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.

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

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

[MENTAL DISEASES.] By CHARLES F. FOLSOM, M.D.

[HYSTERIA.] By CHARLES K. MILLS, A.M., M.D.

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

[CATALEPSY.] By CHARLES K. MILLS, A.M., M.D.

[ECSTASY.] By CHARLES K. MILLS, A.M., M.D.

[NEURASTHENIA.] By H. C. WOOD, M.D., LL.D.

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

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

[HEADACHE.] By WHARTON SINKLER, M.D.

[VERTIGO.] By S. WEIR MITCHELL, M.D.

[TREMOR.] By WHARTON SINKLER, M.D.

[PARALYSIS AGITANS.] By WHARTON SINKLER, M.D.

[CHOREA.] By WHARTON SINKLER, M.D.

[ATHETOSIS.] By WHARTON SINKLER, M.D.

[LOCAL CONVULSIVE DISORDERS.] By ALLAN MCLANE HAMILTON, M.D.

[EPILEPSY.] By ALLAN MCLANE HAMILTON, M.D.

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

[TETANUS.] By P. S. CONNER, M.D.

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

[ALCOHOLISM.] By JAMES C. WILSON, A.M., M.D.

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

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

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

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

[TUBERCULAR MENINGITIS.] By FRANCIS MINOT, M.D.

[CHRONIC HYDROCEPHALUS.] By FRANCIS MINOT, M.D.

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

[SPINA BIFIDA.] By JOHN ASHHURST, JR., M.D.

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

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

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

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

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

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

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

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

[INFANTILE SPINAL PARALYSIS.] By MARY PUTNAM JACOBI, M.D.

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

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

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

[NEURALGIA.] By JAMES J. PUTNAM, M.D.

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

[INDEX]

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.

DISEASES OF THE NERVOUS SYSTEM.

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. 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 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 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.

(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 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 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. 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 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.

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.

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 distinguished mainly by the absence of physical or paralytic symptoms, coinciding with a high rectal temperature. The spleen is often enlarged. Some would add that Bacillus malariæ and pigment might be found in the splenic blood, withdrawn by a long, fine needle.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

II. Sensory Symptoms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

III. Motory Symptoms.

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

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

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

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

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

Common hemiplegia is rarely accompanied by hemianæsthesia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

⁵ Ataxia is greatly aggravated by closing the eyes.

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

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

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