limb paralysis has been hemiplegic, as in
Seeligmüller's twentieth case. A cerebral origin is then always to be
at least suspected.

Barlow[24] has seen 6 cases of paralysis of the facial, but the
histories render a cerebral paralysis more probable in 4 out of those
6. Henoch[25] gives a case of paralysis of left arm, accompanied by
paralysis of corresponding facial nerve. The latter rapidly recovered,
but the paralysis of the arm persisted and was followed by atrophy.
Ross[26] implies that the sides of the neck, face, and tongue are
always at first implicated in spinal hemiplegic paralysis, but do not
remain permanently affected.

[Footnote 24: _Loc. cit._]

[Footnote 25: _Loc. cit._, p. 205.]

[Footnote 26: _Loc. cit._, p. 108.]

That the facial should be affected while the other medullary nerves
escape probably depends on the more anterior position of its nucleus.

The regression of the original paralysis is characteristic, indeed
almost pathognomonic, of the disease. It is on this account that
Barlow has proposed the name regressive paralysis.[27] This author
quotes the case of a boy who at five months was affected with a
universal paralysis, even affecting the neck, but entirely recovered
except in the extensor longus digitorum of the foot. This improvement
constitutes a second apparent convalescence, as deceptive as that
which immediately succeeds the pyrexia. Only in rare cases do all the
{1119} muscles at first paralyzed remain so permanently
(Seeligmüller); nor, on the other hand, do all entirely recover
(temporary paralysis of Kennedy and Frey). Even when an entire limb
appears to be paralyzed, careful examination will usually detect
certain muscles that retain their faradic contractility. Thus the
order of frequency of paralysis in the different limbs must be
distinguished from that observed for different muscles.

[Footnote 27: _Brit. Med. Journ._, 1882.]

Duchenne fils[28] and Seeligmüller[29] have tabulated, for lists of 62
and 75 cases respectively, the general locality of the permanent
paralyses in their order of frequency. The cases of monoplegia are by
far the most numerous. Thus in the table quoted below there are 97; in
Heine's tables (86 cases), 47; in Sinkler's tables (86 cases),
29—total, 173 from a total of 309, or nearly one-half:

                                Duchenne.  Seeligmüller.  Total.
  Left lower extremity              7           27         34
  Right  "       "                 25           15         40
  Right upper    "    |            10           13 |9      23
  Left    "      "    |                            |4
  All four extremities              5            2          7
  Both upper    "                   2            1          3
  Both lower    "                   9           14         23
  Left over and under extremity     1            1          2
  Right "         "         "       0            1          1
  Right over and left under "       2            1          3
  Muscles of trunk and abdomen      1            0          1
                                   --           --        ---
                                   62           75        137

This limitation is all the more noteworthy when compared with the
frequency of general paralysis at the outset.

[Footnote 28: _Archives gén._, 1864.]

[Footnote 29: _Jahrbuch der Kinderheilkunde_, N. H. xii. pp. 338-343.]

The next peculiarity is the great preponderance of paralysis of the
lower over that of the upper extremities. This is noticeable even in
the monoplegias. In Sinkler's cases only two of these affected an arm.
But in bilateral paralysis the predilection is still more remarkable,
paraplegia of the lower extremities being among the most frequent,
paraplegia cervicalis the rarest, form of paralysis. This is not
because a lesion situated in the cervical spinal cord must interfere
with the motor tract going toward the lumbar, and hence nearly always
paralyze all four extremities, if any. Because when this does happen
the upper extremities alone exhibit the atrophic changes
characteristic of anterior poliomyelitis: the lower, though paralyzed,
do not atrophy and retain their faradic contractility. Heine denied
the existence of paraplegia cervicalis. But in the table of
Duchenne-Seeligmüller 3 cases are recorded; Rosenthal[30] relates 1;
Lockhart Clarke, 1.[31] This is the somewhat famous case, described by
Clarke as a progressive muscular atrophy, which contributed one of the
earlier autopsies.

[Footnote 30: _Klinik der Nervenkrankheiten_, 2 Aufl. p. 413.]

[Footnote 31: _Med.-Chir. Trans._, li. p. 219.]

Seeligmüller's case[32] is remarkable in several respects. The
paralysis, occurring after a brief fever in a child seventeen months
old, exclusively attacked the two arms at the moment of invasion, and
never retreated from them, thus offering a double exception to the
usual rule. At four rears of age the arms were much atrophied, and
faradic contractility was lost in their muscles, the legs being
sturdily developed. Nevertheless, {1120} the child constantly fell in
walking, because, observes Seeligmüller, he was unable to balance
himself with his arms, as is habitual with little children learning to
walk.

[Footnote 32: _Jahrbuch, loc. cit._, p. 349.]

The hemiplegic variety of paralysis is again very rare. The
Duchenne-Seeligmüller table contains (out of 137) 3 cases; Sinkler
records (out of 86) 4; West, 5; Heine (out of 86), 1; Leyden, 1;
Duchenne, 1. West's 5 cases all present certain peculiarities, at
least unusual in spinal paralysis. In 2 the paralysis came out
gradually; in 1 succeeded to remittent fever (pigmentary embolism?);
in 1 was preceded by heaviness of the head for several days; and in 1
the leg was paralyzed fourteen days after the arm.[33] It is probable
that in almost all, if not in all cases, hemiplegic spinal paralysis
is the residue of a paralysis originally generalized to all four
limbs, if only for a few hours.[34]

[Footnote 33: In three cases of hemiplegia observed by myself, and
previously diagnosed as spinal paralysis by other physicians, I
doubted the diagnosis from the coincidence of unusual cerebral
symptoms. In the first case the hemiplegia appeared after coma, during
cerebro-spinal meningitis; in the second, after a violent convulsion
the face was drawn to the opposite side, and the patient, a child of
seven, remained for a month in a state of intense maniacal excitement.
In a third case, developed during convalescence from scarlet fever,
the hemiplegia was preceded during two days by hemiparesis, and
accompanied for a year by complete aphasia. Finally, in these cases
faradic contractility persisted in the paralyzed limbs (_Am. Journ.
Obstet._, May, 1874).]

[Footnote 34: Seeligmüller relates one case where hemiplegia,
including the facial nerve, was observed in two days from the
beginning of the fever.]

The question of hemiplegia is closely connected with that of paralysis
of the facial nerve, inasmuch as the existence of the latter often
serves to suggest a cerebral paralysis—a suggestion confirmed later by
the absence of atrophy and of characteristic electrical reactions.
However, in some cases of undoubted spinal paralysis the facial does
really seem to have become involved. Thus in the case just quoted from
Seeligmüller (Case 20 of his table) Henoch[35] relates a case of
paralysis of the left facial coinciding with paralysis of the left
arm. Rapid recovery from facial paralysis: arm atrophied. Barlow[36]
records temporary facial paralysis in six cases, but only two of these
seem to be really spinal. Such temporary paralysis is not altogether
infrequent in the poliomyelitis anterior of adults (Sinkler, Seguin).
Ross[37] implies that the sides of the neck, face, and tongue are
always implicated at first in hemiplegic spinal paralysis, but do not
remain so.

[Footnote 35: _Loc. cit._, p. 203.]

[Footnote 36: _Loc. cit._, p. 76.]

[Footnote 37: _Loc. cit._, p. 108.]

Crossed paralysis is extremely rare. There are 3 cases in the
Duchenne-Seeligmüller table; Leyden[38] has one. But paraplegia of the
lower extremities, coinciding with paralysis of one upper extremity,
is by no means so rare, especially as a residual paralysis.

[Footnote 38: _Archiv Psychiatrie_, Bd. vi.]

Finally, as in cerebral paralysis, the muscles of the trunk, though
often paralyzed at the outset, rarely remain so in children—much more
often in adults. Eulenburg[39] relates one interesting case of
complete paralysis and atrophy of the extensors of the back. Even the
interspinous muscles were involved, as shown by the divergence of the
spinous processes. The paralysis was observed in a girl of fifteen
affected since the age of three, and was completely cured in five
months by daily faradizations of ten minutes each, and two gymnastic
séances, each lasting two hours.

[Footnote 39: _Arch. Virch._, Bd. xvii., 1859.]

{1121} Birdsall[40] has described one case of unilateral paralysis of
the abdominal muscles.

[Footnote 40: _Journal of Nervous Diseases_.]

Study of the precise combinations of the muscles paralyzed has
recently acquired peculiar interest in connection with the
localization in the spinal cord of the motor or trophic nuclei of
their nerves.[41] Several facts have been ascertained: 1st, that, in
notable contrast with progressive muscular atrophy, atrophic paralysis
tends to involve definite groups of muscles; 2d, that this grouping is
not effected in accordance with the proximity to each other of the
muscles on the limb, but with their functional association. Remak
affirms that Charles Bell had already called attention to the fact
that in cases of local muscular paralysis of the extremities the
paralysis does not spread by muscular continuity, but in accordance
with the functional association of muscles. Thus, paralysis of the
thumb is more often associated with that of the forearm than with
paralysis of the other muscles of the hand. 3d. From such grouping may
often be inferred a different localization of certain nerve-nuclei
than would be supposed from the position of the muscles alone. 4th.
That the fibres contained in a single nerve-trunk, but distributed to
different muscles, probably separate from each other within the cord,
to be there distributed to variously-situated nuclei.[42]

[Footnote 41: Ernst Remak, “Localis. der Atroph. lahmung,” _Archiv f.
Psych._, ix., 1879; Ferrier, _Brain_, vol. iv. No. 3; also,
_Proceedings Royal Society_, No. 212, p. 12.]

[Footnote 42: The theory of course assumes the truth of the
demonstration by which atrophic paralysis is rendered symptomatic of
disease of the spinal cord, and the nutrition of a muscle dependent on
the integrity of the muscles of origin of its nerves.]

In the arm two mutually correlative cases are observed: (_a_) Immunity
of the supinator longus during paralysis of the forearm muscles; (_b_)
paralysis of the supinator in association with paralysis of the
deltoid, biceps, and brachialis anticus. The latter constitutes
Remak's upper-arm type of localization, and is exhibited in his first
case.[43]

[Footnote 43: _Loc. cit._; also, cases 1st and 2d by Ferrier, in
which, however, other shoulder-muscles were involved.]

Ferrier has experimentally confirmed this muscular association by
means of isolated irritation of the fourth cervical nerve, which threw
into contraction the supinator longus, together with the deltoid,
biceps, and brachialis internus. At the same time, in the experiment
the flexors and extensors of the wrist were excited, while in the
special form of paralysis noted they were exempt. This electrical
method is a less precise mode of analysis than the pathological, for
the double reason that (_a_) fibres whose nuclei are dissociated may
pass together in the same root; (_b_) because the same muscles receive
fibres from more than one root: thus the flexors and extensors of the
wrist from the fifth as well as the fourth cervical. Thus when the
nucleus of the latter was destroyed paralysis would be averted by
means of the fibres coming from the fifth root.

The experiment and the pathological observation, however, concur in
indicating that the fibres innervating the supinator longus, though
passing to it in the path afforded by the radial nerve, afterward
ascend in the cord to a ganglionic nucleus in close proximity to those
of the upper-arm muscles specified—liable, therefore, to be affected
with them. The purpose effected by such association is the supination
of the arm.

It is excitation of the fourth root in Ferrier's experiment which
gives {1122} results most closely corresponding to Remak's
observations. Excitations of the fifth and sixth root reveal other
combinations, which Ferrier has found realized in adult's spinal
paralysis. Thus in his second case, in addition to the group of
muscles already mentioned, the rhomboid, infraspinatus, and serratus
magnus were paralyzed, the last muscle indicating complication with
the fifth root. In the third and fourth cases muscles supplied from
the sixth root were joined to those innervated by the fourth and
fifth—namely, the pectoralis major and latissimus dorsi.

In this upper-arm type the muscles affected are supplied by three
different nerve-stems—the axillary, musculo-cutaneous, and the radial.
In the forearm type the most common variety consists in paralysis of
the extensors of the wrist, thus exactly imitating lead palsy.[44] The
supinator remains intact, the intrinsic muscles of the hand are
sometimes intact, sometimes paralyzed. Sometimes, however, the
extensors are relatively intact; the interossei are atrophied, and a
clawed hand, resembling that characteristic of cervical hypertrophic
pachymeningitis, is developed.[45]

[Footnote 44: It is on this fact, indeed, that Remak has been led to
argue the spinal nature of saturnine paralysis (“Zur Pathogenie der
Blei lahmung,” _Archiv für Psych._, Bd. vi., 1876).]

[Footnote 45: The march of this disease, together with that of tabes
dorsalis, furnishes data for localizing the nervous nucleus for the
wrist extensors. In both diseases the lesion is ascending: in tabes
disturbance of sensibility occurs first in the distribution of the
sensory fibres of the ulnar nerve; in cervical pachymeningitis the
flexors and intrinsic muscles of the hand are first paralyzed. Hence
it is to be inferred that the central nucleus for the latter muscles
lies in the lower, that for the extensor muscles in the middle,
segment of the cervical enlargement of the cord.]

The much greater frequency of extensor paralysis in the forearm type
of anterior poliomyelitis indicates that the lesion of this disease
begins about the middle of the cervical enlargement (see note).

The foregoing groupings have been made out almost entirely from cases
of adult spinal paralysis or else of lead palsy. In the lower
extremity it is much more difficult to establish such definite
muscular association. Certain laws, however, can be made out: 1st. The
liability to paralysis increases from the thigh toward the foot; thus,
the muscles moving the thigh on the pelvis are the least liable to
paralysis, then those moving the leg on the thigh, while the muscles
moving the foot and leg and thigh are the most frequently paralyzed of
any in the body. 2d. Of the upper thigh-muscles, the glutæi are not
infrequently paralyzed, the ilio-psoas hardly ever, the adductors
rarely except in total paralysis. 3d. Of the muscles moving the leg on
the thigh, the quadriceps extensor is very frequently paralyzed—the
most often, indeed, after the foot-muscles: the sartorius is almost
always exempt; the liability of the hamstring muscles corresponds to
that of the thigh adductors. 4th. At the foot the tibialis anticus
often suffers from isolated paralysis, sharing in this respect the
fate of the deltoid in the upper extremity—a fact already noticed by
Duchenne. On the other hand, (5th) the tibialis anticus often remains
intact while the other muscles supplied by the perineal nerve, the
perineus longus and brevis, are completely paralyzed.[46]

[Footnote 46: Thus Buzzard relates a case of paralysis involving the
quadriceps extensor and peroneal muscles, while the anterior tibial
were intact.]

The remarkable contrast in the morbid susceptibility of the quadriceps
on the one hand, and the sartorius on the other, suggests
dissociations of their nuclei. Remak relates one interesting case
(Obs. 13) where the {1123} sartorius was paralyzed—coincidently with
the quadriceps, it is true, but also with partial paralysis of the
ilio-psoas muscle, which is as rarely attacked as the sartorius
itself. The two facts, taken together, would indicate that the nucleus
of the sartorius lies high in the lumbar enlargement, in proximity to
that of the ileo-psoas. The inference, continues Remak, is reinforced
by functional considerations, since the sartorius, obliquely flexing
the leg on the thigh, is generally in action at the moment that the
psoas flexes the thigh on the pelvis.

Again: according to Remak the tibialis anticus is generally paralyzed
together with the quadriceps extensor, although supplied by a
different nerve.[47] And this should be expected from the necessity of
exciting dorsal flexion of the foot by means of the tibialis anticus
at the moment of extending the leg for the act of walking.[48]

[Footnote 47: Obs. 14, 15, 16, 17, from Remak's essay.]

[Footnote 48: At the moment that the foot is thus flexed, however, to
allow the leg to be swung forward, the thigh and leg are both slightly
flexed.]

Ferrier, from his experiments on the roots of the lumbar plexus, is
inclined to doubt this association of the tibialis anticus with the
quadriceps, and he adduces Buzzard's case, already quoted, to show
coincident paralysis of the quadriceps and peroneal muscles. It is not
improbable, however, that fibres associated together in nerve-roots
may again diverge in the cord, and thus the discrepancy would be
explained.

DIAGNOSIS OF SPECIAL PARALYSIS.—Paralysis of isolated muscles may
sometimes be concealed by the vicarious action of their synergists:
thus of the extensor communis for the tibialis anticus. Paralysis of
both legs and feet may even be partly concealed by the energy of the
thigh-muscles, which, using the paralyzed segments of the limbs as
inert supports, succeeds in effecting locomotion.[49] On the other
hand, in limbs apparently abandoned to total paralysis persevering
search will often discover some muscles or parts of muscles which
respond to faradic electricity: these must be considered as
susceptible of ultimate recovery.

[Footnote 49: Thus in Cornil's famous case, _Soc Biol._, 1863.]

The following table sums up some special diagnostic marks for the
different paralyses[50] afforded by the position of the limb and loss
of movements:

  Upper Extremity. Deltoid. Absence of deformity, which is averted by
    weight of arm. Inability to raise arm. Sometimes subluxation.
    Frequent association with paralysis, biceps, brachialis anticus,
    and supinator longus.

  Lower Extremity. Ilio-psoas. Rare except with total paralysis.
    Associated with paralysis, sartorius. Loss of flexion of thigh.
    Limb extended (if glutæi intact).

  Glutæi. Thigh adducted. Outward rotation lost. Lordosis on standing.
    Frequent association with paralysis of extensors of back.

  Quadriceps extensor. Flexion and adducting of leg (if hamstrings
    intact). Loss of extension of leg. Frequent association with
    paralysis of tibialis anticus.

  Tibialis anticus. Often concealed if extensor communis intact. If
    both paralyzed, then fall of point of foot in equinus. Dragging
    point of foot on ground in walking. Big toe in dorsal flexion (if
    extensor pollicis intact). The tendons prominent. Hollow sole of
    foot (if perineus longus intact).

  Extensor communis. Nearly always associated with that of tibialis
    anticus. Toes in forced flexion.

  Peroneus longus. Sole of foot flattened. Point turned inward.
    Internal border elevated. {1124}

  Sural muscles. Heel depressed. Foot in dorsal flexion (calcaneus).
    Sole hollowed if perineus longus intact; flattened if paralyzed.
    Point turned outward (calcaneo-valgus).

  Extensors of back. Lordosis on standing. Projection backward of
    shoulders. Plumb-line falls behind sacrum (unilateral). Trunk
    curved to side. Trunk cannot be moved toward paralyzed side.

  Abdominal muscles. Lordosis, without projection backward of
    shoulders.

[Footnote 50: See Duchenne, _loc. cit._, and also Roth, _On Paralysis
in Infancy_, London, 1869.]

After the paralysis the most remarkable symptom of anterior
poliomyelitis is the rapid wasting of the paralyzed muscles. The
atrophy begins within a week after the paralysis, and its progress is
even more rapid than that following the section of a nerve. Sometimes
all the flesh on a limb is shrivelled down to the bone; at other times
the muscular atrophy is concealed by an abnormal development of fat,
constituting a pseudo-hypertrophy. When all the muscles surrounding a
joint are equally paralyzed and atrophied, no deformity develops,[51]
unless, indeed, the segment of a limb is used by means of the
non-paralyzed proximate segment. In this case deformities may be
produced by the effect of weight quite irrespective of muscular
action, or in directions opposed to what we should expect from that.

[Footnote 51: Except talipes equinus.]

The weight of the limb or a portion of it, by stretching paralyzed
muscles, often aggravates their atrophy. This is most likely to occur
with the paralyzed deltoid when the arm is unsupported, and with the
anterior tibial muscles when the foot is allowed to drop.

Muscular atrophy occurs in the spinal paralysis of adults as well as
in children; but in the latter alone does the atrophy extend to the
bones and cartilages, tendons, fascia, ligaments, and blood-vessels.
The osseous projections to which the muscles are attached waste; so do
the epiphyses.[52] The long bones are thinner and shorter, the foot is
shorter, and the hand is shortened in paralysis of the upper
extremity, even where this is limited to the upper arm, and the
forearm is scarcely affected (Seeligmüller).

[Footnote 52: Seeligmüller, _Centralbl. f. Chirug._, No. 29, 1879.]

In exceptional cases the limb may become even elongated from passive
extension of the ligaments of the articulation. The bones may become
soft and flexible, and break if pressure be applied.[53]

[Footnote 53: Ch. Salomon, “Des Lesions osseuses et articulaires lieés
aux Maladies du Système nerveux,” _Revue mensuelle_, No. 8, 1878.]

Atrophy of the bones stands in no fixed relation to that of the
muscles, now exceeding, now falling short of that in intensity. This
naturally progresses more slowly; still, within seven or eight months
there may be a centimeter of difference between two limbs.

In marked contrast with this profound trophic disturbance of the bones
is the intact nutrition of the skin. The absence of decubitus is
indeed an important diagnostic mark from ordinary myelitis. The
subcutaneous fat, however, wastes so completely that the skin seems to
be closely adherent to the subjacent tissues, and cannot be pinched up
into folds.

The temperature of the skin always falls; the limb is perceptibly
colder to the touch than its fellow, and is often bluish and cyanotic.
Heine has observed that the temperature diminishes gradually from the
centre to the periphery, and at the coldest point may sink to
14° R.[54] Hammond relates a case where the local temperature was 75°
in an {1125} atmosphere of 72°. The author says that exact
measurements of surface temperature should be taken with Lombard's
differential calorimeter, especially when convalescence is expected,
as then a rise of temperature, however slight, is of most favorable
augury.

[Footnote 54: _Loc. cit._, p. 16. This is not a difference of 14
degrees between the sound and paralyzed limbs, as is erroneously
quoted by Seeligmüller (_loc. cit._, p. 67).]

General factors contribute to the fall of temperature: diminished
blood-supply from shrinkage of blood-vessels, or even atrophy of a
certain number among these; loss of nerve-influence upon the oxidation
processes; loss of muscular contractions, which should attract an
afflux of blood. Among these factors the loss of nerve-supply is
probably the most important, since the others exist in cerebral
paralysis without causing the remarkable coldness characteristic of
anterior poliomyelitis.

The atrophy of the blood-vessels is not always confined to the
terminal twigs. The entire iliac artery, and even the lower part of
the aorta, have been found markedly diminished in calibre.[55] This
shrinkage is unaccompanied by any change in the walls of the
blood-vessels: it is a simple arrest of development. It strikingly
illustrates the dependence of the blood-vessels on the vascular
demands of the tissues they are destined to supply.

[Footnote 55: Charcot and Joffroy, _Archives de Phys._, 1870, case by
Séguin, _loc. cit._, p. 9.]

The changes which take place in the electrical reactions of the
paralyzed limbs rank in importance with their paralysis and their
atrophy. They serve to establish the diagnosis, to decide, to a large
extent, the prognosis, and to measure the degree of nervo-muscular
degeneration.

It is well known that the early diminution, and even entire loss, of
faradic contractility was first emphasized by Duchenne as
pathognomonic of infantile spinal paralysis. Contractility is
diminished in from three to five days after the occurrence of the
paralysis, and by the end of a week is completely lost in those
muscles in which the paralysis is to be permanent. The muscles which
recover spontaneously during the period of early regression recover
their faradic with their voluntary contractility. In others,
persistently but less profoundly paralyzed and susceptible of cure,
the faradic contractility remains simply diminished and in unequal
degrees. Progress to recovery under treatment is usually marked by
progressive increase in the faradic response; but sometimes the power
of voluntary contraction is fully regained, while the faradic response
is still permanently lessened. The loss of faradic contractility is
more complete and permanent in muscles irretrievably paralyzed by
anterior poliomyelitis than in any other disease. These laws have been
generally accepted by late observers.[56]

[Footnote 56: Simon disputes their validity, and declares that the
importance of electricity in the diagnosis of spinal paralysis may
easily be exaggerated (_Union médicale_, 7, 28, p. 942, 1879).]

In 1868, Salomon discovered that muscles in which faradic
contractility had been completely lost were nevertheless capable of
contracting under the stimulus of galvanism—that this contraction is
exaggerated, and sometimes occurs at the opening as well as at the
closing of the circuit.[57] The author remarks that the persistence of
galvanic reaction after the complete loss of faradic contractility is
completely analogous to an {1126} observation of Brucke's on muscles
poisoned by woorara,[58] where the intramuscular termination of the
nerve is paralyzed. It is to be inferred, therefore, in both cases
that the muscular contraction results from direct irritation of the
muscle, and implies the entire loss of influence from the nerve.

[Footnote 57: _Jahrb. f. Kinderheilkunde_, N. F. i., 1868. According
to Erb (_loc. cit._, p. 984) and to Ross (_loc. cit._, p. 111),
Salomon was the first to make this observation. Seguin, however,
attributes priority to Lobb (_Lond. Med. Times and Gaz._, 1863), to
Hammond (_New York Med. Journal_, 1865), and to J. Netten Radcliffe
between 1863 and 1865. These dates precede that of the publication of
Salomon's paper, but the latter seems to have been written without
knowledge of earlier observations. (See also Onimus, _Soc. de Biol._,
1878, who argues that muscle-termination of nerve is partly
destroyed.)]

[Footnote 58: “Ueber den Einfluss der Stromes dauer auf die
Elektrische Bewegung der Muskeln,” _Sitzber. d. k. Akad. d. Wissensch.
in Wien_, 1867, Bd. lxi., quoted by Salomon, _loc. cit._, p. 388.]

Erb has greatly extended these observations, and shown that the
galvanic reactions of paralyzed muscles indicate their structural
degeneration, and are identical with those observed after section of a
peripheric nerve. There are three characteristic peculiarities in the
contractions thus obtained: 1st, they are slow, tonic, long drawn out;
2d, they are more painful than in normal muscles submitted to an equal
amount of electricity; 3d, in complete degeneration the contraction
obtained at anode closure equals or exceeds in intensity that excited
by cathode closure [AnSZ = or > KSZ]. The excitability of the muscle
to the galvanic current remains increased for several months, then
gradually diminishes, and finally falls below normal. The qualitative
alterations persist somewhat longer: finally, the muscle fails
altogether to contract.

Spinal paralysis differs markedly from progressive muscular atrophy in
the absence of constant correlation between the degree of paralysis or
atrophy and of electrical changes.

The last positive symptom to be noted in the paralytic stage of
infantile paralysis is the diminution and ultimate loss of reflex
excitability. This is correlative in time and extent with the loss of
faradic contractility. This seems to be an exception to the usual
rule, which associates loss of tendon reflex with lesion of the
posterior columns or nerve-roots. This is a proof that interruption of
the reflex arc at any point suffices to abolish the tendon
phenomena.[59]

[Footnote 59: Buzzard tested the tendon reflex in the zygomaticus
major in a patient in whom the sensory branch of the fifth nerve had
been stretched, and therefore, to a certain extent insulted. The
reflex response was decidedly lower than on the opposite side
(_Lancet_, Nov. 27, 1880).]

Negative Symptoms.—The negative symptoms of atrophic paralysis are as
important for the diagnosis and pathogeny as are the positive
characters, which have now been sufficiently detailed. The absence of
decubitus or other nutritive lesions of the skin has been already
mentioned. The absence of anæsthesia, or, as a rule, of any marked
degree of hyperæsthesia, is most important as indicating immunity of
the sensory tracts in the cord. Some diffused hyperæsthesia is
sometimes noted during the febrile stage: pain is by no means rare in
adults. But in children this is altogether absent, or else slight and
transitory. On the other hand, the complete preservation of
sensibility constitutes, in children, a serious obstacle to electrical
investigation.

After subsidence of the cerebral symptoms, if any, of the initial
stage, the functions of the brain are always intact[60] and the
disposition of the children apt to be remarkably lively. The general
health is often remarkable for its vigor. The worst, because the most
neglected, cases are naturally most often seen among the poor: the
ranks of professional beggars are largely recruited from among the
victims of infantile paralysis.

[Footnote 60: Practically, it may often be of importance for the
physician to ascertain that an intellectual enfeeblement, or even
idiocy, existing at the time of examination had preceded the onset of
the paralysis by months or years.]

{1127} The chronic stage is marked by the development of a new set of
symptoms—contractions of certain muscles surrounding one or more
joints and deformed positions of the limbs. These symptoms do not
always appear. If all the muscles surrounding a joint are completely
paralyzed and extensively atrophied, and if no weight is imposed on
the limb by the action of a non-paralyzed upper segment, and if the
paralyzed segment be so supported that its own weight does not
approximate the insertion-points of muscles, and thus cause their
passive retraction, then there is no deformity, but a dangling limb, a
membre de Polichinelle.

Laborde states that contractions appeared at the earliest about two
months after the paralysis. Seeligmüller, however, has seen pes
equinus and pes calcaneus develop in four weeks. The date is partly,
at least, determined by the time at which the children try to walk or
otherwise to use the paralyzed limbs; and the deformities are very
much more marked in the lower extremities, proportioned to the much
greater weight which they are obliged to sustain.

All varieties of club-foot, and most frequently equino-varus,
knock-knees, rigid flexions at the knee and hip, cyphosis, lordosis,
and colossal scoliosis may develop as manifold consequences of
atrophic paralysis. That subluxation of the humerus and the claw-hand
may occur in the upper extremities has already been mentioned.

In Seeligmüller's 75 cases, 53, or 71 per cent., exhibited some kind
of deformity. Among these, 43, or 56 per cent., were of the foot; 6
were cases of subluxated humeri; 5, easily-reducible luxation of the
fingers.

The following table contains a summary of the deformities observed as
a consequence of atrophic paralysis. They are distinguishable from
congenital deformities dependent on altered relations of articular
surfaces through defective development[61] by being easily reducible.
This remark especially applies to paralytic club-foot:

            | Equinus.
            | Equino-varus (varus hardly ever alone).
  Foot.     | Calcaneus.
            | Calcaneo-valgus.
            | Valgus.

            | Genu-recurvation.
  Knee.     | Genu-incurvation.
            | Permanent flexion.

            | Luxation.
  Hip.      | Permanent flexion.
            | Permanent adduction.

            | Flexion fingers or wrist (rare).
  Hand.     | Extension of wrist.
            | Claw-hand.

  Elbow.    | No deformity (Seeligmüller).

  Shoulder. | Subluxation humeri.

            | Dorsal scoliosis.
            | Lateral incurvation lumbar region.
  Trunk.    | Cyphosis.
            | Lordosis with backward projection of shoulders.
            | Lordosis without backward projection of shoulders.

[Footnote 61: _Volkmann's Handbuch_, Billroth und Pitha.]

{1128} Mechanism of Deformities.—From what has been said on the cases
in which deformities are absent it is evident that one at least of
three conditions are required for their production: the paralysis must
be unequally distributed in the muscles surrounding a joint; pressure
must be exerted by the weight of the body or traction by the weight of
the limb; effort must be made to utilize the maimed part of the limb
by means of other parts, or even by the muscles of the trunk.

The share taken by these different factors in the production of
deformities has been differently estimated by different observers. The
French surgeon Delpech was the first to explain the phenomenon on the
theory of muscular antagonism. The same theory has been most minutely
elaborated by Duchenne.[62] According to it, the intact or less
paralyzed muscles, in virtue of their tonus, constantly tend to draw
the segment of the limb on which they act in a direction opposed to
that in which it should be drawn by the paralyzed muscles. Since this
action is unantagonized, its influence persists; the insertion-points
of the contracting muscle being permanently approximated, the
nutrition of the muscle is modified: it grows shorter (adapted
atrophy). There results finally shortening and retraction of the
muscles on one side of the joint, over-stretching of those on the
other.

[Footnote 62: _De l'Électrisation localisée_, 1861.]

Duchenne used to illustrate this theory by means of a skeleton
supplied with artificial muscles, whose successive section would cause
the appearance of the corresponding deformity. Werner[63] first
protested against this theory, and the protest has been further
developed and a different theory built up through the efforts of
Hueter[64] and Volkmann.[65] The latter observes that the muscles and
ligaments surrounding a joint normally receive a large amount of the
weight falling upon its articular surfaces. Removal of this elastic
resistance exposes these surfaces to the full force of the pressure,
and thence to almost certain danger of deformity—a danger, therefore,
always incurred after paralysis of the muscles. Thus, the weight of
the body, pressing, unresisted, on the arch of the foot, is able to
displace the bones of the arch from their normal relations and
completely flatten the arch.

[Footnote 63: _Reform der Orthopædie_, 1845.]

[Footnote 64: _Gelenkkrankheiten_.]

[Footnote 65: _Sammlung klin. Vort._, No. 1.]

A position of ease is that in which the movement of the joint has been
pushed as far as possible until limited by the passive resistance of
the ligaments or the conformation of the articular surfaces. The
weight of the body must then be so placed that the line of gravity
falls on the side of the open angle, while the limiting bands stretch
across the base. Thus, a tired man sits with a curved back; the
muscles which may extend the spinal column in a straight line are
relaxed; the column falls forward until arrested by the anterior
vertebral ligaments. Thus, in standing at ease the thigh presses
against the leg, so as to form a wide angle open anteriorly. When the
quadriceps extensor is paralyzed, this position is inevitable and
exaggerated, since the force which might counteract it, contraction of
the thigh extensor, has been removed.

Formerly, the rôle of muscles in this elastic resistance was
under-estimated and that of ligaments exaggerated.

CRITICISM OF THE THEORY OF MUSCULAR ANTAGONISM.—Three considerations
have been urged in objection to the theory of muscular {1129}
antagonism: First, deformities may develop even in limbs totally
paralyzed, provided these limbs be subjected to weight and pressure.
Pes equinus, the most common form of paralytic club-foot, develops
with total paralysis of the muscles of the leg where the child does
not walk, but is carried on the arms of a nurse with its foot
dangling. The part of the foot anterior to the ankle-joint being
longer and heavier than that behind, the point falls; the tendo
Achillis is passively shortened, and by nutritive adaptation to this
position may become permanently retracted. Long persistence in this
position accustoms the dorsal surface of the bones to a less degree of
pressure than the plantar surface: as a consequence, the growth of the
bone becomes more active above, while it is arrested below; the arch
of the foot is increased until the sole is curved into a deep hollow;
and the plantar aponeurosis is correspondingly shortened.

Volkmann relates a case where this same deformity appeared without the
least paralysis, but simply from prolonged passive extension of the
feet in bed. The patient was an adult, and suffered from a severe
typhoid with a double relapse. After recovering from the fever a year
of orthopædic treatment was required to restore the feet to their
normal position.

The second objection is the absence of any proof of such constant
tonus in the muscles as may be sufficiently powerful to determine the
position of a limb. Such tonus exists in the involuntary muscles,
especially in those of the blood-vessels, but there is no evidence
that it exists in the voluntary muscles. To this Seeligmüller has
replied by admitting the objection to the theory as thus proposed, but
substituting the more plausible influence of repeated contractions on
the part of the non-paralyzed muscles. Each contraction draws the limb
in a certain direction, and there it tends to remain, because there is
nothing to antagonize the force which it has obeyed.

The third objection is that examination of individual cases not
infrequently shows displacements in directions opposed to that which
should be determined by muscular antagonism. Volkmann has especially
illustrated the latter assertion by the mechanism of genu-recurvation.
In paralysis of the quadriceps extensor of the tibia the weight of the
body is exercised, not merely from above downward, but from without
inward, falling, therefore, on the inner malleolus. It thus tends to
press the anterior part of the foot outward,[66] and a valgus finally
complicates the calcaneus. Seeligmüller, however, quotes two cases of
pes calcaneus developed in children who had never walked: in one
paralysis of the sural muscles had occurred at the age of four weeks,
and the other case was observed at the age of fourteen weeks.
Seeligmüller remarks that only early examination of the faradic
contractility of a group of paralyzed muscles can decide whether any
among them preponderate during a time sufficient to fix the limb in a
vicious position. Thus in one case of pes calcaneus he found two years
after the occurrence of the paralysis that some contractility still
persisted in the dorsal flexors, but six months later this had quite
disappeared. Had the examination then been made for the first time
when all the muscles were equally paralyzed, it would have seemed
impossible to explain the deformity by muscular antagonism.

[Footnote 66: Sayre asserts that lateral rotation cannot take place at
the ankle-joint, but at the medio-tarsal articulation. Hueter also
refers pes varus and pes valgus to the talo-tarsal articulation.]

{1130} RELATION OF WEIGHT AND MUSCULAR FORCES.—The influences of
weight and of muscular action sometimes concur, sometimes are opposed
to each other. Thus, the weight of the foot alone always tends to
produce equino-varus; it acts therefore to intensify the action of the
sural muscles when the anterior tibial are paralyzed, but to diminish
the influence of paralysis of the gastrocnemius when the foot is being
drawn into dorsal flexion. Hence one reason for the comparative rarity
of pes calcaneus.

Paralytic deformities at the hip and knee are much rarer than those of
the foot. At the hip this immunity is partly due to the relative
rarity of paralysis in the muscles surrounding the joint—still more to
the fact that the weight of the limb tends to correct excessive
flexions. These are therefore more likely to occur in children allowed
to remain in bed than in those who are encouraged to walk by means of
suitable apparatus. The use of crutches, however, favors the
development of deformity, because, since with paralysis of the
thigh- or leg-muscles pes equinus nearly always exists, the thigh is
unduly lengthened. To palliate this inconvenience the patient
instinctively flexes the knee or hip, or both, and the position tends
to become permanent.

When the flexion is rigid and extension becomes impossible, the
gastrocnemii are relaxed until they lose their power of tension, and
thence of fixing or raising the heel. Further, as by the flexion the
limb is moved in front of the body, it is necessary to project the
body forward again over the support. Hence a lordosis is developed, to
be distinguished from that caused by paralysis of the vertebral
extensors (_a_) by the rigid flexion of the thigh; (_b_) by the
facility with which the patient can extend the back as soon as he is
placed in a sitting position.

Although the quadriceps extensor is so frequently paralyzed, rigid
flexion at the knee—such as on the theory of muscular antagonism might
be expected from the action of the hamstring muscles—is very rare. As
already observed, it occurs, if at all, in neglected children allowed
to lie or sit with the leg partly flexed. In those who attempt to walk
the leg is not flexed, but forced into hyper-extension by the
following mechanism: The muscles inserted on the upper part of the
thigh swing the leg forward like a passive support. Afterward the body
bends forward over the support, and its weight, pressing from above
downward and from before backward, and pressing the articular surfaces
of the joint together, forces the head of the tibia backward until the
movement is checked by the posterior ligaments. The deformity is the
same whether the quadriceps or one or all the muscles surrounding a
joint are paralyzed (Volkmann).

DISLOCATIONS.—Dangling limbs are, however, much more frequently the
consequence of total paralysis, with extraordinary relaxation of the
ligaments of the joint permitting dislocation. Reclus[67] has
published several such cases. Verneuil has even suggested that
congenital luxation of the hip-joint always depends on an
intra-uterine spinal paralysis.[68]

[Footnote 67: _Revue mensuelle de Méd. et de Chir._, Mars, 1878.]

[Footnote 68: Quoted from Seeligmüller.]

In the upper extremities rigid contractions are much less frequent,
even in proportion to the number of paralyses. Seeligmüller has seen
five cases of reducible flexion of the fingers, and one of permanent
extension of the wrist and fingers, associated with paralysis {1131}
of all the flexors. In this case, if the arms were so suspended that
the hand hung freely, its weight gradually overcame the action of the
extensors and the fingers fell into flexion. Upon any attempt at
exertion the hyperextension was reproduced.

DEFORMITIES OF THE TRUNK.—Scoliosis will be caused when, with
unilateral paralysis of the extensors of the vertical column, the
lower part of the trunk is drawn to the non-paralyzed side, and the
upper half is bent over the paralyzed side in order to restore the
balance. In bilateral paralysis of the extensors both shoulders are
projected backward, so that a plumb-line dropped from between them
falls behind the sacrum, and lordosis is developed, although the
lumbar column is not projected forward. The same form of lordosis
occurs when the glutæi are paralyzed. When, however, the abdominal
muscles are paralyzed, the lumbar column is really projected forward,
and then a plumb-line dropped from the shoulders passes over the
sacrum.[69]

[Footnote 69: Duchenne, _loc. cit._, 1861.]

PARALYSIS OF THE ABDOMINAL MUSCLES.—Unilateral paralysis of the
extensors of the back is often difficult to detect in young children.
Seeligmüller recommends that the child be laid across the mother's
knees and told to move the trunk from one side to the other while the
pelvis is held firm. If too young to obey the direction, the movement
can be excited by pricking or by electric irritation. It will be seen
that the trunk can be turned only to one side.

In these paralyses of the trunk it is clear that the deformity does
not develop under the influence of muscular antagonism alone, but only
when the non-paralyzed muscles attempt to sustain the superincumbent
weight of the body or a portion of it.

SUMMARY OF MECHANISMS OF THE DEFORMITIES.—We may indeed conclude, as
stated at the beginning, that this complex etiology exists in almost
all cases. When the limb is at rest in bed or the weight of the body
is transferred to crutches, then repeated contraction of the flexus
will suffice to bring the limb into a vicious position (contraction at
knee- and hip-joint). When the foot or hand hangs unsupported, its
weight is sufficient to cause deformity, even when all the muscles are
paralyzed, and sometimes in opposition to the direction of intact
muscles. Thus the weight which is passively borne by the limb, and the
efforts of intact muscles to effect the function of the limb in spite
of the paralysis, both concur in the production of the deformity.

ANATOMICAL LESIONS.—The theory of the anatomical basis of infantile
paralysis constitutes one of the most interesting portions of its
history. It is indeed one of the most instructive chapters of modern
pathology from the rapidity with which in a short time precise
knowledge has accumulated, and for the degree in which this has
revolutionized previous ideas.

Autopsies.—Until 1863 only five autopsies had been made upon persons
affected with infantile paralysis.[70] As the disease was never, of
itself, {1132} fatal, opportunity for pathological investigation did
not present itself, while attention was still vividly attracted to the
paralysis. When this had become a chronic infirmity, and patients had
succumbed to intercurrent disease, the opportunity must have occurred,
but was not then utilized.

[Footnote 70: I believe the first list of modern autopsies was made by
myself in a paper read before the New York County Medical Society,
Dec. 22, 1873. The paper was not published until May, 1874, and in the
mean time Seguin's lecture on “Infantile Paralysis” was published in
the _N. Y. Med. Record_, Jan. 15, 1874, with a tabulated list of 25
autopsies, necessarily almost identical with mv own—cases 9 and 10 are
really identical. A case by Roth is included; 4 negative autopsies are
omitted. In 1880, Seeligmüller, in his elaborate essay in _Gerhardt's
Handbuch_, published a list of 32 cases, including the above, and
adding to them the following: Case by Müller, 1871; 4 cases by Leyden,
1875 (_Arch. de Psych._); 1 case by Raymond, 1874 (_Gaz. méd. de
Paris_); 1 case by Demme, 1876 (_B. med. Bericht über das Jennerischt
Kinderspital zu Bern_); 1 case by Eisenlohr, 1876 (_Tageblatt des
Hamburger Naturforscher Versammlung_); 1 case by Schultze, 1877
(_Virch. Arch._, Bd. lviii.).

To this list we may now add 3 cases by Turner, Humphrey, Taylor, 1881
(_Path. Trans. London_); 2 cases by Dejerine, 1878 (_Progrès méd._),
giving a total of 37 cases with detailed histories and autopsies.]

The first cases affording autopsies in which the spinal cord was
thoroughly investigated, belonged, however, precisely to this class of
extremely chronic lesions, which should be regarded as showing rather
the results of the morbid process than that process itself. Omission
to observe this distinction has been the occasion of several
misinterpretations of the pathological appearances.

Premature Theories.—In the entire absence of evidence it is a little
remarkable that such high authorities as Rilliet and Barthez,[71]
West,[72] Vogel,[73] Eulenburg,[74] should have pronounced
dogmatically that the disease was essential—_i.e._ unaccompanied by
any structural lesion whatever; and that Bouchut,[75] on the strength
of most incomplete examination, should have built up a theory of
myogenic paralysis. It is still more remarkable, after the published
autopsies of Rinecker,[76] Laborde,[77] Cornil,[78] Prévost,[79]
Charcot and Joffroy,[80] Parrot and Joffroy,[81] Vulpian,[82] Roger
and Damaschino,[83] that Politzer in 1866,[84] Brown in 1871,[85]
Barwell in 1872,[86] Kétli,[87] Adams in 1873,[88] should still adhere
to this doctrine. They are, however, entirely in the minority, and all
recent monographs and works published with a view to presenting the
state of science assume the spinal nature of infantile paralysis to be
established beyond possibility of controversy.[89]

[Footnote 71: _Traité des Maladies des Enfants_.]

[Footnote 72: _Diseases of Children_, Am. ed., 1860.]

[Footnote 73: _Diseases of Children_, trans. from 4th ed., 1870.]

[Footnote 74: _Arch. Virchow_, Bd. xvii. 1859.]

[Footnote 75: _Deutsche Klinik_, 1863.]

[Footnote 76: _Gaz. méd._, 1864, Soc. de Biol., 1864.]

[Footnote 77: _De la Paralysie de l'Enfance_.]

[Footnote 78: _Gaz. méd._, 1866, Soc. de Biol., 1866.]

[Footnote 79: _Arch. de Phys._, 1870, p. 134.]

[Footnote 80: _Ibid._, p. 310.]

[Footnote 81: _Ibid._, p. 316.]

[Footnote 82: Bouchut is said by Simon (_loc. cit._) to be alone in
his theory; Kétli, however, agrees with him. Eulenburg, in 1872, in
his systematic treatise, assigns a central origin to infantile
paralysis, but offers no opinion in regard to its nature.]

[Footnote 83: _Gaz. méd._, 1871.]

[Footnote 84: _Jahrbuch für Kinderkrankheiten_, 1866.]

[Footnote 85: _Compend. für Kinderkrank._, p. 161.]

[Footnote 86: _Lancet_, 1872.]

[Footnote 87: _Jahrbuch für Kinderkrank._, 1873.]

[Footnote 88: _Treatise on Club-foot_.]

[Footnote 89: See Seguin, _loc. cit._, 1874; Erb, _Ziemssen's
Handbuch_, Bd. xi.; Seeligmüller, _Gerhardt's Handbuch der
Kinderkrankheiten_; Ross, _Treatise on Diseases of Nervous System_,
vol. ii.; Hammond, _Diseases of Nervous System_, 6th ed., 1881, etc.
etc.]

The following table contains a summary of the seven autopsies in which
the spinal cord is said to have been examined with negative results.
Of these, the only really important case is the third, in which a
microscopic examination, made by so competent an histologist as Robin,
was said to have discovered no lesion of the cord.

{1133} The foregoing autopsies may be tabulated as follows:

TABLE I.—NEGATIVE AUTOPSIES.

No.: 1

Year: 1850 or '51?

Name of Author and Patient: Rilliet and Barthez.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: l. o.

Electric Reaction: ?

Appearances at Autopsy: Negative.

Reference in Literature: _Gaz. méd. de Paris_, 1850 (or '51?) p. 681.

No.: 2

Year: 1850 or '51?

Name of Author and Patient: Rilliet and Barthez.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearances at Autopsy: Negative.

Reference in Literature: _Ibid._

No.: 3

Year: 1867

Name of Author and Patient: Bouchut and Robin. (Angélique Lermain).

Age at time of Paralysis, of Autopsy: 1½, 3

Nature of Symptoms: Suddenly after 3 days' fever.

Limbs Paralyzed: both u.

Electric Reaction: —

Appearances at Autopsy: Negative microscopically.

Reference in Literature: _Union méd._, 1867, No. 130, p. 187.

No.: 4

Year: 1873

Name of Author and Patient: Adams.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Treatise on Club-foot_, p. —.

No.: 5

Year: 1873

Name of Author and Patient: Elischer and Kétli.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Jahrb. Kinderheilk._, 1873.

No.: 6

Year: 1873

Name of Author and Patient: Elischer and Kétli.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Ibid._

Heine, in the absence of autopsies, but arguing from clinical symptoms
alone, already inferred the existence of a spinal lesion as cause of
the paralysis, and believed that it consisted in congestion, or even
in hemorrhagic exudation, capillary or massive, which should compress
the cord and result in partial atrophy. The same opinion is advanced
in 1844 by Brunnière,[90] also by Vogt,[91] in 1868 by Salomon[92] and
Radcliffe.[93] The autopsies contained in the following table, in all
of which vascular lesions are prominent, might be invoked in support
of this view:

TABLE II.—AUTOPSIES SHOWING VASCULAR LESIONS OF CORD.

No.: 7

Year: 1829

Name of Author and Patient: Klein.

Age at time of Paralysis, of Autopsy: 5, 5

Nature of Symptoms: Persistent cerebral symptoms.

Limbs Paralyzed: l. o.

Electric Reaction: ?

Appearances at Autopsy: Congestion of pia around roots of left
brachial plexus.

Reference in Literature: Quoted by Heine.

No.: 8

Year: 1855

Name of Author and Patient: Brund.

Age at time of Paralysis, of Autopsy: 1, 5

Nature of Symptoms: Meningitis?

Limbs Paralyzed: r. u.

Electric Reaction: ?

Appearances at Autopsy: Chronic spinal klepto-meningitis.

Reference in Literature: —

No.: 9

Year: —

Name of Author and Patient: Hammond.

Age at time of Paralysis, of Autopsy: 4 yrs. stand.

Nature of Symptoms: —

Limbs Paralyzed: l. u.

Electric Reaction: ?

Appearances at Autopsy: Encysted clot in left ant. column, lower
dorsal cord.

Reference in Literature: _Journ. Psych. Medicine_, 1867.

[Footnote 90: _Krankheiten des Gehirns und Ruckenmarkes_.]

[Footnote 91: _Lahmung der Kinder_, p. —.]

[Footnote 92: _Jahrb. f. Kinderheilk._, 1865.]

[Footnote 93: _Reynolds's Syst. of Medicine_.]

The first really modern autopsy, that made by Cornil in 1863, agrees
with the two earliest on record in disclosing only an atrophy of the
cord. Some of the other cases, contained in Table III., note in
addition sclerosis of the lateral columns.

In all the remaining autopsies on record are noted atrophy of the
anterior gray cornua and more or less extensive destruction of the
ganglionic cells.

In a certain number of cases the atrophy seemed to be the unique
lesion. But it never was confined to the ganglionic cells, but
included the reticulum of gray fibres in which these were imbedded,
and which {1134} was replaced by a reticulum of connective tissue.
These cases were all examined many years after the occurrence of the
paralysis.

TABLE III.—AUTOPSIES SHOWING ATROPHY OR SCLEROSIS OF WHITE COLUMNS OR
ROOTS.

No.: 10

Year: 1825

Name of Author and Patient: Hutin.

Age at time of Paralysis, of Autopsy: 7, 49

Nature of Symptoms: Convulsions.

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy of cord from below 8th dorsal nerve to
thickness pencil, and of nerves.

Reference in Literature: Quoted by Heine, p. 151.

No.: 11

Year: 1842

Name of Author and Patient: Lunget.

Age at time of Paralysis, of Autopsy: ?, 8

Nature of Symptoms: ?

Limbs Paralyzed: r. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy and brown discol. of ant. roots of
lumbar and sacral nerves going to sciatic.

Reference in Literature: _Anat. et Phys. du Syst. nerveux_, i. p. 358.

No.: 12

Year: 1863

Name of Author and Patient: Recklinghausen.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy of ant.-lateral columns.

Reference in Literature: _Deutsche Klinik_, 1863, Jan. 3.

Seel. says also atrophy of cells; Seguin and J., tubercles.

No.: 13

Year: 1863

Name of Author and Patient: Cornil.

Age at time of Paralysis, of Autopsy: 2, 49

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy antero-lateral columns.

Seeligmüller says also atrophy of ganglion-cells, as if quoting
Charcot.

Reference in Literature: _Soc. de Biol., Comptes Rendus_, 1863.

Infiltration of gray and white corpuscles, with abundant amyloid
corpuscles, especially in anterior gray cornua. These through entire
extent of cord—cells—intact. Paraplegia, but walks by muscles of thigh
and pelvis; leg and foot atrophied.

No.: 14

Year: 1864

Name of Author and Patient: Laborde and Bouvier.

Age at time of Paralysis, of Autopsy: 1, 2

Nature of Symptoms: ?

Limbs Paralyzed: all four.

Electric Reaction: noted.

Appearance at Autopsy: Atrophy antero-lateral columns; nerve-fibres
atrophied and varicose.

Reference in Literature: Laborde, _De la Paralysie de l'Enfance_, pp.
109-119.

No.: 15

Year: 1864

Name of Author and Patient: Laborde and Cornil.

Age at time of Paralysis, of Autopsy: ⅔, 2

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Sclerosis of ant.-lateral columns.

Ganglion-cells normal; sciatic neuritis.

Reference in Literature: Laborde, _loc. cit._, p. 104.

The first group is contained in the following table:

TABLE IV.—AUTOPSIES SHOWING ATROPHY OF THE ANTERIOR CORNUA AND
GANGLION-CELLS.

No.: 16

Year: 1866

Name of Author and Patient: Prévost.

Age at time of Paralysis, of Autopsy: ?, 78

Nature of Symptoms: ?

Limbs Paralyzed: L. u.

Result of Autopsy: Atrophy of left anterior cornu, especially of
ganglion-cells.

Reference in Literature: _Comptes Rendus, Soc. Biol., Gaz. méd._,
1866.

No.: 17

Year: 1870

Name of Author and Patient: Charcot and Joffroy.

Age at time of Paralysis, of Autopsy: 7, 32

Nature of Symptoms: Sudden.

Limbs Paralyzed: All esp. l. u.

Result of Autopsy: Atrophy of cells ant. horns and ant. lateral
columns.

Reference in Literature: _Archives de Phys._, 1870.

No.: 18

Year: 1870

Name of Author and Patient: Parrot and Joffroy.

Age at time of Paralysis, of Autopsy: —, 3

Nature of Symptoms: Unknown.

Limbs Paralyzed: B. l.

Result of Autopsy: Atrophy and partial sclerosis of anterior cornua
and ant. lat. columns.

Reference in Literature: — {1135}

No.: 19

Year: 1870

Name of Author and Patient: Vulpian.

Age at time of Paralysis, of Autopsy: ?, 66

Nature of Symptoms: ?

Limbs Paralyzed: L. l.

Result of Autopsy: Atrophy of ganglion-cells, sclerosis of
antero-lateral columns.

Reference in Literature: _Archives Physiol._, 1870.

No.: 20

Year: 1871

Name of Author and Patient: Müller.

Age at time of Paralysis, of Autopsy: 4, 34

Nature of Symptoms: Fall from bed.

Limbs Paralyzed: L. lower.

Result of Autopsy: Atrophy of ganglion-cells ant. cornua; sclerosis of
anterior roots.

Reference in Literature: Quoted by Seeligmüller, _Gerhardt's
Handbuch_, Tabeln.

No.: 21

Year: 1873

Name of Author and Patient: Lancereaux and Pierret.

Age at time of Paralysis, of Autopsy: 2, 18

Nature of Symptoms: ?

Limbs Paralyzed: L. upper.

Result of Autopsy: Atrophy of external group cells in ant. cornua;
general atrophy of left half of lumbar cord.

Reference in Literature: Petitfils, _Thesis on Atrophie aigue des
Cellules motrices_, 1873, p. 33.

No.: 22

Year: 1875

Name of Author and Patient: Raymond.

Age at time of Paralysis, of Autopsy: ?, 75

Nature of Symptoms: ?

Limbs Paralyzed: R. arm.

Result of Autopsy: Atrophy of ganglion-cells in right ant. horn cerv.
region.

Reference in Literature: _Gaz. méd de Paris_, No. 19, 1875.

No.: 23

Year: 1879

Name of Author and Patient: Taylor.

Age at time of Paralysis, of Autopsy: 1½, 3

Nature of Symptoms: 3 days' fever.

Limbs Paralyzed: L. leg.

Result of Autopsy: Atrophy of left ant. cornua; disappearance of
ganglion-cells; no lesion in white column.

Reference in Literature: _Trans. Path. Soc. London_, 1879.

No.: 24

Year: 1875

Name of Author and Patient: Dejerine.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: R. foot (congenital equinus).

Result of Autopsy: Atrophy of ant. horn right side; atrophy external
group of motor-cells.

Reference in Literature: _Arch. Phys._, 1874.

No.: 25

Year: 1879

Name of Author and Patient: Humphreys.

Age at time of Paralysis, of Autopsy: 1½, 3½

Nature of Symptoms: ?

Limbs Paralyzed: L. leg.

Result of Autopsy: Atrophy of left half lumbar cord; disappearance of
medial group cells both sides; antero-lateral on left side.

Reference in Literature: _Trans. Path. Soc. London_, 1879.

In the remaining cases the ganglion-cells of the anterior cornua had
also disappeared; but in addition to this atrophy excited distinct
evidence of more or less extensive inflammation. This table includes
one case of autopsy at two months (Roger's); one at six weeks after
paralysis (Turner's).

TABLE V.—AUTOPSIES SHOWING EVIDENCE OF MYELITIS, TO WHICH THE ATROPHY
OF THE GANGLION-CELLS WAS CONSECUTIVE.

No.: 26

Year: 1866

Name of Author and Patient: Echeverria.

Age at time of Paralysis, of Autopsy: 3, 10

Nature of Symptoms: Fever.

Limbs Paralyzed: R. arm, R. leg.

Appearance at Autopsy: Granular pigmentation anterior cornua, diffuse
myelitis.

Reference in Literature: Quoted by Seguin, _loc. cit._

No.: 27

Year: 1866

Name of Author and Patient: Echeverria.

Age at time of Paralysis, of Autopsy: 2, 2½

Nature of Symptoms: Febrile diarrhœa.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Ibid.

Reference in Literature: _Ibid._

No.: 28

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 1-5/6, 2

Nature of Symptoms: Scarlatina with second attack.

Limbs Paralyzed: L. arm, then both legs.

Appearance at Autopsy: Foci of softening throughout cord. Atrophy
ganglion-cells and nerve-fibres. Dilatation, fatty degen. vessels.
Sclerosis ant. columns. Atrophy ant. roots.

Reference in Literature: _Gaz. méd. de Paris_, 1871.

No.: 29

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 2, 2½

Nature of Symptoms: Variola.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Foci of softening in ant. cornua. Fatty degen.
blood-vessels, circumscribed myelitis.

Reference in Literature: _Ibid._

No.: 30

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 2, 3

Nature of Symptoms: Fever.

Limbs Paralyzed: Ibid.

Appearance at Autopsy: Foci of softening, as above.

Reference in Literature: _Ibid._

No.: 31

Year: 1873

Name of Author and Patient: Roth.

Age at time of Paralysis, of Autopsy: 1, 2

Nature of Symptoms: Ibid.

Limbs Paralyzed: Ibid.

Appearance at Autopsy: Focus myelitis on both sides. Disappearance
ganglion-cells, abundant exudation corpuscles.

Reference in Literature: _Virch. Arch._, 1873, Bd. lviii. {1136}

No.: 32

Year: 1868

Name of Author and Patient: L. Clarke.

Age at time of Paralysis, of Autopsy: 1, 32

Nature of Symptoms: After inoculation.

Limbs Paralyzed: Both arms.

Appearance at Autopsy: Extensive myelitis ant. and central part gray
matter. Disappearance ganglion-cells.

Reference in Literature: _Med.-Chir. Trans._, li. p. 219.

No.: 33

Year: 1876

Name of Author and Patient: Schultze.

Age at time of Paralysis, of Autopsy: 3, 22

Nature of Symptoms: Acute disease.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Atrophy lumbar cord ant. lat. columns. Atrophy
ganglion-cells. Abundant exud. corpuscles. Proliferation neuroglia.

Reference in Literature: _Virch. Archiv_, Bd. lxviii., 1876.

No.: 34

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 2, 60

Nature of Symptoms: Fall from table.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Circumscribed cicatrix with complete
destruction gray substance. Amyloid degeneration. Atrophy ant. roots.

Reference in Literature: _Archiv f. Psych._, 1876, Bd. vi.

No.: 35

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: ¾, 1¾

Nature of Symptoms: Suddenly.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Atrophy ganglion-cells. Cellular diffused
infilt. (myelitis) gray subst'ce.

Reference in Literature: _Ibid._

No.: 36

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 4, 58

Nature of Symptoms: Sudden over night.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Amyloid infiltration ant. horns, atrophy
ganglion-cells left lumbar horn. Diffuse atrophy gray substance.

Reference in Literature: _Ibid._

No.: 37

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 3, 20

Nature of Symptoms: Ibid.

Limbs Paralyzed: R. leg, L. arm.

Appearance at Autopsy: Sclerotic focus in right lumbar and in left
cerv. region. Diffuse meningo-myelitis. Atrophy ant. lat. columns.
Encapsulated myelitis.

Reference in Literature: _Ibid._

No.: 38

Year: 1876

Name of Author and Patient: Demme.

Age at time of Paralysis, of Autopsy: ?, 3½

Nature of Symptoms: ?

Limbs Paralyzed: —

Appearance at Autopsy: Purulent focus in ant. cornua lumbar region.
Atrophy ganglion-cells.

Reference in Literature: Quoted by Seeligmüller, _loc. cit._, p. 18.

No.: 39

Year: 1876

Name of Author and Patient: Eisenlohr.

Age at time of Paralysis, of Autopsy: ?, ¾

Nature of Symptoms: ?

Limbs Paralyzed: B. legs.

Appearance at Autopsy: Diffuse inflammation anterior horns and ant.
lat. columns.

Reference in Literature: _Ibid._

No.: 40

Year: 1879

Name of Author and Patient: Turner.

Age at time of Paralysis, of Autopsy: 2½, 2¾

Nature of Symptoms: ?

Limbs Paralyzed: —

Appearance at Autopsy: Myelitic disorganization gray substance ant.
cornua lumbar cord.

Reference in Literature: _Trans. Path. Soc. Lond._, 1879.

No.: 41

Year: 1883

Name of Author and Patient: Archambault et Damaschino.

Age at time of Paralysis, of Autopsy: 30 m's, 31 m's, or 26 d'ys fr.
début.

Nature of Symptoms: Malaise and prostration one day.

Limbs Paralyzed: Left leg and right arm.

Appearance at Autopsy: Focus red softening ant. horns left lumbar;
right cervical region. Enormous enlargement vascular network, and
distension blood-vessels; granular corpuscles in lymphatic sheaths;
marked atrophy cells and of myeline sheaths of fibres in ant. roots;
myeline balls in sheath; axis-cylinders disappeared. Lesions more or
less marked throughout cord. Nerves not examined.

Reference in Literature: _Le Union médicale_, 1883.

No.: 42

Year: 1884

Name of Author and Patient: Money.

Age at time of Paralysis, of Autopsy: 2 yrs., 28 m's.

Nature of Symptoms: Fever and vomiting for a week.

Limbs Paralyzed: Paraplegia.

Appearance at Autopsy: Red area both anterior cornua lumbar region.
Here distension and thrombosis vessels; infiltration leucocytes;
absence multipolar cells.

Reference in Literature: _Trans. Path. Soc. Lond._, 1884.

No.: —

Year: 1884

Name of Author and Patient: Money.

Age at time of Paralysis, of Autopsy: Unknown, 7 yrs.

Nature of Symptoms: Unknown.

Limbs Paralyzed: Right leg.

Appearance at Autopsy: Wasting anterior horn almost throughout lumbar
region. Atrophy cells chiefly in ant., ant.-lat., post.-lateral, and
central groups, replaced by dense nucleated tissue.

Reference in Literature: —

It will be useful to add another table, which will group together the
cases in which the autopsies were made within two years after the
occurrence of the paralysis. Of these, all but the two made by
Laborde, in which the cornua are declared to be healthy and the lesion
limited to the {1137} white columns, show traces of destructive morbid
processes in the gray substance of the cord, greatly predominating in
the anterior cornua, but not absolutely limited to them, nor even to
the part of the cord which corresponds to the paralyzed limb:

                           TABLE VI.

  ---------+-----------------+------------------+-------------
  Case No. | Name of Author. | Date of Autopsy  | Year of
           |                 | after Paralysis. | Publication.
  ---------+-----------------+------------------+-------------
     41    | Damaschino.     |    6 weeks.      |   1883
     40    | Turner.         |   26 days.       |   1879
     28    | Roger and       |                  |
           |   Damaschino.   |    2 mos.        |   1871
     42    | Money.          |    4 mos.        |   1884
     27    | Echeverria.     |    6 mos.        |
     39    | Eisenlohr.      |    6 mos.        |
     29    | Roger.          |    6 mos.        |   1871
     31    | Roth.           |    9 mos.        |   1873
     35    | Leyden.         |   11 mos.        |   1876
     14    | Bouvier and     |                  |
           |   Laborde.      |   12 mos.        |   1864
     30    | Roger.          |   13 mos.        |   1871
     15    | Cornil and      |                  |
           |   Laborde.      |   16 mos.        |   1864
     12    | Recklinghausen. |   24 mos.        |   1863
     38    | Demme.          |   24 mos.        |   1876
     23    | Taylor.         |   18 mos.        |   1879
     25    | Humphrey.       |   24 mos.        |   1879
  ---------+-----------------+------------------+-------------

AUTOPSIES OF RELATIVELY RECENT CASES.—In cases relatively recent all
macroscopic changes in the cord may be entirely wanting. There may be
some degree of asymmetry in the surface of section, patches of white
coloration in the anterior gray substance, or of gray or yellow color
in the white columns; the anterior roots may be congested or even
already atrophied.[94] On the other hand, there have several times
been found foci of visible red softening, much more frequently at a
point corresponding to the origin of the paralyzed nerves, but not
absolutely confined to them, and sometimes existing at points where
they have given rise to no symptoms whatever.[95]

[Footnote 94: Roger's first case, No. 28 of Table V.]

[Footnote 95: Case 1st of Roger, Tab. V.]

Microscopic Lesions.—In striking contrast with this paucity of
macroscopic lesions are the interesting structural changes revealed
under the microscope. These lesions are usually comprised within
circumscribed foci whose size may vary from a long diameter of
2 mm.[96] to one of from 10 to 30 mm.[97] Sometimes bilateral foci are
found with monoplegic paralysis; thus one side or the other
preponderates in the morbid process.

[Footnote 96: Case Roth, Tab. V.]

[Footnote 97: Case Schulze, Tab. V.]

In recent cases (Damaschino's, at twenty-six days; Roger's, at two
months; Turner's, at six weeks) patches of red softening existed at
the portions of the cord containing the nuclei of origin of the
paralyzed nerves. In Turner's case the focus contained hemorrhagic
extravasation, and the traces of this were clearly perceptible in
Roger's first case. The blood-vessels are dilated; their lymphatic
sheaths infiltrated with leucocytes and with granular corpuscles;
their walls are thickened, pigmented, or fatty.

{1138} Leucocytes are often disseminated through the diseased area,
and in one case (Demme) were accumulated into a focus of pus. Besides
the leucocytes, the foci are often infiltrated with large round
granular cells that seem to be transformed neuroglia-cells (Leyden).
In one case neuroglia nuclei were accumulated in a ring around the
focus, seeming to indicate the beginning of encapsulation.

The most striking lesion, however, and the one which is common to the
most recent as well as to old cases, is the deformation, atrophy, and
final disappearance of the large ganglionic cells of the anterior
cornua. The first change consists in granular pigmentation;[98] then
the prolongations disappear, leaving the body of the cell shrunken and
deformed; at last the whole cell disappears. Sometimes all the cells
of an anterior horn have disappeared throughout the entire depth of
the focus; quite as often, in certain sections at least, the atrophy
is limited to certain groups, as the external,[99] or the external in
one focus, the antero-lateral in another, situated on the opposite
side of the cord.[100]

[Footnote 98: Case of Echeverria, Tab. V.]

[Footnote 99: Case by Schultze (this is a case of ancient lesion),
Tab. V. (_Virch. Arch._, Bd. lviii.).]

[Footnote 100: Case by Taylor, Tab. IV. (_Path. Trans._, London,
1879.)]

In a case rendered celebrated by Charcot it is stated that in many
sections of the cord atrophy of ganglionic cells constituted the
unique alteration, the tissue immediately surrounding the place whence
they had disappeared being perfectly healthy. It is on this appearance
that has been built up the theory of a primary idiopathic atrophy of
the ganglionic cells as the characteristic lesion of infantile
paralysis. But in other portions of the same cord Charcot himself
describes destruction of the gray reticulum imbedding the cells; and
this destruction is insisted upon in many other observations. In other
words, there is a general disintegration of the gray nervous tissue of
the anterior cornua which contain the focal lesion. The normal tissue
is then replaced by a reticulum of conjunctive fibres, more or less
dense according to the age of the case.

These focal lesions of the cord explain admirably, as will be seen,
the permanent symptoms of the disease. But of great importance for
understanding its initial period is the fact that structural
changes—similar to, but less severe than, those just described—have
beer found diffused throughout the cord. In several cases hyperæmia,
partial atrophy of ganglionic cells and nerve-fibres, infiltration
with exudation corpuscles, in the anterior cornua and even central
gray canal from the lumbar to the cervical region.[101] In
Damaschino's case, besides the focal lesions which corresponded to the
paralyses of the right arm and left leg, were others corresponding to
the left arm and right leg where no paralysis existed.

[Footnote 101: See cases by Leyden, Roth, Schultze, Clarke,
Damaschino.]

This case (1883) is also interesting in bringing out another lesion
not usually noticed. This is the breaking up into balls of the myeline
in the medullated tubes, both of the anterior intraspinal nerve-roots
and of such fibres as traversed the anterior nerves. In balsam
preparations these myeline drops are dissolved; but in osmic acid and
glycerin preparations they appear as black balls all over the field.
The lesion is identical with that already described by Dejerine (1875)
in both nerves, roots, and white columns. The columns of Clarke have
always been found intact.

{1139} In the recent cases no lesions of the white columns have been
observed—a fact upon which reposes the doctrine that such lesions,
when existing, are secondary to those of the cornua.

SECOND GROUP OF CASES.—The next group of cases contains 16, where the
autopsy was made more than two years after the début of the paralysis.

  TABLE VII.—AUTOPSIES SHOWING LESIONS OLDER THAN TWO YEARS.

  ---------+-----------------+------------------+-------------
  Case No. | Name of Author. | Date of Lesion.  | Year of
           |                 |                  | Publication.
  ---------+-----------------+------------------+-------------
     11    | Longet.         |      7 yrs.      |   1842
     27    | Echeverria.     |      7 yrs.      |   1866
     43    | Money.          |      7 yrs.      |   1884
     16    | Lancereaux.     |     16 yrs.      |   1873
     38    | Leyden.         |     17 yrs.      |   1876
     33    | Schultze.       |     19 yrs.      |   1876
     17    | Charcot and     |                  |
           |   Joffroy.      |     25 yrs.      |   1870
     20    | Müller.         |     30 yrs.      |   1871
     22    | Clarke.         |     31 yrs.      |   1868
     10    | Hutin.          |     42 yrs.      |   1825
     13    | Cornil.         |     47 yrs.      |   1863
     36    | Leyden.         |     54 yrs.      |
     34    | Leyden.         |     58 yrs.      |   1876
     19    | Vulpian.        |     64 yrs.      |   1870
     22    | Raymond.        |     70 yrs.      |   1875
     16    | Prévost.        |     76 yrs.      |   1866
  ---------+-----------------+------------------+-------------

The date of these lesions varies from seven to seventy-six years. In
two or three cases, where the autopsy was made on very old people, the
early history of the disease was unknown, but the probable date of the
paralysis was calculated.

In this group of cases patches of atrophy, semi-transparent and
grayish in color, focal or diffused, are clearly perceptible to the
naked eye. As a rule, the atrophy is unilateral, and sensibly affects
the entire half of the cord. In some cases of paraplegia, however,
there is a bilateral, symmetrical shrinkage of the entire lumbar cord,
which has been reduced to the size of a quill.

The atrophy involves, first and most markedly, one or both anterior
cornua; second, the anterior nerve-roots arising from them; third, the
antero-lateral columns.

In both the latter localities the microscope will often find
individual nerve-tubes wasted and deprived of their myeline. The
atrophied patches are generally sclerosed as the seat of a
proliferated neuroglia, coloring deeply with carmine. In Laborde's
cases, published at the very beginning of what may be called the
anatomical period, the atrophy and sclerosis were said to be limited
to the antero-lateral columns and the nerve-roots, while the cornua
remained intact. In all more recent observations, however, the lesion
of the white columns and roots has been found strictly proportioned to
that of the gray horns. The sclerosis extended into the latter,
constituted by a reticulum of connective-tissue fibres, sometimes
fine, sometimes so matted together as to form a dense felt-like
substance, sometimes offering the ordinary aspect of sclerosis.

Amyloid corpuscles have been found infiltrated in great numbers {1140}
through both the gray and white substance in these old cases (case by
Cornil),[102] seeming to replace the infiltration with exudation
corpuscles observed in the more recent ones.[103] When the lesion is
distinctly circumscribed the focus is often surrounded by a zone of
embryonic cells, seeming to indicate a reactive proliferation on the
periphery.[104]

[Footnote 102: _Loc. cit._, _Soc. Biol._,1863.]

[Footnote 103: Seguin (_loc. cit._) observes that the opinion is
gaining ground which ascribes these to a transformation of the
neuroglia corpuscles.]

[Footnote 104: Case by Schultze, _loc. cit._]

As in the relatively fresh cases, the circumstance which has attracted
the most attention is the atrophy of the ganglionic cells from the
sclerosed patches of the anterior cornua. The completeness with which
these have disappeared in any focus seems to be proportioned to the
completeness of the paralysis in the corresponding limb. Partial
atrophy or disappearance of spinal groups of cells from the cornua may
sometimes be correlated with paralysis of special muscles.[105]

[Footnote 105: Thus in Schultze's case, already quoted, the external
group of cells had disappeared from the focus in one gray horn, and
the extensors of the foot were alone paralyzed. This seems to confirm
the opinion advanced by Spitzka, that this external group of
motor-cells corresponds to the extensor, the internal groups to the
flexor muscles.]

Study of the pathology of infantile paralysis is not completed when
the above series of spinal lesions has been enumerated. Most various
interpretations have been made of these lesions as they have been
successively discovered. Thus, after the theory of congestion came the
theory of primary sclerosis, built upon Laborde's two autopsies;[106]
then the theory of primary atrophy of ganglionic cells;[107] then the
theory of myelitis;[108] finally, a theory of complex and variable
lesion.[109]

[Footnote 106: Laborde, _loc. cit._; Cornil, _loc. cit._]

[Footnote 107: Charcot, _Leçons sur les Maladies du Syst. nerveux_;
Prévost, _Soc. Biol._, 1864; Joffroy, _Arch. de Physiol._, 1870;
Petitfils, “De l'Atrophie aigue des Cellules matrices,” _Thèse de
Paris_, 1873.]

[Footnote 108: Schultze, _Virch. Arch._, Bd. lxviii.; Roth, _Ibid._,
Bd. lviii.; Henoch, _loc. cit._, p. 208; Ross, _loc. cit._, p. 125;
Seguin, _loc. cit._, 1877; Erb, _Ziemssen's Handbuch_; Seeligmüller,
_Gerhardt's Handbuch_; Roger and Damaschino, _Gaz. méd._, 1871;
Turner, _Path. Trans. Lond._, 1879; Hammond, _loc. cit._]

[Footnote 109: Leyden, _Archiv für Psych._, Bd. vi., 1876.]

It was Prévost who first ascribed a predominant importance to the
atrophy of the ganglionic cells of the anterior cornua; but it was in
the hands of Vulpian, Joffroy, and more especially Charcot and his
pupils, that the theory was fully developed. Infantile paralysis was
ranked in a newly-formed group of diseases, all characterized by
atrophy of these same cells, and differing from each other principally
in the acuteness of the process and in its complications.[110] Seguin,
in his original lecture in 1874, supported the same views, but in 1877
fully adopted that of myelitis. The objections to this theory are:
1st, that by it two diseases so different in their course,
localization, electrical reactions, and form of paralysis as atrophic
paralysis and progressive muscular atrophy are essentially identified
on account of the identity of one lesion, the atrophy of the anterior
ganglionic cells;[111] 2d, the presence of other lesions or of traces
of them peremptorily proves the pre-existence of a complex {1141}
morbid process which involves the ganglionic cells, but is neither
limited to them, nor, necessarily, originates in them.

[Footnote 110: Thus, acute anterior poliomyelitis, subacute anterior
poliomyelitis, progressive muscular atrophy, amyotrophic lateral
sclerosis, bulbar paralysis.]

[Footnote 111: When this objection is accepted, Barlow's remark falls
to the ground, that “the similarity of lesion found in two such
different diseases as infantile paralysis and progressive muscular
atrophy proves the failure of anatomical characters, taken alone, to
serve as a basis of nosology” (_Brain_, April, 1879, p. 74).]

This inference was drawn by Roger from the hemorrhagic softening,
dilatation, and degeneration of blood-vessels, infiltrations with
exudation-corpuscles, and hyperplasia of conjunctive nuclei present in
his case. Similarily, Schultze, in a case examined nineteen years
after the occurrence of the paralysis, found traces of an extensive
myelitis in the diffusion of the lesions,[112] in the exquisite
cellular infiltration, the proliferation of the neuroglia, and the
atrophy of axis-cylinders of nerve-fibres together with the cells; and
inferred an anterior myelitis, diffused in the long axis of the cord,
but limited to the antero-posterior region. Schultze defines Charcot's
theory to be an hypothesis of such an acute atrophy of ganglionic
cells as leads to a rapid melting down of these bodies, whereby
reactionary inflammation is excited in the surrounding tissue. This
implies that the dying cells are able to act like a virulent substance
on the imbedding tissue, and of this, declares Schultze, “Charcot has
offered no proof.”[113]

[Footnote 112: In this case of paraplegia without lesion of the upper
extremity, to which we have several times alluded, there was bilateral
atrophy of the lumbar cord, atrophy of the right anterior nerve in the
dorsal and lower cervical region, also in the cervical enlargement.]

[Footnote 113: It might be said that the fall of the fever as soon as
the paralysis is declared and the motor cells presumably melted down
should contradict the idea that their dying substance acts as an
irritant upon surrounding tissues.]

A third objection has been brought forward by Leyden, and is really an
enlargement on the second. It is, that various lesions or morbid
processes may underlie the same clinical history. In four autopsies of
cases presenting all the clinical history of acute anterior
poliomyelitis this author has found three different lesions. In one an
extensive lepto-meningitis, together with irregular focal sclerosis of
the white columns, evidently depended upon the latter, and in turn
caused sclerosis of the anterior cornua with consequent destruction of
their cells.[114] In two other cases an anterior poliomyelitis was
accompanied by diffused lesions of the central canal. Finally, in a
fourth case the lesions were limited to the anterior cornua, as is
most usual.

[Footnote 114: This case of Leyden's throws light on the two autopsies
by Laborde with sclerosis of the white columns and intact cornua. It
seems probable that a process originating in the cornua had then been
arrested or had receded, while continuing its evolution in the white
columns.]

The theory of acute atrophy of ganglionic cells is not sensibly
different from that of a parenchymatous myelitis.[115] But all the
objections which can be urged against the former theory apply to the
latter also, with the exception that the hypothesis of inflammation
suggests a cause for the otherwise inexplicable atrophy. Observation
of the pathological appearances alone could not decide whether the
irritation started in the parenchymatous or interstitial tissues.
Reference to the etiology of the disease shows that of the two most
frequent apparent causes, {1142} blood-poisoning and traumatisms, the
first would indicate that the inflammation started in the connective
tissue supporting the blood-vessels; the second suggests that the
irritation began in the spinal elements constituting the origin of the
nerves.

[Footnote 115: Hammond assumes such a form of myelitis in his
classification of inflammations limited to the anterior part of the
gray matter of the spinal cord:

1. Inflammation of motor and trophic nerve-cells: (_a_) Infantile
spinal paralysis; (_b_) Spinal paralysis of adults; (_c_)
Pseudo-hypertrophic spinal paralysis.

2. Inflammation of motor cells: (_a_) Glosso-labia-laryngeal
paralysis.

3. Inflammation of trophic cells: (_a_) Progressive muscular atrophy;
(_b_) Progressive facial atrophy (_Dis. Nerv. Syst._, 6th ed., p.
464).

We think this classification open to several fundamental criticisms.]

Whatever be the starting-point, however, it is very evident that the
morbid process soon involves all the tissues contained in the gray
matter of the anterior horns, and constitutes, therefore, a real
anterior poliomyelitis.

A question of much interest is the relation to this of the lesions of
the anterior roots and of the white columns. Is the atrophy of
nerve-tubes a passive consequence of their separation from the
ganglionic cells, the sclerosis a secondary consequence of this? or is
the sclerosis the cause of the atrophy, itself the result of an
irritation propagated downward from the myelitic focus, according to
the usual law for secondary degenerations in motor tracts? or,
finally, is it a residuum of a leucomyelitis (or of the white
substance), complicating by simple extension the inflammation of the
gray substance?

Review of the autopsies recorded would indicate that the lesions in
question are brought about sometimes in one, sometimes in another, of
these ways—sometimes even, as in Leyden's case, by extension from a
meningitis. That sclerosis of the white columns is most frequently a
secondary degeneration is indicated by the frequency with which it
appears below the lesion of the cornua, by the rarity with which it is
found above, and also by the general proportion between its intensity
and that of the disease of the gray matter.

We have devoted so much space to consideration of spinal-cord lesions,
because they are by far the most constant and the most important;
after these rank the structural alterations of the muscles, which
received for a while such a preponderance of attention.

Hammond has studied the progress of these changes on the living
subject by fragments of fibre successively removed with Duchenne's
harpoon. In an incipient stage of degeneration the fibrillæ are found
to be irregular and torn,[116] the transverse striæ dim; oil-globules
are seen arranged according to the long axis of the fibre. In a more
advanced stage the transverse striæ nearly disappear, the oil-globules
are in large numbers, and fat-corpuscles are also abundant. Finally,
the whole specimen is seen as a mass of air-globules. Six weeks later,
however, these had in turn disappeared, and there remained a mass of
connective tissue.

[Footnote 116: Though, from the method of removal, this appearance
cannot be considered as certainly pathological.]

This series of changes, however, does not always take place, as
Hammond himself recognizes. Laborde[117] first described a granular
form of muscle atrophy, where the muscular substance gradually wastes
away without ever becoming fatty, and leaving a transparent and
hyaline sheath. The two forms of fatty and of simple atrophy can be
distinguished by the naked eye. In the latter the muscle begins by
being thinner or lighter and softer than usual, ultimately turning
light brown. The fatty muscle becomes a homogeneous yellowish-white,
diversified by occasional remnants of reddish fibres.

[Footnote 117: _Loc. cit._, p. 131.]

{1143} Proliferation of the interstitial connective tissue may be
combined with either simple or fatty atrophy. A combination of
abundant sclerosis and abundant fatty infiltration may lead to a
pseudo-hypertrophy of the muscles.

“There cannot be the slightest doubt,” observes Erb, “that the lesions
described constitute a degenerative atrophy similar to what may be
caused by section or sense traumatism of a peripheric nerve.”

The peripheric nerves have been much less thoroughly studied than the
spinal cord. Leyden first directed special attention to the nerves. He
found the sciatic altered in two cases,[118] in the first by an
interstitial neuritis; in the second by partial atrophy. In 1880 the
same writer, in an extensive article on poliomyelitis and
neuritis,[119] greatly extends his views as earlier expressed. Not
only does he claim the coexistence of neuritis with spinal-cord
disease in atrophic paralysis, but thinks that many cases of this, and
also of other forms of paralysis, “lately supposed to originate in the
spinal cord, may really begin in any part of the motor apparatus,”
thence sometimes generalize throughout the whole apparatus, sometimes
remain limited to the original portion affected. Thus, progressive
muscular atrophy may sometimes begin in the nerves, sometimes in the
muscles, and sometimes in the ganglionic cells of the cord; and this
variety of origin explains the discrepancies of opinion which have
been held upon the nature of this disease. Similarly, all forms of
acute or chronic atrophic paralysis in either children or adults may
begin in either the nerves or cord, thence become generalized to both,
or remain limited to one part of the spinal motor system. Cases of
atrophic paralysis which recover are probably not cases of
poliomyelitis at all, but of multiple neuritis, rheumatic, traumatic,
or infectious in nature. The regeneration of peripheric nerves is a
well-demonstrated possibility, but not that of the cells of the cord.
Lead-paralysis is usually confined to the nerves, but sometimes
extends to the cord. In diphtheritic paralysis Buhl has found
injection, thickening, and granular infiltration of nerves at the
union of their anterior and posterior roots;[120] and as long ago as
1876, Dejerine, in a case of atrophic paralysis in a syphilitic woman,
found varicose swelling of the medullary sheath in the nerves of the
paralyzed lower extremities, together with heaping up of the myeline
into large drops, colored black in glycerin and osmic-acid
preparations. Coincidently, in the cord, at the origin of the same
nerves, the number of motor-cells was diminished, and of those that
remained the prolongations, and even the body, of the cell were
atrophied.[121]

[Footnote 118: Cases 34 and 35 of Table V., quoted from _Arch. de
Psychiatrie_, Bd. vi., 1876.]

[Footnote 119: _Zeitschrift für Klin. Med._, 1880.]

[Footnote 120: _Zeitschrift für Biol._, 1867.]

[Footnote 121: _Arch. de Phys._, 1876.]

These views of Leyden's are extremely interesting, and should
stimulate future research into the condition of nerves in all cases of
atrophic paralysis. It is quite incorrect to say, as Archambault and
Damaschino have recently done,[122] that Leyden denies the existence
of anterior poliomyelitis in such cases, especially in such as prove
permanent. He only insists on the frequent coincidence of neuritis, on
a varying point of departure for the morbid process, and on the
probability that in cases of recovery this process has always remained
peripheric.

[Footnote 122: _Le Union méd._, 1883, 7, 35, case quoted in Table V.
It is much to be regretted that Damaschino, who strongly controverts
Leyden's views, did not examine the nerves in his own most interesting
case.]

{1144} The strongest objection to Leyden's theory is the absence in
most recorded cases, either infantile or adult, of the usual signs of
nerve inflammation, local pain, or tenderness. Autopsies of old cases
are not able to differentiate an inflammation from an atrophic process
in the nerves, followed by a secondary thickening of the endoneurium.
This thickening was found in three cases examined by Edmonds in 1882,
whose subjects had suffered from infantile paralysis in early life,
and had had the paralyzed limb amputated at the age of fifteen or
sixteen. Transverse sections were made from the internal popliteal
nerves. The specimens showed some healthy nerve-fibres, presumed to be
sensory; others much smaller, with the axis-cylinders wasted or
degenerated; while strands of connective tissue traversed the
nerve-bundles, resulting from hypertrophy of the endoneurium. The
vessels showed inflammation of their coats, with proliferation of the
endothelium.[123]

[Footnote 123: _Trans. Path. Soc. London_, 1883.]

The brain is usually normal, unless indeed the paralysis has affected
children previously rendered idiotic by congenital atrophia cerebri.
Sandie, however, examined one brain with an interesting positive
result.[124] The brain was taken from a boy of fifteen paralyzed since
the age of three in almost all his muscles, with even paresis of the
muscles of the trunk and neck. The paralysis was more marked upon the
right than on the left side. At the autopsy, in addition to atrophy of
the muscles and of the motor nerves, with exquisite atrophy of the
anterior columns and anterior cornua, was found a decided atrophy of
the left central convolution, and, less marked, of the paracentral
lobule. This was shown by comparative measurements with the opposite
side of the same brain, and also with the corresponding convolution
and lobule in two other brains. The child's intelligence had not been
affected.

[Footnote 124: _Centralblatt f. d. Med. Wissensch._, No. 15, 1875.]

The arrest of development of the bones has been already mentioned, as
well as that of their epiphyses and apophyses. The compact osseous
tissue is atrophied: the medullary, on the contrary, abundantly
developed and rich in fat.

PATHOGENY OF INFANTILE PARALYSIS.—In the pathological anatomy of
infantile paralysis there are two principal facts to be correlated
with its clinical phenomena—namely, the limitation of the myelitis to
the anterior gray horns of the spinal cord; the destruction of the
ganglionic nerve-cells in these gray horns. That the other lesions
observed are subordinate to these is shown by their variableness as
compared with the constancy of the anterior poliomyelitis. These
lesions are, in the cord, the atrophy and sclerosis of the anterior
nerve-roots and white columns; in the muscle, the fatty degeneration
or simple atrophy of the fibre; in the nerve, breaking down, and
finally atrophy of the myeline sheath, sometimes of the axis-cylinder;
proliferation of the endoneurium.

Consequence of Limitation of Myelitis.—Limitation of the morbid
process to a portion of the motor tract, the anterior cornua, and
exclusion of the posterior horns and roots, readily explain the
predominant positive symptom of motor paralysis, together with the
absence of sensory disturbance. The absence of muscular rigidity,
spasm, active contraction, and of exaggerated reflexes is similarly
explained by the immunity from the morbid process of the posterior
white columns and the portion of the {1145} lateral columns
immediately adjacent to them. The motor paralysis resulting from
destruction of the anterior ganglionic cells of the cord is much more
complete than that which depends on simple interruption of the motor
tracts passing from the brain. The manner in which the motor tracts
are connected by a succession of arching fibres with these cells
already indicates that the latter are dépôts for the reinforcement of
the motor impulses. We must believe, indeed, that the centrifugal
impulses reaching the anterior cornua are not yet motor in character,
but to become so must sustain a new elaboration in the ganglionic
cells of this region. Evidently, the network of gray fibres connecting
the arcuate strands of the antero-lateral columns with the cells
become, in virtue of that fact alone, essential to the process. But it
is also probable that the multiplied transmission of impressions,
which lies perhaps at the basis of the process of their higher
elaboration in ganglionic centres, is carried on in the larger network
of gray fibres as well as in the smaller network contained in the
ganglionic cells. Destruction of a portion of this network would
therefore interfere with the elaboration of the motor impulse, in the
same manner, though to a relatively less extent, as destruction of the
ganglionic cells themselves.

Trophic Lesions.—The rapid wasting of the paralyzed muscles, with
their degenerative electrical reactions, seems, however, to be an
effect altogether peculiar to lesions of the ganglionic bodies.[125]
According to Charcot, who has so especially formulated the laws of
amyotrophic paralysis, all the ganglionic cells essential to the
elaboration of motor impulses exercise a trophic influence upon
muscles. The spinal cell, nerve-fibre, and muscle-fibre combine into a
complex indissoluble unity or element. One part of this lesion of
complex elements is necessarily followed by proportionate lesion of
all its other parts.

[Footnote 125: The amyotrophic lateral sclerosis of Charcot exhibits
in an exquisite manner the difference between paralysis without
atrophy, caused by sclerosis of the antero-lateral columns, and
paralysis with atrophy when the morbid process has extended to the
anterior cornua.]

According to Erb, however, who extends Samuel's doctrine of special
trophic nerves, it is not the motor cells which influence the
nutrition of the muscle-fibres with which they are connected, but
special trophic cells lying among the others in the anterior cornua.
This theory is principally based on the existence of muscular
atrophies of central origin (progressive muscular atrophy, bulbar
paralysis), unaccompanied for a long time by paralysis.[126] Hammond
cites as a converse example the anterior poliomyelitis “where the
peripheric disturbance is, in the first place, solely one of motility;
this is paralysis without atrophy. After a time, which may be as much
as six months or even more, the trophic changes begin.”[127]

[Footnote 126: _Ziemssen's Handbuch_.]

[Footnote 127: _Loc. cit._, p. 429.]

But surely this is an exaggerated emphasis on the exception, rather
than the true inference from the rule of rapid wasting in anterior
poliomyelitis—a rule so general as to have originated the title
atrophic paralysis. Erb gives an ingenious scheme (Fig. 55) of the
mental relations of motor and trophic cells with cerebral and spinal
nerve-fibres. It will be seen that isolated lesions of one or the
other trophic apparatus might occur without paralysis of motor tracts,
while simultaneous lesion of the trophic {1146} apparatus and of the
ganglion-cells, or of the latter, involving the tracts coming from the
trophic cells, would cause, as in anterior poliomyelitis, motor
paralysis, muscular atrophy, loss of the reflexes, degenerative
reaction in nerves and muscles.

[Illustration: FIG. 55. _c_, trophic cell for nerve; _a_, cerebral
fibre; _b_, trophic cell for muscle; _d_, ganglionic cell; _s_,
sensory fibre; _f_, trophic path to muscle; _m_, muscle. (From
_Ziemssen's Handbuch der Speciellen Pathol._, Bd. xi. Zweite H.,
Zweite Abtheil, p. 313.)]

Duchenne and Joffroy[128] also argue the existence of special trophic
nerve-cells. The absence[129] of the nutritive lesions of the skin and
cellular tissue which are so conspicuous when the gray matter around
the {1147} central canal or posterior to it is involved,[130] the
dependence of the nutrition of the motor apparatus, nerves, muscles,
bones on the integrity of the anterior horns, are facts which, taken
together, seem to indicate that the maintenance of nutrition depends
on the unbroken continuity of the motor or sensory apparatus from the
periphery to the ultimate central element, rather than on any special
central cells endowed with trophic functions.[131] Erb's hypothesis,
as his own scheme moreover denotes, demands not only trophic cells
distinct from motor cells, but separate trophic cells for the muscles,
for the motor, and for the sensory nerves.

[Footnote 128: “De l'Atrophie aigue et chronique des Cellules
nerveuses,” _Arch. de Phys._, No. 4, 1870.]

[Footnote 129: Money, and also Gowers, have signalized a condition of
the skin resembling myxœdema (_Tr. Path. Soc. London_, 1884, and
_Brit. Med. Journ._, 1879).]

[Footnote 130: Mayer (Herman's _Handbuch Physiol._) sums up the great
mass of evidence now accumulated, which demonstrates the trophic
influence of the central gray mass of the cord upon the tissue.]

[Footnote 131: Nepveu (_La France médicale_, 1879) mentions some cases
of infantile paralysis complicated with trophic lesions of the skin.
The facts, if accepted, could only indicate an extension of the
myelitis to the central and posterior regions of the gray columns. The
relations between non-atrophic paralysis caused by interruptions of
the motor tracts and muscular atrophy dependent on lesion of the
anterior cornua are exquisitely shown in a case reported by Sander. An
adult suffered from chronic motor paralysis, gradually increasing, in
the right arm, with paresis of the lower extremities. In the hand,
arm, and shoulder the paralysis was followed by gradual atrophy and
diminution of the faradic contractility; in the lower extremities no
atrophy occurred. At the autopsy was found a gliomatous tumor seated
in the anterior cornua predominating on the right side, extending from
the level of the sixth dorsal to that of the eighth cervical vertebra.
The ganglion-cells were pigmented and compressed, not altogether
destroyed. The lumbar cord was intact, and the non-atrophic paresis of
the lower extremities evidently resulted from the interruption of the
motor tract above.]

The peculiar grouping of nerve-centres within the cord that seems to
be indicated by some of the groupings of infantile paralysis shows, as
has been said, a probable divergence within the cord of nerve-fibres
which run together in the same nerve-stem. The associations to be
expected from the data of functional association and of clinical
history are by no means fully decided. It is even a matter of dispute
whether the tibialis anticus is functionally more associated with the
flexors or with the extensors of the thigh, and whether its
experimental irritation or clinical paralysis really coincides with
that of the first or of the second group. This entire field of
observation is new and promises fertile results.[132]

[Footnote 132: It is from this field that has come a new argument for
the spinal nature of lead-paralysis, from its peculiar grouping, and
from analogy with that of anterior poliomyelitis of the upper
extremities (Remak, “Ueber die Local. Atropa. Spinal Lahm.,” _Archiv
für Psych._, Bd. ix.; also, Ferrier, _loc. cit._).]

Relation between Limitation of Myelitis and Age.—From the relative
frequency of anterior poliomyelitis in childhood, as compared with its
much greater rarity in adult life, we must infer the existence of some
special conditions in childhood which tend to limit the morbid process
to such a portion of the cord. The theory of a primitive spontaneous
atrophy of the motor cells would serve, indeed, to explain this
limitation. The reasons already alleged for regarding the morbid
process as a systematic myelitis decisively hinder the acceptance of
such an explanation as it stands. On the assumption, however, that the
myelitis is usually of functional origin, and starts, therefore, in
the elements of the anterior cornua essentially involved in the motor
functions, the morbid susceptibility of these elements may be ranked
with the liability to disease of the entire locomotor system which is
known to be so predominant in children. From pathological evidence,
even without anatomical proof, we may reasonably infer an
incompleteness of development in the anterior {1148} cornua of the
cord correlative with that well demonstrated in the bones and
functionally inexperienced muscles. If the antero-posterior fibres
which connect the anterior cornua with the central and posterior gray
masses be also incomplete, the radiation of irritations, and
consequent vascular irritation, would also be arrested within the
boundaries of the original lesion. Thus a peculiarly circumscribed,
instead of the common diffused, myelitis of adults.

Money[133] points out that for the gray matter of the cord, as of the
brain, the centre or maximum force of the circulation is on the
periphery, and the nutritive supply of the centre is thus easily cut
off. Moreover, while the blood-vessels of the cervical and dorsal
regions of the cord pass to it transversely, the vessels of the lumbar
region are compelled to describe a somewhat prolonged vertical course
before reaching their point of distribution. From these circumstances,
even transitory congestions in the circulation of the cord are easily
followed by irreparable injury of its delicate elements.

[Footnote 133: _Loc. cit._, _Path. Trans._, 1884.]

Finally, in all discussions on pathogeny must not be forgotten the
doctrine of Leyden[134] that infantile paralysis, also progressive
muscular atrophy, is a disease which may begin at the periphery and
extend to the centres, as well as the reverse. It must also be
remembered that, as yet, only very scanty evidence exists to support
this, in itself, plausible theory.

[Footnote 134: See _loc. cit._, ut supra.]

COURSE OF INFANTILE PARALYSIS.—The most ordinary course of infantile
paralysis is that already described as typical—namely, extremely rapid
development to a maximum degree of intensity, then apparent
convalescence, retrocession of paralysis, atrophy, and ultimate
deformities in limbs in which paralysis persists.

Several variations from this typical course are observed. Complete
recovery may take place, as in the so-called temporary paralysis of
Kennedy[135] and of Frey.[136] These cases are very rare. But their
possibility seriously complicates the estimate we may make of the
efficacy of therapeutic measures.[137]

[Footnote 135: _Dublin Quarterly Journal_, 1840.]

[Footnote 136: _Berlin. Klin. Wochensch._, 1874. I have described one
such temporary case in the article already quoted. These cases seem
about as frequent in adults. (See Frey, _loc. cit._; also case of
Miles, etc. etc.)]

[Footnote 137: As of the case of complete recovery, the only one the
author had seen, related by Dally, _Journal de Thérap._, 1880, 1,
vii.]

On the other hand, there may be a complete absence of regression; and
this is observed sometimes in cases where the paralysis is originally
limited; sometimes where it is extremely extensive, involving nearly
all the muscles of the trunk or limbs;[138] or muscles or limbs
originally spared may become involved in a fresh attack. Laborde
relates cases of this kind. In Roger's first case paraplegia occurred
under the influence of scarlatina two months after paralysis of one
arm.

[Footnote 138: Thus in Eulenburg's case, quoted ut supra.]

The form of anterior poliomyelitis most frequent in adults is the
subacute, and after that the chronic. Both are extremely rare in
children, the latter excessively so. Seeligmüller and Seguin[139] both
admit the possibility of a chronic form in children, and the latter
has kindly communicated to me one case from his private practice:

{1149} Miss N. D——, æt. 15, paresis in both legs, first at age of
nine, increased at age of twelve, when weakness of vision first noted.
At fourteen both feet in rigid pes equinus, and both tendons achilleis
cut, without benefit. Hands became tremulous, without paresis. On
examination at age of fifteen found moderate atrophy of muscles of
both legs. Tendo Achillis united on both sides, and equinus persists.
Voluntary movement exists, both in anterior tibial and in
gastrocnemius muscles, but diminished in anterior tibial. Faradic
contractility diminished in both sets of muscles; examination
difficult from extreme sensibility of patient. In both hands
interossei, muscles of thumb, and little finger show tremors and
fibrillary contractions. Thenar eminences small, abductor pollicis
nearly absent, not reacting to faradic current. Optic nerves slightly
atrophied. Mind enfeebled, memory poor; articulation not affected.
Five years later the motor paralysis and mental enfeeblement had still
further progressed, but no exact notes exist of this period.

[Footnote 139: _Loc. cit._ (ed. 1877).]

Erb[140] relates a case that he considers unique at the time in a girl
of six. The paralysis began insidiously in the right foot in July; a
fortnight later had extended to the left foot; complete motor
paralysis existed in August, without any lesion of sensibility: after
electrical treatment, then instituted, first return to motility to
peroneal muscles in November; by January child able to walk again and
electrical reactions nearly normal.[141]

[Footnote 140: _Brain_, 1883.]

[Footnote 141: In the same number of _Brain_, A. Hughes Bennett quotes
cases of so-called chronic paralysis in very young children which are
evidently cases of general paresis from congenital cerebral atrophy.
The children were defective in intelligence, could not sit up nor hold
up the head; the electrical reactions were preserved. I have seen a
great many such cases: they are indeed not at all uncommon. Much more
so is Bennett's diagnosis.]

COMPLICATION WITH PROGRESSIVE MUSCULAR ATROPHY.—Raymond[142] and
Seeligmüller describe some rare cases where progressive muscular
atrophy declared itself in persons previously affected with infantile
paralysis in other limbs. Both observers infer a gradual and chronic
extension along the cord of the originally acute anterior
poliomyelitis.[143] Similar cases have much more recently (1884) been
quoted by Ballet as tending to modify the prognosis which has usually
been pronounced favorable quoad life and further spinal accidents.
(See infra.)

[Footnote 142: _Gaz. méd._, 1875. No. 17.]

[Footnote 143: It seems to me that Seguin's case, above quoted, might
be an example of such complication(?). But I have not seen the patient
myself, and describe the case according to the views of the author.]

PROGNOSIS.—The prognosis of atrophic paralysis, quoad vitam, is, as is
well known, extremely good. The prospect of recovery from the
paralysis is variable. It cannot be estimated either by the extent of
the initial paralysis or by the severity of the fever or attendant
nervous symptoms. The electrical reactions alone are of value in the
prognosis, and their value is very great. Duchenne first formulated
their law: “All the cases of infantile paralysis which I have seen
where the faradic contractility was diminished but not lost, and which
could be treated by faradic electricity within two years after the
onset of the paralysis, have completely recovered.”[144] This
encouraging statement must be read as applying rather to individual
muscles than to cases as a whole. Few {1150} complete recoveries of
patients are claimed even by so enthusiastic an electrician as
Duchenne; who nevertheless affirms his not unfrequent success in
re-creating entire muscles out of a few fibres saved from
degeneration.

[Footnote 144: _Loc. cit._]

The persistence of galvanic irritability in muscles which fail to
contract to the faradic current has been shown by Erb to belong to the
degenerative reactions. Hammond, however, without alluding to the
qualitative changes in the galvanic contractions, sees in them the
elements of a relatively favorable prognosis, even when faradic
contractility is lost. Thus, out of 87 cases, in 39 of which the
paralyzed muscles contracted to the galvanic but not the faradic
current, 14 were entirely cured, 28 greatly improved, 30 slightly
improved, 15 discontinued treatment very early.[145]

[Footnote 145: _Loc. cit._, p. 482.]

Examination of fragments of living muscle obtained by Duchenne's
harpoon, though useful, should not be allowed to exaggerate an
unfavorable prognosis. Much fat may be found in such fragments when
the muscle is as yet by no means completely degenerated and can be
made to contract to one or the other current. Erb, however, admits
that the results of treatment have not, in his hands, been brilliant;
but adds that he has had no opportunity to treat any cases which were
not of long standing.[146]

[Footnote 146: _Loc. cit._]

Volkmann[147] considers the paralysis entirely hopeless, and advises
the concentration of all effort upon the prevention or palliation of
deformities.

[Footnote 147: _Loc. cit._]

It seems probable that at the present moment sufficient data do not
exist for formulating a fair prognosis; nor will they until a much
larger number of cases than hitherto have been submitted to all the
resources of a complex and persevering system of therapeutics from the
earliest period of the disease.

SPECIAL PARALYSES.—Among the paralyses, some exercise a more
unfavorable influence on locomotion than others. Thus, paralysis of
the muscles of the trunk is more difficult to palliate, either by
apparatus or by the efforts of the patient, than any paralysis of the
limbs. Similarly, paralysis of the upper segments of a limb is more
crippling than when confined to the lower. Partial paralysis of the
muscles surrounding a joint is often (but not always) more liable to
lead to deformity than total paralysis.

Influence of Neglect.—Apart from the influence of treatment in curing
the paralysis, must be estimated in the prognosis the effect of care
and watchfulness in limiting the disease and in averting many
consequences, even of those which are incurable. The rescue of muscles
only partially degenerated may often serve to compensate the inaction
of those which are irretrievably ruined.

Ballet[148] has recently called attention to the fact that in certain
cases persons who had been attacked with an anterior poliomyelitis in
childhood became predisposed to different forms of spinal disease.
Four have been observed: (1) transitory congestion of the cord,
causing paralysis of a day or two's duration; (2) an acute spinal
paralysis of the form usually seen in adults; (3) subacute spinal
paralysis; (4) progressive muscular atrophy. The author relates cases
under each of these heads, and further quotes one {1151} related by
Dejerine in 1882.[149] The patient, a carpenter aged fifty-five and
with an atrophic deformity of the foot, became suddenly paralyzed in
the four limbs, trunk, and abdomen. The paralysis was complete in a
month, was stationary for three months, then began to improve, and at
the end of six months from the onset of the disease recovery was
complete.

[Footnote 148: _Revue de Médecine_, 1884.]

[Footnote 149: _Revue de Médecine_, 1882.]

The observations of progressive muscular atrophy in persons bearing
the stigmata of an infantile paralysis are quite numerous.[150]

[Footnote 150: Charcot, _Soc. Biol._, 1875, and _Gaz. méd._;
Seeligmüller (4 cases), in _Gerhardt's Handbuch_, 1880; Hayem, _Bull.
Soc. de Biol._, 1879; Vulpian, _Clinique méd. de la Charité_, 1879;
Pitres, new observation, quoted by Ballet in 1884.]

The prognosis cannot be the same for cases where everything is done to
avert malpositions and for those where all precautions are neglected.
Thus, prolonged rest in bed favors pes equinus; the use of crutches
necessitates flexion of the thigh and forced extension of the foot;
locomotion without support tends to displace articulations by
superincumbent weight, causing pes calcaneus, genu-recurvatum.
Finally, compensatory deformities must be averted from sound parts, as
scoliosis from shortening of the atrophied leg, equinus from passive
shortening of the gastrocnemii through flexion of the leg, etc.

ETIOLOGY.—Concerning the etiology proper of infantile paralysis little
definite is known. It is probable, as has been already noticed, that
traumatisms have a much more decided influence than is generally
assigned to them. Leyden particularly insists on this influence, and
on the facility with which a traumatism relatively severe for a young
child may be overlooked, because it would not be recognized as such
for an adult. It must be noticed, however, that children are much more
liable to have the arms wrenched and pulled violently than the lower
extremities; yet in a great majority of cases the lesion is situated
in the lumbar cord.

It has been shown that the myelitis, though so limited transversely,
is often far more diffused in the longitudinal axis of the cord than
might be supposed from the permanent paralyses. This fact corresponds
to the initial generalization of the motor disturbance. It seems
possible that the traumatic irritation, starting from the central
extremity of the insulted nerve, diffuses itself through the cord
until it meets with its point of least resistance, and here excites a
focal myelitis. That this point should most frequently be found in the
lumbar cord would be explained by its relatively less elaborate
development, corresponding to the imperfect growth and function of the
lower extremities.

A second cause of anterior poliomyelitis is, almost certainly, the
presence of some poison circulating in the blood. The frequent
occurrence of the accident in the course of one of the exanthemata is
one indication of this; other indications are found in such cases as
that related by Simon, where three children in one family were
suddenly attacked—two on one day, one, twenty-four hours later.[151]
The same author relates a case of motor paralysis in an adult,
followed by atrophy of left lower extremity, and which occurred during
a fit of indigestion caused by eating mussels.[152] The acute
ascending paralysis of Landry, {1152} with its absence of visible
lesion, has been said to strikingly resemble the effects of poison.
Hydrophobia and tetanus are again examples of the predilection
exhibited by certain poisons for the motor regions of the cord.

[Footnote 151: _Journal de Thérap._, 7, vii., 1880, p. 16. These
children belonged to an American family, but were seen by several
distinguished French physicians.]

[Footnote 152: P. 357.]

The evidence that infectious diseases may constitute the immediate
(apparent) causal antecedent of acute poliomyelitis has led, not
unnaturally, to the theory that all cases of acute infantile paralysis
are due to a specific infecting agent, some as yet unknown member of
the great class of pathogenic bacteria. It may be noticed, however,
that the occurrence of the spinal accidents after the ordinary
infectious diseases, as scarlatina and measles, should as well
indicate that a specific agent proper to itself was at least not
essential to its development.[153]

[Footnote 153: Perhaps the occurrence of diphtheria in the course of
scarlatina and typhoid should indicate a similar lack of real
specificity in the morbid agent of the former disease.]

The influence of exposure to cold, which seems to have been sometimes
demonstrated, must probably be interpreted, as in the case of
rheumatism and pneumonia, as effective by means of some poison
generated in the organism when cutaneous secretion, exhalation, or
circulation has been suddenly checked.

DIAGNOSIS.—The diagnosis of the acute anterior poliomyelitis of
childhood is usually easy, but unexpected difficulties occasionally
arise.

Typical cases are markedly different from typical cases of cerebral
paralysis, but in exceptional cases these differences disappear. This
is shown in the following table:

      SPINAL PARALYSIS.          |     CEREBRAL PARALYSIS.
                                 |
  Paraplegic or monoplegic       | Hemiplegic, (rule). Monoplegic as
  (rule).                        | residuum of hemiplegia or as
                                 | consequence of solitary tubercle
                                 | (exception).
                                 |
  Hemiplegic as residuum from    |
  paraplegia, or original and    |
  involving facial nerve (very   |
  exceptional).                  |
                                 |
  Intelligence free (rule).      | Intelligence depressed (rule).
                                 |
  Intelligence depressed (when   | Intelligence free (exception,
  spinal paralysis has affected  | especially with solitary tubercle).
  imbecile children).            |
                                 |
  Disposition lively.            | Disposition apathetic or cross.
                                 |
  Initial convulsion unique;     | Convulsions repeated; pyrexia
  general symptoms of a few      | prolonged several days or weeks
  hours' duration (rule).        | (rule).
                                 |
  Convulsion repeated during two |
  to three weeks before          |
  paralysis; fever a month (rare |
  exceptions).                   |
                                 |
  Sensibility intact (rule).     | Sensibility intact after initial
                                 | period.
                                 |
  Occasional hyperæsthesia       |
  (exception).                   |
                                 |
  Reflexes cutaneous, and        | Reflexes intact.
  tenderness lowered or lost     |
  (rule).                        |
                                 |
  Reflexes preserved when only   |
  single muscles in groups       |
  paralyzed.                     |
                                 |
  Associated movements of hand   | Associated movements frequently
  absent (Seeligmüller).         | observed in hand.
                                 |
  No rigid contractions of upper | Extensive and rigid contractions of
  extremity.                     | upper extremity very frequent.
                                 |
  Atrophy of paralyzed muscles   | Atrophy very slight.
  and arrested development of    |
  limb, very marked.             |
                                 |
  Faradic contractility          | Electrical reactions normal.
  diminished or lost;            |
  degenerative galvanic          |
  reaction.                      |

Rather singularly, the diagnosis from transverse myelitis is less
liable to error than that from cerebral paralysis:

{1153} ANTERIOR POLIOMYELITIS.   |     TRANSVERSE MYELITIS.
                                 |
  Fever brief or absent.         | Persistent fever.
                                 |
  Sensibility intact.            | Hyperæsthesia, then anæsthesia.
                                 |
  Decubitus absent.              | Presence decubitus.
                                 |
  Reflexes lost.                 | Reflexes increased.
                                 |
  Atrophy of muscles.            | Atrophy of muscles sometimes as
                                 | intense.
                                 |
  Electrical muscular            | Loss of electrical contractility,
  contractility lost.            | but not proportioned to sensory and
                                 | motor disturbance; less rapidly
                                 | completed.

The diagnosis from hæmatomyelitis is almost impossible, and
practically useless. For if the hemorrhage be severe, the child dies
at once, as in Clifford Albutt's case. If less severe, it excites a
myelitis, and the history becomes identical with that of the disease
we are considering; or if the clot beyond the anterior cornua, it is
identified with a vulgar myelitis of traumatic origin.

Progressive muscular atrophy is extremely rare in childhood, but is
occasionally seen under hereditary influence (Friedreich's disease).
In adult cases confusion is not only easy to make, but often difficult
to avoid, especially with the rare, chronic form of poliomyelitis. The
basis of distinction is as follows:

      ANTERIOR POLIOMYELITIS.    |   PROGRESSIVE MUSCULAR ATROPHY.
                                 |
  Onset sudden; maximum of       | March very gradual; maximum of
  paralysis at the beginning.    | disease not attained for years.
                                 |
  Faradic contractility lost     | Faradic contractility not lost
  almost at once.                | until atrophy complete.
                                 |
  Shortening of limbs and        | No arrest of development of limbs.
  atrophy of limbs (in infantile |
  cases).                        |
                                 |
  Functionally associated        | Capricious selection of muscles,
  muscles frequently associated  | but frequent wasting of these at
  in paralysis: hand rarely      | eminences.
  affected.                      |

Paralysis from lesion of a peripheric nerve closely imitates anterior
spinal paralysis.[154] It is distinguished by closely following the
distribution of the injured nerve, and, usually, by concomitant
lesions of the sensibility and of cutaneous nutrition.

[Footnote 154: The importance of this fact has been shown in the
section on Pathogeny. (See also quotations from Leyden and remarks on
lesions of peripheric nerves.)]

The pseudo-paralysis sometimes observed in syphilitic children as a
consequence of a gummatous infiltration of the bones at the junction
of the epiphysis and diaphysis[155] might easily be mistaken for a
spinal paralysis. But it is an affection peculiar to the new-born; the
electrical reactions of the paralyzed muscles are intact; careful
examination will show that the movements of the muscles are not
impossible, but restrained by pain; often other syphilitic affections
are present.

[Footnote 155: Parrot, Wagner.]

The diagnosis from diphtheritic paralysis is embarrassed, from the
fact that true anterior poliomyelitis may develop in the course of
diphtheria as of other infectious diseases. The paralysis of the soft
palate, preservation of faradic reaction, absence of atrophy, and the
usually rapid recovery must establish the differentiation.

In spinal paralysis there is loss of the reflexes,[156] and also of
faradic {1154} contractility, both of which are preserved in hysteria.
In hysterical paralysis, also, there is no wasting of the affected
muscles.

[Footnote 156: See Gowers's monograph on “Spinal-Cord Diseases” for an
excellent summary of the spinal reflexes.]

Various diseases of the bony skeleton or articulations may simulate
spinal paralysis. Congenital club-foot, caused by unequal development
of the bones and cuticular surfaces, is to be distinguished from the
paralytic variety by the date of its appearance,[157] by the deformity
of the tarsal bones, and by the extreme difficulty of reduction.

[Footnote 157: Though in some cases paralysis of the muscles of the
foot seems to take place during fœtal life, and a club-foot result
which is both congenital and paralytic.]

Caries of the calcaneum, leading the child to walk on the anterior
part of the foot to avoid pressure on the heel, may leave after
recovery such a retraction of the plantar fascia as to cause a degree
of equinus and varus, with apparent paralysis of the peroneal muscles.
I have seen one such case.

Congenital luxation of the hip may simulate paralysis; indeed, by
Verneuil, it has been attributed to an intra-uterine spinal paralysis.
There is, however, no change in the electrical reactions of the
muscles surrounding the joint.

In coxitis, however, Newton Shaffer[158] has demonstrated a moderate
diminution of faradic contractility in such muscles, and a
corresponding degree of atrophy; and this fact might complicate the
diagnosis of paralysis from arthritis of the hip-joint. Gibney[159]
has called attention to the facility with which this confusion may
arise, and Sayre[160] relates cases of infantile paralysis mistaken
for coxitis.

[Footnote 158: _Archives of Medicine_.]

[Footnote 159: _Am. Journ. Med. Sci._, Oct., 1878.]

[Footnote 160: _Orthopædic Surgery_.]

In a case observed by myself, which had been previously diagnosed as
coxitis, the mistake was all the more interesting as the paralysis
which really existed seemed to have been caused by a meningitis rather
than primary myelitis of the cornua.[161] It thus corresponded to the
meningo-myelitic case related by Leyden.

[Footnote 161: The details of this case are as follows: C. P——, aged
11, ten months previous to consultation suffered from febrile attack,
accompanied by retraction of head, severe pains diffused through body
and intense at nape of neck; unconsciousness for thirty-six hours;
vomiting; no convulsions. Case diagnosed as cerebro-spinal meningitis
by attendant physician. Convalescence in a week, but with pain in
lumbar region of back, predominating on right side, so aggravated by
standing or walking that both acts impossible. Coincidently, pain in
right calf; exquisite tenderness to pressure even from stocking. No
complaint in recumbent position. Child could not get from floor to
bed, nor raise right leg from ground. As pain subsided walking became
possible, but right leg dragged. Chronic twitchings on left side,
face, arm, leg. These symptoms lasted ten or twelve weeks, but at end
of nine weeks patient could walk up stairs. In ten months power of
walking almost recovered, but there remained a certain amount of
lordosis and oscillation of pelvis, which is jarred on the left side
while the right leg is swung forward. Recumbent, all movements
executed equally well on both sides and passive motion of the
hip-joint perfectly free. Circumference of right thigh and leg
diminished from one-half to one inch as compared with the left.
Faradic contractility diminished on the right side in the gluteal
muscles, vastus externus, and rectus, and in the gastrocnemii. The
sacro-lumbalis muscle was, unfortunately, not examined, but from the
lordosis was probably affected. The remaining muscles were intact.
Pain on pressure persisted over right side of second, third, and
fourth lumbar vertebræ. Diagnosis was made of a limited meningeal
exudation, with compression of anterior part of cord or of a portion
of the lumbar and of the sacral plexus.]

Scoliosis, which may be caused by the relatively rare unilateral
paralysis of some of the muscles of the trunk, may also be simulated
by paralysis with shortening of one lower extremity. To compensate the
{1155} shortening, the trunk is bent over on the paralyzed side; hence
a lateral curvature, easily reducible, but easily leading into error.

It would seem easy to distinguish traumatic cases of subluxation of
the humerus from those due to paralysis of the deltoid. Yet sometimes
only the history will serve to establish, and that somewhat
doubtfully, the diagnosis.[162]

[Footnote 162: A child of four was brought to me with a stiffness and
rigidity of the shoulder-joint which could only very partially be
overcome by passive motion, and not at all by voluntary effort. The
mother stated that several months previously the child had, without
apparent cause, become suddenly unable to move the arm. After two
months' delay it was taken to a dispensary, and told that the arm was
out of joint, and had it reset under ether. From this date the
stiffness had gradually developed. The deltoid was atrophied, with
marked diminution of the faradic contractility. Question: Were these
signs merely symptomatic of an arthritis consequent on a dislocation,
or was the latter the result of a spinal paralysis of the deltoid?]

THERAPEUTICS.—The treatment of anterior poliomyelitis embraces two
stages. In the first it is directed against inflammation of the spinal
cord and the paralysis of the muscles; in the second period the spinal
lesion has run its course and the paralysis is considered incurable.
Treatment is then directed to the prevention or palliation of
deformities or toward facilitating the functions of the limb in spite
of them.

These two periods are not, however, rigidly separated from each other
in chronological order. From the very outset it is important to take
certain precautions to prevent deformities, and while palliating these
with orthopædic apparatus it is important for years to continue
treatment of the paralyzed muscles in the hope that at least a remnant
of them may be saved. To abandon the case to the orthopædic
instrument-maker, or to neglect the problem of dynamic mechanics while
applying electricity and studying the progress of fatty degeneration,
are errors greatly to be condemned.

The treatment of the initial stage is necessarily purely symptomatic
for the fever and convulsions, since the diagnosis cannot be made out
until these have subsided.

As soon as the diagnosis is clear, however, certain measures should be
adopted to diminish the hyperæmia of the spinal cord. Dally[163]
recommends the ventral decubitus; almost all modern authorities advise
ice to the spine and ergot internally or subcutaneously. Thus,
Althaus[164] makes hypodermic injections of ergotin in doses of
one-fourth of a grain for a child between one and two years old;
one-third of a grain between three and five; and one half grain from
five to ten; and these doses repeated once or twice daily. The only
objection to this treatment is the degree of local irritation it can
hardly fail to occasion. Hammond, who “affirms ergot to be of great
service, the only medicine capable of cutting short the disease or of
limiting its lesions,” recommends the internal administration of the
fluid extract—ten drops three times a day for infants of six months,
half a drachm for children between one and two years.[165]

[Footnote 163: _Journ. Thérap._, t. viii., 1880.]

[Footnote 164: _On Infantile Paralysis_.]

[Footnote 165: I have elsewhere quoted one case of early recovery
under the use of ice and ergot; or was this a case of temporary
paralysis?]

The belladonna treatment, at one time so warmly praised by
Brown-Séquard, retains to-day few adherents.

Simon advises cutaneous revulsives to divert the circulation to the
{1156} surface; thus, hot-air baths, mustard powder sprinkled on
cotton enveloping the limbs. Ross advises mercurial inunction along
the spine, followed by iodine and blisters. At the same time, iodide
of potassium should be given internally in large doses. The action of
this drug upon inflammations of the nerve-centres seems, within
certain limits, to be indisputable, but its mode of action is
certainly very obscure. Where the lesion can be attributed to a
meningo-myelitis,[166] the iodide may be expected to facilitate the
absorption of the exudation. In these cases it should be continued for
a long time.[167]

[Footnote 166: As in Leyden's first case, and my own.]

[Footnote 167: Binz explains the local action of iodine by an
exudation of leucocytes which follows the dilatation of blood-vessels.
These elements break down the exudation into which they are poured,
and thus facilitate its absorption.]

Electrical treatment may be begun by the end of the first week after
the paralysis. At this stage Erb recommends central galvanization as
an antiphlogistic remedy for the myelitis. For this purpose a large
anode must be placed over the spine at the presumed seat of the
lesion, while the cathode is applied over the abdomen. By a slight
modification of the method the cathode is placed over the paralyzed
muscles. The application is stabile, and, according to Erb, should
last from three to ten minutes; according to Bouchut, several hours
daily. Erb's method is intended exclusively as a sedative to the local
inflammation. When the cathode is placed on the muscles it is hoped
that the descending current, replacing the lost nervous impulses, may
avert the threatening degeneration of the muscle and nerve.

Faradization cannot modify the inflammatory lesions of the cord. As a
means of averting degeneration in completely paralyzed muscles it is
inferior to galvanism, and should not therefore be used in those
muscles which refuse to contract under its stimulus. Its immense
utility, however, is as a stimulus to muscles imperfectly paralyzed,
but liable to degenerate from inaction and to be overborne by their
antagonists. The excitation of contractions in such muscles is a
powerful local gymnastic, helping to maintain nutrition by
artificially-excited function.

For the same purpose, muscles inexcitable to the faradic current
should be, when this is possible, made to contract by the interrupted
galvanic current. After this treatment has been prolonged during
several months, the faradic contractility often returns, and the
current then should be changed (Seguin).

The value of electrical treatment has been very differently estimated.
Erb remarks that “its results are not precisely brilliant.” Roth,
whose testimony perhaps is not above suspicion, since evidently
prejudiced, insists that numerous cases fall into his hands which have
submitted for months to electrical treatment without the slightest
benefit. On the other hand, Duchenne, as is well known, has expressed
almost unbounded confidence in the therapeutic efficacy of
faradization, declaring that it was capable of “creating entire
muscles out of a few fibres.”

The sensitiveness of children to the electrical current, and their
terror at its application, seriously interfere with its persistent
use; as, if the patience of the physician is maintained, that of the
parents is very likely to fail in the presence of the cries and
resistance of the child.

It is very probable that some of the failures of electrical treatment
are {1157} due to the attempt to rely upon it exclusively, instead of
suitably combining both electrical methods with each other and with
other remedial measures. With our present knowledge it is safe to
assert the desirability of persistent electrical treatment during at
least the first two years following the paralysis. The currents must
never be too strong—the faradic, at least, never applied for longer
than ten minutes at a time. The muscles should be relaxed by the
position of the limbs (Sayre). If the muscles continue to waste, and
especially if they become fatty, the electrical response will grow
less and less, and finally cease altogether.[168] In the contrary case
the galvanic contraction will become normal in quality, and the
faradic contractility will return and increase, while the atrophy is
arrested and the muscle regains its bulk and voluntary powers.
Sometimes, as already stated, the latter is regained, while faradic
contractility remains greatly diminished.[169]

[Footnote 168: Passing through three stages: faradic contractility
diminished, galvanic contraction increased; faradic response lost,
galvanic degenerative; absence of contraction to either current.]

[Footnote 169: Sayre (_loc. cit._) has noticed cases in which the
muscle would contract several times under faradism, then refuse to do
so for a day or two. This observation, if valid and not due to unequal
working of the battery, is a most curious one.]

A succedaneum to electricity that is highly prized by some authorities
is strychnia, especially when subcutaneously administered.
Pelione[170] relates the cure of two cases in children of four and
five years, after three and four years' duration of the paralysis, by
strychnia—one-half milligramme daily. None should be given to children
under six months, but over that age one-ninety-sixth of a grain may be
given (Hammond). It should not be given subcutaneously more than two
or three times a week (Seeligmüller).[171]

[Footnote 170: _L'Union médicale_, 1883.]

[Footnote 171: Duchenne relates a case of a paralysis general at the
outset and remaining so for six months. It was then treated by
strychnine for five or six months, and at the end of that time had
become limited to the lower extremities (_Elect. local._, ed. 1861, p.
278).]

The incidental action of electricity in attracting blood to the
paralyzed muscles may be sustained by several other methods.

Among these the external application of heat, either dry or in the
form of hot douches, alternating with cold, is an adjuvant remedy of
real importance. Beard has suggested tubing, malleable to the limbs,
for the conduction of hot water. It is desirable to employ massage
immediately after cessation of the hot applications.

On the value of massage and passive gymnastics opinion is even more
variable than in regard to electricity. Roth, a specialist in
orthopædics, places it at the head of all remedial measures, and
denounces electricity in comparison. Many professional manipulators,
ignorant of medical science, continually claim wonderful triumphs over
regular physicians obtained by means of systematized massage.
Volkmann, on the other hand, dismisses the pretensions of the
Heilgymnastik with considerable contempt, declaring that faradization
is the only method which can really secure exercise to paralyzed
muscles.

The Swedish movement cure consists in passive movements imparted to a
limb by the manipulator, at the same time that they are strenuously
resisted by the patient. From the nature of this method, and its aim
in stimulating the voluntary innervation of the muscles, it {1158} is
admirably adapted to hysterical paralysis. Theoretically, it is
difficult to perceive the applicability of this method in organic
atrophic paralysis, especially in young children, whose voluntary
efforts cannot be commanded. There are, however, several real
indications for passive gymnastics in the treatment of infantile
paralysis. Surface friction and deep massage have some influence in
dilating the blood-vessels and causing an afflux of blood to the cold
and wasting muscles. A probably more important effect may be produced
upon the contraction caused by malposition and adapted atrophy of
certain groups of muscles. It is these contractions which formerly
constituted the special objection of the orthopædist, and were treated
almost universally by tenotomy. They are in any case the proximate
cause of deformities; and, generally existing on the side of the joint
opposite to the most severely paralyzed muscles, they keep these
over-stretched and prevent them from receiving the benefit of the
electrical treatment. Muscles which will not contract to the faradic
current while thus stretched will often begin at once to do so when
the rigidity of their antagonists has been overcome.

Persevering stretching by the hands will often overcome this rigidity
as completely, and even more permanently, than will the
tenotomy-knife. It is in this part of the treatment that entirely
ignorant and even charlatan manipulations do, not unfrequently,
achieve remarkable results.[172]

[Footnote 172: Of course many of those on record, and to some of which
I have been a witness, relate to hysterical contractions, hysterical
scoliosis, etc.]

It is the retracted tendo Achillis and plantar fascia which most
frequently require this manipulation. In the paralytic club-foot of
young children all authorities agree in the value of repeated
manipulations and restorations of the foot as nearly as possible to a
position where it may be retained by simple bandaging. While turning
the foot out it becomes perfectly white, but on releasing hold of it
the circulation is restored, after which the manœuvre may be repeated
(Sayre).

This principle of intermittent stretching by seizure of the segments
of the limb above and below the joint applies to all forms of
paralytic contraction. In the trunk the pelvis should be held by the
mother, while the manipulator, seizing the thorax of the child between
both hands, moves it gently but forcibly to and fro in the required
direction. Great care is required in these manipulations—not merely to
avoid exhausting the muscles, but even to avoid fracturing atrophied
bones.

It may be laid down as a positive rule that tenotomy should never be
performed in the contractions of spinal paralysis until the resources
of manipulation have been exhausted. It is to be remembered that the
rigidity depends on no active contraction of the muscle, but on its
elastic retraction. The manœuvre of stretching does not appeal to the
force of contractility, which may have been lost, but to the force of
elasticity, which remains and can be made to act in a reverse
direction. Finally, in the cases where the retracted muscles have not
been originally paralyzed, but have lost the power of contracting
during the process of shortening, this power may be restored if the
muscle regain its normal length.

The operation of tenotomy, apparently a far more heroic measure, is
often a less efficacious means of arriving at the results. Unless
followed by the application of apparatus which permits motion in the
joint, section of contracted tendons is only of brief utility.

{1159} Though the edges of the cut tendon have been kept apart until
the intervening space is filled by new tissue, union is finally
effected by the latter, and retraction through elasticity is again
imminent. Often, therefore, the deformity is repeated in spite of
repeated operations; when it is not, the happy issue is due to the
fact that, with increased freedom of locomotion immediately after the
tenotomy, the patient has been enabled to bring the influence of
weight to bear in such a manner as to fix the limb in a new and more
convenient position. Thus, after section of the tendo Achillis for pes
equinus, if the patient begins at once to walk on the paralyzed foot,
the weight of the body, pressing down the heel, may keep the tendon
stretched. So walking immediately after section of the hamstring
muscles will have a tendency to produce genu-recurvation by the same
mechanism which produces it in total paralysis, and the original
deformity will not recur.

Besides the tendo Achillis, the parts which may be occasionally
submitted to tenotomy are the plantar fascia, the peroneal muscles,
very rarely the anterior tibial and extensors, the hamstrings, the
thigh adductors. Section of the external rotators of the thigh or of
the tensors of the fascia lata could hardly ever be required, and
among these operations Hueter[173] rejects that on the plantar
aponeurosis as inadequate. The excavation in the foot it is designed
to remedy depends upon alteration in the form of the tarsal bones, and
can only be cured by means of forcible pressure exerted on their
dorsal surface. Section of the peroneal muscles, often recommended by
Sayre, is considered by Hueter to be superfluous after section of the
tendon achilleis. Paralytic contraction of the hamstrings or of the
hip flexors is rarely sufficiently severe to demand tenotomy.

[Footnote 173: _Loc. cit._, p. 416.]

From what has preceded it is evident that maintenance of locomotion is
of great importance, in order to avoid the deformities which are
threatened by prolonged repose. Locomotion, however, can only be
safely permitted with the assistance of apparatus capable of
restraining the movements liable to be produced by the weight of the
body. The supporting instrument which restrains movement in certain
directions must, however, facilitate it in others: immovable
apparatus, such as is not infrequently applied after tenotomy, is
always injurious.

In young children unable to walk, the development of pes equinus may
often be prevented by drawing down the foot to a sole splint made of
thin wood, gutta-percha, or felt, and fastening it with a flannel
bandage. The point of the foot may be drawn up toward the tibia by a
strip of diachylon plaster. If the equinus has already developed, a
splint of gutta-percha or of felt (Sayre) may be modelled to the leg
and foot while the latter is held forcibly in dorsal flexion. The
splint is attached by means of strips of adhesive plaster. It should
extend as far as the knee, and be suitably padded (Seeligmüller).

In children able to walk a sole splint of thin metal, to which the
foot had been previously attached by a flannel band, should be
inserted in a stout leather boot. On the outer side of this boot
should run a metallic splint, jointed at the ankle and extending to a
leather band surrounding the leg just below the knee. A broad leather
band, attached to the outer edge of the sole anterior to the
talo-tarsal articulation, also passes up on {1160} the outside of the
foot, gradually narrowing until, opposite the ankle, it passes through
a slit in the side of the shoe, to be attached to the leg-splint. This
band tends to draw the point of the foot outward, and thus correct the
varus (Volkmann). Sayre[174] has improved on this shoe by dividing the
sole at the medio-tarsal articulation, in which lateral deviation
takes place, and uniting the anterior and posterior parts by a
ball-and-socket joint, permitting movement in every direction.

[Footnote 174: _Loc. cit._, p. 88.]

The orthopædic boot for the treatment of calcaneo-valgus is
constructed on the same principle. But the splint runs up the inner
side of the leg, and the leather strap passing to it from the edge of
the sole draws the point of the foot inward and raises its depressed
inner border (Volkmann). Essential to the treatment of this deformity,
however, is the elevation of the heel. This is effected by means of a
gutta-percha strap which is attached below to a spur projecting from
the heel of the shoe, and above to a band encircling the leg. If, by
rare exception, a paralytic calcaneus exists in a child unable to
walk, a simple substitute may be found for the shoe in a board
sole-splint projecting behind the heel, attached to the foot by a
strip of adhesive plaster, which finally passes from the posterior
extremity of the board up the back of the leg, and is there secured by
a roller bandage.

The device of the gutta-percha elastic band to replace the
gastrocnemius muscle illustrates a principle of wide application in
orthopædic apparatus. The suggestion to replace paralyzed muscles by
artificial ones was first made by Delacroix[175] in an apparatus
designed for the hand. The suggestion was repeated by Gerdy;[176] and
in 1840, Rigal de Gaillac proposed to exchange the metallic springs
hitherto used for India-rubber straps. Duchenne elaborated the
suggestion in a remarkable manner,[177] using delicate spiral springs
as a substitute for the lost muscles, and taking the greatest pains to
make the insertion-points of these to exactly correspond with the
insertions of the natural muscles. This was effected by means of
sheaths, imitating natural tendinous sheaths, sewed to a glove or
gaiter in which the hand or foot was encased.

[Footnote 175: Article “Orthopédie,” _Dict. des Sciences médicales_,
quoted by Duchenne.]

[Footnote 176: _Traité des Bandages_, 2d ed., Paris, 1837, quoted by
Duchenne.]

[Footnote 177: See chapter on “Prothetic Apparatus” in his treatise
_De l'Électrisation localisée_.]

At the present day the prothetic apparatus the most employed is that
contrived by Barwell.[178] The principle is the same as Duchenne's,
but the artificial muscles are made of India-rubber, to which a small
metallic chain is adjusted, and they are attached to the limb by means
of specially-devised bands of adhesive plaster and pieces of tin
bearing loops for the insertion of the muscle. In this apparatus the
artificial muscles do not attempt to imitate the situation of the
natural muscles with the precision which Duchenne claimed for his.
Barwell's own dressing for talipes valgus consists of two rubber
muscles which pass from the inner border of the foot, one to the
inner, the other to the anterior, part of a band which encircles the
leg just below the knee. For talipes calcaneus another band is
required behind the leg, passing to the heel, as in Volkmann's
apparatus, already mentioned. For talipes varus a rubber band {1161}
should pass on the outside of the foot; for equinus, one or more from
the anterior part of the leg to the sides of the anterior part of the
foot.

[Footnote 178: A tolerably minute account of the Barwell dressing is
given by Sayre, _loc. cit._, p. 84.]

Sayre endorses Barwell's dressing as entirely adequate for the
treatment of any form of club-foot, but modifies it by substituting a
ball-and-socket shoe for the adhesive plaster which should encircle
the foot. The artificial muscles are then passed from the sides of the
shoe to a padded leather girdle encircling the leg. A straight splint,
jointed opposite the ankle, runs up from each side of the foot to this
girdle, and from it two lateral upright bars, jointed at the ankle,
pass to the heel of the shoe; and from below the joint passes forward
on each side a horizontal bar reaching the point of origin of the
artificial muscles and giving attachment to them.

In equinus it is necessary to bind the heel of the foot down firmly in
the heel of the shoe; and this is accomplished by means of two
chamois-leather flaps which are attached to the inside walls of the
shoe and lace firmly across the foot.[179]

[Footnote 179: “The aim of the dressing or instrument is simply to
imitate the action of the surgeon's hand; accordingly, any apparatus
combining elastic force is far superior to any fixed appliance; and,
moreover, that is to be preferred which is the most readily removable.
Shoes, therefore, are better than bandages or splints. A proper shoe
must have joints opposite the ankle and the medio-tarsal articulation;
it must permit the ready application of elastic power; and it must not
so girdle the limb as to interfere with the circulation” (Sayre, _loc.
cit._, p. 91).]

Sayre places so much confidence in the power of this elastic tension
to overcome contractions that he rarely resorts to tenotomy in the
treatment of paralytic talipes. Hueter, however,[180] considers
tenotomy much the speediest, and therefore the most desirable, way of
removing contractions.[181]

[Footnote 180: _Loc. cit._]

[Footnote 181: _Loc. cit._]

Seeligmüller quotes with approval Böttger's method for the treatment
of deformities, where the weight of the body is utilized to stretch
the retracted tendons. Thus, for talipes equino-varus an
over-reduction is effected under ether, and the foot forced into a
position of moderate calcaneo-valgus. In this position it is retained
by the immediate application of a plaster or silica bandage. After
this has hardened the child should be encouraged to walk in the mould,
with the addition of felt shoes having a slanting sole that is
thickened like a wedge at the inner side of the foot and strapped on
like a skate. Then, during the act of walking the body tends to
constantly force down the heel and thus stretch the retracted tendo
Achillis, while the bandage and felt sole (acting like a splint)
prevent the inner side of the foot from slipping up.

For talipes valgus the method is analogous, but the foot is forced
into an equino-varus position, so that the tendo Achillis is
artificially shortened, and ultimately becomes a rigid band, capable,
in spite of the sural paralysis, of sustaining the heel.

A cause of relapse in talipes not unfrequently overlooked is the
presence of even slight contractions of the hip- and knee-joints.
These by shortening the limb tend to the production of equinus, since
the foot points itself in order to reach the ground. These
contractions, whose rigidity is far inferior to that induced by
chronic arthritis, may be overcome by forced extension under ether or
gradually by manipulations, or by the weight-and-pulley apparatus,
applied in the recumbent position, as in morbus {1162} coxarius. The
obvious objection to the latter method is the confinement in bed which
it necessitates in a child enjoying at the time perhaps robust general
health.

The contraction once overcome, the limb must be placed in apparatus
which shall both maintain suitable extension and assist in supporting
the trunk during station and locomotion. The latter purpose is
effected, as in apparatus for chronic joint diseases, by transferring
the weight of the body to steel splints running up each side of the
limb, the outer one as far as a girdle which encircles the hips; the
inner to a band surrounding the upper part of the thigh. Thus is
extended the support which in paralysis limited to the leg-muscles is
given by the steel splints inserted in the side of the club-foot
shoes.

In the simplest form of apparatus locomotion is expected to be
accomplished by the action of muscles inserted above the seat of the
paralysis. Thus, when the muscles passing over the ankle-joint are
paralyzed, the foot is moved as a dead weight by means of the
quadriceps extensor, popliteus, and hamstring muscles inserted at the
upper extremity of the leg. If the quadriceps cruris is paralyzed, the
rotators of the thigh, ilio-psoas, sartorius, and adductor muscles,
passing from the pelvis to the thigh, and which are so frequently
intact in atrophic paralysis, are enabled to move the limb if the
weight of the body is borne by steel splints, if these be light and
properly jointed at the hip, knees, and ankle.[182]

[Footnote 182: Or the joint of the knee may be kept locked while the
patient walks, when extension of the limb is mainly required, during
both the active and passive movements of locomotion, the necessary
flexion being supplied at the hip and ankle. By means of a key the
knee-joint can be flexed during the sitting positions.]

But an important aid to locomotion may be obtained from the artificial
muscles, whose elastic tension is of such value in overcoming
contractions. The quadriceps extensor, the most frequently paralyzed,
may be supplemented by an India-rubber band and chain passing down the
front of the thigh from a point on the pelvic girdle corresponding to
the anterior iliac spine to a point on a leg-band, imitating the
tibial insertion of the quadriceps tendon. Analogous bands stretched
on the posterior aspect of the thigh simulate the hamstring muscles.
When the external rotators are paralyzed, the artificial muscle must
stretch from the pelvic girdle to a band encircling the upper part of
the thigh.

The action of these muscles, apart from their elastic tension of
repose, is thus explained by Duchenne: When any effort is made to move
a paralyzed limb, the intact antagonists to the paralyzed muscles
contract; thus, the flexors of the leg. But this contraction, being
constantly opposed by the elastic tension of the artificial
quadriceps, is restrained and gradual, instead of being brusque,
jerking, and excessive, as it otherwise would be. This is the first
result obtained. In the second place, contraction of the antagonist
having ceased, the artificial muscle which has been stretched returns
upon itself in virtue of its elasticity, and restores the limb to the
position of normal equilibrium.

For the act of walking, however, the artificial quadriceps would
require to be made tense enough to resist flexion, and thus keep the
limb in extension. An artificial anterior tibial muscle, however,
would require to yield to the intact gastrocnemius while the heel was
being raised from the floor; then its elastic force should be
sufficient to retract the point of {1163} the foot in dorsal flexion
during the pendulum movement which passively swings the leg forward.
The tension of the artificial muscle should therefore be so adjusted
that it can only be overcome by the active contraction of the
gastrocnemius, and at the moment of greatest tension, immediately
after stretching, it should be able to quite overcome the
gastrocnemius, then relatively[183] relaxed.

[Footnote 183: We say relatively, believing that the simultaneous
contraction of antagonist muscles has been well established as a
constant normal phenomenon.]

The anterior tibial, gastrocnemius, and many other of the artificial
muscles devised by Duchenne are still in use in the modified form
given to them by Barwell. On the other hand, the action of the long
peroneus in pronating the foot, and which Duchenne imitated by an
elaborate artificial tendon following the exact course of the natural
one, is to-day generally supplemented by the jointed shoe and laced
bandage.

In paralysis of all the muscles surrounding a joint, when the limb is
placid and no retractions by adapted atrophy have taken place, the
artificial muscles can only serve to oppose the malpositions which are
threatened from mechanical influences.

In the upper extremities prothetic apparatus has been principally used
for progressive muscular atrophy. Paralysis of the wrist extensors is
perhaps the only case in which the artificial muscle is required in
anterior poliomyelitis. A string may be necessary to support the arm
in paralysis of the deltoid, to avert luxation of the humerus.

Duchenne's ingenuity did not shrink from the difficult task of
supplementing the muscles of the trunk. This he did by inserting the
elastic spirals in corsets in a direction following that of the
muscles paralyzed. Thus, a unilateral paralysis of the sacro-lumbalis
may be met by a spiral splint running up one side of the spine; below,
to the lateral posterior portion of a pelvic girdle. In bilateral
paralysis two springs are used to antagonize the action of the
abdominal muscles.

In Barwell's apparatus for the trunk[184] India-rubber bands are again
substituted for spiral springs. No attempt is made to imitate the
direction of muscles, but the force is applied in any direction
required to antagonize the pressure producing the deformity.[185]

[Footnote 184: Especially designed for habitual scoliosis, but
applicable also to the paralytic deformity.]

[Footnote 185: Volkmann (_loc. cit._, p. 778) thinks that the force of
Barwell's India-rubber straps, whether for scoliosis or club-foot
apparatus, is inadequate, and much inferior to metallic springs.]

It is always important to remember the rarity of scoliosis caused by
spinal paralysis of the trunk-muscles, and the much greater frequency
with which this deformity occurs as a consequence of the paralytic
shortening of a leg. A high shoe, equalizing the length of the lower
extremities, is then the simple and efficient remedy.

In cases of long standing, even when the scoliosis is due to this
cause, certain muscles on the concave side of the curve may become so
retracted and rigid as to require tenotomy. Before this operation it
is necessary to put the rigid muscles on the stretch as much as
possible; and this may be done, if necessary, by means of Sayre's
hanging apparatus. After this operation the spine may be straightened
out with ease—an important distinction from advanced habitual
scoliosis, where the alteration in the shape of the vertebræ defeats
all attempts at rectification. The position {1164} may be maintained
by elastic straps or corsets and by removing the condition which has
led to the deformity.

Seeligmüller criticises too unfavorably the entire system of elastic
tension in the prophylaxis and treatment of paralytic deformities. He
quotes Duchenne's admission, that in certain cases traction upon
rigidly-retracted tissues becomes insupportably painful, and must be
abandoned. It is in these cases that tenotomy becomes an indispensable
preliminary to the use of apparatus. Sayre insists that the necessity
for tenotomy is indicated when pressure on the rigid muscle is
followed by instantaneous spasmodic contraction in the affected or
neighboring muscles. He declares that such contractions indicate
reflex irritations, show that the muscle has undergone structural
change, and that any attempt to stretch or lengthen it would be
followed by an excess of irritation and pain.

This explanation can hardly be accepted, since muscles, whether
imperfectly or not at all paralyzed, which from position and adapted
atrophy have become retracted, have necessarily undergone structural
changes. The greater these changes, the greater the diminution of
reflex excitability; and in any muscle completely paralyzed and
degenerated this is entirely lost. If, however, the afferent nerves
retain enough vitality, if the muscle be slightly paralyzed or
altogether intact, then irritation of its tendon by stretching may
serve to excite contractions in the belly of the muscle. The
possibility of such spinal reflexes is demonstrated by the now
familiar phenomenon of the tendon reflex in various spinal
diseases.[186] The contractions must be painful from the impediments
offered to the progress of the contracting nerve, and from the
exaggeratedly vicious position into which they tend to force the limb.
Under these circumstances prothetic apparatus must be deferred until
section of the tendons has been made.

[Footnote 186: “Passive muscular tension excites tonic contraction in
a muscle, and this action may, in abnormal conditions, be excessive,
as in the myelitic contractions (so-called tendon reflexes).... The
afferent nerves commence in the fibrous tissues of the muscle, and
seem to be especially stimulated by extension” (Gowers, _On Epilepsy_,
1881, p. 97).]


{1165}


DISEASE OF ONE LATERAL HALF OF THE SPINAL CORD.

BY H. D. SCHMIDT, M.D.


SYNONYMS.—Unilateral lesion of the spinal cord; Spinal hemiplegia and
hemiparaplegia; Unilateral spinal paralysis.

INTRODUCTION.—This disease remained unnoticed until twenty years ago,
when Brown-Séquard, observing that certain lesions of the spinal cord
were accompanied by symptoms resembling those which he witnessed in
animals after section of one lateral half of the cord, recognized it
as a special affection. Although some of the accompanying phenomena of
such a section had likewise been observed by Stilling, Budge,
Eigenbrodt, Tuerk, Schiff, Von Bezold, and Van Kempen,[1] nevertheless
this whole group of symptoms, as belonging to the same disease, was
first clearly recognized and anatomically demonstrated by
Brown-Séquard.[2] According to this physiologist, a section or a
destruction of a small portion of a lateral half of the spinal cord in
its cervical region gives rise to the following phenomena: namely, on
the injured side is observed a paralysis of voluntary motion, of the
muscular sense, and of the blood-vessels; the latter, manifesting
itself by a greater supply of blood and a higher temperature of the
parts, may continue to exist for some years. There is, furthermore, an
increased sensibility of the trunk and extremity to touch, prick,
heat, cold, electricity, etc., owing to vaso-motor paralysis, though
in some cases a slight anæsthesia may exist in a limited zone above
the hyperæsthetic part, and also in certain parts of the arm, breast,
and neck. Besides these symptoms, vaso-motor paralysis of the
corresponding side of the face and of the eye, manifested by an
elevated temperature and sensibility, partial closure of the eyelid,
contracted pupil, slight contraction of some of the muscles of the
face, etc., may also be present. On the opposite side of the injury an
anæsthesia of all kinds of sensation, excepting the muscular sense, is
observed in both extremities; there is also an absence of motor
paralysis. The anæsthesia on this side is owing to the decussation of
the sensory nerves in the spinal cord.

[Footnote 1: Eckhard, “Physiologie des Nervensystems,” in _Handbuch
der Physiologie_, edited by L. Hermann, 2d part of vol. ii. p. 165.]

[Footnote 2: “On Spinal Hemiplegia,” _Lancet_, Nov. 7, 21, and Dec.
12, 26, 1868, reported in _Virchow and Hirsch's Jahresbericht_ for the
year 1868, vol. ii. p. 37.]

If the hemisection of the cord is made in the dorsal region, the
functional disturbances are limited to that part of the body below the
point {1166} of division, and a hemiparaplegia, or paralysis of the
corresponding lower extremity, will be the result.

From these facts it will be readily understood that a lesion occurring
in any portion of one lateral half of the spinal cord of man must be
followed by some or all of the above-mentioned symptoms, and that the
phenomena produced by physiological experiments on animals constitute,
in reality, the pathological basis of unilateral spinal paralysis in
man. They will be more clearly understood by calling to mind the
course of the musculo-motor, vaso-motor, and sensitive tracts in the
spinal cord. Thus, the musculo-motor tracts, after having descended to
the crura cerebri, cross one another in the pyramids of the medulla
oblongata and adjoining upper portion of the spinal cord, forming the
so-called decussation of the pyramids; they then descend through the
spinal cord to supply the muscles of the same side of the body.[3] A
section of one lateral half of the cord therefore causes motor
paralysis on the same side. The vaso-motor tracts remain uncrossed,
and pass, each, through one lateral half of the cord to supply the
vessels on the same side; some regions of the body are stated to make
an exception to this rule. According to Brown-Séquard, the sensitive
tracts conducting the different kinds of sensation, with the exception
of the muscular sense, on the contrary, cross over to the opposite
half of the spinal cord soon after their entrance into it, and thence
pursue their further course to the brain. A section of one lateral
half of the cord, therefore, will be followed by a loss of sensation
of touch, pain, heat, tickling, etc. on the other side of the body.

[Footnote 3: Though, in the majority of cases, a complete decussation
of the motor tracts probably takes place in the pyramids, the
researches of Flechsig have shown (_Die Leitungsbahnen im Gehirn und
Rückenmark des Menschen_, p. 273) that there are a number of others in
which the decussation is not complete, but where a part of these
tracts passes to the spinal marrow uncrossed on the inner surface of
the anterior white columns.]

The symptoms above mentioned must of course vary according to the
extent, the intensity, and the particular nature of the lesion, as
well as the height at which it is located in the spinal cord.

DEFINITION.—The chief characters of unilateral spinal disease are
motor paralysis, hemiplegia, or hemiparaplegia, paralysis of the
muscular sense and of the blood-vessels on the side of the lesion, and
paralysis of sensation with preservation of the muscular sense on the
other side of the body. These symptoms may vary, and be accompanied by
other phenomena according to the particular seat, extent, and depth of
the lesion.

SYMPTOMS.—According to the nature of the lesion, the symptoms of
unilateral disease of the spinal cord may be developed suddenly, as,
for instance, when caused by traumatic injuries; or in a gradual and
slow manner, when they may be preceded by premonitory symptoms, such
as vertigo, pain on the side of the lesion, etc. The most prominent
clinical phenomena, as before mentioned, are motor paralysis on the
side of the lesion, and anæsthesia on the opposite side of the body.
The motor paralysis on the side of the lesion may, according to the
seat of the latter, manifest itself in either the form of a hemiplegia
or hemiparaplegia, and even extend in a light form to the opposite
side of the body. In typical cases, however, in which the injury or
disease is strictly confined to one lateral half of the cord, the
motor power on the other side {1167} of the body remains entirely
undisturbed. At the same time, the muscular sense on the injured side
is paralyzed or considerably diminished, and in some cases (Fieber,
Lanzoni, Allessandrini) the electro-muscular excitability also has
been found lowered, while in others it has remained normal. There is
furthermore observed, on the side of the lesion, a vaso-motor
paralysis, manifesting itself by a greater supply of blood to, and a
higher temperature of, the paralyzed trunk and limbs, giving rise to
an increase of sensibility (hyperæsthesia) of touch, prick, heat,
cold, electricity, etc. in these parts. If the seat of the lesion is
sufficiently high up in the cord, this paralysis extends, moreover, to
the corresponding side of the face and eye, where it also causes an
elevation of temperature, increase of sensibility, partial closure of
the eyelid, contracted pupil, slight contraction of some of the
muscles of the face, etc. In a number of cases at the boundary of the
hyperæsthetic region a narrow anæsthetic zone is observed to exist on
the breast, neck, or arm. This anæsthesia is owing to the division, at
the level of the section, of some nerves of sensation on their way to
the other half of the spinal cord. An increase of the reflex
irritability of the tendons has in some cases (Erb, Schulz, Revillons)
been observed, while in one case (Glaeser) the reflex was found to be
absent. Swelling and œdema of the paralyzed limbs have also been met
with (Glaeser), and in one case (Allessandrini) even swelling and pain
in all the joints of the injured side were observed before death,
while masses of coagulated blood in these joints, particularly in the
knee, were revealed by the autopsy. The inflammatory affection of the
knee-joint of the paralyzed leg has, moreover, been observed by
Viguès, Joffroy, and Solomon.[4] Frequently, atrophy of the paralyzed
muscles takes place, especially in chronic cases. In one case (Fieber)
even atrophy of the upper extremity of the uninjured side of the body
was observed.

[Footnote 4: Erb, “Diseases of the Spinal Cord, etc.,” _Cyclopædia of
the Practice of Medicine_, edited by H. v. Ziemssen, Amer. ed.]

The most prominent symptoms observed on the side of the body opposite
to the seat of the lesion are anæsthesia of every kind of sensation,
preservation of the muscular sense, and absence of motor paralysis.
Reflex action and electro-muscular contractility generally remain
normal, though in one case (Fieber) the latter was found increased.
Although the anæsthesia of the skin generally comprises every kind of
sensation, three cases were observed (Fieber) in which the sensation
of heat remained unimpaired, while the electro-cutaneous sensibility
appeared to be lost. As a general rule, there is no vaso-motor
paralysis on the uninjured side, though in some cases (Erb,
Allessandrini) an elevation of temperature has been observed.

Besides the above symptoms, some others, less characteristic in
nature, are now and then observed in individual cases. They are
painful sensations on one or the other side, or even simultaneously on
both sides of the body, and also a feeling of constriction at the
level of the lesion (Erb). Disturbances of the functions of the bowels
or bladder are also met with, though in other cases they are absent.

PATHOLOGICAL ANATOMY.—The pathological changes taking place in the
spinal cord of patients affected with unilateral spinal paralysis must
vary in different cases according to the particular nature of the
lesion giving rise to the characteristic symptoms. In those cases
reported to {1168} have terminated by a gradual disappearance of the
symptoms with or without therapeutic interference it is very probable
that the exciting cause was a hyperæmia or a myelitis of a small
portion of one lateral half of the spinal cord, sufficiently high in
degree to impair the conducting power of the nerve-fibres passing
through it. In some cases the myelitis may lead to a degeneration of
the nerve-fibres, or even extend to the other half of the cord, and by
calling forth additional symptoms render the case more complicated. In
syphilitic cases the disease depends upon syphilitic deposits or
neoplasms in the affected portion of the spinal cord; these cases,
however, generally yield to treatment. In the same manner may
circumscribed sclerosis give rise to the disease. Another cause may be
found in the compression of the cord caused by meningeal tumors or by
the fractured portions of some of the vertebræ. Chronic disease of the
vertebral bones themselves (Pott's disease) may also, by encroaching
upon the spinal cord, become an exciting cause.

The most typical cases, however, are those depending upon traumatic
injuries, by which one lateral half of the spinal cord is forcibly
divided. These lesions resemble in nature the division of the cord in
the physiological experiments on animals, and are most frequently
caused by a stab from a knife penetrating to the cord through the
intervertebral spaces.

DIAGNOSIS.—In those cases in which the symptoms of unilateral spinal
paralysis appear soon after an external injury to the spine, it
becomes obvious that the latter is the exciting cause. In cases of a
more chronic character, in which the symptoms appear gradually, the
nature of the exciting cause can only be correctly determined by the
observation of certain collateral symptoms characteristic of such
causes as might give rise to the symptoms of the disease in question.
As regards the diagnostic symptoms of unilateral spinal paralysis
themselves, they are sufficiently characteristic to be easily
distinguished from those of other forms of hemiplegia or
hemiparaplegia. Thus, cerebral hemiplegia may be distinguished from
the disease under discussion by the sensory disturbances being either
absent or on the same side as the paralysis; furthermore, by the
one-sided paralysis of the face and of the tongue and by the affection
of various cranial nerves. The hemiplegic form of spasmodic spinal
paralysis is distinguished by the absence of sensory disturbance, etc.
Lastly, hemiplegia depending upon lesion of one side of the cauda
equina is distinguished from unilateral spinal disease by the
paralysis and anæsthesia being confined to the same side, and by
generally affecting certain nervous districts of the lower
extremities.

PROGNOSIS.—In unilateral spinal lesions the prognosis depends
obviously on the particular nature and intensity of the exciting
cause. On the whole, there are quite a number of cases reported, even
of traumatic origin, which have terminated favorably.

TREATMENT.—The treatment of unilateral spinal paralysis depends, like
the prognosis, upon the nature of the exciting cause. The principles
upon which it is to be pursued of course are the same as those upon
which the treatment of the various lesions causing the disease—such as
hyperæmia, myelitis, sclerosis, wound of the spinal cord, etc.—is
based.


{1169}


PROGRESSIVE LABIO-GLOSSO-LARYNGEAL PARALYSIS.

BY H. D. SCHMIDT, M.D.


SYNONYMS.—Chronic progressive bulbar paralysis; Progressive muscular
paralysis of the tongue, soft palate, and lips.

HISTORY.—Although the particular group of symptoms constituting this
disease must have been met with and known to the older medical
observers, they were nevertheless first recognized as a special
variety of paralysis in 1841 by Trousseau,[1] who named the affection
labio-glosso-laryngeal paralysis. But as the memorandum prepared by
this distinguished physician at the time when, in consultation with a
medical colleague, he had observed the particular symptoms of this
affection, unfortunately remained unpublished, twenty years more
elapsed before the first accurate and detailed description of the
symptoms and progressive nature of this disease under the name of
progressive muscular paralysis of the tongue, soft palate, and lips
was rendered by Duchenne. The writings of this author directed at once
the attention of other medical men to this disease, and since that
time a large number of cases have been reported and discussed,[2]
while the microscopical examination accompanying the autopsies of many
of them finally revealed that the seat of the lesion giving rise to
the phenomena of this disease was to be sought in the nervous nuclei
of the medulla oblongata. Hence at the present time the pathology of
this disease is thoroughly understood.

[Footnote 1: _Clinique médicale de l'Hôtel Dieu de Paris_, vol. ii. p.
334.]

[Footnote 2: A very considerable number of cases of this disease, and
discussions thereon, will be found reported in _Virchow and Hirsch's
Jahresbericht über die Leistungen und Fortschritte der Gesammten
Medizin_, for the years 1866-80, vol. ii., section “Krankheiten des
Nervensystems.”]

DEFINITION.—That form of labio-glosso-laryngeal paralysis to be
treated in the following pages is characterized by a progressive
paralysis and atrophy of the muscles of the tongue, lips, palate,
pharynx, and larynx, interfering in a greater or lesser degree with
the articulation of words and sounds and with the functions of
mastication and deglutition—affecting, furthermore, in the later
stages of the disease, the voice and the function of respiration. The
paralysis is caused by a progressive degeneration and atrophy of the
ganglion-cells of those nerve-centres in the medulla oblongata from
which the muscles of the above-named organs receive their supply of
nervous energy, though in most cases the pathological process extends
to, or even beyond, the roots of those nerves {1170} which originate
in these centres and terminate in the respective muscles. In many
cases the pathological process extends to the spinal marrow, and there
causes paralysis and atrophy of the muscles of the trunk, and,
generally, of the upper extremities. Almost in every case the disease,
as its name indicates, slowly progresses until it terminates in death.

There are, however, a number of cases observed which, though
exhibiting the same or similar symptoms, do not, in reality, depend
upon a progressive degeneration and atrophy of the centres and
nerve-roots of the medulla, but, on the contrary, owe their symptoms
to other causes; as, for instance, to tumors, hemorrhages, syphilitic
neoplasms, etc., which, either by pressing upon the medulla from
without, or, if situated within, by deranging in various manners the
individual nervous elements of that part, may give rise to some or
even all of the symptoms of true labio-glosso-laryngeal paralysis.
These symptoms, however, according to the character of the lesion,
may, after remaining stationary for some time, retrograde, and even
disappear, as has been observed in syphilitic cases; or they may
progress, and finally end in death. In order to distinguish these
cases from the chronic or progressive bulbar paralysis some authors
have attached the term retrogressive to this form of the disease.

SYMPTOMS.—As the degeneration of the nerve-centres in the medulla
oblongata, upon which the disease depends, does not proceed in a
regular fixed order, the order in which the clinical symptoms
successively appear also varies in different cases. In the majority of
cases, however, the symptoms appear gradually, manifesting themselves
generally in the form of a greater or lesser impediment in the
articulation of certain sounds or letters depending upon the movements
of the tongue, such as _e_, _i_, _k_, _l_, _s_, and _c_, while at the
same time a difficulty of mastication and deglutition may be
experienced by the patient, due to the progressive development of the
paralysis, which deprives the tongue of its lateral and forward
movements. To this cause also, at this period, the apparently
increased secretion of saliva, running from the corners of the mouth,
must be attributed. With intelligent patients these symptoms are
rendered less prominent by the special effort which they make to
pronounce slowly for the purpose of hiding the deficiency in their
speech. But as the disease advances the difficulty of articulation
increases on account of the paralysis extending to the orbicularis
oris, thus affecting the mobility of the lips and interfering with the
pronunciation of the labial sounds _p_, _b_, _f_, _m_, and _w_. With
the loss of power of articulation the patient's speech becomes
gradually reduced to monosyllables, or even, finally, to
incomprehensible and inarticulated grunts, by which he expresses his
wants to his friends. In consequence of the paralysis of the lips the
patient becomes unable to whistle or blow or to perform any movement
depending upon these organs, while at the same time, through the
disturbance created in the co-ordination of the facial muscles by the
paralysis of the orbicularis oris, the mouth becomes transversely
elongated and drawn downward by the action of the remaining
unparalyzed muscles upon its angles. With the mouth partially open and
the lower lip hanging down, the face of the patient has a peculiar sad
and painful expression, while the voice assumes a nasal sound on
account of the paralysis of the palate.

After a while the difficulty of deglutition, caused by the inability
of the {1171} tongue to properly assist in the formation of the bolus
of food and its propulsion into the pharynx, increases on account of
the paralysis extending to the muscles of the pharynx. The failure of
these muscles in the performance of their special function of grasping
the food and carrying it to the œsophagus obliges the patient to push
it down the pharynx with his fingers. In some cases the difficulty of
swallowing rests with solids, in others with fluids. The defective
deglutition furthermore gives rise to spells of coughing and
suffocation by portions of food getting between the epiglottis and
larynx, while the paralyzed muscles of the palate allow the fluids to
pass through the nose and enter the posterior nares.

As the case slowly proceeds the symptoms grow worse. The paralysis of
the orbicularis oris reaches a point when this muscle is no more able
to close the oral cavity; the mouth of the patient therefore remains
open. The tongue, having now entirely lost its lateral, forward, or
upward movements, rests motionless upon the floor of the mouth,
evincing no other signs of life but occasional slight muscular
twitchings. In some cases a diminution of the sense of taste, and also
of that of touch in the tongue, pharynx, and larynx, has been
observed. Atrophy of the tongue and lips now sets in, and the function
of speech is almost entirely lost. The only letter which the patient
is still able to pronounce is _a_ (broad); all other sounds are
indistinct and can hardly be understood. The paralysis of the tongue
and other muscles of deglutition gives rise, furthermore, to an
accumulation of the now excessively secreted saliva, which, being
retained in the oral cavity, assumes the form of a viscid mucous
liquid dripping from the mouth, extending, in the form of strings or
ribbons, between the surfaces of the lips. Finally, when, through the
progressive paralysis of the orbicularis oris, the patient can no more
close the lips, the flow of saliva from the mouth becomes continuous;
he is then seen engaged in the constant use of his handkerchief for
removing the secretion.

In the latter stages of the disease the pathological process extends
to the centres of respiration, paralyzing not only the muscles of
respiration, but diminishing at the same time the contractile power of
the lungs. A great difficulty of breathing—consisting not only in the
want of depth of the inspirations, but, moreover, in a feebleness of
expiration (manifested by weak, powerless coughing)—then ensues, and
the patient is no further able to blow his nose or clear his bronchial
tubes from the accumulating mucus. The paralysis of the muscles of the
larynx, also occurring at this stage, not only increases the
difficulties of deglutition, but most seriously affects the voice of
the patient by decreasing the innervation of the vocal cords; the
voice then becomes hoarse and weak, to be finally entirely lost.

The decrease in the innervation of the heart—which, lastly, also
occurs—gives rise to irregularities in the action of this organ,
followed by irregularity of the pulse, attacks of syncope, feelings of
extreme weakness, and fears of death; whilst simultaneously the
insufficient performance of the respiratory function renders the
breathing of the patient weaker and weaker. Feelings of great
oppression in the chest then arise, and the patient may die during one
of the now frequent attacks of dyspnœa and suffocation.

No fever or pain is observed during the course of this disease;
sensation {1172} remains unaffected and the mind is perfectly clear.
It is owing to these circumstances that frequently the patient walks
about and attends to the duties of life, until shortly before death he
becomes confined to bed by the great weakness caused by the want of
nutrition. The appetite also remains good, but, unfortunately, in
consequence of the difficulties attending the act of deglutition, the
patient cannot satisfy the demands of his stomach. In the latter
stages of the disease, therefore, when feeding can only be
accomplished by the aid of the stomach-tube, every attempt to relieve
the terrible gnawings and pains of hunger ends in a failure. With
starvation staring in his face, the unhappy victim of the disease
finally sinks into a state of extreme inanition, which, if life is not
suddenly extinguished by an attack of suffocation, slowly leads to
final dissolution.

The symptoms above described are those generally observed in
uncomplicated cases of labio-glosso-laryngeal paralysis. There are,
however, a number of cases reported in which the degenerative process
has passed from the medulla oblongata to the spinal cord, and given
rise to paralysis of the muscles of the neck, especially of the
trapezius, and to those of the shoulders, and even to those of the
upper extremities. Atrophy of the interosseus muscles of the hand,
with those of the ball of the thumb, is not unfrequently observed. In
other cases the disease has been found associated with progressive
muscular atrophy, and in others, again, with paralysis of the lower
extremities, accompanied by contractures and depending upon
amyotrophic lateral sclerosis.

Labio-glosso-laryngeal paralysis is, as before mentioned, slow but
progressive in its course, the duration of which is from one to three,
or even five, years. It always terminates in death within the limits
of this time, either from suffocation, inanition, paralysis of the
heart, or some other intercurrent disease.

PATHOLOGICAL ANATOMY.—The macroscopical and microscopical examinations
made during the last fifteen years of the cerebro-spinal axis in quite
a number of cases of progressive labio-glosso-laryngeal paralysis show
that this disease depends upon a degeneration of the nervous elements
of the nuclei or nerve-centres in the medulla oblongata, involving
also the roots of the nerves arising from the latter, and supplying
with nervous energy the muscles of the different organs paralyzed in
this disease. The exact nature of this degeneration—that is, whether
it represents the sequel of a previously existing myelitis or
originates in a so-called parenchymatous inflammation—appears to be as
yet not definitely settled, though a number of pathologists entertain
the view that it is preceded by a chronic myelitis. This view appears
to be corroborated by the fact that frequently portions of the medulla
oblongata and cervical portion of the spinal cord are found in a state
of sclerosis. The uncertainty in the determination of the exact nature
of the pathological process here concerned chiefly depends upon the
diverse conditions in which the blood-vessels of the medulla are
found. For while, in some cases, perhaps the majority, they have been
found empty and in a normal condition, they have in others been met
with congested with blood—a condition pointing to a chronic
inflammatory process. In other cases, again, their walls have been
found thickened or undergoing fatty degeneration.

At any rate, whether inflammatory or not, the now numerous
microscopical examinations have revealed that the main features of the
{1173} process are a degeneration and atrophy, not only of the
ganglion-cells of the respective nervous nuclei with their plexuses,
but also of the fibres of the roots of the peripheral nerves arising
from these centres; frequently the degeneration extends to some
distance upon the nerves themselves. The microscopical changes in the
ganglion-cells consist of an increase of yellow pigment, a gradual
disappearance of their nuclei, terminating in an atrophy of the
ganglionic bodies themselves, the pathological process leaving,
finally, nothing but irregularly-shaped masses of pigment in the
places of these bodies. The degeneration of the nerve-fibres appears
to consist, as elsewhere, in a swelling of the axis-cylinder,
accompanied by atrophy of the medullary sheath—a condition which
finally leads to the complete destruction of these elements of the
nerve-fibres, so that, at last, the whole nerve is only represented by
the connective tissue of its neurolemma. Besides these changes,
certain pathological products, such as conglomerations of fatty
granules or globules, amylaceous bodies, etc., are also found in the
degenerated nerve-centres and nerve-fibres.

Although in different cases the route which the degenerative process
pursues is not the same, a certain general order, in which the nerves
and nerve-centres are successively affected, and corresponding to the
clinical symptoms, appears, nevertheless, to exist. It is thus that
the nucleus of the hypoglossus has been observed to degenerate before
the other nerve-centres. The nuclei of the spinal accessory and
pneumogastric nerves, and also that part of the facial nucleus from
which the inferior division of the facial nerve arises, appear to be
affected next. The glosso-pharyngeal nucleus appears not to be
affected in all cases, and still less frequently the nuclei and roots
of the abducens, auditory, and trifacial nerves. The fibres forming
the anterior pyramids have frequently been found degenerated
throughout the medulla oblongata and pons; sclerosis also has been met
with in this locality. In many cases, as has been remarked before, the
pathological process descends into the spinal cord. Here, as in the
medulla oblongata, the degeneration is principally confined to the
motor centres located in the anterior horns, while the posterior
horns, together with the lateral and posterior white columns, remain
free from disease. The degree of degeneration taking place in the
fibres of the respectively paralyzed muscles also corresponds to that
of the elements of the nerve-centres from which they are supplied. The
microscopical changes observed in the muscular fibres consist in a
decrease of their diameter, accompanied by an increase in the number
of their nuclei, as well as in the quantity of the connective tissue
surrounding the primary bundles; some authors have observed amyloid
degeneration of the muscular fibres.

ETIOLOGY.—The causes which give rise to the pathological process above
described are but little known. Nevertheless, in a number of cases the
disease has been traced back to taking cold, to physical as well as
cerebral over-exertion, mental excitement, sorrow caused by
misfortunes, poverty of nutrition, excessive use of tobacco, etc. In
some cases the disease commences in the spinal cord in the form of
progressive muscular atrophy or amyotrophic lateral sclerosis, and
gradually extends to the medulla oblongata; in many other cases no
particular cause can be found. The disease is rarely if ever met with
in persons under twenty years of age, but is confined to adult life
and old age. It occurs in {1174} both high and low walks of life,
attacking more frequently men than women.

DIAGNOSIS.—The symptoms of progressive labio-glosso-laryngeal
paralysis are so characteristic in themselves as to exclude any
mistake in the formation of a diagnosis. There are, nevertheless, some
pathological conditions, such as hemorrhages in the medulla oblongata
or thrombosis and embolism of the arteries supplying the latter with
blood, which may give rise to the same or very similar phenomena, and
thus render a correct diagnosis difficult. In such cases it must be
remembered that the cause of true labio-glosso-laryngeal paralysis,
depending upon degeneration and atrophy of the nervous nuclei along
the floor of the fourth ventricle, is very gradual, while the symptoms
produced by the causes before mentioned generally make their
appearance in a more acute and sudden manner. The latter also, if not
remaining stationary for some time, have rather a tendency to
improvement, wanting, therefore, the progressive character of the
former.

Tumors at the base of the brain also, by pressing upon the roots of
the cerebral nerves or upon the medulla oblongata itself, may produce
similar symptoms, which, on account of their comparatively slow and
gradual development, may prove more difficult to distinguish from
those characterizing genuine, progressive labio-glosso-laryngeal
paralysis. Errors of diagnosis, however, may here be avoided by taking
into consideration the special symptoms which generally accompany the
presence of tumors of the brain, such as vertigo, headache, vomiting
or even hemiplegia, and local paralysis. The sensory nerves also may
become affected by the pressure of the tumor upon them. Thus, pressure
upon the trifacial nerve may give rise to neuralgic pains, feelings of
tingling and numbness, or even anæsthesia; while pressure upon the
optic nerves or their tracts, or upon the olfactory and lingual
nerves, will be followed by derangements of vision, smell, and taste.
The symptoms produced by the pressure of a tumor at the base of the
brain, moreover, are not strictly progressive, but may for some time
appear, and disappear again before becoming permanent.

Facial diplegia, in which the expression of the face somewhat
resembles that of a patient affected with labio-glosso-laryngeal
paralysis, is distinguished from the latter disease by the paralysis
affecting both divisions of the facial nerve, while the tongue remains
free and deglutition is undisturbed.

There are still other affections of the cerebro-spinal axis, such as
paralysis of the insane, disseminated sclerosis, etc., which in their
course present some or perhaps all of the symptoms characterizing
labio-glosso-laryngeal paralysis; these may be distinguished from the
latter disease by taking their own special symptoms into
consideration.

TREATMENT.—Although almost all cases of progressive
labio-glosso-laryngeal paralysis terminate fatally, some cases have
been reported by several observers in which a temporary improvement in
the symptoms of the disease, or even a total cure, had been obtained
by treatment. Of course such favorable results can only be obtained in
the initial or earlier stages of the disease. Thus, Kussmaul
recommends in the initial stage, when pains in the head and neck are
present, wet cupping of the nape of the neck in strong persons, also
the use of the shower-bath, while {1175} nitrate of silver may be
given internally. The application of galvanism in an alternate
direction he also recommends—first, through the neck, and later on
through the whole spinal column—and at the same time currents in an
alternating direction from the neck and hypoglossus nerve to the
tongue. Dowse reported a case of bulbar paralysis which he cured by
the application of the constant current upon the paralyzed parts,
subcutaneous injections of atropine and strychnine, with the internal
administration of cod-liver oil, quinine, and phosphorus. He attaches
great importance to the careful feeding of the patient through a tube
passed through the nose, and to the strict application of the galvanic
current; for excessive salivation he recommends atropine. Erb
recommends to regulate the diet and the habits of life of the patient
in such a manner as to avoid every irritation of the nervous system;
furthermore, to generally stimulate the nutrition in order to produce
a tonic effect upon the nervous system. For this purpose he
principally relies upon a cautious hydropathic treatment, to be
continued for a long time and with great regularity. The greatest
importance, however, he attaches to electricity, considering the best
method of galvanism as follows: “Galvanize with stabile application
transversely through the mastoid processes and longitudinally through
the skull, the so-called galvanism of the cervical sympathetic (anode
on the nuchus, and cathode at the angle of the lower jaw), and then
induce movements of deglutition (twelve to twenty at each sitting);
besides this, apply, according to circumstances, direct galvanic or
faradic currents to the tongue, lips, and palate.” The electric
treatment must be continued for some time, with from four to seven
sittings a week. Of the medicines taken internally, Erb recommends
nitrate of silver, iodide of potassium, iodide of iron, chloride of
gold and sodium, ergotin, belladonna, and preparation of iron and
quinine.


{1176} {1177}


DISEASES OF THE PERIPHERAL NERVES.

BY FRANCIS T. MILES, M.D.


The nervous system of the higher animals is the apparatus by which
stimuli coming from the external world or originating in the interior
of their own bodies are perceived (its sensitive functions), or cause
muscular contraction (its motor functions), or, lastly, cause
molecular changes in tissues (its trophic functions).

Besides this power which the nervous system possesses of receiving
impressions originating outside of itself and actively replying to
them, it appears also to possess the power of originating within
itself changes the result of which are sensations, movements, and
trophic alterations. In other words, it can act automatically.

The apparatus for the performance of these various functions consists
of the end-organs, the nervous centres, and the nerves.

The end-organs are peripheral mechanisms for the reception of
impressions. The structure and mode of action of some of them, as the
eye and the ear, are pretty well understood, while others, as those
connected with the sense of touch, temperature, etc., are but
imperfectly known. It is probable that there are also peripheral
mechanisms which facilitate the delivery of the impulses coming from
the nerve-centres to the organs, tissues, muscles, glands, etc.

The nervous centres are made up of nerve-cells variously connected
with each other. They are immediately concerned in receiving
impressions conveyed to them by the nerves and transforming them into
sensations, or transmitting them to other organs, causing reflex
actions, or in originating sensations and impulses.

The nerves are organs which, connected at one extremity with the
end-organs and at the other with the nervous centres, convey
peripheral impressions to the centres, and impulses and influences
from the centres to the various organs of the body.

As it is with diseases of the peripheral nerves that we are now
concerned, let us begin by looking more closely into their structure
and functions.

The nerves appear to the naked eye as white strands of variable size,
which a close inspection shows to be made up of threads or fibrils
(best seen when the cut end of a nerve is examined) bound together by
fine connective tissue and scantily supplied with blood-vessels. A
microscopic examination shows that each of the fibrils visible to the
naked eye is made up of a great number of fibres. These are the
medullated {1178} nerve-fibres, and they extend unbroken between the
nerve-centres, with the cells of which they are connected, to the
various organs and tissues, with which they also enter into organic
union.

If we examine the structure of a medullated nerve-fibre, we find it to
consist of a central thread called the central axis or axis-cylinder,
in which close microscopic investigation shows a longitudinal
striation, indicating that it is made up of fibrillæ. Surrounding the
central axis like a sheath is the white substance of Schwann, composed
of an oleo-albuminous substance, myeline, to which the nerves owe
their white appearance. According to some observers, the white
substance of Schwann is pervaded by a meshwork of fibres. Surrounding
the white substance of Schwann is the sheath of Schwann, a
structureless membrane having at intervals upon its inner surface
nuclei, around which is a small amount of protoplasm.

At intervals along the course of the nerve-fibres are seen
constrictions which involve the sheath and white substance of Schwann,
but which do not affect the central axis, which passes unbroken the
points of constriction. These are the nodes of Ranvier. Each space on
the fibre beneath the nodes of Ranvier contains one of the nuclei of
the sheath of Schwann, and probably, together with the white substance
of Schwann, represents a cellular element. Diseased conditions
sometimes respect the limits of these cellular elements.

The central axis is the true conducting part of the nerve-fibre, and
it is probable that each of the fibrillæ of which it is composed has a
separate peripheral termination and possesses the power of isolated
conduction. The white substance of Schwann and the sheath of Schwann
protect the central axis and seem to be connected with its nutrition.

The fibres in a nerve are bound together by loose connective tissue,
the endoneurium, into the primitive bundles, which are again united by
the perineurium, a membrane of laminated connective tissue, into more
definite funiculi seen by the naked eye, the secondary bundles.

The secondary bundles are tied together by connective tissue, in which
are found fat-cells and in which run the fine blood-vessels supplying
the nerves. This connective tissue has been named the epineurium, and
its condensed outer layers constitute the sheath of the nerve. It is
important to observe that the connective tissue of the nerves is
permeated by lymphatics which penetrate to the nerve-fibres, so that
these are brought in contact with, and as it were, bathed in, the
lymph.

Each nerve-fibre runs an isolated course from end to end, without
anastomosing with other fibres, and near its peripheral termination it
usually divides into two or more branches.

The fibres of the peripheral nerves depend for their integrity and
nutrition upon their connection with central organs. The large
multipolar cells of the anterior horns of gray matter of the spinal
cord preside over the nutrition of the motor fibres; the ganglia on
the posterior roots of the spinal nerves over the nutrition of the
sensitive fibres.

If a nerve be severed from its connection with these centres of
nutrition, it in a short while undergoes degenerative changes which
result in complete destruction of its fibres.

The nerve-fibres when in a state of functional activity conduct
impressions along their length to the end-organs or to the
nerve-centres with {1179} which they are in connection. This property
of the fibres we call their conductivity. Each fibre conducts
impressions in an isolated manner, not communicating them to other
fibres with which it may be in contact. The rapidity of this
conduction in human nerve-fibres is estimated at 33.9 meters (about 38
yds.) per second. This rate may be diminished by cold or by the
anelectrotonic condition which is induced in the nerve by the passage
through it of an electric current.

The nerve-fibres are irritable; that is, the application to them of
stimuli excites their functional activity, and the impression made by
the stimulus is transmitted to their extremities.[1]

[Footnote 1: The nerve-fibres in man do not appear to attain their
full irritability until the fifth or tenth month after birth
(Soltman).]

The natural or physiological stimuli of the nerves act upon their
extremities. Either they act through the peripheral mechanisms, giving
rise to impressions which are conducted centripetally to the cells of
the nerve-centres and there cause sensations or reflex actions, or
they act upon the nerve-centres, giving rise to impulses which are
conducted centrifugally and cause the various phenomena of contraction
of muscles, inhibition of contraction, secretion, etc. Besides the
physiological, there are other stimuli which excite the functional
activity of nerve-fibres when applied at any point along their course.

Mechanical stimuli, blows, concussions, pressure, traction, etc.,
excite the nerves, causing sensations when applied to sensitive
nerves, or contraction of muscles when applied to motor nerves. When
mechanical stimuli are pushed farther, the irritability of the nerves
may be destroyed. The gradual application of mechanical stimuli may
destroy the irritability of nerve-fibres without any exhibition of
excitation, as in paralysis from pressure. In nerve-stretching it is
probable that many of the results depend upon the mechanical
stimulation of the nerve-fibres by the traction. With a certain amount
of force used the irritability of the nerve may be increased; carried
farther, both the irritability and the conductivity may be diminished,
and finally destroyed. As the centripetal fibres are soonest affected
in the stretching, we can see how this proceeding is most beneficial
in neuralgias, where a potent factor, if not the cause of the disease,
is an abnormal excitability of the nerve-fibres. It is to be observed,
nevertheless, that in cases of continued pressure upon mixed nerves
the motor fibres are the first to suffer loss of their conductivity.

Sudden alterations of temperature act as stimuli to nerves. Heat
increases their irritability, but its prolonged application diminishes
it. Cold in general diminishes the nervous irritability, and may be
carried to the point of completely destroying it temporarily.[2]

[Footnote 2: But at a certain age in freezing the ulnar nerve Mitchell
found its irritability notably increased.]

Many substances of widely-different chemical constitution, as acids,
alkalies, salts, alcohol, chloroform, strychnine, etc., act as stimuli
when applied directly to the nerves, apparently by causing in them
rapid molecular changes. Also may be enumerated as chemical stimuli to
the nerves substances found naturally in the body, as bile, bile
salts, urea. The rapid withdrawal of water from nerve-tissue first
increases, and then diminishes, its irritability. The imbibition of
water decreases nervous irritability.

{1180} An electric current of less duration than the 0.0015 of a
second does not stimulate the nerve-fibres. It would appear that more
time is required for the electric current to excite in nerve-tissue
the state of electrotonus which is necessary to the exhibition of its
functional activity. The electric current stimulates a nerve most
powerfully at the moments of entrance into and exit from the nerve,
and the more abruptly this takes place the greater the stimulation.
Thus the weak interrupted currents of the faradic or induced
electricity owe their powerfully stimulating effects to the abruptness
of their generation and entrance into and exit from the nerves. At the
moment of the entrance of the electric current into the nerve—that is,
upon closing the circuit—the stimulating effect is at the negative
pole or cathode; when the current is broken—_i.e._ leaves the
nerve—the stimulating effect is at the positive pole or anode. A
current of electricity very gradually introduced into or withdrawn
from a nerve does not stimulate it. But if while a current is passing
through a nerve its density or strength be increased or diminished
with some degree of rapidity, the nerve is stimulated, and the degree
of stimulation is in proportion to the suddenness and amount of change
in the density or strength of the current. Although with moderate
currents the stimulation of the nerve takes place only upon their
entrance and exit, or upon variations of their density, nevertheless,
with a very strong current the stimulation continues during the
passage of the current through the nerve. This is shown by the pain
elicited in sensitive nerves, and the tetanic contraction of the
muscles to which motor nerves are distributed.

An important factor in electrical stimulation is the direction of the
current through the nerve. A current passed through a nerve at right
angles with its length does not stimulate it. Currents passing through
a nerve stimulate in proportion to the obliquity of their direction,
the most stimulating being those passing along the length of the
nerve. Motor nerves are more readily stimulated by the electric
current the nearer it is applied to their central connection.
Experiments on the lower animals would seem to indicate that the motor
fibres in a nerve-trunk do not all show the same degree of
irritability when stimulated by the electric current.

The irritability of the nerve-fibres may be modified or destroyed in
various ways. Separation of nerves from their nutritive centres causes
at first an increase of their irritability, which is succeeded by a
diminution and total loss, these effects taking place more rapidly in
the portions nearer the nerve-centres. It is important to observe that
an increase of irritability preceding its diminution is generally
observed in connection with the impaired nutrition of nerves, and is
the first phase of their exhaustion.

Prolonged and excessive activity or disuse of nerves causes diminution
of their irritability, which may go to the extent that neither rest in
the one case nor stimulation in the other can restore it. If a
galvanic current is passed through a nerve in its length, the
irritability of the fibres is increased in the region of
catelectrotonus—viz. in the part near the cathode—and diminished in
the region of anelectrotonus—viz. in the part near the anode. Certain
substances, as veratria, first increase and then destroy the
irritability of the nerves; others, as woorara, rapidly destroy it.

{1181} The fibres of the peripheral nerves are divided into two
classes: first, those which conduct impressions or stimuli to the
nerve-centres, the afferent or centripetal fibres; and, secondly,
those which conduct impulses from the centres to peripheral organs,
the efferent or centrifugal fibres. Belonging to the first class are
(1) sensitive fibres, whose stimulation sets up changes in the
nerve-centres which give rise to a sensation; (2) excito-motor fibres,
whose stimulation sets up in the nerve-centres changes by which
impulses are sent along certain of the centrifugal fibres to
peripheral end-organs, causing muscular contraction, secretion, etc.
Belonging to the second class are (1) motor fibres, through which
impulses are sent from the nerve-centres to muscles, causing their
contraction; (2) secretory fibres, through which impulses from
nerve-centres stimulate glands to secretion; (3) trophic fibres,
through which are conveyed influences from the centres, affecting the
nutritive changes in the tissues; (4) inhibitory fibres, through which
central influences diminish or arrest muscular contraction or
glandular activity. No microscopic or other examination reveals any
distinction between these various fibres.

Every nerve-fibre has the power of conducting both centripetally and
centrifugally, but the organs with which they are connected at their
extremities permit the exhibition of their conductivity only in one
direction. Thus, if a nerve-fibre in connection with a muscle at one
end and a motor nerve-cell at the other be stimulated, although the
stimulus is conducted to both ends of the fibre, the effect of the
stimulus can only be exhibited at the end in connection with the
muscle, causing the muscle to contract. Or if a fibre in connection
with a peripheral organ of touch be stimulated, we can only recognize
the effects of such stimulation by changes in the nerve-cells at its
central end which give rise to a sensation.

When we consider the extensive distribution and exposed position of
the peripheral nerves, their liability to mechanical injury and to the
vicissitudes of heat and cold, we cannot but anticipate that they will
be the frequent seat of lesions and morbid disturbances. It may be
that not a few of their diseased conditions have escaped observation
from a too exclusive looking to the central nervous system as the
starting-point of morbid nervous symptoms. This occurs the more
readily as many of the symptoms of disease of the peripheral nerves,
as paralysis of muscles, anæsthesia, hyperæsthesia, etc., may equally
result from morbid conditions of the brain or spinal cord, and not
unfrequently the peripheral and central systems are conjointly
affected in a way which leaves it doubtful in which the disease began
or whether both systems were simultaneously affected.

The elucidation of such cases involves some of the most difficult
problems in diagnosis, and requires not only a thorough acquaintance
with the normal functions of the peripheral nerves, but also the
knowledge of how those functions are modified and distorted in
disease.

The symptoms arising from injuries and diseases of the peripheral
nerves are referable to a loss, exaggeration, or perversion of their
functions, and we often see several of these results combined in a
single disease or as the result of an injury.

The fibres may lose their conductivity or have it impaired, causing
feebleness or loss of motion (paralysis), or diminution or loss of
sensation {1182} (anæsthesia). Or there may be induced a condition of
over-excitability, giving rise to spasm of muscles and sensations of
pain upon the slightest excitation, not only from external agents, but
from the subtler stimulation of molecular changes within themselves
(hyperæsthesia). Or diseased conditions may induce a state of
irritation of the nerve-fibres, which shows itself in apparently
spontaneous muscular contraction or in sensations abnormal in their
character, and not corresponding to those ordinarily elicited by the
particular excitation applied, as formication or tingling from simple
contact, etc. (paræsthesiæ), or in morbid alterations of nutrition in
the tissues to which the fibres are distributed (trophic changes).

If we could recognize the causes of all these varied symptoms and
discover the histological changes invariably connected with them, it
would enable us to separate and classify the diseases of the
peripheral nerves, and give us a sound basis for accurate observation
and rational therapeutics. But, although the progress of investigation
is continually toward the discovery of an anatomical lesion for every
functional aberration, we are still so far from a complete
pathological anatomy of the peripheral nerves that of many of their
diseases we know nothing but their clinical history. We are therefore
compelled in treating of the diseases of the peripheral nerves to hold
still to their classification into anatomical and functional, as being
most useful and convenient, remembering, however, that the two classes
merge into each other, so that a rigid line cannot be drawn between
them, and that such a classification can only be considered as
provisional, and for the purpose of more clearly presenting symptoms
which we group together, not as entities, but as pictures of diseased
conditions which may thus be more readily observed and studied.

It is well to begin the study of the diseases of the peripheral nerves
by a consideration of nerve-injuries, because in such cases we are
enabled to connect the symptoms which present themselves with known
anatomical alterations, and thus obtain important data for the
elucidation of those cases of disease in which, although their
symptomatology is similar, their pathological anatomy is imperfectly
or not at all known.


Injuries of the Peripheral Nerves.

If the continuity of the fibres of a mixed nerve be destroyed at some
point in its course by cutting, bruising, pressure, traction, the
application of cold, the invasion of neighboring disease, etc., there
will be an immediate loss of the functions dependent on the nerve in
the parts to which it is distributed. The muscles which are supplied
by its motor fibres are paralyzed; they no longer respond by
contraction to the impulse of the will. No reflex movements can be
excited in them either from the skin or the tendons. They lose their
tonicity, which they derive from the spinal cord, and are relaxed,
soft, and flabby. As the interrupted sensory fibres can no longer
convey impressions to the brain, we might naturally look for an
anæsthesia, a paralysis of sensation, in the parts to which they are
distributed, as complete as is the loss of function in the muscles.
Such, however, is not the fact. Long ago cases were observed in which,
although sensitive nerves were divided, the region of their
distribution retained more or less sensation, or seemed to recover it
so {1183} quickly that an explanation was sought in a supposed rapid
reunion of the cut fibres. Recent investigations, moreover, show that
in a large number of cases where there is complete interruption of
continuity in a mixed nerve the region to which its sensitive fibres
are distributed retains, or rapidly regains, a certain amount of
sensation, and that absolute anæsthesia is confined to a comparatively
small area, while around this area there is a zone in which the
sensations of pain, touch, and heat are retained, though in a degree
far below the normal condition; in short, that there is not an
accurate correspondence between the area of anæsthesia consequent upon
cutting a sensitive nerve and the recognized anatomical distribution
of its fibres. We find the explanation of this partly in the abnormal
distribution of nerves, but principally in the fact of the frequent
anastomoses of sensitive nerves, especially toward their peripheral
distribution, thus securing for the parts to which the cut nerve is
distributed a limited supply of sensitive fibres from neighboring
nerves which have joined the trunk below the point of section. This
seems proved not only by direct anatomical investigation, but also
from the fact that the peripheral portion of the divided nerve may be
sensitive upon pressure, and that the microscope shows normal fibres
in it after a time has elapsed sufficiently long to allow all the
divided fibres to degenerate, in accordance with the Wallerian law.
Some of the sensation apparently retained in parts the sensitive nerve
of which has been divided may be due to the excitation of the nerves
in the adjacent uninjured parts, caused by the vibration or jar
propagated to them by the mechanical means used to test sensation, as
tapping, rubbing, stroking, etc.[3] It is to be observed that this
retained sensation after the division of nerves exists in different
degrees in different regions of the body; thus it is greatest in the
hands, least in the face.

[Footnote 3: Létiévant, _Traité des Sections nerveuses_.]

As the vaso-motor and trophic nerve-fibres run in the trunks of the
cerebro-spinal nerves, destructive lesions of these trunks cut off the
influence of the centres with which those fibres are connected, and
hence they are followed by changes in the circulation, calorification,
and nutrition of the parts to which they are distributed. Thus, the
loss of the vaso-motor influence is at first shown in the dilation of
the vessels and the unvarying warmth and[4] congestion of the part.[5]
This gives way in time to coldness, due to sluggish circulation and
diminished nutritive activity. Marked trophic changes occur in the
paralyzed muscles. They atrophy, their fibres becoming smaller and
losing the striations, while the interstitial areolar tissues
proliferates, and finally contracts cicatricially. The skin is
sometimes affected in its nutrition, becoming rough and scaly. Other
trophic changes of the skin resembling those produced by irritation of
a nerve are very rarely seen, and they may probably be referred to
irritation of fibres with which the part is supplied from neighboring
trunks.

[Footnote 4: A remarkable exception is seen, however, in the effect of
gradual pressure experimentally applied to nerve-trunks until there is
complete interruption of sensation and motion, in which case the
temperature invariably falls.]

[Footnote 5: In a case of gunshot wound that came under the writer's
care in 1862, the leg and foot, which were paralyzed from lesion of
the popliteal nerve, remained warm and natural in color during
repeated malarial chills, which caused coldness and pallor of the rest
of the body.]

{1184} Anatomical Changes in the Divided Nerve and Muscles.—The
peripheral portion of a divided nerve separated from its nutritive
centres degenerates and loses its characteristic appearance, looking
to the naked eye like a grayish cord, and being shrunken to one-fourth
of its natural size. The changes which take place in the degeneration
of the nerve-fibres, and which proceed from the point of lesion toward
the periphery, are, first, an alteration of the white substance of
Schwann, which breaks into fragments, these melting into drops of
myeline, and finally becoming reduced to a granular mass. The central
axis at a later period likewise breaks up, and is lost in the granular
contents of the sheath of Schwann. Meanwhile, absorption of the débris
of the fibres goes on, until, finally, there remains but the empty and
collapsed sheath of Schwann with its nuclei, the whole presenting a
fibrous appearance. When this has taken place the degenerated motor
nerve-fibres can no longer be excited, and no stimulation applied to
them can cause the muscles to contract. At the same time, the muscles
atrophy and undergo degenerative changes in their tissue. The fibres
become smaller and their transverse striæ indistinct, with the
appearance of fatty degeneration, and finally there is proliferation
of the interstitial cellular tissue. They do not, however, lose their
contractility, and upon a mechanical stimulus being applied directly
to them they contract in a degree that is even exaggerated, but with a
slowness that is abnormal. If, now, we apply the stimulus of
electricity to the muscles themselves, we encounter phenomena of the
greatest interest and importance. The application of the faradic
current, however strong, elicits no contraction; there is loss of
faradic excitability. But if the galvanic current be applied the
muscles contract, and that, too, in reply to a current too weak to
excite healthy muscles to action; there is increased galvanic
excitability. The kind of contraction thus induced is peculiar,
differing from that ordinarily seen in muscles. Instead of its being
short, and immediately followed by relaxation, as when we make or
break the galvanic current in healthy muscles, it is sluggish,
long-drawn out, and almost peristaltic in appearance. This is
characteristic of degenerated muscles, and is the degenerative
reaction. But there is also a change in the manner in which the
degenerated muscles reply to the two poles of the galvanic current.
Instead of the strongest contraction being elicited, as in the normal
condition, by the application of the negative pole to the muscle
(C. C. C., cathode closing contraction), an equally strong or stronger
is obtained by the application of the positive pole (A. C. C., anode
closing contraction), while the contraction normally caused on opening
the circuit by removal of the positive pole (A. O. C., anode opening
contraction) becomes weaker and weaker, until it is at last exceeded
by the contraction upon opening the current by the removal of the
negative pole (C. O. C., cathode opening contractions). In short, the
formula for the reply of the healthy muscles to galvanic excitation is
reversed; there is a qualitative galvanic change in the paralyzed and
degenerated muscles.

If no regeneration of the nerve takes place, the reaction of the
muscles to the galvanic current is finally lost, and they exhibit
those rigid contractions which probably result from a sclerotic
condition of the intramuscular areolar tissue.

After complete destruction of the fibres of a nerve at some point of
its {1185} course, even when a considerable length of it is involved,
and after the consequent degeneration of the peripheral portion has
taken place, we have, with lapse of time, restoration of its function,
consequent upon its regeneration and the re-establishment of its
continuity. The histological changes by which the degenerated fibres
are restored and the divided ends reunited have not been made out with
such certainty as to preclude difference of opinion as to the details.
But the process in general seems to be a proliferation of the nuclei
in the sheath of Schwann, with increase of the protoplasm which
surrounds them, filling the sheath of Schwann with the material from
which the new fibre originates. In this mass within the sheath is
formed first the central axis of the new fibre, which is later
surrounded by the white substance of Schwann. With the regeneration of
the nerve-fibres the functions of the nerve return, but in the order
of sensation first, and afterward the power of transmitting the
volitional impulse to the muscles. Even after regeneration has so far
advanced that the muscles may be made to contract by an exercise of
the will, the newly-formed fibres fail to respond to other stimuli;
thus, the faradic current applied to the nerve does not cause the
muscles to contract; the stimulation is not transmitted along the
imperfectly restored fibres.

It may be here remarked that after regeneration has restored the
functions of a divided nerve the muscles to which it is distributed
may still exhibit for a time the degenerative reaction in consequence
of unrepaired changes in themselves. In the end we may look for
complete restoration in both nerve and muscles.

The time required for the regeneration and reunion of a divided nerve
depends somewhat upon the manner in which the destruction has been
caused. Thus, a nerve which has been divided by a clean cut, and where
the cut ends remain in apposition or close proximity, unites much more
readily than one in which bruising, tearing, or pressure has destroyed
an appreciable length of its fibres or the divided ends have been
thrust apart.

In complete division of a nerve we must not look for regeneration and
restoration of its functions, even in favorable circumstances, before
the lapse of several months, although cases have been recorded where
the process has been much more rapid.

Injuries of mixed nerves, with incomplete destruction of the fibres,
give rise to many and varied symptoms, some of which are the direct
result of the injury—many others of subsequent changes of an
inflammatory character (neuritis) in the nerves or in the parts to
which they are distributed. Pain is one of the most prominent symptoms
immediately resulting from nerve-injury, although as a rule it soon
subsides. There is sometimes merely numbness or tingling, or there may
be no disturbance of sensation at the moment of injury. Rarely is
spasm of muscles an immediate effect. Generally, motion is at first
very much impaired, but if the injury is not grave enough to cause a
lasting paralysis, the muscles may rapidly regain their activity. In
observing the effects of injuries of mixed nerves one remarkable fact
strikes us: it is the very much greater liability of the motor fibres
to suffer loss or impairment of function. Thus, it is common to see
sensation but little or only transiently affected by injuries which
cause marked paralysis of muscles. {1186} So in the progress of
recovery the sensory disturbances usually disappear long before
restoration of the motor function; indeed, sensation may be entirely
restored while the muscular paralysis remains permanent. Direct
experimental lesions of the mixed nerve-trunks of animals give the
same result.[6] For this immunity of the sensitive nerve-fibres no
explanation can be given other than an assumed difference in their
inherent endowments.

[Footnote 6: Luderitz, _Zeitschrift für klin. Med._, 1881.]

According to the amount of damage the nerve has sustained will there
remain after the immediate effects of the injury have passed off more
or less of the symptoms already described as due to loss of
conductivity in the fibres—viz. paralysis of motion, and anæsthesia.
Sometimes the impairment of conductivity in the sensitive fibres shows
itself by an appreciable time required for the reception of
impressions transmitted through them, giving rise to the remarkable
phenomenon of delayed sensation. Degeneration of the nerve
peripherally from the point of lesion, and consequently of the
muscles, will likewise take place in a greater or less degree,
according to the amount of the injury and the subsequent morbid
changes, and give rise to the degenerative reaction which has been
already described. We will not, however, always encounter the
degenerative reaction in the typical form which presents itself after
the complete division of nerves. Many variations from it have been
observed; as, for instance, Erb's middle form of degenerative
reaction, in which the nerve does not lose the power of replying to
the faradic or galvanic current, but the muscles show both the loss of
the faradic with increased galvanic excitability, with also the
qualitative change in regard to the poles of the galvanic current.
Such irregularities may be explained by the supposition of an unequal
condition of degeneration in the nerve and the muscles. A rare
modification has been recorded which has once come under the writer's
observation, in which the muscles reply with the sluggish contraction
characteristic of the degenerative reaction to the application of the
faradic current.

A highly important class of symptoms arise later in injuries of
nerves, due not so much to a loss as to an exaggeration or perversion
of their functions: they are the result of molecular changes in the
nerves, giving rise to the condition called irritation. Irritation of
motor nerves shows itself in muscular spasm, or contractions of a
tonic or clonic character, or in tremor. If the sensitive fibres are
irritated by an injury or the subsequent changes in the nerve
resulting from it, we may have hyperæsthesia of the skin, in which,
although the sense of touch may be blunted, the common sensation is
exaggerated, it may be, to such a degree that the slightest contact
with the affected part gives rise to pain or to an indescribable
sensation of uneasiness almost emotional in its character—something of
the nature of the sensation of the teeth being on edge. There may be
hyperæsthesia of the muscles, shown by a sensitiveness upon deep
pressure, in which the skin has no part. Pain, spontaneous in its
character, is a very constant result of nerve-irritation, whether
caused by gross mechanical interference or by the subtler processes of
inflammation in the nerve-tissue. It is generally felt in the
distribution of the branches of the nerve peripheral to the point of
lesion, although it is occasionally located at the seat of the injury.
Neuralgias are a common result of the irritation of nerves from
injuries.

{1187} Causalgia, a burning pain, differing from neuralgia, and
sometimes of extreme severity, is very frequent after injuries of
nerves, especially in parts where the skin has undergone certain
trophic changes (glossy skin). A number of abnormal sensations
(paræsthesiæ) result from the irritation of sensitive fibres, and are
common after nerve injuries. Among these we may mention a sensation of
heat (not the burning pain of causalgia) in the region of the
distribution of the nerve, which does not coincide with the actual
temperature of the part; it occurs not unfrequently after injury to a
nerve-trunk, and may be of value in diagnosis.

The effect of irritative lesions of mixed nerves upon nutrition is
very marked, and sometimes gives rise to grave complications and
disastrous results. Any or all of the tissues of the part to which the
injured nerve is distributed may be the seat of morbid nutritive
changes.

In the skin we may have herpetic or eczematous eruptions or
ulcerations. It may become atrophied, thin, shining, and, as it were,
stretched tightly over the parts it covers, its low nutrition showing
itself in the readiness with which it ulcerates from trifling
injuries. This condition, called glossy skin, usually appears about
the hands or feet, and is very frequently associated with causalgia.
The hair may drop off, or, as has been occasionally seen, be increased
in amount and coarsened, and the nails become thickened, crumpled, and
distorted.

The subcutaneous cellulo-adipose tissue sometimes becomes œdematous,
sometimes atrophies, and rarely has been known to become
hypertrophied. The bones and joints, finally, may, under the influence
of nerve-irritation, undergo nutritive changes, terminating in various
deformities.

With regard to the trophic changes, as well as to the pain and
paræsthesiæ resulting from nerve-injury, we must bear in mind that
they may be attributed not only to the direct irritation of trophic
and sensitive fibres in the injured nerve, but also, in part, to
influences reflected from abnormally excited nutritive centres in the
spinal cord, and to the spread of the sensitive irritation conveyed to
the brain by the injured fibres to neighboring sensitive centres, thus
multiplying and exaggerating the effect, causing, as it were,
sensitive echoes and reverberations. Indeed, the variety of the
symptoms resulting from apparently similar nerve lesions would seem to
point to the introduction of other factors in their causation than the
simple injuries of the nerve-fibres themselves.

DIAGNOSIS OF NERVE INJURIES.—Although in the great majority of cases
the circumstances attending nerve injuries render their diagnosis a
matter of little difficulty, it is yet important to keep in mind those
symptoms which distinguish them from lesions or diseases of the brain
and spinal cord, inasmuch as in cases of multiple lesion, injuries to
the spinal column, or where the history of the case is imperfect, it
may be difficult to determine to which part of the nervous system,
peripheral or central, some of the gravest resulting troubles are due.
Paralysis, spasm, anæsthesia, atrophy, etc. may be of central or
spinal as well as peripheral origin, and an intelligent prognosis and
rational treatment alike demand that we should distinguish between
them. Moreover, many diseased conditions of the peripheral nerves of
whose pathology we are ignorant, and in which localizing
symptoms—_i.e._ those indicating the exact point at which the nerve is
implicated—are wanting, can only be distinguished as peripheral
affections by the occurrence of symptoms which we {1188} recognize as
identical with those arising from injuries of nerves, in which
definite histological changes are known to occur. Indeed, cases of
disease of the nervous system are not infrequent in which a careful
study of their symptomatology leads to a difference of opinion in the
minds of the best observers as to whether their seat is central or
peripheral. We will notice here some of the prominent symptoms
resulting from nerve injuries which may be useful in distinguishing
peripheral from central lesions, although in many cases it is only by
the careful consideration of all symptoms and the impartial weighing
of all attending circumstances that a probable conclusion can be
arrived at.

The rapid loss of muscular tone and the early atrophy of the muscles
is a mark of paralysis from nerve-injury which distinguishes it from
cerebral paralysis, even when the latter occupies circumscribed areas,
as is sometimes the case in cortical brain lesion. In spinal paralysis
also the muscles retain their tone and volume (the latter being
slightly diminished by disuse), except in extensive destruction of
gray matter, when all tonicity is lost, and in lesions of the anterior
horns of gray matter (poliomyelitis), when there is loss of muscular
tone and marked atrophy. The first of these spinal affections may be
distinguished by the profound anæsthesia and by the paralysis being
bilateral—by the implication of bladder and rectum and the tendency to
the formation of bed-sores; such symptoms being only possible from
nerve-injury when the cauda equina is involved. In poliomyelitis the
complete integrity of sensation—which is almost always interfered with
at some period after nerve-injury—and the history of previous
constitutional disturbance will aid us in recognizing the diseased
condition. While the reflexes are wanting in peripheral, they are, as
a rule, retained, and often exaggerated, in cerebral and spinal
paralysis; the exceptions being in the two lesions of the cord above
mentioned, in which the reflex arc is of course destroyed by the
implication of the gray matter. Loss or alteration of sensation, where
it occurs from nerve-injury, generally shows itself in the
distribution of the nerve, while the sensitive disturbances from
disease or injury of the brain or spinal cord are less strictly
confined to special nerve territories. The trophic disturbances
arising from nerve-irritation are distinctively characteristic of
nerve-injury.

But it is in the behavior of the nerves and muscles to electricity
that we find some of the strongest points on which to base a diagnosis
of nerve-injury, and, although not always conclusive as to the seat of
lesion, it enables us to reduce within very narrow limits the field
for discrimination. The degenerative reaction which we have seen takes
place in muscles the continuity of whose nerves have been destroyed,
or in which degenerative changes have taken place in consequence of
injury to their nerves, is never found in muscles paralyzed from the
brain. In spinal paralysis resulting from transverse myelitis the
electrical excitability of the nerves and muscles may be increased or
diminished, but there is no degenerative reaction. In progressive
muscular atrophy a careful electrical examination may discover the
degenerative reaction in the affected muscles; but it is too obscure,
and there are besides too many characteristic symptoms in that
disease, to allow of a practical difficulty in diagnosis from its
presence. In poliomyelitis anterior (infantile paralysis and the
kindred affection in the adult) we have, it is true, the quantitative,
{1189} qualitative changes of degenerative reaction, such as are seen
after nerve-injury, and in such cases its presence is not conclusive
of peripheral lesion. Here we may be assisted by remembering that
while in poliomyelitis sensation is intact, in nerve-injury it is
almost always affected in a greater or less degree, although it may
have been recognizable but for a short time. In lead paralysis we also
have the degenerative reaction, but whether the seat of lesion in that
affection is central or peripheral is an undecided question.

TREATMENT OF NERVE-INJURIES.—The therapeutics of nerve-injuries belong
largely to surgery. When there is complete division of a nerve the
ends should be united by suture at the time of injury. When this has
not been done, and after the lapse of time no return of function is
observed, the ends of the nerve should be sought for, refreshed with
the knife, and brought together by suture. There is the more hope that
such a procedure will be successful as we know that after a time the
fibres of the peripheral portion of the nerve may be regenerated, even
when there has been no reunion, and thus be in a condition to render
the operation successful. It is a matter for consideration whether in
injuries in which a certain portion of the nerve, not too great in
extent, has been crushed or otherwise obviously destroyed, it would
not be best to excise the destroyed portion and bring the ends
together. Whether the use of electricity, the galvanic current,
hastens the regeneration and restitution of the injured nerves cannot
be affirmed with certainty, although in practice this has seemed to us
to be the case, and the known catalytic action of the current gives us
a possible explanation of such beneficial effects. But, however this
may be, it is certain that with the first symptoms of returning
function in the nerves and muscles the use of electricity obviously
accelerates the improvement. And, again, in the treatment of the
results of nerve-injury, such as paralysis, anæsthesia, pain, it is in
the careful and very patient use of the electric currents, both
faradic and galvanic, that most confidence is to be placed; the
galvanic being generally most applicable and giving the better
results. The symptoms of nerve-irritation are amongst those most
difficult to treat successfully. Counter-irritation, heat, cold,
electricity, may all be tried in vain, and as a last resource against
pain, ulceration, and perverted nutrition we may be obliged to resort
to nerve-stretching, or neurotomy. Under the head of Neuritis much
must be said of treatment applicable to the inflammation, acute and
chronic, resulting from nerve-injuries.


INFLAMMATION OF NERVES.


Neuritis.

Although inflammation of the nerves has been for a long time a
recognized disease, its frequency and the extent and importance of its
results have been appreciated only within a comparatively short time.
The observations upon neuritis were formerly almost exclusively
confined {1190} to acute cases, the results of traumatic lesions or
the invasion of neighboring disease, while the more obscure forms
occurring from cold, toxic substances in the circulation,
constitutional disease, etc., or those apparently of spontaneous
origin, escaped attention, or were classed according to their symptoms
simply as neurosis, functional disease of the nerves, or affections of
the spinal cord. Hence the classic picture of neuritis is made to
resemble exclusively the acute inflammation of other tissues, and
tends to blind as to the subtler but not less important morbid
processes in the nerves which at present we must classify as
inflammation, though wanting, it may be, in some of the striking
features seen in connection with inflammatory processes elsewhere. In
short, we must not look for heat, redness, pain, and swelling as
absolutely necessary to a neuritis.

Entering into the structure of the peripheral nerves we have the true
nervous constituent, the fibres, and the non-nervous constituent, the
peri- and endoneurium, in which are found the blood-vessels and
lymph-channels. Though intimately combined, these tissues, absolutely
distinct structurally and functionally, may be separately invaded by
disease; and although it may not be practicable nor essential in every
case to decide if we have to do with a parenchymatous or interstitial
(peri-) neuritis, it is necessary to keep in mind how much the picture
of disease may be modified according as one or the other of the
constituents of the nerve are separately or predominantly involved.
Thus, a different group of symptoms will be seen when the vascular
peri- and endoneurium is the seat of inflammation from that which
appears when the non-vascular nerve-fibres are themselves primarily
attacked and succumb to the inflammatory process with simple
degeneration of their tissue. Furthermore, it is not too speculative
to consider that the different kinds of nerve-fibres may be liable
separately or in different degrees to morbid conditions, so that when
mixed nerves are the seat of neuritis, motor, sensitive, or trophic
symptoms may have a different prominence in different cases in
proportion as one or other kind of fibres is most affected.

ETIOLOGY.—Traumatic and mechanical injuries of nerves are the most
common and best understood causes of neuritis. Not only may it be
occasioned by wounds, blows, compression, and other insults to the
nerves themselves, but jolting and concussion of the body, and even
sudden and severe muscular exertion, have been recorded as giving rise
to it. We readily understand how neuritis is caused by the nerves
becoming involved in an inflammation extending to them from adjacent
parts, although the nerves in many instances show a remarkable
resistance to surrounding disease. Less easily understood but
undoubted causes of neuritis are to be found in the influence of cold,
especially when the body is subjected to it after violent exertion.
Although the causal connection is unexplained, we find neuritis a
frequent sequel of acute diseases, as typhoid fever, diphtheria,
smallpox, etc. In the course of many chronic constitutional
affections, as syphilis, gout, elephantiasis græcorum, we encounter
neuritis so frequently as to make us look for its cause in these
diseases. Finally, neuritis may develop apparently spontaneously in
one or many nerves.

MORBID ANATOMY.—The macroscopic appearance of nerves affected by
neuritis is very varied, according as the disease is more interstitial
or parenchymatous, acute or chronic. Sometimes the nerve is swollen,
red, {1191} or livid, the blood-vessels distended, with here and there
points of hemorrhage, the glistening white of the fibres being changed
to a dull gray. Sometimes the nerves are reduced to gray shrunken
cords. When the perineurium has been the principal seat of the
inflammation we may have swellings at intervals along the course of
the nerve (neuritis nodosa, perineuritis nodosa acuta) or, as in
chronic neuritis, the trunk of the nerve may be hard and thickened
from proliferation of the connective tissue, sclerosis of the nerve.
The nerve does not always present the appearance of continuous
inflammation, but the evidence of neuritis may be seen at points along
its course which are separated by sound tissue. These points of
predilection are usually exposed positions of the nerve or near
joints. Often the nerve appears to the naked eye normal, and the
characteristic changes of neuritis are only revealed by the
microscope. The microscopical changes in neuritis may extend to all of
the constituents of the nerve, and present the ordinary picture of
acute inflammation, hyperæmia, exudation, accumulation of white
corpuscles in the tissues, and even the formation of pus, the
nerve-fibres exhibiting in various degrees the destruction of the
white substance of Schwann and the axis-cylinder. Or, as in chronic
neuritis, the alterations may consist in the more gradual
proliferation of the peri- and endoneurium, which, contracting,
renders the nerve dense and hard and destroys the nerve-fibres by
compression. In acute as well as in chronic neuritis the perineurium
may be exclusively affected, the fibres remaining normal (Curschman
and Eisenlohr). The nerve-fibres themselves may be the primary and
almost exclusive seat of the neuritis, exhibiting more or less
complete destruction of all their constituent parts, except the sheath
of Schwann, without hyperæmia and with little or no alteration of the
interstitial tissue. Sometimes the fibres are affected at intervals,
the degeneration occupying a segment between two of Ranvier's nodes,
leaving the fibre above and below normal (nèvrite segmentaire
peri-axile, Gombault). All of these lesions of the nerve-fibres may be
recovered from by a process of regeneration, the fibres showing a
remarkable tendency to recover their normal structure and function.

SYMPTOMS OF NEURITIS.—When a mixed nerve is the seat of an acute
neuritis, with hyperæmia of its blood-vessels, it becomes swollen by
inflammatory exudation, and can be felt as a hard cord amongst the
surrounding tissues. It is not only highly sensitive to direct
pressure, but muscular exertion, or even passive movement of the part,
excites pain. Spontaneous pain is one of the most prominent symptoms,
and is sometimes so severe and continuous as to destroy the
self-control of the patient, and demand the employment of every agent
we possess for benumbing sensibility and quieting the excited system.
At first there may be hyperæsthesia of the skin in the region of the
distribution of the nerve, but a much more constant and significant
symptom is cutaneous anæsthesia, which generally makes its appearance
early in the course of the disease. The degree and extent of the
anæsthesia varies very much in different cases, but is seldom total,
except over small areas, even when the inflammation has seriously
damaged the nerve-fibres. This is explained by the sensibility
supplied to the part by neighboring nerves, as already described in
treating of traumatic nerve-injuries. Very characteristic of acute
neuritis are various abnormal sensations (paræsthesiæ) which are
{1192} developed in a greater or less degree during the progress of
the disease, and are described by the patients as numbness, tingling,
pins and needles, burning, etc. In a case of acute neuritis of the
ulnar nerve seen by the writer the patient was much annoyed by a
persistent sensation of coldness in the little and ring fingers, which
caused him to keep them heavily wrapped up even in the warm weather of
summer. When motor symptoms make their appearance they begin with
paresis of the muscles, which may increase rapidly to paralysis. As
this is the result of destructive changes, more or less complete, in
the motor nerve-fibres, we will have, as would be expected,
accompanying the paralysis the symptoms already detailed in the
consideration of nerve-injuries with destruction of continuity—namely,
absence of muscular tone, loss of skin and tendon reflexes, increased
mechanical excitability, atrophy of muscles, and the different forms
of degenerative reaction, with loss of faradic contractility. When
spasm or tremor has been observed in acute neuritis of mixed nerves,
it is a matter of doubt whether it is not to be explained by reflex
action of the cord excited by irritated centripetal fibres. Various
trophic symptoms may show themselves, as herpes zoster or acute œdema.
Erythematous streaks and patches are sometimes observed upon the skin
along the course of the inflamed nerve-trunks. In chronic neuritis,
into which acute neuritis generally subsides or which arises
spontaneously, the symptoms above described are very much modified;
indeed, cases occur which exist for a long time almost without
symptoms. While the affected nerve may be hard and thickened by
proliferation of its connective tissue, pain, spontaneous or elicited
by pressure, is not of the aggravated character present in acute
neuritis, and may be quite a subordinate symptom. It has more of a
rheumatic character, is less distinctly localized, more paroxysmal,
and has a greater tendency to radiate to other nerves. It is probable
that many ill-defined, so-called rheumatic pains which are so
frequently complained of are the result of obscure chronic neuritis.
Anæsthesia and various paræsthesiæ are often more prominent symptoms
than pain. Sometimes there is a hyperæsthesic condition of the skin,
in which touching or stroking the affected part causes a peculiarly
disagreeable nervous thrill, from which the patient shrinks, but
which, however, is not described as pain.

The motor symptoms in chronic neuritis of mixed nerves often remain
for a remarkably long time in abeyance or may be altogether wanting.
They may appear as tremor, spasm, or contraction, these, however,
being probably reflex phenomena. Most commonly there is paresis, which
may deepen into paralysis with atrophy of muscles and degenerative
reaction. The trophic changes dependent on chronic neuritis are
frequently very prominent and important. The skin sometimes becomes
rough and scaly, sometimes atrophied, smooth, and shining (glossy
skin). Œdema of the subcutaneous cellular tissue is often seen, for
example, on the dorsum of the hand, where it may be very marked. The
hair of the affected part shows sometimes increased growth, sometimes
it falls off. The nails may become thickened, ridged, and distorted.
Deformity of joints with enlargement of the ends of the bones is not
infrequently met with as the result of chronic neuritis. In short, we
may meet with all of those trophic changes which have been described
as arising from nerve-irritation, and which occur in chronic neuritis
as the result of compression of {1193} nerve-fibres by the contraction
of the proliferated connective tissue in the nerve-trunk.

The symptom-complex varies greatly in neuritis, so that there is
hardly a symptom which may not be greatly modified or even wanting in
some cases—a fact, which, as we have already said, may be explained by
the morbid process fixing itself exclusively or in different degrees
upon one or other of the component parts of the nerve-trunk, or, it
may be, upon fibres of different functional endowment. Thus pain,
usually one of the most prominent symptoms of neuritis, may be quite
subordinate, or even absent, in cases of neuritis acute in invasion
and progress. In a case of neuritis of the ulnar nerve seen by the
writer, beginning suddenly with numbness and paresis, and rapidly
developing paralysis, atrophy of muscles, loss of faradic
contractility, with degenerative reaction, there was no pain during
the disease, which ended in recovery.[7] On the other hand, in mixed
nerves the sensitive fibres may be long affected, giving rise to pain
and various paræsthesiæ before the motor fibres are implicated, or
these last may escape altogether.

[Footnote 7: “Two Cases of Neuritis of the Ulnar Nerve,” _Maryland
Medical Journal_, Sept., 1881.]

The swollen condition of the nerve, so characteristic in many cases of
neuritis where the perineurium is the seat of a hyperæmia, is wanting
in cases where the stress of the attack is upon the nerve-fibres
themselves. Again, the trophic changes induced in the tissues by a
neuritis may predominate greatly over the sensitive or motor
alterations. Thus, in the majority of cases in which herpes zoster
occurs it is without pain or paræsthesia. Indeed, in chronic neuritis
the symptoms show such variations in different cases that it is
difficult to give a general picture of the disease sufficiently
comprehensive and at the same time distinctive. The prognosis in acute
neuritis is generally favorable, although it must depend in a great
measure upon the persistence of the cause producing it. Thus, if it
has been excited by the inflammation of neighboring organs it cannot
be expected to disappear while these continue in their diseased
condition. In other cases the symptoms may subside with comparative
rapidity; and so great is the capacity of the nerve-fibres for
regeneration that recovery may be complete and nothing remain to
indicate the previous inflammation. The nerve, however, that has once
suffered from neuritis shows for a long time a tendency to take on an
inflammatory action from slight exciting causes. If there has resulted
an atrophy of muscles, we must expect some time to elapse before they
recover their functional activity and normal electric reaction.

Acute neuritis most frequently passes into the chronic form, and it
may then drag on indefinitely, stubbornly resisting treatment and
giving rise to permanent derangement of sensibility, loss of muscular
power, or perverted nutrition. Neuritis shows a tendency to spread
along the affected nerve centripetally, sometimes reaching the spinal
cord, and, as it has appeared in some cases, even the brain, causing
tetanus or epilepsy.

Reflex paralyses, which at one time were believed to be the not
infrequent result of nerve-irritation and inflammation, affecting from
a distance the functions of the spinal cord, have been shown to be the
effect of an extension of the lesion of the inflamed nerve to the
cord, causing organic disease. Instances of the extension of a
neuritis to distant nerves, as those of an opposite extremity, without
the implication of the spinal {1194} cord (neuritis sympathica), are
most probably cases of multiple neuritis, to be considered farther on.

The DIAGNOSIS of cases of traumatic neuritis can scarcely present a
difficulty. Acute neuritis with spontaneous pain, swelling, and
tenderness of the nerve, presents distinctive features hardly to be
confounded with any other affection, although thrombosis of certain
veins, as the saphenous, may present some of its symptoms. To
distinguish chronic neuritis or the cases wanting those obvious
symptoms just indicated (many cases of sciatica) from neuralgia is a
more difficult task. The following distinctive points may be noted: In
neuritis the persistent and continuous character of the pain helps us
to distinguish it from the more paroxysmal exacerbations of neuralgia,
and its tendency, often seen, to spread centripetally spontaneously or
when pressure is made on the nerve, may be also considered as
characteristic of neuritis. Cutaneous anæsthesia, paresis, and atrophy
of muscles are distinctive in any case of a neuritis rather than a
neuralgia. Herpes zoster and other trophic changes speak strongly for
a neuritis.

In the TREATMENT of neuritis the first indication is to get rid, as
far as possible, of such conditions as may cause or keep up the
inflammation, as, for instance, the proper treatment of wounds, the
removal of foreign bodies, the adjustment of fractures, the reduction
of dislocations, the extirpation of tumors, etc. Absolute repose of
the affected part in the position of greatest relaxation and rest is
to be scrupulously enforced. In acute neuritis local abstraction of
blood by leeches and cups in the beginning of the affection is of the
greatest advantage and should be freely employed. The application of
heat along the course of the inflamed nerve has appeared to us
preferable to the use of ice, although this also may be employed with
excellent effect. The agonizing pain must be relieved by narcotics,
and the hypodermic injection of morphia is the most efficient mode of
exhibition. Salicylic acid or salicylate of sodium in large doses
contributes to control the pain. Iodide of potassium in large doses
appears to act beneficially, even in cases with no syphilitic
complications. In subacute or chronic neuritis local bloodletting is
not as imperatively demanded as in the acute form, although it is
sometimes useful. Here counter-irritation in its various forms and
degrees, even to the actual cautery, is to be recommended. An
excellent counter-irritation is produced by the application of the
faradic current with the metallic brush. It appears from general
experience that the counter-irritation has the best effect when
applied at a little distance from the inflamed nerve, and not directly
over its course. In the galvanic current we possess one of the very
best means not only for relieving the symptoms of chronic neuritis,
but for modifying the morbid processes in the nerve and bringing about
a restoration to the healthy condition. Its application is best made
by placing the anode or positive pole as near as possible to the seat
of the disease, while the cathode or negative pole is fixed upon an
indifferent spot at a convenient distance. The positive pole may be
held stationary or slowly stroked along the nerve. Finally, in
protracted cases nerve-stretching may be resorted to with great
benefit. It probably owes its good effects to the breaking up of
minute adhesions which have formed between the sheath of the nerve and
the surrounding tissues, and which act as sources of irritation.


{1195} Multiple Neuritis, Multiple Degenerative Neuritis,
Polyneuritis.

Cases of this important form of neuritis have been observed and
recorded since 1864, but the resemblance of its symptoms to those of
certain diseases of the central nervous system (poliomyelitis,
Landry's paralysis, etc.) has prevented its general recognition, and
it is only within the last few years that its distinctive pathological
lesions have been demonstrated and its diagnosis made with
considerable certainty. We can hardly overrate the importance of this
in view of the great difference in gravity of prognosis between it and
other diseases with which it may be confounded.

Multiple neuritis consists in a simultaneous or more or less rapidly
succeeding inflammation of several or many usually bilaterally
situated nerves, with a greatly preponderating, almost exclusive,
lesion of the motor fibres. Commonly the disease attacks the lower
extremities and progresses upward, although occasionally it has been
seen to begin in the arms. It does not confine itself to the nerves of
the extremities and trunk, but often involves the phrenics, causing
paralysis of the diaphragm, and frequently invades one or more of the
cranial nerves, notably the vagus, thus giving rise to the rapid
heart-beat so often seen in the disease. In the cases of multiple
neuritis observed the muscles of deglutition have never been
paralyzed. The sphincter ani and bladder have likewise escaped. All
degrees of acuteness are observed in the course it runs, from the
cases terminating rapidly in death to those in which the disease
extends over months, slowly involving nerve after nerve, until nearly
all of the muscles of the body are paralyzed, when death may result or
a more or less complete recovery take place. The invasion of the
disease is in most cases sudden, even when its subsequent course is
chronic, and is often marked by decided constitutional disturbance, as
rigors, fever, delirium, albuminuria, etc. Disturbances of sensation
are prominent among the initial symptoms, and are of great importance
for the diagnosis of the disease. Severe, spontaneous, paroxysmal pain
of a shooting, tearing character has ushered in most of the cases on
record, remitting, however, during their progress. Pain is not always
present, nevertheless, and cases not infrequently occur which run a
painless course. In some cases which have come under the writer's
notice spontaneous pain did not occur until some days after the
disease was fully declared by other symptoms. More constantly present,
and more characteristic of multiple neuritis, are the disturbances of
sensation which show themselves in subjective feelings of numbness,
tingling, pins and needles, coldness, burning, and other paræsthesiæ,
which appear at its outset and continue to be present more or less
during its course. Anæsthesia, not of a high degree nor at all
coextensive with the paralysis of the muscles—sometimes, indeed,
confined to very circumscribed areas—may be said to exist always in
multiple neuritis—a fact of great diagnostic value. Hyperæsthesia of
the skin is frequently seen. Hyperalgesia and analgesia are sometimes
observed. Hyperæsthesia of the muscles is a very marked symptom in
almost every case, and shows itself not only upon direct pressure
being made, but also in the pain elicited by passive movements of the
parts affected. Pressure upon nerve-trunks does not cause pain as
{1196} invariably as might have been expected from the location of the
disease. Delayed sensation has been frequently observed.

Paresis of muscles, often commencing suddenly, is early seen in
multiple neuritis, and increases until there is more or less complete
paralysis, the most important feature of the disease. The paralyzed
muscles present the flabby condition characteristic of muscles
deprived of the tonic influence of the spinal cord. Atrophy, which is
not commensurate, however, with the paralysis, soon begins, and may go
on to an extreme degree. As the paralysis develops the tendon reflexes
are lost, and there may be diminution or loss of the skin reflexes
also. The paralyzed muscles lose their faradic contractility, and
exhibit diminution of electric excitability to the galvanic current,
and, finally, the various forms of degenerative reaction. It is
remarkable that neither the impairment of sensation nor the paralysis
is, as a rule, strictly confined to the areas of distribution of
particular nerves, but is diffused over regions of the body. Thus in
the limbs the motor and sensory symptoms are most marked at their
extremities, gradually diminishing toward the trunk. In some cases
multiple neuritis appears to have occasioned the inco-ordinate
movements of locomotor ataxy. In the progress of the disease a
rigidity and contracted condition of muscles may be developed,
occasioning a fixed flexion of some of the joints. Profuse sweating,
œdema of the hands and feet, trophic changes in the skin, mark at
times the implication of trophic and vaso-motor nerves. Bed-sores do
not occur.

The pathological changes in pure cases of multiple neuritis are found
in the nerve-trunks, mainly toward their peripheral terminations, and
in their muscular branches, the evidences of disease diminishing
toward the larger trunks, the nerve-roots being unaffected and the
spinal cord showing no lesions. Sometimes the affected nerves present,
even to the naked eye, unmistakable proof of acute inflammation. They
are reddened by hyperæmia, swollen by exudation, and small
extravasations of blood may be seen among their fibres. The microscope
shows congestion of the blood-vessels, exudation of the white
corpuscles, even to the formation of pus, alteration of the endo- and
perineurium; in short, all the evidence of an interstitial
inflammation, the nerve-fibres being comparatively little altered, and
suffering, as it were, at second hand. In most of the cases, however,
the nerves macroscopically present little or nothing giving indication
of disease. The microscopic changes, however, are extensive, and
pertain almost exclusively to the nerve-fibres themselves. These are
altered and degenerated, giving an appearance almost precisely the
same as already described in treating of the changes occurring in
nerves separated by injury from the centres—Wallerian degeneration.[8]
There is no hyperæmia, thickening, or change in the endoneurium. So
great are these differences in the microscopic appearance of the
nerves in different cases of multiple neuritis that objection has been
raised to classing the two varieties together, and it has been argued
that we cannot with right designate the cases in which hyperæmia and
other evidence of {1197} a general inflammation are absent as
neuritis. It has been, however, argued—apparently, to the writer, with
better reason—that the same morbid influence which at one time affects
the blood-vessels, causing their congestion and the passage through
their walls of the white corpuscles and the exudation of inflammation,
may at another time, by a direct and isolated influence upon the
nerve-fibres, cause their degeneration; in other words, that there may
be a parenchymatous neuritis, which shall affect only the
nerve-fibres. The vastly disproportionate implication of the motor
fibres would point to the fact of a selective infection in multiple
neuritis of certain fibres, as there is a selective infection in
poliomyelitis of the motor cells of the anterior horns of the spinal
gray matter.

[Footnote 8: Gombault's observations (_Arch. de Névrologie_, 1880)
would seem to show that there is a difference in the lesion of the
fibres in neuritis from that in simple Wallerian degeneration,
inasmuch as that in the former the first alteration is seen about the
nodes of Ranvier, and occurs at points separated from each other by
healthy fibre, and also in the more tardy destruction of the
axis-cylinder.]

ETIOLOGY.—Much in the symptomatology of multiple neuritis, especially
of its invasion, strongly urges us to the conclusion that it is a
constitutional disease caused by an unknown morbid influence, the
stress of which falls upon the nervous system. This view receives
strong support from the history of the Japanese kak-ke or Indian
beriberi, a disease at times epidemic in those countries, and which
has the undoubted symptoms and the characteristic pathological
alterations of multiple neuritis. After many acute infectious diseases
neuritis of individual nerves is not uncommon, but the distinctive
characteristics of multiple neuritis have, so far, been observed
almost exclusively after diphtheria, to which it is not infrequently a
sequel. It has been observed as the result at least occurring in
intimate connection with polyarthritis, and the frequency with which
it has occurred in the phthisical is remarkable. There have been not a
few cases of multiple neuritis recorded as having been produced by
chronic alcohol-poisoning. A well-marked case has come under the
writer's observation in which the immediate cause was acute poisoning
by arsenious acid, a very large amount having been taken at one dose
by mistake. The poison of syphilis has been regarded as standing in a
causal relation to multiple neuritis. For the rest, the exciting
causes (probably acting in connection with a peculiar condition of the
system) have appeared to be exposure to cold, great muscular exertion,
direct mechanical injury to the nerves, as the rough jolting of a
wagon, or the inflammation of a nerve which has in some unknown way
extended to others.

The DIAGNOSIS of multiple neuritis in certain cases presents great
difficulty, from the close resemblance of its symptoms to those of
poliomyelitis. The prominent symptoms in the muscular system—viz.
paralysis, atrophy, the degenerative reaction—are the same in both. It
may be remarked, however, that in multiple neuritis the paralysis is
more generally diffused over the muscles of the affected limbs, while
in poliomyelitis it is more confined to the areas of distribution of
particular nerve-branches. Pain is common to the beginning of both
diseases, but it generally passes off more quickly and completely in
poliomyelitis. The persistent hyperæsthesia of the muscles is wanting
in poliomyelitis. But it is in the diminution and alteration of
sensation that we have the surest means of distinguishing between the
two affections. This symptom seldom or never fails to show itself in
multiple neuritis, although its area may be circumscribed and it may
be slight in degree, while it certainly makes no part of the
symptomatology {1198} of poliomyelitis. It has been asserted that the
implication of the cranial nerves so often seen in multiple neuritis
never occurs in poliomyelitis. When we consider the intimate
connection of the anterior horns of the spinal gray matter with the
motor nerve-fibres, it appears highly probable that the same morbid
influence may invade both simultaneously or in quick succession, thus
producing a complex of symptoms rendering a diagnosis very difficult,
and probably giving rise to some confusion in the recorded symptoms of
multiple neuritis. From Landry's paralysis multiple neuritis is to be
distinguished by the impairment of sensibility, the loss of faradic
contractility, and absence of the tendon reflex; from progressive
muscular atrophy, by the loss of sensibility and the much more obvious
degenerative reaction.

The PROGNOSIS of multiple neuritis is in the great majority of cases
not grave, so far as life is concerned, even when there is extensive
paralysis. Death may occur early in the acute form of the disease or
it may take place at the end of chronic cases. When the disease proves
fatal, it is from paralysis of the diaphragm and the other muscles of
respiration. Where the paralysis and atrophy have been great, showing
profound alteration of the nerves, a long time is required for
recovery, and more or less paralysis, contracture, or defective
sensibility may permanently remain.

The TREATMENT consists, at the outset, in rest and position, the local
abstraction of blood (in cases where the nerve-trunk is swollen and
tender), and the administration of such drugs as we suppose act
favorably upon the inflammation of the nerves. Salicylic acid or
salicylate of sodium seem to act beneficially in relieving the severe
pains in the outset of the disease. Iodide of potassium, gradually
increased until large doses are taken, has, in the experience of the
writer, seemed to beneficially modify the course of multiple neuritis.
The necessary relief of pain is best obtained by hypodermic injections
of morphia, supplemented by heat applied to the affected nerves. To
these means may be added rubbing with chloroform and applying to the
painful parts cloths dipped in a 5 per cent. solution of carbolic
acid. After the acute stage has been passed and in chronic cases, just
as soon as we have reason to suppose that the degenerative process in
the nerves has come to a standstill, we possess in the use of
electricity the means of hastening the regeneration of the
nerve-fibres, strengthening the paralyzed muscles, and restoring the
sensation. The galvanic current is to be preferred, and it is to be
applied to the crippled nerves and muscles—sometimes stable for its
electrolytic action, sometimes interrupted to obtain its exciting and
stimulating effect. The excitement to nerves and muscles by the use of
the faradic current has also its uses in hastening recovery.
Protracted treatment and much patience are required to overcome
contractions and restore the nerves and muscles, and the effects of
the disease may be seen for a long time in the weakness and diminished
electric reaction of the muscles.


Anæsthesia of Peripheral Origin.

A prominent and important symptom of the lesion of peripheral nerves
is the diminution and loss of cutaneous sensibility. Besides the
{1199} anæsthesia caused by the affections of the fibres themselves,
which has been touched upon in the preceding pages, it may be produced
by morbid states of the peripheral end-organs or cutaneous
terminations of the nerves. Cold applied to a nerve-trunk may produce
alterations which for days after cause numbness and paræsthesia in the
surface to which it is distributed, and the application of cold to the
surface of the body, as we know from common observation, causes
blunting of the cutaneous sensations, especially that of touch. In
this way, from exposure to the atmosphere at low temperatures, to cold
winds, or by the immersion of the body in cold water, the end-organs
of the nerves in the skin are morbidly affected, and anæsthesia
results, the so-called rheumatic anæsthesia. Many substances, as
acids, notably carbolic acid, alkalies, narcotics, etc., act upon the
cutaneous end-organs in a way to destroy their capacity for receiving
or transmitting impressions and produce a more or less persistent
anæsthesia of the skin. In the anæsthesia so often observed in the
hands and forearms of washerwomen we have an example of the action
probably of several of these causes, as the frequent plunging of the
hands into cold water and the action upon the skin of alkalies and
alkaline soaps. The diminution or interruption of the circulation
through the skin, as in ischæmia from spasm of the minute arteries due
to an affection of the vaso-motor nerves, is also a cause of cutaneous
anæsthesia. In lepra anæsthetica (Spedalskhed) the cutaneous
anæsthesia is dependent upon a neuritis of the minute branches in the
skin. The local anæsthesia met with so often in syphilis, though its
pathology is doubtful, is not improbably sometimes caused by an
affection of the peripheral nerves (neuritis?) and their end-organs.
After many acute diseases, diphtheria, typhoid fever, etc., we have
cutaneous anæsthesia in connection with muscular paralysis, the cause
of both being a neuritis. The patient is made aware of the loss of
sensation by some interference with his usual sensations and
movements. If he puts a glass to his lips, the sensation is as if a
bit were broken out of the rim; his accustomed manipulations are
awkward, because of the want of distinct appreciation of the objects
he holds; he fumbles in buttoning his clothes or he stumbles unless
looking to his steps. An examination, nevertheless, almost always
reveals that the anæsthesia is greater than would have been supposed
from the subjective feelings of the patient; indeed, cases occur in
which he is not aware of an existing defect of sensation. But a
careful examination is not only required to determine the extent, but
by it alone can we arrive at a knowledge of the quality of the
anæsthesia—viz. whether there is a loss of all of the different kinds
of sensation, whether they are affected in an unequal degree, or
whether some have entirely escaped. Thus we must test for the
acuteness of the simple sense of touch by comparing the sensations
elicited by the contact of small surfaces of unequal size, as the
point and head of a pin or pencil, observing the appreciation by touch
of the patient for different substances, as woollen, silk, linen,
cloth, or comparing the sensation of the anæsthesic part with the same
part on the opposite healthy side of the body. The sense of locality
and space may be examined by placing at the same instant upon the skin
of the patient, his eyes being closed, two points (the anæsthesiometer
or the points of a compass), and observing his capacity for
appreciating the impression as double. As there is an enormous
difference of acuteness of the {1200} space-sense in the skin of
different parts of the body (see textbooks of physiology)—ranging from
the tip of the tongue, where the touch of two points separated 1.2 mm.
gives a double sensation, to the thigh, where the points must be
separated 77 mm. to be felt as two—we must be careful to consider in
making the examination the normal space-perception of the region. Care
must be taken not to repeat the test too often, as a rapid education
of the surface to a more delicate appreciation of the impressions is
the result. In certain abnormal conditions from spinal disease we have
a condition of polyæsthesia in which the impression of one point is
felt as two or more. The sense by which we appreciate the pressure of
objects must be tested by placing upon the surface to be examined, in
succession, objects of different weight, care being taken to have the
area which touches the skin and the temperature the same in each. The
parts to be tested must be firmly supported, and all muscular
contraction on the part of the patient prevented. The temperature
sense is examined by the application of hot and cold water or bodies
of different temperature. We sometimes meet with a perversion of this
sense in which the application of a cold surface to the skin gives the
sensation of warmth, and the contrary. In testing the sense of
temperature and the sense of pressure it is not the absolute capacity
of appreciating on the part of the patient that we investigate, but
the power of discriminating between different degrees of temperature
or pressure. The sense of pain must likewise be tested, since morbid
conditions occur in which it may be caused more readily than is normal
by exciting the cutaneous nerves, and that, too, in parts which have
in a great measure or quite lost the sense of touch; or, on the other
hand, touch may be retained, while irritation of the skin can excite
no feeling of pain (analgesia). We have in the faradic current an
excellent means of testing the cutaneous sensibility, inasmuch as it
excites the skin over the various parts of the body about equally, and
it can be employed in very gradually increasing or decreasing
strength. Its effects on the affected part must be compared with those
produced on the healthy surface of other parts of the patient's body
or on healthy individuals.

Frequently accompanying cutaneous anæsthesia, but constituting no part
of it, are various paræsthesiæ, as formication, pins and needles,
burning, etc. Pain, sometimes of great intensity, is not infrequently
connected with it (anæsthesia dolorosa). The paræsthesiæ and pain are
the result of irritation in some portion of the conducting tracts,
and, together with the trophic changes so often seen in connection
with nerve-injuries, they have been already considered under that
head.

It is a very important point to make the diagnosis between central and
peripheral anæsthesia, but it is often a matter of great difficulty,
and sometimes not to be made at all. The history of the case must be
carefully considered, and an examination made for symptoms of brain or
spinal disease, the existence of nerve lesions, or if there is a
history of toxic influences, etc. In peripheral anæsthesia the
reflexes which may be normally excited from the affected surface are
wanting, in contradistinction to anæsthesia of central origin, in
which they are most generally retained or even increased. Concomitant
trophic changes speak strongly for a peripheral origin, as do also
paralysis and atrophy of muscles. {1201} Loss of some of the forms of
sensation, with retention of others—_i.e._ partial paralysis of
sensation—indicate a central origin.

The TREATMENT of peripheral anæsthesia must look, in the first place,
to removal, if possible, of its cause, and the treatment of diseased
conditions, if any exist, of the nerve-trunks, as neuritis, mechanical
injuries, etc. Local applications of a stimulating character may be
advantageously used upon the anæsthesic parts. By far the most
effective stimulant to the diseased nerves is the faradic or galvanic
current, and it should be used in the way that will produce the
greatest amount of excitation in the cutaneous end-organs. This is
best done by applying the faradic current to the dry skin with the
metallic brush, or by allowing the cathode of the galvanic current to
rest upon it for some time.

The PROGNOSIS in peripheral anæsthesia is in the main favorable, but
it must, of course, depend much on the gravity of the lesion causing
it, as mechanical injury, pressure, neuritis, cold, etc. Rheumatic
anæsthesia, the result of exposure to cold, is in general readily
recovered from. Vaso-motor anæsthesia yields in most cases without
difficulty to treatment. Washerwoman's anæsthesia and allied cases are
intractable, and often resist the patient and well-conducted
application of remedies.

As a concrete picture of peripheral anæsthesia we will give a
description of anæsthesia of the fifth nerve—the rather that in its
consideration we meet with some of the most interesting and important
complications occurring in connection with paralysis of sensitive
nerves. The fifth nerve may have either of its three branches
separately affected, giving rise to anæsthesia limited to the
distribution of that branch, or all of its fibres may be
simultaneously involved, giving rise to complete anæsthesia of the
nerve. In the latter case the lesion of the nerve in all likelihood
exists at some point of its course between the apparent origin from
the pons and the ganglion of Gasser, which rests upon the apex of the
petrous portion of the temporal bone. Beyond this point the nerve
divides into its three branches. Amongst the causes of trigeminal
anæsthesia are injuries, tumors, syphilitic thickening of the dura
mater, neuritis, etc., affecting the nerve within the cranial cavity.
In complete anæsthesia of the fifth nerve the parts implicated are the
skin of the forehead to the vertex, the nose, the lips, and chin up to
the median line, the cheek and temporal region, including the anterior
portion of the ear, the conjunctiva, the mucous membrane of the nose,
the mucous membrane of the mouth, and partly of the fauces of the same
side. The tongue is deprived not only of common sensation on the
affected side in its anterior two-thirds, but the sense of taste is
also lost over the same region, by reason that the fibres of the
chorda tympani, the nerve of taste for this region of the tongue, are
derived from the fifth nerve. If the whole thickness of the
nerve-trunk is involved, including the small motor root, there is, in
connection with the anæsthesia, paralysis of the muscles of
mastication on the side affected, which may be distinguished by the
want of hardening of the masseter when the jaws are forcibly brought
together, and by the thrusting of the chin over to the paralyzed side
when the mouth is widely opened, caused by the want of action of the
external pterygoid muscle, which allows the condyle on the paralyzed
side to remain in the glenoid fossa, while the condyle of the opposite
side is pulled forward upon the articular eminence by the sound {1202}
pterygoid. The face is of a dusky or livid color, and cooler than
natural. Ulcers of a stubborn character in the mucous membrane of the
cheek may be caused by the patient unconsciously biting the
insensitive parts. An inflammation of the conjunctiva is frequently
set up, which may extend to the cornea, causing ulceration,
perforation, panophthalmitis, and destruction of the eye (ophthalmia
neuro-paralytica). This has been regarded by some as caused by trophic
changes in the tissues, the direct result of irritation or destruction
of trophic fibres connected with the ganglion of Gasser. Experiments
made upon animals, however, seem to show that the inflammation of the
eye depends upon the irritation caused by the intrusion of foreign
bodies, which, owing to the loss of sensation, are not appreciated,
and which from loss of reflex action are not removed by winking nor
washed away by an increased lachrymal secretion, as in the healthy
eye. It may be that although the latter is the true explanation of the
origin of the inflammation, nevertheless the tissues may have lost
their normal power of resistance to its invasion by reason of
nutritive changes consequent upon the lesion of trophic fibres running
in the trunk of the nerve. The reflexes ordinarily induced by
irritation of the parts in their normal state are lost. Irritation of
the conjunctiva causes no winking of the lids nor secretion of tears,
and titillation of the nostrils no movements of the muscles of the
face nor mucous or lachrymal secretion. The movements of the face are
less lively on the affected side, not on account of paralysis of the
muscles, but from the loss of that constant play of reflex activity in
them which takes place in the normal condition. The loss of the
reflexes distinguishes peripheral trigeminal anæsthesia from that of
cerebral origin, in which they may still be excited by irritating the
anæsthesic surfaces. In trigeminal anæsthesia, which sometimes occurs
from the effect of cold upon the surface of the face, the mucous
surfaces are not affected.

The SYMPTOMS and DIAGNOSIS of peripheral paralysis having been already
given under the heads of Injuries of Nerves and Neuritis, a
consideration of the distribution of any motor nerve will enable us to
anticipate the distinguishing features of the paralysis dependent upon
it. With each the picture will be modified according to the position
of the muscles paralyzed and the motor functions destroyed. It now
remains to give the symptoms, diagnosis, and treatment of the
paralysis of an individual motor nerve, which may serve as an example
and paradigm, in the consideration of which points of interest and
instruction may be touched upon applicable to all other cases.


Peripheral Paralysis of the Facial Nerve (Bell's Paralysis).

Of all the peripheral paralyses, probably that of the seventh is the
one we are most frequently called upon to treat and the symptoms of
which are the most complex and interesting. The frequency of its
paralysis is due to the length and peculiarity of its course, enclosed
as it is in a bony canal which permits no increase of its volume
without compression, the run of its terminal branches through parts
liable to inflammation and disease (parotid gland), and their final
distribution to parts exposed to all vicissitudes of heat and cold and
in constant danger of mechanical injury. {1203} The complexity and
interest of the symptoms of its paralysis depend in a great measure
upon the intimate connections it forms at different points of its
course with the fibres of other nerves of entirely different functions
(acoustic and fifth).

The seventh nerve is liable not only to intercranial compression from
tumors, inflammation of the meninges, syphilitic processes, etc., but
its long course through the petrous portion of the temporal bone
renders it liable to injury from fracture or caries, and its close
proximity to the middle ear causes it often to suffer from the
diseased conditions of the bony walls or mucous lining membrane of
that chamber, its paralysis being not infrequently the result of
simple aural catarrh. After the exit of the nerve from the
stylo-mastoid foramen it is imbedded in the parotid gland, and
sometimes suffers from compression produced by an inflammation or
abscess in that organ or by enlarged lymphatic glands in the
neighborhood. Surgical operations, so often demanded for disease of
the bones or soft parts of the face, may necessitate the lesion of its
trunk or branches. The exposed position of this nerve is sometimes the
occasion of its injury at the very outset of the life of the
individual, when the application of the forceps to the head has been
resorted to in delivery. But the most frequent cause of facial
paralysis appears to be the exposure of one side of the face directly
to cold—as sleeping in a draught of air, sitting at the open window of
a railroad coach, etc. Here the causal connection appears evident from
the rapidity with which the paralysis usually follows, although cases
occur in which an interval of hours or days elapses after the exposure
before the paralysis declares itself. Although this is usually
designated rheumatic paralysis, there is nothing to connect it with
that disease, nor are rheumatics more liable to it than others. Under
such circumstances the paralysis is probably brought about by the
occurrence of a neuritis of the nerve-trunk, which is compressed by
the hyperæmia, and it may be by an inflammatory exudation against the
bony walls surrounding it, until not only does it lose the power of
conduction, but its fibres undergo the degenerative process. In some
cases the neuritis thus excited by exposure to cold attacks the nerve
after it has issued from the bony canal, and then the resulting injury
to the fibres is much less grave. Although in some cases there are
prodromal symptoms, as stiffness or pain in the face, generally the
paralysis occurs suddenly, very often being first observed upon
awaking. The patient may be first made aware of the paralysis by an
inability to drink without the fluid dribbling from the affected side
of the mouth or by the overflow of tears from the eye of the same
side. When the paralysis is recent and the face in complete repose,
there may be little or no deformity to mark the condition of the
muscles. When, however, the patient speaks or the slightest emotional
or reflex movements of the face are excited, as laughing, frowning,
etc., it becomes obvious from the bizarre grimace caused by a
one-sided contraction. After the paralysis has existed for some time
the contrast of the two sides of the face is marked. The paralyzed
side is characterized by a vacancy of expression to which the staring,
unwinking eye contributes. From loss of the tonicity of the muscles
the angle of the mouth droops, and the expressive furrows and lines
about the brow, below the eye, and beside the nose are smoothed out
and obliterated. Speech is affected, inasmuch as the paralysis of the
{1204} lip interferes with the pronunciation of the labials, and all
attempts to purse up the mouth, as in whistling, is abortive. The eye
not only remains open, the lids motionless, but there is partial
eversion of the lower lid (lagophthalmos), and the tears, no longer
directed to the punctum (paralysis of Horner's muscle), flow over the
cheek. The natural impulse to reflex winking caused by evaporation
from the conjunctiva or by the contact of particles of dust is
answered by a rolling of the eyeball upward to wipe the cornea beneath
the momentarily relaxed and drooping upper lid. Excited respiration
causes no movement of the ala of the nose on the affected side, but in
deep inspiration, in contrast to the normal elevation of the ala, it
is flattened down by the suction of the inrushing current of air. In
masticating, the cheek bulges out from want of power in the paralyzed
buccinator to press the food inward against the opposing movements of
the tongue. In persons who have the rather unusual power of
voluntarily moving the ear we may detect the paralysis of the muscles
concerned in those movements—a useful point in diagnosis. Moreover, on
the sound side of the face the features have not entirely the natural
appearance. The angle of the mouth is drawn upward and the naso-labial
line more deeply impressed than natural. This results not from
excessive contraction, but from the muscles remaining in the position
they have taken during contraction, the antagonistic tonic traction
from the opposite side, which would have restored them to their normal
position, being wanting. This may be in a measure remedied by
mechanical appliances which will keep up an elastic pull from the
paralyzed side, or by restoring the muscles after contraction to
position with the hand. The tongue rests symmetrically in the floor of
the mouth, and is thrust out straight, although in appearance it is
pushed toward the side paralyzed—a deceptive appearance produced by
the asymmetrical position of the mouth. In some cases there is partial
paralysis of the velum palati, the half arch on the affected side
hanging lowest, and if we cause the patient to make the sound of _ah_
the opposite side of the palate is alone drawn upward. The uvula may
also participate in the paralysis, but the explanation of its
position, sometimes directed away from, sometimes toward, the side of
the paralysis, cannot be given. In proportion to the amount of the
paralysis of the soft palate will be the prominence of the symptoms
caused by it, such as difficulty in deglutition, a nasal tone in
speaking, and the escape of fluids through the nostril in swallowing.
The sense of hearing is often affected coincidently with facial
paralysis. Thus by reason of their close juxtaposition the same cause
may in common affect the acoustic and the facial, causing imperfect
hearing, subjective noises, etc. The hearing is frequently affected by
diseased conditions of the middle ear, which also cause a facial
paralysis. Still another defect of hearing, however, is caused by the
paralysis of the facial nerve itself. The stapedius muscle, supplied
by a branch of the facial, is the antagonist of the tensor tympani,
and when it is paralyzed the over-tense tympanic membrane vibrates
more readily to sound-waves, and a condition of uncomfortably
exaggerated sensitiveness to sounds is the result (hyperacuisis). The
rarely-occurring symptom of dryness of the mouth on the side of the
paralysis receives its explanation in the well-known fact of the
presence of secretory fibres for the salivary gland in the chorda
tympani, which are derived from the facial. We observe sometimes, in
connection with facial paralysis, that the patient {1205} complains of
certain subjective sensations of taste, as sour or metallic, and an
examination will in some cases reveal that the sense of taste is lost
on the anterior two-thirds of the tongue on the side of the paralysis.
The fibres which convey the sense of taste pass centripetally from the
tongue in the chorda tympani nerve, join the facial just within the
stylo-mastoid foramen, and continue united with it to the geniculate
ganglion of the facial, at which point they leave it to pass in the
great superficial petrosal to the spheno-palatine ganglion, and thence
to the trunk of the fifth nerve. Loss of sensation over the face only
occurs in cases where the fifth nerve has been simultaneously affected
with the facial, which may occur from exposure to cold.

It is obviously of importance in cases of facial paralysis to
determine if they are of central or peripheral origin. The most
prominent symptoms which mark a peripheral paralysis are the
implication of all the branches of the nerve, the loss of the
reflexes, the development of the degenerative reaction, and atrophy of
the muscles. In facial paralysis of cerebral origin the frontal and
orbital branches are not at all or but slightly affected, leaving the
eye with its natural appearance, in contrast to the lagophthalmos, and
the open eye which does not close even in sleep. In cerebral paralysis
the reflexes are normal and the muscles retain their natural electric
reaction. Accompanying brain symptoms assure the diagnosis. In facial
paralysis of bulbar origin the electric reactions are diminished, and
we have a complex of symptoms made up in a great measure by the
implication of neighboring nerves. After the diagnosis of a peripheral
facial paralysis has been made, by a careful consideration of the
symptoms we may with more or less accuracy determine at which point of
the nerve the lesion is situated. If there is paralysis of all the
muscles of the face, without alteration of taste or hearing, the
electric reaction of nerve and muscles normal, the nerve is affected
outside of the stylo-mastoid foramen. This is usually the form of
slight rheumatic paralysis. If we discover that the muscles of the
external ear are paralyzed, it shows that the point of lesion is just
within the stylo-mastoid foramen, where the posterior auricular branch
is given off from the facial. If with paralysis of the face there is
alteration of the sense of taste, with dryness of the mouth, without
interference with hearing, the trunk of the nerve is affected within
the Fallopian canal, involving the chorda tympani fibres below the
point where the stapedius nerve is given off. If to the above symptoms
there is added over-sensitiveness to sounds, hyperacuisis, and there
is no paralysis of the palate, we have the nerve affected still higher
up, but below the geniculate ganglion. If the geniculate ganglion is
involved, there is, in addition to the foregoing, symptoms of
paralysis of the palate. If, now, the lesion is above the geniculate
ganglion, we will have eliminated the symptom due to implication of
the chorda tympani, which leaves the trunk of the facial at the
geniculate ganglion, and the sense of taste is unaffected, while there
remains paralysis of the face, dryness of the mouth (the secretory
fibres run in the trunk of the seventh), hyperacuisis, and paralysis
of the palate.

It was in facial paralysis that the first observations upon the
degenerative reaction in muscles were made, and it is in that
affection that these electric phenomena have been best studied, and
give us the clearest {1206} indications for prognosis and treatment in
peripheral paralysis generally. In rheumatic facial paralysis, the
most common form of peripheral facial paralysis, the electric
reactions of the paralyzed muscles enable us to classify the cases
into three groups, the prognosis and duration of which vary very much.
In the first group are the slight forms of facial paralysis. Here the
faradic or galvanic current, applied to nerve or muscles, causes an
ordinary contraction; the electric reactions are normal. These cases
scarcely require treatment, and recover in two or three weeks. In a
second group are those cases in which within a short time after the
invasion of the paralysis (two weeks) complete degenerative reaction
is observed. This degenerative reaction, with the accompanying
anatomical changes in nerve and muscle, has already been treated of in
this article, and it is sufficient here to say that it is marked by
total loss of electric excitability, both faradic and galvanic, in the
nerve, loss of faradic and increased galvanic excitability in the
paralyzed muscles, with a reversal of the normal reply of the muscles
to the different poles of the galvanic battery. These cases constitute
the severe form of rheumatic facial paralysis, and the prognosis is
grave, recovery takes place only after months, and even after the
lapse of years traces of the disease remain in the imperfect action of
the muscles. A third group of cases are of a gravity intermediate
between these two. In them is present the milder form of degenerative
reaction; that is, there is a diminution, but not a total loss, of
electric excitability in the nerve for both the galvanic and faradic
currents; but in the muscles there is a marked increase of galvanic
excitability, with qualitative change—_i.e._ greater contraction upon
application to them of the positive than of the negative pole. These
cases may be expected to recover in from four to eight weeks, the
muscles still exhibiting the degenerative reaction after voluntary
motion has returned. Among the symptoms to be particularly noticed in
the progress of the severe forms of facial paralysis are spasmodic
twitchings or spasms of the muscles on the affected side of the face,
about the angle of the mouth, and around the eye, occurring
spontaneously or when voluntary movements are made. Also a state of
tonic contraction and rigidity may develop in some of the muscles,
causing a permanent elevation of the angle of the mouth, a narrowing
of the opening of the eye, or a rigidity of the cheek. These symptoms
have been erroneously attributed to the use of electricity in the
treatment, but they occur as frequently in cases in which it has not
been employed. Traumatic facial paralysis, as from wounds, surgical
operations, use of the forceps in delivery, or paralysis from
compression of the nerve, as from tumors, syphilitic thickening of the
dura mater, etc., do not require a detailed mention here, as such
cases come under the head of nerve-injuries, already discussed.
Paralysis of both facials (diplegia facialis), in so far as it is
caused by peripheral nerve lesion, is an accidental occurrence, and
need not be considered as a separate form of facial paralysis. It is
often the result of central disease.

The TREATMENT of peripheral facial paralysis must begin with the
effort to remove its cause. If syphilis is suspected, mercury and
iodide of potassium must be freely used. If the cause is an affection
of the middle ear, this must be treated. Wounds or traumatic injuries
must receive the necessary surgical attention. In addition, in such
cases electricity {1207} must be employed in the manner presently to
be described. In cases of rheumatic facial paralysis the treatment
will vary with their gravity. In the lighter form in which the nerve
is affected outside of the Fallopian canal, recovery takes place in a
comparatively short time, even without treatment, but is hastened by
the use of the faradic or galvanic current daily along the branches of
the nerve. In the severe form we must open the treatment by an attempt
to combat the condition of inflammation—of inflammatory
exudation—which we suppose exists within the Fallopian canal. Local
blood-letting by leeching upon the mastoid process may be
appropriately used in the very first outset of the paralysis. Iodide
of potassium, given persistently in large doses during the earlier
period of the disease, appears to act beneficially independently of
any syphilitic taint. Electricity is the remedy, however, on which
most reliance is to be placed in the treatment of rheumatic facial
paralysis, and the manner of its application may be taken as a model
of how it should be employed in all cases of peripheral paralysis. The
galvanic current, on account of its power of penetrating to the deeper
parts and its catalytic action, is to be preferred for the direct
electrical treatment of the nerve which should be instituted in recent
cases. Its action is best obtained by placing the positive pole behind
the ear on the affected side, the cathode behind the opposite ear, and
passing a moderate current across the base of the skull (the affected
nerve being thus in the course of the current) for one or two minutes.
Occasionally the position of the poles may be reversed. Besides this
direct application of galvanism to the point of lesion, it is
necessary to make a peripheral application of electricity to the
branches of the nerve and to the paralyzed muscles. For this we use
both the faradic and galvanic currents. The galvanic current is used
by applying the positive pole stationary behind the ear, while the
negative pole, with an electrode of suitable size, is stroked over
each branch of the nerve and applied to each muscle, a current being
used sufficiently strong to produce decided contractions. This
peripheral application should be made once daily, the time of
application being from two to five minutes. The application of the
faradic current is made by simply placing one electrode upon an
indifferent spot, and moving the other over the face, with a current
strong enough to cause contractions if the muscles still respond to
it, or if they do not of such strength as the patient can bear without
discomfort. Without doubt, one of the beneficial effects of peripheral
electrization is the reflex excitement of the facial above the point
of lesion through the irritation of the terminations of the fifth
nerve in the skin. A certain advantage derived from it is that it
maintains the tone of the paralyzed muscles, which in the case of the
orbicularis palpebrarum is of great importance in preventing the
eversion of the lower lid and the overflow of the tears. As it is
impossible during the first days succeeding the paralysis to
distinguish severe cases from those of the middle form, it is best to
begin the treatment of all cases in the manner above described. The
use of strychnia in rheumatic facial paralysis, both internally and by
hypodermic injection, may be mentioned on account of the widespread
preposession in its favor, and to point out distinctly its utter
futility.

Mechanical appliances and manipulation are used with advantage in the
treatment of facial paralysis to prevent the paralyzed muscles about
{1208} the mouth and cheek from being drawn out of place and
over-stretched by the action of the sound ones of the opposite side,
thus having their tonicity and nutrition impaired.

Contractions and rigidity of muscles receive little benefit from the
use of electricity, and must be treated by mechanical procedures, such
as stretching, massage, etc.


Neuromata.

The term neuromata was applied to all tumors involving the
nerve-trunks at a time when their histological differences had not
been studied and they were all supposed to be composed of
nerve-tissue; and even yet the name is conveniently retained, because,
although differing widely histologically, tumors situated upon the
nerves have a very similar clinical history.

Neuromas must be divided into true and false, the true consisting of
nerve-tissue, the false, or pseudo-neuromas, being composed of many
varieties, having this only in common, that they are seated upon the
nerves.

The true neuromas are again subdivided into those in which the
nerve-tissue composing them resembles exactly the fibres of the
peripheral nerves, showing with the microscope the double-contoured
white substance of Schwann surrounding an axis-cylinder, and those in
which the tumor is made up of fibres which Virchow has shown to be
non-medullated nerve-fibres—_i.e._ the axis-cylinder without the white
substance of Schwann. These two forms have been distinguished by the
names myelinic and non-myelinic. The true neuromas are non-malignant,
although showing the tendency to recur after extirpation, are of slow
growth, and as a rule do not increase to a very great size. The best
type of the myelinic neuromas is found in the spherical or
spindle-shaped enlargements at the cut ends of nerves, particularly in
the stumps of amputated limbs, where they are found oftenest
intimately connected with the cicatricial tissue, though sometimes
lying free. They consist of true medullated fibres mixed with some
fibrous tissue. The fibres composing them are derived partly from
splitting up and proliferation of the fibres of the nerve itself,
partly are of new formation, the appearances strongly recalling the
process of regeneration in nerves. Myelinic neuromas consist of fibres
and nuclei so closely resembling in microscopic appearance the
fibromas that they have hitherto been confounded with them; and there
is a difference among the highest authorities as to the certainty of
their diagnosis, and, in consequence, of the frequency of their
occurrence. The true neuromas may include in their structure all of
the fibres of the nerve-trunk or only a portion of them (partial
neuroma)—a fact of importance in their symptomatology. Of the false
neuromas, the fibromas are by far the most frequently met with. They
appear as knots, more or less hard, upon the course of the
nerve-trunk, which they may involve completely or partially. They are
often excessively painful to the touch or spontaneously, most of the
so-called tubercula dolorosa belonging to the fibro-neuromas. Fibromas
sometimes occur along the trunk and branches of a nerve, forming a
plexus of knotted cords (plexiform neuroma). Fibro-sarcomas are not an
infrequent form of neuroma.

{1209} Myxomas often occur upon the peripheral nerves, and are
frequently multiple, their points of predilection being the larger
trunks, as the sciatic, ulnar, etc. They show their characteristic
soft structure, and are usually spindle-shape, assuming a rounder form
as they attain a large size. The various forms of sarcoma occasionally
form tumors upon the nerves, attacking generally the large trunks.
Carcinomatous tumors beginning upon the nerves sometimes occur, but as
a rule these growths involve the nerve by extension to it from
adjacent parts.

Syphilitic gummata have been found almost exclusively upon the
intracranial portion of the cranial nerves.

Gliomas appear to affect only the optic and acoustic nerves. Lepra
nervorum (lepra anæsthetica) produces usually a spindle-form
thickening upon the nerve-trunks, but sometimes there are more
distinct knots, which may be felt beneath the skin, bead-like, along
the course of the nerves of the extremities.

Like the true neuromas, the false neuromas, developing from the
neurilemma and perineurium, may involve the whole or only a part of
the fibres of a nerve, or the nerve-fibres may run at the side of the
tumor—different conditions, which may alter materially the effects
produced upon the nerve.

Neuromas, both false and true, may occur not only singly, but often in
large numbers, many hundreds having been counted upon an individual.
Sometimes they are numerous upon a single nerve-trunk and its
branches, and again they may appear scattered over nearly all of the
nerves of the body, even to the cauda equina and roots of the nerves.
According to Erb,[9] isolated neuromas are more frequent in females,
while multiple neuromas are found almost exclusively in men. Neuromas
vary greatly in size, as we might expect from the very great
difference of their nature and structure; sometimes no larger than a
pea, they may attain the size of a child's head.

[Footnote 9: _Ziemssen's Handbuch_.]

ETIOLOGY.—In cases of multiple neuromata it would seem as if there was
a constitutional condition or diathesis as the foundation of the
affection. This we may the more readily believe as there appears good
evidence to show that the tendency to the formation of these
nerve-tumors is sometimes hereditary, and some of them are congenital.

Idiots and cretins have been observed to suffer in undue proportion
with multiple neuromas. We find a direct exciting cause of neuromas in
mechanical injuries of nerves, wounds, blows, pressure, etc. Thus, as
has been already seen, true neuromas occur in the divided ends of the
nerves after amputations or otherwise where a nerve-trunk has been
divided (cicatricial neuroma). As such neuromas are in some degree the
result of inflammation, it is probable that they may sometimes be
caused by chronic neuritis.

For a large number of neuromas no cause can be assigned, and we must
at present consider them as originating spontaneously.

SYMPTOMS.—The position and connections of neuromas being so different,
sometimes simply in contact with the nerve; sometimes situated in the
thickness of the nerve-trunk, the fibres being pressed aside and
spread out upon the surface of the tumor; sometimes involving in their
tissue a part or the whole of the nerve-fibres,—we cannot but expect a
{1210} very marked difference in their clinical history. Not a few
cases occur in which the presence of neuromas, even in large numbers,
gives rise to no symptoms during life, and their existence has been
revealed only upon a post-mortem examination.

The symptom most common to neuromas, and one to be expected from their
mechanical interference with the nerves, is neuralgic pain—sometimes
extreme, local or shooting along the course of the nerves, stubborn,
and hardly to be alleviated by remedies. It is paroxysmal,
notwithstanding the unvarying character of its cause, in consonance
with the tendency to periodical activity which prevails in the nervous
system. Sometimes the pain is increased notably by atmospheric
changes. The pain may sometimes be arrested by firm pressure upon the
nerve above the seat of the tumor. In some cases pressure upon the
neuroma, or even handling it, causes great pain. The intensity of the
pain does not depend upon the size of the tumor, some of the smallest
having earned the appropriate name of tubercula dolorosa. The
continued irritation of a neuroma sometimes produces a condition of
general nervous excitability, which shows itself in hysterical and
even in true epileptic convulsions. Occasionally there are abnormal
sensations (paræsthesiæ), formication, numbness, etc., in the
distribution of the nerve affected, and when from pressure or
histological changes the fibres are destroyed anæsthesia results.

The interference with the conductivity of the motor fibres, which
occurs less frequently than alterations of sensation, shows itself in
cramps, tumors, paresis, and paralysis, according to its degree.

Neuromas may destroy life by the continued excessive pain, which wears
down the strength and depresses the vitality. Death may be caused by
their peculiar situation; as, for instance, upon the cauda equina,
where they produce paraplegia, paralysis of the sphincter and bladder,
and trophic changes.

The DIAGNOSIS of neuromas can only be made when they are sufficiently
superficial to be recognized by the touch, and along with the symptoms
above detailed the tumor is situated upon the known course of a nerve,
to which, moreover, its attachment allows a lateral movement.

The only TREATMENT available for neuromas is extirpation, which must
be conducted with a view to sparing any fibres of the nerve not
involved in the tumor. Where it is necessary to divide the nerve in
the removal of the tumor, as small a portion as possible must be
excised, with the hope of a regeneration and reuniting of the cut
ends. The success of extirpation depends largely upon the nature of
the neuroma. The true neuromas, while they often show a strong
tendency to recur after removal, are benign and show no metastasis.
For the false neuromas the prognosis will be in accordance with their
benign or malignant character.


{1211}


NEURALGIA.

BY J. J. PUTNAM, M.D.


DEFINITION.—It is customary to describe as neuralgic those pains for
which no adequate cause can be assigned in any irritation of the
sensory nerves from outside, which recur paroxysmally, are unattended
by fever, and are distributed along the course of one or more nerves
or nerve-branches.

The general use of the term neuralgia further implies the common
belief that there is a disease or neurosis, not covered by any other
designation, of which these pains are the characteristic symptom. Of
the pathological anatomy of such a disease, however, nothing is known;
and if it could be shown for any given group of cases that the
symptoms which they present could be explained by referring them to
pathological conditions with which we are already familiar, these
cases would no longer properly be classified under the head of
neuralgia.

The attempt has frequently been made, and on good grounds, in
obedience to this reasoning, to cut down the list of the neuralgias,
strictly so called, and to account for many of the groups of symptoms
usually classified under that head by referring them to anæmia or
congestion of the sensory nerves, to neuritis, etc.

One of the best and most recent statements of this view is that of
Hallopeau,[1] who, although he does not wholly deny the existence of a
neurosis which may manifest itself as neuralgia, goes so far as to
maintain that the gradual onset and decline and more or less
protracted course so common in the superficial neuralgias, such as
sciatica, suggest rather the phases of an inflammatory process than
the transitions of a functional neurotic outbreak, and that, in
general terms, a number of distinct affections are often included
under the name of neuralgia which are really of different origin, one
from the other, and resemble each other only superficially. This
subject will be discussed in the section on Pathology, and until then
we shall, for convenience' sake, treat of the various neuralgic
attacks as if they were modifications of one and the same disease.

[Footnote 1: _Nouveau Dict. de Méd. et de Chir. pratiques_, art.
“Névalgies.”]

GENERAL SYMPTOMATOLOGY.—The neuralgias may be conveniently divided
into—1, external or superficial; 2, visceral; 3, migraine and the
migrainoid headaches.


Superficial Neuralgia.

The most prominent symptom of a neuralgic attack of the superficial
{1212} nerves is of course the pain, and sometimes, from first to
last, no other sign of disease is present. In an acute attack the pain
is usually ushered in by a sense of discomfort, which the patient
vainly tries to shake off, or by a feeling of weight and pressure or
of numbness and prickling, or of itching. Sometimes, though far less
often than in the case of migraine, there are prodromal signs of a
more general character, such as a feeling of thirst[2] or of mental
depression or drowsiness.

[Footnote 2: Spoken of by Mitchell's patient with neuralgia of the
stump (see below).]

A dart of pain may then be felt, which soon disappears, but again
returns, covering this time a wider area or occupying a new spot as
well as the old. The intensity, extension, and frequency of the
paroxysms then increase with greater or less rapidity, but, as a rule,
certain spots remain as foci of pain, which radiates from them in
various directions, principally up or down in the track of the
nerve-trunk mainly implicated. The pain rarely or never occupies the
whole course and region of distribution of a large nerve or plexus,
but only certain portions, which may be nearly isolated from one
another.

In an acute attack the affected parts may at first look pale and feel
chilly, and later they frequently become congested and throb. Mucous
surfaces or glandular organs in the neighborhood often secrete
profusely, sometimes after passing through a preliminary stage of
dryness.

The skin often becomes acutely sensitive to the touch, even though
firm, deep pressure may relieve the suffering. Movement of the painful
parts, whether active or passive, is apt to increase the pain. When
the attack is at its height, the pain is apt to be felt over a larger
area than at an earlier or a later period, and may involve other
nerves than those first attacked. Thus, a brachial becomes a
cervico-brachial neuralgia or involves also the mammary or intercostal
nerves. A peculiarly close relationship exists between the neuralgias
of the trigeminal and of the occipital nerves. It is said that when
the attack is severe the corresponding nerves of the opposite side may
become the seat of pain. This is perhaps remotely analogous to the
complete transference of the pain from one side to the other which is
so characteristic of periodical neuralgic headaches, especially if
they last more than one day.

Some cutaneous neuralgias pass away after a few hours' or a night's
rest, after the manner of a migraine or a headache, and patients in
whom this takes place are, as a rule, constitutionally subject to
neuralgia or other neuroses. Toward the end of such an attack there is
often a copious secretion of pale, limpid urine. In a large class of
cases, on the other hand, the attack is of several days' or weeks', or
even months' or years', duration, with remissions or intermissions and
exacerbations, which may be either periodical or irregular.

The most marked periodicity of recurrence is seen with the neuralgias
of malarial origin, which may take on any one of the typical forms of
that disease.

These malarial neuralgias affect pre-eminently, though not
exclusively, the supraorbital branch of the fifth nerve; but it should
not be forgotten that there is also a typically periodical
supraorbital neuralgia of non-malarial origin, of which the writer has
seen several pronounced examples, the pain usually recurring regularly
every morning at eight or nine o'clock and passing away early in the
afternoon. The same periodicity {1213} is seen, though less often, in
other neuralgias. Thus, Trousseau[3] speaks of neuralgic attacks from
cancer of the uterus in a young woman, which recurred daily at exactly
the same hour. Some of the traumatic neuralgias show the same
peculiarity to a marked degree.

[Footnote 3: _Clin. Méd._]

In many neuralgias, on the other hand, the exacerbations are worse at
night, like the pains of neuritis. In the intervals between the
attacks the pain may be wholly absent, or may persist, usually as a
dull aching.

After a neuralgia has lasted a few days—sometimes, indeed, from the
outset if the attack is severe—it is usually found that definite spots
of tenderness have made their appearance at certain limited points on
the course of the nerve. These are the famous points douloureux which
Valleix described with such minute accuracy, believing them to be
invariably present in true neuralgias. This is certainly not strictly
the case, though they are very common. They are not necessarily
coincident with the foci of spontaneous pain, as Valleix supposed, but
do correspond in general to the points at which the affected nerve
emerges from its bony canal or from deep muscles and fascia, and to
portions of its area of distribution in the skin. The spinous process
corresponding to an affected spinal nerve may also become tender, but
this is probably to be looked on, like the same symptom in so-called
spinal irritation, not as a sign of local disease, but as due to a
general reaction on the part of the nervous system, and as a fact of a
different order from the tenderness along the nerve.

The termination of an acute neuralgic attack is usually gradual, like
its onset, although in some cases of headache, and in other neuralgias
to a less degree, there comes a moment when the patient suddenly
declares that he is free from pain.

Neuralgic attacks are usually characterized, besides the pain, by a
highly-interesting series of symptoms, which are in part transitory
and functional, and in part due to structural changes in the
tissues.[4]

[Footnote 4: See Notta, _Arch. gén. de Méd._, 1854; Anstie, _Neuralgia
and its Counterfeits_.]

The spasm and subsequent dilatation of blood-vessels in the affected
area have already been alluded to. A disturbance of secreting organs
in the neighborhood of the painful region, the lachrymal gland, the
skin, the mucous membranes, the salivary glands, is of equally common
occurrence, and is probably in great measure due to direct irritation
of the glandular nerves, since the increased secretion is said to
occur sometimes unattended by congestion.

The hair may become dry and brittle and inclined to fall out, or may
lose its color rapidly, regaining it after the attack has passed.

The increased secretion of urine already alluded to attends not only
renal neuralgias, but those of the fifth pair, intercostal, and other
nerves. There may be unilateral furring of the tongue (Anstie).

The muscles supplied by the branches of the affected nerve or of
related nerves may be the seat of spasm, or, on the other hand, may
become paretic; and this is true even of the large muscles of the
extremities.

Vision may be temporarily obscured or lost in the eye of the affected
side in neuralgia of the fifth pair, and hearing, taste, and smell are
likewise deranged, though more rarely. I am not aware that distinct
{1214} hemianopsia is observed except in cases of true migraine, where
it forms an important prodromal symptom.

In connection with these disorders of the special senses the
occasional occurrence of typical anæsthesia of the skin of one-half of
the body should be noted, which several observers have found in
connection with sciatica. The writer has seen a cutaneous
hyperæsthesia of one entire half of the body in a case of
cervico-occipital neuralgia of long standing. These symptoms are
probably analogous to the hemianæsthesia which comes on after
epileptic or other acute nervous seizures, or after concussion
accidents, as has lately been observed both in this country and in
Europe, and it is perhaps distantly related to the hemianæsthesia of
hysteria. Local disorders of the sensibility in the neuralgic area are
far more common than this, and, in fact, are usually present in some
degree. The skin is at first hyperæsthetic, but becomes after a time
anæsthetic; and this anæsthesia offers several interesting
peculiarities. When this loss of sensibility is well marked, areas
within which the anæsthesia is found are apt to be sharply defined,
but they may be either of large size or so small as only to be
discovered by careful searching (Hubert-Valleroux). The sensibility
within these areas may be almost wanting, but in spite of this fact it
can often be restored by cutaneous faradization around their margins,
and the functional or neurosal origin of the anæsthesia is thus made
apparent. Where the anæsthesia is due, as sometimes happens, to the
neuritis with which the neuralgia is so often complicated, it is more
lasting, but usually less profound and less sharply defined.

These changes may be transient, or, if a neuralgia is long continued
and severe, they may pass into a series of more lasting and deeper
affections of the nutrition.

The skin and subjacent tissues, including the periosteum, from being
simply swelled or œdematous may become thickened and hypertrophied.
The writer has known a case of supraorbital neuralgia, at first
typically intermittent, to lead to a thickening of the periosteum or
bone over the orbit, which even at the end of several years had not
wholly disappeared.

Neuralgias of the fifth pair, which are as remarkable in their outward
results as they are in their severity and their relation to other
neuroses, are said to give rise to clouding and ulceration of the
cornea, to iritis, and even to glaucoma.

Herpetic eruptions on the skin sometimes occur, of which herpes zoster
is the most familiar instance.

Muscular atrophy is very common, especially in sciatica, and in some
cases this occurs early and goes on rapidly, while in others it may be
only slight and proportioned to the disease and relaxation of the
muscles, even where the neuralgia has lasted for weeks or months.

Neuritis of the affected nerve is a common result or attendant of
neuralgia, and may remain behind for an indefinite period after the
acute pain has gone, manifesting itself by subjective and objective
disorders of sensibility, by occasional eruptions on the skin, or by
muscular atrophy.

It is plain that in this list of symptoms a variety of conditions have
been described which would never all be met with in the same case, and
which, as will be shown in the section on Pathology, are probably due
to different pathological causes.


{1215} Neuralgia of the Viscera.

These neuralgias are less definitely localized by the sensations of
the patient than those of the superficial nerves, and it is not
definitely known what set of nerves are at fault.

They are deep-seated and are referred to the general neighborhood of
the larynx, œsophagus, heart, or one of the abdominal or genital
organs, as the case may be.

The pain is usually of an intense, boring character, and does not dart
like the pain of superficial neuralgia, but is either constant or
comes in waves, which swell steadily to a maximum and then die away,
often leaving the patient in a state of profound temporary
prostration.

Deep pressure often brings relief. A patient of the writer, who is
subject to attacks of this kind in the right hypochondrium, will bear
with her whole weight on some hard object as each paroxysm comes on,
or insist that some one shall press with his fists into the painful
neighborhood with such force that the skin is often found bruised and
discolored.

The functions and secretions of the visceral organs are apt to be
greatly disordered during a neuralgic attack, and it is often
difficult or impossible to tell with certainty which of these
conditions was the parent of the other. Undoubtedly, either sequence
may occur, but the pain excited by disorder of function, or even
organic disease of any organ, is not necessarily felt in that
immediate neighborhood. Thus I have known the inflammation around an
appendix cæci, of which the patient shortly afterward died, to cause
so intense a pain near the edge of the ribs that the passage of
gall-stones or renal calculus was at first suspected.

There seems to be as much variation as to modes of onset and duration
among the visceralgias as among the superficial neuralgias, but the
tendency to short typical attacks of frequent recurrence seems to be
greater with the former.

The visceral neuralgias are quite closely enough related to certain of
the superficial neuralgias to show that they belong in the same
general category. The two affections are often seen in the same
person, and not infrequently at the same time or in immediate
succession. Thus in the case of the patient just alluded to above, the
attacks of deep-seated neuralgia in the neighborhood of the right
flank are at times immediately preceded by severe neuralgia of the
face or head. Similarly, intercostal neuralgia may occur in immediate
connection with neuralgias of the cardiac or gastric nerves.

The phenomenon of tender points is not entirely wanting in the
visceralgias, though less constant and definite than in the
superficial neuralgias.

The liver and the uterus especially become the seat of more or less
localized tenderness, and possibly the tenderness in the ovarian
region which is so common, and so often unattended by real
inflammation, is, in part, of this order.

The secondary results of the visceralgias are not easy to study.
Besides the disorders of secretion and function above alluded to,
swelling of the liver with jaundice and paresis of the muscular walls
of the hollow viscera may be mentioned as having been ascribed to
neuralgia.

It is not known to what degree neuritis occurs as a cause or {1216}
complication of these neuralgias, and this is a question which is
greatly in need of further study.


Migraine, or Sick Headache.

This is often classified as an affection of a different order from the
neuralgias, but there seem to be no real grounds for this distinction.

The superficial neuralgias themselves are probably not one, but a
group of affections, with the common bond of severe and paroxysmal
pain.

Neither is what is called migraine always one and the same disease.

Although in its most typical form it presents very striking
characteristics, such as a marked preliminary stage, with peculiar
visual and sensory auras, sometimes occupying one entire half of the
body, a short and regular course and periodical return, deep-seated
pain without tender points, and prominent unilateral vascular
disorders, yet these symptoms shade off by imperceptible degrees into
those of neuralgia of the fifth pair, or more often into one or
another form of unilateral neuralgic headache which stands midway
between the two.

The vascular phenomena of migraine are believed by various observers,
as is well known, to constitute the primary and essential pathological
feature of the disease, and to be the cause of the pain. But this is a
pure hypothesis, and as a matter of fact the cases are abundant in
which no greater vascular changes are present than in other neuralgias
of equal severity.

Migraine seems to occupy an intermediate position between the grave
neuroses, especially epilepsy, and the neuralgias of neurosal origin.

The symptomatology will be described at greater length below.

GENERAL ETIOLOGY.—The causes of neuralgia may be divided into
predisposing and exciting causes.

The most important of the first group are—

1. Hereditary tendencies;

2. The influences associated with the different critical periods of
life;

3. The influences attached to sex;

4. The action of constitutional diseases, such as phthisis, anæmia,
gout, syphilis, diabetes, nephritis, malarial poisoning, metallic
poisoning.

The most important of the second group of causes are—

1. Atmospheric influences and the local action of heat and cold;

2. Injuries and irritation of nerves;

3. Irritation of related nerves (so-called reflex and sympathetic
neuralgias);

4. Acute febrile diseases.

In most cases more than one cause is to blame, and each should be
separately sought for.

PREDISPOSING CAUSES.—1. Hereditary Tendencies.—It is generally
admitted as beyond question that neuralgias are most common in
families in which other signs of the neuropathic taint are prominent.
Such affections as hysteria, neurasthenia, epilepsy, asthma, chorea,
dipsomania, and even gout and phthisis as it would seem, are akin to
the neuralgic tendency.

{1217} The neuropathic family is thought to contain, in fact, a much
larger number of members than this,[5] but there is danger of
exaggerating the importance of an influence of which we know as yet so
little.

[Footnote 5: Féré, _Arch. de Névrologie_, 1884, Nos. 19 and 20, “La
famille névropathique.”]

It should be remembered, moreover, that even where an inherited taint
is present its influence may be but slight as compared with that of
some special exciting cause.

Some neuralgias are more closely associated with the inherited
neuropathic diathesis than others. The connection is especially close
in the case of migraine;[6] then follow other forms of periodical
headache and the visceral neuralgias. Even the superficial
neuralgias[7] are more or less subject to this influence. This is
thought to be especially true of the facial neuralgias.

[Footnote 6: There is a witty French saying (quoted by Liveing), “La
migraine est le mal des beaux esprits;” which might be rendered, “The
disease of nervous temperaments.”]

[Footnote 7: For tables of illustrative cases see Anstie, _Neuralgia
and its Counterfeits_, and J. G. Kerr, _Pacific Med. and Surg.
Journ._, May, 1885.]

Reasons will be offered later for suspecting that many cases usually
classed as neuralgia, and characterized by gradual onset and
protracted course, are essentially cases of neuritis; and there is
need of further inquiry as to how far hereditary influences are
concerned in producing them, and whether such influences act by
increasing the liability of the peripheral nerves to become inflamed,
or only by increasing the excitability of the sensory nervous centres.

2. Age.—Neuralgia is oftenest seen in middle life and at the epochs
marked by the development and the decline of the sexual functions. The
affection, when once established, may run over into advanced age, but
cases beginning at this period are relatively rare and very
intractable (Anstie).

Childhood is commonly said to be almost exempt from neuralgia, but, in
fact, there seems no sufficient reason for withholding this term from
the so-called growing pains of young children[8] so long as it is
accorded to the almost equally irregular neuralgias of anæmia in the
adult. The same remark applies to the attacks of abdominal pain in
children, which often seem to be entirely disconnected from digestive
disorders.

[Footnote 8: Probably due to anæmia or imperfect nutrition (see
Jacobi, “Anæmia of Infancy and Childhood,” _Archives of Med._, 1881,
vol. v.).]

Adolescents and children also suffer from periodical headaches, both
of the migrainoid and of the neuralgic type. These are obstinate and
important affections.[9] Migraine especially, coming on in early life,
points to a neuropathic constitution, and will be likely to recur at
intervals through life, or possibly to give place to graver neuroses.

[Footnote 9: Blache, _Revue mensuelle de l'enfance_, Mar., 1883, and
Keller, _Arch. de Névroloqie_. 1883.]

3. Sex.—Women show a stronger predisposition than men to certain forms
of neuralgia, as to the other neuroses, but it is generally conceded
that whereas neuralgias of the fifth and occipital and of the
intercostal nerves are met with oftenest among them, the brachial,
crural, and sciatic neuralgias are commoner among men. This probably
indicates that the neurosal element is of greater weight in the former
group, the neuritic element in the latter.

4. Constitutional Diseases.—The blood-impoverishment of phthisis and
anæmia, the poison of malaria, syphilis, and gout, and the obscurer
{1218} forms of disordered metamorphosis of tissue, undoubtedly
predispose to neuralgia and the other neuroses, as well as to neuritis
and others of the direct causes of neuralgic attacks.

Anstie regards the influence of phthisis as so important as to place
it fairly among the neuroses. Gout is likewise reckoned by some
observers among the neuroses,[10] but we tread here upon uncertain
ground. Anstie does not regard gout as a common cause of neuralgia,
but most writers rate it as more important, and gouty persons are
certainly liable to exhibit and to transmit an impaired nervous
constitution, of which neuralgia may be one of the symptoms. The
neuralgias of gout are shifting, irregular in their course, and
sometimes bilateral.

[Footnote 10: Dyce-Duckworth, _Brain_, vol. iii., 1880.]

Syphilitic patients are liable to suffer, not only from osteocopic
pains and pains due to the pressure of new growths, but also from
attacks of truly neuralgic character. These may occur either in the
early or the later stages of the disease. They may take the form of
typical neuralgias, as sciatica or neuralgia of the supraorbital nerve
(Fournier[11]), or they may be shifting, and liable to recur in
frequent attacks of short duration, like the pains from which many
persons suffer under changes of weather, anæmia, or fatigue.

[Footnote 11: Cited by Erb in _Ziemssen's Encyclopædia_.]

There are other obscure disorders of the nutrition, as yet vaguely
defined, in connection with which neuralgia of irregular types is
often found. Some of these are classed together under the name of
lithæmia, and are believed to be due to imperfect oxidation of
albuminoid products.[12]

[Footnote 12: See DaCosta, _Am. Journ. of Med. Sciences_, Oct., 1881,
and W. H. Draper, _New York Med. Record_, Feb. 24, 1883.]

Diabetes seems also to be an occasional cause of neuralgia, especially
sciatica, and Berger,[13] who has recently described them, says that
they are characterized by limitation of the pain to single branches of
the sacral nerves, by a tendency to occur at once on both sides of the
body, by the prominence of vaso-motor symptoms, and, finally, by their
long duration and obstinacy. There may not, at the moment, be any of
the characteristic symptoms of diabetes present.

[Footnote 13: _Neurologisches Centralblatt_, 1882, cited in the
_Centralbl. für Nervenheilk., etc._, 1882, p. 455.]

Chronic nephritis also causes neuralgia, either directly or
indirectly; and severe neuralgic attacks may accompany the condition,
which is as yet but imperfectly known, characterized pathologically by
a general arterio-fibrosis and by increased tension of the arterial
system.

True rheumatism does not appear to be a predisposing cause of
neuralgia.

Anæmia, both acute and chronic, is a frequent cause of neuralgia, both
through the imperfect nutrition of the nervous tissues, to which it
leads, and, it is thought, because the relatively greater
carbonization of the blood increases the irritability of the
ganglionic centres.

Even a degree of anæmia which might otherwise be unimportant becomes
of significance in the case of a patient who is otherwise predisposed
to neuralgia; for such persons need to have their health kept at its
fullest flood by what would ordinarily seem a surplus of nourishment
and care.

Under the same general heading comes the debility from acute and
{1219} chronic diseases, and the enfeeblement of the nervous system
from moral causes, such as anxiety, disappointment, fright, overwork
and over-excitement, and especially sexual over-excitement, whether
gratified or suppressed (Anstie), or, on the other hand, too great
monotony of life; also from the abuse of tea, coffee, and tobacco.

Lead, arsenic, antimony, and mercury may seriously impair the
nutrition of all the nervous tissues, and in that way prepare the way
for neuralgia.

IMMEDIATE CAUSES.—1. Atmospheric and Thermic Influences.—Neuralgia is
very common in cold and damp seasons of the year, in cold and damp
localities, and in persons whose work entails frequent and sudden
changes of temperature. Exposures of this sort may at once excite
twinges of pain here and there over the body, and may eventually
provoke severe and prolonged attacks of neuralgia.

The action of damp cold upon the body is complicated, and it exerts a
depressing influence on the nervous centres in general which is not
readily to be explained. One important factor, however, is the cooling
of the superficial layers of the blood, which occurs the more easily
when the stimulus of the chilly air is not sufficiently sharp and
sudden to cause a firm contraction of the cutaneous vessels, while the
moisture rapidly absorbs the heat of the blood. From this result,
indirectly, various disorders of nutrition of the deeper-lying tissues
or distant organs; and, among these, congestion and neuritis of the
sensitive nerves.

Neuralgia often coincides with the presence or advent of storms. A
noteworthy and systematic study of this relationship was carried on
through many years under the direction of S. Weir Mitchell[14] by a
patient of his, an officer who suffered intensely from neuralgia of
the stump after amputation of the leg. The attacks of pain were found
to accompany falling of the barometer, yet were not necessarily
proportionate to the rapidity or amount of the fall. Saturation of the
air with moisture seemed to have a certain effect, but the attacks
often occurred when the centre of the storm was so remote that there
was no local rainfall. It was impossible to study the electrical
disturbances of the air with accuracy, but a certain relationship was
observed between the outbreak of the attacks and the appearance of
aurora borealis.

[Footnote 14: _Am. Journ. of Med. Sci._, April, 1877, and _Philada.
Med. News_, July 14, 1883.]

This patient's neuralgic attacks were almost certainly of neuritic
origin, and it is possible that the exacerbations were due to changes
of blood-tension in and around the nerve-sheaths. It is also possible
that they were the result of circulatory changes and disordered
nutrition of the nervous centres, already in a damaged condition from
the irritation to which they had been exposed.

2. Injuries and Irritation of Nerves.—Wounds and injuries of
nerves[15] and the irritation from the pressure of scars, new growths,
and aneurisms are prolific causes of neuralgic pain, partly by direct
irritation, partly by way of the neuritis which they set up.
Neuralgias are likewise common during the period of the healing of
wounds, as Verneuil long since pointed out. The pain may be near the
wound itself or in some distant part of the body.

[Footnote 15: See S. Weir Mitchell, _Injuries of Nerves_.]

Neuralgia due to the pressure and irritation of tumors, new growths,
{1220} or aneurisms requires a special word. The pain is apt to be
intensely severe, but what is of especial importance is that the
symptoms may not present anything which is really characteristic of
their origin, except their long continuance; and this should always
excite grave suspicion of organic disease.

These attacks of pain may be distinctly periodical; and this is true
whether they are felt in the distribution of the affected nerve or of
distant nerves.

Not only are direct injuries of nerves a cause of neuralgia, but
sudden concussion or jar may have a like effect—whether by setting up
neuritis or in some other way is not clear. Ollivier[16] reports a
case where a blow beneath the breast caused a neuralgia which
eventually involved a large portion of the cervico-brachial plexus;
and the writer has seen a like result from a blow between the
shoulders.

[Footnote 16: Cited by Axenfeld and Huchard, p. 116.]

Peripheral irritations, such as caries of the teeth (see below, under
Facial Neuralgia) and affections involving other important plexuses,
such as those of the uterine nerves, are a frequent cause of
neuralgia, and should always be sought for. They act in part by
setting up neuritis, and in part evidently in some more indirect
manner, since the neuralgia which they excite may be referred to more
or less distant regions, forming the so-called—

3. Reflex and Sympathetic Neuralgias.—The term reflex, as here used,
is ill chosen, and the term sympathetic only covers our ignorance of
the real processes involved, and which we should seek for in detail.
Thus, disease of the uterus or ovaries may cause facial, mammary,
intercostal, or gastric neuralgia.

Hallopeau[17] suggests that some of these results may be brought about
by the pressure of enlarged lymphatic glands attached to the affected
organ.

[Footnote 17: _Loc. cit._, p. 766.]

Another important centre of nervous irritation is the eye. Slight
errors of refraction, or weakness of the muscles of fixation,
especially the internal recti, are a source of frontal headaches and
other nervous symptoms, and even of typical migraine,[18] to a degree
which is not usually appreciated. It is improbable that in the latter
case the irritation acts as more than an exciting cause, but it may
nevertheless be a conditio sine quâ non of the attack.

[Footnote 18: _St. Barthol. Hosp. Repts._, vol. xix.]

Acute and chronic inflammations of the mucous membrane of the frontal
sinuses, perhaps even of the nasal membrane, are likewise important;
and although it is probable that the opinions sometimes expressed as
to the significance of these causes are exaggerated, it is equally
true that obstinate and, as it were, illogical persistence in their
removal will sometimes be richly rewarded.

It is especially worthy of note that there need be no local sign
whatever to call the attention of the patient to the presence of the
peripheral irritation.

Nothnagel[19] has described neuralgias which come on in the first week
of typhoid, and are to be distinguished from the general hyperæsthesia
of later stages. He describes an occipital neuralgia of this sort
which finally disappeared under the use of a blister. Other acute
diseases may have a like effect. The writer has seen a severe facial
neuralgia in the {1221} first week of an insidious attack of pneumonia
in a person who was not of neuralgic habit, and before the fever or
inflammation had become at all severe.

[Footnote 19: _Virch. Arch._, vol. liv., 1872, p. 123.]

PATHOLOGY AND DIAGNOSIS.—In surveying the clinical history of the
neuralgias and the circumstances under which they occur, we have
grouped together a large number of symptoms of very different
character from each other, and we have now to inquire to what extent
these symptoms are really united by a pathological bond.

Two opposite opinions have been held concerning the pathology of
neuralgic affections. According to one opinion, every neuralgic
attack, no matter how it is excited, is the manifestation of a
neurosis—that is, of a functional affection of the nervous centres—to
which the term neuralgia may properly be applied. This view is based
on the resemblance between the different forms of neuralgia, or the
apparent absence, in many cases, of any adequate irritation from
without, and the fact that the persons in whom neuralgias occur
usually show other signs of a neuropathic constitution.

According to the other opinion, the various forms of neuralgia are so
many different affections, agreeing only in their principal symptom,
and are due sometimes to congestion or anæmia of the nerves or the
nerve-centres; sometimes to neuritis, the pressure of tumors, or the
irritation of distant nerves; sometimes, finally, to a functional
disorder of the nervous centres. The arguments in favor of this
opinion are that the difference between the symptoms of the different
neuralgias as regards their mode of onset and decline, their duration,
the persistence of the pain, and the degree to which the attacks are
accompanied by organic changes of nutrition in the tissues and in the
nerve itself, are so great as to make it appear improbable that we are
dealing in every case simply with one or another modification of a
single affection.

This is a valid reasoning, and it is certainly proper to exhaust the
possibilities of explaining the symptoms that we find in a particular
case by referring them to morbid processes which we can see or of
which we can fairly infer the presence, before we invoke an influence
of the nature of which we understand so little as we do that of the
functional neuroses. At the same time, it must be distinctly borne in
mind that the symptoms of certain neuralgias, and the relation which
the neuralgias in general bear to other neuroses, can only be
accounted for on the neurosal theory, and that in a given case we can
never be sure that this neurosal tendency is not present and is not
acting as at least a predisposing cause. It is especially important to
bear this possible influence in mind in deciding upon prognosis and
treatment.

We may now review briefly the signs which should lead us to
diagnosticate or suspect the presence of the various special causes of
neuralgic symptoms.

Neuritis is indicated by the presence of organic disorders of
nutrition affecting the skin, hair, or nails, or of well-marked
muscular wasting; by pain, not only occurring in paroxysms, but felt
also in the intermissions between the paroxysms, or continuous
sensations of prickling and numbness, even without pain; by tenderness
along the course of the nerve; by anæsthesia, showing itself within
the first few days of the outbreak of a neuralgia; by persistent
paralysis or paresis of muscles.

{1222} Neuritis may be suspected, even if one or all of these signs
are absent, in the prolonged neuralgias which follow wounds or strains
of nerves or exposure to damp cold, or which occur in nerves which are
in the immediate neighborhood of diseased organs; also where the pain
is relieved by compression of the nerve above the painful part, or, on
the other hand, where pressure on the nerve excites a pain which runs
upward along the course of the nerve.

It may also be suspected in the large class of superficial neuralgias
which follow a regular and protracted course with gradual onset and
decline, and where the pain is felt not only in the region of
distribution of a nerve, but also along its course—that is, in the
nerve-fibres (either the recurrent nerves or the nervi nervorum) which
are distributed in the sheath of the main trunk or the adjoining
tissues.[20]

[Footnote 20: See Cartaz, _Des Névralgics envisagés au point de vue de
la sensibilité récurrente_, Paris, 1875.]

It must be remembered that the study of neuritis, and especially of
chronic neuritis, is still in its infancy, and that we are by no means
in possession of its complete clinical history.[21]

[Footnote 21: See Pitres and Vaillard, _Arch. de Névrologie_, 1883.]

The presence of congestion of the sensory nerves or nerve-centres may
be inferred with some degree of probability where neuralgic attacks of
relatively sudden onset and short duration occur in parts which have
been exposed to heat or cold, or in connection with suppression of the
menstruation, or, it is said, as a result of intermittent fever. The
exacerbations of pain which take place in cases of chronic neuritis
under changes of weather and after fatigue are very likely due to this
cause; and the same may be true of some of the fleeting pains which
occur in chlorotic and neuropathic persons who are subject to
fluctuations of the circulation of vaso-motor origin.

The same vaso-motor influences which cause congestion may also cause
the correlative state of anæmia, which becomes thus a cause of
transient and shifting though often severe attacks, which may be
irregular in their distribution. General anæmia is also a predisposing
cause of severe typical seizures, as has been pointed out above.

The pressure of new growths or of aneurisms is to be suspected when
neuralgic attacks are unusually severe and prolonged, recur always in
the same place, and occur in persons who are not predisposed to
neuralgias. The pains from this cause are apt to be relatively
continuous, but they may, on the other hand, be distinctly paroxysmal,
and may occupy a part of the body far removed from the irritating
cause.

Bilateral pains should also excite suspicion of organic disease,
though they may be due to other causes, such as gout, diabetes, and
metallic poisoning.

Neuralgic attacks may be supposed to be of neurosal origin when they
are of sudden onset and short duration, or when they occur in persons
of neuropathic constitution, and, by exclusion, when no other cause is
found. These conditions are best fulfilled in the case of migraine and
the visceral neuralgias. It must, however, be borne in mind that the
neuropathic predisposition is sometimes well marked even in the case
of the superficial neuralgias, especially the epileptiform neuralgia
of the face.

GENERAL TREATMENT.—To treat neuralgia with satisfaction it is {1223}
necessary to look beyond the relief of the particular attack and
search out the causes by which it was provoked. As has already been
remarked, these are usually multiple, and among them will be found, in
the great majority of cases, some vice of nutrition or faulty manner
of life.

It is safe to say that any dyscrasia occurring simultaneously with
neuralgia, whether gout, phthisis, malaria, or diabetes, should
receive its appropriate treatment, whatever theory we may hold as to
the real connection between the two conditions.

In protracted neuralgias it is always proper to assume that neuritis
may be present—_i.e._ to treat the nerve itself by galvanism and local
applications. Local irritations, such as diseases of the eye, ear,
teeth, nose, or uterus, should be sought out and removed; and
attention may here be called again to the fact that a neuralgia may be
due to some local condition which does not of itself attract the
patient's attention.

Patients who are subject to pain at changes of weather or on exposure
should be suitably protected by clothing, and should have their
cutaneous regulatory apparatus strengthened by baths and friction. The
best protection, however, is incapable of entirely warding off the
effect of atmospheric changes upon the nervous centres. Vaso-motor
changes of neurotic origin can be, in a measure, prevented by removing
the patient from the influence of irregularity of life and emotional
excitement and through an improved nutrition.

If the patient has been subjected to chronic fatigue or nervous
strain, not only must these be avoided, but their action should be
counteracted by the requisite rest and tonic treatment.

Long hours of sleep at night may often be supplemented to advantage by
rest during certain hours of the daytime. If the patient cannot take
active exercise, massage is indicated, and in some cases of anæmia
this may advantageously be combined with the wet pack, in the manner
described by Mary Putnam Jacobi.[22]

[Footnote 22: _Massage and Wet Pack in the Treatment of Anæmia_.]

Where these measures cannot be carried out, the writer has found it of
much service in these, as in a large class of debilitated conditions,
to let the patient rub himself toward the end of the forenoon in a
warm room with a towel wet in cold or warm water, and then lie down
for an hour or so or until the next meal. If acceptable, the same
operation may be repeated in the afternoon.

Neuralgic patients are apt to be underfed, and even where this is not
distinctly the case, a systematic course of over-feeding,[23] with
nourishing and digestible food, such as milk, gruel, and eggs, given
at short intervals, is often of great service if thoroughly carried
out. The full benefit of this treatment cannot always be secured
unless the patient is removed from home, and, if need be, put to bed
and cared for by a competent nurse.

[Footnote 23: See S. Weir Mitchell, _Fat and Blood; and Nervous
Diseases, especially of Women_.]

A change of climate, and especially the substitution of a dry and warm
for a moist and cold climate, will sometimes break up the neuralgic
habit, for the time at least. In making choice of climate or locality,
however, the physician should keep distinctly in view the end that he
desires to gain. Thus, the debility or anæmia which is the essential
condition of many neuralgias may often be relieved by surroundings
which {1224} would not be thought favorable to the neuralgic tendency
as such. Oftentimes the sedative influence of quiet country life is
all that is required.

Of the tonic drugs, cod-liver oil, iron, arsenic, and quinine are by
far the most important, and it is often well to give them
simultaneously. Iron may be used in large doses if well borne, for a
short time at least. Quinine may be given in small doses as a tonic,
or in larger doses to combat the neuralgic condition of the nervous
system. This remedy has long been found to be of great value in the
periodical neuralgias of the supraorbital branch of the fifth pair,
but its usefulness is not limited to these cases. It may be of service
in periodical neuralgias of every sort, and often even in
non-periodical neuralgia.

When the attacks recur at stated intervals care should be taken to
anticipate them with the quinine by about four hours, even if the
patient has to be waked in the early morning for the purpose. Single
doses of fifteen, twenty, or even thirty grains may check the attacks
where smaller doses have failed. Such doses cannot, however, be long
continued, and are not to be classed as tonic.

Of other remedies which directly influence the neuralgic condition,
the following are the most important: opium, aconite, gelsemium,
phosphorus, belladonna, chloride of ammonium, cannabis Indica,
croton-chloral, electricity, hydropathy, massage, counter-irritation,
subcutaneous injections of water, chloroform, osmic acid, etc.;
surgical operations.

Opium is usually employed only for the momentary relief of pain, but
it has also been claimed that in small and repeated doses it may exert
a really curative action. This should not, however, be too much
counted on. Opium should never be used continuously for the simple
relief of pain unless under exceptional circumstances, the danger of
inducing the opium habit is so much to be dreaded. Moreover, both
patient and physician are less likely to seek more permanent means of
cure if this temporary remedy can always be appealed to. It is best
given by subcutaneous injections of the various salts of morphine. The
dose should always be small at first (gr. 1/12 and upward), unless the
idiosyncrasy of the patient is already known; and there is probably no
advantage in making the injections at the seat of pain or in the
immediate neighborhood of the nerve supplying the affected part,
except such as might attend the injection of any fluid (see below).

Belladonna (atropia), which is so often given with morphine to
diminish its unpleasant effects, seems at times, even when given
alone, to have an effect on neuralgia out of proportion to its
anæsthetizing action, which is very slight. It is considered to be
especially useful in the visceralgias.

Aconite, given, if necessary, in doses large enough and repeated often
enough to cause numbness and tingling of the lips and the extremities
for some days, will sometimes break up an attack, especially of
trigeminal neuralgia,[24] better than any other means; but its use is
liable to depress the heart, and it is a dangerous remedy if not
carefully watched. Some patients complain that it causes a marked
sense of depression or faintness, and a feeling of coldness; and
indeed its full therapeutic effect is sometimes not obtained until
such symptoms as these are induced to some degree. The use of the
crystallized alkaloid, aconitia, has the advantage of ensuring
certainty of dose.

[Footnote 24: See Seguin, _Arch. of Med._, vol. i., 1879; vol. vi.,
1881.]

{1225} The susceptibility of different persons to this drug is so
different that the dose should first be as small as 1/400 gr., but
this may be repeated every three hours, and gradually increased to
1/100 gr., or until its physiological effects are felt. Patients must
sometimes be kept under its influence for weeks together.[25] It is,
however, a remarkable fact that occasionally a few full doses will
secure an immunity from pain for a long period. Although most useful
in facial neuralgias, the writer has known it to be effective in
brachial and mammillary neuralgia. Aconitia can now be had in granules
of 1/400 gr., or can be given in alcoholic solution.

[Footnote 25: See Seguin, _Arch. of Med._, vol. vi., 1881.]

Gelsemium is also occasionally very useful in facial and even in
intercostal neuralgia, and is said to be of special service in the
neuralgia due to carious teeth. The commencing dose of the fluid
extract is five minims, which may be gradually increased to twenty, or
until a slight degree of muscular prostration, ptosis, or dilatation
of the pupil is induced.

The use of phosphorus has been revived of late years, chiefly through
the efforts of J. Ashburton Thompson, and it is at least occasionally
of service. Success is said to be best obtained by full doses (about
1/20 gr. every three or four hours, up to 1/5 or 1/4 gr. daily for
some days), watch being kept for signs of gastric irritation. The best
preparation is an alcoholic solution (Thompson's), such as the
following:

  Rx. Phosphorus,       gr. j;
      Abs. alcohol,     fluidrachm vi.
  Dissolve with heat.
      Glycerin,         fluidounce iss;
      Alcohol,          fluidrachm ij;
      Spts. peppermint, minim v.
                 One teaspoonful represents gr. 1/20.

Electricity, if properly used, is capable of temporarily, and even
radically, relieving the neuralgic state. The forms most often
employed are faradic and galvanic electricity, though frictional
electricity has also been coming into use of late, mainly as a
substitute for faradism. The galvanic current is by far the most
efficacious of all. This probably acts mainly by directly inducing
better nutritive and better functional conditions in the nerves and
nerve-centres, but the fact that it is often of use in cases of
undoubted neuritis seems to indicate that it may also influence the
grosser structural changes in the affected parts, if such are present.
It is impossible to explain its action more exactly, and the teachings
of physiological experiments do not lend us much aid.

It is probably not of much consequence which pole is used in the
neighborhood of the affected nerve. It should be remembered that the
peripheral nerve-trunks are so deeply buried that the electrodes
cannot be directly applied to them, as they are to the exposed nerve
of a frog in the laboratory, and, further, that instead of being
isolated they are surrounded with tissues of good conducting power,
into which the current must rapidly flow off. For these reasons the
nerve near which either electrode is applied is virtually exposed to
the action of both poles in almost equal degree; and although it is
more customary to use the positive pole in the neighborhood of parts
which are considered to be in a state of irritation, yet clinical
experience has not justified the conversion of this custom into a
rule. Neither is the direction of the current of material consequence.

{1226} It is, however, very important in acute cases to take care that
the current-strength should not be rapidly changed; and for this
reason the electrode should be drawn slowly to a distance from the
nerve before it is removed, or left in situ while the current is
gradually diminished by a suitable rheostat. As a rule, the former
method is the more practicable.

In the treatment of acute cases moderate currents and short
applications, frequently repeated, are the best. On the other hand, in
cases of long standing, especially cases of sciatica, strong currents
are sometimes more effective, and even interruptions and reversals of
the current may be in place.

The choice of a battery is not a matter of indifference. Any
stationary battery of high interior resistance will answer the
purpose, but most of the portable (zinc-carbon) batteries in common
use are objectionable,[26] for the reason that their interior
resistance is so low in proportion to that of the body that it may
almost be counted out as a factor in determining the strength of the
current. The latter is liable to rise, therefore, quite suddenly as
the resistance of the body—_i.e._ the vascularity of the skin—becomes
modified. This objection is obviated if a large, constant resistance
(water or graphite rheostat) is attached to the battery and kept
always in the main circuit.

[Footnote 26: _Archives of Medicine_, April, 1884.]

Faradism probably owes its efficiency to the indirect effects of
stimulation of the sensitive nerves of the skin. This may be produced
either by the wire brush, which causes a sharp irritation and
reddening, and is to be compared with the counter-irritants, or by the
milder application of a moist or dry electrode or the hand of the
operator. The latter procedure may be compared to the superficial
manipulation which is sometimes so grateful, especially in nervous
headaches.

The value of electricity as a general tonic should be remembered in
this connection.

Hydropathy.—Douches and baths of various kinds have doubtless proved
of much value in the treatment of neuralgia. The majority of them,
however, are difficult of application for the general practitioner,
and we confine ourselves to mentioning the tonic and soothing action
of the wet pack and of the prolonged warm bath, which should be
followed by sponging with cool water, and used under every possible
precaution against exposure.

Long-continued local applications of gentle heat (bags of sand or
salt, or hot water) are often temporarily grateful, and in the
treatment of chronic cases the daily application of hot water or
ice-bags to the spine is said to have a good effect. In acute and
subacute neuritis, and in those forms of neuralgia in which neuritis
plays a large part, such as sciatica, the persistent application of
ice-bags along the course of the affected nerve, even for days
together, is sometimes of great service. Even where we cannot be sure
that neuritis is present, long-continued applications of ice may be of
use, but alternations of cold and heat, on the other hand, are usually
to be carefully avoided. This treatment is safer in chronic than in
acute cases, though it may be useful in either.

Counter-irritation.—A spray of ether may be substituted for ice when
only a temporary chilling is desired, for its counter-irritant effect.
This {1227} has even been used on the face, the eye being protected by
some suitable covering, and a good deal of benefit is to be hoped for
both from this and from the similar use of chloride of methyl.

Debove[27] has found the chloride of methyl, used in this manner,
singularly effective in the treatment of sciatica. A considerable and
long-continued counter-irritation is thus made over a large surface
and without great pain. The neuralgia is said to be greatly relieved
and a rapid cure sometimes affected.

[Footnote 27: _Bulletin générale de Thérap._, cited in the _Boston
Med. and Surg. Journ._, vol. cxii. p. 210.]

Counter-irritation is also practised by making applications of
cutaneous irritants, such as blisters, mustard, turpentine,
chloroform, or of the actual cautery carried in light superficial
stripes over the skin, and repeated if necessary at short intervals.
As a rule, the counter-irritation is more effective the larger the
surface which is covered.

The use of the cautery and of blisters is in place in almost every
form of neuralgia where the temporary disfigurement is of no
consequence.

Of other cutaneous applications, aconite and chloroform liniments,
menthol in substance or in alcoholic solution (drachm j or drachm ij
to fluidounce j), aconite and veratrine ointments, are the most
useful. A strong aconitine ointment, made with Duquesnet's aconitia
and lard (drachm j to ounce j), has been recommended by Webber[28] to
be used in portions of the size of half a split pea, but, though
effective, it needs to be employed with great caution.

[Footnote 28: _Nervous Diseases_, Boston, 1885.]

These applications act in part as irritants, by keeping up a play of
sensitive impressions in virtue of the lodgment which they effect in
the skin, but also, no doubt, by reducing the sensitiveness of the
cutaneous nerve-fibres, and thus removing one source of excitation of
the diseased nervous centres. The remarkable temporary benefit
sometimes obtained from the instillation of cocaine into the eye in
cases of neuralgia of the ophthalmic division of the fifth nerve bears
testimony in favor of this explanation.

Surgical operations for neuralgia are of three kinds—section
(neurotomy), removal of a piece of nerve (neurectomy), and
nerve-stretching. The two former operations are of course rarely
practised, except upon the purely-sensitive fifth pair of nerves, the
latter upon mixed nerves also.

Neurectomy is now almost always substituted for simple neurotomy, and
sometimes still more effective means are taken to prevent the reunion
of the nerve, such as doubling over the cut end, destroying the nerve
throughout the length of the bony canal in which it lies, and even
plugging the canal with cement.[29]

[Footnote 29: Heustis (_Med. News_, Dec. 8, 1883) found that the
infraorbital nerve could be readily drilled out with a piece of piano
wire.]

The inconvenience following nerve-section is as nothing compared to
the pain of a severe and intractable neuralgia. It has rarely happened
that the disease has been increased by the operation, and under proper
antiseptic precautions the surgical risks are not great. There is some
chance of permanent cure, and a much greater chance of securing an
immunity from pain for a long period.

It is important to remember that when the neuralgia occupies the
distribution of several branches of the fifth nerve, an operation on
the one primarily or most severely affected may relieve the pain in
all. On the {1228} other hand, the converse may be true,[30] inasmuch
as the same district is supplied by recurrent fibres from several
different sources. Before any operation is decided on it should be
remembered that even in apparently desperate cases of trigeminal
neuralgia the persistent and thorough use of tonic and other remedies
may in the end be crowned with success, perhaps at the moment when it
is least expected.

[Footnote 30: Cartaz, _Des névralgies envisagés au point de vue de la
sensibilité récurrente_.]

During the past few years the operation of nerve-section has been to
some degree superseded by that of nerve-stretching, as being less
serious in its immediate (though not necessarily in its remote)
consequences, and sometimes more efficacious. Hildebrandt, indeed,
raises the question whether the traction which is apt to be exerted
when a nerve is cut is not an important element in bringing about the
result. On the other hand, cases are reported where neuralgia which
had not been relieved by stretching was cured by resection.[31]

[Footnote 31: Nocht, _Ueber die Gefolge der Nerven-dehnung_.]

The best showing for the operation is in the treatment of sciatica,
but most of the other superficial nerves, including the intercostals,
have been successfully treated in the same manner.

On the other hand, this treatment is not without its dangers. Apart
from the risks of the operation itself, cases have been reported in
which the spinal cord has been injured, so that chronic myelitis has
been set up, and a greater or less degree of paralysis—rarely
permanent, it is true—may be induced by the direct injury to the
nerve.

This means of treatment is therefore certainly to be thought of in
serious and obstinate cases, but not lightly decided on.

A substitute operation for sciatica is the so-called bloodless
stretching, in which, the patient having been etherized, the thigh is
forcibly flexed on the pelvis, and then the leg extended on the thigh
and the foot on the leg (dorsal flexion), and held for a short time in
this position. A very material degree of stretching of the sciatic
nerve is doubtless possible in this way, and a number of cures have
been thus effected. But, though less dangerous than the stretching of
the exposed nerve, this operation is not a trifling one.

In one case of sciatica the writer has seen a neuritis of some
severity lighted up by this operation, perhaps because the disease was
in too active a state, although it had lasted some months. The
operation is probably most indicated in chronic cases.

The anatomical effects of nerve-stretching are manifold. Nerve-fibres
are usually destroyed in greater or smaller number, and the conducting
power of the nerve correspondingly impaired. Small blood-vessels are
broken and the circulation and nutrition of the nerve-trunks altered,
and it is probable that adhesions in and around the nerve-sheaths,
where such exist, are severed. The nerve-fibres ramifying in the
inflamed sheaths of the large trunks may also be ruptured, and it may
be that the displacement of the fluid contents of the nerve brings
about better nutritive conditions.[32] It is also probable that the
operation either directly or indirectly affects the nutrition of the
nerve-centres,[33] and although this is not without its dangers, the
chances are in favor of a beneficial result.

[Footnote 32: See “Die Rückenmarks-dehnung,” Hegar, _Samml. klin.
Vorträge_, 239.]

[Footnote 33: Hegar, _loc. cit._]

{1229} Another means of directly acting on neuralgic nerves is by
subcutaneous injections of water, chloroform, ether, osmic acid,
nitrate of silver, and other substances. The deep injection of water
over the affected nerve is attended with but little danger, and is
occasionally successful. The similar use of chloroform, in doses of 15
to 30 minims, is much more often effective, but sometimes causes great
pain, and even abscess. It has been mainly used in sciatica, also in
other neuralgias, even those of the fifth pair. In this case the
injection is best made through the buccal mucous membrane. This
treatment is not without danger of causing collapse, or even death,
probably due to the wounding of a small vein. In one case of sciatica
treated by the writer the chloroform probably entered the nerve itself
to some extent, as the injection was followed by very severe pain
lasting for several hours, and eventually by some degree of muscular
wasting. The neuralgic pain, which had continued obstinately for a
long period, was, however, cured, and had not returned at the end of
some days, when the patient was lost sight of.

Osmic acid has been used recently in the same way, and the reports
show about an equal number of successes and failures. The dose is
about 8 minims of a 1 per cent. solution, and the injection may be
repeated at intervals of a few days. It has been used successfully in
various parts of the body, including the face and the fingers. The
injection causes no great pain, but occasionally, though rarely,
excites abscess.

Under the general heading of massage a number of manipulations may be
grouped which are of value in the treatment of neuralgia, even of
long-standing cases of sciatica and the like.[34] When, as often
happens in the case of sciatica, the nerve is the seat of congestion
and exudation, strong and deep kneading along its course, with
vigorous stroking upward in the direction of the lymph-vessels, is the
important part of the treatment. Besides this, however, the prolonged
and gentle manipulation of the painful region may greatly relieve the
patient for a time, apparently by acting on the sensitive nerves and
exerting a sort of inhibitory action, in which it is not at all
impossible that an influence upon the attention analogous to that of
Braidism plays a part.

[Footnote 34: See Reibmayr, _Die Massage, etc._, Wien, 1883.]

A striking instance of the effect of this treatment is seen in the
case of nervous headaches, which are often very greatly relieved by a
series of gentle, monotonous movements of the finger-tips, as well as
by the domestic remedy of gently and persistently combing or brushing
the patient's hair. A still more efficient application of a similar
kind is the regular vibration communicated by a large magnet or by the
instrument devised by Mortimer Granville. A thoroughly satisfactory
explanation of the action of this treatment is yet to be furnished.

There is no doubt that in the treatment of neuralgia a persistent and
thorough use of the remedies suggested is usually the key to success.
Nevertheless, special cases are sometimes reached by special means of
treatment, and the following are appended as occasionally useful:
Ammonio-sulphate of copper (grs. ij-vj, taken in divided doses in the
course of the day); salicylate of soda, in full doses; caffeine; tonka
(fluidrachm j of the fluid extract at repeated intervals of a few
hours); oil of turpentine; muriate of ammonia.


{1230} Special Forms of Neuralgia.[35]

[Footnote 35: Consult, in connection with this subject, the sections
on Symptomatology and Treatment.]

MIGRAINE AND PERIODICAL HEADACHE.—In many of the recent treatises upon
nervous disease migraine and headache are removed from the category of
the neuralgias and placed in that of the functional affections of the
sympathetic vaso-motor system of nerves. This classification is based
upon the fact that in many of these cases marked vascular
changes—congestion or anæmia, as the case may be—are observed in the
external tissues of the affected parts, while the sensations of the
patient often lead us to infer the presence of similar conditions
within the cranium. The pain and the other symptoms of the outbreak,
it is thought, are due to the changes in blood-tension in the cortex
cerebri or in the region of expansion of sensitive nerves, or, in
part, to the spasm of the muscular walls of the vessels themselves.
This theory is seductive from its appearance of pathological
simplicity and exactness, but the writer believes, with Anstie,
Latham, Allbutt, and other observers, that it is not borne out by
clinical experience, and that its adoption tends to cloak the wider
relationship that exists between the sensory neuroses.

Migraine, nervous headache, and the superficial and the visceral
neuralgias hardly differ more fundamentally from each other than
individual cases of either affection differ among themselves. It is
not improbable, as we have seen, that all the phenomena of some
neuralgic attacks are wholly or in part the expression of irritation
of the sensory nervous system from without; but in many cases, on the
other hand, the signs of the neurosal tendency are clearly marked, and
there is hardly one of the symptoms of a typical migraine of which the
analogue may not be found, though perhaps faintly pronounced, in one
or another form of superficial neuralgia, while the relation of both
to the whole family of the neuroses is still more clearly evident.

Migraine is a disease of youth and middle life, characterized, in its
most typical form, by attacks of severe headache of a few or many
hours' duration, of gradual onset and decline, ushered in by
well-marked auras involving one or more of the cerebral functions, and
terminating in nausea or vomiting or profuse secretion of pale urine,
or in some other critical nervous outbreak. The pain is usually, but
not invariably, deep-seated. It may be confined to one side of the
head, most often the left, or may involve both sides, either from the
outset or in the course of the attack. The forehead or temple is
usually the first part to become painful, but in severe or prolonged
seizures the parietal and occipital regions are prone to be affected
likewise.

The auras are manifold and important. On the day before an attack the
patient may feel remarkably well, or may complain only of such
sensations as thirst or giddiness. The attack itself is apt to be
ushered in by visual hallucinations of dazzling and vibrating points
or serrated images, sometimes with prismatic outlines, accompanied by
a loss or obscuration of vision over one-half or some other portion of
the field, which lasts half an hour or more, and sometimes clearing up
in one part while it advances in another. Simultaneously or
immediately after this there may be {1231} tingling and a sense of
numbness of the tongue, lips, hand, or one-half of the body, sometimes
followed by partial hemiparesis, and, if the right side be affected,
by more or less aphasia or mental confusion. Occasionally the other
special senses are affected. Sometimes the aura may constitute the
whole of the seizure.

The writer has observed a case in which migraine was represented
throughout boyhood by repeated attacks of subjective numbness and
tingling of the entire right side of the face, the right arm, and the
right half of the body, with aphasia and hemianopsia, followed during
many years by trifling headache or none at all; later in life by
severe pain. Here migraine as well as neuralgia in other forms was a
well-marked family disease.

These auras are especially worthy of notice, because they occasionally
point to epilepsy, an affection with which migraine is allied.

The pain may begin on the same side with these prodromal symptoms or
on the opposite side. Sometimes drowsiness is a marked symptom
throughout the attack, and this differs in significance from the
sound, refreshing sleep with which the paroxysm often comes to an end.
Sometimes the arteries of the affected side seem strongly contracted,
as shown by pallor and coldness of the face and dilatation of the
pupil (angio-tonic form); sometimes, on the other hand, they are
dilated and pulsate strongly, or the latter condition may follow the
former (angio-paralytic form). The radial pulse may show corresponding
modifications. These vascular phenomena are often, however, entirely
wanting.

Migraine appears to be slightly more common in women than in men. The
liability to the attacks often shows itself in extreme youth, usually
increases at puberty, and generally ceases at the age of forty or
fifty. The attacks sometimes recur at regular intervals of a week, a
month, etc., but, on the other hand, they may remain absent for years
unless brought on by some exciting cause.

ETIOLOGY AND CLINICAL RELATIONS.—Migraine is a directly inheritable
disease, and one which stands in a close relationship to the other
grave neuroses, as well as to the neuropathic temperament. Cases are
occasionally seen in which the migraine of youth gives place to
epilepsy in later years. It is often met with also in families and
individuals of neuralgic tendency, and in fact it shades off into
neuralgia of the fifth and occipital nerves on the one hand and into
periodic nervous headaches on the other. It frequently occurs in gouty
persons, and is thought to be related to the brow ague of malaria. The
attacks may be brought on by any of the causes which depress the
vitality of the nervous system, and by various special irritations,
among which errors of refraction are prominent.

The PROGNOSIS is unfavorable in well-marked cases, in which the habit
of regular recurrence is established, and where the neuropathic
predisposition is pronounced and no special exciting cause can be
found. On the other hand, there are many cases where the tendency is
less deeply rooted, and where with the removal of the exciting cause
or causes the outbreaks cease.

Finally, there is great probability that the disease will cease of
itself with advancing years, not always, however, without having left
its mark on the patient's mental and bodily vitality.

{1232} The TREATMENT should be directed first to the detection and
removal of special sources of irritation, whether in the eye, stomach,
uterus, or elsewhere. Causes of anxiety and mental strain should be as
far as possible avoided, and great caution enjoined in the use of
stimulants and narcotics. The nutrition should be maintained at its
highest level by tonics, and, if need be, by electricity, massage, and
hydropathy. Sometimes, besides this a special diet is advisable, for
it seems beyond question that some patients have fewer headaches if
they abandon all animal food, while others—whether because of a gouty
tendency is not clear—do best on a nitrogenous diet with exclusion of
sugar and starch.

Of the drugs used to control the liability to the attacks, the most
important is cannabis Indica, given in doses of about half a grain of
a good preparation of the extract several times daily for weeks or
months together. Valerianate of zinc and the iodide and bromide of
potassium in full doses are also recommended, but are less
efficacious.

In the treatment of the attack itself, besides absolute rest and
quiet, large and repeated doses of guarana or caffeine, either alone
or combined with drachm doses of bromide of potassium, are sometimes
of use if given at the very outset.

It is thought by some observers that ergot or ergotin is of value if
the vessels are dilated, and conversely nitrite of amyl or glonoine if
they are contracted. It must not be forgotten, however, in case of
doubt, that the throbbing due to the latter drugs may increase the
pain.

The writer has known a strong faradic current applied with the
moistened hand to the back of the neck to relieve an attack, and
prolonged but gentle manipulation of the painful area with the
finger-tips may have a like effect if the pain is not too severe; as,
for example, toward the end of a paroxysm.


Neuralgias of the Fifth Nerve.

Three varieties of these neuralgias may conveniently be distinguished:

1. Ordinary facial neuralgia, analogous to the neuralgias of the other
superficial nerves;

2. Intermittent supraorbital neuralgia, sometimes called brow ague,
though by no means always of malarial origin;

3. Epileptiform neuralgia (tic douloureux).

These varieties are of course closely allied, and have many features
and causes in common.

THE ORDINARY FACIAL NEURALGIA is a painful and obstinate malady,
although not so serious as the typical tic douloureux. The pain may
remain fixed in one position or it may shift from one part of the face
to another; and the latter is especially common in those forms which
occur in anæmic or ill-nourished persons. It associates itself readily
with occipital neuralgia, and sometimes also with neuralgia of the
pharynx and other parts. It occurs most often in persons of neurotic
tendencies or impaired nutrition, and may be provoked by disorders of
the ears, teeth, and even distant organs. The possibility of aneurisms
of the internal carotid or of cerebral tumor should also be borne in
mind, and signs of herpes zoster and locomotor ataxia carefully sought
for.

{1233} The relation of caries of the teeth to neuralgia of the fifth
pair forms a very important chapter, which is admirably treated by
J. Ferrier.[36] Opinions on this subject are conflicting and
unsatisfactory, and the fact that many patients have had nearly all
their teeth drawn in the vain attempt to get cured of one of the
severe forms of facial neuralgia often creates an impatience of
further investigation in the matter. Ferrier points out that as a rule
it is not the severest cases of epileptiform tic douloureux that arise
in this way, but, on the other hand, that it is a mistake to conclude,
because a neuralgia is benefited by medical treatment and made worse
by fatigue, exposure, etc., and because it occurs in a person of
neurotic temperament, that it is not likely to be due to this form of
irritation. The teeth need not themselves be the seat of pain, and the
disease in them may be detected only after diligent search.

[Footnote 36: _Les Névralgies reflexes d'Origine dentaires_, Paris,
1884.]

The most important lesions are said to be caries, exostosis, and other
affections involving the pulp-cavity, exposure of the sensitive
dentine, ulcerations of the gums, injuries caused in extraction, and
other diseases of the alveolar process. The wisdom tooth, by its
pressure on other roots and on the gums, is not infrequently the one
at fault.

Chronic inflammation of the mucous membrane of the nose or pharynx is
said to be an occasional cause of neuralgia of the face, as well as of
the upper portions of the body.

THE INTERMITTENT NEURALGIA OF THE SUPRAORBITAL is an interesting
affection to which too little attention has been paid. One variety
seems to bear a certain relationship to migraine, inasmuch as it
occurs under similar circumstances—_i.e._ in distinctly neuropathic
individuals and families, and in attacks of about the same duration
and periodicity of recurrence.

Another variety approaches the other neuralgias in the longer duration
of the attacks, but is characterized by a daily seizure which recurs
with absolute regularity, coming on usually at about nine in the
morning and increasing in severity for an hour or so, then persisting
unchanged until midday or later, when it gradually diminishes, finally
disappearing in the course of the afternoon. As a rule, it is brought
on by catarrh of the frontal sinuses, often following an acute attack
of coryza. A certain amount of neurosal predisposition is often found
in this form, and the first attacks may show themselves in early
youth, rarely in the decline of life. The writer has seen one family
in which a number of members in at least two generations have been
attacked in this way, the seizures having been brought on by
exhaustion or coryza, or both combined.

This form of neuralgia is often greatly controlled by quinine if given
in sufficiently large doses (15 to 20 or 25, or even 30, grains) and
as long as four hours before the attack.

Lange[37] thinks the action of galvanism is remarkably successful, but
the writer's experience does not fully bear this out.

[Footnote 37: Cited in the _Centralbl. für Nervenheilkunde, etc._,
1881, p. 10.]

Seeligmüller[38] speaks very highly of the effect of the nasal douche,
used for the sake of curing the catarrh of the frontal sinuses, and
potassic iodide may be useful by rendering the secretions more fluid.

[Footnote 38: _Centralbl. für Nervenheilkunde, etc._, June 1, 1880.]

THE EPILEPTIFORM FACIAL NEURALGIA, OR TIC DOULOUREUX, {1234} is a
chronic affliction, characterized by the suddenness of onset and the
severity of its paroxysms of pain, which may recur every few minutes
with lightning-like rapidity, either spontaneously or brought on by
motion of the jaw or the taking of food, and disappear again as
quickly. After a group of such paroxysms as this there may be an
intermission of some hours or days. During the attack the patient is
apt to rub the seat of pain with great violence. The path pursued by
the darts of pain may be either in the direction of the nerve-trunks
or in an irregularly inverse direction.

In spite of their sufferings, these patients may present an appearance
of health. In its worst forms, and especially in advanced life, this
variety of neuralgia may be incurable, and at the best it is sure to
tax the care and skill of the physician. Anstie thinks that it is apt
to be associated with a taint of insanity.

The best TREATMENT consists in the most painstaking attention to
hygiene, in the persistent use of galvanism, arsenic, cod-liver oil,
quinine, aconite (see under General Treatment), and phosphorus. Croton
chloral is occasionally of service.

As a last resort, surgical measures (see above) may be appealed to,
but it should be borne in mind that even when the prospect seems most
hopeless the relief under medicinal and hygienic treatment may really
be near at hand. Where section of nerves is without result, the
operation of tying the larger vessels, the carotid or vertebral, on
the affected side may be tried, and offers some chance of success.

OCCIPITAL AND CERVICO-OCCIPITAL NEURALGIAS are second only to
trigeminal neuralgia in severity, though, fortunately, less common,
and either is liable by extension to give rise to the other.

Neuralgic pains in the occipital region may attend Potts's disease of
the cervical vertebræ; and this is especially important to bear in
mind because the osseous deformity is often wanting for a long time.

The writer has known a persistent pain in this region to be due to
intracranial syphilitic disease, and to cease suddenly with the advent
of more serious cerebral symptoms.

CERVICO-BRACHIAL AND BRACHIAL NEURALGIAS are less often indicative of
the neuropathic taint than the facial neuralgias; and, on the other
hand, they are, like sciatica, relatively often due to neuritis set up
by injury, amputation, strains, enlarged cervical glands,
periarthritis of the shoulder,[39] etc., or associated with herpes
zoster. When not due to an unremovable cause the prognosis is
favorable. The treatment needs no special description.

[Footnote 39: See J. J. Putnam, “A Form of Painful Periarthritis of
the Shoulder,” _Boston Med. and Surg. Journ._, 1882.]

INTERCOSTAL NEURALGIA is a very important form, both on account of its
frequency and obstinacy, and because it is often associated both with
anæmia and chlorosis and with affections of the visceral organs,
especially the uterus. The distressing cardiac palpitation of
neurasthenic patients often associates itself with pain in the left
side, and there is an intimate connection between neuralgia of the
cardiac plexus (angina pectoris; see below) and neuralgia of the
intercostal and brachial nerves.

Pain in this region, often due to neuritis, may accompany acute and
chronic thoracic disorders, and may be the precursor of herpes zoster.
{1235} Caries of the vertebræ and meningitis should be thought of, and
cancer if the neuralgia is very persistent, even if it is paroxysmal
in character.

TREATMENT.—Besides the general indications for treatment referred to
above, it is worthy of special note that nerve-stretching has been
successfully tried for intercostal neuralgia. In one interesting case
seven nerves were stretched at one operation.[40] The reporter
discusses the surgical aspects of the operation, and points out that
the nerves should be sought for, not directly beneath the rib, but
behind and beneath it, and thinks that the failure to bear this fact
in mind might lead to puncturing the pleura.

[Footnote 40: Lesser, _Deutsch. Med. Wochenschr._, Sto. 20, 1884.]

MAMMILLARY NEURALGIA (irritable breast of Astley Cooper), though often
met with in company with intercostal neuralgia, may occur entirely
independently. It is sometimes bilateral, and is apt to be associated
with irregularity of the uterine functions. Cutaneous hyperæsthesia is
often present to a distressing degree, and small tumors of either
temporary or permanent duration may make their appearance (A. Cooper),
which, however, do not affect the prognosis.

There is no especially effective TREATMENT beyond what has been spoken
of. Surgical interference is not especially to be recommended, though
it has occasionally been useful.

LUMBO-ABDOMINAL NEURALGIA, or neuralgia of that part of the lumbar
plexus which supplies the flank and abdomen and the external genital
region. These neuralgias are apt to accompany those of the intercostal
nerves and share in their significance.

The most important facts with regard to them are that they are
intimately associated, in relation both of cause and of effect, with
affections of the abdominal and the pelvic organs and of the testis.
Neuralgias of the terminal branches of the lumbar plexus, the
obturator and anterior crural nerves, though well recognized, are
comparatively rare.

One of the chief respects in which they are important is in calling
attention to the possible presence of disease of the hip-joint or of
periarthritis of the hip, as well as of tumors or inflammation within
the pelvis.

NEURALGIA OF THE SCIATIC NERVE is one of the most severe and common
forms. While sharing in the common etiology and history of the other
neuralgias, it is peculiarly prone to be due to peripheral causes,
which give rise to thickening of interstitial and investing connective
tissue of the nerve. The distribution of the pain may be coextensive
with the whole distribution of the great and little sciatic nerve, but
far oftener the patient indicates certain regions as the seat of his
severest suffering; and these are especially the sacral region of one
side, the neighborhood of the sciatic notch, the popliteal space, the
calf, and the outer side of the foot and ankle. Not infrequently the
whole course of the sciatic nerve is traced out by the darts of pain;
and in this case it is the nerves which supply the sheath of the
sciatic itself which are supposed to be the seat of the neuralgic
process.

Sciatica is usually unilateral, but exceptionally bilateral, or
attacks the two sides alternately. The tender points most often met
with are at the sacro-iliac synchondrosis, the posterior border of the
great trochanter, just beneath the head of the peroneal bone, below
and behind the {1236} external malleolus, but numerous others are
likewise noted by Valleix. Sometimes no tender points can be found.
Sometimes, also, it is one or more of the collateral branches of the
sciatic plexus that are the seat of the neuralgia, and the
distribution of the pain and of the tender points varies accordingly.

It is in sciatica pre-eminently—in part, no doubt, because of the
frequency of neuritis—that disorders of sensibility of the skin are
noticed, as well as muscular paresis or spasm. This anæsthesia has
been studied with great care by Hubert-Valleroux and others, and it
has been shown that it is often confined to limited spots, a
centimeter or so in diameter, within which the loss of sensibility may
be nearly absolute. Nevertheless, their functional origin is proved by
the fact that under faradization they may rapidly disappear.

The duration of an attack of sciatica varies from a week or two to
months or even years, and it shows a marked liability to recur,
especially with changes of weather. First attacks occur pre-eminently,
though not exclusively, in middle life, and oftener in men than in
women, evidently because they are oftener exposed to mechanical injury
and, through their occupations, to sudden changes of temperature and
the like.

The occasional causes are numerous, and include sudden wrenches and
jars, even if not very severe, interpelvic pressure from tumors or
impacted feces, etc. Gout, syphilis, and diabetes may act as
predisposing and even exciting causes, and, it is said, gonorrhœa
likewise. Periarthritic inflammations of the hip-joint and varicose
veins frequently excite pains in the various sciatic nerve-branches
which simulate true sciatica.

As has been indicated, although sciatica may be a pure neuralgia (see
under Pathology), running its course without leading to any
appreciable change in the nerve, yet subacute and chronic neuritis is
very common, either as a primary condition or a complication, and its
presence puts a graver aspect upon the case. The pain of neuritis,
when severe, is relatively constant, remittent instead of
intermittent, dull rather than lancinating, increased by motion and
pressure; whereas the purely neuralgic pains are sometimes relieved by
movement. It is, however, doubtful whether an accurate differential
diagnosis is possible (see above). It is to this neuritis that the
muscular atrophy is due which is often so marked, and it may likewise
give rise to various cutaneous lesions of herpetic character. The
severe pain that accompanies typical herpes zoster of this region is
well known.

The TREATMENT of sciatica must vary with the probable cause of the
disease and its stage of progress. Diathetic taints are to be met if
present, and the greatest measure of physical health secured that the
circumstances possibly admit. It is a good precaution in all cases to
secure free evacuation of the bowels and to guard against hemorrhoidal
congestions.

As against the neuralgia itself, the proper means vary with the
acuteness of the attack and the presence or absence of neuritis. For
the acute stage absolute rest is almost always desirable as a prime
condition. Quinine, belladonna, aconite, and turpentine in full doses
should be thoroughly tried, and special reference had to the
periodicity of the seizures.

Frequent and extensive but superficial counter-irritation (actual
{1237} cautery, blistering, ether, or chloride of methyl) is in place
in this stage, and galvanism (constant current) is often of great
service. It is probable that for the acute stage the prolonged use of
mild currents is the best, whereas in more chronic cases the stronger,
even very strong, currents, brought to bear as accurately as possible
upon the nerve itself, are sometimes more useful.

Hydropathic treatment is in great repute both for acute and chronic
cases, but as success in this way demands care and knowledge, the
reader is referred to the special treatises.

In cases of long standing the continued application of ice-bags along
the length of the limb for days together is often of excellent
service, but this method of treatment is not without its dangers and
needs to be carefully watched.

In chronic cases deep injections are of service, and nerve-stretching
(see above) is in place.

THE VISCERAL NEURALGIAS have not received the attention which is due
them both on account of their intrinsic importance and their
constitutional significance. Not only are they found in common with
the superficial neuralgias in the overtired and the underfed, but they
point more strongly than the latter to the neuropathic diathesis,
alternating with such symptoms as migraine, asthma, nervous dyspepsia,
and insomnia. They occur also in the gouty and among the neuropathic
descendants of the gouty, and as a result of functional and organic
disorders of the viscera.

The pain of these neuralgias, though usually described as vague,
ill-defined, dull, etc., yet often stirs the nervous system to its
depths, causing nausea, faintness, sweating, prostration, reflex
disorders of the secretions, and like symptoms.

ANGINA PECTORIS is a neuralgia probably of the pneumogastric and
sympathetic nervous apparatus of the heart. The pain, which is usually
of a heavy, dull, oppressive, or tearing character, and capable of
rising to intense agony, is usually deep-seated, and felt to the left
of the sternum and beneath the breast, often involving the left arm
and side, and occasionally the left side of the face and neck, and
even the leg of the same side or the right arm. It may also, as the
writer has seen, be confined to the sternal region. In the case
referred to this pain recurred every afternoon and evening with great
regularity. Sometimes instead of pain the arm may be the seat of a
tingling numb sensation only.

During the attacks the action of the heart may continue unchanged, or
it may become slow and feeble or intermittent, yet without necessarily
being the seat of organic disease. The onset of anginic attacks is
usually, but by no means always, sudden, and their duration is
commonly short. All the features of the attack, however, are subject
to considerable variation, and nervous symptoms of a variety of kinds,
which it is not necessary to detail, may precede or attend the
seizure. In severe attacks the patient's anguish and prostration are
extreme; the face and extremities become pale and cold, and a cold
sweat breaks out.

In a large proportion of cases, especially the severest ones, these
neuralgic attacks are associated with organic disease of the heart or
blood-vessels.

A variety of causes have been suggested to account for the seizures,
{1238} prominent among which is a widespread contraction of the
arterioles, bringing a sudden strain upon the left ventricle of the
heart. This theory is especially noteworthy because of the success
which has attended the treatment by nitrite of amyl, which brings on a
rapid vascular relaxation. In other cases spasm of this kind is
manifestly absent. Fraenkel[41] has recently defended the view that a
momentary paralysis and over-distension of the left ventricle is the
exciting cause. In other cases all sign of arterial or cardiac disease
is and remains absent.

[Footnote 41: _Zeitschr. für klin. Med._, 1882.]

In this latter group the tendency to the attacks may cease under
appropriate hygienic treatment. Thus, in an instance known to the
writer a lady of usually good health suffered for several months from
slight attacks of præcordial pain, with pain or a sense of numbness in
the left arm, and often a feeling of breathlessness on very slight
exertion. This condition had manifestly been brought about by
prolonged physical and mental strain, and disappeared completely after
a period of rest. Other such cases are described by Anstie,
Allbutt,[42] and others.

[Footnote 42: _London Lancet_, 1884, i.]

In judging of the significance of anginic attacks in a given case the
signs of circulatory disease should first be studiously sought, and
especially, as more likely to escape notice, indications of cardiac
enlargement or weakness, or of increased vascular tension, or of
chronic nephritis.

Dull pains in the intervals of the attacks are also regarded as
important, as indicating the presence of neuritis of the cardiac
nerves, which without doubt often exists. On the other hand, as
pointing rather to a neurotic origin of the symptoms, a tendency,
individual or inherited, to neuralgias of other forms, to asthma,
migraine, and the other neuroses, is to be looked for.

Heredity plays a certain part in the etiology, and among the special
causes of the non-organic form abuse of tobacco is said to be
important.

The TREATMENT would be likely, of course, to be widely different
according to the nature of the case, being on the one hand addressed
to the circulatory apparatus, on the other to the health of the
nervous system, in both cases following well-known lines.

In the treatment of the individual attacks the diffusible stimulants
and the narcotics are of value when there is time to employ them. With
regard to nitrite of amyl and the longer-acting nitro-glycerin, which
have given so much relief in some cases, it would be premature to
confine their use to the cases of demonstrable vascular spasm or even
organic disease, and they are fair agents for trial in the apparently
non-organic cases as well.

A patient of Romberg's used to get great relief from swallowing pieces
of ice.

When the attacks are long continued or frequent, electricity, either
as galvanism or by the wire brush, is applicable, and also
counter-irritation over the chest, even by vesication.

GASTRALGIA (syns. gastrodynia, cardialgia, gastric colic, cramp of the
stomach, etc.) may be associated with organic disease of the stomach
or may occur as an independent neurosis. It is met with in individuals
and families in which asthma, migraine, gout, etc. are found. In
general it is common in persons of nervous, mobile temperament, and is
moreover apt to point to temporary exhaustion from some cause, though
this is by no {1239} means always true. The writer has seen several
sensory disorders of this class at the period of life of which the
menopause is the chief feature. The pains of apparently
hypochondriacal patients doubtless belong sometimes in this group.

The pain of gastralgia is felt primarily at the epigastrium, whence it
may radiate upward and backward along the œsophagus and through into
the back, as well as laterally in various directions. Allbutt says
that it is sometimes associated with anginiform attacks.

Other associated symptoms are dyspnœa, prostration, faintness,
coldness of the extremities, or reflex changes in the action of the
heart, which may beat feebly, rapidly, and irregularly, or more slowly
than normal.

Apropos of the relation of gastralgia to organic disease, it is
important to recall the fact that some of the organic diseases of the
stomach, notably chronic ulcer and cancer, may fail to reveal their
presence by any physical sign. In a case seen by the writer a
cancerous growth had invaded the entire stomach, causing an enormous
thickening of its walls, yet no tumor was to be felt, and the most
marked symptoms were gastralgia and exhaustion.

The relations of gastralgia to the other purely functional disorders
of the stomach are interesting and peculiar. It is beyond a question
that every variety of digestive disorder, from simply delayed and
painful digestion to pyrosis, the formation of gas, and constant
vomiting, is much more often of purely neurotic origin than has been
supposed.

The DIAGNOSIS of catarrhal gastritis as distinguished from nervous
dyspepsia is indeed often difficult or even impossible. Leube has
recently recorded a case where the matter vomited during life
contained fungoid growths, such as are usually considered
pathognomonic of gastritis, and yet at the autopsy the mucous membrane
appeared perfectly healthy.

With these nervous disorders of digestion, which are by no means
confined to hysterical patients, gastralgia may be variously
associated, or it may occur independently of them all, or vice versâ.
On the other hand, digestion may be attended with a sense of
discomfort, often amounting to severe pain, yet without regular
outbreaks.[43] This symptom is classified by Allbutt as a
hyperæsthesia of the stomach rather than as a neuralgia, but from this
to true gastralgia there is only a sliding scale of difference.
Sometimes a persistent neuralgic habit is set up by a local disorder
which itself passes away entirely.

[Footnote 43: Allbutt, _loc. cit._]

TREATMENT.—In acute attacks the aim is simply to relieve pain by
whichever of the well-known methods promises the best. The real field
for thought and care is in the treatment of the underlying
states—first, those which, like gout, anæmia, syphilis, or nervous
debility, predispose to the attacks; second, the local or special
conditions which act as exciting causes. Sometimes it will be found
that such patients have special idiosyncrasies with regard to the
nature of food or time of meals.

In that condition of the system which is indicated by frequent or
paroxysmal excess of uric acid in the urine a long-continued use of
Vichy water or lithia is sometimes of service. If it be finally
concluded that the stomach is in an hyperæsthetic, not in an inflamed,
condition, it may not be advisable to diminish the amount of food,
but, on the contrary, by one means or another, to increase it.

{1240} NEURALGIA OF THE UTERUS AND OVARIES.—Attention has repeatedly
been called to the fact that affections of these organs may excite
neuralgias in distant parts of the body or in the lumbo-abdominal
nerves; but besides these the uterine and ovarian nerves themselves
sometimes are the seat of neuralgia, and it is claimed that
menorrhagia and metrorrhagia may occur as a consequence.

The other abdominal organs and the testis are occasionally the seat of
neuralgic pains, and attacks which involve the liver may be followed
by swelling of the liver and by jaundice.

It is not always easy to assert with confidence whether an attack of
abdominal neuralgia affects the external or the visceral nerves.

NEURALGIA OF THE ANUS AND RECTUM is a well-marked and painful
affection, and the tendency to it may be hereditary. The seizures
themselves may come on spontaneously, especially after fatigue, or may
be excited by slight irritations, such as the passage of hardened
feces, or may follow seminal emissions. The pain may be accompanied by
quick, clonic spasm of the perineal muscles.

The rapid injection of hot water into the rectum often at once
relieves the attack.

       *       *       *       *       *

We have not space to discuss at length the neuralgiform affections of
the joints and muscles and those due to the metallic poisons and other
causes which do not follow the course and distribution of special
nerves.

In accordance with the belief which we have expressed, that neuralgic
attacks are not always of the same nature, but are the manifestations
of many different conditions, we should be inclined to include many of
these irregular affections under the neuralgias instead of classifying
them apart, as Anstie and most writers have done. Thus, a patient of
the writer, a gentleman of middle life, who has had migraine since
childhood and belongs to a neuropathic family, suffers on the
slightest exertion from violent pain in both thighs, which comes on
very gradually, beginning at the knees and spreading upward,
eventually passing away after a night's rest. One might diagnosticate
this as myalgia if he confined himself to topographical
considerations, but the history of the patient and the regular march
of the attacks point to a different conclusion.


{1241}


VASO-MOTOR AND TROPHIC NEUROSES.

BY M. ALLEN STARR, M.D., PH.D.


DEFINITION.—In the term vaso-motor and trophic neuroses it is intended
to include a number of forms of disturbance of circulation and
nutrition which are caused by disorders of the nervous system. Such
disturbances may occur in any part of the body. They are not to be
regarded as distinct diseases, but rather as symptoms of lesions in
the peripheral or central nervous system. They may present themselves
in various forms, as hyperæmia or anæmia or instability of vascular
tone, as atrophy or hypertrophy or disintegration of normal tissue.
Their consideration cannot, however, be assigned to any previous
department of this volume nor relegated to various divisions of it;
partly because in some cases they are to be traced to lesions of the
sympathetic system, not elsewhere considered; partly because of our
ignorance as to the exact location in many cases of the lesion of
which they are manifestations.

It is probable that at a future time this chapter will disappear from
a system of medicine, as the chapter on ascites has disappeared, and
that the symptoms under consideration will be distributed among
various departments as symptoms of ascertained lesions in various
organs. For the present, however, they demand a separate discussion.

It is not possible to distinguish accurately in all cases between the
vaso-motor and the trophic neuroses, for while in many features they
are distinct, in a large proportion of cases they occur together. But
it is not possible to ascribe all trophic changes to vascular
disturbance, nor all vaso-motor changes to a defect or excess of
trophic action. Hence a separate consideration of these allied
subjects must be given. It is always to be remembered, however, that
each may give rise to the other, and that in their pathology they are
closely connected. Vaso-motor disturbances manifest themselves (1) by
a dilatation of the vessels, producing redness, heat, and rapid
metabolism in the part affected; or (2) by a contraction of the
vessels, causing pallor, coldness, and malnutrition; or (3) by an
alternation of these conditions and consequent temporary disturbance
of function. Trophic disturbances may occur in consequence of such
increase or decrease of blood-supply, or independently of any vascular
change, causing (1) an abnormal production of tissue in an organ, or
(2) a decrease in the size and number of its constituent cells, or (3)
an actual degeneration of the elements which make it up, after which
their place may be taken by another kind of tissue. Under all these
circumstances the function of the part affected will be disturbed, and
symptoms will be produced which will vary with the tissue or organ
involved. Hence a {1242} general consideration of these symptoms must
be given. Before proceeding to a detailed consideration of these
neuroses it is necessary to review the physiology of the vaso-motor
and trophic systems, in order to make clear the manner in which they
perform their functions. And inasmuch as the pathology of these
affections is best understood by comparison with experimental lesions
made by physiologists in investigating their function, it will be
treated together with their physiology.


Vaso-motor Neuroses.

[Illustration: FIG. 56. Vaso-motor Nerves and Ganglia accompanying the
Arterioles in a Frog (Gimbert): _C_, arterioles; _N_, vaso-motor
nerve; _G_, ganglion, from which nerves issue, situated at the point
of anastomosis of several capillaries; _R_, fibre of Remak.]

PHYSIOLOGY.—Local Vascular Tone.—Since changes in the force and
frequency of the heart's action, and variations in the total amount of
blood in the body, affect the body as a whole, the state of
circulation in any one organ or part must be dependent upon the degree
of contraction or dilatation of its own vessels. This is known as the
local vascular tone. It is under the control of a system of
nerve-ganglia with their subservient fibres which are found in the
middle coat of all arterioles (Fig. 56). The energy expended by these
ganglia is manifested by a constant moderate contraction of the
circular muscular coat of the artery—a contraction which is as
constantly opposed by the dilating force of the blood-pressure within
the vessel. An exact equipoise between these two forces never occurs,
since each varies constantly, but in a state of health one never
becomes permanently excessive. Considerable variations, however, in
the local {1243} vascular tone are frequently observed. Thus each
organ is influenced to a certain degree by every other, since an
increase of blood in one part must involve a decrease in all other
parts, the total amount of blood in the vessels being constant.
Alteration in the heart's action is felt more quickly in some organs
than in others, and thus the general blood-pressure by its variations
may cause secondarily a disturbance of local vascular tone. The
variations now under consideration, however, are not of this kind.
They are such as are produced by influences acting directly upon the
ganglia in the vessel-walls.

Local irritation is such an influence, and it may excite the ganglia
to increased activity, so producing a contraction of the vessel and
consequent pallor; or it may suspend the action of the ganglia, so
producing a dilatation of the vessel and consequent flushing.

Another influence is irritation acting from a distance and conveyed to
the local ganglia by nerve-fibres. These nerve-fibres can be
distinguished from all others by their structure, being
non-medullated, and by the fact that they have an indirect course,
passing from the central nervous system to the sympathetic ganglia,
and from these to the local ganglia in the vessels. The impulses sent
along these nerves may affect the local ganglia in one of two ways,
and either cause contraction by exciting the ganglia, or dilatation by
inhibiting the action of the ganglia. The result produced has
determined the names given to the impulse, to the fibre transmitting
it, and to the centre whence the impulse proceeds, and hence
vaso-constrictors and vaso-dilators are distinguished from one
another.

The history of the development of the sympathetic nervous system,[1]
as well as its gross anatomy, affords distinct proof that it is not an
independent system, as Bichat supposed, but is closely connected in
its physiological action with the spinal cord and brain. Impulses
which reach the sympathetic ganglia from a distance along the
vaso-constrictor or vaso-dilator fibres originate in the central
nervous system. The nervous mechanism which controls the local
vascular tone is therefore a complex one, consisting not only of the
set of local ganglia connected with larger sympathetic ganglia, but
also of centres in the spinal cord connected with higher centres in
the brain. The brain-centres in turn are complex, consisting of an
automatic mechanism in the medulla regulating the action of all the
subordinate parts below it, and of a series of cortical centres whose
function it is to stimulate or inhibit the medullary mechanism. It
therefore becomes evident that local vascular tone may be modified by
local causes acting on the ganglia in the vessels—_e.g._ cold or heat;
by changes in the sympathetic ganglia—_e.g._ the hyperæmia of the face
in lesions of the cervical ganglia; by reflex action through the
spinal cord—_e.g._ pallor produced by pain; by reflex action through
the medulla oblongata—_e.g._ glycosuria following sciatica; or by
conscious or unconscious impulses coming from the cortex—_e.g._ the
blush of shame, the vaso-motor paralysis of hemiplegia.

[Footnote 1: W. R. Birdsall, “Embryogeny of the Sympathetic System,”
_Arch. of Med._, vol. i. where a bibliography of the subject is to be
found.]

Vaso-constrictors.—Such a mechanism, however complex in structure,
would be easily comprehended if the constant manifestation of energy
in the maintenance of arterial tone had its only source in the action
of the local ganglia in the vessels, and was affected only
occasionally by impulses {1244} from a distance, as has been thus far
supposed. This, however, is not the case, as has been demonstrated by
a series of experiments beginning with the brilliant researches of
Claude Bernard. The classical experiments of the French physiologist
were made upon the sympathetic cord in the neck of a rabbit. Division
of this was found to produce a dilatation of the vessels of the ear.
Irritation of the peripheral end of the divided cord produced a
contraction of the vessels. Division of the spinal nerves connected
with the cervical sympathetic and of their anterior roots, or
irritation of the cut ends, produced effects similar in character to
those caused by division or irritation of the cervical sympathetic.
Destruction of the spinal cord in the lower cervical region, or
division of the cord at any higher level up to the medulla, was
followed by dilatation of the vessels. If the segment of the divided
cord just below the section was irritated the vessels contracted.
Destruction of the medulla at the calamus scriptorius and above it for
three centimeters produced a general dilatation of all the vessels in
the body, but division above this level had no effect. The initial
congestion produced by these various experiments was accompanied by a
rise of temperature in the part. It was followed after a time by a
partial recovery of vascular tone, which was more complete the farther
the division from the local ganglia. These facts warranted the
conclusion that the energy expended by the local ganglia in holding
the vessels in a state of constant moderate contraction is derived
from the central nervous system, primarily from the automatic centre
in the medulla, which in turn is reinforced by each of the secondary
centres in the spinal cord and sympathetic ganglia; and also that
while the medullary centres control the entire body, the cord and
sympathetic centres control only those parts with which they are
especially related. In order, therefore, to the maintenance of normal
vascular tone the local ganglia must be intact, and they must be in
connection with the sympathetic ganglia; these must be active, and
must be connected with the spinal cord; the cord must be normal, and
its tracts from the medulla must be capable of conduction; the
medullary centre must be active, and not hindered or spurred by
cortical impulses of a conscious or unconscious nature. Any injury to
one or more of these parts will produce a vascular dilatation by
interfering with the transmission of vaso-constrictor impulses from
within outward, and any irritation of one or more of these parts may
cause a contraction of the vessels by increasing the normal stimulus
sent to the local ganglia by the vaso-constrictors.

Vaso-dilators.—The action thus far considered has been wholly of a
vaso-constrictor kind, and the dilatation which has been mentioned has
been due to cessation of the constrictor energy normally passing
outward. This may be termed a passive dilatation. It is the kind
produced by division of any one of the sympathetic ganglia or cords.
But further experiments have shown that another kind of dilatation may
be produced, traceable not to a mere cessation of constrictor
impulses, but to an impulse of a positive kind sent to the local
ganglia and resulting in a sudden suspension of their activity. Such
an impulse is really an inhibitory impulse arresting the action of the
ganglia in spite of the continued stimulus sent to them from the
central nervous system. Its result is a dilatation of the arteries,
produced by the blood-pressure within them, which may be termed an
active dilatation. Thus, Bernard {1245} found that irritation of the
chorda tympani caused an immediate flow of blood to the submaxillary
gland because of the dilatation of its vessels. And Dastre and
Morat[2] have demonstrated a similar effect in the head and
extremities after irritation of portions of the cervical sympathetic
and of the peripheral nerves.

[Footnote 2: See _Archives de Physiologie_, “Vaso-dilateurs,” 1879,
1880, 1882; _Comptes rendus de l'Academie des Sciences_, 1880, pp. 393
and 441.]

Much confusion has arisen from the use of the term active dilatation,
and many explanations of its mechanism have been offered. At first it
was supposed that a system of longitudinal fibres in the vessel-wall
acted as opponents to the circular constrictor fibres. This theory,
originating with Stilling and Duchenne,[3] has been lately revived by
Anrep and Cybulski.[4] They hold that since a vessel elongates as well
as dilates with every heart-beat, its total distension is the result
of two factors—viz. transverse and horizontal distension. If one of
these is neutralized, they claim that the other will be increased.
Longitudinal fibres in the wall by preventing elongation may thus
allow the entire force of the heart to be expended in dilating the
vessel. This theory has not, however, been accepted, and with that of
Schiff, that contractile elements of the connective tissue surrounding
the vessel-walls could pull outward the walls and thus dilate the
vessel, has lapsed, because of lack of demonstration of the necessary
anatomical structure in all arterioles. Another theoretical
explanation, that dilatation of the arteries is caused by contraction
of the veins damming back the blood, is disproved by the fact proven
by Dastre and Morat, that blood-pressure increases instead of
diminishing in the veins during vaso-dilator action. Legros[5] and
Onimus,[6] noticing the normal occurrence of a peristaltic motion of
centrifugal direction in the arteries of the retina, which if
increased produced a certain degree of hyperæmia, attempted to explain
the phenomena of dilatation by supposing a sudden increase of
peristalsis. But Vulpian has proved that the peristalsis is both too
slight and too slow in its effects to account for the rapid action of
the vaso-dilators, and Dastre and Morat have shown that the
peristalsis, not being synchronous with the heart-beat, really impedes
the flow of blood. The last theory to be mentioned has a chemical
basis, and is known as the theory of attraction (Brown-Séquard,
Severini.) According to this, the organs, when active, manifest
increased metabolism, to maintain which the blood is drawn toward them
by the chemical changes in progress. This theory was based on the fact
that irritation of the chorda tympani causes an increased secretion of
saliva as well as a congestion of the submaxillary gland. It is now
known, however, that these two acts are independent of each other, as
either can be suspended while the other continues. Hence this theory
too has lapsed.

[Footnote 3: Von Recklinghausen, _Handbuch der Pathologie des
Kreislaufs und der Ernahrung_, 1883, where a full bibliography is to
be found.]

[Footnote 4: _St. Petersburg Med. Wochenschrift_, 1884, i. 215.]

[Footnote 5: _Des Nerfs vaso-moteurs_, Thèse de Concours, Paris,
1873.]

[Footnote 6: _Des Congestions actives_, Paris, 1874.]

The view already stated, that vaso-dilators act by inhibiting local
ganglia which cause contraction, is now accepted, especially since it
is found that such inhibitory activity is constantly displayed by
other parts of the nervous system, and is competent to explain the
facts. The active dilatation produced by the inhibition of the action
of the local ganglia is {1246} therefore to be clearly distinguished
from the passive dilatation caused by the cessation of normal tonic
impulses sent to them from higher centres. The former is a positive
active vaso-dilator phenomenon. The latter is a negative paralytic
vaso-constrictor phenomenon. The former is more effective, the
dilatation being greater in degree and more permanent than the latter,
and resembles exactly the dilatation produced experimentally by
exhaustion of the activity of the local ganglia by over-stimulation of
the constrictors.[7]

[Footnote 7: Goltz, _Arch. f. d. gesammt. Physiol._, xi. 92.]

An important point of contrast which has been established between
vaso-constrictor and vaso-dilator impulses is that while the former
are constant the latter are intermittent. Hence they cannot be
regarded as opponents of one another. In a normal quiescent state
vaso-constrictor energy is always being supplied to counteract the
continued intravascular pressure ever renewed with the cardiac
systole. The vaso-dilators are inactive. In an organ thrown into
functional activity an increased flow of blood at once takes place,
proportionate to the work being done by the organ. Such a functional
hyperæmia might be produced either by a cessation of constrictor
impulses or by an inhibition of their effects. It is by the latter
means and through the vaso-dilators that it is produced, and it is
probably the chief function of the vaso-dilator nerves to regulate the
blood-supply in accordance with the need of a part. For this reason
these nerves have been supposed to pass with the motor nerves to the
muscles. As few organs exist without a possible use, it is probable
that vaso-dilators pass to all parts of the body, as Vulpian asserts,
though they have not been demonstrated in every organ or every part.

Like the vaso-constrictors, the vaso-dilators can be traced to the
spinal cord, and their centres there are governed by a general centre
in the medulla, which in turn may be affected by impulses from the
cortex. A destructive lesion in any part of the vaso-dilator system
does not produce as marked effects as one involving the
vaso-constrictor system, since the symptoms of such a lesion will only
appear when the vaso-dilators are called into play. When the
vaso-dilator nerve to the submaxillary gland is cut, no change is
observed until by some sapid substance put in the mouth its function
should be excited, when the gland is no longer found to flush with
blood as in the normal state. It is by means of the vaso-dilators that
erectile organs become engorged with blood. Eckhard has shown the
nervi erigentes of the penis to be vaso-dilator nerves. If they are
destroyed, the organs will not respond to the wonted stimulus—a
symptom which, however, would only be noticed at intervals. An
irritative lesion of the vaso-dilator system may produce permanent
congestion of an organ or part, but this seems to be rather more rare
than a congestion from paralysis of the constrictors. It is seen in
injuries of the peripheral nerves.

Origin of the Vaso-motor Nerves.—The exact course of the
vaso-constrictor and vaso-dilator nerves has been traced from various
parts into the central nervous system by the careful experiments of
Dastre and Morat,[8] and more recently by Gaskell.[9] It is now
established that they {1247} exist as separate nerves, although they
often run together, and that they usually enter the spinal cord at
different levels.

[Footnote 8: See _Comptes rendus Soc. de Biologie_, and _Arch. de
Physiol._, 1879-84.]

[Footnote 9: W. H. Gaskell, “On the Structure and Function of the
Nerves which Innervate the Vascular System,” _Journ. of Physiol._,
Jan., 1886.]

If the various spinal nerves be cut singly from above downward, and
the effects noted, and if the peripheral ends be irritated and the
effects noted, and if with proper care the results be analyzed and
compared, it will be found that the anatomical connections of the
segments of the spinal cord with the sympathetic ganglia, which are so
evident at each level, are not the ones by which physiological
impulses pass out at that level. The vaso-constrictors of the head,
which can be traced to the superior cervical ganglion, do not come
from the upper cervical region of the cord, as might be supposed from
the connections of that ganglion, but from the first three dorsal
nerves. They reach the ganglion through the sympathetic cord in the
neck, having traversed the inferior cervical ganglion on the way.
There are vaso-constrictors in the cranial cavity which accompany the
third, fifth, seventh, and twelfth nerves to the eye, face, and mouth.
It is still undecided whether they originate in the cord and medulla,
issue in the spinal accessory nerve, and with it enter the cranium
(Gaskell), or reach those nerves by way of the carotid and vertebral
plexus from the inferior cervical ganglion (Dastre and Morat). The
vaso-constrictors of the arm, which can be traced to the inferior
cervical and upper thoracic ganglia and to the thoracic sympathetic
cord, are derived from the seven upper dorsal nerves. It is true that
division of the roots of the brachial plexus causes a slight
dilatation of the vessels of the arm, but this is so much increased
when the dorsal nerve-roots are divided that it is evident that it is
through them that the constrictor fibres chiefly pass. The
vaso-constrictors of the leg, which can be traced into the second and
third lumbar ganglia and lumbar sympathetic cord, are derived from the
five lower dorsal and first lumbar nerves, and only join the crural
and sciatic nerves after passing through the abdominal sympathetic.
The thoracic viscera are probably supplied partly through the branches
of the inferior cervical and thoracic ganglia, and partly through the
pneumogastric, the latter statement being disputed by Gaskell. The
abdominal viscera are supplied partly through the splanchnic nerves,
which are made up of fibres issuing from the cord in the fifth to the
twelfth dorsal nerves inclusive, and partly through the pneumogastric.
Thus the dorsal region of the cord is the origin of the majority of
vaso-constrictor fibres in the body.

The origin of the vaso-dilators is also to be traced to the dorsal
cord. The vaso-dilators of the bucco-facial region come from the
second to the fifth dorsal nerves, whence they pass to the first
thoracic ganglion, and thence by the annulus of Vieussens into the
cervical sympathetic cord. Those of the eye, head, and ear come from
the same ganglion, but have their spinal origin in the eighth cervical
and first dorsal nerves. Those of the arm are traced into the upper
thoracic sympathetic cord, which they reach from the five upper dorsal
and last cervical nerves. Those of the leg are traced to the first and
second lumbar ganglia and the lumbar sympathetic cord, which they
reach from all the dorsal nerves from the sixth downward. Gaskell
holds, however, that the vaso-dilators of the extremities pass out of
the cord in the cervical and lumbar plexuses and accompany the
cerebro-spinal nerves. The vaso-dilators of the thorax and {1248}
abdomen are supposed to pass in the pulmonary plexus and splanchnic
nerves, but this is not yet fully determined.

Gaskell[10] believes that vaso-motor nerves can be distinguished from
motor and sensory nerves in the spinal nerve-roots by the smallness of
their calibre. He finds such fine fibres only in the spinal
nerve-roots between the second dorsal and second lumbar segments of
the cord (in the dog), and in the three upper roots of the spinal
accessory nerve. According to his account, the vaso-constrictors issue
from the spinal cord in both anterior and posterior nerve-roots as
medullated fibres, and pass to the sympathetic ganglia lying on the
vertebræ (proximal or lateral ganglia); there they lose their
medullary sheath, and either end in cells whence new fibres issue, or
more probably pass directly onward as non-medullated fibres, having a
connection with the unipolar cells of the ganglia only for purposes of
nutrition. The number of fibres issuing from any one ganglion is much
greater than the number entering it from the cord; hence it is
supposed that each medullated fibre splits up into a group of
non-medullated fibres; which is possible, as the researches of Ranvier
have shown that each axis-cylinder is made up of numerous fibrils.
Leaving these ganglia, the nerves pass either to the second series of
ganglia (distal or collateral ganglia), whence they issue in plexuses
to enter the vessels, or to the vessels directly, where they divide in
plexuses. It is in the meshes of the plexus that the local ganglia of
the vessel-walls are found. The vaso-dilators are thought to differ
from the vaso-constrictors in passing directly to the distal ganglia
as medullated fibres, not being connected in any way with the proximal
ganglia. Gaskell makes no statement regarding their limits of origin
from the cord, except to state that the nervi erigentes issue with the
sacral nerves. He agrees with the view that the vaso-dilators act as
inhibitory nerves upon the local ganglia.

[Footnote 10: _Journal of Physiology_, Jan., 1886.]

Vaso-motor Reflexes.—Thus far, reference has been made only to fibres
whose direction of transmission is centrifugal, and whose exit from
the spinal cord is by the anterior nerve-roots. There are other
fibres, however, through which centripetal impulses pass, and these
enter the spinal cord with the posterior nerve-roots. The function of
these fibres is to transmit sensory impulses inward to reflex centres,
and thus set in action motor mechanisms of a vaso-constrictor or
dilator kind whose effects are produced at the periphery. There are,
therefore, vaso-motor reflexes, as well as skin and tendon reflexes,
whose centres are in the spinal cord. These reflex acts may be excited
by impulses reaching the centre not only through the vaso-motor
centripetal nerves, but also through the sensory nerves of the
cerebro-spinal system. The effect of changes of temperature on the
circulation in the skin (if the right hand be plunged in cold water
there is a fall of temperature in the left hand), the effect of pain
upon the color of the face and the size of the pupil, the red cheek on
the affected side in pneumonia, the occurrence of glycosuria during
sciatica,—are all instances of such reflex acts. Many vaso-motor
affections are produced by irritation causing reflex effects at a
distance from the seat of irritation—a fact always to be kept in mind.
The utility of counter-irritation to the surface in diseases of the
internal organs is explained by supposing that vascular changes are
produced in those {1249} organs through reflex mechanisms set in
action by the local irritation. While some of these reflexes may have
their central mechanism in the local ganglia, it is probable that the
majority are to be traced to the spinal cord. It is believed that the
sympathetic ganglia are not the seat of reflex centres.

[Illustration: FIG. 57. Diagram to represent the Mode of Action of
Counter-irritants applied to the Chest (Lauder Brunton). The
irritation of the afferent nerves by the blister on the chest wall
gives rise to a vaso-constrictor reflex in the vessels of the lung.]

Since the vaso-motor nerves are connected almost exclusively with the
dorsal portion of the spinal cord, it is very natural to conclude that
the vaso-motor reflex centres are situated in this region; and the
hypothesis has been advanced by Jacubovitch, and strongly urged by
Gaskell,[11] that the cells of the vesicular columns of Clarke, which
are peculiar to this region, are the seat of these reflex mechanisms.
This hypothesis gains some support from the pathology of
syringo-myelia. In this disease the gray matter surrounding the
central canal and the vesicular columns are destroyed. The
characteristic symptoms are vaso-motor and trophic disturbances,
consisting of changes in the vascular tone, changes of local
temperature, and various eruptions, in some cases going on to
ulceration in the skin and mucous membranes. It is, however, undecided
whether the vaso-motor centres of the cord are limited to the columns
of Clarke, or are situated in the gray matter surrounding the central
canal, since both these parts are destroyed in this disease.[12] That
they are not located in the anterior or posterior gray cornua is
determined by the fact that diseases limited exclusively to these
areas do not cause vaso-motor disturbances. The situation of the
various reflex centres for the various parts of the body is at
different levels of the cord, as has been determined by the
experiments already cited to establish the level of origin of the
vaso-motor nerves. The exact location of the vaso-constrictor and
vaso-dilator reflex centres for definite parts is yet to be
ascertained.

[Footnote 11: _Loc. cit._]

[Footnote 12: See Fürstner, _Arch. für Psych._, xiv. 422.]

Vaso-motor Tracts.—These reflex centres are connected with the medulla
by tracts which lie in the lateral columns of the spinal cord,[13]
although it is not determined in which part of these columns. It is
not possible as yet to separate the constrictors from the dilators in
this tract, nor to determine whether it transmits impulses in both
directions or only from above downward. Nor is the course of
associating fibres between reflex centres at different levels known.
In cases of transverse myelitis the control of the medulla is removed
from the vascular centres below the lesion, and the lack of vascular
tone seen in the paralyzed limbs, together with the susceptibility to
local irritation, is the result of this division of the vaso-motor
tracts.

[Footnote 13: “Owsjanikow and Tschirijew,” _Bull. de l'Acad. de St.
Petersbourg_, xviii. 18.]

{1250} Medullary Centres.—It has been stated already that a general
vaso-motor centre with both constrictor and dilator powers is situated
in the medulla. This lies in two divisions on each side of the middle
line, in or just beneath the floor of the fourth ventricle, from the
calamus scriptorius up to the level of the sixth nerve-nucleus. Each
division governs the vascular tone of its own side of the body,[14]
and lesions in its region in man produce unilateral vaso-motor
symptoms.[15] This centre can be excited to reflex action by strong
irritation locally or through the blood, in which case a general
constriction or dilatation of the vessels of the entire body will
ensue. It seems probable, however, that the general centre in the
medulla is made up of a number of special centres, each of which
governs a definite set of organs. The vascular tone of the thoracic
and abdominal viscera is certainly regulated by a series of such
centres. Brown-Séquard and Schiff have produced hemorrhages in the
lungs, pleura, stomach, intestines, and kidneys at different times by
destructive lesions of the medulla, and the well-known experiments of
Bernard, in which by puncture of the medulla local hyperæmia of the
liver or kidneys was caused, producing glycosuria or polyuria, confirm
this view. Lesions of these parts in man produce similar effects.
Charcot has shown that in cerebral hemorrhage ecchymoses may be found
in the stomach, pleura, and endocardium, and that pneumonia is
especially frequent upon the paralyzed side. De Jonge[16] has been
able to collect thirteen cases of diabetes mellitus in which a lesion
of the medulla (hemorrhage or tumor) was found after death; and
Flatten[17] has proven the existence of similar lesions in diabetes
insipidus. The connection of these centres with the liver and kidneys
has been traced elsewhere.[18] The medulla contains a special centre
for the vaso-motor nerves of the abdomen, which are in the domain of
the splanchnic nerves. This centre is excited reflexly by impulses
reaching it through the depressor nerve of Cyon from the heart; so
that when that organ is overburdened it may be relieved by a fall of
arterial pressure produced by dilatation of the abdominal vessels.
Whether the connection of the medulla with the centres in the
semilunar ganglion which preside directly over these vessels is made
by way of the spinal cord or by way of the pneumogastric nerve is
still undetermined, though the researches of Gaskell favor the former
view. Gastric and intestinal disturbances are certainly produced by
nervous lesions in the medulla, but whether they are due to vascular
changes is uncertain. The vomiting of mucus and blood, and the large
watery evacuations which accompany mental shock or anxiety, as well as
the polyuria associated with mental effort, have been ascribed to
irritation of local centres in the medulla governing the
gastro-intestinal and urinary organs by impulses received from the
cortex above. The spleen is under the control of vaso-motor centres,
since section of the splenic branches of the semilunar ganglia will
produce a great enlargement of the organ, and irritation of the cut
end of these branches will produce {1251} contraction.[19] The medulla
also contains a vaso-dilator centre for the erectile tissues of the
genital organs, irritation of which by mental action or local disease
causes impulses to pass to the nervi erigentes by way of the spinal
cord, resulting in a flow of blood to the parts. Although a centre has
been thought to exist controlling the circulation in the lungs, whose
paralysis has been supposed to explain the occurrence of sudden
pulmonary œdema without other known cause, no definite facts regarding
it are known. That the action of the heart is under the control of the
medulla is a fact too well known to require more than a mention. The
physiology of the nervous control of the heart cannot be discussed
here.

[Footnote 14: Owsjanikow, _Arbeiten aus d. Physiol. Instit. zu
Leipzig_, 1871.]

[Footnote 15: M. A. Starr, “Sensory Tract in Central Nervous System,”
_Journ. Nerv. and Ment. Dis._, July, 1884, pp. 396-398.]

[Footnote 16: _Arch. f. Psych._, xiii.]

[Footnote 17: _Ibid._]

[Footnote 18: See Tyson, “Diabetes Mellitus,” _Pepper's System of
Medicine_, Vol. I. p. 195; Edes, “Diabetes Insipidus,” _ibid._, Vol.
IV. p. 30.]

[Footnote 19: Tarchanoff, _Pflüger's Arch._, viii. p. 97; Ross,
_Diseases of the Nervous System_, vol. i. p. 225.]

While these medullary centres are certainly influenced by impulses
reaching them from the cerebral hemispheres, as is evident from the
vaso-motor symptoms produced by mental action—_e.g._ pallor from
fright, blushing, etc.—it is impossible to state in what portion of
the hemispheres in man the higher vaso-motor centres lie. Eulenburg
and Landois locate them in the motor area in animals.[20] They are
certainly beyond control of the will, and are wholly reflex in their
action, a purely mental act in this case being the excitant of a
purely physical result.[21]

[Footnote 20: _Arch. f. Path. Anat._, Bd. lxviii. p. 245.]

[Footnote 21: In addition to the articles already cited the reader is
referred to Landois's _Physiology_, to Duval's article,
“Vaso-moteurs,” in the _Dictionnaire de Médecine et de Chirurgie_,
vol. xxxviii. (1885), for a summary of vaso-motor physiology, and to
Gerhardt's “Ueber Angio-neurosen,” _Volkmann's Sammlung klin.
Vorträge_, No. 209. Gaskell's researches, published in the _Journal of
Physiology_, are the most recent and satisfactory.]

PATHOGENESIS.—From this review of the physiology of the vaso-motor
system it becomes evident that disturbances of vascular tone may be
produced by many different causes acting upon many various parts. They
may be due to local affections of the part in which the symptoms are
present, as in the case of erythema[22] after burns or frost-bite, or
congestion of any organ after injury. They may be due to affections of
the vaso-motor nerves passing to the part affected, as in the case of
vascular changes due to peripheral nerve lesions.[23] They may be due
to affections of the sympathetic ganglia connected with the part
affected, as in the case of migraine,[24] sudden flushing of one ear,
certain cases of polyuria,[25] and Basedow's disease.[26] They may be
due to lesions in the spinal cord affecting the vaso-motor centres[27]
or compressing the nerve-roots on their way to and from the
sympathetic ganglia,[28] as is the case in the various forms of
myelitis and in Raynaud's disease or symmetrical gangrene, and in
meningitis, tumors of the cord, or Pott's disease. They may also be
caused by such conditions in the cord as cut off the vaso-motor
centres from the medullary centres, such as transverse myelitis from
compression or traumatism.[29] They may be due to lesions of the
medulla oblongata,[30] as is seen in some cases of polyuria and
glycosuria,[31] and in cases of universal erythema[32] following acute
fevers. They may be due to diseases of the cerebral hemispheres, as is
evident from the vaso-motor symptoms occurring in hemiplegia and
hysteria. Finally, they may be of a reflex {1252} origin, dependent
upon some obscure source of irritation in a part quite distant from
the region in which the symptoms appear.[33]

[Footnote 22: Vol. IV. p. 511.]

[Footnote 23: Vol. V., “Neuritis.”]

[Footnote 24: Vol. V., “Migraine.”]

[Footnote 25: Vol. IV., “Polyuria.”]

[Footnote 26: Vol. III. p. 761.]

[Footnote 27: Vol. V., “Syringo-myelitis.”]

[Footnote 28: Vol. V., “Meningitis Spinalis.”]

[Footnote 29: Vol. V., “Transverse Myelitis.”]

[Footnote 30: Vol. V., “Medulla.”]

[Footnote 31: Vol. I., “Diabetes Mellitus.”]

[Footnote 32: Vol. IV. p. 512.]

[Footnote 33: Vol. V. p. 205.]

The DIAGNOSIS of the seat of the lesion in many cases of vaso-motor
neurosis may be made if the organ or the exact limitation of the area
affected be ascertained, and the history of the case, together with
the concurrent symptoms of other kinds, be considered. In some cases
no organic cause can be found, and in these a reflex cause should be
diligently searched for.

SYMPTOMS.—A vaso-motor affection may manifest itself either by a spasm
or a paralysis of the vessels. In angiospasm the part affected becomes
pale, and irritation no longer causes a vaso-motor reflex. It looks
shrunken, and if the skin over it is loose it may be thrown into folds
or shrivelled, presenting the appearance seen in the hands after long
immersion in hot water. The lack of blood in the part arrests the
processes of metabolism which are normally constant, and if the
condition continues this may result in such a disturbance of nutrition
that ulceration, or even gangrene, may ensue. The local anæmia,
combined with the cessation of metabolism, produces a fall of
temperature in the affected part, which is then more easily affected
by the temperature of the air than in a normal state, so that exposure
to cold is very liable to cause freezing. These conditions necessarily
produce an impairment of function, so that if the affection is located
in the extremities, as the fingers, they are soon rendered useless.
The term digiti mortui has been applied to this state. In the surface
of the body angiospasm causes cutis anserina, pallor, numbness,
tingling, slight anæsthesia, and analgesia. If it occurs in a limb,
the finer motions are imperfectly performed, and in time the nutrition
of the muscles may be so impaired as to produce atrophy and paresis.
It may even lead to gangrene. Nothnagel has recorded[34] five cases of
sciatica in which the pain produced a reflex spasm of the vessels of
the leg, which, persisting, resulted in partial paralysis, atrophy,
lowering of temperature, pallor, and sensory disturbances. Ross
mentions[35] the sudden appearance of circumscribed patches on the
hands and forearms of washerwomen, in which there is a pallor,
coldness, and partial anæsthesia. These may be limited to the
distribution of a single nerve, and may be accompanied by trophic
affections.

[Footnote 34: _Arch. f. Psych._, v.]

[Footnote 35: Vol. I. p. 221.]

Spasm of the veins may occur as well as of the arteries,[36] or
independently of them. In the latter case the blood will not pass out
of the capillaries. The part will then be blue, swollen, œdematous,
and painful; the temperature will be lowered by increased radiation of
heat, and all the sensations and functions be impaired in greater or
less degree. If this continues, nutrition may suffer, and in the end
gangrene develop, which will take its course and lead to the throwing
off of the part. Grainger Stewart has described such a condition
occurring in both hands and feet.[37] It may be likened to a severe
form of Raynaud's disease.

[Footnote 36: Weiss, “Symmetrische Gangrän,” _Wiener Klinik_, 1882.]

[Footnote 37: Grainger Stewart, _An Introduction to the Study of
Nervous Diseases_, p. 138.]

Angio-paralysis is more frequent than angiospasm, and may be due
either to paralysis of the vaso-constrictors or to excitement of the
vaso-dilators. It shows itself by a bright-red or mottled appearance
of the skin, and increase of local temperature, and more rapid
processes of {1253} nutrition, together with an increase of secretion
if the part is a gland or a mucous membrane, and an increase of sweat
if it is the skin. In the latter case an increased sensitiveness to
changes of temperature, a subjective sensation of heat, and
hyperæsthesia and hyperalgesia may occur. The hyperæsthesia on the
paralyzed side which is present in hemiparaplegia spinalis is ascribed
to the vaso-motor paralysis. But these symptoms soon give place to
others. The dilatation of the vessels, which at first caused an
increased flow of blood to the part, produces a slowing of the
blood-current in the part, just as a river runs less rapidly where it
becomes wider. The slowing of the current in the skin allows of a more
complete cooling of the part as the radiation of heat and the
evaporation of moisture are increased, and the slowness of the renewal
of blood impairs the processes of nutrition, so that to the first
stage of redness, heat, and increased metabolism there ensues a stage
of blueness, cold, and defective nutrition, and the function of the
part may be impaired. In this stage it usually presents a mottled
appearance, and may be slightly swollen and œdematous, and the
continued increase of perspiration gives it a clammy coldness to the
touch. In all of these conditions severe pain, sometimes of a burning
character, is a very distressing symptom (causalgia). These conditions
are seen in peripheral nerve-lesions, and give rise to the appearances
which have been so admirably described by Weir Mitchell.[38]

[Footnote 38: _Injuries of Nerves_.]

A peculiar combination of symptoms may be mentioned here, to which
Weir Mitchell has given the name of erythromelalgia.[39] This disease
begins with tenderness and pain in the soles of the feet, which are
soon followed by a marked distension of the capillary vessels. The
congestion is attended by a sensation of burning pain similar to that
produced by a blister. The surface is at first of a dull dusky-red
color; later it appears purple. The redness is not uniformly
distributed over the sole, but occurs in patches of irregular shape,
being especially frequent over prominent parts exposed to pressure and
friction, and the attacks seem to be brought on by long standing or
walking. At first there is a rise of temperature in the affected
surface, the arteries pulsate visibly, the veins are swollen, and
there may be some œdema. Later, the foot is cold and pale. Sensations
of touch and temperature are normal, but the part is so extremely
tender that walking is impossible. There is no paralysis. One or both
feet may be affected, but the patches of redness are rarely
symmetrical. The hands are occasionally affected. The condition may
occur in paroxysms or may remain for some time. It resists all known
methods of treatment, although applications of cold relieve the
burning pain to some extent and the tenderness enforces rest.

[Footnote 39: _Amer. Journ. of the Med. Sci._, July, 1878.]

With angio-paralysis may be classed the taches cérébrales of Trousseau
no longer considered diagnostic of meningitis, but denoting a weakened
condition of vaso-constrictor action in the local ganglia of the
vessel-wall which may occur upon local irritation of the skin in any
severe disease affecting the nutrition of the general nervous system.

Actual rupture of the capillaries in the course of vaso-motor diseases
is rarely observed, although the stigmata appearing in hysterical and
cataleptic patients may be ascribed to this cause. In this connection
tabetic ecchymoses may be mentioned, which appear suddenly without
local injury, {1254} and resemble an ordinary bruise, running a
similar course. They occur only in the course of locomotor ataxia.[40]

[Footnote 40: Straus, _Arch. de Neurologie_, tome i. p. 536.]

In addition to these forms of vaso-motor affections there is a
condition of instability of vascular tone which manifests itself by
sudden transient changes in the circulation of various organs. This is
a functional affection, usually due to malnutrition. It is seen in
many cases of neurasthenia and hysteria, and manifests itself by
sudden flushes or pallor, alternations of heat and cold, local
sweating, attacks of mental confusion, and inability to use any organ
continuously from disturbance of the power of the vaso-dilators to
maintain a condition of functional hyperæmia.[41] Little is actually
known about the causes of this state of the vascular system, although
much has been written about it. (For a fuller description the article
on Neurasthenia may be consulted.)

[Footnote 41: Anjel, _Arch. für Psychiatrie_, xv. 618.]

Many functional derangements of the internal viscera have been
ascribed to such vaso-motor instability with more or less
probability,[42] but hypothesis of this kind, however plausible, is
evidently beyond confirmation. It is especially in affections of this
kind that causes of reflex irritation are to be carefully sought.
Cutaneous angio-neuroses, such as have just been described, may affect
any part of the body. They usually appear suddenly, producing much
discomfort and an impairment of function in the part if it is an
extremity. They disappear as rapidly as they come. The duration of
such attacks varies from a few minutes to several days. They are very
liable to recur. If it is the vessels under the control of the
cervical sympathetic which are affected, the symptoms will be those of
migraine or of lesion of the ganglia.[43] If it is the vessels in the
extremities which are involved, the condition of digiti mortui or
erythromelalgia or symmetrical gangrene[44] may be produced.

[Footnote 42: Fox, _The Influence of the Sympathetic System in
Disease_, London, 1885.]

[Footnote 43: See p. 1263.]

[Footnote 44: See p. 1257.]

A singular epidemic occurred in France in 1828 and 1830 which was
termed acrodynia. Many persons were suddenly seized with vomiting and
purging, and soon after the onset the extremities became red or
mottled in blotches, swollen and œdematous, and hot, painful, and
tender. The attacks lasted from a few days to two months, and during
this time the skin became thick and hard, the muscles weak and subject
to spasms, and the general health was impaired. Relapses occurred in
many cases, but all finally recovered, and hence the exact nature of
the disease was not ascertained.

COURSE.—In any case of vaso-motor neurosis the course of the disease
and its termination will depend chiefly upon its cause. If the cause
is some permanent lesion of the nervous system, the condition will
remain, and in this case the termination will depend upon the severity
of the symptoms. Angiospasm may be so severe as to lead to gangrene
ana the separation of the part affected, or may be so slight as to
cause only subjective discomfort and a little pallor. Angio-paralysis
may lead to an extreme degree of congestion, which is attended by heat
and pain at first, later by paræsthesia and coolness, with increased
liability of the part to be affected by changes in the surrounding
air. This stage is succeeded by one of less marked dilatation of the
vessels and a spontaneous partial {1255} recovery, although the more
moderate symptoms may continue indefinitely and seriously impair the
function of the part. If the cause is a temporary derangement of
function in the vascular mechanism, is reflex irritation which can be
removed, or is a curable organic disease, the symptoms will subside
rapidly or gradually and perfect recovery may follow. If the condition
is one of irritability in the vaso-motor centres, producing
alternations of flashing or pallor, such as is observed in nervous
exhaustion, it may recur irregularly for a considerable length of time
until the causative condition can be removed.

PROGNOSIS.—The prognosis must be determined in each case by a
consideration of the cause of the affection, of the nature of the
symptoms, of the severity of the disease, and of the possibility of
success in both symptomatic and causative treatment. In the
angio-paralytic cases an eventual spontaneous relief from much of the
discomfort may be promised, although the duration of the symptoms
cannot be predicted.

TREATMENT.—Treatment must be directed primarily to removing or
diminishing the severity of the cause. A review of the section on
Pathogenesis will indicate how wide a field this may include, and the
reader must be referred to the special articles which are alluded to
in that place for therapeutic measures. Special diligence is to be
shown in searching for a source of reflex irritation. When the cause
cannot be reached, and when the symptoms are of such severity as to
demand immediate attention, treatment may be directed to them.

In all conditions of vaso-motor disease it is important to shield the
part from external injury; for if the vessels are dilated they are
liable to rupture, and any abrasion of the surface may produce serious
inflammation and ulceration; and if the vessels are contracted any
injury will be repaired slowly and imperfectly on account of the
anæmia, and may even hasten the approach of gangrene.

Perfect rest, bandaging with cotton, and even the application of a
light splint to the extremities will be advisable in cases of
angiospasm. It is desirable to retain the animal heat, inasmuch as its
supply is deficient. In angio-paralysis rest in a somewhat elevated
position and applications of mild evaporating lotions are indicated in
the early stage; later, the limb may be bandaged. It is not advisable
to attempt by tight bandaging to counteract the effect of the vascular
paralysis, for the nutrition of the limb is liable to suffer and
gangrene may be induced.

Massage of a part affected with vaso-motor symptoms is of great
service, since the circulation can be increased in the veins, and thus
indirectly in the capillaries, and the nutrition of the part can thus
be favored. It is more efficacious in angio-paralysis than in
angiospasm. Too rough rubbing is of course to be avoided, lest the
skin be injured. All counter-irritation is to be strictly forbidden.

Electricity has been used with varying results. According to Erb,[45]
moderate faradic applications contract the vessels; strong faradic
applications, especially with the brush, dilate the vessels. The
galvanic current at first contracts the vessels, but this is followed
by a secondary dilatation, which will be greater and occur more
rapidly the stronger the current used.[46] Cathodal closures contract
the vessels; the anodal {1256} continuous current dilates them widely.
Stabile continuous currents through a nerve dilate the vessels which
the nerve supplies. Inasmuch as vaso-constrictors and vaso-dilators
pass together in many nerves, and are found together in all parts, it
is impossible to apply electricity to either alone. In those cases,
therefore, in which it has been ascertained which set of vaso-motors
is affected, it is not always possible to produce a direct effect upon
that set by electrical treatment. Erb recommends, in conditions of
vaso-motor spasm a trial of the galvanic current, the cathode on an
indifferent point, the anode being applied over the vaso-motor centres
governing the part, and also over the area of the body which is
affected, and held there while a moderate continuous current is
passing, interruptions being avoided; or, the cathode being placed on
the neck, the anode may be applied to the nerves passing to the
affected part; or a strong continuous current may be sent through the
nerve, its direction being changed several times during a moderately
long application. Finally, the faradic brush applied to the part or a
strong faradic current sent through its nerve may relax the spasm. In
any case, all these methods should be tried before electrical
treatment is abandoned.

[Footnote 45: _Electrothérapie_, 562.]

[Footnote 46: To this statement Lauder Brunton assents—_Pharmacology_,
p. 250.]

In vaso-motor paralysis other methods are used. The cathode is placed
on the part congested, and a weak galvanic current is employed with
frequent interruptions or even with changes of the pole; or the
cathode may be moved about upon the reddened skin while a mild
continuous current is passing. A very weak faradic current with wet
electrodes, or even a weak faradic current applied with a brush, may
be of service. Here, again, various methods may be tried.

If the extremities are affected, it may be well to immerse them in a
basin of water which is connected with one pole of the battery, and
the current directed in the manner just described, according to the
case. It must be confessed that no definite results can be predicted
from the use of electricity in these cases, and much more experience
is needed before definite rules can be laid down. The records show
that in apparently similar cases opposite methods of application have
produced favorable effects, while in other cases all methods have
failed. Too much reliance should not be placed in electrical
treatment. Erythromelalgia is an obstinate affection, and symptomatic
treatment, directed chiefly to quieting the pain by opium and allaying
the sensation of burning by cool baths, must be resorted to.

Internal remedies may be tried appropriate to the condition present.
In angiospasm nitrite of amyl inhaled, or nitro-glycerin 1/100 gr.
t. i. d., may give considerable relief, although both of these drugs
are to be used with caution. Chloral hydrate is also of some service,
and where the patient is in pain and suffers from insomnia this may
fulfil several indications. In angio-paralysis ergot has been used
with advantage. Oxygen inhalations are of service. Chloride of
potassium may also be tried. It is evident, however, that such
remedies, acting as they do upon the general arterial system, are not
to be depended upon in the treatment of local conditions, since they
have no selective action upon the affected part. The majority of the
drugs known as sedatives and antispasmodics have been used in these
conditions, but the records of individual cases show that they are not
of much avail. Theoretical therapeutic measures based upon {1257}
experimentation on animals have been fully discussed by Lauder
Brunton,[47] but practical experience has not yet been sufficiently
extensive to warrant any further statements.

[Footnote 47: _Pharmacology, Therapeutics, and Materia Medica_, pp.
229-360. Lea Bros., 1886.]


Symmetrical Gangrene.

SYNONYMS.—Local asphyxia, Asphyxie locale, Raynaud's disease;
Symmetrische Gangrän.

DEFINITION.—Symmetrical gangrene is an affection of the nervous system
characterized by arterial or venous spasm appearing in symmetrical
parts of the body, especially in the phalanges of all the extremities,
which may result in trophic changes or in gangrene. There are various
stages in the disease, which have given rise to the various names by
which it is known. The stage of local syncope, in which there occurs a
moderate contraction of the arterioles and consequent pallor of the
part, may be followed by a stage of local asphyxia, in which the
complete contraction of the arterioles cuts off entirely the supply of
arterial blood, and the regurgitation of venous blood produces
cyanosis of the part; and this, if continued, may result in the
gangrene of the part, which is then thrown off. Instead of a condition
of local asphyxia, there may be a spasm of the smaller veins,
resulting in a local erythema, which may go on to capillary stasis and
then to gangrene. The spasm of the vessels may cease at any stage as
suddenly as it began; and if this occurs in the first or second stage,
no gangrene results.

HISTORY.—While isolated cases of this affection had been recorded as
curiosities during the past two centuries,[48] the disease was first
studied with care by Raynaud in his _Thèse de Paris_ in 1862. He
collected twenty-eight cases which had been described with accuracy or
had been personally observed in the hospitals of Paris, and after a
thorough analysis of the symptoms defined the disease as “a neurosis
characterized by an exaggeration of the excito-motor power of the cord
presiding over the vaso-motor nerves.” He called particular attention
to the condition of spasm in the vessels, and proposed the name
asphyxie locale to designate the peculiar appearance of the parts
affected. He also noticed the resulting gangrene as a new variety of
gangrene, not dependent upon embolism or upon changes of an
atheromatous nature in the coats of the vessels.

[Footnote 48: Schrader, 1629; Hertius, 1685; Bouquet, 1808; Moulin,
1830; Racle, 1859—cited in full by Weiss, “Symmetrische Gangrän,”
_Wiener Klinik_, 1882.]

The condition was at once recognized by others, and several cases had
been reported prior to 1873, when Raynaud published a more complete
article on the subject in the _Dictionnaire de Médecine et de
Chirurgie_ under the title gangrene symmétrique; in 1874 he recorded
five new cases in the _Archives générales de Médecine_, vol. i. pp. 5
and 189.

The disease, having been thus established as a definite nervous
affection, began to be noticed in other countries than France; and
Billroth in Vienna,[49] Weir Mitchell,[50] Mills,[51] A. McL.
Hamilton,[52] and J. C. Warren[53] {1258} in this country, and many
other careful observers, published cases, together with more or less
complete articles upon the disease. In 1882, Weiss produced a
monograph[54] upon the subject containing references to all the cases
which had appeared; and this is still the most complete article to be
found, although the essay of R. Lauer[55] and the discussion of the
disease by the Berlin Medical Society,[56] as well as the short
articles of Schulz[57] and Lutz,[58] deserve mention, for they contain
additional observations of cases and numerous facts not to be found
elsewhere.

[Footnote 49: _Wiener Med. Wochensch._, 1878, No. 23.]

[Footnote 50: _Amer. Journ. of the Med. Sci._, 1878, July.]

[Footnote 51: _Ibid._, 1878, Oct.]

[Footnote 52: _N. Y. Med. Journ._, 1874, Oct.]

[Footnote 53: _Boston Surg. and Med. Journ._, 1879, No. 3.]

[Footnote 54: Weiss, _Wiener Klinik_, 1882, “Symmetrische Gangrän;”
also _Zeitschrift für Prac. Heilkunde_, 1882.]

[Footnote 55: _Inaug. Dissert._, Strasburg, 1884.]

[Footnote 56: _Zeitschrift für klin. Med._, vi. p. 277, 1883.]

[Footnote 57: _Deut. Arch. f. klin. Med._, xxxv. 183, 1884.]

[Footnote 58: _Bäyr. ärzt Intell. Blatt_, 1884, xxxi. 24.]

SYMPTOMS.—The disease begins suddenly in all cases, and the
constitutional symptoms are less prominent than the local ones. In
some cases there are noticed a certain degree of mental disturbance, a
condition of depression with a tendency to sigh and cry without cause,
disturbed sleep with unpleasant dreams, irritability, and headache. A
loss of appetite and disorders of digestion may follow, and then the
local symptoms appear. In other cases, which seem to be the majority,
the local condition develops without any such premonitory disturbances
of the nervous and digestive systems, although these may ensue. The
local symptoms first noticed may be paræsthesiæ or pain in all the
extremities, usually limited to the tips of the fingers and the toes.
These are continuous and severe, and are immediately followed (and
occasionally preceded) by an appearance of ischæmia or of cyanosis or
of erythema, in the order of frequency named.

(1) The fingers may look pale and dead, presenting the appearance of
the so-called digiti mortui, and may be cold, painful, and anæsthetic.
If this condition is moderate in degree, a certain amount of blood
will continue to flow through the contracted arterioles, and then it
corresponds to the description given by Raynaud of syncope locale. If
it is extreme, the part may be wholly deprived of arterial blood, and
then a true local asphyxia is present. In this stage the patients
usually suffer considerably, although some do not complain of pain
until the next stage. The ischæmia is attended with an impairment of
sensation to touch, temperature, and pain, and finer motions become
clumsy on account of the subjective numbness and actual anæsthesia. At
the same time, the fingers look shrunken, the skin being thrown into
folds, as if the hand had been soaked in hot water, or they may appear
as if frozen, the skin being hard and immovable.[59] The secretion of
perspiration may be increased, and the fingers feel damp as well as
cold, or it may be suspended. The local temperature is lowered. If the
part is cut, little or no blood will flow. At this stage the arterial
spasm may suddenly relax and the part return gradually to its normal
condition, the cessation of the constriction of the arteries and the
return of blood being usually accompanied by burning pain, which may
last for some hours. The duration of such an attack may vary from a
few moments to several days. If it continues longer, this stage is
usually succeeded by the second stage, of cyanosis.

[Footnote 59: Finlayson, _Medical Chronicle_, 1885, No. 4.]

(2) The stage of cyanosis results from one of two conditions: either
the arterial spasm is so complete that no blood passes into the part,
in {1259} which case venous blood from lack of vis a tergo or in
response to gravitation regurgitates into the capillaries, distending
them and producing a state of blueness; or a venous spasm occurs,
preventing the exit of blood from the part, which then becomes
actively congested, and the blood in the capillaries, from want of
renewal, soon becomes venous and produces the cyanotic appearance. The
stage of ischæmia may be so short that it is hardly noticed, so that
the patient's attention is first attracted by the swollen, blue, and
extremely painful condition. The skin may be stretched, the tissue
infiltrated with products of exudation, which can be pressed out, as
can also the venous blood, and the surface may itch as well as be
painful. Anæsthesia is rarely present in this stage, and there may
even be hyperæsthesia. The part is cool from the increased radiation
of heat and cessation of the processes of metabolism, the local
temperature being lowered. The small vessels on the surface will be
visibly injected, and capillary ecchymoses may rarely be seen. There
is less liability to difficulty in movement in this stage than in the
former one, as the sensations of the part are not benumbed, but if
present it is due to the swelling. This condition, like that in the
former stage, may cease suddenly, the recovery of the normal
appearance being, as a rule, slower than after a simple ischæmia. The
duration of this stage has varied from a few seconds to several days.
It is usually followed by gangrene.

(3) The condition of local erythema is described here because it may
lead to gangrene, and has therefore been considered by Weiss as one of
the early stages of the disease. As a rule, however, it is not
followed by the death of the part, and the affection in these cases is
probably one of erythromelalgia rather than of symmetrical gangrene.
Like the stage of ischæmia, the stage of erythema may appear suddenly.
The part presents a bright-red or a mottled appearance—is hot and
swollen, and painful. The vessels are visibly injected, the local
temperature is raised, the secretion of sweat may or may not be
increased, and the patient feels a burning sensation rather than pain.
Hyperæsthesia to touch and temperature and pain is usually present, or
the sensations are normal. The blood can be pressed out, but returns
immediately. In this condition of hyperæmia slight injuries lead
frequently to an inflammatory process, ulcers may form in the pulps of
the fingers or around the nails, and the eschars may appear dark and
even gangrenous; or an actual condition of gangrene may appear in the
tips of the fingers, the exact method of its occurrence being a matter
of dispute. The erythematous condition is much more likely to be
permanent than are the other stages of the disease—another fact which
has led to some hesitation in considering it a true stage. This
condition of erythema may be due to a paralysis of the
vaso-constrictors, the converse of the spasm occurring in ischæmia. It
has also been ascribed to an irritation of the vaso-dilators; and this
appears to be the more probable hypothesis.

(4) The stage of gangrene is always preceded by that of cyanosis, and
the death of the tissue is due to the arrest of nutrition consequent
upon a stasis of the blood. It is not necessary to invoke the injury
of trophic nerves to explain its appearance. In the tips of the
cyanotic fingers, on their palmar surface, beneath the epidermis, a
small blister appears, filled with a dark serous fluid or with pus or
blood. This soon ruptures, and a dark dry scab forms, beneath which an
ulceration may go on destroying {1260} the corium, but not penetrating
deeper. In the majority of cases the gangrene is limited to a small
area of the pulps of the fingers, and only involves the superficial
layers of the corium. The gangrenous spot is surrounded by a purple
margin. When the sphacelus has separated a scar remains which is
frequently insensitive. In other cases when the sphacelus is thrown
off it leaves a deep ulcer, which may look as if the lost tissue had
been cut out with a punch, and this gradually granulates and heals. In
still other cases the entire skin of the terminal phalanx may become
black and dry, presenting a true gangrenous appearance. Then a line of
demarcation is formed, usually at the junction of the terminal with
the middle phalanx; separation of the gangrenous part occurs, and a
stump is left covered with thin, glossy skin. This extensive gangrene,
involving an entire phalanx, is the exception rather than the rule.

While the gangrenous process is in progress in the tip of the finger
the nails cease to grow, and may become bulbous and rigid; the
epidermis elsewhere may become dry and desquamate, and ulceration
around the root of the nail may take place. With the completion of the
stage of gangrene, which may last from one to five weeks according to
its extent, the local symptoms terminate.

It is the symmetrical distribution of the local symptoms just
enumerated which is the peculiar characteristic of the disease. The
fingers of both hands, the toes of both feet, symmetrically situated
spots upon the back, trunk, thighs, legs, forearms, and arms (in the
order of frequency named), are affected either singly or in
combination. In the majority of cases fingers and toes are affected
together, and a few spots are seen on the trunk. In many cases the
toes escape. In a large number of cases the face has been affected,
spots of cyanosis appearing on the nose or ears or lips. As a rule,
the stage of gangrene only ensues in the tips of the extremities, but
a few cases are recorded in which little areas of skin elsewhere have
passed through all the stages of the disease. Pigmentation occurs in
spots upon the body when the process does not go on to gangrene.

Among the rare symptoms which have occurred in some cases are great
impairment of temperature, pain, and electric sensations in the
affected extremities; swelling, pain, redness about, and effusion
into, the joints; considerable loss of motion in the muscles of the
hands and feet, with diminution of electric excitability, but no
qualitative change; and oculo-pupillary changes ascribed to an
irritation of the cervical sympathetic fibres at their origin in the
spinal cord.

In addition to the constitutional symptoms mentioned, which may usher
in the disease and may continue during its course, there have been
observed temporary albuminuria, glycosuria, and hæmaturia. Fever never
occurs as a symptom of the disease, and if present must be ascribed to
some other condition. The special senses have been affected in a few
cases. In one case a spastic contraction of the retinal arteries
alternated with attacks of ischæmia in the extremities.[60] The
intellect is usually unaffected, but Weiss observed a case in which
transient aphasia occurred, which he attributes to local spasm in the
arteries of the cortex. The patient could find words only after long
thought, and spoke slowly and with difficulty.

[Footnote 60: Raynaud, _Arch. gén. de méd._, 1874, p. 11; Galezowski
examined the discs.]

{1261} COURSE AND DURATION.—The onset of the disease is sudden. The
symptoms in the first two stages may last only for a few minutes and
pass off, or the disease may pass through all the stages and terminate
in gangrene. It is usual for the first stage of ischæmia to last
several days, varying in severity; for the second stage to last
several days; and for the stage of gangrene to occupy about three
weeks. The shortest duration of a single attack has been ten days, the
longest five months. If the gangrene begins simultaneously in all the
fingers, the duration will be shorter than if it proceeds to one after
another. In one-third of the cases a recurrence of the disease within
a year of the first attack has been observed, and it is probable that
the proportion would have been larger had all the patients been kept
under observation. In some cases three and four attacks have succeeded
each other with some rapidity, some of the attacks being much less
severe and shorter than others. In some cases the condition of
gangrene has developed only in one out of three attacks. When the
condition is one of local erythema the duration may be indefinite, the
state becoming chronic and lasting for several years.

NATURE.—The nature of the disease is a matter of deduction from the
study of the symptoms, no autopsies having as yet been made. As
already stated, the symptoms are explained on the theory of a
vaso-constrictor irritation in the stages of ischæmia and cyanosis—of
a vaso-dilator irritation in the stage of erythema. Whether this
irritation is the direct result of abnormal processes going on in the
vaso-motor centres in the spinal cord, or is the reflex result of
irritation arising elsewhere, is undetermined. Raynaud held that it
must be of central origin, since in his cases galvanization of the
spinal cord modified the arterial spasm. The latter observation has
not been confirmed by other observers. Weiss believes that the
condition may occur in response to irritation arising in the skin, in
the viscera, or in the brain, and thus prefers the theory of reflex
origin. This theory is adopted by several observers, who find a source
for such irritation in the female genital organs in their cases.

ETIOLOGY.—The disease occurs in adult life, only two cases having been
observed in persons fifty years old. It is most frequent between the
ages of fifteen and thirty, although children and adults beyond the
age of thirty are about equally liable. Females are more liable to it
than males, four-fifths of the recorded cases having been in women. It
occurs more frequently in the winter months, exposure to cold being a
common exciting cause. Other exciting causes are nervous exhaustion,
especially occurring in those who are predisposed to nervous diseases
by heredity; general weakness from anæmia, malnutrition, or the
occurrence of acute fever or exhausting disease; and mental agitation,
a fright having preceded the attack in several cases. In women
menstrual disorders and uterine disease have been considered as
etiological factors. Occupation has something to do with its
occurrence, since washerwomen, waitresses, and chambermaids are the
class most often affected. In many cases, however, no cause of local
irritation can be found.

DIAGNOSIS.—The diagnosis rests upon the development of vaso-motor
symptoms in the extremities, situated symmetrically, going on to
gangrene, in a person not afflicted with cardiac disease or with
endarteritis of any kind, and not having been exposed to frost-bite or
ergot-poisoning. The age of the patient, the symmetrical position of
the symptoms, the {1262} persistence of the pulse in the main
arteries, and the limitation of the gangrene to the tips of the
extremities distinguish it readily from senile gangrene. The history
of the case, the absence of itching, and the presence of pain during
the arterial spasm which passes off when the spasm ceases, serve to
separate it clearly from chilblains. Congenital cyanosis is produced
by cardiac anomalies, and the entire body is affected. Ergot-poisoning
can be ascertained by the history.

PROGNOSIS.—Life is not endangered by this disease, no fatal cases
having been recorded. Recovery from an attack is certain, but the
duration cannot be stated, as it will depend in any case on the
character, the extent, and the severity of the symptoms. The
possibility of a recurrence of the attack should be stated to the
patient.

TREATMENT.—The methods of treatment have varied, and none are wholly
satisfactory. If the causes can be met—_e.g._ anæmia, nervous
exhaustion—they should be treated. If not, the disease itself may be
attacked by means of electricity. Or the symptoms may be treated as
they demand it. Electricity has been used by almost all observers. The
faradic current produces an aggravation of all the symptoms except in
the stage of erythema, and has been discarded. The galvanic current
may be employed in several ways. Two methods are in use. In the first
the positive pole is applied over the cervical region, and the
negative pole over the lumbar region, a descending current being thus
sent through the spinal cord. The current should be of moderate
strength, not above twenty-five milliamperes, few patients being able
to endure the strength implied in Raynaud's statement that he used
sixty-four cells of a Daniel battery. The duration of the application
should be ten minutes, and the electricity may be applied once daily.
In the second method the anode is applied over the brachial or lumbar
plexus, as the case may be, and the cathode passed over the affected
extremity, the current being constant and care being taken not to
break it suddenly. The strength, duration, and frequency should be the
same as in the first method. From these two methods, separately or
combined, Raynaud claimed to have seen favorable results. His
assertions have not been confirmed by other observers who have
followed his directions closely, and hence considerable doubt at
present prevails as to the efficacy of the electric current. The
so-called electrical application to the cervical sympathetic is
certainly useless. In the stage of erythema a very weak faradic
current applied to the hands in a bath may be of service.

Many observers have found that the progress of the case to recovery
was quite rapid if the limb were put at rest in an elevated position,
were kept warm by cotton batting or similar bandaging, and were kept
clean with antiseptic lotions when the stage of gangrene set in.
Massage is to be used in all cases, the limbs or affected parts being
gently rubbed with the dry hand or with aromatic liniments or oils.
All local injury, however, and especially counter-irritation, are to
be carefully avoided. General tonic treatment, especially iron and
cod-liver oil, is to be used in all cases.

The pain occurring in the early stages is often so severe as to
require the use of opium or other narcotics. And when the nervous
symptoms are especially aggravated, and irritability and insomnia give
the patient discomfort, bromide and chloral may be employed.


{1263} Diseases of the Cervical Sympathetic.

ETIOLOGY.—Diseases of the cervical sympathetic ganglia or cord may be
of two kinds—either irritative or destructive.[61] They are produced
by pressure upon the cervical ganglia or upon the sympathetic cord
between these ganglia, by tumors, especially aneurisms, and enlarged
glands; by abscesses; and by cicatrices of old wounds in the neck.
They are also due to extension of inflammation from a thickened pleura
in phthisis and chronic pleuritis of the apex. They may be caused by
injuries, such as stab-wounds, gunshot wounds, etc. Any disease which
produces marked irritation of peripheral branches of the sympathetic
in the neck, or of the cerebro-spinal cervical nerves, may cause
reflex phenomena resembling the symptoms of actual disease. From such
phenomena it is not justifiable to conclude that the sympathetic cord
and ganglia are the seat of lesions, and the only cases which will be
considered here are those in which actual disease was proven to be
present by an autopsy.

[Footnote 61: Ogle, _Medico-Chirurgical Transactions_, xli. 397-440,
1858, 27 cases; Poiteau, “Le Nerf sympathetique,” _Thèse de Paris_,
1869, 19 cases; Eulenburg and Guttmann, _Die Pathologie der
Sympathicus_, 1873; Nicati, _Le Paralysie du Nerf
sympathique-cervicale_, 1873, 25 cases; Seeligmüller, _Inaug.
Dissertation_, 1876; Mitchell, _Injuries of Nerves_; Mobius,
“Pathologie der Sympathicus,” _Berlin. klin. Woch._, 1884, Nos.
15-19.]

Inasmuch as the cervical sympathetic is in close anatomical connection
with the spinal cord, especially with the eighth cervical to the
second dorsal segments (the so-called cilio-spinal centre of Budge),
and as the functions of the sympathetic are dependent upon the
integrity of the spinal cord, it is evident that any lesion of the
nerves uniting it with the cord, or any lesion in the cord itself at
the levels mentioned, may produce symptoms which resemble closely
those of disease of the sympathetic. Thus, cervical pachymeningitis,
myelitis (especially from injury of the cord, or hæmato-myelia), and
diseases of the cervical vertebræ which produce either or both
conditions, may cause a train of symptoms somewhat similar to those to
be described.[62] A careful distinction must be made between primary
and secondary disease of the sympathetic, between reflex and direct
symptoms, between lesions in its substance and lesions in its
governing centres in the spinal cord. The symptoms produced by
affections of a reflex or central nature are rarely as numerous as
those of disease of the sympathetic itself. An example of such a
secondary affection is the combination of sympathetic symptoms
occurring in progressive muscular atrophy. And, finally, since mental
action of an emotional nature may cause flushing or pallor of the
face, with profuse sweating and variations in the size of the pupil
and prominence of the eyeballs, as well as palpitation or arrest of
the heart, there is reason to believe that symptoms of sympathetic
disease may be produced by cerebral lesions.

[Footnote 62: Ross, _Diseases of the Nervous System_, 2d ed., i.
686-688.]

PATHOLOGY.—The pathological anatomy of the cervical sympathetic is
obscure. This is probably owing to the fact that the ganglia are
rarely examined, and pathologists have not been familiar with their
histology. Lesions of the cervical sympathetic have been described in
almost every imaginable form of disease, and at one time, when many
obscure conditions were blindly termed sympathetic, the records were
filled with descriptions of fatty degeneration or interstitial
inflammation or pigment deposit in the ganglia. As no actual symptoms
of disease of the cervical {1264} sympathetic, as now understood, were
present in such cases, it is impossible to believe that the lesion was
other than hypothetical.

The conditions which have been observed in a few carefully-studied
cases of primary disease have been—(1) A parenchymatous inflammation
of the cells of the ganglia, attended by swelling, loss of nuclei,
granular and fatty degeneration, and by atrophy, together with a
degeneration of the fibres issuing from the cells. (2) A sclerotic
process in the connective tissue in and about the ganglia and in the
nerves, resulting in such an increase in the interstitial tissue as to
compress and injure the cells and axis-cylinders. These may be
observed together in the later stages of the disease. (3) In a number
of cases the capillaries within and about the ganglia have been found
dilated, tortuous, and varicose, and hemorrhages from them are not
rare.

SYMPTOMS.—The symptoms of irritation of the cervical sympathetic are
dilatation of the pupil, widening of the palpebral fissure, protrusion
of the eyeball, pallor of the entire side of the face and head, with
slight fall of local temperature and possibly an increased secretion
of perspiration, and an increased frequency of the heart. It is rarely
that these are all observed in any case, dilatation of the pupil with
slight pallor and rapid pulse being the only signs of irritation as a
rule. Such irritation is a less common occurrence than might be
supposed, many lesions which produce pressure even of a slight degree
on the sympathetic having caused symptoms of a suspension of its
function rather than of an increased activity. This is doubtless due
to the non-medullated structure of the fibres, which thus lack
protection from injury.

The symptoms of destructive disease of the cervical sympathetic are
the converse of those just mentioned, and they are all present when
the part is seriously involved. The patient will then have a marked
contraction of the pupil, which no longer responds to light or to
irritation of the skin of the neck, but may change slightly in the act
of accommodation. It resists the action of mydriatics. The vessels of
the choroid and retina may be dilated, as well as those of the iris,
in which case the patient will feel a sense of weariness on any
long-continued attempt to use the eyes. There is no actual disturbance
of vision, and the cornea is not usually flattened, as was formerly
supposed. There is a noticeable narrowing of the palpebral fissure,
the upper lid falling slightly as in a mild state of ptosis, and the
lower lid being slightly elevated. This is due to the paralysis of the
muscles of Müller in the eyelids, which are controlled by the
sympathetic. It is present in 90 per cent. of the recorded cases, and
in many the apparent size of the eye is reduced a half. Retraction of
the eyeball is a less constant symptom, and one which develops only
after the disease has existed some time. It is due partly to the
paralysis of the orbital muscle of Müller, and partly to the decrease
in the amount of fat in the orbit behind the eye. A marked symptom,
and one which is constant, is a dilatation of the vessels of the face,
conjunctiva, nasal mucous membrane, ear, and scalp. This is attended
by redness, a subjective sense of heat, and an actual rise of local
temperature, which may exceed that of the other side by 1.5° F.,
measured in the auditory meatus or nose. This vascular congestion has
persisted in some cases for three years. In others it has been
followed much earlier (in nine months) by a partial or complete return
to the normal condition, and {1265} even when the local temperature
remains higher on the affected side, the visible congestion and the
sensation of heat may have disappeared. The dilatation, succeeded by
the contraction (normal tone), of the vessels has led to a division of
the disease into two stages, and in a few cases the affected side has
become paler than the other in the second stage. In both stages the
part affected is less sensitive to changes in the external
temperature.

An increased secretion of tears and of perspiration has been supposed
to accompany dilatation of the vessels of the skin of the head
inevitably. This is not a constant symptom, as the recent cases have
demonstrated. And no definite statement of the effect of disease of
the cervical sympathetic on the occurrence of dryness or dampness of
the face can be made, both conditions having been observed. A
difference between the degree of moisture on the two sides of the face
on exposure to heat is usually present. Palpitation of the heart has
been an annoying symptom to the patient in many cases, and is usually
associated with a marked slowing of the pulse. This was reduced from
74 to 66 in Möbius' case,[63] and remained slow for some weeks. The
frequency of the heart may, however, be increased after the first
period of slowing, but never reaches a very high rate (88 in the case
cited). A slight atrophy of the affected side of the face has been
observed in several cases, appearing after the disease has existed for
some time. The muscles of the cheek feel flabby and are slightly
sunken; but the condition does not approach in severity true facial
hemiatrophy, nor is it sufficiently rapid to be considered due to a
trophic disturbance. Changes in the secretion of saliva, dryness of
the nasal mucous membrane, and symptoms referable to paralysis of the
intracranial vessels, such as might be expected from the result of
physiological division of the sympathetic, have only been occasionally
observed. Glycosuria has been noted in a few cases.[64]

[Footnote 63: _Berlin. klin. Woch._, 1884, No. 16.]

[Footnote 64: Gerhardt, _Volkmann's Sammlung klin. Vorträge_, No. 209,
“Ueber Angioneurosen,” p. 11.]

COURSE.—The course of the disease has been divided into two stages, as
already mentioned, the majority of the symptoms remaining permanently
from the onset. The second stage is characterized by the cessation of
the dilatation of the vessels, by the appearance of retraction of the
eyeball, and by the development of slight facial atrophy. In the cases
where the sympathetic is extensively destroyed by the lesion no
recovery is possible. When it is simply divided by a wound there has
been a considerable degree of recovery, probably due to a spontaneous
union of the divided ends and re-establishment of the function. From
these facts the prognosis can be deduced.

DIAGNOSIS.—The symptoms are so characteristic that there is no
difficulty in reaching a diagnosis. The most important point in any
case is to determine the cause, care being taken to consider all the
possibilities already mentioned in discussing the causation. The
symptoms of lesion are always unilateral.

TREATMENT.—If the cause can be removed, an indication for treatment is
afforded. Sources of reflex irritation are to be eliminated. If the
sympathetic has been divided by a wound, it may be well to unite the
cut ends, as in suture of other nerves, although this has not yet been
attempted; otherwise there is little hope from any method of
treatment. {1266} Electricity has been applied in vain, and
galvanization of the sympathetic in the neck is now regarded by all
good authorities as useless.

Diseases of the thoracic and abdominal sympathetic ganglia and cords
have been suspected, but nothing definite is known of their symptoms
or pathology; the statements which have recently been made regarding
visceral neurosis not being based upon any cases in which post-mortem
lesions were found.


Trophic Neuroses.

TROPHIC NERVES AND NERVOUS CENTRES.—The nutrition of the body depends
upon the nutrition of the individual cells of which it is made up.
Each cell has the power of appropriating from the blood such
substances as will preserve its existence, enable it to perform its
functions, and produce a successor. Whether this power is inherent in
the cell or is controlled by the nervous system is a question upon
which authorities are divided. Those who hold the first position deny
the existence of trophic nervous centres and of trophic nerves from
those centres to the organs and elements of the body, claiming that
this hypothetical trophic system has not been demonstrated
anatomically, and that the facts urged in its support are capable of
another interpretation. Those who believe in the existence of a
trophic system have been able to demonstrate the existence of fine
peripheral nerve-fibres passing to and ending in individual cells of
the skin, glands, and other organs,[65] and have brought forward a
large collection of facts which merit a careful examination.[66] They
are as follows:

[Footnote 65: _Bericht der Section für Dermatologie, Versammlung
Deutscher aerzte_, Strasburg, 1885; _Vierteljahrschrift für
Dermatologie und Syphilis_, 1885, 4 Heft, S. 683.]

[Footnote 66: “Tropho-neurosen,” _Real Cyclopædie f. d. gesammt.
Medicin_, vol. xiv., 1883; Erb, _Ziemssen's Cyclopædia_, xi. pp.
408-423.]

ATROPHY.—When a nerve is cut certain changes occur in it which are
known as Wallerian degeneration.[67] This affects the peripheral end
of a severed nerve, the peripheral end of a severed anterior
nerve-root, and the central end of a posterior nerve-root. To maintain
its integrity a motor nerve must be in direct continuity with a normal
cell of the anterior cornu of the spinal cord; a sensory nerve must be
in connection with the intervertebral spinal ganglion on the posterior
nerve-root. Nerves which pass between two such ganglia do not
degenerate when cut. The degeneration consists[68] in a coagulation of
the myelin in the medullary sheath, a fatty degeneration of the
coagulum, and a gradual absorption of the débris. The axis-cylinder is
compressed, and finally disintegrated, by a mass of protoplasm which
develops about the nuclei of the interannular segments, and after
undergoing fatty degeneration its débris becomes mingled with that of
the myelin, and is also absorbed. The sheath of Schwann, whose nuclei
have in the mean time increased by a process of subdivision, is partly
filled by the protoplasm (from which the new axis-cylinder develops if
regeneration occurs), remaining as a fine {1267} thread of connective
tissue when all other traces of the nerve-fibre have disappeared.
There may be a proliferation of cells of the endo- and perineurium at
the same time which aids in the transformation of the nerve into a
connective-tissue strand. This process of degeneration involves the
terminal plates by which the nerves join the muscles, but the
terminations of the sensory nerves—_i.e._ tactile corpuscles—do not
appear to be affected. The central end of the cut nerve may display a
similar change for a distance not greater than one centimeter; it
usually develops a bulbous swelling of connective tissue, and retains
its conducting power indefinitely.

[Footnote 67: Waller, _Philosoph. Transactions_, 1850, ii. p. 423;
_Comptes rendus de l'Acad. de Sci._, 1852-55.]

[Footnote 68: Ranvier, _Leçons sur l'Histologie de Système nerveux_,
Paris, 1878; Von Recklinghausen, _Pathologie der Ernahrung_, 1883.]

Degeneration in the tracts of the spinal cord occurs after various
forms of lesion,[69] and is similar in its processes to degeneration
in the peripheral nerves. The increase in the connective-tissue
elements is more noticeable in contrast with the parts unaffected, and
from the density of the tract involved the result has been called
sclerosis. The recent researches of Homen[70] have shown that the
process of degeneration begins in the entire length of the affected
tract, and does not proceed from the point of lesion onward, as was
formerly supposed.

[Footnote 69: See Vol. V., “Myelitis—The Secondary Scleroses,” p. 892;
Schültze, _Arch. für Psych._, xiv. 2.]

[Footnote 70: _Fortschritte der Medicin_, 1885, No. 9.]

When a muscle is separated from its connection with the central
nervous system, either by a division of the nerve passing to it or by
a destruction of the cells in the anterior cornu of the spinal cord
from which that nerve arises, it undergoes an atrophy which is
peculiar in being immediate and rapidly progressive, thus contrasting
strongly with the gradual and slighter atrophy from disuse in cases of
cerebral paralysis where the cells mentioned and the nerve-fibres are
intact. There is at first a simple diminution in the number of the
fibrillæ of which the muscular fibre is made up, together with an
increase in the interstitial connective tissue nuclei. Then an
albuminoid and fatty degeneration of the muscular elements occurs,
with a proliferation of muscle-corpuscles or nuclei, and a gradual
absorption of the débris. The interstitial connective tissue then
increases rapidly, forming fibrous bands through the degenerated
muscle which compress the few muscular fibres remaining, until as a
result the muscle is transformed into a mere ribbon of connective
tissue without any power of contractility.[71] As these changes go on
the electrical reactions change, the three degrees of reaction of
degeneration corresponding to the three stages of atrophy
described.[72] These phenomena of nerve- and muscle-degeneration are
observed in traumatic or idiopathic neuritis, in acute and chronic
poliomyelitis anterior, in general myelitis involving the anterior
cornua, and in bulbar paralysis.

[Footnote 71: Hayem, G., _Recherches sur l'Anatomie pathologique des
Atrophies musculaires_, Paris, 1873; Ross, _Diseases of the Nervous
System_, vol. i. p. 238.]

[Footnote 72: See Vol. V., “Electric Reactions.”]

The influence of the nervous system on the nutrition of the bones has
also been ascertained. When a bone is developing, a lesion of the
nerve to it, or of the deeper portion of the anterior cornua of the
spinal cord from which these nerves arise, will modify and partly
arrest its growth. This is often seen in anterior poliomyelitis and in
hemiatrophy of the face occurring in children. In the adult a no less
marked effect is produced, although the results are less noticeable. A
condition known as {1268} osteoporosis is caused, consisting of an
enlargement of the Haversian canals and an infiltration of fatty
matter into them and an actual decrease in all the inorganic
constituents of the bone, which loses in weight, becomes thinner and
more fragile, so that spontaneous fractures may occur.[73] This
condition has been noticed more frequently in diseases of the spinal
cord than in neuritis; it is said to occur in locomotor ataxia. It has
been found in a few cases of long-standing hemiplegia and also in
dementia paralytica, no explanation of its pathogeny in these
instances, however, being offered. In a case of ataxia with a lesion
in the medulla which involved the nuclei of the fifth, ninth, tenth,
and eleventh nerves on one side, all the teeth of the upper jaw on
that side fell out within a few weeks, those in the lower jaw
remaining.[74] Changes in the nutrition of the bones have also been
recorded in cases of progressive muscular atrophy in the paralyzed
limbs.[75]

[Footnote 73: Weir Mitchell, _Amer. Journ. of the Med. Sci._, 1873, p.
113; Charcot, _Arch. de Phys._, 1874, p. 166.]

[Footnote 74: Demange, _Rev. de Médecine_, 1882, p. 247.]

[Footnote 75: Friedreich, _Progressive Muskelatrophie_, p. 347, 1873.]

The condition of the skin and its appendages is influenced decidedly
by changes in the nervous system, either in the nerves, in the spinal
ganglia, or in the central gray matter. Here it is the sensory nerves
which convey the trophic influence, not the motor nerves, as in the
cases hitherto considered; and when the lesion producing trophic
changes in the skin is central, it is situated in the posterior cornua
of the spinal cord or in the gray matter near the central canal. The
glossy skin seen on the fingers after injuries to the nerves is a type
of such atrophy from disturbance of trophic impulses. Glossy fingers
present a smooth, shining appearance, are dry from the diminution in
the secretion of sweat, feel soft and satin-like to the touch from the
marked thinning of the skin, and frequently show a defective or
irregular growth of the nails, which may be ridged, curved, or
deformed.[76] They are red and mottled from accompanying vaso-motor
paralysis, and are usually hot and painful. Changes in the
pigmentation of the skin and hair are recorded as a not infrequent
accompaniment of severe neuralgia and as a result of great mental
anxiety. Thus in several cases of supraorbital neuralgia the eyebrow
on the affected side has turned white; in infraorbital neuralgia the
beard has become gray; and in both the hair has been observed to fall
out.[77] The sudden turning white of the hair is ascribed to a
swelling of the hair by air within it.[78] In one case, frequently
cited, the hair and nails fell out after a stroke of lightning.

[Footnote 76: Weir Mitchell, _Injuries of Nerves_. See also Vol. IV.
p. 683.]

[Footnote 77: Seeligmüller, _Lehrbuch der Krankheiten d. Peripheren
Nerven_, p. 157, 1882.]

[Footnote 78: _Arch. f. Path. Anat._, xxxv. 5, 575, Landois.]

When a gland is cut off from its nervous connection with the cord or
cerebral axis by section of its nerves, its function is impaired and
its nutrition suffers, so that after a time it loses weight and
undergoes a progressive total atrophy. This has been proven
experimentally in animals in the submaxillary gland. It has been
observed in the testicle in man after division of the spermatic nerve
(Nélaton) and after destruction of the spinal cord by traumatic and
idiopathic myelitis (Klebs, Föster).[79] The sweat-glands are known to
be under the control of a central {1269} nervous mechanism, as cases
of hyperidrosis, anidrosis, and chromiodrosis prove;[80] and an
atrophy of them and of the sebaceous glands has been observed[81]
after nervous lesions.

[Footnote 79: Cited by Samuel, _Realcyclop., loc. cit._ See also
Obolensky, _Centralblatt für med. Wissen._, 1867, 5, 497.]

[Footnote 80: See Vol. IV. pp. 583-586.]

[Footnote 81: See Vol. IV. pp. 683 _et seq._]

Progressive hemiatrophy of the face is treated elsewhere. The
following case of progressive hemiatrophy of the entire body may be
mentioned here: A boy, aged fourteen, dislocated his ankle, which in a
few days became swollen, red, hot, and painful. The inflammation
extended up the leg, but did not involve the knee, and soon subsided.
After a short time the foot began to atrophy. The atrophy extended up
the leg, and involved the thigh; it then progressed to the trunk and
the arm, and lastly to the face on the affected side, until in the
course of two years there had developed a unilateral atrophy of the
entire body. Muscles, fat, and bones were all affected, but no
difference in the skin or hair of the two sides was noticed.
Fibrillary tremors were present in the muscles. The electric reactions
were not altered, but were gradually lost. There was a
hypersensitiveness to touch and to cold, but no other sensory
disturbance. The boy was alive and fairly well when the case was
reported.[82] It is unique.

[Footnote 82: Heuschen, _Schmidt's Jahrbuch._, vol. cxcviii. p. 130.]

These various instances of atrophy cannot be ascribed to simple
disuse, since they differ markedly in their pathological changes and
in the rapidity of their progress from such atrophy. Nor are they to
be referred to vaso-motor disturbances, since in many cases no
vascular changes are evident. Their distribution in the body often
corresponds exactly with that of peripheral nerves, and they accompany
nerve lesions too frequently to be explained on any theory of
coincidence. There are many authorities, however, who refuse to
ascribe them to a lesion of trophic nerves.[83] In regard to the
degeneration of nerves it is said that each nerve axis-cylinder is a
part of the nerve-cell from which it arises, and hence destruction of
the cell or division of the cylinder, by disturbing the unity of
existence, results in the death of the part. The fibre shares all the
changes of nutrition which the nerve-cell undergoes, and if separated
from it necessarily perishes. To this it is replied that trophic paths
and motor paths are distinct at some points in their course, at least
in the central nervous system, since each can be affected alone. Erb,
who has studied this subject carefully,[84] believes that trophic are
distinct from motor centres in the spinal cord, but that both impulses
may be conveyed by the same axis-cylinder in the peripheral nerves—a
middle ground which is widely accepted. It is now known that each
axis-cylinder is made up of several fibrils, so that this theory gains
probability. This would also explain the occurrence of atrophy in the
muscles, the trophic centres being affected when the muscle atrophies,
and unaffected when it is paralyzed without atrophy. Mayer, however,
denies this explanation of the muscular atrophy, holding that the
motor system, cell, nerve, and muscle-fibre, forms a nutritive as well
as functional unit, and that the simple suspension of function, by
interfering with the special {1270} conditions of nutrition attendant
upon physiological excitement, is competent to cause a pathological
change. To this it is replied that the parts of the motor system are
not interdependent, since disease of the muscle does not produce
degeneration of the nerve and of the cell, and the fact of a
degeneration in a peripheral direction alone is evidence of central
trophic influence. The attempt to ascribe trophic changes in the skin,
nails, and hair to vaso-motor disturbance has been equally
unsuccessful in covering all the observed cases.

[Footnote 83: See Handfield Jones, _St. George's Hospital Reports_,
1868, vol. iii. pp. 89-110; Sigmund Meyer, _Hermann's Handbuch d.
Physiol._, ii. Th. 2, “Trophische Nerven,” 1879; Gowers, _Diseases of
the Brain_, 1885, p. 4.]

[Footnote 84: _Arch. f. Psych._, v. S. 445, 1875; also _Ziemssen's
Cyclo._, vol. xiii. p. 117 (Amer. trans.); also _Deut. Arch. f. klin.
Med._, v. S. 54.]

[Illustration: FIG. 58. Diagram of the Arrangement and Connection of
Motor and Trophic Centres and Fibres in the Spinal Cord and Motor
Nerve (after Erb): _a_, motor fibre of spinal cord from the brain to
_d_, the motor cell, which is joined to the muscle _m_ by the motor
nerve; _b_, trophic cell in the spinal cord for the muscle, to which
it is joined by the trophic fibre _bʹ_; _c_, trophic cell in the
spinal cord for the motor nerve, to which it is joined by the trophic
fibre _cʹ_; _s_, a fibre bringing sensory (reflex) impulses to the
cell.

If _d_ is destroyed, the fibres from _b_ and _c_ perish with it, and
the result is paralysis and atrophy of the muscle and degeneration in
the motor nerve—_e.g._ poliomyelitis anterior. If _b_ is destroyed,
the muscle atrophies, and paralysis is a secondary result—_e.g._
progressive muscular atrophy. If _c_ is destroyed, the nerve
degenerates, and paralysis and atrophy of the muscle are secondary
results—_e.g._ neuritis with reaction of degeneration. If _a_ is
destroyed, voluntary power is lost, but reflex power remains, and no
atrophic changes occur—_e.g._ lateral sclerosis. If the motor nerve is
cut between _d_ and _m_, the result is the same beyond the division as
when the motor cell is destroyed.]

{1271} HYPERTROPHY.—Trophic changes are not limited to the process of
atrophy. There are conditions of hypertrophy of supposed nervous
origin. Samuel considers the hypertrophy of one testicle which attends
atrophy of the other from section of its nerve as an example of this.
It has been ascertained that one kidney hypertrophies when the other
is atrophied or extirpated. When the spleen is removed the lymphatic
glands increase in size. But these facts are capable of another
explanation—viz. that increased demand upon the organ leads to its
increased growth. Hypertrophy of the skin and of the tongue is seen in
cretins in contrast with the deformity of the body and atrophy of the
limbs. A hemihypertrophy of the face has been noticed in several
cases, the counterpart of hemiatrophy; and in one case a unilateral
hypertrophy of the entire body was observed.[85] The local thickening
of the skin known as ichthyosis hystrix, and other hypertrophies of
the skin, certain deposits of pigment, and vitiligo, have been
ascribed to nervous causes. Mitchell has recorded cases of abnormal
growth of the nails and hair after injuries to the nerves, and similar
phenomena have followed central lesions. He has also described a
thickening of the skin of the first three fingers and of the back of
the hand following a wound of the brachial plexus. These conditions of
the skin and its appendages indicate an abnormal activity in the cells
of the affected part, a rapid metabolism and reproduction, resulting
in an undue production of tissue, apparently dependent on nervous
impulses reaching the cells from a distance. The insane ear may be
mentioned in this connection as a trophic disturbance due to central
lesion.

[Footnote 85: Ziel, _Virchow's Archiv_, xci., S. 92.]

MYXŒDEMA (cachexie pachydermique) is a disturbance of nutritive
processes characterized by a production of mucin, which is deposited
in all the tissues of the body, but especially in the subdermal
connective tissue.[86] It is considered by the majority of authors a
trophic neurosis, and is therefore considered here.

[Footnote 86: Sir William W. Gull, “On a Cretinoid State supervening
in Adult Life,” _Trans. Clin. Soc. London_, 1874, vol. vii. p. 170;
Ord, “On Myxœdema,” _Med.-Chir. Trans._, 1878, vol. lxi. p. 57;
Mahomed, _Lancet_, 1881, ii. No. 26; Hadden, _Brain_, 1882; W. A.
Hammond, _Neurological Contributions_, 1881, i. p. 36; Ballet,
_Archives de Neurologie_, 1881, vol. iii. p. 30; _Schmidt's
Jahrbucher_, vol. clxxxix. p. 30, and cxcviii. 264; “The Brown
Lectures,” Victor Horseley, _Lancet_, Jan., 1886.]

PATHOLOGY.—In the few autopsies which have been made an increase in
the connective tissue of all the organs has been found, in the meshes
of which a thick, transparent, slimy substance (called animal gum),
consisting of mucin, is present. This may compress and destroy the
parenchyma of the organs involved. There is also found a thickening of
the coats (adventitia and media) of the vessels. An atrophy of the
thyroid gland has occurred in every case, and experimental extirpation
of the thyroid in animals produces symptoms so nearly identical with
those of myxœdema that this is considered the chief pathological
feature of the disease. Whether this atrophy is due to a compression
by the mucin deposited, or is due to a disease of the trophic centres
of the thyroid in the medulla, or is a primary affection of the gland,
remains to be determined.

ETIOLOGY.—The actual causation is unknown. Cold and mental shock have
been considered exciting causes in some cases. Women are much more
liable to the disease than men, and it develops after the age of forty
in the majority of cases. It may occur in childhood and result in a
{1272} cretinoid state. Syphilis and tuberculosis do not appear to be
etiological factors.

SYMPTOMS.—The disease begins gradually, and the nervous symptoms or
the local œdema may appear together or in succession. The patient
notices a thickening of the skin, which becomes dry, rough, and scaly.
The thickening is uniform and involves the entire body. It is most
marked where the subdermal connective tissue is loose, as in the
cheeks, lips, eyelids, and in all parts where the skin is thrown into
folds. The hands and feet do not escape. The thickened skin is hard,
and does not pit on pressure, thus differing from ordinary œdematous
swelling. It appears of a waxy color, and is free from perspiration,
the sweat-glands becoming atrophied from pressure. The hair may fall
out or become woolly and brittle, and may change its color. In a few
cases spots of pigment have appeared on various regions.[87] The nails
are brittle. The teeth are carious. The mucous membranes show similar
changes, and the mouth and tongue, rectum and vagina, may be so
swollen as to impair their respective functions. Digestive
disturbances, constipation alternating with diarrhœa, and uterine
hemorrhages, which occur, are ascribed to this cause. Albumen is
occasionally found in the urine, but is not a constant symptom. The
nervous symptoms are constant. The patients complain of paræsthesiæ
and anæsthesia of the extremities or over the entire body, and the
special senses may be impaired, as well as the tactile sense. They are
very liable to severe attacks of neuralgia. They suffer from
subjective sensations of cold, and are easily affected by changes of
temperature. Motion is interfered with; tremors occur early; movements
become slow and awkward; the gait is unsteady; the voice is rough and
nasal; but no true paralysis or muscular atrophy has been observed.
The patella-tendon reflex is occasionally lost, but not in all cases.

[Footnote 87: Allan McLane Hamilton, _Journ. Nerv. and Ment. Dis._,
1885, April, p. 180.]

These symptoms have been ascribed to the pressure of the mucin upon
the terminal filaments of the nerves, and also to changes in the
central nervous system. That the latter theory is probably correct is
shown by the occurrence of mental symptoms in the majority of cases.
The patients become apathetic and all mental action is slowly
performed. Indifference to surroundings, loss of memory, and inability
to concentrate the attention may be succeeded by transient delirium,
hallucinations, and occasionally by delusions of persecution, and the
patient finally lapses into a state of imbecility. If the disease
develops in early life, education is impossible, and the patient
remains in an infantile condition.

Whether the changes in the nervous system are due to pressure by
deposit of mucin (Hadden), or are due to an altered nutrition of the
most delicate tissues of the body consequent upon the general
metabolic derangement (Horseley), is undetermined. In experimental
myxœdema the degenerative processes have been found in the
nerve-cells.

There are no symptoms referable to the heart or lungs, and if
cirrhosis of the kidney and liver develop, their symptoms supervene
upon and are secondary to those of myxœdema. High arterial tension has
been noticed in the majority of the cases.

The COURSE of the disease is a chronic one, and is progressive. There
are, however, intermissions in the severity of the symptoms in some
cases. Recovery does not occur.

{1273} DIAGNOSIS.—The diagnosis from the accumulation of fat is made
by observing the thickening of the nose, lips, fingers, and tongue,
and the changes in the skin and its appendages. Scleroderma is not
universal like myxœdema. In scleroderma the skin is harder and more
adherent to subjacent parts, is not transparent and waxy, and the
nervous symptoms are wanting. Cretinism seems to be closely allied to
myxœdema, but is only observed before the age of seven and is
accompanied by hypertrophy of the thyroid gland.

TREATMENT.—The treatment is only palliative. Simple nutritious diet,
especially milk diet, with the use of such tonics as iron and quinine,
has been found useful. The progress of the disease is hastened by
exposure to cold, and in a very warm climate the symptoms may remain
stationary for several years. Jaborandi or pilocarpine has been used
in some cases with a moderate degree of success. Nitro-glycerin, gr.
1/100, has also been of benefit. For the paræsthesiæ and anæsthesia of
the early stage the faradic brush has been applied, and for the motor
weakness the faradic current, with the effect of relieving but not
curing these symptoms. During the attacks of neuralgia morphine may be
employed.

Inflammation.—The most important trophic disturbances are those which
consist of an actual disintegration of tissue. These are very
numerous. Herpes zoster, certain forms of eczema and pemphigus, lepra
anæsthetica, scleroderma, acute ulceration of the fingers, perforating
ulcer of the foot, acute bed-sores, keratitis with anæsthesia of the
cornea, sympathetic ophthalmia, and various forms of joint disease,
are examples of such trophic diseases.[88] For the discussion of the
skin and eye diseases mentioned the reader is referred to special
articles on those subjects. In regard to lepra anæsthetica, it may be
mentioned that in this disease lesions have been found both in the
sensory nerves and in the posterior cornua of the spinal cord.[89]

[Footnote 88: Leloir, “Tropho-neuroses,” _Nouveau Dictionnaire de
Médecine et Chirurgie practiques_, 1885.]

[Footnote 89: Virchow, “Nerven Lepra,” _Geschwülste_, ii. 521;
Tschirijew, _Travaux du Laboratoire de Vulpian_, 1879.]

I have reported[90] a case of acute ulceration of the ends of the
fingers and toes occurring in an anæmic girl aged twelve, and
persisting for more than a year, associated with cyanosis of the hands
and feet, and with a tendency to rapid ulceration of any part of the
body which happened to be exposed to pressure. The hair of the
eyebrows, eyelids, and to a less extent that of the scalp, fell out
during the disease. There was no local asphyxia and no appearance of
gangrene; hence the case was not one of Raynaud's disease. Its
symmetrical distribution, the lack of any constitutional organic
disease or of any local cause for the production of the ulceration,
and the anæmic and nervous condition present, all pointed to a
disturbance of the central nervous system. It did not yield to
treatment, either local or general or electrical. Mills has seen a
similar case.[91]

[Footnote 90: _Journal Nerv. and Ment. Disease_, Feb., 1886, clinical
cases.]

[Footnote 91: Mills, _Amer. Journ. Med. Sci._, Oct., 1878.]

Perforating ulcer of the foot begins on the sole, beneath any of the
metatarso-phalangeal articulations, preferably the first or the fifth,
or under the heel, as a small pustule under the epidermis. This
ruptures, and the ulcer which results begins to extend in a direction
vertical to the surface, involving the deeper tissues or even opening
into the joint and destroying the bone. It appears rather like a sinus
than an ulcer, and is {1274} remarkable from the fact that it is not
painful and is insensitive to touch, although it may prevent the
patient from walking on account of extreme tenderness. The epidermis
around the sinus is thickened and insensitive, and there may be
anæsthesia of the entire sole of the foot, and even of the leg,
although this is due to the neuritis present, which is also the cause
of the ulcer, rather than to the ulceration. The circulation is
sluggish in the affected extremity; it becomes cyanotic on exposure to
cold, and seems peculiarly liable to become œdematous. The œdema may
go on to suppuration, and involve the articulations, and ankylosis of
the smaller joints may follow. This, too, is to be traced to the
neuritis. The skin of the foot becomes pigmented, and may be dry or
covered with offensive sweat. As the patient cannot walk while the
ulcer remains, the condition demands treatment. Rest, moist warm
applications, antiseptic lotions, scraping out the sinus, and other
surgical means appropriate to the treatment of ulcers and sinuses do
not often prove of benefit, and in obstinate cases recourse has been
had to amputation of the foot. Electrical treatment has been tried in
vain.

Such perforating ulcers may occur symmetrically on both feet, and may
be numerous. They also occur rarely on the hands. They have been
observed not infrequently in locomotor ataxia, occurring either early
or late in the disease,[92] and have appeared in patients suffering
from dementia paralytica. The only constant lesion found is a
degeneration of the peripheral nerve supplying the affected part.

[Footnote 92: For bibliography see Ross, _Diseases of Nervous System_,
2d ed., i. p. 256, and Blum, _Berliner klin. Wochen._, 1875, Nos.
13-15.]

Acute bed-sores (decubitus) develop in many cases of spinal and
cerebral disease, but not in all. It is argued that anæsthesia of a
part or simple pressure upon a part or irritation of an anæsthetic
part will not explain their occurrence, and that they must be traced
to a destruction of trophic centres in the cord or brain. No amount of
attention to the position and cleanliness of the patient is thought to
be sufficient to prevent them in some cases, and their progress is
often so rapid as to remove them from the category of simple
ulceration. Their most frequent seat is upon the buttocks, over the
sacrum, on the heels, and over the scapulæ; but it is believed that in
the conditions in which they appear in these places pressure on any
part may cause one. They begin within a few hours after the occurrence
of the lesion as irregular mottled patches of redness, in which there
soon appear small or large vesicles filled with dark serum. These
rupture, leaving little areas of ulcerated surface, which soon unite
to form a large ulcer with softened, infiltrated, and bloody base and
ragged edges. The tissues around and within the ulcer have a tendency
to slough and to become gangrenous, and the process goes on rapidly
until a considerable area of the surface is completely destroyed,
together with the deeper structures, fat, muscles, and fasciæ, down to
the bone, which may become necrosed. Acute cystitis is so frequently
associated with acute bed-sore that it is traced to the same nervous
cause, though here, again, another explanation is possible. The
constitutional disturbance produced by these two affections may be
increased by a true septicæmia, to which the patient succumbs; or
metastatic abscesses may be formed, and pyæmia cause death; or,
lastly, the ulcer on the back may lay bare the vertebræ and erode
their ligaments, thus opening a way for the extension of suppuration
to {1275} the meninges of the spinal cord. The duration may be from a
few days to two weeks, and the prognosis is very grave.

Chronic bed-sores develop in a similar manner, although all the
processes described occur more slowly and are much less severe. They
do not show the tendency to extend so widely or so deeply, nor to
become gangrenous. They remain stationary after attaining a certain
size, and the tissues seem to lack all tendency to reproduction and
repair. When the central lesion which they follow begins to pass away
they heal; sometimes local treatment is successful; but in many cases
they persist for years, always threatening the life of the patient
from the possibility of their sudden aggravation or from the
occurrence of the complications already mentioned in connection with
the acute process.

Since neither form of decubitus occurs after lesion of the anterior
cornua of the spinal cord, nor in sclerosis of the posterior or
lateral columns, nor in those cases of locomotor ataxia in which
extensive invasion of the posterior cornua is present, while they are
particularly frequent as a complication of general myelitis,
hemorrhage in the cord, and syringo-myelitis, it is argued that the
trophic centres whose destruction is the cause of these bed-sores lie
in the central gray matter of the cord, near to the central canal. In
unilateral lesion of the cord the bed-sore occurs on the anæsthetic
side of the body—_i.e._ on the side opposite to the seat of the
lesion—a fact which may indicate a decussation of the trophic
nerve-fibres in the cord,[93] but which has also been urged in proof
of the theory that the sore is always due to irritation of an
insensitive surface.

[Footnote 93: Recklinghausen believes that these cases of disturbance
of nutrition can be explained by injury of anæsthetic parts in which
vaso-motor disturbances of central origin exist (_Handbuch d. Path. d.
Ernahrung_, pp. 236, 237).]

The treatment of bed-sores belongs to the domain of surgery, the same
methods being pursued as in the case of any large ulcer. The
application of electricity to the sore has been tried, but the results
are not sufficiently encouraging to warrant its recommendation.

Joint affections of neurotic origin are discussed in the articles upon
Locomotor Ataxia, Hemiplegia, and Hysteria.

It is evident from this review that the nervous centres have some
influence upon the activity of the cells of which the body is made up,
and that they control the processes of growth, function, repair, and
reproduction. The facts are too numerous, too varied, and too positive
to admit of any other explanation. Trophic disturbances must therefore
be considered as a set of symptoms referable to various lesions of the
nervous system. It is evident from the preceding discussion that they
may be produced by disease of the peripheral nerves; by disease of the
ganglionic cells, which nourish those nerves; by disease of the spinal
cord, especially in the region of the central gray matter; and,
finally, by disease of the brain. Whether in the last condition the
effect is a direct one, or is produced secondarily by an irritation of
the spinal centres, cannot yet be determined. There are no trophic
centres as yet localized in the cerebrum, but the pathological facts
already mentioned warrant the conclusion that such centres will not
long elude search. Certain facts observed in cases of infantile
hemiplegia point to the motor area of the cortex as the seat of
trophic centres for the motor mechanisms; since it is found that when
the motor cortex is destroyed in early life the bones and muscles
{1276} which it controls fail to develop properly. Trophic centres for
sensory mechanisms are not yet discovered. Certain investigations of
Luciani recently published[94] point to the cerebellum as the part of
the brain which governs the general nutrition of the body, but these
need confirmation.

[Footnote 94: _Alienist and Neurologist_, July, 1885.]

       *       *       *       *       *

CONCLUSION.—While an attempt has been made here to consider vaso-motor
and trophic neuroses separately, it must be admitted that in very many
conditions the two are coincident. This follows inevitably from what
has been stated regarding the localization of the vaso-motor and
trophic centres in the spinal cord, and regarding the course of the
vaso-motor and trophic nerves from the spinal centres to the
periphery. These two classes of centres and nerves lie side by side in
the central and peripheral organs, and it is less surprising that they
should be jointly affected than that one should ever be involved
alone. In any case of lesion of the peripheral nerves or of the
central nervous system they may be expected. In all cases they are to
be regarded as symptoms of such lesions rather than as distinct
diseases.


{1277}


INDEX TO VOLUME V.


A.

Abdomen, state of, in lead colic, 684
    in tubercular meningitis, 726, 727

Abscess of the brain, 791, 792
  of the spinal cord, 808

Achromatopsia, hysterical, 247

Aconite and aconitia, use of, in neuralgia, 1224, 1227
  hypodermically in exacerbations of cerebral syphilis, 1015

Acoustic sensory disturbances in nervous diseases, 40, 41

Acrodynia, 1254

Acute affections produced by heat, 387
  alcoholism, 586
  cerebral anæmia, 776
  encephalitis, 791
  myelitis, spinal, 810
  poisoning by alcohol in lethal doses, 596
  simple meningitis, 716
  spinal meningitis, 749
    pachymeningitis, 747

Æsthesodic system of encephalon, localization of lesions in, 81
    of spinal cord, localization of lesions in, 69

Affective mental disease, 153

Age, influence on causation of acute spinal meningitis, 750
      of catalepsy, 315
      of cerebral anæmia, 777
      of chorea, 441
      of chronic lead-poisoning, 680, 686, 688
      of disseminated sclerosis, 883
      of embolism and thrombosis of cerebral veins, 951
      of epilepsy, 470
      of family form of tabes dorsalis, 871
      of general paralysis of the insane, 77
      of hæmatoma of the dura mater, 707
      of hysteria, 216
      of hystero-epilepsy, 293
      of insanity, 116, 117
      of intracranial hemorrhage and apoplexy, 927
      of labio-glosso-laryngeal paralysis, 1173
      of migraine, 406, 1230
      of myxœdema, 1271
      of neuralgia, 1217
      of paralysis agitans, 433
      of progressive unilateral facial atrophy, 694
      of syphilitic affections of nerve-centres, 1000
      of tabes dorsalis, 856
      of the opium habit, 650
      of thrombosis of cerebral veins and sinuses, 983
      of tubercular meningitis, 725
      of tumors of the brain, 1029
            spinal cord, 1090
      of writers' cramp, 512
  relation of, to limitation of the myelitis in infantile paralysis,
        1147

Agraphia in hemiplegia, 957

Akinesis in nervous diseases, definition of, 42-44

Alalia (see _Speech, Disorders of_).

Alexia in nervous diseases, 31

Albuminuria in chronic lead-poisoning, 682, 689

Alcohol, influence on causation of acute meningitis, 716
      of cerebral hyperæmia, 765
      of intracranial hemorrhage and apoplexy, 929, 933
      of tabes dorsalis, 854
      of writers' cramp, 512
  use of, in alcoholism, 642, 644
    in cerebral anæmia, 789
    in heat-exhaustion, 388
    in insomnia, 380, 381
    in the chloral habit, 677
    in the opium habit, 673, 675
    in thermic fever, 397

Alcoholic abuse as a cause of epilepsy, 472
  insanity, 175, 202, 630-633

ALCOHOLISM, 573
  Classification, 573
  Definition, 573
  Diagnosis, 637
    of acute alcoholism, 637
    of chronic alcoholism, 638
    of dipsomania, 639
    of hereditary alcoholism, 639
  Etiology, 575
    Alcohol, physiological action of, 580, 586
    Alcoholic beverages, varieties and characters of, 578-580
    Exciting causes, 578
    Heredity, influence on causation, 576
    Moral, social, and personal condition, influence on causation,
          575, 578
    Predisposing causes, 575
  History, 574
  _Pathological Action of Alcohol_, 586
    _Acute Alcoholism_, 586-598
      Symptoms, 587
        Effects in persons of unsound mind, 594
        Effects of different alcohols, 589-591
        of acute narcotic poisoning, 597
        of acute poisoning in lethal doses, 596
        of convulsive form, 593
        of corrosive poisoning, 596
        of irregular form, 592
        of maniacal form, 592
        of ordinary form, 587
      Pathological anatomy, 595
      Varieties, 588
    _Chronic Alcoholism_, 598-633
      Symptoms, anatomical changes, etc., 599
        Alcoholic cachexia in, 616
        Atheroma in, 612
        Biliary catarrh in, 607
        Blood, disorders of, 615
        Blood-vessels, disorders of, 612
        Cerebral, 616
        Delirium, alcoholic, and delirium tremens, 626, 630
        Dyspeptic, 601, 602
        Genito-urinary disorders, 612-614
        Glands, disorders of, 602
        Heart, disorders of, 610-612
        Insanity, alcoholic, 630-633
        Intestinal disorders, 601
        Kidneys, disorders of, 613
        Larynx, disorders of, 607
        Liver, disorders of, 603-607
        Locomotive apparatus, disorders of, 614
        Lungs, disorders of, 608
        Moral sense, perversion of, 624
        Motion, disorders of, 620
        Mouth and throat, disorders of, 599
        Muscles, disorders of, 614
        Nervous system, disorders of, 616
        Obesity in, 615
        Paralysis, alcoholic, 621
        Pleuræ, disorders of, 610
        Psychical disorders, 624
        Respiratory system, disorders of, 607
        Sensibility, general, disorders of, 619
        Skin, disorders of, 615
        Special sense, disorders of, 622
        Spinal disorders, 619
        Stomach, disorders of, 600
        Tremor in, 620
        Visceral derangements, 599
        Will and intellect in, 625
    _Dipsomania_, 635
      Symptoms and nature, 636, 637
    _Hereditary Alcoholism_, _symptoms and forms_, 634
  Prognosis, 639
  Synonyms, 573
  Treatment, 640
    Alcohol, withdrawal of, 642, 644
    Ammonia, use of, 641, 642, 645
    Baths and douches, use of, 641, 642, 643
    Bromides, use of, 642, 645, 646
    Cannabis indica, piscidia, and hyoscyamus, use of, 645
    Chloral, use of, 641, 645, 646
    Coca and cocaine, use of, 643, 646
    Diet in, 643, 644
    Emetics in, 642
    Iron, use of, 643
    Hypophosphites and cod-liver oil, use of, 644, 646
    of acute form, 641
    of chronic form, 642
    of delirium tremens, 644
    of dipsomania and hereditary forms, 645
    Paraldehyde, use of, 641, 642, 645, 646
    Prophylaxis, 640, 642
    Quinia and opium, use of, 642, 643, 645, 646
    Strychnia, use of, 641, 643, 646

Alcoholism, influence on causation of insanity, 119

Allochiria in tabes dorsalis, 832

Alum, use of, in lead colic, 691

Amaurosis in chronic lead-poisoning, 689

Amenorrhœa in the insane, treatment, 136

Ammonia, use of, in acute alcoholism, 641, 642, 643
    in thrombosis of cerebral veins and sinuses, 989

Ammonio-sulphate of copper, use, in neuralgia, 1229

Ammonium chloride, use, in neuralgia, 1229

Amnesia in nervous diseases, 28

Amputation, question of, in tetanus, 559

Amyl nitrite, use of, in angina pectoris, 1238
    in catalepsy, 338
    in cerebral anæmia, 788
    in chorea, 456
    in epilepsy, 502
    in hysteria, 286
    in hystero-epilepsy, 311
    in migraine, 414, 1232
    in vaso-motor neuroses, 1256

Amyotrophic lateral sclerosis, 867

Anæmia as a cause of neuralgia, 1218
    of thrombosis of cerebral veins and sinuses, 984
    of vertigo, 425
  and chlorosis, influence on causation of hysteria, 220
  general, as a cause of spinal anæmia, 806
  of the brain, 774, 777
  of the spine, 805

Anæmic headache, 402

Anæsthesia, hysterical, 246
  in acute myelitis, 819
  in chronic alcoholism, 620
    spinal meningitis, 753
  in hemiplegia, 955
  in hystero-epilepsy, 298
  in injuries of nerves, 1182, 1185, 1186
  in neuritis, 1191, 1192
  in spinal meningeal hemorrhage, 752
    meningitis, 750
    syphilis, 1025
  in symmetrical gangrene, 1259
  in tumors of the brain, 1042
    of the spinal cord, 1092
  in unilateral spinal paralysis, 1166
  of peripheral origin, 1198
    Causes, 1199
    Diagnosis, 1200
    Symptoms, 1199-1201
    Treatment, 1201
  Varieties of, in nervous diseases, 35, 37

Analgesia, definition of, 35
  hysterical, 246

Angina pectoris (see _Neuralgia_).

Angiomata in brain tumors, 1049

Angio-paralysis in vaso-motor neuroses, 1252

Angio-spasm in vaso-motor neuroses, 1262

Anidrosis in progressive unilateral facial atrophy, 696

Ankle-clonus in amyotrophic lateral sclerosis, 868
  in diffuse spinal sclerosis, 888
  in nervous diseases, 54
  in spastic spinal paralysis, 862, 864

Anterior cornua, changes in, in amyotrophic lateral sclerosis, 867
      in infantile spinal paralysis, 1133-1144

Antipyrine, use, in thermic fever, 397, 398

Antispasmodics, use, in hysteria, 278

Anus and rectum, neuralgia of, 1240

Aphasia in nervous diseases, 31
  in cerebral anæmia, 776
    hemorrhage, 941
    syphilis, 1008
  hemiplegia, characters and varieties of, 956, 960
  post-epileptic, 481

Aphonia, hysterical, 239

Apoplexy, 917
  of the brain, meningeal, 710

Apoplectic attack, symptoms of, 933-952
  constitution, peculiarities of, 930

Apoplectiform attacks in tumors of the brain, 1040
  type of acute myelitis, 817

Argyll-Robertson pupil in nervous diseases, 40, 51
    in tabes dorsalis, 830

Arsenic, use of, in chorea, 454
    in malarial form of cerebral anæmia, 790
    in neuralgia, 1224
    in paralysis agitans, 438
    in tetanus, 559
    in tremor, 432
    in writers' cramp, 538

Arteries, cerebral, atheroma of, 991
      in cerebral meningeal hemorrhage, 711
    diseases of, in intracranial hemorrhage and apoplexy, 922

Arterial spasm in spinal anæmia, 806

Arthralgia, the, of chronic lead-poisoning, 684

Arthropathies in hemiplegia of apoplexy and intracranial hemorrhage,
        962
  in tabes dorsalis, 837

Asafœtida, use, in hysteria, 278, 285

Assimilation, alterations of, in nervous diseases, 59

Asthma, hysterical, 245

Asylums in the treatment of opium and alcohol habit, question of, 671
  treatment of insane by removal to, 128, 130-135

Ataxia in tabes dorsalis, 831, 833, 848
  in tumors of the brain, 1041
  in tumors of the spinal cord, 1094
  muscular, in general paralysis of the insane, 189, 193

Ataxic tremor, in nervous diseases, 47

Atheroma, in chronic alcoholism, 612
  of the cerebral arteries, 991

Athetosis, definition and symptoms, 457
  pathology, prognosis, and treatment, 46

Atmospheric and thermic influences as cause of neuralgia, 1219

Atrophy, 1266
  degenerative, in nervous diseases, 54-57
  facial, progressive unilateral, 693
  in amyotrophic lateral sclerosis, 868
  muscular, in chronic lead-poisoning, 687, 688
    in hemiplegia from apoplexy, 962
    in labio-glosso-laryngeal paralysis, 1172
    in nervous diseases, 54
    in neuralgia, 1214
    in tumors of the brain, 1041
    in tumors of the spinal cord, 1054
  of anterior gray cornua in infantile spinal paralysis, 1133-1144
  of bones and muscles in atrophic infantile paralysis, 1124
  of brain, 170, 993, 994

Atropia, use of, in heat-exhaustion, 388
    in labio-glosso-laryngeal paralysis, 1175
    in tremor of spinal sclerosis, 905
    in writers' cramp, 537

Auræ of epilepsy, characters, 475

Aural vertigo, causes and symptoms, 421

Auras in migraine, 1230

Autographic women, 351

Automatism, 228, 331-333


B.

Base of brain, focal lesions of, 91

Baths, use of, in alcoholism, 641, 642, 643
    in chorea, 455
    in heat-exhaustion, 388
    in the opium habit, 672, 673, 676
    in thermic fever, 396, 397, 398
    in tremor, 432
  cold, use of, in spinal sclerosis, 903
  hot, use of, in spinal sclerosis, 900, 903
  sulphur, use of, in chronic lead-poisoning, 691
  value of, in hysteria, 281, 282, 283
  warm, use of, in acute myelitis, 823

Bed-sores, 1274, 1275
  in tumors of spinal cord, 1096, 1098
  malignant, in acute myelitis, 819

Belladonna, use of, in epilepsy, 501
    in infantile spinal paralysis, 1155

Bell's palsy, 1202

Biliary catarrh, in chronic alcoholism, 607

Bismuth, use of, in vomiting of the opium habit, 675

Bladder, disorders of, in chronic alcoholism, 614
    in tabes dorsalis, 829, 834, 836
    in tumors of the brain, 1045
      of the spinal cord, 1096

Bleeding, in acute myelitis, 823
    simple meningitis, 720
  in Bell's palsy, 1207
  in cerebral hemorrhage and apoplexy, 976
    hyperæmia, 774
  in exacerbations of cerebral syphilis, 1015
  in hæmatoma of the dura mater, 710
  in spinal hyperæmia, 805
  in tetanus, 555
  in thermic fever, 398

Blindness, hysterical, 248
  in cerebral anæmia, 776
  word-, in nervous diseases, 31

Blisters, use of, in epilepsy, 502
    in hæmatoma of dura mater, 710
    in tetanus, 555
    in thermic fever, 398, 400
    in writers' cramp, 538

Blood, changes in, in chronic alcoholism, 615, 618
    in the chloral habit, 662
    in thermic fever, 391, 392

Blood-vessels, changes in, in chronic alcoholism, 612

Bluish line upon the gums, significance of, in chronic lead-poisoning,
        682

Blushing, in hysteria, 253

Bones, atrophy of, 1267
  changes in, in alcoholism, 614
  state of, in general paralysis of the insane, 196

Brachial neuralgia, 1234

BRAIN AND SPINAL CORD, ANÆMIA AND HYPERÆMIA OF THE, 763
  _Abscess_, 792
    Diagnosis, 799
    Etiology, 796
    Morbid anatomy, 792
    Prognosis, 799
    Symptomatology, 795
    Treatment, 799
      Medical, 800
        Derivatives, 800
        Mercury, 800
      Surgical, 800
        Emptying contents, 800
  _Anæmia_, 774
    Diagnosis, 787
    Etiology, 776
    Morbid anatomy, 781
      Appearances of, in cerebral anæmia, 781
    Symptomatology, 782
    Treatment, 788
      Alcoholic stimulants, 789
      Amyl nitrite, 788
      Cannabis, 789
      Cold pack, 789
      Massage, 789
      Morphine, 788
  _Hyperæmia_, 763
    Differential diagnosis, 772
    Etiology, 765
    Symptomatology, 768
    Treatment, 773
      Baths, 773
      Bleeding, 774
      Bromides, 773
      Cathartics, 774
      Cautery, 774
      Chloral, 773
      Derivation, 774
      Diet, 774
      Ergot, 773
      Hypnotics, 773
      Pediluvia, 773
  _Inflammation_, 790
    Abscess in, 791
    Acute encephalitis of Strümpell in, 791
      Accompanying endocarditis, 792
      Miliary form, 792
        of septic origin, 792
      Post-paralytic phenomena of, 791
      Sequelæ of, 791

BRAIN AND SPINAL CORD, CONCUSSION OF THE, 908
    Definition and morbid anatomy, 908
    Diagnosis, 909
    Symptoms, 908
      Mental state, 908
      Pulse and temperature in, 909
      Pupils, state of, 909
    Treatment, bromide of potassium, heat and cold, use, 911, 912
      of reaction, 911
      Stimulants, use of, 911

BRAIN, ATROPHY AND HYPERTROPHY OF, 993
  _Atrophy_ during childhood, 993
    Causes, symptoms, and treatment, 994
    of the fully-developed, 994
      Causes, morbid anatomy, and symptoms, 995
      Treatment, 996
  _Hypertrophy_, 996
    Course, diagnosis, prognosis, symptoms, and treatment, 998
    Etiology and morbid anatomy, 997

Brain and its envelopes, tumors of, 1028
  and membranes, changes in, in acute simple meningitis, 719
    in alcoholism, 617
    in cerebral meningeal hemorrhage, 713, 714
    in external pachymeningitis, 705
    in general paralysis of the insane, 196
    in hæmatoma of the dura mater, 708
    in tubercular meningitis, 730-732
  and spinal cord, diseases of membranes of, 703
  lesions of, in insanity, 121
  microcephalic, size of, 139
  softening of, 918, 989
    in children, 990
  state of, in chronic hydrocephalus, 944
  syphilis of, 1003

Brain-cortex, syphilis of (see _Syphilitic Affections of
        Nerve-centres_).

Brain, gross appearances of, in brain tumors, 1050

Brain-tire, treatment of, 358

Breathing, hysterical, 245

Bright's disease as a cause of intracranial hemorrhage and apoplexy,
        930

Bromate of potassium, use of, in epilepsy, 501

Bromide of nickel, use of, in epilepsy, 500

Bromide of potassium, use of, in acute simple meningitis, 721
      in acute spinal meningitis, 752
      in chronic cerebral meningitis, 722
      in concussion of spine, 911
      in hæmatoma of the dura mater, 710
      in hystero-epilepsy, 313
      in insanity, 136
      in melancholia, 160
      in migraine, 1232
      in tetanus, 558
      in tumors of the brain, 1068

Bromides, use of, in alcoholism, 642, 645, 646
    in cerebral anæmia, 789
      hyperæmia, 773
    in chorea, 455
    in epilepsy, 499, 500
    in insomnia, 380, 381, 382
    in migraine, 414, 415
    in spinal sclerosis, 905, 906
    in the opium habit, 674, 676
    in tubercular meningitis, 736
    in vertigo, 427

Bronchi, disorders and lesions of, in chronic alcoholism, 608


C.

Cachexia, alcoholic, characters, 616

Caffeine, use of, in migraine, 1232
    in neuralgia, 1229

Caisson disease, a form of spinal hyperæmia, 804

Calabar bean, use of, in tetanus, 557
    in tetanus neonatorum, 565

Cancer of the brain, 1049

Cannabis indica, habitual addiction to, 667
    use of, in alcoholism, 645
      in brain tumors, 1068
      in cerebral anæmia, 788, 789
      in migraine, 413, 415, 1232
      in the opium habit, 676
      in tetanus, 557

Capillary cerebral embolism, 979

Capsicum, use of, in alcoholism, 642

Carbuncles, as a cause of thrombosis of cerebral veins and sinuses,
        985

Caries of teeth, as a cause of neuralgia, 1229, 1233

Caries of temporal bone, as a cause of tubercular meningitis, 725

Carotids, ligation of, as a cause of cerebral anæmia, 777

CATALEPSY, 314
  Definition and synonyms, 314
  Diagnosis, 334
    from apoplexy and intoxication, 336
    from epilepsy, 335
    from simulation, 337
    from tetanus, 336
  Etiology, 315
    Age, influence on causation, 315
    Imitation, influence on causation, 319
    Reflex irritation, 318
    Sex and puberty, 318
  History, 315
  Pathology and duration, 334
  Prognosis, 337
  Symptoms, 320
    of cataleptoid phenomena in the insane, 327
    of hypnotic catalepsy, 322
    of unilateral catalepsy, 324
    Onset of seizures, mode of, 320
    Pulse, respiration, and temperature in, 321
    Reflex irritability, changes in, 321
    Sensation, disturbances of, 321
    Wax-like flexibility in, 321, 337
  Treatment, 338
    Cold douche, use of, 338
    Electricity, use of, 338
    Nitrite of amyl and nitro-glycerin, use of, 338
    Music, use of, 338
    Purgatives and tonics, use of, 338

Cataleptoid phenomena in the insane, 327

Cathartics in cerebral abscess, 800
    in cerebral hemorrhage, 976
    in cerebral hyperæmia, 774

Cauterization in vertigo, 427

Cautery, use of, in cerebral hyperæmia, 774
    in spinal sclerosis, 905

Cephalic soufflé, diagnostic significance of, 779

Cerebellum, focal lesions of, 90
    tumors of, symptoms, 1062

Cerebral anæmia, 774, 786
    from emotional disturbance, 780
    from ligature of carotid, 776
  Arteries, occlusion of, 946
  Congestion, active, insomnia from, 382
  Hyperæmia in the insane, treatment, 136
  Meningeal hemorrhage, 710
  Meningitis, chronic, 721
  Neurasthenia, 355
  Paralysis, 917
  Pia mater, congestion of, 715
    inflammation of, 716
  Symptoms of thermic fever, 390
  Syphilitic insanity, 202
  Tissue, alterations of, in epilepsy, 491
  Veins and sinuses, thrombosis of, 982
    occlusion of, 918

Cerebro-spinal sclerosis, multiple, 873

Cervical sympathetic, diseases of, 1263
  Etiology and pathology, 1263, 1264
  Course and diagnosis, 1265
  Symptoms, 1264
    Eye and pupil, changes in, 1264
    Heart, disorders in, 1265
    of irritation of, 1264
    of destructive disease of, 1264
    Secretions, changes in, 1265
  Treatment, 1265

Cervico-brachial neuralgia, 1234
  occipital neuralgia, 1234

Charcot's joint disease in tabes dorsalis, 830, 837

Cheyne-Stokes phenomenon, 777
    respiration in tubercular meningitis, 728, 729

Child-bearing and cerebral anæmia, 778

Childhood, headache in, 405
  Insanity of, 171

Children, cerebral hemorrhage in, 928
  Hysteria in, treatment, 275
  Softening of brain in, 990

Chloral, abuse of (see _Opium Habit_).
  use of, in acute simple meningitis, 721
    in alcoholism, 641, 645, 646
    in cerebral anæmia, 789
      hyperæmia, 773
    in chorea, 455
    in epilepsy, 500
    in hysteria, 276
    in insanity, 136
    in insomnia, 380-382
    in migraine, 415
    in tetanus, 558
    in the opium habit, 673, 674, 676
    in tubercular meningitis, 736
    in vaso-motor neuroses, 1256

Chloroform, habitual addiction to, 667
  use of, in hysteria, 286
    in neuralgia, 1229
    in tetanus, 551

Choked disc, in tumors of brain, 1035

Cholesteotomata, in brain tumors, 1049

CHOREA, 439
  Definition, 440
  Diagnosis and prognosis, 453
  Duration, 449
  Etiology, 440
    Age and sex, influence on causation, 441
    Climate, season, and race, 444
    Heredity, influence on causation, 440
    Rheumatism, influence on causation, 442
    Reflex irritation and eczema, 444
    Scarlet fever and pregnancy, 443
    Social condition and over-study, 441
  History and synonyms, 439
  Morbid anatomy and pathology, 450
  Symptoms, 445
    during sleep, 445, 446
    Heart, state of, in, 448
    Mental condition in, 445
    Movements, characters, and description of, 445, 446
    Paralysis and post-paralytic stage of, 447
    Pulse and temperature in, 449
    Sensibility and reflexes in, 448
    Speech in, 445, 448
  Treatment, 454
    Arsenic, use of, 455
    Cimicifuga and conium, use of, 455
    Electricity, use of, 455
    Iron and zinc salts, use of, 455
    Nitrite of amyl, bromides, etc., use, 455
    Strychnia, use of, 455

Chorea, hysterical, 242
  in tumors of the brain, 1039
  post-paralytic, 447, 960

Chronic alcoholism, 598 _et seq._
  cerebral anæmia of adults, 782
    meningitis, 721
  delirium tremens, 630
  hydrocephalus, 740
  lead-poisoning, 678
  myelitis, 886
  spinal meningitis, 752
    pachymeningitis, 748

Cicatrices, myelitic, 815

Cimicifuga, use of, in chorea, 455

Circular insanity, 151

Circulation, obstructed, as a cause of spinal hyperæmia, 802

Classification of alcoholism, 573
  of chronic lead-poisoning, 678
  of mental diseases, 105-109

Clavus hystericus, 252

Cleanliness, importance in cerebral hemorrhage and apoplexy, 977

Climate, change of, value in neurasthenia, 358
      in neuralgia, 1223
      in spinal sclerosis, 903
  influence on causation of chronic lead-poisoning, 680
      of epilepsy, 474
      of hystero-epilepsy, 291
      of thermic fever, 389

Climate and season, influence on causation of chorea, 444
        of hysteria, 218

Climacteric insanity, 173
  period, cerebral hyperæmia in, 771

Climatic and atmospheric conditions, influence on causation of
        tetanus, 544

Clonic spasms, in nervous diseases, 45

Clonus, significance in nervous diseases, 54

Clot, of intracranial hemorrhage, changes in, 920

Club-foot, in family form of tabes dorsalis, 871
  in infantile spinal paralysis, 1127

Coca and cocaine, habitual addiction to, 667
  use of, in alcoholism, 643, 646
    in the opium habit, 676

Cod-liver oil, use of, in chronic alcoholism, 644, 646
        hydrocephalus, 775
      in general paralysis of the insane, 201
      in neuralgia, 1224
      in tubercular meningitis, 735

Cold, influence on causation of Bell's palsy, 1203
      of congestion of spinal membranes, 747
      of neuralgia, 1219
      of neuritis, 1190
      of tetanus, 544
  use of, in concussion of the brain, 911
    in external pachymeningitis, 706
    in thermic fever, 396-398

Cold and wet, as a cause of disseminated sclerosis, 884
      of tabes dorsalis, 855

Cold pack, use of, in cerebral anæmia, 789

Colic, of chronic lead-poisoning, 683

Coma, 382, 785
  alcoholic, characters of, 589, 598
  description of, in nervous diseases, 26-28
  in abscess of the brain, 796
  in acute spinal meningitis, 750
  in cerebral anæmia, 785
  in chronic lead-poisoning, 688
  in tubercular meningitis, 727

Complicating insanity, 174

Complications of hysteria, 258
  of progressive muscular atrophy with atrophic spinal paralysis, 1149
    unilateral facial atrophy, 699
  of tumors of the brain, 1045
    spinal cord, 1106

Compression of nerve-trunks, in hystero-epilepsy, 310

Concussion of the brain, 908
    spinal cord, 912

Condition of brain in sleep, 775

Confusional insanity, primary, 167

Congestion of cerebral dura mater, 704
  of pia mater, 715
  of spinal meningitis, 746

Conium, use of, in chorea, 455
    in paralysis agitans, 438
    in tetanus, 557

Conjunctivitis in the chloral habit, 664, 665

Consciousness, double, in nervous diseases, 28
  loss of, in cerebral hemorrhage and apoplexy, 933
    in nervous diseases, 26
    in occlusion of cerebral vessels, 952
  perverted, in catalepsy, 320

Constitutional diseases, influence on causation of neuralgia, 1217
  affective mental disease, 142

Constipation in chronic hydrocephalus, 743
  in chronic lead colic, 683
  in tubercular meningitis, 725, 729, 736
  in tumors of the brain, 1045

Constriction about waist, sense of, in acute spinal pachymeningitis,
          747
        in disseminated sclerosis, 874
        in spinal meningeal hemorrhage, 752
        in spinal syphilis, 1025
        in tabes dorsalis, 829
        in tumors of spinal cord, 1093

Contact-sense in tabes dorsalis, 833

Contractures, hysterical, 244
  in disseminated sclerosis, 888
  in hemiplegia, 962
  in hystero-epilepsy, 297
  in infantile spinal paralysis, 1127
  in inflammation of the brain, 791
  in secondary sclerosis, 987
  in tumors of the brain, 1039

Convulsions in abscess of the brain, 796
  in atrophy of the brain, 994
  in chronic lead-poisoning, 688
  in hysteria, 236
  in infantile spinal paralysis, 1116
  in spina bifida, 759
  in thrombosis of cerebral veins and sinuses, 986
  in tubercular meningitis, 728
  in tumors of the brain, 1039

Convulsive disorders, local, 461
  form of acute alcoholism, 593

Co-ordination, disturbance of, in tabes dorsalis, 830-833
      in family form of tabes dorsalis, 871

Copodyscinesia (see _Writers and Artisans, Neural Disorders of_).

Cord, spinal, lesions of, in alcoholism, 622
      in tetanus, 549

Corrosive poisoning from alcohol, 596

Counter-irritation, use of, in acute simple meningitis, 721
        spinal meningitis, 752
      in cerebral meningeal hemorrhage, 715
      in chronic cerebral meningitis, 722
        spinal meningitis, 753
      in concussion of the spine, 916
      in external pachymeningitis, 706
      in infantile spinal paralysis, 1155
      in hæmatoma of dura mater, 710
      in neuralgia, 1227
      in neuritis, 1294
      in sciatica, 1262
      in symmetrical gangrene, 1236
      in tubercular meningitis, 736

Coup de soleil, 388

Course of diseases of cervical sympathetic, 1265
  of ecstasy, 343
  of family form of tabes dorsalis, 871
  of general paralysis of the insane, 178
  of hysteria, 258
  of hystero-epilepsy, 307
  of infantile spinal paralysis, 1148
  of insanity, 120
  of myxœdema, 1272
  of simple acute meningitis, 718
  of symmetrical gangrene, 1201
  of the opium habit, 657
  of vaso-motor neuroses, 1254
  of writers' cramp, 521

Cramp, writers', 504

Cranial conformation, vices of, as a cause of epilepsy, 470

Cranio-cerebral topography, in localization of nervous lesions, 93

Cranium, changes in, in chronic alcoholism, 617
    in chronic hydrocephalus, 742, 743

Cretinism, 138

Crises clitoridienne, 836

Crises in tabes dorsalis, 835, 836

Croton chloral, use, in epileptiform facial neuralgia, 1234
    in migraine, 415

Croton oil, use of, in cerebral hemorrhage and apoplexy, 976

Cry of tubercular meningitis, 726, 727

Curare, use of, in tetanus, 556
    in tremors of spinal sclerosis, 905

Cutaneous sensibility, disorders of, in epilepsy, 476, 480

Cyanotic stage of symmetrical gangrene, 1258


D.

Dancing mania, the, 222, 223, 439

Deafness, hysterical, 249
  word-, in nervous diseases, 31

Death, apparent, 385
  mode of, in delirium tremens, 630

Defecation, hysterical disorders of, 240

Definition of alcoholism, 573
  of amyotrophic lateral spinal sclerosis, 867
  of apoplexy, 917, 918
  of athetosis, 459
  of atrophy of the brain, 993
  of catalepsy, 314
  of chorea, 440
  of chronic hydrocephalus, 740
    lead-poisoning, 678
  of eclampsia, 464
  of ecstasy, 339
  of epilepsy, 467
  of hæmatoma of the dura mater, 707
  of hysteria, 205
  of hystero-epilepsy, 288
  of infantile spinal paralysis, 1113
  of insanity, 99
  of labio-glosso-laryngeal paralysis, 1169
  of neural disorders of writers and artisans, 504
  of neuralgia, 1211
  of progressive unilateral facial atrophy, 693
  of spina bifida, 757
  of stigmatization, 348
  of symmetrical gangrene, 1257
  of tetanus, 544
  of trance, 344
  of tremor, 429
  of tubercular meningitis, 723
  of tumors of the brain, 1028
      spinal cord, 1090
  of unilateral spinal paralysis, 1166
  of vaso-motor and trophic neuroses, 1241
  of vertigo, 416

Deformities, in tabes dorsalis, 871
  in infantile spinal paralysis, 1127-1131

Degenerative changes in atrophy, 1266-1277

Deglutition, difficult, in amyotrophic lateral sclerosis, 868
    in Bell's palsy, 1204
    in cerebral hemorrhage and apoplexy, 935
    in labio-glosso-laryngeal paralysis, 1170

Delirium, acute, 163
  chronic, in alcoholic insanity, 632
  in acute simple meningitis, 718
  in alcoholism, 626
  in chronic lead-poisoning, 688, 689
  in nervous disease, 124
  of cerebral anæmia, 785
  tremens, 627

Delusional insanity, secondary, 203
  primary, 167

Delusions, character of, in insanity, 168
  in general paralysis of the insane, 187, 188, 190, 192
  in katatonia, 166
  varieties of, in nervous diseases, 22
  with melancholia, 156, 157

Dementia, in alcoholism, 633
  of general paralysis of the insane, 187
  paretic, in inflammation of the brain, 791
  in spastic spinal paralysis, 863, 865, 866
  and simple, in disseminated sclerosis, 877, 878
  primary, 164
  secondary, 165
  senile, 174
  terminal, 203

Depression in cerebral anæmia, 782, 783
  in mental disease, 20

Dercum and Parker on artificial induction of convulsive seizures,
        213, 529

Development of language, 568

Diabetes, influence on causation of neuralgia, 1218

Diagnosis of abscess of the brain, 799
  of acute mania, 162
  of acute myelitis, 820
  of acute narcotic poisoning from alcohol, 598
  of acute simple meningitis, 729
    spinal meningitis, 751
      pachymeningitis, 748
  of apoplexy, 963
  of anæsthesia of peripheral origin, 1200
  of athetosis, 459
  of Bell's palsy, 1205
  of capillary embolism, 981
  of catalepsy, 334
  of cerebral anæmia, 787
    embolism, 981
    hemorrhage, 963
    hyperæmia, 771
    meningeal hemorrhage, 714
    syphilis, 1112
  of chorea, 453
  of chronic cerebral meningitis, 722
    hydrocephalus, 744
  of chronic lead-poisoning, 690
  of combined form of sclerosis, 870
  of concussion of the brain, 909
      spine, 916
  of congestion of spinal membranes, 747
  of diffuse sclerosis, 890
  of diseases of cervical sympathetic, 1265
  of disseminated sclerosis, 885
  of ecstasy, 343
  of epilepsy, 493-496
  of external pachymeningitis, 706
  of family form of tabes dorsalis, 872
  of functional nervous diseases, 63
  of gastralgia, 1239
  of general paralysis of the insane, 197
  of hæmatoma of dura mater, 709
  of headache, 405
  of hydrencephaloid, 785
  of hypertrophy of the brain, 998
  of hysteria, 260
  of hystero-epilepsy, 307
  of infantile spinal paralysis, 1152
  of insanity, 123
  of labio-glosso-laryngeal paralysis, 1174
  of migraine, 410
  of multiple neuritis, 1197
  of myxœdema, 1273
  of nerve injuries, 1187
  of neuralgia, 1221
  of neuritis, 1194
  of neuromata, 1210
  of organic nervous diseases, 61-63
  of paralysis agitans, 438
  of progressive unilateral facial atrophy, 700
  of simulation of sleep, 775
  of spastic spinal paralysis, 866
  of special paralyses in infantile spinal paralysis, 1123
  of spina bifida, 755
  of spinal meningeal hemorrhage, 760
  of symmetrical gangrene, 1261
  of syphilis of brain-cortex, 1020
  of tabes dorsalis, 857
  of the chloral habit, 665
  of the opium habit, 659
  of thermic fever, 396
  of thrombosis of cerebral veins and sinuses, 987
  of tubercular meningitis, 732
  of tumors of brain, 1051, 1056
      of spinal cord, 1098, 1100
  of vaso-motor neuroses, 1252
  of vertigo, 417
  of writers' cramp, 521
  principles of, in nervous diseases, 59-61

Diaphragm, hysterical paralysis of, 239

Diarrhœal affections of children as a cause of cerebral anæmia, 779

Diet in acute simple meningitis, 721
  in acute spinal meningitis, 752
  in alcoholism, 643, 644
  in apoplexy, 975
  in cerebral anæmia, 790
  in cerebral meningeal hemorrhage, 715
  in chronic hydrocephalus, 745
  in epilepsy, 503
  in external pachymeningitis, 706
  in gastralgia, 1239
  in hæmatoma of the dura mater, 710
  in hyperæmia of the brain, 774
  in the opium habit, 673, 674
  in tubercular meningitis, 735, 736
  in tumors of the brain, 1068
  influence on causation of chronic lead-poisoning, 680

Diffuse myelitis, 886
  sclerosis, 886

Digestive disorders as a cause of headache, 404, 405
    in chronic hydrocephalus, 743
    in neurasthenia, 356
    in tubercular meningitis, 725, 726, 728
    of chronic alcoholism, 599-602, 607
    of the chloral habit, 661, 665
    of the opium habit, 653, 657-659
  symptoms of hystero-epilepsy, 297
    of migraine, 409
    of myxœdema, 1272
    of tetanus, 551
    of thermic fever, 390

Digitalis, use of, in alcoholism, 642, 645
    in epilepsy, 500
    in thermic fever, 397

Digiti mortui, 1252, 1254

Diplopia in disseminated sclerosis, 875, 876
  in nervous diseases, 40
  in tabes dorsalis, 829
  in tumors of the brain, 1042

Dipsomania, 147, 636, 637

Disease of one lateral half of the spinal cord, 1165
  Thomsen's, 461

Diseases, mental, 99
  of nervous system, general semeiology of, 19
  of peripheral nerves, 1176
  of the membranes of the brain and spinal cord, 703

Dislocation in infantile paralysis, 1130

Disorders of sleep, 364
  of speech, 568

Dizziness in general paralysis of the insane, 187, 195

Double consciousness in nervous diseases, 28
  vision in nervous diseases, 40

Doubting insanity, 170

Douche, cold, in catalepsy, 338
    in ecstasy, 338
    in spinal sclerosis, 903

Dreams (see _Sleep, and its Disorders_).

Dropsy of the head (see _Hydrocephalus, Chronic_), 740
  sleeping, 383

Dura mater, cerebral congestion, 704
  cerebral hæmatoma of (hemorrhagic pachymeningitis), 707
    Definition, etiology, and symptoms, 707
    Diagnosis, 709
    Duration and pathology, 708
    Prognosis, 709
    Treatment, 710
  cerebral inflammation of (pachymeningitis), 703
  external pachymeningitis, 704
    Diagnosis and prognosis, 706
    Etiology and symptoms, 704
    Pathological anatomy, 705
    Treatment, 706
  internal pachymeningitis, 706
    Treatment, 707
  spinal, acute inflammation of, 747

Duration of acute mania, 162
  of acute myelitis, 821
  of acute spinal meningitis, 718
  of amyotrophic spinal sclerosis, 868
  of catalepsy, 334
  of chorea, 449
  of chronic hydrocephalus, 743
  of delirium tremens, 629
  of ecstasy, 343
  of family form of tabes dorsalis, 871
  of hæmatoma of the dura mater, 708
  of hysteria, 258
  of hystero-epilepsy, 307
  of progressive unilateral facial atrophy, 699
  of spina bifida, 759
  of symmetrical gangrene, 1261
  of tabes dorsalis, 839, 840
  of tubercular meningitis, 729
  of tumors of the brain, 1045
      of the spinal cord, 1106
  of vertigo, 418
  of writers' cramp, 521

Dyskinesis, definition, in nervous diseases, 47

Dyslalia, 569, 572

Dyspepsia, headache from, 405

Dyspeptic symptoms of chronic alcoholism, 601, 607

Dysphagia, hysterical, 239, 245


E.

Ear affections, hysterical, 249
    influence on causation of acute pachymeningitis, 716
        of external pachymeningitis, 704
  disorders of, as a cause of abscess of the brain, 474
      of epilepsy, 474
      of vertigo, 421
    in progressive unilateral facial atrophy, 698
  middle, disease of, as a cause of thrombosis of cerebral veins and
          sinuses, 985

Eclampsia, 464
  Definition, etiology, and symptoms, 464

ECSTASY, 339
  Definition, 339
  Course, diagnosis, and duration, 343
  Etiology, 341
  History and synonyms, 339
  Prognosis, 343
  Symptoms, 342
  Treatment, 344

Eczema as a cause of chorea, 444

Education, improper, as a cause of hysteria, 218, 220
  of speech in aphasia of hemiplegia, 979
  relation of, to hysteria, 274

Electrical reactions in amyotrophic lateral sclerosis, 868
  in Bell's palsy, 1205, 1206
  in diffuse sclerosis, 890
  in infantile paralysis, 1125
  in spastic spinal paralysis, 864
  of injured and divided nerves, 1184, 1188

Electricity, use of, in Bell's palsy, 1207
    in catalepsy, 338
    in chronic lead-poisoning, 691
    in hysteria, 281, 286
    in hystero-epilepsy, 311-313
    in infantile spinal paralysis, 1156
    in labio-glosso-laryngeal paralysis, 1175
    in migraine, 415, 1232
    in multiple neuritis, 1198
    in myelitis, acute, 824
    in myxœdema, 1273
    in nerve injuries, 1189
    in neuralgia, 1225
    in neurasthenia, 360
    in neuritis, 1194
    in painless facial spasm, 462
    in paralysis agitans, 438
      of intracranial hemorrhage, 978
    in progressive unilateral facial atrophy, 702
    in sciatica, 1238
    in spinal sclerosis, 901, 905
    in symmetrical gangrene, 1262
    in torticollis, 464
    in vaso-motor neuroses, 1256
    in writers' cramp, 534

Emboli, source of, in occlusion of cerebral arteries, 947-950

Embolic origin of abscess of the brain, 799
  theory of origin of chorea, 452

Embolism, capillary, 979
  and thrombosis of cerebral arteries, 946
  of spinal cord, 808, 810

Emetics, use of, in alcoholism, 642
    in hysteria, 285

Emotional attitudes in hystero-epilepsy, 301
  causes of hystero-epilepsy, 293
  state, in general paralysis of the insane, 179
  states, abnormal, in nervous diseases, 19
  strain, influence on causation of insanity, 118

Emprosthotonos in tetanus, 551

Encephalitis, acute, of Strümpell, 791

Encephalic mass, localization of lesions in, 81

Endocarditis, ulcerative, as a cause of abscess of the brain, 799
    as a cause of capillary embolism, 980

Encephalopathy, the, of chronic lead-poisoning, 688

Enchondromatous brain tumors, 1070

Enophthalmos in progressive unilateral facial atrophy, 698

Entero-colitis of infancy, relation to thermic fever, 390

EPILEPSY, 467
  Definition and history, 467
  Diagnosis, 493
    from syncope, 495
    from vertigo, 495
    from uræmic convulsions, 495
    in children, 494
    in malingerers, 496
  Etiology, 468
    Age and sex, influence on causation, 470
    Exanthemata, relation of, to, 473
    Excentric irritating causes, 471
    Exciting causes, 471
    Gastric causes, 474
    Peripheral origin, 474
    Preputial irritation as a cause, 473
    Reflex causes, 472
    Sexual causes, 473, 474
    Syphilis, influence on causation, 470
    Toxic causes, 472
    Traumatic causes, 470, 471
  Morbid anatomy and pathology, 488
    Alterations of cerebral tissue in, 493
    Hughlings-Jackson's cortical theory, 489, 490
    Medullary theory of origin, 489
    Theory of epileptic zones, 489
  Prodromata, 475
    Aural, characters of, 475, 476
    Cerebral disturbances, 475
    Cutaneous disorders, 476
    Hearing and vision, disorders of, 475, 476
    Motor disturbances, 476
    Saliva, increase of, 476
  Prognosis, 496
    Age, influence on recovery, 498
    Menstruation, marriage, and pregnancy, influence on recovery,
          500, 501
  Symptoms, 477
    Frequency of attacks, 482
    of immediate and remote effects of paroxysms, 481
      Physical, 481
      Post-epileptic aphasia, 481
      Psychical, 481
      Tendency to mania in, 482
    of irregular forms, 483
    of light attacks, or petit mal, 477
    of major attacks, 477-479
      Convulsions, characters, 477-479
      Cutaneous state, in, 480
      Duration of attacks, 478
      Eyes, state of, in, 480
      Pulse and temperature in, 480
      Tendon reflexes in, 481
      Tongue-biting, significance, 481
      Urine, state of, 480
    of psychical or masked forms, 483-486
    of sensory epilepsy, 486
      Hallucinations in, 487
  Synonyms, 467
  Treatment, 499
    Abortants, use, 502
    Amyl nitrite, use, 502
    Belladonna and ergot, use, 501
    Blisters, use, 502
    Bromide, use of, 499-501
    Bromate of potassium, use, 501
    Cod-liver oil and hypophosphites, use, 501
    Diet in, 503
    Digitalis, use, 500
    Galvanism, use, 502
    Iodide of potassium, use, 502
    Nitro-glycerin, use, 500, 502
    of status epilepticus, 502
    Strychnia, use, 500
    Surgical measures, 502

Epilepsy, alcoholic, 624
  influence on causation of migraine, 407

Epileptic attacks in cerebral syphilis, 1010
    following hemiplegia, 955

Epileptic insanity, 149

Epileptiform facial neuralgia, 1233

Epistaxis in tumors of the brain, 1044

Ergot, use of, in acute myelitis, 822
    in acute spinal meningitis, 721
    in cerebral hyperæmia, 773
    in epilepsy, 501
    in migraine, 413, 1232
    in infantile spinal paralysis, 1155
    in insanity, 136
    in spinal hyperæmia, 805
      meningeal hemorrhage, 756

Ergotin, use of, in spinal sclerosis, 901

Erotomania, 148

Eruptions in nervous diseases, 57
  simulated, in hysteria, 234

Erysipelas as a cause of cerebral hyperæmia, 765
    of thrombosis of cerebral veins and sinuses, 985

Erythema, local, in symmetrical gangrene, 1259

Erythromelalgia, 1253

Essential vertigo, 426

Ether, habitual addiction to, 667
  use of, in chorea, 455
    in neuralgia, 1229
    in tetanus, 556

Etiology of abscess of the brain, 796
  of acute simple meningitis, 716
  of acute spinal meningitis, 749
  of alcoholism, 575
  of atrophy of the brain, 994, 995
  of Bell's palsy, 1203
  of capillary embolism, 979
  of catalepsy, 315
  of cerebral anæmia, 776
  of cerebral hyperæmia, 765
  of cerebral meningeal hemorrhage, 711
  of chorea, 440
  of chronic hydrocephalus, 741
    lead-poisoning, 679
  of combined forms of sclerosis, 870
  of congestion of the cerebral pia mater, 716
    of spinal membranes, 746
  of diseases of cervical sympathetic, 1263
  of disseminated sclerosis, 883
  of eclampsia, 464
  of ecstasy, 341
  of epilepsy, 468
  of external pachymeningitis, 704
  of family form of tabes dorsalis, 870
  of general paralysis of the insane, 177
  of hæmatoma of dura mater, 707
  of hypertrophy of the brain, 997
  of hysteria, 214
  of hystero-epilepsy, 291
  of infantile spinal paralysis, 1151
  of insanity, 113
  of intracranial hemorrhage and apoplexy, 927
  of labio-glosso-laryngeal paralysis, 1173
  of neural disorders of writers and artisans, 505
  of migraine, 1231
  of multiple neuritis, 1197
  of myxœdema, 1271
  of neuralgia, 1216
  of neurasthenia, 354
  of neuritis, 1190
  of neuromata, 1209
  of occlusion of cerebral arteries, 950
  of progressive unilateral facial atrophy, 693
  of sciatica, 1236
  of spastic spinal paralysis, 864
  of spina bifida, 757
  of spinal hemorrhage, 809
  of spinal hyperæmia, 802
  of spinal meningeal hemorrhage, 754
  of symmetrical gangrene, 1261
  of tabes dorsalis, 851
  of tetanus, 545
  of tetanus neonatorum, 563
  of the chloral habit, 661
  of the opium habit, 649
  of thermic fever, 388
  of thrombosis of cerebral veins and sinuses, 982, 983
  of torticollis, 463
  of tubercular meningitis, 724
  of tumors of the brain, 1028
      of the spine, 1090
  of vertigo, 418
  of writers' cramp, 506
  general, of syphilitic affections of nerve-centres, 999

Exaltation, in nervous diseases, 20

Exanthemata, as a cause of epilepsy, 473
      of vertigo, 419

Excesses, influence on causation of general paralysis of the insane,
            177
        of insanity, 116, 119

Excision of the tumor in spina bifida, 762

Exciting causes of insanity, 118, 119

Exercise, necessity of, in hysteria, 275

Exhausting diseases as a cause of cerebral anæmia, 779
          of tremor, 429

Exhaustion, insomnia from, 380

Exposure to cold and wet as a cause of tabes dorsalis, 855

Eye affections, hysterical, 247
    in progressive unilateral facial atrophy, 698

Eye-strain, headache from, 304

Eyes, state of, in cerebral hemorrhage and apoplexy, 939
    in chronic hydrocephalus, 743
    in epilepsy, 479, 480
    in tubercular meningitis, 725-727, 729
  Disorders of, as a cause of vertigo, 424
    in cerebral anæmia, 783
      hyperæmia, 770, 772
    in diseases of cervical sympathetic, 1264
    in disseminated sclerosis, 875, 877, 878
    in tabes dorsalis, 830-833
    in the chloral habit, 664, 665
    in the opium habit, 657
    in tumors of the brain, 1035, 1042-1044


F.

Facial atrophy, unilateral progressive, 693
  expression in Bell's palsy, 1203
    in cerebral hemorrhage and apoplexy, 939
    in chorea, 445
    in paralysis agitans, 434
  nerve, paralysis of, in atrophic spinal paralysis, 1120
  nerve, peripheral paralysis of (Bell's palsy), 1202
    Diagnosis, 1205
    Etiology, 1202, 1203
    Symptoms, 1203
      Facial expression, 1203, 1204
      Muscles and organs affected, 1203, 1204
      Reactions, electrical, in, 1205, 1206
      Special senses and sensibility in, 1204, 1205
    Treatment, 1206
      Bleeding and counter-irritation in, 1207
      Electricity, 1207
      Iodide of potassium, 1207
      Mechanical appliances and massages, 1207, 1208
  neuralgia, 1232
    epileptiform, 1233
  spasm, painless, 462

Facies hysterica, 230

Faith-cure, 277

Family form of tabes dorsalis, 870

Faradic reactions, significance, in diagnosis of nervous lesions, 66

Fasting girls, 351
  saints, 351

Fatty heart, in chronic alcoholism, 611

Febrile insomnia, 379

Feeding, forced, in neurasthenia, 359

Feet, condition of, in advanced tabes dorsalis, 838
    in diffuse sclerosis, 888

Festination in paralysis agitans, 436

Fever, thermic, 388
  and cerebral anæmia, 779

Fibrillary contractions in nervous diseases, 47

Fifth nerve, neuralgias of, 1233

Flexibility, wax-like, in catalepsy, 321, 337

Fontanels, state of, in chronic hydrocephalus, 741, 742
    in tubercular meningitis, 727

Frauds of hysterical patients, 233, 234

Frequency of epileptic attacks, 483

Friedreich's disease, 870

Front-tap, in diffuse spinal sclerosis, 888

Functional nervous diseases, diagnosis of, 63


G.

Gait in chronic lead-poisoning, 686
  in diffuse sclerosis, 888
  in general paralysis of the insane, 194
  in paralysis agitans, 435
  in spastic spinal paralysis, 863, 864
  in tabes dorsalis, 831

Galvanic reactions, significance of, in diagnosis of nervous lesions,
        66

Galvanism, use in insanity, 137

Ganglionic elements, condition of, in abscess of the brain, 793

Gangrene in vaso-motor neuroses, 1252
  Definition, history, and synonyms, 1257
  Duration, course, and nature, 1261
  Etiology and diagnosis, 1262, 1263
  of Reynaud's disease, 1259, 1260
  Prognosis, 1262
  Symmetrical, 1257
  Symptoms, 1258-1260
  Treatment, 1262
    Electricity, 1262
    Massage, rest, and tonics, use, 1262
    Opium, use, 1262

Gastric crises in tabes dorsalis, 835
  Disorders, as a cause of epilepsy, 474
  Vertigo, 420

Gastralgia (see _Neuralgia_).

Gelsemium, use, in neuralgia, 1225
    in painless facial spasm, 462

General paralysis of the insane, 176

Genital organs, disorders of, in chronic alcoholism, 614

Genito-urinary disorders of the chloral habit, 662, 663
    of the opium habit, 654, 658

Genius, relations of, to insanity, 115

Glandular system, atrophy of, 1268

Gliomatous tumors of the brain, 1046

Gold, use of, in hemiplegia, 970
  and sodium chloride, use of, in hysteria, 278

Gout, relation of, to chronic lead-poisoning, 685
    to hysteria, 215

Guarana, use, in migraine, 1232

Gummatous brain syphilis, 1003, 1014
  brain tumors, 1049

Gums, state of, in chronic lead-poisoning, 684

Gustatory sensory disturbances in nervous diseases, 41

Gymnastics, value of, in hysteria, 275, 280
    in writers' cramp, 536

Gynæcological treatment of hysteria, 289


H.

Habit, influence on causation of alcoholism, 577
  opium, and kindred affections, 647

Hæmatoma of the dura mater, 707

Hæmatorrachis, 754

Hair, changes in, in progressive unilateral facial atrophy, 695

Hallucinations in alcoholism, 626, 631
  in cerebral anæmia, 782, 784, 785
    hyperæmia, 769
  in delirium tremens, 627, 628
  in hystero-epilepsy, 301
  in nervous diseases, 21, 22
  in the opium habit, 655, 658, 659

Handwriting in general paralysis of the insane, 183
  in paralysis agitans, 435

Head, changes in, in chronic hydrocephalus, 742, 743
  retraction of, in acute simple meningitis, 718
  retraction of, in tubercular meningitis, 726, 727

HEADACHE, 401-414
  Diagnosis, 405
  Duration, 401
  Symptoms, 402
    from dyspepsia, 405
    from eye-strain, 404
    from sunstroke, 404
    of anæmic and congestive form, 402
    of hysterical and toxic form, 402
    of organic and neurasthenic form, 403, 404
    of rheumatic, pyrexial, and syphilitic form, 403
    of sympathetic form, 404
  Synonyms, 401
  Treatment, 406, 413

Headache in abscess of the brain, 795
  in acute simple meningitis, 717, 718
  in anæmia of the brain, 783
  in cerebral anæmia, 783
    meningeal hemorrhage, 712
    syphilis, 1003
  in children, 405
  in chronic cerebral meningitis, 722
  in external pachymeningitis, 705
  in hæmatoma of the dura mater, 707
  in hyperæmia of the brain, 770
  in the chloral habit, 663, 665
  in the opium habit, 655
  in thermic fever, 390
  in tubercular meningitis, 725, 726
  in tumors of the brain, 1033
    spinal cord, 1096
  periodical or sick, 1216, 1230

Head-pressure, sense of, in cerebral hyperæmia, 769

Hearing, disorders of, in alcoholism, 623
    in Bell's palsy, 1204
    in cerebral hyperæmia, 772
    in hemiplegia, 955
    in neuralgia, 1213
    in progressive unilateral facial atrophy, 698
    in tumors of the brain, 1030, 1043

Heart, disorders of, in angina pectoris, 1237
    in chronic alcoholism, 610-612
    in disease of cervical sympathetic, 1265
    in labio-glosso-laryngeal paralysis, 1171
    in neurasthenia, 356
    in tabes dorsalis, 836
    in the chloral habit, 662
    in the opium habit, 654, 658, 659
    influence on causation of embolism and thrombosis of cerebral
            veins, 951
        of intracranial hemorrhage and apoplexy, 930

Heat, affections produced by exposure to, 387

Heat-exhaustion, 387
  Pathology and treatment, 388

Heat, use of, in concussion of the spine, 911

Hebephrenia, 171

Hemianæsthesia, hysterical, 247

Hemianopsia in nervous diseases, 39, 40
  in tumors of the brain, 1030, 1042

Hemicrania angio-paralytica, 409, 411
  spastica, 409, 411

Hemiparaplegia in nervous diseases, 44

Hemiplegia, hysterical, 238
  in cerebral hemorrhage and occlusion of cerebral vessels, 940, 954
  in cerebral meningeal hemorrhage, 712
  in infantile spinal paralysis, 1120
  varieties in nervous diseases, 42, 43

Hemispasm in nervous diseases, 45

Hemorrhage as a cause of cerebral anæmia, 776
  cerebral meningeal, 710
  intracranial, 918
  spinal meningeal, 754

Hemorrhages of spinal cord, 808

Hemorrhagic pachymeningitis, 707

Hepatitis, parenchymatous and interstitial, in chronic alcoholism, 604

Hereditary alcoholism, 634
  Ataxia, 870
  Tabes, 870

Heredity, influence on causation of alcoholism, 576
      of angina pectoris, 1238
      of cerebral hyperæmia, 765
      of chorea, 440
      of chronic hydrocephalus, 741
      of copodyscinesia, 513
      of epilepsy, 468
      of general paralysis of the insane, 177
      of hysteria, 214
      of insanity, 113
      of intracranial hemorrhage and apoplexy, 929
      of migraine, 407, 1231
      of neuralgia, 1216
      of syphilitic affections of nerve-centres, 1000
      of tabes dorsalis, 851
      of tremor, 429
      of tubercular meningitis, 724
      of tumors of the brain, 1029

History of alcoholism, 574
  of catalepsy, 315
  of chorea, 439
  of chronic lead-poisoning, 678
  of ecstasy, 399
  of epilepsy, 467
  of general paralysis of the insane, 176
  of hysteria, 207
  of hystero-epilepsy, 289
  of insanity, 109
  of labio-glosso-laryngeal paralysis, 1169
  of neural disorders of writers and artisans, 504
  of progressive unilateral facial atrophy, 693
  of spina bifida, 757
  of symmetrical gangrene, 1257
  of tabes dorsalis, 826
  of the opium habit, 504
  of tubercular meningitis, 723

Home, removal from, question of, in treatment of opium and chloral
        habit, 670, 671

Home treatment of the insane, 128, 130, 131, 133

Homicidal insanity, 146

Hughlings-Jackson on origin of epilepsy, 489

Hydrobromic acid, use, in epilepsy, 501

Hydrocele, spinal, 757

HYDROCEPHALUS, CHRONIC, 740
  Definition and synonyms, 740
  Diagnosis, 744
  Duration, 733
  Etiology, 741
  Pathological anatomy and prognosis, 744
  Spurious, in cerebral anæmia, 785
  Symptoms, 741
  Treatment, 745
    by compression, 745
    by evacuation of the fluid by puncture, 745
    Medicinal, 745

Hydropathic treatment of hysteria, 282
    of neuralgia, 1226

Hydrorachis (see _Spina Bifida_), 757

Hygienic treatment of chronic hydrocephalus, 745
    of hemiplegia, 978
    of hysteria, 274
    of neuralgia, 1223
    of tubercular meningitis, 735

Hyoscyamine, use, in painless facial spasm, 462
  in torticollis, 464

Hyoscyamus, use, in alcoholism, 645
    in brain tumors, 1068
    in paralysis agitans, 438
    in tremor, 432
    in tremors of spinal sclerosis, 905
    in tubercular meningitis, 736

Hyperæmia of the brain, 763
  Spinal, 801

Hyperæsthesia, hysterical, 250
  in acute spinal meningitis, 750
  in acute spinal pachymeningitis, 747
  in chronic alcoholism, 620
  in chronic spinal meningitis, 752
  in multiple neuritis, 1195
  in symmetrical gangrene, 1259
  in tumors of the brain, 1042
    of the spinal cord, 1091, 1092

Hyperæsthesiæ, varieties of, in nervous diseases, 31-33

Hyperkinesis, in nervous diseases, 44-47

Hypertrophy, 1271
  of the brain, 996

Hypnotic catalepsy (hypnotism), 322, 373

Hypnotics, use, in cerebral hyperæmia, 773

Hypnotism, 322, 373

Hypochondriacal form of general paralysis of the insane, 188
  insanity, 150

Hypochondriasis, 154

Hypophosphites, use, in alcoholism, 644, 646
    in general paralysis of the insane, 201

HYSTERIA, 205
  Course, complications, and duration, 258
  Definition, 205
  Diagnosis, 260
    from acute mania, 262
    from general nervousness, 262
    from hypochondria, 262
    from multiple cerebro-spinal sclerosis, 267
    from neurotic temperament, 261
    from neurasthenia, 262
    from spastic spinal paralysis, 267
    from spondylitis, 268
    from true joint affections, 270
    of hysterical blindness and deafness, 271
    of hysterical paralyses, 266
  Etiology, 216
    Age, influence of, 216
    Anæmia and chlorosis, influence of, 220
    Diatheses, gouty and phthisical, influence of, 214, 215
    Education, influence of, 218-220
    Heredity, influence of, 214
    Imitation, influence of, 222-229
    Kidneys, movable, influence of, 221
    Local and sexual irritation, influence of, 220, 221
    Menstrual disorders, influence of, 220
    Race, climate, and social position, influence of, 217, 218
    Sex, influence of, 215
  History, 207
  Pathology, 208-213
  Prognosis, 272
  Symptoms, 229
    Aphonia, 239
    Breathing, peculiarities of, 245
    Chorea, 242
    Clavus hystericus, 252
    Contractures, 244
    Convulsions and general spasms, 235-237
    Dysphagia, 239-245
    Ear affections, 249
    Erotomania, 235
    Eye affections, 247, 248
    Facies hysterica, 230
    Frauds and deceptions, 233
    Insanity, 231-233
    Joint affections, 251
    Local spasms, 244
    Locomotor ataxia, 240
    Mental state, 230
    Nymphomania, 235
    Pain, 250
    Paralyses, varieties and characters, 237-241
    Phantom tumors, 255
    Rectal, 240
    Sensorial affections, 246-250
    Simulating pregnancy, 254
    Smell and taste, perversion of, 250
    Spinal irritation, 251
    Temperature and pulse, 252
    Urinary secretion, state of, 253
    Vaginismus, 246
    Vomiting, 254
  Synonyms, 206
  Treatment, 273
    Baths, use of, in, 282, 283
    Bromides, use of, 276
    Chloroform, use of, 285, 286
    Climatic, 283
    Cold, use of, 282, 283
    Education, necessity of proper, 274
    Electricity, use of, 281-286
    Emetics in controlling seizures, 285
    Exercise and gymnastics, use in, 275, 280
    Gold and sodium chloride, use of, 279
    Gynæcological, question of, 286, 287
    Harsh measures, questionable value of, 276
    Hydrotherapy in, 281, 282
    in children, 275
    Iron and zinc salts, use in, 278
    Massage and Swedish movements, 280
    Metallo-therapy, 284
    Mind- and faith-cures, value of, 277, 278
    Mitchell's rest-cure, 279
    Moral, 276
    Musk, valerian, asafœtida, etc., 278
    Nitrite of amyl, 285
    of contractures, 286
    of paralyses, 286
    of paroxysms, 285
    Opium, use of, 278
    Oöphorectomy, question of, 287
    Prophylactic and hygienic, 274
    Sea-bathing in, 283

Hysteria as a cause of disseminated sclerosis, 884
      of vertigo, 425
  distinguished from brain tumors, 1055

Hysterical headache, 402
  insanity, 148

HYSTERO-EPILEPSY, 288
  Definition and synonyms, 288
  Diagnosis, 307
    from true epilepsy, 308
    from simulation, 310
  Duration and course, 307
  Etiology, 291
    Age, influence of, 291
    Emotional, 293
    Painful menstruation, 293
    Sex, race, and climate, 291
  History, 289
  Pathology, 291
  Prognosis, 310
  Symptoms, 293
    Anæsthesia, 298
    Contracture, 297
    Digestive, 297
    Hallucinations, 301
    Hystero-epileptogenic zones, significance of, 298
    of contortions and great movements, 301
    of delirium, 301
    of emotional attitudes, 301
    of epileptoid period, 300
    of irregular types, 302
    of regular types, 293
    of paroxysms, 293, 304, 306
    Ovarian hyperæsthesia, 298
      pressure, effect of, 299
    Permanent, 307
    Prodromal, 297
  Treatment, 310
    Compression of nerve-trunks, 310
    Electricity, use of, 311-313
    Metallic salts, use of, 313
    Metallo-therapy, 313
    Nitrite of amyl and nitro-glycerin, 311
    Oöphorectomy, question of, 312
    Potassium bromide, use of, 313
    Torsion of abdominal walls to arrest paroxysms, 311
  Varieties, 290


I.

Ice, use of, in acute simple meningitis, 720
    in cerebral meningeal hemorrhage, 715
    in neuritis, 1194
    in tubercular meningitis, 736

Idiocy, intellectual and moral, 138

Ill-health, influence on causation of insanity, 116, 117

Illusions in nervous diseases, 20

Imbecility, intellectual and moral, 138
  in inflammation of the brain, 791

Imitation, influence on causation of catalepsy, 319
      of hysteria, 222-229

Impotence in tumors of spinal cord, 1096

Impulsive insanity, 146

Inco-ordination in nervous diseases, 47-50

Inebriety, trance state in, 346

INFANTILE SPINAL PARALYSIS, 1113
  Anatomical lesions, 1131
    Atrophy of anterior spinal horns, characters, etc., 1133, 1138,
          1139
      nerve-roots and anterior columns of the cord, 1138, 1139
    Autopsies, tables of, 1133-1136, 1139
    Microscopic lesions, 1137
  Theories interpreting the lesions of the cord, 1140-1144
    regarding origin, premature, 1132
  Complication with progressive muscular atrophy, 1149
  Course of, 1148
  Definitions, 1113
  Deformities of atrophic paralysis, 1127
    Criticism of theory of muscular antagonism, 1128
    Dislocations in, 1130
    Mechanism of, 1128, 1131
    Muscular contraction in, 1127
    Relation of weight and muscular forces, 1130
  Diagnosis, 1152
    from cerebral paralysis, 1152
    from diphtheritic paralysis, 1153
    from diseases of bony skeleton and articulations, 1154
    from hæmatomyelitis, 1153
    from lesions of peripheric nerves, 1153
    from progressive muscular atrophy, 1153
    from pseudo-paralysis of syphilitic children, 1153
    of special paralysis, 1123
      Atrophy in, 1124
      Loss of faradic contractility, 1125
      Negative symptoms, 1126
      Temperature of skin, 1124
  Etiology, 1151
    Blood-poisons, influence of, 1151
    Cold, influence of, 1152
    Traumatism, influence of, 1151
  History, clinical, summary of, 1114
  Invasion, mode of, 1115
  Pathogeny, 1144
    Consequence of limitation of the myelitis to anterior horns of
          spinal cord, 1144
    Relation between limitation of the myelitis and age, 1147
    Trophic lesions of, 1145
  Prodromata, 1115
    Acute specific and apyretic diseases, 1116
    Convulsions, 1116
    Fever, duration of, 1115, 1116
    Hemiplegia, 1120
    Immunity of certain muscles and nerves, 1118
    Paralysis, characters of, 1117
      Crossed, and paralysis of trunk, 1120
      Locality of permanent, 1119
      of facial nerve, 1120
      Significance and original extent of, 1117
    Paralyzed muscles, combinations of, 1121-1123
  Prognosis, 1149
  Special paralyses, influence on locomotion, 1150
  Symptoms in detail, 1114
  Synonyms, 1113
  Treatment, 1155
    Belladonna, use, 1155
    Counter-irritation, 1155
    Electricity, 1156
    Ergot, 1155
    Heat, use of, 1157
    Ice, 1155
    Iodide of potassium, 1156
    Locomotion, importance of maintenance of, 1159
    Massage and Swedish movements, 1157
    Mechanical appliances, 1159-1164
    Stretching and manipulation of contracted and atrophied muscles,
          1158
    Strychnia, use of, 1157
    Tenotomy, indications for, 1158, 1159, 1161, 1163, 1164

Inflammation as a trophic neurosis, 1273
  of brain, 790
  of external surface of dura mater of brain, 704
  of nerves, 1189
  of the dura mater of the brain, 703

Injuries, influence on causation of intracranial hemorrhage and
        apoplexy, 931
  of peripheral nerves, 1182

Insane, acute alcoholism in the, 594
  Cataleptic phenomena in, 327
  Temperament, peculiarities of, 140

Insanity (see also _Mental Diseases_).
  Alcoholic, 631
  Cerebral syphilitic, 202
  Chronic alcoholic, 202
  Circular, 151
  Doubting, 170
  Epileptic, 149
  from gross cerebral lesions, 202
  Homicidal, 147
  Hypochondriacal, 150
  Hysterical, 148, 230-233
  Impulsive, 146
  Increase of, question of, 112, 117
  Influence on causation of hæmatoma of the dura mater, 707
      of the opium habit, 651
  Menstrual, 173
  Moral, 143
  of childhood, 171
  of lactation, 782
  Primary, 151
  Primary, confusional and delusional, 167
  Periodic, 150
  Puerperal, 173
  Secondary, delusional, 203
  Suicidal, 146
  Syphilitic, 175, 1017
  Terminations of, in delirium tremens, 630
  Transitory, 164

Insomnia, 379
  in cerebral anæmia, 783
  in delirium tremens, 627, 629
  in the chloral habit, 665
  in the insane, treatment, 137
  in the opium habit, 655

Intellect, state of, in alcoholism, 625
    in symmetrical gangrene, 1260

Intellectual pursuits, as a cause of intracranial hemorrhage and
        apoplexy, 931

Intercostal neuralgia, 1234

Intermarriage, influence on causation of insanity, 115

Intermittent neuralgia of supraorbital nerve, 1233

Intestines, disorders of, in chronic alcoholism, 601, 602

INTRACRANIAL HEMORRHAGE AND OCCLUSION OF THE CEREBRAL VESSELS,
      APOPLEXY, SOFTENING OF THE BRAIN, CEREBRAL PARALYSIS, 917
  _Atheroma of the Cerebral Arteries_, 991
    Diagnosis, 992
    Prophylaxis and treatment, 992
  _Capillary Embolism_, 979
    Diagnosis, 981
    Etiology and morbid anatomy, 979, 980
    Prognosis and treatment, 981
    Symptoms, 980
  _Intracranial Hemorrhage_, 917
    Appearances of old, 921
    Clots, characters of, and changes in, 920
    Definition of apoplexy, 917, 918
    Etiology, 957
      Age, 927-929
      Alcohol, 929, 933
      Apoplectic constitution, characteristics of, 930, 931
      Bright's disease, 930
      Exciting causes, 931
      Heart disease, 930, 931
      Heredity and sex, 929
      Intellectual pursuits, 931
      Narcotic poisons, 933
      Obstruction to circulation, 931, 932
      Season, 931
      Situation of, 918-921, 923, 924
      Traumatism, 932
    Miliary aneurisms, causes, seat, and characters of, 921, 922
    Pathology of hemorrhagic apoplexy, 925-927
    Symptoms, 933
      Consciousness, loss of, onset and degrees of, 933
        temporary loss of, significance and causes of, 942, 943
      Eyes, state of, 939, 941
      Facial expression, 935
      Headache and paræsthesia as premonitory signs, 946
      Hemiplegia, 940
      Mental disturbances and aberrations of special senses, 945
      Muscular relaxation, 935, 939
      Paralysis, 938
      Pulse, state of, 939, 944
      Respiration, 935
      Retinal hemorrhages, 944
      Sensibility, state of, 942
      Speech, 939
      Sphincters, state of, 941
      Swallowing, 935
      Temperature, 935-938
      Tongue, state of, 939
      Vertigo, significance of, 745
      Vomiting, 935
    Vessels, cerebral, state of, in, 922
  _Occlusion of the Cerebral Arteries_, 946
    Diagnosis between hemorrhage, embolism, and thrombosis, 971, 972
      from apoplectiform attacks of intracranial syphilis, 967
      from comatose form of pernicious intermittent fever, 966
      from diabetic coma and sunstroke, 966
      from epilepsy, 965
      from hysteria, 966, 968
      from injuries to the head, 966
      from meningitis of the vertex, 967
      from narcotic poisoning, 964
      from uræmia, 965
      localization of lesions in, 969
    Etiology, 950
      Age, influence of, 951
      Heart and arteries, disease of, 951
      Heart-weakness and hæmic dyscrasia, 951
    Morbid anatomy, 946
      Cerebral substance, changes in, produced by emboli and thrombi,
            949
      Emboli and thrombi, seat of, 947-949
        source of, 947
      Regions of brain usually involved in softening, 949, 950
    Prognosis, 972-974
    Symptoms, 952
      Aphasia, 956-960
      Arthropathies, 962
      Atrophy, muscular, 962
      Chorea, post-paralytic, 960
      Mental condition, 956, 957
      Motor paralysis, duration and course, 954
      Reflexes, increased, rigidity and contracture, 962, 963
      Sensation, state of, 955
      Temperature, 960, 961
      Urine, state of, 961
      Word-blindness, 959
    Treatment, 974
      of cerebral embolism, 977
      of attack, 977
        Prophylaxis, 977
      of cerebral hemorrhage, 974, 975
        Artificial respiration, 976
        Bleeding and purgatives, 976
        Cleanliness, necessity of, 977
        Prophylaxis, 974
        Surgical measures, 977
      of cerebral thrombosis, 977
      of paralysis and later symptoms, 978
        Electricity, use of, 978
        Iodide of potassium and phosphorus, use, 978
        Massage, use, 978
        Silver, gold, and strychnia, use, 978
        Re-education of faculty of speech, 979
  _Softening of the Brain_, 918, 949, 989
  _Thrombosis of the Cerebral Veins and Sinuses_, 982
    Diagnosis, 987
      Localization of the thrombus, 988
    Etiology, 983
      Age, 983
      Anæmia, simple, as a cause, 984
      Carbuncles and erysipelas as a cause, 985
      Ear, diseases of, 985
      of marantic form, 983, 984
      Special diseases most likely to result from, 983
    Prognosis, 988
    Symptoms, 986
      dependent on disturbances of cerebral function, 986
      dependent on congestion and compression of other structures,
            986, 987
    Treatment, 988
      Ammonia, use of, 989
      Prophylactic, 989
      Surgical measures, 989

Iodide of potassium, use of, after intracranial hemorrhage and
            apoplexy, 978
      in acute spinal meningitis, 752
      in Bell's palsy, 1207
      in cerebral meningeal hemorrhage, 415
        syphilis, 1016
      in chronic cerebral meningitis, 722
      in chronic lead-poisoning, 691
      in epilepsy, 502
      in general paralysis of the insane, 201
      in hæmatoma of dura mater, 710
      in multiple neuritis, 1198
      in neuritis, 1194
      in spinal sclerosis, 900
      in thrombosis of cerebral veins and sinuses, 989
      in tubercular meningitis, 736

Iodine, injection of, into sac of spina bifida, 762
  use of, in acute spinal meningitis, 752
    in chronic spinal meningitis, 753
  and iodide of potassium, use of, in spinal meningeal hemorrhage, 756

Iridoplegia in tabes dorsalis, 829

Iron, use of, in alcoholism, 643
    in catalepsy, 338
    in chorea, 455
    in chronic hydrocephalus, 745
    in hysteria, 278
    in hystero-epilepsy, 313
    in neuralgia, 1224
    in spinal meningeal hemorrhage, 756
    in tubercular meningitis, 735

Irritability in tubercular meningitis, 725, 727

Irritable breast of Astley Cooper, 1235

Irritation, local, influence on causation of hysteria, 220, 221


J.

Jaw reflex, in amyotrophic lateral sclerosis, 868

Jerking malady, hysterical nature of, 226

Joint affections, hysterical, 252
    in tabes dorsalis, 830, 837
    of chronic lead-poisoning, 684

Jumpers, the, hysterical nature of, 227

Jumping chorea, 244


K.

Katatonia, 166, 327

Kidneys, disorders of, in chronic alcoholism, 612, 613
    in the chloral habit, 662
    in the opium habit, 654
  movable, as a cause of hysteria, 221

Kinesodic system of encephalon, lesions, 86
    of spinal cord, localization of lesions in, 71

Kleptomania, 147

Knee-jerk, alterations, in general paralysis of the insane, 195
    in amyotrophic lateral sclerosis, 868
    in chorea, 448
    in diffuse spinal sclerosis, 888
    in disseminated sclerosis, 875
    in epilepsy, 481
    in hemiplegia, 962
    in nervous diseases, 152
    in spastic spinal paralysis, 862
    in spinal syphilis, 1025
    in tabes dorsalis, 829, 835, 857, 858
    in the chloral habit, 664
    in tumors of the spinal cord, 1092
  significance in diagnosis of hysteria, 265, 266


L.

Lactation, prolonged, as a cause of epilepsy, 471

LABIO-GLOSSO-LARYNGEAL PARALYSIS, PROGRESSIVE, 1169
  Definition, 1169
  Diagnosis, 1174
  Etiology, 1173
  History, 1169
  Pathological anatomy, 1172
  Symptoms, 1170
    Articulation, difficulty of, characters of, 1170, 1171
    Deglutition, difficult, 1170
    Facial expression, 1170
    Heart, disorders of, 1170
    Paralysis and atrophy of muscles of neck and extremities, 1172
    Respiration, disturbances of, 1171
    Tongue, condition of, 1170-1172
  Synonyms, 1169
  Treatment, 1174
    Diet, 1175
    Electricity, 1175
    Metallic salts and quinine, 1175

Language, development of, 568

Laryngeal vertigo, 425

Larynx, disorders and lesions of, in chronic alcoholism, 607

Lateral sclerosis, 861

Lead, mode of action of, in the system, 689

LEAD-POISIONING, CHRONIC, 678
  Channels of introduction into body, 680-682
  Classification, definition, and history, 678
  Diagnosis, 690
  Etiology, 679
    Age, sex, and diet, influence of, 680
    Exciting causes, 680
    Occupation, influence of, 681
    Season and climate, influence of, 679, 680
  Morbid anatomy and pathology, 689
  Prognosis, 684, 687, 689
  Symptoms, 682-689
    Albuminuria in, 689
    Amaurosis in, 689
    Bluish line upon gums, significance of, 682
    Disturbances of nutrition, 682
    in animals, 690
    of lead colic, 683
    of the arthralgia, 684
    of the encephalopathy, 688
    of the paralysis, 685
  Synonyms, 678
  Treatment, 690
    Alum, use, 691
    Electricity and massage, use, 691
    Opium, use, in colic, 691
    Potassium iodide, use, 691
    Prophylaxis, 690
    Sulphuric acid and magnesium sulphate, use, 690, 691

Lead tremors, 429, 683

Leptomeningitis, cerebral, 716
    spinal, 749

Lesions in the nervous system, localization of, 65

Lethargy, 344, 384
  in cerebral anæmia, 782, 783
  lucid, 385

Levinstein's method of treating the opium habit, 672

Ligation of the sac of spina bifida, 762

Lipomatous tumors of the brain, 1049

Lithæmic insomnia, 379

Liver, changes in, and disorders of, in chronic alcoholism, 603, 607

Local convulsive disorders, 461

Localization of functions of spinal cord, table showing, 77

LOCALIZATION OF LESIONS IN THE NERVOUS SYSTEM, 65
  Cranio-cerebral topography, 93-98
  in base of brain, 91
  in cerebellum, 90
  in encephalic mass, 81-93
  in medulla oblongata, 79, 80
  in peripheral nervous system, 65-69
  in spinal cord, 69-79

Localization of abscess of the brain, 795, 800
  of cerebral hemorrhage and embolism, 969
  of thrombosis of cerebral veins and sinuses, 988
  of tumors of the brain, 1056
      of the spine, 1100

Lock-spasm of writers' cramp, 517

Locomotion, influence of special paralyses of, in infantile spinal
        paralysis, 1150

Locomotor ataxia, 826
    hysterical, 240

Lordosis in atrophic infantile paralysis, 1131

Lumbo-abdominal neuralgia, 1235

Lungs, disorders of, in chronic alcoholism, 608
    in the opium habit, 658

Lupulin, use of, in the opium habit, 676


M.

Magnesium sulphate, use of, in chronic lead-poisoning, 691

Main en griffe in chronic spinal pachymeningitis, 749

Malaria as a cause of cerebral anæmia, 790
  influence of, on the causation of chorea, 444

Malarial epilepsy, 472
  neuralgias, 1212

Male sex, prevalence of hysteria in, 215

Malnutrition of brain in infants, 778

Malt liquors, characters of intoxication from, 591

Mammillary neuralgia, 1235

Mania, 161
  chronic, 163
  following epilepsy, 482
  in alcoholism, 631

Maniacal excitement in general paralysis of the insane, 192
  form of acute alcoholism, 592
    of general paralysis of the insane, 188

Marriage, influence on recovery from epilepsy, 498
  question of, in the insane temperament, 115, 141

Massage, use of, in hemiplegia, 978
    in hysteria, 280
    in infantile spinal paralysis, 1157
    in lead palsy, 691
    in melancholia, 160
    in neuralgia, 1223
    in neurasthenia, 360, 361
    in progressive unilateral facial atrophy, 702
    in symmetrical gangrene, 1261
    in vaso-motor neuroses, 1255
    in writers' cramp, 536

Mastoid cells, inflammation of, as a cause of thrombosis of cerebral
        veins and sinuses, 983

Masturbation, influence on causation of cerebral anæmia, 778
      of epilepsy, 474
      of insanity, 119
  in the insane, treatment of, 137
  of hysteria, treatment of, 276

Mechanical appliances, use of, in infantile spinal paralysis, 1159
      in writers' cramp, 540
  restraint in treatment of the insane, 135, 136

Medulla oblongata, degeneration of, in labio-glosso-laryngeal
          paralysis, 1172
    localization of lesions in, 79

Medullary centres of the vaso-motor system, 1250

Megalopsia in nervous diseases, 40

Melancholia, 155
  agitata, 158
  cerebral nutrition in, 775
  in alcoholism, 631
  in children, 158
  in general paralysis of the insane, 188

Membranes, spinal, congestion of, 746

Memory, loss of, significance of, in nervous diseases, 28-30

Ménière's disease, 422

Meningeal cerebral hemorrhage, 710
  Diagnosis, 714
  Etiology, 711
  Pathological anatomy, 713
  Prognosis, 715
  Symptoms, 712
  Synonyms, 710
  Treatment, 715

Meningeal spinal hemorrhage, 754

Meningitis, acute, 716
    and chronic, following thermic fever, 399
    spinal, 749
  chronic spinal, 752

MENINGITIS, TUBERCULAR, 723
  Definition, synonyms, and history, 723
  Diagnosis, 732
    from acute simple meningitis, 733
    from eclampsia, 734
    from gastro-intestinal affections, 734
    from hydrencephaloid disease, 734
    from typhoid fever, 733
  Etiology, 724
    Age and sex, influence of, 725
    Exciting causes, 725
    Hereditary tendency to tuberculosis and scrofulosis, 724
    Season, influence of, 725
  Pathological anatomy and duration, 729
  Prophylaxis, 736
  Prognosis, 735
  Symptoms, 725
    Abdomen, state of, 726
    Cerebral, 726-729
    Constipation, 725-727, 729
    Cry, 726, 727
    Decubitus, 727
    Eyes, state of, 726-729
    Headache, 725-727
      in the adult, 737-739
    Paralysis and convulsions, 727, 728
    Prodromal, 725
    Pulse, respiration, and temperature, 726-728
    Pupils, state of, 726-729
    Sensitiveness to light, 725-727
    Strabismus, 727
    Stupor, 726-729
    Tongue, state of, 726, 729
    Vomiting, 725, 729
  Treatment, 735
    Bromides, chloral, and hyoscyamus, 736
    Counter-irritation, value of, 736
    Diet in, 736
    Iodide of potassium, use, 736

Menorrhagia and amenorrhœa in the insane, treatment of, 136

Menstrual disorders, influence on causation of hysteria, 220
    in the opium habit, 656, 658
  insanity, 173

Menstruation, influence on recovery from epilepsy, 498
    on causation of cerebral hyperæmia, 766
      of spinal hyperæmia, 802
  painful, influence on causation of hystero-epilepsy, 293

Mental condition in acute spinal meningitis, 750
    in atrophy of the brain, 994, 996
    in chorea, 445
    in chronic hydrocephalus, 742, 743
    in delirium tremens, 628
    in disseminated spinal sclerosis, 877
    in hemiplegia, 956
    in hysteria, 230
    in tabes dorsalis, 836
    in tumors of the brain, 1037
      of the spine, 1096
  Defects and degeneration, states of, 138
  Deterioration, primary, 70

MENTAL DISEASES, 99
  _Insanity_, 99
    Causation, 113
      Age, influence of, 116, 117
      Alcohol and nerve-stimulants, abuse of, 116, 119
      Drugs, abuse of, 119
      Emotions and mental strain, 117, 118
    Classification of, 105, 109
    Definition of, 99-105
    Diagnosis of, 123-125
    Exciting causes, 118-120
      Heredity, 113
      Ill-health, disease, etc., 116, 117, 119
      Intermarriage, 115, 116
      Occupation, 118
      Pulmonary consumption, relation to, 119
      Sex, 118
      Social position, 117, 118
      Vicious early training, 116
    History, 109
    Morbid anatomy and pathology, 121-123
    Prevalence, 110-113
    Prognosis, 125
      Mortality, 126
      Percentage of recoveries, 126
    Treatment, 127
      Asylums, methods of commitment to, 134
        objection to, 127, 130
        question of removal to, 127-135
      Galvanism, use, 137
      Home, removal from, question of, 128, 133, 135
      Home, 131
      Mechanical restraint in, 135, 136
      Medicines, value of, in, 135
      of cerebral hyperæmia in, 136
      of constipation in, 137
      of insomnia in, 137
      of intercurrent diseases in, 136
      of masturbation in, 137
      of menorrhagia and amenorrhœa in, 136
      Preventive, 137, 138
      Rest and sleep, value of, in, 137
      Sedatives and narcotics, use in, 133, 137
  _Insanity complicating_, 174
  _Insanity from Specific Poisons_, 175
  _Organic_, 176
    General paralysis of the insane, 176
      Definition, 176
      Diagnosis, 197
      Etiology, 177
        Age and sex, 177
        Excesses, influence of, 177
        Heredity, 177
        Mental shock, 178
        Syphilis, 178
      History, 176
      Morbid anatomy and pathology, 196
      Prognosis, 200
      Symptoms, 178
        Delusions, characters, 187, 188, 190-192
        Mental, 179, 190-193
        Moral sense, perversion of, 190
        of demented and paralytic form, 187
        of hypochondriacal form, 188
        Onset, mode of, 178
        Physical symptoms, 193
          Ataxia, 188, 189, 193
          Bones, state, 196
          Gait, 194
          Handwriting, 183, 186, 193
          Hyperæsthesiæ, 194
          Knee-jerk, significance, 195
          Pupils, state, 195
          Remissions, 194
          Sexual functions in, 195
          Speech, alteration in, 194
          Urine in, 1195
        Prodromal, 178
        Temperature in, 179
        with melancholia, 188
        with mania, 188
      Synonyms, 176
      Treatment, 201
        Cod-liver oil, use, 201
        Ergot, use, 201
        Hypophosphites, use, 201
        Potassium bromide and iodide, use, 201
        Rest and quiet, value, 201
    Insanity, chronic alcoholic, 202
      from gross lesions of brain, 202
      secondary delusional, 203
    Terminal dementia, 203
      Treatment, 203, 204
  _States of Mental Defect and Degeneration_, 138
    Circular insanity, 151
      Constitutional affective mental disease, 142
      Prognosis, 142
      Treatment, 143
    Epileptic insanity, 149
    Hypochondriacal insanity, 150
    Hysterical insanity, 148, 149
    Idiocy, 138
      Classification, 139
    Impulsive insanity, or instinctive monomania, 146
      Dipsomania, 147
      Erotomania, 147
      Homicidal insanity, 147
      Nymphomania and satyriasis, 147
      Pyromania and kleptomania, 147
        Treatment, 148
      Suicidal insanity, 146
    Insane temperament, 140
      Treatment, 141
    Moral insanity, 143
      Symptoms, 143-146
      Treatment, 146
    Periodic insanity, 150
    Primary insanity, 151
      Prognosis and treatment, 152
  _Psycho-neuroses_, 153
    Affective mental disease, 153
      Prognosis and treatment, 154
    Climacteric insanity, 173
    Delirium, acute, 163
    Dementia, primary, 164
      secondary, 165
        Treatment, 165
    Doubting insanity, 170
    Hebephrenia, 171
      Treatment, 172
    Hypochondriasis, 154
      Prognosis and treatment, 155
    Insanity of childhood, 171
    Katatonia, 166
    Mania, 161
      acute, 161
        Treatment, 161
      simple, 162
        Treatment, 162
    Melancholia, 155
      Agitata, 158
        Duration and prognosis, 159
      in children, 158
      simple, 155
      Treatment, 159
        Asylums, removal to, 159
        Narcotics and sedatives, use, 160
        Tonics, use, 160
      with delusions, 156
      with stupor, 158
    Menstrual insanity, 173
    Primary confusional insanity, 167
    Primary delusional insanity, 167
    Primary mental deterioration or brain atrophy, 170
    Puerperal insanity, 173
    Senile dementia, 174
      insanity, 173
    Transitory insanity, 164

Mental emotion, influence on causation of neurasthenia, 354
  influences as a cause of cerebral anæmia, 780
  shocks, influence on causation of general paralysis of the insane,
        178
  strain, influence on causation of insanity, 118
  symptoms of external pachymeningitis, 705
    of general paralysis of the insane, 190

Mercurial tremor, 429

Mercury, use of, in cerebral hyperæmia, 1016
    in chronic spinal meningitis, 754
    in hæmatoma of the dura mater, 710
    in spinal sclerosis, 900
    in tetanus, 555
    in tubercular meningitis, 736

Metallic salts, use, in catalepsy, 338
      in labio-glosso-laryngeal paralysis, 1175
      in progressive unilateral facial atrophy, 702

Metallo-therapy, use, in hysteria, 284
    in hystero-epilepsy, 313

Metastasis as a cause of cerebral abscess, 796

Microcephalism, 138

Migraine, 406, 1216, 1230
  Diagnosis and prognosis, 410
  Etiology, 406
    Age and sex, influence of, 406
    Heredity, influence of, 407
  Pathology and morbid anatomy, 410-413
  Symptoms, 407
    Circulation, disorders of, 409
    Digestive, 409
    Pain, seat and character, 408
    Paroxysms, characters of, 408, 409
  Synonyms, 406
  Treatment, 413
    Bromides, use, 414, 415
    Caffeine and guarana, use, 414
    Cannabis indica, use, 413, 415
    Climate, change of, 413
    Ergot, use, 413, 414
    Galvanism, use, 414, 415
    in childhood, 415
    Indications for, 413
    Morphia, use, 415
    Muriate of ammonium and chloral, use, 415
    Nitrite of amyl and nitro-glycerin, 414
    Quinia, use, 414

Miliary aneurisms, relation of, to cerebral form of encephalitis, 792
        hemorrhage, 921-923
  tubercles in tubercular meningitis, seat and character, 730, 732

Mimicry in hysteria, 251, 255, 270-272

Mind-cure in hysteria, 277

Miryachit, the, hysterical nature of, 228

Mitchell's rest-cure in hysteria, 279
    in neurasthenia, 358-362

Monoplegia, hysterical, 238
  in nervous diseases, 44

Monospasm in nervous diseases, 46

Moral insanity, 143
  management of spinal sclerosis, 906
  sense, deterioration of, in chronic alcoholism, 624
  treatment of hysteria, 276

Morbid anatomy of abscess of the brain, 792
    of acute simple meningitis, 719
    of acute spinal meningitis, 750
    of acute spinal myelitis, 812
    of amyotrophic lateral sclerosis, 867
    of cerebral anæmia, 781
    of cerebral hemorrhage, 919-927
    of cerebral hyperæmia, 767
    of cerebral meningeal hemorrhage, 713
    of chorea, 450
    of chronic spinal meningitis, 762
    of chronic spinal pachymeningitis, 748
    of congestion of cerebral pia mater, 716
    of congestion of spinal membranes, 747
    of delusional insanity, 169
    of diffuse sclerosis, 886
    of disseminated sclerosis, 874, 880-883
    of external pachymeningitis, 705
    of family form of tabes dorsalis, 872
    of infantile spinal paralysis, 1132
    of insanity, 121
    of internal pachymeningitis, 706
    of neuritis, 1190
    of paralysis agitans, 433
    of secondary scleroses, 893
    of spastic spinal paralysis, 865
    of spina bifida, 759
    of spinal meningeal hemorrhage, 755
    of tabes dorsalis, 840
    of tetanus, 549
    of tubercular meningitis, 729

Morbid anatomy and pathology of chronic lead-poisoning, 689
      of epilepsy, 488
      of writers' cramp, 526

Morbid somnolence, 344

Morphia, use, in acute simple meningitis, 721
    in cerebral anæmia, 788
    in hysteria, 276
    in migraine, 415
    in multiple neuritis, 1198
    in neuritis, 1194
    in spinal sclerosis, 905
    in thermic fever, 398, 399
    in the treatment of the opium habit, 673, 675
    in tumors of the brain, 1068
    in vertigo, 427

Morphœa, in progressive unilateral facial atrophy, 695

Morphine habit, 647

Mortality of chorea, 454
  of insanity, 125, 126
  of tetanus, 553

Motility, disturbances of, in spinal syphilis, 1025

Motion, disorders of, in chorea, 445, 446
    in chronic alcoholism, 620
    in diffuse spinal sclerosis, 888

Motor paralysis in unilateral paralysis of spinal cord, 1166

Motor symptoms of thermic fever, 391
  weakness, in spinal hyperæmia, 803

Motory symptoms of nervous diseases, 42

Multiple and multiple degenerative neuritis, 1195
  Diagnosis, 1197
  Etiology, 1197
  Nature and history, 1195
  Pathology, 1196
  Prognosis, 1198
  Symptoms, 1195
    Onset, 1195
    Pain, characters, 1195
    Paresis and atrophy of muscles, 1196
    Sensation, disturbances of, 1195
  Treatment, 1198
    Electricity, 1198
    Morphia, 1198
    Salicylate of sodium and iodide of potassium, 1198
    Rest, 1198

Multiple cerebro-spinal sclerosis, 873

Muscles, atrophy of, 1267
  changes in, in alcoholism, 614
    in injuries to peripheral nerves, 1182
  degeneration of, in labio-glosso-laryngeal paralysis, 1173
  employed in telegraphy, 508, 509
    in writing, 505, 506
  involved in infantile spinal paralysis, 1121
  rigidity of, in paralysis agitans, 435

Muscular ataxia, in general paralysis of the insane, 188, 189, 193
  atrophy in chronic spinal pachymeningitis, 749
    in nervous diseases, 54
    in poisoning by lead, 687, 688
    in progressive unilateral facial atrophy, 696, 697
    progressive, complicated with infantile spinal paralysis, 1149
  contraction, in acute spinal meningitis, 750
  system, state of, in the chloral habit, 662
  rigidity in diffuse spinal sclerosis, 888

Music, use of, in treatment of catalepsy, 338

Musk, use of, in hysteria, 274

Murmurs, valvular, in chorea, 448

Myelitis, simple acute, 810
  Ascending and descending, 816
  Clinical history, 816
  Diagnosis, 820
  Influence of poisons on cord, 815
  Limitation of inflammatory process, 816
  Myelitic cicatrices, 815
  Morbid anatomy, 812
  Prognosis and duration, 821
  Treatment, 822
    Derivation and bloodletting, 823
    Electricity, 824
    Management of bed-sores, 823
    Management of bladder troubles, 824
    Position, 822
    Rest, 823
    Strychnia, 823
    Warm baths, 823

Myelitis, chronic, 886
  in unilateral spinal paralysis, 1168

Myxœdema, 1271


N.

Narcolepsy, 346

Narcotic poisoning, acute, from alcohol, 597

Narcotics, influence on causation of catalepsy, 319

Narcotics and sedatives, value, in melancholia, 160

Nature of stigmata, 350
  of symmetrical gangrene, 1261

Nausea and vomiting in lead colic, 684
    in the opium habit, 653, 657-659

Neglect, treatment of hysteria by, 277

Nerve-centres, syphilitic affections of, 999

Nerve-roots, degeneration of, in infantile spinal paralysis, 1138-1140
  lesions of, in tabes dorsalis, 840-842

Nerve-section in neuralgia, 1227
  in tetanus, 560

Nerve-stretching in athetosis, 460
  in neuralgia, 1228
  in spinal sclerosis, 903
  in writers' cramp, 538

Nerve-trunks, lesions, in multiple neuritis, 1196
    in neuritis, 1191

Nerves, inflammation of, 1189
  Anatomical changes in divided nerves and muscles, 1184
  Changes in, in chronic alcoholism, 619
  Diagnosis of, 1187
  Divided, pain, seat and characters of, 1185-1187
  Electrical reactions in, 1184, 1188
  Immediate results of injuries to, 1182
  Injuries and irritation of, as a cause of neuralgia, 1220
    treatment of, 1189
  Lesions of, in neuralgia, 1221
  Peripheral diseases of, 1177
    Changes in, in chronic alcoholism, 619
    Injuries of, 1182
  Regeneration and reunion of divided nerves and muscles, 1185
  Sensation, disorders of, 1186, 1187
  Skin, state of, 1183, 1187
  Symptoms of incomplete destruction of, 1185
  Trophic disorders, 1187
  Vaso-motor, origin of, 1246

Nervous diseases, general semeiology of, 19
  disorders of chronic hydrocephalus, 743
    of chronic lead-poisoning, 685-689
    of spina bifida, 759
    of the chloral habit, 663, 665
  symptoms of myxœdema, 1272
  system, disorders of, in alcoholism, 616
      in the opium habit, 656, 658, 659

NERVOUS SYSTEM, LOCALIZATION OF LESIONS IN THE, 65
      Cranio-cerebral topography, 93-98
      in encephalic mass, 81-93
      in systematic lesions, 89
      in focal lesions, 89
          in base of brain, 91
          in cerebellum, 90
      in medulla oblongata, 79, 80
      in peripheral nervous system, 65-69
      in spinal cord, 69-79
        of æsthesodic system, 69
        of kinesodic system, 71

NERVOUS SYSTEM, GENERAL SEMEIOLOGY OF DISEASES OF, 19
      Motory symptoms, 42-54
      Psychic symptoms, 19-31
      Sensory symptoms, 31-41
      Trophic symptoms, 54-59
    Principles of diagnosis in diseases of, 59
        in functional diseases of, 63
        in organic diseases of, 61

NEURALGIA, 1211
  Definition, general, of, 1211
  Diagnosis and pathology, general, of, 1221
  Etiology, general, of, 1216
    Age and sex, 1217
    Atmospheric and thermic influences, 1219
    Constitutional diseases, 1217
    Injuries and irritation of nerves, 1219
    Reflex and sympathetic causes, 1220
  Symptomatology, general, 1211
    of migraine, 1216-1230
    of superficial neuralgias, 1211
      Muscles, spasm and atrophy of, 1213, 1214
      Pain, characters and distribution, 1212
      Periodicity of attacks, 1212
      Points douloureux, 1213
      Secreting organs, disorders of, 1213
      Sensation, altered, 1214
      Skin, disorders of, 1212-1214
      Special senses in, 1213
      Urine, condition, 1212, 1213
      Vision, disorders of, 1213
    of visceral neuralgias, 1215
      Pain, characters, 1215
      Secretion of visceral organs, disorders of, 1215
  Treatment, general, 1222
    Aconite and aconitia, use, 1224, 1225, 1227
    Belladonna and atropia, use, 1224
    Change of climate, 1223
    Cocaine, use, 1227
    Counter-irritation, use, 1226
    Diet, 1223
    Electricity, use, 1225
    Hydropathy, 1226
    Hygiene, 1223
    Injection of water, chloroform, and other substances, 1229
    Iron, arsenic, and cod-liver oil, use, 1224
    Massage, 1223, 1229
    Neurectomy, 1227
    Nerve-stretching, 1228
    Opium, use, 1224
    Phosphorus and gelsemium, use, 1225
    Turpentine, oil of, use, 1229
    Use of ammonio-sulphate of copper, salicylate of sodium, tonka,
          caffeine, and sal ammoniac, 1229
  Varieties, migraine and periodical headache, 1230
    Etiology and clinical relations, 1231
      Age and sex, 1230, 1231
    Prognosis, 1231
    Symptoms, 1230
      Auras and visual hallucinations, 1230, 1231
      Sensation, disorders of, 1230, 1231
      Pain, 1230
    Treatment of, 1232
      Cannabis indica, iodide and bromide of potassium, and caffeine,
            1232
      Diet, 1232
      Electricity, 1232
      Nitrite of amyl, 1232

Neuralgias of the fifth nerve, 1232
  Anal and rectal neuralgia and uterine and ovarian neuralgia, 1240
  Angina pectoris, 1237
  Cervico-brachial and brachial neuralgia, 1234
  Epileptiform, or tic douloureux, 1233
  Facial neuralgia, ordinary, 1232
    Treatment, 1234
  Gastralgia, 1238
  Intercostal neuralgia, 1234
    Intermittent neuralgia of the supraorbital, 1233
  Lumbo-abdominal neuralgia, 1235
  Mammillary neuralgia (irritable breast of Astley Cooper), 1235
  Occipito and cervico-occipital neuralgias, 1234
  Sciatica, 1235
    Treatment, 1236
  Visceral neuralgia, 1237

Neuralgia complicating progressive unilateral facial atrophy, 699

Neuralgias in tumors of the brain, 1041

Neuralgic pains in hemiplegia, 956

NEURASTHENIA, definition, 353
  Etiology, 354
  Symptoms, 354
    Digestive disorders, 356
    Heart disorders, 356
    Muscular strength, loss of, 356
    of brain exhaustion, 355
    Sensation and special senses, disturbances of, 356, 357
    Sexual disorders, 357
    Vaso-motor disturbances, 356
  Treatment, 357
    Change of climate, 358
    Rest-cure, method of carrying out, 358, 362

Neurasthenia as a cause of vertigo, 425

Neurasthenic headache, 404

Neuritis, 1189
  Etiology, 1190
  Diagnosis, 1194
  Morbid anatomy, 1190
  Symptoms, 1191
    Motor, 1192
    Pain, characters, 1191, 1193
    Reflex paralyses, 1193
    Trophic, 1192, 1193
    Sensation, altered, 1191, 1192
  Treatment, 1194
    Counter-irritation in, 1194
    Galvanism, 1194
    Morphia in, 1194
    Salicylate of sodium and iodide of potassium, 1194

Neuritis as a result of neuralgia, 1214

Neuromata, 1208
  Definition, 1208
  Diagnosis, 1210
  Etiology, 1209
    Heredity and traumatism, 1209
  Nature, varieties, etc., 1208, 1209
  Symptoms, 1209
  Treatment, 1210
  in tumors of the brain, 1048

Neuromimesis, 251, 255, 270-272

Neuro-retinitis in tubercular meningitis, 729
    and optic neuritis in tumors of the brain, 1035

Neuroses, trophic, 1266
  vaso-motor, 1242

Nickel bromide, use, in epilepsy, 500

Night-terrors, 370

Nitro-glycerin, use, in catalepsy, 338
    in epilepsy, 500, 502
    in hystero-epilepsy, 311
    in migraine, 414
    in myxœdema, 1273
    in vaso-motor neuroses, 1256

Numbness and formication in nervous diseases, 33
  and tingling in hysteria, 256

Nutrition, bad, influence on causation of catalepsy, 319
  disturbances of, in chronic lead-poisoning, 682

Nymphomania, 147
  in hysteria, 235

Nystagmus in disseminated sclerosis, 877
  in family form of tabes dorsalis, 871


O.

Obesity in alcoholism, 615

Occipital neuralgia, 1234

Occupation, influence on causation of alcoholism, 575
      of chronic lead-poisoning, 681
      of hysteria, 218
      of the opium habit, 650

Ocular causes of vertigo, 424

Œdema as a complication of cerebral anæmia, 782
  in thrombosis of cerebral veins and sinuses, 986

Olfactory sensory disturbances in nervous diseases, 41

Onset of epileptic fit, mode of, 478
  of tetanus, mode of, 549

Opisthotonos in acute spinal meningitis, 750
  in hystero-epilepsy, 295, 296, 301
  in tetanus, 551
  in tetanus neonatorum, 564

Opium, abuse of, as a cause of tremor, 429, 430

OPIUM HABIT AND KINDRED AFFECTIONS, 647
  _Cannabis indica, Habitual Addiction to_, 667
    Treatment, 668, 677
  _Chloral Habit, the_, 660
    Diagnosis, 665
    Etiology and synonyms, 661
    Prognosis, 666
    Prophylaxis, 668-670
    Symptoms, 661
      Circulatory, digestive, and respiratory disorders, 661, 662
      Genito-urinary disorders, 662, 663
      Muscular system, disorders of, 662
      Nervous system, disorders of, 663, 664
      of abrupt discontinuance of drug, 665
      Psychical derangements, 664
      Skin, disorders of, 663
    Treatment, 668, 676
      Curative, 666, 667
  _Chloroform, Habitual Addiction to_, 667
    Treatment, 668, 677
  _Cocaine, Habitual Addiction to_, 667
    Treatment, 668, 677
  _Ether, Habitual Addiction to_, 667
    Treatment, 668, 677
  _Opium Habit, the_, 647
    Diagnosis, 659
    Etiology, 649
      Age, sex, occupation, and luxurious habits, influence on
            causation, 650
      Exciting causes, 652
      Insanity, influence on causation, 651
      Predisposing causes, 649
    History, 647
    Prognosis, 660
    Prophylaxis, 668-670
    Symptoms, 653
      Digestive, 653, 654, 658
      Genito-urinary disorders, 654, 658
      Nervous system, derangements of, 658, 659
      of chronic poisoning, 653
      of withdrawal of drug, 657-659
      Physiognomy in, 654
      Respiratory and circulatory disorders, 654
      Sexual disorders, 656, 658
      Temperature in, 657
    Synonyms, 648
    Treatment, 668
      Abrupt withdrawal of drug, Levinstein's method, 672-674
      Alcohol and stimulants, use of, 673-675
      Baths, use, 674-676
      Bromides, chloral, lupulin, and paraldehyde, use of, 673, 674,
            676
      Coca, cocaine, and cannabis indica, use of, 676
      Curative, 670
      Diet in, 673, 675
      Gradual diminution of drug, 674-676
      of digestive disorders, 672-674
      of nervous symptoms and insomnia, 673, 675, 676
      Opium, use of, 673, in, 675
      Removal from home, question of, 670, 671
  _Paraldehyde, Habitual Addiction to_, 666
    Treatment, 668, 677

Opium, use of, in hysteria, 278
    in insomnia, 380-382
    in lead colic, 691
    in melancholia, 160
    in neuralgia, 1224
    in spinal concussion, 916
    in symmetrical gangrene, 1262
    in tetanus, 577
    in the treatment of the morphia habit, 673, 675
    in tubercular meningitis, 736
  physiological action of, 652

Ophthalmoscopic appearances in cerebral anæmia, 787
    in cerebral hyperæmia, 770
  examination in tumors of the brain, 1035

Optic nerve, atrophy of, in disseminated sclerosis, 879
      in tabes dorsalis, 834

Optic sensory disturbances in nervous diseases, 39, 40

Oöphorectomy, question of, in hysteria, 287
    in hystero-epilepsy, 312

Organic headache, 403
  Mental diseases, 176
  Nervous diseases, diagnosis of, 61-63

Osmic acid, hypodermic use, in neuralgia, 1229

Osteomata in tumors of the brain, 1049

Osteo-myelitis, as a cause of cerebral abscess, 799

Ovarian neuralgia, 1240
  pressure, effect of, in hystero-epilepsy, 298, 299

Over-exertion as a cause of disseminated sclerosis, 884
      of spinal hyperæmia, 802

Over-study, influence on causation of chorea, 441

Over-work, influence on causation of cerebral hyperæmia, 354
      of neurasthenia, 354

Oxygen, inhalations in vaso-motor neuroses, 1256


P.

Pacchionian bodies, seat and nature, in brain tumors, 1050

Pachymeningitis, 703
  Acute spinal, 747
  Chronic spinal, 748
  External, 704
  Hemorrhagic, 707
  Internal, 706

Pain, in angina pectoris, 1237, 1238
  in cerebral syphilis, 1005
  in diffuse spinal sclerosis, 889
  in disseminated sclerosis, 874
  in family form of tabes dorsalis, 871
  in gastralgia, 1238, 1239
  in hysteria, 250
  in injuries of peripheral nerves, 1185-1187
  in intercostal neuralgia, 1234
  in lead colic, 683
  in hyperæmia of the brain, 770
  in migraine, seat, characters, and origin of, 408, 412, 1230
  in multiple neuritis, 1195
  in nervous diseases, varieties of, 33-35
  in neuritis, 1191
  in neuromata, 1210
  in sciatica, 1235
  in spinal syphilis, 1025
  in superficial neuralgia, 1212
  in symmetrical gangrene, 1258-1260
  in writers' cramp, 519
  Influence on causation of the opium habit, 649
  Seat and character, in acute spinal meningitis, 750
        spinal pachymeningitis, 747
      in chronic spinal meningitis, 753
        spinal pachymeningitis, 749
      in external pachymeningitis, 705
      in spinal meningeal hemorrhage, 754
      in tabes dorsalis, 828
      in tubercular meningitis, 725, 726
      in tumors of the brain, 1033, 1034
      in tumors of the spinal cord, 1091-1093

Pain-sense in tabes dorsalis, 833

Painters' colic, 683

Palsy, lead, 685

Pancreas, changes in, in chronic alcoholism, 602

Paracentesis in chronic hydrocephalus, 745
  of the sac in spina bifida, 761

Paræsthesia, hysterical, 250
  in migraine, 1230, 1231
  in nervous diseases, general, 33
  in progressive unilateral facial atrophy, 696
  in spinal syphilis, 1025
  in spinal hyperæmia, 802

Paralalia, 571

Paraldehyde, habitual addiction to, 666
  use, in alcoholism, 641, 642, 645, 646
    in the opium habit, 674, 676

PARALYSIS AGITANS, 433
    Diagnosis, 438
    Etiology and morbid anatomy, 437
    Symptoms, 434
    Synonyms, 433
    Treatment, 438

Paralysis, alcoholic, 621
  atrophic, of infants, 1113
  cerebral, 917
  festinans, 436
  hysterical, 237
  in acute myelitis, 816, 817
  in acute spinal meningitis, 750
  in atrophy of the brain, 994
  in cerebral hemorrhage, 939, 954
    meningeal hemorrhage, 712
    syphilis, 1007-1010
  in chorea, 447
  in chronic hydrocephalus, 743
    spinal pachymeningitis, 749
  in encephalitis, 791
  in hæmatoma of the dura mater, 708
  in infantile spinal paralysis, 1118, 1123
  in nervous diseases, definition of, 42-44
  in spina bifida, 759
  in the chloral habit, 664
  in tubercular meningitis, 727
  in thrombosis of cerebral veins and sinuses, 986
  in tumors of the brain, 1040
    of the spinal cord, 1091, 1093
  Labio-glosso-laryngeal, 1169
  Localized, in nervous diseases, 44
  of chronic lead-poisoning, 685
  of the insane, general, 176
  Spinal spastic, 861
  Spinal unilateral, 1165
  Stage of, in writers' cramp, 518

Paraplegia, hysterical, 238
  in acute myelitis, 817
  in nervous diseases, 43
  in tumors of spinal cord, 1093

Paraplegic spasm in nervous diseases, 46

Paresis in general paralysis of the insane, 189
  and paralysis in multiple neuritis, 1196

Paretic dementia of alcoholism, 633

Paroxysms of epilepsy, characters of, 478
  of hystero-epilepsy, characters, 293, 304, 306
  of vertigo, characters, 417

Patellar reflex, alterations of, in acute myelitis, 818
    in amyotrophic lateral sclerosis, 868
    in chorea, 448
    in diffuse sclerosis, 888
    in disseminated (cerebro-spinal) sclerosis, 875
    in epilepsy, 481
    in general paralysis of the insane, 195
    in hemiplegia, 962
    in spastic spinal paralysis, 862
    in spinal syphilis, 1025
    in tabes dorsalis, 829, 835, 857, 858
    in tumors of the spinal cord, 1092
    significance in diagnosis of hysteria, 265, 266
  tendon reflex in nervous diseases, 52

Pathogenesis of vaso-motor neuroses, 1251
  of infantile spinal paralysis, 1114

Pathological action of alcohol, 586
  anatomy of acute alcoholism, 595

Pathology of athetosis, 460
  of brain syphilis, 1014
  of diseases of cervical sympathetic, 1263
  of catalepsy, 334
  of chorea, 450
  of chronic hydrocephalus, 744
    lead-poisoning, 689
  of hysteria, 208
  of hystero-epilepsy, 291
  of insanity, 121
  of neuralgia, 1221
  of progressive unilateral facial atrophy, 699
  of tremor, 431
  of tubercular meningitis, 729
  of tumors of brain, 1046
    of spinal cord, 1096
  and morbid anatomy of atrophy of the brain, 995
      of general paralysis of the insane, 196
      of hæmatoma of the dura mater, 708
      of hypertrophy of the brain, 996
      of labio-glosso-laryngeal paralysis, 1172
      of migraine, 410
      of multiple neuritis, 1196
      of spina bifida, 759
      of unilateral spinal paralysis, 1167

Perforating ulcer of the foot, 1273

Periodic insanity, 150

Periodicity of attacks of migraine, 407
  of neuralgias, 1212

Peripheral causes of epilepsy, 475
  nerves, diseases of, 1176
    injuries of, 1182
  nervous system, localization of lesions in, 65

Pernicious anæmia, cerebral symptoms in, 779

Petit mal, symptoms of, 477

Phantom tumors, in hysteria, 288

Phosphorus, use, in neuralgia, 1225
    in paralysis agitans, 438
    in sequelæ of intracranial hemorrhage, 978

Photophobia in cerebral hyperæmia, 772

Phthisis, influence of alcoholism on production of, 609
      of neuralgia, 1218
  relation of, to hysteria, 214
    to mental diseases, 119, 142

Physicians, responsibility of, in the formation of the opium habit,
        649, 668

Physiognomy of acute alcoholism, 588
  of acute simple meningitis, 717, 718
  of delirium tremens, 628
  of labio-glosso-laryngeal paralysis, 1170
  of the opium habit, 654
  of tubercular meningitis, 725-727

Physiological action of alcohol, 580

Physiology of dreams, 370
  of spastic spinal paralysis, 865
  of speech, 567
  of tabes dorsalis, 840
  of the vaso-motor neuroses, 1242

Pia mater, cerebral, chronic inflammation of (chronic cerebral
        meningitis), 721
  Congestion of, 715
    Symptoms, morbid anatomy, and treatment, 716
  Inflammation of (acute leptomeningitis), 716
    Diagnosis and pathological anatomy, 719
    Duration and course, 718
    Etiology and synonyms, 716
    Prognosis, 720
    Symptoms, 717
    Treatment, 720
      Bleeding in, 720
      Counter-irritation, use, 721
      Diet in, 721
      Morphia, chloral, bromides, etc., use in, 721
      Quinia, use in, 721

Pigment-scales and flakes, as a cause of capillary embolism, 988

Pilocarpine, use, in myxœdema, 1273

Piscidia, use, in alcoholism, 645

Pleuræ, disorders of, in chronic alcoholism, 610

Pneumonia, in alcoholism, 609

Points douloureux, in neuralgia, 1213

Poisoning of blood, influence on causation of infantile paralysis,
        1151

Polyneuritis, 1195

Polyuria in cerebral syphilis, 1009
  in hemiplegia, 961
  in tumors of the brain, 1044

Porencephaly, 777

Position, influence of, in cerebral anæmia, 780

Post-epileptic aphasia, 481

Post-febrile insanity in cerebral anæmia, 786

Post-mortem examination, methods of, in tumors of the brain, 1050

Post-paralytic chorea, 447

Posterior columns, lesions of, in tabes dorsalis, 840-847

Posterior spinal sclerosis, 826

Pregnancy, influence, on causation of chorea, 444
    on recovery from epilepsy, 498
  Simulation of, in hysteria, 254

Pregnant women, occurrence of hysteria among, 221

Preputial irritation as a cause of epilepsy, 473

Prevalence of insanity, 110

Prevention of insanity, 137
  of intracranial hemorrhage, and apoplexy, 974
  of tetanus neonatorum, 565

Priapism in tumors of spinal cord, 1096

Prodromal symptoms of acute simple meningitis, 717
    of tubercular meningitis, 725

Prodromata of acute myelitis, 821
  of disseminated sclerosis, 874
  of epilepsy, 475
  of general paralysis of the insane, 178
  of infantile spinal paralysis, 1115
  of intracranial hemorrhage and apoplexy, 944-946

Prognosis of acute simple meningitis, 720
    spinal meningitis, 751
    spinal pachymeningitis, 748
  of alcoholism, 639
  of amyotrophic lateral sclerosis, 869
  of apoplexy, cerebral hemorrhage, etc., 972
  of athetosis, 460
  of catalepsy, 337
  of cerebral abscess, 799
  of cerebral meningeal hemorrhage, 715
    syphilis, 1013
  of chorea, 453
  of chronic hydrocephalus, 744
    lead-poisoning, 684, 687, 689
    spinal meningitis, 753
  of constitutional affective mental disease, 142
  of diffuse spinal sclerosis, 890
  of ecstasy, 343
  of epilepsy, 496
  of external pachymeningitis, 706
  of general paralysis of the insane, 200
  of hæmatoma of the dura mater, 709
  of hypertrophy of the brain, 799
  of hysteria, 272
  of hysterical insanity, 149
  of hystero-epilepsy, 310
  of hypochondriasis, 155
  of infantile spinal paralysis, 1150
  of insanity, 125
  of labio-glosso-laryngeal paralysis, 1169
  of melancholia, 159
  of migraine, 410, 1231
  of multiple neuritis, 1198
  of peripheral anæsthesia, 1201
  of primary delusional insanity, 152
  of progressive unilateral facial atrophy, 702
  of spina bifida, 761
  of spinal concussion, 916
  of spinal meningeal hemorrhage, 755
  of symmetrical gangrene, 1262
  of tetanus, 553
  of tetanus neonatorum, 565
  of the chloral habit, 666
  of the opium habit, 660
  of thrombosis of cerebral veins and sinuses, 988
  of torticollis, 464
  of tremor, 431
  of tubercular meningitis, 735
  of tumors of the brain, 1066
    of the spine, 1106
  of unilateral spinal paralysis, 1168
  of vaso-motor neuroses, 1255
  of vertigo, 418
  of writers' cramp, 530

Progressive muscular atrophy in chronic lead-poisoning, 688

PROGRESSIVE UNILATERAL FACIAL ATROPHY, 693
  Definition, synonyms, and history, 693
  Diagnosis, 700
  Duration, termination, and complications, 699
  Etiology, 693
  Symptoms, 694
    Atrophy, seat and characters, 696, 697
    Perspiration, modifications of, 696
    Pulsation of carotids, weakness of, 696
    Sensation, modifications of, 696
    Skin and hair, changes in, 695
    Special senses, state of, 697
    Temperature of affected parts, 696
  Treatment and prognosis, 702

Prophylaxis of abscess of the brain, 801
  of alcoholism, 640, 642
  of cerebral hemorrhage and apoplexy, 974
  of chronic lead-poisoning, 690
  of hysteria, 274
  of the chloral habit, 668
  of the opium habit, 668
  of thermic fever, 396
  of thrombosis of cerebral veins and sinuses, 988
  of tubercular meningitis, 735
  of writers' cramp, 530

Propulsion in paralysis agitans, 436

Psammomata in tumors of the brain, 1049

Pseudo-paralysis in nervous diseases, 44

Psychic causes of epilepsy, 472
  symptoms of nervous diseases, 19

Psychical derangements of chronic alcoholism, 264
    of the chloral habit, 664
  symptoms of syphilis of the brain-cortex, 1017 _et seq._

Psycho-neuroses (see _Mental Diseases_, 153).

Ptosis, hysterical, 238
  in tabes dorsalis, 830

Puberty, influence on causation of catalepsy, 318
      of migraine, 407, 411
  influence on cerebral anæmia, 778

Puerperal insanity, 173
  tetanus, 562

Pulmonary consumption, relation to mental diseases, 119, 142

Pulsation of carotids, weakness of, in progressive unilateral facial
        atrophy, 696

Pulse, state of, in acute alcoholism, 587, 588, 593
    in acute simple meningitis, 717, 718
    in acute spinal meningitis, 750
    in catalepsy, 321
    in cerebral anæmia, 784
    in cerebral hemorrhage and apoplexy, 938
    in chorea, 449
    in concussion of the brain, 909
    in epilepsy, 480
    in hæmatoma of the dura mater, 708
    in hysteria, 252
    in migraine, 409, 411, 412
    in tetanus, 551
    in the chloral habit, 662
    in the opium habit, 654, 657, 659
    in thermic fever, 391
    in tubercular meningitis, 726-728
  and respiration in delirium tremens, 629

Pupils, dilatation of, in migraine, cause of, 411
  hysterical dilatation of, 248
    in acute simple meningitis, 717
    in cerebral anæmia, 775
    in chronic hydrocephalus, 741
    in concussion of the brain, 909
    in diseases of the cervical sympathetic, 1264
    in disseminated sclerosis, 879
    in epileptic fit, 480
    in general paralysis of the insane, 195
    in tabes dorsalis, 829, 830
    in tubercular meningitis, 727, 729
  loss of reflex of, in nervous diseases, 40, 51

Pus, characters of, in abscess of the brain, 793

Pyramidal tract, derangements of, in amyotrophic lateral sclerosis,
        867

Pyromania, 147


Q.

Quinia, use of, in acute simple meningitis, 721
    in alcoholism, 642, 643, 645, 646
    in chronic lead-poisoning, 691
    in intermittent neuralgia of supraorbital, 1233
    in labio-glosso-laryngeal paralysis, 1175
    in migraine, 414
    in neuralgia, 1224
    in paralysis agitans, 438
    in sciatica, 1236
    in spinal meningeal hemorrhage, 756
    in thermic fever, 398
    in vertigo, 427


R.

Race, influence on causation of chorea, 444
      of hysteria, 217
      of hystero-epilepsy, 291
      of thermic fever, 389

Railway sickness, 426

Rectum, hysterical disorders of, 240

Reflex causes of epilepsy, 472
    of neuralgia, 1220
  irritability, changes in, in catalepsy, 321
  irritation as a cause of catalepsy, 318
      of chorea, 444
  movements, abnormal, in nervous diseases, 50
  of patellar tendon in nervous diseases, 52
  paralyses in spinal anæmia, 806
  paralysis in neuritis, 1193

Reflexes, active, in spinal hyperæmia, 802
  exaggerated, in spinal syphilis, 1026
  in acute spinal myelitis, 818
  in amyotrophic lateral spinal sclerosis, 868
  in chorea, 448
  in combined forms of sclerosis, 870
  in diffuse sclerosis, 888
  in disseminated sclerosis, 875, 877
  in hemiplegia, 962
  in spastic spinal paralysis, 862
  in tabes dorsalis, 835
  in tumors of the brain, 1041
    of the spinal cord, 1092, 1094
  tendinous in epilepsy, 481
  vaso-motor, 1248

Religious feeling, extreme, as a cause of ecstasy, 34

Remissions in general paralysis of the insane, 194
  in tubercular meningitis, 727

Respiration, artificial, in cerebral hemorrhage, 976
  in acute spinal meningitis, 750
  in anæmia of the brain, 777
  in catalepsy, 321
  in cerebral hemorrhage and apoplexy, 935
  in concussion of the brain, 909
  in labio-glosso-laryngeal paralysis, 1171
  in the chloral habit, 662
  in thermic fever, 390, 391, 395
  in tubercular meningitis, 728
  in tumors of the brain, 1044

Rest, value of, in apoplexy, 975
    in concussion of the brain, 911
    in hyperæmia of the spine, 804
    in melancholia, 160
    in myelitis, acute, 823
    in neuritis, 1194
    in symmetrical gangrene, 1261
    in writers' cramp, 533
    in vaso-motor neuroses, 1255
  and quiet, value in general paralysis of the insane, 201

Rest-cure, value of, in hysteria, 279
    in migraine, 413
    in neurasthenia, 358, 362

Retropulsion in paralysis agitans, 436

Reynaud's disease, 1257

Rheumatic headache, 403

Rheumatism, influence on causation of chorea, 442, 452
      of meningitis, acute, 716

Rigidity in hemiplegia of intracranial hemorrhage and apoplexy, 962

Rigors in acute simple meningitis, 717
    spinal meningitis, 750

Romberg symptoms of tabes dorsalis, 830


S.

Salaam convulsions, 463

Salicylate of sodium, use, in acute simple meningitis, 721
      in neuralgia, 1229
      in neuritis and multiple neuritis, 1194, 1198

Sarcomatous tumors of the brain, 1048

Satyriasis, 147

Scarlatina, influence on causation of chorea, 443

Schistorachis, 757

Sciatica, 1235 (see _Neuralgia_).

Scleroses, secondary, of spinal cord, 892

Sclerosis of crossed pyramidal tracts as a cause of spastic spinal
        paralysis, 865
  Amyotrophic lateral spinal, 867
    Definition, 867
    Duration, 868
    Morbid anatomy, 867
    Prognosis, 869
    Symptoms, 868
  Combined forms of spinal, 869
  Diffuse, 886
    Morbid anatomy, 886
    Prognosis, 890
    Symptomatology, 888
  Disseminated (cerebro-spinal), 873
    Diagnosis, 885
    Etiology, 883
    Morbid anatomy, 874, 880-883
    Symptoms, 874
  Posterior spinal, 826
  Treatment of, 898
    Climate, 903
    Cold baths, 903
    Cold douches, 903
    Ergot in early stages, 901
    Faradic wire brush, 904
    Galvanism, 901
    Hot Springs, 900
    Management of special symptoms and complications, 905
    Mercury, 900
    Mixed treatment, 899
    Moral treatment, 906
    Nerve-stretching, 903
    Nitrate of silver, 901
    Peripheral treatment, 902
    Static electricity, 906
    Tremors of sclerotic affections, 905

Sclerotic process in tabes dorsalis, 842-847
    in general paralysis of the insane, 197

Scrofulosis, influence on causation of chronic hydrocephalus, 741
      of tubercular meningitis, 724

Scoliosis in infantile spinal paralysis, 1131

Sea-bathing, use, in hysteria, 283

Sea-sickness, 426

Season, influence on causation of chronic lead-poisoning, 679
      of hyperæmia of the brain, 765
      of intracranial hemorrhage and apoplexy, 931
      of tubercular meningitis, 725

Secretions, altered, in diseases of cervical sympathetic, 1265
    in nervous diseases, 59

Sedatives and narcotics, use of, in insanity, 135, 136

Self-concentration, relation to trance and ecstasy, 347

Self-deception of hysterical patients, 233

Semeiology, general, of nervous diseases, 19

Senile dementia, 173
  insanity, 174

Sensation, disturbances of, in catalepsy, 321
    in chronic lead-poisoning, 686, 687
    in hemiplegia, 955
    in injuries to peripheral nerves, 1182, 1185, 1186
    in multiple neuritis, 1195
    in the chloral habit, 664
    in tumors of the brain, 1042
      of the spinal cord, 1091, 1092
  Modifications of, in acute myelitis, 817-819
      spinal meningitis, 750
        pachymeningitis, 747
    in cerebral atrophy and hypertrophy, 942
      syphilis, 1008
    in chronic spinal meningitis, 753
        pachymeningitis, 749
    in neuritis, 1191-1193
    in neuromata, 1210
    in progressive unilateral facial atrophy, 696
    in symmetrical gangrene, 1259
    in tabes dorsalis, 829, 832
  Perversion of, in delirium tremens, 628
    in diffuse spinal sclerosis, 889
    in spinal hyperæmia, 802
      meningeal hemorrhage, 752
      syphilis, 1025

Senses, special, disorders of, in alcoholism, 622
      in cerebral anæmia, 783
      in cerebral hemorrhage and apoplexy, 942
      in cerebral hypertrophy and atrophy, 995
      in nervous diseases, 39
      in neuralgia, 1213
      in neurasthenia, 356
      in progressive unilateral facial atrophy, 697
      in symmetrical gangrene, 1266

Sensibility, alterations of, topographical distribution in nervous
        diseases, 37-39
  Disorders of, in chronic alcoholism, 619
    in chorea, 448
  Loss of, in nervous diseases, 35-37

Sensorial affections of hysteria, 246
    of special senses, in nervous diseases, 39

Sensory disturbances in cerebral anæmia, 783
  epilepsy, 483, 486
  symptoms of nervous diseases, 31

Sequelæ of thermic fever, 399

Serous apoplexy, 783

Sex, influence on causation of acute spinal meningitis, 450
      of catalepsy, 318
      of cerebral anæmia, 778
        hyperemia, 765
      of chorea, 441
      of chronic lead-poisoning, 680, 686, 688
      of disseminated (cerebro-spinal) sclerosis, 883
      of ecstasy, 342
      of epilepsy, 470
      of family form of tabes dorsalis, 871
      of general paralysis of the insane, 177
      of hæmatoma of the dura mater, 707
      of hysteria, 215
      of hystero-epilepsy, 291
      of intracranial hemorrhage and apoplexy, 929
      of migraine, 406, 1231
      of myxœdema, 1271
      of neuralgia, 1217
      of paralysis agitans, 437
      of progressive unilateral facial atrophy, 694
      of simple acute meningitis, 716
      of tabes dorsalis, 852
      of tetanus, 544
      of the choral habit, 661
      of the opium habit, 650
      of tubercular meningitis, 725
      of tumors of the brain, 1029
        spinal cord, 1090
      of writers' cramp, 512

Sexual disorders, of chronic alcoholism, 614
    of hyperæmia of the brain, 778
    of neurasthenia, 357
    of the opium habit, 656, 658
    of tumors of the spinal cord, 1096
  excess, as a cause of spastic spinal paralysis, 864
      of spinal hyperæmia, 802
      of tabes dorsalis, 851, 852
      of vertigo, 420
  excitement, as a cause of ecstasy, 342
  function, in general paralysis of the insane, 195
    in tabes dorsalis, 834
  instincts, perverted, in insane temperament, 146, 148, 161
  irritation, as a cause of hysteria, 221
      of reflex paralysis, 807
  perversions, in general paralysis of the insane, 179, 180

Shaking palsy, 433

Sick headache, 406, 1216, 1230

Silver, use of, in hemiplegia, 978
    in labio-glosso-laryngeal paralysis, 1175
    in spastic spinal paralysis, 901

Simulation of sleep, 775

Simulations of hysterical patients, 230, 233-235

Skin, atrophy of, changes in, in injuries to peripheral nerves, 1183,
        1185, 1186, 1187
  Condition of, in neuralgia, 1212, 1213
  Disorders of, in chronic alcoholism, 615
    in hysteria, 234
    in myxœdema, 1272
    in neuritis, 1192
    in progressive unilateral facial atrophy, 695
    in tabes dorsalis, 837
    in the chloral habit, 663
    in the opium habit, 654, 658
    in vaso-motor neuroses, 1252-1254

SLEEP, AND ITS DISORDERS, 363
  Apparent death, test of, 385
    Circulation of blood in, 774, 775
  Brain, state of, during sleep, 367
  Coma, 382
  Disorders of, in cerebral anæmia, 782, 783
      Hyperæmia, 769
      Syphilis, 1000
  Dreams, physiology of, 368, 369
  Effect of, on choreic movements, 445
  Hypotheses concerning nature of sleep, 364-366
  Insomnia, 379
  in the opium habit, 655
    Febrile form of, 380
    from active cerebral congestion, 382
    from exhaustion, 380-382
    Lithæmic form of, 379
      Treatment, 380, 381, 382
  Lethargy, 384
    Lucid, 386
  Night-terrors, 370
  Sleeping dropsy, 383
  Somnambulism, 371
    Treatment, 378

Sleeping dropsy, 383

Smell, disorders of, in alcoholism, 623
    in hemiplegia, 955
    in neuralgia, 1213
    in tumors of the brain, 1030, 1043
  and taste, perversion of, in hysteria, 250

Social condition, influence on causation of chorea, 441
        of hysteria, 218
        of insanity, 117, 118

Sodium bromide, use, in epilepsy, 500

Softening of the brain, 917, 949, 989
    Red and yellow, in abscess of the brain, 793
  of the cord in acute spinal myelitis, 812
    in spinal hemorrhage and embolism, 809, 810

Somnambulism, 371
  Artificial, 373

Somnolence, morbid, 344
  in tubercular meningitis, 726, 727

Spasm and twitching of muscles in tumors of spinal cord, 1091, 1094
  characters and seat in writers' cramp, 515
  Painless facial, 462

Spasms, general, in hysteria, 236
  in neuritis, 1192
  in tetanus, characters, 549, 550
  Local, in hysteria, 244
    in tumors of the brain, 1038
  Varieties, in nervous diseases, 44-47

Spastic spinal paralysis, 861

Specific poisons, insanity from, 175

Speech, development of, 566

SPEECH, DISORDERS OF, 566
  Classification, 568
    Alalia, 569
      Treatment, 570
    Dyslalia, or stuttering, 572
      Treatment, 572
    Paralalia, or stammering, 571
      Treatment, 571

Speech, disorders of, in amyotrophic lateral spinal sclerosis, 875,
          876
    in Bell's palsy, 1203
    in cerebral hemorrhage and apoplexy, 941
    in chorea, 445, 448
    in disseminated (cerebro-spinal) sclerosis, 875, 876
    in hemiplegia, 957-960
    in labio-glosso-laryngeal paralysis, 1171
    in paralysis agitans, 455
    in the opium habit, 655, 658
    in tumors of the brain, 1038
  Physiology of, 567

SPINA BIFIDA, 757
  Definition, etiology, history, and synonyms, 757
  Diagnosis, 760
  Pathology and morbid anatomy, 759
  Prognosis, 761
  Symptoms, 758
  Treatment, 761
    Excision and ligation, 762
    Injection of iodine, 762
    Paracentesis, 761

Spinal anæmia, 805
    Treatment, 808
  cord, affections of, chronic, inflammatory, and degenerative, 825
    and its envelopes, tumors of, 1090
    Disease of one lateral half of, 1165
      Definition, 1166
      Diagnosis, 1168
      Prognosis, 1168
      Symptoms, 1166
        Anæsthesia, 1166, 1167
        Paralysis, seat, 1166, 1167
      Synonyms, 1165
      Treatment, 1168
    Diseases of membranes of, 703, 746
    Embolism, thrombosis, hemorrhage, and abscess of, 808
      Etiology, 809
      Morbid anatomy of, 809, 810
      Symptoms of, 809
      Treatment, 809
    Localization of lesions in, 69
    Lesions of, in alcoholism, 622
      in tabes dorsalis, 840
      in tetanus, 549
  disorders in alcoholism, 619
  dura mater, acute inflammation of, 747
      Diagnosis and prognosis, 748
      Morbid anatomy, symptoms, and treatment, 748
    Chronic inflammation of, 748
  exhaustion, 802
  hyperæmia, 801
  inflammation, 802
    Irritation, 802
      Etiology, 802
      Hysterical, 252
      Passive, 802
      Symptomatology, 802
      Treatment, 804
        Ergotin, 805
        Local bloodletting, 805
        Rest, 804
  membranes, congestion of, 746
    Etiology, 746
    Symptoms, morbid anatomy, and treatment, 747
    Inflammation and hemorrhage of, 746
  meningeal hemorrhage, 754
    Diagnosis and prognosis, 755
    Pathological anatomy, 755
    Synonyms, etiology, and symptoms, 754
    Treatment, 756
  meningitis, acute, 749
      Diagnosis and prognosis, 751
      Etiology and synonyms, 749
      Morbid anatomy and symptoms, 750
      Treatment, 751
    Chronic, 752
      Diagnosis, prognosis, and treatment, 753
      Symptoms and synonyms, 752
  Myelitis, acute, 810
  Paralysis, spastic, 861
  Sclerosis, posterior, 826
  Syphilis (see _Syphilitic Affections of the Nerve-centres_).

Spine, concussion of, 912
  Diagnosis, 916
  Prognosis, 916
  Symptoms, 915
  Treatment, 916

Spirits, characters of intoxication from, 591

Spleen, changes in, in chronic alcoholism, 607

Springs, Hot, value of, in spinal sclerosis, 900

Staggering, significance, in nervous diseases, 49
    in tabes dorsalis, 831

Stammering, 571

Starvation as a cause of cerebral anæmia, 781
  condition of brain in, 781, 782

Status epilepticus, prognosis of, 498
  Vertiginosus, the, 426
    Treatment of, 428

Stigmatization, 348-351
  Theories concerning origin, 350

Stimulants, use, in heat-exhaustion, 388
    in collapse in opium habit, 673, 675
    in thermic fever, 397

Stomach, disorders of and changes in, in chronic alcoholism, 600

Strabismus in chronic hydrocephalus, 743
  in tubercular meningitis, 727

Strychnia, use, in alcoholism, 641, 643, 646
    in chorea, 455
    in infantile spinal paralysis, 1157
    in intracranial hemorrhage and apoplexy, 978
    in labio-glosso-laryngeal paralysis, 1175
    in paralysis agitans, 438
    in spinal hyperæmia, 805
    in writers' cramp, 538
    Myelitis, acute, 822, 823

Stupor in tubercular meningitis, 727, 728
  Melancholia with, 158

Stuttering, 569, 571

Suicidal insanity, 146
  tendency, in general paralysis of the insane, 191

Sumbul, use, in hysteria, 278

Sun, exposure to, as a cause of acute meningitis, 716

Sunstroke (see _Thermic Fever_).
  headache from, 390, 404
  Influence on causation of cerebral hyperæmia, 764

Superficial neuralgia, 1211

Supposed discharge as a cause of cerebral hyperæmia, 766
      of spinal hyperæmia, 802

Supraorbital nerve, intermittent neuralgia of, 1233

Surgical treatment of abscess of the brain, 800
    of facial neuralgia, 1234
    of tumors of the brain, 1067

Sweating, absence of, in progressive unilateral facial atrophy, 696
    in the opium habit, 657, 658

Swedish movement, use, in hysteria, 280
      in infantile spinal paralysis, 1157

Sympathetic cervical, diseases of, 1263
  headache, 404
  neuralgias, 1220

Symmetrical gangrene, 1257

Symptoms of abscess of the brain, 795
  of acute alcoholism, 587 _et seq._
  of acute cerebral anæmia, 776, 782
  of acute myelitis, 816
  of acute simple meningitis, 717
  of acute spinal meningitis, 750
    pachymeningitis, 747
  of amyotrophic lateral sclerosis, 868
  of angina pectoris, 1238
  of apoplexy, 733
  of athetosis, 459
  of atrophy of the brain, 994, 995
  of Bell's palsy, 1203
  of capillary embolism, 981
  of catalepsy, 320
  of cerebral anæmia, 782
  of cerebral hyperæmia, 768
  of cerebral meningeal hemorrhage, 712
  of cerebral softening, 981, 989
  of cerebral syphilis, 1003
  of chorea, 445
  of chronic alcoholism, 598-633
  of chronic cerebral meningitis, 721
  of chronic hydrocephalus, 741
  of chronic lead-poisoning, 682
  of chronic spinal meningitis, 752
  of chronic spinal pachymeningitis, 749
  of combined forms of sclerosis, 870
  of concussion of the brain, 908
  of concussion of the spine, 915
  of congestion of cerebral dura mater, 704
    of spinal membranes, 747
    of the pia mater, 716
  of delirium tremens, 627
  of diffuse spinal sclerosis, 888
  of disease of cervical sympathetic, 1264
  of disseminated (cerebro-spinal) sclerosis, 874
  of ecstasy, 342
  of epilepsy, 477
  of external pachymeningitis, 704
  of family form of tabes dorsalis, 871
  of gastralgia, 1238
  of general paralysis of the insane, 178
  of hæmatoma of dura mater, 707
  of headache, 402
  of heat-exhaustion, 387
  of hebephrenia, 172
  of hypertrophy of the brain, 944-946
  of hypochondriasis, 154
  of hemiplegia, 954
  of hypertrophy of the brain, 99
  of hysteria, 229
  of hystero-epilepsy, 293
  of infantile spinal paralysis, 1114
  of inflammation of the brain, 791
  of injuries to nerves, 1183, 1185, 1186
  of insanity, 120
  of insomnia, 379-382
  of intermittent neuralgia of supraorbital, 1233
  of internal pachymeningitis, 706
  of intracranial hemorrhage and apoplexy, 733
  of labio-glosso-laryngeal paralysis, 1170
  of melancholia, 155, 156
  of migraine, 407, 1230
  of moral insanity, 143-146
  of multiple neuritis, 1195
  of myxœdema, 1272
  of nervous diseases, motory, 42
      psychic, 19
      sensory, 31
      trophic, 54-59
  of neuralgia, 1213
  of neurasthenia, 354
  of neuritis, 1191
  of neuromata, 1209
  of occlusion of cerebral vessels, 952
  of painless facial spasm, 462
  of paralysis agitans, 433
  of primary insanity, 152
  of progressive unilateral facial atrophy, 694
  of sciatica, 1235
  of secondary scleroses, 987
  of spastic spinal paralysis, 862
  of spina bifida, 757
  of spinal hemorrhage, 809
    hyperæmia, 802
    meningeal hemorrhage, 754
    syphilis, 1024
  of symmetrical gangrene, 1258
  of tabes dorsalis, 827
  of tetanus, 549
  of the chloral habit, 661
  of the insane temperament, 140, 141
  of the opium habit, 653
  of thermic fever, 389
  of Thomsen's disease, 461
  of thrombosis of cerebral veins and sinuses, 986
  of torticollis, 464
  of trance, 344
  of tremor, 430
  of tubercular meningitis, 725
      in the adult, 737
  of tumors of the brain, 1030
    of the spinal cord, 1091
  of unilateral spinal paralysis, 1166
  of vertigo, 416
  of visceral neuralgia, 1215
  of writers' cramp, 514

Syncope in cerebral anæmia, 790
  Treatment of, 790

Syncoptic seizures in cerebral anæmia, 783

Syphilis as a cause of disseminated sclerosis, 886
    of epilepsy, 471
    of general paralysis of the insane, 178
    of insanity, 119
    of spinal meningitis, acute, 749
    of tabes dorsalis, 852
    of tumors of the brain, 1028

SYPHILITIC AFFECTIONS OF THE NERVE-CENTRES, 999
  Brain-cortex, syphilitic disease of, 1017
    Diagnosis, 1020, 1021
    Symptoms, 1017 _et seq._
      Relation to general paralysis of the insane, 1008-1021
  Brain syphilis, gummatous, 1003
    Diagnosis, 1012
    Pathology, 1014
    Prognosis, 1013
    Symptoms and clinical history, 1003
      Aphasia in, 1009
      Epileptic attacks in, 1010
      Eye-ground, changes in, importance of, 1003
      Headache, seat and characters, 1003, 1005
      of cerebral meningeal syphilis, 1003, 1012
      Onset, mode of, 1003
      Paralysis, mode of onset, seat, and characters, 1007-1010
      Prodromes, 1003, 1004
      Psychical symptoms, 1011
      Sleep, disorders of, 1006
      Special senses, modifications of, 1008
    Treatment, 1015
      Aconite, hypodermic use, 1015
      Bloodletting, use, 1015
      Mercurials, use, 1016
      of the accidents or exacerbations of the disease, 1015
      Potassium iodide, use, 1016, 1017
      “Woods,” use, 1016, 1017
  Etiology, general, 999
    Time of development of symptoms after specific infection, 1001
    Spinal syphilis, 1022
      Diagnosis, 1026
      Lesions, 1024
      Relation to acute and subacute myelitis, and to acute ascending
          paralysis, 1022, 1023
      Symptoms, 1024
        Motility, disturbances of, 1025
        Pain in, 1024
        Sensation, perversions of, 1025

Syphilitic diseases of brain, in general paralysis of the insane, 197
  headaches, 403
  inflammation of spinal cord in diffuse sclerosis, 886
  insanity, 175, 1017


T.

Tabes dorsalis, 826
    Diagnosis, 857
    Etiology, 851
    History, 826
    Morbid anatomy of, 840
    Physiology of, 840-846
    Symptomatology, 827
  The family form of, 870
    Diagnosis, 870
    Etiology, 871
    Morbid anatomy, 872
    Prognosis, 871
    Symptoms, 871

Table of 100 cases of brain tumor, 1069
  of 50 cases of spinal tumor, 1107

Taches cérébrales, 1253

Tarantismus, origin and nature of, 223

Taste, disorders of, in alcoholism, 623
    in hemiplegia, 955
    in neuralgia, 1213
    in progressive unilateral facial atrophy, 697
    in tumors of brain, 1030, 1043

Tea and coffee as causes of tremor, 429

Telegraphy, influence on causation of writers' cramp, 507

Temperature in acute simple meningitis, 717, 718
  in cerebral hemorrhage and apoplexy, 937
  in cerebral hyperæmia, 770
  in cerebral meningeal hemorrhage, 713
  in chorea, 449
  in concussion of the brain, 909
  in epilepsy, 480
  in general paralysis of the insane, 179
  in hemiplegia, 960
  in hysteria, 252
  in infantile spinal paralysis, 1115, 1124
  in tabes dorsalis, 833
  in tetanus, 551
  in tetanus neonatorum, 564
  in the opium habit, 656, 657
  in thermic fever, 391
  in tubercular meningitis, 726, 728
  in tumors of the spinal cord, 1095
  of face, in progressive unilateral facial atrophy, 696
  of head, in tumors of brain, 1036

Tendon reflexes in chorea, 448
    in epilepsy, 481

Tenotomy in writers' cramp, 538
  indications for, in infantile spinal paralysis, 1158

Terminal dementia, 203

Termination of chorea, 449
  of progressive unilateral facial atrophy, 699
  of tumors of brain, 1045
    of spinal cord, 1106

TETANUS, 544
  Definition, 544
  Diagnosis, 551
    from hysterical spasm and cerebro-spinal meningitis, 552
    from strychnia-poisoning and hydrophobia, 552
  Etiology, 544-547
    Age, race, and sex, influence on causation, 544
    Atmospheric and climatic conditions, 544
    Theories regarding origin, 546, 547
    Traumatic causes, 545
  Morbid anatomy, 548
  Prognosis, 553
  Symptoms, 549
    Digestive and urinary organs, disorders of, 551
    Mental condition in, 550
    Prodromata, 549
    Pulse and temperature in, 550
    Spasms, seat and characters of, 549, 550
  Treatment, 555-562
    Alcohol, use, 559
    Bleeding, use, 555
    Calabar bean and cannabis indica, use, 557
    Chloral and potassium bromide, use, 559
    Conium, use, 557
    Curare, use, 556
    Mercury, use, 555
    Opium, use, 557
    Preventive, 561
    Surgical measures, 559-562
    Tobacco and anæsthetics, use, 566

Tetanus neonatorum, 563
  Etiology, 563
    Sims on displacement of occipital bone as a cause, 563
  Morbid anatomy, 564
  Symptoms, 564
  Treatment, 565

Tetanus, puerperal, treatment, 562

Thermic fever, 388
  Diagnosis, 396
  Etiology, 388
    Alcohol, influence on causation, 389
    Race, influence on causation, 389
  Post-mortem changes in and theories of the disease, 392
  Sequelæ, 399
  Symptoms, 389
    Cerebral, 390, 391
    Digestive disorders, 390, 391
    Entero-colitis of infancy, relation of, to, 390
    Motor system, disturbances of, 391
  Synonyms, 388
  Treatment and prophylaxis, 396
    Antipyrine, use, 398
    Bleeding, use, 398, 399
    Blisters, use, 398-400
    Cold and cold baths, use, 396, 397
    Morphia, use, 398
    of cerebral, 398
    of pyrexia, 396, 397
    of sequelæ, 398

Thomsen's disease, 461

Thrombosis of cerebral veins and sinuses, 982
  of spinal cord, 808

Tic douloureux, 1233

Tinnitus aurium in hyperæmia, 772
    in nervous diseases, 40, 41
    in tabes dorsalis, 834

Tinnitus in cerebral anæmia, 780

Titubation, in nervous diseases, 49

Tobacco, abuse of, influence on causation of alcoholism, 577
        of tabes dorsalis, 854
        of tremor, 429
        of writers' cramp, 512
  use, in tetanus, 556

Tongue-biting in epilepsy, 481
  state of, in cerebral hemorrhage and apoplexy, 941
    in labio-glosso-laryngeal paralysis, 1171
    in tubercular meningitis, 725, 726, 729

Tonic spasms in nervous diseases, 44

Tonics, use, in catalepsy, 338
    in melancholia, 160

Tonka, use, in neuralgia, 1229

Torsion of abdominal walls in treatment of hystero-epilepsy, 311

Torticollis, 463
  Etiology, 463
  Prognosis, 464
  Symptoms, 463
  Treatment, 464
    Electricity, use, 464
    Exsection of spinal accessory nerve, 464

Toxic causes of epilepsy, 472
  headaches, 402

Tracheotomy in tetanus, 561

Trance, lethargy, and morbid somnolence, 344-348
  Symptoms, 345
  Theories concerning nature, 346, 347

Transitory insanity, 164

Traumatism, influence on causation of abscess of the brain, 797
      of acute spinal meningitis, 749
      of cerebral hemorrhage and apoplexy, 932
      of cerebral hyperæmia, 767
      of cerebral meningeal hemorrhage, 711
      of concussion of the spine, 912
      of copodyscinesia, 514
      of epilepsy, 471
      of external pachymeningitis, 704
      of infantile spinal paralysis, 1151
      of neuritis, 1190
      of progressive unilateral facial atrophy, 694
      of spinal anæmia, 807
      of syphilitic affections of the nerve-centres, 999
      of tabes dorsalis, 855
      of the spinal cord, 1090
      of tumors of the brain, 1029

Treatment of abscess of the brain, 790
  of acute simple meningitis, 720
  of acute spinal meningitis, 752
  of acute spinal pachymeningitis, 748
  of alalia, 570, 571
  of alcoholic insanity, 175
  of alcoholism, 640
  of angina pectoris, 1238
  of athetosis, 460
  of atheroma of cerebral arteries, 992
  of atrophy of the brain, 994, 996
  of Bell's palsy, 1206
  of capillary embolism, 981
  of catalepsy, 338
  of cerebral anæmia, 788
  of cerebral embolism, 979
  of cerebral hemorrhage, 974
  of cerebral hyperæmia, 773
  of cerebral meningeal hemorrhage, 715
  of cerebral syphilis, 1015
  of cerebral thrombosis, 977
  of chorea, 450
  of chronic cerebral meningitis, 722
  of chronic hydrocephalus, 745
  of chronic lead-poisoning, 690
  of chronic spinal meningitis, 753
  of climacteric insanity, 173
  of concussion of brain, 911
    of spinal cord, 916
  of congestion of cerebral pia mater, 716
    of spinal membranes, 747
  of constitutional affective mental disease, 143
  of delusional insanity, 169
  of dementia, primary and secondary, 165
  of disease of cervical sympathetic, 1265
  of disorders of speech, 569, 571, 572
  of ecstasy, 344
  of epilepsy, 499
  of epileptiform facial neuralgia, 1234
  of external pachymeningitis, 706
  of gastralgia, 1239
  of general paralysis of the insane, 201
  of hæmatoma of the dura mater, 710
  of headache, 406
  of heat-exhaustion, 388
  of hebephrenia, 172
  of hypertrophy of brain, 998
  of hypochondriacal insanity, 150
  of hypochondriasis, 155
  of hysteria, 273
  of hysterical insanity, 149
  of hystero-epilepsy, 310
  of impulsive insanity, 148
  of infantile spinal paralysis, 1155
  of insane temperament, 141
  of insanity, 127
  of insomnia, 380-382
  of intercostal neuralgia, 1235
  of internal pachymeningitis, 706
  of intermittent neuralgia of supraorbital nerve, 1233
  of lead colic, 691
  of labio-glosso-laryngeal paralysis, 1174
  of mania, acute, 161, 162
  of melancholia, 159
  of migraine, 413, 1232
  of moral insanity, 146
  of myelitis, acute, 822
  of myxœdema, 1273
  of nerve injuries, 1189
  of neuralgia, 1222
  of neurasthenia, 357
  of neuritis, 1194
  of neuromata, 1210
  of painless facial spasm, 462
  of paralysis agitans, 438
  of perforating ulcer of foot, 1274
  of primary brain atrophy, 171
  of primary insanity, 152
  of progressive unilateral facial atrophy, 702
  of puerperal tetanus, 562
  of sciatica, 1236
  of senile dementia, 174
  of senile insanity, 174
  of somnambulism, 378
  of spina bifida, 761
  of spinal anæmia, 807
  of spinal hemorrhage, 809
  of spinal hyperæmia, 804
  of spinal meningeal hemorrhage, 756
  of spinal sclerosis, 898
  of stammering and stuttering, 571
  of symmetrical gangrene, 1262
  of syncope, 790
  of syphilitic insanity, 176
  of tabes dorsalis, 861
  of terminal dementia, 203
  of tetanus, 555
  of tetanus neonatorum, 563
  of the chloral habit, 676
  of the opium habit, 668, 672
  of thermic fever, 396
  of thrombosis of cerebral veins and sinuses, 988
  of torticollis, 463
  of tremor, 432
  of tubercular meningitis, 735
  of tumors of brain, 1066
  of tumors of spinal cord, 1106
  of unilateral spinal paralysis, 1168
  of vaso-motor neuroses, 1255
  of vertigo, 426
  of writers' cramp, 533

TREMOR, 429
  Etiology, 429
  Symptoms, 430
  Treatment, 432

Tremor, ataxic, in nervous diseases, 47
  hysterical, 244
  in alcoholism, 620
  in delirium tremens, 628
  in disseminated sclerosis, 875, 876
  in nervous diseases, 45
  in paralysis agitans, 434-436
  in spinal syphilis, 1025
  in the chloral habit, 664
  in the opium habit, 655, 658, 659
  in writers' cramp, 518
  muscular, in general paralysis of the insane, 195
  of sclerotic affections, treatment, 905

Trephining, question of, in abscess of the brain, 800
    in cerebral hemorrhage and apoplexy, 977
    in epilepsy, 503
    in tumors of the brain, 1066, 1067

Trismus, 549, 563

Trophic changes in injuries to peripheral nerves, 1183, 1187
  disturbances in tumors of the brain, 1044
    in writers' cramp, 520
    of tabes dorsalis, 837
  lesions in infantile spinal paralysis, 1145
  nerve-centres, 1266, 1275

TROPHIC NEUROSES, 1266
  _Atrophy_, 1260
    of glandular and cutaneous systems, 1268
    of muscles and bones, 1267
    Wallerian degeneration, 1266
  _Hypertrophy_, 1271
  _Inflammation_, 1273
    Bed-sores, acute and chronic, 1274, 1275
    Ulceration of fingers, acute, 1273
    Ulceration, perforating, of the foot, 1273, 1274
  _Myxœdema_, 1271
    Course and symptoms, 1272
    Etiology and pathology, 1271
    Diagnosis, 1273
    Treatment, 1273
      Electricity and tonics, 1273
      Nitro-glycerin, 1273
  _Trophic Nerves and Nervous Centres_, 1266
    Symptoms of nervous diseases, 54-59
      of neuritis, 1192

Tubercles, miliary, seat and character, in tubercular meningitis,
        730, 732

Tubercular brain tumors, 1048
  meningitis (see _Meningitis, Tubercular_), 723
  in the adult, 737
  simulated by cerebral anæmia, 786

Tumor of spina bifida, size, characters, etc., 758

TUMORS OF THE BRAIN AND ITS ENVELOPES, 1028
  Complications and sequelæ, 1045
  Definition, 1028
  Diagnosis, 1051
    from cerebral abscess, 1052
    from cerebral symptoms of Bright's disease, 1053
    from chronic hydrocephalus and softening, 1054
    from dementia and mania, 1054
    from early stage of posterior spinal sclerosis, 1055
    from hysteria and malaria, 1055
    from meningitis, 1053
    from various forms of apoplexy, 1052
    Localization of tumors of brain, 1056-1066
  Duration, course, and termination, 1045
  Etiology, 1028
    Age and sex, influence of, 1029
    Echinococci and cysticerci, influence of, 1030
    Heredity, influence of, 1028
    Injuries, influence of, 1029
    Syphilis, influence of, 1028
  Pathology, 1046
    Methods of making post-mortem examination in cases of brain
          tumors, 1050
    Varieties, structure, seat, and frequency, 1046-1050
    Prognosis, 1066
    Symptoms, 1030
      Apoplectic attacks in, 1040
      Ataxia and muscular atrophy in, 1030, 1041
      Bladder, disorders of, 1045
      Choked disc, neuro-retinitis and optic retinitis in, 1035
      Chorea and choreic movements, 1039
      Constipation in, 1045
      Contractures and rigidity in, 1030, 1039
      Epistaxis and hemorrhages from mucous surfaces in, 1044
      Eye, disorders of, 1030, 1035, 1042-1044
      Headache, characters and seat, 1030, 1033
      Hearing, taste, and smell, altered, 1030, 1043
      Mental disturbances, 1037
      Neuralgias in, 1042
      of multiple tumors, 1031-1033
      Pain on pressure upon head, 1034
      Paralysis, seat and characters, 1030, 1040
      Reflexes, altered, 1030, 1041
      Sensation, perversions of, 1030, 1042
      Spasms, local and general, in, 1030, 1039
      Temperature of head in, 1036, 1037
      Trophic disturbances and disturbances of respiration, 1044
      Vertigo in, 1034
      Vomiting in, 1030, 1034
      Will, impairment of, and defects of speech, 1038
    Treatment, 1066
      Ergot, cannabis indica, and hyoscyamus, use, 1068
      Leeches, use, 1068
      Morphia and potassium bromide, use, 1068
      Surgical, 1066

TUMORS OF THE SPINAL CORD AND ITS ENVELOPES, 1090
  Definition, 1090
  Diagnosis, 1098
    from caries of spinal vertebræ, 1099
    from hysteria, 1100
    from metallic and infectious diseases, 1100
    from spinal congestion, hemorrhage, and meningitis, 1098
    from traumatism, sclerosis, aneurism, and neuritis, 1100
    localization of spinal tumors, 1100-1106
  Duration and termination, 1106
  Etiology, 1090
    Age and sex, influence of, 1090
    Traumatism, influence of, 1090
  Pathology, 1096
    characters, seat, and varieties of tumors, 1096-1098
    vascular changes, 1098
  Symptoms, 1091
    Ataxia and atrophy in, 1094
    Bladder, urinary and sexual disorders, 1096
    Eye disorders, 1096
    Headache in, 1096
    Mental disturbances in, 1096
    Pain, seat and characters, 1091, 1092
    Paralysis and paresis, 1091-1093
    Reflexes, altered in, 1094
    Sensation, alterations of, 1091-1093
    Sense of constriction about waist, 1091-1093
    Spasms and twitchings in, 1091, 1092, 1094
    Temperature of body in, 1095
    Vomiting in, 1096
  Treatment, 1106

Tumors, phantom, in hysteria, 255

Turpentine, use of, in neuralgia, 1229

Tympanites, hysterical, 240

Typhoid fever as a cause of abscess of the brain, 799
      of anæmia of the brain, 781

Typhus fever as a cause of hyperæmia of the brain, 768


U.

Ulcer of foot in tabes dorsalis, 839

Ulcerations in nervous diseases, 58

Ulcers, perforating, of the foot, 1273

Unconsciousness, in cerebral meningeal hemorrhage, 712

Unilateral catalepsy, symptoms, 324
  epilepsy, 482
  facial atrophy, progressive, 693
  preponderance of symptoms in cerebral anæmia, 784
  spinal paralysis, 1165

Urine, state of, in brain tumors, 1045
    in cerebral hemorrhage and hemiplegia, 961
    in chronic lead-poisoning, 682
    in epilepsy, 480
    in general paralysis of the insane, 195
    in hysteria, 253
    in myxœdema, 1272
    in neuralgia, 1212, 1213
    in symmetrical gangrene, 1260
    in tabes dorsalis, 835
    in the chloral habit, 662
    in the opium habit, 654, 658, 659

Uterine and ovarian irritation as a cause of reflex paralysis, 807

Uterus and ovaries, neuralgia of, 1240


V.

Vaginismus, hysterical, 246

Valleix's painful points in migraine, 408

Varieties of hystero-epilepsy, 290

Vaso-constrictors, action of, 1243

Vaso-dilators, action of, 1244

Vaso-motor cerebral disturbances in general paralysis of the insane,
        179
  disturbances in writers' cramp, 520
  nerves, origin of, 1246

VASO-MOTOR NEUROSES, 1242
  Course, 1254
  Diagnosis, 1252
  Pathogenesis, 1242
  Physiology, 1242
    Local vascular tone in, 1242
    Medullary centres in, 1250
    Origin of the vaso-motor nerves, 1246
    Vaso-constrictors, 1243
    Vaso-dilators, 1244
    Vaso-motor reflexes, 1248
    Vaso-motor tracts, 1249
  Prognosis, 1255
  Symptoms, 1252
    Acrodynia, 1254
    Angio-spasm and angio-paralysis, 1252
    Cutaneous angio-neuroses, 1252-1254
    Digiti mortui and gangrene, 1252-1254
    Erythromelalgia, 1253
    Functional, derangements of internal viscera, 1254
    Ruptured capillaries in, 1253
    Sensation, disturbances of, 1252, 1253
    Taches cérébrales in, 1253
  Treatment, 1255
    Amyl nitrite and nitro-glycerin, 1256
    Chloral hydrate and chloride of potassium in, 1256
    Rest, massage, and electricity in, 1255

Vaso-motor and trophic neuroses, 1241
  Definition, 1241
  Reflexes, 1248
  Symptoms of general paralysis of the insane, 189
  Theory of pathology of hysteria, 211
  Tracts of the spinal cord, 1249

Venous congestion in cerebral hyperæmia, 768

Ventricles of brain in cerebral anæmia, 781

Veratrum, use, in tumors of spinal sclerosis, 905

Verbigeration, in katatonia, 166

VERTIGO, 416
  Definition, 416
  Diagnosis, 417
  Etiology, 418
    Blood-poisoning, influence of, 419
    Excessive venery, influence of, 420
    Mechanical causes, 426
    of aural form, 421
    of essential form, 426
    of gastric and senile form, 420
    of laryngeal form, 425
    of neurasthenic, hysteric, and anæmic forms, 425
    of ocular form, 424
  Prognosis and duration, 418
  Symptoms, 416, 420-426
    of aural form, 421
    of essential form, 426
    of gastric and senile form, 420
    of laryngeal form, 425
    of neurasthenic, hysteric, and anæmic forms, 425
    of ocular form, 424
    of status vertiginosus, 421
  Treatment, 426
    Bromides and hydrobromic acid, 426-428
    Cauterization, use of, 427
    Diet, 427, 428
    Morphia, use, 426, 427
    Nitrite of amyl and nitro-glycerin, use, 426
    of aural form, 427
    of gastric and senile form, 426
    of optic form, 427
    of status vertiginosus, 428
    Quinia, use, 427

Vertigo, in abscess of the brain, 796
  in cerebral anæmia, 777, 783
  in tumors of the brain, 1035

Vessels of cerebrum, changes in, in chronic alcoholism, 617
  state of, in cerebral abscess, 793

Violence, significance of, in nervous diseases, 24

Violin-playing as a cause of copodyscinesia, 511

Virchow on origin of progressive unilateral facial atrophy, 700

Visceral derangements of chronic alcoholism, 599
  disturbances in diffuse sclerosis, 889
  neuralgias, 1215, 1237

Vision, disorders of, in cerebral anæmia, 783, 786
    in diseases of the cervical sympathetic, 1264
    in disseminated spinal sclerosis, 878
    in epilepsy, 476
    in neuralgias, 1214
    in tabes dorsalis, 830-833
  hallucinations of, in migraine, 1231

Vitreous degeneration of cerebral cortex in disseminated sclerosis,
        882

Vomiting, hysterical, 254
  in acute simple meningitis, 718
  in anæmia of the brain, 777, 783
  in apoplexy and cerebral hemorrhage, 935
  in cerebral meningeal hemorrhage, 713
  in chronic hydrocephalus, 743
  in chronic lead-poisoning, 684
  in concussion of the brain, 908
  in infantile spinal paralysis, 1117
  in migraine, 409
  in the opium habit, 653, 657-659
  in tubercular meningitis, 725, 729
  in tumors of the brain, 1030, 1034


W.

Wallerian degeneration, 1266

Washerwomen's anæsthesia, 1199, 1201

Wasting diseases, influence on causation of copodyscinesia, 514

Water, hypodermically, in neuralgia, 1229
  influence on causation of chronic lead-poisoning, 680

Wax-like flexibility in catalepsy, 321, 337

Welsh fasting girl, 352

Westphal-Erb symptom of tabes dorsalis, 830

Wet pack, use, in neuralgia, 1223

Will, impairment of, in tumors of the brain, 1038
  and intellect, state of, in alcoholism, 625

Wines, character of intoxication from, 591

Wire brush, faradic, in spinal sclerosis, 904

Witchcraft, hysterical nature of, 226

“Woods,” the, use of, in cerebral syphilis, 1016

Word-blindness, in hemiplegia, 959
    in nervous diseases, 31

Word-deafness, in nervous diseases, 31

Worms, influence on causation of epilepsy, 471

Wrist-drop, 686

WRITERS AND ARTISANS, NEURAL DISORDERS OF, 504
  Definition, history, and synonyms, 504
  Differential diagnosis, 521
    from palsy from pressure, 526
    from paralysis agitans and multiple sclerosis, 524
    from paresis from slight lesions, 522, 523
    from progressive muscular atrophy, 523
    from teno-synovitis, 526
  Duration and course, 521
  Etiology, 505
    Action of muscles used in telegraphy, 508
    Action of muscles used in writing, 505
    Age and sex, influence of, 512, 513
    Cigarette-smoking as a cause of, 512
    Hereditary influence and nervous temperament, 513
    Manner of writing and holding the pen, 506
    Musical-instrument playing, 511
    Telegraphy, 507-511
    Wasting diseases and traumatism, 514
  Pathology and morbid anatomy, 526-530
  Prognosis, 530, 531
  Prophylaxis, 531-533
  Symptoms, 514-521
    Cramp and spasm, characters and muscles affected, 515-517
    Electrical reactions in, 521
    General, 520
    Lock-spasm in, 517
    Pain and modification of sensation in, 519
    Paresis and paralysis, characters and seat, 518
    Tremor in, 518
    Vaso-motor and trophic disturbances, 520
  Treatment, 533, 543
    Arsenic, use, 537, 538
    Atropia, hypodermically, 537
    Electricity, use, 534-536
    Gymnastics and massage, 536, 537
    Local applications in, 538
    Medication, value of, 537
    Mechanical apparatus in, 540-542
    Rest in, 533, 534
    Strychnia, use, 537, 538
    Tenotomy and nerve-stretching in, 538, 540


Z.

Zinc salts, use, in chorea, 455
    in hysteria, 278
    in hystero-epilepsy, 313
  Valerianate, use of, in migraine, 1232



GENERAL INDEX.

A.

Abdominal Glands, Diseases of, ii. 1182

Abortion, iv. 467

Acne, iv. 641
  rosacea, iv. 647

Addison's disease, iii. 939

Alalia, iv. 569

Albinismus, iv. 647

Albuminuria, iv. 34

Alcoholism, v. 573

Alimentation, rectal, ii. 928

Alopecia, iv. 678
  areata, iv. 680

Amblyopia, toxic, iv. 803

Amenorrhœa, iv. 183

Anæmia, iii. 887
  progressive pernicious, iii. 898

Anæsthesia of peripheral origin, v. 1198

Aneurism, abdominal, iii. 821
  thoracic, iii. 801

Angina pectoris, iii. 755

Angioma, iv. 688

Anidrosis, iv. 584

Ankyloglossia, ii. 349

Anthrax, i. 926; iv. 606

Anus, cutaneous eruptions and parasitic conditions of, ii. 892
  syphilis of, ii. 900

Anus and Rectum, Diseases of, ii. 877
  fissure of, ii. 888
  prolapse of, ii. 881

Aorta, aneurism of, iii. 801, 821
  atheroma of, iii. 800
  perforation and occlusion of, iii. 824
  rupture of, iii. 823
  stenosis of, iii. 825

Aortic insufficiency, iii. 659
  obstruction or stenosis, iii. 654

Apoplexy, cerebral, v. 917
  pulmonary, iii. 293

Artery, coronary, diseases of, iii. 828
  hepatic, aneurism of, iii. 840
  inferior mesenteric, diseases of, iii. 839
  pulmonary, diseases of, iii. 833
  superior mesenteric, diseases of, iii. 836

Arthritis, gonorrhœal, ii. 102
  rheumatoid, ii. 78

Ascaris lumbricoides, ii. 952

Ascites, ii. 1153

Asthma, Bronchial, iii. 184
  Hay, iii. 210

Atelectasis, iii. 251

Athetosis, v. 457

Atrophy, v. 1266
  facial, progressive unilateral, v. 694

Auditory canal, external, diseases of, v. 811

Auricle, external ear, diseases of, iv. 810


B.

Baldness, iv. 678

Battey's operation, iv. 290

Barber's itch, iv. 723

Basedow's disease, iii. 761

Bed-bugs, iv. 733

Bell's palsy, v. 1202

Beriberi, i. 1038

Bile-ducts, catarrh of, ii. 1051

Biliary concretions, ii. 1058

Biliary passages, affections of, ii. 1051
    occlusion of, ii. 1082

Biliousness, ii. 965

Bladder, atony and paralysis of, iv. 133
  atrophy and hypertrophy of, in women, iv. 348
  diseases of, iv. 123
  functional diseases of, in women, iv. 349
  hemorrhage of, iv. 134, 340
  hyperæmia of, in women, iv. 339
  inflammation of, acute and chronic, iv. 123, 126, 128, 341
  neuroses of, iv. 132
  new growths of, iv. 136
  paralysis of, in women, iv. 350

Blood and Blood-glandular System, Diseases of, iii. 882

Boils, iv. 604

Bowel, compression and contraction of, ii. 857
  stricture of, ii. 854

Bowels, hemorrhage from, ii. 830

Brain, abscess of, v. 792
  atrophy of, v. 993
  hypertrophy of, v. 996
  inflammation of, v. 790
  softening of, v. 989
  syphilis of, v. 1003, 1017
  and its Envelopes, Tumors of, v. 1028
    Spinal Cord, Concussion of, v. 907
      Diseases of Membranes of, v. 703
      Hyperæmia and Anæmia of, v. 763, 774

Bright's disease, iv. 72

Bromidrosis, iv. 584

Bronchi, Diseases of, iii. 164

Bronchial Asthma, iii. 184
  tubes, dilatation of, iii. 227

Bronchitis, acute and chronic, capillary, mechanical,
        pseudo-membranous, and rheumatic, iii. 169, 170, 171, 172,
        173, 174


C.

Caisson Disease, the, iii. 855

Calculi, hepatic, ii. 1058
  renal, iv. 42

Callositas, iv. 662

Cancrum oris, ii. 338

Canities, iv. 678

Cannabis indica, habitual addiction to, v. 669

Carbuncles, iv. 606

Cardiac murmurs and their relation to valvular heart disease, iii. 651

Cardiac Thrombosis, iii. 718

Cardialgia, ii. 459

Cardicentesis, iii. 798

Caruncle, urethral, iv. 403

Catalepsy, v. 314

Cerebral arteries, atheroma, v. 991
  meningeal hemorrhage, v. 710
  paralysis, v. 917
  veins and sinuses, thrombosis of, v. 982
  vessels, occlusion of, v. 917, 946

Cervical sympathetic, diseases of, v. 1263

Cestodes or tape-worms, ii. 931

Chloasma, iv. 659

Chloral habit, the, v. 660

Chloroform, habitual addiction to, v. 667

Chlorosis, iii. 894

Cholera, i. 715
  infantum, ii. 741
  morbus, ii. 719

Chorea, v. 439
  of the larynx, iii. 76

Chromidrosis, iv. 585

Chyluria, iv. 114

Cimex lectularius, iv. 733

Circulatory System, Diseases of, iii. 599

Clavus, iv. 663

Cocaine, habitual addiction to, v. 667

Cœliac axis, diseases of, iii. 841

Colic, hepatic, ii. 1058
  intestinal, ii. 658
  renal, iv. 42

Coma, v. 26, 382

Comedo, iv. 589

Constipation, ii. 638, 650

Convulsive disorders, local, v. 461

Copodyscinesia, v. 504

Corns, iv. 663

Cornu cutaneum, iv. 663

Coronary artery, diseases of, iii. 828

Coryza, iii. 41

Cough, nervous, iii. 71

Cranio-cerebral topography, v. 93

Cretinism, v. 138

Croup, spasmodic or false, iii. 70, 92
  true, iii. 100

Culex, iv. 733

Cyanosis and Congenital Anomalies of Heart and Great Vessels,
        iii. 687, 712

Cysticercus cellulosæ, iv. 732

Cystitis, acute and chronic, iv. 126, 128
  in women, iv. 341


D.

Deaf-mutism, iv. 840

Deafness after cerebro-spinal meningitis, mumps, scarlet fever, etc.,
        iv. 839

Death, apparent, v. 385

Degenerations, i. 72

Dementia, v. 164

Demodex folliculorum, iv. 732

Dengue, i. 879

Dentition, morbid, ii. 371

Dermatalgia, iv. 711

Dermatitis, iv. 600, 604, 611, 623

Dermatolysis, iv. 675

Dermoid cyst of the ovary, iv. 299

Diabetes insipidus, iv. 27
  Mellitus, ii. 195

Diagnosis, general, i. 148

Digestive System, Diseases of, ii. 319

Diphtheria, i. 656

Disease, causes and prevention of, i. 175

Diseases, General, i. 229

Distomum hepaticum, ii. 1109

Drainage and Sewerage in their Hygienic Relations, i. 213

Dreams, v. 368

Ductus communis choledochus, occlusion of, ii. 1082

Dura mater, cerebral, congestion of, v. 704

Dysentery, ii. 777

Dyslalia, v. 571

Dysmenorrhœa, iv. 192

Dyspepsia, functional and atonic, ii. 436


E.

Ear, internal, diseases of, iv. 835
  middle, diseases of, iv. 817

Echinococcus of the liver, ii. 1101

Eclampsia, v. 464

Ecstasy, v. 339

Ecthyma, iv. 653

Eczema, iv. 625
  marginatum, iv. 718

Effusions, i. 67

Elephantiasis, iv. 675

Embolism and Thrombosis, i. 56
      of the spinal cord, v. 808
  capillary, cerebral, v. 979

Emphysema, iii. 233, 249

Endocarditis, iii. 639, 640, 642, 643

Endometritis, acute and chronic, iv. 460, 462

Enteralgia, ii. 658

Enteritis, Pseudo-membranous, ii. 763

Entero-colitis, ii. 726

Epilepsy, v. 468

Epiglottis, inflammation and erosion of, iii. 109

Epithelioma, iv. 707

Epistaxis, iii. 50

Erythema, iv. 593, 595, 596

Erysipelas, i. 629

Ether, habitual addiction to, v. 667

Etiology, general, i. 125

Eye affections, from diseases of the digestive organs, iv. 749
    diseases of the kidneys and skin, iv. 752
      general system, iv. 800
      nervous system, iv. 771, 796, 797, 799
      respiratory organs, iv. 748
      sexual organs, iv. 755
      spinal cord, iv. 792
    mental affections, iv. 791

Eye-ground and appendages, changes in, from diseases of the
        circulatory apparatus, iv. 738


F.

Facial atrophy, progressive unilateral, v. 694
  nerve, peripheral paralysis of, v. 1202
  spasm, painless, v. 462

Fallopian tubes, dropsy of, iv. 295

Farcy, i. 909

Favus, iv. 715

Fibroma, iv. 686

Filaria medinensis, iv. 732

Fistulo in ano, ii. 897

Flea, common, iv. 733

Flea, sand-, iv. 732

Fluke-worms, iii. 946

Furunculus, iv. 604
  of external auditory canal, iv. 813
  of labia, iv. 362


G.

Gad-fly, iv. 732

Gall-stones, ii. 1058

Gangrene, symmetrical, v. 1257

Gastralgia, ii. 459, v. 1238

Gastric catarrh, acute and chronic, ii. 463, 470

Gastritis, acute and chronic, ii. 463, 470

Gastromalacia, ii. 618

Gastrorrhagia, ii, 580

Genito-urinary System, Diseases of, iv. 17

Glanders, i. 909

Glossanthrax, ii. 368

Glossitis, acute, ii. 354-366
  chronic, ii. 366-368

Glottis, œdema of, iii. 112
  spasm of, in adults, iii. 74

Glycosuria, hepatic, ii. 973

Gnats, iv. 733

Goitre, iii. 974
  exophthalmic, iii. 761

Gout, ii. 108

Graves' disease, iii. 761

Great Vessels and Heart, Congenital Anomalies of, iii. 687

Guinea-worm, iv. 732


H.

Hæmatoma of the dura mater, v. 707

Hæmaturia, iv. 104

Hæmoglobinuria or Hæmatinuria, iv. 104

Hæmopericardium, iii. 788

Hæmophilia, iii. 931

Hæmoptysis, iii. 266

Hæmothorax, iii. 582

Hair, atrophy of, iv. 682
  blanching of, iv. 678

Harvest mite, iv. 731

Hay Asthma, iii. 210

Headache, v. 402, 1216, 1230

Heart, adventitious products of, iii. 637
  aneurism of, iii. 636
  atrophy of, iii. 618
  dilatation of, iii. 630
  diseases of substance of, iii. 601
  fibroid, iii. 607
  hypertrophy of, iii. 619
  malformations of, affecting primarily left side of, iii. 707
  malformations of, affecting primarily right side of, iii. 702
  malpositions of, iii. 601
  murmurs, iii. 651
  neuroses of, iii. 747
  spontaneous rupture of, iii. 617
  Valvular Diseases of, iii. 639
  and Great Vessels, Congenital Anomalies of, iii. 687
  clot, iii. 718
  muscle, degeneration of, iii. 609

Heart's action, functional disorders of, iii. 747

Heat, Acute Affections produced by, v. 387

Hemorrhoids, ii. 882

Hepar adiposum, ii. 1046

Hepatic artery, aneurism of, iii. 840
  calculi, ii. 1058
  colic, ii. 1058
  glycosuria, ii. 973

Hepatitis, interstitial, ii. 990
  suppurative, ii. 1002

Hernia, cysto-vaginal, iv. 377
  pudendal, iv. 398
  recto-vaginal and entero-vaginal, iv. 378

Herpes iris, iv. 609
  simplex, iv. 607
  zoster, iv. 610

Hirsuties, iv. 669

Hodgkin's disease, iii. 921

Hydatid tape-worm, ii. 943

Hydatids of liver, ii. 1101
  pulmonary, iii. 466

Hydrocele or cyst of the canal of Nuck, iv. 397

Hydrocephalus, chronic, v. 704

Hydro-nephrosis, iv. 56

Hydro-pericardium, iii. 789

Hydrophobia and Rabies, i. 886

Hydrothorax, iii. 570

Hygiene, i. 173

Hymen, atresia of, iv. 374

Hyperidrosis, iv. 583

Hypertrichosis, iv. 669

Hypertrophy, v. 1271

Hypnotism, v. 373

Hypochondriasis, v. 154

Hypostatic Pneumonia, iii. 258

Hysteria, v. 205

Hystero-epilepsy, v. 288


I.

Ichthyosis, iv. 666

Icterus, ii. 975

Idiocy, v. 138

Imbecility, intellectual, v. 138

Impetigo, v. 651, 652

Indigestion, ii. 436
  intestinal, ii. 620

Infantile Spinal Paralysis, v. 1113

Inflammation, i. 37; v. 1273

Influenza, i. 851

Insanity, v. 99
  from gross lesions of the brain, v. 202
    specific poisons, v. 175

Insanities, complicating, v. 174

Insomnia, v. 379

Intercranial hemorrhage, etc., v. 917

Intermittent fever, i. 592

Intestinal Affections of Children in Hot Weather, ii. 726
  catarrh, acute, ii. 667
    chronic, ii. 699
  colic, ii. 658
  indigestion, ii. 620
  obstruction, ii. 830
  ulcer, ii. 823
  worms, ii. 930

Intestines, Cancer of, ii. 868
  Lardaceous Degeneration of, ii. 874

Intussusception and invagination, ii. 844

Ixodes, iv. 733


J.

Jaundice, ii. 925


K.

Katatonia, v. 166

Keloid, iv. 685

Keratosis pilaris, iv. 660

Kidneys, abnormalities of, in shape, size, position, etc., iv. 19
  Bright's disease of, iv. 72
  chronic congestion of, iv. 69
  cysts of, iv. 63
  diseases of parenchyma of, iv. 69
  floating, iv. 21
  malignant growths of, iv. 60
  parasites and tuberculosis of, iv. 64
  and Pelvis, Diseases of, iv. 19

Kleptomania, v. 147


L.

Labia, furuncles of, iv. 362
  majora, phlegmonous inflammation of, iv. 391

Labio-glosso-laryngeal Paralysis, Progressive, v. 1169

Laryngismus stridulus, iii. 70

Laryngitis, Acute Catarrhal (False Croup), iii. 92
  chronic, iii. 121
  Pseudo-membranous (True Croup), iii. 100

Laryngoscopy and Rhinoscopy, iii. 19

Larynx, anæsthesia of, iii. 65
  chorea of, iii. 76
  Diseases of, iii. 109
  disorders of motion of, iii. 69
  hyperæsthesia of, iii. 62
  morbid growths of, iii. 127
  neuroses of, iii. 59
  œdema of, iii. 112
  paræsthesia of, iii. 63
  paralysis and paresis of, iii. 78
  perichondritis and chondritis of, iii. 117
  spasm of, in children, iii. 70

Lead-poisoning, Chronic, v. 678

Lentigo, iv. 658

Leprosy, i. 785

Leptomeningitis, v. 716

Leptus, iv. 731

Lethargy, v. 384

Leucoderma, iii. 908

Leukæmia, iv. 697

Lichen ruber and scrofulosus, iv. 623, 624

Lithæmia, ii. 968

Liver, abscess of, ii. 1002
  acute yellow atrophy of, ii. 1023
  amyloid, ii. 1040
  carcinoma of, ii. 1033
  cirrhosis of, ii. 990
  Diseases of, ii. 965
  fatty degeneration of, ii. 1046
  flukes, ii. 1109
  hyperæmia of, ii. 982
  parasites of, ii. 1101
  the, in phosphorus-poisoning, ii. 1030

Localization of Lesions in the Nervous System, v. 65

Lung, Abscess of, iii. 296
  brown induration of, iii. 256
  cancer of, iii. 460
  cirrhosis of, iii. 440
  collapse of, iii. 251
  congestion and œdema of, iii. 258
  gangrene of, iii. 301
  Syphilitic Disease of, iii. 447

Lupus erythematosus, iv. 689
  vulgaris, iv. 693

Lymphangioma, iv. 689

Lymphangitis, simple, iii. 983


M.

Macroglossia, ii. 349

Malarial Fever, Pernicious, i. 605

Malarial Fevers, i. 589
  Hæmaturia and Hæmoglobinuria, iv. 107

Malignant Pustule, i. 926

Mania, v. 161

Mastoid disease, iv. 833

Measles, i. 557

Mediastinum, diseases of, iii. 861

Melæna neonatorum, ii. 832

Melanæmia, iii. 896

Melancholia, v. 155

Menière's disease, iv. 839

Meningeal hemorrhage, cerebral, v. 710
  spinal, v. 754

Meningitis, cerebral, acute simple, v. 716
    chronic, v. 721
    tubercular, v. 723
      in the adult, v. 737
  acute and chronic spinal, v. 749, 752

Menopause, functional disorders in connection with, iv. 432

Menorrhagia, iv. 200

Mental defects and degenerations, v. 138

Mental diseases, v. 99
    organic, v. 176

Mesenteric artery, inferior and superior, diseases of, iii. 836, 839

Metritis, acute, iv. 447
  chronic, iv. 450

Microcephalism, v. 138

Migraine, v. 406, 1216, 1230

Miliaria, or prickly heat, iv. 654

Milium, iv. 592

Mitral regurgitation, iii. 669
  stenosis, iii. 665

Molluscum epitheliale or contagiosum, iv. 661
  fibrosum, iv. 686

Morbid growths, i. 105
  processes, general, i. 35

Morphœa, iv. 672

Mosquitoes, iv. 733

Mouth, hemorrhage from, ii. 370
  and Tongue, Diseases of, ii. 321

Mumps, i. 620

Muscular atrophy, progressive, iv. 540
  system, diseases of, iv. 327

Myalgia, iv. 529

Myelitis, acute simple, v. 810
  chronic, v. 886

Myocarditis, acute and chronic, iii. 604, 607

Myoma, iv. 687


N.

Nævus pigmentosus, iv. 666

Nail, atrophy of, iv. 683
  hypertrophy of, iv. 669

Nasal catarrh, chronic, ii. 42
  passages, diseases of, iii. 42
    morbid growths of, iii. 52

Nematodes or thread-worms, ii. 949

Nephritis, acute diffuse, iv. 82
  acute parenchymatous, iv. 78
  chronic diffuse, iv. 84
    parenchymatous, iv. 80
  suppurative, iv. 99

Nerve, fifth, neuralgia of, v. 1232

Nerves, affections of, in Medical Ophthalmology, iv. 771
    of second pair of, iv. 771
    of third pair of, iv. 780
    of fifth pair of, iv. 785
    of sixth pair of, iv. 789
    of seventh pair of, iv. 790
  peripheral, diseases of, v. 1176
    injuries of, v. 1182

Nervous system, diseases of, general principles of diagnosis of, v. 59
      general semeiology of, v. 19
      motory symptoms of, v. 42
      psychic symptoms of, v. 19
      sensory symptoms of, v. 31
      trophic symptoms of, v. 54

Neuralgia, v. 1212
  of the fifth nerve, v. 1232

Neurasthenia, v. 353

Neuritis, v. 1189
  multiple, v. 1195

Neuroma, iv. 686

Neuromata, v. 1208

Neuroses, Trophic, v. 1241, 1266
  Vaso-motor, v. 1242

Night-terrors, v. 370


O.

Œdema, laryngeal, iii. 112

Œsophagitis, acute and chronic, ii. 409, 416

Œsophagus, Diseases of, ii. 409

Œstrus, iv. 732

Onychauxis, iv. 669

Oöphorectomy, iv. 290

Opium Habit, the, and Kindred Affections, v. 647

Ophthalmitis, febrile and post-febrile, iv. 761

Ophthalmology, Medical, iv. 737

Optic nerve, affections of, iv. 771

Otology, Medical, iv. 807

Ovarian cysts, extra-, iv. 293

Ovarian tumors, iv. 297

Ovaries and Oviducts, Diseases of, iv. 282
  malformations of, iv. 282
  removal of both, iv. 237

Ovaritis, acute and chronic, iv. 283, 284

Ovariotomy, iv. 313

Ovary, cystic tumors of, iv. 301
  dermoid cysts of, iv. 299
  fibroid tumor of, iv. 297
  hernia of, iv. 289
  malignant disease of, iv. 298
  prolapse of, iv. 286

Oviducts, cysts of, iv. 295, 296

Oxyuris vermicularis, ii. 950


P.

Pachymeningitis, acute spinal, v. 747
  chronic spinal, v. 748
  external, v. 704
  hemorrhagic, v. 707
  internal, v. 706

Pancreas, degenerations of, ii. 1128
  Diseases of, ii. 1113
  hemorrhage into, ii. 1129
  morbid growths of, ii. 1123

Pancreatic duct, obstruction of, ii. 1129

Pancreatitis, acute idiopathic, ii. 1118
  chronic interstitial, ii. 1121

Paralalia, v. 571

Paraldehyde, habitual addiction to, v. 666

Paralysis Agitans, v. 433
  Cerebral, v. 917
  general, of the insane, v. 176
  Infantile Spinal, v. 1113
  Pseudo-hypertrophic, iv. 557

Parametritis, iv. 209

Paratyphlitis, ii. 814

Parotitis, i. 620

Parovarium, cysts of, iv. 293

Pathology, General, i. 33

Pediculosis, iv. 728

Pelvic hæmatocele, iv. 239
  Peritoneum and Cellular Tissue, Inflammation of, iv. 208

Pemphigus, iv. 656

Perianal and perirectal abscesses, ii. 985

Pericarditis, iii. 769
  chronic, iii. 784
  tubercular, iii. 793

Pericardium, adherent, iii. 785
  diseases of, iii. 769

Pericardial effusions, operative treatment of, iii. 794

Perihepatitis, ii. 982

Perimetritis, iv. 227

Perinephritis, iv. 102

Perisplenitis, iii. 964

Peritoneum, hemorrhage into, ii. 1180

Peritonitis, acute, ii. 1133
  cancerous, ii. 1168
  chronic, ii. 1161
  local, ii. 1159
  infantile, ii. 1172
  tubercular, ii. 1165

Perityphlitis, ii. 814

Pertussis, i. 836

Pharyngitis, acute, tubercular, chronic, and syphilitic, ii. 390, 400,
        402, 406

Pharynx, Diseases of, ii. 390

Phlebitis, iii. 843

Phlebolithes, iii. 853

Phlegmasia dolens, iii. 843

Phosphoridrosis, iv. 585

Phthisis, fibroid, iii. 440
  pulmonary, iii. 391

Pia mater, cerebral, congestion of, v. 715

Piles, ii. 882

Pityriasis, iv. 621, 622

Plague, the, i. 771

Plethora, iii. 886

Pleura, Diseases of, iii. 483

Pleural cavity, growths in, iii. 583

Pleurisy, iii. 483
  diaphragmatic, iii. 568
  double, iii. 562
  hemorrhagic, iii. 565
  multilocular, interlobular, mediastinal, and rheumatic, iii. 564
  purulent, iii. 539
  tubercular, iii. 569

Pneumonia, catarrhal, iii. 353
  croupous, iii. 307
  hypostatic, iii. 258
  interstitial, iii. 440

Pneumohydro-pericardium, iii. 791

Pneumonokoniosis, iii. 454

Pneumopericardium, iii. 790

Pneumothorax, iii. 573

Polyneuritis, v. 1195

Polyuria or diabetes insipidus, iv. 27

Pompholyx, iv. 655

Portal vein, diseases of, ii. 1095

Pregnancy, disorders of, iv. 405

Prickly heat, iv. 654

Proctitis, ii. 887

Prognosis, general, i. 167

Progressive Muscular Atrophy, iv. 540

Prurigo, iv. 639

Pruritus, iv. 711
  ani, ii. 909
  vulvæ, iv. 362

Pseudo-hypertrophic paralysis, iv. 551
  membranous enteritis, ii. 763
    laryngitis, iii. 100

Psoriasis, iv. 614

Psycho-neuroses, v. 153

Pudendal hernia, iv. 398

Puerperal fever, i. 984
  tetanus, v. 562

Pulex irritans, iv. 733
  penetrans, iv. 732

Pulmonary apoplexy, iii. 293
  artery, diseases of, iii. 863
  embolism, iii. 373
  hydatids, iii. 466
  obstruction, iii. 675
  phthisis, iii. 391
  regurgitation, iii. 676

Purpura, ii. 186

Pyæmia and Septicæmia, i. 945

Pyelitis, calculous and secondary, iv. 47, 53

Pyelo-nephritis, suppurative, iv. 99

Pylephlebitis, suppurative, ii. 1097

Pylorus, hypertrophic stenosis of, ii. 615

Pyopericardium, iii. 790


R.

Rabies and Hydrophobia, i. 886

Rachitis, ii. 137

Rectal alimentation, ii. 928
  pouches, dilatation of, ii. 885

Rectum, abscess about, ii. 895
  effect of certain poisons and remedies on, ii. 911
  hemorrhage from, ii. 890
  inflammation of, ii. 887
  neuralgia of, ii. 909
  non-malignant stricture of, ii. 885
  obstruction of, ii. 889
  polypi of, ii. 882
  rodent and lupoid ulcer of, ii. 889

Rectum and anus, cancer and malignant stricture and ulceration of,
        ii. 902
    Diseases of, ii. 877
    prolapse of, ii. 881
    scrofulous and tubercular affections of, ii. 901
    spasm of, ii. 909
    syphilis of, ii. 900
    ulceration of, ii. 893, 894

Relapsing Fever, i. 369

Remittent Fever, i. 598

Renal calculus, iv. 42
  colic, iv. 42

Reynaud's disease, v. 1257

Rheumatism, acute articular, ii. 19
  chronic articular, ii. 46
  subacute articular, ii. 69
  gonorrhœal, ii. 102
  muscular, ii. 74

Rheumatoid arthritis, ii. 78

Rhinoscopy and Laryngoscopy, iii. 19

Ringworm, iv. 717

Rötheln, i. 582

Round ligament, solid tumor of, iv. 296

Rubeola, i. 557


S.

Sanitary science, i. 173

Sarcoma, iv. 710

Scabies, iv. 726

Scarlet Fever, i. 486

Sclerema neonatorum, iv. 671

Scleroderma, iv. 671

Scleroses of the spinal cord, secondary, v. 892

Sclerosis of the spinal cord, amyotrophic lateral, v. 867
      combined forms of, v. 869
      diffuse, v. 886
      disseminated, v. 873
      posterior, v. 826

Scrofula, ii. 231

Scrofuloderma, iv. 698

Scurvy, ii. 167

Seborrhœa, iv. 586

Semeiology, General, of Diseases of the Nervous System, v. 19

Seminal Incontinence, iv. 137

Septicæmia and Pyæmia, i. 945

Sewerage and Drainage in their Hygienic Relations, i. 213

Simple Continued Fever, i. 231

Skin, atrophies of, iv. 676
  Diseases of, iv. 581
  hypertrophies of, iv. 658
  inflammations of, iv. 593
  neuroses of, iv. 711
  new growths of, iv. 685
  parasites of, iv. 715
  secretions, disorders of, iv. 583

Sleep and its Disorders, v. 363

Smallpox, i. 434

Somnambulism, v. 371

Speech, Disorders of, v. 566

Spina Bifida, v. 757

Spinal Cord, Chronic Inflammation and Degenerative Affections of,
            v. 825
    disease of one lateral half of, v. 1165
    diseases of membranes of, v. 746
    embolism, thrombosis, hemorrhage, and abscess of, v. 808
  Hyperæmia and Anæmia, v. 763
  membranes, congestion of, v. 746
  meningeal hemorrhage, v. 754
  meningitis, acute and chronic, v. 749, 752
  paralysis, spastic, v. 801
  sclerosis, v. 826, 867 869, 873, 886, 892
  syphilis, v. 1022

Spine, concussion of, v. 912

Spleen, diseases of, iii. 962

Splenitis, iii. 962

Stammering and stuttering, v. 571

Steatoma, iv. 592

Stomach, anomalies in form and position of, ii. 617
  atrophy of, ii. 616
  cancer of, ii. 530
  cirrhosis of, ii. 611
  Dilatation of, ii. 586, 610
  functional and inflammatory diseases of, ii. 436
  hemorrhage from, ii. 580
  minor organic affections of, ii. 611
  non-cancerous tumors of, ii. 578
  rupture of, ii. 618
  simple ulcer of, ii. 480
  ulcers of, other than simple, ii. 529

Stomatitis, ii. 321-348

Stomatorrhagia, ii. 370

Sudamen, iv. 586

Suprarenal Bodies, Diseases of, iii. 939, 949

Sycosis, iv. 649
  parasitica, iv. 723

Sympathetic nerve, cervical, diseases of, v. 1263

Symptomatology, general, i. 148

Syphilis cutanea, iv. 699
  hereditary, ii. 254

Syphilitic Affections of the Nerve-centres, v. 999

Syphiloderma, iv. 699


T.

Tabes Dorsalis, v. 826
  the family form of, v. 870

Tabes Mesenterica, ii. 1182

Tape-worm, ii. 931

Tetanus, v. 544
  neonatorum, v. 563
  puerperal, v. 562

Thermic Fever, v. 388

Thomsen's disease, v. 461

Thoracentesis, history of, iii. 586

Thorn-head worms, ii. 949

Thread-worms, ii. 949

Thrombosis, cardiac, iii. 718
  and embolism, i. 56
  of the cerebral veins and sinuses, v. 982

Thrush, ii. 331

Thyroid gland, diseases of, iii. 974

Tinea favosa, iv. 715
  sycosis, iv. 723
  versicolor, iv. 724

Tongue, hypertrophy of, ii. 399
  inflammation of, ii. 354-368
  malignant pustule of, ii. 368
  ulceration of, ii. 369
  vices and abnormalities of, ii. 348
  and mouth, diseases of, ii. 321

Tongue-tie, ii. 349

Tonsils, Diseases of, ii. 379

Torticollis, v. 463

Trachea, Diseases of, iii. 133

Tracheitis, simple and complicated, iii. 133, 136

Tracheotomy, iii. 144

Trematodes or fluke-worms, ii. 946

Tremor, v. 429

Trichinosis, ii. 957

Tricuspid regurgitation, iii. 677
  stenosis, iii. 671

Trophic Neuroses, v. 1242, 1266

Tuberculosis, i. 94
  acute miliary, iii. 472

Tumors of the Brain and its Envelopes, v. 1028
  of the Spinal Cord and its Envelopes, v. 1090

Typhlitis, Perityphlitis, and Paratyphlitis, ii. 814

Typhoid Fever, i. 237

Typho-malarial Fever, i. 614

Typhus Fever, i. 338


U.

Ureters, diseases of, iv. 67

Urethra, dilatation of, in women, iv. 355
  dislocations of, in women, iv. 361
  prolapse of, in women, iv. 362
  stricture of, in women, iv. 363

Urethral, caruncle, iv. 403
  glands, in women, inflammation of, iv. 354

Urethritis in women, iv. 353, 355

Uridrosis, iv. 588

Urinary organs of women, diseases of, iv. 339

Urticaria, iv. 597

Uterine Functions, Disorders of, iv. 182

Uterus, Cancer of, iv. 274
  Diseases of Parenchyma of, iv. 447
  displacements of, iv. 147
  fibrous tumors of, iv. 245
  sarcoma of, iv. 271


V.

Vaccinia, i. 455

Vaccination, i. 465

Vagina, atresia and prolapse of, iv. 376
  cicatrices of, iv. 380
  Diseases of, iv. 367
  double, iv. 381
  growths of, iv. 382

Vaginal cystocele, iv. 377
  rectocele and enterocele, iv. 378

Vaginismus, iv. 384

Vaginitis, iv. 368

Varicella, i. 481

Variola, i. 434

Varioloid, i. 443

Vaso-motor Neuroses, v. 1242

Veins, diseases of, iii. 843

Verruca, iv. 664

Vertigo, v. 416

Vitiligo, iv. 677

Vocal cords, paralysis of, iii. 85, 86

Vulva, atresia of, iv. 373
  diseases of, iv. 388

Vulvitis, iv. 389

Vulvo-vaginal glands, cysts, and inflammation of, iv. 396


W.

Warts, iv. 664

Whooping Cough, i. 836

Wood-ticks, iv. 733

Worms, Intestinal, ii. 930

Writers and Artisans, Neural Disorders of, v. 504

Wry-neck, v. 463


X.

Xanthoma, iv. 687


Y.

Yellow Fever, i. 640



END OF VOLUME V.




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