^iiiliiiliaiiiliil .UC SOUTHERN REGIONAL LIBRARY FACILITY G 000 005 542 6 NERVOUS DISEASES. DANA. Fig. 210.— Composite Photograph SHowi.sf; I;i:i,ati(ivs ok Cranial Fissures and Convolutions (Alec Fra.ser). UIIFACi: 'JO THE TEXT-BOOK NERVOUS DISEASES BEING A COMPENDIUM ■OR '11 IK i;sK oi Students and Practitioners of Medicine Charles L.IDana, A.M., M.D. Professor of Nervous and Mental Diseases in the New York Post-Graduate Medical School, and in Dartmouth Medical College ; Visiting Physi- cian to Rellevue Hospital ; Neurologist to the Montefiore Home ; ex-President of the American Neu- rological Association, etc. WITH TWO HUNDRED AND TEN ILLUSTRATIONS. NEW YORK WILLIAM WOOD & COMPANY 1892 Copyrighted, 1S92, By WILLIAM WOOD & COMPANY ELECTROTYPED AND PRINTED BV THE PUBLISHERS' PRINTING COMPANY 120 & 122 EAST 14TH STREET NEW YORK WL loo Dll It PREFACE. It is the object of the author in this treatise to present the science of neurology in a concise yet as far as possible complete form. Each subject has been taken, all the available facts re- garding it ascertained, the writer's own experience collated, and with the data thus gathered the chapters have been written. The labor involved in such a task has been very great, but I am encouraged to believe that the result will be a useful one ; for the work does not compare or compete with the large treatises which are already in the field nor with the smaller introductory text-books, but I have tried to furnisli a book which will be suit- able for the student and practitioner and not valueless to the specialist. The extreme importance of a knowledge of anatomy has led me to pay especial attention to furnishing in a condensed form the most recent accessions to our knowledge of this subject. Starting with the facts that can be gained in ordinary anatomi- cal works, the student can, I believe, acquire a good idea of modern neuro-anatomy with the help of the anatomical chapters given here. In the classification of nervous diseases and the description of their pathology, I have tried to apply the modern knowledge of general pathology as modified by bacteriology. Tbis I have done conservatively, yet not less than in my opinion is absolutely demanded. A good deal of havoc will be wrought eventually in our conception of the nature of nervous diseases by the newer pathological doctrines; 1 have made as little change as was con- sonant with undeniable facts. The limits placed upon me have made it impossible to furnish a bibliography or to give due credit to every original investiga- IV PREFACE. tor. Full references to literature are to be found in the works of Hirt, Erb, SeeligmilUer, Ross, and Gowers. In many topics I have been much helped by valuable mono- graphs of my American colleagues. While a part of these are credited to their proper source in the text, I feel that I ought to refer here to some of the articles that have been of special service to me. They include monogra^Dhs on Spinal and Brain Tumors by Mills and Lloyd; on Cerebral Palsies of Children by B. Sachs; on Muscular Dystrophies and Writers' Cramp by G. W. Jacoby and by M, Lewis ; on Aj^hasia, Cerebral and Spinal Localizations by M. Allen Starr; on Cranial Temperatures and on ]S'euras- thenia by L. C. Gray; on Degenerative Neuritis by W. H. Les- zynsky ; on Poliomyelitis by Wharton Sinkler ; on Craniometry and Cranial Deformities by F. Peterson and by E. D. Fisher; on Angioneurotic (Edema by Jos. Collins ; on Brain Tumors by P. C. Knapp, and on Sclerosis of the Cord by J. J. Putnam. I am indebted to Tourette's recent treatise on hysteria, to that of Fer6 on epilepsy, and to the annual volumes of Bourneville on these subjects. The masterly lectures of Charcot and the treatises of Ross, Gowers, Hammond, Hamilton, and Putzel have necessarily been freely used. In the anatomical part I have used the works of Edinger, to whose courtesy I am joarticularly indebted, the treatise of Obersteiner, and many monographs by Golgi, Marchi, Cajal, His, Waldeyer, and others. My own work in teaching anatomy and pathology has enabled me to do more than present a compilation. I must finally express my thanks to my publisher, Mr. W. H. S. Wood, for his patience and helpful generosity in my efforts to make my work a production that would be creditable to Ameri- can neurology. To the Student. As a special text-book the present work will be used by two classes of readers, one consisting of those who simply consult it for reference in connection with their cases, the other composed of students who desire to ground themselves systematically in a knowledge of neurology. To this latter class I venture some advice as to the method they should pursue. Neurology is a PREFACE. V difficult branch of medicine to master, nor is there any royal road to it. Still, it can be made comparatively easy if its study is undertaken in a proper and systematic way. In using the present work, the student should first refresh his general knowledge of nervous anatomy as furnished in ordinary text-books. He should then go carefully over the anatomical descriptions here given of the general structure of the nervous system and of that of the nerves, spinal cord, and brain. A thor- ough knowledge of anatomy and physiology makes clinical neu- rology comparatively easy, and in fact reduces much of it simply to a matter of logical deduction. The student should next master the general facts of nervous pathology, symptomatology, and etiology, for he will find com- mon laws underlying apparently the most varying phenomena. Finally, he must begin to study the special diseases. The num- ber of these is very great ; in the present work I have described 17G. Many of these are rare, and it would be wrong for the student to burden his memory with the details about them. He need know only of their existence and general physiognomy. There are, however, according to my enumeration, about 65 ner- vous diseases which are either very common or extremely im- portant, and it is these that the student should master and make part of his working knowledge. Since the distribution and names of the common and rare diseases may be a useful guide, I append here a table and a list : Peripheral. Spinal Cord. Brain. Functional. Totals. Common and im- portant nervous diseases 31 56 27 12 16 10 11 65 Rare 111 87 40 28 21 176 The common or important peripheral nervous diseases are : General. — Neuritis, multiple neuritis, degeneration, neuralgia, parsesthesia (5). Cranial. — Anosmia, optic neuritis, optic atrophy, ptosis, ophthalmoplegia, abducens palsy, headache, migraine, trigem- inal neuralgia, facial spasm, facial palsy, tinnitus, vertigo, ageusia, wry-neck (16). VI PREFACE. Spinal Nerves.— Cervica] neuralj^ia, hiccough, brachial pal- sies, single and combined, brachial neuralgia, intercostal neu- ralgia, herpes zoster, lumbar neuralgia, sciatica, leg palsies (10). Spinal Cord. — Spina bifida, hemorrhage, pachymeningitis, leptomeningitis, poliomyelitis, transverse myelitis, acute and chronic, secondary degenerations, locomotor ataxia, the pro- gressive muscular atrophies, bulbar palsy, muscular dystrophies, spinal irritation (13). Brain. — Malformations, hyperaemia, pachymeningitis, lep- tomeningitis, simple, tubercular, and epidemic, abscess, hemor- rhage, embolism, thrombosis, children's palsies, syphilis (12). Functional. — Epilepsy, hysteria, the tics, chorea, tetanus, neurasthenia, spermatorrhoea, exophthalmic goitre, occupation neuroses, paralysis agitans (10). TABLE OF CONTENTS. PART I. General Description of the Nervous System, ITS Anatomy and Diseases. CHAPTER I. PAGE General Anatomy of the Nervous System, . 1 CHAPTER II. General Description of Diseases of the Ner- vous System. Method of studying, 15 General symptomatology and technical terms, ... 16 CHAPTER III. Diagnosis and Methods of Examination. Pliysiognomy and stigmata, 23 Disorders of motility, 27 Disorders of sensation 34 CHAPTER IV. The Causes and Pathology of Nervous Diseases. Etiology, '^^ Pathology, 43 CHAPTER V. Treatment, Hygiene, Prophylaxis. General hygiene, diet, exercise 47 Hydrotherapy, 49 Climate, 53 Electrotherapy, 53 vm CONTENTS. PART 11. Anatomy and Diseases of the Cerebro-Spinal Nerves. CHAPTER VI. General Diseases Affecti>'g THE Cerebro-Spixal Nerves. Hyperaeinia, anaemia, . Degeneration, Inflammation. Of single nerves, Multiple neuritis, . Functional disorders, . Neuralgia, Paraesthesic neurosis. Aero-neuroses. . Tumors of nerves, . CHAPTER VII. Axatomy of the Craxial Nerves, CHAPTER VIII. Diseases of the Cranial Nerves. Olfactory, Optic, Motor nerves of the eye Trigeminus, . Headaches, Neuralgias, Facial, Auditory, Tinnitus, . Vertigo, , Glosso-pharyngeal Vagus, Hypoglossal, . Spinal accessory, Wrv-neck, CH Diseases of Classification, Anatomy of cervical grouj), Diseases, . \PTER IX. the Spixal Nerves. PAGE 04 Go 68 69 TO 80 81 84 85 02 107 108 11 J 120 121 128 132 •38 138 141 146 ;47 147 48 118 153 153 155 CONTENTS. IX Anatomy of brachial group, Diseases, . Anatomy of dorsal group, Diseases, . Anatomy of lumbar group, Diseases, . Anatomy of sacral group. Diseases, . Tabular summaries, PAGE 158 160 1G8 168 170 170 173 173 178 PART III. AXATOMY A^D DISEASES OF THE SPIXAL CORD. CHAPTER X. AXATOMY AND PHYSIOLOGY OF THE SPIXAL CORD, . 180 Blood supply, 193 CHAPTER XL Diseases of the Spinal Cord. General etiology, symptoms, etc., .... . 196. Classification of diseases . 197 Malformations, .... ... . 197 Spinal hemorrhage, . 200 Caisson disease, . 202 Anaemia and hypersemia, . 203 Meningitis, . 205 CHAPTER XII. Inflammations of the Spinal Cord. Classification, Acute myelitis. Chronic myelitis, . Anterior poliomyelitis, Landry's paralysis, CHAPTER XIII. Degenerations of the Spinal Cord. Classification, Locomotor ataxia. Combined scleroses, Lateral sclerosis, . Secondary degenerations, 210 210 216 220 227 22a 231 248 257 259 CONTENTS. CHAPTER XIV. The Progressive MrscvLAR Atrophies and Dystrophies. PAGE Classification . 261 BuH)ar iiaralysis, . 262 DiH'hemie-Aran type . 263 l-t'y:tyi)o . 268 Auiyotrophic lateral sclerosis . 268 Musi-iilar dystrophies . 209 CHAPTER XV. Tumors and Caa'ities of the Spinal Cord- Functional Diseases. Tmiiors Cavities Syrinj^o-iiiyelia Functional diseases: Spinal irritation Spinal exhaustion 277 280 281 286 288 PART lY. AXATOMY AXD DISEASES OF THE BrAIN. CHAPTER XVI. Anatomy of the Brain, . . .290 Physiology and localization, 317 CHAPTER XVII. Diseases of the Brain. General symptoms, ,329 Malformations ;j33 Meningitis, ;]34 CHAPTER XVIII. Diseases of the Brain Substance. Hypera'mia and anji^nia . 344 Inflammation, abscess^, 340 The ajioplexies : Hi'morrhagc 353 Emiiolism, throndjosj.s 3(jo Children's palsies, 3(j.-) CONTENTS. XI CHAPTER XIX. Deqexeratioxs and Scleroses. Multiple sclerosis, CHAPTER XX. Tumors of the Braix— Syphilis. Tumors, Syphilis of the nervous system, PAGE 374 381 396 PART Y. Functional Nervous Diseases. CHAPTER XXI. Fuxctioxal Nervous Diseases. Classification, The degenerative neuroses: Epilepsy, CHAPTER XXII. The Degenerative 'Nbuhosbs— Continued. Hysteria, The spasmodic tics, Paramyoclonus, . Thomsen's disease, Paramyotonia, Akinesia algera, . CHAPTER XXIII. The Acquired Neuroses. Chorea, Tetanus, Tetany, CHAPTER XXIV. The Acquired Neuroses— Cow^mt^ecZ. Neurasthenia, Nervous women, . Sexual neuroses, . Traumatic neuroses. Exophthalmic goitre, 403 403 416 431 432 433 434 434 436 442 443 446 452 457 460 462 xu CONTENTS. CHAPTER XXV. The Acquired Neuroses— Cow^«mec?. The occupation neuroses PAGE 408 CHAPTER XXVI. The Late Degenerative Neuroses. Paralysis ajjritans, CHAPTER XXVII. Trophic axd Vasomotor Neuroses. Progressive facial hemiatrophy, .... Acromegaly Antrioneurotic cedema 478 484 485 487 CHAPTER XXVIII. The Disorders of Sleep. Insomnia, Niglitmare, Pavor nocturnus. Sleep drunkenness Somnambulism, HypnotisH), . Narcolepsy, . Catalepsy, Sleeping sickness, Sleep-accidents, 490 4913 495 495 49G 497 500 501 502 50a CHAPTER XXIX. Cranio-Cerebral Topography, General index. 505 509 Diseases of the Nervous System. CHAPTER I. GENERAL ANATOMY OF THE NERVOUS SYSTEM. I SHALL describe here, first, the fundamental constituents of the nervous system, and next tlie general facts with regard to their arrangements. The nervous system is derived from the epiblastic layer of the developing ovum, and its constituents are modifications of epi- thelial cells. These cells in the embryo are of tAvo kinds : neuro- blasts, which develop into nerve cells and fibres ; and spongio- blasts, which develop into a supporting structure called neuroglia (His). The nervous system is composed of — (a) Nervous tissue proper, viz. : nerve cells and nerve fibres, forming together nerve units or neurons; and neuroglia. (&) Non-nervous tissue, viz. . connective tissue, blood-vessels, lymphatics, and epithelium. These tissues are united together to form a central nervous system, consisting of the brain and spinal cord, and Bi, peripheral 7iervous system, consisting of nerve fibres, collections of nerve cells called nerve ganglia, and structures attached to the termi- nations of the nerves, called end-organs. The Nerve Cells or Gangliox Cells. — /S/ittpe, — They are of various shapes, differing in different parts of the nervous system. They are oftenest irregularly spheroidal, pyramidal, spindle or flask shaped. They give off processes or poles, and are classified usually in accordance with the number or arrange- ment of these. There are four kinds, viz. : (1) multipolar; (2) bi- polar; (3) unipolar; and (4) small nuclear. The multipolar cells are the common type. iSize.—They vary much in size. The larger cells are about ^i^ inch, the smallest 3 5V0 inch, in diameter. Structure.— The nerve cells are composed of a protoplasmic body, containing a nucleus and nucleolus. The protoplasm of the body appears granular, and sometimes striated or reticulated. 2 DISEASES OF THE NERVOUS SYSTEM. It often contains yellowish pigment. The nucleus is apparently reticulated. The processes are given off in various directions. In all developed nerve cells, one or more of the processes is pro- longed; it then receives a myelin sheath and becomes a nerve fibre. This is called tlie nervous or axis-cylinder process. All nerce fibres are sifnpli/ ])?'oIongations of nerve-cell processes and are really parts of nerve cells. The nervous process sends off Fig. 1.— Mi'LTipoLAR Cell of First or Motor Type OIarchi). showing nervous process and collaterals lateral fibres at right angles as it passes out, and farther on, when It becomes a nerve fibre, it sends off other processes; these are called collaterals (Golgi, Cajal). It ends finally in a brush- like fibrillation called the "end-brush.'' The other processes of nerve cells are called protoplasmic. They connect with the blood-vessels and lymi)hatic spaces and, perhaps, have a nutrient function. They do not, at any rate, connect with other nerve- cell proces.ses. Multipolar cells are said (Golgi, Yon Monakow) to be of two types— motor and .sensory. In the cells of the motor GENERAL ANATOMY OF THE NERVOUS SYSTEM. 3 type the nervous process passes directly into the axis cyhnder of a nerve. In the sensory type the process passes first into a jDlexus of fibres, out of which a single nerve finally emerges. Some multipolar and most bipolar cells give off two nervous processes ; one of these may be medullated, the other not. Many nerve cells of the peripheral ganglia have a membranous sheath or capsule continuous with the sheath of the nerve. The cells Fig 2 —Multipolar Cell of Second or Sensory Type (Marchi), showing nervous process and collaterals of the central nervous system have no capsules. The shape and structure of the various cells are best shown by the accompany- ing cuts. The location of the different kinds of cells is as fol- lows : Multipolar cells are found in the cortex cerebri, basal ganglia, and central gray of the spinal cord and medulla, and in some peripheral ganglia. Bipolar cells in Clark's column and intermediate gray of the cord, and in the posterior spinal ganglia. 4 DISEASES OF THE NERVOUS SYSTEM. Unipolar colls in the posterior spinal and sympathetic ganglia. Small nuclear cells and flask-shaped or Furkluje's celh are found in the cerebellum. Besides these, there are described, in the brain cortex, angular, granular, pyramidal, globose, and spindle cells. Thk nkrvk fibres of the nerve centres are found chiefly in the white tissue or white matter. In the periphery they form the nerve proper of gross anatomy. Tht' peripheral nerve is composed of bundles of nerve fibres // FiQ. 3. Fig. 4. Fig. 3.— Mi'LTipoLAR Cell, showing: processes, reticulum, nucleus and nucleolus. d, Pigment (Nissl). Fio. 4.— MrLTiPoiJVR (PuRKiNJE) Cell from Cerebellum, a, Body; 6, nervous proceiis; c, protoplusinic procfsses. called nerve fasciculi. It is surrounded by a connective-tissue sheath called the sheath of Henle, or epineurium. From this sheath, connective-ti.ssue fibres pass in and surround the fascic- uli. The sheath of the fa.sciculus is called the perineurium. From the i)erin('urium, strands of connective tissue run in among the ultimate nerve fibres, forming the endoneurium. Lymphatic spaces lined with endothelium exist in the layers of the peri- and endo-neural sheaths. In the nerve centres, the nerve fibres have no regular sheaths, but are supported by a connective-tissue and neuroglia framework. The nerve fibre is a long fine strand of GENERAL ANATOMY OF THE NERVOUS SYSTEM. tissue varying in diameter. It may be white or gray according to its structure. It is comiDOsed from within out of (1) an axis cyhnder, (2) a myeUn sheath, and (3) a neurilemma. (1) The axis cylinder is the essential iDart of the nerve. It is the prolonga- tion of one of the processes of a nerve cell and consists of proto- plasm. It is itself made up of fine fibrillse (primitive fibrillae) ^ ^'^^ms^ Fig. 5.— Umpolah Cell, a, Bodj", 6, capsule ; c, process. which run longitudinally. By means of reagents, a transverse striation can be seen also. (2) The myelin sheath, medullary sheath, or sheath of Schwann surrounds the axis cylinder. It is composed of a semi-fluid, fatty substance, which chemically con- sists of lecithin, neurin, and some cholesterin. It varies much in thickness, and this is the jorincipal cause of the different sizes of Fig. 6.— From a Transverse Section through the Sciatic Nerve, ep. Epi- neurium; p, perineurium; n, nerve fibres constituting a nerve bundle or fasciculus in cross-section; /, fat tissue surrounding the nei"ve (Klein). nerves. The myelin sheath is interrupted at regular intervals by constrictions called the " nodes of Ranvier." These constrictions involve the myelin sheath alone. The axis cylinder passes through and the outer sheath (neurilemma) passes over it. There is a lit tie granular matter at the point, called intercellular cement. The nerve fibres, if they divide, always do so at a node (Fig. 10). The 6 DISEASES OF THE NERVOUS SYSTEM. part between two nodes is called a nerve segment. In each sej2:- ment there is an oval nucleus imbedded in the myelin sheath. The nodes are about 1 mm. apart. The myelin sheath is probably de- veloped, like the axis cylinder, from the epiblast, and is closely related nutritionally to the axis cylinder, which it protects and isolates. Be- tween it and the axis cylinder Mauth- ner describes a membranous sheath (a X i s - c y 1 i n d e r sheath). Another sheath is said to be between it and the neurilemma (medullary sheath). By means of certain reagents, oblique lines (incisures of Schmidt) or a retic- ular appearance may be developed (network of Gfedvelst). These appear- ances are, perhaps, artificial. (3) The neurilemma or primitive sheath is a delicate homogeneous covering form- , ing the outermost sheath of the nerve. It is of connective-tissue origin. The sheath is absent in the fibres of the central nervous system and in some fibres of the periphery. Fio. 7.— Diagram showing the Different Parts of the Nerve. From without inward we liave : 1, Nerve with epineurium; 2, nerve fasciculus, with perineu- rium; .3, nerve fibre and endo- neurium: 4, neurilemma, myelin sheath, axis cylinder, primitive fibrilhe. Fio. ^- Fio. 9. Fio. H.— MEDVLLATKn Nerve Fibre, a, Axis cylinder; Fig. 10. I, nucleus ; m, medullary sheath; c, node of Itanvier. Fio. 9.— Medullatei) N'ervk Fibre, showing' axis cylinder, nuclei of medullary she^ith. nodes, and obliciuc incisures of S'chiiiidt. Fig. 10.— Medullated Nerve Fibre, showing mode of division. GENERAL ANATOMY OF THE NERVOUS SYSTEM. Variations in the Types of Fibres. — In accordance with the arrangement of the sheaths of the nerve fibres, several kinds are described. The principal types are the medullated and non- medullated. Medullated nerve fibres make up the bulk of the white matter of the brain and cord and cerebro-spinal nerves. They consist of a myelin sheath and axis cylinder, and may or may not have a neurilemma. Fibres with myelin sheath, but without a neurilemma, make up the white matter of the central nervous system. Non- medullated fibres, or fibres of Re- mak, occur principally in the sympathetic system, but tliey are also found in the cere- bro-spinal nerves. They are grayish and faintly striated, and consist of axis cylin- ders, wath a thin, homogeneous, nucleated sheath lying directly upon them. This sheath, however, cannot often be demon- strated (Schaefer). Naked axis cylinders are found in the peripheral terminations of nerv^es as well as in the brain and cord. Size. — The nerve fibres are of two kinds as regards size. The small fibres are about Y2^o7 inch in diameter, the large y^tu) inch. The small fibres are connected with smaller cells, and either run a shorter course or are distributed to the involuntary muscu- lar fibres of the blood-vessels and viscera. The nerve fibres of the central nervous system give off "collaterals," i.e., small medullated fibres branch out at right angles and pass off to make connections in an un- known way with nerve cells or other fibres. These fibres and those of the nerve roots have no neurilemma, but are surrounded with neuroglia tissue. They always end in a brush-like plexus of i^rimitive fibrils, which surrounds the nerve cells in a netw^ork. The peripheral nerve fibres, except the optic, have no neuroglia ; they terminate in fine fibrillIAORAM .SHOWING THE NeU- noM AND Mode of Connectio.n' between GENERAL ANATOMY OF THE NERVOUS SYSTEM. ceives arterial supply from many different branches, but al- ways from the same general source. The artery passes to the nerve sheath obliquely, then divides dichotomously and sends branches a long distance up and down on the sheath. It may pierce the sheath, however, first, and then divide, as above de- scribed. The dichotomous branches send off arterioles and capil- ATP VTP f$jp Fig. 14. Fig. 13.— Arteries of Sciatic Nerve (Quenu and Lejars). Fig. 14. — Venotts Supply of Posterior Tibial Nerve. N, Nerve ; ATP, VTF, vein; MJP, muscle; B, veins to muscle; C, B, veins to nerve (Que Lejars). artery; nu and laries, which form plexuses about the nerve fascicles. These are "the interfascicular arcades." The arteries subdivide in such a way as to prevent sudden impact of a large blood stream into the tissue of the nerve. In this respect the nerve circulation resem- 10 DISEASES OF THE NERVOUS SYSTEM. bles that of tlu' l.niiii and .'onl. The veins subdivide dichoto- inously, like the arteries. They freely aiKistoniose with the iims- cular veins, so that muscular action helps nerve circulation. The veins of the superlicial nerves connect with those of the deep nerves. The blood-vessels of the spinal cord and brain will be described later. Lymphatic vessels and spaces are found in the epi- neurium and perineurium. There are no distinct lym- phatics in the fasciculi, but lymph spaces probably exist. The General Arraxge- mext axd fuxctioxs of THE Nervous System. Having described the component parts, I shall noAV show the way in which these parts are arranged to form the nervous system. The nervous system, as already stated, consists of— I. A central part, com- posed of the brain and spinal cord. II. A peripheral part, composed of nerves, periph- eral ganglia, and end organs. I. The nerve centres are made up of gray and white matter, inclosed in mem- branes called the meninges. The gray matter consists chiefly of nerve cells ar- ranged in groups or masses. The white matter consists of nerve fibres arranged in tracts, strands, or columns. The gray matter is deposited in five principal places. The niyelon, or central gray matter of the spinal cord, and brain Jixis, extending to the tuber cinereum. The corpora dciitata, ohvary bodies, and red nuclei. The great basal ^'aiiglia, viz., corpora striata composed of lenticular and caudate nuclei, the optic thalami, and the corpora quadrigemina. lKltl-AS( ICI I.AK DlSTRIBl'TION OF AUTERIES (yuENU AND LeJAHS). GENERAL ANATOMY OF THE NERVOUS SYSTEM. 11 Cortex of cerebellum. Cortex of cerebrum. Besides these collections of gray matter, there are minor g:ang:lia in the pons, cerebellum, and cerebrum, which will be referred to later. The white matter connects these various ganglionic de- posits of gray matter with each other and the periphery. 11. The peripheral nervous system is usually described as con- sisting of a cerebro-spinal and a sympathetic part. Both por- tions, however, are alike made up of nerve fibres derived from and dependent on the brain and cord. Both are composed of nerve fibres connected in their course with peripheral ganglia and ter- minating in end organs. These peripheral ganglia consist of three sets- (1) The spinal ganglia, on the posterior roots; (2) the vertebral or sympathetic ganglia, connected chiefly with the an- terior roots; and (3) the peripheral ganglia proper, including vaso- motor and visceral ganglia, with which fibres from both roots are connected. The nerves which run between centre and end organs carry nerve impulses both ways. They are, therefore, divided into the afferent, centripetal or in-going, and efferent, centrifugal or out-going. The old division into motor and sensory nerves will not answer, for we know that there are many out-going nerves which are not motor. The afferent nerves are — 1, The sensory, including: Nerves of general \ Pain nerves or pathic nerves, heat and sensation. ( cold or thermic nerves. f i Contact, Nerves of Tactile, including ^ Pressure, • 1 ' Locality, special -; ^^ ^ , ^ i . I Jserves of muscular sense, sensation. I , , I jserves of special sense of smell, sight, L taste, hearing, and space. 2. Excito-reflex nerves. The efferent nerves are — 1. Motor nerves, going to voluntary or striped muscles, heart muscle, smooth muscle, including the vaso-constrictor and dila- tor nerves. 2. The secretory. These act upon glands. Impulses to the blood-vessels (vasomotor) generally accompany the secretory im- pulses. 3. The trophic. 4. The inhibitory. These nerves control muscular movements, secretion, perhaps also nutrition. We must admit that afferent and efferent impulses take place also between end organs and certain (so-called) sympathetic ganglia. In other words, the cerebro-spinal axis is not always the 12 DISEASES OF THE NERVOUS SYSTEM. only oentre. But these subordinate and peripheral centres are normally in connection Avith the spinal cord and may be influ- enced by it or by hiy;her parts. There are also Inttrrentral or commissural nerves, which connect different ivarts of the cerebro-spinal system together. Some of these con- -^ - nect symmetrical parts on each side together. They have co-ordinat- ing function. Others connect higher with lower centres. These latter ar^ made up of ascending and descend- ing fibres. Higher cen- \ \ ..--' tres send down impulses by the latter, which may stimulate or inhibit lower centres. In the peripheral nervous sys- tem w^e have also end organs. These are deli- cate and in some cases complex arrangements of the nervous and other tissue at the per- iphery of the nerves. Their object is to allows the" nerves to be irri- tated by special stimnH which Avould not other- Avise affect them, e.g., light or sound. Their object is also the proper utilization of efferent impulses upon other tis- sues. There are end organs, therefore, for both sensory or afferent and for efferent nerves. The end organs of the afferent nerves are — I. Eye. II. Ear. III. Taste-buds. IV. Cori)uscles in the Schneiderian membrane. V. Various tactile cells and bodies. VI. The space-sense organ. For the efferent nerves— I. Neuro-muscular corpuscles in the voluntary muscles. II. Local ganglia about the arteries. III. Ijocal ganglia in the glands. Trophic end organs are not known, in many cases the end organ is nothing but the ter- FiG. If).— Diagram showing the Arrangement OF THE NeI-RON-S OR NkRVE UNITS IN THE ARCHITEC- TURE OF THE Nervois Sy.stem. M. N^uroHS I. and //.. Motor neurons; S. Neiirons /., i/., III., sensory neurons; A. Jieuron, associative or commissural neuron. GENERAL ANATOMY OF THE NERVOUS SYSTEM. 13 minal fibres of the nerve. These lose both medullary sheath and neurilemma, leaving only the axillary cylinder. These cylinders split up into terminal plexuses, or else without splitting pass be- tween and around the cells which they are to affect. The nerves, centres, and end organs thus described may be arranged in mechanisms, each mechanism subserving a special function. These form the mechanisms of the nervous system proper, and those of the other organs of the body. They are as follows : f I. The psychical mechanism or mind. Cerebro- spinal. Visceral mechanisms. II. III. IV. V. r The secretory mechanism. ! The trophic mechanism. I The thermic mechanism. [ The vasomotor mechanism. The automatic mechanisms or the mechanism of inherited and acquired aptitudes. The sensory mechanism. The voluntary motor mechanism. The reflex mechanism. Compound neuro- mechanisms. Various of the simpler mechanisms are combined to form those more complex. Thus the automatic and psychical mechanisms embrace in their activity other mechanisms of lower grade. In the same way mechanisms are combined for the regulation of visceral functions. Thus we have — I. The cardiac neuro-mechanism— a combina- tion of automatic, reflex, inhibitory, motor, and sensory fibres and cells. II. The respiratory mechanism. III. The mechanisms of the digestive tract. IV. The renal mechanism. V. The thermal mechanism. VI. The skin and sweat mechanism. VII. The vesical mechanism. I VIII. The sexual mechanism. In the working of these mechanisms the nerve cell is the agent which generates the energy or nerve force, by w^hich impulses are started, controlled, and distributed. The larger the nucleus of the cell in proportion to its protoplasmic body, the more stable or less sensitive the cell. The larger the amount of protoplasm relatively to the nucleus, the more active the discharging power of the cell. The nerve fibres conduct impulses generated by nerves. These impulses travel at the rate of about 100 to 120 feet per second. It is less in visceral nerves (25 to 30 feet per second). There are no electrical currents in normal living nerves (Landois) except when 14 DISEASES OF THE NERVOUS SYSTEM. an iiiipulso travels along them. Then an electrical current travels along with the impulse. It is called the current of negative variation. The irritability or excitabiUty of a nerve is the power it has of responding to a stimulus. When a constant electrical current is passed along a nerve its irritability is modified. This modified condition is called electrotonus. When a nerve impulse passes up an afferent nerve and is then reflected along an afferent nerve, it is called a reffe.v action. The time required for this process is called the reaction time. This averages from 0.125 to 0.2 of a second. CuKMir^THY. — The nervous tissues are alkaline in reaction, but acidity rapidly increases on activity. Acidity is due to lactic acid. It is greater in the gray matter. The percentage of water is shown in the accompanying table, compiled from Hallibur- ton's figures: Percentage of Water. Portion of Nervous System. Fcetus. Age. 20-30. 70-94. Gray matter !- «« ; 83 69 &4 72 White matter 74 68 Nerves have the least water, gray matter of the brain most. Inorganic salts vary in amount, but average 0.5 per cent. PO4 is the largest single constituent of the brain ; potassium is next (Geoghegan). The nervous system is composed of — 1. Proteids, which make up about half the solids in gray mat- ter, one-fourth those in white matter, and one-third those in nerves. 2. Albuminoids, which are neuro-keratin and nuclein. 3. Phosi)horized constituents known as protogon and lecithin. 4. Nitrogenous bodies of unknown composition called, 5, cere- brins; (5, cholesterin, which is a monatomic alcohol abundant in white matter; 7, extractives; and 8, inorganic salts. The following tal)le shows the proportions of the different organic constituents of the brain (Petrowskv): Gray matter. . White matter. Proteids. Lecithiu. Cerebriu 5.5.37 24.7',' 17.24 9.90 0.53 9.55 Choles- terin and Fat. IS. 68 51.91 Other Organic Salts. Mattel-. C.7I 3.34 CHAPTER II. GENERAL DESCRIPTION OF DISEASES OF THE NERVOUS SYSTEM. The Method of Studyixg Nervous Diseases. In studying? the vital phenomena of the human body, we learn first its normal structure and functions. Then when diseased we note the new phenomena which have developed, the causes which produced them, and the anatomical changes lying back of them ; we group our facts and give the disease a name. Finally, we ap- ply the methods by which the disorder can be relieved and future attacks prevented. In fine, we investigate our subject just as we study any branch of natural history. Our study divides itself, therefore, into — Normal Anatomy and Physiology. Symptomatology, a study of the morbid phenomena. Etiology, a study of the causes. Pathology, under which we include a study of the morbid anatomy and physiology. Diagnosis, or the method of differentiating the different groups of diseases. Prognosis, a forecast of the future course of the malady. Treatment and Prophylaxis. Again, although nervous diseases exhibit many phases and have many different morbid changes behind them, there are certain features common to all. It simplifies their study, there- fore, to learn first what these general features are, just as a per- son can better survey and plot out a country in detail if he knows certain general facts about its boundaries and topography. Hence I shall first present in a general way an outline of the fundamental facts that touch more or Jess on all forms of nervous disease. My first chapters will be devoted to — General Anatomy and Physiology, Symptomatology, Etiology, Pathology. Diagnosis, Prognosis, and Treatment. The subject of anatouiy and physiology has already been briefly presented. We shall now take up IG DISEASES OF THE NERVOUS SYSTEM. Symptomatology. I shall bejjin ^vith a definition of certain terms that are fre- quently used. Neuroloyy is the science of nervous diseases. I\sychiatry is the science of mental diseases. A neurosis is a morbid nervous state. The term as sometimes used is restricted to morbid nervous states of functional charac- ter. This is not strictly correct, and in speaking of neuroses I give it the general meaning. A psychosis is a morbid mental state, and is nearly identical with an insanity, but has a broader meaning. The vital activities of the nervous system are shown in the phenomena of the mind, in muscular movements, sensation, con- trol of blood-vessels and secreting glands, in modifications of nutrition, of temperature, and visceral action. The disorder of any one of these functions produces a train of symptoms which receives a name in accordance with its character and class. Disorders of motion are called kinesio-uviiroses; those of sensa- tion, asthesio- neuroses. Correspondingly we have tro2:>ho-neii7'oses, thermo-neiwoses, vasomotor, secretory, and visceral neuroses. When mental or nervous functions are disordered, there is an increase, decrease, or perversion of the special function or activ- ity. Certain Greek prefixes are used to indicate this. They are : " hyper," which mean excess; " hypo," meaning diminution; "a" or " an," which means absence; and " para," which means perver- sion. So we have, for example, hypericsthesiaor excessive sensibility; anfesthesia, which means loss of sensation; parsesthesia, which means perversion of sensation. From the foregoing it will be seen that the classes or kinds of nervous symj)toms are — 1. Mental and cerebral, forming psychoses. 2. Motor and reflex, forming kinesio-neuroses. 3. Sensory, forming sesthesio-neuroses. 4. Trophic, forming tropho-neuroses. 5. Vasomotor and thermic, forming angio-neuroses and ther- mo- neuroses. G. Secretory, forming secretory neuroses. Combinations of these groups of symptoms may affect vari- ous organs. They are called mixed neuroses. A disorder may affect certain parts of the body, like the extremities— it is then called an acro-neurosis ; or certain functions hke the sexual or- gans— it is then called a sexual neurosis. GENERAL DESCRTPTION OF NERVOUS DISEASES. ir K /^ Psychoses Aesthesioneuroses Kinesloneu roses Secretory &iropiii& "\4so«mofor Fig. 17.— Diagram illustrating the Prin- ciple OF THE Classification of Ner- vous Symptoms. Combinations of mental and nervous symptoms form psycho- neuroses. A common and practical division of nervous symptoms is into the objective and subjective. Objective symptoms are those which can be observed and noted by the physician. Subjective symptoms are those which are felt by the patient and give no outward sign. Headache is a subjective symptom; atrophy is an objective one. The particular symptonjs which nervous diseases cause are best described and recorded under the several heads given above. 1. The mental symptoms include all those found in insanity, idiocy, and imbecil- ity, and will not be given in detail here. The common symptoms met with by the neurologist are mental irritability, de- pression, emotional excite- ment, morbid fears, voli- tional weakness and lack of self-control, persistent or fixed ideas, weakness of memory and of power of concentration, and a ten- dency to hypnotic and somnambulistic states. Certain symptoms due to disturbance of brain function are often called cv:/'e6r«/, as distinguished from mental. They are: vertigo, disorders of equilibrium, insomnia, somnolence, stupor, coma. Headache, head pressure, and similar feelings are also often de- scribed under the head of cerebral symptoms. 2. Motor Symptoms. — The symptoms of disordered motility m^y be classified as follows : A. Symptoms of exaggerated motility or hyperkineses. a, fibrillary; [ intentional, or tremor on motion, -] tremor in rest, ( constant, tonic, clonic, f co-ordinate or purposeful. Choreic movements, convulsive tic, athetosis. Muscular tension and rigidity, contracture, myotonia, myo- clonus. Forced movements, associated movements. 2 Tremor : &, tremor proper Convulsions or spasms : 18 DISEASES OF THE NERVOUS SYSTEM. Exaggerated reflexes, clonus, trepidation. B. Symptoms of lessened motility. Paralysis and ^ monoplegia, hemiplegia, paresis: '( paraplegia, diplegia. Loss of reflexes, superficial and deep. Tremor is the result of a disorder in the tonic innervation of muscles. Muscles are kept normally in a state of slight tension by rhythmical impulses from the brain cortex passing down at the rate of about twelve per second. When the rhythm and force of these normal impulses are interfered with we have tremor. The simplest form of tremor is one in which the normal tonic imi)ulses have an apparently exaggerated force. This causes a fine tremor of ten to fourteen vibrations per second. When there is an Interruption to some of the impulses we have a coarse tremor. Here the vibrations are five to eight per second. It is caused by a partial or complete dropping out of the alternate impulse. Various technical names are used in describing the tremors. We have the fine and coarse, as described. Intention tremor is one that occurs on voluntary movement, and is oj^posite in kind to the tremor of rest, which decreases or ceases on voluntary effort. The term paralytic tremor is used to express the tremor of ex- haustion, and the term spastic tremor that of exaggerated motil- ity, as in the tremor of a Chill. Ataxic ti-emor is one in which inco-ordinate movements are combined with the tremor. Fihrillary tremor is a fine twitching of the individual strands or parts of muscles, and occurs usually when they are wasting from lack of neuro-trophic influence. Convulsions consist of abnormal and exaggerated muscular contractions occurring in rapid succession. Convulsions may be clonic, i.e., the muscles rapidly and alternately contract and relax in an exaggerated and irregular way; or they may be tonic, i.e.., contracted steadily and continuously. When a tonic muscular contraction is painful it is called a cramp. Convulsions may be co-ordinate. In this case the patient moves the limbs and body in a more or less purposeful way. He throws himself about the bed, jumps, kicks, strikes, tears the clothes, etc. Convulsions are usually accompanied with loss of conscious- ness. CJioreic momnient.s sa-e sudden jerking, twitching movements of different groups of nmscles. The movements are purposeless and are not under control of the will. Convulsive r/c— When a choreic movement is confined to cer- tain groups of nmscles which work together for a common pur- l^ose, like those of the face, or eyes, or larynx, it is called a " tic." The movements in the " tics " are more definite in character and GENERAL DESCRIPTION OF NERVOUS DISEASES. 19 are limited to muscles physiologically grouped for a definite func- tion. Thus we have tics of the muscles of expression, or of respi- ration, or speech, or locomotion, Atheto.sf'.s.— This is a name given by Hammond to a peculiar form of movement characterized by slow, successive flexion, ex- tension, pronation, and supination of the fingers and hand and arm, or of analogous movement of the toes and feet. The motion rarely ceases in waking hours except for a short time. The con- tractions are forcible, steady, and even, and sometimes painful. The hand assumes characteristic positions. A contracture is a tonic muscular spasm of long duration, i.e.^ days or months. A contracture may be functional or organic ; and in order to test this, one must find whether it ceases during sleep or under an anaesthetic; if so, it is functional (see Hysteria). Fig. 18.— The Haxd in Athetosis (Strumpell). In forced movements the patient suddenly and involuntarily is thrown forward, sideways, or whirled about in various ways. Associated move?nents are those which occur involuntarily in a limb or muscle at rest when the corresponding limb or muscle is moved on the opposite side. Thus in hemiplegia the movement of the normal arm may ex- cite a movement in the one paralyzed. The patient is given a piece of chalk in each hand, and each hand is placed upon a blackboard lying on the table; attempts at drawing lines with the sound arm cause movements of a similar kind, but less per- fect, on the paralyzed side. Paralysis or akinesis is a loss of motor power. Monoplegia is a condition in which one limb is paralyzed ; hemiplegia one in which one-half the body is paralyzed ; and paraplegia one in which the tAvo lower limbs are affected. Sometimes a double hemiplegia or diplegia occurs. The term parpdysis is sometimes used to indicate loss of any kind of function, as jiaralysis of sensation or secretion. Paresis is a term used to indicate a partial paralysis. It is not 20 DISEASES OF THE NERVOUS SYSTEM. to be confoiindtHl with the term ^'eneral paresis, which is a form of insanity. 77/e RtJh.V(s and Th- reflex nerves; 4, motor nerve to muscle; 5, motor nerve cell. In neurology we have to do with four kinds of reflexes: The skin or superficial reflexes. The tendonous or deep reflexes. The visceral reflexes. Idiopathic muscle reflex. All these may be exaggerated, lessened, or absent. Further description of these reflexes will be given under the head of diag- nosis. 3. Sensor)/ symptom.s: Amrathesia is a loss of tactile sensibility. Analgesia, a loss of sensibility to pain. Thermo-anasthesia, a loss of sensibility to temperature. There may be loss of cold-sense or of heat-sense, or, as is usually the case, of both sen.ses. , The term aiuesthesia is often used with a general meaning to GENERAL DESCRIPTION OF NERVOUS DISEASES. 21 indicate loss of all forms of sensibility. Antesthesia in this sense is a symptom referred to the skin, bones, mucous membranes, special senses, or viscera. The muscles have two kinds of sensibility, a sensibility to pain and a special muscle sense. Anaesthesia of the pain sense of muscle is called loss of muscular sensibility or mus- cular analgesia. Anaesthesia of the special muscle sense is one of the factors in causing a symptom known as ataxia. Ataxia is a symptom due to loss of the special sensibility of the muscles, articular surfaces, and tendons. This special sense informs the individual of the degree and strength of muscular movements, and by it definite and co-ordinated movements are made possible. The weight of objects and position of the limbs are also determined by it. In static ataxia there is loss of the power to preserve perfectly the equilibrium when standing. It is due to the form of anaes- thesia just referred to. In locomotor or motor ataxia there is loss of power to co-ordi- nate the limbs properly in motion. In these conditions there is also usually a loss of power to appreciate weights or the position of the limbs. The term muscular ana'sthesia, however, is often used to indicate these latter symptoms. Cerebellar ataxia is a form of inco-ordination due to disease of the central organ of equilibration, viz., the cerebellum. The anaesthesias may be incomplete, and special technical terms are sometimes used to indicate such conditions, but they are not necessary. Hi/jyera'sthesia is an excessive sensibility to touch, contact, and other stimuli. Hyperalgesia is excessive sensibility to pain, and is nearly identical Avith tenderness. Dyscesthesia is an abnormal sensation such as a "thrill" or feeling of discomfort produced by ordinary tactile or painful im- pressions. Paresthesia is a term applied to all the morbid general sensa- tions except pain. The paraesthesias include such feelings as numbness, prickling, formication, flushing, burning, itching, cold- ness, tickling, feelings of weariness, exhaustion, various peculiar visceral sensations. Ordinarily in speaking of paraesthesiae, however, we refer to such feelings as numbness, prickling, and creeping. Delayed sensation is a symptom in which an appreciable time exists, usually one or more seconds, between the time of applying a stimulus and its appreciation in consciousness. Normally a tactile sensation can be felt and responded to in less than one- tenth of a second. Transferred or referred or reflex sensations are those in which 2'Z DISEASES OF THE NERVOUS SYSTEM. the irritation is iiuule at one point and felt at another. Thus an irritation in tlie stomach causes a pain felt in the forehead. The wliole class of so-called reflex pains are realh- transferred sensiitions, since in reality there is no reflex action in the process, as will be seen later. AUochiria is a peculiar form of transferred sensation in which an irritation applied on one side of the body- is referred to a corresponding? point on the opposite side. The special senses when disordered cause symptoms which are given special names. These will be described in connection with the si)ecial subjects. 4. Troph id Bisorde rs.— These are called tropho-neuroses. They consist, so far as relates to neurology, chiefly of hypertrophy and atrophy of nerves, muscle, cutaneous and mucous tissues, joint degenerations, and various skin erui^tions. The tropho-neuroses, if they afTect joints, are called arthro- pathies; if muscles, atrophies, hypertrophies, and dystrophies; or if with atrophy there is a great substitution of fat the condition is known as lipomatosis. When nerves are affected there results de- generation. Tropho-neuroses of the skin produce various symptoms such as herpes, pemphigus, and other eruptions, pigmentation, leuco- derma, alopecia, and bed-sores. 5. Vd.somotor and ^ecretorij St/mj^foms. — The nerves supplying the blood-vessels and secreting glands work together and are usually disordered together. Separate disturbances of the ves- sels and glands, however, occur. AuQW-neurosis is the term given to disorders of the vaso- motor centre and nerves. Angiospasm is a condition in which there is increase of vasomotor tone and spasmodic contraction of the muscular coats of the arteries. Angio-jyaralysis represents the oi)p<)site condition. Such disorders affecting the skin are shown by pallor and coolness or by flushing and heat. Angio- ataxia is a condition of variability and irregularity in the tonus of the blood-vessels. C). The secretory neuroses affect oftenest the skin. Hyperidrosis is an excessive sweating. Anidrosis is excessive dryness. Paridrosis is a perversion of secretion in which peculiar odors or colors are noted. Hainidrosis is the term, applied to bloody sweating. The secretions of the internal organs are controlled by ner- vous influences, but their si)ecial disturbances do not require de- scription here. CHAPTER III. DIAGNOSIS AND METHODS OF EXAMINATION. The diagnosis of a nervous disease may be simply a clinical one; that is to say, one may recognize it as belonging to a certain known and definite group of symptoms. Thus in recognizing the phenomena of epilepsy, one makes a clinical diagnosis. In other cases, and especially in all organic nervous diseases, the physician must make in addition a local, and then a jjathological diagnosis. That is, we must determine the seat and nature of the disease. A diagnosis is made by first getting all the obtainable facts in the i^atient's past history, then by learning from him all his sub- jective symptoms, and finally by making an examination accord- ing to the technical methods to be here described. In examining a patient, it is imperative that a careful search for diseases out- side the nervous system first be undertaken. Then the morbid nervous phenomena should be investigated. The physician should make it an invariable rule to make this examination in a certain fixed and systematic manner. The best method is first to get the family and personal history, and then to go over the mental, cere- bral, and special nervous functions serially in the way indicated under the description of general symptoms, thus : Examine — 1. Physiognomy, general condition of nutrition, complexion, physical defects (stigmata of degeneration), gait, station, i^os- ture, speech. 2. Mental and cerebral symptoms. 3. Motor and muscular symptoms, including muscular and joint atrophies, electrical reactions, and the reflexes. 4. Sensory symptoms, general and special. 5. Vasomotor, troiDhic and secretory. 6. Visceral centres. In investigating the family history, it is often necessary to make very direct and probing inquiries, for patients are, as a rule, inclined to forget or ignore the existence of nervous and mental disease among relatives. The existence of consumption and inebriety, epilepsy and syphilis, in the direct line are very important facts; so also are those concerning birth. The pa- tient should be questioned closely as to his previous diseases, especially syphilis; also as to his habits in relation to sexual indulgence, indulgence in alcohol, and smoking. In women, 24 DISEASES OF THE NEKVOUS SYSTEM. the tea ha])it should be inquired into. The patient may be al- lowed to tell his own story first. Proper queries should be put to supplement this, and tinally the patient should be asked to state those symptoms which to his mind are main and dominant. "NVe will now go over the above points in detail. I. The physiognomy, complexion, posture, and gait being noted, the physician looks next for evidences of imperfect physi- cal development. These are known as the stigmata or marks of degeneration. Marks of Degeneration.— (reweraZ.— Shortness of height, general feebleness of constitution. Left arm and leg larger than right, long fingers. Cranial. — Asymmetry of skull, and especially of frontal bone. Short parietal arc (noted in epilepsy), short "frontal arc (noted in petit mal). Peculiar type of skull, e.g., trigonal, seai:)hocephalic, plagio- cephaiic. High, prominent forehead in women. Heavy jaws, lemurian hyxDophesis, prognathism. Large frontal sinuses, small orbit. High and narrow palate (noted in idiots). Muscular. — Unequal innervation of facial muscles on the two sides. Depression above glabella due to over-action of corrugators (noted in epilepsy). Squints and astigmatism. Ottier J/rt;-A' 6*.— Deviation of nose; ears long, or prominent, or set too far back ; absence of helix, anti-helix, or lobule. Badly set and badly nourished teeth. Crown of scalp double or out of place. Small or deformed genitals, atrophic uterus. Physiological marks are those of deficient vital activity of the organic functions, such as weak heart, low arterial tension, un- stable vasomotor innervation causing coldness and flushing of extremities, weak digestion, constipation, amenorrhoea, sexual weakness or perversion. Psychical marks are those in general of feeble or erratic mental activity, unstable will, deficient moral sense, and lack of emotional control. "While many of the foregoing stigmata have no significance in themselves, yet a combination such as impresses the observer with its preponderance is of great importance, for neuroses or psychoses developed among this class have a much more unfavor- able prognosis. It is especially among neurasthenics, epileptics, severe forms of hysteria, and in the insanities that these signs are to be looked for and studied. Among normal men about two per cent have the stigmata of degeneration; among lunatics, crimi- nals, abortive types of paranoia and primary forms of neuras- thenia, the percentage is about thirty. The accompanying talile will be of help in making the in- vestigations relating to the cranium : DIAGNOSIS AND METHODS OF EXAMINATION. 25 Taken around glabel- la and maximal oc- cipital noint. Measured from b over through bregma to 6, or opposite ext. and. meatus. j Benedict and 1 Hu.schke. fi to a. a to t. From n to lowest point of chin. The empirical greatest heigiit, b p, is ob- tainetl by measuring the sides of the tri- angle in /3 t. •JvCq^si jopua 1 : s •SJBaX o? qwi ^?4 ; q48l Oi q;^ >> fe f- • 1? : : S § 1 : :- i I- 2 fe 1 : %^ '1 i ^ 1 ^ 1 ^' t1 O OO ■ M. 42.0 ''.5 5 700 to 1,000 28.0 F. 84.0 20.0 22.0 7.7 9.0 M. 84.0 20.0 885 to 4.50 22.0 9^0 Physiological Variation. 48.5 to 57.4 28.4 to 35 1,201 to 1,751 28' to 88 10.9 to 14.9 9.1 to 14.4 ](*..5tol9.0 13 to 1G.5 70.1 to 87 10.5 to 14.4 11.5 to 15 70.0 to 74.9 75.0 to 79.9 80.0 to 84.9 over loo to 1.50 t [B ^ ^ 50.0 81.0 1,800 31.0 12.0 11.9 7.1 17.2 14.0 83.8 12.3 s" 52.0 82.0 1,500 32.0 12.5 12.5 7.0 17.7 14.G 82.2 12.37 13.3 1. Greatest circumfer- ence 2. Binauriculararc. . . 3. Volume 4. Naso-occipital arc. . 5. Naso-bregmatic arc G. Bregmat. lamb, arc 7. Lamb, occipital arc 8. A n t e r o - posterior diameter 9. Greatest transverse (Uaiiifter 10. Cephalic or length- brtadlh index 12. Facial length 13. Empirical greatest llri^lit Dolichuccnhalv > X 5s 26 DISEASES OF THE NERVOUS SYSTEM. To nndorstanil it, it is necessary to descriV)e the skull land- marks, and to ^'ive V)rietly the classification and terms used by anthropolot^ists and alienists in describinjj the dimensions and shape of the skull. Dimensions and Shape of ^kvIjI^.— General Classification. —Anthropologists make a general classification of skulls into — Tl)e dolichocephalic, in' which the antero-posterior diameter is to the transverse as 100 is to 75 or less; the brachycephalic, in Mhicli the length is to the breadth as 100 is to 80 or more; the mesocephalic, in which the length is to the breadth as 100 is to 75 to bO. The physiological limits of variation in the ratio of length to breadth are from 100 to 70 to 100 to 90. The dimensions and shape of the skull vary with age, sex, individual, race, and with certain pathological conditions and artificial deformities. In general, liowever, the variations in the shape and size of the Fig. eo.— B,B, Broca's visual plane; vi.^.t, the triangle for ascertaining the empirical greatest height (Benedict). skulls of healthy adults of European and American races are fairly uniform. Variations Df^peuflent upon Age.— The proportions of the skull change most considerably in the first year, and continue to change up to the fourth year. After that, modifications are slight in amount and appear more slowly. Bv the end of the seventh year the skull has nearly reached 'its full size (see table), inore nearly in girls than in boys. The chief measurements dur- ing childhood are given in tlie table. The protuberances and ridges are less marked in children. The female shall is larger posteriorly, is broader, lower, with higher orbital diameter; often it has no'glabella, no super-glabel- lar depression, and is less well marked as to its ridges, promi- nences, and sutures. Variations as Beejards Race.—The length -breadth index and other cranial indices and the volume are the only racial differ- ences so far extensively studied. Even these are^too indefinite factors to be of any practical value. In general, we may say that DIAGNOSIS AND METHODS OF EXAMINATION. 27 the dolichooephalic or long:-lieaded are: the Eng:h.sh, Irish, Scan- dinavians, negroes, 73; Arabs, 74; Chinese, 70. The brachyceph- aUc or broad-headed are : the e-rernians, Si ; Russians, Turks, 81. The mesooephahc or medium-shaped heads are : the American In- dians, 79; Hollanders, Parisians, 71). The Variations Depeyident upon Artificial Deformities, Acci- dents, Fercersions of Growth and Development, and upon Dis- ease. — There ai-e certain more or less jjathological variations in the shape of the skull, due to a premature ossification of a suture, or arrest of development in a centre of ossification, or to a hyperplasia, or aplasia of a part of the skull or of its contents. When one part is shut off from its natural expansion, other parts, as a rule, undergo compensatory development. This principle underlies the pathology of cranial deformities. Those deformitiof! Avhieh it would be well to look for are — The triangular or trigonocephalic skull. The keel-shaped or scaphocephalic skull. The acrocephalic skull. The oxycephalic or steeple-shaped skull. The flat-headed skull. The plagioceph- alic or obliquely deformed skull. Variations in the Insane, Criminal, Epileptic, and other Psy- chopathic Classes Generally. — Minimal measurements of the fron- tal arc {n ji) are oftener found in insane and criminals. The pa- rietal arc is also said to be often shorter in the insane, defective, and delinquent classes and in epileptics. In these classes, how- ever, maximal excesses also often occur. There is, as yet, no acknowledged special variation or type which is, of itself, an indication of a peculiar mental trait or spe- cific pathological condition, although Lombrosoand his followers have tried to make out such. On the whole, it is found that pro- nounced deformities occur often in healthy j^ersons, while in psy- chopathic classes and cnminals there is a large proportion of slight variations generally minimal, i.e., below the mean meas- urements from the normal type. For all ordinary purpose's the only instruments needed in ex- amining the cranium are a tape, a strip of lead to use as a con- form ateur, and a pelvimeter. 2. IXYESTIGATIOX OF SYMPTOMS OF DISORDERED MOTILITY. — The recognition of gross disturbances such as hemiplegia and paraplegia is easy. To determine the exact extent of the paral- ysis, the patient must be made to move the limbs and contract the muscles in every possible way. The degree of paralysis in some groups of muscles can be measured by dynamometers. The ordinary hand dynamometer of Mathieu measures the degree of paralysis in the flexors. It should be graduated accu- rately in pounds or kilograms. I have devised an instrument by which the strength of the extensors of the hand and fingers can be tested. The average power of pressure on the Mathieu dynamometer is, for an adult, forty to fifty kilograms for the right hand, and three to five kilograms less for the left. A woman has about two-thirds of the power of a man. I have had constructed an apparatus by which the strength of the leg-push, i.e., of the extensors of the leg, and foot and the 28 DISEASES OF THE NERVOUS SYSTEM. extensors of the thifxh is tested. The anterior tibial and calf mus- cles can also be tested by means of an instrument called the pe- dometer devised by the late Dr. William R. Birdsall. A good idea of the degree of paralysis can be got by making the patient take the x^hysician's two hands with his own and squeeze each at the same time. A malingerer or hysteric will often in this way unconsciously press much harder than he is aware. The physician's own ingenuity will sug- gest various ways of testing the strength of the leg and thigh muscles, such as making the patient rise on one toe, climb upon a chair, push against an object M'itli his foot. etc. Fig. 21.— Leg Dynamometer. Fig. •2-2.— Foot Dynamometer. Tremor is tested by making the patient hold out the hands and arms at full length, spreading out the fingers at the same time. To determine whether the tremor increases on volitional movement, give the patient a full glass of water, let him hold it out for a moment, then bring it to his mouth slowly. If the ^v-^)(yi^,A^AM^AJy^^'^HVAAA^ iHHHHHmmmmHmimmmtmmmHmmmmHmmmmmmHmmmwmmmmmm, smovd Fig. 23. -Diagram of a Fine Vibratory Tremor. Ten of the divisions on the lower line equal a second. tremor increases with this movement it is called " intentional." As a general rule, the tremor of organic disease is increased by volitional movement, and ceases during rest of the extremity. Functional tremors are usually continuous. In some forms of tremor the hand and arm shake as a whole ; such tremors are called vi])r;itorv. In other forms the tremor in- DIAGNOSIS AND METHODS OF EXAMINATION. 29 volves only the fingers or hand. Such tremors are called oscilla- tory or segmental. The apparent vibration of a tremor may range from five or six to ten or twelve per second. To determine accurately whether the tremor is fine oy coarse special apparatus is needed; but one can with a little experience determine this fairly well by observa- tion alone. Or we can use a sphygmograph as shown by Dr. F. Peterson. This instrument is fixed firmly on the table, and the tremulous forefinger held lightly against the lever. Tremor that is hardly observable by the eye can be felt by placing one's hand against the extended fingers of the patient. Tremor of the tongue and lips and facial muscles must be carefully looked for. It is tested by making the patient close the eyes tightly and show the teeth or protrude the tongue. Tremor of the whole head due to the neck muscles must be distinguished from secondary shaking of the head due to a tremor of the trunk. Fihrillanj tremor, which involves only certain fibres of the muscle, is seen oftenest in the tongue and face muscles of the extremities. Choreic movements, tics, associated and forced movements, and the other forms of motor disturbance can be recognized by simple observation. Myoidema is a tonic spasm of a part of a muscle near its ten- donous attachment. It is produced by a sharp blow upon the muscle near its tendonous insertion. This causes the umscular fibres to bunch up into a small tumor for several seconds. Its pres- ence indicates rapid muscular wasting from exhausting disease. Idiopathic muscular spasm is a phenomenon of a similar na- ture. When the belly of a muscle is struck with a dull instru- ment, a welt of contracted muscle appears and lasts several sec- onds. It indicates an exaggerated muscular irritability. The Examination of the Reflexes.— These, as already stated, are of four kinds : (1) the su^^erficial or skin, (2) the deep or tendonous, (3) the visceral, and (4) the muscle reflexes. 1. A skin or superficial refiex is produced by scratching, tick- ling, pinching, or irritating the skin, with hot, cold, or chemical irritants. The result is a contraction of the muscles supplying the parts near the irritation. The skin reflexes which can be or- dinarily brought out are the plantar, cremasteric, epigastric, ab- dominal, erector spinal, interscapular, palmar, and certain cranial reflexes. The plantar reflex is produced by tickling or scratching the soles of the feet. This causes a quick, involuntary jerking up of the foot and leg. The cremasteric reflex is brought out by scratching the inner side of the thigh or the skin over Scarpa's triangle. It causes a drawing up of the testicle on the same side. 30 DISEASES OF THE NERVOUS SYSTEM. The abdominal reflex consists of a contraction of the abdomi- nal muscles, caused by irritating the side of the abdomen. The epigastric reflex consists of a contraction of the upper fibres of the rectus, caused by irritating the skin of the lower part and side of the thorax. The erector-spinccl reflex consists of a contraction of some of the fibres of the erector spincel, caused by irritating the skin along its outer edge. The scapular reflex consists of a contraction of some of the scapular muscles, caused byirritating the skin over them. The palmar reflex is produced by irritating the palms of the hands. The cranial reflexes are the lid reflex, caused by irritations of the conjunctiva or of the retina: the pupillary-skin reflex, which consists of a dilatation of the pupil caused by scratching the skin of the cheek or chin. The levels of the spinal cord through which the impulse travels are indicated in the accompanying table : Table showi:s'g the Nerves axd Spixal Cord Levels Brought ixto Reflexes. Play ix the Different Superficial Spinal Nerve. 1 2 3 Superficial Reflex. 61 8capul; Spinal Nerve. 81 I 01 I . 10 I ^ V i"l 12 I J n I I 4) 5* J 1 Superficial Reflex. Abdominal Cremasteric Kfiee jerk ^ Gluteal r Ankle clonus 41 5 ^ Epigastric E Plantar DIAGNOSIS AND METHODS OF EXAMINATION. 31 The superficial reflexes that can ordinarily be brought out in healthy persons are the plantar, cremasteric, epigastric, and the cranial reflexes. The palmar reflex is rarely i^resent in healthy people except during sleep, and in children. The superficial re- flexes depend upon the integrity of the reflex spinal arc, and to a less extent upon the degree of cerebral inhibition. When present, they show that the spinal cord at the level through which the impulses travel is healthy. When absent, they do not necessarily Indicate much of anything. For they vary in amount in differ- ent persons and at different ages. In cerebral hemiplegia during and for a time after the acute attack, they are generally lessened or absent on the affected side. Later they may be exaggerated. The deep reflexes are sometimes called tendon reflexes. They are brought out by striking a stretched tendon or muscle or even by tapping a bone or striking the muscular fascia. The deep re- flex in these cases is probably a true spinal reflex, though some assert that it is due to the direct effect of the concussion or sud- den stretching upon the muscle itself (Gowers), which is m a condition of slight tonus. Either view involves the integrity of a reflex arc. The deep reflexes are — The patella-tendon reflex or knee jerk. The ankle reflex or ankle clonus. The wrist reflex. The triceps-tendon reflex or el- bow jerk. The jaw reflex or chin jerk. The light (or pupillary) and accommodation (or ciliary) reflexes. The x>(^teUa reflex or knee jerk consists of a sudden contraction of the quadruceps femoris, vastus internus, and subcrureus caused by striking the patella tendon when the leg hangs loosely at right angles with the thigh. This reflex may also often be pro- duced by striking the lower part of the muscle itself. The ac- tivity of this reflex is increased if, at the same time that the blow is struck, a voluntary contraction of some other muscles is made by the patient. Usually the patient is told to pull on his clasped fingers, or tightly shut the hands. This process is called the re- enforcement of the knee jerk (see Fig. 24). The knee jerk is present practically in all healthy persons ex- cept the aged. Its absence is always of significance. The nerve roots involved are those, in man, of the fourth lumbar pair. The peripheral nerve is the anterior crural. The most essential mus- cle is the vastus internus (Sherrington). Ankle clonus is caused by having the seated patient extend the limb and hold it rather firmly in a semi-flexed condition. The physician takes the foot by the toe and heel and quickly flexes the foot on the leg. He thus suddenly stretches the calf muscles, and they undergo rhythmical contraction. This phe- nomenon does not occur in healthy people. An ankle-tendon re- DISEASES OF THE NERVOUS SYSTEM. flex, however, is brought out in normal conditions Ijy striking the Achilles tendon when the foot is held slightly flexed by the phy- sician. if m f^"^ - r FiQ. 24.— Getting the Knee Jerk by Re-enforcement. DIAGNOSIS AND METHODS OF EXAMINATION. 33 The " paradoxical contraction " is a name given to the tonic contraction of the anterior tibial muscles caused by the physi- cian's suddenly flexing the foot on the leg, thus shortening these muscles. This is a rare phenomenon and never found in health. The wrist reflex is brought out by striking the wrist tendons while the forearm is supinated and held limply on the hand of the physician. The triceps reflex or elbow jerk is brought out by striking the triceps tendon while the arm is sup- FiG. 35.— Getting the Elbow Jerk. ported and the forearm allowed to hang down loosely at right angles to the arm. These reflexes occur in normal individuals. The jaw reflex or jaw jerk is brought out by having the patient open the mouth and leave the jaw relaxed. A flat instrument like a paper cutter is then laid on the teeth of the lower jaw, and if this is struck smartly the elevators of the jaw contract. The light reflex is caused by throwing a bright light into the eye, and the ciliary or acconnnodation reflex by making the pa- tient look at a distant and then at a near object. The pupil 3 34 DISEASES OF THE NERVOUS SYSTEM. normally dilates in the former case and contracts in the latter. When the light reflex is lost while the accommodation reflex re- mains, the condition is called the Argyll- Robertson pupil. The deep reflexes which do not occur in healthy individuals are: ankle clonus, paradoxical contraction, jaw clonus, and usually the wrist reflex. The deep reflexes may be brought out by simply striking the tendon with the side of the hand or the back of a book. For careful work, a percussion hammer is very useful. Fig. 26.— Getting Ankle Clonl's. The Electrical Conditions in Bisturhances of Motility. — These cannot be understood without some description of the methods of using electricity, and hence the technique of electrical exami- nations for purposes of diagnosis will be described under the head of Treatment. 3. EXAMIXATIOX OF THE DISORDERS OF SeNSATIOX.— It should be remembered that sensations are of two kinds, general or common and special. A common sensation is one which is referred to the body. A special sensation is one which is referred to the external world, and in particular to the object which causes the stimulus. The I^ain from a knife cut is referred to the body, and is a common sensation. The coldness felt when a knife blade is laid on the skin is referred to the knife, and is a special sensation. The sensory functions to be examined are : The cutaneous. The muscular, articular, and tendonous. The visual, auditory, olfactory, gustatory, and space senses. Visceral and general bodily sensations. The cutaneous sensations are : (1) The tactile sense, which in- DIAGNOSIS AND METHODS OF EXAMINATION. 35 eludes pressure and contact ; (2) the temperature sense, which in- cludes the heat sense and cold sense ; (3) the pain sense. The first two are special senses, the last is a general sense.* To test the tactile sense, blindfold the patient and use the sesthesiometer. This is an instrument with two rather blunt points, which can be separated or approximated. A hairpin or two ordinary pins can be used in its stead. Its use depends upon the fact that the power to appreciate the contact of two points on the skin gradually approximated varies with the tactile sensi- bility of the patient. The tongue, finger tips, and lips are the most sensitive points. The back, arms, and thighs the least sen- sitive. The following table shows the average distance at which two points are appreciated as such by an intelligent adult : Tip of tongue, . 1 mm. (-V i"-) Tip of toes, cheeks, Tip of fingers, . 2 " eyelids, . 12 mm. Lips, . 3 " TemiDle, 13 " Dorsal surface of Back of hands, . 30 " fingers, . . . 6 " Neck, .... 35 " Tip of nose, . . 8 " Forearm, leg, back of Forearm, . . . 9 " foot, 40 •' Back, . . . 60-80 " Arm and thigh, . 80 " The figures vary somewhat with the thickness or softness of the skin and with the dulness or keenness of the nervous organi- zation. If the distances are double those given above, it may be considered in most cases abnormal. The tactile sense may also be tested by the writing method (Rumpf). Figures or letters are written upon the skin with a hard-pointed instrument, and the patient asked to tell them. The figures drawn are made larger or smaller in accordance with the decrease or increase of sensibility. The following table shows the different sizes as appreciated on the normal skin : Fingertips, 0.5 cm. (| in.) high Palm, 1 Neck 1 Cheeks, 1 Forehead, 1 Arm, forearm, and back of hand, . 1.5 to 3.5 Scapula 1,5 to 3.5 Calf and sole 3 ' (I to I in.) ' (H in.) * Psychologists deny the independence of the pain sense and assert that it is only a quality or modification of other senses. 36 DISEASES OF THE NERVOUS SYSTEM. The sense of contact which is a form of tactile sense is tested by drawing one's finger or a bit of cotton Ughtly over the skin. The sense of locahty or power to localize a point on the skin that has been touched varies with the tactile sense and with the muscular sense. It is tested by placing the finger lightly on a given spot and telling the patient with closed eyes to place his finger on the part touched. He should come with- in 5 cm. of it. In slight degrees of anaes- thesia dependent upon disease of the sensori- motor areas of the cortex of the brain, this is an important test. Further tests may be made by moving points along the skin and asking the patient to indicate the direction of the motion ; or by laying various shaped objects on the skin and asking the patient to tell their shape or position. Still another method is recommended by Oppenheim. It consists in testing at the same time with the festhesiometer symmetrically situated parts of the skin on the two sides of the body. To test the pressure sense, use, if desired, the bar gesthesiometer. A more convenient way is to have the patient rest the hands on a table and then try and determine the weight of different objects. The lightest weight that can be appreciated on the hands or face is one of about 0.03 gram (gr. I). Differences of light weights of 1 and 5 grams and of 25 and 30 grams are about all that can be ordinarily appreciated by the skin. Much smaller differences, of 0.5 to 2 grams, can be detected if great care is used. Weighted rubber balls may be used in the foregoing test. I prefer to use differently weighted metal bodies, held by a wire. Pressure sense is acute on the forearm and abdomen, where locality sense is feeble; also on the brow, temples, and back of the hand. Most of the above tests are not ordinarily needed. With two pins, using the heads, the presence and de- gree of anaesthesia can be detected and approximately measured. The temperature sense is tested by test-tubes filled with hot and cold water, or by using hot and cold spoons, or roughly by breathing and then blowing on the part. A thermo-^sthesiome- ter may be used. This has a round, flat surface 1 cm. in diame- FiG. 27.— Combination ^STHESIOMETER. DIAGNOSIS AND METHODS OF EXAMINATION 37 ter, and contains in its terminals thermometres by which the de- gree and differences in temperature may be noted (Fig. 27). A small heated or chilled surface is appreciated much less easily than a large one. The indifferent range where objects are felt to be neither warm nor cold is from 27" to 30° C. (80. 6"" to 80" F.). Fine differences (0,2° to 1.5° C.) are appreciated above the in- different range. Lower down in the scale, differences from V to 1.8° C. (2° to 8° F.) are appreciable. It may be considered a mor- bid symptom if temperatures of 60° to 65" F. are not felt as cold, or temperatures of 86° to 95° F. are not felt as warm ; also if be- tween the ranges of 1° C. (32° F.) and 40° C. (104° F.) differences of 2° C. are not appreciated. A painful degree of sensitiveness to heat or cold sometimes exists. These conditions are called hyper-thermalgesia and hyper- cyalgesia (Skinner, Starr). When the heat or cold is intense, a sensation of pain is felt. Cold-iDain is produced more easily in some places, such as the elbow, than others, as, for example, the finger tips. Cold-pain is produced by temperatures of from +2.8° C. to —11.4° C. Heat-pain is i3roduced by temperatures of from 36.3° C. to 52.6° C. The pain sense is tested by pricking the skin with needles or the sharp points of an sesthesiometer. The faradic battery with metal points or a wire brush may also be used. Instruments for pinching the skin and measuring the sensibility by the strength of the pinch have been devised. The power of localizing pain is lessened in proportion to the analgesia. The muscular' sensihility, i.e., the general or pain sensation of muscles, is tested by passing the faradic current through the part. Pain and temperature sense are usually affected together. Belayed Sensation.— The time taken for a sensation to be felt and produce a voluntary response is, for — A touch on the hand, about . . .0.12 second " " foot, " ... 0.17 " Hearing, 0.13 " Sight, 0.16 " Taste, 0.15 " The tactile sense, as well as the other special and the general sensations, may show a delay in conduction. The tactile sense especially should be tested on this point. The delay may amount to several seconds. Double Sensations or Polya;st7iesia.— When the touch of one point is felt as two or more, the symptom is known as polyses- thesia. Referred sensations and allochiria are described under Symp- tomatology. 38 DISEASES OF THE NERVOUS SYSTEM. Tests for the Condition of the Special Sense of Muscles, Joints, and Tendons, i.e., for J. toa.'«'«.— Anaesthesia of the special sen- sorv nerves of the muscles, joints, and tendons causes ataxia and inco-ordination. Muscle anaesthesia causes chiefly a loss of iceight stn.se or loss of power to determine Aveights. It is tested by the use of weights suspended by a string so as to exclude pressure sense; also by causing the patient to squeeze a dynamometer up to a certain fixed number. In articular and tendonous anaesthesia there is loss of posture sense. It is tested by the physician's moving the patient's limbs and having the blindfolded patient tell in what direction the movement is made. Or he is told to follow wath one limb the movements which the examiner makes with the other. Muscular, articular, and tendonous an- aesthesia usually exist together; there is then a combined ataxia. Combined ataxia shows itself in standing and in locomotion and other voluntary movements. Thus we have a static ataxia and locomotor or motor ataxia. Static ataxia or inability to stand (or sit) without swaying or irregular move- FlG. No. 1. ^'«- -• 29.— Ataxiagrams. No. 1, Made with eyes open; No. 2, made with eyes closed. ments is tested by making the patient stand with the eyes closed and the heels and toes close together. Normally, the head moves not over an inch in this position, and the patient holds the liead and body more rigid with the eyes closed than with them opened. In ataxic states the reverse is true, and decided swaying or even complete loss of equilibrium occurs with the eyes closed, or even with the eyes open, and the base narrowed by putting the feet together. This phenomenon is called the " Brauch-Romberg symptom." In static ataxia, mus- cular and articular sensations are both involved. The degree of this can be accurately measured by the ataxiagraph. With the DIAGNOSIS AND METHODS OF EXAMINATION. 39 eyes open a healthy person standing erect with feet together tends to sway forward. The antero-posterior excursion of the head averages 3.7 em. (H in.), the maximum being 9 cm.(3i in.). The lateral excursion averages 1.9 cm. (f in.), maxnnum being 5.4 cm. With the eyes closed the antero-lateral excursion averages 3.4 cm. m in.), maximum 3^ in. ; the lateral excursion 1.9 cm. (If in.), maximum (3.8 cm. (2| in.). In other words, the person stands a little steadier with the eyes closed, the average excursion being 1^ x f in. with eyes open, 1^ X f in. with eyes closed (Bullard and Brackett). Ataxia of motion is tested by the gait. The patient can- not walk a straight line and cannot walk without watching the floor with the eyes. The arms cannot be moved in a co-ordi- nate way. With the eyes closed, the patient cannot place the fin- ger on the tip of the nose, or lobe of the ear, or any indicated spot. Ataxia of motion involves especially the articular and ten- donous sensations, but not these exclusively. It may be measured by noting how close the patient keeps upon a given line ten feet long in Avalking; how near he can place the finger upon the centre of a board marked like a target. The patient is placed ten feet away, and made to walk directly at it and place the finger in the centre. To sum up the foregoing, we have : Ataxia Due to Muscular anaesthesia Articular and tendonous anaesthesia. Combined forms, e.g., static ataxia. . . Locomotor ataxia. Tested by Weights, etc. Position of limbs. Co-ordinate move- ments. Station and gait. There are, besides this, certain forms of inco-ordination which are allied to tremor, and are disorders of the sensori-motor corti- cal areas or efferent nerve tracts. Nor is it absolutely established that in the above-described forms of ataxia there is not an in- volvement of the efferent nerve mechanism. Visio7i. — The special modes of examination are given under the head of Diseases of the Optic Nerve and Ocular Muscles. The special points which the neurologist must investigate are visual acuity, astigmatism, errors of refraction, limitation of the visual field, exophthalmia, retraction of the bulb, color-blindness, the state of the pupil and its reflexes. Hearing.— The special methods of examination are given else- where. The points chiefly to be investigated are acuity, range, bone conduction, aerial conduction, electrical reactions. Seiise of S7neU.—See p. 107. Sense of Taste.— See p. 146. CHAPTER lY. THE CAUSES AND THE PATHOLOGY OF NERVOUS DISEASES. General Etiology. The subject of the causes of nervous diseases must be studied from two points of view. First, w^e must learn the predisposing and exciting causes of nervous diseases in general. Second, we must learn the causes of the particular pathological change which constitutes the disease. I. The causes predisposing to nervous disease relate to age, sex, condition, heredity, race, climate, civilization, occupation, habits, diatheses, infections, and poisons. Age and Developmental Influences. — In early age, paralyses and convulsive troubles are more frequent, while sensory neuroses are rare. In adolescence, many severe constitutional neuroses and neuropathic tendencies develop, but organic disease is rare. In adult life, the inflammatory and degenerative troubles are at their height. In old age, those disorders which are dependent on dis- ease of the blood-vessels, such as apoplexies and softening, appear. The special nervous defects and disorders more especially as- sociated with early developmental influences are these (Clouston) : 1. Of the eml^ryonic stage : Acephaly, genetous idiocy. 2. Of the period of most rapid brain growth — birth to seven years: Convulsions, pavor nocturnus, tubercular meningitis, men- ingeal hemorrhage and encephalitis, epilepsy, idiocy, infantile paralysis, neurotic fever, febrile delirium. 3. Of the period of co-ordination of motion and emotion — seven to thirteen: Chorea, epilepsy, asthma, migraine, myopathies, hereditary degenerations of the cord. 4. Puberty and adolescence— thirteen to twenty-five: Epilepsy, neurasthenia, hysteria, migraine, sexual perversions, paranoiac tendencies, hereditary myopathies and myelopathies, insanities. AS'eo?.— Sensory and functional disorders are more frequent in women ; motor and organic disorders more frequent in men. Condition and Occujmtion.—^o general facts will be laid down here. Celibates, however, it may be said, suffer more from ner- vous disorders than married people. It will be shown later that certain occupations entail special nervous disorders, and that in-door life jjromotes functional nervous diseases. CAUSES AND PATHOLOGY. 41 Habits. — Excessive indulgence in alcohol is a most prolific cause of nervous disease, chiefly by the action of this substance on the blood-vessels and the stomach. Excesses in eating, in tea- drinking, irregularity in sleeping, and bad habits of working pre- dispose to nervous disease. Sexual excesses are usually the result rather than the cause of nervous disorders. Heredity.— There are few nervous diseases which are, strictly speaking, inherited. But an over-irritable, unstable, inadequately developed, and badly nourished nervous system — one with a ten- dency to disease— may be inherited. This is known as the neuro- pathic constitution. Excessive intellectual labor and mental strain during the time when children are being i^ropagated tends to produce a neuropathic taint in the descendants. When both parents are themselves of a highly nervous tempera- ment, their children are apt to be more so. The existence of one of the severe forms of constitutional nervous disease, Uke epilepsy or hysteria, in one parent is likely to produce neuro- pathic children. Intermarriage does not cause neuroses, un- less father and mother are of closely alike temf)eraments. Excessive alcoholic indulgence in one or both parents, syph- ilis, injuries or fright to the mother during pregnancy, may result in neurotic children. The mother transmits neuroses and neuro- tic tendencies more than the father. A certain form of nervous disease may not be transmitted in the direct line, but will be found in different branches of the same family, as, for example, in uncle, nephew, and cousin. This is then called a "family dis- ease." Climate and Cimlization. — ]S'ervous diseases are most frequent in temperate climates, and in those which are dry and elevated. They increase with the progress of civilization and the greater strain, complexity, and luxury of modern social life. Those organic nervous diseases which are largely dependent on vascu- lar disease are frequent in the poorer classes among whom syphilis, alcoholism, and bad feeding prevail. Functional and de- generative disorders are frequent in the higher classes. ]S^ervous diseases, if we except those of the degenerative type, prevail more in urban populations. Diatheses. — The rheumatic and gouty diatheses predispose to nervous troubles, more especially those which are of a peripheral and functional nature, Lith^emia, a condition in which the pro- ducts of tissue waste are not properly oxidized and eliminated, has a similar influence. Trauma and Shock. — Hemorrhages and trauma may be a di- rect cause or may predispose to nervous disease. Trauma and shock may cause functional diseases such as neurasthenia, or may lead to the development of insanity or indirectly to degenerative 42 DISEASES OF THE NERVOUS SYSTEM. organic disease. Mental shock, and especially a fright, oftener than severe bodily injury, leads to the development of functional neuroses. Hemorrhages, exhaustion from excessive work, and anxiety are potent causes. Infections.— In comparison with their frequency, the infective fevers are not great factors in producing nervous disease, but practically they often play an important part. Scarlet fever is the most dangerous disorder in this respect. Measles perhaps ranks next, then follow diphtheria, typhoid fever, and pertussis. Among chronic infections syphilis ranks first; malaria, the pel- lagra, and beriberi are also to be mentioned. Poisons. — Alcohol, tea. coffee, and lead, mercury, copper, arse- nic, are to be placed among the frequent causes of nervous disease. Reflex Causes. — Among other causes are local disease of vis- cera, such as renal, uterine, and ovarian diseases, dysi^eptic and liver disorders, visual and auditory troubles. II. The causes of particular pathological types of disease. Inflammatory diseases of the nervous system, as of other sys- tems, are caused almost always by microbic infection. This is brought about directly by injury and exposure to external agen- cies or indirectly through the blood. Inflammatory^ disorders oc- cur oftenest in early and middle life, and in men oftener than in women. Degenerative diseases are observed oftener in middle and later life, and result from excessive nervous strain, syphilis, ex- posures, poverty, chemical poisons, alcohol. Heredity is also an important factor. Diseases of the blood-vessels occur in middle and later life. Bright's disease, the gouty diathesis, alcohol, syphilis, over-feed- ing, and chemical poisons such as lead are among the causes. Functional sjjasmodic diseases usually develop early in life when general in character, like epilepsy and chorea; but later in adult life if local, like writer's cramp and wry-neck. They often follow infective fevers. Hereditary influence is here important. Functional sensory disorders rarely begin before the age of seven to ten, and are more common in women and in temperate climates. A certain class of them, however, like facial neuralgia, develop with the degenerative period of life. General nutritional disorders, like neurasthenia, are more fre- quent in youth and middle life, in active and new civilizations, in temperate climates, especially those which are dry and cool or elevated. Diseases of the peripheral nerves are caused by injuries, and by poisons like alcohol or infections like that of beriberi or by the auto-toxiemia of gout, rheumatism, and diabetes. They occur chiefly in early and middle life. CAUSES AND PATHOLOGY. 43 General Pathology. The nervous system is composed of nerve cells, nerve fibres, connective tissue, the neuroglia, blood-vessels, and lymjphatics. Its disorders involve one or more of the above tissues. The following is a list of the forms of disease which affect the nervous system : 1. Malformations, agenesis. 2. Hyperj^mia, anaemia, haemorrhage, oedema, and arterial and venous diseases. 3. Inflammations. 4. Degeneration and atrophy, softening, sclerosis, gliosis. 5. Tuberculosis and syphilis. 6. Tumors and parasites. 7. Nutritive and functional disorders. I^YFLAMMATiON. — The pathology of most of the above types of disease will be given elsewhere, and does* not call for discussion here. It is, however, of the utmost importance that the student have a clear understanding of the nature of inflammation and degeneration as they affect the nervous tissue. Inflammation is a morbid process which has to deal primarily with blood-vessels, lymphatics, and connective tissue. Inflannuation, teleologically, is the reaction of the organism to an irritant. Wherever there is inflammation, there is irritation. The irritant in inflammation is practically always the product of microbic action or of some irritat- ing product of tissue change. Without some microbic or tissue irritant there can be no inflammation. We make this exception only : that certain chemical substances, such as alcohol, arsenic, and lead, may at times excite a form of inflammation which is, however, probably, primarily a degenerative or destructive pro- cess. Inflammation, when the irritant is removed, tends to sub- side. It is a regressive, not a progressive, process. Bearing these facts in mind, it will be found that inflammations of the nervous tissues never or very rarely occur without the presence of some microbe or some destructive process whose irritant products excite inflammatory reaction. Inflammations may be divided into the (1) exudative and the (2) productive forms (Eelafield). The exudative inflammations maybe simple, without necrosis, with necrosis; purulent; pur- ulent and necrotic. 1. Simple exudative inflammation is accompanied with con- gestion stasis, emigration of white corpuscles, and perhaps diaped- esis of red cells, transudation of blood serum, and formation of fibrin, the total result being an exudate containing white blood cells, now called pus cells, and fibrin in varying proportions. 44 DISEASES OF THE NERVOUS SYSTEM. There is, in some cases, no destruction of tissue ; and on subsi- dence of tlie inflammation the tissue returns to its normal condi- tion. In other cases the inllammatory action destroys some of the nerve tissue. In purulent inflammation there is great accumulation of pus cells and less relatively of fibrin. If the tissue is destroyed, it is nj^in'tilent and necrotic inflam- mation. In some exudative inflammations there is increase of connective tissue from the start, and the process continues till the inflam- mation subsides. Most exudative inflammations are acute or subacute. Inflammatory cedema is a form of exudative inflam- mation. 2. Productive or proliferative inflammation is a process in which there is little congestion and exudation, while new con- nective tissue is slowly formed. Productive inflammation is usu- ally chronic ; tubercular and syphilitic processes are varieties of productive inflammation. The microbes which are known to produce inflammations of nervous tissues are : the ordinary pyogenic streptococcus, the diiDlococcus intra-cellularis, the diplococcus pneumoniae, a bacillus like that of typhoid fever. The bacillus tuberculosis sometimes causes a purulent inflammation. The supposed rabies bacillus, the bacillus of leprosy, the anthrax bacillus, and the micro-organ- ism of infectious multiple neuritis may be added to the list. The principle poisons which may cause chronic productive in flammations are alcohol, lead, and arsenic. Certain irritating auto-toxsemic agents, such as occur in gout, rheumatism, diabetes, and states of inanition, appear able at times to cause productive inflammations. Classificatiox of Ixflammatio^s's. Form. Cause. Simple exudative, with Microbic or toxic, oi- without necrosis. Purulent, with or with- out necrosis. Microbic Microbic Productive or prolifera- Microbic or toxic, tive. Example. Meningitis. Poliomyelitis. Meningitis and encephalitis. Acute purulent myelitis. Chronic menin- gitis. Leprous neuritis. Degenerations and Scleroses.— By degeneration is meant a gradual death of the nerve cells and fiijres, or in other words of the parenchyma of the organ. The cells swell up, becon)8 CAUSES AND PATHOLOGY. 45 granular and fatty, and then either break up and become ab- sorbed or enter into a conditi( )n of a dead coagulum (coagulation- necrosis). Degenerations may be acute or chronic, primary or secondary. Acute degeneration causes a condition known as softening or necrosis. It is due to cutting off of vascular supply, direct injury, and to necrotic and intlanmiatory poisons. Acute degeneration may be folio vved by a reparative process \ldiich is called a repar- ative or reactive inflammation, and which ends perhaps in -pvo- ducing a cicatrix or sclerosis. Chronic degeneration is accompanied and follow^ed by a prolif- erative process which results in the production of connective tis- sue and sclerosis'. Sclerosis is a i^rocess of connective-tissue proliferation, as a result of which the normal or injured parenchyma is supplanted by fibrous tissue. The word sclerosis is usually employed in de- scribing degenerative diseases, though it indicates the result rather than the primary nature of the process. K primary degeneration is one in which the process is due to inherent defect in nutrition or to some poison acting directly on the cell or fibre. A secondary degeneration is one that is due to a cutting off of nerve fibre or cell from its trophic centre, or to an injury or shut- ting off of its vascular supply. Ordinarily, in speaking of second- ary degenerations one refers to those due to the first-mentioned class. Practically, primary and secondary degenerations often occur in the same disease. Degenerations. Forms. Examples. f r Myelomalacia, p . J Progressive muscular ^^^^^^^ 1 atrophy, [ Locomotor ataxia. I ( Chronic myelitis, I Secondary and mixed \ Secondary lateral [ ( sclerosis. Degenerations are caused by certain poisons, such as arsenic, phosphorus, lead, and the poisons of infectious disease. Degen- erations also result from obliterating arteritis such as occurs in old age or from humoral poisons. Degenerations sometimes are due apparently to an inherent defect in the cell nutrition— a pre- mature death of it ; also to causes yet unknown. The question as to whether certain scleroses are forms of productive inflamma- tion or of chronic degeneration is one still undecided. It is probable, however, that many of the so-called chronic inflam- mations of the nervous system are really degenerative processes, and that the primary trouble is in the parenchyma, and not in the connective tissue. Acute and Chronic 46 DISEASES OF THE NERVOUS SYSTEM. Gliosis. ^It is contended by some French pathologists (ChasHn, DC'jerine) that some of the chronic degenerative diseases are the result of a proliferation of neuroglia, not of connectiv^e tissue. This process is called gliosis. Its existence is not yet satisfactorily established. JS'utritive and Functional Disorders.— A fundamental pecu- liarity of nervous tissue of man must here be noted. Nerve cells once destroyed never develop again. The same is true, though not so absolutely, for the nerve fibres running in the central nervous systerii. Peripheral nerves may grow again when cut or destroyed. They always grow from their trophic centre. Nerve tissue in brain, cord, or periphery can never be sutured so that it will functionally unite by direct union. There are a few apparent ex- ceptions. A further peculiarity of nervous tissue is that it is depend- ent for its integrity upon two things, blood supply and trophic influences. The nerve cell is solely dependent on a proper sup- ply of blood, and dies when this is withdrawn. But the nerve fibre is more dependent on the trophic influence of the cell to which it is connected and of which it is a prolongation. It dies when cut off from its cell, but it can get along for a time with but little direct blood supply. Underlying nutritive and functional disorders there exist : A congenital inadequacy of the nervous system to do its work. Dis- turbances in blood supply. Poisonous conditions of the body, due to substances generated within or introduced from without. Reflex irritants. Exhaustive conditions from overwork. CHAPTER Y. HYGIENE, PROPHYLAXIS, TREATMENT. In the treatment of nervous disease, the i^hysician attempts^ 1. To reheve distressing symptoms. 2. To secure radical cure. 3. To iDrevent return. This calls for various measures which may be classed under the heads of general hygiene, diet, ex- ercise, climate, hydrotherapy, massage in various forms, electri- city, drugs, external applications, and surgical intervention. GrENERAL Hygiexe. — To secure and keep steady nerves, and to prevent the supervention of organic nervous disease, would require a considerable reconstruction of the present social system. 1 can only give some hints as to the kind of advice physicians should give to help along the desired end. Thus two people of very nervous temperament should not marry. Children should be brought up to eat slowly a mixed diet, to sleep early and long, to play in the open air, to learn self-control and obedience. Their parents should keep from them all infective fevers. Adults need to keep in mind but two words — moderation, exer- cise. With these they need not fear the use of alcohol, tobacco, tea, coffee, or even occasional irregularities in sleeping and eating. Physical and mental shocks, infective fevers, poisons, and syphilis are prolific promoters of nervous disease. Diet. — For brain-workers in general, the best diet is a nitroge- nous one, but it should contain some fat. Water should be drunk plentifully except by the obese, Avhile the total amount of food should be less than when severe muscular exercise is taken. The best foods are meats, especially fowl; fish, eggs, milk, buttermilk, cocoa, green vegetables, and stale bread with plenty of butter. If there is a tendency to constipation, farinaceous foods and green vegetables may be made the prominent articles of diet in one of the daily meals, and stewed fruit and some alkaline water added. The drinks of brain- workers should be mainly plain and alkaline waters. x\lcohol can be taken in moderation by some brain- workers without harmful results. It may even secure an increased capacity for work. In persons of a sensitive and irritable nervous system, those who are classed joopularly as " nervous," neurasthenic, or hysteri- cal, the above rules apply as to a nitrogenous diet, plus as much 48 DISEASES OF THE NERVOUS SYSTEM. fat as can be digested. There is a class of nervous persons who of themselves find that they cannot take anything sweet without producing headaches, rheumatic pains, and dyspeptic symptoms. These persons should live on meats, fish with butter, oysters, cream and milk, (^od-liver oil, and fat pork. Beef tea with the white of an egg or some peptonoids forms a very nutritious dish. It has been the canon of medicine for many years that animal food must be the soul of the neurotic's diet. Most nervous persons find in addition that green vegetables like spinach agree very well with them. Stale bread can be taken twice a day freely, plenty of butter being used upon it. The dietetic breads from which the starch has been removed are sometimes useful, but are, as a rule, unpalatable, and soon cause disgust. AVhen a rigid diet is to be laid down, there is no better list for nervous invalids than the following: fowl; beef; mutton and lamb; fish, boiled or broiled; oysters; milk; butter; eggs, raw or soft-boiled ; cocoa ; graham bread and gluten bread ; spinach ; Brussels sprouts ; string beans ; stewed fruits slightly alkalinized. Nervous patients, especially hysterical j)atients, should not use alcohol at all. Tea and coffee can be taken in very small amount. The various alkaline mineral waters may be used temperately with impunity, but none of them have much specific effect in re- lieving nervousness or curing the nervous temperament. Water should be drunk between or before meals and a moder- ate amount at meals. At least three pints of liquid should be taken daily. American neurotics do not drink water enough. They have half-desiccated nerves, and desiccation increases ner- vous irritability. An exclusive milk diet is indicated in some forms of hysteria, hypochondriasis, and neurasthenia accom- panied with dyspepsia. KarelFs method is to give four to eight ounces of }varm skim-milk at 8 A.M., 13 M., 4 p.m., and 8 p.m. The amount is gradually increased. Exercise. — As a prophylactic against nervous disorders, the value of exercise, if taken out of doors, can hardly be overesti- mated. Brain-workers are better for moderate exercise, but they do not need much; and after twenty-five, severe intellectual work can rarely be done by persons in athletic training. Before the age of twenty-five, when the system is exuberant with vital- ity, hard study and hard physical exercise can be pursued success- fully together by some. Persons of a neuropathic constitution are benefited by regular exercise only when it interests the mind. In-door gymnasium exercise with the ordinary apparatus does no gootl except through the bath that follows it. In many forms of chronic organic nervous disease exercise is to be prohibited. These will be discussed later. The best forms of exercise are those (1) which take one out of HYGIENE, PROPHYLAXIS, TREATMENT. 49 doors, (2) interest the mind, and (3) call into play the muscles of the chest and arm. Walls:ing fulfils but two and often only one of these conditions. Calisthenics are useful when they interest and are vigorously done. Horse-back riding and bicycling fulfil best the conditions required for a good form of exercise. And bi- cycling is the cheaper, more practicable, and generally better liked of the two. Dr. Graeme M. Hammond has called attention to the special value of cycling in nervous diseases. Lawn-tennis, bad- minton, golf, are all exercises which can be taken up by both sexes and at nearly all ages. Hydrotherapy.— Hydrotherapy is the science of applying water in the treatment of disease. The modes by which it is used in neurological therapeutics are : I. General hydrotherapy : 1. Tonic hydrotherapy. 2. Sedative hydrotherapy. 3. Indifferent baths for mechanical purposes. II. Local hydrotherapy. 1. Tonic Hydrotherapy. — For purposes of stimulating nutri- tion and increasing vasomotor tone we employ cold plunges, the rain bath or shower, the jet, cold sponging, cold sitz-baths, cold sheets, local applications of ice or cold compresses, or cold rub- bing, ice-bags, brine baths, brief cold packs, and sea-bathing. The Cold Plunge.— Th.e patient fills the bath-tub with water at from 60° to 70° F. He then steps in, and at once jumps out and rubs himself vigorously until reaction occurs. The Bain Bath, Jet or JSeedle Bath. — The patient stands in a tub Avitli the feet preferably in warm water, and alloAvs the cold water to fall on the back and rest of the body for one or two minutes. Or a solid jet of cool water is thrown with force upon the back of the patient, by an attendant who stands ten or twelve feet away. The cold jet may be alternated with warm. Cold sitz-baths are taken at a temperature of 70' to 80' F. from ten to thirty minutes. The cold sheet or drip sheet is used by wring- ing a cotton sheet out iik cold water and wrapping it suddenly about the standing patient, w^io is then vigorously rubbed. Ice-bags are worn upon the spine for one or two hours once or twice, or oftener, daily ; or they may be applied for one or two hours at night. Most of these measures have a general stimu- lating and tonic effect. The half -hath and wash-off consists of a tub partly filled with water at a temperaure of 65° to 70° F. The water only half covers the reclining body. While lying in it, the patient is vigorously rubbed. A cold cloth may be laid on the head. After five to twenty minutes, affusions of colder water are poured over the shoulders. The bath may be made as warm as 80 at first. 4 50 DISEASES OF THE NERVOUS SYSTEM. Brine baths contain about two per cent of salt, this being about the amount in sea-water— twenty-five pounds to thirty gallons of water. They are given at a temperature of 100^ F. for twenty to thirty minutes daily, or cool baths at a temioerature of 70' F. may be given for five to ten minutes, the patient exercising meanwhile. Physiology. — Cold applications produce a local contraction of blood-vessels, followed by dilatation. There is usually increased tissue metamorphosis, increased secretion of urine, increased ab- sorption of oxygen, and increased excretion of carbonic acid. In non-febrile persons, cold applications abstract some heat, but they also stimulate the heat-i^roducing centres, so that the total effect is to increase the heat of the body. Only very cold baths lessen heat production as well as excretion of CO2. Cold baths at first accelerate and then tend to retard pulse and respiration. Cutaneous sensibility is at first increased. After a cold bath there is a sense of exhilaration and increased muscular power, provided the bath be not too cold or too long continued. The duration necessary to produce a reaction varies with different people, and some Aveak and sensitive patients never can be made to react. Cold baths systematically taken furnish a kind of vasomotor gymnastics. The neuro-mechanism controlling the blood-vessels becomes more supple, and the tendency to local congestion of the viscera and mucous membranes is prevented. The shower and jet furnish the most valuable means of securing tonic effects in nervous disorders. These are not used with cold water alone. It is often better to api^ly at first a warm stream at 95' or 10."5° F., and then gradually lower it, or to apply the hot and cold jets alternately. In this way tonic effects can be ob- tained even with very feeble persons. 2. Sedative Hydroihercqjy.—ThQ sedative baths are the luke- warm bath, the wet pack, Turkish and Russian baths, the hot sitz-bath, pedal baths, compresses and fomentations, and hot- water bags. Tfie Lukewarm hath is given at a temperature of 95 to 98 F. for ten minutes to half an hour daily. If a slight tonic effect is desired also, the patient should receive an affusion afterward, i.e., basins of cool water at 60^ to 70' F. should be poured over the shoulders. The addition of salt or of pine-needle extract is often useful. The Wet Pack.—K large, thick blanket is spread upon the bed, and upon this is laid a linen or potton sheet wrung out in cold water, 40' to GO' F. The nude patient lies on this, and the sheet is then smoothly wrapped about him, the head and feet not being included. The sheet is carried between the legs and made to lie evenly in contact with the body. Then the blankets are HYGIENE, PPwOPHYLAXIS, TREfATMENT. 51 folded over him, and other blankets may be piled upon this. Sometimes it is well to place hot- water bottles at the feet and a cool compress on the head. The patient lies in this pack for thirty to forty-five minutes and is then rubbed off. A cool affu- sion may be given first. In delicate patients it is well at first to simply wrap the patient in warm flannels until free perspiration results. Then give a cold affusion or wash -off and rubbing. In Turkish batJis the patient is exposed to a temperature at first of 130' or 140' F. for fifteen to thirty minutes, and then to one of 200° F. or 250' F. for a shorter time. This is followed by massage and a cold affusion or plunge or shower. The effects of these baths are somewhat tonic if not too prolonged. The pa- tient should never go into the hotter rooms until he perspires, and he should select bath-rooms that are well ventilated, lliis- sian baths have similar effects, but the bodily temperature is raised to a higher degree in them than in Turkish, owing to the lessened amount of perspiration. Hot /Sit2-Baths.— The patient sits in water at a temperature of 100' to 125° F. for twenty or thirty minutes. Sometimes mustard is added. Hot comjjresses consist of layers of flannels wrung out in hot water and covered with dry flannels and rubber cloth. They are used to relieve local pains and inflammations. They may be applied over the abdomen for insomnia. Hot sprays and douches are used for similar purposes as fomentations. The hot spinal bag is applied at a temperature not above 120° F. Phi/sioh)gij.—\^ Siviii baths, if applied in the form of the moist pack, followed by sponging with tepid water, lessen tem- perature by increasing heat radiation and conduction. If applied so as to iDre vent radiation, the bodily heat is raised. Warm baths increase the circulation of the skin, lessen cutaneous sensibility, withdraw blood from the central organs, increase the exhala- tion of CO 2, but lessen the respiratory activity on the whole. Nitrogenous metabolism is increased from two to three per cent, and more urea is excreted. Pulse and respiration are increased. Nervous excitement is lessened, and the general effect is to cause sedation and a feeling of languor. The wet pack is a most use- ful sedative in neurasthenia and insomnia, and may take the place of medicinal sedatives, like the bromides. It should be given three or four times weekly, or for a short time daily. The luke- warm bath ranks next in its sedative efficacy. It is believed that applications of water to the feet and abdomen especially affect the intra-cranial circulation; given to the thighs and wrists, the pulmonary circulation: cold causing congestion, and heat anae- mia, of the distant parts. Cold to the spine is believed to cause at first constriction, and later dilatation, of the thoracic, abdomi- nal, and pelvic viscera; heat has the opposite effect. Hence cold 52 DISEASES OF THE NERVOUS SYSTEM. applications are used to relieve cold feet and anaemic conditions ot the viscera. The fact must be borne in mind that cold baths and frequent bathing of any kind debilitate some few persons. Massage.— The term massage may be made to include all the manipulations of the body for the purpose of curing disease. The different methods of applying it as classified by Jacoby are: Effleurage or gentle stroking. The maximum force to be ap- plied here should not exceed the weight of the hand. Massage (X friction or rubbing. Energetic strokes with one hand and strong circular or to-and-fro friction with the other. Petrissage or kneading. Tapotement or percussion with the fingers, hands, or instruments. Functional movements, passive, active, and com- bined with movements made by the operator. The physician maybe reminded that a male operator is a mas- seur, a female a masseuse, and that the patient is massed. Massage accelerates the lymph and venous currents, and thus promotes absorption. It increases the rapidity and force of the heart-beat, except abdominal massage, which slows the heart and helps to relieve local congestions and inflammatory deposits. It presses and stretches the terminal nerve filaments, increases the irritability of motor nerves and the contractility of muscles. It may either increase or lessen the irritability of sensory nerves according as it is applied. Of the various forms of massage, ta- potement is the most frequently useful, and is the kind almost exclusively used in neuralgias. It is applied not only with the fingers and hand, but also by the aid of rubber tubes known as muscle beaters, rubber balls with rattan or whalebone handles, percussion hammers and various percuteurs, such as Granville's and Jaeoby's, Massage is of considerable value in certain forms of atonic neurasthenia and hysteria, associated with anaemia, dyspepsia, and feeble circulation, in hemiplegia, in the paralyses of periph- eral origin, in functional spasm, especially in some forms of writer's cramp and allied neuroses, in cerebral hypersemia, in- somnia, constipation, and in headache, and some neuralgias, especially those about the head, neck, and arm. It is contra- indicated in heart disease, arteritis, or where there is danger of dislodging a thrombus. Climate ix Nervous Diseases.— The factors which make up a special kind of climate are : 1. Purity of air; 2, temperature; 3, humidity; 4, sunhght; 5, rarefaction of the air ; 6, ozone ; 7, 'wind ; 8, electricity ; 9, soil ; 10, trees; 11, social conditions. Regarding these points, some facts are very well settled. The air in the country is purer than in cities. The air on the sea and J HYGIENE, PROPHYLAXIS, TREATMENT. 53 at hi^h levels is purer than in other localities. The temperature above the sea-level diminishes about 1° F. for every 300 to 350 feet, and is less the dryer the air. Alterations in temperature are less near the sea and less in the southern hemisphere. The higher the elevation and the colder the air, the less moisture does it con- tain. About the factors of ozone and electricity in the air little definite is known. Climates are classified by Weber into marine, low level inland, and high level inland. These all have great variations in quality, depending upon their temperature, moisture, etc. As a general rule, warm marine climates and sea voyages are best for neuras- thenic invalids of the irritable type. On the other hand, in atonic and an*mic conditions high inland climates are better, at least for a time. Such climates should not be too dry or windy. In organic degenerative diseases of the nervous system, marine climates and low Revels are better. Germany, the Riviera, the Bermudas, the West Indies, Florida, and other Southern States are favorite places for sending neuras- thenic Americans. Camp life in the Adirondacks or other forests is also found most useful. Electricity in Nervous Diseases. Physical. — Electricity is assumed to be a material like a fluid, perhaps a condition of the ether itself. It is not a force any more than water is a force, but it produces force by its move- ments. Electrical phenomena are the result of the strain or stress put upon the electrical fluid. Physicists assume that the electrical fluid exists in two conditions, positive and negative, and we speak of positive electricity and negative electricity ac- cordingly. Under ordinary conditions these fluids are united and in equilibrium; but by certain agencies, such as friction, heat, chemism, etc., they can be separated. We assume that the condition of electrical equilibrium is that of zero, and that the earth's electricity is at zero. Positive electricity is raised above, negative electricity pulled below, this zero point. Electrical phenomena result from attempts of the fluids to become equal- ized or stable again at the zero point, just as the phenomena of heat result from differences of temperature and those of gravity from differences of pressure. The distance to which the electri- cal fluids are separated from the zero point is spoken of as the difference in " potential.*' This potential corresponds to the term " degrees '' in measuring heat. Now, the greater the difference in potential, the greater the effort of the fluids to return to zero. High and low potentials correspond to high or low intensity of heat. Tension is the result of the widely separated fluids striving 54 DISEASES OF THE NERVOUS SYSTEM. to return to the zero point. It is the same thing as difference of potential, and the term may as well be dropped. When the two fluids, at different potentials, attempt to become equaUzed, they pass along certain paths and form electrical currents. Electri- city will pass along any substance, but some substances conduct it more easily than others, and these are known as conchictors. The relative value of different conductors is shown in the follow- ing table : 1. The metals; 2, charcoal, 3, plumbago; 4, dilute acids; 5, sa- line solutions; G, pure water; 7, living animals; 8, flame. Of the metals, silver and copper are the best conductors. The human body would have about the same conductibility as the saline so- lutions, if it were not for the skin, which is a very poor conductor, especially when it is dry. Those substances along w^hich elec- tricity passes with great difficulty are known as non-conductors or inimlators. The following is a list of some of these, the sub- stances arranged in accordance with their relative value : 1. Caoutchouc. 2. Silk. 3. Glass. 4. Wax. 5. Sulphur. 6. Resins, 7. Shellac. 8. Dry air. The electrical fluids may be kept by insulators at different potentials, the insulators preventing them from becoming equal- ized or reduced to the same potential. Electricity in this condi- tion is called static. Its study is called electrostatics. The electric fluid in motion is called dynamical electricity, and its study is electrodynamics. Technical Terms. — There are certain technical terms which it is necessary to understand. Electromotive force (symbol, EMF) is the force which tends to set electricity in motion. An electric current results. The current strength (symbol, C) is the term used to express the capacity of the separated fluids to overcome resistance in their attempts to reach equilibrium or equalization again. This current-strength or simply the current, naturally, is in proportion to the strength of the electromotive force, which is constantly disassociating the electrical fluids and generating the current. If, however, as is always the case, the electrical fluid meets resistance in seeking equilibrium, the resistance dimin- ishes its current. Hence we have the formula known as Ohm's law: ^ Electromotive force EMF Current strength = ; or C = . Resistance R All bodies offer some resistance to electrical currents, and it is important to have some standard unit of resistance for the sake of comparison. Such standard unit has been adopted and is called an oh m. It is the resistance offered to a current by a cer- tain piece of wire of definite size and length. I HYGIENE, PROPHYLAXIS, TREATMENT. 55 A volt is the unit of electromotive force, ^.e., it represents the force which will generate a certain amount of electricity in a second of time. A Daniell cell is of not quite one volt strength. An ampere is the unit of working power or current strength. It is the current strength produced by one volt of electromotive force working against one ohm of resistance. A milliampere is one-thousandth of an ampere. A loatt is the unit of work. Density. — When a given current flows along from a large into a small conductor, the quantity in this latter conductor in a given section is greater and the current is said to be denser. The in- strument by which the strength of a current is measured is known as the amperemeter: in medical practice, only fractions of the ampere are used, and the instrument is called the milliam- peremeter. A rheostat is an instrument for interposing resist- ance in a current. Electrical Appliais^ces.— The batteries used in neurologi- cal practice ai-e of three kinds : the static, the faradic, and the galvanic. The static electrical batteries are mostly modifications of the Holtz influence machine. They are inclosed in glass to prevent the effects of moisture. The instruments made in this country for medical purposes will usually furnish electricity all the year round. A cheaper instrument, made on a different principle by Glaser, of Vienna, is recommended by Lewandowski. The bat- tery accessories consist of an insulated stool and brass-ball elec- trodes with glass handles. The patient is placed on the stool, which is connected by a rod with one ot" the prime conductors. The battery being started, the patient becomes enveloped, as it were, with a layer of electricity which is at a very high potential and constantly flying off, being retained only by the dry, non-conduct- ing air. The electrode held by the operator, and connected directly or indirectly to the other prime conductor, is now brought near the patient. The electrical fluid bounds to the zero point with such force that some of the metallic parts of the electrode are carried off and ignited, causing the disruptive spark. The pa- tient thus is discharged of the fluid ; but it continually reaccumu- lates upon him, and thus one can keep on drawing sparks from all parts of the body. The electric spark causes a muscular contrac- tion and, a little later, a small punctate red spot. There is some pain connected Avith it, but as the electricity penetrates the body for only an infinitesimal period of time, it directly affects the viscera but little, and is not dangerous. Various ingenious electrodes have been devised for modifying the character of the static dis- charge, but they all have much the same effect as the spark. By approximating the prime conductors so that they ahnost touch, and then connecting the outer surface of the two Leyden 56 DISEASES OF THE NERVOUS SYSTEM. jars which hang from the prime conductors with sponge elec- trodes, one gets the static induced current described by Dr. William J. Morton. The special peculiarity of this current, as well as of the spark discharge, is that it is made up of electricity at a very high potential, and that, being composed of oscillating or alternating currents of extremely short duration, the quantity of electricity is very small. The result is that when a muscle de- generates, it loses its irritability to the static current very early. The static current will thus reveal a beginning- degeneration of nerve sooner than the other currents; it also promotes tissue changes more than other forms. It sometimes stimulates a greatly degenerated muscle, so that later the other forms will produce a contraction. It has a powerful psychical effect, and lends itself readily to quackery. In faradic medical hatteries the electricity is produced by in- duction. The chief elements are a cell and two coils of insulated copper wire. One coil is placed around the other, the outer coil being longer and of finer wire. The cell generates a current which in turn " induces '" the electricity which is received hy the pa- tient. The original current is so arranged that it is being con- stantly broken and closed or " made '' again. At both break and make, a current is induced m the inner coil of coiled wire ; this forms what is called the primary induced current and is made up of a succession of short currents. This current, though theo- retically alternating, is really a current of one direction. For the "make" current is opposed and nullified by the original or bat- tery current. The same is true of the secondary induced current which is excited in the outer coil by the currents of the inner coil. Both currents are really composed of a rapid series of single cur- rents going the same way, and they each have a positive and a negative pole. The primary current is one of lower tension, and is rather less strong. It can be used when the resistance of the parts is not great and a very pow^erful current is not needed. The secondary current is one of higher tension, it overcomes resistance better, and can be employed in connection with the wire brush and in auiesthesic conditions. It is also the current used in measuring the strength of the faradic application, as will )je shown later. The current of the secondary coil resembles that of the static induced current. It has, however, a lower potential, vastly slower alternations, and more quantity. It can contract muscle, which the static current cannot affect. The secondary coil should be made of wire of a standard size, length, and layers of coil. A standard coil of wire 800 metres long, .225 mm. in diame- ter, wound on a spool 100 nnn. long, is quite generally adopteil now. Faradic batteries are made with the zinc-carbon or Grenet cell, the Leclancln', the silver-chloride cell, or some modification of HYGIENE, PROPHYLAXIS, TREATMENT. 57 these. For general use, the zinc-carbon cell is the most trust- worthy ; but the dry silver-chloride cell is the most convenient. A dry cell made with muriate of ammonia has of late come into use. Galvanic Batteries.— There are two kinds of these in practical use. The one includes the cells which act as soon as the circuit is closed ; the other includes those which act only when the elements composing the battery {e.g., zinc, carbon, platinum, copper, etc.) are dropped in the exciting fluid. The former class (known as two-fluid cells) are not touched except to renew Avater or add some chemical. In the latter (the single-fluid cells), one of the elements is always taken from the fluid when the current is not in use. The first class of cells has a much weaker chemical Fm. 30.— Author's Electrode Set (H. E. Stammers, New York). action and evolves less electricity in a given time. It includes the Daniel cell, the gravity cell, the Leclanche cell, and the sil- ver-chloride cell. Among the second class or single-fluid cells, the zinc-carbon cell, known as the Grenet or Stohrer's cell, al- ready referred to, is most used. The best portable batteries are made of the zinc-carbon cell or the dry chloride of silver cells. Stationary or office batteries are best made with the Leclanch6 cell or some modification of it; or the dry silver-chloride cell may be used. The electric-light current can be utilized to supply con- tinuous and interrupted currents and for purposes of the cautery. It is expensive. The ordinary accessories to the faradic and galvanic batteries are electrodes, rheostat, and milliamperemeter. The electrodes needed for ordinary purposes are : 1. An indifferent electrode measuring 5 cm. by 10 cm. 2. A normal electrode, 10 sq. cm. 3. A unit electrode, 1 sq. cm. 4. A 58 DISEASES OF THE NERVOUS SYSTEM. soft wire brush. 5. Three handles : one 10 em. and one 40 cm. long, one short handle with an interrupter. G. A milliampere- meter. 7. A rheostat. (See Fig. 30.) Methods of Application.— StsitiG electricity is applied for fif- teen or twenty minutes daily or tri-weekly. For general tonic or sedative effects, sparks are drawn from all parts of the body ex- cept the face. In paralysis or spasm or pain, sparks are apphed to the affected area. For headaches and cerebral paraesthesise, the electrical breeze is very useful, but it must be strong. The faradic and galvanic currents are used for about the same time and intervals as the static. In some cases, however, the galvanic current should be given daily or even two or three times a day. As a rule, a course of electrical treatment should be con- tinued for six to eight weeks, and then discontinued for a time. The special methods used in applying these currents are : 1. General galvanization and faradization or general electriza- tion. 2. Local electrization by galvanization of the brain, of the neck, of the spine, of the special senses, limbs, and viscera. Or by faradization of the neck, spine, limbs, and viscera. 3. The combined faradic and galvanic currents. These are given bj^ means of the De Watteville switch. General and local electrization can be given in this way. 4. The polar method. This is employed chiefly in using the gal- vanic current. The indifferent electrode is placed on the sternum or back, and the other electrode applied wherever indicated. 5. Cataphoric electrization by means of Peterson's electrode. G. Electrolytic applications are used in enlarging strictures and affecting inflammatory deposits and neoplasms. In general electrization, whether galvanic or faradic, the in- different electrode is placed on the sternum, feet or back, and the other pole is carried over the limbs, trunk, neck, and, if in- dicated, the head. In some cases, however, the two electrodes are applied together upon the different muscles of the body. In local electrization, the large electrode may be applied on an indifferent spot, and the other applied to the affected limb or limbs, or the two electrodes may be used together on the same segment of muscles. The details for galvanizing the brain, special senses, and viscera must be obtained from special text-books. When an electrode is held steadily upon a part, it is called stabile ; when it is moved over it, it is called labile. The positive pole is called the anode (An), the negative the cathode (Ca). The size of an electrode is indicated in square centimetres. A formula for applying electricity may be written thus: Anod. galvanization, 10 ma. 5-10 cm. daily, stabile. HYGIENE, PPwOPHYLAXIS, TREATMENT. 59 This means that the positive pole of the galvanic current is to be apphed steadily at a given place daily for five minutes with an electrode of ten square centimetres. The terms "ascending '' and " descending currents" are rarely m Fig. 35. Fig. 33. Fig. 34. Figs. 31 to 36.— Cuts showing Motor Points. The letters refer to points elec- trization of which stimulates certain muscles to contract. These points vary much in different persons. For details see De Watteville's *' Medical Electricity. ' ' 60 DISEASES OF THE NERVOUS SYSTEM. used, the name of the pole being emplo^^ed instead. Thus, anodal galvanization of the brain or arm means that the positive pole is applied at these localities. With the faradic and static currents, neither the pole nor the direction of the current makes much difference. Electro-Diagnosis.— ^\ien a motor nerve is cut off from its centre in the spinal cord, or when this centre itself is diseased, the nerve and later the muscle undergo a degeneration. As a result of this, their reaction to electrical currents is changed, and we get what is termed "partial degeneration reactions" and "complete degeneration reactions " according to the degree of disturbance. These reactions are due mainly, if not wholly, to the degeneration in the terminal nerve fibres and motor end plates in the muscle. When the muscle alone is diseased, the reaction is not changed until very late. The change in irritability is due to the fact that as the nerve fibre wastes it takes an electric current of com- paratively long duration and considerable strength to stimulate it. The first effect is to lose its contractility or reaction to weak cur- rents, then to extremely rapid, short currents like the static, then to the faradic, and last to the galvanic. Such change is known as the quantitative alteration in electric irritability. But besides this, the nerve and muscle are affected in a differ- ent way by the different poles of the galvanic battery. In nor- mal nerve and muscle, a contraction is caused more readily by the negative pole than by the x^ositive. But muscles with degen- erated nerve supply sometimes respond as well or better to the positive pole. This forms what is called the qualitative or serial change in the irritability of the muscle. Finally, degenerated muscles respond more sluggishly than normal to the galvanic and faradic currents. The contraction, in- stead of being sharp and jerky, is sluggish and almost tetanic. This is called the modal change in irritability. The qualitative change is only gotten by placing the active electrode over the muscle, but the quantitative and modal changes may be gotten by placing the electrode over the nerve as well as ov^er the muscle. In describing these changes, the following abbreviations are used : DeR = degenerative reaction. ^ AnCC = anode or positive-pole closure contraction. CaCC = cathode or negative-pole closure contmction. ApOC —■ anode opening contraction. CaOC = cathode opening contraction. Te = tetanus. D = circuit is closed and current flowing. ADTe = tetanic contraction while the positive pole is applied and the circuit closed. HYGIENE, PROPHYLAXIS, TREATMENT. 61 The sii^n > means greater than; <, less than. Thus AnCC > CaCC means anode closure contraction is greater than cathode closure contraction. Degenerations in nerve do not occur except in lesions of the nerve or spinal cord, and In very late stages of primary atrophy of muscles. Hence when one finds degenerative reactions, he can exclude disease of the brain, functional disease, and primary dis- ease of the muscle. The following rules may be formulated for testing for degenerative reactions : Use the faradic current first. The Faradic. Current.— Y^ae a secondary induction coil of .225 mm. diameter, 800 metres long. The distance over which the coil moves is divided into a hundred parts. The strength of current is indicated by percentage or millimetres. In many scales it takes 30 to 40 mm. of CD or coil distance to cause a muscular contraction. Record the minimum necessary for muscular contraction, using the same electrodes and in the same way as in testing with gal- vanism. The Galvanic Current. — 1. Place the indifferent pole over the sternum, and a 10 sq. cm. electrode over the muscle. 2. Pass the current for one minute. 3. Then find the minimum strength needed for a cathode closure contraction. 4. Then for an anode closure contraction. Repeat this test three times. 5. With a given cur- rent, note whether the cathode closure contraction is stronger than AnCC, or otherwise. Test this three times. 0. Note the character of the contraction, if sharp or sluggish. 7. Test nerve in same way. The qualitative changes may be expressed by a formula like AnCC = or > CaCC, i.e.., the positive-pole closure contraction is equal to or greater than the negative-pole closure contraction. Or, better, the minimum strength of current required to cause a contraction in the muscle is recorded for the positive pole and for the negative. Thus : AnCC 5 ma. or 8 cells. CaCC 4 ma. or 6 cells. Blanks for such records are used in the Post-Graduate Clinic, like the following : Record of Electrical Reactions. Case of __ No Muscle. Nerve. Aut. tibial muscle. Reaction to ( Electrode Galvanic Current. ( ....sq. cm. Kierht Side. AnCC 8 ma. CaCC 6 ma. Left Side. AuCC 5 ma. CaCC 7 ina. Reaction to 2d ind. coil. r,ATr Faradic Current. i^ai^.. liight Side. Left 10 CD G-2 DISEASES OF THE NERVOUS SYSTEM. The following: table modified from De Watteville and dia- ^n-am (Fig-. 37) show the diseases in which degeneration reactions may be expected. Table sHOWixa the Lesiox, its Result, the Names of THE Diseases, and the Electrical Reactions. Lesion of- 1 to 2}4. Cortex to cord. 3, 4. and 5. Corniia. Result. Paralysis, traetures. Paralysis, degen- erative atrophy of nerve and muscle. con- 2 to 2}4. Paralysis, 3 to 5. traetures. Lat. cols, and Degenerative at- ant. corn. rophy of mus- cle. 5 to 6. Trophic cord centres. ! Degenerative at- rophy of mus- cle. Paralysis from wasting of mus- cle. Lat1). In this country rheumatism and the infective fevers, especially diphthe- ria, are not infrequent causes, and the metallic poisons, with arsenic leading, come last. ^ex. — Multiple neuritis occurs oftener in the female than in the male. This is due to the fact that alcoholic neuritis, which is the common form, afTects women oftener. Beri-beri occurs much oftener in the male. Age. — Multiple neuritis is essentially a disease of early adult life. Almost all cases occur between adolescence and the period of degenerative changes, twenty to forty-five. Young children are very rarely subject to it. The youngest age reported is fourteen years (Suckling). A few cases have occurred in persons over sixty; but they are but little less susceptible than children. In beri-beri, three-quarters of the cases are between the ages of fifteen and twenty-five, 6% in children, 1.2/^ in old people (Harada). /Season and Climate. — The sporadic forms of polyneuritis from alcohol and various poisons and infections occur without much reference to a seasonal influence. Probably more cases occur in spring and fall, owing to sudden changes in temi^erature. Beri- beri occurs oftener in warm weatlier. Epidemic influences like that causing cerebro-spinal meningitis may increase the number of cases of multiple neuritis. Practically, in this country, the question of drink settles the question of the distribution of poly- neuritis. It is rare in the temperate rural districts and smaller towns, and much rarer in native Americans than foreigners. Sexual excesses, exposure to cold and wet, insufficient diet, are among the helping causes. Symptoms and Course. — Polyneuritis usually begins somewhat acutely, but runs a slow course of several months. Very rarely it runs a sudden course, ending fatally. AVe have, therefore, the ordinarily suhacute multiple neuritis and acute 2)e?micious mul- tiple neuritis. The endemic infectious forms show other types. The following is the classification followed : 1. Subacute, multiple neuritis. Motor type. Sensory type. Endemic forms: Beriberi, etc. Malarial forms. DISEASES OF THE NERVOUS SYSTEM. 2. Acute malignant multiple neuritis. 1. This is the type of neuritis produced by alcohol, infections, poisons, and rheumatic influences. It is usually chiefly a motor trouble, but sometimes takes the sensory or pseudo-tabetic form. Prokromata.—The disease often begins with prodromata last- in"- several weeks. The patient suffers from numbness, slight pains, and weakness affecting especially the lower extremities. In other cases the attack comes on suddenly, and in a short time the most marked symjDtoms^ appear. Onset. — There may be a fever for three or four days, with a temperature of 103^ or 104\ This is not the rule. Numbness and pains attack the feet and legs, rarely ex- tending much above the knees. The muscles and nerves are very tender. The fingers, hands, and arms are often similarly but less af- fected. At the same time the skin becomes reddened or slightly cedematous. The muscles of the legs grow weak, and in a day or two the patient may be unable to stand. In a Aveek or two there may be a comiDlete loss of power in the anterior tib- ial muscles and a lesser de- gree of paralysis in the exten- sors of the hand. Nearly all of the leg and forearm mus- cles become eventually in- volved. Atrophy sets in at the same time and very severe pains are present. The motor cranial nerves are in rare cases affected, and pa- ralysis of the facial or of the third, fourth, or sixth nerve has been seen. When the disease is fully developed, which is within a fortnight, there is paraplegia with foot drop, some degree of wrist drop, muscular atrophy, and slight oedema, especially of the feet. The skin-reflexes are often, the knee jerk and elbow jerk always lost. There is some tactile anaesthesia, often with 4:1— Alcoholic Paralysis, with Foot Drop and Wrist Drop. DISEASES OF THE PERIPHERAL NERVES. 73 hyperalgesia. Temperature and jDain sense are also lessened and slowed in transmission. The anaesthesia occurs in patches or diffusely. Muscle and articular sense are lost in the sensory or pseudo-tabetic form, and are usually somewhat involved in the ordinary paralytic form. Pain and sensitiveness continue. The nerves lose their irritability and the muscles show degen- eration reaction, partial or complete, the characteristic being a great variability of reaction over different groups of nerves and at different stages of the disease, and an early loss of faradic and lessening of galvanic irritability. There is sometimes retinal hy- peraemia and even optic neuritis. Of the visceral nerves, the vagus seems oftenest to show signs of involvement, in rapid pulse and disturbances of respiration. The sphincters are rarely in- volved. In such cases there is, perhaps, involvement of the cord or of the abdominal and pelvic splanchnics. In alcoholic and occasionally in other forms of neuritis, mental symptoms, such as a low, muttering delirium, are very often present, and occasion- ally a well-marked conf usional insanity develops. The disease usually reaches its height in a week or two and then starts on a chronic course ; but it sometimes happens that exacerbations occur, or that a paralysis and atrophy progress for several weeks before regression begins. In alcoholic cases there is often great general prostration; the patients lie for several weeks in a delirious condition, and finally develop pneumonia and die. Some further details should be added. Motor ^ymjytoms. — The characteristic paralysis of multiple neuritis is a quadruplegia, all four extremities being involved. The sj^ecial characteristic is the foot drop, which is indicative of alcoholic neuritis, just as wrist drop is of lead palsy. The paral- ysis is typically a peri]3heral one. It affects the feet and legs, hands and forearms. It usually involves the anterior tibial muscles more than the calf muscles, but sometimes the reverse occurs. The muscles become wasted and flabby. They soon lose in bad cases all reaction to faradism, and they require a strong gal- vanic current to produce a contraction. In anterior poliomyelitis, on the other hand, the diminution in galvanic irritability comes on only after weeks or months. Hence an early loss of galvanic as w^ell as faradic reaction is an important sign of neuritis. As the nerve and muscle recuperate, the galvanic irritability increases. After a time, if the paralysis is great, contractures occur. The feet are extended, the legs are flexed on the thighs, and are al- most immovable, and the patient's condition is most pitiable. Sensory SymjJtoms.—'Numhness, hyperesthesia, severe pains (dull and sharp), burning sensations, great tenderness, all occur, and are very marked symptoms. They are felt mostly in the feet, 7-i DISEASES OF THE NERVOUS SYSTEM. legs, and hands. Hypera^sthesia is usually followed by anaesthesia to touch and somewhat to pain and temperature. The transmis- sion of these latter two sensations is delayed. The anaesthesia sometimes occurs in patches, at other times diffusely over foot, le^^ and hand. Muscular and articular anaesthesia are common, and in the sensory form are the dominant symptom, causing an ataxia of gait and station. The other special senses are not affected except in rare cases, in which there is optic neuritis. Vasomotor and Trophic Symptoms.— There is often osdema, sometimes redness of the skin ; occasionally the epidermis of the soles and palms peels off. Glossy skin and profuse perspiration are rare. Eruptions and ulcers do not occur. Mental Symptoms.— The most common mental disturbance is that so often seen in acute alcoholism, viz., a muttering delirium. This is associated with great general vital depression. If a true insanity develops, it also resembles, as a rule, alco- holic insanity or acute confusional insanity. The characteristic symptoms are a curious degree of forgetfulness, together with many and varying delusions rapidly succeeding each other. These often relate to the pains and parsesthesia from which they suffer. They think that there are gloves on their hands or that something is on their feet. They often think that they have been out walking or riding.. They are talkative, incoherent, and sleepless. Organic Centres.— The bladder is ocasionally affected for a short time, the other centres not at all. This freedom from in- volvement of the sphincters is an important characteristic of the disease in distinguishing it from myelitis. From the foregoing it will be seen that the dominant symptoms are paraesthesia, pains (burning, lancinating, and dull), muscular tenderness, some anaesthesia, paralysis affecting especially the lower extremities and causing foot drop, muscular wasting, with degeneration reactions; with no involvement of the sphincters; sometimes peculiar mental disturbances. The sexsory or pseudo-tabetic type of multiple neuritis is caused less often by alcohol and more often relatively by the me- tallic and infectious poisons. The general course is much like that of the paralytic form, but there is less paralysis, and on the other hand there are more of the burning, tearing pains, a greater degree of anaesthesia, with a very decided muscular anaesthesia causing symptoms of a subacute locomotor ataxia. The paresis, muscular wasting, trophic changes, such as shedding of the epi- dermis and electrical reactions, serve to distinguish the disease. A double facial paralysis somethnes complicates this type. Exdemic and Epidemic Types {Beri-heri or Kakke, Igni- pedites, Acrodynia^ Malarial Multiple JYeu r it is). —Beri-heri or DISEASES OF THE PERIPHERAL. NERVES. 75 endemic multiple neuritis is seen in this country rarely, and only by accident. Beri-beri is the Indian name ; kakke, mean- ing "the leg disease,'' is its Ja,panese name. Ignipedites is a name given by Indian physicians to iDrobably the same disease. French physicians gave the name of " acrodynia " to an epidemic disease which prevailed in France and the Crimea in the early part of this century. It was probably multiple neuritis. There are various types of this disease, in some of which the neuritic symptoms seem subordinate to those of other organs. The forms described by Scheube and Taylor are ; The acute pernicious, the acute or subacute benign, the atro- phic or dry, and the dropsical or wet. The symptoms generally resemble those of multiple neuritis, as already described, plus oedema, extensive serous effusions, and gastro-intestinal disorders. The paralysis affects esi^ecially the lower extremities, but in beri-beri there seems to be an espe- cial tendency also to involvement of vasomotor and visceral nerves. Malarial Multiple Neuritis.— -Jamaica seems to be the only place in which the malarial poison produces an endemic neuritic paralysis (Strachan), and the causation in these cases is not yet demonstrated. Dr. Strachan"s description of the symptoms of what he terms malarial peripheral neuritis shows It to be quite extensive, often involving trunk and cranial nerves, and accom- panied with much x^ain and wasting. Cramps and skin eruptions are often noted, complications that do not occur in the ordinary types. 2. Acute Peris^icious Multiple Neuritis.— There is a form of multiple neuritis which comes on suddenly, progresses rapidl^^, and causes death in a few days or weeks. These cases usually show the ordinary symptoms of neuritic paralysis, w^ith final involve- ment of the cardiac and respiratory nerves, causing death. The agent in these cases is apparently of the nature of sepsis. The neuritis is interstitial and hemorrhagic. Other cases of acute per- nicious multiple neuritis take the form of acute ascending or Landry's paralysis. Here there are few sensory symptoms, no electrical changes or atrophy. The disease is due to an infectious poison which overwhelms the system before it has time to set up any inflammation or organic change. Pathology. — In multiple neuritis the disease affects the per- iphery of the nerves most, and extends up, very rarely reaching the roots. The anterior tibial and musculo-spiral nerves on the two sides are oftenest and most diseased. The process when mild in grade resembles a secondary degen- eration following section of the nerve. In severer cases there is evidence of interstitial inflammation as w^ell as degeneration. 76 DISEASES OF THE NERVOUS SYSTEM. This process, however, varies in degree at different points of the nerve's course. Hence it has been called segmental or dissemi- nated neuritis. In some of these cases and in all acute perni- cious cases there is still more interstitial inflammatory change; small hemorrhages occur, exudation takes place, and collections of leucocytes about the vessel walls and among the nerve fibres are seen. The muscles supplied by the diseased nerves undergo atrophy. This is usually simple and non-inflammatory. But Fig. 44.— Longitudinal Section of a Nerve in ^Multiple Neuritis, showing: rich proliferation of nuclei (Ley den). The process here is inflammatory as well as degenerative. sometimes there is an interstitial myositis with exudation com- pressing the fibres (Senator). The spinal cord is, as a rule, healthy, or presents minor and secondary changes. It will be seen, therefore, that in multiple neuritis there may be : (1) Simple degeneration ; (2) degeneration with some evidences of interstitial neuritis (degenerative neuritis) ; (3) decided intersti- tial neuritis with deger.eration of nerve fibres. The changes occurring in nerve degeneration have been de- scribed. In the second class of cases— degenerative or, as it is sometimes called, parenchymatous neuritis— naked-eye changes rarely occur. Under the microscope many of the nerve fibres are found to have disappeared; there is increase in the connective tissue and hyperjemia. The vessel walls are usually thickened. DISEASES OF THE PERIPHERAL NERVES. 77- The mast cells of Ebrlich are seen, indicating excessive connective- tissue activity. Diagnosis. — Multiple neuritis must be diagnosticated from diffuse or transverse myelitis, anterior poliomyelitis, locomotor ataxia, spinal meningitis, and haemorrhage and Landry's paraly- sis. Practically, diffuse myelitis is the disorder from which it has oftenest to be distinguished. From this it is recognized first by /.■/' <-^, ?--=^ ^'~ Fig. 45. -Diphtheritic Neuritis, Chiefly Interstitial (Siemerling); v\ith secondary degeneration. investigating the cause and onset. Neuritis begins more slowly and with sensory prodromata; it affects the legs and feet, especially the extensors, and if it ascends it skips the hips and trunks and attacks the forearms. There is more muscular atrophy than in myelitis; the knee jerks are absent. It pro- gresses more slowly, and after four or eight weeks gradually regresses. Electrical degeneration reactions are more varied and decided. There are tenderness over the muscles and nerves and peculiar burning, darting pains. The cutaneous anes- thesia, if present, is not so extensive and complete, as a rule, while muscular anaesthesia is more decidedly marked. There is very 78 DISEASES OF THE NERVOUS SYSTEM. rarely involvement of the sphincters, or bed-sores. There may be belt-like constrictions felt round the extremities, but not around the waist. The gradual improvement of the paralysis and atrophy and eventual recovery confirm the diagnosis of neuritis. The presence of neuritis of the cranial nerves would strengthen the theory of a neuritis. From poliomyelitis it is distinguished by the presence of pain and other sensory symptoms, the early fall in galvanic irritabUity, the age of the patient, and the etiology. From locomotor ataxia, neuritis is distinguished by its more rapid onset, the presence of paralysis and atrophy of muscles, paresis, with degeneration reactions, and the absence of involve- ment of the organic centres. Spinal hemorrhage usually leads soon to a secondary diffuse myelitis easily distinguishable from neuritis by the characters above given. Here there is also usually pain in the back. Spinal meningitis is associated with characteristic pain, tenderness, and stiffness along the back. Acute ascending joaralysis in its typical form shows but very slight sensory disorders, and no wasting or change in electrical irritability. The complication of multiple neuritis and myelitis or posterior sclerosis is possible, but is very rare. In the former case the ordinary symptoms of myelitis are added to those of neuritis. In locomotor ataxia there is often some nerve degeneration and occasionally neuritis. The nerve degeneration probably only causes slow atrophic changes and iDaresis; the neuritis causes pains, anaesthesia, skin eruptions, and local troj^hic disorders. Prognosis. — Alcoholic multiple neuritis is a serious disease, because of its associated conditions. Nearly one-half of my pa- tients have died, mainly because they continued the use of alco- hol after paralysis appeared. They do not die of neuritis, but of alcoholism or of phthisis. Other forms of neuritis rarely cause death. The great majority recover almost completely. It may be from six months to two years before all symptoms disappear. The average time is about a year. Treatment.— The patient needs, first of all, rest in bed. The limbs are often extremely tender and the patient's pains ex- cruciating. To relieve these the legs may be painted with menthol and enveloped in cotton batting. In other cases flan- nels wrung out in hot water and renewed every two hours give relief. Internally phenaeetin, antipyrine, salicylate of soda, may be given. In the early stages, salicylate of soda in doses of gr. xx. every two or three hours should be administered. If there is a great deal of depression from alcoholic poisoning, strychnia gr. ^V Q- 3 h. and aromatic spirits of annnonia, 3 ss. q. 3 h., should be used. Nitrate of silver is also useful in the early stage. DISEASES OF THE PERIPHERAL NERVES. 79 After the acute stage is passed the labile galvanic current oc- casionally interrupted may be applied, 2 to 6 ma. for ten minutes three times weekly. Later, by the sixth week, the faradic current, massage, and careful exercise should be given. At this time or earlier (third Aveek), strychnia, iodide of potassium, arsenic, and tonics may be given. In old cases in which a great deal of paralysis and contracture hav^e occurred, forcible extension of the limbs, the use of splints and rubber muscles, are needed. With patience and perseverance the worst cases can eventually be brought to a complete recovery. CoMPLiCATi^s^G Forms of Neuritis axd Neuritic Degen- ERATioi!^. — Neuritis and neuritic degeneration complicate many diseases, but they especially mark and modify subacute and chronic rheumatism, locomotor ataxia, diabetes, paralysis agitans, wasting diseases, and old age. A neuritic degeneration almost always affects the nerves in the neighborhood of an old rheumatic joint. The chief result of this is to produce wasting and some paresis of the muscles mov- ing the joint (Pitres and Vailtard). The iDrocess is a reflex atrophy (see Arthritic Muscular Atrophy). In locomotor ataxia, parenchymatous degeneration is very often present. It does not produce the cardina.1 symptoms of this disease. It does, however, cause some of The anaesthesia, parses- thesia, muscular atrophy, skin dystrophies, and visceral crises. In diabetes, the neuritis takes the form of the sensory type of multiple neuritis, and causes symptoms like those of locomotor ataxia. The patient has sciatic pains, burning or numb feet, loss of tendon reflex, ataxia. The upper extremities are rarely affected. I7i Wasting Diseases and Old Age. — In various wasting dis- eases, such as phthisis, cancerous cachexia, long-continued fevers, marasmus, and in senility, a simple parenchymatous degeneration of nerves, with atrophy, occurs (Arthaud, Koster, Jappa). The symptoms caused by these changes are very slight. They con- tribute to the weakness and wasting. In old age, the atrophy of the nerves is one cause of the lessened sensibility and activity of the skin and its underlying muscles, MoRVA^^'s Disease, Analgesic Paralysis with Whitlow. — (Neuritic type of syringo-myelia.) This is a very rare disease, characterized by a slowly progres- sive paralysis and atrophy of the hands and forearms, with anal- gesia and painless whitlows. It occurs usually in young or middle-aged males. Occupations, such as handling fish, which involve exposure and trauma, pre- dispose to the disease. The symptoms come on slowly, with, at first, severe pains in the arms and hands. The muscles of these parts gradually get 80 DISEASES OF THE NERVOUS SYSTEM. ■weak and atrophy. Ansesthesia and analgesia are present. Usu- ally there is loss of pain and temperature, but not of tactile sense. Whitlows appear which are painless, and one or more of the terminal phalanges may necrose. There is usually a swelling and hard oedema of the parts. Both upper extremities may be affected, and sometimes the feet are also slightly involved. There is sometimes spinal curvature. Hysteria may complicate the affec- tion. The course of the disease is very chronic, but there may be long periods in which the symptoms are quiescent. Pathological examinations always show a neuritis of the parts involved in the disease. In some cases a syringo-myelia has been found. There is, therefore, a Morvan's disease due to syringo-myelia and neuritis, and another type due to a neuritis alone. The prognosis, so far as cure is concerned, is bad, but the dis- ease may remain stationary a long time or improve. The diagnosis is based on the combination of paralysis, atro- phy, loss of pain and temperature but not of tactile sense, and whitlows. Strychnine seems to have stopped the progress of the malady in one case. The treatment in general is only symptomatic. FUNCTIONAL DISORDERS OF THE PERIPHERAL NERVES. These are : 1. Motor forms : tremor, spasm, paralysis. 2. Sensory forms : neuralgia, parsesthesia. 3. Mixed neuroses. 1. Tremor and spasm sometimes occur from peripheral nerve irritation. The cause is over-use of the limbs, and the symptoms are associated with others belonging to the occupation neuroses (see p. 468). Wakixg Numbness (Night Palsy, Recumbext Palsy). This is a disorder characterized by a temporary paralysis of an extremity, with numbness, noticed on first waking, or after lying down for a time. It is a rare disease and little is known of its cause. It occurs in adults and usually in the neuropathic. Sometimes evidence of weak heart or poor innervation of the vessels is present. The symptoms are much like those caused by temporary com- pression of a nerve wlien the leg or arm go to sleep. The paral- ysis is temporary and there is no anaesthesia. It is often very obstinate. DISEASES OF THE PERIPHERAL NERVES. 81 The treatment consists in giving strychnine, mineral acids, and electricity, with occasional courses of bromides; iron and anti- rheumatics may be needed in some cases. 2. Sensory Neuroses. Neuralgia. i)e/z7?,?fww.— Neuralgia is a functional disease characterized by pain in the course of a nerve or of nerves. i^or??i5.— Neuralgias may be idiopathic, t.e., developed sponta- neously, or symptomatic, due to some known toxic influence, re- flex irritant, or organic disease acting on the nerve. Thus a central disease of the nervous system or a tumor pressing on a nerve may cause a symptomatic neuralgia. When, however, there is organic disease of the nerve itself, such as neuritis, the disease cannot be called neuralgia. It is often impossible to draw the lines absolutely. Neuralgias are divided, in accordance with their cause, into the epileptiform, hysterical, reflex, traumatic, gouty, etc. Neuralgias are also divided, in accordance with their anatomi- ical location, into trigeminal, cervico -occipital, brachial, inter- costal, lumbar, crural, sciatic, and visceral. Migraine and headache are not classed among neuralgias. Frequency. — Neuralgias of all kinds make up about ten per cent of the nervous disorders for which the neurologist is con- sulted. The most frequent form is the trigeminal ; next in order come the sciatic, intercostal, cervico-occipital, lumbo-abdominal, brachial, and visceral neuralgias. Etiology: Predisposing Causes. — Neuralgia never affects young children, and, leaving out migraine and headache, it is rarely met with before the fifteenth year. From that time until twenty-five the frequency very rapidly increases. About one- fourth occur betw^een the ages of fifteen and twenty-five; the relative number then slowly decreases to the forty-fifth year, when there is a rapid fall. Neuralgia is very rare in old age. Women are more affected than men in the proportion of five to three (analysis of 887 cases). In New York most cases occur in winter, next in the autumn. More cases occur in temperate cli- mates and in wet and cold regions. Hereditary influence, neurotic constitution, anaemia and de- bility, gouty and rheumatic diatheses, all predispose somewhat to the disease. The exciting causes can be included under the head of toxic agents, infections, exposure, over-exertion, emotional shock, and injuries. Local irritation of nerves may excite neuralgia, direct or reflex in kind. Some help in recognizing the reflex origin of neuralgias and other pains may be gained from the accompanying dia- grams. 6 82 DISEASES OF THE NERVOUS SYSTEM. S>/i7iptoms.— These will be described in detail in the chapters on the special forms. The dominant symptom is, of course, pain. This pain is sharp, dartin^:, boring, stabbing, or burning in character. It comes on in paroxysms of great intensity. In the intervals there may be no pain or it may be simply a dull ache. The pain runs along the course of certain nerves, it is not confined neces- sarily to them, but may be somewhat diffuse. Pain is increased or brought on by cold or heat, or xDressure on the attected part. Fig. 4G.— Diagrams showing the Distribution op the Cerebro-Spinal Strands OF Nerves and the Location op Transferred Pains and Neuralgia. Area I. . . Area II. . Area III. Area IV. Area V. . Area VI. Area VII Strands of Cerebro-Spinal Nerves. Trif^eminus, facial, etc. Upper four cervical. Lower four cervical and first dorsal. Upper si.x dorsal. Lower six dorsal except last. Twelfth dorsal, four lum- bar. Fifth lumbar aud five sa- cral. Distribution. Face and its orifices, anterior scalp. Occipital region, neck. Upper extremities. Thoracic wall. Abdominal wall, upper lumbar, upper lateral thi^^h surface. Lumbar region, upper gluteal, ante- rior and inner thigh and knee. Lower gluteal, posterior thigli, leg. DISEASES OF THE PERIPHERAL NERVES. 83 The skin and nerves are sometimes tender or even exquisitely sensitive. Firm pressure, however, is usually not painful. In about half the cases of long standing, tender x^oi ids may be found which correspond to the exit of nerves from a bony canal or the substance of a muscle or fascia. In rare cases there is ten- derness over the spine corresponding to the point where the affected nerves arise. Besides feelings of pain, there is often a sense of numbness, coldness, tingling, or heaviness of the limb. Vasomotor, secre- tory, and trophic disturbances may occur ; but when these are pronounced, one must suspect neuritis or an organic central dis- ease. Muscular spasm is sometimes present; more rarely there is some muscular weakness. The paroxysms of pain may intermit regularly ; sometimes they come on every day, at the same hour. They are apt to be worse at night. The attacks of the disease often run a course of several weeks or months, and in some forms they last for years. Pathology. — Many cases that used to be called neuralgia are now known to be forms of neuritis, e.g., sciatica and brachial neural- gia. Other forms are sometimes due to impaired nutrition of the nerves from an obliterating arteritis (tic douloureux) ; still others are due to the irritation of nerves from the diathetic poison of gout, rheumatism, and diabetes, or to extrinsic poisons, such as alcohol, lead, and arsenic. In these cases the sensory nerves of the nerve sheaths (nervi nervorum) are affected. There remain many cases in which the trouble shifts from one locality to an- other, or in which no special local or general irritation can be discovered. In these cases we assume that the pathogenic focus is the spinal ganglia or the sensory cells of the posterior horns of the spinal cord. Lesions and irritations of the sensory path above the sensory cells referred to rarely cause pain. There are some forms of neuralgia which may be called " rem- iniscent '' or " hallucinatory.'" The patient, who is an impression- able and sensitive person, has had a genuine cause for neuralgic pains; but this, after lasting some time, has ceased, while the painful impressions continue to remain in the cerebral cortex. The neuralgia is a morbid habit of feeling pain. Such neuralgias are promoted often by the use of morphine. The Diagnosis.— This depends on the fact that neuralgic pains are shifting, paroxysmal, follow the course of nerves, are accom- panied often with tender points and not accompanied with signs of organic nerve disease, such as paralysis and anaesthesia and tenderness over the nerve trunks. Thermic sensations of burning or coldness are rarely neuralgic, but are due to neuritis. The 2)rognosis\s good, except for the reminiscent neuralgias, 84 DISEASES OF THE NERVOUS SYSTEM. the neuralgias of hysterical and neurasthenic persons, who are thoroughly ananiiic, debilitated, and broken down morally and physically. The neuralgias of the degenerative period of life are also very obstinate. The treatment will be discussed under special heads. The Parjesthesic Neurosis (Parjesthesia, JN'umb Hands). This is a not uncounnon disorder, characterized by very per- sistent symptoms of numbness, formication, or burning, with little or no jmin, and with or without motor weakness. It is a trouble allied to the waking numbness just described. Etiologij.—The disease occurs in adult life, and oftenest at or after middle life. Women are oftenest affected, and especially those of nervous temperament, with dyspeptic and rheumatic tendencies. The symptoms are not seen in children or in the aged. They are more marked in the warmer season, and women who wash a good deal are somewhat more subject to them. The dis- order is more frequent in cities. &i/niptoms. — The patients have feelings of numbness, prickling, heaviness, usually in both hands, extending a little way up the forearm. The sensations are, as a rule, diffuse, but may follow the distribution of a nerve, especally the ulnar. In other cases the numbness is sharply limited to the finger-tips or the second and third phalanges. There is no actual pain or tenderness, nor is there any anesthesia, cutaneous or muscular. Instead of or with the numbness there may be burning sensations, especially felt in the palms or soles. There is often a slight degree of paralysis, but rarely any decided vasomotor or trophic changes. The symp- toms exacerbate, being worse at certain periods of the day, usu- ally in the morning. Tliey may increase at night and prevent sleep. The arms are oftener affected than the lower extremities ; and the disease never takes a hemiplegic form, though one arm may be alone involved. The scalp and ears may be involved, though always in a minor degree, the patient complaining of sensations of heat, prickling, flushing, and vertex pressure. Sometimes the knee jerk disappears. The symptoms cause a condition of men- tal unrest and nervousness which add to the sufferings materi- ally. Evidences of overwork, of dyspepsia and constipation, of antemia, or of muscular rheumatism will generally be found. The urine is usually rather light in color and specific gravity (1010 to 1018), slightly cloudy, with excess of phosphates and oc- casional excessive discharges of urates. Pathology. — The pathology is based upon the similarity of the symptoms to those in mild or incipient cases of multiple neuritis DISEASES OF THE PERIPHERAL NERVES. 85 and upon the effects of drugs in relieving symptoms. It is be- lieved that the peripheral nerves are being irritated by some poison circulating in the blood. Co-operating with this are nerves naturally over-irritable, or made so by anaemia, hypertemia, and exposure to cold. Diagnosis.— This disease is to be distinguished from hysteria, neurasthenia, and central organic diseases of cord or brain. In hysteria the symptoms are less diffuse, regular and bilateral, while some anaesthesia is rarely absent. Parsesthesise are very common in neurasthenia, and in some cases here they are due, no doubt, to peripheral irritation. In neurasthenia, the parsesthesise are, however, generally in one extremity, less diffuse and as a rule more temporary. There is no motor weakness, and the head and spine are usually complained of more than the arms or legs. Waking numbness and night palsy are intermittent disorders, disappearing within a short time after waking or rising from a recumbent posture. The numbness that is felt with digiti mortui and Raynaud's disease is accompanied with spasm of the blood- vessels and whitening of the fingers. Prognosis and Course. — The disease, if not treated, runs a course of several months, with some intermissions and relapses. It may disappear, to return the next year. It never progresses to any serious condition, and is in almost all cases eventually cured. Treatment. — The patient should receive alkalies, with bro- mides, pepsin, iron, and strychnia. The f aradic current, massage, and stimulating liniments are useful. Rest and removal from ex- citing causes, such as exposure, are also indicated. 3. Neuroses of Mixed Origin Affecting the Extremities (Acro-Neuroses). There are certain nervous disorders which affect the extremi- ties. They involve the motor, sensory, vasomotor, secretory, and trophic nerves in various degrees. They are sometimes of central and sometimes of peripheral origin ; but as the pathology is lit- tle known, they are best given a clinical classification and placed under the head of peripheral diseases. The acro-neuroses here considered are : Raynaud's disease and digiti mortui. Podalgia, luxation neuralgia. Erythromelalgia. Symmetrical Angio-Neurotic Gangrene, or Raynaud's Disease. (Abortive Form Known as Digiti Mortui.) Symmetrical gangrene or Raynaud's disease is a rare affection characterized by spasm of the vessels of the extremities, coldness, pallor, waxiness of fingers or toes, or by blueness, mottling, swell- 86 DISEASES OF THE NERVOUS SYSTEM. ing, pain, followed often by a dry gangrene of some of the fingers or toes. Etiology. — The disease occurs usually in children and young adults. Women are affected oftener than men. Anaemia, and chlorosis, and neurasthenic states predispose to it. Malarial in- fection, acute infectious fevers, menstrual disorders, fright, oc- cupations that lead to exposure, such as washing, are causative factors. Diabetes and syphilis are also put down as causes. The disease comes on rather suddenly and affects oftenest two or three fingers of both hands. In its early and mild degree there is simply a coldness, numbness, and waxy pallor of the fingers. The skin looks shrunken. There is shght anaesthesia. They feel Fig. 47.— Hand and Foot in the Ga>-grenous Stage of Raynaud's Disease. as if dead. After a few hours this passes away, but returns again and may finally become an almost constant condition. Begin- ning in one or two fingers, it may finally involve all. The toes, tip of the nose, and ears may be similarly affected, though this is rare in the milder form. Exposure to cold, even slight, is the common excitant of this form of the trouble, which is commonly known as " digiti mortui." " dead fingers," or " local syncope." In severer grades the fingers become blue, swollen, and there are burning sensations and much pain, but no anaesthesia. This condition is known as that of " local asphyxia," and it is usually followed by gangrene. In the gangrenous stage small blisters appear on the distal phalanges, which fill with bloody serum, then dry up, and beneath DISEASES OF THE PERIPHERAL NERVES. 87 the scab ulceration begins, which is shallow and soon heals, leav- ing a scar. The process then stops. In very rare cases the whole tip of the finger or toe, including the bone, becomes involved. The process as stated may attack the ears, lips, tongue, and even parts of the trunk. Along with this gangrenous process there is often a hsematuria. The dead-finger trouble may last but a few days or weeks, or it may continue for months. The gangrenous stage lasts about three weeks. It lasts longer if it comes on in one finger after the other. The disease is one of months, and it is liable to recur. The diagnosis must be made from senile gangrene, frost-bite, ergot-poisoning, alcoholic neuritis, endarteritis, and obstruction of nutrient vessels. Pathology. — A neuritis has been found in some cases of so- called Raynaud's disease, but this is secondary. In a few other cases there has been found an obliterating endarteritis (Jacoby). The trouble is in some cases apparently functional and due to the combination of an over-sensitive nervous system and some irritant, such as impoverished blood, malaria, or other toxic agent, which causes spasm of the peripheral vessels. Prognosis. — The cases usually get well. In only the rarest in- stances has death occurred, and then from some complication. Treatment. — Galvanism to the spine and limbs, warm applica- tions, anodynes, tonics, are indicated. Nitroglycerine, the iodides^ chloral may be tried. No specific is known. Paixs i:?^ the Feet of Various Origin (Podalgia). 1. Pains of diathetic, toxic, or neuralgic origin. 2. Pains of reflex origin. i| 3. Pains of mechanical origin. 1. Pedal pains occur in gout, rheumatism, lithaemic states, sjq^hilis, tabes, chronic alcoholism, and diabetes. The pains of latent gout, according to Anstie, are generally located in the dor- sum of the foot. Those of chronic alcoholism have been observed to occur in the wrists and ankles. Those of lithsemia are usually in the heels. In syphilis a node can generally be discovered. A difTerential diagnosis is therefore possible. Erythromelalgia {red neuralgia of the feet, congestive neu- ralgia) is a disease aff'ecting the feet chiefly, and characterized by burning pains and congestion of the parts. The disease occurs usually in men in middle life, after a low fever or severe physical exertion afoot. The disease begins in the ball of the foot or the heel with a pain, which Is worse at night. It increases until nearly the whole sole in the distribution of the plantar nerve is involved, and the 88 DISEASES OF THE NERVOUS SYSTEM. pain, though worse at night, is ahuost continuous. It is much increased by exertion, the feet become very tender, and standing or walking is most painful. Meanwhile there has developed with the pain a flushing of the part upon exertion. In bad cases the parts most atiected are continuously marked by a dull, dusky, mottled redness. The hands may be slightly affected. Slight injuries may cause blisters and even ulcerations. The congestion usually disappears in the horizontal position, and this also relieves the pain. The symptoms are worse in warm weather. The disease is very chronic and, though not dangerous to life, makes life very miserable. Patliology.—ln the cases of erythromelalgia as described by Mitchell and others, there is : (1) A vasomotor neurosis; (2) a plan- tar neuritis; and (8), in rare instances, spinal cord disease. The diagnosis must be made from alcoholic and gouty parses- thesia, podalgia, local disease of bone and ligaments and from reflex pains. Treatment.— WQYSition of the feet and applications of cold give temporary relief. Faradization has sometimes given help ; oftener it has not. There is nothing known which gives perma- nent relief. The physician must rely ujDon rest, bandaging, cold, anodyne applications, hydrotherapy and tonics. The salicylates, turpentine, and mineral acids with strychnia may be given. 2. Reflex or referred pains in the feet are very common. The cause is usually some form of irritation of the genito-urinary tract, such as gonorrhoea, stricture of the urethra, vesical calcu- lus, cystitis, or renal calculus. It may be a misplaced or pregnant uterus. 3. Pains of mechanical origin : (a) Morton's neuralgia. {h) Tarsalgia, or policeman's disease. (a) MoRTOX's NEURALGIA, SO Called, is a neuralgia affecting the metatarso-phalangeal joint of the third and fourth toes, and is due, it is thought, to a slight luxation, with consequent joressure on a digital branch of the external plantar nerve. It sometimes affects other toes, however. It is not always due to a luxation. Incipient fiat-foot may cause it, and I have seen a typical case in a pregnant woman, disappearing after confinement. The trouble occurs generally in Avomen, and if there is a luxation the cause is external injurj^ or shoe-pressure. Treatment is not very satis- factory. It should be directed to giving rest to the foot, and the avoidance of lateral pressure on the joints by wearing a broad- «oled shoe with support to the arcli of the foot. Support may also be given by a broad flannel bandage. Amputation of the toe has cured one case. ip) Tarsalgia {policeman's disease) is a neuralgic affection, DISEASES OF THE PERIPHERAL NERVES. 89 due probably in most cases to an incipient flattening of the foot and stretching of the plantar ligaments. Some have ascribed it to a deep-seated contusion of the adipose cushion covering the os calcis. Probably the condition varies somewhat in difT3rent cases. It is observed in persons who have been in the habit of going barefoot, and have then gone into the army or taken civil posi- tions obliging them to stand or walk a great deal. It occurs in the policemen of Paris, and but few cases have been seen in this country. This is due to the difference in the shoes and in the gait of American and Parisian guardians of the peace. The name tarsalgia was given by Duchenne. Treatment, medical or surgical, seems to do little for the dis- order, which is very chronic. Patients are better in cold weather, and when resting the feet. Leeches, the cautery, the iodides, and broad shoes with rubber heels are serviceable. Tumors of x^erves. These consist of : 1. Nerve hyperplasia. 2. True neuromata. (Single. - Tvr t* ' . o -r. 1 X h ( Malignant. 3. False neuromata. \ t., i. . ■, , -d • ; Multiple, i Benign. 1. Hyperplasia or hypertrophy of nerve trunks is very rare. Generally the increase in size is, in fact, due to increase of the interstitial connective tissue. Sometimes there is an increase in the number of fibres and thickening of the myelin sheath. 2. Trice neuromata are also very rare, and occur almost exclu- sively on spinal nerves. In some there is an increase in medul- lary fibres ; in others only an increase of non-medullated fibres, i. e. , only the axis cylinders and neurilemma increase. They occur either singly or multiply. Multiple neuromata are generally of a neuro-fibromatous character. Neuro-flbromata when multiple may affect the subcutaneous nerves and form growths known £i& fibroma molluscum. Nerve fibres united in a mass by hyperplastic connective tissue form what are called plexiform neurofihromata. Multiple neu- romata may be true neuromatous growths. True neuromata are usually small, ranging from 1 cm. (two- fifths of an inch) to 6 cm. in diameter. They may be much smaller or larger. Neuromata are usually few in number, or at least there is only a local multiplicity of tumors. Multiple (true) neuromata may, however, be very numerous. Gowers estimates in one case that as many as one thousand were present. Even larger numbers have been observed. 90 DISEASES OF THE KERVOUS SYSTEM. 3. False Neuromata.— This term is applied to the various nerve tumors in which a fibroma, myxoma, ghoma, sarcoma, carci- noma, or syphiloma grows upon or in the nerve, Fibro-neuroma is the most common form ; glio-neuroma has been observed on the auditory nerve. Syphiloma occurs only on the intra-cranial or intra-spinal nerves. Carcinoma of nerves may be primary, but is generally secondary, and is of scirrhous or medullary type, rarely the colloid. Leprous neuritis sometimes forms neuro-fibromatous swellings. Tuhercula dolorosa are simply small false neuromata situated subcutaneously on the ends of the sensory nerves. They vary much in histological structure. Malignant Neuromata. — A few cases, about thirty in all, have been observed of multiple malignant neuromata. Trauma and hereditary influence are the etiological factors. The great nerve trunks are of tenest affected, the median, sciatic, and crural rank- ing first. The tum.ors start from the perineurium; they are at first spindle-shaped, and may grow very large. Sarcomatous cells are of tenest found in them ; but they may be myxomatous, fibrom- atous, or mixed. Etiology. — Three general causes exist for the production of neuromata, viz. • 1. A hereditary or a neuropathic predisposition ; this tends to cause the true, the multiple, and the plexif orm neuro- mata. 2. Injuries, surgical operations; these cause especially the fibro-neuromata of which the amputation neuroma is an example. 3. Diathetic, e.g.^ tubercular, influences and whatever produces the various tumor formations, sarcoma, carcinoma, form the third etiological factor. Neuromata of the plexiform type are often congenital. Multiple neuromata may develop early in life. Men are far more subject to multiple neuromata than women. Symptoms. — Neuromata often cause no symptoms. Perhaps the most frequent evidence of their presence, however, is pain and some tenderness. The pain is exacerbating, and may be stopped sometimes by pressure on the nerve above the tumor. Paraesthesia, anfesthesia, paralysis, and reflex spasm may be pres- ent. Some forms of intractable headache are possibly due to multiple neuromata. Multiple and plexiform neuromata cause symptoms less often than a single larger neuroma. A neuroma on the pneumogastric or other splanchnic nerve may cause severe symptoms. Multiple (true) neuromata may last for years and cause no serious inconvenience. Malignant neuromata cause al- ways such symptoms as would naturally follow irritation and compression of a nerve. The diagnosis of neuroma can only be certainly made when the tumor can be felt. In other cases, by exclusion a fairly cer- tain conclusion may be reached. DISEASES OF THE PERIPHERAL NERVES. 91 True neuromata are often multiple ; the false rarely. Idiocy, heredity, neuropathic constitution, scrofula, would all favor the view of the disease being a true neuroma. The treatment is essentially surgical. Internal medication and external applications are of little value. Strong galvanic cur- rents, mercury, and the iodides in large doses may be tried in true neuromata and fibro-neuromata. Both true and false neuromata may return after extirpation. CHAPTER TIL DISEASES OF THE SPECIAL NERVES. The peripheral nerves are the cranial, the spinal, and the off- shoots of the cranial and spinal, known as the sympathetic. I shall take u}) first the cranial nerves. The Craxial ^s^eryes. These consist of twelve pair, viz. : 1. The olfactory. II. The optic. III. The motor oculi. IV. The patheticiis or trochlear. V. The trigeminus. VI. he ab- ducens. VII. The facial. VIII. The auditory. IX. The glosso- pharyngeal and nerve of Wrisberg. X. The vagus. XI. The ac- cessory vagus or spinal accessory. XII. The hypoglossal. The first two are not strictly nerves, but rather parts of the brain. The remainder are analogous to spinal nerves, and arise from the mid and hind brain. AxATOMY AXD PHYSIOLOGY.— I. The olfactoi^ynerve consists: 1. Of [peripheral fibres which are distributed to the superior and middle turbinated bones and upper part of the septum. They are connected with olfactory cells lying in and beneath the mu- cous membrane. They are about twenty in number on each side. They are non-medullated. They pass up through the cribriform IDlate of the ethmoid bone and enter the olfactory bulb (Fig. 48). 2. The olfactory bulb is in man a rudimentary organ containing a few nerve cells,peculiarbodies,perhapsofneurogha tissue, called glomeruli, connective tissue, and nerve fibres. It is analogous to a spinal ganglion or to a nucleus of origin of a nerve in the cord or medulla. 3. The olfactory tract, wrongly called a nerve, is composed of cortical nerve cells and of nerve fibres. It has three roots, the lateral, middle, and mesial. In man, only the lateral is of im- portance. This passes along the margin of the anterior perforated space to the uncinate gyrus, hippocampus, and cornu ammonis. Some fibres also pass inward into the anterior commissure, connect- ing the tract and cortex of the opposite side (Fig. -18). -i. The fourth DISEASES OF THE SPECIAL NERVES. 93 portion of the olfactory apparatus is the uncinate gyrus, hippo- camiDus, and cornu ammonis, and this part is the cortical seat of smell. Further connections by the fimbria, fornix, corpora mam- millaria, and optic thalami are thought to exist (Hill) ; also direct connections with the basal gan- glia. The olfactory fibres do not decussate like the other nerves. Fig. 48. Fig Fig. 48.— Diagram of Olfactory Nerves and Connections. Fig. 49,— The Optic Nervb and its Central Connections (modified from Obersteiner). R, Ketina, darkonthesideconnected with left hemisphere; Ko, optic nerve; C/i, chiasm; Tro, optic tract; CM, Meynert's commissure; CG,Guddeii's com- missure; r/to, thalmus; Cgl, corpus genie, ext.; Qa, corpor. quad.; Ss, optic radia- tions; Co, occipital cortex; iwi, mesial lemniscus. (The shading of the retina and visual field should just reach the vertical lines.) The sense of smell is rudimentary in man, yet it is still the sense by which we can appreciate the most attenuated matter ; for the trillionth of a grain of mercaptan, which awakens a sensation in the mind, has weight and dimensions so infinitely minute as to be quite beyond the power of the imagination to grasp. According to Valentin, we can perceive rsohw^i of a grain of oil of roses. According to Fischer and Penzoldt, one can per- ceive ^TeooV^^Tnr of a grain of mercaptan. I have found that one can perceive the odor from 4 cm. of a solution of oil of cloves 1 94 DISEASES OF THE NERVOUS SYSTEM. to 100,000. Matter to be perceived as odor must be in a gaseous form. Odorous sensations co-operating with taste sensations form " flavor." Variety in odorous sensations depends probably upon the rapidity of molecular vibrations as in the case of light ; and substances having similar relations in vibration have similarity in odor (Haycraft). Males have a more delicate sense of smell than females (Xicolls and Bailey). The keenness of the olfactory sense is lessened in the insane and criminal classes. II. The optic nerve, so called, is really a central tract of the brain, like the olfactory nerve. Traced from without inward, we find the following parts : 1. The rods and cones, with the filaments connecting them to the ganglionic cells of the retina, really form all that there is of a peripheral optic nerve. These rods and cones number about 3,3G0,000. 2. From the ganglionic cells of the retina, fibres collect and pass into the cranial cavity as the optic nerve. This nerve con- tains about 438,000 fibres. They are smaller than other nerve fibres, and are distinguished from them by having a neuroglia imbedding substance and by having no neurilemma. 3. The optic nerves pass to the optic chiasm, where about one- third of the fibres cross, in man. In lower animals the decussa- tion is greater. After leaving the chiasm, the fibres form the optic tract. This tract curves up and back around the crus cerebri, and divides into a lateral and mesial root. 4. These roots connect with the external geniculate body, the anterior tubercles of the corpora quadrigemina, and the posterior ganglion of the thalamus or the jDulvinar. These ganglia are called the primary optic centres. Through the anterior tubercles of the corpora quadrigemina, and by other means, the optic nerve is con- nected with the oeuiomotor nerve, and thus reflex movements of the pupils, lids, and eyeballs are brought about (Fig. 49). 5. From these primary optic centres, fibres enter the posterior part of the internal capsule, curve up and back toward the occip- ital lobes, forming the optic radiations of Gratiolet {8s). 6. They are finally distributed to the cortex of the occipital lobe, and in man chiefly to the cuneus and the upper end of the first occipital gyrus. It will be seen that each retina is connected with the occipital lobe of both hemispheres. It is further known that the outer or temporal half of each retina is connected with the occipital lobe of the opposite hemisphere, and the inner or nasal half of each retina with the occipital lobe of the same side. Further, the upper part of each retina is connected with the lower half of the cuneus, and vice versa (Fig. 49). Other connections exist by which the optic centres on the two DISEASES OF THE SPECIAL NERVES. 95 sides are connected with each other and with other cranial nerves in the medulla. The optic nerve is a nerve of special sense of vision and has no other function except that of an excito-reflex character. III., IV., VI. The motor nerves of the eye are: {a) The third or oculo-motorius, supplying the internal supe- rior and inferior recti, inferior obliquus, the levator palpebr^e, the ciliary muscle, and constrictor of the iris. (&) The fourth or trochlearis, supplying the superior oblique. OVIN Fig. 50. Fig. 51 . Fig. 50.— Diagram showing the Arrangement of the Ncclei op the I\Iotor Nerves of the Eye, and the Decussations of the Fourth and Internal Rec- tus Branch of the Third Nerve. Fig. 51.— Diagram showing the Probable Relations of the Nuclei op the Sixth and op the Internal Rectus Branch op the Third to the Brain. (c) The sixth or abducens, supplying the external rectus. (cZ) The sympathetic, consisting of fibres from the upper cer- vical nerves to the dilators of the iris, to its blood-vessels, and to Miiller's muscle. 2. Motor fibres from the nucleus belonging to the third nerve and running out with the fibres of the seventh (Mendel), supplying the orbicularis palpebrarum. The third and fourth nerves arise from a series of nuclei in the floor of the aqueduct of Sylvius. They leave the brain at the anterior edge of the pons. They run in the cavernous sinus and enter the orbit through the sphenoidal fissure. The sixth nerve arises from a nucleus in the floor of the fourth ventricle. It emerges at the posterior edge of the pons, runs in 96 DISEASES OF THE NERVOUS SYSTEM. the cavernous sinus, and enters the orbit through the anterior lacerated foramen. The nuclear gray matter from which these nerves arise is made up of a series of nests of cells, and each pair supplies a differ- ent set of muscles of the eye, as shown in the diagram. The nucleus of the sixth lies farther back in the floor of the medulla, but it belongs to the same serial deposit of gray matter, and represents the continuation of the anterior horn of the spinal cord (Fig. 51). The motor nerves of the eye, third, fourth, and sixth, are closely connected with each other and other nerves by a long commissure, the posterior longitudinal bundle. The fibres of the third and fourth nerves pass to their nuclei on the same side, then decussate and pass up in the inner part of the crusta to the lower i)art of the central convolutions of the cortex. A few fibres decussate and enter the nuclei of the oppo- site side. They are connected with the internal rectus nucleus. The fibres of the fourth nerve almost entirely decussate, run- ning forward a long distance before they finally reach their nuclei. Thus it api3ears that the abducens is the only cranial nerve except the optic which largely decussates before reaching its nucleus. However, those fibres of the third which sui^ply the internal rectus also decussate, as already stated. The arrangement of the nuclei is believed to be about as fol- loAvs, the upper on the list being anterior : Median line, f Sphincter iridis, Ciliarius. ! Levator palp., Rect. int. ■ ^ ' j Rectus superior, Rect. inf. [^ Obliquus inf. IV. X. - Obliquus superior. VI. y. - External rectus. In order to understand the peculiarities of eye palsies, to be described later, the relations of the sixth to that nucleus of the third nerve which innervates the internal rectus must be under- stood. In turning the eyes to one side, these two nuclei and their nerves act together, causing the external rectus of one eye and the internal rectus of the other to contract at the same time. The impulse from the brain which does this acts first upon the sixth, and through this upon the -internal rectus nucleus of the same side. The fibres from this nucleus cross and emerge in the third nerve fibres of the opposite side to the sixth nerve nucleus. This can be better understood by the diagram. Fig. 51. 1 DISEASES OF THE SPECIAL NERVES. 97 Thus lesions in the brain (at a) cause paralysis of the sixth nerve of the opposite side and internal rectus of the same side. The eyes turn toward the side of the lesion. Lesions in the pons (at b) cause paralysis of the sixth on the same side and internal rectus nucleus of the opposite side. The eyes turn away from the side of tlie lesion. The eye muscles move the eyeball in the following way; The superior rectus elevates the eyeball. The inferior oblique rotates out and up. The inferior rectus depresses the eyeball. The superior oblique rotates out and down. jV. suprairoch. Ohl. swper S. supraorb. Rect. sup, Levator, p.- N- infrafrroch. Pecf, rved, iU #■* Red. inf. N. supramax. Fig. 52.— The Attachment of the Eye Muscles to the Globe (Merkel). The superior and inferior oblique, acting together, rotate in- ward. The external rectus rotates outw^ard. The internal rectus rotates inward. The rectus internus, rectus superior, obhquus inferior, rotate upward and inward. The rectus internus, rectus inferior, obliquus superior, rotate downward and inward. The rectus externus, rectus superior, obliquus inferior, rotate out and up. The rectus externus, rectus inferior, obliquus superior, out and down. The movements of the eyeball are made by the simultaneous action of several muscles. Most of them act as their names indi- cate. But the oblique muscles help to depress and elevate, and 7 98 DISEASES OF THE NERVOUS SYSTEM. then help to rotate in or out according as the internal or external rectus is acting The cortical centres for the eye muscles are not positively known. Lesions in the inferior parietal lobule sometimes cause paralysis of the third nerve. Lesions of the posterior part of the prefrontal lobes also sometimes cause eye palsies, esi^ecially con- jugate deviation. As the optic nerve is the special sensory nerve of the eye, so the third, fourth, sixth, and part of the seventh nerves are the motor nerves. By means of the optic nerve and its receptive and refractive apparatus, the form, color, movement, and, to some extent, rela- tions and distance of objects are determined. The motor nerves I Dental Fig. 53.— The Superiok Maxillary Division op the Trigeminus (Young- Baker). adjust the eye to near and distant objects, inform us as to size and distance, and enable us to follow moving objects and to shift the gaze readily. They also assist in protecting the eye against injury. V. The trigeminus or fifth nerve is one of the most extensively distributed and most delicately sensitive nerves of the body. Its sensory branches represent the atrophied and lost sensory roots of the third, fourth, sixth, seventh, and twelfth cranial nerves (Gaskill). It has a most extensive primary origin by three principal roots : (1) The ascending, which begins in the upper part of the cervical cord at the level of the second cervical segment ; (2) the descend- ing, which rises in the graj^ matter about the aqueduct of Sylvius as high up as the anterior corpora quadrigemina; (3) the middle, which arises from a nucleus in the pons near the level of the DISEASES OF THE SPECIAL NERVES. 99 nerve's exit. The ascending root is mainly sensory; the descend- ing, sensory and trophic ; the middle, motor and sensory. The gray matter from which the trigeminus arises reaches the whole length of the pons and medulla, and is coextensive with the origin of all the other cranial nerves (Fig. 57). Hence the frequency with which its disorders are complicated with those of these nerves. Its cortical origin is jirobably in the lower part of the pre- and post-central convolutions. The trigeminus supplies sensation to the face, nose, the frontal and maxillary sinuses, the teeth, the palate, tongue, and part of the upper pharynx ; also to the scalp as far back as the vertex Gasserian sauglion Foramen oval Fig. 54.— The Inferior Maxillary Division of same (Young). and to the external auditory meatus. It giv^es sensation also to the anterior three-fourths of the dura mater, the falx, and probably the tentorium. The pia and arachnoid are not sensitive. The posterior fossa and the occipital i)art of the dura mater are sup- plied by the vagus. The trigeminus also supplies the above-named parts with trophic, vasomotor, and secretory fibres. The vaso- motor fibres are brought to it from the medulla and cervical spinal cord via the sympathetic ; the secretory fibres have the same origin. Both are reinforced by the four ganglia Avith which this nerve are in close connection. An exception is to be made of the lachrymal fibres which are brought by the motor nerves of the eyeball. The trigeminus supplies motion to the muscles of mastication, viz., the two pterygoids, the temporal, masseter, mylo-hyoid, and anterior belly of the digastric. 100 DISEASES OF THE NERVOUS SYSTEM. VII. The facial nerve has its primary origin in a single nucleus deeply situated in the lower part of the pons. It belongs to the same series of nuclei as the motor nuclei of the vagus, glosso- pharyngeal, and of the spinal accessory; in other words, it is a l^rolongation of the lateral horn of the spinal cord. It has not a nucleus common to it with the sixth, as is usually stated. Those fibres of the nerve which go to the orbicularis, however, appear to come from a nucleus in the third nerve series and to reach the knee of the facial by the posterior longitudinal bundle (Mendel). Tlie deei? fibres of the facial take a tortuous course, l^assing inward, dorsally, then curving down and out around the nucleus of the sixth nerve. The cortical origin of the seventh is in the lower part of the central convolutions, especially the precentral. The fibres pass down in the crusta at the inner side of the pyramidal or motor tract. They decussate and reach the nucleus. The nerve has its exit at the posterior edge of the pons, external to the sixth nerve. It then has to take a long course through a bony canal, during Avhich it receives taste fibres from the second branch of the trigeminus (or the glosso-pharyngeal). These fibres leave the nerve as the chorda tymi^ani, and join the lingual branch of the fifth nerve to supply taste to the anterior two-thirds of the tongue. The facial nerve supplies'motion to all the muscles of the face; to the stapedius, stylo-hyoid, buccinator, and platysma myoid. It also contains trophic and secretory fibres. It does not supply, however, the muscles of mastication. The taste fibres of the facial nerve apparently come in many cases from the second branch of the fifth via MeckeFs ganglion, the large superior petrosal nerve, and geniculate ganglion. In other cases they come from the glosso-pharyngeal nerve via the ganglion petrosum, Jacobson's nerve, tympanic plexus, and genic- ulate ganglion. Some think that the intermediary nerve of Wris- berg, which arises in the upper joart of the glosso-pharyngeal nucleus and connects with the geniculate ganglion, carries taste fibres to the facial. YIII. The auditory or eighth cranial nerve has two different parts. One portion x^asses to the cochlea and utricle and saccules ; it has to do Avith the sense of hearing ; the other goes to the semi- circular canals, and has to do with that sense by which Ave ap- preciate position of our body and its relations to space. The. eighth nerve is thus an auditory and a space-sense nerve. The auditory fibres enter the medulla by two roots, a lateral or posterior and a median or anterior. The lateral root has mainly auditory fibres. The space-sense fibres enter chiefly by the median root. These roots are connected with three nuclei, viz. ; (1) The chief nucleus (dorsal, central, inner nucleus); (2) the DISEASES OF THE SPECIAL NERVES. 101 Carotid Spheno palatine G. larg:e-celled nucleus (Deiter's) ; and (3) the accessory nucleus (ven- tral, anterior, lateral). The chief nucleus (1) is a large mass of gray matter composed of small nerve cells and lies superficially just beneath the floor of the fourth ventricle. The large-celled nucleus (2) lies to the outer side of and below it. The accessory nucleus (3) lies in the substance of the lateral root, and between it and the median root. The lateral root is the one coming chiefly from the cochlea, and is, as stated, mainly a nerve of hearing. It is connected most ex- tensively with the accessory nucleus, but also with the other nuclei. Through the acces- sory nucleus, it con- nects bj^ a few fibres with the superior olives mostly of the opposite side; thence fibres pass up through the lateral lemniscus, to the posterior corpora quadrigemina ; thence to the cortex of the first and second convolutions of the tempero- sphenoidal lobes. Other fibres pass up directly through the lemniscus and the tegmental or sensory tracts to the cortex of the temporal lobes. Connections are numerous, also, with other cranial-nerve nuclei. The lat- eral root also sends fibres to the chief nucleus and (via the stria? acusticse) into the raphe, and thence to the f ormatio retic- ularis and sensory tract. These fibres go also to the posterior tubercles of the cor- pora quadrigemina and thence to the cortex of the temporal lobe. The median root is connected chiefly with the large-cell nucleus (2), but also with the chief nucleus (1). From these nuclei fibres pass up in the posterior cerebellar peduncle through the direct sensory tract of the cerebellum to the roof nucleus or the emboli- form and globose nuclei. IX. The glosso-pharyngeal nerve arises from three nuclei in Glosso-Pharyngeal Nerve (Young). 102 DISEASES OF THE NERVOUS SYSTEM. the medulla: (1) The sensory or perhaps visceral nerve cells an- alogous in character to those of the column of Clark in the spinal cord. (2) A true sensory nucleus consisting of a long, thin de- posit of gray matter continued from the posterior horn of the spinal cord, and associated with a strand of nerve fibres called the ascending root of the vagus and pharyngeal nerves or respi- ratory bundle. (3) A motor nucleus Avhich is called the nucleus ambiguus, and is a continuation of the lateral horn of the spinal cord (Hill, Gaskill). The nerve, therefore, has inotor, sensory, and j^robably visceral fibres. It supplies general sensation to the tympanum and pharynx (in connection with the vagus) and upper part of the larynx; special sensation of taste to the posterior third of the tongue, and motion to the pharyngeal muscles in connection with the vagus. Its cortical re^jresentation so far as taste is concerned is in the hippocampal gyrus. The nerve gives very sensitive reflex fibres to the pharynx and is important in the reflex act of deglutition ; it also carries sensations of nausea from pharyngeal irritation. X. The vagus nerve arises from three nuclei in a way entirely similar to that of the glosso-pharyngeal. 1. The sensory and visceral nucleus. 2. The motor nucleus, called the nucleus ambiguus, which is a prolongation upward of the lateral horn, and is common to it and the glosso-pharyngeal. 3. The sensory nucleus, which gives off the fibres of the as- cending root of the glosso-pharyngeal. The nerve is closely connected with the glosso-pharyngeal above and with the accessory (eleventh) nerve below. The accessory portion of the spinal accessory is practically a part of the vagus, and both in mode of origin and function re- sembles it closely. It arises from a nucleus which lies in the floor of the fourth ventricle, and is continuous brainward with that of the vagus. It consists of small cells giving origin to fibres tha.t are small in size and have sensory, vasomotor, visceral motor, secretory, trophic, and excito-reflex functions. The vagus and accessory part of the eleventh together have an extraordinarily wide distribution and diversity of function. X. First they contain motor, inhibitory, and vasomotor fibres. These fibres go to the pharynx, larynx, trachea, and bronchi ; to the oesophagus, stomach, small intestines, and spleen. 2. Sensory fibres, which go to the occipital and transverse sin- uses and dura mater of the posterior fossa, to the external audi- tory meatus in part, to the pharynx, larynx, and trachea, and to the oesophagus. 3. Excito-refiex fibres, which go to the lungs and heart, DISEASES OP THE SPECIAL NERVES. 103 stomach, and to other or<^ans mentioned as supplied by the vagus with sensation. These reflex fibres stimulate or inhibit the vasomotor centre, the respiratory rhythm, and the cardiac rhythm. They also excite reflexly deglutition and respira- tory movements. The secretory fibres go to the respiratory tract, a3Sophagus, stomach, and pancreas and small intes- tines. C a r d i o -in h i b i t o r y fibres go to the heart, while reflex accelerating fibres and inhibiting fibres go to the lungs. The accessory nucleus supplies the laryngeal adductors and the cardio- inhibitory fibres. XI. The spinal jmrt of the spinal accessori/ arises from the lateral horn and outer part of the anterior horn of the spinal cord. Its fibres of origin extend down as far as the fourth or fifth cervical roots. The fibres unite in the cranium and pass out through the pos- terior lacerated foramen in the same sheath as the vagus. After their exit from the skull, they di- vide into an internal and external part. It is the external branch which contains the fibres of spinal origin. The nerve receives some sensory fibres from the first and sometimes from the second cervical nerve. The terminal branches receive motor fibres from several cervical nerves. The spinal accessory contains large and small or visceral fibres. The spinal part contains only the large fibres. Fig. 56.— The Vagus and Spinal Accessory Nerve (Young). 104 DISEASES OF THE NERVOUS SYSTEM. The spinal accessory supplies the sterno-cleido-mastoid almost exclusively, but only the upper part of the trapezius ; the rest of this muscle is supplied by the cervical and dorsal nerves. The sterno-cleido-mastoid, when innervated, draws the chin up and over toward the opposite side. The upper fibres of the trapezius draw the head back slightly and down toward the same side. Physiologically the spinal part of the accessory nerve is one of the motor cervical nerves ; the accessory or medullary portion is part of the vagus, and has visceral and sensory as well as motor functions.* XII. The hypoglossal nerve arises from a long and large nu- cleus lying in the lower part of the floor of the medulla near the Fig. 5r. — Longitudinal Section showing the Relative Position of the Cra- nial Nerve Nuclei (Edinger). median line and to the outer and ventral side of the central canal. The nucleus is a continuation upward of the anterior horns of the spinal cord and is homologous with the sixth, fourth, and third nerve nuclei higher ui3 (see Fig. 57). It reaches below as far as the decussation of the pyramids and above as far as the glosso-pharyngeal nucleus. A second small-celled nucleus lies just beneath the nucleus proper. Its cortical representation is in the lower end of the central convolutions, to which it is connected by fibres that pass into the raphe and thence to the anterior pyramids. Its fibres pass out between the olivary body and the anterior pyramid. At its origin it is a purely motor nerve ; it receives a few sensory fibres from the cervical nerves and the vagus. It supplies the following muscles : * Dees thinks that the spinal origin of the Eleventh is continuous above with the twelfth, not with the anterior nucleus of the tenth He denies that the medullary- nucleus sends fibres to the larjnix. The internal branch of the eleventh sends motor fibres to the rectus posticus (E. Remak). DISEASES OF THE SPECIAL NERVES. 105 Intrinsic muscles of the tongue : superior and inferior longi- tudinal and transverse. The extrinsic muscles of the tongue; hyoglossus, genio-hyoglossus, and styloglossus. (The palato- Funic, restif. B, VII Fig. 58.— Diagrams showing tue Position of the Cranial Nerve Nuclei and THE Floor of the Fourth Ventricle QIerkle). 106 DISEASES OF THE NERVOUS SYSTEM. glossus and Unguals are supplied by the fifth and seventh cranial nerves respectively.) The depressors of the hyoid: the thyro- hyoid and, with the cervical nerves, the sterno-hyoid and sterno- thyroid. The elevator of the hyoid: genio-hyoid. It is also thought to send fibres to the oral muscles (Tooth). The hypoglossal nerve is concerned in the movements of the tongue and in fixing or depressing the hyoid in mastication and deglutition. When diseased, therefore, speech and deglutition are affected. The small nucleus of the nerve is thought to con- trol the finer lingual movements of articulation. J CHAPTER YIIL DISEASES OF THE CRANIAL XERVES. Diseases of the Olfactory Nerve. The olfactory nerve is affected clinically by loss of function or anosmia, increased sensitiveness of function or hyperosmia, and perversions of function or jiarosmia. Anosmia is far the most common disorder of olfaction. Etiology. — Its usual cause is disease of the mucous membrane of the nose. Injuries, inflammations, and tumors affecting any part of the course of the nerve, its bulb or central fibres, may also cause it. Unilateral cortical lesions in the uncinate gyrus may lead to partial loss of smell. It will be not entire, because each nerve receives fibres from both hemispheres. Paralysis of the fifth or seventh nerve may indirectly cause some anosmia. Primary degenerative changes and excessive olfactory stimula- tion cause anosmia. There may also be a congenital absence of the nerves. Anosmia occurs sometimes as a pure neurosis in hysteria or in neurasthenic states. Diagnosis. — This is made by test odors. To test the sense of smell, a bottle of oil of cloves or of some familiar non-irritating odor may be used. To detect quantitative disturbance one may use six phials containing oil of cloves, in purity and in watery mixture of 1 to 10, 1 to 100, 1 to 1,000, 1 to 10,000, and 1 to 100,000. Special olfactometers have been devised. The sense of smell for any single odor is lost in about three minutes, but returns after one minute's rest. Treatment. — For functional anosmia, snuffs containing str^'ch- nine gr. J^ and gum acacia 3 ij. can be used. Weak galvanic and farad ic currents are recommended. Usually there is in anos- mia a local catarrhal condition of the nose which requires treat- ment. Hyperosmia occurs only rarely and then in neurasthenic, hysterical, or insane persons. In the latter it is more often a psy- chical phenomenon than a peripheral disorder. Hyperosmia can be cultivated, and this is done sometimes by the blind and by those engaged in certain pursuits, such as tea-tasting and wine- tasting. Hallucinations of smell occur in the insane, as just mentioned, 108 DISEASES OF THE NERVOUS SYSTEM. and a few cases of epilepsy are reported in which the cause was a stench. When all olfactory sensations are disagreeable the con- dition is called kakosniia. Parosmia is a not infrequent condition. In it everything smells alike to the patient, and the odor smelled is perhaps a peculiar or offensive one. This condition may be due to local disease, but is often a symptom of hysteria or neurasthenia. Diseases of the Optic Nerve a^d Centres. The optic nerve may be affected by nearly all forms of patho- logical change. For the neurologist, however, the especially im- portant conditions are inflammations, degenerations, injuries, and functional disorders. In order to understand the descriptions of these diseases, it is necessary to define some of the symptomatological terms used : Astheni02)ia is a condition in which exertion of the eyes is wearisome and painful. Amblyopia is a partial loss or dimness of vision in which there are no observable lesions. Amaurosis is a total blindnes.s in which there is no observable lesion. Hemianopsia is blindness of half the visual field. Hemiopia is a condition in which there Is vision in one-half the visual field. Scotoma is a name given to blind spots or areas in the visual field. Inflammation of the nerve, or optic neuritis, may occur as a papillitis or inflannnation of the head of the nerve, a neuro-retini- tis or descending neuritis, a perineuritis or a retrobulbar neuritis. Perineuritis is rare. Neuro-retinitis and papillitis are closely associated clinically and pathologically (Noyes), so that practi- cally only two forms of neuritis need be discussed separately. Papillitis a^'d Xeuro-retixitis.— £'f/o/o^?/.— The causes in general are tumor and inflammation of the brain, poisons, infections, and auto-toxtemic states. In imrticular the causes are tumors, abscess of the brain, meningitis, syphilis, myelitis, nephritis, diabetes, infectious fevers, multiple neuritis, lead, and severe hemorrhages. The disease occurs at all ages and in both sexes. In brain tumors it occurs in two-thirds of the cases, and especially often in cerebellar tumors. It occurs in 80 per cent of cases of tubercular meningitis. Symptoms. — Subjective symptoms are often not present. The vision may remain good for a long time. In other cases there are concentric limitation of the visual field, loss of color sense, and scotomata. For a description of ophthalmoscopic changes, the I DISEASES OF THE CRANIAL NERVES. 109 reader is referred to special text-books. It is in this condition that "choked disc," which is a papillitis with much serous infil- tration, occurs. The changes are less striking in neuro-retinitis. The disease may affect one or both nerves. In brain disease both nerves are usually involved. Pathology and Pathological Anatomy. — The process is usually subacute or chronic. Congestion, exudation, small hemorrhages, and collections of leucocytes occur. The sheath of the nerve just back of the globe is often distended with a serous exudate. After a time the nerve fibres atrophy, connective tissue prolifer- ates and takes their place, and we have a secondary optic atrophy. Fig. 59.— Neuro-retinitis CJakger). The process is essentially peripheral, but it extends back with lessening intensity into the trunk of the nerve. The purely me- chanical theory of neuritis, that it is due to compression, cannot be accepted in the light of modern pathology. It is probable that the neuritis results from an irritating serous fluid which extends down the sheath of the nerve, this sheath being a prolongation of the arachnoid cavity. Mechanical causes lead to constriction, accumulation of the fluid, and compression of the nerve at its periphery, and hence to inflammation. Sometimes, at least, the irritating fluid contains microbes or microbic poisons. Retrobulbar Neuritis.— In this disease the lesion lies chiefly behind the globe. Its causes are especially toxaemia from alcohol and tobacco. It is also due to rheumatic influences, syphilis, lead, and diabetes. 110 DISEASES OF THE NERVOUS SYSTEM. In the acute cases there is usually rather rapid loss of sight, with some pain and tenderness. The ophthalmoscopic changes are relatively slight. In chronic cases, which are usually toxic in origin and due to alcohol or tobacco, oroftenest to both, there are color scotomata or absolute scotomata and amblyopia. There is no pain. The condition is known as tobacco or alcoholic amblyopia. The prognosis of neuritis varies Avith the cause. If this is removable, as in the toxctmiie, recovery is the rule. This is a proof that in neuritis the connective tissue is the part chiefly in- FiG. 60.— Papillitis, "Choked Disc/'' in a Case of Cerebral Tumor. volved, for a destroyed or atrophied optic nerve does not recover. In many cases, however, atrophy follows the neuritis. The treatment is based on the cause. In acute cases one may use cups, salicylates, the iodides, and mercury: later, the iodides and strychnia. Perfect rest to the eyes should be enjoined. Degexeratiox of the Optic Nerve, or Optic Atrophy. — This condition may be primary or secondary. Secondary atro- phy is usually the result of a neuritis. I shall describe h.eve pri- mary optic atrophy. Etiology. — It occurs oftener in men than women (three to one). It occurs as part of locomotor ataiia in less than half the cases ; other degenerative diseases of the cord, like multiple sclerosis, may accompany it. Next to the spinal cord, it occurs oftenest with degenerative diseases of the brain, such as multiple sclerosis DISEASES OF THE CPwANIAL NERVES. Ill and general paresis. Hemorrhages, alcoholism, and lead may be causes. It may occur without known cause. The symptoms are those of gradual decrease of acuity of vision, concentric limitation of the visual field, loss of color sense, dilata- tion and immobility of the pupil. The sense of sight may remain good for a long time. Ophthalmoscopically, the nerve disc is opaque, grayish, or dirty looking, and often has a cup-shaped or " cupped-disc " appearance. The vessels are smaller and few in number. The pathology and pathological anatomy is that of a paren- chymatous degeneration with loss of nerve fibres, which are re- placed by connective tissue. llYie prognosis is almost uniformly bad. The treatment is that usually of the cerebral or spinal disease. Mercury, iodides, strychnia, phosphorus, and iron are given. Warm baths and salicylate of soda sometimes have a temporarily good effect. Strychnia in i)hysiological doses gives, however, the best symptomatic results. Electricity is not of any use. Stretch- ing the nerve does no good. Eserine, pilocarpine, and santonin or nitrate of silver may be tried. The optic nerves and their primary and cortical centres are subjected to various other diseases. So far as these are organic, they will be described in detail under the head of brain dis- eases. But there are certain symptoms often of functional origin which are best described here. These are: (1) Amblyopia and amaurosis ; (2) retinal hyperaesthesia and dyssesthesia ; (3) hemi- anopsia. Amblyopia axd Amaurosis.— ^t^'oZo^/i/.— The causes are inju- ries and shocks, hysteria, migraine, concussion of the brain, light- ning stroke, and severe hemorrhages. There are also certain toxic causes, chiefly alcohol and tobacco, quinine, and salicylic acid. Other causes are glycosuria, uraemia, and reflex irritations, especially of the trigeminal nerve. Night-blindness and snow- blindness are forms of functional amblyopia. The symptoms are diminution or loss of vision, usually sudden, temporary, and involving both eyes. Amblyopia in hysteria is usually greater in one eye and associated with concentric limita- tion of the visual field and disturbance of color sense. Underlying functional amblyopia there may be a peripheral anaesthesia, a psychical or cortical anaesthesia, minute hemor- rhages, causing temporary pressure, vascular spasm, and anemia. The prognosis is usually good. The treatment is purely a causal one. In most cases one must examine for drug poison, uraemia, diabetes, migraine, or a hemor- rhage. Retixal or ocular hyperesthesia is a condition in 112 DISEASES OF THE NERVOUS SYSTEM. . which the eye is abnormally sensitive to hght. It may be due to exposure to extreme hght or to seclusion in a dark room. The neurologist sees it oftenest as a symptom of hysteria {vide Hysteria) and perhaps in hypnotic states. It occurs in mydriasis and al- binism. It is not to be confounded with photophobia due to irritation of the conjunctiva. Nyctalopia, or the sense of seeing better in a dim hght, is a form of the disease. Hemianopsia or half-sightedness may be due to a functional or organic disorder of the nerve or its centres. It is a symptom of many lesions and conditions and can only be described gen- erally here. Etiology. — Its principal functional causes are migraine, lithae- mia, gout. Its organic causes are tumors, inflammations, soften- FiG. 61.— Showing Lateral Homonymocs Hemianopsia. This is not quite complete, there being a space on the blind side where the patient can see (Noyes). ings, or hemorrhages involving part of the optic nerve or its cen- tral connections. ^ymj^toms. — Various descriptive terms are used to indicate the character of the hemianopsia. In lateral hemianopsia a vertical half of the field is involved. In lateral homonymous hemianopsia there is half -blindness on the left or right side of each eye, as the case may be (Fig. 61). In temi^oral hemianopsia the outer half of each eye, and in nasal the inner halves, are involved. The upper or lower segments or irregular segments of the visual field may be involved. These various forms of hemianopsia depend upon the location of the lesion which cuts into and destroys the optic fibres in their course from the eye to the visual centre in the occipital cortex. The mechanism will be understood when it is remembered that each occipital lobe is supplied by nerve fibres from one-half of the retina of each eye. A cut shows this better than any descrip- I DISEASES OF THE CRANIAL NERVES. 113 tion (Fig. 49). In nasal hemianopsia the lesion must be at Ch, in front of the chiasm. In temporal hemianopsia it is at CM., just back of the chiasm. In lateral hemianopsia the lesion must lie farther back than the chiasm, in the tract, the primary centres, the optic radiations, or occipital lobes. In hemianopsia from disease of the nerve as far back as and in- cluding the primary centres in the optic thalamus and corpora quadrigemina, there is a loss of light-reflex when a ray of light is thrown upon the blind side of the retina, but the pupil still contracts when light is thrown on the sensitive side of the retina. This phenomenon is called " Wernicke's hemiopic pupillary re- action." If in hemianopsia the light-reflex is preserved, the lesion is back of the primary centres and involves the optic radiations or cortex. A test for the condition of hemianopsia in its early stage, and one that is useful in stupid or i:>artially comatose patients, is the following : When the finger is suddenly brought in front of the eye on the sound side, there is a wink ; if brought in front from the blind side, the orbicularis does not contract. Hemianopsia is almost always the sign of organic disease. It is not found in hysteria, but does occur in migraine and lithce- mia. It is best made out and recorded by means of the perimeter. Its course and treatment depend ujoon the cause. Diseases of the Motor Nerves of the Eye. The common affections of the ocular muscles are : 1. Paralyses or ophthalmoplegias, which may be acute, chronic, or progressive. 2. Pareses or amyosthenic states, called ordina- rily muscular asthenopias. 3. Spasms, such as strabismus, nystag- mus, and blephorospasm. There are many special terms w^hich are used to indicate the peculiar effects of various paralyses and spasms of the ocular muscles and nerves, and some of these I will define here : Erroneous projection is a condition in which the patient is unable to judge exactly of the relation of external objects to the body. For this relation is determined by the movements of the ocular muscles, and these being weak, wrong sensations are con- veyed to the brain. Vertigo may result from this disturbance of muscular sensation. Diplopia or double vision is a condition due to the erroneous sensation resulting from eye-muscle palsy, and to the fact that the images of the object fall upon non-corresponding retinal fields. Diplopia is simple or homonymous when the false image is seen on the same side as the affected eye. AVhen a red glass is placed over this eye two images are seen, the red one being on the side 8 114 DISEASES OF THE NERVOUS SYSTEM. of the eye involved. Diplopia is heteronymous or crossed when the false image is on the opposite side to the sound eye. Coiijugate deviation of the eyes is a condition in which both eyes turn strongly to one or the other side. It may be paralytic or spasmodic. The mechanism is a complicated one and not Ijerfectly understood. In general, destructive lesions of the brain cause a paralytic deviation toward the side of the lesion. Similar lesions in the pons cause a deviation away from the side of the lesion. The palsy involves the sixth cranial nerve and the branch to the internal rectus from the third. The sixth nerve nucleus is the dominant one, and impulses from the brain go to it first (see Fig. 51). Returning now to the diseases of the motor nerves of the eye, it is found that the paralyses occur in various ways, which may be best grouped as follows : Ophthalmoplegias : 1. Paralyses of the third nerve. ) Acute. 2. Paralyses of the fourth and sixth nerves. ) Chronic. 3. Progressive paralysis of all or part of these nerv^es. The Ophthalmoplegias. I. Paralysis of the -Oculo-Motorius or Third Nerte. — Etiology. — The commonest causes are exposure to cold and syphilis. Other causes are basal meningitis, intracranial tumors, injuries, compression from orbital tumors, the diphtheritic poison, and excessive exposure to light ; excessive use of tobacco, and alcohol, morphine, or other poisons may be a cause. Temporary palsy sometimes occurs in migraine, or it may take the place of an attack of migraine. A palsy of some of the muscles supplied by the third is sometimes caused by cerebral lesions involving the inferior parietal lobule. Partial palsies also occur in loco- motor ataxia and in certain primary mus- cular atrophies. The common causes, how- FiG. 62.— Double Ptosis, ^"^'©r, are, as stated, rheumatic influences and syphilis. There occurs, in rare cases, an acute inflammatory degenera- tion of the nuclei of the ocular muscle nerves similar to acute an- terior polio-myelitis. This condition has been called " polio-en- cephalitis superior." Symj)toms. — When all the muscles supplied by the third nerve are paralyzed, there is dropping of the lid (ptosis) ; the eye can only be moved outward and downward and inward ; there is there- DISEASES OF THE CRANIAL NERVES. 115 fore divergent strabismus and double vision (diplopia). The pupil is somewhat dilated and does not contract to light, owing to paral- ysis of the constrictors of the iris ; and there is loss of power of accommodation, so that the patient cannot read print close to him. The patient suffers under annoyance from the lid drop and the double vision, and there is sometimes vertigo and jihoto- phobia. Only one nerve is involved at a time as a rule. The various eye muscles supplied by the third are rarely all attacked. Fig. 63.— Shutter for Testing Pupil-reflex. The apparatus admits of usingr colored glasses for testing hysteria and maUngering; also of the use of a Maddox prism for testing the eye muscles. The levator may escape almost entirely the ciliary muscle and iris may also be but slightly involved ; but these latter muscles are never involved alone in ordinary types of the disease. The affection usually runs a subacute course, lasting but a few weeks. Functional palsies last but a few days; syphilitic palsies are usually temporary (one to three weeks), but may relapse or become extremely obstinate. Periodical palsies occur every year or six months or even oftener; they last a few days or weeks and are accompanied at first with some pain. They continue to recur for years. 116 DISEASES OF THE NERVOUS SYSTEM. In diphtheritic eye palsies the first three or four nuclei of the series making up the origin of the third nerve are oftenest af- fected, causing paralysis of accommodation, paralysis of the iris and of the internal rectus, the three muscles concerned in accom- modating the eye to near objects (Fig. 62). Pathology. — In the rheumatic palsies there is a low grade of peripheral neuritis, and the same is true of most diphtheritic and other palsies of infectious origin. In syphilitic palsies there is usually a specific basilar meningitis involving the nerve roots. The meningitis may be slight or may amount to gummatous de- posit. In functional and some i^eriodical palsies there is a vaso- motor disturbance causing congestion or anaemia or perhaps sim- ply inhibition of the nuclear centres. Some periodical jpalsies have been found to be due to small tumors involving the nerve root. In rare cases there is primary muscular atrophy of the eye- ball nerves, or primary degeneration of the nuclear centres, or a cerebral lesion of the inferior parietal lobule.* Diagnosis. — One must first determine how extensively the muscles supplied by the third are involved. If only the levator palpebrte, there is simply falling of the lid. If the eyeball muscles are involved, we get the following symptoms. They are : Limitation of movement of the globe. Strabismus and secondary deviation. Erroneous projection. Double vision or dij^lopia, which is either simple or crossed. Paralysis of the iris or iridoiDlegia and of the ciliary muscle or cycloplegia. Concentric limitation of the visual field. All these points must be tested, but the detailed knowledge of them is best gained by consulting ophthalmological works. The extent of involvement of eye muscles can generally be sufficiently tested by making the patient move the affected eye in various directions, and by testing for accommodation and for the pupillary reaction to light. Paralysis of the iris, or iridoplegia, and of the ciliary muscle — cycloplegia. The motor fibres of the third nerve to the iris supply the sphincter, and when paralyzed there is dilatation and immobility of the pupil, a condition known as mydriasis. Fibres from the same nucleus innervate the ciliary muscle, and the iris and this muscle are usually paralyzed together. Paraly- sis of the ciliary muscle is called cycloplegia. In this latter con- dition there is loss of power of accommodation. Iridoplegia and * Some diphtheritic palsies are probably nuclear. DISEASES OF THE CRANIAL NERVES. 117 cycloplegia are usually due to local disease of the eye or to the use of mydriatic drugs. Occasionally they are observed after diph. theria or in multiijle sclerosis. Paralysis of the levator j^alpehrce, csiusing ptosis, is sometimes seen alone, but usually other branches of the third nerve are in- volved. A functional palsy of the lids sometimes occurs in anemic and nervous people at the time of wakmg. It is a temporary mo ru- ing or toaking jJtosis. Paralysis of the sympathetic fibres of the eye causes con- traction of the pupil (myosis) from the unopi)osed action of the third nerve. There is also a slight prominence of the eye and slight ptosis from an involvement of the nerves that supply MuUer's muscle. The pupil does not dilate when the skin of the cheek or neck is irritated. This is a condition known as loss of skin-reflex. In locomotor ataxia there is often a rigidity of the constricting fibres of the iris, while the ciliary muscle continues to act. The IDUpil is then small and does not respond to light, while it does respond to accommodation. This is known as the Argyll-liohert- son pupil. II. Paralysis of the Fourth ]S^erve.— This is a rare affec- tion and not always easily detected. The causes are much the same as those of palsy of the third nerve. The symptoms are slight convergent strabismus when the ej^e is moved downward and diplopia on looking down. There is defect in the movements of the eye downward and outward. Paralysis of the sixth nerve (abducens) is the most fre- quent of eye palsies, and occurs especially often in syphilis and in locomotor ataxia. It causes convergent strabismus and double vision. III. Progressive Ophthalmoplegia. — Besides the palsies already described, there occur certain forms which have a pecul- iar origin and course. They begin sloAvly, as a rule, and steadily progress. In some cases only do they reach a certain stage and then remain chronic. The term " progressive " applies fairly well to them. They often affect the third, fourth, and sixth nerves together. In accordance with the muscles invaded, these palsies are called external, internal, j^artial, and total. Thus if those branches of the third nerve supplying the iris and ciliary muscle are involved alone, it is ophthalmoplegia interna; if the other branches are involved, it is called ophthalmoplegia externa. Definition.— VYOgre^fiixe ophthalmoplegia is a degenerative disease of the nuclei of the motor nerves of the eye. It is in most cases the same disorder as of bulbar paralysis and progressive muscular atrophy. It is sometimes called polio-encephalitis su- perior. 118 DISEASES OF THE NERVOUS SYSTEM. Etiology. — It develops between the ages of fifteen and forty, but may occur later. The sexes are equally affected. Lead, diph- theria, traumatism, syphilis, appear sometimes to be the cause. It may complicate locouiotor ataxia ; more often it forms part of I^rogressiv^e muscular atrophy. The symjJtoms are often not noticed until the disease is far advanced. The vision is not disordered, and there is only a gradual limitation of mobility of the eyeball. A slight drooping of the lids, causing a sleepy look, or a slight squint, usually diver- gent, is noticed. Then upon examination it is found that the eye cannot follow the finger, except to a slight extent. The iris reacts to accommodation and light usually. Double vision may be present. Usually the patient accustoms himself to monocular vision. The disease lasts a long time, and it may become sta- tionary. If complicated with progressive muscular atrophy, however, the course is relatively rapid, death occurring from the latter disease in two or three years. Pathological Anatomy. — In all progressive cases there is a de- generative atrophy of the nuclear cells. In a few rare cases no lesion has been found, and in a few stationary cases the anatom- ical change is that of neuritis. The treatment is that for the disease which it complicates or the condition which causes' it. That is to say, it is the treatment for locomotor ataxia, jDrogressive muscular atrophy, syphilis, or lead-poisoning. Iodide of potassium, strychnia, arsenic, nitrate of silver, and phosphorus may be given. Electricity is of very doubtful value, and only the galvanic current would be indi- cated. General tonic measures and rest to the eyes should be employed. Muscular Asthexopia axd Muscula.r Ixsufficiexcies. — This is a term employed to indicate a lack of equilibrium of the muscles of the eye, as a result of which the visual axes cannot be kept parallel without an effort. This effort is often unconscious, and shows itself only by a ready tiring of the eye on attempting to read, or by the production of headaches and cerebral partes- thesite. Examination of the eye by means of prisms reveals the spe- cial character of the trouble. When the eye muscles act normally the condition is called one of orthophoria. When some of the muscles are weak it is called heterophoria. There are various forms of heterophoria, viz. : esophoria, a tend- ing of the visual lines inward, from weakness of the externi ; ex- ophoria, a tending of visual lines outAvard ; hyperphoria, a tend- ing of visual line of one eye above its fellow\ The condition is tested in various ways. The simplest is this : DISEASES OF THE CRANIAL NERVES. 119 Refractive errors having been corrected, a series of prisms is placed over the eye at first with the base inward while the patient looks at a candle twenty feet distant. The prisms are increased in strength until ttie patient can no longer coalesce the images. The degree of prism is noted, and this indicates the strength of ab- duction or of the externi. The same process is gone through with for the interni, the base of the prism being oat. The externi should overcome a prism of about 8", the interni one of 2?i to 25 or more. There are great individual variations, and there is also considerable variation ni individuals. The above tests measure the amount of abduction and adduc- tion. To test the presence of heterophoria, the writer uses the Mad- dox double prism held in a frame. The line where the bases of the two prisms unite is brought directly over one eye, and is held there in a perfectly horizontal position while the patient looks at a candle twenty feet away. A red glass is at the same time held over the other eye. With the eye covered by the double prism the patient sees double, one flame being above the other, with the other eye he sees a red flame lying just between the two white ones. If the red flame is directly in a vertical line, there is orthophoria , but if it lies to one side or the other, there is ex- ophoria or esophoria according as the red flame was on the oppo- site side to the eye covered with red glass or on the same side. If heterophoria is found, prisms are placed over the eye until the three lights are in a vertical line. The number of the prism re- quired to correct the heterophoria indicates its extent in degrees. By changing the double prism so that its common base line is vertical, the test for hyperphoria can be made.* Muscular asthewypia is said to cause a disturbance of vision, vertigo, migraine, cerebral par^esthesia, and pains in the head, more particularly in the occipital and cervical region. It is be- lieved to be a possible factor in producing choreic twitchings in the face. In neurasthenic persons it may cause a wider range of nervous symptoms. It is said to be an essential factor in caus- ing epilepsy, chorea, and hysteria. The author cannot accept this latter view, and believes that the importance of muscular asthenopia in causing general nervous symptoms is not great. Much of it, if not all, may be relieved by correcting refractive errors and by helping the general health of the patient. The treatment of it, after all myopia, or hypermetropia, or astigmatism, if present, is relieved, consists in the systematic use of prisms for training the muscles, the wearing of proper glasses, *More elaborate and exact methods have been devised by Dr. Stevens and are employed by many ophthalmologists. 120 DISEASES OF THE NERVOUS SYSTEM. and graduated or complete tenotomies according to the method of Stevens. Spasmodic Diseases of the Ocular Muscles. These are- (1) Conjugate deviation from spasm; (2) irregular and associated spasms from convulsive and irritative brain dis- order; (3) nystagmus. Etiology. — iSpas?nodic conjugate deviation occurs from an irri- tating lesion of the ocular nuclei or of the brain in its cortical motor areas and tracts. Irregular spasmodic movements occur in meningitis, hydro- cephalus, and in lesions involving the semi-circular canals. Pecul- iar associated spasms occur in hysterical attacks. Various spasmodic movements and contractions of individual eye muscles occur from ocular disease, errors of refraction, mus- cular weakness and paralysis of certain eye muscles. Rhythmical spasm or nystagmus occurs as the result of hered- itary visual Aveaknesses and refractive errors of various kinds, in albinoes, and in chronic hydrocephalus. It is found usually in neurotic cases associated with ocular defects, in epilepsy, chorea, hj'steria, neurasthenia, and insanity. It occurs in certain degen- erative nervous disorders such as disseminated sclerosis, heredi- tary ataxia, tumors, especially of the cerebellum, and other focal lesions, and in meningitis. It occurs in miners, and is called miners' nystagmus. It may be a reflex symptom from a remote irritation. In nj'stagmus the oscillation of the eyeballs is usually lateral. It may be brought out when slight in degree by causing the pa- tient to look steadily to one side. Vertical and a kind of rotating nystagmus sometimes occur, and are due to much the same causes as those of lateral nystag- mus. Spasj7i of the levator pal pehrce is sometimes seen, and is usually tonic. DISEASES OF THE FIFTH CRANIAL NERVE— THE TRIGEMINUS. The common affections of this nerve are headache, migi*aine, tic douloureux, and various neuralgias. The rarer diseases are anaesthesia, reflex cough and asthma, masticatory paralysis, tris- mus, trophic and secretory and vasomotor disorders. Many of the disorders referred to the fifth nerve are in reality only symptoms of some general neurosis, constitutional disturb- ance, or of some remote local disease. As a matter of conven- ience, however, they may be treated here. DISEASES OF THE CRANIAL NERVES. 121 Headache (Cephalalgia). Headache is the name given to attacks of diffuse pain affecting different parts of the head and not confined to the tract of a particular nerve. It usually comes on in paroxysms at various intervals, but may be continuous. Fig. 64.-SHOWING the Motor anu 8i:nsokv Nerves and the Arteries and Veins of the Face (Merkel). a. Frontal nerve : b, supra-orb. ; c. temporal . a lacrvmal : e. supra- aud inf ra-trochlear : /. auriculo temp. ; g, nasal ; h, malar : t, se^^'^a nerve; k. infra-orbital; m, mental. The veins have longitudinal, the arteries oblique striations. The nerve i is the facial ; all the other branches are trigemmaL 122 DISEASES OF THE NERVOUS SYSTEM. Etiology. — Headache is the most common of nervous symp- toms. Ten to fifteen per cent of school children, twenty-five per cent of men, and over fifty per cent of women are subject to it more or less. The headache ages are from ten to twenty-five and thirty-five to forty-five; most cases occur between the ages of eight and twenty-five, especially in females. The number of headaches in- creases gradually from the period five to ten years up to the period fifteen to twenty, then falls till the thirty-fifth year, and rises again till about the age of forty. Early childhood and de- clining age are practically exempt from chronic functional head- aches. Women suffer from it more than men in the proportion of about three to one. It is more frequent in city populations and among the wealthier classes. Headaches are more common in the spring and fall and in temperate climates. Headaches may be classed, in accordance with their causes, as follows: 1. Hiemic causes, in which impoverished or disordered blood is brought to the brain, as in {a) anemia and congestion; {h) diathetic states: gout, rheumatism, diabetes, ursemia; (c) infec- tions: malaria, fevers. 2. Toxic causes: lead, alcohol, tobacco, etc. 3. Neuropathic states: epilepsy, neurasthenia, hysteria, neu- ritis. 4. Reflex causes ocular, naso-pharyngeal, auditory, dyspeptic, sexual. 5 Organic disease, including arterio-sclerosis, syphilis, tumors, meningitis, and diseases of the cranial bones. The anaemic, dys- peptic, ocular, and neurasthenic are the common forms of chronic and recurrent headache. Symptomatology . — Headaches may be classed in accordance with their location and the character of the pain. We have ac- cordingly; 1. frontal headaches; 2, occipital headaches, 3. parie- tal and temporal headaches; 4, vertical headaches; 5, diffuse headaches and various combinations of the above. The most common form of headache is the frontal, next the fronto-occipital or diffuse, next the vertical, and then the occip- ital. The kind of pain differs with different persons and with differ- ent causes. We have: 1, pulsating, throbbing headache, 2, dull, heavy headache ; 3, constrictive, squeezing, pressing headache ; 4, hot, burning, sore sensations; 5, sharp, boring pains. The first form characterizes headaches with vasomotor dis- turbances, and usually indicates migraine. The second is of a toxic or dyspeptic type. The third is found m the neurotic and neurasthenic. The fourth in rheumatic and an;^emic cases. DISEASES OF THE CRANIAL NERVES. 123 The fifth in hysterical, neurotic, and epileptic cases. The accompanying diagram shows some of the relations of localized pain to the cause. A large experience both in my own practice and in that of others shows it to be approximately cor- rect. Headaches may continue for a day or may last for weeks and months. Some persons have headaches only when constipated or bilious, or when they have an attack of indigestion. Others suffer from a little pain nearly all the time, exacerbations occurring at various periods. Neurasthenic and ocular headaches are gener- ally of this type. When headaches are persistent, examination should be made of the eyes, of the nose and sinuses ; the patient should be questioned as to syphilis, the continuous use of tobacco, and chronic dyspepsia. The possibility of brain tumor, of pachy- Anaemia. Endometritis. Bladder? Constipation. Caries of incisor. Error of eye-refraction, , ^ ^^ # ,- ^ , ^ '/■ vT' /--^ Decayed teeth. Gastric dyspepsia ; --^^^H i ^=-::-f:\ -/rhinopharyngitis, cured by acids ^-^^^ A ]>;!.'" Otitis media. L^ A'W^ Uierine W / 7 Spinal irrita- > y I tion Fig. 65.— Showing the Location of the Pain in Headaches from Different Causes. meningitis from blows, or sunstroke or chronic alcoholism should be considered. The persistent headaches not relieved by ordinary treatment are due to eye trouble, antemia, neurasthenia or spinal irritation, syphilis or pachy-meningitis. Eye strain may cause true migraine or ordinary headache. Eye-strain headache is usually asociated with some weakness of eyesight and pains and discomfort about the globe, besides severer pains at times in the brow or occiput. The cause of the eye strain is usually astigmatism and hyperme- tropia. Occasionally it is due to weakness or lack of balance of the eye muscles. ^limptoms Associated loith Headache.— The symptoms often- est associated with chronic and recurrent headaches are vertigo, somnolence, sensations of heat and pressure (cerebral partesthe- sice), and nausea. Vertigo goes oftenest with headaches of dys- peptic origin: some of the so-called bilious headaches of early life develop later into attacks of vertigo ; this symptom often occurs with frontal headaches. Somnolence occurs oftenest with amemic and malarial headaches; it may develop also with syph- 124 DISEASES OF THE NERVOUS SYSTEM. ilitic head iDains. ;Xausea I have found oftenest with occipital headaches. Pathology. — Headaches are to be distinguished from neural- gias and from a si^ecial and connnon form of head pain known as migraine. Headaches are diffused pains caused, as a rule, by irritations located in or referred to the peripheral ends of the fifth nerve. Their seat is usually within the skull. ^^euralgias, on the other hand, are caused by irritations of the trunks of these nerves. The jDains are local and confined to the single branches of the nerve. Migraine is a periodical neurosis in which there is a discharge of nerve force, not only affecting the trigeminus, but often other cranial nerves as well as sympathetic fibres. It is a general disease of which the headache is only one symp- tom. The nerves of the dura mater are those most involved. Head- aches, when occipital, involve the sensory fibres of the vagus and the upper four cervical nerves. There is no anatomical change in the nerves except in organic headaches. But in many cases the tiiembranes of the brain and their sensory nerves are congested or anaemic. Diagnosis. — Xo symptoiii requires more careful investigation as to its cause than that of headache. The diagnosis is always to be made, not of this symptom, but of its cause. Most of the fore- going description accordingly refers to etiology. It is important, however, to decide whether the case is one of migraine, or neuralgia, or of headache. Headache is usually diffuse and bilateral. It is more or less persistent. Migraine comes on j)aroxysmally, lasts a short time, and then leaves the patient feeling perfectly well or even better than ever. Migraine is often accompanied with nausea, flashes of light, strong pulsations of the head, vertigo, pallor or, more rarely, congestion of the face. Neuralgic pains are sharp and shooting, they run along the tract of the nerve, and often are associated with suffusion of the eye and oedema. Tender points are felt. Treatment.— The constitutional treatment is based upon the etiology. Regulation of diet and digestion, securing a regular movement of the l)owels, attention to ocular troubles, abstention from tobacco and alcohol and overwork are the important points requiring attention. The symptomatic treatment consists in giving antipyrine, anti- febrin, phenacetin, salicylate of soda, caffeine, muriate of annno- nia, and sometimes mori)hine or codeia, and l)romide of ammonia. Antipyrine can be given in doses of gr. v. every twenty minutes I DISEASES OF THE CRANIAL NERVES. 125 till three or four doses are taken. Phenacetin often needs to be ^iven in large doses of ten or even twenty grains. Antifebrin is less trustworthy and must be given in small doses. Exalgin is not a very good or safe remedy. It may be tried in doses of gr. iij. to gr. V. Muriate of annnonia is an excellent remedy given in very large doses, 3 ss. toji., well diluted. Menthol in doses of gr. V. to gr. X. in hot water sometimes stops headaches. In head- aches from anaemia, cafieine and anmionium muriate are best. In headache from nervous exhaustion, similar stimulating anodynes are usually most efficacious. Combination? of caffein citrate and salicylate of soda or benzoateof sodaare of ten better than the sin- gle drug. Caffeine in any case nmst be given in larger doses than is ordinarily done, i.e., gr. iv. or v. Local applications of a twenty-percent solution of menthol, the ice-bag, cloths wrung out in hot water, or a piece of sheet lint soaked in chloroform liniment two parts and tincture of aconite one part are efficacious measures. A cathartic, rest in a darkened room, light diet — all these are measures which many patients themselves learn to adopt. Finally, in headaches from organic disease we have often to resort to iodide of potassium, mercury, and the use of some prep- aration of opium. As will be seen, each case of headache requires special treat- ment and a certain amount of experimentation in order to learn the idiosyncrasy of the patient. Migraine, Sick-Headache, Hemicrania.— Migraine is a constitutional neurosis characterized by periodical attacks of pain chiefly in the course of the fifth nerve. The pain is often asso- ciated with nausea or vomiting, mental depression, vasomotor disturbances such as flushing or pallor of the face, by flashes of light, vertigo, tinnitus aurium, and in rare cases by partial paral- ysis of one oculo-motor nerve. It will thus be seen that migraine is more than ordinary head- ache and unlike an ordinary neuralgia. Etiology.— The disease is very common in civilized countries and is frequent in America. It oczynsky). widely separated, recovery is doubtful unless an operation is promptly done. The treatment consists in electrical applications, mechanical support, with potassium iodide internally and abstinence from alcohol. Local injections of nitrate of strychnine are useful, and massage should be used if it can be applied carefully. In brachial palsies due to severe injuries, dislocations, frac- tures, etc., in which there is evidence, from the extreme atrophy and absence of electrical reaction, that the nerve is entirely cut across and that the ends are not in apposition, a surgical opera- tion is stringently needed. The nerves should be exposed and the ends brought as near together as possible. Decalcified bone- tubes or sterilized macaroni may be used to give a passage for the central end to grow into the peripheral. In these cases, however, it must be remembered that the two ends do not unite : but the DISEASES OF THE SPINAL NERVES. 163 central end grows down into the tract of the old degenerated peripheral stem. The upper -arm type and loioer-ann type palsies are caused l^y much the same factors as the combined palsies ; their symptoms have been indicated above. The upper-arm type is especiaUy frequent in infants and constitutes one of the obstetrical paral- yses. It may in some cases be due to injury or hemorrhage in the cord. A peculiar form of combined nerve pals}^ sometimes occurs, due apparently to d^ primary hrachial neuritis. It begins in the plexus and involves first the nerves of the ux^per cervical roots. It may extend down and involve the ulnar, median, or musculo- spiral. It occurs in adult men generally and in those exposed to rheu- matic influences. Perhaps lead-poisoning may exist. It begins gradually with slight pains and weakness in the shoulder and arm muscles. Atrophy and anaesthesia follow, and degeneration reactions are present. There is not a great deal of pain (Fig. 73). The disease is usually confined to one side. It lasts several months, and nearly complete recovery finally takes place. Relapses may occur. It is differentiated from progressive muscular atrophy by the pain, anicsthesia, and electrical reactions and from arthritic atroi^hy, by the absence of any history of arthritis and the pres- ence of degeneration reactions and anaesthetic areas. Paralyses of Sixgle Nerves.— Paralysis of the Pos- terior Thoracic Xerve.— j£'^/oZo(/^.— This rare trouble usu- ally occurs in male adults and is due to injury or sudden strains. Its paralysis may be part of a progressive muscular atrophy. The nerve goes to the serratus magnus. iSymjjtoms.— When paralyzed, there is difficulty in raising the arm above the horizontal position and the movements of the shoulder are weakened. AVhen the arm hangs by the side the lower angle of the scapula is drawn a little nearer the vertebral column and protrudes slightly. When the arm is held out hori- zontally the inner edge of the scapula protrudes and is drawn toward the middle line. When the raised arm is brought for- ward there is a deep groove formed between the inner border of the scapula and the thoracic wall. The disease often runs a long course and is accompanied with pain. Paralysis of the Circumflex Xerve.— The nerve goes to the deltoid, teres minor, third head of the triceps, and yhoulder joint. It gives sensation to the skin of the shoulder. It is very often paralyzed. The commonest cause is a fall or injury, dislo- ]inimldal tract extends dowai the whole length of the cord and sends its fibres to the anterior horns of the same side. Both of the above tracts are continuations of the anterior pyramids or motor tracts of the medulla. These pyramids divide at the lower end of the medulla, about ninety per cent of fibres crossing over to form the crossed pyramidal tract and ten per cent continuing on the same side. Some of the fibres of the crossed pyramid redecussate (in lower animals) and enter the pyra- midal tract of the side on which thev started (Fig. 88, PT). The direct cerebellar tract begins at the level of the first lum- bar nerves. Its fibres originate in the vesicular column of Clark. They pass up to the cerebellum and go chiefly to the vermis. Most of them then cross over and enter the red nucleus (Fig. 88). The antero-lateral ascending column extends nearly the whole length of the cord. Its fibres come from the posterior commis- sure and the sensory cells of the opposite posterior cornu. They pass up and end in the lateral nucleus (Fig. 88, ALC). The postero-internal column, or column of Goll, is composed of fibres which, originate in the ganglia of the posterior roots, pass inward, and without crossing ascend, to end in a nucleus at the upper limit of the cord, the nucleus of GolPs column (postero- internal nucleus). The column extends the whole length of the cord. It is very small in the sacral region, but increases in size as it passes up (Fig. 88, G). . 1 1 + i There are a few long fibres scattered in the anterior and lateral ground bundles. They degenerate down and are called the an- tero-lateral descending tract. 186 DISEASES OF THE NERVOUS SYSTEM. The names of the short-fibre columns are the anterior and the lateral fundamental columns, the lateral limiting layer, and the column of Burdach. This latter column contains in its cervical part some long fibres which end in a nucleus at the upper limit of the cord, the postero-external nucleus, or nucleus of the col- umn of Burdach (Fig. 82, CB). The Relations of the Different Parts of the Spinal Cord to the Peripheral Serves, to the Brain, and with Each Other.— I will begin with a description of the way in which the anterior and posterior nerve roots are connected to Fig. 85.— Shotvikg the Relations of the Anterior Roots M, W to the An- terior HoRxs; OF the Anterior Horns to the Crossed Pyramidal Tracts and Posterior Roots. Slio-n-iug also the relations of the posterior root fibres : T, to column of Goll and Clark's column; P, to sensory cells and posterior column; J, to sensory cells and antero-lateral ascending column ; R, to anterior horns. S, Sensory root; A, muscle sense; P, pain and temperature sense; T, tactile sense; YR, visceral and reflex fibres. the cord ; then describe the mode in which the different columns and cell groups are connected with each other; and finally I will indicate briefly the connections of the cord with the brain. The anterior nerve roots are connected directly with the an- terior horn cells, of which they are processes. The cells of the anterior horn are surrounded by two sets of "end-brushes,'' one coming from the pyramidal tracts, the other from the posterior horns and roots. Thus these cells are in rela- tion with impulses from the brain and from the periphery. The i)osterior nerm roots originate chiefly in the spinal gan- glia. On entering the cord the fibres divide like a T and pass up and down for one or two inches. They then enter (1) the col- umn of Groll, (2) the anterior or posterior commissure, or (3) the posterior horn. They all send off collaterals, and terminate eventually in end-brushes surrounding nerve cells. There are at least three groups of nerve fibres which enter by DISEASES OF THE SPINAL CORD. 187 the posterior roots and make different connections with the cell groups or columns ; 1. An innermost set. These pass across the postero-external column and enter the median or Goll's column, which they as- cend, to end in the nucleus. 2. A median set. These pass along the inner side of the pos- terior horn, and end either {a) in cells of the deeper part, (5) in the spindle-shaped cells, or (c) go to the anterior horn ; still others (d) cross over in the connnissure to enter the antero-lateral tract. ^^ Fig. 86. Fig. 87. Fig. 86. — Showing the Connections of the Anterior and Posterior Roots AND CoRNUA WITH Each Other (Cajal). A, Anterior root; B, posterior root; «, collaterals; d, end-brushes. Fig. 87. — Showing the Association or Short-Fibre System op the Cord (Cajal). a, Anterior cornua cell; b, c, d, association fibres; e, posterior association fibres. 3. An outer set. These are very fine fibres which enter the tip or outer part of the posterior horn, and then run up and down, forming the rim zone. They eventually connect in the usual way with the sensory cells of the posterior horn (see Fig. 85, A, R). TJie different 'parts of the spiiial cord are connected by the short fibres which unite different levels of the cord, and by com- missural fibres which unite the different halves of the cord. These 188 DISEASES OF THE NERVOUS SYSTEM. s;hort and commissural fibres originate in groups of nerve cells ly- ing in the central parts of the gray matter and called associative nerve cells. They are small and multipolar. Some are distrib- uted sparsely in the white columns. Fibres arise from them, run in the commissures and short-fibre tracts, and end in brushes which put the fibres in relation with vai'ious cell groups (Figs. 86, 87). Physiology.— The detailed facts regarding the functions of the spinal cord may be gotten in physiological text-books. I shall give only those bearing more or less directly on the localization of the functions. The spinal cord is a conductor and centre of nervous action. It represents the lowest evolutionary level of the development of the nervous system. Its functions, so far as they are independent, are stable and w^ell organized, but of a mechan- ical and relatively simple order. Functions of the White Col anins.— The white matter is a con- ductor of nerve impulses, and its functions are relatively simple. We have only to study the direction and kind of impulses carried by its various colunms. The direct eind c rossed 2->yramidal tracts carry motor impulses downward from the brain. A few fibres (two to ten per cent) connect with muscles of the same side; so that in hemiplegia there is usually some weakness on the healthy side. These tracts normally exercise a continual inhibitory in- fluence on the motor cells of the anterior horns; so that when de- stroyed there develop spasmodic conditions of the paralyzed part. The anterior ground bundle, lateral ground bundle, and the lateral limiting laijer have the function of associating different levels of the cord and of connecting it also with nuclei in the medulla and centres in the cerebellum. The columns of Goll conduct special sensations from the mus- cles, articulations, and tendonous sheaths via the root on the same side. When diseased, there is a loss of the sense of position of the limbs, of the power of estimating weights, and of co-ordination of muscular effort (ataxia). The fibres cross over in the medulla. The columns of Burdach conduct to a certain extent tactile sensations coming in from the opposite posterior root. They also contain many associative fibres, connecting different levels. Pain- sense fibres and excito-refiex fibres from the posterior roots run through these columns to reach the commissure or the anterior horns ; othei- fibres run through it to Clark's column and to the column of (roll. Hence it is a pathAvay for all kinds of afferent im- pulses. When diseased, there may be pain, anaesthesia, ataxia, and loss of reflexes. The fil^j-es cross over at once to the opposite side. The antero-lateral ascend i)ig tract conducts sensations of pain and temperature, comini>- in from the opposite side, through the anterior and posterior conmiissure. There are considerable variations in the paths of conduction of tactile tempei-ature and pain sensations, and their exact posi- tion is not positively known. In transverse lesions of the cord these tracts do not genei-ate u])ward so completelv or uniformly as do secondary dej^enerations of otlier long-fibre tracts. Hence they probably receive some interruptions in their course. Automatic Centres.— The nerves and cells of the cord are ar- ranged in complex groups which preside over certain functions or respond in a definite wav to certain stimuli. These are DISEASES OF THE SPINAL CORD. 18^ called the spinal automatic centres, secretory, vasomotor, genital, vesical tant pai-ts of these centres lie deep in the gray matter on either side of the central canal, but nearer the base of the posterior horns. Lesions of the white matter, or of the an- terior or posterior horns, do not directly afiect them. The cillo-spinal centre reaches from the seventh cervical to the second dorsal segment, inclusive. Its stinuilation causes the pupils to contract. The genital centres, including those for erection and ejaculation, reach from the first to the third sacral segment, inclusive. The bladder and rectal centres are in the fourth and fifth sacral segments, extending up and down a short distance, the bladder being perhaps a little lowt r. The spinal vasomotor ceiitres ex- tend from the second dorsal to the second lumbar segments. The vaso-dilator nerves pass out by the anterior, the constrictor by the posterior, root (Gaskiil). The gray matter contsiiuii chiefly cell groups which act as centres and distributors of nerve impulses. In the anterior horns the cells have a motor and trophic function. The larger cells are at the outer parts of the horn and send fibres to the larger skeletal muscles. The more central cells are connected with small muscles and those having more delicate functions and adjust- ments. In the still more central and intermediate parts, also, are sepa- rate trophic cells for the muscles, bones and joints, and cell groups which preside over vasomotor and secretory functions. Among these groups are the spindle-shaped cells, which send fibres to the vaso-con- strictors (Gaskill), through the ante- rior (Hill) and perhaps posterior roots (Gaskill). The cells of Clark's column receive fibres from the vis- cera and blood-vessels. Impulses pass to these cells and thence to the direct cerebellar tract and cerebel- lum. Their function is to conduct impulses from the viscera relating to equilibrium and sense of posi- They are the cillo-spinal, and rectal. The impor- FiG. 88.— Showing the Relation OF THE Arrangement of the Gray Matter, Cell Groups, and White Columns at Four Different Lev- els. Namely, mid-cervical, mid- dorsal, lower dorsal, and upper sacral. (Drawn from specimens.) 190 DISEASES OF THE XERVOUS SYSTEM. tion. They are analogrous to the fibres of the column of Goll. Accord ingr to Gaskill, Clark's column is a centre for the vaso-dila- tors. This is unlikely. The rells of the posterior horns are sensory in function and are connected with the tactile, pain, temperature, and reflex fibres of the posterior roots. The trophic centres for the joints, hones, and skin apparently lie in the posterior horns. Their fibres pass out by the posterior I'oots. ^, . . . -, Topography and Lor-aUzation.—The neurologist and surgeon need to know, for purposes of diagnosis : 1. The relation of the special nerve roots, at their point of origin, to the spinous processes. This is shown in the figure (p. 150). In general it will be seen that the different pairs of nerve roots arise opposite the spinous process of a vertebra one or two segments above those between which it makes its exit. Thus the sixth cervical originates opposite the fourth cervical spine, the sixth dorsal between the third and fourth dorsal spines, the first lumbar between the eleventh and twelfth dorsal spines. There is considerable variation in these relations, as the diagram from Reid shows (Fig. 72). 2. The next points desired are the special function of each pair of nerve roots anterior and posterior, and the level of the various centres in the cord. This is shown in the following table, based on that originally devised by Starr, modified by Mills and myself from personal experiments and the clinical and path- ological observations of Thorburn and others. Localization of the Fttnctions of the Segments of the Spinal Cord. Segment. Muscles. Reflex and Centres. Sensation. First t-ervi- Rectus laterales. cal. Rectus capitis. Aiiticus and posticus. Sternohyoid. Sternn-thyroid. Second tind Sternomastoid. Hyioocliondrium (f). Back of head to vertex third cer- Trapezius. Sudden inspiration and neck. (Occipi- vical. Scaleni and neck. i:)roduced b}' sud- talis major, occipi- Oino-hyoid. den pressure be- talis minor, auricu- Diaphragm. neath the lower bor- laris magnus. super- der of ribs. ficialis colli, and su- praclavicular.) Fourtli cer- Diaphragm. Pupillary (fourth cer- Neck. vical. Deltoid. vical to second dor- Shoulder, anterior Biceps. sal). Dilatation of surface. Coraco-brachialis. the pupil produced Outer arm. (Supra- Supinator longus. by irritation of clavicular, circum- Rhomboid. neck. flex, external mus- Supra- and infra-spi- culo-curaneous, cu- natus. taneous.) Fifth cervi- Deltoid. Satpular (fifth cervi- Back of shoulder and cal. Biceps. cal to first dorsal). arm. Coraco-brachialis. Irritation of skin Outer side of arm and Brachialis amicus. over the scapula forearm to the Supinator longus. produces contrac- wrist. ( Supracla- Supinator brevis. tion or scapular vicular, circumflex. Deep muscles of muscles. external cutaneous, shoulder-blade. Stipimdor longus. internal cutaneous. Rhomboid. Tapping the tendon posterior spinal branches.) Teres minor. of the supinator Pectoralis (clavicular longus produces part). flexion of forearm. Serratus magnus. DISEASES OF THE SPINAL CORD. 191 Segment. Muscles. Reflex and Centres. Sensation. Sixth cervi- Deltoid. Tricex>s (fifth to sixth Outer side and front cal. Biceps. Brachialis anticus. cervical). Tapping of forearm. elbow tendon pro- Back of hand, radial Subscapulai-. duces extension of distribution. Pectoralis (clavicular forearm. (Chiefly external part). Posterior ivrist (sixth cutaneous, internal Serratus magnus. to eighth cervical). cutaneous, radial.) Triceps. Tapping tendons Pronators. causes extension of Rhomboid. hand. Latissimus dorsi. Seventh cer- Triceps (long head). Anterior ivrist (sev- Radial distribution in vical. Extensors of wrist enth to eighth cer- the hand. and fingers vical) . Tapping an- Median distribution in Pronators of wrist. terior tendons the palm, thumb, in- Flexors of wrist. causes flexion of dex, and one-half Subscapular. wrist. middle finger. Pectoralis (costal Palmar (seventh cer- (External cutane- part). vical to first dorsal). ous, internal cuta- Serratus magnus. Stroking palm neous, radial, medi- Latissimus dorsi. causes closure of an, posterior spinal Teres major. fingers. bi'anches.) Eighth cer- vical. Triceps (long head). Flexors of wrist and Ulnar area of hand, back, and palm, in- fingers. ner border of fore- Intrinsic hand mus- arm. (Internal cu- cles. taneous, ulnar.) First dorsal. Extensors of thumb. Chiefly inner side of Intrinsic hand mus- forearm and arm to cles. near the axilla. Thenar and hypothe- (Chiefly internal nar muscles. cutaneous and nerve of Wrisberg or les- ser internal cutane- ous.) Second dor- Inner side of arm near sal. and in axilla. (In- tereosto-humeral.) Second to Muscles of back and Epigastric (fourth to Skin of chest and ab- twelfth abdomen. seventh dorsal). domen, in bands dorsal. Erectores spinee. Tickling mammary running around and region causes re- downward, corre- traction of the epi- sponding to spinal gastrium. . nerves. Abdominal (seventh Upper gluteal region. to eleventh dorsal). (Intercostals and Stroking side of ab- •dorsal posterior domen causes re- nerves.) traction of belly. Vasomotor centres. Second dorsal to second lumbar. First lum- None. Cremasteric (first to Skin over groin and bar. third lumbar). front of scrotum. Stroking inner thigh ( 1 1 i o -hypogastric, causes retraction of scrotum. Patellar. Striking pa- ilioinguinal.) Second lum- Vastus internus. Outer side and upper bar. tellar tendon causes front of thigh. Lum- extension of leg. bar region. ((Jenito- crural. external cu- taneous.) Third lum- Sartorius; adductors Front and outer side bar. of thigh. of thigh. Inner side Flexors of thigh. of leg and foot. Fourth lum- Extensors of knee. Gluteal (fourth to Inner side of thigh. bar. Abductors of thigh. fifth lumbar). Strok- leg, and foot. (In- ing buttock causes ternal cutaneous, dimpling in fold of long saphenous, ob- buttock. turator.; 192 DISEASES OF THE NERVOUS SYSTEM. Segment. Fifth lum bar. 3Iuscles. Outward rotators. I Flexors of knee. I Flexors of ankle. Peronei. Extensors of toes. First and I Calf muscles, st-cond sa- Glutei. cral. Peronei. Extensors of ankle. Small muscles of foot. Third, fourth. Perineal, and fifth !>a- 3Iuscles of bladder, cral. rectum, and exter- nal genitals. Reflex and Centres. Achilles tendon. Over- extension causes rapid flexion of an- kle, called ankle clonus. Plantar (fifth lumbar to second sacral). Tickling sole ot foot causes flexion of toes and retraction of leg. Genital centre. Vesical centre. Anal centre. Sensation. Back of thigh and outer side of leg and ankle ; sole ; dorsum of foot. (External popliteal, external saphenous, musculo-cutaneous, plantar.) Back of buttock and thigh, side of leg and ankle : sole ; dorsum of foot. Circumanal region, anus, rectum, penis, urethra, vagina, per- ineum. (Small sciatic, pu- dic. inferior hemor- rhoidal, inferior pu- dendal.) The blood supply of the spinal cord is a subject of great practical importance; and as our knowledg-e of it has lately been increased, I shall present the matter here in some detail. The spinal cord is supplied with blood by branches from the vertebrals, ascending cervical, and superior intercostal arteries above, and by the dorsal intercostal, lumbar, and sacral arteries below. These send off small branches which enter the spinal canal through the foramen magnum above and the interverte- bral foramina at the sides; they pierce the dura mater and are distributed on the pia mater and in the cord. The arteries that thus supply the cord are these : Primary Arteries. Origin from Ending in Anterior spinal Posterior spinal Lateral spinal Vertebral (from subclav.). Vertebral. Vertebral. Ascending cervical (from sub- clav.). Superior intercostal (from sub- clav.). Thoracic intercostal (from aorta). Lumbar (aorta). Lateral sacral (from int. iliac). Anterior median spinal ar- tery. Lateral spiual Lateral spinal Lateral spinal Lateral spinal Anterior and posterior spi- nal root arteries. Anterior and posterior spi- nal r< lot arteries. Anterior and posterior spi- nal root arteries. Anterior and posterior spi- nal root artei-ies. The anterior spinal arteries are branches of the vertebrals. They unite to form the anterior median artery, which runs down the whole length of tlie cord, receiving re-enforcements from the lateral arteries (Fig. 89). The anterior spinal arteries themselves nourish only a few upper segments' of the cord. The anterior median artery is not, as has been taught, a true prolongation of the anterior spinals, but is really made up bv the lateral .'^pinals. In other words, the vertebral artery tlirough its branches only nourishes the upper cervical region of the cord. The posterior DISEASES OF THE SPINAL CORD. 193 MU ^^ / "^ \ ^ Fig. 89.— The Spinal Cord, Anterior Surface, showing the nerve roots, root arteries, and anterior plexus (Kadyi). 13 104 DISEASES OF THE NERVOUS SYSTEM. spinal arteries are smaller than the anterior and unite on the posterior surface of the cord. They do not continue down as a posterior median arter}'— there is no such artery ; but they help to form two plexuses on the jjostero-lateral surfaces of the cord. The hiteral spinal arteries are derived from branches of the subclavian artery as far down as the second dorsal root ; below this point by the' thoracic and abdominal aorta and the internal iliac. It is an interesting? fact that at or a little below the point where the blood supply changes from the subclavian above the heart to the aorta below, pathological disturbances frequently occur (transverse myelitis). Root Arteries. — The lateral spinal arteries, after they enter the spinal canal, are called the root arteries. They pierce the dura mater and pass, some along the posterior and some along the an- terior roots, to the cord. There are about eight anterior root arteries (five to ten) and about sixteen posterior root arteries (see Figs. 89, 90). The anterior arteries are twice as large (one milli- metre in diameter) and one-half as numerous as the posterior. The root arteries of the cervical region are rather the more nu- merous. There is a large and constant anterior root artery in the trpl- "^'P Fig. 90.— Arterial Supply of Cord, r.a., Anterior root arteiy ; r.p., posterior root arterj-; tr.a., anterior plexus* tr.p. and tr.pl., posterior and lateral plexuses (Kadyi). dorso-lumbar region. The last two lumbar, the five sacral nerves, and the unpaired coccygeal nerve when it exists are accompanied by small root arteries which do not reach up to the cord itself. The lower part of the spinal cord is supplied by large root arte- ries from the lateral spinal arteries. Hence the' theory of Moxon that the circulation here is feeble is not supported by Kadyi's in- vestigations. The Fte.vuses.— The anterior root arteries pass to the anterior median fissure, and then divide, partly to form the anterior me- dian artery and partly to form a rich plexus between the ante- rior roots : this is called the antei'ior arterial plexus. Tne poste- rior root arteries subdivide before they reach the cord, and send twigs to its lateral and posterior surfaces which form the postero- lateral arterial plexus. The posterior root arteries do not anas- tomose to any extent with each other or form a posterior spinal artery, as is done by the anterior root arteries. There are there- fore three relatively independent arterial plexuses: The ante- rior plexus; the two postero-lateral plexuses. Veins.— The veins of the spinal canal outside the dura mater have valves, those within it have none. The veins reach the pia mater and cord by passing along the nerve roots. Hence we have anterior and posterior root veins, corresponding to the root DISEASES OF THE SPINAL CORD. 195 arteries, but more numerous, there being a total of forty or fifty. The anterior root veins are more numerous than the posterior, but smaller (twenty-five to twenty). The veins are a little larger than the arteries, the anterior veins being one-half to one milli- metre, the posterior one and one-half to two millimetres, in diam- eter. Thus we see that the posterior surface of the cord has more and smaller arteries, fewer but larger veins. The posterior sur- face is on the whole more richly supplied with veins, the anterior surface with arteries. The lateral surfaces are the least vascular. Number. Size. Anterior root arteries ■ Anterior root veins 5 to 10. 25 to 30. 16. 20 to 25. 1 nana. Yj, to 1 mm. 1^ mm. 11^ to 2 mm. Vessels of tJie Cord Substance. — The cord is supplid by (1) cen- tral arteries which are branches of the anterior median, and by (2) peripheral arteries which come from the plexuses on the pia mater. These two systems have been called also the centrifugal and centripedal respectively. They are not absolutely indepen- dent, but are in a good measure so. The central arteries nourish chiefly the gray matter, the peripheral arteries the white. Both systems are made of " end arteries," i.e., they do not anastomose with each other. Neither the central nor peripheral arteries are distributed in accordance with anatomical relations or physiolog- ical functions. Each cell group, for example, has a vascular sup- ply from several sources. The central arteries are given off from the branches of the an- terior median at the bottom of the median fissure and number about two hundred, each spinal segment having six or seven. The accompanying central veins are small and their total ca- pacity is less than that of the arteries, so that the central arterial pressure must be high, on account of the poor venous outlet (Kadyi). Some of the blood escapes by the peripheral veins. The peripheral arteries pass into the spinal cord for the most part along the various connective-tissue septa. There they branch and supply chiefly the white matter. They supply the apex and some of tlie deeper substance of the posterior horns and Clark's columns. The arteries of the posterior septum are the largest and most numerous, often reaching to the gray commissure. The peripheral arteries are smaller than the corresponding veins (.04 to .2 mm.). The relation is just the reverse, therefore, of that of the central arteries and veins. The peripheral arteries are small, and after passing into the cord branch into minute vessels which pass up and down and soon become capillaries. The central arteries, on the other hand, continue large, and run up and down some distance before they are subdivided into capillaries. To sum up : the arteries predominate in total capacity in the anterior plexus and central arteries. The veins in the posterior plexuses and peripheral veins. The central arteries are larger and longer than the peripheral. Hence the blood circulates more quickly and under greater pressure in the central gray of the cord. Conditions of enfeebled circulation would affect the pos- terior columns and roots more than the anterior and central parts of the cord. CHAPTER XL THE DISEASES OF THE SPINAL CORD. There are about thirty diseases which may be classified as belonging to the spinal cord. Most of these are organic in char- acter and come under the head of inflammatory and degenerative or system diseases. Functional disorders referable to the cord alone are rare ; while of organic diseases, those that result from injury and inflammation are the most common. Miologi/.— The causes of spinal-cord diseases can nearly all be formulated under the heads of injury, exposure, poisons, auto- toxiemise, infections, and excessive functioning. Persons of mid- dle life are the most predisposed, while heredity does not play an important part. Symptoms. — The symptoms of all disorders of the nervous centres can be included under the heads of those of irritation, depression, and perversion. The princii3al irritative symptoms in spinal-cord disease are pains and parsesthesise of the back and limbs, hypersesthesia and feelings of constriction around the waist, rigidity, spasms, exaggerated reflexes, and irritability of the vis- ceral and vascular functions. The principal symptoms of depres- sion and destruction are anaesthesia, ataxia, paralysis, wasting, and loss of power over visceral centres. The common form of paralysis in spinal-cord disease is paraplegia, in brain disease hemiplegia, in multiple neuritis quadruplegia. Symptoms of irri- tation and depression often accompany each other. The more superficial and meningeal the disease, the more are the symp- toms irritative; the more central and myelonic the trouble, the less the irritation and the more the paralysis and visceral dis- turbance. Thus meningitis, meningeal tumors, and hemorrhages are extremely j^ainful ; w^hile central myelitis is almost painless. Pa^/io/o.^.y.— Inflammations of the meninges of the cord are not rare ; the opposite is true of X3rimary inflammations of the cord itself. As will be shown later, most of the diseases that used to be called chronic myelitis are secondary to injuries and soft- enings. Degenerative diseases of the cord, which include such affections as locomotor ataxia and progressive muscular atrophy, used to be called " system diseases " because they affected certain long-fibre tracts or systems of cell groups. The name implies re- DISEASES OF THE SPINAL CORD. 197 strictions which are not justified in fact, and it can only be re- tained as a matter of convenience. Secondary degenerations alone are aways systemic. The cord is relatively free from ab- scesses hemorrhages, and tumors. Diagnosis. — In making a diagnosis of spinal-cord diseases, one is most helped by a thorough knowledge of the cord functions. In no part of the economy do physiology and anatomy point out more clearly the path to the clinician. Prognosis.— The spinal-cord tissue once destroyed can never be renewed, or only to a limited extent, and that as regards the nerve fibres, not the cells. It has considerable power of adjusting itself to damage; but, on the other hand, serious injury is likely to extend by the process of secondary degeneration. Functional diseases, vascular and nutritive disturbances, of the cord can never be so severe or chronic as to exclude the possibility of re- covery. The special diseases of the spinal cord are the following : 1. Malformations: Myelocele, meningo-myelocele (spina bifida), meningocele, heterojjia, amyelia, micromyelia, macromyelia, double cord. 2. Vascular Disorders : Anaemia, hypersemia, hemorrhage, en- darteritis with aneurism, embolism or thrombosis, oedema. Sec- ondary to these conditions are softenings and sclerosis. 3. Iiiflamniations : Meningitis, myelitis, abscess. Secondarily, softenings, sclerosis. 4. Degenerations : Primary : locomotor ataxia, combined scler- oses, hereditary scleroses, progressive muscular atrophy, and allied types. 5. Tiiherculo.ns : Miliary and solitary. 6. Syphilis : Gumma, meningo-myelitis, vascular disease. 7. Tumors. 8. Functional and toxic disorders. MALFORMATIONS. Spina Bifida (Rachischisis Posterior). Spina bifida is a congenital hernia of the spinal membranes, and sometimes of the cord, through a cleft in the vertebra caused by absence of the vertebral arches. It is really a malformation of the vertebral canal rather than of the cord. Etiology. — The condition is not very rare, about 1 child in 1,200 (French statistics) being affected. It is often associated with hy- drocephalus or with some other defect in development, such as ventral hernia, imperforate anus or pharynx. Hereditary influ- ence is sometimes a factor. It is a true developmental defect, 198 DISEASES OF THE NERVOUS SYSTEM. and is not clue to a primary dropsy of the cord, as was once taught. Forms.— There are three varieties described: 1. Spinal meningocele is a condition in which the spinal mem- branes alone protrude into the sac. 2. Spinal meningo-myelocele is a form in which the mem- branes and cord both protrude. 3. Syringo-myelocele (hydrorachis interna) is a form in which the fluid is in the central spinal canal, and the inner lining of the sac is formed by the meninges and thinned-out spinal cord. Anatomy. — The first two forms are the most common and are called hydrorachis externa. The fluid here lies in the subarach- noid sac, and hence the wall of the protruding cyst is lined with a b ca a bca Fig. 91.- -Meningocele. Meningo-Myelocele. Syringo-Myelocele. a, Vertebral walls; b, cord; c, membranes. the dura and arachnoid. The nerves and cord protrude into the sac in two-thirds of the cases (forming a meningo-myelocele). but in some of these only a few nerves are found. These structures, when present in the sac, lie on \t^ posterior and median surface., sometimes causing a depression there. The tumor contains cer- ebro-spinal fluid, and occasionally connective tissue and fat (Fig.Ol). Symptoms. — Spinal bifida occurs almost always in the lumbar and sacral region, the reason being that the lamina here are the last to solidify. Usually but two or three vertebrie are involved. The tumor varies in size from 3 cm. (one inch) to 15 cm. (six inches) in diameter and may have a broad base or be peduncu- lated. The outer skin is often glossy, or tough, thickened, or ulcerated. Children with spina bifida are usually feeble, badly nourished, and poorly developed mentally. Paraplegia occurs in half DISEASES OF THE SPINAL CORD. 199 the cases, sometimes with anaesthesia and involvement of the sphincters. Tahpes occurs quite often. The prognosis is grave. Most cases die unless treatment is applied, and even then the prospect is not very good. The diagnosis is easy. It is generally only necessary to ex- clude congenital tumors which happen to be located in the lumbo-sacral region. The most important question to decide is whether the cord and nerves are present in the sac. This may be assumed as probable if there is much paraplegia, anaesthesia, and sphincter trouble. The introduc- tion of an insulated needle connected with an electric battery may be tried. The treatment is strictly surgical. At present, injections of Morton's fluid (iodine, gr. x. ; potas. iodid., gr. xxx. ; glycerin, 1 i. Dose, 3 i.) have been most successful. These injections should be made in the lateral portion of the sac, and the child should be kept on the back. Puncture and withdrawal of fluid with compression is not a justifi- able operation The ligature or open- ing and excision of the sac are danger- ous, especially if, as is often the case, part of the cord and nerves lie in the sac. In recent years, surgical results have been more favorable and warrant serious consideration. No surgical treatment should be attempted, however, until two or three months after birth. Fig. 92.— Spina Bifida. Heteropia is a rare malformation in which masses of gray matter are found in abnormal situations. A false heteropia may be caused (Van Giessen) by manipulation of the cord in its removal after death. The displaced masses consist of nerve cells or neu- roglia. Amyelia or absence of the spinal cord can only exist when the brain is absent; but absence of the brain may occur without absence of the cord. In amyelia the spinal nerves are usually present. Amyelic monsters cannot live. Double cord is a very rare defect and involves only part of the cord, except in cases in which there is a double vertebral canal. Double central canal is not rare. It usually involves only a part of the cord. The two canals are side by side. Asymmetry of the cord, usually due to abnormality in the course of the pyramidal tracts, is not extremely rare. Splitting of the cord and defects in development at spe- cial levels are occasionally observed. MiCROMYELY is a condition in which the spinal cord is abnor- 200 DISEASES OF THE NERVOUS SYSTEM. iiially short or small in size, and is not a very rare anomaly. The normal adult cord has a diameter in its various parts of 6 to 9 mm. (dorsal), 8 to 11 mm. (upper cervical), 15 mm. (cervical swell- ing)^ and 12 mm. (lumbar). Spinal Hemorrhage (Spinal Apoplexy). This general name may be given to (1) spinal meningeal hem- orrhage or hiematorhachis, and (2) hemorrhage into the cord sub- stance, or hematomyelia. 1. Spinal meningeal hemorrhage is far the most com- mon form. It may be outside or inside of the dura, the former being rather oftener seen. Etiology.— It occurs in newly born children and in adults, and is more common in men than in women. Injuries, falls, fractures of the spine are the most frequent exciting causes. Severe con- vulsions from epilepsy, eclampsia, tetanus, chorea, or strychnia may be a cause, also severe muscular exertion. Purpura and the blood states following malignant infectious fevers, bursting of an aortic or vertebral aneurism and cerebro-spinal meningitis are rare causes. Symptoms.— \n small hemorrhages there may be no symptoms. In large effusions there are sudden, very severe pains in the back, extending into the limbs, numbness, tingling, hyperesthesia, and muscular spasm, especially of the back muscles. Later there may be weakness or paralysis and anaesthesia, with disorder of the vis- ceral centres. The symptoms reach their height usually in a few hours. Then amelioration may occur, followed by slow recovery or with symptoms of chronic meningitis. Rarely death occurs early from exhaustion. Diagnosis. — A history of injury, child-birth, sudden onset of attack, with symptoms of pain and irritation which rather rap- idly subside, point to extra-dural hemorrhage. In haematomyelia there is less pain and irritation, but more profound paralysis and anaesthesia. The same is true of crush of the cord from fracture or dislocation. In tetanus there is a slower development of the symptoms, and trismus is present. The prognosis is grave in severe cases; but if the patient sur- vives three or four days, the prospect of partial or nearly complete recovery is good. The treatment is perfect rest in bed and the administration of remedies to move the bowels and relieve pain; leeches and other local applications are of doubtful value. It is of no use to give styptics except in purpura, when mineral acids or chloride of calcium may be tried. Later, one may give iodide and mercury and use blisters to the back. DISEASES OF THE SPINAL CORD. 201 Hemorrhage into the Substance of the Cord (Hjema- TOM.YEijiA).—Btiology.—The condition is not very rare. It may- be primary from disease of the blood-vessels or purpura hsemor- rhagica; or it may be secondary to myelitis and tumors. Pri- mary hemorrhage occurs sometimes in infancy, but usually in males between the twentieth and fortieth year. Injuries, over- exertion, exposure, excessive coitus ((iowers), and convulsions are causes. The symptoms develop rapidly, with at first feelings of numb- ness or weakness for one or two hours or longer. Then there is a sudden paraplegia, with anaesthesia or ataxia or both. The sphincters may be paralyzed ; the urine has to be drawn. The reflexes may be abolished at first, but soon return and become exaggerated. There is considerable pain in the back. If the lesion is high up, the arms and thorax are involved. The acute symptoms begin usually to subside at the end of seven to ten days and the disease takes the character of a chronic myelitis. If improvement does not occur, evidences of acute myelitis appear and the patient dies. Pathology. — The vessels involved are the central arteries, which supply the gray matter and are under relatively high pres- sure. The rupture of the vessel, when due to disease, is caused by a fatty degeneration of the coats ; miliary aneurisms, such as are found in the brain, rarely develop in the cord. Hemorrhage often precedes or begins a myelitis, of which it may be the cause or the result. The clot may be absorbed, leaving a cavity as in the brain ; or the broken-down tissue may become the centre of a myelitic focus. The hemorrhage is usually single, but there may be several. Multiple capillary hemorrhages occur, but usu- ally only from asphyxia and convulsions. It is possible that some of the cases of disseminated myelitis occurring after infec- tious fevers start from small hemorrhages. Diagnosis. — The points to be noted are the sudden onset with- out long premonitory symptoms, and the absence of fever, fol- lowed later by gradual improvement. The disease is often mis- taken for acute primary myelitis, which does in fact often follow it. Meningeal hemorrhage is more painful, and there is less paralysis, more spasm, and a more complete recovery later. Prognosis. — This is often serious as regards life, and always serious as regards health. It depends on the extent and seat of the hemorrhages. Dorsal hemorrhages are more favorable, cer- vical the least. Treatment.— Kh^o\\xte rest, ice-bags to the spine, and small doses of aconite given early are all that can be done, except the use of symptomatic remedies. Treatment must be applied at once. The late treatment is the same as that for myelitis. 202 DISEASES OF THE NERVOUS SYSTEM. The Caissox Disease (Diver's Paralysis). Etiology.— The caisson disease is the name g:iven to a more or less complete paraplegia which occurs in persons who work in caissons or diving-bells, and which is brought about by the sud- den return from a condensed air to the normal atmosphere. Per- sons employed in caissons or bells work usually under a pressure of from one to four atmospheres, which means a pressure of from fifteen to fifty pounds to the square inch. Accidents rarely if ever occur when the pressure is not over one atmosphere, and they are also rare if the person has not been subjected to the pressure for at least an hour. DiiTerent persons vary in susceptibility to the effects of this change in the atmospheric pressure, and those unused to the work are more liable to be attacked. The symptoms set in usually very soon after the pafient has come out from the caisson, but they may be delayed for half an hour or more. They consist of intense neuralgic pains in the lower extremities, often affecting especially the joints. There is at the same time epigastric pain. Nausea and vomiting and weak- ness in the lower limbs, amounting in some cases to absolute paral- ysis, very soon appear. There may be headache, dizziness, and sometimes even coma. If the paralysis is considerable, it is usu- ally accompanied with anaesthesia. Disturbances in the sphinc- ters, with retention of urine and constipation, may also be present. The symptoms vary very much in severity, from pain, weakness in the legs, and nausea up to frightful neuralgic attacks and complete paralysis, motor and sensory. The upper limbs are rarely affected. In a few instances hemiplegia, however, has been observed. The disease lasts from a few hours up to several weeks. Death occurs in some of the very severe cases. The symptoms having reached their climax gradually ameliorate, and a complete cure is not infrequent. In some instances, how- ever, the patient is left with a permanent paraplegia and the or- dinary symptoms of a transverse myelitis. Pathology.— V^hew the patient is under atmospheric pressure in the caisson, the blood is driven from the surface of the body, and .the internal viscera, including the brain and cord, are con- gested. The sudden change from the abnormal to normal pres- sure produces a rapid flow of blood from the internal organs to the periphery. The viscera not inclosed in bony cavities are en- abled to relieve themselves of this cohgestion without much harm, but the circulation in the brain and spinal cord is less elastic; that in the spinal cord being less even than that in the brain. The result is that congestions and small hemorrhages ensue, pro- ducing a destruction of the nerve tissue. In other cases there DISEASES OF THE SPINAL CORD. 203 seems to be a blocking up of some of the small vessels, with con- sequent softening of different portions of the cord and to a less extent of the brain. It is supposed that one element in produc- ing the morbid phenomena is the escape of oxygen and carbonic- acid gas from the blood into the tissues or into the blood-vessels. This mechanism, however, has not been absolutely proven. It will be seen, however, that on the w^hole the sudden change in atmospheric pressure leads to vascular disturbances with rupture or obliteration of blood-vessels, with consequent destruction and necrosis of tissue. Following this is a reactive inflammation pro- ducing the phenomena of an ordinary acute myelitis. The treatment is largely prophylactic. The workmen engaged in the occupation should be carefully selected and should accus- tom themselves to their work. They should spend a longer time in coming out of the caisson. If symptoms supervene, it is rec- ommended that they be put back under a slight atmospheric pressure at once until these symptoms disappear. When the disease has developed, it can only be treated by symptomatic remedies. The patient should be kept quiet and given, if nec- essary, hypodermics of morphine. Dr. A. H. Smith recommends the use of ergot. Later on, the various neuralgic and paralytic symptoms may be treated on the same principles as those em- 13loyed in myelitis. Spinal Hyperemia, Acute and Chronic. ^^io?0(7v/.— Acute spinal hypersemia is produced by sexual ex- cesses, violent physical exertion, suppression of menstrual dis- charges, and certain poisons like strychnine. It occurs also in the first stage of acute inflammatory diseases. Chronic spinal hypersemia is, so far as is absolutely known, a very rare condition. Chronic hypersemia of the membranes may be the residuum of a meningitis or of injury, and these are probably the most common causes. As to the causes of the chronic hypersemia of the cord substance itself independent of other diseases, we can say nothing definitely. The symptoms of acute spinal hypersemia are feelings of heavi- ness and weight in the limbs and around the loins, numbness, creeping sensations and actual neuralgic pains, weakness of the lower limbs, with twitchings of the muscles. There may be also some disturbance in the sphincters", though of this one can speak less certainly. The symptoms are nearly always confined chiefly to the lower limbs. The statement that they are increased by lying on the back and ameliorated by lying on the face is not always true, since posture, unless greatly prolonged, influences but very slightly, if at all, the circulation in the spinal cord. 204 DISEASES OF THE NERVOUS SYSTEM. The symptoms of chronic spinal hypersemia, when this hyper- semia involves the meninges chiefly, are probably somewhat iden- tical with those of spinal irritation. They will be described under that head. Pathology. —The circulation of the blood in the spinal cord, as has been shown in the article on anatomy, is one which it is diflS- cult to disturb; but which, once disturbed, is rather slow in being brought back to its normal condition. Thus violent activity of the heart and great increase in the arterial pressure, and the op- posite conditions of weakened heart and lowered arterial tension, appear but little to modify the spinal functions. Hence it is un- likely that the large number of clinical symptoms that have at times been attributed to hypersemia of the spinal cord, or rather to disturbances in the circulation of the spinal cord, have really been due to that cause. Treatment. — The treatment of spinal hyperemia consists in the application of cups to the back, quiet in the horizontal posi- tion, preferably upon the side or face, ice and counter-irritants to the spine, morphine and bromides internally. In the more chronic cases muriate of ammonia, iodide of potassium, and the galvanic current may be used. The use of ergot, which has been recommended, in my experience has been found of little or no value. Spinal Anemia. Even less is known in regard to the etiology and symptoma- tology of spinal antemia than of spinal hypersemia. Undoubtedly severe hemorrhages or diarrhoeal discharges, and an aortic ob- struction which cuts off the circulation of the blood from the spinal cord, will produce a spinal anaemia, and when this is se- vere the functions of the cord are nearly abolished. But prac- tically we do not know of any causes which produce an acute or chronic aniemia leading to serious and prolonged disturbances in the spinal functions, aside from diseases of the arteries of the spinal cord themselves such as occur in advanced life. In the most profound anaemias which must affect equally the spinal cord with other organs very little special disturbance of this organ can be discovered. Here, too, the supposed test of improvement on ly- ing on the back is, in the writer's ojjinion, a fallacious one. It has been customary to associate with spinal anaemia a class of symp- toms characterized by pains in the back of the nature of spinal irritation, weakness of the legs amounting to paraplegia— a type of symptoms that has been called spinal concussion, but it is im- possible in the present stage of science to say that a spinal anaemia actually underlies and causes this condition. DISEASES OF THE SPINAL CORD. 205 INFLAMMATION OF THE SPINAL MEMBRANES (SPINAL MENINGITIS). The meningeal inflammations are : External meningitis. ^ a<¥ +• j.u i x Internal menin|itis. \ ^ffectmg the dura mater. Leptomeningitis. [ Affecting the pia mater. Hypertrophic pachymeningitis. [ Affecting both membranes. External Meningitis, Pachymeningitis Externa (" Compression Myelitis ''). Etiology. — The disease is rare, and always occurs secondarily to some other morbid process. This process is in most cases tuberculosis and caries of the vertebrae. Other causes are sup- purative inflammation in the neighborhood of the vertebrae, psoas abscess, purulent pleurisy, peritonitis, and puerperal pyaemia. When the disease arises from inflammations in the visceral cavi- ties, it is thought to be caused by an ascending neuritis. The Symptoms. — The symptoms are those of irritation of the motor and sensory roots ; later, compression of them and of the spinal cord, local pain in the back, radiating pains, tenderness, hypersesthesia, twitching, paresis, paraplegia, exaggeration of re- flexes, and involvement of the sphincters. Anaesthesia occurs in severe forms. The disease, when chronic, may extend to the other membrane and cord, causing what is termed " compression myelitis." Pathological Anatomy. — The inflammation, if acute, is gener- ally a fibro-purulent one, this being the form usually caused by vertebral caries. The dura mater is covered by a layer of case- ous, semi-solid matter, often very thick and most extensive pos- teriorly. It involves the dura vertically for several inches. In chronic forms the deposit is made up of connective tissue and the cord is compressed. In purely suppurative forms the cellu- lar tissue outside the dura is infiltrated with pus throughout a great part of the canal. The diagnosis is based on the presence of the primary local disease, the kyphosis, the radiating pains, and tenderness, and by the combination of motor and sensory irritation and paralysis. The pro.(/?z-06Z5 is generally bad because the original disease is a serious one. The treatment consists in attention to the local caries or in- flammatory focus. It is therefore purely surgical. Internal Meningitis, Pachymeningitis Interna, Hemorrhagic and Hypertrophic. Inflammation of the inner surface of the dura mater occurs in two forms— the hemorrhagic and the hypertrophic. As the latter IS generally but a sequel of the former, I shall describe the two to- gether under the head of hypertrophic pachymeningitis. 20G DISEASES OF THE NERVOUS SYSTEM. Etiohtgy.— The disease occurs almost always in adult life. A few cases have been reported in children ( Gibney). It usually affects males. Syphilis, alcoholism, exposure, and trauma are ex- citing: causes. jSi/t)ipto /US. —The disease begins gradually with symptoms of irritation (irritative stage). The patient suffers from pain and stiffness in the neck. The pains radiate up to the occiput and down the back; numbness, prickling, and pain are felt in the arms, more in one than the other. The pains exacerbate and are worse at night. Stiffness and cramjjs may affect the arms. Nausea and vomiting sometimes occur. After five or six months, symptoms of paralysis appear (para- lytic stage). The ai-ms are first affected. They become weak, atrophy occurs, associated with contractures and rigidity. There is still pain, and in addition anaesthesia, hyperjesthesia, and trophic changes. Later, paraplegia, with rigidity, exaggerated reflexes, and spinal epilepsy, develop. The patient becomes weaker, and finally dies of exhaustion or from some intercurrent trouble. The disease sometimes takes what is called the periph- eral type. Then the symiDtoms are more localized in the extrem- ities. Usually it is of the cervical type and presents symptoms as described above. In either form the disease is a chronic and painful one. Pathology.— The disease starts as a hemorrhage upon the sur- face of the dura. This leads to a chronic inflammatory process, new hemorrhages occur, and a fresh inflammatory deposit is made until the cord is finally encircled and compressed by a dense con- nective-tissue mass, which involves the pia and to some extent the cord substance. The process is analogous to that of cerebral pachymeningitis hemorrhagica. The cervical region is usually attacked. Prognosis. — A few cases have been reported practically cured. More cases eventually die. Sometimes, however, the disease comes to a standstill for a long time. Diagnosis.— This must be made from tumor, myelitis, Pott's disease, wry-neck, and progressive muscular atrophy. The his- tory of injury, the slow progressive course, and the localization of the symptoms, their bilateral character and the pain, give the most help. It is not always possible to exclude a tumor. Treatinent. — The not rare syphilitic origin of the disease must be borne in mind. Counter-irritants, electricity, hydrotherapy, and symptomatic remedies for the pain and spasms are indicated. It is possible that surgery may help these cases. Acute Spiral Leptomexixgitis (Ixflammatio^^ of the Pia Mater of the Spiral Cord). Etiology. — This is a rare disease, occurring alone, but is com- mon in connection with disease of the cerebral pia mater. Children are oftenest affected, and among adults, males. Al- coholism predisposes to it. The disease is always secondary to an infection or a traumatism. The infections are tubercle, syph- ilis, typhoid fever, and sei)tic{emia. Extension of inflammation from neighboring parts and surgical operations are occasional DISEASES OF THE SPINAL CORD. 207 causes. The cases attributed to rheumatism, exposure, insola- tion, are in reaUty due to some infection, and the virus of cerebro- spinal fever sometimes attacks the cord alone. Symptoms.— The disease begins with pain in the back, radiat- ing along the nerves. There is usually a chill and some fever. The pulse may be fast or slow. The pain increases, and is ac- companied with dorsal tenderness and rigidity of the muscles of the back, amounting sometimes to opisthotonus. The skin is very hyperaesthetic and the reflexes are at first increased. There is constipation, and sometimes retention of urine. After a time symptoms of paralysis come on, with anaesthesia and retention of urine. The patient becomes weaker, bed-sores may form, and death from exhaustion follow. The disease lasts from a few days to several weeks. The dominant symptoms in the first stage are those of irrita- tion, viz. : Pain in back and along the nerves, hypersesthesia, muscular spasm. In the second stage, paralysis, atrophy, and anaesthesia. In the tuhei'cular form of meningitis the symptoms come on more slowly. In septic meningitis the symptoms are of the severe and typical kind described. In meningitis from other infections the symptoms are not so severe as a rule. Pathological Anatomy^ — Acute leptomeningitis shows a some- what different exudate according to the nature of the infecting micro-organisms. The common form is the suppurative exudate which may be due to the streptococcus pyogenes and other pyo- genic micro-organisms, and to the pneumococcus. The purulent matter is usually distributed along the whole length of the cord, but more posteriorly and often more in its lower portion. It may also be localized chiefly at certain levels. The spinal fluid is in- creased in amount. The arachnoid, the inner surface of the dura, and the tissue of the cord itself are usually involved. If the dis- ease lasts several weeks, the purulent matter is absorbed in part and an increase in connective tissue takes place, binding the dura, arachnoid, and pia to the cord. The nerve roots are sur- rounded and compressed by the inflammatory product. In tubercular meningitis there is less exudate. It is more of a fibrinous character, and grayish in appearance. Tubercle gran- ulations are seen distributed over the pia, arachnoid, and inner surface of the dura. Simple exudative meningitis rarely occurs. The inflammatory process often ends in a production of new connective tissue and sometimes the establishment of a chronic leptomeningitis. The diagnosis must be made from myelitis, tetanus, rabies, rheumatism of the dorsal muscles, gonorrhoea! rheumatism, and strychnine-poisoning. In myelitis there is relatively little pain 206 DISEASES OF THE NERVOUS SYSTEM. and much paralysis; in tetanus there is trismus, fever is absent^ and there is a history of trauma. Tubercular meningitis comes on more slowly, is rarely spinal alone, and there may be evidence of local tuberculosis elsewhere. The prognosis is not good, but is especially bad in tubercular meningitis and in cases with high fever, severe pains, and early paralysis. Chronic meningitis sometimes remains after the acute symptoms subside. Treatment.— This, consists first in perfect rest and quiet; leeches should be applied along the spine, then hot poultices or ice-bags; opium is to be given lor relief of pain; mercurial purges and small doses of iodide of potassium or sulphate of magnesium may be given at short intervals. Later, blisters and counter-irritation and lukewarm baths are indicated. Chroxic Leptomexixgitis axd Mexixgomyelitis. Etiology. — This disease, which used to be often diagnosticated, is now believed to be rare, and always secondary to an acute pro- cess or to syiDhilis and jjerhaps chronic alcoholism. It occurs oftenest in adults and in males. Trauma, and especially concus- sion of the spine, used to be thought a frequent cause, but in most of such cases the trouble is simply, a hypera^mia or else neu- ralgic and functional. The symj^tonis gradually develop after an acute meningitis or an injury, and they are the same in character as those of the acute process. There is pain in the back, increased on movement and radiating about the trunk and down the limbs ; tenderness along the spine, stiffness of the back, twitching and spasms in the limbs with some weakness, and later some paralysis, wasting, and anaesthesia, with weakness of the bladder. These jparalytic symptoms, if severe, however, mark an invasion of the spinal cord. Cutaneous eruptions, such as herpes, may appear. The symp- toms run an irregular course, with periods of improvement. They always become less when the patient rests. Pathological Anatomy.— The inflammation consists of a pro- liferation of connective tissue (productive inflammation of Dela- field). The result is a thickening and opacity of the pia mater and arachnoid. The dura mater may be involved, but only in severe cases. The process may invade the spinal cord, causing an " annular ^' or ringlike sclerosis, from which the disease extends into the cord in wedge-shape masses at various parts, causing eventually an involvement of fibre-systems and secondary degen- erations up and down. This somewhat rare terminal condition is called meningo-myelitis. The diagnosis must be made from suinal irritation, locomo- DISEASES OF THE SPINAL CORD. 209 tor ataxia, myelitis, vertebral caries, and torticollis. In spinal irritation there are not the rigidity, severe radiating pains, twitch- ings, atrophy, or paralysis; and neurasthenia or hysteria exists. In locomotor ataxia the knee jerk is lost, there is ataxia, and there is little paralysis, nor is there local tenderness over the spine. In vertebral caries the ])ain and tenderness are much more localized, and there is spasmodic fixation of the trunk. The i^ain is more continuous and dull, and is increased by lateral pressure and lessened by extension. There is usually also some deformity. If compression occurs there is exaggeration of the reflexes and paraplegia, without much anaesthesia. After all, however, with Pott's disease there may be a local meningitis. Treatment.— X% chronic meningitis is usually the product of syphilis or the relic of traumatism or of an acute process, the in- dications for treatment are simple. Rest is the essential thing. With this could be combined the systematic and persistent use of counter-irritants. The hot iron is usually best, because its wounds heal so quickly. Cupping is also useful if done vigor- ously and often. Internally, iodide of potassium, small doses of bichloride of mercury, nitroglycerin, and digitalis may be given ; also the salicylates and ergot. Both the latter drugs should be employed in large doses, if at all. Electricity in the form of gal- vanism and cocaine by local injection, or cata^jhoresis, may be tried. 14 CHAPTER XIL MYELITIS-OFLAMMATION OF THE SPINAL CORD. Myelitis is an inflammation of tlie spinal cord. It may be acute, subacute^ or clironie. It may affect the anterior horns chiefly, when it is called an- terior ^poliomyelitis ; or both the gray and white matter, when it is called diffuse myelitis and transverse myelitis. The forms are still further divided, in accordance with their location, into an- nular or marginal myelitis where the inflammation involves the periphery of the cord; disseminated myelitis where it occurs isolated in different parts of the cord ; x>eriependymal myelitis where it surrounds the central canal. Myelitis is given ditterent names also in accordance with its cause. Thus we have hemor- rhagic myelitis, a form in which the initial process is due to or associated with a hemorrhage; compression myelitis, due to ver- tebral caries, septic or purulent myelitis or abscess of the cord; and tubercular and syphilitic myelitis. For practical x^urposes the following classification is sufficient: Acute myelitis— j 1, Anterior poliomyelitis. "With exudation and necrosis. ( 2. Transverse myelitis. AVith suppuration. - 3. Abscess of cord. ^, . ,.^. (4. Chronic anterior polio- Chronic myelitis— y r if- With necrosis and proliferation. / ^ ^ ^ .... ^ ^ o. Transverse myelitis. f 6. Marginal myelitis. Rare forms. \ I Periependymal myelitis. j 8. Disseminated myelitis. L 9. Compression myelitis. Acute Traxsverse Myelitis (Acute Softexixg of the Spixal Cord). Definition.— Acute myelitis, so called, is generally an acute soft- ening of certain parts of the cord, with secondary inflammatory reaction. It is in extremely rare cases a primary exudative and necrotic inflammation. In other rare cases the inflammation is suppurative, and we then have spinal ab.s-cess. Forms.— Tim common form is one that involves one or two MYELITIS — INFLAMMATION OF THE SPINAL CORD. 211 inches vertically of the spinal cord, and is hence called acttte transverse myelitis. Since both gray and white matter are in- volved, it is also called a diffuse myelitis. Acute transverse myelitis (softening) is the commontype. An acute disseminated myelitis sometimes is met with. Other rarer types are named, in accordance with their location : margi- nal, central, or periependymal. There is also an acute meningo- myelitis, the result usually of a meningitis. Etiology. — Predisposing causes are a neuropathic constitution, the male sex, early adult life, occupations calling for exposure, and muscular strain. The exciting causes are exposure to cold, blows, falls, fractures, strains, extension from neighboring organs, syphilis, infective fevers, and septic infection. Injury is the most frequent cause and syphilis next. But most of these causes pro- duce primarily mechanical destruction, hemorrhages or throm- boses, and the inflammation is secondary. Symptoms. — Prodromal symptoms are rarely present, but there may be slight parsesthesise or pain in the back and limbs. Some- thiies there is a chill, and in a few instances convulsions have been noticed. The initial symptoms consist of feelings of numbness, usually in the feet and legs, which seem heavy and weak. Some pain may be felt about the back. The patient soon finds that he cannot walk easily and that he moves his legs with an effort. In a few hours a paraplegia with anaesthesia has developed, and if the lesion is in the cervical cord the arms are paralyzed also. All these symptoms may come on in the day-time or during sleep. Retention or incontinence of urine and constipation are early symptoms. There may be some fever. Symjytoms of the Attack. — If the patient is now examined, it will be found that he cannot walk or stand, but can move his legs a little. He complains of a sensation like a band around his waist or at the level of the spinal lesion (girdle-symptom). His legs feel numb and heavy, but there is little pain and no tender- ness. Anaesthesia to touch, pain, and temperature exist in vari- ous degrees on the limbs as high up as the lesion. The anaesthe- sia, if not total, is greatest to touch, next to temperature, and least to pain. He has vesical anaesthesia, the urine is retained and he has to have it drawn. The bowels are constipated, but if ene- mata are given the faeces may pass away without his knowledge, owing to rectal anaesthesia. If the lesion is lumbar there is abolition of the sexual power; but if dorsal or cervical, strong erections may occur without the patient's feeling them. When the lesion is above the lumbar cord, also, the bladder may auto- matically and forcibly contract and expel the urine. In time the bowels regain some power. The paralysis in the limbs affects the 212 DISEASES OF THE NERVOUS SYSTEM. flexors of the feet and legs more than the extensors. The patient can push down his hmbs better than he can draw them up. Tiie temperature of the hmbs for a few days is raised, but after this it falls a few degrees below normal. The skin becomes rough, cold, congested; and excessive perspiration may take place. The general bodily temperature is usually normal through- out the disease, but in some cases a fever develops of 102' to 101^ and continues. The prognosis is then bad. Bed-sores may develop early, within a few days or weeks. They appear oftenest upon the buttocks and heels, and are due to trophic disturbance, combined with pressure and pyogenic in- fection of the parts. If the lesion is lumbar, the tendon and skin reflexes are much weakened and the paralysis is somewhat flaccid. The muscles also tend to waste and show degenerative reactions. If the lesion is dorsal, as is more often the case, the reflexes are present, and after a time become exaggerated; contractures and spasms de- velop; the legs may become drawn up and deformities produced. If the lesion is so complete as to entirely cut across the cord, there may still be some excessive muscular tension, but the reflexes will be abolished (Bastian). When the cervical region is attacked the arms are involved as well as the legs, and generally to a severer extent. There may now be also unequal dilatation of the pupils from involvement of the cilio-spinal centre; and optic neuritis from some cause has been known to occur. In extensive involve- inent of the upper part of the cord there may be paralysis of the intercostal muscles and disturbance of the heart's action. The disease having in a few days reached its height, usually remains stationary for a few weeks, and then, should the patient live, improvement slowly sets in. In some cases evidences of ex- tension upward or downward occur (ascending or descending myelitis) ; the symptoms become more severe, and in a few weeks, or oftener months, death occurs. As improvement begins, a return of sensation is first noticed (one to six months); this is followed by return of more or less motion (six to eighteen months). Spasms and contractures now develop, owing to a descending degeneration. A certain amount of ataxia from ascending degeneration, with a little anaesthesia of the skin, may remain, so that if the patient has sufficient motor power to walk somewhat, he presents many features of " ataxic paraplegia " (see p. 249). Some improvement may be expected for from one to two years. A few cases get almost entirely well. The majority become more or less paraplegic and bed-ridden, in which condition they are regarded as cases of chronic myelitis. Fatholoijlral Anatomy.— T\\q early changes found in acute MYELITIS — INFLAMMATION OF THE SPINAL CORD. 213 myelitis are those of inflammation, hemorrhagic extravasation, and softening. Often it is impossible to say whether the i^rimary process was inflammatory or due to a hemorrhage or softening. Macroscopically^ the cord at the affected part appears soft, swollen, and either red and hyperiemic or i^ale and an^enjic. In rare cases no change is apparent to the naked eye. In later stages the parts are white or gray, shrunken, and hard. The cord may be reduced to a thin shred. The meninges about the affected I)arts are often thickened, inflamed, and adherent. Microscopically, if the process is primarily inflammatory we find intense congestion, distended blood-vessels, emigrated Avhite- blood cells in great number, especially in the perivascular spaces, swollen axis cylinders and oedematous swelling of the myelin sheath, red-blood cells, cells filled with fat granules known as compound granular corpuscles, or Gluge's corpuscles. These are leucocytes which have taken up fat granules. A jieculiar form of cell, stellate in shape, known as spider cells or Deiter's cells, may be seen. They are proliferated neuroglia cells. The nerve cells lose their granular or reticular appearance, become homo- geneous, swell up, fat granules appear in them, and a peculiar co- agulation process attacks tlie cell and body. The cell processes retract, become thick, and finally drop off. Vacuoles are sometimes seen in the nerve cells ; but these are very rare if the tissue is prop- erly preserved. Besides the above evidences of vascular and con- nective-tissue activity and of cell destruction, one sees granular matter, broken-down nerve fibres, and other evidences of nerve disintegration. Pigment or extravasations of blood, and in later stages bodies resembling starch granules (corpora amylacea), may be seen. They are probably modifications of the myelin substance. If the lesion is primarily softening there may be much congestion, but the blood-vessels are less distended and fewer Avhite cells are found in the perivascular spaces. The connective-tissue cells are less numerous. The nerve cells are swollen, glassy, and stain badly. There is a great deal of granular matter and nerve detri- tus. It is thought that in inflammatory swelling of the nerve cells they take up the carmine stain, but in degenerative changes they do not.* * lu the different stages of acute degeneration, the nerve cells, particularly those of the anterior horns, show various appearances. These have been described by Friedmann as— 1, homogeneous swelling, hyaline swelling; 2, sclerosis; 3, simple atrophy; 4, fatty and molecular decomposition; 5. cloudy swelling. The degenera- tion begins in the cell body and then involves the processes and the nucleus; finally the whole cell is involved. Nerve cells do not often undergo the acute general death called coagulation necrosis (Friedmann), though the process of sclerosis so called resembles it somewhat. 214 DISEASES OF THE NERVOUS SYSTEM. The connective-tissue changes are most noticeable in the white matter. The axis cylinder and myelin sheath are here often so disintegrated that in thin sections they drop out, leaving holes in the section and giving it a vacuolated appearance. The lesion, whether destructive or inflammatory, may extend up or down the cord, often in the course of certain tracts. Sometimes a de- structive process extends a long way through the central part of the cord (perforating necrosis). After three or four weeks, if the patient lives, the process of absorption and cicatrization begins, and secondary degenerations occur. The granular and fatty matters and leucocytes disap- pear, the blood-vessels are thick-w^alled and distended but less numerous, connective tissue gradually takes the place of the de- stroyed nerve cells and fibres. The axis cylinder is the last to be destroyed and has the greatest power of recuperation. The nerve cell, if once destroyed, is never developed again. The cord at the point or points inflamed or softened becomes reduced to a mass of connective tissue containing, perhaps, a few nerve fibres and cells. In this stage the condition is one that is known as chronic myelitis. In some cases a cyst is formed in the affected region. In fatal cases the inflammation and softening continue ; fresh areas of cord are involved, much meningeal exudation takes place and finally death occurs. The process may in very rare cases be still more acute, suppuration and abscess occur, and here death also rapidly ensues. The inflammatory and softening processes above referred to are described in accordance with their appearance as red soften- ing, yellow softening, white softening. A form of so-called in- flammation known as inflammatory oedema is also described. It js an abortive inflammation, " a lymphatic congestion," analogous to vascular congestion. The diagnosis of acute myelitis must be made from hemor- rhage, acute embolic or thrombolic softening, acute ascending paralysis, multiple neuritis, meningitis, and meningeal hemor- rhage, and hysterical or functional paralysis. Spinal hem- orrhage comes on suddenly and is usually not attended with fever. If meningeal, it is attended with pain. Acute softening cannot be distinguished from acute myelitis, of which it is probably the starting-point in many cases. In acute ascending Ijaralysis the disease is progressive, . there is no involvement of sensation, no atrophy, and little change in the electric irritability. In multiple neuritis the onset is slower, there is more pain and local tenderness and sensory disturbance, and the bladder and rectum are rarely involved. In meningitis there is pain and ten- derness in the back and limbs, rigidity, cramps, a little paralysis, MYELITIS — INFLAMMATION OF THE SPINAL CORD. 215 and no bladder trouble. In hysterical paraplegia there are no marked atroj^hic changes, but little spasm or rigidity, no electri- cal changes, and the stigmata of hysteria may be found. The sensory disturbances are variable and somewhat characteristic. The diagnosis of the location of the lesion is made by studying the height of the amiesthesia, the skin reflexes (see p. 190), and the distribution and extent of the parah^sis. Lesions of the lumbar region involving the gray matter cause very complete paraple- gia with sphincter troubles and degenerative electrical reactions. Lesions in the dorsal cord cause a less complete paraplegia, but, owing to the secondary descending degenerations of the lateral column, rigidity, exaggeration of the deep reflexes, and contrac- tures occur. Lesions of the cervical cord cause paralysis of the arms, with degenerative reactions in the muscles. The paraplegia is spastic and there is not much muscular wasting. If the lesion cuts ofT the cord entirely, the limbs are paralyzed and may be somewhat rigid, but the deep reflexes are absent. Prognosis. — The prognosis is worse the more complete and extensive the paralysis. It is worse in serious motor paralyses than when sensation is chiefly involved. It is best in dorsal myelitis and worst usually in cervical mye- litis, other things being equal. Bed-sores and slight fever are un- favorable signs, so also is severe involvement of the bladder and rectum. Recovery of sensation gives good hope of recovery of some motion. Total absence of recovery of sensation and motion after six months is very unfavorable. Improvement may be ex- pected up to eighteen months after the onset, and in some cases even longer. In compression myelitis there is more chance of recovery than in the other forms. The previous existence of syphilis does not affect the prognosis of cases of true myelitis. Treatment. — In the attack, the patient must be put to bed, leeches or wet cups should be applied to the spine, diaphoresis should be promoted, small doses of aconite and nitroglycerin should be given, and a calomel purge administered. The bladder s'hould be watched. After a week, moderate doses of iodide of potassium should be given. After about three weeks, if there is no fever, electricity may be applied carefully and strychnia ad- ministered. Bed-sores should be guarded against by the use of water beds or cushions, absorbent cotton, bathing the parts with alcohol and weak solutions of tannin. Infusion of buchu, boracic acid, and tincture of hyoscyamus will often help the bladder dis- turbance. After acute symptoms subside, tonics such as arsenic, iron, and strychnia in small doses may be given. Suspension maybe tried carefully; mechanical appliances may be used to help the rigid limbs; lukewarm baths, douches, and massage are helpful to some extent. 21C DISEASES OF THE NERVOUS SYSTEM. Chronic Myelitis (ixcludixg Transverse, Diffuse, Disseminated, and Compression Myelitis). Chronic myelitis is the name given to a disease characterized by a elironic inflammation of the spinal cord and to the chronic reparative i^rooesses which follow acute inflammation, injury, and softening. Chronic myelitis is usually a mixture of inflammatory, reparative, and necrotic processes. i^^07-/?2.y.— Different names are given to chronic myelitis in ac- cordance with the part of the cord affected. Usually the disease affects only certain levels, and then it is called transverse mye- litis. More rarely it is diffuse or disseminated, central or mar- ginal. When caused by pressure from vertebral disease it is called comjyression myelitis. Mioloyy.— The disease maybe either primary or secondary. The 2^rimary form is much the rarer. It occurs chiefly in adults and in early and middle life, and much oftener in males. Expo- sure, shocks, infectious fevers, lead, and syphilis are the chief causes. Syphilis causes it by producing arterial disease and by setting up a specific inflammatory infiltration. Secondary chronic myelitis is the more common form. It is really only the later stage of acute myelitis, softening, hemorrhage, or injury. Meningitis may extend and cause a meningo-myelitis. A neu- ritis may possibly ascend and cause myelitis, but such cases, if they occur, are very rare. Compression myelitis is usually a slowly destructive, not an inflammatory process, and it begins as a meningitis of the dura mater. Symjytoins. — When the disease begins primarily as a chronic affection the symptoms are as follows: The patient notices that his legs are heavy and get easily tired ; prickling and numb sensations are felt in the feet ; occa- sionally a little pain develops in the back or there is a sense of constriction about the trunk. The legs feel stiff, and tests often show that the reflexes are exaggerated. There is but little wast- ing of them, however. The sexual power declines ; the bladder gives some trouble, there being a tendency to retention; the bowels are constipated. xVfter a few weeks or months there is a partial paraplegia, with rigidity of the limbs and exaggerated re- flexes. Some anaesthesia exists, and occasional pain, which is not severe and is felt more in the back than the legs. The muscles have now wasted soniewhat, but show no decided changes to the electrical current. The bladder becomes more in- volved, the urine has to be drawn, it is often alkaline, and unless care is taken cystitis develops. The patient is still able to walk, but he does so with a stiff, shuffling gait which is characteristic J MYELITIS— INFLAMMATION OF THE SPINAL CORD. 217 (Fig. 93). The disease may show signs of slowly extending up and down, more often up. The arms become involved; weak- ness and stiffness, with some wasting, anaesthesia, and pain, de- velop, or the disease may cease its progress and the patient re- main partly paralyzed for years. The general health during the course of the disease deteriorates slowly ; the patients often be- come anaemic and have an unhealthy pallor. Eventually the paraplegia becomes complete, the patient is bed-ridden, the legs are atrophied, contractured, and rigid, with more or less anaesthesia. Cystitis and nephritis develop, or the patient dies from this or from inter- current disease. Chronic secondary myelitis, which is the form commonly seen, presents eventually much the same picture as that just described. In this type, however, the symptoms are worse at first, then improve or regress, then become stationary, and finally grow worse. Symptoms of the Different Forms. —The usual type of chronic myelitis is the transverse dorsal or dorso-lum- bar, and this gives symptoms as above described. If the lumbar re- gion is affected there is more para- plegia, wasting, and involvement of organic centres. If the myelitis is cervical the arms are involved, there may be pupillary changes, and the respiratory muscles are partly para- lyzed ; the paraplegia is not so com- plete and the disturbances of sensa- tion are likely to be more varied. Comj^ression myelitis, so called, is usually only a compression atrophy. It is due, as a rule, to vertebral caries, but its cause may be a spinal tumor, aneurism, and pachymeningitis. Com- pression myelitis is distinguished from other forms by its slow onset and the presence at first of irritative or " root " symptoms. The patient suffers from pain and tenderness localized at a cer- tain point in the spine. The pain radiates about the trunk or down the limbs and is increased on movements. At about the same time some motor weakness develops, usually in the form of paraplegia. The nmscles waste but slightly. The reflexes are exaggerated ; twitchings, sjjasms, and contractures finally oc- -Attitude in Myelitis. Chronic 218 DISEASES OF THE NERVOUS SYSTEM. cur, and there is finally developed a spastic paraplegia or quadru- plegia. Witli this there is usually some anesthesia, though it is not complete. The disease is oftenest in the dorsal or lower cer- vical region, and hence the sphincters escape until late. Locally, evidences of spine disease appear early in the form of a kyphosis. A central ov periependymal myelitis can rarely be recognized with certainty. It produces less pain and irritation, but leads to muscular atrophy, disorders of sensations such as thermo-anccs- thesia, disturbance of vasomotor and secretory nerves and vis- ceral centres. Pathology.— The pia mater is thickened over the affected re- gion and often throughout the cord. The cord itself has a gray, discolored look at the affected level, and is usually shrunken or distorted and hard to the touch. In severe cases of secondary character it is reduced to a small size, and the membranes about it are thick and inflamed. In transverse myelitis a vertical area of only two or three inches is involved. The microscope shows that the prominent changes are loss of nerve structure, great increase of connective tissue, and increase in the number of ves- sels which often have thickened walls. In the more seriously diseased part little is seen but connective tissue. In parts less diseased some nerve fibres are seen, many having evidences of partial disintegration. There is also a good deal of amorphous material studded with nuclei. Stellate cells, granule cells, and nerve cells in various stages of degeneration are present. In the parts less affected the signs of congestion and vascular irritation are more pronounced. Diagnosis. — This must be made from progressive muscular atrophy and amyotrophic lateral sclerosis, pachymeningitis and spinal tumor; from locomotor ataxia and from brain palsies. In progressive muscular atrophy there is a peculiar atrophy without involvement of the sphincters or sensory disturbance. In pachymeningitis there is often a history of an injury; there is more pain in the back and a more marked anaesthesia. The sphincters are not involved. Pachymeningitis is also usually located in the cervical region. Tumors usually cause much more pain; the symptoms come on slowly and are more definitely localized. A spastic paraplegia occurs from brain disease and as a functional trouble. In either case there are no trophic or sensory troubles, nor is there involvement of the sphincters. In locomotor ataxia there is no great degree of motor paralysis, and there are peculiar ataxic and sensory disturbances. Paralysis from brain disease is almost always unilateral, painless, spastic, and free from disturbance of the visceral centres. Prognosis. — Inflammatory processes have a tendency to cease when their reparatory and eliminative work is done. Chronic MYELITIS— INFLAMMATION OF THE SPINAL CORD. 219 myelitis, however, is often, as has been stated, a destructive pro- cess due to some defect in vascular supply or to some mechanical irritation. Besides this, in the spinal cord secondary degenera- tions set in as soon as certain tracts are interfered with. Hence chronic myelitis, after a period of improvement, generally pro- gresses, and the prognosis is not very favorable. Still, patients may live from five to twenty-five years. Dorsal myelitis is the most favorable form; compression myelitis from caries can also often be successfully treated. Those forms which come on rather rapidly are more likely to cease progressing (Gowers). Serious involvement of the bladder is a bad sign, and naturally the prog- nosis is worse the more complete the paralysis. Treatment. — In the earlier and progressive stage of chronic myelitis rest is imperative. The patient should lie down much of the time. Counter-irritation in the form of fly blisters, the cautery, or setons should be applied, and if no improvement results wet or dry cups used. The descending galvanic current along the spine should be tried; faradism and massage being used upon the limbs. Cold baths and cold applications must be prescribed carefully if at all. Lukewarm baths 90^ to 98 ^F. or half-baths with friction at 70° to 80° F. are more likely to be use- ful, but even these must be tried cautiously. The first baths should last not over five minutes and should be repeated only three or four times weekly. In later paraplegic and bed-ridden stages electrical and hydro-therapeutic applications should be followed up patiently and persistently. The patient now may be allowed to remain and exercise in the lukewarm bath for some time. 'Internally, iodide of potassium and mercury should be first given. After thorough trial with these remedies for six or eight weeks, the patient should be given courses of treatment with arsenic, nitrate of silver, phosphorus, and perhaps the chloride of gold. Pills of arsenite of soda, gr. Jq, may be administered three or four times daily for two months; if benefit ensues, the remedy should be resumed after an intermission of three weeks. Phos- phorus is best given in the form of Thompson's solution or Sayres' elixir in doses of gr. -^-^ ter in die increased to gr. ^^o- The remedy should be suspended for three days at the end of each ten days. Silver is given usually in the form of the nitrate (dose, gr. ^ to i). Not more than one drachm should be given without a three- months intermission. Some assert that the hypophosphite of silver and sodium, or the albuminate, are surer preparations. I do not advise the use of ergot. Strychnia in small doses some- times is useful. For the bladder troubles, the internal use of boracic acid, buchu, santalwood, and similar drugs are useful. Mechanical and surgical measures may be of some help. In very ^20 DISEASES OF THE NERVOUS SYSTEM. rare cases suspension does good, but it may do harm. Tenotomy is justifiable for the purpose of straightenino; contracture limbs. In compression myelitis suspension on an inclined plane and the plaster jacket or other support are indicated. Cases have been reported in which surgical operations for the relief of a supposed tumor have cured compression myelitis from Pott's disease. Sea voyages are often useful and are preferable to mountain climates. Rest, quiet, fresh air, and a very regular life are the essentials in all climates. Acute Axterior Poliomyelitis (Ixfaxtile Spixal Paral- ysis, Acute Atrophic Paralysis). Anterior poliomyelitis is a disease of the spinal cord charac- terized by a motor paralysis of rapid onset, followed by muscular wasting, without sensory symptoms. It occurs at all ages, but vastly oftener in infancy ; hence it is often called infantile spinal palsy. Etiology.— The average age at the time of attack is two years. Most cases occur under ten, and four-fifths of these occur under three. It may be congential, i.e., occur in intra-uterine life (Sinkler), and it may occur as late as sixty. Most adult cases occur under the age of thirty.* Rather more of the infantile cases occur in boys, and most of the adult cases occur in males. Race and climate afford no exemption so far as is known. The great majority of cases occur during the hot months of summer (Sinkler), Nearly eightj^ per cent (78.8) occur between June and September, inclusive. Heredity has an influence in only one or two per cent of cases. Over-exercise and chilling of the body Avhen heated are occa- sional causes. Infectious fevers (oftenest measles) precede the attack in about seven per cent (Sinkler). The disease has been reported to have occurred as an epidemic (Cordier). Dentition is rarely an exciting cause, as used to be supposed. Injuries and falls in a few instances appear to be the cause of the disease. The fact that the child is just beginning to walk at the period when most susceptible to poliomyelitis must be considered of importance, since the new movements call for an unusual activity of the spinal centres. * Among 50 personal cases, 39 were in children.. Of the latter there were 24 males, 15 females. Ages: Under six months. !; half to one year. 8; one to two j'ears, 10; two to three years, 5; three to four years. 3: four to six years, 3; six to eight years, 3. Final result was palsy, chiefly in right leg, in 14; chiefly in left leg. in 5; in both legs, 5; in right ami, 4; all four extremities, 1; the remainder in various combina- tions. Disease followed scarlatina in 1, pertussis in 2, cholera infantum in 1, some *' fever " in nearly all cases. MYELITIS— INFLAMMATION OF THE SPINAL CORD. 221 To sum up, age, season, and infectious diseases are the three most important etiological factors. iSy7npto?ns.— There are rarely any premonitory symptoms. The patient is taken with a slight fever, 100' to 102% accompanied with vomiting, diarrhoea, or convulsions. In a few hours or a day paralysis develops ; sometimes the paralysis is as much as a week in developing (" subacute form "). The fever lasts from one to three or four days. The paralysis reaches rapidly its height, then remains stationary for a time; then improvement sets in, vhich reaches a certain point and then stops. We have consequently : 1. A stage of invasion — a few hours or a week. 2. A stationary period — one to six w^eeks, usually two wrecks. 3. A stage of improvement — six months to a year. 4. A chronic stage. 1. The stage of invasion may be so sudden as to suggest hem- orrhage. Sometimes the child, after a restless, feverish night, wakes in the morning paralyzed. Usually the initiatory symp- toms last less than a day. With or before the paralysis there is a fever of 100^^ to 102° P., vomiting, delirium, and, much less often, convulsions, which are not severe. After the general disturbance subsides there may be some pain in the back and limbs for a few days, and in rare cases the bladder is involved so that there is retention of urine. But the dominant symptom is motor paral- ysis. The paralysis is oftenest paraplegia, next one leg, next the arms and legs, and after this various combinations. The eye muscles, laryngeal and respiratory muscles, always escape in in- fants. In older persons the facial nerve may be involved. In certain peculiar cases the cranial nerve nuclei are attacked, in association with the anterior horns. When the eye muscle nuclei are involved it is called " polio-encephalitis suj^erior ; "" when cranial nerve nuclei lower down are involved it is called " polio- encephalitis inferior." 2. The i^aralysis reaches its height in from one to four days. It remains at its height for from one to six weeks, and then improvement gradually sets in. In two or three weeks a wast- ing of the paralyzed limb may be noticed. It is flabby, its tem- perature lowered, and the reflexes are gone. Slight tenderness may be present, but there is no anaesthesia. 3. The stage of regression lasts for from one to six months. There is gradual improvement of the paralysis, beginning in the limbs least affected. This continues until the paralysis has left all but one or two limbs. As a rule, it is the legs alone that are finally left paralyzed. In a quarter of the cases both legs, and in half of the cases one leg, of tener the right, remain affected. The, DISEASES OF THE NERVOUS SYSTEM. inuscles waste and show reaction of deg:eneration, viz., loss of faradie irritability, retention but lessening of '&.— This is a disef.se hav- ino- a type half way Ijetween chronic anterior poliomyelitis and progressive muscular atrophy. The name had best be given to that form of disease which, starting like poliomyelitis, ends as a progressive muscular atrophy. III. Subacute Spinal Paralysis of Pucheniie.— The diseases described under this head are chiefly cases of multiple neuritis. In a very few there are both neuritis and myelitis ; in others the condition is one of minute focal spinal hemorrhages with second- ary myelitis. There is probably no such thing as a " subacute myelitis." Sexile Paraplegia. This is a form of paraplegia occurring in persons over the age of fifty or sixty. It begins A\ith simple weakness of the legs, fol- lowed by wasting and progressive development of a pafraplegia. The sphincters become eventually involved. The disease afTect? the lower extremities first, but gradually extends, and finally involves the arms. The general characters are those of a pro- gressive muscular atrophy; but the disease is distinguished from this by the fact that the sphincters become rather early involved, and that the paralysis and wasting go on together without any fibrillary contractions. The medulla and the facial and ocular muscles do not become involved. Clinicallj' the disease cannot be distinguished from a chronic anterior poliomyelitis which takes upon itself a progressive type. On post mortem, however, it is found that there is a softening of the gray matter in the anterior horns of the spinal cord, more marked in the lumbar swelling. This softening is apparently due to the thickening and oblit- eration of the blood vessels from senile changes in them. Dr. Gowers describes a disease which he calls senile paraplegia in Avhieh there is simple weakness of the legs and slowness of move- ment, without any atrophy, sensory disturbance, or alteration in the reflexes. He considers it to be a form of paralysis agitans. The disease which I have described, however, represents more truly a simple senile paraplegia. Very little can be done for this trouble therapeutically. The use of nitro-glycerin, iodide of potassium, sparteine, digitalis, and general tonic and hygienic measures are indicated. MYELITIS — INFLAMMATION OF THE SPINAL CORD. 227 Acute Ascending Paralysis (Landry's Paralysis). Acute ascending: paralysis is a disease characterized by a rap- idly developing paralysis which begins in tlie legs and then in- volves in turn the trunk, arms, respiratory and throat muscles, usually ending in death. There is little disturbance of sensation, no atrophy or changes in electrical irritability, and no involve- ment of the sphincters. Etiology.— "The disease is a rare one. It occurs chiefly between the ages of twenty and forty; men are affected oftener than women. Exposure is an exciting cause, and it occurs sometimes after acute infectious fevers and syphilis. The form of rabies known as " paralytic " causes a disease which is apparently iden- tical with Landry's paralysis. Symptoms. — There may be slight premonitory symptoms for a few days, consisting of numbness in the extremities, pain in the back or limbs, and malaise. The first definite sign of the disease is weakness in the legs, which rapidly increases until in a day or two the patient cannot walk. The paralysis soon involves the arms and then the muscles of respiration; the medulla is last affected, and then respiration becomes difficult, swallowing and articulation may be impossible. In rare cases there are facial and eye palsies. During the course of the paralysis there is little pain or sensory disturbance, but some degree of ansesthesia may occur. The deep reflexes are abolished. There are no vasomotor and no secretory disturbances, no noticeable atrophy, and no de- generative reactions in the affected muscles. The bladder and rectum are involved only in rare cases. There may be slight initial fever, but none occurs after the disease has well set in. The mind remains clear. The disease, as a rule, ends fatally, and it usually runs its course in less than a week. Death has occurred in forty-eight hours. On the other hand, death has been postponed three or four Aveeks. Variations. — The disease has been known to begin in the medulla or cervical region and descend. Pathological Anatomy. — A number of different diseases have been described under the head of Landry's paralysis, and corre- spondingly a number of different anatomical changes have been found. Multiple neuritis, acute diffuse myelitis and poliomyelitis existed in some cases. In others there was a dropsical exudation in the central canal of the spinal cord, or a hyaline change in the central arteries. In most instances no anatomical change is present. It is probable that in true Landry's paralysis there is no lesion 228 DISEASES OF THE NERVOUS SYSTEM. unless the disease is severe and prolonged. The paralysis is due to a poison of microbic origin. In some eases certainly this poison is that of rabies ; but it is not impossible that other infections may pick out and suspend the functions of the anterior cornual cells, or, as Gowers suggests, the "end-brushes" of the motor tract which connect with these cells. This would ex^Dlain the symptoms. Sometimes the poison may be so great in amount and so irri- tating as to set up a myelitis or perhaps a neuritis. Cases illus- trating these facts have been reported (Eichberg, Rosenheim, Putnam). But in most cases the imtient dies before the toxin can produce any inflammatory reaction. The prognosis is very grave, but not absolutely bad. If there is reason to suspect the case of being one of paralytic rabies, no hope can be offered. Z)/«/7;/06/.y.— This must be made from acute poliomyelitis, acute myelitis, acute multiple neuritis. Its acute ascending course, absence of fever, of an£esthesia, atrophy, decubitus, sphincter troubles, and especially the absence of degenerative electrical reactions are sufficient to enable one to make the diagnosis. Treatment.— Th\^ consists' of warm baths or packs, counter- irritation to the spine, laxatives, and rest. Large doses of ergo- tin, gr. ij., every hour have been successful in one case. Salicylate or benzoate of soda may be tried. i CHAPTER XIII. THE DEGENERATIVE DISEASES OF THE SPINAL CORD. Introductory : The Nature and Types of Degeneration and Sclerosis. The degenerative diseases of the spinal cord are sometimes called " system diseases," and some are often spoken of as scle- roses. There are no true system diseases, however, except loco- motor ataxia, progressive muscular atrophy, and amyotrophic lateral sclerosis. These diseases attack certain columns or parts having a definite jDhysiological purpose. Still, even they are not strictly confined to these parts, and the term " system diseases " is best not used as a basis of classification. The term " sclerosis," also, is somewhat misleading. It is not a proper word to indicate the pathological condition, but it has become generally adopted. Sclerosis is the fibroid (and neuroglia) induration which results from degeneration, destruction, or inflammation. We speak of degenerative sclerosis, of an inflammatory and of a neuroglia sclerosis, or of a sclerosis of mixed origin, according to the nature of the primary disease. The words "degeneration " and '' sclerosis " are often used to indicate the same thing, one being the patho- logical name, the other the anatomical. I shall use the term " sclerosis " here in presenting a classification of the degenera- tions and scleroses of the spinal cord. f I' Posterior spinal sclerosis (lo- I comotor ataxia). J Combined sclerosis. I Multiple sclerosis. I Progressive muscular atro- ( Ascending and descending de- l generations. ( Chronic myelitis and sclero- -! sis following destruction of Primarj^ Spinal scleroses. ^ Secondary. Inflammatory and mixed. cord. I have already described the scleroses following necrosis and mflammation; the secondary degenerations and scleroses con- 230 DISEASES OF THE NERVOUS SYSTEM. nected with these processes are described elsewhere. Multiple sclerosis is a cerebro-spiiial disease and will be discussed in a later chapter. We have therefore now to consider the prim- arj" scleroses. TYie primary degenerative scleroses are due to degenerations which begin in the nerve tissue and end in its atrophy, with sub- stitution of connective tissue. As to their nature so far as the microscope shows us, it is a gradual decay and death of the nerve fibre and cell. In some fibroid processes, like locomotor ataxia, this decay is accomiDanied with the development of irritating products, leucomaines or toxalbumins, which may produce so active a change in the connective tissue as to lead to something resembling a secondary or reactive inflammation. This is never of high grade, however, and in some forms of tabes is very slight. In progressive muscular atrophy the decay and death produce few irritating iDroducts, though enough, perhaps, to account for the fibrillary twitchings and occasional hypertonic condition of the muscles. The ultimate cause of these degenerative processes is not known. The progressive character of the diseases like loco- motor ataxia and progressive muscular atrophy would lead one to think that there is a poison at work and constantly acting on the diseased tissue. So far, all bacteriological examinations have failed to discover any microbe, but the fact that many degenerative processes fol- low infectious fevers or syphilis has led to the suggestion that pathogenic germs have poured into the system a poison, or have so modified the cellular nutrition that there is a poison constantly thrown out which irritates and destroys certain areas of nerve tissue. All the primary degenerations or scleroses have a certain de- gree of kinship. Their causes are in many respects the same, the course of all is uniformly progressive, and one not very infre- quently complicates another. The sharpest distinctions are found between those afTecting the gray matter and those affect- ing the white. Degenerative processes implicating the former tis- sue are nmch rarer and their course is more rapid and fatal. It is the anterior and central parts of the gray matter which are al- most exclusively affected ; consequently we have clinically only progressive muscular atrophy and its allied forms, bulbar pa- ralysis, ophthalmoplegia externa, and amyotrophic lateral scle- rosis. The degenerations of the white matter are more common, slower in course, different in etiology, and nnich more varied in symptomatology. As a rule, the gray matter is not much in- volved except secondarily and late. DEGENERATIVE DISEASES OF THE SPINAL CORD. 231 LOCOMOTOR ATAXIA (Posterior Spixal Sclerosis; Tabes Dorsalis). Definition. — Locomotor ataxia is a chronic progressive disease of tlie spinal cord and peripheral nerves, characterized clinically by inco-ordination, pains, anesthesia, and various visceral, trophic, and other symptoms, and anatomically by a degenerative sclerosis chiefly marked in the posterior columns of the cord and posterior roots, and to a less extent in the peripheral nerves. i^orm.9. -^Besides the common and typical form, there are anomalous and complicated types. r 1. Common form. m 2. Neuralgic. Types. ^ o -n 1 f- [3. Paralytic. i 4. With initial optic atrophy. ( With mu^ular atrophy. Complicated ) ^y -^^^ ^^j^^^. scleroses. forms. / ^vith general paralysis. Etiology. — The disease occurs oftenest in middle life, between thirty and forty, next between forty and fifty. It may occur as early as the tenth and as late as the sixtieth year. In the very early cases it is usually due to hereditary syphilis. It is much more common in males. Hereditary influence is very unimportant and is only indirect, i.e.., the parents may be neurotic. Diathetic influence is slight. Exposures to wet and cold, combined with muscular exertions, are effective causes. Soldiers, travellers, and drivers are rather more susceptible. Excessive railroad travelling, excessive dancing with exposure, favor the development of the disease. Excessive sexual intercourse, combined Avith irregular living, is a predisposing cause. Syphilis is a very important factor. A history of the disease is obtained in from one-half to two-thirds of the cases. In my cases about forty per cent had had syphilis. The patient usually has contracted the venereal disease ten to fifteen years before, and has rarely had noticeable secondary symptoms.* Syphilis is not a direct factor, but pre- pares the system for the degenerative process. Syphilis followed later by excesses — mental or physical— and by exposures espe- * Among 92 personal cases there were 85 males, 7 females. Ages when disease began: Twenty-one to thirty. 15; thirty-one to forty, 38; forty-one to fifty, 29; fift}--one tosixty, 8 ; sixty-one to seventy. 2. Syphilis in 35; doubtful 5 ; denied, 43; un- known, 9. Americans of three generations or more, 15 ; English, 6 ; Scotch. 2. The rest about equally divided between Irish and Irish-Americans, German and German Americans. Among Americans the disease apparently begins earlier, and paralytic forms are more common. The duration when seen had averaged five or six years, ranging from one-half year to twenty- five years. The time between infection and the beginning of the disease ranged from one and a half to twenty-four years, aver- aging thirteen years. 232 DISEASES OF THE NERVOUS SYSTEM. cially tends to produce locomotor ataxia. Lack of proper iodide treatment also favors it. Among other causes are profoundly depressing emotions, acute infective diseases like typhus, pneumonia, and rheumatism, difficult labors with severe hemorrhage, prolonged lactation, in- juries with shock, and excessive smoking. Locomotor ataxia in a somewhat atypical form may result secondarily from gummatous inflammation of the spinal men- inges, from a tumor, and possibly from an ascending neuritis. /Symj^toms.— The disease is generally divided into three stages: the initial or praeataxic, the ataxic, and the paralytic. 1. The initial stage. The patient first notices a slight uncer- tainty in walking, especially at night ; he has numb feelings in his feet, and at times darting pains in the legs or rectum. His sexual function becomes w^eak, his control over the bladder slightly impaired. He has temporary attacks of vertigo and of double vision. A continuous sense of profound weariness oppresses him, even though he has made no exertion. The knee jerk is lost. Such symptoms may last a few months or several years. 2. The ataxic stage. The gait now becomes so unsteady that others notice it ; the patient has to use a cane, and when walking watch his feet and the ground. If he stands with his eyes closed, he totters and may fall. His feet feel as though there was a layer of cloth or cotton between the soles and the ground. Parox- ysms of lightning-like pains attack the legs. Tests show an- aesthesia present in the toes and feet or in xDatches on the legs. A sense of constriction is felt around the waist. The sexual power is often lost ; the bladder is weak, and care has to be taken to empty it. The bowels are constipated ; at times he has attacks of intense pain in the epigastrium, with vomiting and perhaps a diarrhoea coming on without cause. The pupils are small and do not react to light, but do react to accommodation ; vision is still good. The inco-ordination and pain and anaesthesia after a time begin to affect slightly the arms. This stage lasts several years. 3. The paralytic stage. After several years with various re- missions and improvements, the patient loses the power of w\alk- ing altogether. His legs are somewhat wasted, but the muscular strength is fairly good. The anaesthesia and ataxia are very great. The patient does not feel the prick of a pin or touch of the hand ; nor with closed eyes does he know Avhere his legs are. His bladder is anaesthetic and paretic, so that the urine has to be drawn. The pains are much less, but are still present at times. The arms are more involved, but never so seriously as to make them useless like the legs. The intelligence remains good, and the patient may continue bed ridden for years, dying finally from some intercurrent affection. DEGENERATIVE DISEASES OF THE SPINAL CORD. 233 The following table sliows the jjrominent symptoms in the usual order of their aj^pearance : First Stage. (Half to twenty years.) Second Stage. (Two to ten years.) Third Stage. (Two to ten years.') Motor ^j Eye palsies Less Increased Paresis Increased. Paraplegia. Muscular weakness.. . . „ \ Pains Pains Anaesthesia Pain less. Increased. Sensory -J Excito-reflex . . -J Loss of knee jerk A. R. pupil Trophic Arthropathies More rare Rare Visceral - 1 Sexual weakness Vesical weakness Constipation ;- Increased Increased. Special senses. . -| Diplopia Optic atrophy ■ 7 Increased. Tnf rpasiprl I Paralysis of accom- modation. The symptoms must now be analyzed more closely. Locomotor and static ataxia are present very early, but only to a moderate extent. Tests such as making the patient walk and stand with the eyes closed, noting the position of limbs and the weight of objects, will reveal an ataxia due largely to begin- .— Instrument for Testing Tendon Reflexes. ning anaesthesia of the joints and tendons. By the use of the ataxigraph, one can with care assure himself that the patient has an excessive degree of static ataxia. In my experience, when the ataxigraph records over three inches' oscillation, the patient not being paraplegic or under the influence of any drug, it is abnor- mal. Tfie patella-tendon reflex or knee jerk is abolished very early in all typical cases. This constitutes a very important symp- tom, therefore. TJie gait and station in ataxia are characteristic. In walking, the patient keeps his eyes on the ground and on his feet. The latter he throws out rather forcibly, owing to overaction of the extensors of the foot. In watching such a patient walk bare- 234 DISEASES OF THE NERVOUS SYSTEM. footed, the extensor tendons can be seen to stand out with each forward movement of the hmb. The foot is brought down sharply on the heel and the legs are spread apart a little. Turning a corner, turning around, and going downstairs are done awkwardly, and the patient is apt to totter and fall. Walk- ing on a chalked line is very difficult; so also is walking back- ward. The gait improves after the patient walks awhile, and he will generally say that the prac- tice of walking does him good. Still, he soon gets tired (Fig. 98). Severe rectal neuralgia, as- sociated perhaps with haemor- rhoids, is sometimes an early symptom. Persistent neuralgia and functional disturbance of the bladder and rectum should cause suspicion of ataxia. Lan- cinating or lightning pains occur and are very characteristic. The pains dart down th^ legs along the course of the sciatic, or they suddenly appear as patches of pain on the foot or leg or thigh (" spot pains ''). The pain comes unexpectedly and with such se- verity that the patient involun- tarily jumps or jerks the limb. He speaks of his "jerking"'' and " twitching pains.'' The pains may affect the bowels or be felt as a squeezing sensation around the waist (girdle pains). The pains of ataxia are often the most obstinate and distressing symptom. They usually come on in great intensity once or twice a month, and last for two or three days. They then leave the patient for a time. They are often worse in cold and damp weather. In some cases the pains are almost continuous, coming on, if not every day, at least two or three times a week. Such cases are associated with much cutaneous hyperaesthesia, especially during the at- tacks. This type of cases is called " the neuralgic.'' The pa- tients rarely have as much ataxia, paresis, or visceral troubles as do the typical forms, and in certain respects such cases are favorable. The pains of the disease continue well into the second and even Fig. 99.— Showing Station in Second Stage of Locomotor Ataxia. DEGENERATIVE DISEASES OF THE SPINAL CORD. 235 third stage. Meanwhile tlie anaesthesia becomes much more marked. It affects most the feet and next the legs, rarely extending much over the thighs, but passing to the fingers and hands. The anaesthesia is greatest to pain, but touch and tem- perature sense are also involved. There is often delayed conduc- tion and poly^sthesia; many other curious perversions of the cutaneous sense are noted. Some anjesthesia usually develops Fig. 99.— Irregularly, Contracted Visual Field in Case of Tabes with Optic Atrophy, Left Eye (Berger). over the finger tips and hands, and sometimes a band of anaes- thesia develops about the waist. The facial and cranial nerves are not much affected, but there may be trigeminal neuralgia. Optic atrophy occurs in from ten to thirty -five per cent of cases, according to statistics. In my experience the percentage was about ten, the same as that of Gowers. Optic atrophy usu- ally develops in the prseataxic stage. If a patient has reached the second stage without it, he will prohaUy escape it altogether. Cases with ocular paralyses are slightly more disposed to it 230 DISEASES OF THE NERVOUS SYSTEM. (Berger). It attacks the left eye oftener than the right. The atrophy begins sometimes with increased sensibility to light, flashes of light, and muscae volitantes. AVith the failing vision, disturbance of color sense often and contraction of the visual field always occur. This contraction is irregular, with sector-formed defects ; not hemiopic (Fig. 99). The atrophy progresses slowly with slight remissions. It may cease its progress, but this is rare. Blindness comes in about three years. Ophthalmoscoi^i- eally there may be seen slight evidence of congestion in the early stage ; later, pallor of the disc, which finally becomes grayish. Disorders of liearing are frequent in tabes, occurring in about one-fourth of the cases, but in the majority of instances the aural trouble is an accidental complication due to middle-ear disease. Primary atrophy of the auditory nerve is very rare, as juight be expected, since this nerve is structurally not like the optic nerve. Its existence has been inferred on clinical grounds. Another form of tabetic deafness is of trophic origin and due to a sclerotic condition of the middle ear (Treitel). It is caused by involvement of the trophic or vasomotor fibres of the fifth nerve. The senses of taste and smell are rarely affected. The eye muscles are implicated in some way in nearly all cases of tabes. The following are the disorders : 1. Loss of the light-reflex, and myosis. 2. Sympathetic-nerve ptosis. 3. Paralysis of branches of the third nerve. 4. Paralysis of the sixth nerve. Paralyses of the ocular niuscles (third and sixth) occur rather oftener in syphilitic cases. Other ocular troubles are not influ- enced by a preceding syphilis. Ocular palsies occur relatively about equally often at the various ages at which tabes develops. They are early symptoms of the disease occurring as a rule in the praeataxic stage. 1. Loss of light-reflex and pupillary rigidity. The pupils are small and sometimes uneven ; they do not respond to light, but they do to accommodation. This condition is known as the Argyll-Robertson pupil. In early stages the light-reflex may be simply sluggish. In the late stages the accommodation-reflex is also lost. The Argyll-Robertson pupil is practically onh^ found in tabes and in general paresis. The ocular skin-reflex usually disappears early. The myosis in tabes is due to paralysis of the sympathetic dilating fibres. The pupils are sometimes irregular in shape. 2. Sympathetic-nerve ptosis. A slight drooping of one or both lids is not infrequent. It begins early and progresses slightly up to the later stages of the disease. It is due to paralysis of the sympathetic-nerve fibres of the lid. 3. 4. Paralysis of the external eye muscles. The external rec- DEGENERATIVE DISEASES OF THE SPINAL CORD. ^37 tus is oftenest aftected of single muscles, but the various branches of the third nerve taken together are oftener involved than the sixth. Of the third nerve's branches, the levator palpebrse and internal recti muscles are oftenest involved. There may be mul- tiple palsies. These occur oftener in syphilitic cases. Progressive ophthalmoplegia may be associated with tabes. The ocular nerve palsies may be transitory or permanent. Those occurring in the prieataxic stage are usually transitory, taking a few hours, days, or weeks. Cases have even lasted two years and got well. The permanent palsies develop usually in the later stages. The arthropathies of locomotor ataxia. Degenerative diseases of the joints, technically known as ar- thropathies, and spontaneous fractures of bones form important symptoms of tabes. They occur in ten per cent (Char- cot) or five per cent (author) of cases. The arthropathies are three or four times more frequent than the fractures. The joints oftenest af- fected are the knees, an- kles, and hips; but the elbow, shoulder, wrist, and small joints may be attacked. Spontaneous fractures occur oftenest in the shaft and neck of the fe- mur, next in the legs, forearm, humerus, and clavicle. The j^elvis, scap- ula, vertebrae, and undei- jaw may be fractured. Arthropathies are often accompanied with frac- tures, especially of the heads of the bones. The two sides of the body are about equally affected. The arthropathies are characterized by a sudden, apparently spontaneous painless swelling of the joint. The symptoms may develop in twenty-four or forty-eight hours. In rare cases there is a history of some preceding rheumatic pains or of an injury. After a time there is an osseous hyperplasia of the joint, which becomes enlarged to enormous proportions (Fig. 101). There is also a tendency to luxation of the joint. It crepitates on mov- ing. There is no tenderness on pressure, the hand finds Fig. 100. -- Ar- thropathy OF Ankle. Fig. 101.— Arthropathy op Knee (A. S. Egberts). evi- dence of synovial exudation, roughened surfaces, and perhaps 238 DISEASES OF THE NERVOUS SYSTEM. fractures of the enlarged parts. In the milder forms there is simply swelling from synovial exudation and some enlargement of the bones with roughened surfaces. After a few weeks this sweUing may subside and the joint return to nearly its natural size. In other cases the process progresses, the ligaments relax, the bones of the joint can be moved about freely, and luxations are easily produced. There is still no pain, but the limb becomes Fig. 102.— Arthropathy involving Knees and Long Bones of Legs. almost or entirely useless on account of the loose and relaxed con- dition of the parts (Figs. 101, 103). As time goes on, some absorption takes place and the head of the bone may almost disappear. The arthropathies have been divided into benign and malignant; but no sharp line can be drawn or certain prognosis made in the early stage. The arthropathies appear in the i^rodromal and early stage of the disease in over half the cases, and are often at first unrecog- nized. One-third occur after the tenth vear of the disease. DEGENERATIVE DISEASES OF THE SPINAL CORD. 239 The spontaneous fractures are usually brought on by a slight trauma, such as a fall. Violent muscular movements may pro- duce them. They also are painless as a rule. The fractures usu- ally heal well, often with abnormal readiness, but occasionally there is delay, and often healing is accompanied with great throw- ing out of callus. Pathologically the arthropathy is a rarefying osteitis. It does not differ anatomically from arthritis deformans, except that fractures may accompany it. Clinically the chief difference lies in the abruptness, si^ontaneity, and painlessness of the process. The disease, on the whole, cannot be considered specifi- cally different from arthritis deformans, modified by the analgesia of the parts. It is due probably to a degenera- tive change in the nerves supplying the joints and bones. The process may be- gin in the cartilage, bone, or ligaments. Eventually all these parts are involved. There is congestion of the synovial membranes with hydrarthrosis, then atrophy and rarefying hyi:)ertrophy of the epiphyses, relaxation of the ligaments, formation of osteophytes and b o n y- stalactites. There may be a rarefying osteitis of the long bones, without much joint involvement at first (Fig. 102), Various trophic distiirhances of the skin may appear, gener- ally late in the disease. The most common are herx)es and lichen. Besides these, bullae, transitory erythema, urticaria, eczema, pemphigus, ecthyma, ulcers, ichthyosis, and petechice have been described ; but they are rare and often only accidenta 1 complica- tions. A peculiar round, perforating ulcer sometimes develops on the sole of the foot, often as the result of cutting a corn. In rare cases the nails and teeth fall out. In syphilitic cases there is usually baldness. Peculiar " crises " of various kinds occur in tabes. The most common are gastric crises. These consist of attacks of in- tense pain extending from the groin to the epigastrium or encir- cling the waist, accompanied with vomiting and sometimes diar- FiG. 103.— Arthropathy of Elbow CA. S.Roberts). 240 DISEASES OF THE NERVOUS SYSTEM. rhoea. The attacks are usually associated with pains in the legs. They last two or three days, then pass away. Laryngtal crises consist of attacks of spasm of the adductors or paralysis of abductors, with noisy, croupy respiration. The attacks come on suddenly, the patient coughs and struggles for breath, and he may be seized with vertigo and fall down. The pulse may be very fast. The paroxysm lasts for a few minutes to several hours. The symptoms are very distressing, but not dan- gerous. Paroxysms of cough have been described as " bronchial crises." There are also cardiac crises, in which there is dysp- noea and rapid heart-beat and sense of suffocation resembling angina. The heart itself sometimes is diseased, but whether from neurotrophic disturbance or not is doubtful. The pulse is often small, rather rapid, and weak. The laryngeal and heart crises both depend on a degenerative irritation of the vagus, and may be more or less united in symp- toms. Ksense of great weariness and heaviness in the limbs, present constantly, no matter how much rest is taken, is a characteristic symptom, and is due to an irritability of the nerves of muscular sensibility. Iluscular atrophies occur sometimes in tabes. They are of three kinds : 1st, a true progressive muscular atrophy due to de- generation of troi^hic and motor cells; 2d, localized muscular atrophies due to degenerative atrophy of nerves ; 3d, a general wasting. Under the first head one finds ophthalmoplegia, bulbar paral- ysis, and spinal amyotrophy. Under the second, wasting of cer- tain groui^s of muscles in the legs or arms. Besides these, there is a generalized atrophy which occurs in the paralytic stage and is due probably to a slight involvement of the anterior horns in the progressive process that affects the cord. Attacks of hemiplegia in rare instances occur in tabes. They are usually of temporary character and occur early in the disease. They may come on late and are then more likely due to acute softening. Acute paraplegia comes on occasionally also, and this some- times almost disappears. The sexual poioer maybe at first greatly exaggerated; but this is rare, and usually there is progressive weakness and loss of desire. The bladder and sexual functions are rarely entirely lost and rarely equally impaired in this stage ; one may continue good while the other is affected moderately. Usually the sexual func- tion goes first. Some cerebral symptoms occur in tabes, chiefly in the early stage. They are insomnia, which may be very obstinate, and occa- DEGENERATIVE DISEASES OF THE SPINAL. CORD. 241 sional v^ertigo. An irritability of temper and tendency to despond- ency, sometimes _ ,. - noted, cannot be considered unnatu- ral. Apoplectiform and epileptiform at- tacks are described, but are very rare, and should cause a suspicion of a com- plication. The disease in very rare cases terminates in general paresis. Course. — The disease has been termed progres- sive, but it is not so in a large number of cases. With proper treatment the symptoms can often be kept in control for years. The first stage may last twenty years or more; the second stage five to fifteen years. The total duration of the disease varies enormously, ranging between three and thirty years. A few acute cases have been observed, running a course of less than a year. Complications. — These are acute myelitis, gener- ally syphilitic; lateral sclerosis, progressive mus- cular atrophy, hemiplegia from embolism or endar- teritis, general jjaresis, and heart disease. Pathological Anatomy and Pathology .—The GhsiY- acteristic changes are found in the spinal cord and posterior roots, and to a less extent in the periph- eral nerves. The spinal cord usuallv is reduced in size and flattened antero-posteriorly 'i6 Fig. 104.— Showing Columns of Clark. 1, Normal ; 2, diseased, in case of tabes in tliird stage; with degeneration of posterior columns and cerebellar tracts as shown in 3 (Oppenheim). 242 DISEASES OF THE NERVOUS SYSTEM. the pia mater is thickened somewhat. One can see with the naked eye that the posterior columns of the cord are shrunken and have a grayish appearance. Under the microscope it can be seen that the white matter of the posterior columns is very seriously affected ; the nerve tissue has disappeared, and its place is taken by connective tissue through which a few nerve fibres still run. The walls of the h^.R Merve. Fig. 105. Fig. 106. Fig. 105.— Posterior Spinal Gangi!.ion in Third Stage op Tabes. P. R., Posterior A. R., anterior root (Oppenheimj. root Fig. 106, -Healthy Spinal Ganglion, blood-vessels are somewhat thickened, but not remarkably so, nor is there any notable evidence of congestion or excessive vascular irritation. The part of the posterior column first affected is a vertical streak lying in the middle root zone beween the posterior median (col- umns of Goll) and posterior external columns (columns of Burdach) (Fig. 107). The segments first and most affected are those of the upper lumbar and lower dorsal region. Besides this area the rim zone or column of Lissauer is also early involved. x\s the disease DEGENERATIVE DISEASES OF THE SPINAL CORD. 243 Fig. 107. Fig. 108. Fig. 107.— Locomotor Ataxia, showing areas affected in first stage at five different levels. Drawn from specimens in author's possession and from compara- tive study of over thirty other figures. Fig. 108.— Locomotor Ataxia, Second Stage. 244 DISEASES OF THE NERVOUS SYSTEM. Fig. 109.— Locomotor Ataxia, Last Stage. progresses it extends uiDward and spreads laterally so that finally all of the posterior col- umn is changed into a dense connective-tissue mass through which only a few nerve fibres run. The part last and least involved is that lying just pos- terior to the commissure (ante- rior root zone of Flechsig) and that lying just mesial of the posterior horns (external part of the middle root zone). There is sometimes a degeneration of the antero-lateral ascending tract (Gowers' tract) and very rarely of the cerebellar tract. The pyramidal tracts are only involved in complicated cases. The cells and fibres of the col- uilin of Clark are often in- volved in advanced cases (Fig. 104). The gray matter of both the posterior and anterior horns may show some degener- ative changes, viz., decrease of the fibre network and atrophy of the cellular elements. The posterior roots are usu- ally involved, the process ex- tending as far as the spinal ganglia, which also show some degeneration (Figs. 105, 106). The anterior roots are normal. The process begins in the upper lumbar cord ; the sacral cord is usually much less af- fected. However, the exact in- itial point of attack varies, and this accounts for the variation in. the symptoms. Cases that begin with decided bladder and genital symptoms probably start low down ; cases which go for a good while with only ataxia, loss of knee jerk, and DEGENERATIVE DISEASES OF THE SPINAL CORD. 245 pains begin higher ; while in the brachial or arm-type cases the process begins in the cervical enlargement. The peripheral nerves are diseased in a large number of the Fig. 110.— Plantar Nerve Simple Atrophy in Tabes. advanced cases. The nerves of the leg are most involved. The process is a degenerative atrophy or neuritis (Figs. 110, 111). It affects the extremities of the nerves first and slowly extends upward, seldom reaching the large trunks. Fig. 111.— Ulnar Nerve Third Stage Tabes, Atrophy with Proliferation of Connective Tissue (Oppenheim). In the early stage the only nerve that is often affected is the optic. The process here is an atrophy beginning at the periphery and extending brain ward. The third, fifth, and sixth nerves are 246 DISEASES OF THE NERVOUS SYSTEM. occasionally involved ; still more rarely the olfactory and aadi- torv. The vagus nerve and sometimes its nucleus and that of the' glosso-pharyngeal are implicated, it may be, rather early in the disease. It is believed that these facts explain many of the laryngeal and visceral crises. The disease is primarily an irritative degeneration. The nerve fibres of the cord are first involved. Their destruction is not a simple wasting, but is accompanied with evidence of irritation such as swelling of axis cylinders and, secondarily, proliferation of connective tissue and slight congestion. The disease is spoken of by some as a parenchymatous inflammation (Charcot) ; by others as a vascular sclerosis ; by others as a gliosis, i.e., a substitution of neuroglia tissue for nerve fibre. In the light of present knowledge, however, it is safest to saj^ that, through some toxic or diathetic influence constantly acting, there is set up a progressive destructive process which has a selective influence on certain tracts in the posterior columns with their roots and ganglia and to a less extent on the peripheral nerves, particularly the optic. The diagnosis is not difficult in the advanced stages. In the first stage the disease has to be distinguished from multiple neu- ritis, chronic myelitis, spinal tumor, spinal syphilis, general pare- sis, and neurasthenia. Multiple neuritis, in its sensorj^ or pseudo- tabetic form, sometimes resembles closely locomotor ataxia. The differential points are given under that disease. In myelitis there is more paralysis, generallj^ exaggeration of reflexes, and an absence of disturbance of special senses. The diagnostic criteria of locomotor ataxia in all cases are the presence of lightning pains, numbness of the feet, loss of knee jerk, ataxia of station and gait, without much loss of muscular j)ower, the presence of the Argyll-Robertson pupil, the history of syphilis, and the slow onset of the disease. Prognosis. — In the first stage a small percentage may have the disease stopped and get practically well. After the second stage a cure is impossible, but great improvement may be secured and the x^atient made relatively comfortable for years. In the third stage little can be done except relieve the symp- toms, but life may be prolonged. Death usually occurs from some intercurrent malady, or from kidney disease caused by the bladder trouble. Patients very rarely indeed die from the disease itself and its various "crises."' Treatment.— T\ie hygienic treatment consists in enforcing a very regular and quiet life. The meals, sleep, work, and exercise should be taken in the most systematic way. It is often best when possible to have the patient give up business. This is es- pecially necessary if the business involves great mental and phy- DEGENERATIVE DISEASES OF THE SPINAL CORD. 247 sical strain. Absolute rest in bed for several months is often very helpful, especially in neuralgic cases. Out-door country life is better than city life. Climates of low altitude, if not very moist, are better than high altitudes. Sea voyages are often helpful. A diet which is non-fermentative and easily digestible, i.e., a nitrogenous diet, is preferable. The absolute diet of meat with hot Avater seems rarely indicated, and has not proved useful in my experience. Hydrotherapy is much employed in Germany. I have found lukewarm baths at a temperature of 95° F., for ten or twenty minutes daily, helpful in some cases, especially in early stages. Later, cold allusions over the back may do much good. Electricity is of use from its general tonic and reflex effects, and perhaps exercises some direct influence on the diseased pro- cess. Strong galvanic currents (15 to 30 ma.) should be applied along the spine, through the trunk, and down the legs and arms. The combined galvanic and faradic current is even better, given in the same way. The faradic brush should be applied over the extremities and along the back. The actual cautery is efficient in stopping pains. It should be applied to the back as often as once a month at least and sometimes once a week. Dry cups may be applied rapidly and in great number (80 to 100) along the spine and along the course of the sciatic nerves. In very painful cases occasional wet cups and leeches are useful. Blisters and various forms of counter- irritants sometimes do good. Suspension by the neck and arms is helpful, beyond any doubt, in about fifteen per cent of the cases. It is best adapted to per- sons in the second stage and to those who have a good deal of bladder trouble and pain. It is of little value in th.e paralytic stage and must be used with care in the early stage. Suspensions should be given for one to three minutes three times a week until twenty-five or thirty are taken. After three months a second course may be given. The various ingenious modifications of suspension, by which the back is flexed, extended, or stretched by weights and pulleys, have not been shoAvn to have any ad- vantage. Medicinally, for the diseased condition itself it is customary to give iodide of potash, arsenic, strychnine, phosphorus, nitrate of silver, chloride of gold and sodium, ergot, mercury, and chlor- ide of aluminium. I doubt if any of these drugs are of value ex- cept silver, and sometimes the iodide, bichloride of mercury, and gold. Of them silver is the best, and appears undoubtedly to affect favorably the course of the disease. Various salts of silver are used, but none have any special demonstrated value over the 248 DISEASES OF THE NERVOUS SYSTEM. nitrate, which should be given in doses of gr. i to f ter in die for not over two months at a time. Arsenic is recommended by Gowers, but I have not seen it do any good. The same author- ity recommends chloride of aluminium in doses of gr. ij. to iv. Symptomatically the drugs most called for are those which re- lieve pain. Phenacetin and antipyrine stand at the head of the list, but antifebrin, extract of Cannabis indica, codeine, aconitine, exalgin, salicylate of sodium, muriate of ammonia, all may have to be tried. Relief from pain is gotten by using lukewarm baths with pine-needle oil or extract, by aj^plying ice-bags, and by wrapping the limbs in flannel bandages into which sulphur and menthol have been rubbed. Bladder troubles are often much relieved by infusion of buchu 3 ij. and tincture of hyoscyamus TTl X. every three hours, or by sandalwood oil. In vesical and rectal neuralgias, suppositories containing iodoform gr. iij., ex- tract belladonna gr. ^, and codeine or antipyrine may be used. Locomotor Ataxia in Children. The spinal cord of persons under the age of puberty is not subject to primary systemic -degenerative changes. This is a general law to which, aside from the cases of Friedreich's ataxia, there are hardly an}^ exceptions. The posterior columns alone are sometimes primarily affected ; but in almost all instances the disease takes the type known as Friedreich's ataxia, and it may be seriously doubted whether tabes dorsalis ever shows itself in young children in any other way than as hereditary syphilis or as the peculiar form known as degenerative or Friedreich's ataxia. Still, a few cases have been reported in which an apparently typical tabes began between the ages of nine and twenty. THE COMBINED SCLEROSES. By the combined scleroses is meant those forms of degenera- tive sclerosis in which both the posterior and lateral columns are involved. There are several diseases in which combined sclero- sis exists. They are : 1. Ataxic paraplegia 2. Friedreich's ataxia. 8. Complicating scleroses of general paresis. Besides, there are numerous irregular forms. One of these has a tolerably definite clinical course and may be termed 4. Combined sclerosis with terminal softening. It has been described most fully by J. J. Putnam. DEGENERATIVE DISEASES OF THE SPINAL CORD. 249 Ataxic Paraplegia (Progressive Spastic Ataxia). This is a disease characterized by the symptoms of spastic paraplegia and ataxia. Etiologi/.— Ataxic paraplegia is not a special and independent disease. It has not a definite pathological basis. It is a clinical symptom -complex to which a special name is given for the sake of convenience. Nearly all cases of ataxic paraplegia are cases of chronic myelitis of the dorsal region, with secondary degenera- tions, or cases of locomotor ataxia with a complicating or second- ary degeneration in the lateral column. In my experience, ataxic paraplegia is oftenest an atypical form of locomotor ataxia. In some cases a myelitic focus may set up true primary degenera- tive changes in the cord in parts remote from the focus. Bear- ing the above facts in mind, it is unnecessary to go further into the etiology of the disease, it being caused by the same factors that cause chronic myelitis and locomotor ataxia. It is a dis- ease of early and middle life and of men. The symptoms are those of a gradually developing spastic paraplegia plus more or less ataxia. The first symptoms are a heaviness, numbness, and stiffness in the lower limbs. Ataxia develops early. It is shown in standing and walking and in attempting to make co-ordinate movements. It is present even when the mus- • cular sense, as tested by posturing the limbs and by weights, is shown to be good. It involves the arms but little. The gait is a combination of that in tabes and in spastic paraplegia. The heels are brought down first in some cases, in others the toe drags and the heel strikes the floor last. Sometimes the whole foot is planted down at once, and the shoes are worn almost evenly. The deep reflexes are exaggerated and there is trepidation and clonus. Muscular weakness is not very great, but some is present and eventually becomes marked. There is little or no atrophy. There is but little anesthesia and rarely much pain, nor are there often visceral crises. The eyes are rarely involved. There is early loss of sexual power and often considerable bladder trou- ble. The disease after a time may involve the arms. The course is very slow. Some cases eventually lose the spastic symptoms and knee jerks and become typical cases of locomotor ataxia. In other cases the paraplegia increases, con- tractures set in, and the patient resembles a case in the last stage of myelitis. Diagnosis.— The clinical diagnosis is easy and unmistakable. The main question is to determine whether one is dealing with atypical tabes or some form of chronic transverse myelitis or 250 DISEASES OF THE NERVOUS SYSTEM. from a focus of multiple sclerosis. In myelitis the symptoms come on more rapidly, the paraplegic symptoms are more pronounced. In some cases, however, a very good clinical picture of ataxic paraplegia follows an attack of acute myelitis. There are very few arm and no cranial nerve symptoms. In the tabetic cases the onset is slower, there is more ataxia and sensory disturbance, and some eye symptoms are usually present. Pathological Anatomy.— .^^ already stated, the evidence at present shows that ataxic paraplegia of the clinical type described is caused by an extension of the sclerosis of tabes or by a chronic Fig. 11:2.— Distribution of the Lesion in Ataxic Paraplegia of Myelitic Origin. dorsal myelitis. Other conditions causing transverse pressure and destruction of the cord may cause similar symptoms, but they are rare (Figs. 112, 113). The treatment of this trouble does not vary greatly from that of locomotor ataxia or myelitis, and naturally a very important thing is rest. Under this treatment I have seen remarkable amelioration in every symptom. The slight anaesthesia Avhich exists can be made to disappear by the use of electricity. The trembling and trepidation of the limbs at night are often very annoying to the patient. Moderate doses of bromide relieve this. I can strongly recommend the use of orthopaedic appliances for giving support to the shaking knees and hips. Some patients DEGENERATIVE DISEASES OF THE SPINAL CORD. 251 feel better and are even improved by the systematic, careful use of the faradic current, one of hi^h tension or the static current being preferred. No class of patients, in my experience, has re- turned so persistently and faithfully for electrical treatment as those suffering with spastic ataxia or spastic paralysis. A thor- ough course of anti-syphilitic treatment, using inunctions and occasional purges, should be tried if needed, and in later stages very large doses of the iodides are to be tried. In one case, un- doubtedly syphilitic, this certainly did much good. The patient preferred iodide of ammonia. Fig. 113.— Distribution of the Lesion in a Case of Tabetic Origin. Warm baths and cold douches are beneficial, but hot baths are dangerous. The stomach is a thing that must be attended to with great care. Friedreich's Ataxia (Hereditary Ataxia, Friedreich's Disease, Family Ataxia, Generic Ataxia). Friedreich's ataxia is a chronic degenerative disease, affecting the several long-fibre systems of the spinal cord, especially that of the posterior column, and later those of the lateral columns. It begins in the lumbar region and extends up- ward and downward, finally involving the medulla and espe- cially the nuclei of the hypoglossal nerve. It develops in child- 252 DISEASES OF THE NERVOUS SYSTEM. hood, affecting persons with an imperfectly developed spinal cord the result of a neurotic inheritance. Clinically the disease is characterized by ataxia beginning in the lower limbs and grad- ually involving the ui^per limbs and the organs of speech. Cur- vature of the spine, talipes, vertigo, and finally paralysis and contractures appear. The knee jerk is, as a rule, absent. There is but little pain or anaesthesia, and optic atrophy and visceral troubles are usually absent. The disease is rare, only about two hundred cases being on record. Efiolfxj I/.— The fundamental factor in predisposition is an in- herited or connate lack of development of the sjDinal cord, more particularly of the columns of Goll and iDyramidal tracts. This condition is inherited directly sometimes, but indirectly as a rule. That is to say, the parents or other members of the family usually show simply a neurotic history, and it is in only a minor- ity of cases that there is a history of ataxia in the direct line of ancestry. The more frequent condition is this : the patients or grand- parents have some neuroses, such as insanity, inebriety, or great nervous irritability ; the ataxia occurring only in the children of one generation. Sometimes in a single family the uncles and nephews or cousins may be found to have the disease. Hence the name "family ataxia," used by some writers. There are a good many cases in which the parents were apparently perfectly sound and healthy. Yet it is most probable that the sufferers from Friedreich's disease inherit a tendency to degenerative pro- cesses from some of their ancestors. This degenerative tendency may have been shown in those ancestors in a very slight degree. The patients rarely have locomotor ataxia, though this has been observed in a few cases. The children of locomotor ataxies do not have Friedreich's ataxia except in the very rarest instances. Syphilis in the parents is an element in some — perhajos in many— cases. Habitual intemperance in parents undoubtedly is a factor sometimes; much more rarely consanguinity and tuberculosis act as predisposing causes of degeneration. More cases have been observed in America than in any other country; while the fewest have been reported from France. The disease develops at about the time of jDuberty, most cases occur- ring between the ages of six and fifteen years. It is not very rare, however, for symptoms to develop even in infancy, though some of the cases reported at this time were probably of a syphilitic character. In a given family the d,isease, as a rule, strikes the older members first, but the younger members are attacked at a relatively earlier age. The most typical time of development is a rather late one, i.e., after twelve years of age. The disease may come on after maturity. In American cases the age of de- DEGENERATIVE DISEASES OF THE SPINAL CORD. 253 velopnieiit of the disease has been rather earher than the average. The male sex shghtly predominates, its proportion being about sixty per cent. In America the female sex has, however, been more affected (3 to 2). The patients are the children of the la- boring and agricultural classes. They have been found in the country oftener than in crowded cities. The families have often been large, but this is not always the case, especially in American cases. ^S^ursing at the mother's breast is thought to have been an exciting cause. Usually the disease appears after infectious fevers such as diphtheria, variola, and tyi^hoid. Symptoms. — The patient first notices an uncertainty in the gait and some feebleness in the louver limbs. These symptoms gradually increase until they interfere seriously with progression, and force him to leave off active work. With this there may be some slight pains or numbness in the lower limbs, and an exam- ination will shoAv, within a year or earlier, that the knee jerk is gone. After five or six years the arms become affected with inco- ordination, and a little later bulbar symptoms, such as thick or scanning speech, and often nystagmus, appear. During this time the patient suffers little pain and has no trouble with the bladder or rectum. Vertigo and headache are often present (Fig. 114). Dorsal flexion of the toes, talipes varus or some other form of club-foot, and lateral curvature of the spine are often observed. Oscillation of the head and choreiform or inco -ordinate move- ments of the extremities may develop. As the disease progresses the legs become weaker, and finally paraplegia, with contractures and muscular w^asting, sets in. The disease makes slow progress; often it remains almost at a stand-stiil for years, and the patients usually die of some inten-urrent disease, such as phthisis or an infectious fever. Among the rarely observed symptoms are tremor, spasms, de- creased electrical irritability, muscular atrophy, vasomotor pare- sis, polyuria, glycosuria, anaesthesia, fibrillary tremor, choking attacks, ptyalism, strabismus, diplopia, blepharospasm, a slight degree of ptosis, sluggish pupils, tachycardia, profuse sweats, im- potence, slight vesical incontinence, fragilitas ossium. Many of these symptoms are, however, exceptional and accidental. The major and essential symptoms are . (1) ataxia, beginning in the lower limbs and extending to the arms and tongue; (2) pecul- iar rolling, ataxic gait, ataxia gradually involving the arms; (3) disturbances of speech ; (4) talipes and spinal curvatures ; (5) grad- ual development of paraplegia ; (6) loss of knee jerk : (7) absence of cutaneous anaesthesia, of bladder troubles, of eye troubles ex- cept nystagmus, and of severe pains; (8) the development of the foregoing at about the time of puberty. Pathology.— Sixteen autopsies have been made upon cases of 254 DISEASES OF THE NERVOUS SYSTEM. Friedreich's ataxica. The disease in most of the cases had lasted over ten years ; in one, only two years ; in two, eight years. The examinations have led to quite uniform results. The lesions of importance were found in the spinal cord Fig. 114.— Friedreich's Ataxia, Late Fig. 115.— Showing the Distribu- Stage, showing curvature of trunk and de- tion of the Sclerosis at Dtffer- formities of le^. ent Levels of the Cord in Fried- reich's Ataxia. cord was usually small, flattened, and apparently congenitally hnperfect in development. In some cases two central canals have been seen. A sclerosis exists throughout the whole length DEGENERATIVE DISEASES OF THE SPINAL CORD. 255 of the posterior and lateral columns, sometimes extending to the anterior columns (Fig. 115). The sclerosis is most marked in the postero-median columns, which are always affected in toto. The postero-external column is less involved, and there is often a narrow strip of healthy tissue between the posterior horn and the sclerosed area, also between the posterior gray commissure and the diseased i>arts. The posterior column sclerosis is usually most marked in the lumbar region. In the lateral columns the sclerosis always affects the crossed pyramidal tracts. The direct cerebellar tracts and the so-called ascending antero-lateral tract are diseased in some cases, but apparently not in all. In a few instances the anterior median columns are involved. A zone of healthy tissue is often found between the sclerosed pyramidal tracts and the posterior horn. There are no important changes in the gray matter. Some chronic lei^tomeningitis, esiDecially on the posterior sur- face, has been noted. The medulla shows some traces of exten- sion of the sclerosis, but the involvement of the cells of the hypo- glossal nucleus is probably the most significant change. The brain exhibits no changes of importance in relation to the symp- tomatology of the disease. The posterior nerve roots are exten- sively sclerosed, the anterior roots less so, and the peripheral nerves show some degenerative changes. It is thought by some (Dej^rine) that the peripheral nerves are much less involved than in tabes dorsalis. It is also asserted that the sclerosis in the cord is really a neuroglia proliferation — a gliosis. Others assert that Friedreich's ataxia is a primary de- generative disease of the spinal vessels, and that the nervous tis- sue is secondarily involved. Course and Prognosis. — The disease is a progressive one, though it may be stationary for a long time, and may even show temporary improvement. The longest period of duration of the disease on record is forty-six years and the shortest two years, the average being fifteen or twenty years. Death occurs from some intercurrent disorder. Treatment.— A. quiet life, good food, and favorable hygienic surroundings are the main therapeutic helps. Arsenic and vari- ous nerve tonics may be of temporary benefit. My cases and some of the French cases were benefited by suspension by the neck in a Sayre apparatus. If the disease appears in one mem- ber of a family, effort should be made to prevent its appearance in others. The infant should not be nursed by its mother; spe- cial care should be taken to prevent its getting any infectious fevers and to prevent it from receiving any falls or blows. Its life should be exceptionally quiet, so far as physical exertion goes. Hereditary Ataxic Paraplegia.— There is a primary de- 256 DISEASES OF THE NERVOUS SYSTEM. generative disorder of the spinal cord occurring in children, and characterized by symptoms of ataxia with some cutaneous anes- thesia and spasm. The disease develops usually about the time of puberty. It progresses slowly, and takes upon itself the characters such as have been described under the name Ataxic Paraplegia. Such cases may for a time be considered of func- tional or hysterical character. A longer acquaintance with them, however, reveals the progressive and organic character of the disease. Hereditary ataxic paraplegia belongs to the same group as Friedreich's ataxia. It is a primary degenerative disorder, in- volving, no doubt, the lateral and posterior columns of the spinal cord, but with a preponderance of the lesion in the lateral col- unms. The symptoms resemble those of ataxic paraplegia, but the jjrogress is very slow. Cases have been described by Dr. Charles H. Brown. Combined Sclerosis with Terminal Softening. This is a rare disease, described by Dr. J. J. Putnam and later bj'- myself. It is a rather rapidly progressive sclerosis of the cord, ending in a softening which may be due to tubercular or other secondary infection. Etiology.— The patients are in most cases women. The ages range from forty-five to sixty-four years. In some there is a neurotic inheritance, and in several lead has been found in the urine at times. No distinct history of syphilis has been made out in any instance, nor are the patients alcoholic. The disease runs a rather rapid course, varying from nine months to four years and averaging two years. Syuiptoms. — The symptoms begin generally with numbness of the extremities, followed by progressive enfeeblement, and end- ing always in a paraplegia. Grreat emaciation and anaemia are present, and there is often an obstinate diarrhoea. No x:>araly- sis of any special grouj^s of muscles occurs until the final para- plegia sets in. There are in some cases anaesthesia and ataxia, but spastic symptoms, with exaggerated knee jerk and ankle clonus, are the more common. Lancinating or girdle pains are very rare. The arms are affected, but less than the legs. The vision and other special senses and speech are not disturbed. Mental symptoms approaching dementia occur in the terminal stages in some cases. The general course is that of a rather rapidly progressive affection causing pariesthesia and sometimes anaesthesia of the extremities, especially the lower, with progressive weakness of the extremities. This is associated with anaemia, general mus- cular emaciation, diarrhoea, ending in a paraplegia. Pathological Anatomi/.— The pathological appearances of the spinal cord as described by Putnam correspond to my own ob- servations: in all the cases two sets of changes in the cord are recognizable, one of older date, consisting in a relatively dense sclerosis in the posterior columns and in the lateral colunni (mainly confined to the pyramid tracts); and one of subacute DEGENERATIVE DISEASES OF THE SPINAL CORD. 257 character, and evidently of quite recent occurrence. This sub- acute process is, as regards tlie white columns, pp^rtly in new tracts, partly around the borders of the more dense sclerosis, and is chiefly characterized by the peculiar perforated appearance which indicates a somewhat rapid destruction of nerve tubes, with the oedematous distention or destruction of the intervening septa, associated with the formation of granule cells. In the gray horns the degenerative change (partly recent, partly of older date) is indicated by a disintegration of nerve cells. The prognosis is unfavorable. The treatment is purely sustaining and symptomatic. Spastic Spijval Paralysis, Hypertonic Paralysis, Spas- tic Paraplegia (Primary Lateral Sclerosis). Definition. — Spastic spinal paralysis is a disease characterized by rigidity and weakness of the limbs, especially the lower, with- out muscular atrophy and with little sensory disturbance. The disease is described here because it has always been called a "primary lateral sclerosis." No autopsy has as yet, however, proved that such a condition exists, and this name had best be dropped. Etiology. — Spastic spinal paralysis must be considered simply a symptom-complex due to various causes. The principal ones are: 1, chronic dorsal myelitis in adults; 2, double cerebral hem- iplegia in children ; and, 3, a functional cause of unknown char- acter. Rarer causes are multiple sclerosis and spinal tumor. In adults the causes of spinal syphilis and myelitis are nat- urally the causes of this disease. In children the brain lesions of hemiplegia and Pott's disease are causes. The functional and curable form occurs oftener in men and is due to exposures, over- exertion, or other influences, often perhaps of a specific charac- ter. Symptoms. — The general character of the symptoms is that of a slowly developing paraplegia with excessive stiffness of the lower limbs. The reflexes are greatly exaggerated, clonic and tonic spasms occur, forming what is known as spinal trepidation or epilepsy. The muscles feel hard and do not waste ; they may even be slightly hypertrophied. The electrical reactions are not notably changed. The gait is peculiar. The patient takes short steps, pushing the feet along, and the toes cling to the ground. There is a sense of weariness and numbness in the limbs, but rarely any anaesthesia or pain. The bladder and sexual func- tions are usually somewhat involved, and constipation occurs. Later in the disease the arms may be affected, and in rare cases there is involvement of the trunk muscles. The cranial nerves are rarely reached, but sometimes an excessive irritability 17 258 DISEASES OF THE NERVOUS SYSTEM. of the muscles of mastication occurs, and a tap on the chin causes an abnormally quick spasmodic contraction or " chin jerk." In children there is rather less reflex irritability, but a greater ten- dency to contractures and deformities. Course and Prognosis. — The disease, if organic, runs a very long course and has little tendency to shorten life. The ordinary forms are not curable, but their progress may be stopped and improvement occur. In the functional forms a cure may take place. I have observed it to do so in a few months. The pathological anatomy is that of the diseases already men- tioned. In dorsal myelitis there occurs a descending degeneration of the pyramidal tracts. The anterior cornual cells are cut off from the inhibitory influence of the brain, and hence the spasm. On the other hand, these cells in the lower part of the cord are not diseased, and hence there is no muscular atrophy. In double cerebral hemiplegia there is a descending degeneration from the brain along the direct and crossed pyramidal tracts. The pathology of the functional cases is unknown: some of them may be of infectious or toxic origin, and the anatomical condition may be an exudative dorsal myelitis. The diagnosis of the clinical type is easy. It depends on the existence of moderate paraplegia with spasm and exaggerated reflexes, without muscular atrophy or sensory disturbance. The special primary cause is often more difficult to determine. It is especially important to examine for Pott's disease, to ex- clude hysteria and amj'otrophic lateral sclerosis. In Pott's dis- ease there is usually pain, tenderness, and deformity. In hyster- ical paraplegia it is doubtful if there is ever true ankle or rectus clonus (Gowers). Besides, in hysteria the paralysis has a more acute onset and different course. In amyotrophic lateral scle- rosis muscular atrophy soon apijears. In multiple sclerosis evi- dences of sclerotic foci in the bulb and brain appear. The chronic onset of the disease distinguishes it from hemor- rhages, acute softenings, and injuries. The functional form called by Bastian hypertonic: paralysis is of rather acute onset and attended with severer symptoms of motor irritation. The weakness in the legs may be for a time very great, and profuse sweating sometimes occurs. Treat}nent.— This must be directed to the cause. In syphilitic cases iodide of potassium and mercury are to be given. AVarm biths, Turkish baths, massage, and galvanism are recommended. In my experience electrical currents of high tension, static sparks, and the secondary coil have been most useful, though they are condemned by some. Some patients feel better while standing, and they like Avo)-k at a bench or counter. Grymnastic exercises, bicycle-riding, and orthopedic measures help children and very DEGENERATIVE DISEASES OF THE SPINAL CORD. 259 chronic cases in adults. Arsenic, strychnine in quite small doses (gr. Y^o), and the bromides sometimes give relief. Suspension is not often of value, and may do harm. Secondary Degeneratiot^s of the Spinal Cord. When any of the long-fibre tracts of the cord are cut across or destroyed, there soon results a degeneration. This extends Fig. 116.— Showing the Tracts Affected in Secondary Degenerations of the Spinal Cord in Lesions at Different Levels. 1, Descending degeneration after lesion at sixth cervical ; 2, ascending and descending degeneration, lesion at sixth dorsal ; 3, ascending and descending degeneration,lesion at twelfth dorsal ; 4, ascend- ing degeneration, lesion at first sacral. up or down in accordance with the direction in which the tracts carry impulses. Thus when the crossed pyramidal tract is cut across the degeneration extends down ; when the column of Groll is involved it extends up. The degenerative process begins al- most immediately and is complete in a few weeks. The myelin sheath swells, gradually breaks up and disintegrates; the axis cylinder is involved next. At the same time the connective tissue 260 DISEASES OF THE NERVOUS SYSTEM. proliferates and takes the place of the wasted nerves. Finally, long tracts of connective tissue have taken the place of the nerve tissue. The process may not be a complete one if the lesion does not entirely destroy the tract. The short-fibre tracts degenerate only a little way up and down (Fig. 116). Secondary degenerations complicate and add to the patholog- ical change in all organic diseases of the cord. In brain disease, involving the motor tract, as in hemiplegia, secondary degenera- tion extends into the cord and adds to the seriousness of the dis- ease. Degenerations of the spinal cord, however, do not extend up to the brain except in the case of disease of the cerebellar tracts. The accompanying figures show the extent of the secondary degeneration in total transverse lesions of the spinal cord at dif- ferent levels. There is still some doubt as to the degeneration of the antero-lateral ascending tract, which some (Mott) assert is part of the cerebellar tract and goes to the vermis. CHAPTEE XIV. THE PROGRESSIVE MUSCULAR ATROPHIES AND MUSCULAR DYSTROPHIES. The result of modern studies is to show that the anterior cor- nual cells of the spinal cord, the motor nerves and their terminal end-organs, the muscles, form a trophic unit, and that the same degenerative disease may attack either end or any part of this physiological mechanism. There is a clinical and pathological unity in all the different spinal and muscular types of atrophies. 1. 2. Fig. 117.— Showing : 1, Segment of spinal cord with anterior Jiorn cell, end-brush, and lateral tracts, the parts affected in progressive muscular atrophies ; and, 2, the muscle and its nerves, the parts affected in progressive muscular dystrophies. I5ut there are sufficient differences, also, to oblige us for conven- ience' sake to make certain classifications. Thus those disorders which attack chiefly and first the anterior horn cells and the I)yramidal tract are called progressive muscular atrophies; those disorders attacking first the muscle tissue and its nerves are caXVed progressive muscular dystrophies (Fig. 117). The pro- gressive muscular atrophies of central origin may attack the mo- tor nerve cells of the eye, of the throat and lips, of the upper or lower spinal cord. In accordance with the level affected the dis- ease has received a different name. Sometimes the pyramidal tracts of the spinal cord are first and most involved. This has fur- nished excuse for another type. Then, again, while most cases of the muscular atrophy are acquired, there is one type of it which is a hereditary one. Thus we find the disease classified as follows . 262 DISEASES OF THE NERVOUS SYSTEM. f Progressive ophthalmoi^legia. Progr e s s i V e m u s- I Progressive bulbar palsy, cular atrophies of I Progressive muscular atrophy (arm type). central or nervous] Progressive hereditary muscular atrophy origin. | (leg type). t Amyotrophic lateral sclerosis. The progressive muscular dystrophies have also been much subdivided, but they are essentially the same disease, as will be seen later. Of the muscular atrophies, I have already described ophthal- moplegia. Beginning from above I will describe here bulbar paralysis, for though anatomically it belongs to disease of the brain, pathologically and clinically it belongs to the cord. Glosso-Labio-Laryxgeal Paralysis (Progressive Bulbar Paralysis). This is a disease characterized by progressive wasting and paralysis of the muscles of the tongue, lips, palate, and throat, due to an atrophy of the nuclei of the nerves supplying those l>arts. Etiology.— It is a disease of the degenerative, period of life, most cases occurring after forty and between that time and sev- enty. It occurs rather oftener in men than women. A neurotic heredity is sometimes noted. Exposure to cold and excessive use of the muscles, mental strain, debilitating influences, lead, and syphilis are causal factors. Symptoms. — The tongue is the part first affected. The patient speaks indistinctly and cannot articulate the lingual consonants /, V, 11, and t. The tongue cannot be elevated and is protruded only a little distance. It looks scarred and wrinkled. The lips become weak and the patient cannot whistle nor make the con- sonants p, &, m or the vowel o. The saliva begins to dribble from the mouth. Disturbance in swallowing soon develops. Hard solids are taken with difficulty, next fluids, while semi-sol- ids are generally managed best. The lips finally become so para- lyzed that the mouth cannot be shut, and the lower part of the face is motionless and expressionless. The upper face wears an ex- pression of anxiety and suffering, the saliva dribbles constantl5% and the whole physiognomy of the patient becomes characteristic and pitiful in the extreme. The facial nerve may get some- what involved. Articulation becomes almost entirely lost; the voice has a nasal twang from paralysis of the palate. The patient has tired and uncomfortable sensations of dryness and stiffness about the throat. There is no pain or anaesthesia, MUSCULAR ATROPHIES AND DYSTROPHIES. 263 but occasionally there is impairment of the sense of taste. The throat reflex is usually lost, so that tickling it causes no reaction. Electric irritability is at first unchanged, but in the later stages partial degeneration reaction occurs. In rare cases there is a rapid pulse and still more rarely glycosuria. The laryngeal reflex becomes weak, the adductors also, but abductor paralysis is rare. The mind is not affected, but there is often an emotional weakness and tendency to tears — not entirely unreasonable in view of the distressing nature of the malady. The disease is often the terminal stage of spinal muscular atrophy ; it may be associated with the latter, witii amyotrophic lateral sclerosis or with ophthalmoplegia. All these types may occur together. It runs a progressive course, with remissions of a few weeks or months. It lasts from one to three or four years. In one case it has lasted seven years. The termination is eventually fatal. Death occurs through in- terference with swallowing, and inanition or a broncho-pneu- monia or bronchitis may develop which ends the patient's life. Pathology. — The primary lesion is found in the nuclei of ori- gin of the hypo-glossal, glosso-pharyngeal, vagus, and spinal accessory nerves. The raphe fibres and the anterior pyramids are also usually somewhat involved. There is sometimes atrophy of the cells of the facial nerve and of the nucleus ambiguous, which is the motor nucleus of the vagus. The brunt of the disease falls, therefore, upon those more superficial or posterior nuclei which are representative of a continuation of the anterior cornual cells. If the disease is complicated with amyotrophic lateral sclerosis, or progressive muscular atrophy, or ophthalmo- plegia, we find atrophy in the cord or ocular nuclei. The atro- phic process is similar to that observed in the spinal disease. The muscles of the tongue, and to a less extent of the orbicu- laris oris and throat, show evidences of degeneration and atrophy. In some cases the tongue is not shrivelled, owing to the presence of a fatty deposit, and on account of this the disease has been divided into atrophic and paralytic types, but this distinction is unnecessary. A few cases have occurred in which no bulbar lesion was discoverable, even by the microscope. In these cases the disease lay probably in the brain or peripheral nerves. Diagnosis.— Th-e disease must be distinguished from polio- encephalitis inferior, bulbar apoplexy, tumors, and softening, from multiple sclerosis, and from chronic lesions of the cerebral hemispheres causing pseudo-bulbar paralysis. The slow onset, the progressive course, the bilateral character, the absence of in- volvement of sensory nerves, and the degenerative reactions are 264 DISEASES OF THE NERVOUS SYSTEM. always siifficjent for a diagnosis. It is important always to note whether there is ophthalmoplegia and spinal muscular atrophy associated with the disease. Treatment.— T\\e patient should be kept quiet; he must be overfed and given massage and electricity in moderation. The same drug treatment as in the spinal disease is indicated. Small doses of morphine, gr. 2V to 3^, and of atropine may be given also. Electricity should be tried for a short time twice or even thrice daily, if possible. The faradic current may be used, alternating or combined with the galvanic. Galvanization of the neck and medulla appears to do no good. After a time it may be neces- sary to feed with a tube or even to do tracheotomy. Progressive Muscular Atrophy (Progressive Spinal Amyotrophy ; DucHE:NNE-ARA2f 's Disease). This is a disease characterized by a slow, progressive muscular atrophy of the muscles of the extremities and trunk, with conse- quent paralysis, not accompanied with any notable sensory dis- turbance, and due to a progressive atrophy of the motor and trophic cells in the spinal cord. Etiology. — The disease affects persons in the middle period of life (twenty-five to forty-five). The extremes are fourteen and seventy years (Gowers). It is more frequent in males. Heredity is rarely, if ever, a factor. Great mental strain, exposure, trau- matism, excessive use of certain groups of muscles, acute infec- tious diseases — especially typhoid, measles, cholera— child-birth, acute rheumatism, syphilis, and, more than anything else, lead- poisoning are causes. It may complicate locomotor ataxia. The causes, as may be seen, are much the same as those of bulbar paralysis. Symptoms.— The patient suffers at first from slight rheuma- toid pains in the shoulder or arm, associated with some feelings of numbness and weariness. Muscular Avasting then begins to appear, and usually in one hand. The adductor longus pollicis is very early affected, also the thenar muscles and the interossei. The atrophy spreads from muscle to muscle, and does not follow the distribution of nerves, although the ulnar nerve supply is most seriously disordered. The ball of the thumb becomes flat- tened, and the patient cannot abduct or flex it well. When the radial interossei are reached the forefinger cannot be abducted, and this is often an early sign. The disease gradually extends upward, attacking the flexors and extensors of the forearm, then the upper arm and shoulder. Meanwhile the hand has become thin and flattened, flexion of wrist and extension of flngers are lost, and a characteristic " griffin-claw " appearance results. Mean- '/ MUSCULAR ATROPHIES AND DYSTROPHIES. 265 while (three to nine months) the other arm begins to be affected. Occasionally there is a remit-sion for a time. In a few cases the atrophy begins first in the shoulders and arm, attacking the deltoid, biceps, and triceps, then extending downward to the hands. This constitutes the " upper-arm type." If, as is usually the case, the disease continues to progress, it passes from the shoulder girdle to the deep muscles of the back, then downward, involving successively the hip and thigh mus- cles, the glutei, the crural extensors and abductors being oftenest chosen. The leg muscles may be finally involved, but they usu- ally escape. The disease as it descends continues its progress in the trunk, involving the intercostals. It slowly ascends the neck also, and finally leads to paralysis of the diaphragm, or a bulbar palsy may set in. It will be seen that the ordinary course of the disease is from the lower-arm-muscle groups (ulnar and median) up to the shoul- der group (middle cervical nerves), then down through the dorsal and lumbar nerves, rarely reaching the sacral groups. In very rare cases it begins in the legs and ascends. y Along with the wasting there is a corresponding weakness and ^ ^ paralysis, but the paralysis is the result of the atrophy and does not precede it. Fibrillary twitchings of the muscles occur; the idiopathic muscular contraction caused by striking it a blow is very marked ; myoid tumors are easily brought out. In some cases the muscles are flaccid and toneless, and the deep reflexes, knee jerk, and arm jerk disappear early (atonic atrophy), but in other cases the rigidity and tonicity of the muscles are increased, the knee jerks exaggerated, and we have tonic atrophy. This con- dition may be so marked as to give rise to a special clinical type of progressive atrophy known as amyot rovh icJ,ateral scleros is. The electrical irritability of the muscles lessens to both gal- vanic and faradic currents, but no marked qualitative changes occur at first. Eventually we may get partial degeneration reac- tions, but these occur late in the disease, unless this runs a very rapid course, when fairly typical degeneration reactions may be got. A peculiar contraction of the uj)per limbs is sometimes pro- duced by placing the negative pole of the galvanic battery over the fifth cervical vertebra, and the positive in the triangle just below the lower jaw (diplegic contraction of Remak). A peculiar palmar spasm is described by Voeter, caused by suddenly inter- rupting a faradic or galvanic current passed along the affected arm. In typical cases of progressive muscular atrophy there is no anaesthesia; and when such symptoms develop, the presence of jjeripheral disease or of syringo-myelia or spinal tumor must be expected. The patients may suffer from rheumatic-like pains and from parsesthesiae. 266 DISEASES OF THE NERVOUS SYSTEM. The affected pan'ts often show excessive sAveating and con- gestion and evidence of vasomotor disturbance. This may in- volve the face on one or both sides; one pupil may be larger than the other, due to irritation of the ciho-spinal centre. The u'is-reflex, however, is preserved, and the optic nerve is never in- volved. The sexual power is often weakened, but the sphincters are not attacked. The urine shows variations in the amount of urea. There is usually an increase of lime salts. Complications. — The most common complication is an exten- sion of the process to the medulla, causing disturbance of speech and swallowing. Muscular atrophy eompUcates locomotor ataxia, but is rarely complicated by it. A high degree of spasm and rigidity of the legs, particularly, may occur, causing the condition known as amyotrophic lateral sclerosis. Course and Duration. — The disease usually progresses stead- 11}'^ until it has reached an advanced stage, when it may stop. Remissions may occur earlier, however, and even some improve- ment take place ; the disease then ordinarily jjrogresses again. It lasts from two years to thirty or more, but on the average not over ten or twelve years. Death usually occurs from i^ulmonary disease, owing to the weakness of the respiratory muscles. Some- times the extension to the medulla and involvement of the mus- cles of deglutition and of the larynx is the cause of death. Pathology. — The primary anatomical change is a degenera- tive atrophy of the cells of the central parts and anterior horns of the gray matter of the spinal cord. The atrophy gradually extends and involves the whole anterior horn. It also extends vertically, first down, then up. Along with this atrophy are degenerative changes in the lateral columns ; consecutive to this there is atrophy of the anterior roots, peripheral nerves, and the muscles. The disease begins in the deeper parts of the anterior cornua, involving the central and median groups of cells. These are more concerned in nutrition and in the finer muscular movements of the extremities. Hence atrophy alwa3's precedes, or at least keeps pace with, paralysis. The levels af- fected are the lower cervical and upper dorsal; but if the dis- ease is extensive, the dorsal, lumbar, and sacral cord are also in- volved. The affected part is nearly free from nerve cells, and those present are atrophied, their processes are short or absent, and the cell has lost its angular appearance. Sclerotic and pig- mentary changes are observed. The neuroglia and connective- tissue cells are increased in number, but there are no marked changes in the blood-vessels, though these may be much dilated. There is always some degeneration of the lateral columns, and this may be very complete. It is confined chiefly to the j)yra- MUSCULAR ATROPHIES AND DYSTROPHIES. 267 midal tracts, but extends somewhat anteriorly into the mixed lateral column. It does not affect the cerebellar or ascending lateral tracts. The degeneration has been traced up into the brain as far as the internal capsule and ev^en to the cortex. The anterior columns may be slightly affected . The posterior horns, columns, and roots are normal. The affected muscles show various degrees of degeneration. They are pale and streaked with yellow due to fatty deposits. Some fibres may be simplj' narrow and shrunken, others have lost their striatlon and become granular from deposit of fat globules or degenerated muscle elements. Other fibres have lost their striations and look as if filled with a homogeneous, glassy- looking substance containing a few fat granules (vitreous degen- eration); others show a longitudinal striation. The interstitial connective tissue is increased and in places has taken the place entirely of the muscles. The capillaries and small vessels are distended. Healthy fibres may be seen among the diseased. Changes have been found in the sympathetic nervous system, but they are unimportant. The diagnosis has to be made from the progressive muscular dystrophies, chronic poliomyelitis anterior, syringo-myelia, neu- ritis, and neuritic fauuly atroph5^ In the muscular dystrophies there is commonly a history of heredity; the disease begins usually in childhood or adolescence. It attacks the lower limbs oftener ; it is slower in progress ; there are no fibrillary contractions, and the degeneration reaction does not occur. Chronic poliomyelitis anterior begins suddenly and, having reached its height, does not progress, but remains stationary or improves. The paralysis occurs first, the wasting follows. It affects groups of muscles physiologically related, while progres- sive muscular atrophy attacks muscles only anatomically related. There are cases, however, which seem to be on the border line between the two diseases. Syringo-myelia is distinguished by the presence of peculiar sensory and trophic disorders. Neuritis caused by lead-poisoning is detected by the history of the case, its tendency to affect the extensors of the arm chiefly,and the absence of a progressive tendency. Sometimes, however, lead- poisoning and palsy end in true prt)gressive muscular atrophy. Ordinary multiple neuritis is distinguished easily by its rapid onset and the presence of painful symptoms. The hereditary or " leg type " of progressive muscular atrophy is characterized by its beginning in the legs, by a good deal of sensory disturbance, typical degeneration reactions, and heredi tary or family history. 268 DISEASES OF THE NERVOUS SYSTEM. Treatment.— The patient should be well fed and have rest, quiet, and fresh air. Careful local faradization and galvanization of the spine and neck are indicated. Massage does no good. Hypodermic injections of strychnine in the affected member, gr- iu to ^ daily, the internal use of arsenic, phosphorus, iron, quinine, and cod-liver oil sometimes are beneficial. In a few cases with a syphilitic history, mercury and iodide of potash have proved useful. The essentials of treatment are rest, electricity, strychnine locally, the administration of powerful tonics, and over-feeding. Ts^itroglycerin, morphine, atropine, ni- trate of silver, chloride of gold and of barium, and the nitrate of uranium may be tried. Progressive Hereditary Muscular Atrophy of Leg Type (Charcot-Marie Type). This is a hereditary or family muscular atrophy of central (or neuritic?) origin, beginning in the legs and extending uj^ward. It affects males more than females, but the difference is not great. It almost always begins before the age of twenty. It attacks first the muscles of the leg, not the foot, involving the peronei, then the extensors of the toes, then the calf muscles. The thighs escape till later. After some years the upper extrem- ities and small hand muscles are reached. The shoulder and arm, neck and trunk muscles escape. There are occasionally fibrillary contractions ; and always partial or complete degener- ative electrical reactions. The patients comjDlain of some pain and numbness, but there is no anaesthesia. The disease runs a long course, with remissions, and resem- bles in prognosis the dystrophies. The outlook is better than in the arm type, but the disease is not curable. Some authorities assert that the disease is due to a progressive degenerative neuritis. In the writer's ojoinion the anterior horns of the spinal cord are primarily attacked.* The treatment is the same as for the other forms of hereditary muscular atrophy. Amyotrophic Lateral Sclerosis. This is a form of progressive muscular atrophy associated with spastic symptoms and paralysis. It ends in or may be early as- sociated with bulbar paralysis or even with ophthalmoplegia. The etiology resembles that of oixlinary forms of spinal mus- cular atrophy. * The writer has seen the disease in a typical form in one member of the first generation, in two members of the second. A child of one of the latter had, at the age of two years, a typical attack of anterior poliomyelitis. MUSCULAR ATROPHIES AND DYSTROPHIES. 269 The symptoms of typical eases such as were first described by Charcot are those of a slowly developing paralysis. This affects the upper extremities first and spreads diffusely. The atrophy is less marked than the paralysis. There is rigidity, exaggerated reflexes, and sometimes tremor. Fibrillary contractions are pres- ent. There are no notable sensory symptoms. The legs are affected later; the paralysis and spastic condition of the legs are antecedent to the atrophy. The visceral centres are not in- volved. The disease progresses rather rapidly and finally in- volves the medulla, causing bulbar paralysis and death. Some- times ophthalmoplegia is also present. In less typical cases the disease begins with spinal and bulbar symptoms almost simultaneously. In a case under the writer's observation there was ophthalmoplegia, bulbar paralysis, and spinal atrophy beginning at nearly the same time. Ordinary cases of spinal muscular atrophy may also be early associated with rigidity and exaggerated reflexes. The jaw jerk is often increased in this disease, which cannot be said to be really dis- tinct from progressive spinal muscular atrophy ; it runs usually a rapid course, causing death in two or three years. THE PROGRESSIVE MUSCULAR DYSTROPHIES. This name is given to various forms of progressive muscular atrophy in which the disease is hereditary in character and at- tacks primarily the muscles. Although a muscular disease, yet its close relationship with spinal muscular atroi^hies leads us to describe it here. A number of types have been described, the distinctions being based chiefly on the part of the body first affected. These types are not of great importance, but may be enumerated here for convenience : 1. Pseudo-muscular hypertrophy. {a) Leyden-Mobius or hereditary type, appearing in children, beginning in back and lower limbs. 2. Erb's juvenile type, or scapulo-humeral type, beginning in childhood or youth, usually in the shoulder girdle or trunk. 3. Landouzy-Dejerine type, or infantile progressive muscular atrophy of D uchehne, or f acio-scapulo-humeral type. It resembles the preceding form, with the exception that it involves the face. 4. The peroneal or leg type has been classed with the dys- trophies, but is probably of spinal or neuritic origin, and has been described with the atrophies (see page 268). The essential unity of all these different forms is shown by the fact that cases occur in which pseudo-hypertrophy takes place in the scapulo-humeral and other types, by the fact that a dis- 270 DISEASES OF THE NERVOUS SYSTEM. ease resembliug pseudo-hypertrophic paralysis occurs without any hypertrophy, and by the fact that different types occur in the same family. The unity of the spinal and muscular forms is shown bv the same kind of clinical evidence. A. B. Fig. 118. — Showing the Parts First Attacked in the Different Types op Muscular Dystrophy and Muscular Atrophy. The shaded parts iu A show the place of onset of progressive muscular atrophy- of ordinary or Duchenue-Araa type, of leg type, and of tj'pes 2 and 3 in text. B shows place of onset of types 1 and (a) in text. At the same time the classical types of dystrophies are very different clinically from the spinal amyotrophies and hence must be separately described. The differences will be shown under the head of diagnosis. Pseudo-Muscular Hypertrophy (Atrophia Musculorum LlPOMATO^US). This, is a disease beginning in childhood and characterized by a progressive weakness of the legs associated with an apparent muscular hypertrophy due to a deposit of fat in the wasting muscles. MUSCULAR ATROPHIES AND DYSTROPHIES. 271 Etiology.— The disease attacks boys much oftener than girls. It begins, in the vast majority of cases, under the age of ten, often at the close of infancy, very rarely not till after puberty. Heredity is a very important factor (in three-fifths of eases), the hereditary influence being almost always transmitted by the mother. A psychopathic or neuropathic condition is often found in the ancestry. jS^euroses, syph- ilis, intemi^erance, consanguin- ity, are not factors in hereditary causation. Injury and an acute disease sometimes appear to act as exciting causes. JSj/m2Jto?ns. — The first symp- tom noticed is a weakness in the legs, / ^ which shows itself in a peculiar " wad- i ^ dling gait" and a tendency to stumble ]~ and fall. A little later (fifth or sixth W year) an ajjparent hypertrophy of leg muscles, particularly of those of the calves, develops. The extensors of the knee or one of them and the gluteal and lumbar muscles may also be af- fected. Sometimes the hypertrophy is very great, at other times it is barely noticeable (Fig. 119). The affected part has a peculiar, hard, non-elastic feeling to the hand, not like that of normal mus- cle. In the upper part of the body the hypertrophy oftenest attacks the infra- spinatus. The supra-spinatus and del- toid may be somewhat involved. The lower parts of the pectoralis major and latissimus dorsi are also usually atrophied, giving a characteristic appearance to the shoulders. The upper-arm muscles are often slightly wasted, the forearm, neck, and face rarely. The tongue may be hyper- trophied. Along with the pseudo-hypertrophy there occurs an atrophy of certain groups of muscles ; and after a time the pseudo-hyper- trophy disappears and an atrophy takes its place. In the lower limbs the muscles most atrophied are the fiexors of the hips, then the extensors of the knee and those of the hip. The calf muscles fail before the anterior tibial. The atrophy and consequent weakness of the lower-limb muscles causes great difficulty in going upstairs, the gait becomes more waddling, and the pa- tient loses the power of getting up when lying on the floor. These peculiarities are due chiefly to the weakness in the exten- FiG. 119.— Pseudo-Muscular Hypertrophy (Erb). 272 DISEASES OF THE NERVOUS SYSTEM. sors of the knees, the extensors of the hip, and the flexors of the hip. By reason of the same defects, the child wlien standing has an antero-posterior curvature of the spine with the concavity backward (lordosis). This is due to the weakness of the exten- sors of the hips, which, acting from the hips, are unable to tilt the pelvis back. On sitting this lordosis disappears, and is replaced often by a curve in the oj)posite direction due to weakness of the erectors of the spine. There may be some lateral curvature also. In consequence of the weakness and contractures of the leg mus- cles, there early develops a talipes equinus, and later the legs may become flexed on the hips and the forearms on the arms. The muscles show no fibrillary twitchings and rarely any de- generative reactions, but there is sometimes a peculiar tetanic contraction with both the faradic and the galvanic current. The knee jerks and elbow jerks gradually weaken and in time are lost. There is no pain or other disturbance of sensibility. The affected parts feel cold and look reddened as if from defi- cient vasomotor innervation. The organic spinal centres are not involved. Intelligence is usally good. Course. — The disease runs a chronic but variable course. Its progress is at first slow ; after walking becomesi impossible it may progress. It lasts from ten to twenty-five years. In a few cases patients have reached the age of fifty or sixty years, even when the disease began in youth. The earlier the disease begins the more rapidly it extends ; the more pronounced the tendency to lipomatosis, the more rapid is the course. Pathological Anato7ny.— This diseeise, like the other forms of dystrophy, is a degenerative one, the process affecting first the muscle fibres; the connective tissue and terminal nerve filaments being secondarily involved. In the same iDatient and even the same muscle the most varied changes may be noted. In the early stages there is a true hypertrophy of some of the fibres, a condition thought to be characteristic of the muscular dystro- phies in distinction from the spinal atrophies. Besides swelling and hypertrophy of fibres, one sees atrophy of the fibres; the bundles are rounded; there is increase of muscle nuclei, splitting of fibres, vacuolization, and tendency to break up into fibrillse (Erb). The connective tissue at first show^s evidence of irrita- tion and proliferation. Finally, as the muscular atrophy pro- gresses, connective tissue increases and takes its place, until a dense, hard myo-sclerosis results. In some parts there is deposit of fat in the connective-tissue cells, and this may increase until an extensive lipomatosis exists. In the later stage of the disease the fat deposits are absorbed and there is only atrophied mus- cle and connective tissue. The nerves and spinal cord are usu- MUSCULAR ATROPHIES AND DYSTROPHIES. 27: ally normal ; when changes are found they are secondary to the muscular disease (Fig. 120). The process is then, first, hypertrophy of muscle fibre and in- crease of muscle nuclei, swelling and rounding of fibres, and spill- ing of the same; then increase of connective tissue, with corre- sponding atrophy of muscle and deposit of fat. The process is a primary degeneration due to an inherent nutritional weakness of the muscle. In a measure it is true that 'K Fig. 120. — Partially Diagrammatic, showing A, hypertrophied fibres; B, mixture of hypertrophy and atrophy ; C, D, atrophy and fatty deposit ; v, vacuoli- zation ; s, sphtting ; h, hypertrophy of fibres ; g, thickened blood-vessel (Erb). those muscles embryologically latest developed are earliest at- tacked. 2. The juvenile form of Erb or scapulo-humeral form of dys- trophy begins in childhood or early youth, a little later than pseudo-hypertrophy. The shoulder girdle is first affected, later the arm. The forearm and legs are attacked very late. Part of the pectorals, part of the trapezii, latissimus dorsi, rhomboid, upper-arm muscles and supinators are affected, while the supra and infra spinati and forearm and hand usually escape. There may be true and false muscular hypertrophy. There are no fib- rillary contractions or degenerative reactions. j8 274 DISEASES OF THE NERVOUS SYSTEM. 3. The facio-scaimlo-humeral form or infantile progressive muscular atrophy begins in early childhood (third or fourth j^ear) usually, but may develop late. The atrophy attacks first the face, giving a characteristic appearance known as the myopathic facies. There is a weakness of the oral muscle, which causes the lips to protrude and produces a symptom called the "tapir- mouth." The atrophy respects the eye muscles as well as those of mas- tication and deglutition. It extends to the shoulders and arms next, then it pursues the ordinary course of the dystrophies. Fig. v:-2. Fig. 121.— Mcscular Dystrophy uaving Characters of Juvenile Type (2) AND PsEUDO-HyPERTROPHIC TyPE (la) (PUTZEI.). Fig. 122.— Juvenile Type, showing atrophy in shoulder and arms (Erb). Prognosis. — The patient never recovers, but the disease some- times comes to a standstill and there may even be some improve- ment, especially in cases beginning late. Treatment.— T\ie prophylaxis is important. It consists in pre- venting the marriage of women belonging to dystrophic families; if a dystrophy has developed in one child, it would be unwise to take the risk of bringing others into the world. Or if children are already born, they should receive the most careful nourish- MUSCULAR ATROPHIES AND DYSTROPHIES. 275 nient, out-door life should be secured, and the dangers from trauma and the infective diseases be prevented. Infants should not be suckled by the mother if she belongs to the dystrophic family. The moderate use of massage and gymnastics is very impor- tant and useful. All kinds of tonic measures are indicated, such as cold baths, good nourishment, arsenic, strychnine, and phos- phorus and fats. Tenotomy and other orthopedic measures may be useful in the later stages. Fig. 123.— Showing Changes in Arthritic Muscular Atrophy. 1, Normal fibre ; 2, atrophied fibre ; 3, vacuolated fibre ; 4, connective-tissue proliferation ( Darkschewitch). Arthritic Muscular Atrophy. In inflammation of joints the muscles moving are affected by a simple atrophy which is called arthritic. ^^/oZo^^.— Rheumatic arthritis is the commonest cause. Symptoms.— The shoulder-girdle muscles are oftenest affected. Whatever the joint, it is the extensor muscles which are first and most attacked ; the muscles above the joint are more susceptible to the atrophy than those below. The atrophy is rather rapid in the first few weeks and then becomes slower. The muscles 276 DISEASES OF THE NERVOUS SYSTEM. affected waste throughout their whole length. They show no fibrillary contraction and no degenerative electrical reaction. There is often an increased irritability, so that an exaggerated tendon reflex or even clonus may be produced. There is no pain or tenderness or anaesthesia in the muscles. Fatholog I/.— The anatomical change is a simple atrophy and shrinking of the muscle fibres, with some increase in muscle nuclei, little vacuolation, no swelling or splitting of fibres (Dark- schewitch— Fig. 123). There is some increase in interstitial tis~ sue, but this is slight. The nerves and spinal cord are normal. The atrophy is probably due to reflex action. It is a reflex tropho-neurosis. Even a neuralgic joint may cause an atrophy. The prognosis is good. If the arthritis gets well the muscles are also restored. The treatment consists of electricity and gentle massage and exercise. Internal treatment must be directed to the arthritis. Occupation Muscular Atrophies. As a result of constant over-use muscles sometimes atrophy. This applies especially to the smaller muscles of the hand. Thus there occurs an atrophy of the thenar eminence in lapidaries and in persons who constantly use this group of small muscles. The biceps sometimes wastes in smiths, and I have seen atro' phy of the calf muscles in a ballet-dancer. The disease does not tend to extend beyond the muscular group first attacked. Its seat is probably the muscles themselves. The treatment is rest. CHAPTER XY. TUMORS AND CAVITIES OF THE SPINAL CORD. Miology.— Tumors occur rarely in the spinal cord. The largest tables of cases include less than one hundred. The commonest age is thirty to fifty ; tubercle occurs earlier (fifteen to thirty-five — Herter) and lipoma is con- genital. Males are more sub- ject than females. Tuber- culosis, syphilis, and cancer predispose to the disease. Injuries and exposures ap- pear sometimes to excite the growth of spinal neoplasms. Symptoms. — These vary with the location, character, size, and rate of the growth of the tumor. No definite clinical picture can be drawn. The symptoms are such as re- sult from a foreign body slow- ly and iDrogressively irritating and destroying the roots and substance of the spinal cord. Pain appears early and is very constant, continuous, and severe. It is generally re- ferred to nerves running out from the cord in the region of the tumor; a girdle sensa- tion is felt. Numbness, hy- persesthesia, and later anaes- thesia occur. Tenderness over the spine and rigidity are not very frequent. The sensory symptoms are usually more on one side, but may become bilateral. Spasm, contracture, and exaggerated reflexes usu- ally soon develop, involving R Fig. 124.— Showing the Condition in a Brown-Sequard Paralysis due to a Tumor Growing in the Left Side op the Spinal Cord. On the left side, hyperaesthesia, ataxia, paralysis, exaggerated reflexes. At the upper limit is a band of anaesthesia. On right side, anaesthesia. 278 DISEASES OF THE NERVOUS SYSTEM. one or both legs or an arm and leg. Later paralysis, atrophy, loss of control of the bladder and rectum, and bed-sores follow, and death ensues from exhaustion. "When the disease is cervical the four extremities and trunk muscles may be gradually involved, and there is rigidity of the neck and optic neuritis. If lower down, there develops a hemi- paraplegia, later a complete parajDlegia, usually with exaggerated reflexes. If the tumor is in the lumbar region the reflexes are sooner lost and the sphincters early involved. A rather frequent type of symptoms caused by spinal tumors is that known as a Broicn-Sequard paralysis or hemiparaplegia. In a typical case of this kind there is paralysis of motion and muscle sense on the side of the lesion, paralysis of cutaneous sen- sation, especially of pain, and temperature on the opposite side. On the side of the lesion the temperature may be slightly raised ; Fig. 125.— Showing the Mechanism op the Production of a Brown-Seqcari> Paralysis. The shaded part on the left represents the lesion. This involves the pyramidal tract and motor fibres M, causing paralysis and spasm on same side; also the muscle sense nerves M S on same side and the cutaneous sensory nerves C S of opposite side. there is often hypersesthesia, and reflex action is increased. There may be a band of anaesthesia at the level of the lesion and on the same side (Figs. 124, 125). The symptoms vary according as the tumor is outside or in- side the dura. The common extra -dural forms are lipoma, cancer, gumma, and sarcoma. The greater amount of motor and sensory irritation, the evidence of some vertebral disease, existence of malignant tumor elsewhere, the absence usually of hemij^ara- plegia, characterize extra-medullary tumors. The common forms of intra-dural or medullary tumor are glioma and tubercle. In these cases pain and spasm and rigidity are rather less com- mon in the early stage; hemi-paraplegia is more common. A secondary myelitis sometimes develops. The duration of the disease ranges from three months to five years, the average being two or three years. Pathology and Pathological Anatomy.— A\\ forms of tumor occur, but the commonest are gliomata and sarcomata, and after TUMORS AND CAVITIES OF THE SPINAL CORD. 279 this fibromata, myxomata, gummata, and tubercles. Cancer is rare ; ecliinococcus and cysticercus are the only parasitic tumors found. The majority start from the membranes, next from the cord, and fewest from the vertebrae. The meningeal tumors are mostly sarcomata and their various modifications, fibroma, enchon- droma, carcinoma, and lipoma. The myelonic or intra-spinal tumors are commonly glio- mata, sarcomata, tubercle, and syphilomata. Spinal tumors are small in size, ranging from one-fifth to one and one-fifth inches (one- half to three centimetres) in diameter. The glioma may diffuse itself for a long dis- tance through the centre of the cord, forming cavities (syr- ingo-myelia). The sarcomata may likewise be irregularly spread along the surface of the cord. Spinal tumors are usu- ally single, but fibromata, the parasites, and sarcomata may be multiple. The favorite locations for spinal tumors are just below the mid-cervical, the upper and the low^er dorsal regions. The secondary changes produced by tumors are softening, hem- orrhages, secondary degenera- tions, and inflammatory reac- tion. The origin and histology of spinal tumors does not differ from that of tumors elsewhere. The Diagnosis.— Th.Q disease has to be distinguished from vertebral caries, transverse myelitis, and hypertrophic pachymen- ingitis. The points to be noted as regards caries are the absence of an external tumor or kyphosis; the small degree of tenderness and rigidity, the age, and absence of tubercular diathesis. The progressive course, beginning with pain, followed by motor and then sensory paralysis, and the localization of the symptoms ex- cludes myelitis. The differentiation from hypertrophic pachy- meningitis is often very difficult. Fig. 126.— Sarcoma of Spinal Cord, Mid-cervical Region. 280 DISEASES OF THE NERVOUS SYSTEM. The character of the tumor cannot often be determined cer- tainly, Tlie probabihties are in favor of sarcoma or ghoma, es- pecially in middle life. Syphiloma may be suspected from the history and results of treatment. Tubercle is very rare. The 2^rognosis is bad except in syphiloma, and even here it may be serious. Tubercle may perhaps cease to grow. Surgical interference now saves the life of some cases. Treatment. — In syphilitic tumors appropriate remedies may do good and should be vigorously used. In tubercle, tonic treatment, iodine, and cod-liver oil may be of service. In gliomata and sarcomata, nitrate of silver and arsenic may be tried. In other forms, symptomatic treatment is all that can be recom- mended medically. In all cases of spinal tumor surgical inter- ference should be considered ; extra-dural tumors, if taken early, can be removed with great benefit. Even in medullary tumors enucleation may do some good in the early stage. Exploratory operations are justifiable if there is no question as to the diagno- sis of tumor. The mortality from such operation in capable hands is very low, though it is more dangerous than trephining the skull. CAVITIES IN THE SPINAL CORD. The cavities of the spinal cord are known as 1. Hydromyelia. 2. Myelitic cavities. 3. Syringo-myelia. There may be various combinations of these processes, the most common being a combination of hydromyelia and syringo- myeUa. Hydromyelia. This is a dilatation of the central canal of the cord, the cavity being filled with fluid. The condition may be associated with hydrocephalus or with spina bifida, or it may be independent of these conditions. The dilatation may be cystic and irregular or, as is more usual, extend throughout the cord. The dilatation extends more posteriorly, because the posterior columns are formed latest. The abnormality may be slight and give rise to no symptoms. Or a pathological process like a gliomatosis may de- velop upon it. Myelitic axd Hemorrpagic Cavities. Such cavities may be formed in the cord by a central excavat- ing myelitis or by small hemorrhages. These cavities are usually small, irregularly distributed, and are lined with connective tis- sue. They may be formed in rare cases in connection with hy- dromj'elia or neoplasms. TUMORS AND CAVITIES OF THE SPINAL CORD. 281 Syringo-Myelia. Syringo-myelia is a disease of the spinal cord characterized by a development of gliomatous tissue in the central parts, with for- mation of cavities. Clinically the disease is sometimes charac- terized by peculiar disturbances of sensation and nutrition. In many cases, however, the symptoms are atypical and the dis- ease cannot be recog^nized during life. The description here yiven corresponds to the classic mani- festation of the disease, and it is intended to refer to syringo- myelia produced by gliomatosis only. Etiology. — The disease is rare, about two hundred cases hav- ing been reported. It is more frequent than amyotrophic lateral 1. ' 2. Fig. 127.— Distribution of Cutaneous Anesthesia in Syringo-Myelia. 1 shows area of analgesia : 2 shows that of thermo-ana?sthesia. The darker shades show where there is anaesthesia to pain and temperatui*e (Bruhl). sclerosis and rather less frequent than multiple sclerosis. It oc- curs oftener in men than women, and develops early in life, be- tween the ages of fifteen and twenty-five. It occurs especially in persons who follow manual occupations such as butchers, tailors, etc. Traumatism, pregnancy, and in- fectious diseases seem occasionally to give rise to it. Heredity, syphilis, and alcohol are not causal factors. Symptoms.— The disease begins insidiously with some achmg pains in the neck and arms and parassthesia of the hands. There is soon a muscular atrophy of the hands resembling spinal pro- gressive muscular atrophy, with perhaps anaesthesia. As the dis- ease progresses the weakness and atrophy of the hand muscles become more noticeable and gradually extend toward the trunk. The atrophv comes on in both extremities at about the same time. 283 DISEASES OF THE NERVOUS SYSTEM. Fibrillary contractions and partial degeneration reaction may be observed. Cutaneous anaesthesia of the affected hand and arm to temperature and pain, but not to touch, takes place ; and this _ is so marked as to be al- most pathognomonic of the disease (Fig. 127). The legs do not become affected until late, and then generally show a spastic paraplegia. The throat and face are rarely in- volved. There is a scolio- sis of the sjoine. generally in the dorso-lumbar region (Fig. 128). Vasomotor, secretory, and trophic symptoms are prominent. The hands may be oedematous or red and congested. Sweating or dryness of the skin may occur. Eruptions appear on the skin, such as bullae, herpes, and eczema. Pain- less whitlows attack the fingers and may destroy the terminal phalanges. Erosions and ulcerations also occur. The nails be- come dry, brittle, and drop off (Fig. 129). Arthropa- thies and spontaneous frac- tures have been observed. The pupils may be un- equal and the " bulb re- tracted. Late in the disease symptoms of involvement of the medulla develop. At this time also the bladder, rectum, and genital centres are attacked. The disease progresses slowh' for years, with remissions of various degree. The cardinal symptoms are a progressive muscu- lar atrophy, with a pecu- liar partial anaesthesia, trophic disturbances, and scoliosis. Pathological Anatomy. — The seat of the disease is the sub- stance of the cord. On opening it by transverse sections one finds one or more cavities extending in various degrees up and down. The most frequent primary site is the cervical swelHng. From here it usually passes down and may reach the wliole length of the cord. It also extends upward and may involve Fig. 128.— Showing Curvature op Spine in Syringo-Myelia (Erb;. TUMORS AND CAVITIES OF THE SPINAL CORD. 283 the medulla and the nuclei of the cranial nerves. The cavities are of irregular shape, small size, and filled with a liquid like the cerebro-spinal fluid. They are situated oftenest posterior to the commissure and involve one or both posterior horns, but they may be so extensive as to involve almost the whole of the centre of the cord at some levels. The walls are usually lined by a membrane and surrounded by a gliomatous tissue (Figs. 130-135). This membrane is composed of a rather dense gliomatous tis- sue. It may be absent in some parts. The glla cells are in vari- ous stages of development and degeneration. In parts of the cord the new growth may form a large and solid mass occupying Fig. 129.— Showing Hand in Syringo-Myelia op Type of Morvan's Dis- ease (Erb). most of the centl-e of the cord. Small hemorrhages and foci of myelitis may be present. In some cases there is evidence of a dilated central canal, with neuroglia hyperplasia of the walls and a gliomatous infiltration about this. The epithelium of the cen- tral canal mav form part of the wall of the cavity. Pathology^— At about the sixth week of foetal life the central canal of the cord is large, diamond-shaped, and reaches nearly to the anterior and posterior surfaces of the cord. This cavity grad- ually contracts and unites in the middle, the anterior part forming the central canal and the posterior part the posterior septum. The posterior part may, through some embryological defect, fail to close, and a congenital cavity may be left. About this a gli- oma may develop, and we have syringo-myelia. The central canal 284 DISEASES OF THE NERVOUS SYSTEM. may remain imperfectly contracted, and a syring:o-myelia may develop in connection with it. Probably most cases ot syringo- invelia are developed on the basis of an embryological defect. 'Gliomata were formerly thought to be i^ractically identical with sarcomata. It is believed now, however, that they are of _ epiblastic origin, and like ~ nerve cells are modifica- tions of epithelial tissue. This tissue in its normal state is called neuroglia. It is a nervous substance. It is composed of small cells, round or of irregu- lar shape, with a large i- '^^ ^^\ nucleus and fine fi])rillary 'v^^^&**-*E**ms«.j»««^- ^'^ prolongations. In glioma these cells are relatively m u c h more numerous, while the fibrillary net- w^ork is less conspicuous. There is considerable va- riation in the relative richness of cells and fibres, however. When the for- mer are very frequent the term gliosarcoma has been wrongly given to the tumor. The glioma is penetrated by small blood-vessels wdiose walls are often diseased, so that minute hemorrhages oc- cur and the glioma be- comes stained and pig- mented. In other cases it is gray or yellowish in color. The rich cellular pro- liferation in gliomata has suggested an analogy in its growth to that of in- flammation, and the term gliosis is used as analo- gous for neuroglia to inflammation for connec- tive tissue. Gliosis dif- fers from sclerosis, how- ever, in the fact that in the latter process the multiplication of fibres dominates, wdiile in the former it is the cells ; besides this, in gliosis there is a tendency to softening and formation of cavities ; and all nerve fibres dis- appear. In sclerosis some nerve fibres remain, and one observes the presence of granular and amyloid bodies. Peculiar Types. — 1. The disease may be latent, giving rise to very few symptoms or to none that are characteristic. Fig. 131. i^'^'^1^j^^s^:,X Fig. lS-4. Figs. 130-132.— Sections of Spinal Cord at DrF FERENT Levels in Syringo-Myelia (Bruhl). TUMORS AND CAVITIES OF THE SPINAL CORD. 285 2. There may be a period of irritation and pain in the extrem- ities followed by paraplegia, with few sensory troubles, the course suggesting a chronic transverse myelitis or a Brown- Sequard paralysis. 3. There is a type in which bulbar symptoms develop early, but differing from ordinary bulbar paralysis in the in- volvement of the trigeminus and other cranial nerves not commonly at- tacked. 4. There is a form characterized by a rather rapid as- cending paralysis. None of these types can ordina- rily be recogni::ed during life. 5. There is a type c h a r a cterized by the symptoms of muscular atrophy with analgesia and felons (Morvan's disease). In this type there is prob- ably a complicating neuritis. Some as- sert that all cases of Morvan's disease are cases of syringo- myelia, but this is not proven. Diagnosis. — The disease is distin- guished in its clas- sical form by (1) its beginning at the period of adoles- cence, (2) by the progressive muscu- lar atrophy com- bined with the pe- culiar dissociated disturbances of sen- sibility, (3) by the t r o p h i c disturb- ances and scoliosis. It has to be distinguished from progressive muscular atrophy and dystrophy, and amyotrophic lateral sclerosis, hypertrophic cervical pachymeningitis, chronic transverse myelitis, Morvan s disease and anaesthetic leprosy. The sensorv and trophic disorders and scoliosis enable one to distinguish if from progressive muscular atrophy. In leprosy Figs, Fig. 135. 133-135.— Sections op Spinal Cord at Different Levels in Syringo-Myelia (Bruhl). 286 DISEASES OF THE NERVOUS SYSTEM. the dissociation of the sensory symptoms is not present, and the anaesthesia is distributed along 'the course of the nerves or in sharply circumscribed plaques. In some cases the peculiar tu- bercular disease of the skin and the history of the case make the diagnosis easy. In leprosy, also, there is a perineuritis, and the enlarged inflamed nerves may be felt. Portions of the skin may be excised and examined for the leprous bacillus. As regards the' differentiation from Morvan's disease, this cannot often be done. Still whitlows are rare in ordinary forms of syringo- myelia. Morvan's disease begins in one hand and slowly extends, with remissions, to the other. Usually there is loss of tactile as well as thermic and pain sense. The prognosis so far as life is concerned is bad. But the disease has often a long course, ranging from five to twenty years, and periods occur in Avhich the progress of the disease seems arrested and improvement occurs. Treatment. — It is not impossible that we may find some drug which acts specifically on gliomatous tissue, checking its growth. At present we know of only two things which may possibly do this : nitrate of silver and arsenic. These drugs should be given ; and for the rest, tonic and symptomatic treatment are indicated. FUNCTIONAL DISORDERS. Spiral Irritatiox. This name is given to a functional disorder characterized by great pain and tenderness along the spine and associated with a neurasthenic and hysterical condition. The disease has been described as spinal hypersemia (Hammond) and as spinal anaemia. Etiology. — Spinal irritation is far more frequent in women than in men. It occurs between the ages of fifteen and thirty- five chiefly. A neuropathic constitution usually exists. The exciting causes are mental shocks and trauma, which latter need be only slight; excessive physical and mental w^ork in young people ; uterine displacements, sexual irritation, eye strain ; and sometimes infectious fevers. I have seen cases which were the residuum of sporadic cerebro-spinal meningitis. Symptoms.— The disease usually comes on slowly, with feel- ings of tenderness, pain, and burning in the back. Walking in- creases this; sitting and using the arms soon do the same. The neck tires on any exertion; and severe paroxysms of a boring neckache or of headache or backache occur. The patient has to lie down nearly all day, and finally in bad cases remains in bed. There are tender points on each 'side of the spine, generally at about the level of the sixth cervical, fourth to sixth dorsal, and dorso-lumbar junction. These points vary in position and sensi- tiveness. Pressure on them may cause nausea, pulse disturb- ances, parsesthesia, or radiating j^ain. The skin over the back is FUNCTIONAL DISORDERS OF THE SPINAL CORD. 287 sensitive, and there may be sensitive points over the ovaries and epigastrium. The reflexes are exaggerated ; there is some motor weakness, and the patient may be unable to walk, stand, or use the arms very much, but this is due more to the weariness and pain that result than to actual paralysis. Some wasting occurs in the limbs, but degenerative reactions are never found. Occasion- ally the patient has cramps and twitchings in the extremities. Sometimes there occurs in spinal irritation a nearly complete paraplegia. This is usually hysterical and always is functional. When such a combination of spinal irritation and paraplegia is caused by injury, it is called "concussion of the spine." Mental symptoms such as undue despondency, irritability, nervousness, and emotional crises are often present. Neither hysteria nor men- tal feebleness, however, necessarily characterizes spinal irritation. Many patients are unusually bright, hopeful, and intelligently anxious to recover. Sleep is usually poor and disturbed by dreams. The hands and feet are often cold and clammy; the pulse is rapid and of variable tension. The urine is of light spe- cific gravity, with relative excess of phosphates. Visceral symptoms are common in most cases. They consist of sensations of respiratory oppression, palpitations, anorexia, nausea and vomiting, constipation alternating with diarrhoea, attacks of polyuria, and sometimes vesical and genital weakness. The symptoms are usually exaggerated at the menstrual period. The disease runs a chronic course; it always lasts months, often years, depending largely upon treatment and surroundings. Some of the symptoms of the trouble may remain for a lifetime. Pathology.— T\\e symptoms of the disease correspond exactly to what would follow from an irritation of the spinal meninges and posterior branches of the mixed spinal nerves. Hence the name spinal irritation can hardly be improved upon at present. The fact that classical cases follow an acute meningitis leads me to believe that a hypertemia generally underlies the condition. Diagnosis.— Tliis must be made from cervical caries, organic disease of the spine and of the cord. In caries the rigidity, de- formity, and localized pain are generally sufficient helps. Chronic meningitis is distinguished by the history of an acute onset, the symptoms are more stable, there is more rigidity, and the pains are extrinsic and radiating. The hysterical symptoms are absent, and the tendency, on rest, is always toward recovery. If there is a chronic meningo-myelitis or myelitis, the paralyses Avill be per- haps greater, and there may be degenerative muscular changes, anaesthesia, and involvement of the sphincters. In a functional palsy there cannot be complete degenerative electrical reactions or permanent sphincter paralyses. 288 DISEASES OF THE NERVOUS SYSTEM. Prognosis. — Xearly all cases get well eventu ally. Persons with a weak will, feeble body, and neuropathic constitution have the worst outlook. Traumatic cases, if uncomplicated, are not much worse than others. Treatment. — The treatment must be a mental as well as phy- sical one. The patient may be put to bed at first, but she should be kept employed and interested if possible, and she should soon be encouraged to walk and work a little. Her surroundings should be not too sympathetic, and her daily life should be sched- uled exactly for her. She should be well fed, but not stuffed. Internally it is customary to give strychnine, iron, mineral acids, salicine, and quinine as tonics ; moderate courses of bromides in- terrupted at times, or small doses of codeia and valerian, may be used as sedatives. Indian hemp and the analgesics may be of service. I have seen no good from arsenic, nitrate of silver or gold. Iodides and the salicylates, however, are useful. For sleeplessness give a draught of quassia water at night, and make the patient lie on a hop pillow or inhale the steam from boiling water in which hops have been thrown. Locally, counter-irrita- tion along the back must be kept up at stated intervals. For this purpose one may use mustard, iodine, blisters, the cautery, and the galvanic current. The faradic current with a wire brush is most efficacious for removing the cutaneous hypersesthesia (Anstie) if the patient can be persuaded to stand the pain. Cups, leeches, Baumgartism and splints, jackets and braces all may have to be resorted to eventually. A very great deal de- pends upon the perseverance and personality of the physician. Spinal Exhaustiox (Spixal Neurasthexia). This is a condition which is nearly the opposite of spinal irri- tation. It occurs as often in men as Avomen and during middle life or the climacteric. Etiology. — It occurs oftenest in brain-workers and the edu- cated classes. The principal exciting causes are shock, injury, overwork, sexual excesses, and exhausting diseases. The symjytoms, which come on slowly, consist chiefly of a gen- eral motor weakness and condition of exhaustion. The patient cannot walk far or stand long. His reflexes are weak, the mus- cles get wasted and flabby. There are some pains and burning or creeping feelings along the back when any exertion is made. The stomach is weak, the bowels irritable, the sexual power nearly gone. Headaches, insomnia, mental depression, and hypo- chondriasis are present. The disease, in fact, presents many of the spinal and neurasthenic characters of spinal irritation, but the pain is less and the motor weakness much greater. FUNCTIONAL DISORDERS OF THE SPINAL CORD. 289 When this latter reaches the point of paraplegia and follows shock or injury, the trouble is also called "concussion of the spine." Whether an anseniia underlies it we do not know. There is certainly a nutritional defect. The diagnosis, course, and prognosis are much the same as in spinal irritation. Treatment. — The disease may be associated with sprains or surgical injuries which need attention. Aside from this, the treatment must be largely in the nature of the rest cure. Mas- sive doses of tine, nux vomica may be used (ttl xxx. to xl. t. i. d.), combined sometimes with a little opium or codeia. At the same time, electricity, massage, baths, and strong feeding are required. The patients usually improve on first going under treatment, then relapse a little. The physician must keep something in re- serve for these relapses. CHAPTER Xyi. ANATOMY AND PHYSIOLOGrY OF THE BRAIN. Anatomy.— The nervous system is developed from a hollow tube formed bv a folding of the epiblast. The brain or enceph- alon grows out from its anterior part. This swells into three cavities called the anterior, middle, and posterior cerebral vesi- cles. From the anterior a secondary vesicle develops ; the pos- terior divides into two : so that eventually there are five vesicles. Out of them the different parts of the brain are formed. Ccrmniss.pcst Gland.j)ineal. rhugel. CereheUum hijpcphijsenanla^i Fig. 136. Fig. 137, Fig. 186.— The Cerebral Vesicles. Fig. 137.— Fcrther Development of Vesicles into Fore-brain O^orderhirn), TwEEN-BRAiN (Zwischenhirn), Mid-brain (Mittelhirx), Hind-braik (Hinter- hirn), and After-brain (Nachhirn). The cavities (Hohlen) of the vesicles are being formed into the ventricles (Edinger). 1. From the secondary anterior vesicle there grow the cerebral hemispheres, corpus callosum, fornix, anterior commissure, and corpus striatum. This forms the fore-brain. 2. From the primary anterior vesicle, the optic thalami, optic commissure, infundibulum, and corpora albicantia. This forms the 'tween-brain. The olfactory lobes and optic nerves are con- nected with this vesicle. 3. From the middle cerel^ral vesicle there grow the corpora quadrigemina and cerebral peduncles. This is the mid-brain. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 291 4. From the fourth vesicle, the cerebellum and pons. This is the hind-brain. 5. From the fifth vesicle, the medulla, which constitutes the after-brain. The development of these parts is shown in the accompanying diagrams. In man the fore-brain is enormously developed, the Fig. 138.— Still Further Development of Vesicles. The cerebrum is being formed out of the first vesicle 1^ (Edinger). 'tween-brain moderately developed, the olfactory lobes atrophic, the mid-brain almost rudimentary, the hind-brain well developed, the after-brain relatively not much developed. In the process of development of the brain, the neural canal becomes variously enlarged and constricted, until the ventricles of the brain, the foramina of Monroe, and the aqueduct of Sylvius are formed. The ventricles are the two lateral, the third, fourth, and fifth. Fig. 139.— Further Development. The dotted Imes show the oiigmai sub- division into vesicles (Edinger). The foramina of Monroe connect the lateral and third ven- tricles ; the aqueduct of Sylvius connects the third and fourth ventricles. The different segments of the brain as thus enumerated are composed of deposits of nerve cells forming gray matter or gan- glia, and strands of nerve fibres connecting these ganglia. Most of the general description of these parts must be gotten from treatises on anatomy. I propose, however, to enumerate and de- 292 DISEASES OF THE NERVOUS SYSTEM. scribe the various ganglionic deposits found in the brain; then show the way in which they are connected with each other and the spinal cord. The sixteen ganglionic deposits of the brain are arranged in the different segments as shown here : 1. Cerebral cortex. ) 2. Corpus ^ Caudate nucleus. - Fore- brain. striatum. "/ Lenticular nucleus. ) 3. Olfactory lobes. 4. Optic thalamus. 1 5. Corpora genicalata. ^ ^t ween -brain. 6. Corpora mamil. | 7. Luy's body. j 8. Corpora quadrigemina. ) 9. Red nucleus. >- Mid-brain. 10. Substantia nigra. ) 11. Cerebellar cortex. ) 12. Cerebellar nuclei. - Hind-brain. 13. Pons nuclei. ) 14. Olivary body. ) 15. Nodal nuclei. ,- After-brain. 16. Cranial nuclei. ) The Cortex Cerehri and the Convolutions. — The gray matter of the surface of the brain is called the cortex cerebri, and it is by far the largest and most important deposit of nerve cells in the body. The cortex is from 2 to 4 mm. (one-twelfth to one-fifth of an inch) thick, and its total superficial area is 1,800 to 2,700 sq. ctm. The area of gray matter lying in the fissures is about twice that lying on the surface (Donaldson). The cerebral cortex is arranged in folds or convolutions (gyri) separated by fissures or sulci. These fissures divide the brain also into lobes. The fis- sures of the brain are divided into primary and secondary. The former are permanent, and present little change in size, location, or direction. The latter are variable in all these respects, and are often called sulci for purposes of distinction. The primary fissures of the brain are ; The longitudinal. The transverse or choroidal. The fissure of Rolando or central. The fissure of Sylvius. The parietal. The parieto-occipital. The calcarine. The position of these fissures is indicated on the accompany- ing diagrams, which are based on descriptions of Wernicke, Eber- staller, Wilder, Cunningham, and many observations of my own. I have not space to give detailed descriptions. The secondary fissures or sulci will be enumerated in describ- ing the lobes. They are divided into the typical or more or less constant and the atypical or tertiary fissures. The primary fissures divide the cerebrum into various por- tions called lobes. The lobes are : Frontal. The central or island of Reil. Parietal. Olfactory. Temporal. Limbic. Occipital. ANATOMY AND PHYSIOLOGY OF THE BRAIN 293 e 1 T' :S ^ a. ^ .s •?: "S i S r i § - S ^ Si ■^ ^ " rt Si rt -^ '-" .- ;: 3 -g s ^ .'^ ^- s p. -2 -g^ &c o a aj a °, -J P fi; 5 8 S 2 294 DISEASES OF THE NERVOUS SYSTEM. There are eight fissures and seven lobes. TJie frontal lobe is limited behind by the fissure of Rolando, and on the median surface by the calloso-marginal or subfrontal fissure and its ascending- brancii. It has the following sulci; 1. Superior frontal and superior prsecentral. 2. Inferior frontal and inferior prcecentral. 3. Olfactory. 4. Tri-radiate. In the frontal lobe are the following convolutions. 1. Prsecen- tral or ascending frontal, having on its median surface (a) the paracentral lobule. 2. First or superior frontal. 3. Second or middle frontal. 4. Third or inferior frontal (Fig. 140). The jmrietal lobe is limited behind by the parieto-occipital and anterior occipital fissures, below on its outer surface by the Sylvian fissure and a line drawn back from its upper end to the lower part of the anterior occipital. In front it is limited by the fissure of Rolando. On its median surface it is limited in front by the ascending branch of the calloso-marginal or subfrontal fissure, behind by the parieto-occipital, and below by the sub- parietal fissure. Its important sulci are: 1. The parietal or inter- parietal. 2. The post-central. The convolutions formed are, on the convex surface: 1. The post-central or ascending parietal. 2. The superior i^arietal lobule, having on its median surface (a) the quadrate lobule or prsecuneus. 3, The inferior parietal lobule, which is composed of {a) the-&upra_zBiaTgjnal gyrus, (b) the angu- lar gyrus. Tliese latter gyri are variously described, but it is best to regard one, (a) the supra-marginal, as that surrounding the posterior end of the fissure of Sylvius ; the other, (b) tho^^xxgjilsir, as that beginning at the~iTpper^iknrr~oniie first teJi^iporal fissure and extending back as far as the anterior occipital fissure. The Occij^itaJ Lobe. — This is limited on its convex surface, anteriorly, by the parieto-occipital fissure, laterally to this by the anterior occipital and inferior occipital fissures. These in apes form a single continuous fissure sharply separating the occip- ital from the other lobes.* On its median surface the parieto- occipital fissure limits the lobe in front. On the under surface the anterior edge of the tentorium about marks the anterior limit. The sulci are: 1. The transverse occipital (sipe fissure of some writei's). 2. The superior or lateral occipital. 3. The inferior occipital. On the median surface : 4. The calcarine, which joins the parieto-occipital. 5. The inferior occipito-temporal or fourth temporal. The convolutions on the convex surface are -. 1. The superior occipital. 2. The middle occipital. 3. The inferior occipital. 4. The descending occipital. On the median surface we find: 5. The cuneus. 0. Descending occipital. The Temporal Lobe. — The convex or, lateral surface shows the following sulci : 1. The first temporal or parallel sulcus. 2. The second or middle sulcus. On the under and median surfaces are : 3. The third or inferior temporal sulcus. 4. The fourth temporal or inferior occipito-temporal or collateral sulcus, which extends into the occipital lobe. 5. The hippocampal sulcus. The convolutions are: 1. The first temporal convolution. 2. The second temporal convolution. • 3. The third temporal con- volution. 4. The lateral occipito-temporal or fusiform convo- lution. 5. The median occipito-temporal or lingual convolu- tion. 6. The hippocampal convolution, which is an extension of * There is still some doubt about the homology of these tissues. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 295 4 and 5. 7. The uncinate convolution, which is an extension of 6. The Island of Reil (lobus centraUs, lobus caudicis). — This has a circular sulcus surrounding it, and several more or less short sulci dividing it into from five to seven short gyri. The limbic lobe, if described as a separate lobe, is made to in- clude anteriorly the gyrus fornicatus or gyrus cinguli, back of this the isthmus, then the hippo- campal, uncinate, and dentate con- volutions (Fig, 140). The olfactory lobe is rudimen- tary in man. Its position is shown in the diagrams. The operculum is the part of the brain that overlaps the island of i iw_JL4aiii \ Reil. It consists of a fronto-pari- etal part, formed by the lower end s Mf '. .f Fig. 14;^. i^ic 141 Fig. 141.— Section of Cortex of Frontal Lobe Stained by Weigert's Method, showing the fibre systems and laj^ers. 1, 2, 3, 4, The ganglionic cell layers ; a, neuroglia layer; 6, tangential fibres; c, super-radial network; d, outer stripe of Baillarger or Glennari's stripe ; e, inter-radial network ; /, inner stripe of Bail- larger; g, radial fibres of white matter (after Obersteiner and Edinger). Fig. 142.— Section of Cortex of Frontal Lobe (after Golgi). 1, Neuroglia or barren layer ; 2, small pyramidal layer; 3, large pyramidal layer; 4, irregular and spindle-cell layer. At G^, a deposit of granular cells forms a fifth layer in the sensory occipital area of the cortex. 296 DISEASES OF THE NERVOUS SYSTEM. of the two central convolutions, a frontal part formed by the base of the inferior frontal convolution, and a temporal part formed bv the tip of the temporal lobe. The cuneus, prcccuneus and paracentral lobule are important subdivisions on the median surface of the brain. Their position and boundaries are shown in the cuts. Micioscopical Anatomy of the Convolutions.— T\ie cortex of the cerebrum is composed of nerve cells, a network of nerve fibres and processes, and of neuroglia tissue. Superimposed upon it is a very vascular membrane, the pia mater, which sends a rich plexus of' vessels into it. We shall proceed to study : 1st, the structure and arrangement of the nerve and neuroglia cells ; 2d, the arrangement and connections of the nerve plexuses. On both these points new facts are being constantly added, and the present description must be in many respects only provisional. 1st. The cells are arranged to a certain extent in layers. In the outer laver, next the pia mater, is a deposit of neuroglia tissue containing "spider cells.'' Beneath these are small, somewhat irregularlv shaped pyramidal cells (angular cells of Lewis); next come large pyramidal cells ; and deepest of all irregularly shaped cells (including the granule cells of Lewis) and spindle-shaped cells. In the above I have described four layers of cells, and this mav be considered the type. Some anatomists describe five typi- callayers, the fifth being made by a subdivision of the fourth (by Meynert) or of the third (by Lewis). The common four-layer type is found in the central convolutions and frontal lobe. In the occipital region there are six (Lewis) or eight (Meynert) layers described. These are formed by the interposition of granule cells which subdivide the third layer. Various tj^pes of cortex are described depending upon the"^ different degree of develop- ment of the cell layers and upon the fibre arrangements. The common or motor type, as has been stated, has four layers. The large pyramidal cells are here numerous and are arranged in clusters. The sensory type has at least five layers, as described for the occipital cortex,' and here the large j)yramidal cells are few and isolated. The pyramidal cells are arranged with their apices pointing to the periphery. They give off apical, lateral, and basal processes. The basal process of the pyramidal cells is continued as an axis cylinder. Some pass down into the white matter; others turn up and enter the fibre systems of the cortex. The spindle cells point toward the periphery also, except at the bottom of the sulci, where they lie parallel to the surface. Their processes connect neighboring areas and are called associative fibres. The small pyramidal and spindle cells measure about 10 xl8//; the large, 20 x 40,// (y^ott x ^^q in.). There are in the upper central and paracentral convolutions giant cells (of Betz) which measure 125 X 55// ( Yrro X 5^Tj in.). Despite the great variety a.nd complexity of the cortex, it is probable that there are but three principal classes of cells :(1) those which receive nervous impulses 'and which lie chiefly in the second and granule layers; (2) those Avhich associate and co- ordinate these impulses, and which lie in the second and deep in the fourth layers (small pyramidal and spindle cells) ; and (3) those which discharge impulses and which lie in the third layer (large pyramidal cells). ANATOMY AND PHYSIOLOGY OF THE BRAIN. 297 The fibres and plexuses oi the cortex are composed of processes from the nerve cells and terminals coming in from the white mat- ter. They collect into several close networks. One, lying just under the neuroglia layer and running parallel to the surface, is called the tangential layer of fibres ; a second layer runs among the large pyramidal cells, forming the outer stripe of Baillarger; and a third layer, beneath this, is called the inner stripe of Bail- larger. Besides these, there are radiating fibres, running in from the white matter and forming inter-radial and supra-radial net- works (Fig. 142). The cortical gray matter, as will thus be seen, contains layers of nerve cells, into which nerve fibres penetrate. These termi- nate, as do all fibres, in end-brushes, which surround the receptive Fig. 143.— DiAGRAMATic Rkpresentatiun of the Relation of the Cells op THE Cortex to Each Other and to Distant Parts. A, Motor type of cortex. 1, Neuroglia cell; 2, small pyramidal and granule cell; 3, large pyramidal cell; 4, spin- dle cell; o, tangential fibres; 6, stripes of Baillarger; c, associative fibres. B, Sensory type of cortex (Von Monakoff). II., III., V., Second, third, and fifth layers of cor- tex; hx\ large pyramidal cell; sx, granule cells. In A, impulses are received by the small cells 2, distributed and associated by the tangential and other fibres a, b, c and by the spindle cells 4; impulses are emitted by the large cells 3. or sensory cells. An enormous number of fine fi bres are given off by the cells ; some of these form layers in the cortex and con- nect "neighboring parts, others run out and connect more distant parts or pass down to lower levels. There must be three kinds of fibres— afferent, associative, and efferent— just as there are three types of cells (Fig. 143). The different convolutions and lobes of the brain are connected with each other by association fibres and with parts below by projection fibres. The association fibres consist of short fibres connecting neigh- boring convolutions, long fibres connecting neighboring or dis- tant lobes, and commissural fibres connecting the two halves ot the cerebrum. 298 DISEASES OF THE NERVOUS SYSTEM. The short association fibres are numerous ; they lie close be- neath the gray matter and connect convolutions of the same lobes. The course of many of the long association paths is not yet well known, the descriptions commonly given being not alto- gether correct (H. Sachs). The occipital lobe is connected by long tracts to the temporal lobe, and perhaps slightly to the in- ferior i^arietal lobe (H. Sachs). The temporal lobes are con- nected only to the occipital. The frontal lobe is apparently connected with the parietal. Its connection with the temporal is denied (H, Sachs). All the lobes of the two halves of the brain are connected with each other by commissural tracts in the cor- pus callosum and anterior commissures. -^ ^ >r ^y^ Fig. 144. -Nerve Cells of Corpus Striatum with Processes Running into Internal Capsule. I will describe the projection fibres later. The corpora striata are composed of two parts- the caudate nucleus and lenticular nucleus. These two nuclei are separated dorsally by the white fibres forming the internal capsule. Below they are continuous. Their shape and relations are not easily appreciated except by actual inspection of specimens. They are indicated in the accompanying figures (148-150). The head o'f the caudate nucleus is connected with the grav matter of the anterior perforated space. The tail extends into the temporal lobe, where it is continuous with the gray matter of the cortex, called at this point the amygdalum, and with the claustrum. The lenticular nucleus is also continuous with the grav matter of the anterior perforated space. It is divided into three por- tions; the external is called the putamen, the two inner the globus pallidus. These.rparts are separated bv white fibres. The caudate nucleus, putamen, and probably all of the corpus striatum are modifications of the cerebral cortex. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 299 The corpus striatum has (1) fibres which pass to it horn the cortex, (2) fibres which pass through it from the frontal and parie- tal cortex, (3) fibres which originate in it, and (4) fibres connect- ing its different parts. 1. The fibres joining the ganghon to the cortex are few and merely associativ^e. 2. The fibres which pass through it pass chiefly into the dorsal part of the cerebral peduncles (or tegmentum) and are connected with the sensory tracts there. 3. Fibres which originate in the caudate nucleus and putamen collect together and join with the cortical fibres to form the Fig. 145. — Showing the Relations op the Optic Thalamus to Other Parts (Edinger). " lenticular loop " (ansa lenticularis). Some go to the subthal- amus (Luy's body) and optic thalamus; most go to the inferior olives and thence connect with the cerebellum. Some perhaps go to the posterior longitudinal bundle, which is a band of com- missural fibres that connect together the cranial nerve nuclei in the medulla. 4. Fibres connect the caudate nucleus and putamen with the globus pallidus. The corpora striata are relatively rudimentary ganglia in man. They contain sparsely distributed'^multipolar and fusiform cells, YsVo to 5^0 in. in diameter, the larger being in the lenticular nucleus. They are chiefiy of the sensory type (Marchi— Fig. 144). The Optic fJi al a mi.— The^e ganglia form the chief part of the 'tween-brain. They lie at the base of the brain, posterior and in- 300 DISEASES OF THE NERVOUS SYSTEM. ternal to the corpora striata. They are continuous with each other bv means of the middle gray commissure. The upper or dorsal surface forms part of the wall of the lateral ventricles ; the mesial surface forms the lateral wall of the third ventricle. Ex- ternally is The band of white fibres called the internal capsule; below this is a rather large mass, the red nucleus, external to a small grav nucleus called the subthalamic ganglion (Luy"s body). Around and below these is a complex network of fibres called the stratum intermedium. Below this, on the base of the brain, are the corpora mamillaria. The thalamus is composed of four niiclei —the anterior, lateral, and median or posterior. The last is called the pulvinar. Besides these there is on the median surface a small ganglion called the g. habenulse. The optic tracts wind around the posterior and outer edge of the thalamus ; and con- nected with these and the thalamus are two other ganglia, the Fig. 146.— Nerve Cells op Optic Thalamus (Marchi). external or lateral and internal or median geniculate bodies. Thus the thalamus is in close anatomical relations with five small ganglia; three below it — the corpus mamillare, red nucleus, and subthalamus ; two postero-external to it, the geniculate bodies. To these may be added the corpora quadrigemina. The thala- mus is composed of multijDolar nerve cells rather more numerous and larger than in the striatum, but not grouped closely together. Xerve fibres pass in among these cells, which are said (Marchi) to be of the motor type (Figs. 145, 146). The Corpora Quadrigemina.— The mid-brain contains as its chief ganglia the corpora quadrigemina.' These consist of four tu- bercles, two anterior and two posterior (Fig. 145). In man they are rudimentary in structure and relatively unimportant in func- tion. In man also the posterior tubercles are developed more rela- tively than in most lower animals. They together measure about 14 mm. {I in.) in sagittal direction. In front lies the pineal gland and third ventricle; beneath is the aqueduct of Sylvius and the ANATOMY AND PHYSIOLOGY OF THE BRAIN. 301 structures of the upper pons and cerebral peduncles. This inferior boundary is shown by the dotted line in the cut (Fig. 147). Micro- rotj Fig. 147.— Section Through the Corpora Quadrigemina (Q), Tegmentum (TG), AND Cerebral Peduncles. SS, Substantia nigra; Pp, peduncles; AS, aqueduct of Sylvius. scopically the anterior lobes consist of layers suggesting a cortical type (Spitzka) ; the outermost is made up of optic-tract fibres, the next is a thin layer of small nerve cells, then optic fibres again, Fig. 148.— Longitudinal Section, showing the lenticular {In) and caudate nuc/oi icn) separated by the internal capsule (ic). the corpus callosum ice), the anterior commissure iac), the optic tract (II.), the optic thalamus (fii), the corpora genicu- lata Cff), and the pulvinar (p), the crusta icr), the tegmentum (jLg), pons (P), and cerebellum (C); p, putamen ; gr, globus pallodus (G. Stewart). and deepest of all a layer containing a few large cells. The pos- terior lobes are more homogeneous and contain small multipolar cells and a ganglion. 302 DISEASES OF THE NERVOUS SYSTEM. The accompanying figures show the relationships of the basal ganglia and other parts. The Substantia JSigra.— Below the corpora quadrigemina and lying between the upper, sensory part {tegmentum) of the pedun- cles ^of the brain and the lower motor part (crusta) is the sub- stantia nigra. It contains large multipolar, angular, and fusiform cells deeply pigmented (Fig. 147). , . .. The Med Nucleus.— Dorsal to the s. nigra and at about its Fig. 149.— Horizontal Section, showing the frontal (F), temporo-sphenoidal (TS\ and occipital lobes (O), with their gray and white matter, the island of Reil (R), its gray and white substance, the claustrum (cO, the external capsule (ec), the lenticu- lar nucleus (hi), the caudate nucleus (oi), the internal capsule (ic), the optic thalamus QtJi), and pulvinar (p), the corpus callosum ice), the anterior and posterior commis- sures iac and pc), the lateral ventricle (LV), with the choroid plexus (ch) (G. Stewart). middle extent is the red nucleus. It is spherical or oblong, very vascular, and contains numerous sm^ll cells. The suhthalamus (Luy's body) lies more dorsally, but in about the same plane as the substantia nigra. It measures about i by i inch and contains a few cells and a very fine plexus of nerve fibres. The position and relation of these bodies are shown in Figs. 156-158. The nuclei of the pons varolii are irregularly distributed ANATOMY AND PHYSIOLOGY OF THE BRAIN. 303 masses of nerve cells lying deep among the longitudinal and transverse fibres. A special nucleus lying low down in the pons is known as the superior olive. In the after-brain or medulla we have the gray matter of the floor of the fourth ventricle and its cranial nerve nuclei, the olivary bodies, and certain small de- posits of gray matter called the nodal niuilei. The cerebellum in man consists of a median portion or vermis and two lateral hemispheres. It is connected to the cord and rest of the brain by anterior, middle, and posterior peduncles. It is composed of an external layer or cortex of gray matter, of white matter, and central ganglia. The gray matter lies in very close, narrow folds, producing with the white matter an appear- FiG. 150.— Section Through the Middle of the Basal Ganglia, Pr^central (AF) and Part op Post-Central (AP) Convolutions, and (TS) Temporal Lobe. It shows the corpus callosum (cc), the fornix (6), the fifth ventricle (v), lateral ventri- cles (LV), small part of thalamus (f/i), internal capsule (ic), caudate nucleus (en), lenticular nucleus {In), external capsule (ec), claustrum (ec) (6. Stewart). ance on section called the arbor mice. The vermis and hemi- spheres are divided by sulci into a number of lobes and lobules. The vermis is divided into superior and inferior portions. Its further subdivisions and those of the hemispheres are shown in the cuts (Figs. 151, 153). In the white matter of either hemisphere is a nucleus of small multipolar cells, the corpus dentatus or ciliary body. To the median side of this, and belonging structurally to it, is a small nucleus, the emboliform nucleus. In the inferior vermis is a collection of larger multipolar cells, the nucleus fastigium or tegmental nucleus; just to the outer side, between it and the emboliform nucleus, is a small collection of cells, resembling those of the ii. fastigii, called the nucleus globosus. The cortex of the cerebellum is divided from within out mto 304 DISEASES OF THE NERVOUS SYSTEM. a granular layer, a layer of large cells, and a molecular layer. The granular layer is coraposed of minute round cells and larger or Purkinje cells with processes. The cells are all of nervous character; possibly some belong to the neuroglia tissue. They :,.... J Fig. 151.— Showing the Lobes xkd Other Subdivisions of the Cerebellum. Dorsal Surface (Edinger). send up processes into the molecular layer, and some end in a network around the Purkinje cell. The large or Purkinje cells (20 X 30 ^) have very rich branching processes running up into the molecular layer as far as the periphery, where they turn down, and an axis-cylinder process running down into the white matter. The processes do not anastomose and the cells Fig. 152.— Cerebellum, Ventral Surface (Edinger). are not pigmented. The molecular layer contains large and small cells, some of which are multipolar, and send processes which end in a basket-work plexus around the Purkinje cells. Fibres coming in from the white matter appear to terminate also in end-brushes around these cells (Fig. 154— Cajal). The fibres of ANATOMY AND PHYSIOLOGY OF THE BRAIN. 305 the cortex are, as in the cerebrum, radiating and tangential. The tangential fibres are at the level of the Purkinje cells, among the processes of which they run. Just beneath the pia is a thin connective or neuroglia tissue membrane which sends radial fibres down through the gray matter, affording it a support. It will be seen that the general arrangement of the cerebellar cortex is analogous to that of the cerebrum. Associative and re- ceptive cells are found in the granular and molecular layers, and they send processes forming a rich network around Purkinje's cells which are efferent in function. The comparatively small number of the large cells is in harmony with the view that the cerebellum is an organ that receives and adjusts nerve impulses for co-ordinate distribution. All parts of the cerebellar cortex are anatomically alike. Fig. 153. Fig. 154. Fig. 153.— Section Through Middle of Vermis and Pons. Fig. 154.— Cerebellar Cortex of Embryo. D, Furkinje"s cell ; G, granule cell receiving a fibre and sending an end-brush or arborization to the P, Purkinje's cell (Cajal). The white matter of the cerebellum consists of nerve fibres some of which go to form the peduncles. Others form anterior and posterior commissures running through the two extremities of the vermis and connecting the hemispheres. There is also a longitudinal commissure in the vermis. The white matter around the corpus dentatum is called the fleece. Having described the general arrangement of the different divisions of the brain and the collections of gray matter found in them, we are prepared to study the tracts of white matter which connect the different parts. The white matter, as already shown, is made up of : ( Short. 1. Association fibres. < Long. ( Commissural. 2. Projection fibres. 306 DISEASES OF THE NERVOUS SYSTEM. 1. The association fibres of the cortex have been already de- scribed. Besides tiiese, there are association fibres connectin*^ different ganglia of lower levels. They are named . Yicq d'Azyr's bundle, the fasciculus retroflexus or Meynerfs bundle, the teg- mental bundle, the brachia of the corpora quadrigemina and the posterior commissure. These may be called ganglionic associa- tion tracts. Some of these will be described later and indicated in the figures. Commissural association fibres connect similar and symmetri- cal anatomical levels. They are the corpus callosum, the anterior Fig. 155.— Sections of Cortex of Same, but Older. A, Neuroglia layer ; B, zone of bipolar cells; C, molecular layer; D, granular layer; e,/,^. bipolar ceUs of molecular layer ; j, o, y, n, fibres from the white matter which end in end-brushes or arboriza- tions capping the cells of Purkinje ; h, Pm'kinje ceU with axis cylinder and collateral. and middle commissures, the fornix, and the anterior and pos- terior cerebellar commissures. 2. T\\e projection fibres £ive long tracts which connect higher with lower levels. Some of them have a long and some an inter- rupted course. The long projection fibres extend from the fron- tal and parietal cortex down into the spinal cord. They pass as a narrow band of fibres between the lenticular nucleus and the caudate nucleus, helping to form theintenial capsule; thence into the lower part of the cerebral peduncle, forming the crusta ; thence through the i:)ons and medulla. At the lower part of the medulla they form the anterior pyramids. About 90 per cent of the pyr- amids crosses over and passes down in the lateral columns as the crossed pyramidal tract ; the other ten are continued down in ANATOMY AND PHYSIOLOGY OF THE BRAIN. ;07 the anterior column as the direct pj^ramidal tract. Its fibres cross over in the anterior commissure. Both tracts connect with the cells of the anterior horns. The entire traject of fibres from the cortex cerebri to the anterior horns forms tlie voluntary motor tract. The interrupted projection fibres consist of the sensory tracts and the cerebro-pontine tracts. The sensory tracts starting from the brain cortex in part connect with the thalamus, in part pass directly through the posterior portion of the internal capsule, then through the upper part of the cerebral peduncles, forming there the tegmentum, and thence through the pons and medulla as the lemniscus and formatio reticularis. In the medulla some fibres cross over, forming a " sensory decussation," and end in the nuclei of the columns of Goll and i3urdach ; others run in the formatio reticularis, pass down in the posterior and lateral columns, cross ,\_^. Goll. C. Burdadv. ^^D C. Tract Fig, 156.— a, Connections of spinal cord with pons and medulla ; N, nodal nuclei; O, olivary body ; PN, pons nuclei ; L. lemniscus ; 3 to 12, cranial nuclei ; x, decussa- tion ; ST, Sensory tracts ; AFC, anterior fundamental colimins ; LFC, lateral fund, cols. : DC, direct cerebellar tract. over at various levels, and connect with cells of the posterior horns. The cerebro-pontine tracts are described under Fig. 158. Architecture of the Brahi.— The relations of the ganglionic deposits of the brain with the cord and with each other cannot be described in any brief way. But by the aid of the accom- panying diagrams the student can, afte/ some study of ordinary descriptive anatomy, get an idea of the architecture of these parts. It is best to begin from below with the spinal cord, and show first the relations of its different columns to the medulla and pons varolii. In Fig. 156 it will be seen that only the anterior and lateral fundamental columns of the cord are connected with the gray matter of the medulla and pons. The motor and sensory tracts pass through it uninterrupted. The antero-lateral fundamental columns connect with various deposits of gray matter in the me- dulla and pons which are called nodal nuclei. These in turn are connected with the cerebellum and pyramidal and sensory tracts- There is a long band of fibres in the medulla and pons called the 308 DISEASES OF THE NERVOUS SYSTEM. Dosterior lono-itudinal bundle. It is an analogue of the anterior fundamental column of the cord and connects the cranial nuclei. It is connected above with the basal ganglia. Flo- 157 shows the relations of the spinal cord to the cerebruni and c^rebelhim. The pvramidal tracts, having mostly crossed m the lower medulla, go straight up through the internal capsule lo the motor area of the cortex. Fig. 157.— Connections op Spinal Cord with Cerebrum and Cerebellum. Motor tracts go straight to cerebral cortex. Posterc-iuternal and part of postero- external I, sensory) tracts go to their nuclei, then to the cei-ebellum in part, to optic thalamus vand corpora quadrigemina ?) and lenticular nucleus and cerebral cortex. The antero-lateral ascending tracts go i-iaformatio reticularis to optic thalamus and cortex. The direct cerebellar tract to vermis and then rut anterior cerebral peduncle to opposite red nucleus and thalamus. The anterior fundamental and lateral funda- mental columns to pons and nodal nuclei and to cerebellum ANATOMY AND PHYSIOLOGY OF THE BRAIN. 309 The sensory tracts cross in part, while part have crossed al- ready in the cord. They ^o up, forming the inter-ohvary tract, then the lemniscus or fillet. In part then they enter the dorsal portion or tegmentum of the cerebral peduncle, pass through the posterior part of the internal capsule to the motor area of the cortex and parietal lobe. Some fibres enter first the basal ganglia. The cord is connected with the cerebellum by the direct cere- bellar tracts, the posterior columns, and antero-lateral funda- mental columns. All these columns carry afferent impulses ex- cept those of the antero-lateral tracts, which are made up of asso- ciative fibres. Fig. 158.— Connections of Medulla-Pons- Cerebellum with Higher Parts. Nuclei of columns of Goll and Burdach with optic thalamus, lenticular nuclei, and cerebral cortex. Olivary body, with lenticular nuclei and cortex. Pons nuclei with frontal and occipito-temporal cortex. Cei-ebellum, via middle peduncles, to pons nuclei and so to cerebrum. Cerebellum, via anterior cerebral peduncles, to red nucleus, optic thalamus (and corpora striata and brain cortex?), acusticus and tri- geminus, posterior corpora quadrigemina. In general, the spinal cord is connected with the vermis atid fibres surrounding the dentate nuclei, the pons and medulla are connected with the cortex cerebelli and vermis, while the ante- rior peduncles arise chiefly from the dentate nucleus. (Marchi gives other relations.) The connections of the pons, medulla, and cerebellum are shown in Fig. 158. The olivarv bodv is connected with the cerebellum on the one hand and to 'the lenticular nucleus and cortex on the other. It is not connected with the cord. Impulses pass from the cerebellum to the olives, thence up to the bram. JNuclei in the pons are connected with the cortex of the cerebellum ana with fibres running in the ventral part of the cerebral peduncle 310 DISEASES OF THE NERVOUS SYSTEM. on either side of the pyramidal tract, to the frontal and temporal and probably occipital lobes, and island of Reil. The nuclei of the acoustic, glosso-pharyngeal, and vagus, perhaps other sensory nerves, are connected with the cerebellum by a ** direct sensory tract ''which goes to the nuclei of the cerebellum. The nodal nuclei are connected, as has been stated, with the cerebellum. Fig. 159 shows the relations of the optic thalamus and cor- pora quadrigemina to other parts. The corpora quadrigemina, by the posterior tuV^ercles, are connected to the cerebellum and 8.coustic nerve, internal geniculate body and temporal lobes; bv the anterior tubercles to the lemniscus and spinal cord, the Fig. 159.— Relations of Corpora Quadrigemina and Optic Thalamus to Other Parts. OT, Optic thalamus ; CQ, corpora quadrigemina ; KN, red nucleus : S. Luys body, or subthalamus ; SN, substantia nigra ; ON, optic nerve ; AX, acoustic nerve; L, lemniscus; SO, superior olive. optic nerve and optic thalamus, external geniculate body and occipital lobes. The thalamus is connected to the spinal cord by the lemniscus, to the medulla and cranial nerves by the posterior commissure, to the optic nerve and external geniculate body, to the cortex of the frontal, parietal, occipital, and temporal lobes, to the corpora mamillaria and fornix, and to the subthalamus and lenticular nucleus. All its connections cannot be shown or described; but it is the most richly connected ganglion of the brain. Fig. IGO shows the relations of the corpus striatum to the other parts. It is connected with the spinal cord by the lemniscus(?), with the red nucleus, subthalamus and thalamus, with the substantia ANATOMY AND PHYSIOLOGY OF THE BRAIN. ;ii nigra, pons nuclei, and olives. Its connections with the brain cortex are slight and those with the motor tract doubtful. The corpus striatum seems to. have its closest relations with the cere- bellum, partly through the red nucleus, partly through the nuclei of the pons. The Membranes- of the JB rain. —The membranes of the brain are the dura mater, the arachnoid, and pia mater. The dura mater lines the inner surface of the skull. It is attached loosely to the concavity, but closely to the base. It splits into two layers to form the venous sinuses of the skull. The inner of the two layers at certain points projects inward to form membranous V7WM>W^W^^, Fig. 160.— Relations op the Corpus Striatum to Other Parts. septa. These are known as the great longitudinal or cerebral falx, the lesser longitudinal or cerebeUar falx, and the tentorium. Hence both venous sinuses and membranous septa are formed out of the inner layer. The outer layer forms the periosteum of the bone. The dura mater is supplied with sensory nerves chiefly by the trigeminus, but posteriorly by the vagus. The blood sup- ply will be described later. The arachnoid is a thin, transparent, fibrous, non- vascular membrane lying between the pia and dura and continuous with the spinal arachnoid. It bridges over the fissures and the de- pressions at the base of the brain and forms between the pia and itself certain lacunae or spaces. These are the central lacuna found at the beginning of the fissure of Sylvius, the callosal and those of the transverse fissures, and of the lateral aspect of the 312 DISEASES OF THE NERVOUS SYSTEM. l^ons varolii. The space betAveen the dura and arachnoid is called the subdural or arachnoid cavity. It is lined Avith epithe- lium and resembles other serous cavities. The inner surface of the arachnoid is connected with the pia by numerous delicate fibrous x>rocesses. The space between these membranes is called the siiharachnoid spcwe. It counnunicates with the subdural space by means of the foramen of Mag-endie, which lies in the part of the arachnoid that passes over the pons and medulla, closing in the fourth ventricle. The subdural and subarachnoid spaces contain a serous fluid. The normal amount ranges from two drachms to two ounces, it being greater in old people. The arachnoid contains no nerves or blood- vessels. It is described by some as a part of the pia mater. The pia mater lies beneath the arachnoid and is closely applied to the brain in all its folds. It is continuous Avith the spinal pia. It is very vascular and supplies the whole periphery and part of the interior of tlie brain with blood. It consists of two layers : an outer holding the larger vessels, and an inner delicate layer closely associated with the superficial neuroglia of the brain. The pia mater folds upon itself and passes through the trans- verse fissure into the third and lateral ventricles of the brain. These vascular folds form the velum interpositum. which gives off a choroid plexus to the lateral and third ventricles. Another fold, the inferior choroid plexus, is given off to the fourth ventri- cle. The pia mater has vasomotor, but no sensory nerves. Functions of the Brain JLemhrane. — The dura mater, by its outer layer, acts as a perioste"um ; by its inner layer as a lymph sac. It is also, by virtue of its sensitiveness, a protection against injury and disease. The arachnoid forms the inner wall of the lymph sac. The pia mater is a vascular and nutritive organ. It is, however, also closely connected with the lymphatic system of the arachnoid. The Ijlood supply and lymph supply of the brain vary in amount. In congestion the lymph can pass into the spinal canal or be rapidly taken up by the absorbents. In anaemia there may be compensatory increase of lymph. This fluid in dis- ease may accumulate in the arachnoid sac, the subarachnoid space, or the ventricles, these spaces being all in communication with each other. The Blood Supply of the Braix axd its Membraxes. —The vascular supply of the scalp, skull, and dura mater comes from the external carotids; that of the eye, brain, and pia mater from tlie internal carotids and vertebrals. The arrangement is shown here: f Occipital, inferior meningeal, arteries. Posterior auricular. ^ { Ptjsterior. Ascending pharyngeal, posterior meningeal. Internal maxillary, middle meningeal, small t meningeal, f Anterior meningeal. *^ I Posterior communicating. [Anterior choroid. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 313 Vertebral and f \ Posterior meningeal. I Inferior cerebellar. • 1 • «? -^ Anterior cerebellar, basilar give off ] superior cerebellar. [^ Posterior cerebral. The general arrangement and distribution of the arteries of the scalp and dura is shown in the accompanying diagram (Fig. 161). Fig. 161.— Showing the Blood Supply of the Scalp and that of the Dura Mater by the Middle Meningeal. The Mood supjDly of the meninges comes from the anterior middle and posterior meningeal arteries. These all come, except the small anterior meningeal branches and a small posterior branch, from the external carotid. The blood passes into the diploic veins, and from there passes chiefly into the lower occipi- tal and lateral sinuses. Some of it, however, returns in the vena? comites. It all returns down toward the base of the skull, ihe most important of the arteries is the middle meningeal, botii on account of its size and its distribution above important func- tional areas. The blood supply to the pia mater and brain substance comes 3U DISEASES OF THE NERVOUS SYSTEM. from the internal carotid and the vertebral arteries. The branches of the former artery give off the anterior and middle cerebral, the posterior communicating:, and anterior choroid. The vertebral arteries give off the inferior cerebellar, while the basilar branch of the vertebrals gives off the transverse, anterior cerebellar, superior cerebellar, and posterior cerebral arteries i 1 — It Fig. 1G2.— Showing the Arteries at the Base of the Brain. Ou the right side the brain is cut away, showing the cerebral arteries and the course of the pos- terior cerebral. The cerebral arteries, anterior, middle, and posterior, are the three largest and most important. By their anastomoses the circle of Willis is formed. From the circle of Willis and the begmnings of the three arteries mentioned, several groups of vessels, six m all, are given oft". They enter the base of the brain ANATOMY AND PHYSIOLOGY OF THE BRAIN. 315 and supply the great basal ganglia and adjacent white matter. They are called the central arteries, and they are the vessels usually affected in cerebral hemorrhages of adult life. They do not anastomose with each other. The cortical arteries are the terminal branches of the great cerebral arteries. They anasto- mose with each other but slightly. They are distributed very widely and carry much more blood than the central groups. Their distribution is shown in Fig. 163. The cortical arteries are distributed in the pia, and from there they pass in two sets, a superficial and a deep, into the gray matter, and for a short distance into the white matter. They pass straight in at right angles to the surface. They have richly arborescent branches which do not anastomose ; consequently a knife plunged straight into the brain does not cut many vessels. The cortical arteries Fig. 163.— Showing the Distribution of the Artery of the Sylvian Fissure, A Prolongation of the Middle Cerebral. The area iii front of the shaded part is supplied by the anterior cerebral, that behind by the posterior cerebral. probably anastomose somewhat with each other, though not very freely. There is slight if any anastomosis between the cortical and central arteries. The pressure is thought to be less in the vessels of the gray matter. The capillaries are surrounded by spaces called perivascular spaces which serve as lymj)hatic channels. The neuroglia cells send processes which connect with or form passages to the vessel walls (Fig. 164). The blood of the convex and mesial cerebral surface, flowing up from the base, leaves the capillaries and enters veins. Thence it still passes upward, and for the most part enters the longitu- dinal sinus. The most of the vessels enter the posterior portion of the sinus and in a direction forward and upward, i.e., agamst the current in the sinus. The course of the blood current is, therefore, opposed both to gravitation and to the venous flow. 316 DISEASES OF THE NERVOUS SYSTEM. The veins of the cerebrum are : 1, the superficial cerebral ; 2. the deep cerebral veins; and, 3, the cerebral sinuses. The superficial cerebral veins areven?e comites. Those on the convex and mesial surfaces empty chiefly into the superior longitudinal sinus, as described ; those on the basal surface empty into the cavernous and lateral sinuses. These veins have no valves, and their walls are very thin and without muscular fil^res. The deep cerebral veins, or venae (ialeni. receive the blood from the lateral ventricles and from some of the central arteries supplying the basal ganglia. They empty into the straight sinus. The cerebral sinuses are fifteen in number. The importailt ones are the superior and inferior longitudinal, the straight, the lateral, the occipital, the cavernous, and the superior and inferior Fig. 164.— Showing the Nei-roglia Cells of the Brain, their Relation to the Blood-Vessels : also the Sustentacular Processes of the Epithelial Cells OF THE Lateral Ventricle (3Iarchi). A, Epithelial cells lining lateral ventricle ; «, process of same ; 6, spider or neuroglia cell ; c. blood-vessel. petrosal. They carry blood for the most part in a direction from before backward, and convey it eventually to the internal jugular. Most of the blood of the convexity and mesial surface must pass into the longitudinal sinus, but there is a slight connection of some of the veins with the superior ipetrosal and straight si- nuses. The superior longitudinal sinus also communicates slightly with veins of the scalp and with the facial vein. Some of the blood from the mesial surface also goes to the veins of Gralen. On the whole, however, the system of the convex and mesial cerebral surface is a close corporation, the blood having to pass into the superior longitudinal sinus and torcular Herophili, where it meets that of the straight and occipital sinuses, and flows for- ward through the lateral sinuses to the internal jugular. The circulation of the basal surface is less isolated. All the basal si- nuses communicate with each other freely, and there are slight ANATOMY AND PHYSIOLOGY OF THE BRAIN. 317 communications between the veins of the scalp and the cavernous, lateral, and inferior petrosal sinuses. It is safe to tie anv of the sinuses, except the lateral and the posterior part of the longitu- dinal. The cerebellar veins, superior, inferior, and lateral, empty into the straight, the lateral, and superior petrosal sinuses. None of the cerebral veins or sinuses have valves. The pressure in the internal carotid arteries is about 150 mm., that in the cerebral sinuses TO to 80 mm. (Grerhardt), and that in the jugular veins is almost negative. Both arteries and veins are more delicate than the extra-cerebral vessels. Except its gray matter, the brain is not a very vascular organ, but this gray tissue ranks in richness of blood supply with the lungs and liver. The amount of blood in the brain at any one time is only about one to two per cent of the total blood in the circulation, or about four ounces (Ranke). The diameter of the common carotids is 6.7 mm. (Thorne), that of the subclavians 6.2 mm., that of the internal carotids 4 mm., and that of the vertebrals 3.5 mm. (Gerhardt).* The blood to the brain, therefore, has passages three-fifths as great as the total arterial area near the heart, and the blood enters these passages at a pressure (250 to 150) three-fifths as great as that in the ves- sels near the heart. The Functions of the Brain— Cerebral Localization. — The brain is the seat of conscious intelligence and mental activ- ity. It has also control and direction of voluntary movements, it is the seat of instinctive acts, and it regulates in a measure the vasomotor, trophic, and secretory mechanisms of the body. The Pra'frontal Lohes. — The prefrontal lobes, or that part of the brain in front of the prsecentral convolution, are concerned with volition and the j^ower of self-control, concentration of thought and attention. The posterior i3art contains centres for the movements of the head and eyes. Injuries in this part of the brain produce changes of character, indicated by peevishness and irritability of temper, mental enfeeblement, lack of power to con- centrate the mind or to control the acts or emotions. The Central Convolutions, Paracentral and Upper Parietal Lobules. — This part of the brain is called fhemotor area, because it is concerned in the production of nervous impulses which cause voluntary motions of the body. Certain parts of this area are in relation with certain groups of voluntary muscles on the oppo- site side of the body. These areas preside not so much over sin- gle muscles as over those groups of muscles which act together in producing definite purposeful acts. The lower part of the central convolutions, known as the central operculum, is a centre for movements of the larynx, mouth, tongue, and face. Above this area and about the middle third of the central convolutions is the centre for the movements of the shoulder, arm, hand, and fingers. Still farther up, near the longitudinal fissure, and extend- * J. Crichton Brown gives the last two diameters 2.8 and 2.2 mm. respectively. 318 DISEASES OF THE NERVOUS SYSTEM. ing over into the mesial surface and back into the superior parie- tal lobule, is the area for the trunk, hips, legs, feet, and toes. The base of the first and second frontal convolutions is the centre for movements of the head and eyes. The exact arrangement of these centres, which have been determined by experiments upon monkeys and other lower animals as well as by chnical and sur- gical observations on man, is shown in the accompanying dia- grams. Probably the motor area is also the centre for the cuta- neous sensations of the parts corresponding to the muscular groups which it supplies, so that what is called the motor is really a sensori-motor area. The motor area, when irritated by disease, Fig. 1C5.— The Cortical Centres. l^roduces paraesthesiae and convulsive movements in the groups of muscles which it represents. Destruction of it causes not only a i^aralysis, but a certain amount of cutaneous anaesthesia. The various sensori-motor centres are not sharply limited, but lap one over the other, so that the motor area for the forearm, for example, extends over somewhat into that for the shoulder. The corresponding sensory areas are still more diffuse, so that it takes a much more extensive destruction of a certain area of the motor cortex to produce an anaesthesia of the arm than it does to produce a paralysis of the arm (Figs. 165, 166). Bilateral Representation. — Those muscles of the two sides of the body which act together have a double representation in the brain. For example, each group of muscles used in inspiration ANATOMY AND PHYSIOLOGY OF THE BRAIN. 319 has a centre in both hemispheres; consequently, when one centre is destroyed no paralysis results, for the reason that the other centre continues its work. In the same way some of the muscles of the face, such as those for closing tiie eyes, have a double rep- resentation, and a lesion destroying the centre for the orbicularis IDalpebrarum on one side will not usually cause paralysis, because of the continued action of the centre of the other side. The more perfect and habitual the associated action of the muscles of the two sides of the body, the more completely can one centre do the work of its associate. The best examples of the mus- cles having the double representation are the orbicularis palpe- brarum, the muscles of the vocal cords, the muscles concerned in Fig. 1G6.— The Cortical Centres. deglutition and in respiration. The muscles of the viscera and blood-vessels have no known representation in the cortex of the human brain. The special sensations have a bilateral representation also; but the more specialized the sense, the less can one hemisphere take the place of the other. Occipital Parietal, and Temporal Lobes— Centres of Special Sense.— The special senses have two centres— the primary and the secondary. The primary centres are connected with the ganglia at the base of the brain ; the secondary centres are situated in the cortex. The primary centre' for vision is in the posterior part of the optic thalamus, the external geniculate body, and anterior cor- pora quadrigemina. The secondary centre is situated in the occipital lobe, and particularly upon its mesial surface and in that part known as the cuneus. Each occipital lobe is the centre 320 DISEASES OF THE NERVOUS SYSTEM. for visual impulses from the corresponding half of the retina of each eye; for example, the left occipital lobe is the centre for vision of the left half of the retina of each eye. This relation is shown in the diagram (see Optic ^'erve). Total destruction of both occipital lobes, or even of a considerable part of them if the de- struction involves the median surface, will cause blindness. De- struction of one lobe causes only half-blindness or hemianopsia. T\\e primary centre for hearing is in the posterior tubercle of the corpora quadrigemina and the internal geniculate body. The secondary centre is in the cortex of the first and second convo- lutions of the temporal lobe. Destruction of one temporal lobe causes deafness in the opposite ear. This deafness, however, is not complete because the sense of hearing has a bilateral repre- sentation ; each ear, in other words, sends fibres to the temporal lobes of each side, although more fibres cross over than go to the lobe of the corresponding side. The consequence is that the loss of one temporal lobe is in a measure supplied by the other {vide Aphasia). The primary centre for smell is in the olfactory lobes. The secondary centre is probably in the uncus and in part of the hippocamrjal convolution. Whether the tracts for the sense of smell are connected with the. optic thalamus or other ganglia is not definitely known. The primary centre for taste is not known, but sensations of taste may connect with the optic thalamus before passing into the secondary centre, which is in the hippocampal convolution. Centres for Jlemories. — There are certain classes of sensations and perceptions, simple in character and frequently repeated, so that they finally get to be used almost automatically in their work. These impressions relate to the use of the muscles in speech, in writing, and in gesture language, also to other fre- quently repeated purposeful movements of the limbs. The mus- cular movements in writing and speaking are so often repeated that certain areas in the cortex are set apart for the memories of these processes. The visual sensations and ideas elaborated from them, which are frequently repeated in learning to read, have also a centre Avhich is set apart for them. This forms a centre for the visual memories of language. In the same way there are audi- tory sensations and ideas elaborated and so frequently repeated as to be used automatically in acquiring language. These are stored up as auditory memories. We have what may be called motor memories connected with speech and gesture. These spe- cial memories have been found to have a certain localization in the brain. The centre for the memories of the articular move- ments of speech is in the posterior part of the third left frontal convolution ; the centre for the memories of the movements of ANATOMY AND PHYSIOLOGY OF THE BRAIN. 321 writing is not perfectly well known, but is thought to be at the posterior i^art of the second left frontal convolution. The centre for the memories of gesture language is unknown. The centre for the memories of ordinary co-ordinate movements is perhaps in the inferior parietal lobule. The centre for the visual mem- ories of written language is in the angular gyrus, extending back- ward from there into the occipital lobe. The centre for the audi- tory memories of spoken language is in the posterior part of the first and the corresponding upper part of the second temporal convolution. In right-handed people all the memory centres are in the left cerebral hemisphere ; in left-handed people they are in the right hemisphere. The destruction of these memory centres produces different forms of aphasia, as will be described later. In addition to that, disturbances in these centres are produced by lesions which cut off the associating fibres connecting these centres with each other or with motor or sensory centres proper. The Centrum Ovale, Corpus Callosum, and the Associative Functions of the Brain. — The different parts and centres of the brain are connected together by the associating tracts and with lower lev^els by the projection fibres. The simpler and less devel- oped centres of the two halves of the brain are closely connected by fibres that run chiefly in the corpus callosum. The more highly specialized and less simple in function a centre, the less close is its coumiissural connection and the more independent is one-half of the brain from the other. Thus the centres for the movements of the thorax in respiration are closely bound with each other ; those for the purposeful movements of the hands less so ; those for receiving visual impressions are almost independent ; and the centres for the memories, which are still more highly specialized, are practically entirely independent. We infer that the higher mental functions, therefore, work either in one cere- bral hemisphere or in the other, and that the two halves of the brain do not co-operate with each other in much of the higher intellectual work. The corpus callosum is the great commissural tract connect- ing the two cerebral hemispheres and their respective centres. The anterior commissure does some of the same work, being more specially connected with the function of olfaction. The posterior commissure has comparatively few bilateral connecting fibres, its function being more to connect the thalamus with the cranial nerve nuclei and other centres below. The Corpus Striatum.— This ganglion is in close relation with the cerebellum and with nuclei in the pons. It is also in connec- tion with fibres that come up from the muscle-sense tract, in the spinal cord. Its functions are therefore probably connected with securing co-ordinate and purposeful movements. Destruc- 322 DISEASES OF THE NERVOUS SYSTEM. tion, however, of this ganghon in the human brain produces no definite symptoms, and local lesions of it cannot be diagnosti- cated. It is therefore called clinically a latent region. The Thalamus Opticus. — The thalamus is in relation by its projection fibres Avith the frontal, parietal, occipital, and tem- poral cortex. The fibres that go to the occipital cortex are con- nected with the optic tract, and have to do with the function of vision. The fibres that go to the temporal lobe are connected with the auditory tract, and have to do with the function of hear- ing. The optic thalami seem to have some relation to the ex- pression of emotions. In cerebral paralyses in which they are involved, the patient cannot involuntarily express joy, grief, etc. Lesions of the posterior jDart of the thalamus will produce par- tial blindness. Other than this, lesions of the optic thalamus produce no definite symptoms which enable us to make a local diagnosis. Disturbances of hearing have not certainly been traced to lesions in the thalamus. It is thought to be a primary centre for sensations of touch, muscular sense, and perhaps for smell and taste, but no definite facts in human pathology have as yet satisfactorily proved this. Lesions of the thalamus sonie- times produce various forms of mobile spasm, but these are gen- erally attributed to irritation of the fibres of the internal capsule, which go close to it. Hence, aside from disturbances of vision, the optic thalamus also must be considered clinically a latent region. The Corpora Quadrigemina. — The anterior tubercles of the corpora quadrigemina, together with the external geniculate bodies, form part of the primary centres of vision. The anterior tubercles, however, have more to do with reflex movements of the pupil and ciliary muscles than with the actual visual func- tion. The posterior tubercles of the corpora quadrigemina and the internal geniculate body are thought to be connected with the auditory nerve. They also appear to receive some fibres from the cerebellum ; hence their injury or disease j^roduces some dis- turbances in equilibrium and possibly in hearing. Owing to the fact that the nuclei of the third nerves and the red nuclei lie be- neath the corpora quadrigemina, lesions of these latter produce irritations and paralyses of the third nerve, disturbances in equi- librium and forced movements. Lesions in this neighborhood sometimes cause somnolent and stuporous states. The red iniclei are comiected with the anterior cerebellar peduncles on the one hand and with the lenticular nucleus and optic thalamus on the other, and are concerned in securing equi- librium and the adjustment of the body in space. The Cerehellum. — The cerebellum is connected with the pons, the cerebrum, and sjDinal cord. It sends impulses through the ANATOMY AND PHYSIOLOGY OF THE BRAIN. 323 middle peduncles to the gray matter in the pons, and thence down into the antero-lateral columns of the cord. It sends im- pulses to the olivary bodies, and thence up to the great ganglia at the base of the brain, and finally it sends impulses through the anterior peduncles, which cross over, enter the red nuclei, and connect with the thalamus, corpora striata, and perhaps with the cortex of the parietal lobe. It receives impulses from the cortex of the frontal, parietal, occipital, and temporal lobes, which go down into the pons, connect with nuclei there, and thence pass up into its hemispheres. It also receives impulses from the spinal cord, through the posterior peduncles. There is therefore a nervous circuit between the cerebrum, brain axis, and cere- bellum : impulses pass down from the cerebral cortex to the pons, thence to the cerebellum ; and other impulses pass up from the basal cord to the cerebellum. Having received these impulses, it discharges chiefly along the anterior peduncles into the ba- sal ganglia, which act as its end- organ (Fig. 167). The cerebel- lar influences directly affect the spinal cord but little. The cere- bellum has undoubtedly power of securing purposeful move- ments and of enabling us to keep our equilibrium and maintain our relations in space. The v^ermis or median lobe is the part which in man is most important in doing this work. Lesions of the lateral lobes or hemispheres produce few direct symptoms, and they are called latent regions. Injuries of the median lobe, however, produce disturbances in equilibrium, forced movements, and a jDeculiar form of inco-ordination in gait which is known as cerebellar ataxia. Lesions of the middle peduncles produce forced movements also, the forced movements being either to\vard or aAvay from the side of the lesion, accord- ing as it is an irritating one or a destructive one. The pons varolii contains some of the cranial nerve nuclei and collections of nerve cells which are connected with fibres from the cerebral cortex on the one hand and the cerebellum on the other. It also contains the long tracts of nerve fibres that pass from the cerebrum down through into the medulla and spinal cord and transverse tracts of fibres which connect the two hemi- spheres of the cerebellum. Lesions in it cause disturbances in Fig. 167.— Showing the Relations of THE Cerebellum to its End-Organs, the Basal Ganglia, and to Other Parts. 324 DISEASES OF THE NERVOUS SYSTEM. function of the cranial nerves and of the motor, sensory, and commissural tracts. The medulla oblongata contains centres of the cranial nerve puclei, and in it also are various reflex and automatic centres con- trolling and regulating the vasomotor system, respiratory and cardiac rhythm, visceral movements and secretion. The olixary bodies are connected with the cerebellum and basal ganglia, but not Avith the spinal cord. Imj^ulses pass to these bodies from the cerebellum, thence up to the brain. When injured, disturbances of equilibrium and co-ordination occur. The Latent Regions of the Brain.— There are certain parts of the cerebral cortex destruction of which and irritation of which produce no special and distinctive phenomena in man. These are the greater part of the temporal lobe of the right side and a portion of the temporal lobe on the left side. A part of the in- ferior parietal lobule also may be regarded as a latent region. The frontal lobe we have already spoken of as being concerned with certain mental functions, but lesions here often i3roduce no symptoms, and they may be to a certain extent regarded as latent. The corpora striata, optic thalami, portions of the cen- trum ovale, and the two lateral hemispheres of the cerebellum are latent areas. Brain Weight. — The average weight of the male brain is 1,358 gm. ; that of the female, 1,235 gm. The weight varies with age, sex, race, and intelligence, and with a number of other factors. The average weight of the brain at birth is 327.8 gm. ; the brain grows raf)idly until the age of four, then more slowly until the age of seven, then very slowly up to the age of sixteen to twenty. At about the age of forty-five in man and fifty in woman it begins to lose weight slowly, and at the age of eighty or over it has lost about 120 gm. (4 oz.). The brain of man weighs absolutely about nine per cent more than that of woman. Relatively to the body weight, the brain weight of man is about 2fc ; that of woman a very little less. The sexual difference is extremely small.* The brain weighs more in the civilized races, and more in cer- tain of the civilized races than others; the brains of English, Ger- man, and Scotch weigh more than those of French, Italian, and Russian. Some of the African and Australian tribes have the smallest brains, the average negro brain weighing 1 ,250 gm. When a brain weighs less than 1,130 gm. in man or 990 gm. in Avoman, it is called a microcephalic brain; if the weight is above 1.490 gm. in man or 1,345 gm. in woman, it is called a megalocephalic brain. Brain weight has a certain relation to intelligence, which is not, however, an absolute one. Among a hundred men of more than average intelligence, the percentage of large brains Avould be about 25, whereas the percentage of large brains among persons of ordinary or low intelligence would be not more than 4 or 5. In estimating the importance of brain weight, one must consider the height, the weight or volume of body, muscular mass, and * J. C. Brown finds that after making all allowances, woman's brain weighs about one ounce less than man's. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 325 superficial area; these are called the somatic factors. The fol- lowing formula has been devised by Snell for estimating the mental power of different animals: In this formula P represents the psychical factor or the amount of intelligence, H the brain weight, K the body weight, S the somatic factor. The somatic factor has been estimated to be for mammals about 0.666. Applying this formula, we find that, ex- pressed relatively, the intelligence of man equals 0.87; woman, 0.86; the ape, 0.42; the rabbit, 0.59; the birds, from 0.167 to 0.09. The relative weight of different parts of the brain is about as follows: Frontal lobes, 28^/; parietal lobes, 36^; occipital, 10,'^; temporal, 13$:^; lobus caudicis or island of Eeil, 9,^; pons, 1^%. The cerebellum weighs about one-eighth as much as the cere- brum. The proportion of the gray to the white matter in adults is 60 to 40 (Vierordt). The depth of the primary fissures is not quite an inch (20 to 23 mm.). There are one thousand two hundred to two thousand million cells in the cerebrum, and about ten million large cells in the cerebellum (Meynert). About one million cells to a square centimetre is the estimate of Engel. Preserving and Cutting the Brain. The brain should be placed in a gallon of a 2i-per-cent solu- tion of bichromate of potash. This must be changed daily for a week, then twice weekly for a fortnight ; then it should remain in the solution for three or four months, a few crystals of thymol being added. After about three months place the brain in 95^ alcohol. In a few days it will be ready for cutting. In cutting the fresh or preserved brain for the purpose of lo- cating gross lesions, remove the pons, medulla, and cerebellum, place the brain on its base, and make sections in accordance with the directions (Fig. 168). The sectional views exposed are shown in the following series of cuts, which are based upon those of Exner. 326 DISEASES OF THE NERVOUS SYSTEM. ABC D B F a Fig. 168.— Showing the Points at which the Sections are Made, a, 6, Hori- zontal line from base of frontal to base of occipital lobe ; A, vertical section through middle of third frontal convolution : B, through operculum, o ,' C, through superior praecentral and lower end of Rolandic fissures ; D, through re and posterior end of Sylvian fissure ; E, through angular gyrus and anterior occipital fissure ; F. through parieto-occipital fissure. B should be about half-way between A and C ; E half-way between D and F. (See Figs. 169-174.) Fig. 169.— Section Through Line A, Fig. 168. ANATOMY AND PHYSIOLOGY OF THE BRAIN. 327 Fig. 170.— Section Through Line B, Fig. 168. Fig. 171.— Section Through Line C, Fig. 168. 328 DISEASES OF THE NERVOUS SYSTEM. D Fig. 17:2.— Section Through Line D. Fig. 168. E Fig. 173.— Section Throvgh Line E, Fig. 168. F Fig. 174.— Section Through Line F. Fig. 168. CHAPTER XYII. DISEASES OF THE BRAIN AND ITS MEMBRANES. GrENERAL SYMPTOMS. It Tvill add to the intelligibility of descriptions of brain dis- eases and their symptoms if one first makes himself familiar with certain general symptoms that underlie more or less nearly all organic disorders of this organ. Symptoms due to disease of the brain may be placed in four classes : first, general symptoms of brain irritation; second, general symi^toms of brain pressure; third, symptoms of focal irritation or destruction ; and, last, those due directly to the pathological process itself. The symptoms of brain irritation are headache, vertigo, vom- iting, photophobia, mental irritability, insomnia, jDeculiar feel- ings of fulness and pressure about the head, noises in the ears or in the head, tenderness about the scalp, and in severe cases con- vulsive symptoms and delirium. The symptoms of brain com^^ression are headache, vomiting, mental hebetude or dulness, perhaps some form of paralysis, con- tracted pupils, and eventually coma. AVith this there is often constipation and retracted abdomen. The symptoms of brain irritation are often, perhaps usually, associated with a hypersemia. The symptoms of brain compres- sion may be associated with anaemia or oedema, and often in states of malnutrition, where the brain is impoverished, the symptoms resemble much those of compression. Pressure symptoms and irritative symptoms often lap one into the other, and they cannot always be sharply distinguished. Focal symptoms depend almost entirely upon the location of the particular lesion. If it is in a motor area, focal symptoms of irritation Avould be spasmodic phenomena, such as convulsions. If the lesion were destructive, the symptoms would be those of paralysis or anaesthesia. The symptoms due directly to the pathological process itself may be very slight. Thus in case of a tumor of the brain, the symptoms are mainly caused by pressure, irritation, and local disturbance of certain special parts of the brain. In suppuration, however, the process itself may produce general symptoms such 030 DISEASES '3F THE NERVOUS SYSTEM. as are associated usually with sepsis — chills, irregular fever, men- tal hebetude, jDrostration, emaciation, and sweats. Among the symptoms pjrodueed by focal lesions there are a few which deserve some preliminai-y general study because they may be caused by lesions of very different kinds and occur conse- quently in very different forms of diseases. Those symptoms which we wish particulai'ly to study here are hemi^Dlegia and aphasia. These represent the tAvo gi-eat dominating symptoms pertaining on the one hand to motor disturbance and on the other hand to sensori-motor disturbance. Hemiplegia. — Hemiplegia is a paralysis of one-half of the body, involving the side opposite the lesion. The face, arm, and leg are usually all paralyzed; the arm most, the leg next, the face least. Hemiplegia may be either acute in onset or slow and progres- sive. Acute hemiplegia is the result usually of hemorrhages and -oftenings of the brain, more rarely of inflammations and inju- ries. Progressive hemiplegia begins gradually, as its name im- phes, and slowly increases until the height of the disease is reached. It is usually caused by tumors growing in one side of the brain, but it may be caused by a slowly developing patch of sclerosis, which sclerosis may be in turn only a part of a multiple sclerosLS. Further description of the peculiarities of hemiplegia will be given under the head of Special Diseases of the Brain. Aphasia. — Aphasia is a disease of the faculty of language ; and it has a number of varieties, in accordance with the joarticular part of the brain involved and the particular portion of the mechanism of this faculty that is destroyed. By the faculty of language we include the processes by which we hear, see, and at the .same time appreciate the meaning of s\Tnbols. It includes also the faculty of expressing to others, by voice, writing, or ges- ture, our ideas. It has therefore a receptive side and an emissive -ide. We may have lesions in the brain which destroy that part of the language faculty concerned in our power of seeing and understanding written words or the gesture language. In read- ing understandingly one sees certain words ; these words revive certain visual memories connected with past perceptions. Thus one sees the word '' book ; '' this suggests to him past memories of form, color, tactile and other sen.sations associated with the past jjerceptions of books. There is a certain centre in the brain where these visual memories for letters and words are located. When this centre is destroyed the memories are destroyed, and the word '"book" or any other written word conveys no meaning. The patient can spell out the letters, he can see the letters, but he cannot read anymore than if he had never been taught. The condition is known as alexia ovicord-hlindness. Again, a person may have learned to associate certain gestures with definite ideas, DISEASES OF THE BRAIN AND ITS MEMBRANES. 331 as the motion of carrying a glass to the mouth with that of drink- ing, or the motions of using a knife and fork with that of eating, or the motions of the deaf-and-dumb alphabet with certain words and ideas. These memories of gesture language are located in certain regions ; and when they are destroyed the patient is no longer able to understand gestures or the sign language. This condition is known as apraxia. Both apraxia and alexia are forms of aphasia which come under the general head of mind- hlindness. A person hears certain words, as. for example, the word " knife." This conveys to him a certain idea of the form, color, and other properties associated with knife. The memories associated with the auditory perception of different words are stored up in a certain locality which is the centre for auditory memories. When this centre is destroyed the person hears spoken words, but they convey to him no meaning. All that it said to him sounds as if it were in a foreign language : he hears, but he does not understand. This condition is known as word-deafness. So much for the receptive or sensory side of language. In communicating our ideas, we speak, write, and make ges- tures. In speaking we make use of the organs of articulation, and this use involves the fine adjustment of a delicate muscular ajDparatus. In the act of exj)ressing ideas we have to bring into play the memories of the i^ast muscular movements of this artic- ulatory mechanism. These movements were learned by a slow and painful i^rocess during infancy. After the power of speech is acquired, the mechanism works readily and almost automat- ically because we only have to send a stimulus to the centre which presides over the stored-up memories of the impulses to properly innervate the mechanism of speech. There is, there- fore, a centre for the memories of the movements of articulation — a centre which is of course closely connected with the motor areas that directly innervate the larynx, pharynx, and oral and facial muscles. When a lesion destroys this centre for si^eech memories, a person is unable to reproduce the words necessary for expressing an idea; for example, he sees a knife, he knows what it is. but the memory of the motions necessary to express the word " knife "" is gone. To him it seems that the name is gone, and that is the common way of expressing it. He cannot say the word ■' knife." The patient may wish to exj^ress the idea of pain. He feels the pain, he knows that he has pain, but he cannot re- vive those motor memories which are concerned in expressing the word " pain ; '' he cannot tell, therefore, in Avords what is the mat- ter with him. When a person is thus troubled, he is said to have a form of motor aphasia for which the particular name given is aphemia. In the same way there is a centre for the memories of the muscular movements concerned in writing ; and when a lesion 332 DISEASES OF THE NERVOUS SYSTEM. destroys this centre the patient is unable to write, though he may be able to speak. This condition is called agraphia. Fi- nally there is a centre, less well defined, for the memories of the movements used in gesture language, and when this is destroyed the person is unable to express his ideas by gesture or sign lan- guage. This condition is known as amimia. To resume now, Ave have the following divisions of aphasia: Sensory Aphasia. Motor Aphasia. ,r- TIT 1 \ Alexia. Aphemia. Mnid-blmdness. \\^ . k .- ( Apraxia. Agraphia. ,^. , T . ( Word-deafness. Amimia. Mmd-deafness. i ^^ . _ . ( Music-deafness. Parapliasia. There is also a form of aphasia in which the patient misplaces words, often to an extent that makes his speech somewhat inco- herent. This is called j^ciTajjhaaia, and is due to lesions which destroy some of the associative fibre-tracts connecting the special centres for language. Practically we often find mixtures of motor and sensory aphasia, or we have a motor aphasia with paraphasia. Patients may also lose the power of expressing themselves by ordinary speech, but may be able to use signs; they may not be able to write voluntarily, but can write to dictation ; they may not be able to read directly, but can do so when they trace out the letters with a pen. These different forms are due to lesions which destroy various connecting tracts as well as certain of the centres. The commonest form of aphasia is the motor aphasia in which there is aphemia and agraphia; that is, loss of power to speak and write. This may not be complete, and then there will be with the motor aphasia some paraphasia. In examining a patient who has ajDhasia one should note the following points : Whether he can speak, name objects, repeat words after you, write from dictation, copy; whether he can sing or express himself by gestures ; whether he can read, spell, read by tracing letters with the pen, read words that he has written himself ; whether he can understand spoken language or gesture language; whether he can appreciate the nature and use of objects. At the same time he should also be tested for hemi- plegia, deafness in each ear, acuity of vision, hemianopsia, and hemiansesthesia. The location of lesions in the various forms of aphasia has been made out with considerable definiteness. The lesion in aphemia is in the posterior part of the third left frontal convo- lution or Broca's convolution; for agraphia, sometimes in the base of the second frontal convolution, sometimes in the angular gyrus. For gesture language there is no known centre. The DISEASES OF THE BRAIN AND ITS MEMBRANES. 333 lesion in word-blindness and apraxia is in the angular gyrus, ex- tending back into the occipital convolution. The lesion in word- deafness is in the posterior part of the first temporal and upper part of the second temporal convolution. In right-handed peo- ple the lesions are always on the left side ; in left-handed people on the right side (see Fig. 165). Malformations of the Brain and its Envelopes. Congenital malformations of the brain are of little practical importance, for in most cases the monsters cannot live and in all Fig. 175.— Acrania. cases they are better dead. I shall simply give a brief enumera- tion of the important forms. rAnencephal}^ Abnormalities J Porencephaly, of the brain, j Absences or malformations of parts, e.g., Oy- [ ciopia. ^^bnornmlitie. | ^/^f/^^^cele. ?/«i^Si?.SL 1 Encephalocele. us envelopes. [ Hydi^ncephalocele. Anencephaly is always present with acrania. In anencephaly the cerebellum and part of the basal ganglia may be present, in such case the child can live a short time (Fig. 175). Porencephaly is often an artificial condition. It will be ae- scribed later. . . , „-«i^. In cyclopia there is an undivided anterior cerebral vesicle, 334 DISEASES OF THE NERVOUS SYSTEM. the orbits form a continuous cavity with a single rudimentary- eye (Fig. 176) . „ In acrania there is usually anencephaly. Meningocele is a hernia of the brain membranes, arachnoid and dura through a cleft in the skull. In encephalocele the J Fig. 176.— Cyclopia. brain also protrudes. Both these forms occur usually in the occipital region and almost invariably in the median line. In hydrencephalocele there is a sac with fluid contents. Diseases of the Membranes of the Brain. The diseases to be considered under this head are anaemia and hypertemia, inflammation of the dui-a mater or pachymenin- gitis, and inflammation of the pia mater or leptomeningitis. Anaemia axd Hyperemia of the Membraxes of the Brain. — Anaemia of the membranes of the brain is a condition that cannot be separated from anaemia of the brain substance, and will be considered in connection with it. Hyperaemia of the brain membranes, so far as it relates to hyperaemia of the pia mater, must also be considered in connection with hyperaemia of the brain tissue. Dural hyperaemia, or congestion of the dura mater, is a condition which occurs as the result of injuries, sun- stroke, and of certain infective poisons, especially that of syph- ilis. The symptoms are those of pachymeningitis of the slight DISEASES OF THE BRAIN AND ITS MEMBRANES. 335 grade, and will be described under that head. They consist mainly of pain, occasional attacks of vertigo, and sensations of fulness about the head. The treatment is that for the beginning stages of a meningitis. IXFLAMMATIOX OF THE DURA MATER OR PACHYMEXIIS^GI- Tis Exterxa.— It has been the custom to describe two forms of pachymeningitis, the external and the internal. Internal pachy- meningitis, or heematoma of the dura mater, is properly a hemor- rhagic disorder and is described under the head of Dural Hemor- rhages. A true inflammation confined to the internal surface of the dura alone is of extremely rare occurrence. Pachymeningitis externa is a disease that involves, at first at least, the outer surface of the dura, and is usually of surgical origin and interest. Mlologi/.— Accidents, injuries, caries of the i^etrous bone in mastoid disease, of the ethmoid bone in ozsena, necrosis, syphilis, and erysipelas are the usual causes. The symptoms are local headache, fever, delirium, sometimes even convulsions and paralysis. In the severe cases the disease has usually extended and involved the pia. Pus is generally formed, and burrows between the bone and dura. The disease is recognized mainly by the discovery of the local cause. The course is acute or subacute. The treatment is a surgical one. IXFLAMMATIOX OF THE PlA MATER OR LePTOMEXIXGITIS. — Inflammation of the pia mater has the following types : simple meningitis due to some infection, epidemic cerebro-spinal men- ingitis due to a specific general infection, tubercular meningitis, and syphilitic meningitis. All these forms of meningitis may be either acute or chronic; the chronic form being usually simply a sequela of the acute. Acute Simple Leptomexixgitis.—^^/oZo^?/.— Acute lepto- meningitis is always due to an infective process reaching the cer- ebral membranes usually directly from without, but sometimes through the blood. The so-called oedematous inflammation of alcoholism and inanition is the only exception. The most com- mon source of infection is disease of the middle ear and mastoid cells. Disease of the frontal sinuses and upper nasal passages; operations on those parts; disease, injuries, and fractures of the cranial bones — are also common causes. Pneumonia is the most frequent infective disease in which the pyogenic organisms are carried by the blood. After this come pyaemia, septicaemia, vari- ola, scarlet fever, more rarely endocarditis, empyema, rheuma- tism, measles, typhoid fever, and mumps. Occasionally a brain abscess reaches the surface and sets up a meningitis. Insolation can of itself not cause it. The disease is more frequent in males, 336 DISEASES OF THE NERVOUS SYSTEM. and is distributed through all ages of life, though it occurs oftener in the young. Symptoms. — The symptoms in the various types differ some- what, but have a general similarity. They are to be broadly grouped into the prodromal, the irritative, the dei)ressive, and the paralytic stages. Prodromal symptoms are shorter and less marked in simple meningitis than in tubercular. The x^atient suffers from malaise, languor, headache, vertigo, irritability, loss of appetite, and vom- iting. Of these symx)toms headache is the most notable. In the second stage the dominant symptoms are headache, delirium, rigidity of the neck, hypersesthesia of the skin, retrac- tion of the abdomen, vomiting, irregular fever, contracted and often unequal x^upils, sometimes optic neuritis or retinitis. The headache is usually i^ersistent, with exacerbations of great in- tensity. Rather early in this disease the patient's mind begins to wander ; he mutters incoherently ; he may have periods of vio- lence alternating with stupor. In some cases there is a continu- ous low-muttering delirium. Vomiting also occurs early and is of a violent, explosive (projectile) character. This symptom is not always i:)resent. The head is bent back and the X3atient can be lifted from the pillow by j^lacing the hand under the occiput. There is sometimes a general rigidity which resembles catalepsy. Drawing a dull jjoint along the skin causes a red line to appear {tache cerehrale). Pinching or rubbing the skin causes much pain. The abdomen falls in and assumes a characteristic " boat- shape." The pupils are usually contracted and uneven. The eyes are intolerant to light. Optic neuritis occurs often when the inflammation is at the base ; but it is a late symptom. Con- ^Tilsions and local paralyses of the cranial nerves, causing sight strabismus, ptosis, or facial palsy, may occur. The fever is irreg- ular in course and not high— 101° to 103 \ The pulse is usually irregular or rather intermittent. It varies greatly in frequency and may be rather slow — 50 to 70. Respiration is rather quick- ened and sometimes irregular. The bowels are consti^Dated ; the urine small in amount and sometimes albuminous. In the paralytic stage the patient becomes stupid or coma- tose ; there is still some rigidity, except in the very last stages. The abdomen is still greatly retracted, the pupils may now dilate, the skin become moist, and the patient's bowels and blad- der move involuntarily. Death now occurs in one or two days as a rule. When the disease is mainly on the convexity of the hemi- spheres there is more delirium, convulsive and jDaralytic trou- bles; when confined to the base there is less delirium, while paralysis of cranial nerves, optic neuritis, vomiting, and retrac- tion of the head are commoner or more prominent. DISEASES OF THE BRAIN AND ITS MEMBRANES. 337 Course and Duration. — The disease may begin suddenly, and the patient pass at once into the comatose state, dying in a few days. Usually the i^rocess lasts one or two weeks; it may be prolonged for several weeks. The prognosis is very grave, but it is less serious than in tuber- cular meningitis and more serious than in the cerebro-spinal form. The diagnosis is based on the presence of an exciting cause, such as disease of the ear or nose, trauma, infective fevers, and upon the presence of the symptoms given. It is usually easily recognized, the main difficulty being to distinguish it from tuber- cular and cerebro-spinal meningitis. Fatliologij. — The disease is a fibro-purulent or purulent in- flammation. It involves usually the base more than the con- vexity, but the reverse may happen. The ventricles are often involved and may be independently inflamed. There are de- scriptions, therefore, of simple basilar meningitis, meningitis of the convexity, and ventricular meningitis or ependymitis. The inflammatory deposits are most conspicuous along the course of the Sylvian fissure and the vessels branching from it, about the optic chiasm, and at the posterior and under surface of the cere- bellum and the sides of the pons. It may lie only in the sub- arachnoid cavity, but usually the arachnoid and sometimes the dura are implicated. There is increase of fluid in the ventricles and arachnoid cavities, and this fluid may be turbid. The sur- face of the ventricles may show an inflammatory process. The micro-organisms found in meningitis are the pneumo- coccus, streptococcus pyogenes, intracellular diplococcus, the l^neumo-bacillus, and a bacillus resembling that of typhoid fever. Still others have been described, and the process is apparently a mixed infection, though the pneumococcus is found oftenest. Treatment. — Prophylaxis is the most important measure, as there is no specific treatment. Chronic disease of the ear and nasal sinuses should be attended to, and injuries of the skull treated with the strictest regard to antisepsis. The patient should be kept quiet, a dose of calomel given, and small doses of iodide of potassium administered at frequent intervals. An ice cap may be appHed to the head and hot applications to the feet. Hot poultices along the upper spine are useful. Opium must be given for the pain, if needed; and antipyretics or phenacetin sometimes answer, in a measure. The internal use of iodoform has been highly recommended, gr. vi. to gr. xij. daily; shaving the head and rubbing upon it an ointment containing '^^% iodo- form, then covering the scalp with an oiled-silk cap, is a treat- ment highly spoken of. Surgical intervention is sometimes justi- fiable. 338 DISEASES OF THE NERVOUS SYSTE^^ Epidemic Cerebro-Spinal Mexijs^gitis (Spotted Fever). —This is an acute infective disorder and is produced by a special micro-organism. It lias certain peculiar clinical characteristics which lead us to describe it separately. Anatomically the changes involve the spinal membranes as well as the cerebral. Etiology.— The disease most frequently attacks children, but it may occur at any age. Males are affected rather more often than females. It prevails in the form of epidemics which affect cold and temperate climates especially, and which travel from one part of the country to another. It may occur sporadically. It most frequently develops during the winter season, and attacks persons who are living in crowded houses, tenements, or barracks. It is slightly contagious. One attack does not confer an immu- nity against a second. Symj^toms. — The general ajDpearance of a person attacked with the disease is that of one who has been poisoned by some agent which is extremely prostrating to the whole system and at the same time one which has a specific inflammatory effect upon the meninges of the brain and spinal cord. When the disease is rapid and malignant, the patient seems to die of an acute toxaemia be- fore any inflammatory i3rocess has time to develop. In milder cases and those of longer dui'ation the prostration is less, and the evidences of inflammation of the meninges then develop in the typical way. The disease may begin with prodromal* symjitoms of malaise, discomfort, pain in the neck, vomiting, and headache. As it develops, the headache, accompanied with giddiness, in- creases, pain and stiffness in the neck become more violent, pains run down the back and radiate to the limbs ; there is photophobia, and dehrium in many cases is marked. The skin is hyperses- thetic, the pulse rises to 120 or higher, the temperature varies very much and is usually raised to 103^ 104% or even more. The bowels are generally constipated. In most cases there develop certain skin eruptions, usually in the form of purpuric spots; herpes, urticaria, and erythema are occasionally seen. These eruptions vary very much in different epidemics; the purpuric spots are the most important from a diagnostic point of view, and have given to the disease the name of spotted fever. As the dis- ease progresses the symptoms of irritation and pain give way to those of somnolence, stuiDor, and paralysis. Optic neuritis, acous-' tic neuritis, and inflammation of other cranial nerves take place, and paralyses of the limbs may be added. The disease may run a short and malignant course, killing the person in a few hours or one or two days. In moderate cases it lasts about two weeks. A large number of different varieties of the disease are described, such as the abortive form, fulminating form, and typhoid form. The disorder is often complicated with DISEASES OF THE BRAIN AND ITS MEMBRANES. 339 pneumonia and bronchitis, less often with inflammation of the joints and serous membranes. The disease often leaves very seri- ous sequelae, the most important being deafness and spinal irrita- tion or chronic spinal meningitis. A large proportion of deaf- mutes owe their affliction to this disease. Patlioloyical Anatomy.— In the very acute cases the post mortem shows nothing but the evidence of very severe blood- poisoning. In the milder and more chronic cases an inflamma- tion involving the pia and arachnoid of the brain and cord is found. This inflammation is fibrinous or fibro-purulent in char- acter, and may be accompanied with the exudation of a good deal of inflammatory material. Bacteriological researches show that this disease is due to the presence of a specific micro-organism which is apparently very much like that which causes pneu- monia. The diagnosis is based upon the history of an epidemic of the disease being present, upon the presence of the ordinary symp- toms of acute cerebral and spinal meningitis, such as headache, delirium, retraction of the head, the sunken abdomen, hypertes- thesia and pains ; finally, the presence of the peculiar purpuric spots or of herpes of the face will enable one to make a positive diagnosis. One must learn to distinguish the disease from typhus, tetanus, uraemia, pneumonia, and from the other forms of men- ingitis, especially the tubercular. The diagnosis is often made difficult by the fact that cerebro-spinal meningitis may occur in a sporadic form, and it is well known that after a community has been once visited with an epidemic, these sporadic cases are liable to crop up from time to time for many subsequent years. The sudden onset of the disease, the spinal symptoms, the skin eruption, the absence of history of injury or of evidence of tu- berculosis w^ill usually enable one to recognize the disorder. The prognosis varies much with the epidemic, but the disease is always a serious one. The mortality ranges from twenty to eighty per cent ; it is worse when the disease comes on suddenly and severely, with early coma. It is better in persons over the age of ten. Cranial -nerve complications are unfavorable, in that they are apt to leave permanent deafness. Severe spinal com- plications are apt to leave their mark in the form of a chronic meningeal trouble. • Treatme7it.— There is no specific remedy for the disease, and* the ordinary antiphlogistic measures such as mercury and iodides are of less value than in other forms of nieningitis. The patient should be given sustaining food, and everything possible should be done to counteract the depressing effects of the toxaemia. Opium or morphine internally, chloral, digitalis, quinine, ben- zoate of sodium and salicylate of sodium, and alcohol are the 340 DISEASES OF THE NERVOUS SYSTEM. drugs which have been specially recommended. Warm baths, hot moist applications, and leeches have all been tried with more or less good results. Tubercular Mexixgitis (x\cute Hydrocephalus).— This is a form of meningitis due to infection with the bacillus tuber- culosis. It differs pathologically from other forms in the charac- ter of the infective organism ; anatomically, in the fact that the Inflammation is usually and chiefly basilar and never purely pur- ulent; etiologically, in that it chiefly affects young children; and symptomatologically, in the presence of prodroraata and a more irregular course. ^^/oZor/^.— Tubercular meningitis occurs chiefly between the ages of two and ten, sometimes in infancy, rarely in adult life, very rarely after the age of fifty. Males are rather more subject to it. A hereditary history of phthisis, a scrofulous diathesis, bad hygienic surroundings, and the presence of tuberculosis else- where in the body predispose to it. Tuberculous milk, the erup- tive fevers, especially measles, blows on the head, and great emo- tional excitement ajDpear to act as exciting causes. Symptoms. — A knowledge of the prodromal symptoms is espe- cially important. These are paroxysmal and intensely severe headaches and darting pains in the head, vertigo, loss of appe- tite, explosive vomiting without nausea, the vomited matter being usually colorless and watery, constipation, an altered disposition, and irritability. The tache cerehrale or cerebral macule, more rarely ptosis and facial paralysis, may appear early. The pro- dromal stage often lasts, with remissions, three or four weeks. When the disease sets in there is more persistent headache ; vom- iting, fever, and the other symptoms of meningitis already de- scribed appear. The irritative stage gradually passes into the paralytic and comatose. Death occurs in two or three weeks. In infants the disease often runs a very obscure course, the pa- tient show^ing chiefly symptoms of brain compression. Pathological Anatomy. — In rapidly fatal cases, with severe symj)toms, there may be only an intense congestion of the brain with numerous miliary tubercles in the pia mater at the base and over the convexity. Here we must assume that a bacillary toxine causes the symptoms. In most cases there are decided deposits of tubercles at the base, with fibrinous inflammatory deposits about the optic chiasm, along the fissure of Sylvius, at the sides of the pons and elsewhere. Miliary tubercles are seen scattered over the convexit\^ and in the choroid plexus and ventricles. They are generally found in the spinal membranes also, especially over the cauda equina. The tubercles lie beneath the pia sur- rounding the small vessels. They may coalesce into large tuber- cular nodules. There is usually an increase in the arachnoid DISEASES OP THE BRAIN AND ITS MEMBRANES. S-il fluid, and in most cases an increase in the ventricular fluid. Some- what rarely there is very ^reat distention of the ventricles and compression of the convolutions. This condition used to be called acute hydrocephalus. Small spots of softening may be seen from obliteration of the vessels by the tubercles. The bacillus tuberculosis is found in the tubercular nodules. Diagnosis. — As regards the form of the disease, this is based on the hereditary history, the age, the existence of tuberculosis of the lungs or other organs, and the peculiar prodromata of the disease. Occasionally tubercles can be seen on the choroid. Prognosis. — This is usually absolutely bad, yet post-mortem observation of cases dying with practically no inflammatory change makes it seem possible that the disease might be checked, and a good many cases are reported where it apparently has been. Some of these are, however, probably cases of hereditary syphilis. Treatment. — So far as now known, this is not different from that given under the head of meningitis elsewhere. It seems, however, as if in time some anti-toxine may be discovered which will check the progress of the poison and the development of the tubercle ; meanwhile the best thing to do is to give small doses of iodide of potassium at frequent intervals and use symptomatic treatment. Chronic Hydrocephalus. This is a disease mainly of infancy, characterized by a gradual enlargement of the head, with mental deficiency and symptoms of brain irritation caused by an accumulation of fluid in the ventricles of the brain. The old term " acute hydrocephalus " meant an acute inflam- mation with effusion, but the name is not needed and is best dropped. Chronic hydrocephalus is not an inflammatory j^ro- cess, but one due to mechanical causes or to defects in structure or nutrition. The fluid always accumulates in the ventricles of the brain ; hence chronic hydrocephalus is always internal. The so-called external forms of hydrocephalus are inflannuatory or else are secondary to meningeal hemorrhage or brain atrophy. Chronic hydrocei)halus is almost always a disease of infancy and is generally congenital. It may, however, be acquired. In speak- ing of chronic hydrocephalus, we refer to the chronic internal congenital disease. Etiology.— Your out of five cases begin at birth or within the first six months of life. Syphilis (J. Lewis Smith), alcoholism, lead-poisoning m the parents, and some unknown family taint predispose to the disease. Poverty and poor nutrition and rick- ets are also factors. 342 DISEASES OF THE NERVOUS SYSTEM. Symptoms.— T\\e head may be so larg^e at birth that instru- mental help is needed. More often the parents notice a gradual increase in the size of the child's head, beginning soon after birth. The forehead bulges, the occiput stands out, the fontanel] es and sutures widen, and pressure shows evidence of fluctuation. Mean- while the face does not grow^ much and the result is to give a triangular shape to the head. It may measure twenty-four, twenty-seven and one-half (Minot), thirty-two (Bright), and even forty-three inches (Klein) in diameter. These extreme measure- ments are reached only after one or two years. With this abnor- mal growth of the head, mental and physical symptoms appear. The infant is restless and irritable, its appetite may be good, but the general nutrition is poor and its bodily growth is retarded. Fig. 177.— Chronic Hydrocephalus. The mind does not develop ; usually it does not or cannot learn to walk. It may be unable to support the weight of its head. There is strabismus and sometimes optic atrophy. The pressure of the dropsy thins the orbital bones and forces down the axis of the eyeballs (see Fig. 177). Vomiting, coma, and convulsions eventually appear, and the child dies of exhaustion or some in- tercurrent disease in two or three years. In some cases the trouble is less serious, it ceases to progress, the bones solidify, and the child grows up with good intelligence. Chronic hydrocephalus sometimes develops in late childhood and in adult life. It is then due to some tumor or inflammatory process obstructing the vense Galenae and the aqueduct of Syl- vius. The symptoms are chiefly those of brain pressure, and the disease cannot be recognized with certainty. The hydrocephalus which is associated with the brain atrophy DISEASES OF THE BRAIN AND ITS MEMBRANES. 343 of insanity and old age or with general dropsical conditions has no kinship with the process we are now describing. Pathology.— The disease is due to the gradual accumulation of a serous fluid in the ventricles of the brain. The cause of this is an inflammatory or developmental obliteration of the foramen of Magendie and the adjacent lateral foramena of Mierziejewski. This prevents the escape of the ventricular fluid into the general arachnoid cavity. Contributing factors are congenital or ac- quired defect in the absorbents of the ventricles and a rachitic and easily yielding skull. The attempts to make chronic hydro- cephalus an inflammation are failures, though there is at times a thickening of the lining membrane of the ventricles. The lat- eral ventricles are principally and often solely affected, and these are so distended as to press out their cerebral walls, flattening the convolutions, and turning them into a thin shell often less than a quarter of an inch in thickness. Sometimes only one lat- eral ventricle, and in rare cases only the fourth ventricle, is affected with the dropsy. The diagnosis has to be made from rickets and an acute in- flammatory process. In rickets the head is square, the f ontanelle does not bulge, the enlargement is less, and there are signs of the disease in the bones elsewhere. Prognosis. — The congenital cases usually die in a few months, or at least before the third year. Those developing in infancy may live for four to six years; and in mild cases the disease ceases to progress and a fairly healthy adult life is reached. Treatment. — A great many measures have been recommended, but there is no unanimity about any one of them. In such a state of therapeutics it is safe to say that treatment is of little use. The most rational measure is the inunction of mercury and the administration of iodide of potassium combined with tonics. Surgical measures such as tapping the ventricles are irrational and need not be discussed. Quincke's method of tap- ping the spinal canal will not apply in these cases. Though it is a practicable measure as I have found by experiments on the cadaver. Strapping the head with diachylon plaster is recom- mended by Trousseau and by J. Lewis Smith. CHAPTER XYIII. DISEASES OF THE BRAIN. These diseases, like those of other parts of the nervous sys- tem, consist of malformations, vascular disturbances, inflam- mations, softenings, hemorrhages, degenerations and scleroses, chronic infections, tumors, and functional disorders. Cerebral hyper.emia is a condition in which there is an excessive amount of blood in the cranial cavity ; it may be acute or chronic, active or i^assive. Etiology. — In the description which is to follow I shall refer only to those conditions of hypercenua of the brain w^hich are pathological. It is a well -recognized fact that hypersemia of the brain occurs physiologically under excitement and over-activity of the heart and from various stimuli ; l)ut a pathological condi- tion of acute congestion may be induced by sunstroke, certain drugs such as alcohol, and by injuries; also by mechanical causes which prevent the exit of the blood from the cranium. An acute congestion also occurs in mania and in many forms of fevers, as well as in the initial stage of meningitis. A chronic cerebral hy- persemia may be induced by the causes already mentioned as bringing on acute congestion. The prolonged use of alcohol, prolonged mental excitement, overwork, and worry may also lead to this condition. The foregoing causes lead to what is known as active congestion, in which the blood is driven in excess into the brain through the arteries. A passive congestion may exist in which the blood is prevented from leaving the brain and is kept mainly in the intra-cranial veins. The causes of passive congestion are mainly mechanical, such as cardiac disease and mechanical obstructions about the neck from tight clothes and an obstruction to the flow of blood from the lungs by playing on wind instruments. Symptoms. — A great deal has been written regarding the symp- tomatology of cerebral hyperemia, but many of the statements made are nothing but guesswork. Probably the main symptoms produced by an active congestion of the brain are a sense of ful- ness and pressure, a feeling of constriction about the head, some headache which may be vertical, mental excitement or irritabil- ity, confusion of ideas, vertigo, insonmia, ringing in the ears, DISEASES OF THE BRAIN. 345 and pulsating sounds in the head. These symptoms are some- times increased when the patient lies down, and are generally increased when the patient bends the head over so as to prevent the return flow of blood from the brain. It is impossible to diag- nosticate passive hypersenda from active through the symptoms alone, but probably in the former condition the disturbances and symptoms mentioned are less marked; in other words, an active hypersemia produces more phenomena than passive. In either case examinations of the fundus of the eye and of the tym- panum furnish no sure criteria. Pathology.— Qev^hrtxl hypersemia used to be regarded as nearly synonymous with cerebral neurasthenia. In the writer's opinion, it is secondary to the neurasthenic state; and produced, if it exists in that state, by the impaired vasomotor innervation which is characteristic of neurasthenia. It is not wise, therefore, to make the diagnosis of cerebral hyperaemia often as the primary condi- tion. It is only after traumatisms and sunstroke or after a men- ingitis that we can speak of the cerebral hypersemia as being in a certain sense the primary condition to be treated. The state- ment made by some writers that cerebral hypersemia underlies certain conditions of acute delirium, of aphasia, of paralysis, and even dementia or insanity can hardly be supported. In many of the cases of cerebral hyperaemia where symptoms are produced, there is undoubtedly a condition of toxaemia which is a con- tributing factor to many of the symptoms. Treatment. — The specific treatment of cerebral hypersemia, when indicated, consists in giving large doses of fluid extract of ergot and bromide of potassium. One or two drachms of the ergot three times a day and fifteen or twenty grains of bromide of potassium may be prescribed. Wet cups to the back of the neck, the cautery in the same region, ice caps, purgatives, quiet and rest, and a careful regulation of the diet and the bowels are all important measures. Cerebral Anemia.— This condition, like hypersemia, may be either acute or chronic. It occurs among the young ; more often in females than in males. It is seen in early adult life, where it is induced by the various causes producing general anaemia, and again after the climacteric, when it is due to organic changes in the cerebral arteries of the nature of an obliterating endarteritis. Bright's disease and syphilis, exhausting diseases and profuse hemor- rhages, and such disorders of digestion and nutrition as lead to general anaemia produce also cerebral anaemia. A potent cause of acute cerebral anaemia is fright. Si/7nptoms.— The symptoms of acute cerebral anaemia are ver- tigo, confusion of ideas, nausea, faintness or complete syncope. 346 DISEASES OF THE NERVOUS SYSTEM. In chronic cerebral anaemia the symptoms are mental apathy and a teeling of disinclination to work, tendency to somnolence in the day-time and insomnia at nit^ht, mental depression, head- aches which are usually frontal or vertical, occasionally some vertigo and tinnitus. There may be spots before the eyes and undue sensitiveness to sounds. In children some very severe symptoms are attributed to cerebral ansemia, but here, as in hy- peremia, it is probable that there are other causes at work, par- ticularly toxic agents or reflex disturbances. Diagnosis. — A chronic anaemia of the brain can hardly be recognized except through the evidences of a general anaemia. When this is present and there are also symptoms such as have been described, a fairly certain diagnosis can be made. We must look upon cerebral anaemia as being in almost all cases a second- ary phenomenon, except in the aged, and then the trouble is due not alone to poverty of the blood, but to the fact that the circu- latory apparatus is diseased. It is generally believed that in cerebral anaemia the symptoms somewhat improve by the hori- zontal position and are made w^orse by the upright position. It is also asserted that in anaemia the pupils rather tend to be dilated, while in hyperaemia they are contracted. Treatment. — Treatment should be directed toward enriching the supply of blood and toward improving the general nutrition. It consists, therefore, in the administration of preparations of iron and of such tonics as the mineral acids, strychnine, quinine, and nitroglycerin. INFLAMMATION OF THE BRAIN— ENCEPHALITIS. The forms of inflammation of the brain are acute suppurative encephalitis, acute non-suppurative encephalitis, chronic enceph- alitis, chronic polioencephalitis. Inflammations of the brain are analogous to those of the spinal cord ; that is to say, there are acute suppurative inflanniiations or abscesses, and acute exuda- tive inflammations with or Avithout necrosis, and there are chronic inflannnations. The brain differs from the spinal cord, however, in that acute suppurative inflammation is comparatively fre- quent, while the acute exudative inflammations are extremely rare. Chronic inflammation, also, of the brain is rarer than chronic inflammation of the cord, if we except that type which underlies general paresis. Acute Suppurative Excephalitis (Abscess of the Braix). Brain abscess is a suppurative inflammation which affects the parenchymatous and other structures of the organ. It is always a focal disease, but may be single or multiple. DISEASES OF THE BRAIN. 34? Etiology.— ThQ primary cause of all forms of brain abscess is a microbic infection. The form of microbe, its mode of entrance, and the part of the brain attacked vary greatly. The predis- posing causes relate chiefly to age and sex. Brain abscess rarely occurs before the first year or after the fiftieth year of life. It is rather frequent in young people, and occurs on the whole often- est between the ages of ten and thirty. Males are more often affected than females in the ratio of about three to one. The exciting causes are chiefly disease of the ear and of the cranial bones, injuries, and remote suppurative processes. To this may be added infectious fevers and the presence of tumors. Inflam- mation of the middle and internal ear is the most common cause of brain abscess. The disease affects the tympanum and mastoid cells, more rarely the labyrinth. It is usually a sup- purative process of long standing. Caries of the ethmoid and nasal bones and of the orbital cavity leads to brain abscesses in a considerable proportion of cases. After chronic ear and bone diseases, injuries are the most frequent cause. The injury may be a compound fracture with direct infection from the open wound, or the abscess may be the result of contrecoup and may develop in a part of the brain opposite to that which w^as in- jured, or the abscess may develop below the point injured, there being apparently healthy tissue between the surface of the brain and the diseased part. These abscesses develop through lacera- tion of brain tissue and subsequent infection of the wound with organisms. The most common remote suppurative processes which are followed by brain abscess are tubercles, inflammation of the lungs, fetid bronchitis, and empyema. Brain abscess may develop, however, from distant points of suppuration on the ex- tremities or in almost any part of the body. Pyaemia may lead to the production of brain abscess. Among the infectious fevers which are complicated with brain abscess are diphtheria, typhoid and typhus fevers, erysipelas, small-pox, the "grippe." The oidium albicans or thrush may also be a cause. Brain tumors sometimes become surrounded by a suppurative encephalitis or may break down with the formation of mixed suppurative and neoplastic tissue. Tubercular tumors are most frequently accom- panied by suppurative encephalitis. Symptoms.— Br SLin abscesses take sometimes an acute and sometimes a chronic course. In acute cases the symptoms de- velop rapidly and the disease runs its course in a few days or w^eeks. The symptoms come under the general head of those of pressure, those of poisoning from the diseased focus, and local symptoms due to irritation or destruction of certain special areas of the brain. The pressure symptoms are those of headache which is often very severe and persistent, vomiting which is quite 348 DISEASES OF THE NERVOUS SYSTEM. frequent though not invariable, vertigo, and a condition of men- tal dulness wliich may pass into a delirium, ending finally in coma. Optic neuritis often occurs. The pupils are apt to be irregular, but furnish no definite indications. The pulse is usually slow, ranging from 60 to 70, but it varies a great deal. The tempera- ture is normal or subnormal as a rule, but this also varies, and it may rise several degrees above normal, alwaj's running an irregu- lar course. The toxic symptoms are those which we get in septic poisoning; namely, iDrostration, irregular fever, emaciation, ano- rexia, and such mental and sensory disturbances as have already been referred to. As a result of local irritation or destruction, there occur convulsions, paralysis, aphasia, and disorders of some of the special senses. Convulsions are not very common. AVhen they occur they are generally of an epileptic character. The paralysis is usually in the form of hemiplegia. The cranial nerves are not often involved, if we except the oi^tic. The urine is said to show a diminution in chlorides and an increase in phosphates. The patient dies finally in coma from exhaustion. In the chronic form of brain abscess the symptoms may for weeks, months, or years remain practically latent, after the ex- citing cause has been at work and after the abscess has been es- tablished. The patient during this latent stage may suffer from headache, vertigo, mental irritability, and depression ; he may at times have a convulsive attack. Occasionally there will be an exacerbation of the disease, at which time he suffers from intense pain, vomiting, perhaps delirium or a convulsion. From this he recovers and continues in a fairly good state of health again. After a variable period, usually of weeks or months, the terminal stage sets in. This terminal stage of the chronic form may as- sume very much the characters of the acute form already de- scribed. In other cases it shows itself by a sudden apoplectic or epileptic seizure or a sudden attack of coma, in which the patient sinks and rapidly dies. These terminal phenomena are due to the fact that the abscess, which has been previously encysted and quiescent, suddenly breaks into a lateral ventricle or through the surface of the brain, or to the fact that a hemorrhage occurs into the abscess. Complications.— The common complications of brain abscess are a phlebitis of the superior petrosal and lateral sinuses and a meningitis. The phlebitis accompanies abscesses that are caused by disease of the ear. The meningitis may be caused by ear dis- ease, but more frequently accompanies abscesses due to injury. "When phlebitis is present there will be found an oedema about the ear and neck and a hardness of the jugular veins. In men- ingitis there is apt to be more rigidity of the neck, more pain, and there are often cranial-nerve paralyses. DISEASES OF THE BRAIN. 349 FatJiolog I/.— Acute suppurative encephalitis resembles acute suppurative myelitis in the intimate nature of the clianges that take place. Tliere is an intense congestion of the parts, which give it a reddened appearance and Avhicli used to give to this process the name of red sjftening. This condition, however, is only the initial stage of the suppurative inflammation and does not deserve to be ranked as a sijecial form of inflammatory pro- cess. It is possible that in some cases the inflammation may get no further than the stage of red softening. The congestion then gradually disappears, absorption of exudate occurs, and a more or less complete recovery takes place. When the process contin- ues, however, the parts become crowded with leucocytes and infiltrated Avith inflammatory exudate. The nerve fibres and cells are destroyed, in part mechanically, in part by the poison- ous influence of the pyogenic organisms. The nerve cells lose their normal contours, swell uid, and disintegrate ; the neuroglia cells absorb the broken-down detritus and swell up, forming what are known as granular corpuscles ; the leucocytes increase until a purulent mass is formed. The total result is a mixture of broken-down nerve fibres and cells, leucocytes, and granular bodies. Bacteriological tests show the presence of various pyo- genic microbes. The abscess thus formed v^aries in size from one to six or eight centimetres in diameter (two-fifths to three inches). It is generally somewhat round, and if the case is chronic a fibrous wall is formed. It takes from three to four weeks for such a wall to develop (Fig. 178). Brain abscesses are usually single, occasionally there are two or three. In some conditions they are multiple; that is to say, there may be fifteen, twenty, or more. Multiple brain abscesses are always small and are usually due to pyaemic infection. Location. — Brain abscesses involve the cerebrum oftener than the cerebellum, in the proportion of about four to one (Barr). Thej^ occur rather oftener in the right cerebrum. They are very rare in the pons and medulla. The cerebral lobes oftenest affected are the temporal and frontal. In the cerebellum it is the lateral hemispheres that are most frequently attacked. The seat of the abscess has important relations to the cause. Abscesses due to ear disease are almost always either in the temporal lobe or the cerebellum. If the ear disease is in the tympanum, the cerebrum is usually the seat of the abscess. If the disease is in the mastoid cells, the cerebellum is usually the part affected. If the disease is in the labyrinth, the abscess is also more apt to be in the cere- bellum. This distribution of the seat of the disease is due to the anatomical relations of the bony parts to the temporal lobe and cerebellum, respectively. Brain abscesses due to injuries are more frequent in the frontal and temporal lobes. What are 350 DISEASES OF THE NERVOUS SYSTEM. known as idiopathic brain abscesses— that is, those which arise without any known cause— are most frequent inthefrontallobes. This is because most such cases are due to an unrecognized affec- tion of the nasal cavities and ethmoid bone. Brain abscesses due to suppurative processes in the lungs and pleura are probably embolic; and as the emboli are carried up into the middle cere- bral artery, the brain abscesses having this origin are situated in the field supplied by this artery. In children under ten, in whom Fig. 178.— Abscess op Cerebellum. brain abscess is usually due to ear disease, the cerebellum is more apt to be affected. Course. — Acute abscesses last from five to fourteen days, rarely over thirty days. Traumatic cases run the shortest course. Chronic abscesses may have a latent period of Aveeks, months, and in rare cases even one or two years. When terminal symp- toms come on death occurs in a few days. In a few cases brain abscesses have been spontaneously evacuated through the nose. Aside from this, the termination is always a fatal one unless sur- gical interference takes place. There is sometimes a recurrence of the abscess after an operation. Diagnosis.— The diagnosis of brain abscess is based upon the DISEASES OF THE BRAIN 351 history of injury, aural or nasal disease, remote suppuration, upon the general symptoms of sepsis, upon the presence of head- ache, vomiting, slow pulse, normal or subnormal and irregular temperature, a local tenderness of the scalp and rise of tempera- ture over the seat of the lesion, hebetude, delirium, optic neuri- tis, rapid wasting, and diminution of chlorides in the urine. The diagnosis of the location of the abscess is based upon the history of its cause, Avhether from injury, ear disease, emboU from the lungs, or nasal disease ; also upon the presence of hemi- plegia, local convulsions, tenderness and rise of temperature of a certain area of the scalp. As brain abscesses are apt to affect 352 DISEASES OF THE NERVOUS SYSTEM. latent regions like the temporal and frontal lobes, local diagnosis is usually difficult. The diagnosis must be made from tumors of the brain, meningitis, and phlebitis of the sinuses. The differ- ential points are given under the heads of the diseases mentioned. The prognosis of the disease is absolutely unfavorable unless some surgical interference is resorted to. The few rare cases of spontaneous evacuation of the abscess would not lead to any practical modification of this statement. Treatment. — The actual treatment of a brain abscess after it has developed is, as already stated, exclusively a surgical one. The successes so far have not been very great, but they have been sufficient to justify operation and to furnish greater hope for the future, when a more exact diagnosis can be made and a wider surgical experience has been obtained. The accompanying fig- ure shows the points to be located in trephining for abscess from ear disease. Something is due to the patient in the way of pre- vention, especially in cases of persons who have chronic aural or nasal disease with carious processes. These should be carefully watched and treated. Acute Exudative Encephalitis (Acute Bulbar Myelitis, polioe]\"cephalitis superior ak^d ijfferior, infan- TILE Polioencephalitis, Primary Encephalitis of Friedmann). Acute exudative encephalitis is a disease whose pathological existence is probable, but as yet we are not able to establish any definite clinical types associated with the process. An exception to this may be made in the case of acute bulbar myelitis and acute polioencephalitis superior. A third exception is claimed by Strumpell, who affirms the existence of an acute polioenceph- alitis of children. A form of acute non-suppurative and primary encephalitis is described by Friedmann, and illustrative cases are given ; but as yet it is doubtful if we can place this condition in the category of a distinct disease. Acute bulbar myelitis is a disease which is strictly analogous in course to acute myelitis. The special symptoms simply depend upon the peculiar location of the disease. They consist of an acute glosso-labio-laryngeal palsy, and are referred to under the description of bulbar paralysis. Acute iDolioencephalitis superior is a disease in which the nuclei of the nerves supplying th-e eye muscles are involved; it is a disease analogous to poliomyelitis anterior, and has been described under the head of Ophthalmoplegia. The acute polioeDcephalitis of children (Strumpell) is a dis- ease that involves the gray matter of the convexity of one of the DISEASES OF THE BRAIN. 353 cerebral hemispheres. The disease is supposed to be strictly analogous to an inflannuation of the anterior horns of the spinal cord. It attacks children between the first and fourth years of life, with symptoms of fever, delirium, and often of convulsions followed by a hemiplegia. The acute symptoms pass away in a week or two, leaving the child with the hemiplegia which may improve very greatly, but more commonly continues through life. With it later there are developed contractures of the affected side, some atrophy, mental defects, and epileptic convulsions. The real existence of this disease is very doubtful. Chronic Encephalitis.— Under the older views of inflam- mation there were described as chronic cerebritis such lesions as sclerosis and cerebral atrophy. These jjrocesses we now regard as being simply reparative and as the sequelae of acute destruc- tive or inflammatory pro(^esses. They will be described, there- fore, under such heads. The only form of chronic cerebritis for which there is a recognized clinical prototype is the chronic cor- tical cerebritis, which is the basis of general paralysis or paralytic dementia. Even this process, however, is still regarded by many as essentially a degenerative one and not inflammatory. As the symptoms which result from it are those of insanity, the disease will not be described in this work. THE APOPLEXIES. Apoplexy is a condition characterized by a sudden paralysis and shock, usually with loss of consciousness, and due to the breaking or blocking up of a blood-vessel in the brain. Apoplexy is a general term. Its particular forms are . 1. Intracranial hemorrhage, from rupture of blood-vessel. 2. Acute cerebral softening, from embolism or thrombosis. Since both embolism and thrombosis cause a rapid softening in the area supplied by the obstructed vessel, the term acute softening covers both disorders. Apoplexy from Intracranial Hemorrhage (Cerebral Hemorrhage, Hemiplegia). Forms.— There are four groups of blood-vessels in the brain, those of the dura mater, those of the pia mater, and those sup- plying the basal ganglia and white matter. Besides this, we may consider the pons, medulla, and cerebellum which are supplied chiefly by branches of the vertebrals as a separate group, sub- ject to somewhat different mechanical conditions. Correspond- ing to this we have : 1. Dural or pachymeningeal hemorrhages. 2. Pial or subarachnoid hemorrhages. 23 354 DISEASES OF THE NERVOUS SYSTEM. 3. Central hemorrhages. 4. Hemorrhages in the medulla, pons, and cerebellum. It is the central hemorrhages (So. 3) due to rupture of the blood-vessels going to the great basal ganglia, internal capsule, and white matter that cause the great majority of cerebral hem- orrhages seen by the physician. It is this class that I have par- ticularly in mind in the following description. Etiology.— At the time of birth and during infancy there is a slight tendency to intracranial hemorrhage owing to the acci- dents and injuries of labor. After this period the liability is very small, but slowly increases up to the age of forty, when predis- position specially begins. Four-fifths of all cases occur after forty, and the tendency to hemorrhages increases in each decade up to eighty, when it diminishes absolutely and relatively.* Males are slightly more predisposed than females (five to four). Rather moi'e cases occur in cold weather, at high altitades, in the temperate zone, and among civilized races. Heredity has an undoubted, though not great influence in predisposing to cerebral arterial disease. Infective fevers and marasmic states are predisposing causes. Chronic kidney disease is present in one-third of the cases. Chronic alcoholism, syphilis, and gout are powerful predisposing causes. Rheumatism is less impor- tant. Heart disease, fatty and atheromatous arteries, arteritis, and miliary aneurisms may be regarded as more than simply predis- posing — they are determining causes. Leucocythsemia, scurvy, and purpura are conditions which also particularly tend to cause hemorrhage. The so-called apoplectic habit — short thick neck and high shoulders and florid face — has really some importance in the better classes. Congenital anomalies, such as a narrow tho- racic aorta or inherited deficiency in the strength of the walls of the blood-vessels, also play a i^art. Any sudden physical exer- tion, such as straining at stool, the excitement at coitus or of a passion, eating a large meal and drinking a great deal of fluid, especially alcohol, taking a cold bath, all may lead to rupture of an artery. Often the vessel breaks during sleep, owing perhaps to the contracted condition and consequent higher pressure m the arteries, and to the fact that on account of the horizontal position there is more resistance to the return of the blood from the brain. The symjytoms are the prodromal, those of the attack and acute stage, and those of the chronic stage. * Among 53 cases collected by me at Bellevue Hospital, the agres were 10 to 20, 4; 21 to 30, G ; 31 to 40, 10 ; 41 to 50, 11 ; 51 to 60. 7 ■ 61 to 70. 10; 71 to 60, 5 The right side was affected in 23 cases ; left in 25 cases. The location was . Pachymeningeal, 7 ; pial and cortical. 8 ; ventricular, 23 : corpus striatum and vicinit}-, 7 ; optic thalamus, 2 ; corpora quadrigemiua, 1 ; pons, 1 ; cerebellum, 3. DISEASES OF THE BRAIN. 355 Prodromal symptoms are rare except in syphilitic cases. Wlien present the patient suffers from dizziness, numbness of the hand and foot on one side, and a failure of memory for words. He may have " full " feelings or even pain in the head and bad dreams at night. Nose-bleed and irregular heart action sometimes occur. The attack always comes on suddenly and may be ac- comiDanied (1) with convulsions and coma, (2) with coma alone, or (3) without loss of consciousness. 1. Initial convulsions are rare and generally mean a meningeal hemorrhage. When present they are unilateral or partial, as a rule, but may be general. 2. The common mode of onset is with coma. The patient, without w^arning, suddenly becomes dizzy, loses consciousness, and falls. The face is flushed, the pulse hard and rather slow, the breathing is labored and stertorous, the cheek on one side puffs out with each expiration, the eyes are partly closed, the eyeball§ fixed or deviated to the paralyzed side, the pupils are contracted and rigid, the skin is bathed in sweat, the limbs are relaxed, but some evidence of hemiplegia is present ; the urine may be retained or it and the fccces involun- tarily evacuated. The urine is usually of rather high specific gravity and often contains albumin, even when there is no renal disease. The temperature in severe cases may fall below normal during the first twelve hours, even to 96° F., but this is not the rule. It is the rule, however, for the temperature in a few hours to be 1" or 2" higher on the paralyzed than on the sound side. If the case is rapidly fatal coma continues, respiration often assumes a Cheyne-Stokes character, the pulse becomes faster, the tempera- ture gradually rises, and usually reaches 102° or 103° F., until just before death, when it may sink again. Swallowing and speech become difficult, hypostatic pneumonia sets in, and the patient dies in from two to four days. In sloAver fatal cases the patient regains consciousness partially and then enters a condition of stu- por or mild delirium. He is restless and suffers from headache. The temperature may continue normal for a time, but is usually higher on the affected side. At the end of two or three w^eeks it rises higher, pneumonia develops, the patient becomes uncon- scious and finally dies. In the favorable cases, which constitute the majority, coma, if present, gradually passes away in from one to six hours, leaving the patient's mind somewhat w^eak and confused and his speech disturbed, or more rarely the intelligence may not be at all disturbed. During the first few days or weeks after the attack the physician finds that the prominent symptom is the hemiplegia. This affects the arm. and leg most and the face least. Only the lower two branches of the facial nerve are involved, and the patient can shut the eyes. The tongue, if pro- truded, turns to the paralyzed side ; the uvula is turned in various 356 DISEASES OF THE NERVOUS SYSTEM. ways and its position is of no significance. There is often some evidence of cutaneous anaesthesia of the paralyzed side, and less often hemianopsia and disturbances of hearing occur. In right- sided hemiplegia the patient, after recovering consciousness, is often unable to talk or to understand what is said. Examina- tion shows that he has a motor or sensory aphasia (y/fZe Aphasia). The deviation of the eyes and head to one side usually dis- appears in a day or two. Occasionally there is a temporary ptosis. The pupils at first are contracted, that on the paralyzed side the more so ; this condition disappears with returning con- sciousness. The paralysis of the arm and leg is flaccid at first, and the limb falls heavily when lifted ; the reflexes are lessened or abol- ished. Sometimes, however, rigidity sets in at once. This symptom occurs when blood has broken into the ventricles, and also in some meningeal hemorrhages. The skin reflexes are abolished or nearly so on the affected side. The usual course of the temperature is for it to rise on the second and third day to 100' F. or 102 F., being V to 1° F. higher on the paralyzed side. In a few days it gradually falls, so that by the eighth to the tenth day it is normal. If the temperature continues to rise after the fourth or fifth day, it is a sign of an extension or infiammatory reaction of the hemorrhage. Hence the thermometer furnishes a very important criterion of the seriousness of the ease. The varying course of the apoplexy is shown in the following diagram ; Health line. 3. Chronic stage. 4 to 8 weeks. Improvement. Attack.- 1. Death. 2. Death. 2 to 4 days. 2 to 4 weeks. The Chronic Stage, Hemiplefiia.—M the end of a month, if fever and s^^mptoms of cerebral irritation have subsided, the chronic stage may be said to begin. The hemiplegia has improved , the patient can move the leg and arm a little, sensory symptoms DISEASES OF THE BRAIN. 357 have lessened, the mind is clear, headache has disappeared. Im- provement continues, though more slowly, for several months or even one or two years. During this time the patient is " a hemi- plegic." The hemiplegia affects the arm more than the leg and the face least of all. The distal segments of the limbs, the feet and hands, are affected more than those near the trunk. The mus- cles that act bilaterally, such as those of respiration, phonation, and facial expression, are but slightly involved. The paralysis is not strictly a hemiplegia, for the muscles on the sound side are somewhat weakened, as tests will show. In severe cases, es- pecially in old people, even the visceral muscles, especially those of the bladder, are weakened. At the onset of the attack there is sometimes a temporary " initial " rigidity of the muscles on the pai-alyzed side, or an " early '' rigidity may develop in one or two days. There always develops at about the beginning of the sec- ond week a " late '' rigidity. This, which at first is slight, gradually increases, and finally contractures affect the paralyzed limbs. The superficial reflexes, wdiich at first were absent, reappear ; the tendon refiexes become much exaggerated, and clonus can be obtained in the leg and arm. The sound side shares to a small extent in these conditions. The contractures affect the extensors of tlie foot more than the flexors, and bring the toe down and the heel up. The leg is held nearly extended, and the limb in walk- ing is swung around, the toe scraping the ground. The shoulder is adducted, the forearm flexed, and the fingers tightly shut into the palm by the overaction of the flexors. The facial muscles show a slight contraction and drawing to the affected side. The muscles on the paralyzed side do not waste. In infantile hemi- plegia, however, the affected limbs grow less than those on the sound side. The paralyzed lin)bs may be the seat of peculiar disorders of movement. These consist of Associated movements. Tremor. Ataxia. Choreic movements. Continuous or athetoid movements. Spastic movements and cramps. Such movements, aside from those that are spastic, are rarely seen in the hemiplegia of adults. The electrical irritability may be at first sightly increased and diminished, but the change is slight in amount and never reaches the degenerative stage. Hemianj^sthesia, if present at first, disappears to a great ex- tent, leaving only residua about the feet and hands. Paraesthe- 358 DISEASES OF THE NERVOUS SYSTEM. sise are common. In rare cases the patient suffers great pain in the arm and leg. This pain is generally of a burning character and very obstinate and distressing. Cramping pains in the legs and arms are common in the severer cases. During the first five weeks after the onset joint inflammations and bed-sores may attack the affected side. The temperature of the hemiplegic side is usually a very little higher than that of the sound side. ^ Vasomotor disturbances, sweating, skin eruptions, and in- creased growth of hair are some of the rarer symptoms. The mental condition is more or less affected. The patient becomes irritable, cries easily, and is in general more emotional. The memory is impaired, and the poAver of concentrating the attention and carrying on work is less. Sometimes a progressive mental deterioration sets in or insanity develops. The mental disturbance is greater in old people and depends somewhat on the size of the hemorrhage. Those forms which produce serious aphasia especially limit and lessen mental activity. Pathology and Morbid Anatomy. — Spontaneous intracranial hemorrhage is always due to the presence of diseased blood-ves- sels in the brain. This diseased condition consists of 1. A degenerative arteritis' which results in producing small aneurisms. 2. A fatty degeneration of the vessel walls. 3. Be- sides this, in most cases the larger blood-vessels are atheromatous. 1. The arteritis produces small or miliary aneurisms which affect only the smaller arteries, especially those of the central group. They may be fusiform or sacculated in shape ; they range in size from one-fifth to one millimetre (^^o to it i^^-) ^^ diameter. They are usually not very numerous, but there may be as many as a hundred in the brain. They are the results, not of inflam- mation, but of a degeneration which affects first an area in the internal coat; this causes local weakness and consequent dilata- tion ; secondarily there is a periarteritis. These aneurisms occur almost exclusively during the degenerative period of life. 2. Fatty degeneration of the walls of the small cerebral arteries occurs in purpura, scurvy, leucocythsemia, marasmic conditions. and post-infective states, especially in early life, and is the com- mon cause of liemorrhage at that time. 3. Atheroma affects the larger vessels only. It is indirectly a cause of hemorrhage by lessening the elasticity of the vessel wall. Atheroma is present in one-eighth to one-fifth the cases. Hyper- trophy of the heart is a factor in causing hemorrhage, and such hypertrophy exists in about forty per cent of cases. Emboli lodged in the cerebral arteries may cause hemorrhage by sud- denly stopping the arterial circulation and raising the blood pressure. Hemorrhages are found by far the oftenest (twenty per DISEASES OF THE BRAIN. 359 cent) in the caudate and lenticular nuclei and adjacent parts. The lenticular and lenticulo-striate branches of the middle cere- bral are oftenest affected ; next the branches of the anterior cere- bral to the caudate nucleus and the ventriculo-optic branches of the middle cerebral. The branches of the posterior cerebral break more rarely. The parts affected in hemorrhage, in order of frequency, are about as follows ; Caudate and lenticular nuclei. Meninges and cortex. Centrum ovale. Optic thalamus. Pons, cerebellum, medulla. 'Cortex hemorrhages are generally small and may be sub- arachnoid or may break through into the arachnoid cavity. Ven- tricular hemorrhages are almost always secondary to a rupture into the neighborhood of the basal ganglia. Pons hemorrhages occur usually in the median line. Cerebellar hemorrhages are oftenest due to rupture of the superior cerebellar artery. They usually cleave their way externally and break into the fourth ventricle. Dural hemorrhages are due to rupture of the menin- geal veins and arteries and of the vessels in newly organized clots. They lie in the arachnoid cavity and flatten the convolutions. The reparative changes after a hemorrhage take the following course: 1st. Coagulation of the blood, which in a few days be- gins to soften and become absorbed. 2d. Formation of a fibri- nous wall about the clot. This occurs from the seventh to the ninth day. 3d. Formation of a cyst with transparent fluid con- tents, and perhaps fibrous trabecul* running through it, twenti- eth to thirtieth day. 4th. Contraction of the cyst wall, which begins by the fortieth day. 5th. Secondary degenerations begin from the tenth to the fourteenth day. Physiologi/.— The blood pressure of the cerebral arteries is equal to about 150 mm. of mercury. The resistance or support furnished by the surrounding tissue is equal to about 10 mm. of mercury. Hence there is a special liability to rupture of intra- cranial vessels. The middle cerebrals are most often affected, because they are in the most direct line from the heart and are nearest to that organ. The pressure lessens as the arteries subdi- vide and get farther away from the heart (Mendel). The diagnosis must be made from alcoholic coma, uraemic coma, opium coma, epilepsy and hysteria, acute softening from embolism and thrombosis. From alcoholic coma the diagnosis is made by the odor of the breath, the incomplete coma, the equal pupils, the absence of low or unequal temperature. From uremic coma by the absence of albumin and casts in the 360 DISEASES OF THE NERVOUS SYSTEM. urine, though their presence does not surely indicate uraemia; by the unequal pupils, the temperature, the absence of hemi- plegia, and of the physiognomy peculiar to cases of chronic Bright's disease. From opium-poisoning by the history, the stomach contents, the presence of equal and contracted pupils, the slow respirations, the temperature, and the absence of paralysis. From epilepsy by the history of the onset with epileptic cry, the dilated and equal puj^ils, the biting of the tongue, the ab- sence of hemiplegia, the rather rapid return of consciousness. Hysterical attacks present little semblance to that of apo- plexy; hysterical hemiplegia is characterized by its fiaccidity, by its not involving the face, and by the presence of the anaes- thesia and other hysterical stigmata. In embolic softening the earlier age of the patient, the pres- ence of decided valvular heart disease, the parturient condition, the slighter degree and shorter duration of coma, the absence of serious disturbance of temperature, the onset first of paralysis and then of convulsive movements and coma — all lead to a pre- sumjjtion in favor of embolism. The presence, on the other hand, of a congested face, tense pulse, and throbbing carotids favors the existenf'e of a hemor- rhage. From thrombotic softening diagnosis is more difficult. The occurrence of prodromata, consisting of slight seizures quickly recovered from, the slighter degree of coma, the advanced age, hard atheromatous arteries, evidence of anaemia and asthenia, weak or fatty heart, the absence of stertorous respiration, flushed face, and unequal temperature not much lowered or raised, the sHght pupillary disturbance, and absence of convulsions point to thrombotic softening. Evidence of a lesion in the pons or cerebellum suggests hemorrhage, while evidence of lesion in the medulla points almost surely to softening. The chances in any case between the ages of thirty and fifty, if there is no heart disease, are six to one in favor of hemorrhage. Prognosis. — The majority of cases get over the first attack. They are very liable to have another within one to five years. The minority recover from this. Few survive a third attack. The prognosis of the attack itself depends on the severity of the coma and paralysis, the disturbance of temperature and of respiration, the evidence of rupture into the ventricles, the de- velopment of decubitus, the continuance of loss of control over the bowels and bladder. If profound coma continues four days there is little hope; if fever develops and continues steadily, or if there is initial sub- normal temperature, the prognosis is grave. DISEASES OF THE BRAIN. 3G1 If the patient passes the first week with Httle or no fever and consciousness has returned, the prognosis is good. The presence of renal disease and of alcoholism is bad. De- velopment of shght delirium which continues is unfavorable. Cerebellar and pons hemorrhages are very fatal, meningeal slightly less so. The prognosis of the chronic stage has been given under symptoms. Improvement continues rather rapidly for three months, then very slowly. Improvement may continue for one or two years. Complete recovery is very rare. The great danger after middle age is recurrence of the attack. Treatment of the Attack.— The patient should be laid in a hor- izontal position and kept quiet. Ice should be applied to the head and hot bottles at the feet. The feet and legs should be swathed in clothes wrung out in hot water containing mustard, a cupful to a pail of water. A laxative should be given, either one or two drops of croton oil or a quarter of a grain of elaterium. If there is evidence of intense cerebral congestion, the pulse being very full and hard and the heart beating strongly, bleeding eight to ten ounces is justifiable. Ordinarily it is better to give a drop of tincture of aconite every twenty minutes for two or three hours. Pressure on the carotid of the sound side, and even liga- ture of it, has been recommended, but there is no experience yet to justify it. Administration of bromide of sodium and enemata of ergot have been advised, but are of doubtful value. After the first twelve hours treatment must be symptomatic. Should de- lirium and other evidence of mental irritation appear, large blis- ters must be applied at the back of the neck and an elaterium purge given if the patient is not too weak. The use of iodide of potassium or mercury is not indicated unless the case is dis- tinctly syphilitic. The passage of a galvanic current through the brain cannot possibly do any good. Great care should now be taken that the patient does not develop pneumonia. The mouth and pharynx should be cleansed antiseptically, and the patient should not be allowed to remain in one position. If there is sufficient evidence of a meningeal or cortical clot, tre- phining should be seriously considered. At the end of three or four weeks the faradic battery may be used carefully on the affected limbs. A seance of fifteen minutes daily for four to six weeks should be given, then treatment should be suspended for a fortnight, to be begun again and kept up sys- tematically for a year if need be. Massage may be alternated with the electricity. When contractures develop the stabile gal- vanic current may be tried, though it does little good. Static sparks, however, are helpful : lukewarm baths should be tried ; 362 DISEASES OF THE NERVOUS SYSTEM. and measures used to produce liyperextension of the affected parts. Internally during this time the patient is to be given courses of iodide of iDotassiam, tonics, and laxatives if needed. The pa- tient should be made to live a quiet life, preferably in a warm, equable climate. The kidneys should be kept active and arterial tension low. For these purposes nitroglycerin should be given and at times small doses of chloral, and the diet should be simple and rather non-nitrogenous. Strychnine in very small doses (gr. YQo) sometimes helps the contractures; so also do the bromides and physostigma. Acute SoFTE^'ING of the Brain (Embolism, Thrombosis). Acute softening is a condition caused by the plugging of a blood-vessel with an embolus or thrombus, and is characterized ])y a sudden apoplectic seizure ; the symptoms eventually running a course like that of cerebral hemorrhage. Etiology. — Embolism occurs rather more often in women, thrombosis in men. Embolism is rare in children ; it occurs often, est between the ages of twenty and fifty, thrombosis between the ages of fifty and seventy. The most important predisposing factors in embolism are acute or recurrent endocarditis, infec- tious fevers, profound anaemia, pregnancy, and blood dyscrasl^e; in thrombosis, syphilitic, lead, or gout}' arteritis, fatty heart, and blood dyscrasise. The same causes which lead to the arterial dis- ease which produces cerebral hemorrhage also predispose to thrombosis ; though in the latter condition atheroma plaj^s the important part. Symptoms. — In embolism there are rarely any premonitory symptoms ; the onset is sudden ; it may begin with some con- vulsive twitchings, then follow hemiplegia and temporary loss of consciousness. Coma, however, is rarer than in hemorrhage, and if present is usually shorter. There is rarely vomiting, nor do we find the hard, pulsating arteries, flushed face, and severely stertorous breathing. The initial temperature changes are slight, but in a few days fever may develop. In thrombosis premonitory symptoms are frequent. In syphilitic cases there are headaches and cranial nerve palsies. In other cases vertigo, temporary aphasia, transient hemi- plegia, numbness of the hand and . foot, and drowsiness may be present. The onset is more gradual ; the hemiplegia slowly develops, taking several hours, perhaps, for its completion; meanwhile the patient gradually becomes comatose. The at- tack sometimes is rather sudden, with no loss of consciousness, and it may occur in sleep. The teujperature often has a DISEASES OF THE BRAIN. 363 slight initial fall, followed by a rise, just as in hemorrhage. In both embolism and thrombosis the hemiplegia tends to im- prove very much in a few days or weeks unless the vessel ob- literated is a large one. Embohsm is rather more apt to affect the left side of the brain, though the difference is not great. The middle cerebrals are most frequently affected (seventeen out of twenty-seven cases). Softenings affect the vertebrals, basilar, and posterior cerebral arteries more often relatively than do hem- orrhages ; then the initial symptoms may not present the char- acter of hemiplegia, but of a bulbar paralysis. Acute softening may kill within twenty-four hours, but, as a rule, the patient survives the onset, and if he dies it is not for several weeks. After the acute stage is over the patient passes into the chronic stage, which resembles in nearly all respects that of hemorrhage. After an acute softening, however, it is believed that there are more spastic symptoms and a. greater tendency to mobile spasm. In embolism, owing to the youth and freedom from arterial disease, the mind is less affected ; v.diile in thrombosis the contrary is the case. Pathology. — The embolic plug cuts off the blood supply from a certain area of brain tissue. In twenty-four hours this begins to soften. If the area is in the cortex it becomes red (red soft- ening); if in the white and less vascular i^art, it is usually white with a few red punctate spots. The red softening gradually be- comes yellow (yellow softening). The dead tissue softens and is absorbed, leaving a cicatrix or cyst. If the embolus contains in- fective microbes there may be a local encephalitis and abscess. In thrombosis there are usually evidences of extensive athe- roma or of syphilitic arteritis. In those instances in which the thrombosis is caused by the blood state and a weak heart, little arterial change occurs. Atheroma affects chiefly the internal carotids and the large arteries at the base, viz., the middle, an- terior, and posterior cerebrals and the basilar and vertebrals. Thrombosis with apoplexy occurs oftenest in the corpora striata and optic thalamus, next in the pons and medulla. Embolism almost always affects the great basal ganglia or some cortical branch of the anterior and middle cerebrals. The secondary changes after thrombosis resemble those after embolism; a thrombus, however, may lead to supplementary embolism through breaking off of a clot, and both conditions may cause a complicat- ing cerebral hemorrhage. The Diagnosis.— The important points have been gone over under the head of hemorrhage. They may be tabulated in part here. 364 DISEASES OF THE NERVOUS SYSTEM. Hemorrhage. Age, thirty to fifty. Hereditary history of arterial disease. Sudden onset, with coma and paralysis occurring together, the coma deepening. Initial and early rigidity. Very unequal pupils. Stertorous breathing and hard, rather slow pulse. Peculiar alternating conjugate deviation. Early rigidity. Peculiar disturbances of temperature, as described. Acute Softenixg. Earlier or later age. History of syphilis. Premonitory symptoms and more gradual onset, more transi- tory coma, or absence of coma. Initial convulsive movements. Presence of weak heart or endocarditis. Slight hemiplegia Avith anaesthesia. The puerperal state. Embolism is distinguished by the age, the presence of endo- carditis, of the puerperium, or infective fevers, and by the sud- den onset, with perhaps some convulsive movements. Thrombo- sis occurs oftener in the aged, and there are prodromata — a slower onset and evidence of arterial disease and a weak heart. The pi'ognosu- £is regards the attack is somewhat better than in hemorrhage as a rule. In embolism it is good as regards re- currence ; in thrombosis, bad. The mental condition is better in embolism ; usually Avorse in thrombosis. The recovery from at- tacks is more complete in acute softening. After the chronic stage is reached, however, the prognosis is about the same in all forms. The treatment of the attacks consists essentially in rest and such attention to the bowels, kidneys, and heart as may be indi- cated. In thrombosis it may be important to give heart stimu- lants and arterial depressants, and for this purpose I advise the use of alcohol, digitalis, or strophanthus with nitroglycerin. Iodide of potassium and mercury ought to be given if there is the slight- est suspicion of syphilis. Later it is well to give courses of the iodides and mercury and of strophanthus, nitroglycerin, strych- nine, and such tonics as may be indicated. The symptomatic treatment of the chronic stage is the same as in hemorrhage. DISEASES OF THE BRAIN. 365 Cerebral Palsies of Children— Hemiplegia, Double Hemiplegia or Diplegia, a^d Paraplegia. The brain palsies of early life show themselves in the form of . 1, hemiplegias; 2, diplegias or double hemiplegias, in which both sides of the body are involved; and, 3, paraplegias, in which the lower limbs are chiefly or entirely involved. In these palsies, as in the same troubles of adult life, the loss of motor power is always accompanied with a rigidity and with some contractures and exag- geration of reflexes, in this respect distinguishing these paralyses, from those of spinal origin. The seat of lesion in these cases is. in the hemispheres of the brain, and it is the upper motor seg- ment which is involved ; that is to say, that part of the motor tract w^hich extends from the brain cortex dov/n to the spinal cord as far as the anterior horns. The brain palsies of children are therefore disorders of the cortico-spinal segment, while the spinal palsies of children are disorders of the neuro-spinal seg- ment. Etiology, — The disease occurs rather oftener in males than in females, though the difference is slight. The vast majority occur in the first three years of life ; about one-third of them are con- genital. Injuries to the mother during the time of pregnancy, possibly diseases and emotional disturbances at this time, are factors in producing the congenital cases. Those cases that occur at the time of birth are due to tedious labor, the use of forceps, and other injuries at the time of parturition. After birth, the causes are those which lead to the production of intracranial hemorrhages, embolism, and thrombosis; these being injuries and the infectious fevers. Of the latter, pneumonia, whooping- cough, measles, and scarlet fever are the most prominent. Syph- ilis is a rare cause ; cerebro-spinal meningitis and epileptic con- vulsions are also occasional causes. Symptomatology. — The disorder in about one-fourth of the cases begins with a convulsion, which may be unilateral, but is usually general in character, and may last for several hours. At the same time a febrile process develops, and this continues for several days. When these acute symptoms have subsided, or be- fore this, it is noticed that the child is paralyzed upon one side, the paralysis involving the arm, leg, and face as in adult hemi- plegia, or perhaps involving both sides. This paralysis under- goes gradual improvement, the face recovering earliest and most, the leg next, and the arm least. As the child develops it is found that the paralyzed side fails to grow as fast as the other, and there may be half an inch to one or two inches of shortening in the arm or leg. The circumference of the limbs is less, the sur- 366 DISEASES OF THE NERVOUS SYSTEM. face someAvhat colder, and some vasomotor disturbance may be present. With tiie progress of the case a rigidity of the affected limbs develops : the heel becomes drawn up, so that there is talipes equino-varus or equino-valgus. The flexors of the forearm and of the wrist and fingers contract, as do also the adductors of the thighs. In general it will be found that there is a contraction of the flexors and adductors of the affected limbs. With this rigidity and the contractures there is an exaggeration of reflexes and clonus in most cases. In the disordered limbs the peculiar mobile spasms develop. These consist of athetoid, choreic, and ataxic movements, also sometimes tremors and associated Fig. 180. — r THETosis. Beginning in Childhood. movements. The choreic and athetoid movements are the most common (Fig. 180). Along with the development of these symj^toms it is noticed that there are disturbances in the mental condition of the child. It is usually backward in development, this backwardness rang- ing from simply a feeble-mindedness to complete idiocy. Taking all cases, there is about an equal division between feeble-minded- ness, imbecility, and idiocy (Sachs). Perhaps a little over one- fourth of the cases have a fair intelligence. There is usually slowness in learning to talk, and in a small i)roi)ortion of cases there is a decided aphasia. Such condition is rather more fre- quent with right hemiplegia than with left iiemi|>logia, though the rule is not an absolute one. In connection with the mental defect there may develop many of the peculiar moral traits as- DISEASES OF THE BRAIN. 367 sociated with idiocy and low degrees of intelligence. Epilepsy very frequently complicates the disease; nearly one-half of the cases suffer from this trouble. This epilepsy is in most cases general in character; in a few cases it takes the Jacksonian type, in a small number pe^/^ waZ alone is noted. Examination of this class of sufferers reveals, aside from the paralyses de- scribed, various evidences of defective development. These are known as stigmata of degeneration; though they cannot be classed strictly among such, since they are acquired stigmata in most cases, rather than marks which are the result of primary deficiency in development. These stigmata consist of a micro- cephalic or a macrocephalic skull, cranial and facial asymmetry, prognathism, imperfectly develoj^ed teeth, and a high palatal arch. It has been found that, as a rule, in cases of cerebral hemiplegias of childhood the patient eventually has a slight flat- tening of the skull on the side of the lesion (Fisher and Peterson). Finally, in a few cases there may be found defects in the special senses, such as imperfect hearing, deafness, deaf -mutism, and de- fects in vision such as hemianopsia, and perhaps imperfections in smell and taste. Anaesthesia is never observed. The symptoms in the cerebral palsies of children having passed the acute stage and having become somewhat ameliorated, enter into a chronic stage. This chronic stage begins within a few months after birth or after the onset of the disease. Ts^o groat change occurs in the paralyses as the child grows older until he reaches the time of puberty, though there is a slight improve- ment in most cases After the time of puberty, if the mental condition of the child is good, the physical symptoms are apt to improve considerably. Morbid Anatomy. — The primary changes that lead to the cere- bral i)alsies of children are- 1st, simj^le agenesis or lack of brain development, producing localized atrophy of the cerebrum and the condition known as porencephalus. True porencephalas is a condition in which, owing to a congenital defect in nutrition, a cavity or depression exists in the cerebral hemispheres, this cav- ity reaching generally into the lateral ventricle. True poren- cephalus is found in about one-fourth of the cases, tliough no definite statistics can be given, owing to the different interpreta- tions given to this term ; 2d, hemorrhage, which is probably the most frequent of the single causes; 3d, embolism; 4th, throm- bosis; 5th, meningoencephalitis and perhaps polioencephalitis; 6th, a diffuse cortical sclerosis. Many other terms are used to describe the pathological conditions found at the basis of the brain palsies of children; but the principal causes of all are un- doubtedly as has been described— hemorrhages, embolism and thrombosis, and a defective development or agenesis. It is prob- 368 DISEASES OF THE NERVOUS SYSTEM. able that in the heiiiiplegies the original lesion is generally a central hemorrhage, less often a meningeal hemorrhage. After this, iDrobably the most frequent condition is a porencephalus from some intrauterine accident which may have been defective nutrition causing ansemia and softening, or hemorrhage or throm- bosis. Polioencephalitis or inflammation of the cortex of the brain of the kind similar to poliomyelitis is alleged to be a cause in some cases by Strumpell, but this has not yet been proven. In double hemiplegias or diplegias of children the cause is in the Fig. 181.— Atrophied Brain with Sclerosis and a Cyst, from Infantile Cerebral Hemiplegia. Case of vast majority of cases a meningeal hemorrhage due to some in- jury or disturbance at the time of labor. In other cases of di- IDlegia the lesion is a double porencephalus, which may be either the result of an intrauterine hemorrhage or simply a defective development. In the paraplegias the lesion is probably very much the same as in the diplegias, that is to say, either a menin- geal hemorrhage or a true porencephalus. Occasionally a diffuse sclerosis has been found in these cases. Not infrequently, as the result of hemorrhages, there develop cysts which fill up the atro- phied areas of the brain (Fig. 181). It is difficult to present accu- rately and definitely the relations between the pathological DISEASES OF THE BRAIN. 369 change and the chnical result, but it may be shown with some degree of correctness in the following table • Original Lesion. Later Pathological Condition. Clinical Result. Hemorrhage. Embolism. Thrombosis. Agenesis. Atrophy. Lobar sclerosis. Cysts. Porencephaly. Microcephaly. Hemiplegia. Diplegia. Paraplegia. Sensory defects. Mental defects. Epilepsy, etc. Diplegia or Birth Palsies.— That form of the brain pal- sies of childhood characterized by double hemiplegias or di- plegias has certain special characters which lead to its being often classed apart. These diplegias in almost all cases are con- genital and are due either to injuries at the time of birth or to some disorders of intrauterine life. There may be convulsions or a prolonged state of asi^hyxia at the time of birth. After re- covery from this no special trouble is noticed with the child by the mother for some weeks or months, when it will be found that 't does not use its arms or legs. Other convulsions develop, and eventually the features of a double hemiplegia with mental im- pairment and epilepsy are observed (Figs. 182, 183). In these cases the mental defect is much more decided than in the hemiplegias ; indeed, few of these cases ever show any good amount of intelli- gence. Ej)ilepsy is extremely common. The anatomical lesion in the cases is, as already stated, either a meningeal hemorrhage which has pressed upon and injured the cortical motor areas in each hemisphere or it is a congenital porencephalic defect. Spastic Cerebral Paraplegia.— In a few cases the brain lesion is such that there results very little disturbance to the arms or face, and the paralysis is almost entirely confined to the low^er extremities. Such cases w^ere once described as spastic paraplegias of childhood and thought to be due to lesions in the spinal cord. There is little doubt, however, now that the pri- mary trouble is in all cases a bilateral lesion of the cerebral hemi- spheres with a descending degeneration affecting a portion of the lateral columns of the cord. In these cases there are rigidity and contractures, club foot, exaggerated reflexes and spasms of the flexors and the adductors, so that the child's legs cross each other and interfere in its feeble attempts at walking. Spastic para- plegia is usually, like diplegia, a birth palsy and due to the same causes. It seems also to be associated with defective intelligence to about the same degree as with diplegias. Epilepsy also is connnon with this type of the disease. Diagnosis.— The clinical diagnosis of cerebral palsies is to be made from the spinal palsies. The latter are distinguished by the 24 370 DISEASES OF THE NERVOUS SYSTEM. fact that ill the paralyses of spinal origin there is no rigidity or exaggeration of reflexes, and there are electrical degenerative reactions of the muscles and decided wasting of the limbs with shortening. The mode of onset in cerebral palsies and their dis- tribution in the form of hemiplegias in which the face is involved also indicate the seat of the lesion. The pathological diagnosis Fig. 182. Fig. 183. Figs. 182 and 183.— Cerebral Diplegia with Contractures and Talipes. Fig. 182 standing ; Fig. 183 suspended by arms. is bj' no means an easy one. Cerebral palsies occurring at the time of birth and accompanied at that time with general convul- sions or asphyxia may be considered to be due to meningeal hem- orrhage, especially if the delivery of the child has been brought about by the use of forceps or if the labor has been long and tedious. Diplegias and paraplegias which are congenital are probably due to true porencephalus, provided there was no diflBl- DISEASES OF THE BRAIN. 371 culty at the time of labor and no convulsions or other serious phenomena after it. Cerebral palsies occurring after birth in the first, second, or third year of life are apt to be due to hemor- rhage, and less often to embolism, or thrombosis. Hemiplegias developing after infectious fevers are likely to be due to hemor- hage. In diagnosticating the pathological lesion in such cases it must always be remembered that the hemorrhage is much more frequent than embolism, and that thrombosis as a factor has not yet been ve:y clearly established. Course and Prognosis.— In all types of the disease the course is chronic and perfect cure is hardly possible, although in the slighter forms of hemiplegia nearly all traces of the paralysis may be absent. In the hemiplegic form the patient often reaches adult life, and if his intelligence is not defective and he has no epilepsy, the motor trouble improves a great deal and he may live a long and useful life. If epilepsy and mental defect are present, there ensues eventually a further mental deterioration, and such cases rarely live much beyond the i^eriod of adoles- cence, or if they do they pass into the asylums for the idiotic and epileptic. The diplegic and paraplegic cases have a inuch worse prognosis both as to duration of life and as to improve- ment in symptoms. The degree of intelligence and the absence of epilepsy are the two factors wdiich measure the seriousness of these cases, as they do those of the hemiplegias. As regards the significance of individual symptoms, the post-hemiplegic move- ments have a bad import ; the presence of a microcephalic head or of decided marks of degeneration is unfavorable. Treatment. — The treatment, so far as the paralj'sis is con- cerned, is largely mechanical. The i^atient is benefited by occa- sional courses of electrical treatment which stimulate somewhat the nutrition and functions of the muscles. Massage and stretch- ing of the contract ured tendons and limbs also are helpful in my experience. The orthopedic surgeon is able to render valuable assistance by occasional overstretching of the contractured limbs and placing them in splints. Tenotomy may also be resorted to with advantage, as I have had occasion to see. The child should be encouraged above all, however, to use the limb as much as pos- sible. He should be taught gymnastic exercises ; running, walk- ing, and bicycle-riding are all measures wiiich give great help. When the child's intelligence is good and there is little or no epi- lepsy, a great deal can be expected in the way of improvement as the child grows older. So far as the epilepsy is concerned, it should be treated on the same principles as idiopathic epilepsy, except that great care should be had in the use of the bromides; a thorough test must be made in order to determine how much of this drug will sup- 372 DISEASES OF THE NERVOUS SYSTEM. press the fits, and then its use must be graduated in the future in accordance with the knowledge thus obtained. Tlie mental de- fects of the child can only be helped by proper training of the body and careful education of the mind. The question of oper- ative interference in these cases has of late excited much atten- tion. A priori it would not seem as though surgical interference could do good in relieving conditions in which there is destroyed or atrophic tissue. Still the subject must be dealt with em- pirically, and there have been some results which show that apparently a relief is obtained in a few cases by trephining the skull or by Lannelongue's operation of craniectomy. If there is no microcephalus, if the case is one of hemiplegia with imbecility and epilepsy, the surgeon should simply make an exploratory opening. If he then finds any evidences of compression from the presence of a cyst, this may be very cautiously opened. If there is microcephalus, the linear craniectomy is the operation which is indicated. This has been found to be a very serious surgical measure and should only be resorted to with great cau- tion. In all cases, in operating on children, it has been found that it is imperative that the operation be made as short as pos- sible, and that as little be done at any single operation as is con- sistent with the indications. CHAPTER XIX. DEGENERATIONS AND SCLEROSES. Degeneration of the brain tissue, as in the case of the cord tissue, leads to sclerosis. Destruction, necrosis, injuries from any cause, lead also to sclerosis. Sclerosis is sometimes a primary change due to a gradual proliferation and increase of connective tissue and neuroglia tissue. We have, therefore, in the brain primary degenerations and scleroses and secondary scleroses. The primary degenerations are bulbar palsy and ophthalmo- plegia externa, or, as these diseases are sometimes called, polio- encephalitis inferior and polioencephalitis superior; besides these are paralytic dementia, which is a diffuse cortical sclerosis, and disseminated sclerosis; and finally, underlying epilepsy we have, it is believed, a diffuse increase of neuroglia tissue which has been called a neuroglia sclerosis or a gliosis. Secondary scleroses are those which are the result of inflammations, hemorrhages, injuries, embolism, and thrombosis. A secondary sclerosis usu- ally affects certain special areas of the brain and is called a lobar sclerosis. Corresponding to these pathological changes we have certain clinical types of disease. Thus the diffuse cortical scle- roses cause what is known as paralytic dementia ; polioencephali- tis superior and inferior cause bulbar paralysis and ophthalmo- plegia; neuroglia sclerosis is perhaps at the basis of epilepsy and other degenerative disorders ; lobar sclerosis is the lesion in cases of cerebral palsies of children, such as hemiplegias, diplegias, and paraplegias, and many forms of inco-ordination, motor disturb- ance, and convulsive manifestations. Besides the terms that we have used here, there are in medi- cal literature frequently employed the expressions brain atrophy, hypertrophy, porencephaly, chronic cerebritis, tuberous scle- rosis, all of which terms are more or less synonymous with what we have already given and are superfluous to our nosology. There is possibly a primary chronic softening or degeneration of the brain, but if it exists is extremely rare, and occurring in advanced life is probably due to disturbances in the blood sup- ply. 374 DISEASES OF THE NERVOUS SYSTEM. MuiiTiPLE Sclerosis (Disseminated Sclerosis, Ixsular Sclerosis, Sclerosis ex Plaques Dissemixees). Multiple sclerosis is a chronic degenerative disease character- ized by the development of small patches of connective tissue throughout the brain and spinal cord, and by symptoms of paral- ysis, tremor, disturbances of speech and of the eye muscles, and by a number of other symptoms, very variable in character. In America the disease is, in the writer's experience, rare. The diagnosis, to be sure, is often made, but only two cases ver- ified by post mortems have been reported by American physi- cians. ^^ioZo^^.— Heredity is a predisposing cause in a small propor- tion of cases. The disease has been directly inherited; but generally the patient simply inherits a neuropathic constitution. The disease develops in the early part of adult life, oftenest be- tween the ages of thirty-five and forty-five, but it maj' occur in children, and it is probable that a considerable number of cases developing in adult life are cases in which the seeds of the disease were sown during adolesqence. The sexes are about equally affected, the preponderance being rather in favor of the female. The chief exciting cause of most cases is undoubtedly some infective fever, usually typhoid, diphtheria, small-pox, measles, or erysipelas. It has been known to follow an acute attack of hsemoglobinuria and perhaps of malaria. Myelitis and encephali- tis are said to have led to the subsequent development of multi- IDle sclerosis, but this is unlikely. Exposure to cold and wet and traumatisms, especially those which lead to the development of the traumatic neuroses so called, are sometimes the cause of the disease. In fine, acute infections and severe traumatisms involv- ing concussion, co-operating with a neuropathic nervous system, form the most important etiological factors. Syphilis is rarely a cause. Symptoms. — The disease probably has existed a long time be- fore very notable sj'mptoms develop. Among the first things which the patient observes is a weakness in the limbs, usually in an arm or leg ; this is soon accompanied with a tremor which is of a jerky, irregular character. The paralysis slowly extends and the patient becomes partially paraplegic or hemiplegic. He may have some ataxia with the paralysis. At the same time disturb- ances in vision occur, such as amblyopia, spots before the eyes, nystagmus, and diplopia. Defects in articulation develop ; the speech becoming slow and scanning, or " syllabic," as it is called. Attacks of vertigo or apoplectic or epileptic seizures occur. There may be some sensory symptoms, although these are usu- DEGENERATIONS AND SCLEROSES. 375 ally not marked or permanent. When present they consist of pains in the limbs, resembling those of locomotor ataxia, and anaesthesias variously distributed. Mental change is not infre- quent and is somewhat characteristic. The patient's mind is rather dull, but his temper is equable and placid. The memory may become weak ; very rarely insanity develops. The disease runs a very variable course, depending upon the seat of the multiple lesions. In typical forms these lesions are distributed throughout the brain and spinal cord, but chiefly in the brain axis, and consequently in these cases the progress of the symptoms is fairly uniform. We have referred to them in the brief outline of the disease ; they may be enumerated here again. 1st. Paralysis taking the form of hemiplegia, paraplegia, monoplegia, or some cranial nerve paralysis. 2d. A. jerky tremor, often called intention tremor. 3d. Spastic phenomena shown by exaggeration of knee jerks, clonus, and rigidity of limbs. 4th. Cerebral disturbances characterized by vertigo, headache, epi- leptiform and apoplectiform attacks, and the peculiar mental state referred to. 5th. Nystagmus and disorders of vision and of the optic nerve. 6th. Disorders of articulation or scanning speech. 7th and finally, an irregular and intermittent course to the disease. We will take up some of these symptoms now in detail. The l^aralysis is most frequently of the nature of a hemiplegia or paraplegia which is never complete, but rather in the shape of a simple weakness. This paresis is almost always accompanied with a spastic condition, so that there is exaggeration of reflexes and clonus. It is often also accompanied with an inco-ordination, but most frequently of all it is associated with the peculiar " in- tention tremor " referred to. This tremor is coarse in its charac- ter; it ceases when the limbs are at rest and is shown only when voluntary movements are attempted. Thus when the patient tries to raise a glass of water to his lips the jerky trenmlous movements increase so that the water is spilled before it reaches his mouth. The tremor affects the muscles of the neck some- times, so as to cause oscillation of the head ; and sometimes the muscles of the trunk, but rarely if ever the facial muscles. The nystagmus, which is another manifestation of the tremor of the disease, is usually lateral' and is present in about two-thirds of the cases. Eye palsies involving most often the sixth nerve occur in about one-sixth of the cases. The pupillary and ciliary mus- cles are rarely affected, and the Argyll-Robertson pupil is not found in the disease. The disturbance of articulation is very common, ranking in frequency with the nystagmus and tremor. In speaking the patient separates the words into distinct sylla- bles, or he may simply separate the words very distinctly from 376 DISEASES OF THE NERVOUS SYSTEM. each other. Sometimes words are dropped or imperfectly pro- nounced. The trouble seems to be due to inco-ordinate move- ments of the tongue and other muscles and organs concerned in articulation. The cutaneous disturbances of sensation are not very great. They occur in perhaps one-third of the cases, but are often temporary and are perhaps due to a superimposed hys- teria. Severe pain is not a common symptom, but it may exist in the form of neuralgias of the nerves of the limbs or in the shape of girdle pains. The anaesthesias are usually partial and involve only small areas of the limbs. There may be various parsesthesise affecting the paralyzed parts of the body. Of the nerves of special sense the eye is most frequently involved, and a study of its condition is most important. The paralyses of its muscles and consequent diplopia have been referred to. Tem- porary disturbance of vision is not uncommon. Such disturb- ances consist of constriction of the visual field, amblyopia, and scintillating scotomata. The fundus of the eye shows in some cases a slight degree of neuritis, and in the later stages a true atrophy may be present. One eye is usually more involved than the other, and one eye alone may be affected. The oi^hthalmo- scopic changes in the disc are said to be different from those found in locomotor ataxia and in the neuritis of brain tumors. Disorders of the visceral centres producing retention of urine, constipation, and trophic disturbances leading to oedema, skin eruption, arthritis, etc., are relatively rare and occur, if at all, in later stages of the disease. Aborted Types or " Forms frustes "' of Multiple Scle- rosis. — In some cases the nodules of sclerosis are so limited in number and so peculiarly jilaced that they give rise to very atypical fonns of the disease. Perhaps the most common one is that in which the disease takes the type of a progressive spastic paraplegia. The pati nt suffers from weakness of the lower limbs, accompanied with stiffness, cramps, exaggerated reflexes, and disturbances in the bladder and rectal functions. Anaes- thesias, pains, and the girdle symptom may develop. In addition to this, however, a close examination will show some evidence of disease of the optic nerves and perhaps disturbances of the eye muscles. The patient will have nystagmus, diplopia, or other visual disorders. There will also be some attacks of vertigo or of epileptoid convulsions. The combination of the eye symptoms with the progressive paraplegia will often reveal the true char- acter of the disease. A purely sjnnal form of multiple sclerosis has been described; it is probable, however, that multiple sclerosis never affects the spinal cord alone. A cerebral form of multiple sclerosis has also been described, but this usually runs a course very similar to DEGENERATIONS AND SCLEROSES. 377 that of the true cerebro-spinal malady, and it is unwise to at- tempt to make any special clinical distinction, Charcot divides the symptoms into cerebral and sj)inal, and includes under the cerebral the eye symptoms, apoplectic attacks, and speech dis- turbances; under the spinal symptoms, paralysis and tremor. Tremor, however, is often, if not usually, due to a cerebral lesion. Pathology. — Grayish nodules are found distributed through the brain and spinal cord. They vary in size from a millimetre to two or three centimetres in diameter (one- twenty-fifth to one Fig. 184. Fig. 185. Figs. 184 and 185.— Multiple Cerebro-Spinal Sclerosis (Charcot). inch). They are of firmer consistence than the surrounding brain substance, but are not quite so hard as ordinary connective tissue. They consist microscopically of fibrous tissue which does not seem to be connected with the walls of the blood-vessels as a rule. Very often the axis cylinders of nerves can be seen passing through the lesion. The nodules are found most frequently in the white matter of the brain, more especially in the pons, internal capsule, and centrum ovale (Figs. 184, 185). They rarely begin primarily in the gray matter, but may invade it secondarily. The roots of the peripheral, especially of the cranial, nerves occasionally con- 378 DISEASES OF THE NERVOUS SYSTEM. tain or are surrounded by these sclerotic masses. In the spinal cord they may extend up and down the gray and white matter for a considerable distance, or they may involve the whole cord at a certain level, turning it into a fibrous mass. The blood-vessels sur- rounding and in connection with these diseased areas show some evidences of thickening and increased vascularity, but no true inflammatory process. The primary pathological change in mul- tiple sclerosis is as yet unknown ; many things point to its start- ing originally from small emboli or thrombi which lead to minute softenings, with a secondary reparative and sclerotic process. The fact that the disease follows infective fevers makes such an origin of it seem probable. On the other hand, pathological anatomy does not yet bear out this view, and it is possible that m ^.^^Wf^ ••" Fig. 186.— Spinal Sclerosis, J, K, L, M, Sclerotic foci : A. anterior, B, posterior horn (BIoccl)- the disease begins by a primary degeneration affecting first the myelin sheaths of the nerve fibres, this being followed by a neu- roglia and connective-tissue proliferation which ends in the formation of the small islands of sclerosis. An important patho- logical peculiarity of the process is that while it destroys the myelin sheaths of the nerves, the axis cylinders remain intact for a long time, and consequently conduction of nerve impulses takes place imperfectly, directly through the nodular masses. Course and Buratioii.— The disease runs a very irregular course. Its prodromal stage is long and remissions of consider- able length occur. The disease may last from five to fifteen years, the average duration being five or six years. Death sometimes occurs from involvement of the nerves of the medulla, but more often from weakness and exhaustion or some intercurrent malady. DEGENERATIONS AND SCLEROSES. 379 Diagnosis.— The diagnosis in typical cases is not very difficult ; but as, on the other hand, typical cases are not common, the disease has always to be studied with great care before certainty can be reached. The diagnosis is based upon the slow develop- ment of the disease, with attacks of vertigo, weakness, and un- certainty in gait; upon the paralysis of the extremities with intention tremor, ataxia, rigidity, and contractures; upon the disturbances of vision, nystagmus, and the speech troubles. The presence of headache, attacks of vertigo, apoplectiform attacks, and the peculiar mental condition often furnish help. The age of the patient and the cause should also be taken into consider- ation. The disease must be distinguished from Friedreich's ataxia, spastic spinal paralysis, locomotor ataxia, dementia para- lytica, bulbar paralysis, paralysis agitans, chronic meningitis, and hysteria. The points already given and those furnished under the heads of these different diseases must be utilized in making these distinctions. The method of exclusion may be used with advantage in reaching the diagnosis of this protean malady. Prognosis. — The prognosis, while not favorable as regards the ultimate cure, is somewhat favorable as regards the remission and improvement, and the disease on the whole is not so severe as is locomotor ataxia or the other degenerative disorders. Treatment.— In the treatment the same measures recom- mended for other degenerative diseases of the nervous system must be employed. Hygienic aieasures, electricity, and hydro- therapy have some therapeutic value. Internally the use of large doses of iodide of potassium, the hypodermic injection of arsenic, the administration of nitrate of silver and of quinine and other tonics are advised. A very regular, systematic, and quiet mode of life, combined with the use of iodide of potassium and bichloride of mercury, has produced the best results in my experience, even in cases which gave no history of syphilitic in- fection. Hypertrophy and Atrophy of the Brain. These are both terms which can be dropped from neurological nomenclature as representing distinct disorders. Hypertrophy of the brain has been described as a disease occurrmg m child- hood, developing either congenitally or in association with rick- ets. It has been said to produce much the same symptoms ob- jectively as hydrocephalus. There is not sufficient pathological evidence to justify us in saying that the hypertrophy is really a hypertrophy of the brain, rather than a chronic inflammation or gliomatosis or some other tumor formation. Atrophy of the brain may be either total or partial. When total, that is, involving the whole of the encephalon, it is con- genital and is described under the term microcephaly. A slight 380 DISEASES OF THE NERVOUS SYSTEM. decree of general atrophy occurs during senility and in the later stages of chronic insanity. Partial brain atrophy is either con- genital or acquired. When congenital it is due to some intra- uterine inflammation, vascular obstruction, or aphasia ; and when acquired it is due to some of the numerous causes which have been described under the head of infantile and birth palsies. It will be seen that brain atrophy does not have any place as a distinct disease. CHAPTER XX. TUMORS OF THE BRAIN.-SYPHILIS. The kinds of tumor found in the brain are tubercle, syph- iloma, glioma, and sarcoma, which are the common forms; myxoma, carcinoma, fibroma, osteoma, cholesteatoma, lipoma, psammoma, neuroma, vascular tumors including aneurisms, echinococcus, and cysticercus. In fact, all forms of new growths are found in the brain ; but the infectious granulomata, tubercle, and gumma and the sarcomatous type of tumors are the most common. As compared with other organic diseases of the cen- tral nervous system, brain tumors are rare. Etiology. — Brain tumors affect males oftener than females, the ratio being about as two to one (644 : 320). Sarcomata alone seem to affect females about as often as males. Brain tumors occur with about equal frequency throughout all ages of life up to about fifty ; one-third occur under the age of twenty (Gowers). During childhood tumors are about equally distributed through- out all ages (Starr). One-half of all the tumors of childhood are tubercular; after this come gliomata and sarcomata. The gumma, glioma, and sarcoma begin to be more frequent after the age of twenty. Sarcoma and especially cancer occur in the mid- dle and later ages of life; but brain tumors of any kind are ex- tremely rare after the age of sixty. To sum up in tabular form, the relative frequency of the dif- ferent kinds of tumors with regard to age is shown in the follow- ing: Childhood, .... tubercle, parasites. Early life, .... gumma, glioma, parasites. Early and middle life, . . sarcoma, glioma, and gumma. Middle and late life, . . sarcoma, gumma, cancer. Heredity has a slight influence in predisposing to brain tumors. Blows on the head and other forms of injury to the cranium are exciting causes in a small proportion of cases. fSymptoms.— The symptoms of brain tumors vary extremely in accordance with the location, the kind of tumor, the rapidity of growth, and the age of the patient. The general course of a 382 DISEASES OF THE NERVOUS SYSTEM. case of brain tumor in an adult is somewhat as follo\vs The patient first notices a headache which is very intense and persist- ent and which has exacerbations of frightful severity. With the headache or between the attacks vomiting occurs, which is often not accompanied with any nausea. Sensations of vertigo, an- noying parsesthesise, and convulsive movements affecting one or more extremities develop, and there may even be general con- vulsions. The patient finds that his eyesight is weak and pro- gressively deteriorates. The mind becomes more or less dis- turbed, the mental processes are dull and slow, a feeling of hebetude and incapacity to attempt any mental exertion is present. As the disease progresses the intense pains and vomit- ing produce weakness and emaciation. Paralyses of various kinds develop. Blindness may ensue. Convulsions of a local or general character become more frequent, and finally the patient becomes bed-ridden and helpless. The course of the disease is not a steady one, there being often slight remissions, or there may be periods when progress seems to be arrested. After a period of time varying from one to four or five years death occurs from exhaustion or some intercurrent malady. The symptoms thus very briefly outlined are divided into gen- eral and focal. The general symptoms are at first those of cere- bral irritation and of headache, vertigo, and vomiting, optic neu- ritis, convulsions, disturbances of speech, and hebetude. Head- ache occurs in from one-half to two-thirds of the cases ; it is very severe and the pains are of a bo.'ing or lancinating character ; they are so horrible that they often lead the patient to think of suicide. The pains are sometimes periodical, occurring every night or every other day, and suggest by their periodicity a mala- rial character. They are located sometimes in the brow or in the occiput, while sometimes they are diffused all over the head ; they are rather more frequent than otherwise in the neighbor- hood of the tumor. They are more frequent with cerebellar tumors than with those located anywhere else. They are also frequent with tumors of the mid-brain and of the cerebral hemi- spheres. They are less frequent when situated in the peduncles and at the base of the brain. The' pains are due to the increased intracranial pressure and to irritation of the membranes of the brain by the encroachment upon them of the new growth. Head- ache occurs in about the same proportion in children and adults, and it does not seem to bear much relation to the kind of tumor, although the pains are generally less with the gliomata, and they are more frequent with rapidly growing tumors whatever their character. With the pains there is often a local tenderness of the scalp and cranium which may be elicited by percussion, and TUMORS OF THE BRAIN. 383 in most cases there is greater tenderness in that part of the cra- nium lying over the tumor. Vomiting is a symptom which is ahnost as frequent as head- ache. The vomiting is often of a projectile character and not accompanied with much nausea. Vomiting occurs, as does headache, more frequently with cerebellar tumors. It is asso- ciated with rapidly growing tumors such as syphilitic or tuber- cular neoplasms. Vertigo is a general symptom which occurs in from one-third to one-half of the cases. The vertigo may be slight, such as is often felt from ordinary causes. Occasionally it is very severe and accompanied with forced movements. The severer forms and those associated with forced movements occur with tumors of the cerebellum and the parts closely con- nected with it. Optic neuritis is one of the most frequent and important of all the general symptoms of brain tumor; it occurs at some period of the disease in at least four-fifths of the cases, more frequently in cerebellar tumors and in those of the mid- brain and great basal ganglia. It is rare in tumors of the me- dulla. It is less frequent and marked in the slow-growing tumors. The neuritis may run a somewhat rapid course and then improve a great deal or even for a time disappear; but ordinarily the course is progressive and it ends eventually in an atrophy of the optic nerve. Hence the examination of the eyes in brain tumors should be made a number of times in order to note the progress of the trouble. Primary atrophy of the optic nerve does not occur in brain tumors. The inflammation almost al- ways affects both nerves, but it may begin with one and subse- quently affect the other. The cause of optic neuritis in brain tumors has been the subject of a great deal of discussion and theorizing. There are doubtless different factors entering into the mechanism of its production in different cases, but accepting the modern doctrines of inflammation, we must believe that the most probable and most essential cause is an irritation of the nerve fibres by the products of the growth of the tumor which infiltrate into the sheaths of the optic nerves. There are pecul- iar mechanical conditions which tend to hold these products within the sheaths and thus enable them to act more energet- ically as irritants. Simple mechanical processes alone— the ten- sion and pressure— would hardly explain the presence of a genu- ine inflammation. Mental defects are almost always present in tumors of the brain. These defects consist in a slowness of the mental pro- cesses, a condition of hebetude, a tendency to attacks of somno- lence, and sometimes a peculiar childishness and silliness or pecul- iar mental irritability. The memory is also usually someAvhat weakened and the power of attention lessened. Such psychical 3S4 DISEASES OF THE NERVOUS SYSTEM. defects are more frequent with tumors of the fore-brain and more frequent also witli large tumors. General convulsions occur in about one-fourth of the cases and more frequently when the tumors are situated in the cerebral hemispheres and cortex. There may be also apoplectiform attacks, from which the patient recovers in the course of a few days or weeks. More rarely there is a genuine apoplexy from the bursting of a blood-vessel in the neighborhood of the tumor. The speech disturbances are most marked in tumors which affect the pons and medulla and the origin of the cranial nerves. Such siDcech disturbances, when characteristic, are shown by a confluent articulation, that is to say, the patient runs the sylla- bles together. The cranial temperature in brain tumors is in most cases somewhat raised as compared with the normal (Gray, Mills, and Lloyd). The elevation may be several degrees above the normal. The normal average scalj) temperatures (Gray) are from 92^ to 94.5° F., being somewhat higher over the frontal and parietal than over the occipital regions. In brain tumors the temperature has been found raised to 95°, 96°, and 98". The value of thermometric observations, however, in the symptomatology of brain tumors is somewhat doubtful, owing to the variability in the normal tem- perature and the difficulty of getting accurate records. Focal Symptoms. — The symptoms of brain tumor are pro- duced in part by the irritation and pressure, in part by destruc- tion of the normal tissues. The sjauptoms are also modified by variations in the vascularity of the tumors, and perhaps to some extent by direct irritation from products secreted by the tumor cells. Having by a study of general symptoms arrived at a fairly certain diagnosis as to the presence of a tumor, it is necessary to corroborate the diagnosis and to localize the lesion by an exam- ination of the symptoms which are the result of irritation or destruction of certain particular parts of the brain; these are called the focal symptoms. For purposes of special or local diag- nosis we divide the brain into the following parts or areas (Knapp) : 1. The prsefrontal, which includes all that part lying in front of a line that extends fj'om the upper end of the ascending branch of the fissure of Sylvius directly up at right angles to a horizontal line between the frontal and occipital poles of the brain (see Fig. 187). This region includes probably centres for the move- ment of the head and eyes, but it is chiefly concerned with the higher intellectual processes ; its under surface lies on the orbital plate of the frontal bone and upoh the right olfactory lobes. 2. The central region, which is bounded in front by the vertical line just described, behind by a line passing down from the an- terior end of the parietal fissure to the fissure of Sylvius, and TUMORS OF THE BRAIN. 385 above by a line that bounds posteriorly the post-central convo- lution. 3. The parietal lobe. 4. The occipital lobe. 5. The tem- poral or temporo-sphenoidal area. G. The corpus callosum. 7. The great basal ganglia and capsules. 8. The corpora quadri- gemina, deep marrow, and pineal gland. 9. The crura cerebri. 10. The pons and medulla. 11. The cerebellum. 12. The basal surface of the brain. The boundaries of most of these areas are indicated better by the figure than by a description. They correspond to some extent with the cerebral lobes, but not en- tirely so, since the frontal and parietal lobe divide between them the central area. 1. Tumors of the prefrontal area. Tumors in this area often show no particular localizing symptoms, and this part of the brain 25 386 DISEASES OF THE NERVOUS SYSTEM. is consequently put down as a latent one ; nevertheless, in a grood proportion of cases tumors here produce peculiar mental disturb- ances that, taken in conjunction with the general symptoms, enable us to make a local diagnosis. The symptoms are pecul- iar mental hebetude, childishness, irritability, often a kind of, silliness and emotional weakx^ess, a tendency to laugh and cry and to get angry at trifling causes. The entire character and temperament of the man are sometimes changed. Besides this, owing to implication of the olfactory nerve, there may be loss of the sense of smell on one or both sides ; implication of the optic nerves will cause hemianopsia and optic neuritis. If the tumor involves the orbit there will be paralyses of the ocular muscles and protrusion of the globe of the eye. If the tumor grows back- ward there is gradual invasion of motor centres with irritation, showing itself by spasms, convulsions, and later by paralyses. 2. Tumors of the central region. It is in this area that we are often able to make the closest and most accurate diagnosis of the localization of new growths, owing to their involvement of the different motor centres. Through this involvement these centres are at first irritated, with the result of producing local spasms or Jacksonian epilepsy. Such spasms are often preceded by sensory symiDtoms or aurse. As the tumor grows the area of involve- ment becomes larger, spasms become more diffused, and general convulsions may finally appear, with hemiplegia. The motor dis- turbances are not infrequently accompanied with sensory dis- orders. These may be simply feelings of numbness or prickling which either are permanent or simply precede spasms, or there may be hemiansesthesia of a moderate degree to pain, touch, and temperature. The muscular sense also may be somewhat involved. In case of slight sensory involvement the capacity for localizing sensations seems to be most implicated. Besides the symptoms mentioned, there may also be motor aphasia and agraphia. The exact localization must be worked out with the help of the figures and descriptions given under anatomy. 3. Tumors of the parietal area. The symptoms pi-oduced by tumors m this area may be very slight. The most characteristic are disturbances of muscular sense which occur when the supra- marginal gyrus is affected, and word blindness Avhich occurs when the angular gyrus and inferior lobule are affected. When the tumor is higher up near the longitudinal fissure, the muscles of the lower limbs may be involved, and if the tumor encroaches upon the central area spasms and paralyses of various muscular groups ensue. The cortical representation of the third nerve is thought to be in the neighborhood of the angular gyrus, and some cases have been reported in which paralysis of this nerve resulted from tumors in that area. TUMORS OF THE BRAIN. 387 4. Occipital lobes. Tumors in this region, if situated in the cuneus and first occipital convolution, produce homonymous hemianopsia. If the tumor involves the other parts of the occi- jpital lobe and the cuneus is not seriously involved, there may be a condition known as soul blindness or incapacity to understand the nature of the things which one sees. If the tumor extends up chiefly toward the angular gyrus, there may be word blind- ness, along with some hemianopsia. If the tumor extends farther forward into the parietal lobe, there may be hemiansesthesia, hemiataxia, and perhaps a little hemiplegia owing to involvement of the fibres of the internal capsule. 5. Temporal area. The temporal or temporo-sphenoidal area on the right side is very nearly a latent one. On the left side tumors involving the posterior part of the first and upper poste- rior part of the second temporal convolution produce word deaf- ness. Tumors in either lobe when large and extending well down toward the base may produce attacks of vertigo or forced movements, owing probably to irritation of the internal ear. Tumors that involve the hippocampal convolution and the uncus may produce perhaps some disturbances in the senses of smell and taste. 6. Tumors of the corpus callosum. Tumors situated in this area are very rare. Their symptoms have been thought to be somewhat characteristic ; but in the writer's experience they cor- respond closely with tumors situated in the third ventricle and lateral ventricles of the brain; in other words, tumors which, beginning in the central parts of the brain, gradually extend outward toward the periphery. The symptoms credited to tu- mors of the corpus callosum are, first, the general symptoms of brain tumor, to which there are superadded a gradually de- veloping hemiplegia with later a paraplegia. At the same time there is a great deal of mental dulness, stupidity, and drowsiness; the patient often sits for hours mute, refusing to speak, or lies in a half-somnolent condition. There are no paralyses of the oculo- motor nerves or of the other cranial nerves. There is no anaes- thesia. The disease gradually jDrogresses and the patient dies in coma. 7. Tumors of the great basal ganglia and the capsule (the optico-striate region). The general symptoms of tumors of this region resemble in many respects those of tumors of the corpus callosum. The stupidity, however, may be less marked. There is usually a progressive hemiplegia which may be accompanied with anaesthesia and sometimes with choreic movements, if the tumor involves the optic thalamus and adjacent part of the cap- sule. Tumors of the caudate nucleus alone and of the lenticular nucleus alone seem to give rise to no special symptoms, and these 388 DISEASES OF THE NERVOUS SYSTEM. regions are regarded as latent. Tumors of the anterior three- fourths of the optic thalamus alone may cause no sjieeial symp- toms, but in some cases there occur peculiar choreic or athetoid movements. Tliese, however, are probably due to irritation of the fibres of the internal capsule. If the tumor involves the posterior part of the optic thalamus and adjacent areas, there will be a hemianopsia, which may be distinguished from the hemianopsia due to lesions in the occipital lobe by the presence of the hemiopic pupillary reaction, that is to say, a ray of light thrown in upon the insensitive part of the retina will not pro- duce a reflex contraction of the pu^Dil. 8. Tumors of the corpora quadrigemina, deep marrow, and pineal gland. The characteristic symptoms, as shown by ]N"oth- nagel, of tumors of this region are inco-ordination, forced move- ments, and oculo-motor palsies. Together with these there may be hemianopsia or blindness due to destruction of the primary optic centres. It is possible that some degree of deafness or hemi-deafness may be produced by the involvement of the pos- terior tubercles of the corpora quadrigemina. 9. Tumors of the crus. Tumors of the crura cerebri are ex- tremely rare. When present, they cause hemiplegia and i^er- haps a hemianaesthesia, with paralysis of the third nerve upon the same side as the lesion ; in other words, a crossed paralysis. 10. Tumors of the pons and medulla. Tumors in this area necessarily produce very varying symptoms in accordance with their size and location. If the tumor is in the pons it will cause, if situated high up, a palsy of the third nerve upon one side and hemiplegia on the opposite side. If lower down there may be a palsy of the fifth nerve on one side and hemiplegia on the other side. If the tumor is extensive it may pi'oduce not only a hemi- plegia, but a hemianaesthesia. If situated somewhat superficially and on the lateral edge of the pons involving the peduncles, there will be forced movements of the body, either toward or from the seat of the lesion. If the tumor is in the medulla it will produce hemiplegia and hemianaesthesia, with paralysis of the hypoglossal nerve or perhaps some other cranial nerves upon the same side. If large and involving both sides of the medulla, there may be the general symptoms of a progressive bulbar paralysis. One peculiarity of tumors situated in the pons is that they some- times produce a conjugate deviation of the eyes which is away from the side of the lesion. In this respect the symptoms differ from conjugate deviation produced by lesion in the cerebral hemispheres where the head and eyes are turned toward the side of the lesion. 11. The general symptoms of tumors of the cerebellum are, as we have already said, more pronounced than those of tumors of TUMORS OF THE BRAIN. 389 other regions; we more frequently have headache, vomiting, ver- tigo, and optic neuritis from neoplasms here. If the tumor is situated in the lateral lobes of the cerebellum, no localizing symptoms develop until the tumor becomes very large so that it presses ujion the medulla or other adjacent regions. When the tumor is m the middle lobe a peculiar ataxia develops, known as cerebellar ataxia. The gait of the jDatient is a reeling one like that of a drunken man, or in Avalking he takes short steps and spreads his legs as if in fear of falling. This has been called the titubating gait. Besides this, severe forced movements may occur which usually throw him sideways or perhaps forward, very rarely backward. Secondary symptoms from pressure on the medulla often develop in tumors of the middle lobe; such symp- toms being glycosuria and disturbance of the functions of the cranial nerves. Late in the disease hemiplegia and paraplegia and bulbar symptoms may develop from extreme pressure. There may be also hydrocephalus due to pressure on the veins of Gralen and obstruction of the return flow of blood from the cen- tral arteries of the brain. 12. Tumors of the base of the brain. Tumors situated in the anterior fossa produce symptoms very much like those described under the head of tumors of the j^raefrontal area, but there is necessarily destruction of the olfactory lobe and there is more apt to be involvement of the optic and oculo-motor nerves and of the tissues of the orbit. Tumors of the middle fossa. Tumors sometimes involve the hypophysis. Such condition has been found in cases of acro- megaly, and it has been suggested that the tumor of the hypo- physis is the cause of the disease referred to ; but such cannot be the case, since a number of tumors of this region have been de- scribed in which none of the symptoms of acromegaly were pres- ent. Tumors of this region and of the interpeduncular space produce symptoms such as would naturally result from pressure on the optic chiasm, and it is mainly the early presence of optic neuritis and of peculiar forms of hemianopsia which differentiates lesions in this area from those in the anterior fossa. Multiple tumors. About one-seventh of all brain tumors are multiple. Hence in making a diagnosis of the localization of tumors this fact nmst be borne in mind. The tumors which are most frequently multiple are tubercle, cancer, and melanotic growths. P«Y7?o/o^^//.— Tubercle is a form of tumor found oftenest in children and is altogether the most frequent of brain tumors. It is more often located in the cerebellum, but may appear in the pons or other parts of the brain. It may be a single or, as it is then called, a solitary tubercle, or there may be a multiple 390 DISEASES OF THE NERVOUS SYSTEM. growth. The tumor is hregularly round in shape and varies in diameter from one and a half to two inches. It has a grayish- yellow appearance externally; internally, a yellowish or cheesy look. It is not vascular, but is often surrounded by softened or inflamed tissue. There may be an associated meningitis. The tumors, when solitary, usually start from the central parts of the brain, but they also develop on the meninges of the convexity, particularly in the parietal region, and sometimes they develop also at the base. Tubercle always arises from infection by the tubercle bacilli which are carried by the blood to the brain. The tumors develop usually from some infectious focus, starting in a blood-vessel of the pia mater. Microscopically the tumor shows the ordinary appearances of tuberculous growths. It con- tains in its periphery many round cells, nuclei, and giant cells. In the centre there is usually an amorphous substance, the prod- uct of degeneration and the breaking down of the ordinary sub- stance of the tumor. The characteristics of the growth are the presence of the round cells and giant cells, the caseation and soft- ening of the centre, and the absence of vascularization, with the presence of the bacilli. Syphiloma or gumma. 'Gummatous tumors of the brain are usually associated with syphilitic meningitis or some other form of cerebral syphilis such as endarteritis and perhaps inflammation of the cranial nerve roots. Syphilitic growths are usually found upon the brain surface, oftenest on the base, next upon the con- vexity of the frontal and central convolutions. The process ap. pears either in the form of a somewdiat distinct tumor or in the form of an irregular thickened exudate lying upon the surface of the brain and forming what is called gummy meningitis. The gummata uiay attain great size. They start usually from the pia mater and are due, as in the case of tubercle, to the irritative action of some infective organism. The gumma is irregular in shape ; it has a somewhat thick grayish periphery and often a yellowish centre, the appearances differing w'ith the age of the tumor. Microscopically it is found to consist of small round cells and spindle cells with various broken-down nerve-tissue elements. It presents in the interior the evidence of cheesy degeneration, somew^hat like that in tubercle, but less marked. There is a pecul- iar development of fibrous tissue in the syphilitic growths which distinguishes them somewhat. Besides this, the blood-vessels are numerous in the periphery and' show evidences of endarteritis and periarteritis. The distinctions between gumma and tu- bercle are the less amount of cheesy degeneration in the centre of the former, its more irregular appearance, the presence of arteritis and vascularization, the absence of giant cells and of tubercle bacilli. TUMORS OF THE BRAIN. 31)1 Actinomycosis is a form of infectious tumor which sometimes extends from the face and neck into the brain, leading to inflam- matory processes, however, rather than true tumors. No other neoplasms of infections origin attack the brain unless glioma be found to be of that nature. Glioma may occur in any part of the brain, but is most fre- quently found in the cerebrum. It is the only tumor which is peculiar to the nervous centre, being developed from the neu- roglia tissue which forms the supporting structure of these centres. Glioma originates in the white matter of the nerve centre and not from the membranes or fibrous structures. It may grow to a very large size and is the form of brain tumor which becomes the largest. Gliomatous tumors measure from three to eight or more centimetres in diameter. In appearance the glioma can be scarcely distinguished from the brain substance itself, but usually looks like either pale or congested gray matter, or it may have a yellowish or gelatinous a^Dpearance. The tumor is very vascular and it may show the results of hemorrhages. The cen- tral part sometimes breaks down, forming cavities or cysts. The tumor may grow very rapidly, infiltrating the normal tissue. In those cases there is hardly any definite boundary between the tumor and the normal tissue. In other cases the tumor grows slowly, but rarely if ever becomes encapsuled. Microscopically it is found to consist of small cells with delicate fibrous prolonga- tions, these being the glia cells. The tumor is very vascular and its whole appearance is suggestive of an inflammatory pro- cess rather than a new growth ; the inflammatory process being one in which the neuroglia tissue reacts to the inflammatory irri- tant. Gliomata may undergo certain changes, e.g., a mucous de- generation of the cells takes place, forming a myxo-glioma. When there is with the neuroglia-cell i^roliferation a rich proliferation of round cells from the connective tissue it is called a glio-sar- coma. When the tumor is situated near the surface, involves the membranes, and grows slowly, with an increase in fibrous tissue, it is called a fibro-giioma. When the gliomatous growth is very firm and hard, the fibrous portion of the glia tissue predominates ; it constitutes a nodule such as is found in multiple sclerosis, and these hard gliomata are sometimes called neuro-gliomata. Sarcoma. The sarcoma and its various modifications form perhaps the most important and almost the most frequent of the brain tumors. The sarcoma is a tumor of connective-tissue origin ; it develops, therefore, from the brain membranes or from the sheaths of the blood-vessels. Sarcomas may be single or multi- ple. They may be of all shapes and they grow to very varying sizes. They often develop a capsule. They may be either pri- mary or secondary. Their growth is often j-apid. They are 392 DISEASES OF THE NERVOUS SYSTEM. white or grayish in appearance or may be somewhat yellowish, dependent on the iDredominance of the different kinds of cells and blood-vessels. Microscopically they are made up of small round cells, spindle cells, and other cells of various sizes and forms. They contain often considerable fibrous tissue. They contain blood-vessels, but are not richly vascular. The essential characteristic of the sarcoma is the rich development of round cells and spindle cells ; in other words, its rich cellular contents. Sarcomata are peculiar in undergoing many modifications • thus sometimes fibrous tissue develops largely and the tumor is called a fibro-sarcoma ; sometimes the tumor undergoes mucous degen-' eration and is called a myxo-sarcoma. There may be a breaking down of the centre with the formation of cysts. There may be a development of pigment. Xot infrequently a sarcomatous pro- cess invades a glioma and we hav^e a mixture of a sarcoma and glioma. Sarcomatous tumors sometimes have an alveolar struc- ture. These tumors contain endothelial cells derived from the lymphatics and are called endothelioma. When sarcomata de- velop from the dura mater and are slow in growth there may be calcareous deposits in them and they are called psammomata. The fibroma is a very ra^'e brain tumor, unless the pachionian bodies, when enlarged and hardened, may be so considered. Osteoma is not x^articularly rare, developing in the form of bony plates in the dura, falx, or tentorium. Osteomata in the brain substance are merely pathological curiosities. Enchondromata, lipomata, and angiomata are rare and have no practical importance. Occasionally neuromata or false neuromata are found devel- oping on the roots of the cranial nerves. Cancer is relatively a very rare affection of the brain, especially as a primary development. It usually arises from the membranes of the brain. Cancer is not infrequently multiiDle and is usually of the soft or colloid character. Parasitic growths. Parasitic tumors are extremelj^ rare in this country. The only forms which are found are the echino- coccus and the cysticercus cellulosse. The echinococcus produces hydatid cysts which may be large or small, few or many, and are usually all upon the surface of the brain. They are much rarer than the cysticerci. These form cysts which are usually multi- ple, slow in growth, lie upon the surface of the brain or in the ventricles, are encapsuled, and show no symptoms (Fig. 188). Aneurisms are anatomically tumors ; but clinically they pre- sent some special symptoms and hence are described separately. Diagnosis. — It is necessary first to make the diagnosis of the presence of the tumor, next of its location, and finally of its nature. The existence of a brain tumor is determined by the TUMORS OF THE BRAIN. 393 presence of the characteristic general symptoms— headache, vom- iting, vertigo, optic neuritis, mental disturbances, and progres- sive course. The physician must bear in mind the possibilities of meningitis, abscess, lead-poisoning, hysteria, and paretic de- mentia. Ver}'' often a localized basilar meningitis of syphilitic or tubercular origin simulates closely the presence of a tumor. Be- sides the general points referred to, in estimating the probabili- ties of the existence of a tumor we must bear in mind the age of the fjatient and the existence of a tuberculous or syphilitic his- tory, the history of an injury, of local tenderness, and of rise of cranial surface temperature, and the presence of some new growth Fig. 188.— Echinococcus Cyst of the Third Ventricle. in other parts of the body, particularly about the neck or thorax or in the lungs. The diagnosis of the location of the tumor is based upon the rules already given in regard to local diagnosis. The diagnosis of the nature of the tumor can often be made and should be at- tempted. In children, for example, the chances of the tumor being tubercular are very great, particularly if there is a scrofu- lous diathesis or tubercular disease elsewhere. Syphilitic tumors of the brain are almost always accompanied Avith or preceded by manifestations of external syphilis. Gliomatous tumors occur in childhood and early life. They produce, as a rule, fewer irrita- tive phenomena and are accompanied by remissions and by apo- 39J: DISEASES OF THE NERVOUS SYSTEM. plectic or pseudo-apoplectic attacks due to the vascular nature of the tumor. Carcinomata occur late in life and are usually sec- ondary. Prognosis. — In extremely rare cases tumor of the brain ap- pears to stop growing and become encapsulated and atrophied. Such tumors are of a tubercular or syphilitic, perhaps sometimes of a sarcomatous character. As a rule, the brain tumor grows steadily and the symptoms of the disease become more pro- nounced until death occurs. The prognosis is best for tubercle in children and gumma in adults. It is worse in those cases of glioma and sarcoma which have a rapid course. In fact, the sooner serious symptoms develop, the more rapid the general development of the disorder, the sooner does a fatal termination come. The disease lasts on an average two or three years, rang- ing from a month to eighteen years. Treatment. — Something can be done in cases of tuberculous tumors, syphilitic tumors, and iDossibly in the sarcomatous vari- ety. In tuberculous tumors a general constitutional and strength- ening treatment must be resorted to ; fresh air, tonics, and a large amount of food being the main reliance. The utility of any form of tuberculin is as yet doubtful. In syphilitic tumors much can be done by the usual vigorous antisyiDhilitic treatment. In sar- comatous tumors, if they are suspected, some help may be ob- tained from the internal use of arsenic. Symptomatically we must give such drugs as antipyrin, phenacetin, antifebrin, code- ine, and perhaps morphine for the relief of i^ain. The ice -cap and leeching often help the headache also. Should convulsions develop the bromides should be used, just as in idiopathic epi- lepsy. In cases in which the location of the tumor can be made out, the question of surgical interference should be considered. The percentage of cases in which surgery can help is extremely small. It will only include those cases in which the tumor can be located ; of those w^hich can be located, only those which are in an acces- sible region, and finally, of those which are in an accessible region, it includes those which are either superficial, or, if lying in the brain substance, are more or less encapsulated. The removable tumors of the brain amount to less than five per cent. They are, in particular, the sarcomatous, syphilitic, and tubercular tumors lying in the central or occipital areas. In many cases where there is some doubt as to the localization an exploratory trephining is justifiable, and in a few cases in which it is known that the tumor cannot be removed the trephining for the simple purpose of re- lieving pressure is justifiable. It is probable that in adults some tumors from the anterior and middle fossa of the brain can be removed. In children tumors ca-nnot be removed successfully TUMORS OF THE BRAIN. 395 from the cerebellum ; in adults it is perhaps possible. Operations for tumors should be undertaken as early as possible; this is a fact on which too much stress cannot be laid. IXTRACRAXIAL ANEURISMS. Intracranial aneurisms are of two kinds—" miliary " and those of large size. The miliary aneurisms are minute dilatations of the vessels and are always multiple; they have been described under the head of cerebral hemorrhage. Large aneurisms affect only the large cerebral arteries at the base of the brain. The arteries are affected in the following order: middle cerebral, basi- lar, internal carotid, and anterior cerebral. The anterior and posterior communicating^ and vertebral arteries are occasionally involved, the posterior cerebral and inferior cerebellar very rarely (Gowers). M iolog I/.— ^Lales are affected slightly oftener than females. Aneurisms occur at all ages from ten to sixty; before ten and after sixty they are extremely rare. Heredity occasionally plays a part in predisposing to cerebral aneurisms. The exciting causes are embolism, esj^ecially when the emboli contain microbes; syphilitic disease, injuries, and in rare cases senile degeneration. The symjDtoms are very indefinite; they resemble to a consid- erable extent those of tumor at the base of the brain ; headache and vertigo, mental dulness and irritation, cranial-nerve palsies, and occasionally hemiplegia and convulsions are noted. Optic neuritis is rather rare. In a few cases the patient is conscious of a murmur or recognizes the pulsating sensation in the head. Sometimes Avhen the aneurism is in the vertebral artery a mur- mur can be heard between the mastoid process and the spinal column (Moser). The diagytosis is often difficult; it is based on symptoms of tumor at the base of the brain pressing on cranial nerves and on motor or sensory tracts. The effect of carotid compression should be tried. The 2^rog)iosis is not good. In perhaps the majority of cases a rupture of the vessel occurs in a few years ; however, rupture is not the inevitable event, and sometimes the disease becomes sta- tionary or undergoes spontaneous cure. The treatment of the disease, if it can be recognized, is the same as that for aneurism elsewhere so far as drugs are con- cerned ; surgically the common carotid may be tied and perhaps the vertebral if the aneurism is believed to be connected with that artery or with the basilar. 396 DISEASES OF THE NERVOUS SYSTEM. Syphilis of the Nervous System. Syphilis is an extremely important factor in the causation of the organic diseases of the nervous system. Nervous syphilis makes up over ten per cent of all the hereditary forms, and while in adult life the specific virus attacks nerve centres relatively less often, yet it is a factor whose importance is very great. In the previous descriptions of nervous diseases we have referred to the syphilitic element in connection with etiology and pathology; but syphilis produces upon the nervous system certain forms of disease which are characteristic, hence it is best to take a brief survey of the effects of this infection independently. Syphilis is beyond much question the result of an infection by a microbe, and the result of the activity of this microbe upon the nervous centres is to produce a condition which is really a form of inflam- mation. The reader can best understand syphilitic disorders, therefore, by remembering that they are all forms of an inflam- mation. The syphilitic infiltration is simply an exudative in- flammation with a specific exudate; the syphilitic gumma is a deposit of this exudation analogous somewhat to an abscess. Syphilis attacks chiefly the membranes of the brain and spinal cord and the blood-vessels of these organs; in particular the base of the brain and the blood-vessels that supply this region are affected. Syphilis acts on the nervous centres in four ways •. it produces meningeal exudation and inflammation, it forms gum- matous tumors, it causes arteritis, and it leads to degenerations. Etiology. — A neuropathic constitution probably predisposes to the development of nervous syphilis. The age at which it occurs most frequently is between twenty and forty, but it may occur at all periods of life from infancy up. It attacks men oftener than women in the i^roportion of about seven to one. Hereditary syphilis makes up about three per cent of the cases. Inadequate and improper treatment of ttie disease at first favors the develop- ment of nervous syphilis later. The neglect in particular of the early use of iodide of potassium tends to render a i^erson more liable to have the nervous centres attacked. The use of alcohol, excesses in the way of severe bodily exercise, severe mental strain, and overwork predispose to the development of the disease; in- juries undoubtedly haA^e a similar effect. The time after the infection when the disease is most apt to occur is the third year, but it is not infrequent between the second and the tenth years, and it is possible for nerve syphilis to develop from within a few months up to thirty years after the infection. Symptoms. — Since syphilitic changes may attack any part of the nervous centres, the symptomatology of nerve syphilis is TUMORS OF THE BRAIN. 397 necessarily a varied one. The reader can perhaps best under- stand the way in which the disease acts by having presented first a series of tables showing on the one side the clinical symptoms, on the other the chief anatomical changes that underlie them. The first table presents the symptoms of syphilis of the brain, which is unquestionably the most connnon form. The next table shows the symptoms of syphilis of the cerebro-spinal system, a form which ranks second in frequency. Third we have syphilis of the spinal cord alone, which is somewhat rarer, and last and rarest of all we have syphilis of the nerves. In addition to these four forms of syphilitic manifestation we have two diseases which are acknowledged to be sequelae of syphilis and which are called post-syphilitic degenerative processes. I. Syphilis of the Brain. Clinical Symptoms. Anatomical Change. Severe headache, vomiting, vertigo, men- Gummatous inflammation of the base in- tal dulness, and irritability, attacks of volving nerve roots, or gummatous in- somnolence or coma, convulsions, era- flammation of convexity, arteritis, and nial-nerve palsies, optic neuritis, hem- phlebitis, iplegia, polyuria, and polydipsia. II. Cerebro-spinal Syphilis. Many of the brain symptoms as above, Gummatous basilar meningitis ; diffuse, spastic paraplegia with spinal pains disseminated, or localized meningo- and involvement of sphincters. myelitis. III. Spinal Syphilis. Paraplegia with pains, Brown-Sequard Meuingo-myelitis, gumma, localized paralysis. softenings from obliterative arteritis. IV. Syphilis op Nerves. Cranial-nerve palsies, cauda equina Root neuritis, gummatous neuritis, sj'mptoms, local palsies of peripheral nerves. ♦- v.— Post-syphilitic Degenerative Processes. Locomotor ataxia ; general paresis. Taking up these different forms of nerve syphilis in order, I will give some further details with regard to each of them. I. Syphilis of the brain in its most common form shows itself by a gradual development of severe and persistent headache. This is usually associated with vertigo, sometimes with nausea and vomiting. After the headache has developed and has lasted for a time, or even without much delay, there comes on sometimes an attack of hemiplegia. Preceding the hemiplegia, or in some cases without the hemiplegia, there are paralyses of the cranial nerves, more especially of the nerves of the eye. Optic neuritis is somewhat frequent. There may be, before any paralyses de- velop, attacks of epileptic convulsions, either general or partial. 398 DISEASES OF THE NERVOUS SYSTEM. Without any paralyses or with simply cranial-nerve paralyses there may develop attacks of somnolence and coma. Even if such attacks do not appear the patient often shows a mental irri- tability and weakness, a slowness of the reasoning process, and incapacity to fix the attention such as is observed in connection with brain tumors, only with nerve syphilis these symptoms are not usually so marked. Polyuria and polydijDsia are symptoms which are occasionally met with. It will be seen that the syph- ilitic poison produces very various manifestations when it attacks the brain. The characteristic features are this variability in the symptoms and their remittent character. Elaborate systems of clinical classification might be made out of these v^arious groups, but it will be sufficient for the present purpose to call attention to the fact that the intense headaches, optic neuritis, cranial- nerve palsies, attacks of somnolence and coma, and hemiplegia associated with some of the foregoing symptoms are characteris- tic of most of the forms. The reason for the peculiar symptoms in brain syphilis is manifest when it is known that the lesion most commonly found underlying them is a gummatous menin- gitis Avhich has a special predilection for the base of the brain. In particular it seems to attack the interpeduncular space and the neighborhood of the optic chiasm and the surface of the pons Varolii. This gummatous meningitis consists of a syphilitic in- flammatory exudate which surrounds, presses upon, and injures cranial nerves, attacks the arteries of the base, producing an obliterating arteritis and conseqaent softenings, with the hemi- plegia which is so often a manifestation of the disease. Much less frequently the inflammatory j^rocess attacks the coiivexity, and then it assumes the form of a gummatous patch which produces cortical irritation wath headaches, mental disturbances, and convulsions. II. The next form of nervous syphilis is the cerebrospinal. In this we have almost exactly the same conditions and symp- toms so far as the brain is concerned; but in addition there are symptoms due to more or less diffuse syphilitic inflammation of the pia mater of the spinal cord. The syphilitic process often extends into the spinal cord, producing an obliteration of the arteries and softening with the symptoms of a transverse or a central myelitis. Thus we have combined the symptoms of cere- bral syphilis and paraplegia with, as a rule, considerable pain in the back, produced by the involvement of the meninges. III. The third type of syphilis is the spinal form. The symp- toms in spinal syphilis are usually those of a transverse myelitis, involving, in the writer's experience, most often the lower paj*t of the dorsal and upper part of the lumbar cord. This myelitis usually comes on rather slowly with the ordinary symptoms of a TUMORS OF THE BRAIN. 399 chronic or subacute transvei-se myelitis. It is probable that syphilis is a much uiore frequent factor in the production of so- called transverse myelitis than is usually supposed. The ana- tomical process underlying it is that of a meningitis which passes along the septa into the substance of the cord, involves the arteries of the cord, and produces a more or less complete soften- ing of the part. The only truly inflammatory process, therefore, is that which is produced in the meninges, connective tissues, and arteries. The anatomical changes in the cord substance are mainly those of softening with reactive inflammation. Spinal syphilis may show itself also by the development of gummatous nodules which grow from the meninges, press upon the cord, and IDroduce the symptoms of a spinal tumor. Spinal syphilis may also develop itself in three or four different foci, producing the symptomatology of disseminated myelitis. IV. Syphilis of the nerves. Syphilis rarely affects the periph- eral nerves; there are, however, occasional deposits of syphilitic exudate producing the ordinary symptoms of irritation and com- pression of nerves. There is said to be a form of multiple neuri- tis produced by syphilis, but its actual existence has not yet been absolutely demonstrated. Syphilis has been known to attack the roots of the cranial nervcjs, producing a root neuritis; and it is very apt to attack the roots of the spinal nerves when the spinal membranes are involved. V. The post-syphilitic degenerative processes are locomotor ataxia and general paresis. Occasionally it happens that the syphilitic deposits in the spinal cord may produce lesions some- what like those of locomotor ataxia, and in this case there will be a train of symptoms which also resemble this disease. In true locomotor ataxia, however, the process is never in any sense a syphilitic one. The syphilitic poison seems to so affect the ner- vous centres as to predispose them to the peculiar degeneration characteristic of tabes. Syphilis may also produce a chronic meningo-encephalitis which will manifest itself by symptoms re- sembling to a considerable extent general paralysis; but it is very generally conceded that true general paresis is not a syphilitic disorder. Syphilis, however, seems to predispose to it, just as it does to locomotor ataxia. Hereditary ^ijphilis.— Inherited syphilis will lead to anatomi- cal changes and clinical manifestations resembling in all respects those of acquired syphilis. Inherited syphilis, in other words, may produce headaches, cranial-nerve palsies, hemiplegia, epi- lepsy, mental disorders, and paraplegia. The disease probably is the cause of a considerable proportion of the cases of chronic hydrocephalus and of many of the cases of so-called tubercular meningitis. The peculiarities of hereditary syphilis show them- 400 DISEASES OF THE NERVOUS SYSTEM. selves rather more in diffuse symptoms such as would be attrib- uted to a meningitis of the convexity ; in other words, convul- sions and mental weakness are rather more frequent, while hemiplegia and cranial-nerve palsies are comparatively rare. Hereditary syphilis also very rarely indeed attacks the spinal cord, although it is not unlikely that it is a factor in the production of some of the hereditary scleroses of that organ. Hereditary syph- ilis develops at any time from birth to the eighteenth year, but most commonly under the age of five years. Pathology.— I have already given some indications of the path- ological changes produced by syphilis. The disease affects the nervous system (1) by producing a meningitis with infiltration, (2) by producing gummatous masses, (3) by producing an inflam- mation of the arteries, and (4) by so influencing the nervous sys- tem as to lead to the development of degenerative diseases. Of all these forms of anatomical change it is the arteries that are most often affected, and particularly the arteries at the base of the brain. Syphilitic meningitis is characterized by the proliferation of round cells and the preponderance of an exudate which has a tendency to infiltrate into the nervous tissues. The anatomical characteristics of the syphilitic gumma must be studied in special text-books. The inflammation of the arteries attacks first the external coat and adventitia, producmg there an enormous mul- tiplication of round cells. The external coat becomes weakened, and as a result there develops beneath it, between the intima and the elastic layer, another exudate which constitutes what is known as endarteritis. In syphilitic arteritis, therefore, there is both a periarteritis and an endarteritis; the former being usu- ally the primary and most essential process. The endarteritis, however, as it develops gradually produces an occlusion of the arteries. This cuts off the circulation of the blood and leads to softening of the part. There is also a development of a hyaline degeneration in the arteries which some regard as a very essential part of the anatomical change. Diagnosis.— The diagnosis of nervous syphilis is based upon the history of an infection, the irregularity and fugacity of the symptoms, the intense headaches, the presence of an optic neu- ritis, the age of the patient, and the results of treatment. In estimating the importance of the history of infection, it should be remembered that the third year after infection is the serious one for the development in particular of those symptoms produced by obliterating arteritis. In hereditary syphilis the presence of the Hutchinson teeth, the hazy cornea, and deafness or other ear trouble help us in diagnosis. The headache of syphilis is rather characteristic. It may attack any part of the head, but is usu- TUMORS OF THE BRAIX. 401 ally unilateral or irregular, or again it may be bilateral in its dis- tribution. The pain is very intense and sometimes exhibits a certain periodicity. It is usually worse at night. It is apt to last continuously for from five days to three or four ^veeks. Headache of this character, foJlowed by the paralysis of one or more cranial nerves or by an attack of hemiplegia, is extremely suggestive of syphilis. Optic neuritis is very liable to occur when the disease shows other evidences of being situated at the base of the brain. This optic neuritis is associated with contrac- tion of the visual field, and a characteristic feature of this con- traction is that it varies a great deal from week to week. The sex and age of the patient may be taken into consideration in weighing the evidence, and finally the prompt effects of the use of iodide of potassium should have very decided weight. Prognosis.— It is very difficult to give definite facts regarding the prognosis of syphilis. Unquestionably the outlook is much more favorable than it is for any other organic disease of the nervous system. When the syphilitic process has not produced so much arterial disease as to lead to obliteration of vessels and softening, a very great degree of improvement and even a recov ery may be expected. So far as injuries to the nerves or nerve roots go, we can generally expect a great improvement or cure. Lesions of the convexity are usuallj^ amenable to treatment. Syphilitic hemiplegia has a not much better prognosis than hemiplegia from other causes. Syphilitic myelitis has a not very good prognosis, but it is better than that of myelitis due to trauma. Nervous syphilis may last from one to three or four years. The effects of the disease may, if nerve tissue is destroyed, last a lifetime. Treatment.— \b regards the prophylaxis, it is important that persons who have become infected by syphilis should be treated w ith iodide of potassium in the second as well as the third stage of the disease. After the first year at least, the patient should not neglect to take a certain amount of iodide of potassium four times a year, each course of treatment lasting six weeks. The patient should be warned against indulging in alcohol, against all excesses, mental as Avell as physical. A laborious life full of worry and anxiety, in which the patient attempts to help him- self along with stimulants, is surely provocative of the develop- ment of nervous syphilis. The treatment of the disease when it has appeared consists, mainly in the administration of iodide of potassium or sodium. This should be given in beginning doses of ten grains three times a day and increased gradually until the maximum amount which the patient can bear is taken. This maximum is usually between three and four hundred grains a day. In some cases it is un- 26 402 DISEASES OF THE NERVOUS SYSTEM. portant to give luore than this — as much, that is to say, as two liundred grains three times a day, and it is the general experience olf American neurologists that results can be obtained by these large doses which cannot be obtained by smaller ones. In my own experience I have known a i^atient to take five hundred grains three times a day for a considerable time without harm, and indeed with benefit. Usually, however, such extraordinary doses are rarely needed. It is found that, as a rule, patients tol- erate large doses of iodide quite as well as smaller ones, and some- times the iodism produced by small doses disappears when large doses are given. The drug is best administered largely diluted with water or with Vichy or in milk, and taken after meals. Some persons bear it better before meals. It is occasionally ad- visable to combine mercury with the iodide. This may be given in the form of the bichloride or by an inunction. Other drugs which are of value are the ordinary tonics such as iron, quinine, and the bitters and mineral acids. Plenty of good food, out -door air, and all those things which will improve the general health of the patient are indicated. CHAPTEK XXL FUNCTIONAL NERVOUS DISEASES. Functional nervous diseases are those in which no definite known anatomical change underhes the morbid phenomena. On this account it is customary to classify them on a clinical basis. We can, however, also make etiological and pathogenic subdivisions. Applying such a method now, we have two broadly distinguished classes: the primary, or degenerative, and the secondary, or acquired neuroses. Such a classification is suggest- ive and helpful, though not perfectly correct, because several factors often enter into the cause of the same neurosis. Primary neurasthenia, hypochondriasis. Epilepsy. Hysteria major. Hereditary chorea. General spasmodic tics. Myotonia. Primary degenerative ^ neuroses. ' r o m infectious, autocthonous, and mineral poi- sons. Acquired neuroses. Chorea. I Tetanus. J Tetany. I Rabies. Tremor. (^ Neuralgia. Neurasthenia. Exhaustion and shock neuroses. Acquired degener- I Hysteria. ] Exoi>hthalmic goitre. [ Occupation neuroses. r Tic douloureux. \ Local si^asmodic ties, ative neuroses. i j^^^^^^^^^ ^gitans. Miscellaneous. ( Vasomotor, trophic, and ( sleep disorders. THE DEGENERATIVE NEUROSES. Epilepsy. Idiopathic epilepsy is a chronic functional disorder character- ized by periodical seizures attended with loss of consciousness and usually with convulsions. Mental disturbances may accompany or take the place of the convulsions. 404 DISEASES OF THE NERVOUS SYSTEM. Symptomatic epilepsy is a form in which the periodic convul- sive attacks are due to gross organic changes in the brain. Jacksonian or partial epilepsy is a form of symptomatic epi- lepsy usually, and is characterized by periodic convulsions affect- ing only certain groups of muscles, and often unattended by loss of consciousness, Hystero-epilepsy is not ejDilepsy, but a form of hysteria. Eclampsia or acute epilepsy is the name given to a single isolated attack of convulsions. It is generally of the symptomatic type. Reflex epileptiform convulsions are considered to form a dis- tinct tyi3e by some (Starr). In this class of cases peripheral nerve irritations produce severe or mild epileptic attacks which are often very frequent in occurrence. Idioi)athic epilepsy shows itself in three rather distinct types of attacks, viz. : that of severe attacks, called the grand mal ; that of minor attacks, the petit mal; and the rarer larvated forms characterized by acute mental disorder and called psyr^iical epilepsy or the psychical epileptic equivalent. Etiology. — Predisposing causes : Heredity is the most potent of any single influence. A history of epilepsy or insanity is found in the famih'- in about one-third of the cases and rather more on the paternal side. Alcoholism and the intermarriage of neurotic persons contribute powerfully to i^roduce the convulsive ten- dency in children. Powerful emotions during pregnancy, ac- couchement injuries, and syphilis have some influence. More cases occur in the country than the city, more in temj^erate climates, and more among in-bred races. All American statistics (Putzel, Hamilton, Hammond, Starr, and myself — 186 cases) show a slight preponderance among males. European observers find it the other way. Age.—T\ie epileptic age is between ten and twenty, and still more definitely between ten to fifteen. In three-quarters of the cases the disease begins before the age of twenty; in one-sixth of nxy cases before the age of five. After twenty the danger of epi- lepsy is slight, andtwhen it occurs it is usually due to accidental causes, like syphilis, alcoholism, or plumbism. Idiopathic epi- lepsy, however, may develop even after sixty. The accompany- ing table shows graphically the relation of age to the develop- ment of epilepsy, chorea, and neuralgias. Exciting causes. Exciting causes are not present in the ma- jority of cases. The most important are the occurrence of rickets at the time of dentition, fright, injury to the head, sunstroke, in- fectious diseases, especially scarlatina, masturbation, alcoholism, and syphilis. Masturbation is a real but rare cause, so also is syphilis. The so-called reflex causes are ocular and auditory irri- EPILEPSY. 405 tations, worms, dyspeptic states, dental irritations, lesions in- volving peripheral nerves. Some American observers put nmch stress on the importance of ocular irritations; European writers have laid more emphasis on disease of the ear. Probably the gastro-intestinal tract and genital organs furnish the most im- portant exciting irritations. True idiopathic epilepsy may be Percentage of total cases up to end of 5Vr to 7th to 15'^ 20^ to 31'^ to 40^ 4P.^ to. 50^.' 51'.' to 61 ^^ to 60% 50% 40 X 30% r'' ,--^^ \ A^ 20% ; /\ /- "A, J / V \ lOX f^ r^ r^ \ // // / V- V ^ \ Fig. loJ.— Table showing Percentage of Cases of Epilepsy, Chorea, and Neuralgia Occurring at Each Half Decade and (after 20) Each Decade. Double line, epilepsy; dotted line, chorea; single line, neuralgia. brought out by peripheral irritations ; more rarely there occurs only a reflex epileptiform neurosis. SymiAoms of the Convulsion.— The patient often feels some premonitory symjDtoms for a few hours or a day, consisting of general malaise, irritability, or giddiness. The attack begins in about half the cases with a peculiar sensation called the aura. Often also a loud cry is uttered and the patient falls unconscious to the ground. The face is pale, the eyes are open and turned up and to one side and the pupils dilated. The head is drawn back or to one side, and the whole body is in a state of rigidity or tonic spasm. The arms are slightly drawn out from the trunk, the forearms and wrists flexed, the fingers clinched or flexed in other ways, the legs and feet extended. This tonic stage lasts 406 DISEASES OF THE NERVOUS SYSTEM. for fifteen or twenty seconds ; the face becomes congested and then hvid from compression of the veins of the neck and stoppage of respiration. Gradually jerky movements of the face and limbs begin and the stage of clonic spasm sets in. The trunk and limbs are now alternately flexed and extended with violent shock-like contractions, the facial and eye muscles twitch, saliva collects in the mouth, and as the tongue is often bitten, it becomes stained with blood. The moveiaents are sometimes so violent that the patient is thrown about the bed or floor, and occasion- ally a limb is dislocated, usually the shoulder. The urine often, and the faeces occasionally, are passed. The temperature is raised V to 1° F., rarely more. The pulse, feeble at first, becomes frequent and tense, and then, as the attack subsides, becomes feeble again. The clonic spasm lasts one-half to one or two min- utes. It subsides gradually, and the patient sinks into a stupor, from w^hich he can be roused with difficulty. This stupor is suc- ceeded by a heavy sleep of several hours and a feeling of hebetude which lasts all day. Vomiting sometimes occurs as a terminal symptom. Immediately after the attack there is a temporary exhaustive paralysis, with loss of knee jerk. The pui)ils contract again and often oscillate.^ There may be a slight amount of transient albuminuria or glycosuria. The earthy phosphates are found increased; urea is not. There is a distinct lessening of haemoglobin in the blood (Fere) and of haematoblasts. Sometimes the attack is followed by others, and for hours the patient passes from one convulsion into another. This condition is called status epilepticus. It usually la:,ts less than twelve hours, but may last for one or more days and until finally death occurs from exhaus- tion. It only develops in the severer types. Symptoms of the Minor Attacks.— In the minor attacks (petit mal) the patient suddenly stops in anything in which he is en- gaged, the features become fixed, the eyes open, the face is pale, the pupils dilated, often slight twitching of the facial muscles or of the limbs occurs, and consciousness is lost. In a few seconds the attack is over, and the patient, who does not fall, resumes his work or conversation, being unconscious of what has occurred, except that he has had a " spell." Often there is a warning sen- sation or aura. This is felt as giddiness, sense of fear, numb sen- sations of the extremities, flashes of light or blindness, or choking sensations. There may be a cry uttered. The minor attacks are in rarer cases accompanied with sudden forced movements; the patient runs a few steps, or turns round or makes some automatic movements. This is called yrocmrsiiie epilepsy. Symptoms of the Psychical Attacks.— Sometimes the minor at- tacks are followed by outbursts of maniacal excitement or by sudden violent automatic movements, and in these states the EPILEPSY. 407 patient may commit crimes of violence. In rare cases the patient passes into a somnambulic state, during which he performs ac- customed acts, such as driving and walking, automatically and naturally (somnambulic epilepsy). This form of epilepsy may come on without a preliminary minor attack, and then it is to be considered a " psychical epileptic equivalent.'" Minor attacks may end in convulsions of a co-ordinate type in which the patient jumps, kicks, throws the arms about as in hysterical attacks. These are called hysteroid convulsions. The seizure may consist of only a short tonic stage and a few twitchings of the limbs, the whole lasting but a few seconds. This is called an abortive attack. Under the influence of medi- cation, the severe seizures are often reduced to abortive forms. Jaoksonian or partial e%)ilepsy is a form of the disease char- acterized by convulsive attacks affecting only a single group of muscles or a limb, and generally not accompanied by loss of con- sciousness. Jacksonian epilepsy is always symptomatic of some focal lesion afTecting the cortical motor area of the brain. This may be a tumor, inflammation, or injury. This form of seizure is particularly significant of a slowly growing brain tumor or syphilis. The aura usuall}^ consists of a sensation of numbness, prick ling, or of a breeze beginning in the hand or leg and passing up to the head, when consciousness is lost. Still oftener there is a peculiar sensation starting in the epigastrium and passing up- ward. More rarely there are special sense aurse such as flashes of light, noises, or voices, and peculiar tastes or smells. Besides these there occur feelings of giddiness, dreamy states, peculiar sensations in the head, and indescribable general sensations. The aurse may be divided into Visceral — epigastric, laryngeal, cardiac. : Cutaneous sensations. Special senses — flashes of light, etc. Psychical — emotions, dreamy states, etc. Cephalic— giddiness, etc. The aura is thought to indicate the seat of the first discharge of nerve force, and its study is of most importance in connection with symptomatic epilepsies, as Avill be shown later. Relative frequency of the different kinds of attacks. The severe attacks are the most frequent, next come combinations of severe and minor attacks, and next minor attacks alone, while the psychical forms are the rarest. Frequency of the Attacks.— The severe attacks may come on only once or twice a year, and this commonly occurs during the development of the disease. The frequency gradually increases until they occur every month or two or three times a month. 408 DISEASES OF THE NERVOUS SYSTEM. Sometimes the fits occur in groups of four or five every month or two. In very bad cases convulsions occur every day. The petit mal attacks are more frequent and usually occur daily. Time of Attacks. — The moon and the seasons have no influence. More attacks occur during waking hours than during sleep; but two- thirds of the attacks occur between 8 a.m. and 8 p.m. Many patients have their attacks early in the morning just after awaking {matutinal epilepsy). Many attacks occur betAveen 3 and 5 a.m., when the temperature of the body and the vital powers are at the lowest. Practically no epileptic attacks occur between 11 A.M. and 12 M. (only 3 in 1,985— Fere). State of Patient Between Attacks. — Epileptic patients often feel better for a time after the convulsion is over. They not rarely suffer from severe neuralgic headaches; the appetite is capricious, often in children it is voracious, but in older cases their may be anorexia ; the bowels are usually constipated ; the pulse is small, soft, and frequent. 3Iental Condition. — A gradual mental deterioration occurs in the great majority of epileptics; but it is slight in some and not very great in others. It shows itself by feebleness of memory, irritability of temper, selfishness, incapacity to concentrate the mind or to carry out a purpose. In children great mischievous- ness and lack of moral sense, with vicious impulses, may appear. The mental deterioration is dependent on those underlying fac- tors which cause the disease. It is apparently in some cases due to the excessive number of the fits. This is not necessarily the case, nor is it generally true that it occurs more often \vith petit mal. It is more marked in cases beginning very early in life, but this is only true when there are decided marks of physical and mental degeneration present. A certain rather small percentage of epileptics become either demented or insane. True epilepsy is not compatible with extraordinary intellectual endowments. Caesar, ^S^apoleon, Peter the Great, and other geniuses may have had some symptomatic fits, but not idiopathic epilepsy. Physical Condition. — Epileptics are rather undersized and of not very robust constitution (Fere). They always present some of the marks of degeneration, physical, physiological, or mental. Such marks or stigmata are about ten times more frequent than in healthy persons. The physical stigmata are (Fere) short stature, cranial asymmetry (in 71^), short parietal or frontal arc, and triangular skull; in women high prominent forehead; bad teeth badly placed, high jDalatal arch; facial asymmetry; promi- nence of occiput and lemurian hypophisis; differences in color, size, position, and shape of pupils; astigmatism (in 75^ cases); badly shaped and placed ears; misplaced crown of scalp; low vital capacity ; small genitals, atrophic uterus; greater develop- EPILEPSY. 409 ment of left side; long fingers. Cranial deformities of pro- nounced type occur in epileptics associated with idiocy, hemi- plegia, and brain defects of early origin. Sometimes, apparently from a premature ossification of sutures, there are the peculiar shapes of the skull known as scaphocephaly, or steeple skull, and plagiocephaly, or obliquely deformed skull. The physiological marks of deterioration are a lessened mus- cular strength (as 35 to 50), habit choreas, a rather imperfect eye with excessive amount of astigmatism and functional mus- cular weakness. There is a lessened vital capacity, weak and slow digestion, and sexual atrophy or irritability. The excretion of phosphoric acid is below normal as compared with urea. Fig. 190.— Diffuse Neuroglia Sclerosis Fig. 191.— Same, Enlarged (Chaslin). OF the Cortex in Epilepsy. The psychical stigmata are mental feebleness, moral insensi- bility, irritability, wayward and vicious inpulses, lack of will power, and sexual aberrations. Pathology. — The body of the epileptic shows sometimes skin eruptions and ulcers, the result of treatment. There are often evidences of local injuries and fractures due to falls. The organs may show vices of conformation. The uterus is frequently in- fantile or sharply flexed. Deformation of the occipital bone or the atlas so as to produce narrowing of the upper spinal canal has been noticed. The brain may be unduly large or small, but there is nothing constant in this, nor is there an abnormal differ- ence in the weight of the two hemispheres. The convolutions show many anomalies, but there is in them nothing specific. On the whole the convolutional type is a simple one. The patholog- ical change found most constantly in epilepsy is an induration or sclerosis (ghosis). This affects the cornu ammonis rather often (4^ to Wo), more rarely the olivary bodies or cerebellum. Besides 410 DISEASES OF THE NERVOUS SYSTEM. this, small patches of induration occur in the gray matter in vari- ous parts of the cortex. Chaslin finds a diffuse increase of neu- roglia tissue throughout the brain, more marked when the case is older (Fig. 191). Others have found an increase in the neuroglia cells (Kingsbury). In old cases there is often a chronic leptomen- ingitis, and vascular changes due to the frequent congestions of the brain take place. These consist in varicose and fusiform di- latation of vessels, with evidence of small hemorrhages. Slight degenerative changes in the nerve fibres are also observed. Bevan Lewis finds in epileptics with insanity a fatty de- generation of the nuclei of the "angular cells'' of the second layer of the cortex. In the severer and later stages of the dis- ease this nuclear degeneration is increased so that vacuoles are formed. The cells of the deeper layers are also affected, but to a less extent. The change, though not peculiar to epilepsy, is more extensive and pronounced in this disease. To sum up: The anatomical basis of idiopathic epilepsy con- sists in a nuclear degeneration and later a vacuolation of the cor- tical cells, beginning and most pronounced in the cells of the sec- ond layer. Also a proliferation and increase in the neuroglia tissue, this occurring most markedly in various islets or sj^ecial areas of the cortex. The blood-vessels and connective tissue are involved only secondarily and later. Physiology. — The epileptic fits are due to sudden discharges of nerve force. The seat of the discharge is the cortex of the brain. The discharging cells are, in the severe seizures, the large motor cells, the function of which is to store up and discharge nerve force. They are under control of the sensory cells (angular cells) of the second layer, which have an inhibitory power. These being diseased their control is weakened and the motor cells " explode '' iDeriodically. In sensory and psychical epilepsy the same mechanism exists. The more highly organized cells with large nuclei of the second layer are congenitally or otherwise Aveak and diseased, the cells below them are not maintained in stable equilibrium and hence iDeriodically break down and "dis- charge." The diagnosis is based on the character of the attacks and has to be made from hysterical and various toxic and sympto- matic convulsions. The aura, the scream, the quick loss of consciousness, the di- lated pupils, the tonic convulsion, the bitten tongue, the emptied bladder, are all characteristic. The hysterical patient sometimes, but rarely, loses consciousness, the epileptic almost always. Hys- terical patients do not hurt themselves in falling or bite their tongue, and their muscular movements, while irregular and vio- lent in character, are yet co-ordinate, ^.e., they throw themselves EPILEPSY. 411 about, kick, strike, etc. Their attacks often are produced by emotion and are ended by some powerful mental or physical impression. The slight rise of temperature in epileptics rarely occurs in hysterics. Petit mal and epileptic vertigo are distin- guished by the sudden lapse of consciousness and by the sudden pallor and fixation of the eyes, dilatation of the pupils, and slight twitchings of the face. Nocturnal convulsions are usually epileptic. Eclampsia, or acute symptomatic and reflex convulsions, can- not always be distinguished from epilepsy. The history of the case, the irregular and often prolonged character of the fit, may enable one to make the diagnosis. Course and Prognosis. — Epilepsy shortens life to some extent; most cases do not live beyond the age of forty or fifty. About ten per cent become demented or insane. Five or ten per cent get well. The remainder reach a certain stage of severity in their disease and continue in it for years. This severity depends on the treatment, the nature of the attacks, and the extent of de- generation which the organism shows. While unquestionably treatment cures or sui^presses the disease in some cases, it disap- pears spontaneously in others. The prognosis of petit mal is worse than that of grand mal ; that of the two combined is worse still, yet not hopeless. The psychical form of epilepsy is the least amenable to treatment. Epileptic insanity and dementia are in- curable. Death occurs rarely in the attacks except in terminal stages. Yet the status epilepticus is always a source of danger. Epileptics are said rather frequently to suffer from phthisis. This is, however, a matter of infection and can be prevented. It should be remembered that epileptics who have only a moderate number of attacks, six to fifteen yearly, can get along comfort- ably for years, doing their work and enjoying a fair share of the duties and pleasures of life. Finally, the following prognostic rules may be laid down : The prognosis is better in males, better if there is a hereditary history, better if the fits are nocturnal or diurnal alone, better in grand mal, better if fits occur infrequently, better if they begin after twenty, and better if due to extrinsic causes. The prognosis is very bad in post-hemiplegic epilepsy and epilepsy due to organic disease. Treatment.— The first and essential rule of treatment is to take cases early and treat them vigorously from the start. Children who have had a few convulsions during the first three to five years of life should be treated as if they might develop epilepsy between the ages of ten and fifteen or earlier. The recurrence of a fit betw^een the ages of five and ten should excite appre- hension and call for the most diligent treatment. Another rule is that when epilepsy is recognized in children the case should be 412 DISEASES OF THE NERVOUS SYSTEM. treated constantly for at least three years after all attacks have ceased. Conditntional Treatment.— A\on^ with the evolution of epi- lepsy there is probably a progressive diffuse neuroglia sclerosis of the brain. Whether this is primary or secondary, it is at least proper to use those measures which apparently affect this neu- roglia proliferation. ]S^itrate of silver and arsenic and perhaps iodide of potassium are drugs which we have good reason for be- heving affect this. Hence I advise that all epileptics as the basal medication should be given courses of these drugs. Besides this, we should use measures that increase vasomotor tone and strengthen and steady the circulation. Nothing does this better than water. Epileptics should be given showers, douches, cold sponge-baths, or wet-packs according to their needs and opportunities. They should also drink water freely. Again, the nervous system is greatly steadied and quieted by mental occupation that interests one. Nothing is more unfortunate than the idleness often enforced on epileptics. 1 have seen the dis- ease absolutely checked by having a boy learn a trade that he liked. The next most important indication is diet. In petit mal par- ticularly an absolutely noh-irritating diet, such as milk, meat, and bread, will quickly lessen or stop the attacks. Meats can be taken in moderation if eaten slowly. As a rule it is a little safer to keep meat out of children's diet for a time; but in adults it is not necessary. Removal of irritating causes. Malaria if present promotes the con^^lsive tendency ; so also do lead and alcohol ; tobacco does not do this, but its use is better stopped, as it is liable to weaken vascular tone and impair digestion. Syphilis causes epilepsy only through producing organic changes. The rheumatic, gouty, and so-called tubercular diatheses do not stand in any close relation to epilepsy. The condition known as lithaemia, however, in which there is insufficient oxidation and excretion of products of tissue waste, needs attention. Hence the use of bicarbonate of potash, the alkaline mineral waters, and a restricted diet is not rarely indicated. The importance of reflex irritations has been much overesti- mated. Still they must be considered. The most serious are those arising from the gastro-intestinal tract, the sexual organs, and the eyes. Phimosis if present must be relieved, and mastur- bation or sexual excesses stopped if possible. It is admitted now that removal of the ovaries, even if diseased, never cures true epilepsy, though it may help hysterical convulsions. Astigmatism and hypernietropia should be corrected; also ocular insufficiencies if these are pronounced. EPILEPSY. 413 Proper attention to the- frequent constipation and dyspepsia is of course necessary. The use of hot water is often serviceable, a glass being sipped slowly before the niorning and evening meals! This helps also to carry off the bromides and wash out the system generally. To still further promote this, a purge should be given every fortnight or month. Out-door life and active physical exercise are indorsed by Hippocrates. They do not have any specific influence unless associated with some employment. Specific treatment. The drugs which have obtained and held a reputation as anti-epileptics are not numerous. They are the bromides, chloral, chloral-amide, belladonna, zinc, nitro-glycerin antipyrin. Of less value are digitahs, cannabis indica, borax, valerian, and ergot. As adjuvant drugs we have quinine, strych- nia, iron, the phosphates, arsenic, silver, the alkalies and iodides. The most valuable of the specific drugs are the bromides. All bromides act alike in this disease. If one does not cure another will not. Occasionally, changing or mixing reduces the attacks for a time and benefits the stomach. The best bro- mides are those of potassium, sodium, strontium, ammonium, and hydrogen (hydrobromic acid). Bromide of jjotassium is the most trustworthy. Bromide of sodium is more agreeable to the taste, less irritating to the stom- ach and milder in its effects, but is eventually just as depressing as other forms. Bromide of ammonium has a brief stimulant effect on the circulation. Bromide of strontium has no advan- tages that I can discover. Bromide of gold is of no use. Hydrobromic acid is useful in those cases in which there are indigestion and phosphaturia and an alkali is contra-indicated. It produces acne less readily than the alkaline bromides. Bromides should be given in daily doses of 3 i., increased grad- ually until the attacks are suppressed or the dose reaches 3 iv. to § i. daily. Few patients can tolerate more than this latter dose. Thorough bromidization should be always tried if necessary to stop the fits, and it may be occasionally repeated. But bromidi- zation is sometimes injurious, ev^en making the disease worse, and it must always be employed with caution. When the fits are suppressed the bromides should be reduced, but never entirely stopped for at least two years after the last fit. In most cases, and especially in nocturnal epilepsy, an extra .large dose of bromide or bromide and chloral should be given at night. It is very important that the bromides should be chemically pure (most samples are not), that their use should be continued a very long time, and that their depressing effects should be offset by tonics and all possible roborant measures. Bromides lessen the fits in from eighty to eighty-five per cent of cases. They do no good or do actual harm, as regards fre- 414 DISEASES OF THE NERVOUS SYSTEM. quency of attacks, in from five to ten per cent of cases. Bro- mides do no actual good to the patient in a much larger propor- tion of cases. To prevent bromide acne, arsenic, calcium sulphide, baths, and diuretics are the best measures. To prevent bromidization, one should adopt all possible robo- rant measures ; use salt-water baths and regular physical exercise, give black cofTee, caffeine, cocaine, mineral acids, strychnine, bitter tonics, cod-liver oil. In all cases the patient should dilute the drug, preferably with carbonic-acid water or Vichy, in the proportion of six ounces of water to a scruple of the drug. A few drops of phosphoric acid may be added to this. The continuous administration of an alkaline bromide in an alkaline water sometimes affects 'the bladder, and then the bro- mide can be given dissolved in hydrobromic acid. The best substitutes for the bromides, when these do no good or do harm, are belladonna, zinc, strychnine, glonoin, borax, and antipyrin. The best non-specific adjuvants (drugs) to the bromides are potassium iodide (in syphilitic epilepsy), potassium bicarbonate (in lithsemic and rheumatic states), carbonate of ammonium, the hyi^ophosphites, arsenic, iron, and quinine. The best sj^ecific adjuvant to the bromides, as Seguin has shown, is chloral hydrate. By adding five or six grains of this to a mixture the bromide dose can be reduced one-half and the fits still be controlled. Chloral-amide has a similar effect. Both these drugs will sometimes affect the eyes and stomach unfavor- ably. Children bear nearly as large doses of bromide as adults. The remedies that are especially useful in petit mal are, after the bromides, bromide of camphor, belladonna, glonoin, canna- bis indjca, cod-liver oil, ergot, counter-irritation at the back of the neck, and cold spinal douches. For epilepsy in children, besides the bromides it is sometimes advisable to employ milk diet, rest, and oxide of zinc. In hemiplegic and in Jacksonian epilepsy the actual cautery applied over the scalp is beneficial. For nocturnal epilepsy one may increase the dose of bromide at night and add chloral or digitalis. Strychnine is sometimes useful. Raising the head of the bed or making the patient sleep in a chair at night are meas- ures that may be tried. For hysterical and erethitic cases, with or in place of bromides give a diet of milk and vegetables, and try turpentine, valerian, or zinc. Belladonna is usually contra-indicated. Counter-irritation by means of blisters, issues, and setons at the back of the neck is of doubtful value. For the status epilepticus give large enemata of chloral and EPILEPSY. 415 use emetics and purges. Venesection is often efficacious, morphine is dangerous, ciiloroform is only palliative, and nitrite of amyl is of little value. To prevent impending attacks the best remedy is nitrite of amyl, which may be carried in a phial filled with cotton. Inhala- tion of chloroform or ammonia, the internal administration of ammonia, spirits of lavender, or alcohol, a sternutatory, and pressure on the carotids— all are measures which sometimes stop the attack. Alterative and habit-breaking drugs, such as mercury, iodide of potassium, arsenic, and antimony, are useful in epilepsy, especially in acquired forms due to lead, alcohol, and syphilis. Bromides stop the fits oftener if given early in the disease, if given to young children, and if given in cases that develop after twenty-one. Injuries to the head which have caused a fracture or a con- tusion of the brain are the most frequent traumatic irritants. Whenever epilepsy can be distinctly traced to a blow on the head the question of trephining should be brought up. If there is a history of fracture or present evidence of fracture or even evidence of severe head injury, trephining is justifiable. The more marked the evidence of a degenerative constitution and the less marked the evidence of real brain injury, the less hopeful the prognosis. On the whole, surgery can do little for acquired and nothing for idioj)athic epilepsy. CHAPTER XXIL HYSTERIA. Hysteria is a chronic functional disorder characterized by nervous crises of an emotional, convulsive, or other nature and by an interparoxysmal state in which certain marks or stigmata are present. Hysteria is essentially a psychosis, and the dominant symptoms are attributable to disorder of the cortical areas of the brain. Its components are the paroxysms, or " crises " as they are called, on the one hand, and the peculiar symptoms of an interparoxysmal state on the other hand. The disease is to be regarded as a definite one, having a certain, as yet unknown, pathological basis underlying it. The use of the word should be much more restricted and definite than has hitherto been the fashion. There are two forms of the disease, hysteria major and hysteria minor. Etiology. — Of the predisposing causes heredity is the most important. In about seventy-five per cent there is a history of hysteria or some neurosis or psychosis in the i)arents. The disease is transmitted more often by the mother. Heredity is particu- larly apt to be important in the hysteria of children ; it is a much smaller factor in hysteria of adult males. A hereditary history of rheumatism, gout, and tuberculosis is of very doubtful im- portance. Hysteria is a disease of early adult life, most cases occurring between the ages of from fifteen to twenty-five in females ; it occurs later in males. Hysteria attacks children be- tween the ages of eight and fifteen, chiefly between eleven and fourteen. The disease affects Avomen more than men in the pro- portion of four to one, varying much with race, climate, and occupation. Hysteria occurs in all classes of life, but rather less frequently in the middle classes than among the poor and the very rich. Male hysteria is more frequent in the poorer classes who are subjected to the exciting influences of alcoholism, pov- erty, injuries, etc. Hysteria is certainly much less frequent in its severer forms in this country than in some parts of Europe, par- ticularly France. In my experience it is much less frequent than epilepsy in the northern and eastern parts of this country, It occurs, however, quite frequently in the negroes and also in the Latin races of this country. Bad methods of education and bad family training undoubtedly tend to promote the development of the disease. HYSTERIA. 417 The most important single exciting factor is powerful emotion, particularly fear. Other emotions of an allied character— excite- ment, sorrow, anxiety— may bring on attacks. The disease can be developed by imitation. Injuries combined usually with mental shock are fruitful causes of producing hysteria. The infectious fevers, syphilis, diffuse hemorrhages, the poisons— lead, alcohol, mercury, and tobacco— the administration of ether, mental and bodily and sexual excesses are all important agents in developing the disease, SynuJtoms.— The symptoms of hysteria are best described under two general heads— first, those of hysteria minor or the hysterical condition, and, second, those of hysteria major. 1. Hysteria minor is characterized by the interparoxysmal con- dition of emotional weakness, nervousness, hypersesthesia and pains, and by crises of an emotional character. In hysteria minor there are no permanent objective marks like anaesthesia and paralysis, and no decided convulsive seizures. The patient, who is almost always a girl or young woman, gradually develops an undue sensitiveness, the mind is depressed, and she gets easily alarmed. She has feelings of nervousness and lacks control over the emotions, she laughs and cries very easily and yields to every impulse. She suffers from headaches which are usually vertical and often severe and chronic, and from spinal pains. She sleeps as a rule rather badly and often has disagreeable dreams. She has, under any little excitement, sensations of tickling, fulness or choking in the throat, forming the condition known as globus. Excitement also brings on attacks of trembling or chilly feelings which come and go. There is more rarely a considerable amount of vasomotor instability, as shown by flushings and by coldness of the extremities. She has with more or less frequency distinct crises of an emo- tional character, during which she laughs or cries without ap- parent cause, or at least to an extent beyond her control. She may have attacks of vomiting or headache, or of intense mental excitement amounting almost to delirium. In some cases the patient has somnambulic attacks at night, or she may have under a little excitement attacks of cerebral automatism during which she involuntarily does things that she is entirely unconscious of when she comes out of the attack. The crises are followed by a copious discharge of very light urine. Hysteria minor is closely allied to a condition of neurasthenia or of simple nervousness. It is associated with neurasthenia oftentimes, and is to be distin- guished from it chiefly by the peculiar psychical state, the hyper- ^esthesia, and the crises which have been described. Even in hysteria minor there is a degree of that peculiar mental condi- tion which will be described later and which is known as sug- 27 418 DISEASES OF THE NERVOUS SYSTEM. gestibility. Hysteria minor is a disease which belongs especially to childhood and early womanhood. It is very liable to become ameliorated and disappear a little later in life or under the in- fluence of proper treatment, but it may continue or pass into the major form. 2. Hysteria major is characterized by interparoxysmal mani- festations of anaesthesia, paralyses, contractures, tremors, pecul- iar mental conditions, and by paroxysms of an emotional, con- vulsive, or other serious nature. Hysteria major is what is usually meant when one si)eaks of hysteria; it includes also hystero-epilepsy. The onset may be gradual, but not infre- quently it follows some shock, the first symptom being a convul- sion, a paralysis, or some emotional outburst- The symjytoms of the crises are the most striking and will be described first. The most common of the paroxysms of hystei'ia are emotional outbursts of crying or laughing ; after this come motor disturbances in the shape of convulsions of various types. Besides this we have attacks of severe i^ain, forming neuralgic crises ; attacks of nausea, gastralgia, and vomiting, forming gas- tric crises; much more rarely there are prolonged attacks of hysterical coughing, hiccoughing, sneezing, or rapid breathing. The hysterical seizure may also take the form of attacks of trance and lethargy, catalepsy, amnesia, and cerebral automatism. The emotional crises are characterized by ajDpearing without any good cause; the patient laughs Avithout reason, and the laughing continues and is quite beyond her joower of control. In the same way, and rather more frequently, crying attacks or attacks of furious anger and excitement come on. Associated with these outbursts there is almost always a peculiar sensation of something in the throat. It is described sometimes as being a ball or pressure or a squeezing sensation. It is called hysterical globus, and is due usually to a paresthesia of the nerves of the throat and larynx, but occasionally there «ris also a muscular spasm of those parts. Following the crises there is a profuse discharge of pale, limpid urine. Hysterical convulsions have two rather Avell-defined types. One of them is that which comes on also in hysteria minor and is the ordinary form of hysterical convulsions; the other is a much more severe disturbance in every way and is known as a hystero-epileptic or hysteroid attack. In the hysterical convul- sion the patient, under the influence of some excitement, in- jury, or acute gastric disturbance, rather suddenly falls down and begins to go through various irregular movements of the body, such as thrashinu- with the arms, kicking with the legs, throwing the head from side to side, rolling about on the bed or floor. In the more distinctively convulsive seizure the hands and arms HYSTERIA. 419 and fingers are flexed, the legs and feet are extended, the eyes are generally closed, the eyeballs often converged or moved about irregularly, the pupils dilated. There is some lessening of sensa- tion over the body and of the conjunctivae. The patient often utters noises or screams at intervals. She may bite her lips, but does not bite the tongue, nor does she ever hurt herself in her va- rious contortions. The attack may last for half an hour to several hours, unless some measured are taken to break it up. In other forms of hysterical convulsion there is simply a general shaking or trepidation of the body as though the patient had a chill; in other cases again the main type of movement is that of opistho- tonos, the patient rising up upon the head and heels and arching the body as in tetanus. Again the attack may consist simply of a little rigidity of the body, or of a series of rhythmical movements of the head or trunk or limbs, the patient sitting up and oscillat- ing the head or swaying the trunk or moving the arms, uttering at the same time incoherent words. In children the attacks may be associated with peculiar noises and movements in imitation of animals, such as the growling of a dog or the mewing of a cat. This condition is called therio-mimicry. In some instances the attack may be accompanied or may end in a condition of mental excitement approaching delirium. The patients while suffering from these seizures generally appreciate what is going on about them, and will often res^^ond to some stern order for them to cease or will be brought to a state of quietude by pressure upon some part of the body which provokes pain. In Avomen in particular, pressure over the ov^aries or epigastrium will abort the attack; the application of cold water or an emetic will do the same. The Symptoms of the Interparoxysmal State.— Between the crises the patient may be in a fair condition of general health, but usually presents certain definite chnmic manifestations of the disease. The most characteristic are sensory symptoms, paralyses, and contractures. Sensory symptoms. These consist of cutaneous and mucous hyperaBsthesia and anaesthesia and anaesthetic disturbances of the special senses. Cutaneous anaesthesia occurs in three forms : the common form is that of hemianaesthesia involving one-half of the body; next in frequency is the segmental anaesthesia in- volving an arm or a leg or part of the face or head ; rarest of all the forms is a disseminated anaesthesia occurring in the form of patches. These various modes of distribution are shoAvn in the accompanying figures. The anaesthesia is a pain anaesthesia chiefly. The tactile and thermic sensations are less markedly affected. The aucesthesia is in some rare cases transferable by means of magnets or electrical irritants or by suggestion. The anaesthesia can also be lessened or removed temporarily by the 420 DISEASES OF THE NERVOUS SYSTEM. application of magnets or coins or pieces of metal. For example, if a silver coin is fastened upon the anaesthetic area, in the course of a few minutes or a few hours there will be a zone of normal sensation under and around the coin. Sometimes the tempera- ture of the skin upon the anaesthetic part is lowered 3° or 4° F., and upon pricking the skin blood does not flow. The anaesthesia is oftener upon the left side in the proportion of three to one. Hysterical anaesthesias are not accompanied with subjective sen- sations like organic anaesthesias. The skin reflex is usually abol- ished. Anaesthesias of some kind occur in a very large proportion of chronic forms of hysteria major. They are rare, however, in Fig. 192.— The Three Types op Distribution of Anesthesia in Hysteria : Hemianesthesia, iSEGMENTAL, and Disseminated. Z, Hysterogenic zones. children, and are rarer in women than in men in the author's ex- perience. Anaesthesia of the mucous membranes is present chiefly in hemianaesthesia ; it then involves the mucous membrane of the mouth and throat, and to a less extent that of the nose and glot- tis. Hemianaesthesia is usually accompanied with some hemi- plegia and often with some tremor. Segmental anaesthesia is also often accompanied with some degree of paralysis of the part. Visual anaesthesias. One of the most common of the perma- nent stigmata of hy.steria is an anaesthetic condition of the retina. The result of this is the production of a concentric limitation of the visual field and a disturbance in the color sense. Complete loss of this sense may take place or there may be a variation in the way in wdiich the colors are perceived. There may be also 1 J HYSTERIA. 421 a distinct diminution in the acuity of vision or even a complete loss of sight of one eye. The visual disturbance is most common with hemiantesthesia. It is more marked on the affected side, but exists to some extent on the healthy side. The limitation of the fields is shown in the accompanying cut (Fig. 193). Hearing. There is sometimes a diminution in the acuity of hearing of one ear, and this occurs, if present, in connection with hemiansesthesia. There may also be a loss of hearing to high and low notes, while hearing is apparently fairly good to notes of medium range ; and finally there may be a diminution in hearing by bone conduction, while hearing by aerial conduction is but Fig. 193.— Hysterical Loss of Color Sense and Limitation op Visual Field. Color sense absent in left eye and field contracted; in right e5e field less con- tracted ; order of appreciation of colors from without in was yellow, violet, blue, red, green (observation by Dr. E. S. Peck). little impaired, this being due probably to an anaesthesia of the acoustic nerve. Disturbances of taste in the form of anaesthesia or paraesthesia are quite frequent and are important signs in hysteria. The loss of the sense of taste may only involve the back portion of the tongue and the palate ; in other words, the taste field is here limited as it is with hearing and vision. The sense of smell may be abolished, but this usually occurs in connection with hemianaesthesia. Hyperaesthesias and neuralgias. Pure neuralgias are some- what rare in true hysteria, but hyperaesthesia and pains of vari- ous kinds are not at all infrequent. Hyperaesthesia occurs in the form of patches at different parts of the body. These sensitive points may, when pressed upon, bring on paroxysms of various 422 DISEASES OF THE NERVOUS SYSTEM. kinds, and they are therefore called the hysterogenic zones (Fig. 192). The most common seat of these zones in women is over tlie ovaries ; in men, in regions correspondng to the ovaries and on the scrotum. Hysterogenic zones, however, may be found just be- neath the mammary gland, on the epigastrium, along the spine, and in other places. These zones are sensitive areas ; they can be made to disappear by applications of electricity and by refriger- ation and counter-irritation. Hysterical patients often sufTer from local headaches which are apt to be confined to the top of the head or to the sides near the temples. The pain is severe, sharp, and boring, and may exacerbate with such intensity as to jiroduce symptoms almost resembling meningitis. The spot-like pains are known as hysterical clavus. Hysterical jjatients occa- sionally have migraine, facial neuralgia, i nd intercostal neural- gia. Much more often they have pains along the spine, produc- ing symptoms of spinal irritation. Hysterical patients also have at times attacks of palpitation and pains over the heart, consti- tuting what is known as pseudo-angina. Such troubles are much more frequent in women. Motor symptoms. The motor symxDtoms of hysteria are paral- yses, amyosthenia, contractures, tremor, and choreic and ataxic movements. The i^aralyses of hysteria take the form of hemi- plegia, paraplegia, and monoplegias. Hysterical hemiplegia oc- curs usually rather suddenly, often as the result of some severe shock. The left side is more frequently attacked. The arm is most affected, the leg next, while the face is hardly ever in- volved. The paralysis is not an absolute one, and the patient is able to drag himself along. The deep reflexes are usuallj' not exaggerated and they may be for a short time absent. The paral- ysis is thus a flaccid one. The gait of the patient is different from that of hemiplegia due to organic disease ; in hysterical hemi- plegia the patient drags the paralyzed leg after him, in organic hemiplegia the ijatient swings the paralyzed leg around in a half circle. This peculiarity of the gait, the absence of exaggerated reflexes, the absence of paralysis of the face, and the presence very commonly of other hysterical stigmata are sufficient to en- able one to make the diagnosis. Sometimes the face on the affected side is slightly drawn by a spasm so that it appears to be paralyzed, when it really is not (Charcot). Monoplegias affect the arm or leg, very rarely indeed the face, occasionally the eye muscles, and most commonly of all the muscles of the larynx. Hysterical monoplegia is usually 'accompanied with anaesthesia of the affected part and by other symptoms of hysteria. There are no serious atrophic changes or disturbances of the electrical reactions. Hysterical eye palsies show themselves in the form of tenest of an insufficiency of the internal recti, much more rarely HYSTERIA. 423 by a paralysis of the third nerve or some of its branches. In hysterical palsy of the larynx the adductors are involved so that the patient cannot speak aloud, and the condition is called hysterical aphonia. The trouble often comes on suddenly, the patient finding that he cannot speak above a whisper. The paralysis is not so great but that the adductors can be approxi- mated in coughing. The trouble is distinguished from laryngeal inflammation by inspection of the affected part. The abductors of the larynx and the tongue and other muscles of articulation are in very rare cases also involved, and hysteria may produce symptoms resembhng a bulbar paralysis. Paraplegia is a rather common form of hysterical palsy; it is usually brought on by emotions of depressing character, often associated with some slight injury. It may be accompanied with a good deal of pain Fig. 194.— Hysterical Contractures. in the back, and the form of disease which is popularly known as " spinal concussion " consists in many cases of hysterical para- plegia combined with hysterical neuralgia of the spine. In hysterical paraplegia there is very little wasting of the limbs and no change in the electrical reactions. The deep reflexes may be somewhat increased or normal; they are never absent. There is never any prolonged or persistent ankle clonus, but there may be a short or spurious clonus due to a general exaggerated irritability of the nervous system. The sphincters are never in- volved except temporarily or through some complication. Amyosthenia is a frequent, peculiar, and interesting symptom occurring in the interparoxysmal stage of hysteria. It consists in a more or less temporary feeling of weakness of an arm or of the legs. Thus a person in lifting a dish from the table suddenly feels the arm give out, and if not careful the dish is dropped; or while walking the patients suddenly feel as though they had lost all power in the lower limbs. This amyosthenic condition is generally temporary, but it may be so permanent as to produce a 424 DISEASES OF THE NERVOUS SYSTEM. certain degree of monoplegia or paraplegia. The amyosthenic condition generally precedes a paralysis. It presents no objec- tive signs in the way of electrical reaction ; it involves a whole member, not a single group of muscles ; it affects more the anaes- thetic side, and when it exists the deep reflexes are usually exag- gerated (Toui-ette). Contractures. In some forms of hysteria there is a tendency for the muscles to undergo contracture under slight mechanical stimulation such as pressure or a blow. This tendency to con- tracture in hysteria is called the contractural diathesis, and it is an important sign. The contractures may be temporary, disap- pearing soon after the exciting cause ceases, or they may develop independently and last for a long time. They involve the legs, Repose. Movement. Fig. 195.— Illustrating Intentional Tremor in Hysteria (Tourette). arms, and facial muscles, and may be associated with paralysis and anaesthesia. Tremor occurs in hysteria in a considerable proportion of cases, more especially those in which there is hemiplegia and hemi- antesthesia. Hysterical tremor simulates all the various types. The common form is one in which the oscillations occur from five and a half to seven and a half times a second, and it is there- fore a tremor of average rhythm. It ceases for a time when the person is quiet or lies in the horizontal position; also during sleep. It affects the head and tongue as well as the extremities, the latter more upon one side than the other. It may be chiefly in the lower limbs. Sometimes it has the type of an intentional tremor, ceasing on rest of the hand and increasing when the hand is moved, as in raising a glass to the lips (Fig. 195). It then resem- bles exactly the tremor of multiple sclerosis. There may be a slow tremor of four to five and a half oscillations per second ; this per- sists during rest and is but little modified by voluntary move- ments. It imitates the tremor of paralysis agitans. Finally there may be a rapid tremor of eight to nine oscillations per second. This also persists during repose and is but little modi- HYSTERIA. 425 fled by movements. It imitates the tremor of Basedow's disease, alcoholism, and neurasthenia. The mental state in hysteria is characterized by emotional in- stabihty and intense craving for sympathy, weakness of the will, lack of self-control, acuteness of perception, and a constant vari- ability of moods. The hysterical mind is not a dull one, it is not a consciously mendacious or evil one. But there is an abnormal increase of sensibility and an exaggeration of the personal feel- ing or egotism which leads to selfishness and promjjts deceit. The fundamental defect in the hysterical brain is that it is circumscribed in its associative functions; the field of conscious- ness is limited just as is the field of vision. The mental activity is confined to personal feelings, which are not regulated by con- notation of past experiences, hence they flow over too easily into emotional outbursts or motor paroxysms. The hysterical person cannot think. Physiologically the condition is explained by supposing that there is a benumbing of the association fibres which normally connect sensory cortical centres with other parts and enable one to compare and adjust new experiences with old. In other words, to reason and form correct judgments. Underlying the hysterical mental state there is a condition of suggestibility^ by reason of which ideas and impressions easily be- come fixed and dominate the mind. The person becomes self- hypnotized and believes he or she is suffering from things which have no objective existence. The pains, palsies, and anaesthesias of hysteria major are pseudo-delusions, differing from delusions of the insane in that the false belief or idea is a subconscious one. Trophic disorders. In hysterical paralysis a slight amount of atrophy occurs, but only such as would naturally follow disuse of the part. A very few cases have been reported in which a true neurotic atrophy resembling the atrophy that occurs in neu- ritis or progressive muscular atrophy was present, and it is even affirmed that degenerative reactions may be elicited. Cutaneous eruptions and dystrophies practically do not exist, or, if present, are the result of complicating disorders. Visceral symptoms. Hysterical patients often suffer from dyspepsia and constipation, also from anorexia and in some cases from persistent vomiting or regurgitation of food. Occasionally the anorexia and vomiting become persistent; the patient refuses food or rejects all that is taken; she emaciates, becomes weak and bed -ridden, and develops into that particular phase of hys- teria known as " the fasting girl." In these cases, along with the aversion to food and vomiting, there may be a great deal of gas- tralgia. The urine in hysteria is apt to be of low specific gravity. Always after hysterical attacks there is a profuse flow of very 426 DISEASES OF THE NERVOUS SYSTEM light-colored urine having a gravity of only 1,003 to 1,006. Some- times there is retention of urine ; in extremely rare cases there is a condition known as ischuria and anuria, in which for several days extremely small quantities of urine are passed, owing ap- parently to a suspension of the functions of the kidney. Such cases should always be carefully investigated, to see that the patient does not deceive her attendants in regard to the amount of urine passed. Vasomotor symptoms are very common. They consist of flushings and pallor, cold extremities, an 1 at times an (Edematous condition of one or more extremities. This oedema may be of the ordinary pale, waxy character, pitting upon pressure. In other cases it has a i^eculiar bluish tinge and it does not pit; the hands, which are the parts generally affected, are several degrees below the normal in temperature, and the limb resembles in some respects the condition in Reynaud's disease. Gangrene, however, never supervenes. This form of oedema is known as the blue cedema of hysteria. There occur in hysteria febrile attacks, and much has been written upon the subject of hysterical femr. These so-called hysterical pyrexias may resemble in their course typhoid or malarial fever ; as a rule, the temperature runs a very irregular course, and the fever often lasts for weeks or even months. The essentially neurotic origin of these fevers has hardly yet been established, and one can only reach the diagnosis by most care- fully excluding all other possible causes. Anaemia is a very common condition in hysterical patients. Hystero-Epilepsy. — The form of hysteria which shows itself by the development of severe crises known as hystero-epileptic at- tacks is extremely rare in this country, at least in its typical phase. It has been particularly studied by the French waiters Charcot, Richer, and others. Hystero-epilepsy, as this form of the disease is called, is a true hysteria and not epilepsy at all, nor a mixture of hysteria and epilepsy, though the name would suggest that that was the case. The typical attacks of hystero- epilepsy begin with certain prodromata consisting of a feeling of malaise and irritability which may last for several hours or a day. The attack is ushered in often with an aura, the patient utters a cry, falls to the ground, loses consciousness, and enters into the first phase, known as the epileptoid stage. During this she suffers from tonic and clonic spasms very much like those of true epilepsy. The muscles finally relax, and the patient be- comes comatose for a moment and then enters the second stage, that of the contortions and grand movements. In this there is opisthotonos, the body is arched up, and there are violent move- ments of the trunk and limbs, which undergo flexion and exten- HYSTERIA. 427 sion, the movements being all of large range. The next stage is that of emotional attitudes, during which the patient seems to be experiencing intense feelings of anger, joy, or some other violent passion, which she expresses by the postures of her body, the movements of the eyes and facial muscles. This stage over, she enters into the last phase, which is known as that of delirium, during which there is a great deal of mental excitement of a 1 Epileptcid ^Mmym^ymrnxmrnm^^ yimmn.nmnu^.mwmminmv uniiiulinini'iii' Z Grand Movements .._ yf'^^ 3 Passional •"i(lU(lil(l'l(l(|((i/i|ii|||l(, , 4 JJelinctis Fig. 196.— Showing the Different Stages of a Hystero-Epileptic Seizure (after Richer). depressing character, from which she gradually emerges into her normal condition. To recapitulate : we have in a typical attack, first, prodromata ; second, the epileptoid phase, lasting from one to three minutes; third, the phase of contortions and' grand movements, one to three minutes; fourth, the emotional phase, lasting from five to fifteen minutes; and, finally, the stage of delirium, lasting a variable time ; the whole attack lasting from five to twenty minutes (Fig. 196). In this country we occasion- ally see hysterical patients exhibiting one or two of these phases, 428 DISEASES OF THE NERVOUS SYSTEM. but very rarely indeed do they ever go through the whole series. The patients who suffer from hystero-epileptic attacks generally during the interparoxysmal stage present many of the stigmata of hysteria such as paralyses, contractures, and anaesthesias. Hysterical crises which take the form of convulsions or emo- tional seizures sometimes end or are associated with attacks of catalepsy or trance or attacks of amnesia and cerebral automa- tism. As these conditions all occur in other diseases than hys- teria, they will be described elsewhere in connection with the subject of the disorders of sleep and of consciousness. Hysterical persons occasionally are attacked with violent and IDersistent hiccoughing or sneezing. Sometimes also there come on attacks of extremely rapid breathing or hysterical polypnoea, during which the respirations run up to fifty or seventy a minute. A hysterical cough sometimes occurs; it lasts for a long time. CEsoi^hageal spasm with consequent dysphagia is another one of the somewhat rare phenomena of hysteria. Pathology. — There is no known anatomical change at the basis of hysteria. We do not find the marks of degeneration as we do in certain forms of insanity and epilepsy. The pathology of hysteria is really its psychology. It is a brain disease affecting primarily the cortex, while secondarily lower centres are involved. The essential trouble is on the one hand a benumbing of the associative and inhibitory tracts of the brain so that the sensa- tions are dammed up till they promiscuously overflow. On the other hand, the receptive areas are over irritable and sensitive. The field of consciousness is narrowed but exalted in intensity. Diagnosis. — Physicians recognize three different phases of hysteria — a hysterical temperament, hysteria minor, and hysteria major. The hysterical temi3erament is something with which all women and many men are naturally endowed. It is a condi- tion, not a disease, and does not call for description or elucida- tion here. Hysteria minor is the hysterical temperament plus certain stigmata and the crises. One should not make the diag- nosis of hysteria minor unless he can find these factors. The stigmata we have already enumerated, also the peculiar and varied forms in which the crises show themselves. In hysteria major we have a much greater iDreponderance of the stigmata and much severer forms of the crises, these being largely of a motor type. Hysteria simulates many organic diseases, and it is often 'difficult to distinguish surety the real from the spurious thing. The essential characteristics of hysterical forms of dis- ease are the peculiar emotional condition of the patient, the past history of hysterical crises, the presence of the stigmata of hys- teria such as anaesthesias, limitation of the visual field, paralyses, and contractures. The variability of the symptoms, their sus- HYSTERIA. 429 ceptibility to influence under suggestion and rigorous moral measures, the absence of serious disturbance of nutrition, the sex and age, and tlie cause should also have weight in guiding us to our decision. Diagnosis of special forms of hysterical manifestations. Hys- terical paralysis is characterized by the fact that there is no marked degree of wasting of the muscles, no electrical reactions of degeneration, the deep reflexes are preserved or exaggerated, and other marks of hysteria are present. Hysterical anaesthesia can generally be lessened over certain areas by the application of the magnet or ca,n be made temporarily to disappear; it is pecul- iarly distributed in the way described under symptoms and is associated with aneesthesias of the special senses. Hysterical contractures sometimes cease during sleep and always under deep narcosis, and the use of an anaesthetic may clear up the case. They usually follow a fit, an injury, or an oi^eration. They are somewhat increased on attempts to overcome them by force ; they are usually associated Avith paralysis and anaesthesia and other hysterical symptoms. Hysterical convulsions. These differ from convulsions of epi- lepsy in the way best indicated by the following table ■ Hysterical Convulsion. Epileptic Convulsion. Brought on by emotion or injury; no The opposite in all these particulars, aura ; no initial cry ; movements co- ordinate ; tongue not bitten, and pa- tient never injures herself. Duration perhaps several hours with intermis- sions ; consciousness generally pre- served. Micturition and defecation do not occur. No rise of temperature; may be stopped artificially. The hystero-epileptic attacks are so characteristic that a mis- take could not be made. Prognosis.— The prognosis of hysteria in children is good. They generally get well, although in some cases there is a recur- rence later in life. In liysteria minor of young adults the prog- nosis varies with the severity of the disease and with the physi- cal strength, mental endowment, and social environment of the patient. Mild forms of hysteria under proper treatment usually get well. The severer forms are often intractable even under the best treatment. When a severe form of hysteria occurs in a person of feeble frame who is surrounded with a sympathetic family, the task of rescuing her from her disorder is a very ardu- ous one. Traumatic forms of hysteria which are not infrequently associated with some actual physical injury are often difficult to cure. Hysteria which is associated with some organic disease, 430 DISEASES OF THE NERVOUS SYSTEM. such as a severe pelvic disorder or an organic affection of the central nervous system, has a bad prognosis. Hysteria in the male is generally curable, but it requires vigorous treatment, and spontaneous cure is by no means likely to happen. Treatment.— The treatment of hysteria may be divided into the mental, mechanical, dietetic, and medicinal. By all odds the most imi^ortant factor in the treatment of hysteria is the mental treatment, and the most imiDortant meas- ure to be taken is the isolation of the patient. She should be placed where she will not be surrounded by sympathetic friends ; where her life will be a regular one ; where some occupation may be given which will engross her attention, interest her mind, and call into play her physical activities. In the major forms of hysteria associated with anorexia, emaciation, anaemia, and pos- sibly pelvic disorders, the "rest cure" as elaborated and carried out by Weir Mitchell forms by all odds the most successful means of treatment. In many cases of less severe character a partial rest cure in which the patient is separated from her family but is not placed under such severe restrictions may be all that is needed. In the case of children removal from home is often advisable, and the discipline of well-conducted schools is a most excellent measure. The mechanical means used in hysteria are hydrotherapy, electricity, massage, and exercise. Of these measures hydro- therapy and electricity take the first rank. In hydrotherapy the douche or jet to the back, the shower and cold plunge, and the half bath are the most efficacious. The technique of their use is given elsewhere. In the electrical treatment the static and fara- dic currents give the best results. The static sparks often relieve contractures and lessen or I'emove the anaesthesias, and both forms of electricity seem to have a generally beneffcial tonic ef- fect. Massage is of some value in promoting nutrition, and it also has a favorable sedative effect on many cases. Exercise, particu- larly of an active kind such as stimulates the mind and interests one, is a measure of extreme value and one which has perhaps not been sufficiently api^reciated. The use of the bicycle, play- ing tennis, and horseback-riding are measures which cannot be too strongly recommended to hysterical women; in fact, it is probable that some cases which are submitted to the rest-cure treatment might do better by an entirely opposite kind of pro- cedure. The drugs Avhich can be recommended in hysteria are not numerous and their power is limited. Valerianate of zinc, tur- pentine, asafoetida, tincture of sumbul, iron, and the bromides are the most important of the nervines. In hysterical children a capsule containing two grains of valerianate of zinc and one of THE SPASMODIC TICS. 431 sulphate of quinine is often efficacious. Gowers places more reli- ance upon the oil of turpentine in doses which should be increased to the point of strangury. Pitres recommends the wearing of colored glasses in order to keep off hysterical attacks. Some ex- perimentation is necessary in order to see which color is most suited to the case. In the treatment of hysterical convulsions the most efficient measure is the administration of an emetic, and this can be best done by giving hypodermically one- twelfth of a grain of apomor- phine. Convulsions can be stopped sometimes by throwing water in the face or on the epigastrium ; by firm and somewhat long- continued pressure over the ovaries; by the administration of valerian, aromatic spirits of ammonia, or compound spirits of ether. The Spasmodic Tics (Tic Cona^ulsif). Spasmodic tic is a disease to which the name of chorea is often, but incorrectly, given. It is a very chronic disorder, and shows itself in the form of quick, electric-like spasms of certain groups of muscles or single muscles. The s^Dasmodic move- ments are violent, and several rapid contractions succeed each other, after which there is a period of rest. The spasm has a tendency to become localized in certain nerves, especially the facial {mimic tic), or even in a single branch or twig, as that to the orbicularis, the zygomaticus, the diaphragm, or the tensor tympani. Spasmodic tic sometimes involves the muscles of ex- piration and the larynx, and then it has been wrongly called chorea of the larynx. Stuttering is a form of tic. The convulsive movements may take a wide range and affect a number of groups of muscles, producing quick, violent move- ments of the body. They are sometimes accompanied with ex- plosive disturbances of speech. In these cases the patient at the time of the convulsive movement utters some obscene or profane words {coprolalia), or involuntarily repeats the last words of the sentence spoken to him {echolalia), or spasmodically imitates a gesture made to him {echokinesis), or involuntarily exclaims the thought uppermost in his mind, perhaps revealing some secret against his will {tic cle pensee). The peculiar disorder of the Maine "jumpers," characterized by sudden violent movements on being touched or startled, is a form of tic. So also are the similar troubles known as Za/a/?, occurring in Malay, and imjriachit, occurring in Siberia and Kamchatka. Most of the special forms of spasmodic tic (mimic tic, wry- neck, etc.) have been described elsewhere, ISpasmodic tic with coprolalia affects children between the 432 DISEASES OF THE NERVOUS SYSTEM. ages of six and sixteen years, and by preference the masculine sex. There is almost always a neurotic family history, and the children are nervous. The disease begins with attacks of violent and irregular move- ments, affecting generally the head, face, and upper extremities first, then involving the whole body. The movements can be con- trolled for a time by the will, only to break out with increased violence later. They cease entirely during sleep, which is gen- erally profound. After having suffered from the disease for a time, the patient will, with the attacks, utter inarticulate cries, or he may begin to repeat or echo the words that he overhears. All this is done automatically and suddenly, Avith the accompaniment of grimaces and muscular contortions. The special peculiarity of the disease is the sudden interjection by the patient of obscene words and expressions (coprolalia). The disorder is chronic, lasting for years. It is best treated by isolation, tonics, and ordinary antispasmodics. Paramyocloxus MuiiTiPiiEX (Myoclonus Multiplex, CoxvuLsiYE Tremor, Myospasia). Myoclonus multiplex is a rare disease allied in nature to the convulsive tics and characterized by attacks of quick clonic spasms affecting the trunk and sometimes the extremities also. The disease occurs most often in adult males. It is caused usually by fright, injury, or some violent emotion. Very different forms of spasm have been described under the name myoclonus multi- plex, but in the typical disease the patient without warning is seized with sudden and lightning-like contractions of the trunk and hip muscles, which cause his body to be alternately flexed and extended so violently that he is often thrown from the chair or couch on which he is lying. The arms and legs may be also in- volved, and the attack takes on the characteristics of a general tremor in Avhich the Avhole body shakes. The facial muscles may be affected. The spasmodic movements are bilateral, although they sometimes begin on one side. The convulsions differ from those of hysteria in that they affect groups of muscles that have not the same physiological function and produce move- ments which cannot be easily imitated voluntarily. Still this distinction is not a sharp one. The patients are generally neu- rasthenic or hysterical. They hav-e no paralyses, no anaesthesias, very few pains, and their bodily nutrition is not seriously im- paired. The pathology and pathological anatomy are unknown. The diagnosis is based on the peculiar character of the spasm, thomsen's disease. 433 on the fact that the trunk muscles are involved, and that the spasms are bilateral. The disease usually lasts but a few months, but it may extend over a number of years. The prognosis is fairly good. The treatment consists of tonics and the use of chloral. Gal- vanism seems to be very efficient. Atropine and hyoscine are indicated, and hydrotherapy may also be advantageously em- ployed. Saltatory Spasm. This is a curious and rare form of disease characterized by convulsive movements of the legs brought out by touching the feet to the floor. It occurs in both sexes and at all ages, but usually in those of a neurasthenic and hysterical temperament. The phenomena of the disease are exhibited when the jjatient attempts to stand. The minute that the feet touch the floor vio- lent contractions occur in the muscles of the calves and hips, sometimes in the whole body; these cause the patient to jump, and the movements may be so severe as to throw him down. The seizures are only brought on by the exciting effects of the weight of the body on the feet. Saltatory spasm is probably a form of hysterical spasm. It has been described chiefly by the older writers, and its symptomatology and pathology have not been carefully worked out. Thomsen's Disease (Myotonia Congenita). This is a hereditary family disease characterized by the devel- opment of tonic cramps when the patient attempts voluntary movements. The disorder is very rare. About forty cases have been reported, and in this country only three, one of them being a patient of the Avriter's. ^^/oZo^?/.— Congenital myotony is practically always heredi- tary and runs in families. It affects males by preference and de- velops at the time of adolescence. Si/mptoms.— The patient notices that on trying to rise or walk his legs are seized with a painless cramp, which in a few seconds relaxes, but conies on again when the muscular movements have been repeated. If he closes his hands tightly a cramp occurs and he cannot relax the grip. If he shuts his eyes he cannot open them for a moment. The nmscles of mastication may be affected, but the extremities are the parts most involved. The involuntary muscles are spared. The cramps are increased by cold and nervousness; they are lessened by nmscular exercise. The muscles are somewhat hypertrophied, and the patient may present the appearance of a very strong man. The actual strength is fair, but less than would seem. The general health may be good, but the patients sometimes show the signs of low vitality in weak digestion, feeble sexual power, and susceptibility The electrical excitability of the nerves is normal, that of the 28 434 DISEASES OF THE NERVOUS SYSTEM. muscles is increased, and there is produced a contraction tetanus by both currents. In addition Erb describes a xjeculiar reaction produced by a strong stabile galvanic current. It consists in the appearance of wave-like muscular movements passing from cathode to anode. This was not present in my case or Jacoby's. The mechanical excitability of the muscles is also increased, Fatholofji/.— The disease is probably a primary muscular dys- trophy. There may be, however, a i^eculiar defect in innerva- tion, resulting from a congenital anomaly of the motor tracts. The muscular fibres are found to be hypertrophied, the striations indistinct, and the nuclei increased. The diagnosis is easily made by the characteristic tonic cram])s. The prognosis is bad as regards cure, but the disorder does not shorten life. Treatment. — Dr. Thomsen, who first described the disease, states that active muscular exercise benefits patients. No spe- cific measures are known. CoxGExiTAL Paramyotonia. Paramyotonia is the name given to a form of myotonia in which the symptoms deviate somewhat from the typical ones that appear in Thomsen's disease. Paramyotonia occurs symp- tomatically, congenitally, and in a peculiar clinical form known as ataxic. We have, therefore, symptomatic, congenital, and ataxic forms. Symptomatic paramyotonia is noted most characteristically in a certain form of paralysis agitans. Here the patient, when attempting to walk or to rise from the sitting posture, is suddenly seized with an apparent rigidity of the muscles Avhicli prevents him from stirring. The myotonic condition appears also in spas- tic paralyses of spinal and cerebral origin. Congenital paramyotonia is a family affection resembling in this respect Thomsen's disease. The muscular rigidity is brought on not by voluntary movements, but by exposure to cold and often very slight degrees of cold. The tonic spasm is a long one and lasts for from a quarter of an hour to several hours. It affects the arms more than the legs. The facial muscles are prone to become rigid. The attacks are followed by some muscular weakness. In congenital paramytonia the trouble is undoubt- edly a primary disturbance of the muscles; in other words, a myopathy. Ataxic paramyotonia is the name given to a disorder charac- terized by transient spasms like those of Thomsen's disease, as- sociated with distinct ataxia and also with weakness and some anaesthesia (Gowers). This disease is probably located in the spinal cord and should perhaps be considered one of the forms of symptomatic paramyotonia. ISo special treatment can be given for either of the two latter forms of disease, of which very few examples have been observed. • AKi2fESiA Algera (Paix Palsy). Akinesia algera is the name given by Moebius to a peculiar form of paralysis which occurs in psychopathic persons and is due to the fact that intense pains are produced by every muscu- AKINESIA ALGERA. 435 lar movement. The result is that the patient hes helplessly in bed, afraid to stir hand or foot. The disease occurs only in per- sons who have a very unstable nervous system and generally in those who have a paranoiac tendency. It occurs in adults only. Pain-paralysis comes on gradually and affects eventually all the muscles of the extremities and body. There are no objective dis- turbances such as atrophy, electrical degenerations, and anges- thesias. The muscles and skin, however, are somewhat tender to the touch. The disease lasts a long time. The patient some- times improves, in other cases insanity ensues. The disease is essentially a form of insanit5% a pathophobia, and is allied to the disorder knoAvn as mysophobia. The paralysis is the result of pain hallucination, and the patient is afraid to move the arm or leg on account of this hallucination, just as the mysophobic patient is afraid to touch anything on account of the fear of con- tamination. The prognosis is bad, and so far treatment has accomplished little or nothing. CHAPTER XXIII. THE ACQUIRED NEUROSES. Chorea (St. Vitus' Daxce). Under this name various spasmodic disorders have been de- scribed. They are to be classed as follows : I. Common chorea, or Sydenham's chorea. II. Hereditary chorea, or Huntington's chorea. III. The convulsive tics. lY. Hysterical chorea, including so-called chorea major. V. Various local endemic choreas, such as the electric chorea of Dubini and the electric chorea of Bergeron. Chorea of Sydenham. This is the common type of chorea, and is the disease ordi- narily meant when the term chorea is used. It is a subacute dis- order characterized by irregular jerking and inco-ordinate move- ments. The disease is a common one, forming about one-fifth of the nervous diseases of children. Etiology. — Most cases occur between the ages of five and fifteen (see chart, p. 405). It is very rare under five. A few cases occur after twenty, and even up to old age, when a senile chorea is sometimes observed. It affects girls more than boys in the ratio of about 2.5 to 1. In adult life the disproportion is less marked. It is relatively rare in the negro race, especially in those of pure blood (Mitchell). In this country it is more common in children of German, Hebrew, and Portuguese race. It occurs in all climates. Most cases develop in the spring months, next in the autumn, next in winter, and last in summer. The seasonal influence varies in different localities. In Phila- delphia more cases occur relatively in the spring. In New York there is an almost equal increase in the autumn. School attend- ance has something to do with these variations. Choreic attacks appear to be related to increase in storms (Lewis). The disease is more frequent in cities, and probably in the poorer classes. Hereditary influence is slight, bilt it exists. In a small percen- tage of cases one parent has had chorea, epilepsy, insanity, or a decided neuropathic constitution. A phthisical or a gouty his- tory in parents is also not rare. The chief exciting causes are injury and fright, mental worry. CHOREA. 43Y and rheumatism. Fright or some emotional disturbance is a cause in about one-fifth of the cases*. Acute rheumatism is given as a cause in very varying proportions, ranging from five to twenty-five per cent. In this country it ranges from fifteen to twenty per cent (Sinkler, Starr, Sachs, and personal observa- tions). Endocarditis is developed in the course of chorea in a slightly larger proportion of cases. This may exist without any manifestations of rheumatism. Pregnancy is a cause of chorea generally in primipara and always in young women under twenty- five. Chorea sometimes follows infectious fevers, especially mea- sles, scarlatina, and whooping-cough. It has been caused in rare cases by reflex irritation from an injury, from nasal disease, and sexual disorders. Overstudy and the worry of examinations are factors in causing chorea in predisposed and badly nourished chil- dren. Intestinal irritations, such as worms, may excite chorea. Malaria also may aggravate, if it does not produce it. Hamilton describes a form of chorea caused by tobacco-poisoning. Anaemia and malnutrition underlie most cases. Symptoms.— The disease may begin suddenly, but usually it develops slowly, and it is not till one or two weeks that the symp- toms are decidedly i3rominent. It usually begins with irregular twitching of the hand or face on one side. The child winks, grimaces, and drops things from its hand. The foot and leg be- come affected later and the child stumbles in walking. In two or three weeks the opposite side is involved, but usually less than the one originally affected. In three or four weeks the disease reaches its height. The patient's movements are then almost continuous. The hands can hardly be used and the child has to be fed and dressed ; even walking is awkward and diflBcult. Speech is indistinct and confused from the irregular movements of the lips and tongue. The muscles of respiration may be in- volved so that the rhythm is uneven. It is asserted that the heart's action is affected also ; but this is unlikely. • The choreic movements usually occur both when the muscles are at rest and during volitional acts. In some cases the disease is chiefly characterized by inco-ordinate movements when pur- poseful acts are attempted. In other cases voluntary movements can be readily performed, and the muscles twitch only when the limbs are at rest. The movements cease, as a rule, during sleep. But the child sometimes sleeps badly on account of the move- ments. In severe cases attacks of mental excitement and even delirium come on for several successive nights, and this may be so marked a feature as to form what is called chorea insaniens, or maniacal chorea. Apart from such phenomena, the mind in chorea is usually dulled, the temper irritable, and the child much harder to manage. 438 DISEASES OF THE NERVOUS SYSTEM. The appetite is poor and capricious, the tongue coated, and the bowels often constipated. The nutrition fails a little ; there is anaemia and a tendency to loss of flesh. The eyes present nothing abnormal. Hypermetropia, astig- matism, and muscular insufficiencies exist, but not much more than in other nervous children. The child is often worse in the morning and improves toward night. Excitement and physical exertion make the movements worse. There is rarely any pain and never anaesthesia or ten- derness. The muscles are weak but not actually paralyzed. The deep reflexes are somewhat lessened and the knee jerk may be abolished. The electrical irritability of the muscles is, as a rule, increased, but there are no qualitative changes. Nocturnal enu- resis occasionally occurs. The urine contains an excess of urea and phosphates, and at the height of the attack the specific gravity may be increased. Forms. — Maniacal chorea is characterized by great mental ex- citement — especially at night, delirium, with hallucinations and delusions. AHqy one or two weeks the excitement lessens and the patient becomes dull and apathetic. Such cases usually oc- cur in adult women, and they are sometimes fatal. Paralytic chorea. In this form one arm becomes rather sud- denly weak and powerless. A few twitching movements are ob- served. This form occurs only in children and runs the same course as the spasmodic type. Chorea of adult life and senile chorea. The disease when it occurs in the second half of life attacks men rather oftener than women ; it is not related to rheumatism. There is usually a neu- rotic family history and even a hereditary history of chorea. The attack is usually caused by emotional disturbances. It runs much the same course as juvenile chorea, but is rather more apt to become chronic. When it occurs in old men it is called senile chorea. This type is not to be confounded with hereditary or Huntington's chorea. Duration — Relapses. — The disease in this country lasts about ten or twelve weeks, ranging, however, from six weeks to six months. There may be great improvement followed by a relapse, and in this remittent manner the disease may last for years. If it lasts more than six months it should be called chronic. Re- lapses occur in about one-third of the cases, and rather oftener in girls. Relapses occur oftenest within a year of the first attack and much oftener in the spring. After three years relapses prac- tically cease. The number of relapses is usually but one, but the disease may recur eight or nine times. Relapses rarely occur in adults except in the chorea of pregnancy. Pathology.— Th.Q seat of the lesions in chorea is the gray mat- CHOREA. 439 ter of the cortex and its meninges, the pyramidal tract, len- ticular nuclei, and the spinal cord. The lesions are in acute cases of the nature of intense hyperjemia, with dilatation of vessels, small hemorrhages, and spots of softening. There is infiltration of the perivascular spaces with round cells and swelling and pro- liferation of the intima of the small arteries. In chronic cases the evidence of active vascular irritation is less, but there are Fig. 197.— Perivascular Dii^tations in the White Matter of the Convolutions OF A Very Chronic and Severe Case of Chorea. perivascular dilatations and increase of connectiv^e tissue (Fig. 197). The process suggests a low grade or an initial stage of in- flammation. The cause of this is probably either an infective micro-organism or a humoral irritation similar to that causing the rheumatic symptoms and the heart lesions. In a consider- able per cent of cases (ninety per cent— Osier), especially in those of long duration, there are fibrinous deposits on the walls of the heart. The hyperaemic process may not be confined to the men- inges and motor areas of the brain and cord, but it is only from 4:4:0 DISEASES OF THE NERVOUS SYSTEM. the disease in these parts that the symptoms of chorea arise. The presence of points of irritation in the cortex and its men- inges and in the deeper parts excites irregular discharges of nerve force and j^roduces the choreic movements. The interruption of the voluntary nerve impulses by diseased foci makes these move- ments irregular. The apparently special involvement of the len- ticular nuclei may explain some of the inco-ordination. In para- lytic chorea the pyramidal tract is probably more seriously injured by some single large focus of congestion, exudation, or hemorrhage. Indeed, I have seen a true hemiplegia develop in the midst of an attack. In maniacal chorea the meninges and cortex are more involved. Diagnosis. — The disease is easily recognized by the peculiar twitching movements. It is necessary only to distinguish the different forms. It must be distinguished from convulsive tic, electric chorea of Dubini, hysterical spasms which include myo- clonus, saltatory chorea, and chorea major. The distinctions are not difficult and are given in connection with descriptions of these disorders. Prognosis. — As regards life the i^rognosis is very favorable. In this country death from chorea hardly ever occurs in children. It is more fatal in adults. In England the mortality from chorea is about two per cent. Nearly all non-fatal cases eventually get well. Treatment. — The most imjDortant single factor in treatment is rest. The child should not be allowed to take violent exercise or to have any excitement. In most cases he should be taken from school, and in bad cases he should be kept in bed. Cold sponging or the ether spray daily along the back is use- ful. Nourishing food and iron are indicated. As specific remedies, arsenic still heads the list. It should be given in doses of tu v. of Fowler's solution t. i. d., increased by one or two drops daily to fifteen or twenty drops or even more. If this causes nausea and gastric i^ain or headache, the dose should be stopped for a day and then resumed, if i^ossible, where it was left off. Sometimes the suli)hide of arsenic is better tolerated than the arsenite. Next to arsenic come antipyrin (gr. v.), antifebrin (gr. iij.), exalgin (gr. iij.), the doses to be carefully increased if needed. Tincture of cimicifuga sometimes helps when arsenic fails. The bromide or valerianate of zinc is also an excellent remedy, especially when there is a hysterical element. The bro- mides and chloral are useful adjuvants in promoting sleep. Chloral alone is said to be curative if given in doses sufficient to prolong sleep greatly (Bastian). Exalgin given cautiously with iron, in doses increased to fifteen grains a day, is often very use- ful. Hyoscin hydrobromate in doses of gr. yio is occasionally CHOREA. 441 efficacious. Among other drugs of less value are the salicylates, cypropeclium, lobeline, physostigmine, and tartar emetic. In chronic and obstinate cases hypodermic injections of Fowler's solution should be tried. Galvanization of the brain and spine is also useful. Change of air sometimes breaks up an attack. Hereditary chorea was first described by a Lono- Island physician, Dr. Waters, in 1842, later by Drs. Gorman and Lyon and in 1872 by Dr. Huntington. The American cases have been observed chiefly in New York, Connecticut, New Jersey and Pennsylvania. Cases have been reported also from Gerniany France, and England. The disease rarely begins before thirty or after fifty ; it occurs about equally in males and females. It is always directly hereditary, either through father or mother, usually the latter. It begins without known cause by twitchings in the face ; the movements then extend to the arms and legs. It is attended with progressive mental deterioration, with a ten- dency to melancholia, and finally ends in dementia. Its course is chronic and usually very slow, lasting ten or twenty years. Post mortem, chronic pachymeningitis and leptomeningitis with degenerative changes in the cortex have been found. Electric chorea is a name sometimes and wrongly given to very violent forms of ordinary chorea of Sydenham. The term was first applied by Dubini to a peculiar and progressively fatal spasmodic affection which has been observed almost solely in Italy, and which is perhaps of a podagrous or malignant malarial origin. M. Bergeron in 1880 also described an "electric chorea" in which the patients are attacked by sudden rhythmical spasms. This latter disease has a uniformly favorable course. Neither of these diseases resembles true chorea, nor do they have the char- acter of the tics. The term electric chorea, therefore, is one that should be only used, if at all, with a qualifying explanation. Habit Chorea {Tic Coordiue).— There are many persons who go through life with some trick of speech, of gesture, or some peculiar grimace. It may be only a shrug of the shoulder, a twitching of the eyes, or a sniff. These various movements are tics of the co-ordinate kind. The spasmodic motion is of itself normal, but is inappropriate and misapplied. Such movements are often seen in children. They sometimes represent abortive attacks of chorea, and sometimes they are the residuum of old attacks. In many cases they are chronic convulsive tics from the start and have little relationship to Syden- ham's chorea. The condition is to be treated both by moral and medicinal measures. Oscillatory spasms and nodding spasms have been described Procursive Chorea, or Dancing Chorea— haycock^ has de- scribed as a separate kind of chorea a rhythmical or trochaic torm, which he says affects children, principally girls, and shows itseii in spasmodic rhythmical contractions or in sudden rotating or 4:4:2 DISEASES OF THE NERVOUS SYSTEM. procursive movements of the body. This has been called chorea procursive, or chorea festinans, by other writers. In many cases it is accompanied with vertigo, when the condition of the patient is similar to that of a person who has been whirling around a num- ber of times. Such cases always have decidedly hysterical char- acters, although these procursive attacks may complicate ordinary chorea. Chorea major is a manifestation of hysteria, and will be de- scribed under that subject. It is not a chorea at ah. TETANUS. Tetanus is an acute or subacute infectious disease characterized by violent tonic spasms with remissions and exacerbations. It is called idiopathic when no open wound is found and traumatic when such condition is present. When it attacks infants it is called tetanus neonatorum; when the jaws alone are involved it is called lockjaw, or trismus. A form which affects the face and throat is called head or cephalic tetanus. Etiology. — It has a special predilection for new-born children in some countries (West Indies) and to a less extent tor puerperal women. It affects males more than females. After the first month of. life there is practical immunity till after the tenth j'ear. It then increases in frequency up to forty. It is much more fre- quent in dark races and in some tropical climates (West Indies, South and Central America). Symptoms. — The disease sets in from five to fifteen days after infection. It begins with feelings of stiffness in the neck and throat and sometimes with chilly feelings. Gradually tonic spasms develop which involve the trunk muscles, causing opis- thotonos and other forms of rigid spasm. Trismus, or lockjaw, also occurs. The spasms are attended with intense pain. Some- times there is a rise of temperature and this may be very high. The disease lasts for two to five weeks. There is evidence of irri- tation and congestion of the spinal cord and injured nerves, but no special anatomical changes are found. A specific bacillus producing a tetanizing poison has been discovered. The diagnosis is based on the characteristic history and the peculiar spasms. In strychnine-poisoning there is no initial tris- mus or epigastric pain. In rabies there is also no trismus but a respiratory spasm on attempts to swallow. The i^rognosis is bad. About eighty per cent of the traumatic and sixty per cent of idiopathic ca^es die. The treatment consists of complete rest and quiet in a dark room and the administration of chloral, bromide, morphia, and physostigma. Successful results from injection of blood serum of an animal which has had the disease are reported. TETANY. 443 Tetany (Tetanilla). Tetany is a subacute or chronic spasmodic disorder character- ized by intermittent or persistent tonic contractions beginnin<>- in tlie extremities and associated witli pareesthesiie and liypei^ excitability of the motor and sensory nerves. Etiology.— ThQ disease is very rare in this country, but rela- tively common in Europe, especially in Austria. It occurs with frequency during the second, third, and fourth years of life and again at the time of puberty. Its rate of frequency then slowly declines and it is very rare after fifty. It affects' males much of tener than females up to the age of twenty, after that the differ- ence disappears. It occurs mostly in the working classes. In infants rickets is often noted. The exciting causes are exhausting influences like diarrhoea, lactation, se^jsis, fatigue, mental shock, and fevers ; also exposure to cold and m et. Alcoholism, dilatation of the stomach, and intestinal entozoa are also causes. It may be produced artificially by extirpation of the thyroid gland. The disease sometimes appears as an epidemic. ISymptoms. — Tetany begins sometimes suddenly with symmet- rical tonic contractions of the hands ; at other times there are at first sensations of numbness, prickling or pain in the extremities, with malaise and perhaps nausea ; then spasms begin. The at- tacks affect first and most the upper extremities. The flexors of the forearm and hand are usually involved; the fingers are flexed at the metacar[)0-phalangeal joint and extended at the other joints, and the thumb is adducted, producing the " accoucheur's hand." The forearm may be flexed and the upper arm adducted. The knees and feet are extended, the toes flexed, and the foot in- verted. In severe cases the muscles of the abdomen, chest, neck, and face are involved. Opisthotonos and dyspncDea may result. The muscles of the face and eyes develop contractions, and tris- mus sometimes occurs late in the disease. The nmscles of the larynx, oesophagus, and bladder may be affected. Fibrillary tremors are observed in the contracted muscles. The attacks are accompanied by parsesthesise and cramp-like pains. There may be some abolition of sensation in the skin of the parts affected during attacks. The cramps last from a few minutes to hours or days. They occur during day and night and may wake the pa- tient from sleep. Fever is sometimes present in epidemic cases. The disease has a tendency to recurrence. While it lasts, both during and between the attacks peculiar phenomena are observed as follows : 1st. Increased Mechanical IrritaMUty of Motor Nerves— The motor nerves show an abnormal irritability, so that on strikmg the motor point a sharp muscular contraction is brought out. When pressure or a blow is made on the face over or near the exit of the facial nerve from its foramen, contractions of the facial muscles occur, especially those of t\ie lips. This is called the fa- cial phenomenon." Bv pressing on the artery and nerve qt a limb a tetanic attack can be produced in the muscles supp lecL It is probable that it is the pressure on the nerve alone whicii causes the phenomenon which is called " Trousseau's symptom. 2d. The electrical irritability of the muscles and nerves is m^ creased, especially to the galvanic current. Thus a negative^ pole closure contraction (CaCC) is brought out by a very weak; 444 DISEASES OF THE NERVOUS SYSTEM. current ; and if a little stronger, it causes a tonic contraction or cathode' closure tetanus (CaCTe) The positive-pole opening contraction (AnOC) may be tetanic, i.e., (AnOTe), and there may ]3e even a cathode opening tetanus (CaOTe), a phenomenon not seen in any other disease. According to Gowers there may be a reversal of the polar formula, so that a positive-pole closure con- traction occurs earlier than a negative (AnCC>CaCC). This is certainlv rare. 8d. Art increase of irritability of the sensory nerves is shown by pressing upon them, when sensations of i^rickling and formi- cation appear along their course. There is an increase also in the electrical sensibility, shown by appreciation of very Aveak galvanic currents. The auditory nerve reacts to the galvanic current in about fifteen per cent of normal cases, and then only to strong currents and to ohly a i^artial extent; but in tetany it reacts in nearly all cases, and with coniparativeh- weak currents (2 to 5 or 6 lua.) on anode closure, anode fixed, and anode open- uig (AnC Klang, AnDKl, AnOKl) (Chvostek). The iDhenomena of hyperexcitability above described vary considerably and rapidly during the course of the disease, and are not always present. Tyjjes'of the Disease.— The disease varies in intensity and dura- tion. This variation depends much upon the cause, and there have been made a number of types of the disease based on the etiology. Thus we have 1. Epidemic or rheumatic tetany. 2. Asthenic tetany due to lactation, diarrhoea, exhausting dis- eases, etc. 3. Thyroid tetany, due to removal of the thyroid gland. 4. Reflex tetany from gastric dilatation and intestinal worms. 5. Latent forms of tetany in which the phenomena of hyper- excitability and paraesthesia occur with very slight if any con- tractions, and no Trousseau symptom. Infantile tetany should perhaps be separated from other forms. Symptomatic tetany from brain disease is also spoken of. When the spasms are continuous the disease lasts but a few Aveeks; when they are intermittent it may continue for months. Epidemic cases last but a few weeks. The disease may be said in general to last from a few weeks to a few months. Patients are liable to a recurrence on return of the exciting cause. Pathology. — The phenomena of the disease indicate a congested and irritative condition of the gray matter of the spinal cord. The cause of this state is evidently in some cases (epidemic tet- any) an infectious poison; in other cases mucin in the blood (thyroid tetany), and in other cases it may be a rheumatic or some other toxic influence. Ergot is known to produce symptoms resembling tetany. In infantile tetany the irritation is apparently cortical and due to meningitis or to rickets and the reflex irritation of disor- dered bowels. It is doubtful if any reflex influence can be invoked in adults. Tetany is a functional 'disease and the symptomatic expression of a central irritation. This irritation may be of differ- ent kinds, hence tetany has a claim to be called a distinct disease simply on clinical grounds. It has no such definite pathology as chorea or epilepsy. In the very few autopsies Avhich have been made no definite organic lesion has been found. TETANY. 445 Diagnosis.— The disease is usually easily recognized by the character of the spasms, their symmetrical nature, their course, and the phenomena of hyperexcitability of the muscles and nerves. Trousseau's symptom is found in no other disease. The " facial phenomenon," the peculiar electrical and mechanical irri- tability of the muscles and nerves are very rare in other condi- tions. The sensory irritability and especially that of the acoustic nerve are also characteristic. From tetanus the disease is distin- guished by the intermittency of the contractions, their feebler character, the fact that they begin in the extremities and extend to the trunk, and by the absence of trismus at least until late in the disease. Treatment. — The cause should be removed if possible, lactation stopped, diarrhoea and indigestion corrected, worms expelled, rickets, if present, attended to. Rest; nourishing food, and tonics are indicated. Symptomatically, bromide of potash in doses of 3 iss. to 3 ij. daily with chloral furnishes the surest relief. Hyos- cine in doses of gr. y^^ n^ay be tried. Inhalation of chloroform or injections of morphia are needed in severe cases. In nocturnal tetany Gowers advises digitalis. Lukewarm baths may be of service ; so also may ice-bags to the spine. If electricity is used only the weak galvanic current should be employed. CHAPTER XXIV. NEURASTHENIA (NERVOUS EXHAUSTION)-NERVOUS AVOMEN. Neurastheis^ia is a morbid condition of the nervous system of which the underlying cliaracteristics are weakness and exces- sive irritability. The disorder is a functional one. In its typi- cal forms the symptoms are distinctive. £'^/o/o^2/-~^6urasthenia occurs most often between the ages of eighteen and thirty, next between the ages of thirty and forty, and then between forty and fifty. It rarely, if ever, begins be- fore eighteen or after fifty.* It affects men and women almost equally in this country. Pure cases are more frequent in men, while atypical forms in which there are complications of hysteria, spinal irritation, and local disorders are moi'e frequent in women. Americans are, as a race, much affected by it! The cold and dry climates of the temperate zone favor the development of the disorder. So also do high altitudes if they are dry. Hence the climate of this country, as well as its civilization, undoubtedly help to promote the disease. In the West, and especially the Northwest lake region and the Colorado plateau, neurasthenia is said to be rather more prevalent than in the South or East. It occurs in rural as well as urban populations. The educated classes— professional men, business men, and politicians— furnish a large contingent. Heredity is a very important factor in the primary forms. The exciting causes are excessive mental strain, anxieties, sud- den shocks, injuries, sunstroke, excessive child-bearing, sexual excesses— especially masturbation— irregularities and excesses in eating, drinking, and smoking. Overwork does not cause it, pro- vided there is no great mental worry ; and even this can be borne if the patient is regular in eating and sleeping and does not drink or smoke too much. In some .cases it follows some single power- * Among 100 consecutive cases there were 53 women, 47 men. Ages : fifteen to twenty-five. 25 ; twentj^-six to thirty-five, 38 ; thirty-six to forty-five, 25 ; forty-six to fifty-five, 20 ; fifty-six to sixty-five, 2. There are relatively more cases in the adolescence of man and in the later period of life of women. Nativity : United States, 59; Ireland, 29 ; Germany, 12 ; others, 9. NEURASTHENIA— NERVOUS WOMEN. 447 ful physical exertion. Malarial-poisoning, syphilis, and the in- fective fevers are important agents in causing neurasthenia. So also are lithaemic states, gastric dilatation, and dyspepsia. Reflex irritations. There are many persons, with delicately balanced organizations, who only require some single depressing or irritating agent to put them in a pathological state. This is the case in those neurasthenics who are made so by reflex causes, (iiven a neuropathic constitution, neurasthenia may be produced by ovarian and uterine disease. Subinvolution and decided me- chanical displacements are more potent in causing neurasthenia than the chronic inflammatory states. Prostatic and urethral disorders, hemorrhoids and fissures, may excite general neuras- thenic symptoms. Chronic middle and internal ear disease, caus- ing great tinnitus and partial deafness, often aggravates a neu- rasthenia, if it does not excite it. Nasal stenosis and hypertrophic catarrh, acting either directly or by disturbing the visual appa- ratus, may be a cause. Muscular insufficiencies of the eyes, re- fractive errors, especially hypermetropia and astigmatism, are often important factors in the etiology of neurasthenia, but they are not primary or fundamental. Of reflex influences causing and keeping up neurastiienia, disturbances of the stomach, in- testines, and liver are by all odds the most important; next come irritations from the pelvic and generative organs. Symptoms. — In the neurasthenic condition there are certain common symptoms which will be found in all cases, but these symptoms vary in prominence according to the special setting of the case. The modifying elements are these : (1) age, (2) sex, and (3) neuropathic constitution. In ordinary cases the patient after some years of arduous work, anxiety, and irregular habits, during which he has kept himself continually on a strain, begins to have feelings of nervousness, restlessness, and irritabihty which are new to him. He has trouble in sleeping and wakes unrefreshed ; he loses interest in his work, which tires him greatly. His appetite is poor and his digestion disordered; he has vertigoes and peculiar feelings about the head ; and he begins to get alarmed about himself. The symp- toms progress until he finds he can no longer work, he is irritable, depressed, and discouraged, and finally begins to take himself in hand. In some cases, after a sudden fright or injury and shock, all these symptoms develop rapidly. In younger persons the history is somewhat different: the pa- tient has perhaps indulged in sexual abuse; then suddenly learn- ing that it is a very dangerous practice he experiences a fright. He becomes nervous, worried, and mentally depressed. He too has cerebral par^esthesi* and insomnia; he loses interest in his stud- ies, cannot concentrate his mind, broods over his early indiscre- 448 DISEASES OF THE NERVOUS SYSTEM. tions, and is panic-stricken over every nocturnal emission. Getting- some comforting assurances and advice from his physician, he improves and perhaps gets well, but not infrequently has for several years a train of disturbing neurasthenic symptoms. As in older pases, the neurasthenia may come on suddenly from shock, violent physical exertion, and over-use of tobacco. Symptoms in Detail.— T\\Q neurasthenic iDatient suffers from a peculiar feeling of nervousness, discomfort, uneasiness, and sense of unrest; or from feelings of tension, as though under a stimulant. He loses interest in his work, dreads to assume any responsibility, has morbid fears regarding his business, his sexual function, his general health, his future, or some trivial subject. Some idea fixes itself upon him and he cannot rid him- self of it. He has difficulty in concentrating his mind on work. Periods of depression attack him. These mental ^-st at es vary much, and may be so paroxysmal as to form "crises." His sleep is poor, disturbed by dreams, and he awakes unrefreshed; some- times there is a morbid somnolence. Slight attacks of vertigo annoy him. The sensory symptoms consist of feelings of pressure on the top of the head, as of a hand or cajD pressing on the scalp {the helmet symptom); pain or weariness in the back of the neck; numbness of the hands or feet, creeping sensations up the back or limbs, burning feelings in the ears, pricking of the tongue, a sense of oppression of the chest and of "sinking" in the epigas- trium. These form what are termed neurasthenic parcesthesice. ZS'eurasthenics in about half the cases suffer from headaches. These are diffuse and frontal or occipital. The pain is persistent, worse . after exertion, and not very intense. A boring occipital pain, neckache, and neck loeariness are very common, and women often have severe pains along the spine. Intercostal neuralgia, especially on the left side, is common. General neuralgia, aching of all the limbs, feeling of soreness of the scalp or of the mus- cles, as though one had been beaten, are often complained of.* The Special *S'e?^se.S'.— Neurasthenia does not, as a rule, cause very serious visual troubles. There is always some weakness and increased irritability of eyesight. If the patient uses the eyes nmch these symptoms may become very marked. There is a feeling of pressure and discomfort or pain in the eyeballs. Head- ache comes on. Vision gets blurred; there are spots before the eyes; excessive light is annoying and moderate light dazzles. Reading soon tires and causes pain; the lids twitch; the eyes easily redden and water. Examination shows in early life mo- * Neurasthenics with a hypochondriacal tendency sometimes sufifer from a persis- tent delusional pain located in a certain region, such as the arm or back. This con- dition has been called topoalgia. NEURASTHENIA — NERVOUS WOMEN. 449 bile and often dilated pupils ; they are rarely uneven ; there is a sli£,dit lessening of visual acuity. The visual field is normal, but sensation in its periphery tires very easily, so that after long test ing there is apparently a concentric limitation of the.field. The color sense is unaffected. Muscular insufficiencies, especially of the internal recti, often occur. The patient's visual memories are lessened, so that the neurasthenic cannot remember faces and places as he has been accustomed to do. If the patient has any refractive error, especially hypermetropia or astigmatism, his eye symptoms are more marked and cause him so much annoyance that the general symptoms get worse. The eye trouble may thus keep up the neurasthenia, but it will not alone cause it, and treatment of the general and local symptoms by attention to the eyes alone is irrational and disappointing. Neurastlat»nics are often over-sensitive to noise. This is usually simply due to the general mental irritability; but sometimes there is a distinct hyperacousia, and slight noises or even agree- able music drive the patient nearly wild. Subjective disturbances of taste occur in cases complicated with digestive troubles. There are no peculiarities regarding the sense of smell other than a general over-sensitiveness to odors. The general muscular strength is lessened, and the patient very soon tires, or even completely collapses, after slight exertion. Muscular effort or mental excitement causes a tremor of the hands; often this is a persistent symptom. This tremor is "fine "and vibratory in character (about twelve to the second). The skin reflexes and tendon reflexes are exaggerated. There is a slight amount of "static ataxia," i.e., the patient sways more when standing erect with closed eyes than when his eyes are open, the reverse being the case in healthy people. The eyelids quiver when tightly shut. The general nutrition is not usually much affected ; if anything, the patient loses weight. There is decided evidence of loss of vasomotor tone. This is shown in the cold hands and feet, tendency to hyperidrosisof the palms and soles, flushings and pallor of the face, sense of fulness in the head, variations in the specific gravity and amount of the urine. Palpations of the heart easily occur, and examination of the pulse shows it to have frequent and rapid 'variations in ten- sion, there being generally abnormal lowering. The vasomotor reaction produced by drawing a blunt instrument over the skin is more pronounced than in healthy people. A deep red hne appears after pressure, which lasts twenty or thirty minutes. In rare cases an artificial urticaria can be produced. The phe- nomenon is called " dermography." The sexual functions are weakened and irritable, and inter- 29 450 DISEASES OF THE NERVOUS SYSTEM. course is imperfect and exhausting. In the younger and more neuropathic cases emissions occur, and morbid fears regarding this function annoy and depress the patient. These fears and introspections occupy the mind and furnish to the patient the belief that all his troubles hinge upon his early indiscretions or his present rather frequent emissions. Sometimes thei-e is, in fact, such an extreme degree of seminal loss as to keep up the neurasthenic state. The genitals become relaxed, there is a slight discharge of urethral and prostatic secretion, especially after stools. In women dysmenorrhoea, menorrhagia, and slight irreg- ularities in menstruation occur. The digestive organs, including the metabolic tissues of the liver, are almost always at fault. There are a great many ner- vous affections of the stomach, such as gastralgia, gastroxynis, muscular atony, etc. These disorders may be associated with neurasthenia and be the cause of part of the trouble. The gastric trouble in rare cases may even be primary, or hold equal rank with the nerves in the symptom complex. Such, however, is by no means the rule. The nervous asthenia leads to the gastric dyspepsia, and this again makes the neurasthenia worse. The special symptoms caused by the stomach complication are a sense of congestion and f-ulness in the head, dizziness, headache, palpitation, and abdominal pulsation ; belching, feeling of pres- sure and fulness in the epigastrium, nausea, pyrosis, anorexia, and alterations of taste. The hepatic functions are weakened and slowed down ; and a neurasthenic liver is one of the common and fundamental condi- tions of the neurasthenic state. This produces intestinal dyspep- sia, fermentation, and constipation. The blood absorbs an excess of ptomaines and imperfectly oxidized products, causing many of the general nervous symptoms already described, such as the parsesthesi{je, dizziness, somnolence, and head pressure. This condition is called " lithaeinia,''' or nervous gout. It is not so much a distinct diathesis, like the gouty or rheumatic, as it is a morbid condition from accumulation of metabolic products. The intestinal movements are sluggish, and the patient suffers from flatulence and feelings of distention. Sometimes there is a nervous diarrhoea alternating with constipation.* Sometimes the striking sj-mptom in a neurasthenic patient is the disturbance in the heart's action. This shows itself in feeble- * Enferoptosis and Neurasthenia.— A 'form of neurasthenia has been rlescribed by Glennard under the head of enteroptosis, or prolapse of the abdominal viscera. This occurs in women who have lax abdominal walls, with some descent of the stomach and intestines, and stretching of the suspending ligaments and mesenterj'. In these cases there is usually some dilatation of the stomach, atony of the intestinal walls, and consequent symptoms of inuigestion. NEURASTHENIA— NERVOUS WOMEN. 451 ness of the heart beat and heart sounds and sinallness of the pulse. Palpitation occurs on slight exertion, and there may be pseudo-anginal attacks, or sensations of oppression and discom- fort over the heart. The patient also complains of feeling the beating of the heart, perhaps all over the body. The pulse may be very slow, especially in the morning. General neurasthenic symptoms are present. Patients with heart disease are liable to be especially annoyed by various evidences of heart weakness and irregular action. The respirations are normal in number, but shallow, and de- ficient respiratory expansion may be noted. A feeling of pres- sure on the chest is often described. The younger patients and women are generally anaemic, but in middle-aged adults this is not so; the face is full and ruddy and the mucous membranes of good color. The urine in the young and neuropathic cases is variable in specific gravity, but generally low, 1.012 to 1.018; under excite- ment it may drop to 1.002. Phosphates, earthy and alkaline, are excreted in excess, wdiile the nitrogenous solids are often dimin- ished in amount. In older cases with more digestive and hepatic disturbance and lith^mia the urine is heavy, 1.024 to 1.036, quite acid, and contains at times excess of phosphates and urates. Ox- alates are also found, but indicate no more than does excess of urates, i.e., a lithtemic state. The amount of urine passed is variable. At times there is polyuria, but on the whole the total amount is below normal. The Modified Tx-p-K^.— Neurasthenia in Adolescence— De- generative Neurasthenia.— When neurasthenia begins under the age of twenty-five, there is a more distinct evidence of neuro- pathic constitution. The mental symptoms are more marked and approach those of hypochondriasis. There is greater de- pression and greater introspection. 'Morbid sexual ideas, fear of impotence, remorse over past indiscretions in venery ; spermato- phobia; morbid fears of contamination, of being forever inca- pacitated for procreation or sound mental and physical work, annoy the patient. The general nutrition is affected. He is anaemic, has cold extremities, clammy hands, dilated pupils. His urine is of low specific gravity and contains an excess of phos- phates, both earthy and alkaline. Pains, parsesthesiae, vertigo, head pressure, and gastric disturbances are not so marked. This type of neurasthenia is often described as " sexual " or as " primary. '' It is really a manifestation of neurotic degeneracy, and may be looked upon as an abortive form of paranoia. When more fully developed the degeneracy shows itself by such symp- toms as fixed ideas, and morbid fears such as agoraphobia (fear of open places) ; claustrophobia (fear of closed places) ; mysophobia 452 DISEASES OF THE NERVOUS SYSTEM. (fear of eontainination) ; pathophobia (fear of disease); anthro- pophobia (fear of society). Abortive forms of folie du dotcte, or the doubtness-niadness, are also present in this type. neurasthenia of Women in Adolescence. — Young nervous women are usually anaemic, dyspeptic, and constipated; their nutrition is not good; they are thin; they excrete large quanti- ties of limpid urine ; they often have spinal pains and headaches of the migrainous and other types, and almost all of them suffer more or less at the time of menstruation. They have mobile pupils. Their special senses are keen, to the point of hypertes- thesia. The heart is irritable; the vasomotor centres are un- stable. They have cold, clammy extremities. They are vivacious, quick, observant, impatient, living on their " nerves," fond of excitement, and indulging in amusements, for which they pay the penalty by prolonged exhaustion. Neurasthenia of Women in Early and 21iddle Life.— It is the nerv^ous women between the ages of twenty-five years and forty who make up the majority of female neurasthenics. They are, so to speak, the wreckage of the young nervous women and of healthy young women for whom the burden of life and domes- ticity^ was too heavy. For they are usually married and are some- times prolific mothers, though the worst cases are the childless or the " monopsedic.*' The principal symptoms from which they suffer are nervousness, weakness, insomnia, dyspepsia, morbid and depressing ideas, headaches and neuralgias, vertigo, tremor, and vasomotor symptoms. They often have migraine and backaches, but they do not have fully developed spinal irritation ; they suffer from peculiar feelings of numbness in different jDarts of the body ; they often exhibit a marked tremulousness of the hands, Avhile the cold ex- tremities and wet hands are not so commonly observed. They become easily exhausted. They are excessively nervous and irri- table ; slight noises will startle them; they cannot read long with- out gettmg a pain in the head ; they suffer from time to time from attacks of prof ound mental depression, and often have fixed ideas of a melancholy type; they have, at times, "crises," or "nervous storms," which may take the form of a headache, a fit of blues, or a lively domestic disturbance. The dyspepsia they have is not of a very severe type ; it is usually accompanied with fermenta- tion and acid eructations. The urine always varies in quantity and specific gravity. Sometimes they will pass large amounts of limpid urine. Such women are often called hysterical, but the somatic and asthenic symptoms are more prominent than the psychical, and they do not have hysterical stigmata. Climacteric Neurasthenia.— At the climacteric in women, and sometimes at a corresponding age in men, neurasthenic symptoms NEURASTHENIA— NERVOUS WOMEN. 453 develop. In women these symptoms are mostly of a vasomotor character. Hot flashes, flushing, nervous irritai3ilitv, poor sleep oj- morbid somnolence, pains in the back and head, sensations of fainting and sinking, tendency to mental depression, are among the chief symptoms in women, among whom this trouble may be regarded as a climacteric neurasthenia. Evidences of vascular tension and of beginning arterial degeneration will be found. In men the symptoms do not greatly differ from those of the ordinary type. Both in men and women this form of neurasthe- nia runs a comparatively short and favorable course. Course and Z>i^raif/o7Z.— Neurasthenia is a chronic disorder and lasts from one to five or ten years, depending largely upon treatment and habits of life. The forms occurring at the climac- teric are the shortest and most favorable, those occurring in early middle life come next, while those fovms which develop in youth, if dependent upon neurotic constitution, are the most chronic. The disease lasts longer in women than in men. P«^/io^^?/,— Neurasthenia is a condition in which the nutri- tion of the nerve cells is primarily at fault. These cells have lost their power of building themselves up into stable compounds. They easily break down under slight irritation, and send out consequently but feeble impulses. These facts are indicated by the terms " irritability" and " weakness.'" It is thought by some that this dystrophic condition especially involves those parts which make up the vasomotor neuro-mechanism ; and if this be so, it is the nervous tissue of the medulla and central parts of the spinal gray matter that are the most involved. There is lit- tle doubt, however, that the cortical gray matter and higher cen- tres of the brain are also implicated, for the mental symptoms are always prominent. It is certain that the peripheral nerves are not i3rimarily at fault. Since it has been shown that the sympa- thetic system is only an outflow from the cerebro-spinal, and that many of its ganglia are rudimentary and functionless, the idea that neurasthenia is located in the " ganglia " of this system be- comes quite untenable. The view that neurasthenia is usually lithsemia and of gastro-hepatic origin I have tested thoroughly. Patients rarely get any better by treatment based on this hy- pothesis. Vascular changes in the nervous sj^stem take place. These are of the nature of cerebral hyper^emia, and probably hyper- emia of the spinal gray matter. More rarely there is ansemia. The importance and dominance of the vasomotor changes in the skin and internal viscera have been already alluded to under the head of symptoms. This vasomotor disturbance is one char- acterized by a weakness of the inhibitory vasoconstrictor centres. As a consequence the vessels dilate and contract irregularly in 454 DISEASES OF THE NERVOUS SYSTEM. the different systems of the body. Furthermore, they do not re- spond normally to the stimulus of functioning. When brain or stomach acts it calls for a definite and well-regulated supply of blood; in neurasthenia it does not get it, and hence the morbid symptoms. The nervous system controls the metabolic processes of the body, which are especially active in the liver, spleen, and mus- cles. In neurasthenia this process is disturbed, and the liver particularly is atonic or sluggish. This disturbance has already been described under the head of digestion. In other cases metabolism is affected differently ; it seems to be simply too slow. The tissues do not build up and break down at a normally rapid rate. The urine is of low specific gravity and the total solids excreted are less than normal. One exception to this slowness of metabolism occars. In all forms of neurasthenia there is a tendency to excessive breaking up and discharge of the phosphates, both alkaline and earthy. Diagnosis. — Neurasthenia must be differentiated from simple nervousness, degenerative forms of insanity, such in particular as paranoia, from hypochondriasis, from melancholia, hysteria, and spinal irritation. Nervousness may be a natural characteristic, a part of the temperament. As long as the patient does not suffer and is not incapacitated from work and enjoyment, we can somewhat arbi- trarily say it is not neurasthenia. Peculiar sexual perversions, doubting mania, pronounced forms of morbid fears, may be associated with some neurasthenic symptoms, but the diseases mentioned are essentially iDsychical disorders and dependent on a congenitally deficient brain. The hereditary history is usually bad. The clearness and dominance of the mental symptoms are sufficient for a diagnosis. The same remarks apply to hypoGhondriasis. The mental depression and fixed ideas are altogether disproportionate to the other symptoms. In melancholia there are pallor, anaemia, loss of flesh, ano- rexia, insomnia, coated tongue, and constipation, often a lowering of temperature, a profound and constant mental depression. This must often be looked out for in Avomen at the time of the climacteric. The mild types of melancholia are found oftener in women. Hysteria may complicate neurasthenia. It is found much oftener in women, but in the neuroses following shocks and inju- ries it is seen in men. Hysteria is essentially a mental disease involving the emotional faculties and the will, while the bodily condition may be good. It is characterized by various crises of a convulsive or emotional character. There are certain stigmata 1 NEURASTHENIA— NERVOUS WOMEN. 455 almost always present which enable one to recognize it. These are the anaesthesiae of the special and gerieral senses. Spinal irritation is usually a complication of neurasthenia or hysteria, and presents easily distinguishable characters. It may occur quite independently of the distinctive symptoms of the neurasthenic state. The jyrognosis is in general favorable. Most patients get well, or practically well, so that with care they can enjoy life and at- tend to its duties. But the patient almost always has some re- minders that he cannot overtax himself or do quite as much as can a person of strong nerves. This is especially true up to the age of forty-five or fifty. The lessened sensibility of the nerves in the declining years then comes to his help ; he gets the benefit of his past years of regularity and temperance ; his late years are his best, and he lives to enjoy many of them. Neurasthenics, if they get well, get old. ^N^eurasthenia does not lead to insanity or epilepsy or organic disease; but it may be supplanted for a time by an asthma or severe neuralgia or other neurosis. Treatment. — It is of the first importance for the physician to get a firm control of the patient. This can only be done by mak- ing the most careful and scrutinizing examination, and by so acting as to make the patient feel that he understands his case and is master of its character. The patient should then have his course of treatment laid out for him. If he does not follow it strictly all treatment should be stopped. Women are harder to manage at their homes 'than men, and it is better to isolate them somewhere if possible. Rest or lessening of business and domestic duties is fundamen- tal. Travelling is bad, but the patient can be sent to stay at such places as the Azores, West Indies, Bermuda, or to some special point in Southern Europe. A trip along our great lakes, camping out, or long sea voyages in rather warm climates are to be advised. The diet should be rather nitrogenous than otherwise, but fats and green vegetables and certain fruits may be added. Sugars and starches are to be avoided, though malt preparations usually agree. The nutrition of the patient cannot be too carefully watched. He should be weighed and sometimes fattened, using water, malt, oil, and cream for this purpose. The amount and specific gravity of urine must be noted, and his diet regulated accordingly. Neurasthenic patients usually drink too little water or else too much at meal-time. Water should be drunk between meals or half an hour to an hour before meals. Neurasthenics need to be properly fed, but not to be stuffed. In many cases a low diet, but one perfectly digestible, is most indicated. Meals should be taken at fixed hours. A cold sponge bath, or a shower or a strong jet of cold water 456 DISEASES OF THE NERVOUS SYSTEM. on tlie back, or a cold plunge, are measures that are almost in- variably indicated. In irritable cases the Avet pack for three- quarters of an hour, followed by the cool wash-off, has a very quieting effect. A lukewarm bath at 95' to 98' at night for half an hour relieves the paraesthesise and insomnia. The skin should have a thorough rubbing every day. Respiratory exercises for expanding the lungs, light exercise, such as swinging clubs or dumb-bells, throwing balls, swinging from horizontal bars or rings, bicychng, horseback-riding, tennis, rowing, fishing, etc., should be encouraged. The exercise should not be severe ; it should be interesting, it should be done in fresh air, and it should bring into play the lungs and arms more than the legs. Walking does little good, though it is better than nothing. The drugs of most use in neurasthenia are the bromides, nux vomica, mineral acids, quinine, iron, valerian, the hyp- notics, and saline and alkaline laxatives. Many drugs of re- pute, such as arsenic, phosphorus, zinc, cannabis indica, bella- donna, are of no especial value. The bromide of sodium or potassium should be given in doses of fifteen or twenty grains three times daily; it should be kept up for only a week and thei;i gradually reduced to one-half dose once daily. At the same time the patient may be given a tonic mixture containing quinia, strychnia, and, if indicated, iron. Quinine must be given carefully, as it causes increase of nervous- ness in many. Phosphoric and muriatic acids are the two mineral acids most often of use. These acids are usually better given after meals. In mild cases a tonic and sedative may be combined by giving a mixture containing hydrobromic acid with nux vomica and pepsin. As a matter of convenience the bromide of lithium in five-grain doses may be put up in capsules with hydrobromic acid and glycerin. Tincture of nux vomica sometimes acts bet- ter than strychnia, but it must be given in large doses— tti x. in- creased to m XXV. or m XXX. The saccharated carbonate or albu- minate of iron, or Eland's pills, if given, should be given generously, i.e., in doses of thirty grains daily. The insomnia, if present, yields usually to the bromides, but will return unless further treatment is given. After using bro- mides for a time, therefore, it is better to substitute half a drachm of sulphonal or of chloralamide, or gr. xv. of chloral, or a drachm of paraldehyde. Lukewarm baths (95' to 100") may be used as adjuvants. The dose of the hypnotic should be gradually less- ened and not suddenly and irregularly stopped. If the patient is lithsemic or arthritic, he should be made to drink an alkaline water, like the lithia waters or Carlsbad, and his bowels are better kept open by means of salines than pills. NEURASTHENIA — NERVOUS WOMEN. 457 Antipyrin, potassium bicarbonate, and the salicylates often help painful symptoms in such eases. In those forms of nervousness in which there is a great deal of melancholy quinine is of use, and when quinine cannot be borne in ordinary doses the patients will often tolerate Warburg's tincture. In cases in which there is a good deal of cerebral hyperemia and occipital pain, aconitia and cupping or burning at the back of the neck are indicated. In young patients witli seminal troubles, atropia, camphor, and turpentine may be added to quieting mixtures at night. In those with an hysterical element, five to ten grains of valerianate of zinc should be given daily for three or four weeks. Young nervous women require tonics, such as Warburg's tinc- ture and large doses of Blaud's pills, together with systematic cold applications to the spine; and, for certain periods, the bro- mides, valerian, and nervines of that character. Marriage may help them ; but, unfortunately, these women are sometimes very prolific. The cultivation of athletics Avould be the greatest boon that young women could receive. All girls should be examined, shown what deficiencies exist, and taught to make them up by gymnastic exercise. In neurasthenic women with painful backs or with a hysteri- cal complication, much can be said for electricity. General and spinal galvanization and the static sparks are the specially effi- cient forms. General electrization is a decided mechanical tonic and useful in almost all forms of neurasthenia; but it is more useful in cases in early life, in women, in the asthenic, and in those with spinal pains. Electrical treatment should be given three or four times weekly for about six weeks, then suspended. Massage has no special or curative value in neurasthenia, ex- cept as part of the rest-cure. Mildly used it soothes and quiets many patients and has a symptomatic use. Vigorous massage is injurious. The rest-cure, as described by Dr. Weir Mitchell, is indicated for a certain class of neurasthenic Avomen with decided impair- ment of nutrition and a complicating hysteria. The discovery and treatment of the reflex irritations are im- portant. After the stomach and liver, the pelvic organs and the eyes are the most fruitful sources of trouble. The Sexual Neuroses aivd Psychoses. , Of the above disorders the neurologist has to deal chiefly with the vicious habit of masturbation (which may, however, be also a manifestation of disease) and the sexual neuroses, spermator- rhoea and impotence. 458 DISEASES OF THE NERVOUS SYSTEM. Masturbation axd Spermatorrhcea.— Masturbation is the name given to the vicious habit of artificiaiiy exciting the sexual orgasm. It is very common among boys and less common but present among girls and adult men and women. It is usually only a vice due originally to low associations and teachings among children. In some cases it is a disease or the symptom of a neurotic or insane constitution. Etiology. — It is most common between the ages of fourteen and eighteen, but may begin earlier. Even infants and very young children sometimes masturbate, usually as the result of some local irritation which leads them to rub the genitals. A tight prepuce, eczema, or worms may lead to the habit, but it is usually taught by a companion. The practice sometimes at- tacks schools almost like an epidemic, for in every institution a certain per cent of the boys are sexually precocious or vicious, while the others are ignorant and innocent of the evils of the practice.' Masturbation is relatively rare after twenty, but is practised by some throughout life even up to old age. Results. — Masturbation as ordinarily practised leads after a time to a feeling of malaise, mental depression, disinclination to work, study, or to enjoy one's self as before. The appetite is a little impaired, the extremities easily get cold and j^erspire read- ily. Peculiar numb feelings are felt in the hands and feet. There is an unnatural nervousness and irritability, and the power of concentrating the mind is a little weakened. The patients often have dilated pupils and hyperaesthetic skin. After a time noc- turnal emissions occur. The organs become irritable and slight excitement causes erections. These symptoms may be slightly marked and pass away in a day or two, or until another indul- gence occurs. Masturbation is sometimes done to an extraordinary extent, even daily or twice daily for a considerable time. After a while the young man begins to find that he is not well and realizes that this habit is hurting him. Then if he be sensible and of healthy constitution he stops. Others are frightened out of it by friends or by reading the terrorizing stories printed in quack ad- vertisements and circulars. Sometimes the fright thus caused leads the unhappy youth into a condition of hypochondriasis, which is helped on by the occurrence of nocturnal pollutions and the nervous debility resulting from his past indiscretions. In other cases in which there is a decided neurotic history, a genuine neurasthenia of a sexual type develops and annoys the patient for years. Masturbation rarely leads to insanity and is oftener a symp- tom than a cause of such disorder. It is occasionally the cause of epilepsy. When this is the case the convulsive attacks are NEURASTHENIA— NERVOUS WOMEN. 459 likely to put on a hysteroid phase and are accompanied with peculiar co-ordinated convulsions and emotional disturbance. Masturbation is the common cause of hystero-epilepsy in women. Diagnosis.— Isiiu^Y victims of the masturbation habit who have come to recognize its evils and tried to stop it develop a hypochondriacal condition, and feel sure that there is something in their faces which reveals to the world their trouble. This is not the case. But there is a certain physiognomy which in a measure characterizes the masturbator to such an extent that an experienced observer can detect it. The pale, pasty complex- ion, moist, furtive eye, dilated pupil, listless, restless, and de- pressed manner, the wet, flabby palms and hyperaesthetic skin, all help to tell the story. Locally the penis is often reddened and more or less turgid, the scrotum relaxed, and a varicocele may be present. Examination of the urine may reveal spermatozoa. The urine also is almost always of rather low specific gravity, and contains a great excess of phosphates, both earthy and alka- line. Treatment. — The patient must be told plainly the necessity of stopping the practice. He must be impressed, but not terrorized. He should be kept out of doors at vigorous physical exercise, for sedentary and solitary work is always bad for such cases. He should be made to take cold-water baths and should sleep on a hard bed with light covering. He had better sleep with some one whose presence may exercise a controlling influence. He should not eat heartily at night, never just before going to bed, and what is still more important, he should not drink before going to bed. Sometimes it is well to have him wakened at an early hour in the morning, when he should empty his bladder; for emissions occur often early in the morning and are promoted by the irritation of a full bladder. Locally cold-steel sounds may be introduced and allowed to remain for ten minutes three or more times a week, or the psychophor or Ultzman's short catheter may be used. In bad cases w^ith a great deal of prostatic irritation, local applications of nitrate of silver are needed. Internally a mixture of tinct. opii, tinct. camph., and tinct. lupulin may be given at night, the ingredients being somewhat varied in amount to suit the case. Bromides, chloral, atropia, and salix nigra are also drugs which al-e often useful. The mechanical measures which have been devised for preventing erections, such as rings with sharp teeth, are rarely needed and rarely useful. They may even do harm by directing the mind to the affected function. I do not believe it right for the physician to prescribe fornica- tion. It is not safe nor curative, apart from the moral aspect of the matter. It has always struck me also as pretty small busi- 460 DISEASES OF THE NERVOUS SYSTEM. ness for a man to purposely select a wife to relieve him of the results of a weak will and vicious sensual indulgence. If mar- riat'-e comes in the natural course of events, as it often does, so mu'ch the better. But to select a wife as a remedial agent for masturbation is unjust to the woman and a confession of moral and mental feebleness. Man is distinguished from the brute by his self-control. Let him bear this fact in mind and raise him- self above the animals by a determined efTort of the will. Pure thoughts and chaste associations, vigorous physical exer- cise and a resolute effort to act a manly part will always be successful. Traumatic Nervous Affectioxs (Traumatic ^'euroses AXD Psychoses), Spixal Coxcussiox. The present tendency of neurology is to deny the existence of any special nervous affection produced by trauma or shock. There may follow from these causes • 1. Surgical injuries. 2. Neurasthenic states, o. Hysterical states. 4. Hemorrhagic, inflammatory, and degenerative diseases. 5. Combinations of the foregoing. These troubles may follow not only railway but other injuries, but are especially liable to follow those associated with intense fright. 2. Traumatic neurasthenia, or "traumatic neurosis,*' does not differ from forms of neurasthenia produced by other causes, ex- cept that with it there may be certain sprains and surgical trou- bles. Traumatic neurasthenia not infrequently is associated with much spinal pain, and in women especially the clinical symptom group known as " spinal irritation ■' may develop. In other cases there may be more of the features of spinal asthenia. When to these spinal symiDtoms a partial paraplegia is added, we have the disease that has been called " railway spine," or spinal concussion. The anatomical names given to this used to be spinal anaemia, spinal hypersemia, and spinal meningitis. But no evidence has as yet proved the exact nature of the lesion. 3. Traumatic hysteria is a rare affection in this country. It does not differ from hysteria produced by other causes, except for its sudden onset and occasional h«urgical complications. It is usually a hysteria major and has the characteristic stigmata of that type. In this city electrical injuries and frights have pro- duced some classical cases of hysteria major. 4. There is considerable evidence that in some rare cases trau- matism may produce minute multiple hemorrhages throughout NEURASTHENIA— NERVOUS WOMEN. 4G1 the nervous centres. In such cases there are usually neuras- thenic or hysterical symiDtoms and in addition symptoms of organic disease. In the majority of cases the symptom complex is something like this (Knapp) : " The patient has headache and vertigo; he is depressed, irritable, and hypochondriacal, with a diminished power of application; he may have some visual disturbance, he often has a contracted field of vision and occasionally optic atro- phy ; there is some tremor and perhaps inco-ordination ; he has anaesthesia, usually not limited to one-half of the body, and with it numbness and prickling ; his movements are slow and weak ; his tendon reflexes are exaggerated; there is often some lack of control over his bladder; and he may have pain and stiffness in the back from muscular strain.*' The symptoms eventually re- semble a disseminated sclerosis. Massive hemorrhages and serious mechanical injury of the nervous centres may be also produced by injury. Finally, it is a well-known fact that traumatisms may excite in the predisposed locomotor ataxia, inebriety, insanitj^, or may lead to the development of a cerebral tumor. It is the mental impression, the shock, much more than the l^hysical injury, which produces the neurosis or psychosis. The symptoms may appear soon after the accident, or after a period of relative health lasting a few weeks the neurosis grad- ually develops. The most important practical point in connection with the subject is the diagnosis and the elimination of malingering. This is additionally difficult for the reason that the hopes and anxieties depending upon litigation tend to cause introspection, exaggeration of symptoms, and unconscious bias even in the most honest. The opinion among American neurologists tends to favor the seriousness of traumatic neuroses. While malingering is not rare, yet if the patient has really a traumatic neurasthenia or hysteria the disease may not be a trifling one. Careful research, however, often tends to elicit the fact that previous to the in- jury the patient was an alcoholic, syphilitic, or neurotic, and perhaps had already the beginnings of his alleged traumatic disorder. In no part of clinical medicine is a careful and searching examination and weighing of symptoms more ur- gently called for. The methods of carrying out such examina- tions are given elsewhere. Special methods for testing anaesthe- sia are sometimes needed. The two sides of the body should be tested simultaneously with concealed needles, beginning on the trunk, or the faradic current with a double-pointed electrode may be used. There are few patients who can successfully de- ceive in an examination covering all the special senses. 462 DISEASES OF THE NERVOUS SYSTEM. The treatment of the traumatic neuroses calls for no special notice. EXOPHTHALMIC GOITRE (BASEDOW^S DISEASE, GRAVES^ DISEASE). Exophthalmic goitre is a chronic neurasthenic neurosis cliar- acterized by rapid heart beat, enlargement of the thyroid gland, protrusion of the eyeballs, and various neurasthenic and vaso- motor symptoms. JEtwlog I/.— The disease occurs much oftener in women than men (four to one). It is a disease of early adult life, occurring chiefly between fifteen and thirty-five, very rarely in childhood, and never after fifty.* It is apparently more conunon in the Anglo-Saxon race, but is not vei-y frequent in America. There is very rarely any direct inheritance of the disease, but the family is often a neuropathic one. As a rule, the patient is of a neurotic temperament. Anaemia and debilitating diseases pro- mote its development. Goitre and heart disease do not seem to predispose to it. The most frequent exciting causes are power- ful depressing emotions and severe physical exertion. Rarer causes are injuries and infectious diseases, such as measles, scarlet fever, and pneumonia. ISi/m2)toms.— The disease usually begins gradually and the first symptom is in most cases rapid heart beat and palpitations, accompanied with some nervousness and tremor. The next symptom is enlai'gement of the thyroid gland, and at about the same time the eyeballs begin to protrude. This order of devel- opment does not always take place, and occasionally one of the three principal symptoms is not present. The disease is usually one or two years in developing, the heart symptoms being those which continue by themselves longest. With the symptoms mentioned there occur many minor troubles which are more or less characteristic. The patient is usually very nervous and irri- table; a distressing insonniia may be present. There is almost uniformly a fine tremoi- (eight to nine per second) of the hands, less marked in the lower limbs and not present in the face or tongue. The reflexes are exaggerated. There is a tendency at times in walking for the knees suddenly to give way. I'he patient rarely has neuralgias, but does have burning or fever- ish sensations and headaches. The skin is rather reddened and the patient sweats profusely. Pigmentation and vitiligo are sometimes seen, and urticaria may develop. The electrical re- * Among: Sa cases at N. Y. Post Graduate Clinic (Fiske-Bryson) there were 8 males, 25 females. Apes: thirteen to twenty, 8; twenty-one to thirty, 8; thirty-one to forty, 6; forty-one to fifty, 5; fifty-one to sixty, 1. EXOPHTHALMIC OOJTRE. 403 HlHtancAi of th*> body Ik much dijninihh^^], httirig W> U) l,r>fXj oIjjjih ■inHU'.iu\ of 2,fm to :j,(XX). Thara In muntUuu,^ a derii'jotl)io hkiri, a« in other uinxruhthamc ntaUiH. Tlui rcHpiratory furjctjon ii* weakenr^ci and chent exparjHion oftn;. Atta/;kJ^ of a perHiKtr^nt watery diarrhoea mH of the diw^jane are: Ta^ihyeardui and pulsating arUiriea. (ioitre. ExopljtijalnjuB. Tremor. The minor HyrtLpUymx iwft : NervouBneHH. Sweating, Infsfjmnia. JjdHi-^.iKid electrical reBiKtance, UiminiBhe^J renpiratory expannion, HubjacAAvft BenfeationB of heat. J^iarrhoia. Polyuria, Hyrapt/yffvH in haUiil. — Ta/Rhycardia i« the most constant hingle hymptrjin. The pulw^s beats from IW to 120 per minute UHually, but may rise to W) or even 2^XJ. its rhythm is usually steady; but palpitations r>ccur easily, even without exciting cause. TIjc patient may wake up at night with distressing attacks, some- thing like thowi of angina i>e<;toris, but the intenw^ pain and Benwe of impending death are usually abw:!nt. 'J'he ijeart is di- Iate<^l and a Bystrjiic njurmur is oftf^n heard at the baw^ propagatef the gland stand out prominently (Tig. ]Iy8j. Jf only part of the gland is involved it is oftenest the right lobe. A thrill is felt over it and a systolic murmur f^an Ix:; heard. The bulging of the eyes or exophthalmus is usually bilateral and even. If one eye is alone or more affect^^d it is the right. The exophthalmuB varies much in degree. It is not usually very great, but may l>e so exc^sive as to prevent closing of the lid« and to expose* the insertions of the rer^ti. The eyeljall may V>e slightly enlarged Tone-tenth). The pupils are nonual and vision lij not impaired, though myopia rx?ca.siorially occurs. The fundus i64 DISEASES OF THE NERVOUS SYSTEM. and visual field are normal. Paralysis of some of the eye muscles is a rare complication. Weakness of the internal recti ' and ex- ophoria are frequent. The lids show certain peculiarities. One of these, known as Von Graefe's symptom, consists in the in- ability of the lid to follow the downward movement of the eye- ball. When the patient is told to follow the movement of the finger vertically downward the eyeball moves steadily, but the lid catches, as it were, and refuses to follow or does so in a jerky manner. Another symptom, known as /Stellwag's symptom, is a considerable retraction of the lids, especially the upper one. Both this and Yon Graefe's symptom are due to a common tendency Fig. 198.— ExoPHTHALj HE, WITH AND WITHOUT EXOPHTHALMUS. of the lids to retract — due perhaps to overaction of the muscle of Miiller. A tremor of the lids sometimes occurs. Course.— The disease progresses slowly. After a year or two it often becomes stationary for a long time. Cases of gradual spontaneous recovery occur. The natural duration of most re- coverable cases is two to four years. In those which do not re- cover the disease lasts five, ten, or more years. Eventually the patient emaciates, the heart becomes weaker, albuminuria and dropsy appear, diarrhoea sets in, and the patient dies of exhaus- tion or is carried off by phthisis or some intercurrent disease. Other cases having improved up to a certain point remain in this state for years. Complications. — Mental derangement occasionally occurs in the later stages of the disease. Hysterical crises, epileptic at- EXOPHTHALMIC GOITRE. 465 tacks, choreic movements, paralysis of the ocular muscles, mus- cular a,trophy, paralysis agitans, Addison's disease, diabetes, loco- motor ataxia, and local oedema have all been observed. With the exception of hysterical attacks these complications are rare. Abort ive Forms.— TYii^ name is applied to cases in which only a part of the distinctive symptoms develop. Tachycardia al- ways exists ; with it are tremor and moist skin, lessened electrical resistance and nervousness. Or tachycardia and goitre may alone be present. Fathology.— The disease may be regarded as a neurasthenic or atonic condition of the vasomotor centres and of the great vis- ceral nerves, the vagus and spinal accessory. As a result of the first condition the blood-vessel walls are relaxed and the cutane- ous hyperaemia results. The enlargement of the thyroid is ex- plained by a vasomotor paresis of its vessels. It is a kind of erection of the organ. The exophthalmus is also due chiefly to paralysis of the orbital vessels. A tonic spasm of the muscle of Miiller is thought to help in producing this symptom. This muscle consists of unstriated fibres originating in the membranous lining of the orbit and inserted into the lids. It is rudimentary in man, and its influence in causing protrusion of the globe nmst be very small. The deposit of retrobulbar fat is a secondary phenomena. The rapid heart beat is probably due to impair- ment of the inhibitory fibres of the spinal accessory. Thus all the symptoms may be explained on the theory of a vasomotor and cardio-inhibitory paresis. Another theory suggested of late is that the disease is primar- ily an affection of the thyroid gland ; that this organ is overactive and throws into the blood substances that irritate the nerves. More properly the mechanism should be that it withdraws from the blood too much of those substances which are needed for nerve nutrition. The principal substance so far as known which develops in excess when the thyroid fails to act is mucin. In myxoedema the thyroid giand atrophies, and a long list of symp- toms almost directly the opposite of those of exophthalmic goitre occurs. The thyroid theory is weakened by the fact that tachy- cardia and many other characteristic symptoms may develop without a goitre, and that in simple enlargement of the thyroid the symptoms of Graves' disease do not appear. Small hemorrhages and congestion of the medulla have been found in a few cases. Aside from this, no important changes in the central nervous system have been discovered. The heart is dilated and enlarged, endocarditis is sometimes present, oftener not. The arteries are dilated. The thyroid gland is vascular and its arteries dilated; its proper structure is increased in amount. There is increase of fat and vascular dilatation in 30 466 DISEASES OF THE NERVOUS SYSTEM. orbit. The thymus gland is usually present to a greater extent than normal. Prognosis.— Aho\xt one-fifth of the cases get well or practically well. Probably over half the cases, if they can be properly treated, reach a fairly comfortable condition of improvement. The cases in which symj^toms come on quickly have the most favorable prognosis. In those with marked exophthalmus and goitre the prognosis is not so good. Diagnosis.— The disease can be distinguished by the persist- ent tachycardia, with goitre or exophthalmus, and in its early stage by the tachycardia Avith tremor, moist skin, sensations of heat, nervousness, insomnia, lessened respiratory expansion, and electrical resistance. A symptomatic Graves' disease may some- times be caused by a goitre pressing on the vagus or sympathetic and causing irregular heart beat and perhaps exophthalmus. In these cases the history of a long-standing goitre exists, the heart's action is irregular, the exophthalmus is usually partial and one- sided. In abortive forms it is necessary to have tachycardia and at least one other of the four major symptoms to make a diag- nosis. Treatment. — Rest is the most important single thing. The patient should be put to bed or kept on the back for one or more months. Freedom from excitement and worry must be en- joined. No especial diet is needed, nor do climatic influences or baths or mineral waters have much effect. Some cases are said to be improved, however, by removal to heights of one to three thousand feet. In most cases a. sea-voyage is the better change if one is made. The drugs used are numerous. The most efficient are tincture of strophanthus in doses of fifteen to forty drops daily, iodide of potassium or the syrup of hydriodic acid, arsenic and bromide of potassium used together ; quinine, mineral acids, and iron, used together. Other remedies are tincture of aconite in ni v. or aco- nitia gr. ^h^ doses, tincture of belladonna increased to the limit of tolerance, tincture of cactus grandiflorus in tt^ x. to xx. and tincture of veratrum viride, tti x. to xxx. dose, and the picrate of ammonia, gr. i. to ij. t. i. d. Of these drugs, strophanthus, the iodides, bromides, and iron have served me best. Digitalis is of doubtful value. Electricity possesses some utility. It should be given, if possi- ble, two or three times daily in the form of galvanism and in doses of two to six milliamperes for ten minutes. The technique is as follows. Positive pole on back of neck, negative drawn along course of vagi in the neck ; each side two minutes. Same with positive pole placed subaurally one minute; negative pole over thyroid two minutes, negative over cardiac region one min- EXOPHTHALMIC GOITRE. 467 ute, positive pole over eyes, negative over thyroid one minute, two milliamperes. The faradic current may be used for general tonic effects or combined locally with the galvanic. The patient should lie down during treatment and remain quiet for an hour later. For the palpitations, sulphate of sparteine or strophanthus with Hoffmann's anodyne may be used. The ice-bag placed over the heart and neck is helpful and may be used systematically. Tonic hydrotherapy is often useful, but should be carefully em- ployed. Surgical treatment until late years has been unsuccess- ful. Recently several cases have been reported in which cure has been produced by partial removal of the thyroid gland. This measure is yet in an experimental stage. Treatment of the nose has been said to cause disappearance of symptoms, but its utility is very doubtful. Respiratory exercises by which the patient is taught to increase his chest expansion do much good, as shown by Dr. Bryson. Mild compression of the lids at night seems to help the ex- ophthalmus, and slight and steady compression of the thyroid gland sometimes reduces its size a little. CHAPTER XXV. PROFESSIONAL NEUROSES, OCCUPATION NEUROSES (WRITERS^ CRAMP AND ALLIED AFFECTIONS.) Writers' cramp is a chronic functional neurosis character- ized by spasmodic, tremulous, inco-ordinate or paralytic disturb- ance when the act of writing is attempted, and associated with feelings of fatigue and pain. Etiology. — It is a disease of the present century, and has been particularly noted since the introduction of steel pens about the year 1820. A neuropathic constitution is often present, and some- times there is a hereditary history. Men are much more subject to the disease than women. 'The most susceptible age is between twenty-five and forty. It rarely occurs after fifty or before twenty. Clerks and professional writers are naturally much more subject to the disease. Excessive worry, intemperance, and all debilitating influences predispose to it. The chief excit- ing cause is excessive writing. But this is not all. The writing that is done under strain or a desire to finish a set task is the harmful thing. The style of writing is also an important factor. Writing done in a cramped posture Avith movements of the finger alone or with the little finger or wrist resting on the table is most' injurious. Free-handwriting done from the shoulder ac- cording to the American system is least harmful. Shaded or heavy Avriting wdth sharp steel pens is also productive of harm. Copying is much more harmful than composing. x\uthors seldom have writers' cramp. Albuminuria, lead-poisoning, exposure to wet and cold, and local injuries are sometimes exciting causes. SymXJtoms.—S^viiex^' cramp very rarely attacks a person sud- denly. The patient first notices a certain amount of stiffness oc- curring at times in the fingers, or the pen is carried with some uncertainty and jerky movements are made. He feels a sensa- tion of fatigue in the hand and arih, and this may amount to an actual tired pain. The first symptoms may last for months or even years. The hand is rested as much as possible, new pens or penholders and new modes of holding it are tried. Often the patient, fearing the onset of the cramp, and as its result loss of employment, becomes anxious, worried, and mentally depressed. PROFESSIONAL NEUROSES, OCCUPATION Js^EUROSES. 469 Sometimes the trouble is worse when beginning a daily task, and it gradually wears off in a few hours. At other times exactly the reverse is the case. When the disease has reached its highest stage, writing becomes almost or entirely impossible. The mo- ment the pen is taken in the hand and an attempt at using it made, spasmodic contractions of some of the fingers, or even of the arm, occur, the pen flies in any direction, and it is impossible to control or co-ordinate the movements. The rule is that al- though writing cannot be done, all other complex movements are performed as well as ever. Thus the sufferer from writers' cramp may be able to play the piano, or paint, or thread a needle, or use the hand in any complex movements. This limitation, however, is not always present. Telegraphers, who use to some extent the same muscles as in writing, and who also often have to do a great deal of writing, are liable to suffer from both writers' and telegraphers' cramp at the same time. No evidences of actual paralysis are present in the affected muscles, and there is rarely aniesthesia, but the arm aches and is sometimes tender. Sensations of numbness and prickling are present : in rare cases vasomotor disturbances are observed ; associated nmscular move- ments of the other arm or of the neck or face sometimes occur. The hand may tremble on attempting to write or fall almost paralyzed when the pen is taken. Tlie various symptoms occur with different degrees of promi- nence, so that the disease has been classed under the heads of (1) the spastic, (2) the neuralgic or sensory, (8) the tremulous, and (4) the paralytic forms. These forms are, however, often more or less mixed. 1. The spastic form is undoubtedly the most common, and it has given to the disease its name. Cramp of some nmscle or muscles is present in over half of the cases. The muscles of the thumb and first three fingers are of tenest affected, and in some cases the flexors, in some the extensors, are chiefly involved. In telegraphers' cramp it is the extensors, but in writers' cramp the flexors, that are mainly attacked. The thumb or forefinger or the little finger alone may suffer from the spasms. The prona- tors and supinators are quite often involved. The spasm is usu- ally a tonic one. With the spasm there is also inco-ordination so far as writing movements are concerned, and this fact is quite as important in producing the bad writing as the spasm. The inco-ordination is apparently of the motor type, and is not due to anaesthesia of the muscle sense, as in locomotor ataxia. 2. The neuralgic form resembles the spastic plus sensations of fatigue and pain, which are quite severe and are brought on by writing. There may be tenderness along the arm also. 3. The tremulous type, though rare, is very characteristic 470 DISEASES OF THE NERVOUS SYSTEM. when present. The patient when attempting to write observes a tremulous movement of his hand and arm. This ceases when his attempts to write cease. The tremor usually affects most the fingers used in pen-prehension, but it also spreads to the forearm and may even involve the entire extremity. An oscilla- tory or lateral tremor, due to involvement of the pronators and supinators, has been observed. The tremor is of the character known as " intention-tremor,*' such as is observed in disseminated sclerosis. It is shorter in range and more rapid than the tremor of that disease. 4. The paralytic form, or that type in which muscular feeble- ness is the dominant symptom, is said to be rare by Gowers, and this accords with my experience. German writers speak of it as common. In the typical paralytic form the patient, as soon as he begins to write, feels an overpowering sense of weakness and fatigue in the fingers and arm. The fingers themselves loosen their grip and the i^en may drop from the hand. Powerful im- pulses of the will and change in the mode of holding the pen enable the sufferer to continue, but the arm aches and finally is absolutely painful, and weakness and fatigue compel the writer to desist. Sometimes the paretic condition is succeeded by the spastic. Many of the cases 'of paralytic writers' cramp are not true examples of the neurosis, but are rather cases of neuritis of a rheumatic or other type. General Sy)nptoms. — Writers' cramp is essentially a motor neurosis, and its leading symptom is the impairment of a motor function. Other symptoms, however, both general and local, are always associated with it. These are ma^inly (1) psychical and (2) sensory, more rarely (3) vasomotor and (4) trophic. 1. Psychical symptoms. The patient is often nervous, emo- tional, and mentally depressed at times. He suffers from in- somnia and vertigo. Patients are generally unwilling to admit that there is any other trouble than the local one, and only care- ful exammation may bring evidence of constitutional trouble. There are cases of purely mental writers' cramp. 2. Sensory troubles. These consist of pain, sense of fatigue, feelings of numbness, prickling, pressure, weight, tension, con- striction, etc. Hypersesthesia, and more rarely anaesthesia, are also observed. The most common sensory symptom is that of aching and fatigue, and this is usually confined to the arm, and oftenest runs along the course of the radial and median nerves. The cervical vertebrae may be tender, and sometimes pa- tients have a headache in the parietal region of the side opposite the affected arm. 3. Vasomotor, trophic, and secretory disturbances. The con- dition known as digiti mortui has been observed, coming on par- PROFESSIONAL NEUROSES, OCCUPATION NEUROSES. 471 oxysmally. It is a symptom which the general neurasthenic state helps to produce. When the nerves are involved decided vascu- lar changes may occur, such as passive congestion of the hand and arm, with swelling and turgescence of the fingers, and a sensation of throbbing. In bad cases the fingers will look as if they had chilblains. Local sweating, dryness of the skin, and cracking of the nails, all are conditions which may follow impair- ment of writing power from neuritic causes. Electrical Reactions.— The results of observations upon the electrical reactions of the affected parts are somewhat contradic- tory. Ordinary tests will, as a rule, reveal very little change. Sometimes there is a quantitative increase, sometimes a decrease, of irritability to both forms of current. The increase occurs in the earlier stages, the decrease in the later. An increase or modification of electro-muscular sensibility has been noted. The electrical examinations, therefore, are only of value in ex- cluding a neuritis or possibly in determining the stage of the disease. Pathology. — Neuritis is undoubtedly present in some forms of writers' cramp, so called. It is not present, however, so far as external tests go, in the typical neurosis. Nor are there any post-mortem observations throwing light on the anatomy of the disease. We must believe, therefore, that it is a neurosis having no appreciable anatomical basis. The act of writing is a very complicated one, calling into play numerous sets of delicately innervated muscles. These muscles are employed: 1, in pen-prehension; 2, in pen movement; 3, in holding the arm and wrist tense. 1. The muscles employed in pen-prehension are the two outer •lumbricales, two outer interossei, the adductor muscles of the thumb, the flexor longus pollicis; to some extent the deep and superficial, short and long flexors, and the extensors of the thumb. These are supplied mostly by the ulnar (interossei, adductor pol- licis, inner heads of deep flexor of fingers, and inner head of short fiexor of thumb). The rest of the muscles are supplied by the median. 2. In moving the pen, if the writing is done mainly by finger and not by arm movements, the muscles brought into play are the flexor* longus pollicis, extensor secundi internodii poUicis, flexor profundus digitorum, extensor communis digitorum, and to some extent the interossei. The musculo-spiral and ulnar nerves innervate these groups about equally. In moving the pen by the "American'' or free-hand method there is a very slight play of the above muscles, while most of the pen move- ment is done by the muscles of the upper arm and shoulder, viz., the teres major, pectorales, latissimus dorsi, biceps, and triceps. 472 DISEASES OF THE NERVOUS SYSTEM. The spinal centres for these muscles are distributed along the fifth, sixth, and seventh cervical segments of the cord. The cells are larger and situated more superficially in the anterior gray horns. 3. Besides these movements involved in pen-i^rehension and in the letter-making, a certain amount of muscular tension is ex- ercised in " poising " the forearm and hand and steadying the wrist. The biceps and triceps, the supinators and the fiexors, and extensors of the hand are here brought into i^lay. From the foregoing it will be seen that the muscles of pen- prehension are most used in all but the free-hand style of writ- ing, since the same groups have a double duty, that of clasping and of moving the instrument. While writers' cramp is often complicated with some neurotic disturbance leading to associated symptoms of pain, paralysis, tenderness over nerves, vasomotor disturbances, etc., there can be no doubt that the lesion in typical cases is central. Writing is an acquired automatic movement, and it must have as its ana- tomical basis a certain established arrangement of nerve-Cell groups in the cervical part of the spinal cord. The nerve im- IDulses generated in the cerebral cortex pass along the pyramidal tracts and set at work those ganglion groups which, in turn, in- nervate the muscles used in writing with motor impulses. These grovips are themselves innervated also sensorially by the nerves of muscle sense in movement. In writers' cramp tho spinal groups of cells are more or less used up or exhausted, and the motor impulse which naturally would innervate them strikes cells which respond unequally, or it overflows to other cell groups, and hence the spasmodic, irregular movements of the arm. The cerebral centres in the cortex or basal ganglia are closely connected with those in the -cord, and may be said to form part of the writing mechanism. It happens in some cases that this centre too is exhausted and discharges its impulses irregularly. In some cases, therefore, the cerebral, and in some the spinal, cell groups are the more affected, and a diagnosis of the exact condition in each is approximately possible and may be not without practical importance. Writers' cramp is a disorder of efferent paths and stations. The muscular sense does not seem to be involved. The pathology of writers' cramp is that of all the other forms of occupation neuroses, and nothing need be said upon this point regarding them when they come to be considered. The diagnosis of well-marked cases of writers' cramp presents no difficulty. In the earlier stages, however, it may be confounded with a large number of disorders, viz., post-hemiplegic chorea, hemiataxia, progressive muscular atrophy, progressive locomotor PROFESSIONAL NEUROSES, OCCUPATION NEUROSES. 473 ataxia, various forms of tremor, lead paralysis, rheumatoid arthritis, neuritis, cerebral and nerve tumors, and tenosynovitis. In many of these cases it is only necessary to bear in mind the history of the disease in order at once to reach a safe conclusion as to its nature. If there is a great deal of pain in the arm, with tenderness along the course of the nerves; if thei-e is decided change in the electrical reactions ; if there are sensations of tingling, numbness etc. ; and if the patient shows an absolute loss of power in the various groups of muscles, with some incapacity for doing other acts besides the one with which he is specially concerned, then the trouble is undoubtedly peripheral and due largely to an un- derlying neuritis. The prognosis in these cases is much more favorable. If, on the other hand, the disorder comes on in per- sons who have done an excessive amount of writing; if it is associated with nerve strain; if the electrical reactions are but slightly changed, the sensory symptoms slight, and the motor inco-ordination marked, limited to the special class of work, and not accompanied with absolute paresis, the disorder is central and needs both a different treatment and prognosis. It is these cases that form writers' cramp proper, although no doubt neuritic and central forms are associated, or the former may run into the latter. Course and Duration. — Writers' cramp is a chronic disease. It begins insidiously and attacks one group of muscles after an- other as each is brought into play by new methods of writing. If the left hand is used, that, too, is liable to become affected. The course varies, however ; for a time progress may be arrested or improvement set in. When the disease becomes well estab- lished it will most often last a lifetime. Prognosis. — The prognosis is unfavorable, yet not so much so as has once been thought. Undoubted cases of complete recov- ery have been reported, even under unfavorable conditions. The prognosis is much more favorable if the patient begins treatment early and before marked spastic symptoms are present. It is more favorable in the neuralgic forms. Some patients who suffer from a mild form of the trouble manage, by the help of in- struments or special pens, to do their work for years. The more acute the disease and the more evidently peripheral and neuritic its origin, the better the prognosis. In over one-fourth of the cases, patients who use their sound arm will not be affected in it. The facts stated regarding the cause, physiology, and general symptomatology of writers' cramp apply to the other torms ot occupation neuroses. A few special details, however will be given regarding these. The most common and important are musicians' cramp and telegraphers' cramp. 474 DISEASES OF THE NERVOUS SYSTEM. Musicians' Cra mjj.— Vndev this head we mclude pianists' cramp, viohnists'' cramp, flutists' cramp, and the cramp of clar- ionet players. Pianists'' cramp occurs usually in young women who are studying to become professionals or who are especially hard- working and ambitious. The absurd " Stuttgart method '' of teaching the piano, in which the motions are confined as much as possible to the fingers, predisposes especially to this disease. The symptoms are those of fatigue, pain, and weakness. The pains are of an aching character. They are felt in the forearm especially, but extend up the arm and between the shoulders. Sl3asmodic symptoms are rare. The right hand is of tener affected, but both hands eventually become involved. Violinists' cramp may attack the right hand which holds tha bow or the left hand which fingers the strings, but more often the left hand is affected. Clarionet players sometimes suffer from cramp of the tongue and of the laryngeal muscles. Flute players suffer not very infrequently from slight laryn- geal spasms. A similar trouble affects elocutionists. The term mogophonia is applied to this type. Telegraphers' cramp affects especially those operators using the Morse system, an instrument which is still the one most widely in vogue. Contrary to the opinions of previous writers, Dr. Lewis believes that this neurosis is not a rare one and is destined to become more frequent. In this city the cramp is not rare, the proportion being about one in every two hundred. The technical name among operators for the cramp is "loss of the grip." In telegraphing, the extensors of the wrist and fingers are called most into play, and hence are most and earli- est affected. The symptoms come on very slowly, the thumb and index-finger being fij-st affected. The victim finds that he cannot depress the key on account of spasm in these muscles, and he finds most difficulty in making the dot characters, such as h (. . . .), or p ( ), or z (. . . .). When the flexors are most affected the key is depressed with undue force and a dash is made instead of a dot. Sufferers from the " loss of grip " gen- erally suffer from writers' cramp also. While spasm is usually present, the disease may show itself simply in pain, paresis, and incapacity to co-ordinate the muscles. In sewing spastn, which affects tailors, seamstresses, and shoe- makers, clonic and tonic spasms attack the muscles of the hands on attempting to use them in the regular work. Tailors who sit cross-legged sometimes suffer from a peculiar spasm on assuming this position. It is possible, however, that these are cases of tetany, and not the functional neurosis under consideration. Smiths'' spasm, hephcpstic hemiplegia, appears to have been observed only by Duchenne and Dr. Frank Smith. It occurs in persons engaged in pen-blade manufacturing, saw-straightening, razor-blade striking, scissors-making, file-forging, etc. In doing this work they have to use a hght or heavy hammer, with which strokes are delivered very rapidly and carefully. After a time spasmodic movements occur in the arm used, and the arm falls powerless. As in the cases reported there are generally hemi- plegic symptoms, and also neuralgias, vertigo, and other cerebral troubles, the disease cannot be a pure " occupation " neurosis. Drivers'' spasm has been observed in veterinary surgeons by Dr. Samuel Wilkes. PROFESSIONAL NEUROSES, OCCUPATION NEUROSES. 475 Milkers' spasm is an extremely rare affection, which was first described by Basedow and seems to occur in milkmaids never in milkmen. ' Cigar makers'' cramp is very rare. Watchmakers' cramp and photographers' cramp are also to be regarded merely as pathological curiosities. Ballet-Dancers' 6Va/?i/;.— Under this name certain painful and paralytic troubles occurring in ballet-dancers, especially premieres danseuses, have been described by Schultz, Onimus, and Kraus- sold. It does not appear that the trouble is really a co-ordinative functional one, but is rather neuralgic, or the result of local strain upon the parts. The list of professional neuroses is made to include, besides those above given, cramps and co-ordinative troubles affecting artificial-flower makers, billiard- players, dentists, hide-dressers, electrical-instrument makers, stampers, turners, sewing-machine girls, money-counters, weavers, painters, and pedestrians. Prophylaxis and Treatment. — T\\q introduction of type- writers, gold pens, and improved penholders has prevented some- what the increase of Avriters' cramp. Stenographers rarely have it unless they write in long hand. Persons who have to write a great deal should use large cork or rubber penholders and gold or quill pens with smooth paper. The best style of writing is that done from the shoulder, but this is a method that book-keepers and those who have to keep accounts cannot easily adopt. Many nervous persons have a bad habit of gripping the pen very tightly and pressing down on the paper with excessive force. Fatigue soon results and painful sensations develop in the arm. Proper attention should be paid to the position of the paper written upon, the height of the desk, the light, and the sleeves of the coat or dress. The paper should be laid at an oblique angle to the edge of the desk, and not at a right angle as many writing-teachers are accustomed to direct. As some cases of " cramp " are undoubtedly cerebral, it is very unwise to attempt any extraordinary exploits in writing or to work with the ambi- tion to put the writing capacity to the utmost test. Cramp is often dated from days when such extra work is done. When the cramp is fully developed, the most essential thing is rest. This may be secured by getting a new form of pen- holder, holding the pen in a different way, using the unaf- fected arm, using some form of mechanical appliance. The me- chanical appliances are splints, rubber bands around the wrist, and various instruments contrived to prevent spasm and throw the work of writing on new and larger groups of muscles. Instruments for writers' cramp are very numerous. Those that are of some value are Mathieu's, Nussbaum's, and some mod- ification of Cazenave's (see Figs. 199, 200). All the various instru- ments have been of service, or have even been curative ni some 476 DISEASES OF THE NERVOUS SYSTEM. 190.— Mathieu's Ixstrument FOR Writers'' Cramp. special cases, but not too much jnust be expected of them. As a rule they are only paUiative. A cheap instrument that may prove satisfactory is that of Mathieu. In the medical treatment of writers' cram^), the two most im- portant agents are massage and electricity. By massage only very mediocre results were obtained until greater attention was drawn to it by Air. J. Wolff, a Avriting-master of Frank- fort-on-the-Main. This gentleman has cured many cases, though not all that he has treated (Berger), and he has secured many testimonials for his method. The treatment, as described by Schott (G. W. Jacoby), consists of a system of gymnastics and masage. The gymnastics con- sist of movements performed by the i^atient alone and movements executed with the co-operation of the operator. The first are performed by the patient during from twenty to thirty minutes, rarely for forty-five minutes. These movements consist of gym- nastics of the fingers, extension, flexion, abduction, and adduc- tion V^eing performed, and the thumb being exercised separately. xVfter this the same four motions are executed at the wrist joint, then extension and flexion of the forearm, and ulti- mately the arms themselyes are exercised in the same manner and are to l)e lifted over the head. Each single exercise is to be performed from six to twelve times. After each motion a pause is to V)e ob- served. The op- posed movements are to be carried out in the same maimer, except that the operator must carefully resist their execution as though he were endeavoring to force the patient to perform a motion just the reverse of his intentions. Reg- ularity of pressure is to be observed in this, so that the same amount of force is always used and so that the pressure does not A'ary in intensity from moment to moment. The time to be de- voted to these opposed movements sliould be the same as that for the unopposed ones. According to the intensity of the affec- FiG. 200.— Nr./«^M06'/6'.— As hypnotic states maybe imitated and as inju- ries or crimes may be done during this state, it is very important to be able accurately to distinguish it. Since the phenomena are all subjective, this is very difficult. Tlfe methods of value are these : 1. Careful examination of the general phenomena by experts while the subject is in the alleged hypnotic state. 2. Testing the muscular hyperexcitability by percussing motor points. 3. Tests of alleged aniesthesia by sudden burning, or pinching, or injur- ing the subject. 4. Tests of the tetanic muscular rigidity by the revolving tambour. In the hypnotic state the hand may be ex- tended and held with perfect steadiness, while in conscious states a tremor soon appears. 5. Tests with glasses and other appci- ratus may be made to determine alleged ana^sthesiie of the special senses. Therapeutics. — The practice of using major hyjDnotization is injurious, tending to exhaust the nervous force and weaken the will. It should be done only with the greatest care. Its utility in therapeutics I greatly doubt. It may relieve symptoms in the hj^sterical for a time, but it cannot be of permanent benefit and is likely to lead to actual harm. The induction of minor hypnotic states by suggestion is not harmful if carefully and moderately employed. Its practical re- sults, however, are not great, and the method is tedious, uncer- tain, and sometimes ridiculous. It has its value in pedagogy, among children, in neurasthenia and morbid habits. The gen- eral popularization of hypnotism by means of mind-cures. Chris- tian science, etc., accomplishes its results at the expense of mental demoralization; and faith-healing institutes are more pernicious elements in society than gin-mills. Morbid Drowsixess. — This is a very common symptom, which may be due to any one of the following causes : 1. Old age, when there is a weakened heart or diseased arteries, with cerebral mal-nutrition. 2. The diseased vascular conditions which precede cerebral hemorrhage. 3. The cerebral mal-nutrition or inflam- mations occurring before or during certain forms of insanity. 4. Various toxsemiie, e.g., malarial, uremic, choltemic, and syphi- litic. 5. Dyspepsia and gastric repletion. 6. Diabetes. 7. Obe- sity. 8. Insolation. 9. Cerebral anaemia, and hyper^emia. 10. Exhausting diseases. 11. Concussion of the brain. 12. Climatic conditions, cold, etc. 500 DISEASES OF THE NERVOUS SYSTEM. A very common cause of drowsiness is dyspepsia attended with some torpidity of tlie liver, the condition popularly known as *' biliousness/' Another frequent cause is malarial infection, which perhaps acts indirectly by impairing the functional activity of the liver. Drowsiness from these causes oftenest comes on in the afternoon. An;emia is attended with drowsiness during the day, while there is often i^somnia at night. Syphilis is more likely to cause insonniia, but in its third stage somnolent conditions may be produced which are of serious significance. Drowsiness occurs froui the effect^ of severe cold. It sometimes tlevelops when persons change their surroundings, especially on going to the seashore, for low levels and a high degree of atmospheric pressure seem to promote sleep. The drowsy state that some- times follows concussion of the brain is a familiar phenomenon. Some persons, no doubt, acquire the habit of drowsiness. At first the trouble may have been induced by indigestion, " bilious- ness,'' or malarial infection, but it persists after the cause is re- moved. Such persons can hardly sit through a lecture, a church service, or any exercise requiring quiet and attention. As the morbid drowsiness here described is only symptomatic, its treat- ment need not be discussed. Such remedies as coca, coffee, tea, atropia, glonoin, do not produce results equal to expectations. Morbidly Beep ^leep. — Certain persons, when they sleep, pass into an almost lethargic slumber. Persons who sleep in this way often sleep a longer time than normal. They are awakened with difficulty, and then suffer with headache or disagreeable sensa- tions throughout the day. The symptom may be a prodroma of insanity. Instances in which persons retire at the usual hour, but can with great difficulty be roused in time for the ordinary duties of the day, are not rare. Some of these are illustrations of the vice of indolence, but in other cases there is an absolute need of nine, ten, or even fourteen hours of sleep. This disorder of sleep is most liable to occur in the young and in those of nervous temt)erament. It often seems to be a congen- ital condition, for which nothing can be done. In other cases it results from over-feeding and indolent habits. Treatment is much the same as that indicated for sleep-drunkenness and som- nambulism. o. P(trrocess. A line from the upper end of the fissure of Rolando to the point of the process Avould pass through this important sensory area (Fig. 208; see also p. 351). VII. To find the position of the central ganglia, viz., corpus striatum and optic thalamus, draw a line from the upper end of the fissure of Rolando to the asterion, practically a vertical line. This limits the optic thalamus posteriorly. A vertical line par- allel to the first, a little in front of the beginning of the fissure of Sylvius, limits the corpus striatum anteriorly. A horizontal plane 45 mm. (If inches) below the surface of the scalp at the bregma CRANIO-CEREBRAL TOPOGRAPHY. 507 Lmits the ganglia superiorly. The ganglia he about 35 mm. (1| inches) below the superior convex surface of the brain (Per^). VIII. To reach the lateral ventricles: A number of routes may be taken. The lateral is recommended by Keen. Mark a point 1| inches behind the external auditory meatus and 1\ inches above a base line made by drawing a line through the lower border of the orbit and the external auditory meatus. Trephine at this point and plunge the director into the brain in Fig. 209.— SaowTiNG the Relative Position of the Fissures and Cortical Centres of the Brain. the direction of a point 21 to 3 inches vertically above the oppo- site external meatus. The ventricle lies at a depth of 2 to 2^ inches (5 to 5.7 cm.). Mr. Alec Fraser has devised a way of mapping out the fissures by means of a series of composite photographs, so taken as to show the relation of the underlying parts to certain tapes tacked upon the skull. One of his figures is reproduced here (Fig. 210). In applying this method the surgeon tacks the tapes on the shaved scalp. Then looking at the diagram he finds where the point in the brain is that he wishes to reach and notes its rela- 508 DISEASES OF THE NERVOUS SYSTEM. tion to the median lateral or circumferential tapes. Then as the circumference of the illustrated head is to the circumference of the living one, so is the position of the area on the tapes in the illustrated head to the desired position of the same area in the living one. The illustration is a composite of several adult heads varying in circumference from 20^ to 23^ inches. The tapes are divided into inches and half inches. The pri- mary tape is the circumferential passing horizontally round the vault of the head (on the shaven scalp) from the root of the nose (glabella) to the maximum occipital point, which is about one inch above the inion. The tape which thus entirely surrounds the head is divided into four equal parts. The points where the division is made are at the anterior and posterior poles and mid- way on each lateral half of the tape. From these lateral mid- points a tape is run vertically over the top of the head, and other tapes are run anteriorly and posteriorly half-way between the point where the transverse tape crosses the sagittal suture and the anterior and posterior poles. Another longitudinal tape Is run from the anterior to the posterior pole half-w^ay between the sagittal suture and the circumferential tape. INDEX Abdomixal reflex, 30 Abscess of the brain, 346 Acrania, 333 Acroceplialic skull, 27 I Acrodynia, 70, 74 I Acromegaly, 485 [ Acro-neuroses, 85 I Actinomycosis of the brain, 391 , jEsthesiometer, 35 Age, etiological influences of, 40 Ageusia, 14G Agoraphobia in neurasthenia, 451 Agraphia, 333 Akinesia algeria, 434 Alcoholic paralysis, 70 Alexia, 330 Allochiria, definition of, 23 Amaurosis, 108, 111 Amblyopia, 108, 111 Amimia, 333 Ampere, definition of, 55 Amputation neuroma, 90 Amyelia, 199 Amygdalum, 298 Amyosthenia, 423 Amyotrophy, progressive spinal, 264 Analgesia, definition of, 20 Anaemia, cerebral, 345 of the membranes of the I brain, 334 f of the peripheral nerves, 64 spinal, 204 Anaesthesia, definition of, 20 hysterical, 419, 429 Ansesthesia, trigeminal, 131 visual, in hysteria, 420 Angio-ataxia, definition of, 23 Angioma of the brain, 393 Angio-neurosis, definition of, 23 Angio-neurotic cedema, 487 Angio-paralysis, definition of, 33 Angio-spasm, definition of, 22 Anencephaly, 333 Aneurisms, intracranial, 395 Anidrosis, definition of, 23 Ankle clonus, 31, 34 Anode, 58 Anosmia, 107 Ansa lenticularis, 299 Anthropophobia in neuras- thenia, 452 Aphasia, 330 table of forms'of, 332 Aphemia, 331 Aphthongia, 148 Apoplexy, cerebral, 353 spinal, 200 Apraxia, 331 Arachnoid, spinal, 180 Arbor vitse of the cerebellum, 303 Arcades, interfascicular, 9 Argyll-Robertson pupil, 34, 117, 236 Arm, paralyses of the, 160 Arteries of the brain and its membranes, 313 of the spinal cord, 192 Arthropathies of locomotor ataxia, 237 i 510 INDEX. Associative functions of the brain, 321 Asthenopia, definition of, 108 muscular, 118 Ataxia, definition of, 21 family, 251 Friedreich's, 251 generic, 251 locomotor, 231. See Loco- motor ataxia progressive spastic, 249 testing for, 38 Ataxiagraph, 38 Ataxic paraplegia, hereditary, 255 Athetosis, 19 Atrophia musculorum lipoma- tosis, 270 Atrophy, arthritic muscular, 275 of tiie brain, 379 progressive muscular, 261, 2b^4 progressive muscular, of the leg type, 268 Auditory nerve, anatomy a.nd physiology of the, 100 diseases of the, 138 Aura, epileptic, 407 Axis cylinder* 5 Axis-cylinder processes of nerve cells, 2 Baillarger, stripe of, 297 Ballet-dancers' cramp, 475 Bar sesthesiometer, 36 Basedow's disease, 463 Baths, forms of, 49 Batteries, varieties of, 55 Bell's palsy, 134 Beri-beri, 70, 74 Bilateral representation, 318 Birth palsies, 369 Blepharospasm, 184 Blood supply of nerves, 8 of the brain and its mem- branes, 312 Blood supply of the spinal cord, 192 Brachial paralyses, 160 Brachial plexus, arrangement of the, 158 diseases of the, 159 Brachycephalic skull, 26 Brain, abscess of the, 346 actinomycosis of the, 391 acute softening of the, 862 anaemia of the, 345 anatomy of the, 290 aneurisms in the, 395 angioma of the, 392 architecture of the, 307 associative functions of the, 321 atrophy of the, 379 blood supply of the, 312 cancer of the, 892 cutting the, 328 degeneration of the, 373 diagnosis between hemor- rhage and acute soften- ing of the, 363 diseases of the, general symptoms of, 829 embolism of the, 362 enchondroma of the, 392 fibroma of the, 392 functions of the, 317 glioma of the, 391 gumma of the, 390 hemorrhage in the, 353 hypersemia of the, 344 hj^pertrophy of the, 379 inflanunation of the, 346 latent regions of the, 324 lipoma of the, 893 localization, 317 localization of tumors of the, 384 malformations of the, 333 membranes of the, diseases of, 334 INDEX. 511 Brain, membranes of the, func- tions of, 312 motor area of the, 317 osteoma of the, 392 parasitic growths of the, 392 preserving the, 328 red softening of the, 349 relation of the different parts of the spinal cord to the, 180 sarcoma of the, 391 sinuses of the, 316 sixteen ganglionic deposits of the, 292 softening of the, 349, 362 syphilis of the, 397 syphiloma of the, 390 thrombosis of the, 362 tracts of the, 305 tumors of the, 381 weight of the, 325 Brauch-Romberg symptom, 38 Brown-Sequard paralysis, 278 Bulbar myelitis, acute, 352 paralysis, progressive, 262 Burdach, column of, 185, 186, 188 Caisson disease, 202 Cancer of the brain, 392 Capsule, internal, 306 Caput obstipum, 148 Catalepsy, 501 Cathode, 58 Cavities in the spinal cord, 280 Cells, angular, of Lewis, 296 Deiter's, 8 ganglion, 1 granule, of Lewis, 296 nerve, 1 of the cortex cerebelli, 304 of the cortex cerebri, 296 of the spinal cord, 183 Purkinje, 304 spider, 8 spider, of the cortex cerebri, 296 Centres, cerebral, 317 spinal cord, 188, 190 Centrum ovale, physiology of the, 321 Cephalalgia, 121 Cerebellum, anatomy of the, 303 physiology of the, 322 Cerebro-spinal meningitis, epi- demic, 338 Cerebrum, anatomy of the, 290 Cervical nerves, diseases of the, 153 Charcot-Marie type of progres- sive hereditary muscular atrophy, 268 Cltildren, cerebral palsies of, 365 Choked disc, 109 Chorea, 436 dancing, 441 electric, 441 habit, 441 hereditary, 441 Huntington's, 441 insaniens, 437 maniacal, 437 of adult life, 438 of the larynx, so-called, 431 paralytic, 438 procursive, 441 senile, 438 Sydenham's, 436 Choreic movements, 18 Cigarmakers' cramp, 475 Civilization, etiological influ- ences of, 41 Clarionet players' cramp, 474 Clark's column, 183, 189 Claustrophobia in neurasthe- nia, 451 Claustrum, 298 Climate, etiological influences of, 41 therapeutic uses of, 52 Clonus, ankle, 31, 34 51; INDEX. Coccvgodynia, 177 Collaterals of a nerve fibre, 2 Columns of the spinal cord, 184, 188 Compression myelitis, 205, 217 Conductors, relative value of, 54 Conjugate deviation of the eyes, 114 Contractures, 19 hysterical, 424, 429 Convolutions of the brain, 292 microscopic anatomy of the, 296 Convulsions, 18 epileptic, 405, 429 hysterical, 418, 426, 429 • reflex epileptiform, 404 Convulsive tremor, 432 Coprolalia, 431 Cord, spinal, see Spinal cord Corpora quadrigemina, 300 physiology of the, 322 Corpora striata, 298 physiology of the, 321 Corpus callosum, i^hysiology of the, 321 Cortex cerebelli, 303 cerebri, 292 Cramp. 18 ballet-dancers', 475 cigarmakers', 475 clarionet-plaj'ers', 474 musicians', 474 photographers', 475 telegraphers', 474 watchmakers', 475 writers', 468 Cranial measurements, table of, 25 nerves, anatomy and phy- siology of the, 92 nerves, diseases of the, 107 reflexes, 30 Cranio-cerebral topography, 505 Cranium, dimensions and shape of, 26 Cremasteric reflex, 29 Crises in locomotor ataxia, 239 neurasthenic, 448 Current strength, definition of, 54 Cyclopia, 333 Cycloplegia, 116 Cycling, value of, 49 Deafxess, nervous, 138 Degenerations, 44 diseases in which the reac- tions of, may be expected 62 marks of, 24 neuritic, 79 of brain tissue, 373 of nerves, 65 of the sjjinal cord, second- ary, 259 testing for reactions of, 60 Degenerative diseases of the spinal cord, 229 Deiter s cells, 8 Delayed sensation, 37 Deviation, conjfigate, defini- tion of, 114 Diagnosis, electro-, 60 of nervous diseases, 23 Diaphragm, paralysis of the, 15.") Diatheses, etiological influence of, 41 Diathesis, contractural, 424 Diet for brain- workers, 47 Digiti mortui, 85 Diplegia, definition of, 19 in childhood, 365, 369 Diplopia, 113 Divers' paralysis, 202 Dizziness, 141 Dolichocephalic skull, 26 Dorsal nerves, diseases of the, 168 INDEX. 513 Double sensations, 37 Drivers' spasm, 474 Duchenne-Aran's disease, 264 Duchenne, subacute spinal jjaralysis of, 226 Dura mater, inflammation of the, 335 spinal, 180 Dynamometer, 27 Dyscesthesia, definition of, 21 Dystrophies, progressive mus- cular, 261, 269 ECHOKIXESIS, 431 Echolalia, 431 Eclampsia, 18. See Convulsions nutans, 151 Elbow jerk, 33 Electric irritability, alterations in, 60 Electrical currents in nerves, 13 Electricity, definitions of tech- nical terms, 53 methods of application, 58 therapeutic uses of, 53 Electrization, 58 motor points for, 59 Electrodes, 57 Electro-diagnosis, 60 Electromotive force, definition of, 54 Electrotonus, 14 Embolism of the brain, 362 Encephalitis, 346 acute exudative, 352 acute suppurative, 346 chronic, 353 primary, of Friedmann, 352 Enchondroma of the brain, 392 End-brush of a nerve fibre, 2 End organs of nerves, 12 Endoneurium, 4 Enteroptosis, 450 Epigastric refiex, 30 Epilepsy, 403 33 Epilepsy, diagnosis, 410 etiology, 404 hystero-, 426 Jacksonian, 404, 407 laryngeal, 144 mental condition in, 408 pathology, 409 physical condition in, 408 physiology, 410 prognosis, 411 symptoms, 405 treatment, 411 Epineurium, 4 Erb, chronic atrophic paralysis of, 326 juvenile form of pseudo- muscular hypertrophy of, 270 Erb's palsy, 161 Erector-spinse reflex, 30 Erythromelalgia, 87, 177 Etiological table of peripheral nervous diseases, 178 Etiology of nervous diseases, 40 Examination of patients, methods of, 23 Exercise, prophylactic value of, 48 Exhaustion, spinal, 288 Exophthalmic goitre, 462 Eye, anatomy and physiology of the motor nerves, 95 diseases of the motor nerves, 113 muscular asthenopia or in- sufficiencies of the, 118 spasmodic diseases of the nmscles of the, 120 Facial nerve, anatomy and physiology of the, 100 diseases of the, 132 Farad ic current, testing by the, 61 electrical batteries, 56 Feet, pains in the, 87 5U INDEX, Fever, hysterical, 426 Fibres, association, of the brain, 297, 306 connecting different gan- gha of the brain, 306 nerve, medullated and non- medullated, 7 nerve, a prolongation of nerve-cell processes, 2 nerve, structure of the, 4 of the cortex, 297 projection, of the brain, 306 Fibrillary tremor, 18 Fibroma of the brain, 392 Fissures, cerebral, 292 Flute-players' spasm, 474 Formula for applying electric- ity, 58 FothergilFs neuralgia, 130 Friedmann, primary encepha- litis of, 352 Friedreich's ataxia, 251 Functional nervous diseases, 403 Galyaxic current, testing by the, 61 electrical batteries, 57 Ganglion cells, 1 habenulse, 300 Gangrene, symmetrical angio- neurotic, 85 Gedvelst, network of, 6 Geniculate bodies, 300 Gerlier's disease, 144 Giddiness, 141 Glioma of the brain, 391 Gliosis, 46 Globus pallidus, 298 Glosso-labio-laryngeal paraly- sis, 262 Glosso-pharyngeal nerve, anat- omy and physiology of the, 101 diseases of the, 146 Glossoplegia, 148 Grand mal, 404 Graves' disease, 462 Gray matter, five principal de- posits of, 10 Goitre, exophthalmic, 462 Goll, column of, 185, 188 Gout, nervous, 450 Gowers, column of, 185 Gumma of the brain, 390 H.^MATOMYELIA, 201 Hasmidrosis, definition of, 22 Habit chorea, 441 Habits, etiological influence of, 41 Hands, numb, 84 Headache, 121 Hearing, primary centre for, 320 Hemiansesthesia, hysterical, 419 Hemianopsia, 112 definition of, 108 Hemiatrophy, progressive lin- gual, 148 Hemicrania, 125 Hemiopia, definition of, 108 Hemiplegia, 330, 353, 356 definition of, 19 in childhood, 365 Hemorrhage, cerebral, 353 spinal, 200 Heredity, etiological influences of, 41 Herpes zoster, 170 Heterophoria, 118 spinal, 199 'Hiccough, 155 Huntington's chorea, 441 Hydatids of the brain, 392 Hydrencephalocele, 334 Hydrocephalus, acute, 340 chronic, 341 Hydromyelia, 280 Hydrorachis externa, 198 interna, 198 Hydrotherapy, 49 INDEX. 515 Hygiene, 47 Hyperacusis, 145 Hyperiemia, cerebral, 344 of the membranes of the brain, 334 of the peripheral nerves, G4 spinal, 203 Hyperesthesia, auditory, 145 definition of, 21 hysterical, 421 retinal or ocular, 111 Hyperalgesia, definition of, 21 Hypercyalgesia, definition of, 37 Hyperidrosis, definition of, 22 Hyperosmia, 107 Hyperplasia of nerve trunks, 89 Hyperthermalgesia, definition of, 37 Hypertrophy of the brain, 379 pseudo-muscular, 270 Hypnotism, 497 Hypoglossal nerve, anatomy and physiology of the, 104 nerve, diseases of the, 147 Hysteria, 410 amyosthenia in, 423 critical symptoms of, 418 diagnosis, 428 etiology, 41G interjoaroxysmal symptoms of, 419 major, 418 minor, 417 motor symptoms of, 422 IDathology, 428 permanent stigmata of, 419 prognosis, 429 sensory symptoms of, 419 symptoms, 417 treatment, 430 visceral symptoms of, 425 Hystero-epilepsy, 426 Ignipedites, 70, 74 Impulses, rate of travel of, 13 Inco-ordination, testing for, 38 Infantile polioencephalitis, 352 spinal paralysis, 220 Infections, etiological influ- ences of, 42 Inflammations, 43 of nerves, 68 Insomnia, 490 Insufficiencies, muscular, of the eye, 118 Insulators, relative value of, 54 Intention tremor, 18 Iridoplegia, 116 Irritability, electrical, altera- tions in, GO Irritation, sj^inal, 286 Jacksonian epilepsy, 404, 407 Jaw reflex, 33 "Jumpers,'^ 431 Knee jerk, 31 Labile electrode, 58 Laryngeal syncope, or vertigo, or epilepsy, 144 Larynx, chorea of the, so- called, 431 Latah, 431 Lead palsy, 164 Leg, peripheral palsies of the, 173 Lenticular loop, 299 Leptomeningitis, 335 acute simple, 335 spinal, 206 Lethargy, 501 Lid reflex, 30 Light reflex, 33 Lingual hemiatrophy, progres- sive, 148 paralysis, 148 spasms, 147 Lipoma of the brain, 392 Lissauer, column of, 185 Lithsemia, 450 Lobes, cerebral, 294 516 INDEX. Localization, cerebral, 317 of brain tumors, 384 spinal, 190 Lock-jaAV, 132, 443 Locomotor ataxia, 231 arthropathies of, 237 cerebral symptoms in, 240 complications of, 241 course of, 241 crises in, 239 diagnosis of, 246 disorders of hearing in, 236 etiology, 231 eye-symptoms in, 235 forms of, 231 gait in, 233 in children, 248 muscular atrophies in, 240 optic atrophy in, 235 pathological anatomy and pathology of, 241 prognosis of, 246 reflexes in, 233 stages of, 232 symptoms, 232 treatment of, 246 Lumbar nerves, diseases of the, 170 Luys' body, 302 MALFORMATIO^'S of the brain, 333 Massage, 52 Mastodynia, 169 Masturbation, 458 Medulla oblongata, physiology of the, 324 Medullary sheath, 5 Membranes of the brain, anae- mia of the. 334 of the brain, blood supply of the, 313 of the brain, diseases of the, 334 of the brain, functions of the, 312 Membranes of the brain, hyper- semia of the, 334 of the brain, malformations of the, 333 of the brain, symptoms of diseases of the, 329 of the spinal cord, 180 Memories, centres for, 320 Meniere's disease, 141 Meninges, cerebral, see Mem- branes of the brain spinal, 180 Meningitis, epidemic cerebro- spinal, 338 spinal, 205 tubercular, 340 Meningocele, cerebral, 334 spinal, 198 Meningo-myelitis, 208 Meningo-myelocele, spinal, 198 Mesmerism, 497 Mesocephalic skull, 26 Meynert's bundle, 306 Micromyely, 199 Migraine, 125 Milkers' spasm, 475 MilliamiDeremeter, 55 Mimic tic, 132 Mind -blindness, 331 Mogophonia (fiute-pl ay ers' spasm), 474 Monoplegia, hysterical, 422 Morton's neuralgia, 88 Morvan's disease, 79 Motility, symptoms of disor- dered, 27 Motor, area of the brain, 317 points for electrization, dia- gram showing the, 59 Movements, choreic, 18 forced and associated, 19 Multiple neuritis, 70. See Poly- neuritis Muscles, centres for movements of the, 317 Muscular anaesthesia, 38 INDEX. 517 Muscular atrophies and dys- trophies, 2G1, 269, 276 atrophy, arthritic, 275 atrophy, proj^ressive, 264 atrophy, progressive hered- itary, of the leg type, 268 sensibility, testing the, B7 Musicians' cramp, 474 Mydriasis, 116 Myelin sheath, 5 Myelitis, acute, 210 acute bulbar, 352 central, 218 chronic, 216 compression, 205, 217 disseminated, 211, 216 forms of, 210 periependymal, 218 transverse, 210, 216 Myoclonus multiplex, 432 Myoidema, 29 Myosis, 117 Myospasia, 432 Myotonia congenita, 433 Myriachit, 431 Mysophobia in neurasthenia, 451 Narcolepsy, 500 Neck imins, 157 paralysis of the muscles of the, 152, 155 Necrosis, perforating, of the cord, 214 Nerve roots, spinal, 180, 186 Nerves, afferent and efferent, 11 ansemia of, 64 auditory, anatomy and physiology of the, 100 auditory, diseases of the, 138 cervical, diseases of the, 153 cranial, anatomy and phy- siology of the, 92 cranial, diseases of the, 107 degeneration of, 05 Nerves, dorsal, diseases of the, 168 end organs of, 12 facial, anatomy and physi- ology of the, 100 facial, diseases of the, 133 glosso-pharyngeal, a n a t - omy and physiology of the, 101 glosso-pharyngeal, diseases of the, 146 hypersemia of, 64 hyperplasia or hypertrophy of, 89 hypoglossal, anatomy and physiology of the, 104 hypoglossal, diseases of the, 147 inflammation of, 68 inter-central or commissu- ral, 12 lumbar, diseases of the, 170 motor, of the eye, anatomy and physiology of, 95 motor, of the eye, diseases of, 113 olfactory, anatomy and physiology of the, 92 olfactory, diseases of the, 107 optic, anatomy and physi- ology of the, 94 optic, diseases of the, 108 peripheral, functional dis- orders of the, 80 peripheral, relation of the different parts of the spi- nal cord to the, 186 peripheral, table of diseases of, 178 phrenic, paralysis of the, 155 pneumogastric or vagus, anatomy and physiology of the, 102 pneumogastric or vagus, diseases of the, 147 518 INDEX. Nerves, regeneration of, 68 sacral, diseases of the, 173 spinal accessory, anatomy and physiology of the, 103 spinal accessory, diseases of the, 147, 148 spinal, diseases of the, 513 structure of, 1, 4 syphilis of, 398 trigeminal, anatomy and physiology of the, 98 trigeminal, diseases of the, 120 tumors of, 89 Nervous diseases, functional, 403 diseases, methods of study- ing, 15 exhaustion, 44G system, anatomy of the, 1 system, general arrange- ment and functions of the, 10 system, mechanisms of the, 13 tissue, chemistry of, 14 Neuralgia, 81 cervico-brachial, 166 cervico-occipital, 157 congestive, of the feet, 87 digital, 166 epileptiform, 130 Fothergiirs, 130 hysterical, 421 intercostal, 168 mammary, 169 Morton's, 88 of the lumbar nerves, 172 plantar, 177 red, of the feet, 87 sciatic, 174 trigeminal, 128- Neurasthenia, 446 course and duration, 453 climacteric, 452 degenerative, 451 { Neurasthenia, diagnosis, 454 etiology, 446 in adolescence, 451 in adult life, 452 modified types of, 451 pathology, 453 primary, 451 prognosis, 455 ■ sexual, 451 * spinal, 288 symptoms, 447 treatment, 455 Neurilemma, 6 Neuritic degeneration, 79 type of syringo-myelia, 79 Neuritis, 68 complicated forms of, 79 dermatitic intercostal, 170 migrating, 168 multiple, 70. See Polyneu- ritis l^lantar, 177 retrobulbar optic, 109 sciatic, 174 symmetrical spontaneous ulnar, 166 Neuro-fibromata, plexiform, 89 Neuroglia, 8 Neurology, definition of, 16 Neuromata, 89 fl on the roots of the cranial ^ nerves, 392 Neurons, 1 Neuro-retinitis, 108 Neuroses, aero-, 85 degenerative, 403 different forms of, 16 of mixed origin affecting the extremities, 85 parses thesic, 84 professional and occupa tion, 468 sensory, 81 sexual, 457 traumatic, 460 Nictitating spasm, 134 I INDEX. 519 Nightmare, 494 Nodding spasm, 151 Nodes of Ranvier, 5 Nucleus, caudate, 298 fastigium, 303 lenticular, 298 red, of the brain, 302 red, physiology of the, 322 Numb hands, 84 Numbness, waking, 80 Nystagmus, 120 Occupation, muscular atro- phies from, 276 Qildema, angio-neurotic, 487 blue, of hysteria, 426 circumscribed, 487 Ohm, definition of, 54 Olfactory nerve, anatomy and physiology of, 92 nerve, diseases of the, 107 Olivary bodies, physiology of the, 324 Ophthalmoplegia, 114 progressive, 117 Optic atrophy, 110 atrophy in locomotor ataxia, 235 nerve, anatomy and physi- ology of the, 94 nerve, diseases of the, 108 Orthophoria, 118 Oscillating spasm, 151 Osteoma of the brain, 392 Oxycephalic skull, 27 Pachymeningitis externa, 335 spinal, 205 Pain palsy, 434 sense, testing the, 37 Pains in the feet, 87 transferred, diagram show- ing the location of-, 82 Palmar reflex, 30 Palsy, see Paralysis Papillitis and neuro-retinitis, 108 Parsesthesia, 84 definition of, 21 trigeminal, 131 Paradoxical contraction, 33 Parageusia, 147 Paralysis, acoustic, 138 acute atrophic, 220 acute curable atrophic, 225 agitans, 478 alcoholic, 70 analgesic, with whitlow, 79 Brown-Sequard, 278 cerebral, in children, 365 chronic atrophic, of Erb, 226 compression, 164 crutch, 165 definition of, 19 divers', 202 Erb's, 161 facial, 134 from intracranial hemor- rhage, 355 glosso-labio-laryngeal, 262 hereditary ataxic, 255 hypertonic, 257 hysterical, 422, 429 infantile spinal, 220 lingual, 148 night, 80 of the brachial nerves, 160 of the cervical muscles, 152,. 155 of the circumflex nerve, 163 of the diaj)hragm, 155 of the iris, 116 of the lumbar nerves, 170 •• of the median nerve, 165 of the motor nerves of the eye, 114 of the musculo-spiral nerve» 164 of the oculo-motorius, 114 of the phrenic nerve, 155 520 INDEX. Paralysis of the posterior tho- racic nerve, 163 of the suprascaiDular nerve, lU of the ulnar nerve, 166 painful, 4;^4 peripheral facial, 134 peripheral, of the leg. 173 progressive bulbar, 262 recumbent. 80 spinal spastic. 2-57 subacute spinal, of Du- chenne, 226 Paralyzing vertigo, 144 Paramyoclonus multiplex, 432 Paramyotonia, congenital. 434 Paraphasia, 332 Parai^legia, ataxic. 249 definition of, 19 hereditary ataxic, 255 in childhood. 365 senile, 226 spastic, 257 spastic cerebral, of child- hood. 369 Paresis, definition of, 19 Paridrosis, definition of, 22 Parkinson's disease, 478 Patellar reflex, 31 Patholog\', general, of nervous diseases. 43 Pathophobia in neurasthenia. 452 Pavor nocturnus, 495 Pedometer, 2^ Perineurium, 4 Peripheral nervous system, general diseases of the. 64 Petit mal. 404, 406 Photographers' cramp. 475 Phrenic nerve, paralysis of the, 155 Physiognomy, 24 Pia mater, inflammation of the, 335 mater, spinal 180 Pianists" cramp. 474 Plagiocephahc skull. 27 Plantar neuralgia. 177 reflex. 29 Pneumogastric nerve, anatomy and physiology of the. 103 nerve, diseases of the. 147 Podalgia, 87 Poisons, etiological influences of. 42 Policeman's disease, 83 Polioencephalitis. 352 Poliomyelitis, acute anterior. 220 chronic anterior. 224 Poly^esthesia. 37 Polyneuritis, 70 acute pernicious. 75 diagnosis, 77 endemic and epidemic types, 74 etiology, 70 malarial, 75 onset. 72 pathology, 75 prodromas, 72 prognosis, 78 symptoms, 73 treatment. 78 Pons varolii, nuclei of the. 302 varolii, physiology of the. 323 Porencephaly. 333. 367 Potential, difl'erence in. 53 Prtedormitium, 5i)3 Pressure' sense, testing the. 36 Projection, eiToneous, defini- tion of. 113 Prosopalgia. 130 Pseudo-muscular hypertrophy. 270 Psychiatry, definition of. 16 Psychical epilepsy, 404. 406 Psychoses, definition of, 16 sexual. 457 traumatic. 400 I INDEX. 521 Ptosis, 114 morning or waking, 117 Pupillary skin reflex, 30 Purkinje cells, 304 Putamen, 298 Rachischisis posterior, 197 Ranvier, nodes of, 5 RaynaucFs disease, 85 Reaction time, 14 Reactions, degenerative, dis- eases in which they may be expected, 62 degenerative, testing for, GO Re-enforcement of the knee jerk, 31, 32 Reflex action, 14, 20 epileptiform convulsions, 404 irritations, neurasthenic form, 447 pains of the lumbar nerves, 172 Reflexes, 20 deep, 31 examination of the, 29 superficial, 29 table of spinal-cord levels for the superficial, 30 tendon, instrument for test- ing, 23 Regeneration of nerves, GS Representation, bilateral, 318 Retinal hyperiesthesia. 111 Rheostat, 55 Roots, spinal nerve, ISO, 186 Sacral nerves, diseases of the, 173 Salaam spasm, 151 Saltatory spasm, 433 Sarcoma of the brain, 391 Scaphocephalie skull, 27 Scapular reflex, 30 Schmidt, incisures of, 6 Schwann, sheath of, 5 Sciatica, 174 Scleroses, 44 Sclerosis, amyotrophic lateral, 265, 268 disseminated, 374 insular, 374 multiple, 374 multiple, aborted types of, 376 multiple cerebral, 376 posterior spinal, 231 primary lateral, 257 spinal, combined with soft- ening, 256 spinal, forms of, 229, 248 Scotoma, definition of, 108 Secretion, neuroses of, 22 Senile chorea, 438 paraplegia, 226 vertigo, 143 Sensation, delayed, 21, 37 double, 37 examination of the disor- ders of, 134 transferred, 21 Sense, pain, testing the, 37 pressure, testing the, 36 tactile, testing the, 35 temperature, testing the, 36 weight, testing the, 38 Sensibility, muscular, testing the, 37 Sewing spasm, 474 Sex, etiological influences of, 40 Sexual neurasthenia, 451 neuroses and psychoses, 457 Shingles, 170 Shock, etiological influence of, 41 Sick-headaehe, 125 Side pains, 163 Singultus. 155 Sinuses, cerebral, 316 Skin reflex. 29 Skull, dimensions and shape of, 26 522 INDEX. Sleep, accidents of, 503 disorders of, 489 normal, 490 paroxysmal, 500 perversions of, 493 Sleep-drunkenness, 495 Sleeping sickness, 503 Smell, disorders of, 107 instruments for testing, 145 primary centre for, 320 Smiths' spasm, 474 Softening of the brain, red, 349, 362 of the cord, 210 Somnolence, morbid, 500 Spasm, facial, 123 flute-players', 474 idiopathic muscular, 29 lingual, 147 milkers', 475 nodding, 151 of the ocular muscles, 120 oscillating, 151 salaam, 151 saltatory, 433 sewing, 474 smiths', 474 winking, 134 Spasmodic tic, 431 Spasmus nutans, 151 Spastic paraplegia, 249 spinal paralysis, 257 Spermatorrhoea, 458 Spina bifida, 197 Spinal accessory nerve, anat- omy and physiology of the, 103 accessory nerve, diseases of the, 147, 148 amyotrophy, progressive, 264 anaemia, 204, 286 apoplexy, 200 concussion, 460 cord, amyotrophic lateral sclerosis of the, 265, 268 Spinal cord, anatomy of tlie, 180 cord, cavities in the, 280 cord, combined sclerosis with softening of the, 256 cord, hemorrhagic cavities in the, 280 cord, malformations of the, 197 cord, myelitic cavities in the, 280 cord, physiology of the, 188 cord, i)rimary lateral scle- rosis of the, 257 cord, relation of difierent parts of the, to the per- ijDheral nerves, brain, and each other, 186 cord, secondary degenera- tions of the, 259 cord, syphilis of the, 398 cord, tumors of the, 277 exhaustion, 288 hypera^mia, 203, 286 irritation, 286 meningitis, 205 nerves, diseases of the, 153 neurasthenia, 288 paralysis, spastic, 257 Spotted fever, 338 Stabile electrode, 58 Stammering, 148 Static electrical batteries, 55 Status epilepticus, 406 Stellwag's symptom in exoph- thalmic goitre, 464 Stigmata, 24 permanent, of hysteria, 419 Stuttering, 148 St. Vitus' dance, 436 Substantia nigra, 302 Subthalamus, 302 Suggestibility in hysteria, 425 Sydenham's chorea, 436 Syncope, laryngeal, 144 Symptomatology of nervous diseases, 16 INDEX. 523 Symptomatology of peripheral nervous diseases, 178 Syphilis, hereditary, nervous symptoms of, 399 of the nervous system, 396 Syphiloma of the brain, 390 Syringo-myelia, 281 neuritic type of, 79 Syringo-myelocele, 198 Tabes dorsalis, 231. See Loco- motor ataxia dorsalis, pseudo-, 70 Tachycardia in exophthalmic goitre, 463 Tactile sense, testing the, 35 Tarsalgia, 88 Taste, disorders of, 146 instruments for testing, 145 l^rimary centre for, un- known, 320 Telegraphers' cramj), 474 Temperature sense, testing the, 36 Tendon reflexes, 31 reflexes, instrument for test- ing, 233 Tension, definition of, 53 Tetanilla, 443 Tetanus, 442 Tetany, 443 Thalami optici, 299 optici, physiology of the, 322 Thermo-anaesthesia, definition of, 20 Thomsen's disease, 433 Thrombosis of the brain, 362 Tic, convulsive, 18, 431 coordine, 441 de pensee, 431 douloureux, 130 mimic, 132 spasmodic, 431 Tinnitus aurium, 139 cerebri, 139 Tongue, hemiatrophy of the, 148 paralysis of the, 148 spasms of the, 147 Topography, cranio-cerebral, 505 Torticollis, 148 Tracts, cerebral, 306 of the spinal cord, 185 Trance, 497 Transferred pains, diagram showing the location of, 82 Trauma, etiological influence of, 41 Tremor, 18 convulsive, 432 hysterical, 424 testing for, 28 Trigeminus nerve, anatomy and x3hysiology of the, 98 nerve, diseases of the, 120 Trigonocephalic skull, 27 Trismus, 132, 442 Trophic disorders in hysteria, 425 Tropho-neuroses, 22, 484, Tubercula dolorosa, 90 Tubercular meningitis, 340 Tumors of nerves, 89 of the base of the brain, 389 of the brain, 381 of the central region of the brain, 386 of the cerebellum, 388 of the corpora quadrigem- ina, deep marrow, and pineal gland, 388 of the corpus callosum, 387 of the crus, 338 of the great basal ganglia and the capsule, 387 of the occipital lobes, 387 of the parietal area, 386 of the pons and medulla, 388 of the iDrsefrontal area, 385 524 INDEX. Tumors of the spinal cord, 217 of the temporal area, 387 Vagus nerve, anatomy and physiology of the, 102 nerve, diseases of the, 147 Vasomotor symptoms, 23 disorders, 484 Veins of the spinal cord, 194 Vertigo, 141 arterio-sclerotic, 143 auditory, 141 bilious, 142 laryngeal, 144 lithsemic, 142 mechanical, 143 Meniere's, 141 neurotic, 142 ocular, 142 Vertigo, paralyzing, 144 senile, 143 Vicq d'Azyr's bundle, 306 Tiolinists' cramp, 474 Vision, primary centre for, 319 Volt, definition of, 55 Von Graefe's symjDtom in ex- ophthalmic goitre, 464 Watchmakers' cramp, 475 Watt, definition of, 55 Weight sense, testing the, 38 Word-blindness, 330 Word-deafness, 331 Wrist drop, 164 Wrist reflex, 33 Writers' cramp, 468 Wry-neck, 148 ZoxES, hysterogenic, 422 UNIVERSITY OF CALIFORNIA LIBRARY Los Angeles This book is DUE on the last date stamped below. »^- J UN 14 1371 OCTUREBB "MB JUL ^5 Form L9-40m-5,'67(H2161s8)4939 ■ '"I ill ^ IIS^Mr 4291