Chapter I: Front Matter (1)

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.