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.