O' \ THE LIBRARY OF THE UNIVERSITY OF CALIFORNIA LOS ANGELES Gift of Dr. L. C. McLain AN ATLAS OF THE DIFFERENTIAL DIAGNOSIS OF THE DISEASES OF THE NERVOUS SYSTEM (WITH A PHYSIOLOGICAL INTRODUCTION) ANALYIICAL AND SEMEIOLOGICAL NEUROLOGICAL CHARTS BY HENKY HUN, M. D. F ORMERLY PROFESSOR OF THE DISEASES OF THE NERVOUS SYSTEM IN THE ALBANY MEDICAL COLLEGE; MEMBER OF THE AMERICAN MIDICAL ASSOCIATION, THE ASSOCIATION OF AMERICAN PHYSICIANS, THE AMERICAN NEL'ROLOGICAL ASSOCIATION. ETC.; AUTHOR OF "A GUIDE FOR AMERICAN MEDICAL STUDENTS IN EUROPE." -SYLLABUS OF A COURSE OF LECTURES ON THE DISEASES OF THE NERVOUS SYSTEM," ETC. THIRD REVISED AND ENLARGED EDITION ¥' THE SOUTHWORTH COMPANY, PUBLISHERS TROY, NEW YORK 1922 v;: ■' :„/ Copyrighted 1912, 1914 and 1922 by HENRY HUN, M. D. Momedical library 17 1 ^_-, 141 To Thomas Hun a loving father a learned physician a man of wisdom and wit this book is dedicated in most grateful remembrance. »;^(wo35 TABLE OF CONTENTS Preface, Page i PART ONE SEM BIOLOGY S. — Introduction to the Semeiological Charts. Methods of examination of patients suffering from ner\'ous diseases and a discussion of the significance of symptoms. CHART I. II. III. IV. V. VI. VII. VIII. PAGE 39. — Case taking- 57- 61 71 85 95 105 115 IX. 119. examination of patients ; comprising numbers i to 80. . — Analysis of etiological factors; comprising numbers 81 to 194. — Semeid .'\natomical terms ; comprising numbers 460 to 465. 127. X. XI. XII. 133- 141.- 149.- XIII. XIV. 165.- XV. 185.- XVI. XVII. ■95. 205. CVIII. -2I5- XIX. 217. XX. 221 — XXI. 229.- XXII. 239-- FIGURE PAGE I to 5. no. 6. 11.^- 7 to 13. 168. 14. 179. 15 to 17. 250-1 18. 252- 19- 253- 20. 254- 21 to 23. 255- 24 and 26. 256-7 25- 256. 27. 258. 28 to 31. 259. 32. 260. 33- 261. 34- 262. 35- 263. 36. 264. 37- 264. 38. 265. PART TWO Diagnosis -Introduction to the Diagnostic Charts. Clinical classification of nervous symptoms as a basis for diagnosis. -Diseases causing motor paralysis (vifeakness) ; comprising numbers 469 to 557. -Diseases causing convulsion or spasm ; comprising numbers 570 to 632. -Diseases causing perversion of motion (ataxia, tremor, nystagmus, fibrillation, also local palsies and spasms) ; comprising numbers 635 to 733. -Diseases causing disorders of speech and gait ; comprising numbers 735 to 804, -Diseases causing diminution or exaggeration of sensation (anesthesia, hy- peresthesia, etc.) and disorders of special senses; comprising numbers 805 to 928. -Diseases causing perversion of sensation (pain and vertigo) ; comprising num- bers 930 to 1034. -Diseases causing mental disorders; comprising numbers 1036 to 1120. -Diseases causing trophic (change of size) and sympathetic (ganglionic and vaso-motor) disorders; comprising numbers 1121 to 1203. -Diseases caused by syphilis of the nervous system; comprising numbers 1205 to 1217. -Diseases associated with abnormal cerebrospinal fluid; comprising numbers 1220 to 1244. PART THREE LOCAUZATION ■Localization in spinal cord ; comprising numbers 1250 to 1279. •Localization in brain ; comprising numbers 1290 to 1309. General localization from symptoms of paralysis or spasm; comprising num- bers 1310 to 1415. PLATES Erb's motor points for electrical examination. Erb's diagram showing the effects of injury of a nerve. Diagrams illustrating the various laryngeal paralyses. Diagram illustrating the various forms of ocular paralyses. Diagrams of the cerebral hemispheres. Diagram of oculo-motor nucleus. Diagram of nuclei in brain stem. Diagram of section through pons Varolii. Diagrams of sections through the medulla oblongata. Diagrams of transverse sections of the spinal cord. Diagram of nuclei in anterior horns of cord. Schematic representation of the more important diseases of the spinal cord. Schematic representation of some points in the physiology and pathology of the spinal cord and of the peripheral nerves. Diagram showing the motor and reflex functions of the spinal cord segments. Diagram showing the cutaneous distribution of the sensory nerves and nerve roots. Diagram of long motor projection tracts. Diagram of long sensory projection tracts. Diagram showing course of gustatory fibers. Diagram illustrating hemianopia. Diagram showing the nuclei of origin and the distribution of all motor and sensory nerves. INDEX, Page 267 PREFACE The diagnosis of diseases of the nervous system is generally r^arded by medical students as one of the most difficult subjects in their course of study. It is so difficult that many students become discouraged and after a few attempts make no strong, continued effort to master it and, perhaps in consequence, physi- cians generally are weaker in this than in other phases of their work. In the hope of making this task less difficult for both physicians and students this book has been written. If the student can be taught to make the diagnosis of these diseases with comparative ease, it may happen tliat he will be led to under- take those further studies in the finer anatomy and physiology of the nervous system, which are essential for a full understanding of this difficult but fascinat- ing department of medicine. A careful physical examination and history of the case, as complete as can be obtained, are, of course, the essential basis of every diagnosis; but the com- monly employed method of comparing the combination of symptoms thus obtained in any case with the various syndromes characteristic of the different diseases until a similar combination can be found, is not altogether satisfactory. More scientific and instructive are the analysis of each important symptom, its ex- planation in the normal or abnormal activity of the nervous system and the con- sequent ascertaining of the disease which must cause it under the circumstances (the other symptoms) existing in any individual case which may present itself. In spite of its apparent complexity, the diagnosis of nervous diseases lends itself better than that of the diseases of most of the other organs to exact path- ological analysis. Just as a chemist in analyzing a substance of unknown com- position by a series of appropriate tests eliminates from consideration one group of chemical bodies after another until he finally discovers its class and name, so the neurologist subjects a patient to one test after another in definite sequence. As the result of each test he throws out of consideration one or more groups of diseases and assures himself that he has to do with a disease belonging to another definite group. With each successive test the number of diseases constituting a group becomes less, until finally one definite individual disease stands revealed among the few most closely related to it and can be absolutely identified by a com- parison of the remaining symptoms characteristic of each, which are given in the final abstracts. This analytical method is used, I think, by most teachers of neu- rology in demonstrating cases of diseases before their classes of students. It is the crystallization of this teaching into the tabular form which this book attempts to present. In using this book for diagnostic purposes it is important that the "Intro- duction to the Diagnostic Charts" on page 119 should be carefully studied. By means of these charts it is possible to diagnosticate easily and rapidly almost any disease of the nervous system and to localize the lesion, when any lesion exists. If the examiner makes a mistake at any point, the next step in thei process or the abstract of the other symptoms of disease will probably show him that he is in error and that it is necessary for him to retrace his steps. For the sake of completeness certain trophic diseases are included, which, although causing a number of functional disturbances in the nervous system, are not really nervous diseases. As might naturally be expected, the same disease, in so far as it presents many symptoms, appears a number of times in the different charts and even in the same chart; so that, in order to get a more complete idea of its symptomatology, it is essential that the different abstracts of it should all be read. To facilitate this, cross references by numbers within brackets are placed in the text. Many diagnostic and technical terms are used which may not be familiar to the student; therefore these terms are classified, defined and their significance stated, as far as it is known to the author, in a series of semeiological charts pre- ceding the diagnostic ones. Cross reference to these terms also is facilitated by the numbers within the brackets. A very complete index serves this same purpose. The peculiar characteristic of this book on diagnosis is that it gives to the student or physician a key by which, in a comparatively easy manner from one or more important symptoms, he can arrive at a diagnosis. It also has the advantage that it divides the diseases into groups, the members of which have a definite relationship with each other; so that in the process of using the charts the student is constantly catching glimpses of the natural relationships between the different diseases of the nervous system. Although the symptoms of different diseases have often been contrasted in tables of parallel columns, in no other book, known to the author, has the subject been presented as it is here, and this must be his excuse for publishing it and for any defects which it may show, as there was no model which could be followed in preparing it. In the preparation of this book the author ha? received valuable suggestions and aid from several friends and especially from Drs. Archambault, Dawes, Hawn, Mosher, Streeter and Viets. To these, his present friends and former students and assistants, he gratefully acknowledges his indebtedness and returns his thanks. It is very gratifying to the author that the first two editions of five thousand copies have been exhausted, giving him an opportunity of making a complete re- vision of the text, and of making a few additions both to the semeiological and to the diagnostic charts, which seem to him to add much to the value of the work. The criticisms of Dr. Mosher and his untiring aid in putting the three editions through the press are large factors in whatsoever success the book may have. Henry Hun. Albany, N. Y., March 1, 1922. PART I SEMEIOLOGY THE EXAMINATION OF PATIENTS AND A PHYSIOLOGICAL AND PATHOLOGICAL ANALYSIS OF THE RESULTS OBTAINED FROM SUCH EXAMINATION AN ANALYSIS OF THE SUBJECTIVE AND OBJECTIVE SYMPTOMS OF DISEASE Introduction to the Semeiological Charts A Review of the Physiology of the Nervous System (The bracketed numbers refer to the numbers in the body of the book) The diagnosis of nervous diseases, if it is to be at all satisfactory and accurate, must be based on anatomy and physiology. It might seem strange to mention physiology in connection with such a schematic tabulation of diagnosis as this book presents. All of these charts, however, are con- structed strictly on a physiological basis and without such basis they could not have been made or could not be successfully used. The diminution, exaggeration, or perversion of the different phy- siological functions of the nervous system constitutes the scheme of each chart and is the key for the diagnosis of the separate diseases which are their clinical expression. The practitioner is sup- posed to have some acquaintance with these subjects, and the curriculum of the medical college is so arranged that the student is taught them before he commences clinical work. It seems, however, desirable to make here an attempt to present a very brief, but comprehensive, outline of the physiology of the nervous system, including some statements as to its anatomy, which latter can be supplemented by an inspection of the plates at the end of the book. The human being is a unit in the universe which contains him, of which he is a part and with which he is in constant relationship. Life consists in a constant reaction of the organism to the forces of nature which act upon it from all sides. These reactions are called "physiological ac- tivities," and when they become disordered from any cause they are called "pathological activities," or symptoms of disease; when they are altogether absent the organism is dead. The nervous sys- tem is the most important seat of these reactions. Of the numerous forces and forms of energy in the world only a portion can be perceived by man. It is certain that some animals perceive things imperceptible to him. The various forms of energy in nature cannot act directly upon the nervous system to produce sensory impulses; but intermediate organs, "end-organs," or "receptors," are necessary to trans- mute into nervous energy, the external energy (sun's rays, etc.) which comes from the external world. There may be some question whether the external energy passes through the nervous sys- tem to the muscles and from them passes out again to the external world; or whether the external energy (light, etc.), in its action upon the end-organ, liberates the potential energy stored in the end-organ, just as a spark liberates the potential energy stored in gunpowder. The latter assump- tion seems to be the triie one, because the energy imparted to the animal by the stimulus is much less than the consequent energy manifested by the animal. Hence the conclusion, that in virtue of chemical changes the potential energy stored in the end-organ becomes active; the ex- citing cause of this being the external force or foreign irritation. There are doubtless many forms of energy in the world which cannot be perceived by man because he possesses no suitable end-organs to bring about this transmutation. Sometimes this can be accomplished by adding to the end-organs some mechanical contrivance suitable to bring about this transmutation ; as, for instance, the fluoroscopic screen for X-rays. The universal ether is doubtless in vibration far beyond the limits of about four hundred million million per second, which constitute the color red and about seven hundred and sixty million million, which constitute violet; and, indeed, we have reason to believe that the ultra-violet rays have some eflfect upon the human body, but beyond the above limits the vibration of the ether is neither reacted to by our eye nor recognizable by our brain. The sensory apparatus is not perfect. Some time is required for the excitation caused by the external stimulus to pass through the end-organ and the nerve fibers to the cerebral cortex and to excite the latter to action (the initial lag) and the resulting sen- sation persists an even longer time after the external stimulus has ceased (the terminal lag). Things moving very rapidly, as for instance the spokes of a rapidly moving wheel, cannot be seen individually, and a rapidly recurring series of the same sound blends into a musical tone. But, however limited and imperfect the sensory apparatus may be, the end-organs, each of which is specific and can respond to one definite form of energy and to that one only, whether on the sur- face or in the interior of the body, are starting points from which all nervous and mental activity, even the highest, springs. The fundamental function of the end-organ and hence the primary activity of the nervous system is, thus, "receptivity." The fundamental, anatomical element, or unit, of the nervous tissue is the "neuron" (461-4) : & nucleated cell with many processes projecting from it, some short and branching (dendrons) ; one (rarely two or more), often extending a long distance, usually becomes the axon of a medullated nerve fiber, and frequently gives ofif a few collateral branches. Both axons and dendrons are composed of delicate fibrillae which pass directly, without inter- ruption, through the cell body from the tip of a dendron to the tip of the axon. Of these neurons, varying in form and size and supported by the delicate framework of the neuroglia, the entire nervous system is composed. The fundamental physiological characteristics of the nervous tissue are excitability and trans- mission : the power of receiving an excitation and transmitting it from one end of the neuron to the other, and even to other neurons with which the first has anatomical and physiological relation- ship, or contact. By its dendrons the nerve cell receives nervous impulses and by its axon trans- mits these impulses. The transmission of energy from one neuron to another at their synapse, or point of contact, depends, probably, upon differences in the tension of this energy in the two neu- rons. Later observations, however, seem to prove that, at the termination of the axon, its fibrillae jjass directly into the dendron of another neuron, at least in some cases. A neuron is merely a conducting channel. It originates nothing. It merely transmits. The rapidity of conduction of the nervous impulse along a nerve fiber is approximately foui hundred feet per second normally, but varies with the temperature and other artificial conditions. The nervous conduction seems to be a wave of chemical decomposition associated with a local elec- trical current. The transmission of an impulse from one neuron to another is relatively slow. The Centripetal Neurons Cutaneous Sensibility. The surface of the body and the cavities connected with it contain organs: the terminal organs of sense (the sensory "end-organs"), which bring the body into connection with some, but probably far from all, of the forces of nature and these end-organs are so constructed as to transmute physi- cal forces (light in the eye, sound in the ear, heat, cold, touch, pressure and pain in the skin, etc.,) into nervous excitations in the terminal filaments of the peripheral nerves. The skin contains many of these isolated terminal sense organs and, therefore, sensibility is not spread uniformly over the skin, as it appears to be, but is really located in individual points lying close together, but each distinct. From these points of greatest sen- sibility its acuteness diminishes concentrically. In every square centimeter of skin there are, on the average, 12 to 13 points for cold, o to 3 for heat, and 24 for tactile impressions; although these figures vary very greatly for different parts of the skin, the points being most numerous on the finger tips and fewest on the back. Points for tactile impressions vary from 7 to 300 per square centimeter. There are also distinct points for painful sensibility. These points for painful sensibility are much more numerous, but far less sensitive and delicate, than are those for tactile sensibility. The nerve fibers supplying these points of painful sensibility have no end-organs, but end as fine free filaments. Where the skin is stretched over bone ((T.g., the malleoli) tactile sensibility is less distinct, and it is more distinct where the skin is hairy ; a point for tactile sensibility being situated at the base of most, if not of all, hairs. There may be a delay in the conduction of painful impressions through either the neuron or the synapse; so that with repeated pin-pricks the pain becomes more acute (sum- mation of impulses). After section, or injury, of a nerve, the anesthesia and analgesia are never so extensive as is the area of distribution of the nerve, and sensibility often returns before the regeneration of the nerve has completely taken place. This is partly due to peripheral anastomoses with terminal filaments of adjacent nerves and partly, perhaps, to sensory fibers in the motor nerves (recurrent sensibility.) Head and his colleagues, after much experimental work on the subject, arrived at the following con- clusions : There are in the peripheral areas three kinds of sersibility, due to there being three different kinds of nerve fibers supplied to each area : 1st. Deep Sensibility: Muscle sen.se, joint sense, pressure, pain, and vibration sense. This sensibility is conveyed by sensory nerve fibers, more or less deeply situated beneath the .skin, and usually running with the motor nerves. When the nerves of the tendons are cut. these forms of sensibility are lost, but not on section of the sensory nerves of the skin. 2nd. Eficritic Sensibility: Tactile sensibility for slight impressions, form and space sense, sense ot moderate, not extreme, temperatures, (22° to 40° C.) and the precise localization of pain and temperature sense. This area of sensibility is very constant for each individual nerve. The restitution of this form of sen- sibility is very slow and is not complete until several years after the injury to the nerve. 3d. Protopathic Sensibility: Pain and sense of extremes of temperature (below 22° or above 40° C). Disturbances of this form of sensibility are accompanied by paresthesiae and a false localization. This form of sensiblity is best tested on the periphery of the affected area, where the anesthesia is not complete, or over the whole area while the regeneration is taking place. The restitution of this form of sensibility is relatively rapid (7 to 10 weeks). These researches of Head are of great interest and value and have attracted much attention and discussion: but they are not, in their entirety, accepted by all neurologists and more recent investigations seem to show thit after section or injury of a nerve all forms of sensation are practically equally impaired and in cases of re- covery all return with equal rapidity ; so that testing for one form usually suffices for all. The testing of sensi- bility is very difficult, so much depends upon the patient's intelligence, power and quickness of perception and freedom from suggestion. Sensory impulses of all kinds are carried to the central nervous organs by the sensory nerves. Of these, the spinal nerves enter the cord (mainly) through their cell bodies in the spinal ganglia and through the posterior nerve roots (Fig. 26) ; while the fibers of the trigeminal, the great cranial nerve supplying sensation to the face, after passing through their cell bodies in the Gasserian ganglion, enter the pons (Fig. ig). The fibers from the posterior nerve roots, on entering the spinal cord, are sorted ac- cording to their physiological function into three great groups (Fig. 26). One group which conveys most of the tactile, and a part of the pressure and muscle-joint sense impressions, ascends mainly, without decussating, in the posterior columns to the nuclei of the columns of Goll and Burdach, and thence is continued by a new set of neurons (the internal arcuate fibers), which decussate and pass through the median lemniscus (fillet) (Figs. 20-3) to the optic thalamus; whence it is continued, also by another set of neurons (relays), to the parietal cortex. These fibers convey impulses essential to the production of association reflexes. The second group, which conveys impulses essentia! to the maintenance of equilibrium, passes to the cells of the columns of Clarke and thence, mainly without decussating, through the direct cerebellar (posterior, spino-cerebellar or Flechsig's") tract in the outer part of the lateral column and through the restiform body to the vermis or middle lobe of the cerebellum. The third group, which conveys all the temperature and painful impressions, passes through cells in the posterior horn, decussates in the central gray matter of the cord and passes upward through the spino-thalamic tracts and lateral portion of the formatio recticularis, joining in part the median lemniscus, to the optic thalamus and thence to the parietal cortex, and in part coursing backwards to the cere- bellum. The fibers of the first and third group have thus a double ending, one in the optic thalamus and cue in the cortex. A destructive lesion, either in the terminal end-organ or at any point of these sensory tracts or neurons, causes a corresponding paralysis of sensation (anesthesia) : while a slight, irritative lesion may cause hyperes- thesia, paresthesiae or pain in the distribution of the nerve. In addition to the anesthesia, which occurs in organic disease of the nervous system, there is an anesthesia which occurs in hysteria; hysterical anesthesia (415). This hysterica! anesthesia occasionally, but rarely, in- volves the organs of special sense. It more commonly involves cutaneous sensibility and then the anesthesia is not limited to the distribution either of a peripheral nerve or of a nerve root. It may instantaneously disap- pear. It may recur in the same place, or in some other locality. It does not prevent the use of the part in per- forming acts in which sensibility is essential. Upon excitation of the hysterical anesthetic parts vascular re- flexes occur, which is never the case in anesthesia due to organic disease, peripheral or spinal. It is evident that this hysterical anesthesia is a purely mental phenomenon : an imagined idea or delusion. It is due to sug- gestion ; a "fixed idea" is so dominant that the sensation of pain or touch, which should normally result, dots not enter consciousness (see later). The excitation causing the dominant fixed idea inhibits other cortical activity. Pain (374) is an unpleasant sensation which never occurs in health, but only when the body is injured, either mechanically or chemically. It is a signal or warning that the body needs protection. Its intensity de- pends not only upon the intensity of the mechanical or chemical irritation, but also upon the condition (inflam- matory, etc.) of the peripheral nerves or of the cerebral cortex. It is more intense when cerebral cellular activities produce the concepts of fear and apprehension and the condition of "active attention" (see later), which makes the painful sensation more acute. An unexpected wound is less painful than an anticipated one. and a wound is often not at all painful when the cortical activity is greatly excited by some other cause (a battle for instance.) Pain is often associated with the allied perceptions called "paresthesiae" (375), which at times accompany, and at times follow, the pain and which are usually of central origin and are due to irritation of the sensory fibers at some part of their course through the central nervous organs. The Kinesthetic Sense (43). The muscles, tendons and articular surfaces all contain end-organs which send impulses to the central nervous organs whenever the muscles contract or the joints move and cause sen- sations from which the position of the limb in space can be accurately located, even when the eyes are closed or the patient is blind. These sensations are caused by the movement of the part and have much to do with regulating and inciting its further movements. The kinesthetic sense is of the greatest importance in all act- 7 ions and more especially in the automatic and habitual acts, (walking, swimming, talking, singing, etc). The pathways for the nerve fibers conducting "muscle-sense," as it is often called, and which have their origin in the muscle spindles, etc., enter the spinal cord through the posterior nerve roots, mainly pass forwards to the col- Bmns of Lockhart Clarke and thence directly outwards to the direct cerebellar tract (posterior spino-cerebellar tract) and through it to the cerebellum, and in part through the posterior columns to the cerebrum. The corresponding fibers in the cranial nerves enter the pons and medulla. The EquiUbrimn Sense. The three semi-circular canals, each lying in a plane at right angles to the other two, constitute the most important organ for the equilibration of the body. In every movement of the head the endolymph in the canal in the plane in which the head is moved is set in motion and moves also the hair-cells in the canal. The stimulus arising from these irritated hair-cells passes through the vestibular branch of the acoustic nerve to Deiter's nucleus and its neighborhood and thence to the vermis of the cerebellum. The vesti- bular nerve has no direct connection with the cerebral cortex and hence its activity is entirely unconscious. Gustatory Sensation. (Charts Via and XlVe). The mucous membrane of the mouth (in addition to the terminal organs for tactile, pressure, thermic, painful, etc., impressions) contains also the terminal organs of the nerves of taste: the taste-buds or bulbs, so called from their form, embedded in the epithelium of the mucous membrane of the mouth, especially in the tip and edges of the tongue. Excitation of these taste- bulbs gives rise to four distinct gustatory sensations : sweet, acid, salty and bitter, to which may, perhaps, be added alkaline and metallic. Many so-called tastes are really a combination of gustatory and olfactory sensations. The nerve fibers arising from the taste-bulbs on the posterior portion of the tongue pass by the glosso-pharyngeus nerve in a direct manner through the petrous ganglion to their nucleus in the medulla, whence they ascend with the other sensory fibers of the lemniscus to the optic thal- amus, and thence to the cerebral cortex, posterior to the olfactory area, in the gyrus hippocampi, (Fig. i6) ; while the nerve fibers arising from the taste bulbs on the anterior portion of the tongue pass at first in the chorda tympani nerve and run with it through the Fallopian canal to the geniculate ganglion. Here the fibers divide; a part continuing alongside the facial nerve and forming the nervus intermedius, which runs to a nu- cleus in the medulla, close to the glosso-pharyngeal nucleus ; while the rest of the fibers run through the petrosal nerve and join the fifth nerve and pass to the Gasserian ganglion (Fig. 36), and thence to the cerebral cortex (Fig. 16). A destructive lesion at any part of this course will cause unilateral loss of taste (ageusia). When the lesion is in the Fallopian canal, the ageusia may be associated with facial paralysis on the same side. Olfactory Sensation. (Charts Via and XlVe). The mucous membrane of the nose, analogous to that of the mouth, in addition to the end-organs for tactile, thermic, pressure and painful impressions, contains also the end-organs of the nerves of smell. The nerves terminating in these organs pass upward through the crib- riform plate to the olfactory bulb, and thence backward through the olfactory tract; some to the anterior per- forated space and sub-thalamic region (for the olfactor>- reflexes) and others to the cortical centers for smell in the coniu Ammonis (Fig. 16). These fibers do not pass through the internal capsule as do the fibers from all the other organs of sense, with the doubtful exception of the gustatory fibers. Hearing. (Charts Via and XI Ve). The terminal organ for hearing is the organ of Corti in the cochlea within the petrous portion of the temporal bone. In this organ there is a long series of vibratory structures of unequal length supported upon the basilar membrane (membrana spiralis) ; so that among them can be found a representative for every possible tone (produced by single vibrations of any rapidity between 40 and 40,000 per second) with its overtones, or harmonics. The acoustic nerve (cochlear nerve) arising in this organ passes to the ventral and dorsal acoustic nucleus in the pons (Fig. 19). From this nucleus fibers pass upward, some decussating and some not, through the lateral fillet (lemniscus lateralis) to the posterior corpora quadrigemina and the median geniculate body ofthe thalamus and thence through the sublenticular region of the internal capsule, posterior to the fibers for cutaneous sensibility, and reach the cortical auditory area in the anterior transverse temporal convolution immediately below and forming the lower margin of the Sylvian fissure in each hemisphere. A destructive lesion of one acoustic nerve will cause unilateral deafness on the same side, but a lesion of the tract connecting the subcortical with the cortical centers, since this tract contains Ixjth crossed and uncrossed fibers, will not cause any deafness The cortical representation of the au- ditory nerve is bilateral. Deafness results only from ,1 bilateral central lesion affecting the corpora quadri- gemina or the subcortical tracts described above. Even destruction of the acoustic cortical center in both hemi- spheres does not seem always to cause complete deafness. Sight (Charts Via and XIV, b, c, d). The terminal end-organs for sight consist of the rods and cones in the retina. The rods seem to be concerned with seeing in dim, the cones in bright, light. They vary in relative numbers in different animals, according as the latter roam by night or by day. They also vary in man according to their situation. Only cones are found in the fovea centralis. These gradually diminish in num- ber towards the periphery of the retina, where only rods are found. From these structures start the terminal filaments of the optic nerves, which run backward from the eyeballs to the optic chiasm. In the optic chiasm the fibers from both maculae luteae and from the nasal half of each retina decussate; so that in the left optic tract are collected all the fibers from the left half of each retina (right visual field) and those from both maculae luteae ; while in the right optic tract are collected all the fibers from the right half of each retina (left visual field) and those from both maculae luteae. The fibers of the optic tract on each side terminate in 8 the external geniculate body, the pulvinar and the anterior quadrigeminal body of the same side, and are thence continued through the posterior portion of the internal capsule and the fasciculus of Gm- tiolet to the lips of the calcarine fissure on the median surface of the occipital lobe of the same side (Figs. i6 and 37). A destructive lesion of the optic nerve causes blindness of the corresponding eye, but a lesion of any por- tion of the optic tract, or geniculate body, or fasciculus of Gratiolet, or the lips of the calcarine fissure, will cause homonymous hemianopia of the field of vision of the opposite side. A lesion of the central portion of the optic chiasm will cause bitemporal hemianopia; while a lesion of the outer edge of the optic chiasm will cause nasal hemianopia of the field of vision of the opposite side. Internal or General Sensation. In addition to these sensory impulses, which convey to the brain excita- tions from the special sensory organs and hence from the external world, there are others which come from the different organs, or viscera, of the body and, in case they reach the cortex, give rise to what are called in- ternal or general sensations. Some of these internal excitations remain entirely peripheral and affect mainljr the blood vessels; others reach no further than the spinal cord or ganglia at the base of the brain and incite those automatic acts which preserve the nutrition and the life of the individual, and still others reach the cere- bral cortex and at times affect profoundly the processes taking place in it. These general sensations have much influence on a person's moods, thoughts and actions and especially his emotions. Hunger may en- tirely alter the acts of a man or beast. Such internal or general sensations are for the most part ill-defined and ill-localized. They seem to de- pend upon the blood supply and the activity of the different organs and upon the state of contraction of the hollow organs; and they appear to have much to do with our feeling of comfort or discomfort, which latter may amount to great pain. The sensation of hunger seems to be caused by contraction of the empty stom- ach, and the various colics by contraction of the circular muscular fibers of the intestine, the ureter, or the bile duct. But the best understood of all these internal or general sensations is the composite one called "muscle-joint sense," which is mainly made up of impulses from the muscle and its tendon and the articu- lating surfaces and also from impulses from the skin and other tissues in the neighborhood, as these are stretched or relaxed in motions of the joint. The muscle-joint sensory conduction we have already considered under the term of the kinesthetic sense. The centripetal neurons entering the spinal cord through the posterior nerve roots are very numerous, being about one and a third million in man; while the centrifugal neurons leaving the spinal cord through the anterior nerve roots number less than one-half a million. The Centwfugai, Neurons Tlie Louver Motor Neurons. From the nerve cells in the anterior horns of the spinal cord axons pass outwards constituting the anterior nerve roots and run, some to the muscles of the body, others to the ganglia of the sympathetic system and others to the glands. The Upper Motor Neurons. From the nerve cells in the anterior central convolution (precentral gyrus) axons descend through the corona radiata and constitute the anterior two-thirds of the posterior limb of the internal capsule. Thence they descend through the crura cerebn and the pons and constitute the anterior pyramids of the medulla oblongata. Hence these upper motor neurons constitute what is called the "pyram- idal tract," also called the "fasciculus cerebro-spinalis. " From the lower part of the medulla a small part of the fibers of the pyramidal tract pass directly downward throughout the spinal cord, lying on the median sur- face of the anterior colunm (fasciculus cerebro-spinalis anterior or the direct pyramidal tract) ; while by far the larger part of these fibers of the pyramidal tract decussate and pass downward throughout the spinal cord in the lateral column of the opposite side (fasciculus cerebro-spinalis lateralis or the crossed pyramidal tract. The relative size of the direct and the crossed pyramidal tract varies somewhat and, in extremely rare cases, it has been claimed, no decussation of the pyramidal tract occurs. On the other hand in 15% of men decussation is complete and there is no direct pyramidal tract. The fibers of both the crossed and the direct pyramidal tracts (the fibers of the direct tract decussating in the anterior white commissure) finally ramify with the dendrons of the nerve cells in the anterior horn on the opposite side of the body from the cerebral hemisphere in which these fibers originate. The cortico-rubral tract consists of fibers from the cortex of the frontal lobes to the red nucleus. The cortico-pontile tract consists of fibers from the cerebral cortex to the pons. The thalamo-spinal tract consists of fibers from the nerve cells in the optic thalamus, their axons passing downwards and terminating near the nerve cells in the anterior horns. The rubrospinal tract (Monakow's bundle or fasciculus intermediolateralis). From the nerve cells in the red nucleus axons descend, after decussation in the tegmentum, in the contralateral side of the pons, medulla and spinal cord, in which latter they lie in front of the pyramidal tract and hence this tract is some times called the "pre-pyramidal tract" They terminate near the nerve cells in the anterior horns. The tectospinal tract. From nerve cells in the corpora quadrigemina axons descend, decussate beneath the aquaeductus Sylvii and pass downward through the formatio reticularis and the anterior and lateral col- umns of the spinal cord to the nerve cells in the anterior horns. The vestibulospinal or Deiter's tract. From nerve cells in Deiter's vestibular nucleus axons pass down- wards, mainly without decussating, through the anterior and lateral columns of the spinal cord to the nerve cells in the anterior horns. The ponto-spinal tract. From cells of the formatio reticularis axons pass in part directly downwards in the lateral column of the same and of the opposite side of the cord to the nerve cells in the anterior horns. The neurons of the last five of the above mentioned tracts constitute the extra-pyramidal motor tracts. They all terminate in the nerve cells of the anterior horns and have to do with automatic and associated move- ments, and muscle-tone. Lesions of these tracts are apt to cause motor disturbances, such as tremor, rigidity and athetosis, but no paralysis of voluntary motion, as long as the pyramidal tract is normal. Between these bundles of centripetal and centrifugal libers and connecting the former with the latter lie the central ganglionic masses of the spinal cord and brain, which receive the impulses coming through the centripetal fibers and shunt them along various different tracts of the centrifugal fibers, producing the rel- atively simple reactions of the spinal cord and the extremely complex reactions of the brain. Although the cortical motor centers represent almost exclusively muscles lying on the opposite side of the body, it appears from clinical observation and physiological experiment that the muscles of the body have a bilateral cortical representation. By electrical stimulation of the cortex, the muscles on the same side of the body may be made to contract ; although a much stronger irritation of the center is needed than is necessary to cause a contraction of the corresponding muscles of the opposite side of the body. Those muscles on both sides of the body which usually act together (diaphragm, etc.,) have especially well marked bilateral repre- sentation; so that these muscles are rarely completely and permanently paralysed in unilateral cerebral lesions. A cortical paralysis may abolish motion only and may be very circumscribed: two or three fingers, or the thumb alone. The actions which are especially lost in the cortical lesions are the purposeful actions which have been slowly acquired as the result of experience and training : actions which are peculiarly voluntary and skillful. A destructive lesion of either the upper or the lower motor neurons will cause a motor paralysis. If the lower motor neurons are destroyed there will be a paralysis both of voluntary and of reflex acts: a flaccid paralysis with atrophied and degenerated muscles (252) ; while if the upper motor neurons are destroyed there will be a spastic paralysis of voluntary acts without muscle alterations ; the reflex acts persisting and being in- creased : a spastic paralysis (251). (For explanation of the increase of reflex activity just mentioned, see page II). The Sympathetic System is not considered in this brief review of the physiology of the nervous system, because the Sympathetic System, important as it is, plays little part in the diagnosis of nervous diseases (Chart XVIId). Movements (Charts IV, V, X) When a sensory surface is irritated the animal often responds immediately by a comparatively simple movement, or the movement may occur only after a considerable space of time and may be very complicated, or it may never occur. Movements may also apparently occur spontaneously, not being preceded by any sensory irritation in the immediate past; although on careful analysis these spontaneous movements can always be referred back, indirectly, to some sensory irritation. All the actions of man or animal (for the day is past when the difference between man and ani- mals was regarded as fundamental and not merely one of degree) have their origin immediately or remotely in sensory irritation or excitation, and all these different kinds of movements may be di- vided into two great classes : subcortical and cortical reflexes, according as the neurons concerned in the production of these acts have their cell bodies situated in the gray matter of the spinal cord and basjd ganglia or in that of the cortex of the brain. Automatic acts are complicated reflex acts and may be either subcortical or cortical. Subcortical Reflexes and Inhibition (Chart V) The Simple Reflex. The centripetal nerve fibers terminate in the gray matter of the spinal cord and in that of the brain stem. Some of the nerve fibers, those conducting the impressions re- sulting from tactile, and especially those from painful, stimuli, terminate in synapsis with the den- drons of nerve cells lying in the posterior horns of the cord or in the sensory nuclei of the brain stem. Through these latter, the impulse is transmitted to a group of nerve cells in the anterior horns of the spinal cord or in the motor nuclei in the brain stem and along the axons of these lat- ter cells to the muscles, causing tliem to contract and produce a motion which is called a reflex act. This group of nerve cells innervates not one, but a number, of muscles, in varying degree, to produce a definite purposeful movement and this resulting movement is to a degree orderly: "coordinated." The nervous complex ju.st described may occur en- tirely through one segment, or metamere, of the spinal cord and is called the "unconditioned re- flex," t. e., not depending on other complicating factors or conditions. It is so simple that it oc- curs very rarely, perhaps never, in man ; although it does occur in all its simplicity in some of the 10 lower animals. It occurs in frogs and most clearly in those whose spinal cord has been separated from the brain by a transverse cut at any point above the reflex arc involved in the act. A reflex act is a reaction from an irritation, which under like conditions always take place in exactly the same way; it seems purely mechanical, as if a machine were working. The irritation may be a usual (normal or adequate), or unusual (abnormal or inadequate) one; the former being much more effective ; and it may arise from stimulation of the skin, mucous membrane, muscle tendon or fascia, or of any of the organs of special sense. The centripetal neuron, the centrifugal neuron and the connecting neuron joining together the two others form what is called the spinal or, in- cluding the brain stem, the subcortical reflex arc. It is the simplest and most primitive form of nervous reaction and is the type, or pattern, of all other more complex forms of nervous reaction. For its production there is necessary a receptor (end-organ), a conductor (neurons) and cm. effector (muscle or gland). By the neurons the receptor and the effector are brought into inti- mate connection. Usually, if not always, many groups of nerve cells lying in different levels and the coordinating influence of the cerebellum take part in the ordinary reflex activity. Such simple reflex acts are the only ones occurring in the body during the early months of life and are, at first, unconscious acts, and, indeed, many reflex acts occur unconsciously throughout life (pupillary, etc.). Similar reflex acts cause the respiratory and cardiac movements, the flow of saliva and other secretions, the vascularity of organs and consequently the wannth of the body, and in general regu- late the physiological actions of the body. These are called instinctive or hereditary actions; the result of the experience of ancestors and, therefore, called phylogenctic in contradistinction to ontogenetic acts, which are acquired by the education and experiences of the individual. Muscular tonicity is a variety of reflex action and disappears in destructive lesions of anv part of the reflex arc (240). The groups of nerve cells lying in the anterior horns and causing, when in activity, a definite coordinated movement are called "common paths." These are the paths by which nervous impulses coming from different parts of the body leave the spinal cord to produce the reflex act and are the paths which all these nervous impulses have in common ; while the sensory impulse arising from irritation of any one sensory surface is called a "private path," and is at the service of only one group of end-organs. The reflex act is influenced by many other conditions. Slight irritative lesions of the reflex arc cause exaggeration, while destructive lesions cause abolition, of reflex action. If the neurons in the cord are excited by a strong painful irritation of a peripheral nerve, as for instance the bathing of a sciatic nerve of the frog in a strong salt solution, the reflex acts will not take place. It is said to be inhibited. It can also be inhibited by strong impulses coming down to the cord from the higher nerve centers. Finally, a reflex act during its occurrence inhibits, more or less completely, all other reflex activity of the spinal cord, and especially inhibits the activity of the antagonistic muscles. The voluntary abolition of reflex activity (inhibition) may be brought about by a contraction of those muscles which antagonize the muscles taking part in the reflex act, or this latter act may be "inhibited" by a direct action upon the subcortical motor cells restraining them from taking part in it, nullifying their activity. In addition to this voluntary inhibition, a great variety of nervous ac- tivities taking place in almost any part of the nervous system (especially strong, painful impres- sions), and even the normal process of cerebral activity will cause a more or less complete inhibition of reflex activity of the lower parts of the cord. Complete destruction or section of the upper part of the spinal cord is said to abolish all reflexes in the lower part. This phenomenon, if it really exists, except as a temporary one due to shock, etc., has not been satisfactorily explained and is in marked contrast to the exaggerated reflexes found in incompletely destructive lesions of the upper portion of the cord, and appears from the most recent observations to have no founda- tion in fact. Conduction of reflex or other impulses along the peripheral nerves is equally rapid whatever may be the intensity, or quality, of the irritation, but conduction through the gray matter is much slower and varies greatly with the intensity and quality of the irritation. The gray matter also possesses the power of summation ; so that excitations too feeble to give rise to a reflex may be- ll come potent ones by repetition at very short intervals of time. The gray matter immediately fol- lowing its activity shows a "refractory period" of longer or shorter time, during which it is inexcit- able or exhausted. This indicates that the gray matter accumulates energy during rest, which it discharges when in activity. This refractory period may play its part in rhythmical action ; such as the heart-beat. Most reflex acts are purposeful and healthful in their nature. Many of them are absolutely essential for life. They may be divided into the offensive and defensive. A destructive lesion of any pwrtion of the reflex arc causes abolition of the reflex acts, as does also a strong irritation of tlie higher nerve centers. Slight irritative lesions, such as slight inflamma- tions, involving any portion of the reflex arc, vnll cause an exaggeration of the reflex act, as will also, and more commonly, a lesion which interferes with conduction of nervous impulses (in- liibitory impulses) through the central motor (cortico-spinal) neurons. An irritation, especially a continuous one, even if not very intense, wrill often cause a tonic spasm or contracture. Coordination (43, 248, 638) The centripetal neurons, which enter the cord through the posterior horns, in part, as we have just described, run forward and passing through a connecting neuron to a motor neuron in the an- terior horn form a "reflex arc." Other centripetal neurons run upwards in the spinal cord in various tracts, already described on previous pages, to the higher nervous ganglia lying within the skull. Some of these ascending neurons pass, directly or indirectly, to the cerebellum, which is the great coordinating center of the nervous system. As we have learned, the simple reflex act is coor- dinated, a number of muscles being concerned in the act, some contracting powerfully and others with varying degrees of intensity. This is due to the fact that the nerve cells in the anterior horns are arranged in groups, the starting point of the "common path;" the receptive neuron being a "private path." Each of these common paths, when incited to action, produces a definite co- ordinated movement. This coordination is very simple and applies only to one action. Most move- ments of the body consist not of one but of a series of coordinated movements in definite sequence. This complicated coordination, both for reflex and for so-called voluntary acts, takes place in the cerebellum and in lesions of the cerebellum botli these kinds of actions become incoordinate, ir- regular and ineffective. The subcortical reflex is congenitally coordinated (phylogenetic). On the other hand, coordination due to cerebellar influence is acquired by experience, training, practice (ontogenetic). The cerebellum coordinates a series of reflex acts in definite coordinated succession. The mechanism of the action of the cerebellum is very little understood. As already described, the centripetal fibers from Flechsig's tract (the direct cerebellar tract) and from the nuclei of the columns of Burdach and Goll pass through the restiform bodies to the Purkinje cells in the cere- bellar cortex. From the semi-circular canals, through the vestibular nerve, fibers run to Deiter's nucleus. Centrifugal fibers run from the dentate nucleus of the cerebellum to the red nucleus and from the nucleus and from Deiter's nucleus fibers descend to and through the spinal cord in tlie extrapyramidal tracts already mentioned. The cortex of the cerebellum is connected with the cerebral cortex by centripetal fibers through the middle peduncles. Centripetal fibers also run from the dentate nucleus of the cerebellum to the red nucleus and thence to the cerebral cortex of the frontal lobes (the cerebello- nibro-frontal tract). The cerebellum has, therefore, very wide connections. From recent investiga- tions there seem to be definitely localized coordination centers in the cerebellar cortex similar to those long since demonstrated to exist in the cerebral cortex. The Cortical Reflexes In addition to the ascending neurons passing to the cerebellum, others ascend to their final termination in that portion of the cerebral cortex which lies posterior to the fissure of Rolando, being interrupted in their course by various ganglia at the base of the brain. These so-called "sensory projection fibers" which spring from definite sensory end-organs terminate in definite and distinct cortical areas. Thus, the fibers from the retina (optic fibers) terminate in the occi- pital lobe; those from the nose (olfactory fibers)and those from the mouth (gustatory fibers) ter- minate in the cornu Ammonis; those from the ear (auditory fibers) terminate in the anterior trans- 12 verse temporal convolution, those from the skin (tactile fibers) terminate in the posterior central convolution and those from the muscles (muscle sense) terminate in the inferior parietal lobule. These localized areas constitute the anatomical basis of cerebral localization (Figs. 15 and 16). They are all situated in the hemisphere contralateral to the peripheral sensory organs from which their long projection nerve fibers spring (having passed through sub-cortical ganglia in their course). These areas are all connected together by nerve fibers (axons) which connect every portion of the sensory cortex with every other portion. These are called "association fibers." Finally, from each of these localized diflferentiated sensory areas, bundles of axons pass forwards under the fissure of Rolando to the anterior central convolution and its immediate neighborhood (the so-called motor area of the cortex) and come in contact with groups of neurons, the axons of which constitute the pyramidal tract and terminate in those groups of nerve cells in the anterior horns of the cord which we have already described and to which we have given the name of the common path along which impulses pass to the various groups of muscles. These groups of neurons whose cell bodies lie in the anterior central convolution (the motor area) may be called the common path for the impulses coming from the sensory area of the cerebral cortex. It is quite possible, then, for a nervous impulse entering the spinal cord through a posterior nerve root, not only to pass forward to the motor neurons in the anterior horns and produce a reflex act, but also to ascend by the sensory projection fibers to the cerebral cortex posterior to the fissure of Rolando and there to be reflected to a common path in the anterior central convolution and thence downwards along the pyramidal tract to the same common path in the anterior horn through which the spinal reflex impulse passes. The gray matter of the cord is compressed into the center of the cord, of which it forms a long continuous "H" shaped axis. Its transverse area is so small that an impulse entering through the posterior roots finds a sliort and easy route to the common path and passes along it so quickly that it is not apt to be modified or inhibited by any other impulse reaching the common path at the same instant. Subcortical reflexes are, therefore, quickly and definitely performed and are relatively simple in character. The gray matter of the cerebral hemispheres, on the other hand, is not compressed into their centers, but is spread out in a large area over their entire surfaces, which are themselves, greatly increased in extent by their numerous sulci. When an impulse reaches the cerebral sensory cortex through the sensory projection fibers, it may pass, as we have said, to a common path in the motor cortex. It may also pass through the association fibers to many, widely separated, areas of the sensory cortex and set their neurons in activity. Through these latter numerous neurons, impulses may also pass to the same common path, some tending to increase, others to impede or abolish, its activity. The cortical reflexes are, consequentiy, slower than the subcortical and do not follow immediately up)on the excitation. They may, indeed, be delayed days, weeks, even years after the time of the original excitation which was the primary cause of them. They may never occur. They may be exceedingly characteristic individual acts very different from the stereotyped reflex acts and may consist of a great variety of successive acts. Just as the subcortical reflexes, so the cortical reflexes have been the object of much experi- mental work. One of the earliest of these recent series of experiments was performed by Pav- low. His results, stated briefly and without details, are that the salivary secretion of a dog, which is normally caused by food in his mouth, can be excited, after a course of training or edu- cation, by optic excitations (one of various colors or of different intensity of the same color), or by auditory excitations (one of various sounds or different intensities of the same sound), with- out food in any way entering into this final acquired reaction. This reaction will not occur if the corresponding sensory cortical area be destroyed. A very slight sensory excitation occurring at the same time will abolish or impair it. It is a cortical reflex but has in large degree the character- istics of the spinal reflex. It is called the "conditioned reflex" in contradistinction to the "uncon- ditioned" reflex : the normal response to food. The conditioned reflex is not acquired by punish- ment and reward, but merely by association and, when acquired, does not result in pleasure or pain. It is a true reflex with no emotional content. Somewhat analogous reflexes (sometimes called motivated reflexes) have been acquired by 13 animals as the result of long training by means of punishments and rewards: such as rats finding their way through a maze and the training of animals in various ways, and more broadly in "forcing the formation of sensory habits." Much and most fruitful work has been done in this line. The human being undergoes a very similar training, directed by rewards and punishments, in the home, the school and in life. The cortical reflexes, often called the "association reflexes," and known by a still older designation, "voluntary movements," are the result of education. Given the knowledge of a per- son's education, and enviroment in all its details, his acts can be predicted with a great deal of certainty and are practically so predicted by his fellow men, even though they do not know all the details of his heredity, which knowledge is, of course, also necessary for an infallible judgment. (See voluntary movements.) The subcortical reflexes, the simple reflex acts, may be entirely unconscious ones. They are most marked when by a lesion the spinal cord in its entirety or its lower portion is separated from the brain, and in such cases (which are of not infrequent occurrence) the individual has no con- sciousness of the movements of his arms, or legs or sphincters, unless he is looking at them. The cortical reflexes, on the other hand, are usually associated with very remarkable phenomena (including consciousness), which we have next to discuss. Before doing so it may be noted, as a summary of previous statements, that there are three ways, and only three, in which an animal responds to the various stimuli coming from the external world : 1st. Reflex Acts which are centered in the spinal cord and brain stem, and which are relatively slightly, or not at all, modified by other stimuli. 2nd. Automatic Acts, centered in the corpus striatum and nucleus lenticularis and greatly modified by other stimuli including the emotions. 3rd. Volutary Acts, centered in the cerebral ■ cortex and profoundly modified by many stimuli arising from present and past perceptions, matured judgments, habits and emotions. The "So-called" Psychic Functions (Charts III and XVI) So far in our discussion of cerebral activity (the excitation of the sensory cortex and the con- ditioned, motivated and associated reflexes which result), we have been dealing with facts which can be definitely proved by anatomical and physiological investigation. What we have considered however, does not, by any means, include all the phenomena connected with cerebral activity. When a nervous impulse reaches the sensory cortical area it produces, if of sufficient inten- sity, a phenomenon called sensation. Thus, when we are looking at a tree we appreciate something which we call the sensation of the sight of a tree. It is often called the image of a tree although there is in the brain nothing like an image on a photograpliic plate of the tree, but rather a cor- tical activity which is the symbol of a tree. Moreover, while we are looking at the tree, there is tak- ing place another cerebral activity of which we are entirely ignorant and unconscious — a permanent change occurs, whether static or dynamic, which constitutes a memory of the tree; so that when we close our eyes an image of the tree may remain, which we clearly see and which is perfectly true; although it does not possess the quality of reality. This memory of this identical tree re- mains permanently in the brain, potentially, and can at any time be brought into consciousness (a term later to be defined) by a process which is called the as.sociation of ideas (also later to be defined). Sensation and memory are the basic factors in psychology and upon them is built up the elaborate structure of this science, whether it be called introspective or phy.siological psychology. Sensation undoubtedly is a manifestation of force, the product of the oxidation of the nutriment in the blood and ceases as soon as the blood ceases to flow in the corresponding part of the cerebral cortex, but no psychologist or physiologist has ever satisfactorily, or even intelligibly, defined what sensation really is. This is true of many of the other natural forces. To mention only two: gravitation and electricity have never been explained. Their essential nature, after centuries of observations, is not yet understood. This does not prevent our studying them and discovering 14 that they invariably act in certain well defined ways, tliat they follow certain laws ; and by avail- ing ourselves of our knowledge of these laws these forces have become our very useful slaves. It may be that in the future we shall discover the essential nature of these forces more or less com- pletely, but that day is not yet. We may also discover what sensation is, but it can even now be studied, and as a matter of fact this form of energy is being experimented with in every psycho- logical and physiological laboratory in the land. The Psychology handed down to us by our fathers attempts to solve these facts by traditional authority, by abstract reason and by introspection and has introduced the element of the super- natural and of mystery. The result after thousands of years of this study has been far from satisfactory. Our knowledge acquired by these means has advanced little, if at all, beyond that of the ancient Grecian philosophers. To the physiological psychologist of recent years these facts still await solution ; but to him they are the result of cortical activity and do not require, and prob- ably will never require, a supernatural explanation. What sensation is, has not been explained either by the scientist or by the philosopher. To the former, however, it appears to be energy pro- duced by cortical activity. The mystery of the mechanism of the animal body is beirig slowly dispelled by investigation. This investigation has been carried on, and is being carried on, under many difficulties. The dis- section of the human body and experimentation on animals is still repugnant to many. The prej- udices of mankind have to be reckoned with. Many higlily educated men, while granting that most of the organs of the human body are in their activity subject to ordinary physical laws and that the source of their activity is the nutriment in their blood supply, are, yet, unwilling to grant that the activity of the nervous system is to be explained in the same way. They point out that most of the internal organs take certain chemical substances from the blood and convert them only into other chemical substances and that the chemist in his test tubes and other apparatus can imitate these reactions more or less perfectly. They omit to state, however, that there is one set of organs, the muscular system, much more extensive than any other organs in the body, which takes the nutriment from the blood and transmutes it into a form of energy, contractility, and, thus, does exactly what the nervous system does, when it transmutes the nutriment in the blood into forms of energy called the sensation, consciousness, etc. The reason that I am devoting what may appear to be too much space to this subject is that I am desirous of presenting the physiology of the nerv- ous system on a physiological rather than on a mystical basis; and, yet, what is here presented is but a bare outline of the subject and is in need of much amphfication. Sensation and consciousness, whatever their nature may be. are the fundamental elements m any aspect of psychology or of cerebral physiology, if, indeed, any distinction can be drawn be- tween these two sciences. They are the "Axiom" or the "Given" of mathematics, of logic and of psychology. They are self-evident propositions which cannot be further analysed. Sens.\tion (Ch.\rts VI and XIV) When the various impulses originating in the sensory end-organs have passed along the various tracts and have traversed, and been interrupted by, several masses of gray matter, they reach the sensory area of the cerebral cortex and there give rise to a new form of energy called sensation. That is to say, a physical force (as for instance, ether in rapid undulation) is con- verted in a terminal organ into nervous energy, and as such, having traversed the sensory tracts, reaches the cerebral cortex. It is there transmuted into a new form of energy (as for instance the sensation of light). The sensation of light takes place in the brain, not in the eye, and has no similarity to the undulations of ether from which it normally originates, and it may, indeed, be caused not only by these, but also may originate, in perfect darkness, from mechanical irritation of the eye (as by pressure from the finger upon the eyeball) or of the optic nerve. Sensation is, therefore, rather a symbol than a picture (the image of the older psychology) of the external ob- ject, with wliich by experience it is associated. Sensation is thus a special, individual form of energy, similar to electricity, hght, etc., which is produced in the cerebral cortex and which has its special individual characteristics. It has an 15 analogy to electricity produced on amber by friction. Sensations originating from the different organs of sense are located, as we have seen, in different and special portions of the cortex (Figs. 15 and 16) and do not at all resemble the external phenomena causing them. A clap of thunder and a flash of lightning are very different external phenomena, but the reactions in the cortex, which constitute these sensations, probably \^ry in topography rather than in quality. We know nothing more of the essence of this form of energy, which we call sensation, than we do of the essential nature of electricity, or of contractility in the muscle fiber or in the amoeba. We know something of its effects and we know something of the locality of the cerebral cortex in which it occurs (Figs. 15 and 16) and that it is very dependent upon abundant blood supply and we believe that it depends upon physico-chemical actions taking place in the cortex. Conscious sensation, probably, occurs only in those animals which possess cerebral hemispheres. Sensation and all other forms of mental activity are absolutely dependent upon a fairly healthy cerebral cortex and a fairly abundant blood supply to it. When the cerebral hemi- spheres in an animal are removed, or when the cerebral cortex in man is entirely, or mainly, de- stroyed by disease, or in a child the hemispheres are absent or very defective, or when the blood supply is cut off from the cerebral cortex altogether or in large part, then sensation, perception, memory, thought, emotion (and its corporeal expression, except in anger), ethics, association of ideas, voluntary' motion, inhibition, intelligence, personality and consciousness are all lost. Sensation is the simplest manifestation of consciousness (see later) or cognition. For its production a certain degree of intensity of the nervous impulses is essential (the threshold), below this point of intensity the cortex may be in activity, but sensation will not result; the activity vrill be subconscious. A series of slight subliminal impulses. o,uickly repeated, may by summation cause sensation. There is, therefore, a minimum of intensity necessary for sensation ; just as electricity passing through a wire must have a certain intensity before the wire glows and light is produced. There is also a maximum beyond which, no matter how great the irritation, there is no increase of sensation, but rather a diminution from exhaustion of the nerve cells. Between this minimum and maximum point, sensibility increases, or diminishes, not continuously, but by little steps : a definite ratio to the stimulus, in accordance with Weber's law, which, although not absolutely, is approximately, correct, especial'y for stimuli of moderate intensity. Furthermore, a weak or moderately strong excitation may reach the cortex at a time when other portions of the cortex are in such strong excitation that this weak irritation may produce no sen- sation, but remains subconscious, is inhibited by the stronger cortical activity. The line between the con5^ious and the subconscious cannot be sharplv drawn. Subconscious cerebral activity is much greater in volume, although much less in intensity, than is cerebral activity resulting in consciousness. Scnsatior is the intcr-reaction between a relatively strong nervous impulse from an organ of sense and f'' • cortical activities constituting the memories of those previous perceptions, emotions, etc., which rr- the individual's personality. Perceptions and Concepts (Chart VI). A perception consists of a combination of sensations, which are obtained from various sensory end-organs, all of which proceed, usually simultaneously, from the same external object. A percep- tion of an apple is composed of several sen.sory impulses: of visual sensations caused by nervous impulses from the retina, representing the outline and markings and color of the apple; of muscle sensation caused by nervous impulses from the ocular muscles, representing its distance from the eye, its position in relation to other objects and to some extent its form; of tactile sensations cau.sed by nervous impulses from the hand, representing its form, firmness and texture ; and of gustatory sensations caused by nervous impulses from the mouth, representing its taste. The various physico-chemical changes, thus set in activity in the cortex, combine to produce the full perception of the apple, which perception is greatly modified by our emotions, moods, memories and the then present other perceptions, and is not exactly the same, sometimes widely different, in different men. The perception of an apple by Adam was probably very different after the fall of man than before it. For a full and complete perception, consisting as it does of so many ele- mentary sensations, quite an appreciable time, or frequent repetition, is needed. It is quite pos- 16 sible that a full perception may consist both of conscious and subconscious elements. The kinesthetic sense, for instance, is rarely, if ever a conscious sensation. The development of a perception is found by experiment to proceed from generalities to details. A combination of the full perceptions of many apples, each resembling and at the same time in some respects differing from the others, produces the idea or concept of an apple, with which is associated its written or spoken name and any other experiences or knowledge which have become associated during our life with apples. (See also under Association.) A concept is, therefore, an abstraction. Perceptions occur in the cerebral cortex in immediate proximity to the cortical termination of the corresponding projection fibers. Each cortical center consists of a smaller portion, in which the projection fibers terminate, and a larger portion, in which perceptions take place and in which their memories are stored. Thus, the optic fibers terminate in the lips of the calcarine fissure, while the rest of the median and convex surface of the occipital lobe is devoted to optic perceptions and memories (Figs. 15 and 16). When sensations only, but not perceptions, can occur, as when that portion of the center in which the projection fibers do not terminate is diseased, the condition is called, in general, agnosia. When there is a failure of tactile perceptions the condition is called astereognosis; in failure of optic perceptions, soiil-Uindness, or psychic blindness, and in failure of auditory perceptions, sotiU deafness, or psychic deafness, or auditory or sensory apliasia. When that portion of any sensory area of the cortex in which the sensory fibers terminate is diseased, both perception and sensation are abolished. Memory (Chart III) When perception takes place, physico-chemical changes are occurring in a definite portion of the cerebral cortex, which not only produce the perception, but also leave, thereafter, a perma- nent alteration in the cortex (a vestige). The energy derived from the chemical changes taking place in the cortex during an active perception may result in a structural, physical or chemica] change in the nervous elements, or more likely in the storing in them of potential energy, which can be liberated and become actual later. Memories seem to be dynamic changes in nerve cells and fibers which reduce the resistance to subsequent similar impressions or excitations. Cer- tainly, a definite change is brought about which registers a permanent memory of the object per- ceived and subsequently this memory can be latent or active from time to time. Consciousness, the actual perception of an object and its associated active memories (active attention), is a very exhausting, energy consuming process for the cerebral cortex. Subconsciousness, and the pres- ervation of memories, not actually present in consciousness, are not exhausting to the cortex, even though the memories be preserved for many years. In virtue of this change in the cortex, a memory of the corresponding object always results from excitation of this altered cortex. The memory may be aroused, or enter into cog- nition, by the external force which originally caused it and, then, the object will be recognized (re-known), because the actual perception .corresponds perfectly vnth its memory; or the memory may be aroused by way of association fibers which the original perception had previously set into activity. Memories become associated with each other in accordance with the relationship of the objects causing them, as the result of our experiences with these objects. In perception, then, a trace of the cortical excitation remains in the cerebral cortex as a memory, in a sense analogous to the persistence of the after-image in the retina after strong excitation (look- ing for some time at a bright light). The retention of any memory depends upon the frequency of he perception causing it, its interest and its startling nature. The recall of a memory is by ^vay of the association fibers from a perception or some other memory associated with it. In comparing an actual perception of an object, or an experience, with its memory, if the two exactly coincide and resemble each other, there is not only the act of recognition, but also what is called "identification" and "similarity;" whereas if the perception and the memory of a former per- ception do not exactly coincide, there is what is called "non-identity" and "dissimilarity," and this action is called "discrimination." This cerebral activity with its two results: identification or discrimination, is the basis of classification, systematizing and iudgment. 17 Memories are, however, very different qualitatively from the original perceptions. The for- mer have no actuahty. Even though they may be at times very vivid, they never seem real to a normal personality. This is due to the absence of any nervous impulses coming simultaneously from the peripheral sense organ, especially from its musculature, which were present in the original perception. They are never so intense as the original perception. It is almost, if not quite impossible to recall a memory derived from any peripheral organ of sense, while that organ is engaged in producing an actual perception ; the actual perception is much too strong for the mem- ory and the latter is inhibited l)y the former. The cortex of the brain is in great part a huge store-house of memories. The memories of any object vary in different men according to their training, education, attention and former asso- ciations with the object. These memories are grouped together ; so that those which are derived from the same organ of sense lie together in the cortex. This localization of memories has been worked out with great care and is to a considerable extent known. It is shown in figures 15 and 16. A local cortical lesion may thus produce a loss of a group of allied memories. All memories are sensory in character with the excephon of one extremely doubtful group. This group consists of memories of so-called "innervation feelings." When a muscle is con- tracted the person to whom it belongs has a feeling of this contraction and can estimate its strength. Such innervation feelings, if existent, are sensory, but it is difHcult to be conscious of them. They are, in the main, subconscious. This feeling is called an "innerva- tion feeling'' and its memory, it is claimed by some investigators, is stored away in the cortex of the anterior central convolution and especially in the neighborhood in front of it. This innervation feeling, it is claimed, is essential for the voluntary performance of the corresponding act. When, in consequence of a cortical brain lesion in the area in which these memories are stored, a person loses the power of performing certain acts, he often says, "I have forgotten how to do it." These innervation feelings and memories, if they really exist, do not obtrude themselves strongly into our consciousness. They have rather to be sought for. It is, indeed, very difficult if not impossible to be conscious of them. They may, however, be subcon- scious and play their part in the production of complex perceptions. There are many physiologists and psychologists, however, who question whether there are any so-called innervation felings or memories, and regard the cortical motor cells as merely "common paths" similar to those in the spinal cord. However that may be, whether true innervation memories exist or not, the function of this cortical area is an actuality and whenever a portion of the motor cortex is sufficiently excited by a cellular activity, a perception, or a memory, in the sen- sory cortex so-called voluntary, or association, action results. (See Voluntary Movements). CoNSCrOUSNESS AND SUBCONSCIOUSNESS (ChaRTS III AND IV) Con.sciou.sness and subconsciousness are terms used to express the fact that the cerebral cor- tex is in activity. Although convenient expressions, they should not be regarded as representing di.stinct, possibly conflicting, entities. They are both component parts of the personality. The difference between them is only one of degree: the degree of intensity of the local cortical activity which produces them combined, perhaps, with a sense of "friction" which the intense activity meets in passing through the cortical neurons. .A.s this resistance decreases with repeated use an act, at first conscious, may become .subconscious. A person is at times unconscious of his habits : his habitual acts. .\t one instant a sen.sation, a perception, a concept, an idea, a thought, a judgment or some other product of cerebral activity is present in consciousness becau.se of a strong local cortical activity and the next instant the activity becomes less, is replaced by another strong local cortical activity, and the former ceases to be present in consciousness and becomes a part of the subconscious cerebral activity. There is, thus, a constant interchange between local corti- cal activities and consequently the content of consciousness is constantly changing. The fact tliat an intense cortical activity makes its resulting energy an integral part of consciousness, makes it al.so a dominant factor in any judgment or action which may result. Normally, during life, there is constant cortical activity, whether it is an activity resulting in consciousness or subconscious- ness. Furthermore, there are all degrees of intensity of this activity and consequently varying de- 18 grees of consciousness from vivid expectant attention (concentration), to passive attention (rev- erie) to semiconsciousness, to stupor, to dreams (by night or by day), to subconsciousness and, in the absence of all cortical activity, to unconsciousness. What consciousness really is we know no more than we know what it is which is exhibited by amber when it is electrified by friction. Yet we do not hesitate to say that electricity is a form of energy, or force, produced by friction upon amber, by a dynamo, or by numerous other means ; and just as we say that the potential energy of coal may be converted into electricity ; so we may say that the potential energy in the blood (derived from food) is converted in the cerebral cortex into conscious sensations, percep- tions, etc., or, taken collectively, into consciousness. Consciousness consists, at any instant of time, of the then present perceptions and of those past memories wliich are directly or indirectly associated with these present perceptions and which have been awakened by them into activity at that instant of time. Consciousness is thus a form of energy resulting from a high grade of activity of the cerebral cortex. The other memories, at that instant active, but not active with sufficient intensity to enter into consciousness, constitute subconsciousness and may at any time become conscious memories. The content of consciousness embraces only a small fraction of those activities which take place in the brain and indeed only a fraction of those activities which take place in the cerebral cortex at any instant of time. The cortical activities constituting consciousness are very much less numerous and extensive than those constituting subconsciousness. When we first dress each morning, we are conscious of the contact of our clothes with our skin, but soon this sensation ceases, is replaced by others and the cortical activity caused by the contact of the clothes becomes subconsciousness. It still persists, however, and if by way of association fibers its activity be slightly increased it will again enter con- sciousness and the sensation will again arise temporarily. We walk in the street and are conscious of seeing and hearing many things, but many other things cause cortical activity of such low in- tensity that we fail to be conscious of them. They remain subconscious and a faint memory of them persists which may later be brought into consciousness by way of the association fibers, the impulses from wliich may increase the subconscious activity to a degree which constitutes con- sciousness. A familiar example is that of a man whose attention is so fully occupied that he does not hear the striking of a clock, but later recalls the memory of this sound, which memory was ob- tained subconsciously. Consciousness and personality can probably be best studied in their forming in infancy, and in such a study they may well be found to consist essentially in the action and interaction of each new perception on the few other perceptions previously acquired, which at that date constitute the rudimentary personality of the child. A new born babe has, probably, no consciousness. An infant attains consciousness slowly as he gradually obtains perceptions and memories and forms a large number of associations of all kinds. When an infant has his first perception this one percption, together with certain rudi- mentary sensations he may have acquired, constitutes his entire consciousness and his entire in- telligence. It is all he knows. As other perceptions are obtained and associated together his intelligence and his consciousness become larger, more distinct and more complete. The child in his development increases with great rapidity the num- ber of his perceptions, less rapidly and subject to many subsequent corrections his associations, still less rapidly his concepts, even more slowly his ethical and aesthetical ideas, and yet more slowly his abstractions. But at the end of a few years any perception or memory suggesting action is subjected to the interplay of all these activities before the action is done or left undone. In other words, consciousness and the act of thinking and reasoning on which action is based (see Voluntary Motion) are already, even in cliildhood, very complicated, perhaps more so than in later life, when action is mainly determined by habits of thought and by judg- ments firmly established by numerous experiences. Consciousness is a form of energy, such as light and electricity, ivhich is transmuted from other forms of energy by physico-chemical action taking place in the cerebral cortex. Consciousness embraces all those chemical activities which have a certain intensity; below this degree of inten- sity the activities constitute subconsciousness. The process is somewhat analogous to that in an 19 electric light btilb through which an electric current may be constantly flowing, but which only gives forth light when the current has attained a centain intensity. Consciousness is constantly being newly formed and is dependent upon the perceptions, memories, feelings and ideas, ethical and others, present at any one instant. These phenomena themselves constitute and are consciousness. None of them, usually, continues. Others are con- stantly replacing them. None remains constant. The continuity of consciousness is preserved by the mingling of memories of past perceptions with present ones, and by memories of past states of consciousness. Consciousness has narrow limits. It cannot contain many perceptions, ideas, etc., at the same time. We daily take advantage of this. When a child or an adult is conscious of a painful per- ception or idea and is consequently unhappy we suggest to him another perception or idea and emphasize it until it replaces the painful one, which sinks into subconsciousness and is less domi- nant. Just as reflex action taking place in the spinal cord temporarily inhibits more or less completely the activity of the rest of the cord; so a strong activity in the cerebral cortex tends to inhibit the activity of the rest of the cortex and to dominate consciousness. This strong local cortical activity is accompanied by a local increased blood supply, as can be shown by the ther- mopile. The blood supply is, therefore, in constant, more or less rapid (usually rapid) ebb and flow throughout the different areas of the cortex, being most abundant in those areas which are in activity. Consciousness is a condition which, as yet certainly, we do not understand, al- though in a general way we regard it as the result of chemical changes taking place within the cere- bral cortex. The chemical changes themselves are not consciousness, but they produce this form of nervous energy very much as a steam boiler and a dynamo, or a galvanic battery, produces elec- tricity. We are as ignorant of the exact nature of consciousness as we are of that of electricity. These chemical changes produce consciousness (or rather the perceptions and emotions which constitute it), a form of nervous energy; just as the chemical changes taking place in any living cell or tissue of the body produce a form of energy peculiar to itself. Consciousness is thus locally and continually produced in the brain. The cortical activity causing it passes according to definite channels to other regions of the cortex, surges through the brain, awakening memories and ideas and causing actions and reactions. The subject is a most difficult one and is made, in a sense, more difficult by the ambigviities of language, which allow us to replace an idea by a word of somewhat uncertain definition and thus leads to uncertain and faulty reasoning, or to a high sounding sentence which means nothing. Consciousness, or cognition, seems to be something added on to the essential processes taking place in the brain. The various association reflexes occurring in the brain could take place and do take place quite accurately without consciousness, as for instance in the automatic acts of the somnambulist, or in the epileptic trance. That consciousness has any power to influence cerebral activity and the association reflexes is not evident and has not been proved. That frequently it cannot do so is proved by the oft recur- ring condition where an idea is present in consciousness which the person is anxious to dismiss but his consciousness even combined with his so-called will power is unable to dismiss it. Only when by the association fibers a different and stronger local cortical activity is awakened will the distressing idea fade away. The brain is very abundantly supplied with blood, e.specially the cortex, and the latter is very sensitive to any interference with its blood supply. Loss of consciousness, which occurs nor- mally in sleep and pathologically in many conditions, is caused much more frequently by a change in the quantity (anemia) or quality (drugs and poisons, including sepsis and other autogenetic toxic products) of the blood supply than by all other conditions combined. Perver.sions of conscious- ness, on the other hand, seem to depend less upon the quantity of the blood .supply than upon its quality (poisons) and upon changes, organic or functional, in the cerebral cortex, especially upon its exhaustion. Finally it is to be remembered that the cortical cellular activities not only accompany (are the cause of) but precede sensation, consciousness and the other "osychic" functions. The con- 20 ditioned reflexes are cortical activities, but they occur in infants and animals unconsciously and prior to any e^ndence that the "psychic" functions as yet exist. Emotions (Chart III and IV) The great majority of sensations perceived by an individual during his life are followed by the reactions in the nervous system already described. There are, however, sensations and per- ceptions which are accompanied by an emotional content — pleasure or pain, according as their con- tent suggests the well-being of the body, a richer and happier life on one hand; or death, or a re- stricted and unhappy life on the other hand. Heredity, early education, past experiences and asso- ciations, also, influence the emotional content of a perception. Such perceptions with an emotional content, cause an abnormally powerful reaction on the part of the nervous system. The emotional reflexes are among the earliest to be observed in the infant. It appears from experi- ments on animals that the emotions of pleasure are the result of, or at least are influenced by, cortical activity; while the emotions of pain, anger and displeasure occur after the removal of the cerebral hemispheres and are the result of the activity of the basal ganglia. These emotions produce a strik- ing effect upon the functions of the abdominal viscera as has been abundantly proved by animal experimentation and human experience. Thus, pleasant sensations promote the activity of the muscles and glands of the stomach: while unpleasant sensations retard, or entirely arrest, this activity. But, by far, the most striking and important influence of the emotions upon the somatic activities is that manifested by anger and fear upon the secretion of the suprarenal glands and the consequent rapid and excessive production of adrenalin. The emotions of anger and fear are usually followed by violent muscular activity whether in the form of fighting or flight. It has been proved by experimental and clinical evi- dence that adrenalin appears in increased quantity in the blood within a few seconds or a few minutes after the occurrence of violent anger and fear. Furthermore, it has been proved by ex- periment that adrenalin in excess in the blood causes first an increase in the amount of sugar in the blood which is essential for muscular contractions; second, a dilatation of the bronchioles and in- creased rapidity and power of the heart action, thus causing an increased amount of oxygen in the blood which is also essential for muscular contraction ; third, prevents muscular fatigue and re- stores power to exhausted muscles, and fourth, quickens coagulation of the blood. All of these conditions are of great practical value to the angry or frightened animal, whether in a fight or in a flight. In addition to these violent emotions, there are more gentle emotions of pleasure and pain which we call "feelings" and which are due in part to internal, or general, sensations from the body itself and in part from the success or failure of our undertakings in life. When the bodily functions are disordered we have a general feeling of discomfort and when all is working well we have a sense of buoyancy and exaltation; all moves smoothly without friction, as in a well oiled machine. These internal sensations, as was mentioned on a previous page, are ordinarily the dominant factor in our feelings and emotions and greatly influence also our voluntary actions, which for instance may be altogether different in a state of hunger from those in a state of satiety. Indeed the internal sensations, such as hunger, etc., are very often themselves the cause of extensive voluntary acts, which usually result in the relief from this sensation. As these internal sensations vary from time to time, our moods change, and perceptions, which at one time are pleasant, may at another time be unpleasant. Ir- respective of our moods, however, some perceptions are almost always pleasant, others are not. Things which tend towards the preservation and health of oneself and one's family are usually pleasant and vice versa. Perceptions to which we have become accustomed are usually pleasant, and even unpleasant perceptions by frequent repetition at times become bearable and even pleasant. Not a few perceptions are accompanied with relief or discomfort, as when hunger is as- suaged, or we accomplish something desired, or in some way contribute to our well-being or suc- cess and thus give pleasure; while other perceptions act in a contrary manner. These feelings of pleasure and pain may be due in part to the intensity of the sensation or perception ; in part to 21 heredity, as a result of evolution, in the case of objects desirable for the health of the body; but in greater part to associations (see Association) with previous similar perceptions, and in greatest part to feelings of satisfaction or dissatisfaction with the result of one's actions. Sensations of moderate intensity are usually pleasant; sensations of very great intensity which produce abnormally strong reactions in the nervous tissues, are usually unpleasant, while those wliich liave a complicated ratio are usually also unpleasant, which is especially true for musical sounds. Foods which nourished our ancestors usually taste good to us. The child possibly acquires a taste for sweet things from the sugar in its mother's milk. Most of our pleasant and unpleasant sensations are the result of our education. They are, therefore, much more pronounced in adults, especially educated ones, than they are in children ; although the expression or manifestation of them is less pronounced, more inhibited or restrained by other cortical activities. A perception which is associated with, or followed by, pleasure or pain will always, or for a long time, as often as it occurs actually or in memory, be accompanied by a pleasant or painful emotion, whether the memory of the original pleasant or painful result associated with it is present in consciousness or not. On the other hand, our emotions or rather "our moods," depend in great part on our success or failure in life. Mankind does not find itself in this world with all its needs and wants satis- fied; on the contrary, everyone must acquire food, clothes, habitation, warmth and a hundred other necessities. A man who sees his neighbor with something good, which he has not, desires it, or something similar. These wants and desires are the great, almost the only, incentives to volun- tary action. When tliis voluntary action results in success we have in it our greatest pleasure and when it results in failure, our greatest unhappiness. All things connected with our success receive an associated emotion of happiness; while those things connected with our failure receive an associated emotion of grief. In these various ways a certain number of our perceptions have associated with them an emotion (204), or mood, or tone, of pleasure or pain, greater or less, and a series of such emotions, or one long continued, will make us happy or unhappy for a considerable length of time and will constitute what we call our "mood." In certain abnormal states of the cerebral cortex (exhaustion, circulatory irregularities, poison and other less known disorders) the emotions become dissociated from the ideas with which they are normally associated ; so that all cerebral activity' is accompanied by one emotion : in some cases, sadness; in others, fear; in others, joy and in others apathy or absence of all emotion. An emotion is often so strong and so occupies the patient's consciousness that it is im- possible, or nearly so, to attract his attention. Such an abnormal mental condition occurs in some forms of insanity. Association The essential physiological characteristics of nervous tissue are: first, its excitability, its reaction to .stimulation by the discharge of nervous energy stored within it, and second, its transmissibility ; this nervous energy, wherever produced, does not remain localized, but tends to pass along nerve fibers, throughout its own neurons and to other neurons. The channels along which it will pass depend upon the anatomical arrangement of the fibers. In consequence of heredity and evolution, certain channels are easier for the passing of this nervous impulse than are others. This is especially true of certain reflexes present at birth, such as breathing, suck- ing, etc. Other channels are made easy later in life by the constant passage of impulses along them. The more frequently an association fiber and the synapse connecting two fibers are used the better conductors they become. The way that has once been traversed and that has often been traversed becomes the easiest way. It is the way of least resistance and it is a universal rule, whether it be a foot-path or a conductor of electrical or of other force or a nerve fiber or cell or a synapse separating two cells, that the way of least resistance is the easiest way: the way usually followed. When not used for a long time, like a deserted garden path, the cliannel may be obliterated and the association lost. When a perception occurs, impulses radiate out along the association fibers from that por- tion of the cortex which produces it. If at the same time another perception, (usually there are 22 many), or a vivid memory of a perception received a moment before, takes place in another por- tion of the cortex, the association fibers connecting these two or more portions of the cortex, where perceptions are occurring, or have just occurred, being acted upon at both ends, will convey im- pulses to and fro more readily than the other association fibers. The details of this process are ob- scure, but it seems evident tliat the longer and more frequently the association fibers are traversed by these impulses the better conductors do they become and these two perceptions become more and more easily excited the one from the other. They may also be excited through the mediation of a third memory associated with both of the others. The activity in the cortex does not long persist; so that when the associated idea is in consciousness, the original perception which awoke it is al- ready, or soon will be, subconscious. Yet they are firmly associated together; so that whenever in the future one enters into activity it may excite the other. Thus, association between percep- tions of the events and objects received simultaneously, or immediately before or after each other, are formed in a never-ending stream and the events and objects are considered as contemporane- ous and often as related to each other. Subsequent experiences may verify and strengthen some of these associations and may disprove and unmake others. Associations with any one perception may be, and usually are, extremely numerous. There is also an association of words as well as of perceptions and the associations of words have no necessary relationship to the associations of the objects which they represent. Associations may be at first very imperfect and very difficult to form, but with repetition and practice become easy. The work of a child in school is difficult until by repetition he has learned thoroughly his lesson. Then the recitation is easy. Addition subtraction, etc., are at first performed slowly and with difficulty but later, in consequence of fre- quent repetition, rapidly and easily. The association between question and answer becomes firmly established. When a number of perceptions are produced which are very similar and yet show more or less individual variations, as for instance perceptions of men or dogs, from a comparison of them and of memories of others, more or less similar, a concept or idea of a man or a dog is formed which includes all the individuals. From many examples of individual freedom of action, the abstract idea, or abstraction, of liberty is formed. A great many such abstract ideas are gradu- ally formed and this process is facilitated by the use of language. But each idea is the result of experience: the result of a conglomeration or generalization of one or more perceptions and their associations, and, by the aid of language, is given a name. It has been said that "we caa understand only so much of an abstraction as we know individual cases which sustain it." Think- ing and reasoning are much simplified and made more rapid by the employment of these abstrac- tions. A concept, idea, or abstraction, differs in different persons in consequence of their different experiences, of their education and of their associations with the perceptions involved. Ethics Inasmuch as the sensory and motor areas of the cortex are intimately connected together, some perceptions lead to voluntary action, which may result in pain, either directly as physical pain, or indirectly as mental pain, the result of punishment or condemnation ; so that the action and the perception which led to it will become associated with these unpleasant sensations or perceptions, and these associated unpleasant sensations will tend to restrain further similar actions. Such acts, bringing with them a penalty, will be called wrong and there will gradually be formed a large number of associations which will be identified with the ideas of punishment and condemnation and which tend to prevent the performance of wrongful acts : just as another combination of associations which have become associated with pleasure, reward or praise, will be associated with good or right. A person's idea of what is right or wrong will depend upon his education, the result of experience and of teaching, and is the basis of emotions and ethics, and that ill-defined acquisition from teaching and experience, the so-called conscience, and may evolve into very elaborate and very controlling feelings and habits of thought. Accord- ing as education has developed in a person one set of these associations rather than the other, a good or bad character, not from the person's own but from the community's standpoint, is formed. 23 These ethical ideas can of course be imparted from one person to another by language and, indeed, frequently are so imparted, but such etliical ideas are rarely so firm and convincing as those ob- tained from experience. Concentration and Attention It seems to be a general law in the physiology of the nervous system that when there is a stron" activity in one part, the activity of the rest of the nervous system is inhibited. Thus, reflex activity can be inhibited by strong pain ; and the reflex activity of the spinal cord is more or less in- hibited when the brain is in activity. In the brain itself, when a portion of the cortex or a group of ner\-e cells is in activity, the activity of the other cortical areas, as well as that of the lower centers, is inliibited. The stronger the local activity, the greater and more extensive will be the general in- hibition, and consequently the more this local activity will have a free and uninterrupted field. When an unusual or very vivid perception or idea is in consciousness it occupies the center of the stao-e. Consciousness consists of this one vivid idea and its associations; so that milder activities occurring in the cortex at the same time, which should produce, ordinarily, perceptions and asso- ciations, remain subconscious. This phenomenon is called concentration and is a very important function in nervous physiology. When the cause of this concentration is a perception, in ad- dition to this inhibitory influence, impulses from the active sensory cortex radiate to the motor cor- tex and out to the perceiving organ and cause a change in its musculature in the form of greater tension, tonicity, change in its position, etc., which local changes heighten the power of the organ for the perception of stimuli. Concentration is only another name for attention and has been re- garded as an efi^ort, and an expression, of the will or will-power, but the primary and essential factor seems to be unusually strong cortical activity. Not infrequently the concentration is centered about an unpleasant idea, from the thought of which we vainly try to escape; yet it is forced upon our attention and we cannot free ourselves from it in spite of every effort of our so-called will. We are at times in a state of "expectant attention" in regard to some possible unpleasant percep- tion, which state we cannot prevent, try as we may. Reverie and Thought The steady stream of perceptions originating from the excitation of the various sensory or- gans is constantly awakening associated memories, and tliese memories other associated memories, and so, while consciousness remains passive, (does not for the moment contain any strong or im- pelling idea) an ever-varying series of memories, visions, day dreams, etc., flow by. This is called a reverie or a day dream. But during this passive condition, some memory may be awak- ened which will arouse a number of associated memories (strong cortical activities) which will dominate consciousness and may pass to the motor area, producing action. Tliis stronger cortical activity brings the faint or passive consciousness into a strong active condition of attention and the passive reverie will be converted into active thought and this latter condition is called the act of fhmklng or reasoning. The process of thinking is, thus, independent of speech; although speech is essential to its clear expression and certainly facilitates it, especially in its deep and profound forms. The question of attention is one which seems to require a more or less external will to keep the cerebral activity limited to one subject. Attention is, however, a manifestation of the activity of the association of ideas. If many associations at the same time bring into strong con- sciousness the desirability of investigating some one perception, this idea (desirability of investiga- tion), which we may call "a" and which will have widespread associations, will bring into con- sciousness this perception to be investigated, which wc may call "b" with its various associations. If one of these associations leads to others remote and unrelated, and away from "b" it will not go far before it will awaken some of the associations conected with "a," even the absence of "b" from consciousness will do tliis, and "a" will be brought into consciousness and through "a" the investigation will be brought back to "b" again. This action, like other nervous actions, grows stronger by use, just as a machine runs more .smoothly and powerfully after its initial stiffness has been overcome by use; so a trained, educated, cerebral cortex, is able 24 to keep one set of memories present in consciousness (attention), to call up associated memories, to reject some, to keep others active and to compare them all together. When we have forgotten a name, we often cannot by an effort of "will," however strong, re- call it. The desire for the name starts series after series of associations in some way related to the name, which finally bring it into consciousness. Or the attempt may fail and the desire may be unsatisfied at the time. Hours or days afterwards the name may enter consciousness by some chance conscious or subconscious association and be recognized as the desired name. Imagination : Creative Faculty A perception usually calls up memories previously associated with itself or its memory. But unrelated memories may have previously been in consciousness simultaneously, or nearly so, and these memories may associate themselves with it and a combination of ideas and scenes may pre- sent themselves which are not the result of any unmodified previous experience. This is called imagination. Imagination is based upon memory. We can imagine nothing, the elements of which we have not previously perceived. But memory can present elements not previously associated together (men and wings) and these elements may combine themselves to produce a non-existing entity : i. e., men with wings. Things may be so combined and modified as to produce an entity, strange, bizarre and never before perceived. The normal relations of parts may be altered out of all relationship to themselvs to produce something quite different from anything within our ex- perience. Thus, things may be combined, which are the exact opposite of our experience, with very whimsical results. A new and not previously perceived possible grouping of well known elements may lead to experiments and discoveries of important facts, ideas, theories, etc. This is the creative "faculty" which shows itself actively in prose and poetic works of the imagination, in contradistinction to true facts or real liistory, and passively in day dreams. This re- sult of cortical activity may in many persons be facilitated by the action of drugs and may in some cases be the cause of hallucinations and delusions, (as in hysteria, hypochondriasis and insanity). However strange the results of the imagination, the elements of these results (even of some of the most monstrous delusions) are former experiences. Intelligence (Charts III)' Intelligence consists of the contents of object consciousness. It implies accurate formation of associations and their ready future availability. It is absolutely dependent upon memory, without which it cannot exist. The greater the number of memories and the more perfect and easier the recalling of associations, the greater is the intelligence. A person's memories depend primarily on perceptions derived from his sensory organs and on his experiences. The greater the number and the variety of his experiences the greater will be his intelligence, other things being equal. If any one sensory organ is absent or diseased from birth, memories of this sense will not be present and the intelligence will be diminished, unless this defect is in some way compensated for. In- telligence does not necessarily imply keenness of perception. An increase of intelligence, though unusual, is not abnormal. In some cases this increase is due to a greater number of perceptions and ideas (the learned man) ; in some cases to better and vrider associations throughout the entire sensory cortex (the wise man), and in some cases one portion of the cortex is functionally developed at the expense of others (the genius.) A diminution of intelligence may be due to imperfect development, to impaired nutrition or to destructive lesions of the cortex. Perversions of intelligence (insanity), although they may, in part, be caused by peripheral lesions, are fundamentally due to disease or poisoning, or malnu- trition of the cerebral cortex. Personality (Charts III and XVI) Personality is a term used to express all the energy and power which have been stored in the cerebral hemispheres by the activity of the cerebral cortex during the life-time of the individual. It consists of all his memories, sensations, perceptions, concepts, ideas, and their various associations, 25 which vary in character in different individuals. More especially, it consists of those strong as- sociations which have become his habits and his habitual judgments and also of his emotions, and of all else that the cerebral cortex and its association fibers have accumulated within themselves in virtue of their activity resulting from the sensory excitations which it has received during the individual's experiences in his life. The possibility of this accumulation by the cortex and, to some extent, its character depend upon the hereditary structure and functional activity of the nervous system of the individual. Personality is the sum of the conscious and subconscious content of the brain. It expends as this content grows larger and better systematized. It becomes greater as during life a larger stock of energy is accumulated in its associated memories. It is stronger as the consciousness is more intense (\irility). The "Ego" is the result of a long series of experiences (former per- ceptions) by which the body is differentiated from the external world (corporeal ego), and by which the complex of memories and ideas which the cortex has accumulated is differentiated from that of other individuals and is peculiar to itself (mental ego). The totality of one's memories constitutes his experiences. Many similar memories, or ex- periences, are gradually combined into a general idea or principle which becomes a guide, or as- sociation channel, for future judgments and actions and may persist after the individual mem- ories or experiences upon which it was founded have been lost. Cortical excitations of this nature are followed at once by actions which are almost involuntary (habits) and are not the result of a balancing of many former memories and ideas (thought). In this way one's character or personality is built up. Ideas firmly fixed by tradition, education and habit, acquire an overwhelming emotional value. They not only exist in spite of experience _biit_even mould experience into conformity with themselves. Personality is the result of the manifold work- ing of natural forces. Had the natural forces been different the personality would have been different. Each personality has its own history founded on its own personal experiences. A man's personality is not present at birth. It has been acquired or created during and by liis life reactions in a brain whose organization and capacity have been determined by heredity. Personality, being founded on, and consisting of, personal experiences, is strongly individ- ual ; but inasmuch as the large majority of men in the same commimity have very much the same experiences, and as they discuss these experiences with each other, there springs up between them a friendly feeling as beings of the same nature and with the same interests, needs, desires and aims. According to its education from its experiences a personality may keep itself apart from others and strive only for its own well-being and may thus be selfish (an egotist), or it may merge itself into the social life of the community and strive for the well-being of its fellow men as well as its own and thus be generous (an altruist). In spite of much in common, each personality differs from others. Some by their educational experiences become contemplative men, others close observers, others men of action, etc. Some men are of weak character, who have always been indulged and have always followed the path of least resistance; some are of strong character, who have had to endure privation and have learned to control their desires. These different kinds of men cannot by any effort of will change suddenly their character, which has been formed slowly by countless past experiences, acting upon a brain the anatomical struc- ture and physiological activity of which has been determined by heredity. The personality of a child has the jxitentiality of developing in the future, but the kind of development depends as much, if not more, upon the kind of future that is before it. as tipon its heredity. Personality seems to be the energy re.sulting from chemical changes which have taken place and are taking place in the cerebral cortex and to depend absolutely upon the integrity of the latter. When the cortex is exhausted, or diseased, personality may be changed under some un- usual experience, resulting from the undue dominance of some local excitation of the cortex, either permanently or temporarily (double personality), or it may become completely lost (automatism). There is no scientific or trustworthy evidence of the existence of any further factor in the form of any ethereal essence, a "mind" or "soul," as distinguished from what has been de- 26 scribed as "personality." Indeed this assumption rather complicates than simplifies the matter, inasmuch as it is contradictory to one of the must firmly established principles of natural philos- ophy : "the law of the censervation of energy." This law has not only been established by ir- refutable proof in the inorganic world, but also has proved by experiment to be valid in animals and even in man. If the soul can produce, or stop, a cerebral activity of its own volition, thus creating or annihilating force which normally proceeds in an endless chain from one manifes- tation to another, then the law of the conser\'ation of energj' is no longer valid. Mankind has been unwilling to allow that the casualties and laws which prevail in physical activities, can be potent also in the body and still less in the brain and "mind," because this controverts all their preconceived notions of the soul and its relation to God. The pre- judices (pre-judgments) of most men will not permit them to regard the mental activities as the result of the physiological activity of the cerebral cortex, in the same way that the physiological activities of the internal organs of the body produce and cause the function of these organs. They are unwilling to regard psychology as identical with the physiology of the cerebral cortex. In earlier historic times, the winds from the cardinal points of the compass, rippling streams, •cascades, the waves of the sea, growing trees and shrubs, etc., (everything which exhibited mo- tion), were each supposed to be animated by an indwelling spirit, by whom their motion was originated and maintained. At the present time, Naiads, Nereids, Dryads and other Nymphs, charming creatures of the imagination, have all been banished by the advance of knowledge. Only the indwelling, animating spirit of man, the soul, still survives in the belief of many. If a needle, or bar of soft-iron, is rubbed with a magnet, or with a piece of magnetic iron ore, and suspended so that it can turn freely, it will turn towards the north. A philosopher in very ancient times, who saw this phenomenon, would probably have said that this iron bar con- tained an animating spirit that "willed" to turn to the north and when by any cause it was de- flected it still willed and strove to turn again to the north. A modern scientist knows that a magnetized iron rod tends to put itself at right angles to the electric currents, which are always flowing around the earth, and hence it points north to the magnetic pole : one end of the axis around which the earth's electric currents revolve. He has proved these facts by many ex- periments and can prove them again at any time ; although he cannot explain the final cause of the action of the earth's electric currents upon the needle. The "why," he does not know. He does, know, however, that it is inevitable, constant, and not the capricious will of an invisible and unproved spirit. Whether an individual believes in a soul, or not, and explains the phenomena of life in accord- ance with this lielief, depends upon his traditions, his education, his experiences and upon the personality which has been gradually created and developed during his lifetime by the com- bination of all those forces constituting consciousness and subconsciousness, and which per- sonality may, in a sense, be likened to the older conception of the soul. It seems probable that consciousness, intelligence, personality, etc., are forms of energy and may, perhaps, be called spiritual in contradistinction to material. They certainly are absolutely dependent upon the blood supply of the cortex, and when this is arrested, personality with every other manifestation of consciousness ceases; but it still exists potentially and may be reanimated, if the circulation be restored after an interval of only a few minutes. If, however, the arrest of the circulation is so long that the cortex begins to degenerate or die, the personality is lost permanently, both actively and fjotentially. Personality, is then, the energy of cortical activity accumulated during the life of the indi- vidual. It is the sum of all his perceptions, concepts, their associations in abstractions, ideas, moods, and knowledge and the demonstration of all these in manner and method of action. It is the so-called mental content of the individual, or better perhaps, it is the individual, since the functioning of all his organs and his internal secretions are factors in the productions of his moods and are peculiar to him. It is the "Ego." As it is energy, not matter, it may be re- garded as the mystic spirit called the "Soul," whose manifestations have been for ages the rid- dle of the science of psychology and upon whose assumed origin and destiny has been built the faith of religions. 27 Insanity (Charts III and XVI) There is an abnormal as well as a normal cerebral activity. Whether we believe in the ex- istence of a soul within the body or not, certainly insanity is no longer regarded as the posses- sion of the body by an evil spirit (demoniacal possession). This was a well established belief for asjes, but it has long since been abandoned and we now regard insanity as caused by abnor- mal cerebral action. The conception of the control by a spirit, which we have finally rejected as re- gards insanity, the vast majority of mankind still retains for the healthy body, possibly be- cause most of the few men, who really think, have not studied cerebral physiology. We have considered briefly the actions taking place in the sensory area of the normal, healthy, cerebral cortex. In an abnormal cortex these actions are deranged. Local disordered cortical function produces local paralysis, or apraxia, or convulsions, or even hallucinations; while general disordered function produces coma, neurasthenia or insanity. Abnormal structure, whether the alteration be slight or great, and consequent abnormal function, of the cerebral cortex may be either congenital or acquired. The congenital form may be manifest in early in- fancy or may become apparent at any stage of the individual's development, as he successively meets tasks which require more and more intellectual power, when it becomes evident that his intelligence and ethics fall below the commonly accepted standards of the race or community of which he is a member. Insanity is a term applied to those forms of cerebral activity in which the intelligence, con- sciousness, emotions, personality, ethics, etc., one or all, are absent or abnormal. It manifests itself in various forms of cerebral disorder and may be divided into two classes: the organic (or structuraf) and the functional. When the brain is congenitally malformed or defective in con- sequence of disease, or injury, in the mother's womb, or at birth, its action is necessarily impaired and the manifestations of its activity are either absent or abnormal. Such cases are evidently of hereditary or, more accurately, of congenital, origin. If this congenital defect be extreme and the child cannot talk he is called an idiot (1083) ; if the defect be less extreme and the child can talk he is called an imbecile (1090) : a purely arbitrary, but convenient, division. Other cases of congenitally defective brain there are, which are capable of perceptions, memories, associations and consciousness; and of a certain degree of education. Some are even precocious children, but their education cannot be carried very far and at about the age of puberty they show abnormal cerebral responses. They show a difficulty in, or an im- possibility of, acquiring the more complicated concepts of morality, altruism, etc. They cannot form wise and true judgments and they become criminals, moral imbeciles, etc. These cases are classed together under the term the feeble-minded (1094). All these groups of congenitally defective cliildren constitute the class of amentia (1078 — more or less complete absence of a mind which never existed; in contradistinction to all other forms of insanity: those in which intelligence already acquired, more or less perfectly, is lost, more or less completely, and which constitute the class of dementia (1079). Education and training have much to do with the development of the activity of the cerebral cortex and consequently with the individual's intelligence and ethics. There are individuals who, partly in consequence of a defective brain and partly in consequence of defective training and education, do not have normal experiences and form a number of abnormal associations and ideas, especially etliical. Such individuals comprise the majority of criminals and cranks. Such cases bridge over the separation between the congenital and the acquired forms of insanity. It is possible that a person with a normal brain, who is isolated from his fel- low-beings and receives no training or education, will be feeble-minded or even an imbecile. In amentia the cerebral cortex is so structurally or functionally incapable that it cannot pro- duce perceptions, or register memories, or form associations, except of the most rudimentary kind. Persons suffering from this condition, then, have no material for intelligence, conscious- ness or ethics and are either incapable of any, or of only rudimentary, speech. In dementia an originally fairly normal cortex, in consequence of organic or functional disease, can no longer 28 exhibit sufficient activity to bring previously acquired memories into consciousness or to repro- duce formerly acquired associations or to manifest other formerly possible, cerebral activities. The form of dementia (loss of previously acquired intelligence) most closely resembling amentia is adolescent insanity, or dementia precox (1098), wliich occurs in apparently normal youths between puberty and the age of 25 or 30 years. They lose their mental and physical activity, and exhibit marked mental deterioration and consequent abnormality. Some of these cases make a more or less complete improvement and are able to lead a fairly normal life of rather subdued intensity. Other cases grow worse and terminate in dementia and death. Still other cases of insanity exhibit a fairly normal mentality until a fairly advanced age, at which time they exhibit delusions and erroneous judgments, from wliich they construct some- what elaborate systetn-athed delusions. A careful consideration of the history of such cases shows that even from youth they have exhibited a number of abnormal judgments. These cases are cases of paranoia (1116) and are incurable. In addition to the above classes of cases, in which the dementia is usually due to a congenitally defective brain, is a class of cases due to organic disease (lesions) occurring in an apparently nor- mal brain which may, however, have an hereditary tendency to cerebral disease. One of these forms of acquired insanity is senUe dementia (1107), which is due to atrophy of the cerebral con- volutions owing to imperfect blood supply, which is itself often due (secondarily) to atheroma- tous arteries and which is incurable. Another form of organic brain disease eventually cens- ing Atmentia. is general paresis (1106) due to a syphilitic meningo-encephalitis. Brain tumors and abscesses and meningitis, may also in rare cases give rise to symptoms of insanity, probably by causing local or general disturbances of the cerebral circulation. These cases of acquired organic brain disease terminate in dementia and death. Dementia also occurs as a terminal symptom in alcoholic dementia (1103), epileptic dementia (1104), secondary dementia (1105), and in most other forms of insanity which have persisted for years. Exhaustion of the cerebral cortex from worry, anxiety, shock and other causes may cause in- sanity in persons with an unstable brain, as may also an anemic and altered condition of the blood. It is, of course, possible that several of the above causes act simultaneously, or in se- quence, and as a matter of fact they frequently do so. Many forms of insanity are not due to organic brain disease. No lesion can be found after death and they must, therefore, be classed among the functional diseases of the brain. Many of these are due to poisons (alcohol, germ toxins, ptomaines, etc.), others are due to mental strain and especially to all possible forms of worry, in persons with badly educated brains. In most of these functional insanities, acute delirium (1110), delirium grave (1111), con- fusional insanity (1108), delirium tremens (1109), Korsakow's psychosis (1102), acute alco- holic mania (1112), simple delusional insanity (1113), symptomatic mania (1114), symptomatic melancholia (1115), the cardinal symptom is delirium, frequently associated also with an emo- tional disorder. In the other cases of this group there is a profound disorder of the emotions alone without any sufficient rational cause: mania (1118), melancholia (1117), circular insanity (1119), manic-depressive insanity (1120.) We have already considered the emotions at some length. The emotions may at times attain such an intensity as to entirely dominate the personality and to profoundly influence both the thought and the activity of the patient and to produce clinical pictures of mania and melancholia described in Chart XVI. In the functional insanities characterized by delirium we meet with a remarkable class of symptoms called illu.sions (214) and hallucinations (213), which are present usually in pro- fusion. Illusions are always, and hallucinations are frequently, faulty and imperfect percep- tions. Delusions due to faulty logic or faulty premises are common enough in the congenital and organic insanities; but not hallucinations and illusions, although they do occasionally occur. An hallucination is much more vivid than a memory and is not a complete and correct re- production of a former memory, but usually is something strange and bizarre. In some cases the hallucinations do not have the vividness of true perceptions, but seem to be internal voices or 29 suggestions, telephonic communications, or electrical action, etc. The process in the brain which produces an hallucination must be similar to that which produces a perception or memory, but the process is limited to the cerebral cortex, the spino-peripheral neurons playing no part in it, as they do in a perception. Hallucinations and illusions may occur as the result of a local disturbance in a brain which may not be for the moment entirely normal, although the individual is certainly not insane. In such cases, hallucinations and illusions can be quickly dispelled by reason and by proof of their abnormal character. Insane persons, however, in consequence of a diffuse cortical disturbance, cling to their hallucination? and illusions with great tenacity in spite of strong proof to the contrary. They cannot be corrected by the evidence of their other senses or by the evidence and reasoning of their friends. These hallucinations and illusions oc- curring in a brain weakened by nature, poison or disease, naturally lead to abnormal associations and consequently to abnormal ideas (delusions). Abnormal associations will result not only from the strength and vividness of these hallucination.s, but also because from patches of men- ingitis and from patches of atrophy, or other cause, in the brain of an insane man some areas of the cortex have more blood and are more easily excited than others and, therefore, respond more readily to association impulses, near and remote. Moreover, these abnormal ideas, entering into consciousness and coming into conflict with former long established ideas, lead to a condition of consciousness which we call bewilderment, clouded, befogged, confusion, distrust, apprehension, fear, etc. In these cases impulses reaching the cortex normally from the organs of sense are so much weaker than the excitations already there, that they cannot enter into consciousness, but remain subconscious. They may, although subconscious, be registered and may be recalled to consciousness after the attack of insanity is past, but they have no present value and are inadequate to correct the abnor- mal activities and no sane judgment can result. A cortex in which normal perceptions can occur only imperfectly, or not at all, and in which abnormal perceptions, associations and ideas are dominant, will naturally produce abnormal asso- ciation reflexes, or actions. The simplest of these is delirium (217, 1109-10), in which the patient responds by word and act to the many false perceptions and ideas in his clouded and weakened con.sciousness. When the intensity of the process is less the false perceptions and ideas will produce delusions (215, 1097), which will cause abnormal and often dangerous asso- ciation reflexes or acts. These delusions may remain isolated, unsystematized or may be woven in with all the real experiences of the individual's life; so that a systematized delusion, founded upon more or less evidence or reasoning, acting upon a weakened or limited general cortical ac- tivity, and one, therefore, incapable of producing a correct judgment, results. Often in justifying or explaining a delusion a patient will give reasons or cite experiences, which we call false, but which are doubtless experiences, which have been presented to him by his abnormally acting cerebral cortex. These delusions, or false and imcorrectable judgments, naturally lead to acts which are incompatible with an unconstrained life in a reasonable com- munity. Naturally, with all these abnormal cortical activities, not only the ethical ideas of the individual are changed, but al.so the normal emotions associated with normal cortical activity are profoundly altered, whether in the form of exaltation or depression, either continuously or in alternation with each other. In all forms of insanity, in consequence of its abnormal content, consciousness is altered and personality may be changed. There may be a double personality or the individual may imagine that he is dead, an animal, a king, or God, or, in extreme degrees of dementia, the patient may show no consciousness or personality at all. The emotions are also altered (morbid temperaments) in accordance with ideas in consciousness, or may be entirely dissociated from the ideas with which they are normally in harmony, or may be entirely absent in extreme dementia, or may be feebly carried over from former highly emotional states. The emotion most fre- quently present, especially in the early stages of the disease is fear fphobia). Fear and apprehension are prominent, even dominant, symptoms in the early stages of almost every case of insanity. The unusual, often monstrous, phenomena occurring in the cerebral cortex are so different from those previously present and so out of harmony vrith for- 30 mer memories and ideas, that the patients naturally become distrustful, apprehensive and full of fear. Many can hardly believe the information supplied by their own senses, much less the words of their friends^. Some regard themselves as persecuted and as the victims of conspiracies. Fear is the dominant emotion within them. The association reflexes are always altered in insanity in consequence of the abnormal cortical activity. In extreme dementia, voluntary motion is completely abolished. In profound melan- cholia, voluntary acts, as well as thought, are inhibited; while the reverse is true in mania, in which cortical activity, although abnormal, is greatly exaggerated. In consequence of prominent, compulsory ideas, so frequent in insanity, compulsory acts result. Voluntary Action. Association Reflexes The ultimate product of the complex mechanism of the nervous system is an action upon the animal's or man's environment for his benefit. We have already considered this activity in its barest outline under the title of "cortical reflexes." It seems desirable to consider these re- flexes more fully in the light of our knowledge of the "psychic activities" and under the name by which they are generally known, "voluntary acts" or "association reflexes." Activity never normally originates directly or spontaneously in the motor area of the cerebral cortex, but the cortical impulse initiating the movement always originates from the sensory area of the cortex. When a very strong excitation arises in this sensory cortex, as for instance, per- ceptions which are associated with the idea of imminent danger of death, this excitation passes to the motor cortex and thence down through the internal capsule and pyramidal tract and causes movements of flight and self-preservation. This act is as inevitable and as machine-like as is the simplest reflex act. A good swimmer bent on suicide cannot drown himself unless he is weighted or the action of his arms or legs is restricted. Escape from imminent death is for most men an imperative voluntary act. If, however, the danger is less great, as on a battlefield, the excitation leading to flight may still be there, but it may be inhibited by excitation from other associations, such as the idea of shame, love of country, etc., and the two excitations may neutral- ize each other. It is a question in any individual jcase whether the chemico-physical energies representing and causing the fear of death or those representing and causing love of country and honor are based on stronger experiences and wider and stronger associations. Whichever is the stronger prevails. Ordinarily, when a perception, or memory, suggesting action has sufficient intensity to enter consciousness, the excitation is sufficiently strong to pass along the association fibers and awaken into activity the group of motor cells, called the "common paths," lying in the anterior central convolution and, if no other counteracting excitation comes to this latter portion of the cortex, the irritation passes through these great motor cells in the anterior central convolution and down through the internal capsule and pjTamidal tract and the action takes place. Actions resulting from memories are usually weaker than those resulting from the original excitation or perception. When a number of more or less conflicting memories and ideas are in consciousness, some for and some against the action, impulses will be constantly coming to the motor cortex to be either im- mediately inhibited, or strengthened. The play of the diiiferent perceptions, memories and ideas, the play of motives, nmy continue a long time as the person deliberates and exercises his free-mil. This merely means that the sensory activities causing the diflferent memories, together with those causing the ideas derived from the mass of associated memories which constitute our ethics and those which constitute our emotions, have sufficient intensity to act upon the motor cortex, some as excitants, some as inhibitors. Fresh, allied memories constantly enter consciousness, because of their association with those already in it, and take part in this phenomenon. It is like a de- bating society in which arguments for and against are presented almost simultaneously, and the stronger argument rather than the will of the judge is the decisive factor. It is probable also that subconscious activities may play some part in this process and it is certain that the emotions exercise an almost dominant part in it. Eventually the stronger excitation will prevail and the act will be either done or left undone. 31 A voluntary act, depending upon, and being the result of, the association of ideas, may be described as an association reflex. The idea of the apparent freedom of will depends upon the absence of external compulsion and also upon the fact that the action takes place, or does not take place, in accordance with the relative strength of those cortical activities, which cause, also, our ideas and desires. The more perceptions and ideas a person has in his memory, the more learned and intelligent he is. the greater, wider and more protracted will be this "play of motives" and the more difficult will be the choice of the resulting action : the victory of any one set of motives. The very learned man is not the man of action. In a child, or in an ignorant man, with fewer elements of a choice, the association reflex will usually be more prompt. When a decision under the same or similar conditions is made a second time, and, especially, when fre- quently repeated, the association reflex takes place more and more promptly. In the frequent repetition of an act, practice, the same conducting channels and synapses are being constantly traversed and consequently become better conductors, and the act is easier to perform and is more or less automatic. It becomes a habit. A large part of our voluntary acts are habits. It is to be remembered, also, that the internal sensations and secretions which dominate our "moods," exercise a strong influence over voluntary movements which, under changing moods and altered internal sensations and secretions, may be very different at different times, although the causal external sensation is the same. The gray matter, the point of union of the motor and sensory neurons, is in small com- pass in the subcortical centers and hence is well fitted for direct transference: for reflex and auto- matic actions. In the cortical centers, the gray matter is spread over a large surface and per- mits separate, local action, and consequently permits a large number of different memories and ideas, some positive and some negative, to act simultaneously upon the motor cortex and, thus, either cause or prevent a voluntary action. Both voluntary and reflex acts are for the benefit of the individual. The reflex acts depend upon heredity and evolution. They are the result of the experience of the individual's ancestors, of the experience of the race (phylogenetic). Voluntary acts depend upon the individual's personal experience (ontogenetic). The difference between the two depends mainly on difference in anatomical structure. In conditions which are new and in which no experience can guide him, an individual's voluntary acts are quite as likely to be detrimental as salutary. His reflex acts almost without exception are salutary. The innervation memories stored in the motor cerebral cortex are originally acquired from reflex acts. The first voluntary acts of the child (sucking, opening and closing eyes, closing of hand, etc.) are adopted reflex acts, either unmodified or but slightly modified. A young infant does not will to suck milk from his mother's breast. It is a reflex act. But after the infant has experienced the result of this act a sufficient number of times, the sight of his mother, or hunger, may awaken his memor- ^f this act and of the consequent relief from hunger, may awaken his desire, and he will suck the breast voluntarily in consequence of this active memory. Voluntary motions, or association r -I -.xes, occur early and develop rapidly in infantile life, but occur much earlier, though they develop more slowly, in young animals. Chickens run almost as soon as they are born to their mother when she "clucks" for them. The lower animals thus possess at birth, by heredity, a more perfect nervous sy.stem ; while human infants possess at birth by heredity, one less perfect, but capable of a wonderful development, which results in greater part from per- sonal experiences. The Play op Motives The isolated cortical areas, containing the memories acquired by previous experiences, are all brought into activity by association fibers. When any sensory impulse requiring action is brought to the cerebral cortex, conflicting ideas, corresponding to those localized memories, must be brought into unison before any association reflex (voluntary action) can result. The cerebral activity may be compared to a town meeting. At the town meeting a new condition presents itself for action. Shall some action be taken, or postponed, or refused? The subject is discussed from many angles; the result of memories stored in the sensorj^ area of the cortex of the citizens. Many ideas acquired from former experiences 32 are advanced. The clergy bring forth certain moral factors, the result of a long education extend- ing back to infancy when the brain was most impressionable and which have long been pre- served in the brain as fixed principles. The business men advance certain utilitarian factors, ex- periences acquired through many business undertakings and which have been stored in the brain as fixed business principles and are emotionless. The poets and orators present the emotions of patriotism and glory which have been the result of a long education, which has stressed their vital importance for the community and each individual member of it. The shysters and rascals pre- sent ideas of self-interest and pecuniary expediency. Each view advanced calls up another, favor- able or unfavorable. And so the dispute rages. The chairman, or moderator, takes no part in the discussion, wliile all these different ideas are poured in upon him. One by one inadvisable or impractical ideas die away. Their tendency to action is inliibited by the stronger impulse ot the majority of other ideas. A greater unanimity is acquired by the remaining ideas. They pour in upon the chairman with ever greater intensity. He is set into activity and the overwhelming idea or impulse of the assembly for action pours through him to his Sheriff and Policemen: executives who correspond to the groups of motor nuclei which have been trained by previous reflex and voluntary acts to execute the "will," of the individual, which is really the dominant activity of his cerebral cortex. Speech (Charts IVc and XIII) The most complicated and important of all voluntary acts is speech. Although the lower animals can, in all probability, communicate with each other, speech and the allied functions, reading and writing, are peculiar to human beings and are the result of much instruction in the line of imitation and study. These functions, therefore, depend upon a healthy brain. If a child has such an imperfectly formed brain that he is an idiot (743), he consequently cannot speak. The perfection and content of speech, reading and writing depend upon education; being more imperfect the less the education and training and are, therefore, often quite abnormal, or even absent, in the defective and feeble-minded (752, 1090, 1094) and in hysteria (747-8) and in- sanity, especially in adolescent insanity (1098), in dementia (1079), in coma (745) and in in- sanity with diffuse cortical changes in the speech area (1106). The power of speech is of enormous importance in the development of the race, it is the one factor which has enabled the human race to so far outstrip all other animals that it seems to form an entirely different order of beings from them. The spoken, and, still more, the written, word allows man to make his own all the experience, knowledge and wisdom of his ancestors and contemporaries, and raises liim, thus, far above his own limited individual experiences. Like all knowledge, the art of speaking, reading and writing is acquired from sensory im- pressions. The art of speech is not in-born, although its possibility, its meclianism, is. It is derived from the sense of hearing; so that when a child is born deaf, or ac- quires deafness in the first two or three years of life, he is also dumb: a deaf mute (744). A deaf mute can be taught to speak only very imperfectly, and then only by the sense of sight, or much more rarely by touch (Helen Keller). The art of reading and writing is de- rived partly from the sense of hearing and mainly from the sense of sight. If a child is born blind, or acquires blindness in the first few years of life, he can learn to read only books printed in a peculiar way, and then only by the sense of touch and hearing; the sense of touch replacing the sense of sight in these cases. Many persons think that speech comes naturally, or by nature, to a child. Such is not the case. In a home and hospital for infants where the limited number of nurses were so busy in attending to the physical needs of the infants that they had little time for anything else, it was noted with some .surprise that the children, grown to the age of eighteen months and two years, made no effort to speak. It was necessary to bring in some older girls for this purpose and to im- press on the nurses the necessity of devoting attention to teaching children to speak. The first sounds which the child utters, little cooing sounds, are doubtless emotional reflexes, scarcely more complicated than laughing or crying. From the.se sounds, speech is gradually built up by careful training. The mother in her play with the child imitates these sounds and gradually changes them into so-called "baby talk :" into some resemblance to actual syllables or words. The 33 child who is continually being taught to imitate the mother, very slowly changes the simple coo- ing and other sounds into these nearly related ones and finally toward the end of the first, or dur- ing the second, year of life. Da-da is converted into pa-pa, and ma-ma, and other simple words. It is a play and a lesson which is taking place every day in every nursery in the land. It is a slow process, but after a time the child begins to utter words to which he at first attaches no signifi- cance or understanding, but to which he later attaches a more and more definite meaning. Thus, speech, like other activities, is gradually acquired from simple reflex acts. During the first month of its life the child gives utterance only to vowel sounds, especially "oo" and "a." Toward the end of the second month he begins to utter consonants, especially, "m" and "t," followed in the third month by "b"and "g" and "r" and "n," and in the fifth month "k" is added. During the second half of the first year the child holds monologues, as if really talking. Some of the sounds can be represented by letters, others cannot. He shows a strong tendency to repeat the same sound over and over and over again, probably in part, because his vocabulary of sounds is not large. At the beginning of the second year the child is able to repeat with some accuracy the simplest sounds which he hears ; but even when he learns to repeat, with some distinctness, ."♦'mple words as "mama" and "papa'" he attaches at first no meaning to them. At the same time, however, he is beginning to understand certain words that are said to him and in response to the question, "How big is the baby ?" he raises his hands to approximately the level of the top of his head. Thus, at a certain stage of his development the child can speak words which he cannot understand and can understand words which he cannot speak. There is much doubt as to really how much he understands. The raising of his hands may be a conditioned reflex, similar to those already described, and he might raise his hand equally well to the words "How small is the baby?" or even the word "big" or "ig" or even to inflection of the voice with- out any spoken word at all. Thus speech is at first a modified reflex. After this process has gone on for a time the child acquires a great facility in imitating the sound of words, as he does in all kinds of imitation, and will often surprise his mother by uttering a sentence wliich he has never said before, although, doubtless, he has often heard it said by others. However doubtful may be his understanding of words in the early stages of this process, there is no doubt that this understanding is slowly acquired and finally it becomes evident that the child clearly associates an object with a definite sound, or word. He often points to an object, the name of which is spoken, or even leads one to it when he is, as yet. unable to walk alone. It is evident that the perceptions and memories of spoken words are of fundamental import- ance in the art of spenking. These perceptions take place and these memories are stored, in right handed persons, in the posterior half of the left superior temporal convolution and in the posterior portion of the left island of Reil (Fig. 15) ; so that lesions of this area cause a pro- found disorder of speech: sensory aphasia (775-6). From this portion of the cortex impulses pass along association fibers (the fasciculus uncinatus) lying in the external capsule to the base of the left inferior frontal convolution (Fig. 15) and to the anterior portion of the island of Reil. A lesion in this region, also, causes a profound disorder of speech: motor aphasia (774.) The distinction between motor and sensory aphasia is not always easily drawn. In some cases when a patient is unable to speak a desired word it may be very difificiilt to decide whether he has forgotten the innervation memories necessary to speak the word (motor aphasia — 222) or has forgotten the word itself (sensory aphasia — 223). In the latter case he may be able to repeat the word when he hears it spoken. Lesions of the external capsule, in which run the association fibers connecting the centers of sensory and motor speech (the fasciculus uncinatus). also, cause a profound disorder of speech (conduction aphasia). Perceptions of written or printed words are formed and their memories are stored, in right handed persons, in the cortex of the left occipital lobe, and from this area impulses pass along the association fibers lying beneath the angular gyrus to the base of the left inferior frontal con- volution and the base of the loft middle frontal convolution, where are stored the innervation memories of speech and writing respectively. Therefore, deep lesions in the region of the left angular gyrus in right handed persons will cause a complete alexia {ITJ^ and an incomplete 34 agraphia (779). The area of the cortex in the left hemisphere described above, including the bases of the middle and the inferior frontal convolutions, the island of Reil, the posterior half of tlie superior temporal convolution and the angular gyrus, is called "the zone of language" and is the cortical center, or psychic center, for the faculty of language. In addition to its cortical center, speech depends upon the integrity of the muscles and nerves which move the lips, tongue, soft palate, larynx and those concerned in respiration. In lesions of these muscles and nerves and of their nuclei in the medulla and pons and of the pyramidal tract, sp>eech may be abolished (anarthria) or pronunciation impaired (dysarthria), whether in conse- quence of paralysis or of incoordination, or of spasm (as in stuttering). Reading and writing may be similarly abolished or impaired in lesions of the peripheral nerves or of their nuclei in the optic thalamus or in the anterior horns of the cervical enlargement of the cord or of the fas- ciculus of Gratiolet or of the pyramidal tract. Dysarthria might also be due to a cortical tpajralysis of the pneumogastric nerve, but the laryngeal muscles have a bilateral cortical representation; so that if one cortical area be injured the corresponding area of the other hemisphere can carry on the function of speech perfectly. There is, therefore, no laryngeal paralysis, or consequent dysarthria, due to any lesion within the cerebral hemispheres, unless the lesion be very extensive and involves both hemispheres (pseudo-bulbar paralysis). Automatic Movements (Charts III and XVI) This term is applied to two quite different sorts of actions. In one sense automatic, or autochthonous, acts are reflex acts which originate , not from external, but from internal, or or- ganic, excitations or irritations. One of the best examples of this activity is the respiratory act. Another is the gastric and intestinal peristalsis. Such acts are very numerous and carry on the nutritive activities of the body. The name is also applied to voluntary acts which have been learned with more or less diffi- culty, but which have been enacted so often that ihey can be performed without consciousness. Such acts are walking, writing, piano-playing, smoking and many others which can be very i>er- fectly performed unconsciously, although each one can be enacted consciously and usually is so done. The nervous impulses underlying these automatic acts, although they may be entirely un- conscious acts, probably always pass through the cerebral cortex and are never shunted to the ganglia at the base of the brain. Otherwise it is hard to understand why in destructive lesions of the motor cortex, the corona radiata, or the internal capsule these automatic acts are abolished, as they surely are. Involuntary and Abnormal Motor Responses Spasms and Couz'iilsions (Chart IVb). Spasms and convulsions consist in involuntary muscular contraction. They depend mainly upon irritation of the central gray matter, especially the cerebral cortex, and partly upon peripheral irritation. Passive contracture and Thomsen's disease alone are purely of peripheral (muscular) on- gin. Many of the tonic spasms are reflex, some are the result of nerve root irritation (menin- gitis, tumors, etc.) and many are associated with degeneration of the pyramidal tracts. The result of pathological and experimental investigation makes it evident that epileptic and epileptiform convulsions may originate from irritation of the motor cortex. When a slight, but lasting, local irritation of the motor cortex occurs, there results a local spasm, clonic and tonic, which extends from one extremity to another and finally becomes a general convulsion, accompanied in some cases by coma. When the irritation is stronger and especially when it affects both hemispheres there results first a tonic followed by a clonic convulsion and coma. Irritation of other parts of the cortex can also produce epileptic convulsions, if the irritation be strong enough and the motor cortex be intact. Tonic spasms, without clonic ones, may be ob- tained by irritation of many parts of the central nervous system. The epileptiform convulsion caused bv cortical irritation may be accompanied by alterations in the cardiac action, in the respira- 35 tion and in the activity of other internal organs, as in the cases of ordinary epilepsy. Indeed, these changes in the cardiac action and in the circulation through the brain may be more essential factors than is the cortical irritation in the production of some of the symptoms of an epileptic attack. The contractures which accompany cerebral paralyses are due to contraction of the stronger muscles, partly in efforts for voluntary movements from the brain, but mainly reflexly from the spinal cord. The pathogenesis of many spasms and the localization of their origin, especially of the ir- regular spasm, are given in Chart IVb. The various forms of spasms are at times quite difficult to recognize. It requires much experience to be able always to differentiate clonus, tics, athetoid and choreic spasms from one another and from the perversions of motion: tremor, ataxia and apraxia. Tliis is imfortunate because the diagnosis by these diagnostic charts requires that the symptoms be correctly observed and named. The student should compare carefully what he sees with the definitions in the book and should observe as many cases as possible. Ataxia, Apraxia and Tremor {Chart IV c). When an impulse from a cortical motor center passes down to a group of nerve cells in the anterior horns of the spinal cord, it causes a definite synergic contraction of a number of muscles to produce the movements over which the group of nerve cells presides. As soon as this movement commences, a number of sensory im- pulses pass from the muscles and joints involved to the coordinating centers, especially to the cerebellum, and the movement is consequently coordinated and orderly. This coordination of movements is not inborn. It is acquired by experience and practice. The movements of a new bom baby are always ataxic. When the function of the cortical center is impaired there results a paralysis or an apraxia (loss of skill) according to the degree of the impairment and when the coordinating apparatus is functionally impaired there results ataxia. In either rase awkward, ill-adapted and uncertain movements result. In cerebellar lesions there is asynergy: the muscles taking part in the movement do not act together at the proper time and with the proper relative force to produce an orderly movement. The motor apparatus, together with its sensory regulation, may be called the executive apparatus and it may be disordered in various ways: 1st. If the motor portion of this apparatus be injured there results a paralysis or paresis. See Chart IVa. 2nd. If the sensory or regulating apparatus be injured there results ataxia. See Chart IVc. 3rd. If what has been learned has been lost or impaired there results apraxia or dyspraxia. See Chart IVc. Ataxia, incoordination of movement, always depends upon .some disturbance of the sen- sory or regulating apparatus. It occurs in several distinct varieties, depending upon the portion of the sensory nervous system afifected : 1st. Peripheral, or dynamic, due to lesion of the peripheral sensory neurons. 2nd. Cerebellar, or static, due to lesion of the cerebellum or its tracts, including the termin- nation of the auditory nerve in the semi-circular canals. 3rd. Cerebral ataxia, to a lesion of the cerebral hemispheres. 1. Peripheral, or dynamic, ataxia (280, 644) is caused by an impairment or loss of the complicated sensations conveyed by sensory fibers from the muscles, joints and other tissues which is known by the name of muscle-joint sense (43 and 352). It affects all movements of the parts involved. It is associated with hypotonia (240), which allows an abnomial excursion in passive movements without the resistance normally offered under sudden stretching, and which may allow of abnormal positions of the extremities. The loss of the muscle-joint sense can to some extent be replaced by the sense of sight, which allows the patient to guide his movements by his eyes. Cerebellar, or static, ata.via (281, 642) is caused by impairment of the function of the great coordinating organ : the cerebellum. It affects mainly, or only, walking and standing, wliich acts 36 resemble those of a drunken man, or become absolutely impossible. The sense of sight gives very little aid in such cases. Movements of the extremities while the patient is recumbent are fairly normal. With cerebellar ataxia is usually associated vertigo; although this latter symptom may not be pronounced. Cerebral ataxia is due to a lesion of the sensory tracts and centers within the brain. If this lesion involves the sensory tracts in the medulla or pons or crura cerebri, the cerebellar tracts may also be involved and the ataxia may be either cerebellar or dynamic or both. In cases of cerebral hemianesthesia where the lesion is either in the optic thalamus, the internal capsule or the parietal cortex, the ataxia, which invariably results, is of the dynamic variety and is associated with hypotonia. Such cases of ataxia may be slight in degree and may show great and relatively rapid improvement. When the lesion is in the parietal cortex, the center for cutaneous and muscular sensibility, ataxia results, because of the loss of those sensations wliich are essential for the proper guidance of voluntary movements. In tumors of the frontal lobe, whether cortical or sub-cortical, ataxia is a common symptom and is of the cerebellar type; being doubtless due to involvement of the fronto-cerebellar tract. In cerebral ataxia, it is evident that the patient is trying to execute the movements and knows what he wants to do, but he executes them awkwardly. Apraxia (282) may residt from the loss of the purposeful idea which should prompt a given action. In lesions of the posterior central convolution or of the supra-marginal gyrus this idea cannot be formed (sensorial apraxia or agnosia), in which case the action which should follow the idea cannot originate; or when this idea is formed the memory is quickly lost (amnestic apraxia), in which case the appropriate action is begun, but never completed. In lesions of the anterior central convolution, or of the area immediately anterior to it, the purposeful idea may be present, but the innervation memories necessary for the production of the appropriate action are lost; so that the action cannot be performed (motor apraxia). When the association fibers connecting the anterior and posterior central convolutions are the seat of lesions, the appropriate action will not occur, or a somewhat similar action may be substituted for it (associative apraxia). In any organized society much results from imitation and from instruction. Certain complexes of innervation feelings become by practice so firmly united, that what was at first done with difficulty and imperfectly, becomes easily and perfectly performed. These innervation complexes are not inborn (although their anatomical substructure may well be), but are learned and acquired by practice. These innervation complexes become memories (kinesthetic mem- ories). Innervation memories may be conscious in early life when first learned, but may be unconscious later. Many of them may never enter consciousness. As long as these memories persist the corresponding action may be performed, consciously or unconsciously, as the final result of sensory impulses exciting them. Many complicated acts are not performed often enough to form an innervation complex, but must be performed consciously and with constant sensory guidance from many parts of the brain simultaneously (sight, muscle sense, touch, etc.). Tremor (250) may be caused by rapid rhythmical interruptions of the inner\-ation impulses passing to the muscles or by failure of a proper proportion or equilibrium in the innen-ation of the muscles and their antagonists, and is especially characteristic of lesions of the lenticular nucleus and of the red nucleus and rubro-spinal tract. Tremor usually ceases during sleep and is usually increased by mental excitement; although a very powerful emotion may arrest the tremor temporarily. It seems to be always of central origin. Clonic spasm from exaggerated reflexes must not be confounded with a coarse tremor. Athetosis, or mobile spasm, is a slow twisting movement of the fingers and hands, either uni- lateral or bilateral. It often follows a hemiplegia or diplegia, and occurs most frequently in cerebral palsy of childhood. It is characteristic of lesions of the caudate nucleus and of the putamen. Trophic Influences (Chart XVII) The nervous system exercises an important trophic influence over many of the tissues of the body, in addition to influences over their blood supply through the vaso-motor system. 37 This trophic influence can be divided into two great divisions, motor and sensory. When the motor nerve cells of the central or peripheral motor neurons are degenerated or destroyed (as in lesions of the nerve fibers or of the motor cells, of which these nerve fibers are the axons), the nerve fibers springing from such degenerated cells undergo a rapid degeneration, as do also the muscles, in which these nerve fibers terminate ; and in early life when there is motor paralysis, or immobilit)' of parts of the body from any cause, these parts fail to grow normally. When the sensory nerves are degenerated, as in syringomyelia, myelitis, tabes, lesions of the spinal ganglia or of the ganglia at the ba9e of the brain, etc., in consequence of the anes- tliesia thereby produced, the body is no longer protected, by reflex and voluntary acts, from the many traumatisms to which it is frequently subjected and therefore ulcerations, arthropathies, ul- cerations of the cornea and other tropliic lesions result. Some of the ductless glands, especially the pituitary and the thyroid, when hypertrophied or atrophied as regards their glandular structure, also produce widespread trophic disorders. The Cerebro-Spinal Fluid (Charts VIII and XIX) The central nervous organs (brain and spinal cord) are bathed in a fluid called the cerebro- spinal fluid. This fluid is secreted or transudes from the choroid plexus within the ventricles of the brain and thus may contain substances which are in the blood. It passes out of the ventricles at the inferior angle of the fourth ventricle, through the foramen of Magendie. If from any cause (tumor, meningitis, etc.) the foramen of Magendie is occluded, this fluid, con- stantly secreted, cannot escape from the ventricles and dilates these cavities more or less ac- cording as the sutures of the skull are ossified less or more completely ; thus producing internal hydrocephalus. The cerebro-spinal fluid passing out of the foramen of Magendie becomes the subarachnoid fluid, which lies in the meshes of the tissue forming the deeper layers of the arachnoid. In this situation it can receive products of any inflammation of the meninges : albuminous substances (globulin) and cellular structures (leucocvtes in acute, and lymphocytes in chronic, inflammations) ; so much so as to be cloudy or even purulent. The specific germs of the various forms of meningitis can often also be detected, as well as blood in hemorrhage and pus in abscess. In tertiary and quaternary syphilitic meningitis the Wassennann reaction is usually positive. The cerebro-spinal fluid leaves the cranial and vertebral cavities along the cranial and spinal nerves and through the Pacchionian bodies and enters the veins. The cerebro-spinal fluid is obtained by lumbar puncture and the rapidity of its escape is evidence of the tension which it is under, which tension c"an more accurately be measured by a manometer. When the cerebro-spinal fluid is increased in amount, as in meningitis, or when a foreign body, as a tumor, is within the cranial or spinal cavity the tension of the fluid is usually increased. The examination of this fluid is, therefore, of much importance in disease of the cerebral and spinal meninges and in other intra-cranial and intra-spinal conditions. Electricity and the Nervous System (Chart II) Nervous conduction, although it has some analogies with electrical conduction, is due to an entirely difl^erent form of energy. But when nervous action takes place, whether in a peri- pheral nerve or in a central ganglion, there always occurs an electrical current through the nerve or ganglion in the opposite direction. So constant and delicate is this reaction, that it has been used to prove the presence of nervous activity. Moreover the electric current, both Galvanic and Faradic, can be conducted along nerve fibers, and changes in the tension of electricity so con- ducted in the nerve fibers cause contraction of the muscles in which they terminate, as is shown in Oiart VII. The muscle fibers, also, respond directlv to changes in intensity of a Gal- vanic current, but not to those of a Faradic current. Degeneration of a nerve can be shown by its reactions to electricity C Chart VI lb). All forms of electrical energy are excitants for all the sensory organs, acting not so much upon the end-organs as upon the nerves themselves. Other forms of electricity, especially static electricity and high frequency currents, are used as therapeutic measures but have no diagnostic value. 38 CHART I Case-Taking METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES. teisS^^;.^... / Errors in diagnosis result more frequently from imperfect observation than from faulty reasoning. Methods of Examining and Testing Patients Data derived from QUESTIONING INSPECTION PALPATION PERCUSSION ^ ELECTRICITY LUMBAR AND BRAIN PUNCTURE OPHTHALMOSCOPY LARYNGOSCOPY L THERMOMETRY see chart I a. see chart I b. see chart I c. . see chart I d. 39 CHART la Questioning Comprising Numbers 1 to 18 (Note) — The examination of every patient, who is conscious and intelligent, begins with a history of his health and of that of his ancestors. This is an important source of information, although usually less so than are the results of the physical examination. The taking of a reliable clinical history is something of an art, but at best we are absolutely dependent upon the truthfulness of the patient, as we rarely have means to check his statements by informa- tion from other sources. It is important to put the patient at his ease and to gain his confidence. The patient is vitally interested in his own case and it is best to let him tell his own story of his illness in his own way, without interruption. He is eager to tell of his personal sufiferings Jind often becomes impatient and irritable if interrupted by questions as to his hereditary and previous illness, which may better be asked later. When he has finished his own story is the time to ques- tion him about his illness, more especially and fully in regard to the organ probably affected, but also concerning the function of the other organs of the body. This done, he should be questioned as to his previous illnesses, occupations, etc., and finally as to any special prevailing illness in his ancestors or relatives. It is important to ask as few leading questions as possible. Questions in regard to personal habits and venereal diseases should only be asked when absolutely alone with the patient, and then in a manner wliich assumes that all men are guilty of indiscretions. During our taking of the clinical history we should have the patient under close observation and can thus form a good judgment as to his manner and general mental and physical characteristics. 41 Methods of Examination of Patients Suffering from Nenous Diseases QUESTIONING Methods of Testing 11 Allow the patient to tell the story of the illness without interruption (see note on History of pres- preceding page). Then ascertain the exact date and manner of onset (sudden or slow, prodromata, etc.) and tlie exact sequence of symptoms. Inquire into all details which may concern the case (headache, pain, paresthesiae, vertigo, in- somnia, mental condition, emotions, memory, special senses, paralyses, spasms, fits, disturbances of organic reflexes, loss of weight and strength, etc. ), whether of recent or of old date. Seek for any possible cause (injury, poisons, drugs, infections, worry, mental or physical overstrain, shock, etc.). Be careful not to suggest answers to nervous people. Inquire into previous treatment and its effect. ent illness. (Chart II) Family and personal history. (Chart II) 3 Consciou ( Charts XVI) sness. Ill & 4 Sanity. (Charts XVI) III & .\scertain the occurrence in the present, or a past, generation of the family of consanguineous marria-ges, of any nervous diseases, especially the neuroses (neuralgia, epilepsy, hysteria, insanity, suicide, dnmkenness, etc.), or of sypliilis or tuberculosis. Note patient's age, full address, race, his mental and physical development, his school life, injuries at birth, occupation, habits (alcohol, drugs, venery, masturbation, etc.), exhaustion, anxiety, worry, dwelling and previous illness, such as rickets, infectious diseases, chorea, fits, tuberculosis, syphilis (use discretion in this inquiry: ask of women, about sore throat, skin rashes, miscarriages, etc., and, for men, a good question is: "Of course, like all the rest of us you have had the clap. Have you ever had the pox or any sore on the genitals?") This may make confession easier. Ascertain the condition of other organs (cancer and tuberculosis). Psychoanalysis is a part of the personal history. It is a minute and exhaustive inquiry into the patient's previous and present actions, motives and dreams, especially in regard to unhappy and repressive influences in the sexual life, of which the patient is scarcely, if at all, conscious and which have been repressed rather involuntarily than deliberately. The repressed idea may express and reveal itself (to a skilled investigator) in dreams, symbols, phobias, etc. Psy- choanalysis and its concomitant treatment may produce in some cases beneficial results, but equally good results may follow other treatment and the method, fascinating though it be, seems to the author to be fraught vdth danger and is not recommended. Patient may lie in a stupor and make little or no response to questions, noises, shaking, pin pricks, or strong sensory irritations of any kind. He may appre- ciate neither his surroundings, nor his acts, nor the time and place, nor his own individuality. He can remember, after recovery, nothing of what hap- pened while he was uncon.scious. There are all possible grades in impairment of consciousness from complete coma to a slight lack of attention and an inability to collect one's thoughts. This can he learned by conversation. Patient's conversation and manner may show that his brain acts in an abnormal way and that he entertains abnormal perceptions and ideas (hallucinations, delusions, compulsory acts, ideas, etc.). Ascertain if a change has taken place in the patient's normal mental state, and when. Note whether patient is elated, active, loquacious; or dull, inattentive, sluggish, distracted, evasive, suspicious, and why. Some cases may require prolonged observation. At times irritating questions may be desirable, in order to evcile the patient. A2 ] ntelligence. (Charts III, XIII & XVI) Memory and under- standing. (Charts III, XIII & XVI) Emotions. (Charts III & XVI) 8 Speech. (Charts III, XIII & XVI) 9 Reading. (Charts III, XIII & XVI) 10 Writing. (Charts III, XIII & XVI) 11 Stereognosis. (Charts III, VI & XXII) QUESTIONING (Continued) In testing a patient's intelligence, we test his general knowledge by asking him to name the ditiferent days aiad the different months and by arithmetical, geo- graphical, political and historical questions. His power of observation by show- ing him a number of things and asking him later to describe them. His poti^er of attention by asking him to add a long column of figures or underscore a letter wherever it occurs in a page of print. His pozver of comprehension by asking him to e-xplain something he has read or heard. His association of ideas by giving him a word and asking what other ideas it suggests to liim. His mental reaction time by the time he takes to solve problems, or to name an object, the picture of which is shown to him. His moral sense by questions in ethics. .'\n apparent defect in intelligence may be due to lack of attention, or may be shown, by further questioning, by having him repeat long phrases, execute verbal and written commands and name objects shown to him, to be due wholly, or in part, to a loss of memory; either general (amnesia), or local (aphasia), especially to a failure to understand what is said to him (sensory aphasia) ; while reason and judgment are normal. Test memory for remote, as well as for recent, occurrences. Test memory of statements made a few minutes previously, or of events of the day before, or of years before. Patients may show by their conversation, if suitably guided, or by their manner, or by both, whether they are emotional or not. The emotional state of the patient and the mental characteristics discussed just above, can often best be learned from the statements of friends and relatives. Curious fears, the so- called "phobias," (235) are often present. Patients's speech may be entirely absent (anarthria) or altered and very defec- tive, rational or irrational ; there may be a limited vocabulary or use of the wrong word (aphasia), poor articulation (dysarthria), tremor in voice, monot- onous, scanning speech, omissions of syllables and words, and may show indi- vidual peculiarities, all of wliich are to be noted. Speech is tested by interro- gation and spontaneous (voluntary) speech. Test also patient's understanding of letters, words and phrases spoken to him, his executing spoken and written commands, his picking out objects named; and have patient name objects, give sequences, i. e.. numbers, days of week, months, etc., and repeat catch phrases, as "Round the rough and rugged rock the ragged rascal ran," etc. Ask the patient to read aloud, even short sentences, words, or letters only If this be impossible can he read to himself? Can he recite, can he understand what he has read? Can he execute written commands? Ask the patient to write, spontaneously, from dictation and from copy. Have him write the names of objects shown him. Note any defect in the character of the writing or in the ideas expressed. Can he read and understand what he has written ? .^sk the patient to name objects placed in his hand, his eyes being shut, after excluding anesthesia. Even without feeling them all over and without moving them about in his fingers, a normal person should be able to recognize many objects (metals, cloth, etc.) merely laid against the skin of his hand, face, foot, lips, etc. Stereognosis may, therefore, in exceptional conditions, be tested, although less perfectly, in other parts than the hands. 43 12 Sight. (Charts VI & XIV) 13 Achromatopsia. Color sense. (Chart VI) 14 Field of vision for white and colors. (Hemiano- pia) (Qiarts VI & XIV) 15 Hearing and tinnitus aurium. (Charts VI & XIV) 16 Smell. (Charts VI & XIV) 17 Taste. (Charts VI & XIV) 18 Slec->. QUESTIONING (Concluded) Ask the patient to read small print or Jaeger's test type at reading distance (10 to 16 inches, according to age, refractive conditions, etc.) and Snellen's test letters at twenty feet. If patient cannot read the appropriate line at twenty feet the loss of vision is expressed by the number of feet from the chart at which he can read this line divided by twenty. Thus at ten feet the vision would be expressed by -.^- In great defect of vision the patient may be able to see only dimly the hand moved before his eye, or may only be able to dis- tinguish between light and darkness. In testing suspected malingerers, who claim to be blind in one eye, while testing the sight with plain or low-power lenses, both eyes being open, a greatly over-correcting high-power lens should be surrep- titiously placed before the normal eye. Then, if he can read the test-type, he must do so with the eye which he claims to be blind. Ask the patient to match different colored worsteds of various shades by day light. Color blindness may also be detected, and perhaps more accurately, in a dark room with a lantern with colored glass. Place the patient with back to the window or light and have him close his left eye and with his right gaze at the observer's left eye. Then let the observer move his hajids about in a plane mid-way between himself and the patient; so that each should see the hand at the same instant as it comes into the field of vision. The observer can see if the patient's eye wanders from his own and recall it. Test left eye in same way. If any defect in field of vision is suspected, use a perimeter. With a perimeter not only the field of vision, but also, by using different colored papers, the color field can be mapped out. Normally the color field is largest for blue, then for yellow, orange, red, green, etc., in the order named. If tliis order is changed there is said to be an "inversion of the cloror fields" (851-2). Normally the lines limiting the different color fields, when charted, are everywhere separate from each other. If they touch or cross there is "interlacing of the color fields" or "dychromatopsia" (851-2). The patient's hearing may be tested by voice, watch, or tuning fork. Be sure there is no wax in the ear. Ascertain whether he understands what is said to him, i. e., executes spoken commands. Galton's whistle should be used for test- ing high and low notes. Each ear should be tested separately. Bone conduc- tion is tested by holding watch or tuning fork firmly on skull. Normally a tun- ing fork, which, held on mastoid ceases to be heard, can still be heard when held close to meatus (Rinne's test). Normally a vibrating tuning fork, held on center of forehead, is heard equally in both ears. If heard best in the deaf ear (positive) the lesion is in external or middle ear. If heard best in the nor- mal ear (negative) the lesion is in inner ear or in auditory nerve (Weber's test). We also ask about ringing in ears (tinnitus aurium). In testing a malin- gerer, who claims to be deaf in one ear, place in his ears the ear-pieces of a stethoscope with long rubber, not metallic, tubes and speak into the bell (chest- piece) held some distance behind his back. While so speaking compress first one then the other tube a ntmiher of times. It will soon be evident whether he can hear with each ear, since he cannot tell which tube is open and which is shut. Ask the patient to name from its odor any fragrant substance (such as asafoetida, cloves, peppermint, etc.) held for a moment beneath each nostril in turn, the other being closed. Ammonia and acetic acid should not be used in this test. Ask the patient to point to the name on a printed card of the taste of a strongly bitter, sweet, salt or sour solution touched from a medicine dropper, or a camel's hair brash, to one side after the other of the protruded tongue. The tongue should be well washed between each test. The amoimt of sleep which the patient gets in the twenty-four hours is always an important question. Insomnia fagrypnia) is present in many nervous diseases and is apt to be exaggerated by patients; so that their statements should be controlled, when possible, by those of the nurses or relatives. Many symp- toms, especially fears, are worse at night: "Pavor noctumus of children." 44 CHART lb Inspection (mainly) Comprising Numbers 20 to 43. 45 Methods of Examination cf Patients Suffering from Nervous Diseases 20 Facial expres- sion and gen- eral appear- ance and behavior. (Charts XVI & XVII) 21 Walk. (Chart XIII) 22 Skull. (Chart XVI) 23 Vertebral col- umn. (Chart X) INSPECTION Methods of Testing The expression of the patient's face indicates, in most cases, the degree of his intelligence and his emotional state (sad or gay or anxious), and also may suggest the presence of certain diseases and conditions; such as myxedema and cretinism (( 116314). acromegaly (1183), scleroderma (1165), exophthalmic goitre (1193), paralysis agitans (677), myasthenia (554), nasal obstruction, atheroma of temporal arteries, notched teeth, hazy cornea, the saddle- back nose of syphilis, etc. His general appearance and behavior often indi- cate his power of self restraint (inhibitory power, breeding), or the existence of hallucinations (213) of sight, hearing, touch, or of compulsory acts (218). The walk of the patient may suggest the presence of hemiplegia (254), p>ara- plegia (257), local paralysis (259), ataxia (motor or cerebellar) (280-1), spasm (242), atony (252), paralysis agitans (677) and other tremors (250), pseudo- hypertrophic paralysis (500), hysterical paralysis (527), foot drop, (bilateral in multiple neuritis and lead palsy, unilateral in acute anterior poliomyelitis), weakness, exhaustion, etc. The skull should be observed as to type (brachy- or dolicho-cephalic, round or long heads), size (microcephalic — small, macrocephalic — large), rickets (box shaped), general or local hydrocephalus (bulging — posterior or anterior), fontanelles and sutures, asymmetry, tumors, etc- The spinal column should be observed as to curvature (angular or lateral), scoliosis, kyphosis, spina bifida (occultoj, deformity (dislocation). Pott's disease, tumor, tenderness (by palpation), etc. 24 Eye. (Charts V, & XIV) Note the existence of arcus senilis, the condition of pupils (unequal, anisocoria (341), miosis (340), mydriasis (339), and irregularity), the presence of keratitis or iritis, prominence of eyeballs, nystagmus, squint, ptosis, paralysis, etc. 25 Pupillary re- flex to light. (Charts V & XIV) 26 Hemiopic re- flex. Charts V & XIV 27 Pupillary re- flex to ac- commo- dation. (Charts V & XIV) Note whether each pupil, the other eye being covered, dilates and contracts as the eye is alternately shaded by the hand and exposed to light, or an electric light is flashed into it ; vision being constantly fixed upon some distant object. When a pupil contracts to light (direct reflex) the pupil of the other eye also contracts (consensual reflex). Naturally a pupillary reflex will not occur when the 5ris adherent to the lensi (posterior synechia) as the result of a former iritis, which itself is often due to syphilis (in which disease pupillary reflexes are of much importance) or to rheumatism. Note whether the pupil contracts as light is flashed on each half of the retina alternately. A ray of light collected by a lens should be used in this test. This reflex is difficult to obtain, and recent researches indicate that its existence is doubtful. It has been found, however, in a number of cases and verified by post- mortem findings in some of them. Note whether the pupil dilates when the patient looks at a distant object and con- tracts when he looks at one so near his face as to require convergence of the eyes. This test can be made on a blind man by having him first converge his eyes and then make the axis of his eyes parallel, by imagining that he is looking at a near and then then at a distant object. 46 28 Pupillary re- flex to pain. Charts, V, XIV (330) 29 Double vision, diplopia. (Charts VI & XIV) 30 Secondary deviation of the sound eye. (Chart XIV) 31 Nystagmus. (Charts IV & XII) 32 Tremor. (Charts IV & XII) 33 Convulsion and spasm (Charts IV & XII) 34 Paralysis (motor). (Charts IV, & XIII) INSPECTION (Continued) The pupils dilate when the patient suffers acute pain. Therefore, they dilate re- flexly when the skin of the face is sharply pinched, or pricked with a pm, or irritated by electricity. Note which eye deviates, however slightly, from the direct axis of vision and which eye lags more or less on movement of eyeballs in following the moving' finger. Place a colored glass before the affected eye, move a bright object (candle) throughout the field of vision and have the patient note the relative position of the two images. The colored image will of course be the one seen by the affected eye. Hold a card close in front of the sound eye. Have the patient look at an object so held that the weakened muscle must be brought into action. The sound eye covered by the card will be observed to move too far and when the card is re- moved the sound eye will quickly move back into proper position. The oscillation of the eyeball which constitutes nystagmus is often plainly to be seen. Extreme deviation of the eyeballs in one direction or the other makes it more evident, and at times demonstrates a nystagmus not otherwise apparent. If present, nystagmus is usually recognized while making the two tests 29 and 30. It should not be confounded with the irregular jerky motion of a weakened ocular muscle attempting to move the eyeball. Note anv tremor of lips, or other parts of the body. Note its frequency, amplitude, its relation to voluntary movements and whether it is associated with muscular rigidity. In testing for tremor, ask patient to hold arms ex- tended before him or over his head with fingers spread and motionless ; or observe him place his hand in his trousers' pocket. Note any convulsion (269), spasm (245-6), contracture (263-4), athetosis (271), choreiform movement (272), etc., which may be present. These various forms XI of spasm are often difficult to recognize and differentiate from each other. Note any obvious paraJvsis. such as ptosis. Note the naso-labial fold and the height of the angle of the mouth on each side. Wliile under close mspection, patient should be requested to execute every possible motion: i.e., wnnkle forehead (look upward, or open eyelids held closed by obserx-er), frown, open and shut each evelid, move eyeballs up and down and to either side (note whether upper eyelid follows eyeball well downwards), whistle, laugh, distend cheeks, raise upper lip and each angle of mouth, protrude tongue straight and move it in all directions, raise uvula in phonation, close jaws and move chin forwards and jaw laterally, contract strongly all muscles of face at once move head backwards, forwards and towards each shoulder and shake it, bend body in all directions, raise arms vertically, raise shoulder, adduct and fbduct arm flex and extend elbow, wrist and each finger, spread fingers, adduct, abduct, flex and extend thumb, pronate and supinate forearm while elbow is flexed stand on each leg, raise body on tiptoes, adduct and abduct thigh, flex and extend thigh, leg, foot and toes. X 47 35 Paresis. (Charts IV, X & XIII) INSPECTION (Concluded) Make strong resistance to above mentioned movements while patient is executing them: i. e., pull on eyelids, on one angle of mouth, resist movements of jaw, or of bending head, or body, or of flexing, extending, adducting and abducting joints, compare the strength of the paretic muscle with that of a similar healthy one. when possible, with its fellow of the opposite side of the body. For future comparison, etc., the strength of the paretic muscle can be registered by dyna- mometers, of which the most practical is the one for the hand grasp. Or sufifi- dent weights may be placed on hand, foot or head to overcome the attempted movement. By these tests the degree of the paresis can be approximately measured. ^ , . Note whether patient tires easily on repeated or continuous activity of any set of Myasthenia. , (Chart IV) muscles. zf. . Note whether patient can alternately extend and flex joints quickly and repeatedly. (Ch t 1 V^ '^ '^^^' especiaJly rapid alternate supination and pronation. 38 Ankylosis. 39 Contracture. (Charts IV & XI) 40 Muscle tone. (Charts IV & X) Note whether any joint is rigid, so that it cannot be moved. Ascertain the cause of the rigidity, whether bony union, contracted muscle or contracted scar tissue (muscle, ligament, skin, etc.). Note whether any muscle is contractured with consequent impaired motility of the joint and whether this contracture can be overcome by force, with or with- out etherization (active contracture), or not (passive contracture). Note whether muscles are firm or flabby, and whether or not resistance is offered to rapid motions of joints while the patient tries to avoid voluntary resistance. Normally there is slight resistance. In disease the resistance may be altogether absent (atonia), or weak (hypotonia), or strong (hypertonia). 41 Note whether any muscle shows atrophy or hypertrophy, or fibrillary contrac- Irophic lesions, tions, or if there is any arrested development or trophic lesions of other tissues (especially ulcers, herpes, glossy .skin, abnormalities of nails, etc.). (Chart XVII) 42 Coordination (synergy). (Charts IX & XII) 43 Muscle and joint sense. Deep sensi- bility (bath- yesthesia, kinesthe- sia). (Charts VI & XII) Note w'ltther complicated movements are executed in an orderly manner while the patient's eyes are closed. Ask patient to walk, touch point of nose with finger tip, pick up objects, write, touch knee with heel of other foot, hold foot steady in one position, trace a circle in the air with foot, walk backwards, side- ways and along a line, stand on one foot alone or on both feet close together, either side by side or one in front of the other (Romberg's symptom), stand on tiptoes or on heels, stand on one foot and trace a circle on the floor with the toe of the other foot. All these tests should be made both with eyes open and shut. Note whether patient, with his eyes shut, can tell whether his joints are flexed or extended, or can duplicate with one extremity the position in which his other is placed. Note whether he can estimate weights correctly or can grade by weight loaded balls correctly. Note whether he can locate his extremities in space. To test this, his eyes being shut, an extremity after being moved about is held in one position and he is told to turn his head and eyeballs so that when he opens his eyes he shall be looking directly at his thumb or great toe. When he opens his eyes it will be plain to see whether they are ditected right or not. 48 CHART Ic Palpation and Percussion Comprising Numbers 45 to 68 49 Methods of Examination of Patients Suffering from Nervous Diseases PALPATION AND PERCUSSION Methods of Testint. 45 Note the color of the skin, the pulsation of arteries in neck, the condition of the Circulation and jugular veins and the frequency and regularity of respiration, especially Cheyne- respira on. Stoke's respiration (425 ), whether respiration he costal or abnormal, or the dia- phragm be immobile, unilaterally or bilaterallv. (Chart XVII) 46 Note pulse of patient as to frequency, \olunie, tension (best tested by tonometer i^r-u^ \'\ni\ °'' sphygmomanometer) and irregularity in rhvthm and force. ( Chart A. V 1 1 ) 47 Difficulties in sensory testing. (Chart VI) The result of all sensory tests (and the same is true in regard to tests for many mental symptoms) depends upon the patient's truthfulness. Deception is always possible and even with the most truthful patients the tests require much time and the results are often contradictory, especially so, in e^■citable and in uneducated patients, who cannot iix their attention continuously. Notliing should be present to distract the patient's attention and his skin should be warm. In some nervous diseases the patient has occasional, spontaneous sensations which interfere with the tests. Most patients under the education of repeated tests become more acutely sensitive. On the other hand, tests too long continued tire the patient and give rise to contradictory results. It is to be remembered that the sensibility of the skin both for tactile and painful impres- sions varies greatly in diiiferent parts of the body and in different individuals. 48 Tactile sen- sibility. (Charts VI & XIV) With the finger tip (or with a smaller and lighter object, such as the head of a ]>in, a camel's hair bnish, a pledget of cotton, a hair, etc.), touch the patient's skin lightly, having told him to say "yes" every time he feels the slightest touch. Or the patient may describe figures (space sense) traced on his skin with ink (to prevent dispute or doubt). A pledget of cotton is better for accurate testing than is the finger tip or a pin, because with the cotton the pressure sense (49) is eliminated. Of course, during all sensory tests the patient's eyes must be closed or covered. In some cases of hysterical anesthesia, if the patient is told to say "no" when she does not feel the touch, she will say "no" only at the instant she is actually touched within the anesthetic ( ?) area; showing that sensation is not abolished, although it may well be abnormal (Janet's test). Tactile sensibility, or, more properly, ".space sense," or "localiz- ing sense," (.^.3), may also be tested with the esthe.siometer ; a pair of blunt dividers, by which it is noted how far the points may be separated and yet be felt as one. This distance varies greatly in difl'crent parts of the body (at the point of tongue it is one m. m., at finger tips two m. m., along back and on upper part of arm and thigh it is sixty-five m. m. The distance is smaller trans- versely than longitudinally on the extremities. Neither this compass esthesi- ometer. nor Hering's esthesiomcter gives more valuable results than the pin- head tests. When mapping out an anesthetic area commence in the anesthetic area and work towards the normal skin. Do the reverse in mapping out hyperes- thesia; i.e., from normal skin to h\peresthetic area. The electro-cutaneous test can be more accurately measured, but is of little practical value. 50 PALPATION AND PERCUSSION (Continued) 49 Pressure sense. (Chart VI) 50 Painful sen- sibility. (Charts VI & XIV) 51 Retardation of conduction. (Chart VI) 52 Persistence of sensation. (Chart VI) 53 Localization. (Chart VI) 54 Double sensa- tion and polyesthesia. (Chart VI) 55 Temperature sense. (Chart VI) 56 Pallesthesia. (Chart VI) 57 Cutaneous reflexes, (Chart V) Note whether patient can estimate correctly the amount of pressure exercised by the finger pressed against the skin, or by weights laid upon it. Note whether patient feels pain when pinched, or when skin is pricked by finger- nail, pin-point, or other sharp substance. Many instruments have been devised for measuring more or less accurately the intensity of the painful impression. -w Note whether the painful sensation is felt immediately upon, or some seconds after, the painful contact. Note whether the painful sensation persists a longer time, after the painful con- tact has ceased, than is normal. Note whether the point of contact, tactile or painful, can be localized correctly by the patient either by description or by pointing; his eyes, of course, being shut or bandaged. Note whether a single or painful contact causes two (double sensation) or more, sensations (polyesthesia). 58 Touch the sk-in at numerous points alternately with smatl test tubes, one filled with hot, the other with cold, water, or writh hot and cold bodies (spoons) of the same size and form. Certain points of the skin are especially sensitive to heat; others to cold. It is well, therefore, to test for heat and cold separately. Note whether the patient feels the vibration of a tuning fork (vibration sense) pressed so firmly on the skin that the vibration can be transmitted through the underlying bone (osseous sense). Stroke or scratch, as softly as will suffice, with finger nail or head or point of pin, the skin of the sole of the foot (plantar and Babinski), or ai buttock (glu- teal), or the inner side of thigh (cremasteric), or the side of abdomen (umbil- ical), or the hypochondrium (epigastric), or interscapular region (interscapu- lar),' or stroke firmly along the postero-internal border of the tibia (Oppen- heim's reflex^ and note the resulting movement of the great toe. The muscle itself must be felt and watched in cases where the resulting contraction is too slight to move the part. Cpharnygeal), and note the resulting movement. Note the pallor or redness of the skin, also rapid changes and flushings with or Mucous mem- Touch with finger, straw, brush, or probe, the cornea or conjunctiva (conjunc- brane reflexes, ^j ^ ^j. mucous membrane of nose (nasal), or palate (uvular), or pharnyx (Chart V) 59 Vaso-motor ^,,^,.^ ,,.^ ,^^^T^^^vvIT^'' w'thout''irritatbn, such as scratching with a pin or finger-nail (dermographia). (Chart V hysician. Occurs in insanity ( f unctionail ) . Occurs in hysteria and epilepsy (functional). A person performs complicated and apparently intelligent acts, while suffering from loss, or great im- pairment, of consciousness, and retains little or no memorj' of the acts done. Brain is probably anemic or ex- hausted, or the patient is under the influence of a great emotion (fright). Occurs in epilepsy, insanity, hypnotism, and rarely in hysteria (functional); not uncommon in childhood during sleep. 64 Diagnostic Symptoms 202 I N T E L L I G E N C E I M I I S H E D I 211 Amentia 212 Dementia I ^213 Hallucina- tions 214 Illusions 215 Delusions INTELLIGENCE Definition Absence or defect of intelligence, winch is congenital or is acquired in infancy before the intelligence has developed. Absence or defect of intelligence, which is acquired in later life in a person previously intelligent. Significance Due to a malformed or diseased brain. Occurs in idiots, imbeciles and feeble-minded persons. Due to atrophy or functional fail- ure or diminution of blood sup- ply of cerebral cortex. Occurs in insanity and is often its terminal stage. 216 Hypochon- driasis 217 Delirium 218 Compulsory ideas and actions (275) I. Vivid perceptions of sensations (visual, auditory, ol- factory, tactile, painful, etc.) not directly depen- dent upon any external corresponding reality; a sensation without an external object. They may rarely occur in normal individuals and then may be recognized or proved to be false, but they are usually regarded as real and are then associated with defect- ive judgment and mental impairment, and therefore cannot be corrected. Erroneous perceptions. A false interpretation of an actual sensation, which is really of a dififerent nature from that which the patient believes it to be. Fre- quently occurs in rational persons, especially in those with defective terminal sensory organs. In such cases easily corrected. Erroneous judgments (often, but not always, depen- dent upon hallucinations) which can be corrected neither by reason, nor by the evidence of the senses and which are not in accord with universal human experience, and are the consequence of mental en- feeblement. Delusions are systematized or un- systematized according as they are supported or explained by more or less coherent reasoning, or not. The systematized delusions are of much more serious prognosis. Delusions of imaginary symptoms and illness formed on an insufficient basis of abnormal sensations, which cannot be corrected and are associated with much mental depression. Irrational talk, or acts, or both in persons with di- minished consciousness. Probably due in most cases to hallucinations, illusions and mental confusion ; consequently its irrationality may be in part only apparent. Often occurs in fevers. Certain thoughts or questions or doubts, which are for- ever in the patient's mind and cannot be removed. They may be of any nature. Patients are irresistibly compelled by an unknown force to do certain acts or to say certain words, usually quite trivial. Patients recognize the abnormal character of these ideas and acts and are made very unhappy by them, but are quite unable to prevent them. Due to disease of the cerebral cortex, whether functional, cir- culatoTy, toxic or organic Usually symp- toms of insan- ity, or of ex- t r e m e degree o f neurasthe- nia, are also present. In in- sanity these perversions of intelligence can- not be correct- ed by reason and demonstra- tion, and in neu- rasthenia are only rarely and imperfectly so corrected. Methods for the detection of disorders of consciousness and intelligence are described in Chart la. For further discussion of these symptoms and the diseases in which they occur see Chart XVI. f5 CHART Illb Disorders of Memory and Emotions Comprising Numbers 203 and 204 and 220 to 237 67 203 M E M R Y D I M I N I S H E D Analysis of the Symptoms of the Case (Semeiology) MEMORY Definition Significance Inability to recall former perceptions and Functional or organic dis- ideas. Loss of memory in general. May ease of the cerebral cor- be more or less extensive. May affect tex, often anemia, some- memories of the immediate, or of the re- times the result of fright, mote, past. Diagnostic Symptoms 220 Amnesia 221 Inability, more or less complete, to rec- Agnosia ognize objects and acts, their uses and meanings, which were formerly well known ; the sensory nerves and end-or- gans and projection fibers being normal. Such patients perform idiotic and insane acts and put formerly well known objects to absurd uses (urinate in water pitcher, etc.). It may be regarded as a local amnesia. Among the various forms of agnosia are: Asterognosis (230), Alexia (229), Agraphia (228) and the different forms of Sensory Aphasia (223-6). 222 Inability to express by words some idea in Motor _ the patient's mind, although there is no aphasia paralysis of the vocal organs and the (aphemia). patient can usually express the idea by gesture. A loss of memory of how to speak (innervation memories), especially names. A limitation of the vocabulary. 223 Inability to understand (although not deaf) Sensory or spoken words formerly intelligible. Loss Auditory of memory of words formerly heard, aphasia Hence inability to recognize them when (word spoken (233). deafness) 224 Inability to name objects, which the patient Optic sees clearly, although he can name them aphasia after feeling them. Loss of visual memo- ries (232). 225 . . . Mixed Amixttire of the three forms of aphasia just aphasia described. 226 The use of a wrong word, or the omission Paraphasia of a word, or the placing of the right (Jargon word in the wrong place, in speaking, speech) with consequent incoherent speech. Jargon speech is an extreme degree of ithis. 227 The use of a wrong word, or the omission of Paragraphia a word, or the placing of the right word in the wrong place, in writing. 228 Inability to express in writing the idea in Agraphia the patient's mind, although he formerly could do so and his right arm and hand are not paralysed. 229 Inability to read words patient could for- Alexia . merly read, although he sees them clearly (Word and there is no paralysis of his vocal or- blindness) gans. 68 Lesion of a cortical sen- sory center, or of the association fibers con- nected with that center. Lesion in or near base of left inferior frontal con- volution and anterior portion of left island of Reil in right-handed persons, and of the right side in left-handed per- sons. Lesion in or near posterior part of left superior tem- poral convolution and posterior portion of left island of Reil in right handed persons. Lesion of left occipital lobe or of association fibers from this lobe in right handed persons. Any one or a combination of the above lesions, or a lesion of the island of Reil, or of external capsule in right-handed persons, in whom the above lesions are always in the left cerebral hemisphere, or. in slight degree, may result from carelessness, or alcohol- ism, or a mild dementia. Lesion in the base of the middle left frontal con- volution, cortical or sub- cortical. Sub-cortical lesion beneath left angular convolution in right-handed persons. Diagnostic Symptoms 230 Aster e- ognosis 231 Apraxia (282) 232 Psychic blindness 233 Psychic deafness Definition Inability to recognize objects by the sense of touch, although there is no anesthesia present in sufficient degree to prevent it. InabiHty to execute a desired act. Loss of skill in executing acts, although there is no motor paralysis present. Loss of in- nervation memories necessary to perform these acts. Inability to recognize well known objects or to comprehend familiar things by sight, although the patient is not blind. Loss of visual memories, optic aphasia (224). Inability to recognize and comprehend well known words and sounds, although the patient is not deaf. Loss of auditory memories. Includes sensory aphasia (223). Significance Lesion in or near cortex, or sub-cortex, of contra- lateral posterior central convolution. Cortical, or sub-cortical, lesion of motor area of contralateral hemisphere. Cortical, or sub-cortical, lesion of left occipital lobe, except in region of calcarine fissure. Cortical, or sub-cortical, lesion of left superior tempwral convolution in right-handed persons. 204 E M T I N S 234 Sadness (Melan- cholia) 235 Fear (Phobias) D I M I N I S 237 H Apathy E D 236 Joy (Mania) EMOTIONS Without adequate cause the patient is de- pressed and unhappy. There is a great repression of mental and physical activity usually. He can be influenced little, if at all, by reason ; difficult to get his attention. Without adequate cause the patient is in constant fear of an impending calamity, or has an unformulated fear. He has an unreasonable fear of the danger of contamination from filth, germs, etc., (mysophobia). He dreads to cross an open space (agoraphobia), or to enter a small room or confined space (claustro- phobia), or fears a storm (astropholiia ), or syphilis (syphilophobia), or ill-timed urination (urophobia), or everything (pantophobia), etc. Can be influenced httle, if at all, by reason. Frequently has a more or less unconscious sexual basis. Without adequate cause the patient is exhil- arated. There is great exuberance of men- tal and physical activity. Careless and destructive. Can be influenced little, if at all, by reason. Difficult to get his at- tention. Without adequate cause patient is in a dull, stuporous condition. No expression of physical or mental activity. An auto- maton, submitting passively to whatever is done to him. Functional or circulatory disturbance of cerebral cortex, especially cere- bral exhaustion. Occurs in neurasthenia and especially in insanity. Fears and apprehension seem to be the basic symptoms of many forms of incipient in- sanity (Mosher). Methods for the detection of disorders of memory and emotion are described in Chart la. For further discussion of these symptoms and of the diseases in which they occur see Oiarts XIII and XVI. 69 CHART IV Disorders of Voluntary Motion ANALYSIS OF THE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease. 240 DISORDERS OF VOL- UNTARY MOTION The power of executing movements by an effort of will is acquired in early life. The process is quite obscure, but seems to depend upon the existence of innerva- tion memories of past acts, primarily reflex. Voluntary motion de- pends ufKm the integrity of the central motor neu- rons (461 ) and of the peripheral motor neuro-i<: (462). In disease the power of voluntary mo- tion may be diminished, exaggerated or per- verted. MUSCULAR TONICITY Closely connected with the power of voluntary and. involuntary action is the fact that the muscles of a normal person are in a condition of constant, slight, but varying, con- traction. This is called mu.scular tonicity or tone. It is really a re- flex act caused and main- tained by many slight ir- ritations, and can be abolished by cutting the posterior nerve roots. Muscular tonicity is in- creased (hypertonia) in destructive lesions of the central motor neurons and in some functional disorders. It is di- minished (hypotonia), or abolished (atonia). in destructive lesions of the peripheral motor or sensory neurons, in lesions of the cerebellum. in sleep and in narcosis. 241 DIMINUTION also called AKINESIS and HYPOKINESIS 243 PERVERSION also called PARAKINESIS 242 EXAGGERATION also called HYPERKINESIS 71 f 244 PARALYSIS A condition in which the muscles cannot be con- tracted by the strongest effort of the will. As commonly used the term includes : PARESIS A condition in wliich the muscles can be contract- ed only feebly by the strongest effort of the will. f 245 TONIC SPASM A continuous, involuntary, muscular contraction of longer or shorter dura- tion (572). 246 CLONIC SPASM More or less rhythmical alternations of involun- tary, coarse, violent mus- cular contractions and relaxations. Must not be confounded with a coarse tremor (571). 247 IRREGULAR SPASM Tnvoluntarv acts of various L kinds (293-4, 573-4). 248 ATAXIA Disorderly movements due to loss of power of co- ordination (638). Asy- nergia (281-2). Asso- ciated with hypwtonia (252). Dysmetria (289.) 249 LOSS OF SKILL, APRAXIA Awkwardness. 250 ^ TREMOR Involuntary rhythmical os- cillation of some part of the body or of a muscle. I Less pwwerful, more rapid and more rhyth- mical than a clonic I spasm but similar in appearance, especially when coarse. Tremor may be slow (3 to 6 per second) or rapid (8 to 12 per second). It may ^ be coarse or fine (639). 'The conditions under which paralysis or paresis occurs are set forth in Chart IV a The conditions under 'which the various forms of spasm occur are set forth in Chart IV b The condStians undeV "which the various forms of per- version o f motion occur are set forth in Chart IV c. CHART IVa Motor Paralysis Comprising Numbers 244 and 251 to 260 7A Analysis of the Symptoms of the Case (Semeiology) 244 PARALYSIS CHARACTER EXTENT p A H R A A R L- A Y C S T I E S R Diagnostic Symptoms r 251 Spastic, or hyper- tonic, paralysis. (473). (Figs. 24-6) 252 Flaccid, or hypo- tonic, or atonic, or atrophic paralysis (472). (Figs. 24-6) 253 Myasthenic paralysis ('554) MOTOR PARALYSIS Definition A paralysis in which the muscles show in- creased tone and offer much resistance to passive motion, especially rapid motion. The normal excursion of the joint is re- stricted. The muscles have their normal volume and under the microscope their fibers show a normal appearance. The electrical reaction of muscle and nerve is normal (394). The tendon reflexes are increased. Significance Destructive lesion of cen- tral motor neurons(461). It occurs in diseases of the brain or spinal cord, or may be functional. Rarely a reflex spasm (268), especially pre- putial irritation in children, or pain, may simulate this condition. A paralysis in which the muscles have lost their tone and offer little or no resist- ance to passive motion, even when rapid. The joint has a normal or even increased excursion. The muscles ex- hibit a great and rapid atrophy, and under th( microscope their fibers show a loss of their transverse striation and various forms of degeneration (fatty, hyaline, etc.). The electrical reaction of degeneration is present (397). When muscles are completely degenerated (402) pa sive contractures (263) may occur, in which stage the flaccidity and free ( xcursion of the joint are lost. The tendon reflexes are abolished or di- minished. A rapid tiring of muscles ujx)n exercise. A myasthenic reaction to electricity (399.) Muscles show small foci of small round cells. Destructive lesion of peripheral motor neurons (462). It oc- curs in disease of the mus- cles, peripheral nerves, ante- rior horns of cord, or motor nuclei in brain stem. It is never functional, but may be somewhat simulated by joint disease. Hypotonia wnth- out muscular paralysis or atrophy occurs in cerebellar lesions, tabes and other ataxic conditions (240). A lesion of the muscles and often of the thymus gland. 74 Diagnostic Symptoms f254 Hemiplegia (478-9) (Figs. 17-24;^ P A R A Y S I S i 255 Diplegia (478) 256 E X T ^ Crossed E N T MOTOR PARALYSIS (Continued) Definition A paralysis with exaggerated tendon reflexes of one lateral half of the body and extremi- ties limited by the median line in front and behind. It is partial, if limited to arm and leg; complete, if arm, leg, tongue, palate and face are all involved. In some cases of hemi- plegia there are slight weakness and exag- gerated reflexes on the other side of the body also, especially in the leg. Symmetri- cal, bilateral muscles, which have a com- mon function and a bilateral cortical inner- vation, are not paralysed : at most tempor- arily weakened. Such are the ocular, mas- ticatory, laryngeal, respiratory, diaphrag- matic, bladder, rectal, etc., muscles. In cerebral hemiplegia certain muscles are, in most cases, more completely paralysed than others. These "predilection muscles of Wernicke" are the trapezius, the ex- ternal rotators and adductors of the upper arm, the triceps, the supinators and ab- ductors of thumb, the exten.sors of the thigh, the flexors of the leg and the dorsal flexors of the foot. A double hemiplegia involving both sides. May be complete or partial and not infre- quently is limited to the legs, or the face (facial diplegia), etc. paralysis (537-42) ( Hemiplegia alternans) (Figs. 20-1) 257 Paraplegia (480) (Figs. 24-6) 258 Monoplegia (479) (Fig. 15) 259 Local paralysis (481') (Fig. 15) Significance A lesion of the contralat- eral central motor neu- rons (461). H e m i- plegia is usually due to a cerebral lesion, but the partial form may be due to a spinal 'esion, very rarely. Verj' rare- ly, there may be no lesion, except an ex- treme local anemia or edema of the brain as in nephritis (hemiplegia sine materia). A lesion, usually but not always cortical, of the central motor neurons or basal nuclei on both sides. A paralysis of one or more homolateral cranial nerves and of the contndateral arm .'uid leg. Always due to a lesion involving the pyramidal tract with other structures in the brain stem (460) ; either in the medulla (hypoglossal hemiplegia alternans — 1290—1), the pons (facial hemiplegia alternans — 1292), or in the crus cerebri (motor oculi hemiplegia alternans — 129.3). The nuclei, or the neurons, peripheral or central, of the cranial nerves are involved below the decussation of their central neurons. A symmetrical par- alysis of both sides of the body. Usually orly i n- volves the legs and lower part of body, but may involve the arms and even both sides of the face. May occur in lesions of the muscles (dystrophies — 477), or of the peripheral nerves (neuritis — 488-9). or of the spinal cord, or brain stem, or even of the cerebral cortex (bilateral lesion). The distinction between paraplegia and diplegia (255) is not always sharply drawn. In general diplegia is applied to paralyses of cerebral origin, paraplegia to those of spinal or peripheral origin. •A paralysis of one ex- May be due to lesion of motor cerebral cortex, tremity only, or of or of the motor nuclei, or of the peripheral one-half of the face nerves. only. May be due to lesions of muscles or of peripheral nerves, or of spinal cord, or rarely of motor cerebral cortex, or functional. A paralysis limited to one or more muscles of the face, eye, mouth, neck, body or extremities. Less than a whole extremity. Inability to produce vocal 260 sounds. Absence of Aphonia voice, but whispering is [ (737-8) i)Ossible. Methods for the detection of paralysis and paresis are described in Chart I b. For further consideration of these symptoms and of the diseases in which they occur, see Chart X. A variety of local paralysis. Laryngeal paralysis, or- ganic or functional. CHART IVb Spasm Comprising Numbers 245 to 247 and 263 to 276 Analysi> of the Symptoms of the Case (Semeiolo^^y! Diagnostic Symptoms r263 Passive contrac- ture (Figs. 24-6) 264 Active contrac- ture (Figs. 15, 17, 24-6) 245 T N I S P A S 265 Myotonia (590-603) 266 Rigidity 267 Convulsive tics (598) 268 Reflex spasm SPASM Definition A continuous contraction of long duration in which the muscles, tendons and ligaments have become anatomically shortened and cannot be extended by force, even under etherization. The muscle' fibers are degenerated, while the connective tissue of the muscle is hypertro- phied and usually secondarily contracted, as in other newly formed connective, or scar, tissue. A continuous contraction lasting weeks, months, or years, which can be overcome by force, either with or without etherization. Muscles are in a normal condition of nutrition. Most common in the arms, or legs, or neck muscles (torticollis). The active contracture of a hemiplegia is usually that of flexion in the arm and of extension in the leg. An active contracture of brief duration but much longer than a convulsive tic. It may occur at the commencement of voluntary motion (Thomsen's disease, or myotonia congenita) or may be excited by cold (Eulenberg's disease, or paramyotonia congenita). It is frequent in meningitis and tetanus in which it takes many forms, viz: "retraction of head;" "trismus," strong closure of jaw; "opisthotonos," arcliing of body backwards; "pleurosthotonos," bend- ing of body to one side : "emprosthotonos," arching of body forwards and "orthotonos," holding of body rigid and straight. An active contracture of such mild degree that it does not prevent passive, or even voluntary, motion of the part, although rendering it diffi- cult (paralysis agitans, etc. — 677). A violent spasm of momentary duration. If rapidly repeated it must be classed under myo- clonus (270 and .598 to 601). If painful it is called "tic douloureux" (599). A spasm, usually tonic, caused by irritation of some sensory tissue. It is especially common after injury. Many, if not all, of these reflex spasms may be, really, hysterical and can be ci"-c-<^l by suggestion (415). j Significance Due to muscular lesions and to degeneration of the peripheral motor neurons (462). Active contractures occur- ring in hemiplegia affect the muscles not abso- lutely paralyzed. When the contracture is over- come by the application of a plaster of Paris splint, the muscles often show a surprising degree of voluntary motion when the splint is re- moved. These contrac- tures depend in part, on attempts at voluntary movements and on asso- ciated movements, but in greater part on reflex action from sensory irri- tation ; the inhibitory ac- tion of the brain being cut off by the lesion. They never occur in hemiplegia in tabetics and in any case can be relieved by section of the po.sterior nerve roots. Such contractures are always of very bad prog- nosis as to recovery from the hemiplegia. Active contracture is some- times due to paralysis of antagonistic muscles or to muscle lesions. All tonic spasms (not in- cluding pas.sive contrac- ture) are due to a func- tional disorder, or are reflex (especially in chil- dren), or are due to irri- tation (chemical, sen.sory or vascular) of central motor neurons (461). Painful cramps, espe- cially in legs, of the na- iture of myotonia or tics, may be due to a de- ficiency of water in the system, and to cold. 7.S j^IAGNOSTIC Symptoms 246 ^ 269 Gjnvulsion (571) i 270 Myoclonus or convul- sive tics 271 Athetosis or mobile spasm (574) SPASM (Concluded) Definition Significance Violent clonic contractions of man}', or of all the, muscles of the body. Successive clonic contractions of one or of a few adjacent muscles. Repeated convulsive tic. Most common in the face muscles (blepharo- spasm (598). Slow, worm-like, rhythmical movements, often "j associated with transitory contractures (spasmus mobilis), of fingers and wrists and more rarely of toes and ankles. Hyperex- tension is the predominant action. Usually unilateral, but may be bilateral. Much more common in children than in adults. Muscles of the neck, face and of other parts of the body are not infrequently involved. It never occurs in completely paralysed mus- cles. 272 Rapid, irregular, coordinated but purposeless Choreic movements caused by contraction now of one move- group of muscles, now of another, through- ments out the body; bilateral or unilateral (hemi- Chorea minor chorea). Cease during sleep. They often i^^^) render voluntary movements ataxic and are usually associated with a mild degree of paralysis of the muscles involved. 273 Patient performs involuntarily and uncontrol- Chorea ably a complicated and apparently purpose- major or ful movement. Also applied to a coarse tre- magna mor or violent oscillation of a part of the (629) body. 274 Patient frequently performs involuntarily, and Habit usually unconsciously, the same act. Usually chorea a small act. (627) 275 Patient is compelled by some power within him, Compulsory which he cannot understand or explain, to acts (218") perform certain acts against his will. Clonic spasms are usually due to irritation of the cerebral cortex, but may also result from very exaggerated reflexes (clonus). Lesion is usually in the caudate nucleus and putamen of contrala- teral hemisphere and not causing complete paralysis. May occur in diffuse cortical le- sions. Functional disorders, oc- curring in the neu- roses and in insanity. Choreiform movements, as well as athetosis and tremor, may occur in lesions of the corpus striatum. J 276 Associated move- ments (Synkinesis) Unintentional muscular contractions, occurring when movements are executed, or attempted in muscles not directly concerned in the move- ment attempted; often the corresponding muscles of the opposite side of the body, often those of the face. Such associated movements are Bell's phenomenon (4,34), Striimpell's tibialis phenomenon (435), Babinski's associ- ated movements in unilateral paralysis (436). In such cases movements often associated to- gether, but which can be easily dissociated volun- tarily in health, can- not be dissociated in disease which cuts off voluntarv action. Methods of detection of spasm are described in Chart I b. For further discussion of these symptoms, and of the diseases in which they occur, see Charts XI and XII. 79 CHART IVc Perversions of Motion Ataxia, Loss of Skill, Tremor Comprising Numbers 248 to 250 and 280 to 294 81 Analysis of the Symptoms of the Case Semeiology ATAXIA— LOSS OF SKILL [Ataxia is a disorder of one or more synergic units (simple asynergia), or of complex cerebellar synergia (integrative asynergia), or a disorder of the cerebral cortex (apraxia).] Diagnostic Symptoms Definition (280 Motor ataxia (644) ( dynamic ataxia) (Figs. 24-6) 281 Cerebellar ataxia (642) ( static ataxia) (Figs. 19-26) Voluntary movements are executed in an irregular and disorderly manner, which is due to a loss of the co-ordi- nating power. Rarely associated with decided vertigo. Walking and standing are inco-ordi- nate, but other acts are not, or only slightly so. Patient executes simple movements of his legs fairly well when lying in bed, but in walking and standing he lacks synergy of the muscles and staggers and sways like a drunken man. Asynergia major usually associated with vertigo (392). Significance Is due to a loss of muscle sense (43) (deep sensibility). May be due to lesions of peripheral sensory nerves, or of posterior colimins of cord, or of brain stem, or of cerebral cortex posterior to fissure of Rolando, or may be toxic (alcohol), or func- tional. Is due to lack of muscular synergy (42) (asynergy). Due to lesion or functional disorder of the cerebellum or its tracts, including the direct cerebellar tract in brain stem or cord, or to tumors in frontal lobe of brain or to disease of ears or eyes, or to poisons (alcohol, etc.). In lesions of the cerebellar hemisphere the disorder may be transitory; in lesions of the worm it is more per- manent. r 282 Apraxia (Fig. IS) 283 Anarthria (737) 284 Dysarthria (738) 285 Dysphagia 286 Dysmasesis (554) 287 Astasia and Abasia (652 and 795 288 Adiadocoki- nesia {?>7) 289 Dysmetria Inability, or difficulty, in performing a desired and accustomed act be- cause of loss, or derangement, of the innervation memories concerned in that act (Motor aphasia, agraphia, etc.). The voluntary movements are awkward but not exactly ataxic. The patients seem to have lost their initiative to action. Sometimes a de- sired action is replaced bv a different one (231). Loss of skill: Asyner- gia minor. Absence of speech. Speech may never have been acquired, as in idiocy, or may never have been acquired on ac- count of deafness, or it may be voluntarily restrained for a purpose; or it may be more or less involuntar- ily restrained, as in insanity or hys- teria (Mutism 744-7). Such difficulty in articulation that 1 Occur in speech becomes indistinct and blurred, but is probably never so great as to cause complete anarthria (283). Lesion of the cerebral "common paths" or loss of innervation memories, general or partial, due to cortical or subcortical lesions of the anterior or posterior central, or supra-marginal convolutions, or to the association fibers connected with these convo- lutions, or to functional or anemic disorders of cerebral cortex. (See page 37^. May be either functional or organic and, if the latter, may or may not be due to lesions in the peripheral organs of speech. If not, it is called pure motor aphasia or aphemia. Difficulty in swallowing. Difficulty in mastication. Complete inability to .stand or but legs can be moved freely, strongly, when lying or sitting. walk even Difficulty in repeating a movement rapidly, especially .supination. An exaggerated extension of the fingers just previous to grasping an object. 82 esions of the medulla and pons (bulbar paralysis, Figs. 21-3) and of the cranial nerves. Also in diphtheria, hydrophobia, mya.sthe- nia gravis, rarely in trichinosis and frequently in hysteria (globus hystericus). These symptoms are due to a combined disorder of syn- ergic units and of integrative syn- ergia, or to nuclear or cranial nerve paralysis, or are functional. A delusion or auto-suggestion, which occurs in hysteria. May occur rarely in cerebellar lesions. Occurs in lesions of a cerebellar hem- isphere, or is functional. Due to disorder of (282). the synergic units. 250 T R E M R Diagnostic svmptoms TREMOR Definition 290 Involuntary, rhythmical oscillation or Passive trembling of a part which is other- tremor wise at rest. (646 and 647) 291 Intention tremor (645) An involuntary tremor which only occurs when a voluntary motion is made, or is willed and is about to be made. 292 Nystagmus (640) 293 Fibrillary contrac- tion or fibrillation (641) 294 Myokymia (697) Significance Functional. Occurs in paralysis agi- tans, weakness, etc. Functional and organic. Occurs in neuroses and in organic diseases (disseminated sclerosis). It is due to dissociation of synergic units and, therefore, is asynergia rather than tremor. It is caused by lesions of the cerebellum, of the putamen and lenticular nucleus and of the red nucleus and rubro-spinal tract. An involuntary trembling or oscillation of eyeball, usually horizontal, rarely verti- cal, very rarely rotatory. Increased, or only occurs, on voluntary motion of eye- ball, especially on extreme deviation. The rapidity of the oscillations varies from 60 to 200 per minute ; their amplitude from 2 to 4 millimeters. Nystagmus may be oscillatory when the motion in each direc- tion is equally rapid, or rhythmic when it is quicker in one direction than in the other. Ocurs espeially in lesions of the vestibular and other nuclei in the pons, Deiter's nucleus in the cerebellum, the pos- terior longitudinal bundle in the brain stem, in disturb- ances in the semi-circular canals, and in weakness of ocular muscles, and in lesion of ponto-cerebellar angle, also in the caloric reaction (79), and in cerebellar disease (80). It is due to dissociation of synergic units (asynergia.) An involuntary contraction of a bundle Degeneration of those multipolar nerve of fibers of a muscle of short dura- tion. When many occur in adjacent bundles at short intervals, waves of contraction run over the muscle, but do not cause it to contract as a whole. cells in the anterior horns of the spinal cord and brain stem of which the motor nerves supplying the mus- cle are the axons. Rarely occurs in traumatic neuroses. A fibrillary twitching of the muscles Normal. Exhaustion. Following ex- occurring in healthy persons. cessive muscular contraction or ex- posure to cold. Methods of detection of perversions of motion are described in Chart I b. For the further discussion of these symptoms and of the diseases in which they occur, see Chart XII. 83 CHART V Reflex Activity ANALYSIS OF THE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease. 296 REFLEX ACTS [297 CUTANEOUS OR SUPER- 1 FICIAL REFLEXES A reflex act which originates from an irritation of the skin (57). An involuntary movement caused by irritation of a sensory nerve or terminal organ. Although not the result of a conscious in- tention, yet these acts seem purposeful and usually tend towards the protection of the body. In order that a reflex act may take place there musi be a comparatively healthy re- flex arc, consisting of a motoi nerve, a sensory nerve and some gray matter connecting the two; or, in other words, a motor neuron and a sensory neuron connected together di- rectly or by a bridging neuron. Reflex acts are inhibited and modified by inhibitory im- pulses passing down from the brain along the so-called inhib- itory fibers, which are also the central motor neu- rons : the pyramidal tract (472-4, 811). '(Figs. 19, 24). 298 MUCOUS MEMBRANE REFLEXES A reflex act which originates from an irritation of a mucous mem- brane (58). 299 TENDON OR DEEP REFLEXES A reflex act which originates from the sudden stretching of the fibers of a muscle (60-6). 300 ORGANIC REFLEXES A reflex act afi"ecting one of the viscera of the body, especially the bladder or rectum ( 1 ) . 301 VASO-MOTOR REFLEXES A reflex act affecting the arterioles (59). 302 PUPILLARY REFLEXES A reflex act affecting the pupil (25-8). The conditions in which reflex acts are disor- ordered are set forth in Chart V a. The conditions in which the pupillary reflexes are disordered are set forth in Chart V b. 85. CHART Va Cutaneous or | Superficial ^ Reflexes, Mucous Membrane Reflexes, Tendon or DeepIReflexes, Organic Reflexes, Vaso-Motor Reflexes Comprising Numbers 303 to 328 87 Analysis of the Symptoms of the Case (Semeiology) CUTANEOUS REFLEXES Diagnostic Symptoms 303 Plantar 304 Babinsld's 305 Gordon's 306 Oppenhdm's 307 Gluteal 307a Anal 308 Cremasteric 309 Umbilical 310 Epigastric 311 Interscapular 312 Corneal or conjunctival Definition, Elicitation and Location of Reflex Centers. Plantar flexion of tlie toes associ- ated with a contraction of the tensor fasciae femoris (Bris- saud's reflex) when the sole of the foot is irritated. (1st and 2nd sacral segments.) Sluggish extensive dorsal flexion of the great toe when the sole of the foot is irritated. Dorsal flexion of the great toe when deep pressure is made through the calf muscle on the deep flexor muscles beneath ; the leg being completely relaxed. Dorsal flexion of the great toe elicited by firm stroking with a hard object, or finger, just he- hind the postero-internal border of the tibia from above down- wards ; the leg being completely relaxed. Contraction of the buttocks when the skin covering them is irri- tated. (4th and 5th lumbar segments.) Contraction of sphincter ani upon pin pricks of anus. (5th sacral segment.) Drawing up of the testicle when the inner side of the thigh is irritated. (1st to 3rd lumbar segments.) Sudden movement of umbilicus towards the side of abdomen irritated. (8th to 12th dorsal segments.) Sudden retraction of epigastrium when the hypochondrium is irritated. (7th to 9th dorsal segments.) Drawing inwards of the scapula when the skin of the interscap- ular space is irritated. (Sth cervical to Ist dorsal seg- ments.) Closing of the eyelids when the cornea or conjunctiva is irri- tated. (Sth to 7th cranial nucla.) Significance The abnormal reflexes, Babinski, Gordon and Oppenheim reflexes and ankle-clonus, always indicate disease of the central motor neu- rons (461), except in infants, in whom these reflexes (except ankle-clonus) may be pres- ent normally, and in some cases of hysteria, in wliich an imperfect ankle-clonus may rarely be obtained. The Babinski reflex is most reliable in a diagnostic sense. The Oppenheim reflex is sometimes present when the Babinski is absent and vice versa. Ker- nig's sign indicates meningitis or meningis- mus ; it is an important but not certain, diag- nostic sign (320). Alterations in the tendon reflexes are of very much greater diagnostic value tlian are those of the cutaneous (except the Babinski) re- flexes, which are in many cases inconstant, probably because the cutaneous reflex im- pulses may possibly pass through the gray matter of the brain (cerebellum) as well as through a wide area of tliat of the spinal cord. Diminution of reflexes is usually of little diag- nostic value, but their abolition is of great value and may be due to a destructive lesion of any part of the reflex arc (a peripheral motor neuron, a peripheral sensory neuron, or a central bridging neuron). When there is a lesion of the peripheral motor neuron, atrophic motor paralysis is present in ad- dition to the loss of the reflex. When there is a lesion of the peripheral sensory neuron there is usually a sensory paralysis (anes- thesia, etc.) in addition to the loss of the re- flex. Diminution or abolition of reflex activity (cutaneous or tendon) may occur, at least temporarily, in acute diseases or other forms of irritation of the central motor neurons; also in cases of shock, exhaustion, coma, narcotism and after epileptic fits, (except Babinski) ; also by will power and by voluntary movements of the muscles concerned; also (except Babin.ski) in recent cases of complete separation of the brain from the reflex centers in the spinal cord, and, rarely, from increased intracanial pressure, also frequently in fevers. 88 MUCOUS MEMBRANE AND TENDON REFLEXES. Diagnostic Symptoms 313 Nasal 314 Auditory-or- bicularis reflex. 315 Uvular 316 Pharyngeal 317 ■ Ankle-clonus 318 Achilles reflex 319 Knee-jerk Definition, Location of Elicitation and Reflex Centers. 320 Kernig's sign 321 Dorsal foot reflex 322 Elbow and wrist reflexes 323 Maxillary reflex Sneezing when the nasal mem- brane is irritated. (5th to 10th cranial and upper cervical nuclei.) When a loud noise is unexpectedly made immediately behind the patient, his orbicularis muscles contract. This reflex cannot be inhibited and may serve to de- tect simulated deafness. Raising of the uvula in phonation or upon irritation of its mucous membrane. (9th to 10th cranial nuclei.) Retching or gagging when the pharynx is irritated. (9th to 10th cranial nuclei.) Oscillation of the foot when the ball of foot is pressed quick- ly and continuously upwards. (5th lumbar and 1st sacral seg- ments. ) Sudden plantar flexion of foot when the tendo Achillis is sharply struck, patient kneeling. (1st and 2nd sacral segments.) Sudden extension of knee when the ligamentum patellae is sharply struck. When this re- flex is exaggerated it is usually accompained by a contraction of the adductors of the opposite thigh, or even by knee-clonus (61). (2nd to 4th lumbar segments.) Resistance to sudden extension of the knee. Sudden plantar flexion of the toes when the dorsum of the foot over the 4th and 5th metatarsal bones is struck. (5th lumbar and 1st sacral seg- ments.) Sudden extension or flexion of el- bow or wrist when the corres- ponding tendons are sharply struck. (5th to 7th cervical segments.) Sudden closure of jaw when it is sharply struck downwards. (5th cranial nucleus.) Significance The abolition of the knee-jerk is of great diag- nostic importance. It is absent in tabes, neuritis (multiple and crural), acute anterior iwliomyelitis involving the extensor cruris, Landry's paralysis, lesion of the cauda equina or of the lumbar enlargement, during an attack of family periodic paralysis, after an epileptic attack and in cases of muscular dystrophy involving the extensor cruris muscles. It is usually abol- ished in Friedreich's ataxia and combined sclerosis, except in the early stages when it may be increased. It may be absent in cerebral compression (tumor or meningitis) and in some cases of cerebellar disease, and may then be unilateral. It may be absent also in the conditions mentioned in the preceding paragraph. Exaggeration of the reflexes may be due to a mild inflammation, or to any irritation, of any part of the reflex arc. Strychnine in- creases reflex activity by irritating the nerve cells in the anterior horns. More commonly, the refle.xes are increased by any lesion of the central motor neurons, thus cutting off the normal inhibitory influence of the brain, and are then associated with paralysis of voluntary motion. The presence of ankle- clonus, the Babinski reflex and the dorsal foot reflex indicates a lesion of the pyramidal tract much more certainly than does an ex- aggerated knee-jerk, unless the latter is associated \vith an adductor contraction. Very commonly the reflexes are increased in functional diseases (hysteria) and in nervousness. Innervation of the muscles not concerned in the reflex act and diverting the attention increases reflex activity (reinforcement, 68). The paradoxical reflex is of no diagnostic im- portance. It consists in a contraction of the tibialis instead of the calf muscles when ankle-clonus is tested for; also of a con- traction of the flexors instead of the exten- sors of the tliigh when the knee-jerk is tested for. In the dorsal foot-reflex (Mendel-Bechterew) normally there is either no reflex or a dorsal flexion of the toes, but in cases of pyramidal tract lesions a plantar flexion of the toes occurs. 89 ORGANIC AND VASO-MOTOR REFLEXES. Diagnostic Symptoms 324 Bladder or vesical reflex. 325 Rectal reflex 326 Ischemic reflex 327 Paralytic, hyperemic reflex (dermogra- pliia) Definition, Elicitation and Location of Reflex Centers. The retention of urine in the bladder by the splrincter reflex, the expulsion of urine by the detrusor reflex and the syn- chronous relaxation of the sphincter. ( Hypogastric sympathetic gang- glia.) Similar to that of the bladder. (Hemorrhoidal sympathetic gang- lia.) A sudden pallor of the skin fol- lowing an irritation and limited to the area of irritation. Congestion of the skin follow- ing the ischemia due to irrita- tion (taches cerebrales and dermographia). Significance. Inability to void urine, or to retain it, is some- times due to nervousness and sometimes to mechanical obstruction (enlarged prostate or stricture), but any other serious disturbances of the organic reflexes indicate organic disease of the nervous system. It never occurs in diseases limited to the peripheral nerves, except in lesions of the cauda equina, and rarely in cerebral disease. It is most common in spinal disease: sphincter paralysis with empty bladder and constant dribbling of urine in lesions of lumbar en- largement, and detrusor paralysis with dis- tended bladder and often with dribbling of urine in lesions above the lumbar enlarge- ment. (Fig. 28.) Vaso-motor disturbances cause a disturbance of the nutrition of the part. Diseases which result from, or are associated with, disturb- ances of the vaso-motor reflexes are dis- cussed in Chart XVII. 328 By irritation of the skin or deeper tissues of Reflex of the leg, more especially by firm lateral com- spinal pression and powerful flexion of the foot Automatism and toes there results a flexion of all the (Marie) joints of the leg and a withdrawal of it up- Defensive wards. ( Babinski ) Lesion of the pyramidal tract. The methods of eliciting the various reflexes are described in Chart I c. Diseases in which the reflexes are altered are discussed in Charts X, XIV, XVI, XVII. ■.■•'.••.. 90 i: I CHART Vb Pupillary Reflexes Comprising Numbers 302 and 329 to 341. 91 Analysis of the Symptoms of the Case .(Semeiology) 302 P U P I L L A R Y R E F L £ X E S Diagnostic Symptoms r329 Pupillary reaction to light (25) PUPILLARY REFLEXES Definition, Eucitation AND Location of Reflex Centers 330 Pupillary reaction to pain (28, 335) 331 Pupillary reaction to accom- modation (27) 332 Argyll- Robert- son phe- nomenon (437, 891) 333 Immobile pupil (545) 334 Hemiopic reflex (26) Significance Pupil contracts when light is thrown on retina of the same eye (direct reflex), and when light is thrown on retina of opposite eye (consensual re- flex), and dilates when retina is shaded front light (ciliary ganglion). Pupil dilates in pain, pincliing, pin pricks, etc., of skin. The direct pupillary reaction to light is abnormal in lesions of any part of the reflex arc (optic nerve, cor- pora quadrigemina, the VVestphal-Edinger cell group of the motor oculi nucleus, third nerve and ciliary gang- lion). If the lesion is in front of the optic chiasm, there will result blindness of the corresponding eye with loss of the direct, but preservation of the consensual reflex. If the lesion is back of the chiasm there will result a partial, never complete, loss of the field of vision of both eyes, and both the direct and the consensual pupil- lary reflexes will be preserved. If double lesions occur in the proximity of both corpora quadrigemina and total blindness results, both the direct and consensual reflexes are lost. If the double lesions are posterior to the corpora quadrigemina and bilateral heinianopia or total blindness results, and both the direct and consens- ual pupillary reflexes are preserved. Both these reflexes are absent in deep .sleep, narcosis, shock, coma, epileptic, and occasionally in hysterical, attacks; also absent in tabes, in many cases of paresis and in rare cases of syphilis alone ; absent also when the eye is under the in- fluence of mydriatics or miotics. A careful study of tlic pupillary reflexes will serve to detect many cases of malingering. This reflex may be deranged in lesions of the cervical sympathetic ganglia of the same side. Pupil dilates when I>atient looks at a distant object and visual axes are parallel and con- tracts when patient looks at a near ob- ject and eyes con- verge. Pupil does not re- spond to hght, but does respond to ef- forts at accommo- dation. The pupil responds neither to light nor accommodation, but in some cases may still dilate slightly^ on irritation of cervncal s y m p a - thetic. Pupil contracts when light is thrown on the unparalysed half of retina, but does not contract when light is thrown on para- lysed half. The pupillary reaction to accommodation is absent (cyclo- plegia) in lesions of the third nerve, sometimes after diphtheria, occasionallv in alcoholism and when the eye is under the influence of mydriatics or miotics, also in myopia and in cases of deficient convergence. The Argyll-Robertson phenomenon occurs in almost all cases of tabes and paresis (in many of these cases a degeneration of the posterior columns of the cord has been found at autopsy) and very rarely in cases of syphilis in which there are no manifestations of either tabes or paresis for years afterwards. The reverse of the Argyll-Robertson phenomenon, i. e., the preser- vation of the light reflex and the loss of the accommo- dation reflex, occurs occasionally in diphtheritic jjaral- ysis and has been found associated with syphilis, basal meningitis, tumors of corpora quadrigemina and mye- litis. It is extremely rare. Immobile pupil may occur in lesions of the optic nerve or tract or in its nucleus or in that of the third nerve or in the ciliary ganglion or its nerve. It may also be associated with ojihthalmoplegia externa or interna of both. When it occurs alone it is due to lesion in the nucleus. Immobile pupil also occurs in tabes, in epi- lepsy, in some forms of hysteria, in fainting, and in katatonic stupor. The hemiopic reflex occurs only in lesions of the optic tract or geniculate bodies (homonymous hemianopia) or of the central part of the optic chiasm (bitemporal hemianopia). The existence of this reflex is disputed by many obse^'^rs. 92 PUPILLARY REFLEXES (Concluded) Diagnostic Symptoms 335 Cilio- spinal reflex (465, 1191-2) 336 Hippus 337 Westphal's pupil reaction 338 Paradoxical pupillary reflex 339 Mydriasis 340 Miosis Dehnition, Eucitation AND Location of iReflex Centers Significance 341 Unequal pupils or anisocoria dilates when The cilio-spinal pupillary reflex is absent in lesions of skin of the the cervical sympathetic, and in many lesions of the medulla and lower cervical and upper dorsal region of the spinal cord (cilio-spinal center — 465). Pupil the neck on same side is irritated, (cer- \'ical sympathetic ganglion) or when Hippus is usually associated with a general exaggeration cocaine is dropped of reflexes, in the eye. When the eye is sud- Westphal's pupillary reaction occurs in some cases of denly exposed to tabes and in paresis, light, there occurs a series of altern- The paradoxical pupillary reflex is of no diagnostic sig- nificance. It has been observed in tabes and in paresis and is the result of fatigue. ate contractions and dilatations of the pupil, gradu- ally growing less Mydriasis may be irritative or spasmodic, due to irrita- in degree. When patient's eye- lids are held forc- ibly apart and he attempts to close them he not only turns the eyeball upwards (Bell's phenomenon") but also the pupil con- tracts. Pupil dilates ir stead of upon light forts contracting exposure to or upon ef- of accom- modation. Dilated pupils. Contracted pupils. One pupil is larger than the other when the eyes are at rest. tion of the cervical sympathetic ganglion or nerve; or may be paralytic, due to paralysis of the third cranial nerve or the ciliary ganglion ; or may be due to both causes. It occurs in children, and on taking certain drugs (mydriatics). It occurs also from irritation of the cer\'ical sympathetic directly by incipient lesions in the cervical enlargement of the spinal cord and its man- branes, or by tumors in the neck, or by excess of car- bonic acid in the blood as in dyspnoea and indirectly by strong emotions and especially by pain ; also in par- alysis of the sphincter pupillae (iridoplegia) from le- sions, such as optic atrophy, glaucoma, lesions of the third nerve or ciliary ganglion, which break, or im- pair, the refli-'x arc, and which usually cause more or less diminution of vision and a deficient perception of light; also in coma, in cases of increased intra-cranial pressure, and in some other cerebral and meningeal lesions, especially in their later stages. Miosis may be irritative or spasmodic, due to irritation of the third nerve or ciliary ganglion ; or may be para- lytic, due to paralysis of the cervical sympathetic gang- lion or nerve, or may be due to both causes. It occurs in old age, in deep sleep, or on taking certain drugs (miotics) ; also from irritation of the third nucleus or nerve, as in meningitis in early stages and especially in hemorrhage into the pons ; and from excessive use of accommodation, as in watchmakers, etc. ; also from paralysis of the sympathetic in lesions of the neck and of the spinal cord (syringomyelia). It occurs often in tabes, paresis, iritis, irritation of cornea and, tempor- arily, after excision of the Gasserian ganglion. Anisocoria occurs in many conditions and is of little or no diagnostic value. The methods of eliciting the pupillary reflexes are described in Chart I b. Disea.ses in which these reflexes are altered are discus.sed in Chart XIV. 93 CHART VI Disorders of Sensation ANALYSIS OF THE SYPMTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease. 344 DISORDERS OF SENSA- 345 DIMINUTION 1 TION The power of receiving perceptions of the external world and of the occurrences in our own body (the basis of all knowledge) is acquired early in life. The na- ture of the process is entirely unknown, but it rests upon the . power of storing up merrtories and of recalling them. It de- pends upon the integrity of the central and peripheral sensory neurons (463-4), as well as upon that of the terminal sensory or- gans and of the cerebral cortex (47 to 56). This power may be diminished, or exaggerated, or perverted in various diseases. Either no perception or an abnor- mally feeble one follows a sen- sory irritation adequate in health to cause a perception (806, 811). 346 EXAGGERATION An unusually strong perception, as compared with hralth, follows any sensory irritation (807). 347 PERVERSION The occurrence or modification of a perception such as never occurs in health (930). The condiitons under which sensation may be diminished or in- creased are set forth in Chart VI a. The conditions under which sensation is perverted are set forth in Chart VI b. 95 CHART Via Diminution and Exaggeration of Sensation Comprising Numbers 345 and 346 and 348 to 372 91 Analysis of the Symptoms of the Case (Semeiology) SENSATION Diagnostic Symptoms r348 Anesthesia (complete) or Hypesthesia ( partial ) . (Superficial sensibility) 349 Analgesia or Hypalgesia 250 D I M I N U T I N Definition A loss, or diminution, of the normal sensibility to touch upon adequate irritation. Normal sensibility varies in acuteness in dififerent parts of the body and in dilterent individuals. A loss, or diminution, of the normal sensibility to pain, which in heakh varies in different individuals and in different parts of the body. Significance. 350 Thermic Anesthesia or Hypesthesia A loss, or diminution, of the sensibility to variations in temperature. Thir loss may be more marked for cold than for heat and vice versa. 351 Inability to distinguish differ- Loss of pres- ences in the amount of pres- sure sense sure made on the skin. 352 i Loss of muscle and joint sense or Akinesthesia. (Deep sensibility) 353 Apallesthesia or loss of osseous sense or vibra- tion sense. 354 Astereognosis Tnabilitv to tell bow stronglv a muscle is contracted, whether a joint is flexed or ex- tended, or where an extrem- ity is situated in space. A very complex sensation. Inability to feel the vibration of a tuning fork pressed firmly on the skin. Inability to recognize objects bv the sense of touch ; anes- thesia not being present. 355 Deafness or Anakusia or Hypakusia 356 Anosmia or Hyposmia 357 Ageusia or Hypogeusia Ix)ss. or diminution, of sense of bearing. Diminution of sensibility may be due to disease of the terminal end-organs, or to a destructive lesion either of the peri- pheral sensory neurons (464), (in wliich case all forms of sensibility are abolished over an area usually couiciding with, but smaller than, the distribution of the peripheral nerve, and the reflex acts in the same part are also abolished) ; or of the sensory central neurons (463), (in which case frequently all forms of sensi- bility are not abolished, and the anes- thetic area does not correspond to the area of distribution of a nerve, and the reflex acts in the part are not abolished). Sensiliility is abolished in coma, nar- cosis and often, apparently only, in hys- teria. A broad zone of analgesia and, more rarely, of anesthesia also, about the body occurs in locomotor ataxia : "tabetic cuirass." The anesthetic area may coin- cide with the distribution of a peripheral nerve or with that a nerve root (peri- pheral lesion) ; or with the distribution of several nerve roots (spinal lesion) ; or the area may involve one-half the body: called hemianesthesia (cerebral lesion and hysteria). Anesthesia of one side of the face and of the opposite arm and leg, "crossed hemianesthesia," occurs in lesions in the tegmentum of the pons and in the restiform body in the medulla. Anesthesia may involve some portion of the body sup- plied by small branches of many different nerves, such as a hand, a foot, a leg, a foreann, etc., and be .sharply limited: "stocking and glove variety" (hysterical). (Fig. 3.1^ Analgesia, thermic anesthesia and apalles- thesia may be due to lesion of the central gray matter, or of the antero-lateral as- cending tract, of the cord (Fig. 26) or of the peripheral nerves or, very rarely, in hy.steria. (Fig. 26.) Astereognosis always indicates a lesion of the cerebral cortex. (Fig. 15.) Loss, or diminution. of smell. Loss, or diminution, of sense of taste. Anakusia. anosmia, ageusia and blindness, of sense may be due to a lesion of the .sensory terminal organ, of the sensory nerve or tract, or may be functional. But these symptoms may occur in .so many condi- tions unconnected with the nervous sys- tem that they may have very little diagnos- tic value in nervous diseases. 9,S SENSATION (Continued) Diagnostic Symptoms 358 Blindness or Anopsia or Amaurosis 359 Amblyopia Los Definition. of vision. 360 Hemeralopia 361 Nyctalopia 362 Hemianopia Decided impairment, but not complete loss, of vision, especially for colors in the early stages. Usually in such cases the field of vision is made small by the loss of more or less of its periphery or by scotomata. A condition in which the pa- tient sees better in a dim light than in a bright one (day blindness). A condition in which the pa- tient sees well in a bright light but is almost blind in a dim one (night blindness). Loss of one-half of the field of vision. c ^ Homonymous Loss of the same half in both fields. Nasal Loss of the nasal half in each or either field. Bi-temporal Loss of the temporal half in both fields. In almost all cases of hemian- opia a limited area of cen- tral vision is preserved. 363 Loss of an homonymous quad- Tetartanopia '"^^t of both fields of vision. or Ouadrantic Hemianopia 364 Achromatopsia or color blind- ness. Hemi- chromatopsia 365 Dissociation of sensation Inability to distinguish the different colors from each other either throughout the whole, or in one-half, the field of vision. Loss of some forms of cu- taneous sensibility (usually for pain and temperature) with preservation of others (tactile). (Figs. 24-7.) Significance Hemeralopia associated with a central sco- toma for green and red is not uncom- mon in tobacco smokers. In them, when the pupil is dilated in a dim light, the healthy part of the retina can act. Tliis condition is quite different from snow- blindness, where the retina is exhausted by too bright and too long continued light. Nyctalopia is at times associated with con- genital retinitis pigmentosa, with cor- tical (peripheral) cataract and with other defects in the eye, and from exhaustion. Hononymous hemianopia is due to a lesion of the optic tract posterior to the chiasm, of the geniculate bodies, the optic fascicu- lus or the median surface of the occipital lobe of the opposite side of the brain (lips of calcarine fissure). (Fig. 16) Bi-temporal hemianopia is due to a lesion of the central part of the optic chiasm. Nasal hemianopia is due to a lesion of the lateral margin of the optic chiasm. Bi-nasal hemianopia cannot result from one lesion. Tetartanopia is due to a lesion of the upper lip of the contralateral calcarine fissure if it be a lower quadrant of the field of vision and of the lower lip of this fissure if it be an upper quadrant: very rarely to a partial lesion of the geniculate bodies or optic fasciculus. (Fig. 16.) Achromatopsia may be due to a congenital defect or to defective education or may be the early stage of a gradually devel- oping blindness or amblyopia. Due to mild, not completely paralysing, lesions of any portion of the visual tract in the broad sense. Dissociation of sensation always indicates a lesion of the central gray matter (syringomyelia) or of the spino-thalamic tracts, or more rarely at the ponto-cere- bellar angle of the pons at the level of the auditory nerve. It occurs associated with motor paralysis of the opposite side of the bodv in some cases of Brown-Sequard's paralysis. 99 SENSATION (Concluded) Diagnostic Symptoms ''366 Hyperesthesia 346 E X A G G E R A T I N 367 Hyperalgesia 368 Thermic Hyper- esthesia or Hyperalgesia 369 Hyperosmia 370 Hypergeusia 371 Photophobia 1^372 Hyper akusia Definition Increased tactile sensativeness. An unusually slight touch can be perceived. A very rare and even doubtful con- dition. It is usually em- ployed when a touch causes an unusually great, even painful sensation, where hy- peralgesia or haphalgesia (380) would be a better term. Increased sensitiveness to pain. Significance Exaggeration of sensibility of all kinds is usually functional. More rarely it is the result of an irritative, rather than a destructive, lesion of the central or peripheral sensory neurons. It occurs in strychnine poisoning and tetanus. Hyperesthesia occurs as a zone at the upper limit of the anesthesia in many spinal lesions, and on the same side of the body as is the lesion in Brown- Sequard's paralysis. It is usually asso- ciated with increased reflex activity. Increased, even painful, sensi- tiveness to heat or cold, or n. . , , ■ ■ r . • , , ... ' Photophobia is functional, or due to eye strain, or to inflammation of some part of the eye, or optic nerve, or cerebral Increased, even painful, sensi- * tiveness to odors. Increased and unpleasant sen- sitiveness to taste. Increased and painful sensi tiveness to light. Increased, even painful, sensi tiveness to sounds. Hyperakusia is functional, or due to ear diseases affecting the labyrinth, or to cerebral conditions causing hyperemia of the labyrinth (meningitis, encephalitis, tumors, etc.) and to spinal affections. Methods for the detection of these conditions are described in Chart I c. Diseases in which these conditions occur are discussed in Chart XIV. 100 CHART VIb Perversions of Sensation Comprising Numbers 347 and 374 to 392 101 Analysis of the Symptoms of the Case (Semeiology) Diagnostic Symptoms ^374 Pain (Figs. 33, 38) 375 Paresthesiae ,v6 Failure of localization. Topoanesthesia 377 Allocheiria SENSATION Definition Is an unpleasant sensation not felt in perfect health, except in cases of injury. It varies greatly in intensity. It presents different qualities, such as : tearing, cutting, burning, throb- bing, darting, etc. It may be diffuse, or felt in a small area(localized),or may run along a nerve trunk (radi- ating), or may run half way or en- tirely about the body or an extrem- ity (girdle), or it may be felt in an area which is itself anesthetic (an- esthesia dolorosa.) Pains may vary as to time of occurrence, some showing a distinct periodicity (ma- laria, neuralgia and migraine), some occur at menstrual epochs. Some headaches occur in morning (uremic), others in afternoon (ocular) and others towards even- ing and at night (syphilitic). Some pains are increased by pres- sure (neuritis and neuralgia) while some are diminished liy it (lead colic ) . Curious sensations rarely felt in per- fect health, usually unpleasant but not severe enough to be called pain. They are numbness, tingling, formi- cation, heat, cold, heaviness, tired feeling, hunger, etc. When a cutaneous sensation is felt but cannot be localized. 378 Double sen- sation and Polyes- thesia 379 Paradoxical sensation 380 Haphalgesia 381 Retardation of conduc- tion of pain 382 Persistence of sensation When an irritation is not felt at the point of contact, but at a corres- ponding point on the opposite side of bodv. Significance Perversions of sensibility, especially pain and paresthesiae, are often lunctional and are often due to irritation (pressure, chemical, in- flammatory, etc.) of central or peri- pheral sensory neurons. Radiating and girdle pains are usually due to lesions of the nerve roots. Anes- thesia dolorosa is due to a lesion of the central end of a sensory neuron which has been destroyed below this point and therefore can conduct no sensations from below up to the brain. Although pain may be felt as peri- pheral it may be of central origin and due to lesions of central neu- rons within the brain or cord. On the other hand pains due to lesions in the abdominal viscera may be re- ferred to remote part<; of the hnrlv or the head (referred pains — 953). Failure of localization may be func- tional but usually results from lesions of the peripheral sensory neurons (tabes). .'Mlocheiria occurs in hysteria, very rarely in tabes, hemiplegia and sclerosis. Polyesthesia occurs only in tabes and in hysteria. Paradoxical sensation has been met with in a number of spiiial .and cerebral diseases, but is without diagnostic significance. When one contact gives rise to two distinct sensations (double sensa- Haplialgesia occurs in hysteria, tion) or more (polyesthesia). The quality of thermic sensation is reversed, a hot bodv feels cold and vice versa. Retardation of coiuluction of pain occurs only in lesions of [Peripheral sensory neurons (tabes or multiple neuritis), and is therefore, a very imiwrtant diagnostic symptom. A slight tactile impression from cer- Persistence of sensation occurs in tain objects, but not from others, is lesions of the peripheral sensory felt as intense pain. neurons (tabes). The sensation of pain is not felt until Binocular diplopia is due to a weak- an appreciable interval after the ness of one or more of the external time of contact. muscles of one eye, or to displace- ment of one eyeball; so that the The sensation continues an unusually image does not fall on identical long time after the irritation causing spots in the two retinae, it has ceased to act. 102 SENSATION (Concluded) P E R V E R S I ^< 388 Diagnostic Symptoms 383 Binocular Diplopia (818) 384 Monocular Diplopia or Poly- opia (880- 4) C O n c 1 u d e d 385 Metamor- phopsia 386 Micropsia 387 Macropsia Tinnitus Aurium 389 Parakusis 390 I'arosmia 391 Parageusia 392 Vertigo I. Definition Two separate visual perceptions of the same object, the perception from the normal ej-e (true image) being more distinct than that from the abnormal eye (apparent image). A condition in which objects appear double or multiple, e\ei\ when looked at with one eve alone. A condition in which objects appear distorted. A condition in which everything looks much smaller than normal. Significance A condition in which everything much larger than normal. looks A sound of ringing, roaring, whistl- ing, etc., in ears or head. Perversions of hearing, such as hear- ing tones incorrectly or hearing bet- ter when other loud noises are present at the same time, or hear- ing sounds or words for which there is no external cause (hallucina- tion). The perceptions of abnormal odors or of those for which there is no external cause (hallucination). The perception of abnormal tastes or of those for which there is no external cause (hallucination). A feeling as if the person (sub- jective) or as if surrounding ob- jects (objective) were whirling about, or both. Diseases in which these conditions occur are discussed 103 Monocular diplopia may occur in hys- teria, in cases of double pupillary opening, in anomalous refraction (incipient cataract), and irregular- ities in the cornea. Metamorphopsia may occur in hys- teria, also in astigmatism (re- iracrive) and in displacement of the retinal elements (retinal) wliich may ocur in retinitis, choroiditis, and in detachment, or tumor, of retina. Micropsia may occur in hysteria, in paralysis of accommodation and, with distortion, when the retinal elements are spread apart (recent choroiditis or retinitis). Macropsia may occur in hysteria, in spasm of accommodation and. with distortion, when the retinal elements are crowded together ( atrophic stage of retinitis and choroiditis). Tinnitus aurium, parakusis, parosmia and parageusia occur in lesions of the terminal organ of the un- cinate gyrus, and in insanity and functional disorders. They may constitute the aura of an epileptic attack. Vertigo may be functional (hysteria, neurasthenia, traumatic neuroses) ; or may depend on changes in the cerebral circulation, especially anemia and hyperemia (cardiac and arterial diseases, congestion in por- tal or systemic circulation, galvan- ism of head or neck), or toxic (to- bacco, morphine, alcohol, some di- gestive disturbances, etc.) : or may depend on diseases of the cerebel- lum and its tracts, or of the ear or eye. It is the principal symptom in Meniere's disease f aural ver- tigo). Vertigo is closely associated with vomiting. In vertigo associat- ed with lesions in. or pressing upon, a cerebellar hemisphere, external objects seem to whirl in the direc- tion away from the injured hemi- sphere in both conditions, but the subjective vertigo, usually, is away from the injured hemisphere in case the lesion is within it and towards it when the lesion is external and presses upon the hemisphere. in Charts XXIV and XV. CHART Vila Electrical Examination Comprising Numbers 393 to 403 105 Analysis of the Symptoms of the Case (Semeiology) Definition, Significance and Relationship of the Symptoms of Disease 393 ELECTRICAL REACTION OF MUSCLES AND NERVES (70-3) Nerve fibers respond to changes in intensity of both the far- adi' and the galvanic cur- rents. The dianges in intensity are best brought about by making and breaking the current. Muscle fibers respond only to the galvanic current. The muscl- re- sponds to the faradic current only in virtue of the nerve fibi-rs supplied ■ to it. When these nerve fibers are de- generated the muscles can no longer resiiond to Ihe faradic current. Both nerves and muscles have points on the body surface; the so-called motor points (see figures 1 to fi) from which they are most readily excit- able. There- fore, in testing a nerve or muscle by electricity the electrode (pos- itive or nega- tive) is plac*^! on the corre- sponding motor point. (70-3L Name OP THE Reac- tion 394 Normal excita- bility (473) Tis- sue Test- ed 3"J5 Dimin- ished excita- bility 3'.H1 Exag- gerated excita- hilicy 397 Reac- tion tt degen- eration (472) N E R V E A N D M XJ S c L E N E R V E M V S C L E Reaction TO Faradism . Contraction present to a strength of current wliii-h is normal for the nerve and muscle tested. Contraction present but it requires an unusually strong current to produce it. Contraction present to an unusually weak current. Gradual loss of excitability which be- comes com- plete in about two weeks after injury or onset of the disease. < Jr.ndu.-tl loss of excitability which be- comes com- plete in le.ss than two weeks after in.jiiry or onset of the disea.se. Reaction to Galvanism AND FoRMiLA OF Galvanic Reaction Neg.Cl.C. Pos.CI.C. Pos.Op.C. Neg.Cl.Tet. is the normal formula, or in other words Neg.Cl.C. occurs with the weakest cur- rent that will cause an.v contraction. Pos.CI.C. occurs with a little stronger current. Pos.Op.C. occurs with a still stronger current. The explanation of the above formula is as follows : The weakest current that will cause any contraction of the muscle will do so when the negative electrode is on the motor point and the current is closed. (Neg.Cl.C.) A more powerful contraction will take place when a .stronger current is used and then there will also be a contrac- tion when the current is closed and the positive pole is on the motor point (Pos.CI.C). A still more powerful current causes a contraction when the current is opened and the p A.CC The essence of the formula of the reaction of degeneration is A.CC > K.C.C. Character Significance OF THE OF the Contrac- Reaction tion Normal excitability shows a noi"mal condition of muscle and nerve. Diminished excitability occurs in many dis- eases and conditions (thick skin), Quick. especially in lesions of the central motor neu- rons and is not of much value in diagnosis. Exaggerated excitability is a rare condition. It occurs in nervous persons with moist skins and in tetany. The reaction of degenera- tion proves None. that the peri- pheral motor neurons are degenerated and that re- covery will Sluggish. either never take place. Tlie or will be sluggish very slow. character The lesion of the must be muscular either in the <-on tract- perii)heral ion is uer\es or the most nerve roots charac^ or in the teristic anterior thing in horns of the the react- spinal cord ion of or in the degen- motor nuclei eration. in the brain stem. 106 ELECTRICAL REACTIONS (Concluded) Name OF THE Reaction 398 Partial reaction of degen- eration 399 Myas- thenic reaction (553) \ 400 Myo- tonic reaction (613) 401 Neuro- tonic reaction Reaction Reaction Tissue to to Tested . Far.'^dism Galvanism Contractions present, but 1 Nerve require unusually strong I currents, whether far- j adic or galvanic. Contractions Contractions i present only present to j Muscle 'o unusually unusually ! strong cur- weak cur- | rents. rents J Formula of Galvanic Reaction Sluggish. Either the normal form ula, or the formula of the reaction of degeneration, or a combina- tion of the two may be pres- Sluggish ent'. A.C.C. may equal K.C.C. Character OF THE Significance contrac- of the tion Reaction The signifi- cance of this Quick or Nerve and Muscle Nerve and Muscle Contractions quickly grow less strong and soon cease under rapidly repeated excitation. Continuous tonic con- traction lasting some time after the electrical Xormal Normal Quick ; grows rapidly weaker and Curious wave-like contractions occur and last after electrical stimulation stimulation has ceased, has ceased. Nerve Unusually excitable. Te- j tanic contraction persists I after electrical stimula- 1 tion has cea.sed. Positive pole is about equally as potent as the negative. Hence the formula A.C.C. = K.C.C. Continues usually a long time and has a wave-like character. reaction is the same as that of the reaction of degeneration, except that it indicates the lesion is less severe and that all the nerve fibers are not de- generated. Occurs only in myas- thenia gravis (554). Occurs in Thomsen's disease (611). 402 Reaction of com- pletely degenerated muscle (70 to 73) I Muscle Normal. Normal. Muscle None. None. Normal. None. Continuou? None. Occurs in hysteria, amyotrophic lateral sclerosis and chronic bul- bar paralysis. Muscle fibers are entirely degenerated and recovery is impossible. 403 Electrical reaction of the Optic and Auditory Nerves The optic nerve responds to the galvanic f-urrent witli a .«ensation of light, the color of which varies with the pole employed. The auditory nerve responds with a loud sound when the negative electrode is placed in or near the meatus and Uie current closed and with a faint sound when the positive pole is used and a stronger current broken. These reactions are withoait diagnostic importance. The negative electrode placed in front of the ear causes a nystagmus towards the ear testenijlass. Lower bniiich of facial ^i. platysnia niyoiilr-s Muscles of Xhv J root of tonguf ( M. oniohvoideus y. thoracic, anter. (M. pector.) Region of central convolutions Region of the iliird frontal convohit ion . M. temporalis Upper branch of facial in front of ear S. facialis X. aiiriculo. post. Middle branch of faiial Loner br. of facial M. splenius H. sternocleido- luastoideus iV. accessonii.i M. levator anguli sea puke M. cucuUaris N. dnrs. scapulce N. axillnris N. thoracic, long. (M. serratus antic, niflj.) JV. phrenicvs .Suprascapular Plexus point. (Erb's point. brachialis M. deltoid., biceps, brachial, intern, and supinat. long.) Fig. 1 U. lficrp» re?, M, abaitctordigill M, «.-»or digit- min. M. (.pponi-u* dlRli, 111 lit M. tumbilcftles M. supinator lonpos M. pronator teres M flex Ciirpl radi.iliB AVrc mujf iiJonUon/uji M. bicep* brBibli M, lirach inii'iniis M flixoT ' llllUXllM M gistrocnem. (cap lou) M. solmis CHART VIIc ERB'S DIAGRAM SHOWING THE EFFECTS OF INJURY OF A NERVE \<^^*^mLm GiJ>'< t (Galvanic 5:^1 ■« ar&dic f a» w« K. tieatlh '°t?faralysed side and badly towards the healthy side. (incom- plete) Lesion of nuclei in the medulla (706) Alcoholism (1102) Lesion of the corpus callosum (1300) Intra- ventricular lesion (1008) Lesion of tegmentum of pons (1292) Paralysis of cervical sympathetic ganglion (1 191) Hysterical hemiplegia (796) Organic hemiplegia (797) ANATOMICAL TERMS 460 Brain stem 461 Cortico-spinal or upper motor neurons 462 Spino-muscular or lower motor neurons 463 Central sensory or upper sensory neurons 464 Peripheral sensory or lower sensory neurons. 465 Cilio-spinal center (335. 1191-2) Comprises the medulla oblongata, pons VaroHi and crura cerebri. (Figs. 18-23.) Motor cerebral cortex, corona radiata, internal capsule, pyramidal tracts at base of brain, motor decussation and crossed and direct pyramidal tracts in spinal cord. (Figs. 15-26.) Motorial end plates, peripheral nerves, anterior nerve roots, nerve cells in the an- terior horns of spinal cord and the motor nuclei in the brain stem. (Figs. 19, 26.) Sensory cerebral cortex, corona radiata, internal capsule, cerebellum and its jjcduncles, lemniscus and sensory decussation, nuclei of columns of Goll and Burdach, antero-lateral ascending (Gower's) tract, direct cerebellar (Flech- sig's) tract and column of Clark. (Figs. 15-26.) Sensory end organs, peripheral nerves, posterior nerve roots, spinal ganglia, posterior horns and columns of Goll and Burdach in the spinal cord and nuclei of columns of Goll and Burdach. (Figs. 22-6.) Situated in the lateral horn of gray matter in the last cervical and first dorsal segment of the spinal cord and is connected with a higher center in the medulla. Destructive lesions of this center and its nerve roots cause (1st) a paralytic miosis, (2d) a narrovring of the eyelid opening, (3d) an enophthalmos; while irritative lesions (rare) of this center and its nerve roots cause (1st) a spas- modic mydriasis, (2d) an exophthalmos (Homer's Sydrome — 455). 124 PART II Differential Diagnosis A Clinical Diagnostic Analysis of the Symptoms OBTAINED FROM THE EXAMINATION OF PATIENTS 125 Introduction to the Diagnostic Cliarts DIRECTIONS FOR THEIR USE. In using this book for diagnostic purjwses the student, or practitioner, having made a com- plete examination of the patient according to the scheme presented in chart I, should make note of the more important symptoms. Then, selecting any one of these symptoms, he should turn to the table of contents and see which chart treats of the disorders which include this symptom. Finally, turning to the commencement of the chart indicated, he should apply one test after another until he reaches the diagnosis. At the left margin of each chart is placed the symptom to be analyzed; on the right margin are placed all the possible diseases in which this symptom can occur. Proceeding from left to right, in each column a number of alternatives are offered, and by selecting the one appro- priate to the case the diagnostician proceeds from one column to the next, until he reaches the correct diagnosis. In the column immediately preceding the diagnosis is an abstract of most of the svmptoms which may occur at different stages of the disease. The great majority, but not necessarily all, of the symptoms given in the abstract should be present in the history or found in the examination of the case, if the diagnosis be correct. A few practical examples will illustrate the method much better than a long general descrip- tion. Let us, then, consider a few cases as they occur in actual practice. Only the essential symptoms are noted. Case I. Male, aet. 51. — He smoked and chewed tobacco and drank to excess for years. About two months ago he began to have pains at various points in both legs. His legs became slowly weaker and his flesh became tender, but he is able to walk a mile. Organic reflexes normal. Feet cold, and the legs have lately grown smaller. On physical examination the muscles of the lower legs, and less so those of the thighs are weak, tender and somewhat atro- phied. The legs, and especially the feet show slight anesthesia, marked anaigesia and well marked retardation of the conduction of pain. Achilles reflex absent. A slight knee-jerk can be obtained with difficulty. In walking toes drop a little and the knees are raised abnormally high. Important symptoms: Paralysis (weakness!), High -stepping Gait, Anesthesia and Pain. The chief symptom in this case is weakness, and we, therefore, turn to chart X, which dis- cusses "diseases causing motor paralysis." The paresis in this case is continuous and the reflex acts are diminished or absent. We, therefore, have to do with a flaccid paralysis and turn to chart Xa. The presence of muscular atrophy following the paralysis, together with the absence of any apparent hypertrophy, guides us in the second column away from the functional diseases and the muscular dystrophies and to the degenerative atrophies ; while the normal organic refle.xes guide us in the third column away from the spinal cord, and to the peripheral nerve, diseases. The presence of anesthesia, pains, muscle tenderness and other sensory symptoms guides us in the fourth column to the class of neuritis of the spinal nerves. In the fifth column the fact that there are many spinal nerves affected guides us to the diagnosis: Multiple Neuritis, which the history of alcoholic abuse confirms. We can approach this case in another way by considering his abnormal walk. In the table of contents we find that disorders of gait are treated in chart XIII and indeed in chart XIIIc. The walk in this case is evidently "paralytic and flaccid," the tendon refle.xes being diminished. Furthermore it is a high-stepping gait. A comparison of the three possible abstracts with the symptoms of our case makes it evident that the case is one of Multiple Neuritis. We can trace the case also by means of the anesthesia and analgesia : symptoms which are discussed in chart XlVa. The tendon reflexes being diminished and the organic reflexes normal in this case, we are led to three abstracts, only one of which fits our case, and thus the diagnosis of Multiple Neuritis is again confirmed. Finally we may take up the initial symptom in the case: pain in the legs. Pain is discussed in chart XV and pain in the extremities in chart XVc. In our case the pain is bilateral and is associated with anesthesia; so that we are again brought to three abstracts, of which the one of Multiple Neuritis most nearly fits our case. 127 Case II. Female, aet. 23. — Ten years ago she and her brother had simultaneously an attack of headache, backache and fever. Her brother died and she recovered with a paralysis of both legs, which has since improved, rapidly at first, then more slowly. Her legs are still somewhat weak, especially the left one, but she can walk fairly well. No sensory disturbances, organic reflexes normal. On physical examination there is a decided weakness, slight atrophy and slight shortening of left leg. Knee-jerks are absent in both legs. No objective sensorj' abnormalities. !^i?i'' ' ' Important symptom : Par.^lvsis. In the analysis of this case we follow the same path traced in case I until we reach column four in chart Xa. In this case there are no sensory symptoms, the paralysis involves neither the cranial nor the extensor nerves exclusively, and is acute in its origin ; so that the diagnosis must be Acute Anterior Poliomyelitis. Case III. Male, aet. 48. — Had a chancre followed by a cutaneous rash twenty-two years ago. During the past ten years has had "lightning pains" in legs and a girdle sensation, also gastric, vesical and urethral crises. During the past six months, his walking has become diffi- cult and awkward and is much worse, practically impossible, in the dark. Organic reflexes normal, except for some delay in micturition. On physical examination there is no loss of muscular power, but all movements of legs are awkward, violent and excessive. There are marked ataxia, anesthesia in areas and well marked retardation of conduction of pain from feet. Complete absence of knee-jerk. Argyll-Robertson pupillary reflex, Romberg's symptom and loss of muscle sense in legs. Lumbar puncture gave fluid showing the pressure of globulin and lymphocytosis and a positive Wassermann. In walking the patient does not stagger, but flings feet out widely. Important symptoms: Ataxia, Ataxic Gait, Anesthesia. Pain, Abdominal Crises, and Lymphocytosis in Cerebro-spinal Fluid. In tliis case there is no loss of motor-power but well marked ataxia in legs. From the table of contents we learn that diseases cau.sing perversion of motion, including ataxia, are treated in chart Xlla, to which we turn. As the patient does not stagger in walking and the move- ments of the legs are ataxic, not only in walking, but also in other movements, it is certain that the case is one of "motor ataxia." The ataxia is bilateral and the knee-jerks are absent; so that it is evident that we have to do with tabes or multiple neuritis (pseudo-tabes). We differ- entiate these two diseases by comparing the abstracts of their symptoms. As in this case there are no muscular weakness, atrophy and tenderness, it is plain that the diagnosis is Tabes. We may also reach a diagnosis in this case by studying the patient's walk with the aid of chart XIIIc. The gait is ataxic, rather incoordinated than staggering, the knee-jerks are abolished and there is .\rgyll-Robertson phenomenon ; so that the diagnosis of Tabes is con- firmed. Furthermore ve may trace the case by the symptom of anesthesia with the aid of chart XlVa. The terdo i reflexes are abolished. The organic reflexes are not much disordered, but they are slightly. There is no motor paralysis and thus we are led again to Tabes. If we consider the symptom named "Argyll-Robertson phenomenon," which is present in tliis case, we shall find it discussed in chart XI Vd and here again we are led directly to Tabes. If we consider the pains in the legs or the girdle sensations about the body or the abdominal crises, we find them discussed in chart XV and in either case are led to Tabes. If we consider the results of the examination of the cerebro-spinal fluid with the aid of chart XIX, we find the butyric acid test positive, the existence of lymphocytosis, a positive Wassermann, a clear fluid and ataxia, and thus the diagnosis of Tabes is again confirmed. Case IV. Female, aet 19. — Patient's father and mother were first cousins. They had eight children, of whom three died in infancy and four are healthy. Child learned to walk late and with difficulty, frequently stumbled and fell. Was backward at school and when she was nine years old it was evident to all that she was not normal. Patient's movements became gradually and steadily more awkward. Now she cannot walk without aid. General movements are slightly ataxic and simulate somewhat tremor. Movements of the legs are more ataxic and weaker than those of the arms. Her walk is extremely ataxic and staggering. No knee-jerks, Rabinski present. Organic reflexes normal. Internal strabismus. No loss of mu.scle sense. Important symptoms: Ataxia and Ataxic Gait. 128 The most characteristic symptom in this case is ataxia and so, as in case III, we turn to chart Xlla. In this case, the ataxia is mainly on \v;ilkiiig and thtre are no motor paralysis and no loss of muscle sense. We are, therefore, brought to the alternative as to whether the disease occurs in an adult or a child. This case doubtless dates from early childhood. There are no similar cases among her brothers and sisters, but she comes certainly from a tainted family. She has no nystagmus, but has strabismus. As this case began before puberty and has no knee- jerks it is doubtless a case of Friedreich's Ataxia. The strabismus points to Marie's hereditary cerebellar disease and indeed these two diseases are so closely related that there is some ques- tion as to whether they are separate entities. We may approach this case from a different angle. The chief symptom is difficulty in walk- ing. We turn, therefore, to chart XIIc and note that the walking is ataxic. The staggering gait which is permanent, the bad heredity, the absence of knee-jerk and the commencement of the disease in infancy confirms the diagnosis of Friedreich's Ataxia. It may be noted in passing that this case does not show a distinct tremor, or nystagmus, or the blurred speech which symptoms are often present in this disease. Case V. Male, aet. 62. — His disease commenced with difficulty in speaking and swallow- ing about a year ago, and has slowly and steadily progressed. His speech has become so bad that it is unintelligible and he has the greatest difficulty in swallowing, and chokes over his food. There is constant drooling of saliva from his mouth. Cannot protrude his tongue beyond his teeth, cannot raise his arms because of weakness of muscles about the shoulders. His legs are somewhat weak. Fibrillary contractions and great atrophy of muscles of tongue and of shoulder girdle (deltoid, pectorals, etc.). Muscles of hands are not involved. Absence of tendon reflexes in arms. Knee-jerks lively, ankle-clonus and Babinski are present. There are no sensory disturbancesL Important symptoms : Paralysis, Fibrillary Contraction and Muscular Atrophy. The principal symptom in this case is a motor paralysis. We turn, therefore, to chart X. The paralysis certainly is a continuous one and of the three alternatives next offered us we must select the third, inasmuch as we have a flaccid paralysis with muscular atrophy in the head and arms and a mild spastic paralysis in the legs. We turn, therefore, to cliart Xc. In this case the cranial and spinal nerves are involved, next there are no sensory symptoms, next the disease is chronic, and finally the lips, tongue, larynx and pharynx are involved: consequently the diag- nosis is Progressive Bulbar Paralysis. But this diagno.sis does not explain the paralysis and atrophy of the muscles of the shoulder which are supplied by spinal nerves. We turn, there- fore, to the next sub-division, where spinal nerves are alone involved, and follow through, no sensory symptoms and through a paralysis involvincr the shoulder girdle muscles, and reach the diagnosis of Amyotrophic Lateral Sclero'^is. The diagnosis is, then, a combination of two diseases : Progressive Bulbar Paralysis and Amyotrophic Lateral Sclerosis, and we find in the abstracts of these diseases that they often occur together in combination. If we consider the symptom "fibrillary contraction" with the aid of chart Xllb, it is evi- dent that this is an organic and not a functional disease, that there is a marked muscular atrophy and that there are no sensory symptoms, and thus the diagnosis of both Progressive Bulbar Paralysis and Amyotrophic Lateral Sclerosis is confirmed. Finally if we consider the symptom "mtiscular atrophy" with the aid of chart XVITa we find that the atrophy is considerable and of a relatively rapid course, that there are no muscular hypertrophy and no sensory symptoms and thus we are led again to the same diagnosis. Case VI. Male, aet. 12. — During the first year of his life the child had great difficulty in retaining food. At the end of his first year he began to have convulsions with unconscious- ness, and, with the exception of an interval of two years, these have continued up to the present time: the last attack having occurred three weeks ago. The child has a very small head and an idiotic expression of face. He apparently understands most of what is said to him, but he can talk only a very little and only a few words are intelligible. There are no contractions or deformities, and he uses his arms and legs well. Important symptoms: Anarthria and Idiocy. The most striking symptom in this case is that a boy of twelve years can scarcely s|>eak intelligibly. Turning to the table of contents we find that disorders of speech are treated in chart XIII, to which we turn. The loss of speech in this case is so nearly complete that it can 129 be called anarthria, which is discussd in chart Xllla. The disease is evidently congenital, and the expression of the face is idiotic, and reading and writing are impossible; so that the diagnosis is Idiocy. Had we, on the other hand, decided that the child could speak, but very imperfectly and unintelligibly we should have sought for the disease in the same chart Xllla, under the heading of dysarthria. Here the congenital nature of the defect and the absence of cleft palate, etc., would have led us directly to Imbecility. In order to trace the case further let us follow the cross reference after idiocy which is 1081 and which we find in chart XVIc. This case on account of his convulsions might be classed under Epileptic Idiocy or on account of his small head under Microcephalic Idiocy, or under both. Case VII. Female, aet. 53. — Complains of trembling and that she cannot execute any movement quickly, because her arms and legs are stiff and rigid. When walking she has a decided tendency to pitch forward. Feels warm at times when the room seems cool to others. Expressionless face, passive tremor of hands. Propulsion and retropulsion when walking or standing. Rigidity of arms and legs. Difficulty in rising frotn a low chair. Knee-jerks rather increased. Important symptoms: Muscular Rigidity, Tremor and Abnormal Walk. The most characteristic symptom in this case is the rigidity of the amis and legs which is a mild tonic spasm. From the table of contents we learn that diseases causing spasm are treated in chart XI, to which we turn and find that general tonic spasm is discussed in chart Xlb. In this case there is no fever and of the five sub-divisions under this head, this case clearly falls in the second : "rigidity which does not prevent passive or voluntary motions." Of the two alternatives next offered it is evident that we must choose the second, in the abstract of which we find all the symptoms present in our case. The diagnosis is, therefore. Paralysis Agitans. If we follow the symptom "tremor," we find this treated in chart Xllb. It is a passive tremor and, whether it be increased or diminished on voluntary movements, if it be slow, the abstracts show that it is a case of Paralysis Agitans, because the other abstracts do not fit this case at all. If we consider the difficulty in walking in this case we turn to chart XIIIc. In the three great divisions offered this case evidently falls in the third : "paralytic and spastic ;" and of the two sub-divisions next offered we must take "general rigidity" which leads us again to the diagnosis of Paralysis Agitans. Case VIII. Male, aet. 59. — During the past 34 years has had at times attacks of asthma. During the past four years has been troubled by a great many paro-xysmal attacks of vertigo, at irregular intervals ; some are slight, some are so severe as to throw him from a chair half way across the room to the floor, where he must lie for several hours, because when he raises his head from the floor he vomits violently and the dizzim-ss becomes worse. He often has slight attacks of vertigo, which make him stagger when walking. During these four years he has been slowly growing deaf in his left ear; the deafness being now extreme. He has also had during the same time in the same ear, a buzzing and a ringing which is most intense just before an attack of vertigo. He has no paraly.sis and no loss of muscle sense. Bone conduction is absent. He also is much troubled by gastric flatulence, to which he attributes his vertigo, but when he takes digestive medicine and the digestive disturbances arc relieved, the vertigo remains unchanged. His eyes were found to he astigmatic and proper glasses used, but no improvement in the attacks of vertigo followcfl. Three vears after the above record was made the attacks were milder and less frequent, but at that time his left ear was totally deaf and deafness was advancing in his right ear. Important symptoms: Paroxysmal Vertico. Staggering Walk and Deafness. In this case the principal symptom is paroxysmal attacks of vertigo; diseases causing which, we learn, are treated in chart XVd. We see from this chart that vertigo may be caused by digestive disturbances and disease of the eye, both of which were present in this case, but the vertigo persisted when these abnormal conditions were relieved; so that they could hardly be the cause. On the other hand, we find that vertii,'ci is asso<-iate(l with deafness, a prominent symptom in this case, and in looking over the abstract of this form of vertigo we see that it fits the case exactly ; so that the diagnosis is Meniere's Disease. 130 If we consider another symptom, "the occasional staggering in walking," we find this treated in chart Xlla. This patient has no loss of muscle sense and no muscular paralysis. He is an adult and his hearing is abnormal and thus we are led again to Meniere's Disease. Finally if we trace the symptom "deafness" with the aid of chart XlVe we find that the deafness, at any rate at first, was unilateral, that bone conduction is absent, that there is no facial paralysis and that severe paroxysmal vertigo and tinnitus aurium are presei:t ; thus confirming again the diag- nosis. Case IX. Female, aet. 17. — Heredity good. Was well until about three years ago when, at the time of commencing menstruation, she began to have attacks of clonic convulsions with unconsciousness, which have continued up to the present time and in which she has occasionally bitten her tongue. Has also lesser attacks of unconsciousness, or very cloudy consciousness, in which she automatically prays, or says foolish things. Has no memory of any of her attacks. She has an immediate aura of fire before her eyes and of wheels revolving in her head. Some headache follows the attack. The convulsions occur only, and the lesser attacks mainly, at night. Physical examination is negative, urine normal. Fundus of eye normal. Knee-jerks equal. Much acne on face. Important symptoms: Coma and Convulsions. The constant symptom in all her attacks is unconsciousness, or coma, of short duration. This symptom is treated in chart XVIa. There is no history of recent injury, of brain disease, of poisoning, of heart disease, of paralysis, of kidney disease or of fever. Therefore, we are led at once to the diagnosis of Epilepsy or of Eclampsia. The latter can be excluded by the frequently recurring attacks at long intervals. If we next take the symptom of clonic convulsion with the aid of chart XIa, we find that there is no fever and the convulsion is a universal one, and not local at the onset. There is coma and there are no symptoms of disease ol the brain or cord, or of the kidneys, heart or blood, or of poisoning and thus we confirm the diagnosis of Epilepsy. Case X. Female, aet. 34. — Nine years ago one morning, her left arm, leg and side of face felt numb and she could not see things on her left side without turning her head. These symp- toms steadily increased during the day and she could not use her leg, and especially her arm, well. She could always walk, but at first she could walk only with difficulty. This difficulty in walking gradually passed away. She could use her arm, but could not use it well for more than a year, and it is not quite right even at the present time. The numbness of the left side and the inability to see things on her left stiU persist. On physical examination there are found anesthesia and analgesia of the left arm and leg and left side of body and face, (left hemi- anesthesia and hemianalgesia) , also blindness in each eye for all objects to the left of central vision (left homonymous hemianopia). The left arm and leg are a little awkward and a trifle weak; strength of left hand grasp to that of right is as 80 to 105. Knee-jerks lively, perhaps stronger on left side : neither ankle-clonus nor Babinski. Organic reflexes normal. Important symptoms: Hemianesthesia, Hemianalgesia and Homonymous Hemianopia. The principal symptoms of this case are hemianesthesia, hemianalgesia and homonymous hemianopia. These are sensory symptoms and indeed, symptoms of a diminution of sensation. We turn to the table of contents and find that "diseases causing a diminution of sensation" are considered in chart XIV, which we next consult. Starting with disorders of sensation in the first column, we have five alternatives offered us in the second column, among which we ought, without doubt in this case, to select diminution of sensation and following this division we have in the next column three alternatives, among which, undoubtedly, we should select anesthesia and analgesia and turn to chart XlVa. In this chart we have the alternatives of the tendon reflexes being either absent or present. In the above case they are present. The dilemma in the next column is quickly decided because the organic reflexes are normal. The history of a motor paralysis lasting a year oi more and still slightly persisting directs us to the first alternative in the next column, especially as there are no hysterical symptoms present; while the unilateral nature of the symptoms and next the acute onset (one day) brings us to the diagnosis of Cerebral Hemorrhage or Softening. To determine which lesion is present, we follow the first cross reference. No. 503-6, which we find in chart Xb. In looking over the abstracts differentiating cerebral hemorrhage, embol- ism and thrombosis, our case, with its relatively slow onset, its absence of any coma, its absence of any source for an embolism, is probably one of cerebral thrombosis and certainly one of cere- bral apoplexy. 131 The next question is as to the locality of the softening. To ascertain this we turn to the table of contents and find that "localization from symptoms of paralysis" is discussed in chart XXII to which we turn. The reflexes being present in our case, we are brought to the ques- tion : whether sensory or motor paralysis is dominant. In our case sensory paralysis is dominant and we turn to chart XXIIc. Of the first alternative offered us in this chart we must choose the first: anesthesia and analgesia. In regard to the next column, the distribution of the anes- thesia in our case evidently falls into the class: "the (left) arm. leg and face are anesthetic." In our case there is no Jacksonian epilepsy and there is hemianopia, so that the localization of the softening is in the posterior part of the right internal capsule. If we now turn to Fig. 17 we can easily see how a lesion in the posterior portion of the internal capsule can easily involve the sensory fibers from one-half the body and also the optic fibers; the continuation of the optic tract. It is also easy to understand that on account of the wide-spread circulatory disturbances in the early stages of the disease, before a collateral circulation liad, to a degree, reestablished itself in the periphery of the lesion, the motor fibers lying directly anterior should be involved and a more or less temporary hemiplegia should occur, as was indeed the case. It might seem strange that deafness did not occur in this case as it is certain that the auditory fibers also must have been involved in the lesion, but it is well known that central lesions only produce deafness, even unilateral deafness, when the lesion is bilateral (see page S.) Thus we have arrived by means of the charts to the diagnosis of this case of "thrombosis of the artery supplying the posterior portion of the internal capsule " but in order to make this diagnosis doubly sure, let us take another one of the prominent svmptoms, such as homonymous hemianopia, and follow it through the charts. This symptom is also a diminution of sensa- tion and therefore we turn again to chart XIV. Disregarding this time diminution of sensa- tion we follow "disturbances of vision" and "limitation of field of vision" to chart XlVb. Here we find homonymous hemianopia and in the next column there can be no doubt that we must choose the path which hemianesthesia indicates and by it are led to the diagnosis of hemorrhage, or softening, in the posterior part of the posterior limb of the contralateral internal capsule, which is the diagnosis which we had already reached by another road. 132 CHART X Motor Paralysis DIAGNOSTIC ANALYSIS OF SYMPTOMS. Tests Symptoms Analyzed Permanence OF Paralysis 469 MOTOR PAR- ALYSIS OR PARESIS (244) After a careful examination has shown that the paralysis is a true one and is not simulated by any ankylosis or by pain on motion. 470 CONTINUOUS PARALYSIS 471 INTER- MITTENT PARALYSIS. Reflexes in Paralyzed Muscles The reflex acts in the paralysed muscles are absent or decidedly diminished. 472 FLACCID PARALYSIS Lesions of peripheral motor neu- rons. There are hypotonia and changes in the electrical reaction of the nerves and muscles involved in very varying degree from simple diminution in excitability to complete reaction of degenera- tion. No associated movements present. The reflex acts in the paralysed muscles are normal or exag- gerated. 473 SPASTIC PARALYSIS (251) Lesions of central motor neurons. There is hypertonia without altern- ations of electrical reaction of the nerves and muscles. Associated movements (synkineses) may be present. 474 A combination of FLACCID PAR- ALYSIS in the upper part of the paralyzed area and of SPASTIC PARALYSIS in the lower part. All the muscless of the body and head. The muscles of one or both legs, rarely of arms. Commencing in legs, extending to arms. The differential diag- nosis of those dis- seases in which FLACCID PAR- ALYSIS occurs is set forth in CHART Xa. The differential diag- nosis of those dis- eases in which SPASTIC PARAL- YSIS occurs is set forth in CHART Xb. Associated with a cervical rib. 133 The differential diag- nosis of those dis- eases in which there is a combination of FLACCID and of SPASTIC PARAL- YSIS, and of those in which INTER- MITTENT PARAL- YSIS occurs is set forth in CHART X c. L CHART Xa Flaccid Paralysis Comprising Numbers 475 to 477 on left side of Chart and 482 to 500 on right margin y__ -»it€Y DJACNOSTir HYMn-OMS AND TB8TS J7S roncpiiilal or no- A iiiotnr pnrnlriiii ot oiif (infaolilc hcmiiilpctal nr llrmlplegio niiinHl io infnucy. nro t5>mmun nml may tiiii«k iho owiggpraloii rpfir.\r.i or Diplegin nr TJirri- moy !)<• ferpr hihI nt limes Idiory or insanity. Frwmi-iirly Hierr i MonopJesia or iiri"pl<^lic «rnip- wr.brnl illplmin. bulbar •ymprom* (4241 are pr( (2&4-C, S>8) I"'"» "I oinn-i. prpri«iiun«. flc. cno occur inroliinlaril.v, bul no i 'Ss'inptomv "f irrilalioD (convulclons, riciiJily. '■tc.) c |>iiFiiouniT») (Src a loo Srrlneomyella — :i53. $40-1.) 4S0 I-ompMs (2.17) (Si-r> nlM SyrincnmFeiin - 5J3. 840-1.) Alm'«t ntwnyt In adiilii and after mlil'lle lifp. Smlrtrn onwl, or n«), iiSH' Illy vilh (Iff. Mii.t 1037). or nitli hearfai'lie or v«rlli:o niKl nifnlnl. oinfimicm. Not in- fr«|in-iilly llio at- tarli CH.mmi-ne.« wtth a hernipleKJa which may or may not l>e follriiveil liy DIAGNOSTIC AKAXYSIS OF SYMPTOMS ABSTRACT 01.' SYMPTOMS iHilh silica (Little's dlftcnNp) of the body, or ul mie enlreniilj', williont anoMheNia nad witli very tittle mu«culnr ntrophy (from disuse). A squint is common, llie \n% are often maiuly or alone parnlyseH, Iti^dity nnd ronlmctiirps B. In nalkine there is oflMi «ddii>i(ir Bp«sm. "soiMorB itn\t" (70S-808t. Hxlensor spopm is nUo frrtiucnl. Epili'^priform convulsions are commun. both at onset and dnrini: Ihi- wmr^p of the disease. There ia mueli mental weaknem H partial airrsf of arowth of Uie panilyscJ parts. AthelOKis anid post-hem i pi I'pic chorea -and other motor disorders are common. Speech is commonly alTe^tcd (dj-sartliria). Tlie organic reflexes nr* not di^tiirh^. ■M'nt nllhoiit fibrlllnrion nr ttfopby. and •miomiitic und mimilic aclicns are prcservctl. In smh coses the eyeballs will follow a light o<- 'ihcr ohjen. but cnntiot be turned bj ai ii^'hintary motions. Tho skull Is often sm.iller on the side of the a(recSid cen'bral hcmisfdiere. Tbe origin of the disease may he pre-noli1 (ciniseiiitall. nalnl (bemorrhnge) and ponln arc The dinoise i^ ofim the r-snlt of injiu-y nnd even more frequently of syphilis:. When not so. prodmiunl sjinptome (422) are usually present. Connilt.ions jic enmmon. butb at llie onset ami during (he course of the dtaense. (\hicb I" often inlcffiilttcnt. Headache and menial Impairment are frequent. The onset of paralysis is apoidcctiform. It is usually motor only, is rather mild in des-ree uwl is usually Irarwlcnt. Organic refleies normal, fercbro-sninal fluiJ ofli-n bloody. ■ will, and lau^liinir. we(.pli HIS ijf piiriilyhiH are more pronounced than these nf irritation (convulsions may occur, especially in ■■oi'tical leiinns and in hemnrrhaec into Ihc v.'nlfii'lt". ill which riiiac lumbar punclure may yield a bloody lluid.l The paraljHis in in part temporary and in pari piTmniient in varying decree. Slow improvninenl with aliiioat perfect recovery in r.ire cn«c«. More or li'ss lir-minnent mentnl impainm-nl. often very Blifiht, I'liialiy patients are more emotional than previously. ICMCBcriiled reflexes and nnkU-l and tracheal rales arc vi-y iinfiiiorable sympionia. Certain muHdcs are more frn|iienTly an.l severely paralysed in apoplexy than ■Jihet*. Wirnji'kc'* nnilitcclion muwles (2ri4). t of both. t>u-: llinr, in tJi.' I4), Slmihi- to the above, but onset Is more arlcrial ten.sion is nsuntly low. Tlie mon than in hcmorrhas''. hectiunc (he 1 'similar to the above, hut on^el may he I syphilis. Tlie arliirinl Icnsicn is iimin basilar artery or*' ajore frequently nllc beinorrliagc or embolism. I" i> 'ir ..f the body, usually of motion only, rnrel ( )n«ei is iisiiallv acenmpiinled bv prormiiid I Piihe is slow. Slicbl vnriatirn> of lemi I II Hilly high arterial tension. The d irni rontmcturrs, causing (Icsiiin of joinu of arms and extension of joint* of les. ar<' frcfjiient nnd of bad pronrnosii rare ca-sus. The pupils arc usually dilntcti. sometimfis uncfiiial and always, in deep coma, inactive. Certain muse lensalion only, somi'lir (CfK-.l of several hours re about Uie nnrmal point : when the iiatly oeiurs in advanced life. If death dor lower hratinh of the facial ncr.-e is r hut not alwayi. In Itie coma there i^ iriation is esln'mc ilio iirosno'i* is liad. usually more inch mon- completely and perninncntly pan >flen turnini: of the heail. and Cinijuciile ileviu TroilroniBta are rather rare (122). There ar ipmvement in the paralysis: first ii ivery frcm the parnlyvis. Alhelosls and other post- ' more frequcnl'-y and severely paralysed than oUiera: Wcr- 1 inslantiineous and eomn is usually lew profound and sl'orter and frequently is entirely absent. There ise usually occurs in youlli or middle nite, In genenil the symptom* are less severe and lc«s permancn n is more apt Io be cnrticjil. .Multiple (mere than twol r"nirrences are more ctimmon in embolism thai re no pmiTroniata. There is cardiac disease or other source for emboluB. The : than in h'-morrhnge. Convulsion*, aphasia nnd monoplegia ore more corn- in hemerrlmite. >re k-raiiual. althniik'ti still sud'len an't p\ni al titnps ini ■ hifih. .\rtjerinl disease ia common. The disease usua 'd. Kimultaneous paralysis of many cortical functions ProdrnmalB (422) are common. Coma is r I ndvanc-d life, flulhar symptoms are more i inmon than in hemorrhage. Multiple (inin-e ' frequently absent or les men Ilinn in bomorrbace 1 two) recurrences arc im profound. Tlierc is often a history of or emtiolism, because bmncheo of Ihc re common in thrombosis thaa in either Reasory symptoms arf always pres- ent, Oriainic n-- flexes are nor nrndual onoetKitli- mal nr only out cnma, except as sliahlly dl«or'»ec«B. Steadily increasing ia anil nn'ri- or Ir-s menial diillne*9. Focal symplnms, IhiMi iKidic and iiarelylii', are usually present, e.*pecially .Tacksmiian psy r42I,(!0'Jl, Mjirkedly increased tension of cerebrospinal and slow piiUe in -lime of riinipre-Kinn, especially in tumor. li-nds. >rien fever. A source of infrctir tiivved by a rapid li-rminnlion. spinal fluid obtoined hy punet slowly (days) extends. I iraeler "tie svmplefti" re uielnr svinploms beni line Iiilal Pin.il pilrpsy {48a). In early * of muscle sense a Tlirre ii. paralysis always of motion and commonly of •ensalVm. usually in the form of para- plcBiii, mon- nirfly iu the (opin of a spinal hemiplegia (432), which later may breomea para- plecla. The re- Hexed are exasfier- ated. Anitle-elonuf and RabiiLskI are Choreic nymploms. Oninial and spinal nervos arc la- volvwl. Lrms and legs arc paralysed. Pri- apism Is com- mon, also re«- piralory difficul- ty and eariy death. Radiating pains arc com- I I or aooompaniee on attack of hemi-chorea. a-medullary I ivolving the » ' positinn of liic tumor. I produ"e irrtlnlive. ini of ibe bod.v : witli nnalcesia. thermic and sometimes tactile anesthesia nf other side (432). Stationary, or sfendilv pn Thev may lie absent, hut are usually increased on the side of the motor paralysis, nnrt are so greatly increased freque pr-m'-dullnry, |iiiral,vtic symptoms. • ressive ebronic illy as rc«lhe- ■ia. [■ains radlatin; into llie eitrfW- ilien are mmmoB. Legs mainly in- volved. Arms in\-nlvi>d later and sitehtly. If at nil. These dis- eases may occur e may be a history of injury n islory nf ininrv. Little or nn b- a hi. ..ry of r. ex Ira -medullary tumors prodi Eiideiire nf Pott's disNI«e or tumor nain, In coses of compreurinn du* iiti-r<'a«ed |rn>inn and may roniain History of workin:: under ineri'oiied Inlra-meiliillary paralyll nd a fracture of vertebwe with deformity. The knee-jerk^ mi pain. S-nsory symplonis and disorder' of the organir reflex Much girdle pain, Riddlly nnd aoasm in back. Symptoms irritntjvc. intra -medullaiir paralytic. s.\-mptoms. ^Tiiscle spasn ii*m of bnck. Symptm iploms. Muscle spasm ! nt fir^if more ui is characterislic. V be abolished in the early stages. later in-r s are almost alwn.va nrrBcnt. A history or liint-ral. I.ni-nl rmini. Mny b- increasci lenision of ei Rnhinski present. I' li-re toa v he blo od i n Ihe c«rebro-npinal fluid. vidence of syphilis {12(K) Is often present i Patients re nmotional. Very acute onset es of syphi- /Acute onset 1 rhmnic onset rehm-spinal Very chronic onset \*ery acute onset n syphilillc r Acute onset 1 tTirnnic on»et ■■erii.vil recion of spinal eord above cen-lcat en- larcement. (PNg«.24-R.) ; first unilateral. f/>enl pain. The tenai'm of Ihi- cerebro-H|ilnal fluid i is a characteristic symptom. Rnbinslrf is present. > he .P.1, Tn stage*. Very cliri ins Ihe cord, Riddily and sintson in muscle s disense there moy be no aenKory nymptoma I and exhibit lymphocytosis. of l"os und haeli nr Reflexes may be so ' friinirnl. I'sually intense pifn wlien spine is bent nr r ■snsgerated as to conntitute spinal epi]eps;y (fW-l, 43.1). nd cflperi.dly or V according to s DIAnNOSIS Vr.-bral Palsy of ('hi)dliIi>nint;eal .Vpcplexy. Hemorrhage in ^'rebml 502 mnnlnBe*. I'achymeninsitis Interna llemor- rhari'-ii. Amiirism. etc. (.'>SS. tO«S.) (Pigs. 1,-1-111,1 'iT.-bnil HcmorrhiiBe. 504 Cerebral acute f Apiqilexy. > I (147. l."!*. 422, .VM. SJf., SI50-1. 1043. lOiH-fi.l (Fic». ir.l7 1 Cerebral Throinbm «oftening. •N'o fever. No infection, or origin for abscess. Chronic coui-se. Steady progpesslon of all symptoms. Often histnry of previous remote injury. No in- of pellular eb-menls found in the blood or in cerebro-spinal fluid obtained by lumbar puncture, Frenuently symptoms are irritative, rather than lir. I'ercuKsien of skull over region of tumor often shows (endernes«. H>'adaehe is very rarely absent and is usually intense. It may he I or local, hut is of 'ittle or no value in localijiins the tumor. The panilj-sis crmmenecs as a monoplegia nnd very slowly (weeks or months) ex- I. especially suppurative discnsea of the ear. Rapid rcurre. esrepl that a Intent neriod in the progress is common, fol- nelirium is common. Often a flistory of a recent injury. Teumcvlcsis mny be found in the blood and in fh" cerebro- re (741. Frequently sj-mptoms rather paralytic than irritative. The paralysis commences as a monopleein and rather 'cnbnil 'nimnr. Uleuiititie Cyst. (bV.-. nil, .■S.VMMl, r.7S, .1S7. R3«. S,'i2-0-4(2-4-r. 'MS-'X Otll, inai-riO.) (Figs. 16-17.) ■er.tirit .M.-erw .ir |nr:illjie.l Meoinnill., MS (I.V{. 171. l--!. ."uS, ,-,S7. 907. tXll. 1X17, Ifllf).) (I-Vs. 1-V17.) Spinal Tumor or unilateral spinal b-*ion. Brown- 509 Senunt^l - paralysis. (IM. 101. 4.12. +*«. r.lB, GIO. r.4l. .V.2. R2.'^:t!l-44. !)i.*i. 0S2. 100ft. 127il. 1405.) (FIk*. 24-1!.) < hon-ic Paralysis ((^.) &10 l>i seminatetl Sch-nwls, (l.'iO, TiMI. tV<0. OCR. ASS, 511 .■|0. 70.S M>3. 014. inM.) Injury .\c-ule l-um Injury or lieiiwrrliagc in, ,\iiite myelili^ or myelomalarin of. (7itS. Sill) r'lironic myelidi or myelnmalaria c^f. merning. Much cinli" pain and rodlatini: e msy oociir. Orebro-apioot fluid is under Old Bse. aiheromatous arteries. iiapheric pressure. Headache. Terliro nnd vomiting in early ntngc of diaease. I^ler symptoms n irlerial lenslon usually high, loss of memory. l'>iintional and exbiluis mental impairment. Paral.vsis is Tumfr can be seen or felt on back replacing the spines af the vertebrae, fvr not. Clul^-foot is common. r the cleft can tie fell in spine lins and paralysis of legs. Some cases exhibit an apoplectiform course with cmia and death evere. resembles that ot pnrnlyis agitnns without tremor, and rciiexes of all kinds are not much altered There may not he paralysis. Ileflexcs mny be present or exaggerritctl according a* the lumbar enlarHemet <* «rly stBge 'pt perhaps hy lie muliir parnlfl- i i>h)-4irian (imagina diirntion. Orgsiiie nieots (4:ttll | do n In walking Biitewa) ■ilallon predominate over inose of paral>-9i8 Much rigidity, girdle and radiating pains and spasm In back mnsclea. There la usually spasmodic retention of the urine in earlv stasec- Paralssis Is of sudden onset slight ii ■ -ord IS involved. Usually a history of injiirr. Reflexes ex .ggemlwl. I.uml.ar puncture may yield a Woody fluid. Svmptoms vary with nnsition of h-m-rriiage. Pnrnhsis purelj tnotor, a paresis rnlher than a complete paralvVw, very slowly orocr-^ive and oft^n sintinnnrv rliirine lone neriotls. Snasm. rigidilv of leg mnsi-l.-. and later contraclures. Kn-adr exatraerated reflex-s. 10 (.a«ive luollrn. '7r''«n"y wlien rapid Ankle clonus. Rabio«ki nnd ^ninal enllonsv (4331. Or-anic reflexes little if al all disnnlered. Arms usually nnt nffected. but may be sligbtlv so aft^r years. This clinical pirtui 11 M nt '■re!- jT w . wIj 1 "'^'""' ■""■"''"''■'- nlthoiieli in it H>e r-flexe* arc not always irr-atlv exmrgernle-l and the posterior columns ore at time* involved cannot he distinetiv separated from thi" ■ *>■""'''""«• T'"' disease 1- usually of sudden cnsi-i ami ofieu follew< seme powerful cnioliim. It is usually permanent until cured by another Bimnc emotion, which mav be oftrn artifiHnlk pr-slueed by the . .1 paraiyse.1 limb otten olTera great re«istan<-e to pnsnive motion, even to slow mollei., <-..|itrtieiiires ai-" iwnmon. Knee-jerks are usually incr-n-ed. but no true nukle-clenus cr Unbin-'ki. the ankli-.bno^ lielng either ab*cnt nr of riincbis, (n(W, 073.) lal mcmbrani-s. Ilemato- Sil I rarely there r iski prp-ists. 1 j**lhe»ia and analgesia. The tendon reflexes a s'ase of ndnit life, but is analosnus to Friedre Bifonc emotion. i especially from Ihe ge •arly stage*. ,\nkle Spastic I'amplegin or lateral sclerosis (usually 5"J5 symploai iiic nnd part of a mon- extensive lesion, •n.innl or cerebral). (547,800.) (Figs. 24-7.) Ataxic Paraplegia or poslero-Iati>ral .flerosis. 526 (ili». lOn.) (I'lgs. 24-0.) IIy.terinil Paralysis. 527 (747-.'*. 7li2-!H!. WO, lOTU.) stepping laterally along a r.enl pan|i)--e>. IS, 23. 33. 38.) TrniBiyl pnrfllTsiB (2-'>iil<; side. Paralj-si* of h^-poslossiu' of f arm ami li-e of opp "i A disease i-nii:>ed hy r-ntin^' iipi>ilril fiiod (sniisaife. pnrk, cbf'*''' '"' even aplmcia. Tlic nio*l eharaeleritdJc siymplom it oi-idar pnr,i1j e^pci-Ullv Hif exl'muf, are parnlyxiil. At the flulnpty the Ittol' r paiinn i< n pi'irniuettl nyinplim. The disease hoK n very h'^l' The onset of pnrnlyHi-t in sndilen. If the patient d«>"s not die promptly. Inter tlie sjinptoms are rwrrewiive rnthtr than pro- grewive. lliey iin' uKunlly nniliih'ml. but mny }«■ bilateral. A number of motor cianinl nei^rcs nre paralysed, while there is a spnstie pnrnly«i»- more or lew proiioiin<'"'«t in the anna andl'^e^. Verlico iji a eemmon symptom, May be due to n*nite in- Unmmntion. Iiemorrhnse. thiYimbosin. eml>nliEm, or rv>mprearion, Alny oeeur in ncule (interior poliomyelitis. Often due to syphilitic endnrlerttis or syphilitic nouritis. or to aleohol or other piiisens. eil food, pTo.I ond therefore owurs in sroiip* of persons who bni Anihiynpiii. diplopia. pI'isiB and rnydriaHiB are alnnyK pri'sent and often raniiil noelei are found dinensed, but the spinnl nerve ei'llsiiri' not involveyebiill f.Srd. 4th j vision. nyntoBTnus, etc.. may result. 1 Uint ptosix. siguint. double There is paralysJ!: of the lips, toniruc. pharyni and larynx tTih, Olh. lOtb. 11th and 12t(h nerves) with conaetiuent dysa HiPin and dyspbnpin and umially ataxia and respiratory diaturhaneefl. itiliil Thi- c'hprinie fomw of tliese :, with ttie spinal form (fi47-P) the •11 1.-11 airophiw and resemWe the musnilnr d)titropbir»i in that the pnrnly.si': anrl atrophy advance tocether slowly, and it in diflinilt to «ny which is primary, ■niry nlno mnstitiite n group of (Tronic deeonwative atrophies. The paralysis is purely motor. [The paralysis in- « the eye raus- A irrsjdui plesiii I onset of wcnknews of onilar muscles, H may be steadily progreMive ■yriwll". immoliile p"pils. The disease may nttne'; nnly the e»t"mal nm ■miiletii I . Dispnsr may be complicated by biillmr paralysis f."i4'!l and ir, hnvioc procressorl to n certain point, it may remain stntionni ,ele« of the eyeball f"pht!ialmoplo?ia external, or only the ioliTO s iiaunlly niaweiated with mnj'olrophic lateral acleroaiR. Mu^i'lra mny lie attacknl in any order, ptosis, aiulnt, im- mui<-les (ophthnlmoplesin inlernn). or both, (optitbalmo- riir pumlysis in- vf^lven the lips. Ifincue. pharynx and larynx. iiili« Ii«dI fiirward. Tbnre are hulhor symptoms (4"I), Thcr 1. pharynx, Inrynit, etc. Roth facial nerves are invidved in s ■<-ii'-e of advnncod life. Often associated with amytrophie later II due 1.1 leeion« in both eerchrnl hemispheres in r len mnrk-d. Tlicre is more menUil i are ilrcolinir of saliva, dysarlhrin, dj-^phnyin. and nphoi>ia. Paralysis, tremor, atrophy, (ihrillnry cnnlrnctinn of niriselrfi of toncu''. lip*. nic e.iHcs. The pnralj-si^ very simvly pmcressew. There are syTOpiomnnt a mild spasric paraplcRin in lcp« with ankle-clonus and Rnbinski, 1 sclerosis and nt times with proiiressive ophTbalnioplcKia (fWal, In addition to ibe pseiido-biilbnr pamlv^is of mynithonla Bravis (n.'Ml k'hich thcri' li no miincle atri>ph,v, or librillation. and no change in the pleetrienl reaction, but nil Ihe other symptoms of bulbar paralysis i|wiin nt and k renter emotional exeilnbility tlian In true bulbar paral.vsla. 'Pymmetrlcal pnra]- I the Kmnll mnm-le ! of iHuidn or in I Mionlder c i rd 1 e |Synmiotrirnl para- :ly«i;i commeneinc; I in Ihe muscle* of the IMfAs and but- tock*. ^(•le« ,i(Ter'|ed f^hin iie weflkncRS. atrophy, fibrillary contrnciion« and nil doerees of alteration in electricjil «cHtaihil|ty from simple diminution to complete reaction of di^nn.- ration. The pneres m-]ether the Int- ioto^ically, patholoKlenlly nnd elinicnlly. in the brut or second yaf of life, with a oymmetricnl , usrb's exhibit the rcnelloa of deff»neratioii nnd little. y in\o|vment of Ihe pyraniiiial tract. trophy of Ibe muscle" of the thiehs. polvii and bin'li r no, pseudo-hypertrophy. The lesion consists in an .'rndually extending upwards and downwards, finally intolvini: the hulba trophy of the nerve cells in Ihe anterior horns anl a dee^nration in the Ma rkeil scninry •ymptoini an* pres- ent, sueh as pain, parMtlifwae, anes- thriiiiiici,ure!< and mii^i^ilar wus eni|>tionK (herpes, pemphie itrophy in hands, "daw hand." The flexor muscles arc more completely parolysed than the es- •. elc.) are not uncommon. Pert bro- spina I fluid may he under increased tension and show lym- Pi«rebro*pinal flufd mny shoi ical enlarite- 1 of spinal (Pigs;. M-e.) (»; n nf m AM th- miiM-lM of Tlir the body and hefld. mi inwii'iatien of sensniion is the most i-hanicteridic nj-iuptiim and is cnnliinnl with uiiin -ind pa rent hen in e and more or low mnlor paralysis ami atrophy. Trophic le«ions are usually piv>minenl, Pemphinis. uh-emlion and ni'ilil.nii''" of the hanils and Imphic lesions of bones, musclett. and olher lissuex oecii trophip svmiitoms predominate over motor symptoms in Ihe arm^: while thel-i-B nhow a mild fpastic pnrni2,"i). and sraliosis nr k)'rihoi "nui prr*»n! the sj-mplnms may he twth in arms and lees, and the motor ^vrnptcpnis an- iibnul ak pnnnineat a« the sensory nnd may he nnilitr-ml in thi- ear! cerateil In ■■"nlral allfwiis in Ihe cervical or donwl region*. The cen ical form of the di^nii;- runs a chronic course, exlendinc at times ovit dead"*, but r.ipid ennrw, and may exhibit a unilateral, spastic, muscular paralysis nt lea*! in the early slaae*. In sudi eases the lesion cnmmen eii in the Iinulint ■"Ijl,''''''"!, j""" r' **'' '•''"■"■«' '» "'" "pi'l tirine of the mui.-b'« whm in action. Piiiinil can walk w-II at the slnrt. hut after a few forn fow bundredl sfrn. i* Iind eut. The «amp is tnie of all -ithi-r volunliiry acts. Kvuniinnlion of the nius.dr* with el-clricily Kive« the ms-B-lhenii- re- t.fln»l. There I. no DiuHnihir atrophy and no rvnction of de'i-ncration. In the domain of eninhil nerves fin whirti the en.sc usually coinmeneisl there may be ptoslw. diplopiPi. ophlhalmopleBia. diplrgia facialis, dysarthria, dysmasfsia. etc.. and nil the spinal nerv<» may hp affcctod. The Iwad of the ptOHia. "nie nymptomsarc slight in the niornin? and «mw worse during Ihe day. No sensory dislurli.inees cscepl painful cinmp". Organic rcflext-s normal. A tumor is often found in the thymus gland and multiple foci of small round cells (lympbo- e muKciilnr atrophy haK often the location nnd char;< 1 Ihe t.viiP called MonanV disease. In the most comn I mere tb"n half the cases. Pnnidnxicnl fS7I» and -. aees. All forms of ri-flex action are abo|ii;hefl wh^n I iwly prosretses and the anefllhesia at first sliBhl si'ai Uiruemcnl and aetccnds. prodiicinc tlie nymptnms simt" ■riiticB of that of proEre>i>.ive spinal mnseular atrophy (MS). I form Ihe c-nieal reeion Is alone affecteil and si-nsiiry and nianooiis sensations have been noted. When a diBHise clioma is rprvieni and lumbar enlarsemcnts arc Involvetl, hut are exag- i hecomps more nmrh.<1. Tlie diffuse form often runs n fniriy at resemhlinit a very chronic aia'endini: paralysis. I* held reimclivl t\ t lb.' Miuspirs nl the autopsy. Mn«-lp. „t one or holh lees, rarely of lofmiiti Rarely rommnnHnc in lei-i exlendinc to arms. but in Aikocialed with a <-rvinil rib. li«. sk ralsia. .\«n.in(«l will, arterial disMte. ReppBtrn of per ■Ml "V"''" "' !'■''"';'■ ' iIp cmmp. nnd iveakneat of leg or b-s«. cnuwd by nalkina. Putini: the allnck Ihe feet are cold, and there is diminishcil or absent pulcatii-n in arteries of fe*t. aiw>ciat"i with marki^ arterio-srlen'=is of arieriefi of leg .is shown by palpation ami by Ihi e r in-Atf occurs m one or both arms. No sensory distur'ianc*' except painful cneinps. Orgnnic refli-xi". nonnnl. Ancio-spnstic hemiplcKin in which Icmponiry attacks of hemipleeia, sometime^ associaled with aphasia, occur, is probably a variety of this disease. "nil.""'!"' » m!"^!*'*^!"' '■*"" '""'"'''■" "^ '^'' ''■^ usually firnt nnd then of arms, laslinn a th. hours or day-, llie attacks usually ocnirin IJi- morning er after rest. During the attack the left cardiac ventricle mav become icaipornry dilatwl and n murmur mny be beard, Tlie an IU.1 .lunckpu i-hern i* usually well marked heredity, or Ihe dis.'a»e occurs In family «r.'iips. Durine n »cv.-re altnck three is often a diminution or nb«i>n<'e of the i-eflexe* nnd of the fanidic and galvanic excitability of the aerve?. ami of the mechnnical cxdtabiHtv of the tr<.iips 01 lamily perioiju- paniljwis these negnlive symptomh mr not preseul. Soiu?ef thejc cfls,» on apparently dur to malari.i and can Im- curiil by Ihe adutinixlnition of quinine. in «!,' 7"J'' **"'' ""r' '"""u'"' '^''" "^"' """ '''*"*■■ '" """*"•«'"■- ff n-rrii-ol rib, nttncto. o'tnir, hm only afler use ,.f the ana. Tli.-w attacks are i]i.ually unihtteial. ev.n though Ihe extra nh U on both sides. TIip attack ronsists „l ,n,. il V- ' Vli " , "."" .""* ^"^ ""^ " "*""■* •■'"''• "'"'■ '^ ""■ "f '^'' """ '" ■■'">'»""•■''■ ""• «"" "'""vs a dcHdeH panels, which pas,.-- off if Ihe arm U kei.t at r-.t. An ununited fracliire of the clavicl- will rnr.-lv .Miisr simil; . maj w caused by a cervical nh. and is often n'liev.d by elpvalion of the arm and it- n>"'le wocp by motion. In rare cases this parnlj^is. ai first i rl allarln „( trmporary pnml.vsis are very rnrelv met wilh inbv.teria and In eld-rly per«ont with thick-n<-d arte .•Oral oriKin euch paralynwj are of limited extent ; when of spins], gen-ral. See al"o oeeupition neurows (615) . in which cases apopic ly unihiteial. arm U keiit al lermiltont, ma V is probable Inter. Some ci e DIAGNOSIS ni'morriiage softening or anite infiammation in brain-stem R34 l,-.i;t-4. Wtl. 7-I01. Tumor ill or eomprpwinj; the bmin-slem (aFjtl), fi3o Ilcmorriingc or xoflening in crii-i cerebri (r^lS] fiSG Tumor in or comprcHsing cms pprehri (fl5G). M7 Uemorrhagp or softening in puna ('1431 fslS Tumor in or comprcMing pons (tr»0). KW lIoniorrnHgc or softPDing in medulla (544). WO Tumoi in or mmpr^ssing medulla (iKiti). Ml nolulUmus. '142 A.-ui.' t-r Apoplectiform l'nli.irtiiT|.haliti» Superior (Wer 54S iiirkp) (5S4. 104t!-S). Ai-ute or .\poplccliform I'olior-ncophnlitis Inferior. Acute Bui- B14 bar pamlysis (KM. Iftlll-Sl. Prosre^'ivi" nphthnlnioplezia. Polioencephalitis Superior M^ Chronica (often ^ymptoroallc of n Bteadily proBresaivc, moiv widpspicad disra>p, «uch a* labes, tumor, etc.). I'l-o-n-wivp Iliilliar Paralysi... Polioenwpbalili* Inferior 54ii (■|ii>iMit:i. Kihir-glfwopbaryamal Panilysis. (llftt. T'M. commi-nccs in thr small mnflcl.-s of the «B follows and i.s dependent upon the pnral>-»i». wilh ankle-elonus and often nnd of very chronic counie. Mechanic- (illCi. SiHi, llTiOl. Prosressiif Spinal Miiocular Atn^iby. Amn-Pui-hcnnc type MS of muscular ulrophy. Chronic Atrophic Paralyats. Chronic Poiiomypltlis. («ei, soo. iinni. liifnulile. Kamily, Ilcrrdilary Anli-rior Poliomyplitis &1sn ( AV'-iilnig-Hiiffamnii t,\ pe I . y of, or hemorihajie la. Aoutf 'ir dironic mjeliti* i:i;iii). of. <-nfi. R3«. r>-.o be assodatednith ntrcpbj of the paralysln may be due to tempnrary arlr mbncKH, linsling, feclinc of congetrtion, rcdiicK jinptimis. Pain, in Mie form "f a brn'hial n'-u- ■B of thr hand and even of the fori'arm. iai "pnsm in the c-ntral nervoim system. Whpn ArtrrinI diseaic. Piuhynii-ningili" h>perir«iphica i-.-rvicnli*. -wl Tumor ia. or ionipr;«.Miig, is;tll) '*''- SvrinBoinyelia. CVntral alio*i«. MorTan's Disease, (tW:i, Wn 'M)2.4n-2, lIKit). IKi2. IIT". lU'T. i:iin-21. M)ii>thc-iiia travis. Pseiidoliulhar Paralysis. 5.%4 Intrr-niltcnt Limping -r ria.idir.ition D,*-rf.asia Angio- 553 twirioiicn, (iinni. nunily I'lriodi.- Pnral.vhi-, »« Prcur- o( cpr*ks,l rit. M,...n -ub-claviaa artery. 53T CHART Xc Combined and Intermittent Paralyses Comprising Numbers 471 and 474 on left side of Chart and 535 to 557 on right margin 139 cr DIAGNOSTIC SYMPTOMS AND TB6TS ( Etilnlirnl symp- If the parionl doiM not pri>mplly dip. one nr more crnnia] nttyet t^mg. eia (52."i). There hit usually iJjsn" '- ■- ■ • - -■- tomx at fint may be more iinilntenil. DIAGNOSTIC ANALYSIS OF SYMPTOMS .VeiLti ABSTRACT OF SYMPTOMS There is mor'* or Ickk niiirknl simslje pnrsplc- Craalal nerve* nlone ItivoIvmI, (Pies. 18, 23, 33. 38.) f'rniscij ptiralXKii (2.V!) and bulbar i.symphonis (-12'1). TaralysiB of uiie or wore pye muirclus ot o I of ficbl (hntli li'lc mill of ano bdiI li-^ "f n|ipiw branclii-s) ot Irigennmiil mrie ( Hiitlm syui|itiitii» — 134.) Symp- mill 1(^ of opposite sirlc. 1 ami |i>5 of oppi"*ilf *i'l''. i;i'. i"irk, rheene. i-iinned fmifl. cic.) anil ther^torf ooriire in croups of pr>rRors\ fm i- .«-ii|F)r r'>f'''r'''f' Anihl.vfipia, lilplopin. ptosis ani myilriasis are alnnyK pn ■iy llip motor rnininl nui-Iei are fonnc] di^raiwd. biil Ihe apiiinl nerve cellfi n I very hish morlalily. anil in due lo Ibe ingestion of the linriHii* The onset ot parnlytris in sudden. It the patioDi ilo^s not die prnotptiy, later Ilie syTnplonii< are recressive mther than pro- grcBuivc. Tliey are iiminlly nnilnteml. but may lie liilal«tBl. A number of motor cranial nerves are paralysed, while there is a upHstie |inm1>-!ii!^ more or les« piwnoiinn^ in (he arms and b'zK. Verliso 'ia a eommon symplom. May hp due tn rurate in- llammalinn, hemorrhnse, thrombosis. omboli>mi, or onmpreninn. May oef>iir in aeiito antiTior poliomyelitis. Often due to •vphilitic enilnrteritis or syphilitic neuritis, or to nleotiol or other piiisons. raraljuis of hyimclosMi.* <>t riui' sidf an A dijtease rntiacd by i-iilin:; niii'ili'*! fnod (siiiisni;e. ; even apliaRia. Tin- mosl charaetiriHlie -j-mptorn i especially the exli'rnuf. are paralysed. At the mil pfltion it a prominent symptom. The diKease hn\ inset, Regre«»i-e. No optic neuritis. A variety ofapoplexy (3041, No increased tenmon of cerebrospinal fluid, onset. Progressive couree. Optic neuritiK. May be Jnctrased len»ion of cerebrn.^iinal fluid, onset and regressive course. .>o optic neuritis. No increased tension of ce re bro- spinal fluid, ironic onset and progressive course and optic neuritis. May he increased tension ot cercbro-spinal fluid. r.\rni« onset nnd rcgreseive course. No optic neuriti!>. No iuoreui^ed tension of rerohrc-spinal fluid. [chronic onset nnd progressive courae and optic neuritis. May be Incrcnsed tension of cerebroipinnl fluid. tc onset and regressive course. No optic neuritis. No incri-nsed tension of ccrebro-^pinal fluid. Chronic onset nnd progressive course nnd optic neuritis. May lie inoreased tension of eerebro-spinnl fluid. r Annie ( [Ciironic I Chi I'ho ba' .■e eaten tocpfher. The first ajinploms are proalralinn. nau* nd often in an rilreme decree. TTie pupil \9 immobile, i involvefl Hlher clinically or patholngieaHy. There isliHli I nnd vomiline fnl|on'#d by d,vsarthrii) and dj'sphai [■omm™lfl1i'in !■ lost and one or more of ibe rrn-li mi or no, mental diMiirbances or fever, but obslinnle < weles i more or lf«5 pittensive paralysis of the motor n . nystagmus, etc.. may result. "liere is paralysis of the tip*, toneue. pharynx and Inryni tlipin and dysphagia and usually ataxia and respiratnry liMiiir Tti" chronic forms of these (The pnnalysis in- iliiiea>if«, witli the spinal form {fi4T-S) volvca the eye mus- (iinsliliile the procre«olintr of saliva, dysarlhria. d>'sphnsia. and aphoma. PnralysiR, Iri-mor. atrophy, fibrillary oiintrnction of musele*: of tongue. Iip», iiv.il.i. pharyax. larynx, etc. Roth facial nerves an- involved in so-iie c.ise= The pnrnl.v>,ts very slowly proEresses. There are symptoms of a mild spastic parapletria i" lei?< with ankle-rlomis and Babinski. A (llKiaic at adv.iuced life. Oflen awodaled with ani.vtrophie lateral srl"rri;i= nnd nt limes with proure^ive opIiHialuioplegia (fi4Ji1. In nddtiinn to tlic pseudo-biilbnr paralvsis of myasthenia gravis (Ttn4) ther" jK nnrtlier form due to lesiono in both cerebral hemispheres in which Ibere i\ no muBole ain.phy. or filirillfition. and no chanee in (he eli-ciiieol reaction, but alt the other symptoms of bulbar pat^lysis more or lew marli'd. There is more mental impairment and greater emotional excitability than in true bulbar parnl.>-sie. Kya V'-i" moirieal parnl ■ing in the small rmis^le of hands or in Minnlrlpr C irdle Spinal n e r V alone iuvnlveil II-'iRi'. 21-7. The niimeles afTect'^d *hnw ppogresBive weakness, atrophy, filirillai hand", nr. more rnrelv. in the muscles of the slioulder idrdle (aci nlr'iph,v. Tlie Ihumli cannot he brought arroso bnnd lo lonch Ihr Ualiinsht. tmt nnl nlwayn. Tliere arc sr'i^ndnr,v eonlractiirrK. <"^ii »1 irrilaliilily of muscles is inerenseil. Rflrn assoi'ialed with p'""' inil eiiliitiins are invulvi'il or not. I( is diflimlt to dra* any -iicl -Tnie xyniptomK as alxive, but s r other, sympt-ms of lateral sclerosis, Tliis .lini- las Ijc rar.lcd a n ehro ■ polio 'Oie two diseases howei ', differ radically eliologicnlly. pathologically and rlinicnily. I in the muRolp* of t]ie Ibighs nnd but- toelw. tory 1 tiKC commences. In the iirsl nr second year of life, with V year". The niiiseles exhihli ihe reaction of degvnera and willKiut any intolvincnl of the pyraiaidnl tract. symmetrical atrophy iif Ibc muscles of the thichB. pelvis and tiaek gradually extending njiwards and downwards, finally involnne the bulbar niii n nnd little, or no, pseudo-hypertrophy. The leaiou consists in an atrophy of the nerve cells In Ihe anterior horns and a drgeoralion in Ihe nntei Alnrknt seiiMory ipaptomifc an- pres- ent, Niich as pain, pnrcsthewiae, anes- llie...ia. etc, with Ihe motor pamly- Diwioeiafion ot na- wition (Sft-il 1* present. Holh armn and legN are paralysetl. There are tropbic distiirhancefi in Ihe arras and nol in the !<■«■. Pupils are often une()iinl. Reflexes are abolished in the arms and iaiTi-a*er heinE paralysn). Conlrai-Hire^ may he present in Ihe legs. litic iTiyelon [, (Dosl eitonsive in first few days and t . Symptoms continue to extend for s im iialadii (12in. i". intense pain and spann* In arms and nei-k pnuwlc ih' i 1. in the lalcr slllBe^. (pnslic symptoms appear in Ihe legi Mosi of thi*c r-a'fe are the result of chronic s.vphilitie ni" ay slowly improve Inter, May be deformity in cervical region of spine. Knee-jerks may be lime and are fnlrlv Kymmetrieal. Organi"" reflexes disordered. A history or otlier evid-nci absent in early ntages, faimliar piinctun of sj-philis (12(^1 is often found in syplii Very chronic onset nnd a progrcMive n iri'ilalive, Intrn-niertullnry paralytic. ' Fmplni mralysin and c. Culaneniis en ninuilis. Sy-mptomK at flrvt mainly unilateral. Iie< ures and musculnr ; (herpes, pemphig atroT>hy in hands, "claw hand." The flexor miisch s, etc) are not uncommon. Cercbro-spinol fluid r aie more complelely paralysed Ihan Ihe ex- r he under increnseil tension and show lym- ; liilalcral later, Ccrohro^ipinal fluid may shn* reri'ical enlarge- ment of spinal cord. (Figs. M-G,) 9 ot % ■•. the mo«t Trophic liuionh are usually pmmir Irophie *vmiitom» predominate ove pre^iinl the t^^-mploms may be both geniled in e"nlnil uliosls in Ihr- cervical rapid eeiir«e, ami may exhibit » unilate •hamcterislir »j-mptom and Is cunhiricfl with luiiii /'ml pare^lheniae and more nr leirn motor paralysis nnd atrophy. The muscular nirophy has often the location and diarwi-lpriilii-i of Ihal of proErcMive «pinal miiwiilnr alrot)hy (EVtSl, ;il. Pemphigus, ulceration ami mulilalien of ibe band* and trophic lesions of bones, musclrfi, nnd oilier tiwiiies occur in ihe lyne called Morgan's disease. 7n the most common fonn Ihe 0"riical reei-in is alone atfeotpil and sniBory and molor syinptmns in the nrm*: while ibelw -bow a milil (.pailic paraplegia (TiQTt). nnd fN^linsis or kypho-ii: occurs in mere thnti half Ihe rasps. Paradoxical (S71H and spontaneous sensations have been mdnl, When a diffuse clioma is and legs, and Ihe moHir sj-inplonia are iihoTii as prmnincnl an the sensory nnd may be unililoral in Ihe eariy stasies. .VII forms of reflex action are abolished when the cervical nnd Inmhiir cnlnrcemenl* are involved, hut are exae- dorwil regionx. The ceriical form ot Ihe ilisi-nit.- nins a chronic coui-bc. extending al limeji over ilr"ar|n>. Inil -lowly pro^roses nnd the anesthesia at firat slighl sl-a'lily beconup* more mark,r|. The dilfuse form often nins a fairly All Oie mu«-W of T thr body and head. 111. ^aslic, musiiilnr pnralysi agits. In such case); (he lesion comnien''e alaru cl,.1 ,.««.""'' V'"" "^ *^'' '^^'^'"^ '• •*"* ™P''' •i'^nP nf 11"- mnsHes when in aelion, Paliriil can walk well at the slarl, but afd artjoa r.fiHil. There i. no miisnilnr atrophy and no rwiction of dpzeneration. In the donijiin of erulal nerves (in which the ■d an necnunl of the ptiwis. TTic aympinmsare slieht in the morning n.tid grow worse during the day. ilop»y. and nsceiiids, producing the symptoms simewbal resembling a i lation of tlie i-ry chronic Mi-ending pnmlysis. mlti-i rely of Rnrrt> the di-. nl Ihe u-k^ of pijnfiil r forn tow hundred) steps ih tired out. The same ik true of all other volimlnry acts, KKaminntion of the nniscles tvith eleriririty ci «e usually coinmene"*) there may be ptosis, diplopia. O|ilithalmopleuia. diplegia facialis, dysarthria, dytminesia, elc. and all the spinal nenee No sensory ^sTuHiaiices except painful cramps. Organic reflexes normal. A tumor is often found in the thymus gland and multiple foci of i nnislheni'" re- leil. The hi-ad 11 round cells (lympho- e cramp, and weakness of lee or lesi, r both arms. No senmiry diahir'>anei »..! by V •ept poi Ih markeciaied with apbnsi rieriofi of leg as tihown by palpalion and by the X-r Comnienring in legs extending to arm>. rate! 1- rnuBwl by „ cervlfiil rib, and is often relieved by" olevniio e6), llniuormnge or softening in misliilln (Thl-l), Tiimni in or nimpreKsing nitslulla (tkV!). Iloliiliiiniuii, "f .-yeball f.^rd, 'Ith and filh) ; «n that ptnsLs, aiiuinl. double id 12bh nerv(«l with conse<|iienl dysni^ Vcuie <,r .\popleetiform Tolii niekel (3S1, iWi-Rl. ■ or .VpopIecHform PoHnen - i.araljsis (534, HMCrSl. .■iic'phalilis Superior (\Ver- ephaliiis Inferior. .\mte Bul- y contractions nnd all degrees of alteration in electrical «xrftn,hilify from simple dimimilion to complete reoction of deseneration. The progress commences In the small mnacles of the nulo-h'imeral type), is usually fairly s.vmmetrical o-d extends lo the other grmips of miisdies in arms, body nnd even Iocs. The muscular wiaknew fnllon-^ and is dependent upon the lillle finmir. The finsers cannot be spread apart, nor can their ln.«tt two phnlnnices he extended on the (in?l. The le^s shown ni^ld di-gree of spastic pnralynls. with nnkle-eloniis and often ■eiiillv til.- "daw hnn4fll. Some niithors divide this symiiKcm complex into two grmips according a* to w-helher the atrophy or the pnraljtis is primary, and as to whother the lat- di"tiavtinn elinmilly. 'itir one fdrin may he an earlier sta'.-e of ilie iiilier. Tile symplom complex is divided into two groups (&4S) in this chart. i nnd lerminnling fatally nl ilie r nerve roots, without inflnrama- I'rosrci»i\,' Ophthalmopleaia. roUoencephalitis Superior bi't rhninini (ofleri Mymiitomalio of a steadily progressive. mor- widrspivad disfO'C. "nn* as tnhes. luinor, etc.), I'loarvv-ivi. Itiilbar rarnlysi«. Polioencephalitis Inferior Mil Chreuica. I.ahlo-gh-s«.pl.nrynKPaI Paralysis. HifH, im. n.-.n. (mr.. '^Hi. iirifli. Progressive Spinal Muscular Atro|diy, Aran-Diiehennc type T*i^ of muscular ntrnphy, rhronic Atn-phic Paralysis. Chronic Polioniyelilis. (6SK'.. «00. I.IWII. Infantile, li'aiully. Hereditary Aulcrior Puliniujelilis Msa (W-rduig-Hoflmnnn type). Injury of. or hemorrhage in. I'achymininsili* hiperlrophic of. ITOS. S3R. WO alk-ins. rtiirioj; the attnck the feet are cold, nnd there is ditninished or absent piilsalii.n in arteries of feet, awocinteil ifiil cciimp'. OrEanic reflex™ normal, .^mdo-spaxtic hemiplegia in whidi temporary allacks of hemiplegia, sometimeu 7-I"nw »'?* Mn'k "i''*^n."' '■"" "'"*!!.'''* "' ""' ''''" """il'y fi""* and then of arms, ladling a t"*w lioum or days. Tlie allncks usually ocnir in the mornini: cr after nil. Durins Ihe atlnck the left cardiac ventricle may become Icaipororj- dilats-d and a murmur may he beard. Tlic cranial in «em- ™,.!,. Ir f ■l""' '- "'""''' . ,' ™'''<'^ heredity, or Ihe disease .unirs in family inwups. During a severe atlnck there is oflen a diini ien or alienee of ihe i-eflexes and of Ihe fnnidic and galvanic excilahility of t^e nervcc. nn.l of the mwhnaicnl excitability of the mnseles. in «>m croups of family penod.c paralysis these negative symplom. are not prescl. S-m-of lUe.c ra«.K nn. apparently due lo malari.i nnd cm be cnr.-l by the admini-l ration of qninino. ell and mn be swn wxlh the X-ray, In tome cases of rerviml rib. atlnck*- ncrur, but nnlv after use of Ihe arm Tliese niiaikx >in, iiKiinllv nnihiienil. nrii ihoiiirb ibe erlra rib i» on both sides. The attack cnnsisis i,t numbnew. linclini;, feelinc of congwrtion. rednen* of nili-"! fracture of the clavicle will rarely cause similar «.nnpliiin«. Pain, in Hie fonn of a brachial neu- Finent and may be araoolalifl nith atrophy of the musdcK of the hand and even of the forearm. Svringomyelia. CenirnI sliosix. Morvan'* Disease. (fiOS, K« S02-4tl-2. lOon. nr.2, 1170, 11S7, 1370-21. M>asthenin gravis. P'.e.iito-hulbiir Para Inierniltlent l-imping cr Clnn.liniti.ni, Dy»l>aKia Angio- 5fvi si-uroti.-a. mnn). Kamily Pcriti.tii l•ar.^ly^i Pre«-■ forms of tonic spasm occur are set forth in Chart Xlb. 573 CHOREIFORM (272) 574 ATHETOID (271) r Diseases in which choreiform and athetoid spasm occur are set forth in Chart XIc. 141 CHART XIa General Clonic Convulsions Comprising Numbers 571 on left side of Chart and 575 to 596 on right margin Idiopathic epilepsy — 575 Symptomatic epilepsy — 576 to 596 143 DIAGXOSTir SVMI-rnMS AND TRST8 f Ix«s of ponscious- I oeee, (comn or iii>ini'<-i^ma) (SK). Krwiiipnlly hiliDB ft till- toncup or nllirr iDJury. Short I itiiriitiuD. No other ajiDptom of dtspaee except tbe coDvolsion. SfmptomE of seri- ous brain dUeaec. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS ntlnrk flo erjinil mnt). is nt first tonic with ■irr.-.i .,i T.^im ,,ti..ii. Thr fnc 'Imiie ipiKon of lonj::(>r liiirntion (J to 5 rnitini. ■ i uhi [■^y, rPH|iiruliot ,rlinll'li.f,v. ptc.) i-iilhHl tlip "ai'nMiry iiiini" t'l2n) .nnrl j- ..frr u u-ii, i .niiilly ahsent Hiiring anil inimwlinli'ly ofirr thr artjuk. A .I.i- in (III llii" fordieail and fiioo. C'lmiplpti- nmni'sin in rtennl I any p^m <'f thr hoiJy, In som" ra-^os Ihf iitiiickfl oiv-uroiily at iiicht or It nirtliiil. At limes Ihi-re in mircly loss of pnnsi'iousnct wiihr.nr h.'Ii.i lund lepilsin iii'rx'iirsivn rotntorin) or piTformK a siii^- ■■( vis ■ ■ m itin.k of Aoitr fo)l"W(i or ri>plncpH h i?ouviiliivc atiaok ([isychic (H|iiii ili m i In . M pillcDts mo iiMinlly rfull and aliiptd, nfton finstnirtivr -iml .i(i|.,iMrii I. pblcn-Blifin, by the purposeful and linx-ly nnliirc of (he Mttioli. I: mmtial. made hy li A oonvuUiv(>|(aek. r*ip< not repr-ftl irritation [The conniliion Ihf miwdM flt Htmul Ihi- wiroo time (epileptiform ( coni-ulsion). Congenitol or in infancy. Often ferer at onset of first convulsion. Till' disi'o*(> onpnil: tempo n I steadily usually toms. nckf. which arc noahu'we of tbe • syiuptomB of a nt^ttg brntn diBeas^ n-ith Wiuory and psyWilc x.iTitp- rl«ady advance towards Symptom B of dlH- rase of other of cerebro-spinal disease, r Kidney disease. thni the Cardiac d ' Blood dim InlcntiOD Ir r, iconninL; speech, nystagmus. and tb<> Slow' pul'P nupid U-i-t dilation Symptoms ot poi- soning. Appan-nt. but no true, coma (shown by RiiKcplibiiliy to etiBt'ention durine Ibr altnek). No biting of tongue or other injury, l.oni; duration. (■Blue line on Rums, lead in urin. 1 .Mrohnlic odtir of hrenlh and iti'Ti* inmot and ncrvousne I'k irars in itendy gait, motor sod sensory paralysis, many symptoms of I"cbI lesion^, etc. of convulsions, accelerated respiratioo. restlessness, cyiinosis and cotiimctt contains albumen and many casts and is usually scanty. There may be albuminuric retinitis, hexdache, vumitinp, Cheyn^Siokes rc.iiinitlon and somnolence, B£ iDlermiitsion in heart beats associated with coma aud conviilKioos. which pass off after the heart begins beating again. Arteries atheromatous. Advanced life usu •mall volume. Irit there is more or less mcntui impairment (epile|itic dc- ipllcptir etinvnision cloiiely. The diatsnosis of malingering can only be onfci'ioii of Tnalingcrcr. ■inllv common in syphilitic and rachitic diildrc often p"" , associal<usiderablc mental impairment. There is usually dy-»arthria. HeadnHie, vertigo and vomiting. Cbokeil disc or optic neuritis. More or loss of raemor.v. Iioivilixing symptoms are sometimes present. Convtilsi Loss of will power, restlessness. dcliiKions (usually of exaltation) and symptoms of Inianity. Poor jiidgnieni. Good nnturctl but Irascible. Childish. Characl eristic blurred speech, TrcmiT of loner facia] miiscU'«. lips, tongue and band!<. and awkn-ardncAs (ataxia and apraxia). rncqunl and irreaul.ir pupils, Are^'ll-'toberlson pupil, optic neiiri(ihlhalmosi'opic exam eicposed to high tcmpcrnttirea. D?liriitm •r other germ*, may be found lu the cerehr ■ usually present. i-«pinal fluid. There is often an epidemic of the disease (Welch- |Hly relievrti by the uiii ''inf Uie nervous «y^.tem. <•* ialeitiual putrefaction and other if Moi all. of the ger stion of laiulcd meat and other poise ^ and are not to constant as In diarrhoea nod foul s DIAGNOSIS ■ major attack. ■iirring ahn in ndults, especially in pregnancy, altogether similar (epileptifnrml to the ahoic, but o<'curring only once, or in one series, and ABOcialed often with digestive disturbances and abdominal distention aud may be due to poisoning (ptomaine, alcohol, etc.), or U> tli- Mntvs lymphaticus. Slay be due in some children to peripheral Bl Ihe onset of an acute infection. No sharp line can be dravvn Dolween llicse conxiilsions and those of uremia (587), or lead (oS4». or alirohol (OSTi), or nulo-intoxicatioa (506), r begins in early infancy, rnilateral or hilatcrnl convi The shape and site of the akuH cpili-iisy. e|.iif|no- ii |i«vchic [Hiiiivaleiit. e| 1 i.-.a. -lii). ^4:l. niJs. ■pil.pl 7a-s:i, 1101), •erel.nil Pal-«v of niiMbno-l, (.-.111, IVJI. S()L lt>.->l-SSl. Cerebral Tumor lineludllig abneewi and cystl not in or n«ir motor aren of MPtei (507-3r.-7-fl-41. :i'*7. S3C. ftM). ParesU. Itcnerat l*«ne«is. Panilyiic llemenlla, (1.1-.. ISO, 400-12-3. «7o. im. 8!i7. 1052. llOfi. ll'ID. U'ilOI. liiv.emlnal<-d Sclero.i-. (loO. f.n. o-'A (itw. OSS, "raft. "os. -sos. om. IIKMI, Iremic eonvuUion. (103. r.7"!, W-H. W71- .^tokesAdnmi.' Diaense. 14241, imKM. Amniic coonilsion. Lead convulsion. (404. 57(5, lt>5:n. Alcoholic and Narcotic convulsion. (.17(1. ll.'iR, iMB. Patient may fall or glide to the ground but does not hurt herself, itiitudi's, (altitudes pamionellcsl , Patients often "rave'* during !> are forcefln M)l 122 or Difloy timi-« rvpcntwl HliHsm, rarv'Ir om- Irncliiri', of one croup of iiiii»c1p», opciirrinc in pan>x- yKili* wbirh ratlirr tend to viibsiile on voluntary move- uii'dIk. MyiH'Ionua (270). n^KiD! Id oni- linn an.I m.Ip of n.'i-k aoiJ rt"""!* '" '^? "' ^'^'' siili- uod then to opposite side. nore rarely in neok ■I'he siiusms ar^tlaw' "'ways unibteral. and when bilntwaUre not ayiBmelncal. Tlier interf.(t ntj HtHe with volun- tary muvfmeaU. DIAGNOSTIC ANALYSIS OF SYMPTOMS .\BSTRACT OF SYMPTOMS Much pnin in hiad ^iml iivck al ousol. Wnikfipss sL.wly folloi oome \ioipiit and ni'Tp eouiiniiouH. t^ileptiform iitlncks nr Tile spasms seem likp uiimir eeslures and apneas to be rather purpoacful- May Psji-liie disHinifrs have ori^'nat^d from local irritation, Deunistlienic ual hut have fieraiated after the irritation f an emotional e often present. fThe 1 i (endinum. Symploins sliow considerable variation in different cases. In rare oikik there may be iofeclinn, fever and delirium (Hunt). BociDn in side of face or in one arm or Ipit and may e«tend over one, or even hntli sides of body. The spasms are billttral iind fairly »ym- njetrirul. but not (jnchronous. They are irre^ihir In totf nnd rhyliim. and are almost llwiys limited to on.- >sed. >ipa>nus never appear to be purpose- il .No mitvement renullr^. merely indi- dual muscles «princ forth in slronK intniclion. Irritation of Ibe ekin or ti'lons rniiseK paroxysms. I.itlle or no emotional di-tturbanecs. TretDblinc of tnusdes belneen Ihe pnroiysms. The spasms bec«oie less, or entirely cease, during sleep. Re- flexes exaggeratdl. of mufclrt and los* of faradio exeitability. The spasms be- ' arr accomp'injeit hy no pain. See also reflex spasm The contractures art nfiyxTipariir-d hy sharp dirts of pain. The muscles [nvoKed arc attached by one end to tbe trunk of the body. Muscles of Ihe fn^e, hand and forearm, foot and lower legs almost never involved. No "lerediiv. A dlsentc of ndult life. Many casea orcur in the satiie gencralion of a family. The disease beisins i early life and is aR>oaated with epilppsiy and dempniia. hy lyinf; a hand (i!.')illy nt li-ly; bnt usually porHism iaer-nt niu.Hcle* and so ovei r many audi local qpaiims. i mud the extremity as soon tvhi-n Kpat^m ix limited to ( one half Ihe body and then p.is-'< acn IP may occur which will pus* into a IB tbe local ttpasm nprii'ars. f'ansriin c-hnlf the body or to one extremity. ing in pharynx oenophnru*. Rleiilily vf aplnt CerBlmllar nia There is the history of an jnfi-cird wound, or septie childbirth. wllliin n month, unually within two weeks. The iiifectinn may oo-ur llirouith the navel in new horn b.ihies fleinnns neonatorum) jaws, oecitrring in pnroxj-jiins; also riKidity nf facial mmdai priwlunnc "risiis sartlouiniB." In the onset a cradually increasins stiffness nf masticnlory nnd other muscles followed and ncii hclnit held in position of opisthotonos, omprosthotonox, ptmrMtliolonos or ortholonos (2'S). The spasms are associated with profuse mealing. There are no meulnl symptoms nnd no co'iia, very hich, The diacnie vartc- greatly in intensity. The ICD|tr the inmliation p^'riui) ihc milder Ihe disease. Ixica! tetanus ind head lelaniis with local paralysis have been deecribed. There in a history of a bite hy an animal (usually dog or cat) within a year, usually within six months. Tin* most sirikint: failures are irL-mor, rapid pulse, fever, mental depression, fri^^ht. \\"r especially on MBhl of water. Spasmodic closure of phtlTOX find oeuiphnmis, mukini; swallowinit. enppeinlly of fluids, imp >"sil>le. Saliva cannot he swallowed and is expelled from the m*" couch, opisthotonos and genfral spasms are common. Cefl'l i"l^ froin ciitaneoua or speiial sensory wurfnees are creatly i-icrcased, especially lh.it of inspiratory d.vspnoen. Priapisri -i"! liahl nnd aecnnimndalion. Tlie since of exciliment is at timn f''ll'Wcd hy B slace of paralysis and is often preceded by a p-odromal stnee of malaise and of pains, especially in Ihe scar. Hysn noi-is must he made in such i-ases by the preience of hydailctl -yinptoms (425), absence of fever, absence of true rcspirnliry spa^m, and by time. ' both sides, or it may remain a local spasm and pass ide abducted. >r uo. paralys Head, trunk e, Exagcerated reflexes. Little, or no, fever. ind extremities each rotate about lone axio from li'le of l< 1 tc the -ipposite side nnil tbf eyes Riifidlty ratlier Hinn Kpaxm, not slroiig enoiieh le pn'venl paiaivv or voluntary movem^nls f2«i). Apyrexla. If nn-| Fonn-louRten la ' „ pr«-nl. see aloo^ _",".".'!'„" epilepsia media I (57.-.). RxlTrmitio and trunk remaii \»t.\ minutes, hours or days. Rilidily of the action (.Retracliun of ti« hud and opistholonos. flexion of elbows, supination of hands, extension of legs with pointing of loes. Other symptoms of cerebellar disease. tKf potiliun in which they may be plncnl for a surprisingly lona linie. Wax-like resistance to passive motion. Diflirult positions nialniM illiuln, abolition of reflexes, and more or less complete apparent loss of consciousness are usual symptoms. Other bysterieni sj-mplom'^ fii(v. meech monotonous, passive tremor of hands and less, ciharoctcristlc altitude, festinnling gait. Tendency to full backwards or forv ndefinitely without apparent effort. The attack may ifien present, (451). See also epidemic encephalitis continue*), to escape altogether miiteleK of (he faee usually escape altogether. Marki4 h' IV Tiiarki'it hjTHTlmpby, nosely allied to this dlM'ast i« "| insure In ciitd with eonsefluent reflex vaso-molur spo"^ anl ■ailed acfiiiircd form, "myotonia aei]uisila,'" is prolmhlj iv\ n firtt (ii«vi-ni.-nt rifti-p n ri-xt or when action Is done faster. I'atie-it cannot hurry or eJtccute rapid movements. Is liable to li ilitv Mil iii.ii. I ii-.-trical reaction (400). Increasml mechnn'til excitability of muBclc. even slight prowure with tbe finger-tin MIC iMn. I iij -iiiti" fKulenhere's disease) also on an hceditary basis (it has attacked twenty-eight members of a family tiiiiiiiii' iii-iiii!.. cs in Ihe muscles. A myotonia congenita •niermillens and a myotonia congenita atrophica have been d^se iilhiji'tli. ]' ililli-ii'iit disca-ie. :■ possible Ms (077). See also Encephalitis letliargiea (1047). enuiljbrium The arms are le«ui alTi-clnl Ihan Ihe leu'i and ■aui--. a idii&gish, long eontinutsl contractinn. Muscle fiber> in •ix gcneralionsK hut these paroxy3iuil altaeks follow iheil with the rtiantclerislii-s implied in Iheir names, The of opistholonoH (205), Periods of intcrniission with relaxed muscles lasting several minutes. Cutaneous and tendon fnnvulftions, mental defect and partial arrest of BTowth. are common. The contracture and motor paralysis may be unilateral n reflexes increased, bilateral. History or evidence of ttrychni Tetanus (172). Tetanus tmumalicui. Tetani rheuinalictis. Tetanus puerpetnliii, Telani ui'onatorum. Rabies, Ilytropbohia. I.yssa (173). llematorrhaclils (52.1. 07.^1. Lesion of cerebellar hemispheres, Cerubellar fits fiMT, fi8fi, 7P3-*, lOlfi, I2nfi). Le.'^ion of vermis of c>>rcbellijm. Cerebellar fit- {Ml. GSfi. 78.1-4, lOlfi. 12iK). Catalepsy (10(18). Paral^is Aftiinns. Parkinson's disease (20-1. U77. 709. 804). Myntnnia Congenita. Thom»en*» dii>catp (li)il. 2iki. Ilfi71. including Pammyolonin Congenita (Culenberg's diseaae). Spavm mainly con- Rilaternl painful Ionic spasm of muscles of hands and someUinet of feel, latrtinp minules. hours, or rarely days. Hands and fc I drawn inlo smallest voUime possible with hollow deepened (obilptrical hand). Joints of arrat flexed, those of legs extended, fined In bands and Inereaserl mechanical (Trouweau's phenomenon— 140) ana olfelricnl (Erb's sign— 142) excitability of nerves. Facial nerve *i'py irrilable: so that slight blows on it cause spasm of facial miiBi).* (Chvostek's sign — 141), Usually associated with feet, paroxyomal. rii'keiii or dfcrsiite iliwrder^ and intestinal paniHle*. or dlln'oil stomach: often foMows extirpation of panilhyroid glands. Sometimes occurs as a symptom of hydrocephalua. cerebral tumor or other serious brain dispaw in rbildren. It oecure in iafi-ctiouB diseases, in poisoning and in pregnancy and u u occupation neiiniHis (rtlG). This disenae is probably due esi-ntially to destruction of the parathyroid glands nnd may perhaps be cured hy the administration of theHC glands, fienenil painful clonic, followed by tonic. Spasm very general and very painful, malolj in the fonn ■'"'""'• pnisoning. Death usimtly results iq a couple of hours. Renerai permanent eoalrnclnre. Paralj-sis Is coincident with Ihe contnctore. Spnim only oocurg Oeeurs usually in small muscles and in those that have b«n overworhed or improperly worked in doing tbe same act many times. The spa»m is often painhit. and In some eases pain may he the only 8>-mptom (neuralgic form). The spasm Is of I performing graduat onset steadily Rrons worse, and renders tbe apcuUoin*d net diflicult or impo<«ible. It occurs only when the muscles are used. In some eases there is tivmor. in others Incoorijinalion ami in rare eases, paralptis or paresis (paralytic forml le necui>tomMl rather than spasm. Atrophy of the muscles involveil is Gmnmoi. I'atientH are usually neuratthenlc. Many varieties; writer's, telegrapher's, pianist's, violinist's, seamstrees', shoemaker's, etc.. cramp. A shnilar neuiwis occneionally affects the Toice of sineers, public speakers, elc. Telrtny (121. fil.1). sirychninp <(invul5i*.ns (.11.1, S'lO). Ralhi-r brief itpasm A spu*m lasting min urethral spasmodii Im or hours, due to loco! irrllatioD inaeunuibeni( sirlelurr, vesical spasm, lenesmus. etc. S(e also pa III Funclio Tonic spasm, le'Kl. a lirrHixli'Dt A spasm of varying intensity attacking an arm, or leg. orbelti.Tiu permanent A eontmeture of a few or many muscl.si usunllv associaltd with i efforts are miidi- lo o\errome It. No muaele atrophy. Attlm»s i (1174) or may ennsisl in jumping or skipping (sjiltotorr gpumi I (rrfl.0). wkwanlnesB and often preve Many \ idles. Hlepharospiism. loriicollis. spasmodic croup, laryngismus stridulu>rtii'al irrilation spasm (lKt2). Hyslericat contracture (107*1). Posthemiplegic e<.n Irs. ■lure i:m. :. loabilitf to tlaad inlk. Mnre or complete. IVH tin of all II nyonmic alaxi (2S0). nnllnt^rnl, (UcmiBtaxia.) I'ritla(-nl. Illnmial/iiln.) Irrejoilar distrlbiitlnD. I Oemirj at any age. usually Id adults. ' I'liially wnwry BIAGNOSTIC ANALYSIS OP SYMPTOMS ABSTRACT OK SYMPTOMS Patient exhibits the itasgering, irn-inilar gall of a drunlteii man. I.illle ntaxia of niov*mpnt« of hands, or of leea when Ijlng down. Vertigo, vomitini; and heodafiit; nre often present, nystai^us may lip iitesent (tumorel. Knee-jerlis may be presni or nl>*?nt (uion. cnnilguous iracta may niso b" io'ralveil in n*ich cane thrrr \ «en«nry symptning in the arms iind legs and diHlurbancra in the domain of thi- irsninl nerves, miially unilateral, nnd laryioE in character according lo the gent of the lesion. Choked disc or side ns It^ion). >nnn1 pemnn and rill hr motor and No loss of miisrle »i-n«e. No motor , pHro1y«i«, except is late iitat.'V of 050-1, Sinegerinc enti, constantly or psroxj«- j Diplopia mally. Hendsrhe. verlico and vomiting J at limes. No cbokrf disc. Knee-jerks 1 hejifne^h other diBorders of hiBhl. Vertigo ceases when eyes are eloied. il rini;ina in nm- ear. Pniv>ty*nml iiltscks of mtenBC vertigo and defect in l>"nf Occurs in youth. I No lenury aymp- 1 loma. Many seiuory symptoms. Oft'n nnalee»ia and thermic aneatbena. liriiTi ID family groups and ^hows well marked her^'dnv though leit pronounced. A general, conree. irregii'or ii Blstimus is common and speech often defective. Synpicn nr, limulitling jerky choreiform mwementB. Ny- !iri'ient n mixture of weohness and ataxia. rOcciir* after 1 Occurs befor '■ UKDnlly pn puberty. Knee-jerks present. Oculnr parn'j -i' before pDberty. Kneejerkig absent, except i iHy present, Opiic slroi>hy rare. Club-foot cc . of ptipil reftes nnd opti p and m exceptional ca- st ropby >. Babinehi ICvidently organ tc. l^e<> can be mov<^l nisily in nil directions without ataxia wh Simulatea an nprnxia I2:n) rather th»n nn nlnxia. Often May or niny not be motor parnlysi lia while walking. 'ul il lying down, but collapite when tihe tries to walk, or after nalk.ng a few stept. nppnrrnlly from lack of confidence emiilicnal cause and hjDlerical vrap'<>''>3 (415) are present. Both leA are inrolwd. Never hurts herielf Eerlously. of same side with iifialgesta and iher Lou of muscle Nense and §pniiory symptom R umnlly prominent. Knee- jerk imually 1d- When of acule course the condition uiu- ally folloivs an apoplectic attack. Often arlerial dispane is preaeni, When of chmnic cour*e chok'd disc may be present. ■Mnrked uneslhcain wilhoiit analgetiin. No motor [laralysiH. No other symptoms. .Apoplectiform atinck followed by hemiplegia {Keiinory ofti-mr than motor). Other where the motor paraly^iis wa* slight. itesthesia of conlrulatcrnl side. One leg only involved. Very rare. May be the earliest stage of a -ipjnal tiini poBt-hemiple^ic motor disturbance? are often iiresi-nt. reflex will power. No ataxia when moving leg while lying ir. Unilalpral later becoming bilateral. The ataxin ofcnrs iu convulrseence in i Knei'-jerkn normal. No ankte'Clonu*. History of alt'i>liuli>>n There are often niHxiii nnd K nrlhriu and paralysis of v; i^igns of cortical irrilalion (' il and foolish speech. Hli Ala Rincgerated knee- iprh«, nnUeclontis nnd nnblnnki. Knee jerki nnd aii- kl^.-lonu« alwenl. No Rnhinski. Oftm loK» nf munele nenie and retardnlion of roniliiclion of pnin. ireal vari"ly of local «j-mploms. I'sunllv Imih motor and rnumory Nyinptoms. Irregular, jerk.v, alax inientton tremor, scanning upeeeli. nj^lagmu*. espeptnlly on motion of eyeball, nnd ittropliy of op Rarely llie diseuee runs an acute coiira- and has bem called "acule ataxia," of which therp are 18 tiie presence of symptoms only explicablr on the n^umption of Ihe exiateuce of levernl. se[mr if iiMiscle setiRe on one side of body nnd analgesia and Ibcrmii: IS cranial nerves arc UHually present, iilkiuus). Anestbe«ia, cupecinlly loss of muscle sense. Is oflet ;in and other symiilotii's. Temporary ti-emor. mcnl! m^y be crossed parulysi* III me mental disturbance. if both arm« and legs, and movements are !■ nerve. In some ernes huHmr paral.vsis (434* is aneai 'v?r:il varieties (662). In its early stages the diacnoK e. small lesions. I of this discnse i r.ittle \ rombinalion of symptoms of locomotor ataiin (tWl) nnd spastic parnple.-in fH'-in) in veryin:; t'i"l'"i''i usually lost before any nnewtheHia can be deleeleil. In later slnces arms may he somewhat involied. .V riir.- disc jerks may be ahclished towards the end of the disease, but Babinehi persists. This disiase iniiy be caused by pi r nn pnin. WenknesK, slilfness, ninxia, pare^theii ncensionally some involvement of cranial nerves ions and other severe anemiias. I Slight motor iiaraljsU i* present, Miisflen lender and atrophic. Pnin* rardy ' normal. Cranial nerves rnrely Invulved. Usually sensory sj-mptnnis, UbiiiiII I never so chronic as tabes. No globniin or b-mpbm-yiosiN in crrebro-splnal fliii -„„-,,„ I, .J , . rHl«tory of taking dnie«, alcohol, mor- The alaxi .npjerks usually exnirgerated hut no I phine. ver^nnl. cocaine, heroin, etc nnd exc itnbiDski or ankle-clonus. Evidently 1 functional (pseudo-alaxia). 1 Dmorionnl cause. ry severe and partial re.i history of nicohniie nbii" Prognosis is good. of degenenition and retardation of cnndueilon of pi Ii'iitnl dii^turlinnccs in many cases. Ocen«ionnlly the ■iflei leil with tremor and neurasthenic symptom?. Failure ted with c 'Til? ntnxia may appear only when eyes are closed nnd is usually usually collapse on reactiiug a place of anfety. signs of mental impairment. Patients nr^ emotional tcrir-nl symptoms (415) tin pre-sent. Rarely fall, but T^-eaion of ccri'bellum or ita tractsi: if acute in onset, apoplexy: if chronic, tumor, or inllammalion. inoT-'i. ci.-.;j, ftso. Tft4. i>iw. utm. I2fl5i. Ocular ataxia or verticw (1020). .Marl>''s biTpditary cerebellar ataxia (iMH), l'il\. rri'-dnich's Piecise. Ilrredilary Ataxia (104. 124, G71). (187, 705. 7S2). Astoula and Abasia (2S7. 7IW). l.esion of Infernl column of i^iniil cord, ir dircfl cerebellar tract (017. l.'|tin-73. 1100 (f-'ie.. 24-7.) onn em (iri2 IK3 LeHnn of i.'".lerior niluuin of cord (780, I3»]0;t-4. 140H), (KigH. 24-71. Posl-liemiplcaie ataxia (h-siun in or near posterior part of opilc thalamus— 1208. 13981. (Fig. 17). .'Softening, heiuorrhasc nr tumor In brain stem C^M. et. si.i„ S.T.i. T.-ilO-T). (I''!iP>. 10-22). •Softenina or tumor of conlmlateral iiurietal cortex (I30S-75. 1:«12). (Fig, IG). Alcibollo intoxication (lltS. 101-2. {iST., 003. 1173, 1 vpaslic and al.ixic. Very characlcrlHiie are I- often einotinmil and exhihil mental weaknes. exeeed!u;;ly difficult. The most essi'utlnl point le and anesthesia of legs. Vibration sense (50. 353) is Orgnnie reflexes slightly, or not nt all, disordered. Knee- tarely any perninncnl motor paralysis: hut hypnlonln (2.">2). allowing hypcfe.x tension nnd extreme mobility of joints, is common, and tempomry paralysee In thr domain of the crania] nerves fcspecinlly the muscles of eyeball) are not lux-cnimon eiirly symptoms. MovemenlH nre atoxic, ipiick, violent, excess tve and constantly conlrolled by eyesight. The nffeclefl pans ennnoi lie held motionle** in onn position lone. In wnlklnc. legs nre held well ntmri and feel are (luue loo far outwani and too far forwani nnd are brought back hard on heel. Ataxin niiich worse when eyes at* closed. Walking in thr dark or luickwnrds is usunll.v impossible. Romberg's symptom (4:tS). Argyll Unberlson phenomenon (437), luyosis, nnd optic alniphy with concentric liniilation of fii-ld of vision are common. Lighlnin? pains .»f great intensity in tnial! .in-as followed by h.nieralgr*in. girdle senitalioiis and paresllnsiae ar- prominent sympl.mis. (Irgaiiie n>(lpxes, espe<'ially Ihe vesical, nre disordered, Artliropathies (1188) or perforating ulcer or o'lier trophic disonlers may h.- present. Ani'slbesin and nnalgesia in patches and in cuirass, ulnar hypere«t1iesia. Retardation of conduction of pain. Visceral crises (O^^Tl are tinuatly presenl. Townnls the end of the diaease motor pnrnlyiiis may appear. lymphocytosis and globulin In cerebro-spinal (luld. The discnsc is unmetime* dividiil Into tlir.-i. WjiRrs-dst), the neuralgic; (2nd), th" ataxic; (3nn, the paralytic slage. History or other evidences of syphilis or of venepenl disease is iwLiolly present. Positive Wflsirermann also usually prenenl. There are several forms of tnbps. In the cerehrnl form, atrophy of ihe oplie nerve is the prominent symptom nnd the legs show little atnxln. In cervinil tabes the arms are mainly alfeel-d, In the orrlinnry fonn the legs ,irc mainly afftH'iefl, In all forms the knee-jerk, are nb-senl. Babi(i>tki i< present in rnrc cnses. compllcnle.1 hy lat.-rnl sclerosis. In miny case« ef tabes the ataxia is slight and the diniinoslh musi n-sl mainly on the obwnee of the knee-jerk, the Arcyll-Roherlson phenomenon and the ceiebro-»piunl Ijinphocytosis. together with wbatcMT other syiniitom* may bo present. JU*'ioitiati-d Sclirosis. Myelitis Diswminala. Kncephaloin.i-eIlti« (Ml. 5S0, Ot«l, ttSS. 750-68. ^m. 1)14, 1054). Uaxic Paruplegia. rombinnl Sclerosis (:.2tl. TP9). (Fign. 24-«). .ni-i>ni< lor Ataxia. Tnlic« Dopsiilis (i:tj, 1T:i. 123 T.TH. 7«. 820-71-00. fll2-7I)-8S, ItMM, 1172W1. 1217-31). (Figs. 24-6). Mullipli- Neuritis. I'ol.vrn-iinlH. I'si'iido-labes (KV 7SD. s.2ii. niOS. 1117. I.'t27>. r»rug habit (toxic) (482. 058. 707-81). Ilyslerieal Alaila (1070). CHART Xllb Tremor, Nystagmus, Fibrillation Comprising Numbers 639 to 647 on left side of Chart and 666 to 697 on right margin 153 DIAGNOSTIC SYMPTOMS AND TESTS InUDtloo TrMDor (281). tremor; 4 to S jit or is iHiisDy nssiicinK^ ivllh sojmniiiB spre^li. n.vMafmu^. atropliy "f opt nllv a Brmit »*nrii'ty of motnr in'l sensory symptoms iliie to mnni inlly wirh tlieir loss, over a vory vnrinble area. The sensory •jmpl< n symprrtm. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OP SYMPTOMS nene nnd ataxia. Reflexes are ii«unlty exnggersted and ankif-i-lnniis nnd Bnl>in«ki are present. In some caees the deep rellcii-s are early abolished and Ih^ orsanic reflexM dUordered. ns. alihniish all the^e mny hp nbannl. The mntor symptfim^ nirntnente ;ia fntigtie. slowly becoming paresis, rarely paralysis, nrd are u^uiilly as*oeini*«l wirh pjnggerated refleies. ocea- usually in tlie form of paresthesiae, more rnrelj pain followed by Irregular patches of anesthesia. Epileptiform or apiplei'iili>rm atincks tollowod by transitory paralyale are commoo. Oi^cur? in family groups, but Is neithri hereditary nor eoneenital. Occurs in family groups and shows tc^II mnrlcKd heredity. Slarserin;: gaii. Ataxin. NyBiagmns is speech oftno defective. OcTur^ ID yoiirm ppnon?. athptosh. nnd prngresn auiopiiy there is found Tri^noi I nuncinlrd with general wenknt fFine, rapid tremor; S to 12 per aecood. Pawiive Trpnior. I ] iDcreAMM) on rol- J imtiiry motion and | excitement (200). i ^lophtbnltnii:. mnllj- wh*n eo'iitp. tiirhyrardla, vasi-ulnr Ihrobtiing, fluKhing. »npniin'i. ifltient look* dOTt'award (nraete's srmploml. The ^.-^ijiro i nilaleral. rhythmionl tremor, whlcli increjses on voluntary movements. There are, also, djsnrlhria. dyspliasia. mmcular w-ahm'^v «pn»llelty and controoturee. Mpecinlly facial Kriraace* and ,c pmBointion. Thr refleies, superfleini and deep, are normal. The patient is emotional, present* various mental eymploms. a pro?rt-i«ive dementia ind the disease has a fatal termination. .\l the 1 bilateral symuietrioal degenerRtion of the putnmcn and trlobus pntlidus of the nucleus lenticularis. Another lesion, constantly found, is hepntic cirrhosis, which produi^s no symptoms during life. nd exceptional case*. Babinski i» present. Optic atrophy rare. Clnb-foot common. Rfliely sensory sj-mptom: an- prcent. evidence of any organic disease of the nen-ous syntem. Bxhausl4on or holding a limb in n ntraineil position Cnr a long lime cauic* tremor. '^fcilement. polyuria and at limes albuminuria, insomnia and vorli;:o are common symptoms. Tbc upper lid does not fall nor- Oecur after puberty. Ko''' jerks are present. Ocula r paralysis, los« of pi Orrur before puberty. Kii'e jerks arc ah=ent except in early atage or in ra s or K onvalpscnce from nn acute disease. Anemia •> usually present, but rliarriioea, much nrrvniisne's, tremor rspecinlty marked . of tb- porcncbymotouv variety and noed not be large. Ili*tory of ndiicllon to alcohol or liruc*. Mental symptoms are common. arratly at different times, Preiience of hysterical symptoms (4151. Tremor is w-jrwe when ailpotion i Tremor i* m.irk«l tn fncp. lips and touEue : n r^umhnr puncture shows a lymphocytosis and globuli and judgment impair 1 it. Irn>eulnr tremoi I and Hppprh blurred Evidenc"' of great rxh Pati. i and emolinnal. Pupils ictcd i opium <: Qninqunnd'* 'rign (4."iSl in alcoholic cnwv Symptor •, Proures'tivi' mcnbil impairment. Reslless and chlldiiih. W,i5*ern>ann reiction usually positive. Arcyll-Roberlsr ijstem. Often history of slight injury assoeialpd i and letters. Apopli-cliforr Snecrti is slurreti by elision of nyllnbli phenomenon is present. ilb fright, or. more commonly, of tri),'ht alone. and epilpplifonn attacks may oivitr. History of nyphilis Slow tremor of hand and fool of same side. iated with oculo-moir>r pnrn nt tlic oppcsite side. Other sj-mptoi «of a G4(ta Passive Tremor. Diminiibed on vol- untary motion (290). Eithi^T Inlentinn or Always a symptom of organic disease. Very rarely, an hyjiterlcBl clonic ■pasm may aimu late true nyitag- mue (pseudo-nys- tagmus). This ia often vertical and is more rapid and more violent than ny«ta([mu« nod is na5ociateitlioul any tremor fpntiil.'miH asitans ing Inter. Voluntory movoments arc slew, much rcilrfctcd and feehte, but arc never comnlplely paralyned. t entirely hplples^. Marked symptoms of parn agitni :^'iir. not infrciiiicrilly in Encephalitis l.cth- r begins tii late rally. Head is early affected, Nodding movem Slow, coarrie 1 tremor. I'ossive Tremor. f Rotatory or J volved. 1 I A series of . noddin: tremor of head occurrine suddpnly in rickety babies The tremor ceases when the child's eyes are closed. I Iht risidity. Rf eral weakness, .\thpi ' and passing off in ll mntous artorles summer time. Usually accompanied by n.vstagmi jerky treraoni limited to the back, or Involving all ninscle^. enused by cold (physiological) or Infection (pathological) onrl resulting in an inr Not ■eociated with other symptoms. Hereditary basis (a1cohoIi high (evf Impnirment of sight Vertigo is a promt- I Dent symptom, I Coarse, jerky tre- mor is a prominent I symptom. .\taxla J is also present. lent' lal aitflcks of rertico a«sociated with deafness and tinnitus aurium and due to disease of inner ear. Ny or cali-aniKcd. or ear syrinced. or labyrinth In any way irritated. The caloric reaction (70) is absent. Tihlynpia. nyitagmus. tics a ection from the lahiTinth i volved oceun iiilTy when head is rotated vlo- Vertigo, cerebellar alsiin and other sj-mpioms of diniease of the cerehelluin. The nystagmus is ustially towards the side of the lesion. [Occnra In early .vouth. Strong hpredltj'. Knee-jerks nbsent. except in early stage, Rahloski Is present. Optic atrophy rare Muscular vreaknere and contractures are not uncommon Occurs at any age. No heredity Intention tremor. Eiagjiemted knee-jerk, Babinski. optic atrophy and scnnnine speech are common symptoms. Vertiso Is ii5unlly present (0321, r,rfical paralyses common, Orynirs In mi-ninsiris and in local lesions (tumors eapeeially). Nystagmus U commonly present in bulbar lenions, especially in those involving the ccrwbellflr peduncles and tracts and the posterior longitudinal bundle. to be confounded with the deep bowing fSataam crampl which occurs in some idiots and enilepties, with or without Th* nyataemus is most marked when the child's head Is held still and the tremor prei'ented (flTD). nystagmus, RoUiD! of the head may occur In otitis media and in rickety chtldr-n. or more of the recti VIHRII.T.AIIV c-n TR,\(TTION OR PIHUn.I>,\TION Kvidence of orcnnic dUease. DcEenera- atr. I li'm nf peripheral ruli 1 motor opuront. Marked miiscul ly with mi weakness, I. Congenital, Nystagmus ( Marked sensory sjTnptoms, T.a eral oscillating nystagmus associated with jerking movements of the limbs or trunk. osBravatiHl by cold and by percussion. Associated with other ■alescencc frcm ocul.ir palsies or when weakened muscles are stronaly exerted. li'tocw. Bvidence o! func- No muscular atro- tional, not organic, phy or weflkness. .Analgesia and thermic anestheela witti m .Mii« those of multiple sclerosis, but (be ir^oior presents a tnily oscillatory character and there is no real ataxia. Emotional and maniacal attacka may occur and, less c-'mnionl.v. mental confiisiun and hallucinations. Many of the cases r'scmhl' closely, if they are not idenliiml with, dystrophia leotieular**. The lesions iu lhi,s disease vary greatly in the different caies which have been examined after death. In some cases there is utronhy of the cprcbral convolutions, in others degeneration of the Isniicnlttr nucleus and very commonly htions of the glia cells. 'roiire^.iie I,pnticiilar Degeaerntlon. Wilson's Di»i'rt»e, Dystonia (.entlculnris is closely allied to the^e syndrom". Friedreich"* Hereditary Atasin. ir,.*,I. BS7. 7nr«. 7«il. .\sthenio Tnminr or weaknewi, (702). I'Uophthalmic (ioitrc. Rnsedow's (JmvW Disease. (HlB). llj^terinil or N' matic Npup.ist Paralytic liemi' nthenii- L'otlnc. mercury, and also Trau- 1071-71 ■nerat I'arcsis. riiresis. ii7.* (i:iri-77-vt(, .ion-12-a r.Tft. 7««, s!i7, lOfii'. iioti, 12H!, lUrtiJi. ■si >n of th" Criis (Vrchri or Pons Involving the Srf Rubro-'piii.il trwci. (ISl. 1203. 1341), (Figs. 18-30). 'anily*i» .\:itiinv Parkin. (ilKI, 7iM». WMl . IHse 077 Senile Tremor. ' Spasmus Nuttms. Nictilatio Spn»tica, (liWI. t Chills. Risoi^ Shlverine, • Essential Tremor. * Atnblyopla, (3.-i9). ' Albinism. ' Miner's Nystagmus. ' Meuitn-'* Disease, Aural vertlpi. Ijihyrlntliine I Vertigo. (040, ItlS. 1019). rerebellar Di«en*e. (fl07-?. fWO. 7&4, 1016. ISn,*)). i Friedreich** Hereditary Ataxia. (flBl. 170) i DiMeminnted Sclerosis, (086. 7ft lunkr e never acquired, or esrlr j !<■: buDce iDnerratioD memo "j ,, _ ,_ (or spcetb were never " aU'lit. noise but i-uuQOC apeak, .imnj to speak tbrough the j 1401)' looervutJoD inemories uecvssarj for apeccb bave been acquirml but are not available. No bysterical *ymploin». llyatericAl (ymjitouu aud enolo^ical fsctots l>r««eat, Altbougb not alwoya promioeDt. Complete absence of speech, and readiog altad ii impnssiblv. Pnticnt maKes do effort speak or lo coiumuuicate by ueature^. ion of face and actions are idiotic. iuD of face and notions ore normal. Abseiioe of facial expression and of ail volun UCtiOQB, exprension and BCtions are abnormal. Reading and writing after mucb traininf. Paiic&i L-xhibits littie or no intelligence and history shows that be never bad any. Incapable o( any but the moat elementary education, if of any. Soils himself with ucine and feces. PaticDt shon'8 a good intellieence, but can expreK himself only hy eeatures and tbat only aa ttaa result of careful training. Some deaf muteacao be taught to speak, eener&lly Tery imperfectly. ud j-Absenc to \ lary in a deep sleep and cannot be aroused to any expression of r intelligeoce by stimulation of any sensory surface. ilient is evidently insane and has delusions. When recovery has taken place it may be lenraed that bis silence was due to a delusion, usually either of fear or of a divine command (delusional insanity). Hysl si] appearance. Placid and ctntentcd. ■\naribria fl'robnbly only a severe form of hr«erical aphonia. It is a rare condition. [Ciin, by hard urging, be made to whisper some words faintly but distinctly I profound dementia. Idiocy. (10S3). Deaf MuQtdu. Coma. (205. 1037). Insanity, (1041). Apoplectic symi'tiimn \'ocftl orsauB defectlv Vocal organs nnnnol. Will neither wbiaper nor speak. Can whisper faintly but distinctly. j Mny mutter but cannot articulate distincQj; Sudden imsct, usually followed by speed.v death. Paralysis of motion or sensation or of both in the extremities. Loss of speech may be complete or patient ^yln- ublp to ssy one or two words distinctly. There may. or may not be, paralysis of motion, ot sensation, or of both in the eilremities. Wi>ids imperfectly formed, also a nusai voice. An exatfbltionof the vocal organs shows no paralysis, but a developmental d'->fe<'t : such its deft palate and «mitar malformation. U'urds imperfectly formed and usually a very limited nhbulsry- Intelliuence very defective. Paralysis, usually of the spaati'- variety, may be present in tbe extremides. Siilisiitution of one letter for another. An exnniinaiioa gt the vucal organs shows no defects or parnlyais. Patients exhibit a nither childish or affe<^ied form of 9ijee< iralysed cord. .ill tbe laryngeal muscles. Cada- reme abduction). In phonatlon, median line to reach the LinRuals cannot be clearly spoken. This dlGBoulty is usually temporary. Nasal voice. Liquids may regurgitate through nose. Nasal voice. Indistinct articulation, which ia improved when head is thrown backwards. Voice bourse. In swallowing, larynx is not well closed; so timt food enters it, causing cough, dyspnoea and possibly deglulitioQ pneumonia. Aplionia. weak cough and snoring breathing if bilateral. Weak, hoarse voice if unilateral. If bilateral the cords are ducktd together during inspiration, giving rise to a slight stridor. Other fuHal muscles are paralysed. May he evidence of injury or pressure upon bypoglossus netre. May follow dipbtberia. Liquids may regurgitate through note. May foHow dipbtberia. Paralysis of Poeial nerve. (708. ftSS. 1383). Paralysis of Hypoglossus nervf. (TOtf). Paralysis of Levator Palatl. Paral.vsjs of Superior Laryngeal N"er%'e. irl'^- The labials, the linptols or tbe vowel Ronndi or nil of them cannot he properly pro- nounred. A care- ful exnmlnntion r^- veJil* a parnlysli or n paresris within , the drimsin of tlie fncial. the hypo- Slo^ttl or tie pne ti m g a s t i c 1(1 111 MUf ur both vocal cords from paraiysi? ofcnoi >r cords lie near the median line (extreme nidation r ■mailer on Inspiration. of one or both vocal coi-ds from pnrnlysi -8t«rIcat Aphonia. (748), Tremor and Ataxia.- Tn-miilous rqi) slovenly «peech, words are badly formed, lellem and syllables are Evidfut left out both !d speaking and writing. '■-'■'L''"oti. Scanning speed). Monotonous speech, ■Ortntu letlere (con Ulternnce Is arrested by a spa-m of snit. lentat de- Spc-ch i I. re are aphonia or boari-uess niid nasal speech and some dysphagia. There may be respira- rMay he evidence of injury or of pressure upon pneumogastric nerve, tory dyspnoea ond deglutition imeumonia. If both nerv.s are slightly affected there may be rapid and irregular cardiac afiion and slow and irregular respiroiion ; if severely affected, •' [*ulbar symptoms (424) with hemiplegia or paniplegria and exaggerated tendon reflci death occurs. In pseudobulbar paralysis (546. 5531 the speech is also thick and indistinct ' In myastliinia gravis (554) dysarthria results from '-oolinueil speaking. foreign bodfhas ia the mouth (hot potato speech! (i-id fi«iuently changes in pitdi, lenomenon (ft"l- History of syphilis. Lui CbildWini* and steadily progressive demt of hereditary ataxia. In cerebellar lesiims. the spi'i>oh i» o(i>'n slow, labored aud irregular and pbonntion Is affected. ttacks mav ,.^o„; Oi,il,lld.n«» and ^t^-,a\U- r^r^^l ~ ■ ' a~ '~^f^ puncture show* globulin and lymphoeyioii.. Patients are restless and especially irriiahle and violent, iiHI.ougb usually amiable. .Apoplectiform aud epilei.iiform tracKs ma,\ nccui. (.iiil<]t>Jini)» ana sieadUy progressive dementia. Wii'sermann usually positive. Alcoholic history. .I'li'-ir.me:. trtfor nod breath. Temporary nature. r..olii.h speech and actions. Intention Tremor. Grent variety of widespread mol« and sensory -ymptoms. NysUgmus. e.ta^emted knee-jerk. Habinski. The speech is Jerky and -omewhat resembles the scanning of ver.e. Passive T«mor. Rigidity of mnsdes and slisl.t fle*n of most joints. Attit..de is tbat of bending fomatd. Mask-like face. Fes tina ting gait. Speedi aUo shows fe.tinatlon at times. See al*. Encephalitis Lethargies (1047). spoken with difficulty and are repeated many times imperfectly b*re they are finaUy utUred explosively. Speech U explosive and filll of repetition of certain sounds. that words can be uttered. The same is repeated several times hiT»r«- .) « .« .h. „;^ .J." ioiViVh^n' ei,',S«?r.",."n«l';nTitM""' " "*''"""^" <«"i'«'«»in-). Tbm i. i:m^,u, « „i..i„8 a, ™.cu .p.™ a be spoken. Thi^ more the attention Paralysis of Pneumognstric Nerve trunk, (7041. Bulbar Paralysis, {424. 544. 540. 60*. TW. IIM)- Frledreich's aud Marie's Hereditary Ataxia, (10424. (VW-l-fift-70-87. 7S2-3). _ ,„,^ _^, Paresis. (185. 180. 579, 676. 803, 1(W2. 1106. 1216. 1230) Alcoholism. (5K5. 058, 063. 673. 7S1. ftM. 7031. tfl.m MuS "ofo'Snated Sclerosis, (.-ill, 580, OT.il. CC6. ftW, 750. SOS. ni4. 10541. rnmlysis Agitans. (Bin. «,,. 904>. Stammering {Annrthrla Liternlis). (720). Siultpring (Anarthria Si,aimodicft or articulalive tics). (729). L CHART Xlllb Amnesia and Aphasia Comprising Numliers 739 on left side of Chart and 772 to 780 on right margin 169 TEST 739 AMNESIA AND (220 to 229). APHASIA XoiK! of these conditious con- stitiiles a disease, but is ralliiT one symptom of a more complex disease. Each is a form of dementia, or more accurately, amnesia in the l)road sense of the term and consists in a loss of general or special memories. See also .\narthria and Dysarthria (737-8). Ill I'xaininins patients for am- nesia or aphasia, it is most iiiipiirtant to first ascertain to what ilesree. if at all, they are deaf. DIAGNOSTIC ANAL-: AMNESIA. APHASI ABSTRACT O The loss of memory may not be accompanied by any, the names of persons is rather common and of no diaj less distant past, are referred by the memory to the in cerebral concussion and compression (1042-3), especia little time immediately previous to the injury and frig! Examination of the patient shows a loss of memory, espe in old people and in the insane, and is usually associat Patient is incapable of normal speech .. <-Ian express ideas by gestures, but cannot name objects \J Patient is capaule of normal speech but exhibits a decided loss of memory. (s[H)ntaneous, repeatius after dictation, reading aloud) for want of innervation memories of a few or many spoken words. Patient is incapable of normal speech for w.iiit of auditoi-y memories of spoken words. I'atient is incapable of normal speech for want of \'isual memories of objects. I'.itieut is incapable of normal speech for want of visual memories of written or printed words. Patient is incapable of normal speech, be- cause of a faulty co-operation of the various cortical centers concerned in speech. verbs better than nouns and proper names. IlecogniZi tieut is frequently at a loss for a word, llis vooabular phasia — 7TS) but is often conscious of his mistake if h matismus), but can often repeat sequences of numbe from copy, but makes many mistakes in spontaneous w with right-sided hemiplegia in right-handed persons and PatieL. fails to understand more or less of what is said what he repeats. Cannot execute verbal commands, bi; conscious of tliis mistake even when his attention is cal Patient cannot name objects seen, but may, at times, r^ aphasia has been classed under the complex term "moti; Patient cannot read written ov printed letters or words, use a wrong word and, wiien they do so, are conscious, many mistakes in spontaneous writing. I'atients cann. Patients suffering from this defect exhibit a combination i groups. First, those in which the symptoms of motor £ combination, incomplete, of the symptoms of motor an group (Transcortical motor aphasia) spontaneous sp( of the year, the alphabet, numerals, etc.) are little, if group (Transcortical sensory aphasia) there is more oi (days, mouths, etc.,) are possible; although these wore glee of both sensory and motor aphasia. Spontaneous three groups resemble those occurring in gradual recov impossible or defective. The patient omits words in sj so that the speech or writing, wueu po.ssible at all. oft Patient is incapable of spontaneous writing for want of simply cannot W'rite. A very rare condition uucoi left frontal convolution is iimuediately above the motor printed matter into script. His copying is purely mecl Patient omits words in writing, uses the wrong words, mi The .subject of aphasia, in its various forms and subdivisions, is a very complicated one and is, as yet, far from being solved. Too few Broca, in ISOl. published a case of motor aphasia with a lesion at the base of the left inferior frontal convolution and thereby laid t Wernicke (vvliose studies have contributed greatly to the comprehension of aphasia) divided motor and sensory aphasia into three sub- 1st. Cortical Motor Aphasia, in which the patient is unable to speak, write or read ahnid correctly, or to speak or write correctly 2nd. Subcortical Motor Aphasia, in which the patient can neither speak spontaneously nor from dictation nor read aloud correctly 3rd. Transcortical Motor Aphasia, in which the patient can neither speak nor write correctly, but CJin speak and write from diets 1st. Cortical Sensory Aphasia, in which the patient can speak (with paraphasia) and copy, but can neither write, nor speak, no 2nd. Sub-cortical Sensory Aphasia, in wdiich the patient can speak quite perfectly, write, copy, read aloud and understand writii 3rd. Transcortical Sensory Aphasia, in which the patient can speak (with parapliasia) and write (with paragraphia), can copy, Wernicke also recognizes a Conduction Aphasia, in which the patient can speak, write and read and undersUind correctly, but exhibit Marie considers all forms of aphasia as resulting from a greater or less degree of a general intellectual impairment i-ather than from lo aphasia wit:h didiculty of arlii'ulalion (anarthrin or dysarthria). Whether he is altogether riglil in this or not. certainly our conccpfir nicke's ideas, neither of which is pre bably altogether false. It is to be renieml>ered. however, that many cases of dejnentia, in all stages of acteristie. defects of one or more of the component parts of the complex phenomenon of speech. This strongly indicates a loss of some tion is, at the present day, too firmly proved to be easily abandoned. .\<;i:apiii\. Palicni's -pecch is imninil, Iiut his writing is abnormal. i OF SYMPTOMS LND AGRAPHIA lYMPTOMS 3y very little, iutelloutiuil imijaii-iuent iu other respects. To a certain degree the loss of memory of ;ic or prognostic value. "Retroactive amnesia"' is where events, which occurred in the more or iate past, as in Korsakoff's psychosis (1102). "Itetrograde amnesia" occurs in some cases of iiose associated with fright. In it, memory is lost of those events which occurred during some DIAGNOSIS .\mnesia. y for recent events, impaired judgment and a rith mental depresj^ion. ;eneral failure of mental powers. Very common Dcinentia (1079). 773 or at all. Patient knows the idea he wislies to express, but cannot put it into words, ('an u.se le desired woi-d when it is spoken to him and can often tlieu pronounce it. In speaking, the pa- limiti-d often to one or two words, or even to none (anarthria — 737). Uses a wrong word (para- ttentiou is called to it and often when it is not. Cannot construct sentences correctly (agram- lays, months, etc., and can sing songs. When his arm is not paralysed patient can usually write ig (paragraphia — TSti). Can usually read but not aloud. The condition is usually associated e-vei-sa. im. Cannot repeat what is said to him, or if in rare cases he can do this, he does not understand adily executes wricteu ones. In speaking, the patient frequently uses a wrong word and is not :o it. Can write spontaneously and from copy but not from dictation. He can read well. Moi.ir .Vphasia or Aiiheniia (222, 771 1402). Sensory Aphasia. Auditory Aphasia. Word Deafness (222-33, 13S2-82a). Visual or Optic Aphasia (224. 232, 13.57). Alexia. Word Blindness (220. 13S2a, 1403). 77(! Transcortical Aphasia. Mixeii 77S Aphasia (22f)1. Paraphasia (22(1). lize and name objects which he touches and feels. His defect in speech is not great. V'isual ihasia," of which it may form a not inconsiderable part. cannot execute written commands, but readily executes verbal ones. In speaking, patients rarely lieir mistakes. Patient can write from dictation imperfectly, but not at all from copy and makes lad what they have written. otor (774) and sensory (775-0-7) aphasia in varying degree and can be classified into three sia predominate. Second, those in which the symptoms of sensory aphasia predominate. Third, a nsory aphasia. A sharp line, however, cannot be drawn between these three groups. In the first is disturbed; buc repeating after dictation and reciting of serials (days of the week, the months .D, impaired. Cases in tliis group run rather a rapid course towards recovery. In the second 3 fully developed sensory aphasia and the repeating after dictation and the reciting of serials •e not understood when .spoken by themselves or others. In the third group there is some de- ech is very imperfect; while the reciting of serials is well preserved. The symptoms in all from pure motor or sensory aphasia- In all three groups reading aloud and writing are either ing or writing, or uses a wrong word (paraphasia), or puts a right word in a wrong place; lecomes quite incoherent (Jargon speech). necessary innervation memories. His arm and luuul are nut paralyzed for other movements. He cated by motor aphasia, because the cortical area tor writing being at the base of the second :ech center. A patient with agraphia may be able to copy print or script, but lie cannot copy cal. A patient may be able to write letters, sponlauoously. Ijut not words and sentences. up words in the sentences so that writing becomes incoherent. He can, however, write. les. scientifically observed, have come to autopsy. oundation, not only of the modern ideas about the faculty of speech, lint al.so of cerebral localization. sions each : n dictation, or to read with full understanding, but can copy correctly and understands what is said to him. t can read, write and undei-stand what is said to him. 1, can copy, can read aloud, and can understand speech and writing. ipy from dictation, nor read aloud perfwtly. nor understand speech or writing. lilt cannot speak or write from dictation, nor understand speech. e and speak from dictation, and read aloud but all without understanding, and cannot undei-stand either speech or writing iraphasia and paragraphia. •erebral lesions, especially not to those of the left inferior frontal convolution. He considei's motor aphasia to be a combination of sensory if aphasia previously to Marie's article had been growing too schema 'ic. The truth pi-obably lies somewhere between Marie's and Wer- ■oliipment. exhibit no aphasia. Furthermore, cases of aphasia arc rarijy permanently complete (anarthria), but show varying, even ehar- nent of a composite whole and each of these elements may, in time, be more certainly localized. The theory of a cerebral corticil localize- AL-nipliia (227. 13S!)). Paragraphia ("226). 770 7Sl) CHART XIIIc Disorders of Gait; Ataxic, Paralytic and Flaccid, Paralytic and Spastic Gaits Comprising Numbers 736 to 742 on left side of Chart and 781 to 804 on ri^ht margin (Note) — -In addition to tlie diseases mentioned in this chart, pain, whether in the joints (rheumatism, gout, arthritis, morbus coxae, etc.), or in the muscles (rheumatism myositis etc.), or in the bones (caries, etc.), or in the nerves (sciatica, etc.) will cause a limping gait. The gait of a patient suffering from weakened arches in the feet is very characteristic in advanced cases and this common disease should always be thought of in any disturbance of gait and in any painful affection of the legs or lower back. 171 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANAI DISOEDEE ABSTRACT ( cli-:onlor is (if a temporni'y nature. Pnlipnt's sprwh is liUuTeHi.) 742 Paralytic and spastic (Stiffness is the most prom- inent symptom.) 'There Is a strong heredity disease occurs in family groups ; in youtli. Nystagmus. No heredity. Uccui-s at any age. IncoonlinatMl Cait. (Stainpiic.; (iait.) Waddling Gait. I'alienI (lni>s ncit \\;ilk liki' a ilninken man. but Uirinvs his legs alxHit in ai anil excessive nianurr. .\ll movemeuis of logs are ataxic. In well markei are raised li'igh. Muug outwards and forwards excessively and brought ba< ground with hard st.-inip on heel. The eyes are employef alculiiilic ahuso. •Occurs before puberty. Knee-jorks usually ab^ieni. i 'niitraoture and ilerorruity nf fiT-r. liaKiuski \ present. Oef-urs after puberty but in yiiulb. Ivufe-jerks usually present aud exaggerated. Oculo-uioior paralysis and optic atrophy. KelraitiiiM nf ln-ail. eerebellar lits auatient pushi's himself up with his hands and crawls up upon his own legs. (A similar gait is ibdomnl ttimors.) rilateral but may be unilateral. Xo change in the muscles. Hip joints unusualy mobile. X-ray e of acetabulum. the walk. Muscular weakness, tenderness and atropliy. Knee-jerks absent. Many sensory 11 as foot-drop. History of colic and of exposure to lead. [liseular atrophy williout tenderness. Electrical reaction of degenreation. No sen.sory symptoms. .. Organic and peripheral relh'xi's normal. Xo sensory paralysis. Tipheral reflexes disordered (lost). Sensory paraly.sis. Patients, even with cniti-hes. ar.> rarely Loss of memory and mental impairment. Reflexes normal or increa.swl. Uy when lying or sitting. Patii'Ut apparently makes no effort to w.ilk. lycgs collapse. Ap- rgr"s side gait — 450) . ds and outwards alwut the normal leg as a pivnt and is set down in advance i>f lliis latter strongly extendiHl at the km-e and the whole sidi' of the body is i-igid and swings forward as a ling kitenilly) along a line the patient moves well towaiils the paralysed side, but badly to- ide gait l.">(;). Orgiinic reflexes are di.sordered, and si'usory symptoms are present, N'o ata.xia. Organic reflexes may or may not be disordered, sensm-y symptoms. e to forw.ird movements; I Marked ataxia, srs mtisl often be bent far I,egs freiiueutly show forward. Thighs are ad- together or even crossed ious, or some other form pVdult. Organic reflexes not disordered. No sensory J symptoms. No ataxia. 1 ' Youth. Siassiirs es {cm, 7.">0, 827, SiKi. f)7i), 7R5 OSS, 1004, 1217, 12S1). (Figs. 24-7). Ijesions of posterior columns of 7SG spinal cord ((VU. 1271. i:'.G0-?,-4. l-itim. (Figs. 24-G). .Muscular Dystrophies (477. Il."i4). 787 Congenital Di.slocat.ion of the 7SS Hip. Multiple Neuritis (4.SS, G02. '<2.">. 7.S9 lOOS. 1147, 1327). Lead Palsy (4!I4. .">S4, 10.",:!). 7!M) Aiaite Anterior Poliomyelitis 701 (40."'>, 1148, 12.'?:!). (Figs. 24-7). Weakness (G71 ) . 702 Myelitis or Myelomalacia in VO:! lumbar enlargement of ccu'il {4.S.J, S27, 1140, i:«OL Senile Paraplegia (.";22). 701 Astasia and .\basia (2S17. G,">2). 70." Hysterical Hemijilegia or Mono- 70ii plegia (.")27, 1070). Organic Hemiplegia nv Mono- 71)7 plegia. (Ai)oplexy. Cerebral or Spinal Tumor or .\bscess). M.yelitis or Myelomalacia above 70,'* lumbar enlargement. including Comiiression Mvelilis ( .''>i:i-4-7-20-o0, 8.31 ) . ( Figs. 24-7 ) . Ataxic Paraplegia 700 (."i2i;. G(50). (Figs. 24-7). Spastic Paraplegia (.">2."i), incliid- ,800 ing .'Amyotrophic Lateral Sclerosis (.547), Cerebral Diplegia 801 (478, 501, .577, 10.51). S.vringomyelia (5.53, G93, 840-2, 1000, 802 11.52, 1170, 1187, 1370-2), Disseminated or Multiple 803 Sclero.sis (oil, 580, C.59, G(!(!, 088. 7.59, 70.8, 914, 1054). Paralysis .Vgitans (Old, i;77. 7G0). 804 CHART XIV Disorders of Sensation DIAGNOSTIC ANALYSIS OF SYMPTOMS DISORDERS OF GENERAL SENSATION AND OF THE SPECIAL SENSES Symptom Analysed Alterations in Sensation r806 Diminution of Sensation. 807 Exaggeration of Sensation. 805 I>isorders of Sensation. (See also Perversion of Sensa- tion Chart XV). 808 Disturbances of Vision. 1^811 Anesthesia and Analgesia. 812 Dissociation of Sensation. 813 Loss of Muscle Sense. \ See Chart XIV a. 814 Numbness. 815 Hyperesthesia. 816 Perversion. 817 • See Chart XIV b. Limitation of field of vision, j 809 Disturbances of Hearing. 810 Disturbances of Taste and .Smell. 818 Double vision (Diplopia). ■ 819 Conjugate Deviation of Eyeballs. 820 Pupillary Abnormalities. 821 Ophthalmoscopic Exami- nation. 822 Deafness (anakusia). 823 Hyperakusia (oxyakoia'l or 1^ Parakusia. • See Chart XIV c. i^ See Chart XIV d. ■ See Chart XIV e. 173 CHART XlVa Disorders of Sensation Comprising Numbers 806 to 814 on left side of Chart and 824 to 844 on right margin V" .J 175 S06 DIMINrTIONOP CDTANICdllS 8ENSIBII,ITY (130). IJIAUNOSTIC SYMPTOMS AND TESTS Ml ANIOSTHKKTA usiinlly com- liiiipd Willi »onii- ANAI,CJB8IA niirl THRRMIO ANIWTllIfl- KIA. nup^i^Inllr tn •ovi-ri' wmpm of the diiensc {Si&-50). (Vis». 26, S3). 'IVudon ri'llrntfl diumialicd nliM'iil (Ii-«ioa of peripheral, leusory neurons — 472). I (Irk'niiio relicsea inonnnl (300). 1 (Pigs. 24-0). The nnMlhexin or Ira pn>ii-8arthria and dysphngin. fo ml>^•^ pnrnly^a, nnesclioaia limited lo anal and ssenital re^iion and vicinity. Occuiionalty dissociation of sensation nceuis. poiener. Reilexex In lens normal. Incontini-niv nf uri Assoaati'd witli or symptoms. Organic reHexc'S usually norm III. very rarely dinor- derrf (300). bilateral mid s|int). bntli of periphe i-cnti-nl Bcniiory n il and of tlightly urons. (300). I pains. hyiH'ralgeBla. dioreir und othetnid movements and nta^i'i in one . with •*r'a«tii' piiralyKis in lens. Bladder lliiecid pavalysiB and mnaoulnr nlrojihy I dribbling. Constipation, Pupils ari' i iii'niit hitcrni half of the body, /-Symptoms bilnli 'Syniptonii* nwiinl ud ft I jMii'eslheNiae in arms SeoliORia and kypho)i nd hands arc prominent symptoms, i in neck and upper dorsid ri'glon. MoMr wcabnens and lr.>nior of nnns. Spastic symptoms In lees. Organic : Nei DIAGNOSIS (1^1, W2. !)41. ll-lin. I17a. 1321-71. .Multiplu Neurilii. (4SS, m'i. TSO, 1008, 1147, 1327). (.eaion of I'oitterior Nerve Root or of Spiuiil Se?menl (laa'i). Myelitis or Myelomalacia in I.iiuibur Enlnrgrmcut (485, "US. 1320), Tumor in Lumbar Kiilann-meut (4S0. 1320). Tubes, Locomotor Aiairia ('Htl. 7.'>0. 7.'<5. MIH. 0711. '.»W, 1004. 1217. 1231). Myelitis or Myelomalacia In Upper Oervical Resion (513-1). Myelitis ur Myelomalacia in Dor^l Ri>^iou (fll7-5). I.esloo In Brain Stem (535, iViOl. lesion of conns tcmiinalia of Spinal Cord. <-eivbml MeniOiiilU (.".0,S. ."00. (ItlT.. UKW. IIM.-.. tlHtS-lt. l^'i*'.)!. (Vr.>l.nil ll.'iii.in-liii^e i.i- S..tt.'nlu«: (.^4, 5S>*. MIO-I. HV);{, limLi;). Cerebr.il Tuaior {iW7. fiSO-JS. TiI9, .1S7. M2-n. (IT,, *«2, flOS, Wll. ir>riO). ■^yinpt.ao!- iisimlly unilii(er.il, .\iie.«tlie'iin usually in form of tiemianesChesia. which may be ti-nnsferri-ii in wnie msii. Anesthesia often diarply boundei] by a prominent anatiiniiciil bmdmark (knco, hip, dhow, etc.) and not by nerve or root dtstributlun. The niiesthi-siii i* ununlly unknown to the patient ami Li discovered upon physical examination, but when discovered is usually more (.i>mplete tluin that present in ctise^ of organic diaeuBe. The anesthesia is not rivil. The putieut tan button clothes, write, etc.. with anesthetic hands without looking. No evidence of any oreanic di'wise. Aneslhesin is from Buegcstlon. II ,»n-»llu-»ia Dolorosa {I,eHii ( Opiic Thalnaius) (ia«). .Myelitis or Myelonuilacin in Ceivinil Kularavuiejit (VA laVM. r»m..riu iVrvical Ki.l,ir=eraent (T.:.'2. V.m\. Muscular ati«ftexes u!-vtlM"iilics. till with fltnjla and anesthesia. It ociiiw hi mullipli' neuritis, tabes, and in I'-sIons of posterior culvimim of spinal cord, of bniin stem, of posterior third of iwsterior limb of internal capsule and ■ much 90 thnt "dioked tliap" and other symptoms of cerebral liminr should be Boufht for in mich cnses- CTiostie mine, ivilli the esee|ition of the jipoe of hyperealhcsin. limiting iihnvc rhe iine*ibesin in iniuBierwo ni.v.liiis or m.v*vrinKomyclia in I.umhar I3DlarBi>o*leii..r. Cerehrilar Artery {1200-1). r.i-.iwn-Se(|iiard PniTilyBia (MV2. ."Hi!!, lisijt. (|--ii:>.. :;4r.l. of the parietal cortex. Unilateral mimbneiw at band nnd toot. Meadlly proCTCHsive. with slowly progrinii Biltitenil nuiubness ig of no diacnxtttic importnncr. It may he either of nervJii* CHART XlVb Disturbances of Vision Comprising Numbers 808, 816, 817 on left side ot Chart and 845 to 871 on right margin Blindness may be caused by a solitary lesion in the eye, or optic nerve, or optic chiasm Heniianopia may be due to a lesion of the optic tract, or geniculate bodies, or fasiculus of Gratiolet, or of the carcarine fissure region on the median surface of the occipital lobe. The cortical center of sight is the cortex of the occipital lobe. The fibers of the optic nerve having their origin in the lower left quadrant of the retinal of both eyes finally terminate in the lower margin of the calcarine fissures of the left occipital lobe (Fige. 16 and 37), and tlie fibers from the upper left quadrant of the retinal of both eyes terminate in the upper margin of the calcarine fissure of the left occipital lobe ; and the same relationship exists between the fibers from the right side of the retinal of both eyes and the calcerine area of the right occipital lobe. The central fibers of the optic nerve having their origin from the small area of clear vision may possibly terminate in, or near, the geniculate bodies, but more probably pass in the fasiculus of Gratiolet to the occipital lobe and terminate either in the floor of the calcerine fissure or more widely in the occipital cortex. 177 DIAGNOSTIC SYMPTOMS DIAGNOSTIC AN. DISTURBANI ABSTRACT < A yellow color of all objects seen irrespective of tlicir true color: xanthopsia (ye A red color (erythropsia) of all objects seen irrespective of their true color (rerl v I SOS DISTURBANCES - (IF VISION. PERVRRSION. SI 7 AliSKNCE OR I.IMITATION (IK KIKI.n OF VISION (35S to 3(>2-3). A green color of all objrcis seen irrespective of tJK'ir true color (green vision). Muscae volitaiiti'.s. twisted threails and irregular s|)ots moving aliout in field of v Flashes nf liulit and ilark sim.Is siirn.unded by a briglit zone (glittering scotoniatji Achromatopsia (;j('>4) and lieniicln'omatopsia occur in slight lesions of the geniculal |.llysterical syniiitoms (41.'")) are presei .Vn inversion (red having a larger field than the blue — 14) and an interlacing T flioked e. fOcidar lesions, such as cataract, optii (Jninine. in t'lyic doses, may cause inl dilnlalinn td' tlic pupil. In either Ilil.iteral. Nr lesinti in eye. Pupillary reflexes r No lesicin in eye. Optic neuribis ma; Unilateral 1 Nfp Irsimi in rye. No optic neuritis. I max be slu>\vn Hint the blindness is Xii hemiiiiiir |)n|)illary rellrx. No he Homonymous Tcl.arlanopi.a ov (.Quadrant cir oilier paralysis. May or may n( 1 lemiamiiMa. disc. Very rarely occmrs in lesions ( i>r optic fasciculus of opposite side. 'No lii'iiil.-ini'sllii'sia. Nn heniiopic pu] (2(!). No uili Homonymous heininnopi.T (14. 3(i2, 1:137) may very rarely be bilateral, due I.I doiilib' lesion. Ileniiaiiesthesin. May or may not be a hemiplegia. [)ui)illar.v reMe.v. Paralysis of moi abducens nerve or butli. Bitemporal hemianopia (3(i2, 1.3.3.")). r j Slow onset, progressive coi;rse, tcrmina in complete blindness. Clioke<] disc, pupi]|;ii\v iM'fiex. Occurs in lesions of tJie retina, or of IMiesc may occur as (lie result of sma neig'liborhooased tension of On opi eyeball. Il.vsterical symiitiinis (41.")) are prese .Symptoms of l.'ilics are present, especi or no alaxia. History of Syphilis. Nasal li.inian.ipin (302, 13.30). Horizontal hernia nopin. llninonymous scotomnta. Concentric limitation of field of vision. even to complete blindness. {SIS OF SYMPTOMS i OF VISION SYMPTOMS I vision ) . I'). I. Sci'ii rs.|icciiill.v when eyi's aro (iiriipil towanls a bi-ij;lit lislit. iiiMiiily .ippoariiii;' iiud clisippearini; in tlic field of visimi. iilii's. ,il' tlio optic fii^ciciiliis and especially of llie calcariiic riortex. disease are present. The color field becomes normal after the in- d. (Cushins.) uritis, retinitis. srlaciCTmia. etc., may cause blindness. ? spasm of the retinal arteries. Belladonna may cause extreme blindness, or semi-blindness, may resnlt. mal. Uri'mic aniiiiirosis may be in this class (edema). present. I'upiUary reflexes absent. pillary ri tlexes normal. Hysterical symptoms. By tests (12) it real. DIAGNOSIS Jaundice, or Santonin. Amyl Nitrite. Cannabis S45 Indica or Picric Acid Poisoning. Xeiirasthenia, Hysteria, great emotional excitement S4() and after cataract operations; also after the eye has been exposed for a long time to an electric or oUier bright light (snownblindness). Diseases of optic nerve and retina and after eata- S47 ract operations. N(Mirastheuia, circulatoi-y distnrban<'es in brain and 848 digestive disturbances. Migraine and Aura of Epilepsy and circulatory 849 disturbances in brain (575, S.5S. 1028-61). Acliromatopsia (364). 850 Hysteria (lOTfi). 851 Cerebral Tumor (830). 852 Ocular lesions. 852a Drugs. S52b Lesion or edema of both occipital lobes. 853 Cesion of optic nerve or cliiasni (^!I4). 854 Hysterical .Vniblyopia. 855 nesthesia rl^pper homonymous cpiadraiit of ear-h fielil of vision. p choked -' >tic tract I Lower homonynnms (juadvani of each field of vision. T.esion of lower lip of contralateral calcarin" fissure. 856 r.esion of upper lip of contralateral calcarine fissure. 857 |- Sudden onset and of short duration. Often more marked in, or limited to, one eye. No other s.vmp- I toms except nervousness. Oireiilntory disturbances. ry reflex -| Clinked disc. Slow onset. Pivigressive course of tlie aralysis. ; disease. I No clmked disc. Rapid onset. Pennanent, not pro- t gressive, or rarely shows a regressive course. .\o hemiopic pupillary n-IIex. .N'o choked disc. Re- gressive coui"se. Aura of migraine. 858 lemiopic oculi or usually lemiopic iChoki'd disc. Slow onset. Progressive No choked disc. Rapid onset. S.vmptoms of menin- gitis may be present. ^r.ilal,.ral. T'nilateral. Tumor involving median surface of contralateral K'lll occipital lobe cjr fasciculus c]f (Jraliolel (i:{78). Hemorrhage or softening in or near contralateral c-;il- 8611 canine fissure or optic fasciculus of Gratiolet (1378). Hemorrhage or softening in the posterior part of SiCI posterior limb of confalateral internal capsule. Tumor involving contralateral optic tract or genie- 802 ulate bodies (S9o, 1337). NcHiritis or lesion of contralateral optic tract (895, St!,'? 1337) Tumor compressing central part of optic chiasm 801 (894, 13.35). (Enlargeil and unequal, of disc. moscopic I'xamiuation the optic papilla shows atrophy. Glaucoma (944). Optic .itrophy (S9S). Pfl8 80!) H.vsleria (1070). Argyll-Rorbertson phenomenon anr uueqiial ijupils (339-41). AliXORMALITY OF I'UI'IL. S90 The hemiopic pupilliiry re- flex (■?). (30). S91 The Argyll- RolltMiSOIl , phi'linllirlioll t-l;l7 Bitemporal homianopia (362, 1335). 1 liii.iciiymcus ln'iniauopia (•W'2. 13;'.7i. Histoi-y of syphilis. I.yiiiiilnnyli.sis in (■iTt'biM-spinal Uuid. I'lisitivi' VVasscrmann. Tii'linitis. No markpd symp- toms of cerebral disoase. DIAGNOSTIC ANAL' PUPILLARY ABNORMALITIES ANI ABSTRACT () These phenomena occur in too mauj Their significance has been discussi Choked disc. Symptoms progressive, Often hemiplegia or paralysis of era history of syphilis. Very rarely ii (Ataxia. Absence of knee-jerk. Light Mental impairment. Blurred speech. Rarely occurs. Xo ataxia. Knee-jerks Albumeai and casts in urine. Sugar in urine and in blood. Lead in urine. Examination of the blood shows a condition of severe anemia. Urine and blood normal. 821 ABNORMALITY OP PAPILLA. Disfovered by Ophthalmoscopic Examination. S02 0|>tif neuritis. Clioked disc. 893 Opiie .-ilvopliy. Bilateral. No retinitis. Marked cerebral symptoms, espec- ially headacie. Well marked history of traumatism ii paral.vsis. Increased size of head and fontanelle be increased in size, the pressure Retraction of head. Cerebro-spinal General convnlsiou or Jacksonian epi lepsy is common. May be loca paralysis. Reflexes usually in creased. Cenliellar. but no motor ataxia. Ce Unilateral. Local inllnMiiiinli(iii can usually bt discovered by examining the e.ve and or ("Secondary. Bilateral. Unilateral. It may be the terminal stage of a neuritis and hence f Traces of the active inflammation (old hemorrhages : Old age. Usually atheromatous arteries and high arte Loss of knee-jerk. Miosis. Lightning pains. Bladder UneqimI pupils. Impairment of speech. Tremor. Men ( Characteristic tremor or other s.ymptoms of this di.seasc Local indniuuinliim or lesion can usually be discovered on careful examinati Primary. No signs of a former in- flammation. OF SYMPTOMS 'TIC NEURITIS AND ATROPHY lYMPTOMS itions to be of umcli diagnostic importauce. Chart Vb. ninating in blindness. Often associated with acromegaly. Tumor compressing 1335-G). DIAGNOSIS ihe optic cliiasm (So-i. S(>4-">, nerves. Optic neuritis or symptoms of meningitis. At times a ant hemianopia in partial lesions of the geniculate bodies. pains. GirJle sensation and tabetic cuirass. raxia. Restlessness. Childishness. Uncontrollable. sent. May be no mental impairment. Normal speech. No apraxia. Headaches, especially in morning. Usually edema o£ some part of Brlght's Disease, body. Dyspnoea on exertion and loss of strength. Lesion of coutoalateral optic tract or geniculate bodies (W)2-3, 1337). Tabes (611, 829, 912). Paresis (913, llOfi). Syphilis (1205). (Kgs. 24-7). Great thiret and Diabetes llellitus (1174). ['rogressive emaciation and loss of strength, polyuria. Large appetite. Dry skin. Blue line on gums. History of lead colic. Wrist-drop. History Lead Poisuiiing (4'.i4. of exposure to lead poison. 10.")o). Dyspnoea on exertion and progressive weakness. Pallor of skin Anemia or LouUimia. and mucous membranes. 7<;, TiSl, 71(;. 7!M). 989, History of syphilis. Argyll-Robertson pupillary reflex. LymphO' cytosis in cerebro-spinal fluid. Positive Wassermann. Syphilis (1205). ich the nerve has been injured. Usually complicated with facial Injury. 894 895 896 897 898 899 900 901 902 903 9(H d sutures open in the young. In adults, in whom the skull cannot Ilydrocppbnlns (901). reater and tlie optic neuritis and headache are more intense. nphocytosia. Fever. May or may not be fever. At times a latent period. Primary supp\iratiou of bones of skull or elsewhere. Optic neuritis pres- ent in abimt 53% of cases. No fever. Usually steady progression. Optic neuritis present in about 80% of all cases ; almost invariably present in tumors in the posterior fossa and in those associated with internal hydro- cephalus. Tumors in pituitary gland, corpus callosum and in the central convolutions, especially extra-cerebral tumore, often show no optic neuritis. ;llar fits. Meningitis (.-*0. 005). Cerebral .Misress or Sinus TbrrnnUosis (.508). <^M■^llr;l] T'lmmr f."07. 7S). Cerebellai- Tumor or Abscess (fi07-S-53-S0, 784. 1016, 1295). 905 906 907 90S 909 iw any of the causes of neuritis mentioned above, exudates, etc.) can usually be seen. ten-iion. iturbance. impairment. Restlessness. Unreasonsbleness. OhiUlisihi'.ess. n usually be discovered on careful examination. Terminal stage of Optic Neuritis (S09). Senile Optic .\tropby. Tabes (829). (Figs. 24-7). Paresis (1100). Disseminated Sclerosis (000). Disease of the eyeball or orbit (IS-SS). 910 911 912 913 914 915 CHART XlVe Abnormalities of Hearing, Taste, and Smell DIAGNOSTIC ANALYSIS OF SYMPTOMS Diagnostic Symptoms and Tests 809 D I S R D E R S ' F H E A R I N G 822 D E A P N E S S A N A K U S I A (355) I. Usually unilat- eral. May be bilat- eral. A perma- nent symp- tom. Bone tion' f^"^ im- P^.*"^- paired.y^'^- Abstract of Symptoms 'Severe paroxysmal vertigo and I tinnitus aurium. I No vertigo. May be heredity. Locomotor ataxia or dissemi- l,nated sclerosis may be present. Diagnosis Meniere's or 918 Labyrinth disease (649, 685, 1019). Atrophy of aud- 919 itory nerve. Bone May be i May be history of syploilis, con- asso- | symptoms of meningitis, symjj- toms of tumor at base, optic neuritis, etc. due- tion not ciated with facial im- paral- paired. ysis. Tumor or inflam- mation involving auditory nerve trunk. I Disease of, or injury to, middle Lesion of ear. i^or outer ear; cerumen- 920 921 Usually bilateral. Very rarely unilateral, and then only a transitory symptom. r Associated with symptoms of lesion of the I fKjns or crura cerebri. Associated with symptoms of lesion of the cerebral cortex. Complete deafness does not always occur in a bilateral lesion of the temporal cortex. Bilateral lesion 922 of the lemniscus. (Fig. 20). Hysterical symptoms (415). No symptoms of organic disease. Lesion of the temporal cortex on both sides. (Fig. 15). Hysterical deaf- ness (1076). Deafness may be caused by lesions in the ear or auditory nerve or by bilateral lesions in the brain stem. There is reason to believe that the cortical center (or area) for hearing is in the anterior transverse tecporal convolution which is situ- ated in the percular (upper) surfaec of the superior temporal. Innervation may bilateral. WORDS ONLY. Sensory aphasia (223) is present. 923 924 924a 823 HYPERA- KUSIA, OXYAKOIA OR PARA- KUSIA (372, 389). 810 DISORDERS OF SMELL AND TASTE f Hysterical symptoms are present. Inflammatory lesions of ear or its neighborhood are present. Facial paralysis is present. Low notes are especially painful. Tinnitus aurium is present. Very little, if any, diagnostic significance can be attached to disturbances of smell and taste. The cortical area for .smell seems to be in the comu Ammonis; while that for taste is probably slightly posterior and ex- ternal to the olfactory area; but no case has been re- corded where loss of taste or smell has been proved to be due to anv cortical lesion. Lesion of transverse temporal convolution Lesion of left 925 superior temporal convolution. (Fig. 15). Hysteria (1076). 926 Hyperemia of 927 inner ear. Facial paralvsis 928 (1333). 181 CHART XV Perversion of Sensation: Pain and Vertigo DIAGNOSTIC ANALYSIS OF SYMPTOMS DISORDERS OF SENSATION— PERVERSION Symptoms Analysed r931 PAIN (374). 930 PERVERSION OF SENSATION IN NERVOUS DISEASES (347). Location of Pain r933 PAIN IN NERVE Pain limited to the trunk and branches of one nerve in any part of the body, except that at the height of the attack, there may be a mild radiation of the pain into corresponding nerve of opposite side or into adjacent nerves. 934 PAIN IN HEAD. HEADACHES IN NERVOUS DISEASE After a careful examination with suitable instru- ments has proved the absence of glaucoma, jiritis, muscular insufficiencies and i other diseases of the eye, of the nose and its sinuses, of the teeth, of the ear, of the scalp (rheuma- tism) or of the crjmial bones (periostitis, caries). 935 PAIN IN TRUNK IN NERVOUS DISEASE After a careful examination has proved the ab- sence of Pott's disease, rheumatism of spine or trunk muscles, arthritis, disease of breast, peri- carditis, pleurisy, aneurism, pleurodynia, peri- ostitis, cancer and other tumors, colic (intes- tinal, uterine, biliary, renal) dyspepsia, pan- creatitis, appendicitis, peritonitis, gastric ulcer, gastritis, enteritis, hernia, floating kidney, tubal pregnancy, pelvic inflammation, intestinal obstruction, etc. 936 PAIN IN EXTREMITIES IN NERVOUS DISEASE After a careful examination has proved the ab- sence of any disease of the bones, muscles, joints, blood vessels or skin of the arms and legs. Flat foot must Iw excluded. See Chart XV a. 932 VERTIGO L(392). See Chart XV b. See Chart XV c. See Chart XV d. 185 CHART XVa Pain in Nerve, Pain in the Head, Headache Comprising Numbers 933 to 934 on the left side of margin and 937 to 968 on the right margin 187 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANAITSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS Tl. iJjiTrnnlml diamnsie be- incoii ni'iirilis aiul upuralgriii I'flDnut nitvays be mnile clio- )call7. l%e itiapiMis is Mf\ by the experience Ihat certain oervM. such s« llie sdatic. neuritis; ( the Ul- lore prone to I. 33. 3St. A history uf herrfilj' or other evi- dence of n neuro- palhic preriiniioaitioD. ronton iliil nr nc- iIuIrMl. iB ciimoion. Pflin \s unilnlcral and is iDcri'ANvl bj move- ment tind by eipo- Mirc to colli or wind nnil [a S'lmctimes niwnciDled nilti mus- di' ■rpRnm. Vmi- mnior nml irapbic dUriirliiini'i"< nrv ofteo prpwnt Poin. uoctumal. Moall area ai •pressing. Pnin loalixcd in l<]vii1eiio; at polMODlng. SIny ill- i'omt vnso-motnr '"" "o tropliitr ilistiirbnncc. excppt rnrely a bIow blancbing ot tlic hail. Ne?er Jiny oliH-lricnl reaction of deecncration. Patient naually anemie Certain points on Hip ncrie are usuollj tender Vpoinls of Valletx). Freqiii-ntly the parts supplied by Hie nerve are hyperestlietie Neimilgia (llfi. ]71l. ami local spasms occur. The neuralgia may be only one aymplora ot a more gcaenil duiease (aymptomatic neuralgia) or tndepeod- ent ot any oth'ir rtisrnse (idiopntbie neuralcia). ConlimiouR pain i eiacerbatioDB. Pain limited t« the whole or a portion of Che trunb and dia- trihutioa of the trige- minal (prosopalgia) or occipital nerves. Dl»- cases ot the eye, the nose and Its sinnae*, the teetli, the ear, the scalp and tbc bonea must first be excluded. (For the dlagnosia bctn'eea neuritis and neuralgia see 933). Pain strictly limited to one lateral halt of the head. Pain as if atU -were bdi driven tbroiifli the skull. History or other evi- Pair dencc of Bjrpbilis (not always obtainable). May be boll vnso-motor and trophic j tender! disturbanO'a and there may also be i the electifcal reaction ot degenera-i lioo. Geieral health usually good. Nerve whi !A tumor may Ix; felt or rarely seen witJt X-ray on nerve, A tumor or n displaced Iwnc or other Bubataiices may be felt or aeon with X-ray oear. and corapressii liash or herpes lin)itf1). Compresiion Neuritis. IliTpeliu G.intfHonii is or Neuritis (H1-3-5-5I -8-06-88-94. 078. 1188. 1235). —V Neuritis (489. 4itt. 834). Radiculitis. at the supra-orbitfll notch. The eyeball may he pnlnfal and TIic pain is felt below the eye in the cheek and sidi- of nose and radiates into the teeth The pain Is felt in the lower jaw and ita teeth and gums and in the aide ot toneue, in the ci The pain is felt in two or three of the eltnationa described above. The pain is momentary in duration and is associntofl with a dtmii', or a series of clonic, spasi if the upper jaw. The tender point is at the infra-orbital foramen. lie car and in the temporal rogion. The tender points are at the me s felt in the occipital region running up aloni one side .it the scalp to liie verli'x. T*be neck Is stiff. T^c tender points an' bi'liind lln' innitoid luvci arly sjinplcm in neurasthenia and nerrmis break riown. In many eases the pain is dull and is a sense of strong prc'isure raiher than poin. , behind the middle of the sterno-deido-maEtoid muscle and on the parietal eminence. This is i Infra-orbital Neuralgia or Neuritis. Infra -maxillary Nenralgla or Neuritis. Trigeminal Neunlds or Nearltis. Tic DouIour«us (fiOO). Ocdpllal Neuralgia or Neuritis. reriodicnl attacks (often occurring at menstrual cpixA) ot sevre i-i crania nngio-paralyticn) or pallor, coldness and dilated impils (Ik ilolor or sensory aphasia may be present in the attsek. as well a age and often shows a direct inheritance, "Symptonuitic" miiia Pain of great intensity in a smalt spot anywhere ou acalp ivith the feelini; as it a nail was being driven tbrouifh the akull at tins point. 'Die region is tender. Hysterical symptoms (■115) mre present. I'ain may be felt at any time but is worse in evening oi night, quent. Cranium is often tender at points. Pain may 'be due ir oenirs only at night, or in the early morning hou>«. It follows no nene distrlbulioa but is felt over a amall area and extends overa wider and wider circle. Argyll- Robertaon phenomenon Is fre- o periostitis. Lumbar puncture may show lymphooytorfs or positive Wnssermnnn. Optic neuritis may be present. bend or body. Exogenetlc. Autn-genelic. (Cerebral byiirren; Cerebral anemia. n,-adnohi Frontal headache may be due to gastric dyspepsia and constipatian, ns well as to disease of the eye or caries of teeth. Occipital headache and temporal heaitacbe may be due to disease to pelvic disease. These referred pains are associatvl with hypiTnlceRin of skin ot same region, which may be as constant and imnort^int vvmiilnms nv is the pain. The pain of eye howevin-. should not be nttacheil to those referred psins in diniotisis. ("Occurs after the ingestion of narcotics. Does not conw on Itnmeiliatcly. often not (ill the next day. lOccuTB as the result of breathing for hours foul air in UDveotllatod ronms. especially if patient is accustomed to pure air. Transitory. rOceurs as Uie result of constipation, espi^cinlly where the bowels usually net freely, Tliis headache is usually most marked in the frontal re;;ion. t Occun in Bri):ht*s disease, usually is worse when patient lirst v Urine Is usually scanty and contains albumen and ea^^t^. Kdcnm and gastric dint irbances n Headache with fulness and throbViiug In hood, acimivated by cough. The congestion may bo active (after takinfr amyl nitrite) or pas* may be followed hy o i^erehral hemorrhage, nendni^iM occnrrinj; at the lime of puberty "r of menstruntion may well he eonjrestive. ! (heart diseasel. Vertigo and vomiting may he present. High arterial tensim iften associated with albuminuria and occasionally with i-asts. Headache, most co posture. In this monly at vertex, with fnintintt, Dsrkness befcire eyes, fold hands and feet. Cardiac or arterial disease present, A series of such headaches may be followed by i as in other forms of headache, aevsrtl etiological fncinrs may be present. iiri'-p issoctateil with phobias and tremors and inKomnIn i williiu the akull, eapeHally preasore in oi-cipital t mptomi of neurasthenia. Pain grows less t"ward« evcnini; and is iisimlly felt In the occiput or vertex. Feeling a region. Headaches resulting from ov er strain (merilJil or physiral. espwlnlly eye strain) may well be of this nntur it a tishi band i ■crehral thrombosis. The re upon the head {cawiue Evidence of serious brain disease. Hesd- nehe often associated with vomiting, or ver- tigo, or both. Chronic headache. Pain constant with cxBcerbatlons. Evid'^nce of infection. Optic nenntu chofeed disc. or IProcressive nymploms, motor or sensory or both, first of irritation. Inter of pantljTiis. In ease of abscess there may he n latent period and. in llie a over the seat of the lesion. Lumbar puneliire shows greatly In<'ren>red pressure of cerehro -spinal fluid. Surfi headaches can be relieved by "ic Orebellar, without motor, ataxia Is present. Vertiiro. Cerebellar tits. ■ver, Heailanhe v "dectimpression." . is iirton present. TiiiiiituK ;iuiiiiTn, A serie« -if surti headaches hnndadic may be relieved by the recumbent neumsthcnlque). Ofti'n a sense of fulness and nir.' .■a*es the vikiill nia.v lie lenili-r ..n pi-r.-.i^ion Intractable, incurable, more or less constant headachw. No cause or stretching of the dura mater by tumor, hydrocepholus. etc. Evidence of rheuma- tism elsewhere. DilTuse pain and tenderness of scalp. Pnin rTemporatj. Occurs during the first few days or But I Pennanent, lie n-sisned. r may be pru movement of fronto-oecipital muscle. Hay he e other eereheal '■ No ..pii<- 1 rili-.. I,u vill I lally vho- Evidence of exposure to hiRh temperntu llI«torr of exposure i Relieved often by nppHcatlon of warmth. At times siuat 'k of almost any (ever (typhoid). Ruah headaches may he du" lo the a.-ti Occurs throughout t*e disease and Is associated with muscle spasm and paralysis and local edema of tlie scalp (sinus Suppuration elsewhere In head er body. Latent stage. Convulsions and coma, high temperature. Headache otten folIowc-1 by coma and convulsions. li'iiiler nodules can he fell, and hence the eondition has been ca I of the toxic sulistanec dir-'"tly upon the brain or Indirecll.v irombosiH). Coma. Lumbar puncture will show tymphocytui nnphocytdsii!. ,\popTeetic attach'* may lied "indurative headnehe." by niiislne vnao-pBralylic congestion lis and globulin in cerebro-spinal tluld. Trigeminal 9Vi Neuralgia iomeiimes on one side, sometimes on the other side of the craniiun. Skin Is very hyperalgcsic and vaso-motor disluihancea, either in the form of flushing, sweating and contracted pupils (heml- -ania aniiio-spasticn) are often present. Often ushered in by vlsunl hallucinations in the form of flashes of light, speetrn. etc., or by paralytic phenomena, such ns hemlanopia. and sootomata. insitory local paralyses, especially in the domain of the cranial nerve.«. TowbrI* the end of the attack there are vomiting and nausea. The disease usually commences in early life, ceases in old is not intre<|uent in tabes, paresis, brain tumor and epilepsy. Migraine or Hctnlcranla. Idiopathic and symptomatic (8in, )=FvS. 1020), of the eye, ICPlh. pharynx or ear. Vertex headache may be due to anemia or trail) iirowsworse mwards evening, or follows reading. Too much importance. Ciavus, Hysteria (lOTfi). Syphilitic Neurnlgin (meningitis). Referred Pains nr Rymplomatie Neurnlria (374). AlcDhelic or Mini>hine Ilendndie. Foul Air Headache, Constipation Headache. Uremic Hsadache. Congestive and High Teusion Headache. Anemic Headache, Neurasthenic Headadie (IflTll. rerebral Tumor, or Abv.-pwi, or Hydrocephal (HOT. 1506,967). r.T-lv-llar Tumi.r (Il«l!H , PachymeBinptls and (^ir..nic Meningitis (588, S90). Rheumatism of Scalp. Infectious or Toxic Hendaelie. .Icute Uenlnptis and Sinns l^romhoals (590,] Cerebral AbsceM (961). Sunstroke (G8». 1070). CHART XVb Pain in Trunk Comprising Numbers 935 on left side of Chart and 970 to 991 on right margin 189 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANALYSIS PAIN IN TRU: ABSTRACT 01- SYJ f Evidence of rPain and tender- r l'liubi;is aud nervous oxiuiuslion, paiu and sense of pressure most marked neurotic tempera- ment. No evidence of organic disease. Pain in back." 935 PAIN IN TRUNK IN NIi;RVOUS DISEASES. Pain in thorax and abdomen. uess of spinousJ processes. [Hysterical symptoms (llfi). Much tenderness of spinous processes, espei Pain and tender- Severe pain in coccyx witliout evidence of any disease of it. Pain iucreas .ness of coccyx. Evidence of organic disease. Pain, tender- May follow ness and traumatism. rigidity of spine. Vertebral ciilumn is ankylosed. Unilateral. bysterical symptoms (415) are present. Severe and constant piiin in back and radiating about body and into extrcm -Mucb spasm of spinal muscles. Exag-gerated reflexes. Little or no para and if any, it is of a transitory nature. Hyperesthesia and hyperalgesia Slowly increasing motor and sensory symptoms, irritative and paralytic iugeal, when paralytic symptoms are more prominent, the tumor is in th( more girdle pain aud pain radiating into extremities than in meningitis It may be possible to feel exostoses on vertebrae. Unilateral or bilateri lesions in other parts of the body. X-ray examination makes the c Girdle pain (374). No other symp- toms. Many other symp- toms. Bilateral usually. - No other symp- toms. .\t first unilateral and later bilateral. In mammary gland. Hysterical symp- toms. Dhl age. disease. .Arterial In prccordia and- arm. .\ny age. No arter- ial disease. Pain shoots around chest, following the course of an i costal nerve, Or may be limited to a small area o nene : pleurisy, pericarditis, pneumonia, pleurod periostitis, etc.. having been excluded by a careft amination. Loss of knee-jerk. Argyll-Robertson phenomi-non. syphilitic infection. There is a zone of hyi)erosthesia where the girdle pa may be severe. History of other evidence of syphilis. Lumbar pui Slowly increasing motor and sensory symptoms, at fii Paroxysmal attacks of pain in one mammary gland, gland can be detected. Pain is usually in the left Paroxysmal attacks of pain in precordia shooting u in sternal regicm. of suffocation and impending de Pain similar to the above, but no arterial disease, gestion, tobacco, overwork, etc. Not infre^ Neuralgia o. Neuritis of Ulnar, 00. at base of neck and in axilla, and a ce'ical tti^^^ o-^^in^ oltl^S: ' ''"' ''"""""'' '" "" '"^t"'^>'«- 99(i a of the sciatic nerve. Little, if any, anesthesia or motor paral- Sei-itici (T^O) affected side semi-flexed, thigh slightly abducted, inclines his ' ' ' " '" -ender points over the sciatic notuh (gluteal point), above the Ileal point). In neuritis, the nerve, wherever felt, is tender, i-ialica is mueh more frequently a ueiiritis than a neuralgia. A always be made. The tendo Aebillis reflex is often abolished the anterio. surface of the thigh and inner surface of leg to the fnirnl Neuralgia or Neuritis .v.- ■ ot knee and at internal malleolu.s. Extensors of thigh may be '^'ni.u^m oi i>Lunti.s. .).), anterior surface of thigh and inner side of leg in neuritis. May herpes along the course of the nerve. hernia and other diseases have been excluded. A rare form of Obturator Neuralgia. 99S 999 1003 1003a t'""l ^ Probab./ always associated with, and is caused by, Meral»ia Paresthetica pic of this disease than is the pain, which is often entirely '''"°^'' ^ iiestnetica. I Us much more sensitive than Uie articular surface. No evi- Arthralgia „r Hysterical .Tuint. 1000 May follow gonorrhea, malaria, gout, broken arches or injury. AchiUodyuia. lOQ] e cases are cured by anti-rheumatic medicine, others by sur- Talalgia or Calcanodvnii irMV> upporting the weakened arches. laiai^ia oi Laicanofiynia. 1002 lly following an injury. Usually occurs in women. The joint Mela tarsalgia or Morton's Too. •hidrosis and vaso-motor disturbances. Usually caused by Causalgia or Thermalgia. ry of syphilis usually, always loss of knee-jerk, cerebro-spinal Tabes Neur.iKic sta-e (a^^) 1lv^A 1 and deep, often followed by hyperalgesia over same area. -XemaUic sta^e ((,(,]). 1004 'nu^rj!'^'^'''' ^,° Argyll-Robertson's phenomenon. I.eu- Spinal Meningitis (GOT., !)74, 120,-!^) lOOT the cord is secondarily compressed or involved "paraplegia teral, later bilateral. Increased pressure of cerebro-spinal Spinal Tumor (509. 82S, 839-44, 97.5). 1006 eases the domain of the anterior crural nerves. Abolition of Lesions of Cauda Equina (487) (Fig 29 ) 1007 b.inces. Anesthesia in perineum and genitals and much pain (rig. „i.i jihi, and extending towards body. Muscular weakness, atrophy Multiple Neuritis (488) inos lesiae in toes and fingers and often with fever. -^euu^s ^*^^,). lOOS • anesthesia. Trophic disturbances and mutilations. These Syringomyelia (553 093 840-" 115" 1170 11S7 1000 r,'ia in legs. The pains often resemble the pains of tabes, 1370-2) er with pallor, shrinking and wrinkling of the same parts. Erythromelalgia (1198). 10l5 n: so that fingers and toes become purplish and even bl.-ick. Kaynaud's Disease (1195). 1011 .ages ':lrL:lZ':7:rJ'r '^ ™"^"''^''^'^"- ""■" "-^«""- -^"'P-- D°'— Dercum-s Disease (1175). 1012 CHART XVd Vertigo Comprising Numbers 932 on left side of Cliart and 1015 to 1034 on right margin 193 DIAGNOSTIC SYMPTOMS AND TESTS Motor Ataxia is present. Cerebellar Ataxia is present 932 B T I G O (392) Crossed Paralysis. Vertiao on niovoincnt of lieaj. Di'afiHss .iiiil syni|il(iiiis nf aural diseasp. l>iliN>lii:i niKl symptoms of ocular disease. Position and nujving^ Symptoms of cir- culatory or digest- ive disturbances. I'xliaustion. Digestive dis- orders. Cardiac and hemic disease. .Vtlieromatous arteries. High blood tension. Aiir)plexy. Rpilepsy. Migraine. Toxic. Symptoms of cerebral disease (headache, etc.). Organic. Functional. DIAGNOSTIC ANALYSIS OF DISORDERS OF SENSATION; PERV] ABSTRACT OF SYMPl In tlicse cases the vertigo is not a prominent symptom. In some cases, iu consc' of falling and fears that he will fall and experiences some vertigo ; while in oth lesions in the brain stem and elsewhere. The diagnosis is made from the pres Any disease of the cerebellum, especially tumors, may cause vertigo, which is m of the hemispheres. The diagnosis is made from the absence of paralysis, the and, in tumors, the optic neuritis and failure of sight. Lesions of tlie brain stem may involve the tracts from the cerebellum and cause made by the motor or sensory paralysis or both, which occurs in the form of 1 paralysis in the domain of the cranial nerves (crossed paralysis, etc.). (B'igs. Cysts and tumors suspended free in the fourth ventricle cause intense dizziness t drome). Except for this symptom the diagnosis is e-xtromely difficult or impossi the position in which the head is held. Choked disc is common. .\ steadily, progressive deafness of one car associated with tinnitus in that ear, a may throw patient to the ground. Kaisiug the head from the ground may cau: or loss of bone conduction and loss of power of hearing high notes are usually the paro.\ysmal attacks. Suppurative and other diseases of the ear may be p when the ear is completely deaf, but then may commence in the other ear. Alt may cause vertigo by affecting the semi-circular canals or vestibular nerve dii laesa). It is difficult to draw the line between these cases of aural vertigo cover all these conditions. Strictly speaking Meniere's disease apiilies only to a Uammation of the labyrinth causing vertigo is called Voltoni's disease. D.Hible vision and weakness of ocular muscles and eye strain may cause vertigo. IS relieved by closing the defective eye, even when it is not caused by the dip! When patient's head is bent down for a long time and then is suddenly raised, ' enees vertigo. A blow on the head will cause vertigo, probably in consequeuci of back of head or moving head quickly may cause vertigo. A similar vertigf rent to the head. Great weakness, especially in the convalescence from disease, is a common cause When, iu cousefjuence of the congestion due to digestive disorders, the portal ciiN aie anemic. These digestive disorders may also produce abnormal chemical s diagnosis is made by the presence of the digestive disorder and by the cure of In all forms of cardiac disease the brain may receive an insullicient and irregular : frequent in aortic disease. The diagnosis is made from the presence of cardiac to the altered quality than quantity of the blood supply (1030). Atheromatous arteries interfere with the normal blood supply both as to amount cause vertigo. This is especially common in elderly people. The diagnosis is m; usually, an increased arterial tension. Fulness of head, headache, mental confusion, tinnitus aurium, palpitation of hen \'ertigo is a common initial symptom of apoplexy of all forms (ccr'bral hemorrha rhage) and may be the only symptom of a slight attack. Usually the sequence o \'ertigo may constitute the aura which may or may not be followed by a full at tiicks. In some cases a severe subjective sensation of vertigo, frequently foUowc attack. Vertigo is not an uncommon symptom in the interval between the atta Vertigo may be the initial symptom or may accompany an attack of migraine. Th makes the diagnosis plain. I Abnormal conditions of the blood, as in Uie early stages of infectious diseases a I Various toxic substances, such as tobacco, alcohol, coffee, morphia, m tlie application of a galvanic cur- h of vertigo and ataxia. Exhaustion Vertigo. 1022 tiou is engorged with blood, the cerebral vessels ^^^^^ Cerebral Anemia from digestive disorders, 1023 .ances which rn^iy produce a toxic vertigo. The j^j.,,.,,,^, hemorrhage, etc. vertigo when the indigestion is cured. ily of blood and vertigo may result. This is most cin-ovAc Cerebral Anemia from bl„n<| :,„,! cardiac 1024 }ase. In hemic diseases tlie vertigo is aue rather j. siseases.- as to uniformity of distribution and hence may Chronic Cerebral Anemia from atheromatous nrfer- 1025 linm the presence of atheromatous arteries with, • „ /^..^i-r.-e, Its ^ Sjr pll 1 1 lb _) . Jyspnoea on exertion, and high blood tension. Cerebral Congestion. ]02« embolism and thrombosis, and meningeal hcmor- . , ,. . t-rn\ ii'io? her symptoms makes the diagnosis clear. . The diagnosis is m.ide from the epileptic at- ,.:,,i],.pgv (57.-,, lOCl, 1073). 102.S ' vomiting, may be the equivalent of an epileptic ' > - ^ and may continue during minutes or hours. micrania, the much more prominent symptom, :\[if;i.aine (S49-.5S. 950). 102S n leukemia, melanemia, gout, diabetes, etc. t^^j^ y„.y„„ (io24). 1030 cause vertigo, probably by aflceting the oircula- jy Vertigo • 1031 ingestion of the substances before each attack of lies It consi.sts in attacks of vertigo, with dim- Gerlier's Vertigo. Vertige Pnralvsant. 1032 unction or act of the arms, simulating hysteria. iecially inflammations and syphilitic lesions) is Cer,>hral Meningitis an.l Tumor (Syphilis) (.%OS, 1033 both by irritation of the meninges and by trans- 530-42) irritation of the cerebro-cerebellar tract. The vomiting, slow pulse, etc., which are frequently B the result of psychic traumata, acute and Neurasthenia. Traumatic Neuroses anriii£ sod after Bbtorr, Of oUier iTid^ncc of rt'Ci-nt fV)nviil»itinii rare. injur; to bead. f I'lipils imiinlly crtDtmcrrc i reapoud heiHy to llsbt. Pupils dilated. ofU-n unoqual, i ' uBuallf do not respond to light. T'nlicnl iiiKy In- i-omiilrtoly uiir..n«diiui for n s'l"''' tune, nflor wbidi lie r.'in/iit Symptoms follow thi' Injury iomrflately- Rnroly any pnralysla. Ofti-u i DIAGNOSTIC ANALYSIS OF SYKPTOMS ABSTRACT OP SYMPTOMS 1 n ilaioil oondilioD for a time, or he may be onlyl;!'! May bi' conttiriun of scalp. Minx iisunlly M\<> I symptnuiM, Ofi tlif iiijiirj iininHli"i'^l>~' but flot Alnnys; thi>r.> luiiy in- it '■IuckI intTvnl." («s|iPdnUy in extra-dura! hemorrliiiE^l. Profound comii, aterlnmus liri>atliing, puls^ slow, refl>ii<>9 :itiM|isbfd. iiicrpnsod irnaion of ccrebro-spiaal fluid b T ponjiii:in» dcvialinn of the hoad and eyes. Ofifii piiriilynin in rlic form of more or li-BS complete hemiplegia, t^it'ltier witli Baliiuski reflcv ami some ^tinrai. Often relrogniile umuc^ft (772). ConvuIaiODS a r p frequently preaont. Thr aymploma an- Ib-'w of n Iol'oI mcoincitis (507, 1048) or obscess (50*^, 1(H9) wlHi innnlly hieli fever and chills (both may be abaenti occurring in n cachectic, anemic, or Snfcclfd patient, eBpecinlly in one with carie* of bone of skull (otiliil. Ileadsebc, vomiting. nu>lir»i8 of superior longilMdiunl sinus there may be epistazlB miil nicma in root of nimc. \Micn Ihe cnvemous sinus is involved thew may be cirma of eyelids and conjunclivar-. diohod di^cs. prominence of (he«y«ball« "H'l oculo-motor nnd abduccns pnralysis. When the transverse sinun itt involved there may be wlemn over mnstofd and pnlpnble tbmmbosla of inttrnul jui:ulnr viin in uppi-r part of neck. DtAONOSIS I CvuiprL-Miion 1043 Occbml ComprciuioH 1043 ("■ntusioii niid hemorrhngt') ■ s ThromliOBla. fimO). 1044 liich mny be cloudy, give globulin "nn of neck and oplstbotonoti. revcr. hrndadic, delirium. ConvnIiioiiB and reirnction of nMnmon. Paralysis of cranial nerves. ICemig's sign, Lumbar puncture and examination of the fluid, Irritation followed by those of paralysis. Pulse usually small, irreg^lcir md rapid, except in terminal stage when it may be slow. Optic neuritis i> riir.'ly present. An acute disease chnraeHrlKed by prmcrat symptoms ; anch as fever with sloir pulse, bcndache and vomiting, convulsions (especially In children), m-ntnl confusion, delinuni, drowim-s* and I cephalitis bns been aubdlvided Into n number of special forms ot dlse:iw« detcrihe>l •■ls<-whcre in these ch^irts. See 40ii (encephalitic fonn),r>42. ri43. CM. 1047. 104S. The dl'ease often folliiws no attack of influenza, and is of acute or sub-ncmi- onset Hii mr.sc striking feature Is profound somnolence, from which the patient, williout much dillicuJty. can be an)U5>>d to fairly cliNir coneciousix'vs. tempomrily. With this snini-eomn lire nssociatetl a pHmlyais ot one or "j mow of the mot-T cranial nuclei, especially of the motor nculi, and a i>rolaund vfivil.Ti"=i, The sensory cranial nuclei are not affected. There is no pnnilyxis 771. No preceding injury or disuse. History of a previous lilneas. of which (he coma is only one symptom, and often the Icrminai one ; or the prcaenee of an Inflammation of the scalp (erysipelas, -m.purritloul. or of the bones of the kull f.^ries and especially suppuration II llie hones of the ear). niatory or other idcnce of poison- | log. I . Convulsions absent. ICvidcnce of a .Hr- Often a slight inad»iuacy. npasm or riiddily during the attack. After UDCerinin prodromata, coma and paralysis with fever appear and death r«n two or three weeks. The diaeaae uau&lly occurs in young persons and seems to be due to poisoning, especially alcoholic. Optic r polioencephalitia superior hemorrhagica acuta) or may he in the form of a hcmipl''^in. partial or complete. turitis may be pri'si TIic p;>rilysiB may attack the eye muscle* (Wernicke's A.m.- Multiple KnivphaliUs. (496, 643^). I'M^ Headache, vertigo and romitinv. Often mild delirium. A recent, infected wound orotln' general and reseralile those of a rapidly growing ;umor. Choked disc occunrathw mi Headache, vertigo and vomiting. May be a history of former injury. No (evsr. Ocmi-^e tumors at the base are more likely to cause paralysis of one or more ■ mtinl nen -. Memtplegia or diplegia ocriirrioe in early infancy is common. .\ motor monopl^a ' feet. Itpileptiromi convultinns, unilateral or bilateral, are frequent. HemtntheliK iiisp. or origin, for snppura The general symptoms ai Moderate, irregular, often absent, fever. Course is progressive but may be very acute or eitrcmely chronic and often almwB a latent period. Tin; symptoms are both local ai re prominent than the local. Suppuration of the middle ear and of the mastoid cells must be carefully e.tcluded. especially in oltildrcn (see 50S1, Pulse usually regular and full. Mental deterioration, but local symptoms are often as prominent as the general, Convulsions, especially Jacksoninn epilepsy, are common, f s very common (see .107. S071. especially when the tumor is situated in the posterior fossa of the skull. larthria, etc.) is rare. Usually some arrest of development of the paralysed part and of the sliull. Little or no niusculm and hemichorea freaaently complicate the disease and cnntractuii's occur In nimofct every case. rophy, and refl-xe* liecially ivhen tumor ta in or near the CFirtei; while Ankle-clnau* and Unblnski. Tsunlly tome mpiital de- IVoBr^Birive mi-ntal impairment, childtsbness. restlcMness, amiable hut irrilabK Stendily increasing di-mentia. Blurted speech. Tremor of lipa. tongue and hnnda. Tenninnl dementia. Inability to repent diflirult phraaea, due partly to parnphaKln, partly to loss of memory. Wriline imperfect : wobK ayllablea and letter« are left out and letters doubled. Apopleciitonn and .'orniilslve attacks. Ahnormntitics of pupil. Areyll-Robertson'a reflex. Lumbar puncture gives globulin and lymphocytosis in cen^ro -spinal fluid, iliitory of syphili*. ro.«itivc Wassermnnn reaction. Ilislorj- of lead poisoning, of lead colic, of wrist-ilrop. rtc. Blue line on ::UDs. OanvnUions. Lead can be found !n the urine, especially after the .idminislration of K. I. Intention tr#mot. Scanning dpeedi. Many motor and ncnsory symptoms. SMgeoroted reflexes. Ataxia, Nystagmus, The convulsive attacks may he epileptiform, npoplcctiforru or myol-nlc. Headache, ivunpulsory acta and slight dementia arc not uncommon symptonis. Ilendaehe, increnBimr fever, potyclandulnr enlargement, difficulty In walk ind epecch, lethargy, increasing dmwsinoes. passing into coma and death. Trypanosomes arc found in blood, cercbro-flnld and irlanda. Disease Is almost invariably ronfim-d to Nrgrom and Is due to the bite of the TNoslse fly liy which to'panosomea enter the blootl and multiply there during yean before symptonis of the disease manifest thnmselves. At the autopsy a nieniiiiio-enceiihiLlo.myelitls is found. Often tremor or twitching, nistory or evidence '■.-r-bnil Absi-ew, 1040 nri inl tension, sleafliiy BTttwiin; ■npnble. RpAplratlon is slow and stertorous. Face is congested: skin cold and clammy. Pulse is first slow, but later, especially i fatal ( . bcni t rapid, Flislor jvldei, • of patient's hai :vml gas. He is cyanotic with rapid, irregular pulse. He often vomit* and exhibit* r Oflel pre. edcfl by tinnihrs annum, dimness of vision, cold sweats, and t: ir altacfcx of syncope have been described as occurring, very m M«ca, Slinht Hpnsm orrlgidity Is freqin ly. in Raynaud's Dlaeiisc. clonic spasm, t durinc e attack, in intermil hen ,■ the onset of the coma Is more t^adunt, I'uNe Is linolt or meri' Sudden attack of coma ot short du- ration with or without n convul- sion. Tlnually a history of similar attacks and often of remote injury. Convulsions almost nlways present and are usually the most striking aymiitom ot the disease, but not so chamcteristic as umvnseiousness, which is at times the only symptom of the attack. lower. iviih coma and slielit spasm. Slow pulse, atheromatous nrleres. tlaunll.v occurs in ndvancml ngc. miulsicn lasts only two or three minutes and is nccnmpanied iind followed by a conin which cmdually pas-scs into n itei-p. This post-opllentic cniuii is S'uneiimes iit'irnt and is sonn-time* replaced by unconscious ac- en iitncfc of ceni'riil oinvulsions Is called "the major attack" or "le grand mil." At iiuie* such an alL-ick follow* nu'itlier immedintely lliponghout a |..ue series fsialii-* epilcptl.-usl. Al other times there Is only (,.u ; uncimmou nii^vements of lips nnd jaws beins cmmcn. This is cnllwl "the minor nttnck" or "le petit nml." R-s. and in tliem the patients le«e their foraaer Indivlluallty. In sonic of tbc^e attacks (ambulatory automatismi the patients .•r .ill iillnik.. there is amne-in. A rare form of epilepsy is one in wiiieh llie pnllent falls suddenly to the ground and get* up again !mm'd=nie!y wttltiiu! anv »ppr.>ciil>te lo»« of eonscioosnesa fvertiirinousl. The mxciou^nesj diirinz it nnd the complete or almost complete absence of any meuwry of it. In the interval helween lb- itttnck«. which at tlm-s exteniN on r mouths and yctrs. the patient may be entirely normal. Fre- rtreme dementia, especially if ihe attacks are freiruent and rest on a strong lieretlitnry basis. This condition is not to ba eonfepHuWI with ih.* transitory mental Impairment due to bromide given them- The attack usually commences with a convulsion, as described in Chart X. 575, "Hie e lion. sfmellmcTi iriiinl. sometimes a deed of violence f post-epileptir in=aiiily). Such uncijn«eioii.nes9 and no convulsion and cither no action or som.. trivia' ot fooliili net reidneei the eonviilaive attack and is called the "iisyebic couivalent" and is altogethe wander about and take joumej-s and are lost to iheir friend« nnd to theBwelveB, ,\f essential charaet~ri«tic r,f tin epileptic attack is ihe complete or almost woiplete unc luenlly he is irrJlahle nnd shows some mental weakness which may slowly im-renie peuticnlly. On the other hand, many epileptics have attacks during raanj years and yet shinv little, or no, mental impairment. I^pilepsy beginning in a patient over forty .v s of tir- should sugci'st the possibility of a corehral tumor. Sudden attack of unilateral paraly- sis. Rarely the pn- j rnlysia comes on I slowly. stMdily in- j creasing during I honra or days : TngmTesceDl apo- plexy." In tuch s Ihe c Albumen and cflzta, or sugar, or all three. In urine. (Convulsions arc rare, but both tonic and clonic spasms may o(vur. in vol v- ini; one-half of the h<'dy when the lef.if.u is cortical. or involving hot* Bide, of the body when the hemor- rlin;:e oecurs In the bruin stem (4ti0) or ruptures into a ventride. No convulsions. Convulsions usu- ally. I The alt'H'k is nlloncther similar to the major attack nf epi|pp«,v. but it does not n-ctit. Tl distendrd abdomen, fi.ul smelling feces, vomltinc. diarrhoea, etc.. and ceiwt wheo llic Sudden attack of tickling end burning in larynx, suffocation nnd striduloiB bmotbing. falling to the ground unconacious for a taw minutei I usually be r-fcrred to a A rare form of tabetic crisis {Iaryni:enl i The coma comes on instantly or in the course of n f(,w hourii. There arc >tertOTOiiR flaccid paralysis in tlje form of bemlplogio. The hilaiernlly inmrvateil muiclw [upp, lar.vnEcal, respiratnr.v. nhdominal. micturition, defefralion. ctc.t .>8cnpe peniLanrat ent from Ihe start. The other reflexes may. durinc the coma, b- nbollshfl. Ut^ 1.1 may die In coma or the coma may pass awny after sevi-rnl ho 11* or days. The low paralysed. Tontue protruded towards the paralysed side. Usually there Is alsn ni diinpneaw. hut which may be permnnent, in whieh latter e«*e the mntnr paraljiis Iinpmv.-m-nt uMially besins in flie face, next in lea and finally In llie arm. !„ en,, tMeiiires appear In aim and extensor contracture in leg. Pr.*! hemipleiric motor band. Some mental impairment persists. I-ocal sj'mptoms sneh as aphasia may or lesion may cause an exacerbation ot the symptoms In the sccmd week. RepeAtsd a ronvulsioM". inri of the huily or 10 iiiUy ,Ti. •|.\v (Itill 4t#d »||), J of this nature. Imi in these ease, convulsions are Tare, and the cause may eonilst In History or evidence of expomire to itreat heat. Absence of pereplratlon. Thecoma co I lymptoms (paralytic) occarionnlly oecur. labored nnd may show "air hunger." Sugar and almost always albumen iind Cfists also in nnne. Pulse ot high tension. History usually ot headache. TOmtdng. dyspnoea and dimness of vision. Ophthalmoscopi acute Indigestion with foul smollinc fece=. Hish fever is common. Often history of improper food. The a failing cirnilatlou (cerebral anemia). mi's on rapidly but not instantaneously and Is preci-ded by many prodromata: \f bIi'iw albuminuric retinitiii. In nirc ciises there may be bemipleein or other paralysis. Urine con- ■hich occnrs in the course of, and especially towards Ihe end of acute Infectious fevers Is probably headache, mental confusion, mnrkcd disturbance ot i-ixion. parvnthesiae. weaknces. etc. Delirium In a common symptom. Local ecping Sickness. Aleoliolic Coma. ("tl7l NiLre.itiKm ftnm opium, etc. (054). Illuminating or coal gaa poisoning. Syncope. Internal Hemorrhage. Sii>)(es-.\dams' Diseaae. (426, 5S!). l-:pilep«y. (111-27. 420, 575, 849. miiv 73 W, 111*4). HBO 1057 IfttS lino I0(»i flexor con- 1 ly ocfur. especially in Prodromal *yni|>lonis present. Rllgbt c -- -- .,, . ... eur. A reactive inflammation about the trausilnry f..rni. with tendency to relapses and without contracture, is Ibc so-ealled lacunar hcmipl(«sia." in which not one large focus, but numerous minute toci ot Hacks at varying Intervals nre common. 1 softenine occur in the cortical nre.i involved. l-:.larop«a, (57rt). 1002 Tabes, (001)- Uryogeal cris**). lOflEi Pn<'liyiueningitis Internn llemorrhaKiert I'll!'l (502. 588). Ceriibral Hemorrhage. "^M (1+7. 405-0. noi, r.lairon, (n«fl. (HW). lOTO CHART XVIb Pseudo-coma, Double Personality and Weakened Mentality Comprising Numbers 1038 to 1040 on left side of Chart and 1071 to 1077 on right margin 199 DIAGNOSTIC SYMPTOMS AND TESTS 1038 rSEUDO-OOMA. UODBLE PERSONALITY AND AUTOMATISM (209). Hysterical symp- toms (415). Hysterical symp- toms (415). Epileptic symp- toms (575). Convulsions and Spasms frequent. Convulsions frequent. IMO WEAKENED MENTALITY. Patients appear to be intelli- !;ent, but incapable of Ions sustained effort, and of self- i-ontrol, often foolisb and un- reasonable. The different dis- eases in these groups merge into each other and no sharp line can be drawn between them. They all rest on a neu- rasthenic basis, and in all suggestion plays a great part. .\ppreheiLsion and various prominent symptoms. In phobias are consequence of their weakenixl mentality, these patients cannot rid themselves, by rea- soning, of their uureasonable bensions and fears. appro- DIAGNOSTIC ANALYSIS OF S PSEUDO-COMA, DOUBLE PERSONALITY, AND These diseases merge into eadi other and into iusai cases occur and in all suggestion (auto- and foi ABSTRACT OP SYMPTO Occurs usually in girls and women of an emotional nature, be stopped by a strong and continued pressure on ovaries tion will usually show that she is attentive to her surroui from external causes, or auto-suggestion (hypnotism, so •Patient seems at times to be in a hypnotic state, or in an a' and in that state to lead a life carried on from former sin states from auto-suggestion, patients often act like autom ception and in some hysterical patients may well be due 1 While in an unconscious state patient often performs compli has no memory. Whether in such unconscious state he ca doubtful. While unconscious, epileptics often perform at The symptoms are tho.se of a general exhaustion of the nerv bility, especially of the lower centers. It is common in i or tire easily. Every task looms as a mountain before t! ory and will power are both poor. They feel nervous, irri (agoraphobia, claustrophobia, mysophobia, etc.). Almost lack of will power. The patient also suffers much from p ralgias and digestive disturbances. The essential symptc is employed to designate the most intense degree of neur perative ideas and acts. The patient, usually a male, is in a condition of extreme ne consciousness in which the attention is firmly and perman pressed because of a delusion in regard to a supposed disi delusion has its origin in abnormal sensations. On medi idea, but the false idea cannot be dispelled from the patie strous, fantastic and impossible. At times they seem like and apprehensive, and their attention is firmly fixed on tl even grotesque delusion that some organ of the body is d The di>ort:inl diagnostic symiitivm (415). The result of an accident. IPTOMS WEAKENED MENTALITY and many transitional, i) is a large factor. ;Iid-i are closed and resist attempts to open tliera. Coma can usually 2vcn in tbe apparent coma the patient is suggestible and close observa- gs and therefore not truly comatose. Such a condition may result mbulism. trance). eouditiou from auto- or foreign suggestion, or from wilful deception. • states quite distinct from the normal life. In the hypnotic or allied [S. This is a very rare condition and offers much opportunity for de- aconscious suggestion on the part of the physician. i acts and leads a life, during hours, days or ■weeks, of which he later ■member what happened in previous similar states is, to say the least, atic acts. systnm, especially of the brain, associated with an increased irrita- but more so in women. The patients are either incapable of exertion so that they are discouraged before they undertake it. Their mem- :, appi'oliensive and have a number of peculiar fears ; phobias — 235 iarncteristic of neurasthenia as are the phobias, are indecision and atii'ii, vaso-motor disturbances, paresthesiae, headache, backache, neu- )f neurasthenia are apprehension and fear (phabias). Psyohasthenia jnia and exhibits a bad heredity, morbid ideas and impulses and im- DIAGNOSIS Hysterical Coma (1076). 1071 Hysterical .Vutomatism (]07l>). 1072 Rpilepsy (lOGl). 1073 Neurasthenia, Psychasthenia (114, 1074 1.3S, 1527. .586, 018, 620, 064-74. 747-8. 702, 7*!, 837, SAO, Sol, 870-80, 924. 926, 951, 971, KHMl. 1034, 1071-2. 1077). 1076 ;reat fright, or in some accidents from fright alone without physical a been received. It is especially common in railroad accidents and in injury; although it occurs also in cases where there is no hope of re- rasthenia and hysteria and it may present any of Uie symptoms de specially after exertion, vertigo, parosthesiae, neuralgic pains, local isturhances are common symptoms. Unpleasant, horrible and vivid racteristic of the disease are insomnia, especially in the early morn- Most, if not all, of these symptoms can be simulated, and as many rally more or less of conscious and unconscious simulation. Simula- the key to which lies rather in "suggestion," as in hysteria. In ttbiiiation of chronic mental anxiety, strain and worry and of acute as been called "shell shock" — a poor and inadequate name for it. uess of the mental powers, varying In degree, but always decided. Traumatic Neuroses. Sometimes cnllid Traumatic Hysteria (1.57, (11.5. 674. 1034). 1077 CHART XVIc Insanity Comprising Numbers 1041 and 1078 to 1082 on left side of Chart and 1083 to 1120 on right margin 201 y^ V DUGNOSTJC SYMPTOMS AND TESTS DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS A coDditioD Id ^icb (hi- mind hna sot fl078 Amenria (211). Man or lew eomptete. (A mental dp- fN:t either con- ireniliil «t moii- ifonK^ in in- (aneyl- dcrtloped wiUj nilrancinK a disease of tta» bntio, cilbi or acquirM io iofnocx- nif'ntal defect, tliesp pnt prpneut mnuy find Tflrio 'IffecW nnd dciormities »i (unnmt skull, p'>«l«rior liy hiah pnlaline iirth. coHrsi formed •■nr*. etc. The mni' I'lther ijcncml or pnrtinl, n ilB sliebt di'sreex may bf lo di>foctivi> tninini;. sge, due to >r conseoital Besides tlie ionis oftt'D u» plifsienl iiph ai: de- iitin tnny be diir- in nart I'liiieiila aliou little vt nulk. U!' : eiliil geiicc. They ore inwipable of inueb edueutiun. The, eon form (." abalru u cuiuuiun and aesual insunct is ofteu strongly dsTeloped. DiAQNoeia Hydrt)eeplinlic Idiocy (11,120). ■, Bpileptic Idiocy, II. 101. MicrucAphuIli; Idiocy. Amaurotic Idiiicy, r>iri>ucepbttlic Idiocy. Idiopathic Idtoey. Idiocy (101. 743) 1080 1080 1087 1088 Leir ui'lt* iiu evident tliuuijli low degree of iatelli- i;eptiL>jj» and uu bigb iiiuinl iikus. .Masturbation I'ulienb) show a degree of intelligence oppr eatiou. even Uioujiti m general amiable, Turtar-like exprcsaiou of the eouutetiijn muy be due in some cat>ea to poison, aui. >iicliiui; the normal bat are evidently hi'luw the Hliitidurd. when aubjeeleil to tbe Biuet- .'mjuii.' children d^'^elup up lo a certain puait. but theu litup aud uir\er advance further ' . ^luijting e^es. tlileb Uaaureu tongue. auU ^liort, atubby bn^ecs. I'bey puaseu gtea' 1 ui vviue or tobjcco, iiuiiple iutuutili&ui ia utten culled "uteleiuBis, f Alt the clusaca above given under idiocy but witb Uns ezttems 'iieniul defvcLa. I 1 ery delckiive lulclligeace in genera], but in cectum directions lusuully uiu^ic or mathematics) maj bIiow great nkill. •{ A^ocJated with destruction or atrophy of the thyroid gland. Arreat of gi-uwlb. Thick, dry and 8>.iily akiu. Course feature* (lllJ4). [ Associated with no speual diacacli!TUitii,'&. or otiier menial tests. They cannot be educated beyond u certain point. They are ofteu ohatiDule and of violent temper upon provo- .tilismuBj. In eouie cai^es ol infant ill am us, theie la a defective ^runib u: the body wiib ii id "progeria." Idiupalhie Imbecility. 1000 Imbecility. (101) Coctain feeble-minded persoDB seem incapable of uppiefiend'Hg Uie aimpleat iiionil ideas, although their tueutal defect is not ao oix i in other directions. Uu closer cKaminatiou, however, a general mental defect becomes evideni 1079 Dementia (212) More or Ick complete. (A lots of men- tality, previous- ly oequireil. Srst mnntfested after infancy). 1011 I A condition In which tbe mind bai rli>vcloped to a cer- tain, even a IiIrIi. dejtrec of intelH- gencp and then, in conBequenee of dis- ease of the brain (functional or or- fanii'l, nil mental deri'lopment haa not only ceased, but there liaa been a diRtinot retro- CfMsIon which may Ro on to a com- plete Io»» of intel- Iijri>nce. Memory. rmotioRB and In- lefi-«t ore all loit. Paliput become apathetic, reacts to no slim it 1 n 1 1 o n . •oiN himself and doM not even cat. ' Complete apathy, coming on more u and will respond to no stjmulatio i-ellexea are exaggeratud. The ct leas acutely ivitb iiwoui.iia >ii the eaily muges. ijui • Appears lo he antsthetic uiid .malgeaic. lialliici irsc ot tbe diiictise U tniMiupied at iluiea by pL-riuin till us aud deluaious \it tieitement, Muri I'utient incapable of any mental ellocl. Iu a dreum-tike state, immobile aud doi-a nut aiiiirvciate what i» guioi; i lire not prominent syuptxma ; although the diaeosc shows much relationship to cunfusiouul miMuity (llUK). Tbe c thou half of such cuaes n^cui cr alter sevenil months. ) lOM The I FeeUft- I Minded rat ImhecllltyorllnbitiinlCriminnlK. J <101) aiury IK^nientia iinil Stupi.r, rariiol Qpulby. ratienis are dull and lUipid bm euuclnutaeu Is fairly dear and th'-y uppreiiate whai 'm un ubacuce ul euiotiuus mid of inteicnt lu aii.viliitig, .Vnesthesia and analgeaia. ibey are uuwillin; They perform frcjuently >.puuirtiieoiis, impulon.'. -illy acts. They often repeat the same act ur tbe i vl u phrase which tliey have juai beard or ^pukcu (eclmlalia), or repeat ubseeoc wi'i'ds tcuprulaliu), X'he vncieties under tbia head merge into eacli ether, and all show, as prominent sjmpcoius, impulsive t itieni, llailuciualious and delusiuus are common. There lit iiud uUer ri>isliinc\.' when forced to do it (negativism). lies istercotjpy). They also often repeat the last woixl bupraiLiaj. or remain iu any given posture (catalepsy). c pcognoisis r Illsiory of alcoholism and i and space. iated > 1 luullilile very i ideas and a re eases. A peculiar loss of memory with a bringing of memories ol the ceiuoie past , at times permanent, often luiupornry. com- Hebephrenic form. :i Uie Hallo. lediate past (cet [vgr.'viive mentui deteiioratix S at puherlj. u^ cuuditions of stupor and exdteiueut, negativism, stvreuiypy, euhololla t'uUj tueutal deterioration, at tim<',s permanent, often temporary. iiii'Us and partially syateuiatined delusiuus witb steady mental deterioration. Usually ocvur- rinp in ndult life after 2£i je^n, but may occur in youtb. I Occuriing In old nge. Hidiocy of alcoholism extending ovec many yei amounts Qf alcohol. The aymptoms at limes Tremor. Dysarthna. huatt uf memory and power of attention and mental power. Delusions are frequeut. >>urmul and ethical ideas blunted. Irritobb mhle lliu*^- ol paresis illtKi) (pscudo-puresis), but tbe dementia is less pronouuced, the cetcbro-spinal fluid is normal and improvement follows ab>liii History of very u epileptic a (Gradual loa of m>'iiiory and lUL'utal power. .MasturhuLiun i cuuimou. Usually stea>lily progressive and iucuruble, but this dementia may ( iiiipli-te losa of intelligence. I'utienls muy carry oier iutu this stage some traces >f the e Jj, failure to appreciate the celaiions of time ry susceptible to the eHecls of smalt n eliildliood and way be traualtory, in wblcb cose It may be cured by bromide. J delusions of ibo former psychosis. They usually sit motiouIeB* amiiesia- aeniimenlal and often ' ncc from alcohol. I'aninoid form. Ivorsakow's PaychosU. lOD.^ 1099 .Xdoleaeent Infinity ; tbe ao- f-.,ll«l Dementia Precox or 1100 Mchisophrenia — a splitting of the p^che (terms of lery doubt- UCri fal value), 1102 Ilialory of a previous psychosis which baa gradually pasted into a couJitiun ol apathy and niur.' oi (apaUietic dementia) but some cases show great restlessDCW (a^itutitl dementia^ History of syphilis. Lumbar puncture shows flobulin ud lymphucyto'ia in d-rcbru-spiual tluid. Wussermauii usually positive. .Argyll Huberisoi is pheut'Uiciiou and often un ijuul pupils. Tremor of 'Ips, tuiigia- aud bands. Lose of memory, loss of aelf-rcatraiut, ina- bility for contiounos menial concntratioo. reukles»ooiKjuid clmuge in cfaaructer are early symptoms. Speech blurred, slovenly aud tremulous. Words, sylbiblcs and letten left out iu speaking and in writing. I{<-«llcw, cxclt^le and irritable, with exaltation or at least cheerfulness, in spile ot the illuoss which patient roreiyrec -guuea us ccisteat. liraudiuse delusions, silliness aud iueonsiateucy in sinking •uuiru^i wiih iuonliuate preteasiou^. Gradually increasing pbyaiuil ami eipeciuUy menial weakness up to comidete dementia. No paralysis, but much pai'i-am and especially aprnxia (231. 'Si>'-). ty'areli"<^, inconsidcr.ite, slovenly clothi«, etc. Apoplectiform and epileptiform aeisurea are uaually present in the coui'se of dia 'iL«e. Incurable, but remissions. Freijueutly aswciatnl with t^>eB, more rarely witb various forms of spinal sclerosis, .Associated with physical weakness and with atheromatous arferies. The dementia varies from day to day greatly iu degree aud may lead tbe patient to do very foolish things (often erotic), while api>ai-eutly »une. Loss of will power (drunkenness). Depn-ssion and loss of memory, especially for recent events, with retentiou uf past uieraoriea. Dread of impending poverty. Desire to go home, imagining himself to be in a strange place. Ucstleas at night, ossoci itcd with hallucinations and delusions, .\tiack8 of excitement. Alcoholic Dementia. (058, 1100-12). ICpilepiir Dementia, (375, 10(11). Tvrminol or Secondary Dementia. low Hslluclnatioos are abuodaot and doml- Dsnt. Hallueioatory Inannitr (213-71. or I).-lirium. 1081 DeluBion» are present and dominant. Delu- aionnl Insanity (215) 10S2 An eiaggeraled emo- tional state is tbe dominant sympt o m . Kmotional Insanity (2041. The insanities of the neuroses have been considtr^ under epi- lepsy, hysleria and hyporhondriaiis. \ t^'iidilioii in which the pntient is constantly rr«iTin(! faUe perceptWiN from his different si-ntw: either visual, auditory, olfactory, gastatory. tactile or painful. r.i from several ur all combinpil. Asooeinted with this Is al- ways a certain desree of impaimieni of con- arlousness. whicJi weakens his judgment and does not permit htm to dpcide that these baltudnetions are false. \ cindition in which ibc patieui has formed a false juditmenl about things which concern him. The basis of thcKe false judgmenU ia partly n congrnitally defective brain and part- ly baltucinations. AMOclaied with these de- lusions there Is always present n varyiug de-. Itft'e of impairment ol intelligetice. which pre- v.-nis the patient from recogniKioi: the false- nens of the delniion when cvideuee is pre- »-nt«i to him which would be ndniiuaic for a liuniml man; although many of these pa- tients lo their own wny reason shrewdly. These delusions lead to irrational eoudurt on till' part of the patient which would not be inalloiial were Uic delusions Irue, \ ilieul is overwhelmed by a lai-ge number of bn Unci nations and illusions which cunn that of those about liim, aud cspi-cially doubts their intentions towaid uim. He dot witb his previous experiences. He, rother slowly, becomes cnfused. frightened and timid. Dols : ich mlgtii be rational were his hallucinations true. May be the early stage of other forma of lusauit, Utslory of alobollaiu. dent. Oreut frigbl. iilions and illusious are of all kiuda but are usually visual and cuneeru suakes, spiders and uther small griitesiine and repulsive uuimals. Tactile haltudnaii :i escape from bis enc'ii^es, I'rvuounced, continuous treiuor and insomnia. Diseaee usually lasts liss tliau a week and usually terminates in recovery. Many otlier poisons besides alcohol : cither exogcnetic, such as belliidouua, salicylic add, etc. ; or autugeuelic, such as uremia, chol.sterin, plomaims ; ur septic, especially when the potsou acU upon t a mild hallucinatory Insouity or delirium, which may lait a few hours or days or may continue during weeks, months or years. To this group belong the "puerperal i ut appreciate bis s , Probably n form IIS, shown by fumbling of the liugers, also t . exhausted nervous system (post-febrile iua ise commences with fever, beadocbe, dased feeling and delie \ own identity and « uBuulIy very eri- uity), may produce iteks. "arrsis, (jeneriil I'ar (KV.Hi. 409-l2-ia. 1-Jlfl. 1230). Senile Dementia. roiifiiKional Iniuinily. Delirinm Tremens (llWtl2). 11(M HOG 1107 llOS noo , followed by violent excitement aud violent actions. Many hallucinations. Speech is continuous, violent and incoherent. Disease usually terminati.'S fatally in two or three ' History of alcoholism. Patient bos formed, on ll>e basis of ballucinollous, more or less permanent delusions, especially of jealouay aud persecution. These are often so exaggerated and monstioun as to be grotesque. A very common delusion wives are unfaithful. Patients often net violently, gome alcubulic tremor. Curable, and usually lusts lesa than a month after uleohol has been withheld. Patient has delusions upon which he hasce his actions. These delusions are not associated with any decided emotional manifestations and are at times permanent, at times changeable; but they arr nm reao»^ merely profoundly depressed vrith inhibition of uU action (melancholia uttcnllal. At times the intensity of their grief drives them to frenxy and breaks IbroLigb their inhibition L (MP'us melaoetiolicus). Oceaaionally there is restlessness (melancbo Aeuie Delirium. Toxic. Sepiic Febrile or Post- lUO febrile and Puerperal. Delirium Crave. Ull aglta All these conditions seem to be the direct result of delusions Jiuch patients ore very prone to s 1 men is that Uieir ( mi-lnncholia cum stupore) or impels them to deeds of violence Acute AleoboHc Msnii. Alcoholic Halludni: (n08-9). Symptomatic or Delusional Mania. .'Symptomatic or Delusional Melancbolin. 1114 U18 Paiieni has many delusions which arc often the result of ballueinatlons. They ore fit.-d, pirmanent oud are reasoned upon. Newspoper paragraphs on inditFercni subjects and various drcumstiiiK are wovm in with the delui-ioos in the attempt at an explanation of Uic curious things which are buppeuiug lo the patient. Tiieae patients reus .n very cleariy and if their premises ore granted i' tbiw syslemotlised and some wild theory is evoHeu to explam ti.em. The most triiial happeuings, even in the remote past, are fitted into Ibis system In the most surprising and ludicrous way. T ■kuble person because so many persona buff themselvM al.xut his affairs, lu typltal ,-ases the patient evolves first a delusi'm of observation (all things, even thi- most indifferent and remoti> ■ ' - to try hU character), and bnally a delusion of Enindeiir (he mual have a great destiny when ao many persons si-ek to injure bim or to tempt him. In the latter ca. :x,ii»:Tnttuii of tlie someiimM natural fetliai: ot cndnoss or discouragement wiih life. An lureditary pnTdUpudiiion >■ frenneul. -xaL-B'' ration of the autiirnl fpeling of happening is to injure bim s in the entire life of the patient are more or less distorted and almost impossible lo answer their argumeniA, The delusions are e general rnuh is that the patient regnnis himself as a most re- lave refcreucf to him) : neit, a delusion of persecution (every to prove him unworthy). i.y the paiirnt to explain the melancholy; />;; "'J^',,;;^ :„); very prone to suicide. Their circulation and their iW"'y eh there is no discuverable adeiiiiatc cause — "a doud Bcttic" •'\'-r ilie mind." A pewslmlst. No hallucinations, no delusions, except xurb n« tiar>Jonab1e sin, etc. There is an inhibiLioo of mental and phy^iial activity. Patients withdraw themselves aa much as possible from tbe i ire greatly dlsorderi^I. f^irable. The secondary form of melancholia aistie. They have no hallueiuniioui a severe form (frensy). t'uiable. and melancboUl «'»'' usually, but not always, a eomparotlveiy normal period between the 1 joyous and exdted ^o^.^^^.^f ""» ,Jj-';overable adeToiiii. Mania is often syrop- Primary Mania. f Alterations at long intervnla ot mania and melancnoi- "■'•■ u-.m.,,-. oui uoi aiways. a eomparotlveiy normal period between the i wo. The duration and the intensity of tlie attaeks and the duration of tbe Interval arc very varying. , , K 1- I Attacks of excitement or ..f depression may recur (>"*^'°' insanity), or may alternate, after a longer or shorter interval (drcular insanliyl. In suin« cuseM tbe exdted and depressed phases are commingled, or thr nlterolions are momentary, giving a "mixed form." ano meianciiolm. J Kmepelio has incorporated nil of lht*c forms under wc term manic-depressive insanity" but the permanence of thla term isdoubtful. Ills classificuUcn involves a recasting of the nomendsture uf mental dlseoBes, and It U doubtful If the time Is yet ripe for nicfa I. an attempt. 1 c'irciilnr Insanity, :Mnnii' Depressive Insanity. 1118 ino C^ CHART XVII Trophic and Sympathetic Disorders DIAGNOSTIC ANALYSIS OF SYMPTOMS TROPHIC DISORDERS AND DISORDERS OF THE SYMPATHETIC SYSTEM TissxJES Involved 1121 Trophic Lesions. 1122 Disorders of the Sympathetic System. Symptoms Aanalysed r 1123 Muscular Tissue. See Chart XVIIa. 1124 Cutaneous and Sub-Cutaneous Tissue. See Chart XVIIb. 1125 Fatty Tissue. 1126 Bone Tissue. 1127 Joint Disease. 1128 I Other Trophic Lesions. 1129 Ganglionic Disorders. 1130 . Vaso-Motor Disorders. See Chart XVIIc. V See Chart XVIId. 203 r CHART XVIIa Muscular Atrophy and Hypertrophy Comprising Numbers 1123, 1131 and 1132 on left side of Chart and 1146 to 115S on right margin 205 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANALYSIS ( MUSCULAR ATROPHY AND ABSTRACT OF SYl Muscular atropliy. Lesion in peri- pheral motor neurons. [1131 I ATKOr I IV. 1123 MUSCULAR TISSUE Atrophy is rela- tively rapid in on- set ami usually great in de?ree. 1132 iivi'i:i!'ri;iinn .\tropby is very slow of onset ami often slight in de- gree. Increased or nor- mal strength. 1 Decreased I strength. Muscular atrophy and hypertrophy combined. r.esion in muscles. Lesion in central motor neurons. No lesion. Lesion in muscles. Acute and sub- acute coui-se ( inflainniMtory lesions). Chronic couree (degenerative lesions) . I'aralysis is the primary s.vmptoni and atrophy is secondary to it. .V trophy is tlie pri- mary symptom and the paralysis is secondary to, and consequent upon, it. Associated witli chronic .ioint disease, especially he found. -Musflcs of face (Landouzy-Dcjcrine type), or ol are lir.st affected. Some nl^^ch»> apparently h hypertrophied, with increase of interstitial fa \'ery slow course. Paralysis is pri- mary and atrophy is secondary. Muscular fibers normal. A true hypertrophy. I The hyperlniphy is the result The hypertr(i|)hy is due to mi heredity. Calf niiiscles. infra-spinatus. deltoid and some oti muscles are both weak and atrophied. No fib some hypertrophied and much interstitial fat. affected. SYMPTOMS rPERTROPHY UMS lete or par- •li-ctri(;ii ou of eratiou. iiition of the ical pxcitabil- iit uo reaction 'eneration. 'ilistory of injury, wound or scar. Limited to distribution of one nerve (simple neuritis) or many nerves (multiple neuritis). Usually asso- ciated with sensory symptoms: pain and anesthesia, nerve and muscle tenderness. (iroups of muscles attacked not corresponding to the dis- tribution of an.v nerve. No sensory symptoms, except some pain at onset in back, joints and muscles. Very rarely nerve and muscle tenderness. Globulin and lymphocytosis in eerebro-spinal fluid in acute stage. Atrophy affects either the arms or the legs. Sensory and other symptoms of myelitis are present. Organic re- fle.xes are more or less disordered. Superficial and deep reflexes are abolished in the paralysed area. Atrophy commences in the small muscles of hands, or muscles of shoulder girdle, aud extends and is asso- ciated with fibrillary contractions. Mild spastic para- plegia (52.5, SOO) in legs. .\trophy affects the muscles of tongue and lips and is as- sociated with fibrillary contractions. Mild spastic para- plegia (52.0, SOO) in legs. Atrophy affects the hands usually. Is associateil with dissociation of sensation aii ABSTRACT C 1124 CUTANEOUS AND SUB- CUTANEOITS TISSUE Aln.pliy 1134 Hypertrophy. 113') Eruptions. 113(J I'Iccralions. Tlii' skill is iiiuisunll.v .suii iitli ;iiul lliin. Tlie tiugers become pointed. The OL't'iirs iiuite frequently in niTvous iliseascs, especially in those in whi The hair falls out, either all over head, face and body (as in syphilis), o is not changed in appearance, .\llied to this condition is the turnin; of severe pain, or psychic shock, or unknown cause (loss of hair dye) .\trophy of the normal pigment of the skin; so that patches of clear whi sons of dark complexion. The edge of the patch is more deeply pigmcu .See also facial hemi-atrophy, 117!). f The skin and mucous membranes everywhere appear thickened, as if i I I slightly, on pressTire. The skin is sallow, dry and scnly. Patients features are enlarged. Nails, teeth and hair break and fall out. The and hoarse. Response is slow and iutellectu.ality very sluggish and at atrophied, or destroyed, b,y disease. The disease may follow removal i and intestitial nephritis may be present. Is more common in women tl time of the climacteric. When it occurs in children th y lieconu' dwarj sence of the secretion of the thyroid gland and it can be cur''d or ben* roid gland. The skin is thickened, generally or locally, infiltrated, very firm and ban at their ends, and the fingers become much shortened and abnormally' men and seems to be allied to myxedema. The disease often couuuenci ends with an atrophy of the indurated patch (stadium atrophic urn). . Clusters of vesicles filled with clear fluid, each cluster upon a patch of re( nerve roots and strictly limited to their distribution. The eruiition d accompanied, preceded and followed by .severe pains in the nerve, along i for months after the rash has disappeared. Rarely, in severe cases, m I Lymphocytosis has been found in the cercbro-spinal fluid in some caseS. In some fiu'ms of nervous disease (especially in hysteria) elevated patches when the skin is irritated (urticaria scripta, dermographia — 2vements are heavy. Voice is slow j « disordered. The thyroid gland is he thyroid gland. Arteriosclerosis - in men, and frequently occurs at the The cause of the disease is the ab- ■d by the administration of the thy- Occurring in Cretinism and Dwarfs (1002. 11 77 1. 1104 children. rhe bones of the phalanges become absorbed, especially Selenideriiia ami Sclerodactyly. 116u able. The disease is more common in women than in 5 a local patch of edema (stadium oedema tosum) and imes patches are pigmented. ed skin; the clusters following the course of one or two Herpes Zoster. Herpetic Ganglionitis or Neuritis. IKiO up and disappears after a week or two. It is usually (!)-K)-7s. 12;ij). course of which it is situated. The pain may continue and sensory paralysis may be associated with herpes. hite or red, appear, at times spontaneously, and always Urticaria (1201). 1167 ■h patches of urticaria sometimes itch and sometimes ly size, api)car on the skin and mucous membranes. Sev- Pemphigus. 1168 ways some burning sensatiim and the pain nyiy be in- , legs. The disturbances are limited to the area of dis- Leprous Neuritis. ll(i!l ire nerves. All forms of sensibility are abolished. Small ng the nerve trunk, together with other manifestations 3, when, as is usual, the trophic disturbances are limited Syriim'(jniyrliM or Morvan's diseise (.")."p3, tJ'cK}. 1171.1 Pain and temperature sense lost, with persistence of 840-2. Kmit, ll."2. 1187). (Pigs. 2.5-7). r affected area. Kyphosis and spondylitis are common the skin and occurring only in bed-ridden patients usu- Bed Sores. Decubitus. 1171 reurring almost always on parts subjected to much pres- arts are not kept scrupulously clean. ot growing larger superficially, but slowly and painlessly Perforating Ulcer of Tabes and (rarelyl Syringo- 1172 irough the foot and appears on its dorsum. Such an ices as a corn, which ulcerates and the pus, escaping, upillary reHexes and other symptoms of tabes are pres- je urine in a small minority. atism. In cases of arsenical neuritis, the skin is often Neuritis (4SS-02, 824, 940-9, 1147). ]17ii CHART XVIIc Trophic Disorders of Fat, Bone and Joints Comprising Numbers 1125 to 1128 and 1137 to 1141 on left side of Chart and 1174 to 1188 on right margin 209 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANALYSIS TROPHIC DISORDERS OF ABSTRACT OP SYJ 112C RONR TISSTTR. 1127 JOINT DISRASE 1128 OTHER TRO- I'lIIC LESIONS. fn37 1125 FATTY TISSUE. .\trophy. 1138 Hypertrophy. fll3Sa Failure in flevplopinent. 1139 Atrophy. 1140 Hypertrophy. 1141. Fragility. One of the ("iirliest symptoms of diabetes mellitus is an inability of the body to de excess of fat had been deposited. Patients lose weight and if the disease is lor urine shows the constant presence of sugar. Atrophy of fat and emaciation o r.arye and tender deposits of fat, in lumps or in layers, widely diffused over arms Arms and legs painful and tender, especially in the acute stage when the fat is frequently m middle aged women (often alcoliolie or syphilitic). Excessive accumulation of fat, especially on buttocks, pubes and breasts. Deedenc Many cases occur, either congeuitally or acquired in early life, in which the bony so that the individuals remain throughout life of abnormally small stature. Tin ^ due to atrophy or loss of function of the pituitary gland. Some of these individi (simple dwarfs or decidedly undersized menl. while others show many pliysic elsewhere, under infantilism and mongolism (lOr*.".), cretinism (10!l.'), IKy.) an dro-dystrophia fo-talis) there is a dystrophy of the epiphyseal cartilases, in couse in length ; so that dwai-fism results. The head is relatively long, the bridge of t) their proximal si'gment, the hand is short, the fingers broad, of almost equal lem pelvis contracted, legs often bowed or knock-kneed and joints ab normally lax. Adults, as well as diildren, not Infrequently become shorter in consequence of e: as in rickets, osteitis deformans (11S2), osteomalacia (1185), etc., and in conse (•In cases of extensive acute anterior poliomyelitis and of cerebral palsy of childhoa growth or very slow growth of the part from disuse. * One side of the face is much smaller than the other, due to atrophy of all the tiss and fat. The process is usually progressive. It seems to be caused by injury,; geminal neuritis. Dryness, scaliness and loss of color of the skin are common "syi which a small area atrophies, which atrophy gradually extend-^ laterally over^ bones. The process continues until the entire half of the face is atrophied and,i even to other parts of the body. One side of the tongue is usually atrophied. F accompanies the atrophy. 'One side of the face is much larger than the other, due to enlargement of all the t ally progressive, and seems in some cases to be due to a periostitis. The bones of the head and face are enlarged, diffusely or nodulated . and may cause them. Headache, neuralgia, blindness, deafness and facial paraljsis are, thus, ' are not enlarge3), can be produced by the i be curwl by extirpation of the thyroid. Paroxysmal spa.sm or congestion of the hroncliioles, often reflex from nasal disea nervous temperament of most asthmatics, together with the very rapid onset ai may be due to a disturbance of the thoracic sympathetic. The paroxysmal aft.' prolonged expiratory murmur, nnike the diagnosis easy. Asthma is associated he in part voluntary, in part reflex; also is usually associated with bronchitis. 'Paroxysmal attacks of sub.iective and objective coldness and pallor ("dead linger) or tip of nose or of eai-s or of all together. These attacks may last a few minu lowed by an attack, in which the same parts become dusky blue, or purplish bl This is associated with pain. This attack may pass off, after several hours, wi tion of them, nuiy become gangrenous and finally slough off. The necrosis dot The disease is usually s.vmmetrical. It is more common in cold weather and is b.v working with hands. Paroxysmal hemoglobinuria and evidence of cong&stii tacks. A hemiplegia and in other cases a coma, both transitory, have bein desc .Vnalogous to Ra.vnaud"s disease is gangrene of extremities occurring in many met old age; either without the local syncope or local asphyxia, or wilh only slight : j Parox.vsmal attacks of formication, tingling, numbness and other parestbesiae in fi tervals and exclusively in women. They seem to he brought on b.v overwork ai J diirin;; the attack the skin becomes pale and blue. Similar symptoms sometlm I Paroxysms of severe pain in one foot, rarely in both, rarelj' in hands and very ri I increased b.v allowing foot to hang down, or by motion of it, or by cold. The p; re."i). 1101 Iiilation of pupil (mydriasis), exophthalmos, eyelid when eye is turned downward (Graefe's :his disease and in exophthalmic s(iitre (1193). !scpnt of upper eyelid when e.ve is turned dowu- d systolic murmur in vessels of neck and over ough many of its symptoms may be referred to on of the thyroid iiland. Many of its symptoms, nistration of thyroid gland, and the disease can hriliiticm of Cervical SyiU]inlbelic. l'".xopliihalniic Coitre (UTi'). 1192 11!):! Freedom from symptoms in llie interval. The .\s ssation of the attack, indicates that the disease of dyspnoea, with the abundant dry rales and strong contraction of the diaphragm, which may (r.ic.t. ll'.M "local syncope") and tingling of fingers or toes ov hours and then may pass off, or may be fol- ("local asj)hyxia or cyanosis") from congestion, bundant sweating, or the parts, or a small por- it usually involve the whole of the cyanotic area, f'n brought on by putting hands in cold water, or if other internal organs may occur in some at- d in a few cases of this disease. ■s of a family at varying ages from childhood to .■ations of these conditions in some of the cases. ■s and hiLnils. The attacks occur at irregular in- y having the hands in cold water. In some eases ccur in t:he early stages of acromegaly (1183). ■ in face, lasting a few minutes or a few hours. except in the earliest attacks, is accompanied by >n only, and is generally due to a neuritis, rarely ith atheromatous arteries. lainful cramp occurs in muscles of legs after a short rest to return if walking is resumed. Dur- in the dorsalis pedis or posterior tibial artery. on. The disease not infrequently precedes gan- y due to arteriosclerosis associated with vaso- U;lyii:iiiir> I loll I. Disease Svmnietrical (Jangrene Hit." Family (iangrene. .Vcrnparesthesia. Krythrnnielal-ia nOHH. Intrrniiltei'l Limping or Aiigiiisrlerotic'.M i"C<) . 119(1 1197 11 OR Claudic.'ition. Dvsbasia 1100 lines appear for a few secomls white, but soon DernHigr.-ipbia (o'iti. IIIIT). 1200 ig localized with pyrexia or gastric disturbance. d, sometimes general. .\ngio-Neurotie Edem.i ami T'rticnrin. (11071. 1201 (Juincke's Diseasi'. Milroy's or Meig's Disease. Trophcsleiua. 1202 Ilyperhiilrnsis. Excessive Sweating. 12(K! M CHART XVIII Syphilis of the Nervous System Comprising Numbers 1205 to 1217 213 DIAGNOSTIC ANALYSIS SYPHILIS OF THE WEI DIAGNOSTIC SYMPTOMS AND TESTS 1205 SYnilLIS OF THE NERVOUS SYSTEM. History o£ personal, or hered- itary, syphilis. Physical evi- dence of syi)hilis ; such as Wa.ssermann reaction, a chancre or its scar, indura- tion, raucous patches, a syphi- litic rash or its copper colored scars, hazy cornea, notcheh- Symptoms of spinal meningitis, or of pachymeningitis (551, 605, ro- 974. 1005). Rigidity of back. Girdle pains and r.iidiating pains, par e.\ai;gerated rcliexes in legs. Some of these cases present the symptoms of i>ri>gressive spinal muscular atrophy (548), )h- .V combiuatioii of the aliove .symptoms, noted under 1208-9-1.3, in lal very varying extent and intensity. .\ clinical picture comprising cerebral and spinal symptoms ami presenting great variations, which are impossible to describe in a few words. he Symptoms of neuritis (4SS-92, 824^, 940-8). Spinal Syphilitic Endarteritis and 1211 Thrombosis. Rrb's Syphilitic Lateral Sclerosis. 1212 Syphilitic Meningitis of Cord and 1213 of Nerve Roots. (Meningo-raye- litis. Pacliymeningitis Cervicalis Ilypertropbica.l Cerebro^Spinal Syphilis. Syphilitic Neuritis. 1214 1215 Symptoms of general paresis (1106). Symptoms of locomotor ataxia (661). Paresis. 1216 Locomotor Ataxia. Tabes. 1217 (Fig. 27.) CHART XIX Abnormal Cerebro-Spinal Fluid Comprising Numbers 1220 to 1244 215 ri22i Globulin test positive. Wiiite cells increased. 1223 Leucocytosis. 1224 Lymphocytosis. 1220 ABNORMAL CEREBRO- SPINAL FLUID. 1222 Globulin test negative. (.White cells not increased. DIAGNOSTIC ANALYSIS OF ABNORMAL CEREBROSPI] TESTS Weichselbaum's diploooccus in- tra-cellularis meningitidis or rarely Pneumococcus. Weichselbaum's diplococeus, Pneumococcus, Pfeiffer's ba- cillus, Streptococcus, Staphy- lococcus, Typhoid bacillus or Bacterium coli, etc. Tubercle bacillus. Tubercle bacillus. AND DIAGNOS Fluid may be clea Tension increase< Fluid usually cloud liisli tension. Fluid usunlly clea cate coagulum high tension. Wassermann and Colloidal Gold reactions positive. Fluid clear bacteria. and [Wassermann and Colloidal Gold reactions negative. Tension is usualli but not very high 1225 No lymphocytosis. No leucocytosis. No bacteria and Wassermann negative. Fluid clear with inc si on. :oMs LUID HNS udy. Ocours iu fpiiloiii- DIAGNOSIS Symptoms of epidemic Cerebro- I'Ipitlemic Cerebi-o-spinal Meniu- 12li%». 1254 I Sacral 1255 V Lum- bar Paralysis Muscles of anus. Muscles of bladder. Muscles of genitals. Pyriformis. Abductor halluds. Flexor hallucis ■i brevis. T-IV dorsal interossei. I -1 1 1 plantar interossei. III-IV lum- bricales. Abductor minimi dijfiti. Onponens . minimi digiti. Paresis 1 Muscles of anus and rectum. Muscles of bladder. Muscles of genitals. Pyriformis. Biceps femoris. Flexors of toes. Peroneus longus. Peroneus brevis. Gluteus maj^mus. Obturator intemus. Gemellus superior. Gluteus medius. Gluteus minimus. Biceps femoris. Semimembranosus. Semitendinosus. Popliteus. Gastrocnemius. Soleus. Tibialis f)osticus. Peroneus longus. Peroneus brevis. Flexors of toes. Extensors of toes. Gemellus sui)erior. Gemellus inferior. Gluteus medius. Gluteus minimus. Semimembranosus. Semitendinosus. Gluteus miximus. Tensor fasciae femoris. Gastrocnemius. iSoleus. Extensors of toes- Tibialis anticus. Actions lost or impaired Absent . Anesthesia In- with a zone of creased hyperesthesia in surrounding partial it or limiting lesions it above tu Retention of feces. Retention of urine or dribbling. Erection and ejacu- lation impiossible. Outward rotation of thigh im- paired. Internal rotation impaired. Flexion of knee difficult. Plantar flexion of foot. Raising inner mar- gin of foot. Raising outer mar- gin and dorsal flexion of foot. Flexion and extension of toes, adduction of great toe, abduction of little toe, etc. Defecation. Micturition delayed, dribbling. Erection and ejacu- lation impossible. Outward rotation of thigh very difficult. Inward rotation impaired. Flexion of knee difficult. Retraction of thigh very difficult. Flexion of foot barely possible. Flexion of toes impossible. Extension of toes weak, except great toe, which may be dorsally flexed. Raising inner margin of foot difficult. Raising outer mar- gin of foot im- possible. Plantar None weakened. Achilles- tendon reflex. Ejaculation. Erection. Micturition. Defecation. Gluteal. As above, and a strip on posterior and outer surface of lower legs and of dorsum of foot and especially of toes. Ejacu- Plan- As above, and lation. tar. back of thighs Erection. Tendo- and legs and Achil- inner and outer Us- margin and Micturition. sole of feet. Defecation. Gluteal. 221 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS AT DIFFERENT LEVELS OF THE CORD (Continued) Modified from Wichman Segment Reflex Sensory Involved Motor Conditions Conditions Conditions -( In- creased in > Anesthesia with a zone of hyperesthesia surrounding Actions lost or partial it or limiting Paralysis Paresis impaired Absent lesions it above Muscles of rec- Defecation, with Patellar Plan- As above, and tum and anus. fecal incontinence. may be tar. inner side of Muscles of Micturition, with wanting. lower l^s and bladder. dribbling. dorsum of feet Muscles of Erection and ejacu- and strip on genitals. lation impossible. outer posterior Obturator Outward rotation o; E surface of internus. Obturator thigh weak. thighs. Pyriformis. internus. Inward rotation Gemelli. impossible. Gluteus Retraction of thigh medius. impossible. 1256 Gluteus Flexion of knee IV minimus. lost. Lum- Gluteus Plantar flexion of bar maximus. Biceps femoris. Semi- membranosus. Semi- tendinosus. Popliteus. Gastrocne- mius. Soleus. Flexors of toes. Extensors of toes. Peroneus brevis. Peroneus lonsTis- Tihialis anticus. Rectus femoris. Vastus extemus. Va.stus intemus. Adductor magnus. Adductor brevis. Adductor minimus. Gracilis- foot lost. Flexion and exten- sion of toes lost. Raising outer mar- gin of foot. Raising inner mar- gin. Extension of thigh weak. Adduction difficult. Muscles of Vastus internus. All movements of Patellar Ankle- As above, and anus, bladder Rectus femoris. legs are lost, except and clonus whole of legs and genitals. Crureus. that extension of cremas- may except a tri- Outward ro- Adductors of thigh . legs is barely pos- teric. exist. angular area on tators of Flexors of thigh sible and that the front of thigh thigh. at the hips. thigh can be flexed with base at It! ward rota- on body by the Poupart's 1257 tors of thigh. psoas and iliacus. ligament. Retractor of Defecation and mic- III (flexor) thigh. turition are de- Lum- Flexors of knee. stroyed. bar Plantar flexors Urine and feces of foot. dribble and cannot Flexors of toes. be retained- Extensors of foot. Vastus extemus. 222 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS AT DIFFERENT LEVELS OF THE CORD (Continued) Modified from Wichman Involved Segment Paralysis Motor Conditions sisaaBj Actions lost or impaired Reflex Conditions In- creased in partial Absent lesions 1258 Paralysis of •SBOSJ II all muscles Lum- bar of lower extremity, except psoas. 1259 Total paralysis I of whole lower Lum- extremity. bar psoas included. Paralysis of lower extrem- 1260 ity, and gluteal XII region. to III Paralysis of Dor- abdominal sal and dorsal regions, gradu- ally added as the site of the lesion ascends. 1261 As in 3d II dorsal. Dor- sal 1262 All muscles Flexion of fingers. I of trunk and Muscles of the little Dor- lower ex- finger. sal tremities. Ill and IV inter- SBOS(j Complete paralysis of legs, rectum and bladder. As above. As above. ossei. Lumbricales. Pronator quadratus. Lower part of pec- toralis major. Lower part of pec- toralis minor. As above. As above and weakness in flexion of fingers. Pronation dis- turbed. PateUar, Achilles and cremas- teric. Achil- les may be in- creased. Plantar. Sensory Conditions ^ Anesthesia with a zone of hyperesthesia surrounding it or limiting it above Whole of legs and pelvis. (Testicles not sensitive to pressure.) As above, and paralysis of mus- cles of respiration causes diaphragm- atic breathing and dyspnoea. Cremas- Patel- teric and lar ab- Achilles. sent or "in- creased. Epigas- Patel- tric and lar, umbilical cre- reflex. mas- teric, Acliil- les and plan- tar. All below lost in complete division of cord. All subja- cent re- flexes. Oculo- All pupillary subja- symp- cent toms. re- ■■ * flexes- All below lost in complete division of cord. As above, and groins and front of scrotum and penis. As above, and a band running around body about two seg- ments below the one in- volved and limited above by a narrow zone of hyper- esthesia. As above, and a strip on the inner side of the upper arms. As above, and a strip on the inner side of the forearms. 223 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS AT DIFFERENT LEVELS OF THE CORD (Continued) Modified from Wichman Segment Reflex Sensory Involved Motor Conditions Conditions Conditions Anesthesia with a zone of In- creased hyperesthesia ■^ in surrounding it or limiting Actions lost or ^ in >artial Paralysis Paresis impaired Absent esions it above Paralysis of Flexors of the lit- .\s above. Oculo- All As above, and muscles of tle finger. pupillary below. the fingers, trunk and Opponens minimi symp- except volar lower extrem- digiti. toms. surface of the 1263 ities. Flexor subl. digi- thumb and the Vlll Abductor of torum. ulnar surface Cer- little finger. Flexor pro fun. digi - All below of the little vical Adductor of torum. lost in finger. thumb. Flexor carpi ulna- complete Flexor of the ris. division The cervical little finger. Extensors of the Hand weak. of cord. sensory nerve Opponens thumb and fingers. roots supply the minimi digti Triceps (slight). Extension of arm. same area of the III and IV Latissimus dorsi Int. rotation and skin in common, interossei. (lower part). retraction of arm. especiallv in the Lumbricales. Pectoralis major. Pectoralis minor. Scalenus medialis. Scalenus posticus. Adduction of arm hands and fin- gers. Hence the anesthesia is slight and un- certain. Lower ex- Extensors, As above and Arm All As above, and tremities and Flexors Hand very weak. reflexes, below. most of the trunk. and Retraction and in- Forearm hands and a Flexor pro- Abductors ward rotation of reflexes. .small strip on fundus digi- of thumb. arm. Palmar the anterior. 1264 torum (ulnar Exte:isor indicis. (Winged scapulae" ) reflex. another on the VII side). Extensors of the posterior, sur- Cer- Flexor carpi fingers (movements face of the vical ulnaris. barely possible). All below foreanr). Small hand Supinator longus. lost in muscles. Biceps (very slightly complete Pronator paretic. ) cord quadratus. Triceps Pectoralis major. Serratus magnus (slight). Latissimus dorsi. Teres major. division. 224 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS AT DIFFERENT LEVELS OF THE CORD (Concluded) Modified from VVichman Se NSORY Reflex Conditions Conditions Motor Conditions Conditions Sensory ^ Anesthesia t -*■ In- with a zone of creased hyperesthesia surrounding f "^ in Actions lost or partial it or limiting Paralysis Paresis impiiired Absent lesions it above. Muscles of Coraco-brachialis. As above and Arm All As above, and lower extrem- Biceps. movements of fin- reflexes, below. whole of hands ity and trunk. Bracliialis anticus. gers and thumb Extensor and fingers and ^luscles of Supinator brevis. impossible. forearm radial side of fingers (in- Deltoid. Extension of fore- reflexes. forearm. 1265 cluding thumb) Scaleni. arm. VI and hand. Splenii. Flexion of forearm Cer- Triceps. Deep head and weak. All below xncal Pectoralis neck muscles. Supination very lost in major. weak. complete Latissimus Adduction of arm cord dorsi. and inward rota- division. Teres major. tion. Infraspinatus. Adduction, retrac- Serratus tion and external ro '- magnus. tation. (Winged scapulae.) Raising of arm. Rotation of head'. Fatal in a few days or weeks. Muscles of Levator anguli As above and Scapular .All As above, and lower extrem- scapulae. shoulders raised and below. whole of arms, ities and Scaleni. with difficulty tendon except tip of trunk. Diaphragm ( be- Rotation and flex- reflexes of shoulder. .■Ml the mus- cause of filaments ion of head. paralysed cles of the from V cervical seg- Dyspnoea. muscles 1266 arm. forearm, ment to phrenic Fatal in a few in arms. V hand and fin- nerve), or spread of hours or days. Cer- gers; even the injury from 5th vical deltoid, to 4th cervical -All below coraco- segment. lost in brachialis and Trapezius and complete brachialis sterno-cleido-mas- cord anticus. toid are int.ict. divi-sion. Deep cervi- cal muscles. Intercostals. 1267 Total cross-lesions from the fourth cervical segment upward are rapidly fatal, because iV-I of complete paralysis of the diaphragm and intercostals. Cer- vical Total cross-lesions of the brain-stem are rapidly fatal for the same reason. 22: B.— TABLE OF SYMPTOMS ACCORDING TO AREA INVOLVED IN TRANSVERSE SECTION OF THE SPINAL CORD 1268 Lesions of anterior horns, i Acute anterior poliomyelitis (495, 789, 1148, 1233, 1324.) Chronic atropluc paralysis (547-8, 695, 1150, 1324.) 1269 Lesions of posterior horns; sensory disturbances (1322.) 1270 Lesions of pyramidal tract; Spastic Paraplegia (525-47, 800, 1212, 1384-6-9, 1406.) 1271 Lesions of posterior columns; Tabes (661, 785-6, 1322, 1360, 1363-4, 1406.) 1272 Lesions of direct cerebellar tracts; Hemiataxia (653.) 1273 Lesions of postero-lateral columns; Ataxic Paraplegia (526, 660, 799, 1360, 1406.) 1274 Lesions of spino-thalamic tract; Dissociation of sensation (812, 1369.) 1275 Lesions of anterior gray commissure; Syringomyelia (552, 693, 798, 840-2, 1370-2.) 1276 Lesions of entire lateral half ; Brown-Sequard paralysis (442, 509, 844, 975-82.) 1277 Lesions of posterior spinal ganglion; Herpes Zoster (940, 978, 1166, 1235.) 1278 Lesions of posterior nerve roots; Tabes a:id Herj>es Zoster. 1279 Lesions of anterior nerve roots; Atrophic paralysis. 226 CHART XXI Cerebral Localization Comprising Numbers 1290 to 1309 227 CHART XXIa Cerebral Localization in the Medulla and Pons* Ganglia at Base Comprising Numbers 1290 and 1292 229 Seat of Lesion 1290 r.esion involving latoral half of the Medulla Oblonsata : Avellis' syndrome. Babinski (427). and Nageotte's Bulbar Syndrome. liarc because of the small transverse area of the ni-^^ 'Lesion BUateral. more May be blind- Movement Pupil Usually May be Normal. Nystagmus (at confined or less exten- ness without of eyeball. reflex lost absent. absent. times vertical). to sive, of all ocu- choked disc or to both squint, pupils anterior lar muscles. other lesion. light and often unequal. pair except the accommo- (nates). abducens. dation. May be slow, Lesion None or may May be deaf- None, Normal. Usually Present. Normal. rhythmic confined be slight ness, if lesion except present. Of cere- tremor of arm to paralysis as be bilateral. chewing bellar and leg of posterior above, or of at times. type. opposite side. pair trochlearis. especially on .(testes). voluntary motion. None. None. Walking Normal Usually Cere- Normal. Nystagmus and or present. bellar (SO), tendency standing slightly exagger- ated. R.irely abolished. ataxia wiUi hypo- tonia almost always present. to fall to one side, occipital headache is frequent, cerebellar fits may occur. None. None. Walking, Normal Usually Usually Normal. Tendency to standing or present. present fall or to turn and slightly with eyes, head or sitting. exagger- ated. hypo- tonia of the cere- bellar type. body to one side. Rotatory movements, more or less pronounced, choreic-spasms in homolateral Lesion of iiif(>rior cerebellar pedu Qcles cause lateropulsion ; those of the su- half of body. perior ■erelu'llar peduncles cause choreiform movements and cerebellar and vertical ataxia. divergence o£ the eyeballs sometimes occur. Fractures, tumors, etc., at base of skull may cause many of the above symptoms according to their position, but their early and characteristic symptom is paralysis of one or more of the cranial nerves. Symptoms of pa- ralysis predominate over those of irritation. Small lesions, not so extensive as to involve the entire lateral half of the brain stem, may occur at any point. The symptoms of these lesions depend upon the function (physiology) of the part affected and will naturally vary greatly. The location of such a lesion in a transverse section will depend upon what longitudinal fiber tracts are involved, and in longitudinal section upon what cranial nuclei and nerve tracts are involved, aa shown by the symptoms present in any case. A study of the figures at the end of this book is essential for the localization of such lesions and will serve this purpose better than a long verbal description. 231 CHART XXIc Cerebral Localization: Ganglia at Base LOCALIZING SYMPTOMS IN LESIONS OF GANGLIA AT BASE OF BRAIN Seat of Lesion 1298 Optic Thalamus. (Fig. 17) (837a) Nucleus Lentic- ularis and Nucleus Cauda- tus. 1299 Corpus Stri- atum. (Fig. 17) Inter- nal Cap- sule. 1300 Corpus Callosum. 1301 Island of Riel Qau strum and External capsule. (Fig. 17) 1302 Pituitary Gland. 1303 Pineal Gland. Diagnostic Symptoms Is the highest and most important center for complicated automatic actions. It is the seat of the emotion of anger and probabl}', in large part of pleasure and well being. Disease of tliis organ may give rise to few characteristic symptoms. There may be hemiaiiopia (pulvinar and external geniculate involvement) vrith hemiopic pupillary reaction and contralateral sensory disturbances with conse- quent incoordination. In lesions of the optic thalamus occasionally a slight irri- tation of the skin is not felt at all, while a stronger one is felt inordinately. Absence of emotional expression in face, even when not paralysed. Vaso-motor disturbances may occur in opposite side of body. Isolated analgesia and thermic anesthesia do not occur in lesions above the optic thamus. In rare cases a lesion of the nucleus lenticularis may be of such a form as to injure the anterior and posterior part of the posterior limb of the internal capsule, while its middle part escapes. In such cases there results a hemiplegia which involves the leg and face more than the arm. Dysarthria is a not uncommon symptom and in some cases the symptoms of sensory irritation and incoordination described under lesions of the optic thalamus have been present. When the ganglia on both sides are affected, voluntary voiding of urine may be impossible, while au- tomatic involuntary voiding may occur at regular intervals. The most characteristic s\Tnptoms due to lesions in the corpus striatum are rigidity ( Park- inson's disease^— 677), choreiform movements (Huntington's chorea — 624) and athetosis ( Post-hemiplegic — 632 and Bilateral — 631). These symptoms aisp form part of the syndromes known as : pseudo-sclerosis — 667, progressive lenti- cular degeneration and dystonia lenticularis (668). ' Lesions in the anterior limb of the internal capsule cause either no symptoms or a paralysis of contralateral half of face. There may be ataxia and athetoid move- ments. Lesions in the anterior two-tliirds of the posterior limb of the internal capsule cause a total contralateral hemiplegia of the body. This hemiplegia consists purely of a muscular paralysis and never produces a paralysis of the cortical functions such as aphasia, alexia, etc; but may produce dysarthria. Lesions in the posterior third of the posterior limb of the internal capsule cause hemianesthesia and loss of muscle sense on the opposite side of the body. Lesions at the extreme posterior end of the posterior limb of the internal capsule, in addition to hemianesthesia, cause contralateral hemianopia, deafness, only if the lesion be bilateral, and often the symptoms of motor irritation, described under lesions of optic thalamus. No diagnostic symptoms. Symptoms of ingravescent character, gradual develop- ment of hemiplegia, with slight hemiplegia of the other side also, drowsiness, dysarthria and anarthria. Death in coma (Bristow's syndrone). Lesions in this area produce disturbances of speech, grouped under the general term paraphasia, and may produce anarthria, the result of complete aphasia. Hypertrophy, tumor, hemorrhage and some other lesions of the gland associated with excess of secretion may cause acromegaly or gigantism, in addition to a progressive bi-temporal hemianopia, terminating in blindness. A defect or atrophy of the gland associated with a diminution of secretion in early life may cause dwarfism and may produce pituitary eunuchismus or adiposogenital de- generation with excess of fat and a defect in the formation of the genitals. In any case of pituitary disease there may be polyuria, polydipsia and occasionally glycosuria and very rarely an escape of cerebro-spinal fluid from the nose (hydrorrhoea nasalis). In some cases of pituitary disease there are no symp- toms. Abnormal growth of hair and deposition of fat. Abnormalities of genitals (at times with attacks of sexual excitement, eunuchismus). Excessive growth in height of body (dyspinelismus). In consequence of involvement of adjacent tissue, bilateral ocular paralysis, nystagmus, pupil abnormalities, ataxia, and per- haps disturbances of hearing may be present. 233 CHART XXId Cerebral Localization: Lobes of Brain LOCALIZING SYMPTOMS IN LESIONS OF CEREBRAL HEMISPHERES Seat of Lesion 1304 FRONTAL LOBE Contains the centers for all the skilled acts, especially the left lobe. Large lesions in the frontal lobes may cause a change in character and disposition of the patient. Many lesions, especially tumors, cause Jacksonian epilepsy, especially when sit- uated in posterior part of lobe ; while lesions in anterior part of lobe may cause epileptiform convulsions. Ataxia sometimes occurs in tumors in the fron- tal lobe. (Fig. 15) rThe ascending frontal convo- lution. Lesions in this region may cause awkward- ness ( cortical ataxia or apraxia) rather than paralysis. Diagnostic Symptoms Lesions in the upper fourth of this convolution may cause Jacksonian epilepsy commencing in, and motor paralysis of, the contralateral leg. Very large lesions (hemorrhage, tumors, etc.) in tliis region may cause also paralysis of the homolateral leg in a lesser degree. Lesions in the middle half of the convolution may cause Jacksonian epilepsy commencing in, and awkwardness of or loss of skill or complete paralysis of the contralateral arm. Very minute lesions in the upper part of this region may affect only the shoulder ; in the lower part, only the hand. Lesions in the lower fourth of this convolution may cause Jacksonian epilepsy commencing in, and paralysis of, the contralateral half of face and neck. Very minute lesions in the upper part of this region may affect only the eyes; in the lower and anterior part, the tongue and larynx. The base of the middle left fron- tal convolution. Small lesions in this area may cause in right-handed per- sons, agraphia, and in many cases Jacksonian epilepsy, commencing in the contralateral arm. The base of the Small lesions in this area may cause, in right-handed per- inferior left fron- sons, motor aphasia, and in many cases Jacksonian tal convolution. epilepsy, commencing in the right side of the face. f 1305 PARIETAL LOBE Contains the centers for cutaneous and muscular sensation. Many lesions, espe- cially tumor, cause Jacksonian epilepsy when situated in the anterior portion of this lobe ; while lesions in posterior portion may cause epileptiform con- vulsions. (Fig. 15) The ascending parietal convo- lution. [^ Lesions in the upper fourth of this convolution may cause some blunting of cutaneous sensibility, and especially I astereognosis in contralateral leg and foot. I Lesions in the middle half of this convolution may cause i some blunting of cutaneous sensibility, and esi>ecially I astereognosis in contralateral arm and hand. I Lesions in the middle half of this convolution may cause j some blunting of cutaneous sensibility, and especially L astereognosis in contralateral half of face. The left ang- ular gyrus. The rest of the t parietal cortex. 1306 TEMPORAL LOBE Contains, on the left side, the centers of sensory speech. Lesions may cause epileptiform con\'ulsions. (Fig. 15) Lesions in this region may cause loss of muscular sense and motor ataxia in the contralateral arm and leg. Deep lesions in this region in right-handed persons may cause alexia and hemianopia. Lesions in the posterior portion of the left superior tem- poral convolution in right-handed persons, mav cause sensory aphasia (psychic deafness.) 235 LOCALIZING SYMPTOMS IN LESIONS OF CEREBRAL HEMISPHERES (Concluded) Seat of Lesion Diagnostic Symptoms 1307 OCCIPITAL LOBE Contains the centers of sight. Lesions may cause epilepti- form convTilsiohs. (Fig. 15) Neigh- borhood of calcarine fissure. I Rest of occipital (^ lobe. Lesions in this area cause contralateral homonymous hemi- anopia. A lesion limited to the superior lip of this fissure causes quadrantic hemianopia or tetartanopia of the con- tralateral lower quadrants of field of vision. A lesion lim- ited to the inferior lip of this fissure causes loss of contra- lateral upper quadrants of the field of vision. Lesions in this area may cause loss of power of recognition of persons and things (psychic blindness). 1308 Many lesions cause a mixutre of paralysis and convulsions over a limited area Cortical Lesions. which in some cases may slowly grow larger. The intelligence of the patient is (Fig. 15) always more or less impaired. 1309 1-ocalized lesions in the white substance of the brain (centrum ovale) may involve Sub-Cortical the fibers of the corona radiata. Such lesions when lying close to the cortex will Lesions. cause the symptoms characteristic of lesions of the overl}'ing cortex, but are not quite so sharply defined. In especial, Jacksonian epilepsy and mental symptoms are less pnonounced than when resulting from cortical lesions. 236 CHART XXII Cerebro-Spinal Localization TOPICAL DIAGNOSIS LOCALIZATION OF LESIONS FROM ANALYSIS OF SYMPTOMS ri314 _ 1 Sensation alone, in all its forms is lost or impaired 1310 PARALYSIS The most important of all localizing symptoms. 1312 The reflexes in the para- lysed area are abolished (except in 1310 and 1329) A lesion of the periphera] neurons. 1315 Motion alone is lost oi impaired. 1316 Both motion and sensa- tion are lost or impaired J I See Chart XXII a. 1313 The reflexes are preseni (except in 1357 and 1359) A lesion of the centra! neurons. 1317 Special forms of " pheral paralyses. 1318 Sensory paralysis nant. Little or no paralysis. peri- See Chart XXII b. domi- raotoi See Chart XXII c. See Chart XXII d. 1319 Motor paralysis domi- nant. Little or no sen- sory paralysis. 1320 Both motor and sensory i >■ paralysis well marked. I See Chart XXII e. 1311 I Jacksonian Epilepsy, together with other symptoms of cerebral disease. j For diseases and lesions accompanied by motor paralysis see 469, by motor spasm see 570, by ataxia see 638, by tremor see 639, by nystagmus see 640, by fibrillation see 641, by local para- lysis see 636, by local spasm see 637, by disorders of speech see 735, by disorders of gait see 736, by anesthesia and analgesia see 811-15, by disorders of special senses 808-10, by pain see 931, by vertigo see 932, by mental disorders see 1036, by trophic disorders see 1121, by vaso-motor dis- orders see 1130, by ganglionic disorders see 1129, by syphilis see 1205, by abnormal cerebrospinal fluid see 1220. 237 CHART XXIIa Cerebro-Spinal Localization Paralysis with Abolished Reflexes R E F Ti E X E S A B O Ij I S E D 1314 Sensa- tion alone, in all its forms, is lost or im- paired. I 1315 Motion alone is lost or im- paired. 1310 Both motion and sensa- tion are lest or im- paired. TOPICAL DIAGNOSIS LOCALIZATION OF LESION FROM ANALYSIS OF SYMPTOMS Diagnostic Symptoms and Tests Localization Area of anesthesia. Onset etc., lies within ni-nte the area of distri- or sub- bution of one or acute, more nerves. Area of anesthesia. Onset etc., lies within nciite the area of distri- nr bution of one or chronic. more nerve roots. Nerve involved, if palpable, is Lesion is in one or more sen- 1321 The paralysis is limited to mnsclM supplied by ouc or more nerves. (Figs. 19-21.) Tbn paralysis is limited to muscles supplied by one or more nerve roots. (Figs. 19-21) Onset .icutp or sub-acute. No fever at onset. Onset :.o). •esent. svidence of disease within orbit. Lesion is within the orbit (915). 1338 nerves paraivsed. Lesion of 3rd cranial nerve truuk or nucleus (TOO). 1339 (Fig. IS). jposite side. Lesion involving one cms cerebri (676). 1340 posite side present at rest and exaggerated on Lesion of red nucleus or rubro-spinal tract on same side 1341 as motor oculi paralysis (4.'^1, G76). ■anial nerve CTOO). Lesion of 3rd cranial nucleus, in whole or in part 1342 (700). (Fig. IS). nerves paralysed, especially the facial. Lesion of fith cranial nerve or nucleus (1346-7). 1343 (Figs. 19, 20). ith hemianesthesia of opposite side. Loss of Diffuse lesion of Pons Varolii (53S, 885). (Figs. 1344 1 of eyes to right or left. Facial or auditory 19, 20). he brain present. Electrical reaction of degen- Lesion above nucleus of facial nerve in cerebral hemi- 1345 xes present. spheres or in crura cerebri. (Figs. 15, 10). josite side. Often abducens paralysis. Lesion in Pons Varolii. (Figs. 19, 20). 1346 usually. ■ Other cranial nerves, especially audi- Lesion of nucleus of facial nerve. (Figs. 19, 20). 1347 ffected. ess anrl vertigo without di.sease of the ear. Lesion of facial nerve trunk at liase of brain (Fig. 19). 1348 d tinnitus aiirium, due to stapedius paralysis. Lesion of nerve above geniculate ganglion (928). 1349 li notes also, are painful to hear. No loss of (Fig. 36). cretion of tears. aterior two-thirds of tongue of same side. Lesion of facial nerve between geniculate ganglion and 1350 stapedius branch. (Fig. 36). 1 anterior two-thirds of tongue of same side. Lesion of facial nerve between stapedius and chorda 1351 tympani branches. (Fig. 36). e. Tenderness near stylo-mastoid foramen. Lesion of facial niTve below chorda tvniiiani branch. 1352 (Fig. 36). CHART XXIIc Cerebro-Spinal Localization Comprising Numbers 1318 and 1353 to 1359 on left side of Chart and 1360 to 1383 on right margin 243 TOPICAL DIAGNOJ LOCALIZATION OF LESION FROM AN ANESTHESIA WITH EXAGGERAT DIAGNOSTIC SYMPTOMS AND TESTS r Marked ataxia. r Limited to one or both legs. Limited to one arm. In both arms and both legs. 1353 ANESTHESIA with or with- i out ANALGESIA. lu arm and log of same side. Slight ataxia. Slight ataxia. Marked ataxia. ["Marked ataxia. ^ Slight ataxia. In arm and leg of one side and Moderate ataxia, in other side of face. In arm, leg and face nf same side. Slight ataxia. 318 EN SORT ARALTSIS •OMINANT. JTTLE OR fO MOTOR ARALYSIS. ENDON .EFLEXES RESENT OR iXAGGBRATED. 1354 ANALGESIA with THER- MIC ANESTHESIA, but little or no tactile anesthesia, is present. DISSOCIATION OF SENSATION. rt'sually unilateral. In one or both | legs. 1 t Usually bilateral. In one or both arms. Usually unilateral. Leg of .same side also involved. Usually bilateral. Legs of normal sensibility. Anesthesia marked, bilateral. Ma of muscle sense. Anesthesia slight and most market be cerebral symptoms, Jacksonji .Anesthesia slight, most marked other cerebral symptoms (Jac paralysis. May be other spinal symptoms, in arms and legs. May be other spinal symptoms, in arm and leg. -\nesthesia slight, most marked i May be other cerebral symptoi May be paralysis of other cranial of the eyeballs. No Jacksonian epilepsy. Hernial Jacksonian epilepsy common. N; No trophic disturbances. No ( ataxia. Trophic disturbances in legs. Oi usually abolished, especially in No trophic disturbances. Often i Trophic disturbances in arms. ' especially in advanced cases. In arms, or legs, or both. Rilateral nsunlly, marked ataxia. TJnilatpral, slight ataxia. 1355 HOMONYMOUS HEMIANOPIA. 135C HOMONYMOUS TETARTANOPIA, QUAD- R.VNT HEMIANOPIA. 1357 PSYCHIC BLINDNESS. 1358 SENSORY APHASIA. .\uditory. Visual. 13.59 ASTEREOGNOSIS. May be other spinal symptoms, paraplegia). llemianopia and anesthesia usua .lacksonian epilepsy and other c thesia present. Symptoms of Thrombosis of the I In contralateral arm and leg witl Idenlical halves of each field of vision (right or left) are blind. No licmiopic pupillary of the occipital lobes may be present. Identical quadrants of each field nf vision (right or Icflt arc blind. No hemiopic pupill anesthesia or other paralysis. May be other cerebral syinplimis of lesion of the occipi Patient is not blind, but cannot recognize things by sight, though lie may by touch or hei Patient is not deaf, but cannot underetand words spoken to him, allhou^li he nnderslaiid; memory for spoken words. Patient is not blind but cannot umlerstand written words, although he understands them memory for written words. Alexia. Patient is not anesthetic, or very slightly so, but cannot recogniz e objects by the sense sight. YSIS OF SYMPTOMS REFLEXES LOCALIZATION ! other spinal symptoms, especially loss Lesion in one or both posterior columns of cord in dorsal region. Same 1360 side if unilateral (054, 7SC). (Figs. 24-6). . foot. -Vlmost always unilateral. May Lesion in upper one-fourth of posterioi- central convolution in contralateral 1361 jpilepsy, etc. cerebral cortex. (Fig. 15). hand, ascereognosis marked. May be l-Ksiou in middle one-half of posterior central convolution in contralateral 1362 aian epilepsy). Usually some motor cerebral cortex. (Fig. 15). 'Pnoea common. Loss of muscle sense Lesion of posterior columns of cord iu cervical region (654, 786). 1363 (Figs. 24-6). ;pnoea common. Loss of muscle sense Lesion of posterior column of cord on s;ime side, in cervical region (654, 1364 7S6). (Figs. ^-6). and and foot. Astereognosis marked. Lesion in upper three-fourths of posterior central convolution of contra- 1365 especially Jacksonian epilepsy. lateral cerebral cortex. (Fig. 15). rves. Paralysis of conjugate deviation Lesion in tegmentum of pons Varolii on same side as the facial anesthesia 1366 (885). (Fig. 20). » common. Lesion of posterior part of internal capsule of contralateral hemisphere 1367 (801, 1299). (Fig. 17). mianopia. Mental deterioration. Lesion of superior parietal lobule of contralateral hemisphere (657). 1368 (Fig. 15). rbance of organic reflexes. Usually Lesion in periphery of opposite lateral column of cord in dorsal region 1369 (1372). (Figs. 24-0). c reflexes disordered. Tendon reflexes Lesion in central gray matter (anterior commissure) of cord in lumbar en- 1370 •anced cases. (B^gs. 24-6). largement. In central gliosis the lesion may extend upwards to the cervical enlargement and involve the arms secondarily (840-2, 1372). a without loss of muscle sense. Lesion in periphery of the opposite, or of both, lateral columns of the cord 1371 in the cervical region (1373). (Figs. 24-6). on reflexes usually abolished in arms, Lesion in central gray matter (anterior commissure) of the cord in cervical 1372 enlargement (Syringomyelia) (553, 693, 840-2, 1009, 1152-70-87, 1370). (Figs. 24-6). Iways some motor paralysis (spastic Lesion of lateral columns of cord (053, 1212, 1309, 1371, 1400). (Figs. 24-0). 1373 present. Other cerebral symptoms. Lesion of posterior part of contralateral interu.il capsule (801). (Fig. 17). 1374 ral symptoms usually present. Ancs- Lesion of inferior parietal lobule of contralateral hemisphere (0.^)7). 1375 (Fig. 15). rior. Inferior Cerebellar Artery (1291). Lesion (softening) of the lateral half of the pons (1291). 1376 .fness. Lesion of ponto-cerehellar angle on side of deafness (428). 1377 ;. Other cerebral syniplonis of lesions Lesion of edges of calcarine fissure of occipital lohe, or of fasciculus of 137S Gratiolet of contralateral cerebral hemisphere (302, 817, 890, 1307-19-21). (Fig. 10). :eflex. No hemi- jbes. Lower quadrant of Lesion of upper lip of contralateral calcarine tissure (363, 817, 1307-19-21). 1379 field of vision. Upper quadrant of Lesion of lower lip of contralateral calcarine fissure (363, 817, 1307-19-21). 13S0 field of vision. (Fig. 10). He has forgotten what he has seen. Lesion of cortex of occipital lobe of left cerebral hemisphere (232, 1307). 13S1 (Fig. 16). n when he sees them written. Has no Lesion of cortex or subcortex of posterior part of left superior temporal 13S2 convolution or in the association fil)ers connecting the superior temporal with the inferior frontal convolution (222, 775). (Fig. 15). u he hears them spoken. He has no Subcortical lesion of the Angular Gyrus (777. 1403). 1382a )uch, although he can by the sense of Lesion in cortex or subcortex of the posterior central convolution of con- 13S3 tralateral hemisphere (229, 354). (Fig. l.T) 4 i CHART XXIId Cerebro-Spinal Localization Comprising Numbers 1319 on left side of chart and 1384 to 1403 on right mars^in 245 TOPICAL DIAGNO LOCALIZATION OF LESION FROM AI MOTOR PARALYSIS WITH EXAGG DIAGNOSTIC SYMPTOMS AND TESTS Limited to one or f Symptoms bilateral usually. May be otliei- spinal symptoms. Often at both legs. Organic J of sensation in legs. reflexes not dis- 1 ordered. [Symptoms unilateral usually. May be other cerebral symptoms, especi b'psy. Limited to both arms and both legs. Organic reflexes not disordered. 'No sensory paralysis. No cerebral symptoms. Often ataxia and dissoci arms and legs. Usually some sensory paralysis. Dysarthria and dysphagia. Paralysis ol ing with position of lesion. Limited to one Occasionally some slight sensory pariil.vsis. Jacksonian tpilepsy and oth arm. common. Limited to arm and leg of same side. Dissociation of sensation and ataxia may be present. Organic reflexes cerebral symptoms. Usually some sensory symptoms. Dysarthria and dysphagia common, crania! nerves frequent. ../..iLi.^ .Usually some st-asory symptoms. Jacksonian epilepsy and other sympton l.iTiiiti'ak. .YSIS OF SYMPTOMS ATED REFLEXES LOCALIZATION . and dissociation Lesion of homolateral, or of both lateral, columns of cord in dorsal region (1369 13S4 1371-3). (Figs. 25-7.) Jacksonian epi- Lesion of upper part of anterior central convolution of contralateral hemi- 1385 sphere, cortical or subcortical (leg center)- (Fig. 15). 1 of sensation in Lesion of lateral columns of the cord in the cervical region (525). (Figs. 25-7.) 13SH! nial nerves vary- Lesion of the brain stem (involvement of pyramidal tract in the medulla, pons 1387 or crura cerebri). (Figs. 19-22.) irebral symptoms Lesion in corte.x or subcortex of middle one-half of anterior centra! convolution 1388 of contralateral hemisphere (arm center). (Fig. 15.) disordered. No Lesion of contralateral lateral column of cord in cervical region. (Figs. 25-7.) 1389 iralysis of some Lesion in the brain stem (involving the pyramidal tract). (Figs. 19-22.) 1390 cortical disease. Lesion in cortex or subcortex of upper three-fourths of anterior central con- 1391 volution of contralateral hemisphere (Fig. 15.) t Lesion in cortex or subcortex of inferior part of anterior n'utral convolution 139-'' of contralateral hemisphere (face center). (Fig 15) cortical disease ! *^"'- I Lesioii of cortex or subcortex of lower three-fourths of anterior central convo- 1393 lution of contralateral hemisphere (arm and face centers). (Fig. 15.) and dysphagia. [ ^"'(Fil "n")^""" "'' ^^"^^ ^'"^^ "^ ^^^ hypoglossus paralysis (rare condition). 1394 imon, especially 4 I Lesion in bridge portion of pons on same side as the facial paralysis. (Fig. 20.) 1395 )f other cranial Lesion in pes cruris cerebri on same side as the motor oculi paralysis. (Fig. 19.) 139i! ■ sensory symp- Lesion in anterior part of posterior limb of internal capsule of opposite hemi- 1,'?97 sphere. (Fig. 17.) f emotional ex- i.f^iou in posterior part of optic thalamus and corpus striatum of opposite 139S "-• hemisphere. (Fig. 17.) ^'^^^^- I^esion throughout anterior central convolution of contralateral hemisphere 1399 (cortex or subcortex). (Fig. 15.) Lesion in tegmentum of pons or me- areas, and the location of the cortical functions. See 1304-9-61-2-S-8-72-81-3-5-8-91-2-3-9, 1401-3-10-S. 250 Fig. 1 6 Schematic representation of tlic median surface of the left cerebral hemisphere. U. L. Q. qiuulrant of both retinae. I,. L. U. — Lower left ciuadrant of both retinae. See S56-7-60, 1307-7S-80, T412. Upper left FACIAL \ ARM LEG HYPOGLOSSAL Fig. 17 Horizontal Section through Right Hemisphere showing the principal tracts situated in the Internal Capsule; Kn, Genu of Corpus Callosum ; F, Fornix; NC, Caudate Nucleus; NL, Lenticular Nucleus; OT, Optic Thalamus, Sp, Splenium of Corpus Callosum. See 1298-9, 1367-74-97-8. 251 Nucl. Comiss. post, ot ] I.TSC. long, dors, i F.isc. long dors. Kk'nurll Oculorn.-Kern •M Ifv.ilor palpcbr.ie. M. obliquus inferior M. rectus superior. M rectus internus. M jectus inferior. Fic. iS Sclicmatic reproeiil.iti'in ui ilu- niulel siliialcd liciie.itli the- ilcior of the Sylvian aqueduct, showing the origin of the posterior commissure, the oculo-motor and trochlcaris nerves, as well as the nuclear localization of the centers for tlie individual ocular nuiscles (after Edinger.) See 692, 700, 818, 1332. 252 post. root P'-Cerv. root 1 Cerv. Fig. 19 Schematic representation of brain stem ; showing nuclei and nerve roots. The sensory nuclei and nerve roots are colored red, the motor blue. See 1 32 1 -4-39-48-66-87-90, 1408. 253 '< <: •Deiter's pucV -spinal V -subst.gelat., anterolat. tn (Gowers) superi or oli Fig. 20 Diagrammatic transverse section through the pons at a level slightly posterior to the superficial origin of the trigeminus- See 1292, 1321-4-43-7-66-9S, 1401-8. rned. raphe I post lonr. fasc. -N soli tar. -V. spiral rt -subst.gelat. --N.am'big. dir.cerebel tr (Flechsig) - ant.lateral tr. (Gowers) — \nt arcuate fibres Fig. 21 Diagrammatic transverse section through the medulla, approximately near its middle. See 1290-1, 1321-4-94, 1401-8. 254 col. Go^l n. gracilis "Col.Biarda.c'h n.cuneatus - "Spinal V --subst .gelat,. " "TTit. arcuate fr. — ant.Viorn -lemniscus — olive Fig. 22 Transverse section of medulla just above motor decussation and just above line of junction with tlie cord showinii; tbe sensor\' decussation and the topography of the lowest level of the medulla. See 1290-1. Transverse section of the cord just at the line of iuncti m with the medulla. sIiowuil; the motor decuss' tion and the topography of the uppermost level of the cord. See i2go-r. 255 Fic. DfAORAMMATIC SECTION OF THE SPINAL CORD TO ILLUSTRATE ITS PHYSIOLOGY Left side shows situation nf lesions causing disorders of motion and sensation. Right side -jIiou s situation of lesions causing disorders of reflex activity. Destructive lesiniis at .M or E cause diminution, slijjht irritative lesionr.. exaggeration, of motion. Destructive lesions at S cause pennanent anestliesia, analgesia, thermic anesthesia and loss of muscle sense. Destructive lesions at T cause analgesia and thermic anesthesia. Destructive lesions at P cause ataxia. De- structive lesions at K cause loss of muscle sense, ataxia and anesthesia. Irritative lesions at S. K, T, or P, may cause exaggeration, or perversion, or both, of sensation. Destructive Ic^inns at D cause diminution, and at E, exaggeration, of reHex activity. Slight irritative lesions at D cause exaggeration, and at E diminution, of reflex activity. Symptoms of lesions at .\I are described in 252, 26,3, 41(5, 547-8, 791, 1 148-0, 12.VS and 1324: at E in 251, 254. -'56- j^S-f*- 70Q-800. IJ12 and 1384-6-9: at S in 826; at T in 1,169-71,1; at P in 281, 642-5,1; at K in 280, 654, 786, 1322-60-.V4 and I40(.i. The results of lesions at D and E are discussed in Chart Va. Cervical Enlargement Lumbar b'nlargenient Fir,. 25 LOCALIZATION OF NUCLEI IN THE ANTERIOR MORNS OF THE SPINAL CORD (After Edinger modified from Sano.) 256 Fig. 26 A SCHEMATIC REPRESENTATION OF A TRANSVERSE SEt'TION OF THE SPINAL CORD. SE\'ER \E LEVELS BEING COMBINED INTO ONE DfvSCnNDING Tr,.\CTS V. S. T.:^ vestibulo-spiiial tract T. S. T. = tecto-spinal tract D. P. T.= direct pyramidal tract / corlico-spinal C. P. T. = crossed pyramidal tract \ tract N. S. T. = rubro-spinal and thalanici spinal tracts S. C. ^ Schultze's comma ASCENDJNC. Tr.ACTS S. T. T, = spino-thalamic tract A. S. C. T. = anterior spino-cerebellar tract \ P. S. C. 'T. = posterior spino-cerebellar tract (Flecbsig's tract) C. C. ^ Clark's cokniin (Cowers' tract) On tbe left side of the cord are represented the nerve roots and tliose bnndles of long fibers in the white columns which carry impulses downward from the brain to the spinal cord, and on the right side are represented these bundles of long fibers in the white columns which carry impulses upward from the spinal cord or spinal ganglia to the brain. It hardly needs to be stated that, although in this figure these long bundles of fibers are represented on one side only, they are really situated symmetrically on each side of the cord. The short fibers which connect ditiferent levels of the cord together are not represented in the figure. Lesions involving the pyramidal tract give rise to a spastic paralysis described under 251, 254, 525-6, 547, 660. 799-800, 1212 and 1.S84-6-9. Lesions involving the anterior horns give rise to atrophic paralysis, the acute forms of which are described under 495, 791, 114S, 1233 and 132.J : while the chronic forms are described under 547-8. 695, 1150 and i,'^24. Lesions involving the posterior horn give rise to symptoms described under r322. Lesions of posterior columns give rise to symptoms described under 785, 1302, 1347, 1350-1 and 1396. Lesions of the spino-ccrebellar tract give rise to symptoms described under 281 and 653. Lesions of the spino- thalamic tr;ict and of the anterior commissure of the giay ma'ter give rise to symptoms described under 365, 812 and I3=;.t. Lesions of the whole of one lateral half of the cord give rise to symptoms described under 442. 509, 840, (>8r and 1405; while lesions of the whole transverse section of tiie cord give rise to symptoms described under 485, 513-4-17-8, 520-T-50-3, 793-8, 827-30-1-8, 980, 1149, 1329-30 and 1404-7- Lesions of posterior spinal ganglion give rise to symptoms described imder 040-78, 25; Fig. 2-/ Sclu'malic representation of the more important diseases of the spinal cord. Locomotor Ataxia (lumbar region) See 248, .M5, 409-12-3-23, 661, 75g, 7S5. ^.ii}. 8gi, .894, 912, 979, 988, ior(lrnlh. Compression Myelitis with the ecmse- ([nent A^cendini,' and Descending Dejjcni'r.ations. See 520, 7'AS. No 3 shows the point of the compression with the whole transverse section of the cord the scat of an inflammation. No. I shows ascending degeneration of the colnnnis of (loll, nf the spino-thalamic tracts, and of the .intcrinr ;nid posterior spino-cerc- hellar tracts. No. 2, close to the lesion, shows in addition a slight degeneration of the cohmnis of Bnr- dach. Nos. 4-6 show degeneration of the crossed and direct pyramidal tracts, of the vestibulo- spinal, rubro-spinal, and thalamo-spinal tracts and of Sclnilt/c's comma. The tipper series faces uj) and the lower down. UsJolla lamballJ 258 SCHEMATIC REPRESENTATION OF SOME POINTS IN THE PHYSIOLOGY AND PATHOLOGY OF THE SPINAL CORD AND PERIPHERAL NERVES Fic. 28. Diagram to illustrate the mechanism of the bladder reflex. Fig. 28 B represents the bladder. S C rep- resents the reflex centre, with its motor and sensory neurons, for the sphincter of the bladder, which is ex- cited to action by urine in the neck of the bladder or in the prostatic ure- thra. DC represents the reflex centre, with its motor and sensory neurons, for the detrusor of the bladder, which is excited to action by the distention of the walls of the bladder. These two reflexes are antagonistic and the sensory surface irritated being much larger in the latter (DC), than in the former (SC), reflex, the de- trusor reflex will eventually over- power the sphincter reflex under normal conditions. S T represents the sensory tract connecting the blad- der with the brain, by means of which the individual is informed as to the degree of fulness of the blad- der. M T represents the motor tract conecting the cerebral with the spinal centre by means of which the indi- vidual can inhibit the activity of either centre ( up to a certain degree) and increase the activity of the an- tagonistic centre. Fig. 29 illustrates effects of lesions of Cauda equina. If the lesion is at "A" there is complete motor paralysis of both legs, and complete anesthesia of thewhole of both legs and of the perin- eum, buttocks, scrotum and penis, and all reflexes of the legs are abolished. If the lesion is at "B" there is complete motor paralysis of both legs, except tiie flexors of the thigh and the extensors of the leg, and complete anesthesia of the perineum, buttocks, scrotum and penis, and of the pos- terior surface of the thighs, the posterior and lateral surfaces of the legs, and all of the foot, except a small area on its inner surface. All the re- flexes of the legs except the knee-jerks are abolished. In both cases the muscles atrophy, there is no zone of hyperesthesia above the anesthesia and the bladder and rectum show a motor and sen- sory paralysis. If the lesion is limited to the conus medullaris there is a paralysis of the rectum and bladder and an anesthesia of the penis, scrotum, perineum, one inch about anus, and the upper two-thirds of the posterior surface of the thighs. Otherwise there is no paralysis of motion or sensation. L.III. N.crur. D.XI. , D.xn. L.II. m L.nr. l.IV. ■'After Fr. S c 11 u 1 : J e - K 5 st e r. Fig. 29 ■*k^ 30 Showing the innervation of musales through more than one nerve root, so that the destruction of one nerve root or of one group of nerve cells does not cause a com- plete and permanent paralysis. 259 Fig. 31 A diagram showing that a given sensation area of the skin is sup- plied by filaments from several nerve roots ; so that division of one root does not necessarily produce total anesthesia. It also shows the peripheral overlapping; so that the area supplied by one nerve can be almost completely supplied by neigh- boring nerves. Motor and Reflex Functions of the Spinal-Cord Segments (Modified AFTER Starr and Edinger) Segment Cervical Muscles 2-3 i r 6-i 17- 8 Dorsal 1 2-12 Lumbar '.! ■3-^ Sacral 1-2 3-5 Stemomastoid Trapezius Scaleni Small rotators of head Diaphragm Lev. ang. scap. Rhomboids Spinati Deltoid Supinat. long Biceps Supinat. brev. Serrat. mag. Pectoralis (clav.) Teres minor Pronators Brachialis ant. Triceps Long extensors of wrist and fingers Pectoralis (costal) Latiss. dorsi Teres maj. Long flexors, wrist and fingers Extensors of thumb Intrinsic hand-muscles Dorsal and abdominal muscles Abdominal muscles Iliacus Psoas Sartorius Flexors of knee Quad, femoris Int. rotators of thigh Adductors of thigh Abductors of thigh Tibialis ant. Calf-muscle,s Ex. rotators of thigh Extensors of toes Peronei Long flex, of toes Intrinsic foot-muscles Perineal muscles i;i Reflexes Dilatation of pupil by irri- tating side of neck, 4 cer- vical to I dorsal Scapular reflexes, 5 C-I D Supinat. long., 5 C Biceps, 5-6 C Triceps, 6 C Posterior wrist, 6-8 C Scapulo-humeral, 7 C Anterior wrist, 7-8 C Palmar, 7 C-I D Epigastric, 4-7 D .Abdominal, 7-1 1 D Cremaster, 1-3 L Patellar, 2-4 L Bladder, 2-4 L Rectal, 4 L-2 S Gluteal, 4-5 L .Ankle-clonus. I c Achilles, \ '"-^ * Plantar, 1-2 S Anal. ) (. Virile, f •' ■ ^ Fig. 32. 260 261 ■|1 sir T. c•^o.Sp;^«.«T,..ct- Fig. 34 LONG MOTOR PROJECTION TRACTS For lesions involving these tracts see under Fig. 26 262 Fic- 35 LONG SENSORY PROJECTION TRACTS For lesions involving these tracts see under Fig. 26 263 Gasseriafv OtmyUon.' Vnerye- /sensory root/ a/'^^ / Tongue 1 ^ICenicuiate Canylu>nj Stylorrmw^tctd fortimen -PosterwrAurCcular "^losso pharyngeal FiC. 36 DIAGRAM OF TRIGEMINAL, FACIAL AND GLOSSOPHARYNGEAL NERVES, SHOWING COURSE OF TASTE FIBRES. (After Pun-es Stewart) Optio RadltUont Corpiu Callotum Optic ThaUmus Corp. genic exC Optic IVsct Optic Nerve iiual Word Centre S Auditory Word-CeiiCre Kftriciculus Uoranatu* Vocal Word.C«ntre Lesion at i produces blindness of one eye. Lesion at 2 produces bi-temporal hemianopia. Lesion at 3 produces bi-nasal hemianopia. Lesion at 4 produces R. hemianopia with hemiopic pupil reaction *^mu»-^ Fic. 2,7 DIAGRAM ILLUSTRATING HEMIANOPIA (Modified from Vialet) Lesion at 5 produces R. hemianopia with normal pupil reaction. Lesion at 6 produces R. hemianopia with normal pupil reaction. Lesion at 7 produces psychic blindness. j,„K" ■"■- - Lesion at 8 produces Alexia. The heavy black lines represent the fibers from the m.-iciila lutea in each retina, the point of central or clearest vision. 264 INDEX INDEX Roman numerals indicate charts. Arabic numerals indicate marginal numbers. Arabic numerals preceded by "p" indicate pages. Abasia : See Astasia Abdomen, Boat-shaped retraction of, XI, 605 Abdominal reflex : See Umbilical reflex Abdominal spasm or cramp, XII, 732 Abducens nucleus, Conjugate deviation in lesions near the, XIV, 885; XXII, 1344 paralysis. XIV, 872; XXII, 1343 Abductor laryngeal paralysis, XIII, 759 Abscess, Cerebral ; See cerebral Spinal : See spinal Abstraction, p. 17 Accommodation reflex : See pupillary reflex to accommodation Achilles reflex, I, 62; V, 3:8 Acliillodj-nia, XV, looi Achondroplasia, XVII, 1177 Achromatopsia, I, 13; VI, 364; XIV, 850 Acromegaly. I, 20; XVII, 1197 Acroparesthesia, XVII, 1197 Action, p. 10 Association, p. 22 Autochthonous, p. 35 Automatic, p. 14, 35 Involuntary, p. 35 Reflex: See Reflex Voluntary, p. 14. 31 Active contracture, I, 39; IV, 264; XI, 572. Acute alcoholic mania. XVI, 1 109-12 anterior poliomyelitis : See poliomyelitis apoplectiform polioencephalitis inferior, X. 534-44 superior, X. 534-43; XVI, 1046-7-8 ascending paralysis, II, 170; X, 482 ataxia : See ataxia atrophic paralysis : See poliomyelitis bulbar paralysis, IX, 424; X, 534-43-4; XVI, 1046-7-8 delirium, XVI, iiii encephalitis, multiple, XVI, 1046-7-8 Adams-Stokes' disease, XI, 58; XVI, 1060 phenomenon, IX, 426 Adiadocokinesia, IV, 288 Adiposis dolorosa, XV, 1012 ; XVII, 117S Adiposogenital dystrophy, XVII, 1176; XXI, 1302 Adolescent insanity, XVI, 1098 Adrenalin, Action upon nervous system of, p. 21 Aesthesiometer, L 48 African lethargy, II. 142; XVI, 1055 Age in nervous diseases, II, 86 Ageusia, p. 10; VI. 357; XIV, 810 Tests for, I, 17 Agitated dementia, XVI, I IDS melancholia, XVI, 1115 Agnosia, p. 17, III, 221 Agoraphobia, III, 235; XVI, 1074 Agraphia, p. 35; III, 228; XIII, 779-8o; XXII, 1401 localization of, XXI, 1304; XXII, 1401 Agrypnia. I, 18 Akinesia, IV, 241 Akinesthesia, I, 43; VI, 352; XIV, 813 Albinism, XII, 683 Alcoholic coma, XVI, 1056 convulsion, XI, 576-85 dementia, XVI, 1103 hallucinosis, XVI, 1 112 headache, XV, 954 intoxication, XI, 585; XII, 658-63-73; XIII, 767, 781 mania, acute, XVI, 1 109-12 neuritis (or paralysis), X, 488 tremor, XII, 673 vertigo, XV, 1031 Alcoholism, I, 2; II, 116-61-2; XII, 658; XIII, 767-81 Alexia, p. 35 : HI, 229 ; XIII, 777 localization of. XXII, 1403 Allocheiria, VI, 377 Alopecia. XVII, 1161 Altruism, p. 28 Amaurosis, VI, 358 Uremic, XIV, 853 Amaurotic idiocy, XVI, 1087 Amblyopia, VI, 359; XII, 682 Hysterical, XIV, 855 Ambulatory automatism, XVI, 1061-71-3 Amentia, p. 28; III, 211 Diseases causing, XVI, 1078 Amnesia, I, 6; III, 220; XIII, 739-72 Retroactive, XIII, 772: XVI, 1102 Retrograde, XIII, 772 Amyl nitrite poisoning, XIV, 845 Amyotonia congenita, II, 105 ; X, 483 Amyotrophic lateral sclerosis, X, 547; XI, 695: XIII. 800: XVII, 1 150 Anakusia, VI, 355; XIV, 822 Diseases causing, XIV, 822 Tests for. I, 15 Anal reflex, V, 307a Analgesia, VI, 349 Diseases causing, XIV, 811 Localization of lesions causing, XXII, 1354 Tests for, I, 50 269 INDEX Anarthria, p. 35; IV, 283; XIII, y^y-T^ Diseases causing, XIII. Ji'j literalis, XIII, 770 spasmodica, XIII, 771 Anatomic introduction, p. 5 Anemia, cerebro-spinal fluid in, XIX, 1244 Optic neuritis in, XIV, 902 Vertigo in, XV. 1021-5 Anemic convulsion, XI, 583 lieadache, XV, 950-3-9 Anesthesia, p. 6; VI, 348; XIV, 811 Diseases causing, XIV, 811 dolorosa. VI, 374 Glove form of, VI, 348; IX, 415 Hysterical, p. 7: VI, 348; IX, 415; XIV, 837; XVI. 1076 Laryngeal, XIII, 757-63-4 Localization of lesions causing, XXII, 1353 Stocking form of, VI, 348 ; IX, 415 Tests for, I, 48 Thermic, VI, 350; XIV, 8ri Tests for, I, 55 Aneurism, Cerebral, X, 502 Angina pectoris, XV. 984 Anginal crises, IX, 423 Angio-neurotic oedema, XVII, i2or -paralytic hemicrania, XV, 950 -sclerotic dysbasia, X, 555; XVII, 1 199 -spastic hemicrania. XV, 950 hemiplegia, X, 555 Angular gyrus, Symptoms of lesions of, III, 229; Xin, ^TJ■, XXII, 1382a, 1403 Anisocoria, I. 24; V, 341 Ankle-clonus, V, 317 Tests for, I, 60 Ankylosis, Tests for, I, z?- Anopsia, VI, 358 Anosmia, VI, 356 Tests for, I, 16 Anterior central convolution: See localiza.- tion commissure of cord : See localization crural neuralgia or neuritis, XV, 997 horn, or column or nerve root: See spinal cord Apallesthesia, VI, 353 Tests for, I, 56 Apathetic dementia, XVI, 1097, 1105 Apathy, III, 237 Ape's hand. XII, 714 Aphasia, I, 6; III, 222-3-4-5-6; XIII, 739 .'\uditory, lU, 223; XIII, 774 Broca's scheme of, XIII, 739 Conduction, p. 34; XIII, 778 Cortical motor, XIII, 774 sensory, XIII, 775-6 Diseases causing, XIII, 739 Marie's theory of, XIII, 739 Mixed, III, 225; XIII, 778 Aphasia, Motor, III, 222; XIII, 774; XXII, 1402 Localization of, XXI, 1304; XXII, 1402 Optic, III, 224; XIH, 776; XXII, 1357-81 Sensory, p. 17; I, 6 ; III. 223-4; XIII. 775-6-7 Localization of, XXI, 1306; XXII, 135882 Sub-cortical motor, XIII, 739 sensory, XIII, 739 Trans-cortical motor, XIII, 778 sensory, XIII, 778 Visual, in, 224; XIII, ^^(, Wernicke's theory of, XIII, 739 Aphemia, III, 222; XIIL 774; XXII, 1402 Aphonia, IV, 260; XIII, 757-8, 60-1-2-3-4 Hysterical, XIII, 747-8-62 Aphthongia. XII, 729; XIII, 771 Apoplectiform polioencephalitis inferior, II, 118-69; X, 495, 534-44; XVI, 1046-7-8 superior, II, 118-69; X. 495, 534-43; XVI, 1046-7-8 Apoplexy, II, 147, 189; IX, 422; X, 504; XI, 5&S; XIV. 835-60-1; XV. 1027; XVI, T043-63-4-5-6 Athetosis after, X, 503; XI, 632 Cerebral, X. 504; XI, 588; XIV, 835; XVI, 1043-63-4 Ingravescent, XVI, 1043-63-4 Meningeal, X, 502-24; XI, 588; XVI, 1063 Pontine. XIII. 740 Prodromata of, IX, 422 Vertigo from, XV, 1027 Apraxia. p. yj: III, 231 ; IV, 249-82; XVI, 1106 Association, p. },y Motor, p. yj Aran-Duchenne type of muscular atrophy, X, 548; XII, 695; XIII, 800; XVII, 1 1 50 Arcus senilis, I, 24 Argyll-Robertson's pupillary reflex, V, 332; LX, 437 Diseases causing, XIV, 891 Arm-center, Symptoms of lesion of, XXII, 1 362-5-83-8-9- 1 -3-9, 141 1 Paralysis of, XII. 708 to 13 Spasm of muscles of, XII, 733 Arsenical neuritis, II, 158; X, 488 .Arterial disease in etiology of nervous di- seases, II, 97 cause of transient motor paralysis, X, 558 Arthralgia, XV, 1000 Arthritis deformans, XV, 976 Arthropathy of tabes, XVII, 1186 Articulative tics, XIII, 771 Asphyxia, local, XV, ion; XVI, 1059; XVII, 1 195 Associated movements, IV, 276 Association of ideas and memories, p. 22 Tests for, I, 5 fibers, p. 13 reflexes, p. 14. 31 270 INDEX Astasia and abasia, IV, 287; XII, 652; XIII, 795 Astereognosis, p. 17; III, 230; VI, 354; XXII, -'35t^-83 Tests for, I, 11 Asthenic tremor, XII, 671 Asthma, XI, 616; XVII, 1194 Astrophobia, III, 235 Asynergia, p. 36; IV, 248 Major, IV, 281 Minor, IV, 282 Ataxia, p. 36 ; I, 21-42 ; IV, 248-80-1 ; X, 488 ; XII, 638; XVI, 1 104; XXI, 1290-6 Acute, X, 488; XII, 659-62 Aural, XII, 649 Cerebellar, p. 37 ; I, 21 ; IV, 281 ; XII, 642-50-69; XXI, 1290-6, i?04 Cerebral, p. 'S^ Diseases causing, XII, 638 Dynamic, p. 36; IV, 280; XII, 644 Friedreich's hereditary, II, 104, 124; XII, 651-70-87; XIII, 765-82 Hysterical, XII, 664 Locomotor : See Tabes Marie's hereditary cerebellar, II, 124; XII, 650-69; XIII, 783 Motor, p. 36; IV, 280; X, 488; XII, 644; XXI, 1290 to 97 Ocular, XII. 648 Post-hem-plegic, XII, 655 Static, p. 37 ; IV, 281 ; IX, 438 ; XII, 642 Vertigo with. XII, 648-91; XV, 1015-20 Ataxic gait. Diseases causing, XIII, 740 paraplegia, X, 526; XII, 660; XIII, 799 Ateleiosis. XVI, 1095 Atheromatous arteries. Vertigo from, XV, 1025 Athetoid spasm. Diseases causing, XI, 574 Athetosis, p. 38; I, Zi\ IV, 271; X. 501-4; XI, 574 after apoplexy, X, 504 ; XI, 632 in cerebral palsy of childhood, X, 501 ; XI, 631 Congenital, X, 501 ; XI, 630 Athlete, Muscular hypertrophy in, XVII. 1156 Atonia, I. 40; IV, 240 Atonic paralysis. I, 40; IV, 252; X, 472 Atrophic paralysis, IV, 252; X, 472-6-7, S47-8 Atrophies, Degenerative, X, 476 Localized, XVII, 1188 Atrophy, Arthritic, XVII, 1127-53-86 of bone. Diseases causing, X"VII, 113^79 fat. Diseases causing, XVII, 1 137 joints, XVII, 1 153 muscles, I, 41; X, 476-7; XVII, 1131 skin. Diseases causing, XVII, 1 133 Attention, p. 24 Tests for power of, I, 5 Attitudes passionelles. XI, 586; XVI, 1076 Attonita melancholica, XVI, 11 15 Auctioneer's cramp, XII, 726 Audition, Cortical center of, p. 8 Auditory aphasia. III, 223; XIII, 775 nerve. Deafness in atrophy of, XIV, 919 Electrical reaction of, VII, 403 Lesions of, XIV, 920 -orbicularis reflex, V, 314 Aura of epilepsy, IX, 420; XIV, 849 Glittering scotom.ata as, XIV, 849 of migraine Glittering scotomata as, XIV, 849 Hemianopia as, XIV, 858 Aural ataxia, XII, 649 headache XV, 953 vertigo, XII, 649-85; XIV, 918; XV, 1019 Autochthonous acts, p. 35 .Automatic acts, p. 14, 35 Automatism. Ill, 210; XVI, 1038-9 Ambulatory, XVI, 1061-71-3 Diseases causing, XVI, 1038-9 Epileptic, XI, 575; XVI, 1061-73 Spinal reflex of, V, 327a Auto-suggestion in hysteria, IX, 415; XVI, 1071-2-6 Auto-toxic coma, XVI, 1069 convulsion, XI, 576-96 : XVI, 1069 Avellis' syndrome, IX, 449; XII, 706; XXI, l2go Awkwardness : See apraxia Axon, p. 6 Babinski and Nageotte's bulbar syndrome; IX, 427; XXI, 1290 Babinski's associated movements of trunk and thigh. IX. 436 reflex, V, 304, 328 Tests for, I, 57 Backache, Diseases causing, XV, 935 Barany's test, I, 79 Barlow's disease, X, 495 Basedow's disease, II, 132 ; XII, 672 ; XVII, "93 Tests for, I. 20 Bathyesthesia, I, 43 Bechterew's reflex : See dorsal foot reflex Bed sores, XVII, 1171 Bell's palsy, XII, 703 phenomenon, IX, 434; XII, 703 Benedykt's syndrome, IX, 431; XXI, 1293; XXII, 1341 Beri-Beri : See neuritis, multiple Bewildered mental condition, III, 207 Biemacki's sign, IX, 439 Binocular diplopia, V, 383; XIV, 818 Biot's respiration, IX, 425 Bi-temporal hemianopia, VI, 362 ; XIV, 817- 64-94; XXII, 1355 Bladder reflex, V, 324 Blepharospasm, XI, 598, 615-6; XII, 726 Blindness. V. 329; VI. 358; XIV. 853-4-5; XXII, I33I-55-6-7 271 INDEX Blindness, Color, VI, 364 Day, VI, 360 Diseases causing, XIV, 817 Night, VI, 361 Psychic, p. 17; III, 224, 32; XIII, 776-7; XXI, 1307; XII, 1357 Snow, VI, 360; XIV, 846 Word, III, 229; Xni, 777 Localization of, XXII, 1403 Boat-shaped retraction of abdomen, XI, 605 Bone, atrophy of, Diseases causing, XVII, 1139-79 conduction. Tests for, I, 15 Failure of development of, XVII, 1138a Fragility of, XVII, 1141-85 Hypertrophy of, Diseases causing, XVII, 1 140, 1 180 to 84 tissue, trophic lesions of, Diseases caus- ing, XVII, 1 126 Boston-Kocher sign, XVII, 1192 Botulismus, X, 542 Brachycephaly, I, 22 Brachial plexus, Neuritis or injury of, IX, 444-5 ; X, 490 Paralysis of, IX, 444-5; X, 490; XXII, 1326 Spasm or cramp of, XII, 733 Symptoms of lesions of, XXII, 1326 Bradycardia, XII. 728 Brain, congenitally defective, p. 29 puncture, I, 75 stem, definition of, IX, 460 Lesions of, U, 147-89; X, 534 to 46; XII, 656: XIV, 832; XV, 1017; XXI, 1290 to 97; XXII, 1321 to 4, 1387-90-4-6, 1400-8 Localization : See localization Tumor of, X, 535-7-9-4' ; XII, 656 Vertigo in lesions of. XV, 1017 Bright's Disease, Optic neuritis in, XIV, 899 Brissaud's lefiex, V, 303 Bristow's syndrome, IX, 452; XXI, 1300 Broca's scheme of aphasia, XIII, 739 Brown-Sequard's paralysis, IX, 432; X, 509; XIV, 844; XV, 982; XX, 1276; XXII, 1405 Brudzinski's leg sign, IX, 447 neck sign, IX, 446 Brun's syndrome, IX, 453 Bulbar paralysis, IX, 424; X, 544-6; XII, 694; XIII, 759-64; XVII, 1 151 Acute, X, 544 Chronic progressive, X, 546; XII, 69)4: XVII, 1 151 Pseudo-. X, 554 Symptoms of, IX, 424 Burdach's column and nucleus: See spinal cord Caisson disease, X, 521 Calcanodynia, XV, 1002 Calcarine fissure. Symptoms of lesions of, VI, 364; XIV, 850-6-7-9-60; XXII, 1378 to 80 Caloric reaction, I, 79; XII, 685 Cannabis Indica poisoning, XIV, 845 Capsule, External : See external Internal : See internal Caput obsticum paralyticum, XII, 705 spasticum, XII, 705-30 Cardiac disease, Vertigo from, XV, 1024 Caries of the spine, 11, 122 Case taking, I Casque neurasthenique, XV, 960 Catalepsy, XL 609; XVI, 1098 Cataract, Diplopia in, XIV, 882 operation, Perversion of vision after, XIV, 846-7 Catatonia, XVI, iioo Cauda equina, Paralysis of, X, 487; XII, 721 Symptoms of lesions of, X, 487; XII, 721; XV, 1007; XXn, 1328 Causalgia, XV, 1003a Central Convolution, Anterior, Symptoms of lesions of, XXII, 1385-8-91-2-3-9, 1410- 1-2 Posterior, Symptoms of lesions, of XXII, 1361-2-5-83 Motor (cortico-spinalj neurons, IX, 461 Diseases of, X. 473 Location of lesions of, XXII, 1313 Sensory neurons, IX, 463 Centrifugal neurons, p. 9 Centripetal neurons, p. 6 Cephalagia : See headache Cerebellar abscess, XIV, 909 artery, posterior inferior. Thrombosis of, XXL 1291 ataxia, p. 37; IV, 281; XII, 642-50-69; XXI, 1290 to 1304 Diseases causing, XII, 638 Marie's hereditary, II, 124; XII, 650-69; XIII, 783 fits, XI, 607-8; XXI, 1295 nystagmus. I, 24-31-80; XXI, 1295 peduncles. Symptoms of lesions of the middle. XXL 1296 tract (direct). Lesion of the, XII, 653; XX I L 1369-73 tumor, IV, 909 Cerebellum, Diseases of the, VI, 392 ; XI, 607- 8; XII, 647-69-86; XIII, 783-4; XV, 1016; XXL 1295 Lesions of the, XII, 647-69-86; XIII, 783- 4 hemispheres, XI, 607 vermis, XI, 608 Localization in : See localization Physiology of, p. 12 272 INDEX Cerebral abscess, II, 153, 174, 184; X, 508; XI, 578, 587; XIV. 907; XV, 961; XVI, 1049 Cerebro-spinal fluid in, VIII, 405 ; XIX, 1238 Headache in, XV, 961-7 activity. Diseases causing weakened, XVI, I 040- I anemia. Vertigo from, XV, 1021-2-3-4-5 aneurism, X, 502 ataxia, p. yj apoplexy: See apoplexy, cerebral hemor- rhage and softening compression, XVI, 1043 concussion, XVI, 1042 congestion, XV, 958-1026 contusion, XVI, 1043 cortex. Symptoms of lesion of the, XXI 1308 Conjugate deviation of the eyeballs in irritative lesions of, XIV, 819 cyst: See cerebral tumor decompression, XV, 961 diplegia, II, 117; IV, 255; X, 478, 501; XI, 577, 614-31 ; XIII, 801 ; XVI, 1051- 88 disease. Nystagmus in, XII, 689 edema, Cerebro-spinal fluid in, VIII embolism, X, 505; XIV, 835-60-1; XVI, 1065 endarteritis. Syphilitic, II, 178; XVIII, 1207 gumma, isolated, XVIII, 1206 hemorrhage, II, 147, 189; X, 503; XI, 588; XIV, 835-60-1 XVI, 1043-64 Cerebro spinal fluid in, VIII, 405-6; XIX, 1242 into ventricles, X, 504 localization : See localization meningitis : See meningitis, cerebral palsy of childhood, II, 117; X, 501; XI, 577; 614-31; XIII, 801; XVI, 1051-88 softening, X, 505-6 ; XIV, 835-60-1 ; XVI, 1043-65-6 syphilis, XV, 1033; XVIII, 1205 Cerebro-spinal fluid in, VIII, 412-3-4; XIX, 1230-1-2 thrombosis, X, 506 ; XIV, 835-60-1 ; XVI, 1066; XVIII. 1207 tumor, II, 125, 152, 191 ; X, S07-35-7-9-4I ; XI, 578-87; XIV, 836-52-9-62-4-5, 908; XV, 961;, 1033; XVI, 1050 Cerebro-spinal fluid in, VIII, 405-12-3; XIX, 1237 Coma in, XVI, 1050 Headache in, XV, 961 Optic neuritis in, XIV, 908 Perversion of vision in, XIV, 852-9-62- 4-5 Vertigo from, XV, 1033 Cerebration, Disturbances of, III. 200 Diseases causing disorders of, XVI, 1036 Tests of I, 3 to II Cerebro-spinal fluid, p. 38; I, 74; VIII, 404; XIX. 1220 Abnormal, XIX, 1220 in abscess. XIX, 1238 Albumen in, VIII. 411 in anemia, XIX, 1244 Bacteria in, VIII, 409; XIX, 1223-4 Blood in, VIII, 406 Butyric acid test in, VIII, 412; XIX, 122r-2 Cellular elements in, VIII, 409; XIX, 1223-4 in cerebro-spinal meningitis, XIX. 1226-33 clear with coagulum, VIII. 408; XIX, 1223-4 Cloudy, VIII, 407; XIX, 1223 Colloidal gold test in, VIII, 414 Globulin in. VIII, 412; XIX. 1221 in hemorrhage in spinal membranes, XIX, 1240-2 in herpes zoster, XIX, 1235 in hydrocephalus, VIII, 405; XIX, 1239 Leucocytosis in, VIII, 409; XIX, 1223 Lymphocytosis in, VIII, 409; XIX, 1224 in meningitis, VIII, 405-9- 10- 1 -2 ; XI, 590; XVIII, 1208-9-13-4; XIX. 1226-7-8-9-32 Noguchi test in, VIII, 412 Nonne-Apelt test in, VIII, 412 Obtaining of, I, 74 in paresis, VIII, 409-12-3-4; XIX, 1230 poliomyelitis, VIII, 409-12; X, 495; XIX. 1233 purulent meningitis, XIX, 1227 Red or reddish color of the, VIII, 406 in serous meningitis, XIX, 1241 sporadic purulent meningitis, XIX, 1227 Sugar in. VIII, 410 in syphilis, VIII, 409-12-3-4; XVIII, 1206 to 17; XIX, 1230 to 32 tabes, VIII, 409-12-3-4; XVIII, 1217; XIX, 1231 Tension of the, VIII, 405 in tumor of brain or spinal cord, VIII, 405- XIX, 1237 typhus fever, XIX, 1236 tuberculous meningitis, XIX, i22»-9 uremia, XIX, 1243 Wassermann test in, VIII, 413 ; XIX, 1224 Cerebro-spinal syphilis, II, 108, 175 to 80; XVIII, 1214; XIX, 1232 Cervical region and enlargement: See spinal cord rib, Symptoms of, X, 557 ; XVII, 1 143 Disorders of, XVII, 1122 sympathetic. Irritation of, XVII, 1192 Paralysis of, XVII, 1 191 Cervico-brachial neuralgia, XV, 995 273 INDEX Charcot's disease, XVII, 1186 Charcot-Marie-Tooth's type of muscular at- rophy, X, 496; XII, 731 Chasmus, XII. 73i Cheyne- Stokes' respiration, I, 451 IX, 425; XII, 728; XXI, 1290 Chills, XII, 680 Choked disc, Diseases causing, X, 507-8; XIV, 892 Chondrodystrophia foetalis, XVII, 1177 Chorea, I, 33; II, ii3> ^^b; IV, 272; XI, 573 Degenerative, XI, 625 Electrical, XI, 597. 628 Dubini's, XI, 597. 628 gravidarum, XI, 622-3 Habit, IV, 274; XI, 627 Herai-, IV, 272; X, 510; XI, 573, 622 Hereditary, II, 103; XI, 624 Huntington's, II, 103; XI, 624 Hysterical, XI, 629 Infectious, XI, 622-3 Insaniens, XI, 623 major or magna, IV, 273; XI, 629 minor, IV, 272; XI, 622 mollis, X, 510 Post-hemiplegic, X, 501 ; XI, 629 in pregnancy, XI, 622-3 Pseudo-chorea, XI, 573 Rhythmical; Xi, 629 Senile, XI, 625 Sydenham's, XI. 622 Choreic movements, I, 33; IV, 272 paralysis, X, 510 Choreiform spasms. Diseases causing, IV, 372; XI, 573 Chromatopsia, Tests for, I, 13 Chronic atrophic paralysis, X, 548; XII, 6SH- 5; XIII, 800; XVII. 1150-1 bulbar paralysis, X, 546; XII, 694; XIll, 759-64; XVII, 1 151 Chvostek's sign, IX, 441 ; XI, 612 Cilio-spinal center, IX, 465; XVII, 1191-2 reflex, V, 335 Circular insanity, XVI, 1119 Circulation, Tests for, I, 45 Circulatory disturbances. Perversion of vision in, XIV. 848-9 Claudication, Intermittent, II, 190; X, 555; XVII, 1 199 Claustrophobia, III, 23S; XVI, 1074 Claustrum and external capsule, Symptoms of lesions of, XXI, 1301 Clavus, XV, 951 Claw-hand, X. 547; XII, 715 Cleft palate, XIII, 75' Clitoridian crises, IX, 423 Clonic spasm, IV, 246 Diseases causing, XI, 571 Clubbed fingers and toes, XVII, I184 Coal gas poisoning, XVI, 1058 Coceygodynia, XV, 972 Coffee vertigo, XV, 1031 Cold as an etiological factor, II, 100 Colic, Lead, II, 159; XV, 989 Colloidal gold test VIII, 414 Color blindness, VI, 364 fields, inversion of and interlacing of, I, 14; XIV, 851-2 sense. Tests for, I, 13 Coma, I, 3; HI, 205; XIII, 745; XVI, 1037 Alcoholic, XVI, 1056 from cerebral compression, XVI, 1043 concussion, XVI, 1042 Diabetic, II, 194; XVI, 1067 Diseases causing, XVI, 1037 Epileptic, XI, 575 ; XVI, 1061 Hysterical, XVI. 1071 in internal hemorrhage, XVI, 1059 Laryngeal, XVI, 1062a Narcotic, XVI, 1057 Pseudo-, Diseases causing, XVI, 1038 Toxic and auto-toxic. XVI, 1069 Uremic, I, 103 ; XVI, 1068 vigil. Ill, 206 Common paths, p. II Comprehension. Tests for power of, I, 5 Compression of brain stem, X, 535-7-9-41 Cerebral, XVI, 1043 myelitis, II, 122; X, 520; XIII, 798 neuritis, XV. 939 Compulsory acts and ideas, p. 10; I, 4; III, 218; IV, 275; XVI, 1098 Concentration, p. 24 Concentric limitation of field of vision, IX, 415; XIV, 817, 868 to 71 ; XVL 1076 Concepts, p. 16 Concussion, Cerebral, XVI. 1042 Conduction of pain. Retardation of. I, 51 ; VI, 381 of motor impulses, p. 9 sensory impulses, p. 6 Confusional insanity, XVI. 1108 Congenital dislocation of the hip, XIII, 788 Congenitally defective brain, p. 29 Congestive headache. XV, 958 vertigo, XV, 1026 Conjugate deviation of eyeballs. Lesions caus- ing, XIV. 819-85-7 Conjunctival reflex. V, 312 Tests for, I, 58 Consanguineous marriages in nervous dise2ses, I, 2; n, 81 Conscience, p. 23 Consciousness, p. 18 Disturbances of, I, 3; III, 201; XVI, 1036 Consensual pupillary reflex, I, 25 ; V, 329 Constipation headache, XV, 953-6 Continuous paralysis. Diseases causing, X, 470 Contraction, Fibrillary, IV, 293; XII, 641 274 INDEX Contracture, Active, I, 39; IV, 264; XI, 572 Dupuytren's, XI, 621 Hysterical, XI, 6i8 Passive, I, 38; IV, 263 Post-paraplegic, X, 480, 516 to 520; 549 Post-neuritic, X, 621 Post-paraplegic, X, 480; 516 to 520; S49 to 52; XI, 620; XIII, 742 Tests for, I, 38-9 Contusion, Cerebral, XVI, 1043 Conus terminalis of spinal cord. Lesion of XIV, 833 Convergence, Deficient and cycloplegia, V, 331 Conversation in diagnosis, I Convulsions, p. 35; IV, 242-69; XI, 57c- 1 ; Sec epilepsy Alcoholic, XI, 576-85 Anemic, XI, 583 Auto-toxic, XI, 576-96; XVI, 1069-70 Cerebellar, XT, 607-8 Diseases causing, XI, 571 Epileptic, IX, 420-1; XI, 575; XIV, 849; XV, 1028; XVI, 1061-73-85, 1104 Febrile or toxic, XI, 595-6 Hysterical, IX, 415 ; XI, 586 ; XVI, 1076 Lead, X, 4941 XI, 576-84-5 Location of lesions causing, XXII, 1311 Narcotic, XI, 585 Strychnine, XII, 613 Toxic or febrile, XI, 595-6 Uremic, XL 576-81 Convulsive tics, IV, 267-70; XI, 598 to 602, 616; Xn, 726 Coordination, p. 12 Tests for, I, 42 Coprolalia. XVL 1098 Cornea. Diplopia, astigmatism and monocular diplopia in irregularities of the, XIV, 8S^ Corneal reflex, I, 58; V, 312 Comet player's cramp, XI, 615; XII, 726 Corpora quadrigemina, Localization in : See localization Corpus callosum. Symptoms of lesions of, XXI, 1300 Striatum, Localization in : See localiza- tion Cortical lesions : See localization Cortical reflexes, p. 12 Cortico-rubral tract, The. p. 9 Cortico-pontile tract, The, p. 9 Cramp, XI, 615-6: See also spasm Cranial asymmetry, I, 22 fontanel les, I. 22 hyperostosis, XVII, 1 181 nerves : See nerves nuclei : Sec nuclei sutures, I, 22 tumors, I. 22 Cranium, Localization at base of: See locali- zation Creative faculty, p. 25 Cremasteric reflex, V, 308 Tests for, I, 57 Cretinism, XVI, 1092; XVII, 1164 Crico-arytenoid, posterior. Paralysis of, XIII, 759 Crico-thyroid. Paralysis of, XIII, 757 Criminals, Habitual, p. 28; XVI, 1106 Crises, Tabetic, IX, 423; XV, 988; XVI, 1062a Crossed hemianesthesia, VI, 348; XXI, 1292 paralysis, IV, 256; X, 537 to 42; XV, 1017; XXI, 1290 to 3: See also Brown- Sequard's paralysis Croup, Spasmodic, XI, 616; XII, 728 Crura cerebri, Hemorrhage or softening in, X, 536-53 Localization in : See localization Symptoms of lesions of th», X, 536-7-43; XII, 656-76; XXI, 1293 XXII, 1340-1-2-5-87-96, 997, 1408 Crural neuralgia, XV, 997 paralysis. XII, 717; XV, 997 Cutaneous lesions. Diseases causmg, XVII, 1 124 reflex acts, I, 57 ; V, 297 sensibility, p. 6 tissue. Atrophy of, XVII, 1 133 Eruptions of, XVII, 1135 Hypertrophy of, XVII, 1134 trophic lesion of. Diseases causing, XVII, 1124 ulcerations of. Diseases causing, XVII, 1 136 Cyanosis, Local, XV, loii ; XVI, 1059; VII, 1 195. See also Raynaud's disease Cycloplegia, V, 331 Cyst, Cerebral : See tumor Dazed mental condition. III, 207 Dead fingers, XVII, 1195: See also Raynaud's disease Deaf-mutism, XIII, 744 Hysterical, IV, 283; XIII, 747; XVI, 1076 Deafness, p. 8; VI, 355; XIV, 822 Cortical center involved in, XFV, 924a Diseases causing, XIV, 822 Hysterical, XIV, 924 Psychic, p. 17; III, 223, 233; XIII, 775; XXI, 1306 Tests for, I, 15 Word. Ill, 223-33; XIII, 775 ; XXL 1306 Decompression. Cerebral, XV, 961 Decubitus, XVIII, 1171 Deep reflex acts. I. 60 to 68; V, 299 sensibility, p, 6 Tests for, I, 43 Defectives, p. 28; XVI, 1095 Defensive reflex (Babinski), V, 328 Degeneration, Electrical reaction of, VII, 397- 8, 402 27: INDEX Degenerative atrophies, X, 476 Chorea, XI, 625 Deiter's nucleus, p. 12 tract, p. 9 DeHberation, p. 31 Delirium, p. 29; III, 217; XVI, 1080 Acute or grave, XVI, iiii tremens. XVI, 1103-9-12 Delusional insanity, III, 215; XIII, 746; XVI, 1081, 1113 Diseases causing, XVI, io8i Delusions, p. 29; I, 4; HI, 215 of grandeur, XVI, 1 106-16 observation, XVI, TI16 persecution, XVI, 11 16 in hysteria, IX, 415 Systematized, p. 29 Dementia, p. 28; III, 212; XIII, 773; XVI, 1079 Agitated, XVI, 1105 Alcoholic, XVI, 1 103 Apathetic, XVI, 1097. iioi-S-7 Diseases causing, XVI, 1079 Epileptic, XI, 575; XVI, 1061, 1104 Paralytic: See Paresis precox, p. 29; XVI, 1098 Primary, XVI, 1097 Secondary, XVI, 1105 Senile, XVI, 1107 Terminal, XVI, 1105 Demoniacal possession, p. 28 Dendrons, p. 6 Dercum's disease, XV, 1012; XVII, 117S Dermographia, I. 59; V, 327; XVII, 1 167, 1200 Deviation of the eyeballs, conjugate, Diseases causing, XIV, 819 Secondary, of the sound eye, I, 30; XIV, 818 Tests for, I, 30 Diabetes mellitus. Coma in, II, 194; XVI, 1067 Fat atrophy in, XVII, 1174 Optic neuritis in. XIV, 900 Perforating ulcers in, XVII, 1172 Diadocokinesia, I, 37 Diagnostic charts, Introduction to, p. 127 Diaphragm, Paralysis of, XII, 707 Spasm of, XII, 72^ Digestive disturbances. Vertigo in, XV, 1023 Perversion of vision iru XIV, 848 Diphtheritic paralysis, X, 488; XIII, 756-7 Diplegia, IV, 255 ; X, 478, 501 ; XII, 703 Cerebral: See Cerebral Facial, XII, 703 Infantile; See infantile Diplopia, I, 24, 29; XIV, 818 Binocular, VI, 383; XIV, 8r8 Diseases causing, XIV, 818 Hysterical, XIV, 880 Monocular, VI, 384; XIV, 818 Tests for, I, 29 Displacement of eyeball, XIV, 879 lens, XIV, 883 retina, XIV, 883 visual axis, I, 29; XIV, 818 Disseminated myelitis or sclerosis: See sclerosis Dissociation of personality. III, 209 ; XVl, '039 sensation, VI, 365 ; XIV, 812 Diseases causing, XIV, 812; XXII, 1334 Disuse, Bone atrophy from, XVII, 1 178 Muscle atrophy from, XVII, 115S Diver's paralysis, X, 521 Dolicocephaly, I, 22 Dorsal foot reflex, I, 63 ; V, 321 Double persoriality. III, 209; XVI, 1039 Diseases causing, XVI, 1039 pupillary opening, XIV, 881 sensation, I, 54; VI, 378 vision : See diplopia Drug habit, I, i, 2; X, 482; XII, 658,63; XIII, 767; XV, 1031 poisoning, II, 165 vertigo, XV, 1031 Drunkenness in nervous diseases, I, 2; II, 116 Dubini's disease, XI, 597, 628 Dupuytren's contraction, XI, 621 Dwarfism, II, 109; XVII, 1164-77 Dynamometer, Testing with, I, 34 Dysarthria, p. 35; I, 8; IV, 284; XIII, 738 Diseases causing, XIII, 738 Localization of lesions causing, XXI. 1299; XXII, 1387-90-4-5, 1400 Dysbasia angio-sclerotica, II, 190; X, 555; XVII, 1 199 Dyschromatopsia, I, XIV, 851-2 Dysmasesis, IV, 2S6; X, 554 Dysmetria, IV, 248-89 Dyspepsia, Headache in, XV, 953 Dysphagia, IV, 285 Localization of, XXII, 1387-90-4-5, 1400 Dyspinelismus, XXI, 1303 Dystonia lenticularis, XII, 668 Dystrophia adiposogenitalis, XVII, 1176; XXI, 1302 Dystrophies, Bone tissue, XVII, 11 26 Cutaneous, XVII, 1124 Fatty tissue, XVII. 1125 Joint, XVII, 1127 Muscular, II, 107-28; X, 477; XIII, 787; XVn, 1123 Ear disease as cause of headache, XV, 953 Deformity of, XVI, 1078 Hyperemia of inner, XIV, ga? Lesion of, XIV, gi8 to 921-7 Echolalia, XVI, 1098, iioo Echopraxia, XVI, 1098, 1 100 Eclampsia, XI, 576; XVI, 1062 Edema angio-neurotica, XVII, 1201 Localized, of scalp, XVI, 1044 276 INDEX Edinger-Westphal nucleus, V, 329 Effectors, p. II Ego, The, p. 26 Egotism, p. 26 Elbow reflex, I, 64; V, 322 Electrical chorea, XI, 597, 628 motor points, I, 70; VII, 393; Vllb reaction, I, 70 to yz\ VII, 393, 395a of auditory nerve, VII, 403 degeneration, VII, 397-8, 402 Diminished, VII, 395 Exaggerated, VII, 396 Formula of degenerated nerve and muscle, VII, 397 of normal nerve and muscle, VII, 394 of muscles and nerves, I, 70 to Ti\ VII, 393, 395a Myasthenic, VII, 399 Myotonic, VII, 400 Neuritic, VII, 401 Normal, VII, 394 Electricity and the nervous system, p. 38 in examination of nervous patients, I, 70 to n, VII Embolism, Cerebral, X, 505 ; XIV, 835-60-1 ; XVI, 1065 Emotions, p. 21 Emotional insanity. Diseases causing, XVI, 1082 Emotions, Disturbances of, I, I ; III, 204 Tests for, I, 7 Emprosthotonos, IV, 265 ; XI, 590, 603 Encephalitis, XVI, 1046 Acute multiple, X, 495, 543-4; XVI, 1048 Epidemic, lethargic, XII, 677; XVI, 1047, 1234 Encephalomyelitis, XII, 659 Endarteritis, cerebral, sj-philitic, II, 178; XVIII, 1207 : See softening Spinal, syphilitic, II, 175; XVIII, 1211 : See spinal cord Syphilitica, II, 178; XVIII, 1207-II Endocrinopathies, XVIIb End organs, p. 5 Enophthalmos, XVII, 1191 Enteralgia, XV, 989 Epicritic sensibility, p. 7 Epidemic cerebro-spinal meningitis: See Ccrcbro-spinal meningitis Epigastric reflex, V, 310 Tests for, I, 57 Epilepsy, I, 2; II, iii-27-45a; IX, 420; XI, 575; XV, 1028; XVI, 1061-73 Amnesia in, XI, 575 Aura of, IX, 420; XIV, 849; XVI, 1061-73 Automatism in, XI, 575; XVI, 1061-73 Double personality in. III, 209; XI, 575; XVI, 1039 Glittering scotoma as sura of, XIV, 849 Idiopathic, XI, 575; XVI, 1061-73 Epilepsy, Jacksonian, IX, 421 ; XI, 587-8, 602; XXI, 1304; XXII, 1311 Major attack of, XI, 575; XVI, 1061 Media, XI, 575 Minor attack of, XI, 575 ; XVI, 1061 Nocturnal, XI, 575; XVI, 1061 Procursive, XI, 575 Psychic equivalent in, XI, 575 Rotatory, XI, 575 Spinal, I, 60-1; IX, 433; X, 509-20; XIV, 839-40 Symptomatic, XI, 576-87-8-95-6 Epileptic aura, IX, 420; XIV, 849; XVI, 1061- 73 coma, XI, 575; XVI, 1061-73 convulsion, IX, 420; XI, 575; XIV, 849; XV, 1028; XVI, 1061-73-85, 1 104 cry, XI, 575; XVI, 1061 dementia, XI, 575; XVI, 1061, 1104 idiocy, XVI, 1083 insanity, XI, 575; XVI, 1061-85, 1104 state, XVI, 1061 vertigo, XV, 1028 Epileptiform convulsion, XI, 571 Equilibrium, Sense of, p. 8 Erb's juvenile form of muscular dystrophy, X, 499; XIII, 787; XVII, 1 154 paralysis, IX, 444; X, 490 sign, IX, 442; XI, 612 syphilitic lateral sclerosis, X, 525; XVIII 12X2 ' Erotic excitement in dementia, XVI, 1107 Erroneous personality. III, 208 Eruptions, Cutaneous, Diseases causing, XVII, 1135 Erythromelalgia, XV, loio; XVII, 1198 Erythropsia, XIV, 846 Essential tremor, XII, 681 Ethics, p. 23 Etiology of nervous diseases, I, i ; II, 83 Eulenberg's disease, II, 106; IV, 265; XI 611 • XVI, II 57 Eunuchismus, Pituitary, XVII, 1176; XXI, 1302 Examination of patients Brain puncture, Id Electricity, Id Inspection, lb Laryngoscopy, Id Lumbar puncture. Id Ophthalmoscopy, Id Palpation, Ic Percussion, Ic Questioning, la Thermometry, Id Excessive sweating, XVII, 1203 Excitability, Nervous, p. 6 Excitation, Maniacal, XVI. 1 1 18 Exhaustion in etiology of nervous diseases, n, 95; Xin, 761 Vertigo from, XV, 1022 27; INDEX Exophthalmic goiter, 1, 20; II, 132; XII, 672; XVII, 1 193 Extension of inflammation in etiology of nerv- ous diseases, II, 90 External capsule, Symptoms of lesions of the, XXI. 301 rectus, Paralysis of the. XIV, 872 Exudative disorders. Diseases causing, XVII, 1145 Eye as cause of headache, XV, Q43-53 in disease, I, 24 Secondary deviation of sound eye, I, 3° Eyeball, Conjugate deviation of, XIV, 819 Displacement of the, XIV, 879 Limitation of motion of the, XII, 1700; XIV, 818 Optic atrophy in disease of the, XIV, 910-S Paralysis of external rectus, XIV, 872 inferior oblique, XIV, 877 rectus, XIV, 875 internal rectus, XIV, 873 superior oblique, XIV, 876 rectus, XIV, 874 Spasm of the muscles of, XIV, 878 Face center, Symptoms of lesions of, XXII, 1329-3-5 Facial expression in disease, I, 20 diplegia, XII, 703 hemiatrophy, XVII, ii79 hemihypertrophy, XVII 1180 monoplegia, XII, 703 nerve. Localization of lesions of, XXII, 1333-48 to 52 nucleus. Symptoms of lesions of, XXII, 1333-45-7 paralysis, XII, 703; XIII, 754; XIV, 928; XXII, 1333 spasm or cramp, XII, 726 Facio-scapulo-humeral type of muscular dis- trophy, X, 487; XIII, 7^7 ■• XVII, 1 154 False image. Position of, XIV, 818 Family gangrene, XVII, 1 196 history of nervous patients, I, 2 myoclonus epilepticus, XI, 601 periodic paralysis, X, 556 Faradism in examination of nervous patients, I, 70-2 ; VII, 393 Fatty tissue, Diseases causing atrophy of, XVII, 1:37 hypertrophy of, XVII, 11 38 trophic lesions of, XVII, 1125 Fear, III, 235 Feeble-minded, p. 28; XVI, 1094 Febrile or toxic convulsion, XI, 595-6 Festinating gait (festination), XI, 610; XII, 677; XIII, 769, 804 Fibrillary contraction (fibrillation), IV, 293 Diseases causing, XII. 641 Field of vision. Limitation of the, IX, 415 ; XIV, 817-68-71 ; XVI, 1076 Diseases causing, XIV, 817 Tests for, I, 14 Fits, I, I : See also convulsion and spasm Cerebellar, XI, 607-8; XXI, 1295 Flaccid paralysis, IV, 252 Diseases causing, X, 472 Tests for, I, 34 to 41 Foot drop, I, 21; II, 159; X, 488-94; XIII, 789-90; XVI, 1063 Formication, VI, 375 Formula of electrical reaction of degeneration, VII, 397 normal electrical reaction, VII, 394 Foul Air headache, XV, 955 Fourth ventricle. Vertigo from lesion within, XV, 1018 Foville's paralysis, IX, 454; XXI, 1292 Fragility of bone, XVII, 1141-85 Free will, p. 32 Frenzy, Maniacal, XVI, 11 18 Friedreich's hereditary ataxia, II. 104-24; XII; 651-70-87; XIII, 765-82 paramyoclonus multiplex, XI, 600 Froehlich's syndrome, XVII, 1176; XXI, 1302 Frontal convolution. Symptoms of lesions of the inferior. XXII. 1402 middle, XXII, 1401-g headache, XV, 953 lobes. Symptoms of lesions of the, XIV, 886; XXI, 1304; XXII, 1401-2 Gait, Diseases causing ataxic, XIII, 740 disorder of, XIII, 736 in disease, I, 21 ; XIII, 736 Festinating, XII, 610-77; XIII, 769, 804 High stepping, X, 488; XII, 662, 720; XIII. 789-91; XV. 1008; XVII, 1147-8; XIX, 1233; XXII, 1327 Mowing, XIII. 797 Paralytic and flaccid, XIII. 741 Spastic, XIII. 742 Scissors, X, 501 ; XIII, 798 to 803 Gallon's whistle, I, 15 Galvanic excitation of nerves and muscles, I, yz; VII, 393 Galvanism in examination of nervous patients, I, 71-2 Ganglionic disorders. Diseases causing, XVII, 1122-9-30 Gangrene, Family, XVII, Iig6 Symmetrical, XV, loii; XVII. 1195 Gastralgia, XV, 987 Gastric crises, IX, 423 General appearance in disease, I, 20 General paresis : See paresis sensation, p. g Cieniculate bodies. Lesions of, XIV, 862-93 ; XXII, T337 278 INDEX Genital neuralgia, XV, 991 Gerlier's vertigo, XV, 1032 Gigantism, II, 109; XVII, 1183 Girdle pain, VI, 374 Diseases causing, XV, 976 to 82 Glaucoma, XIV, 868; XV, 944 Glioma, II, 125 Central, X, 553 Glittering scotomata, XIV, 849 Globus hystericus, IX, 416; XI, 586; XVI, 1076 Glosso-pharyngeal paralysis, XII, 703a spasm or cramp, XII, 727 Glossy skin, I, 40; XVII, 1160 Glove form of anesthesia, VI, 348; IX, 415 Gluteal paralysis, XII, 719 reflex, V, 307 Tests for, I, 57 Gordon's reflex, V, 305 Graefe's symptom, XII, 672; XVII, 1192-3 Grandeur, Delusion of, XVI, 672; XVII, 1192-3 Grand mal (le), XI, 575; XVI, 1061 Grasset and Gaussel's phenomenon, IX, 448 Gratiolet, Lesions of the optic fasciculus of, XIV, 859-60; XXII, 1378 Graves' disease, I, 20; II, 132; XII, 672; XVII, 1 193 Green vision, XIV, 847 Gumma, II, 175 Isolated cerebral, XVIII, 1206 Spinal. XVIII, 1210 Gustation, Cortical center of. p. 8; XIV, 810 Gustatory sensations, p. 8 Habit, p. 26, 32 chorea, IV, 274; XI, 627 spasm, IV, 274; XI, 627 Habits, Sensory, p. 14 Habitation as cause of nervous diseases, I, 2 ; II, 89 Habitual criminals, p. 29; XVI, 1096 Hallucinations, p. 30; I, 4-20; III, 213 Hallucinatory insanity, Diseases causing, XVI, 1080 Hallucinosis, Alcoholic, XV, 112 Hand, Ape's, XII, 714 Claw, X, 547; XII, 71S Obstetrical, XI, 612 Paralysis of muscles of, XII, 714-6 Trident shaped, XVII, 1177 Haphalgesia, VI, 380 Hare's eye, XII, 703 Head in disease. The, I, 22; XVI, 1078 Head's researches on sensibility, p. 6 Headache, I, i ; XV, 934 Alcoholic, XV, 954 Anemic, XV, 950-3-9 Aural, XV, 953 in cerebellar tumor, XV, 962 in cerebral abscess, XV, 961-7 Headache, Congestive, XV, 958 Constipation, XV, 953-6 Diseases causing, XV, 934 Dyspeptic, XV, 953 Foul air, XV, 955 Frontal, XV, 953 High blood-tension causing, XV, 958 Hydrocephalic, XV. 961 Indurative, XV, 964 Infectious, XV, 965 Meningitic. XV, 963-6 Menstrual. XV, 950 Migraine, XIV, 849-58; XV, 950. I029 Vertigo in. XV, 1029 Morphine. XV, 954 Vertigo from, XV, 1031 Neurasthenic, XV, 960 Occipital, XV, 949-53 Ocular, XV, 953 Pachymeningitic. XV. 963 Pelvic. XV, 953 Rheumatic, XV, 964 Sinus thrombosis causing, XV, 966 Sunstroke causing, XV, 968 Temporal, XV. 953 Toxic. XV, 965 Tumor causing, XV, 961 Uremic, XV, 957 Vertex, XV, 953 Heatstroke or sunstroke, XI, 589; XV, 968; XVI, 1070 Hearing, p. 8; I, 15; HI, 223-33; VI, 355-72- So; XIII, 744-75; XIV, 809-22; XXII, 1382 Cortical center of. p. 8; XIV, 822; XXII, 1382 Diseases causing disorders of, XIV, 809 Loss of, XIV, 822 Tests for, I, 15 Hebephrenia. XVI, 1099 Heine-Medin's disease, X, 495 Hematorrhachis, X, 524; XI, 606; XV, 973 Cerebro-spinal fluid in, XIX, 1240 Hemeralopia, VI, 360 Hemianesthesia altemans, or crossed, VI, 348; XXI, 1292 dolorosa, XIV, 837a; XXI, 1298 and hemianalagesia, VI, 348 ; IX, 4IS ; XIV. 843; XXI, 1290-3 Hysterical. VI, 348; IX, 41S : XIV, 837 Transference of, IX, 415; XIV, 837 Hemianopia, VI, 362; XIV, 817-58-63-90 as aura of migraine, XIV, 858 Bi-temporal, VI, 362; XIV, 817-64-94; XXII, 1335 Diseases causing, XIV, 817 Homonymous, VI, 362; XIV, 817, 59 to 63-95; XXI, 1298, 1307, 1337; XXII, 1355-78 Diseases causing, IV, 817-90 279 INDEX Hemianopia. Horizontal, XIV, 866 Localization of, XXI, 1298, 1307; XXII, I 355-6 Nasal, VI, 362; XIV, 8i;-65; XXII, 1336 Diseases causing, XIV, 817 Quadrantic, VI, 363; XIV, 816, 856-7; XXI, 1307; XXII, 1356 Tests for, I, 14 Hemiataxia, XII, 653 to 57 Hemiatrophy, Facial, XVII, 1179 Hemicrania, XV, 950 angio-paralytica, XV, 950 spastica, XV, 950 Hemichorea, IV, 272; X, 510; XI, 573, 622 Hemichromatopsia, VI, 364; XIV, 850 Hemihypertrophy, Facial, XVII, 1180 Hemiopic pupillary reflex, V, 334 Diseases causing, XIV, 817-90 Tests for, I, 26 Hemiplegia, I, 21; IV, 254; X, 478-9-81 altemans, or crossed, IV, 256; X, 537 to 42; XV, 1017; XXI, 1290 to 93 Facial, IV, 256; XXI, 1292 Hypoglossal. IV, 256; XXI, 1290-1 Oculo-motor, IV, 256; XXI, 1293 Angio-spastic. X, 555 Complete, IV, 254; XXI, 1299 Diseases causing, X, 478-9-81 ; 534-41 ; XII, 653-5-6; XXII, 1384-5-88 to 99 Homolateral, IV, 254; XXI, 1299 Hysterical, XIII, 796 Infantile: See cerebral palsy of childhood Lacunar, XVI. 1066 Organic, XIII, 797 Partial, IV, 254 Spinal, IX, 432; X, 509; XIV, 844; XV, 982; XX, 1276: See also Brown-Se- quard's paralysis Hemorrhage (or softening), in brain stem, X, 534; XII, 656: XIII, 749; XIV, 832 XII, 1290 tfi f:;; Cerebral, 11, i-<7-S9; X, 503; XI, 588 XIV, 8.r=;-f.n-i XVI, 1043-64 Cerebro-spinal fluid in, VIII, 405-6 XIX, 1242 into ventricles, X, 504 internal, Coma in, XVI, 1059 Vertigo in. XV, 1023 Meningeal cerebral, II, 147-89; X, 502; XI, 588; XVI, 1043-63 Cerebro-spinal fluid in, VIII, 405-6; XIX, 1241-2 Spinal, X, 524 of spinal cord (or injury) above cervical enlargement, X, 512; XIV, 830 in cervical enlargement, X, 547 dorsal region, X, 516 lumbar region, X. 484 in cms cerebri (or injury of), X, S36; XH, 656; XXI, 1293 Medulla, X, 540-4; XHL 749; XXI, 1290 pons, X, 5.38-43; XIII, 749 Hepatic crises, IX, 423 Hereditary ataxia, II, 104-24; XII, 651-69-70- 87; XIII. 765-82-3 chorea : See chorea infantile poliomyelitis, X, 5483 Heredity in nervous diseases, I, 2; II, 81 Herpes, I, 40: XI, 590; XIV, 834 zoster, XV, 940-8; XVII, 1166; XIX, 1235 Cerebro-spinal fluid in, XIX, 1235 Herpetic ganglionitis or neuritis, XV, 940-78 Hiccough, XII, 731 High blood-tension. Headache from, XV, 958 Vertigo from, XV, 1026 High stepping gait, X, 488; XII, 662, 720; XIII, 789-91; XV, 1008; XVII, U47-8; XIX, 1233; XXII, 1327 Hip, Congenital dislocation of, XIII, 788 Hippus, V, 336 History taking, I, i Homonymous hemianopia : See hemianopia scotomata, XIV, 867 Homer's syndrome, IX, 455; XVI, 1191 Hunger, p. 9 Huntington's hereditary chorea, II, 103 ; XI, 624 Hydrocephalic cry, XI. 593 idiocy, II, 120; XVI, 1084 Hydrocephalus, I, 22; II, 120; XIV, 905; XV, 961; XVI, 1084 Cerebro-spinal fluid in, VIII, 405; XIX, 1239 Headache in, XV, 961 Optic neuritis in, XIV, 905 Hydrophobia, II, 173; XI, 604 Hydrorrhoea nasalis, XXI, 1302 Hypakusia, VI, 355 ; XIV, 823 Hypalgesia, VI, 349; XIV, 81 1-2 Hyperakusia, VI, 372; XIV, 823 Hyperalgesia, VI, 367 Tests for, I, 50 Thermic, VI, 368 Hyperemic reflex, V, 327; XVII, 1200 Hyperesthesia, VI, 366; XIV, 815 Tests for, I, 48 Thermic, VI, 368 Hypergeusia, VI, 370 Hyperhidrosis, XVII, 1203 Hyperkinesis, IV, 242 Hyperosmia, VI, 369 Hyperostosis cranii, XVII, 1181 Hypertonia, I, 39; IV, 240; X, 473 Hypertonic paralysis, IV, 251 ; X, 473 Hypertonic pulmonary osteo-arthropathy, XVII, 1 184 Hypertrophies, Localized, XVII, 1188 Hypertrophy of bone, Diseases causing, XVII, 1 140 of fat. Diseases causing, XVII, 1138 muscle, 1. 40 Diseases causing, XVII, 1132 in an athletic,, XVII, 1156 skin. Diseases causing, XVII, 1134 280 INDEX Hypesthesia, VI, 348; XIV, 811 Thermic, VI, 35° Hypnotism, XVI, 1071 Hypochondriasis, III, 216; XVI, 1075 Hypogeusia, VI, 357; XIV, 810 Hypoglossus paralysis, XII, 706; XIII, 755 spasm or cramp. XII, 729 Hypokinesis, IV. 241 Hyposmia, VI, 356 Hypotonia, I, 39; IV, 240; X, 472, 483 Hypotonic paralysis, IV, 252; X, 472 Hysteria, I, 2; II, 1 12-29-31-54-82; IX, 415; X, 527; XIV, 846-S1-70, 926; XV, 951- 71-2-6-7 Auto-suggestion in, IX, 415 ; XVI, 1071-2- Concentric limitation of field of vision in, IX, 415; XIV, 870 Perversion of vision in, XIV, 846-51 Traumatic, XVI, 1077 Vertigo from, XV, 1034 Hysterical amblyopia, XIV, 855 anesthesia, p. 7; VI, 348; IX, 415; XIV, 837; XVI, 1076 Tests for, L 48 aphonia, XIII, 747-8-62 ataxia, XII, 664 backache, XV, 971 chorea, XI, 629 coma, XVI, 1 071 contracture, X, 618 convulsion, IX, 415; XI, 586; XVI, 1076 deafness. XIV. 924 delusions, IX, 415 diplopia, XIV. 880 hemianesthesia, VI, 348; IX, 415; XIV, 837; XVI, 1076 hemiplegia, XIII, 796 hyperakusia and parakusia, XIV, 926 joint, XV, 1000 monoplegia, X, 527; XIII. 796 mutism, IV, 283; XIII, 747; XVI, 1076 neuralgia, XV, 951-71 paralysis I, 21; IX, 415; X, 527; XIII, 747-862-96; XIV, 880; XVI, 1076 spasm, IV, 268; IX, 415; XI, 616-8; XII, 637; XVI, 1076 suggestion, IX, 415; XVI, 1071-2-6 symptoms, IX, 415 tremor, XII, 674 Hystero-epilepsy, XI, 586 Hysterofrenic areas, IX, 418 Hysterogenic areas, IX, 417 Ictus, X, 479 laryngeal, IX, 423 Ideas, p. 17. 23 Idiocy, p. 38; II, loi; XIII, 743; XVI, 1083-9 Idioglossia, XIII, 753 Idiopathic epilepsy, XI, 575; XVI, 1061-73 idiocy, XVI, 1083-9 imbecility, XVI, 1090-3 muscular dystrophy, X, 498 neuralgia, XV, 937 Idiots savants, XVI, 1091 Illuminating gas, poisoning, XVI, 1058 Illusions, p. 291 ; III, 214 Imagination, p. 25 Imbecility, p. 28; II, loi : XVI, 1090 mattoids, XVI, 1095 moral, XVI, 1096 morons, XVI. 1095 Imagination, p. 25 Immobile eyeball, X, 545 pupil, V. 333 ; X. 545 Indurative headache, XV, 964 Infantile diplegia, II, 117; X, 501; XI, 577. 631 ; XII. 801 ; XVI, 1051-88 hemiplegia, II, 1 17; X, 501; XI, 577, 631; XIII, 801; XVI, 1051-88 hereditary family poliomyelitis, X, 548a paralysis: See poliomyelitis Infection, XVI, 1095 Infectious chorea, XI, 622-3 headache, XV, 9<^5 nervous diseases, I, i ; II, 93 Inferior oblique muscle. Paralysis of, XIV, 877 rectus muscle, paralysis of, XIV, 875 Inflammation in brain stem, X, 534-43-4; XII, 656 . . Cerebral : See meningitis, encephalitis and abscess of nerves: See neuritis spinal cord: See spinal cord Infra-maxillary neuralgia or neuritis, XV, 946 -orbital neuralgia or neuritis, XV, 945 Ingravescent apoplexy, XVI, 1063-6 Inherited nervous diseases, II, 84 tendencies to, II, 85 Inhibition, p. 11 Injury, I, I ; H, 136-46 of Cauda equina, X, 487 brachial plexus, X, 490 nerve, X, 489-92; XIV, 824; XVII. 1 146-7 optic nerve, XIV, 904; H. 147-89; X, 524; XIX, 1242 or hemorrhage, of spinal cord cervical enlargement, X, 549 cervical region, X, 512 dorsal region, X. 516 lumbar region, X, 484 Innervation feelings, p. 18 Insanity, p. 28; I, 2; II, 110-30-5S; XVI, 1041 Acquired, p. 29 Adolescent or juvenile, XVI. 1098 Alcoholic, XVI. H02-9-12 Catatonic, XVI. iioo 281 INDEX Circular, XVI, 1 1 19-20 Confusional, XVI. 1108 Congenital, p. 29 Delusional, III, 215; XIII, 746; XVI, 1081, 1 1 13-4-5-6 Dementia, XVI, 1097. 1 103 to 07 Dementia precox, XVI, 1098 Emotional, Diseases causing, XVI, 1082 Epileptic, XI, 575; XVI, 1061-85, II04 Febrile and Post- febrile, XVI, 11 10 Hallucinatory, XVI. 11 12 Diseases causing, XVI, 1080 Hebephrenic, XVI. 1099 Korsakow's psychosis, X, 488; XVI, 1 102 Maniacal, XVI. 1 12-4-8-20 Manic-depressive, XVI, 1120 Melancholic, XVI, III5-7 Paranoia, XVI, 11 16 Pananoid, XVI, iioi Paresis, p. 29, II, 135-80; VIII, 409-12-3-4; XI, 579; XII, 675; XIII, 766; XIV, 897, 013; XVI, 1052, 1 106; XVIII, 1216; XIX, 1230 Post-epileptic, XII, 575; XVI, 1061 Puerperal, XVI, mo Recurrent, XVI, 1120 Septic, XVI, mo Tests for, I, 4 Toxic, XVI, mo Insolation, XI, 589; XV, 968; XVI, 1070 Insomnia, I, 18 Inspection in diagnosis I, 20 to 43 Insufficiency of ocular muscles, XII, 692; XIV, 818 Intelligence, p. 25 Disturbances of, III, 202 Tests for, I, 5 Intention tremor, IV, 291 ; XII, 645 Diseases causing, XII, 645 Intercostal neuralgia, XV, 977 spasm or cramp, XII, 732 Interlacing of color fields, I, 14; XIV, 851-2 Intermittent limping or claudication, II, 190; X, 555; XVII, 1 199 Internal capsule. Symptoms of lesions of, XIV, 861; XXI, 1279; XXII, 1367-74-97 rectus muscle. Paralysis of, XIV, 873 sensations, p. 9 Interscapular reflex, V, 311 Tests for, I, 57 Intoxication, Alcoholic, XI, 585; XII, 658-63; XII, 767-81 Inversion of color fields, I, 14; XIV, 851-2 Involuntary motions, p. 35 Iridoplcgia, V, 339 Iritis, I, 24 Irritation of sympathetic ganglia. Diseases causing, XVII, 1143 Ischemic reflex, V, 326 Island of Reil, Symptoms of lesions of, XXI, i3or Jacksonian epilepsy, IX, 421 ; XI, 587-8 Location of lesions causing, XXI, 1304-5; XXII, 131 1 Janet's test, I, 48; IX, 415 Jargon speech. III, 226; XIII, 778 Jaundice, Yellow vision in, XIV, 845 Jaw, Paralysis of muscles of, XII, 702 reflex, V, 323 Tests for, I, 65 Spasm of muscles of, XII, 725 Jendrassik's method of reflex reinforcement, I. 68 Joint sense, I, 43 Joints, Diseases causing trophic lesions of, XVII, 1 127 Joy, III, 236 Juvenile insanity, XVI, 1098 Kahler's disease, XVIII, 1209 Kak-ke : See multiple neuritis Kalmuck idiots, XVI, 109S Keratitis, I, 24 Kernig's sign, V, 320 Tests for, I, 66 Kinesthesia, p. 7; I, 43 Tests for, I, 42-3 Knee-clonus, I, 61 -jerk, I, 61 ; V, 319 pendular, I, 6i Tests for, I, 61 Knowledge, Tests for general, I, 5 Klumpke's paralysis, IX, 445 ; X, 490 Korsakow's psychosis, IX, 451; X, 488; XVI, 1 102 Kyphosis, I, 23; XVII, 1183 Labyrinth disease and labyrinthine vertigo, XII, 649-85; XIV, 918; XV, 1019 Labio-glosso-pharyngeal-laryngeal paralysis, IX, 412; X, 546; XII, 694; XIII, 759- 64; xvn, I IS I Lacunar hemiplegia, XVI, 1066 Lagophthalmos, XII, 703 Lalling, XIII, 753 Landouzy-Dejerine type of muscular atrophy, X, 497; XVII, HS4 Landry's paralysis, II, 170 ; X, 482 Lang's colloidal gold test, VIII, 414 Language, Zone of, p. 35 Laryngeal crises, IX, 423 ; XVI, 1062a exhaustion, XIII, 761 Nerve, Paralysis of superior, XII, 704; xm, 757 inferior (Recurrens") XII, 704; XIII. 7S8 vertigo, IX, 423; XVI, 1062a Laryngismus stridulus, XI, 616; XII, 728 Laryngitis, XIII, 760 Laryngoscopy in examination of nervous patients, I, 77 282 INDEX Larynx, Anesthesia of, XIII, 757-63-4 paralysis of, XII, 704; XIII, 757-8 spasm of, XII. 728; XIII, 757-8 Lasegue's symptom, IX, 419 Lateral column : See spinal cord sclerosis, X, 525-47; XIII, 800 Amyotrophic, X, 547; XII, 695; XIII, 800; XVII, I ISO Erb's syphilitic, X, 525; XVIII, 1212 Lateropulsion, XXI, 1292-5-6 Lead colic, II, 159; XV, 989 convulsion, X, 494; XI, 576-84 palsy, II, 159; X, 494; XII, 716; Xin, 790; XVI, 1053 poisoning, Optic neuritis in, Leg center: See localization paralysis of muscles of, XII, 717-21 spasm of, XII, 733 Le grand mal of epilepsy, XI, 575 ; XVI, 1061 Lemniscus, Lesion of, causing deafness, XIV, 922 Lenticular progressive degeneration, XII, 668 Le petit mal of epilepsy, XI, 575 ; XVI, 1061 Leontiasis ossea, XVII, 1181 Leprous neuritis, II, 141; XVII, 1169 Lethargic encephalitis, XII, 677; XVI, 1047; XIX, 1234 Lethargy, African, II, 142; XVI, 1055 Leucoderma, XVII, 1162 Levator palati. Paralysis of, XIII, 756 Limping, Intermittent, X, 555; XVII, 1 199 Lisping, XIII, 753 Little's Disease : See Cerebral palsy of child- hood Local asphyxia. XV, loii ; XVI, 1059 cyanosis, XV, roii; XVI, 1059; XVIL 1 195 paralysis, IV, 259 ; X, 481 ; XII, 700 to 721 spasms, XI, 571-2; XII, 637 syncope, XVII, 1195: See also Raynaud's disease Localization, p. 13; XX, XXI, XXII at base of cranium, XXI, 1297 by Jacksonian epilepsy, XXII, 131 1 by paralysis, motor and sensory, XXII, 1310 Cerebellar, XXI, 1295 direct tract, XII, 1295 hemispheres, XI, 607 peduncle (middle), XXI, 1296 vermis, XI, 608 Cerebellum, Symptoms of lesions of, XXI, 1295 Cerebral, XXI, 1290 to 1309 brain stem, X, 5,34-45 ; XII, 656 ; XIV, 832; XXI, 1200 to 97; xxn. 1321-4-87-90-4-6, I 40 I -8 abducens nucleus, XIV, 872; XXII, 1343-4-46-7 corpora quadrigemina, XXI, 1294 Localization, crura cerebri, X, 536-7; XII, 676; XII, 1293; XXII, 1340-5-96, 1408 dysarthria and dysphagia, XXII, 1387-90-4-5, MOO facial nucleus, XXII, 1345-7 fourth ventricle, XV, 1018 ganglia at base, XXI, 129 to 1303 lemniscus, XIV, 129 922 medulla oblongata, X, 540-1-4; XII, 656; XIII, 749; XXI, 1290; XXIL 1387-94, 1400-8 motor cranial nuclei, XXII, 1324 pons Varolii, X, 538-9-43; XIV, 843- 85; XXI, 1292; XXII, 1344-66-76- 95, 1401-8 ponto-cerebellar angle, XXII, 377 red nucleus, XXI, 1293; XXII, 1341 rubrospinal tract, IX, 431; XII, 676; XXI, 1293; XXII, 1341 sensory cranial nucleus, XXII, 1343 sixth cranial nucleus, XXII, 1343 hemispheres agraphia. III, 228; XXI, 1304; xxn, 1377 alexia. III, 229; XIII, ^^T, XXH, 1403 angular gyrus, XXII, 1493 aphasia, motor. III, 222; XIII, 774; XXI, 1304; XXII, 1402 sensory, III, 223; XIII, 775-6; XXI, 1306; XXII, 1358-82 arm center, XXII, 1362-6-83-8-91-3-9, 141 1 astereognosis. III, 230; VI, 354; XXII, 1359-83 blindness, psychic. III, 232; XXI, 1307; XXII. 1357-81 calcarine fissure, XXII, 1378-9-80 central convolution, anterior, XII, 1 385-8-91 -2-3-9, 1410-I- posterior, XXII, 1361-2-5-83 claustrum, XXI, 1301 corpus callosum, XXI, 1300 striatum, XXI, 1299; XXII, 1398 cortical lesions, XXI, 1308 external capsule, XXI, 1301 face center, XXII, 1392-9 facial fibers, XXII, 1545 frontal convolution, inferior, XXII, 1402 middle, XXII, 1401-9 frontal lobe, XIV, 886; XXI, 1304; XXII, i40t-2 geniculate bodies, XXII, 1337 ganglion, XXII, I349-50 hemianopia, homonymous, XIV, 817 ; XXI, 1298, 1307, 1337; XXII, I35S- 6: See also hemianopia 283 INDEX Localization, internal capsule, XIV, 86l ; XXI, IZ99; XXII, 1367-74-97 island of Reil, XXI 1301 leg center, XXII, 1361-5-8-75-85-91-9, 1412 nucleus caudatus, XXI, 1299, lenticularis, XXI, 1299 occipital lobe, XIV, 850-3-6-7; XXI, 1307; XXII, 1378-9-80-1 optic fasciculus of Gratiolet, XIV, 850-9-60; XXII, 1378 thalamus, XXI, 1298, XXII, 1398 parietal lobe, XII, 657; XXI, 1395; XXII. 1368; 1413-5 lobule, inferior, XXII, 1375 superior, XXII, 1368 pineal gland, XXI, 1303 pituitary gland, XXI, 1302 Reil, island of, XXI, 1301 temporal convolution or lobe superior, XIV, 923-243.-2$; XXI, 1306; XXII. 1358-82 cranium, at base oi, XXI, 1297 Failure of, VI, 376 Motor paralysis, XXII, 1315-16-17-19-20 Neurons, central, XXII, 1313 peripheral XXII, 13:2 brachial plexus, XXII, 1326 Cauda equina, XXII, 1328 chorda tympani, XXII, 1351-2 cranial motor nerves, XXII, 1323 sensory nerves, XXII, 1321 facial nerve, XXII, 1333-48 to 52 hemianopia, XXII 1331 : See also Hemianopia lumbar plexus, XXII, 1326 optic chiasm, XIV, 854-64-5-94; XXII, 1335-6 nerve, XIV, 847-54-66; XXII, 1334 tract, XIV, 862-2-3-95; XXII, 1337 orbit, XIV, 915; XXII, 1332-8 ponto-cerebellar angle XVII, 1377 sixth cranial nerve, XXII, 1343 spinal nerves, X, 489; XIV, 824; XXII, 1323 to 8 third cranial nerve, XXII, 1339 sensory paralysis, XXII, 1314-16-17- 18-20 Spinal cord, XX, 1250 to 79 anterior commissure, XX, 1275 ; XXII, 1370-2 horn, XX, 1268; XXII, 1324 nerve roots, XXII, XXII, 1324 Burdach's column, XXII, 1322 central gray matter, XXII, 1370-2 cervical enlargement and region, XXII, 1330-63-4-71-2-86-9, 1407 direct cerebellar tract, XII, 653 ; 1272 dorsal region, XXII, 1360-9-84, 1404 I Localization, lateral column, XXII, 1369-71- 3-84-6-9, 1406 li'mbar enlargement, XXII, 1329-70 posterior column, XII, 654; XIII, 786; XX, 1271; XXII, 1322-60-3-4,1406 horn, XX, 1269; XXII, 1322 nerve roots, XX, 1298-9; XXII, 1322 Segments cervical ; 8th, XX, 1263 7th, XX. 1264 6th, XX, 1265 5th, XX, 1266 4th to 1st, XX, 1267 dorsal ; I2th to 3d, XX, 1260 2d, XX, 1261 1st, XX, 1262 lumbar; 5th, XX, 1250 4th, XX, 1251 3d, XX, 1252 2d, XX, 1253 1st, XX, 1254 vision, Dusturbances of, XIV, 808; XXII, 1331 Localized atrophies and hypertrophies, XVII, 1188 Lockjaw: See tetanus Locomotor ataxia : See tabes Long thoracic nerve. Paralysis of, XII, 709 Lower motor neurons, p. 9; IX, 462 sensory neurons, IX, 464 Lumbar enlargement : See spinal cord plexus, spasm or cramp of, XII, 733 symptoms of lesions of, XXII, 1326 puncture, I, 74; XI, 590 Technic of, I, 74 Results of, XIX, 1220 Lumbo-abdominal neuralgia, XV, 990 Lyssa, II, 173; XI, 604 Macrocephaly, I, 22 Macropsia, VI, 387 Major attack of epilepsy, XI, 575; XVI, 1061 Mania, p. 29; III, 236 Acute alcoholic, XVI, 1 109-12 Epileptic, XI, 575; XVI, 1061-85, 1 104 Primary. XVI, 11 18 Symptomatic, or delusional or secondary, XVI, 1 1 14 Maniacal excitation, XVI, 11 18 frenzy, XVI, 1 1 18 Manic-depressive insanity, XVI, 1120 Marie-Tooth-Charcot's type of muscular atrophy, X, 496; XII, 696 Marie's hereditary cerebellar ataxia, II, 104- 24; XII, 650, 69; XIII, 783 ideas of aphasia, XIII, 739 reflex of spinal automatism, V, 328 284 INDEX Mask-like face, XI, 6io; XII, 677; XIII, 769, 804 Mastodynia, V, 983 Masturbation in nervous diseases, I, 2 Mattoids, XVI, 1095 Maxillary reflex, V, 323 Mechanical irritability of nerves and muscles, I, 67 Median paralysis, XII, 714 Medulla oblongata, Hemorrhage or softening in, X, 540-1-4; XII, 749 localizing symptoms : See localization Tumor of, X, 541; XII, 656; XIII, 749 Meig's disease, XVII, 1202 Melancholia, p. 29; III, 234 agitata, XVI, 11 15 attonita, XVI. 1115 cum stupore, XVI, 1115 Primary, XVI, 11 17 raptus, XVI, 11 15 Secondary, or sympathetic, or sympto- matic, or delusional, XVI, 1 1 15 Memor>',p. 17 Disturbances of, I, i ; III, 203 Tests of, I, 6 Mendel-Bechterew's reflex : See dorsal foot reflex Meniere's disease, XII, 649-85; XIV, 918; XV, 1019 Meningeal apoplexy, II, 147-89; X, 502-24; XI, 588 ; XIV, 1063 Meningismus, XI, 594 Meningitis, II, 119-23-48-67-76-86-92; X, 508; XI, 590-1, 605; XVI, 1045 Cerebral, X, 508; XI, 590, 605; XFV, 834; XV, 1033; XVI, 1045; XVIII, i2o8-9r 14-^6 to 29 Vertigo in, XV, 1033 Cerebro-spinal, XI, 591, 605; XVIII, 1214; XIX. 1226 to 29 fluid in, VIII, 405-9-10-1-2; XIX, 1226 to 29, 1332 gummosa, II, 176; XVIII, 1208-9-13-14 Headache in, XV, 963-6 Localized, X, 508 Optic neuritis in. XIV, 906 Purulent, II, 192; XI, 592; XIX, 1227 Cerebro-spinal fluid in, XIX, 1241 Spinal, acute and chronic, XI, 605 ; XV, 974, 1 105; XVIII, 1213-4 of spinal cord and nerve roots, XVIII, 1213 Syphilitic, XV, 981 ; XVIII, 1208-9-13-14 Tuberculous, II, 119-23-92; XI, 593; XIX, 1228-9 Cerebro-spinal fluid in, XIX, 1228-9 Meningocele, II, 102 Mental activity, Disturbances of, I, I ; III, 200; XVI, 1036 Diseases causing disorders of, XVI, 1036 Reaction time. Tests for, i, s Mentality, Weakened, XVI, 1040 Meralgia paresthetica, XV, 999 Mercurial tremor, II, 160; XII, 673 Metamorphopsia, VI, 385 Metastasis in nervous diseases, II, 98 Metatarsalgia, XV. 1003 Microcephaly, I, 22; XVI, 1084 Micropsia, VI, 386 Microsmia, XVII, 1177 Migraine, II, 1 15 ; XV, 950, 1029 Glittering scotomata in, XIV, 849 Hemianopia in, XIV, 858 Vertigo from. XV. 1029 Millard-Gubler's s>'ndrome, IX, 429; XXI, 1229 Milroy's disease, XVII, 1202 Miner's nystagmus, XII, 684 Minor attack of epilepsy, XI, 575 ; XVI, 1061- 73 Miosis, I, 24; V, 340; XII, 661; XVII, 1191; XXI, 1290 Mixed aphasia. III, 225; XIII, 778 Mobile spasm, IV, 271 Mongolism, XVI, 1095 Monocular diplopia, VI, 381 ; XIV, 818 Monoplegia, IV, 258; X, 478-9-81, 527; XIII, 796 Diseases causing, X, 47S-9-81 Hysterical, X, 527; XIII, 796 Organic, XIII, 797 Moral imbecility and insanity, p. 28; XVI, 1096 sense, Tests for, I, 5 Morons. XVI, 1095 Morphine headache, XV, 954 vertigo, XV, 1 03 1 Morton's toe, XV, 1003 Morvan's disease : See Sj'ringomyelia, Motion, Diseases causing diminution of, IV, 244; X, 469; XXII, 1315-6-9-20 Exaggeration of, IV, 245-7; XI, 570; XXII, 1311 Perversion of, IV, 243; XII, 635 Disorders of voluntarv-, IV, 240; X, 469; XI. 570 ; XII, 635; Xni, 735 Involuntary', p. 35 Motives, Play of, p. 33 Motor aphasia, III, 222; XIII, 774 Localization of, XXI, 1304; XXII, 1402 Ataxia, IV, 280; X, 488; XII, 644; XXI. 1290 to 97 Diseases causing, XII, 644 Impulses, Conduction of, p. 9 Neurons, p. 8, 9 Diseases of the, X. 469: XI, 570; XII, 635-7 -oculi. Paralysis of, XII, 700 paralysis, IV, 244 : X. 469 Diseases causing, X, 469; XXII, 1315-6- 9-20 Localization of, XXII, 1310 Tests for, I, 34-5 285 INDEX paresis, IV, 244; X, 469 points, electrical, I, 70-1 ; VII, 393 Movements, p. 10 Association, p. 22 Autochthonous, p. 35 Automatic, p. 14, 35 Involuntary, p. 35 Reflex : See reflex Voluntary, p. 14, 31 Mowing gait, XIII, 797 Mucous membrane reflex acts, V, 298 Tests for, I, 58 Multiple encephalitis. Acute, X, 495, 543-4; XVI, 1046-7-8 Myelitis : See sclerosis Neuritis : See neuritis Sclerosis : See sclerosis Muscae volitantes, XIV, 848 Muscle degeneration, IV, 252; XVII, 1131 -joint sensation, p. 9 sense, Loss of, XI, 352; X, 488; XII, 661; XIV, 813 Diseases causing, XIV, 813 Tests for, I, 43 tone, I, 40; IV, 240 Muscles and nerves, Electrical reaction of, I, 72 : VII, 393 Mechanical excitability of, I, 67 trophic lesions of, Diseases causing, X, 476-7; XVII, 1 123 Muscular atrophy, I, 41 Aran-Duchenne's type of, X, 548; XII, 694-5; XIII, 800, XVII, iiso-i Charcot Marie-Tooth's type of, X, 496; XII, 696 in chronic paralysis, XVII, 1155 Dise-ases causing, X, 476-7; XVII, 1131 from disease, XVII, 1155 Idiopathic. X, 498 Landouzy-Dejerine type of, X, 497; XVII, "54 Peroneal type of, X, 496 ; XII, 696 "~ Progressive, spinal, X, 547-8; XII, 695; XIII. 800; XVII. 1 150 Spinal or neuritic, X, 496; XII, 696 Muscular coordination, I, 47 dystrophies, II. 107-28; X, 477; XIII, 787; XVII, 1 154-8 dystrophy, Erbe's juvenile form, or scapu- lo-humeral type, X, 499; XIII, 787; XVII. 1 154 in disease, X, 477 Landou7y-Dejerine's form, or facio- scapulo-humeral type, X, 497; XIII, 787; XVII, 1 154 Pseudo-hypertrophic form, I, 21 ; X, 500; XIII, 787; XVII, 1 158 Simple or idiopathic, X, 498; XIII, 787; XVII, 1 1 54 Muscular hypertrophy, I, 40 in athletes, XVII, 11 56 Diseases causing, XVII, 1132 Muscular insufficiency, ocular, I, 24; XII, 692; XIV, 818 rigidity, I, 31 : See also paralysis agitans tonicity. I, 39; IV, 240; X, 472-3 Musculo-cutaneous paralysis, XII, 713 -spiral paralysis, XII, 716 Mutism, Deaf, IV, 283 ; XIII, 744 Hysterical, IV, 283; XIII, 747; XVI, 1076 Insane, IV, 283; XIII, 746; XVI, 1097, 1104-5-15-17 Myasthenia gravis, X, 554; XIII, 764 Tests for, I, 36 Myasthenic electrical reaction, VII, 399 paralysis, IV, 253; X, 554; XIII, 764 Myatonia congenita, II, 105 ; X, 483 Mydriasis, I, 24; V, 339 Myelitis or Myelomalacia, II, 122-49-68-87 in anterior horns : See poliomyelitis cervical enlargement, X, 550; XIV, 838; XVII, 1149; XXII, 1330 region, X, 413-4 Compression, II, 122; X, 520; XIII, 79$ Disseminated : See sclerosis in dorsal region, X, 517-8; XIV, 831 above lumbar enlargement, X, 513-14-17- 18-20-50; XIII, 708; XIV, 830-1-8 in limibar enlargement, X, 485; XIII, 793; XIV, 827; XVII, 1 149; XX, 1339 Multiple: See sclerosis Transverse, XV, 980 Myoclonia, XII, 697 Myoclonic nystagmus, XII, 691 Myoclonus, IV, 270; XI, 600-1 epilcpticiis, XI, 601 Myokimia, IV, 294; XII, 697 Myopia and cycloplegia, V, 331 Myotonia, IV, 265 acquisita, XI, 611 atrophica, XI, 611 congenita, II, 106; IV, 265; XI, 6ri ; XVII, 1 1 57 intermittens, XI, 6tl Myotonic electrical reaction, VII, 400 Mysophobia, III, 235; XVI, 1074 Myxedema, I, 20; XVII, T163 Nageotte and Babinski's bulbar syndrome, IX, 427: XXI, 1290 Nanosmia, XVII, ii77 Narcotism, II, 165; XI, 585; XV, 954; XVI, 1057 Nasal hemianopia, VI, 362; XIV, 817-65; XXII, 1336 reflex, V, 313 Tests for, I, 58 Neck, Paralysis of muscles of, XII, 705 Spasm of Muscles of, XII, 730 286 INDEX Negativismus, XVI, 1098 to iioi Nerves and muscles, Electrical reaction of, I, 71-2; VII, 393 Injury of, X, 489-92; XIV, 824; XVII, 1 146-7; XXII, 1323-7 Nerves and muscles, Symptoms of lesions of nerves, Motor cranial, X, 452 ; XXII, 1323-7 Facial, XII, 703; XIII, 754; XIV, 928; XXII, 1333-48 to 52 Sixth (abducens), XIV, 872; XXII, 1343 Third. XII, 700; XIV, 873 to yT, XXII, 1339-42 Root, anterior, XX, 1279 ; XXII, 1324 posterior, XIV, 826; XX, 1278; XXII, 1322 sensory, cranial, XXII, 1322 spinal, X, 489; XIIc and d; XIV, 824; XXII, 1323-5-7 : See also neuralgia, neuritis and tabes Nervous system, Physiology of, p. 5 Neuralgia, I, 2; II, 1 15-71; XV, 933-37 Achillodynia, XV, 1001 Angina pectoris, XV, 984 Arthralgia, XV, looo Calcanodynia. XV, 1002 Causalgia, XV, 1003a Coccygodynia, XV, 972 Cervico-brachial, XV, 995 Crural, XV, 997 Enteralgia, XV, 989 Erythromelalgia, XV, loio; XVII, 1 198 Gastralgia, XV, 987 Genital, XV, 991 Herpetic, XV, 940-78 Hysterical. XV, 951-71, 1000 Idiopathic, XV, 937 Infra-maxillary. XV. 946 Infra-orbital, XV, 945 Intercostal, XV, 977 Intestinal, XV, 989 Joint, XV, 1000 Lumbo abdominal, XV, 990 Mastodynia. XV. 983 Meralgia paresthetica, XV, 999 Metatarsalgia, XV, 1003 Neurasthenic, XV, 960-70 Obturator, XV, 998 Occipital, XV, 949-53 Pelvic, XV, 953-91 Phrenic, XV, 986 P.seudo -angina pectoris, XV. 985 Sciatica, XII, 720; XV, 996 Spinal, XV, 971 Supra- orbital, XV, 944 Symptfmatic, XV, 937-53 Syphilitic, XV, 952 Tabetic, XV, 979-88, T004 Talalgia, XV, 1002 Thermalgia, XV, 1003a Neuralgia, Tic douloureux, IV, 267; XI, 599; XII, 726; XV, 948 Trigeminal, XV, 943 to 47 Neurasthenia, II, 114-56-62-64-81-3 ; XV, 560- 70; XVI, 1074 Perversion of vision in, XIV, 846-8 Neurasthenic backache, XV. 970 headache, XV, 960 tremor, XII, 671-4 vertigo, XV, 1034 Neuritic electrical reaction, VII, 401 or spinal muscular atrophy, X, 496; XII, 696 Neuritis, II, 141-3-5-51-66-77-88; X, 488-9-92; XIV, 824; XV, 933-41-9, XVII, 1147-73; XXII, 1321 to 27 Alcoholic: See multiple neuritis Anterior crural, XV, 997 Arsenical, II, 158: See multiple neuritis Brachial plexus, X, 490 Causalgia, XV, 1003a Compression, XV, 939 Crural. XV, 997 Diabetic. II, 194: See also multiple neuritis Diphtheritic, X, 488; XIII, 756-7: See also multiple neuritis Erythromelalgia, XV, loio; XVII, 1198 Herpetic ganglionitis or neuritis, II, 141-3- 5-51-8-66-88-94; XV, 5WO-78, XVII, 1 166 Cerebro-spinal fluid in, XIX, 1235 Infra-maxillary, XV, 946 -orbital. XV, 945 Leprous, II. 141; XVII, 1169 Multiple, II, 140- 1 -58-61 -77-94; X, 488; XII, 662; XIII, 756-7-89; XIV, 82s, XV, 952-1008; XVII, 1 147; XVIII, I2is; XXII, 1327 Occipital, XV, 049 Optic, X, S07-8; XIV, 892. 910 tract, XIV, 862-3-95; XXII, 1337 Simple XV, 933-41-9; XVII, 1 147-73; XXII. 1321 to 27 Supra-orbital, XV, 944-53 Syphilitic, II, 177; XVIII, 1215 Trigeminal. XV, 943 to 48 Neuroma. X, 491 ; XV, 938 Neurons, p. 6 Centrifugal, p. 9 Centripetal, p. 6 Diseases of the, central, X, 473-4; XXII, 1313 motor, p. 8, 9; IV, 251-2; IX, 461-a X, 460-72-3; XVII, 1 131 peripheral. X, 472-4; XIV, 805; XXII, 1312 sensory. VI. 344: IX. 463-4; XIV, 805 Neuroses, II, 133-8 Occupation. II, 144: XI. 615 Traumatic. II. 157; XII, 674; XV, 1034; XVI, 1074-7 287 INDEX Neurotonic electrical reaction, VII, 401 Nicotine tremor, XII, 673 vertigo, XV, 1031 Nictitation, XII, 726 Nictitatio spastica, XII, 679-90, 726 Nocturnal epilepsy, XI, 575 ; XVI, 1061 Nonne-Apfelt test, VIII, 412 Nuclei, Symptoms of lesions of cranial, X, 493; XXII, 1321-2-4 motor, X, 493; XXII, 1324 Facial, XXII, 1347 Sixth, XXII, 1343 Third, XXII, 1339-42 sensory, XII, 1322 Spinal motor, XXII, 1324-7 : See poliomyelitis sensory, XXII, 1322-7 : See tabes Nucleus caudatus and lenticularis : See locali- zation Numbness, VI, 375; XIV, 814 Nyctalopia, VI, 361 Nystagmus, I, 24, 31; IV, 292; XXI, 1294-5 Cerebellar, I, 80 Diseases causing, XII, 640 Miner's, XII, 684 Myoclonic, XII, 691 Tests for, I, 24, 31, 80 Observation, Delusion of, XVI, 1 1 16 Tests for power of, I, s Obstetrical hand, XI, 612 paralysis, IX, 444-5 ; X, 490 Obturator neuralgia, XV, 998 paralysis, XII, 718 Occipital headache, XV, 949-53 lobe, SjTnptoms of lesions of, XIV, 850-3- 6-7; XXI, 1307; XXII, 1378-9-80-1 neuralgia or neuritis, XV, 949-53 Occupation in nervous diseases, I, 2; II, 90 neuroses, II, 144; XI, 611 Ocular ataxia, XII, 648 headache, XV, 953 muscles. Insufficiency of, XII, 692; XIV, 818 Paralysis of, XII, 700; XIV, 818-72-7; XXII, 1332 Spasm of, XI, 590; XIV, 818-78 vertigo, XII, 648; XV, 1020 Oesphageal spasm, XI, 616 Olfaction, Cortical center, p. 8 Olfactory sensation, p. 8 Ontogenetic acts, p. II Ophthalmoplegia completa, X, 545 externa, X, 545; XI, 590; XIV, 872 interna, X, 545; XI, 590; XIV, 873 progressiva, X, 545 sympathetica, XXI, 1290 Ophthalmoscopic examination. Diseases re- vealed by, I, 76; XIV, 821 Opisthotonos, IV, 265 ; XI, 590, 603-13 Opium poisoning, XVI, 1057 headache from, XV, 954 tremor from, XII, 673 Oppenheim's disease, X, 483 reflex, I, 57; V, 306 Optic aphasia. III, 224; XIII, 776 atrophy, XIV, 893, 911 chiasm, p. 8 symptoms of lesions of the, XIV, 854- 64-S; XXII, 1335-6 fasciculus of Gratiolet, Lesions of the, XIV, 850-960; XXII, 1378 nerve. Lesions of the, XIV, 847-54-66; XXII, 1334 neuritis. Diseases causing, X, 507-8; XIV, 892 atrophy following, XIV, 910 papilla, Abnormalities of, XIV, 821 thalamus. Symptoms of lesions of, XII, 655; XXI, 1298; XXII, 1398 Localization in : See localization tract, p. 8 Symptoms of lesions of, XIV, 862-3-95; XXII, 1337 Orbit, Symptoms of lesions within, XIV, 915 ; XXIL 1338 Organic diseases, II, 137-9 hemiplegia, XIII, 797 reflex acts, I, i ; V, 300-24-5 ; X, 476 ; XIV, Sii Orthotonos, IV, 265 ; XI, 590, 603-13 Oscedo, XII, 731 Osseous sense. Loss of, VI, 353 Tests for, I, 56 Osteitis deformans, XVII, 1182 Osteo-arthropathy, Hypertrophic pulmonary, XVII, 1 184 Osteogenesis imperfecta, XVII, 1185 Osteomalacia, XVII, 1185 Osteopsathyrosis, XVII, 1 185 Ovarian tenderness, IX, 415 Oxyakoia, XIV, 823 Pachymeningitis, X, 502 ; XI, 588 ; XVI, 1063 Headache in, XV, 963 hypertrophica cervicalis, X, 551 interna hemorrhagica, X, 502; XI, 588; XVI, 1063 Paget's disease, XVII, 1182 Pain, p. 7; I, I, 50; VL 374-80 Diseases causing, XV, 931 in abdomen, XV, 935 back, XV, 935 extremities, XV, 936 head, XV, 934 nerve distribution, XV, 933 thorax and abdomen, XV, 935 trunk, XV, 935 Girdle, VL 374; XV, 976 to 82 Persistence of, I, 52; VI, 382 288 INDEX Pain, Radiating, VI, 374 Referred, VI, 374; XV, 953 Retardation of conduction of, I, 51 ; VI, 381 Palatine arch, High, XVI, 1078 Pallesthesia, Loss of, V, 353 Tests for, I, 56 Palpation in examination, Ic Palsies, Local, IV, 259; X, 481; XI, 571-2; XII, 636 Pantophobia, III, 235 Papilla : See Optic papilla Paradoxical pupillary reflex, V, 338 reflex, V, 318-9-38 sensation, VI, 379 Parageusia, VI, 391 Paragraphia, III, 227; XIII, 780 Parakinesis, IV, 243 Parakusis, VI, 389; XIV, 823 Diseases causing, XIV, 823 Paralysis, I, 1-21 ; IV, 244 Abducens, XII, 701 ; XIV, 872 Abductor laryngeal, XIII, 759 Acute ascending, II, 170; X, 482 Agitans, I, 20-1; XI, 610; XII, 677; XIII, 769, 804 Alcoholic : See multiple neuritis Arsenical : See multiple neuritis Atonic, IV, 252; X, 472 Atrophic, IV, 252; X, 472-6-7, 547-8 Acute: See poliomyelitis Chronic : See chronic atrophic and bulbar paralysis Axillary, XII, 712 Bell's, XII, 703 Brachial plexus, IX, 414-5; X, 490; XXII, 1326 Brown-Sequard's, IX, 432; X, 509; XIV, 844; XV, 982 Bulbar, IX, 424; X, 544-6; XH, 694; XIII, 759-64; XVII, 1 151 Cauda equina, X, 487; XII, 721; XV, 1007; XXn, 1328 Cervical rib, X, 557 sympathetic, IX, 455; XVII, 1191 Choreic, X, 510 Chronic bone atrophy in, XVII, 1139 Muscular atrophy in, XVII, 1155 continuous, Diseases causing, X, 470 Crico-ar>-tenoid, XIII, 759 -thyroid, XIII, 757 Crossed, IV, 256; X, 535 to 41 ; XV, 1017; XXI, 1290 to 93 Crural, XII, 717; XV, 997 Diaphragmatic, XII, 707 Diphtheritic, XIII, 756-7: See also mul- tiple neuritis Diseases causing, IV, 244; X, 469; XIV, 805; XXII, 1310 Diver's, X, 521 iParalysis, Erb's, IX, 444; X, 490 I External rectus, XII, 701; XIV, 782 Facia'., XII, 703; XIII, 754; XIV. 928; XXII, 1333-45 to 52 Family periodic, X, 556 Flaccid, IX, 252 Diseases causing, X, 472 Test? for, I, 34 to 41 Foville's, IX, 454; XXI, 1292 Glosso-pharyngeus, XII, 703a Gluteal, XII, 719 Hand, XII, 714-16 Hj-pertonic, IV, 251 ; X, 473 Hypoglossal, XII, 706; XIII, 755 ?lypotonic, IV, 252; X, 472 Hysterical, I, 21; IX, 415; X, 527; XIII, 747-S-62-96; XIV, 880; XVI, 1076 Infantile : See poliomyelitis and cerebral palsy of childhood Inferior oblique, XIV, 877 rectus, XIV, 875 Intermittent, X, 471 Internal rectus, XIV, 873 Klumpke's, IX, 445 ; X, 490 Labio-glosso-ipharyngeal-laryngeal, IX, 412; X, 546; XII, 694; XIII, 759-64; XVII, 1151 Landry's, II, 170; X, 482 Laryngeal nerve. Recurrent, XIII, 758 Superior, XIII, 757 Lead, II, 159; X, 494; XII, 716; XIII, 790; XVI, 1053 Levator palati, XIII, 756 Local, IV, 259; X, 481; XI, 571-2; XII, 700 to 721 Localization of lesions causing, XXII, 1310 Median, XII, 714 Motor, IV, 244; X, 469; XXII, 1315-6-9- 20 Tests for, I, 34-5 Motor-oculi, XII, 700; XIV, 873 to JT, XXII, 1339 to 42 Musculo-cutaneous, XII, 713 -spiral, XII, 716 Myasthenic, IV, 253; X, 554; XIH, 764 Neck muscles, XII, 705 Obstetric, IX, 444-5 ; X, 490 Obturator, XII, 718 Peroneal, XII, 720 Phrenic, XII, 707 Pneumogastric, XII, 704; XIII, 763 Posticus laryngeal, XIII, 759 Pseudo-bulbar, X, 554; XIII, 764 -hypertrophic, X, 500; XIII, 787; XVn, 1 158 Pterygoid, XII, 702 Radial, XH, 716 Rectus externus, XIV, 872 inferior, XIV, 875 oblique, XIV, 877 intemus, XIV, 873 289 INDEX Paralysis, Rectus, superior, XIV, 874 oblique, XIV, 876 Recurrens, XIII, 758 Sciatic, XII, 720 Sensory, Diseases causing, VI, 345 ; XIV, 805, XXII, 1314-6-8-20 Serratus, XII, 709 Spastic, IV. 251 ; X, 473 Spinal accessory, XII, 705 Sub-scapular, XII, 711 Superior larjngeal nerve, XIII, 757 oblique, XIV, 876 rectus, XIV, 874 Supinator longus, XII, 716 Supra-scapular, XII, 708 sympathetic ganglia, Diseases causing, XVII, 1 142-91 Tests for, I, 34-5 Thoracic (anterior and posterior), XII, 710 Long, XII, 709 Thyreo-ary-epiglottis, XIII, 757-602 Tibialis, XII, 720 Trigeminus (motor branch), XII, 702 Trochlearis. XV, 701 Ulnar, XII, 715 Vagus, XII, 704; XIII, 763 Vaso- motor, V, 327 Paralytic dementia : See paresis and flaccid gait, XIII, 741 spastic gait, XIII, 742 vaso-motor reflex, V, 301-27 Paramyoclonus multiplex, XI, 600-1 Paramyotonia congenita, II, 106; IV, 265; XI, 611 Paranoia, XVI, 11 16 Paronoiacs, p. 29 Paranoid form of insanity, XVI, iioi Paraphasia, III, 226; XIII, 778 Paraplegia, I, 21 ; IV, 257; X, 480 Ataxic, X, 526; XII, 660; XIII, 799 Diseases causing, X, 474-80-1-2-84 to 88; XIII, 741-2; XV, 975-80; XXII, 1384-7 dolorosa, XV, 975 Senile, X, 522; XIII, 794 Spastic, X, 525-47; XIII, 800 Paresis, p. 29; II, 135-80; XI, 579; XII, 675; XIII, 766; XIV, 897; XVI, 1052, 1106; XVIII, 1216; XIX, 1230 Cerebro-spinal fluid in, VITI, 409-12-3-4; XIX, 1230 Motor, Diseases causing, IV, 244; X, 469 Tests for, I, 35 Optic atrophy in, XIV, 913 Paresthesiae. p. 7; VI, 375 Parietal lobe and lobule : See localization Parkinson's disease: See paralysis agitans Parosmia, VI, 390 Passive contracture. I, .38; IV, 263 Tremor, IV, 290; XII, 646, 646a Diseases causing, 646, 646a Pelvic neuralgia, XV, 953-91 Pemphigus, XVII, 1 168 Pendular knee-jerk, I, 61 Perceptions, p. 16 Percussion in examination of nervous diseases, Ic Perforating ulcer, XVII, 1172 Periodic family paralysis, X, 556 Peripheral neurons. Disorders of, X, 472-4; XIV-80S Location of lesions of, XXII, 1312 Motor neurons, IX, 462 Diseases of, X, 472-4 Sensory neurons, IX, 464 Diseases of, XIV, 805 Peroneal paralysis, XII, 720 Peroneal type of muscular atrophy, X, 496; XII, 696 Persecution, Delusion of, XVI, 1 1 16 Persistence of sensation, I, 52 ; VI, 382 Tests for, i, 52 Personal factors in nervous diseases, I, 2; II, 82 Personality, p 25 Double, III. 209; XVI, 1039 Diseases causing. XVI, 1039 Erroneous, III, 208 Diseases causing : See insanity Pes calcaneus et valgus, XII, 720 equino-varus, XII, 720 Petit mat (le), XI, 575; XVI, 1061 Pharyngeal crises, IX, 423 reflex, V, 316 Pharynx, Spasms of muscles of, XII, 727 ' Pharynx, Paralysis of, XII. 703a spasm of, XII, 727 Phobias, III, 235; XVI, 1074 Photophobia, VI, 371 : XII, 683 Phrenic neuralgia, XV, 986 paralysis, XII. 707 spasm or cramp. XII, 731 Phylogenetic acts. p. 11 Physical exarrination of patient, I Physiological introduction, p. S Pianist's cramp. XI. 615 Picric acid poisoning, XIV, 845 Pill-rolling movement of fingers, XII. 677 Pineal gland. Diseases of, XXI. T303 Pituitary gland. Diseases of the, XXI, 1302 enlarged. Symptoms of, XIV, 864 Kunucbism from disease of, XVII, 1176; XXL 1302 Plantar reflex, V, 303 Tests for, I, 57 Play of motives, p. 33 Pleasure, p. 21 Plcurosthotonos, IV, 265 ; XL 590. 603 Plexuses. Brachial and Lumbar, Symptoms of lesions of, IX, 444-51 X, 490; XII, 733; XXII, 1326 290 INDEX Pneumogastric paralysis, XII, 704; XIII, 763 spasm or cramp. XII, 728 Points of Valleix, XV, 937-43-49-7"-90-5-7 Poisons, I, l; II, 92, 165; X, 482; XII, 633; XIV, 845; XVI, 1058 Polioencephalitis inferior. Acute, X, 534-44 Chronic, X, 546; XII, 694; XIII, 764; XVII, nsi superior. Acute, X, 543 ; XVI, 1046-8 : See also Botulismus and encephalitis chronic, X, 545 Poliomyelitis, Acute anterior, II, 118-69; X, 1(^5; XIII, 797; XVII, 1148; XIX, 1^33 Cerebro-spinal fluid in, VIII, 409-12; X, 495; XIX, 1233 Chronic, X, 548; S48b Infantile hereditary, (family), X, 548a Polyesthesia, I, 54; VI, 378 Polyneuritis, II, 140-1-58-61-77-94; X, 488; XII, 662; XIII, 756-7-89; XIV, 82s; XV, g;52-ioo8; XVII, 1147-69; XVIII, 1215; XXII, 1327 Polyopia, VI, 384 ; XIV, 881 Pons Varolii, Hemorrhage or softening in, X. 538-9-43; XIII, 749; XIV, 843-85; XXI. 1292 Localizing symptoms of: See localization Symptoms of lesions of, XIV, 843-85; XXII, 1344-46-66-76-95, 1401-8 Tumor in, X. 539 ; XII, 656 Ponto-cerebellar angle. Symptoms of lesions of, IX, 428; XXII, 1377 Ponto-spinal tract, the, p. 10 Porencephalic idiocy, XVI, 1088 Porencephaly, II, 117; X, 501; XI, 577, 631; XIII, 801 ; XVI, 1088 Position sense. Tests for, I, 41 Post-epileptic insanity, XI, 575; XVI, 1061 coma, XI, 575; XVI, io6i -febrile insanity, XXI, 1 1 10 -hemiplegic ataxia, XII, 655 athetosis, XI, 631-2 chorea, X, 501 ; XI, 626 contracture, X, 501-4; XI, 577, 614-9 -neuritic contracture, XI, 621 -paraplegic contracture, X, 480, 516 to 20; 549 to 52; XI, 620; XIII, 742 Posterior column or horn: See Spinal cord inferior cerebellar artery, Thrombosis of, XXI, 1291 longitudinal bundle. Lesion of, XIV, 885 spinal ganglion, Lesion of, XX, 1277 Postero-lateral sclerosis, X, 526; XII, 660; XIII, 799 Posticus (laryngeal) paralysis, XIII, 759 Pott's disease, I. 23 ; II, 121 ; X, 520 Predilection muscles (Wernicke's). IV, 254 Predisposing factors in nervous diseases, II, 82 Preputial irritation, IV, 251 Pressure sensation, p, 6 Pressure sense. Loss of, VI, 351 Tests for, I, 49 Priapism, X, 512-5-49-52; XI, 604; XIV, 830 Primary dementia, XVI, 1097 Procursive epilepsy, XI, 575 Prodromata of apoplexy, IX, 422 of epilepsy, IX, 420 Progeria, XVI, 1095 Progressive bulbar paralysis, IX, 424; X, 546; XI], 694; XllI, 759-64; XVII, 1151 lenticular degeneration, XII, 668 muscular atrophy, X, 547-8; XII, 695; XIII, 800; XVII, 1150 ophthalmoplegia : See polioencephalitis superior chronica Propulsion, XI, 610; XII, 677; XIII, 769, 804 Prosopalgia, XV, 943 to 48 Prosopoplcgia, XII, 703 Protopathic sensibility, p. 7 Pseudo-angina pectoris, XV, 985 -bulbar paralysis, X, 546, 554; XIII, 764 -chorea, XI, 573 -clonus, IX, 415 -coma, Diseases causing, XVI, 1038 -hypertrophic paralysis, I, 21; X, 500; XIII. 787; XVn, 1158 -nystagmus, XII, 640 -paresis, XVI, 1103; XVIU, 1208 -ptosis, XVII, 1191; XXI, 1290 -tabes : See multiple neuritis Psychalgia, XVI, 11 17 Psychasthenia, V, 970; XVI, 1074 Psychic blindr.ess, p. 17; III, 232; XXI, 1307; XXII, 1357 deafness, p. 17; III, 223-33; XIII, 775; XXI, 1306 equivalent of epilepsy, XI, 575 ; XVI, 1061 functions. The, p. 14 trauma, XVI, 1072-6 Psychoanalysis, I, 2 Psychosis, Korsakow's, IX, 451; X, 488; XVI, 1102 Ptarmus, XII, 728 Pterygoid paralysis, XII, 700 Ptosis, I, 24; XII, 700 Puerperal insanities, XVI, mo Pulmonary osteo-arthropathy, XVII, 1184 Pupillary abnormalities, I, 24; XIV, 820 opening, double. XIV, 881 reflex acts Argyll-Robertson, V, 332; IX, 437; XIV, 891 Accommodation, I, 27; V, 331 Consensual, I, 25 ; V, 329 Direct, I, 25 ; V, 329 Hemiopic, I, 26; V, 334; XIV, 890 Indirect, I, 25; V, 329 Light. I, 25-7; V, 329 Pain, V, 330 Paradoxical, V, 338 291 INDEX Pupillary reflex acts. Pathology of, V, 302 Physiology of, V, 302 Westphal's, V, 337 Pupils, Iirmobile, V, 333; X, 545 Unequal, V, 341 Pulse in nervous diseases, I, 46 Purulent meningitis, XI, 592; XIX, 1227 Cerebro-spinal fluid in, XIX, 1227 Pyramidal tract, Lesion of, XX, 1270 Quadrantic hemianopia, VI, 363; XIV, 816-56- 7; XXI, 1307; XXII, 1356 Quincke's disease, XVII, 1201 Quinine vertigo, XV, 1031 Quinquand's sign, IX, 443 Rabies, II, 173; XI, 604 Race in nervous diseases, II, 88 Radial paralysis, XII, 716 Radiculitis, XV, 942 Raptus melancholicus, XVI, 1115 Raynaud's disease, XV, loii; XVI, 1059; XVII, 1 195 Reaction of completely degenerated muicle, VII, 402 of degeneration. Electrical, VII, 397-8 Reading, Diseases causing disorders oi, XIII, 735-77 Tests for, I, 9 Reasoning, p. 33 Receptors, p. 11 Recognition, p. 17 Rectal crises, IX, 423 reflex, V, 325 Rectus extemus oculi. Paralysis of, XIV, 872 inferior, XIV, 875 obliquus. XIV, 876 internus, XIV, 873 superioris, XIV, 874 obliquus, XIV, 876 Recurrens paralysis, XII, 704; XIII, 758 Recurrent insanity, XVI, 1 1 20 Red nucleus. Symptoms of lesions of, IX, 431 ; XXI, 1293; XXII, 1341 vision, XIV, 846 Referred pains, VI, 374 Reflex Achilles, I, 62; V, 318 Acts, p. 14; V, 296 abolition of. Diseases causing, X, 472; XIV, 811; XXII, 1312 exaggeration. Diseases causing, X, 472; XIV, 8ri; XXII, 1313 Inhibition of, V, 296-7 Reinforcement of, I, 68 Anal, V, 307a Ankle, I, 60; V. 317-8 arc, p. 10; V, 296 Argyll-Robertson, V, 332; IX, 437; XIV, 891 Association, p. 14, 31 Reflex, Auditory-orbicularis, V, 314 Babinski's, I, 57; V, 304, 328 Bechterew's, I, 63 ; V, 321 Bladder, V, 324 Brissaud's, V, 303 Cilio spinal, V, 335 Conjunctival, I, 58; V, 312 Corneal, I, 58; V, 312 Cortical, p. 12 Cremasteric, I, 57; V, 308 Cutaneous, I, 57; V, 297 Deep, I, 60 to 68 ; V, 299 Defensive (Babinski), V, 327a Dorsal foot, I, 63 ; V, 321 Elbow, I, 64; V 322 Epigastric, I, 57; V, 310 Gluteal, I, 57; V, 307 Gordon's, V, 305 Hemiopic, I, 26; V, 334; XIV, 890 Hyperemic, V, 327; XVII, 1130 Inhibition of, p. 10 Interscapular, I, 57: V, 311 Ischemic, V, 326; XVII, 1 130 Jaw, I, 65; V, 323 Kemig's, I, 66; V, 320 Knee, I, 61 ; V, 319 Pendular, I, 61 Marie's, of spinal automatism, V, 328 ; Maxillary, I, 65 ; V, 323 Mendel-Bechterew's I, 63; V, 321 Mucous membrane, I, 58; V, 298 Nasal, I, 58; V, 313 Oppenheim's, I, 57; V, 306 Organic, I, i ; 300-24-5 ; X, 476 ; XIV, 811 Paradoxical, V, 318-9-38 Pharyngeal, I„ 58; V, 303 Plantar, I, 57; V, 303 J Pupillary, I, 25-7-8; V, 302 to accommodation, V, 331 light, V, 329 Pain, V, 330 Rectal, V, 325 Reinforcement of, I, 68 Spasm, IV, 268; XI, 616-8; XII, 637; XVII, 1 194 spinal automatism (Marie), V, 328 Sub-cortical, p. 10 Superficial, I, 57; V, 297 Tendon, I, 60-6; V, 299; X, 472-3; XIV, 811 Umbilical, I, 57; V, 309 Uvular, I, 58; V, 315 Vaso- motor, I, 59; V, 301-27 Vesical, V, 324 Westphal's pupillary, V, 337 Wrist, I, 64; V, 322 Reil, Island of. Symptoms of lesions of, XXI, 1301 Reinforcement of reflexes, I, 68 Renal crises, IX, 423 292 INDEX Respiration, Biot's, IX, 425 Cheyne- Stokes', IX, 425; XII. 728; XXI, 1290 Tests for, I, 45 Retardation of conduction of pain, I, 51 ; VI, 381 Retching, V, 316 Retina, Perversion of vision in diseases of, XIV, 847-83 Retroactive amnesia, XIII, 772; VI, 1102 Retrograde amnesia, XIII, 772 Retropulsion, XI, 610; XII, 677; XIII; 769; 804 Reverie, p. 24 Rheumatism of scalp, XV, 964 Rhythmical chorea, XI, 629 Rigidity, I, 31; IV, 266; XI, 590, 603-S-10-12; XII, 677; XIII, 769, 804 Rigors, XII, 680 Rinne's test. I, 15 Risus sardonicus, XI, 603 Romberg's symptoms, I, 41 ; IX, 438 Rosenbach's sign, XVI, 1063-6 Rotatory epilepsy, XI, 575 Rubro-spinal tract, The, p. 9 Symptoms of lesions of, IX, 431 ; XII, 676; XXI, 1293; XXII, 1341 Salaam cramp, XII, 690 Saltatory spasm, XI, 618 Sanity, Tests for, I, 4 Santonin poisoning or jaundice, XIV, 84S Scalp, Localized edema of, XVI, 1044 Rheumatism of, XV, 964 Scapulo-humeral type of muscular atrophy, X, 499; XII, 787; XVII, 1 154 Schiiller's side gait, IX, 456; XIII, 796-7 Sciatic plexus. Spasm or cramp of, XII, 733 Sciatica, XII, 720; XV, 996 Scissors gait, X, 501; XIII, 798 to 803 Schmidt's syndrome, IX, 450; XII, 706 Sclerodactyly, XVII, 1165 Scleroderma, I, 20; XVII, 1165 Sclerosis, Amyotrophic lateral, X, 547-8; XII, 695; XIII, 800; XVII, 1150 Combined, or postero-lateral, X, 526; XII, 660; XIII, 799 Disseminated, or multiple, II, 150; X, 511; XI, 580; XII, 659-66-88; XIII, 759- 68, 803 ; XIV, 914 ; XV, lois ; XVI, I0S4 Optic atrophy in, XIV, 914 Vertigo in, XV, 1015 Lateral, X, 525-47 ; XIII, 800 Syphilitic of Erb, X, 525; XVIII, 1212 Postero-lateral, X, 526; XII, 660, XIII, 799 Scoliosis, I, 23 Scotomata, Glittering, XIV, 849 Homonymous, XIV, 867 Scurvy, X, 495 Seamstress' cramp, XI, 615 Secondary dementia, XVI, 1105 deviation of sound eye, XIV, 818 Tests for, I, 30 Secretory disorders, Diseases causing, XVII, 1 145 Semeiological charts. Introduction to, p. S Semi-coma, III, 206 Diseases causing, XVI, 615 Senile chorea, XI, 625 dementia, p. 29; XVI, 1107 optic atrophy, XIV, 911 paraplegia, X, 522 tremor, XII, 678 Senility, Fragility of bones in, XVII, 1185 Sensation, p. 6, 15; VI, 344; XIV, 805; XV, 930 Auditory, p. 8; I, 15; HI, 223-33; VI, 355-72-89; XIII, 744-75; XrV, 809; XXII, 1382 Conduction of, p. 7 Cutaneous, p. 6 Deep, p, 6 Difficulties in testing, I, 47 Diminution of, I, 47; VI, 345; XIV, 806-II Diseases causing, XIV, 806; XXII, 1314-16-18-20 Disorders of, VI, 344; XIV, 805; XV, 930 Dissociation of. III, 209; VI, 365 Diseases causing, XIV, 812; XXII, 1354 Double, I, 54; VI, 378 Equilibrium, p. 8 Exaggeration of, VI, 346; XIV, 807 Diseases causing, XIV, 807 General, p. 9 Gustatory, p. 8; I, 17; VI, 357-70-9I ; XV, 810 Hearing, p. 8 Internal, p. 9 Kinesthetic, p, 7 Light, p. 10, I, 12; VI, 358 to 64-71-83 to 87; XIV, 808 Disorders of, XIV, 808 Localization of, I, 531 XXII, 1310-14-16- 18-31 Muscle-joint, p. 7; I, 43; VI, 352; X, 488; XII, 661 ; XIV, 813 Olfactory, p. 8; I, 16; VI, 356-69-90; XIV, 810 Painful, p. 7 ; VI, 374 ; XV, 930 Paradoxical, VI, 379 Persistence of, I, 52; VI, 382 Perversion of, VI, 347 Diseases causing, XIV, 816; XV, 930 Pressure, p. 6; L 49) VI, 351 Sight, p. 8 Summation of, p. II Tactile, p. 6; I, 48; VI, 348-66-76 to 82 Temperature, p. 6; I, 48-SS ; VI, 350-68-79; XIV, 81 1 -2 Visual, p. 8 293 INDEX Sensibility, Deep, p. 6; I, 43 Epicritic, p. 7 Head's researches on, p. 6 Protopathic, p. 7 Sensory aphasia, p. 34; I, 6; III, 223-4; XIII, 775-6-7 Locahzation of, XXI, 1306 ; XXII, 1358-82 Septic insanity, XVI, mo Serous niening^itis, XI. 594; XIX, 1241 Cerebro-spinal fluid in, XIX, 1241 Serratus paralysis. XII, 709 Sex in nervous diseases, II, 87 Shaking palsy : See paralysis agitans Shell shock, XVI, 1077 Shivering, XII, 680 Shock, I, I Shoemaker's cramp, XI. 615 Side gait, Schiiller's, IX. 456; XIII, 796-7 Sight, p. 8; I, 12 Cortical center of, p. 8; XXI, 1307 Loss of, VI, 358 to 64; XIV, 808; XXII, 1331-S-6-7 Perversion of, XIV. 808; XXII, 1331-2-S- 6-7 Simple delusional insanity, XVI, 1 1 13 idiopathic muscular dystrophy, X, 498; XIII, 787; XVII, 1154 Singer's cramp, XI, 615 Singultus, XII, 731 Sinus thrombosis, II, 185; XV, 966; XVI, 1044 Headache in, XV, 966 Sixth cranial nerve or nucleus (abducens), Symptoms of lesions of, XIV, 872 ; XXII, 1343 Skill, Loss of: See apraxia Skin, Diseases causing atrophy of, XVII, II33 eruptions of, XVII, 113S hypertrophy of, XVII, 1134 trophic lesions of, XVII, 1 124 ulcerations of, XVII, 1136 Glossy, XVII, 1 160 Skull in disease, I, 22; XVII, 1181: See also cranium Sleep, I, 18 Sleeping sickness, II, 142 ; XVI, 105S Smell, p. 8 Cortical center of, XIV, 810 Loss of, VI, 356 Perversion of, VI, 369, 390 Tests for, I, 16 Sneezing, V, 313; XII, 728 Snow blindness, VI, 360; XIV, 846 Softening, Cerebral, X, 505-6; XIV, 835-60-I ; XVI, 104.V65-6; XVIII, 1207 Brain stem, X, 534; XII, 656 Crus cerebri, X, 536-43 Medulla, X, 540-4; XIII, 749 Pons, X, 538-43; XIII, 749 Spinal. II, 189a; X, 485-513-4-7-8-50; XIII. 793-8; XIV, 827-30-1-8; XV, 080; XVIII, 1211 Somnambulistic state. III, 210; XVI, 1061-72- 3-5 Somnolence, II, 142; III, 207; XVL 1055 Sopor, III, 207 Spasm, I, 7; XI, 570: See also reflex acts or cramp, p. 35 ; IV, 242 abdominal, XII, 732 asthmatic, XI, 616-8; XVII, 1194 athetoid, IV, 271 ; XI, 574 Auctioneer's, XI, 615; XII, 726 Blepharospasm, XI, 598, 616; XII, 682, 726 Brachial, XII, 733 Choreic, IV, 272; XI, 573 Clonic, IV, 246 ; XI, 571 Cornet player's, XI, 615; XII, 726 Diaphragmatic, XII, 731 Facial, XII, 726 Glosso-pharyngeal, XII, 727 Habit. IV, 274; XI, 627 Hypoglossal, XII, 729 Hysterical, IV, 268; XI, 586-618-20; XII, 637-732; XVI, 1076 Intercostal, XII, 732 Irregular, IV, 247 Jacksonian epilepsy, IX, 421 ; XI, 587-8 602-17; XXI, 1304-5; XXII, 131 1 Jaw muscles, XII, 725 Laryngismus stridulus, XI, 616; XII, 728 Local. XI, 571-2; XII, 637 Lumbar, XII, 733 Mobile, IV, 271 Neck muscles, XII, 730 Nictitans, XII, 726 Nutans, XII, 679-90 Occupation, XI, 615 Ocular muscles, XL 590; XIV, 818-80-7 Oesophageal, XI, 616 Phrenic, XII, 73l Pianist's, XI, 615 Pneumogastric, XII, 728 Reflex. IV, 268; XI, 616-8; XH, 637; XVII, 1154 Salaam cramp, XII, 690 Saltatory, XI, 618 Sciatic, XII, 733 Seamstress, XI, 615 Shoemaker's, XI, 615 Spinal accessory, XII, 731 Telegrapher's, XI, 615 Tests for. I. 33 Tic, articulative, XIII, 771 convulsive, IV, 267-70 ; XI, 598 to 602- 16; XII, 726 douloureux, IV, 267; XI, 599; XII, 726; XV, 948 Tonic, IV, 245; XL 572 Torticollis, XI. 618; XH, 730 Trigeminal, XII, 725 Typewriter's, XI, 615 Urethral, XI, 616 294 INDEX Spasm. Vesical, XI, 6i6 Whooping cough, XI, 6i6 Writer's cramp, XI, 615 Spasmus glottidis, XI, 616; XII, 728 mobilis, IV, 271 : See athetosis nictitans, XII, 679-90 nutans, XII, 679-cp Spastic hemicrania, XV, 930 paralysis, I, 33-9; IV, 251; X, 473 paraplegia, X, 525-47; XIII, 800 Special senses, Disturbances of, I, I ; XIV, 805 syndromes and sypmtoms, IX Speech, p. 33 Disorders of, 11, 222 to 33; XIII, 735 Diseases causing, XIII, 735 Tests for defects in, I, 8 Sphygmomanometer, I, 46 Spina bifida and occulta, I, 23; II, loz; X, 523 Spinal abscess, II, 153-74-84 Cerebro-spinal fluid in, XIX, 1238 accessory paralysis, XII, 705 spasm, XII, 730 automatism (Marie), V, 327a caries, II, 122 column in disease. See vertebral cord, endarteritis and thrombosis and hemorrhage of, II, 147, 189a, X, 48s, 512-4-7-8-24-50; XIII, 793-8; XIV, 827-30-1-8; XV, 980; XVIII, 1211 Localization in: See localization Symptoms of lesions of, above lum- bar enlargement, X, 513-4-8-7-20- 50; XIII, 798; XIV, 8301-1-8; XV, 980 anterior commissure, XX, 1275 ; XXII, 1372 : See syringomy- elia horn, XX, 1268; XXII, 1324: See poliomyelitis and progressive muscular atrophy nerve roots. XX, 1279; XXII, 1324: See herpes zoster. Burdach's column and nucleus, p. 12; XII, 654; XIII, 786, XX. 1271 ; XXII, 1322-60-3-4, 1406 Cauda equina, X, 487 ; XII, 721 ; XV, 1007; XXII, 1328 cervical enlargement, X, 549 to 52; XIV, 838 to 40; XXII, 1330 region, X, 512 to 15; XIV, 830; XXII, 1407 conus terminalis, XIV, 833 direct cerebellar tract, XII, 647- 53; XX, 1272; XXII, 1369-73, 1406 dorsal region. X, 516 to 19; XIII, 798; XIV, 831; XXII, 1404 Goll's column and nucleus, p. 12 Spinal, lateral column, X, 525-47; XII, 653-60-95 ; XIII, 800-1 ; XVIII, 1212; XX, 1270-1-3-4; XXII, 1369-71-3-84-6-9, 1406 lumbar enlargement, X, 484 to 86; XIII, 793; XIV, 827-8; XVII, 1 149; XX, 1329 posterior column, X, 526; XII, 654-60; XIII, 786; XX, 1271- 3; XXII, 1360-3-4, 1406 horn, X, 1269; XXII, 1322 nerve roots, IV, 826; XX, 1278; XXII, 1322 postero-lateral columns, X, 526 ; XII. 660; XIII, 799; XX, 1273; XXII, 1406 pyramidal tract, XX, 1270: See also lateral column spino-thalamic tract, XX, 1274; See also lateral column epilepsy. I, 60-1 ; IX, 433: X, 509-20; XIV, 839 to 40 ganglion, lesion of, XX, 1277: See also herpes zoster gumma, XVIII, 1210 hemiplegia, IX. 432; X, 509; XIV, 844; XV, 982; XX, 1276: See also Brown- SequardTs paralysis meninges. Hemorrhage in the, II, 147 memingitis. Acute and chronic, XI, 605; XV, 974, 1005; XVIII, 1213-4 muscular atrophy. Peroneal type of, X, 496; XII, 696 Progressive, X, 548 Neuralgia. XV, 971 ; XVI, 1076 or neuritic muscular atrophy, X, 496; XII, 696 nuclei : See nuclei segment, Lesions of, XIV, 826 Localization in: See localization syphilis, XVIII, 1210-6 tenderness, IX, 425; XVI, 1076 tumor. II. 152; X, 486. 509-15-19-41-52; XIV, 828-39-40; XIV, 975-82 Spondylitis deformans, XV, 976 Squint: See diplopia Stammering. XII, 729; XIII, 770 Static ataxia, I, 42; IV, 281; IX, 438; XII, 642 Status epilepticus. XVI, 1061 Stellwag's sign, XVII, 1 192-3 Sternutatio spastica, XII. 728 Stereognosis, Tests for. I, n Stereotypy. XVI, 1098, iioi Stocking form of anesthesia, VI, 348; IX, 415 Stokes-Adams disease, XI, 582 ; XVI, 1060 phenomenon, IX, 426 Strabismus convergens, XIV, 872 deorsum vergens. XIV, 874-7 divergens. XIV, 873 sursum vergens, XIV, 875-6 295 INDEX Strumpel's tibialis phenomenon, IX, 435 Strychnine poisoning, V, 297; VI, 366; XI, 613 Stupor, III, 206; XVI, 1097 Stuttering, XII, 729; XIII, 771 Subconsciousness, p. 18 Subcortical lesions, XXI, 1309 Subscapular paralysis, XII, 711 Suggestion. Susceptibility to, in hysteria, IX, 41s; XVI, 1071-2-6 Suicide in nervous diseases, I, 2 Sulfonal poisoning, X, 482 Sunstroke or heatstroke, XI, 589; XV, 968; XVI, 1070 Convulsion in, XI. 589 Headache in, XV, 968 Superficial reflex acts, I, 57 ; V, 297 Superior laryngeal paralysis, XIII, 757 oblique muscle. Paralysis of, XIV, 876 rectus muscle, Paralysis of, XIV, 874 Supinator longus. Paralysis of, XII, 716 Supra-orbital neuralgia or neuritis, XV, 944*53 -scapular paralysis, XII, 708 Surface thermometers, I, 78 Sweating, Excessive, XVII. 1203 Sydenham's chorea. II, 113, 126; XI, 622-3 Symmetrical gangrene. XV, ion; XVII, 1195 Sympathetic ganglionic system. Irritation of the, XVII, 1143-92 Diseases of the, XVII, 1 122-9-30 Paralysis of the, XVII, 1142-91 Symptom complexes and special syndromes, IX Symptomatic neuralgia, XV, 937-53 epilepsy, XI, 576 to 596 mania. XVI, 11 14 melancholia, XVI, 11 15 Syncope, Coma from, XVI, 1059 Local, XVII, 1105: See also Raynaud's disease Syndromes and special symptoms, IX Synergy, I, 42; IV. jS:-2 Synkinesiae, X, 47,; Syphilis, I, 2: See al«'. cerebro-spinal syphilis Argyll-Robertson phenomenon in, V, 332; IX, 437; XIV, Sgt Cerebro-Spinal, II, 108, 175 to 79, 180; XVIII, 1214; XIX, 1232 fluid in, VIII, 409-12-3-4; XVIII, 1205; XIX, 12,30-1-2 Optic neuritis in, XIV, 903 Vertigo in, XV, 1025-33 Endarteritis and thrombosis in, II, 175 ; XVIII, 1207-11 Lateral sclerosis in, X, 525; XVIII, 1212 Syphilitic Meningitis. IT. 176; XV, 952-81; XVIII. i2o8-f)-T.vr4 Cerebral of base, XVIII, 1209 of convexity, XVIII, 1208 Cerebro-spinal, XVIII, 1214 Spinal. XVIII, 1213 Sj-philitic, nervous diseases, II, 94, 108; XVIII, 1205 neuralgia, XV, 952 neuritis, II, 177; XV, 952; XVIII, 1215 Syphilophobia, III, 235; XVI, 1074-S Syringomyelia, X, 553; XII, 693; XIII, 802; XIV, 840-2; XV, 1009; XVII, 1151- 70-87; XXII, 1370-2 Tabes dorsalis, II, 134-79; VIII, 409-12-13; IX, 423; xn, 661; XIII, 759-85; XIV, 829-71- a5, 912; XV, 979-88, 1004; XVIII, 1217; XIX, 1231 Argyll-Robertson phenomenon in, V, 332; IX, 437; XIV, 891 Arthropathy in, XVII, 1186 Cerebro-spinal fluid in, VIII, 409 to 14; XVIII, 1217; XIX, 1231 Crises in, IX, 423; XV, 988; XVI, 1062a Cuirass in, VI, 348; XIV, 829 Optic atrophy in, XIV, 912 Perforating ulcer in, XVII, II72 Vertigo in, XV, 1015 vision, Limitation of field of, in, XIV, 871 Tachycardia, XII, 704; XVII, 1193 Taches Cerebrales, V, 327 ; XI, 590 Tactile saisations, p. 6 Tests for, I, 48 Talalgia, XV, 1002 Tapir mouth, X, 497 Taste, I, 17 ; VI, 357-70-91 ; XIV, 810 Cortical center for, XIV, 810 Diseases causing disorder of, XIV, 810 Tests for, I, 17 Tecto-spinal tract. The. p. 9 Telegrapher's cramp. XI. 615 Temperature sense, p. 6 Exaggeration of, VI, 368 Loss of, VI, 350 Tests for, I, 55 Temporal convolution, Lesions of the superior, XIV. g25; XXI, 1306; XXII, 1382 Lesions of. causing deafness, XIV, 1306 ; Localization in : See localization Sensoiy aphasia in. XXII, 1358-82 Tendon reflex acts, V, 299 exaggerated, Diseases causing, X, 473; XIV, 8ii diminished, X, 472; XIV, 811 Tests for, I, 60-6 Tenesmus, XI, 616 Terminal dementia, XVI, 1105 Tetanus, II, 172; XI, 603 neonatorum, XI, 603 Tetany, U, 121 ; XI, 612 Tetartanopia, VI, 363; XIV, 856-7; XXI, 1.307; XXII, 1356 Thalamo spinal tract. The, p. 9 Thermalgia, XV, 1003a Thermic anesthesia, VI, 350; XIV, 81 1-2 hyperalgesia, VI, 368 296 INDEX Thermic, hyperesthesia, VI, 368 hypesthesia, VI, 350 Thermometry in examination of nervous dis- eases. I, 78 Third cranial nerve nucleus, Symptoms of lesions of, XXII, 1339-42: See also localization Thomsen's disease, II, ic6; IV, 265; XI, 611 Muscular hypertrophy in, XVII, 1157 Thoracic paralysis, XII, 709-10 Thought, p. 24 Thrombosis, Cerebral, X, 506; XIV, 835-60-1; XVI, 1066; XVIII, 1207 Posterior inferior cerebellar artery, XXI, I2gi Sinus, II, 185; XV, 966; XVI, 1044 Spinal, XVIII, 121 1 Thymus gland. Lesion of, IV, 253; X, 554 Thyroid gland, Lesion of, I, 20; II, 132; IV, 253: Xn, 672; XVn, 1 193 Thyreo-ary-epiglottis paralysis, XII, 757-60-2 Tibialis paralysis, XII, 720 Tic, articulative, XIII, 771 convulsive, IV, 267-70; XI, 598 to 602, 616; XII, 726 douloureux, IV, 267; XI, 599; XII, 726; XV, 94S Tingling, VI, 375 Tinnitus aurium, I, 15; VI, 388 Tobacco vertigo, XV, 1031 Toes, Clubbed fingers and, XVI, 1184 Tongue, Paralysis of, XII, 706 Spasm of muscles of, XII, 729 Tonic spasm, IV, 245 Diseases causing, XI, 572 Tonicity, Muscular, I, 40; IV, 240; X, 472-3 Tonometer, I, 46 Tooth-Charcot-Marie type of muscular atro- phy, X, 496; XII, 696 Topoanesthesia, VI, 376 Torticollis, XI, 598, 618; XII, 730 Toxic coma, XVI, 1069 convulsion, XI, 595-6 headache, XV, 965 insanity, XVI, mo nervous diseases, II, 92 tremor, XII, 673 vertigo, XV, 1030 Trance. XVI, 1071 Transcortical aphasia, XIII, 778 Transference of hysterical anesthesia, IX, 415; XIV, 837; XVI, 1076 Transmission, nervous, p. 6 Transverse myelitis, XV, 980 : See myelitis Traumatic nervous diseases, I, i ; II, 91, 136-46 hysteria, XVI, 1077 neuroses, II, 157; XII, 674; XV, 1034; XVI, 1077 vertigo from, XV, 1034 tetanus, XI, 603 Tremor, p. 37; II, 163; IV, 250; XII, 639; XXI, 1292-4 Alcoholic, XII, 673 Asthenic, XII. 671 Diseases causing, XII, 639 Essential, XH, 681 Hysterical, XII, 674 Intention, IV, 291 ; XII, 645 Diseases causing, XII, 645 Mercurial, II, 160; XII, 673 Neurasthenic, XII, 671-4 Nicotine, XII, 673 Opium, XII, 673 Passive, IV, 290; XII, 646-61 Diseases causing, XII, 646-61 Senile, XII, 678 Tests for, I, 32 Toxic, XII, 673 Trident shaped hand, XVII, 1177 Trigeminal or trifacial neuralgia or neuritis, XV, 943 to 48 paralysis, XII, 702 spasm or cramp, XII, 725 Trional poisoning, X, 482 Trismus, IV, 265; XII, 725 Trochlearis paralysis. XII, 701 Trophic influences, p. 38 lesions, Diseases causing, XVII, 1121-8 Tests for. I, 41 Trophedema, XVII, 1202 Trousseau's sign, IX, 440; XI, 612 Trypanosomiasis, II, 142; XVI, I055 Tuberculosis in nervous diseases, I, 2 Tuberculous meningitis, II, 119-23-92; XI, 593; XIX, 1228-9 Cerebro-spinal fluid in, XIX, 1228-9 Tumor, II, 152-91 of brain stem, X, 53S-7-9-4I-2; XII, 656; XIII, 749 Cerebellar, XIV, 909 Cerebral, II, 125-52-91; X, 507-35-7-9-4I ; XI. 578-87; XIV, 836-52-9-62-4-5, 908; XV, 061 : XVI, 1033-50 Cerebro-spinal fluid in, VIII, 405-12-3; XIX, 1237 Coma in, XVI, 105c Headache from, XVI, 1050 Perversion of vision in, XIV, 852-9-62- 4-5 Vertigo in, XV, 1033 Spinal cord, II, 152-91; X, 486, 509-15-19; XIV, 828-3Q-40-2 : XV, 975-82, 1006 of cervical enlargement, X, 552; XIV, 839 region of spinal cord, X, 509-15-19 dorsal region, X, 519 lumbar enlargement, X, 486; XIV, 828; XXII, 1329 cms cerebri, X, 537; XII, 656 medulla oblongata X, 541 1 XII, 656 optic chiasm, XIV, 864-5 297 INDEX Typewriter's cramp, XI, 615 Typhus fever, Cerebro-spinal fluid in, XIX, 1236 Ulcer, Perforating, XVII, 1172 Ulcerations, Diseases causing cutaneous, XVII, 1136 Ulnar paralysis, XII, 715 Umbilical reflex, V, 309 Tests for, I, 57 Unconsciousness, I. 3 ; III. 201 Understanding, I, 6; III, 202 Unequal pupils, V, 341 ; XIV, 820 Unverricht's family myoclonus epilepticus, XI, 601 Upper motor neurons, p. 9; IX, 461 sensory neurons, IX, 463 Uremia, II, 193 Cerebro-spinal fluid in, XIX, 1243 Uremic amaurosis, XIV, 853 coma. I, 193; XVI, 1068 convulsion, IX. 576-81 headache, XV, 957 Urethral crises, IX, 423 Urethral spasmodic stricture, XI, 618 Urophobia, III, 235; XVI, 1074-5 Urticaria, XVII, 1167 Angio-neurotic. XVII, 1201 scripta, XVII, 1167, 1201 Uvular reflex, V. 315 Tests for, I, 58 Vagus paralysis, XII, 704; XIII, 763 spasm, XII, 728 Valleix, Points of. XV, 937-43-9-77-90-5-7 Vascular disorders. Diseases causing, XVII, 1144-S Vaso-niotor disorders, Diseases causing XVII, 1 130 reflex acts, V, 301-27 Tests for, I, 59 Venery in nervous diseases, I, 2 Vertebral column in disease, I, 23 Vertex headache, XV, 953 Vertige paralysant, XV, 1032 Vertigo, I, I : VI, 392 ; XV, 932 Alcoholic, XV, 103 r Apoplectic, XV, 1027 Atheromatous, XV, 1025 Aural, XII, 649-85; XIV, 918; XV, 1019 in brain stem lesions, XV, 1017 Cardi.ic, XV, 1024 in cerebellar disease, XV, 1016 cerebral anemia, XV, 1021-3-4-5 congestion, XV, 1026 tumor, XV, 1033 CoflFec. XV, 103 r in digestive disturbances, XV, 1023 Diseases causing, XV, 932 Drug, XV, 1031 Vertigo, Epileptic, XV, 1028 Exhciustion, XV, 1022 in fourth ventricle lesions, XV, 1018 Gerlicr's disease, XV, 1032 Hysterical, XV, 1034 Labyrinthine, XII, 649-85; XIV, 918; XV, 1019 Laryngeal, IX, 423; XVI, 106a Meniere's, XII. 649-85; XIV, 918; XV, 1019 in meningitis, XV. 1033 Migrainous, XV, 1029 Morphine, XV, 1031 Neurasthenic, XV, 1034 Nicotine, XV, 1031 Ocular, Xn, 648; XV, 1020 Paral>sing, XV, 1032 Quinine, XV, 1031 Tabetic, XV, 1015 Tobacco, XV, 1031 Toxic, XV, 1030 in traumatic neuroses, XV, 1034 tumor, XV, 1033 sclerosis (disseminated), XV, 1015 Syphilitic, XV, 1025-33 with ataxia, XII, 648-9; XV, 1015-20 Vesical crises, IX, 423 reflex, V, 324 spasm, XI, 616 Vestibulo-spinal tract, The, p. 9 Vibration sense. Loss of, VI, 353 Tests for, I, 56 Violinist's cramp, XI, 615 Visceral crises, IX, 423 Vision, Diseases causing disturbances of, XIV, 808; XXII, 1331 Double, XIV, 818: See also diplopia Green, XIV, 847 Limitation of field of, IX, 415; XIV, 817- 68 to 71 ; XVI, 1076 Localization of lesions causing disturb- ances of. XXII. 1331 Loss of. XIV, 852a to 55; XXII, 1334 Perversion of, XIV, 816 Red, XIV, 846 Tests for, I. 12-3-4, 29 Yellow, XIV, 945 Visual aphasia, III, 224; XIII, 776 axis, displacement of, I, 29; XIV, 818 Vitiligo, XVII, 1 162 Vocal cords. Paralysis of, XIII, 757-9 Voltoni's disease, XV, 1019 Voluntary motion, p. 14, 31 Disorders of, IV, 240; X, XI; XII; XIII Vulvo-vaginal crises, IX, 423 Walk, Inability to, in disease, I, 21 ; XIII Wasserniann reaction, VIII, 413 ; XII, 66r ; XIII, 78s; XIV, 829, 871, 912; XV, 9791, XIX, 1232 298 INDEX Weakened mentality, Diseases causing, XVI Weakness, XIII, 792 Tremor from, XII, 671 Weber's law, p. 16 syndrome, IX, 440; XXI, 1293 Tests, I, IS Werding-Hoflfman type of poliomyelitis, X, 548a Wernicke's polioencephalitis superior hemor- rhagica acuta, X, 543; XVI, 1048 predilection muscles, IV, 254; X, 504 scheme of aphasia, XIII, 739 Westphal-Edinger's nucleus, V, 329 pupillary reflex, V, 337 pseudo-sclerosis, XII, 667 Whooping cough, XI, 616 Will, p.io Free, p. 10 power, p. 10 Word blindness, III, 229; XIII, 777; XXI, 1307; XXII, 1381 deafness. III, 223-33; XIII, 775; XXII, 1306; XXII, 1382 Worry, I, I Wounds as etiological factors, II, 146 Wrist-drop, X, 494; XI, 584; XII, 716; XIII, 790; XVI, 1053 reflex, V, 322 Tests for, I, 64 Writer's cramp, XI, 615 Writing, Diseases causing disorders of. III, 227-8; XIII, 735-79-80; XXII, 1401 Tests for defects in, I, 10 Wry neck, XII, 730 Xanthopsia, XIV, 845 1 Yawning, XII, 731 Yellow vision, XIV, 845 Zone of language, p. 35 UNIVERSITY OF CALIFORNIA LIBRARY Los Angeles This book is DUE on the last date stamped below. JC/N i 1 6 Btc:o Form L9-100m-9,'52(A3105)444 D 000 113 212 5