ANALYTICAL and DIFFERENTIAL DIAGNOSIS ofNERVOUS DISEASES HENRY HUN. M.D. *v^T «* mf.< Columbia SUntoertfitp mtljfCttptjflftoiork THE LIBRARIES jftlebical ilibrarp Given by Dr. Oliver S. Strong AN ATLAS of the m-^w.^sv. DIFFERENTIAL DIAGNOSIS OF THE DISEASES OF THE NERVOUS SYSTEM ANALYTICAL AND SEMEIOLOGICAL NEUROLOGICAL CHARTS BY HENRY HUN. M. D. FORMERLY PROFESSOR OF Til I I 111: NEKVOCS SYSTEM IN Tilt AI.HWY KKMCAX OOLUBCUS, MEMBER Of TBI \MII1H\N MEDICAL ASSOCIATION, THE ASSOCIATION OF AMERICAN PHYSICIANS, THE UOnUCAM Ml oi.K \l Ifli .oil.vlloN, FTC, AUTHOR OF "\ i.cihi: FOB \\n Ki' >.n mfihcal stidfnts IN M 10.11:." "BTXLABUB OF A 001 If Tin. skiiviiis 81 "Ml REVISED AND ENLARGED EDITION T«« 8oot»wo»tii I ■.«!•«■. i. I'l IBUSZM1 TROT, N*W YnKK 1014 H H Copyrighted 1912 and 1914 by HENRY HUN, M. D. *%fr~~f To Thomas Hun a loving father a learned physician a man of wisdom and wit this book is dedicated in most grateful remembrance Preface, Page 1 CHART I. II. III. IV. V. VI. VII. VIII. IX. TABLE OF CONTENTS PART ONE Semeiology Introduction to the Semeiological Charts PAGE 31. — Case taking — examination of patients; comprising numbers 1 to 79. 49. — Analysis of subjective symptoms; comprising numbers 81 to 190. 53. — Semeiology of disordered mental activity; comprising numbers 200 to 237. 63. — Semeiology of disordered voluntary motor activity; comprising numbers 240 to 293. 77. — Semeiology of disordered reflex activity; comprising numbers 296 to 341. 87. — Semeiology of disordered sensory activity; comprising numbers 344 to 392. 97. — Electrical examination; comprising numbers 395 to 405. 107. — Examination of cerebro-spinal fluid; comprising numbers 410 to 420. ... I Special syndromes; comprising numbers 425 to 458. | Anatomical terms; comprising numbers 460 to 464. PART TWO Diagnosis Introduction to the Diagnostic Charts X. 125. — Diseases causing motor paralysis (weakness); comprising numbers 469 to 556. XI. 133. — Diseases causing convulsion or spasm; comprising numbers 570 to 631. XII. 141. — Diseases causing perversion of motion (ataxia, tremor, nystagmus, fibrillation), also local palsies and spasms; comprising numbers 635 to 7.;.; XIII. 155. — Diseases causing disorders of Speech ami gait; comprising numbers 736 to 800. XIV. 163. — Diseases causing diminution or exaggeration of sensation (anesthesia, etc.) and disorders of special senses; comprising numbers 804 to 927. XV. 175. — Diseases causing perversion of sensation (pain and vertigo); comprising numbers 930 to 1033. XVI. 185. — Diseases causing mental disorders; comprising numbers 1036 to 1117. XVII. 193. — Diseases causing trophic (change of size) and sympathetic (ganglionic and vaso- motor) disorders; comprising numbers 1120 to 1202. XVIII. 203. — Diseases caused by syphilis of the nervous system; comprising numbers 1205 to 1217. XIX. 205. — Diseases associated with abnormal cerebro-spinal fluid; comprising numbers 1220 to 1242. PART THREE Localization XX. 209. — Localization in spinal cord; comprising numbers 1250 to 1287. XXI 217. Localisation in brain; comprising numbers 1268 to 1285. XXII. 227. -( iemral lorali/.itiou from symptoms of paralysis or spasm; comprising numbers 1290 to 1405. PLATES Erb's motor points for electrical examination. Erb's diagram Bhflffl mg the effects of injury of a nerve. j illustrating laryngeal paralyses, ' ii ins of ocular paralyses. ns of the cerebral hemispheres. I ulo-motor nucleus, Diagram of nuclei in brain i ion through pons Varolii. ii the medulla oblongata. I I if the spinal cord, 1 1 f nuclei i Sobemal the more important diseases of the spinal cord. Schematic repi points in the physiology and pathology I diagram showing the motor and n H of the spinal cord segments. I diagram showing the cutaneous distribution ol tl rvesand nen e Diagram ol long n d loi j projection Diagram showing course ol gustatorj fibers. I Hagram illustrating I showing llie nurlei of origin and the .1 sen INDEX. Page 387 FIGCRE 1 to 5. 103 3. 6. 106. 7 to 18, 158. 14. 169. 15 to 17. 340 1. 18 2 12. 19 213. 30 211 346. 2 1 and 26. 346 7 2fi 2 16. 348 38 to 31 340. 83. 380. 381. 84. 383. 86. 364. 37. 384. PREFACE The diagnosis of diseases of the nervous system is generally regarded 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 that 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 is the analysis of each important symptom and the consequent ascertaining of the disease which must cause it under the cir- cumstances (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 iu 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 eaofa successive test the number of diseases constituting a group becomes less, until finally one definite individual disease stands revealed among the few moai closely related to it bya comparison of the remaining symp- toms characteristic of each, which are given in the final abstracts. This analyt- ical method is used, I think, by all great teachers of neurology in demonstrating cases of disease before their classes of students. It is the crystallizat ion 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 I tiagnostio ( 'harts" on page 1 LQ should be carefully studied. By means of these charts it is possible to diagnosticate easily and rapidly 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 the process or the abstract of the other symptoms of the 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 symptoma- tology, 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 signifi- cance stated, as far as it is known to the author, in a series of semeiological charts preceding the diagnostic ones. Cross reference to these terms also is facilitated by the numbers within the brackets. A very full index, in the prepa- ration of which the author has received much assistance from his friend, Dr. Dawes, also 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 differ- ent 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 the charts the author has received valuable sugges- tions and aid from several friends and especially from Drs. Mosher, Gordinier and Archambault, while for the plates he is greatly indebted to Drs. Streeter and Hawn. 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 edition of two thousand copies has been exhausted in eighteen months, giving him an opportunity of making a complete revision of the text, and of adding a few plates and also intro- ductions 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 both editions through the press are large factors in whatever success the book may have. Henry Hun. Albany, N. Y., August 1, 1914. 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 SEMEIOEOGICAL CHARTS The diagnosis of nervous diseases, if it is to be at all satisfactory and accurate, must be based on anatomy and physiology. The practitioner is supposed 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 brief, but comprehensive, outline of the physiology of the nervous sys- tem, including some statements as to its anatomy, which latter can be supplemented by an in- spection of the plates at the end of the book. The fundamental element, or unit, of the nervous tissue is the neuron (461-4) a cell with many processes projecting from it; some short and branching (dendrons), one (rarely two) which often extends a long distance and usually becomes the axon of a medullated nerve fiber, and which, in some cases, gives off a few collateral branches. Both axons and dendrons are com- posed of delicate fibrillae which pass directly without interruption through the cell body. Of these neurons, varying in form and size and supported by the delicate framework of the neuro- glia, the entire nervous system is composed. The fundamental physiological characteristics of the nervous tissue are excitability and transmission: the power of receiving an excitation and transmitting it from one end of the neuron to the other and of transmitting it to other neurons with which the first is in anatomical and physiological relationship or contact. By its dendrons the nerve cell receives nervous impulses and by its axon it sends out its own impulses. There is experimental evidence which tends to prove that the activity of a nerve cell is the result of chemical reactions (consumption of rhromatophilic substance, etc.), while the conduction along nerve fibers is mainly a physical process. The transmission of energy from one neuron to another in contact with it serins to depend upon differences in the tension of this energy in the two neurons. The cellular activity is, therefore, easily exhausted, while the activity of the nerve fiber is not easily exhausted. 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 nerve to produce sensory impulses, but intermediate organs, "end-organs," are necessary to transmute the external energy into nervous energy. In virtue of chemical changes the potential energy stored in the end-organ becomes active; the inciting cause of this being the external or foreign irritation. There are, doubtless, many forms of energy in the world which cannot be perceived, because there are no suitable end-Organs to bring aOOUl this transmutation. Sometimes this can lie 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 for us the color red, and about seven hundred and sixty million million, which constitute violet; and indeed we have reason to believe thai the ultra-violet rays have some effect upon our body, but beyond the above limits the vibrations of the ether are not recognizable by our eye and brain. The absence of a sensory end-organ limits the number of perceptions and consequently the content of consciousness, but this content is or can be. much larger at the present time than in times past. Many new forces I X-ray, etc.) are now perceptible by the organs of -m-e which were before itipercept ible. The seti-ory apparatus also is not absolutely perfect. Things moving very rapidly cannot be seen. The -poke- of a rapidly revolving wheel cannot be -, , n The Origin and Transmission of Sensory Impulses Cutaneous and muscle-joint sensation (Chart Via). The surface of the body and the cavi- ties 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 which "end-organs" are so constructed as to transmute physical 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, but is located in individual points. From these points of greatest sensibility, its acuteness diminishes concentrically. In every square centimeter of skin there are, on the average, 12 to 13 points for cold, to 3 for heat, and 24 for pressure, 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. Most observers maintain that there are distinct points also for pain- ful sensibility. Where the skin is stretched over bone (the malleoli), sensation is less distinct and 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 of several seconds in the conduc- tion of painful impressions, and there may be a summation of painful impressions; so that with repeated pin-pricks the pain becomes more acute. After section or injury of a nerve, the anes- thesia and analgesia are never so extensive as is the area of distribution of the nerve, and sensi- bility often returns before the regeneration of the nerve has taken place. This is partly due to peripheral anastomoses and partly to recurrent fibers of the sensory nerve. Head and his colleagues, after much experimental work on the subject, arrived at the fol- lowing conclusions: There are in the peripheral areas three kinds of sensibility, due to there being three different kinds of nerve fibers supplied to each area. 1st. Deep Sensibility. Muscle sense, pressure sense, pressure pain and localizing 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 motor nerves of the muscle tendons are cut, these forms of sensibility are lost. 2nd. Epicrilic Sensibility. Tactile sensibility for slight impressions, form and space sense, sense of 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 sensibility is very slow and is not complete until after several years. 3rd. Protopathic Sensibility. Pain and sense of extremes of temperature (below 22° or above 40° C). These symptoms are accompanied by paresthesiae and a false localization. This form of sensibility is best tested on the periphery of the affected area, where the anesthesia is not complete, or over the whole area while 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 atten- tion and discussion, but they are not, in their entirety, accepted by all neurologists. Sensory impulses of all kinds are carried to the central nervous organs by the sensory nerves. Of these, the spinal enter the cord 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 supply- ing sensation to the face, after passing through their cell bodies in the Gasserian ganglion, enter the trigeminal sensory nucleus in the pons (Fig. 19). The fibers from the posterior nerve roots, on entering the spinal cord, are sorted according to their physiological function into three great parts (Fig. 26). One part, which conveys tactile, 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 (Figs. 20-3) to the optic thalamus, whence it is continued, also by another set of neurons (relays), to the parietal cortex. The second part, which conveys impulses for co-ordination, passes to the cells of the column of Clarke and 6 thence, mainly without decussating, through the direct cerebellar tract in the outer part of the lateral column and through the restiform body to the cerebellum. The third part, which conveys temperature and painful impressions, passes through cells in the posterior horn, decus- sates in the central gray matter of the cord and passes upward in the antero-lateral column through the spino-thalamic tract and lateral portion of the formatio reticularis to the optic thalamus, and thence to 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 hyperesthesia, paresthesiae or pain in the distribution of the nerve. In addition to the anesthesia, which occurs in organic disease ot the nervous system, there is an anesthesia which occurs in hysteria: hysterical anesthesia. This hysterical anesthesia, occasionally but rarely, involves the organs of special sense. It more commonly involves cu- taneous sensibility and then the anesthesia is not limited to the distribution either of a peripheral nerve or of a nerve root. It may instantaneously disappear. It may recur in the same place, or in some other locality. It does not prevent the use of the part in performing acts, in which sensibility is essential. Upon excitation of the anesthetic parts vascular reflexes occur, which is never the case in anesthesia due to organic disease, peripheral or spinal. It is evident that this hysterical anesthesia is the result of imagination or delusion. It is purely psychic. 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 of warning that the body needs protection. Its intensity depends not only upon the intensity of the mechanical or chem- ical irritation, but also upon the condition (inflammatory, etc.) of the peripheral nerves and of the cerebral cortex. It is more intense when accompanied by fear and apprehension. An unexpected wound is less painful than an anticipated one. Pain is often associated with the allied perceptions called ''paresthesiae" (375) which at times precede, 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 neivous organs. Gustatory sensation (Chart Via). The mucous membrane of the mouth (in addition to the terminal organs for tactile, pressure, thermic, painful, etc., impressions) contains also the term- inal 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 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 miumer through the petrous ganglion to its nucleus in the medulla, whence they ascend with the other sensory fibers of the lemniscus to the optic thalamus, and thence to the cerebral cortex posterior to the gyrus hippocampi (Fig. Hi); while the nerve fibers arising from the taste bulbs On the anterior portion of the tongue pass at first in the lingual nerve and, soon leaving this. form the chorda tympani, which joins the facial nerve and runs with it through the fallopian canal to the geniculate ganglion. Here the fillers divide; a pari continuing alongside the facial nerve and forming the nervus intermedins, which runs to a nucleus in the medulla dose to the glosso-pharyngeal nucleus; while the reel of the fibers run through the petrosal nerves and join the fifth nerve and pass to the Qasserian ganglion (Fig. 38), ami thence to the cerebral cortex ii'n. A destructive lesion at any point of this course will cause unilateral loss of taste ia). When the lesion is in the Fallopian canal tl maj be associated with facial paralysis on the same side. Olfactory ttntaUon (than Via). The mucous membrane of the nose, analogous to that of the mouth (in addition to the terminal organs for tactile, thermic, pressure, painful. impressions), contains also the terminal organs of the nerves of smell. The nerves terminating in these ornan- pass upward through the cribriform plate t<> the olfactory bulb, ami thence back- ward through the olfactory tract: some to the anterior perforated space and Bub-thalamic region (olfactory reflexes) and some to the cortical center for smell in the gyrus hippocampi (olfactory perceptions) (Fig. 16). Each olfactory bulb is connected through the anterior commissure with both cortical centers. Hearing (Chart Via.) 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 lengths; so that on them can be reproduced every possible tone with its over-tones or harmonics. The auditory nerves terminating in this organ pass to the ventral and dorsal auditory nuclei in the pons. From these nuclei fibers pass upward, some decussating and some not, through the lateral fillet to the corpora quadrigemina, and thence through the sub-lenti- cular region of the internal capsule, posterior to the fibers for cutaneous sensibility, and reach the cortical auditory center in the anterior part of the superior temporal convolution (Fig. 15). A destructive lesion of one auditory nerve will cause unilateral deafness on the same side, but a lesion of the tract connecting the sub-cortical with the cortical centers, since this tract con- tains both crossed and uncrossed fibers, will not cause any deafness. Deafness results only from a bilateral central lesion affecting the corpora quadrigemina or the sub-cortical tracts described above. Even destruction of the auditory cortical center in both hemispheres does not seem to cause complete deafness. Sight (Chart Via). The terminal organs for sight are the rods and cones in the retina within the eyeball. The rods seem to be concerned in seeing in dim, the cones in bright, light. They vary in relative numbers in different animals, according as they roam by night or by day. From these structures start the terminal filaments of the optic nerves, which run backward from the eyeballs. 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 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 Gratiolet to the lips of the calcarine fissure on the median surface of the occipital lobe of the same side (Fig. 37). A destructive lesion of the optic nerve causes blindness of the corresponding eye, but a lesion of any portion of the optic tract, or geniculate body, or fasciculus of Gratiolet, or of the lips of the calcarine fissure will cause homonymous hemianopia of the field of vision of the opposite side; while a lesion of the central portion of the optic chiasm will cause binasal hemianopia. Internal or general sensation. In addition to these sensory impulses which convey to the brain excitations from the special sensory organs and hence from the external world, there are others which come from the different organs of the body and, in case they reach the cortex, give rise to what is called internal or general sensation. Some of these internal excitations remain entirely peripheral and affect mainly 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 nutri- tion and the life of the individual; while others reach the cerebral cortex and at times affect profoundly the processes taking place in it. These general sensations have much influence on a person's emotions, moods, thoughts and actions. Hunger may entirely alter the normal acts of a man or beast. Such internal or general sensations are for the most part ill-defined and ill-localized. They seem to depend upon the blood supply and upon 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 even severe pain. The sensation of hunger seems to be caused by contraction of the empty stomach, 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- 8 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 in connection with the conduction of tactile sensory impulses. To these internal sensations must be added also, probably, the cortical innervation feelings (see later) inasmuch as a person often feels that he is moving, or feels that he knows the position of, a paralysed or even amputated limb. Sensation (Chart VI) When these various impulses 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 converted 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 sen- sation 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 of the external object, with which by experience it is associated. Sensation is thus a special, individual force, similar to electricity, light, etc., which is pro- duced in the cerebral cortex and which has its special, individual characteristics. A complex manifestation of this force constitutes consciousness and personality. 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 reac- tions in the cortex, which constitutes these sensations, probably vary in topography rather than in quality. We know nothing more of the essence of this form of energy, which we call sensa- tion, 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 that it must result from 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 hemis- pheres in an animal are removed, or when the cerebral cortex in man is entirely or mainly destroyed by disease, OX in B 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), 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, below this point of intensity the cortex may be in activity, but sensation will not result; the activity will be sub-conscious, A series of these alight impulses quickly repeated may by summation cause sensation. There is, therefore, a minimum of intensity necessary for sensation; jusl a- elec- tricity passing through a wire must have a certain intensity before the wire glows and lighl IS produced. There is also a maximum beyond which, no matter how great the irritation, then is no increase of sensation, hut rather a diminution from exhaustion of the nerve cell-. Between (hi- minimum and maximum point, sensibility in creases , or diminishes, not continuously, hut by little steps; a definite ratio to the stimulus (Weber's law). 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 sensation, but remain Bub-oonsdous. The line between the oonsoioufl and the sub-conscious cannot be sharplv drawn. 9 Perceptions and Concepts (Chart VI) A perception consists of a combination of sensations, which are obtained from various sen- sory end-organs, but all of which proceed, usually simultaneously, from the same external object. A perception of an apple is composed of several sensory impulses: of visual sensations from the retina, representing the outline and markings and color of the apple; of muscle sensation from the ocular muscles, representing its distance from the e} r e, its position in relation to other objects and to some extent its form; of tactile sensations from the hand, representing its form, firmness and texture; and of gustatory sensations from the mouth, representing its taste. The various physico-chemical changes, thus set in aetivitj- in the cortex, combine to produce the full percep- tion of the apple. For a full and complete perception, consisting as it does of so many elemen- tary sensations, quite an appreciable time, or frequent repetition, is needed. 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 other, produces the idea or concept of an apple, with which is associated its written and spoken name and any other experiences or knowledge which have become asso- ciated during our life with apples. (See also under Associations.) 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 optical percep- tions 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 optical perceptions soul-blindness, or psychic blindness, and in failure of auditor}' perceptions soul-deafness, or psychic deafness, or auditory or sensory aphasia. When that portion of the cortex in which the sensory fibers terminate is diseased, both percep- tion and sensation are abolished. Emotions (Chart III) Certain activities of the brain are accompanied by feelings of pleasure or discomfort or even pain, and usually also, if these feelings are moderately intense, by changes in the func- tional activity of the internal organs, especially in the circulatory and respiratory systems, but also in the alimentary canal and in the other viscera and glands of the body. These feel- ings are due in great part to the internal or general sensations. 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 vol- untary acts, which have for their aim 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. Irrespective of our moods, however, some perceptions are almost always pleasant, others are not. Things which tend toward the preservation and health of one's self and his 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 of discomfort, as when hunger is assuaged, or we accomplish something desired or in some way contribute to our well-being or success 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 heredity, as a result of evolution in case of objects desirable for the health of the body; but in greater part 10 to associations (see Associations) with previous similar perceptions, and in greatest part with the feeling of satisfaction or dissatisfaction with the result of one's actions. Sensations of moderate intensity are usually pleasant; while sensations of very great in- tensity, which produce abnormally strong reactions in the nervous tissue, are usually unpleas- ant. Sensations originating from sets of vibrations having a simple ratio to each other are usually pleasant, while those which have a complicated ratio are usually unpleasant. Foods which nourished our ancestors usually taste good to us. The child probably acquires a taste for sweet things from the sugar in its mother's milk. Most of our pleasant and unpleasant sensations arc the result of our education. They are, therefore, much more pronounced in adults, especially educated ones, than they are in children. 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. Mankind does not find itself in this world with all its needs and wants satisfied; on the con- trary everyone must acquire food, clothes, habitation, warmth and a hundred other necessi- ties. A man who sees his neighbor with something good, which he has not, desires it, or some- thing similar. These wants and desires are the great, almost the only, incentives to voluntary action. When this 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 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 con- stitute what we call our "mood." In certain abnormal states of the cerebral cortex (exhaustion, circulatory irregularities, poison and other less well 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 thai it is impossible, or nearly so, to attract his attention. Memory I ( 'mart III) When perceptions take place, chemical changes are occurring in a definite portion of the cerebral cortex, which not only produce the perception, but also leave thereafter a permanent alteration in the cortex. The force derived from tin- chemical changes taking place in the cortex during an active perception may n^ult in a structural, physical or chemical change in the nervous element-, or more likely in the storing in them of potential energy, which can lie liberated and become actual later. Memories are dynamic changes in nerve cells and fibers which reduce the resistance to subsequent similar impressions or excitations. Certainly, a definite change is brought about which registers a permanent memory of the object perceived and subsequently this memory can be latent (sub-COnscioUS), OT active (cOUBCioUs), from time to tune. 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. Bub* consciousness 1 the preservation of memories, not present in consciousness, is not exhausting to the cortex, even though 1 he memories be preserved tor many years. In virtue of this change in the cortex, a memory of tin- perception always results from irritation of this altered cortex. This memorv ma\ l>e arOUSed, or enter into munition, by the external force which originally caused it and, I hen. the object will be rfnujriizr.l i re-kno\vn ), because 'he actual perception cone-ponds perfectly with its memory; or the memory may be aroused by way of those association fibers which it had previously set into activity. Memories become associated with each other In accordance with the relationship of the objects causing 11 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 per- sistence and after image in the retina after strong excitation (looking for some time at a bright light). These memories are, however, very different qualitatively from the original perceptions. The former have no actuality. Even though they may be at times very vivid, they never seem real to a normal personality. The whole cortex of the brain is in great part a huge store-house of memories. 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 Figs. 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 exception of one doubtful group. This group consists of memories of so-called "innervation feelings." When a muscle is contracted the person to whom it belongs has a feeling of this contraction and can estimate its strength. This feeling in called an " innervation feeling " and its memory is stored away in the cortex of the anterior central convolution and of the neighborhood in front of it. This innervation feeling seems to be 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 do not obtrude themselves strongly into our consciousness. They have rather to be sought for, but they usually can be observed, except in those actions which follow very rapidly upon the perception, or memory, causing them. There are many physiologists and psychologists, however, who question whether there are any so-called inner- vation feelings or memories in consciousness. 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 perception, or a memory, from the sensory cor- tex, a so-called voluntary, or association, action results. (See Voluntary Movements.) 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, whenever produced, does not long remain localized, but tends to pass along nerve fibers, throughout its own neurons and to other neurons. The chan- nels along which it will pass depend upon the anatomical arrangement of the fibers. In con- sequence 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, sucking, etc. Other channels are made easy later in life by the constant passage of impulses along them. The more frequently an association fiber is used the better conductor it becomes. 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, 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 channel 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, or a vivid memory of a perception received a moment before, takes place in another portion of the cortex, the association fibers connecting these two portions of the cortex, where perceptions are occurring, or have just occurred, being acted upon at both ends, will convey impulses to and fro more readily than the other association fibers. The longer and more frequently the asso- ciation 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. The activity 12 in the cortex does not long persist; so that when the associated idea is in consciousness, the original perception which awoke it is already, or soon will be, sub-conscious. Yet they are firmly associated together; so that whenever in the future one enters into activity it may excite the other. Thus, association between perceptions of the events and objects received simul- taneously, or immediately before or after each other, are formed in a never-ending stream and the events and objects are considered as contemporaneous 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 frequent repetition, rapidly and easily. 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 grad- ually 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 can understand only so much of an abstraction as we know individual cases which sustain it." Thinking and reasoning are much simplified and made more rapid by the employment of these abstractions. 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 ami there will gradually he formed a large number of associations which will be identified with t he ideas of punishment and condemnation and which tend to prevent the performance of wrongful nets; just as another combination of associations which have become associated with pleasure, reward or praise, will be associated witli 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 ami ethics, and of that ill-defined function, the so-called conscience, and may evolve into very elab- orate and very controlling feelings and habits of thought. According as education has devel- oped one set of these associations rather than the other, a good or bad character, not from his own hut from the community's standpoint, is formed. These ethical ideas ean of course he imparted from one person to another by language and, indeed, frequently are so imparled, hut such ethical ideas are rarely so firm and convincing as those obtained from experience. ( on. km u\ i ion \\i> Amis iion It seems to be a general law in the physiology of the nervous system thai w hen there is a strong activity in one part, the activity of the resl of the nervous system is inhibited. Thus, reiiex activity ean be inhibited by strong pain; and the reflex activity of the spinal cord is more or less inhibited when the brain is in activity. In the brain itself, when a portion of the cortex or a group of nerve cell,, fa in activity, the activity of the other cortical areas, as well a- that ia of the lower centers, is inhibited. The stronger the local activity, the greater and more exten- sive will be the general inhibition, and the more this active portion will have a free and unin- terrupted field. Naturally, consciousness remains limited to this strong activity for a long time. When an unusual or very vivid perception or idea is in consciousness it occupies the center of the stage. Consciousness is limited to 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 associations, remain sub-conscious. This phenomenon is called concentration and is a very important function in nervous physiology. When the cause of this concentration is a perception, in addition to this inhibitory influence, impulses from the active sensory cortex radiate to the motor cortex and out to the perceiving organ and cause a change in its muscula- ture in the form of greater tension, tonicity, change in its position, etc., which local change heightens the power of the organ for the perception of stimuli. Concentration is only another name for attention and has been regarded as an effort, and an expression, of the will or will- power, but the primary and essential factor seems to be the cortical activity. (See Will.) 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 atten- tion" in regard to some possible perception, 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 organs is constantly awakening associated memories, and these memories other associated mem- ories, and so, while consciousness remains passive, an ever-varying series of memories, visions, day dreams, etc., flow by. But consciousness may be active, and just as cerebral activities may cause either action or inhibition in the sub-cortical centers, so the whole mass and content of consciousness may to a certain extent strengthen certain memories and weaken others. This action of consciousness, like other nervous actions, grows stronger by use. So that a trained, educated, intellectual man, is able to keep one set of memories present in consciousness (atten- tion), to call up associated memories, to reject some, to keep others active, to compare them all together. This is called the act of thinking or reasoning. The process of thinking is thus inde- pendent 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. Atten- tion is, however, in part a manifestation of the association of ideas. If many associations at the same time bring into strong consciousness the desirability of investigating some one per- ception, this idea which we may call "a" and which will have widespread associations, will bring into consciousness this perception to be investigated, which we 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 connected with "a;" even the absence of "b" from consciousness will do this, and "a" will be brought into con- sciousness and through "a" the investigation will be brought back to "b" again. When we have forgotten a name, we often cannot by an effort of "will," however strong, recall 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 association and be recognized as the desired name. Imagination: Creative Faculty Although usually one perception calls up its associated memories and keeps repeating them, in recalling again and again past events; yet unrelated perceptions and ideas may be present simultaneously, or nearly so, in consciousness and may be artifically associated together so that by such combinations ideas and scenes may present themselves, which are not the result 14 of our experience; or our former experiences may be changed or modified out of all relation- ship with themselves. This is called imagination. It is the creative faculty which shows itself actively in prose and poetic works of the imagination, or passively in day dreams; in con- tradistinction to true facts or real history. Consciousness (Chart III) Consciousness consists, at any instant of time, of the then present perceptions and of those past memories which are directly or indirectly associated with these present perceptions and which have been awakened by them into activity. Consciousness is thus a form of energy resulting from activity of the cerebral cortex. The other memories, not at that instant active, constitute sub-consciousness 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. The activity within the cerebral cortex must reach a certain intensity in order to produce sufficient energy to constitute consciousness. When this cortical activity, although existent, is less intense, we call the result of this activity sub-consciousness. Such sub-conscious activity may leave an ill-defined memory as the result of its action. The conscious and sub-conscious content of the brain together constitute a personality. 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 perception, together with certain rudimentary sensations he may have acquired, constitutes his entire consciousness and his entire intelligence. 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 number of his perceptions, less rapidly and subject to many subsequent corrections, that of his associations, still less rapidly his con- cepts, even more slowly his ethical and aesthetical ideas, and yet more slowly his abstractions; but at the end of a tew 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, con- sciousness and the act of thinking and reasoning on which action is based (see Voluntary Motion) are already, even in childhood, very complicated, perhaps more so than later in life, when action is mainly determined by habits of thought: by judgments firmly established by numerous experiences. Consciousness is a form of energy or force, such as are light and electricity, which is transmuted from chemical action taking place in the cerebral cortex. Consciousness embraces nil these ch activities which have " certain intensity; below this degree of intensity then activities constitute .sub- consciousness. The process is somewhat analogous to that in an electric-light hull) through which an electric current inai/ be constantly flowing, but Which only gives forth light when the cunt tit has attained a certain 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 long in con- sciousness. Others :ire constantly forcing them out. None remain- constant. The continuity of consciousness is preserved by the mingling of memories of past perceptions with present ones, and by memories of past state- of consciousness. Consciousness is an active procest and depends upon the integrity and the blood supply of the cerebral cortex. This blood supply is in constant ebb and flow throughout the different areas of the cortex; being at any instant most abundant iii those area- which are in activity. Consciou a condition which, a- yel certainly, we d t understand, although in a general way we regard is ai the result of chemical changes taking place within the cerebral cortex. The chemical changes themseltk an not conectoueneee, but they produce this form of nervous energy very much as a steam boiler and i dynamo, or a galvanic battery, produce electricitj W% Iff are as ignorant of the exact nature of consciousness as we are of that of electricity. These chemical changes produce consciousness; a form of nervous energy; just as the chemical changes taking place in the muscles produce muscular force; a form of mechanical energy; just as chem- ical changes taking place in any living cell or tissue of the body produce a form of energy pecu- liar to itself. Consciousness thus locally produced, and thus continually produced, in the brain, passing according to definite channels to other regions of the cortex, surges through the brain, as memories and ideas are awakened and cause action and reaction. The subject is a most difficult one and is made, in a sense, more difficult by the faculty of language, which allows 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 as accurately without consciousness, as for instance in the automatic acts of the somnambulist, or in the epileptic trance. The brain is very abundantly supplied with blood, especially the cortex, and the latter is very sensitive to any interference with its blood supply. Loss of consciousness, which occurs normally 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. Per- versions of consciousness, 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. Personality (Chart III) Personality is the sum of the conscious and sub-conscious content of the brain. It expands 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 (virility). 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 experiences, are gradually combined into a general idea or principle which becomes a guide, or association 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 over- whelming emotional value. They not only exist in spite of experience but even mould experi- ence into conformity with themselves. Personality is the result of the manifold working 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 per- sonality has been created during and by his life, in a brain whose organization and capacity have been modified by heredity. Personality, being founded on, and consisting of, personal experiences, is strongly individual; but inasmuch as the large majority of men in the same community 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, 16 each personality differs from others. Some by their educational experiences become con em- plative men, others close observers, others men of action, etc. Some men are of weak char- acter, 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 structure and physiological activity of which has been modified by heredity. The personality of a child has the potentiality of developing in the future, but the kind of de- velopment depends more upon the kind of future that is before it, than upon its heredity. Personality seems to be the energy resulting 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 ial 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). Intelligence (Chart III) Intelligence consists of the content of object consciousness. 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 experi- ences. The greater the number and the variety of his experiences the greater will be his intel- 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. 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 wider 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, although they may, in part, be caused by peripheral lesions, are fundamentally due to disease, or poisoning, or malnutrition of the cerebral cortex. Soul and Mind All of these physiological activities of the cerebral cortex, which we have considered and which are popularly called "mental" or "spiritual," although they depend upon an inherited anatomical structure of the bruin, are mil preaenl at birth. They are acquired, or created, during life by experience and by education in its broadest sense. They are the result of phymologico- chemical activity within the cerebral cortex. 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 described above as "personality." Indeed this assump- tion rather complicates than simplifies the matter, inasmuch as it is contradictory to one of tin- most firmly established principles of natural philosophy: "the law of th mservat ion of energy." This law has not only been established by irrefutable proof in the inorganic world, but also has been proved by experiment to be valid in animals and even in man. If (' can produce or stop a cerebral activity of its own volition, thus ci mnihilating force which normally proceeds in an endless chain from one manifestation of force to another, then the law of the conservation of energy is no longer valid. Mankind has been unwilling to allow that the causalities and laws, which prevail in physi- cal activities, can he potenl 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 preju- pre-judgments) of mOSl men will not permit them to regard the mental activities as the 17 result of the physiological activity of the cerebral cortex, in the same way that the physiological activities of the other internal organs of the body produce and cause the functions of these organs. They are unwilling to regard psychology as identical with the physiology of the cere- bral 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., were each sup- posed to be animated by an indwelling spirit. 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, remains. Whether an individual believes in a soul or not, depends upon his traditions, his education, his experiences and upon the personality which has been gradually created and developed during his lifetime by the combination of all those forces constituting consciousness and sub-conscious- ness, and which may, in a sense, be likened to the older conception of a soul. It seems probable that consciousness, intelligence, personality, etc., are forms of energy and force and may, per- haps, be called spiritual in contradistinction to material. Whether this energy or force, which is gradually accumulated during life, persists after death, we do not know. It certainly is abso- lutely 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 potentially. Our knowledge in comparison with the wonders of the Universe is infinitely small. We know the relation of things, not their essence. But our knowledge is increasing and it is to be hoped that our children's children may have a higher point of view and a clearer vision. Insanity (Charts III and XVI) Whether we believe in the existence of a soul within the body or not, certainly insanity is no longer regarded as the possession of the body by an evil spirit (demoniacal possession). This was a well established belief for ages, but it has long since been abandoned and we now re- gard insanity as caused by abnormal cerebral action. The control of the body by a spirit, which we have finally rejected as regards insanity, the vast majority of mankind still retains for the healthy body, possibly because 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 struc- ture, whether the alteration be slight or great, and consequently abnormal function, of the cerebral cortex may be either congenital or acquired. The congenital form may be manifest in early infancy 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. The greatest degree of absence of intelligence is idiocy (1081), which shows itself almost at birth. In this disease the brain is so functionally incapable that it cannot produce perceptions, or register memories, or form associations, except of the most rudimentary kind. These persons, then, have no material for intelligence, consciousness or ethics and are incapable of speech. Next to this extreme degree is imbecility (1088), which may show itself at any time from birth to early childhood. In this class, simple perceptions, memories, associations and speech are possible, but only very imperfectly, and there is very limited material for consciousness, intelligence or ethics. A still slighter degree of this condition is only manifested when a considerable degree of intelligence or ethics is imperatively required, especially at the so-called critical periods of life, as at puberty (some forms of adolescent insanity — 1096). Although individuals of this 18 class have memories, associations and consciousness, their intelligence, ethics and judgment are found to be inferior to those of their fellows educated under the same conditions and they are called feeble-minded and defectives (1092) in varying degree. In the slighter forms of this class only the higher and more complicated ideas, such as altruism and morality, are absent or impaired (moral insanity and some criminals). In the severer forms, the loss is more profound and involves all the cortical functions. In other cases of congenitally defective brain the defect is very slight, but some of the asso- ciation channels are more patent than others, and than is normal; so that certain associations and ideas are constantly being presented to consciousness and are called up by all kinds of un- related associations and cannot be corrected, and consequently the cortical actions are distorted and twisted and irrational. To this class belong the paranoides (1113). Education and training have much to do with the development of the activity of the cere- bral cortex and consequently with the individual's intelligence and ethics. There are individ- uals who, partly in consequence of a defective brain, but mainly in consequence of?a defective training and education, do not have normal experiences and form a number of abnormal asso- ciations and ideas, especially ethical. Such individuals comprise the majority of criminals and cranks. Such cases bridge over the separation between the congenital and the acquired forms of insanity. Of course, it is possible that a person with a normal brain, who is isolated from his fellow beings and receives no training or education, will be feeble-minded or even an imbecile. All these congenital forms of insanity may be broadly classed under the term amentia (211, 1076) in its widest sense: the mind never having fully developed. On the other hand all the acquired forms of insanity may be broadly classed under the term dementia (212, 1077) in its widest sense: since there is always present a certain mental weakness not previously present, a falling off in greater or lesser degree from the previous more perfect cortical activity. Acquired, disordered activity of the cerebral cortex resulting in insanity primarily also depends upon a defective brain, either hereditary or acquired, but secondarily upon many in- citing causes. It may be due to a general deficiency in the blood supply consequent upon athero- matous arteries, as in senile dementia (1105); or may be due to an irregular cortical circulation consequent upon chronic meningitis; the most striking example of this class being paresis (1 Id! i. Various poisons (alcohol, etc.), endogenous or exogenous, are responsible for other forms of insanity which are usually, but not always, of comparatively short duration. Local lesions of the brain, surh as abscess, tumors, etc., may in some cases alter the circulation of blood through the cortex generally and thus cause insanity. Exhaustion of the cerebral cortex from worry, anxiety, shock and other causes may cause insanity 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 sequence, and as a matter of fact they frequently do so. In most of the forms of insanity the altered cortical activity manifests itself in certain striking and unusual phenomena. One of these is hallucinations (2i:>, L078), which are abnormal perceptions. In hallucinations the symbol occurring in the cortex does not correspond to any external phenomenon, bul is purely subjective, and is due to disturbances in the cortex itself, not in the peripheral sense organs. The hallucinations may occur in any of the special sensory regions of the cortex and hence may be either olfactory, gustatory, visual, auditory, tactile, or even visceral. The process in the brain which produces an hallucination must he similar to that which produces a perception. An hallucination is much more vivid than a memory and an hallucination is not a complete and correct reproduction of a former memory, but usually is Something strange and hi/.arre. In some cases the hallucinal ions do not have tin- vivido true perceptions, bu1 seem to lie internal voices of suggestions, telephonic communications or electrical action, etc. An illusion i .1 |i i- also a false perception, but it originates from an external reality which is misinterpreted in the brain: the symbol in the cerebral cortex is not such as is usual]} dated by the average man with the external object, hut rather a symbol usually associated 19 with a quite different object. 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 hallucinations and illusions with great tenacity in spite of strong proof to the contrary. These hallucinations and illusions occurring in a brain weakened by nature, poison or disease, naturally lead to abnormal associations and consequently to abnormal ideas. Abnormal associations will result not only from the strength and vividness of these hallucinations, but also because from patches of meningitis, or other cause, some areas of the cortex have more blood 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 sub- conscious. They may, although sub-conscious, be registered and may be recalled to conscious- ness after the attack of insanity is past, but they have no present value and are inadequate to correct the abnormal 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 association reflexes, or actions. The simplest of these is delirium (217, 1107-8), in which the patient responds by word and act to the many false perceptions and ideas in his clouded and weakened consciousness. When the intensity of the process is less the false perceptions and ideas will produce delusions (215, 1079), 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 life; so that a systematized delusion, founded upon more or less evidence or reasoning, acting upon a weakened or limited general cortical activity or 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, the symbols of which have occurred in his abnormally acting cerebral cortex. These delusions, or false and uncorrectable 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 also 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 the 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 frequently present, especially in the early stages of the disease is fear (phobias). 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 with former 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 conspira- cies. Fear is the dominant emotion within them. 20 The association reflexes are always altered in insanity in consequence of the abnormal cortical activity. In extreme dementia, voluntary motion is completely abolished. In pro- found melancholia, 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. Movement (Charts IV and V) When a sensory surface is irritated the animal often responds immediately by a compara- tively 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 occur spontane- ously, apparently 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 these different kinds of movements are divided into three great classes: reflex, voluntary and automatic. Reflex Action and Inhibition (Chart V) A reflex act is a reaction from an irritation, which under like conditions always takes place in exactly the same way; it seems purely mechanical, as if a machine were working. The irri- tation may be a usual (normal or adequate), or an unusual (abnormal or inadequate), one; the former being much more effective, and it may affect the skin, mucous membrane, or muscle, tendon or fascia, or any of the organs of special sense. The impulse starts in the end-organ of a sensory nerve supplied to the sensory organ affected and passes centripetally along the peripheral sensory nerve fiber, or fibers, to the spinal or cranial ganglion, situated on the pos- terior spinal, or the cranial, nerve root. Thence it passes forward through the posterior horn to the anterior horn of the spinal cord, or through the brain stem to a cranial motor nucleus, and thence along a motor nerve root and peripheral nerve to a muscle or muscles, striated or unstriated, in which it causes a contraction, or to a gland in which it causes an alteration in its secretion (Fig. 24). Muscular tonicity is a variety of reflex action (240). The various nervous elements traversed by the nervous impulses, as just described, con- stitute what is called "the reflex arc" (296). Slight irritative lesions of the reflex arc cause exaggeration, while destructive lesions cause abolition, of reflex action. This is the simplest form of nervous reaction and this is the simplest expression of it. Such simple reflex acts are the only ones occurring in the body during the early months of life and are unconscious acts. Similar reflex acts cause the respiratory and cardiac movements, the Bow of saliva and other secretions, the vascularity of organs and the warmth of the body, and in general regulate the physiological actions of the body. When the nervous impulse reaches the gray matter of the central nervous organs so many ways of transmission are open to it that it can pass by longer or shorter arcs or by several of them. The shortest possible reflex arc is through a peripheral ganglion (as in the vaso- motor reflexes). The next shortest is through the spina] cord. A longer one is through the spinal cord and the ganglia at the base of the brain. The longest is through the cerebral cortex. Some reflex acts, such as the pupillary (302), remain unconscious acta throughout life. On the other hand, most of the sensory impulses described al>ove, when they have tra- versed the sensory nerves and have reached the senary ganglia, pass in part as described above to the motor nuclei, but pan also in part up the central sensory conducting tracts to the higher gan glia :,1 the base of the brain; where they may cause more complicated reflex acts and pass still higher to the sensory cerebral cortex; where they may give rise to sensations and percep- tions (Fig. 36). Here the impulses may apparently stop, or they may be continued from the BenBOiy OOrteX tO the motor cortex and thence a new impulse may pan downward along the pyramidal tract, and thus the involuntary reflex act may be increased or replaced by a volun- tary act, or may be abolished (inhibited), voluntarily. ■J I This voluntary abolition of reflex activity (inhibition) may be brought about by a contrac- tion 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 sub-cortical motor cells taking part in it. In addition to this voluntary inhibition, a great variety of nervous activities taking place in almost any part of the nervous system (especially strong, painful impressions), and even the normal process of cerebral activity, will cause a more or less complete inhibition of reflex activity. It seems as though two impulses acting upon a cell at the same time under certain conditions may mutually counteract each other. Therefore, reflex activity is more active in animals in which the brain (or even other parts of the nervous system) is separated from the spinal cord or reflex centers and in human beings when the same result is accomplished by disease (isola- tion). Curiously enough, when the human spinal cord in its upper part is completely destroyed the reflex activity of the lower parts of the cord is abolished. This phenomenon has not been satisfactorily explained and is in marked contrast to the exaggerated reflexes found in incom- pletely destructive lesion of the upper portion of the cord. Conduction of reflex or other impulses along the peripheral nerves is equally rapid what- ever 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 inactive excitations may become active ones by repetition. The gray matter immediately following its activity shows a "refractory period" of longer or shorter time during which is it inexcitable 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. 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 the defensive. A destructive lesion of any portion of the reflex arc causes abolition of the reflex acts, as does also a strong irritation of the higher nervous centers. Slight irritative lesions, such as slight inflammations, will cause an exaggeration of the reflex act, as will also and more commonly a lesion which interferes with conduction of nerve impulses (inhibitory impulses) through the central motor (or cortico-spinal) neurons. An irritation, especially a continuous one, even if not very intense, will often cause a tonic spasm or contracture. Voluntary Action, Association Reflexes (Chart IV) The anterior portion of the cerebral cortex, which contains innervation (kinesthetic) memories, or motor centers, is connected through bundles of association fibers with the pos- terior portion of the cortex, in which are memories obtained from the organs of sense. Activity never normally originates directly, or spontaneously, in the motor cortex, but comes to it from the sensory cortex. When a very strong excitation arises in this sensory cortex, as for instance perceptions 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 knees 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 battle- field, the excitation leading to flight may be still 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 neutralize each other. It is a question which idea: the fear of death or the love of country and honor, is based on stronger perceptions 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 corresponding innervation memories and, if no other counteracting excitation comes to this latter portion of the cortex, the irritation passes through the great 22 motor cells in the anterior central convolution and down through the internal capsule and pyra- midal 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 immediately inhibited, or strengthened. The play of the different perceptions, memories and ideas: the play of motives, may continue a long time as the person deliberates and exercises his free-will. This merely means that the different memories, together with the ideas derived from the mass of associated mem- ories which constitute our ethics and those which constitute our emotions, have sufficient in- tensity to act upon the motor cortex, some as excitants, some as inhibitors. Fresh, allied mem- ories constantly enter consciousness, because of their association with those already in it, and take part in this phenomenon. It is like a debating 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 sub-conscious activities may play some part in this process. Eventually the stronger excitation will prevail and the act will be either done or left undone. 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 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 association reflex, 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 tewer elements of a choice, the association reflex may be more prompt. When a decision under the same or similar conditions is made a second time, and especially when frequently repeated, the asso- ciation reflex takes place more and more promptly. In the frequent repetition of acts: prac- tice, the same association conducting channels are being constantly traversed and consequently become better conductors, and the acts become easier to perform: become more or less auto- matic. It becomes a habit. A large part of our voluntary acts are habitual. It is to be remem- bered also that the internal sensations, which dominate our "moods," exercise a strong influence over voluntary movements which, under changing moods and altered internal sensations 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 sub-cortical centers and hence is well fitted for direct transference for reflex and automatic actions. In the cortical centers the gray matter is spread over a large surface and permits 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 experiences of the individual's ancestors, of the experience of the race (phylo- genetic). Voluntary acts depend upon the individual's personal experience (ontogenetic). The difference between the two depends mainly on differences in anatomical structure. In con- ditions 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 firM voluntary acts of the child (BUCking, opening ami closing eyes, closing of hand, etc.) are adopted reflex acts, either unmodified or but slightly modified. A young infant doei not will (o suck milk from his mother's bre.i-i |i \ a reflex act. Hut after the infant perienoed the result of this act B lufficianl number of times, the sight of oil mother, or hunger, may awaken his desire and he will suck the breafll voluntarily in consequence of this 23 active memory. Voluntary motions, or association reflexes, occur early and develop rapidly in infantile life, but occur much earlier, though the}' develop much slower, 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 system; while human infants possess at birth by heredity, one less perfect, but capable of a wonderful develop- ment, which results in greater part from personal experiences. A normal voluntary motion depends not only upon a fairly healthy cerebral cortex (which implies a certain degree of intelligence) and a normal muscle, but also upon the integrity of the two motor neurons: the central (corticospinal) and peripheral (spino-neural) , or the upper and lower (461-2). The impulse causing the voluntary contraction starts (as regards its purely motor function) in the cell body of the central motor neuron lying in the anterior central con- volution (Fig. 15). It passes along the axon of the cell, which becomes the axis cylinder of a nerve fiber, through the corona radiata, the anterior portion of the posterior limb of the internal capsule (Fig. 17), and emerges from the cerebral hemisphere at the base of the brain in the pes cerebri. It is then covered by the transverse fibers of the pons Varolii, from the lower edge of which it emerges to help form the anterior pyramids of the medulla oblongata (Figs. 20-22). At the junction of the medulla with the spinal cord, these fibers of the anterior pyramids in great part decussate; the completeness of this decussation varying somewhat in different indi- viduals (Fig. 23). Usually the great majority of the fibers decussate and run down through the spinal cord in the posterior part of the lateral column (crossed pyramidal tract), a small minority of the fibers running down in the anterior column of the same side as the pyramid and close to the anterior median fissure (direct pyramidal tract) (Fig. 26). In certain extremely rare cases no decussation takes place. The fibers from both the direct and the crossed pyramidal tracts pass to the groups of motor nerve cells lying in the anterior horns (Fig. 26), and to these cells they communicate their impulses. (The course of these central motor neurons is shown in Fig. 34.) From the group of nerve cells in the anterior horns of the spinal cord, these impulses, thus communicated, pass out along the axons of the cells, which axons become the axis cylinders of the anterior nerve roots, and thus pass along the peripheral motor nerve fibers to the group of muscles innervated by this group of nerve cells in the anterior horn. These impulses enter the muscles by the motor end plates and cause a muscular contraction. 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 on the opposite side of the body. Those muscles on both sides of the body which usually act together have especially well marked bilateral representation; so that these muscles are rarely completely and permanently paralysed in unilateral cerebral lesions. A cortical paralysis may affect motion only and may be very circumscribed; two or three fingers, or the thumb only. The actions which are especially lost in the cortical lesions are the purpose- ful actions which have been slowly acquired as the result of experience and training: actions which are peculiarly voluntary and skilful. A destructive lesion of either of these types of motor neurons will cause a motor paralysis. If the peripheral motor neurons are destroyed there will be a paralysis both of voluntary and of reflex acts: a flaccid paralysis (252), while if the central motor neurons are destroyed there will result a paralysis of voluntary acts only; the reflex acts persisting and being even increased: a spastic paralysis (253). (For explanation of the increase of reflex activity just mentioned see page 22.) The Will and Will Power The term "voluntary" motion implies "volition" or "will": some attribute of the individual or personality which controls or regulates the cerebral activities. The will and the freedom of the will stand, however, in direct contradiction both to the law of preservation of force or energy 24 and to the law of causality. Moreover, we have just learned on page 23 that voluntary motion results from the play of motives and that the strongest sensory cortical activity prevails and causes the resulting motion which seems to be due to our will power only because the percep- tion or memory in consciousness resulting from this "strongest sensory cortical activity" is, in virtue of its strength, in accordance with our so-called will or desire. It seems, therefore, better to call these actions which result from the strongest sensory cortical activity "association re- flexes" rather than voluntary acts. As the result of experience in life we acquire desires (see page 11) and each desire can only be satisfied by action. The presence in consciousness of a desire to obtain a certain end or result; which desire is itself the result of cortical activity will by this intense cortical activity excite, influence and usually control those cortical activities, which produce action, thought, study, etc. It is the cortical activity causing the desire which does this, not some external entity: the will. The act of concentration or attention seems also to call for a will power, but we have learned on page 14 that concentration depends primarily on a strong cortical activity, which the so- called will power and our desires are often incapable of controlling. What has been called the will is probably the dominant cortical activity present in consciousness at any given moment. It depends upon the personality which rests upon many experiences and upon many crystal- lized experiences in the form of judgments, habits, prejudices, etc., which give our actions stability and consistency; and this sum of consciousness, or even one strong idea in conscious- ness, the result of a strong cortical activity, may modify the association of ideas and may control both them and the resulting action. Nevertheless, both in voluntary actions and in efforts of attention, the individual, or the personality, does not seem to himself to be a mere passive spectator, but feels that, although he may be somewhat bound down by experience and habit and prejudice, yet he does exercise a very real and decisive influence upon both these processes, and at least modifies if he does not actually control them. Everyone feels conscious of this power, and it is not altogether satis- factory to dismiss this feeling as a delusion existing in the mind of every member of the human race. It is indeed quite possible that the personality, which is a force produced by chemical process taking place in the sensory cerebral cortex: the result of cellular activity, may in the motor cortex be transmuted back into cellular activity, and thus may promote or inhibit motor action. Just as an electric light, produced by chemical activity within a battery, may be trans- muted again upon a photographic plate into chemical action; or as the light of the sun acting upon the chlorophyl in green leaves may break up the molecule of carbon dioxide into its con- stituent parts: carbon and oyxgcn. Personality is a force, and it is hard to conceive of an immaterial spirit as anything else than a force The primary and essential element in the process still remains the activity of the neuron, and we have already seen that the force generated by one set of neurons may in turn generate, or modify, the activity of another set of neurons. Thus, the personality, which is gradually built up during the life of an individual, may play an active, not a passive, role in the phenomena constituting his conscious life and activity. This statement of what constitutes the will and will-power is in harmony with the subjective feelings of mankind; and yet it is but a restatement in other words of what has been said in the preceding paragraph that " the will is the dominant cortical activity present in consciousness at any given moment," because the personality is also the expression of the sum of the cortical activities present at any given moment. Spasms am> Convulsions (Chabt iy> Spasms and convulsions consist in involuntary muscular contraction. They depend mainly upon irritation of the central ^ray matter, especially the cerebral cortex, and partly upon peri- pheral irritation. Passive contract lire and Thomsen's disease alone are purely of peripheral (mUSOUlax) origin. Many of the tonic spasms are reflex, some are the result of nerve root irritation (meningitis, tumor . etc.) and many an associated with defeneration of the pyramidal tract-. 25 The result of pathological and experimental investigation makes it evident that epileptic and epileptiform convulsions 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 obtained by irritation of many parts of the central nervous system. The epileptiform convul- sion caused by cortical irritation may be accompanied by alterations in the cardiac action in the respiration and in the activity of other internal organs, as in 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 actual production 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 irregular spasm, are given in the chart. 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. This is unfortunate because the diagnosis by these diagnostic charts requires that the symptoms be correctly ob- served and named. The student should compare carefully what he sees with the definitions in the book and should observe as many cases as possible. Apraxia, Ataxia and Tremor (Chart IVc) 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 mus- cles to produce the movement over which this group of nerve cells presides. As soon as this movement commences, a number of sensory impulses pass from the muscles and joints involved to the co-ordinating centers, especially to the cerebellum, and the movement is consequently co-ordinated and orderly. This co-ordination of movements is not inborn. It is acquired by experience and practice. The movements of a new born 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 co-ordinating apparatus is functionally impaired there results ataxia. In either case awkward, ill-adapted and uncertain movements result. 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: inco-ordination of movement, always depends upon some disturbance of the sen- sory or regulating apparatus. It occurs in several distinct varieties, depending upon the por- tion of the sensory nervous system affected. 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 termi- nation of the auditory nerve in the semi-circular canals. 26 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 (42 and 352). It affects all movements of the parts involved. It is associated with hypotonia (240), which allows an abnormal 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, ataxia (281, 642) is caused by impairment of the function of the great co-ordinating organ: the cerebellum. It affects mainly, or only, walking and standing, which acts 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 centers for cutaneous and muscular sensibility, ataxia results, because of the loss of those sensations which 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 evi- dent that the patient is trying to execute the movements and knows what he wants to do, but he executes them awkwardly. Apraxia (282) may result 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 libers 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 done. These innervation complexes are not inborn (although their anatomical Bub-Structure may well be), but are learned, are 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 ladr. Many of them may never enter consciousness. As long as these memories persisl 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 guidance from many parts of the brain simultaneously (sight, muscle sen -e, touch, etc.). Trttnor (250) may bfl camed by rapid rhythmical interruptions of the innervation impulses - to the muscles or by B failure of a proper proportion or equilibrium m the innervation of the muscles and their antagonists. Tremor usually ceases during sleep and is usually in 27 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 con- founded with a coarse tremor. Speech (Charts IVc and XIII) The most complicated and important of all voluntary acts is speech. Speech and the allied functions: reading and writing, are peculiar to human beings and are the result of much instruc- tion 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 (750, 1088, 1092) and in hysteria (747-8) and insanity, especially in adolescent insanity (1096), in dementia (1103), in coma (745) and in insanity with diffuse cortical changes in the speech area (1104). 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 him, 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 derived from the sense of hearing; so that when a child is born deaf, or acquires 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 derived 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 replac- ing the sense of sight in these cases. It is evident, then, that the perceptions and memories of spoken words are of fundamental importance in the art of speaking. 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 (772). 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 (771). 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 difficult to decide whether he has forgotten the innervation memories necessary to speak the word (motor aphasia — 221), or has forgotten the word itself (sensory aphasia — 222). 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 convolution and the base of the left middle frontal convolution, where are stored the innerva- tion 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 (773) and an incomplete agraphia (776). The area of the cortex in the left hemisphere described above, including the bases of the middle and the inferior frontal convolution, the island of Reil, the posterior half 28 of the 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 pyra- midal tract, speech may be abolished (anarthria) or pronunciation impaired (dysarthria), whether in consequence of paralysis or of inco-ordination, or of spasm (as in stuttering). Read- ing 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 fasciculus of Gratiolet or of the pyramidal tract. Dysarthria might also be due to a cortical paralysis 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 hemispheres can carry on the function of speech perfectly. There is, therefore, no laryngeal paratysis, 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 autochthonus, acts are reflex acts which originate, not from external, but from internal, or organic, excitations or irritations. One of the best examples of this activity is the respiratory act. 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 they can be performed without consciousness. Such acts arc walking, writing, piano-playing, smoking and many others which can be very perfectly performed unconsciously, although each one can also be enacted consciously and usually is so done. 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. 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 (a8 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 litters terminate; and inearly life when there is motor paralysis, or immobility 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 base of the brain, etc., in consequence of the anes- the-i.i, tin' I. oily is no longer protected, by retlex and voluntary acts, from the many traumatisms to which it is frequently BUbjected and therefore ulcerations, arthropathies, ulcerations of the Cornea and other trophic 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 disorder-. Tut: CeBEBRO-SpINAL li.rin (CHARTS \lll am. XIX) The central nervous organs (brain and spinal cord i 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 Mood, it passes out of the ventricles at the inferior angle of the fourth ventricle, through the foramen of Magendii It from any Cause (tumor, meningitis, etc.) the foramen of Magnidir is occluded, this Quid, con- stantly secreted, oannol excape from the ventricles and dilates these cavities more or l< 29 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 sub-arachnoid 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 (leucocytes 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 Wasserman reaction is usually positive. 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 can 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 ajjd the Nervous System Nervous conduction, although it has some analogies with electrical conduction, is due to an entirely different 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 elec- tricity so conducted in the nerve fibers cause contraction of the muscles in which they termi- nate; as is shown in Chart VII. The muscle fibers also respond directly to changes in intensity of a galvanic current, but not to those of a Faradic current. 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. 30 CHART I Case-Taking METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES Errors in diagnosis result more frequently from imperfect observation than from faulty reasoning. Data derived from f QUESTIONING see chart I a. INSPECTION see chart I b. PALPATION PERCUSSION ELECTRICITY LUMBAR AND BRAIN PUNCTURE. OPHTHALMOSCOPY LARYNGOSCOPY ITHERMOMETRY Methods of Examining and Testing Patients - see chart I c. see chart I d. 31 CHART I a 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 thai of his ancestors. This is an importanl source of information, although usually less so than arc the results of the physical examination. The taking of a reliable clinical history is something of an art, but at best we arc absolutely dependent upon the truthfulness of the patient, as we rarely have means to check his statement- 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 bis own ease and it is best to let him tell his own story of his illness in his own way, without interruption; then to question him further about his 01- oess, more especially and fully in regard to the organ probably affected, bu1 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 importanl to ask as few leading questions as possible. Questions in regard to personal habits and \renereal diseases should only be asked when absolutely alone with the patient, and then in a manner which assumes that all men are guiltv of indiscretions. During our taking of th^ 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. 33 METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES QUESTIONING Methods of Testing 1 Allow the patient to tell the story of the illness without interruption. Then History of pres- ascertain the exact date and manner of onset (sudden or slow, prodroraata, ent illness. etc.) and the exact sequence of symptoms. Inquire into all details which may (Chart II) concern the case (headache, pain, paresthesias, vertigo, insomnia, mental condition, emotions, memory, special senses, paralyses, spasms, fits, disturb- ances 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 Family and personal history. (Chart II) Consciousness. (Charts III & XVI) 4 Sanity. (Charts III & XVI) Intelligence. (Charts III, XIII & XVI) Ascertain the occurrence, in the present, or a past, generation of the family, of any nervous diseases, especially the neuroses (neuralgia, epilepsy, hysteria, insanity, suicide, drunkenness, etc.), or of syphilis, or tuberculosis. Inquire as to consanguineous marriages. Note patient's age, full address, race, his mental and physical development in school life, occupation, habits (alcohol, drugs, venery, masturbation, etc.), dwelling and previous illnesses, such as rickets, infectious diseases, chorea, fits, tuberculosis, syphilis (use discretion in this inquiry: ask about sore throat, skin rashes, miscarriages, etc.), and injuries at birth or later. Ascertain the condition of other organs (cancer and tuberculosis). 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 unconscious. There are all possible grades in impairment of consciousness from complete coma to a slight lack of attention and an inability to collect his thoughts. This can be learned by conversation with him. 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 and 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 excite the patient. In testing a patient's intelligence, we test his general knowledge by asking him to name the different days and 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 power 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 power of comprehension by asking him to explain something he has read or heard. His association of ideas by giving him a word and asking what other ideas it suggests to him. 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. Memory and understand- ing. (Charts III, XIII & XVI) Emotions. (Charts III & XVI) An 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 his 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 the}' 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. 34 Speech. (Charts III, XIII & XVI) 9 Reading. (Charts III, XIII & XVI) 10 Writing. (Charts III, xni&xvi) 11 Stereognosis. (Charts III, VI & XXII) 12 Sight. (Charts VI & XIV) 13 Color sense. (Chart VI) 14 Field of vision for white and colors. (Hemianopia) (Charts VI A: XIV) 15 Hearing and tinnitus annum. a VI & X 1 V | Hi Smell. VI & XIV) 17 Taste. \ I A MY, is Bleep. QUESTIOXIXG (Continued) Patient's speech may be entirely absent (anarthria) or altered and very defec- tive, i.e., rational or irrational; there may be limited vocabulary or use of wrong word (aphasia), poor articulation (dysarthria), tremor in voice, monot- onous, scanning speech, omissions of syllables and words. Speech is tested by interrogation and spontaneous (voluntary) speech. Test also patient's understanding of letters, w r ords 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. Note any defect either in utterance or understanding. 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. Ask 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 .-kin of his hand, face, foot, lips. etc. Stereognosis may, therefore, in exceptional conditions, be tested, although less perfectly, in other parts than the hands. 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 I 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 £#. I n P' l:lt defed 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. Ask the patient to match different colored worsteds. 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 hands 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 Bee it' 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 this order is changed there is said to be an "inversion of the color fields" (849). Normally the lines limiting the different color fields are everywhere separate from each other. If they touch or cross there is "in- terlacing of the color fields" or "dyschromatopsia" (849). The patient's hearing may bi' tested by voice, watch, or tuning fork. He sure there is no wax in the ear. Galton's whistle should be used for testing high and low notes. Each ear should be tested separately. Hone conduction is tested by holding watch or tuning fork firmly on skull. Normally a tuning fork, which, held on mastoid Ceases to be heard, can still be heard when held dose t" meatus (Rhine's test). Normally a vibrating tuning fork, held on .•enter of forehead, is heard equally in both ears. If heard best in the deaf ear (positive) the lesion is m externa] or middle ear. If heard best in the nor- mal tive) the lesion is m inner ear or in auditory nerve (Weber's We also ask about ringing in ears (tinnitus aurium). Ask patient to name from its odor any fragrant substance (such as a-afoetida, cloves, peppermint, etc) held for a moment beneath each no~tril in turn, the other being dosed, Ammonia ami acetic acid should not be used in tl Ask the patient to point to the' name on a printed card of the taste of a stron.dy bitter, sweet, salt or sour solution t -lied from a medicine dropper, or a camel's hair brush, to one side after the other of the protruded ' le should be well Washed belweell each tot. The amount of sleep which the patient L'ets in i he twenty-four hours is always an Important question. Insomnia (agrypnia) is present in many nervous ad i j apt to be exaggerated bj patients; so that their statements should be controlled, when possible, by those of the nurses or relatives. Many sympl i ially fears, are worse at night ; " Pavor noctumus of children." CHART lb Inspection (mainly) Comprising Numbers 20 to 42 37 METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES INSPECTION Methods of Testing 20 The expression of the patient's face indicates, in most cases, the degree of his Facial expres- intelligence and his emotional state (sad or gay or anxious), and also may sion and gen- suggest the presence of certain diseases and conditions; such as myxedema eral appear- and cretinism (1163-4), acromegaly (1183), scleroderma (1165), exophthalmic ance and goitre (1193), paralysis agitans (677), myasthenia (553), nasal obstruction, behavior. atheroma of temporal arteries, notched teeth, hazy cornea, and the saddle- (Charts XVI back nose of syphilis, etc. His general appearance and behavior often indi- & XVII) cate his power of self restraint (inhibitory power, breeding), or the existence of hallucinations (213) of sight, hearing, touch, or of compulsory acts (218). 21 The walk of the patient may suggest the presenoe of hemiplegia (254), para- Walk, plegia (257), local paralysis (259), ataxia (motor or cerebellar) (248), spasm (Chart XIII) (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. 22 The skull should be observed as to type (brachy- or dolicho-cephalic, round or Skull. long heads), size (microcephalic — small, macrocephalic — large), rickets (box (Chart XVI) shaped), general or local hydrocephalus (bulging — posterior or anterior), fontanelles and sutures, asymmetry, tumors, etc. 23 The spinal column should be observed as to curvature (angular or lateral), scoliosis, Vertebral col- kyphosis, spina bifida (occulta), deformity (dislocation), Pott's disease, tumor umn. tenderness (by palpation), etc. (Chart X) 24 Note the existence of arcus senilis, the condition of pupils (unequal, anisocoria Eye. (341), myosis (340), mydriasis (339), and irregularity), the presence of keratitis (Charts V, VI or iritis, prominence of eyeballs, nystagmus, squint, ptosis, paralysis, etc. &XIV) 25 Note whether each pupil, the other eye being covered, dilates and contracts as Pupillary reflex the eye is alternately shaded by the hand and exposed to light, or an electric to light. light is flashed into it; vision being constantly fixed upon some distant object. (Charts V & When a pupil contracts to light (direct reflex) the pupil of the other eye also XIV) contracts (consensual reflex). 26 Hemiopic re- flex. (Charts V & XIV 27 Pupillary reflex to accommo- dation. (Charts V & XIV) 28 Double vision, diplopia. (Charts VI & XIV) 29 Secondary deviation of the sound eye, (Chart XIV) 30 Nystagmus. (Charts IV & XII) 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 not entirely reliable. Note whether the pupil dilates when the patient looks at a distant object and contracts 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 patient first con- verge his eyes and then make the axes of his eyes parallel, by imagining that he is looking at a near and then at a distant object. 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 removed 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 appar- ent. If present, nystagmus is usually recognized while making the two tests 28 and 29. It should not be confounded with the irregular jerky motion of a weakened ocular muscle attempting to move the eyeball. 38 31 Tremor. (Charts IV & XII) 32 Convulsion and spasm. (Charts IV, XI &XII) 33 Paralysis (motor). (Charts IV, X & XIII) 34 Paresis. (Charts IV, X & XIII) 35 M jthenia. (Chart IV) 36 Diadocoki- nesia. (Chart IV) 37 Ankylosis. INSPECTION (Continued) Note any tremor of lips, tongue, 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. Note any convulsion (269), spasm (245-6), contracture (263-4), athetosis (271), choreiform movement (272), etc., which may be present. These various forms of spasm are often difficult to recognize and differentiate from each other. Note any obvious paralysis, such as ptosis. Note tin- naso-labial fold and the height of the angle of the mouth on each side. While under close inspection, patient should be requested to execute every possible motion: i.e., wrinkle forehead (look upward, or open eyelids held closed by observer), frown, open and shut each eyelid, 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 abduct 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. 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 anil abducting joints, compare the strength of the paretic muscle with that of a similar healthy one, when possible, with its fellow of the opposite of the body. For future comparison, etc., the strength of the paretic muscle can red by dyna- mometers, of which the most practical is the one for the hand grasp. Or suffi- cient weights may be placed on hand, foot or head to overcome the attempted movement. Note whether patient tires easily on rep.:. ted or continuous activity of any set of muscles. Note whether patient can alternately extend and flex joints quickly and repeat- edly. Test especially rapid alternate supination and pronation. Note whether any joint is rigid, so that it cannot lie moved. Ascertain the cause of the rigidity, whether bony union, contracted muscle or contracted Boar tissue (muscle, ligament, skin, etc). Note whether any muscle is contraotured with consequent impaired motility of the joint and whether this contracture can lie overcome by force, witli or with- (Charts IV & XI) out etherization (active contracture), or not (passive contracture). 39 Note whether muscles are linn or flabby, and whether or not resistance is offered Muscle 'one. to rapid passive motions of joints while the patient tries to make no voluntary IV & X) resistance. Normally there is slight resistance. In disease the resistance may l.e altogether absent (atonia), or weak (hypotonia), or strong (hypertonia). Xote whether any muscle shows atrophy or hypertrophy, or fibrillary contrac- tions, or if there is any arrested development or trophic lesion- of other I (especially ulcers, herpes, glossy skin, abnormalities of nails, etc.). Xote whether 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, writ.', touch knee with heel of other foot, hold foot iii one position, trace a circle in the air with foot, walk backwards, walk along a line, stand on one fool alone, or on both feet close together, either side de or one in front of the other (Romberg's symptom), stand on or on heels, stand oil one foot and trace a circle Oil the tloor with the toe of the Other foot. All should be made both with e\,s o|vii and shut. Note whether patient, with hi- eyes shut, can tell whether his joints are flexed tended, or can duplicate with one extremity the position in which his other is placed. Note whether he 0811 estimate weights correctly or can eight loaded ball* correetlj Note whether he can locate hi- extremities being shut, an extremity after being n about is held in one position and he is told to turn his head and eyeb that when he opens hi eyes he -hall l.e looking directly at hi- thumb 01 lor. When he opens hi- e\es it Will be plain to see whether they are directed riL'ht or not. 39 38 Contracture. 40 Trophic XVII) •tl Co-ordination (Chart- IV A \ I I 42 Muscle and joint Deep ' ti-ihil- lt V (l.athves- thesia, I the VI A \[li CHART I c Palpation and Percussion Comprising Numbers 45 to 68 II METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES PALPATION AND PERCUSSION 45 Circulation and respiration. (Chart XVII) 46 Pulse. (Chart XVII) 47 Difficulties in sensory testing. (Chart VI) 48 Tactile sen- sibility. (Charts VI & XIV) 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) Methods of Testing Note the color of the skin, the pulsation of arteries in neck, the condition of the jugular veins and the frequency and regularity of respiration, especially Cheyne- Stokes' respiration (435), whether respiration be costal or abdominal, or dia- phragm be immobile, unilaterally or bilaterally. Note pulse of patient as to frequency, volume, tension (best tested by tonometer or sphygmomanometer) and irregularity in rhythm and force. 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 excitable and in uneducated patients, who cannot fix their attention continuously. Nothing 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 different parts of the body and in different individuals. With the finger tip (or with a smaller and lighter object, such as the head of a pin, a camel's hair brush, 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 ab- normal. Tactile sensibility, or, more properly, "space sense," or "localizing sense," (53), may also be tested with the esthesiometer; 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 different 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 aesthesi- ometer, nor Herring's aesthesiometer 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 hyperesthetic area. The electro-cutaneous test can be more accurately measured, but is of little practical value. 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. 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. Note whether a single tactile or painful contact causes two (double sensation) or more, sensations (polyesthesia). 42 PALPATION AND PERCUSSION (Continued) 55 Touch the skin at numerous points alternately with small test tubes, one filled Temperature with hot, the other with cold, water, or with hot and cold bodies (spoons) of the sense. same size and form. Certain points of the skin are especially sensitive to heat; (Chart VI) others to cold. It is well, therefore, to test for heat and cold separately. 56 Note whether the patient feels the vibration of a tuning fork (vibration sense) Pallesthesia. pressed so firmly on the skin that the vibration can be transmitted through (Chart VI) the underlying bone (osseous sense). 57 Stroke or scratch, as softly as will suffice, with finger nail or head or point of Cutaneous pin, the skin of the sole of the foot (plantar and Babinski), or a buttock (glu- reflexes. teal), or the inner side of thigh (cremasteric), or the side of abdomen (umbil- (Chart V) ical), or the hypochondrium (epigastric), or interscapular region (interscapular), or stroke firmly along the postero-internal border of the tibia (Oppenheim's 58 reflex) and note the resulting movement. The muscle itself must be felt and Mucous mem- watched in cases where the resulting contraction is too slight to move the part. brane renexes.fp oucn ^.j^ fi n g eri straw, brush, or probe, the cornea or conjunctiva (conjunc- (Chart V) tival), or mucous membrane of nose (nasal), or palate (uvular), or pharnyx 59 (pharnygeal), and note the resulting movement. Vaso-motor reflexes. Note the pallor or redness of the skin, also rapid changes and flushings with or (Charts V& XVII) without irritation, such as scratching with a pin or fingernail (dermographia). 60 With leg relaxed, semi-flexed and well supported, strike or press the sole of the Ankle-clonus. foot quickly, firmly and continuously upwards and note whether the foot (Charts V&X) oscillates or not. This clonus occurs at times spontaneously when the toe and not the heel rests on the floor ("spinal epilepsy"). 61 While patient is sitting on a chair with legs crossed, or better on a table with Knee-jerk. legs hanging free, or is lying in bed on his back with knees flexed, strike the (Charts V&X) ligamentum patellae a sharp blow with the finger, edge of hand, book or percus- sion hammer and note whether the foot flics forward. The amplitude of the excursion of the foot is not alone a safe guide to infer increase of knee-jerk, but rather its vigor, its quickness, and the presence of two or three additional oscillations as the foot falls back again. Even a continuous oscillation, or clonus, occurs in some cases (the so-called "spinal epilepsy"). More common than this clonus is a simultaneous contraction of the adductors of the other thigh when the knee-jerk is exaggerated. In order to obtain this reflex the ob- server must make sure that the muscles of the legs are completely relaxed. The extensor femoris muscle must be observed and felt in those cases where the resulting contraction is too faint to move the leg. Knee-clonus may be obtained in suitable cases by grasping the patella from above and pullim: it Q2 sharply downwards. Achilles reflex. While patient is kneeling in a chair with his feel projecting free, the tendo- (ChartS V & X) Achillis should be Strongly struck with B percussion hammer and the movement g, of plantar flexion noled. Where the patient cannot kneel the leg may be sup- r> , , . ported in any position which relaxes it and the teiido-Achillis struck. reflex. When the dorsum of the foot is struck sharply over the 4th or 5th metatarsal (Chart V) hones, note the dorsal (normal) or plantar (pathological) flexion of toes t;1 (Mendel-Bechterew's reflex — 320). Elbow and I reflexes. The arm helm,' relaxed, well supported and semi-llrxed at elbow the tendons at (Chart V) elbow or wrist are sharply struck. 65 Tlie patient's ohm is firmly grasped with finger and thumb or a Hat stick is placed The jaw nflex. iii thc> patient's Tin nit li resting on his lower teeth, the mouth being half open, (Chart V) and then the stick or the hand holding chin is .-truck sharply downward and aa the Closure Of the mouth noted. Kernig's reflex. With thigh flexed at hip and leg Hexed at knee, the patient either sitting or lying, (Chart* V & X) the leg should be quickly extended at knee join! and a strong resistance to ,.- such extension noted, it' pit Mechanical Strike the nerve or muscle sharply with the finger or permission hammer or press irritability. the nerve trunk or its t. aider points. 88 The tendon, and to some extent the cutaneous reflexes, can be made stronger Reinforcement, and oan be often made to appear when apparently absent, by diverting the patient's attention in any way, usually by having him pull strongly on his • d hands, hi eyes being turned to the oeiling or to a picture at the instant the reflea is tested (Jendre 18 CHART I d Electricity, Lumbar Puncture, Brain Puncture, Ophthal- moscopy, Thermometry, Caloric Reaction Comprising Numbers 70 to 80 METHODS OF EXAMINATION OF PATIENTS SUFFERING FROM NERVOUS DISEASES ELECTRICITY AND LUMBAR PUNCTURE 70 Farad ism. (Chart VII) 71 Galvanism. (Chart VII) 72 Muscle and nerve. (Chart VII) Methods of Testing The electrodes should be kept well moistened with warm .salt water during the testing. The larger electrode is placed on sternum or back of neck or sacrum; while the smaller electrode, provided with an attachment for making and breaking (opening and closing) the current, is placed over the motor point of nerve or muscle. The secondary current of a faradic battery should be employed and the current should be gradually increased in strength by methods which vary in different batteries, until the faintest distinct contraction of the muscle occurs whenever the current is suddenly closed, the negative elec- trode being over the motor point. The test should be repeated several times. As the skin becomes moister a less strong current becomes necessarj'. It is important to make sure of the exact position of the motor point in each case by some preliminary tests and not to let the electrode slip away from this point during the testing. With the electrodes arranged as above, first the negative, later the positive, electrode should be placed over the motor point of nerve or muscle and the strength of the current slowly increased by means of the rheostat until the faintest distinct contraction of the muscle occurs whenever the current is closed. The strength of the current causing this contraction, with each elec- trode in turn over the motor point, should quickly be read from the galvano- meter, even before the needle has quite ceased its oscillations. In the same way read from the galvanometer the strength of the weakest current which will cause the faintest distinct contraction, when each electrode in turn is on the motor point and the current suddenly opened. In all cases both the muscle and the nerve supplying it should be tested both by faradism and galvanism. 73 Note the character of the muscular contraction, whether quick or sluggish (de- Character of the generative), or showing any peculiarity, and whether it is unusually persistent contraction. (Chart VII) 74 Lumbar puncture. (Charts VIII & XIX) (myotonic), or whether it rapidly grows feebler under repeated tests (myasthenic). The patient's body should be bent strongly forwards. Patient should, if possible, sit, but may be lying down. The skin having been thoroughly washed with alcohol, a horizontal line should be drawn from the posterior spine of one ilium to the other and a sterilized fine needle three or four inches long, preferably of platinum and with rather a short bevel, should be inserted between the laminae of the vertebrae immediately below or above this horizontal line. The needle may be inserted in the median line or a little to one side of it and pushed steadily forward and slightly upward until it enters the arachnoid sac when usually the cerebro-spinal fluid will escape in drops. If the needle be pushed too far it can be felt as it strikes the body of the vertebra and it should then be with- drawn about half an inch. It is rarely necessary and sometimes dangerous to attach a syringe and aspirate the fluid. If the needle becomes occluded clear it out with the stylet. It is better not to withdraw more than half an ounce of the fluid. Note the rapidity of escape, whether by drops or in a fine stream (tension), its appearance (cloudy, bloody, purulent). The fluid may be examined chemically (for albumen, sugar, cholin, etc.). A portion of the fluid, especially that containing the fine coagulum which frequently forms, is centrifuged, the clear fluid is carefully poured off and the bottom of the tube scraped and aspirated with a capillary pipette, the content of which is spread on a slide, fixed, stained and examined for cells (lymphocytes, leucocytes, bacteria, etc.). The cerebro-spinal fluid should also be tested for an increase of globulin, indica- tive of the presence of a syphilitic infection, of ancient or recent date, or of a meningitis, according to the method suggested by Noguchi (419). After lumbar puncture patients should remain quiet in bed during twenty-four hours. Even so, they are apt to suffer from headache, especially if much fluid has been with- drawn, or withdrawn too rapidly. Sometimes the nerve trunks of the cauda equina are injured, causing pain in the legs, but such pains are rarely severe and are of short duration. In some cases, in consequence of the withdrawal of the cerebro-spinal fluid, the medulla and cerebellum have been drawn down into the foramen magnum and death has resulted promptly. Such an acci- dent is only possible in cases of cerebral tumor situated in the posterior fossa of the skull, and therefore lumbar puncture should not be performed in such cases. 46 BRAIN PUNCTURE, OPHTHALMOSCOPY, LARYNGOSCOPY, THERMOMETRY, AND THE CALORIC REACTION 75 This operation consists in trephining (with avoidance of the sinuses and large Brain puncture arteries) a small button from the scalp and bone, inserting a very thin needle canula and aspirating a small quantity of the brain substance, or tissue of a tumor, or fluid from a cyst. It has been many times performed and the results have been somewhat encouraging, but it is an operation which should be per- formed only by an experienced surgeon or neurologist and its detailed descrip- tion is hardly in place here. 76 Ophthal- moscopy. (Chart XIV) 77 Laryngoscopy. (Chart XIII)" 78 Thermometry. 7! i Caloric reaction. (Chart XII) 80 Cerebellar nystagmus. (Chart XXI; 1272) Examine the eyes for choked disc or optic neuritis, and for optic atrophy, reti- nitis, miliary tubercles, etc. Examine the larynx for evidence of paralysis of one or more or of all its muscles. It is often necessary to ascertain the temperature of the patient. The thermom- eter should be well washed in cool water both before and after taking the tem- perature. In taking the temperature in the mouth, the bulb of the thermometer should be placed well under the tongue and it should be noticed that the lips are held tightly closed during the two minutes that the thermometer is left in the mouth. In taking the temperature in the axilla, the axilla should first be wiped dry from sweat and care should be taken that the thermometer be surrounded by skin and not at all by clothes; the patient should be rolled over on his side in order to press arm firmly against chest and the thermometer should be left in position eight minutes. In taking the tem|x>rature in the rectum, a little vaseline or soap-suds should be put on the bulb before inserting it into the rectum, where it should remain two minutes. Instruments have been invented for taking the surface temperature of the skin of any part of the body, but they have not proved to be of much practical value. When one ear of a normal person, with head held upright, is syringed out with cool water there results a horizontal and rotatory nvst agmus towards the other ear; when water warmer than the body is used, the nystagmus turns towards the syringed ear. This reaction does not occur in cases of destruction of laby- rinth, <>r of paralysis of the vestibular nerve. In lesions of the ri^ht cerebellar hemisphere, nystagmus to the right may only lie M-ni. or may be made more marked, when the patient lies on the left side, and vice-versa. 17 CHART II Analysis of the Subjective Symptoms of the Case Comprising Numbers 81 to 190 I-.' ANALYSIS OF THE SUBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) List of diseases most likely to occur as the result of the etiological factors obtained from the history of the case. '101 Idiocy and Imbecility 102 Spina Bifida and Meningocele 103 Hereditary (Huntingdon's) Chorea 84 Inherited Organic 104 Hereditary (Friedreich's) Ataxia 81 Heredity, Diseases Diseases 105 Myatonia Congenita including con- 106 Myotonia Congenita (Thomsen's Disease) sanguineous 107 Muscular Dystrophies marriages in ^108 Syphilis of the Nervous System neuropathic families '109 Insanity (Predisposing 110 Epilepsy cause) 111 Hysteria 85 Inherited Neuroses 112 Chorea Tendencies 113 Neurasthenia 114 Neuralgia and Migraine. ^115 Drunkenness (Alcoholism) '116 Cerebral Palsy of Childhood 117 Acute Anterior Poliomyelitis 118 Meningitis (tuberculous, etc.) Tnfancy and Childhood 119 Hydrocephalus 120 Tetany And all the inherited diseases except 103 and 106 121 Caries of Spine and Compression Myelitis ,86 Age 122 Meningitis (tuberculous, etc.) ' 123 Hereditary Ataxia Childhood and 124 Glioma Youth -! 125 Chorea 126 Epilepsy 127 Muscular Dystrophies 128 Hysteria .129 Insanity ^Adult J All other forms of Nervous Diseases and many of those above given 130 Hysteria 'More common i 131 Exophthalmic Goitre in women 1 . 132 Neuroses 82 Personal 87 Sex Factors 133 Locomotor Ataxia (Tabes) (Predisposing More common „ 134 Paresis causes) . in men 135 Injuries .136 Organic Diseases r Jewish & Latin 137 Neuroses 88 Race -Anglo-Saxon 138 Organic Diseases '139 Beri-Beri 89 Dwelling 'Tropical < 140 Leprous Neuritis Place, 141 Sleeping Sickness Habitation ..Dampness 142 Neuritis 90 Occupa- (-Overstrain 143 Occupation Neuroses - tions ^Poisons 144 Neuritis 50 r 145 Wounds and Injuries 146 Hemorrhage in Brain, Cord or Membranes 147 Meningitis 'Physical 148 Myelitis 149 Disseminated Sclerosis 150 Neuritis 151 Tumors '91 Trauma- - .152 Abscess tism fl53 Hysteria Psychical, Acute J 154 Insanity & Chronic 1 155 Neurasthenia v 156 Traumatic Neuroses 83 Etiological Factors (Inciting causes) 92 Poisons Toxic 93 Infec- tions 94 Syphilis rl57 Arsenical Neuritis Metallic J 158 Lead Palsy, Colic, etc. 1 159 Mercurial Tremor Alcoholic j J60 Multiple Neuritis ( 161 Neurasthenia Tobacco, Tea f 162 Tremor or Coffee 1 163 Neurasthenia Narcotic 164 Drug Poisoning; Acute or Chronic 165 Neuritis 166 Meningitis 166 Myelitis Germs and J 167 Acute Anterior Poliomyelitis Toxines 1 168 Landry's Paralysis 169 Neuralgia 170 Tetanus .171 Hydrophobia (172 Gumma 173 Meningitis Gummosa 174 Neuritis Syphilitica 175 Endarteritis Syphilitica \ 176 Locomotor Ataxia < 177 General Paresis J 178 Neurasthenia 1 179 Hysteria 95 Exhaus- tion 96 Extension Of Inflam- mation Post-Syphilitic Infections From Illness, Overstrain, Worry From Venery and Masturbation Caries of Skull or Vertebrae 97 Arterial I H us Metastasis from I >ther Organs ISO Neurasthenia f ISl Cerebral or Spinal Abse. ■ L82 Sums Thrombosis is:; Meningitis 1st Myelitis I lv"> Neuritis 186 tpopli mors (188 Tuberculous and Suppurative Meningitis 99 I H of Other Organs Bright 'a I tiseasa 189 ' tamis j Diabi I Mellitus I '.in Diabetic Coma .inn Cold is a doubtful direct, but probably an auxiliary stioli 51 CHART III Disturbances of Mental Activity ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease. 200 Disturbances of Mental Activity. 201 CONSCIOUSNESS The appreciation of one's existence and ' individuality as separate from the rest of the universe (Subject con- sciousness). The content of conscious- ness is the sum of the present percep- tions of the various sensations (Object consciousness), together with the memories of past perceptions and judgments (Experience) (Chart XVI) 202 INTELLIGENCE The power of ascertaining facts and rea- soning upon them. The power of dis- covering the relation of things and of acquiring knowledge (Chart XVI). 203 MEMORY The power of retaining in the mind and of recalling at will perceptions and ideas formerly received. The more striking the perception and the more frequently it is repeated or recalled, the better becomes its memory (Chart XIII). 204 EMOTIONS An emotion is a state of conseioiisnesH accompanied by a feeling of pain, pleasure, fear, anger, wonder, worn, etc In health ■ person's emotion is usually in harmony with hie environ- ment, bu1 in diapasoH may be quite in- dependent of 1 1 »« - environment (Chart XVI). In disease, consciousness and intelli- gence may be either diminished or perverted as is set forth in Chart III a. Neither intelligence nor consciousness is exaggerated or increased in disease, although the latter may be apparently so (Self-consciousness). In such cases, however, there is a concentra- tion or limitation of consciousness rather than an increase of it; an exaltation of the subject, with a lowering of the object, consciousness. In disease, memory may be diminished in whole or in part, and the emotions may be either diminished or exagger- ated as is set forth in Chart III b. .Memory is never increased in disease, although certain memories may be accentuated and others lost. 53 CHART III a Disorders of Consciousness and Intelligence Comprising Numbers 201 and 202, and 205 to 218 66 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) 201 C N S c I u s N E S S Diagnostic Symptoms f205 Coma CONSCIOUSNESS Definition The patient lies in a profound stupor from which he cannot be aroused by irritation of any sensory organ (eye, ear, skin, mucous membrane, etc.)- No voluntary acts are per- formed and the reflexes are abolished or diminished, except the circulatory and res- piratory, which are often, but not always, deranged. Patient is unable to swallow. Lips and cheeks puff out during expiration. 206 The patient is apparently in a coma but by Semi-coma strong sensory irritation can be aroused to or some manifestation of consciousness. No Stupor voluntary acts are performed, but the re- flexes are usually present. Patient can swallow. Patient may lie apparently awake, but really unconscious, with a low mutter- ing delirium (Coma vigil). 207 Dazed, Be- The patient lies in a deep sleep or moves wildered, about automatically. Can be rather easily Somno- aroused, but does not fully appreciate his lence or surroundings. Can speak more or less in- Sopor telligently. Significance These three conditions are not always sharply differ- entiated, but may merge into each other. They are due to loss or di- minution of brain func- tion in consequence of pressure upon the brain or of circulatory dis- turbances in it, or of poisons, etc. Occur in traumatism, and in many organic diseases of the brain and its membranes and especially of its blood vessels; also when toxic substances (morphia, etc.) or toxins (fever, etc.) are in the blood; also in Bright 's disease and diabetes mellitus. Rarely the condition is functional. f208 Erroneous A mental condition in which a person imagines himself personal- to be different from what he really is ; sometimes an ity animal, sometimes a famous character in history, sometimes God, etc. P E R V E -I R T E D 209 Double personal 210 Auto- matism Somnam- bulism At intervals the patient is in a sort of somnambulistic state and presents an abnormal consciousness and personality. His memory at times changes with his personality, in which case he remembers only occur- ences in former similar conditions and not those of his normal state, and vice versa. This is a very rare condition and offers much opportunity for decep- tion, and in some cases of hysteria may well be sug- gested by the examining physician Occurs in insanity (functional). 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 memory 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, hyp- notism, and rarely in hysteria (func- tional) ; not uncommon in childhood during sleep. 56 Diagnostic Symptoms 211 Amentia 212 Dementia f213 Hallucina- tions INTELLIGENCE Definition Absence or defect of intelligence, which is congenital or is acquired in infancy before the intelligence has developed. Significance Due to a malformed or diseased brain. Occurs in idiots, imbeciles and feeble minded persons. Absence or defect of intelligence, which is acquired in later life in a person previously intelligent. 214 Illusions 215 Delusions Due to atrophy or functional failure or diminution of blood supply of cerebral cortex. Occurs in in- sanity and is often its terminal stage. Vivid perceptions of sensations (visual, auditory, ol-~ factory, tactile, painful, etc.) not directly dependent upon any external corresponding reality; a sensation without an external object. The}' are usually re- garded as real and are then associated with defective judgment and mental impairment, and therefore cannot be corrected. Erroneous perceptions. A false interpretation of an actual sensation, which is really of a different nature from that which the patient believes it to be. Fre- quently occur in rational persons, especially in those with defective terminal sensory organs. In such cases easily corrected. 216 Hypochon driasis 217 Delirium 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 cn- 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 in persons with diminished COnSCioUS- 11688. Probably due in most eases to hallucina- tions, illusions and mental confusion; consequently its irrationality may be in part only apparent. Often occurs in fevers. •J is Certain thoughts or questions or doubts, which arefor- Compulsory ever in the patient 's mind ami cannot be removed. ideas and They may be of any nature. Patients are irresistibly actions compelled by an unknown force to « l < » certain acts or (275) to say certain words, usually quite trivial. Patients hize the abnormal character of these ideas and act, and are made very unhappy by them, but are quite unable to prevent them. Methods for the detection of disorders "f consciousness and intelligence arc desoribed in Chart la. POT further discussion of these symptoms and the which they occur see Chart XVI. Due to disease of the cerebral cor- tex, whether functional, cir- culatory, toxic ororganic. Usu- ally symptoms of insanity, or of extreme degree of neurasthenia, are also present. In insanity these perver- sions of intelli- gence cannot be corrected b y jon a n d demonstration, and in neuras- thenia only rarely and im- perfectly. :.7 CHART III b Disorders of Memory and Emotions Comprising Numbers 203 and 204 and 220 to 237 59 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Diagnostic Symptoms MEMORY Definition '220 Inability to recall former perceptions and Amnesia ideas. Loss of memory in general. May be more or less extensive. May affect memories of the immediate, or of the remote, past. 221 Inability to express by words some idea in the Motor patient's mind, although there is no paraly- aphasia sis of the vocal organs and the patient can usually express the idea by gesture. A loss of memory of how to speak (innervation memories), especially names. A limitation goo °f tne vocabulary. Sensory or Inability to understand (although not deaf) Auditory spoken words formerly intelligible. Loss aphasia of memory of words formerly heard. Hence (word inability to recognize them when spoken deafness) (233). 203 M E M R Y D I M I N I S H E D 223 Optic] aphasia 224 Mixed aphasia 225 Paraphasia (Jargon speech) 226 Paragraphia a word, or the placing of the right word in the wrong place, in writing. 227 Agraphia Inability to name objects, which the patient sees clearly, although he can name them after feeling them. Loss of visual memo- ries (232). A mixture of the three forms of aphasia just described. The use of a wrong word, or the omission of a word, or the placing of the right word in the wrong place, in speaking, with consequent incoherent speech. Jargon speech is an extreme degree of this. The use of a wrong word, or the omission of Inability to express in writing the idea in the patient's mind, although he formerly could do so and his right arm and hand are not paralysed. 228 Inability to read words patient could formerly Alexia read, although he sees them clearly and (Word there is no paralysis of his vocal organs, blindness) 229 Inability to recognize objects by the sense of Astere- touch, although there is no anesthesia pr- ognosis sent in sufficient degree to prevent it. 230 Inability to execute a desired act. Loss of Apraxia skill in executing acts, although there is no motor paralysis present. Loss of innerva- tion memories necessary to perform these acts. 231 Inability to recognize objects through some Agnosia organ of sense which is itself normal. This may be due to failure of full perception or to loss of special memories. 232 Inability to recognize well known objects or Psychic to comprehend familiar things by sight, al- blindness though the patient is not blind. Loss of visual memories, optic aphasia (223). 233 Inability to recognize and comprehend well Psychic known words and sounds, although the deafness patient is not deaf. Loss of auditory memo- ries. Includes sensory aphasia (222). 60 Significance Functional or organic dis- ease of the cerebral cor- tex, often anemia, some- times the result of fright. Lesion in or near base of left inferior frontal con- volution and anterior por- tion of left island of Reil in right 'handed persons, and of the right side in left-handed persons. 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 re- sult from carelessness. Lesion in the base of the middle left frontal convo- lution, cortical or sub- cortical. Sub-cortical lesion beneath left angular convolution in right handed persons. Lesion in or near cortex, or sub-cortex, of contralat- eral posterior central con- volution. Cortical, or sub-cortical, lesion of motor area of contralateral hemisphere. Cortical, or sub-cortical, lesion of sensory area of cortex of contralateral cerebral hemisphere. Cortical, or sub-cortical, lesion of left occipital lobe, except in region of calcarine fissure. Cortical, or sub-cortical, lesion in left superior temporal convolution 'n right handed persons. Significance EMOTIONS Definition Without adequate cause the patient is de- pressed and unhappy. There is a great re- pression 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 con- stant fear of an impending calamity, or has an unformulated fear. He dreads to cross an open space (agoraphobia), or to enter a small room or confined space (claustropho- bia), or fears a storm (astrophobia), or syph- ilis (syphilophobia), or ill-timed urination (urophobia), or everything (pantophobia), etc. Can be influenced little, if at all, by reason. Frequently has a more or less un- conscious sexual basis. Without adequate cause the patient is exhil- arated. There is great exuberance of mental and physical activity. Careless and destruc- tive Can In' influenced little, if at all. by reason. Difficult to get his attention. Without adequate cause patient is in a dull stuporous condition. No expression of phys- ical or mental activity. An automaton, sub- mitting passively to whatever is done for him. Methods for the detection of disorders of memory and emotion are described in Chart I a. For further discussion of these svmptoms and of the diseases in which they occur see Charts XIII ami XVI. Diagnostic Symptoms '234 Sadness (Melan- cholia) ' E 235 X Fear A (Phobias) G G E -i R 204 A E T M E D T - I 236 D Joy N I ( Mania) S M I - X I 237 s Apathy H 1. D Functional or circulatory disturbance of cerebral cortex, especially cere- bral exhaustion. Occurs in neurasthenia and espe- cially in insanity. Fears and apprehension seem to be the basic symptoms of many forms of incipient insanity (Mosher). 61 CHART IV Disorders of Voluntary Motion ANALYSIS OF THE Definition, Significance 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 de- pend upon the existence of innervation memories of past acts, primarily re- flex. Voluntary motion depends upon the integ- rity of the central motor neurons (461) and of the peripheral motor neurons (462). In disease the power of voluntary mo- tion may be diminished, exaggerated or perverted. 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 muscular tonicity or tone. It is really a reflex act caused and maintained by many slight irritations, and can be abolished by cutting the posterior nerve roots. Muscular tonicity is increased (hypertonia) in destruc- tive lesions of the central motor neurons and in some functional disorders. it i diminished (hypo- tonia,) or abolished (ato- nia,) In destructive lesions of the peripheral motor or sensory neurons, in lesions of I be cerebellum, m sleep and in narcosis OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) and Relationship of the Symptoms of Disease. - 211 PARALYSIS A condition in which the muscles cannot be con- 241 DIMINUTION also called AKINESIS and HYPOKINESIS 242 EXAGGERATION also called HYPERKINESIS 243 PERVERSION also called PAR ^KINESIS contracted by the strong- est effort of the will. As commonly used the term includes: PARESIS A condition in which the muscles can be contrac- ed only feebly by the strongest effort of the will. r245 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 (571). Must not be confounded with a coarse tremor. 247 IRREGULAR SPASM Involuntary acts of various kinds (292, 573-4). r248 ATAXIA Disorderly movements due to loss of power of co- ordination (638). Asyner- gi:i. Associated with hypotonia (252) 249 LOSS OF SKILL. LPRAXIA Awkwardness. 260 TREMOR involuntary rhythmioal os- cillal ion of some the bodj or of a muscle. I e powerful, more rapid ami more rhythmical than a clonic spusin Kilt similar in appearance, especially irhen coarse. [Yemor ma] be slow (8 to Q per second lor rapid • 12 per It may l"- coarse or line The conditions under which paralysis or paresis occur 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 conditions under which t he various fornix of per- version o f motion occur are set forth in Chart I\ ■■ CHART IV a Motor Paralysis Comprising Numbers 244 and 251 to 260 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) 244 PARALYSIS \ INTENT™ 11 C H A R A -{ C T E L R Diagnostic Symptoms 251 A Spastic, or hyper- tonic, paralysis. (473). (Figs. 24-6) MOTOR PARALYSIS Definition 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 elec- trical reaction of muscle and nerve is nor- mal (396). The tendon reflexes are in- creased. 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 preputial irritation in children, or pain, may simulate this condition. 252 A Flaccid, or hypo- tonic, or atonic, or atrophic paralysis (472). (Figs 24-6) 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 the 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 (399). When muscles are completely degenerated (404) passive contractures (263) may occur. The tendon reflexes are abol- ished or diminished. Destructive lesion of peripheral motor neurons (462). It oc- curs in diseases 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 without muscular paralysis or atrophy occurs in cerebellar lesions, tabes and other ataxic con- ditions (240). 253 A rapid tiring of muscles upon exercise. A Myasthenic myasthenic reaction to electricity (401). paralysis Muscles show small foci of small round (553) cells. A lesion of the muscles and often of thymus gland. MOTOR PARALYSIS (Continued) Diagnostic Symptoms Definition f 254 A paralysis with exaggerated tendon reflexes, Hemiplegia of one lateral half of the body and extremi- (478-9) ties limited by the median line in front and (Figs. 17-24) 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 exagger- ated reflexes on the other side of the body also, especially in the leg. Symmetrical, bi- lateral muscles, which have a common func- tion and a bilateral cortical innervation, arc not paralysed; at most temporarily weak- ened. Such are the ocular, masticatory, laryngeal, respiratory, 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 external rotators and adductors of the upper arm, the triceps, the supinators and abduc- tors of thumb, the extensors of the thigh, the flexors of the leg and the dorsal flexors of the foot. 255 A double hemiplegia involving both sides. Diplegia May be complete or partial and not infre- (478) quently is limited to the legs, or the face (facial diplegia), etc. Significance A lesion of the contralat- eral central motor neu- rons (461). In extremely rare cases the lesion may be homolateral (homo- lateral hemiplegia), in which cases the pyra- midal tract may not decussate in the med- ulla. Hemiplegia is usu- ally due to a cerebral lesion, but the partial form may be due to a bulbar or spinal lesion, very rarely. Very rarely, there may be no lesion, except an extreme local anemia or edema of brain as in nephritis (hemiple- gia sine materia). A lesion, usually but not always cortical, of the central motor neurons or basal nuclei on both sides. 256 A paralysis of Crossed one or more paralysis homolateral (537-42) cranial nerves (Hemiplegia and of the alternans) contralateral (Figs. 20-1) arm and 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 (1268)), the pons (facial hemiplegia alternans (1269)), or in the cms cerebri (motor oculi hemiplegia alternans (1270)). The nuclei, or the neurons, peripheral or central, of the cranial nerves are involved below the decussation of their central neurons. 257 A symmetrical par- 1'araplegia alysis of both (480) sides of the body. (Figs. 24-6) Usually only in- volves the legs and lower pari of bod] . lint 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, para- plegia to those of spinal or peripheral origin. 2">s A paralysis of one ex- Monoplegia t remit y only, Or of one i 179 (Fig. 15) 200 Local paralysis i Mi (Fig. 16) 200 Aphonia (787 B) half of the face only, \la\ be due to lesion of motor cerebral i Or of the motor nuclei, or of the peripheral nerves. A paralysis limited to one or more muscles of the face, eye, mouth, neck, bod] or extremitic I i than a whole extremity. May be due to lesions of muscles or of peripheral net vm, or of spinal cord, or rarely of motor cerebral cortex, or functional Inability to produce vocal sound- Absence of voice, but whispering is pos- sible. A \ ariety of local pai alysis. Laryngeal paralysis, o;- ganio Or functional. Methods tor the detection of paralysis and paresi bedinCharl I b. For further consideration of these symptoms and of the diseases in which th X. r.7 CHART IV b Spasm Comprising Numbers 245 to 247 and 263 to 276 O'.i ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) SPASM Diagnostic Symptoms Definition 245 T O N I C S P A S M ' 263 A continuous contraction of long duration in which Passive the muscles, tendons and ligaments have be- contrac- come anatomically shortened and cannot be ex- ture tended by force, even under etherization. The (Figs. 24-6) muscle fibers are degenerated, while the connec- tive tissue of the muscle is hypertrophied and usually secondarily contracted, as in other newly formed connective, or scar, tissue. 264 A continuous contraction lasting weeks, months, Active or years, which can be overcome by force, either contrac- with or without etherization. Muscles are in a ture normal condition of nutrition. Most common in (Figs. 15, the arms, or legs, or neck muscles (torticollis). 17, 24-6) The active contracture of a hemiplegia is usually that of flexion in the arm and of extension in the leg. 265 An active contracture of brief duration but much Myotonia longer than a convulsive tic. It may occur at (613) the commencement of voluntary motion (Thorn- sen's disease, or myotonia congenita) or may be excited by cold (Eulenberg's disease, or para- myotonia congenita). It is frequent in menin- gitis and tetanus in which it takes many forms, viz: "retraction of head;" "trismus," strong closure of jaw; " opisthotonus," arching of body backwards; " pleurosthotonus," bending of body to one side; " emprosthotonus," arching f body forwards and " orthotonus," holding f body rigid and straight. 266 An active contracture of such mild degree that it Rigidity does not prevent passive, or even voluntary, motion of the part, although rendering it diffi- cult (paralysis agitans (612)), etc. 267 A violent spasm of momentary duration. If rapidly Convulsive repeated it must be classed under myoclonus tics (270 and 601-4). If painful it is called ' tic (601) douloureux " (602). 268 Reflex spasm A spasm, usually tonic, caused by irritation of some sensory tissue. 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 n 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 hem- iplegia in tabetics and in any case can be re- lieved by section of the posterior nerve roots. Such contractures are always of very bad prog- nosis as to recovery. Active contracture is some- times due to paralysis of antagonist muscles or to muscle lesions. All tonic spasms (not in- cluding passive contrac- ture) are due to a func- tional disorder, or are re- flex (especially in chil- dren), or are due to irrita- tion (chemical, sensory or vascular) of central motor neurons (461). Painful cramps, espe- cially in legs, of the na- ture of myotonia or tics, may be due to a defi- ciency of water in the system. 70 Diagnostic Symptoms SPASM (Continued) Definition 246 C 247 I R R E G U L A R S P A S M S 269 Violent clonic contractions of many, or of all the, Convulsion muscles of the body. (571) 270 Successive clonic contractions of one, or of a few Myoclonus adjacent muscles. Repeated convulsive tie. or Most common in the face muscles (blepharo- convul- spasm (601)). sive tics '271 Slow, worm-like, rhythmical movements, often " Athetosis associated with transitory contractures or mobile (spasmus mobilis), of fingers and wrists and spasm more rarely of toes and ankles. Hyperex- (574) 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. 272 Rapid, irregular, co-ordinated, but purposeless Choreic movements caused by contraction now of one move- group of muscles, now of another, throughout ments the body; bilateral or unilateral (hemichorea). Chorea minor Cease during sleep. They often render volun- (573) tary movements ataxic and are usually asso- ciated with a mild degree of paralysis of the muscles involved. Patient performs involuntarily and uncontrol- ably a complicated and apparently purposeful movement. Also applied to a coarse tremor or violent oscillation of a part of the body. Patient frequently performs involuntarily, and usually unconsciously, the same act. Usually a small act. 273 Chorea major or magna (628) 274 Habit chorea (626) 275 Patient is compelled hy some power within him Compulsory which he cannot understand or explain to acts (218) perform certain acts against his will. 276 Muscular contractions, occurring when movements Associated are executed <>r attempted, in muscles not di- move- rectlv concerned in the movement attempted; ments often the corresponding muscles of the opposite side of the body, often those of the face. Such associated movements are Hell's phenomenon i III Strumpell's tibialis phenomenon ill.".-, lialnnski's associated movements in unilateral paralysis (•( 16). Significance Clonic spasms are usually due to irritation of the cerebral cortex, but may also result from very exag- gerated reflexes (clonus). Lesion is usually in pos- terior part of optic thal- amus or corpus striatum of contralateral hemi- sphere and not causing complete paralysis. Le- sion may involve the fibers connecting the optic thalamus with the cerebral cortex. May oc- cur in diffuse cortical lesions. Functional disorders, occur- ing in the neuroses and in insanitv. In such cases movements often associated together, but which can be easily dissociated voluntarily in health, cannot he disso- ciated in disease which cuts off voluntarv action. Methods of detection of spasm are described m ('hart I b. For further discussion of these symptoms, and of the diseases in which they occur. BOS Charts XI and XII. 71 CHART IV c Perversions of Motion Ataxia, Loss of Skill, Tremor Comprising Numbers 248 to 250 and 280 to 293 73 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) ATAXIA— LOSS OF SKILL Diagnostic Symptoms 280 Motor ataxia (644) (dynamic ataxia) (Figs. 24-6) Definition 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. 2S1 Walking and standing are inco-ordi- Cerebellar nate, but other acts are not, or only ataxia slightly so. Patient executes simple (642) movements of his legs fairly well (static when lying in bed, but in walking ataxia) and standing he lacks synergy of the (Figs. 19-26) muscles and staggers and sways like a drunken man. Usually associated with vertigo (392). 282 Inability, or difficulty, in performing Apraxia a desired and accustomed act because (Fig. 15) of loss, or derangement, of the innervation memories concerned in that act. Loss of skill. Significance Is due to a loss of muscle sense (42) (deep sensibility). May be due to lesions of peripheral sensory nerves, or of posterior columns of cord, or of brain stem, or of cerebral cortex posterior to fissure of Rolando, or may be toxic (alcohol), or functional. Is due to a lack of muscular synergy (41) (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 is transitory; in lesions of the worm it is more permanent. Loss of innervation memories, general or partial, due to cortical or sub- cortical lesions (anterior or posterior central, or supra-marginal convolu- tion) or to functional or anemic disorders of cerebral cortex. (See page 26-7). May be either functional or organic and, if the latter, may or may not be due to lesions in the organs of speech. If not, it is called pure motor aphasia or aphemia. 283 Absence of speech. Speech may never Anarthria have been acquired, as in idiocy, or (737) it may be voluntarily restrained for a purpose; or it may be more or less involuntarily restrained, as in insanity or hysteria. 284 Such difficulty in articulation that Dysarthria speech becomes indistinct and (738) blurred, but is probably never so great as to cause complete anarthria (283). 285 Difficulty in swallowing. Dysphagia 286 Difficulty in mastication. Dvsmasesis (553) 287 Complete inability to stand or walk Astasia and but legs can be moved freely, even Abasia strongly, when lying or sitting. (653 and 792) 288 Difficulty in repeating a movement Occurs in lesions of a cerebellar hem- Diadocoki- rapidly, especially supination. isphere, or is functional. nesia (36) 74 Occur in lesions of the medulla and pons (bulbar paralysis, Figs. 21-3) and of the cranial nerves. Also in diphtheria, hydrophobia, myasthe- nia gravis, rarely in trichinosis and frequently in hysteria (globus hystericus). A delusion or auto-suggestion, which occurs in hysteria. May occur rarely in cerebellar lesions. 250 T R E M O R TREMOR Diagnostic Symptoms Definition 289 Involuntary, rhythmical oscillation or Passive trembling of a part which is other- tremor wise at rest. (646 and 647) 290 Intention tremor (64.5) 291 Nystagmus '(640) An involuntary tremor which only occurs when a voluntary motion is made, or is willed and is about to be made. An involuntary trembling or oscillation of eyeball, usually horizontal, rarely verti- cal, very rarely rotatory. Increased, or only occurs, on voluntary motion of eyeball, especially on extreme deviation. The rapid- ity 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 direction is equally rapid, or rhythmic when it is quicker in one direction than in the other. Significance Functional. Occurs in paralysis ti- tans, weakness, etc. Functional and organic. Occurs in neuroses and in organic diseases (disseminated sclerosis) Occurs especially in lesions of the vestibular and other nuclei in the pons, Deitcr'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). 292 An involuntary contraction of a bundle I ibrillary of fibers of a muscle of short dura- contrac- tion. When many occur in adjacent tion or bundles at short intervals, waves of fibrillation contraction run over the muscle, but (641) do not cause it to contract as a whole. 293 Myokymia A fibrillary twitching of the muscles occurring in healthy persons. Degeneration of those multipolar nerve 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. Normal. Exhaustion. Following ex- cessive muscular contraction or ex- posure to cold. Method- of detection of perversions of motion are described in ('hart I b. For the further discussion of these symptoms and of the diseases in which thev 0CCU1 Chart XII. 78 CHART V Reflex Activity ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the symptoms of disease. f297 CUTANEOUS OR SUPER- FICIAL REFLEXES A reflex act which originates from an irritation of the skin (57). 296 REFLEX ACTS An involuntary movement caused by irritation of a sensory nerve or terminal organ. Although not the result of conscious in- tention, yet these acts seem pur- poseful and usually tend towards the protection of the body. In order that a reflex act may take place there must be a compara- tively healthy reflex arc, con- sisting of a motor nerve, a sen- sory nerve and some gray mat-- ter connecting the two; or, in other words, :i motor neuron and a sensory neuron connected together directly or by a bridg- i ri ti neuron. Keflex acts are in- hibited and modified by inhib- itory impulses passing down from the brain along the so- called inhibitory filler.--, which are also the central motor neu- rons (the pyramidal tract) (472- 4, 810). (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 affecting one of the viscera of the body (1), especially the bladder or n ctum. 301 VASO-MOTOR IM II I \l s A reflex act affecting the arterioles (59). 302 PUPILLARY EU I LEX A reflex act affecting the pupil (25-7). The conditions in which reflex acts are disor- ordered are set forth in Chart Y a. The conditions in which the pupillary n arc disordered I forth in Chart V b. :: CHART V a Cutaneous or Superficial Reflexes, Mucous Membrane Reflexes, Tendon or Deep Reflexes, Organic Reflexes, Vaso-Motor Reflexes Comprising Numbers 303 to 326 7'.. ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) CUTANEOUS REFLEXES Diagnostic Definition and Location of Symptoms Reflex Centers 303 Plantar flexion of the toes when Plantar the sole of the foot is irritated. (1st and 2nd sacral segments.) 304 Sluggish extensive dorsal flexion Babinski's of the great toe when the sole of the foot is irritated. 305 Dorsal flexion of the great toe Gordon's when deep pressure is made through the calf muscle on the deep flexor muscles beneath ; the leg being completely relaxed. 306 Dorsal flexion of the great toe Oppenheim's elicited by firm stroking with a hard object, or finger, just be- hind the postero-internal border of the tibia from above down- wards ; the leg being completely relaxed. 307 Gluteal 307a Anal 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.) 308 Drawing up of the testicle when Cremasteric the inner side of the thigh is irritated. (1st to 3rd lumbar segments.) 309 Sudden movement of umbilicus Umbilical towards the side of abdomen irritated. (8th to 12th dorsal segments.) 310 Sudden retraction of epigastrium Epigastric when the hypochondrium is irritated. (7th to 9th dorsal segments.) 311 Drawing inwards of the scapula Interscapular when the skin of the interscap- ular space is irritated. (5th cervical to 1st dorsal seg- ments.) 312 Closing of the eyelids when the Corneal or cornea or conjunctiva is irri- conjunctival tated. (5th to 7th cranial nuclei.) 313 Sneezing when the nasal mem- Nasal brane is irritated. (5th to 10th cranial and upper cervical nuclei.) Significance The abnormal reflexes, Babinski, Gordon and Oppenheim reflexes and ankle-clonus, always indicate disease of the central motor neurons (461), except in infants, in whom these re- flexes (except ankle-clonus) may be present normally, and in some cases of hysteria in which an imperfect ankle-clonus may rarely be obtained. The Babinski reflex is most re- liable in a diagnostic sense. The Oppenheim reflex is sometimes present when the Bab- inski is absent and vice versa. Kernig's sign indicates meningitis or meningismus; it is an important, but not a certain, diagnostic sign. Alterations in the tendon reflexes are of very much greater diagnostic value than are those of the cutaneous (except the Babinski) re- flexes, which are in many cases inconstant, probably because the cutaneous reflex im- pulses may even pass through the gray matter of the brain (cerebellum) as well as through a wide area of that of the spinal cord. Diminution of reflexes is usually of little diag- nostic value, but their abolition is of great value and maybe 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, atro- phic motor paralysis is present in addition to the loss of the reflex. When there is a lesion of the peripheral sensory neuron there is usually a sensory paralysis (anesthesia, etc.), in addition to the loss of the reflex. 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 Babinski) in cases of complete separation of the brain from the spinal cord, and, rarely, of increased intra- cranial pressure, also frequently in fevers. The abolition of the knee-jerk is of great diag- nostic importance. It is absent in tabes, neuritis (multiple and crural), acute anterior poliomyelitis involving the extensor cruris, Landry's paralysis, lesion of the cauda equina or of the lumbar enlargement, during the attack of family periodic paralysis, when exhausted 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. 80 MUCOUS MEMBRANE. TENDON, ORGANIC AND VASO-MOTOR REFLEXES Diagnostic Symptoms 314 Uvular 315 Pharyngeal 316 Ankle-clonus 317 Achilles reflex 318 Knee-jerk 319 Kernig's sign 320 Dorsal foot reflex Definition and Location of Reflex Centers 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. (1st to 2nd sacral segments.) Sudden extension of knee when the ugamentum patellae is sharply struck. When this reflex is ex- aggerated it is usually accom- panied 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 <>f jaw when it is sharply struck downwards. (61 ii oranial nucleus.) The retention of mine in the blad- der by the sphincter reflex, and i (pulsion of urine by tin- de- trusor reflex and the synchro- nous relaxation of the sphincter. (Hypogastric sympathetic ganglia.) Similar to that of the bladder, orrhoidal sympathetic lia.) den pallor of the skin follow- ing an irritation and limited to the area of irritation. Significance 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 reflexes are increased by any lesion of the motor central 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 with 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 thigh when the knee-jerk is tested for. In the dorsal foot-rellex i Mendel-Bechterewt 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. 321 Elbow and wrist reflexes 322 Maxillary rellex 323 Bladder or vesical reft x ;!-' I Rectal 325 Ischemic reflex 326 Para!' hyperemic Congestion <>f the skin following p fl( \ the ischemia due to irritation ; (dermogra- (t&chee oerebralea and dermo- phiai graphia). The thoda of eliciting 'he various n ed in Char) 1 o. isee in which the reflexes are altered are discussed in Charts X. \i\ 81 Inability to void urine, or to retain it. is some- times due to nervousness and sometimes to mechanical obstruction (enlarged pro- 1 stricture), imt any other serious disturbance of the Organic reflexes indicates organic dis- ease of t he nervous system. 1 1 never occurs in diseases limited to the peripheral nerves, ex- o pt in lesions of the cauda equina, and rarely in cerebral disease. It i- most common in spina] disease, Bphincter paralysis with empty bladder and constant dribbling of urine in ne of lumber enlargement, and detrusor paralysis with distended bladder and often with dribbling of urine in lesions above the lumbar enlargement. (Fig. 28 Vasomotor disturbances cause a disturbance of the nutrition of a part. Diseases which re.Milt from, or are associated with, disturb- anoes of the vaso-motor reflexes an 1 in Chart \ \ II. XVI, \ \ 1 1 CHART V b Pupillary Reflexes Comprising Numbers 302 and 330 to 341. 83 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Diagnostic Symptoms 330 Pupillary reaction to light (25) PUPILLARY REFLEXES Definition and Location of Reflex Centers Pupil contracts when light is thrown on retina of the same eye (direct reflex), and when light is thrown on retina of opposite eye (con- sensual reflex), and dilates when retina is shaded from light (ciliary ganglion). 331 Pupillary reaction to accom- modation (27) Pupil dilates when pa- tient looks at a dis- tant object and vis- ■ ual axes are parallel and contracts when patient looks at a near object and eyes converge. 332 Argyll- Robert- son's phe- nomenon (447, 891) Pupil does not re- spond to light, but does respond to ef- forts at accommo- dation. 333 The pupil responds Immobile neither to light nor pupil accommodation, but (545) in some cases may still dilate slightly on irritation of cer- vical sympathetic. 334 Pupil contracts when Hemiopic light is thrown on reflex the unparalysed (26) half of retina, but does not contract when light is thrown on para- lysed half. Significance The pupillary reaction to light is diminished or absent in lesions of the reflex arc (optic nerve, corpora quadri- gemina, the Westphal-Edinger cell group of the motor oculi nucleus, third nerve and ciliary ganglion), espec- ially in lesions of the ciliary ganglion. When the op- tic nerve or corpora quadrigemina are involved the consensual reflex can not be obtained from the other (healthy) eye. It is absent in blindness, 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 eye is under the influence of mydriatics or myotics. The pupillary reaction to accommodation is absent (cyclo- plegia) in lesions of the third nerve, sometimes after diphtheria, occasionally in alcoholism and when the eye is under the influence of mydriatics or myotics, also in myopia and in cases of deficient convergence. The Argyll-Robertson's 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's phenomenon, i.e., the preser- vation of the light reflex and the loss of the accommo- dation reflex, occurs occasionally in diphtheritic paral- ysis and has been found associated with syphilis, basal meningitis, tumors of corpora quadrigemina and myelitis. 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 ophthalmoplegia externa or interna or both. When it occurs alone it is due to a 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 observers. 84 PUPILLARY REFLEXES (Continued) Definition and Diagnostic Location of Symptoms Reflex Centers 335 Pupil dilates when Cilio- neck on same side spinal is irritated or when reflex cocaine is dropped (465, in the eye. (Cer- 1191—2) vical sympathetic ganglion.) 336 When the eye is sud- Hippus denly exposed to light, there occurs a series of alternate contractions and dilatations of the pupil, gradually growing less in degree. 337 When patient's eye- Westphal's lids are held fore- pupil ibly apart and he reaction attempts to close them he not only turns the eyeball upwards (Bell's phenomenon) but also the pupil con- tracts. 338 Pupil dilates instead Paradoxical of contracting upon pupillary exposure to light or reflex upon efforts of ac- commodation. 339 Dilated pupils. Mydriasis 1 340 Contracted pupils. Myosit :* II One pupil is largi i Unequal than the other when pupils t>r the eyes are al aniaoooria Significance The cilio-spinal pupillary reflex is absent in lesions of 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). Hippus is usually associated with a general exaggeration of reflexes. Westphal's pupillary reaction occurs in some cases of tabes and in paresis. 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. Mydriasis may be irritative or spasmodic, due to irrita- 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 cervical sympathetic directly by incipient lesions in the cervical enlargement of the spinal cord and its mem- 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 reflex 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. Myosis 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 lie ilue to both causes. It occurs in old age, in deep sleep, or on taking certain drugs (myotics); 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 ami of the spinal cord (syringomyelia). It occurs often in tabes, paresis, iritis, irritation of cornea and, tempor- arily, after excision of the Gasserian ganglion. Aniscoria occurs in many conditions and is of little or no diagnostic value. The methods of eliciting the pupillary reflexes are deseribed in Charj I b Diseases in which these reflexes are altered are discussed in Chart X I V 85 CHART VI Disorders of Sensation ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease. 344 DISORDERS OF SENSA- 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 memories and of recalling them at will. It depends 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. 345 DIMINUTION Either no perception or an abnor- mally feeble one follows a sensory irritation adequate in health to cause a perception (805, 810). 346 EXAGGERATION An unusually strong perception, as compared with health, follows any. sensory irritation (806). 347 PERVERSION The occurrence or modification of a percept ion such as never occurs in health (930). The conditions 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. 87 CHART VI a Diminution and Exaggeration of Sensation Comprising Numbers 345 and 346, and 348 to 372 89 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) SENSATION Diagnostic Symptoms Definition 348 A loss, or diminution, of the Anesthesia normal sensibility to touch (complete) or upon adequate irritation. Hypesthesia Normal sensibility varies in (partial). acuteness in different parts (Superficial of the body and in different sensibility) individuals. 349 Analgesia or Hypalgesia 350 Thermic Anesthesia or Hypesthesia A loss, or diminution, of the normal sensibility to pain, which in health varies in different individuals and in different parts of the body. A loss, or diminution, of the sensibility to variations in temperature. This loss may be more marked for cold than for heat and vice versa. 353 Apallesthesia or loss of osseous sense or vibra- tion sense. 354 Astereognosis 355 Deafness or Anakusia or Hypakusia 356 Anosmia or Hyposmia 357 Ageusia or Hypogeusia 358 Blindness or Anopsia or Amaurosis 359 Amblyopia Significance Diminution of sensibility may be clue to disease of the terminal end organs, or to a destructive lesion either of the peri- pheral sensory neurons (464), (in which case all forms of sensibility are abolished over an area usually coinciding with, but smaller than, the distribution of a 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). Sensibility is abolished in coma, nar- cosis and often apparently in hysteria. A broad zone of analgesia and, more rarely, of anesthesia also, about the body occurs in locomotor ataxia: "tabetic cuirass." The anesthetic area may coincide with the distribution of a peripheral nerve or with that of a nerve root (peripheral lesion); or with the distribution of sev- eral nerve roots (spinal lesion) ; or the area may involve one-half the body: called hemianesthesia (cerebral lesion and hys- teria). 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. 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 forearm, etc., and be sharply limited "stocking and glove variety" (hysterical). (Fig. 33.) 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.) Loss, or diminution, of sense Astereognosis always indicates a lesion of of hearing. the cerebral cortex. (Fig. 15.) 351 Inability to distinguish differ- Loss of pressure ences in the amount of pres- sense sure made on the skin. 352 Inability to tell how strongly a Loss of muscle muscle is contracted, wheth- and joint sense era joint is flexed orextended, or Akinesthe- or where an extremity is sit- sia. (Deep uated in space. A very corn- sensibility) plex sensation. Inability to feel the vibration of a tuning fork pressed firm- ly on the skin. Inability to recognize objects by the sense of touch; anes- thesia not being present. Loss, or diminution, of sense of smell. Loss, or diminution, of sense of taste. Loss of vision. Decided impairment, but not complete loss, of vision, espe- cially 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. Anakusia, anosmia, ageusia and blindness, 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 diagnostic value in nervous diseases. Hemeralopia associated with a central sco- toma for green and red is not uncom- mon in tobacco smokers; so that when the pupil is dilated in a dim light the health part of the retina can act. This 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. 90 SENSATION (Continued) Diagnostic Symptoms f 360 Hemeralopia 361 Nyctalopia 362 Hemianopia Definition 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. 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. 363 Tetartanopia or Quadrantic Hemianopia Loss of an homonymous quad- rant of both fields of vision. 364 Inability to distinguish the Achromatopsia different colors from each or color blind- other either throughout the ness. Hemi- whole, or in one-half the chromatopsia field of vision. 365 Dissociation of sensation 366 Hyperesthesia 367 Hyperalgesia 368 Thermic Hyper- -ia or Hyperalgesia 360 Hyperosmia 870 llyprrgcusia 371 Photophobia 872 Byperakusia Loss of some forms of cutane- ous sensibility (usually for pain and temperature) with preservation of others (tac- tile). (Figs. 24-7.) Increased tactile sensitiveness. An unusually slight touch can be perceived. A very rare and even doubtful con- dition. It is usually employed when a touch causes an un- usually great, even painful sensation, where hyperalge- sia or haphalgesia (380) would be a better term. Increased sensitiveness to pain. Increased, even painful, sensi- tiveness to heat or cold, or both. Increased. e\en painful, sensi- tiveness to odoi ed and unpli asant Ben* Bitivenesfl to taste. Significance Homonymous 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 lateral col- umns of the spinal cord, or more rarely a lesion in the ponto-cerebellar angle of the pons at the level of the auditory nerve. It occurs associated with motor paralysis of the opposite side of the body in some cases of Brown-Sequard's paral- ysis. i at ion of sensibility of all kinds is usually functional. More rarely it is the result of an irritative, rather than a destructive, lesion of the oentral or peripheral sensory neurons. It occurs in Strychnine poisoning and tetanus. Byperesthesia 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- S&ruard'a paralysis. It is usually asso- ciated with increased reflex activity. Photophobia is functional, or due to eye strain, or to inflammation of some part of the eye, nr optic nerve, or cerebral menu ed and painful sensi- \ [ vperakiisia is functional, or due to ear tiveneas to light, 'diseases affecting the labyrinth, or to cerebral conditions causing hyperemia of ed, even painful, send- the labyrinth (meningitis, encephalitis, tiveneSS to sounds. tumors, etc) and to spinal affections. Methods f<.r the detection of these conditions an di scribed to chart [o. Diseases in which these conditions oocui ed in Chart XIV. CHART VI b Perversions of Sensation Comprising Numbers 347 and 374 to 392 93 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Diagnostic Symptoms 374 Pain (Figs. 33, 38) 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 (radiat- ing), or may run half way or entirely about the body or an extremity (gir- dle) , or it may be felt in an area which is itself anesthetic (anesthesia dolo- rosa). Pains may vary as to time of occurrence, some showing a distinct periodicity (malaria, neuralgia and migraine), some occur at menstrual epochs. Some headaches occur in morning (uremic) , others in afternoon (ocular) and others towards evening and at night (syphilitic). Some pains are increased by pressure (neuritis and neuralgia) while some are dimin- ished by it (lead colic). 375 Curious sensations rarely felt in per- Paresthesiae feet health, usually unpleasant but not severe enough to be called pain. They are numbness, tingling, formi- cation, heat, cold, heaviness, tired feeling, hunger, etc. 376 Failure of When a cutaneous sensation is felt but localization cannot be localized. (Topoanesthesia) 377 Allocheiria 378 Double sen- sation and Polyes- thesia 379 Paradoxical sensation When "an irritation is not felt at the point of contact, but at a correspond- ing point on the opposite side of body. Where one contact gives rise to two distinct sensations (double sensation) or more (polyesthesia). The quality of thermic sensation is reversed, a hot body feels cold and vice versa. 380 A slight tactile impression from certain Haphalgesia objects, but not from others, is felt as intense pain. 381 Retardation The sensation of pain is not felt until of conduc- an appreciable interval after the time tion of pain of contact. 382 The sensation continues an unusually Persistence long time after the irritation causing of sensation it has ceased to act. Significance Perversions of sensibility, especially pain and paresthesiae, are often functional 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. Although pain may be felt as peri- pheral it may be of central origin and due to lesions of central neurons within the brain or cord. On the other hand pains due to lesions in the abdominal viscera may be referred to remote parts of the body or the head (referred pains 952). Failure of localization may be func- tional but usually results from lesions of the peripheral sensory neurons (tabes). Allocheiria 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 spinal and cere- bral diseases, but is without diag- nostic significance. Haphalgesia occurs in hysteria. Retardation of conduction of pain occurs only in lesions of peripheral sensory neurons (tabes or multiple neuritis). Persistence of sensation occurs in lesions of the peripheral sensory neurons (tabes). Binocular diplopia is due to a weak- ness of one or more of the external muscles of one eye, or to displace- ment of one eyeball; so that the image does not fall on identical spots in the two retinae. 94 SENSATION (Continued) Diagnostic Symptoms 383 Binocular Diplopia (816) 384 Monocular Diplopia or Poly- opia (878- 82) 385 Metamor- phopsia 386 Micropsia 387 Macropsia 388 Tinnitus Aurium 389 Parakusis Definition Two separate visual perceptions of the same object, the perception from the normal eye (true image) being more distinct than that from the abnormal eye (apparent image). A condition in which objects appear double or multiple, even when looked at with one eye alone. A condition in which objects appear distorted. A condition in which everything looks much smaller than normal. A condition in which everything looks much larger than normal. A sound of ringing, roaring, whistling, etc., in ears or head. Perversions of hearing, such as hearing tones incorrectly or hearing better when other loud noises are present at the same time, or hearing sounds or words for which there is no external cause (hallucination). 390 The perceptions of abnormal odors Parosmia or of those for which there is no external cause (hallucination). 391 The perception of abnormal tastes Parageusia or of those for which there is no external cause (hallucination). 392 A feeling as if the person (subjective) Vertigo or as if BUrrounding objects (objec- tive) were whirling about, or both. Significance 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 hysteria, also in astigmatism (refractive) and in displacement of the retinal ele- ments (retinal) which may occur in retinitis, choroiditis, and in detach- ment, 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 and in insanity and functional disorders. They may con- stitute the aura of an epileptic attack. Vertigo may be functional (hysteria, neurasthenia, traumatic neuroses); or may depend on changes in the cere- bral circulation, especially anemia and hyperemia (cardiac ami arterial diseases, congestion in portal orsys- temic circulation, galvanism of head orneck), or toxic (tobacco, morphine, alcohol, some digestive disturbances, etc.) ; or may depend on diseases of the cerebellum and its tracts, or of the ear or eye. It is the principal symp- tom in Meniere's disease (aural ver- tigo). Vertigo is closely associated with vomiting. In vertigo associated with lesions in. or pressing upon, a cerebellar hemisphere, externa] ob- jects seem to whirl in (lie direction away from the injured hemisphere in both conditions, hut 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 t he hemisphere. hi < :i . mi winch these condition- occur are discussed in Charts XIV and XV 95 CHART VII a Electrical Examination Comprising Numbers 395 to 405 97 ANALYSIS OF THE OBJECTIVE SYMPTOMS OF THE CASE (SEMEIOLOGY) Definition, Significance and Relationship of the Symptoms of Disease Name Tis- Reaction OF THE sue to Reac- Test- Faradism tion ed 395 '396 - 'Contraction " ELECTRICAL Normal present to REACTION excita- a strength OF MUSCLES bility of current AND NERVES (473) which is (70-3) normal for Nerve fibers thejnerve respond to N E and muscle changes in tested. intensity of R both the far- V Cont raction adic and the 397 E present but galvanic cur- Dimin- A it requires rents. The ished N an unusually changes in excita- D ' strong intensity are bility M current to best brought U produce it. about by s making and c L E breaking the current. Muscle fibers 398 respond only Exag- gerated to the galvanic Contraction current. The excita- present to an muscle re- bility unusually sponds to the weak faradic current .current. only in virtue of the nerve fibers supplied to it. When these nerve fibers are de- Gradual generated the loss of muscles can no excitability longer respond which be- to the faradic f N comes com- current . Both E plete in nerves and R about muscles have V E two weeks points on the after injury body surface; 399 or onset of the so-called Reac- the disease. . motor points tion of . (see figures 1 to degen- Gradual 5) from which eration loss of they are most (472) M U s excitability readily excit- which be- able. There- c comes com- fore, in testing L plete in a nerve or .. E less than muscle by two weeks electricity the after injury electrode (pos- or onset of itive or nega- the disease. tive) is placed on the corre- sponding motor point (70-3). Reaction to Galvanism and Formula of Galvanic Reaction Neg.Cl.C. Pos.Cl.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 any contraction. Neg.Cl.C. Pos.Cl.C. with a little stronger current. Neg.Cl.C. Pos.Cl.C. Pos.Op.C. 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 contraction when the current is closed and the positive pole is on the motor point (Pos.Cl.C). A still more powerful current causes a con- traction when the current is opened and the positive electrode is on the motor point (Pos.Op.C). With such powerful currents and the negative pole on the motor point there results a tetanus or continuous contraction when the current is closed, (Neg.Cl. Tet.) ; so that the muscle cannot relax to contract again when the current is opened- There is, therefore, in health no reaction corresponding to " Neg.Op.C" No reaction. After the first two weeks the muscle responds to unusually feeble gal- vanic currents and the normal form- ula is reversed; the positive pole be- ing more potent. Pos.Cl.C. Neg.Cl. C. Pos.Op.C Neg-Op.C (which last reaction never occurs in health). It is usual to express the formula for the normal reaction and for the reaction of degeneration in the Ger- man language in which Kathode means the negative electrode and Anode means the positive electrode. The usual normal formula is K.C.C, A.C.C, A.O.C, K.C.Te. The reaction of degeneration is A.C.C, K.C.C, A.O.C, K.O.C The essence of the normal formula is K.CC>A.CC The essence of the formula of the reaction of degen- . eration is A.CC>K.CC 98 Character Significance of the of the Contrac- Reaction tion "Normal excitability shows a normal condition of muscle and nerve. Diminished excitability occurs in many dis- eases and conditions, especially in lesions of the central motor neu- rons and is not of much value in diagnosis. Quick. None. Sluggish. The character of the muscular contrac- tion is the most charac- teristic thing in the reac- tion of degen- eration. Exaggert ted excitability is a rare condition. It occurs in nervous persons with moist skins and in tetany. The reaction of degenera- tion proves that the peri- pheral motor neurons are degenerated and that re- covery will either never take place, or will be very slow. The lesion must be either in the peripheral nerves, or nerve roots, or in the anterior horns of the spinal cord, or in the motor nuclei in the brain stem. ELECTRICAL REACTIONS (Continued) Character Name Reaction Reaction Formula of OF THE .Significance OF THE Tissue to to Galvanic Contrac- of the Reaction Tested Faradism Galvanism Reaction tion Reaction ■ Contractions present, but " Either the Quick or The signifi- Nerve require unusually strong normal form- sluggish cance of this currents, w tiether faradic ula, or the reaction is 400 Partial or galvanic- formula of the the same as reaction of that of the reaction " of degen- eration Contractions Contractions _ degeneration, reaction of present only present to or a combina- degeneration, Muscle to unusually unusually tion of the two Sluggish. except that it strong cur- weak cur- mav be pres- indicates the rents. rents ent*. A.C.C. may equal K.C.C. lesion is less severe and that all the nerve fibers are not de- generated. 401 Myas- Nerve Contractions Normal Normal. Quick, Occurs only thenic and quickly grow grows in myas- reaction Muscle less strong rapidly thenia gravis (553) and soon cease under rapidly repeated excitation. weaker and ceases. (553). 402 Myo- Nerve Continuous Curious Positive pole Continues Occurs in tonic and tonic con- wave-like is about usually a Thomsen's reaction Muscle traction contractions equally as long time disease (613) lasting occur, and potent as the and has a (613). Bome time last after negative. wave-like after the electrical Hence the character. electrical stimulation formula stimulation has ceased. A.C.C. = K.C.C. has ceased. 403 Neuro- tonic reaction 'Nerve Unusually excitable. Te- tion has ceased. 404 Heart ion pletely lerated muscle (70 to 73) Muscle Normal. Muscle None. tame contraction persists I after electrical stimula- V Normal. I Normal. None. Nunc Continuous None. Occurs in hysteria, amyotrophic lateral sclerosis and chronic bul- bar paralysis. Muscle fibers are entirely degenerated and r ecove ry is impossible. W5 Electrical reaotion of the i ipticand Auditory Nerves •The optio nerve reapondi to the garranio current with :i teniatlon of light, the ootor <>f whiob ranee with the pole empli The auditory nerve reaponda with ■ loud Kundwbeo the Motive electa tho meat hi and the current do ed end with ;i feint sound wood the poeltive pole la need end i itrooger current broken. Theee reaction* are withou Importance. The negative electrode placed in front of thai I when the current M'i.>.-.| mlintl ppoeite direction when the ourrenl e. broken The p • electrode < Ij the revet ■ direction, in which the caloric U and is "Inch the electric teal tii 1 \ certain thai the lesion is in the labyrinth and not m the oerve If there is qo ri pon e to either the calorie or the electric test the lesion is in the oerve or its nuoleus. 99 CHART VII b Erb's Motor Points for Electrical Examination of Nerves and Muscles The motor points arc the areas upon the surface of the body at which the individual nerves and muscles can be most easily excited by electricity. For the nerves, these points coincide with those al which the nerve lies most superficially or where it can be pressed against a resisting tissue; for the muscles, they lie over the point of entrance of the nerve into the muscle. Comprising Figures 1 to 5 101 ERB'S MOTOR POINTS M. orbic. palpebr. Muscles or the ( nose \ M. zygoruatici M. orbicul. oris< Middle branch of facial M. niasseter M. levator rocnti M. quadr. menti M. triang. menti JV. hyyixilosx. JjOtcer branch of facial M. platysma mvoides Muscles of the f root of tongue \ M. omobyoideus JV. thoracic, anter. (M. pector.) N. phrenicus Suprascapular poiDt. (Erb's point. M. deltoid., biceps, brachial, intern, and supinat. long.) Rg.i third frontal convolution, M. temporalis Upper branch of facial in front of car X. facialis N. auriculo. post. Middle branch of facial Loner br. of facial M. splenitis M. sternoeleido- mastoideus N. accessorius M. levator anguli scapulae M, cucullaris JV. dors, scapula? N. thoracic, long. (M. serratns antic, maj.) M. >leltoideua M )Dist>ric»te* ERB'S MOTOR POINTS (Continued) Fig. 3 U kdtludor magnua M. .idduct. longu;, M 'vim l»ternui M. tensor facie lit* Fig. 4 M blcrp* tm tor bAllitfn h,(. r . CHART VII c ERB'S DIAGRAM SHOWING THE EFFECTS OF INJURY OF A NERVE V,lu»^- > — *■ — ," — ^ , ,. V i » » — v — ,., — ^ i ealtk. i? 11 A Wy K Health ^WZZr y3trot)h 1) ^^-o| 1 ( t r6tio i ,offniwle,C»rrkosis &±£ §lGa.lv4nic M.u) . £:|f&ride 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 righl even at the present lime. The numbness of the left side and the inability to see things on her left still persist. (In physical examination there is found anesthesia and analgesia of the left arm and leg and of left side of body and face, (left heini anesthesia and hemianalgesia), also blindness in each eye for all objects to the left of oentral 128 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 Bahinski. 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 or 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. 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 had 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 seems 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 8). Thus we have arrived by means of the charts to the diagnosis of this case of "thrombosis oi 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 symptoms, 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 opposite sided internal capsule, which is the diagnosis to which we had already reached by another road. 124 CHART X Motor Paralysis DIAGNOSTIC ANALYSIS OF SYMPTOMS. Tests Symptoms Analyzed Permanence Reflexes in Paralyzed Muscles of Paralysis 'Abolition or diminution of both voluntary and reflex acts in the muscles involved. 472 469 MOTOR PAR- ALYSIS OR PARKS IS (244) After aoarefol ex- amination has shown that the paralysis is a true one and is not simulated by any ankylosis or by pain on motion. 470 CONTINUOUS PARALYSIS 171 INTER- Ml [TENT PARALYSIS. FLACCID PARALYSIS (252) 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. Abolition or diminution of volun- tary, with persistence or even exaggeration of reflex, acts in the muscles involved. 473 SPASTIC PARALYSIS (251) lesions of central motor neurons. There is hypertonia without altera- tions of electrical reaction of the nerves and muscles. ■171 A combination of FLACCID PAR- ALYSIS in the upper part of the paralyzed area, and of SPASTIC PARALYSIS in the lower part. All the muscles of the body and ■ head. The mUSOleS Of one or both leps. rarely of arms. Commencing in legs, extending to arms ted With a cervical ril «. 125 The differential diag- nosis of those dis- eases in which FLACCID PARAL- YSIS occurs is set forth in CHART X a. The differential diag- nosis of those dis- eases in which SPASTIC PARAL- YSIS occurs is set forth in CHART X b. The differentia] diag- nosis Of those dis- eases in which there is a combination of l l \ccil> and of SPASTIC PARAI Ysis. and of those In which INTER- MITTENT I'M: LL YSIS occurs forth in ni \i;t \ o. CHART Xa Flaccid Paralysis Comprising Numbers 475 to 477 on left side of Chart and 482 to 500 on right margin I-'". DIAGNOSTIC SYMPTOMS AND TESTS 47.", No muscular atro- 1'hy, except rarely in chrome cases. Reflexes may be diminished only, not abolished. ("Paralysis beginning I in the feet and as- | rending to the head I in adults. No true paralysis great hy] ' in infants. iXO I but great hypoto- nia i r The organic r flexes a r e permanently disordered (I and 47U Muscular atrophy, usually great, fol- lowing the paralysis after the second week of the disease. Paralysis primary. The Degenerative Atrophies. (See also .Syringomyelia 552, 837-3.) The organic reflexes are normal or show " only transitory dis- turbances (1 and 323-4), 'I he paralysis is in the form of a paraplegia, commencing in the feet aj ing bulbar symptoms (434), and causing death usually in the seconc are pronounced the disease is probably a neuritis (488). The spleen , dry's paralysis and in addition hematoporphyrinuria. (Compare caret Occurs usually congenitally, rarely during the first year of life. No he in very abnormal positions. The child cannot use the Blight powei nuts, no disturbances of organic reflexes. Electrical reaction much c" rVery acute onset. Sympton Marked sensory symptoms, such as pain, | thesia. May be blood in ci paresthesiae, anesthesia, etc., are pro- i . , , . senl with the motor symptoms. The Ac "'°' sub-acute or dm.,,,,, , legs only are paralysed and exhibit! °wier evidence of syphilis i trophic disturbances. There is incon-1 Very chronic and progressive tinence of urine and the bladder is empty or nearly so. Very acute, acute or sub-acu I of the cord. Fibrillation < [ perineum, genitals and moj There is usually a history of acute, sub-acute and elm 'Many spinal (very and arms (long neurons) I 'Sensory symptoms, rarely cerebral) weakness, atrophy and tei such as pain, nerve nerves are affected. duction of pain and loss o and muscle tender- form of Korsakow's psycl ness, paresthesiae, form rarely runs an acute anesthesia, etc., are J ical form exhibits many s. present. The motor and The paralysis is CO- sensoiy paralysis In very exceptional incident with the (anesthesia) may cases sensory symp- distribution of one, be slight and the toms may be prac- rarely of a few spi- pain great. The tic-ally absent, [nal nerves. motor paralysis is usually greater than the sensory. Occurs must commonly in inj For special forms of neurits No Sensory symp- toms, except rarely pain and tender- ness over the nerve trunks in early stage. The paralysis is co- incident with the distribution of one, rarely of a few spi- nal nerves. ■The paralysis is confined to the dis- tribution of one or more cranial nerves. Extensor muscles are alone affected. A paralysis of acute onset, usually con- fined to the arms and legs, geneially to a portion of one or both; in rare cases involves the cranial nerves. \ chronic form, may occur exceed- ingly rarely. Nerve Atn The rr ban 1 < Ine o The paralysis is usual)} mon Usually confined to the extei lead poisoning. Previous The paralysis (which is alwa\ sinus. Rarely there is sligi so in children. The pararj In infants ami young chil neuritis with predominate turns are common and thi of functionally related mu Tin- muscles of I In- | runi and scurvy ( Barlow's disc. (4) encephalitic form, (5) CI i ionic atrophic paralysis (." i( lompare carefully with l v A paralysis of chronic onset commencing The di: in peronei muscles and extending sym- mucl metrically. Intrinsic muscles of the app feel affected. .nil 177 A combination of muscular atrophy and apparent hy- pertrophy. Paralysis secon- dary. The Muscular Dys- A chronic disease commencing in childhood or youth and usually showing marked heredity, It exhibits a progressive muscular atrophy, usually Combined with some hypertrophy, hence called muscular dystrophy. In time all the muscles become atrophied. The organic reflexes arc normal and there are no sensory symptoms whatever and no motor paralysis, except such as would result from the muscular degeneration, Even the ap- parently hyperl lophied muscles are weak. Tendon reflexes are early much diminished and finally absent in the affected muscles. There are no liluil- lary contractions. The course of the disease is progressive, but very chronic, lasting many years, from iis point of commencement i he atrophy ex- tends ii igboul the body. It produces a marked lordosis. Although the muscular dystrophies are divided into three groups, there are many transitional and mixed tonus, and the examination of the excised muscles also shows mixed forms. The disease is i extremities, muscles shov wilh a mixti trophy in di! eni parti of i More or less The disease, is i Inanities. E: cles shows de mixture of a and especial! tcrstitial fat. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS DIAGNOSIS ■ ascending the legs and body. Before the legs are completely paralysed the paralysis appears in the hands and rapidly ascends the arms. The ascending paralysis reaches the medulla and pons; produc- Acute Ascending (Landry's) Paralysis, ough some rare cases may recover. The organic reflexes are usually normal, except as affected by weakness of the abdominal muscles. There is little pain and little or no anesthesia. If sensory symptoms enlarged. There is rarely fever, and no electrical reaction of degeneration (3991 Certain drugs especially the prolonged use of trional or sulfonal, may cause symptoms closely resembling those of Lan- 4SS and 495.) luscles exhibit extreme want of tone and flabbiness. The legs are always, the arms are often, affected but in less degree. The mobility of the joints is greatly increased and the extremities can be placed Myatonia Congenita. Amyotonia Congenita. ary muscular contraction still remaining to any advantage. The child can neither sit, stand, nor walk without assistance. Tendon reflexes absent, no muscular atrophy, no fibrillation, no sensory disturb- but no reaction of degeneration. The tendency of the disease is towards improvement, but not to complete recovery. days and may improve later. May be deformity in lo of the vertebral column. The anesthesia always present is not preceded by hyperes- not preceded by hyperesthesia. A history or ' Injury of, or hemorrhage i Lumbar en ment of spina! (Figs. 24-7.) ymptoms continue to extend for some time and are fairly symmetrical. Fibrillation may bo present. The anesthesia usually present often found in syphilitic myelomalacia (1211) which is not as frequent in the lumbar enlargement as it is higher in the spinal cord. Symptoms at first mainly unilateral, becoming bilateral later. Cerebro-spinal fluid is usually under increased tension. usually sub-acute. Much pain in perineum and genitals. May be deformity in lumbar region of spine. Bed-sores are less common and symptoms less symmetrical than in lesions n the peronei muscles. When the lesion is low down the muscles on anterior aspect of thigh are not paralysed and knee-jerks are normal. The anesthesia always present in the extensively over legs, is often preceded by hyperesthesia. alcohol, etc.) or infection (diphtheria, etc.). The paralysis is usually in the 'form of a paraplegia and increases in intensity during the first few weeks, but in some cases reaches its height in a few days; s. The extensors are usually weaker than the flexors and the consequent foot-drop causes, when walking is possible, a high stepping gait. The paralysis commences at the distal extremity of the legs ids towards and often involves those of the body. The cranial nerves are rarely affected and then especially the long ones (phrenic, pneumogastric, facial, etc.). The most characteristic symptoms are of the muscles affected, at first the small muscles of the hands and soles of the feet. In addition, there are usually pain, paresthesiae, mixture of hyperesthesia and anesthesia, ataxia, retardation of con- sense. Edema and trophic disturbances are common. The atrophy and emaciation are often extreme. Not infrequently there is fever, and in alcoholic cases there are mental disturbances usually in the '0). No globulin or leucocytosis in cerebro-spinal fluid. Great variations in type occur. Some cases may be purely motor (diphtheria, etc.), others mainly sensory and others mainly ataxic. This last '' acute ataxia." The diphtheritic form may involve the muscles of Ihe extremities, but it always first appears in, and is usually limited to, the uvular and ciliary (accommodation) muscles. The arsen- sory disturbances and a peculiar bronzing or pigmentation of the skin. (Compare carefully with 482 and 495.) * when it can be felt and is usually the seat of various paresthesiae and of intense pain. In severe cases a complete, or partial, electrical reaction of degeneration and trophic disturbances are present. lie muscles involved and subsequent active or passive contractures of the antagonists may occur. For description of special forms of neuritis or injury, see Chart XII c. sensory symptoms coincide with the area of distribution of one or more nerves entering into the brachial plexus. Muscles of shoulder and upper arm, 5th and 6th cervical (Erb's paralysis); or muscles of earm with oculo-motor symptoms at times, 7ih and Sth cervical and 1st dorsal nerves (Klumpke's paralysis, 454-5)). nder tumors can be felt on one or on many nerves, which are usually the seat of paresthesiae and of more or less pain, often severe. tsure to cold, extension of inflammation, syphilis and tumor at base of br; y see Chart XII c. The paralysis is not accompanied by symptoms of centrai disease. All the muscles supplied by the nerve are usually paralysed. ead and accompanied by other symptoms of central disease. Only a portion of the muscles supplied by the nucleus may be paralysed. May be : 'in ted with atheromatous arteries or infectii he wrist and fingers causing wrist -drop. Supinato lead colic, arthralgia, etc. Lead can be detected i the i not involved (716). Rarely the muscles of dorsal flex rine after the administration of iodide of potassium. olved, causing foot-drop. Blue line on gums. History of exposure to motor and never sensory, except temporarily in the legs in very rare eases) and muscle tenderness. Lymphocytosis and globulin in cerebro-spinal fluid itest during the first week or two and may improve rapidly at first and late: parts may remain more or less undeveloped. The vast majority of cases o- symptoms. Deformities, contractures, subluxation of joints from relaxed lay rarely come on abruptly, but is usually preceded by fever and signs of meningeal irritation, exceptionally even conyi.il- the acute stage. In a small percentage of cases the disease rapidly terminates fatally. The onset is always acute, especially lore slowly, but recovery is usually only partial; some or many muscles remaining paralysed and atrophied throughout life. ,r in the first three years of life, but the disease may occur in adults and then may, in rare cases, closely resemble multiple contractured muscles and ligaments, and arrest of growth are common in young children. Trophic and vaso-motor symp- atrophy is usually extreme. The paralysed parts are usually cold and cyanotic, and the paralysed muscles exhibit the reaction of degeneration. The paralysis may have any distribution, but groups always affected. The more widespread the paralysis, the greater will probably be the improvement. The legs are more frequently affected than the arms and the extensors more than the flexors. l paralysed. Cranial nerves rarely affected (acute encephalitis). An infectious disease which may occur in epidemics, especially in warm weather. In young children the gums must be carefully examined be carefully excluded. Poliomyelitis lias been divided into a number of different forms which are partially described by their names (1) spinal form, (2) Landry's paralysis form, (3) brain-stem form, •ebellar form, (6) neuritic form, in which form slight muscle tenderness may occur, (7) meningitic form, (8) abortive form. Some cases of porencephaly (501.) may have the same etiology and pathogenesis. possibly be regarded as a chronic form of this disease with a very different etiology and pathology. Whether there is a true chronic anterior poliomyelitis is very doubtful. If it exists it is certainly very rare. ally commences before the age of twenty years and was formerly considered one of the muscular dystrophies as there is often a well marked heredity. Usually the paralysis and atrophy do not extend :he knees. In the later stages of some rare cases symptoms of atrophic paralysis have developed in the hands and arms. The muscles obtained by harpooning show simple degenerative atrophy, and no tertrophy. In rare cases there may be pain. Fibrillary contractions and reaction of degeneration are present. Club-foot is common. Leyden has described a form of hereditary muscular atrophy with- }hy, attacking the legs in the first ten years of life, in which the atrophy involves especially the muscles attached to the pelvis. ■ked in the upper ation of excised aration of fibers :ophy and hyper- "* iers and in differ- degenerated fiber, ial fat is present. rked in lower ex- Dn of excised mus- m of fibers with a and hypertrophy, quantities of in- The disease usually commences between the ages of 15 and 35 years. The atrophy begins in the orbicularis oris and extends to the other muscles of the face, to the shoulder girdle and finally to the legs. Patient cannot whistle, nor speak well, nor drink easily. Lips are thin and protrude: " tapir mouth." When smiling the mouth elongates only, its corners are not raised. Some muscles of shoulder are often apparently hypertrophied at first and later atrophied, or may be atrophied from the start. 'he disease usually especially the triceps between the ages of 12 and 15 years. The pectorals, trapezoid, deltoid, etc., are often hypert.ro phied at first and later atrophied. The biceps and atrophied from the start. Motion of shoulder and arm much impaired. The face muscles are not involved until late in the disease, if at all. The disease usually commences between the ages of 2 and 7 years, but sometimes much later. The calf muscles first show r apparent hypertrophy, followed by the extensor cruri infra-spinati, deltoid, etc. Other muscles are atrophied. AH muscles finally become atrophied. Even hypertrophied nrascles are weak, but not so weak as those which are atr phied. Marked lordosis and weakness of serratus magnus muscle. In rising from the ground patient has to push himsfelf up with his arms and crawl up upon himself. Waddlir gait. Deformities and contractures occur in the later stages and the lordosis is later replaced by a marked kyphos' ■ute or chronic myelitis or myelo S25, 1148a, 1309). imor in, or compressing lalacia of (791, L Tumor in, or compressing, (826, 1309). Lesions of the cauda-equina (1007, 130S). (Fij Multiple Neuritis. Polyneuritis. Pseudo-tabes. (662, 787, 823, 100S, 1147, 1307). (Figs. 33, 38). Neuritis or injury of a spinal nerve (sciatica, etc.), (822, 941, 1146-7, 1173, 1303-5-7). (Figs. 33, 3S). Neuritis or injury or tumor of brachial plexus \ lirb's or Klumpke's paralysis), (454-5). (Figs. 33, 38). Single i nultiple Neuromata, (93S). (Figs. 33, 38). 491 Injury or inflammation of one or more motor cranial nerves (facial paralysis, etc.), (1301-7). (Fig. 19.) Inflammation, softening or hemorrhage involving one or more motor cranial nuclei (motor oculi paraly- sis, etc.), (1304). (Figs. 18-21.) Lead Palsy, (584, 7S8, 1050). Acute Anterior Poliomyelitis. Myelitis of the An- terior Horns; Infantile Paralysis. Acute Atro- phic Paralysis. Heine-Medin's Disease, (789, 1148, 1233). (Figs. 24-6.) Spinal or Neuritic Muscular Atrophy. Peroneal type, and Charcot-Marie-Tooth's type, of muscular atrophy, (696). Facio-scapulo-humeral type, Landouzy-Dejerine type, dystrophy, (1152). Scapulo-humeral type, or Erb's juvenile form, of dystrophy (7S6, 1152). J Pseudo-hypertrophic Paralysis, (780, Hob) 498 Simple Idiopathic Muscular Dystrophy CHART Xb Spastic Paralysis Comprising Numbers 178 to 481 on left side of Chart and 501 to 527 on right margin DIAGNOSTIC SYMPTOMS AND TESTS 473 S P A S T I C P A R A L Y S I s 47S Hemiplegia or Diplegia or Monoplegia (254-5, 258) 479 Hemiplegia, or Monoplegia J.. I, "258) (See also Syringomyelia — 552, 837-9.) 480 Paraplegia C.V.7) (See also Syringomyelia- 552, 837-9.) 481 Paralysis of any ex- tent : local] mono plegia, hemiplegia, or paraplegia Congenital or ac- quired in infancy. There may be fever or apoplectic symp- toms at onset. Almost always in adults and after middle life. Sudden onset, or stroke (ictus), usu- ally with coma (205 and 1037), or with headache or vertigo and mental con- fusion. Not infre- quently the attack commences with a hemiplegia which may or may not be followed by coma. A motor paralysis of one (infantile hemiplegia) or both sides (Little's dis are common and may mask the exaggerated reflexes. In walking then and at times idiocy or insanity. Frequently there is a partial arrest ol of cerebral diplegia, bulbar symptoms (434) are present without fibrilli expressions, etc., can occur involuntarily, but no voluntary motions. T" Symptoms of irritation (convulsions, rigidity, etc.) are The disease i more pronounced than are symptoms of paralysis. ache and i Symptoms of paralysis are more pronounced than those of irritation (convulsions may occur, especially in cortical lesions and in hemorrhage into the ventricles, in which ease lumbar puncture may yield a bloody fluid). The paralysis is in part temporary and in part per- manent in varying degree. Slow improvement with almost perfect recovery in rare cases. More or less permanent mental impairment, often very slight. Usually patients are more emotional than previously. Exaggerated reflexes and ankle-clonus are present after coma has cleared up. Babinski is present from the start. Puffing, stertorous respiration is common. Cheyne-Stokes respiration (435) and tracheal rales are very unfavorable symptoms. Gradual onset with- out coma, except as a terminal symp- tom. There is paralysis always of motion and commonly of sensation, usually in the form of para- plegia, more rarely in the form of a spinal hemiplegia (442), which later may become a para- plegia. The re- flexes are exagger- ated. Ankle-clonus and Babinski are present . Spasms and contractures and bed sores are often present. The organic reflexes are disordered. The motor paralysis is permanent or lasts a very long time. Sensory paralysis may be slight and transitory and may be altogether ab- sent. The anesthe- sia is often limited above by a narrow zone of hyperesl he- sia. Paralysis limited by some prominent anatomical land- mark. Sensory symptoms are always pres- ent. Organic re- flexes are normal or only slightly disordered. Brain symptoms. Steadily in- creasing psychic disorder, and local motor and sensory disturb- ances over the same area. A sudden att the upper, balls, awaj arterial (lis face, then hemiplegic Similar to th arterial tei mon than Similar I" t li syphilis. k basilar art hemorrhag Headache, v mon. Clio more rarel mental du usually pr< increased t cempressio Spinal symptoms. Paralysis of motion and sensation on oppo- Characterise site sides of body. Symptoms spinal epil The paralysis is only slight and follows or accomp a paralysis (chorea mollis). Intention tremor, nystagmus, scanning speech, ata r There may be a history of injury and a fracture ol No history of injury. Little or no pain. Sensor syphilitic myelomalacia (1211). May be history of remote injury. Much pain radia spinal fluid. There may be a history of injury and a fracture o No history of injury. Little or no pain. Sensory f tic myelomalacia (1211). May be a history of remote injury. Much girdle pa Evidence of Pott's disease or tumor compressing t pain. In cases of compression due to Pott's die uniler increased tension and may contain globul History of working under increased atmospheric pi Old age, atheromatous arteries, arterial tension usu Tumor can be seen or felt on back replacing the is involved, or not. Club-foot is common, Signs of irritation predominate oyer those of par unless the cord is also involved. Usually a hist Paralysis purely motor, a paresis rat passive motion, especially when r: N " 'lav. a. a mu i liple Xerosis (659). Krb's s; This disease may be simulated, in There is a combination of motor pai IX|:| ' In s e cases, especially inward Tl e motor paralysis is usually accompanied by a great variety of sens y the physician (imaginary or delusional paralysis). A paralysed limb retention of urine is common. Hysterical symptoms (42.5). Impossil this is sometimes of value in diagnosis. Choreic symptoms. Cranial and spinal nerves are in- volved. Arms and legs are paralysed. Pri- apism is com- mon, also respira- tory difficulty and early death. Radiating pains are common. Legs only are par- alysed. Girdle sensation and pains radiating into the extrem- ities are common. Legs mainly in- volved. Arms involved later and slightly, if at all. These dis- eases may occur in severe ane- mia. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS the body, or of one extremity, without anesthesia and with very little muscular atrophy (from disuse). A squint is common. The legs are often mainly or alone paralysed. Rigidity and contractures l adductor spasm, "scissors gait" (795-9). Extensor spasm is also frequent. Epileptiform convulsions are common, both at onset and during the course of the disease. There is much mental weakness of the paralysed part. Athetosis and post-hemiplegic chorea and other motor disorders are common. Speech is commonly affected (dysarthria). The organic reflexes are not disordered. In some cases atrophy, and automatic and mimetic actions are preserved. In such cases the eyeballs will follow a light or other object, but cannot be turned by any effort of the will, and laughing, weeping, emotional is often smaller on the side of the affected cerebral hemisphere. [he result of injury. When not so, prodromal symptoms (432) are usually present. Convulsions are common, both at the onset and during the course of the disease, which is often intermittent. Head- npairment are frequent. The onset of paralysis is apoplectiform. It is usually motor only, is rather mild in degree and is usually transient. Organic reflexes normal. Cerebrospinal fluid often bloody. laralysis usually of one-half of the body, usually of motion only, rarely of sensation only, sometimes of both. The lower branch of the facial nerve is much more completely and permanently paralysed than lay lie normal. Onset is usually accompanied by profound coma (205) of several hours or days duration, but not always. In the coma there is oftenjurning of the head, and conjugate deviation of eye e hemiplegic side. Pulse is slow. Slight variations of temperature about the normal point; when the variation 1 nephritis and usually high arterial tension. The disease usually leg and lastly in arm. Contractures, causing flexion of joints of a: is1 urbances occur in rare cases. extreme the prognosis is bad. Prodromata are rather rare (432). There is often ._ advanced life. If death does not occur in the coma, there is usually more or less improvement in the paralysis; first in the and extension of joints of leg, are frequent and of bad prognosis as regards recovery from the paralysis. Athetosis and other post- but onset is more often instantaneous and coma is usually less profound and long and frequently is entirely absent. There are no prodromata. There is cardiac disease or other source for an embolus. The jsually low. The disease usually occurs in youth or middle age. In general the symptoms are less severe and. less permanenMhan in hemorrhage. Convulsions, aphasia and monople; - - •rhage, because the lesion is more apt to be cortical. Multiple (more than two) recurrences are more common i i embolism than in hemorrhag but onset may be more gradual, although still :rial tension is usually high. Arterial disease uore frequently affected. Simultaneous paralysis of olism. smiting and convulsions, general or local, are com- or optic neuritis is usually present in tumor, much cess. Steadily increasing inertia and more or less Focal symptoms, both spasmodic and paralytic, are specially Jacksonian epilepsy (431,605). Markedly f cerebro-spinal fluid and slow pulse in stage of ially in tumor. sudden and even at times instantaneous. Prodromata (432) are common. Coma is more frequently absent or less profound. There is often a history of is common. The disease usually occurs in advanced life. Bulbar symptoms are more common than in hemorrhage or embolism, because branches of the is of many cortical functions is more common than in hemorrhage. Multiple (more than two) recurrences are more common in thrombosis than in either No fever. No infection, or origin for abscess. Chronic course. Steady progression of all symptoms. Often history of previous remote injury. No in- crease of cellular elements found in the blood or in cerebro-spinal fluid obtained by lumbar puncture. Frequently symptoms irritative, rather tha paralytic. Percussion of skull over region of tumor often shows tenderness. Headache is very rarely absent and is usually intense. It may t local, but is of little or no value in localizing thetumor. The paralysis commences as a monoplegia and very slowly (weeks or months)extends, be or months)exten< Often fever. A source of infection, especially suppurative diseases of the ear. Rapid course, except that a latent period in the progress is common, fol- lowed by a rapid termination. Delirium is common. Often a history of a recent injury. Leukocytosis maybefound in thebloodand in thecerehro- spinal fluid obtained by puncture (74). Frequently symptoms rather paralytic than irritative. The paralysis commences as a monoplegia and rather slowly (days) extends. 3ms are motor paralysis, loss of muscle sense and ataxia on one side of the body; with analgesia, thermic and sometimes tactile anesthesia of other side (442). Stationary, or steadily progressive chronic course. ii" bilateral Reflexes vary with the position of the tumor. They may be absent, but are usually increased on the side of the motor paralysis, and are so greatly increased frequently as to cause 3). DIAGNOSIS Cerebral Palsy of Childhood. Porencephaly. Acute encephalitis. Infantile hemiplegia or diplegia (Little's disease). (577, (130, 70S, 104S, 10S6.) (Figs. 15-16.) Meningeal Apoplexy. Hemorrhage in cerebral meninges. Pachymeningitis Interna Hemor- rhagica. Aneurism, etc. (5S8, 1060.) (Figs. 15-16.) Cerebral Hemorrhage. 1 504 Cerebral Apoplexy. (432. 5SS, 832, 856-7, 1043, 1060-3.) (Figs. 15-7.) Cerebral Thrombosis softening. Cerebral Tumor, including Cyst. (536-42, 578, 587, 833. 849, S55-61, 892, 908, 960, 1047.) (Figs. 15-17.) Cerebral Abscess or localized Meningitis. (578, 587, 907, 960, 965, 1045-6.) (Figs. 15-17.) Spinal Tumor or unilateral spinal lesion, Rrown- Sequard's paralvsis. (442, 4Sli, 515, 519, 542, 551, 826, 830-40, 975. 9.81, 1003.) (Figs. 24-6.) 506 507 attack of hemi-ehorea, involving the same side of the body. Sympto nay be bilateral, but are then difficult of recognition. In many cases the hypotonia (almost invariably present) may simulate Choreic Paralysis. (622.) zularly distributed motor and sensory paralysis. -ae with deformity. The knee-jerks may be abolished in the early stages, later increased. There may be blood in the cerebro-spinal fluid. Much pain and rigidity and spasm of back. Symptoms at first more unilateral. Local pains. May be i ased tension of cerebri Very acute onset j Acute onset ) Chronic onset Very chronic onset -ae with deformity. The knee-jerks may be abolished in the early stages, later increased. There may be blood in the cerebro-spinal fluid. Very acute onset is and disroders of the organic reflexes are almost always present. A history or other evidence of syphilis (1205) is often present in cases of syphili- ) Acute onset ) Chronic onset dity and spasm in back. Symptoms at first unilateral. Local pain. The tension of the cerebro-spinal fluid may be increased. Very chronic onset Cervical region of spinal cord above cervical en- largement. (Figs. 24-6.) Dorsal region of spinal cord. (Figs. 24-6.) lg.. Much girdle pain and radiating may occur. Cerebro-spinal fluid is Compre . Rigidity and spasms in muscles of legs and back are frequent. Usually intense pain when spine is bent or moved and especially on getting out of bed in the mo: jre may be no sensory symptoms. Reflexes may be so exaggerated as to constitute spinal epilepsy (60-1, 443), but vary according to seat of lesion. Contractu ymphocytosis. Headache, vertigo and vomiting in early stage of disease. a, loss of memory. Emotional and exhibits mental impairment. Paralysis is not severe, resembles that of paralysis agitans without tremor, and reflexes of all kinds are not much altered. if the vertebrae, or the cleft can be felt in spine without any visible tumor (occulta). There may or may not be paralysis. Reflexes may be present or exaggerated according as the lumbar enlargement earlv Paralysis is of sudden onset, slight in degree and disappears soon, Much rigidity, girdle and radiating pains and spasm in back muscles. There is usually spasmodic retention of the urine ir injury. Reflexes exaggerated. Lumbar puncture may yield a bloody fluid. Symptoms vary with position of hemorrhage, a a complete paralysis, very slowly progressive and often stationary during long periods. Spasm, rigidity of leg muscles and later contractures. Greatly exaggerated reflexes. Legs offer great resistance to Ankle-clonus, Babinski and spinal epilepsy (443). Organic reflexes little if at all disordered. Arms usually not affected, but may be slightly so after years. This clinical picture is at limes the early stage oi spinal paralysis, although in it the reflexes are not always greatly exaggerated and the posterior columns are at times involved, cannot be distinctly separated from this disease, except perhaps by its etiology. nild form, with exaggerated knee jerks, but without ankle clonus or Babinski, and with marked stiffness of legs, as the result of reflex action from irritation, especially from the genitals. ind marked ataxia which develop very gradually and slowly. Some moderate pain and Tarely there may be anesthesia and analgesia. The tendon reflexes are exaggerated. Ankle-clonus and Babinski. d of the disease the reflexes may be abolished, but the Babinski persists. It is a disease of adult life, but is analogous to Friedreich's ataxia (652). :oms. The disease is usually of sudden onset and often follows some powerful emotion. It is usually permanent until cured by another strong emotion, which may be ofte: rs great resistance to passive motion, even to slow motion. Contractures are common. Knee-jerks are usually increased, but no true ankle-clonus or Babinski. Organic rette> ^plaining all of the symptoms by any one organic lesion. The paralysis is not limited to one muscle, or to the distribution of nerve. Associate. 1 movements do not occur i artificially produced by is rarely disturbed, but hysterical paralysis, and Disseminated Sclerosis. (580, 659, 668, 688, 756, 765, 799, 913, 1051.) Injury or hemorrhage in, Acute myelitis or myelomalacia of, (795, S2S.) Chronic myelitis or myelomalacia of, Tumor in, Injury or hemorrhage in, Acute myelitis or myelomalacia of, (795, S29.) Chronic myelitis or myelomalacia of, Tumor in, l Myelitis. (795.) (Fig. 27.) Caisson disease or Diver's paralysis. Senile Paraplegia. (791a) Spina-bifida. Hemorrhage in spinal membranes. Hemator- rhachis. (973.) Spastic Paraplegia or lateral sclerosis (usually symptomatic and part of a more extensive lesion, spinal or cerebral.) (797.) (Figs. 24-7.) Ataxic Paraplegia or postero-lateral sclerosis. (660, 796.) (Figs. 24-6.) Hysterical Paralysis. (747-8, 759, 793, 878, 1074.) 512 513 514 515 CHART Xc Combined and Intermittent Paralysis Comprising Numbers 171 and 174 on left side of Chart and ">:r> to 656 on right margin 131 DIAGNOSTIC SYMPTOMS AND TESTS 474 C O M B I N E D P A R A L Y I S Cranial and spinal nerves involved. (Figs. 1S-23, 33, 38.) Sensory symptoms present usually. 'Bilateral symp- toms. Crossed paralysis (256) and bulbar symptoms (434). Spinal nerves alone involved. (Figs. 24-7, 33, 38.) No sensoiy symptoms. No sensory symptoms. If 1 1 io patient does not promptly die, one or mot gia (525). There arc usually dysarthria, dysp] toms at first may lie more unilateral. Paralysis of one or more eye muscles of one side Paralysis of facial (both upper and lower branch- Paralysis of hypoglossus of one side and of arm The onset of paralysis is sudden. If the patient sive. They are usually unilateral, but may Ik paralysed, while there is a spastic paralysis in .May he duo to acute inflammation, hemorrhai myelitis. Often due to syphilitic endarteritis i Chronic — The chronic forms of these diseases, with the spinal form (547), constitute the progressive muscular atrophies and resemble the muscular dystrophies in that the paralysis and atrophy advance together slowly, and it is difficult to say which is primary. They also constitute a group of chronic degenerative atrophies. n Symmetrical para!- The muscles affected show progressive weakness, ysis commencing in or, more rarely, in the muscles of the shoulder the small muscles of thumb cannot be brought across hand to tone hands or in shoul- but not always. There are secondary contract dex girdle muscles. of muscles is increased. Often associated umns are involved or not. It is difficult to di ' The paralysis in- volves I lie eye mus- cles. The paralysis in- volves the lips, tongue, pharynx I and larynx. P Th< Marked sensory symptoms are pres- ent, such as pain, paresthesiae, anes- thesia, etc., with the motor paraly- Dissociation of sen- sation (3C5) is pres- ent. r ery acute onset . Sympti may yield a bloody fiuii Acute, sub-acute or chroni litic m\ elomalacia i,l-l 1 Chronic course, intense pa common. Cerebro-spina Very chronic onset and a All the muscles of the body and head. Muscles of one or both legs, rarely of Commencing in legs extending to arms. Associated with a cervical rib Both arms and legs are paralysed. There are trophic disturbances in the arms and not in the legs. Pupils are often unequal. Reflexes are abolished in the arms and increased in the legs. Bab- inski and ankle-clonus are present. The bladder is usually more or less dis- tended; its detrusor being paralysed. Contractures may be present in tin' legs. Dissociation of sensation is the most characteristic symptom and is co Trophic lesions are usually prominent. Pemphigus, ulceration and trophic symptoms predominate over motor symptoms in the arms; present the symptoms may be both in arms and legs, and the mote aggerated in central gliosis in the cervical or dorsal regions. The cer fairly rapid course, and may exhibit a unilateral, spastic, muscular ] The characteristic sign of the disease is the rapid tiring of the muscles when in activity. P»1 (401). There is no muscular atrophy and no reaction of degeneration. In the domain ol i usually held retracted on account of the ptosis. The symptoms are slight in the morning Intermittent attacks of painful muscle cramp, and weakness of leg or legs, caused by walkinf Rarely the disease occurs in one or both arms. No sensory disturbances except painful crai Recurrent attacks of paralysis of the muscles of the legs usually first and then of arms, las nerves are not attacked. There is usually well marked heredity, or the disease occurs in 1 but in some groups of family periodic paralysis these negative symptoms are not present. A cervical rib can be felt and can be seen with the X-ray. In some cases of cervical rib, att; skin which comes on after the arm has been used a short time, and, if use of the arm is co be Caused by a cervical rib, and then is often relief by elevation of the arm and is made V DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS No optic neuritis. A variety of apoplexy (504). No increased tension of cerebro-spinal fluid. al nerves are paralysed. There is more or less marked spastic paraple- f Acute onset. Regressive c taxia, anesthesia and often vertigo. (Bulbar symptoms— 434.) Symp- \ [ Chronic onset. Progressive course. Optic neuritis. May be increased tension of cerebro-spinal fluid. arm and leg of opposite side. igeminal nerve on one side and of arm and leg of opposite side. ; of opposite side. {Acute onset and regressive course. No optic neuritis. No increased tension of cerebro-spinal fluid. Chronic onset and progressive course and optic neuritis. May be increased tension of cerebro-spinal fluid. f Acute onset and regressive course. No optic neuritis. No increased tension of cerebro-spinal fluid. [ Chronic onset and progressive course and optic neuritis. May be increased tension of cerebro-spinal fluid. {Acute onset and regressive course. No optic neuritis. No increased tension of cerebro-spinal fluid. Chronic onset and progressive course and optic neuritis. May be increased tension of cerebro-spinal fluid. ; so that ptos: There is more or less extensive paralysis of the motor nerves of eyeball (3rd, 4th and t vision, nystagmus, etc., may result. 3t die promptly, later the symptoms are regressive rather than progres- :al. A number of cranial nerves, either motor or sensory, or both, are ess pronounced in the arms and legs. Vertigo is a common symptom. ^ ■mhosis, embolism, or compression. May occur in acute anterior polio- I There is paralysis of the lips, tongue, pharynx and larynx (7th, 9th, 10th, 11th and 12th nerves), with consequent dysar- litic neuritis. L thria and dysphagia and usually ataxia and respiratory disturbances. onset, of weakness of ocular muscles. It may be steadily progressive or, having progressed to a certain point, it may remain stationary. Muscles may be attacked in any order, ptosis, squint, im- yeballs, immobile pupils. The disease may attack only the external muscles of the eyeball (ophthalmoplegia externa), or only the internal muscles (ophthalmoplegia interna), or both, (ophthalmo- impleta). Disease may be complicated by bulbar paralysis (54G) and is usually associated with amyotrophic lateral sclerosis. s bent forward. There are bulbar symptoms (434). There are drooling of saliva, dysarthria, dysphagia, and aphonia. Paralysis, tremor, atrophy, fibrillary contraction of muscle of tongue, lips, harynx, larynx, etc. Both facial nerves are involved in some cases. The paralysis very slowly progresses. There are symptoms of a mild spastic paraplegia in legs with ankle-clonus and Babinski. e of advanced life. Often associated with amyotrophic lateral sclerosis and at times with progressive ophthalmoplegia (545). In addition to the pseudo-bulbar paralysis of myasthenia gravis (553) another form due to lesions in both cerebral hemispheres in which there is no muscle atrophy, or fibrillation, and no change in the electrical reaction, but all the other symptoms of bulbar paralysis less marked. There is more mental impairment and greater emotional excitability than in true bulbar paralysis. y, fibrillary contractions and all degrees of alteration in electrical excitability from simple diminution to complete reaction of degeneration. The process commences in the small muscles of the hands, scapulo-humeral type), is usually fairly symmetrical and extends to the other groups of muscles in arms, body and even legs. The muscular weakness follows and is dependent upon the atrophy. The ittle finger The fingers cannot be spread apart, nor can their last two phalanges be extended on the first. The legs show a mild degree of spastic paraplegia, with ankle-clonus and often Babinski, specially the" claw hand." The head is usually bent forward and there is much deformity about shoulder and other parts. A disease of adult life, and of very chronic course. Mechanical irritability agressive bulbar paralysis (54G). Some authors divide this symptom complex into two groups according as to whether the atrophy or the paralysis is primary, and as to whether the lateral col- i such distinction clinically, The one form may be an earlier stage of the other. most extensive in first few days and may slowly improve later. May be deformity in cervical region of spine. Knee-jerks may be absent in early sto Lumbar punetu Symptoms continue to extend for t Cervical ment of spinal cord. (Figs. 24-6.) : time and are fairly symmetrical. Organic reflexes disordered. A history or other evidence of syphilis (1205) is often foundin syphi- and neck precede the paralysis and contractures and muscular atrophy in hands, " claw hand." Cutaneous eruptions (herpes, pemphigus, etc.) are not un- may be under increased tension and show lymphocytosis. Most of these cases are the result of chronic syphilitic meningitis. ssive course. Symptoms at first mainly unilateral, becoming bilateral later. Cerebro-spinal fluid may show increased tension. with pain and paresthesiae and more or less motor paralysis and atrophy. The muscular atrophy has often the location and characteristics of that of progressive spinal muscular atrophy (547). ion of the hands and trophic lesions of bones, muscles, and other tissues occur in the type called Morvan's disease. In the most common form the cervical region is alone affected and sensory and he legs show a mild spastic paraplegia (525), and scoliosis or kyphosis occur in more than half the cases. Paradoxical (379) and spontaneous sensations have been noted. When a diffuse glioma is itoms are about as prominent as the sensory and may be unilateral in the early stages.. All forms of reflex action are abolished when the cervical and lumbar enlargements are involved, but are ex- >rm of the disease runs a chronic course, extending at times over decades, but slowly progresses and the anesthesia at first slight steadily becomes more marked. The diffuse form often runs a s, at least in the early stages. i walk well at the start, but after a few (or a few hundred) steps is tired out. The same is true of all other voluntary acts. Examination of the muscles with electricity gives the myasthenic reaction nerves (in which the case usually commences) there may be ptosis, diplopia, ophthalmoplegia, diplegia facialis, dysarthria, dysmasesia, etc., and all the spinal nerves may be affected. The head is jw worse during the day. No sensory disturbances except painful cramps. Organic reflexes normal. ng the attack the feet are cold, and there is diminished or absent pulsation in arteries of feet, associated with marked arterio-sclerosis of arteries of leg as shown by palpation and by the X-ray. rganic reflexes normal. Angio-spastic hemiplegia in which temporary attacks of hemiplegia, sometimes associated with aphasia, occur, is probably a variety of this disease. few hours or days. The attacks usually occur in the morning or after rest. During the attack the left cardiac ventricle may become temporarily dilated and a murmur may be heard. The cranial groups. During a severe attack there is often a diminution or absence of' the reflexes and of the faradie and galvanic excitability of the nerves, and of the mechanical excitability of the muscles, of these cases are apparently due to malaria and can be cured by the administration of quinine. :cur, but only after use of the arm. These attacks are usually unilateral, even though the extra rib is on both sides. The attack consists of numbness, tingling, feeling of congestion, redness of the d,the arm shows a decided paresis, which passes off if the arm is kept at rest. An ununited fracture of the clavicle will rarely cause similar symptoms. Pain, in the form of a brachial neuralgia, may >y motion. In rare cases this paralysis, at first intermittent, may become permanent and may be associated with atrophy of the muscles of the hand and even of the forearm. Hemorrhage, softening or acute inflammation in brain-stem 535 (543-4, 656). Tumor in, or compressing the brain-stem (656). 536 Hemorrhage or softening in crus cerebri (543). 537 Tumor in, or compressing 'crus cerebri (656). 538 Hemorrhage or softening in pons (543). 539 Tumor in, or compressing pons (656). 540 Hemorrhage or softening in medulla (544). 541 Tumor in, or compressing medulla (656). 542 Acute or Apoplectiform Polioencephalitis Superior (495, 535, 543 1064). Acute or Apoplectiform Polioencephalitis Inferior. Acute Bui- 544 bar paralysis (495, 535, 1064). Progressive Ophthalmoplegia. Polioencephalitis Superior 545 Chronica (often symptomatic of a steadily progressive, more widespread disease, such as tabes, tumor, etc.). Progressive Bulbar Paralysis. Polioencephalitis Inferior 546 Chronica. Labio-glosso-pharyngeal Paralysis, (G94. 761, 1150). Amyotrophic Lateral Sclerosis. Progressive Spinal Muscular 547 Atrophy. Aran-Duchenne type of muscular atrophy. Chronic Atrophic Paralysis, (095, 797, 1149). ' Injury of, or hemorrhage in, 548 Acute or chronic myelitis or myelomalacia of, (795, 835, 1310). 549 Pachymeningitis hypertrophica cervicalis. 550 .Tumor in, or compressing, (836) 551 Syringomyelia. Central gliosis. Morvan's Disease, (693, 552 837-9, 1009, 1150a, 1170, 11S7, 1357, 1359). Myasthenia gravis. Pseudo-bulbar Paralysis. Intermittent Limping or Claudication. Dysbasia Angio- 554 sclerotica, (1199). Family Periodic Paralysis. Pressure of cervical rib upon sub-clavian artery. CHART XI Convulsion or Spasm DIAGNOSTIC ANALYSIS OF SYMPTOMS Tests SYMPTOM Analyzed Character Extent .571 CLONIC mainly (246) ' GENERAL CONVULSION LOCAL i CLONIC .SPASM 570 CONVULSION OB SI 'ASM (242) 572 TONIC mainly (245) * 'general TONIC SPASM LOCAL TONIC .SPASM J 573 CHOREIFORM (272) - 574 Diseases in wbio arc sit forth in VHIITOID I (271) Diseases in which convulsions occur set forth in Chart XI a. Diseases in which local clonic and all forms of tonic spasm occur are set forth in Chart XI b. 188 CHART XI a General Clonic Convulsion ( !omprising Numbers 571 on left side of Chart and 575 to 596 on right margin L35 DIAGNOSTIC SYMPTOMS AND TES1 S (-Repeated attacks. The convulsion commences in all the muscles at about the same time (epileptiform convulsion). 671 G E N E R A L C L O N I C C o N V u L s I o N Apyrexia. Loss of conscious- ness, (coma or semi-coma) (205). Frequently biting of the tongue or other injury. Short duration. No other symptom of disease except the convulsion. Symptoms of seri- ous brain disease. One attack or one ^series of attacks. Congenital or in infancy. Often fever at onset of first convulsion. In youth or more .often in adults. Symptoms of cerebro-spinal disease. f Kidney disease. Symptoms of dis- ^ S l°L°} ] i e lZ TgaDS j Cardiac disease. (.Blood disease. than the brain followe I i. hi of tile, au tendon spots a pressur spasm around attack Such p observ; A con villi and nc periphe The disea rarely are ran Between are foil of the sympti disease psychic vance 1 Intent ior There an and th Slow pul: Rapid fc culatio o . _ , • ( Blue line on gums, lead in urint Symptoms of poi- ) b ' sonin S- I Alcoholic odor of breath and g( Apparent, but no true, coma (shown In- susceptibility to suggestion). No biting of tongue or other injury. Long dura- tion. Symptoms of hys- The attai teria 1 125). Such very ii attacks have been usually called hystero-epi- orbital lepsy. tomfl | The convulsion always commences in one group of muscles and later extends over the whole or part of one side of the body and often over both sides. Jacksonian epilepsy (431). ■s Hyperpyrexia. Epileptiform convulsion. If the convulsion remains unilateral, con- sciousness may or may not be lost, usually not, but it is always lost when the convulsion becomes bilateral. Coma during and after the convulsion. There a present of scriou: ease, always. Occurs s Pyrexia. See also 577. Lumbar puncture gives a clear bloody or purulent, fluid, unde pressure containing globulin polymorphonuclear leucocyte.' Lumbar punct ure gives a clear f increased tension and contaii ulin and many mononucleai cytes, and if the disease polymorphonuclear leucocytes Lumbar puncture gives a clear f increased tension, but no ii cellular elements. . . . ( May occur in children at the onset of any infectious disease, especially in < •convulsion. | j s tng resu i t of some unusU al metabolic changes within the body, and espe 'Epileptiform con- convulsion. Comat during and usually after the convulsion. Headache, backache and radiating pains, delirium, vertigo and vomiting, espe- cially on change of posture, hyperalge- sia (spinal and elsewhere), photophobia, etc., are early symptoms. Retraction of head, opisthotonus, etc. (265). Pa- ralysis of cranial nerves (squint, etc.), cutaneous eruptions (herpes), t&ches cer<5brales and Kernig's symptom (319). Tonic spasm and paralysis are more common in basic inflammations, and clonic spasm in cortical inflammations. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS : with arrest of respiration. The face, at first pale, soon .becomes pushed and^cyanoth .*,. The pupil is dilated and inactive. This tonic state is quickly the major attack (le grand mal), is at first onic with arrest of respiration The face at first pale ; soon ™ ™- , tongue, which isoften bitten during the attack. There is often lateral devia- , minute) by clonic spasm of longer duration (i to 5 minutes) with noisy respiration and irotl on 1 ps o Iten mo J twi , chir | of cer t ain muS cles, " motor aura," or by a sensory hallucination (tac- and eyeballs and nystagmus At t.mes urine and feces are passed during he attack. The attack s ° f ' en preceuea J » temperature of the body is raised and albuminuria is frequent. The risual, olfactory, etc.) called the "sensory aura" (430) and is often usheied '" ^ a "^ ' *' ie «P''f P'l ,^/^^" weakness (stage of exhaustion) often follow the attack. After a violent atlack purpuric are occasionally absent during and immediately after the attack. A deep sleep an 1 some ™* cular ^ at varving in.ervals, but attacks can neither be brought on nor arrested by nf'LTthe ^^^J^-^^-^^^-^^^-^^^ lV"o C i,;Jl enllensv)? The attacks vary Jreatly in character. A1 times there is merely rigidity without clonic media). At times there '- ~ ace Complete amnesia in regard to it always follow an attack. There are recurrences at varying intervals oui. jiuu c, » ihMta%"^y a^ghtor while asleep by day (nocturnal epilepsy; .The attacks ; vary -greasy ,r ^ a ™te, A , » media). At times tliere is merely loss of consciousness without action or with some automatic art: he minor at ack e pe Mmal^ At a.mesjhe patient is ^cS^re^^ unconscious and runs forwards ana turns an act of violence (epileptic mania). At times an more or less mental impairment (epileptic dementia). The diagnosis of malingering can only be made by long m in syphilitic and rachitic children, but occurring also in adults especially in P« g --y altogether similar (epileptiform) to the above but occ urring only °nce or ck, especially common ed. Associated often w,,.. .... ition and at the onset of an acute infection. No sharp line can be drawn between these convulsic . h . mit)leeia or diplegia, with cons derable mental impairment. There is usually dysarthria, genital or begins in early infancy Umlatera or b.'atera convu sions occur ^^J^^fZre orTs complete a?re!t of development, physical and mental. The shape and size of the skull often post-hemiplegic motor disturbances: athetosis, rigidity anrl contractures, i requemiy lueie is, «■•« " r xl. Cases of epileptic idiocy may belong to this class, even though they present no paralysis. Headache, vertigo and vomiting. Choked disc or optic neuritis. More or less motor ™d sensory paralys. loss of memory. Localizing symptoms are sometimes present. Convulsions are often local. ,. ■„ .i j i • r, „„ll„ „f wiiaiinnl and ™mntoms of insanity. Poor judgment. Good natured but irascible. Childish. Characteristic blurred Loss of will power, restlessness, delusions ^^Jf^^^PX^^'^^ a nd apraxia). Unequal and irregular pupils, Argyll-Robertson's pupil, optic neu- speech. Tremor of lower facial muscles, lips, tongue and hands, and aokoaraness (aiaxu j™^ ^ ^ J , .,._ i. t . ,,._;,,..,; u -. J,.,-!,,-,,,,, ve:,ctii,n i41fl-20i. ritis or atrophy. L History of syphilis. Lumbar puncture shows lymphocyto vulsive attacks, which ■ a temporary weakness s involved, there are steadily progressing brain rally motor, sensory and Dms, and a steady ad- ;oma or dementia. more or less complete arrest of development, physit Mental inertia (apathy) and increasing mental weakness and cerebrospinal fluid, globulin and a positive Wassermann reaction (419-20). , scanning speech, nystagmus, unsteady gait, motor and sensory paralyses, many symptoms of Ideal lesion, etc. g intermission in heart beats associated with coma and convulsions, which pass off after the heart begins beating again. Arteries atheromatous. Advanced life ;e of small volume. Insufficient amount of blood or of red cells and hemoglobin. Pallor, dyspnoea esent. Often the result of one large or of repeated hemorrhages. aking K.I. Wrist-drop. History of lead colic and of exposure to lead. emor and nervousness. Muscular tenderness. History of alcoholic abuse. DIAGNOSIS Idiopathic Epilepsy (including the major attack, the minor attack, epilepsia media, nocturnal epilepsy, epileptic automatism, epileptic mania, psychic equivalent, epileptic dementia), (110, 126, 430, 846, 1027, 1058, 1071, 10S3, 1102). Eclampsia, (1059). Cerebral Palsy of Childhood. Porencephaly. 577 (501, 630, 798, 104S, 10S6). Cerebral Tumor (including abscess and cyst) not in 578 or near motor area of cortex (507-8, 587). Paresis. General Paresis. Paralytic Dementia, 579 (134, 177, 416, 419-20, 675, 763, 895, 1049, 1104, 1216, 1230). Disseminated Sclerosis, 580 (511, 659, 668, 68S, 756, 765, 799, 913, 1051). usually high, the heart hypertrophied, Uremic convulsion, (576, S50, 956). usually, exertion and strabismus are common. Often severe digestive disorders with congested portal i ■ays in the presence of an audience. There is always a warning in the form of globus hystericr, and violent and many of the movements seem purposeful and to be theatrical posing crucin long time, especially if the audience be excited. Eyes are usually closed and the eyeballs tun etc., especially if the audience be sent from the room. Moderate pressure upon these parts Vbundant limpid urine after the attack, but urine and feces The convulsion often commences with a motor (twitching), rarely with a sensory (tingling), aura. It spreads first through the whole of the part first attacked and then in a definite order from face to arm, or from arm to leg or face, or from leg to arm according to the anatomical arrangement of the cortical motor centers; hence never from leg to face without the arm being involved. The convulsion is followed bya hemiplegia, sometimes transient, sometimes permanent and progressive. There may be muscular rigidity in the intervals between the convulsive attacks. mlnitation etc Patient may fall or glide to the ground but does not hurt, herself. The convulsion is 'on et! and assumed attitudes, (attitudes passioneltes). Patients often "rave" during the attack, which upwards if eyelids are forced open. Attack can usually be arrested by pressure on ovarian region, supra- lay cause an attack. Great variety of sensory symptoms, never passed Involuntarily during an attack. The reflexes Occurs in youth or middle age and often after traumatism of old date. Headache, ing. Usually choked disc or optic neuritis. Symptoms sum, lily progressive. out choked disc may occur in localized meningitis or other irritative lesions lr Occurs in old age and often after recent injury. Alcoholism, atheromatous arteries and insanity are common Sudden apoplectic attack with improvement later. No choked disc. Symptoms pro- gress paroxysmally, and after each paroxysm there is marked improvement Anesthesia is usually present. Hysterical symp- ! not abolished during the attack as may occur in epilepsy (1058). r ertigo and vomit- lilar attacks with- : lesions in the cerebral cortex. Stokes-Adams' Disease, (430, 1057). Anemic convulsion. Lead convulsion (494, 576, 1050). Alcoholic convulsion, (576, 658, 663, 764). Hysterical convulsion, (1074). Cerebral Tumor (including abscess and cyst) in or near motor area of cortex. Jacksonian Epilepsy. (431, 507-8, 605.) (Figs. 15-16.) Hemorrhage in or near motor area of cortex (pachy- meningitis, etc.). Jacksonian Epilepsy. (502, 1060.) (Figs. 15-16.) after some prodromal symptoms such as headache, poor eyesight, etc., y, (By lumbar punct ure, Weichselbaum's diplococcus almost always, o :d I (Weichselbaum's diplococcus). Strong retraction of head. n persons who have been exposed to high temperatures. Delirium is usually present, rarely the pneumococcus or other germs, may be found in the cerebrospinal fluid. There Sunstroke i epidemic of the dis Heatstroke, (966, 1068). 1214, Cerebrospinal Meningitis, 1226). By lumbar puncture, pyogenic bacteria may be found in the cerebrospinal fluid. Suppuration or an infected wound may be present, especially in the head. Suppurati. [ or in nasal sinuses, carbuncle or erysipelas of head or neck. Retraction of head may be less marked. liddle ear or mastoid, Purulent Meningitis, (1227). ob- By lumbar puncture tubercle bacilli may be found in the cerebrospinal fluid. A tuberculous process may be found in some other part of the body. Gr! ho- Choked disc and choroid tubercles may occasionally be seen by ophthalmoscopic examination. Tuberculin skin test will be positive. ite, der By lumbar puncture no bacteria can be found in cerebrospinal fluid. Many, if not all, of the general symptoms of meningitis may be present, but they i of as in the other forms and are promptly relieved by the withdrawal of a moderate amount of the cerebrospinal fluid. rig of teeth and hydrocephalic cry. Tuberculous Meningitis (1228-9). : not so severe and are not so constant ecting the nervous system. of intestinal putrefaction and other abnormal processes, often started by the ingestion of tainted meat and other poisons. Vomiting, tympanites, diarrhoea and foul smelling feces. Serous Meningitis, Meningismus. (1239). Febrile or toxic convulsion Auto-toxic convulsion, (576, 1067). CHART XI b Clonic or Tonic Spasm Comprising Numbers ">72 on left side of Chart and 600 to 621 on right margin (Note) — Many of the spasms, especially the tonic spasms, are associated with pain, and are then called "cramps." 1:1: DIAGNOSTIC SYMPTOMS AND TESTS 571 L Pyrexia in very O acute cases. C C L A "NT L JN I c ■ c L s N p I A C S Apyrexia M s p A 572 T O N I C Pyrexia L O c A L T N I c s p A S I M A pyrexia. Shock-like spasms similar to that pro- duced by an electric shock Begins in one arm and side .side and then to opposite A~single]_or many times repeated spasm, rarely con- tracture, of one muscle or of a group of muscles, occurring in parox- ysms which rather tend to subside on voluntary move- ment s. Myoclonus. (270.) Spasm commenc- ing in jaws. Spasm commenc- ing in pharynx and oesophagus. 'Occurs in face and more rarely in neck The s and arms. am Begins in arms and may extend to legs, The but almost never to face. Often the mi tendons play as in subsultus tendinum. ax< Begins in side of face or in one arm or The leg and may extend over one, or even fir: both sides of body. There is the history of an r infected wound, or septi of jaws, occurring in paroxysms; also rigidity t body being held in posilion of opisthotonus, on becomes very high. The disease varies greatly There is history of a bite by an animal (usually especially on sight of water. Spasmodic closur cough, opisthotonus and general spasm are cor light and accommodation. The stage of excitt diagnosis must be made in such cases by the I Spasm commences in back of neck and in back. There may be more or less symptom. Lumbar pui fThe Apyrexia. If un- consciousness i s present. See also epilepsia media 1(575). 'Cerebellar ataxia is present (281). A tonic spasm of sudden onset, the face \ not being affected. dell Retr Extremities and trunk rem attack may last minutes Rigidity rather than spasm, not strong enough to prevent passive or volun- tary movements (266). (Rigidity of all muscles, mr Spasm passes away as the action is continued, to the muscles of the face usually escape altogetl fibers show marked hypertrophy. Closely alii* low exposure to cold with consequent rellcx VI The so-called acquired form, " myotonia acqui Bilateral painful tonic spasm of muscles of hands tended. Increased mechanical (Trousseau's pi dated with rickets or digestive disorders and i It, occurs in infectious diseases, in poisoning a; General painful clonic, followed by tonic, Spasm very general and v spasm. ni, ,' c poisoning. Death h General permanent contracture. Paralysis is coincident will Spasm only occurs Occurs usually in small muscles and in those Iha when performing gradual onset, steadily grows worse, and rendei some accustomed rather than spasm. Atrophy of the muscles i act, the voice of singers, public speakers, etc. Spasm only at com- mencement of any action. Spasm mainly con- fined to hands and feet, paroxysmal. Rather brief spasm muscles. More permanent spasm. A permanent or, at least, a long con- tinued, contracture. The muscles are anatomically short- ened, i n later stages. of one or more A spasm lasting minutes < cough, oesophageal spas A contracture of a few or many muscles usually efforts are made to overcome it. No muscle at bling (674) or may consist in jumping or ski I A hemiplegic con- fTendon reflexes air incrflG fracture. i and lasts for years. Usi A paraplegic con- tracture. I Tendon reflexes are increaijl I follows an attack of par A local contracture. Absence of reflexes. Muel i ^ traction of tendon and I DIAGNOSTIC ANALYSIS OFf SYMPTOMS ABSTRACTS OF SYMPTOMS ck and extends to leg of same Much pain in head and neck at onset. Weakness slowly follows the spasms. At times there is wastin spasms become violent ar.d more continuous. Epileptiform attacks are common. Death results in a few nlonths uscles and^loss of faradic excitability. The Dubii DIAGNOSIS Electrical Chor. s are almost always unilateral, ri bilateral are not symmetrical. is are bilateral and fairly sym- , but not synchronous. They -ular in force and rhythm, and lost always limited to one The spasms seem like mimic gestures and appear to be rather purposeful. May have originated from local irritation, but have persisted after the irritation has ceased. The spasms never appear to be purpose- ful. No movement results, merely indi- vidual muscles spring forth in strong contraction. Irritation of the skin or tendons causes paroxysms. ychic disorders of an emotional or neurasthenic nature often present. The contractures ; (617). : accompanied by no pain. i also reflex spasm Convulsive Tic (blepharospasm, torticollis, etc.), 601 (267, 270, 617, 726). The contractures are accompanied by sharp darts of pain, emotional disturbances, f The muscles involved are attached by one end to the trunk < Trembling of muscles between the paroxysms. The spasms become ler~ or entirely cease, during sleep. E irated. Muscles of the face, hand and forearm, foot and lowe never involved. No heredity. A disease of adult life. Many cases occur in the same generation of a family, begins in early life and is associated with epilepsy and i are always unilateral at The spas may extend to adjacent muscles and so over one half the body and then pass across and involve both sides, or it may remain a ocal spasm and V in a short time. After many such local spasms, one may occur which will pass into a general convulsion. A general convulsion can some- times be averted by tying a band tightly around the extremity as soon as the local spasm appears Consciousness is always lost when the convulsion extends to both sides of the body; but usually persists when spasm is limited to one-halt the body or to one extremity, lbirth within a month usually within two weeks. The infection may occur through the navel in new born babies (tetanus neonatorum). The characteristic symptom is rigid spasmodic closure 1 , «, k , . 1 , cm E " nsus saXiicus " In the onset a gradually increasing stiffness of masticatory and other muscles followed and accompanied by paroyxsms of painful tome spasms; , he Clonus pieSrosthd"onus d, ^ orthotonus (265). The spasms are associated with profuse sweating. There are no mental symptoms and no coma. Towards the fatal termination the temperature ensity. ' The longer the incubation period the milder the disease. Local tetanus and head tetanus with local paralysis have been described. ■ cat) within a year usually within six months. The most striking features are tremor, rapid pulse, fever, mental depression, fright, horror and extraordinary emotional excitement, even mania, harynx ad Oesophagus mldng swallowing, especially of fluids, impossible. Saliva cannot be swallowed and is expelled from the mouth with difficulty. Spasm of muscles of respiration, hie- Eeflex acirtrom cutaneous or special sensory surfaces are greatly increased, especially that of inspiratory dyspnoea; and priapism occasional!* occurs. The pupils are dilated and respond to is aftlmes followed lb} 'a si "age of paralysis and is often preceded by a prodromal stage of malaise and of pains, especially in the scar. Hysterical persons at times simulate hydrophobia. Ihe :e of hysterical symptoms (425), absence of fever and by time. rbance, or loss, of consciousness. Tonic retraction of neck, opisthotonus and boat-shaped retraction of abdomen. Slight irritation will] cause, s; shows increase of cells in cerebro-spinal fluid , except in serous meningitis. For different varieties see 590-4. nities on the same side as the lesion are adducted, on the opposite side abducted. Head, trunk and extremities each rotate about long axis fro\ towards the same direction. of the head and opisthotonus, flexion of elbows, supination of hands, extension of legs with pointing of toes. Tic Douloureux, (267, 726, 947). 602 Friedreich's Paramyoclonus Multiplex. 603 Unverricht's Family Myoclonus Epilepticus. 604 Jacksonian Epilepsy, (431, 587, 1282-3, 1291). 605 Tetanus, (170). Tetanus traumaticus. Tetanus 606 rheumaticus. Tetanus puerperalis. Tetanus neonatorum. , any position in which they may be placed for a surprisingly long time. Wax-like resistance to passive motion. Difficult positions mainta s or days. Anesthesia, abolition of reflexes, and apparently more or less complete loss of consciousness are usual symptoms. Other hysterical " e face, speech monotonous, passive tremor of hands and legs, characteristic attitude, festinating gait. Tendency to fall backwards or forwards l on first movement after a rest or when action is done faster. Patient cannot hurry or execute rapid movements. Is liable to lose equihbnu ilarked heredity. Myotonic electrical reaction (402). Increased mechanical excitability of muscle, even slight pressure wilh the finger-tip causei his disease is "paramyotonia congenita" (Eulenberg's disease) also on an hereditaiy basis (it has attacked twcniy-eight members of a family inr itor spasm and nutritive disturbances in the muscles. A myotonia congenita intermittens and a myotonia congenita atrophica have been descnb is probably an altogether different disease. sometimes of feet, lasting minutes, hours, or rarely days. Hands and feet drawn into smallest volume possible with hollow deepened (obstet enon (450)) and electrical (Kill's sign (452)) excitability of nerves. Facial nerve very irritable; so that slight blows on it cause spasm of facia lal parasites, or dilated stomach; often follows extirpation of parathyroid glands. Sometimes occurs as a symptom of hydrocephali pregnancy and as an occupation neurosis (616). In some cases this disease may be due to destruction of the parathyroid glands and linful, mainly in the form of opisthotonus (265). Periods of intermission with relaxed muscles lasting several minutes. Cutaneous and tendon results in a couple of hours. u-ii.iv; contracture. Convulsions, mental defect and partial arrest of growth, are common. The contracture and motor paralysis may be unilateral or D 1 been overworked or improperly worked in doing the same act many times. The spasm is often painful, and in some cases pain may be the c accustomed act difficult or impossible. It occurs only when the muscles are used. In some cases there is tremor, in others ^incoordination ed is common. Patients are usually neurasthenic. Many varieties: writer's, telegrapher's, pianist's, violinist's, seamstress, shoemakers, ned indefinitely without apparent effort, s jrmptoms are often present, (425). ebra I y peihaj Headache, backache, delirium, Kernig's ;ide of lesion to the opposite side and the eyes 577). The arms are less affected than the legs and sluggish long continued contraction. Muscle generations), but these paroxysmal attacks fol- 1 with the characteristics implied in their names. Hydrophobia. Lyssa. Rabies, (171). Meningitis, Cerebral and Spinal, (508, 590, 831, 974, 1005, 1032, 1045, 1208-9-13). Lesion of cerebellar hemispheres, (648, 686, 783, 1016, 1272). Lesion of vermis of cerebellum, (648, 686, 7S3, 1016, 1272). Catalepsy, (1096-8). Paralysis Agitans. Parkinson's disease, (677, 766, 800). Myotonia Congenita. Thomsen's disease, (265, 1155), including Paramyotonia Congenita (Eulenberg's disease). irs, due to local irritation in neurasthenic patient ethral spasmodic stricture, vesical spasm, t Functional in its nature. Many varieties. Blepharospasm, torticollis, spasmodic croup, la etc. See also the convulsive tics (601). liated with anesthesia of the part. Usually there is a combination of spasm of flexors and extensors, such as is not seen in organic disease. A f if. At times may be cured by ovarian pressure or by faradization. Other hysterical symptoms (425). Hysterical spasms are not always in the ; (saltatory spasm). ■hen the spasm does not prevent their occurrence. Little or no muscular atrophy. The spasm is limited to the arm and leg of the same side a there are flexion of elbow, wrist and fingers, and extension of knee. Is associated with a sclerosis of the pyramidal tract and indicates a hopeless hen the spasm does not prevent their occurrence. a. It is of very bad prognosis. icular atrophy. Is limited to the distribution of one i rather than of muscle. (hand). Joints of arms flexed, those of legs ex- Tetany, (120, 616). muscles (Chvostek's sign (4.51)). Usually asso- umor or other serious brain disease in children. , be cured by the administration of these glands, flexes increased. History or evidence of strych- iateral. ly symptom (neuralgic form). The spasm is of rare cases, paralysis or paresis (paralytic form) lamp. A similar neurosis occasionally affects aus stridulus, bronchial asthma, whooping Strychnine convulsions. (314-7, 3( Cerebral palsy of childhood, (116, 501, 577, 630, 79S, 1048). Occupation Neuroses, (143, 614). 615 615a ctional spasm, which becomes greater the more of contracture. They may consist in trem- follows an attack of apoplexy, by a few weeks gnosis as to recovery from the hemiplegia. Little or no muscular atrophy. The spasm, which is often not so continuous as in the hemii »ic form, consists in flexion of both knees, and more nerves. Folio of nucleo-peripheral moto Occurs in fingers. puytren's contracture seems to be due to con- Reflex spasm, (601, 637, 1194). 617 Hysterical contracture, (1074). 618 Post-hemiplegic contracture, (501, 504, 577, 615a). 619 Post-paraplegic contracture (512-20, 548-51, 795). 620 Post-neuritic contracture. Dupuytrcn's contrac- 621 ture. i CHART XI c Choreiform and Athetoid Spasms I lomprising Numbers ~>~'-'< and 57 I on [efl ride of < Ihari ■Mill 622 i" ii:;i on right margin I3U CHART XII Perversion of Motion and Local Palsies and Spasms DIAGNOSTIC ANALYSIS OF SYMPTOMS Symptom Analysed Character -638 ATAXIA (248) 635 PERVERSIONS OF MOTION (243) 639 TREMOR (250) 640 NYSTAGMUS (291) 641 FIBRILLARY CONTRACTION OR FIBRILLATION (292) The diseases in which ataxia occurs are set forth in Chart XII a. The diseases in which tremor, nystagmus, or fibrillation occurs are set forth in Chart XII b. 636 LOCAL PALSIES 637 LOCAL SPASMS LOCAL PALSIES AND LOCAL SPASMS See Chart XII c. See Chart XII d. 141 CHART XII a Ataxia Comprising Numbers (ills and 642 to 64 I on left side of Chart and 648 to 664 on right margin L43 DIAGNOSTIC SYMPTOMS AND TESTS 63 A T A X 1 A (248) 642 Ataxia mainly upon standing ,' or walking. Stagger- ing gait. Static ataxia. Cerebellar ataxia. (281). 043 Inability to stand or walk. More or less complete. No loss of muscle sense. No motor paralysis, except in late stage of 651-2. f Bilateral. Unilateral. I (Hemiataxia ) ^Unilateral. (Hemiataxia.) 044 Ataxia of all move- mei. -j Bilateral Dynamic ataxia. Motor ataxia (280 j. Irregular ^-distribution. ("Occurs at any age, usually in adults. I Usually sensory symptoms Occurs in youth. No sensory symp- toms. Many sensory symptoms. Often analgesia and thermic anesthesia. Sight and hearing normal. Sight or hearing abnormal. Patient e; nystaga ; Hypotoi very mi mally. at time normal. Occurs in family groups and si though less pronounced. A ge mus is common and speech oi (230) r; No loss ol lying dc Evidently func- tional. Evidently organic. Loss of muscle When of acute course the condi sense and sensory symptoms usually prominent. Knee- jerk usually in creased. ally follows an apopleci ic atl Si arterial disease is pre chronic course choked disc present. Knee-jerks normal. No ankle-clonus. History c ("Great variety of local symptom are intention tremor, Bcanrjnf I ness. Rarely the disease run J essential point is the presenc< A combination of symptoms of usually lost before any anrstl Knee-jerks may be abolished "Rarely any permanent motor p; ball) are not uncommon earn held well apart and feet are fl symptom (448), Argyll-Robert: sensations and paresthesias a gesia in patches and in cuirat in cerebro-spina] Quid. The i Positive Wassermann also urn mainly affected. In the ordii and the diagnosis must rest m Slight motor paralysis is presen normal. Cranial nerves rarer never so chronic as tabes. Ni Knee-jerks usually exaggerated, but no J Babinski or ankle-clonus. Evidently ■< functional (pseudo-ataxia). [ j-;,, 10 ti nal Exaggerated knee- jerks, ankle-clonus and Babinski. Knee-jerks and an- kle-clonus absent. No Babinski. Often loss of muscle sense and retardation of conduction of pain. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS s the staggering, irregular gait of a drunken man. Little ataxia of movements of hands, or of legs when lying down. Vertigo, vomiting and headache are often present. Choked disc or nay be present (tumors'). Knee-jerks may be present or absent (usually present). Cerebellar fits (609-10) may occur. Symptoms may be bilateral or unilateral (same side as lesion). i present, also a diadocokinesia (36) due fcoalong continuanceof muscular contraction. Patients can he on back with legs flexed at hips and knees much longer than a normal person and onger than patients with dynamic ataxia. t, constantly or paroxys- f Diplopia or other disorders of sight. Vertigo ceases when eyes are closed. lache, vertigo and vomiting < :> choked disc. Knee-jerks [ Deafness and ringing in one ear. Paroxysmal attacks of intense vertigo and defect in bone conduction are frequent symptoms. well marked heredity usually. Staggering gait, but ataxia also in armsj , coarse, irregular tremor, simuhil ing jerky choreiform movements. Nystag- iefective. Symptoms present a mixture of weakness and ataxia. Occurs after puberty. Knee-jerks present. Ocular paralysis, loss of pupil reflex and optic atrophy common. early stage and in exceptional cases. Babinski reflex power. Simulates an apraxia Occurs before puberty. Knee-jerks absent, except usually present. Optic atrophy rare. Club-foot loved easily in all directions without ataxia when patient is lying down, but collapse when she tries to walk, apparently from lack of confidence and w than an ataxia. Often has an emotional cause and hysterical symptoms (425) are present. Both legs are involved. icle sense. May or may not be motor paralysis of same side with analgesia and thermic anesthesia of contralateral side. One leg only involved. No ataxia when but marked ataxia while walking leg while Marked anesthesia without analgesia. No motor paralysis. No other symptoms. Very rare. May be the earliest Apoplecf iforrn attack followed by hemiplegia (sensory oftener than motor). Other post-hemiplegic motor disturbances are often present. The ataxia occur cases where the motor paralysis w r as slight. spinal tumor. Unilateral later becoming bilateral. conv;dL'scence in be j There are often ataxia and loss of muscle sense on one side of body and analg I arthria and paralysis of various cranial nerves are usually present. . and thermic anesthesia on the other side. There may be crossed paralysis. Dysphagia and dya- LSigns of cortical irritation (convulsions). Anesthesia, especially loss of muscle sense, is often present. Headache common. May be some mental disturbance. • Imli- Blurred and foolish speech. Ataxia and other sympta Temporary tremor. 'sually both motor and sensory symptoms. Irregular, jerky, ataxic movements of both arms and legs, and movements are slow. Gait is often both spastic and ataxic. Very characteristic ;eh, nystagmus, especially on motion of eyeball, and atrophy of optic nerve. In some cases bulbar paralysis (434) is an early symptom. Patients are often emotional and exhibit mental weak- acute course and has been called "acute ataxia," of which there are several varieties (662). In its early stages the diagnosis of this disease is often exceedingly difficult. The most lymptoms only explicable on the assumption of the existence of several, separate, small lesions. motor ataxia (661) and spastic paraplegia (525) in varying proportions. Little or no pain. Weakness, stiffness, ataxia, paresthesiae and can be detected. In later stages arms may be somewhat involved. A rare disease. Occasionally some involvement of cranial nerves. Orga; rds the end of the disease, but Babinski persists. This disease may be caused by pernicious and other severe anemias. of legs. Vibration sense (56, 353) is reflexes slightly, or not at all, disordered. sis; but hypotonia (252), allowing hyperextension and extreme mobility of joints, is common, and temporary paralyses in the domain of the cranial nerves (especially the muscles of eye- iptoms. Movements are ataxic, quick, violent, excessive and constantly controlled by eyesight. The affected parts cannot be held motionless in one position long. In walking, legs are too far outward and too far forward and are brought back hard on heel. Ataxia much worse when eyes are closed. Walking in the dark or backwards is usually impossible. Romberg's phenomenon (447), myosis and optic atrophy with concentric limitation of field of vision are common. Lightning pains of great intensity in small areas followed by hyperalgesia, girdle ominent symptoms. Organic reflexes, especially the vesical, are disordered. Arthropathies (11S6), or perforating ulcer or other trophic disorders may be present. Anesthesia and anal- nar hyperlhesia). Retardation of conduction of pain. Visceral crises (9S7) are usually present. Towards the end of the disease motor paralysis may appear. Lymphocytosis and globulin se is sometimes divided into three stages — (1st), the neuralgic; (2nd), the ataxic; (3rd), the paralytic stage. History or other evidences of syphilis, or of venereal disease is usually present, present. There are several forms of tabes. In the cerebral form, atrophy of the optic nerve is the prominent symptom and the legs show little ataxia. In cervical tabes the arms are form the legs are mainly affecled. In all forms the knee-jerks are absent. Babinski is present in rare cases, complicated by lateral scleroses. In many cases of tabes the ataxia is slight ' on the absence of the knee-jerk, the Argyll-Robertson phenomenon and the cerebro-spinal lymphocytosis, together with whatever other symptoms may be present. luscles tender and atrophic. Pains rarely very severe and partial reaction of degeneration and retardation of conduction of pain often present. Organic reflexes normal. Pupil reaction r olved. Usually sensory symptoms. Usually history of alcoholic abuse. Mental disturbances in many cases. Occasionally the disease runs an acute course, "acute ataxia," (659) and is bulin or lymphocytosis in cerebro-spinal fluid. Prognosis is good, ing drugs, alcohol, etc. The ataxia is usua and excitable. ?iated with tremor and neurasthenic symptoms. Failure of memory and other signs of mental impairment. Patients are emotional The ataxia may appear only when eyes are closed and but usually collapse on reaching a place of safety. usually associated with cortical anesthesia. Hysterical symptoms (425) are present. Rarely fall, DIAGNOSIS Lesion of cerebellum or it; tracts; if acute in onset, 648 apoplexy; if chronic, tumor, (609-10, 654, 686, 783, 1016, 1272). Ocular ataxia or vertigo, (1020). 649 Aural ataxia or vertigo. Meniere's Disease, 650 (685, 91S, 1019). Marie's hereditary cerebellar ataxia, 651 (669, 782). Friedreich's Disease. Hereditary Ataxia, 652 (670, 6S7, 762, 781). Astasia and Abasia, (2S7, 792). 653 Lesion of lateral column of spinal cord, involving 654 direct cerebellar tract, (64S, 1356, 1360, 1396). (Figs. 24-7.) Lesion of posterior column of cord, (785, 1350-1 654a 1347, 1396). (Figs. 24-7.). Post-hemiplegic ataxia (lesion in or near posterior 655 part of optic thalamus (1275). (Fig. 17.) Softening, hemorrhage or tumor in brain srem, 656 (535 et. seq., S30, 1268-71). (Figs. 19-22.) Softening or tumor of contralateral parietal cortex. 657 (1355, 1362). (Fig. 15.) Alcoholic intoxication, (663, 673, 764, 780). 658 Disseminated Sclerosis. Myelitis Disseminata. 659 Encephalomyelitis, (511, 580, 668, 688, 756, 765, 799, 913, 1051). .taxic Paraplegia. Combined Sclerosis, (526, 796). (Figs. 24-6.) Locomotor Ataxia. Tabes Dorsalis, (433, 756, 784. 827, 894, 979, 987, 1004, 1217, 1231). (Figs. 24-6). Multiple Neuritis. Polyneuritis. Pseudo-tabes, (4S8, 787, 823, 1008, 1147, 1307) Drug habit (toxic), (482, 658, 764, 7S0). Hysterical Ataxia, (1074). CHART XII b Tremor, Nystagmus, Fibrillation Comprising Numbers <>:i'.i t<> 647 on left side of Chart and litis in 697 on right margin II.'. DIAGNOSTIC SYMPTOMS AND TESTS o:?9 T R E M R (250) 640 N Y S T A G M U s (291) ■645 Intention 290). 646 Passive Tremor. In- creased on volun- J tary motion a n d excitement (289). G47 Passive Tremor. Diminished o □ voluntary motion (289). fC'oarse, irregular tremor; 4 to 8 per second. Fine tremor. Pine, rapid tremor; « S to 12 per second. | Slow tremor; 3 to G i it second. Slow, fine tremor; 3 to G per second. Tremor is usually associated with scanning speech, nystagmi Usually a greal variety of motor and sensory symptoms d sionally with their loss, over a very variable area. The i Vertigo is a very common symptom. Occurs in family groups and shows well I Oecurs after pul marked heredity. Staggering gait, j Ataxia. Nystagmus is common and 1 speech often defective. [ Occurs before pu Tremor is associated with general weakness or convalescence Exopblhalmus, goitre, tachycardia, vascular throbbing, Bus when patient looks downward (Graefe's symptom). The g History of addiction to alcohol or drugs. .Menial symptom* greatly at different t imes. Presence of hysterical symptoms (425). Tremor is worse wh Tremor is marked in fare, lips and tongue. Progressive roei cytcsis and globulin in cerebro-spinal Quid. Wassermann i Slow, coarse tremor. Either Intention or Passive Tremor. Always a symptom of organic disease. Very rarely, an hysterical clonic spasm may simu- late true nystag- mus (pseudo-nys- tagmus). This is often vortical and is more rapid and more violent than nystagmus and is associated w i t h other hysterical symptoms (425). 'No weakness of any rectus muscle. Weakness of one or muscles. Slow tremor of hand and foot of same side, associated with ( Tremor, which is associated with muscular rigidity and mask-li involves the other side. The tremor is mi si marked in tin acteristic attitude (head and body bent forward, elbows lit ilar tendency to run backwards (retropulsion). The attitu The disease often commences with a stiffness and slowness no sensory symptoms except the set sation of rigidity and Tremor begins bilaterally. Head is early affected. Nodding Rotatory or nodding tremor of head occurring suddenly in ri involved. The tiemor ceases when the child's eyes are clo A scries of jerky tremors limited to the back, or involving al Not associated with other nervous symptoms. Hereditary b f Defective vision from whatever cause, { Due to lack of pigment in iris, choroid ( ^Yorkers in mines. Due to working ii Paroxysmal at tat violently, or ga . Vertigo, cerebellfl Coarse, jerky tre- mor is a prominent j Occurs in early y symptom. Ataxia j is also present. I Occurs at any ag Cerebral symptoms occurs in mening present . Rickety baby in Most marked whi winter. ing of the heat , Congenital. Lateral oscillating more of the recti Nystagmus occurs in convalescence frc Impairment of sight. No impairment of ■ sight. Vertigo is a prom- inent symptom. 641 FIBRILLARY CON- Ti: \i in in in: FIBRILLATION (292 . Evidence of organic disease. Degenera- tion of peripheral motor neurons. Evidence of func- tional not organic diseases. Marked muscular atrophy with muS- - cular weakness. No muscular atro- phy or weakness. 'Marked sensory symptoms. Analgesia and the f Muscular atrophy No sensory symp- { Mllscular , tril| ,i iy toms. r J [ Muscular atrophy Occurs usually in DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS phy of optic nerve and ataxia. Reflexes are usually exaggerated and ankle-clonus and Babinski are present. In some cases the deep reflexes are early abolished and the organic reflexes disordered, lany local lesions, alt In nigh all these may be absent. The motor symptoms commence as fatigue, slowly becoming paresis, rarely paralysis, and are usually associated with exaggerated reflexes, occa- r symptoms are usually in the form of paresthesiae, more rarely pain followed by irregular patches of anesthesia. Epileptiform or apoplectiform attacks followed by transitory paralysis are common. Knee-jerks are present. Ocular paralysis, loss of pupillary reflex and optic atrophy are common. Knee-jerks are absent except in early stage or in rare and exceptional cases. Babinski is present. Optic atrophy rare. Club-foot common. Rarely sensory symptoms are present, n acute disease. Anemia is usually present, but no evidence of any organic disease of the nervous system. Exhaustion or holding a limb in a strained position for a long time causes tremor. veating, diarrhoea, much nervousness, tremor especially marked on excitement, polyuria and at times albuminuria, insomnia and vertigo are common symptoms. The upper lid does not fall normally of the parenchymatous variety and need not be large. mmon, moral sense and judgment impaired and speech blurred. Patient is restless and emotional. Pupils contracted in opium cases. Quinquand's sign (453) in alcoholic cases. Symptoms vary ntion is directed to it. Irregular tremor. Evidence of great exhaustion of the nervous system. Often history of injury associated with fright. History of syphilis. Lumbar puncture shows a lympho- airment. Eestless and childish. Speech is slurred by elision of syllables and letters. Apoplectiform and epileptiform attacks may < usually positive. Argyll-Robertson's phe: ator paralysis of the opposite side. Other symptoms of a severe brain Ie, May be associated with hemiplegia, sensory or motor. Tremor ceases during sleep and i Teased in excitement. , consists of "pill re ; and hands; the hi lees slightly flexes t and mask-like fa ement of one novements of fingers and general tremor, which commences in one extremity, later extends to the other extremity of the same side (rarely to that of the opposite side), and finally 1 body escape, except in very rare cases. Disease commences after forty years of age and progresses slowly. The tremor usually becomes coarser in the later stages. Char- les! in;it inn L r :iii or pp.pulMon: a tendency to fall forward winch compels patient to walk faster and finally to run until he falls forwards or against, an obstacle. He has a sim- dl due in inuscul.ir rigidity which is more characteristic of the disease than is the tremor, and in rare cases occurs alone without any tremor (paralysis agitans sine agitatione). id, simulating a mild paralysis, the tremor appearing later. Voluntary movements are slow, much restricted and feeble, but are never completely paralysed. There are of heat, which are frequent and distressing symptoms. Patient slowly becomes entirely helpless, tent. No rigidity. General weakness. Atheromatous arteries, tabies in the winter time and passing off in the summer time. Usually accompanied by nystagmus which grows worse when the child's head is held still. Occas ally other muscle groups are Multiple Sclerosis. Disseminated Sclerosis, (511, 580, 659, GSS, 756, 765, 799, 913, 1051). Marie's Hereditary Cerebellar Ataxia, 669 (651, 7S2). Friedreich's Hereditary Ataxia, 670 (652, 6S7, 762, 7S1). Asthenic Tremor or weakness, (790). 671 Exophthalmic Goitre. Basedow's Disease. 672 Graves' Disease, (1193). Toxic Tremor (alcohol, opium, nicotine, mercury, 673 etc.), (658, 663, 780). Hysterical or Neurasthenic Tremor and also Trau- 674 matic Neuroses, (1072-5). Paralytic Dementia. General Paresis. Paresis, 675 (570, 763, 895, 1049, 1104, 1216, 1230). Lesion of the Crus Cerebri or Pons involving the 676 Rubro-spinal tract, (441, 1270, 1325). (Figs. 1S-20). Paralvsis Agitans. Parkinson's Disease, 677 (612, 766, S00). Senile Tremor. 67S Spasmus Nutans. Nictitatio Spastica, (690). 679 les, caused by cold (physiological) or infection (pathological) and resulting in an increase in the body's temperature and may be followed by high fever. coholism in ancestors, etc.). May be local or general. Usually in advanced age. ital or acquired, in early childhood. Often associated with blepharospasm and oscillation of head. Usually associated with photophobia. light and looking sideways constantly while at work. 'ertigo associated with deafness and tinnitus aurium and due to disease of inner ear. Nystagmus in the opposite direction from the labyrinth involved occurs occasionally when head is rotated id, or ear syringed, or labyrinth in any way irritated. The caloric reaction (79) is absent. a and other symptoms of disease of the cerebellum. The nystagmus is usually towards the side of the lesion. Strong heredity. Knee-jerks absent, except in early stage. Babinski is present. Optic atrophy rare. Muscular weakness and contractures are not uncommon. i heredity. Intention tremor. Exaggerated knee-jerk, Babinski, optic atrophy and scanning speech are common symptoms. Vertigo is usually present (932). d in local lesions (tumors especially). Nystagmus is commonly present in bulbar lesions, especially in those involving the cerebellar peduncles and tracts and the posterior longitudinal bundle. child's head is held still and the tremor prevented (679). Not to be confounded with the deep bowing (Salaam cramp) which occurs in some idiots and epileptics, with or without nystagmus. Roll- occur in otitis media and in rickety children. igmus associated with jerking movements of the limbs or trunk, aggravated by cold and by percussion. Associated with other congenital defects, liar palsies or when weakened muscles are strongly exerted. nesthesia with only slight anesthesia, or none at all. Trophic disturbances and mutilation. Slight tactile impressions are often painful. ibrillary contraction of tongue and lips, dysarthria, dysphagia and spastic paraplegia. ibrillary contraction of small muscles of hands and of shoulder girdle combined with spastic paraplegia. ibrillary contraction of the peronei muscles. Rarely there are pain, muscle twitching and anesthesia. alaris palpebrarum but may occur in any muscle. It consists in a quivering of the muscle fibers and occurs in neurasthenic and exhausted persons. 6S2 683 6S4 Labyrinthine 685 Chills. Rigors. Shivering. Essential Tremor. Amblyopia, (359). Albinism. Miner's Nystagmus. Menidre's Disease. Aural Vertigo, (650, 918, 1019). Cerebellar Disease, (609-10, 648, 7S3, 1016, 1272). 686 Friedreich's Hereditary Ataxia, (670). 0S7 Disseminated Sclerosis, (668, 765). GS8 Cerebral Disease (especially of the brain stem). 6S9 Spasmus Nutans. Nictitatio Spastica, (679). 690 Nystagmus-myoclonus. 691 Ocular Muscular Insufficiency, (810). (Figs. 14, IS). 092 Syringomyelia, (552, S37-9, 1009, 1170, 1187, 1357-9). 693 (Figs. 25-7.) Chronic Bulbar Paralysis, (540, 1150). (Fig. 21-2) 694 Amvotrophic Lateral Sclerosis, (547, 797, 1149). 695 (Figs. 24-6.) Spinal or Neuritic Muscular Atrophy, (496). Myokymia. Myoclonia, (293). 696 097 CHART XII c Local Palsies Comprising Numbers 700 to 721 on right margin ite) — The anesthesia accompanying these palsies can be seen from the areas of cutaneous distribution of these nerves depicted in the plates at the end of the book (Figs. 33-8). In mild lesions of the nerves anesthesia is either absent or much less marked and less extensive than the motor parah 117 Inability to Move, More or Less, Muscles of J A W DIAGNOSTIC ANALYSIS OF SYMPTOMS LOCAL PALSIES Abstract of Symptoms There are ptosis and strabismus divergens and the pupil is dilated and immobile both to light and accommodation (this condition of the pupil may occur as an isolated paralysis, — 333). The eye- ball can be moved in no direction except outward (abducens),and outward and downward with rotation of eyeball (superior ob- lique). For symptoms characteristic of the isolated paralysis of each ocular muscle see Chart XIV c, 816. When the superior oblique muscle is paralysed the levator palpebrae superioris is paralysed with it and ptosis results. ^ The ocular muscles, except the levator palpebrae superioris, have a bilateral cortical representation. Hence ocular paralyses, except ptosis, almost never occur in lesions above the oculo- motor nucleus, except in bilateral lesions. The cortical repre- sentation of the ocular muscles seems to be very diffuse or multiple. Conjugate deviation may result from supra-nuclear lesions. For the symptoms of paralysis of the trochlearis (patheticus) nerve and of the abducens nerve, each of which produces a strabismus convergens, see 816. The muscles of mastication of one side, rarely of both sides, are paralysed and in severe cases atrophied. The temporal and masseter muscles cannot be felt firmly contracting when efforts are made to chew. The jaw cannot be closed tightly or opened strongly or moved laterally towards the healthy side (external pterygoids), or the chin pushed forwards (internal pterygoids). Mastication of food is difficult or impossible; dysmasesis (286). The jaw reflex (322) is abolished. In some cases one side of the soft palate (tensor veli palatini) is paralysed and in some the hearing of low tones is unpleasant ■f (tensor tympani). In trigeminus lesions there is unilateral abolition of the con- junctival, corneal, sneezing and palatal reflexes; and the secretion of tears is at times affected. There is no irritation, or tears, from inhaling ammonia or acetic acid. There is also loss of sense of taste, and dilatation of the pupil, narrowing of the eyelid slit, even enophthalmus, are present. Heat and redness of skin in recent cases and coldness and cyanosis of skin in old cases. The salivary secretion and taste are affected when either the proximal or the distal end, but not the middle, of the nerve is affected. The muscles of expression of one side (rarely of both sides) of the face are paralysed. The forehead cannot be wrinkled and the eye appears larger than normal and cannot be closed (lagoph- thalmus, hare's eye). When attempts are made to close the eyelids the eyeball turns upward, the cornea disappearing behind the upper lid (Bell's phenomenon). The angle of the mouth is lower than normal and cannot be raised. The naso-labial fold is obliterated. The lips cannot be firmly closed; so that whistling is impossible and speech is impaired. Mastication is difficult be- cause the weakened buccinator muscle allows food to collect be- tween the jaws and the cheek. The platysma is also paralysed; so that the angle of the mouth cannot be drawn downwards. Tears may flow from the eye and irritate the cheek and saliva from the angle of the mouth. The conjunctiva may become in- flamed and the cornea ulcerated, because the eyelid cannot wink and keep the conjunctiva clean. In some cases the facial paral- ysis may be preceded and accompanied by pain. In severe cases the paralysed muscles exhibit the electrical reaction of degen- 148 Diagnosis Paralysis 700 of Motor Oculi. (Figs. 14, 18). Paralysis 701 of Troch- learis and of Abducens. Paralysis 702 of motor ) branch of $ Trigeminus. Facial 703 Paralysis. Bell's palsy. Prosopo- plegia. Facial Monoplegia. Facial Diplegia, (751, 928, 1317). Inability to Move, Moee or Less, Muscles of THE F A C E LOCAL PALSIES (Continued) Abstract of Symptoms Diagnosis eration. Hearing and taste are frequently impaired and disor- dered. When taste is affected the salivary secretion is also affected In the earlystages of the disease the face isdrawnover toward the healthy side by the unantagonized healthy muscles. In the later stages the face may be drawn back again perma- nently towards the paralyzed side by the contracting newly formed connective tissue in the degenerated muscles. Also in the early stage of recovery the face may be drawn towards the paralyzed side by over-innervation of the muscles form- erly paralyzed, and may exhibit temporary contractures and spasms, possibly "associated movements." These spastic symptoms may be due to irregular regeneration of the nerve. The upper fibres of the facial nerve have a bilateral cortical representation as do the laryngeal nerves. Hence lesions of the cerebral hemispheres paralyse mainly the lower branch of the facial; the eye on the paralysed side can be closed but is easily forced open. For the localization of the differ- ent forms of facial paralysis, see 1317. Paralysis of the pneumogastric nerve is discussed under 760. In Pneumo- 704 addition to the laryngeal paralysis there is often present dis- gastric order of the respiratory act and of the heart beat (tachycardia). Paralysis (760). When the tip of the shoulder sinks downwards and forwards and Paralysis 705 the arm cannot be easily raised, there may be a paresis of the of the trapezoid muscle. When this muscle is paralysed on both sides, Spinal the head tends to fall forward. When the head is drawn towards Accessory, one shoulder and the chin turned upwards and towards the other, the sterno-cleido-mastoid muscle is paralysed on that side ■{ toward which the chin turns. This posture is called caput obsti- pum spasticum, when the muscle is atrophied and secondarily contracted and the deformity can no longer be corrected by passive motion. Caput obstipum spasticum occurs also and is more pronounced in torticollis from spasm of the muscle (730). When the sterno-cleido-mastoid muscle is paralysed on both sides, the head tends to fall backwards. The tongue when protruded (urns towards the paralysed side. Hypo- 706 When both sides are paralysed the tongue cannot be protruded glossus at all, and in such cases, apeech, mastication and deglutition are Paralysis. difficult and imperfect. In lesions of the nucleus of the hypo- (546,752). glossus nerve there is also B mild paresis of the orbicularis oris muscle. Intracranial lesions involving the hypoglossals and other nerve roots at the base of the brain may cause Avelli's syndrome: pharyngo-laryngeal or glosBO-phaxyngo-laryngeal paralysis (old); or may cause Schmidt's syndrome: the above and also sterno-cleido-mastoid and trapezius paralysis. phragm is paralysed on one or lioth sides, causing dyspnoea Phrenic 707 on exertion and unking in of the epigastrium on inspiration, 1'aralysis. ■ iallv on deep Inspiration. The lower part of the lung a drawn upwards and atelectasis and pneumonia may air. He- sides the usual o and neuritis, tins paralysis may also occur in pleurisy, peritonitis, trichinosis and in bulbar and spinal lesions. The paralysed diaphragm shows l.ittt phenomenon. The supra-.'tnd infra spmatus musclefi are paralysed: BO thai rota- Supra- 708 tion of the arm out ward and rai^iiu; it in abduction are impaired. Scapular Muscles involved are atrophic and ulnar side of hand is turned I'arah forwards. Thcserratus anticus major [a paralysed: BO that when the scapula Long TOfl is raised, its lower angle approaches the vertebrae and the inner Thoracic margin of the scapula does nol !"■ do e to the thorai and. on Paralysis, movements of the arm upwards and forwa from the Berratus thorax like a (ring. The arm cannot lie raised heyond a hori- Paralysis. ■Ontal line. 1 19 Inability to Move, More or Less, Muscles of the LOCAL PALSIES (Continued) Abstract of Symptoms Motion of the arm inward and forward is impaired. Hand cannot be placed on opposite shoulder. Diagnosis Anterior and Posterior 710 Thoracic Paralysis. Rotation of the arm inward and motion of the arm backward are impaired. Sub-Scapular 711 Paralysis. The deltoid and teres minor are paralysed: so that the arm can- not be raised. The combined paralyses of the brachial plexus: Erb's and Klump- ke's paralysis, are discussed under 454, 455 and 490. Axillary 712 Paralysis. The biceps, brachialis anticus and coraco-brachialis muscles are Musculo- 713 more or less completely paralysed; so that flexion of the arm at Cutaneous elbow is more or less impaired, especially in supination (very rare). Paralysis. The pronators and flexors of the hands and fingers, the muscles of the ball of the thumb and the first and second lumbrical muscles are paralysed. The hand can neither be flexed nor pronated. The thumb cannot be brought across hand to touch the little finger, but remains close to the index finger (ape's hand). The first (proximal) phalanges of fingers can be flexed, but not the second and third phalanges. The interossei, the third and fourth lumbricals, and the muscles of the little finger are paralysed. The proximal phalanges can- not be flexed, the other phalanges cannot be extended and the little finger cannot be moved. The fingers cannot be spread. When muscle atrophy and contracture occur "claw hand" results. The extensors and supinators of the hand and fingers, and the ab- ductor pollicis longus, are paralysed. The thumb is adducted and can neither be abducted nor extended. Wrist-drop and slight pronation. Wrist and fingers cannot be extended completely. The wrist-drop differs from that of lead palsy (494) in that the supinator longus is paralysed. Therefore, if the forearm is held midway between supination and pronation and the elbow strongly flexed against a resistance offered, the belly of the supinator longus will not stand out firmly contracted as it will in lead paralysis and in health. The extensor femoris is paralysed; so that flexion of the thigh on the body and extension of leg on thigh are impossible or difficult. Standing and walking are difficult, and ascension, jumping and running impossible. The adductor muscles of thigh are paralysed; so that adduction of leg, pressing of thighs together and crossing of legs are im- possible. The glutei muscles are paralysed; so that walking, ascending stairs, straightening up of body, abduction and rotation of thigh are impaired. Generally much muscular atrophy. Foot and toes are paralysed ; the leg cannot be flexed on thigh and rotation of the thigh is impaired. In cases of isolated tibialis paralysis there is absence of plantar flexion of foot, and of plantar, flexion, spreading and adduction of toes (Pes calcaneus et valgus). In cases of isolated peroneal paralysis there is absence of dorsal flexion and abduction of foot and its adduc- tion impaired — absence of dorsal flexion of toes. There are foot- drop, high stepping gait and Pes equino-varus. For paralysis from lesions of the cauda-equina, see 487, 1007 and 1308. 150 Median 714 Paralysis. Ulnar 715 Paralysis. Musculo- 716 Spiral and Radial Paralysis. Crural 717 Paralysis (997). Obturator 718 Paralysis. Gluteal 719 Paralysis. Sciatic 720 Paralysis. (996) Cauda Equina Paralysis* (Fig. 29). 721 CHART XII d Local Spasms Comprising Numbers 725 to 733 on right margin l.M DIAGNOSTIC ANALYSIS OF SYMPTOMS LOCAL SPASMS Abstract of Symptoms The jaws are held tightly shut and the masseter and temporal mus- cles can be felt to be contracted (lock jaw), usually bilaterally. The spasm may be "tonic," as in tetanus (606), tetany (614), irri- tation of teeth (wisdom teeth) and certain unilateral lesions of the pons and medulla; or "clonic," as in chills and in rare cases of paralysis agitans and hysteria. When the pterygoid muscles alone are in spasm the mouth is held open and cannot be closed. ' Spasms of one or more muscles of expression of the face, unilateral or bilateral, are relatively common, as in convulsive tic (601) and tic douloureux (602). These spasms are often a mixture of tonic and clonic contractions, the clonic predominating. They may affect all the muscles or only one, as in tonic spasm of the orbicularis palpebrarum (blepharospasm) (601, 617), or in clonic spasm of this muscle (spasmus nictitans: nictation). The platysma myoides often takes part in these spasms and very rarely the muscles of the soft palate and the internal and external ear mus- cles. Very rarely spasm of some of the facial muscles about the mouth constitute an occupation neurosis or cramp, as in the "Auctioneer's cramp" and "Cornet player's cramp." These facial cramps may be symptomatic directly of lesions of the cort- ical facial center, of the facial nerve in its course, and reflexly of the trigeminal nerve or its terminal filaments in the eye, nose, mouth or ear. There is also to be remembered the passive con- tracture of the degenerated muscles and the active contracture due to over-innervation of the convalescing muscles in facial paral- ysis. Causeless and uncontrollable laughter must also be classed among the facial spasms. This condition, similar to the allied state of causeless and uncontrollable crying, occurs especially in hysteria and in lesions of the optic thalamus. ' Spasm of the pharynx of a tonic nature preventing swallowing and of a clonic nature repeating the act of swallowing with great fre- quency occur. The former occurs in hydrophobia (607) and some- what also in tetanus (606) ; while the latter, associated with coma, frequently occurs in mild epileptic attacks. The spasm also occurs from irritation of the pharynx in hysteria and very rarely, as one of the crises in locomotor ataxia (433). Spasm of the oesophagus is not uncommon in hysterical persons and makes the swallowing of food very difficult. Spasm of the muscles of the larynx (spasmus glottidis, false croup, laryngismus stridulus), causing noisy and difficult breathing, is a not uncommon and occasionally a dangerous condition. It occurs almost exclusively in children and is often associated with rickets and with digestive disorders. Occurs also in general diseases such as hydrophobia, hysteria, epilepsy, chorea, tabetic crises, etc. Sneezing (sternutatio spastica, ptarmus) and coughing, reflex acts implicating both the pneumogastric and the intercostal nerves, are often due to pathological conditions and irritation of the nervous system. Bradycardia, Cheyne-Stokes' respiration and cerebral vomiting are symptoms of irritation of the pneumo- gastric nucleus, but are not characteristic and are of little diag- nostic value. r Spasm of the tongue is very rare, especially so the tonic form. Dur- ing the attack speaking and swallowing is impossible. Very rarely a tonic spasm of the tongue occurs when the patient attempts to speak (stuttering and aphthongia). Spasm of the tongue is some- times associated with facial spasm and with spasm of the sub- maxillary muscles. These spasms may be due directly to lesions of the cortical tongue center, of the hypoglossus nerve in its course, or reflexly, especially from lesions of teeth, mouth and nose. 152 Diagnosis Trige- 725 minal Spasm or Cramp. Trismus. Facial 726 Spasm or Cramp (267, 601). Glosso- 727 Pharyn- geal Spasm or Cramp. Pneumo- gastric Spasm or Cramp. 72S Hypo- glossus Spasm or Cramp. 729 Spasm of Muscles of I) I A P II R A G M A B I) M E N LOCAL SPASMS (Continued) Abstract of Symptoms Spasm of the neck muscles, especially the sterno-cleido-mastoid : caput obstipum (spastic wry neck), is sometimes congenital and is sometimes acquired in later life. In these cases the head is drawn toward the shoulder of the affected side and the chin is turned toward the other side and slightly elevated and the sterno-cleido-mastoid muscle can be felt to be firmly contracted. When the trapezius is the seat of the spasm the occiput is drawn backwards and turned toward the shoulder of the affected side and the edge of the muscle can be felt to be firmly contracted. Spasm of the muscles is sometimes tonic, sometimes clonic and often both. The cause of these spasms is often neurotic and often rheumatic. Rarely it is some disease of the eye or of the ear (torticollis ab oculo laeso, ab aure laesa) or of the cervical vertebrae. Usually many muscles are involved, although one or two more prominently than the others. Tonic spasm of the diaphragm, either unilateral or bilateral, occurs very rarely and produces dangerous dyspnoea. It sometimes occurs as one symptom of a general disease : tetanus, hydrophobia, hysteria, etc. Clonic contractions are common and cause hic- cough (singultus), always a distressing and at times a dangerous symptom, which occurs occasionally in brain and spinal cord lesions and frequently in irritation of the pneumogastric nerve, especially from the gastric mucous membrane. A similar but slower contraction of the diaphragm associated with facial spasm (opening of mouth) causes the act of yawning (oscedo, chasmus) which is sometimes frequently repeated as an aura of apoplexy or epilepsy and occurs also in hysteria, digestive disorders, drowsi- ness, etc. ("Tonic and clonic contractions of some or all of the abdominal mus- ■l cles occur with extreme rarity, and are usually, if not always, hysterical. Diagnosis Spinal 730 Accessory Spasm or Cramp (601). Phrenic Spasm or Cramp. rai Inter costal Spasm. Abdominal Spasm. 732 A i; M \ N D I. I <; Tonic and clonic spasms of the muscles of the arm and shoulder Brachial, 738 or of the leg, with the exception of the secondary contractures or Lumbar, due to lesions of the pyramidal tract and of the peripheral nerves, or Saiatio arc very rare They usually are due either I" deficiency of Plexus, water in the system, and often occur in disease in which much Spasm or water is lost, as cholera, diarrhoea, etc, or to hysteria, or to Cramp rheumatic factors, or are reflex. The deformity resulting in each case can be predicted from the function of the muscle involved. 153 CHART XIII Disorders of Speech and Gait Symptoms Analysed 735 DISORDERS OF SPEECH, READING AND WRITING. 736 DISORDERS OF GAIT. DIAGNOSTIC ANALYSIS OF SYMPTOMS Character of Disorder 737 ANARTHRIA (283) Inability or unwillingness to speak. No disease of vocal organs or peripheral nerves. This condition may result from a complete aphonia (260) or complete aphasia (221) or complete dysarthria (284). The diseases in which Anarthria and Dysarthria occur are set forth in Chart XIII a. 73£ DYSARTHRIA (284) Ability to express thought by speech but articulation is defective. 739 APHASIA (221) Articulation normal but expression of nor- mal thought is defective. 740 ATAXIC 741 PARALYTIC AND FLACCID 742 I'M: A LYTIC AND SPASTIC The varieties of Aphasia and the conditions under which they occur are set forth in Chart XIII b. Tin' dfaeBBM in which Disorders of Gail occur arc set forth in Chart XIII o. I :.: CHART XIII a Anarthria and Dysarthria Comprising Numbers 737 and 738 on left side of Chart and 743 to 768 on right margin 157 737 ■Result "t" ■ ! A infancy, or congen- .\ ital. A R 'I' -i, II i; A Result of disease in '"adult life. DIAGNOSTIC SI MPTOMS AM) TESTS Auditory memorii ng | May make noises bul i spoki'ii v.i ! .(■!• acquired, or were earrj lost through disease; hence innervation memories ■ i were never learned. Innervation mi ssary for spcccli ha acquired but are no) available. No hysterical symp toms. Can be t r:t i hoi 1 to speak through tl Bight. Complete absence of speech, and ren is impossible. Patient i speak hi- in communicate by gestui 'Congenital. Defective Education. 738 D Y S A R T II R I A 284, 188 Paralytic. Hysterical symptoms and etiological although nut always prominent. Apoplectic symptoms (504 I, I Vocal organs defective. normal. Vocal organs normal. The labials, the Un- guals nr i hi- vowel sounds or all nf them cannot be properly pronounc- ed. A careful ex- ■ i ion reveals a paralysis i.r a sis within the do- main of the facial, the hypoglossal or the pneumog nerve. No symptoms of any central disease. Will neit her « hisper nor speak. I Can whisper faintly but distinctly. May iniitti r but cannot artioi Words imperfectly formed, also a nasal voice. An Words imperfecta formed and usually a very limib Substitution of one letter for another. An examinai speaks the vowels correctly but has difficul 'Patient cannot whist le or close lips tightly, Tongue is not protruded straight but devi Soft palate is not raised (bilateral) or not raise Anesthesia of larynx. Paralysis of crico-thjm on lower level) and of thyreo-ary-epiglottis Immobility of one or both vocal cords from par vcrie position of cords (between extreme addi in cases of unilateral paralysis, the healthy cord n paralysed cord. Immobility of one or both vocal cords from pal cord or cords lie near the median line (extra become smaller on inspiration. Immobility of one or both vocal cords from pa arytenoid lateralis muscles) and in some CS ■ and hoarse. Cords are wide open (abduction) i May be symptoms rj n j] atera j or bilateral paralysis of the soft palate, ol l.ol central disease, n .i ■ , , i .l all the laryngeal muscles and anesthesia of larynx Slow and clumsy speech. Cerebellar gait. Speech sounds as if a force Tremor and Ataxia.- Rigidity. Spasm. Tremulous and slovenly spi ton !. letters and syllables are left out both in speaking and writing. ! Argyll-Robertson's phenol Evident mental do- I attacks may occur r terioration. [ Alcoholic history, appear ng speech. Intention Tremor. M'.n I'onous speech. Passive Tremor. Great variety of widespread Rigidity of muscles and slight fli D letters (consonants) are spoken with difficulty and are repeated many times imperfectly bi mce is arrested by a spasm of one or more of the muscles concerned in speech, such as the hy] I is directed to the speech the worse it becomes. Singing is usually not at all affected. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS Expressions of face and aclii of Expressions of face and actii • idiotic. ; normal. npossible. are possible Patient exhibits little ntelligence and hi but the most elementary education, if of any. Soils himself with urine and feces. Patient shows a good intelligence, but can exp suit of careful training. Some deaf mutes loud f Absence of facial expression and of all volu t to j tary actions. [ Facial expression and actions are abnormal. . a deep sleep and cannot be aroused to any expression of consciousness Patient is evidently insa usually either of fear i t and has delusions. When recovery has taken place it : of a divine command (delusional insanity). Anarthria i itory shows that he never had any. Incapable of any ess himself only by gestures and that only as the re- can be taught to speak, generally very imperfectly. or intelligence by stimulation of any sensory surface. ly be learned that his silence was due to ilso common in profound dementia. delu Hysterical appearance. Placid and contented. (Probably only a severe form of hysterical aphonia. It is a rare condition. Most cases Can, by hard urging, be made to whisper some words faintly but distinctly. ly. Sudden onset, usually followed by speedy death. Paralysis of motion or sensation or of both in the extremities, ation of the vocal organs shows no paralysis, but a developmental defect; such as cleft palate and similar malformations, abulary. Intelligence very defective. Paralyses, usually of the spastic variety, may be present in the extremities. t be persuaded to whisper a few n : the vocal organs shows ng certain consonants e i defects or paralysis. Patients exhibit a rather childish or affected form of speech. Some substitute "W" for "R", others use "TH" for "S", etc. In idioglossia a child substitutes others for them; thus apparently invents a new language. This speech usually becomes normal as the child grows older. ;ide, or cannot be protruded at all. lly (unilateral) in phonatii ical cords not tense in phonation and ottis immobile). ost all the laryngeal muscles. Cada- extreme abduction). In phonation, icross the median line to reach the Labials cannot be clearly spoken, especially when the paralysis is bilateral. Li'nguals cannot be clearly spoken. This difficulty is usually temporary. Nasal voice. Liquids may regurgitate through nose. Nasal voice. Indistinct articulation, which is improved when head is thrown backwards. Voice hoarse. In swallowing, larynx is not well closed; so that food enters it, causing cough, dyspnoea and possibly deglutition pneumonia. are sucked together during inspiration, giving a slight stridor. Other facial muscles are paralysed. May be evidence of injury or pressure upon hypoglossus nerve. May follow diphtheria. May follow diphtheria. 4 m 1 1 V \ — v -<. fill \-M\ p \\ \ \£ J/f & Liquids may regurgitate through nose. Tumor or lesion along course of, or in, recurrent laryngeal nerve, espe- cially lesions of the aorta or lungs. Voice very little altered. If bilateral, there is great inspiratory dyspnoea with stridor. ico-arytenoid poslerior muscle. The in) leaving narrow slit which may one or both the adductors (thyro- Is as well. Aphonia, or voice is weak part of, their course. Edges concave. here are aphonia or hoarseness and nasal speech and some dysphagia. There may be respira- tory dyspnoea and deglutition pneumonia. If both nerves are slightly affected there may be rapid and irregular cardiac action and slow and irregular respiration; if severely affected, death occurs. as in the mouth (hot potato speech) and frequently chi May'be a tumor or lesion along the recurrent nerve. May be the first symptom of an entire recurrent paralysis, or one symptom of a more general disease (bulbar paralysis, tabes, multiple sclerosis, etc.). Evidence of inflammation of the larynx. History of over use of the voice. Hysterical symptoms. of pressure upon pneumogastrie nerve. ulbar symptoms (434) with hemiplegia or paraplegia and exaggerated tendon reflexes. In pseudo-bulbar paralysis (54G, 553) the speech is also thick and indistinct. 7). History of syphilis. Lumbar puncture shows globulin and lymphocyt and steadily progressive dementia. Wassermann usually positive. pitch. Symptoms of hereditary ataxia. 'atients are restless and especially i ritable and violent, although usually amiable Apoplectiform and epileptiform r and breath. Temporary nature. Foolish pp3ech and actions. and sensory symptoms. Nystagmus, exaggerated knee-jerk, Babinski. The speech is jerky and somewhat resembles the scanning of verse. 3n of most joints. Attitude is that of bending forward. Mask-like face. Festinating gait. Speech also shows festination at times. e they are finally uttered explosively. Speech is explosive and full of repetition of certain sounds. lossus (aphthongia). There is difficulty in relaxing the muscle spasm so that words can be uttered. The same word is repeated several times before others can be spoke Idiocy, (1081). Deaf Mutism. Coma, (205, 1037). Insanity, (1041). Hysterical Mutism, (1074). Hysterical Aphonia, (750, 107-1). Apoplexy in pons or medulla. Cleft Palate, etc. Imbecility, (10SS). Lisping and Lalling and Idioglossia. Paralysis of Facial nerve, (703, 928, 1317). Paralysis of Hypoglossus nerve, (70G). Paralysis of Levator Palati. Paralysis of Superior Laryngeal Nerve. Paralysis of the entire Recurrent Laryngeal Nerve (Reeurreos Paralysis). Paralysis of Crico-Arytenoid Posterior^Nerve (Abductor or Posticus Paralysis). Hysterical Aphonia, (748). Paralysis of Pneumogastrie Nerve trunk, (704). Bulbar Paralysis, (434, 544, 546, 694, 756, 1150). Friedreich's Hereditary Ataxia, (652, 670, 687, 7S1). Paresis, (134, 177, 579, 675, 895, 1049, 1104, 1216, 1230) Alcoholism, (585, 65S, 663,673, 780,953, 1030, 1053, 1101, 1107, 1109). Multiple or Disseminated Sclerosis, (511, 5S0, 659, 668, 6SS, 756, 799, 913, 1051). Paralysis Agitans, (612, 677, 800). Stammering (Anarthria Literalis). Stuttering (Anarthria Spasmodica or articulative tics). 749a 750 CHART XIII b Amnesia and Aphasia ( 'oni|>ri.sing Numbers 7:W on left side of ( iharl and 769 to 777 on righl margin 1 59 DIAGNOSTIC A AMNESIA AND \PII.\H \ 221 to 227) None "i these conditions constitutes a disease, bu1 is rather one sj mptom of a more complex disease. Each is a form of de- mentia in the broad sense of the term and consists in a loss of general or i memories. See also Vnarthria and Dysarthria 7:;s-s Patient is capable of normal speech but ex- hibits a decided Ins.- of memory. Patient is incapable of normal speech for want of innervation memories of a Few or many spoken words. Patient is incapable of normal speech for want of auditory memories of spoken words. Patient is incapable of normal speech for want of visual memories of written or printed words. AMNESIA, ; U'.sti; I he loss of memory may not be accompanied by any, i of the names of persons is rather common ami of no or less distant past, are referred by the memory to I cerebral concussion and compression (1042-3 ! little time immediately previous to the injiin and Eri I Examination of the patient shows a loss of mei in old people and ill the insane, and i- usual] Can express ideas by gestures, but cannot name object when it is spoken to him and can often then pronou one or two weirds, or even to none (anarthria). I sei and often even when it is not. ( 'anno! const rui s- i 1 1 ii songs. When his arm is not paralysed patient Can usually read but not aloud. The condition is u Patient Tails to understand more or leSS of w li.it is said what he repeats. Cannot execute Verbal CO] and-. COnSCioUS of this mistake even when bis attention i- i Patient cannot name objects seen, or read written 01 p ('annot execute written commands, lint readih I MCU Can write from dictation imperfectly, lint noi at all AGHAPill \ Patient is incapable of normal speech from loss of innervation memories and of auditory Patient memories of spoken words. ,i I, called Patient is incapable of normal speech from loss of proper associations and of appreciation of Patient I the memories concerned in speech. exhibi I Patient is incapable of writing for want of the B< Patient B Bpeech is normal, but his writing is abnormal. J condition uncomplicated by tor aphasia. (.Patient omits words in writing, usee the wrong words, i Broca, in 1861, published a case of motor aphasia with a lesion at the base of the left inferior frontal convolution and thereby laid I Wernicke whose Btudies have contributed greatrj to the comprehension of aphasia) divided motor and sensory aphasia into threi l-t. Cortical Motor Aphasia, in which the patient i- unable to speak, write or read aloud correctly, or to speak or writ 2nd. Sub-cortical Aphasia, in which the patient can neither speak spontaneously nor from dictation nor read aloud co 3rd. Transcortical Motor Aphasia, in which the patient can neither speak nor write correctly, but can speak and write iron 1st. Cortical Sensory Aphasia, in winch the patient can speak (with paraphasia) and copy, but can neither m 2nd, Sub-cortical Sensor} Aphasia, in which the patient can speak quite perfectly, write, copy, read aloud and undei 3rd, Transcortical Sensor) Aphasia, in which the patient can speak (with paraphasia) and write (with paragraphia) i m cop Wernicke also recognizee a Conduction Aphasia, in which the patient can -peak, write and read and understand correctly, bu Mane considers all form- iii aphasia as resulting from a greater or less degree of a general intellectual impairment rather than phasia with difficulty of articulation dysarthria). Whether he is altogether right in this or not, certainly our concept - ipn.i-ia with difficulty ni articulation (anarthria oi neither of which i- probably altogethei falsi LYSIS OF SYMPTOMS 1ASIA AND AGRAPHIA T OF SYMPTOM- ill-- by very little, intellectual impairment in other resp I . in degree the loss of memory or prognostic value. "Retroacti ; iccurred in thi mmediati past, as in Korsakoff's psychosis (1100 unnesia" occurs in some i ted with fright. In it, memory is losl of those events which occurred during iaQv for recent events, imp leral failure of mental powers. Very common 1 wiili mental depression. •II oral all. Can use verbs better than nouns and proper names. Recognizee the desired word it In speaking, the patienl is frequently at a loss for a word. His vocabulary is limited often to paraphasia 775) but is often conscious of his mistake if his attention is called to it . agrammatisrnus), bul canoften repeal sequences of numbers, days, months, etc., and can write from ropy, but makes many mistakes in spontaneous writing (paragraphia t>-i| with right-sided hemiplegia in right-handed persons and vice-versa. J "" epeat what i- said to him, or if in rare cases he can do this, he dor- not understand ittcn ones In speaking, the patienl frequently uses a wrong word and is not d I., n < an write spontaneously and from copy but not from dictation. He ran read well. ■'d-. but may at times recognize and name objects which hi touches and feels, H-rl.al ones In speaking, patients rare conscious of their mistakes a copy and make man) mistakes in spontaneous writing. Cannot read what they have writ! nam.- objects nor understand words spoken to him. In speaking, patient is frequently wrong one and is then unconscious of his n a when attention is ' Hi in ,-, oi may not l»' able to read and writing is impossible or very defective. DIAGV'-I- n Is in speaking, uses the wrong word, puts words m a wrong place in the aentenci and even jargon on memories. Ili> arm and hand are nol paralysed for other movements. \ ' pp words in the -■ □ i it writing bi mes incoherent. : 1077 Motor Aphasia ti to 742 on left side of Chart and 780 to 800 on right margin Note) — In addition to the diseases mentioned in this chart, pain, whether in the joints (rheumatism, gout, arthritis, morbus coxae, etc.), or in the muscles (rheumatism, myositis, ■ tc or in the bone- (caries, etc.), or in the nerves (Bciatica, etc.) will cause a limping unit. The gait of a patienl suffering from weakened arches in the feet is very characteristic in advanced and this common disease Bhould always be though! of in anj disturbance of gail and in any painful affection of the legs or lower back. 161 DIAGNOSTIC ANALY S DIAGNOSTIC SYMPTOMS AND TESTS The disorder is of a temporary nature Patient's speech is blurred and foolish. 710 \i.i\i:i In- coordination is tlic must prominent symptom. Staggering Gait. (Reel- Disease of permanent nature. Patient Bways from side to side and lurches like a drunken man. The ataxia is almost entirely limited to walking (_ and standing. There is a strong heredity and di ea ie occurs in family groups and in youth. Nystagmus. I No heredity. Occurs al anj age. DISORDE ABSTRACT Marked men Ooours liefoi Occurs aftei optic atri Retract ion o [nooordi- nated I rail Stamping gait.) Waddling Gait. Patient does not walk like a drunken man, but throws his lens about in an awkward and excesi manner. All movements of legs are ataxic. In well marked cases legs arc raised high, II outwards and forwards excessively and brought back and down to ground with hard heel. The eyes are employed to control the movements and walking in the dark is very perfect Or impossible. Muscular atrophy and pseudo-hyper- trophy. Muscles normal. General weakness, especially of extensors High-step- r In walking patient throws body from side i" side lil weak. In rising patient pushes himself up with fa tumors. Similar walk. Congenital. Usually bilateral but ma of hip and absence of acetabulum. Bilateral. May be si ataxia in the walk. Mil DISORDERS OF GAIT. 7)1 Paralytic nine Gait (Weakness of extensors only. Bilateral. Blue line on gums. Wrist-drop as well as foot-dro] and flaccid. ' CWeaknt Variable distribution. Weakness, especially of extensors, often unilateral. Muscular atro] the most pro- minent >v '" 1 ' 1 Feel drag to walking all muscles of leg: -,,„ nvi'i ground. too weak to raise feet. No tremor or spasm. Steps short. Hysterical symp- Inabilitv to V""; I'!'"-'',',"' Both '"- -.and on one -aek of will power. or both fee. Knee-jerk may be -; increased. Ankle- clornis nsuallv clonus usually, Babinski always absent. i ine leg Unilateral. 742 (BtiaSStM. *«& Legs hi„^,J r'^' 1 w»dfre- '""- quently minent ' , ■• . remble. symptom. Tendon reflex. creased. Ankle- , and Bab inski pre i at ("Temporary condition following .linos. Organic and Permi nt condition, Organic and peripheral reflexes 1 disease. 1 Advanced Age, atheromatous aj teries Loss of memo Legs can be moved freely and normally when lyii walk or has forgotten how to walk The weak leg is drawn along after the strong oni Strength in leg than would be necessary for wa I Sclmllor's side gait I. The weak leg is usually Swung forwards and oiit\ leu is usually strongly extended at the face and laterally) along a line the patient moves well bo The lens are rigid and offer resistance to forwar. walking, bodj and -boulders .nils, often be !»■ legs forwards. Legs frequentl} show tremblin forward. Thighs are adiiucleii BO that knees a ! in walking (scissors gait). Pernici of severe, anemia maj be present, i rigidity. Patient is slightly bent forward and all bis joints slightly Hexed. enq to Staggci backwards l':i> sivc . rumor Fes tin 5 OF SYMPTOMS OF GAIT SYMPTOMS disorder and history of alcoholic abuse. Aberty. Krfee-jerka usually present. Contracture and deformity of feet. Babinski present. jberty but in youth. Knee-jerks usually present and exaggerated. Oculo-motor paralysis and •ml, cerebellar fits and other cerebellar symptoms may be present. f Knee-jerks abolished. Argyll-Robertson's phen imenon, optic atrophy. History of syphilis usually. A common disi Knee-jerks are usually present. May be no other symptoms than ataxia and anesthesia, or may bo all the spinal symptoms of locomotor ataxia but none of the crania , especially no eye symptoms, A rare disease. i duck. Marked lordosis. Atrophy of some muscles, apparent hypertrophy of others, but all are .anil- and crawls up his own legs. A similar gait is Been al times in pregnancy and in abdominal DIAGNOSIS Alcoholic Intoxication (658, 663, 780 673, 764 . Friederich's or Hereditary Ataxia 781 (652, urn 687, 762 Marie'- or Hereditary, Cerebellar 782 Ataxia 651 rebellumoritBtractE (609-10. tils 686, 1016, 1272 661, 766, 827 894, 979, 784 'is;, nmt. 1217, 1231 24-7. Lesions of p isterior columns of 786 spinal cord (654a, 1347, 1350-1, Muscular Dystrophi L152). 786 teral. No change in the muscles. Hip joints unusually mobile X-ray shows dislocation lar weakness, tenderi and atrophy Knee-jerks absent. Man] sensory symptoms. if colic and of exp '-'in- in lead. without tenderness Electrical reaction of degeneration. No sensory symptoms Sexes normal. No sensory paralysis ! lost . Sensory paralysis Patients, even with crutches, are rarely able to walk in this in. I mental impairment. Reflexes normal or increased. •r sitting Patient apparently makes no effort to walk. Legs collapse. Apparently is afraid to ntal Dislocation of the 786a Hip. Multiple Neuritis 188, 662, 823, 7s7 1008, 1117. 1307 . Lead Palsy 194, 1050 , 7ss Acute Anterior Poliomyelitis 1 195, 789 11 Is. I Weakness 671 790 Myelitis or Myelomalacia in 7"* • 1 lumbar enlargement of cord is". 825 Senile Parapli gi 522). 791a i and Vbasia 287 653 792 aslvai - beyond it. In some action- when taken unawares the patient shows more g. In walking sideways stepping laterally) along a line patient moves badly in each direction 1 Hemiplegia legia 1 1074 it the normal leg as > pivot and i- set down in advance of tin- latter (mowing gait The • whole side of the body i- rigid and swings forward as a whole In walking sideways stepping il.- the paralysed Bide, but badlj towards the healthy Bide (8chuller , « side gait), Organic reflexes are disordered, and sensor] symptoms are present, No Aramenl ' o t b- t in Organic reflexes maj or may not be disordered, sensor] symptoms r-kwards to' pull lien brought u-ld tiuhl togcthei ■ ,. iii n f Organic reflexes no di Bj mpi (■At ■ \diilt mill. Scissors < hut. Intention tremor, marked ataxi i. at times staggeriE ■n md prop ni i' ever increasii ipul lion ■ tend- jplegia or Monop- 794 plexy, < 'erebral or Spinal. Tumor 01 Myelitis or Myelomalacia above 796 lumbar enlargement, including Compression Mvelitts (517-20, J 1-7 includ- 797 ing Vmyotrophii i ■ 17 Cerab lllls 1170,1187, i or M iltipl Sclerosis (511 580 688, I CHART XIV Disorders of Sensation DIAGNOSTIC ANALYSIS OF SYMPTOMS DISORDERS OF GENERAL SENSATION AND OF THE SPECIAL SENSES Symptom Analysed Alterations in Sensation '810 Mil Disorders of Sensation. (See also Perversion of Sensa- tion (.'hart 805 Diminution of Sensation. 806 Exaggeration of Sensation. 807 Disturbances of Vision. SOS I •isturlianccs of Beating. 809 Anesthesia and Analgesia. 811 Dissociation of Sensation. 812 . Loss of Muscle Sense. 813 Hyperesthesia. fS14 Perversion. 815 Limitation of field of vision. . 816 Double vision. 817 Conjugate Deviation of Eyeballs. 818 Pupillary Abnormalities. 819 < >!>litimlinoscopic Exami- nation. . See Chart XIV a. See Chart XIV b. tSee Chart XIV <■. See Chart XIV .1. f820 Deafness (anakusia). 821 Hyperakusia (oxyakoia) or See Chart XIV .-. Disturbances of Taste and Smell. I Parakusia. 163 CHART XIV a Disorders of Sensation < lomprising Numbers 806 to 812 on left side of chart and 822 to 841 on righl margin I US DIAGNOSTIC SYMPTOMS AND TESTS ■Tendon reflexes diminished or absent i lesion of peripheral sensory neurons — 472). SOS DIMINUTION OF CUTANEOUS SENSIBILITY (345 . Sill \\l VI 'llKSIA\"usu:illv n.m- bitoed with Borne ANALGESIA and THERMIC ANESTHE- Sl \. especially in severe cases of the disease (348^0). (Figs. ■Ji;, 33). Organic reflexes normal (300). (Figs. 24-6). Organic reflexes disordered (300) (Figs. 21-7 Organic reflexes disordered: it may I ni\ slightly (300). (Figs. 19-30.) I 'I'll. Tendon reflexes normal or ex- aggerated in arms or legs ■ or both (lesion of central sensory neurons — 473). f Ass, mi il Organic reflexes usually normal very rarely disor- dered (300). Tendon reflexes absent in arms; exaggerated in legs. Lesion both of peripheral and of central Bensorj neurons. < trganic slightly (300). reflexes lisordered Ml ANALGESIA and THERMIC ANESTHESIA with little or no TACTILE ANESTHES1 \ DISSOCIATION OI SEN- SATION (365). BIO AKINES1 III -I \ Tendon reflexes usually exag- gerated in legs I 173). < trgamc - relieves little 01 not al a] disordered (300). Arms affected. Leg affected. A hyst ton I'M \ NUMBNESS. 806 EX UJGERATIONOl < i TANEOUS SENSIBIL1 I 5 Motor paralysis and hyper opposite sale of i he bod) Loss of muscle sense is usually associated with ataxia and an pai ietal cortex. Unilateral numbness of hand and foot, steadily progressive, Bilateral Dumbness i- of no diagnostic importance It may Hyperesthesia and hyperalgesia ari myelitis. if little or no diagnostii DIAGNOSTIC ANALYSIS OF SYMPTOMS ANESTHESIA AND ANALGESIA ABSTRACT OF SYMPTOMS esthesia corresponds to the distribution of a nerve or to that of one of its branches, though usually less extensive. In case of spinal nerves there is also a paralysis of motion, is pronounced, in the distribution of the nerve (Figs. 33-38). esia, pain and muscular paralysis, tenderness and atrophy widespread and symmetrical in the distribution of spinal nerves. Usually a history of alcoholic abuse. esthesia corresponds to the distribution of a nerve root, but is less extensive. Central symptoms often present (Figs. 33-38). ted with flaccid paralysis, muscular atrophy and trophic disturba iling. Incontinence of feces. Bedsores. legs. Bladder empty and j Symptoms bilateral. Acute or sub-acute. [_ Symptoms mainly unilateral, at least at first. Very slow progressive course. tor paralysis, but marked ataxia and loss of muscle sense. Romberg's symptom, Argyll-Robertson's pupil. Tabetic cuirass. Retardation of conduction of pain. Optic atrophy ent. Ulnar hypesthesia and paresthesiae. ted with spastic paralysis, without muscular atrophy, ii il anesthesia bounded above by a zone of hyperesthesia. and legs, or in legs alone. Bi- f S P astic Paralysis in both arms and legs, (Spastic paralysis in both legs. ted with paralysis of cranial nerves, ataxia, symptoms unilateral, at least in early stages, dysarthria and dysphagia. tor paralysis, anesthesia limited to anal and genital region and vicinity. Incontinence of urine and fece3. Impotence. Reflexes in legs Priapism. Disturbances of respiration. ted with .ymptoms ted with :al symp- 25). nly irri- ( Motor spasm {retraction of neck and opisthotonus) and convulsions. Acute onset with fever. Kernig's sign. Lumbar ( puncture shows globulin and increase of cellular elements in cerebro-spinal fluid. Herpes facialis. Motor paralysis, which may be temporary. Often hemianopia. Usually ataxia and loss of muscle sense. Cerebral symptoms. Post-hemiplegic motor disorders. Symptoms unilateral. Mainly para- f Acute onset. I lytic. J ^Chronic onset. Symptoms usually unilateral. Anesthesia usually in form of hemianesthesia, which may be transferred in some cases. Anesthesia often bounded by a prominent Hysterical Anesthesia (1074). anatomical landmark. The anesthesia is usually unknown to the patient and is discovered upon physical examination, but when discovered is usually more com- plete than that present in cases of organic disease. The anesthesia is not real. The patient can button clothes, etc., with anesthetic hands without looking. No evidence of any organic disease. Usually motor paralysis. Convulsions, local or general. Jacksonian epilepsy (587, inertia and impairment. Choked disc or optic neuritis. DIAGNOSIS Neuritis or Nerve Injury (489, 492, 941, 1146-7, 1173, 1301-7). Multiple Neuritis (4SS, 662, 787, 1008, 1147, 1307). Lesion of Posterior Nerve Root or of Spinal Segment (1302). Myelitis or Myelomalacia in Lumbar Enlargement (4S5, 791, 1309). Tumor in Lumbar Enlargement (486, 1309). Tabes. Locomotor Ataxia (661, 753, 784, 894, 979, 937, 1004, 1217, 1231). Myelitis or Myelomalacia in Upper Cervical Region (513-4). Myelitis or Myelomalacia in Dorsal Region (517-8). Lesion in Brain Stem (535, 653). Lesion of conus terminalis of Spinal Cord. Cerebral Meningitis (508, 590, 60S, 1032, 1045, 120S-9, 1228-9). Cerebral Hemorrhage or Softening (504, 5SS, S32, 856-7, 1043, 1060-4). Cerebral Tumor (507, 536-42, 578, 587, 833, S49, 855, 861, 892, 90S, 960, 1047). 824 S25 830 830a 831 832 833 834 ted with flaccid paralysis and muscular atrophy in arms, with spastic paralysis in legs. Bladder /Symptoms bilateral and acute or sub-acute, ided and dribbling. Constipation. Pupils are unequal often. ^Symptoms mainly unilateral, at least at first. Very slow progressive course. nd paresthesiae : mds and arms chronic course. arms and hands are _ prominent symptoms. Motor weakness and tremor of arms. Muscular atrophy, with fibrillation late stages. Scoliosis and kyphosis in neck and upper dorsal region. Spastic symptoms in legs. Organic reflexes normal. tabetic-like) and paresthesiae in legs and feet. Le<*s exhibit a steadily f Reflexea increased spasm predominates over paralysis in early stage. Babinski usually on both sides, but in ising paralysis, which may he unilateral in the ,-arlv stage.. Organic J unecmal de S ree - Organic reflexes slightly disordered. es are more or less disordered. Chronic or sub-acute course. , t> n i u r u i t ■ r * u ■ i ^ -a i i n j- j j (.Reflexes early abolished. Tropic disturbances in legs. Organic reflexes early and greatly disordered. lesia on one side of the body and extremities; analgesia and thermic anesthesia and at times also tactile anesthesia on the Much girdle pain and spinal epilepsy are com- ul extremities. mon symptoms. Myelitis or Myelomalacia in Cervical Enlargement (549-50, 1310). 835 Tumor in Cervical Enlargement (551, 1310). 836 Syringomyelia or Morvan's Disease (cervical type) (552, 693, 1009, S37 1150a, 1170, 1187, 1357-9). (Figs. 24-7.) Syringomyelia or Central Gliosis in Dorsal Region. (552). 838 Syringomyelia in Lumbar Enlargement. (552). 839 Brown-Sequard Paralysis (442, 509, 981). (Figs. 24-8.) 840 hesia. It i multiple neuritis, tabes, i lesions of posterior columns of spinal cord, of brain stem, of posterior third of posterior limb of internal capsule and of the or in such cases, due, with the exception of the zone of hyperesthesia, limiting above the anesthesia in transverse myelitis or myelomalacia. In such cases it marks the upper limit of the h slowly progressive mental dulness is suggestive of cerebral tumor. So much so that "choked disc" and other symptoms of cerebral tumor should be i either of nervous, or of vascular, origin. CHART XIV b Disturbances of Vision Comprising Numbers 807, 814, 815 on left side of < Jharl unci M'J to 866 on right margin DIAGNOSTIC SYMPTOMS WD fESTS DIAGNOSTIC ANALY DISTURBANCE ABSTRACTS i' 814 l-i.i:\ ERSION 307 DISTURBAV OF VISION 815 ABSENCE OB LIMITATION OF FIELD OF VISION (368 to 364). \ yellow color of .'ill objects seen irrespective of thru- true color: xanthopsia (yello A red color (erythropsia) of all objects seen irrespective of their true coloi red vi A green color of all objects seen irrespective of their true color (green vision). Muscae volitantes, twisted threads and irregular spots moving about in Geld of v j Flashes of light and dark spots surrounded by a bright zone (glittering jcotomata Achromatopsia (364) and heinichromatopsia occur in slight lesions of the geniculate An inversion (red having a larger field than the blue — 14) and an interlacing, of the color fields (Dyschromatopsia). Blindness (358, r Bilateral. 1318). No lesion -\ TT •■ . , -mlI uu Unilateral within orbit Bilateral. Homonymous Tetartanopia or Quadrant Hemianopia. ("Hysterical symptoms (425) arc present. | Choked disc and other symptoms of br I creased intra-cranial pressure is relie No lesion in eye. Pupillary reflexes not No lesion in eye. Optic neuritis may b No lesion in eye. No optic neuritis. 1 k shown that the blindness is not real. No hemiopic pupillarj reflex. No hen or other paralysis. May or may not disc. Very rarely occurs in lesions of or optic fasciculus of opposite side No hemianesthesia. N »^XS Homonymous hemianopia (14, 362, 1321). May very rarely be bilateral, due to double lesion. Bitemporal hemianopia (362, L319). Nasal hemianopia 362, 1320). Horizontal hemianopia. Bomonymous seotomata, Hemianesthesia. May or may not be a hemiplegia. pupillary reflex. Paralysis of mote :il>duccn> ner\ e or both. Slow onset, progressive course, terminal in complete blindness. Choked disc pupillary reflex. Occurs in lesions of the retina, or of opt, These may occur as the result of small neighborhood of the calcarine fissure. ("Increased tension of eyeball. Excavati t'upph Concentric limitation of field of vision, J N ? ««™wed ***** of eye- On ophl even to complete blindness. Hysterical symptoms (425) are present Symptoms of tabes are present, esp no ataxia. History of Syphilis. ' [lob OF SYMPTOMS DF VISION rMPTOMS poo d especially when eyes arc turned towards a bright light, iddenly appearing and disappearing in the field of vision, lies, of the optic fasciculus and especially of the calearine cortex. ire present I'h ilor lield becomes normal after the in- < Pushing.) I remic amaurosis may be in this class (edema). Pupillary relic Uary reflexes normal. Hysterical symptoms. By tests it may be luadrant of each field of vision. i I Lowei In u'li field of i DIAGNOSIS Jaundice, or Santonin, Arayl Nitrite, Cannabis 842 Indica or Picric Acid Poisoning. Neurasthenia, Hysteria, great emotional excitement 343 and after cataract operations; also after the eye has been exposed for a long time to an electric or other bright light (snow-blindness). Diseases of optic nerve and retina and after cataract 844 operations. Neurasthenia, circulatory disturbances in'brain and 845 digestive disturbances. Migraine, and Aura of Epilepsy, and circulatorv 846 disturbances in brain. Achromatopsia Hysteria (1074). Cerebral Tumor (833). Lesion or edema of both occipital lobes. Lesion of optic nerve or chiasm. Hysterical Amblyopia 847 848 849 B60 851 851a Lesion of lower lip fissure. 852 Lesion of upper Up of contralateral calearine fissure. I Sudden onset and of -hort duration. Often more | marked in, or limited to, one eye. No other syuip- '•xcept nervousness. Circulatory disturb Choked disc. Slow onset. Progressive course of the ' disease. No choked disc. Rapid onset. Permanent) not pro- hows a regr ess ive - No hemiopio pupillary reflex. No choked disc. Re- gressive course. miopia mil or •' N ■ . No ohoked disc Rapid onset. Symptoms of menin- l gitis may be present. 1 involving their upper or lower p ■ 'IIS ill tfa Aura of migraine. 854 Tumor involving median surf:. occipital lobe or fasciculus of Grate Hemorrhage or softening in or near contralateral cal carin ciculus of < Irat orrhage or softening in the posterior pari ol terior limb of contralateral internal capsule. Tumor involving contralateral optic tract or geni ulate bodies Neuritiaor lesion of contralateral optia tract [898 Tumor oompi tral part of (8!>l\ I pituitary.) Tumor compressing homolateral outer part of optic sci 392, i I !0 I >|ila Horn i tnd final atrophy ptic nerve. Pupi aid mutual , i MS), '"-'"I' > aniin ition ti ptic papilla ihowa itrophy. Optio atrophy. 864 ■gvii-i; h.'m ' - in' i phenomenon and ibseno eof reflex and lymphooytosia In cerebro-apinaJ fluid. Little or CHART XIV c Disturbances of Vision DIAGNOSTIC ANALYSIS OF SYMPTOMS Character of the Diplopia Secondary Deviation of Sound Eye (29) Inward. 807 l> I S I I K B \ I l. I v 1 s I N S16 Double ■. iaion. Diplo- pia (Fig. 18) The images separate and come together again when the eye- lolls are from one side to the other, or upward or down- ward and back again. Displace- ment of Visual Axis (28) Inward. Strabis- mus convergens. Outward. Outward. Stra- bismus diver- gens. Limita- tion Outward. Inward. Graphic Represen- tation op the Diplopia. Broken Line is the False Image Upward. Down- ward Down- ward and inward. Upward and inward. The A together eyeball* are i ur I. 1 low nward. Strabismus deorsum ver- gens, slightly divergens. Upward. Stra- bismus sursum vergens, slightly divergens. None or slightly upward and in- ward. Strabis- mus sursum ver- gens, slight ly convergens. None or slight ly downward and inward. Stra- bismus deorsum vergens, slightly convergens. May be variable. Position of False Image (See 28) On the same side as the affected eye. On the oppo- site side to the affected eye. Upward Above and on and opposite side somewhat to the affect- inward, ed eye, image tilted top in- ward. Down- Below and on ward and opposite side somewhat to the affect- inward, ed eye, image tilted top out- ward. Rotation Below and on downward same side as and the affected somewhal eye, image outward, tilted top in- ward. Rotation Above and on upward same side as and the affected hat eye. image outward, tilted topout- ward. FUt. ii The limitation of motion and the ] of the I ! ! he reverse of those in paralyeis. There may be present irritation, especially in t be nose or teeth, which wonl.l cause a reflex spasm. The spasm is usually more transient tl are MM internal rectus and the inferior oblique. a u u a I k 1 i I >i 1 I e 1 K i <> i Diagnosis Ex- 870 ternal Rectus. In- 871 lernal Ueci us. Su- 872 perior P Rectus. A H A L Y S I S Y In- 873 ferior Rectuv Su- 874 perior Ob- lique. fa- ST. - . ferior Ob- lique. The whole eyeball can he seel, to he displaced. r/No changes visible in eye. Hysterical sympti represent. "Two openli en in pupil. MONO- Cl LAB ill eve Spasm of the B7fl ooular n. Displaoemenl ^77 ol eyeball. ioal ->7^ diplopia. Double pupd- B78 By oblique illumination the lens can be Cataract. teen to be opaque in p Examination show- dislocation of lens. Dislocation sxi Examination shows astigmatism and an irregular contour of the cornea. Dislocation of lens, [rregularit B17 i onjugate deviation • l » ith oiler m m.jr the anterioi 883 Deviat in I u i llj do pn snt portion of the pons (otphs when the eyeballi are at rest. A vertical deviation I) to the abduoens du itcil with a lesion "t the corpora clous, involving pos terior quadrigemin i I w it h other symptoms ol ol ill.- b i tl.e longitudinal bundle. aj 884 part of brain, espsoially, In ■ r part of frontal loin' e lesion In cortex. CHART XIV d Abnormalities of Pupil and Optic Papilla Comprising Numbers 818, 819, 890, 891, 897 and 898 on left ride of ( 'hart and 890 to 914 on right margin 171 DIAGNOSTIC ANA J Ms ABNORMALITY OF PUPIL 819 U3NORM \l.l I 5 "I PAPILLA Result of i tphthalmoscopii I lamination. DIAGNOSTIC SYMPTOMS \NI> TESTS Disordered pupillary reflex to light and accommodation (330-1). Mydriasis, myosis or unequal pupils (339-41), Sill I The hemiopic pupillary reflex [26). 891 The Argyll- Robertson phenomenon (447). Bitemporal bemianopia (362, 1319). Homonyi is hemianopia (362, L321). History of syphilis. Lymphocj toai in cerebrospinal fluid. Positive Wassermann. 897 i Iptic neuritis. Choked disc. Bilateral trophj . i oilateral Bilateral. I Inilatera PUPILLARY ABNORMALITIES A ABSTP. k.CT OF S These phenomena oocui in to< Their significance ha b< ( 'linked disc. Symptoms prof i M'tcu hemiplegia oi pararj - history oi syphilis \ erj rai Vtaxia. Absence of knee-jerk. -j Menial impairment. Blurred 6 I Rarely occurs. No ataxia Kn Albumen and easts in urine. Sugar in urine and in bl I Retinit i \ arked symp- toms nf cerebral disease. No retinitis Marked cerebral symptoms. Lead in urine. Examination of the blood ■hows a condition of severe anemia. I line and blood norm d I Well marked history of traiiinatis in. rea ed size of head, and fonti Retraction of head. Cerebro-ap General eonvidsieu of Jai lepsy is common. Maj be paralysis, Reflexes usual! creased. Local inflammation can usually be made out by examining thi i rai Secondary. tt may be the terminal stage of a neuritis and Traces of the active inflammation (old hemorr ' Old age I sually at heromatous arteries and liiu Primary. No signs | LoBS ** kn oe-J erk ' Myosis. Lightning pains. "i a former inflam- Unequal pupils, [mpairment of speech. Tremo matioti. , .. , r , I liildislmess. 1 lharacteristic tremor or other symptom ol thU Local inflammation or lesion can usually be made out on careful exam SIS OF SYMPTOMS I OPTIC NEURITIS AND ATROPHY PTOM8 Iny conditions to be of much diagnostic importance based in < Jhart Vl>. Ire, terminating in blindness. Often associated with acromegaly. ■nuii.-il nerves, Optic neuritis or symptoms of meningitis. At times a d quadrant hemianopia in partial lesions of the geniculate bo lies. Ightning pains. ( lirdle sensation and tabetic cuirass. •Ii. Apraxia. Restlessness. Childishness. Uncontrollable. rks present. Maj be no mental impairment. Normal speech. No apraxia. Headaches, especially in i ning. Usually edema of some part of body. Dyspi a on exertion and loss of strength. Progressive emaciation and lose of strength. Greal Hurst and polyuria. Large appetite. Dry akin. Blue line on gums. Kistorj of lead colic. Wrist-drop. History of exposure to lead poison. Dyspj ■< on exertion and progressive weakni Palloi of skin :iik1 mucous membi DIAGNOSIS Tumor compressing the optic chiasm 851, B60-1 892 1319-20 - Lesion of contralateral optic tracl or geniculate 898 bodies 868-9, 1321 . Tabes (661, 827 Figs _M-7. v.u 110 1 gag Syphilis (1206). 8 96 Bright's Disease. 899 Diabetes Mellitus 1 1 175). , ;kx) Lead Poisoning 1 194, 576 584, 788, 988, 1060 . 901 Anemia '>r Leukemia. 902 of syphilis. Argyll-Robertson's pupillary reflex. Lympho oytoau in cerebrc-epinal fluid. Positive wassermann. « hich the nerve 1 1 - * ~ been injured I 'sim ■j and sutures r » j ..-11 in the young, tymphi irer. Dmplicated with facial paralysis. a. 11 nun noi l„- fever. \t times a latent period Primary ?uppu«tion .nil or elsewhere. < (ptic 1 litis present in about 53' of ca No fever I sualrj steady progre ion I Iptii 1 iiriti present in about mi', ol all cases; almost invarial in tumors in the posterior fossa. Tumors in pituitan gland, corpus oallosum and in the central convolutions, especiallj extra-cerebral ti often show no optic neuritis. Syphilis (1206). 903 Injury. . IIM Hydrocephalus 960 90S Meningitis (590, 608) 906 Cerebral Uwcess or Sinus Thrombosis ■>n: < larebral Tumor (507, 578 908 '' follow anj "I the causes ol neuri , 1 above, s and exudates, etc can luniallj bi (<■ri.il tonsion. der diatui Mental impairment 1:. tl< m duuaaonab bi m tdi out roful examination 1,111 1 • " al ' ige ..1 1 Iptii Neurit! 86 ■ Senile 1 Iptio Itrophy. 1 1 mi 668 .'I III. I Mil, II 910 •hi 912 •11 I 91 1 CHART XIV e Abnormalities of Hearing, Taste, and Smell DIAGNOSTIC ANALYSIS OF SYMPTOMS Diagnostic Symptoms and Tests 808 D I S R D E R S F H E A R I N <; f820 D E A F N E S S A N A K U S I A (355) -Usually unilat- eral. •w May be bilat- R eral. A " D perma- S nent .symp- A tom. N. D Bone con- No due- facia tion paral- im- ysis. paired. Abstract of Symptoms Severe paroxysmal vertigo and tinnitus aurium. No vertigo. May be heredity. Locomotor ataxia or dissemi- nated sclerosis may be present. Bone con- duc- tion not im- paired Maybe fMay be history of syphilis, asso- symptoms of meningitis, symp- ciated with facial paral- ysis. I to n is of tumor at base, optic < neuritis, etc. I Disease of, or injury to, middle [or outer ear; cerumen. Usually bilateral. Very rarely unilateral, and then only a transitory symptom. C Associated with symptoms of lesion of the pons 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. No symptom WORDS ONLY. Sensory aphasia (222) is present. Hysterical symptoms (425). of organic disease. 821 HYPERA- KUSIA, OXYAKOLA OB PAB \- Ki BIA ByBterical symptoms are present. Diagnosis Meniere's or 918 Labyrinth disease (650, 685, 1019). Atrophy of aud- 919 itory nerve. Tumor or inflam- 920 mation involving auditory nerve trunk. Lesion of ear. Bilateral lesion of the lemniscus. (Fig. 20.) Lesion of the temporal cortex on both sides. (Fig. 15.) ByBterical deaf- 1074). 921 922 923 92 1 Lesion of left 926 superior temporal eon volution. (Fig. 15.) Hysteria (1074). 926 927 Inflammatory lesions of ear or its neighborhood are Hyperemia of present. inner ear. Facial paralysis is present. Low notes are especially Facial paralysi painful. Tinnitus aurium is present. (1317) B09 DISORDERS Very little, if any. diagnostic significance can be attached OF SMELL to disturbances of smell and taste WI) TASTE. 173 CHART XV Perversion of Sensation: Pain and Vertigo Symptoms Analysed f931 PAIN (330). 930 PERVERSION SENSATION IX XKKVOUS DISK ASKS (306). DIAGNOSTIC ANALYSIS OF SYMPTOMS DISORDERS OF SENSATION— PERVERSION Location of Pain 933 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, iritis, muscular insufficiencies and other diseases of the eye, of the nose and its sinuses, of the teeth, of the ear, of the scalp (rheumatism), or of the cranial bones (periostitis, eariee). 935 PAIN IX TRUNK IX 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, perio- stitis cancer and other tlimOTS, colic (intestinal, uterine, biliary, renal) dyspepsia, pancreatitis, appendicitis, peritonitis, gastric ulcer, gastritis, enteritis, hernia. Boating kidney, tubal p nancy, pelvic inflammation, intestinal obstruc- tion, etc. 986 PAIN i\ EXTREMITI] - LN M RVOUS DISEAS1 After a careful examination has proved the ab- sence nt' any disease of the bones, mu joint-. Iiliinil vessels Or -km of the arms and I Ia1 font mUSl lie excluded. See Chart XV a. See Chart XV b. 932 VKRTKio See Chart \\ i . See Chart XV ,1. 17.5 CHART XV a Pain in Nerve, Pain in the Head, Headache < lomprising Numbers 933 and 934 on the left side of ( 'hart and 937 to 966 <>n the rijiht margin ::; DIAGNOSTIC SYMPTOMS AND TESTS 933 The differential diagnosis be- P tween neuritis and neuralgia A cannot always be made clin- I ically. The diagnosis is aided N by the experience that certain nerves, such as the sciatic, are I more prone to neuritis; while N others, such as the trigeminal, are more prone to neuralgia. N (Figs. 33, 38). 'A history of neurotic heredity or other evi- dence of a neuro- pathic predisposition, congenital or ac- quired, is" 7 common. Pain is unilateral and is increased by move- ment and by expo- sure to cold or wind, a n d is sometimes associated with mus- cle spasm. Vaso- motor and trophic disturbances are often present. rParoxysmal pain with free intervals. I Continuous pain with exacerbations. fPain limited to the whole or a portion of the trunk and distribu- tion of the trigeminal o r occipital nerves. Diseases of the eye, the nose and its sinu- ses, the teeth, the ear, the scalp and the bones must first be excluded. (For the diagnosis be- tween neuritis and neu- ralgia see 933.) Pain strictly limited to one-half the head. Never any motor paralysis or persis- tent anesthesia or loss of reflexes. May be motor paralysis or anesthesia or loss of reflexes or all combined. May be some v. of the hair. or neurastheni May be both vi disturbances a the electrical tion. General 'The pain is felt above the eye in the forehead, in the ten If tension of eyeball be increased, examine eye for glauc The pain is felt below the eye in the cheek and side of nc The pain is felt in the lower jaw and its teeth and gums : The pain is felt in two or three of the situations describe! The pain is momentary in duration and is associated wit] The pain is felt in the occipital region running up along oi and early symptom in neurasthenia and nervous breaki Periodical attacks (often occuring at menstrual epoch) of crania angio-paralytica) or pallor and dilated pupils (h there are vomiting and nausea. The disease usually e< Pain as if nail was being driven through the skull. Pain of great intensity in a small spot anywhen Pain, nocturnal, small area spreading. Pain localized in ..small area. Evidence of poisoning. Evidence of circula- tory disorder. Evidence of nervous exhaustion History or other evi- dence of syphilis. Disease exists in organs within the head or body. Exogenetic. » Auto-genetic. Cerebral hyperemia. i Cerebral anemia Evidence of brain disease. Chronic headache. Pain constant with exacerbations. PYREXIA. Evidence of infect ion. Headache. HYPER- PYREXIA..^ Evidence of exposure to high temperature. Pain may be felt at any time but is worse in evening or i Cranium is often tender at points. Pain may be due t \ Frontal headache may be due to gastric dyspepsia and co to pelvic disease. These referred pains are associated v f Occurs after the ingestion of narcotics. Does not come on [ Occurs as the result of breathing for hours foul air in unve Occurs as the result of constipation, especially where the t Occurs in Bright's disease, usually is worse when patient I Headache with fulness and throbbing in head, aggrava aches may be followed by a cerebral hemorrhage. Hoa< Headache, most commonly at vertex, with fainting. Dai In this as in other forms of headache several etiologica Headache associated with phobias and tremors and insomnia and other symptoms i pressure within the skull, especially pressure in occipital and cervical region. Hi Progressive symptoms, motor or sensory or both, first of i cussion over the seat of the lesion. Lumbar puncture si Intractable, incurable, more or less constant headaches. I stretching of the dura mater by tumor, hydrocephalus, < Diffuse pain and tenderness of scalp. Pain on movement f Temporary. Occurs during the first few days or first \ [ Occurs throughout the disease and is a, [Permanent. \ [ Suppuration elsewhere in head or bod} History of exposure to high temperature. Headache oft Optic neuritis or choked disc. May follow trauma- tism. Evidences of rheuma- tism elsewhere. DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS trophic disturbances, except rarely a slow blanching Certain points on the -motor but -- ver any electrical reaction of degeneration. Patient usually anemic lerve are usually tender (points of Valleix). Frequently the parts supplied by the nerve are hyperesthetic and local spasms occur. The neuralgia may be only one symptom of a more general disease (symptomatic neuralgia) or independent of any other disease (idiopathic neuralgia). -motor and trophic there may also be iction of degenera- jalth usually good. j and i Nerve neither swollen nor tender. f A tumor may be felt or rarely seen with X-ray on nerve. I with X-ray near, and compressing, the nerve. A tumor or a displaced bone or other substance may be felt i Rash of herpes limited to distribution of nerve. Nerve wherever it can be felt is swollen and tender. There may be an inflammatory focus near to and involving the nerve, back as the vertex. It is most severe along the nerve trunk but extends also beyond it and on each side. The tender point is at the supra-orbital notch. The eyeball may be painful and tender. and radiates into the teeth of the upper jaw. The tender point is at the infra-orbital foramen. I in the side of tongue, in the ear and in the temporal region The tender points are at the mental foramen and in the temple. bove. clonic or a series of clonic spasms of a facial muscle. side of the scalp to the vertex. The neck is stiff. The tender points are behind the mastoid process, behind the middle of the sterno-cleido-mastoid muscle and on the parietal eminence. This is a common n. In many cases the pain is dull and is a sense of strong pressure rather than pain. v -ere pain, sometimes on one side, sometimes on the other side of the cranium. Skin is very hyperalgesic and vaso-motor disturbances, either in the form of flushing, sweating and contracted pupils (hemi- crania angio-spastica) are often present. Often ushered in by visual hallucinations in the form of flashes of light, etc., or by paralytic phenomena, such as hemianopia. Towards the end of the attack nences in early life, ceases in old age and often shows a direct inheritance. "Symptomatic" migraine is not infrequent in tabes, paresis, brain tumor and epilepsy. n scalp with the feeling as if a nail was being driven through the skull at this point. This region is tender. Hysterical symptoms (425) are present. Neuroma, (491). Compression Neuritis. Herpetic Neuritis. Neuritis, (489, 492, 822). Supra-orbital Neuralgia or Neuritis. Infra-orbital Neuralgia or Neuritis Infra-maxillary Neuralgia or Neuritis. ] Trigeminal Neuralgia or Neuritis. J Tic Douloureux (602). Occipital Neuralgia or Neuritis. Migraine or Hemicrania. Idiopathic and symptomatic, (846, 854, 1028). Clavus. Hysteria, (1074). 942 J, Trigeminal 944 Neuralgia or Pros- 945 it, or occurs only at night, i icriostitis. Lumbar punctu: • in the early morning hou i may show lymphocytosis It follows ■ positive Was; distribution but is felt over a small area and extends ( Optic neuritis may be present. ■ a wider and wider circle. Argyll-Robertson's phenomenon is frequent. Syphilitic Neuralgia (meningitis ipation, as well as to disease of the eye or caries of teeth. Occipital headache and temporal headache may be due to disease of the eye, teeth, pharynx i hyperalgesia of skin of same region, which may be as constant and important a symptom as is the pain. The pain of eye strain grows worse towards miediately, often not till the next day. lated rooms, especially if patient is accustomed to pure air. Transitory. els usually act freely. This headache is usually most marked in the frontal region. t wakes up in the morning. Urine is usually scanty and contains albumen and casts. Edema and gastric disturbances ; • ear. Vertex headache may be due to anemia i ening, or follows reading. by cough. The congestion may be active (after taking amyl nitrite) or passive (heart disease). Vertigo and vomiting may be present. High arterial t •lies occurring at the time of puberty or of menstruation may well be congestive. retinit's is often present. Tinnitus aurium. A series of such head- ess before eyes. Cold hands and feet. Cardiac t actors may be present. ■ arterial disease present. A series of such headaches may be followed by a cerebral thrombosis. The headache may be relieved by the recumbent posture. neurasthenia. Pain grows less towards evening and is usually felt in the occiput or vertex. Feeling as if a tight band or cap were upon the head (casque neurasthenique). Often a sense of fulness and aches resulting from overstrain (mental or physical, especially eye strain) may well be of this nature. Eation, later of paralysi; •s greatly increased pre n case of abscess there may be a latent period and, in the active stage, fever. Headache is constant with intense exacerbations. In rare cases the skull may be tender c i of cerebro-spinal fluid. Such headaches can be relieved by the operation of "decompression." cause can be assigned. May be some mental deterioration or other cerebral symptoms. No optic neuritis. Lumbar puncture will usually show lymphocyto . Fever may be present in rare sub-acute cases. Apoplectic attacks may < fronto-occipital muscle. Relieved often by application of warmth. At times small tender nodules can be felt, and hence the condition has been called "indurative headache." eek of almost any fever (typhoid). Such headaches may be due to the action of the toxic substance directly upon the brain or indirectly by causing vaso-paralytic congestion, ciated with muscle spasm and paralysis and local edema of the scalp (sinus thrombosis). Coma. Lumbar puncture will show lymphocytosis and globulin in cerebro-spinal fluid. Latent stage. Convulsions and coma, followed by coma and convulsions. Referred Pains or Symptomatic Neuralgia, (374). Alcoholic or Morphine Headache. Foul Air Headache. Constipation Headache. Uremic Headache. Congestive and High Tension Headache. Anemic Headache. Neurasthenic Headache, (1072). Cerebral Tumor, or Abscess, or Hydrocephalus, (507, 508, 965). Pachymeningitis and Chronic Meningitis, (5S8, 590). Rheumatism of Scalp. Infection or Toxic Headache. Acute Meningitis and Sinus Thrombosis, (590, 1044). Cerebral Abscess (960). Sunstroke, (589, 106S). 957 958 959 I CHART XV b Pain in Trunk Comprising Numbers 935 on left side of < lharl and 970 to 990 on right margin L79 DIAGNOSTIC SYMPTOMS AND TESTS ("Evidence ol neurotic I tempera- ment. No I evidence of Pain iii back, organic 1 disease. i Evidence ol organic disease. Pain, tender- ness and rigidity of spine. PAIN I\ TRUNK IN NERVOUS DISEASES. Girdle pain (374). Pain in thorax and abdomen. (Tain and tender- ness of spinous pro- I cesses. Pain and tender- I ness of coccyx. May follow traumatism. ""Vertebral column is ankylosed Unilateral. Bilateral usually. Plmli'as ami nervous exhaustion, pain and sen-e i if pressure most in Hysterical symptoms (426). Much tenderness of spinous processes, Severe pain in coccyx without evidence of any disease of it. Pain ii symptoms i4'2.">) are present. Severe and constant pain in back and radiating about body and Much spasm of spinal muscles. Exaggerated reflexes. Little or i if any, it is of a transitory nature. Ilyperes hesi.i and hyporalge- Slowly increasing motor and sensory symptoms, irritative and parah . paralytic symptoms are more; prominent, the tumor is in the cord ' and pain radiating into extremities than in meningitis usually. It may lie possible to feel exostoses on vertebrae. Unilateral or bib other parts of the body. X-ray examination makes the diagnosis | Pain shoots around chest, following the course nerve, or may be limited to a small area of the pericarditis, pneumonia, pleurodynia, periost been excluded by a careful examination. .Many other symp- | toms. No other s; toms. \t tn-st unilateral and later bilateral. Loss of knee-jerk. lit if infection. Argyll-Robertson's phenon Mill. Ill mamillary gland. In precordia and Along attachment of diaphragm. In abdomen. In all these rare forms of neuralgia organic abdominal disease' must be carefully and thoroughly excluded, I is sterical toms. rOld age, disease. Sj lllp- Aiterial \n> age. No arter- ial disease. In genitals. There is a zone of hyperesthesia where the gir severe. History or other evidence of syphilis, l.umba Slowly increasing motor and sensory symptoms Paroxysmal attack- of pain in one mammary g can be detected. Pain is usually in the left I Paroxysmal attacks of pain in precordia shooti region, of sulTocation and impending death. Pain similar to the above, but QO arterial disea tobaCCO, overwork, etc. Pain felt in lower anterior part of chest, also in same side of neck 'render points are along the attachment of the diaphragm and bel t rouiely rare disease. 'Paroxysmal attacks of pain in epigastrium often occurring at the sa ach or neighboring viscera, especially no gall stones. May be BBS Similar paroxysmal attacks of severe pain, occurring irregularly at p Paroxysmal attacks of severe pain in abdomen occurring with some Pain relieved by pressure. Blue line on edge of villus, wrist-drop Pain in hip, groin, liypogaslrium and genitals. Tender points near Neuralgic pains and irritability in the pelvic viscera, the bladder, rec pains at limes occur during years in one testicle or one labium n OSTIC ANALYSIS OF SYMPTOMS PAIN IN TRUNK 0STRACT OF SYMPTOMS DIAGNOSIS ■d in cervical spine ;ui'l occiput. Neurasthenia (1072). 970 aeially in mid-dorsal region; ovari le - 8 also common "vJotT' ^"^ S " mihrA " 71 Bed '>• motion, touch, defecation', etc. In most cases there is a history of injury. Often hysterica] Cocoygodynia. >»72 (Injury. Very sudden onset. Lumbar puncture maj show bloody fluid. Retention Hematorrhaohis (524). 973 exIiemilH - "I urine. History of infection septic, syphilis etc. . Lumbar puncture shows globulin and M'-"'"K''^ s i""^'r. "'/';' ]- ""» men,, lellular elements m cerebrospinal fluid, gj p^V '"""' ( [paraplegia dolorosa). When irritative symptoms are very prominent the tumor is meningeal, when Spinal Tumor (509, S-'ti. 976 -tupt. nii~ .it first usually unilateral, later bilateral. Less pain and spasm in back, more girdle pain 836-40, 981, 1006). 2 1-7. I 'il girdle pains at level of thi disease. Rarely any paralytia symptoms. Usually bone lesions in Spondylitis Deformans. 978 we. Arthritis 1 leformans, (Tender points of Valleix: one, two inches from posterior median line; another, two [nteroostal Neuralgia. 977 ii intercostal inches from anterior median line; and a third, in mid-axillary line, Other points ■vc; pleurisy, on nerve may also be hyperalgesia Pain is paroxysmal. Respiration, cough, having sneezing, etc lire painful. Rash "t herpetic vesicles along course of nerve. Herpetic Neuritis (940 . 978 n. Lumbar puncture gives lymphocytosis. Uaoria. Lightning pains in legs, History of syphi- Tabes (827, 661 (Fig 27 979 in, I below a bilateral anesthesia, which may !»■ Blight, and a motor paralysis, which may be Transverse Myelitis Figs 980 J 17 gtcture gives lymphocytosis. Pains worse at night. Syphilitic Meningitis, 980a first irritative, Liter paralytic, Brown-Sequard'e paralysis at first (442), Spinal Tumor (976 981 I, iiikI, al times, radiating beyond the l ts of the breast. No tumoi oi other disease of the gland Mastodynia, 982 ■ to left ihoulder and even down left arm and. at times, both arms Sense of oppression in Bternal UigiiMrPectoris. ■rial ti lee, ii ,- usimlh high \ie i ol cardiac dulneas usually increased Neurotic nilivelu.il who has ivn overstrained heart, \t tunes the result of gastric indigestion, Pseudo-Angina-Pectoi 984 t frequently on left side, lircuthing, sneezing, coughing, etc., painful. Pain Phrenic Neuralgia, 980 : mIitmi .-,l.-i, |, i mi i . .i, i muscle No sign of pulmonarj pleural, cardiac or othi In ex- ill> in tin- e:nl\ iiinriiiiig. No diKeshve disturbance* or evidence of urn disease of atom- Gaatralgia. 986 Ii cont met ion of il mpty stomach and consequent feeling of hunger. eck of bladdei uciated with symptoms of tabe 861 987 odicity, when biliary, renal mid other forms of colic appendicitis, diverticuUti i, etc have been excluded Enteralgi i Lead Coli eti 986 id in mine nfter administration ol l\ I ie, on en il i.i ilium, inner pun of groin, etc Lumbo-abdominal Neuralf i, (torus, vagina and urethra, but these an rare and relatively unimportant conditions Neuralgic Pelvic Neuralgia. 990 mi i ti i- pomi the pain may radi CHART XV c Pain in Extremities i !omprising Numbers 936 on lefi side of < lharl and 905 to 1012 on right margin 181 DIAGNOSTIC SYMPTOMS AND TESTS ." 1 *;i i ii iii arm. Pain limited to the trunk and distribu- tion of the sciatic, anterior crural or ["Unilateral. Any of obturator nerve, these forms of neu- ritis nia\ be asso- ciated with, or pre- ■', cede, or foDow a rash "i herpes: her- petic neuritis. Pain limited to I ige :;:;. 38 . outer surface of thigh. 936 PAIN IN EXTREMITIES !\ NERVOl - DISEASES. Pain in a joint. Pain at insertion of Achilles tendon. Pain in heel I Pain in toe. Willi girdle pains. and lumbar punc- ture gives lymphocytosis. \\ nh am Bilati \\ nh dissociation ..I sensation. \\ it Ii vaso-motoi disturbances DIAGNOSTIC ANA ABSTRACT With fat Pain radiates along one or all of the nerves of the arm. Te other points where nerves are superficial. Vaso-motor di paralysis; hut movements of arm are impaired by the pain pressure on nerves must he carefully excluded. Pain shooting along the trunk, or over small areas ill tin' dish but the pain may prevent motion. Patient holds knee of the opposiie side and bears his weight on the healthy leg. major i trochanteric point) and in popliteal space (popntea may be decided muscular weakness and atrophy. Sciatica tinn for any possible pressure upon the nerve should al\\a> Pain along the trunk and distribution of the anterior crural ankle. Tender points on anterior aspect of the hip joint, paralysed and atrophied and knee-jerk lost and anesthesia i be secondary to diabetes and injury. There may he an en Pain along inner side of thigh, along course of obturator ner .. neuralgia and is usually associated will' paralysis of the ai Pain is assoeiated with paresthesia!' (['specially uumbiie-- an. The paresthesia!' are more characteristic of this di-< Pain in a joint, usually the knee-joint, increased on motion. dence of any disease of tic joint. Many hysterica] symp Severe pain at insertion of Achilles' tendon on walking and Pain m lower surface of heel, especially when walking removal of the sub-calcaneal bursa, or of exostoses, others Pain in the nietatarso-phalangcal joint, especially of the fourl is lowered from "breaking" of the arch transversely. I With Romberg's symptom, ArgyhVRobertson's phenomenon, J lymphocytosis and lightning pains over am ill With pain ami rigidity in back and in extremities. Exaggei ("Steadily progressive motor ami Bensorj symptoms, al first mi Brown-Sequard's, paralysis (442). Motor paralysis and anesthesia over whole of both legs, exci •J peripheral and organic reflexes. Muscular atrophy and ti m lower back and radiating into legs- Motor and sensory paralysis commencing at the distal end i 1 and tenderness. The disease usually commences with pah Pain and parest hoMae, analgesia and thermic anesthesia wit symptom- are usually limited to arms with symptoms of s] ire milder Extreme pain in soles oi feel associated with redness and swell foot must be excluded Pallor and coldness of fingers and toes followed l>y cyanosis In extreme cases a larger or smaller slough forms as Marked Increase in fat, either diffuse or in separate tumors with it. and the fatts masses are tender, especially in SIS OF SYMPTOMS TREMITIES SYMPTOM.- DIAGNOSIS H supra-clavicular fossa, in axilla a) head ol radius and at Cervico-brachial Neuralgia or Neuritis of Dinar, 00.5 ■anees. Fibrillar] contractions :i' timi scur. There is no motor Median Radial, etc "uuiors at base of neck :ni'i in axilla, and a ■ 556), causing [on of the sciatic nerve. Little, if any, anesthesia or motor paralysis, Sciatica 720 996 ted side semi-flexed, thigh slightly abducted, inclines lii> body to id.T points over the sciatic notch gluteal point . above the trochanl lint . In neuritis, the nerve, wherever felt, is tender, and then there much more frequently a neuritis tluui a neuralgia. A rectal examina- I made. ,•<■ .hi the anterior surface of the thigh and inner surface of leg to the Crural Neuralgia or Neuritis. 997 it side ol knee tnd at internal malleolus. Extensors of thigh maj be be mi anterior surface of thigh and inner side of li'ii in neuritis. May on nf herpes along the irse of the nerve. after hernia and other diseases have been excluded. A rare form of Obturator Neui 998 (tors. iclnmi and is frequently associated with, and is caused by, flat foot Meralgu Paresthetica 999 the pain, which i- often entirely absent. In- »kin i- much more sensitive than the articular surfaces. No evi- Arthralgia or SystericaJ Joint 1000 - I.'.", dmu. Maj follow gonorrhea, malaria, gout, broken arches or injury. AohiJlodynia 1001 leumatic medicine other- i>\ Burgical Talagia or Calcanodynia. 1002 supporting 'he weakened arches, lally following an injury. Usually occurs in women. I "he joint Metatarsalgia or Morton's rot 1003 tory of syphilis usually, always loss ol knee-jerk, cerebro-epinal Tabes Neuralgic stage 661 "Nil terficial and deep often followed by hyperalgesia over same \,. ,i.i\ii No Irgyll-Robertson's phenomenon, Spinal Meningitis 608 974 1005 ■ unilateral, later bilateral Increased pressure ol cerebro-epinal fluid Spinal rumor 509, 826, 836-40, 976J i |HN ' the domain of the anterior crural nerve- Abolition ol Lesions ol I auda Equina 187 Fig -"' 1007 . i. -He -i,i iii perineum and genitals and much pain tremitii - mil extending towards bodv Muscular weaki atrophy Multiple Neuritis i ss 1008 ■ ml fingers and often with fever iio|ilne disturbances and mutilati Syringomyelia 1150a, 1 1 7< •. 11^7. 1009 i be pains often resemble the pains of tabes, but 1357-9 in, I luter with pallor, shrinking and wrinkling ol thesame parts I lit Erythromelagjs 1198 1010 Congest • i lt ■ i - i'i-i toes i", 'I urplish m,| even black Raynaud's Disease 1195 l'Mi in- ml lenH. but ti"i elsewh pain tasooiated \ to L033 on right margin DIAGNOSTIC SYMPTOMS wi> I i:sts Motoi Uaxia is present. Cerebellar Ataxia is present. 932 V ]•: R T I G o (392 I irossed Paralysis. \ ertigo ;iinl aun emcnt ol head Deafness and symptoms of aural dis Diplopia and symptoms of ocular disease Position and moving. Symptoms "I circulatory disturbances Digestive dii orders. ( '.-inline and hen disease. \i herqmatous arteries. 1 1 i k h blood tension. Apoplexy. Epileps; Migr: Toxic Organic Symptoms ol cerebral di , te Functional. DIAGNOSTIC AN DISORDERS OF SENSAT A.BSTB \* i In these cases the vertigo is not a prominent symptom. In - of falling and fears that he will fall and experiences some vert lesions in the brain stem and el en here. The diagnosis is made \n\ disease of the cerebellum, especially tumors, max cause vertig tin 1 hemispheres. The di >m I hi absence of p and, III III 'S, the Optic lnairil is ami failUTI Ol Lesions of the brain stem may involve the tracts From the cerebell made by the motor or sensory paralysis or both, which occur it paralysis in the domain of the cranial nerves (crossed paralysis Cysts and tumors suspended free in the fourth ventricle cause in1 the diagnosis is extremely difficult or impossible. The vertigo i held, i Ihoked disc is common, \ steadily, progressive deafness of one ear associated with tinnitt may throw patient in the ground. Raising the head from the | or loss nf bone conduction and loss of power of hearing high m theparoxj mal attacks. Suppurative and other diseases of the the ear is completely deal', but then may commence in tl th cause vertigo by affecting the semi-circular canals or vesl laesa). It is difficult to draw the line between these case all these conditions. Strictly speaking, Meniere' disease appl Bammation of the labyrinth causing vertigo is called Voltonrs Double vision and weakness of ocular muscles and ■ ■■ strain ma; is relieved by closing the defective eye, even when it is not cau When patient's head is bent down for a I id then is sudd vertigo A blovi on the head will cause vertigo, prol back of head or moving head quickly may cause vertigo. A B\ to the head. Great weakness, especially in the convalescence from disea When, in consequence of the congestion due to digestive di are anemic. These digestive disorders ma\ also produce abno diagnosis is made by the presence of the digestive disorder and 1 In all inn us of cardiac disease the brain maj receive an insufficien frequent in aortic disease. The diagnosis is made From the pn to the altered quality than quantity of the blood supply i 1029 Atheromatous arteries interfere with the normal bl 1 supply bot cause vertigo. This is especially common in elderly people. T usually, an increased artei ial tension. Fulness of head, headache, mental confusion, tinnitus auriui tension. Vertigo is a common initial symptom of apoplexy of all form ■ ■ rhage) and may be the only .symptom of a slight attack. Isua Vertigo may constitute the aura which may or may no! be Follow© In some cases a severe subjective sensation of vertigo, frequently Vertigo is a not uncommon symptom in the interval between tl Vertigo may be the initial symptom or may accompany an attaol mal es the diagnosis plain, Abnormal conditions of the bl I, as in the early stages of the in Various toxic substances, such as tobacco, alcohol, coffee, morphia, of the cerebral or cerebellar cortex. The diagnosis is made by thi \ di-ea e endemic in Switzerland and occurrii nJ n war! ness of vision, ptosis, often diplopia without strabismus, and a Pain in back of neck, attack lasts a fen minutes. In addition h apoplexy, any irritation of the meninges itumorsji oiated with tevere vertigo, especially on change of position. Ti pressure on I he CI n bl Hum, or, i l ated in the frontal lul oade by the numerous other symptom of these di ea with the vertigo, which is less severe in the recumbent posture Vertigo is a not uncommon symptom in those functional nervous • in h i- neurasthenia, the traumatic neuroses and hysteria. Thi VerUgO is never very severe and often resembles rather syncop: YSIS OF SYMPTOMS ••I; PERVERSION: VERTIGO d SYMPTOMS ■s. in consequence of the incoordination, the patient is in danger while in other cases the vertigo may be the direct result of the m the presence of motor ataxia. Iiirh is more permanent in lesions of the vermis than in those ol pis, the presence of cerebellar ataxia, headache, and vomiting DIAGNOSIS Tabes, Disseminated Sclerosis and other disease 1015 with ataxia. Cerebellar Disease (609-10, 648, 686, 7s:;. 1272). loin Bid cause ataxia and, less frequently, vertigo. The diagnosis is ,e form of hemiplegia with increased reflexes, and also of local D . Fig 19-22.) Dizziness only when head is moved. Except for this symptom vary greatly in intensity with the position in which the head is Lesions of the brain Btem WO, 535-46,656,830, 1017 L268-74, 1301-4, L375, 1378, 1382-4, 1388, i:J98). Lesions within the fourth ventricle. (Kg, 19.) 101s 1 that ear, and with paroxysmal attacks of severe vertigo which r,d may cau-e vomiting. \t tacks vary in severity. Impairment ure usually present. Vertigo 1- usually entirely absent between may be present but usually arc not. Disease usually ceases when I-. \im 1 e 01 functional disturbance of the ear may ir nerve directly or indirectly (aural vertigo or vertigo ab aure vertigo ami Meniere's disease, which latter is often used to cover : ge into the semi-circular canals. In- Meuiere's Disease. Voltoni's Disease \ural Vertigo. Vertigo ab aure laesa (650, 685,918) 1019 li BUI imetimes on railway trains by tin- diplopia alone. ■used, or when patient's body is rotated rapidly, he experiences ol vaso-motor reflex disturbance. Lying on one side of tcvertigo rom the application of 1 galvanic current rhe vertigo Ocular Vertigo. Vertigo ah oculo laeso (649). 1020 \cute ( lerebral Anemia 1021 niiili cause lioth of vertigo and ataxia. Exhaustion Vertigo he portal circulation is engorged with blood, the cerebral vessels Acute Cerebral Anemia from digestive disorders 1023 I chemical substances which may produce a toxic vertigo. The hemorrhage, etc vertigo when the indigestion i- cured. -I irregular supply of 1.1 1 and vertigo may result. Tin- i- most in hemic diseases the vertigo is due rather ( 'lironic ( 'erebral Anemia I n >m diseases. ilood and cardiac io uniformity of distribution anil hence ma\ ('lironic ('erebral \nemia from atheromatous alter- 1025 m de from the pr< »encc ol atheromatous arteries with, ies (syphilis palpitation of heart, dyspi a on exertion, ami high blood Cerebral Congestion I hemorrhage, embolism and thrombosis, and meningeal hemor- kpoplexy (504). i. :n i full attack. The diagnosis is made from the ep cks Epilepsy (575, 1058, 1071 il iwed bv vomiting, maj he the equivalent of an epileptic attack. ntinuc durum mmute- or hours. migraine. The hemicrania, th< much more prominent symptom, Migraine B46, 854, 949 mil in leukemia, melanemia gout, diabetes, etc. go in.' I bablj bj affecting the circulation Drug Vertigo 1080 ii f of the ingestion ol the sub of vertigo. r n hot ortigo, with dim Gerliei Vertigo Vertige Paral 1031 ■ ■ .i, ..i net ..I the firms, simulating bj I inflammation Cerebral Meningitis and Tumor Syphilis 508, i" ; -' ci of the meiimce- ami h\ li in mitted b\ direi tct The diagni iting, dow pul-e, etc., which aiv frequently a sociated cute and chronic, Neurasthenia, rmumntic Nei ' !..■! . hart I in- 101 CHART XVI Disorders of Cerebral Activity DIAGNOSTIC ANALYSIS OF SYMPTOMS Symptoms Alterations in Analysed Mentality '1037 Coma. See Chart XVI a. 1036 Disordered Mentality. 1038 Pseudo-Coma. 1039 Double Personality. 1040 Weakened Mentality. 1041 .Insanity . "See Chart XVI b. See Chart Wl o. 1H-, CHART XVI a Coma ( Comprising Numbers L037 on left side of Chart and 1042 to 1068 07, 1045) or abscess i/iOS, the coma are common. There may be local symptoms, both irritative a be edema of eyelids and conjunctivae, choked disc, prominence of the ey Retraction of neck and opisthotonus. Fever, headache, delirium. Convul tation followed by those of paralysis. Headache, vertigo and vomiting. Often mild delirium. A recent, infectei general and resemble those of a rapidly growing tumor. Choked disc Headache, vertigo and vomiting. May be a history of former injury. No tumors at the base are more likely to cause paralysis of one or more ci A motor monoplegia (anarthria, etc.), rare, hemiplegia or diplegia occurrii defect. Epileptiform convulsions, unilateral or bilateral, are frequent. Progressive mental impairment, childishness, restlessness, amiable but irri syllables and letters are left out and letters doubled. Apoplectiform an History of lead poisoning, of lead colic, of wrist-drop, etc. Blue line on g Intention tremor. Scanning speech. Many motor and sensory symptom Headache, increasing fever, difficulty in walk and speech, tremor, increasi Patient can usually be aroused from his coma sufficiently to speak and his alcoholic abuse. Pupils are contracted and do not respond to light (if opium). Patient is other narcotic. { Patient is in a confined space or room in which there is a strong smell of il Sudden attack of coma with pallor and weak or absent cardiac action of si extremities cold, restlessness, yawning. Low arterial tension, steadily g Sudden intermission of heart beat during a considerable fraction of a mini 'The attack usually commences with a convulsion, as described in Chart X, 5 sometimes trivial, sometimes a deed of violence (post-epileplie insanity) sciousness and no convulsion and either no action or some trivial or fool the convulsive attack ami is called the "psychic equivalent" am! is altoj and take journeys ami are lost to their friends and to I hemselves. After a an epileptic attack is the complete or almost complete unconsciousness i some mental weakness which may slowly increase to mild Or extreme de epileptics have attacks during many years ami yet show little, or no, I The attack is altogether similar to the major attack of epilepsy, but i distended abdomen, foul smelling feces, vomiting, diarrhoea, etc., and Thecoma comes on instantly or in the course of a few hours. There are tert in the form of hemiplegia. 'The bilaterally innervated muscles (upper fa ion-, abdominal, micl tuition, defecation, etc.) escape permanent paralysis. reflexes may, during the coma, be abolished, later exaggerated (Rosenba pass away alter several hours or days. The lower branch only of the fa i he paralysed side. Usually there is also at first a sensory hemiplegia > in which latter ease the motor paralysis greatly improves or entirely disi in leg and finally in the arm. In case recovery does not take plai in leg. 1'osl hemiplegic motor disturbances may occur, especially in h: toms such as aphasia may occur. A reactive inflammation about 'he lei second week. Repeated attacks at varying intervals are common. After uncertain prodromata, coma and paralysis with fever appear and de. . encephalitis superior hemorrhagica acuta) or may be in the form of a he Patient emaciated. Acetone odor of breath. Pulse is email and rapid, ski Onset usually gradual. Some edema, cyanosis, restlessness, rapid noisy resj albumen and casts. ' Occurs at the onset of acute infections, especially in children. Often associ hut in these eases convulsions are rare, and the cause may consist in a fa History or evidence of exposure to great heat Absence of perspiration. symptoms (paralytic) occasionally occur DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS DIAGNOSIS Cerebral Concussion. r a short time after which he remains in a dazed condition for a time, or he may be only dazed from the start. Pallor, low blood tension, vertigo and vomiting are common symptoms. May be contusion of scalp. Symp- irely any paralysis. Often retrograde amnesia (769). jiately but not always; there may be a "lucid interval," (especially in extra-dural hemorrhage). Coma, profound stertorous breathing, pulse slow, reflexes abolished, increased tension of cerebro-spinal fluid are the usual )f hea'd and eyes' Often paralysis in the form of more or less complete hemiplegia, together with Babinski reflex and some spasm. Often retrograde amnesia (769). ) with usually high fever and chills (both may be absent) occurring in a cachectic, anemic, or infected patient, especially in one with caries of bone of skull (otitis). Headache, vomiting, restlessness and delirium preceding ralytic. A very characteristic symptom is a localized edema of the scalp. In thrombosis of superior longitudinal sinus there may be epistaxis and edema at root of nose. When the cavernous sinus is involved there may ind oculo-motor and abducens paralysis. When the transverse sinus is involved there may be edema over mastoid and palpable thrombosis of internal jugular vein in upper part of neck. and retraction of abdomen. Paralysis of cranial nerves. Kernig's reflex. Lumbar puncture and examination of the fluid, which may be cloudy, give globulin and increased cellular elements in it. Symptoms of cerebral irri- Meningitis, (590, 608). Cerebral Compression (contusion and hemorrhage). Sinus Thrombosis, (964). nd or other cause, or origin, for suppuration. Moderate, irregular, often absent fever. Course is progressive but may be very acute or extremely chronic and often shows a latent period. The symptoms are both local and rather rarely. The general symptoms are more prominent than the local. Suppuration of the middle ear and of the mastoid cells must be carefully excluded, especially in children (see 508). Course is progressive. Mental deterioration, but local sympto erves. Choked disc is very common (see 507, 897). often as prominent as the general. Convulsions, especially Jacksonian epilepsy, are common, especially when tumor is muscular atrophy, and reflexes exaggerated. Ankle-clonus and Ba or near the cortex; while ski. Usually some mental genitally, or in early infancy are common. Usually some arrest of development of paralysed part and of skull. Little athetosis and hemichorea frequently complicate the disease and contractures occur in almost every case. 6teadily increasing dementia. Blurred speech. Tremor of lips, tongue and hands. Terminal dementia. Inability to repeat difficult phrases, due partly to paraphasia, partly to loss of memory. Writing imperfect: words, vulsive attacks. Abnormalities of pupil. Argyll-Robertson's reflex. Lumbar puncture gives globulin and lymphocytosis in cerebro-spinal fluid. History of syphilis. Positive Wassermann reaction. Convulsions. Lead can be found in the urine, especially after the administration of K. I. :aggerated reflexes. Ataxia. Nystagmus. The convulsive attacks may be epileptiform, apoplectiform or myotonic. Headache, compulsory acts and slight dementia are not uncommon symptoms. 'Wsiness, passing into coma and death. Trypanosomes are found in blood and in cerebro-spinal fluid. i is characteristic of intoxication; being indistinct, blurred and foolish. Pupils are dilated and respond to light. Flushed face and conjunctiva, and stertorous respiration. Often tremor or twitching. History or evidence of Cerebral Abscess, (152, 181, 508, 578, 587, 907, 960). Cerebral Tumor, (151, 507, 536-42 578, 5S7, S33, S49, S55, S5S, 861,892, 960). Cerebral Palsy of Childhood. Porencephaly, (116, 501, 577, 630, 798, 10S6). Paresis, (1104). Lead Palsy, (158, 494, 584, 788). Disseminated Sclerosis, (668). Trypanosomiasis or African Lethargy. Alcoholic Coma, (764). 1049 1 1050 1051 1052 1053 *-sy, and mentally incapable. Respiration is slow and stertorous. Face is congested. Pulse is at first slow, but later, especially in fatal cases, becomes rapid. History or evidence of patient's having taken morphii Narcotism from opium, etc. 1054 ating or coal gas. He is cyanotic with rapid, irregular pulse. He often vomits and exhibits more or less tonic or clonic spasm. uration. Often preceded by tinnitus aurium, dimness of vision, cold sweats, and nausea. Slight spasm or rigidity is frequent during the attack. In internal hemorrhage the onset of the coma is more gradual. Pulse is small, g lower. more with coma and slight spasm. Slow pulse, atheromatous arteries. Usually occurs in advanced age. ^he convulsion lasts only two or three minutes and is accompanied and followed by a com; .h an attack of general convulsions is called "the major attack" or "le grand mal." At til tion; unconscious movements of lips and jaws being common. This is called "the minor to the post-epileptic insanity. These attacks may last minutes, hours, or days which gradually passes into a sleep. This post-epileptic coma is sometimes absent and is sometimes replaced by unconscious action, res such an attack follows another immediately throughout a long series (status epilepticus). At other times there is only uncon- attack" or "le petit mal." Sometimes the attacks occur only at night (nocturnal epilepsy). At times an attack of insanity replaces d in them the patients lose their former individuality. In some of these attacks (ambulatory automatism) the patients wander about fks there is amnesia. A rare form of epilepsy is one in which the patient falls suddenly to the ground and gets up again immediately without any appreciable loss of consciousness (vertiginous). The essential characteristic of il and the complete or almost complete absence of any memory of it. In the interval between the attacks, which at times extends over months and years, the patient may be entirely normal. Frequently he is irritable and shows :i, especially il the attacks are frequent and rest on a strong hereditary basis. This condition is not to be confounded with the transitory mental impairment due to bromide given therapeutically. On the other hand, many I impairment. Epilepsy beginning in a patient over forty years of age should suggest, the possibility of a cerebral tumor. Illuminating or coal gas poisoning. Syncope. Internal Hemorrhage. Stokes-Adams' Disease, (436, 582). Epilepsy, (110, 126, 430, 575, S46, 1027, 1071, 10S3, 1102). ecur. There is only one attack or a series of attacks at short intervals. It can usually be referred to an irritation of some part of the body or to some form of poisoning when these conditions are removed. It is most common in children. It is often :iated with digestive disturbances, Eclampsia, (576). respiration and a slow full pulse. Usually paralysis Jcular, masticatory, deglutition, laryngeal, respira- iski reflex usually present from the start. The other ign). Patient may die in coma or the coma may decidedly paralysed. Tongue protruded towards quickly disappears, but which may be permanent, rs. Improvement usually begins in the face, next itraetures appear in arm and extensor contractures Some mental impairment persists. Local symp- ray cause an exacerbation of the symptoms in the d later in disease. Hemiplegia disappears quickly ted with cerebral miliary aneurisms). Permanent, or Prodromal symptoms (headache, vertigo, etc.) common. Convulsions, especially Jacksonian epilepsy (431), at onset and completely. Prodromal symptoms may or may not be present. Profound and long coma usually. High arterial tension (: long continued hemiplegia. Aged patient. Presence of interstitial nephritis. No prodromata. Youthful patient. Cardiac or pulmonary disease, sepsis or aneurism. Existence of embolism elsewhere in body. Slight or absent coma. Pulse not so slow. Hemiplegia not so permanent. Paralysis of some cortical function; aphasia, hemianopia, etc. Spasms not infrequent. Prodromal symptoms present. Slight or no coma. Atheromatous arteries or history of syphilis. Paralysis of some cortical function; aphasia, hemianopia, etc. A mild, transitory form, with tendency to relapses and without contracture, is the so-called "lacunar hemiplegia," in which not one large focus, but numerous minute foci of softening occur in the cortical area involved. Pachymeningitis Interna Hemorrhagica, (502, 5SS). Cereln-al Hemorrhage, (146, 411-13, 503, 58S, 832, 856-7). Cerebral Embolism, (505, 832). Cerebral Thrombosis, (506, 832, 1207). asulti gia, partial two or three weeks. The disease usually occurs in young persons and seems to be due to poisoning, especially alcoholii 1 "- complete. Optic neuritis may be present. The paraly Breathing is labored and may show "air hunger." Sugar and almost always albumen and casts also in urine. Pulse of high tension. History usually of headache, vomiting, dyspnoea and dimness of vision. Ophthalmoscope may show albuminuric retinitis. In ra may attack the eye muscles (Wernicke's polit tinitis. In rare cases there may be hemiplegia or other paralysis. Urine contains "circuhtion Tcere e bra° n an 'n' f ? U ' smelling feceSl High fever is common. Often history of improper food. The coma which occurs in the course of, and especially towards the end of, acute infectious fevers is probably of this nature, . comes on rapidly but not instantaneously and is preceded by many prodromata; such as headache, mental confusion, marked disturbances of vision, paresthesiae, weakness, etc. Delit symptom. Local Diabetic Coma. Uremic Coma, (576, 581, 850, 956) Toxic or Auto-Toxic Coma, (596). Sunstroke or Insolation, (589, 966). 1055 1056 1057 1058 1059 10 50 1061 1062 1063 Acute Multiple Encephalitis, (495, 543-4). 1064 1065 106P 1067 100S CHART XVI b Pseudo-coma, Double Personality and Weakened Mentality ( lomprising Numbers 10:iS to 1040 on left side of < Iharl and 1069 in l()7."> on ri^ht margin IS'.t 1038 PSE1 I id-COMA. HI AGNOSTIC SYMPTOMS AND TESTS Hysterica] symp- toms (425). /-Hysterica] symp- ' loins i 125). DOU BLB PERSONALITY .VXD AUTO- M \ II sm (209). Epileptic symp Items (575). ( lonvulsiona and Spasms frequent. ( ionvulsions frequent. DIAGNOSTIC ANA f PSEUDO-COMA, DOUBLE PERSON \BSTK.\CT Occurs usually in girls and women ol an emotional be stopped by a strong and continued pressure o vation will usually show that she is attentive to from external causes, or auto-suggestion ihypnoti ("Patient seems a1 tunes to be in a hypnotic .stall-. 09 ami in that stall- lo lead a life carried on from 6 states from auto-suggestion, patients often act like tion and in some hysterica] patients max well In- .I While in an unconscious state patient often perform has no memory. Whether in such unconscious st doubtful. While unconscious, epileptics often pel Apprehension and various phobias are prominent symptoms. In consequence of ^flidjr 1 /v'e\*ene3^ OnJktiljJ ""these f panwm cun^yt rid^lrcm^l+eA.Ajy^rea- soning, of their unreasonable appre- bans^E^W bdii /jflurioH-rctS alduoG ^ilfrtnaM licil'J lo 1040 WEAKENED MENTALITY. Patients appear to be intelhgent, but incapable of king sustained effort, and of self- control, often foolish and unreasonable The different diseases in these groups merge into each other and no sharp line can be drawn between them. They all rest on a neurasthenic basis, -ml in all suggestion plays a greai part. twj* kwmhirxci u yijrjtiicj, i ) nwjipMtbk ana incredible. No certain evidence ot any organic disease; although almost every disease can be more or less per- fectly simulated (425). The symptoms are those of a general exhau especially of the lower centers. It is common in easily. Every task looms as a mountain before I will power are both poor. They feel nervous, ir phobia, claustrophobia, etc. I. Almost as eharacl The patient also suffers much from palpitation, five disturbances. The essentia] symptoms of m The patient, usually a male, is in a condition of exfa consciousness in which the attention is firmly and pressed because of a delusion in regard to a suppo fi!f'Win r hi*fiFl? I r'WP™i abnormal .sensations. I ' J M-VV,uf the rjaWMea Cannot be dispelled from strous, fantastic and impossible. At times they S and apprehensive, and their attention is firmly li even grotesque delusion that some organ of the l> .The disease occurs almost exclusively in women and M1 ^H# N I X T E L L I G E N C E 1076 Amenlia (211). More or less complete 1077 Dementia (212) More "i' less ^complete. 107S Hallucinations are abundant and domi- nant. Hallucinatory Insanity (213). 1079 Delusions are present and dominant. Delu- sional Insanity (215) 1080 An exaggerated emo- tional state ie thi mptom. Emotional I of flu' have been condition in which the mind has not developed with advancing age, due to a disease of the brain, either congen- ital or acquired in infancy. Besides the mental defect, these patients often present many and various physical and deformities such as: de- formed skull, posterior hydrocephalus, high palatine arch, coarse body, de- formed ears, etc. The amentia may be either general or partial, and some of its slighter degrees may be due in part to defective training. Occurring in youth, at puberty or before 25 or 30 years. A condition in which the mind has developed to a certain, even a high, degree of intelli- gence and then, in consequence of disease of the brain (functional or organic), all mental development has not only leased, but there has been a distinct re- nin, which may go on to a complete loss of intelligence. Memory, emotions and interest are all lost. Pa- tient becomes apathet- ic, reacts to no stimula- tion, soils himself and does not even eat. Usually occur- ring in adult life alto- l:."i years, but may OCCUT in youth. Occurring in old age. Patients Bhow little or no intelligence. Are unable to urine and feces. About their only desire is thai J Most of these patients exhibit frequent and violent Patients can talk and are more or less cleanly in their They are incapable of much education. They can f and the sexual instinct is often strongly developed. Patients show a degree of intelligence approaching tE children develop up to a certain point, but then si ing eyes, thick fissured tongue, and short, stubby fins tobacco. Simple infantilism is often called " atele Certain feeble-minded persons seem incapable of appi Complete apathy, coming on more or less acutely. O tion. Appears to be anesthetic and analgesic. The cases recover after several months. Partial apathy. Patients are dull and stupid but consc is an absence of emotions and of inte.jst in anythir They perform frequently spontaneous, impulsive, sil! of a phrase which they have just heard or spoken (e The varieties under this head merge into each other 'History of alcoholism and usually associated with mult History of alcoholism extending over many years. T: amounts of alcohol. The symptoms at times resemb History of very numerous epileptic seizures. Gradua' History of a previous psychosis which has gradually pr (apathetic dementia) but some cases show great rest History of syphilis. Lumbar puncture shows globuli inability for continuous mental concentration, reel at least cheerfulness, in spite of the illness which pail dementia. No paralysis, but much paresis and esj tabes, more rarely with various forms of spinal scle: Associated with physical weakness and with atheroma loss of memory, especially for recent events, with ret' Blood tension often high. A condition in which the patient is constantly receiving false perceptions from his different senses: either visual, auditory, olfactory, gustatory, tactile or painful, or from several or all combined. Associated with this is always a certain degree of impairment of conscious- ness, which weakens his judgment and does not permit him to decide that these hallucinations are false. A condition in which the patient has formed a false judgment about things which concern him. The basis of these false judgments is partly a congenitally defective brain and partly hallucinations. Associated with these delusions there is always present a vary- ing degree of impairment of intelligence, which pre- vents the patient from recognizing the falseness of the de- lusion when evidence is presented to him which would be adequate for a normal man; although many of these patients in their own way reason shrewdly. These delu- sions lead to irrational conduct on the pari of the patient which would not be irrational were the delusions true. •Patient is overwhelmed by a large nun intentions towards him. He does fo' History of alcoholism. Patient's halli Great fright. Violent attempt to ei Many other poisons besides alcohol: i produce a mild hallucinatory insanity Disease commences with fever, headacl •History of alcoholism. Patient has for men is that their wives are unfaithfu Patient has delusions upon which he b is not built upon them. Curable in Patient has a number of delusions, u: systematized or nearly so but whi( are strong enough to influence his coi duct and bearing. Curable in most case Patient lias many delusions which arc c and are woven in with the delusions ill Bions are thus systematized and some himself as a mosl remarkable person delusion of persecution (every happ Exaggeration of the sometimes natural oi discouragement with life. Exaggi ra i natural feeling of Patient is constantly in a depressed and painful frami by the patient to explain the melancholy: the co are very prone to suicide. Their circulation and are constantly in a joyous and excited mood I and due to delusions (1111). Mania is dh idi 4 | son, i {Alternations at long intervals of mania ami melanrhoB of excitement or of depre ion n icui Kraepelin has incorporated all of th rider the tei DIAGNOSTIC ANALYSIS OF SYMPTOMS ABSTRACT OF SYMPTOMS ik intelligibly, but are often noisy. Many are unable to walk-. Usuallysoil themselves with ood. They can do no act requiring intelligence and are incapable of sustained attention, reaks of anger. Many of them are undersized. I Associated with hydrocephalus. Fontanelles and sutures are unusually open and broad. Bra I culous sclerosis with nodules. | Associated with epilepsy. ■{ Associated with a very small skull. Brain usually weighs loss than 1000 grammes, or 33 ounces. j Occurring in family groups, with blindness and optic atrophy and dark red spot in place of macula lutea. Associated with congenital hemiplegia or diplegia and with rigidity and convulsions (501). { Associated with no special characteristic. f All the classes above given under idiocy but with less extreme mental defect. ■t„ Thev exhibit in their acts an evident though low degree of intelligence. J Very defective intelligence in general, but in certain directions (usually music or mathematics) may show great skill, few abstract conceptions and no high moral ideas. Masturbation is common 1 Associated with destruction or atrophy of the thyroid gland. Arrest of growth. Thick, dry and scaly skin. Coarse features (1164). ( Associated with no special characteristics. ■mal but are evidently below the standard. They cannot be educated beyond a certain point. They are often obstinate and of violent temper upon provocation, even though in general amiable. Some nd never advance further (infantilismus). In some cases of infantilismus, there is a defective growth of the body with a email head and a peculiar characteristic Tartar-like expression of the countenance, slant- They possess great faculty of imitation (Kalmuck idiots or mongolismus). This disease presents many resemblances to cretinism (1090, 1164). Infantilism may be due in some eases to poison, such as wine or " Infantilism with premature senility is called " progeria." iding the simplest moral ideas, although their mental defect is not so obvious in other directions. On closer examination, however, a general mental defect becomes evident. ousness is obscure. Patient incapable of any mental effort. Is in a dream-like state, immobile and does not appreciate what is going on about him. Will answer no questions and will respond to no stimula- e no hallucinations or delusions. The cutaneous reflexes are lost and the tendon reflexes are exaggerated. The course of the disease is interrupted at times by periods of excitement. More than half of such shows a tuber- Hydrocephalic Idiocy. Epileptic Idiocy. Microcephalic Idiocy. Amaurotic Idiocy. Porencephalic Idiocy. Idiopathic Idiocy. Imbecility Idiot Savants. 14). Cretinism. Idiopathic Imbecility. 1081 Idiocy (743) 10SS Imbecility. Moral Imbecility or Habitual Criminals. Primary Dementia and Stupor. 1092 The Feeble- Minded 1083 1084 10S5 1086 1087 1088 1089 1090 1091 1094 1095 ness is fairly clear and they appreciate what is going on about them. Hallucinations and delusions are common. There rSimple progressive mental deterioration, at times permanent, often temporary, com- inesthesia and analgesia. They are unwilling to perform any act and offer resistance when forced to do it (negativism). mencing at puberty. its. They often repeat the same act or the same words many times (stereotypy). They also often repeat the last word ■< Alternating conditions of stupor and excitement, negativism, stereotypy, echolalia lia), or repeat obscene words (coprolalia), or repeat an act (echopraxia), or remain in any given posture (catalepsy). with steady mental deterioration, at times permanent, often temporary, all'show, as prominent symptoms, impulsive ideas and acts. The prognosis is uncertain. [Hallucinations and partially systematized delusions with steady mental deterioration. leuritis, except in very rare cases. A peculiar loss of memory with a bringing of memories of the remote past up to the immediate past (retroactive amnesia — 769), failure to appreciate the relations of time and space. '. Dysarthria. Loss of memory and power of attention and mental power. Delusions are frequent. Normal and ethical ideas blunted. Irritable, sentimental and often very susceptible to the effects of small Dse of paresis (1104) (pseudo-paresis), but the dementia is less pronounced, the cerebro-spinal fluid is normal and improvement follows abstinence from alcohol. of memory and mental power. Masturbation is common. Usually steadily progressive and incurable, but this dementia may occur in childhood and may be transitory, in which case it may be cured by bromide. into a condition of apathy and more or less complete loss of intelligence. Patients may carry over into this stage some traces of the emotions and delusions of the former psychosis. They usually sit motionless ess (agitated dementia). I lymphocytosis in cerebro-spinal fluid. Wassermann usually positive.. Argyll-Robertson's phenomenon and often unequal pupils. Tremor of lips, tongue and hands. Loss of memory, loss of self-restraint, less and change in character are early symptoms. Speech blurred, slovenly and tremulous. Words, syllables and letters left out in speaking and in writing. Restless, excited and irritable, with exaltation or rarely recognizes as existent. Grandiose delusions, silliness and inconsistency in striking contrast with inordinate pretensions. Gradually increasing physical and especially mental weakness up to complete y apraxia (230, 2S2). Careless, inconsiderate, slovenly clothes, etc. Apoplectiform and epileptiform seizures are usually present in the course of disease. Incurable, but remissions. Frequently associated with Hebephrenic form. Catatonic form. Paranoid form. Korsakow's Psyche Alcoholic Dementi; 1096 1097 Adolescent Insanity or the so-called Dementia Precox 1098 (a term of very doubtful value). 1099 1100 1101 (65S, 1107, 1109) Epileptic Dementia, (575, 1058). Terminal or Secondary Dementia. Paresis. General Paresis. Paralytic Deineniia, (134, 177, 416, 419-20, 579, 675, 763, 895, 1049, 1216, 1230). 1102 1103 arteries. The dementia varies from day to day greatly in degree and may lead the patient to do very foolish things (often erotic), while apparently sane. Loss of will power (drunkenness). Depression and n of past memories. Dread of impending poverty. Desire to go home, imagining himself to be in a strange place. Restless at night, associated with hallucinations and delusions. Attacks of excitement. Senile Dementia. 1105 nd especially doubts their of hallucinations which cannot be reconciled with his previous experiences. He becomes confused, frightened and timid. Doubts his own identity and that of those about hii acts which might be rational were his hallucinations true. May be the early stage of other forms of insanity. Probably a form of moderate delirium. ions are of all kinds but are usually visual and concern snakes, spiders and other small grotesque and repulsive animals. Tactile hallucinations, shown by fumbling of the fingers, also are usually very evident. : from his enemies. Pronounced, continuous tremor and insomnia. Disease usually lasts less than a week and usually terminates in recovery. • exogenetic, such as belladonna, salicylic acid, etc.; or autogenetic, such as uremia, cholestrin, pti lelirium, w r hich may last a few hours or days or may continue during weeks, months or years. • septic (post-febrile insanity), especially when the poison acts upon an exhausted i Confusional Insanity. Delirium Tremens (1101, 1109). Toxic, Septic or Post-febrile Insanity. lazed feeling and delirium, followed by violent excitement and violent actions. Many hallucinations. Speech is continuous, violent and incoherent. Disease usually terminates fatally u , on the basis of hallucinations, more or less permanent delusions, especially of jealousy and persecution. These are often so exaggerated and monstrous as to be grotesque. A very common delusion atients often act violently. Some alcoholic tremor. Curable, and usually lasts less than a month after alcohol has been withheld. • three weeks. Acute Delirium or Delirium Grave Acute Alcoholic Mania. Alcoholic Hallucinosis (1101, 1107). These delusions are not associated with any decided emotional manifestations and are at times permanent, at times changeable; but they are not reasoned upon shrewdly and a systematic theory Simple Delusional Insanity. These delusions are of a pleasant exhilarating nature impelling to action, to talk and incidentlyto the disregard of the right of others. These patients are usually violent and dangerous to themselves and others. These delusions are of a depressive nature and tend to inhibition of action and speech, to self-abasement and to self-destruction. The patients sometimes seem to be in actual stupor (melancholia cum stupore) or merely profoundly depressed with inhibition of all action (melancholia attonita). At times the intensity of their grief drives them to frenzy and breaks through their inhibition and impels them to deeds k. ot violence (raptus melanchohcus). Occasionally there is restlessness (melancholia agitata). All these conditions seem to be the direct result of delusions. Such patients are very prone to suicide. the result of hallucinations. They are fixed, permanent and are reasoned upon. Newspaper paragraphs on indifferent subjects and various circumstances in the entire life of the patient are more or less distorted ji tempi el an explanation ,,t i lie curious things ulueli are happening to the patient. The patients reason very clearly and if their premises are granted it is almost impossible to answer their arguments. The delu- i nieoij is e\t.iv,.,| lo explain lliein. 1 lie most trivial happenings, even in the remote past, are fitted into this system in the most surprising and ludicrous way. The general result is that the patient regards Jiise so niai,\ persons busy themselves about his affairs. In typical cases the patient evolves first a delusion of observation (all things, even the most indifferent and remote have reference to him); next, a to injure nun or to try his character), and finally a delusion of grandeur (he must have a great destiny when so many persons seek to injure him or to tempt him). ind for which there is no discoverable adequate cause— "a cloud settles over the mind." A pessimist. No hallucinations, no delusions, except such as are secondary to the depressed frame of mind and invented ifrlilv ■ ' ".'l ,a ""'" ;i1,11 ' sm, etc. there is an inhibition of mental and physical activity. Patients withdraw themselves as much as possible from the world. They sit quiet and are pictures of woe. They 'Ociuy functions are greatly disordered. Curable. The secondary form of melancholia, due to delusions, has been described under 1112. Symptomatic or Delusional Mania. Symptomatic or Delusional Melancholii Primary Melancholia. iut any discoverable adequate cause. Optimistic. They have a mild form (maniacal excitation) and a severe form (frenzy) h usually, but not alwayi Mania is often sympto- Primary Mania comparatively normal period between the two. The duration and the intensity of the attacks and the duration of the interval i WnSi L™ iy - !lltm,at '; •• , , er A ,' onger or sl,orte , r interval (circular insanity). In some cases the excited and depressed phases are commingled, maniacal depressive insanity but the permanence of this term is doubtful. His classification involves a recasting of the nomenclature of mental dis, ■ the alternations are momentary, giving a ses, and it is doubtful if the time is yet ripe for s lixed form." lan attempt. Circular Insanity. Maniacal Depressive Insanity 1106 1107 1107a 1108 1109 1111 1112 1116 1117 CHART XVII Trophic and Sympathetic Disorders DIAGNOSTIC ANALYSIS OF SYMPTOMS TROPHIC DISORDERS AND DISORDERS OF THE SYMPATHETIC SYSTEM Symptoms Analysed 1120 Trophic Lesions. 1121 Disorders of the Sympathetic System. Tissues Involved fll22 Muscular Tissue. 1123 Cutaneous and Sub-Cutaneous Tissue. 1124 Fattv Tissue. 1125 Bone Tissue. 1126 Joint Disease. 1127 .Other Trophic Lesions. rll28 Ganglionic Disorders. 1 1129 (.Vaso-Motor Disorders. See Chart XVII a. See Chart XVII b. ■See Chart XVII c. VSee Chart XVII d. 193 CHART XVII a Muscular Atrophy and Hypertrophy ( lomprising Numbers 1 122, 1 130 and l 131 on left aide of < hart .■mil 1 1 It; to l L56 on righl margin DIAGNOSTIC ANAL I HI \<;.\<>STIC S\ M1TDMS \\H 1 I r face (Landouzy-Dejerin form) are first affected Some a atrophied, a few hypertrophied, Paralysis Is and is secon Very slow course. Muscular fibers normal, A true hypertrophy. The hypertn Tin- hypertn ( 'alf muscles, infr:i-s|)ili:i1 trophy. ( Hlicr muscles are botl generation: some atrophied, atrophied. Legs are early and i IS OF SYMPTOMS ND HYPERTROPHY SYMPTOMS m < omplete 01 par- ri' i tial electrical hi- reaction of degeneration nc! linn; electrical excitabil- i >■ 1 it] . hill DC "i degeneration: History of injury, wound, bruise or scar. Limited to distribution of one nerve (simple neu- ritis) or many nerves, (multiple neuritis). Usu- ally associated with m'Iisoia -\ inptoins: pain and anesthesia, nerve and muscle tenderness. (I roups of muscles attacked not corresponding to the distribution of any nerve. No sensory symptoms, except some pain at onset in back, joints and muscles. Very rarely nerve and muscle tenderness. Globulin and lymphocytosis in cerebrospinal fluid in acute \tlophv affects either the alius or the leji>. Selixin and other symptoms of myelitis ale present. Organic reflexes are more or less disordered. Superficial and deep reflexes are abolished in the paralyzed area. Vtrophy Commences in the small muscles of hands. Or muscles of shoulder girdle, and extends and is ■led with fibrillary contractions. Mild spastic paraplegia 525, 797) in leys Atrophy affects the muscles of tongue and lips and ociated with fibrillar] contractions, Mild spastic paraplegia (525, 79?) in leys Airophj affects the hands usually. Is associated with dissociation of sensation and often with on uid mutilation. DIAGNOSIS Injury of nerve (489, 822). 1 I 16 Neuritis (488-92, 822, 1)40-8 ). 1147 (Figs. 33, 38.) Vcute anterior poliomyelitis 1 1 t^ (495,789). (Figs. 28-7.) Myelitis of Cervical or Lumbar 1 1 18s Enlargement (48.5, 549) Amyotrophic lateral sclerosis 1149 (547 695, 797) (Figs. 26-7.) < limine bulbar paralysis (646, 1 150 'I'M Figs 21-2.) Syringomyelia (552,693, 837-9, 1150a 1009, 1170, 1357-9). especially with ankylosis, Many of these cases are neuritic, but in > s no Arthritic atrophy. of shoulder girdle i Krli.- juvenile type . or of legs (pseudo-hypertrophic es apparently hvperi rophicd Excised muscle fibers show degeneration: some increase of interstitial fat No fibrillary contractions. ,h3 The atrophj entirely to ■■ No electrical reac- tion of degenera- tion. The reflexes are exaggerated Ankle-cl i ind are present when legs are affected, unless prevented b] conl rat I uret Muscular dystrophies (477 786, 1152 1156) A paralysis of long standing, 1163 especial!] one from infano] result of much exercise, is due to irring at the commencement ol voluntary motion Strong man or al hlets 1 1" 1 1 Thomsen's diss ise (613 1 166 id -nine other mils' ll rge, but are w< ■ 1 1 • n i hyper- Ik and atrophied No fibrillar] contraction Excised muscle Boers show de- vpei trophied and much interstitial fat l\ affected. out • \ll muscles are finallj Pseudo-hj pertrophic 500 and the iiiii- ul ii d\ - trophies (118 CHART XVII b Cutaneous and Sub-cutaneous Trophic Disorders Comprising Numbers 1 123 and 1 132 to 1 L3S on left Bide of Cnarl and 11(30 to 1173 on right margin 197 DIAGNOSTIC ANAL il CUTANEOUS AND SUB-CUTANEt DIAGNOSTIC SYMPTOMS AND TESTS 112.3 CUTANEOUS AND SUB- CUTANEOUS TISSUE 1132 Atrophy. L133 Hypertrophy. 1134 Eruptions. 1135 ABSTRACT ( [The skin is unusually smooth and thin. The fingers become pointed. change occurs quite frequently in nervous diseases, especially in t.l . The hair falls out, either all over head, face and body (as in syphilis) I skin is not changed in appearance. Allied to this condition is thi I consequence of severe pain, or psychic shock, or unknown cause JAtrophy of the normal pigment of the skin; so that patches of clear j persons of dark complexion. The edge of the patch is more deep] '-See also facial hemi-atrophy, 1179. The skin and mucous membranes everywhere appear thickened, as if ii slightly, on pressure. The skin is sallow, dry and scaly. Patient body and features are enlarged. Nails, teeth and hair break ai heavy. Voice is slow and hoarse. Response is slow and intellect disordered. The thyroid gland is atrophied or destroyed by I re val of t lie thyroid gland. Arterio-sclerosis and interstitial in Common in women than in men, and frequently occurs at the time in children they become dwarfs. The cause of the disease is th thyroid gland and it can be cured by the administration of the thy The skin is thickened, generally or locally, infiltrated, very firm an especiallj at their ends, and the fingers become much shortened ! in women than in men and seems to be allied to myxedema. Tin dis ocdematosum) and ends with an atrophy of the indurated patch (, Clusters of vesicles filled with clear fluid, each cluster upon a patch i or two nerve roots and strictly limited to their distribution. Th' It is usually accompanied, preceded and followed by severe pain in pain may continue for months after the rash has disappeared. In some forms of nervous disease (especially in hysteria) elevated pa always when the skin is irritated (urticaria scripts dermographia sometimes do not. Successive crops of bullae, which are at first small vesicles and inereu- Several vesicles may coalesce. There may or may not be fever may be intense. A very fatal disease. No spa the a With much loss of tissue. 'Ulcerations larger and smaller with sloughing and loss of phalanges and even whole lingers and toes. The whole process is painless and may in part be the result of traumatism in the analgesic parts. scum! IHTVi Spastic turb: tore over syni] With small loss of tissue. See also Raynaud's, diseasi 1 L95). Large, deep, sloughing ulcers commencing wi patients usually suffering from motor and .- subjected to much pressure (sacrum, trocha pulously clean. \n uli .ration usually commencing on the bal and painlessly extending deeper, until in u on its dorsum. Such an ulcer very rarely which ulcerates and the pus escaping forn lary reflexes and other symptoms of tabes ai in the urine in a small minority. Ulcerations more or less severe, the result ( Bkin is often bronzed. Symptoms of neurit . IS OF SYMPTOMS 5 TROPHIC DISORDERS I SYMPTOMS k curved and are striated. This in which the peripheral neurons are degenerated. <>nly in patches, usually on the head and face. The rnmsi white of the hair in patches, or universally, in i of haii dye itc appear. They are, of course, most noticeable in igmented than the surrounding skin. DIAGNOSIS Glossy skin. Alopecia, (general <>r areata). Vitiligo and I.eucoderaaa. 1160 1161 UG2 rated, and do nol pit, or pit but e very sensitive to cold. The all out. The movements are ty very sluggish and at times i-e. The disease may follow it is may lie present. Is more ie climacteric. When it occurs isence of the seeretioli of the ! gland. < lecturing adults. ( Iccurring in children. ird. Tic bones of the phalanges bee ime absorbed, abnormally movable. The disease is more common often i urn-ices :is :i loc:d patch of edema stadium limn atrophicum). At times patches are pigmented. I lene I skin; tin- clusters following the course of one uption dm-, up ami disappears after a week or two. nerve, along the com 1 which it is situated. The Myxedema. Cretinism and Dwarfs (1090, 1177). Scleroderma ami Sclerodactyly. Herpes Zoster. Herpetic Neuritis 1163 1164 1165 t, white or red, appear, at time- spontane tusly, and Such patches of urticaria sometimes itch and Urticaria (1201). 1167 an\ Bise. appear on the skin and mucous membranes. burning sensation- and the pain symptoms in legs. The disturbances are limited to tribution ol one or more nerves. All forms of V are abolished. Small tumors may occur along the inks, together with other manifestations of leprosy. nptoins m legs, when, a- is usual the tropin. • di -- s are hunted to hand- and arms I'am ami teinpeia- il tactile Bensibilit] , usuallj rea Kj phosit ind spondylitis are common Pemphigus. Leprous Neuritis Syringomyelia or Morvan's disease (562, 693, lis: (Figs. 26-7.) 1168 llti'.i 1170 nd occurring only in bed-ridden iry paralysis, and occurring almost al - ,U: n hi a the parts are not kepi Bed Sores. | decubitus, the foot, not growing larger superficially, but slowlj il cxtoml ■pi!'-' through the fool illy commenci - jerk. urgyll-Robertson's pupil- rencnl in the majoril hile sugar is pi Perforating Ulcer of Tabes and (rarely) Syringo myelia and I linbi j ighl traumal ism In I iraeni al neuritis, the ■ it . Neuriti I 8, II I7i CHART XVII c Trophic Disorders of Fat, Bone and Joints Comprising Numbers 1124 to 1127 on lefl side of Chart and 117") to NSs on ri<;ht margin 199 DIAGNOSTIC ANAL^ TROPHIC DISORDER! DIAGNOSTIC SYMPTOMS AND TESTS ABSTRACT < 1124 FATTY TISSUE. 1136 Atrophy. | 1137 ^Hypertrophy. 'Failure in development. 1125 BONK TISSUE. 1138 Atrophy. 1139 Hypertrophy. 1140 Fragility. One of the earliest symptoms of diabetes mellitus is an inability of the l excess of fat had been deposited. Patients lose weight and if the dise urine shows the constant presence of sugar. Atrophy of Fat and emaa Large and tender deposits of fat, in lumps or in layers, widely diffused c Arms and legs painful and tender, especially in the acute stage when tl frequently in middle aged women (often alcoholic or syphilitic). Many eases OCCUT, either eongenitally or acquired in early life, in which so that the individuals remain throughout life of abnormally small si a due to atrophy or loss of function of the thyroid, or pituitary, gland. mally formed (simple dwarfs or decidedly undersized men), while ot tl described elsewhere, under infantilism and mongolism (1093), erelinisi (chondro-dystrophia foetalis) there is a dystrophy of the epiphyseal <■ normally in length; SO that dwarfism results. The head is relatively li especially their proximal segment, the hand is short, the fingers broad, lordosis, pelvis contracted, legs often bowed or knock-kneed and joi developed. Adults, as well as children, not infrequently become shorti in the legs, as in rickets, osteitis deformans (1182), osteomalacia (11!- kyphosis, etc. In cases of extensive acute anterior poliomyelitis and of cerebral palsy of cl or very slow growth of the part from disuse. One side of the face is much smaller than the other, due to atrophy of al fat. The process is usually progressive. It seems to be caused by inji neuritis. Dryness, scaliness and loss of color of the skin are common small area atrophies, which atrophy gradually extends laterally over il process continues until the entire half of the face is atrophied and, in parts of the body. One side of the tongue is usually atrophied. I'a the atrophy. One side of the face is much larger than the other, due to enlargement of progressive, and seems in some cases to be due to a periostitis. The bones of the head and face arc enlarged, diffusely or nodulated, and them. Headache, neuralgia, blindness, deafness and facial paralysis are not enlarged. Forehead is bulging and head is often of great size Disease commences late in life with slight pains, especially in legs. Th jaw is not enlarged. The head enlarges, the legs and vertebral coliiii patients become shorter (even as much as a foot or more) and their w: Symmetrical enlargement of all the tissues, but especially the bones of tin etc. It, comes on gradually, patient requiring larger and larger gloves Shouldered" (kyphosis). These changes arc often associated with bib head and joints is a common symptom. The disease is caused l.\ lr in early life, before the epiphyses arc joined by bone to shaft, gigantis The hands and feet are enlarged, and the lingers and toes "clubbed." Th by the X-ray. These symptoms arc associated with chronic puhnonan * toms vary greatly in degree and extent; the mildest form being "clubl In some persons the bones are unusually brittle and break upon the sligh of these cases occur in old age (senility), others occur in middle life, du malacia), while others occur in children. The disease causing it thvrosis, etc. 1120 JOINT DISEASE. 1127 OTHER TRO- PHIC LESIONS. Joints painless, enlarged, abnormally movable, especially liy perextc nsinii, cartilages eroded, effu- sion of synovial Quid, exostoses of bone. The exciting cause for these changes is often painless traumatism, at least in part. (■Joint involvement not un- Knee-jcrl- common. Usually in legs. Bladde ! Joint involvement rare. Usu- Knee-jcrl tally in arms. Loss ol 1141 Atrophy and hypertrophy. Atrophy OT hypertrophy of different organs (mammary glands, tongue, etl quently met with and may be due to disordered nervous action, but tin S OF SYMPTOMS F FAT AND BONE SYMPTOMS t • > deposit fat in the tissue, although previously often bo is long continued Inn. mi- emaciated. Examination of the mi occur in fevers and in many other conditions. arms and legs. Face, feet and hands not much involved. it i- being deposited. Locomotion impeded. Occurs most DIAGNOSIS Diabetes Mellitus (900, 1172). 1175 Adiposis Dolorosa. Dercum's Disease (1012). 1170 ■ bony framework of the body does not develop normally; - reason to believe that some of these cases are individuals are merely small but otherwise nor- show many physical deformities. Some eases have been kMO, 1164) and microcephaly [1084). In Achondroplasia ■gas, in consequence of which the bones do not increase the bridge of the nose depressed, the arms and legs short. ■most equal length and divergent undent shape), lumbar aluiormally lax. The muscles are rather unusually well i consequence of excessive bowing of weakened long hones etc. and in consequence of curvature of the spine, 08 in hood occurring in infancy there is often an arrest of growth even of the hones, and especially of the skin and or cold and in some cases is due to a trigeminal (Btoms. The process commences in the skin, of which a vin and inward to the fat, muscles and even In. lies. The beyond the median hue and even to other n the trigeminal nerve usually precedes and accompanies. Dwarfism, Microsmia, Nanosmia, Achondroplasia 1177 (1164). Disuse from Paralysis. Facial 1 temiatrophy. 1178 1179 Lilly of the hones. The process i.- usually v cause pressure symptoms on the nerves running through I thus, common symptoms. Lower jaw and extremities Facia] I [emihypertrophy. Hyperostosis Cranii or l.eontiasis Ossen. 11S0 1181 >rics of the hod> become enlarged and soft, hut the lower ■come Lent and bowed (spondylitis and kyphosis). The ted. nils and feet, lower jaw, and .-termini, also ears, tongUO, I -hoe-. Thorax is much enlarged and patient is "round iral hemianopia, follow Pain in trophy of the pituitary body. If the disease commences isteaii ..1 pes of the fori -a i d ften enlarged, as can be shown eptii "i tuberculous nature usually. Thesymp- violcnce. oven on turning the patient over in bed. Borne softening of the hone and diminution of lime sal' •en variously named: osteogenesis imperfecta, o Osteitis Deformans. Paget's Disease. Acromegaly and Gigantism, I ragilita I Issium. < toteopsath] rosi 1182 lis:: Hypertrophic I'ul nary < Osteoarthropathy. 1 1 s i liv. ire absent Pains in lee-. Ataxia without paralysis. .■inpti.m- \re\ ll-lo.l.ei i-un's pupil rellex. I'am- in aim I' o ,1 1 .,f arm- (alight I. infill and thermic, with persistence <>f tactile, sensibility. or other part • nt i»»l\ hands, fingers, i to I, are not infre- r, ..i ob cure lignificance and are without diagnostic value. Arthropathy of Tabes (661 I. (Charcot's Discaai 1 186 l Kins Byring yelia (562, 603, 1170) (Fl§«. 24-7.) " s " Localised Hypertrophies and Atrophies, symmet- 1188 rioaJ and asymmetrical CHART XVII d Ganglionic Disorders, Vaso-Motor Disorders < omprising Numbers 1128, L 129 and l ill' to 1145 on left aide of Chan and 1191 to L203 on right margin 101 DIAGNOSTIC ANALY GANGLIONIC AND VASO DIAGNOSTIC SYMPTOMS AND TESTS rll42 Parah I ii 1128 GANGLIONIC DISORDERS. 1143 Irritative. lilt Vascular 11 _".i VASO-MOTOB DISORDERS. 1 1 1-', Exudative Secreton ABSTRACT OF Ptosis "I eyelid, although patient can raise it perfectly l>y an effort of will fj not dilate when shaded, although it contracts briskly when eye is exposed sure with retraction and lowering of eyeball (enophthalmus). Intra-oc abolished, flushing of skin and absence 01 sweat on the affected side of fac( third rib. The symptoms are exactly opposite to those of paralysis of the cervical syn widening of the palpebral fissure (Stellwag's sign) and delayed d< ■ The Boston-Kocher's sign, an amplification of Graefe's sign, may occur in Exophthalmus, tachycardia, goitre, flushing, sweating, tremor, nervousness, ward (Graefe's sign), widening of the palpebral fissure (Stellwag's sign), thl The d -ease occurs much more frequently in women than in men and althi the cervical sympathetic ganglia, yet it is really due to excessive secretion the reverse of those of myxedema (1163), can be produced by the adrnini extirpation of the thyroid. Paroxysmal spasm or congestion of the bronchioles, often reflex from nasal nervous temperament ot most asthmatics, togetherwith the very rapid on may be due to a disturbance of the thoracic sympathetic. The paroxyBn prolonged expiratory murmur, make the diagnosis easy. Asthma is assocL be in part voluntary, in part reflex; also is usually associated with bronch Paroxysmal attacks of coldness and pallor ("dead fingers," "local syncope" of all together. These attacks may last a few minute- or hours and then the same parts become dusky blue, or purplish black ("local asphyxia or c This attack may pass off, after several hours, with abundant sweating, or grenous and finally slough off. The necrosis does not usually invol metrical. It is more common in cold weather and is often brought on bj Hematuria and evidence of congestion of other internal organs may occur Analogous! to Raynaud's disease is gangrene of extremities occurring in mam old age; either without the local syncope ot loci,] asphyxia, or with only s Paroxysmal attacks of formication, tingling, numbness and other p intervals and exclusively m women, They seem to be brought on by ovei cases during the attack the skin becomes pale and blue. Similar symptoms Paroxysms of severe pain in one foot, rarely in both, rarely in hand- and ver creased by allowing foot to hang down, or by motion of it, or by cold. Tl redness and swelling of the whole, or part, of the sole of foot. Usually a to a simple va-o-motor neurosis. The neuritis, when present, is often a8S0 Occurs in middle aged or elderly persons and is associated with arterial disease walk and increases so that walking becomes impossible. It passes off after attack the feet are cold and then' is absent or greatly diminished pulsation i alcohol and tobaCCO and injur\ seem to he common cause- of this condition feet. The arms are rarely involved. In many diseases if lines or writing lie traced on tin' skin with a sharp point, t to lines of bright redness, which persist for minutes or hours. rParoxysmal attacks of localized edema of sub-cutaneous or sub-mucuou a few hours or days. The extent of the edema varies greatly. I' ! extremity, or even more. It ma\ cause death when occurring in the larynx -ure. They occur in hysteria and are usually associated with a neiiiasihei ociated with symptoms of digestive disorder, thej an' called urticaria cept the itching. The disease often show.- a strong heredity ami at timet Edema of the lege, unilateral bet ling bilateral, bad heredity. The edema i being a sudden demarcation at the level of the joint, The edema may be ai Some cases present paroxysmally or constantly a profuse -wealing, usually loca OF SYMPTOMS OTOR DISORDERS fMPTOMS l>I VGXOSIS ido-ptoeis). Contraction of pupil (myoeis), which does Paralysis of Cervical Sympathetic. liulit and on convergence, narrowing of palpebral fis- t<-ri^i< >n diminished. The cilio-epinal reflex 3353 is d also mi aide of neck, or of arm and thorax above the ll'.tl lulu Dilatation of |iu|nl (mydriasis), exophthalmic, ■r eyelid when eye is turned downward I ri -■■ ami in exophthalmic goitre (1 L93 ■ i-iii ot upper eyehd when eye \i turned down« and systolic murmur in vessels of neck ami in thyroid. • it it- symptoms may In- referred i<> disorder of mid gland. Many df n- symptoms, which are ti.m df thyroid gland, and the disease '-an In- cured by Irritation of Cervical Sympathetic. Exophthalmic Goitre. Freedom from symptoms in the interval. The and cessation of tin- attack, indicates that the disease ol dyspnoea, with the abundant drj rale- ami with strong contraction of tin- diaphragm, which may \stlima 617). tingli il; of fingers or toes or tip of nose or of eat - oi iff, or may In- followed byan attack, in which from congestion. Tin- is associated with pain. 'I t Ik-mi. may liccomc gan- be cyanotic .ilea. I ' i usually svm- hands iii cold water, or by working with hand-. • e-k- iioiii childhood to indicati conditions in -ome of the cases. i Angei occur at irregular k ami by having the hands in cold water In some occur in tin- ■ romegaly 1 183 I ice. last inn a feu minutes "i a few hours, m- am. except iii the earliest attacks is accompanied bj only, ami i- generally due to a net • I with atheromatous artei ul cramp occur- in mi rfter a Bhort • to return if walking i- re-uined. Dunn- the ■ i- pedi oi posterior tibial artery, Syphilis, infrequent!) pre 'odes ■-• ingrei f the Raynaud's Disease, Symmetrical Gangrene Mill . 1195 I'amilx i iangrene \i i < i|>:u i —i besia. I i\ thromelalagia 1010) Intermit tent Limping Vngio-Sclerotica 554 [ication Dyabasia 1199 bul i change Dermographia (326, 1167). I _'l N I iher white or red, lasting tape-Neurotic Bdema and Urticaria. 1167), 1201 ■hall inch in din ijun, inditioi i in clor itch and Iraw ii between the two di I" limited above bj the ankle, knee "i groin; then \hlrm oi ' ' phoden Hyperhidi ive Sweating CHART XVIII Syphilis of the Nervous System I !omprising Numbers 1205 to 1217 DIAGNOSTIC SYMPTOMS AND TESTS DIAGNOSTIC ANAI SYPHILIS OF THf 1205 S"5 I II I LIS 01 THE NERVOUS SYSTEM. Hi- tory of personal, or hered- itary, syphilis. Physical ev> dence of syphilis; such as W assei 1 1 1 : 1 1 1 1 1 reaction, a chancre or its scar, indu- ration, mucuous patches, a syphihtic rash or ite copper colored scars, hazy cornea, notched teeth, furrows about angle of mouth, saddle nose, ptosis, iritis, enlarged glands, pi i iosteal nodes, etc. 'Syphilitic Nervous Diseases. Symptoms of syphilis of the nervous system are very variable from day to daj transitory and manifold. They consist of paresis, rather than of complete paralysis. They usually show rapid im- provement under K.I. and Hg. or Salvarsan. Nocturnal headache is common, as are also the Argyll-Robertson's pupillary reflex, unequal pu- pils and optic neuritis. i lerebral symptoms. Although these symptoms can lie divided into several, more or less well defined, groups, yet a combination of several or all of the lesions, in varying intensity, is not infrequent; so that a combi- nation of the symptoms of several or all of the groups may be present in one case. Pure, uncomplicated cases "i each type are, however, com- monly met with. Spmal symptoms. i Both forms of spinal syphilid may occur together i ( lerebral and spina symptoms. 'Little or no ivii in cerebro-spinal lumbar puncture. ( llobulin and d "i \ tOSis is foil spinal Moid (jiuneture. eeid. lid ii from No globulin and lit lymphocytosis I'mni cerebro-spinal fluid lumbar puncture. ( llobulin ami decide oeytosis found in spinal fluid from puncture. ( llobulin and decide oeytosis in cerebro fluid. 1 ■''' Peripheral symptoms. Wassermann reactio blood. Normal eerebi Hind. Post-, or Met.,-, syphilitic ("Cerebral symptoms. nervous di-ease. spmal symptoms. I increased lymphoqj fcerebro-spinal fluid. SIS OF SYMPTOMS ERVOUS SYSTEM from Vlliph- rebro- imliar ABSTRACT OF SYMPTOMS Symptoms of cerebral tumor (507, 636). Other syphilitic ptoms may be present. Rapid course with irregular remissions and intermissions. The symptoms of cerebral compression are much less pronounced than in non-syphilitic tumors. Very amenable to anti-eyphilitic treatment. Symptoms of cerebral thrombosis (506). The attacks occur rather early in adull life. There are manj prodromata Nocturnal headache is common. The p noderate in degree, variable in intensity and often temporary Mental derangements, often in the form of trance-liki frequently occurs. Branches of the basilar arterj are in- volved most frequently, and the attack often occurs during sleep, or without coma during the day. ^Symptoms of cortical irrita- tion (Jacksonian epilepsy, local headache and tender- id paralysis of cortical function mono- Mental de- rangement is comi and often takes the form of pseudo-paresis), but ible to anti-syphilitic treatment. Symptoms of meningitis (590, hi is*, which ma} be very slight and very variable. \\ ill, severe headache noi there may |„ and vomiting. Little or no elevation of temperature or So tuberculi dence of tuberculosis. This hildren. mptoms of cortical a or paralysis ol functions, r "i cranial nerves (e | 'i oulo-motoriue ■ irregular distribu- tion and m varying degree. Drowsiness and stupor are .common, ,, r do f^ynptoms of Brown-Sequard's paralysis, or later of para- plegia II.'. 509, 840, 981 ptonru of myelomalacia 185, 513-4, 517-8, 549-50). mptoms of lateral scl mpn- mlial Symptoms of spinal menin pachymeningiti Rigiditj of back. Girdle pain radiating pains, exaggerated reflexes in legs S i theBe '"'-'- present the symptoms of progressive spinal mils. ' A combination ol the '- mptuim 12084, 1213 in intensity \ clinical picture compri pina) symptom and presenting hich arc impo Bible to describe in a leu WOI DIAGNOSIS Isolated Cerebral Gumma Cerebral Syphilitic Endarteritis 1207 and Thrombosis Syphilitic Meningitis of Con- 1208 verity of Brain. Syphilitic Meningitis of B Brain, including K I liscase. L209 Isolated Spinal I .11111111:1 Spmal Syphilitic Endarteritis and Thrombosis. I. ii.'s Syphilitic Lateral IOSIS Syphilitic Meningitis of Cord and ..I \. 1 \ e Root \lniiii- go-myelitis, Pachymeningitis < lervicalis ll\ pertrophica.J 1210 L211 1212 1213 the Sympton pinal ■ I, 940-8 1 loi nptotns of be tor atari i 661 < 'erebro-Spinal 83 philis Syphilitic Neuritis Looomotoi Marin 1 ibei I'.c '. 1215 i.'i.. IJI7 CHART XIX Abnormal Cerebro-Spinal Fluid Comprising Numbers 1220 to 1242 •jii: L223 Leucocytosis 1221 Butyric acid tesl positive. l2 20 \n\m;.\i \i. I EREBRO- 8PINAL I l.i ID 1224 Lymphocytosis. L222 Butyric acid tesl negative. DIAGNOSTIC ANA1 ABNORMAL CER1 Weichselbaum's diplococcus intra-cellularis meningitidis or rarely Pneumococcus Weichselbaum's diplococcus. I'ncuiiineoccus, Pfciffcr's bacillus. Streptococcus, Staphylococcus, Typhoid bacillus. Bacterium coli, etc Tubercle bacillus. "i (■Tubercle bacillus TESTS AND I> Fluid im.-iv be Tension mere Wassermann tive. •Iloll posl- \\ assei 111:11111 react ion nega- tive. 1225 No Lymphocytosis or Leucocytosis No bacteria and \\ ossermi negat ive Fluid usual!} under high tei Fluid usually cate coagulu liii;li tension. Fluid clear bacteria. Tension is us but not very Fluid cIcm tension; in bloody 5IS OF SYMPTOMS *0-SPINAL FLUID tNOSTIC 8IGNS DIAGNOSIS i or cloudy. Occurs in epidem- Symptoms of epidemic Cere- Epidemic Cerebro-epinal Meningitis. 1226 1 usually. bro-spinal meningitis (591). loudy and < Iccurs .-( ior;n I- ically. Symptoms of sporadic or Sporadic Purulent Meningitis. purulent cerebro-epinal men- ingitis (592). 1227 r with deli- and under I Acute course. ( 'limine course. f Acute, or sub-acute Tuberculous Ma Symptoms of tuberculous ■ Meningitis, meningitis 59 Chronic Tuberculous Meningitis [Tremor and mental Sympl b of Paresis (1104). Paresis. symptoms. free from . Ataxia Symptom.- of Tabes (661 1. Tabes. Symptoms not typically characteristic of paresis Cerebro-spinal Syphilis (1208-9, 1213- or tabes, being due to a cerebro-spinal menin- 14). *■ gitis. Motor paralysis. Symptoms of acute anterior Acute Anterior Poliomyelitis. poliomyelitis i 195). I Figs. 26-7 1228 1229 1230 1231 1232 Herpetic rash Symptoms of herpes Boater Herpes Zoster - 1 166). l-pid.i High Symptoms of Typhus. fever. T\ phus Fevei Choked disc usually Symptoms of cerebral or Tumor present spinal tumor 507, 678, 587). Symptoms of cerebral or Abscess spinal abscess .Mis, ,"i7s, 587). t 'lioked disc mi I., pn cut Headache Apo w Sj mptoms of hydrocepl 1 1 ill. no:,, 966). ' this Hydrocephalus. Symptoms of serous menin- Serous Meningiti tin- (594 Symptoms of cerebral or He rrh spinal hemon li i' i A U him i. r , [examination of the nunc I remia albumen and casts 1 !• mi, headache, dj spnoi n etc usuallj present Anemia I Examination -leu anemia, Anemia pallor, etc . or anii,' infec- tions, "i tome similai con ditions vs.\:, 1236 1237 1238 1239 1240 PART III LOCALIZATION OF LESIONS WITHIN THE NERVOUS SYSTEM BY A CONSIDERATION OF THE PARALYTIC AND IRRITATIVE SYMPTOMS RESULTING FROM THEM CHART XX Spinal Localization Comprising Numbers 1250 to 1267 90S TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD Modified from Wichman Segment Involved Reflex Sensory Motor Conditions Conditions Conditions , Anesthesia In- with a zo^e of creased hyperesthesia _x in surrounding it or limiting Actions lost or partia Paralysis Paresis impaired Absent lesions it above 1250 None. Coccygeus. Elevation of Anal. None. Skin over sac- V coccyx. rum and anus. Sacral 1251 Coccygeus. Levator ani. Elevation of Erection None. Slightly larger IV coccyx. of penis area than above Sacral Sphincter ani. Elevation of anus. dimin- extending over Detrusor urinae. Sphincter ani. ished. inner portion Transversus perinei . Ejection of urine. of gluteal Erector penis. Vaginal constriction . region. Compressor urethrae. r Sphincter ani Rectum. Defecation dis- Ejaculation As above, and Levator ani. turbed. lost. perineum, gen- Detrusor Retention of urine, Erection itals and upper 1252 urinae. later followed by diminished. part of inner III - Transversus dribbling. Tendo- surface of Sacral perinei. Erector penis Compressor ■ urethrae. Ejaculation lost. Erection possible Achillis. thighs. (Testicle sensi- but paretic. tive to pressure.) f Sphincter ani Pyriformis. Outward rotation Ejacula- None. As above, and Levator ani. Obturator internus of thigh. tion. the posterior Gemellus superior. Retraction of thigh Erection. surface and Gluteus maximus. Flexion of knee. Plantar outer surface Biceps femoris. Plantar flexion of weakenec of thighs. 1253 Gastrocnemius. foot. n H Soleus. Standing on the toes Sacral Tibialis posticus. Raising inner margin Detrusor urinae of foot. and other All the small mus- Defecation and muscles as in cles of foot. Retention of urine . 3d sacral. as in 3d sacral. 210 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD (Continued) Modified from Wiehman Segment Involved Motor Conditions Reflex Conditions 1254 I Sacral Paralysis Muscles of anus. Muscles of bladder. Muscles of genitals. Piriformis. Abductor hallucis. Flexor hallucis brevifl. 1-1 V dorsal interossei. I-III plantar interossei. 111-IV lum- bricales. Abductor minimi digiti. < )|>ponens I. minimi digiti. Paresis Actions lost or impaired Absent Sensory Conditions Anesthesia with a zone of creased hyperesthesia in surrounding partial it or limiting lesions it above In- Retention of feces. Retention of urine or dribbling. Plantar None. Erection and ejacu- weakened. lation impossible. Achilles- Gluteus maximus. Obturator internus. Gemellus superior. Gluteus mediae. Gluteus minimus. Biceps femoris. S( 'in i - membranosus Semi-tendinosus. Popliteus. Gastrocnemius. Soleus. Tibialis posticus. Peroneus longus. Peroneus brevis. Flexors of toes. Extensors of toes. tendon reflex. Ejaculation. Erection. Micturition. Defecation. Gluteal. 1 •_».-.:. Y Lum- bar Muscles of anusGemellus superior. and rectum. I is of Madder. Muscles of genitals. Pyriformis. Biceps femoris. Flexors of Peroneus longus. Peroneus brevis. Gemellus inferior. Gluteus medius. Gluteus minimus. Semimembranosus Semi-tendinosus. Gluteus maximus. Tensor fasciae femoris. Gastrocnemius. Soleus Extensors of toes. Tibialis anticus. 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 gnat toe, abduction of little toe, etc. Defecation. Micturition delayed, dribbling. Erection and ejacu- lation impossible. ( hit ward rotation of thigh very difficult. Inward rotation impaired. Flexion of knee difficult. Retraction of thigh ('.luteal very difficult. Flexion of fool barely possible. Flexion of toes impossible. Extension of toes weak, except great toe, which may he dorsallv flexed. Raising inner margin df fool difficult. Raking outer mar- gin of foot im- I ile. As above, and a strip on posterior and outer surface of lower legs and of dorsum of foot and especially of toes. Ejacu- lat on. Plan- tar. A< above, and hack of thighs Erection. Tendo- and legs and Achil- inner and outer lis. margin and Micturition. sole of feet. Defecation. -Ml TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD Modified from Wichman Segment Involved Reflex Motor Conditions Conditions (Continued) Paralysis Paresis Muscles of rec- tum and anus. Muscles of bladder. Muscles of genitals. Obturator internus. Obturator Pyriformis. internus. Gemelli. 1256 Gluteus IV medius. Lum- Gluteus bar minimus. Gluteus maximus. Biceps femoris. Semi- membranosus. Semi- tendinosus. Popliteus. Gastrocne- mius. Soleus. Flexors of toes. Extensors of toes. Peroneus brevis. Peroneus longus. Tibialis anticus. Muscles of Vastus internus. anus, bladder Rectus femoris. and genitals. Crureus. Outward ro- Adductors of thigh, tators and Flexors of thigh thigh. at the hips. Inward rota- tors of thigh. 1257 Retractor III (flexor) thigh. Lum- Flexors of knee, bar Plantar flexors of foot. Flexors of toes. Extensors of foot. Vastus externus. Rectus femoris. Vastus externus. Vastus internus. Adductor magnus. Adductor brevis. Adductor minimus. Gracilis. Actions lost or impaired Absent Sensory Conditions , Anesthesia In- with a zone of creased hyperesthesia in surrounding partial it or limiting lesions it above Defecation, with Patellar Plan- fecal incontinence, may be tar. Micturition, with wanting, dribbling. Erection and ejacu- lation impossible. Outward rotation of thigh weak. Inward rotation impossible. Retraction of thigh impossible. Flexion of knee lost. Plantar flexion of 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. All movements of Patellar Ankle- legs are lost, except and clonus that extension of cremas- may legs is barely pos- teric. exist. sible and that the thigh can be flexed on body by the psoas and iliacus. Defecation and mic- turition are de- stroyed. Urine and feces dribble and cannot be retained. 212 As above, and inner side of lower legs and dorsum of feet, and strip on outer posterior surface of thighs. As above, and whole of legs except a tri- angular area on front of thigh with base at Pou part's ligament. TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD (Continued) Modified from Wichman Segment Involved Motor Conditions Paralysis Paresis 1258 Paralysis of ] 11 all muscles Lum- of lower bar extremity, except psoas. 1259 Total paralysis I of whole lower Lum- extremity, bar psoas included. Paralysis of lower extrem- ity, and gluteal 1260 region. XII Paralysis of to III abdominal and Dor- and dorsal sal regions, gradu- ally added as the site of the lesion ascends. 1261 As in 3d II dorsal. Dor- sal 1262 All mil 1 of trunk and 1 Dor- lower ex- 1 sal tremitiee. Psoas. ;s Reflex Senbobt Conditions Conditions * Anpsfhesin Absent Patellar, Achilles, and cremas- teric. In- with a zone of creased hyperesthesia in surrounding Actions lost or impaired Complete paralysis of legs, rectum and bladder. As above. partial it or limiting lesions it above Achil- Whole of legs les and pelvis, may (Testicles not be in- sensitive to creased, pressure.) Plantar. Cremas- Patel- As above, and teric and lar ab- groins and front Achilles, sent or of scrotum and in- penis. creased. Epigas- Patel- As above, and trie and lar, a band running umbical ere- around body reflex. mas- about two seg- terie, meiits below Achil- the one in- les and volved and Plan- limited above tar. by a narrow zone of hyper- esthesia, All below All As above, and losl in subja- a strip on the complete oeni inner side of the division re- upper arms. of conl. flexes. Flexion of fingers. Asal»>ve and weak- Oculo- All As above, and Muscles of the little oesa is flexion of papillary Bubja- a strip on the finger. fingers. symp- sent inner side of the 1 1 1 and IV inter- Pronation dis- toins. re- forearms. ossei, turbed. All below Sexes. Lumbric losl in Pronator quadratua. complete Lower part of pec division totalis major. of cord. Lower pan of pea toralil minor. As above, and paralysis of mus- cles of respiration causes diaphragm- atic breathing and dyspnoea. As above. .- 1 3 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD (Continued) Modified from Wichman Segment Invol VED Reflex Sensory Motor Conditions Conditions Conditions , Anesthesia In- with a zone of creased hyperesthesia A in surrounding 1 it or limiting Actions lost or partia Paralysis Paresis impaired Absent lesions it above Paralysis of Flexors of the lit- As 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 ities. Flexor subl. digi- thumb and the Abductor of torum. ulnar surface little finger. Flexor profun. digi- All below of the little Adductor of torum. lost in finger. 1263 thumb. Flexor carpi ulna- complete VIII Flexor of the ris. division The cervical Cer- little finger. Extensors of the Hand weak. of cord. sensory nerve vical Opponens thumb and fingers. roots supply the minimi digiti. Triceps (slight). Extension of arm. same area of the Ill and IV Latissimus dorsi Int. rotation and skin in common, interossei. (lower part). retraction of arm. especially in the Lumbricales. Pectoralis major. Pectoralis minor. Scalenus medialis. Scalenus posterior. 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 (Winged scapulae.) Forearm hands and a Flexor pro- Abduct ins Retraction and in- reflexes. small strip on fundus digi- of thumb. ward rotation of Palmar the anterior, torum (ulnar Extensor indicia. arm. reflex. another on the side). Extensors of the posterior, sur- 1264 Flexor carpi fingers (movements face of the VII ulnaris. barely possible). All below forearm. Cer- Small hand Supinator longus. lost in vical muscles. Biceps (very slightl; y complete Pronator paretic). cord quadratus. Triceps. Pectoralis major. Serratus magnus (slight). Latissimus dorsi. Teres major. division. 214 TABLE OF SYMPTOMS IN TRANSVERSE LESIONS OF THE CORD (Continued) Modified from Wichman Segment NVOLV ED Reflex Slnsory Motor Conditions Conditions Conditions A Anesthesia In- with a zone of creased 1 hyperesthesia A in partial surrounding ' Actions lost or it or limiting Paralysis Paresis impaired 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. Brachialis anticus. gers and thumb Extensor and fingers and Muscles of Supinator brevis. impossible. forearm radial side of fingers (in- Deltoid. Extension of fore- reflexes. forearm. cluding thumb)Scaleni. arm. 1265 and hand. Splenii. Flexion of forearm VI Triceps. Deep head and weak. All below Cer- Pectoralis neck muscles. Supination very lost in vical major. weak. complete Latissimus Adduction of arm cord dorsi. and inward rota- division. Teres major. tion. Infraspinatus. Adduction, retrac- Serratus tion and external re i- 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. 1266 All the mus- cause of filaments ion of head. paralysed V cles of the from V cervical scg ;- Dyspnoea. muscles Cer- arm, fi meat to phrenic in arms. vical hand and fin- gers; even th( nerve), <>r spread • injury from 6th f deltoid, to ith oervioal All below loraco- segment . Fatal in a few lost in brachialia and Trapezius and hours or days. complete braohialis Bterno-cleido cord antirus. toid are intact. division. I leep oervi- oal Mm dee. IntfP I2t i ir ataxia be present. Sbcretobi iMi ( iiiu.ii Drsn mi u»a - Myosis :inil pseudo-ptosi - (ophthalmoplegia sym- patbica) and salivation are common. Cheyne- Stokes's respiration inking, •mei is aJf Of lateral Tendon reflexes increased with Babinski and ankle- clonus mi opposite siilr. Cutani • reflexes may 01 maj not be incn < ifii'ii present. No motor, bul there may !»■ cere- bellar, ataxia. Conjunctivitis is frequent in eye of same side. May be :i tendency to fall «>r to turn tu iini- siilc Salivation. ■:iln n, nt- Of Normal >.r slieliiU exag- gerated us above. I -ii.illv present . I mall} present on the Borne aide as the lesion, i.'ii ,ni i In- same side as thr lesion. < Soniunctivitis is frequent in the eye of the same aide Salivation. Tendon reflexes incre ised I ifteo with Babinski and ankle- clonus "N the oppo !'• side, Cutaneous reflexes may or maj not l>" increased. No motor, may It Normal cerebellar, ataxia I Iceratii t cornea maj occur Ma) be a tendency i" fall "i turn i le sidi jugtite Normal or maj be it«l ■ liL'liil\ Present M:i\ be motor ai iiTilii-llal at \:tl.i Lost "ii iIh- sain" — i ■ 1 < - as ill" lesion. Ulceration of ill" <■■ >rnt-:i ma] rarely occur \ slow rhj iliini" tremor "t tin- arm and l"g of oppo- site side maj be present CHART XXI b Cerebral Localization: Ganglia at Base TABLE Or SYMPTOMS D " TRANSVERSE LESIONS OF BRAIN STEM AND CEREBELLUM Actions Secretory Paralysis of Paralysis of Lost or Reflexes Ver- Muscle and Other Seat of Lesion Motion Sensation Impaired Altered tigo Ataxia Sense Disturbances Some, or all, of None. Movement Tendon Usually None. Normal Tremor the ocular mus- of eye- reflexes absent. resembling cles (except ball. Use increased, that of external rectus) of contra- with paralysis on the same lateral Babinski agitans 'Lesion side, combined half of the and ankle- (Benedikt s confined with a contra- body. clonus, on syndrome). to the lateral hemiple- opposite (441) pes or foot. gia, usually side. complete. Cutaneous Hemiplegia reflexes 1270 alternans may or Crura oculomotoria. may not Cerebri (Weber's syn- drome, 440). Contralateral hemianesthesia, or hemianalge- be in- creased. A slow, rhythmic Lesion One or more sia and thermic Movement Tendon Present. Cere- Im- tremor of confined ocular muscles, hemianesthesia, of eyeball. reflexes bellar paired. arm and leg to the except the or both. Deaf- normal. type. of opposite tegmen- abducens. ness may be side may be tum. present, if lesion be bilateral. present . 'Lesion Bilateral, more May be blind- Movement Pupil reflex lost Usually May be Normal Nystagmus (at confined or less exten- ness without of absent. absent. times vertical), to sive, of all ocu- choked disc or eyeball. to both squint , pupils anterior lar muscles, other lesion. light and often unequal. pair except the accommo- 1271 Corpora (nates). abducens. dation. May be slow. Quadri- Lesion None or may May lie deaf- None, Normal. Usually Present . Normal rhythmic gemina. confined be slight ness, if lesion except present. Of cere- tremor of arm to paralysis be bilateral. chewing bellar and leu of posterior as above, or of at times. type. opposite side, pair trochlearis. as] tally on ^(testes). voluntary motion. 1272 None. None. Walking Normal Usually Cere- Normal Nystagmus Cere- and or present. bellar (80), tendency bellum. standing. slightly exagge- rated. ataxia with to fall to one side, occipital hypo- headache it Rarely tonia frequent . abolished almost always ■ Hai- ti!. s may 1273 None. None. \\*;i Ikiri^r, Normal Usually Usually Normal Tendency to Middle standing or present fall or to turn cere- ami ■lightly with Bad or bellar sit tins. exagge- hypo- bo.ly to one peduncles. tonia side. 1; i>f tin' movements, more oi bellai pronounced) type choreii in homolateral of inforifir ccrebcl ar pedunelei ■ion ; those half of body. »f the superior cerebelku peduncli - neiform move- ami vertical menta and divergence of tin- eyeballs imes occur, 1274 Fracturt he above syn ling to their po but their early and paralysis ol aptoms Cranium of paralysis predominate irritation. Involve 1 1 ntire lateral half of tin' In • it any point I in- ymptoms of tbi lepend upon the f tlon (physiology) ol the pari affected and will natur ally \ rhe location "i ruch ■ lesion in a ti ,; « "ill depend upon what longitu- dinal Boer tracts an Involved, and In longitudinal Notion upon what cranial nuclei and nt Involved, as shown bv the symptom present in the end of this book ■ntfa] for the localisation of sue! l »iii serve 'in- purpose description 221 CHART XXI c Cerebral Localization: Ganglia at Base LOCALIZING SYMPTOMS IN LESIONS OF GANGLIA AT BASE OF BRAIN Seat of Lesion 1275 Optic Thalamus. (Fig. 17) ' Nucleus Lentic- ularis and Nucleus Cauda- tus. 1276 Corpus Stri- atum. (Fig. 17) Inter- nal Cap- sule. 1277 Corpus Callosum. 1278 bland of Kiel. Claustrum and External capsule. (Fig. 17) L279 1'ituitarv Gland. 1280 Pineal Gland. Diagnostic Symptoms Symptoms are variable and uncertain. May be hemianopia (pulvinar, and external geniculate involvement) with hemiopic pupillary reaction, contra- lateral hemianalgesia. Rigidity, choreiform movements, athetosis, and incoordination of contralateral leg, arm, and half of face may be present. The above mentioned motor disturbances occur also in lesions just external to the optic thalamus which involve the fibers connecting the thalamus with the cerebral cortex. Sensory disturbances (pain, hemianesthesia dolorosa, anesthesia, loss of muscle sense) may be present in the same parts. Occa- sionally a slight irritation of the skin is not felt at all, while a stronger one is felt inordinately. Absence of emotional expression in face, even when not paralyzed. Vaso-motor disturbances may occur in opposite side of body. Isolated analgesia or thermic anesthesia does not occur in lesions above the optic thalamus, but other forms of anesthesia do. No diagnostic symptom except the hemiplegia due to the involvement of the internal capsule. 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 symp- toms of sensory irritation: muscle spasm 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 auto- matic involuntary voiding may occur at regular intervals. 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 movements. Lesions in the anterior two-thirds of the posterior limb of the internal capsule cause a total contralateral hemiplegia of the body. This hemiplegia con- sists 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. Lesions in this area produce disturbances of speech, grouped under the general term paraphasia, and may produce anarthna, the result of complete aphasia. Hypertrophy, tumor, hemorrhage and some other lesions of the gland asso- ciated with excess of secret ion may cause acromegaly Or gigantism, in ad- dition to a pr o gr essi ve hi temporal hemianopia, terminating in blindness. \ defect or atrophy of the gland associated with a diminution of secretion m early life [nay cause dwarfism and may produce pituitary eunuchiamua or adiposogenital degeneration with excess Of fat and a defect in the formation of the genitals, in any case of pituitary disease there may be polyuria. polydipsis and occasionally glycosuria and very rarely an escape of cerebro- spinal fluid from the nose (hydrorrhoea nasalis). In some oases of pituitary disease there are no symptoms. Abnormal growth of hair and deposition of fat. Abnormalities of genitals tat times with attacks of seMlal e\cit etuent I xcessive growth in height of body (dyspinelismus). In consequence of involvement of adjacent tissue. bilateral ocular paralysis, nystagmus, pupil abnormalities, ataxia, and |wr- haps disturbance* of hearing may be present. CHART XXI d Cerebral Localization: Lobes of Brain LOCALIZING SYMPTOMS IN LESIONS OF CEREBRAL HEMISPHERES Seat of Lesiox 1282 FROxNTAL 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 Jack- sonian 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) 1283 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 berior portion may cause epileptiform con- vulsion.-. (Fig. 15) Diagnostic Symptoms 'Lesion 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 this 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 ascending frontal convo- lution. Lesions in this region may cause awkward- ness (cortical ataxia, apraxia) rather than paralysis. The base of the Small lesions in this area may cause in right-handed per- middle left fron- sons, argaphia, and in many cases Jacksonian epilepsy, tal convolution. 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. 'Lesions in the upper fourth of this convolution may cause some blunting of cutaneous sensibility, and especially astereognosis in contralateral leg and foot. The ascending parietal convo- lution. 1284 TEMPORAL LOBE • lontains, on the left side, tin- o< of Bensory speech. Lesions may cause epileptiform convulsions. Lesions in the middle half of this convolution may cause some blunting of cutaneous sensibility, and especially astereognosis in contralateral arm and hand. Lesions in the lower fourth of this convolution may cause some blunting of cutaneous sensibility, and especially bereognoeis in contralateral half of face. The left ang- Deep lesions in this region, in right-handed persons may ular gyrus. cause alexia and hemianopia. The reel of t lie Lesions in this region may cause loss of muscular sense and parietal cortex, motor ataxia in the contralateral arm and leg. i esione in the posterior portion of the left superior tem- poral convolution in right-handed persons, may cause sen- Bory aphasia (psychic deafness). 1286 OOCIPITA] LOBE ( Sontaine i he centers of Bight . Lesions may cause epilepti- form eonvul (Fig Neigh- borhood of oaloarine occipital . lobe. ■ in this area cause contralateral homonymous hemi- anopia. A lesion limited i" 'lie superior lip <'t" this i iiadrantio 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 lOBB of contra- lateral upper quadrants of the field of vision. Lesions in this area may cause loss of power of recognition OJ OS and things (psychic blind:. 1286 Man\ lesions cause ■ mixture of paralysis and convulsions over ■* limited area Cortical Lesions. which in some cases maj slowly grov larger. The intelligence of the patient (Fig. 15) is always more or lest impaired. CHART XXII Cerebro-Spinal Localization TOPICAL DIAGNOSIS LOCALIZATION OF LESIONS FROM ANALYSIS OF SYMPTOMS T1294 1292 The reflexes in the para- lysed area are abolished (except in 1310 and 1329) < A lesion of the peripheral neurons. 1290 PARALYSIS The most important of all localizing symptoms. Sensation alone, in all its forms is lost or impaired. 1295 Motion alone impaired. is lost or 1296 Both motion and sensa- tion are lost or impaired. „ •See Chart XXII a. 1297 Special forms of pheral paralyses. pen- 1293 The reflexes are present (except in 1357 and 1359) - A lesion of the central neurons. 1298 Sensory paralysis domi- nant. Little or no motor paralysis. 1299 Motor paralysis domi- nant. Little or no sen- sory paralysis. 1300 Both motor and sensory . paralysis well marked. See Chart XXII b. See Chart XX 11 c. See Chart XXII d. Bee Chart XXII e. 1291 "iiian Epilepsy, together with other symptoms <>f cerebral disease. I ox diseases and lesions accompanied l>y motor paralyrit see 469, l>y motor spasm see 570, by ntiiriii see 638, by tremor see 889, by nystagmus Bee 840, by fibriDaHon Bee 841, by local paralysis Bee 636, by local spasm sec (i.'iT, by disorders <»/ speech sec 735, by disorders <>/ gasi see 73ti. by anesthesia and anatgosia see 810-12, by disorder* of special senses see 807-9, by paw see 881, by vertigo see 982, by menial disorders gee 1038, by (ropnie disorders see 1120, by raso-motor disorders • • 1129, by ganglionic disorders Bet 1128, by syphuie Bee 120">. l>v abnormal eerebro-epinal ,'/uin righl margin TOPICAL. I LOCALIZATION OF LESION FF , 1315 I DISTURBANCES OF VISION. (807.) 1297 SPECIAL FORMS OF PERIPHERAL PAR- ALYSIS. REFLEXES < \l'.' ILISHED IN PAR- ALYSED AREA, EX- < KPT IN 1329. 1316 PARALYSIS OF OCU- < LAR MUSCLES (700). 1317 FACIAL PARAL- '•YSIS (703). PERIPHERAL PARALYSIS W I DIAGNOSTIC SY.M (. 'Blindness of entire field of vision of one eye is present n light. Bitemporal hemianopia is present. The outer baU of eai 9 is present. Nasal hemianopia is present. The inner half of field of is present. Homonymous hemianopia is present. Identical halves (r I pupillary reflex is present i.e. reflex is absent when para 'All muscles of one eye paralysed. Eyeball protruded or I rNo hemiplegia. Other crani All muscles supplied by i third cranial nerve are J Paralysis of arm and lee of oi paralysed at once. Tremor of arm and leg ol op I causing ataxia. Partial or progressive paralysis of muscles supplied by thir No hemiplegia. Other crani J Paralysis of external rec- tus muscle. 1 Hemiplegia often combine,. of conjugate deviation of I be involved. Lower branch of facial Other symptoms of : only, or mainly, paralysed. tion never present Reflex 'Paralysis of arm and lei: of oj No hemiplegia. Chronic col and abducens, ma Associated with unilateral di Both lower and upper brandies of facial nerve equally paralysed. No deafness but hyperakusis notes, and often the high i times absence of secretion Hyperakusis. Loss of tasti il No hyperakusis. Loss of Last No hyperakusis. No loss of t GNOSIS 1 ANALYSIS OF SYMPTOMS H ABOLISHED REFLEXES ItSANDTESTS LOCALIZATION tic n.-rve is atrophied. Pupil does not respond to Lesion in optic nerve (887-8). I ;is id of vision is blind. Bemiopic pupillary reflex Lesion is in the central part of ootie chiasm 362 L3tfl 815. 860, 892 on of one eye is blind. Hemiopic pupillary reflex Lesion is in outer margin of optic chiasm (362, 1320 815, 861 or left) of each field of vision is blind. Hemiopic Lesion is in the optic tract or external geniculate 1321 I "J! ol retma is excited by light. body of opposite side 858 cr evidence of disease within orbit. Lesion within theorbil 91 1 1322 lerves paralysed. Leaion of 3rd cranial nerve trunk or nueleua (700) 1323 Fig is Lesion involving crus cerebri (676 1324 present at rest and exaggerated on motion, Lesion of red nucleus or rubro-epinal tract on >.• 1325 side as motor oculi parol; 1 '""'■''' "" rv " ' 7I, ° Lesion of 3rd crania) nucleus, in wl ■ or in part 1326 (700) (Fig is fcrves paralysed, especially the facial. 1. ion of 6th cranial nerve or nuoleus 1330-1) 1327 (Figs 19, -'11 ) hemianesthesia of opposite side. Loss of power Diffuse lesion of Pons Varolii (539,883) fFias 1328 ight or left Facial or auditory nerve may 19,20.) • brain present. Electrical reaction of degenera- Lesion above nucleus of facial nerve in cerebral 1329 hemispheres or in crura cerebri. (Fig 15 lands Often abducens par Lesion in Pons Varolii Figs 19,20.) 1330 Omially Other cranial nerves, especially auditorj Leaion of nucleus of facial nerve Figi 19,20 L381 land vertigo without disease oft] u Leaion of facial nerve trunk at base of brain (Fig ""." auriurn, due to stapedius parol i Lou Leaion of nerve above geniculate ganglion (9281 1833 ire painful to bear. No lo tl 1 1 gmgnon u_m. i.u.i |N«two-»Wi l 1. acial nerve between geniculate ganglion and stapedius branch 1 1 ■■ IQ nnt-rmr two-thirds of tongue of an 1 1 facial nerve between stapedius and 1 tymp i , :,, I Tenderneaa near stylo mastoid foramen 1 , ,,,,,,,1 facial nerve below chorda tympani bi inch 1 I3fl (Fig CHART XXII c Cerebro-Spinal Localization I Comprising Numbers 1298 and L340 to 1346 <>n Kit side of Charl and 1347 to iHti'.i on ri^lit margin. L340 ANESTHESIA with without ANALGESIA. DIAGNOSTIC SYMPTOMS AND TESTS Marked ataxia. Limited to one or both legs [Slight ataxia. Limited to one arm. Slighl ataxia In both anus and both legs. Marked ataxia Marked ataxia. In arm and leg of SO mi' side. Slighl ataxia. TOPIC/ LOCALIZATION OF LESION ANESTHESIA WITH Anesthesia marked, bilateral. of muscle sense, Anesthesia slighl and most mt be cerebral symptoms, Jacks* Anesthesia slight, most marked cerebral symptoms (Jackson i May lie other spinal symptom in arms and legs, May la- other spinal symptom in arm and leg. Anesthesia sli«;ht. moat marked i he other cerebral symptoms, irs&lfjsr «* +■ >%%%s«- — I In arm. leg and face of same Slighl ataxia side. 1298 s i:\sojn PARAL1 SIS DOMINANT. LITTLE OR NO MOTOB PARAL- VS1S. TENDON REFLEXES PRE- SENT OR EXAGGERATED. L341 ANALGESIA unh THER- MIC ANESTHESIA, l>.n litl li oi no tactile anesthesia, is present. DISSOCJ ATION id SI NSATION. In oi r both legs. Usually unilateral. Usually bilateral. I No Jacksonian epilepsy Hernia Jacksonian epilepsy common. No trophic disturbances. \i Trophic disturbances in legs. usually abolished, especially (Tsnally unilateral. Leg of No trophic disturbances Ofti nn mi > on i< a L, , in.', J. ... I In one or both , s: '""' sil1 '' als " involved In arms, or legs, or both, I'sualh bilateral. Legs of Tropin,- disturbances in arms -normal sensibility. especially in advanced [Bilateral usually, marked May I ther spinal symptom. ataxia. plegia). f Eiemianopia and anesthesia ii in J Jacksonian epilepsy and other e< ] present 1342 HOMONYMOUS 1IKMI Wtil'l \ 1343 HOMON1 Mors TETARTANOPIA, QUAD- RANT HEM! ANOP1 \ 1344 P8YCHIC HI. I. \ dm SS "l:> APHASIA, 1346 AS! I REOGNOSI8. H'nilateral, slight ataxia. Jn contralateral arm and leg with ''''■""'^ ll:ilv " s *' r '■"■>' field of visi righl or left) are blind. No hemiopic pupillarj i M "' l, "; : l ' 1 quadrants of each held of vision (right or left) are blind. No hemiopic pur, anesthesia or other paralysis. May be other cerebral symptoms. Patienl is not bhnd, bul cannot recognize things by sight, though he may by touch or N P me^or^ n fOTs J p^k , en >U woX 0i wdm>mA worda s,, " k "" '" ll ""' ttlthou 6« '" Patient is not anesthetic, or very slightly so, bul cannot recognize objects by the IAGNOSIS 3M ANALYSIS OF SYMPTOMS GGERATED REFLEXES LOCALIZATION spinal symptoms, especi -IK loss Lesion in one or both posterior columns of cord in dorsal reg Same ride if unilateral 1347 34-6.) m foot. _ Aim,,.., always unilateral. May Lea^r^in upper^ne-fourth of posterior central convolution in contralateral cerebral 1348 fed, astereognosis marked. May be other Lesion in middle one-half of posterior central convolution in contralateral cerebral cortex I34i) Depsy). Usually some motor paralysis. (Kg. 15 luuTuawsrai cereorat conex. i.i.i ksarmoea common. Loss of muscle sense Lesion of posterior columns of cord in cervical region (654a 785 Figs. 24^0 1350 kpnoea common. U ! muscle sense Lesion of posterior column of cord on same aide, in cervical region (654a, 785 Pip 24-6.) 1361 "' i', 1 " ', '"".'■ ^tereognoae marked. May Leaion in i a three-fourths of posterior central convolution of contralateral cerebral 1352 Bally Jacksonian epilepsy. cortex. (Fig. 15 '' IJ '"•" '•'- , - "'" Pml y** of conjugate deviation of Lesion in tegmenl , B Varolii on same ride as the facial anesthesia 883). L353 "'""""""' l -'-| M " of posterioi pari of internal capsule of contralateral hemisphere (857, 1276). 1354 hianopia. Mental deterioration. Lesion of superior parietal lobule of contralateral hemisphere 657). Fig 15 i:;.v, Uee of organic reflexes. Usually ataxia. Lerion in peripherj of opposite lateral column of cord in dorsal region 1360 1358 24-6 l,.:,"! 1 : .;,, | rcndon reflexes ***■ * t^ r: ni iM " : """ n " r uni f ure - r ••' m lumb « ™iw»™ - tn im central gliosis the lesion may extend upwards to the cervical enlargement and involve the arms secondaril] (837-9, 1359 i f* ""' ' '"" "' rnu8cle WMe ' l ' 1 "- 1 "" '" periphery of the o] rite, orol both, lateral unns of the cord in theoervii il I 158 regio igf S4-6.) "'"" , '" 11 "''- "- ||:ilK abolished ii as, Lerion in central gray matter (anterior commissure) of the cord in cervical enlanremenl 1358 652, 693 837,-9 1009, 1170, lis?. 1367) (Figs. 2 ' ' »W» spastic para- Lerion of lateral columns of cord 664,1212,1366,1368,1396) Figs. 2 1360 Other cerebral symptoms. Lesion of posterior pari ntralateral internal capsule 867 Fig 17.) 1361 fa symptoms usually present Vneel is Lesion of infer arietal lobule of c alateri misphen 651 Fig 16. 1362 1 • on ol ponto ■ rcbi II ir angle on ride of deafness 138 i ;,, . : ' 0t »>w oerebral symptom. I.,. irine fissure of occipital lobe, o. ol fascioulus of Gratiolet of eon- 1364 tteral cerebral hemisphere 362,815 890 1286 Fig 16 Lower quadrant ol Lesion of upper lip of contralateral 1285 I ,■■ n. n,;-, ' i;i'" •'"" ll " ,l " : I ■'■ ""' ol lower Iq sonti ilateral calci ■ fissure I i i ;,,,, field of visi L "' '•' ' '""' "*»' , " 1 " I occipital lobeoflrfl cerebral hemisphej , -.„; '""' "'" "" " I oi pari ol l.ii rior temporal convolutioi 15 0U * hh8 « n b ' r«ght. I. , nvo , ,. r:i|;lli , , , phen CHART XXII d Cerebro-Spinal Localization Comprising Numbers i-".*'.i on lef1 side of chart and L372 to L391 on right margin. 235 TOP / LOCALIZATION OF LESI ( MOTOR PARALYSIS DIAGNOSTIC SYMPTOMS AND TESTS I"/'";' 1 to one or fSymptoms bilateral usually. May be other spinal symptoms '"; h "*s- Organic * of sensation rnlegs. reflexes nol dis- ordered. LSymptoms unilateral usually. May be other cerebral symptoms, es] Limited to both f No " insulv paralysis. No cerebral symptoms. Often ataxia and arms and both legs J : "'" ls : ""' le ss L299 MOTOB PAR- ALYSIS DOMIN- ANT LITTLE ok NO SEN- SORY PARALY- SIS. TENDON REFLEXES PRESENT OH EXAGGERATED i Irganic reflexes not 1 ,. ,, disordered. i ' M1 ' ■ """"' -^''ison paralysis. Dysarthria and dysphagia. Paral I ing with position of lesion. Limited to one arm. Occasionally some slight sensory paralysis. Jacksonian epilepss ai common. r Dissociation of sensation and ataxia may be present. Organic n cerebral symptoms. Limited to arm and , ■ ,, leg of same side. ^ Usually some sensory symptoms. Dysarthria and dysphagia not | crania] nerves frequent. U'sually some sensory Symptoms, .lacksonian epilepsy and othi Limited to lower branch of facial nerve. Limited to arm and lower branch of facial nerve i Jacksonian epilepsy and other syna common. Often complicated with of same side. Limited to arm and leg of same side and hypo-") glossus nerve of opposite side. Usually some sensory symptoms. ..,., . , r Paralysis of some other crania Limited to arm and leg ol same side and lower abducens paralysis branch of facial nerve of opposite side J Limited to arm and leg of same side and motor Usually some sensory symptoms ocuh nerve ol opposite side. nerves common ("Usually other cerebral symptoms pn fSymptomsof paralysis rather | , "" 1S ' Limited t< i arm and t lian of irrit.it ion Not pro- 1 ni . leg and lower gressive. Often sensory symptoms present. P branch of facial < ' pression on opposite side of nerve on same side .... .symptoms ol irritation No objective sensory symptoms, ofi I .lacksonian epilepsy. m SARTHRIA Paralysis of some of the cranial nerves and usually of arm and lee also and DYSPHAG] \ VOL' M'JIIA Loss of power Of Writing, although arm is nol paralysed l.o.ss oi power of peaking .some or all words. Limited voi HlUSCleS Ol Speech nol paralyzed. Inability to read, although patient can see and can speak MOTOB \l'll \H \ VLEXIA unary iL DIAGNOSIS FROM ANALYSIS OF SYMPTOMS rH EXAGGERATED REFLEXES LOCALIZATION itaxia and dissociation Um^thgmOM^ a^tbath lateral. columns „f cord in dorsal [372 Oly Jacksonian epilepsy. Leaon of upper part of anterior central convolution of contralateral hemisphere 137 ; cortical or sub-cortical (leg center). fFig. 15.) ociation of sensation in Lesion of lateral columns, of the card in the cervical region (626 1 igs 36-7 1374 '"' "" rv "~ v:i,v " '"oi :;;,,'^^)' West - " ""-"■' •?- h *■ >** »■>., m her cerebral symptoms Lesion in cortex or QiddJ ,e*alf of anterior central convolution i 176 of contralateral hemisphere arm center] Fig 15 a ■...! disordered. No I mtralateral lateral column of cord in cervical region (1131, 1141). 1377 -- i- I some Lesion in the brain stem in vohring the pyramidal tract). (Figs 19-22 1378 ortical disease. Lesion in carta or sub-cortex of upper three^ourths of anterioi central con- 1379 rotation of contralateral hemisphere. (Fig 15.) rLeaon in cortex or sub-cortex of inferior pari of anterior central convolution 1380 U of cortical disease , 0I contralateral hemisphere (face centei Fig 1". «.r apbi Lesion o cortex or sub-cortex of lower three-fourths of anterior central oonvota- 1381 (. uon or contralateral hemisphere (arm and Fig i.-, rtbria and dysphagia '™ 2] """'""•'' "" " ^ M "'" ***>&*«* ***&* rar odition). 1382 •s common, especially Lesion in bridge portion of pons .... same side as the racial paralysis. (Fig. 20 1383 ' other cranial Lesion ia pee cruris cerebri on same side as the motor oc aralysis. (Fig. 19 1384 aMOT3 « ■ l -' l ;;;;:;,.'" : ";';;r^ ''""' a | "" , " , " ,r l "" 1 ' " f n**™* capsule at ,.,,,„,„.,■ 1„ „„,- ." ' " * , "Ci;:i,. , ;;: , " , r;,",r rf ■ »* a - d *■ -* *. «■ '"" t " r "' Uaon throughout ai ral convolution of contralateral hemisphere oor- 1387 lex "i sub-cortex I ig i". Lesion in tegmentum of pons or i lulls 284-6 Figa 20-1.] L388 ■ or subcortical lesion al base of middle frontal oonvolution of left 1389 u hemuphen in righl banded person 227, 77'. I be made and Corti. „i or sub-, urtical fan , ,,,... ,„■ „„,,„„ ,,.,, ,„„ lta| ,,„„.„,„„„„ „, ni;l „ , banded i.-, *"l\ j ""' '"" «n«ulai rolution in righl banded p CHART XXII e Cerebro-Spinal Localization 1291 J A C K S <) N I A N E P I L E p s X TOPICAL DIAGNOSIS LOCALIZATION OF LESION FROM ANALYSIS OF SYMPTOMS MOTOR AND SENSORY PARALYSIS WITH EXAGGERATED REFLEXES JACKSONIAN EPILEPSY r Limited 1300 to both Both legs. motor and sen- sory paraly- sis well marked. Reflexes Limited present to both or exag- arms gerated , and \ except both in 1396. .legs. Diagnostic Symptoms and Tests ' Paralysis severe. No ataxia. Organic reflexes much disordered. Some of the trunk reflexes are lost. Vertical extent of lesion is shown by the ab- sence of the different trunk reflexes. Upper limit of lesion shown by the zone of hyperesthesia, limiting the anesthesia above. Paralysis not so extreme. Marked ataxia. Loss of muscle sense. Or- ganic reflexes not at all, or slightly, disordered. Trunk reflexes not abol- ished. Knee-jerks and other leg re- - flexes may be increased or abolished. ("No involvement of cranial nerves. Priapism. Dyspnoea. Very dan- j gerous, usually fatal. Involvement of some cranial nerves. Dysarthria and dysphagia. Very '-dangerous, usually fatal. Spasmodic twitching of head and eyes to one side. Twitch- ing may remain limited to these muscles or may extend to other muscles of face and neck and arm and later to leg of same side or may finally extend to muscles of both sides of body. Spasmodic twitching commences in one side of face. Twitching may remain limited to these muscles or may extend to others as above. Spasmodic twitching in hand or arm. Twitching may remain limited to these muscles or may extend to face Or to leg or to both simultaneously of same side and may later extend to muscles of other side of body also. Spasmodic twitohing of foot or leg. Twitching may re- main limited to these muscles, or may extend to arm ;ind later t<> face of same side and later to muscles of other side of body. (Figs. 15, 16). Spasmodic twitching, commencing simultaneously, In arm and face of lame Bide, whioh later extends to muscles ill the \>x of the same side and still later to muscles of the opposite side of the body. Spasmodic twitohing commencing In arm and leg of same side, which may later extend to face Of same side and may later extend to muscles of the other side of body. Localization Transverse lesion of spinal 1395 cord in dorsal region. (Myelitis.) (516-9, 829). Lesion both in lateral and 1396 posterior columns of cord. (Ataxic Paraplegia.) (526, 660. 796) (Figs. 25-7.) Transverse lesion of spinal 1397 cord in cervical region. (512-5, 828) (Figs. 25-6). Lesion on both sides of 1398 brain stem (medulla, pons or crura cerebri, accord- ing to cranial nerves in- volved). (Figs. 19-21). Lesion in or near base of 1399 middle frontal convolution of contralateral hemisphere. (Fig. 15). Lesion in or near lower 1400 quarter of the central con- volutions of contralateral hemisphere. (Fig. 15). Lesion in or near middle 1401 half of the central con- volutions of contralateral hemisphere. (Fig. 15). Lesion in or near upper 1402 quarter Of central convo- lutions or paracent ral lob- ule of Opposite hemisphere. Lesion near and equally 140:? distant from motor area of face and arm in contra- lateral hemisphere. ( Fin- 15)- Lesion near and equally 1104 distant from motor ana Of arm and lee; in emit rs lateral hemisphere. ( Fie; 15), Spasmodic twitohing commencing in face and arm and lesion in inferior parietal l i' 1 ^ lee, of same side, which may later extend to muscles lobule of cunt ralati I] al of opposite side, hemisphere. (Fig. 15). 287 PLATES Schematic representation of the convex surface of the left cerebral hemisphere, showing t lie motor and and the location of the cortical functions. See 1282-6, 1348 9, 1352, L355, 1362, 1367 9, 1373, 1376, L379, 1380 I. 1387, 1389 91, 1 loo 5. 21(1 Fio. 10 Schematic representation of the medial the lefl cerebral hemisphere U. L. Q. Upper left quadrant of retina 1. I. Q Lower left quadrant "i retina Bee 852-3, 856, 1285, 1364-6, 1 102 PACIAL \ ARM Lt HYPOGLOSSAL i ra 17 Horizontal Section thro I lemisphcre showing the principal I psule; Kn. Genu oft laic Nucleus; \l Lenticulai Nuclei! ''I Optic I'hulnmuji Bp, Splenium ol Corpi 'II Nuil. Comiss. post. et | fasc long, dors, i Fasc. long iters Klrfnzcll. Oculom.-Kern M. levator palpebral: M. obltquus inferior M. rectus superior :.^.A.^. "'$ *^/ M. rectus inleriius M jcctus inferior Fig. 18 Schematic representation of the nuclei situated beneath the floor of the Sylvian aqueduct, showing the origin of tlie posterior commissure, the oculo-motor ami trochlearis nerves, as well as the nuclear localizatii I the centers for i hi' individual ocular muscles (after Edinger). s,r. 692, Tim. 816, 1316. 242 I n. L9 Schematic representation of brain stem; showing nuclei and nerve roots. The sensory nuclei and nerve roota are colored red, the motor blue. S«e 1301-1. 1323-32, 1353, 1375, 1378, 1398. 248 - -Deiters nucV pyramid Diagrammatic transverse section through the pons at a level slightly posterior to the superficial origin ot the trigeminus. See 1269, 1301-4, 1327-30, 1353, 1383, 1388, 1398. rued, raphe i post. long", fasc. -N.sohtar. - -V. spinal rt - -subst.gelat. ---N.arrVbig. « dir.cerebel tr. (Flechsig) - -ant lateral tr. (Gowers) x — int. arcuate fibres Fig. 21 Diagrammatic transverse section through the medulla, approximately near its middle. See 1268, 1301-4, 1382, 1388, 1398. 244 coVG'oYl -Ti. gracilis col.Burdach -n cuneatus - "Spinal V — subst . gel at,. ■ -mt.arcuatefr. —n — ant.Viorn — lemniscus olive Fio. 22 TranEveree section of medulla just above motor decussation and just above line of junction with the cord, showing the sensory decussation and the topography of the lowest level of the medulla. See 1268 Fio. 23 Transverse section of the cord }uft at tin- lirn- of junrtion with the medulla, showing the motor decussation and the topography of the uppermost level of the cord. Bh L208 24fi Fig. 24 DIAGRAMMATIC SECTION OF THE SPINAL CORD TO ILLUSTRATE ITS PHYSIOLOGY Left side shows situation of lesions causing disorders of motion and sensation. Right side shows situation of lesions causing disorders of reflex activity. Destructive lesions at M or E cause diminution, slight irritative lesions, exaggeration, of motion. Destructive lesions at S cause permanent anaesthesia, analgesia, thermic anesthesia and loss of muscle sense. Destructive lesions at T cause analgesia and thermic anesthesia. Destructive lesions at P cause ataxia. Destructive lesions at K cause loss of muscle sense, ataxia and anaesthesia. Irritative lesions at S, K, T, or P, may cause exaggeration, or perversion, or both, of sensation. Destructive lesions at D cause diminution, and at E, exaggeration, of reflex activity. Slight irritative lesions at D cause exaggeration, and at E diminution, of reflex activity. Symptoms of lesions at M are described in 252, 263, 495, 547, 789; 1148-9, 1233 and 1304 at E in 251, 254, 256, 525-6, 796-7 and 1212, 1372-4-7; at S in 824; at T in 1356-8-60; at P in 281, 654; at K in 280, 654a, 785, 1302, 1347 and 1350-1, 1396. The results of lesions at D and E are discussed in Chart V a. Cervical Enlargement Lumbar Enlargement Fig. 25 LOCALIZATION OF NUCLEI IN THE ANTERIOR HORNS OF THE SPINAL CORD (After Edinger modified from Sano.) 246 I to. 26 I SCHEMATA REPRE8EN1 VTION OF \ TRANS\ ERS1 SECTION OF THE SPINAL CORD; SEVERAL LEA ELS BEING COMBINED IN DO ONI ' '.ITS \ S i - vest ibulo-epinal 1 1 I 8 I U pina] trad 1 1 I' I direct pyramidal I spinal i I', i .1 t racl * trad ■illllil \-i i NS1NG lie ICTBJ - i i jpino-thalamic i rad V.S.C.1 interior spino eerebeU Gowers trad) P.S.C l. posterior Bpino-cerebellar trad Flei ('.('. ( 'lark's column On the left side of the cord are represented the nerve roots and those bundles of long fibers in r 1 1 « - white col- umns which carrj impulses downward from the brain i" the spinal cord, and on the right Bide are represented those in the white columns which carrj impulses upward fi or spinal ganglia i" n li hardly needs to be stated that, although In this figure these long bundles of fibers are repn mi one side only, the) are really Bituatcd Byniini each side "i the cord. Hie short fibers wluch conned different levels ol the cord together are not represented in the figi us involving the pyramidal tract Lim- bed under 251, 254 1212 and 1372-4-7. Les - involving tin- anterior horns give rise to atrophic paralysis, "I" ol which Bribed under 196, 789, 1148, 1233 md 1304 ; while the ol tie formi i lesoribed under .Mr. 895, 1149 and 1304 Lesioru involving the posterior horn column cribed under 786, 1302, 1 3 17, I860 ribed under 281 and 664. Lesioi f the spino-tha of the anterioi ymptorus described under 305, 811 ami i 6-00 I the whole of one lateral half of thi cribed undor 142,609, 840 ind 981 ; while lesions of the whole ti cti i the cord givi ptomi described under 185, 513 I, 617 S md 980, U48a, i 109-10, i 247 Fig. 27 Schematic representation of the more important diseases of the spinal curd. See 345. 416, U9 20, 133, 661, 756, 784, 827, 891, 894, 911, 979, 987, Hint. 1015, 1172, Use, 1217 and 1231 Locomotor Ataxia (lumbar region) Amyotrophic Lateral Sclerosis Acute Stage Chronic Staff Anterior Poliomyelitis See 116, 419, 495, 789 1 1 Is and 1233 LoCOmotOl \la\ia (cervical region) See 547, 695, 707, 1149; and 525, 670 and 797 Descending Degeneration of Pyramidal Tracts Syringomyelia See 552, 693, 837-9,1009, 1150a 1170, 1IS7, 1357 and 1359 Mr,luii4 rmlcilli, Compression Myelitis with the conse- quent Ascending and Descending Degenerations. See 520, 795. No. 3 shows the point of the compression with the whole transverse section of the cord the Beat of an inflamma No. 1 shows ascending degeneration of the columns of Goll, of the spino-thalamte tracts, and of the anterior and posterior spino-cerebellar I raets. No. 2, close to the lesion, shows in addition a slight degeneration of the columns of Burdach. Nos. 4-6 show degeneration of the crossed and direct pyramidal tracts of the vestibulo- spinal, rubro-spinal, and I halamo spinal tracts and of Schultze's comma, The upper series face up and the lower down. 248 M. .hill. II. SCHEMATIC REPRESENTATION OF SOME POINTS IN THE PHYSIOLOGY AND PATHOLOGY OF THE SPINAL CORD AND PERIPHERAL NERVES. Fig. 28. Diagram to illustrate the mechanism of the bladder reflex 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 excited to action by urine in the neck of the bladder or in the prostatic urethra. DC represents there- flex centre, with its motor and sensory neurons, for the detrusor of the bladder, which is excited to action by the disten- tion of the walls of the bladder. These two reflexes are antagonistic and the sen- sory surface irritated being much larger in the latter (D C), than in the former (S C), reflex, the detrusor reflex will eventually overpower the sphincter reflex under nor- mal conditions. S T represents the sensory tract connecting the bladder with the brain, by means of which the individual is informed as to the degree of fulness of the bladder. M T represents the motor tract connecting the cerebral with the spinal centre by means of which the individual can inhibit the activity of either centre (up to a certain degree) and in- crease the activity of the antagonistic centre. Fig. 29 illustrates effects of lesions of cauda equina. Fig. 28 If the lesion is at "A" there is com- plete motor paralysis of both legs, and complete anesthesia of the whole of both legs and of the perineum, 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 the 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 reflexes 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 sensory 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 thigha Otherwise there is no paralysis of motion or sensation. See 487, 721, 1007, 1308. D.XL Fio. 80 Showing the inncrvaiion of muscles through more than one nerve root, so that the destruction of one nerve root or of OM group ol iiitvo cells does not oauaa a OOmpUta and permanent paralysis. Fio. 31 \ diagram ahowina that -tv area ol the skin la lappuM l>y Bla menta from several nerve roots; so that dividon ol one root does not necessarily produce total anesthesia. It alao shows tho peripheral overlapping; so that the upplied by ono nerve cun bo almost completely supplied I'.v neighboring 249 Motor and Reflex Functions of the Spinal-Cord Segments (Modified after Starr and Edinger) Segment Muscles Reflexes Cervical Sternomastoid Trapezius 2-3 | Scaleni Small rotators of head Diaphragm Lev. ang. scap. Dilatation of pupil by irri- Rhomboids tating side of neck, 4 cer- 4 Spinati Deltoid vical to 1 dorsal Supinat. long Scapular reflexes, 5 C-l D Biceps Supinat. long., 5 C 5 Supinat. brev. Serrat. mag. Pectoralis (clav.) Biceps, 5-6 C Teres minor Triceps, 6 C Pronators Posterior wrist, 6-8 C 6' Brachialis ant. Triceps Scapulo-humeral, 7 C Long extensors of wrist and Anterior wrist, 7-8 C 7 fingers Pectoralis (costal) Latiss. dorsi Palmar, 7 C-l D Teres maj. | , Long flexors, wrist and fingers Epigastric, 4-7 D Dorsal 1 1 1 { Extensors of thumb 1 Intrinsic hand-muscles Abdominal, 7-11 D 2-12 Dorsal and abdominal muscles Lumbar Abdominal muscles Cremaster, 1-3 L r H Iliacus Psoas Patellar, 2-1 L 2 Sartorius Flexors of knee Quad, femoris Bladder, 2-4 L Int. rotators of thigh f Adductors of thigh Rectal, 4 L-2 S 4 Abductors of thigh Tibialis ant. Gluteal, 4-5 L f Calf -muscles 5 Ex. rotators of thigh Extensors of toes Achilles, 1 1 ** S Ankle-clonus, J Sacral Peronei " \ Long flex, of toes Plantar, 1-2 S Intrinsic foot -muscles ¥&> }«■ 3-5 Perineal muscles Fig. 32 250 251 *V VcSC-6vf.-Sp.naf TVact V R U «re-S pl «(T,att y Tfcaf-^c -Sp.xif T.«.cT Fig. 34 LONG MOTOR PROJECTION TRACTS For lesions involving these tracts see under Fig. 26. 252 Fig. 86 LONG SENSORY PROJECTION TRA< Pfl For lesions involving these tracts sec umler Fig, 28. 263 Tontfue Stylomastoid foramen steriorAuruuIar Glosso pharyngeal Fig. 36 DIAGRAM OF TRIGEMINAL, FACIAL AND GLOSSO-PHARYNGEAL NERVES, SHOWING COURSE OF TASTE FIBRES. (After Purves Stewart) Optic lUdlalioni Corpui Calloiurn Optic Thalamus Corp. genlc ext. Optic Tract optic Nerve Viaual Word Ceutre 8 Auditory Word-Centre Fasciculus IJorinatu* Vocal Word-Centre mv> Fig. 37 DIAGRAM ILLUSTRATING HEMIANOPIA (Modified from Vialet) ... , Lesion at 1 produces blindness of one eye. Lesion at 5 produces R. hemianopia with normal pupil reaction. Lcaion at 2 produces bi-temporal hemianopia Lesion at produces K. hemianopia with normal pupil reaotion. Lesion at 3 produces bi-nasal hemianopia Lesion at 7 produces psychic blindness. Lesion at 4 produces R. hemianopia with hemiopic pupil reaction. Lesion at 8 produces Alexia. The heavy black lines represent the fibers from the macula lutea in each retina, the point of central, or clearest vision. 254 S ES ° 3 fe cp t* £ £ fs £ * -J J? !"vr fc: 0. IS a?3 pa 5 g z &: IP L UJ^i $ k INDEX INDEX Roman numerals indicate charts. Arabic numerals indicate margin numbers. Arabic numerals preceded by " p " indicate pages. Abasia : See astasia Abdomen, Boat-shaped retraction of, XI, 608 Abdominal spasm or cramp, XII, 732 .' bducens nucleus, Conjugate deviation in lesions near the, XIV, 883; XXII, 1328 paralysis, XII, 701 Abductor paralysis, XIII, 756 Abscess, Cerebral : See cerebral Spinal : See spinal Abstraction, p. 13 Accommodation reflex : See pupillary and reflex Achilles reflex, I, 62; V, 317 Achillodynia, XV, 1001 Achondroplasia, XVII, 1177 Achromatopsia, I, 13; VI, 364; XIV, 847 Acromegalia, I, 20; XVII, 1183 Acroparesthesia, XVII, 1 197 Action, p. 21 Association, p. 22 Autochthonous, p. 28. Automatic, p. 28 Reflex: See Reflex Voluntary, p. 22; IV, 240 Active contracture, IV, 264 Acute alcoholic mania, XVI, 1 109 anterior poliomyelitis : See poliomy- elitis or apoplectiform polioencephalitis inferior, X, 544 superior, X, 543; XVI, 1064 ascending paralysis, II, 168; X, 482 ataxia: See ataxia atrophic paralysis : See poliomyelitis bulbar paralysis, X, 544 delirium, XVI, 1108 encephalitis, multiple, X, 495; XVI, 1064 Adams-Stokes* disease, XI, 582; XVI, 1057 phrnomenon, IX, 436 Adiposis dolorosa, XV, 1012; XVII, 1176 Adiposogenital degeneration, XXI, 1279 Adolescent insanity, XVI, 1096 Aesthesiometer, I, 48 African lethargy, XVI, 1052 Age in nervous disease, II, 86 ■<■ p. 7 ; vi, 357 Tests for, I, 17 Agitated dementia, XVI, 1103 melancholia, XVI, Ilia Agnosia, p i<>. III. -'.u Agoraphobia, III, 235; XVI, 1072 Agraphia, p. 28; III, 227; XIII, "6 localization of, XXI, 1282; XXII, 1389 Agrypnia, I, 18 Akinesia, IV, 241 Akinesthesia, I, 42; VI, 352; XIV, 812 Albinism, XII, 683 Alcoholic coma, XVI, 1053 convulsion, XI, 576, 585 dementia, XVI, 1101 hallucinosis, XVI, 1 109 headache, XV, 953 intoxication, XII, 658, 663, 673; XIII, 764, 780 mania, Acute, XVI, 1107, 1109 neuritis, X, 488 tremor, XII, 673 vertigo, XV, 1030 Alcoholism, I, 2; II, 115; XII, 658; XIII, -64, 780 Alexia, p. 28; III, 228; XIII, 773 Localization of, XXII, 1391 Allocheiria, VI, 377 Alopecia, XVII, 1161 Altruism, p. 16 Amaurosis, VI, 358 Uremic, XIV, 850 Amaurotic idiocy, XVI, 1085 Amblyopia, VI, 359; XII, 682 Hysterical, XIV, 851a Ambulatory automatism, XVI, 1058, 1069-71 Amentia, p. 19; III, 211 Diseases causing, XVI, 1076 Amnesia, I, 6; III, 220; XIII, 770 Retroactive, XIII, 769; XVI, 1 100 Retrograde, XIII, 769 Amyl nitrite poisoning, XIV, 842 Amyotonia congenita, II, 105; X, 4^.1 Amyotrophic lateral sclerosis, X, 54;; XII, 695; XIII. 797; XVII, 1149 Anakusia, VI, 355; XIV, 820 Diseases causing, XIV, 820 Tests for, I, 15 Ana' reflex, V, 307a Analgesia, VI, 349 Diseases causing, XIV, 810; XXII, 1341 Tests for, I, 50 Anarthria, p. a6; IV. jS* ; XIII, 737, 771 Disease* causing, XIII, 737 literalis. XIII. r< 7 spasmodica, XIII. j6t Anemia, Cerebrospinal fluid in, XIX. 1343 850 INDEX Anemic convulsion, XI, 583 headache, XV, 949, 958 optic neuritis, XIV, 902 vertigo, XV, 1021-5 Anesthesia, p. 7; VI, 348; XIV, 810 Diseases causing, XIV, 810; XXII, 1340 dolorosa, VI, 374 Glove form of, VI, 34s ; IX, 425 Hysterical, p. 7; VI, 345; IX, 425; XIV, 834 of larynx, XIII, 754. 7°o-I Localization of, XXII, 1340 Stocking form of, VI, 345 ; IX, 425 Tests for, I, 48 Thermic, VI, 350 ; XIV, 810 Tests for, I, 55 Aneurism, Cerebral, X, 502 Angina pectoris, XV, 983 Anginal crises, IX, 433 Angio-neurotic edema, XVII, 1201 -paralytic hemicrania, XV, 949 -sclerotic dysbasia, X, 554; XVII, 1 199 -spastic hemicrania, XV, 949 hemiplegia, X, 554 Angular gyrus, Symptoms of lesions of, XXII, 1391 Anisocoria, I, 26; V, 341 Ankle-clonus, V, 316 Tests for, I, 60 Ankylosis, Tests for, I, 37 Anopsia, VI, 358 Anosmia, VI, 356 Tests for, I, 16 Anterior central convolution : See localiz- ation 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, 1095, 1103 Apathy, III, 237 Ape's hand, XII, 714 Aphasia, I, 6; III, 221; XIII, 739 Auditory, pp. 10, 28; XIII, 772 Conduction, p. 28, XIII, 739 Cortical motor, XIII, 739 sensory, XIII, 739 Diseases causing, XIII, 739 Mixed, III, 224; XIII, 774 Motor, III, 221 ; XIII, 771 Localization of, XXI, 1282; XXII, 1390 Optic, IN, 223; XIII, 773 Sensory, pp. 10, 28; I, 6; III, 222; XIII, 772 Localization of, XXI, 1284; XXII, 1345 Aphasia, Sub-cortical motor, XIII, 739 sensory, XIII, 739 Trans-cortical motor, XIII, 739 sensory, XIII, 739 Visual, III, 223; XIII, 773 Aphemia, XIII, 771 Aphonia, IV, 260; XIII, 744, 754, 756-60 Hysterical, XIII, 747-8, 759 Aphthongia, XII, 729; XIII, 767 Apoplectiform polioencephalitis inferior, X, 544 superior, X, 543 Apoplexy, II, 186 Athetosis after, X, 503; XI, 631 Cerebral, X, 504; XI, 588; XIV, 832; XVI, 1043, 1061-3 Ingravescent, XVI, 1060-3 Meningeal, X, 502, 524; XI, 588; XVI, 1060 in pons Varolii, XIII, 748a Prodromata of, IX, 432 Vertigo from, XV, 1026 Apraxia, pp. 26-7; III, 230; IV, 249, 282; XVI, 1 104 Association, p. 27 Motor, p. 27 Aran-Duchenne type of muscular atrophy, X, 547; XII, 694; XIII, 797; XVII, 1149 Arcus senilis, I, 24 Argyll-Robertson's pupillary reflex, V, 332; IX, 447 Diseases causing, XIV, 891 Arm-center, Symptoms of lesions of, XXII, 1349, 1352, 1369, 1376, 1379. 1381 Arsenical neuritis, II, 157; X, 488 Arterial disease in etiology of nervous diseases, II, 97 Arthralgia, XV, 1000 Arthritic atrophy. XVII, 1151 Arthritis deformans, XV, 976 Arthropathy of tabes, XVII, 1186 Articulative tics, XIII, 768 Asphyxia, Local, XVII, 1 195 Associated movements, IV, 276 Association of ideas and memories, p. 12 Tests for, I, 5 Association reflexes, pp. 22-3 Astasia and abasia, IV, 287; XII, 653; XIII, 792 Astereognosis, p. 10; III, 229; VI, 354; XXII, 1346, 1369 Tests for, I, 11 Asthenic tremor, XII, 671 Asthma, XI, 617; XVII, 1194 Astrophobia, III, 235 Asynergia, p. 26; IV, 248 Ataxia, p. 26; I, 21, 41; III, 248; X, 488; XII, 638; XXI, 1268-73 Acute, X, 488; XII, 659, 662 Aural, XII, 650 260 INDEX Ataxia, Diseases causing, XII, 638 Dynamic, p. 26; IV, 280; XII, 644 Cerebellar, p. 26; I, 21; IV, 281; XII, 642; XXI, 1268-73, 1282 Cerebral, p. 26 Friedreich's hereditary, II, 104, 123 ; XII, 652, 670, 687, XIII, 762, 781 Hysterical, XII, 664 Locomotor : See tabes Marie's hereditary cerebellar, XII, 651, 669; XIII, 782 Motor, p. 26; I, 21; IV, 280; X, 488; XII, 644; XXI, 1268-74 Ocular, XII, 649 Post-hemiplegic, XII, 655 Static, p. 26; IV, 281; IX, 448; XII, Vertigo with, XV, 1015 Ataxic gait, Diseases causing, XIII, 740 paraplegia, X, 526; XII, 660; XIII, 796 Ateleiosis, XVI, 1093 Atheromatous arteries, Vertigo from, XV, 1025 Athetoid spasms, Diseases causing, XI, 574 Athetosis, I, 32; IV, 271; X, 501, 503 after apoplexy, X, 507; XI, 631 in cerebral palsy of childhood, X, 501 ; XI, 630 Congenital, X, 501 ; XI, 629 Athlete, Muscular hypertrophy in, XVII, "54 Atonia, I, 39; IV, 240 Atonic paralysis, I, 39; IV, 252; X, 472 Atrophic paralysis, IV, 252; X, 472, 547 Atrophies, Degenerative, X, 476 Localized, XVII, 1188 Atrophy, Arthritic, XVII, 1 126, 1151 of bone, Diseases causing, XVII, 1138 fat. Diseases causing, XVII, 1136 muscles, Diseases causing, I, 40, X, 476-7; XVII, 1 130 skin, Diseases causing, XVII, 1132 Attention, p. 13 Tests for power of. I, 5 Attitudes passionellcs, XI, 586 Auctioneer's cramp, XII, 726 Audition, Cortical center of, p. 8 Auditory aphasia, p. 10; XIII, 772 nerve, Deafness in atrophy of, XIV, 919 Electric reaction of, VII, 405 Lesions of, XIV, 920 ■enaction, p. 8 Aura of epilepsy, IX, 430 Glittering scotoma as, XIV, 846 of migraine, rlemianopia as, XIV, 854 Aural ataxia. XII, 650 vertigo, XII, 650, 6B5; XIV, 018; XV, 1019 Autochthonous acts, p. 28 Automatic acts, p. 28 Automatism, III, 210 Ambulatory, XVI, 1058, 1069-71 Diseases causing, XVI, 1039 Epileptic, XI, 575; XVI, 1058 Auto-suggestion in hysteria, IX, 4_'5 ; XVI, 1069-71 Auto-toxic coma, XVI, 1067 convulsions, XI, 596 Avelli's syndrome, XII, 706 Awkwardness : See apraxia Axillary paralysis, XII, 712 Axon, p. 5 Babinski and Nageotte's bulbar syndrome, IX, 437; XXI, 1268 Babinski's associated movements of trunk and thigh, IX, 446 reflex, V, 304 Tests for, I, 57 Backache, Diseases causing, XV, 935 Barlow's disease, X, 495 Basedow's disease. XII, 672; XVII, 1193 Bathyesthesia, I, 42 Bechterew's reflex : See dorsal foot reflex Bed sores, XVII, 1171 Bell's palsy, XII, 703 phenomenon, IX, 444; XII, 703 Benedykt's syndrome, IX, 441 ; XXI, 1270 Beri-Beri : See neuritis, multiple Bewildered mental condition, III, 207 Biernacki's sign, IX, 449 Binocular diplopia, VI, 383; XIV, 816 Biot's respiration, IX, 435 Bitemporal hemianopia, VI, 362; XIV, 815, 860, 892; XII, 1319 Bladder reflex, V, 323 Blepharospasm, XI, 601, 617; XII, 682, 726 Blindness, VI, 358; XIV, 850-1; XXII. 1318 Color, VI, 364 Diseases causing, XIV, 815 Psychic, III, 232; XXI, 1285; XXII. 1344 Snow. VI, 360; XIV, 843 Word, III, 228, 233; XIII, 773 Boat-shaped retraction of abdomen, XI, 608 Bone, atrophy of, Diseases causing. XVII. 11. iS, 117.) conduction, Tests for, I, 15 Fragility of, XVII, 1140, 1185 Hypertrophy of, Diseases ctnaing, XVII. 1x39 tissue, trophic lesions of, Diseases canting, xvn. 1 u; Boiton ECocher'a rign, XVII, 1192 Rrachycephali.i Brachial plexus. Neuritis or injury of, X. 400 .-■< INDEX Brachial plexus, paralysis, IX, 454-5; X, 490; XXII, 1306 Sjasm or cramp, XII, 733 Symptoms of lesions of, XXII, 1306 Bradycardia, XII, 728 Brain puncture, I, 75 stem, Definition of, IX, 460 Hemorrhage, inflammation, or softening in, X, 535; XII, 656 Lesions of, XIV, 830; XV, 1017 Localization in : See localization Symptoms of lesions of the, XXII, 1301-4, 1375, 1378, 1382-4; 1388. 1398 Tumor of the, X, 536; XII, 656 Vertigo in lesions of, XV, 1017 Bright's disease, Optic neuritis in, XIV, 899 Brown-Sequard paralysis, IX, 442; X, 509; XIV, 840; XV, 981 Brudzinski's neck sign, IX, 456 leg sign, IX, 457 Bulbar paralysis, IX, 434; X, 544, 546; XII, 694; XIII, 756, 761; XVII, 1 150 Acute, X 544 Chronic, X, 546; XII, 694; XVII, 1 150 Progressive, X, 546; XII, 694; XVII, 1150 Pseudo-, X, 553 Symptoms of, IX, 434 Burdach's column : See spinal cord Caisson disease, X, 521 Calcanodynia, XV, 1002 Calcarine fissure, Symptoms of lesions of, XIV, 847, 852-3, 855-6; XXII, 1364-6 Caloric reaction, I, 79; XII, 685 Cannabis Indica poisoning, XIV, 842 Capsule, External : See external Internal: See internal Caput obstipum paralyticum, XII, 705 spasticum, XII, 705, 730 Cardiac disease, Vertigo from, XV, 1024 Caries of the spine, II, 121 Case taking, I Casque neurasthenique, XV, 959 Catalepsy, XI, 611; XVI, 1096-8 Cataract, Diplopia in, XIV, 880 operation, Perversion of vision after, XIV, 843-4 Catatonia, XVI, 1098 Cauda equina, Paralysis of, X, 487 ; XII, 721 Symptoms of lesions of, X, 487; XV, 1007; XXII, 1308 Central convolution, anterior, Symptoms of lesions of, XXII, 1373, 1376, I379-8I, 1387; 1400-5 Central convolution, posterior, Symptoms of lesions of, XXII, 1348-9, 1352, 1369 motor neurons, IX, 461 Diseases of, IX, 473, XVII, 1153 Location of lesions of, XXII, 1293 sensory neurons, IX, 463 Cephalalgia: See headache Cerebellar artery, posterior inferior.Throm- bosis of the, XXI, 1268 ataxia, IV, 281; XII, 642, 669; XXI, 1268-74, 1282 Diseases causing, XII, 642 Marie's hereditary, XII, 651, 669; XIII, 782 mystagmus, I, 80 peduncles, Symptoms of lesions of the, XXI, 1273 tract (direct), Lesion of the, XII, 654; XXII, 1356, 1360 Cerebellum Diseases of the, XII, 686 vertigo in, XV, 1016 Lesions of the, XII, 648; XIII, 783; XXI, 1272 vermis of the, XI, 610 hemispheres of the, XI, 609 Localization in : See localization Cerebral abscess, II, 152, 181; X, 508; XI, 578, 587; XIV, 907; XV, 960; XVI, 1046 Cerebro-spinal fluid in, VIII, 411; XIX, 1237 Headache in, XV, 960 activity, Diseases causing weakened, XVI, 1040- 1 anemia, Vertigo from, XV, 1021-5 aneurism, X, 502 apoplexy : See hemorrhage and soft- ening compression, XVI, 1042 concussion, XVI, 1043 congestion, XV, 957, 1025a contusion, XVI, 1043 cortex, Symptoms of lesions of the, XXI, 1286 Conjugate deviation of eyeballs in the irritative lesions of the, XIV, 817 cyst: See tumor decompression, XV, 960 diplegia, X, 478, 501; XI, 577; XIII, 798; XVI, 1048 disease, XII, 689 edema, Cerebro-spinal fluid in, VIII, 411 embolism, X, 505 ; XIV, 832 ; XVI, 1062 endarteritis, Syphilitic, XVIII, 1207 gumma, Isolated, XVIII, 1206 262 INDEX Cerebral hemorrhage, II, 146; X, 503; XI, 588; XIV, 832, 856-7; XVI, 1043. 1061 Cerebro-spinal fluid in, VIII, 41 1-3; XIX.I240 into ventricles, X, 504 localization : See localization meninges : See hemorrhage meningitis: See meningitis, cerebral Cerebro-spinal fluid in, VIII, 410; XIX, 1226-9, I2 39 Headache in, XV, 961, 964 palsy of childhood, II, 116; X, 501; XI, 577, 630; XIII, 798; XVI, 1048, 1086 softening, X, 505-6; XIV, 832; XVI, 1062-3 syphilis, XVIII, 1206-9 Cerebro-spinal fluid in, VIII, 410; XIX, 1230-2 thrombosis, X, 506 ; XVI, 1063 ; XVIII, 1207 tumor, II, 151; X, 507, 536-42; XI, 578, 587; XIV, 833, 849. 855-61, 892; XV, 908, 960; XVI, 1047 Cerebro-spinal fluid in, VIII, 411, 419; XIX, 1236 Headache in, XV, 960 Optic neuritis in, XIV, 908 Perversion of vision in, XIV, 849 Vertigo from, XV, 1032 Cerebration, Disturbances of, III, 200 Cerebro-spinal fluid, p. 29; I, 74 Abnormal, VIII, 410; XIX, 1220 in abscess, XIX, 1237 Albumen in, VIII, 418 in anemia, XIX, 1242 Bacteria in, VIII, 416; XIX, 1223-4 Blood in the, VIII, 412-3; XIX, 1225 Butyric acid test in the, VIII, 419; XIX, 1221-2 Cellular elements in the, VIII, 416 in cerebro-spinal meningitis, XIX, 1226 clear with coagulum, VIII, 415; XIX, 1223-4 cloudy. VIII, 414: XIX, 1223 in epidemic cerebro-spinal menin- gitis. XIX. 1 '-•'■ Examination of the, I, 74; VIII, 410 Globulin in the, VIII, 410 in hemorrhage in cerebral or spinal meninges or in ventricles, XIX, i.- 1' 1 in herpes zoster, 1234 in hydrocephalus, XIX. [338 Leucocytosis in, V11I, 416; XIX. 1 -'-'3 Cerebro-spinal fluid, Lymphocytosis in, VIII, 416; XIX, 1224 in meningitis, VIII, 410; XI, 590; XVIII, 1214, 1226-9, 1239 Noguchi test in the, VIII, 419, XIX, 1221 Obtaining of, I, 74 in paresis, VIII, 420; XIX, 1230 poliomyelitis, VIII, 416, 419; X. 495; XIX, 1233 purulent meningitis, XIX, 1227 Red or reddish color of the, VIII, 412-3 in serous meningitis, XIX, 1238 sporadic purulent meningitis, XIX, 1227 Sugar in, VIII, 417 in syphilis, VIII, 410; XVIII, 1214 tabes, VIII, 420; XIX, 1231 Tension of the, VIII, 411 in tumor of brain or spinal cord, XIX, 1236 typhus fever, XIX, 1235 tuberculous meningitis, XIX, 1228-9 uremia, XIX. 1241 Wassermann test in the, VIII, 420; XIX, 1224 Cerebro-spinal syphilis, XVIII, 1214 Cervical region and enlargement : See spinal cord rib pressing upon subclavian artery, X, 556 sympathetic, Irritation of the, XVII, 1 192 Paralysis of the, XVII, 1191 Cervico-brachial neuralgia, XV, 995 Charcot's disease, XVII, 1186 Charcot- Marie-Tooth's type of muscular atrophy, X, 496; XII, 696 Chasmus, XII, 731 Cheyne-Stokes' respiration, I, 4?; IX, 435; XII, 728; XXI, 1268 Chills. XII, 680 Choked disc, Diseases causing, XIV, 897 Chondrodystrophia foctalis, XVII, 1177 Chorea, II, 11 2. iaSi IV, 272; V Degenerative. XI, 624 Electrical, XI, 600, 627 gravidarum, XI, 622 Hal.il. IV. .7. 1 ; XI, 626 Hcnii-. IV, 27a; X, 510 Hereditary, II, 103; XI Huntington's, 11, 103; \ Hysterical, XI, 628 Infectious, X major or m.iRna, IV, 273; XI. minor. IV. . mollis, X, 5:0 263 INDEX Chorea, in pregnancy, XI, 622 Rhythmical, XI, 628 Senile, XI, 624 Sydenham's, XI, 622 Choreic movements, I, 32; IV, 272 paralysis, X, 510 Choreiform spasms, Diseasescausing, XI, 573 Chvostek's sign, IX, 451 ; XI, 614 Chromatopsia, Tests for, I, 13 Chronic atrophic paralysis, X, 547; XII, 694; XIII, 797; XVII, 1 149 bulbar paralysis, X, 546; XII, 694; XVII, 1 150 Cilio-spinal center, IX, 465 reflex, V, 335 Circular insanity, XVI, 1 116 Circulation, Tests for, I, 45 Circulatory, disturbances, Perversion of vision in, XIV, 845-6 Claudication, Intermittent, X, 554; XVII, 1199 Claustrophobia, III, 235; XVI, 1072 Claustrum and external capsule, Symptoms of lesions of, XXI, 1278 Clavus, XV, 950 Claw-hand, X, 547; XII, 715 Cleft palate, XIII, 749 Clitoridian crises, IX, 433 Clonic spasm, IV, 246 Diseases causing, XI, 571 Clubbed fingers and toes, XVII, 1 184 Coal gas poisoning, XVI, 1055 Coccygodynia, XV, 972 Coffee vertigo, XV, 1030 Cold as etiological factor, II, 100 Colic, Lead, II, 158; XV, 988 Color blindness, VI, 364 fields, Interlacing, and inversion of, I, 14; XIV, 849 sense, Tests for, I, 13 Coma, I, 3; HI, 205; XIII, 745 ; XVI, 1037 Alcoholic, XVI, 1053 Diabetic, II, 190; XVI, 1065 Diseases causing, XVI, 1037 Epileptic, XI, 575; XVI, 1058 Hysterical, XVI, 1069 in internal hemorrhage, XVI, 1056 pseudo-, Diseases causing, XVI, 1038 Toxic or Auto-toxic, XVI, 1067 Uremic, XVI, 1066 Vigil, III, 206 Comprehension, Tests for power of, I, 5 Compression of brain stem, X, 536, 538, 540, 542 Cerebral, XVI, 1043 myelitis, II, 121; X, 520; XIII, 795 neuritis, XV, 939 Compulsory acts and ideas, I, 4; III, 218; IV, 275 Concentration, p. 13 Concentric limitation of field of vision, IX, 425; XIV, 815 Concepts, pp. 10, 13 Concussion, Cerebral, XVI, 1042 Conduction of pain, Retardation of, I, S 1 > VI, 381 of motor impulses, p. 24 sensory impulses, p. 6 et seq. Confusional insanity, XVI, 1106 Congenital dislocation of hip, XIII, 786a Congestive headache, XV, 957 Conjugate deviation of eyeballs, Lesions causing, XIV, 817 Conjunctival reflex, V, 312 Tests for, I, 58 Consanguineous marriages in nervous diseases, I, 2 ; II, 81 Conscience, p. 13 Consciousness, p. 15 Disturbances of, I, 3 ; III, 201 Consensual pupillary reflex, I, 25 Constipation headache, XV, 955 Continous paralysis, Diseases causing, X, 470 Contraction, Fibrillary, IV, 292; XII, 641 Contracture, Active, I, 38; IV, 264 Dupuytren's, XI, 620 Hysterical, XI, 618 Passive, I, 38; IV, 263 Post-hemiplegic, X, 504; XI, 577, 619 Post-neuritic, XI, 621 Post-paraplegic, X, 480, 548-5 1 ; XI, 620 Tests for, I, 32, 38 Contusion, Cerebral, XVI, 1043 Conus-terminalis of spinal cord, lesion of, XIV, 830a Convergence, Deficient and cyclopegia, V, 331 Conversation in diagnosis, I Convulsions, p. 25; IV, 269; XI, 570-1; XVI, 1037 Alcoholic, XI, 576, 585 Anemic, X, 583 Auto-toxic, XI, 596 Diseases causing, XI, 571 Epileptic, XI, 575; XVI, 1058 Febrile or toxic, XI, 595-6 Hysterical, XI, 586 Lead, XI, 584 Location of lesions causing, XXII, 1291 Strychnine, XI, 615 Tests for, I, 32 Toxic or febrile, XI, 595 Uremic, XI, 576, 581 Convulsive tics, IV, 267, 270; XI, 601, 617; XII, 726 264 INDEX Coordination, Tests for, I, 41 Coprolalia, XVI, 1096-8 Cornea, Diplopia in irregularities of the, XIV, 882 Corneal reflex, I, 58; V, 312 Tests for, I, 58 Cornet players' cramp, XII, 726 Corpora quadrigemina, Localization in : See localization Corpus callosum, Symptoms of lesions of, XXI, 1277 Striatum, Localization in : See localiz- ation Cortical lesions : See localization Cramp, XI, 616; See also spasm Cranial asymmetry, I, 22 fontanelles, I, 22 hyperostosis, XVII, 1181 nerves : See nerves nuclei : See nuclei sutures, I, 22 tumors, I, 22 Cranium, base of, Localization of: See localization Creative faculty, p. 14 Cremasteric reflex, V, 308 Tests for, I, 57 Cretinism, XVI, 1090; XVII, 1164 Crico-arytenoid posterior paralysis, XIII, 756 Crico-thyroid paralysis, XIII, 754 Criminals, Habitual, XVI, 1094 Crises, Tabetic, IX, 433 Crossed hemianesthesia, VI, 345 paralysis, IV, 256; X, 537-42; XV, 1017; XXI, 1268-70 Croup, Spasmodic, XI, 617; XII, 728 Crura cerebri, Hemorrhage or softening in the, X, 537 Localizing symptoms in the : See localization Symptoms of lesions of the, XII, 676; XXII, 1324, 1329, 1384, 1398 Tumor in the, X, 538 Crural neuralgia, XV, 997 paralysis, XII, 717; XV, 997 Cutaneous eruptions, Diseases causing, XVII, 1134 reflex acts, V, 297 Tests for, I, 57 sensibility, p. 6 tissue, atrophy of, XVII, 1132 Hypertrophy of, XVII, 1133 trophic lesions, Diseases causing, XVII, 1123 ulcerations, Diseases causing, XVII, 1X35 Cyanosis, Local, XVII, 1193 Cycloplegia, V, 331 Cyst, Cerebral : See tumor Dazed mental condition, III, 207 Dead fingers, XVII, 1195 Deaf-mutism, XIII, 744 Deafness, p. 8; VI, 355; XIV, 820 Diseases causing, XIV, 820 Hysterical, XIV, 924 Psychic, p. 10; III, 222, 233; XIII, ^2 Tests for, I, 15 Decompression, cerebral, XV, 960 Decubitus, XVII, 1171 Deep reflex acts, I, 60-6; V, 299 sensibility, p. 6 Defectives, p. 19; XVI, 1093 Degeneration, Electrical reaction of, VII, 399, 400, 404 Degenerative atrophies, X, 476 chorea, XI, 624 Deliberation, p. 23 Delirium, p. 20; III, 217 Acute or grave, XVI, 1108 tremens, XVI, 1107 Delusional insanity, XIII, 746; XVI, 1 109-13 Diseases causing, XVI, 1079 Delusions, p. 20; I, 4; III, 215 in hysteria, IX, 425 of grandeur, XVI, 11 13 observation, XVI, 11 13 persecution, XVI, 11 13 Dementia, p. 19; III, 212; XIII, 770 Agitated, XVI, 1103 Alcoholic, XVI, 1101 Apathetic, XVI, 1095, 1103 Diseases causing, XVI, 1077 Epileptic, XI, 575; XVI, 1102 Paralytic : See paresis precox, XVI, 1096 Primary, XVI, 1095 Secondary, XVI, 1 103 senilis, XVI, 1105 Terminal, XVI, 1103 Demoniacal possession, p. 18 Dendroni, p. 5 Dercum'i disease, XV, 1013; XVII, 1176 Dermographia I, 59; V, 326; XVII, n<>7, 1200 Deviation of the eyeballs, conjugate, Dis- eases causing. XIV, 817 Secondary, of sound eye, I, 29; XIV, 816 Tests for, I, 29 Diabetes mellitus, Coma in, II, 190; XVI, 1065 Fat atrophy in, XVII, 117s ( >|>tii- neuritis 111. XIV, 900 Perforating ulcers in, XVII, 1172 I tiadoookynctU, IV, 288 Tests for, I, 36 »6S INDEX Diagnostic charts. Introduction to, p. 1 19 Diaphragm, Paralysis of, XII, 707 Digestive disturbances, Vertigo in, XV, 1023 perversion of vision in, XIV, 845 Diphtheritic paralysis, X, 488; XIII, 753-4 Diplegia, IV, 478; X, 478; XII, 703 Cerebral : See cerebral Infantile : See infantile Diplopia, I, 24, 28; XIV, 816 Binocular, VI, 383; XIV, 816 Diseases causing, XIV, 816 Hysterical, XIV, 878 Monocular, VI, 384 ; XIV, 816 Tests for, I, 28 Displacement of eyeball, XIV, 877 of lens, XIV, 881 of visual axis, I, 28; XIV, 816 Disseminated myelitis or sclerosis: See sclerosis Dissociation of sensation, VI, 365 ; XIV, 811 Diseases causing, XIV, 811 Disuse, Bone atrophy from, XVII, 1178 Diver's paralysis, X, 521 Dolicocephalia, I, 22 Dorsal foot reflex, I, 63 ; V, 320 region of cord : See spinal cord Double personality, III, 209; XVI, 1039 Diseases causing, XVI, 1039 pupillary opening, XIV, 879 sensation, VI, 378 Tests for, I, 54 vision : See diplopia Drug habit, I, 1, 2; X, 482; XII, 663 poisoning, II, 164 vertigo, XV, 1030 Drunkenness in nervous diseases, I, 2; II, "5 Dubini's disease, XI, 600, 627 Dupuytren's contracture, XI, 621 Dwarfism, XVII, 1164, 1177 Dynamometer, Testing with, I, 34 Dysarthria, p. 28; I, 8; IV, 284; XIII, 738 Diseases causing, XIII, 738 Localization of, XXI, 1276; XXII, 1375, 1378, 1382-3, 1388 Dysbasia angio-sclerotica, X, 554; XVII, 1 199 Dyschromatopsia, I, 14; XIV, 849 Dysmasesis, IV, 286; X, 553 Dyspepsia, Headache in, XV, 952 Dysphagia, IV, 285 Localization of, XXII, 1375, 1378, 1382-3, 1388 Dyspinelismus, XXI, 1280 Dystrophies, Muscular, II, 107, 127; X, 477; XIII, 786; XVII, 1152 Ear disease as cause of headache, XV, 952 Deformity of, XVI, 1076 Hyperemia of inner, XIV, 927 Lesion of, XIV, 921, 927 Echolalia, XVI, 1096-8 Echopraxia, XVI, 1096-8 Eclampsia, XI, 576; XVI, 1059 Edema angio-neurotica, XVII, 1201 Localized, of scalp, XVI, 1044 Ego, The, p. 16 Egotism, p. 16 Elbow reflex, V, 321 Tests for, I, 64 Electrical chorea, XI, 600, 627 motor points, I, 70; VII, 395; Vllb reaction, I, 70-1 ; VII, 395 of auditory nerve, VII, 405 of degeneration, VII, 399, 400, 404 Diminished, VII, 397 Exaggerated, VII, 398 formula of degenerated nerve and muscle, VII, 399 of normal nerve and muscle, VII, 396 of muscles and nerves, I, 70; VII, 395 Myasthenic, VII, 401 Myotonic, VII, 402 Neurotonic, VII, 403 Normal, VII, 396 Electricity and the nervous system, p. 29 Electricity in examination of nervous patients, I, 70-1; VII, 395 Embolism, Cerebral, X, 505; XIV, 832; XVI, 1062 Emotion, p. 10 Emotional insanity, Diseases causing, XVI, 1080 Emotions, Disturbances of, I, 1; III, 204 Tests for, I, 7 Emprosthotonus, IV, 265 ; XI, 590, 606 Encephalitis, Acute multiple, X, 495, 543-4; XVI, 1064 Encephalomyelitis, XII, 659 Endarteritis, cerebral, Syphilitic, II, 175; XVIII, 1207 spinal, Syphilitic, II, 175; XVIII, 121 1 syphilitica, II, 175; XVIII, 1207, 1211 End-organs, p. 5 Enophthalmus, XVII, 1191 Enteralgia, XV, 988 Epicritic sensibility, p. 6 Epidemic cerebro-spinal meningitis : See cerebro-spinal meningitis Epigastric reflex, V, 310 Tests for, I, 57 Epilepsy, I, 2; II, no, 126; XI, 575; XV, 1027; XVI, 1058, 1071 Amnesia in, XI, 575 Automatism in, XI, 575 266 INDEX Epilepsy, Double personality in, III, 209; XI, 575 Glittering scotoma as aura of, XIV, 846 Idiopathic, XI, 575 Jacksonian, IX, 431; XI, 587, 605; XXI, 1282-3, 1291 Major attack of, XI, 575; XVI, 1058 media, XI, 575 Minor attack of, XI, 575; XVI, 1058 Nocturnal, XI, 575 ; XVI, 1058 Procursive, XI, 575 Psychic equivalent in, XI, 575 Rotatory, XI, 575 Spinal, I, 60-1; IX, 443; X, 509, 520; XIV, 838 Symptomatic, XI, 576-96 Epileptic aura, IX, 430; XIV, 846 cry, XI, 575; XVI, 1058 dementia, XI, 575; XVI, 1058, 1102 idiocy, XVI, 1083 insanity, XI, 575; XVI, 1058 state, XVI, 1058 vertigo, XV, 1027 Epileptiform convulsion, XI, 571 Erb's juvenile form of muscular dys- trophy, X, 499; XIII, 786; XVII, 1151 paralysis, IX, 454; X, 490 sign, IX, 452; XI, 614 syphilitic lateral sclerosis, X, 525; XVIII, 1212 Erotic excitement in dementia, XVI, 1105 Erroneous personality, III, 209 Eruptions, cutaneous, Diseases causing, XVII, H34 Erythromelalgia, XV, 1010; XVII, 1 198 Erythropsia, XIV, 843 Essential tremor, XII, 681 Ethics, p. 13 Etiology of nervous diseases, I, 1; II, 83 Eulenberg's disease, IV, 265; XI, 613 Eunuchismus. Pituitary, XXI, 1279 Examination of patients, I Excessive sweating, XVII, 1203 Excitability. Nervous, p. 5 Excitation, Maniacal, XVI, 1115 Exhaustion in etiology of nervous dis- eases, II, 95; XIII, 757 Vertigo from, XV, 1022 Exophthalmic goitre, I, 20; II, 131; XII, 672; XVII, 1 193 Extension of inflammation in etiology of nervous diseases, II, 96 External capsule, Symptoms of lesions of the, XXI, u;3 External rectus. Paralysis of the, XIV, 870 Eye as cause of headache, The, XV, 943, 952 in disease, I, 24 Eyeball, Conjugate deviation of the, XIV, 817 Displacement of the, XIV, 877 Limitation of motion of the, XIV, 816 Optic atrophy in diseases of the, XIV, 914 Paralysis of external rectus of the, XIV, 870 of inferior oblique of the, XIV, 875 rectus of the, XIV, 873 internal rectus of the, XIV, 871 muscles of the, XIV, 816 superior oblique of the, XIV, 874 rectus of the, XIV, 872 Spasm of muscles of the, XIV, 876 Face center, Symptoms of lesions of; XXII, 1380, 1381 1383 Facial expression in disease, I, 20 diplegia, XII, 703 hemiatrophy, XVII, 11 79 hemihypertrophy, XVII, 1 180 monoplegia, XII, 703 nerve, Localization of lesions of, XXII, 1317 nucleus, Symptoms of lesions of, XXII, 1329-31 paralysis, XII, 703; XIII, 751 1 XIV, 928; XXII, 1329-36 spasm, or cramp, XII, 726 Facio-scapulo-humeral type of muscular dystrophy, X, 497 False image. Position of, XIV, 816 Family gangrene, XVII, 1 196 history, I, 2 myoclonus epilepticus, XI, 604 periodic paralysis, X, 555 Faradic excitation of nerves and muscles, I, 70-2; VII, 395 Faradism in examination of nervous patients, I, 70-2; VII, 395 Fatty tissue, atrophy of, Diseases causing, XVII, 1136 hypertrophy of, Diseases causing, XVII, 1137 trophic lesions of, Diseases caus- ing, XVII, HJ-t Fear, 111. Feeble-minded, i> [9; XVI, 1092 Febrile or toxic convulsion, XI, 595 Fcstinating gait (Festinationl, XI, 612; XII. 677; Mil, ;«), 800 Fibrillar] (Fibrillation), IV, 292 Diseases causing. XII. 641 267 INDEX Field of vision, Limitation of the, IX, 425 Diseases causing, XIV, 815 Tests for, I, 14 Fits, I, 1 : See also convulsion and spasm Flaccid paralysis, IV, 252 Diseases causing, X, 472 Tests for, I, 39 Foot drop, I, 21 ; X, 488, 404; XIII, 788 Formication, VI, 375 Formula of electrical reaction of degenera- tion, VII, 399 of normal electrical reaction, VII, 396 Foul air headache, XV, 954 Fourth ventricle, lesion within, Vertigo from, XV, 1018 Foville's paralysis, XXI, 1269 Fragility of bone, XVII, 1185 Free-will, pp. 23-4 Frenzy, Maniacal, XVI, 1115 Friedreich's hereditary ataxia, II, 104, 123; XII, 652, 670, 687 ; XIII, 762, 781 paramyoclonus multiplex, XI, 603 Frontal convolution (inferior), Symptoms of lesions of the, XXII, 1390 (middle), Symptoms of lesions of the, XXII, 1389, 1399 headache, XV, 952 lobes, Symptoms of lesions of the, XIV, 885 ; XXI, 1282 Gait, ataxic, Diseases causing, XIII, 740 in disease, I, 21 ; XIII, 736 disorder of, Diseases causing, XIII, 736 Festinating, XII, 677; XIII, 766, 800 High-stepping, X, 488; XIII, 787-9 Mowing, XIII, 794 Paralytic and flaccid, XIII, 741 and spastic, XIII, 742 Scissors, XIII, 742 Galton's whistle, I, 15 Galvanic excitation of nerves and muscles, VII, 395 Galvanism in examination of nervous patients, I, 71 Ganglionic disorders, Diseases causing, XVII, 1 128 Gangrene, Family, XVII, 1196 Symmetrical, XV, ion; XVII, 1195 Gastralgia, XV, 986 Gastric crises, IX, 433 General appearance in disease, I, 20 General paresis : See paresis sensation, p. 8 Geniculate bodies, Lesions of, XIV, 858; XXII, 1321 Genital neuralgia, XV, 990 Gerlier's vertigo, XV, 1031 Gigantism, XVII, 1 183 Girdle pain, VI, 374 Diseases causing, XV, 935 Glaucoma, XIV, 864; XV, 943 Glioma, II, 124 Central, X, 552 Glittering scotomata, XIV, 846 Globus hystericus, IX, 426; XI, 586; XVI, 1074 Glosso-pharyngeal spasm, or cramp, XII, 727 Glossy skin, I, 40; XVII, 1160 Glove form of anesthesia, VI, 345 ; IX, 425 Gluteal paralysis, XII, 719 reflex, V, 307 Tests for, I, 57 Gordon's reflex, V, 305 Graefe's symptom, XII, 672; XVII, 1 192-3 Grandeur, Delusion of, XVI, 1 1 13 Grand mal (le), XI, 575; XVI, 1058 Grasset and Gaussel's phenomenon, IX, 458 Gratiolet, Lesion of the optic fasciculus of, XIV, 855-6; XXII, 1364 Grave's disease, XII, 672; XVII, 1193 Green vision, XIV, 844 Gumma, II, 172 Isolated, cerebral, XVIII, 1206 spinal, XVIII, 1210 Gustation. Cortical center of, p. 7 Gustatory sensations, p. 7 Habit, p. 16 chorea, IV, 274; XI, 626 spasm, XI, 626 Habitation in nervous diseases, I, 2; II, 89 Habitual criminals, XVI, 1094 Hallucinations, p. 19; I, 4, 20; III, 213 Hallucinatory insanity, Diseases causing, XVI, 1078 Hallucinosis, Alcoholic, XVI, 1109 Hand, Ape's, XII, 714 Claw, X, 547; XII, 715 Obstetrical, XI, 614 Trident shaped, XVII, 1177 Haphalgesia, VI, 380 Hare's eye, XII, 703 Head in disease, The, I, 22; XVI, 1076 Head's researches on sensibility, p. 16 Headache, I, I ; XV, 934 Alcoholic, XV, 953 Anemic, XV, 952, 958 Aural, XV, 952 in cerebral abscess, XV, 960, 965 Congestive, XV, 957 Constipation, XV, 952, 955 Diseases causing, XV, 934 Dyspeptic, XV, 952 Foul air, XV, 954 Frontal in disease, XV, 952 High blood tension causing, XV, 957 268 INDEX Headache, Hydrocephalic, XV, 960 Indurative, XV, 962 Infection, XV, 963 Meningitic, XV, 961, 964 Menstrual, XV, 949 Migraine, XIV, 836, 854; XV, 949, 1028 Morphine, XV, 953 Neurasthenic, XV, 959 Occipital, XV, 952 Ocular, XV, 952 Pachymeningitis XV, 961 Pelvic, XV, 952 Rheumatic, XV, 962 Sinus thrombosis causing, XV, 964 Sunstroke causing, XV, 966 Temporal, in disease, XV, 952 Toxic, XV, 963 Tumor causing, XV, 960 Uremic, XV, 956 Vertex, in disease, XV, 952 Heatstroke or sunstroke, XI, 589; XV, 966; XVI, 1068 Hearing, p. 8 Cortical center of, p. 8 Diseases causing disorders of, XIV, 808 Loss of, XIV, 820 Tests for, I, 15 Hebephrenia, XVI, 1097 Heine-Medin's disease, X, 495 Hematorrhachis, X, 524; XV, 973 Hemeralopia, VI, 360 Hemianesthesia, alternans or crossed, VI, 345; XXI, 1269 dolorosa, XXI, 1275 and hemianalgesia, VI, 345; IX, 425; XXI, 1268-70 Hysterical, VI, 345 ; IX, 425 ; XIV, 834 Transference of, IX, 425; XIV, 834 Hemianopia, VI, 362; XIV, 815, 800 Bi-temporal, VI, 362; XIV, 815, 860, 892; XXII, 1319 Diseases causing, XIV, 815 Homonymous, VI, 362; XIV, 815, 800; XXI, 1285; XXII, 1342 Diseases causing, XIV, 815 Horizontal, XIV. 862 Localization of, XXI, 1275, 1283, 1285; XXII, 1315. J342-3 Nasal, VI, 362; XIV, 815; XXII, 1320 Diseases causing, XIV, 815 Quadrantic. VI. 363; XIV, 815; XX, U85; XXII. 1343 Tests for, I, 14 Hemiataxin. XII. 654-7 Hemiatrophy, Facial, XVII, ii;j Hemicrania. XV, >>vi angio-paralytica, XV, 949 iii',1, XV, tj.|'> borea, IV, 27a . X, 5x0; XI. 573 Hemichromatopsia, VI, 364; XIV, 847 Hemihypertrophy, Facial, XVII, 1180 Hemiopic pupillary reflex, V, 334 Diseases causing, XIV, 890 Tests for, I, 26 Hemiplegia, I, 21; IV, 254; X, 478-9 alternans, IV, 256; X, 537-42; XV, 1017; XXI, 1268 Facial, IV, 256; XXI, 1269 Hypoglossal, IV, 256; XXI, 1268 Oculo-motor, IV, 256; XXI, 1270 Angio-spastic, X, 554 Complete, IV, 254; XXI, 1276 Crossed : See H. alternans Diseases causing, X, 478-9 Hysterical, XIII, 793 Infantile : See cerebral palsy of child- hood Lacunar, XVI, 1063 Organic, XIII, 794 Partial, IV, 254 Spinal, IX, 442; X, 509; XIV, 838; XV, 981 Hemorrhage in brain stem, X, 535; XII, 656 Cerebral, II, 146; X, 503; XI, 588; XIV, 832, 857; XVI, 1043, 1061 cerebro-spinal fluid in, VIII, 41 1-3; XIX, 1240 into ventricles, X, 504 internal, Coma in, XVI, 1056 Vertigo in, XV, 1023 Meningeal, cerebral, II, 146; X, 502; XVI, 1060 Cerebro-spinal fluid in, VIII, 41 1-3; XIX. 1240 Spinal, II, 146; X, 524 Cerebro-spinal fluid in, VIII, 41 1-3; XIX, 1230-40 or injury of spinal cord, above cervical enlargement. X. 51a in cervical enlargement. X. 548 dorsal region, X, 516 lumbar region, X, 4S4 or softening in cms cerebri, X, 537 in medulla. X, 541 pons, X, 539 Hepatic crises, IX, 433 Hereditary ataxia, II, 104. 123; XII, 651-2, "■) ;■•, us r: xiii. 76a, 781-3 chorea: See chorea 1 1 iniiity in nervotu diseases, l. a; II, 81 Herpes, I, 40; XI, ggo; X r. Herpes zoster, XVII. 1166; XIX. 1234 Cerebro-spinal fluid in, XIX. 1934 Herpetic neuritis, XV, 940, 978 li, XII, 73] High stepping gait, X, 4SN; Xll. 710; XIII. 741 269 INDEX High tension headache, XV, 957 vertigo, XV, 1025a Hip. Congenital dislocation of, XIII, 786a Hippus, V, 336 History taking, I, 1 Homonymous hemianopia: See hemi- anopia Scotomata, XIV, 863 Hunger, p. 8 Huntington's hereditary chorea, II, 103; XI, 623 Hydrocephalic cry, XI, 593 idiocy, XVI, 1082 Hydrocephalus, I, 22; II, 119 Cerebro-spinal fluid in, VIII, 411; XIX, 1238 Headache in, XV, 960 Optic neuritis in XIV, 905 Hydrophobia, II, 171 ; XI, 607 Hydrorrhoea nasalis, XXI, 1279 Hypakusia, VI, 355; XIV, 820 Hypalgesia, VI, 349; XIV, 810 Hyperakusia, VI, 372; XIV, 820 Hyperalgesia, VI, 367 Tests for, I, 50 Thermic, VI, 366 Hyperemic reflex, V, 326 Hyperesthesia, VI, 366; XIV, 813 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 Hypertrophic pulmonary osteo-arthro- pathy, XVII, 1184 Hypertrophies, Localized, XVII, 1188 Hypertrophy of bone, Diseases causing, XVII, 1139 of fat. Diseases causing, XVII, 1 137 muscle, I, 40 Diseases causing, XVII, 1131 in an athlete, XVII, 1154 skin, Diseases causing, XVII, 1 133 Hypesthesia, VI, 348; XIV, 810 Hypnotism, XVI, 1069 Hypochondriasis, III, 216; XVI, 1073 Hypogeusia, VI, 357; XIV, 809 Hypoglossus paralysis, XII, 706; XIII, 752 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, ill, 128, 130, 153, 179; XIV, 843, 848, 866, 926; XV, 950, 971 ; XVI, 1070, 1074 Concentric limitation of field of vision in, IX, 425; XIV, 866 Perversion of vision in, XIV, 843, 848 Traumatic, XVI, 1075 Vertigo from, XV, 1033 Hysterical amblyopia, XIV, 851a. anesthesia, p. 7; VI, 345; IX, 425; XIV, 834 Tests for, I, 48 aphonia, XIII, 748, 759 ataxia, XII, 664 backache, XV, 971 chorea, XI, 628 coma, XVI, 1069 contracture, X, 618 convulsion, XI, 586 deafness, XIV, 924 diplopia, XIV, 878 hemianesthesia, IX, 425 ; XIV, 834 hemiplegia, XIII, 793 hyperakusia and parakusia, XIV, 926 joint XV, 1000 mutism, XIII, 747 neuralgia, XV, 950 paralysis, X, 527; XIII, 747-8, 759, 793; XIV, 878; XVI, 1074 spasm, X, 618 symptoms, IX, 425 tremor, XII, 674 Hystero-epilepsy, XI, 586 Hysterofrenic areas, IX, 428 Hysterogenic areas, IX, 427 Ictus, X, 479 laryngcus, IX, 433 Ideas, pp. 10, 13 Idiocy, p. 18; II, 101; XIII, 743! XVI, 1081 Idioglossia, XIII, 750 Idiopathic epilepsy, XI, 575; XVI, 1058, 1071 idiocy, XVI, 1081 imbecility, XVI, 1091 muscular dystrophy, IX, 498 neuralgia, XV, 937 Idiots savants, XVI, 1089 Illuminating gas poisoning, XVI, 1055 Illusions, p. 19; III, 214 Imagination, p. 14 Imbecility, p. 18; II, 101 ; XVI, 1088, 1091 moral, XVI, 1094 Immobile eyeball, X, 545 pupil, V, 333; X, 545 Indurative headache, XV, 962 Infantile diplegia, X, 501 hemiplegia, X, 501; XI, 577, 630; XIII, 798; XVI, 1048 paralysis : See poliomyelitis 270 INDEX Infantilism, XVI, 1093 Infectious chorea, XI, 622 headache, XV, 963 nervous diseases, I, I, II, 93 Inferior oblique muscle, Paralysis of, XIV, 875 rectus muscle, Paralysis of, XIV, 873 Inflammation of brain stem, X, 535; XII, 656 Cerebral : See meningitis and abscess of nerves : See neuritis spinal cord : See spinal Infra-maxillary neuralgia or neuritis, XV, 94S orbital neuralgia or neuritis, XV, 944 Ingravescent apoplexy, XVI, 1060-3 Inherited nervous diseases, II, 84 tendencies, II, 85 Inhibition, p. 22 Injury, I, 1; II, 135 Injury of cauda equina, X, 487 brachial plexus, X, 490 nerve, X, 489, 492; XIV, 822; XVII, 1 146 optic nerve, XIV, 904 or hemorrhage of spinal cord, cervical enlargement, X, 548 cervical region, X, 512 dorsal region, X, 516 lumbar region, X, 484 spinal cord, XIV, 838 Innervation feelings and memories, p. 12; III, 221 Insanity, p. 18; I, 2; II, 109, 129, 154; XVI, 1041 Adolescent or juvenile, XVI, 1096 Catatonic, XVI, 1098 Circular, XVI, 1 116 Confusional, XVI, 1106 Delusional, XIII, 746; XVI, 1079 Emotional, Diseases causing, XVI, 1080 Epileptic, XI, 575 ; XVI, 1058 hallucinatory, Diseases causing, XVI, 1078 Hebephrenic, XVI, 1097 Maniacal depressive, XVI, 11 17 Paranoid, XVI, 1099 Pott-epileptic. XI. 575; XVI, 1058 febrile, XVI, 1107a Recurrent, XVI, 1 117 Septic, XVI, 1107a Tests fur, I, 4 \VI, 1107a Insolation, XI. 589; XV. 966; XVI, 1068 Insomnia, I, 18 Inspection in diagnosis, I. Insufficiency of ocular muscles, XII, 692 Intelligence, p. 17 1 titturbancei "f, lit, 202 Tests for, I, 5 Intention tremor, IV, 290; XII, 645 Diseases causing, XII, 643 Intercostal neuralgia, XV, 977 spasm or cramp, XII, 732 Interlacing of color fields, I, 14; XIV, 849 Intermittent limping or claudication, X, 5541 XVII, 1199 paralysis, X, 471 Internal capsule, Symptoms of lesions of the, XIV, 857; XXI, 1276; XXII, 1354, 1361, 1385 rectus muscle, Paralysis of, XIV, 871 sensations, pp. 8, 10 Interscapular reflex, V, 311 Tests for, I, 57 Intoxication, Alcoholic, XII, 658, 663; XIII, 764, 780 Inversion of color fields, I, 14; XIV, 849 Iridoplegia, V, 339 Iritis, I, 24 Irritation of sympathetic ganglia, Diseases causing, XVII, 1143 Ischemic reflex, V, 325 Island of Reil, Symptoms of lesions of, XXI, 1278 Jacksonian epilepsy, IX, 431 ; XI, 587, 605 Location of lesions causing, XXI, 1282-3; XXII, 1291 Jargon speech, III, 225; XIII, 775 Jaundice, Yellow vision in, XIV, 842 Jaw reflex, V, 322 Tests for, I, 65 Jendrassik's method of reflex reinforce- ment, I, 68 Joints, trophic lesions of, Diseases causing, XVII, 1 126 Joy, III, 236 Juvenile insanity, XVI, 1096 Kahler's disease, XVIII 1209 Kak-ke : See neuritis, multiple Kalmuck idiots, XVI, 1093 Keratitis, I, 24 Kernig's sign, V, 319 Tests for, I, 66 Kinesthetic memories, pp. 1., 97 Knee-clonus, I, 61 Knee-jerk, V, 318 Tests for, I, 61 Knowledge, Tests for general, I. 5 Klumpke's paralysis, IX, 455; X, 490 Korsakow*s psychosis, X, 488; XVI, 1100 Kyphosis, I, 83; XVII, It 83 Labyrinth disease, XIV, 918 Labyrinthine vertigo, XII, 685 Labio-glosso-pharyngeal pvalytit, X, 546 Lacunar htjnlplegia, XVI, 1063 271 INDEX Lagophthalmus, XII, 703 Lalling, XIII, 750 Landouzy-Dejerine type of muscular atrophy, X, 497, XVII, 1151 Landry's paralysis, II, 168; X, 482 Language, Zone of, 6. 28 Laryngeal crises, IX, 433 exhaustion, XIII, 758 nerve, Paralysis of superior, XIII, 754 vertigo, IX, 433 Laryngismus stridulus, XI, 617; XII, 728 Laryngitis, XIII, 757 Laryngoscopy in examination of nervous patients, I, 77 Larynx, Anesthesia of, XIII, 754, 760, 761 Lasegue's symptom, IX, 429 Lateral column : See spinal cord sclerosis, X, 525; XIII, 797 Amyotrophic. X, 547; XII, 695; XVII, 1 149 Erb's syphilitic, X, 525 Lateropulsion, XXI, 1269, 1272-3 Lead colic, II, 158; XV, 988 convulsion, XI, 576, 584 palsy, II, 158; X, 494; XIII, 788; XVI, 1050 poisoning, Optic neuritis in, XIV, 901 Leg center: See localization Le grand mal of epilepsy, XI, 575; XVI, 1058 La petit mal of epilepsy, XI, 575 ; XVI, 1058 Lemniscus, Lesions of, causing deafness, XIV, 922 Leontiasis ossea, XVII, 1181 Leprous neuritis, II, 140; XVII, 1169 Lethargy, African, II, 141 Leucoderma, XVII, 1162 Levator palati, Paralysis of, XIII, 753 Limping, Intermittent, X, 554; XVII, 1 199 Lisping, XIII, 750 Little's disease, X, 501 Local asphyxia, XVII, 1195 cyanosis, XVII, 1195 paralysis, IV, 259; XII, 636 spasms, XII, 637 syncope, XVII, 1195 Localization, p. 12; XX, XXI, XXII at base of cranium, XXI, 1274 by Jacksonian epilepsy, XXII, 1291 by paralysis, motor and sensory, XXII, 1290 cerebellar, XXI, 1272 vermis, XI, 610 Direct, tract, XII, 654 hemispheres, XI, 609 peduncle (middle), XXI, 1273 Cerebral : brain stem, X, 535-46; XII, 656; XIV. 830; XXI, 1268-71; XXII, 1375, 1378, 1398 Localization, cerebral, abducens nucleus, XIV, 882; XXII, 1328 corpora quadrigemina, XXI, 1271 crura cerebri, X, 537-8; XII, 676; XXI, 1270; XXII, 1324-29. 1384, 1398 dysarthria and dysphagia, XXII, 1375, 1378, 1382-3, 1388 facial nucleus, XXII, 1329-31 fourth ventricle, XV, 1018 ganglia at base, XXI, 1268-80 lemniscus, XIV, 922 medulla oblongata, X, 541-2; XXI, 1268; XXII, 1375, 1382, 1388, 1398 motor cranial nuclei, XXII, 1304 pons Varolii, X, 539-4° ; XIV, 884; XXI, 1269; XXII, 1328-31, 1353, 1383, 1388, 1398 ponto-cerebellar angle, XXII, 1363 red nucleus, XXII, 1325 rubro-spinal tract, XII, 676; XXII, 1325 sensory cranial nuclei, XXII, 1302 sixth cranial nucleus, XXII, 1327 third cranial nucleus, XXII, 1323, 1326 hemispheres : agraphia, XXI, 1282; XXII, 1389 alexia, XXII, 1391 angular gyrus of, XXII, 1391 aphasia, motor, XXI, 1282; XXII, 1390 sensory, XXI, 1284; XXII, 1368 arm center, XXII, 1349, 1352, 1369, 1376, 1379. 1381, 1387, 1401 astereognosis, XXII, 1346, 1369 blindness, Psychic, XXI, 1285; XXII, 1344, 1367 calcarine fissure, XXII, 1364-6 central convolution, anterior, XXII, 1373. 1376, 1379-81, 1387, 1400-5 posterior, XXII, 1348-9. 1352, 1369 claustrum, XXI, 1278 corpus callosum, XXI, 1277 corpus striatum, XXI, 1276; XXII, 1386 272 INDEX Localization in cerebral hemispheres: cortical lesions, XXI, 1286 external capsule, XXI, 1278 face-center, XXII, 1380-3 facial fibers, XXII, 1317 frontal convolution, inferior, XXII, 1390 middle, XXII, 1389, 1399 frontal lobe, XIV, 885; XXI, 1282; XXII, 1389-90 geniculate bodies, XXII, 1321 ganglion, XXII, 1333-4 hemianopia, homonymous, XXII, 1342-3 internal capsule, XIV, 857; XXI, 1276; XXII, 1354, 1361, 1385 Island of Re:l, XXI, 1278 leg center, XXII, 1348, 1352, 1355, 1362, 1373, 1379, 1387, 1402 nucleus caudatus, XXI, 1276 nucleus lenticularis, XXI, 1276 occipital lobe, XIV, 850-6; XXI, 1285; XXII, 1367 optic fasciculus of Gratiolet, XIV, 855-6; XXII, 1364 optic thalamus, XXI, 1275; XXII, 1386 parietal lobe, XII, 657; XXI, 1283; XXII, 1403-5 lobule (inferior). XXII, 1362 (superior), XXII, 1355 pineal gland, XXI, 1280 pituitary gland, XXI, 1279 Reil, Island of, XXI, 1278 temporal convolution (superi- or), XIV, 925; XXI, 1284; XXII. 1368 cranium, At base of, XXI, 1274 Failure of, VI, 376 neurons, Central, XXII, 1293 Peripheral, XXII, 1292 Peripheral : brachial plexus. XXII, 1306 cauda equina, XXII. 1308 chorda tympani, XXII, 1335-6 cranial motor nerves, XXII, 1303 sensory nerves, XXII, 1301 facial nerve. XXII, i,u;, 1332-6 hemianopia, XXII, 131 lumbar plexus, XXII. 1306 ocular muscles, XXII, 1316 optic chiasm, XIV, 851, 860-1, 892; XXII, 13.0-20 nerve, XIV, BSI; XXII, 1318 tract XIV, 858-9, 893; XXII, I.U'I Localization, peripheral, orbit, XXII, 1322 sixth cranial nerve, XXII, 1327 spinal nerves, XXII, 1303-8 third cranial nerve, XXII, 1323 sensation tests for, I, 53 Spina! cord : anterior commissure, XXII, 1357-9 horn, XXII, 1304 nerve roots, XXII, 1304 Burdach's column, XXII, 1302 central gray matter, XXII, 1357-9 cervical enlargement and region, XXII, 1310, 1350-1, 1358-9, 1374, '377, 1397 direct cerebellar tract, XII, 654 dorsal region, XXII, 1347, 1356, 1372, 1395 lateral column, XXII, 1356, 1358, 1360, 1372-74, 1377. 1396 lumbar enlargement, XXII, 1309, 1357 posterior column, XXII, 1347, I350-I, 1396 horn, XXII, 1302 nerve roots, XXII, 1302 Segments : cervical ; 8th, XX, 1263 7th, XX, 1264 6th, XX, 1265 5th, XX, 1266 4th to 1st, XX, 1267 dorsal ; 12th, to 3rd, XX, 1260 2nd, XX, 1261 1st, XX, 1262 lumbar ; 5th, XX, 1255 4th, XX, 1256 3rd, XX, 1257 2nd, XX, 1258 1st, XX, 1259 sacral ; 5th, XX, 1250 4th, XX, 1251 3rd. XX. iasa and, XX, 1253 1st, XX, [354 vision, Disturbances of, XXII. 1315 Localized atrophies and hvpertrophies, XVII, : 188 Lockjaw: See tetanus Locomotor ataxia: Sec I Long thoracic nerve, r.ir.ilv -i~ of. XII, 709 Lumbar enlargement: See ipinal plexus, spasm or cramp of, XII, 733 symptoms, of lesions of, XXII. tJOO puncture, I, 74, XI, 590 ■ of, I. n INDEX Lumbo-abdominal neuralgia, XV, 989 Lyssa, XI, 607 Macrocephalia, I, 22 Macropsia, VI, 387 Major attack of epilepsy, XI, 575; XVI, 1058 Mania, III, 236 Acute alcoholic, XVI, 1 109 Epileptic, XI, 575 Primary, XVI, 11 15 Symptomatic, or Delusional, or Sec- ondary, XVI, mi Maniacal excitation, XVI, n 15 depressive insanity, XVI, 1117 fre.izy, XVI, HIS Marie-Tooth-Charcot's type of muscular atrophy, X, 496 Marie's hereditary cerebellar ataxia, XII, 651, 669-70; XIII, 782 idea of aphasia, XIII, 739 Mask-like face, XI, 612; XII, 677; XIII, 766, 800 Mastodynia, XV, 982 Masturbation in nervous diseases, I, 2 Maxillary reflex, V, 322 Mechanical irritability of nerves and muscles, I, 67 Median paralysis, XII, 714 Medulla oblongata, Hemorrhage in or softening of, X, 541 Localizing symptoms : See localization Tumor of, X, 542 Meig's disease, XVII, 1202 Melancholia, III, 234 agitata, XVI, 1 1 12 attonita, XVI, 11 12 cum stupore, XVI, 1 1 12 Primary, XVI, n 14 raptus, XVI, 1112 Secondary or Sympathetic, or Symp- tomatic, or Delusional, XVI, 1112 Memories, Innervation, III, 221 Memory, p. II Disturbances of, I, 1 ; III, 203 Tests for defects in, I, 6 Mendel-Bechterew's reflex: See dorsal foot reflex Meniere's disease, XII, 650, 685; XIV, 918; XV, 1019 Deafness in, XIV, 918 Vertigo in, XV, 1019 Meningeal apoplexy, II, 146; X, 502, 524; XI, 588; XVI. 1060 Meningismus, XI, 594 Meningitis, II, 118, 122, 147, 166, 183; XI, 590, 608; XVI, 1045 Cerebral, X, 508; XI, 590, 608; XIV, 831; XV, 1032; XVI, 1045; XVIII, 1208-9 Vertigo in, XV, 1032 Meningitis. Cerebro-spinal, XI, 591. 608; XVIII, 1214; XIX, 1226-9 fluid in, VIII, 410; XIX, 1226-9, 1239 Gummosa, II, 173; XVIII, 1208-9, 1213-4 Headache in, XV, 961, 964 Localized, X, 508 Optic neuritis in, XIV, 906 Purulent, XI, 592; XIX, 1227 Cerebro-spinal fluid in, XIX, 1227 Serous, XI, 594; XIX, 1239 Cerebro-spinal fluid in, XIX, 1239 spinal, Acute and chronic, XI, 608; XV, 974, 1005; XVIII, 1213-4 of spinal cord and nerve roots, XVIII, 1213 Syphilitic, XV, 980a; XVIII, 1208-9, 1213-4 Tuberculous, II, 118, 122, 188; 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, 5 Mentality weakened, XVI, 1040 Meralgia paresthetica, XV, 999 Mercurial tremor, II, 159; XII, 673 Metamorphopsia, VI, 385 Metastasis in nervous diseases, II, 98 Metatarsalgia, XV, 1003 Microcephalia, I, 22; XVI, 1084 Micropsia, VI, 386 Microsmia, XVII, 1177 Migraine, II, 114; XV, 949 Glittering scotoma in, XIV, 846 Hemianopia in, XIV, 854 Vertigo from, XV, 1028 Millard-Gubber's syndrome, IX, 439; XXI, 1269 Milroy's disease, XVII, 1202 Mind, p. 17 Miner's nystagmus, XII, 684 Minor attack of epilepsy, XI, 575 ; XVI, 1058, 1 07 1 Mobile spasm, IV, 271 Mongolism, XVI, 1093 Monocular diplopia, VI, 384 Monoplegia, IV, 258; X, 478-9, 481 Diseases causing, X, 478-9, 481 Moral imbecility, XVI, 1094 sense, Tests for, I, 5 Morphine headache, XV, 953 vertigo, XV, 1030 Morton's toe, XV, 1003 Morvan's disease: See syringomyelia 274 INDEX Motion, Diseases causing diminution of, IV, 244; X, 469; XXII, 1294- 1300 exaggeration of, IV, 245-7; XI, 570; XXII, 1291 perversion of, IV, 243; XII, 635 Disorders of voluntary, IV, 240 Motives. Play of, p. 23 Motor aphasia, III, 221 ; XIII, 771 Localization of, XXI, 1282; XXII, 1390 ataxia, IV, 280; XII, 644; XXI, 1268-74 Diseases causing, XII, 644 impulses, conduction of, p. 24 neurons, Diseases of the, X, 469; XI, 570; XII, 635-7 oculi paralysis, XII, 700 paralysis, IV, 244; X, 469 Diseases causing, X, 469 Localization of, XXII, 1290 Tests for, I, 33-4 paresis, IV, 244; X, 469 points, Electrical, I, 70-1 ; VII, 395 Movements, p. 21 Association, p. 22 Autochthonous, p. 28 Automatic, p. 28 Reflex : See reflex Voluntary, p. 22 Mowing gait, XIII, 794 Mucous membrane reflex acts, V, 298 Tests for, I, 58 Multiple encephalitis, Acute, X, 495, 543-4 neuritis: See neuritis sclerosis : See sclerosis Muscae volitantes, XIV, 845 Muscle degeneration, IV, 252; XVII, 1130 -joint sensation, pp. 6, 8 sense, Loss of, VI, 352; X, 488; XII, 661; XIV, 812 Tests for I, 42 Diseases causing, XIV, 812 tone, I, 39; IV, 240 Muscles and nerves, Electrical reaction of, I, ;->; VII, 395 Mechanical excitability of, I, 67 trophic lesions of. Diseases causing, X. 47'. 7; XVII, 1122 Muscular atrophy, I, 40 Aran-Duchenne's, type of, X, 547; XII, 604; XIII, :>,:; XVII, 1149 Charcot-Marie-Tooth's type of, X, 496; XII, 695 Diseases causing, X, 476-7; XVII, 1 130 in chronic paralytia, XVII, 1 153 Peroneal type of, X, 496 Muscular atrophy, Progressive spinal, X, 547; XII, 694; XIII, 797; XVII, 1 149 Spinal or neuritic, X, 406; XII, 696 coordination, I, 41 dystrophies, II, 107, 127; X, 477; XIII, 786; XVII, 1152, 1156 dystrophy, Erb's juvenile, or scapula- humeral type of, X, 499; XIII, 786; XVII, 1 152 in disease, X, 477 Landouzy-Dejerine, or facio-scap- ulo-humeral type of, X, 497; XIII, 786; XVII, 1151 Pseudo-hypertrophic form of, X, 500; XVII, 1 156 Simple or idiopathic X, 498; XIII, 786, XVII, 1 151 hypertrophy, I, 40 in athletes, XVII, 1154 Diseases causing, XVII, 1131 insufficiency, Ocular, I, 24; XII, 692; XIV, 816 rigidity, I, 31 : See also paralysis agitans tonicity, I, 39; IV, 240 Musculocutaneous paralysis, XII, 713 -spiral paralysis, XII, 716 Mutism, Deaf, XIII, 744 Hysterical, XIII, 747 Myasthenia gravis, X, 553 Tests for, I, 35 Myasthenic electrical reaction, VII, 401 paralysis, IV, 253; X, 553 Myatonia congenita, II, 105; X, 483 Mydriasis, I, 24; V, 339 Myelitis or Myelomalacia, II, 148, 167, 184 in anterior horns: See poliomyelitis cervical enlargement, X, 549-50; XIV, 835; XVII. ii4^a region, X, 513-4; XIV, 828 Compression, II, 121; X, 520; XIII, 795 Disseminated : See sclerosis in dorsal region, X, 517-8; XIV, 829 above lumbar enlargement. X. 513-4; XIII. 795 in lumbar enlargement, X, 485; XIII, 7»i; XIV. Xj 5 ; XVII, 1148a Multiple: See sclerosis Transverse, XV, 980 Myoclonia, XII, 697 Myoclonic nystagmus, XII, 691 Myoclonus, IV, 270; XI, 601-4 epileptieUi f Myokymia, IV. .■■/.; ; XI] Myopia and cycloplegia, V, 331 Myosis, 1 p; XII, 66i; XVII, iigij XXI, rati! 275 INDEX Myotonia, IV, 265 acquisita, XI, 613 atrophica, XI, 613 congenita, II, 106; IV, 265; XI, 613; XVII, 1155 intermittens, XI, 613 Myotonic electrical reaction, VII, 402 Myxedema, I, 20; XVII, 1163 Nageotte's and Babinski's bulbar syndrome, IX, 437; XXI, 1268 Nanosmia, XVII, 11 77 Narcotism, XV, 953; XVI, 1054 Nasal hemianopia, VI, 362; XIV, 815 reflex, V, 313 Tests for, I, 58 Negativismus, XVI, 1096-8 Nerves and muscles, Electrical reaction of, I, 72; VII, 395 Injury of, X, 489; XIV, 822; XVII, 1 146 motor cranial, Symptoms of lesions of, X, 492; XXII, 1303-7 Facial, XXII, 1331-6 Sixth, XXII, 1327 Third, XXII, 1323, 1326 root, anterior, Symptoms of lesions of, XXII, 1304 posterior, Symptoms of lesions of, XIV, 824; XXII, 1302 sensory cranial, Symptoms of lesions of, XXII, 1301 spinal, Symptoms of lesions of, X, 489; XIV, 822; XXII, 1303-S-7 Nervous system. Physiology of, p. 5 Neuralgia, I, 2; II, 114, 169; XV, 933, 937 Achillodynia, XV, 1001 Angina pectoris, XV, 983 Arthralgia, XV, 1000 Coccygodynia, XV, 972 Cervico-brachial, XV, 995 Crural, XV, 997 Erythromelalgia, XV, 1010; XVII, 1198 Gastralgia, XV, 986 Genital, XV, 990 Herpetic, XV, 940, 978 Hysterical, XV, 950, 971 Idiopathic, XV, 937 Infra-maxillary, XV, 945 Infra-orbital, XV, 944 Intercostal, XV, 977 Intestinal, XV, 988 Joint, XV, 1000 Lumbo-abdominal, XV, 989 Mastodynia, XV, 982 Meralgia paresthetica, XV, 999 Metatarsalgia, XV, 1003 Neurasthenic, XV, 959, 970 Neuralgia, Obturator, XV, 998 Occipital, XV, 948 Pelvic, XV, 990 Phrenic, XV, 985 Pseudo-angina pectoris, XV, 984 Sciatica, XV, 996 Spinal, XV, 971 Supra-orbital, XV, 943 Symptomatic, XV, 937, 952 Syphilitic, XV, 951 Tabetic, XV, 979, 987, 1004 Talalgia, XV, 1002 Tic douloureux, XI, 602; XV, 947 Trigeminal, XV, 942, 946 Neurasthenia, II, 113, 155, 161, 163, 178, 180; XV, 970; XVI, 1072 Perversion of vision in, XIV, 843, 845 Neurasthenic backache, XV, 970 headache, XV, 959 tremor, XII, 671, 674 vertigo, XV, 1033 Neuritic or spinal muscular atrophy, X, 496; XII, 696 Neuritis, II, 142, 144. 150, 165, 185 ; X, 489, 492; XIV, 822; XV, 933. 94i; XVII, 1 147. ^73 Alcoholic, X, 488 Anterior crural, XV, 997 Arsenical, II, 157; X, 488 Brachial plexus, X, 490 Compression, XV, 939 Crural, XV, 997 Diphtheritic, X, 488 Erythromelalgia, XV, 1010 Herpetic, XV, 940, 978 Infra-maxillary, XV, 945 -orbital, XV, 944 Leprous, II, 140; XVII, 1169 Multiple, II, 139. 160; X, 488; XII, 662; XIII, 787; XIV, 823; XV, 1008; XVII, 1 147; XXII, 1307 Occipital, XV, 948 Optic, X, 507-8; XIV, 897 tract, XIV, 859 Simple, XV, 941; XVII, 1147 Supra-orbital, XV, 943 Syphilitic, II, 174; XVIII, 1215 Trigeminal, XV, 942, 946 Neuroma, X, 491 ; XV, 938 Neurons, p. 5 Central, Location of lesions of the, XXII, 1293 Motor, IV, 251-2; IX, 461-2 Diseases of the, X, 469; XVII, 1 130 peripheral, Location of lesions of the, XXII, 1292 Sensory, IX, 463-4 Diseases of, XIV, 804 276 IXDEX Neuroses, II, 132 137 Occupation, II, 143; XI, 616 Traumatic, II, 156; XI, 616; XII, 674; XV, 1033; XVI, 1075 Neurotonic electrical reaction, VII, 403 Nicotine tremor, XII, 673 vertigo, XV, 1030 Nictitation, XII, 726 Nictitatio spastica, XII, 679, 690 Nocturnal epilepsy, XI, 575; XVI, 1058 Noguchi's test, I, 74; VIII, 419 Nuclei, cranial, Lesions of the, X, 493 motor. Symptoms of lesions of the, X, 493; XXII, 1304 facial, XXII, 1331 sixth, XXII, 1327 third, XXII, 1323, 1326 sensory, Symptoms of lesions of the, XXII, 1302 spinal motor, Symptoms of lesions of, the, XXII, 1304 sensory, Symptoms of lesions of, XXII, 1302 Nucleus caudatus and lenticularis, Localiz- ation in : See localization Numbness, VI, 375; XIV, 841 Nyctalopia, VI, 361 Nystagmus, I, 24; IV, 291; XXI, 1271-2 Cerebellar, I, 80 Diseases causing, XII, 640 Miner's, XII, 684 Myoclonic, XII, 691 Tests for, I, 30 Observation, Delusion of, XVI, 1113 Tests for power of, I, 5 Obstetrical hand, XI, 614 paralysis, IX, 454 Obturator neuralgia, XV, 998 paralysis, XII, 718 Occipital headache, XV, 948, 952 lobe, Symptoms of lesions of the, XIV, 850, 855; XXI, 1285; XXII, 1364-7 neuralgia or neuritis, XV, 948 Occupation in nervous diseases, I, 2; II, 90 neuroses, II, 143; XI, 616 Ocular ataxia, XII, 649 muscles, Insufficiency of the, XII, 692 Locationof paralysisof the, XXII, 1316 Paralysis of the, XII, 700; XIV, 816 Spasm of the, XI, 590; XIV, 816, 876 vertigo, XII, f>40 ; XV, 1020 Oesophageal spasm, XI, 617 Olfaction. Cortical center of, p. 8 Olfactory sensation, p. 7 Onotogenetic acts, p. 23 Ophthalmoplegia completa, X, 545 externa, X, 545; XI, 590 interna, X, 545; XI, 590 progressiva, X, 545 sympathica, XXI, 1268 Ophthalmoscopic examination, Diseases revealed by, XIV, 819 Ophthalmoscopy in examination of nervous patients, I, 76 Opisthotonus, IV, 265; XI, 590, 606 Opium poisoning; XVI, 1054 tremor, XII, 673 Oppenheim's reflex, I, 57; V, 306 Optic aphasia, III, 223; XIII, 773 atrophy, XIV, 865 Diseases causing, XIV, 898 Senile, XIV, 910 chiasm, p. 8 Symptoms of lesions of the, XIV, 851, 860, 892; XXII, 1319-20 fasciculus of Gratiolet, Lesion of the, XIV, 855-6; XXII, 1364 nerve. Lesion of the, XIV, 851, 862 Perversion of vision in diseases of the, XIV, 844 Symptoms of lesions of, XXII, 1318 neuritis, Diseases causing, X, 507-8; XIV, 897 followed by optic atrophy, XIV, 909 thalamus, Symptoms of lesions of the, XII, 655; XXI, 1275; XXII, 1386 Localization in the: See localiz- ation tract, p. 8 Symptoms of lesions of the. XIV, 858-9, 893; XXII, 1321 Orbit, Symptoms of lesions within the, XIV, 914; XXII, 1322 Organic diseases, II, 136, 138 hemiplegia, XIII, 794 reflex acts, I, 1 ; V, 300, 3J3-4 ; X. 4;--; XIV, 810 Orthotonus, IV, 265; XI, 590, 606 Oscedo, XII, 731 Osseous sense, Loss of, VI, 353 Tests for, I, 56 Osteitis deformans, XVII, 1182 Osteo-arthropathy, Hypertrophic pulmon- ary, XVII, 1184 Osteogenesis imperfecta, XVII, 1185 Osteomalacia. XVII, 1185 Osteopsathyrosis. XVII, 1185 Ovarian tenderness, IX, 425 Oxyakoia, XIV. B» 277 INDEX Pachymeningitis, X, 502; XI, 588; XVI, 1060 Headache in, XV, 961 hypertrophica cervicalis, X, 550 interna hemorrhagica, X, 502; XI, 588; XVI, 1060 Paget's disease, XVII, 1182 Pain, pp. 6, 7, 11; I, 1, 50; VI, 374 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, VI, 374 Diseases causing, XV, 935 Persistence of, I, 52 Radiating, VI, 374 Retardation of conduction of, I, 51; VI, 381 Palatine arch, High, XVI, 1076 Pallesthesia, Tests for, I, 56 Palsies, Local, IV, 259; XII, 636 Palpation in examination of nervous patients, I, c Pantophobia, III, 235 Paradoxical pupillary reflex, V, 338 reflex, V, 318 sensation, VI, 379 Parageusia, VI, 391 Paragraphia, III, 226; XIII, 777 Parakinesis, IV, 243 Parakusis, VI, 389; XIV, 821 Diseases causing, XIV, 821 Paralysis, I, 1, 21 ; IV, 244 Abducens, XIV, 870 Abductor, laryngeal, XIII, 756 Acute ascending, II, 168; X, 482 agitans, I, 20, 21; XI, 612; XII, 677; XIII, 766, 800 Alcoholic, X, 488 Arsenical, X, 488 Atonic, IV, 252; X, 472 Atrophic, IV, 252; X, 476-7. 547 Acute: See poliomyelitis Chronic: See chronic atrophic and bulbar Axillary, XII, 712 Bell's XII, 703 Brachial plexus, IX, 454-5; X, 490; XXII, 1306 Brown-Sequard's, IX, 442; X, 509; XIV, 838 Bulbar, IX, 434; X, 546; XII, 694; xiii, 761 ; xvii, 1150 Cauda equina, X, 487; XII, 721; XV, 1007; XXII, 1308 Paralysis, Cervical rib, X, 556 sympathetic, XVII, 1191 Choreic, X, 510 chronic, Bone atrophy in, XVII, 1 178 Muscular atrophy in, XVII, 1153 continuous, Diseases causing, X, 470 Crico-arytenoid XIII, 756 Crico-thyroid, XIII, 754 Crossed, IV, 256; X, 537-42; XV, 1017; XXI, 1268-70 Crural, XII, 717; XV, 997 of diaphragm, XII, 707 Diphtheritic, X, 488; XIII, 753-4 Diseases causing, IV, 244; X, 469; XIV, 804; XXII, 1290 Diver's, X, 521 Erb's, IX, 454; X, 490 External rectus, XIV, 870 Facial, XII, 703; XIII, 751; XIV, 928; XXII, 1317 Family periodic, X, 555 Flaccid, IX, 252 Diseases causing, X, 472 Tests for, I, 33, 39 Gluteal, XII, 719 Hypertonic, IV, 251 ; X, 473 Hypoglossal, XII, 706; XIII, 752 Hypotonic, IV, 252; X, 472 Hysterical, I, 21; X, 527; XIII, 747-8, 759, 793; XIV, 878; XVI, 1074 Infantile: See poliomyelitis and cere- bral palsy of childhood Inferior oblique, XIV, 875 rectus, XIV, 873 Internal rectus, XIV, 871 Intermittent, X, 471 Klumpke's, IX, 455; X, 490 Labio-glosso-pharyngeal, X, 546 Landry's, II, 168; X, 482 Laryngeal nerve ; Recurrent, XIII, 755 superior, XIII, 754 Lead, II, 158; X, 494; XIII, 788; XVI, 1050 Levator palati, XIII, 753 Local, IV, 259; XII, 636 Localization of lesions causing, XXII, 1290 Median, XII, 714 Motor, X, 469 Diseases causing, XXII, 1295-6, 1299, 1300 Tests for, I, 33-4 Motor oculi, XII, 700 Musculo-cutaneous, XII, 713 -spiral, XII, 716 Myasthenic, IV, 253 Obstetric, IX, 454 Obturator, XII, 718 Phrenic, XII, 707 278 INDEX Paralysis, Pneumogastric, XII, 704; XIII, 760 Posticus laryngeal, XIII, 756 Pseudo-bulbar, X, 553 Hypertrophic, X, 500; XVII, 1156 Pterygoid, XII, 702 Radial, XII, 716 rectus, External, XIV, 870 Inferior, XIV, 873 Internal, XIV, 871 Superior, XIV, 874 Recurrens, XIII, 755 Sciatic, XII, 720 sensory, Diseases causing, XXII, 1294- 6, 1298-1300 Serratus, XII, 709 Spastic, IV, 251 Diseases causing, X, 473 Spinal accessory, XII, 705 Sub-scapular, XII, 711 Superior laryngeal nerve, XIII, 754 oblique, XIV, 874 rectus, XIV, 872 Supinator longus, XII, 716 Supra-scapular, XII, 708 sympathetic ganglia, Diseases causing XVII, 1142 Tests for, I, 33-4 Thoracic, anterior and posterior, XII, 710 Long, XII, 709 Thyreo-ary-epiglottis, XIII, 754 Tibialis, XII, 720 Trigeminus (motor branch), XII, 702 Trochlearis, XV, 701 Ulnar, XII, 715 Paralytic dementia : See paresis and flaccid gait, XIII, 741 spastic gait, XIII, 742 vaso-motor reflex, V, 326 Paramyoclonus multiplex, XI, 603 Paramyotonia congenita, IV, 265 ; XI, 613 Paranoia, XVI, 11 13 Paranoiacs, p. i<) Paranoid form of insanity, XVI, 1099 Paraphasia, III, 225; XIII, 775 Paraplegia, I, 21; IV, 257; X, 480 Ataxic, X. 526; XII, 660; XIII, 796 Disease cutting, X, 480 dolorosa, XV, 975 Senile, X. 522; XIII, 791a Spastic, X, 525; Mil. 797 II 134, 177; XI, 570; Ml. 675; XIII. 763; MV. 895; XVI, 1 1.. i XVIII, iai6; XIX, 1390 Cerebri. Ipiliaj fluid in, VIII, 416, 419- 20; XIX, 1230 Paresis, Motor: Diseases causing, IV. 244; X, 469 Tests for, I, 34 Optic atrophy in, XIV, 912 Paresthesiae, p. 7 ; I, 1 ; VI, 375 Parietal lobes and lobule : See localization Parkinson's disease: See paralysis agitans Parosmia, VI, 390 Passive contracture, IV, 263 Tremor, IV, 289 Diseases causing. XII, 646-7 Pelvic neuralgia, XV, 952, 990 Pemphigus, XVII, 1168 Perceptions, p. 10 Percussion in examination of nervous patients, I, c Perforating ulcer, XVII, 1172 Periodic family paralysis, X, 555 Peripheral neurons, Disorders of. X. 472. 474; XIV, 804 Location of lesions of, XXII, 1292 motor neurons, IX, 462 Diseases of, X, 472. 474 sensory neurons, IX, 464 Diseases of, XIV, 804 Peroneal paralysis, XII, 720 Peroneal type of muscular atrophy, X. 496, Persecution, Delusion of, XVI, 11 13 Persistence of sensation, VI, 382 Tests for, I, 52 Personal factors causing nervous diseases, II, 82 Personality, p. 16 Double, III, 209; XVI. 1039 Diseases causing, XVI, 1039 Erroneous, III, 208 Pes calcaneus et valgus. XII. 720 Pes equino-varus, XII, 720 Petit mal (Le), XI, 575; XVI, 1058 Pharyngeal crises, IX, 433 Pharyngeal reflex, V, 315 Tests for, I, 58 Phobias, III, 235; XVI, 1072 Photophobia, VI, 371; XII, 683 Phrenic neuralgia, XV, 98s paralysis, XII, 707 spasm or cramp, XII, 731 Phylogcnctic ads, p. 23 Physical examination of patient. I Physiological in tro d uction, p. 5 Pianist's cramp. XI, 616 Picnic acid poisoning. Xl\ Pill rolling movement of fingers, XII, 677 Pineal gland Diaeaac of tin-. XXI 1270 Pituitary gland Diseaaei ■ if the. XXI. 1279 cunuchismu-. \ \ I Plantar reflex, V, 303 Tests for. I, 57 Pleasure, p. 1 1 TO INDEX Pleurosthotonus, IV, 265; XI, 590, 606 Plexuses, brachial and lumbar, Symptoms of lesions of, IX, 454-5; X, 490; XXII, 1306 Pneumogastric paralysis, XII, 704; XIII, -60 spasm or cramp, XII, 728 Points of Valleix, XV, 937, 942, 948, 977, 989, 995-7 Poisons, I, 1; II, 92, 164; X, 482; XIV, 842 Polioencephalitis inferior, Acute, X, 544 Chronic, X, 546; XII, 694; XVII, 1 150 superior, Acute, X, 543; XVI, 1064 Chronic, X, 545 Poliomyelitis, Acute anterior, II, 117, 167; X, 495; XIII, 789; XVII, 1 148; XIX, 1233 Cerebro-spinal fluid in, VIII, 416, 419; X, 495; XIX, 1233 Polyesthesia, VI, 378 Tests for, I, 54 Polyneuritis, II, 139, 160; X, 488; XII, 662; XIII, 787; XIV, 823; XV, 1008; XVII, 1147; XXII, 1307 Polyopia, VI, 384 Pons Varolii, Hemorrhage or softening in, X, 539 Localizing symptoms in : See local- ization Symptoms of lesions of, XIV, 883 ; XXII, 1328-31, 1353, 1383, 1388, 1398 Tumor of, X, 540 Ponto-cerebellar angle, Symptoms of lesions of, IX, 438; XXII, 1363 Porencephalic idiocy, XVI, 1086 Porencephaly, II, 116; X, 495, 501; XI, 577, 630; XIII, 798; XVI, 1048 Position sense, Tests for, I, 41 Post-epileptic insanity, XI, 575; XVI, 1058 ; 1 102 coma, XI, 575; XVI, 1058 febrile insanity, XXI, 1107a hemiplegic ataxia, XII, 655 athetosis, XI, 630-1 chorea, XI, 625 contracture, X, 504; XI, 577, 619 neuritic contracture, XI, 621 paraplegic, contracture, X, 480, 548-51; XI, 620 Posterior column or horn : See spinal cord, inferior cerebellar artery, Thrombosis of, XXI, 1268 Postero-lateral sclerosis, X, 526; XII, 660; XIII, 796 Posticus paralysis, XIII, 756 Pott's disease, I, 23; II, 121; X, 520 Practice. Effect of, p. 13 Preputial irritation, IV, 251 Pressure sensation, p. 6 Pressure sense, Loss of, VI, 351 Tests for, I, 49 Priapism, X, 512-5, 548-51; XI, 607; XIV, 828 Primary dementia, XVI, 1095 Procursive epilepsy, IX, 575 Prodromata of apoplexy, IX, 432 epilepsy, IX, 430 Progeria, XVI, 1093 Progressive bulbar paralysis, X, 546; XII, 694; XVII, 1 150 muscular atrophy: See amyotrophic lateral sclerosis ophthalmoplegia: See polioencepha- litis superior chronica Propulsion, XI, 612 ; XII, 677 ; XIII, 766, 800 Prosopalgia, XV, 942 Prosopoplegia, XII, 703 Protopathic sensibility, p. 6 Pseudo-angina pectoris, XV, 984 bulbar paralysis, X, 546, 553 clonus, IX, 425 coma, Diseases causing, XVI, 1038 hypertrophic paralysis, I, 21; X, 500; XVII, 1 156 nystagmus, XII, 640 paresis, XVI, 1101; XVIII, 1208 ptosis, XVII, 1191; XXI, 1268 tabes : See neuritis, multiple Psychasthenic XV, 970; XVI, 1072 Psychic blindness, p. 10; III, 232; XXI, 1285; XXII, 1344 localization of, XXI, 1285; XXII, 1344 deafness, p. 10; III, 222, 233; XIII, 772; XXI, 1284 equivalent of epilepsy, XI, 575 ; XVI, 1058 trauma, XVI, 1070 Psychosis, Korsakow's, X, 488; XVI, 1 100 Ptarmus, XII, 728 Pterygoid paralysis, XII, 702 Ptosis, I, 24 Pulmonary osteo-arthropathy, XVII, 1 184 Pupillary abnormalities, I, 24; XIV, 818 diseases causing, XIV, 818 opening, Double, XIV, 879 reflex acts, V, 302 Argyll-Robertson, V, 332; IX, 447; XIV, 891 Accommodation, V, 331 Tests for, I, 27 Consensual, I, 25 ; V, 330 Direct, I, 25 ; V, 330 Hemiopic, I, 26; V, 334; XIV, 890 Indirect, I, 25; V, 330 Light, I, 25; V, 330 Tests for, I, 25-7 280 INDEX Pupillary reflex acts, Paradoxical, V, 338 Pathology of, V, 302 Physiology of, V, 302 Westphal's, V, 337 Pupils, Immobile, 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 Quadrantic hemianopia, VI, 363 ; XIV, 815; XXI, 1285; XXII, 1343 Quincke's Disease, XVII, 1201 Quinine vertigo, XV, 1030 Quinquand's sign, IX, 453 Rabies, II, 171; XI, 607 Race in nervous diseases, II, 88 Radial paralysis, XII, 716 Raptus melancholicus, XVI, 1112 Raynaud's disease, XV, 1011; XVII, 1195 Reaction of completely degenerated muscle, VII, 404 of degeneration. Electrical, VII, 399, 400 Reading, Diseases causing disorders of, XIII, 735 Tests for, I, 9 Reasoning, p. 14 Recognition, p. 11 Rectal crises, IX, 433 reflex, V, 324 Recurrens paralysis, XIII, 755 Recurrent insanity, XVI, 1117 Red nucleus, Symptoms of lesions of, IX, 441; XXI, 1270; XXII, 1325 vision, XIV, 843 Referred pains, VI, 374; XV, 952 Reflex, Achilles, I, 62; V, 317 acts, p. 21 ; V. 296 abolition of, Diseases causing, X, 472; XIV, 810; XXI, 1292 Localization of diseases caus- ing, XXII, 1292 exaggeration of, Diseases causing, X, 472; XIV, 810; XXI, 1293 localization of lesions causing, XXII, 1293 Inhibition of, V, 296-7 Reinforcement of, I, 68 Anal, V, 307a Ankle, I, 60; V, 316-7 arc, p. 21 ; V, 296 Argyll-Robertson, V, 332 Physiology and pathology of, V, 332 Association, p .•_• Reflex, Babinski's, V, 304 Tests for, I, 57 Bechterew, I, 63; V, 320 Bladder, V, 323 Cilio-spinal, V, 335 Conjunctival, I, 58; V, 312 Corneal, I, 58; V, 312 Cremasteric, I, 57; V, 308 Cutaneous, V, 297 Tests for, I, 57 Deep, I, 60-6; V, 299 Dorsal foot, I, 63; V, 320 Elbow, I, 64; V, 321 Epigastric, I, 57; V, 310 Gluteal, V, 307 Tests for, I, 57 Gordon's, V, 305 Hemiopic, V, 334 Tests for, I, 26 Hyperemic, V, 326 Interscapular, I, 57; V, 311 Ischemic, V, 325 Jaw, I, 65; V, 322 Kernig's, I, 66; V, 319 Knee, I, 61 ; V, 318 Maxillary, I, 65 ; V, 322 Mendel-Bechterew, I, 63; V, 320 Mucous membrane, V, 298 Tests for, I, 58 Nasal, I, 58; V, 313 Oppenheim's, I, 57; V, 306 Organic, I, 1 ; V, 300, 323-4; X, 472; XIV, 810 Paradoxical, V, 318, 338 Pharyngeal, I, 58; V, 315 Plantar, V, 303 Tests for, I, 57 Pupillary, V, 302 to accommodation, V, 331 Tests for, I, 27 to light, V, 330 Tests for, I, 25 Rectal, V, 324 spasm, IV, 268; XI, 617; XII, 637 Superficial, I, 57; V, 297 Tendon, V, 299; X, 472-3; XIV, 810 Tests for, I, 60-6 Umbilical, I, 57; V, 309 Uvular, I, 58; V, 314 Vaso-motor, V, 301 Tests for, I, 59 Vesical, V, 323 Westphal's pupillary, V, 337 Wrist, I, 64; V, 321 Riil, Island of, Symptoms of lesions of, XXI, 1278 Reinforcement of reflexes, I, 68 Renal crises, IX. 4,(3 Respiration, Tests for. I, 45 281 INDEX Retardation of conduction of pain, VI, 38i Tests for, I, 51 Retching, V, 315 Retina, Perversion of vision in diseases of, XIV, 844 Retroactive amnesia, XIII, 769; XVI, 1100 Retrograde amnesia, XIII, 769 Retropulsion, XI, 612; XII, 677; XIII, 766, 800 Reverie, p. 14 Rheumatism of scalp, XV, 962 Rhythmical chorea, XI, 628 Rigidity, I, 31; IV, 266; XI, 590, 606, 612, 614; XII, 677; XIII, 766, 800 Rigors, XII, 680 Rinne's test, I, 15 Risus sardonicus, XI, 606 Romberg's symptom, I, 41 ; IX, 448 Rosenbach's sign, XVI, 1060-3 Rotatory epilepsy, XI, 575 Rubro-spinal tract, Symptoms of lesions of, IX, 441; XII, 676; XXII, 1325 Salaam cramp, XII, 690 Saltatory spasm, XI, 618 Sanity, Tests for, I, 4 Santonin poisoning, or jaundice, XIV, 842 Saturnine : See lead Scalp, Localized edema of, XVI, 1044 Rheumatism of, XV, 962 Scapulo-humeral type of muscular atrophy, X, 499; XVII, 1 151 Schuller's side gait, XIII, 793 Sciatic plexus, Spasm or cramp of, XII, 733 Sciatica, XII, 720; XV, 996 Scissors gait, X, 501 ; XIII, 795-9 Schmidt's syndrome, XII, 706 Sclerodactylia, VII, 1165 Scleroderma, I, 20; XVII, 1165 Sclerosis, Amyotrophic lateral, X, 547 ; XII, 695; XIII, 797; XVII, 1149 Combined or postero-lateral, X, 526; XII, 660; XIII, 796 Disseminated or Multiple, II, 149; X, 511; XI, 580; XII, 659, 668, 688; XIII, 756, 76s, 799; XIV, 913; XIII, 796 Optic atrophy in, XIV, 913 Vertigo in, XV, 1015 Lateral, X, 525; XIII, 797 Syphilitic, of Erb, X, 525 Postero-lateral, X, 526; XII, 660; XIII, 761 Scoliosis, I, 23 Scotoma, Glittering, XIV, 846 Homonymous, XIV, 863 Scurvy, X, 495 Seamstress' cramp, XI, 616 Secondary dementia, XVI, 1 103 deviation of sound eye, XIV, 816 Tests for, I, 29 Secretory disorders, Diseases causing, XVII, 1145 Semeiological charts. Introduction to, p. 5 Semi-coma, III, 206 Diseases causing, XVI, 1037 Senile chorea, XI, 624 dementia, p. 19; XVI, 1105 optic atrophy, XIV, 910 paraplegia, X, 522; XIII, 791a tremor, XII, 678 Senility, Fragility of bones in, XVII, 1185 Sensation, p. 9 Auditory, p. 8 Conduction of, p. 6 et seq. Cutaneous, p. 6 Difficulties in testing for, I, 47 Diminution of, I, 47 ; VI, 345 ; XIV, 80s Diseases causing, XIV, 805; XXII, 1 294- 1 300 Disorders of, VI, 344; XIV, 804 Dissociation of, VI, 365; XIV, 811 Diseases causing, XIV, 811 Double, I, 54; VI, 378 Exaggeration of, VI, 346; XIV, 806 Diseases causing, XIV, 806 General, p. 8 Gustatory, p. 7 Internal, pp. 8, 10 Light, p. 8 Localization of, I, 53; XXII, 1290 Muscle-joint, p. 6 Olfactory, p. 7 Painful, p. 6 Paradoxical, VI, 379 Persistence of, I, 52; VI, 382 Perversion of, VI, 347 Diseases causing, XIV, 814; XV, 930 Pressure, p. 6; I, 49 Summation of, p. 9 Tactile, p. 6 Temperature, p. 6; I, 55 Tests for, I, 48 Sensibility. Deep, p. 6 Epicritic, p. 6 Head's researches on, p. 6 Protopathic, p. 6 Sensory aphasia, pp. 10, 28; III, 222; XIII, 772; XXII, 1345, 1368 localization of, XXI, 1284; XXII, 134S, 1368 Septic insanity, XVI, 1107a Serous meningitis, XI, 594; XIX, 1239 cerebro-spinal fluid in, XIX, 1239 Serratus paralysis, XII, 709 282 INDEX Sex in nervous diseases, II, 87 Shaking palsy: See paralysis agitans Shivering, XII, 680 Shock, I, 1 Shoemakers' cramp, XI, 616 Side gait, Schiiller's, XIII, 793 Sight, p. 8 Cortical center of, p. 8 Loss of, VI, 357 Tests for, I, 12 Simple delusional insanity, XVI, mo Simple idiopathic muscular dystrophy, X, 498 Singer's cramp, XI, 616 Singultus, XII, 731 Sinus thrombosis, II, 182; XV, 964; XVI, 1044 headache in, XV, 964 Sixth cranial nerve or nucleus Symptoms of lesions of, XXII, 1327-8 Skill, Loss of. III. 230; IV, 249, 282 Skin, atrophy of, Diseases causing, XVII, 1132 eruptions, Diseases causing, XVII, "34 Glossy, XVII, 1 160 hypertrophy of, Diseases causing, XVII, 1 133 Trophic lesions of, XVII, 1123 ulcerations of, Diseases causing, XVII, "35 Skull in disease, I, 22; XVII, 1181: See also cranium Sleep, I, 18 Sleeping sickness, II, 141 Smell, p. 7 Diseases causing disorders of, XIV, 809 Loss of, VI, 356 Tests for, I, 16 Sneezing, V, 313; XII, 728 Snow blindness, VI, 360; XIV, 843 Softening, Brain stem, X, 535; XII, 656 Cerebral. X, 505-6; XIV, 832; XVI, 1062-3 in crus cerebri. X, 537 or hemorrhage in brain stem. X. 535 in medulla, X, 541 in pons, X, 539 Somnambulistic state. Ill, jno, 210 Somnolence, III, 207 Sopor, III, 207 Soul l in-, p, 17 blindncn, p 10 deafm i, p i" Spasm, p. j? ; I. 1 ; XI 570 abdonnn.il, XII. 732 in asthma. XI. t,\- athetoldi 1 '■ tag, XI. 57.1 • doneer**, Ml. 736 Spasm, Blepharospasm, XI, 601, 617: XII, 682. 726 Brachial, XII, 733 choreiform. Diseases causing, XI, 573 Clonic, IV. 246; XI, 571 Diseases causing, XI, 571 Cornet player's, XII, 726 or cramp, XI, 570 Diseases causing, XI, 570 Facial, XII, 726 Glosso-pharyngeal, XII, 727 Habit, IV, 274; XI, 626 Hypoglossal, XII, 729 Hysterical, XI, 618 Intercostal, XII, 732 Irregular, IV, 247 in Jacksonian epilepsy, IX, 431 ; XI, 587, 605 Laryngismus stridulus, XI, 617: XII, 728 Local, XII 637 Lumbar, XII, 733 Mobile, IV, 271 Occupation, XI, 616 Ocular muscle, XIV, 876 Oesophageal, XI, 617 Phrenic, XII, 731 Pianist's, XI, 616 Pneumogastric, XII, 728 Reflex, IV, 268; XI, 617; XII. 637; XVII. iiy 4 Salaam cramp or, XII, 690 Saltatory, XI, 618 Sciatic, XII, 733 Seamstress', XI, 616 Shoemakers', XI, 616 Spinal accessory, XII, 730 Telegraphers', XI, 616 Tests for, I, 32 Tic convulsive, XI, 601 douloureux, XI, 602 Tonic, IV, 245; XI, 57a Diseases causing. XI. 57 j Torticollis. XII, 730 Trigeminal, XII, 725 Typewriters', XI, 616 Urethral, XI, 617 Vesical, XI, 617 Violinists', XI, 616 Whooping cough, XI. 617 Writers', XI, 616 Spasmus glottidis, XI. oi;-; XII. ;vS mobilis, IV, .71 ni. in. ins. XII. 736 nutans. XI I. (71). 690 Spastic hemicrania, XV. 111 par.ih -■ . I • for, I. .1.1. .v) paraplegia, X. 5.7; XIII. 7.17 283 INDEX Special senses, Disturbances of, I, I Special symptoms and syndromes, IX Speech, p. 27 Disorders of, XIII, 735 Diseases causing, XIII, 735 Tests for defects* in, I, 8 Sphygmomanometer, I, 46 Spina bifida and occulta, I, 23; II, 102; X, 523 Spinal abscess, II, 152, 181 accessory paralysis, XII, 705 spasm or cramp, XII, 730 caries, II, 121 column in disease : See vertebral cord, Endarteritis and thrombosis of the, XVIII, 1211 Hemorrhage, softening or injury of, II, 146 localization : See localization Symptoms of lesions in, above lumbar enlargement, XIII, 795 anterior commissure, XXII, 1357, 1359 horn, XXII, 1304 nerve roots, XXII, 1304 Burdach's column, XXII, 1302 cauda equina, X, 487; XV, 1007; XXII, 1308 cervical enlargement, X, 548-9, 551; XIV, 835-6; XXII, 1310 region, X, 512-5; XIV, 828; XX, 1397 conus terminalis, XIV, 830a dorsal region, X, 516-9; XIV, 829; XXII, 1395 lateral column, XII, 654; XVIII, 1212; XXII, 1356, 1358, 1360, 1396 lumbar enlargement, X, 484-6; XIII, 791; XIV, 825-6; XXII, 1309 posterior column, XII, 654a; XIII, 785; XXII, 1347. 1350-1, 1396 horn, XXII, 1302 nerve roots, XXII, 1302 epilepsy, I, 60-1; IX, 443; X, 509, 520; XIV, 838 gumma, XVIII, 1210 hemiplegia, IX, 442; X, 509; XIV, 840; XV, 981 meninges, Hemorrhage in the, meningitis, Acute and chronic, XI, 608; XV, 974, 1005; XVIII, 1213-4 muscular atrophy, Peroneal type of, X, 496; XII, 696 progressive, X, 547 nerves : See nerves Spinal neuralgia, XV, 971 or neuritic muscular atrophy, X, 496; XII. 6o6 nuclei : See nuclei segment. Lesions of. XIV, 824 Localization in : See localization syphilis, XVIII, 1210-6 tenderness, IX, 425 tumor, II, 151 ; X, 486, 509, 515, 519, 5+2, 55i; XIV, 826, 836, 838; XV, 975. 981, 1006 Spondylitis deformans, XV, 976 Squint: See diplopia Stammering, XII, 729; XIII, 767-8 Static ataxia, IV, 281; IX, 448; XII, 642 Status epilepticus, XVI, 1058 Stellwag's sign, XVII, 1 192-3 Sternutatio spastica, XII, 728 Stereognosis, Tests for, I, 11 Stereotypy, XVI, 1096-8 Stocking form of anesthesia, VI, 345 ; IX, 425 Stokes-Adams disease, XI, 582; XVI, 1057 phenomenon, IX, 436 Strabismus convergens, XIV, 870 deorsum vergens, XIV, 872, 875 divergens, XIV, 871 sursum vergens, XIV, 873-4 Strumpel's tibialis phenomenon, IX, 445 Strychnine poisoning, V, 297; VI, 366; XI, 615 Stupor, III, 206; XVI, 1095 Stuttering, XII, 729; XIII, 767-8 Subscapular paralysis, XII, 711 Suggestion, Susceptibility to, in hysteria, IX, 425 Suicide in nervous diseases, I, 2 Sulfonal poisoning, X, 482 Sunstroke or heatstroke, XI, 589; XVI, 1068 Headache in, XV, 966 Superficial reflex acts, I, 57; V, 297 Superior laryngeal paralysis, XIII, 754 oblique muscle, Paralysis of, XIV, 874 rectus, Paralysis of, XIV, 872 Supra-orbital neuralgia or neuritis, XV, 943 Supra-scapular paralysis, XII, 708 Surface thermometers, I, 78 Sweating, Excessive, XVII, 1203 Sydenham's chorea, XI, 622 Symmetrical gangrene, XV, ion; XVII, "95 Sympathetic ganglionic system, Irritation of the, XVII, 1 143, 1 192 Diseases of the, XVII, 1128, 1143 causing disorders of the, XVII, 1121 Paralysis of the, XVII, 1142, 1191 284 INDEX Symptom-complexes and special symptoms, IX Symptomatic neuralgia, XV, 937, 952 epilepsy, mania, XVI, im melancholia, XVI, 11 12 Syncope, XVI, 1056 Local, XVII, 1 195 Syndromes and special symptoms, IX Synergy, I, 41 Syphilis, I, 2: See also cerebro-spinal syphilis Argyll-Robertson phenomenon in, XIV, 891 Cerebro-spinal, XVIII, 1214 of nervous system, XVIII, 1205 Cerebro-spinal fluid in, VIII, 410; XIX, 1232 Optic neuritis in, XIV, 903 Vertigo from, XV, 1025, 1032 Syphilitic endarteritis and thrombosis, II, 175; XVIII, 1207 Cerebral, XVIII, 1207 Spinal, XVIII, 1211 lateral sclerosis, XVIII, 1212 meningitis, II, 173; XV, 980a; XVIII, 1208-9 Cerebral, of base, XVIII, 1209 of convexity, XVIII, 1208 Cerebro-spinal, XVIII, 1214 Spinal, XVIII, 1213 nervous diseases, II, 94, 108; XVIII, 1205 neuralgia, XV, 951 neuritis, II, 174; XVIII, 1215 Syphilophobia, III, 235 Syringomyelia, X, 552; XII, 693; XIII, 798; XIV, 837-9; XV, 1009; XVII, 1150a, 1 170, 1 187; XXII, 1357, 1359 Tabes dorsalis, II, 133, 176; XII, 661; XIII. 756, 784; XIV, 827, 867, 894; XV, 979, 987. 1004; XVIII, 1217; XIX. 1331 Argyll-Robertson phenomenon in, XIV, 891 Arthropathy in, XVII, 1186 Cerebro-spinal fluid in, VIII, 416, 419- 20; XIX, 1231 Optic atrophy in, XIV, oil Perforating ulcer in, XVII, 1172 Vertigo in, XV, 1015 Tabetic crises. IX, 4.13; XV, 087 cuirass, VI, 345 Tachycardia, XII, 704, XVII, 1193 Tachcs cerebrates, V, 326; XI, 590 Tactile sensations, p. 6 Talalgia, XV, 1002 Tapir month, X. .107 Taste, p. 7 Diseases causing disorders of, XIV, 809 Tests for, I, 17 Teeth as cause of headache, XV, 952 Telegraphers' cramp* XI, 616 Temperature sense, p. 6 Loss of, VI, 350, 368 Tests for, I, 55 Temporal convolution, Lesions of the superior lobe, XXII, 1368 Lesions of, causing deafness, XIV, 923 Localization in : See localization Sensory aphasia in, XXII, 1368 Tendon reflex acts, V, 299 exaggerated, Diseases causing, X, 473; XIV, 810 diminished, Diseases causing, X, 472, XIV, 810 Tests for, I, 60-6 Tenesmus, XI, 617 Terminal dementia, XVI, 1103 Tetanus, II, 170; XI, 606 neonatorum, XI, 606 Tetany, II, 120; XI, 614 Tetartanopia, VI, 363; XIV, 815; XXI, 1285; XXII, 1343 Thermic anesthesia, VI, 350; XIV, 810 hyperalgesia, VI, 367 hyperesthesia. VI, 366 hypesthesia, VI, 350 Thermometry in examination of nervous patients, I, 78 Third cranial nucleus: See localization. nerve or nucleus, Symptoms of lesions of, XXII, 1323, 1326 Thomsen's disease, II, 106; IV, 265; XI, 613 Muscular hypertrophy in, XVII, "55 Thoracic paralysis, XII, 709-10 Thought, p. 14 Thrombosis, Cerebral, X, 506; XVI, 1063; XVI II, 1207 Posterior inferior cerebellar artery, XXI, 1268 Sinus, II. 183; XV, 064; XVI. 1044 Spinal. XVIII. 1211 Tibialis paralysis, XII, 7^0 Thymus gland) lesion of. IV, 853 Thyreo-ary-epiglottia paralysis, XIII. 754 Tic. articnlative, XIII. 768 convulsive, IV, 267. 270; XI. 601, 617; xii. ja6 douloureux. IV, -•< 7. XI. 60a; XII, 726; XV, 017 Tingling, VI. 373 Tinnitus annum, 1. 15; VI, 388 Tobacco vertigo, XV, 1030 INDEX Tonic spasm, IV, 245 Diseases causing, XI, 572 Tonicity, muscular, I, 39; IV, 240 Tonometer I, 46 Tooth-Charcot-Marie's type of muscular atrophy, X, 496; XII. 696 Topoanesthesia, VI, 376 Torticollis, XI, 601, 617; XII, 730 Toxic coma, XVI, 1067 convulsion, XI, 595-6 headache, XV, 963 insanity, XVI, 1107a nervous diseases, II, 92 tremor, XII, 673 vertigo, XV, 1029 Trance, XVI, 1069 Transverse myelitis, XV, 980 Transmission, nervous, pp. 5, 6 Traumatic nervous diseases, I, 1 ; II, 91, 135 hysteria, XVI, 1075 neuroses, II, 156; XI, 616; XII, 674; XVI, 1075 Vertigo from, XV, 1033 Tremor, pp. 26-7; II, 162; IV, 250; XII, 639; XXI, 1269-71 Alcoholic, XII, 673 Asthenic, XII, 671 Diseases causing, XII, 639 Essential, XII, 681 Hysterical, XII, 674 Intention, IV, 290; XII, 645 Diseases causing, XII, 645 Mercurial, II, 159; XII, 673 Neurasthenic, XII, 671, 674 Nicotine, XII, 673 Opium, XII, 673 Passive, IV, 289; XII, 646-7 Diseases causing, XII, 646-7 Senile, XII, 678 Tests for, I, 31 Toxic, XII, 673 Trigeminal or trifacial neuralgia or neu- ritis, XV, 942, 946 paralysis, XII, 702 spasm or cramp, XII, 725 Trional poisoning, X, 482 Trismus, IV, 265; XII, 725 Trochlearis paralysis, XII, 701 Trophic influences, p. 29 lesions, Diseases causing, XVII, 1120, 1 127 Tests for, I, 40 Trophoedcma, XVII, 1202 Trousseau's sign, IX, 450; XI, 614 Trypanosomiasis, XVI, 1052 Tuberculosis in nervous diseases, I, 2 Tuberculous meningitis, II, 118, 122, 188; XI, 593; XIX, 1228-9 Cerebro-spinal fluid in, XIX, 1228-9 Tumor, II, 187 of brain stem, X, 536 Cerebral, II, 151; X, 507, 536-42; XI, 578, 587; XIV, 833, 849. 855, 861, 892, 908; XV, 960; XVI, 1047 Cerebro-spinal fluid in, VIII, 411, 419; XIV, 1236 Coma in, XVI, 1047 Perversion of vision in, XIV, 849 Vertigo in, XV, 1032 of cervical enlargement of spinal cord, x, 551 ; xiv, 836 region of spinal cord, X, 515 crus cerebri, X, 538 dorsal region of spinal cord, X, 519 lumbar enlargement of spinal cord, X, 486; XIV, 826 medulla, X, 542 optic chiasm, XIV, 860-1 spinal, II, 151 ; X, 509 ; XIV, 826, 836, 838; XV, 975, 98l, 1006 Typewriters' cramp, XI, 616 Typhus fever, Cerebro-spinal fluid in, XIX, 1235 Ulcer, Perforating, XVII, 1 172 Ulcerations, Diseases causing cutaneous, XVII, 113S Ulnar paralysis, XII, 715 Umbilical reflex, V, 309 Tests for, I, 57 Unconsciousness, Tests for, I, 3 Understanding, Tests for defects in, I, 6 Unequal pupils, V, 341 Unverricht's family myoclonus epilepticus, XI, 604 Uremia, II, 189 Cerebro-spinal fluid in, XIX, 1241 Uremic amaurosis, XIV, 850 coma, XVI, 1066 convulsion, XI, 576, 581 headache, XV, 956 Urethral crises, IX, 433 Urethral spasmodic stricture, XI, 617 Urophobia, III, 235 Urticaria, XVII, 1167 Angio-neurotic, XVII, 1201 scripta, XV, 1167 Uvular reflex, V, 314 Tests for, I, 58 Vagus paralysis, XII, 704; XIII, 760 spasm, XII, 728 Valleix, Points of, XV, 937. 942, 948, 977, 989, 995-7 Vascular disorders. Diseases causing, XVII, 1 144 286 INDEX Vaso-motor disorders. Diseases causing, XVII, 1129 reflex acts, V, 301 reflexes, Tests for, I, 59 Venery in nervous diseases, I, 2 Vertebral column in disease, I, 23 Vertex headache, XV, 952 Vertige paralysant, XV, 1031 Vertigo, I, 1; VI, 392; XV, 932 Alcoholic, XV, 1030 Apoplectic, XV, 1026 Atheromatous, XV, 1025 Aural, XII. 650, 685; XIV, 918; XV, 1019 in brain stem lesions, XV, 1017 Cardiac, XV, 1024 in cerebellar diseases, XV, 1016 in cerebral anemia, XV, 1021, 1023 Coffee, XV, 1030 Diseases causing, XV, 932 Drug, XV, 1030 Epileptic, XV, 1027 Exhaustion, XV, 1022 in fourth ventricle lesions, XV, 1018 Gerlier's disease, XV, 1031 Hysterical, XV, 1033 Labyrinthine, XII, 650, 685; XIV, 918; XV, 1019 Laryngeal, IX, 433 Meniere's, XII, 650, 683; XIV, 918; XV, 1019 in meningitis, XV, 1032 Migrainous, XV, 1028 Morphine, XV, 1030 Neurasthenic, XV, 1033 Nicotine, XV, 1030 Ocular, XII, 649; XV, 1020 Paralysing, XV, 1031 Quinine, XV, 1030 Tabetic, XV, 1015 Tobacco, XV, 1030 Toxic, XV, 1029 in traumatic neuroses, XV, 1033 tumor, XV, 103? sclerosis, disseminated, XV, 1015 Syphilitic, XV, 1025, 1032 Vesical crises, IX, 433 reflex, V, 323 spasm, XI, 617 Vibration sense, Loss of, VI, 353 Tests for, I, 56 Violinist's cramp, XI, 616 Visceral crises, IX, 433 Wlion, Concentric limitation of field of, IX. 435; XIV. 866; XVI. 1074 disturbances of, Diseases causing, XIV. 807 Vision, Double, XIV, 816 Tests for, I, 12, 13. 14 field of, Tests for, I, 14 Green, XIV, 844 limitation of field of, Diseases causing, XIV, 815 localization of, Disturbances of, XXII, 1315 Loss of, XIV, 850-1 Perversion of, XIV, 814 Red, XIV, 843 Tests for, I, 12, 13, 14 Yellow, XIV, 842 Visual aphasia, III, 223; XIII, 773 axis, Displacement of, I, 28; XIV, 816 Vitiligo, XVII, 1 162 Vocal cords, Paralysis of, XIII, 753-60 Voltoni's disease, XV, 1019 Voluntary motion, p. 22 Disorders of, IV, 240 Vulvo- vaginal crises, IX, 433 Walk, Inability to, in disease, I, 21 Wassermann reaction, VIII, 420 Weakness, XIII, 790 Tremor from, XII, 671 Weber's law, p. 9 syndrome, IX, 440; XXI. 1270 tests, I, 15 Wernicke's polioencephalitis superior hemorrhagica acuta, XVI, 1064 scheme of aphasia, XIII, 739 Westphal-Edinger nucleus, V, 330 Westphal's pupillary reflex, V, 337 Whooping cough, XI, 617 Will, p. 24 Free, pp. 23-4 -power, p. 24 Word blindness. III, 228. 233; XIII, 77J deafness, III, 222; XIII, 772 Worry, I. 1 Wounds, II. 145 Wrist-drop. X. 404; XI. 584; XII, 716 reflex, Y, 331 Tests for, I. 64 Writer's cramp. XI, 616 Writing, Diseases causing disorders of, XIII. 735 Tests for defects in, I, 10 Wrv neck, XII. ;.!<> Xanthopsia, XIV, *i awning, XII, 731 yellow vision, \i V, 842 47 COLUMBIA UNIVERSITY LIBRARIES This book is due on the date indicated below, or at the expiration of a definite period after the date of borrowing, as provided by the library rules or by special arrangement with the Librarian in charge. DATE BORROWED DATE DUE DATE BORROWED DATE DUE ' C28I3-52) IOOM