JOHN J. MaePt Wwiwmim Iritoi No. HL Date NATIONAL LIBRARY OF MEDICINE Bethesda, Maryland Gift of Edward B. Schlesinger A MANUAL OS DISEASES OF THE NERVOUS SYBTfc BY THE SAME AUTHOR A Manual of Diseases of the Nervous System. Vol. II.—Brain and Cranial Nerves: General and Func- tional Diseases of the Nervous System. Second Edi- tion. Octavo. With 182 Engravings. Cloth, $4.00 ; Sheep, $5.00 ; Half Russia, $6.00. Clinical Lectures on Diseases of the Nervous System. 8vo. Cloth, $2.00. Diagnosis of Diseases of the Brain. Second Edition. 8vo. With Engravings. Cloth, $1.50. Syphilis and the Nervous System; being a Revised Reprint of the Lettsomian Lectures for 1890. 8vo. Cloth, $1.00. Epilepsy and other Chronic Convulsive Diseases. Second Edition. 8vo. In preparation. A Manual and Atlas of Medical Ophthalmoscopy. Third Petition. Edited hy Dr. Gowers with the assistance of Marcus Gunn, m.b., f.rc.s. With Coloured Plates and Woodcuts. 8vo. Cloth, $4.00. The Dynamics of Life: an Address delivered before the Medical Society of Manchester, Octoher 3, 1894. Crown 8vo. Cloth, 75 cents. These prices are net. Note.—The illustrations of which the source is not stated arc oriainal, and part of the copyright of the hook. A MANUAL OF DISEASES OF THE NERVOUS SYSTEM BY SIR W. R. GOWERS, M.D., F.R.C.P., F.R.S. CONSILTING PHYSICIAN TO UNIVERSITY COLLEGE HOSPITAL; PHYSICIAN TO THE NATIONAL HOSPITAL FOR THE PARALYSED AND EPILEPTIC, QUEEN SQUARE TTbtrfc Edition REVISED AND E N LARGED EDITED BY SIR W. R. GOWERS AXD JAMES TAYLOR, M.A., M.D., F.R.C.P. SENIOR ASSISTANT PHYSICIAN TO THE NATIONAL HOSPITAL FOR THE PARALYSED AND EPILEPTIC, QUEEN SQUARE; PHYSICIAN TO THE NORTH-EASTERN HOSPITAL FOR CHIL- DREN AND TO THE NATIONAL ORTHOPAEDIC HOSPITAL VOLUME I DISEASES OF THE NERVES AND SPINAL CORD WITH ONE HUNDRED AND NINETY-TWO ILLUSTRATIONS PHILADELPHIA P. BLAKISTON'S SON & CO. 1012 WALNUT STREET 1899 4 I /;JtP/ PREFACE TO THE FT"RST EDITION. This volume contains the first part of an attempt to give an account of diseases of the nervous system, sufficiently concise to be within the compass of the time-pressed student or busy practitioner, and yet adequate in its outline of a subject which has become wide and deep beyond any other part of medicine. Success m both aims can scarcely be more than approximate. Most of the illustrations are printed from blocks prepared from original drawings by phototype processes, and I am in- debted to Messrs. A. and W. Dawson, of the Typographic Etching Company (by whom most of the work has been done) for the care they have taken in the reproduction. The casual reader may perhaps miss subsidiary letters in the illustrations of the lesions of the spinal cord. The omission of these is intentional. A knowledge of the structural topography of the cord is the first requisite in the study of its morbid anatomy, and when this knowledge is gained, the figures will be understood without difficulty. Familiarity with unlettered illustrations facilitates the comprehension of sections of the spinal cord. Qulen Anne Steeet, London August, 1886. PREFACE TO THE THIRD EDITION. In the present edition every chapter has been subjected to careful revision, and numerous additions have been made em- bodying the results of personal experience and the more important facts ascertained by others. We are indebted to Dr. Bertram Abrahams for assistance in the revision of the section on the Anatomy and Functions of the Spinal Cord, and to Dr. F. E. Batten for the appendix on the Muscle-spindles. W. R. GOWKRS. JAMES TAYLOR. January, 1899. CONTENTS. INTRODUCTION . . . Classification of Diseases of the Nervous System, 2 PART I.—GENERAL SYMPTOMATOLOGY Symptoms and their Investigation Motor Symptoms ' Inco-ordination of Movement, 10 Sensory Symptoms ..... Tactile Sensibility, 13; Sensibility to Pain, 15; Sensibility to Temperature, 15 ; Muscular Sensibility, 16 Reflex Action ..... Cutaneous Reflex Action, 19; Muscle Reflex Action— " Ten don-reflexes," 20; Paradoxical Muscular Contrac- tion, 27 Changes in Nutrition ..... Electrical Irritability ..... Muscles : their Action and Paralysis Muscles moving the Upper Limb, 31; the Lower Limb, A't The General Constitution of the Nervous Systkm . PART II.—DISEASES OF THE NERVES General Pathology . Structure of Nerves, 62; Physiology of Nerves, 63; Lesions of Nerves, Secondary Degeneration, 65 Symptoms of Nerve-injury and Degeneration Electrical Changes, 71; Sensory Symptoms, 78; Reflex Action, 79 ; Vaso-motor and Trophic Disturbance, 79 Injuries of Nerves . Compression, 80 Inflammation of Nerves : Neuritis Causes, 82; Pathological Anatomy, 83 ; Symptoms, 85 ; Dia- gnosis, 87; Prognosis, 87; Treatment, 88 Vlll CONTENTS. PAOK Morbid Growths in Nervks : Nkuroma . • .90 Causes, 93; Symptoms, 94; Diagnosis, Prognosis, and Treat- ment, 95 Diseases of Special Nerves . . • .96 Phrenic Nerve, 96; Nerves of Upper Limb, 98; Combined Palsies of the Nerves of the Arm, 110; Diagnosis, 113; Treatment, 114; Nerves of the Lower Limb, 114; Diagnosis, 117; Treatment, 118 Brachial Neuritis . H9 Causes, 119; Symptoms, 119; Diagnosis, 121; Prognosis, 122 Sciatica . . . . . .123 Causes. 124; Symptoms, 126 ; Pathology, 129 ; Diagnosis, 130; Prognosis, 131; Treatment, 131 General Crural Neuritis , - . 133 Neuromyositis ...... 134 Multiple Neuritis . . . .188 Varieties, 144; Symptoms, 152 ; Course, 161 ; Cause of Death, 162; Complications, 163; Pathological Anatomy, 161; Pathology, 169; Diagnosis, 172; Prognosis, 178; Treat- ment, 181 Acute Mi-ltiple Myositis - . . 185 Endemic Neuritis . , . . .185 Malarial Neuritis . . . . .185 Beri-beri ...... 186 Symptoms, 187; Pathological Anatomy, 189; Pathology, 190 ; Diagnosis, 191; Treatment, 191 Leprous Neuritis . . . 192 Symptoms, 193 ; Pathology, 195 ; Diagnosis, 196 ; Prognosis, 196; Treatment, 196 Herpetic Neuritis . 196 Causes, 196; Pathological Anatomy, 197; Symptoms, 198; Prognosis, Treatment, 198 PART III.—DISEASES OF THE SPINAL CORD. Introduction—Anatomy of the Cord . . 199 Structure of the Cord ... 200 Grey Substance, 203 ; White Substance, 207; Commissure of the Cord, 223 Blood-supply to the Cord . 226 Functions of the Spinal Cord Motor Conduction, 228; Representation of Movements in the Cord, 230; Sensory Conduction, 233; Reflex Action, 238; Adaptation to Posture, 241; Co-ordination of Movement,' 242; Influence on Nutrition, 244; Visceral Control, 245- 228 CONTENTS. IX Functions of the Spinal Cord (continued)— page Mutual Relation of Functions, 249; Diagrams of Sensory Areas of Skin corresponding to Spinal Segments, 2-50. 251 ; Table showing approximate relation to the spinal nerves of the various motor and reflex functions of the spinal cord, 252 Symptoms of Disease of the Cord . . . 253 Indications of the Seat of the Lesion : Anatomical Diagnosis : Motor Symptoms ..... 254 Loss of Motor Power, 251; Motor Over-action—Spasm, 255 ; Muscular Contractions, 256; lnco-ordination of Move- ment, 257 Sensory Symptoms .... 258 Increased Sensitiveness, 259; Pain, 260; Spontaneous Sen- sations, 261 Rejlex Action . . . . • 262 Loss, Excess, and Reflex Spasm, 262—264 Vaso-motor and Trophic Disturbance . . 265 Visceral and other Disturbances .... 267 Paralysis of Sphincters, 267; Pyrexia, 268; Convulsions, 269 Combination of Symptoms .... 269 Total Transverse Lesion, 269; Unilateral Lesion, 272 General Pathology and Etiology: Indication of the Nature of the Lesion : Pathological Diagnosis . . 274 SPECIAL DISEASES OF THE CORD . , .281 Diseases of the Vertebral Column , . . 281 Injuries of the Spine ..... 281 Dislocation, 281 ; Fracture, 282 Caries of the Spine . . . 286 Causes, 286; Pathological Anatomy, 287; Symptoms, 289; Complicat'ons. 292 ; Course, 292 ; Diagnosis, 294 ; Prog- nosis, 296 ; and Treatment, 297 Tumours and other Diseases of the Spine . 299 Growths in the Spinal Column .... 299 Etiology and Symptoms, 300; Diagnosis, 302; Prognosis, 303; Treatment, 304 Vertebral Exostoses Syphilitic Disease Erosion by Aneurism . Hydatid Disease Diseases of the Articulations Lateral Curvature, 307 ; Vertebral Arthritis, 307 304 305 305 306 307 DISEASES OF THE MEMBRANES OF THE CORD . , 308 Spinal Meningitis : Inflammation of the Membranes . 309 External Meningitis ... 309 Cause, 309; Pathological Anatomy, 310; Symptoms, 311; Diagnosis, Prognosis, 312 ; Treatment, 313 X CONTENTS. Spinal Meningitis (continued)— page Internal Meningitis ..... 313 Acute Internal Meningitis .... 313 Causes, 313 ; Pathological Anatomy. 315 ; Symptoms, 317 ; Diagnosis, 319 ; Prognosis, 321; Treatment, 321 Chronic Internal Meningitis .... 322 Causes, 323; Pathological Anatomy, 324 ; Symptoms, 328; Diagnosis, 330 ; Prognosis, 332 ; Treatment, 333 HEMORRHAGE INTO SpiNAL MEMBRANES : SPINAL MENINGEAL HEMORRHAGE : HlMATORRHACHIS . . . 334 Causes, 334; Pathological Anatomy, 335; Symptoms, 336; Diagnosis, 337 ; Prognosis, 338; Treatment, 338 DISEASES OF THE CORD . . . . .339 Anemia and Hyperemia ..... 339 Anaemia, 340; Hyperemia, 342 Inflammation—Myelitis ..... 343 Acute Myelitis ..... 344 Etiology, 344 ; Pathological Anatomy, 348 ; Symptoms, 358 ; Varieties. 365 ; Pathology, 367; Diagnosis, 368; Proe- nosis, 372 ; Treatment. 373 Abscess ...... 377 Embolism ...... 377 Chronic Myelitis ..... 378 Etiology, 379 ; Pathological Anatomy, 382 ; Symptoms, 386 ; Diagnosis, 387 ; Prognosis, 388; Treatment, 389 Compression ...... 390 Causes, 390; Pathological Anatomy, 390; Symptoms, 393; Diagnosis, 394 ; Prognosis and Treatment, 395 Anterior Polio-myelitis : Atrophic Spinal Paralysis . 395 Acute Atrophic Paralysis (Infantile Palsy) . . 396 Etiology, 397 ; Symptoms, 399 ; Pathology, 409 ; Diagnosis, 416 ; Prognosis, 418 ; Treatment, 419 Subacute and Chronic Atrophic Spinal Paralysis . . 424 Acute Ascending Paralysis .... 427 Causes and Symptoms, 427, 428 ; Pathology, 430 ; Diagnosis and Prognosis, 431 ; Treatment, 432 Paralysis from Lessened Atmospheric Pressure—Divers' Paralysis—Caisson Disease . 433 Symptoms, 433 ; Pathology, 434 Hemorrhage into Spinal Cord—IIjematomyelia . . 437 Etiology, 437; Pathological Anatomy, 43S; Symptoms, 439; Diagnosis, 441 ; Prognosis and Treatment, 441 CONTENTS. XI PAGE DEGENERATIONS OF THE CORD .... 442 Locomotor Ataxy—Tabes Dorsalis . . . 444 History, 444; Causes, 445; Symptoms, 448; Motor, 449; Sensory, 450; Reflex, 454; Eye, 415; Sphincters, 458; Vaso-motor and Trophic, 459; Visceral, 461; Course and Termination, 463 ; Complications, 465 ; Pathological Ana- tomy, 467; Pathology, 474; Diagnosis, 480; Prognosis, 483; Treatment, 484 Primary Spastic Paraplegia—Primary Lateral Sclerosis . 489 General Pathology, 489; Causes, 492; Symptoms, 493 ; Patho- logical Anatomy, 497 ; Diagnosis, 500; Prognosis and Treat- ment, 502 ; Family form, 503 Ataxic Paraplegia . . . . .503 Causes, 504; Symptoms, 505; Pathological Anatomy, 507; Pathology, 508; Diagnosis, 510; Prognosis and Treatment, 511 Sclerosis of Cord from Toxic Blood-states . .511 Pfllagra . . . . . 511 Causes and Symptoms . . .512 Sclerosis from other Toxic Blood-states . . . 513 Symptoms, 514; Morbid Anatomy, 515; Pathology, 516; Diagnosis, Prognosis, Treatment, 518 Hereditary Ataxy—Friedreich's Disease . . • . 519 Symptoms, 520; Pathological Anatomy, 525 ; Pathology, 528; Diagnosis, 529; Prognosis and Treatment, 530 Simple Senile Paraplegia . . . 530 Chronic Spinal Muscular Atrophy: Progressive Muscular Atrophy . . . . . . 531 Causi-s, 533; Symptoms, 534; Varieties and Complications, 542, 543; Course. 543; Pathological Anatomy, 545; Path- olog}T, 551; Diagnosis, 555 ; Prognosis, 556 ; Treatment, 557 Arthritic Muscular Atrophy . . . 559 Pathology, 560; Diagnosis and Prognosis, 5G0; Treatment, 55 02/ 536 536 537 546 517 547 548 48 XVI LIST OF ILLUSTRATIONS. Fig. *agr 154. Progressive Muscular Atrophy ; Degeneration in Medulla and Cord 549 155, 156. Pseudo-hypertrophic Paralysis . °'Q 157. „ ., Partial Enlargement of Rectus . 570 158, 159. „ „ Absence of Latissimus Dorsi ; Enlargement of Infraspinatus 571 160, 161. „ „ Mode of rising . . 572 162. „ „ Late Stage; Muscular Contrac- tion and Wasting . . 574 163. Pseudo-hypertrophic Paralysis; Weakness of the S;>inal Muscles . 575 164. „ „ Enlargement of the Vasti . 576 1(15, 166. „ „ Muscular Alterations . 577, 578 167. Section of a Myolipoma attached to the Spinal Cord . . 580 168. Simple Idiopathic Muscular Atrophy. . . . 584 169—171. Idiopathic Muscular Atrophy affecting the Face . . 589 172. „ ,, showing Lordosis . . . 590 173. Advanced Muscular Atrophy, probably of the " Peroneal Type" . 595 174. Myolipoma of the Spinal Cord .... 608 175. Tumour growing from the Dura Mater . . . 611 176. Sarcoma between the Arachnoid and Pia Mater . . . 611 177, 178. Tumour growing from the Dura Mater . . 611. 612 179. „ of the Cauda Equina . . . .612 180. Neuromata of the Cauda Equina .... 612 181. Central Tumour of Spinal Cord . . . .613 182. Syphiloma in the Spinal Cord . . . 614 183. Central Canal in Normal Cords .... 630 184. Syringomyelia from a Child .... 631 185. „ with extensive Gliomatosis . . . 632 186. „ with Tumours of the Pons and Cauda Equina . 633 187. „ associated with Multiple Growths . . 635 li"8 „ with Haemorrhage into the Cavity . . 636 189. „ with Irregular Cavities in the Spinal Cord . 639 190. Spina Bifida; sections of Spinal Cord . . 649 191. Diagram of Muscle-spindle .... 672 192. Transverse Sections of Normal Muscle snindle . . 673 DISEASES OF THE NERVOUS SYSTEM. INTRODUCTION. A classification of Diseases of the Nervous System, at once scientific, exact, and convenient for systematic description, is not at present possible. If we attempt to classify the diseases according to either seat or nature, we are met at once by difficulties which prevent any complete arrangement. These difficulties arise from the fact that many diseases affect more than one part of the nervous system, that the precise seat of other maladies is unknown, and that we are still ignorant of the nature of a considerable number of diseases. A rough division is often made into two broad classes of "organic" and "functional" disease. The first class, that of "organic diseases," comprehends those in which there is always a visible lesion, manifesting sometimes the morbid process which constitutes the disease, sometimes only the ultimate result of that process. The second class, that of " functional diseases," is less definite, comprehending (1) those diseases that consist only in a disturbance of function, and are there- fore properly so designated; and (2) many diseases which have this in common with true functional disease, that they are transient and not permanent, and that they are not known to depend on organic changes. But there is also a large class of diseases in which no constant lesion has been discovered, but which are not transient, and cannot well be placed in either of these classes. This simple classification is therefore inadequate. It may be well to consider in what respect it needs alteration to meet the requirements of our present knowledge. The term "organic disease," as commonly used, means visible disease. But visibility is relative; it depends on the means of vision. The application of the microscope to pathology immediately increased the range of organic disease, and a similar increase has resulted, in our own day, from the use of staining agents, which render visible many changes that could not before be seen. Still it remains true that the degree of alteration determines visibility. Molecular changes in nutrition, considered as such, must be colossal to be detected. Such Vol. I. 1 2 INTRODUCTION. alterations, not sufficient to be seen, but still considerable, probably constitute the morbid process in many diseases that are commonly classed as "functional." Hence we may distinguish a class of "nutri- tional diseases " as to a large extent distinct from those that consist m a mere derangement of function. While distinguishing these two classes, we cannot entirely separate them; nutrition and function are mutually dependent, and prolonged functional disturbance must deter- mine nutritional change. Visible disease varies much in nature and degree. Some forms can always be seen with the unassisted eye; they change the shape or colour or consistence of the part. Other forms can be detected only with the aid of the microscope; while many may be seen with the unassisted eye when their degree is considerable, and only by means of the microscope in their early stage or when in slight degree. It is convenient to term such alterations, the visibility of which is alto- gether a matter of degree, "structural diseases." Thus we may dis- tinguish four pathological classes of disease of the nervous system: 1. Organic disease (or "coarse" organic disease); such as tumour, haemorrhage, softening. 2. Structural disease; such as most forms of sclerosis. 3. Nutritional disease; such as general paralysis of the insane, paralysis agitans. 4. Functional disease; such as reflex convulsions, and many forms of hysteria. In the first class the morbid process always begins outside the nerve-elements themselves. In the second class it may begin in them or outside them. In the third and fourth classes these elements are probably always primarily affected. Such a classification helps us to obtain clearer views of the primary relations of disease, but is not convenient for systematic description. For this a hybrid system is necessary, in which organic and structural diseases are classified according to their seat,—in the nerves, spinal cord, or brain. With each group may be placed some nutritional or functional maladies of local incidence. The bulk of these diseases are, however, best considered separately, after the organic diseases have been described, since many of them are of wide distribution or uncertain seat. Classification has two purposes to serve. It serves to bring out the differences in the nature of disease, and thus to define our conceptions and make clear our distinctions. But this purpose is less obtrusive than the second,—to furnish us, as it were, with shelves on which to place our conceptions, and labels with which to ticket them, so that we may find them when we need them and study them in a useful order with the least loss of time. Even if our knowledge were perfect, it is not likely that any scientific INTRODUCTION. 3 classification founded on natural distinctions would serve the prac- tical needs of an arrangement for use. Our present knowledge is un- questionably so very far from perfect as to be inadequate even for a complete natural classification; while an attempt to construct one of this character that shall be also of practical convenience is a mere waste of time. For use, we must divide where we ought only to distinguish; and we have to place near together, for convenience' sake, maladies that should be not only far from each other, but sometimes far from all others. Yet it is useful to attempt, if not to classify, at least to distinguish tht. chief pathological groups of the morbid processes that are commonh regarded as diseases of the " nervous system," and are so designated Unserviceable as a practical division, the attempt affords a general vier^ of the nature of the maladies, including the various influences to whiwi they are due, and therefore by which their nature is determined. The view that is obtained is not less useful because the groups that are, in the mass, well defined, are perceived to have connecting links when their borders are scrutinised, or are even found here and there to blend in places where a demarcation can only be artificial. We perceive thus that elements are common to more than one, and such elements may be thus more clearly discerned, and their importance is more ckavly re- vealed. The first great distinction, which is indeed a cleavage running through all the varieties distinguished for practical convenience, is that of primary seat. Some diseases begin in the nerve-elements, others outside them, in other structures. These structures have widely different pathological relations. The bones which protect, the fibrous tissues that invest and support, the vessels which convey the blood to or from the nerve-structures, bring the diseases of these structures into connection with most chronic and acute constitutional diseases; the blood itself, altered by numerous and widely different affections, frequently produces disturbance of function or of structure, and multiplies the relations of disease of the nervous system to an extent that is to us indefinite, and potentially is all but infinite. Not only does the blood cause disease by the direct influence of its changed constitution or the morbid agents it bears, but the physical conditions of the circulation, by excess or deficiency of force, and the passage in it of bodies that can obstruct the arteries, involve a direct relation to morbid states of the heart, which is frequently obtrusive. The affections which constitute connecting links between the two general classes of disease, those in which the nerve-structures suffer primarily and suffer secondarily, deserve a general notice. Some of them present to view certain pathological features which are of great importance, and which we have only lately become able to perceive dis- tinctly if not yet clearly. 4 INTRODUCTION. The various morbid growths are also, for the most part, diseases only in, not of, the nervous system, although one variety of neoplasm affords another illustration of the connection between the two classes; gliomata connect extrinsic growths with diseases that are primarily of the nerve-structure. The supporting neuroglia, different from the nerve-structures as it seems, and indeed is, consists of a residue of the embryonal tissue from which the nervous elements were developed. In its nutritional tendencies it presents a relation to the nerve-structures which, though definite, is opposite; it overgrows when the latter decay, and thus gives rise to the condition of secondary " sclerosis." Its growth seems normally to be restrained by the vitality of the higher tissue, and becomes exuberant as soon as that of the latter is lessened. It may persist in tracts, large or small, when there is a congenital arrest of development, such as gives rise to the cavities called " syringo- myelia ;" this persistence is especially important because the tissue may cease to be quiet, may grow and develop into the definite and dangerous condition known as " central gliomatosis." But the neuroglia, as the " connective tissue " of the central structures, shares the lower morbid tendency of the interstitial tissue of all organs. It is by an overgrowth of this, in random foci, presenting at first some of the features of inflammation, that " insular sclerosis " develops, while the neuroglia also takes a chief part in all forms of interstitial inflammation in the brain, cord, and nerves. Its secondary overgrowth in degenera- tion of the nerve-structures varies in amount and in energy; even when secondary, it seems occasionally to assume an independence which makes it excessive, and an energy which involves some of the features of inflammation. We have to distinguish from the primary interstitial changes, those acute processes in which the nerve-structures suffer primarily, but with rapidity. When they undergo slow decay we call it " degeneration," but an acute destructive change may take place so rapidly as to resemble "parenchymatous inflammation"—i. e. inflammation in which the primary element is in the proper functional structures of an oror n. Such changes belong to the group of diseases that are truly of the nervous system, but are not always readily distinguished from the inter- stitial inLammations, since the interstitial tissue and vessels may parti- cipate in the more intense processes. Their course presents all gradations, from the most acute to chronic forms, but even in the former it is often remarkable how small is the share the connective- tissue elements take. These processes have become, of late, very im- portant, on account of the extent and degree to which they can be traced to toxic influences. They constitute, in slow form, the systemic degenerations of the central nervous system, and also, in both slow and rapid forms, the varieties of toxic peripheral " neuritis." The former as well as the latter, have been extensively traced to the influence of blood-states. But as chronic " degeneration," they are also often due to defective vitality, or imperfect vital endurance, senile or premature INTRODUCTION. 5 occurring in late life before other structures decay, or as isolated failure soon after development is complete. The latter class is represented by the diseases of which " hereditary ataxy " is a type. The toxic influences which are thus effective seem, so far as we can trace their nature, to be chemical. They may be metallic poisons—or the simpler chemical substances of organic origin, as alcohol —or com- plex organic compounds, either received from without or, more often, formed within the body. They are often formed within the body by the organisms that give rise to " acute specific diseases," as has been clearly proved in the case of diphtheria; to the same mechanism many nervous sequelae of acute diseases are apparently due. These poisons, especially those of organic origin, present the remarkable feature of a special tendency to influence certain nerve-structures, that we are only able to distinguish from others by their difference or function; underlying this must be some minute difference of consti- tution which renders them more susceptible to the particular chemical compounds. These structures suffer most where their vitality is least,— for instance, the ends of the nerve-fibres,—the parts farthest from the nerve-cell of which they are the processes. Thus many toxic agents act on the extremities of the long sensory or motor nerves in the limbs, causing " degenerative peripheral neuritis," while a similar degeneration of the fibres of the pyramidal tracts of the spinal cord (the processes of the motor cells of the cortex) constitutes " lateral sclerosis." The motor fibres of the limbs are processes of the cells of the anterior grey matter of the cord; the sensory fibres proceed from the cells of the ganglia in the posterior nerve-roots. Of the latter, those which seem most prone to suffer are the afferent fibres from the muscles. In loco- motor ataxy these nerves suffer first, apparently from a toxic agent which is a result of syphilis, and acts also on the other processes of these ganglion-cells —those which become the fibres of the posterior median columns. These ascend the cord, but depend for their vitality on the cells of the posterior ganglia. Thus the degeneration in the spinal cord, the " posterior sclerosis," and the changes in the peripheral nerves, are but parts of the toxic effect on one set of "neurons." The afferent nerves from both skin and muscle suffer, moreover, from many other toxic causes, and, alike in alcoholic neuritis and in diphtheritic palsy, we may have a close resemblance to locomotor ataxy. A corresponding lesion underlies the correspondence of symptoms. The special susceptibility of the muscle nerves is the cause of the frequency, and early date, of the loss of the knee-jerk, and of the significance of the symptom. Other toxic agents influence, not the peripheral ends of the chief processes of the cells, but the structures in which nerve-energy is produced in the central mechanism. Such, for instance, is strychnine, and the strychnine-like products of the organism of tetanus ; while ore element in the production of the curious disturbance of chorea seems to be the action on the elements of the motor cortex of some 6 INTRODUCTION. poison allied to, but not identical with, that which causes acute rheumatism, and is probably a complex organic chemical compound. Eelative deficiency in the power of resisting toxic agents must be ascribed to imperfect vital energy, a lower degree of the energy of life that maintains nutrition. Such imperfection is manifested by a class of cases in which failure of nutrition occurs spontaneously in certain structures, either in late life, as in many cases of senile muscular atrophy, or labio-glossal paralysis, or senile brain failure, or paralysis agitans,—or else soon after complete development is achieved, as in the so-called " hereditary ataxy " and its congeners. Moreover it is possible that a slight difference in the power of vital endurance in some structures, causes a greater readiness to suffer degenerative changes in middle life under acquired influences. The toxic agents which can thus act on the nerve-structures and impair their nutrition and function are numerous and varied. They may be derived directly from without, may be produced within the body by the organisms of disease, and may be produced by disordered chemical processes apart from external influence, or by an external influence that becomes effective through a peculiar predisposition. They present relations to those rheumatic poisons which act on the fibrous tissues and on other structures. Exposure to cold, apparently the same, may cause in different persons—a general catarrh, local inflfl.TriTna.tinn (as tonsillitis), acute rheumatism (with or without endocarditis), spinal myelitis, or peripheral neuritis, apparently according to the nature of the toxic agent generated, determined by the constitution of the indi- vidual. A slight difference in the initial effect may determine a divergence in the chemical processes under the influence of life, and the ultimate result is the same in no two individuals, and may be very different. GENERAL SYMPTOMATOLOGY. SYMPTOMS AND THEIR INVESTIGATION. The nervous system is almost entirely inaccessible to direct obser- vation. The exceptions to this are trifling: the termination of one nerve, the optic, can be seen; some of the nerve-trunks in the limbs can be felt, either in the normal state or when enlarged by disease.* As a rule, the state of the nervous system can be ascertained only by the manner in which its work is done, and morbid states reveal their presence by the derangement of function which they cause. The functions of the nervous system are often divided into mental, motor, and sensory; but they are far more extensive than those words denote. The functions of all the organs of the body, all states of the blood-vessels and hence of the circulation within them, and even all processes of nutrition, are under the control of the nervous system. The disturbance of nerve-function produced by disease is conterminous in extent with the human organism. Our knowledge of these symptoms is constantly increasing in range and in degree. They differ, however, very much in relative importance. Some occur more frequently than others, and are more direct in significance. Many have a special relation to certain parts of the nervous system, while others occur in diseases of all parts. It may be well, at the outset, to describe the characters of some of the most frequent symptoms; while the more special symptoms can be conveniently considered when we deal with diseases of that part. Motor Symptoms.f—Disturbance of motion is one of the most • To the new X rays, unfortunately, the nerve-centres are opaque and inacces- sible, and the nerves differ too little in transparency from the other tissues to permit them to be seen, while their course is seldom such as to bring them into conspicuous distinction from other structures. f Some modification of the word kinesis (akinesis, &c.) is sometimes used to designate motor symptoms. These words seem to me to add nothing to our know- ledge or to its clearness—certainly nothing to compensate for their cumbersome character; and the definite addition all new words make to the information that has to be acquired is not always sufficiently weighed against their supposed advantage. 8 SYMPTOMS. common effects of disease. Movement is produced by muscles, but the muscles are excited to contraction by the nervous system. Most alterations of motility, both defect and excess, are due to its derange- ment. The conditions are very few in which motor changes originate in the muscles themselves. Defect of movement is of muscular origin only in some cases of primary alteration in the nutrition of the muscles. When there is a general impairment of nutrition, the muscles participate in this; they are ill-nourished, and therefore feeble. Such a condition is met with in chronic wasting diseases, in anaemia, and as an acute affection in all acute febrile diseases. This is the chief cause of the muscular weakness that so often results from fevers; it may even proceed to the degree of causing visible changes in the aspect of some fibres. In a few chronic diseases the muscles undergo a primary altera- tion. One is the disease known as " pseudo-hypertrophic paralysis," a special form of a wider malady, in which there is atrophy of the muscles, due to their own defective power of vital maintenance. Rheu- matic and other inflammations, commonly interstitial, may greatly impair their power, first by the pain contraction causes, and then by damage to the nerves in this tissue, a state to be distinguished from the primary affection of these endings themselves. In almost all other conditions, loss of power in the muscles is dependent on the state of the nervous system, either directly or through defective nutrition of the muscles, or both. The nutrition of the muscular fibres depends on the motor nerves, although we are still ignorant of the precise nature of that dependence. The subject will be referred to again in the special account of the changes that result from injuries to the nerves. So also with increased and involuntary muscular action. We know little of what has been termed " idio-muscular contraction,"—that is, contraction originating in the muscle itself. Whenever the whole of a muscle contracts, the contraction is due to an influence acting on all the fibres, and this is generally from the nerve-centres. Even muscular " tone" is dejiendent on the connection of the muscle with the nerve-centre, since it ceases when the connection is de- stroyed. It is possible that the extreme degree of the contraction in cramp is the effect of a tendency in the muscle itself. When the shortening exceeds a certain degree it becomes fixed in a peculiar manner, which seems as if it were due to a tendency in the fibres to pass beyond the power of relaxation. Contraction of the whole of a muscle may also result from mechanical influences acting on every part equally, as in traction. But these exceptions occur under special conditions. The partial contractions that are termed "fibrillary" are probably local, since they are so readily produced by mechanical stimulation, such as a tap on the muscle. Yet fibrillary contractions, although sometimes local, may be often of central origin. This is also true of the flickering contractions that are so common in persons whose MOTOR. 9 nervous system is enfeebled, the " live flesh" of popular language. They may occur in any muscle, from the orbicularis palpebrarum (in which they are most common) to the gluteus maximus. After damage to the nerve-fibres to the muscle they occur in special degree; they are often frequent for years in the calf muscles after sciatic neuritis. Paralysis.—Defect of movement may present every degree from slight weakness to absolute loss. There may be inability even to make the muscle contract, or the voluntary contraction may occur, but be too feeble to move the parts to which the muscle is attached. The latter difference is to some extent relative, since it varies with the readiness with which the part can be moved—i. e. with the resistance to be overcome. A contraction that will flex a finger may be insufficient to flex the wrist. The difference may vary in the same part according to position. A degree of power in the flexors of the hip, that will move the leg when the patient is lying on his side, may be insufficient to do so when the patient is lying on the back. This difference is even more conspicuous in some other muscles ; paralysis of the extensors of the elbow may be discovered only on an attempt to raise the hat: in many positions extension is due to the weight of the arm, much more than to the muscles, so that considerable weakness may be unobserved. The term "paralysis " has long been applied to all degrees of defect of power, a distinction being made between complete and incomplete paralysis. Partial loss of power is also sometimes termed " paresis." The advantages of "paresis" over the word "weakness" are chiefly psychical, and depend on the popular horror of " paralysis," which has become specially associated with complete loss of power, and the idea of incurability seems inseparably attached to the term. Our means of estimating defects of muscular contraction are very imperfect, in consequence of the peculiar and various forms of move- ment which are produced. An instrument to measure the force exerted is called a " dynamometer," but any simple form of instrument can have only limited application. Several have been devised, but that in general use consists of an oval steel ring, which can be narrowed either by compression applied to its smaller diameter or by traction applied to its longer diameter. The change in the shape of the dynamometer, and therefore the force exerted, is shown by the movement of an index on a scale that has a double graduation, a closer for com- pression, which is easy, and a wider for traction lengthways, which is difficult. This form of dynamometer is known as " Charriere's," from the name of its first maker. Another less convenient form was devised by Duchenne. These instruments are chiefly used for the measurement of the grasp. The estimation of the strength of other movements is practicable, but not easy. The observer opposes the movement by means of the instrument, and notes the resistance that can be overcome. Thus pressure applied through it just above the patella, to force down the raised thigh in the sitting posture, shows 10 SYMPTOMS. the power of the flexors of the hip. The wide variations in strength among different persons renders absolute estimation possible only when the defect is considerable. Slight changes are recognised by comparing the power on the two sides. It should be remembered that the limbs on the right side are normally stronger than those on the left, the rela- tion being about as five to four. Care must be taken to secure uniformity of the conditions under which the observations are made. A careful search would doubtless reveal average proportions between other movements that can be measured. Thus the strength of flexion of the hip, estimated in the way just mentioned, often corresponds to the strength of grasp on the same side. Inco-ordination of Movement.—By this term is meant a defect in the relative time and degree of the muscular contractions by which a move- ment is produced. Every movement is due to the contraction of a series of fibres, which may or may not correspond to the series massed together in a " muscle." Movements, not muscles, are represented in the structure of the brain, and the fibres which, together, cause a simple movement may be in more than one muscle, or may be only part of a muscle. The synergic action of the several fibres, in a definite degree and at a certain time, is essential for the movement. So also is the simultaneous contraction of the opponents of these acting muscles, which are thus steadied; this antergic * contraction is essential for the exertion of force, and must be often great in degree when strength rather than amount of movement is required. It must also be lessened automatically to permit movement. (The process will be considered in connection with the functions of the spinal cord.) Defect in the opponents does not interfere with movement, but it prevents the exertion of force, by permitting the movements to be too great. It is not customary to apply the term " inco-ordination" to any derangement of movement except that which is irregular in time. There may be also irregularity in degree, but it is when the contractions have not the normal duration, or are not synchronous, or not in due sequence, that the conspicuous irregularity occurs to which the term is applied. This is also often called " ataxy." Its manifestations differ in character according to the character of the movement. The variations are so great that it is not practicable to describe them, nor is it necessary, since all have the general nature just stated. It is also not easy to estimate the inco-ordination so as to permit definite record. When the movement of the arm is affected the degree may be estimated by making the patient try suddenly to touch, with the point of a pencil, a spot on a sheet of paper placed before him, his eyes being closed at the moment of the attempt. After a certain number of attempts the average distance from the spot of the dots he has made is ascertained, and this, compared with the result * I use this term because we have none to express antagonistic co-operation. This is synchronous with that of the acting muscle, but not synergic. MOTOR. 11 given by a normal individual, affords a numerical indication of the degree of inco-ordination.* The method is effective, although the result is perhaps scarcely worth the trouble. Whenever there is inco-ordination, spontaneous movements occur if the patient tries to hold the limb in a certain posture; the variation in muscular contraction prevents fixation as well as disorder in movement; co-ordination is as essential for steadiness of uniform contraction as for the steadiness of the varying contractions of movement. These involun- tary movements constitute a delicate test for the presence of ataxy. All spontaneous muscular contractions derange those that are due to the will, and movement is disordered by any "tremor" which co-exists. The slight rapid contractions that cause " tremor " may, indeed, occur only as voluntary movement, and there is a gradation of disorder from simple inco-ordination to that which may be called " tremulous." So also more extensive spasm disturbs movement with which it coincides, and energetic contractions of involuntary nature may be excited by a volitional impulse. Hence, just as simple ataxy may pass into tremor, so, on the other hand, there is a gradation by " jerky inco-ordination " to wide sudden movements, the violence of which obscures the element of mere disorder. It is necessary to distinguish co-ordination and the direction of movement to a definite end. The motor process for the latter depends on sensory guidance, chiefly on the senses of touch and sight. A semp- stress with loss of semaion in the fingers cannot sew unless she constantly watches them. A compositor, whose sense of touch is dulled upon the tips of thumb and index finger, cannot pick up the type, or if he does pick it up may drop it again, unless he constantly watches the movement. There is also a guidance from the afferent nerves of the muscles, but this is related to co-ordination proper rather than to the direction of movement, and it will be more conveniently considered in connection with the functions of the spinal cord. Indeed, the mechanism of co-ordination, and its special factors, can only be discussed in that connection. Spasm.—Involuntary muscular contraction, when considerable in degree, termed spasm, is always due to the influence of the nervous system. It is a frequent symptom of disease. Three chief varieties may be distinguished, but intermediate and combined forms are often met with. (1) We may have, first, a single isolated very brief contraction of one or more muscles. (2) Separate contractions may occur in rapid succession, a second commencing as soon as there is relaxation of the muscle from the first contraction. This is termed " clonus," or " clonic spasm." The relaxation of one is often incomplete when the next con- traction begins. (3) There may be a persistent contraction in which no relaxation can be perceived. This is termed "tonic spasm." (1) It will be remembered that muscles, as long as they are connected * Blix, «Neur. Centralb.,' 1884, p. 83. 12 SYMPTOMS. with the nerve-centres, are never in a state of perfect relaxation. There is always a certain degree of persistent slight contraction of the fibres, which keeps them adapted to the distance between their attachments, so that the substance of the muscle presents always a similar degree of firmness. This physiological " tone " is due to a continuous action of the centre on the muscles, through the motor nerves ; but this action is apparently determined, in degree at least, by the sensory impressions from the parts, and especially from the muscles.* Tonic spasm may be regarded as an augmented degree of this state, due to various causes. Although it necessarily depends directly on the action of the centres in the spinal cord, this may be due to the augmenting influence of the cerebral centres, or to diminution of the latter, permitting insubordinate activity, and is often clearly the result of a reflex process. It must be distinguished from structural shortening of the muscle. The distinction is easy, because tonic spasm can always be overcome by gentle, steady traction, while structural shortening cannot be thus removed. The latter may result from long-continued tonic contraction; nutritional changes alter the structure of the muscle and fix the elements, especially the interstitial tissue, in the state of contraction. It occurs whenever muscles for a long time are unextended by their antagonists, and so results from the long-continued maintenance of a certain posture, and also in extreme degree from paralysis of opponents. Its influence on the joints and the parts moved causes the various de- formities that result from local palsy. The tonic spasmodic shortening which can be overcome is often spoken of as " spastic." It is some- times also distinguished as " contracture," the term " contraction" (which really includes all forms of spasm) being then applied in a narrow sense to the fixed shortening. (2) Single muscular contractions vary much in extent and duration; when partial they sometimes, as already stated, seem to be of local origin. When more extensive they depend on the nerve-centres. (3) Clonic spasm consists of a series of brief contractions, each of which corresponds to that which is caused by a single induction-shock applied to the nerve. This has a definite duration of one tenth to one twelfth of a second, but it is often prolonged by the force which the contracting muscle has to overcome. In the serial contractions to which the term " clonus " is applied there is also an interval between the end of one and the commencement of another, occupied by the process of stimula- tion. The "foot-clonus" to be presently described, which consists of a series of such contractions, varies in frequency from five to eio-ht or ten per second. The contractions in " tremor," as seen for instance in " paralysis agitans," have a somewhat greater average frequency. * Jendrassik ('Neur. Centralbl.,' 1896) has endeavoured to estimate the degree of tone by the resistance of the muscles to passive extension, and finds it greater in spastic paraplegia, and less in tabes than in normal states. The latter, however, pre- sented such wide variations as to preclude absolute inferences. The amount of tVi extending force applied seems to need more careful adjustment. SENSORY. 13 Tetanic spasm is produced by the blending of clonic contractions which may be so fused that the contraction is uniform, and is then identical with tonic spasm; or there may be commencing relaxation of one before the next contraction supervenes. This is chiefly seen as such spasm develops or lessens. The passage of tonic into clonic spasm is well seen in the severe epileptic convulsion, in which the fixed spasm becomes first vibratory, then intermittent, and at last remittent. Sensory Symptoms.—Altered sensation is another very common symptom. It has often to be searched for, because a significant defect may be unknown to the patient. Each form of sensation, touch, temperature, and pain, must be separately tested, since one may be affected and not another. The affection of one form only is sometimes of important diagnostic significance. Sensibility to Touch. —The structures that subserve tactile sensibility are stimulated chiefly by motion—by change in contact. Prolonged contact, uniform in its degree and place, is perceived but little, and only by close attention. It is the change that excites a nerve impulse; the commencement of contact is more effective than its cessation, but in each case rapidity of change chiefly determines the result. a firm pressure may be scarcely noticed if produced very gradually, while a sudden touch is observed, however light. In testing tactile sensibility care must be taken that the instrument employed does not give an impression of heat or cold, lest the patient perceive by the sense of temperature that which he cannot perceive by the sense of touch. The observer's finger may be used, if it is not cold, or the skin may be touched with a feather, a piece of string, of india rubber, &c. The eyes of the patient should be closed during the examination, and, since he is apt to fancy that he feels a light touch when he does not, he should occasionally be asked if he can feel, when no contact is made. But it is easy to make the test too fine. Where the skin is thick, or sensibility is normally low, a light touch with a piece of string or a feather may normally be unperceived. Loss of sensibility to touch is termed " anesthesia," but this word is often applied loosely to all forms of impaired sensibility. In examining the tactile sensibility it is important to ascertain not only whether the patient can feel, but whether he is able to" recognise the place touched,—whether he can correctly " localise " the sensation. For this he must be asked not only whether he feels the touch, but also to say or point out where he feels it. The part touched should be frequently varied. Another test for tactile sensibility depends on the fact, ascertained by E. H. Weber, that the distance apart at which two points are discriminated is nearly the same in different individuals in the same part of the body, although it varies much in different parts of the body. The normal distance being known, the increased distance at which the points have to be placed for their discrimination is a measure of the degree of defect. The points should not be so 14 SYMPTOMS. sharp as to occasion pain. Common compasses may be employed, but the most convenient" sesthesiometer " is one contrived by Sieveking, in which the points are attached to a graduated bar. The greater the degree of tactile sensibility, the nearer together can the points be, and still be discriminated. The distance at which they are normally distin- guished must be known before any inference can be drawn. The most important average distances, ascertained by Weber, are as follows:— The distance is smallest, i. e. the sensitiveness is greatest, at the tip of the tongue, where the points are discriminated when only 1*5 mm. apart. Then come, in order of sensitiveness, the finger tips, 2 to 3 mm.; the lips, 4 to 5 mm.; the tip of the nose, 6 mm.; the cheeks and the backs of the fingers, about 12 mm.; the forehead, 22 mm.; the neck, 34 mm.; the forearm, lower leg, and back of foot, 40 mm.; the chest, 45 mm.; the back, 60 mm.; the upper arm and thigh, 75 mm. Slight variations exist in different individuals, and a deviation from the normal that is uniform in degree throughout the body is probably physiological. In using this test it is necessary to touch the skin with the two points at the same moment, and with equal pressure. The examination requires time and patience, and the results are considerably modified by the intelligence of the patient. Moreover the power of discrimination is increased by practice. It is rare to obtain a con- clusive result unless there is a degree of defect that causes a slight absolute loss. For these reasons the practical value of the test is less than was at first anticipated, and it is not often employed. It is most useful for the estimation of changes of sensibility in the same person and the same part. Curious modifications of tactile sensibility are sometimes observed. In one of these, a single touch is felt as if it were two or even three, a condition that has been termed " polyesthesia " (Fischer). In another, an impression on one part is referred to some other part, usually in the same limb, rarely in another limb.* In another variety, an impression on one part has been referred to the corresponding place on the opposite side of the body; this has been termed " allocheiria" (Obersteiner). Perception of the degree of pressure on the skin is probably sub- served by the nerves for tactile sensibility. It may be estimated by simple pressure applied through any instrument, or by small weights, or by an instrument contrived for measuring the tension of the pulse in which, by means of a spring, the part tested must be supported, so that the muscles are not brought into action. The point to be ascertained * In most persons there are spots in the skin whence a painful sensation seems to dart to a distant place; e.g. a. prick on the thigh in a limited area may be felt also as a sharp pain near the scapula. This shows how structural connections must exist favouring the " reference " of sensation to a distance from the nerve stimulated Another instance of the same perverted reference is presented by the frequent neuralgic pain in one jaw due to a carious tooth in the other jaw, which seems painless. SENSORY. 15 is the minimum variation that can be recognised. In health this is about one twentieth of the total pressure, whatever the latter may be (Weber). The sensation in the skin caused by electricity, especially by faradism, does not always correspond to that due to other stimuli. It has been thought to depend on a special form of sensibihty, but the evidence of this is insufficient. Its features and their meaning have yet to be ascertained. Sensibility to pain is subserved by what are called nerves of " common sensibihty." It may be tested by a prick or a pinch. For a prick, too fine a point must not be used, not only because a sharp point may penetrate the skin, but because, in the less sensitive parts of the skin, where the nerve-endings are not close together, a fine point may be unfelt at one spot, although felt readily at a place close by. Nothing answers better than the point of a quill pen. The faradic current may be employed to test sensibility to pain, wire terminals being most suitable for the purpose. Its advantage is the delicacy with which it can be graduated; but it does not furnish any absolute standard, and needs more study before it can be usefully employed. Sensibihty to pain may be changed with or without sensibihty to touch. Its loss is termed "analgesia," but is often included in the general term " anesthesia." A painful sensation may be felt more intensely than normal ; this is usually called " hyperesthesia "—a general term for increased sensitiveness ; sometimes, with more pre- cision, " hyperalgesia." Occasionally a touch on the skin gives rise to pain, but it is probable that this is due to the stimulation of the over-sensitive nerves of common sensibility, and is not an intensification of a tactile sensation. The fact that touch may be perfect, although no pain can be caused, makes it difficult to conceive that the nerves of touch can subserve pain. Both tactile and painful impressions may produce sensations that are abnormal in character, described as " thrilling," " tingling," &c. This perverted sensation has been termed " paresthesia," or " dysesthesia," words that have also been applied to purely subjective sensations. When a prick is perceived as touch, pain being lost, care is needed that the patient shall clearly know what is desired. Since there is often delay, when there is not loss, he should be told to say " touch " or " prick " the instant either sensation is perceived. When sensibihty to pain is diminished but not lost, the test must be kept uniform. Another source of error is then occasioned by the readiness with which the patient may mistake the degree of pain he is required to recognise, and by the fact that his idea often varies in the course of the examina- tion. He may thus deny that he feels a prick as such at a part where presently he says he does, and this quite honestly, the sensation being really the same. It is probable, indeed, that this is the most frequent cause of the conclusion that the state " varied in the course of the examination," or that "the patient's answers were unreliable." Sensibility to temperature is usually affected with sensibility to pain, 16 SYMPTOMS. but often not in the same degree, and one may be impaired without the other. There may be an absolute inabihty to recognise either heat or cold as such, or slight degrees of each may be unperceived while con- siderable degrees are recognised correctly. In the latter case there is impairment of the power of perceiving differences in temperature, analogous to the defect in the perception of differences in pressure. There may be also perverted sensibility, whereby hot objects feel cold, and cold objects hot. The pain which extreme degrees of temperature normally produce may be felt with undue readiness, or less readily than normal. When the interval is increased that elapses before a sensation of pain is felt, there is a similar delay in the sensation of temperature. It must be remembered that, in health, this sensation is less quickly produced than that of pain, because time is required to raise the temperature of the skin sufficiently to enable the heat to stimulate its nerves. For rough examination, hot and cold spoons may be employed, or a hinged tongue depressor, one half of which is warmed, or two similar test-tubes, one containing hot and the other cold water. Both heat and cold must be sufficient in degree to be unquestionable, so that the doubt of a patient is certainly pathological, and not due to uncertain " lukewarmness." For ascertaining the power of differential discrimination, large test-tubes may contain water at known temperatures, indicated by a thermometer in each. It is always necessary to test separately the sensibility to heat and to cold, as there is reason to believe that they are subserved by different nerves. If very minute points of the skin are examined, it has been found that at some points only heat, at others only cold, is perceived. The stimulation of points of the skin by electricity is said also to show that at some points the peculiar electrical sensation is produced, at others a sensation of cold, at others one of heat. Further, the points identified as " cold points " and " warm points " by the one method are said to correspond with those ascertained by the other.* The conclusion from these observations is confirmed by the fact that in disease the sensibility to heat and to cold may be affected in different degrees. Commonly, however, the defect in the two corresponds; accuracy in the comparison is beset with great difficulty. Muscular Sensibility.—The term "muscular sense," as often used, includes more than one form of sensation. There is, first, a true muscular sensibihty. The muscles are abundantly supplied with sensory nerves, which end in the interstitial tissue between the muscular fibres in special structures, fusiform in shape, and hence termed "muscle spindles." These have long been known, but have lately been investigated by Sherrington, Batten, and others. They are of considerable length, some nearly half an inch long, and have a special relation to the afferent fibres, which seem to begin in them, * Blix,' Zeifcehr. f. Biologie,' Bd. xx, p. 141; Eulenberg, * Zeitschr. f. klin. Med.,' Bd. ix, Heft 2. The observations have also been corroborated by Goldscheider and Herzen, but the subject deserves further investigation. SENSORY. 17 although the strange fact that they contain striated muscular fibres makes it probable that motor fibrils may enter them. Their relations, degenerative and morbid, have yet to be worked out, but we may assume that it is probably in them that the afferent impulses arise. Such impulses are excited especially by pressure, and by traction on the muscle. Thus a squeeze of the calf causes a muscular sensation of an undeniable quality, and strong passive flexion of the foot on the leg causes a sensation which is distinctly produced in the muscle. The nerves are, moreover, strongly stimulated when the fibres are widened by the extreme contraction of "cramp," which causes acute pain. It must be ascribed to the compression of these nerve- endings, since no afferent impressions seem to come from within the fibres. It is thus a proof of their susceptibility to pressure-excita- tion. After cramp, moreover, the nerves are left in a state of such exalted excitability that even slight extension of the muscle gives rise to pain, although such extension has no sensory effect in the normal state. Every one has experienced the effect. We shall afterwards see the importance of the fact that the nerves are chiefly stimulated by these two mechanical processes. The muscular pain caused by electrical stimulation, as distinct from the pain felt in the skin, may be due to the stimulation of the afferent nerves in excessive degree, or to the effect on them of the muscular contraction that is produced; the former is the more probable. But these sensations of pain, although due to "muscular sensibihty," are not included in the term " muscular sense." They are, however, of great importance on account of the conclusive evidence they afford that afferent impulses come from muscles and as to the way in which they are produced. The chief knowledge that is ascribed to the " muscular sense " is that of the character of movement and posture due to the action of the muscles, of the degree of movement and energy of contraction, and also of the character of passive movement (by an external force) and of posture when the muscles are at rest. It is evident, however, that here we have two very different conditions, in one of which there is much activity of all the motor elements, nervous and muscular, while in the other these are almost at rest, only such gentle action persisting as maintains the " tone." Except in absolute relaxation, there is probably continuous stimulation of the afferent nerves by this tonic state of the muscular fibres. In active contraction, this stimulation is far greater, and activity of the motor nerve-centres is added. Hence two elements are comprehended in the term, and must be separately considered. Our knowledge of active states of the muscle is due, at least in some measure, to the effect on consciousness of the activity of the nerve- structures causing the movement. The proof of this consists in three facts. (1) In palsy of an ocular muscle, objects seen are referred to the position (in relation to the body) that they would occupy if the movement corresponded to the innervation; it is the latter, i. e. the VOL. I. 2 18 SYMPTOMS. activity of the centre, to which the perception corresponds. (2) After amputation of a hmb, a person who makes an effort to move the lost part seems to feel as if he did move it. (3) In some convulsions beginning locally, slight attacks may be attended with a feeling that the arm is raised above the head, or otherwise moved, when it is hanging by the side. These facts show that the central motor process is an important source of our knowledge. But to its effect must be added that of the impulses from the muscles, about to be described. Our knowledge of rest-posture and passive movement must be derived from incoming impulses. These are not from the skin; the sense of posture may be lost when cutaneous sensibility is normal, and perfect when this is much impaired. This is observed in unilateral lesions of the spinal cord, and in other diseases. The chief source of these perceptions must therefore be the deeper afferent nerves, those of the muscles and joints, perhaps chiefly of the muscles. These afferent impulses are no doubt continuously generated, but do not influence consciousness as definite sensations. They certainly in- fluence the activity of the motor centres of the spinal cord, and there is reason to think that they pass, in part, to the cerebellum, and act through it on the cerebral cortex, determining and assisting in regu- lating its activity. This influence on the motor centres, by the effect it produces, is apparently one chief cause of the perceptions of these passive states. The active state of the motor centres of the cortex, however it is produced, has an effect on consciousness and enters into perceptions though no sensation results. This may be combined either with true sensation from the parts concerned, or with the result of still shghter impulses, to be discerned only by close attention, to the joints, skin, &c, of which we seem, at first, to be altogether unconscious. We are thus led to refer our perceptions of passive posture in part to the same structures as give rise to our perceptions of active posture. Our knowledge is the result of such perception, and not of true sensation proper ;—we perceive and know that which we do not feel. Our recognition of resistance to contraction affords one of the most delicate tests for " muscular sensibihty." It is ascertained by testing the ability to detect differences of weight, i. e. variations in the resistance to contraction. In this examination the patient's eyes should be closed, and the objects used should be of uniform size. Leather balls like small cricket balls, containing various wei«-hts from two drachms to two pounds, are in use at the Queen Square Hospital for this purpose. To ehminate as far as possible the stimulation of the cutaneous nerves, we may (1) reduce it to a minimum area, placing the weights in a bag suspended by a string to the part to be tested, so that only a small area of the skin shall be pressed upon; (2) increase the area (Hitzig), and thus diffuse it in diminished degree; (3) increase the weight, and therefore the pressure in both area and decree, so that the addition to be discerned shall bear only a small proportion to the total stimulation. REFLEX. 19 Thus we may test muscular sensibility:—(1) by the power of discriminating weight. This is greater than in the case of the nerves of the skin, since a difference of one fortieth of the total weight can be recognised under normal conditions; (2) by the sensitiveness of the muscles to pressure and traction; (3) by their sensitiveness to electrical stimulation. It is difficult to test accurately the electro- sensibility unless the sensitiveness of the skin is lost, or is removed, as by the injection of cocain. The power of recognising passive posture is also regarded as a test for muscular sensibility, but it may mean much more, afterwards to be considered. If cutaneous sensibihty is normal, the parts handled must be grasped firmly, and pressed on both sides, so that the direction of pressure may not suggest the posture. The patient should be asked to indicate the sensation by putting the limb of the other side into the same posture. Several observations should be made to eliminate the chance of accidental error. Reflex Action.—Many symptoms of disease of the nervous system are due to derangement of the various reflex actions. These are numerous, and we can now only consider their general characters. Each action is effected through afferent sensory nerves, efferent motor nerves, and a system of nerve-cell-processes, and intervening sub- stances,—the "reflex centre." The centre is usually complex and often extensive, and in it are paths of different "resistance," deter- mining the form of reflex action and its extent, according to the source and intensity of the sensory impression. The reflex centre is between the roots of the sensory and motor nerves concerned, and with them it constitutes what may be termed a "reflex arc." The sensory impulse may not only excite a motor process, it may also pass up to the brain, and influence consciousness as a sensation. It is probable that the two effects are subserved by the same nerve-fibres, so far as the cutaneous nerves are concerned, but some fibres from the muscles pass up the cord without connection with the spinal centres. Further, the reflex centre of the spinal cord is to some extent under the control of encephalic centres—a point of very great importance. Two forms of reflex action must be distinguished. The first is that excited chiefly by stimulation of the nerves of the skin; the second is produced by the stimulation of deeper nerves, chiefly those of the muscles, in the manner just described. This form is caused, among other ways, by tapping a tendon, and therefore was at first, and still is sometimes, called " tendon-reflex action "—an undesirable name. Cutaneous Beflex Action.—The reflex movements obtained from the skin are excited rather by a gentle stimulation, as a touch, than by a strong, painful impression. They consist of a single movement in most instances, either quick or slow, but often complex, and extensive in proportion to the character of the stimulation effected, the nature of the central mechanism, and the state of the centre. Often muscles at 20 SYMPTOMS. a distance are influenced by a powerful stimulation, either with others or alone. A strong impression may cause a reflex action so wide as to involve most of the muscles of the body. As a rule a painful impres- sion causes quick flexion of a limb, such as to withdraw it from the cause of the pain. Thus a prick near the knee causes a reflex flexion of the hip. In other cases, where withdrawal is impossible, a protective movement results, as in the case of the eyelids. The slighter degrees of excitation cause a contraction in the muscles close to the part of the skin that is stimulated, the impulse passing, in the spinal cord, only to the related motor centres. This limitation of the process renders them important in diagnosis, especially when lost on one side (see the chapter on the functions of the spinal cord). The cutaneous reflex actions may be excited at almost any part of the skin, but at some parts they are very definite in cha- racter, and are distinguished by special names. The most important are the "plantar reflex," from the sole; the " gluteal reflex," a contrac- tion in the gluteus when the skin over the muscle is stimulated ; the " cremaster reflex," a retraction of the testicle on stimulation of the skin on the inner part of the thigh; the " abdominal reflex," in the muscles of the abdominal wall when the skin over the side of the abdomen is stroked; the upper part of this reflex is a very definite contraction at the epigastrium, and has been termed the " epigastric reflex." A series of reflex actions may be obtained in the muscles of the back, the highest being in the muscles of the scapula. Others have been distinguished and named, but this process may easily be carried too far. These spinal reflex actions vary in their excitability in different individuals, and are always more readily produced in the young than in the old. They may be increased or abohshed by disease. In the region of the cranial nerves the most important reflexes are those of the eye,—(1) the conjunctival reflex ; (2) the contraction of the pupil on exposure of the eye to light; (3) dilation on stimulation of the skin of the neck. Muscle-reflex Action; "Tendon-reflexes.'"—The second group of phenomena which depend on reflex action were first systematically studied by Erb and Westphal more than twenty years ago. Attention was called to them in this country by Grainger Stewart and Buzzard in 1878. They have since been the subject of a vast amount of study and discussion. All occur in muscles that are in a state of slight tension, and are produced by a sudden increase of this tension or by some other sudden mechanical influence, but voluntary contraction superadded to passive tension, diminishes or prevents them. They are distinguished according to their seat, and vary in distinctness, conspicuousness, and the ease with which they are produced according to the mechanical conditions of the muscles and their attachments. The first of these is the jerk of the leg which occurs when the patellar tendon is tapped. It has been called the " knee-phenomenon " REFLEX. 21 by Westphal, the "patellar tendon-reflex" by Erb, the "knee-jerk" by myself. To obtain the jerk, the knee must be flex3d so that the quadriceps femoris is gently extended. If then the patellar tendon is struck, the quadriceps contracts, and the lower leg is jerked forward if free to move. The blow is given over the space above the tibia where the tendon can yield, so that there is a sudden increase in the tension of the muscle. The most convenient position is with the knee to be tested flexed nearly, but not quite, at a right angle, by being placed over the other knee as the person sits (Fig. 1). But if the leg to be tested is stout, its tension in this position may be too great to Fig. 1.—The Knee-jebk. Fig. 2.—The Knee-jeuk. The dotted line indicates the movement Method of obtaining it when it which follows the blow on the patellar is not readily produced in the tendon. ordinary way. permit of any movement. In such case the observer may place his arm beneath the patient's thigh, just above the knee, and rest his hand on the patient's other knee (Fig. 2). Muscular relaxation is sometimes more readily obtained when the legs hang vertically ; or the foot may re^t on the floor, and the contraction be felt by the hand placed on the muscle; the effect of the recoil and of the muscular contraction must then be carefully distinguished. If the bent fingers of each hand are hooked together, the hands pulled strongly, and the eyes closed, the movement is increased in degree—" reinforcement," it has been termed.* It is essential that the flexors also should be free from voluntary con- traction. This contraction may be ascertained by feeling the hamstring tendons, and pressure on these by the fingers often helps to secure re- laxation. The blow may be given by the side of the hand, a percussion hammer (Fig. 2), or a stethoscope with an india-rubber edge to the ear-piece. If the jerk is doubtful, the skin should be bared. * A useful device suggested by Jendrassik. 22 SYMPTOMS. The same contraction may be obtained by other modes of suddenly increasing the traction on the muscle, especially when this excitabihty is abnormal in degree. A blow on the tibia may be effective, but a method which has much practical convenience is this. When the patient is lying with the muscles relaxed, the patella is displaced downwards by a finger placed across its upper edge; a tap on the finger in the direction of pressure, so as suddenly to increase the tension, excites the contraction of the muscle whenever there is even slight increased excitabihty. If the tension is maintained when the excitabihty is much greater than normal, the single contraction is immediately succeeded by a second, and this by a third, and so on—a series of quick clonic contractions, or " clonus,"which will be considered presently in more detail. It may continue as long as tension is kept up, but instantly ceases when the muscle is relaxed. Similar contractions can be obtained by similar measures in many other muscles. That in the muscles of the calf, which causes a move- ment at the ankle-joint, is especially important. If the calf muscles, which are connected with the Achilles tendon, are made tense by gently pressing up the foot, and this tendon is tapped, the muscles contract, causing a slight extension movement of the foot; just as the muscles of the thigh contract when the patellar tendon is struck. The tendon is unsupported just as is the patellar tendon, and so yields before the blow increasing suddenly the tension on the muscles. A tap on the side of the tendon is equally effective; but if the tendon is so firmly supported on the other side that it cannot yield, a tap which before caused the contraction will not do so. This is evidence that it is not the mere percussion of the tendon, but the increased tension, which constitutes the stimulation. In cases in which the excitabihty is excessive—just as sudden tension in the thigh muscles will cause a con- traction, followed by others in a continuous series—so, in such cases, if the calf-muscles, which extend the ankle-joint, are suddenly put on the stretch by pressing the hand against the sole of the foot (Fig. 3), the first contraction is followed by another, and they recur as long as the tension is maintained. This series of contractions, the "foot-clonus" or "ankle- clonus" (or " foot-phenome- Fig. 3.—Method op eliciting the non —Westphal), is a very Foot-clonus. important symptom. The movement is remarkably uni- form under the same conditions, varying from six to nine contractions per second. By attaching a writing point to the foot, and making it REFLEX. 23 trace a line on a revolving cylinder covered with blackened paper, tracings may be obtained (Fig. 4), which are almost as regular as Fig. 4.—Tracing of the Foot-cxontjs in Paraplegia. (The tracing reads from right to left.) those of a tuning-fork.* The clonus in the extensors of the knee has the same time, and the two are of the same nature. A clonus quite similar may sometimes be obtained in other muscles—peronei, flexor brevis pollicis. Similar contractions may be obtained in the muscles of the arms. Normally those most distinct are (1) in the biceps and supinator longus, obtained by a tap at the wrist, especially on the radius, to which the biceps tendon is attached; and (2) in the triceps, by a tap on its tendon above the olecranon. When excessive, and there is persis- tent contraction in the flexors of the fingers, a similar contraction can be obtained in them, or in the supinators, and even a clonus, by maintain- ing the increased tension. With the increased excitabihty of disease, a contraction can easily be obtained in the masseters by tapping the chin when the jaw is depressed, and a clonus may occasionally be produced in these muscles, and even in the trapezius. When a tendon is tapped, and its muscle contracts, the occurrence has so much the aspect of a true reflex action that it was generally assumed to be such, the stimulus being the excitation of nerves in the tendon. This view received apparent confirmation by the discovery of certain facts. (1) That there are nerves in tendon. (2) That these phenomena depend for their occurrence on the integrity of the reflex path to, through, and from the spinal cord, and are arrested by a lesion in this path. By experiments on animals (in whom similar contractions may be obtained) it has been found that they are pre- vented by division of the nerves to the muscles, by division of either the anterior or posterior roots of the spinal nerves, or by destruction of the spinal cord.f These experimental facts are abundantly confirmed by those of * Other illustrations will be found in the writer's paper (' Med.-Chir. Trans.,' 1879), " The so-called Tendon-reflex Phenomena." Since then tracings have been published by Charcot and many others. t See Tschirjew, 'Archiv fur Psychiatric' Bd. viii, Heft 3, 1878, and many subsequent investigations, among which the most important are those of Waller (« Journ. of Phys.,' 1896) and Sherrington (' Proc. Roy. Soc.,' 1893). They do not involve practical questions, such as to make their description needful here. 24 SYMPTOMS. disease, conspicuously in peripheral neuritis. They unquestionably show that some reflex action is essential; but (as Westphal main- tained from the first) they do not prove that the contractions depend on a simple reflex action. From the fact that the contraction is caused by a tap on the tendon, the conclusion that the contraction was a simple reflex effect of the stimulation of its nerves seemed obvious, so the name " tendon-reflex" was given by Erb, and its simplicity and correspondence with the conspicuous facts made it at once current, and it has remained so. Yet the theory it embodied is not only erroneous, but it obscures the general relations of these phenomena, which are of great importance for the comprehension of the symptoms of disease. Hence it is necessary to explain the evidence in some detail, and the facts show, usefully, that that which is "obvious" may, as the origin of the word suggests, be a cause of stumbling. (1) The contractions occur equally when the connections of the tendon and all its nerves have been divided. (2) They occur only when the muscle is in a state of slight passive tension, and the tap on the tendon can increase this. With a relaxed muscle, a pinch of the tendon produces only a wide reflex action, like that from a pinch of the skin; indeed, this follows a pinch that can be felt when the muscle is tense. Definite stimulation of the nerves of the tendon never acts on its muscle only. (3) Not only must the tap increase the tension, but (as we have seen when these phenomena are excessive) any similar sudden increase has the same effect, e. g. a tap on the bone to which the tendon is attached. That on the depressed patella (p. 22), has the same effect as a tap on the tendon below. When there is extreme excess, the readiness with which a tap on the bone is effective has led to the idea that the stimulus is from the periosteum, but the tap is only effective when it can act mechanically on the muscle. It must be on the bone to which the muscle is attached, and in the direction to increase its tension. The evidence is conclusive that the contractions are not excited by stimulation of the nerves of the tendon; the stimulus originates in the muscle, the tendon being only a means by which that stimulation is produced. If so, is not the contraction itself a reflex effect ? It was suggested by two of the earliest investigators, Tschirjew and Westphal, that the contraction is local in production, due to the influence of the stimulus on the whole of the muscular fibres when they are rendered specially excitable by the reflex influence of the tension acting through the spinal cord. A reflex action takes a certain time, which is needed for the impulse to travel to and from the cord, and for the reflex process to occur in the centre. According to received physiological data, an interval of at least one fifteenth of a second would be needed for the knee-jerk if it were a reflex process, and rather more for the movement at the ankle I have found that when the Achilles tendon or the front of the leg is REFLEX. 25 tapped, the resulting contraction occurs in about -033 sec* The interval for the knee-jerk has been found by most to be about -04 or -033 or 022 sec.f Grotch found it to be -025 sec, and that between the tap on the tendon and a true reflex contraction of the opposite quadriceps to be Tl sec.J But it is certain that some reflex process is concerned in the pheno- mena. We have still to account for the irritability which permits the local stimulus to cause a contraction. This irritability is developed by passive tension. If the muscle is relaxed, the fibres may contract if they are struck directly, just as do the fibres of a separated frog's muscle, but no contraction can be produced by striking the tendon. Hence we must assume that the tension excites, by a reflex influence, a state of irritability to local mechanical stimulation,—such as that of a tap on the muscle, on its tendon, or even the vibration from a tap on the bone or on adjacent parts. But only that form of mechanical stimulation is effective which suddenly increases the previous tension. It is only because the tap on the tendon does this so readily that the tendon is the means by which the contractions are most easily pro- duced, and through which they have been chiefly studied and pre- maturely named. If the tension put on a muscle is gentle and gradual, it may only develop the irritability, and an additional local stimulation is necessary to produce a visible contraction. If, however, the tension is sudden and forcible, it not only develops the irritability, but pro- duces visible contraction in the muscle thus rendered irritable—as in setting up the foot-clonus. I have shown that the relaxation of the muscle, between the successive contractions, is not complete: there is persistent residual contraction, i. e. a tonic contraction on which the clonic contractions occur. When one clonic contraction is over, the tension continuing, a second is instantly developed. The production of the clonus seems thus to depend on the limited dura- tion of single muscular contractions (such as are obtained by a single induction shock§), the effect of sudden tension being exerted on all the fibres of a muscle at the same time. In the state of excitability produced by the moderate tension its effect on the relaxing fibres is * ' Med.-Chir. Trans.,' 1879, p. 292. An erroneous distinction between the nature of the knee-jerk and foot-clonus was made in this paper. t -039 sec, Burckhardt; -032—*034 sec, Tschirjew ; *04 sec, Brissaud ; -03—-04 sec, Waller; *03 sec, Eulenberg. Some of my own measurements ('Med.-Chir. Trans.,' 1S79, p. 275) gave a longer interval when the movement of the foot was taken as the indication of the commencing contraction. "Load" will increase greatly the period of latent stimulation, probably by causing the initial contraction to expend itself on the elasticity of the muscle. The measurements given above were obtained by recording the commencing contraction of the muscle. t * Journ. of Phys.,' 1896, vol. xx, p. 322. In the rabbit he found the interval for the tendon-contraction to be only -005 sec, and compares this with Tigerstedt's measurement of the interval when the nerve is stimulated (-01 sec, twice as great), and concludes that the contraction can only be direct. § See Foster's ' Physiology,' 1888, pt. i, p. 78. 26 SYMPTOMS. that of a fresh stimulus, and they contract again. We have no facts to suggest that such serial contractions could each be produced through a reflex mechanism. We have seen that the afferent nerves of muscles are especially excited by tension (see p. 17). If there were reason to regard each contraction as reflex we should have to regard these nerves as the seat of the excitation. The facts on all relations are better explained, and some pathological facts are only explained, by the assumption that the tension causes by reflex action this irritability. It seems, therefore, that the term "tendon-reflex" is altogether inaccurate. The phenomena are, according to the explanation above given, dependent on a " muscle-reflex " irritability, which has nothing to do with the tendons. If each contraction is reflex, it must be generated by an afferent impulse from the muscle-nerves, not from the tendon-nerves. This fact seems conclusive and inevitable. Hence if we wish to describe them by a general term, it is best to employ one which does not involve any special theory of their nature. They have been termed "tendon-muscular phenomena," but the intervention of tendons is not necessary for their production; the one condition which all have in common is that passive tension is essential for their occur- rence, and I have suggested* that they be termed myotatic contractions (rondos, extended). The irritability on which they depend is due to and demonstrative of a muscle-reflex action which depends on the spinal cord. It is highly probable, as Tschirjew suggested, that the condition on which the myotatic irritability depends is identical with muscular "tone." Since the experiments of Heidenhain it has been generally admitted that "tone" depends on tension, and is a reflex process.! A true "tendon-reflex" may be excited by pinching the tendon, but this is a start of the whole limb, precisely such as results from a pinch of the skin. It is an instance of the pain-reflex described above. The importance of discarding the tendon-reflex theory (and therefore the name) is great, for it prevents the comprehension of the true nature of other phenomena of great importance. Chloroform first increases and then abohshes the irritability; in ether narcosis (except when extremely deep) it is increased: % asphyxia has a similar effect, at first increasing, then abolishing, while oxygen simply augments the excita- * ' Diagnosis of Diseases of the Spinal Cord,' 2nd edit., 1881, p. 29. t By some interesting researches recently published, Mommsen has reached the same conclusion, that muscular tone is dependent on a muscle-reflex action excited by tension acting on the sensory muscle-nerves (' Virchow's Archiv,' Bd. ex, p. 22). The view given above has been recently advocated by Gotch as the result of his experiments ('Journ. of Physiology,'1896), and is indeed now generally accepted by physiologists. % ' Diagnosis of Diseases of the Spinal Cord,' 1883, p. 31; observations by Horsley. REFLEX, 27 bility.* The relation of these contractions to the nerve-centres will be considered in connection with these. Paradoxical Muscular Contraction.—This name has been given by Westphal f to a slow tonic contraction occurring in a muscle when its attachments are suddenly brought nearer in some morbid states. It is best seen in the tibialis anticus; if the foot is grasped, and passively flexed on the leg, the tibialis anticus contracts, sometimes after an appreciable interval; its tendon stands out, and the contraction keeps the foot flexed for a time, which may be some minutes (in one case for twenty-seven) : the relaxation is slow. Repetition lessens the con- traction. The contraction is not voluntary (although a voluntarv contraction may simulate it). It may occur on one side only. The contraction produced by brief f aradism may be similarly prolonged in the same case. A similar contraction may be observed in the extensors of the toes, sometimes in the flexors of the knee, rarely in the arm muscles. It seems to be an excessive manifestation of a physiological relation by which suddenly diminished tension increases as increased tension lessens the activity of the motor centres. Tension stimulates the afferent nerves, and the relaxation of the opponents of a contracting muscle during movement seems to be thus produced, as is made probable by the absence of descent of the upper lid in palsy of the inferior rectus.| Sherrington has shown that if the nerve to a muscle is cut and its central end stimulated the opponents relax.§ Con- versely we can understand that diminished tension may induce over- action. It seems to be an excess of the contraction by which a muscle adapts itself to passive shortening of its course. In the cases that have presented, this phenomenon there has been no muscular rigidity, and no great excess (even sometimes a loss) of the myotatic irritability. It may occur in the early stage of tabes, and in some other affections, but its significance is not known. A phenomenon somewhat similar occurs in hvsteria (Fere) ; it seems, indeed but an isolated and imper- fect instance of the condition that, when universal and perfect, consti- tutes the flexi/Alitas cerea of catalepsy, i. e. an unrestrained spinal reflex process in the centres concerned in the states of the muscles. Changes in Nutrition.—The nutrition of all the tissue elements is largely under the influence of the nervous system. Whether this influence is exerted through special "trophic" nerves, or through the motor, the sensory, and especially through the vaso-motor nerves, is a question that has been much discussed in the past. The balance of evidence is against the existence of special trophic nerves or centres. The fact reo-arding these changes that is clearest and most important is * Risien Russell (' Proc. Roy. Soc.,' vol. liii, p. 430). t 'Arch. f. Psych.,' Bd. x, p. 243. J See the Author,' Med.-Chir. Trans.,' 1879. § «Brit. Med. Journ.,' 1893. 28 SYMPTOMS. that acute disturbance of nutrition is the result of irritative changes in the nutrition of the nerves, and is in proportion to the intensity of that irritation. If a thread is passed through each sciatic nerre, and one is also irritated by the application, from time to time, of irritant liquids, trophic changes occur in that limb with greater rapidity and far greater intensity than in the other (Lewaschew). The same fact is frequently indicated by the extreme readiness with which trophic lesions of the skin, and even cellular tissue, occur in certain forms of inflammation of the spinal cord, especially in those that have a strong tendency to spread in the cord, and to the nerves, if they reach the centres of them. The only apparent explanation of the various facts is that the nerve-endings are related to the tissues in such a way that the nutrition of the molecules of the tissues is determined in its character by that of the nerves. The process of irritation descends the nerves ; it passes from them to the tissues, and extends to all that are in continuity. Thus we can understand equally the acute changes in the muscles, which will be described as resulting from disease of the motor nerves, and also those in the skin and othei tissues that are under the influence of the sensory fibres. Nutritive changes in the shin are easily recognised, but they diffei much in their character according to their acuteness. When they are rapid, and due to very acute irritation of the nerves or the spinal cord, such as those just mentioned, the temperature of the limb is raised, the vessels readily dilate, and remain dilated for a long time, bullae form, containing a dark-coloured liquid, and slight pressure occasions a slough. These changes sometimes seem to occur spontaneously, but are more often excited by some cutaneous irritation, and very slight irri- tation of the skin will suffice to produce them. Trifling pressure will set up a slough, and extensive vesication may result from the applica- tion of a hot-water bottle that is not more than pleasantly warm to a healthy hand. When the nerve irritation is intense, effusion may occur into the joints. In the case of the fifth nerve, acute trophic changes occur in the eyeball, chiefly when the disease involves the G-asserian ganglion, or the nerve in front of it. To produce the same effect, a lesion behind the ganglion has to be more irritating than one in front of it, and a similar relation obtains in the case of the spinal nerves and the spinal ganglia. The cells of the ganglia govern the nutrition of their processes in each direction, i. e. of the whole neuron, and we can understand that they have some power of hindering the propagation of irritative changes, while, if these invade the ganglion, they pass thence with special energy. Very intense changes in nutrition may thus pass to the skin in acute inflammation of the spinal cord. The alterations in nutrition in chronic lesions (which have been carefully studied by Paget and Weir Mitchell) differ considerably from those that result from acute irritation. There is a slow chano-e in the nutrition of the skin, which becomes red, thin, and shiny—the " glossy REFLEX. 29 skin" of Paget. The subcutaneous tissue also wastes, so that the finger tips become pointed. The growth of the hair and nails is altered, and the latter become brittle. The bones may suffer in their nutrition, and may break more easily than in health. If the lesion occurs during the period of growth, this is retarded.* These changes seem to depend on slower change in the nutrition and vitality of the tissue elements corresponding to a slower change in that of the nerves, an atrophy rather than a degeneration, f The muscles suffer from lesions of the motor nerves ; the minute changes are described with the latter. At first there may be merely flabbiness, and an appearance of wasting that is not confirmed by measurement, but there is soon an actual diminution in the circum- ference of the limb. In extreme cases all the muscular tissue dis- appears, and the contour of the limb is considerably changed. In comparing the size of the limbs on the two sides it should be remembered that the limbs on the right side are normally some- what larger than those on the left side, and that the difference varies according to the occupation of the individual, and the degree in which this involves a greater use of the limbs on one side. In measuring, great care is necessary to secure, as nearly as pos- sible, the same conditions on each side, both as regards the state of the muscles and the place of measurement. It is best, wherever possible, to take the maximum measurement in each part, rather than to attempt to make the measurement in the same place. In the calf the maximum circumference should always be taken. In the thigh accurate measurement is extremely difficult, because a maximum cannot be taken. We may endeavour to measure at the same point in the thigh at the same distance from the condyles, but it is very diffi- cult to be exact, and a more accurate comparison can often be made by taking the minimum circumference above the knee, in spite of the fact that the muscular tissue there is small, and the difference less than it is elsewhere. In the forearm the best result is obtained by taking the maximum measurement around the muscular prominence below the elbow, over the supinator longus. In the upper arm, the circum- ference is nearly the same in the middle third, and the measure- ment may be made halfway with httle risk of error. In all cases care must be taken to draw the tape equally tight at each place. It is easier to do this with a flexible steel measure than with an ordinary tape measure. Exactness is best secured by having a spring at one extremity of the tape with an index that will show the tension. Electrical Irritability— The nerves and muscles are excitable by electricity, and the excitabihty is changed by disease, of which the » But the subject of hindrance to growth is complex, and still not clear. See the account of infantile paralysis. t Cf. Marinesco on degeneration and atrophy (" La Theorie des Neurones," «Presse Med.,' 1895). 30 SYMPTOMS. change is often an important symptom. It indicates the state of nutrition of the nerve-fibres and muscles, and from this we can often draw important inferences regarding the condition of the centres. In the normal state nerve-fibres are stimulated by either the induced or the voltaic current, the stimulation of the motor nerves being shown by contraction in the muscles supplied by them, that of the sensory nerves by the sensation that is caused. The contraction of the muscles is continuous when the faradic current is applied, but if the isolated shocks of which the current consists are separately passed, each causes a brief, momentary contraction. When the voltaic current is applied, contraction occurs, with a current of moderate strength, only when the strength of the current is changed, and chiefly when the current commences or ceases to pass, i. e. when the circuit is "made" or "broken." The stimulation of the sensory nerves is greatest at those times, but occurs also, in a slighter degree, during the whole time that the voltaic current is passing. Hence this is probably the case also in the motor nerves, although the stimulation is too feeble to produce a contraction in health with a strength of current that can be borne. In proportion as the nutrition of the nerve-fibres is impaired, their excitabihty is lowered, and a stronger current of each kind is required to excite them and cause contraction in the muscles they supply. When their nutrition is much impaired—i. e. when the fibres are "degenerated"—no contraction can be obtained even with the strongest currents. The changes in the excitability of the muscles are less simple, because in them there are two excitable structures—the terminal branches of the nerves, and the muscular fibres themselves. Of these the nerve- fibres are the more sensitive to faradism, and the faradic stimula- tion of a muscle, under normal circumstances, is by means of these motor nerve-endings. Thus we find that its excitabihty corresponds in degree to that of the motor nerve supplying it. The muscular fibres themselves are, even in the normal state, less sensitive to faradism than the nerve, apparently because they are incapable of ready response to a stimulus so very short in duration as are the shocks of which the faradic " current" consists. The proof of this consists in the fact that under the influence of curara, which removes the excitabihty of the terminations of the motor nerves, the muscle requires a stronger faradic current to stimulate it than in the normal state. But under the influence of curara, or when the nerve is degenerated, the slowly inter- rupted voltaic current stimulates the muscle as readily as in the normal state ; a contraction occurs when the circuit is completed or broken— slower than that which occurs when the nerve-fibres are intact, and due to the stimulation of the protoplasm of the muscular fibres them- selves. The fact that, under normal circumstances, the contraction which is caused by the voltaic current is as quick as that produced by the faradic shock, is ground for believing that, in health, the voltaic as well as the faradic current causes the muscle to contract by exciting REFLEX. 31 the motor nerve-endings. When the motor nerve is degenerated, and will not respond to faradic or voltaic stimulation, the apphcation of the former to the muscle ceases to cause contraction. Apparently, the nerve-degeneration is accompanied by changes in the nutrition of the muscular fibre, by which any power of response to faradism, which it \ ossessed in the normal state, is lost. But not only does the response to the voltaic current remain; it becomes more ready than in health, doubtless in consequence of nutritive changes just mentioned. More- over there may often be observed a change in the readiness of response to the two poles of the voltaic current—a "qualitative " change, as it is termed. In health, the first contraction to occur, on gradually increasing the strength of the current, is at the negative pole when the circuit is closed, and a stronger current is required before closure- contraction occurs at the positive pole. But, in the morbid state we are considering, closure-contraction may occur at the positive pole as readily as at the negative, or even more readily,—and contractions, when the circuit is broken, occur far more readily than in the normal state. This condition, then—faradic irritability lost, voltaic irritability increased and often changed in quality—is termed the " degenerative reaction," because it occurs when the nerve-fibres are degenerated; if we test them we shall find no response to any stimulus, voltaic or faradic. It thus indicates loss of excitabihty in the motor nerves within the muscles, or a change in their endings on the fibres, by which these cannot be excited, either by electricity or by nerve-impulses, in the fibres. It occurs when the latter has been produced by some toxic agent, or the fibres also are degenerated in consequence of their damage between the muscle and the ganglion cells of the cord of which they are part, or destruction of the cells. But the motor nerve-celis and fibres often undergo changes in nutrition of a much more chronic character. In this condition the excitability of the fibres is lessened gradually and slowly. The irrita- bility of the intra-muscular nerve-endings is lowered in the same degree as that of the nerve-trunks, and we have a similar diminution to both faradism and voltaism. The nutrition of the muscular fibres is slowly, gradually impaired; and when the nerve-fibres are much affected the muscular fibres are also. There is no stage in which the nerve-fibre excitability is lost, and the muscle-fibre excitabihty retained; hence there is no condition of lost faradic and increased voltaic excitabihty such as characterises the degenerative reaction just described. Excitabihty is changed to the one form of stimulus just as to the other. Between these two forms there are intermediate conditions. For instance, the nerves may present normal irritability, while in the muscle there is often increased voltaic excitability and a changed order of polar reaction. In these cases some nerve-fibres are degene- rated, and lead to the increased excitabihty of some muscular fibres. In both nerve and muscle the character of the reaction is manifested 32 SYMPTOMS. by the more excitable structures ; hence it is normal in the nerve and altered in the muscle—this has been termed by Erb the " middle form of degenerative reaction," It is more accurate to call it the " mixed form." Another common intermediate form is due to the degeneration of the nerves, although slow, being less slow than in the condition described above. Hence the nutrition of the muscular tissue and its excitability (by voltaism) persist longer than those of the nerves, and although lowered, are diminished less than the faradic excitability of the nerves at each stage. When the latter is lost, voltaism will still cause a shght contraction in the muscles, which may occur first at the anode instead of the cathode. Every gradation, moreover, is met with between this and the true reaction of degeneration. This will be intelligible on consideration. It depends chiefly on the rate at which the nerves degenerate. The lowered excitability of the nerves, due to degeneration, is often preceded by a slight increase of irritability, very transient when the degeneration is acute, of longer duration when the degeneration is of the slower variety j ust noticed. In some morbid states, again, in which the change of nutrition in the cells and fibres is extremely shght, an increase may alone be discovered. I have found such an increase, for instance, in diseases regarded as functional, as paralysis agitans and chorea, and it is an interesting proof of the molecular changes which underlie, or result from, so-called " functional " maladies. The various changes in irritability were formerly thought to indicate the existence, and various affection, of separate centres for the nutri- tion of the nerves and muscles, apart from, though acting through, the motor nerve-cells. Remembering that the fibres of the nerves and muscles suffer in different degrees, as above described, the phenomena may all be explained on the simpler principle stated, without the assumption of these special centres, of the existence of which there is, indeed, no evidence. Special trophic nerves and centres for muscular nutrition have quietly disappeared from physiology, and are now only matters of interest to the student of its history, and to those whose memories reach further than two decades. It is, however, important to remember that such alterations in nutrition and excitability as occur in the whole course of the motor fibres when the cells are affected (of which they are the prolonged processes) may have a different origin at the periphery. They are the same in "degenerative peripheral neuritis," which begins in the extremities of the fibres (where vital resistance is least in consequence of distance from the cell body), and extend for a variable distance upwards. But this condition is seldom, if ever, so slow as to permit the equal loss of nerve and muscle excitability met with in the central degenerations. MUSCLES OF UPPER LIMB. 33 THE MUSCLES: THEIR ACTION AND PARALYSIS. Disease of the motor nervous system is largely manifested by loss of muscular action. Individual muscles, as well as groups of muscles, are often separately affected. Hence it is desirable to consider the symptoms of the paralysis of the more important muscles, before we enter on the study of special diseases. The symptom of the palsy of any muscle is a loss of its normal action, and a knowledge of this action is essential for the comprehen- sion of those symptoms. The two must therefore be considered together. They are positive and negative aspects of the same facts. It may be well, at the same time, to mention the nerve by which each muscle is supplied, and also the spinal roots from which the fibres come. These cannot be ascertained by dissection. Of the several roots that join to form the cord of the plexus from which the nerves to two muscles come, fibres from all may pass into one nerve, and from only one or two of the roots into another. The facts have been learned from experiment and the effects of disease and injury. Their practical importance is great. The action of muscles is threefold. (1) By their tonic contraction they maintain the parts in a certain posture, independently of volun- tary effort. By actual contraction they (2) produce certain move- ments, and also (3) oppose the action of other muscles by a feebler contraction, and thus steady the movement that results. The complex way in which muscles act together, and modify each other's effect, renders the subject a very large one. Here only an outline can be given of the more salient facts concerning the most important muscles. The reader who desires to pursue the subject further can do so in the ' Physiologie des Mouvements' of Duchenne, whose investigations by means of faradism and his observations on disease were so careful and so extensive as to leave little but confirmation to subsequent workers. In the following account the nerve that gives the branch to the muscle is first given, and then the number of the nerve-root or roots— (C)ervical, (D)orsal, or (L)umbar—from which the nerve-fibres come. Special Thoracic Muscles. The Diaphragm (C. 4 chiefly, phrenic nerves), although a double muscle with two nerves, habitually acts as a whole, the two halves contracting simultaneously and diminishing each lateral curve of the arch. The central tendon descends but little. The abdominal viscera are depressed, and the parietes protruded. If the hand is placed beneath the ribs, the descent of the viscera beneath the diaphragm can be felt. When the diaphragm contracts alone, as when the intercostals are paralysed, or the phrenic nerve is faradised, the ribs to which VOL. I. 3 34 ACTION AND PARALYSIS OF MUSCLES. the muscle is attached are slightly raised during its action, and this elevation causes a slight expansion of the thorax. In ordinary breathing this expansion is lost in the action of the intercostals. In paralysis the inspiratory protrusion of the upper part of the abdomen is lost; it even recedes during inspiration instead of advancing, and a descent of the viscera can no longer be felt by the hand. There often results an alternation in the respiratory movements of the thorax and abdomen, retraction of the one corresponding to protrusion of the other. Steeno-mastoid (spinal accessory nerve C. 2 —5 or 6, also branches from upper cervical plexus), passing from the sternum and adjacent part of the clavicle to the mastoid process, inclines the head towards, and rotates the face from, the side on which the muscle contracts. Both muscles together support the head in the vertical position, and if it is bent back, they bring it forwards into, but not beyond this position. Paralysis of one muscle has no influence on the position of the head, and but little on its movements. Other muscles supplement the loss. There is no such thing as a "paralytic torticollis." In palsy of both muscles the head can be balanced in the vertical position, but if it falls back it can be brought forward only with great difficulty. Each sterno-mastoid is associated in action with the muscles of the other side; it is a " contra-lateral muscle." For instance, in using the right arm, the head is turned to the right by the left sterno-mastoid. This association is sometimes reproduced in disease. Muscles moving the Upper Limbs. Muscles moving the Scapula and Shouldek-joint.—The Trapezius spinal accessory (C. 2 to 6, whether also the lowest C. and upper D. is doubtful)* consists of three parts. The first, from the occipital bone to the outer end of the clavicle, is rarely used except in breathing (respiratory portion—Duchenne). Fig. 5.—Paralysis and wasting of tra- FiG. 6.—Ditto when the arms are pezius; alteration in contour of raised (the right one being aided shoulder at rest. by another person). The second part is that which passes from the lig. nuchse, lowest cervical, and upper three dorsal spines, downwards and outwards to the acromion and outer * Anatomists now believe that the twigs from these nerves only pass through the muscle, and that it is wholly supplied by the spinal accessory. This agrees with the fact that its action is chiefly with the arm. MUSCLES OF UPPER LIMB. 35 part of the spine of the scapula. The lowest part passes from the dorsal spines below the third, outwards and partly upwards, to the inner half and base of the spine of the scapula. The second part is the chief elevator of the scapula and shoulder. With the third part it brings the scapula towards the spine, and puts the shoulder back. Both parts tend to rotate the scapula—acromion up, lower angle out. By this rotation the arm is carried above the horizontal level to which the deltoid raises it. Paralysis of the highest part has little influence on the movement of the scapula, but causes a change in the contour of the neck (Fig. 5) especially conspicuous on deep inspiration. The change in the shape of the neck is very great, when the arms are raised, if the whole trapezius is wasted (Fig. 6). In palsy of the middle part the elevation of the shoulder is imperfect; in that of the third part the scapula is farther from the spine than normal. In palsy of all parts the scapula becomes rotated (acromion down, inferior angle in) by the weight of the arm and the contraction of the opponents (Fig. 7). The rotation may mask the displacement outwards, due to the paralysis of the lowest part. If the clavicular part remains, there may be no rotation, but the scapula is lower than normal. The Rhomboids (a nerve that passes through the scalenus—C. 4 and 5) first rotate the scapula on the outer angle, moving the lower angle inwards, and then move the whole scapula upwards and inwards. In strong elevation they aid the trapezius, which prevents the rotation of the scapula. The rotatory action aids forcible depression of the raised arm. The muscles also fix the scapula for the action of the teres major. Their tone helps to keep the scapula against the thorax (opposing the pectoralis) and in its vertical position (opposing the serratus), and hence, in paralysis, the edge of the scapula, at rest, stands out a little, leaving a furrow, and the scapula is slightly rotated (lower angle out). Movement is but little interfered with by the paralysis of the rhomboids; but the movement backwards of the raised arm by the teres and deltoid is feeble for want of the fixation of the scapula. The Levator angidi scapulse (direct branches from C. 3 and4or 5) first rotates the scapula on the outer angle and then raises it. The muscle is usually paralysed with the trapezius, and then the scapula falls, but the special effect of its palsy is lost in that of the trapezius. If the levator is preserved, and the trapezius paralysed, there is great rotation of the scapula, which is, as it were, suspended by its inner angle (Fig. 7). Serratus magnus (posterior thoracic nerve—C. 5 and 6) carries the scapula outwards, forwards, and slightly upwards when the arm is put forwards. It tends to rotate the scapula on the inner angle (acromion up), the lower fibres most powerfully, but this rotation is prevented by the rhomboids and levator anguli. It does not raise the shoulder when the arm is hanging. It helps to fix* the scapula when the posterior fibres of the deltoid move the raised arm back. If the scapula is fixed by the rhomboids, the serratus can act on the ribs,'and aid forced inspiration. It has most inspiratory effect when the arms are elevated. In paralysis there may be little change in the position of the Fig. 7. — Paralysis and wasting of deltoid and trapezius j rotation of scapula, from weight of arm, in consequence of the paralysis of the tra- pezius; progressive mus- cular atrophy. 36 ACTION AND PARALYSIS OF MUSCLES. scapula at rest, but often there is slight rotation (lower angle in) from the unopposed tone of the rhomboids. When the arm is moved forwards by the anterior part of the deltoid, the scapula, no longer held against the thorax and moved forwards by the serratus, is rotated on its vertical axis by the action of the anterior part of the deltoid on the humerus, and of the middle part on the scapula. Thus the posterior edge recedes from the thorax, leaving a groove into which the hand can sometimes be placed (Fig. 8). The scapula is at the same time rotated, lower angle inwards and upwards. Elevation of the arm above the level of the shoulder is much weakened, but can be imperfectly effected by the middle part of the trapezius. Loss of the serratus weakens other movements, but does not abolish any. Inspiratory expansion of the thorax, when the arms are raised, is distinctly less on the paralysed side (Poore). Fig. 8.—Paralysis of the serratus magnus; FiG. 9. —Paralysis of right deltoid; ele- eversion and rotation of scapula when vation of shoulder by trapezius on an the arm is put forwards. attempt to raise the arm, which is slightly abducted by the supraspinatus. The Deltoid (circumflex nerve, from the brachial plexus posterior cord—C. 4 and 5) abducts the humerus, the anterior and posterior fibres also moving the arm forwards and backwards respectively. The arm is raised least by the posterior, and most by the anterior fibres, but even the latter only elevate it to a right angle with the trunk. Hence, if raised by the anterior fibres, and then moved back by the posterior, it is at the same time depressed. Elevation above a right angle is by rotation of the scapula (trapezius and serratus). These muscles also fix the scapula for the deltoid, preventing the rotation (acromion down, lower angle in) that the deltoid acting alone would cause. In paralysis, abduction of the arm, direct, forwards, and backwards, is almost lost. All the abduction that remains is a trifling movement by the supraspinatus. Au attempt to abduct results in rotation of the scapula and elevation of the shoulder (Fig. 9) from an excessive innervation of the associated trapezius and serratus, which, as we have seen, fix the scapula when the deltoid acts. Para- lysis of single parts of the deltoid causes loss of the corresponding movements of the arm, but if the middle part only is paralysed, there is still a limited MUSCLES OF UPPER LIMB. 37 power of direct abduction by the conjoined contraction of the anterior and posterior parts, aided by the supraspinatus. The Supraspinatus (suprascapular nerve—C. 4 and 5) abducts the arm, moves it forwards, and rotates it in. It thus aids the d 'ltoid. Isolated para- lysis of the supraspinatus has little influence on movement or position ; but if the deltoid is also paralysed, the head of the humerus falls away from the acromion far more than when the deltoid is paralysed alone. The Infraspinatus (suprascapular nerve—C. 4 and 5) rotates the humerus outwards, and in paralysis this movement is lost. A difficulty in writing is produced, the movement along the line being by this rotation of the humerus. The Teres minor (circumflex nerve—C. 5) has a similar action to the infra- spinatus, and its palsy has a similar effect. The Subscapulars (short subscapular nerve, from the fifth and sixth cervical) rotates the humerus in, and its paralysis lessens this movement. The Latissimus dorsi (long subscapular nerve, from the brachial plexus, posterior cord—C. 7) lowers the raised arm, and puts it back; the upper part adducts the scapula, the lower depresses the shoulder by acting on the humerus, which it tends to drag out of the socket. It inclines the trunk a little, and both muscles together extend the trunk. In paralysis, forcible backward depression of the raised arm is lost, and the shoulder cannot be put back without being also raised (by the trapezius). The Pectoralis major (anterior thoracic nerves from the brachial plexus, outer and inner cords—C.5, 6, and 7) consists of two muscles, the action of the clavicular and sternal parts being different. The clavicular (which arises also from the highest part of the sternum), if the arm is hanging, brings the shoulder forwards and upwards, as if shivering; if the arm is raised, it is brought forwards and lowered to the horizontal position. The muscle is thus concerned, Duchenne says, in the " cut " of the swordsman and the benediction of the priest. The sternal portion lowers the raised arm from every position, and if the arm is hanging, it draws the shoulder down. Paralysis of the upper part has little effect on the movement of the arm, because the anterior fibres of the deltoid have the same action. It is easily recognised by making the patient put his arms in front of him and press the palms together. In paralysis of the lower part, even with the latissimus, the raised arm can still be lowered accu- rately by the weight of the arm and relaxation of the elevators, but it cannot be lowered against even a slight resistance. Thus a blacksmith with this defect could wield a heavy hammer, but could not blow the bellows by pulling down- wards a cord (Duchenne). The Teres major (short subscapular nerve from the brachial plexus posterior cord—C. 7) approximates the humerus and the outer edge of the scapula, by bringing the former to the side of the trunk, and rotating the latter. The simultaneous contraction of the levator anguli and rhomboids, fixing the inner angle, causes this rotation to raise the prominence of the shoulder. Hence, in a forcible elevation of the shouldei-, the arm is pressed against the side, the lower fibres of the latissimus and pectoralis major aiding the adduction. The teres cannot alone put the arm behind the trunk. In paralysis, the eleva- tion of the shoulder, with the arm against the side, is lost. Muscles moving the Foeeaem.—Triceps (musculo-spiral nerve—C. 6 and 7).—The long head has an action similar to the teres, but feebler. It contracts when the arm is forcibly lowered, and prevents the displacement downwards of the head of the humerus by the actual depressors, the latissimus and pectoralis. All parts extend the elbow, the long head with less force than the others, but its 38 ACTION AND PARALYSIS OF MUSCLES. action on the shoulder-joint, just mentioned, is important, because forcible depression of the raised arm is often associated with extension of the elbow. In paralysis of the triceps the elbow can only be extended by the weight of the fore- arm, and extension against gravitation is impossible. Thus a man with paralysis of the triceps cannot raise his hat in the customary manner. Flexion of the elbow is uncertain, on account of the loss of the antagonistic steadying force. The Brachialis anticus (musculo-cutaneous and musculo-spiral nerves) flexes Triceps (long head) — Triceps (inner head) Ulnar n. < Flex, carpi ulnar. Flex. dig. profund. Flex. dig. sub. (II & III) Flex, digit, sub. (l&IV) Ulnar n. Palm brev. Abd. minim, digit. Flex. min. dig. Oppon. min. dig. Lumbricales Deltoid (ant. half) Mus.-cut. n. Biceps Brach. ant. > Median n. Supinator long. Pronator teres Flexor carpi radialis Flex, digitor sublim. Flex. long, pollicis Median n. Adductor pollicis Opponens pollicis Flex. brev. pollicis Adductor pollicis Fig. 10.—Motor points for the arm, inner side (from Erb). The points at which the muscles and nerves can most effectively be stimulated. MUSCLES OF UPPER LIMB. 39 the elbow simply. Its rare isolated palsy has little effect, since it is supple- mented by the biceps and supinator longus. The Biceps (musculocutaneous nerve—C. 4, 5, and 6) supinates the forearm if it is pronated, and then flexes the elbow. In paralysis the flexion can still be effected, but the traction on the humerus causes pain at the shoulder, from the loss of the support of the long head of the biceps. The Supinator longus (musculo-spiral nerve—C. 4 and 5) places the forearm midway between pronation and supination, and then flexes the elbow. If it is paralysed there is a tendency for supination to accompany flexion (biceps) ; and if the brachialis anticus is also paralysed, the elbow can only be flexed when the forearm is supinated. If the three direct flexors of the elbow are paralysed, feeble flexion is still possible by the extensors of the wrist, which cross the elbow-joint, but only after the forearm has been pronated and the wrist over-extended. De'.toid (posterior half) Musc.-spiral n. Brachialis ant. Supinator longus Extensor radial, long. Kxteusor radial, brev. Extensor digit. < —----------f- Extensor indicis- Ext. os. met. pol. — Extensor pr. intern, pol.--- Dorsal interosse (1 and II) Triceps (long head) i- Triceps (outer head) Extensor carpi uln. Supinat. brev. Extens. minim, digiti Extensor indicis L Extens. long. poll. Abduct, minim, digiti "1 Dorsal interossei } (III and IV) FiG. 11.—Motor points for the arm, outer side (Erb). 40 ACTION AND PARALYSIS OF MUSCLES. The Supinator brevis (musculo-spiral nerve by posterior interosseous branch — C. 5) is the only simple supinator. If it is paratysed, supination can still be effected by the biceps, and also by the supinator longus as far as midway between pronation and supination. Pronators.—The^- teres and p. quadratus (median nerve—C. 6 and 7) both pronate strongly, and their palsy causes loss of this movement, but pronation to the mid-position is still possible by the supinator longus. Muscles moving the Hand.—Flexors of Wrist.—The F. carpi ulnaris (ulnar nerve) and F. carpi radialis (median—C. 7 and 8) flex the wrist. The ulnar flexor tends to turn the supinated hand still morn out, but neither moves the wrist-joint laterally. Flexion indeed hinders the lateral movements of the wrist, in consequence of the shape of the articular surfaces. The f. c. ulnaris flexes the fifth metacarpal bone on the carpus as well as the wrist-joint. In paralysis, flexion of the wrist can only be effected by the* flexors of the fingers when these are extended. Extension of the wrist is unsteady from the loss of the antergic contraction of the flexors (see p. 10). Extensors of Wrist.—Extensor carpi radialis brevis et longus ; E. c. ulnaris (musculo-spiral nerve and its posterior interosseous branch—C. 6 and 7). The short radial is a direct extensor; the long radial and the ulnar move the hand laterally as well. In para- lysis of all three extensors the wrist can only be extended by the extensors of the fingers when the phalanges are flexed. In loss of the short radial, direct extension is still possible by the long radial and ulnar, and lateral extension by one of these alone. If either is paralysed, together with the short radial, direct extension is lost, and only lateral extension, in the direction of the remaining muscle, is possible. Paralysis of either lateral extensor, long radial or ulnar, leads to permanent deviation of the wrist in the direction of the remaining muscle (Fig. 12). Fig. 12. — Paralysis of The loss of the long radial is more serious than the long radial ex- that of the ulnar, because the radial lateral move- tensor of the wrist in a ment is of more importance bein„ needed for the young child; habitual . ,. .' , , ° deviation of the hand convenient motion ot the hand to the mouth. Para- towards the ulnar side. lysis of the extensor impairs flexion of the fingers, (After Duchenne.) from the great shortening of the course of the ten- dons by the flexion of the wrist that occurs. The ulnar extensor acts also synergically with the extensor of the metacarpal bone of the thumb, as may be noted if the finger isplaced on the tendon beneath the styloid process of the ulna. Hence, in paralysis of this extensor, the hand deviates laterally when the thumb is strongly extended. Extensors of the Fingers.—Extensor communis digitorum; E. indicis • E. minimi digiti (musculo-spiral nerve—C. 6 and 7). The common extensor moves the fingers and then the wrist. When the muscle is faradised, the extension begins at the distal phalanges, and these become flexed again, when the hand is extended beyond the plane of the forearm, by the tonic force of the flexors, the course of their tendons being elongated by the extension of the wrist. Moreover the muscle has little action on the last two phalanges, since they cannot be extended by the long extensor, if the interossei, their proper extensors are paralysed. During extension by the communis the fingers are separated from the second. The extensors of the first and last fingers have a similar MUSCLES OF UPPER LIMB. 41 extensor action, but, in addition, they adduct their respective fingers towards the middle finger. In paralysis, the extension of the fingers is impossible ; but if the proximal phalanges are passively extended, the middle and distal joints can be extended by the interossei. For the lateral movements of the digits, exten- sion of the proximal phalanges is essential, and hence these movements are lost, but they can be performed if the proximal phalanges are passively extended. The posture of the fingers due to contraction of the palmar fascia resembles that in palsy of the long extensor (see Fig. 13), but an examination of the palm shows the cause of the flexion. Flexors of Fingers.—F. sublimis (median nerve—all fibres C. 7 and 8); F. profundus (median and ulnar nerves). These muscles flex chiefly the- second and third phalanges, the first phalanx being flexed by the interossei. The superficial muscle flexes the second phalanx on the first, the deep flexes both. The action on the first phalanx is con fined to extreme flexion of the fingers, and is the less, the more the wrist is flexed. But if the flexion of the middle and distal phalanges is prevented the first is strongly flexed. In extreme shortening of the course of the tendons by flexion of the wrist, the action on the fingers is very feeble, evidence of a normal antergic action of the extensors of the wrist. Fig. 13 Fig. 14. FiG. 13.—Posture of the hand in contraction of the palmar fascia, resembling that in paralysis of the long extensors of the finger. Fig. 14. — Paralysis of the fibres of the flexor sublimis which act on the two middle fingers: twelve years' duration. The second phalanges of these fingers are bent backwards and subluxated from the contracture of the unopposed interossei, while the last phalanges are kept in position by the unaffected flexor profundus. (After Duchenne.) When the extensor of the fingers is in strong action, extending the proximal phalanges, the action of the flexors on the second and third joints is very strong (tearing position). In paralysis of these muscles the power of flexing the last two joints is lost, but the interossei still flex the metacarpo-phalangeal joints. Paralysis of the deep flexor alone causes merely loss of the power of flexing the distal joint, but this impairs many movements, such as playing on the piano. In paralysis of these muscles, the unopposed tone of their opponents, the interossei, which extend these joints, leads in time to over-extension, and, with repeated passive pressure in using the fingers, may even produce a sub- luxation backwards. In palsy of the sublimis this effect is chiefly seen at the middle joint (Fig. 14), in that of the profundus at the distal joint. Interossei and Lumbricales (ulnar nerve, except the outer two lumbricales, which are supplied by the median—C. 8 and D. 1).—The interossei abduct and 42 ACTION AND PARALYSIS OF MUSCLES. adduct the fingers, but only when these are extended at the metacarpo- phalangeal joints, and some effort is required for adduction, since the tendency of the long extensor is to separate the fingers, and this influence has to be overcome. They also extend the second and third phalanges on the first, and flex the first on the metacarpal bones. The lumbricales aid the flexor-extensor action of the interossei, but do not move the fingers laterally. The opposite action of the forearm muscles and of the interosseous extensors and flexors is very important. Their synergic action steadies movements, and in many actions they contract alternately. Thus in making a down-stroke with a pen or pencil the long flexors bend the last two joints; while in making an up-stroke these are extended, and the metacarpo-phalangeal joint is flexed, by the interossei. In paralysis of these muscles the lateral movements are lost, but a slight abduction and adduction of the index can still be effected by its long extensors. Only the first phalanx can be extended, and flexion is almost confined to the last two phalanges. The first two lumbricales, being supplied by the median nerve, often escape when the other muscles are paralysed by an injury to the ulnar nerve, and they aid the others when these are merely weak; hence the index and middle fingers seem to recover before the others (Fig. 15). The position of Fig. 15. Fig. 16. Fig. 15.—Recent incomplete paralysis of the interossei from a punctured wound of the ulnar nerve at the wrist: attempt to extend fingers. The loss of extension of the last two phalanges is chiefly marked in the third and fourth fingers, from the influence of the lumbricales (supplied by the median) on the others. (After Duchenne.) Fio. 16.— Paralysis of the interossei (ulnar nerve) slight in degree: attitude of fingers at rest. the hand at rest becomes altered. Normally there is slight flexion at all joints by the tone of the muscles, interossei and long flexors. In paralysis the first phalanx is in a line with the metacarpal bones, while the other phalanges are flexed, the middle more than the distal (Fig. 16). In action this flexion is always increased, the metacarpo-phalangeal joints become over-extended, and the other joints strongly flexed (Fig. 17). Gradually the hand assumes this posture even at rest (Fig. 18), and ultimately the posture becomes warped into a deformity by the over-extension of the first phalanges, and extreme flexion of the others, due to the contracture of the long extensor and of the flexors; the tendons of these muscles stand out conspicuously on the back and in the palm, and a claw-like attitude is developed, the " main en griffe " (Figs. 19 and 20). Changes in the articulations may ultimately limit even passive movement. Muscles of the Thumb.—Extensor secundi internodii pollicis (musculo- spiral nerve, posterior interosseous branch —C. 8 and D. 1) extends both phalanges, and moves the whole thumb backwards and from the fingers, so as to bring it behind the plane of the metacarpus. It may ultimately extend the wrist-joint, but it never supinates. It is not used in extending the thumb when MUSCLES OF UPPER LIMB. 43 this is opposed to the first finger. In paralysis, the metacarpal bone of the thumb is slightly flexed on the carpus, and is inclined forwards. The second phalanx is flexed on the first, and can only be extended (by the abductor and outer part of the short flexor) when the metacarpal bone is adducted and the first phalanx is flexed. The constant flexion of the second phalanx interferes with the movement of the index finger, unless the patient remembers to move the thumb out of the way by the extensor of the metacarpal bone. Writing is not interfered with because the muscle is not concerned in extension with opposition. Fig. 17 Fig. 18. Fig. 17.—Attempt to unbutton waistcoat by the hand shown in the last figure; extreme flexion of the last two phalanges, and extension of the first, on the attempt to use the fingers. (From nature.) Fig. 18. —Old-standing palsy of interossei and thenar muscles, showing the Over-extension of the first and flexion of the last two phalanges. Fig. 19.—Paralysis of all the intrinsic muscles of the hand and of the long flexor of the thumb, in consequence of an injury to the brachial plexus in dis- location of the shoulder. The fingers present the claw-like attitude; the thumb is in extension. (After Duchenne.) Fig. 20.— Paralysis of the ulnar nerve from a wound at the wrist (indicated in the figure). Extreme claw-like hand from the unopposed contraction of the common extensor and long flexors of the fingers and thumb. (After Duchenne.) The Extensor primi internodii pollicis (musculo-spiral nerve, post-inteross. branch—C 8 and D. 1) is the true abductor of the thumb. It moves the metacarpal bone outwards, and extends the first phalanx. It would move the whole hand in the same direction as the thumb, were not this tendency counter- acted by the antergic contraction of the extensor carpi ulnaris (q. v.). It does notpronate or supinate. In paralysis abduction of the metacarpal bone is less than normal. There is an undue flexion of the first phalanx, and the meta- carpal bone is flexed on the carpus, so that the thumb is drawn towards the palm. The loss of this muscle is, however, compensated to a considerable extent by other muscles. 44 ACTION AND PARALYSIS OF MUSCLES. The Extensor ossis metacarpi pollicis (musculo-spiral nerve, post-inteross. branch —C. 8 and D. 1) is really the long abductor of the thumb. It moves the metacarpal bone outwards and forwards, flexing it on the carpus, and then flexes the wrist with slight pronation. It thus moves the thumb as much forwards as outwards. In paralysis the metacarpal bone is, at rest, less inclined forwards than normal, and somewhat abducted, but the first phalanx is in its normal position. Movement of the thumb is but little interfered with. In combined palsy of the extensors of the first phalanx and of the metacarpal bone the thumb becomes adducted, and is parallel to the radius. The first phalanx is slightly flexed by the thenar muscles. The Thenar muscles constitute two groups: (1) The short abductor and outer portion of the short flexor (median nerve—0. 8 and D. 1) move the metacarpal bone forwards and inwards (flexing the first phalanx), incline it outwards, and rotate it inwards, so as to place its palmar aspect opposite the fingers. The second phalanx is ultimately extended. If the metacarpal bone is previously abducted the movement is greater, and amounts to circumduction. (2) The adductor and inner part of short flexor (ulnar nerve—0. 8 and D. 1) go to the inner side of the first phalanx. The metacarpal bone is moved towards that of the second finger: if previously flexed, it is extended; if pre- viously opposed to the index, it is moved a little outwards. The phalanges follow the movements of the metacarpal bone, but the first is slightly flexed and the second is extended, as the fingers are by the interossei. The Opponens pollicis (median nerve—C. 8 and D. 1) flexes the metacarpal bone on the carpus, and abducts it, but this movement is insufficient to oppose the thumb to the index; the conjoint action of the abductor is necessary (see above). Fig. 21. Fig. 22. Fig. 23. Fig. 21.—Normal position of the thumb (for comparison with the succeeding figures). Fig. 22.—Position of the hand in long-standing paralysis and wasting of the thenar muscles. Under the influence of the long extensor the metacarpal bone oi the thumb has been brought into the same position as the other metacarpal bones, being rotated slightly, so that the back of the thumb is in the plane of the back of the hand, like the hand of the ape. (After Duchenne.) Fig. 23, from another case, shows the same condition, but still greater dis- placement of the metacarpal bone has taken place, from the greater contraction of the extensor. (After Duchenne.) The Flexor longus pollicis (median nerve—C. 7 and 8, and D. 1) flexes the second phalanx forcibly and the first feebly. It has no action on the metacarpal bone. It is used in writing (making a stroke towai'ds the body) and in picking up a small object, &c. In paralysis this flexion is lost, and with it these actions; if an object is held between the tips of the thumb and forefinger, the last MUSCLES OF LOWER LIMB. 45 phalanx of the thumb is bent back. Other movements of the thumb are not interfered with. If all the thenar muscles are paralysed the metacarpal bone is in the plane of the index, and drawn towards it by the extensor of the second phalanx, which moves the metacarpal bone inwards and backwards. The whole thumb corre- sponds with the metacarpal bone in position, the phalanges being normal. In paralysis of the short abductor and flexor the second phalanx cannot be extended unless the metacarpal bone is abducted. These short muscles normally prevent the abduction that the extensor of the second phalanx tends to produce. The latter, moreover, prevents undue adduction when the special abductors are paralysed, but brings the metacarpal bone into the plane of the index. Thus the posture of the hand at rest resembles that of the hand of an ape (Figs. 21 and 22). If the abductor and opponens are paralysed, the tips of the thumb and fingers can only be brought together by flexing the last phalanges of the digits (Fig. 24). Then the thumb can be brought into contact with the finger by means of the short flexor, which inclines the metacarpal bone sufficiently to effect this, although not enough for the tip of the first finger to touch the thumb when its phalanges are extended. If the short flexor is paralysed, the thumb can still be opposed to the first two fingers by the abductor, but it cannot be opposed to the last two fingers on account of the defi- cient lateral inclination of the thumb, which should be produced by this muscle. Writing is easy by means of the short abductor, whereas if this is lost, although the thumb can be opposed to each of the fingers, writing is much interfered with. If all the thenar muscles are paralysed, a certain amount of opposition of the thumb and fingers is still possible, by means of the flexion of the last phalanges of the thumb and fingers. If all are paralysed except the adductor, objects can still be held between the thumb and side of the palm. Fig. 24.—Paralysis of the ab- ductor brevis and opponens pollicis. From the want of these muscles the thumb can only be brought in contact with the tip of the index by strong flexion of the last two phalanges of the fingers, other- wise the tip of the thumb only reaches the middle of the second phalanx. (After Duchenne.) Muscles of the Lower Limb. Muscles moving the Hip-joint.—The Gluteus maximus (inferior gluteal nerve, small sciatic, and a special branch from sacral plexus—L. 4 and 5, S. 1) extends the hip-joint, and freely rotates the thigh outwards. It is the most powerful extensor of the hip, and it is chiefly used when a forcible extension is required, and the joint has been previously flexed. It is employed, not in standing, or in walking on level ground, but in going upstairs, or uphill, and in rising from a seat When it is paralysed these movements are difficult. The Gluteus medius (gluteal nerve—L. 4 and 5, S. 1) is the chief abductor. All parts of the muscle have this action, but in addition the anterior third 46 ACTION AND PARALYSIS OF MUSCLES. moves the thigh forwards and rotates it inwards, while the posterior third moves it backwards and rotates outwards. The successive action of the several parts causes circumduction. The Gluteus minimus (gluteal nerve) has pro- bably the same action. In paralysis, abduction and circumduction are lost; in Crural n.--- ---i Obturator nJ~W~ Pectineus-yi—© Adductor mag.1—p Adductor long.- - I > Tensor vaginae femoris. 7" Sartorius. Quadriceps. Rectus femoris. Vastus extern. FiG. 25.—Motor points on the front of the thigh (Erb). standing on the other foot the pelvis is inclined on the affected side, and hence, in walking, there is an oscillation of the trunk, which becomes very con- siderable if the muscles of both sides are affected. Moreover the unopposed tone of the outward rotators produces a permanent rotation of the leg, so that the toes are directed outwards, and, from the altered position of the foot, the propulsion of the body in walking is deficient. The Pyriformis, Gemelli, Obturator internus, and Quadratus femoris (special nerves from the sacral plexus, but from L. 5) all rotate the thigh out- wards, and the first-named muscle, in addition, carries the thigh obliquely backwards and outwards, in the same way as the posterior fibres of the gluteus medius. In paralysis of these muscles external rotation is impossible, and the unopposed tone of the internal rotators (anterior fibres of the gluteus medius and minimus) causes the leg and foot to be habitually turned inwards. The Psoas (special lumbar nerve, L. 2 and 3) and Iliacus (anterior crural nerve L. 2 and 3) flex the hip-joint, and, in doing so, cause also a slight rotation outwards. In paralysis, flexion is lost, and the use of the leg in walking becomes impossible. The Tensor vagina femoris has a slight power of flexing the hip, and at the same time rotates the thigh in. It normally counteracts the tendency of the MUSCLES OF LOWER LIMB. 47 ilio-psoas to rotate outwards. If it is paralysed, there is a tendency for the foot to turn out when it is being brought forward in the act of walking. Adductors of the Thigh (all are innervated from the same roots, L. 2 and 3). —The Pectineus (obturator nerve) causes an oblique movement forwards and inwards, i. e. a combined flexion and adduction, as in crossing the legs. It also rotates outwards. The Adductor longus, and probably the Adductor brevis (obturator nerve), have the same action, but the flexion is less than by the pectineus. The Adductor magnus (obturator and great sciatic) causes a similar adduction, but while its upper fibres rotate outwards its lower fibres rotate in, and are employed in keeping the foot straight during adduction in riding. This is very difficult if these fibres are paralysed. The foot then turns out when the hip is flexed, either in the recumbent posture or in walking, from the preponderance of rotation out by the other adductors. When all the adductors are paralysed, not only is adduction lost, but in flexion of the hip the foot is moved forwards and outwards, instead of directly forwards, showing that there is normally a synergic action of the abductors and adductors with the flexors in this movement. Muscles moving the Knee.—Extensors: Pectus, Vasti, and Crureus, together called the E. quadriceps (ant. crural nerve, L. 3 and 4).—The vasti act solely on the knee-joint; the rectus also aids in flexing the hip, but chiefly when the knee is bent. Inconsequence of its passage over the hip-joint, more- over, the force with which it extends the knee is increased by the simultaneous extension of the hip. This effect is useful in the propulsion forwards of the body in walking. The crureus is unimportant. In paralysis of the extensors of the knee, standing is still possible if the knee is extended, since the arrangement of the articulation renders a contraction of the extensors unnecessary. But secondary shortening of the flexors is apt to occur, and then standing becomes impossible because the knee cannot be perfectly extended. In the same way, walking is possible if the leg is not moved forward beyond the vertical position ; if it is, the knee becomes flexed by the weight of the leg and foot, and the patient falls when he attempts to rest upon it. Rising from the kneeling posture in the ordinary way is impossible. In partial paralysis of the muscles, as in pseudo-hypertrophic paralysis (q. v.), the exten- sion of the knee, in rising, is facilitated by placing the hand upon it, and so bringing the centre of gravity of the body near the fulcrum of the lever formed by the femur. If the vastus internus and rectus are paralysed, the vastus externus may dislocate the patella by the obliquity of its traction. The vastus internus never does so in the opposite condition, because its action is less oblique. Flexors of the Knee.—These are all supplied from the same spinal roots, although through various nerves—L. 4 and 5, S. 1.—The Sariorius (ant. crural nerve) flexes the hip- and knee-joints, and has a feeble power of rotating the thigh outwards and the knee inwards. It is a muscle of small importance. The Gracilis (obturator nerve) adducts the thigh more powerfully than it flexes the knee. It rotates the leg inwards. The Sendtendinosus, Biceps, and Semimembranosus (great sciatic nerve) are not only flexors of the knee but extensors of the hip-joint, and are the muscles that extend the hip during ordinary walking, the gluteus maximus (q. v.) being called into action only during special efforts. The leg is rotated inwards by the semitendinosus, outwards by the biceps. In paralysis of the flexors the resulting loss of the power of flexion interferes 48 ACTION AND PARALYSIS OF MUSCLES. with walking, since the knee-joint cannot be bent, in the forward movement of the le°-, until the thigh is flexed sufficiently to permit the weight of the foot to flex the knee. To prevent the toes striking the ground the foot is unduly flexed on the leg. The loss of the support that the flexor tendons give to the knee- joint leads to an undue strain on the ligaments, which become stretched, and slight retroflexion of the joint may occur. In paralysis of the muscles that extend the hip, there is a tendency to fall forwards in walking. To counteract this the trunk is carried backwards, and a fatiguing strain on the flexors of the hip results. In paralysis of the biceps, the leg, during flexion, is rotated inwards ; when the biceps remains and the other muscles are paralysed, there is an undue rota- tion outwards. The effect of these abnormal movements on the ligaments of Tibialis anticus--- Extensor digit. Peroneus brevis Extensor long. poll. Dorsal interosse Ext. poplit. n. \—Gastrocnem. (outer head). Peroneus longus. Soleus. Flexor long, pollicis. Extensor brev. digit. Abductor minim, digit. Fig. 26.—Motor points of leg, outer side (Erb). the joint is such that, after a time, the amount of rotation becomes greater than is possible in health. The Popliteus (internal popliteal nerve) has but a feeble power of flexing the knee. Its chief action is to rotate the leg inwards when the knee-joint has been flexed. Muscles moving the Foot.—Extensors of Foot on Leg*—The Gastro- cnemius and Soleus (internal popliteal branch of the sciatic—L. 5 and S. 1) * These muscles are sometimes termed " plantar flexors," because they are homo- logous with the flexors of the wrist. The term is a bad one, since it involves a use MUSCLES OF LOWER LIMB. 49 have the same action. They extend the hinder part of the foot and draw down the outer side of the forepart of the foot, but very little the inner side. Hence the foot is rotated, so that the dorsum looks outwards, while the whole foot is Sciatic n. Biceps (long head) Biceps (short head) Ext. poplit. n. Gastrocnem. (ext. head) Soleus Flexor long. poll. § \ Gluteus maximus. • Adductor magnus. ~"1 Semitendinosus. %~t---Semimembranosus. Int. poplit. n. Gastrocnem. (int. head). Soleus. Flexor digit, comm. Tibial n. FiG. 27.—Motor points, back of thigh and leg (Erb). turned inwards on the axis of the leg. The peculiar inversion and adduction that thus accompanies extension is due to the form of the articular surfaces. The gastrocnemius has very little power of flexing the knee, but the extension of the word "flexor" in absolute contradiction to its proper signification. We ought not to frame a descriptive term such as this on an analogy which involves a contradiction to the description. Flexion is bending, a movement from a straight line; and extension is less bending, a movement towards a straight (stretched, extended) line. To call a movement toward a straight line " flexiou," because in the arm the similar movement produces this effect, is a process that is not description, but the statement of an analogy—the worst possible kind of nomenclature. Names should be descriptive or they should be arbitrary. Neither theory, nor analogy, nor homology should have any part in them. What we call homology is merely a species of analogy; it rests on inference and reasoning, not on simple absolute aspect. Nothing that rests on reasoning is inherently stable and free from change. VOL. I. 4 50 ACTION AND PARALYSIS OF MUSCLES. of the knee increases the effect of the muscle on the ankle-joint, especially in walking, just as we have seen that the extension of the hip augments the force with which the contracting rectus extends the knee. For direct extension of the ankle, the peroneus concurs and opposes the inversion. The only difference between the gastrocnemius and soleus is that the latter, having no attachment to the femur, can extend the ankle when the knee is flexed as well as when it is extended. In paralysis of these muscles, extension of the ankle (by the peroneus longus and flexor longus digitorum) is extremely feeble, and the foot can scarcely be carried beyond a right angle. Walking is greatly interfered with; standing on tiptoe is impossible. The unopposed peroneus longus causes eversion of the foot, lowers the head of the first metatarsal bone, and deepens the plantar arch. In time the ankle-joint becomes over-flexed, the heel considerably lowered, and the plantar muscles and fascia become shortened. The resulting deformity is termed talipes calcaneus (Fig. 28). FiG. 28.—Talipes calcaneus from atrophic paralysis of the calf muscles, with flexion of the middle and distal phalanges of the toes, from paralysis of che interossei. The peroneus longus (musculo-cutaneous nerve, from external popliteal of sciatic—S. 1 and 2) everts the foot, lowering the inner border, narrowing the foot, and increasing the plantar arch. It also turns the whole foot out on the axis of the leg. It has a very feeble power of extending the ankle. It keeps down the inner part of the foot during extension by the calf muscles, as in walking. In paralysis of this muscle the inner part of the front foot is not supported during extension, and yields to slight force. The foot becomes adducted and rotated, so that the sole is directed inwards, in consequence of the unopposed action of the sural muscles. The inability to press the inner part of the ball of the foot firmly against the ground leads to over-action of the flexors of the great toe. The plantar arch is lessened ; there is " flat-foot." Flexors of the Foot.—(Both are supplied by the anterior tibial branch of the external popliteal nerve—L. 5 and S. 1.) The Tibialis anticus produces simul- taneously three movements: it elevates the inner part of the front foot (oppos- ing the peroneus longus) ; it flexes the ankle-joint, and adducts the foot. The Extensor longus digitorum, besides extending the toes, flexes and abducts the foot. The abduction is in consequence of the outward position of its tendons beneath the annular ligament. These two muscles together produce direct flexion of the foot, or flexion with adduction or abduction, as the force of one or the other preponderates. Paralysis of either weakens flexion, and the corre- sponding lateral movement is lost, flexion being accompanied by the deviation effected by the muscle that remains. The defect in flexion is greatest in para- lysis of the tibialis, and the loss of the instinctive flexion, when the leg MUSCLES OF LOWER LTMB. 51 is brought forward in walking, causes the foot to catch against the ground. Paralysis of the flexors is followed by secondary contracture of the extensors, PlG. 29.—Talipes equinus, due to atrophy of the tibialis anticus and secondary contracture of the calf muscles. In A the foot is shown at rest; there is slight equino-varus. In B it is shown during flexion, and the varus is changed to valgus by the action of the peroneus longus. Note the increased extension of the toes in b from the com- pensatory over-action of the long extensors of the toes. (After Duchenue.) and talipes equinus results (Fig. 29), which is the greater the longer the palsy has lasted (Fig. 30). Its occurrence is facilitated, in many cases of palsy, Fig. 30. Fig. 81. Flff. 30.—Extreme talipes eqninus from old-standing palsy of the tibialis anticus (infantile paralysis) and extreme contraction of the calf muscles. No flexor movement was possible. Fig. 31.—Paralysis of the interossei and the adductor and short flexor of the great toe. The first phalanges are over-extended and the second are flexed, while the hollow of the sole is increased. (After Duchenne.) by lessened growth of the bones of the leg, so that the ball of the foot only touches the ground when the foot is extended. There is usually slight rotation inwards of the foot at rest, even when the tibialis is paralysed (see Fig. 29, a), because such rotation is produced by the sural extensors (p. 42); but in this case the slight valgus at rest is changed to varus on an attempt to flex the ankle (Fig. 29, B). 52 ACTION AND PARALYSIS OF MUSCLES. The Peroneus brevis (musculo-cutaneous [peroneal] branch of ext. popliteal nerve—S. 1 and 2) abducts the foot and rotates it, raising the outer edge. The Tibialis posticus (posterior tibial nerve from int. pop.—L. 5 and S. 1) adducts the foot and curves it, rendering the outer border and instep more convex. Its power of adduction is greater than that of the tibialis anticus, and it does not rotate the foot in the same manner. These two muscles alone have the power of adducting and abducting without flexing or extending; and in their paralysis these simple movements are lost. I f one only is paralysed, a deformity develops corresponding to the action of the other muscle,—talipes valgus in paralysis of the tibialis posticus; t. varus in that of the pei'oneus brevis. The muscles moving the toes present, in their mode of action, a close corre- spondence to those of the fingers. The Extensor longus digitorum and the Extensor longus pollicis (anterior tibial nerve—L. 5 and S. 1) extend chiefly the first phalanges, while the Flexor longus digitorum and Flexor brevis (posterior tibial nerve—S. 1 and 2) flex the last two phalanges. The Lumbricales and the Interossei (post, tibial nerve by ext. and int. plantar—S. 1 and 2), together with the Abductor and Flexor brevis minimi digiti, oppose both the other extensor and flexor muscles, flexing the first phalanx and extending the others. This action is of great importance in walking, since they give the last propulsion to the body as the ball of the foot leaves the ground. The Abductor, Adductor, and Flexor brevis pollicis (plantar nerves from post, tibial—S. 1 and 2) have a similar action on the great toe, but with adduction or abduction respectively. The interossei also produce a lateral movement of the toes, but this action is of little practical importance. In paralysis of the common extensor of the toes, and of the proper extensor of the great toe, the tonic force of the interossei and analogous muscles produces persistent flexion of the first phalanges and extension of the others. If the conditions are reversed, and the latter muscles are paralysed, the first phalanges are over-extended, sometimes even subluxated, and the two other joints are flexed, so that a claw-like form of foot is the result (Figs. 31 and 28). The final propulsion in walking, above described, is much interfered with, and the attempt is painful because the ends of the toes are turned towards the ground. Other examples of the effects of paralysis of the muscles of the arm and leg are given in the illustrations to the chapter on Infantile Paralysis (Acute Polio-myelitis). 53 THE GENERAL CONSTITUTION OF THE NERVOUS SYSTEM.* Our conceptions of the elementary arrangement of the ner1 ous system have been changed during the last nine years by important histological discoveries, which clear many obscurities, give new signi- ficance to facts before imperfectly perceived, and involve new patho- logical conceptions, general and special. Although new difficulties have arisen, as they must do at each step forward, numerous facts, which before were mysterious, become intelligible, and their elucidation con- stitutes confirmation of the truth of the discoveries. The evidence has been received as adequate by all physiologists. Pathologists must therefore accept them, and reconstruct their conceptions. It is accordingly necessary to give an outline of the constitution of the cerebro-spinal nervous system as at present discerned, even of that which is not of direct present application to pathology, but which may become so and is essential for the perception of the whole. The facts have been found also to be true of the sympathetic system.f These discoveries are the result of a method of metallic staining, first devised in detail by G-olgi of Pavia, in which silver is reduced in the structures that have been impregnated with chromium during hardening, and usually also acted on by osmic acid. It displays the minute structure of the grey matter with a distinctness and in a manner that reveal facts before altogether unseen. Almost the first definite steps were the results obtained in the Inver- tebrata by Nansen, before he turned his face from polar cells to Polar seas. But the first important disclosures, which involved the radical change in conception, were due to Ramon y Cajal of Barcelona J and to the veteran v. K6lliker,§ supplemented and diffused by Waldeyer.|| Since 1890 there has been incessant work at the subject, and y Cajal has presented to us the chief facts that had then been ascertained, in the Croonian Lecture to the Royal Society in 1895. All nerve-fibres are prolonged processes of nerve-cells They consist of an axis, with a " medullary sheath " around it when the course is long, either within or outside the central organs. Most cells have but * The interpolation of this account of the recent revolution in fundamental elements of our knowledge, although not quite consistent with the plan of the book, seems the most convenient way of presenting the facts to the reader. They pass below, and rise above, the range of practical knowledge which can be used in common work, and yet are changing our physiological and pathological conceptions in a manner and degree which must be adequately recognised, although much of their effect is still uncertain. t v. Kolliker, " Histol. Mittbeil.," ' Wurzburg. Sitzungsb.,' Nov. 23rd, 1889. + Previously, ' Internat. Monatschr. f. Anat.,' 1890, Bd. vii. § Loc. cit. || ' Berlin, med. Wochenschr.,' 1891, No. 28. 54 ACTION AND PARALYSIS OF MUSCLES. one such meduUated process, larger than the others ; some have two. The other processes are short; they soon divide and branch within the grey substance: the long meduUated processes also at last end by dividing and ramifying. The conception formerly held may be thus stated. Of the ultimate divisions of the short, quickly-branching processes in the grey matter, some had been thought to join the terminations of similar processes from other cells, either neighbouring cells in the grey matter, or the terminal branches of meduUated nerve-fibres, processes of cells far away. Thus, of the motor cells of the spinal cord, some of the processes, passing backwards, were believed to join those of sensory cells in the posterior cornua, of which the meduUated process was a fibre of the posterior root. The constituent elements of the nervous system thus formed, by branch union, one continuous complex net- work, with paths for the nerve-impulses, due to union and continuity of the cell-processes. The paths in actual use were determined not only by such union, but also by differences in " resistance" among those which continuity provided. The " resistance," which thus per- mitted an energetic impulse to spread more widely than a slighter one, was varied in degree by functional activity; it was diminished by the repetition of the same activity, and it was also varied myste- riously by other nerve-impulses from various sources It might thus be increased so as to "inhibit" action. In so far as any attempt was made to conceive its seat, it was thought of as in the cells, or in the feltwork of uniting processes in the grey substance, called " spongy," from its blending trabeculse. Much of this conception is retained. But the more the methods of examination were improved actual union of the branches of cell-processes became less perceptible under the microscope. The development of the use of staining agents, especially metallic, has increased the power of discrimination. Variety of aspect can be thus produced in structural elements that before were indistinguishable. By the use of such methods, and especially that of G-olgi, the branches of the processes and fibres have been clearly traced, and they have been found not to unite. They are distinctly seen to end in the structural material in which the nerve-cells lie, sometimes by an enlarged knob-like extremity, sometimes by a point. Often the branches cross and even interlace, with the semblance of union, but close observation shows that it is a semblance only. Discontinuity is found to be the general rule. Whether invariable or not is still undecided; it is most difficult to exclude union in the dense felt of fibrils which the branching processes form in some parts, the " neuro-pilema " of His, and, moreover, the general rule of free endings is compatible with occasional actual union.* From this it follows that the " nervous system " consists of discon- * Cf. Masius, 'Arch, de Biol.,' 1892; Fritsch,«Brit. Assoc. Report,' 1892. GENERAL CONSTITUTION OF THE NERVOOS SYSTEM. 55 tinuous elements, each a cell-body with its processes, long and short. For these elements the name "neuron," proposed by Waldeyer,* has been all but universally adopted; for distinctiveness, its plural is formed according to the living language, and not the classical form—■ in English it is " neurons," in G-erman, " neuronen," in French, " neurones." The chief process, the medullated, or axis-cylinder process, is called the " axon," or " axis-process." f The branching processes in the grey matter are termed the " dendrons," the branches of these " dendrites." J From the axons there often spring fine fibres, which pass off at right angles, termed " collaterals " by Ramon y Cajal, the relations of which are imperfectly known. They have been seen to end by a T-like division and ultimate branching. The definite and extended discernment of another fact deepens the importance and application of that just described. Thirty years ago § Max Schultze discovered and depicted the fact that the axis-cylinder is compound and not simple, that it consists of a large number of fibrils,—" primitive fibrils," he termed them. He pointed out that they could be traced throughout the fibre, separated by a finely granular substance. They could be well seen where the axis-cylinder widens in joining the nerve-cell, that is, where the cell narrows into its chief process. Others could not see the significant striation, among them Ranvier, whose work domi- nated science throughout the next fifteen years, || and the fact was practically ignored. The axis-cylinder was regarded as simple and integral, until recent methods have enabled the clear establishment of the correctness of Max Schultze's observations. The number of fibrils that constitute an axis-cylinder is considerable. Obersteiner has found that there are about fifty in an axis-cylinder of the sciatic nerve of the frog.^T * Loc. cit. t Because the " axon" is the separate " nerve," when one exists, an attempt has been made to make current the use of " neuron " for this alone. But etymo- logical consistency has little influence on the vitality of names. The use of " neuron " for the whole element has become so general that resistance to it is futile. Moreover, the conception attached to it in use is already definitely detached from its etymology. Lastly, although the cell-body and its processes are one, to have only the word " cell" for the whole element, a word that will still, inevitably, be applied to the cell body, leaves the latter without nominal distinction from the other two parts of the element—the neuron and the dendrons. Hence the word " neuron " is here used in the established senses. X "Dendrite " has also beeu used as equivalent to "dendron," and still is; but the need for distinguishing the t«ij:s from the process itself makes it highly probable that this convenient separation of the words will become universal. § In 18G8 ; see Strieker's ' Histology' (NTew Syd. Soc. trans.). The observations were confirmed by Babuchin in 1868 and 1869. || See further on Structure of the Nerves, p. 62. ^f Personal communication. 56 ACTION AND PARALYSIS OF MUSCLES. These fibrils consist of a conducting substance, the " hyaloplasm " of Leydig and Nansen (so termed from its greater translucency in hardened tissue). This is isolated by a slightly granular material, distinguishable chiefly by its difference of aspect and staining after the changes produced by hardening agents. It has been termed the " spongioplasm "—" plasm " because it also has a soft consistence, " spongio " because it is said to form trabecule, which constitute the chief element in the ground substance, or matrix, of the " spongy " grey substance* in which the cells lie and their processes branch. From this compound constitution of the axis, we must infer that its terminal division into branches is merely the separation of these fibrils, first into groups, and at last into single fibrils—" primitive fibrils." It is so at the periphery and in the grey matter. The final twigs may be termed " axites," if a special designation seems needed.f The short branching processes have been found to consist of similar fibrils, and this is true also of those supposed to be extensions of the substance of the cell, and therefore called " protoplasmic processes." This name should be given up with the conception attached to it. The opinion that their function is to convey nutritive material to the cell-body was, indeed, never more than an hypothesis, resting on no real foundation. J With the recognition of the fibrillary constitution of the axon and dendrons, has been associated an equally important recognition of the fact (most clearly depicted by Max Schultze §) that their fibrils pass through the body of the nerve-cell without interruption. Those of the axon diverge to pass to the several dendrons, but those of the latter do not pass all to the axon. Some pass directly to other dendrons, so that, in such, there must be conduction from the cell as well as towards it.|| Moreover, both y Cajal and Kolliker have observed, in certain cells of the cerebellum, all the fibrils of an axis-cylinder pass directly to a dendron, scarcely entering the body of the cell. Twigs from such processes of small cells, especially in the Inver- tebrata, have been said to join the elements of the neuroglia.^" Tie * Apathy, 'Biol. Centralbl.,'1889. The term "spongy grey substance" wns before in use on account of the sponge-like interlacement of the cell-processes. The conception attached to it has thus become somewhat confused. t Especially since one writer has termed them neurites, which would be confusing unless the axis-process were termed the " neuron," as it certainly will not be. The only proper use of this word (neurites or neuronites) would be for the terminal twigs in general. X That these dividing branches, long, and not obviously permeable, should be the channels by which the cell receives that which could pass directly through its walls, was simply a positive inference from the negative fact that no other function was obvious. That we must cease to consider these processes " protoplasmic" and nutritional was insisted on in 1890 by Rabl Ruckhardt (' Neurolog. Centralb.'). § Loc. cit. || v. Kolliker, ' Wuitzburg. Sitzungsb.,' Nov. 23rd, 1889. T Among others by Ladowsky, ' Verhandl. Med. Congress,' Berlin, 1890, ii, 92. GENERAL CONSTITUTION OF THE NERVOUS SYSTEM. 57 fact is in harmony with the origin of both from the same embryonal tissue. The differentiation of the nerve-elements from this, may leave some blending of structure. It must be remembered that there is much uncertainty regarding the nature of many of the smaller cells, and it is conceivable that some are nervous and some neuroglial, and that there may not be always actual separation of their connections. An essential difference between the axon and the dendrons cannot as yet be established. Branching does not differentiate them, for the axon also branches after a longer course. Nor does either multiplicity or length. The cells of the posterior ganglia of the cord have but one axon and one dendron, united for a short distance as the single process of the " unipolar " cell. These two processes are of nearly equal length in the case of those cells that give rise to the fibres of the posterior median column ; these, reaching the cord by the posterior roots, ascend to the level of the medulla, while the other division of this cell-process probably comes from a muscle as far away. We see also, in this instance, the absence of any real distinction from the direction of con- duction. Although the axons of the motor cells conduct from these, so also must some of those dendrons to which fibrils pass from others. Moreover, in the case of the posterior root-fibres which go to the local grey matter, the long fibre from the periphery conducts towards the cell ; the shorter fibre, which soon branches in grey substance, con- ducts from it. Opinions may differ as to which should be regarded as axon and which as dendron, but analogy suggests that the latter should be that which soon ends in the grey substance. But it is difficult to avoid regarding each fibre of the cells related to the posterior median column as an axon. There is no reason for regarding either a dendron or an axon as an essential element of a cell. Yet the distinction is necessary, and the general application of the names is justified by the common difference between the one meduUated process, which passes out of the grey matter, and the other numerous processes, which are not medullated, and soon divide within the grey substance. The extent to which the physiology of the nervous system is inferred from its minute anatomy, is illustrated by the revolution in our con- ceptions produced by the discovery of the discontinuity of its elements, the fibrillary constitution of the conducting structures, and the course of the fibrils. These, passing through the nerve-cells, without inter- ruption, can merely conduct through the cell-body as they do elsewhere in their course. With this fact disappears the old idea, so simple, apparently so adequate and reasonable from its superficial analogies—the idea that the nerve-cells are the seat of the production of nerve-impulses, that in them " nerve force " is generated from the latent energy stored in the nutritional compounds which have entered into their constitution. But we cannot have such generation where the fibrils are continuous. For it, we must look to their extremities, formerly supposed fo be in the cell-body, now perceived to be in the 58 ACTION AND PARALYSIS OF MUSCLES. " spongy grey substance." The process must be where the continuous fibrils begin in the centre, as it is in the skin and other parts of the periphery, in the case of fibrils that conduct thence. As all the nerve- impulses that reach the centres, through which external influences act, and the environment is perceived, originate in the minutely separate nerve material at the extremity of the afferent fibrils, so all the out- going impulses, and those which pass from one part of the centres to another, originate in their special form at the analogous extremities of the fibrils in the grey substance. We must conceive these impulses arising in the extremities of the " cellulipetal" dendrites (to use the somewhat cumbersome term of v. Kolliker), being excited m some way by the stimulus of the impulses which reach the contiguous extremities of other " cellulifugal" fibrils, dendrites or branches of the axon of a distant cell. The incoming impulses may excite those that go out, as impulses are excited at the periphery by other forms of energy ; or there may be a process of conduction, through the intervening ground-substance,—the matrix in which the cells lie and the dendrites end. For the increase in the amount of nerve- energy which often takes place, there must be more than conduction, its production must be " excited " by that which is conducted. We can conceive such excitation without continuity, especially when we con- sider that the stimulation of muscular protoplasm is by the impulses in nerves which terminate on the fibres, and not in continuity with the contractile substance—indeed, separated from it by a structure apparently quite different in its simpler nature. If this conception of the origin of the impulses in the terminations of the fibrils seems less easy than their origin in the more massive nerve-cells, we must remember how multiplicity neutralises minuteness. Indeed, the minuteness of the conducting fibrils almost involves a multiplicity of minute sources of nerve-impulses,—which must, more- over, be far from minute in comparison with the molecules, from the latent energy of which the impulses proceed. All modern discoveries prepare us for finding every mass to be an aggregation, and each perceptible quantity of energy to be made up of minute constituents, every one of which is definite, both in its separate character and in its contribution to the effect of the whole. The finely divided nerve- substance will constitute a total source of energy, as adequate in extent as a nerve-cell, with a more obvious facility for the renewal of the molecules lost in functional action, and far greater opportunity for varying relation to the structures from which the impulses are received. What, then, is the function of the nerve-cell ? The one certain fact, established by evidence that is secure, is that on it depends the life of the nerve-fibres—the vitality of all the processes, equally that of the dendrons and of the axon. The evidence of this, the immediate deo-ene- ration of any separated part, is well known. It is less conspicuous in the case of the dendrons, but sufiiciently certain. How the influence GENERAL CONSTITUTION OF THE NERVOUS SYSTEM. 59 is exerted we can only surmise. The nucleus of every cell is its life centre, and in some way the nutrition of the protoplasm is determined by it. The cell-body has a complex structure, dimly perceptible by the help of reagents, at present beyond our practical comprehension. One distinct fact, however, is that the protoplasm of the cell, extend- ing into the narrowing axon, thins away between the outer sheath and the white substance, becoming unrecognisable until one of the many nuclei is reached. Each of these is surrounded by like protoplasm, also thinning off along the fibre until invisible. It is certain also that if the cell-body and nucleus are destroyed, or the fibre separated, the pro- cess of degeneration begins by changes in these nuclei. They seem to be concerned in carrying on the influence of the distant cell, and it is not easy to conceive any other path for this influence than a thin layer of protoplasm, within the sheath, continuous from nucleus to nucleus, vitally influenced by these, and conveying, by its own nutri- tional state, that of the cell. A space, in this position, is rendered visible by reagents which make the contents of the sheath shrink. Indeed, coagulated material, in small quantity, can be seen within it.* This has been regarded as evidence of the presence during life of such a space as is here assumed to contain connecting proto- plasm. Many facts, previously obscure, become more intelligible in the light of the new discoveries. The knowledge that the cell governs the nutrition of the fibre, and the belief that from it proceeded the nerve- impulses, involved a correspondence in the direction of nutritional in- fluence and of conduction, and it was found, in fact, that conduction and degeneration were in the same direction as a rule—but only " as a rule." It was untrue of the sensory nerves. These, coming from the cells of the ganglia on the posterior spinal roots, degenerate downwards, but they conduct upwards—an anomaly which had to be simply ignored. The fact is now seen to be in harmony with others. The arrest of secondary degeneration in the grey matter, the fact that the degeneration of the fibre which enters the grey matter never passes on to the next nerve-cell, through which conducted impulses must pass, was mysterious when they were believed to be in continuity. The discontinuity explains it at once. The degeneration is limited to the single neuron. The division of the axis-cylinder at its terminal ramification, whether that of the sensory nerve in the skin or of the motor nerve in the muscle, was scarcely intelligible when the axis-cylinder was regarded as a single conducting path ; it is so when we perceive that the apparent division is simply the separation of its constituent fibrils, each a dis- tinct conducting path. This fact is, moreover, especially important in relation to the minute localisation of the various forms of sensation in * Schiefferdecker, ' Arch. f. mik. Anat.,' xxx, 1887. 60 ACTION AND PARALYSIS OF MUSCLES. the skin. The sensory nerve-fibres themselves are not numerous enough to subserve this localisation, which could not result from the division of an axis-cylinder that conducted as a whole. The fact that the special form of energy termed a " nerve-impulse " may arise in a fibre in its course under the action of a stimulus, that the capacity of the fibres is not limited to " conduction," is less surprising if we conceive all such impulses as produced at their extremities. While old difficulties thus disappear, and many facts become more readily intelligible, so great a change of our conceptions involves new difficulties. Not only are the structures concerned most minute, but their discernment depends on the use of reagents which reveal them by developing differences in aspect due to chemical changes; new physical characters have been produced by other agents of the same nature. There seems but little original difference in consist- ence between the material that constitutes the conducting axis of the " primitive fibrils," and that of the separating substance. Both are apparently almost diffluent during life, and are indistinguishable physically until their difference in constitution is revealed by the action on them, first of the chemical agents that harden, and then of those that stain.* Both processes involve molecular chemical changes, which multiply initial differences, and leave the actual amount of these more obscure than we are apt to think. The conducting element of the fibrils, the " hyaloplasm," or " kine- toplasm," is said to be more diffluent than the separating " spongio- plasm," but the difference may be chiefly due to the hardening agents used. Continuous within the tubules, and through the cell-body into the dendrons, it has been said that beyond these it is also continuous with similar material in the matrix of the spongy substance Into this also the spongioplasm. is said to pass and form a trabecular structure. The fact that the fibrils, as stained by Oolgi's method, apparently end, must indicate that these elements, if continuous with those of the matrix, are different in nature in some degree. The difference may be much exaggerated by reagents, and yet sufficient to constitute the functional discontinuity which is generally assumed to be as structur- ally absolute as it appears in the sections. Until we knbw what the structure of the matrix is, we can scarcely conjecture the nature of the process that occurs in it between the dendrites. " Conduction" may have been too readily regarded as * In connection with the fact that molecular differences between substances apparently the same, even when examined with the utmost minuteness, may be revealed by staining, the facts of the colour photography of Cassagne may be noted. The waves of light which differ only in rapidity and length, but by this excite different elements of the retina, reduce a special silver salt in the gelatine film in different degree. Extremely slight as must be the resulting difference in the molecules which is produced, it apparently suffices, augmented by some additional chemical process, to make each of them retain some stains and not others. , GENERAL CONSTITUTION OF THE NERVOUS SYSTEM. 61 impossible, and it is not clear that actual conduction of nerve-impulses is incompatible with the augmentation we include under the term "excitation." An increase must occur when, for instance, in many reflex actions the afferent impulse that reaches the spinal cord is minute in proportion to that which leaves the centre. We seem thus to have a process of stimulation comparable to that in the cutaneous nerves (themselves apparently analogous to dendrites), under the influence of some other form of energy from the outside. In this connection it is especially noteworthy that many dendrites terminate in knob-like enlargements, suggesting receptive functions. We do not know the nature of a "nerve-impulse." We must, however, assume that it is energy in some form of motion, released from that previously latent in the nerve-substance, apparently the "kinetoplasm" or "hyaloplasm." Chemical change occurs by which simple compounds are formed, as in all similar processes, and the simplest conception is that the process is like that in a train of explosive material, modified, restricted, but perhaps accelerated by the influence of life.* The motion of a touch, which acts upon the nerve-endings in the skin, reaches them by passing through the skin as the simplest form of motion; so also pass the special forms of wave motion that con- stitute electricity and heat. A differentiation of the nerve-tissue in the ending seems to enable their molecules to receive one special form of motion most readily. Hence our " special senses." The manner in which the equilibrium of the nerve-substance is disturbed in each doubtless differs much, but it is instructive to note in connection with the theory of the nerve-impulse just suggested, that the wave-motion of light seems first to induce recognisable chemical changes in material of unknown nature. * This view has been developed at length in the writer's ' Dynamics of Life/ London, Churchill, 1894, but was clearly stated by Herbert Spencer, 'Elem. Biology,5 vol. i, 1864. 62 DISEASES OF THE NERVES. GENERAL PATHOLOGY. Stetjctubb.—Each individual fibre consists of a central core, or "axis-cylinder," surrounded by the "medullary sheath," or "white substance of Schwann," and a delicate membranous sheath enclosing it. The axis-cylinder is the func- tional element, that which conducts the nerve im- pulses. It was long thought to be homogeneous, conducting as a whole, like an insulated wire, but it is now recognised to be a compound structure, in consequence of the recent researches of which an account has j ust been given. The separate " primitive fibrils " of which it consists are sufiiciently numerous to be of great physiological importance, an axon according to its size, containing apparently from thirty to fifty (see p. 55). They were, as has been stated, described thirty years ago by Max Schultze; but, although his observations were not unconfirmed, those investigators whose work had most influence, notably Eanvier, failed to recognise them. The axon has been practically regarded as simple until the last few years. Indeed, the methods of histological inves- of the structure tigation by which its fibrillary structure can be of nerve-fibres. I recognised are still outside the range of ordinary fated III™non- microscopical pathology. For this, that which was meduUated fibre; before discerned retains its importance, because it S, sheath; M, js g^rj a]i ^^ can ^e appiied to morbid changes. iuvgIih or wintc substance of The "medullary sheath" (M, Fig. 32) consists of Schwann; kc.axis- myelin, a liquid fatty material, supported by a fine rfeus-^N "node1" network of horny substance, "neurokeratin." This IS, incision Schmidt. _(From foe sympathetic. the nerve-fibre of fne white substance, the " primitive sheath," or a frog, stained with " neurilemma," or " sheath of Schwann " (S). Nuclei o-mic aci .) ^ ^[q at intervals within the sheath, between it and the myelin. The white substance is interrupted at regular distances by what are termed " nodes,"—sometimes, from their discoverer, "nodes of Ifcanvier" (1ST). The end of each portion, or "inter- node," is enclosed by the sheath, through which the axis-cylinder passes. Between the incurved extremities of the sheath is a little Atj Fig. 32.—Diagram of sheath is absent in the " non-medullated " fibres of A delicate membrane surrounds PHYSIOLOGY OF NERVES. bd clear cementing substance, shown by the fine dotting in the figure. There is one nucleus (n) to each internode, about its middle; hence they are sometimes called "internodal nuclei." Around the nucleus is a little protoplasm, and it is probable that a very thin layer of protoplasm everywhere lies between the sheath and the myelin connecting that of the adjacent nuclei, and these with the protoplasm of the nerve-cells (see p. 59). The internodes are shorter towards the termination of a nerve. It is important not to confound these divisions with other imperfect indentations (IS, Fig. 32, I), often called the " incisions of Schmidt," or " indentations of Lautermann." * These are oblique, incomplete divisions of the white substance. Many exist in each node. They are believed by some histologists to be of artificial origin, but their uniformity is in favour of their dependence on some structural feature. The myelin, Eanvier suggests, must protect the axis-cylinder, since its almost liquid consistence will diffuse pressure on the nerve. Other possible uses it subserves may be suggested, but we have no proof of them. The nodal segmentation evidently permits nutrient material to reach the axis-cylinder. The "grey fibres," or "non-medullated fibres," consist of an axis- cylinder, sheath, and nuclei (Fig. 32, III), but contain no myelin. They constitute the sympathetic nerves, but some (also probably sympa- thetic fibres) are found in all the spinal nerves. They are absent from the nerves of special sense except the olfactory, which contains no other fibres. The nerve-fibres are united into " fasciculi" by delicate nucleated connective tissue, and these fasciculi are similarly connected into larger bundles, while the whole nerve is surrounded by a dense connective- tissue sheath or " perineurium." Under this sheath, and extending between its lamellae and amongst the individual nerve-fibres, there is a lymph-space lined by flattened endothelial cells, which probably plays an important part in the propagation of inflammation. From the perineurium a very delicate "sheath of Henle" extends on to the ultimate divisions of the nerve. All these tracts of connective tissue and spaces are continuous, and they convey the blood-vessels. They also contain nerve-fibres, " nervi nervorum," which are derived from the nerve itself .f The sheath and connective tissue of each nerve are thus part of the area of distribution of its own fibres. Physiology of Nerves.—The first great fact to be kept in view is that the axis of each nerve-fibre is the prolonged process of a nerve-cell, the wall of the cell and process being continued as the sheath of the nerve-fibre, the protoplasm of the cell becoming less and less as the process narrows, and the white substance, the medullary sheath, making * They were first described by Schmidt of New Orleans, and afterwards by Lautermann. f Horsley, Roy. Med. and Chir. Soc, January 22nd, 1885. 64 PHYSIOLOGY OF NERVES. its appearance when the narrowing has reduced the process almost to the width of the fibre. This medullary sheath begins in the layer of protoplasm which surrounds the axis within the neurilemma, and which can be traced, lessening as the myelin increases, for some distance. Probably it does not entirely cease on either side of the myelin (see p. 59). Thus, in the meduUated fibres there is a continuity with the cell of the axis, the neurilemma, and probably the protoplasm, and this continuity proceeds from the fact that the fibre is by development a part of the cell; while it .is moreover found to be so vitally, throughout life. It shares all modifications in the nutrition of the cell, never preserving a perfectly normal state if the nutrition of the cell is changed. Tet the relation is less simple than it seemed when the axis was believed to be but an attenuated prolongation of the substance of the cell. It has been pointed out in the last chapter that the fibrils which constitute the axis pass through the cell and, although they must be considered part of the cell, we are led to look rather to the protoplasm, prolonged along the fibre, for the element of vital integrity—a conclusion in harmony with much elsewhere. The function of nerve-fibres is seen in a different aspect under the light of the new investigation. As already explained, it was formerly thought that the cells produce and the fibres conduct what is termed " nerve-energy," although fibres also can generate this when they are stimulated, and cells conduct the impulse that passes through them.* The fact is now seen to be that the nerve-fibrils simply conduct when they pass through the cell-body, as they do elsewhere; and it is con- spicuous when, for instance, a bundle of fibrils simply skirts the edge of the cell-body at one corner in passing from one process to another, as may occasionally be observed. That which is true of one fibril must be true of all. The relations are too fundamental for the conception of differences. If any fibrils began or ended in the cell-substance, all would do so. If it is true of some, it must be true of all, that the function of the cell is vital nutrition. Where the fibrils begin as such, as conducting structures with the constitution susceptible to the same changes throughout, whether this " beginning " is a change of constitution or of structure —there we must look for the source of the energy that is conducted. But we have not yet learned how to look. The division of nerve-fibres where they terminate, as in muscle, or begin, as in the skin, must be regarded as separation or union of axis- * The double similarity of the function of the cells and the fibres was further insisted on in the last edition of this book in words that are worth quoting, because they show how significant are the facts of function as well as of structure:__ "The process of the cell itself must conduct, and the cell must itself conduct. Each motor cell of the cord is part of the path through which the nerve-ener^v from the brain passes. That which passes through must be conducted, however it may be changed in amount. Even if it is renewed, we cannot so distinguish this function of the cell from that of the fibre as to say that there is not conduction." LESIONS OF NERVES. 65 fibrils or of groups of them. This has been already explained, and other points have been mentioned in the last chapter which concern the action of the nerves, in so far as this can be discerned with distinctness. Lesions of Nerves.—Secondary Degeneration.—A nerve-fibre undergoes destructive changes whenever it is separated from the cell from which it springs, i. e. the body of the cell of which it is vitally a part. Formerly, importance was attached to the fact that as a rule the degeneration is in the direction of conduction, i. e. from the cell from which the nerve-fibre conducts nerve-impulses. This must be so because each fibre belongs only to one cell. The fact is, however, conspicuous, because it is only in the long axis-processes that the direction of degeneration can be observed. The short dendrons degenerate from, though they usually conduct towards, the cell-body ; and so also do the long sensory fibres, axis-processes of the cells of the spinal ganglia. These were formerly regarded as inexplicable excep- tions to the correspondence, when the impulses were thought to be produced in the cell. We can now see that they are instances of the general condition. The degeneration is commonly termed " secondary," because it is dependent on a "primary" lesion of another kind—as division or destruction of the cell-body of the nerve. Degeneration also follows many slighter lesions such as nerve compression, transient or exten- * sive, or local inflammation and the like ; and this may differ only in degree from that which follows division. It must be more than a difference of degree, however, when there is no recovery. The secondary degeneration is often called " Wallerian," from the name of the pathologist who first studied it. It is of great importance practi- cally and theoretically The medullary sheath breaks up into segments, and these into smaller and smaller fragments, and the minute globules and granules are ultimately removed from the nerve-sheath, and when the degeneration is complete the axis-cylinder also perishes. The process is not one of mere decay, but is an active one in which the nuclei of the fibre, and their protoplasm, assume an exuberant energy of growth, while the protecting myelin sheath and the essential conducting axis perish, apparently at the same time. In connection with this it may be remembered that in the central organs, the connective tissue overgrows as sclerosis when the fibres decay. Developmental relations justify us in connecting the two sets of facts. In all organs, indeed, we can perceive the fact, though most clearly in the nerve-structures, that "parenchymatous " decay and adventitial growth go hand in hand. In nerve-fibres the aspect of the process of degeneration can be better perceived than in any other structures, and it has been carefully studied in animals, chiefly by Ranvier. The most important facts are illustrated in Fig. 33, in which the examples have been selected from Ranvier's figures and reduced to one tint. First of all the nuclei are increased in size (A n, Bn); the amount of protoplasm about VOL. I. 5 66 LESIONS OF NERVES. them is greater than normal, and is granular; there is in places a local increase in the amount of protoplasm within the sheath, com- Fm. 33. Fig. 34. Fig. 33.—A-J, degeneration of nerve-fibres (osmic acid and carmine staining). A, from sciatic of rabbit four days after section; B, C, same, fifty hours alter section; D, a fibre stained with carmine only, to show the axis-cylinder; E, F, G, fibres from pigeon three days after section; H, two fibres from pneumngastric of rabbit six days after section; J, a lymphatic cell from interstitial connective tissue, containing globules of myelin which it has taken up. In all the figures— n, n, nuclei; x, x, constrictions of the myelin produced by the growth of the protoplasm; ac, axis-cylinder. K, L, regeneration of nerve-fibres. K, from pneumogastric of rabbit seventy-two days after section; L, from sciatic of rabbit ninety days after section; e, rounded end of white substance of central end of nerve; *, sheath; na, new axis-cylinder. In L are two globules of myelin remaining from the degeneration of the old fibre. Fig. 34.—Degenerating fibres from cutaneous nerves of man. (After Pitres and Vaillard.) A, from near a bedsore in a case of fracture of the skull; B, C, D, from the fifth nerve in a case of neuralgia and ulceration of the lip; n, n, nuclei. In A the protoplasm and nuclei are increased, and the myelin is breaking up, the processes having proceeded furthest in the neighbourhood of the nucleus in the middle of the fibre; in B the segmenta- tion has gone on to the formation of globules, which in C are, for tlie most part, small, and many have been removed, so that the fibre is narrow; while in D all the products of degeneration have been removed from con- siderable tracts of the sheath. pressing the myelin (A x, B x, C x). The nuclei then become detached from the sheath; the protoplasm everywhere increases, and encroaches on the myelin, until here and there it meets across the tube, com- GENERAL PATHOLOGY. 67 pletely separating the myelin (A, lower part; B, upper part), and with the myelin the axis-cylinder (D). This process then goes on with increased rapidity ; the myelin is broken up into smaller and smaller fragments (C, E,F), which become globular in the watery protoplasm, just as oil forms globules in water. The nuclei meanwhile continue to enlarge, and then divide, first the nucleolus and then the whole nucleus (F). The two nuclei may again divide, until (as in G-) there are four or more nuclei in each internode, instead of one only as in health. The small globules of fatty myelin seem to become changed in chemical composition, since they are stained l^ess deeply by osmic acid. Eanvier suggests that their fatty matter may undergo a process of saponification. Ultimately they seem to pass through the sheath, are taken up by con- nective-tissue cells and lymphatic cells in the vicinity (as in J), and are gradually, for the most part, removed. By the time the myelin is in small globules the nuclei cease to multiply. On the removal of the products of degeneration the sheath shrinks, and looks empty in places; but here and there it is enlarged by the nuclei, protoplasm, and a few remaining myelin globules (H). Hence in transverse section many small sheaths are seen, with a few of larger size where they have been cut across at these swellings. In the rabbit the first changes are visible at the end of twenty-four hours ; the first complete interruption of the myelin and axis-cylinder occurs about the end of the second clay; the process of destruction is considerably advanced at the end of the fourth day, and is finished, and the multiplication of the nuclei ceases, towards the end of the second week. In peripheral nerves the changes seem to progress from the lesion to the periphery, but within the central nervous system they are said to begin at the same time in all parts of the fibre. It is uncertain to what extent this difference is real or is only apparent, but the process goes on most rapidly at the periphery. At the end of the second day, in the rabbit, stimulation of the nerve by electricity below the lesion no longer causes muscular con- traction, the disappearance of electrical excitability coinciding with the first complete segmentation of the myelin and axis-cylinder. A curious fact, unfortunately more interesting in pathology than in practice, is that the degeneration of a divided nerve does not occur if the ends are brought quickly into perfect apposition. It is so in animals, and probably also in man.* Immediate replacement may occur in some incised wounds, and thus the fact is explained that simple division is a less serious injury than a grave contusion. The axis-cylinder seems thus to undergo these changes as a whole, although we know that it is a group of fibrils. But we have seen that the conducting substance of these fibrils, and that which separates it (and may be conceived as analogous to the mye^n around the whole axis-cylinder), differ but slightly in consistence. Both are nearly fluid, * See Bowlby,' Injuries and Diseases of Nerves,' p. 32. 68 LESIONS OF NERVES. and so break up into globules, although they differ in constitution in a manner and degree that subserve entire difference in function, and permit reagents to produce artificial differences in aspect and cha- racters misleading if simply transferred to the living state, and yet the revelation of an essential difference of absolute importance. The process is thus the result of an active growth of the nuclei and protoplasm of the nerve, i. e. of the cellular elements of which the nerve is composed. Why does this occur ? The determining cause is the interruption of the continuity with the cell-body or the destruction of this. Eanvier connects the destructive growth of the protoplasm with the loss of function in the axis, and suggests that normally the activity of this restrains the vital energy of the cell-elements. These changes are often attended with others outside the fibres, such as we regard as evidence of inflammation. Several observers have described increase of nuclei and accumulation of leucocytes in the interstitial connective tissue, and even in the nerve-sheath, with dilatation of the blood-vessels. Such changes are, indeed, intense at the primary lesion; their degree in the nerve below the lesion varies and seems to be proportioned to that in the primary process. This is another mode of stating the important fact that the irritative character of the secondary process is determined by the irritative nature of the primary disease. We may say, if we like, that in the slighter degrees it is distinctly inflammatory in aspect in proportion to the signs of inflammation at the primary lesion. But this is only another mode of stating one part of the general fact, and the importance of the transmis- sion of the character of the process cannot be too strongly insisted on. The process of secondary degeneration occurs more slowly in the rabbit than in a bird, and seems to be still slower in man, in whom it is probable that complete segmentation does not occur until between the fourth and eighth days. It is certain than an identical process occurs in man. Changes in peripheral nerves near bedsores and in the fifth nerve, found by Pitres and Vaillard, are shown in Fig. 34, a comparison of which with Fig. 33 will show the identity of the process. It is highly probable that after complete division of a nerve in man the changes are the same as in animals. But the most common lesion is, or involves, inflammation, and the process of degeneration is thus greatly modified by the character of the primary lesion, and in time as well as in character. In the latter cases, which are chiefly those of focal neuritis, the process cannot be the same as that which follows sec- tion of a nerve. The change in irritability, which will be more fully described in the account of the symptoms, is a slow depression, some- times moderate in degree. The depression may be preceded by an increase in irritability. In such cases there can be no complete seg- mentation of the nerve-fibres. There must be a gradual alteration in the molecular nutrition of the axis-cylinder, changing its excitability. Even in severe cases there is not usually a sudden loss of irrita- bility ; the current necessary for stimulation has to be made stronger, GENERAL PATHOLOGY. 6tf until at last in seven or eight days the strongest endurable current fails to cause muscular contraction. But we cannot infer, from this alone, that there is an actual interruption of the axis-cylinder. A stronger current might still excite the nerve, because, as we shall presently see, when a nerve is being regenerated, an axis-cylinder may conduct, and still not be excitable by currents of ordinary strength. All severe changes in the nutrition of the fibres involve the intra- muscular nerve-endings in the same degree.* The evidence of this is that the faradic irritability of the muscles (which depends on the nerves within them) presents changes quite similar to those of the nerve-trunk. But this is not always true in slight changes of nutrition of the nerve. We shall presently see that the slight alterations of irri- tability in the nerve and muscle do not always correspond. The nerves terminate in structures of special nature, and these may well have some shght degree of nutritional independence. These secondary destructive changes occur in the peripheral part of . the divided nerve. But the part that remains continuous with the cell does not always preserve a normal state. Changes occur in it, espe- cially near the lesion, which are still the subject of study, and of which more must be known before their significance can be determined. In a divided nerve the changes, which are mainly those of ordinarv, often incomplete, degeneration in isolated axis-cylinders, affect the centripetal (sensory) fibres far more extensively than the centrifugal. Later on the cells connected with both suffer, the nucleus shrinking and the protoplasm to some extent becoming disintegrated.! Regeneration may occur in the nerve after the degeneration is over. It is a slow process, occupying the second, third, and fourth month after division. According to Eanvier, and as Waller thought, it occurs always by the growth of new axis-cylinders from the central end of the nerve (see Fig. 33, K and L), which ultimately become covered with myelin. One or more new fibres may spring from each central fibre, and these may subdivide. All are enclosed in a sheath which is con- tinuous with that of the central end (Fig. 33, K, s.). We must assume that only some of these axis-cylinders persist and achieve functional permanence. But the whole of this subject needs re-investigation in the light of the multiple constitution of the axis-cylinder. J Some- times these fibres twist about, and even turn back and grow upwards, probably in the direction of least resistance. In animals new fibres * Fully described and figured by Babes and Mariuesco, ' Babes' Atlas Path. Histol. des Nervensystems,' part i. t See Hoinen, ' Ziegler's Beitrage,' viii, and 'Babes' Atlas,' part 2. R. A. Fleming (' Brit. Med. Journ.,' 1896, ii, p. 918) lays great stress on the degeneration of the fine (vaso-motor ?) fibres above the lesion, and describes also a considerable con- nective-tissue overgrowth in the same part. X The precise renewal of these fibrillary conducting paths cannot be ascertained in animals, and in man the amount of damage that is renewed is far smaller. Facts are needed regarding minute differential localisation after recovery from an injury, compared with the normal. 70 LESIONS OF NERVES. may grow through a considerable extent of cicatricial tissue between the divided ends of a nerve, but in man it is doubtful whether regene- ration of a divided nerve occurs unless the extremities are brought in contact, or at least close proximity. Some investigators believe that there is a formation of fibres in the peripheral extremity independ- ently of the growth of new fibres from the central end.* In cases of slight injury, regeneration occurs more readily ; in these it is probable, as we have just seen, that degeneration has been incomplete. The regenerated nerve-fibres regain some conducting power while they are still much narrower than normal, and before they can be excited by electricity, f Muscles.—The degeneration of the motor nerves is attended by changes in the nutrition of the muscles. These commence in or after the second week. The muscular fibres become narrower, and may be reduced, ultimately, to one third of their former width. An increase in width has been said to precede the narrowing for a few days.J The transverse striation becomes less distinct, and the striae seem to be nearer together than in health. The fibres may become cloudy or granular, but do not present actual fatty degeneration except in some very acute cases. If no regeneration of the nerve takes place, the transverse striation gradually disappears, and may be replaced by a longitudinal striation, or the fibres may undergo certain chemical changes, and pre- sent a peculiar glassy appearance, which has been called "vitreous * E. g. Neumann, Mayer, i i ta 13 14 M .. .y ,-'"' ..... ..... — — -*--•■"■ ,eKr V ........ ....... --- «•'*♦ S..JJ- i---; '--- ----- i p .....................iiiiiiiiiniiiiii.......iiiiiiiiiiiiiiiiniiiMiiimtJllI FiG. 35.—Type of degenerative reaction in a case of nerve-injury of mode- rate severity. (After Erb.) Muscle irritability lowered from middle of first week; faradic, extinct in middle of third, reappearing in ninth; voltaic, increased from middle of second week until tenth, then de- pressed until fourteenth. Nerve irritability (changed alike to both currents) is lowered from middle of first week, lost at end of second, reappearing at seventh. Power lost until end of fifth week. muscles at once become flabby from loss of tone, and to this atony actual wasting is added in the course of a few weeks. The wasting is due to the reduction in size of the muscular fibres. If the sensory nerve-fibres are not interrupted, the muscles become tender to the touch, and pain is caused by their strong contraction, due probably to the effect of interstitial inflammation on the sensory nerves, which end in the connective tissue. The most important symptoms are those that are afforded by elec- 72 LESIONS OP NERVES. trical examination of the muscles and nerves, since they enable the degenerative changes to be ascertained and followed during life.* The alterations in the electrical reaction, consequent on this degeneration, have been already briefly mentioned (p. 29),"'but must now be described in greater detail. The rapid degeneration of a nerve, which follows a severe lesion, is attended by a loss of irritability on electrical stimula- tion, the loss being the same to faradism and voltaism. After such lesions as are common in man—neuritis, for instance,—there is no sudden loss, such as occurs after injury of a nerve in an animal, when the nerve becomes segmented, but there is a more or less rapid diminution of excitability, and this goes on until no stimulation can be produced, even by a strong current. The progressive changes in irritability may be conveniently represented on a chart. Fig. 35 shows the typical course of the changes of irritability in a case of moderate severity. In the muscle (M) a fall of irritability (due to the degeneration in the nerve-endings) occurs simultaneously with that in the nerve-trunk (N), and the faradic excitability becomes extinct at the same time in both nerve and muscle. The fall in voltaic irritability is quickly arrested by the change in the muscular fibres, through which they soon become more excitable than normal to the voltaic current. This change usually occurs during the second week, and the irritability continues to increase during the third and fourth weeks. At its maximum it may amount to three, four, or five cells of the battery, i. e. contraction can be obtained in the paralysed muscles with a current weaker by so many cells than is necessary to cause contraction in a corresponding un- affected part. The further course of the changes in irritability depends on the severity of the lesion and the intensity of the degeneration. In a case of moderate degree, such as is shown on the chart, nerve irrita- bility reappears about the end of the second.month, usually after some voluntary power is regained. It is at first low, so that a strong current is required. It gradually increases, but for a long time continues a little below the normal degree. This return of nerve irritability is accompanied by a corresponding return of faradic irritability in the muscles (i. e. in the intra-muscular nerves). The increase of voltaic irritability often persists long after recovery of power, but it lessens as faradic irritability returns, and, as shown in the chart, it may fall below the normal before it ultimately regains its original degree. Slight changes in irritability can be ascertained only by a comparison with the corresponding part on the other side in the same individual. Moreover, when we speak of excitability being " lost," we mean that we can obtain no stimulation by any strength of current that can be borne. The sensitiveness of the skin varies in different persons and in different part's. The resistance of the skin also varies j the greater it is * For a careful analysis of abnormal electrical reactions in muscle and nerve see Doumer, ' Bulletin Offic. de la Soc. franc^ d'Electrotherapie,' 1897. The author lays especial stress on the importance of recording the nature of the excitation and the character of the muscle-curve produced. SYMPTOMS. 73 the stronger must be the current used to secure the action on the nerves below. Hence the importance of ascertaining what current is actually passing by the use of a galvanometer. It may be used once to gain in- formation as to the significance of the number of cells that constitutes the evidence of the difference between the two sides when the sensitive- ness to the pain which is caused prevents the use of the instrument in all measurements. If the lesion is very severe, so that there is no recovery, and no re- generation of the nerve, the loss of nerve irritability, and of the faradic muscular irritability, is permanent. The increase in voltaic irritability persists for months, and then gradually falls as the muscular fibres waste, and becomes lower and lower (see Fig. 36), WEEKS) 3 10 20 30 40 SO 60 70 80 90 M f--- ■.F .......... ........... ;,**■«» line. N fine- 1 P Fig. 36.—Type of reaction in a case of complete and permanent damage to a nerve. (After Erb.) Early course as in the last diagram; no return of power, nerve irritability, or faradic irritability in the muscle. The early increase in voltaic irritability gradually lessens, and at the end of ten months falls below the normal, hut is not extinct until nearly two years. In this and the following: figures the normal degree of irritability (ascer- tained from the healthy side) is represented by the finely dotted horizontal line (n.l.) ; faradic irritability, F, by a line of larger dots; voltaic irritability, V, by a broken line; M, muscle; N, nerve; P, power of voluntary contraction, its degree shown by the vertical lines; the asterisk marks the occurrence of the lesion. The vertical divisions represent time intervals. (Many of these iudicatiug letters are given only in subsequent figures.) until ultimately no reaction can be obtained, the fibres having perished. It does not become extinct until at least a year has elapsed, and some- times (as in the chart) only towards the end of the second year. Often, when no contraction can be produced on the first attempt, after two or three applications, distinct contractions are obtained. The changes we have hitherto considered are in the degree of irrita- bility, " quantitative " changes. But the quantitative increase in the muscular irritability is often accompanied by a change in the order of response, according to the pole that is applied and the strength of current—a " qualitative " or " polar " change. We have already con- sidered its general characters (p. 31), and have seen that it consists in an undue readiness of response at the positive pole (anode) com- pared with that at the negative poll (kathode) (Fig. 37, B and C), the muscle being normally the more sensitive to the latter (Fig. 37, A). Writing CI. for the closure of the circuit, O. for its opening, and C. for contraction, the normal reaction is— 74 LESIONS OF NERVES. 1. K.C1.C.; 2. | ^ qc V 3. K.O.O. In disease— 1. I ff^Q1. 2. An.O.C.; 3. K.O.C.: or even 1. An.Cl.C.; 2. K.C1.C.; 3. K.O.C; 4. An.O.C. This qualitative change is at times absent, especially in cases of neuritis. It may be slight, and only amount to an equal kathodal and anodal excitability. It is practically constant when a nerve has been actually destroyed. On the other hand, it may be present and significant where less acute disease has not yet caused obtrusive wasting. Even when there is a marked quantitative change, the kathodal closure contraction may still occur first. When the change is present it is only in the muscles, and it mast depend on the muscular fibres themselves. In the motor nerve the kathodal response is always the first, although a qualitative change has been detected in degenerated sensory nerves. The muscular contractions which occur thus with undue readiness differ from normal contractions, excited through the nerves, in their distinctly deliberate character. Instead of the quick, lightning-like Fig. 37.—Tracings of the muscular contractions in nerve degeneration. (After Erb.) Ka, kathodal closure contraction; An, anodal closure contraction. A, tracing in health; Ka much stronger than An; contractions sudden. B, tracing in nerve-degeneration with moderate current. An much greater than Ka, the latter scarcely visible. Contraction slower, shown by the more sloping upstroke. C, the same, with a stronger current. Ka greater, but still less than An; the slow character of the contraction and its long duration well marked. contraction, the movement is distinctly longer in reaching its maximum and longer in its duration. The recognition of this feature is easy, and often of practical importance when there is doubt whether the SYMPTOMS. 75 voltaic current is acting through the nerve-twigs, or on the muscular fibres themselves. Sometimes a slight abnormal tetanic contraction during the passage of the current also occurs. During the period of increased voltaic irritability the mechanical excitability of the fibres is often increased. If they are directly percussed, they respond with a distinct slow contraction (Erb). Such are the changes in irritability which occur in cases of nerve- lesion and degeneration of moderate and considerable degrees of severity. Certain variations are occasionally met with, and these occur especially in cases of neuritis of slight degree. In severe cases the fall in nerve irritability, which usually commences in the middle of the first week, may not take place until the end of this week, although it may then progress so rapidly that no response to stimulation can be obtained at the end of the second week. An example of this is shown in Fig. 38.* The same chart, and some of those that follow it, illus- trate another very common variation from the type above described. There may be no fall in the voltaic excitability of the muscles before the commencement of the degenerative increase. Indeed, this initial fall is as often absent as present. The ehange in the nutrition of the muscle may then coincide with, instead of succeeding, the degeneration of the nerve-endings (Figs. 38, 40). Sometimes, if the degeneration is rapid, there is an interval of a few days before the secondary changes Fig.C3. tVKS. i -'.'' .....thi IN fW.T.-. n> P NONE. Pays a. Fig. 39. II 14- 16 18 20 2a 1\ 36 Ig 30 33 V,.I < ... *••• ••., '....■ -TV *5** 'ft rr* •-*•* -.r -.-. -.-: P III III JJJJ ill uu I'l ill mi Fig. 38.—Severe neuritis, paralysis complete for mouth*; recovery imper- fect. Irritability of nerve normal during first week; fell rapidly during the second; lost at its close. Simultaneous increase in voltaic irritability. The divisions on the left side represent cells of the voltaic battery, and half- centimetres of the secondary coil of Stohrer's induction apparatus, in this and the following charts. Fig. 39.—Slight neuritis; slight return of power on seventh day, slowly in- creasing; normal in fifth week. Muscle: faradic irritability lessening from fourth day, lost on fifteenth, reappearing on twentieth. Voltaic irritability normal till twelfth day, then augmented. Nerve-trunk: lowered from fourth day without initial increase, reappearing on twenty-third day; changed alike to faradism and voltaism. in the muscle have reached the degree necessary to produce increased irritability. In a slight degree of degeneration the increase in the voltaic irritability of the muscles maybe postponed for a week or more after the nerve irritability begins to fall, and until the rise occurs the * This and the following charts are from cases of neuritis of the facial nerve. 76 LESIONS OF NERVES. voltaic irritability of the muscles may remain normal, even when their faradic irritability falls with that of the nerve-trunk. An instance of this is shown in Fig. 39. When the nerve-lesion is very slight in degree, the fall in nerve irrita- bility may be preceded by a rise, which mayiie far greater in degree than the subsequent fall. In slight cases the fall may indeed be not only slight, it may be altogether absent, so that the rise consti- tutes the only symptom. This initial increase in irritability is important as the manifestation of the slightest degree of altera- tion in the nutrition of nerve- FlG. 40.—Slight neuritis; power not entirely fibres.* It may last for a few rVK& t 3. 3 4- 5 6 ' ' '1 i M «'...„ '.;;v: "•'•'•"'•' .......... """ '- N [n.r .....•■*< ::?_*: '^'L'Ji **■*-■* «* .».«.•.*£ p ......II Willi mull 1111 n\\ mini mini and I have once known it to con- tinue for five weeks (Fig. 41). Although the change in irrita- bility of the nerve is usually the same to both currents, a partial exception to this rule is presented by the increase in irritability we are now considering. The change is not always quite equal to WKS. i 2 3 4 5 6 7 8 9 10 H n IS 14 IS <6 17 l& 19 ao developed during second week, and con- tinued till seventh. Nerve irritability increased during second week, _ passing during the third into transient depres- sion, the voltaic irritability falling more than the faradic. . j - ?. ... ... ... v.". » — -- "- —- "- --■ ••• V » :r. r-v ;;r .TV, .~ 1 71,. 1 '+* ++ ■*^ • *.. ■ 1 • . . . . . . • • • • ... . . - P __U iuuU ill! 11111 CON TIN IED NOI .MA L Fig. 41.—Slight neuritis; quick recovery of power during third and fourth weeks. Degen. react, in muscles present at the end of the second week, slowly lessening, but present in slight degree until the fourth month. Considerable increase in irritability in the nerve-trunk at the end of the second week, greatest to the faradic shock (crosses), and lasting until the fifth week. faradism and to voltaism, and it is frequently much more marked to the isolated faradic shocks than it is to either the voltaic current or the rapid succession of shocks that constitutes the faradic current. This is shown very strikingly in Fig. 41, and in less degree in Fig. 43. In the former the irritability to the two currents was the same ; in the latter that to voltaism was distinctly the greater. I have once met with a slight but distinct and prolonged diminution in faradic irrita- bility when no change could be found to voltaism (see Fig. 42). * A similar change is met with in some central diseases, as chorea and paralysis aaritnns. SYMPTOMS. 77 Lessened irritability to faradism with distinct increase to voltaism has been observed in an ulnar nerve, the seat of traumatic paralysis (Bernhardt). In one case of extensive peripheral neuritis of obscure toxic origin, in which the face on both sides was paralysed for a time— a peculiar nutritional change in the nerves, where the action of the Fig. 42. WEEKS 12. 3 V 6 6 Fig. 43. DAYSl 4- 6 8 to <1 14 -jn.l. ™ r~rt-» tlST .;.. :N _—._ _—._ .-__. -.-..».» .—. _ .._ —. P U11U1U muii IHIIII in in III 11 M I__ •.T.irT' T.T 'AT '•• :N .Th. L-.. L;^.tt *y ?"•* 7*< P mi Llil Hll Fig. 42.—Slight neuritis: power regained during the second week. Deg. react, in muscle distinct on eighth day, lessening during second and third weeks. Nerve : lowered faradic, normal voltaic irritability. Fig. 43.—Very slight neuritis. No change in muscular irritability; irri- tability of nerve-trunk increased from fourth to eighth day, most to faradic shock (crosses), least to faradic current. toxic agent was less than at their extremities, and made the nerves in- sensitive to the momentary induced current,—the voltaic excitability of the facial nerves was not lessened, although faradic irritability was lost to such a current as could be borne. The electrical excitability of a nerve and its power of conduction are usually lost together. But when a nerve is recovering from a local lesion, and regeneration is in progress below, some power of conducting the impulse that is excited above the lesion may return in the peripheral portion before it becomes excitable by any form of electricity. This is true of the impulse from the brain, and that excited by electricity. This seems to show that the nerve-fibres can conduct— that is, pass on the nerve-force they receive as such, before they can produce nerve-energy in response to the influence of a " stimulating " force acting on them. Another rare anomalous condition has been noted by Bernhardt and G-riinberg in cases of recent nerve injury. When the lesion arrests all conduction of the voluntary stimulus a strong faradic stimulation of the nerve above the lesion may still cause slight contraction in the paralysed muscles. Recovery of the nerve is attended by gradual restoration of power over the muscles, the nutrition of which slowly improves ; but if the wasting has been considerable, a long time elapses before they regain their normal size. Indeed, as already stated, they may be always somewhat smaller than the corresponding muscles on the unaffected side. Curious secondary spasmodic symptoms are common after palsy of the facial nerve (q. v.)— contractures, spontaneous contractions, and associated over-action of different muscles. The last is very rarely met with after palsy of the nerves of the limbs, but coarse, fibrillary, 78 LESIONS OF NEKVES. muscular contractions, and a tendency to cramp, are not uncommon, and may persist for years. (See also Neuritis.) Sensory symptoms also result from lesions of the nerves that contain sensory fibres. The interruption of the fibres arrests conduction, and causes loss of sensation in the part supplied by the nerve, just as it causes motor palsy. But a slight lesion of a mixed nerve may cause persistent muscular paralysis, and sensation be unaffected, or impaired only in slight degree and for a short time. This result is so frequent that we cannot ascribe it to a difference in the relative damage to the motor and sensory fibres. It must be due either to the fact that the sensory fibres recover more readily, or that a slight degree of conduction may suffice for the stimulation of the sensory centres in the brain, and not for that of the muscular fibres. There is also a third hypothesis, and that is a difference in the sensory and motor impulses in physio- logical character.* In another class of cases, however, we must seek a different explanation of the persistence of sensibility in the area supplied by the nerve. There may be no loss even when a nerve is completely divided. This is observed chiefly near the extremity of a limb. It can only be explained by what is termed " recurrent sen- sibility." Anastomoses exist between the terminal fibres of different nerve-trunks, and it would seem that this contiguity of sensory fibres suffices for conduction. Individual differences are seen to exist in this. Thus, of two persons in whom the ulnar nerve at the wrist has been divided, one may have total anaesthesia in the fingers supplied by the nerve, and in the other there may be little or no loss. The peripheral segments of the sensory fibres degenerate, like the motor nerves. We cannot test them, and ascertain the degeneration in the same way, at least in severe lesions, because their stimulation cannot be perceived. Nevertheless an altered polar reaction has been observed in slight cases, analogous to that which occurs in the muscles. A sensation is produced with the positive voltaic pole by a weaker current than is required with the negative pole. In some cases of nerve injury and neuritis a delay in conduction of pain maybe observed. Increased and disordered sensitiveness in the area of distribution of the nerve, with or without spontaneous pain, is very common in cases of partial lesions of nerves. It must be referred to the morbid changes in their fibres, alterations in the nutrition of the axis-cylinder or nerve- endings, probably analogous to the slight changes in the motor nerves which increase their excitability. Pain and tenderness of the nerve- trunk are also frequent in the same cases, due no doubt to the increased sensitiveness of the " nervi nervorum " distributed in the sheath. The sheath of each nerve is part of the distribution of its own fibres, and those that end in the sheath seem to be very readily deranged. We shall see the importance of this consideration in relation to neuritis and * The experiments of Leuderitz (' Zeitschr. f. klin. Med.,' Bd. iii) merely confirm the observed fact, and do not really explain it, as he and others have assumed. SYMPTOMS. 79 neuralgia. The pains, both local and distant, are sometimes very severe and persistent. llcflex Action.—All lesions of nerves abolish reflex action in the area of the distribution of the nerve affected, except those that involve so slight a change as to cause increased sensitiveness. Myotatic irri- tability is also lost, from damage to either the motor or sensory fibres concerned, and this loss may persist long after the other symptoms. Vaso-motor and trophic disturbance is a common consequence of lesions of nerves. It is most severe in those that are inflammatory in part or altogether. The vaso-motor nerves run in the mixed nerve- trunks, and suffer with the other fibres. The general character of the disturbance has already been described (p. 27). When the lesion is acute and irritative, vascular dilatation and an increase of temperature occur at first, and are followed by passive hyperaemia and lowered tem- perature. There may be oedema, and an increased secretion of sweat. The changes in the skin, acute and chronic, are those that have been already described. " G-lossy skin," red, smooth, and thin, is especially common, and is frequently accompanied by atrophy of the subcutaneous tissue, and perhaps of the bone, so that the finger-tips become narrow, and present an aspect that is very characteristic. Burning pain, with tenderness, often accompanies the change, and may continue for long. Occasionally, instead of becoming thin, the epidermis increases in thickness, the nails often become thick and rough, and present trans- verse or longitudinal furrows.* In parts where there is much sub- cutaneous tissue this may also become thickened and have a peculiar doughy feel, resembling that met with in myxoedema. The growth of the hair may be lessened or increased. Sloughing of the skin is far less common than in central diseases, but eruptions, particularly of the nature of erythema, eczema, herpes and pemphigus, may also be met with. Yesication occurs with extreme readiness, and sometimes vesicles or bullae appear to form spontaneously. Ulcers result which erode and destroy the tissues, especially of the finger-ends. Mustard plasters also blister the skin more readily than in health. It is im- portant to remember these facts, because the affection is one in which hot applications are often recommended. A gentleman dislocated his shoulder, and either by the displaced bone, or in the reduction, the brachial plexus was seriously injured. The muscles of the hand wasted, and the skin became glossy. He was advised by a surgeon to bathe the hand daily in hot water. One day his wife bathed it in water which to her was pleasantly warm, and which caused him no discomfort, but the result was that the hand was covered with blisters, and ulcers were left which did not heal for months. * Several excellent illustrations of these chauges are given by Bowlby, loc. cit., where also a full account of traumatic lesions is given. The observations of Bern- hardt (' Virchow's Archiv,' 1886) appear to show that the retarded growth of the nails is independent of the influence of the particular nerves. Great individual vacations are found with identical lesions. 80 COMPRESSION. The joints often suffer in their nutrition. Acute inflammation, such as occurs sometimes in spinal affections, is rare, but chronic changes in the joints are frequent, with much tenderness; alterations in the articular surfaces, and fibrous adhesions result, which limit movement. When the muscular wasting is slight, the condition may resemble a pri- mary joint affection, and this mistake in diagnosis is sometimes actually made. INJURIES OF NERVES: COMPRESSION. Traumatic lesions of nerves are in the province of surgery. They belong to the physician only in so far as their effects are produced by the agency of a neuritis, the mechanical origin of which may escape notice. Neuritis is described in the next section. A word is needed, however, on the subject of simple, slow compression of nerves, not because the symptoms are grave, but because they often give rise to very grave mental concern on the part of the patient, and to occa- sional doubts in the mind of his medical attendant. Compression of a nerve may be sudden or slow. Sudden compression bruises the nerve-fibres, producing definite lesions, and also sets up neuritis. Symptoms often occur too soon to be explicable as neuritic. A slight degree of these is familiar as a result of pressure on the sciatic nerve in the act of sitting. There is first tingling in the region of distribution of its fibres, often with a sense of warmth, with disordered sensations and even a loss of sensibility in the skin. Often this is accompanied by an inability properly to put in action the muscles that are supplied by the nerve. All the symptoms pass away in a few minutes, a sense of cold and an inability to direct movements being often the last effects. If they do not pass away, the persistent effects are ascribed to a neuritis such as is produced by any other cause. But neuritis is not the primary lesion, and the initial symptoms are not produced by the agency of inflammation. Hence, when they persist, it is doubtful whether we should ascribe them to the inflammation unless they occur after an interval. The mechanism by which the tingling and early anaesthesia are produced, probably causes also the lasting symptoms. The compression no doubt causes anaamia, but the known sensitiveness of nerves to mechanical stimulation makes it probable that the effects are chiefly produced by the mechanical influence of the pressure on the elements of the nerve-fibres, and that a compression for a few hours has such an effect in separatino- the molecular elements of the white substance, as to set up a secondarv degeneration of the same character as that which results from division of a nerve. The neuritis is thus no more the cause of symptoms in compression than in division. In each there is a displacement of molecules interrupting conduction. This is also the conclusion of Weir Mitchell, who found that a pressure of eighteen to twenty inches COMPRESSION. 81 of mercury for twenty seconds abolished the power of conduction, though only for a few minutes, in spite of conspicuous change in the white substance. The latter is still greater, and the effects more enduring, in a contusion. The cause of the tingling in the region of distribution of the sciatic nerve is, as already said, readily recognised when it is due to pressure by sitting. But it is otherwise when the pressure is on the nerves of the arm and is produced during sleep. The tingling may be felt in the region of the ulnar nerve, in consequence of flexion of the elbow, or in the whole hand, from the pressure on the nerves of the brachial plexus on the side on which the patient is lying. Waking up with the tingling, and sometimes with cramp or powerlessness in the hand, he is naturally alarmed. The diagnosis, however, is rendered easy by the unilateral character of the symptoms, and by the fact that they are always felt on the side that is bearing the weight of the body. There may, however, be great difficulty in diagnosing this form of compression from actual contusions. The symptoms are produced much more readily when the general health is bad; they last longer, and more often end in neuritis. Gradual compression may result from continuous pressure, such as that of a crutch or the growth of an adjacent tumour, or from the implication of the nerve in a cicatrix or callus. Of new growths com- pressing nerves, exostoses and aneurisms are most frequent. The symptoms of this form approach those of neuritis; they may be sensory, motor or trophic. They are ushered in by hyperesthesia, which is followed by anesthesia, seldom complete in degree or quality, tactile and muscular sensibility being usually retained when other forms are lost. Intense and persistent hyperesthesia or complete anesthesia point to neuritis. Motor weakness and trophic changes appear; there may be atrophy or hypertrophy of the nails, trophic ulcers, or joint affections. Among rarer symptoms are local spasm with fibrillary twitchings and reflex convulsions. In simple com- pression the symptoms, as a rule, disappear after the removal of the cause; the subjective sensations are the first to vanish, then the anesthesia goes, and lastly—in severe cases not till after some months —the motor disturbances. In rapid compression there may be, according to the duration of the injury, merely congestion at the affected spot or peripheral degeneration starting from it. A nerve which has been long compressed is narrow at the affected part, where it may even be flattened into a ribbon; above and below it is normal or swollen. The compressed portion may be white from anemia or red from congestion. Eventually degene- rative or neuritic changes may develop, and the former are sometimes found above the lesion as well as below Treatment is essentially surgical, but the physician must aim at maintaining the nutrition of the muscles by the usual means during the recoverv of the nerve, when this can be released frpm compression. VOL. I. 6 82 NEUitlTIS. INFLAMMATION OF NERVES: NEURITIS. Neuritis, or inflammation of nerves, presents various characters, which have led to the distinction of numerous forms. The inflam- mation of single nerves usually begins in the outer sheath of the nerve, and this has been distinguished as "perineuritis." It may involve also or chiefly the connective tissue between the bundles of nerve-fibres ("interstitial neuritis"), or the nerve-fibres themselves ("parenchy- matous or degenerative neuritis"). Some forms of neuritis have a tendency to ascend the nerve, and this variety has been termed ''ascending neuritis" or "neuritis migrans." One nerve-trunk may be primarily affected, or many nerves may suffer at the same time. The latter condition, " primary multiple neuritis," is of great import- it nee, and will be described in a separate section. Most forms of neuritis may be either acute or chronic. Acute neuritis usually subsides into a chronic stage, and its symptoms may thus persist for a long time. Other varieties that have been distin- guished depend upon the cause to which the inflammation is secondary. Thus we have cancerous, syphilitic, gouty, diabetic, and other forms. Causes.—Injury causes more or less inflammation, which occurs readily, and follows very slight damage. Neuritis may thus be set up by all sorts of wounds, by contusions, by compression from with- out or by adjacent structures, and by over-extension of the nerves. Those nerves that pass by joints are liable to injury from dislocations, either by the displacement of the bones, or during reduction. In fractures the nerves may be injured directly, or may be compressed by the callus that is formed. Nerves are sometimes damaged by a violent contraction of the muscles through which they pass. It is probable also that muscular effort excites neuritis in other situations, especially in persons who are predisposed. Moreover, a strain on the fibrous tissues of joints, fascie, &c, may set up inflammation in them, which may spread to the nerves. Neuritis may arise by extension from adjacent inflammation; this is particularly seen in the case of phlebitis. The nerves near suppu- rating joints may be involved, and even, it is said, those that pass by a joint the seat of simple inflammation. The latter is certainly rare. The intercostal nerves have been affected by extension from an in- flamed pleura. The cranial nerves and the spinal nerve-roots are involved by extension from the membranes. Exposure to cold is another cause of neuritis. It is then often called " rheumatic." The nerve, or rather its sheath, may be primarily affected, or the first effect may be inflammation of the fascie, from Avhich the inflammation spreads to the nerve-sheath. Persons who are liable to muscular rheumatism, and those who are gouty, suffer PATHOLOGICAL ANATOMY. 83 thus with especial frequency. But exposure to cold and the toxins of gout and rheumatism also act in another way, by causing a blood-state which acts on many nerves at the same time. Many general diseases have a similar power of causing either an isolated or a multiple neuritis. It is through this agency that diphtheritic paralysis is produced, and the same effect may be due to the presence of other toxic material in the blood, metallic poisons, alcohol, &c, an account of which will be found in the section on Multiple Neuritis. When an isolated neuritis occurs during an acute disease it is probably produced through the agency of compression, unnoticed during the prostration. Neuritis has also been found in the vicinity of bedsores (Pitres), and though probably due to pressure may be part of the mechanism by which they are caused. Some chronic general diseases cause only isolated neuritis,—either simple, as that which is due to gout (when the general disease must be regarded chiefly as a pre- disponent); or special, as syphilitic, cancerous, or leucocythemic neuritis, in which there is an infiltration of the nerve with the special tissue-element characteristic of the general disease. The characters of the simple isolated form constitute the chief subject of this section. Pathological Anatomy.—The changes differ according as the inflammation affects primarily the adventitial connective tissue, " adventitial neuritis," or the fibres themselves in the " paren- chymatous " form. Isolated neuritis is generally adventitial, and will be first described. In acute inflammation the affected part of the nerve is red, softened, and swollen. The redness depends on distended vessels, which may be visible on the surface; in more acute cases it may result from the presence of minute hemorrhages. The swelling is due to oedema, or to a sero- fibrinous exudation, sometimes jelly-like in aspect. The micro- scope shows leucocyte-like cor- puscles surrounding the vessels, infiltrating the sheath (Fig. 44) and a ecu nulating between it and the nerve. There may be even small extravasations of blood. Suppuration is extremely rare Fig. 44.—Neuritis: degeneration of nerve- fibres, the myelin broken up into masses, globules, and granules. Accumulation of leucocytes in uerve-sheath. From a case of multiple neuritis. (After Leyden.) These changes may be limited to the sheath in what is called "perineuritis," or may extend into the substance of the nerve in " interstitial neuritis." In the latter case the lymphoid corpuscles infiltrate the septa, and may even be seen in the substance of the fasciculi, between the nerve-fibres. These changes 84 NEURITIS. may be continuous along a considerable tract of the nerve (diffuse neuritis), but more frequently they are chiefly marked at certain places, which are separated by portions of the nerve which are so little affected as to appear to the naked eye to be normal (" focal" or "disseminated neuritis"). The foci of inflammation are chiefly situated at places where the nerve turns round a bone, or emerges from canals or fascie, or divides. The extent to which the nerve-fibres suffer varies much. They usually present little change when the inflammation is limited to the sheath, unless the nerve lies in a bony canal, or in rigid fibrous tissue, within which the sheath cannot expand; its swelling then exerts pressure on the fibres. When the inflammation is interstitial the fibres suffer more readily, although not invariably. On the other hand, they are sometimes found much altered, when the connective- tissue elements are but little affected. In this case the inflammation is " parenchymatous " and begins in the nerve-fibres, the interstitial tissue being secondarily involved or unaffected. The changes in the fibres are almost the same as in degeneration (Figs. 33 and 34). It was pointed out how closely the two processes of inflammation and degeneration are connected, and how difficult it is to separate, or even to distinguish them, in many cases. The myelin of the white substance first breaks up into segments, more or less elongated, often with smaller globules of myelin between or beside them. The masses are cloudy or finely granular in aspect. The axis-cylinders are inter- rupted where the myelin is divided. The nuclei of the sheath are increased in number, and the protoplasm around them is increased in quantity. Next the myelin is divided into smaller globules and granules, and the axis-cylinder is no longer recognisable. The myelin then disappears in parts of the tubes, while it remains at other parts, but is still more finely divided. Lastly, the sheaths become empty and very narrow, containing only nuclei at intervals, with here and there a little finely granular material, or sometimes some brownish pigment granules. The process may thus go on to complete destruc- tion of the fibres. These commonly suffer unequally; fibres that have a normal appearance are scattered among those that are much altered. In chronic interstitial neuritis the axis-cylinders often suffer less than the white substance. The latter becomes atrophied, so that the fibres are smaller than normal. If the interstitial inflammation is very intense the fibres may break up as above described. As the inflam- mation subsides, the new cellular elements that have made their appearance assume the aspect of fusiform cells, and fibrous tissue is developed, either from these cell-., which become less numerous or from the intercellular exudation. This fibrous tissue surrounds and encloses the fasciculi, a condition that has been termed " sclerosis of the nerve." A firm fusiform swelling may remain at the affected spot and this may be adherent to adjacent structures. The axis-cylinders SYMPTOMS. 85 are unequally affected. Those which are involved undergo typical degeneration. Sometimes fat is ultimately formed in the new con- nective tissue, a condition that has been rather unnecessarily termed " Hpomatous neuritis " (Leyden) ; the fatty deposit does not seem to be related to any special form of neuritis. Occasionally the connective tissue overgrowth is so extensive that the whole nerve is converted into a sclerotic cord (Virchow's " proliferative " form). In syphilitic neuritis, which affects chiefly the cranial nerves, there is a cellular growth in the sheath and interstitial tissue similar to that which constitutes other syphilitic new formations, with a variable amount of alteration of simpler inflammatory character. The growth in the sheath may amount to a distinct syphilitic tumour, with or without interstitial changes. In cancer, nerves adjacent to the new growth may present simple interstitial neuritis, or may be infiltrated by a growth of cancer-elements spreading to the nerve by direct extension. In leucocythemia there is a dense infiltration of the nerve with leucocytes. The destructive changes in the nerve-fibres extend down the nerve to the periphery in a process of secondary degeneration, more or less inflammatory in nature, as already described in secondary degeneration. Usually the central portion of the nerve remains free, the alterations ceasing a short distance above the seat of the primary inflammation. In rare cases an ascending neuritis (n. migrans) passes up the nerve, and may spread, at a plexus, to other nerve-bundles and other nerve- trunks. The formation of fibrous tissue in the inflamed part, and the cicatricial contraction of this tissue, often prolong the irritation of the nerve-fibres and the symptoms due to this, and a state of " chronic neuritis " is said to be left. Symptoms.—The symptoms of neuritis vary extremely according to its intensity, its extent, and the nerve that is affected. In three places, the brachial plexus, the sciatic nerve, and the crural nerves, the sym- ptoms are sufficiently special to make their separate description desirable, although the general account applies to them also. The onset of the acute form is sometimes attended by some con- stitutional disturbance, especially when many nerves are affected. The chief symptoms are local. The most prominent is pain, felt in the inflamed part of the nerve, and also often in the part to which it is distributed (see p. 78). Sometimes the pain involves the whole limb, and in severe cases it may be most intense, burning, boring, rarely darting, in character ; it is usually worse at night and increased by movement, by postures that involve tension or pressure on the nerve, and by whatever causes passive congestion of the limb, such as the act of coughing. Sometimes it seems to radiate into distant parts, and not rarely pain is also felt in the corresponding region of the opposite limb. The sensitiveness of the whole of the affected region is increased, and even the bone may be tender, so that at first attention may not be directed to the nerve, but when this is pressed great pain 86 NEURITIS. is always produced. In slighter cases the pain is usually limited to the nerve and its distribution. It may, indeed, be absent when the nerve or branch is chiefly motor, a fact difficult to explain unless the sheaths of such nerves contain fewer sensory fibres than usual. If the nerve is accessible to direct examination it may be felt to be distinctly swollen at the affected part. Occasionally the skin over it has been observed to be red, and rarely there has been slight oedema. Spontaneous sensations may be felt in the region supplied by the nerve, tingling, &c, and the skin may be hyperesthetic. After a time, as the nerve-fibres suffer, sensation may be perverted, or even lessened; complete anesthesia is usually confined to small areas. The muscles supplied by the nerve become weak in various degree, tender, and present fibrillar twitchings; they are seldom powerless, but pain may prevent their contraction. They present the altered electrical reac- tions characteristic of nerve-lesions. Increased perspiration has been observed in the part of the skin supplied by the inflamed nerve, very rarely it is arrested, and sometimes, although rarely, eruptions occur. Herpes is not common from ordinary acute neuritis. The epidermis may become thickened into a state like ichthyosis, or may atrophy and appear as " glossy skin." Effusion into joints has been observed in .very rare cases. The constitutional disturbance which may attend the onset subsides in the course of a few days, but the pain and other symptoms usually persist in undiminished severity for several weeks. They ultimately slowly subside into a chronic stage, and may continue as a secondary neuralgia due to a habit of over-action set up in the centre. In the chronic form constitutional disturbance is absent, and pain is the prominent symptom from the first. The affection of motion and sensibility, and the trophic changes, are similar to those met with in the acute form. In both forms the muscles may waste, and present the reaction of degeneration when they are tested with electricity (p. 73). In slight cases the initial increase of excitability in the nerve is often well marked. Trophic changes in the skin are very common; so is alteration in the nutrition of the joints, and adhesions form, limiting the movement, and fixing the parts in the position corre- sponding to the muscular inaction. When neuritis ascends a nerve, the symptoms gradually extend in area; and if it reaches the plexus from which the nerve proceeds, they may extend to most or all the nerves of the limb. This " ascending neuritis" is not rare in man, may even reach the spinal canal, and there produce various disturbances. The inflammation may spread in the tissue outside the dura mater, or may extend to the cord, and cause subacute or chronic myelitis with or without meningitis. The paralysis that occurs secondarily to some visceral diseases, as those of the bladder, and commonly regarded as reflex paralysis, is probably produced through the agency of an ascending neuritis. Lastly, the inflammation may extend to the nerves of the DIAGNOSIS---PROGNOSIS. 87 other side, usually to those that correspond to the primary seat of the disease. Such extension may be through the spinal cord or the membranes, but in some cases symptoms occur in the nerve of the opposite side, without any indication of an affection of the centres. Experiments on animals have demonstrated that such implication of the opposite nerve may occur when the centres are unaffected. It has been called " sympathetic neuritis." We have seen that reflected pains are occasionally felt in the corresponding nerve on the opposite side, and it is probable that, as in neuralgia, vaso-motor disturbance in the nerve-sheath may accompany such pains, and, in a predisposed person, may cause actual neuritis. The Duration and Course of neuritis vary much. A slight acute neuritis may run its course in a few weeks and then subside. Much more commonly the affection persists in a chronic stage for many weeks, or even months, and slowly passes off The rheumatic and gouty forms are as a rule much more tedious than those that result from injury, although traumatic neuritis is sometimes very insidious and may last a long time ; it may ascend the nerve from its starting- place and become localised in certain situations, where it may develop afresh, and give rise to symptoms that often seem to be independent of their cause. In the predisposed, it can set up troublesome local functional disturbance, hysterical contracture, and the like. Diagnosis.—The diagnosis of neuritis depends, first on the localisa- tion of the symptoms to the distribution of a certain nerve-trunk, and secondly on the pain and tenderness in the nerve. The diffuse pains that attend the onset may be readily mistaken for the pains of acute rheumatism, or for those due to an inflammation of the bone, but in the course of a day or two the localisation of the symptoms declares their nature. The chronic form is easily and often mistaken for neuralgia, and the diagnosis is the more difficult because many so-called neu- ralgias are really due to neuritis. The distinction can only be fully discussed when we have considered the symptoms of neuralgia, but it rests chiefly on the fact that in neuralgia the pain intermits more completely than in neuritis, there is not the same initial tenderness in the nerve-trunks, and the tender spots have a more uniform localisation. Lessened sensibility or change in the muscles, showing organic damage to the nerve-fibres, are conclusive evidence of neuritis. The pains in some central diseases, chiefly those of the spinal cord, may be thought to be due to neuritis, but there is not the local tenderness of the nerve-trunk, and the pain is not limited to the distribution of a single nerve. As we shall see presently, the diagnosis of multiple neuritis from affections of the cord is far more difficult. Prognosis. —The gravest form of simple neuritis is that in which the nerve is affected secondarily to a local suppurative inflammation. The prognosis is best, as a rule, in traumatic neuritis, but the rule is one to which the exceptions are occasionally very considerable in degree. A neuropathic disposition makes the prognosis worse. In all cases 88 NEURITIS. the intensity of the symptoms, and the evidence of descending degene- ration, furnish a more trustworthy guide to prognosis than does the mere form of the affection The effects of complete degeneration always endure for some months. Regeneration does not occur until the original cause has ceased to act, and then occupies many weeks in its progress to the restoration of functional competence. In all forms pain is apt to linger on, and the longer the older the patient is. Treatment.—The first consideration in the treatment of neuritis is the removal of its cause, if this can be discovered. A wound or injury or local inflammation adjacent to the nerve must be dealt with by appropriate measures. Any constitutional cause, such as gout, must be treated. For the inflammation of the nerve, it is of the first importance to secure to the part as perfect rest as possible. Move- ment causes mechanical irritation of the nerve, and involves functional stimulation of its fibres, both of which are injurious. The nerves of a limb run between muscles, and the contraction of these muscles causes pressure on the inflamed nerve, and irritates it, as the pain thus produced sufficiently shows. Pain is indeed a useful indication of the harmful influence of movement, since the stimulation of the nerves of the sheath, in which the pain is produced, doubtless has also a reflex effect, increasing the vaso-motor element in the inflammation Hence it is most important that all movement that causes pain should be avoided. The posture of the limb should be such as to involve the least pain and the least danger of secondary contracture. The general treatment of an acute neuritis must be that suitable for any acute local inflammation, whatever its seat,—an unstimulating diet, an aperient, and diuretics. In gouty cases a brisk purgative may, with advantage, be given. General diaphoresis is useful in cases that are due to cold, and in others local sweating is often of distinct service. The limb may be steamed, or exposed to hot air. This should be followed by hot fomentations applied along the course of the affected nerve, and these by linseed-meal poultices. Leeches may also be employed at the onset of severe cases. When the inflammation results from injury, cold may be applied along the course of the nerve instead of heat; both probably modify the vascular disturbance of inflammation in a similar manner. Counter-irritation may be used at the onset of slight cases; but when the inflammation is severe, this agent is more effective during the subsidence of the inflammation than during its active stage Blisters, repeated mustard plasters, or stimulating liniments may be used, but care must be taken not to blister skin that is anesthetic, or troublesome ulceration may be caused. The same caution is necessary in regard to hot applications, as is shown by the case mentioned on p. 79. Spontaneous pain requires sedatives, of which the hypodermic injec- tion of morphia is by far the most potent. It should be used only for spontaneous pKin, and not to enable the patient to use the limb in a way that would produce pain if morphia were not given. Mechanical TREATMENT. 89 irritation may be equally injurious, although the pain which it would cause is obviated by the sedative. Moreover it should only be used as a last resort, when the agent to be mentioned next is inadequate. Morphia has little influence on the morbid process; it lessens the effect of the disease on the brain only by acting on the brain. In cocaine we have an agent capable to a large extent of replacing morphia, and of a greater therapeutic capacity. Although it has less power of relieving pain, it is capable of doing much more than that. It arrests the local transmission of the impulse- that cause pain, and so, at a limited region, it does lessen pain and often remove it for a time, and the local character of its action enables it to exert a simul- taneous influence on the morbid process. It prevents the irritative influence on the inflamed structures of the impressions that are felt as pain, which we have just considered; and the entire arrest of the influence, even though the region is small, seems to produce a much greater effect on the process than might be anticipated. It is in- structive to note the opposite influence, revealed by the occasional redness of the skin and subcutaneous oedema, along the course of the inflamed nerve. The injection should be made at one of the seats of pain. In the rheumatic form salicylate of soda has been given, but is of doubtful value. Iodide of potassium sometimes seems to be useful, but no agent has so distinct an influence on the process of inflam- mation in the nerve as small doses of mercury. A grain of blue pill may be given once or twice a day; and if morphia has to be injected at the same time, the mercury is useful also in correcting the constipating influence of the morphia. In the chronic stage or form, counter-irritation, by blisters or cautery, is of great value. So also is electricity, which has little influence during the acute stage. The voltaic current should be used. The positive electrode may be placed over the inflamed part of the nerve, or over the seat of pain, and kept there for ten minutes at a time, the strength of current being slight, such as the patient can just perceive. In very chronic cases a stronger current, sufficient to cause actual pain, is of service, applied in a similar n anner, but for a shorter time. It has probably chiefly a counter-irritant influence, and faradism may be used in the same way. All painful impressions on the skin lessen, for a time, the nerve-pain. The muscles supplied by the inflamed nerve may be left alone, unless their wasting is marked, or the degenerative reaction shows serious damage to the motor fibres. In cases of moderate severity thev will recover when the nerve recovers. All that is desirable is that they should be gently rubbed once or twice a day. If the Avasting is considerable, however, or there is degenerative reaction, they should be stimulated to gentle contraction by a weak, slowly interrupted voltaic current. They should on no account be faradised during the active stage of the affection, even if they act to faradism. The acute pain that the faradic stimulus causes, and the increased tender- 90 NEUROMA. ness that lasts for hours afterwards, are evidence of its injurious effect. In all cases attention to the general health is of great importance. Tonics are needed during the chronic stage. Change of air will some- times remove, in a few weeks, symptoms that have previously been stationary for months. The modifications of treatment that are rendered necessary by the position of the neuritis will be considered when we come to speak of the affections of the several nerves. The pathological varieties of neuritis only need special treatment in so far as they depend upon special causes, and this point, as already mentioned, must always be one of the first considerations. MORBID GROWTHS IN NERVES : NEUROMA. The term " neuroma" has been applied indiscriminately to all morbid growths situated on the peripheral nerves. The discovery, by Virchow, that many of these consist of a growth of nerve-fibres, while others consist of heterologous tissue such as constitutes morbid growths elsewhere, has led to the distinction of the former as " true neuromata " and the latter as " false neuromata," or " pseudo-neuro- mata," and even to the limitation of the term " neuroma" to a growth of nerve-tissue, whether in the central or peripheral nervous system, the heterologous growths being called by the names they bear in other situations, as " fibroma," " sarcoma," &c. The latter system of nomenclature, although certainly more consistent, has not become current in this country. The true neuromata may consist of meduUated or of non-medullated nerve-fibres, termed " myelinic " and " amyelinic " forms by Virchow. The latter were for a long time regarded as fibrous. The occurrence of ganglion-cells has been proved in only one or two instances. There is connective tissue between the nerve-fibres, which varies in amount and in character, and hence the firmness of these tumours also vajies. This interstitial tissue may be so abundant as to constitute an inter- mediate form between the true and false varieties. This is probably the condition in most cases of multiple neuromata. The " false neuro- mata " may be of various nature, but fibrous growths, " fibromata," are far more common than any other kind Myxoma occasionally occurs, the new mucoid tissue growing from the neiwe-sheath. In one case* a myxo-fibroma as large as a goose egg involved the * Schuster, • Zeitschr. f. Heilkunde,' 1886, vii. NEUROMA. 91 sheath, and pressed on the median nerve, a piece of which, when resected with the tumour, showed hyaline degeneration of the medul- lary sheath, the axis-cylinders persisting in a slightly swollen condi- tion. Glioma is very rare on the peripheral nerves, although occa- sionally found on the auditory nerve; it should be remembered that this form of growth arises from the same embryonal tissue as true neuroma. Various forms of sarcoma have been met with. Carci- noma also occurs, very rarely as an isolated growth, but not un- commonly as a more or less diffused or nodular infiltration of the nerve, arising by extension from a contiguous growth.* Syphilitic growths are common on the cranial nerves within the skull, but are rare elsewhere. In lepra anesthetica the nerves are infiltrated with fibrous tissue, enlarging them to many times their normal size. The enlargement is rarely nodular, and is rather a chronic cirrhotic inflammation than a growth. (See Leprous Neuritis.) A curious variety of neuroma, consisting of interlacing cords, more or less nodular and tortuous, is termed plexiform neuroma. The disease commonly begins in foetal life, and is most common on some branch of the fifth nerve in the orbit or the upper eyelid, but has been met Avith over the temporal bone, in the lumbar, cervical, brachial, and solar plexuses, on the penis and the mamma. It may be quite superficial or deeply seated. The cords, from 1 mm. to seve- ral centimetres in diameter, consist of a clear outer zone of concentric fibrillar connective tissue, of inner looser nucle- ated tissue, and, in the middle, a bundle of nerve-fibres, some normal, others de- generating. The cords are connected too*ether by loose tissue, sometimes myxomatous, separated from the proper tissue of the cords by an epitheliated space. The growth of this form is extremely slow, but it may exert compression on adjacent structures.! A remarkable case of extensive myxomatous disease of the nerves of the forearm, congenital in origin, pre- senting analogies to plexiform neuroma, is recorded by Mr. Be Morgan. J * A unique case of rhabdomyoma occurring in a nerve is recorded by Orlandi (' Arcb. p. 1. sc. rued.,' xix, 5). t Marchand, ' Virchow's Archiv,' Bd. lxxvi, p. 36. X ' Path. Trans.,' vol. xxvi, p. 2. FiG. 45.— Plexiform neuroma from the orbit. (After Mar- cband.) The connective tissue surrounding the cords has been removed except at a.and irregular,cylindrical, nodular cords are seen anastomosing. A nerve passes into the tumour and suddenly becomes enlarged. 92 NEUROMA. The subcutaneous extremities of sensory nerves are sometimes enlarged into minute tumours which, when painful, have been termed " tubercula dolorosa." Neuromata in the skin may co-exist with similar tumours on the nerve-trunks. Those shown in Fig. 46 are from the same case as the tumours represented in Figs. 47—49. The size attained by growths on nerves varies from that of a child's head to a nodule only just visible. They rarely exceed the dimensions of the closed fist. The variation in size of multiple neuromata is illustrated in The large tumour (Fig. 47) was the size 0 FiG. 46. —Cutaneous neuromata from skin of abdomen. (After Smith.J Figs. 47—49, after Smith.* of a lemon, but in the same case a growth from the sciatic plexus Fig. 47. Fig. 48. Fig. 49. Fig. 50. FiG. 47.—Right elbow of a man, set. 30, with multiple neuromata; those on the nerves of the arm are visible beneath the skin as mouiliform series of swellings along the course of the nerves (After Smith.) Fig. 48.—Part of the brachial plexus and nerves of the arm. Fig. 49.—Neuroma of the posterior tibial nerve, same case. The tumour wos the size of a lemon, and could be felt in the popliteal space. The flattened buudies of fibres of the nerve were separated and passed over the surface of the tumour. The portion of nerve to the right is a piece of the external popliteal. The tumours caused no in'eif'erence with function. The patient died of enteric fever. One large tumour filled the pelvis. Fig. 50.—Small neuroma of popliteal nerve laid open. It is seen to lie within the sheath. It caused no symptoms during life. (After Smith.) almost filled the pelvis. They may occur on any nerve in the body, cranial or spinal, and are sometimes numerous on the pneumogastrics, spinal roots, and sympathetic plexuses. When neuromata are multiple * R. W. Smith, ' Treatise on Neuroma,' 1849. Many instructive cases have been collected by Bowlby (' Diseases and Injuries of Nerves'). CAUSES. 93 they are often extremely numerous, and almost every nerve in the body may be transformed into a chain of growths. In the case figured more than 200 were counted in the right arm alone, and the total number of growths in the body cannot have been less than 1000, while in another 3020 were counted.* These multiple neuro-fibromata have a great tendency to undergo sarcomatous degeneration. They have hence been termed " secondarily malignant neuromata."t The tumours are almost always within the sheath of the nerve (Fig. 50). Sometimes they are on one side, and the nerve may pass by unchanged. More often the substance of the nerve is involved, and the fibres may be separated and spread out on the surface (Fig. 49). Even then they may not be damaged. They suffer far more in heterologous growths than in true neuromata Causes.—The causes of neuroma are generally obscure. Multiple neuromata are sometimes hereditary, and are probably due, in most cases, to a congenital tendency of tissue growth. Plexiform and multiple neuromata have been met with in the same family. They are said to be sometimes the result of general neurotic predisposition, and evidence of this is found in the occasional occurrence of neuro- mata in the subjects of cretinism or idiocy, of which some remarkable examples have been recorded. It is now generally held that multiple and plexiform neuromata, together with the affection known as ele- phantiasis neuromatodes, are results of the same congenital process.X Multiple neuromata are said to be almost confined to men. The isolated form is not uncommon in women. They may occur at any age. Virchow believes that they are unusually common in the phthisical and scrofulous. Of traceable immediate causes the most frequent is traumatic injury. Pressure, punctured wounds, or division of the nerves may give rise to them, apparently by a perversion in the process by which cicatrisation takes place. A well-known instance is the formation of the so-called " amputation neuromata," or " bulbous nerves," round or oval growths, the size of a bean or larger, which form on the divided extremities of the nerves in the stump left after an amputation. The occurrence of new growths containing nerve-fibres may seem to be very remarkable. We must remember, however, how frequently they are connected Avith traumatic causes, i. e. take origin in cicatricial processes. In such processes the nerve-fibres present a remarkable power of groAvth. Ranvier has shown that from the end of each old fibre several new fibres grow, only one of which probably ultimately persists. Under apparently mechanical influences some of these fibres may twist about, and even turn and grow upAvards. It is thus not * ' Med. Times and Gaz.,' 1883, i, p. 152. t Garre, * Beitrage z. klin. Cbir./ ix; Sclieven, ibid., xvii. X See especially Finotti, ' Virch. Arch.,' cxliii. Some go so far as to include molluscum fibrosum in the same category (Soldau, * Inaug. Diss.,' Berlin, quoted in ' Virch. Jabrb.,' xxx, i, p. 231). 94 NEUROMA. difficult to understand that a true neuroma may result from injury to a nerve; it is said, indeed, that the ends of the nerves in amputation stumps are generally enlarged into minute bulbs, which contain more fibres than do the nerves on which they are situated.* Symptoms.—These may be entirely absent, especially in the case of multiple (true) neuromata, which are sometimes discovered post mortem when their existence has not been suspected. Often, how- ever, they cause marked symptoms. The most frequent is pain seated in the tumour (which may be extremely tender) or referred to the distribution of the nerve, often acute, burning, or darting, and frequently intermittent. It may be increased by pressure on the tumour. In the case of the terminal neuromata local pain may be the only sensory symptom; but when the nerve-fibres suffer, parsesthesise, numbness, or formication may be complained of, and ultimately sen- sation may be lessened or lost. Paralysis of the muscles supplied by the nerve is occasionally met with, the region paralysed corresponding to the distribution of the nerve on which the tumour is situated, except in the case of neuromata in the cauda equina, from which paraplegia may result, with flexor spasm. A neuroma of the pneumo- gastric may cause grave cardiac disturbance, sometimes increased by pressure on the tumour. More common motor symptoms are reflex spasms in adjacent or even distant muscles. For instance, in a case of " bulbous nerves " in the stump after amputation at the shoulder-joint, the muscles on that side of the neck were in constant clonic spasm. Occasionally epileptiform convulsions are produced, and have been known to cease when a painful neuroma had been excised. The occurrence of these symptoms has little relation to the size of the tumour. When the neuromata are in accessible situations they may be felt. Sometimes they give rise to visible tumours, and in multiple neuroma the course of the superficial nerves may be marked out by lines of bead-like swellings, as in Fig. 47. The cutaneous neuromata also cause visible swellings. The whole abdomen was covered with such nodules in the case recorded by Smith (Fig. 46). They are sometimes not sensitive, sometimes exquisitely tender and most painful, especially when closely united with the skin. Pressure on the nerve above the tumour commonly lessens the pain. Plexiform neuroma rarely causes other symptoms than the signs manifesting its local presence. The functions of the nerve-fibres involved are not usually interfered with. Once or twice anaesthesia of the skin has been observed. Course.—The growth of neuromata varies greatly in rapidity. When symptoms occur they most commonly last for a long time, increasing in severity, and f lorn the long-continued pain the patient may ultimately be worn out. In other cases the symptoms show * Bowlby, loc. cit., p. 20. DIAGNOSIS—PROGNOSIS—TREATM ENT. 95 little tendency to increase, and in rare instances they may lessen in severity and even disappear. Diagnosis.—The recognition of the existence of a neuroma depends on its superficial position, or on the production of symptoms of damage to the nerve. The latter, when existing alone, are equivocal, since they may be due to pressure on the nerve from an adjacent growth, or even to neuritis. The disease may be suspected if symptoms—pain, numb- ness, weakness—occur, limited to the distribution of a nerve-trunk, and no cause of external pressure can be discovered, and the long course of the symptoms makes it unlikely that they are due to neuritis. The diagnosis can, however, only be certainly made when the tumour can be felt. Secondary subcutaneous sarcomata may very closely resemble neuromata. The diagnosis of the kind of neuroma, whether " true " or " false," i.e. composed of nerve-fibres or other tissue, is very difficult. Multiple neuromata are usually true, and of very slow growth; false neuromata are rarely multiple unless they are of infecting nature and rapid in development. The existence of idiocy, or other neuropathic indication, is in favour of the neural nature of the tumours. The lateral position of the growth on the nerve is in favour of its " false " character. The diagnosis of plexiform neuroma is only possible when the tortuous nodular cords can be felt. Prognosis.—This depends on the existence of symptoms. If these are absent, unless the tumour is of rapid growth, there is good reason to hope that they will not occur. In multiple (true) neuromata the nerve is less likely to suffer than in isolated growths. If symptoms are present the prognosis is less favorable, and depends on the ten- dency which they exhibit to increase. Treatment.—Medicines are useless except in the syphilitic forms of nerve-tumour, not here considered. Extirpation is the only remedy. If the tumour is lateral, and can be shelled out, the removal entails little risk. If, however, the growth infiltrates the substance of the nerve, the affected part must be excised, and the ends brought together. The risk of permanent loss of function in the nerve is great, and in deciding on such an operation, the urgency of the symptoms, and the importance of the function of the nerve, must be taken into consideration. After the extirpation of such tumours, the tendency of cicatricial processes in nerves to go on to the formation of similar growths (seen in " bulbous nerves ") renders the chance of relapse considerable. The operation reproduces conditions favorable for the activity of whatever predisposing influence aided in the original development of the disease. When neuromata are multiple, surgical treatment is out of the question, except for isolated tumours that cause distress. In the case of terminal neuromata—whether the cutaneous " tuber- cula dolorosa " or the amputation neuromata—excision is practicable, and it is unattended with the risks attending interference with a 96 SPINAL NEKVES. nerve in its continuity. In amputation flaps the chance of a relapse is considerable. In plexiform neuroma excision is undesirable, and no other treatment is of any use. Pain, and the reflex spasm, that are so distressing in amputation neuromata, need relief when attempts to cure have failed. By nerve- stretching we may perhaps give relief without the effects that follow excision, and in cocaine we have a means of arresting for a time the ingoing impulses that play an important part in generating the symptoms. The rest thus given to the centre is absolute, and its degree and frequent repetition may compensate for its brevity. DISEASES OF SPECIAL NERVES. The diseases of the cranial nerves may be most conveniently considered in connection with the diseases of the brain. Here, therefore, only the affections of the spinal nerves will be described, in so far as they present special features. The effect of paralysis of the individual muscles has been already described in detail, and need not be here repeated, except in general terms, or in so far as the association of palsies resulting from a nerve-lesion presents a parti- cular character. Phrenic Nerve.—Impaired function of the phrenic nerve is commonly the result of disease of the spinal cord, or of the roots of the nerve—the third and fourth cervical trunks—from disease of the membranes or the bones. The deep position of the nerve-trunk pro- tects it from injury, but it is occasionally damaged in wounds of the neck, and in its course through the thorax it may be compressed by tumours, aneurisms, &c, or involved in inflammations of the pleura. Paralysis of one nerve sometimes follows exposure to cold, and is ascribed to neuritis. That of both has been met with in multiple neuritis; it has also been observed following diphtheria and influenza, in the course of tabes (Cerhardt) and progressive muscular atrophy, and in poisoning by lead and alcohol. In disease of the spinal cord and membranes both nerves are usually paralysed; causes acting on the nerve-trunk usually affect one only. The effect and symptom of paralysis is inaction of the diaphragm (see p. 33). If one nerve only is affected, the diaphragm does not descend on that side, but the movement of the other side lessens the resulting defect of movement, and it can then be detected only by close <" uservation. The loss of the action of the diaphragm has little effect on the respiratory functions while the patient is at rest, but dyspnoea is said to be readily pro- duced by exertion; the breathing then becomes quick and the voice NERVES OP THE ARM. 97 feeble. At the same time this is probably chiefly because too much and too constant work is thrown on the upper thoracic muscles of extraordinary breathing. Any lung disease, such as an attack of bronchitis, is rendered far more serious by the diminished breathing power. When the diaphragm is paralysed, the movement of the thorax is often increased, and the expansion of the lower part may draw forwards the adjacent abdominal wall. This must not be mis- taken for the effect of the descent of the diaphragm. Paralysis has to be distinguished from (1) abnormal ner o is breathing. The dia- phragm is used little in extraordinary breathing, which is chiefly by the upper part of the thorax, of the " superior costal type," as it is called. Hysterical and nervous patients will often breathe, for a time, only in this manner, even when at perfect rest, especially when they are under observation. Such breathing is no doubt facilitated in women by the fact that the diaphragm is habitually used by them less than by men. Repeated examination may be necessary to deter- mine wl let her there is any real paralysis of the diaphragm in these cases. A single diaphragmatic inspiration settles the point. The patient's attention should be distracted, and she should not be aware of the object of the examination. (2) Inflammation of the diaphragm may arrest its movement, and so also may diaphragmatic pleurisy or peritonitis—each distinguished by the fact that it is usually secondary to adjacent inflammation, and any movement causes characteristic pain. (3) A primary and isolated degeneration of the muscular fibres of the diaphragm has been described by Callender and others as com- mon after death, but it has not yet been proved to cause symptoms, and needs further investigation. Paralysis may be due to disease of the nerve, its roots, or of the spinal cord. In the latter case other muscles always suffer; in the former the diaphragm usually suffers alone, the result of peri- pheral neuritis. The distribution and the course of the other palsies are distinctive. By far the most common cause is disease of the spinal cord, local or ascending from below and adding this final effect to the preceding palsy of the intercostals. In disease of the nerve-roots there are other indications of the position of the disease. The affection is often overlooked because not searched for, especially in local disease of the cervical cord. The observer forgets that its associations are not with the lower dorsal muscles, and he omits to look for it in cases in which the cervical cord is suffering and other respiratory muscles act well. If there is reason to suspect partial neuritis as from cold, hot fomentations at first, and afterwards counter-irritation, should be applied over the lower and inner part of the anterior triangle of the neck. The only other special point in treatment is the apphcation of electricity. The nerve may be stimulated by pressing the rheophore deeply outside the lower part of the clavicular portion of the sterno- mastoid. The other pole may be placed at the epigastrium or over the VOL. i. 7 98 SPINAL NERVES. corresponding half of the diaphragm. But the influence of electricity on paralysis of the diaphragm is not sufficient to make its use desir- able. In the cases in which such treatment could do good the affec- tion is transient and comparatively unimportant. In central disease electricity has very little influence. Nerves op the Upper Limb. The nerves of the arm and shoulder are derived from the five lower cervical and the first dorsal nerves. These interlace in the brachial plexus in such a complex manner that most of the nerves of the arm are derived from many spinal roots. The nerve-roots form, by their union, three trunks, which we may indicate by Roman numerals. They are formed thus :—I, by the branch from the fourth, and the roots of the fifth and sixth cervical; II, by the seventh ; and III, by the eighth cervical and the first dorsal. Each trunk divides into two parts, and the union of these divisions forms the three cords of the brachial plexus from which the nerves of the arm proceed. But before the primary trunks divide, certain nerves arise, the origin of which is thus less doubtful. The fifth and sixth cervical roots give origin directly to the posterior thoracic nerve for the serratus, and from the cord formed by their union springs the supra-scapular nerve. The three cords of the plexus have the following relations:—The posterior is derived from all three primary trunks, and gives rise to the subscapular nerve, the circumflex, and the musculo-spiral (or radial, as the whole nerve is sometimes termed). The upper or outer cord is derived from the two upper primary trunks, i. e. from the fourth, fifth, sixth, and seventh cervical roots, and from it proceed one anterior thoracic and the musculo-cutaneous nerves, together with the outer head of the median. The inner or lower cord is derived only from the lowest primary trunk, i. e, from the last cervical and first dorsal, and gives rise to the ulnar, the inner head of the median, the internal cutaneous, the intercosto-humeral, and to the second anterior thoracic nerves. It may be convenient to put these coarse anatomical relations in the form of a table. Nerves. Primary Trunks. Subscapular Circumflex Musculo-spiral 3 Post. cord I. 4, 5, and 6 C. II. 6 and 7 C. III. 8 C> Nerves. /8C.\ IidJ . Upper cord Lower cord ["External ant. thoracic. -| Musculo-cutaneous. [Outer head oi~\ r median. Inner head of J Ulnar. Internal cutaneous. Intercosto-humeral. Internal ant. thoracic. These anatomical facts, however, give us little help in tracing the relation of the nerves to the spinal roots. The investigations of Ferrier and Yeo,* who * 'Proc. Roy. Soc./ March 2Lst, 1881. Careful dissections by Herringliam (cf. March 25th, 1887) give somewhat different results, but this method of investigation is open to more uncertainties than that of stimulation. Herringham's conclusions should, however, be noted by future investigators. NERVES OP THE ARM. 99 ascertained the movements produced by faradising the several spinal roots in the monkey, show us the way in which the movements, muscles, and nerves are represented in the spinal roots. Their results are therefore of great interest, although we are not justified in transferring the facts to man except in so far as they receive confirmation from human anatomy and pathology* Subject to this reservation, the chief results are important, and may be thus stated :f The roots to which the several nerves are thus traced are as follows:—Sub- scapular, 6 and 7 C.; circumflex, 4 and 5 C.; musculo-spiral, 4, 5, 6, 7, 8 C.; musculo-cutaneous, 4, 5 C.; median, 5, 6, 7, 8 C.; ulnar, 8 C, 1 D. Still more important are their observations on the relation of various move- ments of the arm to the nerve-roots, and these are as follows: Cervical 4 — Elevation and retraction of the arm, flexion and supination of the forearm; by the rhomboids, supra- and infra-spinatus, biceps, brachialis, and supinators. Cervical 5.—Similar to the last, but without retraction of the arm, and with -extension of the wrist and first phalanges; by the deltoid, serratus, flexors of elbow, extensors of wrist, and long extensors of fingers. Cervical 6.—Adduction and retraction of the upper arm, extension and pro- nation of the forearm, flexion of the wrist; by contraction of the pectoralis, latissimus dorsi, triceps, flexors of wrist, pronators. Cervical 7.—Adduction and rotation inwards at the shoulder-joint, flexion of the wrist, and of the fingers at the second phalanx; by the teres major, latissimus dorsi, subscapulars, triceps, and long flexors of the fingers. Cervical 8.—Flexion of fingers and thumb so as to close the fist; flexion of wrist towards the ulnar side, pronation of forearm, extension of elbow; by the intrinsic muscles of the hand, the long flexora of the fingers and thumb, the flexors of the wrist and the triceps. Dorsal 1.—Adduction of the thumb, flexion of the fingers at the metacarpo- phalangeal joints ; by the interossei, &c. Thus most movements are related to many spinal roots. The nerves supplying each muscle have a correspondingly multiple relation to the spinal roots. It cannot be traced anatomically, but has been ascertained by comparing the results of experiments on animals with those of disease and injury in man, and (in the case of sensation) of the division of roots for the treatment of some forms of disease. The facts thus ascertained have been confirmed by cases of disease of the spinal cord itself, which, when sufficiently limited to be significant, have been found to agree closely with observations on the roots. The con- stituents of each nerve-root come from a definite part of the cord, which is termed the corresponding spinal "segment." A single muscle is seldom related to a single segment; usually its nerve-fibres come from parts of two segments, or even from three. Its representation in the grey matter of the cord corresponds to its relation to the nerve-roots, and has often a considerable vertical extent. The most important relations are these : that of the deltoid, rhomboids, supra- and infra-spinatus, flexors of the elbow, and supinators to * In the case of the leg there are some important discrepancies between the results in the ape and the conditions that obtain in man. These will be noticed in their proper place. t Ferrier has since stated that the relations he gave (followed in the text) were all one nerve too high (' Proc. Roy. Soc.,' 1883, vol. xxxv, p. 229), but this would make the innervation of the intrinsic muscles of the hand from the second dorsal nerve, which is certainly not the case in man. 100 SPINAL NERVES. the fourth and fifth cervical; that of the adductors of the arm and extensors of the elbow to the sixth and seventh nerves; pronation to the sixth and eighth; extension of the wrist to the fifth ; flexion to the eighth ; extension of the first phalanx to the fifth; flexion of the fingers to the seventh and eighth, and the action of the intrinsic muscles of the hand to the first dorsal. These facts will probably, in the future, find important practical applications. Regarding the relation of the sensory branches to the nerve-roots, we have, besides the facts of anatomy, only the evidence furnished by rare cases of injury or disease in which the lesion and its effects are well defined.* Few facts of this character are, however, so conclusive as that illustrated in Fig. 51, in which the area shaded by slanting lines was rendered anaesthetic by the division of the posterior roots of the last cervical and first dorsal nerves. The general indications are that the distribution of the sensory fibres of the nerve-i'oots is along the axis of the limb, and not across it. The last two pairs of nerves supply the ulnar side of the limb and the finger tips, the fifth pair the radial side and the middle roots of the brachial plexus, the middle zone of each side of the limb and the thumb.f Fig. 51.—Area of impaired sensation after division of the posterior branches of the 8th C. and 1 D. nerves, by Professor Horsley for inveterate paroxysmal neuralgia in that region. Paralysis of the nerves of the upper limb may be due to disease of the nerve-roots, of the plexus, or of the trunks that arise from these. It is convenient to consider first the diseases of the nerve-trunks, and afterwards those of the nerve-roots and of the plexus. From the roots themselves only one important nerve-trunk is derived:—the pos- terior thoracic nerve. The others spring from the plexus. The morbid influences that affect the nerves of the arm are very varied. The brachial plexus passes close to the shoulder-joint, and hence dislocation often damages the nerves, sometimes one only, some- times several, and occasionally all the trunks. In fractures of the * Instructive facts of this charactpr will be found in papers by Thorburn 'Brain,' January, 1887, and October, 1887, Allen Starr ('American Journal of the Medical Sciences/ 1892), and Head (' Brain,' 1893 and 1894), who has mapped out the areas representing the segmental distribution of the sensory fibres of the spinal cord by means of observations on superficial tenderness accompanying visceral disease, on cases of herpes zoster, and on cases of spinal cord disease. (See diagrams at end of Chapter on " Functions.") t This is due to the mode of growth of the arm-bud in the embryo as shown by Ross in a most instructive paper, ' Drain,' January 7th, 1888. See also chapter on the Functions of the Spinal Cord. NERVES OF THE ARM. 101 bones the nerves adjacent may be torn, or may be compressed by the ends of the bone, or by the callus that is formed, especiallv by the exterior " fibrous callus." The musculo-spiral nerve is most prone to suffer from its proximity to the humerus, and in one such case the nerve, when exposed, was found not only to be embedded in the callus tissue, but to have been divided for about one-third of its diameter, opposite the fracture. Bandages that are applied are occasional sources of compression, and there is especial danger of harm from those that secure a splint applied to prevent motion in cases of neuritis. Unless loss of sensation draws attention to it, the injury is generally only dis- covered when the splint is given up, and therefore its possibility should be remembered. The course of certain nerves is, in some parts of tin- arm, especially apt to be directly involved in wounds of various kinds, or they may be compressed by the cicatricial fibrous tissue when the wound is merely near the nerve. The position of some exposes them to pressure against the unj lelding bone. Even slight pressure on these nerves is effective when prolonged, as it often is during sleep, when warning sensations are unperceived. The sleep induced by alcohol is especially apt to be attended by this accident. Hence there is a group of " Sleep-palsies" of the arm, chiefly of the musculo-spiral and median nerves, rarely of the plexus itself. One nerve, the musculo-spiral, passing between the bone and the triceps, is occasionally bruised by the contraction of the muscle. Primary neuritis may involve any nerve, or the brachial plexus, or the nerve-roots ; certain nerves are also particularly prone to suffer in peripheral neuritis. The inflammation of the plexus, which is a unilateral perineuritis, is separately described (Brachial Neuritis) ; the latter is considered in the general account of Multiple Neuritis. Secondary neuritis, set up by injury or by adjacent inflammation, may extend upwards, and, reaching the plexus, spread to other nerves. Neuromata are rare. Various morbid processes in the neck may involve the nerve-roots. Posterior Thoracic Nerve—Nerve to the Serratus.—In consequence of its position and long course, the nerve to the serratus often suffers. After being formed in the substance of the scalenus medius muscle, by the union of branches of the fifth and sixth cervical nerves, it passes behind the brachial plexus and along the side of the chest to the lower border of its muscle. It is in the neck that the nerve is most often injured ; injury to the axilla less often implicates it. It may be damaged in the neck by direct pressure—as in carrying on the shoulder a heavy sharp-cornered object—or by severe muscular efforts, such as carrying a weight that does not press into the neck, wielding a heavy hammer, or long-continued exertion with the raised arm, as, for instance, in whitewashing a ceiling. In such cases a traumatic neuritis is set up by the violent compression of the nerve consequent on the forcible or prolonged contraction of the muscle through which it passes. When 102 SPINAL NERVES. the onset of the palsy occurs immediately on the exertion, a paralysing injury to the nerve must have occurred, which will be followed by secondary neuritis. Falls and blows on the neck and shoulder are occasional causes ; there is usually much bruising of the adjacent parts. Punctured and gun-shot wounds occasionally involve the nerve, which may also be affected in or after typhoid fever, influenza, and diphtheria. The least frequent cause is exposure to cold, such as a draught on the neck, or sleeping on damp earth. I have once known it to follow par- turition, developing four days afterwards, doubtless from neuritis excited either by the muscular exertion or by exposure of the neck to cold during the labour. An hysterical paralysis in the distribution of the nerve has been described by Verhoogen. The serratus suffers also in central disease, chiefly in progressive muscular atrophy and dys- trophy and infantile paralysis ; but in these it is always associated with palsy of other muscles. Isolated paralysis of these nerves is nine times as frequent in men as in women. It occurs chiefly in muscular workers, and during the active period of life, twenty-five to forty. The immediate causes sufficiently explain this relation to age and sex, and they also account for another fact—that it is far more frequent on the right side than on the left. It is sometimes bilateral, but the two nerves are never damaged at the same time. One man was affected on the right side after carrying heavy beams on the shoulder; he then carried them on the left shoulder, and the left serratus became paralysed. Severe neuralgic pains in the neck and about the shoulder commonly precede and accompany the onset of the affection when due to neuritis. The symptoms of the paralysis of the serratus have been already de- scribed (p. 35). It is readily recognised by the recession of the posterior edge of the scapula from the thorax when the arm is put forwards (Pig. 8, p. 36). In severe cases the muscle is found to have lost faradic irritability, although it may still contract to the voltaic current. The course of a severe case is always tedious. Months may pass before improvement is manifested, and the paralysis is sometimes per- manent. In treatment it is desirable to maintain the nutrition of the muscle, as far as possible, by electrical stimulation, and its superficial situation renders this easy. If counter-irritation is desirable, it should be applied over the position of the scalenus, since the lesion of the nerve is commonly at this place. The use of the arm should be limited. When practicable, the elbow should be carried in a sling of such a length as slightly to raise the shoulder. All movements that may involve contraction of the scalenus, i. e. all movements needing elevation of the shoulder, must be prohibited. The supra-scapular nerve arises from the trunk formed by the union of the sixth, fifth, and a branch of the fourth cervical nerves, but its fibres come from the fifth and partly from the fourth. It is occasionally damaged, alone or with the circumflex, in dislocation of the humerus, and by falls on the shoulder, and by carrying heaw weights. In some cases the injury may be to the upper part NERVES OF THE ARM. 103 of the plexus (see p. Ill), which may recover except this nerve It suffered with the circumflex, in a case recorded by Eemak, from acute limited inflammation of the plexus, due to exposure to cold after over- use of the arms. Bernhardt has seen it following a fall upon the hand. The result of its disease is palsy of the supra- and infra- spinatus (p. 37). The latter is the more important, and causes a defect of the rotation outwards of the humerus, interfering with many movements, and, among others, with the movement of the pen along the line in writing. Undue work is thrown on the posterior part of the deltoid and the teres minor; the deltoid may become hypertrophied, and its posterior edge is conspicuous against the wasted infra-spinatus. The scapula is rotated, so that the lower angle is moved upwards and inwards. The paralysis of the supra-spinatus is unimportant, except that the humerus is less firmly fixed and the deltoid more readily fatigued. It can, in very slight degree, supplement the deltoid, and if paralysed with the deltoid, the head of the humerus falls more than it does when the deltoid is paralysed alone. Some anaesthesia over the scapula often results from disease of this nerve ; early in the affec- tion there is frequently severe pain in the region of the shoulder-girdle. The Circumflex nerve, although arising from the posterior cord of the plexus, seems to derive its fibres from the same source as the supra-scapular, the fourth and fifth cervical nerves. It supplies the deltoid and teres minor, and the skin over the deltoid. The course of the nerve renders it very liable to injury from dislocations and falls on the shoulder, and from the pressure of a crutch. Simple neuritis and so-called " rheumatic palsy " are rare, but the nerve has been affected in some acute diseases, possibly from pressure, and in rheumatic fever, perhaps by inflammation extending from the joint; typhoid and diabetes may also give rise to circumflex paralysis. It suffers, with other nerves, from disease of the upper part of the brachial plexus, and the chief symptom is paralysis of the deltoid (p. 36), which abolishes almost all power of raising the arm, a very trifling deo-ree of abduction by the supra-spinatus alone remaining. The shght nerve-supply that the fore-part of the deltoid receives from one of the anterior thoracic nerves is insufficient to mitigate the effect of the paralysis of the circumflex, although it may maintain shght power of voluntary contraction in the anterior fibres, and this sometimes gives rise to an erroneous impression that the paralysis of the circum- flex nerve is incomplete. The effect of the conjoined palsy of the teres minor is unimportant. The wasting of the deltoid causes a change in the shape of the shoulder (Figs. 7 and 9). Sensation may be lost in the skin over the lower part of the muscle, and the loss sometimes extends on to the shoulder (Pig. 52) ; Hitzig pointed out many years ago that the anaesthetic area is often the seat of vaso-motor paralysis. In some cases there is no anaesthesia, even when the muscle is wholly paralysed; we have seen that this is often the case in nerve lesions (p. 78). Adhesions are apt to form in the shoulder-joint, in 104 SPINAL NERVES. Fig. 52.—Disease of the circumflex nerve from pressure neuritis during acute illness ; wasting of deltoid. The dotted line indicates the area of cu- taneous anaesthesia. part probably the result of trophic changes, since the circumflex supplies the articulation as well as the chief muscle that moves it. The diagnosis of the paralysis of the circum- flex nerve is easy. The only condition readily mistaken for it is anchylosis of the shoulder- joint in a stout individual, in whom the state of nutrition of the muscle is not readily per- ceived. The risk of error is increased by the fact that arthritis and paralysis may result from the same cause—a fall on the shoulder. Passive movement at once solves the problem. The scapula moves with the arm in anchylosis, and not in palsy. Furthermore, attempts at voluntary contraction leave the muscle flaccid, while if the affection is in the joint the muscle- fibres be orne rigid in the attempt to contract. The importance of examining the joint is very great in all cases of interference with move- ment of the shoulder. A patient had an epileptic fit which was supposed to have left brachial monoplegia, merely because he fell on the shoulder, and the movement of the arm was lessened first by pain, and then by arthritic adhesions. In dia- gnosing the lesion from those of other nerves, the electrical reactions and the area of anaesthesia may be important. The Musculo-cutaneous nervi supplies the chief flexors of the elbow and the skin over the radial side of the forearm. It is scarcely ever paralysed alone, but often suffers, with other nerves, in disease of the brachial plexus. In the few recorded cases the cause has been traumatic,* but in Eemak's case of t aralysis of the supra-scapular and circumflex nerves on the right side, from limited neuritis of the plexus, therp was complete palsy of this nerve on the left, thought to be due to a still more limited inflammation in the left brachial plexus.f The symptoms correspond to its function; there is paralysis of the biceps and brachialis anticus (see pp. 38, 39), the effect of which is especially conspicuous when the arm is supinated and the supinator longus cannot flex the elbow. There may also be anaesthesia of the radial side of the forearm. The Musculo-spiral nerve is more frequently paralysed alone than any other nerve of the arm. Arising from the posterior cord of the brachial plexus, it seems to derive its motor fibres from all the nerve-roots that enter the plexus except the first dorsal. It supplies the triceps, all the muscles on the back of the forearm, the extensors of the wrist and fingers, both the supinators, also the skin on the radial side of the back of the hand, the back of the thumb, index * See Bernhardt, ' Erkrank. peripher. Nerven.,' 1897, p. 329. t ' Neur. Centralbl.,' 1896, p. 578. NERVES OF THE ARM. 105 finger, and half the middle finger. It is thus the extensor nerve of the arm, and has a more complete relation to a single function than is common among the nerves of the limbs ; a fact that has given rise to diagnostic error, since a palsy limited to a single function suggests a central cause. The frequency with which this nerve suffers is due to its course. As it leaves the brachial plexus to wind round the bone, its position exposes it to injury in dislocation or from the pressure of a crutch; the most common form of " crutch palsy " is paralysis of this nerve Lying as it does close to the humerus, it is readily torn in fracture, or compressed by callus, and it suffers gravely from even temporary pressure against the hard bone. Such pressure is often exerted during sleep, especially that induced by alcohol. The nerve may be paralysed by the pressure to which it is exposed when the body, with the arm beneath it, rests on the ground or on a hard bed. Thus a man slept all night on a bench, lying on his right side with his arm beneath him, and woke in the morning with this nerve paralysed. Curiously, a precisely similar event had occurred to him three years before. In other cases the pressure on the nerve is that of a hard and sharp object over which the arm is placed during sleep, as the edge of a chair or the side of a couch. The Continental custom of tying together, behind the body, the arms of a prisoner, often causes paralysis of this nerve, sometimes on both sides. In Eussia it is not uncommon in infants, from the popular practice of binding the arms to the body and then laying the child to sleep on its side. I have three times met with paralysis from a violent contraction of the triceps, once during the act of pulling on a tight pair of boots, once from throwing a stone with energy, and once from grasping a lamp-post to avoid a fall during a severe attack of giddi- ness. In each the nerve was at once completely paralysed ; and in the second, in which the palsy was severe, a bruised appearance was ob- served over the lower part of the triceps. Neuritis due to cold is often assumed to be a cause, and is possibly sometimes effective, but the exposure has usually been during alcoholic sleep, and it is probable that the paralysis is due to compression rather than to cold. The same influence may also have been operative in cases in which the nerve has been paralysed during an acute disease. Although in a case of para- lvsis during typhus, described by Bernhardt, neuritis was found after death, this was at the spot at which pressure is usually effective, and the inflammation was probably thus excited. Pressure always sets up neuritis, and the diagnosis of a primary neuritis is never justified if the spot affected is one liable to compression. Paralysis of this nerve, with others, has followed the use of an Esmarch's bandage; and a partial palsy sometimes results from the habitual or even occasional injection of ether beneath the skin of the posterior part of the arm. The symptoms of disease of the musculo-spiral nerve are paralysis of the extensors of the elbow and of the wrist, the long extensors of the fingers and thumb, and the supinators (see pp. 37—40). All these are 106 SPINAL NERVES. paralysed by a complete lesion of the nerve near the brachial plexus. When the lesion is near the middle of the humerus, as it is in most cases of compression, the triceps generally escapes, but not always. The supinator longus is usually paralysed, but escapes if the lesion is below the origin of its branch, and may also escape if the injury to the nerve is incomplete. In sleep palsy it usually suffers, but I have seen it unaffected, in a case in which the ext. carpi radialis was also but little affected, and Bernhardt has noted the escape of the supinator in an otherwise complete paralysis from dislocation of the humerus. The extensor palsy causes characteristic wrist-drop, and loss of the power of extending the first phalanges of the fingers and the thumb (see p. 40). There is sometimes a gradation of palsy from the first finger, in which it is least, to the fourth, in which it is greatest (Fig. 53). The same gradation is seen in lead palsy, and other forms of Flff. 53.—Paralysis of the musculo-spiral nerve; maximum extension of wrist and fingers. The extension of the fingers progressively diminishes from the first to the fourth. (From a photograph.) peripheral neuritis. It is not easy to explain. The action of the flexors is feeble, from the loss of antergic support; in most cases of complete palsy I have found the power of flexion reduced from this cause to one third of the normal. The loss of the power of supination is a grave inconvenience. If an object is grasped firmly the arm becomes pronated. The patient tries to compensate for the loss by putting the elbow against the side and rotating the humerus. Fig. 54.—Prominence at back of hand from para- The pronators may ulti- lysis of the extensors The patient was suffering mately become shortened. from wrist-drop due to silver poisoning (see vol. J , ii, •' Argyria"). The over-flexion of the carpus, and its deficient support by the extensor tendons, lead to a prominence of synovial sacs, and perhaps of the bones, at the back of the carpus (Fig. 54). In severe cases the muscles waste, and the maximum circumference of NERVES OF THE ARM. 107 the limb below the elbow may be a quarter or half an inch less than on the other side ; at the same time there may be thickening of the tendon-sheaths at the back of the hand. The electrical reaction depends on the severity of the lesion of the nerve; commonly there is well-marked degenerative reaction. The affection of sensibility in the area supplied by the nerve is very variable. The skin of the upper arm rarely loses feeling; in the hand sensation may be normal although the muscular paralysis is complete. There may be sub- jective "tingling" in the part although there is no loss of sensibility. The elbow- and wrist-jerks may be lost even when the reaction of degeneration is not present. The diagnosis is easy in most cases. The affection is distinguished from lead palsy by its common limitation to one arm, by the affec- tion of the supinator, and often by the sudden onset; that from lead is gradual. The latter is further characterised by the early onset of the degenerative reaction in the affected muscles. These characters, and the commonly obtrusive cause, always suffice for the diagnosis. Et must be remembered, however, that this nerve is one most fre- quently affected in many other forms of multiple neuritis (q. v.). The prognosis in disease of the musculo-spiral nerve depends on the severity of the lesion, as indicated by the electrical reaction. When there is evidence of nerve degeneration the paralysis usually lasts for some months. Eecovery ultimately occurs in almost all cases. The treatment is that for neuritis, already described, but attention should be paid to the posture of the limb, so as to avoid tension on the affected part of the nerve. For this reason, and also because strong contraction of the triceps may further injure the nerve, extension of the elbow should be avoided in cases of lesion of the nerve as it winds round the humerus. The Median nerve supplies the pronators, the radial flexor of the wrist, the palmaris longus, the flexors of the fingers (except the ulnar half of the deep flexor), the muscles that abduct and flex the thumb, and the two radial lumbricales. Its motor fibres seem to have an exten- sive origin from all the cervical roots that enter the brachial plexus. It subserves sensation on the radial side of the palm, on the front of the thumb, of the first two fingers, and of half the third finger, and also, at least in many persons, on the back of the last phalanx of the index and middle finger; sometimes also on the adjacent part of the back of the ring finger and the back of the last phalanx of the thumb. Isolated palsy of this nerve is not frequent, and generally results from wounds of the forearm, or fractures of the forearm bones, rarely from injuries in the upper arm. The nerve is occasionally the seat of neuritis, which may be induced by compression, especially in those who, in their work, have to hold an object between the hand and upper arm. Occupation paralyses of this nerve have been observed in ironers, locksmiths, joiners, cigarette makers, and once in a dentist. The nerve may also suffer as the result of pressure of the head of the 108 SPINAL NERVES. humerus in sleep or narcosis, while in former days it was not infre- quently injured by unskilful venesectors. I have known it to be paralysed at the wrist a few hours after a severe sprain of this joint. Webber has recorded a case in which it seemed to be injured by a violent contraction of the pronator teres. When there is com- plete damage to the nerve, pronation is impossible beyond the mid- position, to which the supinator longus can bring the forearm, and an attempt is made to supplement this by rotating the humerus inwards, and separating the elbow from the side. The wrist can only be flexed with a strong inclination towards the ulnar side. The thumb is in persistent extension and adduction (like the thumb of the ape, Figs. 22 and 23, p. 44), and cannot be opposed to the tips of the fingers. The power of flexing the second phalanges on the first is lost, and also that of flexing the distal phalanx of the first and second fingers, but this phalanx can still be flexed in the third and fourth fingers by the ulnar half of the flexor profundus (see p. 41). Inter- osseal flexion of the first phalanx is still possible, and the unopposed extensor action of the interossei on the middle and distal phalanges tends to cause a subluxation of the articulations concerned. The wasting of the thenar muscles is usually conspicuous. The resulting condition is very characteristic; but if the damage is at the wrist, flexion of the wrist and distal phalanges remains. The sensory loss is variable; it may be absolute or absent. If there is anaesthesia it is greater on the palmar surface, and will often be found also on the dorsal aspect of the extremities of the first two fingers. Trophic changes of the skin and nails are not uncommon. The Ulnar nerve comes, through the inner cord of the plexus, from the last cervical and first dorsal roots, and its origin from the lowest part of the cervical enlargement gives it an important relation, since it is the first of all the brachial nerves to be affected by disease that ascends from the dorsal to the cervical region of the spinal cord. The nerve supplies the ulnar flexor of the wrist, the ulnar half of the deep flexor of the fingers, the muscles of the little finger, the interossei, some of the lumbricales, the adductor, and inner head of the short flexor of the thumb. Its sensory area is the ulnar side of the hand, back and front, generally more extensive on the back (two fingers and a half) than on the front (one finger and a half). The course of the nerve, superficial behind the elbow and at the wrist, renders it liable to separate injury. It is often implicated in wounds of the forearm, and about the elbow-joint, by dislocations of the shoulder and elbow, enlargement of the elbow bones, and by fractures of the bones of the forearm. It is occasionally the seat of neuritis, and, like the musculo- spiral nerve, it is sometimes paralysed by pressure. At the elbow the projecting bones preserve the nerve from direct pressure; although Duchenne describes paralysis in men who, while at work, rest the bent elbow on a hard substance, this mechanism is certainly rare. It is much more common for the nerve to suffer in long-continued flexion of the NERVES OF THE ARM. 109 elbow, without external pressure; and from this cause the nerve is sometimes paralysed during sleep.* I have three times seen a sleep palsy of the ulnar nerve. The tension may set up neuritis, and is especially effective if the resistance of the tissues to morbid influences is lessened by general ill-health. Many persons must have noticed that if, when out of health, they sleep with the elbow bent, they wake with tingling, and even loss of feeling, in the region supplied by the ulnar nerve, although this may not happen when they are in good health. If the ill-health is profound, as in an acute illness, local neuritis of considerable intensity may be set up. Thus a lady, a few days after childbirth, who was prostrated by a long, exhausting labour, noticed tingling in the side of the hand, and whenever she bent her elbow, a sensation " as if she had knocked her funny-bone." Paralysis of the muscles supplied by the ulnar nerve followed in a few hours, and in a fortnight there was distinct wasting. When I saw her, six months later, the ulnar nerve behind the elbow was distinctly thickened. She had had a similar but more transient attack after a previous con- finement. A similar palsy has occurred during the course of typhoid fever, and both nerves have been known to suffer (Bernhardt). In such conditions not only is the tissue health lowered, but warning sensations are often unperceived. Actual cysts of the nerve have been described by Bowlby and zum Busch. The importance of the interosseal flexion of the fingers for many actions, such as writing, renders palsy of the ulnar nerve peculiarly dis- abling. Several illustrations of the symptoms have already been given (pp. 42 and 43). In flexion of the wrist the hand deviates towards the radial side, and persistent distortion may take place. Adduction of the thumb is lost, and so are most movements of the little finger. The fingers cannot be flexed at the first or extended at the other joints, but the loss is slighter in the first two fingers than in the others, because their lumbricales are supplied by the median nerve. In time the opponents of the interossei, by their contracture, lead to over-exten- sion of the first phalanges and flexion of the others ; the " claw-like hand " is produced (see p. 43), but this is less complete than in cases of progressive muscular atrophy, on account of the escape of the first two lumbricales. When the palsy is imperfect it may be possible to extend the second and third phalanges, if the first can be over-extended and an advantage thus given to the interossei by the lengthening of the course of their tendons, just as in partial paralysis of the long extensors they may be able to extend the digits if the wrist is flexed, but not if it is extended. In lasting damage the hypothenar eminence may disappear, the palm is hollow, the thenar muscles that remain * H. Braun (' Deutsch. med. Woch.,' 1894) believes that in sleep the nerve is compressed, not at the elbow but at the shoulder, particularly when the arm is abducted and carried backwards, so that the bands are crossed behind the head. A similar effect may result from the arm being held in this position iu an operation, e.g. the removal of a breast. 110 SPINAL NERVES. stand out, and the opponens may cause a slight forward rotation of the thumb. The loss of sensation, as in the case of the other nerves, varies much, both according to, and irrespective of, the degree of lesion of the nerve. Subjective sensations are common, with and without anaes- thesia, and those who have had neuritis are sometimes unable to bend the elbow for a few minutes without a sensation of tingling in the area supplied.* The diagnosis of disease of the ulnar nerve is easy. A difficulty is occasionally caused by the circumstance already mentioned, that dis- ease at the lowest part of the cervical enlargement may cause sym- ptoms limited to the region of this nerve, but a knowledge of the fact is usually sufficient to prevent an error.f Combined Palsies op the Nerves of the Arm.—Paralysis in the region of two or more of the nerves of the arm is very common, and results from many causes. It may be due to disease of the spinal cord or of the nerve-roots within the spinal canal, but with these we are not now concerned. The most frequent causes outside the spinal canal are the following:—(1) Morbid processes in the neck, affecting the nerve-roots outside the spine or the upper part of the brachial plexus, especially growths and exostoses. (2) Diseases of the plexus itself, neuritis or injury, dislocations of the shoulder, the stretching by a sudden wrench of the arm, J or actual rupture of the nerves entering the plexus by great local violence. § (3) Fractures of the bones. (4) Neuritis, which may ascend a nerve of the arm to the part of the plexus whence it comes, and there spread; or neuritis of the plexus may be primary and of various extent, "neuritis migrans." The last, ascending neuritis, occurs when an injury of a single nerve is followed by an extension of the motor and sensory symptoms to the regions supplied by other nerves. This can only be explained by an ascending neuritis reaching the junction of the nerves at the brachial plexus, and there spreading, often in what seems a random manner. Thus a lady cut her wrist so as to leave a scar an inch long, over the position and in the direction of the median nerve. The injury caused paralysis and wasting of all the muscles in the hand * Anaesthesia of the region supplied by the ulnar and external popliteal nerves is a not infrequent symptom of general paralysis of the insane and tabes. In the ulnar it was first described by Biernacki, 'Neurol. Centralbl.,' 1894, in the external popliteal by Sarbo. See Sarbd and v. Deky, * Pest. Med.-Chir. Presse/ 1897. t Poncet ('Comptes Rendus,' 1888) describes a manual paralysis in glass-blowers (ho iked-hand, main en crochet) which closely simulates ulnar palsy, from which it is to be distinguished by the freedom of the thumb and the absence of anajsthesia. X Bowlby, loc. cit., p. 225. § Rieder ('Munch, med. Wochenschr.,' 1893) describes a paralysis affecting mainly the circumflex and musculo-spiral nerves of the left arm, and occurring especially in bricklayers from the pressure of the hod upon the shoulder. NERVES OF THE ARM. Ill supplied by this nerve. This palsy was followed by a gradual loss of power, with diminished faradic irritability, in the long extensor of the fingers, the ulnar flexor of the wrist, and also by defect of sensation in the skin supplied by the ulnar nerve. Hence the neuritis must have ascended to the plexus and there have spread along each root of the median nerve. Again, a woman cut her right hand with a broken stone bottle, along the hypothenar eminence. Three weeks after- wards the muscles of the hand supplied by the ulnar nerve gradually became paralysed, with wasting and loss of irritability, and in the area of the skin supplied by the nerve there was first tingling and then diminished sensibility. Burning pain spread up the front of the forearm, and inner side of the upper arm to the axilla; all the fore- arm muscles lost power, the flexor carpi ulnaris, and the flexor sublimis digitorum in greatest degree; the tingling and lessened sensibility spread to the fingers supplied by the median nerve, and the abductor pollicis wasted. In this case also there must have been an ascending neuritis of the ulnar, spreading to the median at the brachial plexus. The extension is sometimes only in the neighbourhood of the cause. A whitlow on the thumb was followed by extreme wasting, with reaction of degeneration in all the thenar muscles supplied by the median. But a case is on record in which a nodular inflammation commencing in the ulnar nerves apparently spread up to the sympathetic* The brachial plexus is occasionally the seat of a primary neuritis. This is described in a separate section (p. 119), as it is a defined and important disease. In dislocation of the shoulder the displaced head of the humerus may damage the nerves. In subcoracoid dislocation they are necessarily compressed. The extent of injury varies greatly; only one nerve may suffer, or not one may escape. Every muscle of the arm may be para- lysed, from the deltoid downwards. In most cases the injury is severe in degree; there is rapid wasting of the muscles, with the reaction of degeneration, and there is a great tendency to the occur- rence of trophic changes in the skin. It was in a case of this character that the forearm and hand were covered with blisters from the apph- cation of water that seemed merely warm to a healthy hand (p. 79). Fracture of the humerus may damage both the musculo-spiral and ulnar nerves, rarely the median. Fracture of the bones of the forearm often injures both the median and ulnar nerves. Injuries to the neck sometimes cause a partial paralysis of the arm of peculiar distribution, the special characters and significance of which were first made known by Erb.f A similar paralysis may come on apart from injury. The muscles affected are the deltoid, often the supra-spinatus and infra-spinatus, the biceps and brachialis * Remak, «Deutscb. Klinik,' 1864, p. 159. t Heidelberg Society, 1874, 'Ziemssen's Handbuch,' 1874, Bd. xii, pt. 2, p. 509; see also Bernhardt,« Zeitsch. f. kl. Med.,' 1882, Bd. iv, p. 415. A previous descrip- tion by Duchenne in 1885 had escaped notice. 112 SPINAL NERVES. anticus, and the supinators. Erb found that there is one spot between the scaleni, corresponding to the sixth cervical nerve, at which electrical stimulation puts all these muscles in action. Hoedemaker, who has described two cases of this palsy, finds the motor point in a iine drawn from the sterno-clavicular articulation to the seventh cervical spine, 1-5 centimetres from the edge of the trapezius. The palsy is appa- rently dependent on disease of the roots of the &-t\ and sixth cervical nerves, and the fifth, it will be remembered, receives a twig from the fourth.* Biidingerf and GauppJ have recently shown that in forcible elevation of the arm some backward rotation of the clavicle occurs, Fig. 55. Fig. 56. Fig. 55.—Combined palsy of deltoid, supra-spinatus, and infra-spinatus, from a fall on the shoulder. Figs. 56, 57.—Left hand of a patient suffering from agrowth beside the lower cervical spine compressing the nerve-roots. There was anaesthesia of all parts supplied by the brachial and cervical plexus. The arm was addueted, the elbow flexed, the hand in the posture shown, flexion of first, extension of second, strong flexion of last phalanges, the first phalanx of the thumb over-extended, the second flexed. Rigidity extreme, and an attempt to overcome it caused great pain. There was also some contracture of the foot (equino-valgus). compressing the fifth and sixth cervical nerves against the first rib. The fact that in this case the nerve-fibres are simply contused and not broken will no doubt account for the frequency of recovery from this form of paralysis. Besides injuries, this group of palsies may result from non-traumatic processes, probably from neuritis, and also from * Erb referred the palsy to disease of the sixth nerve. The experiments of Ferrier and Yeo point to the fifth and fourth roots as those innervating these muscles, but his subsequent correction indicates the fifth and sixth (see p. 99, foot- note). t 'Arch. f. klin. Chir.,' 1894. X ' Centralblatt f. Chir.,' 1894. NERVES OF THE ARM. 113 growths in this situation. Duchenne, Seeligmiiller, and others have also described paralysis of similar distribution produced in infants during birth, either by pressure from the position of the arm, or by traction on the neck with the finger or hook during turning. Dis- location of the shoulder during delivery may cause very extensive damage to the plexus. Permanent paralysis of each arm was the result of bilateral dislocation caused by a midwife dragging a child out by the two arms.* Most obstetrical cases slowly recover. Those due to injury in adult life are often severe; the symptoms continue for a long time, and may be permanent. A paralysis complementary to that of Erb, in which the muscles escape which suffer in that form, results from disease of the nerve- roots below, f It is often associated with ocular symptoms, such as narrowing of the pupil and palpebral fissure. Morbid processes connected with the bones of the cervical spine sometimes produce combined symptoms of irritation and palsy of the nerves of the arm, pain, hyperesthesia, anaesthesia, paralysis of muscles, and extreme muscular contractures, often very irregular in distribution (such as are shown in Figs. 56, 57). I have several times known sensory symptoms in the arm to be due to a cbronic syphilitic cellulitis beside the vertebrae, causing deep-seated induration and severe compression of the nerves; in each case it was completely removed by antisyphilitic treatment. Growths at the part may also compress the subclavian artery, and the weaker pulse may aid the diagnosis. J Diagnosis.—The diagnosis of diseases of the nerves of the arm has been for the most part sufficiently considered in connection with the special nerves. It consists chiefly in an apphcation of the facts there stated. One or two more general considerations deserve, however, a brief mention. Some diseases of the spinal cord are first manifested in the arm, by muscular palsy, wasting, or by anaesthesia. The risk of error is prevented, in most cases, by the absence of any corre- spondence between these symptoms and the functions of special nerves, by the absence of any indication of morbid processes in- the neighbourhood of the nerves, and by the presence of other signs of disease of the spinal cord. It has been mentioned that disease in the lowest part of the cervical enlargement may be manifested only in the region of the ulnar nerve, the lowest in origin of all the brachial nerves. Such disease is, however, usually bilateral, and secondary to disease in the dorsal region of the cord, the indications of which have * Danchez, ' Ann. de Gyn.,' &c, Oct., 1891. Double palsy in adults is occasionally seen, as in a case recorded by Bernhardt, in which the arms were pulled on for an hour to steady the patient during the operation of oophorectomy. t It has been termed " Klumpke's paralysis," because investigated in Vulpian's laboratory by Mdlle. Klumpke in 1885 (see ' Zeitsch. f. Nervenh.,' 1891) ; it had, however, beeu described long previously, notably in 1827 by Flaubert. X Bowlby, loc. cit. VOL. I. 8 114 SPINAL NERVES. preceded the symptoms in the arm. A knowledge of these facts, an a careful consideration of the distribution and course of the symptoms, will rarely leave the observer in doubt. Treatment.—There is little in the treatment of the diseases of the nerves of the arm that requires special mention. The chief measure is the treatment of the cause of the paralysis. Any present source of pressure must be removed as far as possible. The ends of a divided nerve must be sutured. It is remarkable how quickly this has some- times been followed by the restoration of conducting power. The posture of the arm must, in all cases, be such as to avoid tension on an injured or inflamed nerve. The treatment of neuritis is described in the next section. Electrical stimulation of the muscles is of great importance in all cases of severe damage to the nerves. Even in old and stationary cases it sometimes starts some improvement. Nerves of the Lower Limb. Disease of these nerves is far less common in the lower than in the upper limb, with one important exception,—the primary disease of the sciatic nerve that goes by the name of " sciatica." This affection is reserved for separate description. The nerves of the leg are derived from the lumbar and sacral plexuses. The lumbar plexus, consisting of the first three and a half lumbar roots, supplies the skin of the lower part of the abdomen, of the front and sides of the thigh, of the inner side of the lower leg and foot. It supplies also many muscles—the cremaster, those that flex and adduct the hip-joint, and those that extend the knee. Its branches for the leg are the obturator and anterior crural nerves. The sacral plexus consists of the fifth lumbar root and half the fourth (lumbo-sacral cord) and the first four sacral nerves, of which, however, only the upper three have to do with the leg. This plexus innervates the extensors and rotators of the hip, the flexors of the knee, and all the muscles that move the foot, together with the skin of the gluteal region, the back of the thigh, the outer side and back of the lower leg, and most of the foot. Its chief nerves are branches to the outward rotators of the hip, the gluteal nerve, and the small and great sciatic. The results obtained by Ferrier and Yeo (see p. 99) on stimulating the roots of the lumbar and sacral plexuses in the monkey may be thus summarised: Lumbar I and II. Lower abdominal muscles (not cremaster). III. Psoas and iliacus, sartorius, extensors of knee; (flexion of hip and extension of leg). IV. Glutei, adductors, extensor cruris, peroneus longus; (extension of hip and knee, elevation of outer side of foot). V. Glutei, hamstrings, and all the muscles in front and back of lower leg; (rotation of thigh outwards, flexion and rotation inwards of leg; extension of foot with elevation of outer edge ; flexion of distal phalanges of toesj. NERVES OF THE LEG. 115 Sacral I. Hamstrings, calf muscles, long flexor of toes, intrinsic muscles of foot; (slight outward rotation of thigh, flexion of knee; extension of foot, adduction of great toe, flexion of first phalanges of all toes and of both phalanges of great toe). II. Intrinsic muscles of foot; (" interosseal" flexion of toes, similar to the last). These results cannot be simply applied to man. For instance, it is certain that in man, one flexor of the hip, the psoas, and the cremaster, are largely innervated from the second lumbar, but no indication of the action of either of these could be observed on stimulating this root in the monkey. The distribution of the sensory fibres of the nerve-roots is considered in the chapter on the Spinal Cord. The Lumbar plexus itself is sometimes damaged by growths in the abdomen (especially by those that spring from the lumbar glands) and by psoas abscess, while the nerve-roots may suffer in disease of the bones of the vertebrae and in meningitis. The plexus may also be in- vaded by inflammation ascending the lumbo-sacral cord from the sacral plexus, and it is occasionally the seat of spontaneous neuritis. The obturator nerve is rarely affected alone; it has been sometimes damaged in the course of parturition. The anterior crural nerve has suffered from the same cause, and is sometimes injured by wounds of the groin or thigh, or by dislocation of the hip-joint. Symptoms may be limited to it in disease of the nerve-roots, and as in injury or growths of the vertebrae, its paralysis occasionally follows acute or subacute inflam- mation of the knee-joint. Of the interference with movement that may result, the paralysis of the flexors of the hip depends on the position of the disease. This paralysis is total only when the lumbar plexus is damaged. Disease of the anterior crural nerve, within the abdomen, does not affect the psoas, but may paralyse the iliacus, and so weaken, without abolishing, the power of flexion. The chief symptom of disease of this nerve is the loss of power in the extensors of the knee, and the wasting of these muscles, together with loss of the knee-jerk which results from the interruption of the reflex arc. The effect of these palsies on movement is very serious (see pp. 46, 47). Anaesthesia involves the whole of the thigh (except a strip along the middle of the back), the inner side of the leg and foot, and the adjacent side of the first and second toes. In many cases the paralysis is incomplete, and the symptoms present corresponding variation. Irritation of the nerve may cause severe pain in the region supplied by it. This is sometimes an early symptom of a growth near the spine. The pain in neuritis of the plexus may extend along the course of the ilio-hypogastric, ilio-inguinal, and genito- crural nerves, to the lower part of the abdomen and groin. Impairment of sensation in an area on the front of the lower half of the thigh is occasionally met with as an isolated symptom, usually in men in the second half of life. It comes on without pain, and may pass away after months, or may persist for years. The loss is greatest in the 116 SPINAL NERVES. middle of the region, but the transition to normal sensibility is well defined; its origin and nature are mysterious, except that the subjects of it are usually gouty. It seems to have little significance. Paralysis of the obturator nerve causes a loss of the power of adduc- tion of the thigh, so that the patient cannot put one leg across the other. Rotation of the thigh outwards is interfered with, but in slighter degree than adduction. The effect of these palsies (described on p. 47) is far less serious than is the disability which results from disease of the anterior crural. There is disturbance of sensation along the inner side of the thigh and knee ; an obturator hernia may press upon the nerve, giving rise to paresis of the muscles which it supplies, and burning pains in the region of its sensory distribution. The superior gluteal nerve occupies an intermediate position between the two plexuses, arising as it does from the lumbo-sacral cord, which descends from the fourth and fifth lumbar roots. Its disease, which is very rare in isolated form, causes paralysis of the gluteus medius and minimus, with a loss of abduction and circumduction of the thigh (see pp. 45, 46). The Sacral plexus is sometimes damaged by growths in the pelvis, by pelvic inflammation of various kinds, and by compression during parturition. In the child it may be damaged by traction on the legs. It is also often the seat of neuritis, which, however, less frequently begins in the plexus than ascends to it from the sciatic nerve. Apart from spontaneous neuritis, which will be separately described, the sciatic nerve outside the pelvis is occasionally injured by wor>uds, rarely by dislocations of the hip, often by disease of the bone, and by adjacent morbid growths. It is also a relatively frequent seat of neuroma. Of the terminal branches, the external popliteal, by its superficial course, and proximity to the hard bone, suffers from traumatic lesions of various kinds; it is also prone to spontaneous neuritis. This nerve is homologous with the musculo-spiral nerve of the arm, and presents an analogous liability to disease ; it occasionally suffers in persons whose occupations entail much kneeling. The pos- terior tibial nerve is more secure in its deeper course, but may be damaged by fracture of the bones. The symptoms of palsy of the sciatic nerve vary much in their character, according to the position of the disease. The small sciatic is implicated only when the mischief involves the pelvic plexus, and it scarcely ever suffers alone. The effect is palsy of the gluteus maximus, which interferes with rising from a seat more than with walking (see p. 45). There is also anaesthesia of the skin in the middle third of the back of the thigh, and in the upper half of the calf. A lesion of the sciatic nerve, near the sciatic notch, paralyses the flexors of the leg (which are also extensors of the hip ; seep. 47), and ail the muscles below the knees. Often the lesion is below the upper third of the thigh, and then the flexors of the leg escape. Even when all the muscles below the knee are paralysed, walking is still possible, the foot NERVES OF THE LEG. 117 being raised by over-flexion of the hip. The anaesthesia that results from a lesion of the nerve below the origin of the small sciatic, involves the outer half of the leg, the greater part of the dorsum of the foot, and all the sole, but the leg may escape, perhaps through union with other nerves. The symptoms of disease of the branches are as follows: That of the external popliteal or peroneal nerve causes paralysis of the tibialis anticus, long extensor of the toes, peronei, and extensor brevis digitorum. The effect of this is a loss of all power of flexing the ankle and of extending the first phalanx of the toes (see p. 50). The foot cannot be raised from the ground in walking, and talipes equinus ultimately results (Fig. 30, p. 51), which may be attended with persistent flexion of the first phalanges of the toes from contracture of the unopposed interossei. There is also anaesthesia on the outer half of the front of the leg, and on the dorsum of the foot.* Disease of the internal popliteal nerve paralyses the popliteus, calf muscles, tibialis posticus, and long flexors of the toes, as well as the muscles of the sole. In addition to the disability which characterises paralysis of the plantar muscles, there is loss of the inward rotation of the flexed leg if the disease is so high as to involve the branch to the popliteus, and there is also loss of the power of extending the ankle- joint. Talipes calcaneus results (Fig. 28, p. 50). The sensory loss is on the outer lower part of the back of the leg, and on the sole, but varies much. The plantar nerves rarely suffer alone. A lesion of the internal nerve causes anaesthesia on the inner part of the sole, and plantar surface of the three inner toes and half the fourth, together with paralysis of the short flexor of the toes, the plantar muscles of the great toe (except the adductor), and of the two inner lumbricales. Disease of the external nerve produces anaesthesia of the skin on the outer half of the sole, the little toe and half the fourth, paralysis of the flexor accessorius, the muscles of the little toe, all the interossei, the two outer lumbricales, and the adductor of the great toe. The effect of this palsy (see p. 52) is serious, since the toes cannot take their proper share in propelling the body forward in walking, and they gradually become flexed at the last two joints and extended at the others, from the contracture of the opponents of the interossei,—a position of the toes that causes serious inconvenience in walking. Diagnosis.—The diagnosis of diseases of the nerves of the leg is determined by the same general principles as those that have been mentioned as applicable to the nerves in general, and to the nerves of the arm in particular. The limitation of the symptoms to the functional areas of individual nerve-trunks, the evidence afforded by nutrition, irritability, and reflex action that the muscles are separated * Anaesthesia in the district supplied by this nerve may be a symptom of various progressive nervous diseases j it was first described in this connection by Sarbo (see p. 110, footnote). 118 SPINAL NERVES. from the spinal cord, the implication of the sensory functions, and often the tenderness of the affected nerves, indicate, in most cases, the seat of the disease. To these signs are often added other indica- tions of a local cause, corresponding, in its position, with the nerve to which the symptoms point. The relation of nerve-trunks to nerve-roots, although by no means simple, is certainly less complex in the case of the nerves of the leg than in those of the arm. This is especially the case in the lumbar plexus, and it leads to an occasional difficulty in diagnosis. Pressure on the spinal cord, for instance, at the level of the origin of the fourth lumbar roots, may cause symptoms identical with those of a partial lesion of the anterior crural nerve. For instance, I have known para- lysis of the extensors of the knee, loss of the knee-jerk, with anaesthesia in the front of the thigh, to be the result of a gumma at the side of the cord at this level. But other evidence of a spinal lesion is rarely absent under such circumstances, and in this patient a foot-clonus, due to the pressure on the pyramidal fibres, left no doubt as to the situation of the disease. Another difficulty arises from the long course of the nerve-roots in the cauda equina, disease of which may simulate that of the nerves of the leg. Implication of this region is most commonly due to syphilis, trauma, congenital defects (spina bifida), or new growths.* But the symptoms are commonly bilateral in consequence of the prox- imity of the nerve-roots of the two sides. In all cases in which symptoms are bilateral (unless there is evidence of a disease known to cause symmetrical lesions, such as multiple neuritis)-, the suggestion is that the disease is situated where the motor or sensory paths of each side are so near that they can be affected by a single lesion, i. e. that the disease is within the spinal canal. But here, as in other cases, we cannot reverse our diagnostic rules. Disease of the spinal cord does not always cause bilateral symptoms. A limited lesion of one anterior cornu may be so placed as to paralyse the muscles supplied by a single nerve, and a doubt may be felt as to the central or peri- pheral origin of such palsy. The muscles supplied by the anterior crural nerve, and the muscles in the front of the lower leg supplied by the external popliteal, are those of which the central palsy most often leads to doubt. The mode of onset, the presence or absence of sensory symptoms, the rarity of acute spinal palsy except in child- hood, and of nerve-lesions except in adult life, the wider initial pre- valence of the palsy in acute, and its later extension in chronic cornual disease,—these suffice as a rule to remove any doubt. It is important to remember that the pressure of a growth may cause either a chronic or an acute affection of the nerves. The chronic symptoms result from compression; the acute from a neuritis set up by the pressure and irritation. Treatment.—The treatment of disease of the nerves of the leg * See Thorburn, ' Brain,' 1888 ; Fr. Schulze,' Deutsche Zeitschr. Nervenheilk.» 1894, vol. v. BRACHIAL NEURITIS. 119 does not differ from that of disease of the nerves of the arcn. More care, perhaps, is needed to avoid increasing present mischief, or inviting a relapse, by exposure to cold or by fatiguing exertion. More care is also needed to obviate the tendency to secondary contractures in the case of palsies of long duration, and in those attended by pain in which the patient seeks ease in postures to which the muscles only too readily adapt themselves. The contraction of the hamstrings, from con- stant flexion of the knees, occurs very readily and is most troublesome ; that of the calf muscles, which occurs when the flexors of the ankle are paralysed, also constitutes a serious obstacle to walking after recovery. A little timely care, by attention to posture, will often save a vast amount of later trouble. That of the calf muscles, however, which is due to the extension produced by the weight of the foot as the patient lies, cannot always be entirely, prevented, but may be lessened by a board or large sand-bag against which the feet can rest. An outline is given elsewhere of the forms of local inflammation of these nerves, with special reference to the morbid process, on account of its important practical relations. (See Crural Neuritis, p. 133.) BEACHIAL NEURITIS. Besides the forms of inflammation of the nerves of the arm already described, a primary inflammation of the brachial plexus occurs in a form as well defined as sciatica, and equally meriting a separate description. This, however, need only include its special features; those that are common to other forms of neuritis have been already described. It is closely analogous to sciatica, and is usually a peri- neuritis, — a primary inflammation of the sheaths of the branches that enter and form the brachial plexus. Cases occur, however, in which the symptoms correspond in general character to the rest, but in which their distribution suggests that the nerve-roots rather than the plexus are the seat of the inflammation, and pain about the spine supports the opinion. This form may be called Radicular Neuritis. Although its existence has not been established by pathological evidence, the symptoms mentioned admit of no other explanation. A knowledge of their significance is of great practical importance on account of the closeness with which they may simulate those of organic disease of the bones of the spine, or a growth in the spinal membranes. Causes.—The influence of gout in causing local neuritis is very conspicuous in the brachial form, with the special characteristic that this occurs chiefly late in life, verv often from the inherited disease, 120 BRACHIAL NEURITIS. and with greater frequency in females than any other form of neuritis; their liability is at least equal to, if not greater than, that of men. Five sixths of the cases occur after fifty, and it may be met with up to extreme old age. In men there have usually been the ordinary manifestations of gout, but in women the tendency is often only indicated by the family history, and by previous muscular rheuma- tism, especially lumbago and sciatica,—which have seldom been ab~ ont in either sex. In one case the onset of the brachial neuritis occurred immediately after an attack of sciatica. Neuritis of the brachial plexus may also arise from trauma or the pressure of new growths, e. g. of a pressure on the posterior surface of the clavicle Symptoms.—Pain, the great symptom of the inflammation of all mixed and sensory nerves, is greater in this than in most forms of neuritis. It is usually the first symptom, and lasts long after the inflammation is over; its severity, coupled with the age of most sufferers, renders the malady one of a peculiarly trying character. The first pain is often referred to a distance from the seat of the inflammation, perhaps because this begins at the plexus, where, at divisions, it is facilitated by motion, and the conducting fibres are readily reached and early irritated. Frequent seats for the first pain are the region of the scapula (sometimes beneath the bone) and the wrist or back of the forearm, with or without the hand. In other cases, however, the first pain is at the plexus itself, above the clavicle or in the axilla, and these are the places in which it is commonly most intense throughout the attack. As the pain increases it extends along the course of the nerves of the arm, which the patient will often accu- rately indicate with his finger when tracing the lines of pain. The pain is sometimes sudden in onset and severe from the begin- ning ; more often it is at first occasional, or felt on certain movements, but, as it increases, it becomes more continuous, with variations that soon become paroxysmal. Ultimately there is always more or less dull wearying pain in the whole arm, but especially in the region of the plexus, varied by attacks of great severity. In these the pain is acute and lancinating, or stabbing, or burning ; it usually takes the course of the nerves, diffusing itself from them, and often passing to the side of the chest and to the neck,—seldom to the head. The pain often varies in character according to intensity; at the height of the paroxysm it may be sharp and stabbing, or such darting pains may be superadded to a more diffused burning pain, which lasts lono-er than the acute pain, and may be followed, as the paroxysm subsides, by general tingling of the skin of the whole limb. The paroxysms are induced by movement or occur spontaneously. In slighter cases the pain is paroxysmal only, and then the relation to movement is a very conspicuous feature. Although it is seldom confined to movement, this never fails to induce severe pain, and the patient avoids the slightest use of the limb. Elevation of the arm especially causes distress. With the pain there is usually undue sensitiveness of the skin DIAGNOSIS. 121 which may be much increased during and after the paroxysms. Loss of sensation is rare, and is met with only in cases that are not only severe but prolonged. The two may concur, as " anaesthesia dolorosa." The muscles usually present the flabbiness and slight wasting common in neuritis, but the damage to the motor fibres is seldom sufficient to cause considerable atrophy. Sometimes, however, there is enough damage to cause wasting of some group of muscles, with the reaction of degeneration. This is most frequent in the radicular form, in which the damage is to the upper part of the plexus and nerve-roots. There may then be anaesthesia of the skin over the affected muscles. It is difficult to ascertain the existence or the amount of motor weakness; effort induces pain so readily that the patient can seldom be induced to make an attempt to exert force. Power is often said to be almost lost,-when it is probably greater than is believed. Besides the muscles, the subcutaneous tissue of the limb may also waste, and the skin may become thin and shining, and present the aspect already described. Subcutaneous oedema is also common, and in one case erythema nodosum was found.* Arthritic changes in the joints of the fingers are almost constant in the cases that occur in later life ; the adhesions may be permanent. Diagnosis.—Few maladies, as a fact of experience, give rise to greater diagnostic difficulty. This is due to several causes: the affection is rare; its symptoms are sometimes equivocal; the subjects are usually in the degenerative period of life, when many obscure diseases attended with pain in the arm occur to the mind of the physician; and lastly, the distinction between neuralgia and neuritis is often difficult, although less so than is supposed. The last is, indeed, the mosi frequent source of error. The most severe and characteristic cases of brachial neuritis are frequently mistaken for pure neuralgia, on account of the paroxysmal character of the more severe pain, and because the characters of neuritis are unfamiliar. The points to deter- mine the diagnosis are those described in the sections on neuritis and neuralgia;—the degree of persistent tenderness of the nerves and the influence of movement, together with the history of the attack, the locality of the pains, and especially any evidence of damage to the fibres. A history of neuralgia in the person or the family is of slight weight only; the tendencies to true neuralgia and to neuritis are often combined, and each is a frequent result of gout. A far greater diffi- culty is presented by the cases in which the inflammation remains slight and is confined to the plexus, affecting branches where the con- ducting fibres can be so irritated as to cause distant pain, which then becomes the leading symptom. This is often paroxysmal, and, when on the left side, may radiate to the chest and be associated with dis- turbed action of the heart. Angina pectoris is often thought of. in such cases; and here again the degenerative age may increase the difficulty by leading to the presence of some coincident disease of the * v. Frankl Hochwart, * Wien. klin. Wocbenschrift,' 1897, No. 1. 122 BRACHIAL NEURITIS. heart, or by making true angina not unlikely. The distinction afforded by the nerve-tenderness is then of great importance, because the dis- proportionate amount of tenderness (compared with the amount of pain) is more emphatic in slight than in severe cases. Persistent tenderness with only paroxysmal pain should always suggest neuritis. When the position of the pain is carefully examined, its relation to the plexus and branches is often clear. It is important to remember that all nerve-pains in the brachial region on the left side have a tendency to resemble anginal pain in distribution, and to be associated with cardiac distress. Probably there is some peculiar tendency for pains in this part to disturb the action of the heart; a common physio- logical relation may underlie both the nerve-pains of cardiac angina and the cardiac symptoms of nerve-pains. Hence this secondary dis- turbance does not neutralise the significance of the special signs of neuritis. In some cases of the slighter class, the pains suggest the idea of an aneurism; in many cases of brachial neuritis this diagnosis has been made, and the patient has had to endure months of mental distress, for which no real cause was in existence. Such a suspicion, in the absence of special signs, such as pressure-symptoms, should only be entertained if the pains are persistently and increasingly severe, and unaccompanied by any considerable amount of tenderness. In all these cases, moreover, the presence of the gouty diathesis may be allowed weight in the diagnosis. The muscular wasting, slight in degree, added to the arthritic changes, gives rise to a condition which may b3 mistaken for a primary joint affection with secondary " arthritic atrophy " of the muscles. It is only in the chronic stage that this error is possible. A careful attention to the history of the case will show its real nature, but with- out this attention the mistake is easy, and it is often made. Prognosis.—Except in its most trifling degree, brachial neuritis is a tedious malady ; the duration of every severe case is to be measured by months, and often more than a year elapses before the patient is free from pain. Post-neuritic pain is always more prolonged in the old than in the young, and the age of the subjects, together with the amount of damage to the nerves, causes suffering to last longer than in almost any other form. To these causes also must be added the degree of sensitiveness of the affected nerves, exceeded only by that of the fifth nerve, and also the mobility of the parts in which the plexus lies ; this involves a continued cause of irritation, brought into play as soon as the diminution in the severer pain permits the patient to employ the long useless arm. Relapses, moreover, are not uncommon. Recurrence may take place after moderate attacks, but seldom occurs after those of extreme severity. Recovery from the consequences of the inflammation is not always complete. The limb often remains smaller and feebler, with a liability to tingling and to cramp, and also to neuralgic pains under the in- fluence of changes in the weather, &c. But the most serious conse- SCIATICA. 123 quences are the alterations in the joints. These are very frequent: the fixation occasioned by the pain permits, and the tendency to perverted nutrition produces, adhesion between the articular surfaces, in consequence of which the movement becomes permanently re- strained. It is probable, moreover, that the constitutional state which underlies the primary malady often increases the degree of these joint-alterations. The shoulder, wrist, and fingers are the joints that are most frequently thus rendered stiff. The interference with the movement of the fingers is especially troublesome ; the joints become painful in consequence of the unavoidable strain on the tissues when an attempt at use is made. Treatment.—The treatment that has been described, as needed in neuritis generally, is suitable also for this form, and its details need not here be repeated. Abstinence from movement is of great import- ance ; the occurrence of stiffness of the joints in consequence of the immobility of the limb must be risked. It is doubtful, indeed, whether the tendency to this is much increased thereby, for the effect of pain, in preventing sufficient movement to maintain the normal state of the joints, is not materially increased by rest otherwise enforced; while the difference between a little movement and none, during the acute stage of the affection, is enough to make a considerable difference in the effect on the inflammation of the nerves. The influence of cocaine, injected under the skin, is very beneficial, but it is needed frequently in severe cases, and two injections (each -^—£ gr.) may be given daily during the height of the disease. It is important that the nerves should not be irritated by massage in the state of active inflammation; indeed, no therapeutic measure which occasions prin can do as much good as harm. After the tenderness has subsided, gentle rubbing, such as is agreeable, may be employed with advantage. Electricity is only needed for muscles that present the reaction of degeneration, or to aid in removing after-pains. In one severe case, associated with multiple neuromata of the skin, relief resulted from excision of the outer and inner cords of the plexus. The excised portions showed some interstitial neuritis.* SCIATICA. The most frequent of all forms of inflammation of a single nerve, unilateral, and primarily of the connective-tissue elements, and especially of the sheath, is that of the sciatic. The fact, coupled with the prominent character of the painful and disabling symptoms, have raised " sciatica " into a conspicuous position among diseases of * Maury and Jiibriug, ' Ainer. Journ. of Med. Sci.,' 1874; a similar case of septic origin recorded by S.mds and Seguin was not cured by excision of the plexus. 124 SCIATICA. the nerves, and indeed among diseases generally. This renders desirable a specially full description of the malady, fuller than strictly corre- sponds with its subordinate position as a variety of neuritis. As the word " sciatica " is commonly used, it is a general designation for all affections of which the chief symptom is pain in the region of the sciatic nerve. In a stricter use of the word, however, it is applied to painful affections of the nerve not due to any morbid pro- cess outside it; thus limited, it practically corresponds to inflamma- tion of the nerve. Two varieties may be distinguished, however, according as the process in the nerve is excited by primary disease in its vicinity, "secondary" sciatica; and "primary" sciatica, when the pain is the expression of disease beginning in and related to the nerve itself. Primary sciatica is sometimes regarded as a neuralgia. This view is in the main erroneous; the vast majority of cases of sciatica are really cases of true neuritis. Causes.—Sciatica is far more frequent in males than in females ; the proportion has been very variously estimated. The best evidence of the incidence of the disease is that presented by the patients treated at the Devonshire Hospital, Buxton, of which an analysis of 1000 cases has been made by Dr. E. V. Gibson.* The percentage of males is 88-4, of females ll"6,f giving a ratio of 5 to 1, which is probably very near the truth. The disease is unknown in childhood, and rare in the second decade of life. It does not, indeed, occur under fifteen; in more than half the cases it begins between thirty and fifty, and between fifty and seventy in a quarter. Having regard to the smaller number of persons living, the frequency of its occurrence must be regarded as at least as great in late as in middle life. J No special influence of sex is distinguishable in the decade forty to fifty: the proportion of males to females is that of the whole series. Under forty a smaller, and over fifty a larger proportion of females suffer. Exposure to the exciting causes is probably more common in males during middle life, when also the malady is promoted by the various accelerating influences which aid the active development of its chief constitutional cause—gout. But it must not be forgotten how comparatively small is the actual number of cases in women. Underlying most cases of sciatica is either the state of definite gout, or that rheumatic diathesis in which the fibrous tissues suffer, especially those that are connected with the muscles, a form closely connected with common gout by co-existence or descent. It occurs frequently in those who are themselves gouty, who present the personal characteristics of the disease, and have fostered it by mode of life. It occurs also in those of * Dr. E. Valentine Gibson, ' Lancet,' 1893, vol. i, p. 860. t 884 females, 116 males, in the 1000. X The percentage distribution of the 1000 cases at Buxton is as follows:—The age is taken at which the first attack commenced. Between 15 and 20, 14 cases; 21 to 30, 159 cases; 31 to 40, 310 cases; 41 to 50, 248 cases (one quarter of the whole); 51 to 60, 187 cases; 61 to 70, 71 cases; 71 to 80, 11 cases. CAUSES. 125 gouty inheritance, but who themselves have been abstemious, and sometimes present a weakly constitution—thin, pallid, neurotic. The latter have often suffered from acute articular rheumatism in earlier life. It is among them that the most severe cases are met with, in "which the inflammation spreads to other nerves, or involves the sheath of the sciatic with other structures, and that it develops early in life, during, for instance, the second fifteen years. This constitutional state, with all its effects, is sometimes met with when there is only trifling evidence of inheritance. Some unknown influence seems to determine its development in intense degr. e as a congenital tendency, manifested by rheumatic troubles, various and severe, early in adult life—the sporadic occurrence of that which is usually inherited. There is no evidence of a direct causal relation to other consti- tutional diseases. Syphilis has been supposed in some cases to give rise to it, but the cases are rare, and the common cause can seldom be excluded. An exciting cause is to be traced in many of the cases. Exposure to cold is the most frequent. It is usually local exposure, as by wet boots, standing in water, &c.; sometimes, however, a general chill of the body determines an attack. The exposure to cold may be even more direct, as by sitting on wet grass. Draughty water-closet seats are answerable for some cases. The neuritis often arises by the exten- sion of an adjacent rheumatic affection of the fibrous tissue, especiallv of that form of " lumbago " which involves the fibrous attachments of the muscles at the back of the sacrum, less commonly in its ordinary lumbar seat. This affection passes down from the sacrum, extendino- along the fasciae, to the nerve-sheath in the neighbourhood of the sciatic notch; or passes forwards, over the crest, to the front of the iliac bone, and spreads in the tissue about the lumbar plexus, and descends to that which covers the mass of sacral nerves from which the sciatic proceeds. (The fact is of much interest, because it shows that this form of fibrous rheumatism, of which we have only a very vague pathological conception, must be regarded as inflammation, since positive neuritis results from it.) The rheumatic pain has usually existed for a few days only before the extension occurs, but sometimes a chronic affection, after existing as such for several weeks, spreads acutely. Mechanical disturbance sometimes excites the disease, and often co-operates with other influences. The pressure of the edge of the chair, in those who sit much, is the most frequent. Muscular over-exertion, suddenly compressing the nerve in the thigh, is occa- sionally effective. If the nerve is already tender, a strong contraction of the muscles at the back of the thigh, especially when the knee is flexed, and the muscles can freely shorten and widen, may produce acute pain in the nerve, evidently by its compression. This cause is probablv effective only in a predisposed person, or when there is already com- mencing neuritis 126 SCIATICA. Various morbid processes within the pelvis may cause sciatica by compressing the sacral plexus, or by exciting inflammation which invades the nerve. Rectal and other tumours give rise to progressive pressure, and the inflammation excited descends the nerve, resembling the primary form. It may be an early symptom of a growth springing from the bone, as an enchondroma arising at the sacro-iliac synchon- drosis. Pelvic inflammation and injury during labour are occasional causes. A loaded rectum may be the excitant, but is a rare cause, although apt to be recurrent when once effective. Lastly, the sciatic nerve may be secondarily involved in mischief that is outside the pelvis. The most frequent cause of this is disease of the bone, as disease of the hip-joint, especially senile rheumatic inflammation (Gibson). The proclivity of the fibrous tissue of this nerve to suffer primarily is due to its position and the exposure this involves, and to its con- nections, which facilitate the passage of inflammation to it. But there are cases with a strong disposition for fibrous rheumatism to fix itself in the tissues of the pelvis, sacral and lumbar regions; the nerves cannot escape implication; whether the sciatic suffers early or late, and in what degree, depend on secondary conditions, but it is specially liable on account of the anatomical relations of its origin. The mass of the " sacral plexus " is prolonged into it, and the mem- branes covering this, and its branches, including the lumbo-sacral cord, are very liable to be the seat of such inflammation, wide-spread, fixing itself irregularly on the various nerves, but in special degree on the sciatic. In these cases the pain is extensive, and often severe in the front of the thigh, but the symptoms of descending neuritis are prominent chiefly in the sciatic. Symptoms. — The two nerves suffer with nearly equal frequency, but Gibson found, in his extensive series, that the left was a little the more liable, in the proportion of 48 to 44 per cent. In about 7 per cent. both were affected simultaneously—a striking indication of the smaller relative part played by the general blood-state, compared with poly- neuritis, and the preponderant influence of local excitants. The chief symptom of primary sciatica is pain along the course of the nerve-trunk, often also along that of its branches; pain in the area of its distribution is sometimes subsequently developed. The affection may begin suddenly, especially in cases of rheumatic origin, —as suddenly as lumbago. Some movement seems to excite it, but there has usually been slighter rheumatic pain in the neighbour- hood for a day or two, generally about the hip or sacrum. More frequently the onset is gradual; slight pain is felt along the back of the thigh, on movements and in postures that make the nerve tense, or cause pressure upon it. This pain, due to a slight degree of inflammation, has generally existed for some weeks, increasino- in degree until a considerable severity is attained, or suddenly becoming intense under the influence of some exposure or over-exertion. At SYMPTOMS. 127 * last the patient is easy only when at rest, and when the leg is in a certain posture. Any movement that makes the nerve tense causes pain, and to avoid this the knee, in walking, is kept slightly flexed. and the leg held stiffly so as to avoid stretching the nerve. * As the pain on movement increases, spontaneous pain is added, at first chiefly felt in the nerve-trunk, but soon spreading to its branches and distri- bution. It is usually most intense in certain spots—(1) above the hip-joint, near the posterior iliac spine, (2) at the sciatic notch, (3) about the middle of the thigh, (4) behind the knee, (5) below the head of the fibula, (6) behind the external malleolus, (7) on the back of the foot. The pain may radiate over the whole distribution of the nerve, but it is often so distinctly limited to the course of the trunk and branches, that the patient points these out with exactness when he indicates its course. The chief intensity of the pain is usually down the back of the thigh It may be dull or acute, is often burning in character, and worse at night. It may seem to dart downwards, starting from the highest point. As the pain on movement increases, the nerve-trunk becomes extremely tender to pressure. Even before the tenderness becomes considerable in the thigh, pain may often be produced in the following manner:—Let the patient sit on a chair with the knee at a little more than a right angle, and the body bent forward, so as to lengthen the course of the nerve at the hip- and knee-joints. If the finger is then pressed into the popliteal space, so as to make the nerve a little more tense, a pain is felt in the course of the nerve at the back of the thigh or above the sciatic notch, and behind the hip. It is due to the sensitiveness of the nerve to tension, and is a very useful test, especially when the part inflamed is high up within the pelvis. It may reveal the affection of the nerve here, by making it more tense, when there is no tenderness to pressure at the back of the thigh. Abnormal sensations other than pain are often felt in the area of distribution of the nerve,—tingling, formication, and the like; and in severe cases there may be diminished sensibility on the back of the thigh, on the leg, or the foot. The affection of sensibility at the back of the thigh indicates that the disease extends up the nerve, above the sciatic notch, to the origin of the small sciatic, or that this is involved in a simultaneous neuritis. In severe cases the muscles supplied by the nerve become flabby, tender to the touch, and sometimes distinctly weak and wasted. This is chiefly noticeable in the calf muscles, and in the group supplied by the external popliteal nerve. A tendency to cramp in the muscles is often very marked. There may be an alteration in the electrical irritability, usually a slight ■ increase to each form; it is considerable, and amounts to a distinct degenerative reaction, only in very severe cases. Slight fever and corresponding constitutional symptoms may attend an onset that is acute, when the inflammation is intense. Chronic cases, however, are usually not attended by elevation of temperature. 128 SCIATICA. The duration and severity of the affection are extremely variable. They depend on its intensity, and on the amount of rest given to the limb in the early stage, and on the constitutional state of the patient. The inflammation may be trifling in degree, causing pain on move- ment only, which may pass away in the course of a few weeks. On the other hand, the spontaneous pain may be so continuous and intense that sleep can be obtained only by the help of narcotics, and the disease may continue for many months, and even for a year. In most cases that last more than a year there is partial recovery and relapse. Improvement is shown first by the subsidence of spontaneous pain, followed by the slow diminution of the pain on movement, and then of the tenderness of the nerve. The muscular wasting, which occurs in severe cases, may last long after the active stage is over; fibrillary contractions in the muscles that have been affected may continue for years, and are often accompanied by a strong tendency to cramp, which may be excited by voluntary contraction. Occasionally a secon- dary neuralgia is set up, which may be very enduring, may involve the entire length of the nerve, and may be wide in distribution, ex- tending outside the sciatic area. The disease is prone to relapse, and still more prone to recur after recovery. A second attack may occur in the same or in the other leg, but both legs are scarcely ever affected at the same time. At last, however, the tendency of the sheath to be inflamed seems to become exhausted, and the liabitity to cease. The cases of secondary sciitica depending on disease outside the nerve, compressing or irritating it, differ, in some respects, from the primary form. The early pain is felt less in the nerve-trunk than in its distribution, especially when the nerve suffers first by pressure; interference with the conducting functions is more conspicuous in the early stage. The primary form may be afterwards closely simulated, because secondary inflammation may descend the nerve and induce the same tenderness of the nerve-trunk. The course of the secondary cases is more progressive, but it depends on that of the original disease. Complications of sciatica are rare, but one or two deserve mention. Cutaneous eruptions, usually herpetic in character, have been occa- sionally met with. These may heal slowly, but, in themselves, they are unimportant. Sometimes the epidermis exfoliates; oedema of the limb occurs in rare cases. These are, however, rather effects of the neuritis than complications, and so also is the muscular wasting that is occasionally pronounced. The trophic changes in the skin are the expression of a peculiarly irritative character of the inflammation. Occasionally the symptoms of inflammation of one sciatic nerve are attended by bilateral symptoms, especially at the onset, such as tingling or pains in the feet and the soles, or some weakness of the flexor muscles of both ankles. These indicate an associated poison ; it mav be alcohol causing its own peculiar bilateral peripheral neuritis, and PATHOLOGY. 129 aiding in the generation of their acute gouty effects on the sciatic. Such a combination may puzzle the observer. A rare complication is a tendency of the mischief to ascend the nerve. Thus symptoms may spread from the region of the sciatic to that of the lumbar plexus ; the pain may spread to the front of the thigh, and the extensors of the knee may become flabbv and weak. This is probably due to the passage of an ascending neuritis up the lumbo-sacral cord. In extremely rare cases the morbid pro- cess has apparently reached the spinal cord, and indications of cord disease (e. g. disordered sensibility in the soles) have thus succeeded those of a primary and apparently simple sciatica. There may even be symptoms of lateral sclerosis (excessive knee-jerk, rectus clonus, &c), such as develop in some cases of arthritis and other conditions of pro- longed pain. The wider distribution of the pain and other symptoms, when a rheumatic inflammation is extensive from the first, may have the aspect of a complication, but often' the involvement of the sciatic does not dominate the case, which is then rather one of general crural neuritis, the result of the affection of the fibrous tissue of the floor of the pelvis where numerous nerves arise. The position of some of them determines the frequency with which they suffer specially, but the size of the sciatic nerve-mass necessarily causes its affection to be chiefly conspicuous. That of some of the lowest branches of the lumbar plexus also determines the common seats of the effects of extension upwards. In spreading cases, one effect of extension is of particular import- ance—the paralysis of the bladder that may result from extension to its nerves. The nearer part of the lumbar plexus is often then involved, and pain is felt in the front and outer part of the thigh, and even in the groin and lower part of the abdomen The vesical nerves from the pelvic plexuses of the two sides are near together, and the palsy of the bladder is often complete, and of long duration, outlasting, it may be, all other symptoms. Fortunately, it is a very rare complication. Pathology. — The evidence of pathological changes is .scanty. Rheumatic inflammation of the nerve is scarcely ever met with in its active stage ; the disease is not one which is even attended by death from other causes, and the morbid changes are a matter of inference. There is, indeed, hardly any organic disease so common as sciatica, of which, in its various degrees, opportunities for pathological observa- tion are so few and so meagre. Signs of inflammation have been found, chiefly conspicuous in the sheath of the nerve, and invading the interstitial tissue in more severe and prolonged cases. They are such as are met with in all forms of perineuritis—swelling and redness, most distinct opposite the middle of the thigh—thickening of the sheath, invading the substance of the nerve. Microscopical changes have been found, similar to those in acute neuritis elsewhere, in the rare opportunities for observation that have been met with. VOL. I. 9 130 SCIATICA. The existence of neuritis in all severe cases admits of no doubt; the symptoms—wasting of the muscles and anaesthesia—indicate structural damage to the nerve-fibres, and preclude any other explana- tion. There is every gradation between these severe forms and those which are slight, and the symptoms in the latter are identical with those of the earlier stage of the severe cases. The early local tender- ness proves the initial affection of the sheath and fibrous tissue. All cases of definite persistence and prolonged course are inflammatory. Only transient pains coming and going, associated with neuralgia else- where, can be regarded as of neuralgic character. These are often the sequel to a true neuritis, or are, not seldom, the manifestation of a tabetic neuralgia, the pain of which may recur during years in a neuralgic form, and even be influenced in its incidence by change in the weather, so as to receive a rheumatic character. The symptoms are explained by the morbid process, and the facts of neuritis in general, already described, apply to this disease in every point. It is primarily a perineuritis; the pain m the nerve and its tenderness are due to irritation of the sheath-nerves. The pain re- ferred to the distal portions of the nerve is due to the irritation of its conducting fibres by the interstitial inflammation, while their greater damage explains the sensory impairment and muscular wasting. The disease, like other forms of irregular neuritis, is not one essentially of the nervous system. It is a local effect of the con- stitutional malady, gout, or the fibro-rheumatism which results from the inherited diathesis, and each seems to depend on the presence of chemical toxines in the blood, generated in the body by abnormal metabolic processes. Uric acid is probably only one of these, and not the most harmful, or that which has the most special influence. But the nature and origin of these is still one of the most obscure as it is one of the most important problems of pathology, and we must assume that it acts upon tissues disposed to degraded nutrition by the influence of inherited tendency. Diagnosis.—The distinction between a sciatic neuritis and a sciatic neuralgia is sometimes difficult, although less frequently than might be inferred from current accounts of these diseases, in which the history of the neuralgia has been written from the symptoms of the neuritis. If we recognise that all cases of sciatica with persistent tenderness of the nerve are really neuritic, cases of sciatic neuralgia become extremely rare. The two diseases occur usually under different conditions : the subjects of neuralgia have often suffered from neuralgia elsewhere, and are generally weakly and anaemic. The pain is from the first spontaneous ; it occurs as part of more extensive and severe attacks ; posture has little influence upon it; movement is not itself painful, although it may excite paroxysms of pain. The pain is referred to the branches and distribution of the nerve rather than to its trunk, or it darts up or down the trunk ; and tenderness of the nerve, if it exists, is altogether subordinate to the spontaneous pain. TREATMENT. 131 When the nerve is only one of many localities in which the pain is felt, and the patient is an adult, the possibihtv of its tabetic nature must be remembered. This is practically certain if the knee-jerks are assuredly absent, but of this fact there must be no question. The " lightning " character of the pain is an important diagnostic feature in such cases; although the presence of this character has almost pathognomonic significance, pain of less acuteness and brevity is often significant. It is an instance in which a certain feature has great significance, but its absence is of relatively small value. Secondary sciatica is usually produced by disease of bone about the hip-joint, or of the joint itself, or by disease in the pelvis. In the former case a careful examination (never to be omitted in any case of sciatica) at once reveals the mischief. When the disease is within the pelvis, and is not primarily connected with the nerves (as the pressure of a growth), the tenderness of the trunk of the nerve is slight in pro- portion to the pain felt in its distribution; this circumstance should always lead to a careful search for any indication of pelvic mischief. In any case of doubt, or of prolonged course with steady increase in the symptoms, a rectal examination should be made. Sciatic pain occurs in some diseases of the bones of the spine, in lesions of the cauda equina, and occasionally in disease of the spinal cord itself. In these cases we have little or no tenderness of the nerve; the pain is chiefly peripheral, and very often bilateral. Double true sciatica is so rare that bilateral pain should always suggest disease of the nerve-roots; but the pain in these cases is generally irregular in its distribution, and considerable in other nerve areas in the leg or neighbourhood of the hip, and is often increased much by movement of the spine. These cases of "secondary sciatica" are of much practical import- ance, because their nature is usually mistaken; for a long time the patient is thought to be the subject of the ordinary more common form, and is treated accordingly, even when the character of the pain should raise a suspicion of the nature of the case. Prognosis.—The prognosis of sciatica, not secondary to disease outside the nerve, is good as regards ultimate recovery, but is very uncertain as regards severity and duration. As a general rule, these features are proportioned, but both are influenced by the practicability of adequate rest. Irritating exertion may lengthen the duration of the disease by many months, and indeed relapse may follow each partial recovery for one or two years. Spontaneous pain, and that which is referred to the distribution of the nerves, make the prospect less favourable. Treatment.—The principles of the treatment of sciatica are those of neuritis already described, and only the points of special character need be here repeated. In all cases rest to the limb is important beyond any other measure, and its urgency is proportioned to the acuteness and severity of the symptoms. Many slight cases are converted into 132 SCIATICA. severe ones by unwise exertion. Every posture that induces pain, and all movements which increase that which exists, should be avoided. The same is true of pressure on the nerve by a hard seat, and by strong contraction of the flexors of the knee. Pain may be thus suddenly brought on in severe degree, and may endure. In more positive treatment the causes of the disease must be remembered, and, among these, the frequency with which it is related to a gouty or rheumatic blood-state. In gouty cases saline purgatives are often of signal service, and are distinctly useful in preventing attacks in those who are liable. In the acute stage of a severe attack, hot linseed-meal poultices should be applied along the course of the nerve. Counter-irritation is of great value, and cannot be employed too early. A commencing attack may often be cut short in a few days by rest, and a series of mustard plasters or small blisters applied over the seats of pain, moved as this changes under their influence, chasing it, as it were, from one spot to another, until it disappears. Internally, whenever there is reason to believe that active inflammation exists, mercury should be given—a grain of blue pill twice daily; nothing else seems distinctly to influence the process. Salicylate of potash or lithia, and nitrous ether, should also be given at the onset—soda salts being avoided. Spontaneous pain can only be relieved by sedatives. Morphia is the surest, but it should only be used for the relief of severe spontaneous pain. Cocaine often proves of great service, if it can be combined with rest, and injected at the actual source of the pain. It should be injected pretty deeply at this place, but not into the nerve. One twelfth of a grain may be first used, increased rapidly to a third or half a grain. It generally relieves, although not in the same degree as morphia, but it seems to have more influence in promoting the subsidence of the inflammation, as described in the account of neuritis, apparently because it has a more distinct influence on the conduction of irritating impulses along the nerves. Morphia, although equally effective elsewhere, may also be injected with advantage over the inflamed part of the nerve, so as to combine the counter-irritation of cutaneous acupuncture with some local as well as general sedative influence. Simple acupuncture along the course of the nerve has been recommended: it gives temporary relief to the sciatic pain, as to any superficial pain, but the cases are very few in which it has a permanent effect. Sedative or counter- irritant liniments and ointments may also be applied along the course of the uerve; the most useful are belladonna liniment mixed with an equal part of chloroform liniment, and aconite ointment, rubbed in until distinct tingling is produced. Electricity is chiefly useful in the later stages; its method of use has been described in the account of the treatment of neuritis. In very obstinate cases, nerve-stretchino- has done good; sometimes, perhaps, by releasing the nerve from compressing adhesions, but probably more often by effectinc an energetic counter-irritation, and enforcing a beneficial rest. It has GENERAL CRURAL NEURITIS. 133 ceased to be the fasliion it was a few years ago, proof of its limited power. Forced movement of the joints, followed by rest, has been sometimes employed. In severe cases absolute rest in bed, and, if necessary, the application of a splint to ensure this, has been recom- mended. Weir Mitchell* has urged the use of a long splint, reaching from the axilla, jointed, so that the hip and knee-joints may be slightly varied in position, and the combination with this of a soft flannel bandage to the limb. The latter should be reapplied twice daily, from the foot to the groin, to lessen the amount of blood in the limb. If further measures are necessary, the application of the Paquelin cautery to the tender points, or of tin splints filled with ice water, is recommended, and after recovery massage with plentiful feeding. To prevent recurrence the causes of gout should be carefully avoided, and any signs of a gouty state lessened by an appropriate regimen. Habitual saline aperients are very important; the "flush out" clears away bile that would be reabsorbed, and the result is the same as increased secretion from the liver. Slight pain, threatening a recurrence, should be met by more rest, by counter-irritation with sina- pisms, and the careful avoidance of sudden movements, and indeed of all exertion that causes or increases pain. If this is considerable, or the nerve is distinctly tender, complete rest for a day or two may obviate the subsequent need for weeks of rest. If there is the sacro- lumbago that often precedes sciatica, the pain produced by sudden movement may often be lessened by a few moments' rubbing. General Crural "Neuritis. In rare Cases. " rheumatic" inflammation of the fibrous tissue covering the lumbar and sacral plexuses is so extensive that many or most of the nerves to the leg are involved, in consequence of the affection of their coverings at their origin. That of the sciatic may preponderate, as already mentioned in the section on Diagnosis, where the general characters of this form are referred to, and its secondary origin by extension, in some cases of primary sciatic neuritis. The cases in which the affection of the fibrous membranes is extensive give rise to such wide-spread symptoms, pain taking the course of many nerves and accompanied by the tenderness of descending neuritis and impairment of movement, often chiefly from the inhibitory influence of the pain it causes, attended by moderate muscular wastino-. There is usually slight increase or decrease in the electric irritability in some group of muscles, with increased knee-jerk, very rarely the reaction of degeneration where the nerves have suffered severely, and then the knee-jerk may be lost if these are the extensors of the knee. In cases of general crural neuritis the extent of the symptoms causes them to simulate such as are caused by disease of the spinal cord, * Weir Mitchell,' International Clinic,' 1891. 134 NEURO-MYOSITIS. and the distinction may be one of real difficulty. But it usually suffices to be aware of its occurrence and general characters, especially the moderate degree of the objective symptoms, and the existence of tenderness of some nerve-trunks near the pelvis. The diagnosis is also aided by the fact that it occurs chiefly in those who present a gouty or rheumatic disposition, acquired or inherited. The difficulty may be increased by the occasional presence of reflected pain on the opposite side, distinguished, however, by its slighter character, and correspondence in seat to that which is most severe on the side chiefly affected. The course of these cases is often prolonged, and months may pass before improvement commences, especially when the under- lying constitutional state is not recognised, the treatment of which, as in sciatica, is of primary importance. Anterior Crural Neuritis.—Such an affection of the fibrous tissue may be limited to that related to a single nerve, or some other branch of the sacral or lumbar plexus may be the seat of a neuritis like that which underlies sciatica. The anterior crural, or a branch, suffers most frequently, with resulting symptoms in the front of the thigh, or in the outer part. These are chiefly sensory ; motor symptoms are seldom conspicuous in cases so limited in area. The outer part of the thigh, in the upper two thirds, is a specially frequent seat of pain and occasionally of diminished sensibility. Anaesthesia in this region sometimes develops in a very chronic manner, without pain, as an isolated but curiously enduring symptom, usually stationary when discovered, and apparently the result of a limited neuritis of chronic form. It seems to have no sinister significance, but has little tendency to yield to treatment. NEURO-MYOSITIS. The term " neuro-myositis" is perhaps the most convenient by which to designate an affection, usually confined to a single limb, generally the arm, in which symptoms indicating an interstitial rheumatic inflammation of the muscles are the leading feature. They become tender, but the especial character is the pain caused by contrac- tion of the fibres, i. e. by the stimulus which, normally, generates afferent impulses. The adjacent fibrous tissue may also suffer, and especially that about the joints, while the condition of the nerve trunks may be such as to give rise to symptoms like those of simple brachial neuritis; but in such cases the affection of the nerves is subordinate to the peculiar state of the muscles. The affection has thus fairly well-defined features related to the tissue in which the afferent impulses originate, and these are common to all cases, however widely the rheumatic affection may spread, and however severe the NEURO-MYOSITIS. 135 additional symptoms which partake of the characteristics of other allied diseases. Hence the suitability of the name " neuro-myositis." in spite of some limitation of meaning which this use implies.* The affection occurs chiefly in patients in the second half of life, and under the same general conditions as brachial neuritis. It is, however, met with mere frequently in young persons, sometimes even in children, especially as a troublesome sequel to rheumatic fever, limited to the structures and muscles of the hand. More often it commences in the neighbourhood of the shoulder, in the deltoid and upper arm muscles, and passes down the arm to become more severe in the hand than at the elbow. Slight changes usually occur in the articulation of the shoulder, but more troublesome arthritic adhesions form in the finger-joints and at the wrist, as is common when mus- cular pain interferes with movements in rheumatic persons. This lasts so long in the intrinsic muscles of the hand, and tissues about the tendons, that the fixation of the joints becomes permanent before there is time for the restoration of the muscles, and some oedema in the acute stage is followed by the characteristic changes in the nutrition of the skin, peeling of the epidermis and wasting of the subcutaneous structures. But the affection of the muscles is the characteristic feature. The symptoms clearly indicate a rheumatic interstitial inflammation, affecting the tissue in which the afferent nerves begin, and the impulses they convey originate, perhaps, in the mysterious " muscle- spindles." In this tissue the impulses, unfelt in health, are generated by tension and compression, and become painful in some conditions, as after cramp. Then, if the muscle is stretched in extension, or the interstitial structures are compressed by muscular contraction, considerable pain is readily produced. Simple muscular rheumatism, transient, such as the common form of lumbago, seems an affection of this interstitial tissue too slight to persist as permanent inflam- mation. The chief feature of the form now under consideration is the production of pain by those forms of stimulation to which the nerve-endings normally respond (see p. 58), compression by voluntary contraction, and the passive tension in the antagonist. Pain is caused also in the structures about the joints, especially in the capsules, when the limit of movement is reached which the state of the various structures permits. Even passive movement induces a sudden contraction of the muscles, partly reflex, partly voluntary, which causes pain. This pain spreads widely in the mus- * It has indeed been proposed by Senator to use it to designate another disease, the rare acute symmetrical myositis (described further on), which is like multiple neuritis in toxic causation, and distal bilateral distribution (' Deut. med. Wochen- schr.,' 1893). The term has not, however, come into use for this affection, and seems not needed for it. " Acute myositis " or "polymyositis," the names employed in Germany, are sufficiently adequate to leave to its present application the term " neuro-myositis." 136 NEURO-MYOSITIS. cles, as those adjacent contract to stop the movement to which the pain seems due, and it is produced with readiness in the morbid state. Hence arises the characteristic feature. Muscular contraction, the great cause of pain, results from any movement, active or passive, and the patient acquires the conviction that no passive movement of the limb is possible without the production of pain in the muscles. Such pain does actually occur whenever an attempt is made to move the joints, as the shoulder and elbow, even in slight degree, or the wrist-joint, if with any suddenness. It is first and most felt not in the neighbourhood of the joints, but in the muscles. Afterwards some may be felt in the structures about the joint. On close and careful observation it will be found that the pain is related much more to the expectation of passive movement than to that which takes place. Before any movement is produced, the muscles contract in order to control and restrict the source of expected suffering. The pain coincides with this contraction, which is unconsciously volitional and reflex, rather than really voluntary. But with the help of some patience and perseverance it is possible to get the limb quite passive, resting without effort in the observer's hands, and to make gentle slow passive movement of the joints without the occurrence of this inhibitory contraction of the muscles. The patient is often astonished at the painless movement of joints wh<-n he thought great suffering would result from the least displacement of the parts. But if then a more sudden movement is made, and the alarm and perhaps slight pain cause sudden spasmodic muscular contraction, the pain felt in the muscles is great. There is usually some tenderness on sudden compression of the muscular substance, and this may be considerable and produced with some readiness, but often the sensibility to pressure is inconspicuous. We know, from the state left by common cramp, how easily pain is produced in the muscle by contraction; when this is sudden and considerable the pain may be shared by the nerves ; as already stated, those of the brachial plexus above the clavicle and in the axilla, present the same tenderness as is met with in simple brachial neuritis, although in slight and subordinate degree, manifestly from the inflammation of their sheaths. Other structures suffer, as already stated. The result is a considerable amount of fixa- tion of the limb from the pain which is produced by movement; this has more than one source, and it may be difficult at first to discern that from which the chief suffering proceeds. The arthritic changes within the joints produce adhesions which, with the alteration in the capsule, fix the joint in an abnormal posture, generally that which falls short of complete extension. The contraction of the muscles to inhibit movement tends to be more and more persistent and continuous, and this state of rigidity is prone to cause some shortening of their structures; nutritional change fixing the functional states assists in producing the slight deformity and fixed posture of the joints that are frequently observed. NEURO-MYOSITIS. 137 The malady is commonly of very prolonged duration, developing insidiously even after recovery from an initial, more acute attack of local rheumatism, especially when slight persistent pain on move- ment is maintained by the neglect of needed, rest. The affection is usually unsymmetrical, affecting one side only, after the fashion of these rheumatic affections of the fibrous tissues, of sciatica, or of brachial neuritis. Nevertheless, in moderate typical form, the manner in which it presents itself as an affection of the interstitial tissue of the muscles and their nerves justifies the view which is expressed in the designation given to it; and the peculiar implication of the afferent muscle-nerves, in consequence of its interstitial localisation in the muscles, justifies its inclusion among the maladies here described. This is further warranted by the condition which commonly results. The duration of the affection and the changes which ensue in the sub- stance of the muscles and the tissue about the joints, and the fixation of these during the time that elapses before the cessation of pain permits freedom of movement, by that time mechanically hindered, bring the cases into the class of residual consequences of nerve lesions. The resulting interference with use of the part is greater than is proportionate to the amount of rheumatic inflammation, being espe- cially great when much sensitiveness has proceeded from the long- continued pain, and fear of its induction outlasts the danger and exceeds it in degree. Some chronic neuralgic pain is apt to remain, due in part to the predisposition to neuralgia which most patients of this class possess. Another curious sequel hinders the return of mobility in these cases. Passive movement is difficult out of proportion to any pain produced, although this results if the attempt is persevered in and its strength increased. The common effect is a peculiar rigidity of the limb, such as at first suggests firm adhesions at the joints—an impression that may be easily retained if the examination is hasty. Its nature is rendered clear by sufficient patience and close observation; passive movements must be attempted with the utmost gentleness and slow- ness, and the attention of the patient turned to some other part during their course, while the observation of the examiner remains fixed. The same care is necessary in local therapeutic measures if these are to be successful. Gentle upward rubbing to the muscles should be afterwards combined with slow passive movement, at first scarcely appreciable in degree, and continued with the endeavour to keep behind the production of the muscular spasm. This will often permit good to be effected by local applications of heat, dry or moist, liniments, nst itutional disturbance as indicate an acute morbid blood-state. But this diagnosis often rests chiefly on the exclusion of other causes; if these are absent, the fact that neuritis is known to result from obscure blood-poisons may be allowed weight, especially if the symptoms begin in the legs or in all parts of the limbs simultaneously, and do not affect VuL. 1. 12 178 MULTIPLE NEUKITIS. exclusively at first the extensors of the extremities. Sensory symptoms in these cases at the early stage often take the form of tingling and "numbness," and the pains so characteristic of the alcoholic form are frequently absent, or are represented only by dull aching. In slight cases of this type sensations of numbness and "pins and needles" in the legs, with readiness of fatigue and loss of the knee-jerk, may be the only symptoms. The facts that the nature of toxaemic causes is to a large extent unknown, and that the poison may probably be acquired from without, make it necessary to be prepared to find this cause of multiple neuritis under almost any circumstances. Residence abroad should suggest an inquiry for exposure to malarial influences. The possible significance of tubercle as a cause should lead to a careful exa- mination of the lungs; but the possibility that phthisis may be an effect, and not a cause, of multiple neuritis must be borne in mind. Prognosis.—The danger to life is in proportion to the acuteness of the malady, to its severity as measured by the extent of the para- lysis, and to the degree in which the strength of the patient is impaired by other maladies, or by the cause of the neuritis. It is important also to remember that when the affection has increased up to the time that the patient comes under treatment, it generally does not respond immediately to the arrest of its cause, such as the with- drawal of alcohol, but continues to increase for two or three weeks. It is this temporary progressive tendency that constitutes the graver element in the disease, and must be taken into account in every initial prognosis. Hence the forecast must be guarded in all cases that are severe when the patient comes under treatment, and most so if there has been a rapid increase in symptoms that had existed for a long time in slight degree. If the extensors of hands and feet are powerless, and the muscles connecting the limbs with the trunk are distinctly enfeebled, unless the disease has clearly begun to lessen, there is danger that a further extension may involve the muscles of respiration; this is especially great when the muscles moving the shoulder are considerably weakened. It obviously follows that the danger is still greater if the muscles of the trunk, and especially of the chest, have already given evidence of changes in their nerves. Pain in the trunk of the same character as that in the limbs is also a grave symptom if the motor power of the limbs has become small, or the case is one unusually general in its distribution, because where the sensory fibres are suffering the motor fibres are in danger also. Paralysis of the diaphragm adds considerably to the danger, and its power should be carefully watched in the manner and with the precautions mentioned in the account of its paralysis (p. 33). It may become paralysed without the fact coming to the conscious- ness of a patient lying quietly in bed, but a slight weakness of the intercostals will then cause considerable difficulty of breathing and an accumulation of mucus in the lungs, a condition predisposing to definite bronchitis, by which the patient may be quickly suffocated. PROGNOSIS. 179 The importance of this point is great, since respiratory palsy is one of the most common immediate causes of death. It is probable also that deficient breathing power is one of the causes, perhaps even the chief cause, that lead to the development of the chronic phthisical lung disease that comes on in so many prolonged cases. Especially important, also, is any indication that the nerves of the heart are suffering. In an acute increase due to continued use of alcohol the vagus sometimes suffers severely before other nerves, and increasing frequency of the pulse is then of most serious significance. The prognosis should be guided by the motor rather than by the sensory symptoms. The latter may improve while the former increase with- out lessening the gravity of the latter indication. Persistent oedema is of bad omen, and so also are other indications of considerable blood- change. When once the malady has become stationary, and its cause has definitely ceased, the danger to life is small, except in severe cases, in which the pains are intense, the patient helpless, or the heart is feeble, and the pulse persistently frequent, or there are signs of lung disease. In these, as in all cases, moreover, the danger is much increased by any indication that the spinal cord is involved. The tendency to re- covery is far less in the cord than in the nerves; and retention of urine (with all its secondary consequences), bedsores, &c, are prone to occur, and to involve their own danger even if the disease in the cord does not increase. The prognosis as regards life in cases of moderate severity depends, indeed, as much on complications as on the state of the nerves. Signs of chronic cerebral meningitis, of degeneration of the walls of the heart, of disease of the liver and of the kidneys, also lessen the prospect of escape with life. The danger is, however, greatest, and the mortality highest, in the acute cases that are due to some toxaemic state or to cold, and it must be estimated by the rapidity with which the paralysis develops and spreads. Whenever it becomes considerable in a few days, the danger of early extension to the mechanism for respiration is very great. In these cases, also, pneumonia frequently occurs, concomitant with the early symptoms, and few cases thus complicated recover. In cases that are not fatal the full development of the symptoms is followed by a stationary period, which lasts for one or two months before improvement begins, and for this the patient or friends should be prepared. The course of restoration is always extremely slow; the muscles least affected regain power in from two to four months, but it is usually six months or more from the onset of improvement before the extensors are fairly strong, if their palsy was considerable or complete. The intrinsic muscles of the hand are still longer in recovery. The improvement in the nutrition of the muscles follows that in then- power, so that they remain smaller than normal, long after they have reo-ained strength. It may, indeed, be years before the muscles whose size can be well seen, such as the abductor indicis, are of normal size. 180 MULTIPLE NEURITIS. It is seldom that any permanent weakness is left unless the spinal cord is diseased, and when a patient is distinctly improving a good ultimate prognosis may be given, provided there are no complications to inter- fere with it. In no case with distinct spinal symptoms can we feel confident that restoration of power will be complete ; and in cases in which there are indications of considerable damage to the cord it is almost certain that some lasting weakness will be left. The electric irritability of the muscles and nerves may be expected to return to the normal more slowly than their capacity of response to the will, but sooner than their nutrition. The conditions that are ob- served in these cases are the same as in the isolated form of neuritis, in which, although the primary change is in the connective tissue, the symptoms depend on the secondary changes in the nerve-fibres. Hence the statements made on p. 71 are equally applicable to multiple neuritis. The reactions often furnish important information, especially soon after the onset; the more the irritability deviates from the normal the greater will be the subsequent wasting, and the longer the duration of the palsy. When some faradic irritability returns in both nerve and muscle it may be regarded as a sure indication of advancing restoration of structure, which is certain to involve a progressive in- crease of conduction of voluntary impulse, and response to it. If the trunk nerves are not involved, the prognosis in severe cases is a little better when the arms are chiefly affected than when the legs have suffered most. The sensory disturbance may be expected to follow a course on the whole similar to that of the motor symptoms. A diminution in the spontaneous pain may be anticipated sooner than in the tenderness of the nerves and muscles, which usually lasts, in lessening degree, until the muscles have regained some power. The extreme tenderness, indeed, passes away with the spontaneous pain, but some degree of over-sensitiveness continues for a long time. Happily the tendency to persistent neuralgia, seen after the isolated form, need not be antici- pated after multiple neuritis. We find the explanation of this in the absence of the new formation of connective tissue from the inflamma- tory products, which in the isolated form perpetuate, by cicatricial con- traction, the irritation to which inflammation gave rise. There is little difference in the prognosis, as regards recovery, in the different forms of neuritis. The anticipations that may be formed are governed in all by the rules just mentioned, and the risk to life has been already considered. In all, however, it may be repeated the extent to which the cause is under control forms an essential element in the problem, and must influence the conclusion in every case. The prognosis, however, is better in the sensory than in the motor form better when the arms escape than when all the limbs are involved and better in cases of chronic than of acute onset, and better if an apparently acute onset is really such than if it succeeds slio-ht sym- ptoms of longer duration. When the malady follows an acute specific TREATMENT. 181 disease, the severity of the latter is no guide to the course of its sequel; severe neuritis may follow a mild attack of the acute specific. Treatment.—The different classes of multiple neuritis here con- sidered need treatment that in some respects varies, and in others is the same in all forms. Tn all it is essential to discover, if possible, the cause of the neuritis, and to remove it or arrest the continuance of its action. This obviously should be the first consideration in cases due to alcohol, in which it is sometimes of great difficulty. It is desirable, as a rule, that alcohol in all forms should be given up entirely, but often this has to be done by degrees, a great reduction in amount pre- ceding entire abstinence from it. With patients who are " their own masters " the reduction is often most difficult to secure, and it is neces- sary to give a warning that not only will life be in danger, but that the pains will certainly increase, and continued indulgence will entail sufferings so great that any sacrifice would be made, or deprivation endured, if their intensity could be realised. With every female drinker, deception should be considered not only possible but probable; those who are under the control of relations or of a husband have generally had a long training in duplicity in order to procure stimulants, and it is easy for them to continue it, even when kept in bed, if they are attended by their own servants. These are corrupted, and alcohol is taken in secret when the fact is being stoutly denied. If a case does not present the arrest or improvement that might reasonably be expected from the withdrawal of the cause, such continued drinking should always be suspected. Hence it is of great importance that such patients should be, whenever practicable, under the immediate care of trustworthy trained nurses, rather than of their own servants or of relatives who may be improperly influenced or persuaded; if the patient's means do not permit this, removal to a hospital or some public institution is desirable. When the heart is too weak to permit the entire withdrawal of stimulants, the amount taken must be regulated solely by the state of the pulse. In such cases total abstinence is attended with some danger of the cardiac failure which has been mentioned as one of the causes of death. When the disease is due to cold, the patient should be carefully preserved from risk of further ex- posure, which during the early stages may convert a slight into a severe attack. Even in alcoholic cases a chill will cause a rapid increase in the symptoms, and both this and fatigue should be carefully guarded against. In other forms, also, these measures, adopted in the stage when pains and tenderness are the only or chief symptoms, would often prevent the further development of the disease. Physical rest is of great importance, and in all cases, except the slightest, rest in bed is desirable The excitation of the nerves caused by movement tends to intensify the morbid process in them, and what- ever produces pain has the same effect. If the patient is in bed, local treatment can be more readily employed, and the restraint facilitates the necessary control over habits. The feeding of the patient is an impor- 182 MULTIPLE NEURITIS. tant part of treatment, especially when the stomach has been deranged by alcohol. At the outset, warm fomentations should be applied over any tender nerves. Care must be taken in their use over the region supplied by the affected nerves, on account of the danger of vesica- tion ; troublesome ulcers may be caused by even moderate degrees of heat, as in the case mentioned on p. 79. Such applications, and also counter-irritants, have less effect in the parenchymatous forms than when there is a tendency for the connective tissue and sheath to suffer, and for their vessels to be involved in the process. A warm bath, for fifteen or twenty minutes daily, is often of service if the patient is able to bear the necessary procedures. Care should be taken that the patient does not habitually assume a posture that will promote the occurrence of deformities The dropping of the feet is the greatest danger, and should be prevented by a large and heavy sand-bag about nine inches in diameter, which may be adapted to the position of the feet, or by a board placed across the bed. Frequently such a boot as that figured (Fig. 61) is of great service in preventing or minimising contraction of the gastrocnemii. Another danger is the habitual flexion of the knees, permitting a contraction of the hamstring muscles, and due to the discomfort that is caused by extension of the knees ; this should, however, be insisted on, because the initial discomfort soon passes away if extension is adopted from the outset. The extension of the knees involves that of the hip-joint, and prevents contraction of its flexors. No drug has any very marked influence on the morbid process. It has been seen that multiple neuritis tends to lessen after its cause has ceased to act, and under such conditions it is easy to come to the con- clusion that drugs do good which merely do not hinder. Mercurv which is certainly useful in isolated perineuritis, has little influence on the parenchymatous form, but it may be tried in any case in which it seems probable that the sheaths are primarily affected, and in which pain or tenderness in the larger nerve-trunks is a prominent svm- ptom. During an acute febrile onset the treatment should be that * For full description of this simple apparatus, see«Clinical Juurnal,' March 6th, 1895. TREATMENT. 183 adapted to the general state, and must differ according to its cause. In such an onset of an alcoholic neuritis, citrate of potash, nitrous ether, and compound tincture of cinchona are suitable, with a little digitalis if there is feebleness of the pulse. When due to cold, sali- cylate of soda may be given, or, if the attack has been predisposed to by alcohol, salicylate of potash may be substituted so as to avoid the retention of uric acid in the system by the soda. The probability of a gouty state of the system should be remembered in all cases in which there is a history of alcoholism. In the toxaemic forms in which there is a suspicion of a blood-state allied to that of septicaemia, no drug affords such a prospect of influence as the tincture of the per- chloride of iron in full doses, 20—30 minims three or four times a day. Afterwards, when the actual onset is over, and from the first in the more chronic cases, tonics answer best—iron, quinine, or small doses of strychnine. Iodide of potassium, for some reason, seems to do good only in the chronic sensory form. In this also arsenic has been found useful, but arsenic should be given with caution, and in small doses ; there is some danger that large doses may intensify the malady, since polyneuritis is one of the effects of chronic poisoning by arsenic, and has actually been produced by the medicinal use of the metal. Cod-liver oil is useful in the later stages, especially if there is impairment of general nutrition. In alcoholic cases the addition of cocaine, TV to } grain to each dose of whatever is taken, aids in lessen- ing the craving for stimulant. When due to malarial poisoning, quinine may be given freely. The complications of multiple neuritis do not need other treatment than that suitable to them when they occur alone, nor do they indicate any special imodification in the treat- ment of the disease of the nerves. In most cases the pain is such as to render anodynes necessary. Of these, morphia, by hypodermic injection, is the most effective, but should be employed only as a last resource, and so regarded will not often be found necessary. Its danger is the readiness with which those persons who were previously alcoholic become habituated to it. It may be given by the mouth with less risk, but in other drugs we may find a substitute that is effective in most cases. Injections of cocaine beneath the skin over the seat of pain often afford considerable relief, and cocaine may thus be given instead of by the mouth, securing the double object of lessening at once the local pain and the craving for stimulant—which is relieved almost as effectually when cocaine is given by the skin as by the mouth. Atropine may also be given hvpodermically. In antipyrin and acetanilide we have drugs of another nature, that often give great relief to spontaneous pain. Indian hemp may also be given regularly without harm, and without interfering with the occasional administration of other anodynes ; while to procure sleep, if pain is slight, reliance may be placed on bromide, sulphonal, trional, or chloralamide. Antipyrin also often gives a patient « -rood night in spite of some pain. When there is mental excitement 184 MULTIPLE NEURITIS. hyoscine is useful, especially by hypodermic injection in doses of 4^y to iio or t^o of a grain. The application of electricity to the paralysed muscles is important in order to maintain their nutrition in as good a state as possible during the process of recovery of the nerves. Only voltaism has the power of doing this, and should be applied daily, large sponge-holders being employed so that the current may reach as much muscular tissue as possible; only such a strength should be employed as will produce visible contraction and cause no after-pain. Voluntary mus- cular action constitutes a more effective stimulus to nutrition ; but if, although the muscle can be put in action by the will, there is loss or great diminution of faradic irritability, or an excess of voltaic irri- tability shows that some fibres are in an abnormal state in consequence of the degeneration of their nerves, voltaism may still be applied with advantage. There is no evidence that the application of electricity to the nerves has any influence on their regeneration. Shght sensory loss is sometimes lessened in the chronic stage by the application of faradism by the wire brush. The tender limbs may be wrapped in cotton wool, with or without a covering of oiled silk. Massage is of service in the later stages of the disorder for its influence on the nutrition and circulation in the affected limbs. An upward movement of the pressing hand helps the circulation of fluid in the vessels and in the tissues. It cannot be borne during the acutely painful stage, and, indeed, as long as it gives pain it probably has more capacity for harm than for good. In the later stages it helps to overcome the contracture of the muscles, which should be gently extended at the same time as they are rubbed, —pressure, for instance, being made upon the ball of the foot at the same time as the calf muscles are rubbed. The very long course of all severe cases makes a heavy demand on the patience of the sufferer and the perseverance of the medical practi- tioner ; but the prolonged convalescence has the advantage, in alcoholic cases, of enabling a habit of abstinence to be formed. This, with the recollection of what has been endured, renders multiple neuritis more often a cure of intemperance than any other of the many maladies to which alcohol gives rise. During the slow recovery, the measures above indicated—tonics, electricity, and massage—should be con- tinued. As already stated, the power of standing is interfered with for a time after the muscles have regained adequate strength, by the contraction of the gastrocnemii, causing a degree of talipes equinus. This is often so considerable as to suggest the desirability of dividino- the tendo Achillis, but the operation is seldom if ever necessary. The attempt to stand and walk constitutes a powerful means of extension of the calf muscles, before which they soon yield sufficiently to permit the balance of the body to be maintained, and then progress becomes more rapid. The contraction at the knee and hip is more difficult to get rid of, but generally yields in time to persevering and gentle efforts. ENDEMIC NEURITIS. 185 Acute Multiple Myositis. Acute Polymyositis. In rare cases there occurs an acute interstitial inflammation of the muscles, which presents a general resemblance in distribution, and in toxic causation, to the acute polyneuritis we have just considered, but differs in the facts that the affection of the nerve-fibres is trifling and evidently subordinate, and that the subcutaneous fibrous tissue is usually also inflamed, causing oedema and erysipelatoid dermatitis. This is sometimes absent while the nerves are occasionally inflamed in greater degree, precluding an absolute separation, although most cases present a sufficiently uniform difference to make a distinctive type. The malady is so uncommon, and the cases that have been met with have varied so much in severity and precise causation, that they hardly do more than illustrate the variety of special form which may be as- sumed by such toxic maladies, and which indicate corresponding features in the poison which causes them. The symmetry of its mani- festations is conclusive evidence that the blood is its vehicle, and the facts that a source of definite poisoning can often be traced, while the distal parts of the limbs are commonly the first to suffer, constitute a conspicuous connection with polyneuritis. Although not a primary affection of the nervous system, its relations justify its mention here, especially since its features have enough in common with the acute form of multiple neuritis to involve some risk of confusion in diagnosis. ENDEMIC NEURITIS. Malarial Neuritis. The clear evidence that has accumulated, showing the dependence of multiple neuritis on toxic blood-states, some connected with an organismal virus, prepares us to find that it often results from the pro- ducts of the growth of organisms of endemic character, such as cause the malarial fevers of which we are able to discern a variety of forms. Conspicuous among them is the malady known generally by the name of " beri-beri," but a simpler form of neuritis palsy is more common, although absolutely infrequent. Yarious forms, however, result from the untypical varieties of malarial disorder, and their occurrence, causation, and relations are still only imperfectly discerned, met with, as they are, chiefly in tropical countries The characteristic form involves chiefly the motor nerves, usually of the legs, and is met with especially in India and on the coasts of Africa. The arms suffer only in severe and prolonged cases. It is usually subacute in course, and the resulting disability entails early removal from the causal conditions, which lessens much the danger to 186 MULTIPLE NEURITIS. life that is involved. Secondary contracture in the muscles is especi- ally common, and constitutes a troublesome sequel, prolonging ^ for months the inability to walk, unless prevented by the means described elsewhere. Sensory symptoms of various characters may be the leading features in other cases in which the organisms are peculiar in their nature, and these give rise to symptoms which are prone to set up special diffi- culties in diagnosis, unless their probable nature is suspected, and the significance of the exposure to the cause is perceived, and receives due weight. Beri-beri. Beri-beri, the Kak-ke of Japan, is also known by various popular names in the several countries of which it is native.* It is a wide- spread disease, passing by a contagion that is readily conveyed and propagated, having apparently its chief homes in Japan, the Eastern Archipelago, India, New Zealand, Ceylon, the South Pacific Islands, and the coast of Brazil. It is especially prevalent in the Dutch East Indies, among the soldiers and in the prisons, and this led to its systematic investigation under the direction of the Netherlands Government. Through this our knowledge of the malady was much increased, especially by the investigations of Pekelharing and Winkler,f who had a large number of cases under their observation both during life and after death. Still more recently a troublesome outbreak occurred at a lunatic asylum at Dublin. Opinion as to its nature and cause has varied much, and still is far from uniform among those who have studied it; but there is a strong preponderance of evidence that it depends on a specific organism, and that symmetrical peripheral neuritis is the common effect of the virus, and the mechanism by which its chief symptoms are produced. The organisms found J are in the form of rods and cocci, but it is probable that these are only * Beri-beri is probably a modification of the Cingalese name for the disease, balir- bari = extreme weakness. Kak-ke is the old Chinese name for it, by which it is mentioned in their medical works since 200 B.C.; it is derived from two words, meaning "legs" and "disease." The affection disappeared from China two cen- turies ago, remaining in Japan, where it continues a most serious endemic malady. f Pekelharing and Winkler, 'Onderzoek naar den aarden de oorzaak der Beri- beri,' Utrecht (sep. publication), 1889, analysed in the 'Centralbl. f. Nervenkr.,' 1889; also ' Weekblad f. Nederl. Geneesk.,'1888, and * Deut. med. Wochenschr.,' 1888, No. 30. Other important contributions to the subject are by Balz, 'Zeitschr. f. kl. Med.,' 1881; Scheube, ib., 1882; Weintraub, ♦ Wien. med. Wochenschr.,'1888, Nos. 23—44.; Van Eecke, 'Tijdschr. v. Nederl. Indre,' 1887, p. VI; Wernich, 'Virchow's Archiv,' Bd. lxxi; Miura, 'Virchow's Archiv/ Bd. cxi and cxiv, whose conclusions, however, differ from those of most investi- gators; Seguin, ' Phil. Med. and Surg. Rep.,' 1888; and Springthorpe, 'Australian Med. Journal,' 1889. Balz, in 1881, expressed the opinion that the disease was a specific " panneuritis." X First described by Balz and Scheube, and since by Pekelharing and Winkler Eigkman, Weintraub, Springthorpe, and others. BERI-BERI. 187 different stages in the development of the same species. They have been cultivated, and peripheral neuritis of nearly the same distribution as in beri-beri has been produced by their inoculation. Eepeated in- oculations are, however, necessary for this result to be produced; and hence, from this and the phenomena of the disease, it is assumed to be not a simple infectious malady, capable of being induced by a single exposure to its cause, but one in which repeated opportunities for infection are necessary. In harmony with this are the facts that sufferers acquire the disease from residence in certain infected houses, or places in which it is supposed that the soil is saturated with the organisms; that they may rapidly recover on removal to a district that is free, and relapse only on returning to an infected place; that it prevails where persons are gathered together, as in barracks and prisons; and that the air of these places is found to contain the organisms which, collected from it, will cause the disease in animals, from whom it is transmissible to others by further inoculation. The serious extent to which it may spread among those who live together under conditions favouring its extension, is shown by the instance of a ship arriving in Japan from New Zealand after a voyage of 272 days. The disease spread on board so rapidly that altogether 169 cases occurred, with twenty-five deaths. In 1878 no less than 38 per cent, of Japanese soldiers were affected. It is probable that the in- halation of dried organisms floating in the air as part of " dust," is the chief way in which the disease is propagated. By some it has been thought that a nitrogenous diet induces or predisposes to the disease, and facts apparently supporting the opinion have been adduced ; an exclusive fish diet has been thought to cause it, and so also has a rice diet. A remarkable outbreak in Manila in 1880 followed a period of rice-eating during a cholera epidemic. These influences probably merely produce susceptibility.* It is a remarkable fact that Europeans seldom suffer. Males are more liable to the disease than females, and it is chiefly prevalent during the hot season. Symptoms.—Peripheral symmetrical neuritis is a constant feature of the malady, which is usually chronic in course and gradual in onset, but prone to undergo acute exacerbations. These have been generally regarded as acute forms of the disease, but it is said by Pekelharing that the symptoms of neuritis may always be discovered before the onset of the definite symptoms, and this when the patient is ignorant of their existence and feels quite well. Most observers have failed to recognise this, and it is probably true only under certain conditions, and persons suddenly exposed to an intense infec- tion may suffer acutely from the very commencement. Occasionally * Putnam ('Boston Med. and Surg. Journal,' 1890) and Birge, in the same periodical, describe a form of neuritis very like beri-beri occurring in men long at sea engaged in fishing, with poor food. In some of the cases scurvy was also present. 188 MULTIPLE NEURITIS. the malady develops with extreme rapidity and severity. On the other hand, many cases are chronic throughout, and last for months. The leading symptoms are those of multiple neuritis (chiefly affecting the legs and the cardiac branches of the vagus), dropsy, and symptoms of cardiac failure. The amount of urine is generally lessened, and its secretion may be almost suppressed in acute cases. A " critical" increase in the secretion may mark the commencement of improve- ment. It is unchanged in character, and does not contain albumen. The dropsy is a very variable symptom, and this has led to the dis- tinction of two forms, the dry and the dropsical. Pekelharing and Winkler, however, found some effusion of fluid almost invariably after death, and it is probable that its conspicuous presence or absence depends chiefly on the state of the heart (conditioned by that of its nerves), and partly on the trophic and vaso-motor disturbances due to the local neuritis. One very constant symptom is said to be a dis- agreeable epigastric sensation, variously described as pain, drag- ging, &c, sometimes very severe.* The earliest symptoms are a change in the electrical excitability of the peroneal nerves and the flexors of the ankles (which suffer most throughout)—a slight degree of the reaction of degeneration, quantita- tive and often qualitative. These are often to be found before there are any subjective symptoms, which begin as a sense of heaviness of the legs, readiness of fatigue, dyssesthesise and diminution of tactile sensibility in the lower limbs, palpitation and undue excitability of the heart. The electrical changes may be met with in slight cases which proceed no further, f and have shown that some patients, supposed to be shamming, were real sufferers. To these subjective symptoms are added other objective signs,—oedema along the edge of the tibiae, a peculiar pasty and stiff aspect in the face, an increase in the cardiac dulness to the right, roughness of the first and accentuation of the pulmonary second sound. These symptoms may increase slowly, or rapidly in the form of an acute stage. The degenerative reaction becomes complete in the muscles first affected, and they become para- lysed and undergo the characteristic atrophy, while other nerves and muscles progressively suffer in the same manner,—the calf muscles, the extensors of the knee, the adductors of the thigh, and, lastly, the flexors of the thigh and the abductors of the hip. In the trunk the abdominal muscles and intercostals may be involved, and in severe cases the arms are paralysed, first the extensors of the wrist and fingers, later the flexors, and sometimes most of the muscles, may be so atrophied as almost to disappear. The face often suffers: the diaphragm may become paralysed, and also the larynx (the inferior before the superior laryngeal nerve) ; while grave cardiac weakness .and increasing dilatation of the heart testify to the serious implica- tion of the cardiac branches of the vagus. Simultaneously, sensory * Von Tuzelmann, * Lancet,' 1894, vol. ii, p. 1467. t Pekelharing and Winkler, Eigkman (1889), &c. BERI-BERI. 189 symptoms develop, corresponding in distribution to the more severe motor symptoms ; sensibility to touch is lessened or lost (first on the inner side of the lower limb), while that to pain usually remains, and sometimes is augmented to the degree that constitutes what has been termed " anaesthesia dolorosa." The temperature-sense may be diminished to either heat or cold or both in various parts, and there is often considerable loss of cutaneous sensitiveness to faradism. There may be tingling, formication, and other dysaesthesiae, together with tenderness of the nerves and muscles, but far less in degree than in most forms of polyneuritis, and chiefly marked in the early stage of the disease. The oedema that is so common begins in the legs, usually spreads widely, and involves not only the subcutaneous tissue but the cavities of the peritoneum, pleura, and pericardium: in the last it seriously impedes the action of the already dilated and feeble heart, It is to cardiac failure that death is commonly due ; the other chief cause is failure of the respiratory muscles, aided generally by effusion into the pleural cavities, and accompanied by the indications of cardiac weakness, and of dilatation of the right side of the heart. From this cause the cardiac dulness sometimes increases rapidly, even in a few hours. The oedema is usually attended by increasing anaemia, which doubtless facilitates its occurrence. These symptoms are always later in development than are those due directly to the neuritis. In the most acute cases the definite symptoms take commonly six or eight weeks to run their course, and the usual duration of the malady is several months. Death from the heart failure is usually prolonged, and accompanied by much distress. Occasionally a very acute form prevails, in which rapid failure of the heart and various effusions lead to death in about a fortnight, and cause a mortality of 60 and 70 per cent. Pathological Anatomy.—The only constant changes are in the nerves, but some serous effusion is almost invariable. Thus Pekelharing and Winkler found an excess of fluid in the cellular tissue in 83 out of 85 cases—about 97 per cent. The pericardial fluid was increased in 67 per cent, of the cases, in about 23 per cent, there was hydrothorax, and ascites in 14 per cent. The changes in the nerves are often indistinct to the naked eye, although always conspicuous under the microscope. They are met with in both motor and sensory branches, and, in advanced cases, in the nerves of the vessels. They are always greatest at the terminal portions, lessening upwards, while the nerve-roots and spinal cord are always normal, with the doubtful exception of vacuolation of the motor cells,* and some degeneration of the fibres of the posterior column in a few cases.f The first change is an increase in the seg- mental nuclei, shrinkage of the medullary sheath at the nodes, and a * Miura, loc. cit. t Van Eecke, loc. cit. 190 MULTIPLE NEURITIS. peculiar "lumpy" degeneration of the medulla, sometimes replaced by a " foam-like" appearance in it, concealing the axis-cylinder. Both changes are often accompanied by the formation of granule corpuscles. These slighter changes are found chiefly where the lesion is commencing, and especially in the vagus and phrenic nerves, in which, necessarily, a considerable degree of change is incompatible with life. They have been seen in the branches within the heart, in some of the fibres of the trunk, and in the laryngeal nerves. Where the change in the nerves is more advanced, the white substance is entirely broken up, and the axis-cyUnder presents segmentation or irregular swellings, or has disappeared, and the increase in the nuclei of the neurilemma sheath is still greater than before. The blood- vessels of the nerves are but little changed in the early stage ; after a time they may present some thickening of the wall, accompanied by a general increase in the amount of the interstitial tissue; but, as a rule, there is an absence of any signs of interstitial inflammation—the changes are essentially parenchymatous. In the muscles there may be at first a cloudy opacity with indis- tinctness of the transverse striae, going on to granular degeneration; or the fibres may simply become narrow, preserving their striation. The nuclei of the fibre-sheath are always increased in number, but the interstitial tissue is generally but little altered. Pathology.—The characteristic organisms have been invariably found in the blood, and, what is a remarkable instance of their slow action, and of the cumulative influence needed to generate the malady, Pekelharing and Winkler * found them in the blood of all the inhabitants of an intensely infected place, whether these had or had not symptoms of the disease, and failed to find them in the blood of persons living in places free from infection. Cultures from the blood reproduce the malady, and so do cultures from the animals thus infected. The organisms have not been found in special associa- tion with the morbid process in the nerves. It thus appears that the malady bears a close resemblance, in its essential features, to cases of multiple neuritis due to a chronic blood-poison such as alcohol, and still more to that which, as we shall see, is presented by chronic arsenical poisoning. There is a slow accumulation in the blood of a virus that has a specific action on the peripheral nerves, and like some others, first and chiefly on the nerves of the legs, but with a greater affinity for the vagus, especially for its cardiac branches, than most others. Although invariably associated with the presence in the blood of a special organism, the absence of this in the vicinity of the lesion, taken in conjunction with modern researches in bacteriology, makes it probable that the virus is a chemical substance produced by the organism in its growth. This brings the disease into close affinity with some other forms of multiple neuritis, on which it throws sufii- * Also Ogata (1888) and others. They have also been found sparingly in the organs, even in the spinal cord, which is commonly free from disease. BERI-BERI. 191 cient light to justify this somewhat full account of a malady that is not likely practically to concern many readers. If we regard, as appa- rently we must, the cardiac failure as the result of the cardiac neuritis, and the dropsical effusion as the combined result of this and the local trophic and vaso-motor influence of the neuritis (to which, perhaps, the change in the blood should be added), we have a remarkable illus- tration of the extent, variety, and degree of the secondary processes of disease which multiple neuritis may produce. The Diagnosis can only be a matter of difficulty in a very early case, or in a patient who is not known to have been exposed to the infection, or in consequence of ignorance of the disease. Doubt may exist, however, whether in a given case the malady is alcohohc neuritis or beri-beri. The former is probable if the arms are involved at the same time as the legs, still more if they suffer first; also if pains are severe, oedema absent, and the heart unaffected. The con- verse would make the endemic malady probable. Beri-beri has cer- tainly been intensified by alcohol in some cases, and the symptoms then presented are a combination of the two,—pains, associated with the weakness and enlargement of the heart and the widespread tendency to dropsical effusion met with in beri-beri. In most cases some other indication of the influence of alcohol, especially enlarge- ment of the liver, will assist the diagnosis. Prom other forms of multiple neuritis it is unlikely that the diagnosis would have to be made. Prom affections of the spinal cord the distinction (chiefly needed in the chronic " dry " variety) depends on the points already mentioned in the account of multiple neuritis. Acute cases with much oedema and weakness of the heart, and enlargement of the right side, may be mistaken for primary heart disease; but if the symptoms of beri-beri are known, the affection may be recognised by the absence of any indications of primary valvnlar disease; while an examination of the legs will reveal the weakness of the flexors of the foot and lessened tactile sensibility in the skin over them. Treatment.—Beri-beri is one of those diseases for which it is probable that a method of at least prophylactic inoculation will be discovered in the future. At present the destruction of the organisms by disinfecting agents, or, better, the removal of a person to an unin- fected district, constitutes the only means of preserving him from the continued entrance of the poison—a measure essential for successful treatment, and, in many cases, all that is really necessary. The limits of disinfection are, however, reached with the dwelling-house; and the great difficulty presented by the disease is the manner in which whole districts are capable of giving rise to it, probably by the infection of the soil, which cannot be rendered innocuous. However, even within the narrow limits of personal use, disinfection has achieved some remarkable results, and in few diseases has the lio-ht of pathology given more useful guidance to the hand of the practitioner 192 MULTIPLE NEURITIS. In most respects the treatment of the symptoms of beri-beri does not differ from that of alcoholic neuritis. A special point, however, is that the strengthening of the heart by digitalis or strophanthus is more often of urgent importance, and requires greater care lest the feeble fibres be overtaxed. Small doses should therefore be given— three or at most five minims of the tincture of digitahs. Bodily rest is of paramount importance to the weak organ, in order that there may not be any demand on its energies for other work than that involved in the maintenance of what may be termed static nutrition, and that it may be spared the increased work necessi- tated by muscular exertion. Strychnia, quinine, &c, may do good, but their use in this disease does not differ from that in the more common forms of multiple neuritis. Leprous Neukitis. Far removed as leprosy may seem to be from the malady last described, both by its general character and extremely chronic course, it is certainly also an endemic disease; its cause must be sought in local influences; and it agrees with beri-beri in the nature of those influences. Since the researches of Carter, Hansen, and Neisser showed the constant presence of a specific bacillus in all the new formations met with in the disease, their observations have received abundant corroboration ; the disease was indeed one of the first to be proved to depend on living organisms. The virus resembles that of beri-beri in being transmissible from individual to individual, but differs in its capability of passage by inheritance, in the less readiness with which it passes from person to person, and in the extreme slow- ness with which it commonly develops to the degree necessary to cause symptoms. Years may elapse after the last possible exposure, before distinct symptoms of leprosy appear. In the case from which Fig. 63 was taken the sufferer was a European of healthy parentage, who could not have been infected within ten years of the first sym- ptoms. In one case of infection from adult to adult, nine years elapsed after the death of the leper before the man who had lived with him began to suffer. When, indeed, a large quantity of the virus is received, the malady develops much more rapidly. But leprosy differs from beri-beri, and from most other forms of multiple neuritis, in the fact that although inflammation of many nerves is frequently a part of the disease, it is not an essential part or a constant feature of the affection. On the contrary, it is only one Df an extensive series of lesions, inconstant, not only in its occur- rence, but in its seat and extent. It characterises a special variety Df the disease, the " anaesthetic leprosy," in which not only areas of the skin become insensitive, but the ends of the fingers mav suffer such an impairment of their nutrition that they are lost. Moreover LEPROUS NEURITIS. 193 as we have seen in the introductory section, the want of strict sym- metry is associated with an important difference from the symmetrical forms—the neuritis is not a parenchymatous or degenerative form, but is a perineuritis and interstitial neuritis, and the damage to the fibres is secondary. This change in the connective tissue is asso- ciated with the actual presence of the organisms in it. The neuritis thus seems to be due to the direct action of the bacilli on the affected tissues, and not, as in beri-beri, to a virus circulating in the blood— not to a product of the organisms, but to the organisms themselves. This fact enables us to understand better its peculiar features, and especially its irregular distribution; the inflammation occurs where the organisms happen to fix themselves in the connective tissue, and although certain common conditions on the two sides may detennine a partial correspondence in the nerves affected, there is not the sym- metry that results from an action on like structures on the two sides, equally accessible to the virus. In this, and in its connective-tissue seat, the neuritis of leprosy resembles more the isolated neuritis of syphilis, rather than the common varieties of the multiple form.* The symptoms of the malady are extensive and various, but only those that consist in derangement of the functions of the nervous system concern us here, and it is alike needless and impracticable to describe the others. The nervous symptoms of leprosy depend almost exclusively on inflammation of the nerves. These symptoms are muscular wasting and anaesthesia, greatest in degree towards the ex- tremities of the limbs, but more or less irregular in situation, and in the region of the distribution of nerve-trunks, which, if accessible, are obviously diseased. The symptoms are not confined to the limbs, but are also met with in the face, where an affection of the fifth nerve may cause anaesthesia, and movement may suffer from involvement of the trunk of the facial nerve, so that the eyelids cannot be completely closed. The form of sensibility that is impaired also varies; sometimes touch, sometimes pain is lessened in greater degree, but usually all forms are implicated to some extent. The legs often suffer before the arms, but a special order of affection cannot be distinguished. There may be unpleasant tingling sensations, but pains are usually trifling, perhaps because the process is extremely chronic. In some cases there may be severe pain in the position of the nerves or deeply seated in the limbs. The inequality of the affection of the fibres of the same nerve is shown by the fact that the knee-jerk may persist although the extensors of the knee are partially paralysed. Fig. 62 shows the distribution of anaesthesia in the hands in a well-marked example of this disease which came under my observation some years ago. The patient was a Creole of Mauritius, who had come to England in early childhood, and presented the first distinct symptoms at • Gerlach ('Virch. Arch.,' cxxv, 'Neur. Cent.,' 1891, p. 464) says infection is from skin, branches of nerves being then affected and finally the nerve-trunks, so that skin may be seen infiltrated when nerves still remain free. VOL. I. 13 194 MULTIPLE NEURITIS. twelve years of age—changes in the pigmentation of the skin, anaes- thesia, and muscular wasting. They steadily increased during the next four vears, the anaesthesia extending each half-year from one finger to another. There was also patchy anaesthesia of the legs below the knee. As the figure shows, the loss of sensation does not correspond in area to nerve distribution. This depends on the fact that even when all the nerves, in- cluding those of the fingers, are diseased, all the fibres may not be destroyed in any one nerve, so that some sensibility exists in each nerve area. Yarious perversions of sensibility, spon- taneous " dysaesthesiae," ting- ling, formication, and the like, may precede the loss. The latter usually occurs gradually, but sometimes so suddenly as to suggest some secondary vascular lesion, haemorrhage or thrombosis, in the vessels of the nerve that is the seat of the process —a possible result in its early and most active stage. It must be remembered that in all inflammations of the sheath and interstitial tissues this proceeds to a considerable degree before the fibres of the nerve suffer, and thus sudden loss of sensibility does not show that the nerve was previously healthy. This occasionally sudden onset is of much practical importance; one case was sent to me from a place in which the disease is endemic, by a doctor well acquainted with it, who had not suspected leprosy because the anaesthesia came on almost suddenly. Accompanying anaesthesia there is usually some muscular wasting, which may be great. In the case figured it was considerable, although only in the small muscles of the hands wras it comparable to that of progressive muscular atrophy. The electrical excitability of the mus- cles was greatly lowered to each current, and this is perhaps the most common condition ; either the damage to the nerves is so chronic that the fibres undergo slow changes pari passu with those in the nerves and their endings, or the patient comes under observation at a late stage in the local affection, at which the changes present in the earlv stage have disappeared; sometimes, indeed, all irritability has vanished. In cases that are seen soon after the onset of the lesion of the nerves, there may be the reaction of degeneration in the muscles, either partial Fig-. 62.—Distribution of anaesthesia in a case of lepro>y. The black areas indicate the loss. LEPROUS NEURITIS. 195 or complete, and there is often a conspicuous exaltation of the mechanical irritability of the nerve-trunks. When the facial nerves are affected this may be well seen, and may resemble that met with in tetany.* The thickening of the nerve may be felt when that which is affected is accessible. The state of myotatic irritability varies accord- ing to the distribution of the neuritis; it is lost at places where the sensory or motor fibres are involved, but those supplying the front of the thigh and its muscles often escape, and the knee-jerk is preserved. Anchylosis of the joints may occur, as in other forms of neuritis The "mutilations" of leprosy, by which the ends of the fingers and toes are lost, are also regarded by some as a consequence of the neuritis. The nume- rous other symptoms of the disease are indepen- dent of the nerves (except perhaps the pigmentation of the skin), and are be- yond the province of this book. The neuritis of leprosy is typically adventitial (Fig. 63). The primary sheath and the secondary sheaths of the fasciculi are greatly increased in thickness, and consist of nucleated fibrous tissue arranged concentrically (a, b). From the sheath, tracts extend into the in- terior of each fasciculus (b), isolating the groups of nerve-fibres. The in- crease of tissue even ex- tends between the fi'res themselves (c), and these undergo slow wasting; many of the fibres in the figure are seen to be distinctly narrower than normal. The concentric growth of fibrous tissue may even invade the whole area of the fasci- culus, all the nerve-fibres perishing before it (d). The characteristic bacillus of leprosy is found abundantly, in recent cases, in the new tissue of the nerves. Peculiar cells are met with, infiltrated with the * Schultze,'Deut. Arch, f.kl a Med.,'1888, Bd. xliii. FiG. 63.—Sections of nerves from a case of anaes- thetic leprosy, under the care of Dr. Buzzard. A, median nerve at wrist x 5; B, portion of same more highly magnified; c, part of a less diseased fasciculus from the ulnar nerve; D, a small fasciculus from median in which the con- centric fibres have invaded the whole area of the fasciculus. 196 MULTIPLE NEURITIS. organisms. As the fibrous tissue develops and contracts, the bacilli seem to perish, and ultimately can no longer be discovered. The diagnosis depends on the occurrence of irregular areas of anaes- thesia, generally associated with irregular patches of pigmentation and pallor in the skin, and often with muscular atrophy, in a person who has been exposed to the risk of infection, generally by having lived in a district in which the disease is endemic. The irregularity of distribution and the limitation of considerable sensory changes sufficiently distinguish it from other forms of neuritis. The spinal affections with which the mixed anaesthesia and wasting are most likely to be confounded are, as Schultze has pointed out, cases of syringomyelia in which the distension of the central cavity damages the grey matter, and may cause similar symptoms of irregular distri- bution—muscular atrophy, sensory impairment, trophic disturbance.* But these are limited to the arms; and if the legs suffer it is in a different way—as simple paraplegia with excess of myotatic irritability that may go on to spasm. The prognosis of the disease in the simple anaesthetic form is grave only when the sufferer is still exposed to fresh infection, or in cases of considerable severity. But it must be remembered that, just as the disease may develop long after exposure to its cause, so it may slowly increase for a long time after this exposure has ceased. The treatment of the affection is beyond the scope of this work ; in so far as the nerve symptoms require special measures, these are the same as in ordinary neuritis. A trial may be made of the stimula- tion of the muscles by whatever form of electricity they will respond to, and of the anaesthetic areas in the skin by the wire brush and faradism. HEEPETIC NEUEITIS. Among the cutaneous eruptions occurring in acute neuritis, that which characterises " herpes zoster " has been mentioned. This affec- tion always presents a correspondence in area with nerve distribution; a definite neuritis has been found in the rare cases which have afforded an opportunity for pathological investigation; and pain with other nerve symptoms is common, and may be conspicuous. Hence herpes, although usually described as a skin disease, is really the manifestation of a form of neuritis which is sufficiently individual in course and features to merit a separate description.f Causes.—Our knowledge as to the aetiology of the neuritis which underlies the most common form of herpes is still very incomplete. An important clue is, however, afforded by the fact, first pointed out by Mr. Jonathan Hutchinson, that the disease may be induced by the * See " Morvan's Disease," later. t The first suggestion as to the nervous origin of herpes seems to have been made by Richard Bright, 'Reports of Medical Cases,' 1831, vol. ii, part 1. HKRPKTIC NEURITIS. 197 presence of arsenic in the blood. This indicates that it may be due to a chemical toxic agent in the circulation, and suggests that as its common cause. But the nature of the agent is still quite un- known. The careful researches of Rendu cast doubt upon the aetio- logical importance once attributed to gout, although a causal connection can occasionally be traced, as in a well-known case of Trousseau's. Ebstein * records the case of two brothers who, after eating mussels, developed the one urticaria, the other herpes. The affection has been traced to malaria by Winfield.f We know, furthermore, that some of the many varieties of rheumatic toxins may act upon various parts of the nervous system, in a manner not unlike that seen in poisoning by arsenic, so far as concerns the characters of the nerve inflammation. Herpetic neuritis may thus probably be produced by toxins introduced from without, or manufactured within the body ; it may even assume an epidemic form We do not know why it should usually be unilateral and show a predilection for certain regions ; the reason is probably a local one, and it may be noted that herpes has been seen to develop in the scar of a burn, and to reappear in those left by a first attack forty-six years previously. Neither age nor sex seems to have much influence in relation to the disease. Pathological Anatomy.—The indications of inflammation have been found especially in the ganglia on the posterior spinal roots ; they tend to spread centrally towards the cord, rather than peripherally. The G-asserian ganglion, which corresponds to that of a posterior root, is similarly affected in herpes frontalis. Although these inflammatory changes were first described (by von Biirensprung) as long ago as in 1861, our knowledge as to their exact nature is still meagre. We can state, however, that they affect primarily the intercellular material, and that they are ordinarily very severe, frequently inducing haemor- rhagic exudation; the swelling and injection of the gangha and adjacent nerve-trunks are usually macroscopically evident. We must distinguish from this primary form those in which the eruption is only a conspicuous symptom of inflammation communicated to the nerve, or clearly secondary to some other cause. Thus Wagner records in one case purulent pachymeningitis and swelling of the spinal gangha of the affected area. The occurrence of bilateral herpes is explained by Kaposi X on tne ground of primary affection of the spinal cord, but no anatomical proof of this is adduced, and it seems more reasonable to look to the general action of the toxic agent in the blood as the cause. As to the nature of this agent we are, except in the case of the special poisons already mentioned, absolutely ignorant. This point has already been discussed in connection with neuritis. With regard to distribution, although practically any sensory nerve * 'Virchow's Archiv,' vol. cxxxix. f ' New York Med. Journ.,' 1895. + Eulenherg's ' Real Encyklopadie,' art. " Herpes." 198 MULTIPLE NEURITIS. may suffer, the main incidence is upon the intercostals, and particu- larly those of the lower dorsal region; the fifth nerve, in any of its branches, but particularly the first and second, and the branches oc the cervical plexus, giving rise to the occipito-cervical form, the small occipital and great auricular nerves being most affected. The lower part of the leg is an occasional seat; the arm very seldom suffers. The inflammatory process may spread to the adjacent motor nerves (see later), or into the spinal cord, leading in one case to death from ascending myelitis.* The herpes itself is commonly ascribed to im- plication of trophic nerves, but Ebstein (loc. cit.) regards it as due to inflammatory irritation of the vaso-dilator fibres. Symptoms.—The description of the herpetic eruption falls properly within the province of dermatology. Areas of congestion appear with oedema passing on into inflammation with effusion; the epi- dermis is raised, and pus may ultimately form. The conspicuous commencement in certain foci is probably to be referred to the affection of terminal nerve divisions, or their corresponding ganglionic cells. It is significant of a general toxic cause that the attack may be ushered in by gastric prodromata, particularly vomiting, with con- comitant fever. Of the neuritic symptoms the most conspicuous is pain, which will be more fully considered under the head of neuralgia; it will here suffice to note the distinctions between the pre- and post- herpetic pains, the former of which usually abates with the appearance of the rash, while the latter is both more severe and of longer duration. Either anaesthesia or hyperaesthesia of the region served by the affected nerve frequently follows the eruption ; there is in some cases per- sistent interference with conduction. Motor affections are also not uncommon. These may be simply immobility from hyperaesthesia or true paralysis from spreading of the neuritis to motor nerves. In the latter case there is some muscular atrophy with more or less perfect reaction of degeneration. Ebstein has collected twenty cases of herpetic palsy, of which at least two were simply hyperaesthctic immobility; in three of the others the paralysis preceded the erup- tion. The facial nerve is the one which most commonly suffers, and its palsy may supervene upon herpes of the trigeminal or occipito- cervical type. In a case recorded by Lesser, frontal herpes was succeeded by paralysis of the fourth cranial nerve, the inflammation having, it is suggested, spread from one nerve to the other in the cavernous sinus. As regards prognosis, all that need be said is that the severitv and persistence of the neuritis usually vary directly with the age of the patient. The question of the treatment of herpes does not fall within the scope of this book; it may, however, be mentioned that the pain is frequently alleviated by galvanism, failing which cocaine may be tried. * Hardy, ' Gaz. des Hdpitaux,' 1876. PAET Til. DISEASES OF THE SPINAL CORD. INTRODUCTION. ANATOMY OF TEE SPINAL CORD* The spinal cord, it will be remembered, is much shorter than the spinal canal, reaching only to the second lumbar vertebra. Hence the nerve-roots descend to their foramina of exit. The lower they arise, the longer is their intra-spinal course. All those below the second lumbar pair leave the canal below the lowest portion of the cord. It is customary to speak of the portion of the spinal cord from which each pair of nerves arise as the corresponding " segment" of the cord. The segments are longest in the dorsal region, and shortest in the lumbar enlargement. They are also called " metameres." The only parts of the spinal column that we can usually feel are the vertebral spines. Many of these are not on a level with the bodies of their vertebrae. It is important, therefore, to know the relation of the spines to the bodies of the several vertebrae, and of these to the origin of the nerves. These relations are shown in the accompanying figure (Pig. 64). Of the Membranes, the pia mater closely invests the surface, and is continuous with the tracts of connective tissue that pass within the substance of the spinal cord. It is also prolonged along the nerve- roots as their sheaths. The arachnoid forms a much less close invest- ment. The dura mater is not in contact with the bones as it is in the cranium, but a layer of fat and a plexus of large veins intervene * The following outline of the anatomy of the spinal cord is intended merely to place before the reader those points that are essential, or likely to become so, for understanding the functions of the organ and the symptoms of its disease. It does not profess to be exhaustive even in outline, and is designedly kept as free as possible from whatever, in either the substance or terminology of recent science, does not come within the scope of those objects. Many of the results reached by modern investigators are mutually incompatible, and where a choice has been necessary the observers have been followed who possess the greatest authority and whose conclusions best agree with facts previously ascertained. 200 SPINAL CORD. between the two. It thus forms a loose sheath for the cord, and variations in the amount of blood in the plexuses outside it permit corresponding (but inverse) varia- tions of the amount of cerebro-spinal fluid within it. An extension of the 1 C dura mater passes along each nerve-root, ~ and blends with its sheath. Structure of the Spinal Cord.— " 4 The general form of the cord, the enlarge- ments it presents, and its constitution of 6 white and grey substance, are too well 7 known to need description here. The 8 white substance surrounds the grey, ex- " | D cept at the two points at which the - 2 posterior horns come to the surface ... (Fig- 65). It consists of meduUated nerve-fibres, chiefly longitudinal. The posterior cornua isolate the posterior 5 columns from the rest of the white sub- '" 6 stance. These columns are separated by - 7 a " posterior median septum " of connec- tive tissue, and a little distance from this another incomplete septum, "posterior — 9 intermediate septum," corresponding to ___ 10 a depression on the surface, marks off iu i^'2^jTTTl a portion next the median septum, the " OX* 'Wi\ U " Postero-median column," or " column J2 fxl*lw=±=;'"' """'..... 12 °^ ®°^>" from the part next the pos- terior horn, " postero-external column," L/ a c° FiG. 64.—Diagram (framed from an original in- vestigation) showing the relation of the verte- bral spines to their bodies and to the origin of the several nerve-roots. It will be seen that the ends of the vertebral spines are opposite the middle of their own bodies only in the lumbar region; they correspond to the lower edge of their own bodies in the cervical and the first two dor.-al vertebrae, and to the upper part of the body below in the rest of the dorsal region. Each cervical spine is nearly opposite the lower roots of the nerve below; the vertebra prominens is opposite the first dorsal roots, and from the 3rd to the 10th dorsal the spines correspond to the second root below; the 11th spine corresponds to the 1st and 2nd lumbar nerves, the 12th to the 3rd, 4th, and 5th; the 1st lumbar to the 1st, 2nd, and 3rd sacral nerves, while the tip of the cord is opposite the upper part of the 2nd lumbar. or "column of Burdach," the part of which next the cornu is called the "posterior root-zone," because many fibres of the STRUCTURE. 201 posterior root pass through it. The rest of the white substance is divided, in the middle line in front, by the anterior median fissure, Fia. 65.—Diagram of a section of the spinal cord in the cervical region. A. C, anterior commissure; P. C, posterior commissure; I. g. s., intermediate grey sub- stance; p. Cor., posterior cornu; c. c. p., caput cornu posterioris; L. n. L., lateral limiting: layer; a.-l. a. t., antero-lateral ascending tract, which extends along the periphery of the cord. down which the pia mater and blood-vessels pass, and at the bottom of which is the anterior or white commissure. Between the anterior median fissure and the posterior cornu the white sulstance is con- tinuous and undivided, extending round the front and side of the cord. It is artificially divided into an anterior and a lateral column, the line of division being the outermost of the anterior nerve-roots, which pass through the front of the cord; but there is no corre- sponding distinction of structure, and hence it is often termed the " antero-lateral column." The white substance varies in amount in different parts of the cord, but, as a whole, lessens gradually from above downwards (see Fig. 66). It is everywhere composed of meduUated nerve-fibres, which, however, possess no neurilemma-sheath. In carmine-stained sections the axis-.cylinder is seen within each fibre, not always in the centre, and around this are concentric cloudy lines due to the irregular refraction of the white substance. Between the fibres is a peculiar substance, the " neuroglia," or nerve-cement. It appears to consist of nucleated branched cells ("spider-cells"), whose long, delicate processes form the fibres of the neuroglia. The cells, stellate on section, are found in the larger interspaces between the nerve-fibres. The fibres of the neuroglia branch and interlace, forming a very fine network; some of them 202 SPINAL CORD. are arransed radially; starting centrally from the outer ends of fie ciliated epithelial cells which line the cerebro-spinal canal, they diverge, branching as they go towards the surface of the cord. This neuroglia is developed from the same (epithelial) embryo- logical elements as the nerve- structures—an important fact, because it enables us to under- stand the fact that, in defective development of the nerve-struc- tures, the neuroglial tissue is ex- cessive in amount. But its differ- entiation in development involves also its chemical nature, since it contains far more of a material like that of hair or horn, and hence called " neurokeratin." The nerve-fibres, thus con- nected, lie in a coarser network, formed by branching processes of septa that proceed inwards from the pia mater. In these septa blood-vessels run, and some are occupied by nerve-fibres that have a horizontal course. The septa consist of fine fibres of ordinary connective tissue from the pia mater, and of neuroglial material, which forms also a layer between the membrane and the nerve-fibres in the intervals be- tween the septa. This layer varies considerably in thickness. Many of the septa pass through the white substance to join projec- tions from the grey substance, which cause the irregularity of the outline of the latter. These processes, outside the neck of the posterior cornu, are broad, and join each other so as to form a sort of network, the meshes of which en- close columns of nerve-fibres. This is called the " lateral reticular for- mation " (Fig. 65, right side ; also 66, c 2-8). The substance of the D Fm. 66.— Diagram showing the relative size and shape of the cord and grey matter at dillerent levels. ' STRUCTURE. 203 horn behind the caput is sometimes broken up in the same way—■ the " posterior reticular formation." The grey substance varies in shape and size in different parts of the cord, being largest in the cervical and lumbar swellings, and corre- sponding to the number and size of the nerve-roots given off. The variations in shape and size are indicated in the accompanying figure (66), and will be readily understood by an examination of this. The division into anterior and posterior horns or cornua is familiar. The part on each side that intervenes between the two horns may be conveniently termed the " intermediate grey substance " (I. g. s. in Fig. 65). In the dorsal region a projection from this extends into thfe lateral column (Fig. 66, r> 2, 5, and 8), and has been termed the "lateral horn"). It is customary to divide the grey matter into two varieties, "spongy" and "gelatinous." The latter forms a cap on the posterior horn, and a layer immediately around the central canal, and is named on account of its naked-eye aspect. It consists largely of neuroglia, traversed, however, by nerve-fibres, and with numerous nerve-cells scattered through it. The spongy substance, which forms the rest of the two cornua, consists mainly of an exces- sively fine felty network of very narrow meduUated nerve-fibres, naked axis-cylinders, and fine nerve-fibrillae which arise, in part at least, from the dendrites of the nerve-cells, and in part by a division of the axis-cylinders of the nerve-fibres. These structures are em- bedded in a supporting neuroglia. Through it course many larger meduUated nerve-fibres, passing to or from the white columns and nerve-roots. In it also lie many nerve-cells of various sizes. Those in the anterior cornu are, for the most part, large " ganglion-cells ; " each contains a large nucleus, and usually a mass of pigment, and Fig. 67. Fig. 68. Fig. 69. Gerlach.) 204 SPINAL CORD. sends out several processes. One process, the axon, is continuous with the axis-cylinder of a nerve-fibre (Fig. 67), and can be sometimes traced into a fibre of an anterior root (Fig. 68). The other processes, or dendrons, after a longer or shorter course divide and subdivide, their ramifications ending in minute knobs in the sponge-like matrix of the grey substance. In this they are probably brought into close contiguity with the terminal ramifications of other neurons (Fig. 69). These cells lie in groups, between and through which course tracts of fibres, chiefly from the anterior roots. Other fibres come from the anterior commissure, white columns, and posterior horn. The axons of these cells are certainly motor in nature, and become the motor fibres of the spinal nerves. Similar cells are also found in varying numbers at the anterior periphery of the cord, and even among the fibres of the already descending anterior roots.* Birge, in a careful investigation, found that in each segment of the spinal cord of the frog the number of nerve-cells in the anterior cornu nearly corresponds to the number of fibres of the anterior roots arising from that segment. Each cell is traversed by many nerve-fibrillae, such as are discerned in a cell-process or in the axis-cylinder of a nerve-fibre. These cross and intermingle in the middle of the cell, but pass along the margin from one process to another. By this arrangement impulses entering the cell by one process may leave it by many.f The arrangement of the nerve-cells of the anterior cornu is of some practical importance, on account of the frequency with which this part is the seat of limited lesions. They form, as already stated, certain groups, but these groups vary in different regions of the cord, partly under the influence of the shape of the horn, partly irrespective of this ; and they even vary in parts of the cord that ate near together. They are influenced by the course of the tracts of fibres of the ante- rior roots, which may pass through a group and break it up into smaller groups, although in a neighbouring section it is undivided (see Fig. 70, the cervical groups). Hence very different descriptions have been given of these groups, and the process of distinction has sometimes been carried too far. The groups that can most readily be recognised are the following:—In the inner anterior angle of the cornu is a small group, the inner or median group. This is one of the smallest, and is absent in some parts of the cord, especially in the lumbar region. A much larger group lies near the anterior edge of the horn, in the * Hoche, 'Neurol. Centralbl.,' 1891. f Kronthal,' Neur. Centralbl.,' 1890, p. 40. Impulses may thus be diffused, even if there is no junction of fibrillae or passage of impulses from one fibril to auother. This arrangement provides a mechanism by which the nerve-cells may conduct and diffuse impulses, but such a mechanism does not exclude (as has been assumed) the reinforcement or origination of such impulses, and their discovery leaves untouched the facts which demonstrate the trophic influence of the cells, and the manner in which they arrest secondary degeneration. These functions are indicated by facts of a totally different nature. Kronthal's observations are of great importance, and appear trustworthy. STRUCTURE. 20.1 middle, or a little to the outer side of the middle, the anterior group. External to this, in the outer extremity of the front part of the horn, is another group, the antero-lateral group. '1 hese two groups are often blended, so that the anterior group cannot be separately distin- guished, as in the right-hand mid-cervical figure. A fourth group, usually the largest, lies in the outermost part of the horn, behind its front, usually in the posterior outer angle; it may extend inwards, halfway across the horn. It is called the external or postero-lateral, group (p.-l., Fig. 70). These three are the most important groups. Upper Dorsal 1st Lumbar. Mid-Lumbar. Fig. 70.—Diagrams of the groups of nerve-cells in the anterior cornu. Groups :— 1., inner or medial; A., anterior; A.-n., antero-lateral; p.-l., postero-lateral; i. L. p., intermediate lateral process; p. v. c, posterior vesicular column or tract. The two mid-cervical sections are only a few millimetres apart, and show how the anterior group, separate in the onp, may be blended with the antero-lateral group in a neighbouring part of the cord. There is in some parts also a central group, occupying nearly the centre of the horn. In the small cornu of the dorsal region often no wel - defined groups can be made out, but when any can be recognised, they are generally the anterior and external. Similar cells, usually smaller in size and isolated, are scattered through the intermediate grey matter, and a group of cells occupies a projection outwards into the lateral column in the lower cervical and upper dorsal regions. It was termed by Lockhart Clarke the inter- medio-lateral tract, but is better designated the intermediate process (or lateral horn), and the cells the intermediate group (i. l. p., Fig. 70). 206 SPINAL CORD. Nerve-cells also lie in the grey matter of the reticular formations, lateral and posterior, and are sometimes described as special groups. Many isolated cells, medium and small in size, also lie in the posterior horn. These are probably connected with some of the fibres of the posterior roots. They extend back into the caput cornu posterioris.* Throughout the dorsal and in the upper lumbar cord a group of nerve-cells hes in the inner part of the neck of the posterior horn, the posterior vesicular column of Lockhart Clarke (sometimes tailed "Clarke's column") (p. v. c, Fig. 70; see also Fig. 80). Most of these cells are fusiform in shape, but are placed vertically, so that they appear round or oval in transverse section, and their processes are not seen. Some, however, present processes that run forwards or back- wards. Nerve-fibres pass into and by it, which we shall consider sub- sequently. Although this tract is chiefly developed in the lower dorsal and upper lumbar cord, a few nerve-cells of similar character are met with in the same position in other parts, and are occasionally suffi- ciently numerous to form a small group. The " gelatinous" grey matter, grey substance of "Rolando, which forms a cap on the posterior horn, caput cornu posterioris (c. c. p., Fig. 65), differs considerably from the spongy substance. It has been described as made up of granules, but, according to later researches, consists of a peculiar translucent material forming an excessively fine network, which, like the rest of the neuroglia, behaves to reagents like horny material. In the embryo it is continuous with that which surrounds the central canal,f but from this it becomes separated in the course of development. Its basis substance is thus of neuroglial nature. Numerous nerve-fibres pass through it from the posterior roots, and these, coursing forwards, seem to divide it into columns, as it is viewed in transverse section. A few small ganglion-cells lie in this gelatinous substance, chiefly on the inner side; it also contains many minute cells, some of which are nerve-cells, while others belong to the neuroglial tissue. From the nerve-cells axons have been traced into the posterior column and horn, the posterior root-zone and the lateral column. J Bundles of vertical fibres are also seen in transverse section, and these are often numerous just above the caput, especially on the inner side of the horn. Most of these are fibres of the posterior nerve-roots that have a vertical course for a short distance. In Fig. 80 the axis- cylinders of these fibres are seen to be changing from the horizontal to the vertical direction, and their relation to the posterior root- fibres can be distinctly traced. The hinder part of the gelatinous * It is generally believed that their branching processes enter into the plexus of fibrillse in the grey matter, and thus bring these cells into relation with those of the anterior cornua, and also with fibres that cross by the posterior commissure and form the ascending sensory path to the brain. f Cf. Corning, 'Arch. f. mikros. Anat.,' xxxi, 1888. X Starr, ' Atlas of Nerve-cells,' p. 28 ; Lenhossek, * Der feinere Bau des Nerven* system*,' pp. 120 et seq. STRUCTURE. 207 substance is less dense in structure than the rest, and is sometimes distinguished from it as the " spongy zone."* The gelatinous sub- stance contains many vessels, running for the most part vertically. 117/ He Substance.—We may now examine, in greater detail, the con- stitution of the white columns of the cord, and the probable course and function of the fibres they contain. Their analysis has been greatly aided by three facts,—continuity of degeneration, difference in time of development, and the variation in the size of the fibres of the different tracts. 1. It was discovered by Tiirck that in certain tracts in the white substance the nerve-fibres undergo secondary degeneration when separated from their cells of origin, a degeneration analogous to that which, as we have already seen, occurs in the nerve-fibres outside the cord. This mode of investigation has of late acquired a fresh impetus from the new means of staining degenerated nerve-fibres devised by Marchi. 2. In the developing cord the fibres of different tracts acquire their white substance at different periods, and the study of these differences (first by Flechsig and later by Bechterew and others) has not only confirmed, but also extended, the differential indications afforded by disease. It enables us to make a distinction between fibres that do not degenerate separately, or not through a sufficiently long tract to enable us to distinguish them. The groups into which this method enables us to divide the fibres, and the order in which the medullation takes place, are as follows : (1) Anterior and posterior root-fibres. (2) -\ r inner anterior column. (3) C Ground-fibres of the \ postero-external column. (4) ) C outer anterior and lateral column. (5) Lateral limiting layer and antero-lateral ascending tract. (6) Postero-median column. (7) Direct cerebellar tract. (8) Lateral and anterior pyramidal tracts (which in man are first meduUated at the time of birth).f It may be s'ated as a general rule that the shorter the course of a tract within the central nervous system, the earlier do its fibres acquire their medullary sheaths. 3. The size of the nerve-fibres varies in different tracts, but the full significance of the variations has still to be ascertained. Even in the same tract of the cord considerable variations are met with, which probably correspond with differences in function. When a tract dege- nerates, it is common for the degeneration to be incomplete; fibres remain intact among those that perish: this indicates a difference in function, and with it the difference in size usually coincides. It is also possible that some of the small fibres seen among larger ones may be due to the division of the latter (Sherrington); but such division * So that in some descriptions the posterior horn i< divided into (1) spongy sub- stince of the horn itself, (2) gelatinous zone of the "caput," and (3) ^0 ,gy zone at the tip of the horn. See Lissauer, ' Arch. f. Psych.,' 1886. f See Obersteiner, loc. cit., p. 192. 208 SPINAL CORD. has not been actually demonstrated, and is probably not frequent. The variation in size is from 1 to 25 /* (-^i^ to y^V^ inch). The variations are especially great in the fibres of the pyramidal tract, and it is in these that division has been thought to occur. Those of the direct cerebellar tract are uniformly large, while most of those that constitute the postero-median column are small. It will facilitate the detailed study of the tracts if we consider first those that undergo secondary degeneration for a considerable distance, as our knowledge regarding these is the most complete. STRUCTURE. 209 These degenerations are both ascending and descending. Only one important set of fibres degenerates downwards through a considerable extent—those that continue through the cord the anterior pyramids of the medulla. They commence still higher, in the motor region of the cortex of the cerebral hemisphere, passing thence by the " internal capsule " between the two parts of the corpus striatum, &c, to the cms and pons; they are the chief, perhaps the sole conductors of voluntary impulses. They are termed the pyramidal tracts because they constitute the anterior pyramids of the medulla. They are shaded by short horizontal lines in Fig 71; compare also Fig. 65. At the decussation of the pyramids about three quarters of the fibres usually cross to the other side. These pass down the cord in the lateral column, and constitute the lateral (or crossed) pyramidal tract. Those which do not decussate, pass down their own side of the cord, m the inner part of the anterior column, at the side of the anterior median fissure, and constitute the anterior (or direct) pyra- midal tract. Flechsig has found that the decussation is subject to many variations. In the majority of cases the decussating fibres are between 70 and 80 per cent, of the whole. Sometimes they con- stitute a still larger proportion, and in one case (of 60 examined) all the fibres crossed. Sometimes fewer fibres decussate, only one half or even less than half; in one case 35 per cent., in another only 10. No case has yet been met with in which no fibres crossed.* A con- siderable number of fibres decussate above the medulla, terminatino- around the cells which give origin to the motor cranial nerves. The lateral pyramidal tract occupies the posterior half of the lateral column, outside the posterior cornu. It extends down to the end of the cord, even when it is originally small. Hence those fibres that do not cross at the medulla must do so lower down in the cord. Through the greater part of the cervical and dorsal regions this lateral tract is separated from the surface by a narrow layer of fibres, the direct cere- bellar tract In the upper part of the cervical region (third cervical segment) this tract Hes farther forwards, so that the pyramidal tract comes up to the surface close to the posterior cornu (Fig. 71, c. 3); and here, if the tract is small, there may be a depression on the sur- face. In the lower part of the dorsal cord there is a similar move- ment forwards of the cerebellar tract, so that the pyramidal tract again comes in contact with the surface posteriorly (Fig. 71, d. 12), and, as the cerebellar tract ceases at the first lumbar nerve, the pyra- midal tract extends up to the surface throughout the lumbar enlarge- ment (Fig. 71, L. 4). The inner side of the tract is in contact with the hinder part of the posterior cornu, near the surface, throughout the * In the 'Neur. Cent./ 1898, p. 202, Dr. Philip Zenner describes a case of tumour of the left side of the brain in which the paralysis was on the left side of the body. The post-mortem examination showed that there was "absence of the pyramidal decussation." It is not stated whether Marchi's method was used in the examination. VOL. 1. 14 210 SPINAL CORD. entire length of the cord, but further forwards it is separated from the neck of the cornu and intermediate grey substance by a layer of nerve- fibres, termed by Flechsig the lateral limiting layer (l. l. l., Fig. 65). Among the fibres of the pyramidal tract, in the dorsal and cervical regions, degeneration reveals a few other fibres that belong chiefly to the cerebellar tract. The lateral pyramidal tract diminishes in size from above downwards as its fibres end by entering the grey matter; those that extend lowest (for the leg) occupy the posterior part of the tract in the cervical region. The fibres curve inwards along the septa that extend from the grey matter into the lateral column, and they enter the grey matter between the anterior and posterior cornua. They pass inwards and forwards in the anterior cornu, and are then lost in the complicated structure of the grey matter. Their probable termination will be considered presently. The anterior or direct pyramidal tract (called also the " column of Tiirck ") descends the cord in the inner part of the anterior column, adjacent to the anterior median fissure. Its exact form and size vary : usually it bounds the fissure on each side; some- times it forms only a small tract at the posterior part of the fissure ; when large, it not only reaches forward to the front of the cord, but may cause a prominence on the surface bounded by a distinct sulcus. Its extent down the cord probably varies according to its size. It steadily lessens in area, and, if originally small, may not extend beyond the middle of the cervical en- largement ; if originally large, it may be traced as far as the lumbar enlarge- ment and even into the cord at the level of the fourth pair of sacral nerve- FiG. 72.—Ascending and descend- ing degenerations from myelitis of the mid-dorsal region; the upper section is from the lower cervical, and shows the ascending degeneration of the post.-median column spreading out against the roots (* ag- 72); when bearing the commissure. The other figure is usual proportion to the lateral tract %£&?«&'£%& H «eases atout the mid-dorsal region. tracts, anterior and lateral. Most of the fibres pass through the anterior commissure to the opposite side, either entering at once the grey matter, or passing first to the lateral tract.f The latter is probably the course of most of the fibres when the pyramidal decussation is small. Whether any fibres end in the grey matter on the same side of the cord we do not know. Disease of the brain destroying the motor cortex, or the fibres which * Dejerine and Thomas, ' Compt. Rend.,' 1896, p. 157. Russell traces it to the 5tii segment. f Although this is probable there is no definite evidence of it except in the sacral region (Russell,' Brain,' 1898). STRUCTURE. 21] descend from it to the pyramids, usually limited (at least in conspicu- ous degree) to the related pyra- midal tracts,—anterior on the same side, lateral on the opposite side (Fig. 73). But in many cases slight degeneration has been also found in the lateral tract on the same side, extending into the lumbar region. Hence it is probable that some fibres of each anterior pyramid find their way to the lateral tract on the same side, and descend to the corresponding limbs, especially to the leg. This degeneration of the lateral tract on the same side as the lesion is sometimes very marked just below the decussation of the pyramids, and is therefore not due to any lower re-decussation in the cord.* Muratoff has shown, by extirpation of the cortical areas for the extremities, that a bundle from the bulbar pyramid descends into tho lateral pyramidal tract of the same side. This has been con- firmed by Rothmann and also bv Melius and by Sherrington, who for- merly held a different view.f That there is such a physiological relation is clearly indicated by clinical facts. We shall afterwards see that there is abundant evidence that each hemisphere of the brain is con- nected with both legs, although chiefly with that of the opposite side. There is also a similar and even more equal connection with the trunk muscles, and a slighter con- nection with certain muscles of the arm. Such muscles invariably re- gain some power on the paralysed side, even with a complete inter- causes descending degeneration, Fig. 73.—Descending degeneration of the pyramidal tracts in a case of hemiplegia from disease of the right cerebral hemisphere. (From sec- tions prepared by Dr. Mott.) * Pitres,'Arch, de Physiologic,'1S74; Hadden and Sherrington,'Brain,'Jan., 1886. An illustration of this bilateral degeneration will be found in the section on Diseases of the Brain, Vol. II. t Muratoff, 'Neur. Centralbl.,' 1893; Melius, ' Proc. Royal Society,' 1894; Sher- 212 SPINAL CORD. ruption to the motor path, and they are weakened on the unparalysed side. The subject is considered further in Yol. II. On the whole, the facts hitherto ascertained suggest that the arrangements which subserve this relation vary in different persons, just as does the chief decussation of the pyramids. The fibres probably in some cases continue downwards on the same side until they reach the level of grey matter for which they are destined.* In other cases most or many of them cross at the bulbar decussation Lastly, there is the possibility that a connection between the motor cells or structures of the two sides may supplement the decussation.f How do the fibres of the pyramidal tract end ? They seem all to pass into the intermediate grey matter, and forwards into the anterior cornu, among the motor nerve-cells. There they are lost in the plexus of the spongy substance. There is strong indirect evidence that they divide and subdivide, and that their ramifications come into relation with the plexus of nerve-fibrillse constituted by the dividing processes of the ganglion-cells. The evidence of this is twofold. As far as is at present known, only one process of a ganglion-cell becomes an axon; the others divide. The axon passes into an anterior root; it can be seen to do so in the case of some ganglion-cells (Fig. 68), and, as we have seen, the number of ganglion- cells and anterior root-fibres is nearly the same in the frog, and therefore, presumably, in man also. Since some root-fibres are not motor, the number of motor cells may safely be assumed to be at least not smaller than that of the motor fibres; thus each fibre will have at least one cell related to it. If so, since the pyramidal fibres are certainly connected with the ganglion-cells, the connection can only be by the dendrons or ramifying processes of the cells, and this involves a division of the nerve-fibre. The dividing fibre isolated by Gerlach, and shown in Fig. 69, may have been a branch of a pyramidal fibre. The second point in evidence of division is the fact that the nerve-cells and root-fibres must be many times more numerous than the fibres of the pyramidal tract.X But all (or at least most) of the motor root-fibres may be stimulated through the pyramidal fibres, and therefore each of the latter must be con- nected with several ganglion-cells. Physiological considerations sug- gest the same conclusion, which is fully confirmed by the new histo- rington,'Lancet,' 1894, vol. i; Rothmann, 'Neur. Centralbl.,' 1896; Redlich, ibid., 1897. Their results, obtained by the method of degeneration, have been further borne out by the ingenious experiments of Wertheimer and Liepage ('Arch de Physiol.,' 1897). * Dejerine and Thomas have traced homolateral fibres as low as the 4th sacral root (' Compt. Rend.,' loc. cit.), Russell to 5th root (' Brain,' loc. cit.). t Broadbent, Hadden. In a unilateral lesion of the cord the paralysed foot may move with the other. Such a connection of nuclei was originally suggested by Broadbent to explain the association of bilateral movements. J The total area of the anterior roots of the cord is probably at least five times as great as that of the pyramidal tracts in the upper cervical region. STKUCTUKE. 213 logical methods to which reference has already been made.* curious fact that the degeneration method of Marchi does not reveal this wholesale passage of the pyramidal fibres into the anterior cornua. This is probably due to their passing in in the form of non-medullated collaterals. Let us now consider, for a moment, the whole motor path, from the cortex of the brain to the muscles. We may regard it as composed of two neurons, an upper and lower (Fig. 74j. Each consists of a ganglion-cell above, an axon, and the terminal ramification of the latter. The upper, " cerebro-spinal " neuron consists of the cortical ganglion-cell with its dendrons, and the " pyra- midal" axon which proceeds from the cell, passes through the brain and cord, and ends in the grey substance by division and terminal inter- lacement with several nerve-cells. The lower, " spino-muscular" neuron consists of the spinal motor cell with its dendrons and the axon pro- ceeding from it, which passes through the an- terior root and nerve-trunk to the muscle, where it divides and ramifies on the muscular fibre. The elements of the two neurons do not corre- spond in number, since, as we have just seen, each cerebro-spinal element is connected with many spino-muscular elements. So, too, each motor axon is connected with a considerable area * Gad and Flatau ('Neurol. Centralbl.,' 1897, p. 481) huve endeavoured to mark out the localisation within the motor tracts of the fibres for different parts of the body. Their method consisted in cutting across the cords of dogs and immediately applying to different parts of the cross- section of the lower segment stimuli of varying strength and duration. They found that in general the fibres nearest to the anterior grey matter supplied the body at or near the level of the section, while those for other regions rau more posteriorly and superficially. This is, however, only what would follow from the fact that the axons of the upper neuron (v. infra) terminate by interlacing with the dendrons of the ganglion-cells in the anterior cornua, from which the lower axons to the region supplied by the segment arise. It is a 4dJrHmf- Fig. 74.—Diagram of an element of the motor path. Show- ing cortical cell, pyramidal fibre, anterior horn cell, nerve- fibre, and muscle. More than one anterior horn cell should, strictly speaking, be shown coming into relation with the terminal ramifications of one pyramidal fibre. To show this, however, would have needlessly complicated the diagram. M 214 SPINAL CORD. Fiff. 75.— Decent ration of the antero-lateral ascending tract in a case of locomotor ataxy (q. y. figure), showing its position in the upper cervical region, where the direct cerebellar truct passes outside it into the restiform body. Cb Db La Fig. 76.—Ascending de^ene- raton in the postero-medina column and antero-lateral ascending tract. The cord was crushed at the first lum- bar segment. FiG. 77. —Degeneration after injury to the eauda equina. C a, b, c, upper middle and lower cervical; D a, upper ; b, c, lower dorsal; L a, upper; and L b, middle lum- bar region. (After Schult/e.) of excitable muscle-tissue. It will be found that this conception of the motor path conduces to clearer ideas of many facts of disease, and it is STRUCTURE. 215 important to grasp it firmly. We shall see, for instance, that diseases involving any part of a neuron produce similar effects, however diverse their nature; while there is a fundamental difference between the effects of disease of the two neurons.* Fibres that degenerate downwards through the greater part of the cord are also scattered through the antero-lateral column, in a zone that extends beneath the surface between the direct pyramidal tract and the direct cerebellar tract. Some are mingled with the fibres of the ascending antero-lateral tract presently to be described ; others lie beneath this. It is possible that they really belong to the crossed pyramidal tract. They have been termed by Foster the descending antero-lateral tract.f Bechterew has pointed out that the crossed pyramidal tracts as mapped out by the degeneration and embryological methods do not correspond. In other words, the area of non-myelinated nerve-fibres found at birth is much greater than that degenerating as the result of section of the pyramidal tract high up. Boyce and Sakowitsch have shown independently that the axons of the remaining area— which is situated at the anterior end of the crossed pyramidal tract —descend from the posterior corpora quadrigemina.J Fibres degenerate upwards in both the lateral and the posterior columns. We may consider the latter first. Each posterior column, as we have seen, is divided by the imperfect "intermediate septum" into two parts,—a narrow " postero-median column," and a wider " postero-external column" (Fig. 65). In the lumbar and sacral regions it is not possible to separate the postero- external from the postero-median column, as can be clone in the dorsal and cervical regions. The differentiation is not completed below the level of the eleventh dorsal segment. Secondary degeneration con- * This conception of the motor path was published iu its present form (except, of course, that the neuronic nomenclature had not then been intn duced) in the first edition of this book in August, 1886. By a curious coincidence nearly the same idea was stated (no doubt independently), and even the same terminology employed, by Dr. v. Renz in the 'Centralblatt f. Nervenkr.,' October 15th, 1886. t Foster, ' Physiology,' 1890, p. 873. See also Hadden and Sherrington, 'Brain,' vol. viii; and Tooth, ' Secondary Degeneration of the Spinal Cord,' 1889. Luciani and Marchi state that this tract is mainly composed of axons descending from the cerebellum, a view which is upheld by Biedl ('Neurol. Centralbl.,' 1895). Russell denies this, and states that these axons are derived mainly from Deiter's nucleus in the medulla, a view with which Mott agrees. Held has shown that fibres derived from the red nucleus pass into the lateral column of the cord ('Archiv f. Anat. u. Physiol.,' 1892). X See Bechterew, 'Neurol. Centralbl.,' 1897, No. 23, where a tract in the anterior ground bundle descending from the anterior corpora quadrigemina is also de- scribed. The term " retrograde degeneration" has been applied by Sottas and others to an ascending change which occurs in certain cases in the pyramidal tracts. This degeneration is slow in developing, and undergoes gradual diminution in intensity and extent as it ascends. A similar condition has been found in the posterior columns after cerebral lesions (Durante, 'Rev. uenrologique,' 1898), and in the direct cerebellar tract alter a cerebellar lesion (Campbell. ' Brain,' 1897). 216 SPINAL CORD. firms this distinction. If the posterior columns are interrupted anywhere in their course, ascending degeneration results; and this, a short distance above the lesion, is confined to the posterior median column (Figs. 72, 76, 77), in which the degeneration continues upwards to the medulla oblongata, and ends there at the grey matter of the "nucleus gracilis." The fibres of these median columns degenerate in the same way when the lesion is not in the cord, but in the posterior nerve-roots (as of the cauda equina, Fig. 77). Hence it is clear that these fibres are continued upwards from the posterior nerve-roots without interruption. The contrast Fig. 78. FiG. 7;». Fig. 78.— Degenerations after a lesion of the cord in the lower part of the cervical region. A, highe>t cervical; b, middle cervical 1£ cm. above lesion. Degtneration of the posterior median columns, spreading slightly in A and widely in b into the post. ext. col. The nature of the circumferential degeneration is uncertain ■ it is probably a partial ascending degeneration set up by peripheral myelitis. c, upper dorsal 2 cm. below lesion. Degeneration of the lateral pyramidal tracts ; "comma-shaped" degeneration in front of the post. ext. col.; slight defenera- tion of the anterior ground-fibres. (Schultze.) FiG. 79.—Ascending degeneration after injury to the lowest part of the spinal cord and sciatic nerve-roots arising from it. A, cervical; B, lower dorsal; c, junction of dorsal and lumbar regions ; D, middle of lumbar enlargement. (After Schultze ) between these degenerated columns and the undegenerated external columns through the greater part of the cord above the lesion (Fig. 76) is very striking. But just above the lesion the degeneration is not confined to the median columns ; it spreads out into the external columns, especially towards the hinder surface, and the more exten- sively the nearer to the lesion, until close above this the deo-enerated fibres occupy the whole extent of the posterior column, except a small area close to the posterior cornu. This is due to the fact that the STRUCTURE. 217 fibres pass to the median column through the hinder part of the external column. It is the same whatever is the seat of the lesion, whether it is in the cervical (Fig. 78), dorsal, or lumbar (Fig. 79) parts of the cord; and if it is in the Cauda equina, the degeneration spreads out in the same way in the lumbar enlargement (Fig. 77). This shows clearly that all the way up the cord fibres pass to the median column from the external column, and that these are uncrossed fibres from the posterior roots.* As the fibres ascend the cord in the median column, they come to he posteriorly in proportion as their source is lower. Those from the sciatic nerves, for instance, in the lower cervical cord only occupy the posterior half of the columns (Fig. 79). Those from the whole lumbar enlargement, or whole cauda equina (Fig. 76), reach forward to the commissure in the lower cervical region, spreading out a little near the commissure, where, however, the degeneration is much less dense than it is behind Above the middle of the cervical enlargement the degeneration from a lesion in the dorsal or lumbar regions does not extend forwards beyond the junction of the anterior and middle third of these columns; but if the lesion is in the cervical region the degeneration extends up to the commissure, even at the level of the second cervical segment (Fig. 78, a), showing that the fibres from the cervical roots occupy the anterior portion of these columns. It is now known that most if not all root-fibres divide on entering the posterior columns into ascending and descending branches With the course of the former we have just been occupied ; the latter run but a short way down in the cord and terminate by turning into the posterior cornu and inosculating with the cell-dendrites there found. It is important to remember that the root-fibres that pass to the median column through the external column do not decussate. This is not, however, the only source of fibres to the median column. Fibres pass to it (1) from the neck of the posterior horn, across the anterior part of the external column, curving backwards (Fig. 80, x) ; many of them extend almost to the postero-median septum. They are "endogenous," i. e. they arise from cells of the posterior cornua. In the posterior columns they bifurcate into ascending and descending portions, the former of which may in certain parts of the cord form short but definite tracts, such as the "comma" tract of Schultzef and that in the lumbo-sacral region referred to below. These descending fibres terminate in all probability by again turning into the grey matter of the posterior cornua. (2) From the posterior commissure in the middle line (Fig. 80). These are very numerous and conspicuous in the lumbar enlargement. They course backwards in the septum * Except in cases in which the cervical roots are affected in which degeneration is restricted to the postero-external column terminating in the cuneate nucleus. Gombault, 'Bull, de la Soc. d'Auatomie,' 1891; Sottas, 'Rev. de Med,,' 189:5; Dejerine and Thomas, ' Compt. Rend.,' 1896; Souquez, ' Compt. Rend.,' 1895; Russell, ' Brain,' 1896. f * Arch, f. Physiol.,' 1883. 218 SPINAL CORD. and tlvm pass outwards on each side into the adjacent column. They come from the posterior and lateral columns of the opposite side, decussating in the septum. Some arise from posterior root- fibres, others from cells in the posterior cornua. In the lumbo-sacral region there is a narrow tract of fibres close to the posterior median septum, that is apparently of different nature from the rest of the column. It is lenticular on transverse section, and is indicated by the clear area in l. 4, Fig. 71, and faintly in L b, Fig. 77; it is best seen from the third lumbar to the second sacral segments. It is distinguished by a difference in time of development (Flechsig), and by freedom from the secondary degeneration that involves the rest of the column. It has been observed to undergo descending degeneration in a certain number of cases, and its fibres appear to terminate in the posterior horn of the same side. Their origin is uncertain, but they are probably endogenous and not directly connected with the posterior root.* A careful study by Pineles has shown that they fail to degenerate in tabes, and they also escape in the degeneration associated with anaemia.f This tract is possibly identic al with Flechsig's " oval field," and is also known as the septo-margL.al tract (see p. 220). FiG. 80.—Posterior cornu and column at the last dorsal segment, p. M. 0., postero- median column; P. E. c, postero-external column; p. M. s., posterior median sep- tum ; P. c, posterior commissure; v, commissure vein. p. v. c, postei ior vesicular column; c. C, caput cornu; p. B., posterior root; a, an artery; d, d, d, adjacent to a strip of the lateral column, indicate the tracts of fibres passing from the viciuity and interior of the posterior vesicular column along the septa of the lateral column, to form the direct cerebellar tract; x, x, tracts of fibres passing from the neck of the horn, near the post, vesic. col., to the post-median column. * See Hoche, 'Neurol. Centralbl.,' 1896; Bruce and Muir, « Brain,' 1896. t For an illustration of this tract see later, where the degenerations associated with anaemia are referred to. STRUCTURE. 219 It is very doubtful whether all the fibres that enter the postero- median columns continue in these to the medulla. Some certainly do, but the upward increase in size of the columns seems to be far too small for the accommodation of all the fibres that seem to pass to them. At the same time we have, at present, no indication of the mode in which fibres leave these columns. At the medulla oblongata this column becomes filled with nerve- cells, the post-pyramidal nucleus, so called because the highest por- tion of this column has been termed the posterior pyramid of the medulla. It is also called the nucleus gracilis. The discovery that the fibres of this column are continuous with the nerve-roots invests the post-pyramidal nucleus with considerable importance, since its nerve-cells are the first with which these root-fibres are related, and secondary degeneration hence stops here. The upward degeneration of the median fibres implies upward conduction ; their probable function will be considered in the next section. It is now known that not all of them end in the gracile nucleus ; some enter into the external arcuate fibre-system, while others run in the restiform body to the cerebellum. The postero-crternul column (" column of Burdach," containing the "posterior root-zone" of Charcot) consists chiefly of vertical fibres. Many of the posterior root-fibres pass through it, horizontally or obhquely (Fig. 65). These either curve inwards to the posterior horn (some first inclining upwards), or pass obliquely upwards and inwards to the median column and constitute the fibres of this column that are continued from the nerve-root. Across the anterior part fibres also pass, as just described, between the neck of the posterior horn and the median column. The vertical ground-fibres of the external column have apparently only a short course, since they degenerate for only a few centimetres above or below a lesion. The longest descending degeneration is of a " comma-shaped tract," in the middle of the anterior third of the column in the dorsal region, which may degenerate downwards for eight or ten segments* (Fig. 78). These vertical fibres, of short course, may connect the grey matter of the posterior horn at different (but adjacent) levels; this is rendered probable by the fact that they degenerate in transverse lesions of the cord but not in those of the posterior roots.f This column is larger in the swellings than it is in the dorsal region, chiefly in consequence of the larger number of root-fibres that pass through it. Above, it also ends in a grev nucleus, the pos I ero-external nucleus or cvneate nucleus. Both these posterior nuclei are connected directly with the cortex of the opposite hemisphere, and chiefly with the ascending parietal convolution. Fibres also pass from them to the cerebellar hemisphere * Hoche, ' Arch. f. Psych, u. Nervenkrank.,' xxvii. t Gomhault and Philippe, 'Sem. Med.,' 1894. This is only true of experimental division of the posterior roots, not of two cases described by Dejerine and Thomas ('Compt. Rend.,' 185_ sel, each continuous with a corresponding branch from the next commis- sural artery above and below—the anastomotic artery. This effects a vertical continuity of anastomoses within the cord, like that of the anterior spinal artery outside the cord. The peripheral arteries pass inwards from the surface. A posterior me- dian artery courses in the median septum, giving branches to each side, and an intermediate septal artery passes in the cor- responding septum out- side the post-median column. Midway be- tween this and the root- furrow a branch enters and passes through the postero-external column to the posterior horn, which it enters in front of the caput and chiefly supplies—the vosterior cornual artery; while a posterior radicular artery passes in on the inner side of the posterior root, and is distributed to this and the caput. A series of anterior radicular arteries enter with the anterior roots, and between them and the posterior horn are anterior, middle, and posterior lateral arteries in corresponding parts of the lateral column. The branches into the lateral column do not reach the grey substance; the branches in the grey substance extend into the inner part of the lateral column. The veins of the cord correspond in the main to the arteries, but a large proportion of the blood passes into the peripheral system. Some, especially those of the white substance, pass outwards along Fig. 83.—Semi-diagrammatic representation of the arteries of the spinal cord; as, anterior spinal. Central arteries.—a m, anterior median; c a, be- tween the right and left commissural arteries; a, anastomotic artery, divided transversely, tc which a branch goes from the commissural artery, which then divides into a c, anterior cornual, and m c, mid-cornual arteries. Peripheral arteries.— p m, posterior median ; p i, post-intermediate ; p c, posterior cornual; p r, posterior radicular; p I, m I, a I, regions of the posterior, middle, and anterior lateral branches; a r, anterior radicular. In the right half of the figure the more deeply shaded part indicates the region supplied by the central arteries. 228 SPINAL CORD. the septa; and those on the surface of the sides and back of the cord are gathered into a posterior spinal vein. Others, especially of the grey matter, pass inwards to a large vertical vein that lies in the grey commissure, a httle distance from the central canal on each side (v. Fig. 80; compare also Fig. 65), from which branches pass forwards to the anterior median fissure, and through this to an anterior spinal vein. The anterior and posterior spinal veins deliver their blood, through communicating veins, into the large venous plexuses that lie outside the dura mater, and which receive blood also from the bones, and from the structures and skin behind the spine. But the veins of the spinal cord cannot be injected from these plexuses, not because there are valves in the connecting branches, but apparently because they form so trifling a proportion of the total connections. From the plexuses blood passes to the various vertebral, cervical, and intercostal veins. Although there is a vertical continuity of the vessels of the cord, it is probable that the course of the circulation is, in the main, hori- zontal. From the very tortuous course of the path by which arterial blood enters the cord, it is evident that the pressure to which the arteries of the cord are exposed must be far lower than that in the arteries of the brain, and hence they are far less liable to degeneration and to rupture. On the other hand, the conditions that prevent an injection of the plexus of veins outside the dura mater from passing into the veins of the cord, must save the latter from the extreme over- distension to which they would otherwise be liable when there is a hindrance to the return of blood from the plexus. FUNCTIONS OF THE SPINAL CORD. "We are now in a position to consider the functions of the spinal cord, and the structures by which they are subserved. The functions are these: (1) The spinal cord conducts motor nerve impulses from the brain and sensory impulses to it. (2) It constitutes a series of centres for reflex action. (3) It contains certain centres that ulti- mately govern nervous action in structures under the immediate control of the sympathetic system, the bladder, rectum, blood-vessels, &c. (4) It influences the nutrition in all parts to which its nerves extend. Motor Conduction.—The chief facts regarding the physiology of the motor path have been necessarily considered in the account of its anatomy. We have already seen that the path of motor impulses is through the pyramidal fibres (in the anterior and lateral pyramidal tracts), the anterior cornua, and the anterior nerve-roots. The gan- FUNCTIONS. 229 glion-cells form part of the path, and so also probably does that part of the plexus of fibrillae in the cornu which intervenes between the pyramidal fibres and the ganglion-cells. We have seen that the crossed relation of the cerebral hemisphere with the limbs is sub- served by the decussation at the pyramids, and apparently to a slight extent above the chief crossing, since some degenerated fibres have been seen in the anterior pyramid opposite to the lesion of the brain. We have seen also that we are still ignorant of the mode of connection of the motor cells with the cerebral hemisphere of the same side in the case of the muscles that habitually act with their fellows on the opposite. These can be acted on by either hemi- sphere in degree that approaches equality in proportion as they act together, and is almost complete in muscles such as the intercostals, which can only act together. It is great in the case of all the trunk muscles and of those of the leg, less in those of the arm. This relation is further considered in the account of hemiplegia in Yol. II, to which it specially pertains. The variations in the decussation of the chief set of fibres suggest that the variations in observed facts bearing on the question may merely represent variations that exist in nature. The connection may be subserved by the fibres already mentioned that never decussate, but pass into the lateral pyramidal tract of the same side. The large fibres of the anterior motor nerve-roots are far more numerous than the fibres of the pyramidal tracts, and so also are the cells of the anterior horn, from which the large root-fibres proceed. Nevertheless it is probable that all these cells and root-fibres can be excited through these tracts. Hence many cells must be related to each of the pyramidal fibres. A complex mechanism is no doubt established by the interlacement of the terminal fibrillae of the pyramidal axons with the dendrites of the anterior cornual cells. This mechanism is such that the stimulation of certain pyramidal fibres excites to action a much greater number of nerve-cells, so con- nected and arranged as to produce, through the related nerve-root i, a complex movement, in which many muscles may take part. The nerve- cells thus connected may not all be at precisely the same level, and only some of those at a given level may be thus associated. The simpler the movements, and the fewer their possible variations, the fewer pyramidal fibres may suffice for the production of the move- ments. Thus it is conceivable that for such movements as those of the intercostal muscles, which are simple and constant, very few pyramidal fibres may suffice, whereas a much larger number must be necessary for the highly variable movements of the hand. It is pro- bable also that the pyramidal impulses influence other neurons than those directly subserving muscular contraction. By means of such intermediate or associational neurons these impulses are enabled to effect a more complex and varying movement than could otherwise be produced. 230 SPINAL COFD. Representation op Movements in the Spinal Cord.—It important to inquire how far we can identify these various motor mechanisms of the anterior grey matter. There are several sources of information on this subject. We have already seen that the arrange- ment of fibres in the anterior roots is such as to associate certain move- ments with certain nerve-roots, and it is a reasonable assumption that this corresponds, to some extent at least, with the arrangement in the grey matter. The sources of our information on this point are the limited facts of anatomy, rare cases of restricted disease of the nerve- roots in man, and especially the experiments of Ferrier and Yeo on monkeys. We have already considered the indications that these experiments afford, and their suggestiveness, and we have seen that their value is relative rather than absolute. As regards the grey matter, we must remember also that there may not be a strict horizontal corre- spondence between the nerve-roots and the nerve-cells, because it is probable that some root-fibres enter the antero-lateral white columns, and are connected with nerve-cells at a higher or lower level than that at which they leave the cord. Another source of information is the degeneration of nerve-cells that follows slowly on an amputation of a limb, and the condition of the spinal cord in congenital absence of part of a limb. The last and most important source of information is supplied by cases of limited disease of the anterior cornua, in which the position of the lesion and the distribution of the resulting palsy can be compared. Destruction of nerve-cells causes degeneration of the motor fibres proceeding from them, and wasting of the muscles to which those motor fibres proceed. This alone affords us certain know- ledge. Cases of clear significance are, however, rare, and it will be long before our knowledge can be complete. Meanwhile we may learn something of the central association of muscles by observing what muscles are most frequently paralysed together by such disease. This subject has been carefully studied by E. Eemak* and by Thorburn,f and many valuable isolated observations have been pub- lished. It is only the associations which are frequent that can be allowed significance, because it is not uncommon to have more than one focus of disease in the grey matter. The following summary presents the conclusions that seem probable from the evidence at present available.]: The various facts for the most part fully confirm the conclusion of * 'Archiv f. Peychiatrie,' vol. ix. t 'Brain,' January 7th, 1887, and October, 1888. The facts were observed on cases of injury. He associates each muscle with a single spinal nerve, but these nerves are only collections of roots that are severally continuous, as are the groups of nerve-cells within the cord, and it is certain that the roots related to many of the muscles go into adjacent spinal nerves. X A useful summary of the evidence up to the middle of 1884 was given by Dr. Allen Starr, in the 'American Journal of Neurology,' Aug. and Nov., 1884. The subject is a tempting one for theory, but it is very important to keep to the solid ground of facts, however limited it may be in extent. FUNCTIONS. 231 Remak, corroborated by the experiments of Ferrier and Yeo, that most movements and muscles are represented in vertical tracts, and the whole anterior grey matter, at any one nerve-segment, contains cells that are concerned with different movements. An extensive lesion of small vertical extent may thus weaken many movements, but abolish none. The special representation of the muscular functions, i. e. of definite movements, is no doubt related to special groups of nerve- cells, but a single group may be concerned in more than one associated movement. Different groups are probably intimately connected, because we know that the contraction of any muscle is accompanied by a slighter but proportioned contraction of its antagonists. Anato- mical connections in both spinal cord and brain doubtless underlie this association. Cervical Region.—The highest cervical region apparently contains centres for the small rotators of the head, and the depressors of the hyoid bone were found by Beevor and Horsley to be related to the first two pairs of nerves, the sterno-hyoid and sterno-thyroid chiefly to the first and the omohyoid to the second.* The upper part also contains centres for the muscles of the neck, especially for the sterno-mastoid and upper part of the trapezius. The dia- phragm is probably represented in the grey matter at the level of the roots of the phrenic nerve, the fourth cervical. In the brachial region of the cervical enlargement, the muscles of the shoulder are represented chiefly in the upper part; the intrinsic muscles of the hand in the lower part. The flexors of the elbow are represented above its extensors, and the supinators and extensors of the wrist above the flexors of the wrist. Deltoid, scapular muscles, pectoralis, and serratus.—The fifth and sixth segments, for the most part the sixth, and probably the outer group of nerve- cells.f The centres for the two parts of the pectoralis are separate, and are associated—the clavicular with that of the serratus magnus, the costal with that of the latissimus dorsi (see p. 37). These associated muscles are repre- sented near together, but not at the same spot; the association is often reproduced in disease of the anterior cornu, the clavicular part being affected together with the serratus, but one muscle may suffer without that which is commonly associated with it. The Flexors of the elbow and supinators probably correspond nearly in level with the deltoid. The whole of this series of muscles may be affected alone by disease of the nerve-roots (see p. 38) or of the grey matter, and then we have the " upper arm type " of palsy, described first by. Erb. Extensor of the elbow (triceps) : probably the middle of the brachial region, chiefly the seventh segment, extending down to the eighth, and perhaps up to the sixth, possibly chiefly in the outer group of nerve-cells. The Extensors of the wrist are represented above those of the elbow ; probably chiefly at the sixth or sixth and seventh segments, and not from the » Cbieriy the posterior belly of the muscle, by a branch joining the glosso- pharyngeal. The other muscles named (including slightly the anterior belly of the omohyoid) are innervated from the first cervical by a branch joining the hypoglossal. f Thorburu (loc. cit.) refers the infra- and supra-spinati with much probMbihty to the fourth pair of ner\ es. 232 SPINAL COItD. postero-external, but from the other groups. Flexors of the ivrist: below the extensors, nearly on the same level as the extensors of the elbow, at the seventh and eighth segments, and probably also from one of the outer groups of cells. The pronators have nearly the same representation as the flexors of the wrist. Long Extensors of the fingers: upper part of the brachial region, about the level of the sixth or between it and the seventh segment; probably from one of the anterior groups (not from the postero-lateral group). Long flexors of the fingers: below the extensors; probably seventh or eighth segment. Intrinsic muscles of the hand: lowest part of the brachial region, and the thenar muscles a little higher than the interossei; the latter being represented in the first dorsal segment.* The intrinsic muscles (like the long extensors) are probably related less to the outer than to the inner and anterior groups. The two sets of muscles are related both in action and in central connection, as was illustrated by a case of concussion-lesion under my care, in which the two outer interossei were paralysed and wasted, and also the part of the long extensor supplying the two outer fingers, but no other muscles. Lumbar Enlargement-—Our knowledge of the representation of muscles in the lumbar enlargement is very slight, and we have scarcely any definite facts concerning their relation to the cell-groups. The postero-external group pre- ponderates over the others in size, even more than in the cervical cord, and doubtless also in importance. The few pathological observations of changes in the several groups are not altogether consistent. The chief facts available relate to the probable segmental level and association of the centres, and are as follows: Cremaster, second lumbar segment. Psoas, second, iliacus, third lumbar; the two muscles (one in function) are probably related to a group of cells ex- tending through both segments. Adductors, fourth lumbar segment. Gluteal muscles (extensors of hip)', fourth and fifth lumbar segments. Extensors of knee, third and fourth lumbar segments, probably from the same group as the flexors of the hip ; the two sets of muscles are often affected together, and sometimes the abductors suffer with them. The Sartorius is probably related to the third segment, but not to the same cell-group as the extensors of the knee (to which, indeed, it does not belong; see p. 47). It usually escapes in atrophic palsy of the extensors. Flexors of knee, fifth lumbar and first sacral segments. Their centre is thus below and certainly distinct from that of the extensors. The muscles of the lower leg, moving the foot and toes, are related to the fourth and fifth lumbar and the first sacral segments. The calf muscles, the tibialis anticus, and the peroneus longus have certainly separate centres, and are often affected separately. The tibialis anticus may suffer alone, or may alone escape when the other muscles in front of the leg are paralysed. The muscles of the calf may be affected when those in front of the leg are not. It is probable that the peroneus longus is the highest in central representation, and is related to the fourth lumbar segment. The intrinsic muscles of the foot, especially the interossei, are the lowest in * This is the indication of the majority of cases. Nevertheless Sahli has recorded a case of atrophy of all the intrinsic muscles of the hand, in which the lesion did not extend below the seventh segment; the eighth and first dorsal were perfectly normal. I have seen a case of atrophy limited to the deltoid and intrinsic muscles of the hand, due to an acute process, probably hseni 'rrhau'e, but in this case there may have been two lesions. FUNCTIONS. 233 central relations, being connected with the second sacral segment. The position of their centres, in the lowest part of the lumbar enlargement, thus corresponds to that of the analogous muscles of the hand, in the lowest part of the cervical enlargement. Sensory Conduction.—Our knowledge of the sensory path in the cord is far less definite than that of the motor path, in spite of the fact that it has been the subject of a large number of experimental investigations. The subject is a very difficult one for experimental solution, on account of the difficulty of ascertaining the condition of sensation in animals. The indications afforded by disease are equivocal for another reason. We have seen (p. 78) that, in the sensory nerves, a lesion which permanently interrupts motor conduction may scarcely affect sensory conduction, and the same thing is apparently true of the spinal cord. If loss of feeling results from an acute lesion, it often q uckly passes away, although motor palsy remains complete and absolute, and this when all the elements of the cord seem equally implicated in the morbid process. In cases of such chronic disease as compression, which when slow must act on all the structures in nearly equal degree, the same escape of sensory conduction is often observed. Difficulties are encountered whatever mode of interpretation of the phenomenon we adopt, and the fact of importance to our present problem is that we are not yet able strictly to compare structural and functional damage when the former is moderate. When the damage has been slowly produced it may be apparently great, and yet function may not be much impaired, especially the lower function of conduction of nerve-force. The significance of these facts as regards the problem of sensory conduction in the cord is that we must be cautious in drawing any conclusion from the persistence of sensation We cannot infer, because supposed sensory tracts are visibly diseased in a case in which there was no loss of sensibility, that these tracts have not the function assigned to them, unless we can feel sure that all the axis-cylinders are destroyed. This we can seldom do; and for this reason, and because morbid processes are often wide in distribution, the evidence that can be obtained by comparing the position of lesions with the sensory symptoms they produce is limited and uncertain. Other sources of information are the effect of partial lesions of the cord, intense in degree, but limited in area, especially traumatic lesions affecting one half of the cord or part of one half. Cases of this kind are of high value, but in few, at present, have the extent of lesion and the range of symptoms been accurately ascertained. Hence physiologists have relied chiefly on the results of experiments on animals. Unfortunately the help these can give is also reduced to a literal minimum by the difficulties of experimentation and of interpretation—the physical difficulties on the one hand, the functional perplexities on the other. Some clear facts have been ascertained, and other results have been obtained that still wait certain interpretation. It seems certain, in the first place, that sensation in any particular region of the skin is associated with the functional 234 SPINAL CORD. activity of a definite portion of the opposite cerebral cortex. Anatomical evidence shows that the axons belonging to different centripetal tracts cross the middle line at various levels in the cord, medulla, and mid-brain. The early experiments of Brown-Sequard led him to conclude that the chief part of the sensory path decussates soon after entering the cord, and with this view pathological facts in general agree. The consensus of evidence, however, points to a less sudden and uniform crossing than was formerly assumed. The axons entering from the periphery do not as a rule pass directly across the cord, but break up in the grey matter, whence, possibly after one or more relays, the conducting path is continued on the opposite side. It will be seen that these considerations suggest that sensory conduction is a function of the lateral and antero-lateral tracts rather than of the posterior columns, which run uncrossed to the region of the medulla. This is quite in accordance with what is found both clinically and experimentally. For the posterior median fibres may be extensively degenei-ated when sensation is unimpaired, a fact of which we shall see the probable meaning presently; and, on the other hand, Osawa has shown that section across the whole cord, with the exception of the posterior column, completely abolishes sensation. That this abolition is incomplete unless the grey matter is completely divided was found also by Schiff; the important part played by the grey matter in sensory conduction is thus confirmed. The subject, however, at the present time is too far from even the semblance of settlement to make a discussion of the evidence worth the space it would need, especially in a work dealing with practical medicine.* It is only desir- able, therefore, to point out certain leading facts and leading considerations. Clinical evidence, largely based upon cases of syringomyelia, points to the grey matter as the seat of conduction of painful impressions. Experiments suggest that impressions which act upon the vaso-motor centre pass up in the lateral columns—in animals chiefly on the side of the cord opposite to that on which they are produced, slightly on the same side. Sensations of touch appear to be conducted mainly in the lateral columns and grey matter. In man the paths for both touch and pain are on the opposite side of the cord. We may accept as certain the fact that the tactile or painful impulse we feel crosses the middle line soon after entering the cord ; it is probable that some impulses that we do not feel do not cross. We must never forget that there is sti-ong reason to believe that only a minority of the impulses that traverse afferent nerves affect our consciousness. The participation of the grey matter in the conduction of afferent impressions has been fully confirmed by the facts as to the course of centripetal fibres in the cord revealed by the recent improvements in histological technique. That sensation escapes in anterior polio-myelitis points to the posterior part of the grey matter as the seat of this conduction, and this again is in agreement with both histological and experimentalf evidence. The assumption that a certain number of centripetal axons exist in the central grey matter is of great.service in studying the problems of sensory conduction. Still, they are not numerous enough to save us from the difficulty that the * Thus, for-example, two of the latest series of experiments upon monkeys, those of Mott and Turner, yield conflicting results. The latter are mainly confirmatory of those of Brown-Sequard; while, according to the former, touch and the muscular sense are mainly transmitted up along the side of the cord at which they enter, but the paths of pain and temperature pass up on both sides. t E. g. the researches of Schiff and Ciaglinski (see later). FUNCTIONS. 235 fibres we can look to are, taken altogether, insufficient in number to subserve the marvellous differentiation of sensation in the periphery—differentiation in quality of feeling and especially in locality of feeling. But a difficulty may become inoperative, without ceasing to exist, by being absorbed in a still larger difficulty of the same kind. If we avail ourselves of all the structures of the spinal cord that can conceivably subserve upward conduction, we fail to find room for the separate conduction of impulses which, nevertheless, the spinal cord must separately convey. On only one hypothesis is it possible to conceive such conduction. It has already been pointed out that the increased power of the microscope has shown us that each axis-cylinder, so called, is not a simple body, but a compound structure, composed of fibrillse, and comparable, in point of fact, to a bundle of nerve-fibres. What was formerly regarded as division of an axis-cylinder is now known to be the separation of its ultimate fibril la?, and this has been shown to occur in both motor and sensory axons, and, to a certain extent, along their course (collaterally) as well as at their terminations. It seems to follow of necessity that each sensory area of distinct perception must be subserved by one of these fibrillse. It is conceivable that the impulses may keep each to its own fibrillary path, however many fibrilhe an axis-cylinder may contain. We have, indeed, seen that such fibrillse keep separate even in traversing a nerve- cell. It is only by such an arrangement that it seems possible for the sensory impressions from skin and tissue, of touch, pain, and temperature, to be carried to the brain so as separately to excite certain nerve-cells of the cortex. If these considerations have weight we cannot exclude the lateral and posterior columns from the function of sensory conduction on account of the scanty fibres we can discern to subserve the function, and may consider what evidence on the point disease and injury afford in man. Unilateral lesions of the spinal cord, which cause loss of sensibility of the skin, do so on the side opposite to the lesion. This is true of all forms of sensibility. They thus prove, beyond doubt, the de- cussation in the spinal cord of the path from the cutaneous nerves of pain, of touch, and of temperature. An analysis of the cases in which both effect and lesion have been exactly ascertained—which will be considered more fully when these lesions are described—sug- gests certain other conclusions regarding the position of these paths. The facts suggest, first, that the paths for sensations of pain and of touch are not near together. Sensibility to pain has been lost in almost all recorded cases, but that to touch in only two thirds. They suggest, secondly, that the two paths for tactile sensibility are nearer together than are the two paths for pain. In no case of chiefly unilateral lesion has sensibility to pain been lost on both sides, whereas in two recorded cases sens.b lity to pain was lost on the side opposite to the lesion, while that to touch was lost on both sides.* * It is possible that tactile sensibility may have been lost, in other cases, on the second side, i. e. on the side of the lesion, and the loss may have escaped notice in consequence of the exaltation of sensibility which is commonly present, and which is presumably due to the nerves of common sensibility. 236 SPINAL CORD. These conclusions, moreover, are supported by the facts of two impor- tant cases of injury to the cord which afford direct localising indica- tions. One is a case, recorded by myself,* in which the spinal cord in the upper cervical region was damaged by a small spiculum of bone being driven against it by a bullet, which, entering the mouth, lodged in the body of the third cervical vertebra. The extent of the lesion of the cord is shown in Fig. 81. The chief injury is clearly to the lateral column and grey matter, the posterior column being merely swollen, appa- rently by oedema. The affected part was the seat of haemorrhage and hemorrhagic infiltration. The effect was entire loss of sensibility to pain on the opposite side without any im- pairment of tactile sensibility. To this the other case, recorded by Miiller,t is almost a complement. A Fl». 84.—Section of spinal cord be- . , , -,. .-, -, ,-, , , « „„„ tween the second and third cervical stab-wound divided the whole of one nerves, contused by gunshot injury, half of the cord, including the poste- rior column, and also the posterior column of the other side almost up to the nerve-roots; the grey matter of this side escaped. The whole of both postero-me lian columns was thus divided. The effect was loss of sensibility to pain on the side opposite to the lesion, and of that to touch on both sides. Thus there is strong reason to believe that the path for sensibility to pain does not pass in the posterior columns. The evidence of disease (syringomyelia) points to the grey matter as at any rate the main seat of this path. We have already seen that the escape of sensation in anterior polio-myelitis indicates that it must pass along the posterior part of the grey matter, and this accords well with experimental evidence. Thus Schiff found that section through the whole cord except the posterior columns abolished sensation to pain below the lesion, whereas if a trace of the posterior part of the grey matter was left this sensation was still transmitted, though delayed. Ciaglinski J describes an ascending tract, found experimentally in the dog and verified histologically in man, between the postero-median column and the central canal, and regards this as the path for impres- sions of pain and temperature. As to the path of tactile sensibility we must wait for further evidence. The fibres that degeneiate upwards in the median columns, passing to them from the external posterior columns, and constituting so large a proportion of their * ' Clinical Society's Trans.,' vol. xi, 1878, p. 24. f ' Beitrage zur path. Anat. und Phys. der Ruckenm.,' Leipzig, 1871. Abstracts, which supplement each other, and, together, give a full account of the case, will be found in Kobner's article on unilateral lesions, ' Dent. Arch, f. klin. Med.,' 1877, Bd. xix, p. 190; and in * Virchow's Jahresbericht,' 1871, Bd. i, p. 152. X Cia.'linski, 'Neurol. Centralbl.,' 1896. FUNCTIONS. 237 mass, apparently come from the muscles. We may, however, re- member that many fibres pass to the posterior columns from the grey matter, and also from the posterior commissure in the middle line; some of the former may also come from the posterior commis- sure, and both these sets of fibres may have crossed in the middle line. It is possible that these fibres conduct tactile sensibility, and that they are mingled with those that conduct muscular sensibihty. This theory, however, can only be regarded as a suggestion for future observations; it must be confessed that the results of experiment, which are, however, for reasons already stated, not so valid as clinical observations, tend to indicate the implication of the lateral and antero- lateral columns in the conduction of tactile sensations. The conduction of impulses from the muscles is certainly in the posterior median columns. This is clearly shown by the facts of the pathology of tabes. The function of the direct cerebellar tract has still to be demonstrated. There are certain resemblances between its fibre-relations and those of the posterior median columns which give countenance to Flechsig's theory that it conveys impressions from the muscles of the lower part of the trunk and between the trunk and lower limbs. But the origin of its fibres from the cells of the poste- rior vesicular column, and the mystery attaching to the latter, give additional obscurity to this structure. The fine nerve-plexus between the cells seems connected with fibres of the posterior roots, and this plexus is said to atrophy early in locomotor ataxy.* The obscurity will, indeed, be dispelled if we can accept the speculation of Sher- rington that this cylinder is really part of the series of ganglia on the posterior nerve-roots, which occupies a position within the spinal cord, and is continuous instead of broken into ganglia. The path for sensations of temperature is still unknown. The fact that this sense is frequently impaired with sensibihty to pain suggests that the two paths may be near together in the grey matter. More than this cannot be said. But we have to consider another problem in our study of the sensory path. The same impression that is felt may excite a reflex action. For this, afferent root-fibres must end in the grey matter of the cord. Are the two functions subserved by the same or by different fibres ? A similar question presents itself with regard to the muscle nerves. If the ascending degeneration in the postero-median column, when the cauda equina is diseased, is admitted, as it must be, as proof that these root-fibres pass up without interruption, the muscle- reflex action must be subserved by other fibres. For it, however, comparatively few may suffice. With regard to the other sensory fibres, the evidence at present suggests that all undergo interruption in the spinal cord, since no other paths have yet been found degene- rated when a lesion has been confined to the nerve-roots. If so, the * Lissauer, Oppenheim, &c. See Mott, " Bipolar Cells of the Spinal Co d," 1 Brain,' part lii, 1890. 238 SPINAL CORD. same fibres probably subserve sensation and reflex action, the den- drites of the nerve-cells providing a mechanism for the division of the path and diversion of the impulses. No impression, in health, causes a true reflex action that does not also produce a conscious sensation. Our knowledge of the serial representation of cutaneous sensibihty in the spinal cord has of late been much increased by the careful researches of Head, Thorburn, Starr, Dana, and others. It is probable that there is a progressive representation of the skin in the posterior nerve-cells without relation to the nerve-trunks, and with only a slight relation to the nerve-roots. Correspondence with the latter must not be assumed. In the roots the serial representation is along the axis of the limb, not across it, as it probably is in the nerve-cells. In the dorsal cord, ascending disease often causes an affection of sensation which extends around the trunk at higher and higher levels. In the limbs we have indications of the same arrangement: the soles and palms may be affected alone, and anaesthesia may extend on the limb to a certain level, irrespective of nerve distribution. This is often seen in the legs. I have known anaesthesia in the arms, due to disease of the cord, to cease midway between shoulder and elbow, at the same level around each arm. Disease of the cord may affect sensation on the tips of the fingers only. It is probable that the ascending course of many of the root-fibres subserves a rearrangement of representation in the cells, and provides also for a special connection of the tactile nerves from each part of the skin with the motor cells for the muscles beneath— so conspicuous in many of the cutaneous reflexes. Reflex Action.—The grey matter of the spinal cord constitutes a series of reflex centres, some of which must be of considerable ver- tical extent and much complexity. They are subserved not only by the grey matter, but by the short fibres that in the several white columns connect the grey matter at different levels. The passage of the root- fibres upwards and downwards in the cord, before they turn into the grey matter (conspicuous • in the posterior roots), also, as we have noted, constitutes an arrangement for spreading the afferent impulses through a considerable vertical extent of the cord. We have already seen (p. 19) that we must distinguish two forms of reflex action—the cutaneous reflex action and the muscle-reflex action, the latter producing the " myotatic irritability " which, as we assume, determines the so-called " tendon-reflex contractions." The first form of reflex action is not, however, limited to impressions on the cutaneous nerves. It may be produced by stimulation of the nerves supplying the deeper structures, including those of the tendons and muscles. The attempt to obtain the knee-jerk may cause a true reflex action as well as its special effect, the two being separated by an appreciable interval of time (see Locomotor Ataxy). Reflex action from the skin is apparently subserved by all the sensory nerves, since it may continue, although the nerves for either pain or touch have ceased to act, in consequence of those degenerative processes by FUNCTIONS. 239 which function is sometimes abolished in as complete degree and with as precise limitation as the physiological inquirer could desire. The central process concerned in reflex action must take place between the posterior nerve-roots, by which the sensory impulses reach the cord, and the anterior roots, *by which the motor impulses leave it. The motor ganglion-cells form part of the reflex centre, and the rest of the centre is doubtless constituted by the fibrillary plexus formed by the inosculation of their dendrites and those of the sensory nerve-cells. The whole path between and including the in- and out- bearing nerves may be spoken of as the " reflex arc ;" the grey matter concerned being called the " reflex centre." In this " centre " the sensory impulse is transformed into—or rather gives rise to—a motor impulse, usually much greater in the degree of its energy. Within the centre there are paths established by the connections between the nerve structures, of which only a few are in functional use. It is easy to conceive that the functional action takes place more readily in some lines than in others, and these lines of easiest action are often spoken of as " lines of least resistance," and are said to determine the form of the reflex action. In its simplest form a " reflex arc " con- sists of two neurons, a centripetal and a centrifugal, between the dendrites of which the transformation of the impulse takes place. More powerful stimulation brings also into action the dendrites of the centripetal neuron which are associated with other neurons than the centrifugal already mentioned, and hence conduces to a wider area of motor discharge. The stronger (within limits) the afferent stimulus, the more widely does the process spread in the centre, and the more extensive is the movement produced. Thus a slight touch on the sole may cause only a movement of the foot, while a prick may cause a movement of the whole limb. At the same time there is much more than degree involved in the difference between these two stimuli. The impression that is felt as pain causes a quick simple movement of the part, in which chiefly the flexors are involved. It is a movement obviously to withdraw from harm, and it is proportioned, in energy and extent, to the intensity of the stimulation. To this, however, there is one limitation:—a strong impression of pain may prevent all reflex movement by exerting an inhibitory influence on the centres. On the other hand, a tactile impression causes a much more complex movement, which does not bear a simple relation, in extent and energy, to the degree of the sensory impulse, but is also influenced by the quality of the impression at the place at which it is produced. Thus the reflex move- ment produced from the palm or sole is especiallv elaborate; it may present an indication of the central relations by which the purposed use of the extremities is facilitated. The effect of all painful impressions is similar, whether these are produced through the nerves of the skin or those of deeper structures. The reflex action caused by pinching a tendon is just the same as that caused by a pinch of the skin over 240 SPINAL CORD. the tendon. Even impressions from the afferent muscle-nerves cause a similar reflex movement. Thus there is no real distinction between the deep and superficial true reflex action. The muscle-reflex action which is assumed to exist between the afferent and efferent nerves of a muscle (and to underlie the myo- tatic irritability which permits the knee-jerk, &c.) has been already considered in discussing the theory of this irritability. It is appa- rently a uniformly simple relation between the two sets of nerves for the same part of a muscle; the reflex action is confined to these, and does not spread through a wider extent of the grey matter, as that from the skin frequently does. When a muscle is made tense, or its tendon is tapped, the mechanical stimulation influences all the afferent nerves or all the muscular fibres, and the whole muscle neces- sarily responds. The motor ganglion-cells of the anterior horn must form part of the centre for each form of reflex action, but that portion of the centre which intervenes between the afferent nerves in the posterior root and the motor cells must be distinct in part or altogether. Beyond this we can say nothing of the relation of the two centres. These reflex centres are subject to control by higher centres, as are all lower centres in the nervous system. All true reflex action, e. g. that from the skin excited by a touch or prick, is controlled and kept mode- rate by an influence from the brain, for it becomes excessive when the influence of the brain is stopped, as by a lesion interrupting the spinal cord; it is increased in all parts that are connected with the cord below the lesion. We have no precise knowledge of the seat of the controlling centre or of the path by which the control is exerted. In frogs, however, the restraint seems to be exerted by the optic lobes; in man it is less likely to be exerted by the homologous corpora quadrigemina than by the optic thalamus. The mechanism must, however, be complex, since the restraining influence may be increased by disease in some parts of the brain; many cerebral lesions which cause hemiplegia cause also a diminution of cutaneous reflex action on the paralysed side. The effect seems to indicate that the cerebral centre which controls reflex action is itself habitually controlled by a higher centre, perhaps in the cortex. When this is destroyed, or the path from it is interrupted, the controlling centre passes into a condition of increased activity, and the reflex action is lessened. This is a theory only, but it seems impossible otherwise to explain the facts. The muscle-reflex centres seem also to be under the control of other centres, because, if there is disease of the cord higher up, they also pass into a condition of increased activity. But the phenomena of their disturbance present three important points of difference from those of common (e. g. cutaneous) reflex action. (1) We know with certainty the path disease of which determines their excess : it is the pyramidal tract. (2) Disease of the brain does not cause a permanent dimiuu- FUNCTIONS. 241 tion in the action of the muscle-reflex centres, as it so frequently does in the case of the centres for cutaneous reflex action.* On the contrary, disease of the pyramidal fibres in the brain causes the same excess of this form of reflex action as does disease of the pyramidal fibres in the cord. (3) The excess does not, as a rule, quickly follow an interruption of the path from the brain, as does the excess of superficial reflex action. There may, indeed, be an immediate, usually temporary, excess, coinciding with " early rigidity " from the irritation of the pyramidal fibres, but the permanent excess comes on at the end of a week or ten days, and gradually increases. The explanations may be these. The slowness with which the reflex action usually becomes excessive is conspicuous, and its significance must be considerable. The lesion of the pyramidal fibres causes their degeneration below the lesion, and this must involve their termination in the grey matter. The excess of action of the centres may be the result of the degeneration of the terminal structures, which may con- stitute a controlling mechanism that normally restrains the activity of the muscle-reflex centres. The interval which elapses before the excess is manifested may be due to the fact that there is little tendency to increased activity; that but slight control is habitually exercised or needed ; and that the capacity for over-action is gradually developed and gradually increases—increasing capacity being deve- loped by the increased activity. It is probable that the voluntary impulses pass from the termina- tion of the pyramidal fibres to the motor cells through structures of which this muscle-reflex centre forms part, and that therefore its elements must be in part excited to action by pyramidal impulses—a conclusion quite compatible with a restraining influence exerted by these fibres or their endings when no volitional impulses descend them! The chief local forms of superficial and muscle-reflex action have been already described (see p. 19, et seq.). Their centres are found in the corresponding segments of the cord shown in the table at p. 252. Adaptation to Posture.—Every difference in posture involves a difference in the distance between the attachments of the muscles of the part. When the muscles are at rest they present always a certain state of "tone," which, being equal in every posture, must vary auto- matically with every change of posture, however brought about. In passive movements the muscles that are elongated and those that are shortened adapt themselves to the change as it proceeds. Apparently the increased tension on the former makes them yield to the move- * A very rare exception to this rule will he mentioned when the functions of the brain are consideied. Moreover the knee-jerk is abolished in some cases of tumour of the cerebellum, a phenomenon to be remembered in connection with the fact that, while oue part of the afferent impulses from the muscles acts on the cord, another part apparently passes up to the cerebellum. See the account of co- ordiuation of movement on the next page. VOL. I. 16 242 SPINAL CORD. ment, and the lessened tension on the latter makes them contract, each set thus preserving its proper tone. The tone of a muscle seems to be produced by a reflex process, due to a certain state of the motor cells regulated by the impressions from the afferent muscle-nerves. These, as we have seen, are produced by two mechanical influences, the lateral pressure of the fibres (as in the pain of cramp) and the tension on the muscle. An increase of the latter, in passive move- ment, seems to lessen the activity of the cells and permit the fibres to elongate; a diminution increases the activity of the cells and causes the fibres to shorten. It further appears that the tone of a muscle is influenced through the spinal cord by the condition of its antagonists. Thus the knee-jerk may be increased by cutting the sciatic nerve—i. e. the nerve to the flexors, or diminished by stimulating it. An increase similarly results when the hamstring muscles (the antagonists of the quadriceps) are relaxed by flexion of the knee.* Co-ordination of Movement.—The co-ordination of muscular contractions, which results in the ordination or ordering or arrange- ment of movement, has been already described (p. 7), so far as its general features are concerned. We cannot ascribe to the spinal cord any process that can be designated the arrangement of movement; since the muscular contractions correspond to the activity of the motor cells of the cerebral cortex, and to the corresponding impulses along the pyramidal fibres. These determine the initial activity of the motor cells of the cord, both for the muscles that move a part and for those that oppose the action of the others and give steadiness and uni- formity to the movement. But these impulses from the brain descend on spinal cells that are not in a passive, inactive, functionless state. Such a state probably never exists, for even when there is no voluntary activity there -must be the activity on which the tone depends,—that, as we have just seen, must exist in all postures of the limbs. ■ This state of the cells preceding voluntary activity is determined by the afferent impulses, chiefly by those from the muscles. Through these the muscles are adapted to posture, and in the mechanism for adapta- tion to posture we may trace also a mechanism for part at least of the co-ordination effected in the spinal cord. This seems to consist of two parts. (1) An automatic variation in the state of muscles, per- mitting the ordered performance of intended movements. The state of the afferent impulses acting from the muscle on the motor cells must be at once altered by the effect of the voluntary activity of the muscles, since this will alter the impulses in the muscle-nerves by the changed and changing pressure and tension on the tissues in which these nerves end—the pressure of the contracting and widening fibres and the tension in the antagonists that oppose the motion, but do not prevent it, and are made more tense by the muscles they are opposing. These impulses pass to the cord, and there act on the motor cells, and influence their state in a way that we can at present only guess at, but * See Sherrin.r on, 'Brit. Med. Journ.,' 1893, vol. ii, p. 685. FUNCTIONS. 243 which must be of the utmost importance. There must of necessity be a definite relation between certain states of the muscle and the strength of afferent impulse produced thereby. If we conceive that an increase in the impulse (making it greater than corresponds to the degree of activity of the motor cells), such as must result from the increased tension on the muscle, lowers the activity of those cells, we can understand the way in which the contracting antagonists relax to permit movement which tends to occur. As soon as the resistance begins to yield, the tension-stimulus will be increased, and the total afferent impulse become disproportionately great in relation to the degree of activity of the cells ; as a result, this activity is lessened and the muscles yield. This involves a constant regulation of the activity of the various motor cells by the afferent impulses. A like but opposite effect must be produced on the cells of the muscles producing the movement. This effect on the cells will, of course, blend with that of the voluntary impulse from the brain that is causing the movement. Thus the spinal muscle-reflex process permits the desired movement to take place, as it could not do if the state of the cells were not thus automatically regulated. (2) Relations between the various reflex processes are doubtless established by the repetition of movements, and thus planned mechanisms, as it were, are established in the cord ; within their range the various movements occur. The state of the muscles in standing, for instance, is almost perfectly reproduced by the extensor spasm that occurs when the muscle-reflex processes are in great excess. Thus we have a mechanism by which a relatively simple voluntary impulse may produce an extensive co-ordinated movement. But what we can discern shows that we must regard spinal co-ordina- tion as essentially a reflex process, chiefly due to the impulses from the muscles. The correctness of this view can hardly be doubted when we come to see its perfect harmony with the phenomena and the con- ditions of spinal inco-ordination. Still it must be always remembered that this spinal process is of the nature of a subordinate mechanism, determining the precision of form rather than the actual arrangement and order of the muscular contraction. This is done by a higher process, a co-ordination which consists in the form of action of the motor cells of the cerebral cortex that is produced by still higher volitional processes. These, however, as we shall see, are themselves subject to a like influence and the seat of an analogous regulation, chiefly, it is probable, by impulses proceeding from the cerebellum, which are also due to the varying excitation of the muscle-nerves. That the nerve-fibres which pass up the posterior median columns conduct impulses from the muscles that determine cerebral co-ordination scarcely admits of doubt. Interrup- tion of this path in any part of its course causes a defect of co- ordination, which resembles that due to cerebellar disease with sufficient closeness to add weight to other facts suggesting that it is through the cerebellum that the impulses carried by this path act on the 244 SPINAL CORD. cortex, regulating and determining the activity of its cells and the resulting movement.* The impulses may reach the cerebellum, us we have seen, from the grey matter of the post-pyramidal nucleus in which these fibres end.f But this primary co-ordination is not a function of the cord, although it may be lost in consequence of disease of the cord. • The direct cerebellar tract may constitute a similar path, but of this we have only the evidence of destination and analogy. It is probable that the mechanisms just alluded to, as constituted by the functional relations between the motor and sensory structures in the cord, very much facilitate the execution of many movements, and especially of those that are the more simple in their character. The less variation a movement is capable of, or needs, the more largely may the spinal mechanism be concerned in its arrangement; and hence such actions as standing and walking may be effected through a comparatively small number of the pyramidal fibres, and, as we shall see, they may still be performed when there is disease that would prevent a more elaborate action. It is also probable that in animals such spinal mechanisms are developed to a greater extent than in man, and care must be taken in drawing inferences from one to the other. The impulses from the muscles that determine the muscle-reflex action and the spinal co-ordination, must pass by nerves that end in the grey matter and come into relation with nerve-cells, at or near the level at which they enter the cord. We do not know whether it is through these fibres, or through those that pass upwards without interruption, that the impulses are conveyed which, when excessive in degree, give rise to muscular sensations. But attention may again be called to the important evidence, afforded by such sensations, of the abundance of upward impulses of which we are normally unconscious. These nerves, it will be remembered, begin in the connective tissue of the muscles, and probably also in the muscle-spindles, and the acute pain of cramp, and the muscular tenderness in such affections as multiple neuritis, afford indirect evidence of impulses which we do not usually observe, and might almost doubt; while the manner in which such pain is excited is very clear evidence of the sensitiveness of the nerves to the modes of stimulation that have been assumed as effective. We have already seen (p. 17) that it is through such unfelt impulses that we probably derive the chief part of our conceptions of posture, a subject that must again be considered in connection with the brain. Influence on Nutrition.—The nutrition of the muscles is under * This has been experimentally confirmed by Bechterew, who finds that section of the posterior columns, in various animals, above the lumbar enlargement causes a defect of co-ordination similar to that produced by loss of the cerebellum (Bechte- rew, ' Wjestnik psich. i. nevropat.,' 1889, vii, 1; and ' Neur. Centralbl.,' 1890 p. 82.) f A connection since confirmed by Brosset, * Des Connexious du Cervelet' Paris 1891. FUNCTIONS. 245 the control of the anterior grey matter, and probably of the motor nerve-cells. The influence is exerted through the motor nerves, and indeed consists in the normal integrity of the fibres (see p. 29). The nutrition of the bones and joints is also under the control of the cord, and probably is exerted through the posterior roots. It is true the growth of the bones is hindered when the anterior cornua are diseased, but no atrophic change seems then to occur in the osseous structure, and the influence of the paralysis may be indirect. A true trophic change, and an alteration in the joints, may occur in locomotor ataxy, in which the disease is of the posterior nerve-fibres. The nutrition of the skin seems also to depend on nerves that have their course in the posterior roots. The clearest fact is that irritation of the nerve-structures has far more effect than simple loss of function. It is when the cord or nerve-roots are the seat of irritative inflam- mation that the most acute trophic changes occur, while mere degene- ration of these nerves induces slower and slighter changes (see p. 28). In a dog in which the spinal cord below the cervical region was removed piecemeal, trophic changes in the skin followed the section, but not the subsequent removal. It is hence doubtful whether trophic fibres actually take origin (i. e. have " centres ") in the cord; in all cases it is difficult to exclude the effects of the fall of blood- pressure.* Visceral Control.—Although the viscera are under the immediate control of the sympathetic system of nerves, they are related to centres in the spinal cord, and it is from these centres that the controlling influence is really derived, probably by means of the finer fibres of the anterior roots. The relation is the most direct and important, so far as concerns the diseases of the spinal cord, in the case of the organs over which the will has an influence, the rectum and the b 'adder. The centres for these are in the lumbar enlargement, but we do not know their exact position. They are probably complex reflex centres. We can best understand their action by studying them when voluntary influence is lost. The centre for the sphincter ani is the more simple, but the system of action of each is probably similar. In the wall of each viscus we have muscular fibres to expel the contents, and at the mouth a sphincter arrangement to prevent continuous evacuation. Faeces or air in the rectum, and urine in the bladder, may excite the lumbar centre, and cause two effects—contraction in the wall and relaxation of the sphincter. This process can be controlled by the will to a consider- able extent, although we are still ignorant of the precise mode in which the voluntary influence is exerted. But if the volitional path in the cord is interrupted above the lumbar centres, the will can no longer control the reflex processes; as soon as fa3ces irritate the rectum they are expelled by the reflex mechanism; as soon as a sufficient quantity of urine accumulates in the bladder a reflex contraction of the detrusor * Goltz and Ewald, 'Arch. f. d. gesammt. Physiol.,' 1896. 246 SPINAL CORD. and relaxation of the sphincter cause its escape. The affection of the voluntary path for the sphincter is not always proportioned to that for the legs. If the damage to the cord involves also the sensory tract, the patient is unconscious of the action of the bladder or bowel. If the sensory tract is unaffected, the patient is aware of the process, but cannot control it. It is often said that there is permanent relaxation of the sphincters, but this is true only when the lumbar centres are inactive or destroyed. In this condition evacuation occurs as soon as faeces or urine enter the bowel or rectum. The urine escapes continuously, instead of being expelled at intervals. The condition is less obvious in the case of the rectum, because there is no such con- tinuous passage of fasces into the rectum as there is of urine into the bladder. We may, however, distinguish between the two states of the rectum by the introduction of the finger. If the lumbar centre is inactive, there is a momentary contraction, due to local stimulation of the sphincter, and then permanent relaxation. If, however, the reflex centre and motor nerves from it are intact, the introduction of the finger is followed, first by relaxation, and then by gentle, firm, tonic contraction. I have verified this by introducing an india-rubber Fig. 85.—Tracings oe the Action op the Sphinctee Ani. The vertical lines represent seconds of time. 1. Effect on contraction of sphincter of the injection into the rectum of a small quantity of air at *. a, fall in pressure due to the inhibition of the contrac- tion; b, rise due to the slowly returning contraction. 2. Effect of the intro- duction of the instrument, a, sudden rise of lever at moment of introduction, due to the exposure of the instrument to the pressure of the sphincter (the top of this line represents the degree of previous contraction); 5, initial rise due to increased contraction; c, fall from partial inhibition; d, subsequent contrac- tion, rising to a greater degree than the initial contraction, and subsequently falling slightly. 3. Effect of cough, a, pressure of tonic contraction of sphincter (the slight irregularities are due to pulse-waves); b, fall in pressure, due to the movement of the instrument by the cough; c, initial contraction • d,relaxation of inhibited sphincter; e, e, e, rhythmical variations in subsequent rise. (From the ' Proc. Royal Society,' 1877.) cylinder instead of the finger, and registering the pressure on the cylinder by connecting it with a recording apparatus. The relaxation is then found to be preceded by a very slight brief contraction, and 021962� FUNCTIONS. 247 to be followed by unbroken tonic contraction. The relaxation may also be readily produced by any impression on the mucous membrane above the sphincter. Fig. 85 shows some of the tracings obtained. The action of the bladder mechanism can be best understood by assuming that the motor centre really consists of two parts, one (ms, Fig. 86) maintaining the contraction of the sphincter, the other md) exciting the contraction of the detrusor fibres, and that these two parts are antagonistic; when one acts the other is inhibited. Thus, in normal rest, the sphincter centre is active, the detrusor at rest. Apparently, the process of micturition is effected by the automatic contraction of the wall, when the sphincter is re- laxed. The sphincter is certainly under the influence of the will, which is able to maintain and increase its contraction, but it is doubtful whether the mere ces- sation of the voluntary influence is alone the cause of its relaxation. The elements of the process can be best discerned when it is weakened by slight disease. It is then clear that, in addition to the cessa- tion of voluntary contraction, the relaxa- tion is due to the sensory impulses from the mucous membrane at the neck of the bladder, but these do not seem to in- hibit the spinal centre directly. This only becomes inactive when the afferent impulses act on the sensory centres in the brain, and it may be essential for the influence on these centres to be increased by the lowering of resistance involved in conscious "attention." If the sensation is not attended to no relaxation may occur. The effect may be, indeed, due to an automatic cerebral influence, main- taining the action of the spinal centre, which is only "taken off" when the sensory impression causes its full effect on the cerebral processes. The elements of the mechanism are scarcely to be discerned in health, but may under exceptional conditions be clearly perceived. Although no other part of the alimentary canal is under voluntary influence, all parts are probably related to the spinal cord, by means of the connection between the sympathetic system and the nerve- roots. Constipation is extremely common in disease of the spinal cord, and is often greater than can be accounted for by the mere Fig. 86.—Diagram showing Probable Plan of the Centre for Micturition. MT, motor tract; ST, sensory tract in the spinal cord; MS, centre, and ms, motor nerve for sphincter; mb, centre, and md, motor nerve for de- trusor; s, afferent nerve from mucous membrane to s, sen- sory portion of centre; B, bladder. At r the condition during rest is indicated, the sphincter centre in action, the detrusor centre not act- ing. At a the condition during action is indicated, the sphincter centre inhibited, the detrusor centre acting. 248 SPINAL COP.D. loss of power of the abdominal muscles. The pain in the back that is so common in disease of the stomach has been regarded as a reflected pain, due to this connection. The uterine functions are probably independent of the cord in greater degree than those of any other organs under the influence of the sympathetic. The function of menstruation goes on independently of cord disease, and may be regular although there is absolute arrest of all conduction, sensory and motor. Pregnancy and labour may proceed in normal course, in spite of such disease of the cord as causes complete motor paraplegia. Sexual Functions.—The activity of the sexual organs depends on the integrity of the reflex loop to and from a special centre, also situated in the lumbar enlargement, but the due action of this centre depends on cerebral (psychical) as well as on reflex influences. Dis- ease of the centre, or of the nerves leading to or from it, abolishes sexual action. The sexual reflex is, however, one of the cutaneous reflexes, and it shares the condition of these rather than of the muscle- reflex processes. It has been stated that in tabes loss of sexual power is associated with loss of tactile sensibility of the glans penis.* The centre is probably double, and its action is impaired by inter- ference with either half. When, by disease higher up, the connection with the psychical centres is interrupted, the sexual act cannot be perfectly performed. If the path from the controlling centre (p. 20) is unimpaired, the reflex sexual processes are not in excess, and may even be diminished ; but if the path from this controlling centre is also interrupted, the reflex sexual processes are in excess like the other superficial reflexes, and priapism results. If the reflex centre, or connecting paths, are partially diseased, the sexual process may be impaired and imperfect, but not abolished. Vaso-motor Centres.—The sympathetic nerves to the vessels are influenced from the spinal cord. It is probable that the path is by the fine fibres of the anterior roots, and that most of the constrictor fibres leave the cord between the third dorsal and tie second lumbar, while the dilator fibres are more widely scattered, many arising in the upper dorsal region, while others leave the cord in its lumbar and sacral portions ("pelvic outflow"). Some facts of disease suggest that the subsidiary vaso-motor centres are situated in the intermediate grey matter; and this conclusion is supported by the important researches of G-askell, which refer the function to the small cells of the intermedio-lateral tract, which he traces upwards to the vaso-motor centre in the medulla. The action of the vaso-motor nerves may be deranged by disease of the cord. It is probable that such a relation exists between all parts of the vaso-motor 'system of nerves and the cord, and that the relation obtains between each segment of the cord and the vascular nerves to the corresponding part of the trunk and limbs. This derangement in disease may take a part in the production * 8ee Brown, ' Laucet,' 1898. FUNCTIONS. 249 of the changes in nutrition, but it is probably not the sole mechanism by which these changes are produced. There is a special connection between the sympathetic and the cervical region of the spinal cord. This region contains the path to the visceral nerves that control the sugar-forming functions of the liver. The lower part of the cervical enlargement contains also an important centre which controls the sympathetic nerves for the vessels of the head and face. The path of central influence for the radiating fibres of the iris passes also from the region of the third nerve nucleus, down the cervical cord, by the lowest cervical or first dorsal nerve, to the sympathetic, and then ascends the cervical trunk, and passes along the fibres which accompany the internal carotid artery to the nasal division of the fifth cranial nerve. In this the fibres run for some little distance, ultimately reaching the dilator muscle as the long ciliary nerves. Fibres also pass from the cervical cord to the sym- pathetic, through which the action of the heart is accelerated. Mutual Relation of the Functions or the Spinal Cord.—It may be well to present, in the form of a table (p. 252), the relation of the motor and reflex functions of the cord, as far as our knowledge of these relations extends. Many points are still uncertain. The sensory relations will be sufficiently obvious from the figures. The table does not need any detailed explanation. It is merely a comparative collection of the facts that have been stated in the preceding pages. We shall find the value of this collocation of functions when we consider the effects of transverse lesions of the cord at different levels. 250 SPINAL CORD. Fig. 87. Figs. 87 and 88.—Dr. Henry Head has been kind enough to permit the use of these. researches, mainly on cases of herpes zoster and of localised spinal cord lesions. It majority are approximately so, and, in any case, they will serve as a substantial FUNCTIONS. 251 Fig. 88. Sac. 2 They were devised by him, and the sensory areas are marked out as a result of his Is not claimed that all the areas are absolutely correct. It is believed that the basis for future research. 252 SPINAL COED. Tahle showing approximate relation to the spinal nerves of the motor and reflex functions of the spinal cord. The sensory areas are indicated with sufficient clearness in Figs. 87 and 88. C 1 1 I Small rotators of head. 2 f Depressors of hyoid bone. Sterno-mastoid, upper neck muscles, upper part trapezius Lower neck muscles, middle «j part trapezius REFLEX. Scaleni. Lev. ang. si ' Diaphragm [■ I Pectoralis (clavicular part) } \ Serratus Flexors of elbow 1 Pronators, triceps Deltoid and other shoulder ■ muscles, and ■ sternal part of pectoralis D Extensors of wrist and fingers V Flexors of wrist and fingers 1 Muscles of hand , y / Extensors of thumb . Lower part trapezius and back muscles 3 4 5 6 7 8 9 10 11 . 12 L. 1 Intercostals . 1 • Abdominal muscles Ileo-psoas . r Lumbar muscles Peroneus, f flexor of ankle, J extensor of | ankle l 1 Cremaster , , o f Flexors of hip . . 1 Extensors of knee . . J Adductors of hip . V Extensors and abductors of hip 51 > Flexors of knee . ?. l\ > Intrinsic muscles of foot . 2 J Si 4 y PerinaBal and anal muscles, I 5 J >J Dilatation of pupil. Scapular. • 1 }■ Epigastric. > Abdominal. > Cremasteric. Knee-jerk. Gluteal. \Foot- Plant SYMPTOMS. 253 SYMPTOMS OF DISEASE OF TSE SPINAL CORD: INDICATIONS OF TSE SEAT OF TSE LESION: ANATOMICAL DIAGNOSIS. The symptoms of disease of the spinal cord consist in derangement of its various functions; the loss of some, the exaltation and perver- sion of others. We have already considered these functions, and the parts of the cord by which they are subserved. We may now briefly consider the general character of their derangement, and its signifi- cance in regard to the position of the disease. The combination of symptoms indicates the seat of the lesion; we infer its nature from their mode of development, and other considerations, which will be subsequently discussed. It is always important to keep these two elements of the diagnosis distinct in the mind. A common feature of the symptoms of disease of the spinal cord is their bilateral character. This depends on two causes, of which, however, only the first is peculiar to the cord, and can be regarded as the special cause of this feature of its diseases. The structures in each half of the spinal cord are in such close proximity, that any random process, such as haemorrhage or inflammation or pressure, readily affects both halves—can, indeed, hardly fail to do so in some degree, and usually to such an extent as to cause the bilateral cha- racter of the symptoms to be obtrusive. Secondly, morbid processes that commence in the nerve-elements and affect them according to their function (" system diseases ") usually involve the corresponding structures of the two sides, and the spinal cord contains many struc- tures that are liable to such processes. Hence a large proportion of the diseases of the spinal cord involve both sides and cause symptoms that have a corresponding range The leading fact that results from this is, that the characteristic type of palsy is " paraplegia." The word means literally paralysis of the parts beneath or beyond a certain locality, and involves the distinction of a motionless part of the frame, which no doubt arose from the variable extent of this, in comparison with the uniformity of the region affected in " hemiplegia." But the second condition causing the bilateral character of the symptoms is shared equally with those outlying parts of the spinal cord—the peripheral nerves ; and as this condition obviously determines a stricter svmmetry than does the first, it follows that this character is not, alone, of much significance, and is indeed least significant when most complete In the affections that are strictly symmetrical, therefore, other features must also be taken into account. Another character of spinal symptoms, not shared by those of the nerves, consists in their variation in vertical extent according to the position or extent of the lesion. But we must distinguish two classes of symptoms within the region in which they exist. (1) Those which depend on the interruption of the conducting path to or from the brain, 254 SPINAL OORD. and involve the whole region below the disease. (2) Those which depend on damage to the central structures in the cord and nerve- roots, which are present only at the level of that damage, i. e. in the parts functionally related to that part of the cord. The two sets of symptoms may be distinguished as " conducting " and " central;" but in many diseases those at the level of the lesion are chiefly due to the irritation of the nerve-roots, and these are most usefully designated " root symptoms." Disease of the cord does not always cause bilateral symptoms. A little consideration will show that this must be so. A random process, of small extent, may damage one side only. It may affect one or several structures on one side or all of them. Nevertheless it is very rare for such a process to spare the other side altogether, and practically no lesion affects all parts of one side without damaging, in some degree, the other side, at any rate for a time. In very rare forms of traumatic lesion, however, the damage to the other side is almost imperceptible. Again, " system diseases," in quite exceptional cases and for unknown reasons, are limited to one side; much more frequently they may affect one side earlier and more than the other. Such unilateral symptoms indicate a condition awkwardly termed " hemi-paraplegia." Motor Symptoms.—Loss of motor power results from interference with the motor path in any part of its intra-spinal course,—pyramidal tracts, anterior grey matter, anterior nerve-roots. We have seen that the path may be divided into two segments, upper and lower (see p. 213). The spinal cord contains a considerable portion of the nerve- fibres of the upper segment, and their lower termination in the grey matter, but only the commencement of the lower segment, the motor ganglion-cells, and root-fibres proceeding from them. The chief part of the lower segment is outside the spine, in the nerve-trunks. So far as the loss of power is concerned the effect is the same, in whatever part of the motor path the interruption is situated; but the other symptoms that accompany the loss of power differ very much accord- ing as the interruption is in the upper or lower segment. The lower segment influences muscular nutrition, and forms part of the path of reflex action. Hence, as we shall presently see, the muscles waste, and reflex action is lost, when this is diseased; but when the upper segment is damaged there is no muscular wasting, and reflex action, insfead of being lost, is commonly increased. The symptoms produced by disease of either segment are essentially the same, whatever part of the segment is diseased, whether the cell at the upper extremity, the fibre, or the ramification at the lower extremity of the fibre. If, for instance, the intra-muscular nerve-endings are paralysed by curara the symptoms produced are the same as if the motor fibres in the nerve- trunks are divided or their cells in the cord are destroyed. Disease of the termination of the upper segment in the grey matter of the cord must, of necessity, produce the same effect as disease of the pyramidal SYMPTOMS. 255 fibre itself, or the cell in the cerebral cortex from which the fibre springs. We shall afterwards see that this consideration has very im- portant applications. If a fibre of either segment is seriously damaged, it degenerates below the division, since its nutrition depends on the influence of the cell from which it has sprung. If damaged only by pressure, however complete may be the evidence of degeneration, regeneration is possible, even after one or two years. It is possible that such regeneration also occurs when the damage is by inflammation. The nutritional stability of the fibre, or rather of its essential element, the axis-cylinder, becomes less, and more easily deranged, the greater the distance from the parent cell, and it is least in the terminal ramification of each segment. This is probably the reason why curara acts chiefly on the intra-muscular nerves, and it explains the influence of many poisons on the peripheral nerve-endings, and the facts of nerve-degeneration in tabes and multiple neuritis, &c. The law is probably also true of the upper segment; and if so, many facts of pathology become clearer to us, as will be seen in the chapter on spastic paraplegia. It may thus be taken as a general law of the utmost importance that the vitality of the processes of a neuron and their power of resisting morbid influences diminish in proportion to their distance from the cell body of which they are really part. A lesion of the pyramidal tract causes loss of power in all parts below the level of the disease—that is to say, of all parts the fibres for which are interrupted. A lesion of the grey matter, or of the anterior roots, causes paralysis only of those parts which are functionally on the level of the lesion. The two mechanisms often coincide. A transverse lesion in the cervical enlargement, for instance, may cause paralysis of the arms from the damage to the grey matter and nerve- roots, and paralysis of the legs from damage to the pyramidal fibres. The disease involves, primarily in the former case, the commencement of the second segment of the motor path for the arms ; in the latter, the middle of the upper segment. The associations of the paralysis differ accordingly. The parts affected by a lesion at any level will be readily ascertained by an examination of the table of functions on p. 252. It is important to note that the affection of motor power is often incomplete. It may then involve one set of muscles more than another. The flexors or the extensors may be chiefly paralysed. In disease of the dorsal cord, it is very common for the flexor muscles of the hip and knee to suffer more than the extensors. Why this should be we do not know, but the fact is important, because con- siderable weakness of the flexors of the knee is readily overlooked. In examining motor power each set of muscles should be separately tested. Motor over-action; Spasm is frequent in disease of the spinal cord and its membranes. It may present the form of tonic spasm, which 256 SPINAL CORD. when persistent is termed rigidity; or of clonic spasm, which is usually transient and paroxysmal. Tonic spasm, persistent, and involving only a certain group of muscles, causes distortion of the parts to which they are attached, and is often termed contracture.* Tonic spasm, paroxysmal or persistent, is far more frequent than clonic spasm, which occurs chiefly in association with tonic spasm as the muscular clonus described at p. 22, or as a consequence of certain functional derangements. Tonic spasm may be the result of direct irritation of the motor structures, or may depend on over-action of the reflex centres, due not to irritation, but to deficient control. Either form may be acute or chronic. The acute irritation which causes spasm is generally inflammation of the membranes, rarely an acute lesion of the substance of the cord. The chronic irritation is chiefly due to compression of the motor fibres—either of the pyramidal tracts, when there may be persistent unvarying spasms in the parts below the disease, related to the fibres irritated,—or of the nerve- roots, when similar spasm is produced in the parts at the level of the lesion. The spasm that depends on reflex action is seen chiefly in the legs and trunk, but especially in the former. It may preponderate in either the flexors or extensors, so that the legs, when rigid, may be drawn up or straight out. The flexor spasm seems to be due to an over-action of the centres for cutaneous reflex action, the extensor spasm chiefly to that of the centres for muscle-reflex action, although it may also be excited indirectly by a cutaneous impression. This form will be considered in connection with the reflex over-action. Muscular Contraction.—The actual shortening of muscles, by which they cannot be passively extended to their normal length, is due to tissue changes fixing the active persistent tonic spasm or contracture just mentioned. The rapidity with which it occurs depends on the uniformity of the spasm, and we may distinguish three modes in which it arises, which differ in the time required and degree attained. (1) When one set of muscles is paralysed, their opponents, never being extended, quickly become fixed in the contracted condition which they assume in virtue of their power of adaptation to posture. Thus in palsy of the flexors of the ankle, the calf muscles quickly become contracted, so that the foot cannot be flexed on the leg even up to a right angle. The same thing happens by a similar mechanism, when one posture is unceasingly maintained and one set of muscles is never extended, e. g. persistent flexion of the knee leads quickly to structural shortening of the hamstring muscles. (2) Where there is unchanging active contracture from chronic irritation of the motor fibres by a growth, or permanent reflex contracture, as when reflex flexor spasm keeps the hip and knee permanently flexed, similar structural changes occur, so that passive elongation soon, becomes * The reverse of this condition, loss of muscular tone pi rmitting unusual freedom of passive movement, is described in tabes under the name of hypotonic muscvlaire (Frenkel). SYMPTOMS. 257 impossible. (3) In paroxysmal tonic spasm of intense degree, if one set of muscles is stronger than their opponents, their action may so preponderate as to lead to a greater active contracture than their opponents present, and permanent shortening may occur ; although it does so slowly and to a slighter degree than in the other forms because the muscular action is more or less paroxysmal and varying, and the muscles are at times extended by their opponents. Thus in paroxysmal extensor spasm in the legs, no shortening occurs in the muscles moving the knee, because they are equally balanced, but the calf muscles, being stronger than the flexors of the ankle, contract the more, and extend this joint, whenever a paroxysm of spasm comes on, and, after a time, may undergo slight structural shortening, so that the foot cannot be flexed on the leg beyond a right angle. It is of great importance to distinguish the shortening of muscles due to tissue changes in them, from the active contracture that may closely simulate it. In the latter, gentle extension, kept up for a few minutes, restores the muscle to its normal length. The importance of the distinction is due to the fact that the structural shortening can be removed by tenotomy or forced extension, while these measures are useless in the case of active contracture, which would subsequently reassert itself. Tremor is a symptom which should be mentioned, for it is at least associated with disease of the spinal cord in insular sclerosis (see Yol. II). It also occurs in degenerative diseases, such as paralysis agitans or general paralysis, and as the senile tremor of old age. In these conditions it probably depends upon changes in the cerebral cortex. It is characteristically present in toxic conditions manifesting themselves chiefly in affections of the peripheral nerves, such as those arising from alcohol, lead, and mercury. The spontaneous twitchings of muscular fibres known as "fibrillary twitchings " occur especially in association with degenerative disease of the anterior cornual cells. Inco-ordination of movement, although motor, depends usually on disease of afferent fibres. Its characters have been already described in outline (p. 10). It occurs in three forms, of which the third differs entirely from the others in aspect and nature, and alone is a true motor symptom. The two chief forms are the following:—(1) Simple disorder of voluntary muscular contractions, which, when considerable, amounts to a wild irregularity of movement, and when slight is only manifested by slight irregularity when the guidance of vision is withdrawn—as in the inabihty to maintain the muscular contractions in the perfect uniformity needed for equilibrium when the base of support is ren- dered small by the juxtaposition of the feet. The delicacy of the test is increased by the removal of the firm base afforded by the boot, and by closure of the eyes. The increase in unsteadiness when the eyes are closed is sometimes termed "Romberg's symptom." This con- dition results from interruption of the afferent path from the muscles VOL. I. 17 258 SPINAL CORD. to the spinal cord, including the fibres that ascend the cord and those that subserve the muscle-reflex process at the level of entrance. The effect of the loss of the latter is a cessation of the chief part of spinal co-ordination, which, as we have seen, depends on those processes, co-operating with the voluntary impulse. Hence it is associated with loss of the knee-jerk. The loss of other forms of reflex action does not seem capable of causing inco-ordination. In complete interrup- tion of the root-fibres from the muscles the mechanism of the next form is necessarily conjoined. (2) Inco-ordination resembling the slighter degrees of that just described, and consisting especially in such a defect of equilibrium as results from disease of the middle lobe of the cerebellum, is produced by disease of the posterior median columns above the lumbar enlargement, or, if it extends into the latter, leaving the root-zones free so as not to impair muscle-reflex action. This is apparently produced by interru ] >tion of the path by which impressions from the muscles are conveyed to the posterior nuclei of the medulla, and probably thence to the cerebellum (p. 244). The effect is to deprive the motor cortex of the guidance afforded by these impulses. The difference between this form and the slighter degrees of the first is that the muscle-reflex action is not lost, the knee-jerk being preserved. They are both spoken of as ataxy also. (3) Irregular compression of the motor fibres in the cord apparently causes the peculiar jerky inco-ordination seen in disseminated sclerosis, which is supposed to depend on unequal and irregular conduction along the fibres, due to their compression. This form, however, needs further study. Sensory Symptoms.—Loss of sensation is a very common effect of disease of the spinal cord. It may be total, and involve all forms of sensibihty, or partial, and affect only some forms. The statements made on pp. 13—19 regarding impairment of sensation generally, and ' the method of ascertaining it, apply to that which results from cord disease, and need not be here repeated. It has been also pointed out (p. 78) that loss of sensation occurs less readily than loss of motor power. In cord disease it is common for muscular paralysis to exist with intact sensibility. This may partly depend on the fact, ascer- tained by experiments on the effect of local anaemia of the cord, that the sensory fibres, of the nerve-roots at least, seem to have more resisting power than the motor fibres. Sensation may be impaired by disease of any part of the sensory path—posterior roots, probably also the posterior cornua and commissure, or the conducting tracts up the cord. A division of the sensory path into upper and lower seg- ments is conceivable, analogous to that of the motor path, although we have not the same clear ground for the distinction into simple segments of similar composition. Histological researches show that most of the centripetal neurons have short axis-cylinders, and sugo-est that upward conduction is subserved by a number of relays. Disease of the posterior nerve-roots causes loss of reflex action as well as impairment of sensation, just as disease of the anterior roots SYMPTOMS. 259 interferes with reflex action as well as with motor power. Interrup- tion of the sensory conducting tracts higher up leaves reflex action unaffected. But a focal lesion, such as transverse myelitis, may damage both the conducting tracts and the nerve-roots at the level of the lesion, or may affect only one of these. Disease outside the cord, compressing it, may have the same double effect. Hence it is impor- tant to test sensation at the level of the lesion, as well as in the parts below, and to remember that the "level of the lesion" may involve the limbs or the trunk. Areas of anaesthesia may thus be found on the trunk when there is none on the legs, and may be of considerable diagnostic importance, e.g. in spinal caries. Random disease of the nerve-roots outside the cord usually impairs all forms of sensibihty, although shght damage may arrest the conduction of tactile impressions, and not those of pain, which are probably more energetic. Disease of the roots within the cord often causes only partial loss, because the fibres which conduct different impressions have a different course. But loss of one form of sensi- bility from disease of the root-fibres or nerve-fibres usually depends on the kind of disease, and is especially due to degenerative changes, the result of some present or past local influence. Disease higher up the cord still more frequently causes partial loss; either sensibility to pain or to touch may be impaired. That to temperature is rarely affected without that to pain. We do not yet know precisely the significance of this special form of loss, because, as we have seen, we are still uncertain as to the path for each form of sensibility. It is highly probable, however, that loss of sensibility to pain is produced by disease of the grey matter immediately anterior to the postero- median column. Disease of the posterior median column, and possibly that of the direct cerebellar tract, certainly impairs the conduction of impressions from the muscles. It probably abohshes the " muscular sense " of posture and movement, although this does not entail a distinct sen- sory loss. But there may be also a greater loss of muscular sensibihty, so that the normal sensitiveness to pressure and passive extension (and even at last to electrical stimulation) may be impaired or lost. The " common sensibility " of muscles is probably lost only when the disease of the nerves is greater than suffices to abolish what is termed the " muscular sense." Interference with this path in the nerves or roots outside the cord abolishes muscle-reflex action, and also causes more pronounced symptoms (ataxy, &c.) than disease higher up the path within the cord. Increased sensitiveness, hyperaesthesia and hyperalgesia, are also common in disease of the spinal cord, and usually depend on irritation of the conducting fibres in some part of their course. Probably the irritation produces the effect by intensifying the impulse as it passes, since the phenomena of stimulation of nerves show that their axis- cylinders have some power of transforming other forms of energy intc 260 SPINAL CORD. nerve-force, i.e. of evolving nerve-force, and therefore of increasing the strength of that which passes along them. The term " hyperaesthesia" is commonly used in the sense of "hyperalgesia." In the strict sense of the word, hyperaesthesia is seldom observed or even searched for. When the sensibihty to touch is " increased " there is some perversion of the sensation, not a simple increase. The sensation may be felt as " thrilling" or " shock-like sensations." When there is an extreme increase, pain may be pro- duced by a touch, but it is more probable that the touch stimulates the over-sensitive nerves of common sensibihty, than that actual pain is produced through the tactile nerves. A touch may cause pain when it is not felt as a touch, as in the condition termed "anaesthesia dolo- rosa." Delayed sensibihty to pain, or temperature especially, is common in tabes, and is occasionally met with as a result of other changes in the spinal cord. Impairment of sensibihty for pain and temperature with retention of ordinary tactile sensibility is charac- teristically met with in syringomyelia. Other forms of altered sensi- bihty have been already described. Pain, referred to the spine, occasionally present in organic disease of the cord, is more frequent in disease originating in the meninges or bones. But the frequency with which spinal pain is present in abdominal, especially gastric disease, and in neuralgic affections, lessens its significance when it exists alone. In meningitis, acute or chronic, and in meningeal growths, spinal pain is frequent, and in organic disease of the bones of the vertebral column it is an almost constant symptom, and is combined with local tenderness. The same combination of local pain and tenderness frequently occurs in cases of neuralgic pain, " rachialgia,"—a condition that is often loosely termed "spinal irritation," especially when it succeeds, as it often does, concussion of the spine. Such pain is usually felt through a consider- able extent of the vertebral column, or has more than one place of chief intensity and tenderness. That which is due to organic disease is usually fixed and unchanging. In organic disease of the cord itself pain is more often referred to the neighbourhood of the spine, to the loins or the sacrum, than to the spinal column itself. Still more important are the pains that are referred to the parts to which the sensory nerves are distributed, and have hence been termed " excentric" or " radiating" pains. They are of two kinds : (1) those due to the irritation of the posterior nerve-roots in their passage through the intervertebral foramina, through the membranes, or through the posterior columns of the cord; (2) those produced by irritation of the sensory conducting tracts. The pains of the first class are called " root-pains," and are often intense. They correspond in level to the disease. Those of the second class are sometimes acute, especially in lesions that irritate the conducting tracts by pres- sure, e. g. growths. More often they are dull pains, closely resembling rheumatism, and frequentlv mistaken for rheumatism by the patients SYMPTOMS. 261 themselves and their medical attendants. The mistake is the more easily made, because other symptoms suggestive of spinal disease may be inconspicuous, and the rheumatoid pains in chronic cases may be influenced by weather, being muJh more troublesome in damp and cold than in fine and dry weather. In all cases, persistent rheumatic pains in the limbs should suggest the possibility of spinal disease, and watch should be kept for such symptoms as local loss of power, or alterations in reflex action. There is a third class of pains—resem- bling root-pains—which depend on degenerative changes in the nerve- fibres ; the molecular alterations that result give rise to upward impulses of considerable intensity. They are met with in locomotor ataxy and in multiple neuritis, and may be dull as well as acute. The position in which these various radiating pains are felt—legs, trunk, or arms—depends upon the seat of the disease. Although often produced in the root-fibres, these pains may also be due to the peri- pheral nerves. It is especially important to note that the root-pains are frequently felt as a sense of constriction, a painful sense of tightness, as if a band were tied tightly around the part—the " girdle-pain," as it is called. When there is transverse damage to the cord, at the lowest part of the healthy region there is a state of irritation of the sensory nerves, and this irritation (referred to the nerve-endings) causes the girdle-pain. It is named from its frequency at the level at which a girdle is worn, the middle of the trunk, which depends on the dorsal region being the most common seat of disease; but it may be felt lower down, about the groins or even the legs, or higher up, in the arms. In the limbs it is a mere sense of tightness. The girdle-pain is a symptom chiefly of inflammatory and degene- rative processes within the cord. Pressure on the nerve-roots usually causes acute pain, but the most severe root-pains are those met with in disease of the bones of the spine. These have also, more than any other kind, the characteristic that they are increased by movement, and in growths commencing in the bones (which are usually malig- nant) this feature is of considerable diagnostic importance. The suffering in such cases is so great as to have gained for the resulting symptoms the ominous designation of paraplegia dolorosa. The pain in this condition may have a localising value, that in carcinoma being frequently referred to the neighbourhood of the column, while in caries it seems more frequently to affect the side of the chest. Spontaneous sensations, other than pain, are very common in disease of the spinal cord, and are often of considerable diagnostic im- portance, but suggestive rather of the presence of a morbid state than of its nature. They may present many varieties of character, but the familiar sensation produced by pressure on a nerve-trunk, when the part is said to be "asleep," or to have "pins and needles," is the most common and the most significant. It may occur in functional disturbance of the cord as well as in organic disease, and also is very 262 SPINAL CORD. common in peripheral neuritis. It depends on over-action of the sensory structures, but it has at present no special significance as to the locality of disease. It may be excited by contact when it is not spontaneous, and probably represents the highest degree of excess of impressions conveyed by the nerves of tactile sensibility. The still vaguer feeling called " numbness " is also common, and may occur, in slight degree, in diseases of which all other symptoms are purely motor. But this word is used in so many different senses that the meaning in which the individual uses it should always be ascertained as far as possible. Sometimes it signifies distinct loss of sensibility; more often a feeling as if there ought to be loss when there is not. Our sensations altogether transcend our vocabulary, but the observer must try (without leading) to ascertain the character of the sensation experienced. Reflex Action.—Loss of reflex action indicates an interruption of the reflex arc concerned. This interruption may be anywhere between the peripheral endings of the motor and sensory nerves, and thus is not necessarily within the spinal cord, or even within the spinal canal. [t is as constant in peripheral neuritis as in any spinal disease. The position of the interruption must be determined by the associated symptoms ; if it is in the centripetal portion of the reflex arc, there is impairment of sensation, since the interruption will equally arrest conduction to the brain. If it is in the centrifugal portion of the arc, there is a corresponding interruption in the path of the voluntary im- pulse, and loss of motor power. Moreover disease of the motor centre or motor nerves causes also degeneration of the nerves and wasting of the muscles. Any considerable disease of the nerves abolishes all reflex action from the part they supply, but disease limited to the motor structures may permit a reflex movement to take place at a distance, although preventing it at the part stimulated. Disease of the motor centre or nerves causes loss of all forms of reflex action, the simple form and the muscle-reflex that underlies myotatic irritability. Partial disease of the afferent path may impair one and not the other, may abolish the muscle-reflex action (myotatic irritability) and not the superficial reflex action, since the afferent nerves for the two are distinct, coming in the one case from the muscles, in the other from the skin. When one only is lost it is generally the muscle-reflex action ; the nerves for this seem more sus- ceptible, and to have less power of resisting morbid influences. Loss of all reflex action may occur as a transient symptom, imme- diately after the onset of an acute lesion of the cord, apparently from irritative inhibition of the centres. Cutaneous reflex action may be lessened permanently in some cases of brain disease on the side of the motor palsy, even when the muscle-reflex action is increased. Indeed, this opposite change in the two forms of reflex action co-existing on the same side always suggests intra-cerebral disease. It may be well again to remind the reader how difficult it often is to be sure whether SYMPTOMS. 263 the lcnee-jerk is present or is lost, on acccount of the readiness with which its occurrence may be prevented by inability to relax the muscles, and its presence may be simulated by a true reflex action (see p. 238). Excess of reflex action implies, of necessity, the integrity of the reflex arc concerned, and shows that organic disease, if it exists, is higher up the cord. Each form of reflex action is often increased. In some acute diseases, as acute meningitis, and probably also in some chronic diseases, the increase may be due to an irritation of the centres, but in most forms of chronic disease it is apparently the result of a loss of control, and indicates disease between the centre concerned and the brain. We have already considered (p. 240) the probable mechanism, and have seen that the excess of the muscle- reflex action is related to disease of the pyramidal fibres, and espe- cially to the loss of the terminal part of these fibres, within the grey matter, adjacent to the centres concerned.* This is the significance of considerable excess. Degeneration of the terminal portions of the fibres is commonly due to a descending degeneration of the fibres them- selves. It is possible, however, that the degeneration of the endings of the pyramidal fibres may be primary, as is that of the nerve-fibres. (See Primary Spastic Paraplegia.) The increase of reflex action is chiefly manifested in the legs, in which reflex action is normally more active and important than in the arms. The increase in the cutaneous reflex action is shown by its occurrence on a shghter stimulation of the skin, and by a greater degree and extent of the muscular contrac- tions produced. In these the flexors usually predominate, so that the leg is drawn up in a strong movement. As the action of the -sexual organs depends, in part, on superficial reflex processes, priapism is common when the reflex excess is great. The increase of the muscle- reflex action is shown by an increase of myotatic irritability, and therefore of the so-called " tendon-reflex contractions,"—the increased knee-jerk, rectus-clonus, foot-clonus, wrist-jerk, elbow-jerk, jaw-jerk, jaw-clonus, &c. These have been already described. As already stated, the excess of this irritability is at first moderate, and slowly increases. A high degree of over-action is never suddenly attained, as it may be in the case of cutaneous reflex action. It would seem as though, in the centres liberated from control, a capacity for excessive action is slowly developed, which ultimately results in tonic spasm. Not only is the common cause of this excess damage to the pyra- midal tracts higher up the cord, entailing their secondary degenera- tion; but if such disease higher up—as, for instance, primary myelitis * It is interesting- to note the analogy between the effects of degeneration of the termination of the two segments of the motor path. The increased activity of the muscle-reflex centres, which results from degeneration of the termination of the upper segment, presents some similarity to the increased voltaic irritability of the muscular tibres which results from degeneration of the termination of the lower sejrment. 264 SPINAL CORD. or injury to the cord—is followed by abolition of the muscle-reflex action in the parts below, it is the result of inflammatory damage to the lower part of the cord in which the centres are situated, generally by a descending myelitis. Sometimes the original myelitis involved the whole or a considerable part of the cord below, and the indications of a transverse lesion were merely those of the upper limit of the disease. It is not uncommon for the secondary myelitis below an original transverse lesion to succeed it, and abolish the reflex action which was at first unimpaired. I have several times met with such a sequence. A primary dorsal myelitis has left reflex action in the legs unimpaired and tending to excess, with the sphincter ani in its condi- tion of uncontrolled automatic action, when after a few days, a week or more, indications of a recurrence of myelitis have been attended by abolition of all reflex action, including the knee-jerk, by flaccidity of the muscles, with rapid development of the reaction of degeneration in them, and by complete relaxation of the sphincter ani. This is the state from the first in the cases in which the primary myelitis involves the whole lower part of the cord. Sometimes, indeed, such descend- ing inflammation is limited to the grey matter or to the posterior columns, with corresponding limitation of the symptoms, but with a similar abolition of reflex action. Of course, such descending inflam- mation is a very differ^ at thing from the secondary descending degeneration of the pyramidal tracts* Over-action may perhaps be also produced by a state of irritation propagated from above, as in the " early rigidity " of hemiplegia; we have seen that the motor impulses probably pass from the pyramidal fibres through part at least of the muscle-reflex mechanism. Primary over-action seems also to occur, although apparently it only attains a shght degree. It is probably the cause of the trifling excess met with in cases of defective nutrition of the spinal cord or of the nervous system generally. Reflex spasm.—We have seen (p. 26) that the muscular state on which myotatic irritability depends, assumed to be due to a muscle- reflex action, is probably identical with physiological tone. When- ever there is a considerable increase in the irritability there is a tendency to tonic sp;ism, in which there is a balanced contraction of the muscles, fixing the limbs in the position of extension. At first there is merely slight stiffness of the legs, especially felt on waking from sleep; afterwards the legs, when extended, become distinctly stiff, although they may be quite supple when flexed. If gradually * In consequence of the occurrence of this inflammation in the lower part of the cord having been overlooked, it has been thought that a transverse lesion higher up has the power of abolishing r.flex action below, where the cord is not damaged except by descending degeneration. See, however, p. 272, note. In one case how- ever, described by Bruns ('Arch. f. Psychiatrie,' vol. xxv), the knee-jerk was absent although the grey matter was found to be unaltered. There was abolition of faradic irritability in the legs ascribed to oedema. SYMPTOMS. 265 extended, when near full extension the spasm suddenly comes on and completes the movement, as the blade of a pocket knife moves under the influence of the spring. Hence this has been termed " clasp- knife rigidity." Ultimately the extensor spasm may be so great that, when it occurs, both legs are rigid,4and are so firmly connected with the pelvis that if one is lifted from the bed the other is moved also. This is only met with in or^unic, disease, and is an important diagnostic indication. Paroxysms of spasm may be brought on by any impression on the sensory nerves, a prick on the skin, or an attempt to obtain the clonus. The extreme spasm prevents any clonus being obtained, and it may be necessary to flex the limb before an attempt to obtain it is successful. As violent spasm is passing off, moreover, the tension of the muscles may alone set up a clonus, so that the paroxysm of tonic spasm passes into clonic spasm, a phenomenon that was termed by Brown-Sequard " spinal epilepsy," on account of the superficial resemblance to the sequence of spasm in an epileptic fit. This clonic spasm may often be arrested by any strong painful impression on the sensory nerves, a pinch of the skin, or painful flexion of the big toe; the strong stimulation of the nerves of common sensation inhibits the reflex centre concerned in the clonus. There is always much weakness of the legs when there is much spasm, and there may be ahrlost complete paralysis. Hence the condition has been termed " spastic paraplegia." It is probable that the central reflex mechanisms concerned in the production of this extensor spasm are those that subserve the act of standing. The spasm often enables a paraplegic patient to stand, when his voluntary power is quite insufficient for the act. In advanced cases the extensor spasm may be varied by attacks of flexor spasm, which at first come on chiefly during sleep, but after a time preponderate, and may ultimately be permanent; this is always an unfavorable symptom, since, for some reason not yet understood, this flexor spasm indicates a condition of the spinal cord from which recovery is rare. Vaso-motor and Trophic Disturbance.—Changes in Nutrition.— Considerable wasting of the muscles indicates disease of the motor nerve-cells, or of the nerve-fibres proceeding from these cells. If the disease is acute there is rapid degeneration of the nerves, with the reaction of degeneration in the muscles (seep. 71). The wasting in these cases is always great, and there is always loss of reflex action. Occasionally some fibres of the nerve and muscle suffer and others do not, causing the ,: middle" or "mixed " form of reaction (see p. 32). In rare cases, in which the nerve degeneration set up is of an intensely irritative character, the muscles may rapidly lose all irritability in consequence of true degeneration of the fibres. I have observed this, for instance, in a growth in the lumbar region. In other cases of disease, however, there is a slighter degree of wasting of the muscles ; there is no loss of irritability in the nerves; the irrita- bility may be slightly increased or lessened, but is changed in the 266 SPINAL CORD. same way to each form of electricity. In this condition reflex action is not lost, but, on the contrary, is often increased. The change is apparently the result of a peculiar alteration in the nutrition of the nerve-cells. It is usually the effect of an irritative degeneration of the pyramidal fibres, which influence's in a peculiar manner the nutrition of the motor cells. The changes in the nutrition of the skin, if slight and chronic, resemble those produced by disease of the nerves (see p. 79), and are probably produced through the agency of the posterior roots. Per- forating ulcer and the trophic disease of joint known as " Charcot's joint " are met with especially in tabes. They also occur in syringo- myelia. Sometimes, however, these changes are most acute. Very slight pressure, continued for a few hours, causes vesication, and even sloughing of the skin. Sometimes bulla? form where there has been no pressure. Occasionally there is inflammation of the joints. Such intense changes are only met with when the morbid process in the cord is irritative in its character, especially in hemorrhage, and in spreading or disseminated myelitis. The points on which sloughing occurs with greatest readiness are the heel, over the malleoli, the trochanters, and the sacrum. The position of the bedsores in para- plegia, usually over the sacrum, is different from that in hemiplegia, generally over the gluteal region on the paralysed side. The tendency to trophic disturbance probably favours the occurrence of cystitis from retention of urine, and the readiness with which the inflammation invades the kidneys. I have seen a low form of suppurating subperi- toneal pelvic cellulitis, in a case of disseminated myelitis with cutaneous sloughs, in which no other cause for the cellulitis could be found. Vaso-motor disturbance is common in slight degree, irrespective of the seat of the disease, but, like the trophic changes, which probably depend in some degree upon it, it is always most intense in irritative lesions of the cord. The slighter and common degree consists merely in increased warmth of the limbs, in which the vessels dilate too readily; while, at a later period, the limbs are colder, paler, and often livid at the extremities. In rare cases intense flushing of the skin has been observed, or copious and long-continued perspiration. When the disease is in the lower cervical region, flushing and perspiration may occur on the face and head. Disease of the cervical cord or nerves is sometimes attended by a change in the pupil, on one side only. It is due to the fact that the dilator is innervated from the cervical sympathetic through the last cervical nerves. There may be contraction, from paralysis of these radiating fibres, or there may be persistent dilatation from their irrita- tion. There may also be narrowing or enlargement of the palpebral fissure from the same cause. The cause of the double myosis, so common in some degenerative diseases of the cord, is uncertain ; it is associated with loss of the light-reflex, and also of the reflex dilatation produced by stimulating the skin of the neck. SYMPTOMS. 267 The frequency of the heart's action is often permanently increased in locomotor ataxy, but we do not know by what mechanism. In disease of the cervical cord (perhaps also in that of the cervical nerve- roots) the heart may be slowed to forty, thirty, or twenty beats per minute, usually only for a time. This is frequently met with in fracture dislocation in this region. The effect may perhaps be due to a loss of the influence of the nerves which, when stimulated, quicken the heart. In acute disease of the upper dorsal region the heart's action may be persistently frequent. Visceral Disturbance.—Various disturbances in the alimentary canal occur in disease of the spinal cord, and are no doubt due to the fact that the sympathetic nerves immediately controlling the canal are under the influence of the cord, and may be exciied to abnormal action by its irritation, or may underact when its influence is lessened. Difficulty of deglutition is observed in some cases of acute disease of the upper cervical region. Vomiting occurs also in disease of the same part, especially in fracture of the cervical verttb.'ae. Constipa- tion is extremely common in disease of the cord above the lumbar enlargement. The "gastric and laryngeal crises" of tabes are espe- cially frequent in cases in which the disease is situated high up in the cord. When rectum and bladder are affected, the disease must be lower. Paralysis of the Sphincters.—Incontinence of urine and faeces may be due to disease of the centres that control the action of the sphinctei ani and the muscular mechanism of the bladder respectively, or it may be due merely to disease of the path (probably the pyramidal tract) through which voluntary control is exerted. In the latter case the sphincter ani acts in an automatic reflex manner, as already ex- plained. If the finger is introduced within it, the initial relaxation is felt to be succeeded by a firm tonic contraction. This proves that the anal centre in the lumbar enlargement, and the nerves proceeding from it, are intact. If this centre is destroyed, or the nerves interrupted, no tonic contraction can be felt; there is complete and persistent relaxation. I have more than once observed a dorsal transverse myelitis arrest the voluntary influence and leave the sphincter in its condition of simple reflex action, and, a week or ten days later, the extension of the myelitis into the lumbar region, to be attended by (among other signs) perfect inaction of the sphincter. A rectal examination will then often give important information regarding the extent of the disease downwards. The sphincter of the bladder is not accessible to such direct examination, and the mechanism seems to be more complex, but we may distinguish conditions corresponding to those of the rectum. If the lumbar centre is destroyed the sphincter is permanently relaxed; mine dribbles out of the bladder as fast as it enters it; there is simple incontinence. If there is an interruption of the voluntary path above the centre, the sphincter may act automatically: when a 268 SPINAL CORD. certain amount of urine has collected in the bladder it excites the muscular fibres in the wall to contract; the sphincter relaxes, and the urine escapes,—there is intermittent incontinence. In this condition the mechanism is excited to action by any pressure on the bladder; a movement, or the act of coughing, will make the urine come away. But the muscle of the wall of the bladder is indirectly under the influence of the will; when the sphincter is voluntarily relaxed the detrusor fibres in the wall contract. Loss of voluntary power seems to lead to weakness in the wall of the bladder, so that the bladder is never perfectly emptied, and ultimately the detrusor cannot contract to expel the urine, even when the sphincter is relaxed. Hence reten- tion of urine occurs. When a certain degree of distension of the bladder is attained, the pressure becomes sufficient to force the urine out whenever the sphincter relaxes, and such relaxation is continually occurring under the high pressure that is repeatedly renewed in consequence of the flow from the kidneys. Hence incontinence results,—"overflow incontinence" (see p. 247). The retention often develops very gradually and insidiously when the voluntary power is only lessened; the residual urine is at first small in amount, but gradually increases as the detrusor fails to contract adequately against the resistance. It is important, if the urine comes away involuntarily, to ascertain which form of incontinence exists; since overflow incon- tinence, and the retention it indicates, have much graver consequences than simple incontinence. The permanent distension of the bladder constitutes a permanent hindrance to the flow of urine from the kidneys, and serious kidney disease may result. This is a not uncom- mon cause of death in spinal disease. Moreover, whenever the bladder is habitually emptied imperfectly, decomposition is apt to occur in the residual urine. The decomposition is often aided by the lessened acidity, or even actual alkalinity, of the urine. This change in the composition of the urine excites inflammation of the bladder; pus is formed by the mucous membrane, and this, in its turn, increases the decomposition of the urine. The damage to the kidneys, by the hindrance to the flow of urine from them, may be increased by inflammation ascending the ureters from the bladder. Pyrexia.—The initial elevation of temperature in some spinal lesions may be due to them directly, but sometimes it is due to a blood-state of which the cord disease is a result. This is probably the case in polio-myelitis. The temperature is sometimes raised in dis- ease of the cord apart from the influence of morbid process. Disease of the upper cervical cord, like that of the medulla, may cause hyper- pyrexia, and this may also result from acute central lesions that occupy a considerable vertical extent, such as a central haemorrhage, although by what mechanism these act we do not know. Slio-ht variable elevation of temperature sometimes occurs in disease of the dorsal cord, and is probably due, in some way, to the disturbance of its functions rather than to any influence of the morbid process. For SYMPTOMS. 269 instance, in one case of hemorrhagic myelitis with damage from the third dorsal to the second lumbar segments, every application of electricity to the legs was followed by slight pyrexia. Convulsions.—Lastly, convulsive attacks have been known to attend the onset of acute lesions in various parts of the cord, in adults as well as in children. They are most frequent in disease of the cervical cord, but I have known a convulsion to occur in an adult at the onset of myelitis in the lower dorsal region. The convulsions are general. Their mechanism is unknown, and in some cases, especially of infan- tile polio-myelitis, they may, like the initial pyrexia, be the result of general disturbance of the system by an acute morbid blood-state. Optic neuritis has been met with, especially in connection with disease in the cervical region of the cord, and in cases in which careful examination of the brain post mortem failed to reveal any cerebral disease. Combination of Symptoms.—Certain symptoms are frequently combined, and their combination has a definite localising significance. Loss of motor power occurs in two different associations, according to the position of its cause in the motor path. It may be combined with muscular wasting, loss of electric irritability, and loss of all reflex action. In this case the disease is in the anterior cornua or nerve-roots, the lower segment of the motor path. (But the same symptoms are produced by disease of the nerves themselves—in multiple neuritis.) On the other hand, there may be no wasting, no change in irritability, and, instead of a loss of reflex action, the myo- tatic irritability is increased. The interruption of the motor path is then in the upper segment, usually in the pyramidal tracts. It may be a focal lesion of the cord, or a primary degeneration of the tracts. The distinction is that, in the latter case, there is nothing more than the muscular weakness and increased myotatic irritability. In the former case there are, or have been, indications that the lesion has extended beyond the purely motor elements. The symptoms caused by disease of the several elements of the cord have now been described, but it is necessary to consider further the combination of symptoms that results from a total transverse lesion of the cord, and from a unilateral lesion. A total transverse lesion, however limited in vertical extent, sepa- rates from the brain all parts below it, and hence, so far as will and feeling are concerned, it produces the same effect as if the whole of the cord below the lesion were destroyed. Compression of the cord in the middle of the cervical enlargement, for instance, abohshes motion and sensation in all parts below the distribution of the cervical plexus. A transverse lesion at the second dorsal nerve causes motor and sensory palsy of the trunk and legs, leaving the arms unaffected. But the same loss, motor and sensory, results from disease which damages the whole cord up to the level indicated. Hence the extent of the motor and sensory paralysis indicates only the upward limit of the 270 SPINAL CORD. lesion; how far it extends downwards is shown by the interference with the central and especially the reflex functions of the cord. The upward level is indicated not only by the loss of conduction, but also by the position of the girdle-pain and radiating pains, or zone of hyperaesthesia, which are due to the irritation of the lowest sensory nerves in the upper portion. It is desirable to know the symptoms of impaired conduction that occur when a transverse lesion is at different levels in the spinal cord. They may readily be ascertained by an examination of the table and figures given at pp. 250—252. There is, however, some uncertainty as to the effect on sensation in the limbs produced by disease at different parts of the lumbar and cervical enlargements, since, as we have seen, the exact representation of sensation in the cord is still uncertain. The upper hmit of the lesion is shown by the upward extent of the motor and sensory loss. The lowest nerves supply the anus and peri- neum. Those that supply the skin and muscles of the leg and foot arise from the fourth lumbar to the second sacral segments, and are damaged by a lesion involving the lower part of the lumbar enlarge- ment. In the middle of the lumbar enlargement the nerves arise which enter the lumbo- sacral cord, and these are probably destined for the flexors of the knee, and for the hip muscles supplied by the sacral plexus, the glutei, quadratus, and gemelh, and for the skin of the lower part of the gluteal region. These parts then will be para- lysed by disease in the middle of the lumbar enlargement, while the muscles and skin in front of the thigh are unaffected. The latter suffer when the disease affects the upper part of the lumbar enlargement, the origin of the anterior crural (rectus, &c), and obturator (adductors). The skin on the upper and outer parts of the thigh loses sensibility, with the part adjacent to the scrotum, and in the groin, only when the disease damages the highest part of the lumbar enlargement, from which the second and third lumbar nerves arise, and then the flexors of the hip become paralysed. In proportion as the disease is higher in the dorsal region we have the symptoms ascending higher up the trunk, and marking accurately the height of the lesion by the loss of cutaneous sensibility, and by the impairment, first of the abdominal muscles, and then of the in- tercostal muscles. The umbihcus corresponds to the tenth dorsal nerves, and the ensiform area to the sixth and seventh. When the disease reaches the lowest part of the cervical enlargement (the first dorsal nerves) we have the first symptoms in the upper extremity; but these are not, as might be expected, in the muscles moving the shoulder-joint, but in the hand. The first numbness is complained of in the little finger, and the first weakness is in the intrinsic muscles oi the hand. Ascending higher, the symptoms pass up the arm with some uniformity, and without respect to nerve distribution. When the middle of the cervical enlargement is reached (the fifth, sixth, and seventh cervical) the shoulder muscles and the serratus macnus be- SYMPTOMS. 071 L. I I come paralysed, and there is general loss of power and sensation. (For details see table, p. 252, and also pp. 250 and 251.) Above the level of the sixth pair the trapezius and sterno-mastoid become somewhat weakened, for the fibres of the spinal accessory which supply them un- doubtedly arise in part from this region of the cord. At the fourth and fifth cervical the lower part of the neck becomes anaesthetic, and the diaphragm ceases to act. Here our localisation might cease, for total transverse lesions, at this spot necessarily cause death. For a little time the sterno-mastoids and scaleni can still get some air into the chest, rarely in sufficient amount to maintain life for more than a few days. But limited lesions may occur higher up, and then we have complete powerlessness of the muscles moving the head, upper part of trapezius and sterno-mastoid, and other muscles attached to the occipital bone, and interference with sensation in the neck and parts of the head, which are not supplied by the fifth nerve. The extent downwards of the lesion, its vertical extent, is thus not indicated by the impairment of the conducting functions, by the motor or sensory paralysis; to ascertain it we have to examine the functions of the cord as a central organ, and to ascertain how far they are impaired in the paralysed region—to examine especially muscular nutrition and reflex action. The state of muscular nutrition and irritability indicates how far the anterior cornua are injured. The relation of the several groups of muscles to the cord is shown in the first column of the table. The integrity of reflex action indicates the integrity of the reflex loops, and the study of the superficial reflexes of the trunk is especially instructive in this respect. The series of reflexes, and the relation of each to the cord, are shown in the second column of the table ; the muscle-reflex contractions are printed in italics in the position which corresponds to the centres and nerve-roots which are essential for their production. Excess of superficial reflex action indi- cates loss of the cerebral control exerted on the reflex centres, and con- siderable excess of the muscle-reflexes implies impaired function of the lowest part of the pyramidal tracts, and generally shows the existence of a descending degeneration in the lateral columns. Reflex action in the legs may be abolished for a few hours by acute disease or injury above the lumbar enlargement, in consequence of inhibitory shock, but soon returns if the lumbar centres are intact. As already explained (p. 264), if there is no return of reflex action or myotatic irritability, their absence shows that the lumbar region is involved in the primary lesion; secondary extension to this is indicated by loss of lvflex action distinctly subsequent to the onset. If such loss occurs without wasting and loss of faradic irritability in the muscles, it shows that the disease in the lumbar region is limited to the posterior columns or cornua.* * A few cases have been met with in which a transverse lesion of the dorsal cord, especially a transver.-e concussion-myelitis, without post-mortem signs of lumbar inflammation, has caused a persistent loss of reflex action in the legs. In 272 SPIJS'AL CORD. The fact of chief importance is that dorsal cord disease, the most common form, causes no persistent loss of reflex action in the legs, and that for such loss special causes must be sought. Unilateral lesions interrupt the motor path to the muscles on the same side as the lesion, causing one-sided palsy, termed " spinal hemi- plegia " when the disease is so high as to affect both arm and leg, " hemiparaplegia " when it is lower, and affects one leg only. There is often some loss of power on the opposite side, which may be due either to slighter damage to the other side of the cord ("since few lesions are strictly unilateral) or to damage to non-decussating fibres. Conversely, the paralysis of the leg may be incomplete when that of the arm is complete, owing to the escape of the fibres for the leg which cross lower down the cord. Sensation is affected on the opposite side, but not quite up %to the level of the lesion, because the decussation of the sensory tract is not immediate, but occurs somewhat itfbove the entrance of the nerves. The upper level may vary for different forms of sensibility, in consequence probably of the level of crossing (in rela- tion to entrance) being different for the several paths. A lesion in one side of the lumbar enlargement often affects sensation on the same side as motion, because it damages the sensory path before it has crossed. In all cases of crossed motor and sensory paralysis the sensibility of the muscles differs from the other forms of sensibility; and if it is affected on one side, this is the side of the motor palsy, and not of the cutaneous anaesthesia.* The crossed affection of cutaneous sensibility may involve all forms of sensation or only some of them. Sensibihty to pain is almost in- these cases, however, there has been not only loss of the muscle-reflex action, but also of the skin reflexes, a clear indication of an exceptional condition. Moreover there has also in other cases been loss of faradic irritability and rapid muscular wasting,—in short, there have been all the indications of a lumbar myelitis. The most probable explanation of these cases is that the descending degeneration of the pyramidal tract has been more than usually irritative in nature, so as practically to amount to a parenchymatous inflammation, and that this has invaded the motor structures as a nutritional change, sufficient to abolish their function, without, however, destroy- ing their form. In one such case it was noted that the lumbar nerve elements were extremely granular in aspect. For a different explanation of these cases see Bastian, 'Med.-Chir. Trans./ 1890; Bruns,«Neurol. Centralb.,' 1895, and 'Arch. f. Psych.,' xxv j and Egger, ' Arch. f. Psychiat.,' xxvii; see also note, p. 264. * This was first pointed out by Brown-Sequard in his important study of these cases. Scepticism has been expressed as to the fact, based on a denial that the test commonly employed, recognition of posture, is significant. Experiments on animals, even monkeys, are inconclusive, but the evidence from cases in man is very strong, not only of the occurrence of the loss, but of the significance of the test. In some cases, moreover, the muscles were insensitive to pressure. One recorded instance is the following :—A stab in the dorsal region caused loss of cutaneous sen- sibility in the right leg and motor palsy in the left. On the left side, on which cutaneous sensibility was normal, the sense of posture was absolutely lost, while it was present on the right side, on which cutaneous sensibility was impaired. The patient often thought the left leg was flexed when it was extended. Ultimately this leg presented distinct ataxy. (Gilbert, 'Arch, de Nevrologie,' 1882, p. 275.) SYMPTOMS. 273 variably impaired. The temperature sense is usually affected with that for pain; in only two of twenty recorded cases (in which the affection of sensibihty was carefully noted) was the sense of tempera- ture normal, and that of pain impaired, and in neither of these cases was the sensibihty to pain actually lost. On the other hand, in one third of the cases tactile sensibility was unaffected, and in about one tenth of the cases it was impaired on both sides. Cutaneous sensibihty is sometimes impaired in a zone at the level of the lesion, and on the same side, in consequence of the damage to the nerve-roots entering the cord, and above this there may be a narrow band of hyperaesthesia from irritation of the roots at the upper part of the lesion. On the side of the lesion, below the anaes- thetic zone, there is, in most cases, a remarkable hyperaesthesia, corre- sponding in distribution with the anaesthesia on the opposite side. Painful impressions are felt most acutely, and even a touch on the skin, or warm or cold bodies, produce pain. The cause of this hyperaesthesia is obscure. Both it and the opposite loss of sensibility may last for twenty years, and it cannot be ascribed therefore to any irritation by the morbid process. It is perhaps due to an altered action of the cerebral centres on the opposite side of the brain. There is much evidence of an intimate connection between the sensory centres on the two sides, and it is conceivable that the altered func- tional state of the centre on the side of the lesion, to which impressions cease to come, may induce in the opposite hemisphere a condition expressed as hyperaesthesia. The condition may be thought of in relation to the peculiar phenomena of transfer in hysterical hemi- anaesthesia. Eeflex action is increased in all its forms on the side of the lesion, but the increase only occurs after some days. At first it is lessened or even abolished, no doubt from the inhibitory influence of the irritation of the morbid process. The side below the lesion is at first, for some days or even weeks, warmer than the other, the difference being usually about a degree Fahrenheit. In the course of time this difference passes away, and the side may even be colder than the other. These symptoms may be shown in the form of a table: Zone of cut. hyperaesthesia. ----------anaesthesia. Motor palsy. Hyperaesthesia of skin. Muscular sense impaired. Reflex action first lessened, then increased. Temperature raised. LESION, i Muscular power normal. Loss of sensibility of skin. Muscular sense normal. Reflex action normal. Temperature same as that above lesion. VOL. I. 18 274 SPINAL CORD. The vertical distribution of the symptoms varies according to the vertical position of the lesion. Their relations are best marked when the lesion is in the dorsal region of the spinal cord. When it is in the cervical or lumbar enlargement the upper limit is less distinct because of the complex representation of skin and muscle in the nerve-roots. GENERAL PATSOLOGYAND ETIOLOGY: INDICATIONS OF TSE NATURE OF TSE LESION: PATSOLOGICAL DIAGNOSIS. The kinds of disease to which the spinal cord is liable are not specifically numerous, but those which are common present several varieties. The processes are congestion and anaemia, haemorrhage, inflammation, degeneration, and growths. Haemorrhage and growths are, on the whole, rare. Congestion plays an uncertain part in the production of symptoms; its influence has been certainly overrated by some writers, and perhaps under-estimated by others. Anaemia is now known to be sometimes associated with certain definite changes in the spinal cord, and it is possible that it may occa- sionally give rise to symptoms without producing gross disease. The most frequent lesions are inflammation and degeneration. These two processes, distinct in their typical forms, blend in their intermediate varieties. Inflammation varies much in character and course. Its effects are in some cases produced with great rapidity, in other cases with extreme slowness. It probably commences in most instances outside the nerve-elements, which are secondarily involved. Perhaps some acute processes in the nerve-elements themselves are most accu- rately regarded as a parenchymatous inflammation, analogous to that which we know occurs in the fibres of the peripheral nerves. Degene- ration consists of two processes, a wasting of the nerve-structures, cells and fibres, and an overgrowth of the connective-tissue elements. The latter leads to the condition termed sclerosis. The name has been given to it, apparently, because the process is one that, in other organs, increases their consistence. In the cord it has not often this effect. The newly formed connective tissue is rarely of greater firm- ness, and is often less firm, than the nerve-elements it replaces. In sclerosis, however, we must distinguish two types. In one the process is limited to structures that have the same function; the process begins as a degeneration of the nerve-elements, and the overgrowth of the connective tissue is a consequence of their wasting— the affection is essentially " parenchymatous." The so-called " secondary degene- rations " are of this character ; but similar changes are often primary, and affect the structures that have the same function, often through a considerable extent of the cord. Hence they are termed " system diseases." In the other type the morbid changes are not distributed PATHOLOGICAL DIAGNOSIS. 275 according to function. They are apparently random in incidence, and involve adjacent structures in consequence of contiguity. These begin in the connective tissue and not in the nerve-elements, which suffer secondarily. They are essentially interstitial processes. Insular sclerosis is an example of this type. The position of the islets of selei'osis has no relation to the function of the parts, and may involve parts of adjacent structures that have no common func- tion. Areas of diffuse sclerosis are also met with which have not the sharp limitation of the insular form, and are regarded by some as of the nature of chronic sclerotic inflammation. If such a lesion is so situated as to involve fibres thai? undergo secondary degeneration, this necessarily results when the damage to the fibres is sufficiently great. We have then a combination of the random and systemic forms of sclerosis, but one that has no real pathological significance. There are, however, other relations between the two types that deserve attention. These will be considered in connection with the special morbid processes that present them, but a brief mention of them here may make some factsof other diseases more intelligible. The process of secondary degeneration and secondary sclerosis varies in its character, presenting in some cases a greater amount of vascular disturbance than in others. It seems to partake of the character of the lesion causing it, as we have seen (p. 73) the process of secondary degeneration in the nerves may do. The same difference is seen in the primary degenerations, such as occur in tabes. This difference is analogous to that which, as already described, occurs in some varieties of multiple neuritis. We can indeed see the difference in the eye: tabetic optic nerve atrophy, in most cases, presents no sign of inflammation, while in others the early stage may be accompanied by distinct slight neuritis, to be Been with the ophthalmoscope. Secondly, the chronic inflammations, with the diffuse limitation, extending to adjacent structures irrespective of function, have yet sometimes a marked tendency to be localised in structures of definite function. Thus there is sometimes diffuse sclerosis of the lateral pyramidal tracts and posterior median columns, not sharply limited to these, and yet with a correspondence and symmetry not to be overlooked. Thus the two processes tend to meet; the systemic degeneration or sclerosis to be diffuse; the diffuse inflammation or sclerosis to be systemic; and it is sometimes not easy to say, from mere microscopic examination, to which class a lesion belongs. Lastly, there is a curious fact, which has been strangely overlooked although attention was first called to it by Charcot—that inflammation may extend from a primary lesion along a tract that undergoes secondary degeneration, but in the opposite direction to that of the degeneration. It is very common for the inflammation at a given place in the cord, especially that due to compression, to extend farthest along certain tracts, irrespective of their secondary degeneration, and in some cases this extension occurs through a con- siderable extent of the cord. An ascending inflammation limited to the pyra- midal tracts may, for instance, be traced through several segments. The fact suggests that the neuroglial elements may share to some extent a difference that obtains between the fibres of different tracts, and it may easily lead, and probably has led, to erroneous conclusions. Softening of the spinal cord is very common. Whenever the nerve- fibres are broken up into disconnected globules of myelin, separated 276 SPINAL CORD. by serum in a sort of emulsion, the consistence of the part is neces- sarily lessened. Acute inflammation always causes such a breaking up of the nerve-fibres, and hence inflammation always causes softening as its first effect. The separate particles are augmented by leucocytes, which escape abundantly into the tissue. Ultimately connective-tissue elements are formed, which increase the consistence, it may be up to, and even beyond, the normal degree. In a very chronic inflammation the formation of new tissue may proceed pari passu with the destruc- tive process, and there may be at no time much diminution of consistence. It is in these cases that it is difficult to draw the line between inflammation and degeneration. Does such softening of the cord occur apart from inflammation ? The question is not easy to answer. In the brain necrotic softening is very common as a consequence of arterial obstruction—is indeed the common form of softening. But in the spinal cord we have no such distinct evidence of the occurrence of necrotic softening. If embolism occurs, it is excessively rare. The course of the vessels does not favour the passage of a plug into them, while the vertical connection in the anterior spinal and anastomotic arteries (see p. 227) will prevent damage from obstruction in the central system unless this is situated in the terminal vessels of the grey matter. Arterial thrombosis, due to atheroma of the walls of the vessels, such as is so common in the brain, probably does not occur in the cord. The arteries are smaller than those in which atheroma is met with in the brain, and the low- ness of the blood-pressure within them involves the absence of the chief cause of atheroma. It is likely that spontaneous thrombosis occurring in vessels affected with syphilitic endarteritis sometimes sets up the changes that are now regarded as those of primary inflamma- tion; and such a lesion has actually been met with, but we have no evidence of its frequency.* Besides the morbid processes to which the cord itself is liable, it suffers also in consequence of disease outside it. It may be com- pressed by growths springing from the membranes or bones, and by products of inflammation within the spinal canal. Compression not only causes degeneration of the nerve-elements, but usually excites actual inflammation. This " compression-myelitis " may attain a degree and an acuteness out of all proportion to the causal compres- sion. The membranes may be the seat of haemorrhage which com- presses the cord, or inflammation which irritates it, even when the organ is not invaded in appreciable degree. The series of recognised lesions of the spinal cord, obvious or micro- scopic, does not by any means exhaust the list of its morbid states. Changes may occur in the nutrition of its elements interfering with their function, which are, and are hkely to remain, altogether beyond our means of detection. Such morbid states are often called " func- tional diseases," but when prolonged they are probably more accurately * Williamson, ' Lancet,' 1894. PATHOLOGICAL DIAGNOSIS. 277 conceived as nutritional diseases (see p. 1). Derangements of function that we can regard as purely such are few and rare. But disturbances of function may be due to organic disease in some other part of the nervous system, and they may also be the result of toxic agents. Lastly, functional action in all organs is attended with increased blood-supply; and when excessive, the vascular disturbance may go on to a condition indistinguishable from inflammation, with escape of leuco- cytes, &c. The prolonged experimental stimulation of sensory nerves has actually produced myelitis in the related portion of the cord. In connection with the general pathology of diseases of the spinal cord, it is important to note certain general facts of their causation:— (1) Neuropathic disposition.—An inherited tendency to disease of the nerve-elements, manifested by such affections as epilepsy and insanity. This cause is chiefly influential in producing the structural and nutritional diseases, beginning in the nerve-elements, and especially, among structural diseases, the " system-degenerations," as they are called. (2) Prolonged mental distress sometimes sets up degenerative changes in some elements of the cord, especially in persons who are predisposed by (1). (3) Injury.—A severe concussion of the cord may cause (a) instant grave damage, usually haemorrhage. Or (b) it may cause no immediate effect, but symptoms may come on at the end of a few days and progress slowly or rapidly. Such symptoms are usually due to inflammation, secondary to minute spots of injury, too small to cause direct symptoms. Lastly, (c) the concussion sometimes seems to pervert the process of nutrition in the nerve- elements. Slow symptoms of impaired function may result, and these may progress until, after months or years, there is actual structural disease. Similar effects, especially the graver varieties, are met with as a result of lessened atmospheric pressure in divers and workers in caissons. (4) Exposure to cold.—Wet cold is especially effective. The most frequent effect of a severe exposure is acute inflammation, but habitual exposure may produce chronic inflamma- tion, or degenerative disease. The exposure that is effective may be general, or chiefly of the feet and legs, occasionally of the back. (5) The spinal cord appears also to be the seat of primary infection as in epidemic cerebro-spinal meningitis, tetanus, and possibly acute anterior polio-myelitis. (6) Toxic agents that can act on the cord are numerous, and are seen in alcoholism and lathyrism. (7) Other diseases may also induce morbid changes in the spinal cord. The primary malady may be an acute specific disease, or some more obscure blood-state, the precise nature and relations of which are still undecided. It is probable that certain blood-states due to an organ- ised virus excite some forms of inflammation of the cord and of its membranes, just as it may cause inflammation of the peripheral nerves. Septicaemia may excite meningitis, or even abscess of the cord itself. Tubercle is common on the membranes, but seldom produces inflam- 278 SPINAL CORD. mation. Diphtheria may cause acute changes in the nerve-ce1!* and nerve-roots. Gonorrhoea * has produced myelitis, and such diseases as variola, typhus, &c, have been followed by cord inflammation. Syphilis is a very frequent cause of disease, and may act in several ways. The demonstrated mechanisms are (a) by a syphilitic growth compressing or invading the cord, (b) by changes in the cord resulting from thrombosis occurring in diseased vessels, and (c) by chronic syphilitic meningitis, damaging the cord and the nerve-roots. But (d) acute and chronic inflammations of the cord are often met with in syphilitic subjects, and have been thought to be, in many instances, of syphilitic origin. It is doubtful whether they present any syphilitic characters, i. e. any histological features by which they differ from non-syphilitic inflammations. The evidence of dependence on syphilis is stronger in the case of chronic and subacute disseminated inflammation than in the case of acute myelitis. It may be, however, that inflammations due to other causes, e. g. exposure, run a more acute course when they affect syphilitic subjects. The part thus played by syphilis in lessening the resisting power of the organism may be shared by other factors, such as malnutrition and excesses of various kinds. Lastly, (e) certain degenerative diseases of the cord are verv commonly preceded by syphilis ; one of them, locomotor ataxy, so frequently that a causal relation between the two can scarce ly be doubted. But these degenerative diseases are certainly not syphilitic in nature; they differ in no respect from the similar morbid processes that occur in individuals who have not had syphilis, and are probablv the consequence of some toxin left behind by the moibid agency to which the constitutional malady is due. (8) Excessive muscular exertion has been held to play a part in the generation of chronic disease oi the cord. This view has of late derived some support from experiments upon animals.f (9) Pathological changes in the cord are known to result from the amputation of limbs. These have, however, no clinical significance. The outline just given of the general pathology and etiology of diseases of the spinal cord will enable us to consider the last element in diagnosis, the nature of the lesion. The seat of the disease is indicated by the combination of symptoms; its nature can onlv be determined by considering, separately and together, several other points:—(1) The way in which the symptoms came on. (2) The causes that can be traced, taken in conjunction with the known effects of those causes. (3) The seat of the disease, taken in conjunction with the known liability of certain structures to certain lesions '1 he most important of these elements is the mode of onset, and the other indications should only be used in strict subordination to this. * Gowers, 'Clinical Lectures on Nervous Diseases,' p. 119; also Leyden and Goldscheider, 'Die Erkrankungen des Riickenmarkes,' p. 369. t Independently by 0. Rosenbach and Kdinger (see Edinger and Htlbin Vascular lesions. Acute [ (tew hours or days) J ~| ''Subacute (one to six weeks) ^Inflammation. essure and , Suhchronic growths (six weeks to six months) J 1 Chronic >Degen [_ (more than six months) J eration. A lesion of sudden occurrence, the symptoms developing in the course of a few minutes, is almost always vascular, commonly haemor- rhage, sometimes perhaps vascular obstruction. But a vascular lesion may occupy a somewhat longer time in development—a few hours or days. In acute and subacute inflammation the symptoms come on in the course of a few hours, a few days, or a few weeks. Subacute and chronic inflammation occupies from a few weeks to a few months. Degeneration, in which there is no adequate evidence of any inflam- matory process, occupies many months, or it may be years. The sym- ptoms produced by tumours which invade or compress, and by simple pressure (traumatic causes excluded), are never sudden or very acute, and rarely very chronic; the time occupied by the development of the symptoms varying, according to the nature of the cause, from a fort- night to six months. It is necessary to consider, however, not merely the whole time occupied by the development of the disease, but also the uniformity of its course. Two or more morbid processes may concur. An initial myehtis, for instance, may lead to a secondary degeneration; and on the other hand, in degenerated tissues, sudden vascular lesions oc- casionally occur. Pressure produces local myelitis, which may be independent of the pressure in its development, and have an acute or subacute onset. The whole course of the disease must be ascertained before an inference is drawn, and the possibility of a double process must always be kept in view. The onset and course of the symptoms thus sometimes enable us to decide at once that a lesion is of a given character, as that one which occurs instantly is vascular, or that one which takes years for its development is degenerative. Mure frequently they enable us to exclude certain morbid processes, and to restrict the possible lesion to two or three forms. For instance, a lesion which conies on in the 280 SPINAL CORD. course of a few hours must be either vascular or inflammatory. Between these we have to decide by attention to other indications. In actual diagnosis it is convenient to consider next the indication afforded by the position and distribution of the disease. We consider what diseases occur in this situation, and then which of them have the mode of onset that has been ascertained. This indication involves a knowledge of the various diseases and their seat. The most important consideration is that a wide range of symptoms of uniform character indicates the affection of a definite system of structure, and in most instances a disease commencing in the nerve-elements, and if the onset be chronic we may feel sure that it is a degeneration. On the other hand, the involvement of many functions suggests a random process, such as inflammation or pressure. But this indication is always to be subordinated to the mode of onset. Thus the hmitation to a single structure does not exclude inflammation: this may affect, for instance, the anterior grey matter only, and cause corresponding symptoms. The symptoms may indicate a morbid process limited to one half of the cord, but this does not materially modify the diagnostic method. Almost any process may, in rare cases, be thus limited. System degenerations and acute inflammations are least frequently unilateral, and they never reach a considerable degree of intensity on one side without some affection of the other side. On the other hand, tumours and foci of chronic myelitis are often one-sided, and still more often affect one half of the cord first and then the other. Indication of disease outside the cord, irritation of certain nerve- roots, causing severe local pain, often precedes the symptoms of com- pression, and is an important aid to diagnosis. It shows the existence of a morbid process outside the cord before the cord is involved. But we cannot use even this indication except in dependence on the mode of onset. A disease, as a growth outside the cord, may, as we have seen, not only compress the cord, and cause slow loss of power; it may excite inflammation and cause rapid palsy. The last element in the pathological diagnosis is the detection of any influence which can be regarded as the cause of the disease in the spinal cord, or any associated condition which may indicate an active morbid process. We have seen that the mode of onset may help us to limit the disease to certain possible forms of lesion; the distribu- tion of the affection may render it probable that it is one or other of these forms; and the detection of a cause and the knowledge of the lesion which that cause produces may help us to carry the diagnosis still further. The most important general causes of disease of the cord, and the processes to which they chiefly give rise, have been already mentioned. The causal element in diagnosis is chiefly an application of those facts. The morbid process outside the spinal cord that most closelv simu- lates its disease is, unquestionably, parenchymatous multiple neuritis. INJURIES OF THE SPINE. 281 The diagnosis depends on a thorough knowledge of the varied sym- ptoms of the latter, since its elements vary according to the different manifestations of the disease of the nerves. For these, and for any general diagnostic principles, the reader is referred to the account of that disease. The only sure ground for diagnosis is a thorough knowledge of the various morbid processes and their symptoms ; and the only safe plan is to work by these, from symptom to seat and onset to nature, treating every case as a problem to be worked out to a definite diagnosis, and only then comparing the result with the types of disease. To one of these the case may or may not conform ; if it does not, the comparison with types as a means of diagnosis will only leave the observer stranded and powerless. The distinction of functional and nutritional disease from organic lesions may conveniently be postponed until the symptoms of the former are specially described. SPECIAL DISEASES OP THE SPINAL CORD. DISEASES OF THE VERTEBRAL COLUMN. Diseases of the bones of the spine fall for the most part within the province of surgery. But there are few of these diseases that do not, among their most frequent effects, interfere with the functions of the spinal cord. Hence an account of the diseases of the cord would be incomplete without some mention of the morbid states that begin in its bony case. INJURIES OF THE SPINE. Injuries to the spinal column may consist of punctured wounds (which need not be considered here), concussion (the effects of which on the cord will be considered later), and fracture or dislocation of the vertebrae. It may, however, be useful briefly to describe the more salient features of the last two conditions, their relation to the damage the cord sustains, and the symptoms thus produced. Dislocation. Simple dislocation occurs in the cervical region, most frequently at the fifth and sixth vertebrae. It may take place gradually or suddenly: Gradual displacement is always secondary to disease of the bones ; 282 SPIXAL CORD. sudden displacement may occur in disease or from injury. The damage to the cord is always greatest in traumatic displacement of healthy bones, because the force needed to produce the dislocation is much greater, the displacement is more considerable, and the effect on the canal and the contained cord is greater. Displacement may occur in any direction: it usually involves both vertebral articulations, but, in rare cases, it is oblique, involving one articulation only. The common causes are violent blows or falls on the head, rarely sudden rotation of the head while a weight is carried upon it. The symptoms are a lateral or forward or backward displacement of the head, so that the chin is in contact with the shoulder or the chest, or the occiput with the nape of the neck. There is also irregularity of the vertebral spines, usually readily detected. The cord is damaged in most cases, and the symptoms are those of a total transverse lesion in the situation of the luxation. It may be merely compressed, especially in cases of disease, in which the displacement has occurred with little force. The symptoms of paralysis have been known to pass away, in such a case, on the reduction of the dislocation. More commonly the cord is also bruised, with extravasation of blood, and secondary myelitis occurs later. In such cases, if the patients live, there may be anaesthesia or hyperaesthesia below the lesion, with total paralysis of the limbs, and excess of reflex action. In rare instances the cord has been completely divided. In still rarer instances of slight displacement it has not been injured. Rupture of the transverse ligament which retains the odontoid process may permit the latter to compress the cord, and thus to cause instant death. This often results from sudden suspension by the head, as in criminal executions. One of the curiosities of surgical literature is a case related by Petit in which a man, playing with a neighbour's child, lifted it up by the head, and caused instant death by rupturing the transverse ligament. The father of the child, entering at the moment, stabbed the man with a knife, the blade of which passed in between the first and second cervical vertebrae, divided the spinal cord, and the man also fell dead. Rupture of the ligament has also resulted from raising a heavy weight with the head. The treatment of dislocation is too purely surgical to be described here. Fracture. All organic diseases of the bones, weakening them, predispose to fracture. Among these, one is of special medical interest; the ver- tebrae, especially in the lumbar region, may share the rarefaction and weakening of the osseous tissues occasionally produced in tabes, and then a very shght traumatic influence, a blow or wrench, may cause fracture. The force needed is often so shght as to fail to cause dis- placement or other symptoms except local pain, and symptoms may only supervene at a somewhat later date. Apart from disease, the INJURIES OF THE SPINE. 283 accident is most common in adults, the greater elasticity of the verte- bral column in children giving to them a comparative immunity. Its cause is a blow or fall on the spine, or sudden forcible flexion. In extremely rare cases a fracture, usually slight, has resulted from severe muscular exertion. This is an important fact, showing that muscular exertion may injure the spine, and may lead to symptoms at a later date. Symptoms of such injury, in slight degree, are not uncommon. Fracture may occur at any part of the spine, but is most frequent at the fifth or sixth cervical, and at the last dorsal or first lumbar vertebrae. In the dorsal and lumbar regions the bodies are broken in two thirds of the cases, but in the cervical region the arches alone are fractured in one half. Usually there is a displacement of the vertebral column at the seat of fracture. Rarely the bodies may be crushed without displacement. The displacement of the bone involves a narrowing of the canal and, usually, compression of the cord. This may also result when the arches only are driven in. But the cord may be seriously damaged when there is no permanent narrowing of the canal, as in Figs. 89 and 90. The dura mater is rarely torn except FiG. 89.—Fract ure of the first lumbar vertebra. D M. Dura mater. There was no pennantnt narrowing of the canal, but, nevertheless, the spinal cord was greatiy damaged at the spot; see next figure. b,- a splinter. Blood is almost always extravasated outside the dura mater, often in considerable quantity, from the rupture of the large veins in this situation. There are usually only small extravasations in the pia mater. The cord is, in most cases, bruised and compressed by the lower fragment (Fig. 91). Sometimes it is flattened, and it may even be divided, all nerve-substance being squeezed out of the pia-matral sheath at the spot. In the case shown in Figs. 89 and 90 the cord appeared to have been split longitudinally at the spot, perhaps by the mere force of the concussion. It is very common to have local myelitis, opposite the fracture, without any permanent narrowing of the canal or compression of the cord; the inflammation seems to be 284 SPINAL CORD. the direct result of the concussion. Blood may be extravasated into the bruised part, sometimes in minute spots, sometimes in larger haemorrhages, and even into the central canal. These changes are usually limited to the spot directly damaged, but secondary myelitis may be set up, and sometimes extends beyond the contused area. It Fig. 90. Fig. 91. of the cord itself are chansred beyond the possibility of identification. The ascending degeneration is shown in Fig. 76. Fig. 91.—Fracture of the body of the fifth dorsal vertebra and of its processes. (After Gurlt.) may even extend through the whole length of the cord below the injury, and then its central functions are abolished. In cases of some duration the usual ascending and descending secondary dege- nerations are also found. It is important to note, moreover, that the secondary degenerations have sometimes the irritative character already described (p. 272, note), and that an ascending inflammation may for a short distance above the lesion be limited to a tract that degenerates downwards (see p. 275). Fig. 76, p. 214, represents sections of the cord from the case of fracture figured above. Occa- sionally the injury leads to secondary caries of the bone, with all its consequences. Symptoms.—Three classes of symptoms result. (1) The local indica- tions of the injury to the spine. (2) There may be certain nervous symptoms not distinctly due to the damage to the cord. One of these is general shock, which may be so great as to entail transient loss of consciousness. Vomiting occasionally occurs. There is great pain in the position of the fracture, rendered very intense by pressure, and often radiating along the nerves which come from this part, the roots of which are compressed. In rare cases epileptiform con- vulsions have followed fracture, usually at an interval of some davs (3) Symptoms which result from the damage to the cord, and con- sist in paralysis of the parts below the injury. Its character depends INJURIES OF THE SPINE. 285 on the amount of damage. If this is considerable, there is both motor and sensory paralysis up to the level of the lesion, with loss of power over the sphincters. Reflex action is lost at the level of the lesion, and the examination of the trunk-reflexes often gives important information regarding the extent of the damage, when this is in the dorsal region. Below, reflex action is usually diminished or lost, probably because the centres are impaired by descending myelitis. Spasmodic twitchings sometimes occur in the limbs immediately after the injury, and priapism is the rule, especially if the lesion is cervical. The pains are severe in the arms when the fracture is opposite the cervical enlargement, and in the legs when at or below the lumbar enlargement, so as to damage the nerve-roots. In these cases there may be rapid wasting of the muscles, with loss of electric irritability. There is usually at first incontinence, afterwards retention of urine, but the former is persistent if the lumbar centres are damaged. Cystitis, bedsores, &c, may supervene. Ultimately, if the damage is above the lumbar enlargement and the patient lives, there may be increased myotatic irritability in the hmbs, progressing to spasm, so that spastic paraplegia results. In many cases in which the knee-jerk is at first lost it may be months, or even years, before it returns. Special symptoms result when the injury is in certain parts of the spine. Fracture of the first two cervical vertebrae causes instant death, unless the displacement is very slight, and even then there is imminent danger of further displacement, with the most serious consequences, on any incautious voluntary movement. With slight displacement persons have been known to live for weeks, and then die from secon- dary myelitis; they have even recovered altogether. Now and then there is no compression of the cord, although there is distinct displace- ment, even sufficient to be recognised in the pharynx (Leyden). In such a case death has resulted at a later period from caries. The characteristic symptoms are local pain, increased by all movements (which are rendered almost impossible), displacement, and spinal symptoms. The latter may be slight—merely difficulty in breathing or swallowing—or considerable, and involving the trunk and limbs. Sometimes there is hyperpyrexia. Not more than one case in fifty recovers. Middle Cervical Vertebras.—The third, fourth, and fifth vertebrae are most frequently fractured, When the injury to the cord is consider- able, death usually occurs very rapidly, because the roots of the phrenic nerve are involved, the intercostals being necessarily paralysed with the parts below. In some cases there is little immediate displacement, and the symptoms are slight until further displacement occurs in some movement. Thus a man who had met with an injury of this kind went to be shaved; during the proceeding, his head was turned on one side by the barber, with the unexpected result of causing dis- placement of the fracture, and immediate death. When the fracture is at the cervico-dorsal region, opposite the lower part of the cervical 286 DISEASES OF THE SPINE. enlargement, the arms frequently escape at first, the early paralysis being confined to the legs and muscles of the trunk. Respiration is diaphragmatic only. After a few days the arms become involved, but their paralysis is often partial, affecting, for instance, only certain muscles, as the extensors of the hand, and it is often accompanied by local spasmodic movements. Movements and pressure cause pain, and there is local muscular rigidity. The head may be in normal or in abnormal position. Yaso-motor disturbance in the face and general hyperpyrexia have been observed. There is not unfrequently altera- tion in the joints, especially the knee-joints, apparently the result of the presence of fluid in them. In fracture of the dorsal vertebras (2—11) the arms escape, the legs are paralysed, and the trunk-muscles up to the height of the lesion. The pain in the trunk may be very severe. There is hyperaesthesia or anaesthesia in the parts below. The reflex action in the legs is exces- sive ; that in the trunk is abolished at the level of the lesion. The last dorsal and first lumbar vertebrae are fractured more frequently than the others, and there result paralysis of the legs, complete or irregular, severe pains, tingling, &c, sometimes followed by hyper- esthesia or loss of sensibility, and by rapid disturbance of nutrition, in both the muscles and the skin. In fracture of the lower lumbar vertebras the symptoms are often slight; below the extremity of the cord the nerves occupy a smaller space in the canal, and so may escape compression by a moderate displacement. If they suffer, the fractured vertebrae unite very slowly. A false joint is occasionally formed. Secondary myelitis and its consequences are frequent causes of death at a variable period after the injury. CARIES OF THE SPINE. Caries of the bones of the spine is a frequent cause of paraplegia. It is often termed "Pott's disease," from the English surgeon, Percival Pott, who first described it (in 1779) as a cause of paralysis. Causes.—Males are said to be rather more liable than females, but the difference in sexual incidence is not great. It is more common in childhood (after three), and next in early adult life, but it may occur at any age, and is perhaps more common in the second half of life than any other scrofulous lesion. I have known it commence at fifty, and it has been met with as late as seventy. It is distinctly a manifesta- tion, of the tubercular and scrofulous diathesis, and evidence of such inheritance is to be traced in most cases. Occasionally the sufferer himself presents such indications, e. g. lung disease, or caries of other bones. It occasionally develops simultaneously with other signs of acute general tuberculosis. Injuries seem frequently to excite the bone mischief in the spine, as they certainly do analogous bone disease CARIES. 287 elsewhere, in those who are predisposed; possibly, sometimes, in healthy persons. Falls, blows on the back, and severe strains are the most frequent traumatic antecedents. The last may act by straining the ligaments and setting up inflammation, which spreads to the bones directly or through the intervertebral cartilages. There is usually an interval, sometimes of many mouths, between the injury and the definite symptoms of bone disease. Other causes besides scrofulous disease have occasionally been known to cause breaking down of the bodies of the vertebrae with angular curvature and all its consequences. Soft growths in the spine and, in rare cases, syphilitic formations have had the same effect. Osteitis, due to extension from adjacent inflammation, is a rare cause; thus caries of the cervical spine has been secondary to a primary retro-pharyngeal abscess. The disease sometimes follows septicaemia, probably in consequence of a secondary septicemic abscess in the bone. This was the case in a surgeon about sixty years of age, in whom symptoms of blood-poisoning followed an injury to the ankle They were succeeded by paraplegia of rapid onset, and this by the development of angular curvature in the lower dorsal region. In a large number of cases no exciting cause can be traced. Pathological Anatomy.—The changes in the bones need not detain us, siin-e they belong to surgical pathology, except in so far as they lead to damage to the cord. There is inflammation of the bodies of the vertebrae, and of the intervertebral substance, often at first with enlargement, afterwards with breaking down of the substance of the bone, which gives way under the pressure to which it is exposed, so that deformity of the spine results. Products of inflammation and destruction of tissue, more or less purulent in character, accumulate either inside the canal or outside the vertebral column. In the latter situation they are increased in quantity by the inflammation they excite, and the well-known forms of abscess result. Within the canal the inflammatory products have a firmer con- sistence. Although the inflammation extends to the loose cellular and adipose tissue between the bone and the dura mater, and often to the dura mater itself, it has little tendency to spread as a purulent menin- gitis, or even to penetrate the dura mater, the outer layer of which becomes irregularly thickened in the neighbourhood of the disease (see Fig. 93), while the inner surface of the membrane remains normal. The firm consistence of the inflammatory products, often caseous in character, is an important pathological feature, because this material is so often the agent by which the cord is compressed. The displacement that results from the disease varies according to the extent and character of the disease. Occasionally there is simply a lateral displacement—one spine is a little to one side of that above it. More commonly the collapse of the bodies leads to "angular curvature," the spinal column is bent forwards at an acute angle, and one or two vertebral spines are much more prominent than the 288 DISEASES OF THE SPINE. others. There is often, however, a less abrupt bend; the curvature may extend over four or five vertebrae. Less commonly one spine projects more than the others without any curvature. The nerves, as they pass through the membranes and intervertebral foramina, are irritated by the inflammation, and often compressed by the thickening of the dura mater which sheaths them, and those passing by the seat of compression may also suffer from the narrow- ing of the canal. They may be found red and swollen, or shrunken and grey. They may be damaged when the cord is normal, or but little affected when this is compressed. The damage to the spinal cord depends on the secondary conse- quences of the caries, and is variable and uncertain in both occurrence and character. The mechanism of the damage is twofold—compression and inflammation. The relation between the two is considered more fully in a subsequent chapter (Compression of the Spinal Cord). Slow compression may be attended by chronic inflammation, secon- dary not only in character but in course, or by an acute inflammation out of proportion to the com- pression, alike in degree of severity and in rapidity of development. It is important to recognise these differences. The mechanism of compression varies. The most frequent is the collection of inflammatory products outside the dura mater and the thickening of this mem- brane. Less commonly the cord is compressed by the displace- ment of the bone, or by frag- ments of bone that are pushed into the canal. Often both these causes are influential, as in the case shown in Fig. 92, in which the compression (at s) is between displaced bone in front and in- flammatory products (e) behind. Probably an inflammatory swell- ing or abscess of the bone is sometimes the mechanism of compression, since the signs of pressure have disappeared when an abscess has formed outside the spine, or even when defor- mity has come on—the breaking down of the bodies having relieved the compression produced by their enlargement. Fig. 92.—Caries of the spine, mid-dorsal region. The spinal cord is much nar- rowed and discoloured at s from com- pression between the displaced bone and a mass of inflammatory products, B, outside the dura mater, n m, the inner surface of which is normal. (After Leyden.) CARIES. 289 Symptoms.—Caries of the spine causes symptoms of three classes: (1) those of the bone disease ; (2) the effects of damage to the nerve- roots; (3) those due to the changes in the cord itself. Only the symptoms due to the damage to nerves and cord come within the special province of this book, but the bone symptoms are of much importance, as on them the diagnosis of the cause of the nervous symptoms often depends. It is this which gives the subject its high medical importance, and brings the symptoms and recognition of bone disease into the province of practical medicine. Symptoms of Bone Disease.—The first is pain in the spine, chiefly felt at the affected spot, increased by movement, and especially by pressure on the bone. The local tenderness is a very important sign. It is elicited both by direct pressure on the spines and by lateral pressure; if they are grasped and pressed to one side considerable pain is usually produced. Nevertheless tenderness is occasionally absent, not only in cases of slight character and doubtful nature, but also in those in which paraplegia has come on some time after local curvature. The increase of pain by movement is greatest when the disease is in the more mobile parts of the vertebral column, especially when it is in the cervical region. Movement of the head occasions pain, and there is an instinctive fixation of the head, which is sometimes inclined to right or left, less commonly backwards. It may thus produce the aspect of torticollis, which differs from that due to muscular contrac- tion in that the sterno-mastoid is tense on the side towards which the head is turned, the muscle being simply stretched by the deviation of the head. The deformity of the spine is a later symptom than the tenderness, and usually comes on gradually. Its characters have been already described. It is often absent when the disease is in the cervical region. In this part there is usually another symptom—thickening of the tissues about the spine, which is rare in other parts. In any region an abscess may form in the neighbourhood of the disease. Those which come backwards, or descend to the groin by the psoas muscle, can be recognised externally. Those that form in front of the diseased vertebrae may give rise to symptoms that are puzzling, if the existence of spinal caries is not known. Thus a retro-pharyngeal abscess may cause difficulty of deglutition, and one in the dorsal region may cause symptoms of oesophageal obstruction. Increased pain and tenderness in the vertebral column often precede the indications of damage to its contents. The symptoms due to in- terference with the nerve-roots are very variable, and may be severe or absent; usually they are moderate in degree, and consist of pain on move- ment along the course and in the distribution of the nerves that emerge at the affected region, often hyperaesthesia of corresponding extent, sometimes with spots of anaesthesia. There is also muscular weakness and sometimes muscular wasting. These symptoms are more fully described in the chapter on Compression. Here it may suffice to VOL. I. 19 290 DISEASES OF THE SPINE. say that they are conspicuous only in the minority of the cases, and chiefly occur when there is pachymeningitis. The motor symptoms are most marked when the disease is in the cervical region, and the nerve-roots for the muscles of the arms are damaged, since slight and limited impairment is more readily recognised in the arms than in the trunk. If the disease is in the highest part of this region, the pains may be referred to the occiput. Herpes zoster has been occasionally met with along the course of the irritated nerves. Spasmodic contrac- tion in the muscles supplied by the affected roots is extremely rare in cases of caries. Reflex action is abolished in the affected parts, and the change in the superficial reflexes of the trunk sometimes gives important diagnostic information. Disease of the lower cervical roots may cause symptoms of deranged action of the sympathetic on that side of the head, occasionally shown in the pupil, more often in the vessels. I have seen persistent sweating on one half of the forehead from this cause. The symptoms of interference with the functions of the spinal-cord itself are chiefly due to impairment of its conducting power, causing paralysis below the lesion. As the disease is most frequently in some part of the dorsal region, paralysis of the legs is the common effect. But the symptoms vary in their characters, according not only to the position of the disease, but also to the immediate process of damage to the cord. The signs of caries may have existed for years before paralysis comes on. Angular curvature may even come on in early childhood, and paralysis not till adult life More commonly the interval between the two is not long, varying from a few months to one or two years, but either may first be conspicuous. The cases are numerous in which caries is not suspected until the paralysis leads to an examination of the spine, and it is not uncommon for the signs of bone disease to remain equivocal for some time after paraplegia has developed. The cord symptoms vary much in their mode of onset. Usually there is no exciting cause, but sometimes a strain of the back or exposure to cold seems to excite a change in the condition of the bones, in consequence of which the cord suffers. It is easy to conceive that, when the conditions are favorable, a very slight strain may be effective, even as slight as the sneezing in the case mentioned below. When the cord symptoms have commenced, they may develop quickly or slowly. As instances of chronic onset may be mentioned cases in which the symptoms reached a considerable degree of intensity at the end of nine months, four months, and two months, after their com- mencement. But the onset is sometimes much more rapid; in one case there was complete paraplegia at the end of three weeks. Some- times it is still more acute, and in such cases, when there is no corre- sponding change in the bone, acute myelitis set up by slight pressure is probably the mechanism by which the cord suffers. Thus, in one patient, a child of three, slight weakness existed for three weeks, anr1 CARIES. 291 then the power of standing was lost in a single night. In another child, aged eight, who had presented for two years indications of disease of the cervical vertebrae, the power of moving the legs was lost in the course of twenty-four hours; during the second day the left arm became paralysed, and, at the end of a week, the right arm. Very rarely the onset is instantaneous, probably from sudden dis- placement. A child with angular curvature was walking across the room, when she fell, and on being lifted up the legs were powerless. The more rapidly compression occurs, the slighter is the amount necessary to abolish conduction. Both legs usually suffer together; rarely one is paralysed before the other; very rarely one leg suffers much and the other little or not at all. Thus in one case angular curvature developed in childhood ; at sixteen there was an attack of weakness in the legs, which passed away at the end of three weeks. At 17| the patient sprained his back; pain in it followed, and six weeks later the right leg gradually became weak, and a year afterwards presented intense spastic paralysis, the left leg being very httle affected. He ultimately recovered. An instance in which one leg became affected before the other is that of a woman, forty-five years of age, who suffered from pain in the spine, and one day, when walking, sneezed violently three times, and imme- diately felt " pins and needles " about the right knee, and presently in the foot. The leg became almost powerless during the next three days. A fortnight afterwards she felt similar tingling in the left knee, and at the end of another week in the foot, and during the next three weeks this also lost power, so that at the end of six weeks from the onset both legs were motionless. The diagnosis was verified on her death, six months later. The characters of the paralvsis in relation to the seat of the disease are described in the chapter on Compression. In the most frequent cases the dorsal cord is damaged, and whenever the compression is above the lumbar enlargement the condition of the legs is that of " spastic paraplegia." If it is situated in the cervical region there may be muscular atrophy in the arms, sometimes palsy without atrophy, according to the seat of the disease. When, as is com- monly the case, the arms suffer from damage to the nerve-roots, they suffer before the legs, but if the disease is so high up that the arms suffer from the damage to the cord, the legs may be paralysed before the arms, as in the case of the child mentioned above. In this case the muscles of the shoulder were wasted, the disease being at the level of their nerves, while the forearm muscles were not wasted. In this case, as in others of similar seat, the diaphragm was paralysed. The muscular part of the spinal accessory may be involved, and the power of supporting the head may be almost lost. Yery rarely, from the disease of the highest cervical vertebrae, other nerves of the medulla are implicated, especially the hypoglossal and the fibres of the spinal accessory for the palate. 292 DISEASES OF THE SPINE. Sensory symptoms due to the disease of the cord are less common than motor palsy. The onset of paraplegia may be preceded by subjective sensations in the legs. Dull aching pain in them is also not uncommon. Often there is no loss of sensation; in other cases there are various degrees of loss. Touch or pain may be impaired alone, or there may be absolute loss of sensibility up to the level of the lesion. Partial loss is more common. Reflex action in all forms is excessive (unless the disease involves the lumbar enlargement), and great excess of the superficial reflex action is a common and important feature. The legs are often cold, and sometimes perspire continually. The sphincters are often affected, sometimes early, but they may escape even where there is complete motor palsy of the legs. Complications.—Among common complications are bedsores, cystitis, various secondary effects of the bone disease, such as abscess, local scrofulous disease elsewhere, and general tuberculosis. Tubercular tumours in the brain occasionally coincide with the caries. In very severe cases peculiar secondary mischief has occurred in the spinal cord, and has run an independent course, giving rise to very anomalous symptoms.* Thus a descending myelitis may invade the lumbar enlargement in its entirety and abolish its central and reflex func- tions, causing rapid wasting of the muscles and acute trophic changes in the skin. Inflammation may ascend the pyramidal tracts and thus paralyse the arms—an instance of the strange limitation of inflamma- tion to functional tracts when it passes in a direction opposite to secondary degeneration. Ascending degeneration of the posterior median columns may spread to the postero-external columns, and cause symptoms of ataxy by invading root-fibres at a higher level. Ataxy may come on as the power returns, when the disease is in the dorsal region, probably by damage to the path from the muscles to the cerebellum. Lastly, myelitis may occur in disseminated foci in various parts of the cord, and even in the medulla, giving rise to scattered symptoms of anomalous character. Course.—The bone disease may heal, union occurring between the altered tissues, or it may persist with continued formation of pus, or may become quiescent with occasional periods of renewed activity. The cord mischief is influenced by the state of the bone disease, although its progress may be to some extent independent. Thus inflammation in the cord, in excess of the compression, may subside in spite of the continuance of the bone mischief. Pressure on the cord may be relieved, although the bone disease continues, and even some- times as a result of the increased breaking down of bone and exit of pus by another channel. A case is mentioned below in which para- plegia passed away as angular curvature developed. Hence there is no strict correspondence between the course of the bone mischief and that of the cord disease. In some cases the paralysis, motor and sensory, persists. More often the sensory loss passes away, while * See Charcot, 'Lecons sur les Mai. du Syst. Nerv.,* torn. ii. CARIES. 293 motor paralysis remains, usually as spastic paraplegia, and, in severe cases, flexor spasm comes on with muscular contractions. Life may be prolonged in that condition for years, but often, in such cases, bedsores form, or cystitis leads to kidney disease, or other tubercular disease develops and leads to death, or the lessened respiratory power renders an attack of bronchitis fatal. Ln many cases, again, the paralysis gradually passes away even when the compression continues, and the cord is found considerably narrowed if the patient dies from some other cause. It is possible that such compression is sometimes produced slowly without impairment of conduction. In children re- covery occurs far more readily than in adults. Even in adults, how- ever, recovery may occur from palsy that has lasted for more than a year, with all the signs of descending degeneration in the cord, amounting to severe spastic paraplegia. Usually rest on the back or mechanical supports are necessary to secure recovery, but it occasionally occurs without these measures. A youth acquired angular curvature at sixteen; at twenty paraplegia came on slowly, and pro- gressed with some variations during the next seven years. There was then absolute motor palsy in the legs, and sensation was lessened. He refused to rest, and continued to follow his occupation, which was however a restful one, that of a tailor; he took cod-liver oil and iron, and gradually regained useful power, so as to be able to walk about. Such a case, however, is exceptional. Relapses sometimes occur in cases that improve, although they are certainly not nearly so frequent as might be expected from the nature of the disease. In the majority of cases recovery, once obtained, is permanent. In a minority the paralysis returns when some exciting cause renews activity in the bone disease. The tendency to relapse and the possibihty of repeated recovery are very strikingly shown by the following case. In a girl of fifteen, paraplegia developed during nine months, slowly at first, more rapidly towards the end of that time. She came under my care six months later, having been unable even to move her legs for that time. Bone disease had not been previously suspected, but there was slight tenderness and enough lateral irregu- larity of the lower dorsal spines to show the nature of the case. Rest in bed and tonics were soon followed by improvement; in six weeks she could stand, and in four months was able to walk well. As she gained power, angular curvature came on, prominence of the seventh and eighth dorsal spines. Five months after her discharge she fell and struck her back; the curvature increased, and her legs gradually became weak again. Seven months after the fall she was readmitted, unable to stand, although the paralysis was not absolute. There was foot-clonus on each side. Sensibility was lessened below the ensiform cartilage. Rest on the back was again followed by slow improvement. In three months she could just walk. She was then suspended, and encased in plaster of Paris. At the end of another month she could walk about the room, and no clonus could be obtained. She was soon 294 DISEASES OF THE SPINE. afterwards discharged, and her progress continued, so that, at the end of nine months, she could walk five miles, and there was no trace of clonus, although there was still some excess of the knee-jerk. She soon afterwards married, and bore a child, which died two years and a half after her discharge. She caught cold at the funeral, and a fort- night later again began to lose power; in six weeks the legs were almost motionless, with marked foot-clonus ; sensation to touch was lost up to the umbilicus, that of pain being preserved. Neither rest nor encasement caused any improvement. After some months sulphide of calcium was given, and in a few days power began to return; in a month she could take a few steps, and in four months she could walk about the ward without difficulty. She made another good recovery. Some years later, however, paralysis again came on, and this attack proved permanent. Several cases have come under my notice in which the subjects of caries in early life, which healed without damaging the cord, have at some period in adult life presented the symptoms of primary lateral sclerosis—simple spastic paraplegia, without any root symptoms or evidence of renewed activity of the bone disease. If there is a con- nection between the two, it is probable that the cord has suffered compression so slowly that its functions have not been interfered with, but, nevertheless, the vitality of the pyramidal fibres has been rendered less enduring;. It is important to remember that the deviation is often lateral,* and the chief difficulty is due to the fact that a slight lateral deviation or slight prominence is not unusual in normal spines Hence it is important for the student to make himself familiar with the degrees of deviation that occur in health. At the same time it must not be forgotten that a deviation not greater than occurs in health mav be due to disease. If it coincides with distinct tenderness, and especially also with the position of root symptoms, it may be accepted as evidence of disease, probable or certain, according to the character of the symptoms. The pathology of the affection only concerns us so far as it relates to the effect on the spinal cord, and this is considered in the chapter on Compression. Diagnosis.—When clear indications of caries precede the paralysis, the nature of the case can hardly be mistaken. The obvious inference, that the affection of the cord is secondary to that of the bone, is scarcely ever wrong. When the two develop together, mistakes in diagnosis are often made, but are usually due to the want of repeated examinations of the spinal column. It is when the root or cord symptoms precede distinct evidence of bone disease, and when the latter is so slight as to be equivocal, that the chief real difficulty in * To discover lateral deviation it is well to make an ink-dot on the skin over the middle of the tip of each spine, care being taken that the skin is not stretched to one side. The ink-dots may be copied on tracing-paper. CARIES. 295 diagnosis occurs; the affection is apt to be mistaken for a primary disease of the cord or its membranes—a transverse myelitis when the dorsal region is affected, a progressive muscular atrophy, or primary pachymeningitis, when the disease is in the cervical region. A correct diagnosis can only be made in these cases by recognising the signifi- cance of the slight bone symptoms that are always present, the deep tenderness, and often slight irregularity. Even slight irregularity derives significance from tenderness, limited in extent and correspond- ing in position to the deviation. The irregularity may be a,bsent at first, and then its development is doubly significant. An observed increase in the amount of displacement gives significance to even a slight irregularity. The early excess of the cutaneous reflex action (from the sole, for instance), while not conclusive, adds weight to the other symptoms of bone disease. It may be very marked even while the patient is able to walk about. Distinct root pains are always of great significance, and this is increased by the detection of spots of anaesthesia along their course. All these symptoms derive additional weight from their coincidence in level with the spinal irregularity. It is this which enables the pains to be distinguished from the con- dition for which they are most frequently mistaken—a trunk neuralgia. This error is especially common when the pain is chiefly unilateral. In all such cases the spine should be carefully examined, and any tender- ness of the bone at the level of the pain should excite suspicion. I have also known unilateral abdominal pain due to caries to be mis- taken for that of renal calculus. When damage to the cervical roots causes muscular wasting in the arms, the case may be mistaken for one of progressive muscular atrophy, but differs m the distribution of the wasting, in the pains, and the impairment of sensation. These occur in primary cervical pachymeningitis, which is distinguished by the absence of the signs of bone disease, and in the wider extent through which the root symptoms extend. In the first half of life the recognition of bone disease is practically tantamount to the recognition of caries. In the second half, however, the relative infrequency of caries, the greater frequency of growths in the bone, and the occurrence of eroding aneurisms, introduce a fresh diagnostic problem. The absence of any other indication of a tumour or an aneurism is the first distinction; and the second is the fact that in both these diseases the root pains commonly reach a degree of severity scarcely ever attained in caries, and are especially increased by movement. When there are merely tenderness of the spine and slight weakness of the legs, the question may arise whether there is organic disease, or merely the condition termed "spinal irritation," or mere functional pain and tenderness and weakness of the legs. In these cases the tenderness is usually found over a considerable area of the spinal 296 DISEASES OF THE SPINE. column, with more than one point of special intensity; it is superficial as well as deep, and may change its seat; there are no root pains or spots of anaesthesia. There is more danger that caries of the spine in a young woman may be passed as hysterical paraplegia than of the opposite error. Especially when the subjects of caries present distinct symptoms of hysteria, there is risk, as experience shows, that un- equivocal symptoms of caries may be overlooked. Some other diagnostic indications are mentioned in the chapter on Compres- sion. Prognosis.—Our ignorance of the precise character of the morbid process which is damaging the cord renders the prognosis, in every case of caries, a matter of much uncertainty. Nevertheless there is no disease of the cord in which symptoms of equal gravity so often pass away. The cases are few, therefore, in which hope is unjustified, but they are equally few in which we are warranted in a confident expectation of recovery. In childhood the prospects of recovery are certainly better than in adult life, and they are least in declining years. Damage to the cord between the enlargements is less serious than when these are affected, because the strong tendency to trophic changes constitutes a grave danger when the lumbar enlargement is diseased, and the diminished breathing power an equally serious danger in disease of the cervical enlargement, especially when this is high enough to entail the additional danger of paralysis of the diaphragm. But how perilous a condition may be recovered from is shown by the fact that the child mentioned on p. 291 had paralysis of all four limbs, the diaphragm, and weakening of the intercostals, and yet recovered. Still more striking is a case narrated by Dr. Buzzard, in which disease in the region of the third cervical vertebra caused almost complete palsy of arms, legs, intercostals, and diaphragm, respiration being carried on by the accessory muscles of the neck- Yet the child recovered in spite of the occurrence of an attack of pneumonia when the paralysis was at its height. A girl of thirteen, whose cervical caries was accompanied by all the symptoms of cere- bellar tubercle, recovered. All these, it will be noted, were children. Neither rapidity nor slowness of onset affords any guide to prognosis, nor does the relative order of paralysis and curvature, or the degree of palsy. Severe spastic paraplegia may pass away entirely, provided it remains extensor in character. The prognosis is perhaps a little better when there is no loss of sensation, since this proves that the damage to the cord is moderate in degree; but even complete anaes- thesia does not preclude recovery, as the cases mentioned show. The danger to life is dependent in considerable degree on the evidence that the scrofulous or tubercular tendency is active elsewhere, and also on any difficulty in securing proper treatment. The prognosis is, more- over, still in a transitional state on account of the uncertainty regard- ing the range of successful surgical treatment. CARIES. 297 Treatment.—The first and chief element in the treatment of paralysis is that of the bone disease which causes it, and for full details of this the reader is referred to treatises on surgery. It includes both the older means of securing an arrest of the morbid process, and the still recent measures of operative treatment. If the bone disease heals, the spinal cord, in most cases, will recover. The two most potent therapeutic agents are persistent recumbency and tonics, especially cod-liver oil and iron. In the cases that have done best, these, and these alone, have been the effective agents. Rest should be maintained for months. The posture that an w.'is best is upon the back, on account of the greater ease with which immobility of the bone is secured and maintained, and the great importance of this element in treatment; this position is also the most comfortable, and local pain probably interferes with the sub- sidence of local inflammation. If no improvement occurs after some months' rest, suspension may be tried. It is said to be sometimes attended by instant improvement, especially in children; but this result is rare, and can only occur in the cases, not very common, in which displaced bone compresses the cord. In cases in which there is reason to suspect that this is the cause of paralysis, it may be well to see the effect of suspension before rest is commenced. The moulded jacket is an inefficient substitute for rest, and an unnecessary con- comitant—to be adopted only when rest cannot be secured, or after rest alone has apparently done all that it can achieve. If, for instance, power gradually returns during rest, but the improvement after a time ceases, and the bone disease seems inactive, the patient may be sus- pended, encased, and then permitted to stand and walk; improvement may be renewed and power may rapidly increase. In caries of the mobile cervical spine, even during the period of rest, fixation of the head is necessary. Extension of the spine in the recumbent posture has also been employed, sometimes with apparent benefit. The head of the patient is fastened to the head of the bed by an elastic band attached to a strap passing beneath the occipital protuberance and round the patient's head. A weight of from 4 to 12, or even 20 lbs., is fastened to a band passing round the patient above the hips. Con- tinuous extension is thus obtained.* More recently sudden forcible extension of the spine and immediate reduction of the deformity has been recommended as a mode of treatment for spinal caries. In some cases in which paraplegia was present, rapid return of power in the paralysed limbs has occurred after this treatment; but it is obvious that such a method has inherent in it certain dangers which are at least minimised in less heroic treatment.f The influence of cod-hver oil and iron is as marked in this as in other scrofulous diseases. They constitute an indispensable adjunct • Fleming,« Lancet,' April 27th, 1889. t Discussion at Clinical Society of London, 'Lancet,' Nov. 12th and 26th, 1897. 298 DISEASES OF THE SPINE. to rest, and may be effective even alone, as is shown by the case men- tioned on p. 293. But rest should always be secured if possible. Counter-irritation, opposite the seat of caries, has sometimes appeared to do good, perhaps acting especially on the process of myelitis which attends compression. The actual cautery, in mild form, is that which has been most frequently found useful. Instances of speedy improvement are on record, but it is not always effective, nor can indications for its use be laid down. Sulphide of calcium, which is said to influence scrofulous processes, deserves further trial, although I have not found it so apparently effective in any other case than that mentioned on p. 294. Benefit can only be expected from its use when, as is often the case, inflammatory products constitute the compressing agent. Extreme care in general management, to avoid bedsores, bladder trouble, and bronchitis, are of great importance. In manv cases there is a tendency to improvement after a time, especially when the bone disease is stationary, or the cord has been inflamed, and in these the mere maintenance of life may result in recovery of strength. When power has returned, but the use of the limbs is restrained by the muscular contractions which come on during the paralysis, the ability to stand and walk may be quickly restored by tenotomy, and more slowly by the use of extending splints, &c. Electricity is useful only to maintain the nutrition of the muscles when these are wasting, in consequence of damage to their nerves. The behef expressed in the first edition of this work, that the cases are numerous in which relief to the compression may be afforded by the surgeon, has been fully realised. The path was, indeed, being then opened up by McEwen of Glasgow, who has shown, with others, especially Victor Horsley, how safe and successful the operative treatment is in properly selected cases; and these, indeed, include a large proportion of the cases in which other measures have failed to give relief and must probably have remained unsuccessful. The operation is contra-indicated in cases of rapidly advancing general tuberculosis (to which most deaths after operation have been due, and also, as a rule, in children, in whom other measures are, as has already been stated, usually successful) When the indirect con- sequences of the disease have greatly reduced the patient's strength, the question of an operation may still be entertained if it is a dis- tinct alternative to a speedy death, provided the peril is such as a restoration of the functions of the cord might possibly remove. On the other hand, the operation ought not to be regarded as the first resort in the majority of cases. The large number of cases that recover under the treatment described above make it certain that, in most cases, these measures should first be tried; and this conclusion is the clearer since the duration of paraplegia, for a year or more, seems to interpose no appreciable barrier either to recovery or to the relief that can be given to the pressure. On the contrary, indeed, the prospect of recovery is better if the bone disease has become quiescent, GKUWTHS IN THE SPINE. 299 or the caries has actually healed, processes that must be furthered by the preliminary rest. The operation of laminectomy has the best pro- spect of success in the cases, fortunately very numerous, in which the products of inflammation outside the dura mater compress the cord. These, whether caseous material or a mass of connective tissue into which the inflammatory products have been changed, can be readily removed without opening the dura mater. Even if displaced bone is the source of pressure, the removal of the arches affords relief to it. The chief obstacle to success is the extent to which myelitis has proceeded out of proportion to the compression. This, necessarily, no removal of the pressure can relieve. In proportion as the inflammation has been acute without evideuce of rapid compression, relief is unlikely. But this is not the only cause of a rapid onset, and a difficult question arises in such cases, whether the mechanism is not such that an immediate operation is justified. It may be due to sudden displace- ment of bone or to sudden escape of pus into the canal, as well as to myelitis, and in the two former cases it is possible that relief may sometimes be given, and an immediate operation may be wiser than delay. An operation is suggested whenever a sudden increase in the curvature or severe root-pains coincide with the acute onset of paralysis. Without these symptoms, the rapid onset is probably due to acute myelitis, and then an operation cannot be expected to lessen the interference with the conducting fibres. It is also called for in cases in which the disease is high up, and by its interference with the respiratory mechanism is threatening life. To justify surgical inter- ference, however, the existence of caries must be beyond doubt. The operation involves a small danger to life, although it may not be great, and this fact must always receive due consideration in regard to the certainty of diagnosis as well as the prospect of rehef. TUMOURS AND OTHER DISEASES OF THE SPINE. Growths in the Spinal Column. The bones of the spine are sometimes the seat of primary or secondary growths, and less commonly are invaded by tumours springing from the various structures and even organs in front of the spine. They may also undergo changes as the result of the obscure condition known as osteomalacia, and these changes may occasion pres- sure on the cord, and so give rise to paraplegia.* Cancer (scirrhous * Koppen, 'Arch. f. Psych.,' xxii. 800 DISEASES OP THE SPINE. and encephaloid) and sarcoma are the most common forms of growth; myxoma has been also met with. Cancer is sometimes secondary to a primary growth elsewhere, in the breast, stomach, &c. A primary growth usually begins in the bodies of the vertebrae, and spreads from one to another. The bodies may collapse, because the soft tissue which replaces the bone yields under the weight it has to bear, and thus angular curvature may occur, or some other abrupt deviation from the normal line. From the bodies the growth may extend into the lateral processes, enlarging them, and narrowing the intervertebral foramina through which the nerves pass. It may extend into the arches, and even into the spines, and may also grow into the muscles and tissues beside and behind the vertebral column. The nerve-roots suffer (1) by pressure, (2) by simple inflammation, (3) sometimes by cancerous infiltration. They may thus be found reddened, swollen and soft, or grey and atrophied, or enlarged and hardened. The growth, cancer especially, is apt to spread in the adipose tissue between the bone and the dura mater, and may even entirely surround the dura mater and cord. The cord may suffer compression, but this is less frequent than in caries, even when curvature occurs. On the other hand, it is often inflamed, sometimes acutely; considerable inflamma- tion without compression is far more frequent than in caries. The myelitis occurs without any perforation of the dura mater by the growth. The cause of this tendency to acute local inflammation is not known; once excited, it may spread in the cord upwards and downwards. The growth never invades the cord itself. Etiology.—The general causes are the same as those of similar growths elsewhere. Males suffer, however, more frequently than females, and the morbid growths, taken together, are most common between forty and fifty years of age. An injury has been supposed sometimes to be the exciting cause in this as in other situations. Symptoms.—There may be direct symptoms of the presence of the growth—pain in the spine, usually severe, occasionally absent; local tenderness, and occasional interference with movement of the vertebral column apart from pain. A palpable tumour is never an early sym- ptom, but ultimately a deep-seated hard swelling may be felt on one side of the spine, most readily and earliest when the disease is in the cervical region, where it is occasionally perceptible in the posterior triangle of the neck. The angular curvature which sometimes occurs does not differ from that of caries in its external characters, except that it is more frequently a rounded prominence than a sharp angle, and it may be accompanied by the indications of a tumour, never by those of an abscess. The affection of the nerves is almost invariable in spinal growths, and gives rise to the symptoms that are the most distressing, and also the earliest and most constant,—radiating pain in the course of the nerves that emerge at the part, and due to their irritation by pres- sure or inflammation. Such pains are far more prominent symptoms GROWTHS IN THE SPINK. 301 in this disease than in caries. At first slight, they gradually increase to extreme intensity. It was this feature that led Cruveilhier to call the disease paraplegia dolorosa, a name it has since commonly borne. The pain at first intermits, but subsequently is constant, with paroxysms of greater suffering from time to time. It is usually a sharp and lancinating pain, and its special characteristic is the degree in which it is increased by movement. Even slight movements of the trunk induce the paroxysms. The distribution in the arms, trunk, legs, depends on the seat of the disease. It is extremely rare for these pains to be absent, but they occasionally occur late instead of early.* On the other hand, they may precede other symptoms for months. Cutaneous hyperesthesia usually accompanies them, and spots of anaesthesia often develop, after a time, in the areas to which the fixed pains are referred. Corresponding damage to the motor roots may cause painful muscular contracture (Pigs. 56 and 57, p. 112), paralysis, and wasting. Contractures may also occur in the parts below the disease, produced by the persistent irritating pressure on the motor tract in the cord. Paroxysms of spasm often attend the pains, especially in the abdominal muscles when the disease is in the dorsal region, and are apparently reflex in nature. The damage to the cord causes symptoms similar to those in caries, and described more fully in the chapter on Compression. The chief difference from caries is the greater frequency of a rapid onset of the paraplegic symptoms, due to the invasion of the cord by acute inflammation. All power in the legs is often lost in twelve or twenty- four hours, and this when no curvature has taken place. Such acute paraplegia is not uncommonly preceded for a week or so by retention of urine, probably indicative of shght pressure on the cord. Displace- ment of bone has also been known to cause rapid paralysis.t On the other hand, especially in very slowly growing tumours, the onset of the palsy may be gradual. I have known it to occupy several years in reaching a considerable degree. Probably in these cases the mechanism is a simple slow compression. Thus, compared with caries, the onset is more often rapid, and occasionally much more deliberate. The characters of the resulting paralysis are, as a rule, similar to those in caries, but are more frequently modified by the spread of inflammation, immediate or subsequent. Hence the central and reflex functions of the lumbar enlargement, although the bone disease is some distance above it, may be lost at the onset, or they may be at first normal or excessive, and afterwards lost. In a man with a growth in the mid-dorsal region, paraplegia came on rapidly, evidently from myelitis, and was followed by foot-clonus, &c. But a few weeks later the clonus suddenly ceased, the muscles became toneless, with loss of faradic irritability, and the skin began to slough; the inflammation * The pains succeeded curvature in a case described by L. Humphry ('Lancet,' 1SS4. i, p. 15). t Humphry, loc. cit. 302 DISEASES OP THE SPINE. had spread down into the lumbar enlargement. In many cases, how- ever, there is no descending inflammation, and the reflex actions are in persistent excess, so that spastic paraplegia results. Sensation is lost rather more frequently than in caries. Other symptoms are the same as in compression from any cause. The course of the disease is from its nature progressive; occasionally, however, some improve- ment succeeds a rapid development of palsy, and is due to the partial recovery of a cord damaged disproportionately by inflammation. It is seldom, however, that life is prolonged for a sufficient length of time for this to occur. Much more rarely the pains lessen, although the growth spreads—perhaps from destruction of irritated nerves. The duration of the disease varies according to the nature of the growth. In cancer it is to be measured by months. In slowly growing tumours the symptoms may last for years. Death may be due to bedsores, &c, to cystitis and kidney disease, to growths else- where, or the patient may be simply worn out by the prolonged agony. In one curious case a growth from an intervertebral cartilage caused characteristic symptoms for thirteen years, and then death by meningeal haemorrhage.* Diagnosis.—The recognition of the disease is only a matter of cer- tainty when signs of a tumour are present, but the probability almost amounts to certainty when such symptoms as those mentioned follow a primary growth elsewhere. Such pain as that above described, occur- ring in a person from whom a malignant tumour has been removed, should always be regarded with grave suspicion, and the grounds for this are not lessened by either an interval of several years since the removal of the tumour, or by the completeness with which this was effected. Especially is this true of cases of mammary cancer. The pains should lead to careful and repeated examination of the spine and a search for any abrupt deviation, of any kind, and in any part of the vertebral column; while the cervical spine should be examined at the sides and from the posterior triangle of the neck, the character of the bony prominences on the two sides being minutely compared. Indi- cations of a growth may often be thus discovered long before they are obtrusive. It is also important to remember the fact that acute transverse myelitis may be an early effect of the disease, and if this lesion, in such a subject, coincides with marked local tenderness, the probability of secondary growth in the bone is very great; it is rendered still greater by preceding pains, and certain by coincident deformity. It must be remembered that similar root symptoms are sometimes due to an aortic aneurism, or to a growth in front of the vertebral column, commencing, for instance, in the glands, and irritating the nerves as they emerge from the intervertebral foramina. From intercostal neuralgia, the influence of movement on the pain is usually a sufficient distinction, even when cord symptoms are * Boivert, 'Arch, de Phys.,' 1887, No. 8. GROWTHS IN THE SPINE. 303 absent. The commonly bilateral character of the pain is a further difference. The symptoms of a growth in the lower cervical region are sometimes very closely simulated by symptoms which, from their character and course, are probably due to radicular neuritis. There are severe root-pains, referred to one arm (or less commonly to both arms), increased by movement and without marked tenderness of the plexus of nerve-trunks. The subjects are also in the later period of life. The distinction rests on the absence of the signs of a growth, on the slighter effect of motion on the pains, on the absence of any progressive tendency, and on the common presence of a history of gout, and especially on the absence of any symptoms of compression of the cord even after the nerve-roots have suffered for some months. Sometimes it is necessary to wait and watch the course of the sym- ptoms. It is necessary to be very careful in assessing the value of slight irregularities; the vertebra prominens is apt to be thought to project too much even for its designation, and a deep bilateral swelling is readily assumed, under normal conditions, when the head is bent forward. The chief difficulty in diagnosis is the distinction from caries when distinct evidence of a growth is absent. In the first half of life caries would alone be thought of in such a case, but in the second half the two diseases are about equally frequent. One distinction—suggestive, not absolute—is the intensity of the pain in tumour, taken in conjunction with its great increase when the patient moves. It is true that the root-pains of caries are said to be sometimes most severe, but such severity is not frequent enough to destroy the significance of intensity. I have not, for instance, seen a single case of caries (of a large number) in which the pain was com- parable to that in most of the cases of growth that have come under my observation. Therefore, while absence of pain is of slighter dia- gnostic value (in favour of caries), great severity, and agonising increase by movement, are strongly in favour of vertebral growth. In each disease there may be angular curvature; but this, in growths, is usually soon succeeded by other signs of tumour. In caries these signs are absent, and an abscess often develops. A history or indica- tion of tubercle is almost conclusive evidence of caries. These points will, I believe, avail for the distinction in most cases. In a few it is necessary to wait and watch before an opinion can be formed. Among other diseases with which these growths may be confounded is the dorsal form of tabes, in which severe radiating pains occur in the trunk and not in the legs. But the wide extent of the root symptoms, the slight effect of movement, and the fact that the knee-jerk is lost, suffice for the distinction. There is also usually more extensive dis- turbance of sensation on the trunk. The distinction from tumours of the spinal cord and membranes is considered in a later chapter. Prognosis.—The prognosis scarcely requires formulating. The chief differences are in the time that life is likely to last. The pains 304 DISEASES OF THE SPINE. usually persist, in spite of the progress of the disease, although there is a bare possibility of their subsidence. The chance of any return of power in the paralysed part is small, although not quite absent if the palsy develops in a manner to suggest a secondary myehtis, and the progress of the growth itself is slow. Treatment.—Possibly in a few cases a growth may be so placed as to be removed, and an exploratory operation would be justifiable in any case that might prove suitable; otherwise treatment must neces- sarily be confined to the relief of pain, and to the avoidance of bed- sores and other results of the cord disease. Morphia is alone powerful for the rehef of pain, but unhappily the dose has to be quickly increased, and the power of the drug is lessened by custom. It becomes a race between dose and pain, in which, if life lasts long, the pain not uncommonly gets in front of the narcotic. Cocaine, however, affords some relief in many cases, and may, with other anodynes, at least prolong the influence of moderate doses of morphia. Vertebral Exostoses. Exostoses sometimes grow from the bodies of the vertebrae into the spinal canal, and may compress the cord or nerves. They are, how- ever, exceedingly rare. The symptoms may be those of slow compres- sion of the cord, or of irritation, expressed chiefly by pain. They usually resemble those of a tumour of the cord or membranes rather than of the bones, but the pain is occasionally much increased by move- ment. Their chief characteristic is extreme chronicity. In one case the patient suffered frequent intense paroxysms of pain in the right groin, which had persisted for two years, with occasional intervals of freedom. There was some weakness of the legs, but no considerable paralysis. Ten years before, he had had some loss of sensibility in each thigh, which had passed away. An intra-spinal tumour was diagnosed; the post-mortem examination revealed exostoses from the bodies of the ninth and tenth dorsal vertebrae, slightly compressing the cord. Although extreme chronicity may raise a suspicion of exostosis, it is doubtful whether a confident diagnosis is ever justified except in the cases in which there are similar exostoses elsewhere. This rare indication existed in a patient, under the care of my col- league Dr. Barlow, who presented multiple exostoses, and paraplegia of gradual onset, which was supposed during life, and found after death, to be due to a similar exostosis within the spinal canal. It had sprung from one of the lumbar vertebrae, and had compressed the nerves of the Cauda equina. Exostoses constitute a more promising field for the surgeon than other kinds of vertebral tumour. Many of them are so placed that their removal is feasible. If situated in front of the cord, the division of some nerve-roots, at least in the dorsal region, might permit access to the growth. EROSION BY ANEURISM. 305 Syphilitic Disease. Syphilitic caries of the bodies of the vertebrae is a rare variety, the symptoms of which do not differ from those of the scrofulous form. It has been observed in the cervical region, secondary to deep syphihtic ulceration of the pharynx. Nodes of the vertebrae, within the canal, are occasionally presumed to exist and to compress the cord, but I do not know of any pathological observation confirming the assumption, and it is probable that most of the supposed instances have been cases of syphihtic gummata in the meninges. Deep-seated thickening of the tissues about the cervical vertebrae sometimes occurs in syphilitic subjects. It may develop on one side or both, and is apparently dae to a syphilitic cellulitis. The swelling may be felt either on each side and behind the upper cervical spine, or deep in the posterior triangle of the neck. It may damage the nerves before they enter the brachial plexus, causing a defined palsy, as in one case of the lower arm muscles. Movements of the neck may be interfered with, and irrita- tion of the nerves may cause neuralgia-like pain, generally felt clown the arm, and often very severe. Except by the absence of nodula- tion, it is scarcely to be distinguished from a deep-seated growth. The spinal cord does not usually suffer. All the symptoms pass aw;;y under antisyphilitic treatment. In one late case, however, iodide had no influence, although mercury quickly cured. Erosion by Anetjbism. Bones, like other structures, may atrophy and waste before the pressure of an aneurism, and the bodies of the dorsal, or rarely of the lumbar vertebrae may be thus eroded by aneurisms of the aorta. The pressure and absorption take place from the left side. Two or three vertebrae usually suffer, and the bodies more than the inter- vertebral cartilages. The periosteum becomes thickened, and may resist the pressure and to some extent protect the cord. Sometimes, however, the cord becomes compressed, or the periosteum may come to form part of the wall of the aneurism, and may give way before the blood-pressure, so that rupture occurs into the spinal canal. The symptoms vary much. Pain along the nerve-roots is usually severe, but this may attend aneurisms that merely compress the nerves after their emergence, and do not damage the bone. The process of erosion is usually attended by severe pain in the spine. But in the case of a patient under the care of Dr. Hughlings Jackson, an aneurism of the arch of the aorta had eroded the spinal column, caused pressure myelitis, which gave rise to complete paraplegia and paralysis of the sphincters, without causing any pain. The patient died of kidney disease secondary to cystitis. When the cord is reached, compres- sion causes the usual paraplegic symptoms, of slow or rapid onset. Rupture into the canal is attended by sudden complete paraplegia and VOL. I. 20 306 DISEASES OF THE SPINE. death, either immediate, or in the course of a few hours, from ascending paralysis, due to the haemorrhage around the spinal cord. The diagnosis is scarcely possible unless other indications of aneurism are detected, since the symptoms closely resemble those of a growth in the bone. The nature of the disease may, however, be suspected if such symptoms as have been described are succeeded by sudden paraplegia followed quickly by ascending paralysis. Hydatid Disease. Hydatid cysts sometimes develop in the loose adipose tissue between the dura mater and the bone, and it is believed that they sometimes form in the substance of the bones themselves. About a dozen cases have been collected by Leyden.* As the cyst grows, the bone of the arches sometimes becomes atrophied by pressure, and the cyst may develop outside the canal, so that there is a double cyst, outside and inside, connected by a narrower part. Occasionally the cyst develops also in front of the spine, in the thorax or abdomen. The internal cyst necessarily compresses the spinal cord, which often also becomes inflamed. The usual paraplegic symptoms develop, both motion and sensation being usually lost. Radiating pains along the nerve-roots are frequent. The symptoms, in themselves, resemble too closely those caused by other diseases of the spinal column to permit a diagnosis to be made, unless similar disease elsewhere suggests the nature of the spinal lesion, or unless the cyst can be felt in the back, when a puncture may prove its nature. All the cases hitherto recorded have terminated fatally, but if removal can be effected a cure may be possible. In one case, however, a girl aged twenty-two, in whom a small tumour beside the last dorsal and first lumbar spines was opened (on account of complete palsy of legs, bladder, and rectum), a con- tinuous discharge of echinococcus cysts occurred, more than a hundred escaping in the course of four months, when the patient died in conse- quence of ascending damage to the cord. The tumour had been noticed for eight years before death, during four of which it produced sym- ptoms of irritation of the nerves, and finally prominence of the vertebral spines developed.f But in a case under my care, with svm- ptoms of an intra-spinal tumour in the lumbar region, Mr. Horsley trephined the spine and found a quantity of hydatid cysts compressing the cord. These were removed, and the patient recovered, but the damage was too great to allow the recovery of the extensive atrophic paralysis produced in the right thigh and hip muscles. Numerous small cysticercal vesicles have also been occasionally found within the dura-matral sheath. In one case several such vesicles were attached to nerve-roots, one to each, in the lumbar region, while a considerable number on the cervical enlargement were * 'Klinik der Riickenm. Krankh.,' Band i. t Tedjkovv, 'Med. Obos.' (Russ.), xxviii; and ' Cent. f. Nerv.,' xii, 271. VERTEBRAL ARTHRITIS. 307 beneath the pia arachnoid.* Such cysts may compress the cord, producing paraplegia, and even death. As in other forms of com- pression, the paraplegia may come on suddenly.f Diseases of the Articulations. Lateral Curvature of the Spine seldom affects the functions of the cord. Even when shght compression has occurred, the slow- ness of its production has apparently prevented interference with function. In very rare cases some weakness of the legs has been present, possibly, but not certainly, the result of the curvature. Occa- sionally the intervertebral foramina have been narrowed, and the pressure on the nerves has caused radiating neuralgic pains. Vertebral Arthritis.—In chronic rheumatoid arthritis the inter- vertebral articulations are sometimes involved. The symptoms are local pain, tenderness, and limitation of movement, which may go on to absolute fixation, especially in the cervical region, if anchy- losis occurs. I have known the whole neck to be rigid from this cause, in a case in which also the movement of the lower jaw was much reduced. More frequently, movement is restricted by pain before the mechanical limit is reached. Sometimes an occasional clicking sound occurs. Enlargement of the ends of the bones may occur, and, in thin persons, may even be felt. The pain is increased by movement, and often by changes in the weather, and by fatigue. It is often felt through a considerable extent of the spine, and may extend to the back of the head. The cord is scarcely ever compressed, but the narrowing of the foramina may damage the nerve-roots. The articular processes, it will be remembered, form one side of the inter- vertebral foramina, which are thus encroached on by any enlargement of the bones. The nerves may thus be compressed and irritated, and radiating pains are produced, sometimes even a descending neuritis. The nerve-trunks in the limbs may then become tender as well as painful; muscular atrophy may even occur, and, when the disease is in the cervical region, there may be symptoms of disturbance of the sympathetic. Spasmodic torticollis is said to have been caused by this disease in the cervical region. The atlo-occipital articulation has been affected alone, or with the adjacent vertebrae, and peculiar interference with the movement of the head has resulted. Sometimes the foramen magnum is narrowed, or the odontoid process projects into the canal. Symptoms of damage to the nerves of the medulla have also been produced (Solbrig). In the dorsal region the sym- ptoms produced are slighter in degree, but similar in general cha- * Hirt, 'Berl. kl. Wochenschr.,' 1887, No. 3. The relation of the symptoms to the parasitic disease is doubtful in a degree that makes it useless to mention them. t As in a case recorded by Wiegand (' Warsaw Med. Ob.;' and ' Cent. f. Nerv.,' 1888, 665). 308 SPINAL MEMBRANES. racter, although the local symptoms usually preponderate over those of irritation of the nerves. The whole spine may even become rigid. The degree in which the morbid process causes symptoms varies, however, very much in different cases, and it has occasionally been found out at the post-mortem examination without being suspected during life. It is usually associated with distinct evidence of a rheu- matic diathesis, and commonly with obvious arthritis elsewhere. This is the most important diagnostic indication as to the cause of the spinal symptoms, but it must be remembered that the vertebral affection sometimes exists alone, and it may cause symptoms during many years, often when their nature is unsuspected. It occurs in both sexes, and is met with in young women, in whom the symptoms are often ascribed to hysteria. The treatment is the same as that of the general disease, nerve symptoms alone needing special treatment, such as is described in the section on diseases of the nerves. The most important point in regard to the malady is its diagnosis, because distant nerve-pain is liable to be regarded as unconnected with local disease, or the disease to be thought far more serious than it really is, and especially to be mistaken for chronic meningitis or malignant disease, or even tubercular mischief. DISEASES OF THE MEMBRANES OF THE SPINAL CORD. The general arrangement of the membranes of the spinal cord has been already mentioned (p. 199). The pia mater closely invests the cord, while the arachnoid forms a loose sheath around it, and the two membranes are connected by trabeculse and membranous expansions of fine connective tissue, which occupy the " subarachnoid space." Each surface of the dura mater is covered by a layer of epithelium. The outer sheaths of the nerves are continuous with this membrane; the connective tissue, within the outer sheath, is continuous with both the pia mater and arachnoid. The blood-vessels of the cord ramify, as we have seen, in the pia mater, and the lymphatic canals of the two are continuous. Most of the cerebro-spinal fluid within the vertebral canal is contained in the subarachnoid space, but there is a little fluid between the dura mater and the arachnoid. Both membranes are supplied with nerves, but those of the pia mater are the more abun- dant. The morbid processes that involve the membranes are chiefly three —growth, haemorrhages, and inflammation. Tumours of the mem- branes may be conveniently considered in connection with those of the spinal cord. Inflammation and haemorrhage will be here described. EXTERNAL MENINGITIS, 809 SPINAL MENINGITIS: INFLAMMATION OF THE MEMBRANES OF THE SPINAL CORD. Inflammation of the membranes may be acute or chronic, and may begin, and affect chiefly, the dura mater (pachymeningitis, i. e. inflam- mation of the firmer membrane), or the pia mater (leptomeningitis, inflammation of the softer membrane). The arachnoid usually suffers with the pia mater, but is sometimes the seat of inflammation that affects the pia mater but httle, a form that has been termed arachnitis. Acute inflammation, beginning in one membrane, usually spreads to the others. Chronic inflammation may remain limited to one mem- brane, dura mater or pia mater. All forms of acute inflammation, wherever they begin, cause similar symptoms. It is only when the inflammation is chronic that the symptoms may differ sufficiently to allow of a precise diagnosis. Spinal meningitis may be conveniently divided into two forms, which depend on the situation of the inflammation in regard to the dura mater: (1) that which begins outside this membrane, and some- times arises by extension from some adjacent focus of inflammation ■—external meningitis; (2) that which begins within the dura-matral sheath, and is often primary—internal meningitis. EXTERNAL MENINGITIS. External meningitis is thus an inflammation of the dura mater. It has been termed external pachymeningitis* peripachymeningitis, and -perimeningitis. The inflammation involves not only the membrane, but also the connective tissue outside it, in which are the venous plexuses and adipose tissue. This connective tissue may be inflamed before the membrane itself. The morbid process usually remains limited to the outer surface of the dura mater, even when the inflam- mation is acute and intense, passing through it only in rare cases. Causes.—External meningitis is generally due to extension from some contiguous disease, especially of the bones of the spine, caries of which is the most frequent cause of the affection. It results also from other forms of bone disease, and a syphihtic inflammation is probably, in rare cases, associated with syphilitic disease of the vertebrae. Such secondary external meningitis is generally limited in extent and chronic in course. Deep sacral bedsores, however, sometimes cause • Pachymeningitis interna hsemorrhagica has also been described,—an inflam- mation affecting the inner surface of the dura mater, giving rise to a fibrinous membrane studded with minute haemorrhages. It is found in general paralysis, and also associated with alcoholism, with cerebral tubercular meningitis, and as a result of injury. But in such conditions the pia arachnoid is also usually involved (see Internal Meningitis). 310 SPINAL MEMBRANES. an acute inflammation, which may spread widely. An ascending neuritis has been supposed in some cases to set up local inflammation. Suppuration adjacent to the vertebral column is sometimes associated with a general acute purulent meningitis, and has generally been regarded as the cause of the latter; but careful observations have rendered it probable that in most cases the external suppuration has been the consequence, and not the cause, of the meningitis. It is certain that acute general external meningitis occurs as a primary disease, and may run an intensely rapid course with profuse suppura- tion between the membrane and the bone. The subjects have gene- rally been young, ill-nourished adults, and when any exciting cause has been traced, this has usually been exposure to cold. In some cases the pus has worked its way backwards between the vertebral arches (sometimes through the foramina), and has spread among the muscles of the back, sometimes forming also collections at one or more spots, either at the back or in front of the spine,—under the pleura, for instance, or behind the. peritoneum. Such local collec- tions of pus were also formerly regarded as the cause of the menin- gitis. It is still possible that this mechanism is effective in some instances, as when a retro-pharyngeal abscess is followed by the meningeal affection; but it is certain that in many cases the actual relation is the reverse, and that the external suppuration, in acute cases, is often secondary.* Hence it is probable that this is true of all cases in which the evidence of primary external disease is not con- clusive. At the same time further observations are needed to decide the point. Pathological Anatomy.—The inflammation is sometimes simple, but much more frequently purulent or semi-purulent. If simple, the dura mater may be merely reddened and opaque, with a httle lymph on the surface ; when purulent, the surface is covered by a layer of pus. In the more common semi-purulent form, such as is common in caries of the spine, a layer of inflammatory products covers the outer surface of the dura mater, soft, semi-caseous or firm caseous material, sometimes with liquid pus here and there in the firmer substance. Often the inflammatory products undergo development into fibroid tissue, a mass of which then lies between the dura mater and the bones. Such a layer, caseous or fibroid, may sometimes be half an inch thick (see Fig. 92, p. 288). It may either surround the dura mater, or be chiefly on one side. Sometimes there is an irregular nodular thickening of the outer layer of the membrane (Fig. 93). In most cases the inner surface is normal, even when the cord itself is inflamed. Occasionally the inner surface of the dura mater is also inflamed, and then the internal membranes are involved and adhe- sions form between them. In all forms of external inflammation, the fat outside the dura * Two instructive cases are recorded by Dr. W. H. Spencer,' Lancet,' 1879, vol. i, and Dr. Maguire, ib., 1888, vol. ii. EXTERNAL MENINGITIS. 311 when secondary to mater quickly becomes absorbed, and the membrane may ultimately become adherent to the bone, or connected with it by intervening fibrous tissue of inflammatory origin. The vertical extent of the disease varies much: caries the inflammation is usually limited to the neighbourhood of the bone disease. When acute and general, as in the primary form, the space between the membrane and the bone is filled with pus through the whole length of the canal. Occasionally the pus only lies behind the membrane, between it and the arches of the vertebrae, apparently determined in posi- tion by gravitation. It ceases in the upper cervical region, Avhere the dura mater is in closer contact with the bone, its ascent being perhaps also hindered by gravitation as t"ie patient hes with the head raised. As already stated, pus is often found among the muscles of the back (having escaped between the arches), and sometimes collections are found in front of the spine. The amount outside is no doubt increased rapidly by the local suppu- ration excited by the presence of the pus. In these cases the membrane itself is swollen, and has a sodden aspect, resembling a piece of wash-leather, being softened in proportion to the duration of the affection. The inner sur- face is usually normal, and the pia mater is either unchanged or merely congested. Symptoms.—In different cases of external meningitis the symptoms vary much, and they are usually complicated with those of the cause of the inflammation. Those that occur in caries have been already described. In most acute cases the symptoms are nearly the same as those of internal meningitis, although they are subject to greater variations, and more frequently have unusual and anomalous manifestations, presently to be described. The chief symptoms are pain in the back, often referred to the loins, increased by movement, accom- panied by stiffness of the muscles of the spine, severe root-pains, and cutaneous hyperaesthesia. The pains are usually associated with spasm ; the hyperaesthesia may be followed by anaesthesia, and some- times by paralysis of the muscles supplied by the irritated and damaged nerves. When there is a rapid formation of pus, the func- tions of the cord itself are rapidly interfered with in consequence of its compression, and the symptoms of irritation are to a large extent replaced by those of paralysis, beginning in the legs and ascending. Fig. 93 —External pachy- meningitis ; nodular thickening of outer layer of dura mater in caries of the spine. 312 SPINAL MEMBRANES. The motor palsy is accompanied by flaccidity of the muscles and loss of all reflex actions. Sensation may also be lost, or may be preserved or changed. The sphincters are usually paralysed. Bedsores form rapidly if life is sufficiently prolonged. A peculiar lividity of the skin has been sometimes noted. In these acute cases there is much constitutional disturbance, rigors, profuse sweating, and high fever, in one case amounting to 110° (Maguire). In local secondary forms the symptoms differ in character according to the acuteness of the inflammation, and in distribution according to its seat. Although, as a rule, pain is considerable, other signs of irritation, stiffness and muscular spasm, are generally inconspicuous, and the symptoms resemble, and are merged in, those due to the disease by which the meningitis is produced. Diagnosis.—The most important indications of the chronic form are the vertebral pain and the radiating pains, with other symptoms of irritation of the nerve-roots, combined with the signs of pressure on the cord. These symptoms are seldom distinct from those of the cause of the external inflammation; the meningitis is indeed the chief mechanism by which the local disease causes its nerve manifestations. The acute form causes symptoms that have much in common with those of internal meningitis. It is indeed doubtful whether the diagnosis can be made from the character of the nerve symptoms alone. The special indication of the seat of the process is furnished by evidence of its extension to or from the structures outside the spine. Lf such acute symptoms are secondary to external disease that clearly preceded the meningeal inflammation, this may safely be assumed to be outside the dura mater. In a case of apparently primary meningitis a careful watch should be kept on the tissues of the back; any sign of deep oedema among the muscles beside the vertebral column, in such a case, is probable evidence of commencing purulent inflammation extending from within, and the development of acute local inflammation in either the pleura, posterior mediastinum, back of the abdomen, or behind the pharynx, has the same signifi- cance. It is important that the nature of such symptoms should be kept in mind, as otherwise the occurrence increases the perplexing character of the case. It is probable that the nature of many cases, which remain undecided during life, would be rendered clear by repeated careful observation. Prognosis.—The acute affection is exceedingly grave. Recorded cases have ended in death, but this termination has been a condition of the diagnosis ; and it is possible that some cases which have recovered, in which the exact seat of the inflammation was uncertain, may have been instances of this form, and that the fatality of the disease may not be so great as published facts suggest. But on this point only future observations can throw light. Chronic external meningitis which results from caries is only serious in the compres- sion it exerts on the cord. INTERNAL MENINGITIS. 313 Treatment.—The local form alone affords an opportunity for effective treatment. The first and most important element is the treatment of the original cause of the disease, the caries, &c, to which the meningitis is secondary. Any accessible collection of pus should be opened, and if acute local symptoms, in a case of bone disease, suggest the passage of pus into the vertebral canal, the propriety of immediate trephining should be considered. Rest, counter-irritation to the spine, especially the actual cautery, sedatives to relieve the pain, and tonics are the most important measures in chronic cases. So far as the acute form is open to treatment, the measures suitable are those for the internal variety. In a subacute case, a free exit should be afforded to the pus. An opportunity for this very seldom presents itself, but may perhaps be furnished by sufficiently frequent examination more often than has hitherto been the case. INTERNAL MENINGITIS. Internal meningitis, inflammation beginning within the dura-matral sheath, may be either acute or chronic. The acute form usually com- mences in the pia mater and arachnoid; the chronic forms may begin in these membranes, or in the inner surface of the dura mater. Little is known practically of any separate affection of the arachnoid. Acute Internal Meningitis. Internal meningitis, for the reason already mentioned, has been termed "leptomeningitis," but the acute form only remains limited to those membranes when of slight degree. In some cases the inner surface of the dura mater is also inflamed. Frequently the inflam- mation extends rapidly to the cord, and to such cases the term " meningo-myelitis " is often applied; in other cases, strange to say, no extension to the cord takes place. The inflammation may be either simple or purulent, or it may be secondary to tubercle. It also occurs in conjunction with cerebral meningitis in the epidemic form. Acute simple spinal meningitis is a rare disease. The immediate causes that have been traced are in part such as have a local action; in part they are general morbid influences, such as give rise to other internal inflammations, and have been effective in causing meningitis in consequence either of some personal predis- position, or in consequence of a peculiarity in the agent, which led to a specific action on these structures. (a) The local causes may be—(1) Injuries to the spine, severe or sliglit. from fracture to simple dislocation; concussion; surgical procedures, such as an operation on the vertebral column, or the 314 SPINAL MEMBRANES. puncture of the sac in spina bifida. (2) The exposure of the back to cold has been the apparent cause in rare cases; and still more rarely the prolonged exposure of the spine to the sun, " spinal insolation," has seemed to be effective. (3) Adjacent inflammation has sometimes caused internal meningitis, but in such cases external meningitis has of necessity been first produced, and the inflammation has passed through the dura mater. Hence all the causes of acute external meningitis are also occasional causes of the internal form. But, as al- ready stated, such extension through the sheath is very rare, and there is some doubt as to the precise nature of many of the cases in which it has been supposed to occur. We have seen that in many of the instances in which external meningitis has been ascribed to adjacent suppuration, the latter has been secondary, and the meningitis has been the result of a primary blood-state. When in such cases there has been both internal and external meningitis, it is probable that the former has not been due to actual extension through the dura mater, but that both have been the simultaneous result of a general cause. (b) In a few cases acute internal meningitis is due to the extension of inflammation from the cerebral membranes. Such extension is rarely traced, however, except in two classes of cases :—(1) Those in which shght meningitis is found in the upper cervical region, as far as gravitation favours the descent of sohd particles in the cerebro- spinal fluid as the patient hes in bed. The inflammation ceases when the spine becomes horizontal: for the most part symptoms are slight or absent in such cases. (2) In cases in which a general spinal meningitis has been secondary in point of time to inflammation of the cerebral membranes the affection has generally been due to some cause capable of acting upon both, such as the local presence of tubercles or a morbid blood-state of the character to be immediately mentioned. (c) The most acute and severe forms of internal meningitis are due to a morbid blood-state, either septicaemia or a virus allied to that which causes the cerebro-spinal form. Purulent meningitis occurs in cases of surgical and puerperal septicaemia, both with and apart from a similar affection of the cerebral membranes. Acute inflammation, purulent when intense and prolonged, occurs also as an isolated malady, sometimes without apparent exciting cause, sometimes after exposure to cold. In such cases organisms have been found in the spinal fluids, analogous to those of the cerebro-spinal form, in connec- tion with which the pathological relations will be more fully con- sidered. It probably results from a blood-state not far removed from those which cause some other forms of internal inflammation, and which give rise to acute articular rheumatism. General exposure to cold must be assumed to cause so special an effect only through the agency of toxaemia, such as that which has been already con- sidered as underlying the rheumatic form of acute polyneuritis. Such exposure has been apparently rendered effective in some instances by INTERNAL MENINGITIS. 315 coincident menstruation, which may have produced a special suscepti- bility to the attack, or favourable conditions for the development of some organised virus, such as seems to be the essential factor in the causation of these forms. The exposure to cold that has been effective has presented all the variations that are met with in the case of other diseases thus produced, variations which are common to so many maladies that they can have no special relation to any one of them. Lastly, as a crucial example of this origin of the disease, is the important fact that it may follow, or occur in the course of, certain acute specific diseases, as one consequence of the virus that produces them. Pathological Anatomy.—Internal meningitis is usually of wide extent, since the inflammation spreads readily in the loose tissue of the arachnoid. Probably also the movement of the cerebro-spinal fluid aids in the extension of local forms and in the descent of intra- cranial inflammation by conveying irritant material. In the case of a patient who had been in bed for some time the precise level at which such slight descending meningitis ceases may be that at which the vertebral column becomes horizontal. In the earliest stage the only change is congestion in the pia mater, which is reddened from vascu- larity, and may be dotted with ecchymoses. The inner surface of the dura mater, and the substance of the spinal cord, may be similarly con- gested. When the inflammation is further advanced, in the stage in which the condition most often comes under observation, the pia mater and arachnoid are opaque and thickened, and an " exudation " of inflammatory products, greyish yellow in tint, may cover the pia mater and occupy the meshes of the arachnoid, forming a layer over the cord. This exudation varies in its consistence, and may be semi-purulent in aspect; in the suppurative form the membranes are infiltrated with pus, which also covers their surface. The inner surface of the dura mater usually presents similar changes, a,nd the inflammatory products may fill up the whole space between the dura and pia mater, thus connecting the two membranes and surrounding the nerve-roots (Fig. 94). The microscope shows abundant leucocytal elements, and the larger round and spindle cells that are common in all inflammatory products. The former corpuscles, which resemble, and are probably identical with pus-corpuscles, may be abundant, even when the exudation has not a distinctly purulent aspect; when it has, they constitute almost the whole of the material, lying among the fibres of the arachnoid (Fig. 95). The vessels are dilated, and their sheaths distended with cells. The spinal fluid is increased in quantity, and turbid from flocculi, or even purulent in aspect. The nerve-roots are covered with exudation, and are often swollen and reddened from invasion by the inflammation. But they do not always suffer, even in purulent meningitis, as Fig. 95 shows, in which a nerve-root is almost normal in aspect, and its sheath is unaffected, although it is surrounded by pus-cells. The spinal cord 316 SPINAL MEMBKANES. is often invaded by the inflammation; it is then reddened, pale, and softened, and the microscope shows the tissue changes common in E.g. is of the Cord from Toxic Causes." 342 SPINAL CORD. which occurs from the same cause, in which there may be no visible morbid change, or inflammation may be found, sometimes succeeding the loss of sight, and therefore to be regarded as a result of the derangement of the nerve-elements, or of the influence to which this is due, rather than as the cause of the amaurosis. The treatment of the symptoms due to general anaemia is of course essentially the improvement of the blood-state. Symptoms which can be ascribed, with probability, to vaso-motor spasm may be prevented by drugs that cause a more uniform arterial tone, such as digitalis or belladonna, coupled with nux vomica or strychnia, to render the effect permanent. Hyperemia of the Spinal Cord. The conditions of the return of venous blood from the cord probably shield it effectually from the mechanical congestion from which almost every other organ of the body suffers when the movement of blood through the thorax is hindered. The chief mechanical congestion to which the cord is liable is that which results from the influence of gravitation, and occurs when a person is lying on the back. The dis- tension of the veins outside the dura mater, and also of those of the pia mater, which occurs when the heart has ceased to act, and the blood is free to obey the only mechanical force which then acts upon it, sufficiently proves the power of gravitation to congest the cord. But it is not probable that gravitation has anything like the same influence during life, counteracted, as it then is, by many other forces. Some persons with imperfectly nourished cords (easily fatigued, liable to tingling, &c, in the legs) suffer from aching in the legs or spine when they lie on the back. Since this ceases when the posture is changed, it is probably due to the mechanical congestion of the cord or membranes. It is doubtful whether any other symptoms can be, with confidence, assigned to mechanical congestion. Of active congestion our definite knowledge may be summed up in the statement that it occurs in the early stage of inflammation. We know nothing of it as an independent condition. Nevertheless many pages might be filled by the enumeration of the various symptoms of congestion of the spinal cord,—in which the unrestricted play of " scientific " fancy has elaborated a symptomatology for the separate congestion of every part of the spinal cord. Probably the only case in which we are warranted in suspecting a primary active congestion of the cord or membranes, is that in which symptoms identical with those of commencing myelitis, and following a cause of myelitis, pass away in the course of a few days. These cases will be mentioned in the account of inflammation of the cord. An active congestion, which may be called secondary, seems to result from prolonged and violent action of the nerve-elements of the spinal cord. Thus local dilatation and distension of vessels, migration of MYELITIS. 343 leucocytes into the sheath and into the adjacent tissue, and even small extravasations, are found in some cases of hydrophobia, of tetanus, acd of strychnine poisoning, and it is probable that a similar con- gestion attends all violent physiological activity, violent and continued muscular exertion, coitus, &c. Coitus several times repeated has been known to cause haemorrhage within the cord which must be preceded by an intense congestion. Vascular dilatation, with an increased blood-supply, is the physiological attendant of functional activity in all organs, and doubtless also in the cord, but it is morbid only when excessive. It is doubtful whether it causes symptoms unless it goes on, as it probably may, to actual inflammation. INFLAMMATION OF THE SPINAL CORD; MYKL1TIS. Inflammation of the spinal cord is a common lesion in the acute, subacute, and chronic forms. It usually causes a considerable diminution of consistence, and hence the term " softening of the spinal cord " has been used as a synonym for it. But the term is not accurate, because inflammation does not always cause softening, and a diminution of con>istence may occur without inflammation.* The spinal cord differs from most other structures in that its power of recovering functional capacity after damage by inflammation is comparatively small. The symptoms persist for a long time, and are not unfrequently permanent. Hence the distinction between acute and chronic inflammation is to be drawn, not from the whole course of the disease, but from the mode of onset. It is this which indicates the character of the morbid process. Acute 'myelitis is that form in which the symptoms indicating inflammation of the cord come on rapidly and reach a considerable height in a short time, in less than two weeks. When the onset occupies from two to six weeks the inflammation is regarded as subacute. When a still longer time elapses before the symptoms reach a considerable degree of intensity the myelitis is termed chronic. There is, of course, no sharp distinc- * Oppenheim, Pierre M.irie, and Bruns have been especially identified with objections which have been raised to the nomenclature in cases of myelitis. They allege that many cases of so-called myelitis are due to softening from vascular thrombosis and to other causes not strictly inflammatory in character. They even allege that compression or pressure myelitis is a misnomer. There is, no doubt, much truth in what they allege in reference to softening, but it is not easy to understand an objection to naming the condition myelitis which occurs, at least in many cases of compression, and the views as to what constitutes true inflammation are so con- flicting that little alteration has been made in this edition in the point of view from which myelitis is regarded in earlier editions of this work. 344 SPINAL CORD. tion between these classes. The subacute and acute forms may be conveniently described together. Other varieties are based on the distribution of the disease. The grey matter may be affected only or chiefly, polio-myelitis (from iruXios, grey), a form that has distinctive characters which make its separate description desirable. When the whole thickness of the cord is affected in a small vertical extent the myelitis is said to be transverse. This is one of the most common forms. When an extensive area of the cord is continuously inflamed the myelitis is said to be diffuse; when one small area is affected the inflammation is called focal; when there are many foci contiguous or distant the myelitis is said to be disseminated, and when such foci are present in the brain and pons, as well as in the cord, the condition is spoken of as disseminated encephalo-myelitis. Inflammation of the grey matter, around the central canal, extending into the intermediate grey substance and to a less extent into the cornua, has been termed central myelitis. A further important distinction is that between parenchymatous myelitis, an acute affection beginning in the nerve- elements, and the interstitial form, which begins either in all the elements or in the connecting tissue, and in which vascular disturbance takes a prominent part. The latter is the common form of myelitis, whether transverse or disseminated, but the former is of importance on account of the limited class of symptoms to which it gives rise and of its special causal relations. This distinction is already familiar in regard to multiple inflammation in the nerves. Acute Myelitis. Etiology.—Remote causes.— Little is known of the influence of hereditary predisposition, but myelitis is sometimes met with in members of families in which other evidence of a neuropathic tendency can be traced. Males suffer more frequently than females. It may occur at all ages, but the form which occurs in young children is usually confined to the anterior cornua; other forms of myelitis are most common between ten and forty years. Immediate causes.— Myelitis, acute and subacute, is readily pro- duced by injuries to the cord of all kinds,—lacerations, bruises, and punctured wounds. It also seems to follow simple concussion, but in many of these cases there have been minute foci of structural damage. The myelitis produced by concussion is often, however, f?r more extensive than the primary lesion, for the latter may cause few symptoms, and a few days later a complete transverse myelitis may develop. Haemorrhage into the cord, especially of traumatic origin, may have a similar effect; it may be followed after a short interval by extensive myelitis. In cases in which an interval of more than a few days elapses, pain in the spine may show that a morbid process is going on by which the myelitis is produced. Thus, in one case of amte myelitis, two weeks after a fall, there was continuous pain ACUTE MYELITIS. 345 during the interval, corresponding to the seat of the later inflamma- tion. Concussion also sets up the subacute form of myelitis, and this is especially common after railway accidents (see Traumatic Lesions). Allied to injury as a cause is violent action of the muscles attached to the spinal column, which has sometimes appeared to be the sole agent in producing an acute inflammation in the adjacent part of the spinal cord. The disease has been known to follow a single violent contraction of the dorsal muscles, as, for instance, a successful but violent effort to prevent a fall. It is possible that there is an actual injury to the cord in these cases, but more probably inflammation is set up in the fibrous tissues of the vertebral column or nerve-roots, and spreads to the cord. It is also possible that compression of the vessels may be concerned in the mechanism. In several cases the disease has resulted from attempts to lift heavy weights. Thus a man, two days after such an attempt, became rapidly paraplegic, and ultimately died; softening of the cord was found at the level of the fifth and sixth cervical vertebrae. Slow compression (q. v.) is con- stantly attended by inflammation in the compressed part; the myelitis thus set up may have an independent course, acute or subacute, and may not be proportioned to the pressure. In cancer of the vertebral bones, for instance, very slight pressure may cause an acute inflammation; there is probably sometimes an extension of inflammation to the cord from the external disease, but such extension is not necessary for the occurrence of the myelitis; the inner surface of the dura mater is often normal. Acute myelitis also results from internal meningitis, in which some degree of invasion of the cord is almost invariable. Another exciting cause is exposure to cold, especially when the body is heated, lying on damp grass or on snow, bathing in cold water, &c. This cause has been supposed to act by suppression of the functions of the skin, since myelitis has been produced by varnishing the skin of animals,* but it is unlikely that this is the sole mechanism. Exposure of the back to cold sometimes seems especially effective. Myelitis has been produced experimentally in rabbits by freezing the skin of the back with ether spray (Feinberg) and by painting the cord itself with Fowler's solution (Leyden). It is probable that cold usuallv acts by the mechanism of a morbid blood-state, such as that which causes rheumatic fever, but which certainly varies greatly in its precise character and pathogenetic power. It is also certain that local exposure frequently causes inflammation in organs corre- sponding to the part of the surface that is especially chilled, although this influence may be chiefly to determine the incidence of the effect of the blood-state. In myelitis from cold, local exposure can seldom be traced, and the common mechanism is probably that of a blood- * Feinberg, ' Virchow's Archiv,' Bd. lix. In Vulpian's laboratory similar experi- ments failed. 34b' SPINAL CORD. state. It is instructive to compare the analogous facts regarding the causation of multiple neuritis. Over-exertion is another powerful cause, and is especially effective when combined with insufficient food and exposure to cold. The sudden suppression of the menses and of other habitual discharges has been supposed to cause the disease. In most instances of the kind there has also been exposure to cold, to which the sup- pression and the myelitis may both have been due, and it is impos- sible to say how far the former has been concerned in the process. Thus, a girl sat on wet grass during menstruation, which was immediately arrested, and myelitis followed, a day or two later. It is conceivable that the sudden arrest of the discharge may lead to a morbid state of the blood, or modify that which a chill alone is capable of producing, and that the derangement of the uterine func- tions may have a direct influence on the cord and dispose it to suffer. It is noteworthy that, in the case referred to, the inflammation was in the part of the cord to which the pelvic organs are related, the lumbar region. Functional over-action of the cord may cause inflammation in the part that is thus over-exerted. It has been already mentioned that long-continued stimulation of the sensory nerves may cause myelitis at the spot related to the nerves stimulated. As we have just seen, active function everywhere involves vascular dilatation, which, if excessive, amounts to active congestion, and, when prolonged, is attended by the escape of leucocytes that renders the condition one of inflammation. However excited, such a process has a tendency to independence of course, and to proceed beyond the degree corre- sponding to its cause. It is especially local functional over-action that has a tendency to cause myelitis. Thus the affection seems to be sometimes produced by sexual excesses. Occasionally, however, general over-action of the cord, -as in severe, long-continued exer- tion, has been followed by the disease. In one case it was due to lving at rest on damp ground, after an unusually long walk on a hot day. Toxic blood-states constitute a well-marked class of causes, and their influence is rendered the more distinct by the analogous causa- tion of multiple neuritis. They may be acute conditions due to some organised virus, perhaps allied to those that produce the acute specific diseases.* Inflammation of the cord occasionally comes on in the course of, or after, typhus, typhoid, erysipelas, malaria, and especially variola and measles, as well as acute rheumatism and severe puerperal diseases. The onset may be during the acute disease, at any period after it has existed for about a third of its duration, or it may occur during convalescence, or a month or more after the disease is over. * See Buzzard and Risien Russell ('Trans. Clin. Soc./ 1897), who describe a case ot nieningo-myelitis in which a diplococcus was found in the membranes, and cultures on nutrient media showed the presence of an identical organism. ACUTE MYELITIS. 347 Whether syphilis is a cause of acute myehtis is a question on which opinions differ. Attacks of acute myelitis are not uncommon in syphilitic subjects, and it seems on the whole probable that the mechanism is by disease of the vessels, such as is found in the pia mater in some cases.* The myelitis that occurs in acute specific diseases is probably due to the virus of the primarv disease, to a product of it, or to a secondary infection engrafted on the first. Thus Marinesco found streptococci in the spinal cord in a patient in whom paralysis came on in the course of smallpox. The fact that the inflammation is commonly disseminated, suggests that some specific organisms have a tendency to fix themselves in the spinal cord and set up inflammation. In diphtheritic paralysis, the cells of the cord may present changes that amount to a parenchymatous myelitis. The fact that chronic changes in the cord may be a late effect of syphilis (as in tabes) makes it the more easy to conceive that acute processes should sometimes occur in an earlier stage of the disease.f In another class of diseases, a special influence of the virus appears to be associated with the results of functional over-action. This effect is especially seen in hydrophobia and in tetanus. In some cases of this disease, foci of a somewhat diffuse myelitis of slight degree are conspicuous on microscopical examination. Still more intense myelitic changes are sometimes met with in the chorea of the dog, although, in other instances, the cord is normal. Chronic blood-states and constitutional conditions may also cause acute myelitis. Alcoholism is an occasional cause, and frequently produces the subacute form. Gonorrhoea has also been shown by Leyden,£ Gowers,§ Barrie, and others to be a cause of myelitis.|| The most potent agent of this class is gout. This is known to be a frequent cause of inflammation in various structures,—of the nerves among the rest; and cases of acute and subacute myelitis are met with, especiallv of the disseminated and relapsing forms, for which no other cause can be discovered. In one such case the patient had but lately recovered from a severe and prolonged attack of gouty inflammation of several intra-ocular structures. Like other, chronic general causes, gout probably often acts as a predisponent when the malady is excited by some other cause. Irritation and inflammation of peripheral organs, as the uterus, bladder, kidneys, intestine, &c, have been supposed to be an occasional cause, but this influence is exceedingly doubtful, except in the rare * Sudden paraplegia occurred in a case in which there was diffuse arteritis, sup- posed to be syphilitic (Sohmaus, 'Arch. f. kl. Med.,' 1889); see also Williamson, 'Lancet/1894. f Bourget (' Arch, de Med. exper.,' 1893) found acute myelitis almost destroying the lumbar enlargement, produced by the injection of the streptococci of erysipelas. J 'Zeitschr. f. klin. Med./1892. § 'Clinical Lectures,' G<.wers. || Compare with this a condition of neuritis resulting from gonorrhoea (p- 147). 348 SPINAL CORD. cases in which inflammation of a nerve ascends to the cord. In a considerable number of cases we are able to discover no cause to which myelitis can be ascribed. Many of these are probably due to a blood-state which may have no other consequences or may also cause simultaneous inflammation elsewhere.* Pathological Anatomy.—In recent acute inflammation of the cord, the pia mater, at the affected part, is usually red and vascular, and the cord itself may be slightly swollen. Its tissue is reddened and often marbled from distended vessels, and the distinction between white and grey matter is indistinct or lost. The diminution of consistence which occurs in acute inflammation may be so great that the affected part is diffluent, like cream, and flows out when the pia mater is divided. It does not follow that the consistence is lessened to this degree during life; post-mortem soft- ening occirs more readily at an inflamed part. When the vascular disturbance and extravasation are considerable, the condition is termed " red softening;" so much blood may be effused into the tissue that the part looks as if there had been an actual haemorrhage, and in some cases an extensive extravasation does actually exist; this form is termed " haemorrhagic myelitis " If the inflammation has existed for some time, the effused blood is altered in tint, and the colour of the softened part may be rather chocolate than red. After a longer time the changes in the blood-pigment cause the colour to be lighter, "yellow softening." In many cases the breaking up of the nerve- elements (partly, as just stated, post mortem) is out of all proportion to the extravasation of blood, so that the softening is " white." It is said that red and yellow softening may ultimately become white from the removal of the blood-pigment, but the evidence of this is inade- quate. The period at which these changes of colour are found varies according to the amount of extravasation at the onset. At a later period the yellow or white opaque aspect is changed to a grey trans- lucent appearance, from the absorption of the fatty products of degeneration, and an increase in the connective tissue. If the myelitis is very limited in extent, cavities may be formed within the cord. The microscopical appearances in myel'tis vary much according to the duration and form of the inflammation. In the fresh state the most conspicuous objects are the products of degeneration of the fibres, granules and masses of myelin, and granule corpuscles, with, in older, cases, the peculiar bodies termed "corpora amylacea" (Fig. 97). With these are numerous red blood-discs, leucocyte- * Thoinot and iUasselin ('Rev. de Med.,' 1894) injected pure cultures of Staphy- lococcus aureus and Bacterium coli commune into rabbits, producing paraplegia, the result of spinal cord changes. The grey matter was chiefly affected, and the micro-organisms could be found in the cord as long as six months later. They regard so-called reflex paraplegia as almost certnin]y the result of some infective cond'tion similar to that which they produced artificially. ACUTE MYELITIS. 349 like corpuscles, and, after the first week, distinct cells, round, oval, spindle-shaped, or angular, with nuclei which resemble leucocytes in size, and are readily mistaken for them. Fragments of axis-cylinders may also be seen, granular in aspect, and with irregular swellings (Fig. 97). The softened and even diffluent state of the tissue prevents us from learning much, by microscopical examination, of the condition of the parts in which the inflammation is intense and diffuse, because the breaking up of the tissue and separation of the fragments renders it impossible to obtain sections of the hardened organ. It is only where the inflamma- tion is less intense, or less uni- formly diffused, that a thorough examination can be made. The products of degeneration are best seen in the fresh state or in sections mounted in glycerine (Fig. 97). The fragments and globules of myelin in part occupy the position of the nerve-fibres from which they have come, in part are aggregated into masses. In sections rendered trans- parent in the ordinary way, the fatty products of the de- struction of the nerve-elements are invisible, and the most con- spicuous alterations are the dila- tation of vessels, which is often very great, and the accumulation of leucocytes and other cell- elements in the tissue, and especially about the vessels. In the white substance the larger vessels are conspicuous by their enlargement, and in the grey substance the dilated arteries and capillaries may occupy a considerable part of the tissue (Figs. 98, 99, a). The nuclei of the capillaries are large and numerous. The walls of the smaller arteries are encrusted with leucocytes in the early stage, and, later on, in both white and grey substance, are much thickened by cells, the nuclei of which are often elongated and more or less concen- tric to the lumen of the vessel (Fig. 102, d). Outside this thickened wall the perivascular sheath is enormously distended, at first by leuco- cytes, among which, afterwards, other cells are mingled—round, fusiform, angular, with leucocyte-like nuclei (Fig. 102). In transverse section this distended sheath may look, at first sight, like an enormously Pia. 97.—Myelitis, a, an irregularly swollen axis-cylinder. b, section of nerve-fibre with swollen axis-cylinder. c, section of white substance, with granule-masses and atrophied nerve- fibres, d, corpora amylacea. (From Leyden.) 350 SPINAL CORD. thickened wall. Red blood-corpuscles distend the vessels and are .seen also in the adjacent tissue, sometimes uniformly scattered through it (Fig. 102, f), sometimes aggregated in small extravasations due to the rupture of minute vessels. The grey substance is densely set with round corpuscles, staining deeply, many of which are the nuclei of small fusiform or angular cells (Figs. 99, a, 101, b), while the inter- vening substance is much more granular than in health. The nerve- FlQ.. 98.—Subacute myelitis, lumbar region; both white and grey sub- stance uniformly affected. In the latter the numerous distended vessels appear as lines; here and there a larger one is visible. FiG. 99.—Portions of the section shown in the last figure, more highly magnified. A, from the left ant. coruu; distended capillaries with numerous nuclei; larger vessels with slight distension of perivascular sheaths; numerous round and stellate cells; ganglion-cells, swollen, with shrivelled processes. C, from front of post. column; scattered nerve-fibres separated by amorphous material in which small cells can be seen, round and irregular, some distinct, others indistinct, vessels with thickened walls. B, from near the posterior surface, shows similar changes but with more open spaces from which nerve-fibres have perished. (From sections prepared by Dr. Money.) ACUTE MYELITIS. S5J cells are much swollen and granular, often contain distinct globules strongly refracting, and probably fatty. The cell-processes appear shrivelled or lost (Fig. 99. a). In slight cases the margins of the cells may be less sharply defined than in health, and the bodies then may contain large vacuoles, sometimes wholly within the cells, some- times partly within and partly outside them in an adjacent albuminous- looking substance.* In some cases, however, especially those of disseminated interstitial myelitis of moderate degree, the nerve-cells appear little changed in hardened and cleared specimens, although a granular condition can usually be seen in the recent state. In the white substance, cleared sections show a great increase and alteration in the interstitial tissue. The change may be uniformly distributed, or greatest in the neighbourhood of the vessels (Fig. 102, c). The increase is due in part to an amorphous material, contain- ing nuclei here and there, some of which belong to cells such as have been described in the grey substance ; and these may constitute extensive tracts between the spaces where nerve-fibres once existed (Fig. 102). In older cases the tissue may have a fibrous aspect in places. The large cells, with many processes called " spider cells," or " cells of Deiters," are often conspicuous objects (Fig. 100). The processes extend between the nerve- fibres. We have seen that their existence in the normal cord has been doubted, but in the inflamed cord, in which they are enlarged, their pre- sence is distinct. The changes in the nerve- „. . m. Fig. 100.—Subacute dis>eminated myelitis; fibres vary much. Ihey part of the posterior column. Nerve-fibres always suffer destructive separated by granular material and products Changes, but the products of of. ^generation and by numerous large ° .r spider cells. Ine myelitis in this case was their degeneration, above attended by optic neuritis. (From a sec- described, are scarcely to be tion lent by Dr. Dreschfeld.) seen in cleared specimens. The slightest change in the myelin appears to consist in an alteration in its chemical nature, in consequence of which it stains more readily than in health. Fibres are thus changed adjacent to any increase in the interstitial tissue, and they contrast with the unstained healthy fibres in the vicinity (Fig. 101, c). With or without this change in the myelin, there is an irregular swelling of the axis-cylinders, such as is seen on examination in the fresh state. If the fibres are divided * The significance of this vacuolation has been much discussed. It is probable that the vacuoles form after death, perhaps during the process of hardening, but that they do not form unless the cells have been altered by disease. They have thus some pathological significance. 352 SPINAL CORD. transversely at the places where the axis-cylinder is swollen, this appears much larger than normal (Fig. 97, b). Examples of this will be found in most of the figures. These intense degenerative changes cause the breaking up of the myelin, and may involve the destruction of the fibre, the space occupied by it being left empty. In other cases, however, the axis-cylinder persists and remains sur- FlG-. 101.—Acute transverse myelitis, fatal in three weeks. Carmine preparations. A, section through most diseased part, at first lumbar segment. Foci of inflammation scattered through the whole area of this cord, most abundant in the posterior columns (the apparent enlargement of which is probably due to the direction of the section). Dilatation of the central canal. B, from the anterior cornu at A, b, a distended vessel; the tissue crammed with lymphoid and other cells, among which run normal nerve-fibres. C, from the posterior column, A, c. The areas staining deeply are seen to consist of thickened trabecule, lymphoid cells, amorphous tissue, and also of nerve-fibres, the white substance of which stnius with carmine while that of the neighbouring healthy fibres does not.* • I am indebted to Dr. Dreschfeld for the section from which these drawings are made. The patient was a girl aged twenty-three; paralysis, motor and sensory, was complete at the end of two days; the application by her mother of hot bottles to the feet caused such extensive sloughing ulcers that amputation of one leg was deemed nececsary three weeks after the onset, and the patient died the next day. ACUTE MYELITIS. 353 rounded by a narrow zone of myelin. Often a large number of such shrunken fibres may be found in a part which at first sight appeared devoid of fibres. This shrinking of the fibres occurs not only as the result of pressure on them by the connective-tissue elements, but also where there is httle interstitial change and no compression. The relative amount of change in the nerve-elements and in the interstitial tissue varies very much. In some cases the interstitial changes are evidently primary, and the fibres at first present httle change in slight cases, but afterwards are altered secondarily, being narrowed, and even destroyed, as they are surrounded and enclosed by the products of the inflammation. In other places, or even other parts of the same section, there is but httle increase in the neuroglia, although the fibres have suffered extensively; empty spaces are limited by septa but Httle thicker than normal, although with more nuclei, and often with numerous granules, the nature of which is uncertain. Occasionally there is a more diffuse change in the white substance; the neuroglial tissue is increased by small cells and amorphous material in such a manner that all appearance of septa and spaces is lost; a few nerve-fibres are included in it, and the spider cells are very conspicuous objects, their processes apparently representing the septa that exist in the normal condition (Fig. 100). The distribution of these changes is very variable. The whole thickness of the cord is uniformly affected in pressure-myelitis (see "Compression of the Spinal Cord"). In transverse myelitis the changes may be so intense in all the structures at the affected level that the cord is diffluent, and, as already stated, only separated pro- ducts of degeneration and inflammation, and blood-corpuscles are to be seen. In slighter cases the alteration is seldom distributed uni- formly, and in either a single section, or a series of sections taken near together, each part may present variations in the damage, which may, however, be such that no part escapes in all (see Fig. 102). In meningo-myelitis the periphery of the cord is always most affected, and in old cases the thickened pia mater may send tracts of dense tissue into the interior of the cord, from which branching processes of tissue may pass on all sides. The condition is similar to that met with in chronic myelitis. A similar extension is often conspicuous in cases in which there is no special inflammation of the membranes, and the interstitial changes often extend from the septa that normally pass into the cord and from the walls of the vessels, the course of which may thus be marked out when the vessels cannot be seen. Hence the white columns may be broken up by lines of tissue passing from the surface of the cord towards the grey substance. In disseminated myehtis the foci of inflammation may exist through a wide extent of the cord, and appear on the surface as reddish-grey areas, closely resembling those of disseminated sclerosis, but less sharply outlined. Under the microscope, in the early stage, smaller foci stud the grey and white substance irregularly, sometimes ex- VOL. I. 2:J 354 SPINAL CORD. Fia. 102. *■"> > *x \ : ■ %f^ " ;^:- "4 *£&' D fen i;i^^ -/a, -/;.^ -r^-w ' ACUTE MYELITIS. 355 tending into larger tracts. They may be most abundant in the grey or the white substance. At first the vascular changes are the more conspicuous, but afterwards the evidence of destruction of nerve- elements and the inflammatory products, exudative and cellular, described above, characterise these foci, while ultimately a condition of irregular focal sclerosis remains. In central mvelitis there is a great increase in the nuclei about the central canal, with vascular changes in the commissure adjacent, but there may also be evidence of slight widely diffused myelitis. It is necessary to remember that the nuclei around the central tissue vary much in number, and that it is easy to mistake a normal for a diseased condition. Little is known of the morbid appearances in the parenchymatous forms, except that in a variety of anterior polio-myehtis, and in diphtheritic and other toxic paralyses, the nerve-cells present granular changes, and the interstitial grey substance may be but slightly affected. The nerve-roots coming from a much inflamed part are usually damaged, and may present histological changes similar to those within the cord—distension of vessels, increase of nuclei and of con- nective tissue about the vessels, breaking up of the myelin, swelhng of the axis-cylinders. Degenerative and neuritic changes may descend the motor nerves, although rarely to the same degree as in polio- myelitis, except in the cases in which there is extensive inflammation in the lumbar or cervical enlargement. From the foci of inflammation, ascending and descending degenera- tions pass along the tracts of long fibres that have been already described, downwards in the pyramidal tracts, upwards in the poste- rior median columns, the direct cerebellar tracts, and the antero- lateral ascending tract. In cases of transverse myelitis, moreover, changes that are definitely inflammatory in nature may be traced in certain tracts for a short distance above or below the chief lesion; they may accompany the secondary degeneration, or may be found extending along a tract that degenerates in the opposite direction. Thus distinct inflammation may pass, for a short distance, up the Fig. 102.—Acute transverse myelitis; from a case fatal in a month. A, B, C, neighbouring sections from the inflamed part, in the mid-dorsal region, to show the varying distribution of the inflammation.' (Stained with aniline blue-black.) Distended vessels are all surrounded by thick zones of clear tissue, in places divided obliquely, while outside this, ramifying tracts of darker tissue extend into the white substance. In D, from the front of the posterior column, the changes are shown more highly magnified. The zone around the vessels is seen to consist of the perivascular sheath distended by cellular elements, round, oval, fusiform, angular. The white substance is crammed with similar cells, and hardly any trace of nerve-fibres or of normal structure can be perceived. In E, from a less affected part of the lateral column, stained with carmine, the alveoli remain, although the tissue between them is thickened, and in many places studded with refracting granules and larger nuclei. In many spaces nerve-fibres are seen much smaller than normal in consequence of the wasting of the white substance. F represents a similar condition, with fewer nerve-fibres, and extensive infiltration of the alveoli with blood-corpuscles. (From sections prepared by Dr. Money. For the specimen I am indebted to the late Dr. Hadden.) 356 SPINAL CORD. pyramidal tracts, so that, an inch or two above the upper limit of the general inflammatory changes, an ascending inflammation of these tracts may be combined with an ascending degeneration of the tracts that always present secondary ascending degeneration. If the patient survives, the new interstitial tissue slowly undergoes changes which give it a fibroid aspect, although for some time cell- forms may preponderate in it. We know very little of the nature of the process that occurs in the cases which slowly recover, and sub- serves restoration of function. The fact that a long period of total palsy may be succeeded by the slow return of considerable power, shows that even greatly damaged fibres may regain functional capacity. It is easy to conceive that the fibres which are only so far changed that the axis-cylinders are swollen, and the myelin stains readily, may speedily recover. "We can also understand that the fibres in which a very narrow layer of myelin remains around the axis-cylinder may also regain the power of conducting. We must presume that in these fibres there is no interruption of the axis- cylinders, but there are cases in which we can scarcely believe that the axis-cylinders retain their continuity, although conducting capacity is ultimately restored. An absolute motor palsy of twelve months' duration must depend on changes that involve an absolute inter- ruption of the fibres, and yet in such a case some return of power may occur. Is this effected by a growth of new fibres such as occurs in nerves ? In the lower animals such a growth of fibres has been proved to occur; in man it has not yet been demonstrated, but it is difficult to conceive any other explanation of the clinical facts. The very interesting appearance presented by the section of a cord shown in Figs. 103, b, and 104 suggests strongly a process of regeneration. The cord was crushed in the mid-dorsal region by a fracture of the spine, and motor and sensory paralysis remained absolute, up to the level of the lesion, till the patient's death, six months later. At the seventh cervical (Fig. 103, a) the cord presents only the usual as- cending degenerations, but at the eighth cervical (Fig. 103, b) opaque tracts extend through the grey and white matter, and adjacent to these there is everywhere an extensive destruction of nerve-fibres. In these tracts within the lateral columns a large number of very minute nerve-fibres can be seen, each consisting of a fine axis-cyhnder sur- rounded by myelin (Fig. 104, c). The fibres are smaller than any met with in the normal cord. The appearance is as if there had been an irregular ascending myelitis, which had extended up the cord as high as between the seventh and eighth cervical segments, and from the lower extremity of the normal fibres there had occurred a growth of new fibres such as effects the regeneration of nerves.* We seem to have here an actual process of renewal of fibres that had been destroyed by such inflammation as has caused the empty spaces * For these sections I am indebted to Dr. F. G. Penrose. Unfortunately I have been UDable to obtain any other sections of this part of the cord. ACUTE MYELITIS. 357 Pig. 103.—Ascending myelitis from fr.ictureof spine completely destroying the cord i'i the mid-dorsal region. A, from the seventh cervical, presents only ascending degenerations in post. med. col., direct cerebel. areas, and ant.-lat. ascending tract. B, from the eighth cervical, presents also numerous areas of finely granular aspect under a low magnifying power, the finer structure of which is shown in Fig. 104. Fig. 104.—From the outer part of the front of the lateral column in B, Fiy which their myelin stains more deeply than normal; afterwards they become narrowed, and the axis-cylinder is often irregularly enlarged. Ultimately many or all the fibres disappear from the affected area. Here and there the destruction of fibres may be out of proportion to the increase in the interstitial tissue, so that thickened and often granular trabeculae enclose empty spaces. This is seen in the lower small illustration in Fig. 108 ; it is apparentlv the result of the participation of the nerve-fibres in the inflammatory process during a more general stage, in which all the elements of the tissue were involved. In the recent state, products of degeneration, granule corpuscles, &c, may be found abundantly in the altered * From a section by Prof. Pierret, kindly lent me by Dr. Drcschfeld. 384 SPINAL CORD. regions. The walls of the vessels are thickened, and by this thickening the cavities of the arteries may be ultimately lessened; those of smaller size may even be closed. Not only is the wall of the arteries thickened, but around them the increase of inter- stitial tissue is often greater than elsewhere, so that the appearance is as if it had spread thence into the adjacent structures. Undue signi- ficance has been attached to this condition, especially in old patients with arterial degeneration; it has been regarded as evidence that arterial disease sets up the myelitis, but it is a common appearance in all forms of chronic myelitis, and also in the later stages of acute inflammation. It is probably due to the greater activity of the process in the immediate vicinity of the vessels, and to the share taken by escaped leucocytes in the formation of new interstitial tissue. The peripheral arteries, moreover, occupy tracts of neuroglial and fibrous tissue proceeding from the pia mater, and the increase of interstitial tissue is connected with these; some of it is, on this account, found in the vicinity of the arteries. In the grey substance there is a similar increase of connective- tissue elements, so that the altered part takes a deeper stain with carmine than the normal grey substance, and has a denser structure, from the greater amount of supporting tissue. The nerve-elements become atrophied; the ganglion-cells, at first swollen and rounder, afterwards shrink, until ultimately they may be reduced to small angular bodies, and they even may disappear. The nuclear corpuscles about the central canal are often increased in quantity, and the canal obliterated, but this condition is so common in otherwise normal cords that no importance can be attached to it. A considerable increase of tissue about the central canal, closing it below and causing it to be dilated above (Fig. 109, " syringomyelia"), has been ascribed to chronic inflammation around the canal, but the abnormal tissue is probably always of gliomatous nature, consisting of a development of tissue that is in congenital excess, owing to an arrest of develop- ment. The pia mater is greatly thickened over the inflamed parts, as already stated, and in some cases the affection of the membrane is general, and that of the cord most intense beneath it—a condition termed " chronic meningo-myelitis." It is this form that is shown in Fig. 109. The tracts of new tissue that pass into the cord are dense and wide. As already mentioned, this change may be accompanied by a deeper and sometimes a more diffuse inflammation, as in a, Fig. 109, in which the affection of the cord is greater and that of the mem- branes less than in b. The chronic myelitis that occurs in syphilitic subjects may present no specific characters. In some cases, however, the cell-formation has been abundant, and has been associated with a tendency to fatty degeneration in the older portions of the lesion, and with a similar degenerating hyperplastic inflammation of the pia mater. The condition is, however, clearly one of chronic inflamma- CHRONIC MYELITIS. 385 tion, and not of a syphilitic growth.* Nevertheless an actual growth does sometimes co-exist with a focus of syphilitic myehtis ; it is pro- PlG. 109.—Chronic meningo-myelitis, due to alcoholism. Syringo-myelia, congenital, with central gliomatosis. A, lowest part of cervical enlarge- ment ; pia mater thickened, and from it tracts of tissue extend into the cord. The greater part of the section is the seat of a diffuse myelitis, in which the nerve-fibres could be seen with difficulty, and were sepa- rated by inflammatory products. The grey matter was also affected, and the nerve-cells much changed. The clear spaces in the right ant. cornu appeared occupied by products of degeneration. Central canal greatly dilated and surrounded by new growth, which in B (lumbar sec- tion) has obliterated the canal and thus caused its dilatation above. In this section the myelitis is chiefly peripheral, and the grey matter has, for the most part, escaped. bable that in such cases the growth is usually the primary change. This may be distinguished by the indications of compression and displacement of the adjacent elements of the cord, a condition which shows that there is an actual new formation. The more recent the inflammation, the larger is the proportion of cells and nuclei in the interstitial tissue; the longer it has existed, * See Moxon, « Guy's Hosp. Reports,' 1871, and Charcot and Gombault, 'Arch. de Physiologie,' 1873. VOL. I. 25 386 SPINAL CORD. the greater is the amount of fibrillation it presents. The very chronic indurating forms are sometimes called " sclerotic myelitis," or "focal sclerosis of the cord." From the various areas of inflammation secon- dary degenerations proceed, ascending or descending, and these may complicate the aspect of the disease—a fact which has not always been sufficiently considered in interpreting the morbid appearances. Symptoms.—The symptoms of chronic myelitis vary much according to the character of the morbid process. For the most part they cor- respond in character to those that are produced by acute inflamma- tion, differing, however, in their mode of onset. It is therefore not necessary to repeat them in detail. Different cases may manifest almost every symptom that can be produced by disease of the spinal cord There may be various motor and sensory paralyses, contrac- tures, and even muscular atrophy, but their common feature is their gradual, and often successive development. In the most common form, focal myelitis of the dorsal region, partial or transverse, the symptoms are paraplegic. They differ but little whether there is a single area of disease, or whether several foci near together implicate adjacent structures. Motor power is usually impaired far more than sensi- bility. Subjective sensations are often prominent and early symptoms, whether there is anesthesia or not,—tingling, " pins and needles " in the legs, a sensation as if fur or wool covered the skin, sometimes with dull pain in the legs and back, especially after exeation, and commonly also with a well-marked girdle pain at the level of the chief lesion. Some loss of sensibility, partial in kind or in seat, will often be found if carefully searched for, but there is not often absolute loss of sensa- tion except in the rare cases of intense local sclerotic myelitis, by which conduction may be arrested as completely as by a growth. The onset of the motor weakness is gradual; many months may pass before the power of walking is considerably impaired. As the le^s get weak, excess of reflex action is developed (unless the reflex struc- tures are damaged). The knee-jerk is increased; foot-clonus occurs when the legs are in certain positions ; and a tendency to spasm gradually develops, and increases to the condition typical of " spastic paraplegia." The sphincters frequently share the impairment of voluntary power. Co-ordination of movement is sometimes affected, usually manifested as general unsteadiness, and defect of equilibrium, rather than as pure ataxy. The symptoms may come on simultaneously in the two legs, or one may be affected before the other, and occasionally the paralysis reaches a high degree in one leg while the other still possesses fair strength. When one half of the cord is affected almost alone (as in the lesion shown in Fig. 109), there may even be a crossed paralysis of motion and sensation. Chronic polio-myelitis is often regarded as a distinct variety, but much confusion has arisen from the fact. If chronic myelitis de- velops in the cervical and lumbar enlargement, muscular wasting is CHRONIC MYELITIS. 387 usually added to the other symptoms. Similar atrophy occurs also in the widely diffused form of chronic myelitis, in which almost all parts of the cord suffer, and it may, indeed, be the most conspicuous symptom. It is always irregular in distribution in these cases, and it may be combined with other symptoms, palsy and anaesthesia, also irregular in extent and seat. The muscular wasting varies in the rapidity of the development, according to the character of the inflam- mation, and there are corresponding variations in the relations to it of the loss of power in the muscles, and also in the electrical reactions they present. In very chronic cases there is a slow failure of electrical irritability to both currents ; in others of more rapid course the voltaic irritability persists longer than the faradic irritability, and there may be a distinct degenerative reaction. The symptoms may com- mence in the arms or in the legs, but they ultimately become general in most cases, and, according to the place of their commencement, may seem to have an ascending or descending course. Occasionally the disease begins in the dorsal region, and after a time, perhaps years, it spreads to the enlargements, and the muscular wasting is added. The course of chronic myelitis is usually slow and progressive. The symptoms often increase so gradually as only to attain a considerable degree at the end of two or three years. At any stage the progress of the disease may cease. The chronic course may be varied by occasional more rapid increase of the symptoms, due to subacute or even acute processes in the diseased parts. Every degree of chronicity is met with, and subchronic cases, in which the symptoms develop in the course of a few months, effect a gradation to the acute and sub- acute forms of myelitis. The duration of the disease varies from six months to ten years or more. Thus in one case the symptoms slowly increased during about seven years, and then became stationary, and the patient died twenty-three years after the onset. Diagnosis.—The diagnosis of chronic myehtis rests on the slow deve- lopment of symptoms indicating a random process in the spinal cord, i. e. a process which damages irregularly structures of various functions, and thus cannot be looked on as a " system disease." The maladies from which it has to be distinguished differ according to the seat and character of the inflammation. Dorsal transverse or focal myelitis may be confounded with compression of the cord, with a tumour in it, and with primary lateral sclerosis. The distinction from pressure rests on the absence of a cause of compression, such as bone disease, —especially the absence of the signs of a morbid process outside the cord, preceding those of damage to the cord itself, e. g. the pains that indicate irritation of nerve-roots. A tumour within the spinal cord also causes, in most cases, more irritation of the root-fibres than does chronic myehtis. If myelitis involves one half of the cord much more than the other, the symptoms may closely resemble those of an intra-medullarv growth. But a tumour never causes much 388 SPINAL CORD. damage to one half of the cord without interfering considerably with the functions of the other half, and the symptoms in chrome myelitis may be strictly unilateral. The distinction from primary spastic paraplegia, the so-called " primary lateral sclerosis," is often one of some difficulty. The motor state of the legs may be identical in the two diseases ; in each there is the same extensor spasm, and in each there is a slow, gradual, and apparently simultaneous onset of the weakness and spasm. The distinction is that in primary spastic paraplegia the symptoms are purely motor; there is no indication that the lesion extends beyond the motor structures. In chronic myelitis, on the other hand, there is such indication, either by the impairment of sensation, or by the presence of a girdle pain. This distinction is sufficient in the majority of cases. The distinction from insular sclerosis is in many cases difficult. By Oppenheim and others, indeed, it is asserted that most cases described as chronic myehtis are really cases of disseminated sclerosis. The presence of cerebral or bulbar symptoms would naturally suggest such a diagnosis in a given case. But in insular sclerosis any very obvious affection of sensation is unusual. The form that involves the grey matter has to be distinguished chiefly from pachymeningitis and degenerative muscular atrophy. In pachymeningitis the muscular wasting may be similar, but anaesthesia is usually much more considerable in range and in degree, and there is more pain in the limbs. If there are similar symptoms in both arms and legs, myelitis is far more probable than pachy- meningitis, since the chronic inflammation of the membranes is less extensive than that of the cord. From progressive muscular atrophy, the chief difference is in the random distribution of the wasting, the absence of symmetry, and indications of irregular damage to other structures in the cord, as the occurrence of pain and of loss of sensation. But it must be remembered that, by some authorities, most cases of chronic spinal muscular atrophy are regarded as due to chronic myelitis. For the distinction from other less common diseases, the reader must be referred to the description of them. Like all other organic diseases, cases without wasting of the muscles, occurring in females, are often regarded as " hysterical paraplegia; " the distinction rests on the points already described. It is, however, one of the diseases in which the least excusable enors in diagnosis occur, and in which their effects are often the most disastrous. Pbognosis.—Chronic myelitis is a very grave disease, on account of the intractability of the morbid process, its frequently progressive tendency, and the persistence of damage which is slowly produced. But cases vary widely, especially in the two former features, and it is a disease in which general prognostic rules can scarcely be formulated. The observed tendency of an individual case is alone a trustworthy guide. Arrest of the disease is often obtained, but actual recovery CHRONIC MYELITIS. 389 is rare. The prognosis is little affected by the seat or extent of tie process, except that the implication of the grey matter of the enlarge- ments is generally an unfavorable indication. The severity of the lesion, as shown by the degree of the symptoms, is significant chiefly in cases of long duration, and is subordinate to the course and mode of onset. If it can be arrested, the prospect of improvement is better in proportion to the slowness with which the disease has developed and the shortness of the time the symptoms have lasted. In general, more- over, the prospect is better, the fewer the foci of inflammation, in males than in females, and in cases of uniform than in those of recurrent or relapsing course. Preceding syphilis does not materially modify the prognosis ; hence the great importance of the diagnosis from syphilitic growth, in which suitable treatment has a most certain effect. The ultimate danger to life is least in focal myelitis in the dorsal region ; it is greatest in the disseminated form, especially in the less chronic cases with a tendency to sloughing of the skin, and in the more chronic forms with muscular wasting. The indications drawn from the invasion of the respiratory muscles, and from the presence of any of the complications that so often terminate life, are the same as in other diseases of the cord. Treatment.—The first and most important measure is the improve- ment of the general health, by rest, change of air, and tonics. All causes of physical and mental depression must, as far as possible, be removed. Over-exertion, and even fatigue, should be avoided, and the patient should be kept, as far as possible, from exposure to cold. Absolute rest for a short time is often useful at the outset of the treatment, especially when there has been a somewhat rapid develop- ment of symptoms. In cases of purely chronic course absolute rest should not be maintained for more than a few weeks, or the patient may find it hard to regain his former muscular power. Counter- irritation at the situation of the disease is often useful, and most so in cases in which there is spinal pain or tenderness. Repeated sinapisms or blisters may be employed, but a mild form of the actual cautery is on the whole the most useful. A superficial burn or even slight vesication is sufficient on each side of the spine opposite the affected part, and it is best effected by means of the Paquelin cautery. It should be repeated as soon as the skin has healed, and if linear cauterisation is adopted the fresh line can be made beside the old one. A hot douche to the back, at a temperature of 103° or 104° F., applied daily, has been strongly recommended by Brown-Sequard. Warm brine baths, and various thermal mineral waters, have been also said to do good. A sea voyage is often of service, combining as it does the maximum of fresh air with the minimum necessity for exertion. Drugs, unfortunately, often fail to influence the morbid process, but nevertheless they are occasionally useful, so as distinctly to justify their careful trial in most cases; and it is important to remember that those that are useless in one stage or period of the disease may yet be of 390 SPINAL CORD. unquestionable service at another stage. Tonics, as quinine and iron, should be given if indicated. Most of the measures recommended, and precautions advised, in the treatment of acute myehtis are needed in the chronic form, and it is therefore superfluous to repeat them. Those drugs that most deserve a trial are arsenic, small doses of mercury (such as ^V gr- of the red iodide), and iodide of iron. Energetic mercurial treatment rarely does good, even when the patient has had syphilis, and sometimes it does harm. Iodide of potassium seems to have little influence on the disease. Nitrate of silver, ergot, and phosphorus have been recommended. Strychnia is chiefly useful in cases in which there is muscular wasting, but is of far less value than in the degenerative muscular atrophy. The treatment of other symptoms is that suitable in primary spastic paraplegia or progressive muscular atrophy, and described in the account of those diseases. COMPRESSION OF THE SPINAL CORD. Compression of the spinal cord is a common consequence of various morbid processes. Inflammation is almost always excited by the pressure, and interference with function occurs, partly from the pressure and partly from the resulting myelitis. The symptoms pro- duced have, in different cases, many characters in common, although they vary according to the mechanism of the compression and the acuteness of the inflammation. It is only when there are indications that an acute myelitis has damaged the nerve-elements that we are justified in regarding the interference with function as an effect of the inflammation. Causes.—The morbid processes that may compress the cord are those that involve an encroachment on, or occupy part of, the vertebral canal. The chief are the following:—Disease of the bones of the spinal column, especially caries ; growths in the spine ; aneurism eroding the bones and then compressing the cord; growths in the membranes; thickening of the dura mater. These processes have usually only a small vertical extent, and the pressure they exert rarely extends over more than a few inches. PathologicAL Anatomy.—The cord usually presents evidence of the compression it has endured in considerable narrowing at the spot, where it may be indented and flattened, or cylindrical. Sometimes the reduction in size is extreme ; for an inch or so the cord may be reduced to one thiid of its normal diameter, and it has even been found no thicker than a crow-quill. An example of flattening is COMPRESSION. 391 J, itt. shown in Fig. 110. On the other hand, there is sometimes very little narrowing to be discerned. At the compressed part the cord is usually red in tint if the com- pi essio 1 is recent, but grey if it has lasted for so.ne time ; its consistence is lessened in early cases, and increased in those of long duration. The change in colour and con- sistence is due to the inflammation of the substance of the cord which always results from pressure, and may often be traced for some distance above and below the com- pressed part. When there is much com- pression there is always much inflammation, but considerable myelitis may occur when the amount of compression is slight. The inflammation may be chronic and slow, developing in proportion to the pressure, or it may be subacute or acute, even when the pressure is gradual. The signs of inflam- mation are very distinct on microscopical examination, and resemble those in other forms of myelitis. There is a general in- crease in the interstitial tis-ue; in this, at first, various cell-forms may l>e found, but it ultimate]v presents the appearance of a dense reticulum. The nerve-elements un- dergo degeneration, and abundant masses of myelin, granule corpuscles, and corpora amylacea are visible in the fresh state or in glycerine preparations of the hardened cord (Fig. Ill, c). Many nerve-fibres per- sist, however, with a narrowed sheath of Fig. 110.—Compression of the spinal cord and pres- sure-myelitis, in a case of caries of the spine. I>, mid-dorsal region, mar the chief point of greater compression; the cord is narrowed from before backwards, and is uniformly damaged by inflam- mation, so that the grey substance can scaret ly be distinguished. C, 1£ inches higher up, shows a slighter degree of myelitis, still extending through the whole thickness of the cord. B, first dorsal; the myelitis is much slighter and the chief disease is in the posterior columns, in which ascending degeneration occupies the post.-median columns and extends outwards into the post.-external columns. E, H inches below the point of greatest pressure; inflammation still extending through all the elements of the cord. F, 2 inches lower down, shows only descending degeneration in the pyramidal tracts, anterior and lateral, and also the "comma-shaped" descending degeneration in the anterior part of the post.-external column. In G, at the lowest part of the dorsal region, the comma- shaped degeneration has ceased, and only that of the pyramidal tracts remains. (From preparations by Dr. F. G. Penrose.) 302 SPINAL CORD. myelin, and it is probable that these regain the power of conducting, in spite of the persistence of considerable, and even dense sclerosis in Fig. 111.—Pressure-myelitis; portions of the section D in Fig. 110 more highly magnified. A, from the grey matter, numerous angular end fusiform cells; vessels with walls thickened by a growth of cells, nar- rowing the cavity, which in some is obliterated. B, from the white columns ; thickening of the interstitial tissue, nerve-fibres in part destroyed, in part narrowed; a vessel with thickened walls. C, glycerine preparation from white substance; abundant products of degeneration of the nerve-fibres, in part aggregated into granule masses. D, section of a nerve-root passing by compressed area; increase of interstitial tissue, many nerve-fibres narrowed, some with swollen axis-cylinders. the part. In extreme cases all the fibres seem to be destroyed at the point of chief compression, but there is never an actual division of the cord itself. The grey matter can scarcely be distinguished from the white, even with the microscope, and the ganglion-cells become shrunken and atrjphied. The walls of the small vessels are often thickened by spindle-cells, disposed more or less concentrically to the cavity, which is encroached upon and may be obliterated (Fig. Ill, a, b), a process that must add to the degree of damage to the cord. The signs of inflammation gradually lessen above and below the compressed part, but often extend for some inches in each direction. Beyond its limits the usual ascending and descending degenerations may be traced (Fig. HOj. The nerve-roots passing by the seat of compression suffer from the pressure, and from interstitial inflammation excited in them. They are usually grey in tint and ultimately waste, and may even be reduced to fibrous threads. The microscope shows increase of the interstitial tissue, wasting of many nerve-fibres (Fig. Ill, d), and enlargement of some axis-cylinders. COMPRESSION. 393 Symptoms.—The effects vary much according to the degree of pressure, its rapidity, its direction, the amount and character of the inflammation produced, the amount of damage to the nerve-roots, and the position of the disease. The symptoms in most cases enable the fact of slow compression to be inferred, even when there is no indication of the cause. They are of two classes: (1) interference with the function of the nerve-roots at the level of the morbid process; (2) interference with the functions of the cord itself. The cord symptoms consist chiefly in impaired conduction, manifested in the parts below the lesion. The central functions of the cord (reflex action, &c.) at the level of the lesion are abolished by the pressure, but the symptoms of this abolition are often lost in those of the damage to the nerve-roots. Of the root symptoms the most constant is pain, extending along the course of the nerve-fibres, and through the area of their distribu- tion. The seat of these pains depends on the position of the disease; they may be felt in the arms, around the thorax or abdomen, or in the legs. They are usually sharp pains, resembling neuralgia in character, sometimes accompanied by tender points. Occasionally, when felt in the limbs, they are referred especially to the joints. The pain may be intermitting or constant. It may even be absent, as in a case of aneurism of the arch of the aorta already referred to. It may exist alone, for a long time in a disease that increases slowly, and sometimes may be the only symptom, although some compression of the cord occurs. With it there is usually hyperesthesia of the skin, often intense. After a time anaesthesia develops in irregular areas, in spite of the persistence of the pain,—the condition termed " anaesthesia dolorosa." Irritation of the motor nerve-roots may cause painful contracture of the muscles, but this is, on the whole, rare, and the chief motor symptoms are due to the interruption of the fibres—- muscular weakness, gradual in onset, and accompanied by wasting. The rapidity of the atrophy varies much, and with it the electrical reaction. When slow, there may be merely a progressive diminution in irritability to faradism and voltaism ; when rapid, there is often the degenerative reaction, and sometimes the " mixed form," from the partial damage to the fibres that supply a muscle. These local root symptoms are usually the first, and to them are added, after a time, the indications of interference with the function of the cord itself. There is weakness in the parts supplied from the cord below the lesion. The loss of power is usually gradual, but sometimes comes on rapidly, even in the course of a few hours, when an acute myehtis is set up by the compression. With the weakness there is a marked and early increase in the superficial reflex action, more constantly conspicuous than in most other diseases of the cord, and therefore of some diagnostic importance. The myotatic irrita- bility is also increased, a foot-clonus being almost always pi-esent. Pains in the legs may occur, even when the disease is above the 391 SPINAL CORD. lumbar enlargement, usually dull and aching. There is often formica- tion and tingling. There may be no impairment of sensibihty in the parts below the lesion, even when there is complete motor palsy; in many cases, however, there is some sensory loss, complete only when the spinal lesion is very severe. Conduction of painful impressions may be delayed, sometimes for thirty or even forty seconds. When the pressure is lateral, one leg may be first and most affected, but the other side is usually soon involved, since neither the mechanical effect nor the inflammation remain limited to one side of the cord. The sphincters are often affected. The tendency to the formation of bed- sores is rarely great, unless the lumbar enlargement is compressed or myelitis descends into it. The course of the symptoms varies according to that of their cause. When an acute myelitis has been set up, improvemsnt may occur for a time even if the cause of pressure is slowly progressive. This is true also of root symptoms when they are rapidly developed. If the compression ceases to increase, the cord may recover its conducting function, although it remains narrowed. Sensation is often regained in the legs when motion remains absent, but both motion and sensation may be regained although the narrowing of the cord persists. It has even been found no larger than a goose-quill at the compressed spot, although the paraplegia had passed away. In such a case many narrowed nerve-fibres are found in the section of the comp/essed portion, and it is probable that many axis-cylinders persist, with an envelope of myelin so narrow as to be recognised with difficulty, but which suffices for their conducting function. Under slow pressure the axis-cylinders may not suffer interruption, although the myelin dis- appears. Regeneration of axis-cylinders, as in the peripheral nerves, is also possible. In some cases, especially when a considerable myelitis has been set up, the motor path may recover, but the posterior columns remain affected, so that power returns, but without co-ordination,— " secondary ataxy " resulting. The Diagnosis of slow compression rests on the root and cord symptoms already described, and especially on their coincidence with a cause of compression. Of the former, the sensory symptoms are the most characteristic. In many cases other indications of the compressing disease assist the diagnosis. These vary in character; the most frequent is considerable local tenderness of the spine. If root symptoms are absent the diagnosis is much more difficult, unless the morbid process manifests itself externally. If there is a suspicion of compression in a case of slow paraplegia, an early and considerable excess of superficial reflex action gives additional weight to the suspicion. Even without any other symptoms to indicate com- pression, this is suggested by symptoms which begin on one side and gradually spread to the other. The chief disease from which compression of the spinal cord has to be distinguished is a subacute or subchronic transverse myehtis. ACUTE ATROPHIC PARALYSIS. 395 Besides the indications of a cause of compression already mentioned, the chief distinction depends on the presence of symptoms indicating irritation of the nerve-roots, and especially on the fact that these sym- toms precede those of the lesion of the spinal cord itself. Although a very chronic myelitis is occasionally attended by much irritation of the nerve-roots, the symptoms of this succeed, instead of preceding, the damage to the cord, and the course of chronic myelitis is often much slower than is that of most forms of slew compression. The distinction from a growth within the spinal cord rests chiefly on the early occurrence of impairment of the central and conducting func- tions of the cord, and also on the partial distribution, and often slower course, of the symptoms. The effects of an intra-medullary growth vary widely in different cases, and if there is an early irritation of root- fibres, the distinction may have to depend on the presence or absence of the signs of an external compressing process. The diagnosis of the cause of compression is often much more difficult than that of its occurrence The facts that the patient is in the first half of life, and that he inherits a tubercular tendency, suggest caries. Slightness of root symptoms is also in favour of caries or a tumour within the spinal cord; the presence of these symptoms does not, however, render caries less likely, unless the pain is extremely severe and is greatly increased by movement,—characters that should always suggest a growth in the bones of the spine Root symptoms extending over a considerable vertical area suggest pachymeningitis. Additional details of the differential diagnosis will be found in the account of the several compressing diseases. Prognosis and Treatment.—The prognosis depends on the cause, and the amenability of this to treatment. As a general rule, however, the more rapidly the cord symptoms develop, the more chance there is of improvement, because the greater share does inflammation take in their production. The treatment is that of the cause of the com- pression, and that of myelitis. ANTERIOR POLIO-MYELITIS; ATROPHIC SPINAL PARALYSIS. In certain diseases of the spinal cord, wasting of the muscles is a prominent symptom. In these the lesion involves, exclusively or in part, the anterior grey cornua, and the muscular atrophy depends on the destruction of the nerve-cells, from which the motor nerve-fibres proceed, and on the consequent degeneration of the fibres. The mus- cular wasting does not depend on the nature of the lesion; it occurs equally whether the nerve-cells are destroyed by haemorrhage, by in- 396 SPINAL CORD. flammation, acute or chronic, by slow degeneration, or by pressure. But the rapidity with which the destruction occurs influences the character of the symptom. Time is required for the change in the nutrition of the muscles; one or two weeks elapse, even in the most acute cases, before wasting is distinct. The nerve-cells also form part of the voluntary motor path, and their disease at once interrupts this ; hence, in acute cases, paralysis is rapidly developed, and the atrophy succeeds it after an interval. In chronic lesions, on the other hand, the changes in the cells and muscles progress so slowly that the weakness and wasting appear to come on together. The wasting may even seem to precede the weakness, but a careful examination will show that power is defective as soon as there is distinct atrophy. It is customary to separate the two groups by terming those in which the palsy precedes wasting, " atrophic spinal paralysis; " and those in which wasting is apparently simultaneous with weakness, " spinal muscular atrophy." The atrophic paralyses are due to an acute or subacute process in the anterior cornua. The lesion is probably, in most cases, inflamma- tory in character, a cornual myelitis, or "polio-myelitis" (Kussmaul). In some cases, which differ chiefly in the suddenness of the onset, it is probable that the lesion is hemorrhage and not inflammation. The chronic atrophies are due to a slow degeneration of the cells and fibres. Between the two forms, however, we meet with others of inter- mediate course, subacute or subchronic, due to processes of correspond- ing character,—usually inflammation. Acute Atrophic Paralysis ; Acute Anterior Polio-myelitis. Infantile Paralysis ; Essential Paralysis of Children. Acute atrophic paralysis is a disease in which voluntary power is lost in the course of a few hours or days, and in which some of the paralysed muscles undergo rapid wasting while others recover. The onset of the palsy is often preceded or accompanied by indications of general disturbance. The muscles which waste usually remain weak, and contraction of their opponents may lead to permanent distortion of the paralysed limbs. Although it is usually a form of acute myelitis, its characters and course are sufficiently special to make its separate consideration desirable. The disease is the most common form of paralysis in young children, and has hence received the name of " infantile paralysis." Before anything was known of the lesion on which it depends, it received (from Billiet and Barthez) the unmean- ing designation of the " essential paralysis of children," a term that is falling into merited disuse. The spinal lesion was first demonstrated by Prevost (1865), and soon afterwards by Lockhart Clarke and by Charcot and Joffroy. Its constancy has been abundantly proved by numerous observations during the last thirty years. The occurrence of ACUTE ATROPHIC PARALYSIS. 397 similar symptoms in adults was noted by Yogt (1658) and Duchenne (1864). Etiology.—The disease occurs at all ages, but is ten times as frequent in the first decade as in all the rest of life. It is, moreover, especially a disease of later infancy. Of the cases in early life, three fifths occur in the first three years of life, nearly one fifth in each year. The numbers in each successive year (of 214* cases of which I have notes) were—in the first 54, the second 58, third 39, fourth 17, fifth 23, sixth 8, seventh 4, eighth 6, ninth 5. Of the cases that begin during the first year, nearly all begin in the second six months ; the earliest of the series occurred at two months, but one at the twelfth day is described by Duchenne. The friends often date the disease from birth, but there is no real evidence of its intra- uterine development. After childhood it is most frequent between ten and twenty, and very rare over forty. One case, however, occurred at sixty-three. Many supposed subacute cases in adults have been examples of multiple neuritis. In childhood the two sexes suffer nearly equally (males 133, females 103, in 236 cases), but after ten the malady is almost confined to the male sex. The influence of heredity is small, but a family tendency to suffer may now and then be traced; two and even three brothers or sisters have been affected (Seeligmiiller, &c). One of my own patients had a sister, and another two cousins, affected with the same disease. When more members of a family than one are affected, they usually suffer simultaneously. The inherited tendency may be indirect; of a patient in whom the disease came on in adult life, two brothers had suffered from hemiplegia and an uncle from paraplegia. The disease presents a remarkable relation to season, occurring far more frequently in summer than in winter. Sinkler, who first called attention to the fact, found that in Philadelphia four fifths of the cases commenced in the five hot months, May to September. In this country the relation is equally apparent; three quarters of the cases occur during the hottest third of the year, June to September. The distribution of 160 cases was as follows:—3 occurred in January, 5 in February, in April 2, May 3, June 22, July 32, August 37, September 25, October 15, November 8, December 8. In many cases the weather was very hot at the time; in some, however, the disease came on in cooler weather after a hot period. It would therefore seem that the heat generally acts as a remote cause, and is only occasionally concerned directly in the exciting mechanism. The fact is the more important because cold has long been regarded as the most potent exciting cause. That exposure to cold is an occasional cause is certain, although the number of cases in which it can be traced is not large ; and it is usually a general and not a local exposure, and has not often been immediately preceded by exposure to heat. Exceptions are * Of these 214 cases 116 were seen and analysed by Sir W. Gowers, and 98 by Dr. James Taylor. They include both hospital and private cases. 398 SPINAL CORD. chiefly met with in adults. Thus one patient, aged sixteen, when perspiring from a long ride after the hounds on a hot day in September, lay down on a sofa beneath an open window from which a draught blew on his back. Two days afterwards the first symptoms com- menced. In another case the onset followed a day on a steamer in cold, wet weather, preceded by much paddling in the sea during extreme heat. I have several times known the disease to be due to sitting on damp grass. Two or three days is the interval which usually elapses between the exposure to cold and the onset of the symptoms, but great variations are met with, and the constitutional disturbance may commence within twenty-four hours of the exposure. Over-exertion in walking seems occasionally to aid in exciting the disease; in some cases the child has walked far more than was proper the day before the onset, and in others habitual over-exertion has been permitted. A traumatic influence, such as a fall, occasionally pre- cedes the onset in such a way as to make its influence probable. Thus, in one severe case, a boy eight years old was thrown over the head of a donkey, and the onset occurred five days afterwards. A girl of four fell off a chair, striking her head, and was stunned for a moment; two days later she was sick and feverish; the temperature (101°) continued raised till the sixth day, when general loss of power was found, and the residual state was atrophic palsy of both legs and the right deltoid. The cases following falls and over-exertion present the same relation to season as do the rest. There is no proof of any relation between the disease and the process of dentition The period of dentition coincides with the rapid functional development of the nervous system which succeeds its structural development in the first few months of life. Moreover this period is often one of deterioration of health, in consequence of changes of diet and other causes. The disease occurs before and after the period of teething, and it exhibits no increase in frequency at the period of the second dentition. Many children are perfectly well at the time when the disease occurs. A few are in conspicuously defective health. Thus in one case the child had been rendered feeble by long-continued diarrhoea. I have only once seen the disease in the subject of inherited syphilis. It has been thought to be occasionally secondary to acute febrile diseases, but the frequency of the relation has been unquestionably overrated; in some supposed cases in adults there has been multiple neuritis only, and in children initial general disturbance is constantly mistaken for an independent general disease, and the opinion is often maintained after the discovery of the paralysis, which is then sup- posed to be of secondary origin. Thus in one case initial pyrexia, headache, and vomiting were supposed to indicate scarlet fever. Paralysis of all four limbs came on, with difficulty in swallowing, and the latter was supposed to render certain the diagnosis' of scarlet fever, although there was no sore throat or rash. In older children ACUTE ATROPHIC PARALYSIS. 399 and adults the disease is often thought to be secondarv to rheumatic lever, in consequence of the rheumatoid character of the pains. The error is the more likely to occur if the symptoms follow exposure to cold. It is conceivable that catarrhal affections may be produced by the exposure to cold which induces the disease; but of the 214 cases referred to above, not one was related to any acute specific disease, or to rheumatic fever. Chronic alcoholism has been thought to be a cause in adults, but it is probable that most cases supposed to be due to this influence have been instances of multiple neuritis. Symptoms.—The general characters of the symptoms have been already mentioned—an acute onset, often with constitutional disturb- ance ; paralysis, at first wide-spread, afterwards passing away, except from a region in which the muscles rapidly atrophy, and in which, although partial recovery may occur, more or less weakness and wasting persist. The general disturbance, which is apparently due to a morbid blood-state, may be severe or slight. In most oases there is pyrexia, with its usual accompaniments, headache, prostration, loss of appe- tite, restlessness. Vomiting is very common, and often causes the illness to be mistaken for stomach disturbance. Occasionally there is also diarrhoea. These symptoms of general disturbance usually last for a few days, sometimes for only a few hours, and they are occasionally, but not often, absent. The palsy develops in most cases in the course of this disturbance. A common history is for a child to seem ill and feverish, to be put to bed, and the next morning to be found to have lost power. In other cases the febrile disturbance lasts for several days before the paralysis comes on. But the relation of the general disturbance to the onset of the paralysis presents great variations, which appear (from a comparison of cases) to be independent of any variations in, or special features of, the spinal symptoms. The constitutional symptoms occasionally succeed the onset. Thus a child, well one day, was found next morning to have both legs paralysed, and was feverish and sick ; the general disturb- ance continued for a week. The elevation of temperature is usually moderate in degree; an example of its character, in what may be regarded as a fairly typical case, is that of a child whose tempera- ture on the second day of illness was 101-2°; on the third, 101°; the fourth (on which the palsy developed), 100°; the fifth, 99'5° ; the sixth, 98°. It is usually, as in this case, highest at the commencement, and sometimes reaches 103°, 104°, or even in rare cases 105°. The constitutional symptoms are present in most of the cases in which a fall appears to excite the disease, and are of the usual character ; they are as marked in the cases that appear to be spontaneous as in those that follow exposure to cold. Convulsions occasionally attend the onset, chiefly in young children. In some instances, moreover, the initial symptoms are those of severe cerebral disturbance. Thus one child had repeated general convul- 400 SPINAL CORD. sions during thirty hours, and afterwards was in a state of deep coma for thirty-six hours, the temperature at the onset being 105°. This was succeeded by slighter pyrexia and prostration for three weeks, and it was only at the end of that time that general loss of power was found to have come on. The arms recovered, but atrophic palsy per- sisted in the legs. In another case, a child of seven months became ill, febrile (1028°) and comatose with pin-point pupils; it remained in that state for four or five days, and then gradually recovered, but with general powerlessness, rigidity of the legs, and tenderness of legs and back. The rigidity and pain passed away, but the right deltoid and, to a less degree, the biceps and triceps, and the whole of the right leg remained paralysed, and presented characteristic atrophy. In adults there is sometimes marked somnolence before the onset, and occasionally slight cerebral symptoms, such as diplopia, giddiness, or (very seldom) delirium. A medical student found, one day, that he saw double; on the next day he felt giddy, and became feverish (102°); he slept for forty-eight hours, and on the fourth day found his right arm was weak; atrophy of the deltoid, &c, followed. The cerebral symptoms usually pass away together with the indica- tions of general disturbance, and hence are probably due to the blood- state, but occasionally slight facial weakness has persisted for several wetks. In rare cases the onset is accompanied by symptoms of slight transient spinal meningitis, which must be regarded as a coincident effect of the cause, since the membranes may be affected early. Thus a child, after being feverish and vomiting for two days, became universally rigid, so that strychnine poisoning was thought of. The rigidity passed away two days later, when the right arm and leg were found to be paralysed. Another child presented all the sym- ptoms of spinal meningitis a week after the onset of paralysis of the' arm, and as they passed off the leg also was found affected When the general illness is severe, the paralysis is often not discovered for some time, especially in a child; the immobility of paralysis is often mistaken for the inertia of prostration. In older children and adults another common initial symptom is the pain already mentioned, sometimes referred to the muscles, some- times to the limbs generally, occasionally to the course of the nerves. It is often absent, but may be very severe and accompanied by extreme tenderness of the limbs. In such cases the pain may be supposed to be in the joints, because it is produced by moving them, when it is really in the nerves, which are mechanically disturbed by the move- ment of the joints. In these cases there is neuritis, which may come on at the same time as the palsy, although independent of it. The joints themselves may be the seat of pain, and, when the exposure to cold has been severe, inflammation of one or more joints has been known to come on soon after the onset. Pain may be felt also in the back, usually dull and aching. It maybe severe, especially when there are symptoms of spinal meningitis. Instead cf being initial, pain in ACUTE ATROPHIC PARALYSIS. 401 the limbs may succeed the onset of paralysis, and it occasionally con- tinues for several weeks, especially when seated in the nerve-trunks. In some cases in which the onset and course are characterised by severe pains, the motor effects have entirely disappeared in course of time, indicating that the condition was one of neuritis. Tingling or formication in the limbs may be described by older patients, but sen- sation is seldom affected, even temporarily. The paralysis is almost always rapidly developed. It varies much in its initial range. Only part of a limb may be affected, or there may be universal loss of power; but in the majority of cases the para- lysis is intermediate between these extremes. Two or three limbs are affected—both arms, both legs, or the legs and one arm. When all four limbs are paralysed the neck muscles also may be weak, and even swallowing may be impaired. The other muscles supplied by the cranial nerves escape, as a rule, and the sphincters are seldom involved. Occasionally there is retention of urine, sometimes incontinence, chiefly in severe cases, and it may then last a long time. For instance, a child aged two and a half years woke up one morning with headache, fever, and weakness of the legs, which rapidly increased to complete paralysis. Four days later the arms also became weak, and in a day or two more the urine escaped involuntarily. The arms began to recover in six weeks, and were well in six months: both legs wasted and remained permanently paralysed; the incontinence of urine lasted for a year. In another case, with incontinence for a few weeks, the residual palsy was in the lower legs. As in these instances, the symptom is met with chiefly when the lumbar region is diseased. The paralysis may commence in one limb and quickly spread, reaching its maximum extent in a few hours to a few days, but very often the actual onset is so rapid or so escapes careful observation in consequence of the general illness that all the parts first affected are found to be paralysed when it is discovered. Occasionally the onset is in two distinct stages, separated by a few days; sometimes the loss of power develops slowly in the course of one or even two weeks, in cases that must be regarded as " subacute," but do not differ in other respects from the ordinary form. Examples of the common onset have been already given; as another, may be mentioned the case of a boy, aged a year and four months, who one day seemed ill, was sick, and was put to bed. The next day he could scarcely stand alone; on the following day he could neither move the legs nor sit up in bed. In about ten days the left leg began to improve, but there was enduring paralysis and wasting of the whole of the right, and of the lower part of the left leg. In another case, a child seemed ill, and was kept in bed for five days; on the third day it was noticed that the left arm was not moved so much as the right, and by the fifth day the arm was quite powerless; at the end of a fortnight improvement commenced. In the adult, the mode of onset presents nearly the same characters. A lady, twenty-five years of age, sat down for some time on wet grass. VOL. I. 26 402 SPINAL COUD. Two days later general rheumatic pains came on, which were very severe in the legs on the following day, and the legs were distinctly weak. In the course of the next forty-eight hours the arms also became feeble, and at the end of a week she could scarcely move her arms, and her legs were absolutely paralysed. In a fortnight improvement commenced, first in the arms and then in the feet; but the hip and thigh muscles remained paralysed and rapidly wasted. Cases are sometimes seen similar in other respects to those now under consideration, but in which the paralysis comes on suddenly, and without general disturbance. Thus a child, aged two, was walking along, when he suddenly could not stand, and fell down on his knees; both legs were powerless. Slow improvement followed in the left leg, and wasting in the right. The suldenness of the onset makes it probable that the lesion is hemorrhage, and not simple inflammation. Spinal haemorrhage is known to occur in early childhood. Hence, while we must class these with the other acute spinal atrophies, we are not justified in regarding them as cases of polio-myelitis, since we do not know whether the haemorrhage is secondary to commencing inflam- mation or is primary. The former is probable, because the two sets of cases occur under the same general conditions of onset, and hence they cannot be separated. Moreover, constitutional disturbance is more often absent in cases of actually sudden onset than in others, although it is sometimes considerable. Thus a child had been ill for two weeks, when, being able to walk about, it suddenly fell to the ground; the left leg was found powerless, and the right weak. It is probable that a sudden onset is more frequent than is suggested by the facts that can be ascertained, since the palsy often comes on during the night or during rest; for instance, in one case a child sat on a chair for an hour, when the left leg was found powerless. In some cases of sudden onset the initial palsy is universal, and in such cases as the following it is probable that a limited haemorrhage in the cervical region causes rapid pressure on all the adjacent structures, which afterwards recover from the effects of the pressure. A girl, aged seventeen, suddenly felt tingling in the left hand. In a few minutes the whole arm was powerless, and then the right arm became paralysed. She had a strange sensation at the back of the neck, and went upstairs; as she was going up, her legs became weak, first the left and then the right. In less than half an hour from the time of the first symptom, there was absolute universal paralysis, with difficulty in breathing and in swallowing. Improvement (in the opposite order to the onset) commenced the same evening and was complete in about six weeks, with the exception of the muscles of the left forearm and hand, which rapidly wasted and were permanently paralysed and atrophied. Another girl, while walking across a road, suddenly felt a " sort of shock " as if someone had given her a knock between the shoulders. She became giddy, and instantly felt tinglino- in both arms, especially in the right, which became weak before she ACUTE ATROPHIC PARALYSIS. 403 had got to the other side of the road. Ultimately the arms recovered, but permanent paralysis and wasting of the intrinsic muscles of each hand were left. The initial loss of power is as a rule far more extensive and severe than the permanent affection; in a small number of cases the two correspond. But the extent of the early palsy, that of the enduring atrophy, and the relation between the two, vary extremely, so that no general or even common laws can be discovered. Indeed, in all features of the disease variability prevails to such an extent as to baffle attempts to describe them in general terms, and a better conception of the malady can be gained from such illustrative instances as are here given than from general descriptions. One general fact is unfortunately true of almost all cases, namely, that the palsy scarcely ever passes away entirely, and that where wasting occurs, wasting remains. After the paralysis has reached its height and ceased to increase or spread, whether the point is attained suddenly or rapidly or slowly, it remains stationary for a time, which varies from a few days to six weeks, and then lessens. The improvement occurs first in the parts last affected, and gradually spreads until, usually at the end of from one to three months, all parts have recovered except those which are to be permanently affected. In these the muscles are toneless and flaccid from the first, and in two or three weeks there is distinct wast- ing, which rapidly increases, until the shape of the hmb is changed, and, in extreme cases, scarcely any of the volume of the muscle can ultimately be detected. In fat children the appearance of the limb may be less altered, and it seems that, in some of these, an interstitial growth of fat makes up for the diminution of muscular tissue. In older children and adults the muscles are often tender to the touch during the process of wasting. When the atrophy is distinct the muscles no longer contract to faradism, and, if the motor nerves are tested, they also will be found to have lost irritability. The change depends on degeneration of the nerves, and the muscles usually present the "degenerative reaction " in its characteristic form. The loss of faradic irritability is distinct, in severe cases', as early as the end of the first week, and even by the fifth or sixth day. In a patient, for instance, who is universally, and apparently uniformly, paralysed, one or more groups of muscles may be found to have lost irritability, and in these we know that there will be lasting paralysis and wasting, while the other parts will recover. In a severe case, in which the muscles most affected atrophy completely, the loss of faradic irritability may be permanent. The voltaic irrita- bility remains, increased in degree, for two, three, four, or six months, then slowly falls, as the muscular fibres themselves degenerate, and ultimately, at the end of one or two years, it disappears. It may, however, persist for a long time, if the fibres are stimulated by elec- tricity,—even for three or four years, although the paralysis remains 404 SPINAL CORD. absolute. In rare cases, electrical irritability quickly disappears, even to the voltaic current, from the destructive degeneration of the muscular fibres. More commonly, after six or twelve months, some faradic irritability returns. It may be slight, due to the recovery of a few fibres, insufficient in number to restore any bulk or power, but the new fibres which recover do so perfectly, so that the irritability becomes normal in degree, although the contraction which can be thus produced is very slight' in amount. In other cases considerable recovery occurs, so that some power and volume are regained, although the muscles remain below the normal size. In the muscles which are weak but do not waste there is no degenerative reaction, although there may be slight diminution of excitability to each current. The paralysis, as a rule, is motor only. Sensation is impaired only in extremely rare cases (about 1 in 50), in which inflammation in the lumbar region is so intense as temporarily to impair all the conduct- ing functions of the cord. Thus, in a girl aged five, in whom the permanent state was a symmetrical atrophy of all the muscles below the knees, with a slighter affection of the thigh-muscles and flexors of the hips, the initial general loss of power in the legs was accompanied, for a few days, by complete loss of sensation below the knees. In the similar but more severe case of a boy, aged four, in whom the lasting palsy was general throughout both legs, the anaes- thesia continued for two months. In many cases there is a history of temporarily disturbed sensation attending the onset, probably the result of oedema around the inflammatory area. When sensation is lost there is always incontinence of urine. Keflex action necessarily ceases in the parts related to the affected muscles. That from the skin is at first lost where there is weakness, but it returns with or soon after the recovery of power in the less affected parts. Where there is persistent paralysis it remains absent. The myotatic irritability is lost in the same or even greater degree. For instance, no knee-jerk can be obtained if the extensors of the knee are affected even in shght degree. The loss depends on the interruption of the muscle-reflex centre by the disease in the grey matter. In rare cases of severe cervical polio-myelitis, the inflam- mation spreads beyond the grey matter to the lateral white columns ; there is wasting of the arms, but paralysis without wasting in the legs, and in the latter the myotatic irritability may be increased above the normal, so that the foot-clonus may be obtained. In the course of a few months, however, the condition of the legs becomes normal. A common effect of the disease is to retard the growth of the bones in the affected limb, so that these gradually become shorter than their fellows, and the difference in size increases with the amount of general growth. Hence, it is greater, the younger the patient at the onset of the disease. If one part of a limb is more affected than another, the ACUTE ATROPHIC PARALYSIS. 405 corresponding bone suffers most in growth. The effect is sometimes considerable, when the atrophy is slight. Seeligmiiller has described the opposite effect—an actual elongation of the bones, attributed to the fact that the growing epiphyses suffer traction instead of the normal compression, but this is extremely rare. Those joints that depend for their support on tendons which pass over them become lax when the muscles are paralysed, and the articular surfaces may be no longer kept together. Thus when the deltoid is wasted the head of the humerus may fall out of the glenoid cavity. The head of the femur may fall from its proper position in the acetabulum, and actual luxation may occur when the paralysis of the muscles is unequal, and the less affected unopposed muscles undergo the secondary contracture immediately to be described. That of the abductors and rotators may cause infra-pubic dislocation, and that of the adductors iliac dislocation.* I have known the patellar tendon to be greatly elongated, from the unopposed action of the extensors of the knee, so that their contraction caused the patella to rise three inches above its normal position.f During the chronic stage of the disease there is great tendency to the occurrence of permanent shortening of muscles, with consequent displacement of the parts to which they are attached. Grave de- formities are thus produced. It occurs only when the several muscles acting on a joint are unequally paralysed; the less affected muscles are no longer subject to the normal extension by their opponents, and hence gradually become contracted, and the contraction is fixed by tissue changes in them, so that they cannot be passively extended. It may occur in muscles which are unaffected, and it is uncertain how far it is favoured by a slight degree of paralysis. Posture also aids the production of those muscular contractions, and so also in the case of the foot does the relative shortening of the limb. Bedsores are almost unknown, even in the acute stage of the disease. A shght local elevation of temperature in the most affected parts has been observed in the early stage, but subsequently the affected limb is colder than the other. This is due, in part at least, to the want of the aid to the circulation which is, in health, supplied by the muscular action. The persistent paralysis may occupy the whole or part of one or more limbs. The legs suffer three times as frequently as the arms; the respective percentage being 21 and 68. It is less frequent for both legs or for one arm to suffer, and still rarer combinations are those of both legs and one arm, of both arms, of the arm on one side and the leg on the other, while the rarest of all is the affection of leg and arm on the same side. The limbs on the left side of the body are more often permanently affected than those on the right; the difference is • See Karewski,' Archiv f. klin. Chir.,' Bd. xxzvii. t In a case shown me by Mr. Heather Bigg. 406 SPINAL CORD. The left leg is paralysed alone greater in the leg than in the arm. twice as often as the right. When the paralysis of a limb is incomplete, the part involved varies much in different cases, and as different parts of two or more limbs may be affected, the combinations of palsy which result are extremely varied. The grouping of adjacent muscles is sometimes distinctly that of functional association; often it is random ; but the most frequent condition is to have an irregular affection of the muscles that are associated in the centre. While the grouping is that of function, some of the muscles are only slightly affected, and others suffer with them that are not functionally associated. In the legs, the paralysis, in very severe and fortunately very rare cases, may be absolute, involving all the muscles of both limbs. Usually it is partial, and then the muscles below the knee suffer more often than those above the knee. The calf muscles are affected less frequently or in less degree than the muscles in front of the tibia or the peronei. Hence talipes equinus is a common defor- mity, and its occurrence is FiG. 112.—Old atrophic spinal paralysis. Talipes valgus in the right leg from para- lysis of the anterior tibial; t. varus in the left, from paralysis of the peronei. Fig. 113.—Atrophic spinal para- lysis, affecting chiefly the calf muscles, with resulting contrac- tion of the flexors of the foot, causing talipes calcaneus. aided by the shortening of the limb, in consequence of which the foot has to be extended to bring the ball to the ground. Either the tibialis anticus or the peronei maybe more affected, with the result, m the former case, of talipes valgus, in the latter of talipes varus. In the case shown in Fig. 112 the peronei have suffered most in the left leg and least in the right, producing an unsymmetrical but ACUTE ATROPHIC PARALYSIS. 407 corresponding distortion of the feet. This affords an illustration of another fact, namely, that when there is a partial affection of both legs the paralysis may be unsymmetrical in the two. Much less commonly the calf muscles suffer more than the others, and there results talipes calcaneus, as in the case shown in Fig. 113, and the intrinsic muscles of the foot often suffer with those of the leg. In the thigh, the ex- tensors of the knee are affected more frequently than the flexors, and hence flexor contraction is very common, and may even cause subluxation of the joint. The flexors of the hip often suffer, generally with the extensors of the knee. Less commonly the glutei are involved, but never alone. In the arm, almost all the muscles are sometimes affected, as in the case shown in Fig. 114, but all are seldom entirely paralysed. The intrinsic muscles of the hand often suffer; either the thenar muscles or the interossei may be most damaged. An instance of such para- lysis of the interossei is shown in Fig. 115. The forearm muscles are frequently affected, but the supinators may escape when the other muscles are involved. The deltoid suffers more fre- quently than any other single muscle of the arm. It may be paralysed alone or in association with other muscles ; occasion- ally the deltoid, supra- and infra-spinatus, biceps, and supinators are all involved in the " upper arm type" of palsy of Erb* (see p. 111). But other muscles than these may be Fig. 114.—Atrophic spinal para- lysis, infantile form. Wasting of all the muscles of the left arm from the deltoid down- wards, and of the right ser- ratus magnus. Fig. 115.—Atrophic spinal paralysis (adult form) affecting the interossei and thenar muscles, and also the deltoid. See a paper by Dr. Beevor, ' Med.-Chir. Trans./ 1885. 408 SPINAL CORD. associated with the deltoid. The irregularity of the grouping is shown by the fact that the triceps is often affected with these muscles. In the case shown in Fig. 115 the deltoid and intrinsic muscles of the hand were wasted, and no other muscles. The serratus magnus is occasionally affected as in Fig. 114; in this case, although the left arm had suffered severely, as the figure shows, on the right side only the serratus was involved. With the serratus, the upper part of the pectoralis major is sometimes associated in paralysis (as it is in normal function, see p. 37), the lower part being unaffected; it was so in this patient. The middle part of the trapezius and other scapular muscles are occasionally involved. The neck muscles rarely suffer, but the diaphragm is occasionally paralysed. Although the intercostals and other trunk muscles are so often weakened in the early stage, con- siderable permanent atrophy is very rare. Curvature of the spine is sometimes produced in consequence of th^ patient being allowed to sit up while the muscles are weak. It may be a lateral or an antero- posterior curve, according as the weakness is on one or both sides. I have met with considerable depression of the lower part of the wall of the thorax on the left side from paralysis of the intercostal muscles at the spot, perhaps combined with hindered growth of the ribs. The muscles supplied by cranial nerves are scarcely ever affected. I have once seen complete paralysis of one side of the face, associated with wasting in the limbs, in an otherwise characteristic case, and an instance of affection of the face and tongue has been recorded by Pasteur.* The Course of the disease has been already sketched. There are (1) an initial stage of paralysis, rapidly increasing, often accompanied with fever ; the duration of this stage is from a few hours to a week or even more ; (2) a stationary period, which lasts for a week to a month; (3) a stage of " regression," during which the palsy passes away, except from certain parts in which wasting occurs; this regressive period usually occupies from one to six months; (4) a chronic stage (overlapping the last), during which atrophy con- tinues; slight improvement may occur, but contractures and de- formities are developed. The duration of this stage is indefinite, because, wherever muscular tissue remains and some voluntary power returns, this slowly improves, by increased development of the muscle under the influence of use, and this continues in slight degree for years. This gain is often, however, more than counterbalanced by the interference with growth, and by the occurrence of deformities. Even in the slightest cases complete recovery is extremely rare, and the limb remains smaller than its fellow. On the other hand, death from the disease is equally uncommon, and occurs chiefly in the early stage. It is not improbable that some children die from the * «Lancet/ 1887, vol. ii. It is probable that when the cranial nerve nuclei are affected, the vital centres become involved iu most instances, so that the patients do not survive. ACUTE ATROPHIC PARALYSIS. 409 initial disturbance before its nature is recognised. Now and then death occurs at the end of the first week or ten days, from universal paralysis or from some such severe cerebral disturbance as existed in the cases mentioned above, or as followed the spinal lesion in a case in which paralysis in the arms came on upon the third day of the initial fever and reached its height on the fifth day, faradic irrita- bility being lost by the seventh in many muscles of the left arm; a little rigidity of the neck then occurred, and on the tenth day the patient began to vomit, complained of increased headache, and had hallucinations; on the eleventh day he became comatose and died. Bronchial catarrh is an occasional cause of death, when the respira- tory muscles are weak. Relapses are very rare, and occur chiefly in the form of a separate later extension of the disease. Second attacks are almost unknown; one instance only was met with in the series of 214 cases. Sequelae, beyond those mentioned as part of the symptoms of the disease, are also very rare. As a rule the general and nervous health of the patients, and the duration of life, are uninfluenced by the local palsy. In a few cases, however, some other chronic affection of the spinal cord has come on when the subjects of infantile paralysis have reached adult life. Progressive muscular atrophy has been several times observed to start from the paralysed limb, and even to be apparently excited by a fracture of the bone.* Acute and subacute polio-myelitis in adult life have also been observed as a sequel, and I have twice*seen the symptoms of lateral sclerosis slowly developed, in one case at seventeen, in the other at twenty-eight. In the spinal cord of the subject of old infantile paralysis there seems thus to persist some disposition, slight though it be, to fresh disease, and the cases of lateral sclerosis mentioned show that the liability to disease is not limited, as has been thought, to the grey matter.f The altered structure of the bones has been known to facilitate their fracture; in one case the bones in the affected limb were broken on three separate occasions (Dutil). Pathological Anatomy.—For a long time, infantile paralysis was believed to be a peripheral affection, having its seat in the muscles. But improved methods of examining the nerve-centres have shown changes in the spinal cord which have the characters of an acute inflammation of the grey substance of the anterior horns. The correspondence between the infantile and adult forms makes it certain that the latter are, in most instances, of the same nature. Subacute atrophic para- lysis in adults has been found, however, to depend on disease of the nerves in some forms that were thought to be spinal, but in these the palsy is strictly symmetrical, and when it is irregular in distribution the disease is certainly identical with the infantile form. Observations on the changes in the spinal cord in the early stage * Raymond, 'Prog. Med./ 1889; Dutil, 'Gaz. .Med. de Paris,' 1881. f Compare Ballet and Dutil, 'Revue de Medecine/ Jauuarj, lbSl, p. 18. 410 SPINAL CORD. are few. A case recorded by Dr. D. Drummond, in all probability one of this disease, is by far the earliest on record, and is indeed the earliest .possible.* A child, five years old, died after a few hours' acute illness. The spinal cord, in the region of the fourth and fifth cervical nerves, presented undue redness of the anterior grey matter. The vessels running from the surface to the cornu were distended with blood. The microscope showed distension of capillaries and minute extravasations in the grey substance, swelling of the neuroglial elements and of the ganglion-cells, which were granular with indistinct processes. Another important early observation is that of Dr. Charlewood Turner,f six weeks after the onset (Fig. 116). In this and other somewhat later cases, acute changes have been found in the anterior cornua, more advanced than in Drum- mond's case. They are often widely spread in slight de- gree, and attain considerable intensity in one or more foci, usually in the cervical or lumbar enlargements or both. At these spots the anterior horn is softened ; sometimes there.is haemorrhagic infiltra- tion (Fig. 117), sometimes an actual cavity (Fig. 116, A, b). The microscope shows extra- vasated blood often massed along the vessels (Fig. 116, c), and scattered through the grey matter with other cells such as are met with in mye- litis. There are also granule corpuscles and other products of degeneration of the nerve- elements. These elements, Fig. 116.—Acute anterior polio-myelitis in a child 2£ years old, six weeks after the onset. (After Charlewood Turner.) A. Section through the lowest part of the lumbar en- largement, showing a cavity visible to the naked eye, ou the left side. B. Left ante- rior half of the cord under a low magnify- ing power, showing destruction of almost the whole anterior cornu. c. Portion of anterior cornu in the upper part of the lumbar enlargement. Numerous corpuscles lie in the granular protoplasm and reticulum of fine fibres. A small artery is encrusted with several layers of corpuscles and nuclei. and especially the motor nerve-cells, have almost entirely disappeared. Where the change is slighter in degree there is a leucocytal infiltration, a few granule corpuscles are seen, while the nerve-cells may be structurally intact, * ' Brain,' April, 1885. f < Path. Trans./ vol. xxv, p. 203. ACUTE ATROPHIC PARALYSIS. 411 but swollen and granular. The morbid appearances may be con- fined to the anterior cornua, or may extend in slighter degree into Fig. 117.—Acute anterior polio-myelitis in a child 14 months old. Dr. F. E. Batten's case. The affection commenced in the legs, but there were electrical changes and paralysis in the arms as well. The child died suddenly on the fourteenth day of the illness. The section made and lent by Dr. Batten shows marked engorgement of vessels, with occasionally actual extravasation, small-celled infiltration, and changes in the anterior horn cells. the adjacent lateral column, in which the nerve-fibres near the grey matter may undergo destructive degeneration, and other signs of 412 SPINAL CORD. inflammation may be seen. The posterior columns are always un- affected. In very severe cases there may be signs of slight local meningitis corresponding in position to the region chiefly affected. This region corresponds to the origin of the nerves supplying the muscles in which there is most wasting, and the anterior nerve-roots which arise from this part present the signs of acute degeneration. Such changes indicate a general or interstitial inflammation of the grey matter. But some observations have revealed only alterations in the motor nerve-cells, which have presented granular degeneration, the matrix between them being quite unaffected.* This suggests that there may be a form of polio-myelitis in which the changes are essentially parenchymatous and not interstitial. At a later period, years after the onset, the appearances presented accord with those described as commonly found in the early stage, allowance being made for the difference in time. The anterior cornu at one or more places is shrunken (Fig. 118), and in part stains Fig. 118.—Atrophic spinal (infantile) paralysis. A. First lumbar; the left anterior cornu is smaller than the right, and its ganglion-cells have disappeared with the exception of the inner group. B. Fourth lumbar; the whole left half of the cord is smaller than the other, in consequence of the diminution in size of the ant. horn. Of the ganglion-cells only a few remain, belonging to the antero-lateral group. Similar changes existed throughout the lumbar enlargement^ deeply with carmine, in consequence of its nervous structures being replaced by connective tissue, in part less deeply in consequence of "granular disintegration" of the substance. The motor nerve-cells are absent, partially or entirely. Sometimes a few shrivelled cells remain, sometimes one or more groups may be unaffected ; or one or two nerve-cells of normal appearance may alone remain (see Fig. 118). Small foci of disease may be seen in the unaffected part of the grey matter, and in these the motor cells may be smaller than normal; the intervening plexus may have perished. When one horn is much damaged, the other may merely present fewer nerve-cells than * Rissler,' Nord. Med. Ark./ xx. t For these sections I am indebted to Dr. H. Humphreys, of St. Leonards. The paralysis came on at one and a half years of age, two years before death, and involved most of the muscles of the left leg, those of the calf in greatest degree, so that talipes calcaneus had developed. ACUTE ATROPHIC PARALYSIS. 413 normal, with perhaps a little condensation of the interstitial tissue. The antero-lateral column is usually lessened in size, and may present Blight sclerotic changes, especially in a zone contiguous to the grey substance, whence thickened septa may radiate into the white column. This is apparently due to the extension of an intense inflammation of the grey substance to the adjacent part of the white column. Sometimes a shghter sclerosis can be traced through the lateral column; this is seen chiefly in cases of long duration, and is probably secondary. With extreme damage to both cornua there may be ultimately great wasting of the white columns on each side.* In consequence of these alterations, the affected half of the cord is conspicuously smaller than the other, even to the naked eye, and the difference is greatest where the damage to the grey matter is most intense. The anterior nerve-roots at the most affected part are small and grey, and the degeneration of the motor fibres may be traced down the nerve-trunks. Often a few fibres present a normal appearance although the rest have perished; possibly from the sym- pathetic system. The muscular fibres, in early cases, have beeu found narrower than normal, and in a state of granular degeneration, with an increase in the nuclei of the sheath and of the interstitial tissue. Granules and pigment masses accumulate between the sarcolemma sheaths. In extreme cases (those in which all electrical excitability is early lost) the degeneration proceeds to complete disappearance of the fibres, the place of which is occupied by fibrous tracts, developed partly from the sarcolemma sheaths and partly from the interstitial connective tissue. It is common to find, here and there, a fibre presenting normal appearances. Sometimes fat accumulates in the interstitial tissue, so that the reduction in the bulk of the muscle may be less than that of the fibres. In slighter cases, in which partial recovery takes place, some of the fibres probably regain their normal appearance, even though they have undergone slight granular degeneration. Usually, however, many fibres perish; those which recover are smaller than normal, and the original volume of the muscle is rarely regained. Although there may be a permanent increase in the interstitial tissue, this undergoes contraction and comes to occupy but a small bulk. Muscular fibres are often seen that are larger than normal, and this is not (as has been thought) a transient condition, for it has been observed seventy and forty-five years after the onset.f It is perhaps sometimes a true hypertrophy. J The bones have been found not only shorter than normal, but also • See * British Med. Journal/ 1887, p. 187. t Joffroy and A chard,' Arch, de Med. exp./ 1889; Dejerine and Huet, 'Arch. de Phys./ 1888. % Dejerine. It is said to have been met with in muscles totally paralysed; bat it is doubtful whether ** total palsy" of a muscle excludes voluntary contraction of some fibres in it. 114 SPINAL CORD. smaller, with their angles rounded, the compact substance more uniform, and the Haversian canals smaller (Joffroy and Achard). The brain has been almost always found normal. In one case with extensive paralysis, of long duration, some atrophy was found in the motor region of the cortex (Sanders). It is probable that some acute changes would be found in cases that die with the cerebral sym- ptoms already described. No observations have as yet been made on the acute primary poly- neuritis that seems occasionally to coincide with the inflammation of the cord, perhaps sometimes to exist alone without any cord affection.* It is probable that, in the cases in which the nerves are tender in the middle of their course, the sheath will be found inflamed, and only the motor fibres will present such signs of secondary degeneration as always result from the lesion of the cord. Pathology.—Both the character of the lesion and its mode of onset suggest that it is inflammatory in the majority of cases. In rare instances, as already stated, the almost instantaneous onset makes it probable that the lesion is different in character, is vascular in its nature, probably hemorrhage. It is likely that these cases are really haemorrhagic myelitis, in which the usual initial vascular dis- turbance is so severe as to produce an extravasation. Signs of inflam- mation do not precede the sudden onset. The symptoms are well explained by the pathological facts that have been ascertained, extended by the simple inferences that are indicated by the symptoms. The lesion interrupts the motor path, causing immediate palsy, which results from damage to the cells and nerve-plexus of the grey matter, whether slight or severe. The recovery of the slightly damaged structures restores the voluntary path, and even if the fibres from the cells degenerate, they seem to regain normal nutrition by regeneration when the cells recover. But when the motor cells are destroyed the fibres from these degene- rate permanently. As the slighter damage is usually far wider than the destruction, the initial palsy is more extensive than the persistent atrophy, and the extent of such is purely a matter of this relative area of trifling and severe degree of lesion. Nerve-cells that are destroyed are never renewed, and hence the permanence of the muscular wasting that depends on such destruction. When a few nerve-cells escape destruction, a few nerve-fibres recover and a little muscle-tissue remains, too slight, it may be, to be of use. The occasional interference with the conducting tracts in the white columns is explained by the obvious extension of the inflammation, which, when very intense, may even spread through all the structures of the cord, as in the rare cases in which sensation, as well as motion, is lost. But such cases, which are most rare, differ from true transverse myelitis in the rapidity with * As was probably the case in two cases of paralysis in children shown to the Harveian Society of London by Dr. Leonard Guthrie, 'Lancet/ 1897, vol. i, p. 448. ACUTti ATROPHIC PAKALYSIS. 415 which the damage restricts itself to its special seat, and sensory con- duction is restored. The fact that the disease of the sensory tracts is only secondary and trifling, is emphasised by the fact that even in these cases there are never the acute bedsores that would surely ensue in a case of true transverse or total myelitis of corresponding seat. The observations mentioned on p. 412 suggest that there are two varieties of the inflammation of the grey matter, such as we have recognised in myelitis g nerally; a parenchymatous inflammation consisting in a primary change in the nerve-cells, and an interstitial or general inflammation, as in the common forms of myelitis, in- volving the nerve-cells only as one of many structures equally damaged by a process that has no special relation to the nerve-elements. The distinction is important, because we should expect to find, in the former cases, a wider slight initial affection than in the others, and finally a more definite relation to function in the parts diseased. The true pathology of the malady, its relation to its causes, is still obscure. The one salient fact that we can discern, though scarcely define, is the evidence of a blood-state afforded by the general sym- ptoms. That these symptoms are not the consequence of the local inflammation is shown by their disparity in degree, and difference in time. It is probable, therefore, that the spinal lesion is not the cause of the constitutional disturbance, but is rather an effect of the cause of the latter. It seems impossible otherwise to understand the extreme variation in the two forms of disturbance. But we have no evidence as to the nature of the blood-state, and there are no other effects, commonly associated with the myelitis, to indicate the general patho- logical tendency of its cause. The closest analogy is with some forms of neuritis, and this, as we have seen, may co-exist with the spinal lesion, as a consequence, at any rate, of exposure to cold. Indeed, it is probable that the inflammation of the nerves is the chief or even the only morbid process in some of these cases. On the other hand, it must be noted that in the epidemics of the disease, there were, besides cases of spinal cord disease, simultaneous cases in the same places in which the evidence pointed to an analogous inflammation in the cere- brum. In one epidemic, the American one, the lower animals also suffered (see p. 416). The variations, alike in the general symptoms and in the inflammation of the cord, and especially the indications that the latter may be either parenchymatous or interstitial, suggest that the causal blood-state also varies in different cases. We have no indication of the way in which the remarkable relation to season is produced, whether by predisposing the individual or favouring the development of some toxic agent. We must, however, recognise as an essential element the predisposing influence of age, which we may associate with the facts that the structural development of the nervous system is complete, but the function of the nerve-elements must lack the stability that comes only from continued use, and that the period is generally that which coincides with the first serious demand on the 416 SPINAL CORD. functional energy of the grey matter of the cord. We may remember also the vascular activity that all function entails, and the readiness with which the vaso-motor system of children is disturbed. Lastly the occurrence of the disease in more than one member of the same family indicates a congenital disposition of the system to react in a similar manner to certain external agencies, while a special feature in the latter may perhaps explain the occasional epidemic character of a disease, and furnish grounds for ascribing to it an " infective" character.* The evidence available suggests that it is probably due to some chemical change in the blood analogous to that which seems to cause rheumatic fever, though probably distinct from it—a change excited by cold, disposed to by the effect of heat, the result of some derangement of metabolism which we cannot yet understand, and perhaps having underlying these effects some organismal cause. This hypothesis does not exclude the action of traumatic influences in determining the disease. Such a glimpse of its pathological relations is all that we can at present obtain. Diagnosis.—This rarely presents any difficulty except in the early stage. When the initial paralysis is passing away, and the wasting is distinct, the nature of the case is sufficiently evident, and is cor- roborated by the electrical reactions, by the loss of reflex action, and by the absence of any impairment of sensibility. At the onset, however, the symptoms may readily be misinterpreted. The most common error is to attach too much importance to vomiting, and to regard the attack as simply gastric. General disturbance is naturally ascribed to some general cause until nervous symptoms manifest themselves. Even then there is risk of error. On the one hand, as we have seen, a diagnosis of a general disease is not always relinquished when paralysis appears, but the latter is regarded as secondary. On the other hand, especially in young children, the existence of paralysis is often overlooked at first, and it is supposed that the child do s not move because it is prostrate. This error will not be made if it is remembered that mere prostration seldom causes total immobility, and a fortiori it does not produce local immobility. When the pyrexia ceases, and the loss of power persists and increases, the existence of paralysis is always unmistakeable. The initial general disturbance must then be regarded as part of the disease unless there is the clearest evidence of its independent nature. In adults, the danger of mistaking paralysis for prostration is con- siderably less, but, on the other hand, the general symptoms are as likely to be misinterpreted as in the case of children. The rheuma- toid pains, which are so common, are usually regarded as evidence of acute rheumatism, especially when the affection follows exposure to cold. Whenever rheumatoid pains are not localised in the joints * See Medin, ' Neur. Cent./ 1896, p. 1120 j Buccelli, ' Neur. Cent./ 1897, p. 798 ; Sowerby, ' Journ. Am. Med. Assoc./ January, 1896; Pasteur, «Trans. Clin. Soc * 1897. ACUTE ATROPHIC PARALYSIS. 417 and especially when they are spontaneous, and not influenced by move- ment, the possibility of their spinal (or nerve) origin should be remem- bered ; and other indications of spinal mischief, such as local loss of power, tingling or formication, should be carefully watched for and receive due weight. Of other spinal cord diseases, all chronic lesions are distinguished at once by the onset. From other acute diseases, moreover, the dis- tinction is only difficult in the early stage. As soon as the initial palsy begins to lessen, and the muscles in one part lose faradic irrita- bility and begin to waste, the nature of the case admits of no doubt. The diagnosis may be made with certainty after the end of the first week by the electrical reaction. Lf we find loss of faradic irrita- bility, it is certain that the characteristic alteration in voltaic irrita- bility will follow. The isolated induced shocks should be used instead of the serial "current," because any harmful stimulation of the sensory nerves is thereby avoided. (See Diseases of the Nerves.) Acute transverse myelitis is only simulated when the inflammation of the grey matter is bilateral and so intense as to extend to the white columns, but the age of the patient generally suggests correctly the nature of the disease. The myehtis of childhood is polio-myelitis. The pseudo-transverse variety—polio-myelitis, transverse through its intensity—is seated in one of the enlargements, usually the lumbar; the true transverse form usually occurs in the dorsal region. Real difficulty is confined to adults, in whom there is extensive cervical or lumbar myehtis involving the grey matter. In young adults, polio- myelitis is more hkely ; this is indicated also by what is best described as a regressive onset in contrast to one that is progressive. In the former a wide extent is quickly reached, and the symptoms then tend to lessen; in the latter the morbid process is a longer time reaching its height: in the former the symptoms clearly show that the most severe affection is of the anterior grey matter; in the latter, severe anaesthesia or trophic disturbance usually points to an equally intense lesion of the other parts of the cord. The separation of subacute from acute myelitis of the grey substance is, to a large extent, arbitrary. The symptoms are similar, but the onset is less rapid and occupies more than a week. The distinction of multiple neuritis is from the subacute rather than the acute spinal atrophies, and is considered elsewhere. The diagnosis from paralysis of cerebral origin is usually easy. In cerebral palsy there is never loss of faradic irritability or extreme muscular wasting, or loss of the muscle-reflex action. In the spinal affection there is no trace of the mobile spasm that is common after infantile hemiplegia. Any cerebral symptoms which may attend the onset of polio-myelitis are subordinate in significance to the state of the muscles as evidence of the permanent lesion. Convulsions at the onset of infantile spinal paralysis are general; those that result from a cerebral lesion are usually unilateral or commence locally. The chief VOL. I. 27 418 SPINAL CORD. difficulty arises when arm and leg are involved on the same side. These cases are rare, and present no difficulty if attention is paid to the nutrition and reaction of the muscles. The exceedingly slow onset of pseudo-hypertrophic paralysis, developing gradually, as it does, with the child's growth, ought to render its confusion with poho-myelitis impossible. A reasonable doubt can only arise in a slight case in which the onset was unnoticed or forgotten. I have once known slight atrophic palsy of the exten- sors of the knee to induce the habit of putting the hand on the knee in rising from the ground—an action often thought to be peculiar to the pseudo hypertrophic disease, but acquired when weakness of the extensors occurs in early childhood from any cause. Diseases outside the nervous system which have been mistaken for infantile paralysis are chiefly those in which local pain interferes with the movement of the limbs, and the child is young. I have known, for instance, the mistake to be made in the case of hip-joint disease, necrosis of the femur, and the affection termed " scorbutic rickets," in which there is enlargement of the shafts of the long bones, extreme pain on movement, and spongy gums. In all these cases a careful examination will show that movement is interfered with only by the pain; there is no actual paralysis, and there is no interference with reflex action. The preservation of the knee-jerk is often of great significance ; it at once excludes atrophic palsy in any case in which the extensors of the knee seem feeble. The points above described should always enable the diagnosis to be made. It is impracticable to enumerate the distinctions from every disease with which confusion is possible, for experience shows that there is no form of palsy with which a common disease, such as this, is not at some time confounded. Prognosis.—The danger to life is probably greatest when there is severe constitutional disturbance, which may even precede the develop- ment of the characteristic paralytic symptoms. In the stage of paralysis there is peril only when the chief disease is in the cervical region, and respiration is interfered with; but this danger is small unless an attack of bronchial catarrh is intensified by the palsy. Definite cerebral symptoms involve danger proportioned to their character and degree, but it is generally less in reality than in appear- ance. In the vast majority of cases the disease involves no immediate danger to life. But children are left with little power of resistance to other morbid influences, and occasionally succumb to some other illness, as an acute specific disease, or an attack of bronchitis, a few weeks or months after the onset of the paralysis. As soon as the paralysis has become stationary, i. e. has not increased for twenty-four hours, the danger of further extension is small. But the question at once arises, and is anxiously asked,— What will be the permanent condition ? Will there be lasting paralysis ? An answer cannot be given until the. end of the first ACUTE ATROPHIC PARALYSIS. 419 week or ten days, and then only by means of an electrical examina- tion. Whatever muscles, at the end of that time, have lost faradic irritability will certainly waste, will remain for a long time paralysed, and will probably be permanently affected in some degree, slight or severe. On the other hand, if there is no loss of irritabihty at the end of ten days, but it is apparent at the end of a fortnight or three weeks, the wasting will be slighter in degree, and some ultimate recovery may be anticipated even in the most affected part. Where there is no loss of irritability the paralysis will pass away in the course of a few weeks, or at most of a few months. When faradic irritability is lost early and completely, the wasting will be rapid and great, and it is unhkely that there will be much recovery. The return of faradic irritability that has been lost is a favorable indica- tion; it signifies nerve-regeneration, and will be followed by an increase in voluntary power. Without an electrical examination it is necessary to wait longer before a prognosis can be given, until distinct wasting on the one hand, or improvement on the other, indicates the regions in which the paralysis will persist and in which it will pass away. Even then the prognosis cannot be so definite. In the chronic stage the prospect of ultimate recovery depends on the rate at which wasting developed, on the electrical reaction, and on the duration of the case. Where there is no sign of returning power at the end of three months very httle recovery will occur; the nerve-cells are destroyed, their renewal is impossible. The preservation of voltaic irritability (that of the muscular fibres) is so far satisfactory that it shows there has been no destructive degeneration of the muscles; and if voluntary power is increasing, it indicates favorable conditions for its exertion, but it does not lessen the grave significance of persistent palsy and the absence of faradic irritability, which indi- cate persistent nerve-degeneration. On the other hand, if, at the end of one or two months, some faradic irritability can be still detected, although low in degree (i. e. elicited only by a strong current), improvement is probable, and may become considerable. It is neces- sary, in the case of children, to remember, and it is important to warn the friends, that the growth of the most affected limb will be hindered, and that this, in the case of the leg, may render the effect of the paralysis more obtrusive by its interference with the gait. Otherwise they are distressed by what seems to them an increase in the disease, but is really compatible with continued improvement. Treatment.—The treatment of the acute stage of the disease is essentially the same as that of myelitis, already described, and the rules and principles already stated need not be here repeated. In the initial stage it should be that of the general state, guided by any special causal indications that may be detected; such as free sweating, followed by salicylate of soda or salicin, in a case distinctly due to exposure to cold. We may hope that future observations will afford us some indications regarding the means of counteracting 420 SPINAL CORD. other blood-states that apparently exist at the onset, and are con- cerned in the production of the lesion. At present we are without this help, and can only treat the initial stage as we should any other local inflammation, directing our treatment to the symptoms that may be present, and the conditions that apparently underlie them. The child should be kept at perfect rest, on the side, so that the spine is not the most depending part. Warmth may be applied over the affected part of the cord by poultices or fomentations. The marked relief these give, when there is spinal pain, make it probable that they exert a beneficial influence in all cases. In such a disease—in which there is a natural tendency for the morbid process to cease to spread, and then to lessen in extent—the difficulty of ascertaining the effect of treatment on the lesion of the spinal cord is very great. Full doses of belladonna or ergot have been credited with the control and arrest of the morbid process, but only on the evidence of a coincidence in isolated cases, the value of which is small in a disease so irregular in its course. Either may appa- rently be employed, however, without fear of harm. But probably the measures mentioned above directed to the local inflammation have far more influence than drugs on the morbid process. As in all acute diseases of the nervous system, the chief room for effective treatment rests with the practitioners who see the cases in the early stage. When the acute onset is over and the spinal lesion has become stationary the careful management of the early stage should be con- tinued for a time, because a relapse or recurrence, however rare, is not entirely unknown. Such care is especially needed in cases in which the constitutional disturbance has been prolonged, or has continued after the onset of the spinal symptoms, or in which the latter have come on in distinct stages. Under these circumstances, perfect rest should be maintained for one or two weeks more. The same prolonged care is needed when there is persistent tenderness in the limbs, or any indications of an independent neuritis. Where wasting is taking place, some slight tenderness of the nerves and of the muscles must be expected to accompany the process, and this, being purely secondary in nature, does not call for special treatment. When the acute stage is over, and the condition of the patient is stationary or improving, tonics are generally both useful and needed, especially iron and quinine. Strychnia may be given in all cases, but it should be commenced only three or four weeks after the disease has become stationary. Although clear proof of its utility is not forth- coming, and cannot indeed be expected in a disease in which merely damaged nerve-elements always tend to recover, the drug has a definite influence on the nutrition of the structures that are specially affected, and it is reasonable to suppose that it promotes their recovery, and is capable of rendering this greater. But an agent that has so powerful an influence on function (and therefore on nutrition) is likely to do harm, rather than good, until normal conditions are ACUTE ATROPHIC PARALYSIS. 421 being restored. If function cannot respond properly to a stimulus, it is not hkely that nutrition can be influenced aright. Hence, the more severe the lesion the longer time should elapse before strychnia is commenced, and the smaller the dose that should at first be given. It is probably never either necessary or desirable to give it by hypo- dermic injection in this disease. The disease frequently occurs at the age at which any illness causes the hindrance to general development that constitutes the condition known as rickets, and this fact should be remembered in treatment. In the case of children who are still in the period of the first denti- tion, it is, therefore, wise to anticipate the danger by giving, during convalescence, those agents that have most influence in counteracting the tendency, especially cod-liver oil and iron; the lacto-phosphate of lime and iron is especially useful. The use of electricity is an important part of the treatment, although for reasons very different from those that first led to its use, and it is desirable that they should be clearly comprehended to secure its benefit and prevent its harmful or useless employment. There is no evidence that it can or does influence the process of recovery of the damaged elements in either the spinal cord or the nerves. Moreover, as long as the nutrition of these is actively disordered, its stimulating influence is hkely to increase the derangement rather than promote the restoration of a normal state. The reasons for its use depend on the fact that the disease entails nerve-degeneration, and are essen- tially the same as those that justify and determine its employment in other nerve lesions, and have been already explained. The muscular fibres whose nerves are degenerated suffer changes in nutrition, and ultimately perish if no nerve-regeneration occurs. While the influence normally exerted by and through the nerve-fibres is in abeyance, the muscles are destitute of this influence, and without any functional stimulation. If they are excited from time to time by electricity, their sensitiveness to stimulation is distinctly increased, and this not only to electricity, but to the voluntary stimulus. This is clearly shown by cases that have been untreated; the muscles may not respond at all to the first application, but when they have been galvanised two or three times a distinct contraction may be obtained, and, within a week, some voluntary power may return. Wherever cell and fibre have perished, nothing that electricity effects can be of service ; but where there has been damage, not destruction, and the nerve-fibres slowly recover, but regain their influence on nutrition, and their capacity for conveying impulses, only after some months, the failure of muscular nutrition may be disproportionately great, and may even render useless some regained nerve-power. This result electricity is probably able to prevent. It does not, as far as we can perceive, prevent or even lessen the visible wasting of the muscles ; it is powerless to counteract the effects of a destructive lesion ; but it does seem to hasten recovery from the effects of partial 422 SPINAL CORD. damage, and to lessen the ultimate degree of this damage. It does so solely by its influence on the muscular tissue, and only voltaic elec- tricity can stimulate this tissue when the nerve-fibres are degenerated. The mode of application should be the same as for nerve lesions. The muscle is only stimulated when the circuit is interrupted, as by repeatedly stroking the muscles with one terminal (a sponge, or con- ductor covered with water-holding material, well wetted with salt and water), which should be lifted from the skin between each stroke. The other terminal is kept still; it may be placed on the upper part of the muscle, where its nerve enters it. By some this terminal is placed on the spine over the affected region (and then a larger flat terminal is employed), under the impression that the electricity may influence the morbid process in the spinal cord; but there is no evidence even that the spinal cord is reached by electricity so applied. When applied to the muscles, the strokes may be made with the negative terminal, since each pole will influence the tissue, and the normally greater irritability to the negative often persists. The appli- cation can be made perfectly well by an intelligent nurse, since the diffusion of the voltaic current is so great that it is sure to reach the affected muscles. Each time the sponge is placed on the skin the affected muscles should be seen to move or swell up in slight contrac- tion, and it is desirable to use as many cells of the battery as will produce this result. Sometimes this cannot be done without causing so much pain as to distress the child, but in many instances the distress is really due to a needlessly strong and painful current having at some time been used, and an amount of alarm produced that the child never gets over. It is on this account that it is so important to make a test examination with great care, and to employ the less painful faradic shock. Emotional disturbance may generally be avoided by commencing with a very weak current. It is better, indeed, to commence with no current at all, applying the sponges in the way directed, so that the child may be familiar with them, and cease to fear them. Then two or three cells may be used, and the strength gradually increased day by day. In this way a current strong enough to cause contraction will often be tolerated. If, however, in spite of these precautions, this strength cannot be employed without distressing and disturbing the child, the attempt to obtain muscular contraction should not be persevered in, but only such a current employed as does not disturb the child. An influence on nutrition, if slighter, is still exerted, and if the application is con- tinued for a longer time it is probable that equal good is done. The electrical treatment may be commenced at the end of the fourth week after the onset. It should not be used earlier, lest it excite increased disturbance in the spinal cord. The application need only be made to those muscles in which faradic irritabihty is lowered or lost. Other mus- cles will recover without its aid, or will be uninfluenced by electricity. Another measure which should be employed is systematic rubbing ACUTE ATROPHIC PARALYSIS. 423 of the limbs. This stimulates the circulation, which is always defec- tive, as the blue, cold surface shows. It no doubt also increases the movement of the fluids in the tissues outside the vessels, and so probably increases the interchange of material, and promotes nutri- tion. The muscles should be daily rubbed and gently kneaded, upward rubbing being especially useful. No liniment is required ; the uncovered hand answers best. Cod-liver oil is sometimes rubbed on; a minute quantity is probably rubbed in, without good or harm. Great care should be taken at all times to keep the affected limbs as warm as possible. In all cases in which the trunk muscles are weak, even in slight degree, bronchial catarrh must be guarded against with great care. In such cases the muscles of respiration are weakened, and although normal breathing may not be impaired, the diminution in strength may render an acute bronchial catarrh rapidly fatal, and this even months after the onset of the paralysis. When some voluntary power is regained the systematic use of the muscles is of great service, and should be carefully attended to. Systematic planned movements may generally be adopted, and an improvement of muscular nutrition and power may be secured much earlier than if the limbs are left to the chance influence of such move- ments as a child spontaneously adopts. Most of the good that is done by " movement cures " may be obtained by such simple mus- cular exercises as can be readily arranged with the help of a little consideration on the part of the doctor, and can be efficiently carried on at home, given the necessary perseverance on the part of those who have charge of the patient, and which, unfortunately, is less often forthcoming. Such movements need to be specially arranged to meet the exigencies of each case, so as to call into action those muscles that are weak but not powerless, or that may supplement the muscles that are paralysed. A very important element in the management of the chronic stage is the prevention and treatment of the muscular contractions, and of the deformities to which these give rise. The contractions cannot be entirely hindered, but they may often be prevented reaching a high degree by careful attention to the position of the limbs, and by watching for and treating the earliest indication of shortening of the muscles. It is needless to discuss in detail the varied influence of post ure in these cases ; careful and frequent examination of the patient will show whether any deviation from normal relations is being deve- loped, and its counteraction is chiefly a matter of common sense and a little practical ingenuity. Of especial importance, however, are the prevention of the curvatures of the spine which are caused by allowing the patient to sit up before the back muscles have regained the neces- sary power, and the prevention of the shortening of the flexors of the hip and knee joints that occurs when the patient is allowed to lie in bed with the legs drawn up. More difficult of prevention is the con- 424 SPINAL CORD. traction of the calf muscles, often aggravated in consequence of the lessened growth of the limb. Something may be done during the process of rubbing for the prevention of deformities. While the con- tracted muscles are rubbed upwards they should be extended gently but firmly. Thus, if the calf muscles are shortened, the foot should be steadily pressed upwards while the calf is rubbed. A slipper with elastic straps to a knee-band may be worn at night, often with great benefit. For developed deformities, due to great shortening of the muscles, surgical treatment by splints or tenotomy is usually necessary, and is often important because it enables the patient to use the limb in ways that would be impossible without it. For this and other reasons mechanical appliances are of unques- tionable value. Counteracting deformities and supplementing weak muscles, they often enable a child to walk who could not do so without their aid, and power is often increased to a remarkable extent in indirect ways. In all these cases, however, the instruments require frequent attention and alteration to adapt them to the changes due to growth, and patience is required in the management of these cases through their long and tedious course. Two facts deserve a final emphasis. At the end of six months all possible i ec >very is nearly completed, and certainly at the end of a year the lesion has become a cicatrix, and further improvement will be merely by the slow growth of the muscle that has recovered, under the stimulus of use. Secondly, this process of slow improvement as the result of use will go on for years,—will go on whatever treatment is adopted, and whether special measures are employed or not. The therapeutic specialist who carries on his treatment month after month will claim it as his achievement, but it would occur equally without his aid. From its nature, however, as already stated, it may probably be always augmented by some contrivance to increase the influences that are really improving the power of the muscles. Subacute and Chronic Atrophic Spinal Paralysis (subacute and chronic polio-myelitis). Under this designation cases have been described of a miscellaneous character, in which paralysis, followed by muscular atrophy, comes on less rapidly than in the acute form, its development occupying from ten to thirty days in the cases which are termed " subacute," and from one to six months or even more in those which are called " chronic." Many cases included under this name differ much in their characters, and are sometimes described as " chronic myelitis; " but among the cases placed, even until lately, in this group, are forms of multiple neuritis. Most subacute atrophic palsies are due to nerve disease ; almost all, indeed, which present symmetrical palsy. The cases of spinal atrophic paralysis, in which the onset is not acute, may be placed in four classes. ACUTE ATROPHIC PARALYSIS, 425 (1) Cases of subacute poho-myelitis which differ from the acute form, already described, only in their less rapid development. They present the same initial general disturbance and wide distribution, and the same recovery, except in a limited region in which muscular wasting occurs. They are thus distinguished from polyneuritis, and also by the irregular distribution of the symptoms. Most of the suf- ferers have been adults. Little is known of the exciting cause of this form further than that it certainly sometimes follows exposure to cold, and is probably sometimes the result of a toxemic influence. The symptoms and general history of these cases present no important difference from the acute form. (2) Cases are met with that differ from the type just described in the fact that their course is progressive. The onset is subacute or sub- chronic, occupying from a fortnight to several months, but instead of arrest followed by improvement, the more or less rapid onset is fol- lowed by slower gradual increase, until at last wide-spread chronic muscular atrophy is developed. Many of these are really cases of progressive muscular atrophy with a subacute onset. For example, I have more than once known a case of this disease, ultimately typical, to begin by a subacute atrophic paralysis of the extensors of the wrists. These cases will be considered in the account of that disease. Others present differences from that malady and symptoms of more irregular character, which show that the lesions are distributed through various structures in the cord, and these must be regarded as cases of chronic myelitis involving the anterior cornua. This form also is chiefly confined to adults. It occasionally results from cold, and sometimes from injury, as a fall on the back. Intemperance and venereal excesses are also said to cause it. The wide-spread muscular atrophy which sometimes results from lead-poisoning is probably of this nature. The muscles at first present the degenerative reaction, or normal faradic irritability with increase to voltaism; sometimes, however, there is a loss to both faradism and voltaism. The sphincters usually escape. In many cases the affection exhibits a persistently progressive character; muscular atrophy slowly increases and ex- tends, until the case ultimately resembles one of progressive muscular atrophy, and the patient dies at the end of one or two years from exhaustion, or from interference with the respiratory movements. In other cases the atrophy, after slowly progressing for many months, becomes stationary, and considerable improvement may ultimately take place. This course is seen especially in traumatic cases. Few observations on the pathological anatomy of the affection have been made. Cornil and Lepine found, in one case, at the end of four years, softening of the lower part of the spinal cord, chiefly in the anterior cornua, disappearance of the ganglion-cells, increase of the connective tissue, and sclerosis of the white substance around the anterior horns. The diagnosis from the first form rests on the slow onset and pro- 426 SPINAL CORD. gressive course of the disease. Although the degenerative electrical reaction may be found, it is frequently absent, and this is another distinction from the acute variety. On the other hand, the fact that paralysis precedes wasting is a distinction from progressive muscular atrophy. In the most chronic form, however, this distinction fails, and cases are met with which present a gradation between the two diseases. The prognosis is grave except in traumatic cases, but is influenced by the observed rate of progress, and the presence or absence of any indications of arrest. When the result of injury, considerable im- provement is not uncommon, and it is remarkable how great a degree of paralysis and atrophy may, in these cases, ultimately pass away almost completely. The treatment of the disease must be influenced by the rapidity of its onset. In the subacute stage and form it should be conducted on the same principles as that of acute cornual myehtis. In the chronic form the treatment must be the same as for progressive muscula.r atrophy. (3) Many subacute and chronic cases, which have been described as atrophic spinal paralysis, are peripheral, not central in their nature, and are cases of multiple neuritis, the symptoms and diagnostic indications of which have been already described. The history of the subacute spinal disease has been largely written from cases of multiple neuritis. In the statements just made this fact has been kept in view. While multiple neuritis may simulate closely chronic poho- myelitis, it is certain that the converse is also true, and the central affection has been sometimes thought to be peripheral. The facts at present available suggest that the central and peripheral structures of common function possess common susceptibilities to the action of morbid influences, and there is still danger that the two classes may be confused. The most important criterion is the greater irregularity in distribution of the central disease,—the more perfect symmetry of the peripheral affection. The presence of tenderness of the nerve- trunks, and of the structures to which the nerves are distributed, is of more value, when it exists, than is the suggestion afforded by its absence that the disease is central, because, in the periphery, only fibres of one function may suffer: we may then have none of the symptoms that we commonly associato with neuritis, and look for as proof of its existence. In purely motor neuritis there may be no tenderness or pain. But such an affection is either unilateral or perfectly symmetrical. Imperfect symmetry indicates an affection of the cord. (4) A family form of slow muscular atrophy in children with changes in the anterior horn cells has been described in the last few years by Hoffmann and others. It will be referred to when we come to speak of the myopathic atrophies with which it has some affinities. ACUTE ASCENDING PARALYSIS. 427 ACUTE ASCENDING PARALYSIS. Ascending paralysis, which commences in the legs and ascends to the muscles of the trunk, the arms, muscles of the neck, the diaphragm and the pharynx, is a feature of several diseases—meningeal haemor- rhage, ascending myelitis, &c.; but it occurs also in cases in which the spinal cord, after death, appears healthy to both naked-eye and microscopical examination. Such cases have, however, certain charac- teristic features which make it desirable to distinguish the condition from other diseases, and the affection has, therefore, been provisionally, termed " acute ascending paralysis," in the absence of any evidence of its nature. It was first described by Landry in 1859, and hence is often called Landry's paralysis. Acute ascending paralysis is a most formidable malady, most cases proving fatal in a few days. Its nature is mysterious, but recent discoveries regarding multiple neuritis have disclosed instructive analogies between the two affec- tions. These have, indeed, led some observers to the opinion that this ascending paralysis, without organic central lesion, is an affection of the nerves.* As we shall see, it is not probable that this opinion is correct, although it is possible that the nerves, as well as the centres, are sometimes affected. Causes.—The etiology of the disease resembles, in general, that of acute multiple neuritis more nearly than that of any other affection. The disease affects males more frequently than females. It occurs chiefly between twenty and forty years of age, but has been observed in rare cases in older and younger persons, and even in children. Some sufferers have been the subjects of alcoholism. Severe exposure to cold has been the apparent cause in many instances. In other cases the disease has occurred under conditions such as cause toxaemic states, or after the occurrence of some known blood disease. Thus it has occurred during convalescence from some general disease, smallpox, diphtheria, typhoid fever. It has also followed influenza and febrile diseases of obscure nature. In these cases, it should be noted, the disease has followed at an interval of a week or a few weeks. It also sometimes succeeds some traumatic process, such as a wound, and here also after an interval, and usually when the wound was apparently healed. I have known it thus to follow an attack of pelvic cellulitis. In these respects it closely resembles polyneuritis; and it has been observed, in severe form, in the subjects of old alcoholic neuritis. The disease has been repeatedly observed in the subjects of syphilis, and has apparently been arrested by the treatment for this disease f The circumstance that when some malady or wound pre- * See Ross and Judson Bury, 'Treatise on Peripheral Neuritis.' f Much weight should not be placed on this fact as proof of causal relationship, because (apart from the fallacy of independent cessation) it is probable that the treatment that is effective against the virus of syphilis is also effective against other blood-states that depend on agents of similar nature. 428 SPINAL CORD. ceded the disease, the former was often of a trivial character, prevents surprise at the fact that, in many cases, no influence could be traced to which the disease could be ascribed. Symptoms.—Premonitory symptoms have been noted in some cases —o-eneral malaise, pains in the head and back, tingling in the extremi- ties — for a few days or a week before the onset. The first definite symptom is usually weakness of the legs, often commencing in one and spreading to the other. The weakness increases rapidly, so that the power of standing is lost, sometimes in a few hours, sometimes at the end of two or three days ; it goes on to complete paralysis, with relaxation of the muscles. As the legs become motionless the muscles of the trunk become weak, first of the pelvis, loins, and abdomen then of the thorax. The weakness next invades the arms ; either the upper arm muscles or those of the forearm and hand may be first attacked, and one arm is often weakened before the other. The paralysis of the arms may become absolute, like that of the legs, or some power of movement may remain. The diaphragm and neck muscles then suffer, and difficulty of swallowing comes on, sometimes with paralysis of the muscles of the palate, and often speech becomes difficult, nasal, and indistinct. The inabihty to swallow may become so great that the patient has to be fed through a tube, and the para- lysis may involve the muscles of articulation to such an extent that utterance may be altogether unintelligible. There is often dyspnoea from the weakness of the muscles of respiration, or from interference with the respiratory centre in the medulla., and the cardiac centre may also be involved. The affection of the bulbar nerves is determined by functional relations; thus the lips may be paralysed with other muscles of articulation when the upper part of the face is unaffected. In rare cases the eye muscles are paralysed in some degree, usually manifested only as loss of accommodation, inequality or dilatation of the pupils, impaired reaction to light, or sliglrMctrabismus. The tingling and analogous subjective sensory disturbance has been followed, in some cases, by hyperesthesia of the skin and tenderness of the muscles, but it is probable that in such cases there has been multiple neuritis. There may be some blunting of sensibihty in the extremities, but there is definite loss of sensation only in some severe cases of the typical disease. A firm touch can usually be per- ceived anywhere; perception of painful impressions and of heat or cold is sometimes delayed. At first, reflex action is lost in the affected limbs, both cutaneous reflex action and myotatic irritability. In cases rapidly fatal the loss has continued till death. In cases that have recovered reflex action has returned, but recorded cases have presented considerable differences in this respect, and, as there is some doubt as to the nature of many non-fatal cases, there is some uncertainty as to this point. In some the myotatic irritability has soon returned, and has even become excessive. In the majority it has remained absent, ACUTE ASCENDING PARALYSIS. 429 and not until all paralytic symptoms have disappeared has the knee- jerk returned. In spite of the early flaccidity of the muscles, if life is prolonged they rarely present either wasting or change in electrical irritabihty. A trifling reduction in size may occur, but there is no muscular atrophy such as occurs in polio-myelitis, and even after several weeks the most careful examination fails to reveal any abnormal electrical reaction— a very important feature of the disease. Exceptional cases, which do present the degenerative reaction in the muscles, seem more closely allied to a universal polio-myelitis, from which, indeed, this disease cannot be sharply separated. The sphincters, moreover, escape in the vast majority of cases, but not in all. There is no tendency to the occurrence of bedsores. The cerebral functions are not usually involved, and the state of the patient who, with unimpaired intellect, cannot express himself either by speech or gesture, is painful in the extreme. In exceptional cases, however, there is mental dulness or slight delirium, as if from the influence of a blood-state on the brain. In girls this may take the form of hysterical manifestations, by which the nature of the disease may be masked. As a rule there is no elevation of temperature, even during the rapid development of the symptoms, but in one or two cases, which were not fatal, brief pyrexia attended the onset, and in a few others moderate febrile disturbance (2° or 3°) occurred at a late period. Profuse sweating has been occasionally noted. Enlargement of the spleen (first noted by Westphal), such as occurs in other acute diseases, is very frequent. Thus the chief feature of the disease is an almost purely motor paralysis, progressive in character, with relaxation of the muscles during the acute stage of the disease. It usually has an ascending course, but irregular cases are met with in which the order of invasion is varied. Thus the arms are occasionally involved before the legs, the diaphragm before the intercostals; the bulbar symptoms have been known to precede the others, and I have seen them reach a high degree with a fatal involvement of the cardiac centre before the upper muscles of respiration were affected, or the hands quite powerless. Analogous cases have been recorded by others, the special features and course being those characteristic of the disease, In some cases, however, of irregular course, changes have been found in the electric irritability of the muscles; it is probable that, in such cases, the peri- pheral nerves are affected, although we cannot, on this account, at present separate these from the typical cases of the disorder—a point that will be explained in connection with its pathology. The disease varies considerably in the rate of its progress. It may run its course and end fatally in forty-eight hours. Death usuallv results from either respiratory or cardiac paralysis—the latter in the cases of irregular course. A large proportion of the fatal cases last less than a week. On the other hand, the disease may only attain its 430 SPINAL CORD. height at the end of two, three, or even four weeks. In some cases, apparently of the same character, the paralysis of the limbs has not been complete. There may be a rapid extension of the paralysis to a certain point, and it may then cease to spread, and the limbs last and least affected may slowly regain power. A patient may hie for days in a condition of universal palsy, save for a httle respiratory power, and then improvement begin. As a rule, the order of recovery of the muscles is the opposite to that of their invasion. In favourable cases the recovery of power is usually slow; two or three months often elapse before the weakness entirely disappears. Occasionally there has been a more rapid improvement, and the patient has been well in a few weeks. Pathology.—The most careful and skilled examination has often failed to discover any morbid appearance in the spinal cord, nerves, or muscles. Minute haemorrhages, met with occasionally, have probably occurred during the last moments of life. In other cases, apparently similar to the others, vascular engoragement has been found in the grey matter of the cord, the significance of which is increased by leucocytal accumulations around the vessel. Changes in the ganglion-cells in the more acute cases have also been found, swelling and blurred outline.* Of late attention has been paid to the peripheral nerves and shght indications of acute changes, both parenchymatous and interstitial,! have been found in them, but only in exceptional cases, and peripheral neuritis seems to play no part in the typical disease, although sometimes simulating it. In addition to the enlargement of the spleen observed during life, and found also after death, the mesen- teric glands have been found swollen, and also the closed follicles of the intestines. Organisms have been found in the glands,^ and culture of portions of the nerve-centres yielded, in one case, a bacillus resembling, but not identical with, that of splenic fever. § Other observers have searched for them without success in all cases of typical character. These negative facts, taken in conjunction with the conditions under which the disease occurs, and with the course of the malady, have suggested the idea of a toxic influence acting on the nerve-centres • and this idea receives support from the discovery that acute swelling of the spleen is common, and of the lymphatic glands not rare- lesions that indicate a morbid blood-state. The limitation by func- tion of many toxamiic palsies, e. g. that of accommodation, supports this view, since the isolated acute paralysis of functional centres, not anatomically separate from others, is known only as a consequence of a toxic influence. Further confirmation is afforded by the fact that cases of acute multiple neuritis, certainly due to a toxaemia, may run a * Immermann, Marinesco and Marie, Bailey and Ewing. t Eisenlohr,' Dent. med. Wochenschr./ 1890, No. 38. X Baumgarten. § Marie and Marinesco. ACUTE ASCENDING PARALYSIS. 431 similar course. It has, indeed, been conjectured that the nerves are always the structures impaired, but this exclusive view is disproved by the normal state of the nerves in cases in which the grey substance of the spinal cord has been found to be changed and by the common absence of altered excitability of the muscles, since the motor nerves seem never to escape invariably in peripheral neuritis of any variety, however common their freedom from affection in the type. But the nerves suffer also in some cases, and there seem to be gradations to the cases of acute multiple neuritis of ascending course described at p. 162. All the facts point to the conclusion that the disease is due to a toxin which has a specific action on the motor neurons in the spinal cord, chiefly on the anterior grey matter, sometimes also affecting the motor nerve-fibres proceeding from them. Sometimes it has a wider influence on the spinal cord, and its effects can be traced into the white substance or the posterior horns, possibly as an extension of the inflammatory changes it induced. These are similar to those that attend any acute disturbance of function; the toxic influence is mysterious in nature and origin, but seems to resemble that which causes polio-myelitis, in which the morbid process presents variations and may also involve the nerves. The toxine may be pro- duced by the agency of bacteria, but the evidence of this is incon- clusive; some casos have followed exposure to cold. Diagnosis.—The disease is recognised by the rapid development of paralysis, usually but not invariably ascending, with relaxation of the muscles, and with loss of reflex action, without considerable pain or, generally, any loss of sensation, and if the patient survives, without wasting of the muscles or change in electrical irritability. The latter characteristic distinguishes the disease from acute atrophic paralysis, while the absence of pain in the back and of spasm is a distinction from meningeal haemorrhage. The diagnosis from general ascending myelitis has been already considered; it rests especially on the in- volvement of all the functions of the cord in inflammation. The distinction from multiple neuritis has been mentioned in the account of that disease (p. 174), but, it may be, is not always absolute, since the nerves probably suffer, as well as the cord, in some cases of ascending paralysis. Further, the cases of multiple neuritis simulating this affection, the nature of which has been demonstrated pathologi- cally, have usually run a more prolonged course, several weeks or even months. The distinction from polyneuritis, founded on the course of the ascending form, is subject, however, to the reservation that while ascension to the arm through the trunk is a feature of the central disease, this is not excluded by a more irregular course, and the character of the individual symptoms must be taken into consideration (see also p. 429). Prognosis.—The affection is one of extreme gravity. The danger to life is in proportion to the interference with respiration and with the functions of the medulla oblongata, especially with the cardiac 432 SPINAL CORD. centre, and also to the rapidity with which the palsy comes on. But the cases which develop with comparative slowness are not devoid of danger. Even when the symptoms only reach their height at the end of three or four weeks, death may occur in the same way as in the more rapid cases. On the other hand, recovery has been known although the patient has lost all power of motion at the end of the second day. The danger is great as long as the symptoms are in- creasing, and only when distinct improvement can be recognised is it justifiable to anticipate recovery. The earlier the bulbar symptoms appear, the more serious is their significance. Mental symptoms also increase the gravity of the prognosis, as they usually indicate a severe blood-change, the effects of which on the nervous system are hkely to reach a high degree. Treatment.—During the early stage of an attack of acute ascend- ing paralysis, in the absence of other indications, the treatment should be that suitable for myelitis, since, at the onset, the diagnosis between the two diseases can never be certain. A warm bath, or still better, a vapour bath, should be given if the symptoms followed exposure to cold. It should be followed by counter-irritation over the spine by a long, narrow mustard plaster. More energetic counter-irritation, even the actual cautery, has been recommended. The body should be kept in as perfect rest as possible, and on the side rather than on the back. In very few cases have drugs appeared to exert any influence on the course of the disease, and the malady is so rare that experience accu- mulates slowly. Salicylate of soda seems to deserve a trial in cases that follow exposure to cold. Ergotin has been given, and one case in which it was used deserves special mention. The patient was a man aged fifty-seven, who, a week after exposure to cold and wet, com- plained of a feeling of weight and weakness in the legs ; the temperature rose to 103°; the loss of power gradually became complete in the legs and spread to the arms, without loss of sensation. At the end of the second day there was difficulty in swallowing, in articulation, and in breathing, and death seemed near. Ergotin was given every hour, and during the night the patient took twenty grains. In the morning the bulbar symptoms were better, the arms stronger, and there was a trace of motor power in the legs. The patient rapidly improved, and at the end of a week was well. If swallowing becomes difficult, care must be taken to administer a sufficient amount of nourishment either by the rectum or by the nasal tube. A few cases have been recorded in persons who had had syphilis, in whom arrest of the disease followed the administration of iodide of mercury. The chief lesson of modern research is certainly that we must look for the means of effective treatment to the neutralisation of the toxic influence on which the malady apparently depends, but at present nothing has been ascertained regarding antidotal agents available in the acutely active stage of these toxaemic states. It is, however pro- bable that mercury is capable of doing good, and that when the causa- divers' paralysis. 433 tion is obscure, and the disease develops slowly enough to permit mercurial treatment, it is wise to adopt this irrespective of the fact of preceding syphilis. In cases that follow traumatic lesions, especially if there have been any indications of septicaemia, full doses of per- chloride of iron offer, I believe, the best means of destroying the activity of the blood-state. The general and local treatment should be the same as in acute myelitis. PARALYSIS FROM LESSENED ATMOSPHERIC PRES- SURE; DIVERS' PARALYSIS; CAISSON DISEASE. Divers, and especially those who work in caissons, at such a depth beneath water that they are exposed to considerable pressure, may be- come paralysed soon after their return to the surface.* Apoplectic attacks and hemiplegia also sometimes occur, sometimes transient mental disturbance, or deafness, or bleeding from the nose, but para- lysis of the legs is by far the most common effect, and it is, therefore, clear that the spinal cord suffers in greater degree than any other part of the nervous system. Miners have been said to suffer also, but this is doubtful, because a pressure equal to at least an additional atmosphere seems necessary for the production of the symptoms. Most of the subjects of the disease have worked at a depth of from forty to ninety feet below the surface of water, and under a pressure of two to four atmospheres. In the extensive works involved in laying the foundations of bridges, in which many men have been employed, a considerable proportion of the workers have suffered in some measure; but severe degrees of affection are rare, because the conditions under which they occur can be avoided. They only occur in those who have been exposed for more than a certain time, which is the shorter the greater the pressure. At a depth of ninety feet beneath the surface immunity from severe symptoms (and commonly from all symptoms) is obtained by reducing the periods of work to an hour. The danger is greater in those who have had several previous periods of work on the same day, and especially if slight symptoms have been experienced after one of these. It is also greater in those unaccustomed to the conditions. I have met with one case of hemiplegia hi a diver after only half an hour's work in a well at ninety-six feet, but the man had been down twice before with only intervals of rest of half an hour, and the attack passed off in the course of an hour. In another case paraplegia occurred after working for an hour under only fifty feet of * See, on this subject, Babington and Cuthbert, ' Dubl. Quart. Journ./ 1863, p. 312 (cases at Londonderry); Eads, ' Med. Times and Gaz.,' 1871, p. 291 (cases at St. Louis); Leyden, 'Arch. f. Psychiatrie/ix, Heft 2; and Moxon, 'Lancet/ 1881, ii, 529. VOL. I. 28 434 SPINAL CORD. water, but the man had worked on the preceding day at a depth of one hundred and twenty feet below the surface. It is evident, there- fore, that the power of resisting the dangerous influence varies, and that predisposition to suffer may be caused by the conditions which also induce an attack. It is not during exposure to the abnormal conditions, but on return- ing to the normal atmospheric pressure, that the symptoms come on; often immediately, and always within half an hour or at most an hour of the return to the surface. The onset is usually preceded by other symptoms, and especially by pains in the ears and in the joints. The latter are very common, and occur after a much slighter degree of exposure than is needed to produce paralysis. They are felt chiefly in the larger joints, and may continue for days and even longer. Yery rarely there is also swelling of the joints. The deafness occasionally observed has been usually bilateral, often persisting-in one ear, but passing away in the other. It has even been attended by severe vertigo. The severer degree has been ascribed to haemorrhage into the labyrinth, but no pathological facts are at present available. It is important to note the conditions under which the symptoms come on. Not only do those who are unused to such work seem especially liable to suffer, but there are also considerable individual variations in the degree of liability. Paraplegia or hemiplegia may occur, but the former is far more common. The onset of the paralysis is sudden. The legs feel heavy and are found to be weak, and in a few minutes the patient is unable to move them. Sensation is often lost as well as motion, and in all severe cases the sphincters are affected. The arms are seldom involved. In slight cases the loss of power is incomplete, and one leg may be more affected than the other. The impairment of sensa- tion is often imperfect or irregular. If the paralysis is incomplete the power may return in the course of a few days, but in severe cases the palsy usually lasts for weeks or even months, and it may be permanent. Death may occur at the end of a week or more, in the same way and from the same causes as in acute myelitis. When the paralysis is hemiplegic it is generally moderate in severity and transient, passing off in a few hours or days. It may be even still more brief, as in the case referred to above, in which a diver, after half an hour's work ninety-six feet below the surface, suddenly felt tingling across his loins, and that his right arm and leg were almost powerless ; in half an hour he had recovered sufficiently to walk home. If cerebral symptoms are more intense, they are generally very severe. with sudden loss of consciousness, continuing as deep coma, irregulai breathing, and indications of cardiac paralysis. Such cases usually end in death in the course of a few hours. Pathology.—The most probable explanation of these cases ascribes them to the escape from the blood of gases, with which it has become DIVERS' PARALYSIS. 435 charged during the exposure to the high pressure. It is certain that a great excess of gas must be dissolved in the blood during the expo- sure, and that the amount, at least of oxygen and of carbonic acid, contained in the blood when the person emerges from the caisson must be vastly greater than normal. It must, moreover, be greater the longer the exposure, since the absorption of the excess will be a gradual process, taking place through the lungs in respiration, but it will be more rapid as the pressure is greater. These conditions agree with observed facts. After returning to the normal atmospheric pressure, the excess of gas probably passes off gradually by the lungs in most instances ; but if extreme, gas may escape from the blood within the body. The occurrence of this has been proved experimen- tally (Hoppe-Seyler and P. Bert). Gas, so escaping, is no doubt quickly reabsorbed, but must exert a pressure capable of arresting the function of the structures of the nervous system. If abundant, it may conceivably rupture these. Further, the special effect on the nerve-centres may be connected with the position of these within cavities that are practically closed. These conditions, coupled with the extremely circuitous course of the blood from the cord, may explain the incidence of the effects on the nervous system. The few ascertained facts harmonise with this pathology. Such escape of gas has been proved to result from diminution of the atmospheric pressure.* In many cases no visible lesions have been found, and it is obvious that gas, widely effused, may exert dangerous pressure, and yet may be speedily removed, so that no indication may remain of the cause that has completely arrested function. It was once thought that the symptoms were due to local haemor- rhages, but extravasations are seldom met with, even in the results of experiment, and it is certain that they take but a trifling part in the production of symptoms. The only positive pathological observation agrees with the opinions above stated. Leyden f found (in a case of characteristic paraplegia) small irregular fissures in the mid-dorsal region, chiefly within the posterior and hinder parts of the lateral column. The fissures were filled with round-cells, but contained no red blood-corpuscles, and from their well-defined edges they were cer- tainly not produced by the infiltration of the cells found within them. The only explanation that is satisfactory, or in any harmony with their features, is that they were produced by the sudden escape of gas, and were afterwards occupied by the round-cells.J The physical firmness of the cord is far less in the dorsal region than in the en- largements ; and probably, as Leyden suggests, this is the reason why the dorsal region suffers structural damage from the escape of gas * Hoppe-Seyler, 'Mailer's Archiv/ 1887; P. Bert, 'Coinptes Rend./ 1871-2. t ' Arch. f. Psych./ ix, Heft 2. X The clinic il condition of transient hemiplegia, which has been observed in empyema as occurring during irrigation, and thought by some to be the result of air or pas embolism, may be of similar nature. 436 SPINAL CORD. more than other parts. It is evident, however, that such escape may occur in the brain, for instance, even to a fatal degree, and leave no traces unless it occurs so rapidly as to cause laceration of the tissue. The absence of haemorrhage of the ordinary character may be further explained by the fact that the effused air will resist the effusion of blood. Some other anomalous features, such as the transient cha- racter of the symptoms in some cases, are also explained by the peculiar nature of the lesion, which may exert a wide-spread and considerable influence, and in a short time may have vanished by the reabsorp- tion of the compressing air. Haemorrhage must be regarded as an accidental consequence, and the production of such fissures as were found by Leyden may not be a necessary part of the lesion, even in grave cases The mechanical effects of the gas may be considerable, and arrest the function of the nerve-elements, without the passage of the gas outside the capillary vessels. The fact that the spinal cord suffers more than other organs may be partly due to the plexuses through which the blood can return only slowly to the lungs, where its relief from the surcharge of gas is effected. The same considerations apply to the brain. In both organs the escape of air is more instantly disastrous than elsewhere, and, indeed, may not only occur, but act in a peculiar way, on account of the posi- tion of the organs within chambers that are, to a large degree, closed. The conditions are too complex to permit us to follow them in detail, or analyse fully the mechanisms that determine the effect on the nerve-centres. The escape of the excess of gas in the lungs can only take place gradually, as successive quantities of the surcharged blood pass through the capillaries of the air-cells. If, in consequence of the slowness of the circulation in the cord, any escape of air occurs in its capillaries, the effect of this will be still further to hinder the local circulation, and to favour the further escape of gas. In this way we are able to discern something of the mechanism which determines the special affection of the spinal cord. The less the external support the less will be the resistance to the escape of gas, and the incidence of the lesion on the posterior part of the cord may be, in part at least, determined by the adoption of the recumbent posture when the first symptoms are perceived. At the onset, when the first symptoms are experienced, it is probable that a return to a greater degree of pressure might arrest the develop- ment of the mischief. It is certain that, in all cases of exposure to a high degree of pressure, the transition to the normal pressure should be made gradually. When developed symptoms indicate that a definite lesion of the cord has occurred, the further treatment must be conducted on the same principles as in acute myelitis—the morbid process that has, in fact, been set up. H.EMORKHAGE, 437 HEMORRHAGE INTO THE SPINAL CORD; HJEMATOMYELIA. Primary haemorrhage into the spinal cord, sufficient to cause sym- ptoms, is a very rare disease, and it is even more rare than is suggested by the cases now and then recorded as such. We have already seen that haemorrhage may accompany myehtis; a considerable extravasa- tion may occur when the inflammation is only commencing, during the state of congestion, and while the symptoms are shght. Such cases are easily mistaken for primary haemorrhage. The risk of error is not always removed by pathological examination. Inflammation results from haemorrhage, and when indications of myehtis are found about a clot, it may be impossible to say whether these are primary or secondary. It is probable that many cases of secondary myelitic haemorrhage have been regarded and described as primary, and it is possible that a few cases of primary haemorrhage have been regarded as secondary. One writer, Hayem,* goes so far as to deny the occur- rence of primary non-traumatic haemorrhage; but such an exclusive view is unwarranted. It is certain, however, that the history of primary haemorrhage has been largely written from uncertain data, and will need extensive revision when a sufficient number of exact observations have accumulated. It is probable that the causal influences constitute the surest guide. When haemorrhage occurs under conditions which usually induce myelitis, the extravasation must be regarded as the result of the vascular disturbance of com- mencing inflammation. Etiology.—The rarity of haemorrhage into the cord is especially great in comparison with the frequency of haemorrhage into the brain. The difference probably depends on the tortuous and long course of the arterial path to the cord, whereby the vessels are preserved from the high pressure which is the chief cause of the degeneration, dilata- tion, and rupture of the cerebral arteries. Miliary aneurisms are not found within the spinal cord. Haemorrhage is far more common in males than in females. It may occur at any age, and has been met with in young children, even so early as seven months, f while some of the subjects have been in advanced life; but it is most common between twenty and forty, i. e. during the first half of adult life. Many cases occur in young adults apart from injury or obvious exciting cause, and apart also from initial myelitis, which accounts, however, for some of the cases. It has been met with as a conse- quence of a haemorrhagic tendency, as in a case in which it succeeded * ' Des He"morragies intra-rachidiennes/ Paris, 1872. t Clifford Allbutt,' Lancet/ 1870, vol. ii, p. 84. Numerous haemorrhages were observed in the grey matter of the lumbar and cervical enlargements (probably polio-myelitic, but occurring the day after a fall) in a child of four by Chaffey (' Path. Trans.,' 1885). 438 SPINAL CORD. severe epistaxis, to which the patient, a young man of twenty-four, was liable* Of immediate causes, injury is the most frequent, especially falls which involve a severe concussion of the spine ; the spinal column may or may not be injured at the same time. Over-exertion and exposure to cold have in rare cases preceded the onset. Chronic alcoholism and sexual excess have been thought to predispose. In one case within my knowledge, an extensive haemorrhage into the grey substance at the top of the lumbar enlargement resulted from coitus four times repeated, the symptoms commencing suddenly during the fourth act. Minute extravasations are often found after death from diseases which interfere with respiration and cause venous congestion, and they are especially frequent in maladies which at the same time cause func- tional excitement of the cord, as tetanus and all severe convulsions. They cause no symptoms, and are probably produced during the last moments of life. They have been termed " accessory.1' The diseases of the cord that lead to secondary haemorrhage are chiefly inflamma- tion, tumours, and cavities in the cord. The last-named condition is especially important. It is probable that haemorrhage occurs more readily if the spinal cord contains a congenital cavity or fissure, due to an arrest of development, and surrounded by embryonal neuroglial tissue. Hence this condition will be found in disproportionate fre- quency in cases of haemorrhage. Pathological Anatomy.—The minute extravasations just men- tioned, as met with after asphyxial and convulsive diseases, are found in both the grey and white substance, but especially in the former. They are usually microscopic, or visible to the naked eye as minute red points, distinguishable from distended vessels only by their slighter resistance to a stream, of water. The extravasation may occupy the perivascular sheath, or the cavity in which the vessel lies, or extend between the nerve-elements. The larger non-traumatic haemorrhages, which cause symptoms, always begin in the grey substance, and are often confined to it, extending into the white columns only when large in size. The vessels of the grey substance are more numerous than those of the white, have less external support, and probably undergo more considerable changes in state. The effusion forms a cavity in the cord, sometimes rounded, sometimes irregular in transverse section, and half an inch or more in vertical extent. The cord is enlarged at the seat of the haemorrhage, and this may be visible externally as a dark swelling the size of a nut or a bean. Yery rarely the haemorrhage tears the layer of cord which limits it, and blood, usually only in small quantity, escapes into the membranes. The tissue adjacent to the clot is usually broken down, stained, and softened, and inflammatory changes may be recognised in it with the microscope, just as in the neighbourhood of haemor- rhages into the brain. As in the latter, the effused blood slowly * Sinclair, ' Lancet/ 1885, ii, p. 1043. HEMORRHAGE. 439 undergoes changes in tint, becoming first rusty and then yellow, and ultimately a cyst may remain. Several extravasations may co-exist, usually in the same part of the cord. In contrast to this focal haemorrhage there may be an infiltration of the grey matter with punctiform extravasations, which may appear, until closely examined, to be a single haemorrhage. The tissue between these small extra- vasations is broken down. It is probable that this form is always secondary to myelitis, as in the case mentioned in the foot-note on p. 437. In such secondary cases a careful microscopical examination usually reveals indications of inflammation much more extensive than the area affected by the haemorrhage. A growth into which haemor- rhage occurs is usually a glioma, unaffected parts of which will be found in the neighbourhood of the extravasation. The cavities in the cord into which blood may escape are sometimes of considerable vertical extent. I have known a fissure in the posterior column to be filled with blood through almost the whole length of the cord. This condition thus favours both the occurrence and the extension of haemorrhage. Symptoms.—Slight symptoms, " prodromata," haAre been observed in some cases, chiefly in the form of trifling sensory disturbance, tingling, &c, in the limbs afterwards paralysed. They have existed for a few hours or days, or even for two or three weeks before the onset. It is probable, however, that these have been cases of secondary myelitic haemorrhage, and that there are no premonitory symptoms in primary extravasations. The actual onset is always sudden ; the symptoms attain a considerable degree in the course of a few minutes, but they sometimes increase during one or two hours, when the haemorrhage is from a small vessel and slowly increases in size—probably augmented by the rupture of other vessels which are torn in the tissue lacerated by the blood. Occasionally there has been transient loss of consciousness without any cerebral lesion, probably from the upward influence of the shock. Rarely the onset has been by a series of sudden augmentations of the symptoms. Sometimes the symptoms come on during sleep. The suddenness of the onset is the characteristic of the disease. The symptoms which thus develop vary according to the seat and extent of the extravasation. In the majority of cases there is para- plegia, complete motor and sensory paralysis up to the level of the lesion, with loss of power over the sphincters. Pain commonly but n< >t invariably accompanies the sudden palsy; it may be felt in the spine or in the sacrum, round the trunk, at the front of the thorax, or at the epigastrium, sometimes seeming to pass thence through the trunk to the spine, or it may be felt in the legs. If in the spine it is local, and does not extend through a considerable length of the spine, as in meningeal haemorrhage, and there is not the initial spasm and rigidity which characterise the latter disease. This pain may precede the palsy, even for half an hour or an hour ; it begins suddenly, 440 SPINAL CORD. and is no doubt due to the first slight extravasation, which afterwards increases (when some resistance yields), and effects the compression that produces the paralysis. Thus a girl aged fifteen was seized with sudden sharp pain, referred to the sternum at the mammary level, and to the corresponding region of the spine; this continued for half an hour, when the legs suddenly became powerless and insen- sitive. It is highly probable that when there is such initial medial or bilateral pain the haemorrhage occurs in the central region of the grey matter, perhaps from one of the commissural or anastomotic arteries (see p. 227), and that the pain is due to the irritation of the fibres of the posterior commissure, in which the paths for pain cross the middle line. The spinal column may be tender opposite the affected spot. Usually the paralysed muscles are relaxed. Some- times they are the seat of early clonic contractions, or these may come on a few days after the onset. When the haemorrhage is in the cervical region all the limbs are powerless ; one arm is often affected before the other. The state of reflex action varies according to the seat of the disease; if it is at first abolished it quickly returns in the legs (unless the haemorrhage is in the lumbar enlargement), and it soon becomes excessive unless destroyed by secondary myehtis—a not unfrequent consequence. In one case there was a remarkable initial increase of myotatic irritability a few hours after the onset, probably irritative, and quickly giving place to loss.* Yaso-motor and trophic changes in the skin are common and often intense; there is often vascular dilatation ; bedsores readily form, and cystitis may result. Frequently the secretion of sweat is increased for a time. The temperature is normal at the onset, but it generally rises in the course of a few days from secondary inflammation in the cord. The palsy developed at the onset usually continues for a week or ten days, although the pain may lessen. The symptoms do not always increase during the stage of inflammation, perhaps because this only involves the structures which are already impaired by pressure ; but if the patient has been brought near to death by the primary haemor- rhage, the secondary inflammation may end life. Occasionally, more- over, symptoms of an ascending or descending myelitis may come on, and the former may cause death by its interference with the muscles of respiration. This extension is greatest probably in cases of myelitic haemorrhage, in which the extravasation is merely an incident in the course of a commencing inflammation, but it seems also to occur in cases of primary haemorrhage. The slow extension upwards of the symptoms during the first week may be very distinct; and the occur- rence of descending inflammation may be shown by the loss of reflex action, and by the failure of electric irritability in the muscles, sometimes only in those supplied from the upper part of the lumbar enlargement. The symptoms pass into a chronic stage, improvement being usually slow. Some lasting loss of power remains in most cases, and there is " Sinclair, loc. cit. HEMORRHAGE. 441 often some permanent muscular wasting on account of the frequency with which the haemorrhage is in the cervical or lumbar grey matter. Occasionally there is rapid recovery up to a certain point; a haemor- rhage of small size may abolish conduction in the white columns by the suddenness with which it compresses them, and the effects of the pressure may quickly pass away, while those remain that are due to the destruction of the grey matter. Diagnosis.—The diagnosis rests on the actually sudden onset of the symptoms, and on the occurrence of pain, in a limited region, as part of these. The former is evidence of a vascular lesion (rupture or closure), and the latter shows an acute irritation of the nerve- elements, such as may be produced by their laceration, but not by mere deprivation of blood. It must be remembered, however, that we cannot assume that symptoms which come on during the night's sleep are of sudden onset. Neglect of this consideration sometimes causes a mistake in diagnosis. The mode of onset is a sufficient distinction from all other organic diseases, except haeraorrhagic myelitis and meningeal haemorrhage. The former (really a variety of haemorrhage) is distinguished by the existence of slight symptoms before the sudden attack. We are not justified in regarding as primary haemorrhage any case in which premonitory symptoms existed for more than a few minutes, unless such symptoms were so pronounced and sudden in onset that they might have been due to a definite extravasation, afterwards increasing. Initial fever (within the first six hours) always makes myelitis probable, provided there is no other cause for it. The distinction from meningeal haemorrhage has been mentioned in the account of the symptoms, and in the description of that disease. Prognosis.—In all cases in which the symptoms are considerable in degree or wide in range, the danger to life is great, and remains great until they begin to subside. The prognosis is better when the disease is in the dorsal region than when it is in the enlargements, for the same causes as influence the prognosis in myelitis. It is better when sensation returns in the course of a few days, but if the enlargements are affected other sources of danger remain considerable. Early trophic changes also render the prognosis worse, for they show an intensity of degree that may involve grave danger. After the onset is over, the forecast must be guided by the general principles that deter- mine the prognosis in acute myehtis. Treatment.—The treatment of haemorrhage into the substance of the cord is the same as that of haemorrhage into the membranes (p. 339; The measures requisite are few, simple, and all-important. Absolute rest and the prone position are to be secured before anything else is thought of. Ice should be applied to the spine over the seat of the haemorrhage. The bowels should be opened freely, and full doses of ergot or ergotin may be given: 5SS of the liquid extract or five grains of ergotin may be given by the mouth, or three grains of ergotin 442 SPINAL CORD. may be injected under the skin, and the dose may be repeated two or three times, at intervals of two hours. A few large doses are probably more effectual than smaller doses continued for a longer time, since the haemorrhage probably does not go on for long. The after-treat- ment must be that for myelitis. The disease is one of those in which most of the good that can be done by treatment—and in few diseases is the opportunity more urgent—rests with those in whose hands the patient is immediately after the onset. DEGENERATIONS OF THE SPINAL CORD. A large and important class of diseases of the spinal cord consists of those in which there is a slow degeneration of the nerve-elements, with an overgrowth of connective" tissue, and in which structures are affected that have a common function, while others that have a different function escape even when they are adjacent to the elements that are diseased. Affecting thus functional " systems," they are termed '• system diseases." This term has been used in several senses, more or less special (even based on the developmental relations of the structures), and hence the question whether a given malady is a " system disease " or not, is one to which various answers have been given. The term is here used in its widest and simplest sense, as meaning an affection of the structures that have a function either the same, or so far allied that they work together as parts of one system, distinguishable as such from other sets of structures. A " system disease " may involve all the structures of the system, or only some or one of them ; its chief distinction is from a random disease that involves structures irrespective of function—merely, for instance, because they are contiguous, or supplied by the same artery. In " system diseases " the primary change is, as a rule, in the nerve-elements, and the overgrowth of interstitial tissue is secondary. The process is analogous to that which occurs in the secondary degeneration of nerve-fibres, in which the first change is certainly in the nerve-elements, the destruction of which is followed by an over- growth of nuclei and supporting tissue, amounting ultimately to a " sclerosis," as it is termed. The process is by some regarded as a chronic parenchymatous inflammation, an inflammation beginning in the proper functional elements of the organ, but it seems undesirable thus to widen and loosen our conception of inflammation ; so far as the process is concerned the question is one of name rather than of nature. Another question of much greater interest is the relation of the two elements in the process, the wasting and the growth, the atrophy of the DEGENERATION. 443 nerve tissue, the hypertrophy of the connective tissue. The failure of nutrition in the one causes an increased energy of nutrition in the other. We have seen this relation in the nerve-fibres. The degene- ration of a fibre is attended by an active growth of its nuclei and protoplasm. The nutrition of the two elements, the neural and the adventitial, is evidently connected in the closest manner, but in inverse course. It is important to recognise the fact that the process of growth of the connective-tissue elements is an active manifestation of nutritional energy, which, when once excited, may be to some extent independent of its cause. It may, when very active, pass beyond its proportional limits, and be greater than corresponds to the nerve atrophy that causes it, invading adjacent structures as if an inde- pendent process. It may, when very rapid, have some of the cha- racters of an interstitial inflammation, and even an acute inflamma- tion. Such excess is quite unusual; as a rule the secondary process is subordinate and proportioned to the primary change. These degenerative diseases fall into certain types so far as the spinal cord is concerned, but they are subject to some variety of combination even there, and to great diversity of association with degenerative changes elsewhere. The affection of the cord is of either the sensory or the motor elements, or both. The type of the former is tabes ; of the latter, either spastic paraplegia or muscular atrophy, according as the lower segment of the motor path is affected, or the upper. Other combinations of affection will be better understood when the diseases are described. The degenerative diseases are not numerous, but they are of great importance. They are, degeneration of the anterior cornua and anterior root-fibres, causing muscular atropliy; degeneration of the posterior columns and posterior root-fibres, causing locomotor ataxy; and degeneration of the pyramidal tracts, causing spastic paraplegia, a disease the exact pathological position of which is not quite certain. These degenerations may be variously combined, and some combina- tions need separate description. Their causes are various. In some the nutrition of the nerve- elements fails soon after they have achieved maturity, and this is prone to occur in members of the same family. In other cases, which present a contrast to those just mentioned, and yet are allied, there is a senile degeneration, apparently in consequence of less vital endur- ance in these elements of the nervous system than in the other structures of the body. In such ■ ases the local degeneration merely anticipates the somatic death which it too often induces. In these we must assume an inherent deficiency of vital endurance in the struc- tures that fail. A similar assumption seems to be the only explanation for the cases in which degeneration of certain elements of the central nervous system occurs in middle life, between thirty-five and fifty, usually as a result of depressing emotion, or of some influence which lessens the general nutrition. Lastly, we are confronted with a large 444 SPINAL CORD. and varied class of cases, in which similar degenerations seem to result from toxic agents present in the blood. These may be received from without, or generated within the system, and an especially potent source of such toxins seems to be the development of the organisms of some specific diseases. LOCOMOTOR ATAXY; TABES DOESALIS. The malady thus named is the most common chronic disease of the spinal cord. It consists in a degeneration in the posterior columns of the spinal cord, or the peripheral sensory nerves, or both. According to the current views, it is the expression of impaired nutritional in- fluence of the sensory neurons of the spinal cord, primarily of those related to the afferent muscle-nerves, but often also other afferent nerve-systems, including those from the skin. The nutritional centre is in the posterior ganglia, and the toxin apparently acts first on the extremity of the sensory fibres, and also on those that pass into the cord. The effect is manifested, when considerable, by inco-ordination of movement, peculiar pains, defective sensibility, and loss of the myotatic irritability (muscle-reflex action), of which the knee-jerk is the most convenient manifestation. When slight in degree, the sym- ptoms may be limited to the pains and the loss of the knee-jerk. The name "locomotor ataxy" was given to the disease by Duchenne; "tabes dorsali.s," or "wasting of the back," is a term applied by Hippocrates to certain symptoms supposed to be due to venereal excess, and long ago limited in Germany to symptoms believed to depend on atrophy of the spinal cord. It then included all chronic paraplegias, but was further restricted to this disease by Romberg. It has lately obtained wider use on account of the discovery that inco- ordination may be absent when the disease is slight in degree. The symptoms vary much in different cases. Besides the varieties thus produced, there are two allied affections that ought not to be classed with it. One is the so-called "hereditary ataxy." The other is that in which both weakness and inco-ordination co-exist from the first; " ataxic paraplegia " it may be called. Each differs from other varieties with sufficient constancy to merit separate consideration. These forms are not included in the following account. History.—The inco-ordination of movement and other symptoms of the disease were frequently noted, during the first third of this century, in cases of disease of the spinal cord, but such cases were not distinguished from those with actual loss of power. The inco-ordina- tion was found to be associated with disease of the posterior columns by Stanley* The first really exact account of the disease was pub- * ' Med. Gazette,' Feb., 1840, and ' Med.-Chir. Trans./ vol. xxiii. LOCOMOTOR ATAXY. 445 lished in 1847 by Todd,* who distinguished the cases with inco-ordina- tion and without weakness, from simple paraplegia, and, apparently not aware of Stanley's observation, he inferred (from the character of the symptoms and his theory that the posterior columns contain fibres connecting segments of the cord at different levels) that the posterior columns would be found diseased; and he verified this inference by finding in two cases disease of these columns. The credit of the discovery of the disease belongs, if to anyone, unquestionably to Todd, and few diseases can with greater truth be said to have been "discovered." Four years later (in 1851) Romberg described the disease and the lesion in the posterior columns, but he failed to exclude loss of power from the symptoms. Russell Reynolds, in 1855, gave an accurate description of the symptoms, and, in attributing the ataxy to muscular anaesthesia, was the first to give what we must now regard as the true explanation of the chief symptom.f A series of cases was described by Gull in 1856 and 1857. Tiirck first observed with the microscope the wasting of the fibres in the posterior columns. Duchenne in 1858-9 published an independent and very able analysis of the symptoms of the disease, and gave it the name "locomotor ataxy." He obtained for it (with the help of Trousseau's " Lectures ") the recognition that previous descriptions had failed to secure, and achieved such a degree of success that the malady is called in France " Duchenne's disease." If any name is attached to it, that of Todd alone can be right. Causes.—The disease is much more frequent, in this country at least, in urban than rural populations. Inherited influence is to be traced only in a small proportion of the cases, perhaps in not more than 10 per cent. It is usually a general neurotic heredity, manifested by such diseases as insanity, epilepsy, and other degenerative diseases of the nervous system. Instances of this are—father epileptic; father insane; two sisters insane. But in this small percentage the influence becomes insignificant in the presence of the chief cause, to be mentioned presently, since in many instances its coincidence must be accidental. Direct inheritance of the disease is extremely rare (the special hereditary form being always excluded). A boy with distinct symptoms and optic nerve atrophy was the son of a man who pre- sented characteristic indications of the early stage of tabes (Remak). In most instances of this character the inheritance is not direct, being effected by means of syphilis. The inherited disease is probably the only cause of the juvenile form of tabes. Males suffer far more frequently than females, the proportion being about ten to one, and this seems to imply some proclivity inherent in * ' Cyclopaedia of Anatomy and Physiology/ vol. iii, p. 721. t Reynolds, 'Diagnosis of Diseases of the Brain, &c./ 1855, "Anaesthesia Mus- cularis." Certain words are worth quoting :—" It appears most probable that the centripetal tract of fibres is affected, and that the locality of lesion is very variable " (p. 165). 446 SPINAL CORD. the male sex. A like preponderance of males obtains in a disease that has a close alliance with tabes—general paralysis of the insane. It is, however, not certain that the sexual difference may not be connected with the wider dissemination of the chief cause—syphilis—among men, and with some peculiar power of resistance to its influence on the part of women. The middle period of adult life is that in which locomotor ataxy usually commences. No less than half the cases begin between thirty and forty, one quarter between forty and fifty, and rather less than a quarter between twenty and thirty. It rarely begins after fifty, but I have once known it to develop at sixty-six. Under twenty it is still more rare, but cases are met with as early as ten, and even in quite young children, the subjects of the cause next described. Among the individual causes, one overshadows all the rest—the influence of syphilis. A very large proportion of the sufferers have had, at some previous time, constitutional syphilis, either distinct secondary symptoms or an indurated sore. The proportion is almost as large in the upper and middle classes as in the lower. Of 175 consecutive cases of the disease in men, seen in private practice (in which the past history can be rehed on with more confidence than in hospital patients), no less than 114 of the cases, or 69 per cent., gave a history of a chancre known to be hard, or of secondary sym- ptoms ; and twenty-two others had had a venereal sore of unknown nature. The percentage of those with a history of syphilis or a hard chancre is 77. In another 13 per cent, there was a history of gonorrhoea, in some cases of repeated attacks ; this involves exposure to the risk of syphilis. Patients with unquestionable secondary syphilis are often ignorant of any primary sore. When a disease is a distinct sequel of syphilis in so large a proportion of cases as 69 per cent., we are justified in assuming a similar relation in at least a majority of the cases in which infection cannot be excluded. Gonorrhoea emphasises the inability to exclude syphilis, but in no less than 3 per cent, of the total number of cases was there no exposure to the risk of contracting syphilis in the common way. In the lower classes the pro- portion is higher, and has been estimated at 80 per cent., or even more. The ascertainable facts are certainly below the real facts, as I have pointed out elsewhere.* When a deduction is made for possible accidental coincidence, there remains at least one half of the cases in which numerical coincidence must depend on causal relationship. It is probable, indeed, that, taking all cases, a causal proportion of three quarters would be nearer the truth. In women also antecedent syphilis can often be traced, although rather less frequently than in men. At the same time the facts are even more difficult to ascertain, since in married women syphilis so often runs a latent course. But in the cases of tabes that succeed syphilis the lesion is not syphilitic in histological character; it is as degenerative as in the cases in which syphilis can be excluded, and it is not influenced by the treatment for syphilis. Hence * ' Lettsomiau Lectures/ 1889. LOCOMOTOR ATAXY. 447 it must be regarded as a degenerative sequel of syphilis rather than as a true syphilitic disease. If is probably the influence of syphilis that determines the greater incidence on the urban than on the rural popula- tion, and the preponderance of cases in middle life. Inherited syphilis is also capable of causing the disease, and is to be traced (as far as 1 have seen) in all cases in children. After the acquired disease the interval between primary syphilis and the first symptoms of tabes varies from one to twenty years. It is, however, rarely less than three years, and in most cases it is between six and twelve years. In rare cases the first symptoms occur during the active stage of syphilis.* It is probable, however, that syphilis is not the only cause of the disease. In a few cases, less than 10 per cent of the whole, it can be excluded with confidence. The causes operative in these can be traced also in some of the patients who present a history of syphilis, and in such cases the causation of the malady is probably complex. Hitzig and Buzzard have suggested that a toxin having a similar degenerative action may arise from soft sores. One of these causes, which can sometimes be clearly traced, is injury, such as involves concussion of the spine. The immediate results of the injury, whether slight or grave, transient or lasting, are followed by the symptoms of the degenerative malady. In one case a man fell from a height on to the deck of a ship; transient paraplegia resulted, but six weeks after the accident the man presented extreme ataxy, with good power, and no knee-jerk (Arnold). I have known the symptoms to develop gradually a, few months after a fall from a horse. Exposure to cold and wet has occasionally preceded the onset so directly that it must be regarded as, at least, an exciting cause. There is a history of syphilis in the majority of cases in which the manifestation of tabes follows some immediate cause. In other cases * Although an occasional relation to syphilis had been noted by several preceding observers, Fournier was the first (in 1876) to assert the wide extent of this relation. His statements were received with doubt (because syphilitic patients constituted his field for observation), but they were confirmed from tbe neurological side by myself (' British Med. Journal,' March 1, 1879) and Erb (' Arch, f. klin. Med./ July, 1879) ; while abundant corroboration has been since afforded. Many who at first doubted have been convinced by fresh observations. Facts collected without reference to any point at issue are generally worthless, and freshly collected facts have thrown a new light on the subject. The proportion of cases with previous syphilis neces- sarily varies according to the absolute frequency of syphilis. The difference in the character of the lesion from that of changes known to be syphilitic was urged as an objection, but such considerations are theoretical, and must yield to facts ; instead of denying that this or that lesion can be produced by a given cause, we may have to widen our view of the operation of that cause. Other degenerations of the nervous system seem also to have a relation to syphilis, as I pointed out some years asjo ('Lancet/ Jan. 15, 1881). As will be shown in the section on Pathology, recent discoveries lessen very much the difficulty of comprehending the relation- ship by demonstrating the profound influence on the nervous system of chemical toxins generated by the organisms which we have learned to discern as the materies morhi of specific diseases. 448 SPINAL COKD. the disease has succeeded excessive fatigue and over-exertion, and also certain acute diseases, especially (it is said) acute rheumatism and typhoid fever; it perhaps follows diphtheria in rare cases, but most cases have been examples of the ataxic form of diphtheritic paralysis, ultimately passing away. Alcoholic excess has been noted in some instances, but' most recorded instances have been due to peripheral neuritis, involving chiefly the afferent muscle-nerves. Sexual excess has been supposed by some to be a cause ; but its influence can rarely be detected, and its significance is uncertain, since sexual excitement is undoubtedly sometimes an early symptom of the disease. Secondary Tabes.—Symptoms of locomotor ataxy sometimes succeed other diseases of the spinal cord, and such sequence is especially common in syphilitic subjects. Myelitis and syphilitic gummata may be thus succeeded by tabes. An officer in India, who had had syphilis, having suffered for a day or two from pains in the back, took a bath in snow water, and in a few days his legs were absolutely powerless. He gradually recovered power, but could not co-ordinate the movement: as power returned, lightning pains came on, and a year afterwards he presented the typical condition of locomotor ataxy. Again, a man, twelve years after syphilis, had a severe fall, followed by gradual loss of power, so that at the end of three weeks he could scarcely stand. The legs remained weak for a month, and then im- proved, but ataxy came on; three months later, power was good, inco- ordination extreme. In many cases, however, the ultimate condition is one of combined weakness and ataxy. Symptoms.—A typical case of developed tabes presents certain motor, sensory, and reflex symptoms. There is inco-ordination of movement of the legs, sometimes of the arms also, without loss of power or muscular wasting. There are pains in the affected parts, especially sharp momentary " lightning " pains ; there is some loss of sensation; there is often loss or diminution of reflex action from the skin, and almost always entire loss of the myotatic irritability that is revealed by the so-called " tendon-reflexes," and especiallv by the knee- jerk; there may be retention or incontinence of urine, constipation, and often loss of sexual power. Of this group of symptoms, two usually precede the others—the pains, and the loss of the knee-jerk. These may exist alone, even for years, before inco-ordination comes on. Thus the symptoms are far wider in range than the name "ataxy" suggests; and while inco-ordination, if it exists, is the most obtrusive objective symptom, it may never be developed. Hence physicians have extensively fallen back on the older term "tabes dorsalis." But recent expansion of our knowledge, especially the discovery of the extent to which the symptoms may depend on disease of the peri- pheral nerves, shows that even the qualifying " dorsalis " narrows the term unduly, and "peripheral neuro-tabes" has been added to the terminology of the disease. Besides the symptoms above enumerated, others are occasionally LOCOMOTOR ATAXY. 449 present. Of these the most important are atrophy of the optic nerve (and occasionally of other cranial nerves); trophic changes in the skin, the bones, and the joints; peculiar paroxysmal visceral disturbances and occasionally motor paralyses and muscular wasting. The com- binations of symptoms present in different cases vary much. It will be convenient to consider first the individual symptoms in their various degrees, and then their grouping and sequence. Motor Symptoms.—The characteristic inco-ordination of movement develops gradually. It is usually increased (as Romberg pointed out) by closure of the eyes, and at first may only exist when the guiding influence of vision is thus withdrawn. Before it causes ataxy of movement it may render difficult the maintenance of equilibrium when the base of support is narrowed by the feet being placed close together, toes and heels; if then the eyes are closed the patient sways, and tends to fall. The effect of closure of the eyes is greatest when sensation in the soles of the feet is defective, but does not depend on this defect; it may be marked when sensation on the soles of the feet is perfect. The early defect in co-ordination may be discovered by the patient when he walks in the dark or backwards, or, not un- commonly, when he shuts his eyes in the process of washing the face. In a further degree of inco-ordination there is inability to stand with the feet together, even when the eyes are open, and the patient is only steady when the feet are wide apart. If the feet are bare, the diffi- culty is greater, because muscular action has to replace the rigid base of the boot. The irregular contraction of the muscles is shown by the conspicuous movement of the tendons on the back of the feet. The patient may oscillate from toes to heels before he comes to rest. As the defect progresses, uncertainty is felt in walking even with full visual guidance, especially on uneven ground, or on a very smooth surface. A shght visible alteration in gait is then appreciable, the feet are not placed on the ground quite as in health, or there is distinct difficulty in maintaining equilibrium when the patient turns quickly, and he has to put a foot down suddenly to keep from falling. As the inco-ordination increases, the change in gait becomes greater, but varies much in its precise characters, according to the muscles that are most affected. Often the feet are raised too high, thrown for- wards too far, brought down too suddenly, and the whole sole comes in contact with the ground at once. Often the foot becomes inverted when it touches the ground. Efforts to correct error in movement have themselves to be corrected. In other cases the defect in main- taining equilibrium is greater than the actual disorder of movement of the legs, and the patient sways about in the manner of one who has cerebellar disease; this probably depends on a preponderant affection of the muscles of the hip-joint. As the defect progresses, the patient is only able to walk by steady- ing himself with a stick, or by taking hold of the arm of another person or of adjacent objects At first a very slight degree of this help is VOL. l. 29 450 SPINAL CORD. sufficient; guidance rather than support is needed. Afterwards, however, considerable support is necessary, and ultimately the patient may be unable to stand even with help. When he attempts to rise, the legs move hurriedly forwards and backwards, and if the upright posture is at last achieved, the legs slip forward, and only strong support saves the patient from a fall. The ataxy is manifest also in other movements of the legs. If the patient, when lying, tries to touch an object with his foot, the leg is moved irregularly, goes beyond the place, and then is brought too far back, and only at last does it come in contact with the object, often with unintended, force. This inco-ordination, like that in standing, is much greater if the eyes are closed. The arms may present similar inco-ordination, although they often escape, even when the affection of the legs is extreme; very rarely the arms suffer before the legs (brachial tabes). In one such case there was loss of sensation to touch, not only in the arms, but on the trunk between the epigastric level and the distribution of the cervical plexus. The commencing defect is revealed by delicate movements, such as writing. When slight, it may be conspicuous if the patient tries, with closed eyes, to touch some object, such as his own nose, or, having abducted his arms, tries to bring the forefingers together. As it increases, all movements become irregular; it is impossible for the pafient to button his coat, or to pick up a small object from the table; the fingers twist about in the attempt. The grasp is not sustained; first one finger is felt to relax and then another. If the patient attempts to hold out his hand in a fixed posture, it is seen that the same irregularity obtains; instead of a uniform balanced contraction the muscles contract and relax involuntarily, and slow unintended movements of the fingers result, sometimes closely resembling those of athetosis. The same spontaneous movements may also be observed in the legs. They cease at once when the muscular effort is relinquished. Occasionally the muscles of the trunk present inco-ordination. Thus one patient could sit steadily on a chair when his eyes were open, but if he closed them would at once fall off. The movements of the head, face, tongue, and eyes escape the characteristic derangement. Even with extreme inco-ordination, the power of the muscles mav be unimpaired. Occasionally some group of muscles, as the flexors of the ankle, become weak for a little time and then strong again, just as may the eyeball muscles, as we shall presently see. In some cases motor power in the limbs remains unimpaired to the end; more often, when the ataxy has become great, some muscular weakness supervenes, with or without wasting of the weak muscles There is a distinct group of cases in which weakness and ataxy come on together, but these are considered separately (" Ataxic Paraplegia"). Sensory symptoms are prominent in most cases,—subjective sensa- tions, especially of pain, and loss of sensibility. Spontaneous pains are present in some degree in nine tenths of the cases of tabes. The LOCOMOTOR ATAXY. 451 most frequent and characteristic are the sudden and lancinating pains called " lightning pains." They occur chiefly in the legs, but may be felt in the trunk, arms, and even in the head and face. They are usually paroxysmal, and apt to come on at night; attacks of such pains last for some hours or for a day or two, varying in seat, but often felt in the same part throughout an attack, or through many attacks. Sometimes they are felt in a limited area of the skin; at others they seem more deeply seated; sometimes they dart down the limb. They may correspond to a nerve-trunk (especially the sciatic), but more frequently have no relation to the nerves. They may be felt near joints, but are seldom referred to them. Although the pains are usually acute and " stabbing," they are sometimes of different cha- racter. They may be compared to bad toothache, even when lasting only a second or two. In one patient the sensation was as if both legs were for a moment on fire. The pains in the trunk sometimes correspond in seat to a zone of hyperesthesia, especially when there is a marked " girdle pain." When the pains are referred to the skin, this often becomes tender after the pains have been felt for a time; the contact of the bedclothes cannot be borne, and even a breath of air can scarcely be endured. Curiously, this may be the case when there is impaired sensibihty to pain, but not to touch. When the pain is in the face it may closely simulate trigeminal "tic;" only it is on both sides, and such symmetrical facial neuralgia is very suggestive of a tabetic origin. When pains continue at one spot for some days, vascular or trophic changes may occur there,—ecchymoses have been observed, and I have known the growth of the hair to be changed where pains had been felt in the scalp; each hair bent and broke off near the skin, over an area the size of half a crown; after the pains ceased the growth of the hair became normal. A sharp pain may be accompanied by a sudden reflex spasmodic movement of the legs, or by inhibitory weakness. Thus, in one case, a sudden pain would often make the patient fall on his knees. The pains may be so severe as to prevent sleep. Other kinds of severe pain, less brief than the lightning pains, occur in some cases, and are described by various epithets, as " burning," "tearing," "gnawing." Burning pain in the toes distressed one patient. Much more common, and occurring with other pains, are slighter dull pains like those of rheumatism, for which they are often mistaken, an error that is facilitated by the circumstance that any of the pains of tabes may be influenced by weather, being especially in- creased by damp cold. Indeed, this occurrence on any sudden change in weather is often a marked feature. It is not uncommon for a patient to describe them as " equivalent" to a barometer. They may also be excited by indigestion. Dull pains sometimes precede the sharp pains, occasionally for years. A painful sense of constriction " girdle-pain," is also common, and may be felt around the trunk or in the legs, groins, &c.; it is sometimes referred to a considerable area— 452 SPINAL CORD. the patient may feel as if the whole trunk were tightly enveloped in a cuirass of metal. Darting pains also may be felt in the trunk and not in the legs. Such a sense of constriction is sometimes referred to the legs, especially to the knees, but sometimes to the feet. One patient described this sensation as if an iron band were around each foot. In the arms and hands the pains are usually slight in degree, and seldom cause real distress; they are often felt chiefly in the ulnar region. Visceral pains may also occur, usually paroxysmal, and referred to the stomach, bladder, rectum, &c. Pains are not only the most common, they are often the earliest indication of the disease, and may be the only subjective symptoms in shght and stationary cases. They bear no proportion to the other symptoms, and are sometimes trifling—occasionally altogether absent. They seem sometimes to occur alone; I have seen several patients who suffered lightning pains, characteristic in features, course, and general associations, both with and without the pupil symptoms common in tabes, but with no loss of the knee-jerk. The pains are then usually superficial, and the cases may be termed " cuta- neous neuro-tabes." Ataxy may supervene, with loss of the knee- jerk. Sensations other than pain are also common. They are various in character, described as " tingling," " pins and needles," " creeping," and very often as if the skin, especially of the soles, were covered by some soft substance. Sensations of cold or of heat are also common; the feet may feel as if the legs are always in cold water; a sensation of cold about the testicles is occasionally complained of. Similar cutaneous sensations are also common in the hands. They are espe- cially common in the distribution of the ulnar nerve. Here also there may be impaired sensibility, especially for pain and temperature, when the sensory condition elsewhere in the arm is normal. The ulnar nerve has also been found insensitive to pressure (Biernacki). Increased sensitiveness to pain may also exist, especially on the soles of the feet, and often accompanies lessened sensibility to touch. A diminution of sensibility is also present in most cases of the developed disease. It may involve all forms of sensibility, but seldom equally; some forms may be impaired and others normal. Either pain or touch may be affected alone; the most frequent change is loss of sensitiveness to pain. Delay of the perception of painful stimuli is a common early symptom, as will presently be described. A firm touch (i. e. slight pressure) may be felt when a slight touch is unper- ceived. When a touch is felt, the power of localising it may be im- paired. Temperature sensations are rarely affected without other forms of sensibility, but they are often impaired with that of pain when tactile sensibility is normal. On the other hand, there may be extensive loss to pain without any defect of the temperature sense. A prick may then cause only a sensation of heat or burning, and extreme degrees of heat or cold cause pain less readily than normal. LOCOMOTOR ATAXY. 453 The temperature loss may be partial,—either cold or heat may be unperceived while the other is recognised. When touch is slightly impaired, there may be an inabihty to discriminate differences in the degree of pressure on the skin. Accompanying the diminution or increase of sensitiveness there are sometimes curious changes in the sensation produced. One of these is a delay in the perception of pain, which may amount to several seconds. The greatest delay I have met with amounted to seven seconds, but one of fifteen seconds has been described (Eulenberg). The contact of a point may be felt at once, the pain only after a considerable interval. When felt it may be excessive in degree. Often there is an after-pain, lasting sometimes for a quarter or half a minute or longer, and the maximum sensation may not be attained until several seconds after the pain is first felt. Thus, in a case in which there was a delay of seven seconds, the maximum sensation was only felt twenty-five seconds after the prick (Obersteiner). Often there is a second or third maximum, a sort of rhythmical recurrence of sensation, quick or deliberate. A delay greater than normal may also attend the sensation of heat, but this is less easy to recognise on account of the time normally required to raise the temperature of the skin. The localising power is sometimes strangely perverted. A touch on the toe may be referred to the back of the foot even when there is no ataxy. A touch or prick on one leg may be referred to the other, sometimes with singular uniformity in position (" allocheiria," p. 14). A prick in one spot may be felt in many places (" polyses- thesia") on the same, or on both legs. There may also be impair- ment on the face corresponding roughly to divisions of the fifth nerve. Occasionally a patient feels as if the face were covered by a mask, stretching and compressing the skin, a symptom named by Charcot " Hutchinson's mask." The reaction of the sensory nerves to elec- tricity may be changed in the same way as that of the motor nerves when they are degenerated; instead of the earliest sensation, on closure of the circuit, occurring at the kathode, it occurs at the anode (Men- delssohn) . Impairment of sensation is a very variable symptom. It may be absent even when the spontaneous pains are severe. It is most fre- quent, and usually greatest, in the lower part of the legs and feet. It may even be limited to the soles, and usually then ceases at the outer sharp edge of the foot, but extends for an inch or so up the inner side. Touch or pain may be lost on the sole only, and even, strange to say, the form of sensibihty that is lost on the sole may alone persist in the legs. Although the sole is usually most affected, sensation may be perfect on the sole when lost elsewhere. One leg is often more affected than the other. The loss may extend to the trunk, and over part or the whole of it. Defective sensibihty to touch is sometimes met with around the anus, perinaeum, scrotum, &c, and sexual loss is said to be usually associated with loss of sensibility in 454 SPINAL CORD. the glans penis.* The characteristic pain which pressure on the tes- ticles produces is frequently absent, In the upper limbs the impair- ment of sensation is usually greatest on the hands ; it often commences on the palmar aspect of the fingers, and may be limited to this aspect of the hands, just as it is to the soles of the feet. Sensation may be lost on the trunk and not on the limbs—an important fact, because the anaesthesia may then readily be overlooked. The impair- ment on the trunk frequently ceases when the level of the third rib is reached. On the head, loss of sensation is rare and usually partial. But almost universal defect of sensitiveness to pain over the whole head is sometimes met with. The loss of sensibility is not confined to the skin, but affects the deeper tissues also in many cases. The contraction of the muscles on electrical stimulation may be unfelt, and the muscles may be less sensitive than normal to pressure or forcible extension. It is only from intelligent patients that this can be distinctly ascertained; but some degree of defect is probably an early change. In a case in which the inco-ordination was much greater in one leg than the other, in the more ataxic leg the muscles were insensitive to traction, which excited a definite sensation on the other side. The muscles may indeed be quite insensitive when cutaneous sensibility is little or not at all impaired. It is probable that the sensibility of the joints, fibrous tissues, and tendons is also involved. The sense of posture may be lost when cutaneous sensibility is intact. The anaesthesia may extend to the viscera when the trunk is involved. In consequence of the loss of sensation, grave injuries to the limbs, such as burns, may be unper- ceived, and visceral disease may be unattended with the customary pain. Pleurisy, for instance, may be absolutely painless. But impairment of sensation is not invariable. There may be no loss even in patients who present considerable inco-ordination, and in those who suffer severe pains, as well as in those who have had none. But it is very rare to have no sensory defect when inco-ordination is considerable. Reflex action from the skin is usually impaired in proportion to the loss of cutaneous sensibility, and especially to the loss of tactile sensi- bihty. It may be normal when pain is unfelt. The plantar reflex is most frequently impaired, and the progress upwards of the disease may be attended by a progressive loss of the gluteal, cremasteric, and abdominal reflexes. On account of the variations met with in health, it is uncertain whether reflex action is ever lessened when there is no impairment of sensation. On the other hand, in the early stage of the disease there is sometimes a considerable and even extreme excess of all cutaneous reflex action. Loss of sexual power is an exceedingly common and often an early symptom of the disease, and may precede any impairment of sensory or reflex functions. As has already been stated, the loss is said as * Brown,' Lancet,' 1898. LOCOMOTOR ATAXY. 455 a rule to be accompanied by loss of sensation in the glans penis. Yet in such cases nocturnal emissions may occur, sometimes very frequently. On the other hand, exceptions are met with in which sexual power persists to a late period of the disease, even until after the patient has lost the ability to walk alone. If the condition of cutaneous reflex action is somewhat inconstant, this is not the case with the reflex process on which the myotatic irritability depends. A loss of the knee-jerk, as Westphal first pointed out, is one of the earliest and most constant symptoms of tabes. With it disappear also all other indications of this irritability. In cases with great excess of cutaneous reflex action the knee-jerk is lost as in other cases, and the contrast between the two forms of reflex action is very striking. It is exceedingly rare for the knee-jerk to be obtained in any case of true tabes, but an early case is sometimes met with in which it is not lost, although diminished, and commonly unequal on the two sides. In one or two cases I have found it slight on one side and lost on the other when distinct ataxy was present, and have observed its subsequent disappearance.* In one case, in which the jerk was lost in one leg only, lightning pains were confined to this leg. Very rarely the knee-jerk persists and is equal, although there are characteristic pains, loss of the iris reflex, and a history of syphilis. The loss often precedes for many years the development of inco- ordination. It is important to remember that a true reflex action may simulate the knee-jerk when it is lost. It is distinguished by the con- spicuous interval between the blow and the movement, by the wide range of this, and by the fact that a similar effect can be produced by a prick on the skin over the patellar tendon. Eye Symptoms.—The functions of the internal muscles of the eye are often affected in tabes. In more than five sixths of the cases f the reflex action of the iris to light is lost; rarely the action remains perfect throughout. In most cases of reflex loss the contraction on accommo- dation is preserved, as first noted by Argyll Robertson. Often also (as Erb has shown) the dilatation that occurs on painful stimulation of the skin of the neck, itc, can no longer be produced. Sometimes the ciliary muscle is also paralysed, causing loss of accommodation. Very rarely there is loss of accommodation and of the associated contraction of the iris, without loss of the light-reflex. When reflex contraction is not lost it may not be maintained; the pupil again enlarges ; an actual inverted reaction to light and darkness has been observed.J The pupils are often very small (" spinal myosis "), especially when there is loss of the reflex dilatation from the skin, a loss which seems to be accompanied by atony of the radiating fibres supplied by the sympathetic. The pupils are not always small; they may be of a * Its return on the paralysed side in a tabetic patient who became lieiniplegic, has been recorded (Hugblings Jackson and James Taylor, ' Brit. Med. Journ.,' vol. i, 1894). f Berger says 97 per cent. X L'Abundo,' La Psychiatria/ 1889, vii, p. 28(5. 456 SPINAL CORD. medium size or still larger, and then I have usually found that the skin-reflex can be obtained, although the light-reflex cannot. They are often not perfectlv circular, and are frequently unequal. Both eyes are usually affected in the same manner ; occasionally the reflex action is lost in one and only lessened in the other; this is true also of accommodation ; indeed, almost every possible condition is occasionally met with. On the other hand, the intra-ocular muscles may be unaffected even in advanced cases. According to Berger the ocular tension is often lessened. Paralysis of the external ocular muscles is also common in tabes, and occurs in several forms. (1) Transient weakness lasting a few Fio. 120.—Double tabetic pto-is.* days or weeks, and then passing away. (2) Permanent paralysis, complete or incomplete, of a single nerve or part of a nerve. Either form may occur at any stage, but the first is most common in the early, and the second in the later stages of the disease. The transient palsy renders diplopia a common symptom in the early period; any muscle may be affected, but the external rectus is that which' most frequently suffers. Transient ptosis may precede an almost complete external ophthalmoplegia. The persistent palsy may affect one or more muscles; often the levator is involved, causing what has been termed "tabetic ptosis" (Figs. 119 and 120). S .inetimes the whole third nerve is paralysed. (3) There may be a combined palsy, suggesting a central * From a Salpetriere photograph, for which I am indebted to M. Charcot. LOCOMOTOR ATAXY. 457 origin—as, for instance, loss of the movement of convergence asso- ciated with loss of accommodation, although the internal recti act in the movement towards one side. (4) Many or all the muscles of both eyes may gradually become paralysed—" progressive ophthalmoplegia," internal or external, a condition that is more fully described in the account of ocular palsies in Vol. II. Atrophy of the optic nerve is the most serious ocular complication of tabes. Its frequency is difficult to ascertain, but is certainly less than is often supposed; it does not occur in more than one case in ten. Atrophy is generally an early symptom, usually commencing before inco-ordination is developed, and in a large number of cases ataxy does not supervene ; if it does, the arms are frequently affected before the legs. There seems a tendency for the spinal malady to become stationary when the optic nerve suffers. The disc becomes pale, and its substance shrinks, so that recession begins at its edge instead of at the central " cup," as may readily be perceived by the course of the vessels. The failure of sight usually commences with a peripheral limitation of the field and loss of colour vision, but sometimes central acuity fails early. When this remains good, the peripheral loss may reach a considerable degree before it is suspected by the patient. Rarely there is a symmetrical sectorial defect in the fields. The visible pallor of the optic disc is not always proportioned to the failure of sight; the change in tint depends on wasting of the capil- laries, and this does not always correspond to the wasting of the nerve- fibres. The ultimate tint is grey, or a whitish grey, especially as seen by the direct method. When the disc was very vascular before the atrophy, the grey tint is generally deepest. The vessels are but little narrowed. Occasionally there are slight signs of congestion in the early stage, and then some tissue of gelatinous aspect may develop in the disc, and the vessels may appear somewhat compressed.* The course of the atrophy is usually slowly progressive, and in most cases it ends in total or almost total blindness. It may, however, cease to progress, and even undergo slight improvement. The onset is not always gradual; sometimes sight fails considerably in the course of a few days, without ophthalmoscopic changes to account for it. 1 have met with one such case in which double temporal hemianopia indicated disease at the optic chiasma. In such cases the secondary interstitial process probably assumes inflammatory intensity (see p. 443). The atrophy is often more advanced in one eye than in the other, and very rarely one eye only suffers. Flashes of light are occasionally experienced in the course of the atrophy, comparable to the lightning pains in the limbs, but they are not common. Deafness, having the characters of nerve-deafness, is met with in some cases, sudden or gradual in onset, transient or lasting. The persistent deafness has been attributed to an atrophy of the auditory nerve, analogous to that of the optic nerve, but certainly in many # Further details will be found in ' Medical Ophthalmoscopy.' 458 SPINAL CORD. cases without sufficient reason.* Only when there is a progressive limitation of the range of hearing, analogous to the peripheral limitation of the field of vision, are we justified in assuming nerve atrophy. I have seen two cases of this kind. In each there was also optic nerve atrophy, and the other symptoms of tabes were distinct.f Attacks of vertigo are frequent in the cases attended by deafness, and seem to depend on the disturbance of the labyrinth or auditory nerve, and to be thus connected only indirectly with the primary disease. But chronic slight vertigo from this cause increases very much the tabetic unsteadiness. Anosmia occasionally occurs, and is probably not infrequent. It is apparently due to an atrophy of the olfactory nerve similar to that of the optic. The functions of the other cranial nerves are not often affected. Pains may be felt in the region of the fifth nerve, and there is occa- sionally loss of sensation in some part of the area supplied by it, on one side or both. Unilateral atrophy of the tongue has been sometimes noted. In the larynx, besides the spasm to be presently described, paralysis of the vocal cords is met with, both as an isolated symptom and also after attacks of spasm have occurred for a long time. Both posterior crico-arytamoids may be paralysed, and in one case paralysis of one posticus occurred very early in the disease (Eemak). Sphincters.—The functions of the bladder are frequently deranged; there may be either sluggish micturition or a tendency to incontinence, and very often the bladder is not perfectly emptied. These symptoms frequently occur early in the disease, and it may be indeed only for them that the patient seeks medical advice. The retention may become absolute, or there may be overflow incontinence ; there is rarely paralytic incontinence. The imperfect contraction, even when slight, miy have serious effects. The residual urine tends to decom- pose, and gradually induces over-distension; cystitis is apt to occur, and secondary renal disease may develop insidiously, and is a not uncommon cause of death when the difficulty in micturition has been insignificant. Slight intermittent febrile disturbance is a frequent consequence of this bladder incompetence ; it may cease entirely if the catheter is regularly used. The sphincter ani is often also weak, so that a loose stool can be retained with difficulty; but its paralysis rarely reaches a high degree. Constipation is extremely common. * It is very difficult to distinguish an affection of the nerve from one of the labyrinth independent of the nerve. Even in a case of bilateral deafness coming on in the course of tabes, in which the patient could hear.only a loud voice, and deep notes better than high ones, in which atrophy had been diagnosed, Lucae found calcareous masses in each of the labyrinths, and the auditory nerves were quite normal. f In one, only notes between W- and D could be heard. In the other the patient, when first examined, was absolutely deaf to notes above E2 and below G . A few months later the restriction had confined the range of hearing to the octave in the treble clef between E2 and E1, even E£i being inaudible. Thus the loss occurred chiefly from below upwards. Ultimately no note could be heard. LOCOMOTOR ATAXY. 459 7 aso-motor and trophic disturbances constitute an important group of symptoms, and may reach a considerable degree without a coinci- dent increase in the other symptoms. Local sweating has been noted, confined, for instance, to the palms and soles, or to one side of the he:ul. The ecchymoses and altered growth of hair, in connection with attacks of pain, have been already mentioned. Pigment may disap- pear from the skin and hair in isolated spots. Herpes of the skin is not uncommon, and usually occurs in association with attacks of pain. A peculiar association was present in one case; attacks of limited scrotal pain were accompanied by a " rash " on the foreskin. The epidermis of the sole becomes thickened; blisters readily form beneath it, and may lead to indolent ulcers. The curious affection known as Fig. 121. — Perforating ulcer of the foot in tabes. (From a Salpetriere photograph.) " perforating ulcer of the foot" has been found to be almost confined to cases of tabes. Troublesome ulceration of the toes, especially about the nails, is also occasionally met with, and may necessitate amputation. The growth of the nails of the feet, and sometimes of those of the hands, may be changed; they may be thickened, and the surface furrowed or irregular. The nails may even fall off and be slowly renewed. The teeth sometimes decay quickly, and may drop out. One patient, who had previously lost many of his nails, found that all the teeth of the upper jaw fell out in the course of three days, without any pain or decay. Wasting of the muscles occurs only as a complication in the later stage of the disease. Changes in the nutrition of the joints and bones have attracted much notice since attention was directed to them by the careful investigations of Charcot, whose name is sometimes connected with the condition. They are not very common, but are sufficiently frequent and well marked to place their relation to the disease beyond doubt. The bones may become brittle, and may break readily, in so-called " spontaneous " fractures. The process of union is attended with the formation of a large amount of callus. Sometimes there is also ossi- fication or calcification of the structures adjacent to injured bones, and even of the fibrous tissues independent of the joints, such as the 460 SPINAL CORD. intermuscular and subcutaneous tissues. These may be rapidly in- flamed, and extremely quick swelling may occur, followed by indura- tion. As the inflammation subsides, there is a remarkable tendency for ossification to occur even in the newly formed inflammatory tissue beneath the skin. Such subcutaneous changes occur most frequently in the foot or thigh, especially near joints, but sometimes in the deeper fibrous tissues between the muscles. In the joints the changes consist of erosion of the cartilage, wasting of the heads of the bones, and ossification of the ligaments; sometimes irregular bony growths form, and occasionally the head or shaft of a long bone may undergo an extraordinary increase in size by the development of new osseous tissue on the surface. The joint changes may thus assume an atrophic or hypertrophic character, and the movement may be either too free or too limited. Wasting of the head of the femur often renders dislocation of the hip easy. With such changes, and often fiill on it. One condyle of the humerus and olecranon were found, after death, to have been broken off. Several separate pieces of new bone had formed in the capsule of the distended joint. when they are slight in degree, there may be great effusion within the joints and oedema outside them. The larger joints are those most commonly diseased—knee, hip, ankle, elbow,—but the small joints of the fingers have been known to suffer (Westphal). The relative fre- quency with which the chief joints are affected is approximately indicated by the following percentage: *—knee, 45 ; hip, 20; shoulder, 11; tarsus, 8; elbow, 5; ankle, 4. They often occur during the pre-ataxic stage. The lesions are sometimes excited by injury, and the extraordinary changes that may follow traumatic influences, or occur alone, afford a conclusive indication that abnormal trophic in- fluences are at work. Fig. 122 represents the arm of a man who fell and struck his elbow, fracturing the olecranon and condyle. This was followed by extreme painless swelling, and bony masses could be felt, gradually increasing in size. After death the fractures of the bones were found, and masses of new bone had formed in the capsule of the joints. The arthropathic changes occur also, however, without * Obtained by combining the collections of cases of Weizsacker (Bruns' ' Beitr. z. kl. Chir.,' 1887) and Rotter ('Arch. f. kl. Chir.,* Bd. xxxvil LOCOMOTOR ATAXY. 461 Fig. 123.—Locomotor ataxy ; retro- FiG. 124. — Tabetic foot. (From a photo- flexion of knee-joints. graph b^ Mr. Marriott, B.Sc.) the muscular tendons that pass by them. The knee-joint may thus become so lax that when the patient stands, the joint may become retroflexed, as in Fig. 123. No doubt also this is the result to some extent of the want of tone in the muscles, which has been called by Frenkel hypotonic musculaire. Changes in the tarsal bones and articu- lations may cause the foot to become flat, with a projection inwards or backwards of the tarso-metatarsal articulations, and of the (often enlarged) tarsal bones. The condition has been called the "tabetic club-foot" by Charcot and Fere.* In some cases there is painless loss of teeth, and this may be accom- panied by the presence of troublesome ulceration of the mouth, re- garded by some as analogous to the perforating ulcer of the foot. Visceral symptoms of peculiar character occur in many cases of tabes.f They consist almost entirely of paroxysmal disturbance of function, usually attended with great pain, and have been termed, * The trophic changes in bone and joint have been regarded by some as simple chronic osteo-arthritis, without causal relation to the nerve disease in their subjects, but the evidence is altogether opposed to this view. The arguments that can be adduced in support of it will be found in some of the speeches delivered at a dis- cussion at the Clinical Society, Nov. and Dec, 1885. t The occurrence of attacks of vomiting, sometimes early in the disease, was pointed out by Topinard, but thought by hiin to be a mere complication. (Topinard, » De l'ataxie locomotrice,' Paris, 18R4, p. 273.) 462 SPINAL COED. by the French, crises, with qualifying adjectives according to the seat of the symptom. There is a tendency to over-elaborate this terminology. The most frequent seat of such disturbance is the stomach, and these attacks are called gastric crises. They consist of paroxysms of severe gastric pain, felt in the epigastrium and often passing through to the back. The pain is accompanied by vomiting, with or without nausea. The vomiting is often incessant, and is first of food, then of clear liquid, which may be very abundant; ultimately bile is vomited, and sometimes blood, which may be altered in colour; it has been ascribed to simultaneous vaso-motor disturbance in the mucous membrane. Retardation or irregularity of the action of the heart has sometimes attended such an attack, and rarely pyrexia has been noted. I have known frequent hiccough to accompany the vomiting. Such an attack lasts for some hours or days, and then subsides, to recur in a few weeks. During the intervals the functions of the stomach may be performed in a perfectly normal manner. Although pain and vomiting usually occur together, some patients have attacks of pain without vomiting, and in others there is vomiting without pain. It may occur on first rising in the morning, and be relieved by recumbency. Barely there is nausea alone. A temperate man, in the early stage of tabes, suffered during three years from frequent attacks in which, for several days, he had intense nausea each morning, passing away in the afternoon, and succeeded in the evening by an inordinate craving for food. He never vomited unless he made himself do so, in the vain hope of thus obtaining relief. After two years, attacks of laryngeal spasm were added to the nausea. Occasionally gastric attacks coincide with paroxysms of pain in the trunk. I he chief intestinal disturbance is constipation, but paroxysmal diarrhoea has been supposed to be of vaso-motor origin, and connected with the disease (Pierret). Paroxysms of rectal pain (rectal crises) may occur, and may be accompanied by distressing tenesmus, some- times by a sensation as if there were a foreign body in the rectum. In rare cases paroxysms of pain have precisely the character of attacks of renal colic (nephralgia crises), or are felt in the neck of the bladder or along the urethra or at the meatus (vesical or urethral crises). These may be attended by an intense desire to micturate, although the bladder may be empty and only a few drops of urine may be expelled. In one patient such pain was repeated several times an hour, and each attack lasted for several days. Blood may be passed after an attack. Laryngeal crises are, perhaps, after those of the stomach, the most common. They vary much in character. The most common form is a true laryngeal spasm, with noisy inspiration and expiration, cough, and often considerable dyspnoea. The paroxysms may resemble those of whooping-cough or of laryngismus stridulus, and seem to be due to spasm of the adductors. Pressure on the superior laryngeal nerve at LOCOMOTOR ATAXY. 463 its entrance into the laynx, or on the trachea, or the introduction of a sound, will sometimes induce an attack. The spasm may last for a quarter of an hour or for some hours, but rarely continues so long as the gastric crises. In most if not all these cases of adductor spasm there is permanent weakness of the abductors, which when consider- able constitutes a very grave complication. Whenever there is a history of laryngeal spasm, the respiratory sound should be carefully observed to detect any inspiratory stridor. In one recorded case the spasm spread to the pharynx, making swallowing impossible ; a violent attack extended to the muscles of respiration, and the patient died asphyxiated. Death from these attacks is, however, rare. Paroxysms of rough cough have been termed "bronchial crises;" in one case such attacks ceased when the patient began to suffer from gastric crises. Such paroxysmal cough, sometimes ending with a " whoop," is more frequent than definite laryngeal spasm. The definite crises are, how- ever, often early symptoms, and they may continue for many years. I have seen a patient, still in the first stage, who gave a history of gastric crises during the preceding eighteen years. Anginous attacks have also been described. Acceleration of the pulse is common, and cardiac disease, especially aortic, by no means rare. Comparable to these paroxysmal visceral disturbances, although very different in character and more alarming in aspect, are cerebral symptoms; but these are, fortunately, very rare. They resemble the attacks that are common in general paralysis of the insane, and con- sist of transient apoplectiform seizures, of transient hemiplegia, or of convulsions, general or one-sided. They may occur early in the course of the disease. The alarm they occasion is not without foundation, since death has been known to occur during an attack of apoplectic aspect. Occasionally an actual lesion occurs (probably thrombotic softening), causing persistent hemiplegia, which is probably only coincident with the chronic disease of the nervous system. Paroxysms of vertigo sometimes occur, but their nature is uncertain. They pro- bably frequently depend on derangement of the auditory nerve or labyrinth. Cerebral symptoms may also be superadded, especially in cases which terminate as general paralysis. Course and Termination.—It is convenient to divide the course of the disease into three stages:—(1) In which there is no alteration in gait, the common indications of the malady being the loss of the knee-jerk and the pains, often associated with loss of the light-reflex of the iris, and unsteadiness on standing with the feet together and eyes shut. (2) That in which there is distinct affection of gait, slight or considerable, but in which the patient is still able to walk, alone or with the aid of one or two sticks. (3) In which walking is possible only with the aid of another person, or it is impossible for the patient to walk or to stand. The first stage is not always present; inco-ordi- nation may be developed simultaneously with the loss of the knee- jerk, as one of the earliest symptoms. 461 SPINAL COI?D. The course of the symptoms is extremely variable. The inco-ordi- nation usually supervenes gradually in the course of months, but it sometimes develops very rapidly. I have known it to become extreme in the course of a fortnight from its onset, after the first stage had existed for a considerable time. The epithet "progressive,'* given to the malady by Duchenne, expresses a characteristic of a large propor- tion of the cases in which ataxy is developed, and he knew no other cases of the disease. The inco-ordination, once developed, often increases slowly or rapidly, until it reaches a moderate or a consider- able degree, and the sensory loss shows a like tendency. The local onset of the ataxy seems to be sometimes excited by a peripheral influence, such as injury ; in one case an injury to the left hand was followed by inco-ordination in that limb, afterwards general and cha- racteristic. Still more common is a rapid increase in the symptoms after such a disease as influenza, or in consequence of alcoholic excess. In such cases careful inquiry will generally elicit evidence of preceding symptoms. The pains seldom correspond to the other symptoms in degree or course. They are often very severe in the early period of the disease, and may either lessen or continue unchanged as the loss of sensation develops. Their persistence, even in severe degree, does not show progress in the disease ; once set up, they may continue for years without any increase in the other symptoms, and seem in this to be analogous to neuralgia, being evidence only of functional activity in the altered nerves. The power of recognising the first stage of the disease, which we owe to Westphal's discovery of the loss of the knee-jerk, has enlarged, and in enlarging has to some extent modified, our conception of the general tendency of the disease. It is exceedingly common for the first stage to remain stationary for a long time, for ten, twenty, and even,, in one case I have known, for twenty-five years, if the duration of the lightning pains may be accepted as proof of its existence. When all cases are taken together, and if the patients are subjected to careful treatment, the disease probably shows a progressive tendency in less than one half of the cases. The other symptoms also do not always progress pari passu. Sen- sibility may fail although inco-ordination does not increase. Con- versely, the ataxy may become greater, although sensation remains the same, and even when it shows a distinct improvement. To this we shall return in considering the pathology of the disease. The contrast between the course of different symptoms in some cases is very marked. If optic nerve atrophy develops, the spinal symptoms often remain stationary, and this is also true of visceral crises; I have known gastric crises to cease when inco-ordination came on. In on*1 patient all the symptoms of tabes passed away, optic nerve atrophy ceased to advance, and even the knee-jerk returned, when the patient became insane. The atrophy of the optic nerves, although generally progressive to blindness, also may become arrested. It may remain LOCOMOTOR ATAXY. 465 limited to one c/s, and even when bilateral and very definite, it may cease to increase. The rate of increase in the symptoms of tabes, when this occurs, varies much. Sometimes it is so slow that the ataxy is considerable only at the end of several years. On the other hand, it may be so rapid that in a few months the patient is scarcely able to walk. More commonly the course is variable; periods in which the disease is almost stationary alternate with others in which the symptoms increase rapidly. The exacerbations may seem spontaneous, or may be dis- tinctly excited by some prejudicial influence—a chill, a fall, or some excess, alcholic or sexual. They are sometimes very acute; a marked change may occur in the course of a few days, or even in a few hours. Thus I have known a patient to pass, in the course of twenty-four hours, from a condition in which he could walk fairly well to one in which he could scarcely stand. The symptoms suggested that local myehtis had occurred in the degenerating cord. Muscular power may lessen in such a sudden exacerbation, or the increase may be confined to the special symptom of the disease—the ataxy. The conditions thus developed may pass away again, leaving the patient on a little lower level than before, but they often persist without any considerable recovery. There is nothing in the nature of the disease, in most cases, to produce death. The only direct effect of the malady, which has ended life, is laryngeal spasm or paralysis. Even the gastric symptoms, prostrating as they are, are never fatal. Patients who have reached the third stage have lived, bedridden, for twenty years. Death often results from intercurrent maladies, some of which are more dangerous to these sufferers than to others because they may develop painlessly, and attain a serious degree before their existence is suspected. But many patients die from indirect results of the disease. Kidney com- plications are the most common; they often develop insidiously, and only manifest themselves when life is in peril, as, for instance, by acute febrile symptoms, the exact nature of which may be unsuspected until the urine is examined. I have known a patient, still in the first stage, die thus after a few days' illness. Whenever obscure pyrexia is met with in diseases of the spinal cord, interference with the function of the kidneys, due to retention of residual urine, should always be suspected and looked for. Bedsores and pyaemia occasionally cause death, although far less frequently than in most other diseases of the spinal cord. Complications.—Occurring, as most cases do, in syphilitic subjects, tabes is sometimes complicated by true syphilitic lesions of the brain or ccrd, generally the later lesions, such as gummata, or sudden palsy from the disease of a cerebral vessel. Acute or subacute myelitis may occur during the course of the disease with characteristic symptoms. Such a complication must not VOL. I. 30 466 SPINAL CORD. be confounded with the simple acute exacerbation in the special symptoms, which sometimes occurs with remarkable rapidity. Other system diseases of the cord may develop as complications of tabes. The lateral columns may be diseased with the dorsal posterior columns, giving rise to " ataxic paraplegia,," but this is a distinct affection, and will be so described. Another occasional complication is muscular atrophy, both the local atrophy already mentioned (espe- cially frequent in the tongue), and general atrophy, such as is met with in the pure spinal form. Thus a gentleman, who had had hemiplegia from syphilitic vascular disease, developed the first stage of tabes—pains, loss of knee-jerk, loss of the iris-reflex, and sliglit unsteadiness. He had two courses of mercurial treatment at Aix-la- Chapelle, and at the end of the second, atrophy began in the muscles of the hands, and spread during two years until almost all the muscles of the arms, shoulders, and back became extremely wasted. Local muscular wasting (according to the researches of Dejerine *) is usually the result of degeneration of the peripheral nerves; it is generally symmetrical. The extensive wasting, as in the case just mentioned, is probably due, as a rule, to degeneration in the anterior cornua of the spinal cord. In rare cases the legs present the symptoms of tabes, while in the arms there is the jerky inco-ordination of disseminated sclerosis, and the co-existence of the two lesions has been demonstrated, but is very rare. Another very important and frequent complication of tabes is general paralysis of the insane. The two diseases have many alliances. It is probable that syphilis is the chief cause of general paralysis, as well as of tabes. Reflex iridoplegia is common in both diseases. The two maladies are often combined, and the symptoms of one or the other may preponderate. Thus many general paralytics present sym- ptoms of tabes, and its characteristic lesion is found after death. On the other hand, cases of tabes may present slight symptoms of general paralysis, perhaps only slight optimism and mental weakness, which may remain subordinate, or may increase to a pronounced and pre- ponderant degree. It may be difficult to say in which category a case should be placed. It is sometimes said that the disease may com- mence as ataxy, and may change to general paralysis, but a more correct expression of the facts is the co-existence of the two affections, and the dominance of the symptoms of one or the other. Of complications of tabes outside the nervous system, besides the indirect consequences of the malady, valvular heart disease is, perhaps, the most important, and usually develops without any of the usual antecedents, and at an age at which degeneration is unlikely. It is not improbable that the coincidence is really one of cause, the valvular disease being the result of a syphilitic process. Other * Dejerine, 'Revue de Med.,' 1889. LOCOMOTOR ATAXY. 467 complications are so rare as only to deserve notice when a causal con- nection can be traced or reasonably suspected. Coincident glycosuria has been ascribed to an affection of the medulla oblongata (or may be pro- duced through the cervical spinal cord), but it is extremely rare. But sclerosis of the posterior columns has been shown by Williamson to occur in diabetes.* Pathological Anatomy.—In most cases the spinal cord presents changes visible to the nakod eye. The poste- rior columns have a grey translucent appearance, which is due to the loss of the nerve-fibres, and to an increase of the connective tissue (" grey degene- ration "). The whole of the posterio columns may be thus changed, or only parts of them, the distribution of the visible alteration being that of the histological changes revealed by the microscope and presently to be de- scribed. In the hardened cord the difference of tint in the diseased areas is even more distinct than it is in the fresh organ. The posterior columns are also smaller than normal, because the bulk of the connective tissue is less than that of the normal fibres: hence the shape of the cord is shghtly changed. Fig. 125.—Locomotor ataxy involving: the legs only. Sclerosis of the whole posterior columns in the lumbar region, gradually becoming limited, in the lower dorsal re- gion, to the root-zone and posterior median column. The latter only is affected in the upper half of the cord (ascending degenera- tion). There isalso conspicuous degeneration in the antero-lateral ascending tract. This is rather greater on the left side, while the post.-median degeneration is greater on the right, in harmony with the fact that the latter consists of fibres which do not decus- sate. • « Lancet,' 1894. 468 SPINAL CORD. In a section of the cord stained with carmine or similar reagent, and examined under the microscope, the affected areas are conspicuous by the deep staining of the connective tissue. The position of the excess of this tissue, of the " sclerosis," as it is termed, indicates the place in which the nerve-fibres have degenerated. In the most frequent condition, in which the legs only are affected, the sclerosis occupies the whole of the columns in the lumbar region (Fig. 125), but it is often slight in the anterior parts of the postero-external columns, which may even be free from sclerosis; also in the middle of these columns many more nerve-fibres may be seen than elsewhere. The sclerosis is most dense in the part adjacent to the posterior cornu, through which the posterior root-fibres run, and near the surface of the cord (Fig. 125, d 12). Above the lumbar enlargement the affection of the postero-external columns gradually ceases, but the degeneration is intense in the postero-median columns, and has the distribution of an ascending degeneration, as it in fact is, receding from the commissure in the upper cervical region. (Compare Fig. 125 with Fig. 77, p. 214.) In other cases the external band of sclerosis, adjacent to the cornu, continues separate through the dorsal cord and even through the cervical enlargement (Fig. 126); the median degeneration then extends Fln the former of which the knee-jerk <" pend ac- cording to the theory maintained on an earlier page. The detection of this degeneration, among the unchanged motor fibres of the nerves, is very difficult, and this explains the paucity of evidence of it. The peripheral degeneration is found most commonly in the legs, but is met with also in the arms when these are the seat of symptoms. The change in the nerves bears no relation to that in the spinal cord in degree, or even in existence, for extreme alterations have been found in the nerves when the cord was quite normal. On the other hand, in some cases, the nerves have been healthy. * The first observation was made by Westphal, but the extent and significance of the change in the nerves was pointed out by Pierret (1880), and his observation was soon after confirmed and extended by Dejerine and Pitres. t Schmaus,' Dent. Arch. f. klin. Med.,' 1890. Ml' u~ /.;' J a. 130.-- Osseous lesions in tabes. (After Charcot.) A. Atrophy of the head of the femur. B. Exces- sive formation of callus after so-called "sponta- neous " fracture of the ulna and radius. 474 SPINAL CORD. The optic nerves, when atrophied, present wasting of the nerve- fibres, and usually a remarkable increase in the interstitial connective tissue, which constitutes thick tracts of gelatinous aspect. Dege- neration of the ascending or descending roots of the fifth nerve has been repeatedly found (first by Westphal in 1864) in cases in which symptoms were present in the area of its distribution. Similar changes in the roots or nuclei of other cranial nerves have also been found. Pierret has described, as common in cases with vaso-motor and visceral svmptoms. a degeneration of the intermedio-lateral tract and adjacent nerve-fibres in the upper part of the cord, traceable up the medulla oblongata in the region of the so-called " slender column," adjacent to the accessory, glosso-pharyngeal, and pneumogastric nuclei, from which it is supposed that the chief visceral and vaso- motor influences are exerted. The sympathetic has been examined in several cases, and found healthy, with one exception, in which the sympathetic on the left side of the neck was degenerated in associa- tion with left exophthalmos. In the diseased bones or joints conspicuous changes are found after death. There is occasionally an extraordinary wasting of the articular ends of the bones, which seems to begin by rapid erosion of the cartilages, extending quickly to the bone beyond, the extremity of which may be much reduced in size and altered in form. In the hip- joint, for instance, in a case recorded by Charcot, the edges of the acetabulum had been removed, and the whole of the head of the femur and most of the trochanter had disappeared (Fig. 130). Similar changes have been found in most of the larger joints. In the bones the compact tissue has been found thinner and more porous than normal. At the seat of old fractures a large amount of bony callus is forme 1 (Fig. 130), and sometimes new bone is found in the capsule of joints that have been injured. Pathology.—The great fact of the pathology of tabes is that it is a neural degeneration in the sensory nervous system, peripheral and central. In both peripheral nerves and spinal cord, the incidence of the disease is almost exclusively on the structures concerned in afferent conduction. The cerebral system suffers in far less degree than the spinal, and in more irregular manner, but in the occasional peripheral degeneration of the optic nerve, and the central changes in the roots of the fifth, we may trace the same law of distribution. It is less dominant, however, than in the spinal system, since some of the cranial nerve symptoms are exclusively motor. The motor character of the leading symptom, ataxy, is, as we shall see, only an apparent and not a real exception to the general sensory character of the malady. The degeneration commences in the nerve-elements themselves; the overgrowth of connective tissue, which gives to the lesion its obtrusive character, is secondary. This fact has been observed in LOCOMOTOR ATAXY. 475 the peripheral nerves ; as regards the spinal cord it rests on inference scarcely less certain. That it is true of the spinal cord has, indeed, been doubted, chiefly on the ground of the thickening of the walls of the vessels seen in some cases, and the manner in which the increase of tissue seems to start, from them. But the " system " character of a disease, the limitation of a wide-spread lesion in its early stage or slight degree to structures having a common function, is probably in all cases proof of its neural origin, i. e. its origin in the nerve-elements themselves. In tabes the disease of the peripheral nerves depends on decay of the fibres, and the partial character of the sensory loss indicates the limitation of the chief lesion to fibres of one sensory function. There is every gradation, moreover, between the cases in which the interstitial and perivascular disease is considerable, and those in which it is so sliglit that there is nothing to suggest a primary interstitial process The change in the vessels may reach a high degree in the posterior median columns when their degeneration is purely secondary, and certainly commences in the m ve-fibres, being the result of a focal lesion; a similar thickening of the vessels has also been met with in secondary degenerations in other parts. It is most important to remember that the overgrowth of the neuroglia is a pathological process of growth distinguishable (and to a large extcut distinct) from the defeneration of the nerve-fibres that excites it. It may vary in degree in different cases, and, even in the secondary degeneration of peripheral nerves, may assume an independent energy and even present an inflammatory character. Once excited, the process of tissue-growth may be largely independent of its cause Secondary vascular disturbance may attend it, and thus a sub-inflammatory con- dition (or even a true inflammatory condition) is probably sometimes developed; it may invade the pia mater, and through this may spread widely. The chief causal fact regarding the disease is its common relation to svpliilis. Tabes is generally, although possibly not invariably, a post-syphilitic disease ; certain elements of the nervous system degenerate in consequence of the influence on them of previous syphilis. There may be indeed, present and active syphilis, but, generally the active sb.ge of the disease is over. Syphilis is often a prolonged malady, in which the results of its earlier activity sometimes coincide with its later specific effect. The elements that suffer have some special liability to degeneration, their nutrition may fail from other causes, but they seem to possess a special susceptibility to the influence of syphilis. The usual symmetry of tabetic lesions indicates that the mechanism by which syphilis affects the nervous system is a blood-state. The manner in which the peripheral nerves suffer in many cases, brings tabes, in spite of its chronicity, into analogy with the more acute forms of peripheral neuritis, such as are due to toxic agents, sometimes the result of acute specific diseases. The long interval which elapses between syphilis and tabes and the common 476 SPINAL CORD. slowness of the tabetic process are only in proportion to the ckronicity of the causal malady, compared with the acute specific diseases that have neuritic sequelae Further, the considerations mentioned in the account of multiple neuritis, which suggest that its immediate cause, when it is due to an acute blood disease, is a product of the growth of the organisms of the primary malady, rather than the organisms themselves, hold good also in the case of syphilis and tabes. The degenerative changes in the nervous system differ from the lesions of active syphilis, both in character and in time, in such a way as to make the assumption reasonable that they depend upon some product of the growth of the syphilitic organisms, a product which is probably a chemical toxine, a suggestion first made by Striimpell, and widely held regarding other analogous mala dies. Recent research is bringing into ever greater prominence the important part played by such products in the generation and course of diseases. In the specific diseases that have these sequels, there may be more than one such product of their organisms, causing more than one kind of consequence. The differences between such nerve degenerations as those of tabes, and other late effects of syphilis, is at least not difficult to comprehend on this hypothesis; neither is the fact—which has been so great a difficulty to many—that the treatment which has so speedy an effect on syphilis itself, is generally without influence on the tl generative processes that sometimes follow it. Tabes is probably a rare sequel, when regarded from the side of syphihs. But the occurrence of such consequences in some instances and not in others has analogies in the case of almost all the acute specific diseases that have similar sequelae, and must be taken as evidence of variations in the precise character of the primary disease. The virus of syphilis is doubtless organismal; this has not, indeed, been demonstrated, but the analogy it presents-with other specific diseases precludes doubt on the subject. Similar variations in the sequelas are familiar to us in the case of other diseases. They some- times have, and at other times have not, consecutive effects upon the nervous system, as in the familiar instance of diphtheria. Diph- theritic paralysis is a result of the disease, most irregular in occurrence and degree. But it deserves note that its dependence on a chemical toxin, the indirect result of the organisms, has been conclusively proved by Sidney Martin. The significance of the fact is the greater, inasmuch as its effects sometimes closely resemble the symptoms of tabes. These considerations receive a notable emphasis from the occur- rence of tabes in children who are the subjects of inherited syphilis, to whom the disease in early life is probably confined. It has been present in all the cases that have come under my notice. But the sequel differs much from those that are related to other diseases. Its occurrence is quite independent of the thoroughness of treatment of the primary disease. LOCOMOTOR ATAXY. 477 The pathological facts already known enable us to understand many of the symptoms of the disease. There may be an interruption of the sensory path in one or both of two places, in the peripheral nerves, and in the posterior root-fibres as they enter the cord, and an inter- ruption of the fibres in either place will explain the loss of sensibility which is so frequently present. The pains may most reasonably be ascribed to the molecular changes in the peripheral nerve-fibres. The intensity of a sensation is no measure of that of the process that causes it. Whether the affection of the cells of the posterior ganglia, or of the posterior cornua of the cord* takes part in the production of the symptoms we cannot tell. These cells are the nutritiona'l centres of the sensory " neurons," within the influence of which are the struc- tures that degenerate. It is noteworthy that the affection of «the peripheral nerves must involve the structures by which the nerve- impulses of sensation are normally generated by mechanical and other processes. The long persistence of pains without any increase in the symptoms, shows that they may be due to the action of structures that are changed, but not changing. The loss of reflex action from the skin is explained by the interruption of the sensory path, and an increased irritability of the sensory nerves, the result of even shght degenerative changes, sufficiently explains both the hyper- aesthesia and the increase of reflex action sometimes observed. Whatever theory of the nature of the so-called " tendon-reflex" action is held, the loss of the knee-jerk must be explained by an interruption of the sensory path. On the theory I have advanced, the arrest of impressions from the afferent muscular nerves abolishes the muscle-reflex action on which the local irritability depends (see p 25). Many other facts of disease show that this irritability is easily lost, and that a very slight change in any part of the reflex arc, too slight to cause other symptoms, is sufficient to arrest the k nee- jerk, f Hence we can understand that this loss should be constant and early. It is not improbable, moreover, that these nerves suffer in special degree. The muscles may be insensitive to pain, e. g. that of electrical stimulation Pressure and extension, which in health are painful, sometimes cause no sensation, even when the skin is sen- sitive. The mechanism of the muscular inco-ordination, which is the obtrusive symptom of the disease, has been the subject of much dis- cussion. Two fundamental facts, however, limit the problem. First, the ataxy cannot be primarily due to the loss of cutaneous sensibility. * In disease of the nerve-roots of the cauda equina there is always ascending degeneration of the posterior median columns, but not of the antero-lateral ascend- ing tract. Hence the root-fibres from which the path is continued by this tract must end in nerve-cells in the posterior cornua, and the degeneration of this tract in tabes is proof of the degeneration of these sensory cells. See the * Lancet,' June 19th, 1886. t E.g. its loss after diphtheria when there are no other symptoms. 478 SPINAL CORD. Disease of the conducting path in the cord may cause absolute anaesthesia of the skin without the least ataxy. Although this does not prove that interruption of the sensory path in the nerves, between the skin and the reflex centres, may not cause inco-ordination, this element seems to be excluded by the fact that there is no relation between the ataxy and the loss of feeling in the skin. There may be, in tabes, much ataxy without any cutaneous anaesthesia, and vice versa. The second fact is that ataxy may exist in considerable degree when the lesion is solely one of the peripheral nerves, or nerve-roots, and the posterior columns of the cord are free from disease.* These two facts, taken together, seem to show that the ataxy may be pro- duced by one mechanism, even operating alone, the disease of the afferent muscle-nerves. If the loss of the knee-jerk in tabes is to be taken, as I believe it may, as an indication of the disease of these nerves, the constancy of the loss shows the constancy of the presence of this element, in some degree. As just stated, a very shght degree of disease may abolish the knee-jerk; it is probable that a greater degree is needed to cause inco-ordination, and a still greater change to produce actual insensibility to pressure or extension. In unilateral lesions of the spinal cord, as we have already seen (p. 272), there may be loss of the sense of posture, with intact cutaneous sensibility, on the side of the lesion, and no loss of this sense on the opposite side, on which cutaneous sensibility is lost. In such a case marked ataxy has been observed on the side on which the sense of posture was lost, when motor power returned.f Whatever effect in causing ataxy is produced by disease of the path of muscular sensi- bility in the spinal cord must also be produced by interruption of the path between the muscles and the cord. The latter must also arrest whatever reflex action depends upon these muscle-nerves, J and it is possible that such reflex action takes some part in the mechanism of muscular co-ordination. In this connection it is important to note that the fibres that pass up by the posterior median columns seem to constitute the path from these nerves. The root-fibres to the columns pass up, as the path is * Apart from the evidence of this from cases of characteristic tabes, a very instructive case has been recorded by Dr. Hughes Bennett, in which all the sym- ptoms of tabes were present in a case of multiple tumours of the posterior nerve- roots (' Clinical Soc. Transactions,' vol. xviii). Ataxy has also resulted from other processes, such as injury, that have caused extensive damage to the posterior roots alone. t Gilbert; see foot-note, p. 272. X In a case in which the incoordination was much greater in the right leg than in the left, and cutaneous sensibility was equally impaired in the two, a strong trac- tion on the calf muscles, by forcible passive flexion of the foot, produced a distinct sensation in the extended muscles of the left leg, and no sensation in those of the right. In another case, in which the skin was sensitive to the slightest touch, the patient was unconscious of a vigorous extension of the toes produced by faradic stimulation of their short extensor. LOCOMOTOR ATAXY. 479 proved to do, without decussating, and they may be diseased in intense degree when there is no loss of cutaneous sensibility.* This tract is affected in almost all cases of tabes in which there is a lesion in the cord, and in all such cases in which there is ataxy. This fact suggests that the lesion is first and chiefly of the nerve-fibres from the muscles, f The posterior median columns (extensively connected with the cere- bellum) and the direct cerebellar tract, probably conduct to the cere- bellum the impressions from the sensory muscle-nerves. If so, the disease of these tracts and nerves must interfere with the co-ordinating action of the cerebellum, and cause some part of the loss of function which results from disease of the cerebellum itself. There is another mechanism which may co-operate in increasing ataxy. The vertical fibres of the postero-external column have only a short course, and some probably connect the posterior grey matter at adjacent levels. The affection of these fibres seems to be proved by the fact that the comma-shaped bundle of fibres in the front of the postero-external column may be specially degenerated. This lesion may impair the association of the sensory structures, and so cause a want of harmony in the central mechanism. The theory that the ataxy was due to such a mechanism was advanced by Todd in 1847. It is not probable that, if effective, it has more than an intensifying influence, since ataxy may exist when the posterior columns are throughout unaffected. The discovery that ataxy may result from alcoholic peripheral neuritis confirms the view of its origin above stated. Although cutaneous anaesthesia cannot alone produce ataxy, it may reasonably be assumed to increase that which already exists. Sensa- tions from the skin furnish important guidance to the motor cerebral centres, and are probably also concerned in such reflex muscular actions as that of standing. Similar guidance to the cerebral co-ordinating centres is also afforded by visual impressions, the loss of which distinctly augments the defect of co-ordination. The varying characters of the ataxy in different cases probably depend on the local variations in the degree of change in the muscle-nerves. The special effect of the disease of other elements of the cord, related to the posterior roots (as the posterior vesicular column, Clarke's column), has still to be ascertained. It is probable that co-ordination is chiefly an automatic process depending partly on muscle-reflex actions, and on the connection of neighbouring sensory structures in the spinal cord, but chiefly on the function of the cerebellum, determined by the connection of the * Tliis posterior tract is most diseased on the side opposite to that on which there is most degeneration of the antero-lateral ascending tract. f The opinion that the ataxy depends on impairment of the muscular sense was put forward in 1855 by Dr. Russell Reynolds; see p. 445. Dejerine has also asso- ciated the ataxy with the degeneration of the peripheral sensory muscle-nerves (' Archives de Physiologic,' 3rd series vol. iii, p. 231). 480 SPINAL CORD. muscles with it, and that the interruption of this connection is the chief element in the inco-ordination of locomotor ataxy. It is probable also that the automatic processes are in part under cerebral control, guided by sensory impressions which do not enter the sphere of consciousness, and that the derangement of this control will intensify inco-ordination, though incapable of producing it. We do not at present know to what extent, in any given case, the symptoms are due to the cord disease or to the peripheral nerve lesions. Apparently pains, ataxy, and anaesthesia may be due to either. The question can only be decided by the comparison of symptoms and pathological changes in a large number of cases. That anaesthesia may be due to the peripheral changes is proved by the observed correspondence of the two in distribution (Dejerine). The trophic changes in the skin, bones, and joints are probably due to the process of degeneration in the peripheral nerves. The degenera- tion has been found in all cases of the kind in which it has been looked for, and found also in the nerves of diseased joints. The pathology of the muscular wasting has been already mentioned. The pains in the region of the fifth nerve are explained by the lesions in it root, especially in its ascending root, which, coming up from the medulla, is homologous with the posterior spinal roots. This nerve, indeed, as Pierret has pointed out, represents the sensory roots of almost all the motor cranial nerves. The degeneration of the optic nerve is fairly comparable with that of the peripheral spinal nerves. Considering the special character of the optic nerve, the absence of degeneration of the retina does not seem to destroy the analogy between the two. Regarding the pathology of the visceral crises we know but little. The transient motor symptoms in the limbs, and in the eyeball muscles, are apparently of functional origin. They must be distin- guished from the lasting palsies, which are probably due to degene- rative processes in the nerves or nuclei. Such transient paralysis may precede enduring paralysis due to nuclear degeneration. The loss of function of the internal ocular muscles, being persistent, must be ascribed to degeneration of the related centres. But even the light-reflex may return (jn rare cases) after it has been absent for years, and its loss must therefore depend, at least sometimes, on molecular changes capable of recovery. It is, indeed, important to remember that tabes is a disease which begins as a derangement of molecular nutrition, which is probably only to be discerned when relatively great in its degree. If we also remember that this derange- ment is the result of some toxic material or virus circulating in the blood, we can understand better the leading facts of the disease, and especially the variations in its course, its degree, and the precise character of the symptoms. Diagnosis.—The diagnosis of tabes rests on the combination of symptoms already descrihed. In the early stage, the loss of the knee- LOCOMOTOR ATAXY 481 jerk, together v th pains, or unsteadiness on standing with the feet together and the eyes closed, justifies a diagnosis of the commencing affection, provided we can exclude toxic peripheral neuritis (especially that due to alcohol), diabetes, and diphtheritic palsy. A lesion of the anterior cornua or nerve-roots is excluded by the absence of wasting of the muscles or change in their irritability. The diagnostic value of the loss of the knee-jerk can hardly be overrated. It is probably never absent in health. If there is doubt as to its loss, the precautions recommended on p. 21 should be adopted. When it is lost, and reflex action is in excess, a true reflex movement may sometimes simulate the jerk; the distinction is that the tap sometimes causes a movement and sometimes does not; that an interval, brief but appreciable, elapses before the movement occurs; that a similar movement is caused by a prick on the skin, and that the delayed contraction some- times occurs in the other leg, or in the adductors of both legs.* In cases in which the knee-jerk is present, the diagnosis of tabes is only justified by distinct and characteristic inco-ordination. In the few cases of this kind that have come under my own observation, the knee- jerk has been either unequal on the two sides, or has been lost on one. Such abnormality is probably the rule in these cases, and the diagnosis is thus facilitated. In a case with lightning pains, but neither inco- ordination nor loss of knee-jerk, a suspicion of tabes would be justified by the presence of some other symptom, such as retention or incon- tinence of urine, loss of sexual power, or loss of the iris-reflex. As we have seen, it is probable that cases occur in which these pains exist alone,—a condition that may be termed " tabetic neuralgia." The loss of the iris-reflex is of great diagnostic importance. It shows that a degenerative process is at work in the nervous system, and it suggests, therefore, that other symptoms are also due to de- generation. But since the iris-reflex is not always lost in tabes, the negative significance of a normal reflex is far less than is the positive significance of its loss. The practical value of this symptom can hardly be overrated. It puts the observer, so to speak, on the track of nerve degeneration. Its loss is, moreover, so often due to preceding syphilis, that it should always suggest this antecedent. There are certain diseases with which tabes is especially liable to be confounded. One of these is multiple alcoholic neuritis. The ordinary form of this disease is readily distinguished by the symme- trical paralysis which is its chief manifestation. But the variety which closely resembles locomotor ataxy is the "alcoholic pseudo- tabes" (p. 159), in which the diagnosis maybe very difficult. This is not surprising, because it resembles tabes pathologically; the lesion is a "parenchymatous neuritis," a subacute degeneration, beginning in the nerve-fibres, and similar to the peripheral form of tabes. It * It is impossible to exaggerate the difficulty presented by some patients in ascer- taining whether the knee-jerk is or is not lost, and the care needed. Repeated observations are desirable in doubtful cases. VOL. I. 31 482 SPINAL CORD. often affects, however, in some degree, the motor as well as the sen sory nerves, and there is then some weakness in the distal portions of the limbs. An altered electrical reaction may be found in the muscles (never in the weakness sometimes met with in early tabes), and there is generally marked muscular tenderness, scarcely ever present in tabes. The pains have not the "lightning" character, and the sphincters escape. The pupils act normally, but this is not an abso- lute distinction, since they may be unaffected in tabes. A history of alcoholism may help the diagnosis, and so may improvement when alcohol is withdrawn. By attention to all these points, a diagnosis can generally be made without much difficulty. When the symptoms and lesion of tabes are combined with those of general paralysis of the insane, it may be doubtful in which cate- gory a case should be placed. The question is rather one of the pre- ponderance of the symptoms of one or the other malady than of absolute distinction between them. In most cases, however, in which this combination exists, the symptoms of general paralysis become more pronounced as time goes on, and the spinal symptoms, which at first were the most conspicuous, pass into the background. All common forms of paraplegia are distinguished by the early loss of power, and by the persistence of the knee-jerk, often emphasised by its excess and by the occurrence of a clonus in the extended rectus or calf muscles. If weakness supervenes in tabes, it is usually late in the course of the disease, and the other symptoms have been and are well marked. If the knee-jerk has been once lost in this disease, it is not reproduced by secondary lesions of the cord which ordinarily increase the knee-jerk.* The same distinc- tions usually suffice for the diagnosis from the combined form of paralysis and inco-ordination that I have termed " ataxic paraplegia." In this the knee-jerk is excessive, and there is foot-clonus, while pains and anaesthesia are absent; spasm supersedes ataxy. In other forms of combined disease of the cord the diagnosis depends chiefly on the recognition of union. Acute lesions of the cord, probably situated in the postero-external column, may produce inco-ordination and pain, but the suddenness of the onset, the limitation of the symptoms, and their tendency to sub- side, usually suffice for the distinction. Symptoms from this cause are far more common in the arms than in the legs. Ataxy in one limb may also be produced by a tumour growing in the posterior column, but other symptoms indicate the invasion of adjacent struc- tures, as was conspicuous in the case figured in the chapter on tumours of the cord. All these cases present the characteristics of a focal lesion with random consequences, rather than of a system disease with limitation to a special function. The loss of perception of pain, with preserved tactile sensibility, * See, however, an exception to this, referred to on p. 455. The paper referred to mentions others. LOCOMOTOR ATAXY. 483 when it involves the hands, may arouse a suspicion of syringomyelia. But the loss of the knee-jerk in tabes, and the absence of the momen- tary pains in syringomyelia, will enable a correct diagnosis to be made even without corroborative symptoms. In diphtheritic paralysis occurring long after the sore throat, or in which the nature of this was not recognised, the loss of the knee-jerk may cause tabes to be suspected ; but the nature of the case is almost always rendered clear by the paralysis of accommodation and of the palate which precedes the ataxy, and should be suggested by the absence of pains and the presence of weakness. If true tabes follows diphtheria, with lasting ataxy, it is so rare as to be of little practical importance. When the dorsal region of the cord is chiefly affected, the severity of the pains in the trunk may lead to a suspicion of disease of the vertebral bones, but in the latter the pain is local and fixed, and this, with the characteristic increase of pain when the patient moves, should prevent error. It is still more frequent to mistake such cases for neuralgia of the intercostal nerves, but even if there are no pains in the legs to suggest tabes, the knee-jerk and the light-reflex of the iris are lost in tabes. Experience shows that the most frequent errors in diagnosis are due to a mistake as to the nature of the pains, which are mistaken for rheumatism, especiallv when influenced by weather, or for sciatica when referred to the region of the sciatic nerve, or for some form of gout if the disease exists in the patient or his family, or in the mind of the physician.* In the rare cases in which the cranial nerves are disordered and pains are felt in the head, the symptoms may be mistaken for trigeminal neuralgia. The obscurity of the symptoms may be increased in such cases by a sense of painful con- striction in the face, analogous to the girdle-pain felt around the trunk (see p. 453). The only organic intra-cranial disease that may be taken for tabes is tumour of the cerebellum. In some cases of tabes the unsteadiness resembles that of cerebellar origin. Loss of the knee-jerk is strongly in favour of tabes ; in cerebellar tumour increase of the jerk is the rule, and loss is only to be regarded as not absolutely incompatible. Anaesthesia and lightning pains are conclusive evidence of the spinal disorder, while in cerebellar tumour severe occipital headache is almost invariable, and considerable optic neuritis is extremely common. Optic nerve atrophy is primary in tabes, post-neuritic in tumour. The various visceral crises are often mistaken for primary disorders of the deranged organs. Recurring attacks of the character described should always arouse suspicion of their possibly tabetic nature, and an examination of the knee-jerk will usually decide the point. * In one case, in which tabetic trunk-pain was chiefly felt at the level of the epigastrium, a physician of repute not only made a diagnosis of gastric gout, but refused to modify his opinion when loss of the knee-jerk was discovered, and the patient became unsteady in gait. 484 SPINAL CORD. Prognosis.—The prognosis in tabes corresponds with the facts stated as to the course of the disease. It does not, as was once thought, deserve the epithet " progressive," given to it before the pre- ataxic stage was known and before the disease had been widely observed. Arrest is frequent, and considerable improvement is not rare. The earlier the stage of the disease the better is the prognosis. In the first stage the disease often becomes stationary. When ataxy is developed the prospect of arrest is less than in the first stage, but is still considerable. Occasionally, even in the typical form of the disease, the amount of improvement is very great. One patient was scarcely able to walk across the room, in consequence of the inco-ordination, when he came under treatment, and at the end of six months his gait was scarcely distinguishable from that of a healthy person. When the third stage is reached the possibihty of improvement is far less, but is not quite absent. A woman suffering from pure tabes, when admitted to hospital, had been unable even to stand for six months, on account of the extreme ataxy ; but she improved so much that in a few months she was able to walk about the room without help, and has con- tinued, now for six years, to do her household work without difficulty, and even to walk some miles with the aid of a stick. On the other hand, in some cases the malady increases in spite of every effort, and even when there is permanent arrest or improvement it is rare for all symptoms to disappear. The knee-jerk generally remains absent, and often attacks of pain continue to occur. It is difficult to find any trustworthy indications to guide the prognosis in an individual case. The fact of preceding syphilis has Httle influence on the prognosis. Only when the symptoms have developed rapidly and the syphilis is recent is there any possibihty of benefit from antisyphilitic treatment. In all cases, however, in which the onset of symptoms is acute there is more prospect that they will pass away than if they develop slowly. In most cases the only trustworthy guide to prognosis is the observed tendency of the individual case. Of special symptoms, the pains are often the most distressing, and unfortunately they are the most obstinate symptom of the disease. They may persist in undiminished severity when other symptoms lessen; and, on the other hand, they may become trifling when the disease increases. Diminution of the pain is a good sign if other symptoms are stationary, but not if these increase. It is often, how- ever, a solace to the patient to know that persistence of the pains does not mean progress in the disease. The optic nerve atrophy is usually progressive, but not invariably, as is often asserted. Occasionally its progress is arrested, and more frequently when it is greater in one eye than when both are involved. Strange to say, the occurrence of optic nerve atrophy makes the prognosis as to the spinal symptoms better; in most cases the spinal lesion remains in the first stage. Treatment.—The disease is one in which treatment often has a very clear influence, not only in relieving suffering, but in determining LOCOMOTOR ATAXY. 485 the arrest or diminution of the disease. This is true especially of treatment by drugs. But the first care should be to secure freedom, as far as possible, from all influences capable of increasing the disease, and from whatever is hkely to depress the nervous system. Excessive mental work, anxiety, and physical fatigue are all harmful. In severe and acute cases, absolute rest for a week or two is often useful at the onset of treatment. If the patient walks about, exercise should always stop short of fatigue. Care should be taken to avoid the risk of falls; a severe concussion of the spine will sometimes excite to fresh activity a stationary disease. Exposure to cold is also injurious ; a severe exposure may cause acute mischief. If practicable it is well that the winter should be spent in a warm and dry climate. A sea voyage is sometimes useful, combining, as it does, a maximum of fresh air with a minimum of exertion; it has, however, less actual effect than might be expected. If there is much ataxy, the risk of falls from the motion of the ship must be taken into consideration. It is the most useful in cases that are already stationary; such patients often return with a diminution in all their symptoms. When the disease is advancing, a voyage often does harm rather than good. The digestive organs should be kept in careful order; an attack of indigestion or constipation is often attended by lightning pains, which cease when an aperient has acted. Food should therefore be light in quality, and easily digestible. The change from an active to an inactive life, which tabes often causes, may lead to the develop- ment of gout in an individual predisposed to it, either by inheritance or by his previous mode of life; and the tendency must, as far as possible, be obviated by regulation of diet and by frequent aperients. Smoking should be either avoided or limited to a small amount. Alcoholic excess is especially harmful; it sometimes excites a very severe exacerbation of the symptoms; this is not surprising, since, as we have seen, chronic alcoholism may cause a disease resembling tabes in its symptoms and pathology. Sexual excess is also most injurious. Many patients are preserved from this danger by the disease itself, but it is not always so. Excess seems to have a special influence on the optic nerve atrophy. Several very painful instances of this have come under my notice. A man in the early stage of tabes, with shght atrophy, some peripheral limitation of the fields, but little impairment of acuity of vision, started on a voyage from Austraha to England. The day before he started he married, and when he reached this country he was quite blind. The influence of drugs on the disease is unquestionable in many cases, and if they are used wisely, the more a physician sees of the disease, the more highly is he likely to esteem them. There is no specific for the malady, and in some cases the morbid tendency over- powers every influence that can be brought to bear upon it. Moreover, the influence of drugs is variable; that which seems to do much good in one case has no influence on another, and this is true also of the 486 SPINAL CORD. same case at different periods. Hence the therapeutic statements that have been made by various observers are somewhat discordant. The first question is the influence of antisyphilitic agents. In tabes such influence is distinct only in rare cases, chiefly under the conditions mentioned in the section on prognosis. In those circum- stances full doses of iodide of potassium should be given, and if the interval since the primary disease is short, mercury may be rubbed in until the gums are slightly affected. In cases of slow development, several years after primarv syphilis, such treatment seldom does good, and sometimes does harm. But so widely spread is the opinion that every consequence of syphilis is amenable to treatment, that it is often well to avoid the suspicion of neglect, and to clear the therapeutic ground, by a course of iodide of potassium for five or six weeks. Very small doses of mercury, such as Tx¥ grain of the red iodide, may also be given for a longer time, and may often be conveniently com- bined with other drugs. It seems sometimes to have a tonic influ- ence in these cases. But in such late cases, and in all the late nerve degenerations that follow syphilis, energetic mercurial treatment only does harm. Its depressing influence seems to increase the degenera- tive tendency, and to hasten the progress of the disease,—sometimes even to induce its extension. Of drugs that have been recommended for tabes, those that are most useful are arsenic, iron, quinine, aluminium, nux vomica and strychnia, nitrate of silver, Calabar bean, belladonna, ergot, phos- phorus. Of these arsenic is certainly that which most frequently does distinct good. Most of the cases in which I have known the greatest improvement to occur, have been taking it at the time. In several of these cases there was no other change in the conditions of life to which the improvement could be ascribed. The form in which arsenic is given matters little; rr\iij to vt{ vij of the Liq. Arsenicalis may be given in a mixture, or ^ gr. of arseniate of soda in a pill. Iodide of arsenic has no special advantage, and is not so well borne. This or any other drug must be continued for at least six weeks before an opinion of its influence can be formed. Rapid improvement can never be expected in so chronic a disease. But it is not well to continue any drug for more than about three months at a time. Most good is effected by alternating two or more ; the return to one that had ceased to do good is often beneficial. In connection with the influence of arsenic, it is interesting to note the well-known effect of the drug in improving the nutrition of the skin, and the frequency with which the cutaneous nerves are degenerated in tabes. Quinine, or the extract of nux vomica, may be usefully combined with arsenic; or a small dose of mercury may also be given, n\xv of Liq. Hyd. Bicblor. with n\v of Liq. Arsenicalis, or -^ gr. of the red iodide with -± gr. of arseniate of soda in a pill. Occasionally arsenic seems to irritate the nerve-centres, but smaller doses may then be borne, and may be useful. "Nitrate of silver and phosphorus are less effective, but may some- LOCOMOTOR ATAXY. 487 times be given alternately with arsenic. The chloride of aluminium is another agent that I have found of distinct service, 2—4 gr. twice or three times a day. It certainly diminishes the severity of the pains and the tendency to them. Calabar bean has been recommended as producing temporary im- provement in many chronic spinal diseases. Its influence in tabes is not great. Ergot has been esteemed highly by some, but is seldom distinctly effective. Belladonna is sometimes useful, especia'lv when there is a tendency to incontinence of urine. Strychnia in the same cases sometimes produces marked improvement, especiallv combined with a small dose (-2 J^ gr.) of nitro-glycerine, which causes the blood containing the tonic to pass more freely to the nerve-centres. Counter-irritation to the spine, by blisters or the actual cautery, is often useful, chiefly in the cases just mentioned, in which the dis- ease develops, or the symptoms increase, rapidly, or in which there is spinal pain or tenderness. It is not probable that it influences the process of degeneration, but it may lessen any secondary inflammation. Of special symptoms that require treatment, the pains are the most important. Unfortunately they are often very obstinate, and their variability renders it difficult to estimate the influence of treat- ment upon them. Severe paroxysms may yield only to hypodermic injections of morphia, but this should be reserved for the most intense attacks, since its use is undesirable for a recurring symptom which may continue for years. Indian hemp is often effective ; gr. \ or | should be given every three or four hours during an attack. But the most ureful agents for relieving a paroxysm are antipyrine and acetanilide. One or the other of these seldom fails; should they do so, exalgin or phenacetin or migranin may succeed. Hypodermic injections of cocaine generally arrest, for several hours, pains that are superficial in character, especially if accompanied by hyperaesthesia of the skin. The injec- tion should be of £ to } of a grain, at the upper part of the region to which the pain is referred. Cocaine has no influence over the deeper pains. Superficial pain is also relieved by the local applica- tion of chloroform sprinkled on spongiopiline (or lint and oiled silk). Occasionally the pains are lessened by a warm bath. Counter-irritation to the spine, as by repeated sinapisms, may give some relief. These measures, however, only relieve paroxysms, and do not prevent recur- rence. Chloride of aluminium is of considerable service in lessening the tendency to the occurrence of the pains. Two to four grains may be given three times a day. It is readily soluble, and may be given in combination with other drugs. Paroxysmal visceral symptoms often yield to antipyrine or aceta- nilide, but when severe, morphia alone mitigates their intensity. Slight gastric crises may be relieved by simultaneous sinapisms to the epigastrium and neck. Laryngeal spasm is usually at once relieved by nitrite of amyl or nitro-glycerine; the local application of cocaine is also useful. Weakness of the bladder is sometimes lessened by 488 SPINAL CORD. strychnia or belladonna Strychnia may be given by hypodermic injection, as recommended in the chapter on muscular atrophy. Blisters or sores on the feet should receive careful local treatment until they are well. If neglected they may become very troublesome. The patients should be cautioned never to cut a corn; a perforating ulcer is often set up by a corn being cut too deeply. The epidermis should be softened with an alkali and rubbed off with pumice-stone. Attention to the bladder is one of the most important elements in the treatment of tabes, as in that of all diseases of the spinal cord, chronic and acute. If there is any reason to believe that the bladder is imperfectly emptied, a catheter should be passed ; and if residual urine is found, the' bladder should be emptied perfectly and washed out every day or every other day. No hesitation need be felt in the use of the catheter in these cases, provided very strict antiseptic pre- cautions are taken. Many patients die every year from want of the catheter, because it is thought that all is right since they pass urine freely. The residual accumulation, or the slight cystitis, sets up chronic pyelo-nephritis, which develops insidiously, and is unsuspected until mysterious febrile disturbance occurs, chronic or acute, and leads to death. It is probable that the onset of the final acute disturbance is sometimes determined by the passage of a catheter, just as this will cause a rigor or transient hematuria in a healthy person I have seen many melancholy instances of death from the consequences of un- suspected retention, while the early and frequent use of the catheter is comparatively innocuous. It is especially important to insist on the danger that the practitioner may be misled by the patient, who thinks that because he passes urine freely he necessarily empties his bladder perfectly. Electricity has little influence on the chief symptoms of tabes. The voltaic current is powerless over either the pains or the ataxy, whether it be applied to the spine or the limbs. Faradisation of the skin by the wire brush has been recommended for the defect of cutaneous sensibility, but it has little if any influence. Temporary improvement in gait, and sometimes a little permanent improvement, may be obtained by faradisation of the muscles; the stimulation of the afferent muscle-nerves is probably the mechanism of its action, but I have not met with permanent good from its influence. When the bladder or its sphincter is weak, faradisation from the hypogastrium to the perineum may be employed, and occasionally seems to do some good. In secondary wasting of the muscles an attempt may be made to maintain their nutrition by stimulating them with whatever current they respond to, but the central nature of the cause usually renders local treatment ineffective. Massage also has been recommended, and possibly may be beneficial in some cases. It is most useful if com- bined with the systematic use of the exercises in co-ordination devised by Fren-.ol.* * 'Deutsch. med. Wochenschr./ 1896. PEIMARY SPASTIC PARAPLEGIA. 489 Nerve-stretching was fashionable a few years ago, the operation being usually performed on the sciatic nerve. In the first case in which it was employed (by Langenbuch) the procedure was followed by remarkable and mysterious improvement, not only in the pains, but also in the inco-ordination. The patient subsequently died under chloroform, administered in order that the nerves of the arms might be stretched. The spinal cord was found by Westphal to be healthy. Although the nerves were not examined, there can be little doubt that it was one of the cases in which the nerves alone are diseased. The operation has since been performed in a large number of cases, but without results that have secured its survival, and it is passing into merited disuse. Its place was taken by extension, of the spinal column. In this procedure the patient is suspended in such a manner as to allow the weight of the body to rest on the head and shoulders, and head alone, alternately, and the ligaments of the spinal column are supposed to be so stretched that the spinal cord and its nerve-roots are elongated. The chief effect is produced on the ligaments of the upper part of the spine, but the actual amount of elongation of the spine is exceedingly slight and insignificant, as has been proved by experiments on the dead body. It is difficult to conceive any mecha- nism by which it can do the good in tabes which was at first ascribed to it; and the careful observations by Russell and Taylor on a large number of cases at the Queen Square Hospital * seem to show conclu- sively that it has no real power of permanently influencing the disease. It is important that the patient should avoid falls as far as possible, and likewise exposure to cold and wet. Both of these influences occa- sionally excite an acute exacerbation of the pre-existing malady. PRIMARY SPASTIC PARAPLKGIA (primary lateral sclerosis). The morbid state thus designated is one that has been, and still is, the subject of much discussion. Its relations are complex, and a somewhat lengthy pathological introduction is necessary. General Pathology.—We have seen that in every kind of trans- verse lesion of the spinal cord, provided this is situated above the lumbar enlargement, the paralysis of the legs is soon accompanied by excess of myotatic irritability (increased knee-jerk, foot-clonus), and that the muscle-reflex action on which this irritability and muscular tone seem to depend, gradually increases to tonic spasm, so that a condition develops to which the term " spastic paraplegia " is applied. A condition quite similar to that which is thus secondary to a trans- verse lesion often develops gradually, without any indication of a * Russell and Taylor, ' Brain,' Summer Number, 1890, vol. xiii, p. 206. 490 SPINAL CORD. primary focal disease, and without any sensory symptoms to indicate that the mischief extends beyond the purely motor elements of the cord. We have also seen that these symptoms indicate disease of the upper segment of the motor path, the cortico-spinal segment (p. 213), which extends from the motor cortex through the pyramidal tracts, and ends in the grey matter of the cord, doubtless by a subdivision and ramification of the nerve-fibres in the fibrillary network of the spongy substance. From the gradual onset and limitation of the symptoms in these cases it has been assumed that the disease consists of a primary sclerosis of the pyramidal tracts, i. e. in a degeneration of the fibres of this upper segment. Since these tracts run chiefly in1 the lateral columns the disease has been termed " lateral sclerosis." The clinical features presented by these cases, and their probable significance, were first pointed out by Erb.* Degeneration of the pyramidal tracts had been already observed by Turck (1856) and Charcot (18G5). Erb's inference as to the nature of these cases was supported by the independent (and indeed previous) researches of Charcot on cases of muscular atrophy; he showed that in such cases muscular rigidity coincides with degeneration of the pyramidal tracts. Pathologists have since been searching for confirmation of the hypothesis—for evidence that the symptoms, in their pure form, without muscular atrophy, depend on degeneration limited to the pyramidal tracts. Such degeneration in slight degree, associated with slight symptoms, has been found in cases of general paralysis of the insane (by Westphal and others) ; but in all other cases that have been examined either other parts of the white substance have been degenerated, or the disease has involved also the anterior cornua.t In some cases, as one published by Dreschfeld (of which a figure is given at page 497), the change in the anterior cornua has been so slight that the required conditions are nearly fulfilled. J Although absolute demonstration has not yet been furnished, the indirect evidence of the correctness of the pathological hypothesis is very strong, and the only open question is whether, when there is no disease of the motor nerve-cells of the anterior cornu, the degenera- tion is so limited to the pyramidal tracts as to constitute a system disease in the strict sense of the word. It is not surprising that demonstration of the nature of the pure cases is not forthcoming, since, as we shall see, the disease has little tendency to shorten life. It is only recently that it has been shown that the wasting in the anterior horn cells which underlies progressive muscular atrophy is * In 1875, 'Berlin, klin. Wochenschr.,' No. 26; 1877, 'Virchow's Archiv,' Bd. lxx. f Iu a case recorded by Stofella no other part than the pyramids tracts could be seen diseased on naked-eye observation, but no microscopical examination was made. X The same is true of several cases published recently. One of Strumpell's (' Deut. Ztschr. f. Nervenheilk.,' 1894, v) very nearly fuelled the requisite condi- tions. PRIMARY SPASTIC PARAPLEGIA. 491 not necessarily invariably associated with lateral sclerosis, and there seems no reason why a similar degeneration should not exclusively affect the upper segments of the motor path just as it, rarely no doubt, affects only the lower segment. In the majority of instances, of course, both upper and lower segments are affected in the condition known as amyotrophic lateral sclerosis (q. v.). It should, moreover, be noted that cases which present this group of symptoms may be very various in nature. We have seen (p. -254) that, in each segment of the motor path, the same symptoms are produced by disease of any part of the segment. In the upper segment, with which we are now concerned, the symptoms are the same, whether the disease is in the cortex of the brain, the internal capsule, the pyramids of the medulla, or the pyramidal tracts of the cord ; and they must also be the same if the disease is limited to the termination of the segment in the grey matter of the cord. In cerebral hemiplegia the state of the arm closely resembles that present when primary spastic paraplegia involves this limb. The leg in hemi- plegia presents a less close resemblance to its condition in spinal disease, because the leg is innervated from both cerebral hemispheres, and the supplementary influence of the hemisphere of the same side lessens the effect of the disease of the hemisphere of the opposite side. But if there is disease of the leg-centres in both hemispheres, the state of the legs may be identical with that resulting from disease of the spinal cord. Such bilateral disease often results from injury during birth, — meningeal haemorrhage over the upper part of the central convolutions. This resulting condition is termed "congenital spastic paraplegia." (See Vol. II.) On the other hand, it is extremely probable that degeneration begins in the termination of the fibres in the grey matter, just as it does in the extremities of the peripheral nerves, in each case that part of the neuron furthest from its nutritive centre. It may even be limited to these terminal parts, as the extremity of the lower segment is paralysed alone by many agents, typically curara. In such disease the white columns would be found normal, as in one recorded case in which the symptoms of spastic paraplegia existed during life, and no anatomical change was discovered after death. The detection of the disease of the terminal portion in the grey matter is extremely difficult, perhaps im- possible, because the structure must consist of nerve-fibrillse that interlace with others that are unaffected. This view is supported by the fact that in other cases some degeneration has been found in the lateral pyramidal tracts in the lumbar region slighter than the in- tensity of the symptoms suggested, and gradually lessening, to cease higher up the cord. Such a condition is comparable to the degenera- tion of the lower portion of the second segment of the motor tract in some cases of peripheral (degenerative) neuritis, in which there is a degeneration of motor nerve-fibres, greatest in their extremities, ex- tending for a variable distance up the nerves, but lessening long before 492 SPINAL CORD. the spine is reached. It is highly probable that the toxic agents which cause lathyrism and pellagra (q. v.) act on the extremities of the pyramidal fibres as curara does on the nerves; among the spinal symptoms of lathyrism are paralysis of the legs with rigidity and contractures, and increase of myotatic irritability—foot-clonus, &c.* Both clinical and pathological evidence shows that the morbid state often occurs also as part of a more extensive degeneration. Degene- ration may occur in both lateral and posterior columns, giving rise to combined paralysis and ataxy—" ataxic paraplegia," sufficiently definite in its clinical characters and course to make its distinction convenient; it is therefore separately described. The following account of the clinical features of spastic paraplegia is founded on cases in which the motor paralysis and spasm existed alone, with no definite sensory loss, in which they came on gradually, with nothing in the state of the patient or the history of his symptoms to suggest either a focal lesion or an acute process. Causes.—An inherited neuropathic tendency is to be traced occa- sionally in this as in other chronic spinal diseases. Thus in one case there was a history of insanity in uncle, aunt, and two cousins. The disease affects both sexes in almost equal frequency, presenting in this a contrast to posterior sclerosis. 1 he period of life at which it most frequently begins is between twenty and forty ; about three quarters of the cases begin in these two decades, and about an equal number in each. Cases frequently commence, however, in the second decade of life, chiefly in its latter portion. After forty they become much less common; the latest age at which I have known a typical case to commence is sixty-one. The disease sometimes follows syphilis in a way to suggest a causal relation, even when all cases are excluded in which there is any reason to suspect a focal lesion. In one case the symptoms commenced six months after the primary disease.f But this antecedent is not fre- quent, and in this respect also the disease contrasts with posterior sclerosis. Proximate causes are to be traced only in a minority of the cases. The most frequent is concussion of the spine, such as a fall on the back. Some time, often two or three years, elapses between the fall and the first pronounced symptoms of the disease, and hence focal lesions due to the fall can be excluded. Next in frequency is repeated exposure to wet cold. Very rarely the symptoms have slowly followed some acute illness. In several cases the disease has succeeded prostration after childbirth or abortion, or has commenced during lactation. In one case an attack of arthritis in the knee and ankle of one leg was the immediate antecedent, and this leg was the first to become weak. In another case the symptoms followed sub- acute arthritis of both knee-joints, apparently rheumatic in nature. * See Marie, ' Prog. Med.,' 1883, No. 43. f The cord lesion was found 10 be sclerosis, but the direct cerebellar tract was also degenerated (Minkowski). PRIMARY SPASTIC PARAPLEGIA. 493 The possibility that a joint inflammation may be of spinal origin must be borne in mind in considering the significance of such cases, but it is on the whole probable that a primary joint affection is an occasional cause of the spinal disease.* (Acute arthritis, certainly of spinal origin, has only been observed in severe' myelitis.) The cause of the congenital form is always injury to the brain during birth, in most cases meningeal haemorrhage, causing compression of the motor cortex. Symptoms.—Weakness of the legs, of very gradual development, is the first symptom. The patient finds that he gets tired more readily than before, and that the legs feel heavy; sometimes one leg becomes weak before the other. The progress of the weakness is very variable, but it is slow in all characteristic cases. In many instances the patient is still able to walk a mile or two, even after the disease has lasted for several years, slowly increasing. On the other hand, walking power may be almost lost at the end of six months. It is doubtful whether more acute cases belong to this category. The early weakness is often accompanied by slight unsteadiness, chiefly subjec- tive. When the patient seeks advice, it will generally be found that there is very distinct loss of power in the flexors, often greatest in the flexors of the hip, but consider ible also in those of the knee and ankle, and occasionally much greater in the last than elsewhere. The knee-jerk is excessive and quick; the rectus contraction can be obtained, as the patient lies, by tapping the depressed patella, and a rectus-clonus is often obtainable by sudden depression of the patella. The foot-clonus is usually also obtained with readiness. In rare cases, in which the upper part of the legs sutiers most, there may be a rectus-clonus, but only slight indications of a foot-clonus, two or three movements quickly ceasing. The tendency to spasm is at first noticeable as slight stiffness of the legs on first rising in the morning, but it gradually increases in degree as power lessens, until at last the legs, whenever extended, pass into a condition of strong extensor spasm, rigidly fixing them to the pelvis, so that, as the patient hes, if one leg is lifted from the couch by the observer, the other leg is moved also. The spasm may be such that the knee cannot be pas- sively flexed by any force that can be applied to it until the spasm has become less. When flexed the limb is comparatively supple ; but if it is then extended, the spasm instantly returns, making the limb rigid, and often completing the extension, just as the blade of a knife opens out under the influence of its spring, "clasp-knife rigidity." The spasm is, roughly speaking, proportioned to the loss of power, and its extensor character may enable the patient to stand, the legs being fixed and rigid, when muscular power is quite insufficient to support the body when it is unaided by the spasm. In a still greater degree a voluntary effort may only excite general spasm of the hmb instead of causing a definite movement. Occasionally there are also paroxysms * See Arthritic Muscular Atrophy. 494 SPINAL CORD. of brief flexor spasm causing the legs to draw up. This occurs chiefly when the patient is in bed, and especially during sleep. When the spasm is great, a paroxysm may pass into violent clonic spasm, but this is merely the same clonus that can be produced by passive exten- sion, excited by the tension of the spontaneous spasm (see p. 263). Reflex action from the skin is also usually excessive, and the stimulus excites an attack of spasm. The gait of the sufferers from spastic paraplegia is very character- istic. The legs seem to drag behind the patient, and, in walking, each is hauled forwards as a rigid whole, the toes catching against the ground, and, when the ball of the foot rests on the ground, the limb may shake from the clonus developed by the extension of the calf muscles. When the patient sits, a similar trepidation occurs until the patient pushes the leg forwards so that the heel rests also on the floor. The muscles of the legs are usually large and well nourished. They often seem, indeed, to be hypertrophied, and perhaps are really so; the contraction of spasm constitutes a physiological stimulus to growth, just as does voluntary effort. But they are not always large; they are sometimes moderately wasted. The electric irritabihty is usually perfectly normal, but in the muscles that present the shght wasting just mentioned there may be a trifling diminution of irrita- bility to faradism and voltaism alike. When the patient ceases, or almost ceases to walk, contracture sometimes occurs in the calf muscles. An active contracture is indeed common, preventing at first passive flexion of the ankle beyond a right angle; but if the pressure is maintained, the muscles yield and full flexion is possible. But in some cases there is the fixed contracture described on p. 257 (form 3). Flexor contraction at the hip or knee may occur also in the same cases under the influence of posture, but is on the whole rare, the tendency to it being counteracted by the extensor spasm. The arms are often unaffected, but they suffer in some cases, and present the same progressive weakness and excess of myotatic irrita- bility. Vigorous contractions are elicited by a tap on the tendon of a muscle, or on the bone to which the tendon is attached, provided the muscle is extended. A clonus can sometimes be obtained in the flexors of the fingers. There is less paroxysmal spasm than in the leg, but much rigidity of the limb, from active muscular contracture, flexing the elbow and flexing the fingers at all the joints, as in the " late rigidity" of hemiplegia. The difference in the form of spasm in the arm and leg is no doubt connected with existence of a reflex extensor mechanism, in the lumbar centres, concerned in the act of standing. The muscles of the arm are often as well nourished as those of the leg. The affec- tion of the two arms is very rarely equal; it is common for one arm to be almost normal when the other is much affected and both legs are equally involved. Sometimes, however, the arm and leg on one side are paralysed, and the limbs on the other side are so slightly involved that, in comparison with the palsied members, they seem PRIMARY SPASTIC PARAPLEGIA. 495 normal; the patient often believes that they are unaffected, but examination always reveals some weakness and an abnormal degree of myotatic irritability. The muscles of the trunk may also suffer. A subjective " feeling of weakness " in the back is often complained of early, but seems to be as much a sensory as a motor symptom. Painful spasm of the abdominal muscles may occur in severe cases, and I have even known attacks of tetanoid rigidity of the back to be produced by attempts to move. It is not common, in typical cases, for the symptoms to extend into the region of the cranial nerves, but, in rare instances, difficulty of swallowing and of articulation has existed, due to a similar palsy of the bulbar nerves. Excessive myotatic irritability has also been observed in the muscles of mastication, so that a tap on the chin causes a vigorous elevation of the depressed jaw (Beevor). Sensory symptoms are often entirely absent, with the exception of slight dull pains in the legs, or more frequently in the back. The sensation of weakness in the back, already mentioned, occasionally reaches an intense degree. Rheumatoid pains may be troublesome, but sharp pain is rare, except in untypical cases to be presently mentioned. In such cases also there may be very sliglit defect of sensibility—such, for instance, as blunting of tactile sensibility on the finger-tips. Subjective sensations of "numbness," tingling, formication, are more common. They may exist for years without the development of any other anaesthesia, in spite of the progress of the motor symptoms. The sphincters are sometimes affected, occasionally very early; often, however, they escape even to an advanced stage. Sexual power may be lost, or may remain, even when the spastic paraplegia has reached a high degree. The nutrition of the skin and joints under- goes no change. Ocular symptoms are rare, with the exception of nystagmus, which will often be found if searched for. The action of the pupils is usually perfect, and I have only once seen optic nerve atrophy in an uncomplicated case. The infantile form may resemble very closely that which occurs in adults. There are the same extensor spasm and increase of all forms of reflex action. As the child sits on the knee or a chair any sensory stimulus will make the legs shoot out in spasm (Fig. 131). But the rigidity does not reach the extreme degree often attained in the common form. The excess of the knee-jerk is always distinct, but a foot- clonus is not often to be obtained, perhaps because the muscle-reflex mechanism related to the calf muscles has not received the functional development that must result from the process of walking, with its recurring sequence of tension and contraction. The active contracture in the calf muscles, which most cases present, is a serious hindrance to walking even when the muscular power is sufficient, and it is long 496 SPINAL CORD. before the attempt overcomes the contracture. In most cases, how- ever, the child ultimately gains the power of walking, although much later than normal, and often with some peculiarity of gait, sometimes a tendency to "cross-legged progression," in which one foot gets over or in front of the other (Fig. 132), or with a swinging oscillation of Fig. 132. FiG. 131.—Congenital spastic paralysis (cerebral). Extensor spasm in the legs excited by a sen-ory impression. (Drawn by Dr. H. R. Spencer, from a photograph by Mr. Hyde Marriott.) Fig. 132.—Infantile spastic paralysis of cerebral origin : cross-legged progression. (Drawn by Dr. Spencer, from a photograph.) the body, which may persist to adult life. The growth of the legs is often hindered. The arms do not present tonic spasm such as is seen in adult cases. Tin r .• may be a choreoid disorder of movement, spontaneous irregular movements with inco-ordination, but in the cases that can fairly be called " spastic paraplegia " the arm symptoms are slight. When considerable the condition is often termed " double athetosis." Its characters are described in Vol. II. Transitional forms are met with which constitute gradations between primary spastic paraplegia and other degenerations of the spinal cord. Slight inco-ordination may co-exist in cases approximating the " ataxic paraplegia " described in the next section. Cases may begin as pure tabes, and indications of lateral sclerosis may be superadded. Slight muscular wasting in the arms may be associated with indications of lateral sclerosis in the legs, and constitute a transition to the form of spinal muscular atrophy to which the name "amyotrophic lateral sclerosis" has been given. Very rarely considerable muscular wasting succeeds spasm in the same part. Spastic paraplegia also is often the early stage in cases which afterwards develop other symptoms characteristic of disseminated sclerosis. Nystagmus, how- PRIMARY SPASTIC PARAPLEGIA. 497 ever, as has already been stated, may occur in cases otherwise offering no symptoms except those of lateral column affection. Unequivocal symptoms of syringomyelia have also been known to develop in a case which presented in its earlier stages the characteristic signs of primary lateral sclerosis.* Lateral sclerosis of the spinal cord (like posterior sclerosis) often forms part of the morbid process that underlies general paralysis of the insane. In some cases of this character the mental symptoms are extremely slight, and the case may have the aspect of a primary spinal dis- ease, with slight mental failure complicating it. The course of characteristic cases of primary spastic para- plegia is thus very chronic. The malady may, at any stage, cease to advance. Shght symptoms may remain stationary for twenty years. Often, however, arrest only occurs when the disease has reached a considerable de- gree. It is perhaps the least dangerous to life of any chronic spinal disease. Even secondary kidney trouble scarcely ever oc- curs ; perhaps the excessive re- flex action may save the bladder from injurious over-distension. It is when other elements of the cord suffer that dangerous complications ensue. Pathological Anatomt.—In the fact just stated we probably have an explanation of the silence of morbid anatomy on the subject of uncomplicated lateral sclerosis. " Nee silet mors," the apt motto of the Pathological Society, is true chiefly of disease that kills. Complete degeneration of the pyramidal tracts, anterior as well as lateral, is met with chiefly in cases in which the anterior ganglion-cells and motor nerves are also diseased, although in some instances the amount of this disease is small, and limited to the cervical region. An instance * Charcot, ' Progres Medical,' 1891. t I am indebted for these sections to Dr. Dreschfeld, who has published the case (• British Med. Journal..' Jan. 29th, 1881). VOL. 1. 32 FiG. 133.—Sclerosis of the lateral and (in the cervical region anterior) pyramidal tracts, with slight degeneration of the anterior cornua. A, cervical; B, dor- sal; C, lumbar sections.f 498 SPINAL CORD. of such degeneration is shown in Fig 133. The degeneration in the lumbar enlargement is usually limited to the lateral tract, but the anterior tract may be affected higher up the cord, as in Fig. 133, a. The lateral sclerosis is bounded externally, in the dorsal and cervical regions, by the normal direct cerebellar tract, and internally by the narrow " lateral limiting layer " which intervenes between the pyra- midal tract and the intermediate grey matter There is the usual increase of connective tissue and wasting of nerve-fibres. In many cases granule-cells are abundant in the affected area. They are always present in cases of short duration, and indicate the stage rather than the nature of the process. The degeneration probably begins in all cases in the nerve-elements themselves. In most cases many nerve-fibres can still be seen, scattered through the sclerosed area; most of them are fibres which lie in the pyramidal tract, but do not belong to it. The degeneration of the tract has been traced through the medulla, pons, and cerebral hemispheres to the motor cortex, in which indications of degeneration have also been found. This degeneration through the brain was traced in one case in which the disease of the anterior cornua was slight, the wasting was limited to the hand muscles, and the spastic paralysis began in the legs and then invaded the arms.* Such a case is almost a pure degeneration of the whole of the first segment of the motor path. Fig. 134.—Sclerosis of the pyramidal tracts, lateral and anterior: dorsal region. From a case of muscular atrophy. The degeneration of the pyramidal tracts is well shown in Fio-. 134, from a case of progressive muscular atrophy. The anterior and lateral tracts are entirely degenerated, and the sclerosis stops ab- ruptly at the outer margin of the lateral, but in front extends for- * Kojewmkoff, 'Arch, de Neniologie,' 1883, No. 18. PRIMARY SPASTIC PARAPLEGIA. 499 wards, probably in the short fibres that connect the anterior cornu at different levels. In other cases, in which the anterior ganglion- cells were normal, the sclerosis has not been limited to the pyra- midal tracts ; the anterior columns have been also sclerosed in the lumbar region of the cord.* The direct cerebellar tract and pos- terior vesicular columns have been also found degenerated with the pyramidal tract, and an annular sclerosis of the periphery of the antero-lateral column has been found in several cases.f More frequent still is a combination with degeneration of the posterior columns, described more fully in the next section. In most of these combined cases the degeneration has lessened in the upper part of the cord. In one case, at least, the white columns of the cord have been found healthy. The probable significance of this fact has been already stated (p. 491). It should be remarked, however, that there seems sometimes to be a tendency for the morbid process to extend beyond the pyra- midal tracts in a manner that suggests a greater tendency for the secondary connective-tissue changes to take on an independent invasive activity than in other system diseases. (See also Ataxic Paraplegia.) Another point that deserves mention is the occasional occurrence of lateral sclerosis in association with insular sclerosis. In some cases of this character the degeneration of the pyramidal tracts is purely secondary, the result of the damage to the pyramidal fibres by an islet of sclerosis situated in some part of their course. But it does not appear that this explanation can be given of all cases. In some instances the sclerosis of the pyramidal tract appears to be inde- pendent and coincident. A similar association of insular and posterior sclerosis has also been observed; and such combinations receive additional emphasis from the fact that insular sclerosis may be accompanied by a primary atrophy of the optic nerve, similar to what occurs in tabes, although probably not identical. These facts make it probable that lateral sclerosis, although a system disease, is often one of less strict features than tabes, having some tendency towards chronic myelitis. We shall see that this is true also of ataxic paraplegia. The probable mechanism of the symptoms that give the dominant characters to the malady have been considered in the general account of the symptoms of disease of the spinal cord. The most important fact is that the degeneration, whatever its upward extent, always involves the lowest part of the pyramidal segment, because it seems to begin in this and ascend the fibres. Hence the intra-cornual termination must always be involved. This, it is assumed, is the structure that * As in a case recorded as one of spastic paraplegia by Hopkins ('Brain,' Oct., 1883), but this was an example of combined lateral and posterior sclerosis (ataxic paraplegia). An illustration of the changes in this case is given in the next section. t Direct cerebellar and pyramidal tracts in a case by Minkowski, in which the disease rapidly succeeded syphilis; annular sclerosis by Westphal (see Ataxic Paraplegia). 500 SPINAL CORD. controls the muscle-reflex centre, and the consequent loss of control explains the excess of myotatic irritability and the progressive spasm, progressive by what may be termed a functional hypertrophy result- ing from continuous over-action. When there is the rare consecutive wasting of muscles we must conceive that the degeneration involves also the ganglion-cells and lower segment of the motor path ; when there is coincident wasting of other muscles than those that are the seat of spasm, it would seem that some elements of this lower segment are the seat of a primary degeneration. The slighter muscular wasting without, or with only trifling, change in electrical irritability, is the expression of a slighter alteration in the nutrition of the cells and fibres, without actual destructive degeneration. Diagnosis.—The diagnosis rests on the combination of weakness, excess of myotatic irritability, and spasm—on the gradual onset of these symptoms—and also on the absence of indications of a focal lesion. An acute onset, occupying a few days or weeks, is pmna facie evidence of a lesion that takes the case out of the category of degenerative disease. In most acute cases there is other evidence of a focal lesion, extending, at some level, beyond the limits of the motor path. Such indications are initial impairment of sensation, or a girdle-pain. The latter indicates irritation of the posterior root-fibres at a certain level, and proves that at that level the disease extends beyond the limits of the pyramidal tracts. Spastic paraplegia is common after such lesions, but is secondary and not primary. Although marked sensory symptoms, in a case that presents the symptoms and course of primary lateral sclerosis, are thus evidence that the sclerosis extends beyond the motor tracts, and that the case is not one of pure lateral sclerosis, it is doubtful what significance is to be attached to very slight sensory symptoms, such as slight sub- jective sensations of dull pain, formication, &c, when they exist alone. It is possible that they are due to functional disturbance in the sen- sory nerve-elements, and do not imply structural disease outside the motor area. They are not followed by any more pronounced sensory symptoms. The absence of objective unsteadiness is the chief distinction from ataxic paraplegia (q. v.). When this is slight it may be difficult to say in which class a case should be placed. There are no doubt intermediate cases in which there is a very shght degree of the additional lesion that exists in ataxic paraplegia, but the distinct objective character of the ataxy is the best criterion. Considerable muscular wasting in any part is commonly regarded as bringing the case into another category, that of " amyotrophic lateral sclerosis " ; but some cases of the kind, in which the wasting is confined to a few muscles, resemble more closely the cases we are now considering than they do those with wide-spread and extreme muscular atrophy. These cases are further considered in the account of progressive muscular atrophy. Primary spastic paralysis is not uncommon in those who are at the PRIMARY SPASTIC PARAPLEGIA. 501 age and of the sex at which hysteria prevails, and there is no form of cord disease that is so often mistaken for hysterical paraplegia. The mistake is facilitated by the perfect muscular nutrition. But the mistake ought not to occur, as the peculiar extensor character of the spasm, lessening with flexion, is distinctive; nothing resembling it ever occurs in hysterical paraplegia. When the spasm is trifling or absent, as in shght and early cases, the diagnostic difficulty is much greater, and is increased by the fact that sliglit excess of myotatic irritability occurs in some cases of so-called hysterical paralysis. But this scarcely ever reaches the degree necessary to give rise to a true foot-clonus or a rectus-clonus. There may be a slight clonus pro- duced through a voluntary depression of the foot of the patient in response to the passive flexion of the ankle, and readily recognised ; or a true clonus may be obtainable during hysterical contracture, but apart from such contracture a true foot-clonus or a rectus-clonus deserves the greatest weight, as all but conclusive evidence of organic disease. I have known many mistakes in diagnosis, in which lateral sclerosis was mistaken for hysterical paraplegia owing to disregard of the evidence afforded by this symptom, but I have never known the opposite error from undue regard to this symptom. Moreover an excess of myotatic irritability in so-called hysterical paralysis must depend on more than functional disease. There must be changes in nutrition, and consequent persistent defective control of the muscle- reflex centres. On the hypothesis that I have advanced, this control is exerted by the termination of the pyramidal fibres, i. e. of the upper motor segment, by the structures degeneration of which probably causes spastic paraplegia. A case is actually on record (the case of lateral sclerosis described by Charcot in 1865) in which an initial hysterical paraplegia, cured suddenly and relapsing on emotion, passed ultimately into lateral sclerosis. Similar cases of initial hysterical paraplegia frequently develop all the characters of dis- seminated sclerosis. When the arm and leg suffer on one side only, the disease may be mistaken for cerebral hemiplegia. There is not, however, any affection of the face, which, although theoretically conceivable, is, as a matter of fact, always absent. The limbs on the other side are never quite normal, but present slight symptoms—weakness and an excess of myotatic irritability—similar to those on the affected side, which indicate the nature of the malady. The diagnosis of the congenital infantile form is only difficult when the observer is unaware of the occurrence of these cases. A slight degree of inco-ordination in the hands will usually be found if they are carefully watched while the patient takes hold of some object. The wide separation and irregular movement of the fingers is very charac- teristic. Chronic primary cord diseases are almost unknown in young children. Caries of the spine is, in them, the chief cause of para- plegia ; and the definite onset of the paralysis, in a previously healthy 502 SPINAL CORD. child, is an absolute distinction from the cases of birth-palsy. Other diagnostic indications are described in Vol. II (Infantile Meningeal Haemorrhage). A definite onset also distinguishes glioma of the pons, which may likewise cause spastic paralysis of arms and legs. Prognosis.—In primary lateral sclerosis there is some prospect of arrest, and even of improvement, if the disease has not reached an advanced stage. Actual recovery is rare, but does sometimes occur in early cases. When the spastic state is well developed and has lasted for some time it is very rare to obtain more than arrest. This is, perhaps, due rather to the tendency of the disease than to its degree, since a similar condition that is secondary to a focal lesion often passes away completely; and many facts show that it is not likely that there is anything in the nature of the lesion to preclude the restoration of a normal condition until dense connective tissue has replaced the nerve-elements. In the cases that improve most, it is possible that the disease is limited to the terminal structures. We have not, at present, any guide to the prognosis in an individual case, besides its duration and degree, except its observed tendency, especially under treatment. The prognosis of the infantile form is considered in Vol. II. Treatment.—So far as drugs are concerned, the treatment is, to a large extent, the same as that of posterior sclerosis, already described. The drugs most useful are the same, but, unfortunately, their influence is less frequently appreciable. Nux vomica and strychnine have, how- ever, to be given with caution, and in very minute doses, as they have a tendency to increase the spasm. In severe cases this is a most distressing symptom, and often not amenable to any influence. Bromide sometimes lessens it slightly, but even large doses of bromide have but a trifling effect. Indian hemp, belladonna, and Calabar bean may be tried, but seldom have a distinct influence. One of them may be combined with arsenic, or whatever metallic agent is employed. Absolute rest is sometimes of service, and occasionally seems to produce improvement, which all treatment failed to effect while the patient was walking about. The avoidance of fatiguing exertion is a very important element in treatment, and often seems to permit medicines to do good, which before were counteracted. Rub- bing is also beneficial in some cases. Its influence on the spasm is often very distinct during the process, and a long course of rubbing has produced a permanent improvement in the spastic condition. Upward rubbing seems to have more influence than kneading the muscles. If there is contracture of the calf-muscles, the foot should be pressed up while these muscles are rubbed. When there are facilities for it, the rubbing may advantageously be combined with sweating in the Turkish bath. In one case, of moderate degree, almost all the symptoms passed away after a long course of Turkish baths, arsenic being also given. The patient, who could at first walk scarcelv half a mile, became able to walk several miles without fatigue, and the ATAXIC PARAPLEGIA. 503 improvement was permanent. Electricity is useless in the pure disease. Faradism and all painful applications are harmful, stimulating further the already excessive excitability of the reflex centres. The constant current to the muscles, or from the spine to the muscles or to the feet in water, has no distinct influence in either lessening the spasm or improving the strength. The actual cautery is in many cases most beneficial. In the infantile form, drugs are useless. Rubbing is desirable, and can be efficiently performed by the nurse or mother. Carefully planned gymnastic exercises are also useful. The tendo Achillis is sometimes divided for the contracture of the calf muscles, but the operation is useless and ought never to be performed. Supports help the child to walk somewhat sooner than it would without their aid, and so hasten improvement, but they should only be employed when there is sufficient power and control to make them useful by enabhng the will to effect ordered movements. Family Form op Spastic Paralysis. Cases in which the usual symptoms of spastic paralysis have been present in several members of the same family, occasionally in different generations, have been described by Erb,* Striimpell.t Bernhardt,]: Newmark,§ Eaymond, Sougues,|| G-ee,^" Tooth,** and others. Occa- sionally to the symptoms of the cord affection evidence of bulbar involvement has been added, and the condition has probably been dependent upon some congenital weakness of the pyramidal tracts and their correlated structures, predisposing them to premature decay. Optic atrophy has also been met with. The condition is f urther briefly alluded to in the chapter on Hereditary Ataxy (q. v.). ATAXIC PARAPLEGIA. (combined lateral and posterior sclerosis.) The term ataxic paraplegia seems the most accurate clinical designa- tion for a disease of the spinal cord which presents a combination of the symptoms of paraplegia and ataxy, and consists in combined * « Deut. Ztsch. f. Ncrveuheilk.,' Bd. vi. f Ibid., Bd. iv. X ' Virch. Archiv,' cxxvi. § 'Amer. Journ. Med. Sci.,' 1893; 'Med. News,' 1897. || ' Sem. Med.,' 1896. *[ 'St. Bart.'s Hosp. Reports,' x\v. ** Ibid., xxvii. 504 SPINAL CORD. disease of the posterior and lateral columns. Although its clinical features present some varieties, and may approach those of each of its constituent forms of disease, yet in the majority of cases the symptoms are uniform, and sufficiently characteristic to justify the distinction of the disease and its separate description. As early as 1867 West- phal described comb ned sclerosis of lateral and posterior columns in general paralysis. Erb, von Leube, Prevost, Pierret, and others, during the next ten years, published cases definitely showing the simultaneous occurrence of sclerotic changes in the lateral and pos- terior columns. Von Leyden, in his book on spinal cord diseases in 1875, briefly referred to the condition as one of " combined sclerosis of the posterior and lateral columns," and mentioned a case which he had seen. The first systematic description of the condition, however, was that given in 1877 by Kahler and Pick in an article on "Com- bined System Affection of the Spinal Cord." C. Westphal next pub- lished a paper on "Combined Affection of the Tracts of the Spinal Cord," in which five cases were described. Later Dana, in America, described similar cases; Grasset, going on clinical features, described a similar condition as " ataxo-spastic tabes " and Dejerine as " ataxo- paraplegic tabes."* In the first edition of this book, published in 1886, a condition, similar both clinically and pathologically, of which the writer had seen several cases, was described under the name of ataxic paraplegia, a descriptive title indicating the combination of paraplegic weakness with ataxy. Causes.- Neurotic heredity is to be traced only in a small propor- tion of the cases—about one tenth. A history of syphilis is as rare as it is frequent in pure tabes. Males suffer much more frequently than females. The disease usually commences between thirty and forty, but I have known it to begin as early as nineteen and as late as fifty-two, while commencement at fifteenf and at sixty-onej is on record. Exposure to cold is to be traced occasionally as an exciting cause. In one young lady the symptoms commenced after a season of balls, at which when heated she would habitually sit at open windows, and often sleep in clothes saturated with perspiration. In a few cases, severe exertion, such as excessive athletics, has been the apparent cause. A severe concussion of the spine has sometimes pre- ceded the first symptoms by a few months. The disease may also follow great sexual excess. In many cases no cause can be traced, immediate or remote. Its general etiology thus resembles that of simple spastic paraplegia. * See Prevost, ' Arch, de Physiologic't. iv ; Pierret, ib.; Babesieu, ' Vircbow's Archiv,' Bd. lxxvi; Kahler and Pick, 'Arch. 1. Psychiatrie,' Bd. viii; Westphal, ib., lid. viii and x ; Dana, ' New York Med. Record,' July 2,1887 ; and Clarke,' Brain,' 1890. As to Dejerine's description see Ladaine, 'Brain,' 1890, p. 530; Grasset, ■ Maladies dn Systeme nerveux ;' Montpellier, 1804. t Oppenheim, ' Neur. Cent.,' 1888, p. 647. Such early cases are generally isolated forms of " Hereditary Ataxy." X Suckling. 'La-cet.' lS^'i. ATAXIC PARAPLEGIA. 505 Symptoms.—The onset of the disease is usually slow and gradual, two or three vears passing befoie walking power is much impaired; it is rarely subacute, so as to reach a considerable degree in two or three months. The early symptoms resemble those of spastic paraplegia, with the addition of ataxic unsteadiness, which may be at first the most prominent symptom. The legs suffer first, often alone, or the arms may also be involved. The patient finds that he tires more readily than before, and also becomes unsteady on turning or walking in the dark, and these symptoms gradually increase. The weakness may be slight, but if all the movements are tested, a defect in power will be found in some, often most in the flexors of the knee and hip, and frequently more in one leg than the other. The patient is unsteady when he stands with feet together, and he tends to fall if the eyes are then closed. If the feet are bare, the irregular action of the muscles is shown by the movement of the tendons on the dorsum of the foot, as in tabes. In early cases, the inco-ordination is revealed by the patient's gait, which is distinctly unsteady. There is rarely the high movement and sudden descent of the feet often seen in tabes, but (as in many cases of tabes) the patient is unsteady, reels on turning, and has often to bring his foot suddenly to the ground to maintain his equilibrium. He may even have to steady himself with a stick, or to catch hold of some adjacent object, to save himself from falling. The ataxy is equally evident when he lies, and attempts, his eyes being closed, to touch some object with his foot. The sensorv and reflex symptoms present a marked contrast to those of tabes. Lightning pains are almost always absent; I have only met with them in one case, and in this they were a transient symptom. Sometimes there is a slight dull pain in the legs, felt especially on fatigue. Dull pain in the sacral region or in the spine is not uncommon, and is often an early symptom. The sacral pain, indeed, is sufficiently frequent to deserve special note. A girdle-pain is met with onlv in rare cases. As a rule there is no loss of sensation either on the legs or trunk. Hyperaesthesia is equally rare. Keflex action from the sole may be normal or increased; less commonly it is diminished. The cremasteric and abdominal reflexes are sometimes lost. The most striking difference from tabes, however, is in the con- dition of mvotatic irritability, which, in the vast majority of cases, is greatlv inereased. The knee-jerk is quick and extensive; it can be obtained from above (see p. 22), and there is generally a distinct rectus-clonus. The foot-clonus is also commonly to be obtained. This myotatic excess persists and increases, and when the arms are involved thev present symptoms similar to those in the legs—inco-ordination, weakness, and marked excess of the myotatic irritability. There may be conspicuous ataxy of the hands, and a tendency to cramp-like spasm on an attempt to use them. The muscles in both arms and legs are usually well nourished. Sexual power is often lost early in the disease. The sphincters may 506 SPINAL CORD. be impaired, sometimes early, but they also often escape. As in other diseases, inability to empty the bladder is apt to develop insidiously, without the patient's knowledge, and the organ may thus become habitually distended. The iris usually acts to light, but I have seen loss of the light-reflex in two or three cases, and have once known accommodation to be lost, the action to light leing normal. These symptoms occur chiefly in cases following syphilis. Optic nerve atrophy occurs only in rare cases, far less frequently than in tabes; I have seen one case in which there were indications of a retro-ocular axial neuritis. The external ocular muscles are unaffected as a rule, except for nystagmus, which often exists on movement of the eyes, but seldom when they are at rest. Slight impairment of articulation is not uncommon; sometimes there are irregular tremulous movements of the face resembling those of general paralysis, and this in cases in which there is no mental change. Westphal has observed marked ataxy of the facial muscles. As a rule the mental state is either normal, or there is merely slight failure of memory. As the disease increases, the muscular weakness and reflex spasm become more and more considerable; while the ataxy, after reaching a certain degree (not sufficient to prevent locomotion), necessarily sinks into the background as the paralysis increases. With the increased weakness, the aspect of the patient comes to be that of spastic paraplegia, described in the last section. Indications of unsteadiness may still be observed in isolated movements. The arms, if previously free, may begin to suffer, but sometimes they escape altogether. The motor weakness may go on to complete paralysis. This is quickly reached in some cases, but so slow is the usual progress of the disease that one patient, in whom the disease was at no time absolutely stationary, was still able to stand, after eight years. In spite of the progress of the weakness, sensation remains unimpaired, and the cranial nerves do not suffer. The symptoms present, in some cases, variations from this type. Sensation on the legs may be impaired, and the knee-jerk may be lost. These cases are, however, very rare, and are probably cases of true tabes with lateral sclerosis added Other cases occur in which a srirdle- pain, impaired sensation, &c, suggest extensive changes in the cord, although the state of the legs is that common in the disease. Such cases, as we shall see, are probably examples of chronic myelitis, or are intermediate between that and the disease now under consideration. Ataxic paraplegia has little tendency to cause death. Indeed, the fatal cases have, for the most part, been untypical, and do not convey an accurate idea of the characters of the disease. The chief danger to life is from the accidents common to all chronic spinal affections, —bedsores, and especially kidney disease, from undiscovered or untreated imperfect action of the bladder. ATAXIC PARAPLEGIA. 507 Among complications the most important are mental changes resembling those of general paralysis of the insane, of which indeed this combined sclerosis may form part. Slight muscular atrophy sometimes occurs. Arthritis of doubtful significance has been ob- served. A patient of Westphal's presented derangement of the sympathetic, and died from peculiar spasm of the muscles of respira- tion. Visceral crises, however, are praetically unknown. Pathological Anatomy.—In all cases, the spinal cord has pre- sented sclerosis of both posterior and lateral columns ; but the precise extent and degree of the degeneration are subject to considerable variations. As a general rule, the sclerosis of the posterior columns differs from that of tabes in two particulars. First, it is not more intense, and often it is less intense, in the lumbar than in the dorsal region of the cord. Sometimes, indeed, as in the case shown in Fig. 135, in the middle and lower parts of the lumbar region, the posterior columns may be free from sclerosis, although it is considerable in the dorsal region and at the junction of this with the lumbar enlargement (b). The second difference is that the sclerosis has not that special intensity in the root-zone of the postero-external column which characterises the lesion of tabes. In rare cases the whole posterior column in the lumbar region is diseased. The part of the external column near the commissure and near the neck of the posterior horn usually remains free. Sometimes the degeneration does not extend up to the posterior surface of the cord; for instance, as in the case figured, it affects chiefly the middle three fifths of the posterior columns. When the degeneration is considerable, the posterior median columns, in the upper part of the cord, may present the usual ascending degeneration of secondary origin. When the lesion is slight in degree in the lower half of the cord, there may be only a diffuse degeneration of the columns in the cervical region, similar to that below, and not the more intense limited affection of the median part which occurs when there is a typical ascending degeneration from a considerable lesion of the column lower down. The degeneration in the lateral columns is also variable in extent and position, and is often not strictly " systemic" in character, i. e. is not strictly limited to a single system of fibres, although the pyra- midal tracts are chiefly affected. In one or two cases, indeed, the whole pyramidal tract, and this alone, has been degenerated ; but more often the sclerosis, while intense in this tract, also extends in front of it into the mixed zone of the lateral columns (Fig. 135, a, b). A similar extension, however, is usually met with in the sclerosis that attends degeneration of the anterior cornua; compare Fig. 133. The lateral limiting layer, between the pyramidal tract and the grey matter, mav be also invaded. The direct cerebellar tract often escapes, as in Fig. 135 a (b is below its level of origin), but it is affected in some cases. Occasionally a zone of sclerosis has existed in the whole periphery of the cord, extending deeply into the lateral column in the position of the 508 SPINAL CORD. v^-' pyramidal tract. This tract has been found diseased, in some degree, in all cases, and in several the extent of its degene- ration has been greater in the lower part of the cord than in the upper. The direct (anterior) tract may be affected as well as the lateral, and is commonly in- volved when the lesion is consi- siderable in the upper part of the cord. As in most other de- generative diseases of the cord, there may be some increase of connective tissue in the un- affected columns. Asa rule no morbid change has been recog- nised in the grey matter or in the membranes. In one case only was there slight meningitis. Disease of the ascending root of the fifth has been found in some cases ;* in one there was also atrophy of the cells of the oculo- motor nucleus, and the case thus differed considerably from the type. The muscles have been found normal. Pathology.—The double le- sion in the posterior and lateral columns supplies an explanation of the two sets of symptoms which characterise the disease. F'uJS^^L^:S:£i. To " Jhe *»-<»*»«&» ™»t be re. dorsal; B, last dorsal; C, mid-lumbar. ferred to the disease of the pos- The posterior columns are free from terior columns, which, greatest sclerosis in C, except in their anterior ° parts; in B the disease involves the middle and anterior parts of both post.-med. and post.-ext. columns except in the neighbourhood of the neck of the horn; in A the sclerosis is slighter and is con- fined to the middle three fifths of these columns. The sclerosis of the lateral columns in C is limited, on the right, to the pyramidal tract, on the left it extends m front ot this; in B it is very dense in the whole lateral column, involving not only the pyramidal tract but the limiting layer, and part of the "mixed zone •" in A it is similar in extent but slighter in degree. There is some increase of tissue throughout the anterior columns, and a focus of sclerosis near the auterior fissure. on the right m A and B, on both sides in C.f * Oppenheim, 'Neur. Cent.,' 1888, p. 647. t I am indebted to Mr. J. Hopkins for the opportunity of drawing these sections. The patient was a man aged twenty-one, in whom weakness of the legs commenced ATAXIC PARAPLEGIA. 509 in the dorsal region, involves there the fibres that conduct impulses from the muscles, probably to the cerebellum.* The effect must be to lessen the cerebellar guidance, and this explains the resemblance of the inco-ordination to that in cerebellar disease. The fact that the disease does not extend into the lumbar root-zone accounts for the integrity of the muscle-reflex action, and enables us to understand this marked difference from tabes. Disease of the direct cerebellar tract probably has an influence similar to that, of the posterior median columns. That interruption of the conducting path in the cord will produce inco-ordination is, as we have seen (p. 258), well established. The sclerosis in ataxic paraplegia occupies also the region of the cord in which the short vertical fibres run, connecting the posterior grey matter at different levels, and it is possible that the damage, to these fibres may contribute to the ataxy. The only recognisable lesion that can be regarded as the cause of the paralysis is the degeneration of the pyramidal tract. The state- ments made regarding spastic paraplegia apply also to the disease, and need not be repeated. The lesion has been found greater on the side on which one leg was weaker than the other. The variations in the amount of disease, which does not always correspond to the degree of palsy, are probably due to the fact that the latter may be caused by degeneration of the termination of the fibres, which may be much greater than that of the fibres higher up the cord. In most cases that have been examined, the visible disease was greater in the lower than in the upper part of the cord, increasing from above downwards, a fact which suggests that the maximum lesion is at the lowest part- in the terminal ramification within the grey matter. The chief pathological difficulty arises from the fact, which we have already considered in connection with spastic paraplegia, that the morbid process often extends beyond the limit of the tracts chief!v diseased. It tends to assume a diffuse character, so that it has at twenty, after a wetting, improved, and then slowly increased. He was admitted a year after the onset, with considerable weakness of the legs, a reeling, unsteady gait, increased knee-jerk, foot-clonus, but with no anaesthesia, wasting of muscles, pains, or affection of the arms. The symptoms slowly increased, paraplegia became absolute, and the spasm very intense, sometimes flexor and sometimes extensor. There was a doubtful impairment of sensibility to touch on the legs, but no loss to pain. The sphincters became affected, bedsores formed, and the patient died two years after the onset. Puller details will be found in ' Brain,' October, 1883, p. 383. * Much evidence has been obtained of the connection of the posterior median columns with the cerebellum through the grey matter of its bulbar nucleus, and also of the effect of interruption of these columns in the dorsal cord, in causing inco-ordination like that of cerebellar disease. Besides the experiments of Bech- terew on the latter point already mentioned (p. 215), a recent important investiga- tion into the connections of the cerebellum fully confirms that with the post.- pyramidal nucleus (lirosset, 'Contrib. a I'etude des Connexions du Cirvelet,' Paris, 1891). 510 SPINAL CORD. been regarded by some as rather a chronic myelitis than a system degeneration. It may occupy an intermediate position, and illustrate the fact that there is a close connection between the primary decay of nerve-elements and the growth of the connective-tissue elements that replace the former. In a pure secondary degeneration this growth is limited to the tract affected, but even in tabes it may manifest some degree of independence, which seems to be still greater in ataxic paraplegia. Sometimes, indeed, the primary morbid tendency may be double, involving both the nerve-elements and interstitial tissue. If it so far preponderates in the latter as to cause considerable changes outside the tracts specially diseased, and marked symptoms, such as a girdle-pain or loss of sensation, the condition is really one of chronic myelitis, and the cases should be so classified.. This is probably the true solution of the problem, which has been much discussed, whether the malady is or is not a system disease. It is so in typical cases, but it is on the border of the group of system diseases, and intermediate cases connect it with diseases of diffuse character and non-systemic nature. Diagnosis.—The diseases from which ataxic paraplegia has to be distinguished differ according to the stage of the disease at which the diagnostic problem presents itself. The dominant symptom in the early period is the inco-ordination; in the later period, the spastic palsy. Hence the disease in the early stage is liable to be confounded with pure locomotor ataxy, but the condition of the knee-jerk, lost in the one, excessive in the other, is distinctive. In the rare cases of early tabes in which it is not lost, it is never increased. In tabes, there is not the loss of power which will always be found in ataxic paraplegia, and when a clonus and extensor spasm are added, there should be no risk of confusion; but it is necessary to emphasise the distinction, because cases with much unsteadiness are frequently described as tabes with preserved knee-jerk. From primary spastic paraplegia the diagnosis depends on the presence of inco-ordination, or in a history of it, if voluntary power has become too slight to be susceptible of derangement. Ataxic paraplegia is spastic paraplegia plus inco-ordination. The so-called "hereditary ataxy" presents a close resemblance to ataxic paraplegia, and is, indeed, as we shall see, intermediate between the disease and true tabes. It is distin- guished by its occurrence in several members of the same family, and by the common loss of the knee-jerk; while the presence of nystag- mus, of some impairment of articulation, and of other svmptoms described in the account of the disease, distinguish the isolated cases that are sometimes met with.* The distinction from diffuse or focal chronic myelitis depends chiefly on the extent of the symptoms in the former, and their limitation in * The condition closely resembles that met with as a result of toxic influence probably, in conditions of anaemia, debility, &c. Some of the cases described aa ataxic paraplegia have doubtless been of this nature (see next section). SCLEROSIS FROM TOXIC BLOOD-STATES. 511 the latter. The subacute forms of myelitis are also distinguished by their more rapid onset.* The greatest difficulty is presented by cases which have a subacute onset, and the distinction from a local mvelitis involving the posterior and lateral columns may be very difficult. It depends chiefly on the progressive tendency of the symptoms, which contrasts with the regressive tendency of myelitis. It is possible that when there is a degenerative tendency, a focal myelitis may set up a progressive degeneration in the columns concerned, as it certainly may set up a degeneration limited to the posterior columns A tumour in the middle lobe of the cerebellum may cause unsteadi- ness, closely resembling that of some cases of ataxic paraplegia, and it may also cause weakness of the legs with increased knee-jerk, from the pressure on the pyramidal fibres as they pass through the pons. In such cases, indeed, we probably have the two elements of the disease, produced in a different manner, by lesions of different posi- tion. We have a degeneration of the lateral columns which is secon- dary instead of primary, and we have disease of the co-ordinating centre instead of interruption of the path to it. But the weakness in the legs is never great in cerebellar tumour, and special symptoms of this are never absent. Occipital headache, vomiting, and optic neuritis are present in most cases. In a case in which the pons is compressed, some cranial nerves are usually also damaged. Prognosis.—The prognosis in ataxic paraplegia is similar to that in the spastic form, and depends on similar considerations, which need not be here repeated. Treatment.—The treatment of ataxic paraplegia is the same as that of the allied diseases, and especially of spastic paraplegia, to the account of which the reader is referred. SCLEROSIS OF THE CORD FROM TOXIC BLOOD- STATES. Pellagra. Pellagra is an endemic malady which, though fortunately unknown in this country, deserves mention here on account of the incidence of its effects on the spinal cord. Its chief anatomical lesion is a degeneration of the lateral and posterior columns of the cord, corre- sponding closely to that of ataxic paraplegia, and, as in that disease, with a greater affection of the lateral than of the posterior columns. It differs, however, in the fact that some atrophy of the large nerve- cells of the anterior cornua is common, and also in the constancy with * For some instructive notes on this point in diagnosis see Dreschfeld, ' Brain,' January, 1888. 512 SPINAL CORD. which chronic inflammation of the pia mater is met with, sometimes accompanied by the formation of bony plates in the arachnoid. The Cause of the disease appears to be the action, on the elements of the spinal cord, of an organised virus (or of some product of this) which is taken into the system with diseased or unripe maize. Even spirit distilled from such unripe maize err—-_ ^._ ^ r) may cause the disease. The distri- ct ~:r'~->"""T"'-y ~C'-Tr^"/^ bution of the disease in the north of Italy, where the maize is frequently gathered unripe, is significant. The virus has been thought by some (as Lombroso) to ba a fungus growing in the maize ; by others to be specific micro-organisms of other than fun- goid nature, present in the maize, which develop in the system and pro- duce there the toxic agent that has a special action on the nerve-elements (Belmondo). The researches of Tuc- zek* have clearly shown that the change is a sclerosis of the cord de- pendent upon some toxic substance occurring in diseased or unripe maize. The effects of the poisons fall, not on the peripheral nervous system, but on the spinal cord, and, as is usual in such conditions (see previous section), the sclerosis induced is symmetrical, and, as will be seen from the illus- trations (Fig. 136), in its distribution is very similar to that met with in conditions of anemia and debility (p. 513). The Symptoms resemble very closely those of ataxic paraplegia. There is weakness in the legs, with in- creased myotatic irritability going on to spasm; unsteadiness of movement, especially in the early stages, sometimes accompanied by tremor. Sensibility may be normal, or the perception of touch or pain may be increased or lessened. Belmondo, from an important series of investigations^ has arrived at the conclusion that the symptoms depend on a primary systemic degeneration of the nerve-elements of the pyramidal tracts and posterior columns, determined by the influence of the toxic agent. The course of the disease is chronic, but sometimes an intensely acute * Tuczek,' Klinische u. Anatomische Studien iiber die Pellagra,' Berlin, 1893. t ' Riv. Speriinent.,' 1889-90, xv and xvi. <imple tabes, resembling the former in the common affection of the lateral and posterior columns, and the consequent weakness with ataxy—resembling it also in the imperfect limitation of the changes, and in the intensity of those in the middle of the pos- terior columns in the dorsal region ; but it differs from this, and resembles tabes, in the degree of affection of the posterior columns in the lumbar regions, the extension in slight degree into the root- zones, and the affection of the posterior roots : with these the loss of tho knee-jerk and the affection of sensation are apparently connected. The isolated cases, occasionally met with, present the same combina- tion of spinal symptoms. The precise origin of the affection of articulation and of the nystagmus has not yet been traced. The age at which the disease commences, long before the period at which ordinary degenerations occur, and its family grouping, suggest that its ultimate cause is a congenital tendency of develop- ment, by which the affected elements have a briefer period of vital endurance than the other tissues of the organism. MObius has suggested that there is an actual arrest of development of these structures, but it is evident that their development suffices for perfect function during the early part of life, and that their functional capacity undergoes subsequent failure, which can only be due to a process of structural change. It is possible that we have here, again, a double morbid process, and that a tendency to early degeneration in the nerve-elements is associated with a converse tendency to over- growth of the interstitial tissue, analogous to that which we have in the muscles in pseudo-hypertrophic paralysis (q. v.). In this con- nection it is important to note that in one case the neuroglial over- growth suggested a pure increase of the normal tissue, rather than a result of inflammation; and the peripheral sensory nerves, although * ' Nonne, 'Arch. f. Psych.,' xxii, 1891. " HEREDITARY ATAXY." 529 not degenerated, contained a considerable number of embryonal nerve- fibres in the fasciculi* Dejerine would regard the neuroglial increase as the sole element in the morbid process; but the fact last mentioned, as well as the preponderant affection of certain tracts, makes it improbable that this exclusive view is correct. Although we have here only to consider hereditary cerebellar ataxy and similar conditions, in relation to Friedreich's ataxy, it may be stated that in this disease also we probably have to deal with a developmental defect or perversion, as has been indicated in con- sidering the morbid anatomy. And the same may be said of the family form of spastic paralysis. It might already seen as if we had a series to deal with, with Friedreich's ataxy at one end and family spastic paralysis at the other, the intermediate space being occupied by cases like those of Sanger Brown, in which spasticity and ataxy are combined, and in which the underlying anatomical condition as regards the cord is one of sclerosis affecting lateral and posterior tracts fairly equally, while in Friedreich's disease we have to deal with a condition in which the posterior columns suffer most, and in family spastic para- lysis with one in which the lateral columns may be exclusively affected. Diagnosis.—In most cases the inco-ordination is sufiiciently pre- dominant to suggest that the disease is a form of ataxy, and the unsteadiness of the head, the affection of articulation, the nystagmus, and the age at onset, suffice for the distinction from ordinary tabes. The common form of ataxic paraplegia bears a close resemblance to this disease, a resemblance that is more than superficial, although the excessive knee-jerk and foot-clonus, almost always present in ataxic paraplegia, are usually absent in hereditary ataxy; much spasm is always absent, and nystagmus is common. The difference in the state of myotatic irritabihty is, as we have seen, not absolute; cases of combined lateral and posterior sclerosis occur, of tabetic type, in which the knee-jerk is lost, and in at least one case of hereditary ataxy the knee-jerk has been excessive. The age of onset and family multiplicity may decide the question, but the isolated cases, which are by no means rare, commencing soon after puberty, are not dis- tinguishable from the hereditary disease; they seem to be analogous to the isolated cases of pseudo-hypertrophic paralysis. A greater diffi- culty is presented by cases of slight tabes in children, the subjects of inherited syphilis, in whom it is not uncommon for some weakness of the legs to co-exist, or speech to be disordered, in consequence of some early lesion of the brain. The loss of the iris-reflex should suggest inherited syphilis, and other indications of this will often decide the nature of the case. Disseminated sclerosis presents inco-ordination, nystagmus, and impaired articulation, but the ataxy of the arms differs in the wide range and violent character of the disordering jerks which characterise this disease; while simple unsteadiness of the legs is very rare, and • Anscher, ' La Semaine Med.,' 1890, No. 32. VOL. I. 34 530 SPINAL CORD. the course of the malady is more rapid. The affection of speech differs from that of hereditary ataxy in being simply " staccato," with undue separation of syllables, in the marked cases. In many in- stances, however, the articulatory defect is similar in the two dis- eases. The cases are always isolated. Cerebellar tumour and hereditary ataxy can hardly be confounded, in spite of the fact that the unsteadiness in walking is very similar in the two diseases; the common affection of the arms in the one, and the conspicuous head symptoms (severe pain, optic neuritis, &c.) of the other, sufficiently distinguish them. It is very common for the tremor of the head to be at first ascribed to mere " nervousness," and also for the isolated form, in girls, to be regarded as hysterical. The presence of nystagmus should at once decide the question; it is absolute proof of definite disease. Prognosis.—The prognosis in every case is very serious, since the disease, being a developmental affection, is essentially progressive; but life may be prolonged for many years, and in sliglit cases the malady may interfere comparatively little with the patient's occupation. Thus I have known a man, with very marked symptoms, follow his business as a tradesman for many years. The only guide to individual prognosis is the observed rate of progress, which has little relation to the age at which the symptoms commence. Treatment.—As in other diseases that depend on a congenital tendency, treatment is almost powerless. The measures recommended for ordinary locomotor ataxy (apart from those suggested by the special symptoms of tabes) are those most suitable to the hereditary form. Arsenic, phosphorus, and nitrate of silver deserve a trial; now and then they seem to check the progress of the disease for a longer or shorter time, but its individual tendency determines its course, almost irrespective of treatment. SIMPLE SENILE PARAPLEGIA. This name seems the most unobjectionable for a condition, some- what rare, which appears hitherto to have been unrecognised.* It is confined to late life, occurring in those over 40, and especially over 50. Its characteristic is simple weakness of the legs, with some slowness of movement, but without wasting, sensory disturbance, or reflex altera- tion. The knee-jerk is normal, and there is no foot-clonus. The malady develops very gradually and is slowly progressive, although it seems seldom to attain such a degree as to prevent standing. The condition of the legs resembles that in cases of paralysis agitans with- out tremor, in which the malady is manifested only by weakness, and * A note upon it by myself appeared in the 'Centr:ilbl. f. Nervenkr.,' 1890. CHRONIC MUSCULAR ATROPHY. 531 stiff slowness of movement of the limbs, face, and trunk. Cases are met with in which the condition of the legs above described is asso- ciated with slight symptoms in the arms and face, such as characterise these cases of paralysis agitans. Thus senile paraplegia is probably a partial development of the morbid process of that disease; instead of being general, it is limited to the structures for the legs. If, as the condition seems to suggest, paralysis agitans depends on peculiar changes in the nutrition and function of the motor cells of the cortex cerebri (which impair the power and alter the action of the cells, but do not usually go on to such destructive alteration as entails secondary degeneration of the pyramidal fibres), we can readily conceive that such a process may be sometimes limited to the leg-centres, and may cause the symptoms. If so, the malady is a cerebral and not a spinal one, but it is mentioned here on account of its paraplegic features, and their resemblance to those of disease of the spinal cord. Degene- rative changes may, however, be various in kind and degree, especially in late life; cases occur, similar to these, but with myotatic excess con- necting them with the destructive changes of lateral sclerosis, while others present such symptoms as nystagmus or impeded articulation— evidence that the altered nutrition is wider in its range. CHRONIC SPINAL MUSCULAR ATROPHY. (PROGRESSIVE MUSCULAR ATROPHY; WASTING PALSY; AMYOTROPHIC LATERAL SCLEROSIS; CHRONIC POLIO-MYELITIS). The disease which has long been known by the names " progressive muscular atrophy" and " wasting palsy" is characterised by slow wasting of the muscles, beginning in some one part, and usually spreading and increasing until it is wide in extent and extreme in degree. The changes in the muscles depend on changes in the spinal cord, a slow degeneration of the ganglion-cells of the anterior cornua, accompanied by a similar degeneration in the motor nerve-fibres which spring from the cells. With this degeneration of the cells and peri- pheral fibres there is usually also associated a degeneration of the pyramidal tracts in the cord, sometimes, at least, to be traced up to the motor cortex of the brain. According to current views, there is a decay of the spinal motor neuron, and often also of the upper neuron, which has its nutritional centre in the cells of the motor cortex. Chronic muscular atrophy was separated from primary paralysis by Sir Charles Bell, and was afterwards described more fully by Aran * * Aran, "ltecherches, &c., sur Paralysie Musculaire Atrophique," 'Arch. gen. de Med.,' 1850. 532 SPINAL CORD. ani Cruveilhier.* Bell and Cruveilhier regarded it as a spinal disease. Aran (who first called it " progressive muscular atrophy ") thought that it was primarily a disease of the muscles, a view that was after- wards held by Duchenne,f and subsequently also by Friedreich. This opinion was supplemented by a theory that the wasting was due to a disturbance of the sympathetic. Luys J first discovered the disease of the grey substance of the spinal cord, and Charcot especially associated the atrophy with the wasting of the ganglion-cells. When the con- stancy of the spinal lesion was demonstrated, it was thought that every form of chronic muscular atrophy was of spinal origin; but this view has proved erroneous, and it has been shown that there are forms of muscular atrophy which are purely local and idiopathic. The morbid process is not confined to the spinal cord. Atrophy of the nerve-cells from which the motor bulbar nerves arise often accompanies that of the spinal cells, and "progressive bulbar paralysis" is then associated with " progressive muscular atrophy: " it often comes on after the dis- ease has existed for some time, and ends life; occasionally it initiates the malady. Two varieties of the disease have been distinguished by Charcot, who has been followed in this by most subsequent writers. In the one variety the disease is manifested only by the wasting of the mus- cles—the "Aran-Duchenne type;" in the other there are, in parts other than those much atrophied, the indications of degeneration of the pyramidal tracts of the cord. In the latter cases, Charcot re- garded the degeneration of the pyramidal tracts as the primary lesion, and the affection of the cornua as secondary. He therefore termed the cases of the first class " protopathic," and those of the second class " deuteropathic," and gave to the latter the name " amyo- trophic lateral sclerosis." In Germany, however, and especially by Leyden, doubts have been expressed as to the validity of the dis- tinction between the two classes of cases, and as to the sequence of the lesions in the second class. These doubts are not without founda- tion. The subject will be discussed when the pathology of the disease is considered, and reasons will then be given for the course here adopted of considering the two varieties together as essentially one disease. But cases are also met with (although not frequently) that present * Cruveilhier, 'Arch. gen. de Medecine,' 1853. Hence the disease has been often termed " Cruveilhier's atrophy." + Duchenne, 'Bull. gen. de Therap.,' 1853. J In 1860. Lockhart Clarke described in 1861 changes (lacunae) in the spinal cord, but in the anterior horn cells only pigmentation, not atrophy. Other details of the history of the distinction of the distase and the discovery of its nature will be found in ' A History of the Chronic Degenerative Diseases of the Central Nervous System,' by T. K. Monro, M.A., M.D., Glasgow, 1895, an admirable account of the stages of the discernment of all these diseases. To this book the reader may be referred for more particulars regarding the subject than can be given here, not only in regard to this affection but to all others of a degenerative character. CHRONIC MUSCULAR ATROPHY. 533 every gradation to subacute polio-myelitis in one direction, and per- haps also to polyneuritis in another. Attempts are being made to classify these, but types may be multiplied indefinitely from the inter- mediate forms, and many more pathological and clinical observations are necessary before a useful classification of the cases can be made. In the following description the common forms are chiefly considered. Causes.—The disease is more frequent in males than in females, the proportion being about three to one. It is chiefly a disease of adult life, commencing usually between twenty-five and forty-five. I have known it to begin at fourteen, and as late as seventy, and a case is recorded in which it began at twelve; * there was wasting and rigidity in the limbs, tongue, lips, and lower face. But most cases of muscu- lar atrophy in early life are myopathic, and not spinal. Heredity is to be traced only in less than half the cases, and generally as an indirect neuropathic disposition. Rarely there is direct inheritance of the disease. Among instances that I have met with are a lady whose mother died from a similar atrophy, and another case (from which Fig. 146 is taken) in which a brother had died from some chronic disease of the cord, attended with wasting; but three cases with bulbar sym- ptoms have been recorded, two of whom were cousins, the children of two sisters : the third, who had had syphilis, was a cousin, but his affection was untypical.f Direct inheritance seems to be most common in cases that occur late in life. When many members of a family suffer from muscular atrophy, the malady is nearly always myopathic and not spinal. The affection occurs in all classes of society, and it is doubt- ful whether workers with the muscles furnish a larger proportion of the cases than can be accounted for by their greater exposure to certain exciting causes. Of these more direct causes one of the most frequent is mental distress and anxiety, and this is especially met with in females and in late life. A severe fright has been thought to excite it. Another cause is exposure to wet cold, which is also a cause of many other chronic spinal diseases. Sometimes the exposure has been habitual; sometimes a single exposure has been effective, and some neuralgic pains, indicative of the deleterious influence on the nervous system, have followed the exposure and connected it with the later wasting. The pain has been either in the part afterwards wasted, or in some other, more common, seat of neuralgia. Thus one patient, after remaining in wet clothes for twelve hours, suffered for six weeks from severe neuralgia in the left side of the face, and then the muscles of the left shoulder began to waste. Although excessive use of individual muscles may cause them to waste, it is doubtful whether this influence produces general muscular atrophy. Injury to the cord, such as results from concussion of the spine, is a rare cause. It more often produces disseminated myelitis, which may be manifested by muscular wasting * H. Blumenthal, " Inaug. Diss.," ' Neur. Cent.,' 1884, p. 376. t ' Vhvhow's Archiv,' 188D, p. 115. 534 SPINAL CORD. combined with other symptoms. In a few instances I have known progressive atrophy, of typical characters, to slowly follow a concus- sion, as if this had set up a perversion of the nutrition of the nerve- elements. Still more rarely a fall, injuring one limb, has been followed by muscular atrophy commencing in this limb and becoming general. Thus a woman fell downstairs, and pitched on her left hand and wrist; she had pain in the arm for a long time; two years after the fall this arm began to waste, and the atrophy ultimately became general. The relation might be passed as an accidental coincidence, were it not that in other central diseases—even, for instance, in para- lysis agitans—the symptoms may commence in an injured limb. In rare cases, the disease develops, during adult life, in a subject of old infantile palsy (polio-myelitis), and may start from the most affected part (see p. 409). The disease sometimes succeeds syphilis, and no other cause may be traceable. As with other degenerative diseases, an interval of years elapses between the primary disease and its nervous sequel. The cases that I have seen after syphilis have been typical in course, and evidently degenerative in nature. That syphilis has some share in the causation of these cases is probable from its relation to other diseases, such as tabes; but it is noteworthy that in one case the wasting commenced during, and in another directly after, an energetic mercurial course. This relation is intelligible if the disease is due to a toxine, a result of syphilis, and not to the organisms themselves (see Tabes). Occasionally syphilis and a neurotic heredity can both be traced. In the cases in which atrophy has followed an acute specific disease, especially measles, and has begun in early life, it is probable that the malady is a chronic neuritis and not the central affection now under consideration. Such cases are known as of the "peroneal type " or " neuritic form of muscular atrophy," from the muscles in which wasting in general is first obtrusive, and are separately de- scribed at a later page. General muscular atrophy may result from lead poisoning, but this form is not, as a rule, progressive in character when its cause has ceased to act. It resembles the ordinary form of progressive muscular atrophy, however, in seat and features, and thus differs from the common atrophic palsy of the extensors that is pro- duced by lead. In many cases of progressive muscular atrophy no cause for the disease can be traced. When obtrusive symptoms have followed some adequate cause, it is not uncommon for this to have been pre- ceded by slight symptoms, which show that the malady already existed. A careful inquiry for such symptoms should never be neglected. Symptoms.—The definite symptoms of the disease are occasionally preceded by dull aching in the part afterwards wasted. Sometimes there is such pain in the spine or elsewhere, especially, as already stated, in the cases that are due to exposure to cold. Rarely some sensation other than pain precedes the local symptoms. Thus in one case a sense of coldness preceded the atrophy in each limb that was CHRONIC MUSCULAR ATROPHY. 535 attacked. Weakness and wasting usually come on together, but either may first attract the attention of the patient. In the shoulder and back the loss of power is usually first noticed, and in such covered parts the wasting may become considerable before it is observed. In the hand the wasting is often first noticed, but sometimes it is the impairment of some delicate action, such as writing, that draws atten- tion to the part. The affected muscles lose their proper shape, and there is flattening, or even a depression, where there should be a prominence. If a patient is fat, however, the wasting may cause at first very slight alteration in the external part, especially in the lower limbs. The disease commences in the arm in nine tenths of the cases, and as frequently in one arm as in the other. It begins with almost equal frequency in the hand and in the shoulder muscles. From the part first affected the disease spreads to other parts of the same linib. Before it has attained a considerable degree in one limb, it usually shows itself in the corresponding limb on the other side; often in the muscles corresponding to those in which it commenced, sometimes to those affected second in order of time. As the muscles waste paralysis results of various character and degree, corresponding to the atrophy. In the hand the thenar muscles and interossei are usually the first to suffer. The thenar eminence becomes flattened, and the base of the first metacarpal bone becomes prominent. Of the interossei, the atrophy of the abductor indicis is especially conspicuous; the normal prominence gives place to a hollow beside the metacarpal bone when the thumb is abducted. Depressions form between the meta- carpal bones on the back of the hand, and also between the flexor tendons in the palm in consequence of the wasting of the lumbricales. The forearm muscles may be next involved, the flexors usually before the extensors; and with the flexors the supinators may suffer, or they may escape until the biceps is involved. Occasionally the dis- ease begins in the forearm, and then especially in the extensor muscles of the fingers, sometimes in those of the thumb, especially of its phalanges. The several parts of the long finger muscles may suffer unequally ; the ulnar extensors usually suffer most. Of the shoulder muscles, the deltoid is generally the first to manifest the disease, and in some cases which begin in the hand the deltoid suffers before the forearm muscles. The rounded contour of the shoulder becomes changed (Figs. 7, 144, 145), and the head of the humerus can be recognised beneath the acromion. It is not rare for part of the del- toid to suffer and part escape: we have seen (p. 36) that the several portions have different functions and associations, and this probably involves a relation to separate groups of nerve-cells. The wasting of the deltoid is soon followed by that of the other muscles of the upper arm and of the scapula. The triceps usually suffers less and later than the biceps, but sometimes the reverse is the case. The supra- and infra-spinati are often affected with the deltoid. In exceptional 536 SPINAL CORD. instances the deltoid or hand muscles escape, and there are cases (perhaps a special group) in which the upper arm and shoulder muscles waste even to an extreme degree, and the forearm and hand muscles escape entirely. In most cases, the wasting early involves the muscles of the back, and it sometimes begins in them. The middle and lower parts of the trapezius usually suffer first; the rhomboids and erectors of the spine at a later date. The affection of the trapezius is readily recognised if the patient tries to put the shoulder back (Fig. 145). Thehighest FiG. 144.— Progressive muscular atrophj. Wasting of the mus- cles of the back and arms; in the forearm scarcely any muscular tissue can be recog- nised, and in the hand all the muscular pro- minences have van- ished. (Drawn by Dr. H. R. Spencer.) FlG.145.—Progressive muscular atrophy. Wasting of right trapezius complete (the rhomboids remaining), of the left trapezius partial. On each side the upper part of the trapezius is wasted, and the contour of the neck is cor- respondingly changed. Both deltoids are also atrophied. (Drawn by Dr. Spencer.) part of the trapezius presents a remarkable indisposition to atrophy ; it often remains intact to the last, and then may contrast with the wasting below it, standing out on each side, like a cord passing from the occiput to the shoulder. Hence Duchenne termed this part the ultimum moriens. I have, however, seen several otherwise typical cases, (beginning either in the deltoids or in the hands,) in which the highest parts of the trapezii suffered before the middle parts. The levator anguli scapulje also generally escapes, even when all the CHRONIC MUSCULAR ATROPHY. 537 muscles about it are wasted. The serratus, latissimus, and pectoralis major are usually affected later. They may escape wholly or in part; isolated bundles of the pectoral's may waste, the intervening parts escap- ing, or either the upper or lower part of the muscle may atrophy alone. According to the affection of the muscles that are attached to the scapula, the position of the bone changes, and it becomes rotated under the influence of the muscles that are unaf- fected and unopposed (Fig. 7, p. 35). The muscles that extend the Fig 146.—Progressive muscular atrophy. Weak- ness of the innscles of the neck. A, habitual posture of the head, inclined backwards. B, posi- tion into which it (alls if the patient attempts to keep it in the normal balance. (Drawn by Dr. Spencer.) head on the spine often suffer in con- siderable degree, and from this there results a difficulty in the carriage of the head (Fig. 146). It is habitually inclined back- wards, so as to balance it on the spine with but little muscular exertion; if moved forwards, it falls so that the chin touches the chest. It can be brought back into its former position only with diffi- culty ; the patient has to incline the trunk backwards, so as to bring the head nearly into the vertical position, and then, with a sudden contraction of the sterno-mastoids, and a jerk, the head goes back into its former posture. The increased innervation of the weak extensors of the head often causes a synergic over-action of the frontalis muscles, which are normally associated with the extensors (so that the eve- brows are raised when the head is put back to look upwards.) The skin at the back of the neck lies in transverse folds when the neck is extended. The patient may be unable, when lying in bed, to move the head from side to side. The sterno-mastoids also are often wasted ; either the sternal or clavicular part may be most affected. In striking con- trast to the general wasting of the neck is the condition of the platysma myoides, which always escapes, and may become hypertrophied in a vain attempt at compensation. The muscles of respiration suffer in the majority of cases, and their impairment constitutes a grave source of danger to life. The inter- costals rarely escape altogether; the diaphragm is involved in many cases, and respiration is then carried on by the intercostals and superior thoracic muscles. On the other hand, the intercostals may suffer much and the diaphragm remain free; respiration is then purely abdominal, and the walls of the thorax may be almost motionless in breathing, or there may be merely a slight movement of elevation of the upper ribs. The chest becomes flattened in front, and narrow from 538 SPINAL CORD. before back, from the influence of atmospheric pressure on the ribs, unopposed by the intercostals. Either the upper or lower intercostals may suffer most. When the diaphragm is paralysed the upper chest muscles often suffer more than the lower, and a compensatory increased movement of the lower ribs carries forward the abdominal wall, and may suggest that the diaphragm is acting when it is not. A careful examination will always prevent the error. The muscles of the abdo- minal wall occasionally waste, but far less frequently than those of the thorax. Wasting in the legs is much less common than in the arms, and if it occurs is usually slighter in degree ; but occasionally the disease first manifests itself in the legs, and is more intense in them than elsewhere. The glutei, extensors of the knee, and the muscles in the front and on the outer side of the lower leg, are those that are most affected. We shall presently see, however, that the legs are often paralysed when they are not wasted, and sometimes they are the seat of wasting which differs in certain features from that which is the especial characteristic of the disease. The face almost always escapes the general atrophy, and its normal appearance may present a striking contrast to the rest of the body. In some cases, however, the lips are paralysed as part of the bulbar palsy that so often accompanies the spinal disease. A remarkable case in which the face shared the atrophy of the limbs, and the tongue escaped, has been recorded by Langer ;* on the other hand, the tongue has been the first part to suffer, the arms being affect',id a month later.f Bulbar paralysis, however, often runs its course without muscular wasting in the limbs, and when the latter supervenes it is generally quite subsidiary. The like statement may be made of the converse relation, although it must be remembered that the anterior nerve-cells and those of the bulbar nuclei are analogous structures, and may be similarly and even simultaneously affected. As the wasting progresses, the appearance of the parts in which it is most advanced becomes extremely changed. All trace of muscle may disappear from parts of limbs or even from an entire limb (Fig. 144); and there is usually a wasting of the adipose tissue as well as of the muscle, so that the bone seems to be covered only by fascia and skin. The transverse processes of the vertebrae may be felt in the hollow beside the spine, and the bony prominences about the shoulder may be almost as conspicuous as in a skeleton, so that beneath the acromion there may be a groove, into which the finger can be placed, in consequence of the descent of the head of the humerus from the glenoid cavity. The unequal affection of antagonistic muscles leads to various contractions and deformities. In the hand, especially, distortion is apt to occur; from preponderant paralysis of the interossei and contraction of the long flexor and extensor muscles, * Vienna Medical Society, March 17th, 1882. t Birdsall, ' Journal of Nerv. and Ment. Dis.,' 1887, xiv, p. 256. CHRONIC MUSrULAR ATROPHY. 539 the "claw-like hand" develops in extreme degree (Figs. 19 and 20, p. 43). If all the muscles of a part are equally and simultaneously affected, no deformity results unless an unsupported part yields to the influence of gravitation (Fig. 144). Lordosis is very common in cases in which the trunk and hip muscles are involved. It is often the indirect result of the weakness of the extensors of the hip-joint. It is produced in the manner described in the account of pseudo- hypertrophic paralysis, in which it is almost constant. The electrical irritability of the wasted muscles presents changes which vary in character in different cases. When the wasting is slow, there is usually a diminution in both faradic and voltaic irritabihty, similar in character to each current. But the amount of contraction that can be produced is far less than normal, and progressively lessens The irritability fails with the muscular nutrition, and when the wasting is great, only a slight contraction can be obtained, even with a strong current. When the wasting is extreme, irritability at last becomes extinct, but the voltaic irritability of the muscular fibres persists long after the faradic irritability has disappeared. It may be normal in degree, or lowered, but is seldom increased in such cases. The quality of the voltaic irritability may also be normal, but some- times ACC (anodal closure contraction) occurs as readily, or more readily, than KCC. Tetanic contraction during the passage of the current is produced with undue readiness compared with the closure contractions, and opening contractions are often caused by currents but little stronger than those that cause closure contractions. Thus there may be the qualitative change of the reaction of degeneration without the voltaic increase (see p. 74). When there is the rapid and considerable paralysis described on p. 544, either at the onset or during the course of the disease, the palsy being followed by rapid wasting, there may be quick extinction of faradic, with actual exalta tion of voltaic irritability, and the reaction of degeneration may be present in all its characteristics. Between these forms every inter- mediate condition may be met with, including the mixed reaction described on p. 32. The mechanical irritability of the muscles is considerably increased; a tap causes a local contraction of the fibres struck. Moreover, spontaneous flickering contractions of parts of the muscles are very common, now of one bundle, now of another, conspicuous to the eye, although scarcely felt by the patient. This " fibrillation," as it is termed, is not invariable, nor is it confined to this disease. It may sometimes be observed in muscles that are not yet invaded by the wasting, but where it is observed, in this disease, atrophy usually follows. In the parts affected by the characteristic wasting, all reflex action is abolished, clearly in consequence of the damage to the motor part of the reflex arc ; the afferent portion of the arc is unaffected, for, as we shall see, there is no loss of sensation. The myotatic irritability 540 SPLNAL CORD. (" tendon -reflex action ") is also lost, and lost early. The knee-jerk, for instance, disappears as soon as there is even a slight diminution in the bulk of the thigh muscles, in cases in which the legs are the seat of primary wasting. The muscles are flaceid and toneless—a condition that may be termed " atonic atrophy." To this common rule, however, exceptions are sometimes met with ; there may be from the first rigidity of the affected muscles. When this is the case, the wasting does not go on to the entire destruction of the muscle; often it is considerable, but not extreme, and it may be trifling. With this rigidity there is a preservation or even increase of myotatic irritability. We may term this "tonic atrophy." It is generally associated with spastic para- lysis, without wasting, in some other part. For instance, in one case the forearms and hands were the seat of this tonic atrophy, and in the legs there was simple spastic paraplegia. We shall presently consider the pathology of this condition.* Sensory symptoms are always subordinate and usually very slight. They are confined to pain, usually dull and rheumatoid in character, felt chiefly in the limbs in which the malady is most active. Such pains are common at the onset, as we have already seen, and they may recur from time to time during the course of the disease. Sometimes vague feelings of "numbness" or " deadness " are complained of, but cutaneous sensibility is never impaired. (When anaesthesia accom- panies muscular wasting, both symptoms are due either to chronic meningitis, damaging the nerve-roots, or to disseminated focal myehtis, syringomyelia, or multiple neuritis.) Nor do the muscles lose such sensibility as they normally possess. Perception of posture persists, and the muscles continue sensitive both to pressure and to exten- sion. When the arms are the seat of such atrophy as has been described, the legs, if not also wasted, may be normal, or they may be slightly affected, the thighs thin, and the knee-jerks lost. Often they are the seat of gradual loss of power without wasting, and with an increase of myotatic irritability. The knee-jerk is excessive; a clonus can readily be obtained, and the reflex over-action of the muscles may increase to actual rigidity and spasm, so that there is the condition of spastic paraplegia described in a preceding chapter. It is rare, however, for the spasm to reach the higher degree of intensity, and for the muscles to present the massive firmness that characterises the simple form of spastic paraplegia. On the other hand, there is often some diminu- tion in the size of the muscles, and thus we have a gradation to the condition of tonic atrophy just described. In this condition, moreover, * It should be noted, however, that, in the muscles that are the seat of toneless wasting, when the atrophy has attained an extreme degree, slight rigidity may develop, accompanied by tenderness of the muscle. It is probable that this rigidity is myopathic, and due to the structural changes in the muscles presently to he described. This condition is rare : the early Haccidity is usually maintained to the last. CHRONIC MUSCULAR ATROPHY. 541 there is usually only a moderate diminution in electrical excitability, which does not go on to extinction. The one condition does not seem to pass into the other ; the state of rigidity and myotatic excess does not give place to muscular relaxation ; atonic atrophy does not succeed the tonic wasting. In very rare cases, of which I have seen a few instances, there is a similar condition in the hands when the shoulders are the seat of simple atonic atrophy. The forearms are then rigid, moderately wasted, with myotatic excess, while the muscles of the shoulders are extremely wasted and absolutely flaccid. In still more rare cases the whole arms are thus affected, are thin and rigid, and in no part is there atonic atrophy. In one remarkable case of this character, the muscles of the trunk participated in the spasm; after coughing or yawning, respiration would be checked for a few seconds by general spasm, and whenever the patient was raised from the bed, the arms, legs, back and neck became stiff in tetanoid rigidity, the head being bent backwards. The combinations of the ordinary atonic wasting, and loss of power without wasting and with increased myotatic irritability, are exceed- ingly numerous and variable. The most frequent, as already stated, is flaccid atrophy in the arms and spastic paralysis in the legs; but I have twice seen atonic atrophy below the knees, with weak but well-nourished thigh muscles and much increased knee-jerk. The variable combination of these conditions gives rise to differences that are more apparent than real, and may easily be allowed undue weight in classification. Their explanation will be considered presently. The extreme emaciation of the most affected parts shows that the adipose tissue wastes as well as the muscles. Indeed, the sufferers usually become generally thin, often to an extreme degree. The atrophied limbs are usually cold, and may be livid or pale, but there is no tendency to acute vaso-motor disturbance in the ordinary form of the disease. I have known the skin of the face to become thin and smooth, so that, in one instance, the dark iris could be seen through the closed eyelids, but such a change is quite exceptional. In another patient there was a very remarkable form of local atrophy. Certain areas of muscles underwent wasting, the rest being normal; the affec- tion commenced by a livid discoloration of the skin, and the wasting seemed to involve the skin, subcutaneous tissue, and muscle, causing local depressions. Considerable tracts of the trapezii were thus affected, and smaller spots in the arms and legs. The patient was a sino-le woman of thirty-five, and the disease, which did not show a strongly progressive tendency, is probably a special affection, perhaps of the nature of scleroderma. The functions of the sympathetic are not, as a rule, deranged. Dilatation or contraction of one pupil has been frequently observed, chiefly in association with atrophy of the muscles that are supplied from the lower part of the cervical region; and it no doubt depends on the disease of the spinal cord, and not of the sympathetic itself. 542 SPINAL CORD. The reflex action of the iris is usually normal, and optic nerve atrophy never occurs.* Nystagmus is present in rare cases. The visceral functions are usually little disturbed. Sexual power is often lost. The sphincters rarely suffer, even when the wasting is general and extreme; occasionally they are involved, and they may even suffer early. In other cases, in which the legs become weak after the wasting sets in in the arms, the affection of the sphincters may coincide with that of the legs. In the composition of the urine, slight changes have been found, but not constantly. Urea has been increased in some cases, lessened in others, f The quantity of lime has been found to be increased (Fromman), that of kreatin diminished, even to one tenth of the normal (Rosenthal, Langer). Glycosuria has been observed in association with bulbar symptoms. J The lungs may suffer from the impairment of breathing power, when the intercostals and diaphragm are weakened. Varieties.—The chief varieties of the disease depend on the relative distribution of the three conditions: (1) atonic atrophy, becoming extreme ; (2) muscular weakness with spasm, but without wasting, or with only slight wasting; and (3) tonic atrophy, rarely extreme in degree, with myotatic excess. The commonest condition is to have atonic atrophy in the arms and upper part of the trunk, with simple weakness and spasm in the legs. Atonic atrophy in both arms and legs is less common, and the least common is tonic atrophy alone, in the arms, or universal. The last is, indeed, extremely rare. It is important to note, however, that these conditions may coexist in every degree and combination; between universal atonic atrophy on the one hand, and universal spastic paralysis without wasting on the other, there is every gradation. The latter does not come into the category now under consideration, but similar cases are met with in which there is atrophy of a few muscles (as, for instance, of the hands only), which complete the series. The varieties due to the different combinations of atrophy and paralysis have been already alluded to. A peculiar form of muscular atrophy has been mentioned, first * I have once met with a remarkable reflex fixation of the eyeballs in a case of advanced progressive muscular atrophy. If the patient, looking to one side, was suddenly told to look at an object on the other side, his head was instantly turned towards the second object, while the eyes remained fixed on the first, by a movement corresponding to that of the head but in the opposite direction, and then, after a few seconds, they were slowly moved towards the second object. The phenomenon continued to the end of the patient's life. As I pointed out in an account of this curious condition ('Brain,' vol. i), it is interesting evidence of a normal reflex mechanism in the fixation of the eyes; this was, as it were, isolated by disease, which lessened voluntary control over it. t In a patient who weighed 7 st. 13 lbs., and whose urine varied between 760 and 960 cubic centimetres, 1 found the daily excretion of urea to vary between 10*7 and 15 grammes, the average being 13 grammes. This is just half the normal average Por a man of that weight, which would be (according to Parkes) 24 grammes. X Rovighi and Melotti, 'Riv. Sper.,' 1888, p. 315. CHRONIC MUSCULAR ATROPHY. 543 conspicuous in the peroneal regions * and spreading thence to other muscles of the leg and to the hands. It is characterised by occurrence in early hfe, and often in several members of the same family, and has been termed the " peroneal type " by Dr. H. Tooth, the " neuritic (neurotische) form" of Hoffmann. It is probably not dependent on the spinal cord, and is considered more fully at a subsequent page. Complications.—Progressive muscular atrophy is occasionally accom- panied by the symptoms of some other degenerative disease of the spinal cord. The paralysis with spasm, already described, can scarcely be regarded as a complication: it is rather part of the disease, and its relation to the other symptoms will be considered when we discuss the pathology of the affection.' In rare cases, muscular atrophy in the arms is accompanied by the symptoms of locomotor ataxy in the legs. By far the most frequent complication is bulbar paralysis, weakness of the lips, tongue, pharynx, and often of the laryngeal muscles. It is the expression of a degenerative process in the medulla, similar to that which, in the spinal cord, causes the affection of the limbs. It may come on at any stage of the disease, may precede the sp nal symptoms, or only come on when these have attained a con- siderable degree. In characters, the bulbar palsy may resemble perfectly that which occurs in isolated form, and will be described among the diseases of the brain. Frequently, however, there is but little paralysis of the tongue, even when swallowing and articulation are much impaired. There may also be slight interference with articu- lation when there is no marked bulbar palsy. A minor complication is the neuralgic pain, which, as already stated, is sometimes trouble- some in the early stage of cases that are due to cold. In several patients I have known headache to be frequent and severe throughout the course of the disease. General paralysis of the insane has been met with as an exceptional complication.f Course.—The malady, in most cases, is steadily progressive, as its name implies, but in the rate of its progress it varies in different cases, and in the same case at different periods. It may, moreover, become stationary (sometimes as the result of treatment) at any period in its course, and when once actually arrested, it does not usually again become active. Unfortunately, the tendency to cessation is greatest in the later stages of the disease, when there is little except life to be preserved. Sometimes progress ceases at an earlier stage, and chiefly, I think, in those cases in which the atrophy is strictly symmetrical, and develops simultaneously, or almost simultaneously, on the two sides. Thus I have met with several cases in which there was symmetrical wasting in the two hands, or in certain muscles of the two forearms or of the two upper arms, and in which the atrophy, * Cases, however, have been described more recently in which the upper limbs suffered first or simultaneously (Hoffmann, 'Deutsch. Zeitschr. f. Nervenheilk.,' 1891, i). t Tambroui, ' Riv. Sper. de Ficn., &c.,' 1887, xiii, p. 184. 544 SPIXAL CORD. after attaining a considerable degree in its limited seat, had become stationary and continued so Occasionally some symptom (as weak- ness of the sphincters) may pass away, although the atrophy pro- gresses. When the progress at the commencement is rapid, it usually con- tinues rapid, until the disease has attained a wide extent, although the acute local onset mentioned below may be followed by slow extension. When it begins slowly, it is usually slow throughout. Although the disease sometimes commences in the second arm very soon after its onset, it more commonly makes some progress in its primary seat before beginning on the second side, and the interval that elapses varies with the rate of extension. It often happens that a year intervenes between the affection of the two arms, and I have known, in a very chronic case, the atrophy to slowly progress in one arm for seven years before it showed itself in the other. It is not common for the arms to be reduced to practical helplessness in less than two or three years, but the hands may become useless in as short a time as six months, while in one case the wasting, commencing at the shoulder, had invaded the whole arm in the course of a month. The shortest time in which I have known a patient to reach the last stage of the disease is nine months. With any rate of general progress, the otherwise uniform course of the disease may be broken by the occurrence of almost sudden palsy in a certain group of muscles. Considerable loss of power, it may be absolute paralysis, comes on in a few days, or even in a few hours. It may occur at the onset of the affection. The extensors of the wrist and fingers are the muscles most commonly thus affected. The weak- ness is usually followed by a well-marked degenerative reaction in the muscles. I have seen several eases which began by such subacute or even acute paralysis of the extensor muscles, first in one arm and soon afterwards in the other; the initial condition closely resembled the paralysis from lead poisoning, even to the escape of the supinator longus and ext. ossis met. pol. This cause was, however, excluded, and soon the muscles of the shoulder and back presented commencing slow progressive atrophy, followed by wasting of the interossei until a typical state was reached. In another case, the quick loss of power was confined to the extensors in one arm, which were already weak and slightly wasted, most of the other muscles of the upper limbs having been long atrophied. When there is weakness of the legs without wasting, the onset of this may coincide with the atrophy of the arms, or may succeed it at any interval. In one case five years elapsed, after the arms began to waste, before the legs became weak. It is very rare for the paraplegic weakness to occur first. The chief danger to life is from pulmonary maladies, rendered grave from the weakness of the muscles of respiration. The common com- plication of bulbar paralysis is another frequent cause of death, either by the interference with swallowing and nutrition, or by the laryngeal CHRONIC MUSCULAR ATROPHY. 545 paralysis. Less commonly, death results from bedsores and septicaemia, or from intercurrent maladies. Pathological Anatomy.—The wasting of the muscles is as evident after death as during Hfe. They are reduced in size and pale in colour. Sometimes there is little in the tint of what remains to suggest muscular tissue. Parts of a muscle may be hardly dis- tinguishable from adjacent fat. On the other hand, the bulk of the muscle may be dark, and pale streaks in it may mark the position of local degeneration. Under the microscope the fibres present various changes, and of these four are well defined. (1) There may be simple narrowing of the fibres, without any considerable change in their striation (Fig. 147), although the striae often seem to be further apart than normal, and sometimes the fibrillary segmentation is unusually distinct. (2) Simple fatty degeneration, in which the transverse striation gives place to a granular appearance (Fig. 148), the granules become larger and fewer (Fig. 147) until ultimately distinct globules are scattered through the sheath. Where the muscle resembles fatty tissue to the naked eye, the microscope may show only sarcolemma sheaths containing groups of globules. (3) Muscular fibres are seen in which the sheath contains only a clear material enclosing a few fatty globules, and a few transverse striae, faint, as if fading away. It is probable that this is not the result of fatty degeneration, but of a different process, which has been termed "vitreous degeneration"—a sort of dissolution of the striae, indicated by the appearance of such fibres as are shown in Figs. 147, 148, 149. (4) A longitudinal striation develops in the fibre, and at first co-exists with the trans- verse striation ; but ultimately the latter becomes indistinct, and the fibre looks like a fasciculus of longitudinal connective-tissue fibres (Fig. 150). Sometimes, with the longitudinal striation, the fibre presents a transverse striation very much finer than normal, the striae being narrower and nearer together, as if from a division of the " sarcous elements." This change may sometimes be seen alone, and may be present in only one part of a fasciculus. Thus at one place the number of striae in x J0 0- inch was only seven, while in another region of the same fasciculus seventeen were to be counted in the same space. A tendency to transverse fissuring has also been described, but this is probably artificial. Fatty globules accumulate between the fibres (Fig. 150), accompanied in some cases with granules and masses of reddish-brown pigment. There is often also an increase of the nuclei (Fig. 148), and sometimes of the fibres of the interstitial tissue. Two or three rows of nuclei may he between the fibres. The capil- laries may be dilated and distended. It is very common to see muscular fibres that are much altered side by side with others that present a nearly normal appearance. Ultimately the sheaths become empty and shrink, and may be scarcely distinguishable from the interstitial fibrous tissue. The peripheral nerves contain many degenerated nerve-fibres, and VOL. I. 35 546 SPINAL CORD. the terminal branches for the muscles a still larger number. If the nerves are traced up to the cord it is found that the degenerated fibres come only from the anterior roots. These are conspicuously changed to the naked eye, small and grey. They may resemble fine threads of connective tissue, and under the microscope no nerve-fibres may be found in them, or only a few may remain of normal aspect, the rest being in various stages of degeneration, or represented only by their empty sheaths. The degree of affection of the anterior roots corre- Fig. 117. Fig. 143. Tk.. (49. Fio. 150. Fibres op Wasted Muscles in Progressive Muscular Atrophy. Fig. 147.—Narrowed fibres with nearly normal striation; others clear,containing a few fat globules, and a few faint transverse striae and some longitudinal striation; large globules of fat lie in the interstitial tissue in front of one narrowed fibre. Fig. 148.—Granular degeneration: a fibre with normal transverse striation presents also indications of longitudinal striation. Increase of nuclei of interstitial tissue. Fig. 149.—Two normal fibres and one presenting the clear homogeneous aspect, with a few fat globules and some faint striation. Fig. 150.—Several fibres similar to that of the last figure, witb globules of fat between them. On the right is a fibre which has undergone complete longitudinal striation, the normal striae liaving disappeared, so that it resembles the adjacent interstitial fibrous tissue. Other fibres in the same muscle were in intermediate stages of degeneration, some transverse striation co-existing with the longitudinal striation. sponds to the wasting in the parts supplied by them. The posterior roots are normal. The spinal cord is often softer than natural at the affected part, and the white substance of the lateral columns may be grey and translucent in aspect, especially in the cervical enlargement. Under the microscope morbid changes are seen in the anterior cornua, CHKONIC MUSCULAR ATROPHY. 547 and also in most cases, in the antero-lateral white columns. The change in the anterior cornua corresponds in its intensity to the origin of the nerves to the most affected parts, and since the latter are usually the arms, the disease is generally most intense in the Fig. 151. Fig. 152. Fig. 151.—A normal anterior cornu for comparison with the next figure. Fig. 152.—Progressive muscular atrophy; anterior cornu, cervical region. (From drawings by Dr. H. R. Spencer.) cervical enlargement. In stained sections the grey matter of the horn is less deeply tinted than normal, but in some parts it may stain more deeply, especially in the circumference of the cornu and the processes of grey matter which project into the white column. Occasionally, L CORD. larger areas have a dense aspect and stain deeply, but the central part of the cornua is generally pale and wasted in aspect. Most of the large nerve-cells have disappeared; many entirely, while others are re- presented only by small angular bodies. Not a single large cell may be seen in a section which, in a normal cord, would contain a consi- derable number. Frequently, how- ever, a few large cells can still be seen, but most of these have lost their processes and are more glo- bular than normal. The inter- stitial tissue is also changed. The nerve fibrillae waste with the cells, Fig. 153.—Progressive muscular atrophy; degeneration of the anterior cornua and pyramidal tracts. A, medulla oblongata, complete degeneration of the anterior pyramids, A p j B, at the upper part of the decussation of the pyramids ; D, the decussation of the degenerated fibres; A p, the pyramids, still incomplete. C, cervical, D, dorsal, E, lumbar sections. The degeneration of the anterior cornua is complete in C, but in £ a few cells remain, for the most part without pro- cesses. In C and D the degeneration of both anterior and. lateral pyramidal tracts is conspicuous; in E the anterior tract has ceased, and the lateral tract extends up to the surface of the cord, from which it is separated in C and D by the undegenerated direct cerebellar tract. In C and D the degeneration extends forwards in front of the lateral pyramidal tract, but gradually ceases. The fibres of the anterior commissure are also degenerated.* * In this case the arms were greatly wasted and fbiccid; the legs were para- lysed, rigid, with moderate wasting. The muscles of the back were also atrophied. In the arms the weakness and wasting came on at the same time, in the right arm some time before the left. The shoulder muscles suffered first, but the atrophy quickly spread, and was ulti- mately extreme in the muscles of the Bhoulders, forearms, and hands. The dis- ease ran a rapid course; death occurred two years after the gradual onset. CHHOiNIC MUSCULAR ATROPHY". 549 and there is an increase of the small, angular, and stellate cells and other connective-tissue ele- ments. The larger vessels are dilated and surrounded by un- duly wide spaces, but there is no considerable distension of the capillaries. The cornu as a whole is not usually changed either in size or shape. Similar alterations may be traced through the dorsal region. In the lumbar enlargement the grey matter may be normal, even when it is much altered in the cervical region; but if the legs are wasted there are changes similar to those al- ready described. When the atrophy begins in the legs, the disease may be more intense in the lumbar than in the cervical enlargement; but more often any degeneration that exists is slighter, and a larger number of normal or slightly changed cells Fiq. 154.— Progressive muscular atro- phy. A, medulla oblongata ; degene- ration of the anterior pyramids, A P. B, cervical, C, first dorsal, D, first lumbar, E, mid-lumbar sections. The nerve-cells have disappeared from the anterior cornua, except in E, in which a few remain. There is com- plete degeneration of the pyramidal tracts, anterior and lateral. The de- cussation at the medulla was unequal in this case; of the left pyramid fewer fibres crossed than of the right, and hence the left anterior pyramidal tract is larger, while the right lateral tract is smaller than normal, and, moreover, has ceased at the middle of the lumbar enlargement, to which the left anterior tract extends.* * The patient was a man forty-eight years of age. The disease followed a severe exposure to cold. The wasting of the arms was extreme, and they were absolutely powerless. The legs were much less wasted than the arms, but proportion to the wasting. weak, the loss of power being out of 550 SPINAL CORD. can be seen. Sometimes certain groups of cells are little affected while others are much atrophied. The degeneration may involve to some extent the intermediate grey matter between the cornua, but here it ceases; the posterior horn is always normal. There is distinct degeneration of the anterior root-fibres passing from the cornu through the anterior column. A few fibres may remain, but whole fasciculi appear to be replaced by fibrous tissue. There is also degeneration of the fibres of the anterior commissure, in consequence of which it stains much more deeply than normal, in the regions in which the grey matter is considerably diseased. In the white columns there is usually considerable, and often almost complete degeneration of the pyramidal tracts, anterior and lateral.* The area of sclerosis, resulting from the degeneration of the two tracts, varies in extent according to the size of the anterior tract, and to the distance which it extends down the cord. In Fig. 154 this is illustrated in an unusual manner, in consequence of an inequality in the decussation of the pyramids at the medulla, fewer fibres of the left pyramid having crossed than of the right, so that the left half of the cord contains more than its proper share of the fibres, and the anterior tract extends into the lumbar region even further than does the lateral tract. Where the direct cerebellar tract exists, this, always unaffected, limits the sclerosis of the lateral tract on the outer side. On the inner side, the " lateral limiting layer " (see p. 221) is usually much less degenerated than the pyramidal tract, and intervenes be- tween the latter and the grey matter; but this layer suffers in some degree, perhaps by the affection of outlying pyramidal fibres con- tained in it. The sclerosis does not usually cease at the anterior extremity of the pyramidal tract, but extends forward in the " mixed zone" of the lateral column, lessening in intensity, and ceasing usually opposite the outer part of the anterior cornu. It is here most intense close to the grey substance, and ceases before it reaches the surface of the cord, the antero-lateral ascending tract being unaffected. This sclerosis may be due to the degeneration of the short vertical fibres that pass between adjacent regions of the anterior cornu, and which share the degeneration of the nerve-cells. Occasionally it extends, in slighter degree, into the anterior columns. The posterior columns are always free from definite degeneration, but there may be some general increase of connective tissue throughout the whole cord. The degeneration of the pyramidal tracts is usually * I have not yet met with a single case of progressive muscular atrophy in which the pyramidal tracts were unaffected. Such cases are extremely rare. One has been published by Strumpell ('Zenker's Zeitseh.,' 1887, and 'Neur. Centralbl.,' 18s8, p. 139) which was characterised by the general wasting of the arm, a very slow course, and the absence of leg symptoms. The spinal nerve-cells and motor nerves were degenerated. Other cases have been described by Villiers ('Journ. med. de Bruxelles,5 1897) and by Beevor in a communication to the Neurological Society of London in 1896. CHRONIC MUSCULAR ATROPHY. 551 considerable in degree; often most of their fibres seem to have perished. If it is incomplete in the cervical region, it may be slight in the lower part of the cord, the degenerated fibres being chiefly those that end in the cervical enlargement and dorsal region. When the sclerosis is intense it is not confined to the cord; it can be traced up through the decussation (Fig. 153, b) and through the medulla oblongata, in which, as Figs. 153 and 154 show, the whole of both pyramids maybe degene- rated, so that they .stain deeply, and no nerve-fibres can be dis- tinguished in them.; The degeneration of the pyramids has been found in several cases to extend through the pons and crus to the internal capsule, and even through the white substance to the cortex. Above the capsule, however, the pyramidal fibres are so mingled with others that their degeneration is no longer recognisable by the deeper staining of a definite tract; but it has been detected by the presence of abundant products of degeneration in the path of the fibres. In the motor cortex the large ganglion-cells have been found fewer than normal and distinctly degenerated, many having lost their processes ; and, in the interstitial tissue, the spider-cells and other connective- tissue elements are increased in number.* But the degeneration of the pyramidal tracts has also been found to cease at the crus f and at the decussation.X In cases in which the symptoms of bulbar paralysis were present during life, the motor nuclei of the medulla have presented changes corresponding to those of the grey matter of the spinal cord, with a similar degeneration of the nerve-cells. In other instances the degeneration of these nuclei has been slight, but in such cases the degeneration of the pyramids has been intense, and doubtless involved the fibres connecting these nuclei with the cortex of the brain. The sympathetic nerves and ganglia, when examined, have been found normal, or have only presented such changes as are common apart from symptoms of disease of the nervous system. Pathology.—The theories, according to which the disease was regarded as primarily one of the muscles or of the sympathetic nerves, have now only an historical interest. The constancy of the changes in the ganglion-cells of the spinal cord, the degeneration of the motor root-fibres, and the analogous effects of acute lesions of the anterior cornua, leave no doubt of the relation of the muscular wasting to the disease of the grey matter, and essentially to that of the ganglion-cells, and the fibres proceeding from them. The slowness of the change causes the impairment of the nutrition of the muscular fibres to pro- ceed pari passu with that of the nerve-elements, and the interference with motor conduction to be proportioned to both. We are thus able to understand the condition of electrical excitability, and its slow * Koschewnikoff, 'Archives de Neurologic,' 1883, No. 18; and 'Centralbl. f. Nerveukr.,' 1885, p. 409; Marie, ' Neur. Centralbl.,' 1884, p. 61. t Ilovighi and Melotti, loc. cit.; Dombluth, 'Neur. Centialbl.,' 1889, p. 377. X Moeli, 'Arch. f. Psych.,' x, 718. 552 SPINAL CORD. failure, as nerve and muscle degenerate together. It is only when the slow degeneration is varied by a more acute process of destruction of cells and more rapid degeneration of fibres that the muscular tissue is for a long time less damaged than the nerve-fibres, and presents paralysis in excess of the wasting, with a voltaic irritability in excess of the faradic irritability of the nerve-endings (p. 30). Thus the essential lesion of the disease is a slow decay of the lower segment of the motor path, the segment which consists of the ganglion-cells and their prolongations in the axis-cylinders of the nerve-fibres (seep. 213). To this the conspicuous symptom, the muscular wasting, is secondary. It is perhaps better thought of as a degeneration of the whole segment than as simply a lesion of the ganglion-cells, although the latter being the element on which the nutrition of the segment depends, the two views are merely different modes of stating the same fact.* But the disease is rarely limited to the lower segment of the motor path. The cases mentioned in the note on p. 550 are an example of such rare limitation—an " exception that proves the rule."f We have seen that the pyramidal tracts are commonly degenerated, and it is probable that the degeneration often extends throughout their entire extent, and involves the motor cells of the cortex. J Thus the upper segment is often degenerated as well as the lower segment. In the presence of that complete degeneration of the lower segment which causes the atonic atrophy of the muscles, the degeneration of the upper segment can cause no symptoms. The loss of power that it would produce is also caused by the degeneration of the lower segment, and the latter abolishes the myotatic irritability, excess of which is the characteristic indication of disease of the upper segment. Hence the degeneration of the upper segment of the motor path for the muscles that present the atonic atrophy cannot as a rule be recog- nised during life, for it cannot produce its characteristic symptoms. What is the relation between the degeneration of the two segments, between the lateral sclerosis and the affection of the ganglion-cells ? We cannot assume (as some have been inclined to do) that the affection of the upper segment is secondary to that of the lower, because a * In a few anomalous cases, degeneration of the motor cells of the cord has been met with when no degeneration could be detected in the peripheral mixed nerves (see Kronthal, 'Neur. Centralbl.,' 1891, p. 133). The interpretation of these cases is at present uncertain. Possibly complete disappearance of some fibres left the rest apparently normal, although the skill of the investigators renders this explana- tion difficult to accept. Many more observations, however, are needed to justify a modification of current views. t Moreover the fact that these cases may not be primarily spinal must be borne in mind. J At the same time we have seen (p. 255) that the nutritional stability of nerve- fibres is less in their lower than in their upper part3, and that their isolated degene- ration may be greatest in the lower parts. That this may sometimes also be the case in these pyramidal fibres is suggested by the fact already stated that the degeneration may extend no higher than the decussation of the crura cerebri. CHRONIC MUSCULAR ATROPHY. 553 primary lesion of the grey matter, such as occurs in polio-myelitis, does not cause ascending degeneration of the related pyramidal fibres. Moreover, even a complete interruption of the pyramidal tracts is followed by no degeneration of their upper parts. Hence the intense degeneration met with in progressive muscular atrophy cannot be regarded as secondarv. Neither, when there is atonic atrophy, can we consider the affection of the upper segment to be the primary lesion, and to be the cause of that in the lower. In the seat of slight atrophy there are, as a rule, no indications of the preceding degeneration of the upper segment, which would certainly exist if this lesion were the primary change. Moreover degeneration of the upper segment does not necessarily cause any degeneration of the lower. It is a matter of every-day observation that intense degeneration of the termination of the upper segment may occur, from dorsal myelitis, for instance, with- out any considerable wasting of the legs, and such degeneration has never been known to excite the complete degeneration of the lower segment which causes atonic atrophy. Hence the only adequate explanation of the facts is that the degeneration of the upper and lower segments is simultaneous, or if not simultaneous, at least so far independent that neither is the cause or consequence of the other; both are the results of the same tendency to degeneration of the motor path.* Atonic muscular atrophy is thus, at least in many cases, the visible expression of a tendency to decay of the whole motor path from the cortex of the brain to the muscles. The weakness of some parts, as the legs, with excessive myotatic irritability, often going on to spasm, is explained by the degeneration of the pyramidal fibres for the legs, the lower segment being unaffected. It is easy to understand that the affection of the upper segment, and escape of the lower, or the affection of both, may vary much in relative extent, and give rise to !.he multiform varieties already mentioned. In such a case the nerve-cells for the part thus paralysed are normal. This weakness of the legs usually succeeds the wasting in the arms, and in most cases in which spastic paraplegia is followed by atrophy in the arms, the latter have not shared the spastic palsy. When this condition is associated with slight wasting of the legs, without con- siderable change in electrical irritability, the condition exists that we have more than once considered, in which we must assume that the motor nerve-cells of the cord, while structurally intact, undergo slight changes in nutrition. In this condition there are many nerve-cells of normal appearance in the grey matter; the alterations in nutrition are too slight to cause changes in aspect, or if there are such changes we have not vet learned to detect them. They are perhaps results of the degenerative changes in the termination of the upper segment; when such degeneration is secondary to a focal lesion of the cord or brain, the changes in nutrition of the cells seldom attain such a degree as to * See case published by Mott Brain,' 1895. 554 SPINAL CORD. arrest the mvotatic irritability, or to cause wasting such as attends the destruction of these cells. In some cases, however, the muscular wasting may be great, although the increase of myotatic irritability persists. In these cases, as we have seen, there is considerable rigidity of the muscles throughout the whole course of their wasting, the condition that we have termed "tonic atrophy " In such a condition it is common to find that many nerve-cells have disappeared or are very small, but others remain normal or slightly changed in aspect. Apparently, in addition to the degeneration of the upper segment and to the nutritional changes just mentioned, we have then a considerable degeneration of many, but not destruction of all, the elements of the lower segment. We cannot regard this as simply secondary to the degeneration of the upper segment, for the reasons already given. It must be the expression of a distinct pathological tendency similar to that which elsewhere causes the atonic atrophy and total wasting, but slighter in extent and later in time—insufficient to prevent the less affected cells from causing rigidity under the influence of the degeneration of the upper segment. It is doubtful whether the tonic atrophy ever goes on to atonic atrophy. Theoretically conceivable, it is certain that if it ever occurs it is extremely rare. Nor does it seem that atonic atrophy ever gives place to tonic atrophy with excessive myotatic irritability. The rigidity of tonic atrophy is due to the degeneration of the upper segment, but the effect is not produced if the lower segment is already the seat of such extensive degenerative changes as abolish myotatic irritability. The pyramidal fibres for the parts that are the seat of atonic atrophy are constantly found degenerated, although the muscles have been flaccid to the last. In the rare cases (mentioned on p. 540) in which muscles with atonic atrophy become rigid towards the end of the process, it is probable, as the tenderness suggests, that the rigidity is idiopathic, due to the changes in the muscles, and is not dependent on the central nervous system. It mav be the result of the increase in the interstitial connective tissue, and the longitudinal division and fibrillation by which the muscular fasciculi come to resemble bundles of connective-tissue fibres. It is also possible that similar idiopathic muscular changes may ultimately, in tonic atrophy, maintain and increase the rigidity that is primarily dependent upon the spinal cord. It has been mentioned that the cases in which the legs present the simple palsy and spasm, or the tonic atrophy, which indicate degeneration of the pyramidal tracts, have been separated by Charcot, and termed " amyotrophic lateral sclerosis," the separation being based on the assumption that in such cases the primary lesion is the degene- ration of the pyramidal tracts, and that the affection of the grey matter is secondary or " deuteropatnic," even where the atrophy is atonic. We have seen also that this assumption is unwarranted so far as the atonic atrophy is concerned. It is probable that the pyramidal CHRONIC MUSCULAR ATROPHY. 555 tracts are degenerated, if not constantly, at any rate in such a very large proportion of the cases of progressive muscular atrophy, that Charcot's distinction is, in effect, giving a new name to an old disease, and that the sequence is not that indicated by the name. Whether there are indications of lateral sclerosis or not depends on the circumstance whether the degeneration of the pyramidal fibres is or is not more extensive than the complete degeneration of the nerve-cells that causes atonic atrophy. If the latter is universal the pyramidal tracts may be totally degenerated, and yet there may be none of the characteristic indications of smli degeneration. On the other hand, both arms and legs may be the seat of the spastic paralysis that indicates pyramidal degeneration, and atonic atrophy may be hmited to a few muscles of the hands. Between these we have every grada- tion, in degree and distribution, of atonic atrophy, spastic paralysis, and tonic wasting. The process in the grey matter has been regarded by some as a chronic inflammation. The occasional rapid increase in the symptoms may be thought to be justification for this view; but the process in general is at the degenerative extremity of the series of nerve lesions. The principle involved in this question has been already discussed, and we have seen that, whatever be the nature of the primary process, we must recognise secondary tissue changes of independent energy, and that a distinct process of inflammation may occasionally form part of these (see p. 443). The significance of the occurrence of inflamma- tion may therefore easily be overrated, so far as concerns the question of the process, and the tissue-elements in which the disease begins. Diagnosis.—The simultaneous and gradual onset of weakness and wasting, the slow but progressive increase and extension of the symptoms, render the diagnosis of the developed malady simple and easy. At the onset, when only a single muscle or group of muscles is affected, the question arises whether the atrophy is local or is the commencement of a wider affection. Local atrophy is said sometimes to occur from great over-use of a muscle, especially one of the small muscles of the hand; but such a cause is extremely rare, and only to be suspected on the clearest indications. As a rule, the local atrophy from which the affection has to be dis- tinguished is that due to disease of the nerves. The wasting from disease of single nerves or at a plexus (as the brachial) is sufiiciently distinguished by its limitation, coupled with its rapid onset and associated sensory symptoms. Much more difficult is the distinction of some forms of multiple neuritis. The difficulty presents itself chiefly in two forms: ^i) when the spinal affection begins as sub- acute atrophic palsy (see p. 544); (2) when neuritis affects chiefly motor branches, as in the arms in lead poisoning, or in the legs in alcoholism, &c. In the first case it is necessary to wait for signs of slower wasting in other parts than those first affected before a diagnosis can be made. In the second, a careful search will generally 550 SPINAL CORD. reveal other symptoms of neuritis, and a known cause is usually obtrusive. In pachymeningitis of the cervical region, with considerable damage to the nerve-roots, the wasting in the arms may resemble that of progressive muscular atrophy, and there is often weakness with rigidity in the legs; but the wasting is less chronic in onset, and is always accompanied by distinctive sensory symptoms,—by acute pains, and usually by anesthesia, irregular in distribution. The same dis- tinctions suffice for the diagnosis in diseases of the ne:ve-roots of the cauda equina, as by a tumour. This may cause slow wasting in the legs, but there is always severe pain and loss of sensibility. Chronic disseminated myelitis may cause wide-spread muscular atrophy, but is distinguished by the presence of symptoms of irregular damage to other structures in the cord. The diagnosis from syringomyelia will be considered in the account of that disease. From primary muscular atrophy, " idiopathic atrophy," a variety of " muscular dystrophy," as it has been termed, the diagnosis is some- times easy, sometimes very difficult. It is easy in the pseudo-hyper- trophic form, and often also in the atrophic variety (the cases in wbieh no muscles are large), on account of its characteristic distribution, its course, the age at which it begins, and the tendency to affect many members of a family, and males more than females—features that will be presently described. Whenever several cases of muscular atrophy occur in a family, or during childhood or youth, the probabihty is great that they are idiopathic and not spinal. Indeed, the idiopathic form is to be suspected whenever muscular atrophy begins under twenty, unless there are distinctive spinal symptoms. But cases are sometimes met with in which idiopathic atrophy begins in adult life, and the distinction of such cases may be very difficult, and will be better understood after a perusal of the account of that disease. Prognosis.—The progressive character of the malady renders the prognosis, in every case, grave and uncertain. The chief guide is the observed tendency of the morbid process, both the fact of its actual advance and the energy it manifests. At the same time there is a possibility of arrest, greater in middle life than in old age. Some in- crease of atrophy in the parts already affected may occur for a short time after the process in the cord has ceased to spread—i he muscular wasting going on until it corresponds to the changes in the nerves that have already taken place. The prospect of arrest seems to be greater in the cases in which the wasting is strictly symmetrical and nearly simultaneous on the two sides than in those in which it is irregular, and attacks the second side when it has attained a marked degree in the first. Spontaneous cessation unfortunately seldom tends to occur until an advanced stage is reached; but, as the result of treatment, arrest may take place at any stage. The danger to Hfe is chiefly pro- portioned to the interference with the muscles of respiration, and to the indications of implication of the medulla. Bulbar symptoms CHRONIC MUSCULAR ATROPHY. 557 increase the gravity of the prognosis, especially when definite weak- ness can be recognised. Slight vague difficulty in articulation may remain stationary for years, and does not necessarily render the prognosis worse, especially if the atrophy elsewhere does not increase rapidly. If the malady ceases to advance, the prospect of any recovery depends on the rate at which the disease has progressed. Recent rapid loss of power may be to some extent recovered from, especially when the muscles present the degenerative reaction. Wasting that has existed for six months will probably persist unchanged. In a typical chronic case there is httle hope of any actual recovery of tissue or power. The effects depend on a slow destruction of nerve-elements, the renewal of which seems to be impossible. Treatment.—The first important element is to secure favorable con- ditions of life, and to maintain the general health in as perfect a state as possible. Fresh air and gentle exercise are important, but all fatiguing exertion should be avoided, and likewise all mental strain. When the patient becomes helpless, great care is necessary. Bedsores in this disease mean inattention, and may always be avoided. Only one method of treatment has, in my own experience, shown itself capable of arresting the disease, not indeed in all, but in more than half the cases in which it has been employed.* It is the admin- istration of strychnia by hypodermic injection. In seven almost con- secutive cases, in middle life, this treatment has been followed by arrest within a month of its commencement, and the arrest has been permanent in all the cases but one. In the senile cases the treatment has failed, but in most of them the disease was in an advanced stage, and the lumbar cord had begun to suffer. In some of the cases in which the result was prompt and distinct, strychnia given by the mouth had failed. It is conceivable that the different result is due to the fact that the agent is brought into more rapid contact with the nerve-elements, perhaps in purer form. Its action may possess greater momentum, as it were, and may tbus exert an influence on the nutrition of the nerve-elements much more considerable than when it is slowly absorbed from the alimentary canal. One injection daily has been given, at any convenient place. The nitrate is the most convenient salt, one fiftieth of a grain at first, quickly increased to one twentieth or one fifteenth. The injections need to be continued for months. When the malady is apparently arrested, it is well to intermit the injections for one week in three or four. Other nervine tonics seldom exert a distinct influence, but those that are useful in other degenera- tive diseases, as tabes, such as arsenic, may be given by the mouth at the same time as the injections are employed. In a malady so grave * At tirst I regarded the apparent result with doubt, but careful and repeated observations have made it impossible to consider the arrest of the disease as other than the direct effect of the treatment. It may be asked, Why should not a larger dose by the mouth be equally effective P It does not seem to be, is the only answer that can be given. 558 SPINAL CORD. it is desirable to neglect nothing that may possibly exert a beneficial influence. Local treatment of the muscles has very little influence on the wasting, as may, indeed, be expected from its nature. The most sedulous and skilful use of electricity, voltaic or faradic, fails, as a rule, to produce alone any effect on the course of the disease. If the malady is progressing at the same rate in each arm, and the muscles of one arm are regularly treated with electricity, while those in the other arm are left alone, no difference can be detected in the rate of wasting on the two sides. It is possible, nevertheless, that electricity some- times does a little good. In cases in which a rapid loss of power has occurred, and weakness is out of propoition to the wasting, some re- covery is possible, and there is no doubt that the excitability of the muscular tissue is maintained for a longer time by galvanism, although the bulk of the muscle may not be influenced. In other cases all that can be said is that the influence of electricity, properly applied, is in the right direction. Moreover the disease is one of those in which patients find it hard to believe that electricity cannot help them, and the probability is that their conviction will be fostered by some medical adviser. It is one of the diseases in which unjustifiable assertions are too often made that early electrical treatment would have been suc- cessful. It may be well, therefore, if only to satisfy the patient that nothing has been left untried, that a careful course of electrical treatment should be adopted. Faradism may be used if the muscles are sensitive to it, but if they present any greater irritability to voltaism it is better to use this. It is immaterial whether the appli- cation be confined to the muscles or whether one electrode be placed over the affected part of the spinal cord. The latter method has no disadvantages, but my own observations have failed to confirm the confident statements sometimes made regarding its superiority. It is very important that the current strength employed should be moderate. Strong applications often cause much subsequent pain, and even increased disability, and should be carefully avoided. I have known a rapid increase of weakness follow a strong application in a way that convinced the patient, at least, that the two were connected. Rubbing and massage of the muscles have been frequently employed, and of this treatment also it may be said that its influence is in the right direction, although usually inappreciable so far as the muscular atrophy is concerned. Combined with passive movement, the influence of rubbing in preventing and diminishing deformities is more distinct. No special bath treatment is of service. When the disease occurs in the subjects of syphilis, specific treatment invariably fails, and I have even known the progress of the disease to be distinctly accelerated by an energetic course of treatment both with iodide and with mercury. It is important that all treatment should be pursued in moderation, and that its effects should be carefully watched. ARTHRITIC MUSCULAR ATROPHY. 559 Arthritic Muscular Atrophy. Articular inflammation is almost invariably attended with rapid wasting of the muscles that move the joint. This occurs equally, whatever be the cause of the inflammation, and whether this is spontaneous or traumatic. It attends chronic as well as acute inflam- mations, and occurs in animals if joint inflammation is produced in them.* The muscles that waste are chiefly those which extend the affected joint. The atrophy is well seen in the muscles in front of the thigh when the knee is inflamed. If the ankle is affected, the calf muscles chiefly waste ; if the hip, the glutei; if the wrist, the extensor muscles of the forearm; the triceps when the elbow is affected ; the deltoid when the shoulder-joint is inflamed. In rheumatoid arthritis of the finger- joints such wasting is usually very conspicuous in the interossei, and especially in the abductor indieis. The atrophy, however, sometimes involves the flexors as well as the extensors, and rarely muscles of the limb that are near but do not move the affected joint. In very rare cases all the muscles of a limb have presented some wasting. Cases in which the atrophy is unusual in distribution, and especially when it is on the distal side of the affected joint, must be regarded with some suspicion, because inflammation may have spread from the joint to a nerve, and distant wasting may have been thus produced. It is said that there is sometimes, at the onset, a considerable weakening of the muscle, interfering with movement more than can be accounted for by the pain in the joint which movement causes, and that such initial palsy is transient (Yaltat, Duchenne). But the pain, by its inhibitory influence, usually obscures such palsy, which is indeed con- fessedly rare. The atrophy, on the other hand, may be regarded as almost con- stant. If the onset of the joint affection is acute, the wasting occurs rapidly; in a week or ten days a difference in the circumference of the limb may be detected by measurement. However long the affected muscle may be, the wasting involves the whole length of it, and not merely the part in the neighbourhood of the diseased joint. The degree varies ; usually moderate, and sometimes slight, it is occa- sionally considerable, so that the femur may be readily felt when the quadriceps femoris is the seat of the wasting; or the head of the humerus may be distinct, and the acromion prominent, if the deltoid is affected. Although the whole length of the affected muscle is always involved, if the muscle is a wide and compound one some parts may suffer chiefly. Thus in the thigh all parts of the extensor * Valtat, 'Archives generales,' 1877, tome xxx pp. 159 and 321. The subject has been discussed by Vulpian (' Lecons sur l'App. Vaso-moteur,' 1875, t. ii) and by Paget (' Lancet,' 1873, vol. ii, p. 727, in a lecture republished in ' Clinical Lectn-es and Essays,' 1875, p. 208). 560 SPINAL CORD. may waste equally, or the rectus or vastus interims may suffer more than the other parts. The wasting increases during two or three weeks, then becomes stationary, but continues as long as the joint disease lasts. When the joint has recovered, the muscles in most cases slowly regain their normal size. Occasionally, especially when the arthritis has lasted a long time, the wasting may continue for months or years after the joint disease is at an end. The electrical irritability of the atrophied muscles may be normal, but is often slightly lowered, equally to faradism and voltaism. The change is trifling, to be recognised only by comparison with the other side. There is generally a distinct and sometimes a considerable local increase in mvotatic irritability; the knee-jerk is excessive if the thigh muscles are affected, and a rectus-clonus can sometimes be obtained. A foot-clonus may be elicited when the ankle-joint is affected. Occasionally the increased irritability extends beyond the region of atrophy, so that, for instance, a foot-clonus may be obtained when the knee-joint and thigh muscles are affected, although there is no wasting b. low the knee. As an example of this, which illustrates also the occasional persistence of the atrophy, may be mentioned the case of a young man who jumped over a hoarding and twisted his left leg in doing so. He felt immediately severe pain in the knee, the joint quickly swelled, and became the seat of an acute inflammation which lasted for several weeks, and then slowly subsided. During the inflammation the thigh wasted. I saw him two years after the onset, and there was still considerable wasting, involving the whole of the extensor of the knee. The minimum circumference of the left thigh above the knee was three quarters of an inch less than that of the right, although there was no difference between the two legs below the knee. There was a slight diminution in faradic and voltaic irritability in the affected muscles. The knee-jerk was much more considerable on the left than on the right side, and there was well-marked foot- clonus in the left leg, but none in the right. A year and a half later the symptoms were unchanged. Yery rarely some contracture occurs in the opponents of the atrophied muscles. Sensory symptoms are as a rule absent, but there may be slight tingling in the skin during the acute stage ; it is said that areas of anaesthesia sometimes develop, but probably in such cases, inflammation has extended to a nerve iu the vicinity of the joint. Pathology.—Few facts have been ascertained regarding the con- dition in man. In one case, carefully investigated, the only change was in the muscles, and consisted merely in a narrowing of the fibres, one half of which were below the normal average, while no less than 84 per cent, fell short of a standard which, in health, only 21 per cent. failed to reach.* A few presented longitudinal striation (as in Fig. 150), and some of normal width were unduly tortuous; other- wise their aspect was normal. The sheath nuclei were proliferated in * Darkschewitsch, ' Neur. Cent.,' 1891, p. 353. ARTHRITIC MUSCULAR ATEOPHY. 561 places, and apart from this change the intermediate substance pre- sented local increase in quantity, especially where the fibres were narrower than normal. This observation agrees with those that have been made on animals, in which the condition has been produced, and in them, moreover, the motor nerves have been found normal (Valtat).* Indications of inflammation have been found in the joint nerves,f as might, indeed, be expected, whatever the mechanism of the atrophy. Visible changes in the spinal cord have never been discovered, but this does not exclude nutritional changes. We may, therefore, exclude from the possible causes, all forms of motor neuritis, both simultaneous, due to the cause of the joint inflammation, and consecutive, communicated to the adjacent nerve from the joint. The latter (a secondary extension of inflammation to the nerve) would manifestly not explain the affection of the whole of a muscle on the proximal side of the affected joint—as, for instance, atrophy of the whole extensor in arthritis of the knee— although the extension does occur, and must be recognised as an occasional event.J We must also recognise the possibility of a simul- taneous neuritis, with acute changes in the nerve-fibres, manifested by the reaction of degeneration in the muscles. The event is, how- ever, exceptional. It is certainly separable and to be separated from the common arthritic atrophy; but it is not easy to keep apart the two varieties of neuritis—the simultaneous and the consecutive__ when a case is seen only long after the onset, because a neuritis that arises by extension may travel along the nerve and present an ulti- mate distribution quite different from that which it possessed at the onset. For ordinary arthritic atrophies we must seek some other explana- tion. The nature of their cause long ago suggested to Paget a " reflex influence" on the muscles as the probable mechanism, and Yulpian and Charcot have suggested a similar hypothesis, assuming a derange- ment of the nutrition and influence of the motor cells of the cord, to be determined by the morbid impulses from the joint nerves, and to determine the alterations in the muscles. The theory receives impor- tant support from the fact that the wasting of the muscles is pre- vented by previous division of the posterior spinal roots (Raymond), which amounts, indeed, to an indirect demonstration of the fact that a reflex process § underlies the phenomena. It is doubtful whether we can go much further than this. By preceding hemisection of the cord it is increased on the side of the operation; but the conditions • Valtat, 'De l'Atrophie Muse, &c.,' Paris, 1877. See also Deroche, 'Etude cliu. et exp.,' Paris, 1890. t See Duplay and Cazin, 'Arch, gen.,' January, 1891. J E.g. to the ulnar, in rheumatoid arthritis of the hand (Bury, 'Med. Cbron.,' 1888, p. 182). See on this subject A. E. Garrod, 'Med.-Chir. Trans.,'Ixxi, 265; also Pitres and Vaillard, * Eev. de Med.,' 1887, No. 6. § R.ymond, 'Rev. de Med.,' 1890, 374. vol. I. 36 562 SPINAL CORD. are here more complex, and the demonstration of the reflex relation less simple, than in the result of division of the roots. The increased knee-jerk, &c, that attend the wasting, and the curious fact that arthritis may set up a degeneration of the spinal cord, apparently beginning in the termination of the pyramidal fibres (see p. 493), should be kept in mind. They are certainly significant, and suggest that the influence from the joint nerves acts on the " con- trolling structure " of the muscle-reflex centre (see p. 240) ; but more facts are needed before a valid hypothesis can be framed. Diagnosis.—The moderate degree of the wasting, with correspond- ing change in electrical reactions, coupled with the wide extent of the alteration, embracing the whole of the muscles involved, constitute a distinctive characteristic—distinctive, at least, when taken in con- nection with the preceding joint affection which is the cause of the atrophy. A primary neuritis, causing secondary arthritic adhesions, has its own features—their wider range, so far as function is concerned, and especially their limitation to nerve distribution. Hardly any other malady is likely to be confused with it, except some graver disease, while still in an early sta~* ; but such an affection can only be dis- tinguished by waiting until the nature of the malady has had time to show itself. Prognosis.—When the inflammation of the joint is brief in dura- tion, recovery of the muscles may be anticipated with confidence. In children, even after prolonged joint disease, the muscles usually regain their normal bulk. In adults the wasting often lasts for a long time after the joint is well, and a cautious prognosis should be given if the arthritis has lasted long. Even if slight wasting is persistent, normal power is usually recovered; but, as the case mentioned above shows, the symptoms sometimes continue for years. The prognosis should be especially cautious where there is a marked increase in myotatic irritability, or if the atrophy shows a disposition to involve other muscles of the limb than those concerned in moving the affected joint. Treatment.—The chief treatment is local,—electrical stimulation of the muscles, and gentle rubbing. It is doubtful whether drugs have any influence on the condition, but small doses of strychnia may be given, or added to whatever agent is giveu for the joint affection. As long as the joint is inflamed, treatment rarely causes any increase in the bulk of the muscle. It is of great importance to secure the early recovery of the joint, and to avoid all influences that cause pain in it, since, as we have seen, it is apparently through the sensory nerves that the joint affection exerts its injurious influence. When the arthritis has ended> the muscles usually, recover slowly without assistance, but it is probable that the local treatment accelerates the process. The form of electricity is of little consequence; either faradism or voltaism may be employed, but snould only be used in sufficient strength to cause gentle contraction. The muscles act MUSCULAR DYSTROPHIES. 568 readily to faradism, and a mild faradic current is, as a rule, the best to employ. All painful stimulation of the sensory nerves should be avoided. Muscular Atrophy from OvER-r^E. Muscles that are much used sometimes waste. The effect is seen most frequently in the small muscles of the hand, especially in persons of weakly constitution, who use these muscles unduly. Thus a young lady devoted many hours a day to "illuminating," during several years, and then some muscles of the thenar eminence began to waste, and became considerably atrophied. Such wasting is scarcely ever met with in the larger muscles, but has been observed in the biceps, consecutive to hypertrophy, in Sheffield smiths (Frank-Smith;. The electric irritability is gradually lowered in this local wasting, equally to both currents, as it is in progressive muscular atrophy. We do not know whether this wasting from over-use is purely local, or whether the related ganglion-cells of the spinal cord fail first, and the muscular wasting is secondary to their atrophy. Gull said many years ago, "it is as reasonable to infer a lesion of the grey matter from overwork as of the muscles."* The wasting often persists when the over-use of the muscles is discontinued. Hyper- trophy from over-use does not usually give place to atrophy. These two facts are somewhat in favour of the view that the lesion is primarily of the nerve-cells. The wasting in these cases shows no tendency to extension beyond its original limits. The treatment is, first, the cessation from the excessive exertion of the muscles; secondly, the improvement of the general health, and the adminis- tration of nerve tonics, especially of strychnine; and thirdly, the gentle electrical stimulation of the muscles by either faradism or voltaism. THE MUSCULAR DYSTROPHIES. Idiopathic atrophy, which is primarily muscular, although it is not one of the diseases of the nervous system, is commonly described with them, because it frequently presents so close a resemblance to the spinal atrophy just described as to be distinguished with some diffi- culty. Moreover, even the varieties that do not present this close resemblance were for a time, and indeed until lately, believed to be of central nature, to depend on the spinal cord, and to be rightly included among its diseases. Hence the custom of thus describing them has become established, and has now to be followed, although we know that it is based on a mistaken theory. At the same time, not only * ' Guy's Hosp. Reports,' 1862, p. 246. 564 SPINAL CORD. has the method the advantage of convenience, but it has also some measure of scientific justification. The muscles are more closely allied to the nerves than to any other structures, as regards both physiological properties and pathological susceptibility, and it is doubtful whether any other association would better befit these diseases. The idiopathic myopathies have received much attention during the last few years, and many new facts have been ascertained with regard to the different varieties and their relations to each other. The treatise by Erb * has had the effect of giving unity and cohesion to what was formerly a collection of disconnected types, and has con- clusively demonstrated the essential identity of the different varieties hitherto described. The so-called pseudo-hypertrophic variety of muscular affection has been recognised under this name ever since its graphic description by Duchenne.f The features of this were muscular weakness associated with enlargement of muscles, sometimes a few, sometimes many. He also described in the same work J another form of paralysis which he supposed to be similar in its etiology to the progressive muscular atrophy of adults, and which he named " atrophie musculaire progressive de l'enfance." This was characterised by wasting of the muscles of the face as well as of the limbs, and also by its tendency to affect more than one member of a family. Leyden in 1875 § proposed to separate the hereditary forms of muscular atrophy from those of the Aran-Duchenne type. He pointed out that the hereditary form tends to commence in early life, to affect several members of the same family, especially the males, and he directed attention to the resemblance between the hereditary form and the pseudo-hypertrophic of Duchenne. In 1879 || Gowers in a clinical lecture gave a full description, from numerous clinical observations, of pseudo-hypertrophic paralysis, and also set out all that was known of its pathological anatomy, and in this lecture clearly recognised that hypertrophy and atrophy may be combined in different proportions, and that there are cases that connect the two extremes—in some enlargement of many muscles, in others wasting in all. Such a view affords a glimpse of the group which Erb % afterwards clearly outlined under the name of the "juvenile form of progressive muscular atrophy." From a consideration of the characters and histories of these cases Erb concluded that the three varieties—the juvenile form, the here- ditary form of Leyden, and pseudo-hypertrophic paralysis—were all varieties of one condition, for which he proposed the designation • 'Dystrophia muscularis progressiva,' Leipzig, 1891. t • Electrisation localise^' 3rd edit., p. 595. I Ibid., p. 518. § ' Klinik der Ruck. Krank.,' ii, p. 525. || ' Lancet,' 1879. % ' Deutsch. Arch. f. klin. Med.,' Bd. xxxiv, g. 4G7. MUSCULAR DYSTROPHIES. 565 " dystrophia muscularis progressiva." The next important step in the development of our knowledge took place in 1885, when Landouzy and Dejerine pubhshed* an exhaustive paper on what they named. '' Myopathic Atrophique." It dealt with observations of an exceed- ingly interesting group, the essential characteristics of which were wide-spread muscular atrophy commencing in the face, and without hypertrophy. These cases were really identical with those described by Duchenne as "atropine musculaire progressive de l'enfance," but the later observers completed the description by the discovery from post-mortem examination that it did not depend upon, nor was it associated with, changes in the spinal cord, but that it was a muscular affection without detectable nervous lesions. They regarded their cases as constituting a distinct and separate variety of myopathy, relying upon the commencement in the face and the absence of hypertrophy, and they refused to recognise the essential identity of their cases with those of Erb, in spite of the fact that in one of their quoted cases the face was not affected, and considerable enlargement of the calves, if it was not present at the time, had been a few years before. The latest and most important contribution to the elucidation of this disease is the work of Erb already alluded to.f In this he subjects to close examination numerous clinical records of cases of the different varieties already referred to, and makes it clear by the observation of cases of different types among members of the same family, by the description of cases which form distinct connecting links between the different varieties, and by the observation of the histo- logical conditions in the affected muscles, that all four varieties— pseudo-hypertrophic paralysis, the juvenile form of Erb, the Lan- douzy-Dejerine type,—identical with the atrophie musculaire pro- gressive de l'enfance of Duchenne—are but branches of a parent stem, and essentially the same disease. He proposes a division into two main groups, viz. (1) children, (2) adults; and in the former he would distinguish two varieties, the hypertrophic and the atrophic. In the hypertrophic he would further distinguish those with pseudo- hypertrophy and those with true hypertrophy, and in the atrophic variety those with, and those without involvement of the face. Such a division is of course an arbitrary one, for even between the two chief varieties no hard and fast line can be drawn ; and the same is true in a greater degree of the minor divisions. It has, therefore, seemed best to describe the disease on the same lines as have been followed in previous editions of this book, with a due recognition of the fact that any particular case met with may partake of the characters of simple atrophy and also of pseudo-hypertrophic atrophy, and indeed may at one time be regarded as belonging to one group, and at another to the other. All the diseases of this class seem to depend on a defective tendency in * ' Rev. de Medecine,' 1855. f * Dystrophia muscularis progressiva,' Leipzig, 1891. 566 SPINAL CORD. the development of the germinal tissue which forms muscles; they are essentially congenital diseases. Although they are, in most cases, merely potential maladies at the time of birth, and sometimes for years afterwards—even occasionally during a considerable part of life,—the morbid tendency does sometimes attain actual development in the earlier years. But we know nothing, or almost nothing, at present, of any other cause than this developmental tendency; we know nothing of these diseases as acquired maladies, the result of influences acting on a healthy and normal organism. Another fact of their general pathology is analogous to that which we have already considered in connection with developmental diseases of the central nervous system. It depends on the double constitution of muscular as of nervous organs, on the presence of interstitial con- nective tissue between the contractile elements, and on the relation of both to trophic tendencies. An overgrowth of the interstitial tissue may concur with wasting of the fibres, and this overgrowth may be abnormal in its features. Hence Erb has chosen the term, already referred to, " muscular dystrophy," as a more precise designation for the class—a term which is likely to obtain general acceptance. The important fact to recognise is that there may be either a simple defect in the growth of the fibres, ultimately leading to their disappearance, or there may be, with this, an overgrowth of the connective tissue, either a simple hyperplasia, or a perverted growthin which fat-cells form. These cells increase its bulk, but are ultimately removed. The muscular fibres also sometimes present hypertrophic enlargement, but simple wasting is the most common change. The symptoms by which these changes are manifested vary accord- ing to the nature and seat of the alteration. In all cases muscular power fails as the contractile fibres waste. The chief difference in aspect, however, depends on the seat of the affection and the effect of the interstitial changes, and especially on the frequent enlargement of muscles from the formation of fat in the fibrous tissue. This produces the semblance of hypertrophy that has led to the name "pseudo- hypertrophic paralysis " being applied to the cases in which it is present. The amount of enlargement varies much ; the fibrous tissue alone may cause none, but it is sometimes great and wide-spread in the cases in which fat is formed. In all, however, a primary shrinking of the muscles, often preceded by a true enlargement of the fibres, is due to the wasting of their proper substance, the result mainly of a defective tendency of vital endurance or growth, and only in a slight degree to the influence of the interstitial tissue when this is increased in quantity. Thus certain varieties are constituted by the external manifestation of the muscular changes. Even in the class in which pseudo-hyper- trophy occurs there may be no change, or only diminution in the size of the muscles, but with increased firmness, as the accompaniment of the lessened power. When there is enlargement, this may or may PSEUDO-HVPERTUOPHIC MUSCULAR PARALYSIS. 567 not correspond in time to the loss of power, since the muscular fibres may waste either during interstitial growth, or after this tissue has undergone the atrophy which ultimately supervenes. Thus we may have two classes of cases belonging to this type, one with enlargement of muscles, few or many, the other with only wasting of muscles, the two corresponding in position and in the general course and relations of the affection. In another form there is never an interstitial growth of fat, and probably no considerable increase of fibrous tissue; simple atrophy of the fibres is its pathological characteristic, while primary shrinking of the muscles is its external manifestation. The shoulder muscles are prone to suffer most, and in some cases there is a peculiar affection of the face. These cases are also more variable in the time of life at which the symptoms begin. But these varieties, as we have already state 1, are connected by cases which to some extent combine the various features. Such combined forms forbid the separation of the types, which, nevertheless, frequently maintain so distinct a course in many members of a family, even through several generations, that we are compelled to recognise their distinctness, although we cannot divide them altogether. . The essential element in the disease has been spoken of as a " quali tative" defect, which entails an imperfect development, manifested sooner or later by the defective vitality of the proper elements of the tissue. Bat there is reason to believe that the defect is not always merely qualitative. In some cases the defect in certain muscles is so absolute at so early a period as to make it almost certain that these muscles or parts of muscles are congenitally absent, and that the germinal effect is thus quantitative as well as qualitative. The muscles in which this apparent failure is observed vary in the several forms, and will be mentioned in the account of these. The peculiar form of atrophy, which differs from the others in the early affection of the muscles supplied by the peroneal nerve, is separately described, and its features are not included in these remarks. Pseudo-hypertrophic Muscular Paralysis (Lipomatous Muscular Atrophy, &c). The affection thus designated usually manifests itself during the later developmental period of childhood, and clearly depends on a morbid developmental tendency, which is often present in several members of the same family. It is characterised by a progressive change in the size and diminution in the power of many muscles. The apparent cause of the change has been already mentioned. Isolated cases, which can now be recognised as examples of this disease, were recorded in England in lH'M) (Sir Charles Bell) and in 568 SPINAL CORD. 1847 (Partridge), and in Italy in 1838. A series of cases was described by Meryon in 1852, and Oppenheim in 1855, but enlarge- ment of the muscles was not conspicuous in these.* Several remarkable examples had already come under the notice of Duchenne, who was busy exploring the field of muscular paralysis with the aid of " localised electrisation." He recognised its novel features, and pub- lished an account of it in 1861, under the name by which it has since been generally known. Etiology.—Our knowledge of the causes of the disease is limited to a few general facts. Males furnish the majority of the cases ; they suffer at least four, and perhaps seven times as frequently as females. In the latter, moreover, the malady is slighter in degree, later in development, and less frequently causes death. The disease occurs rather less commonly in isolated cases than in family groups. The number in a family has varied from two to eight. As many as eight brothers suffered and died in the family described by Meryon, while all the daughters escaped. In a family known to the writer, four sons have suffered and none of the daughters ; in another instance two daughters are affected and no sons. Thus there may be a tendency in a family to the affection of one sex, and not the other; but, on the other hand, children of both sexes may suffer in the same family. In many instances in which several members of one generation are affected, no antecedent cases can be traced in the family; the malady, while congenital, is not hereditary. In other families antecedent cases can be traced, and these are invariably on the mother's side. The disease is thus transmitted by women who are not them- selves its subjects. In a case in which four brothers suffered, the mother's brother and sister were likewise affected. Again, a brother and sister were diseased, one daughter of a second sister, and three daughters of a third sister. In another instance a boy suffered, and his sister, unaffected, had two sons diseased and a daughter free, of whose children two sons were the subjects of the malady. Thus the congenital tendency is exclusively due to the maternal element in the embryo. This is also shown by a fact many times observed, that the children of the same woman, by different husbands, suffer in the same way. Indirect hereditary tendencies such as are indicated by the occur- rence of diseases of the nervous system, can be traced so rarely that it is doubtful if they have any influence. Neither the age of * Nevertheless Meryon's cas-es (' Med.-Chir. Trans.,' 1852) certainly belonged to this variety. Conclusive proof of the fact is afforded by cases in collaterals which have come under the writer's observation in near and distant branches of the same family. Other evidence of the fact is described in a 'Clinical Lecture on Pseudo- hypertrophic Paralysis' (London, Churchill, 1879). The chief literature is referred to in that lecture; the numerous papers that have appeared since have added chiefly to our knowledge of the characters of the allied forms of idiopathic atrophy, &c, and the relations of these to the pseudo-hypertrophic variety, and are referred to on a later page. PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 569 parents, nor their intemperance, appears influential, and their con- sanguinity becomes effective only when raised in energy by repetition. Thus, in a family known to me, the intermarriages during five genera- tions were very numerous, and of eight children in the present family five are albinos, and two of these are the subjects of pseudo-hyper- trophic paralysis. In another family of eight, whose parents were double first cousins, six children suffered from muscular dystrophy, different forms being represented in different members of the family. The disease always manifests itself during the period of development, sometimes in the early stage of growth, at the close of infancy, often only during mid-childhood, rarely not until growth is nearly ended. In a third of the cases the first symptoms are noted when the child first attempts to walk, which is usually a little later than in healthy children; very rarely indeed the child has never walked. In about another third the child seems well until it is four, five, or six years old, and then impairment of power attracts attention. In three quarters of the cases the disease manifests itself before the tenth year. Rarely the patient is conscious of no symptoms until after puberty, at the age of eighteen or twenty; but in such apparently late onset there has been enlargement of muscles long before power became impaired, and the disease began much earlier than it seemed to do. One patient, for instance, in whom weakness was only noticed when she was twenty, had been often " chaffed," when a young girl at school, on account of her " tea-kettle calves." Neither social state nor general constitutional condition seems to influence the occurrence of the disease, but its manifestation has sometimes been apparently accelerated by influences that disturb the general health ; it has been first noticed, for instance, during convalescence from some general illness. Symptoms —Impairment of power usually attracts attention before any change is observed in the size of the muscles, or if these are noticed to be large, it is with feelings of parental pride rather than with suspicion, in spite of the fact that the children often walk clumsily, fall with ease, and rise with difficulty. The act of going upstairs is especially difficult to them; the child has to take hold of the banisters and pull himself up. The muscles may at first present nothing unusual, especially in slight cases, or if the child is fat, as is frequently the case. But at the age of five or six years an unnatural enlargement of certain muscles is usually conspicuous, especially when there is a contrast between these and other muscles which are small. If enlargement is almost universal, it is Ubually great and conspicuous. The enlarged muscles usually for a time become still larger in comparison with the others, but afterwards they cease to increase and ultimately become smaller, first relatively and then absolutely. This change occurs earlier in some muscles thau in others, and it may result in a condition of distinct atrophy. 570 SPINAL CORD. Among muscles that are most frequently large, those of the calf take the first place. They sometimes attain a remarkable size. I have measured a calf 14^ inches in circumference in a boy of twelve. The muscles in front of the lower leg are less frequently enlarged, but sometimes project beyond the edge of the tibia. The extensors of the Fio. 155. Fio. 156. Fio. 157. Figs. 155 and 156.—Two brothers, aged four and seven, suffering from pseudo-hypertrophic paralysis. Fio. 157.—Partial enlargement of rectus, the vasti being small. knee are often big; occasionally the rectus or vastus internus is alone increased in size (the rectus in Fig. 157), and the other parts may be normal or small; less frequently all parts are small. The flexors of the knee commonly escape. The glutei are frequently conspicuously large; the flexors of the hip are, of course, inaccessible to observation, but they are usually feeble, and no doubt diseased; there is generally enlargement of the lumbar muscles, and disease of a peculiar and important character in those of the shoulder. Of all the muscles of the body, next to those of the calf, no one is enlarged more frequently or in greater relative degree than the infra- spinatus. It often stands out so conspicuously that its edge is apt to be mistaken for that of the scapula (Figs. 158 and 159). The supraspinatus is sometimes also prominent, but its condition is usually concealed by the trapezius, which is little involved. The deltoid is also frequently large; the serratus rarely. The pectoralis is never enlarged, but, on the other hand, its lower half is wasted or absent PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 571 in a large proportion of the rases, and with this the latissimus dorsi, which has the same action in depressing the raised arm (see p. 37). The teres major may share the wasting of the latissimus. The other muscles of the arm suffer in diminishing degree and fre- quency from above downwards. The triceps and biceps are sometimes enlarged, the former more frequently than the latter, but occasionally only in one part. Both t^ese muscles are sometimes wasted. The forearm muscles suffer in only a small minority of the cases, and the intrinsic muscles of the hand usually escape altogether. This usual escape of the intrinsic muscles of the hand affords a very marked contrast to spinal muscular atrophy, in which they suffer early; Fig. 15s.- Pseudo-hypertrophic paralysis Absence of latissimus dorsi, enlargement of infraspinatus. (From a photograph.) Pig. 159.—Wasting of latissimus dorsi and serratus; enlarge- ment of infraspinatus, suprn- spinatus, and deltoid; atrophy of biceps and triceps. (By Dr. H. R. Spencer, from a photo- graph.) but no rule is free from exception, and although the escape of the hands in the idiopathic affections is almost constant, it is not quite invariable; slight (or commencing) implication of the intrinsic muscles has been met with in very rare instances that were otherwise typical,* * E.g. Sachs, 'New York Neurol. Soc.,' Oct. 2nd, 1888; Baumler, ' Sudwest. Neurol. Ver.-amml.,' Freiburg, 1888. I have once met with wasting of the extensors of both phalanges of one thumb, and enlargement of the abd. indicis has been observed (Taylor. Clin. Soc, April 24th, 1891),and fatty growth in the thenar muscles (Berger, ' Aicli. f. Psych.,' Bd. xiv). 572 SPINAL CORD. and quite distinct from the "peroneal type" to be presently men- tioned. The muscles of the neck are very seldom affected, but I have noted, in a few cases, wasting of the clavicular part of the sterno-mastoid. Those of the face do not suffer except in extremely rare cases intermediate between this and the third type (see also "Westphal, ' Charite Annalen,' 1887, xii, p. 477), but in the patient shown in Fig. 162 there was considerable enlargement of the masseters. The tongue has been increased in size in a few instances. The other muscles supplied by the cranial nerves always escape. The diseased muscles are weak, but the impairment of power is to some extent irrespective of the change in size. The muscles that are abnormally small are generally weaker than those that are abnormally large; and in the latter the weak- ness increases with the wasting. In the legs the greatest weakness is in muscles that are inaccessible to ex- amination—the flexors of the hips; next in order of weakness come the Fia. 160.—Mode of obtaining extension of hips in pseudo-hypertrophic paralysis. F, ful- crum of the lever formed by the femur. P. mean position at which the power is applied by contraction of the quadriceps femoris. W", position of weight in the ordinary mode of rising, to, the place to which part of the weight is transferred by putting hands on knees. FiG. 161.—Mode of rising from the ground in pseudo-hypertrophic paralysis. extensors of the knee and the extensors of the hip. The muscles below the knee usually retain considerable power for a long time and the extensors of the ankle fail before the flexors. In the upper limbs the depressors of the arm are usually alone weakened during the early period of the disease, but subsequently the shoulder muscles suffer PSEDDO-HYPERTROPHIC MUSCULAR PARALYSIS. 573 then the triceps and the biceps, while the muscles that move the hand commonly retain good power to the last. The distribution of weakness in the legs causes certain peculiar defects of movement which are very characteristic, and some are even all but pathognomonic of the disease. The difficulty in going upstairs is especially due to the weakness of the extensors of the knee and hip. The defect of the extensors of the hip causes the gait to have a peculiar oscillating character, in which the body is so inclined as to bring the centre of gravity over each foot, on which the patient suc- cessively throws his weight, because the weak gluteus medius cannot counteract the inclination towards the leg that is off the ground unless the balance is exact. The greatest defect, however, is in the power of rising from the floor, and the most characteristic peculiarity is the mode in which this is achieved, if it be still possible, and no objects are near by which the patient can aid himself. He commonly has not sufficient power to extend the knees when the weight of the trunk is on the upper extremity of the femur, which is then a lever in which the power, applied between the fulcrum and the weight, acts at least advantage. He therefore places his hands on his knees, as in Fig. 160 ; and his arms thus bring much of the weight of the upper part of the trunk on the femur close to the fulcrum, between this and the power, which can then act at greater advantage. Moreover the mere weight of the head which is in front of the arms tends to aid the extension. This, indeed, may effect the extension of the knee without the aid of the extensor muscles, as any one may ascertain by observing the mobility of the patella in this attitude. When the knees are extended the power of the extensors of the hip may be sufficient to raise the body into the upright position, or the patient may aid them by an upward push with the hand as he takes it off. If, however, these extensors are weak, the hands are often moved higher and higher up the thighs, grasping alternately, and thus pushing up the trunk. To get thus the requisite support, the knees must not be quite extended ; and if their extensors have no power the device cannot be employed, and the patient is altogether unable to rise. In many cases, especially when extension of the hip is easy, the patient achieves the extension of the knees in another way; he puts the hands on the ground, stretches out the legs behind him far apart, and then, the chief weight of the trunk resting on the hands, by keeping the toes on the ground and pushing the body backwards, he manages to get the knees extended, until the trunk is supported by the hands and feet, all placed as widely apart as possible (Fig. 161, 2). Next the hands are moved alternately along the ground backwards, so as to bring a larger portion of the weight of the trunk over the legs. Then one hand is placed upon the knee (Fig. 161, 3), and a push with this, and with the other hand on the ground, is sufficient to enable the extensors of the hip to bring the trunk into the upright position. The shortening and contraction of certain muscles lead to another 574 SPINAL CORD. group of symptoms—distortions due to permanent alteration in the position of joints. Some of these are produced, as are distortions in other forms of muscular weakness, by shortening of the less affected opponents of the weaker muscles. Thus the knee-joints become fixed by the contraction of the flexors, and the elbow by the contraction of the biceps when the triceps has lost all power. These contractions only occur late, and are usually facilitated by the habitual flexion of the knee- and elbow-joints. But the deformity at the ankle-joint, which results from contraction of the calf muscles, commences earlier, before their opponents are weak, and is the result of shortening of the muscles. As a consequence of it, the patient cannot get the heels well upon the ground, and the foot cannot be flext \ passively beyond a right angle. The gradual increase of the contraction results in considerable " talipes equinus; " and as power lessens, the patient is able to walk less, and the consequent loss of the extension involved in the act permits a rapid increase in the contrac- tion. Ttie feet, as Fig. 162 shows, soon assume a pos- ture of extreme extension, the dorsum being in a line with the front of the leg, or forming tvith it a convex curve. A subluxation of the ankle-joint takes place, and the articular surface of the astragalus, its anterior extremity, and that of the os calcis, form three prominences under the skin. When this reversal of the ankle occurs, the tibialis anti- cus can no longer act as a flexor. Another deformity, which is due chiefly to muscular weak- ness, is curvature of the spine. An antero-posterior curve, with the concavity backwards, is an early symptom of the disease, and it may become extreme, the upper part of the trunk being carried so far back that a vertical line from the scapula falls an inch or more behind the sacrum. It is due not to the weakness of the trunk muscles, but to that of the extensors of the hip, in consequence of which the pelvis is inclined forwards, carrying with it the lower lumbar vertebrse; hence the upper part of the trunk has to be held far back to keep the centre of gravity of the body over the feet. The proof of this mechanism is that when the patient sits, and the pelvis is supported on the ischial tuberosities, Fig. 162. —Late stage of pseudo-hypertro- phic paralysis; a boy fourteen years old, with muscular contraction and wasting, and lateral curvature of the spine. PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 575 the lordosis disappears. It is, indeed, replaced by an opposite curve, in which the back becomes convex, clearly due to the weakness of its extensor muscles. This curve may become very great, as in the case shown in Fig. 163. The weakness of the spinal muscles also permits the occurrence of lateral curvature (Fig. 162), influenced, in its direc- tion, by the habitual posture and the preponderance of weakness on one side or the other. Fio. 163.—Lad aged fifteen; late stage; wasting of thighs; inability to sit upright in consequence of the weakness of the spinal muscles. The electric irritability of the muscles is only altered when distinct weakness or wasting has set in, when it is lowered alike to faradism and voltaism. There is never any trace of degenerative reaction. The knee-jerk may be at first normal, but as the extensors of the knee become feeble, it is always lessened and gradually disappears. It is never excessive, and in all advanced cases it is lost. Sensation is unaffected, and so also are the sphincters in the vast majority of cases Very rarely there has been, towards the end, a slight difficulty in the retension or expulsion of urine, to be regarded, perhaps, rather as a complication than as an effect of the disease. All other functions of the nervous system are commonly normal, including those of the sym- pathetic. The mental development of the subjects of this disease is generally beyond that of other children of the same age, doubtless on account of the indirect influence of a malady which withdraws them from active amusements; mental defect is a pure complication. The rate of progress of the disease and its duration vary much. After some years, often between ten and fourteen, the power of standing 1 >ecomes lost in consequence of the increasing weakness and the con- traction of the calf muscles. When the patient ceases to walk the muscular disease makes more rapid progress, deformities become greater, and the patient may become almost helpless, except in the hands, and yet live on for several years. Death is sometimes due to 576 SPINAL CORD. some intercurrent malady, as an acute specific disease; but generally the lessened respiratory power causes some chest affection to develop, or one that should be trifling, to become grave. Life is thus ended by acute pneumonia or bronchitis, or by chronic lung disease—a form of pneumonic phthisis or broncho-pneumonia, which develops gradually, with little febrile disturbance. There is never sufficient paralysis of the respiratory muscles to cause death directly. The duration of the stage of helplessness depends very much on the care which the patient can obtain. In the cases in which muscular power remains good until after puberty, the progress of the disease is generally slow. The patient may reach the age of thirty before power is much impaired. It is possi- ble that, in some cases, the disease never attains a considerable degree. More frequently, however, after slight symptoms have lasted for some years, a rapid increase occurs, and very few patients reach the age of forty. The course of the disease is slower in girls than in boys, and females furnish a relatively large proportion of the late cases. Varieties.—The chief varieties of the disease depend on the age at which it commences, and on the condition of the muscles, whether they are large or small. In rare cases a single muscle may be large, and the rest small, as in Fig. 164, in which only the vasti were increased in size. Or everywhere and from the first the muscles are smaller than nor- mal, and they progressively waste. Such cases are not uncommon ; in the first group of cases described (by Meryon), enlargement of muscles was inconspicuous. Many cases in which all muscles are small belong properly to the form considered in the next section. But it must be remembered that there are intermediate cases which form links between the two chief types. The cases described by Meryon must be regarded as examples of the pseudo-hypertrophic form (see p. 568), but they present many points of resem- blance to the " simple atrophy " described further on. Complications.—Congenital mental weakne ss, due apparently to defective development of the brain, sometimes complicates pseudo-hypertrophic paralysis. In rare cases there have been indica- tions of some other morbid condition of the central nervous system, such as epilepsy. It is uncertain in what light the slight occasional affection of the bladder is to be regarded, whether as an invasion of the vesical muscles or as a central complication. Vigoroux has recorded a case in which the symptoms of pseudo-hypertrophic paralysis were combined with the peculiar rigidity of Thomsen's disease. Of course the subjects of the disease are liable, like other children, to various Fig. 161.—Enlarge- ment of the vasti and not of the rectus. In this case all other muscles were below normal size. PSKUDO-HYPKRTROPHIC MUSCULAR PARALYSIS. 577 affections of the nervous system; I have seen both chorea and polio- myelitis as merely accidental complications. Pathological Anatomy.—It is rare at the time of death for any muscles to be actually larger than natural. Sometimes, however, they are enlarged, and the fibres themselves have been found hypertrophied, just as they have been in excised parts. There has also been found a great increase in the nuclei, atrophy of the fibres, vacuolation, and division of fibres. Most of those that are affected are below the normal size. They are pale and yellowish in colour, and often, to the naked eye, resemble perfectly masses of adipose tissue. The resemblance is not merely one of aspect. As seen under the micro- scope, it may be difficult for the observer to realise that he is not looking at a fatty tumour. Nothing may be at first visible but fat- cells, precisely like those of adipose tissue. Among the cells, however, are tracts of nucleated fibrous tissue, and a closer examination of these shews that the tracts contain also muscular fibres (Fig. 165), most of FiG. 165.—Gastrocnemius muscle; muscular fibres, irregularly nar- rowed and in part degenerated, lie among tracts of nucleated fibrous tissue, separated by adipose tissue. them much narrower than normal. They are also irregular in width ; a broad fibre, for instance (as in the figure), suddenly becoming narrow. The fibres for the most part preserve their transverse striation, but where they are narrowest this may have in part disappeared, either by granular degeneration, or, more commonly, by a simple fading of the striae. In the narrowed fibres the striae are sometimes farther apart than normal. In other parts broad fibres may be seen, normal or VOL. I. 37 578 SPINAL CORD. nearly normal in aspect (Fig. 166), coursing among the fat-cells, and accompanied by a smaller amount of fibrous tissue. Fibres occasion- ally present fatty degeneration, a longitudinal striation or Assuring, vitreous ("waxy") degeneration, or vacuolation, but these are rare. Some empty sarcolemma sheaths may be seen where the narrowing of the fibres is greatest. In muscles that still preserve some red tint the amount of fat is less, and there is often a relatively larger amount of interstitial fibrous tissue. Very rarely, in some part of a muscle there has been only wasting of the fibres, without the interstitial change, present elsewhere (Singer, in the triceps). FiG. 166.—Gastrocnemius muscle; two nearly normal muscular fibres, accompanied by fibrous tissue, surrounded by fat-cells. In some of these the interstitial tissue may be almost entirely fibrous, a few fat-cells only being visible here and there. In such muscles it is common to find the fibres more damaged than in those in which the growth is partly fatty. It is chiefly in the latter that many normal fibres are seen. Muscular fibres larger than normal are sometimes found after death. Such fibres have been seen in frag- ments removed during life by excision, or by a "harpoon-trocar." It has been stated that the increased size was perhaps due to a vital contraction under the mechanical stimulus involved in the extraction. Sometimes, however, the enlargement has been unquestionable (see note, "Muscular Hypertrophy"). The motor nerves, when examined, have been found normal. The condition of the sensory muscle-nerves (which terminate in the interstitial tissue in which the primary morbid process occurs) has not been ascertained in any instance. The spinal cord has been found perfectly normal in most cases in which it has been examined. In a few there have been slight and irregular degenerative changes, as in one examined by Lockhart Clarke and myself ;* but the anterior grey • 'Med.-Chir. Trans.,' vol. lvii, p. 247. In this case the cervical and dorsal regions were normal, with the exception of here and there slight accumulations, at PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 579 matter was unaffected, and the changes were probably merely asso- ciated, and not the cause of the symptoms. Haemorrhages have been occasionally found. Probably they have occurred late in life in the degenerated tissue. The neuroglial cells have been found increased in number, and the fibres of the white substance have been found irregu- larly changed, in a few cases, without any constancy in the seat of the alteration. Pathology.—The common integrity of the anterior grey matter of the cord, and especially of the motor nerve-cells, seems conclusive evidence that the disease of the muscles is not due to a primary lesion of the spinal cord. The slight irregular changes occasionally found are probably consecutive to the long inaction of the cord and deformity of the spine. Pseudo-hypertrophic paralysis is not, therefore, as was at first thought, merely a form of spinal muscular atrophy with a special muscular change. The significance of the pathological anatomy is that the malady is a primary disease of the muscles, consisting in an altered condition of the muscular fibres, leading, it may be, to enlargement and subsequently to wasting and associated overgrowth of the connective tissue, in which fat may or may not be deposited. The indication of the conditions under which the disease occurs is that it is congenital, the result of a perverted tendency of growth, inherent in the embryo, and derived from the germ from which the embryo proceeds. In this connection it is instructive to note that there is one form of congenital tumour, the structure of which is almost exactly the same as that of the muscles in pseudo-hypertrophic paralysis. Fig. 167 might be a fragment of a muscle in this disease, but it is a section of a myolipoma, the congenital character of which is emphasised by the fact that it was attached to the conus medullaris of the spinal cord of a patient whose muscles were healthy. (The tumour is shown also in Fig. 174.) It must have been due to the misplacement of some of the embryonal elements from which muscular tissue is developed, and it shows that, from such elements, the struc- tural condition found in pseudo-hypertrophic paralysis may arise. The points of chief importance in the general pathology of the disease have been mentioned in the introductory remarks. The difficult ques- tion of the precise mechanism by which the muscular fibres suffer must be regarded as an open one. We may assume a defective vitality in them, but the conspicuous lesion is the growth of connective tissue, and by this the fibres are doubtless damaged, whether fatty tissue is formed or not. Indeed, the fibres seem to suffer more when there is the bottom of the fissures, of products of degeneration, probably derived from the perivascular erosion common at all ages. At the last dorsal segment, however, there was an area of granular disintegration in the intermediate grey substance on each side, in front of the posterior vesicular tract. This part was unduly translucent for half a centimetre in vertical extent, and in the middle of this area the disintegration had produced an actual cavity, across which the fibres for the cerebellar tract ran unchanged. 580 SPINAL CORD. only fibrous tissue than when there is the fatty deposit, although it is chiefly the fat that causes the enlargement of the muscles. There seems to be a tendency to the formation of fat in the early stage of the disease, and to its removal in the later stage, since in the former the - -::-- - - - "- - ,:- \ - y, ~ y • w ^yl FiG. 167.—Section of a myolipoma which was attached to the spinal cord of a man suffering from locomotor ataxy, for comparison with Figs. 165 and 166. muscles may often be observed to increase in size, and in the latter they become smaller, partly from some removal of fat and partly from the increasing atrophy of the muscular fibres. It is then that the greatest impairment of power occurs. In the cases in which the muscles are small from the first, the tendency to the deposit of fat seems slight, and the condition is an almost pure muscular sclerosis. The late shortening which occurs seems to be due to the contraction of the interstitial fibrous tissue, and it often coincides with the shrinkage from the removal of some of the fat, and the atrophy of the muscular fibres. If it be true that the latissimus dorsi and lower half of the pectoralis are sometimes congenitally absent in pseudo-hypertrophic paralysis, the fact is quite consistent with the explanation of the nature of the disease given above. These two muscles stand perhaps lowest, in functional importance, among the muscles of the body, being used chiefly for the rare depression of the arm against a resistance (see p. 37). It is readily intelligible that a defect in the embryonal tissue of the muscular system should be quantitative as well as qualitative. The loss of the knee jerk is sufficiently explained by the lesion of the muscles. According to the theory that the irritability on which the jerk depends is due to a muscle-reflex action, the loss is readily intelligible, since the afferent influence is due to the stimulation, by tension, of the sensory muscle-nerves, and tliese end (or begin) in the interstitial tissue, which is the seat of the primary morbid process in PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 581 this disease. But the wasting of the muscular fibres must also be capable of abolishing the knee-jerk when the atrophy reaches a considerable degree, and it is also possible that the motor nerve- endings share this structural damage. On any theory of the nature of the knee-jerk, this will explain its loss. It is only when the muscular changes have attained a considerable degree that the loss occurs. The fact therefore does not, in itself, suggest any lesion of the spinal cord. If the malady is thus one of a morbid developmental tendency, it is not surprising that a tendency to analogous developmental diseases should be sometimes present in the nervous system, and that thus imbecility and epilepsy on the one hand, or albinism on the other, should be occasionally associated with the disease. Diagnosis.—The diagnosis of the disease is usually easy if its characters are known. The peculiarity of gait and the mode of rising from the floor, the age of the patient, and the progressive character of the impairment, are in themselves sufficient to suggest the affection, and examination reveals enlargement and often contraction of the calf muscles, and a change in the size of others, which confirm the diagnosis. The mode of rising is not absolutely pathognomonic, and it has misled even good observers; it is occasionally acquired in other diseases in which there is a gradual weakening of the extensors of the hip and knee. It is met with equally in the simple idiopathic atrophy, but is so rare from any other cause as to be of very great diagnostic suggestiveness. Of the condition of the muscles, that which is most characteristic is the combination of enlargement of the infraspinatus with a wasting of the latissimus and lower part of the pectoralis. I pointed out some years ago * that this condition, which is seldom absent, is of very high diagnostic importance, and subsequent observations have fully confirmed the opinion. Next in importance is the enlargement of the calf muscles, especially in combination with contracture that cannot be overcome. In general, the enlargement and diminution of neighbouring muscles is very significant, but it must be remembered that they may be gravely diseased, and yet of normal size, or from the first smaller than normal. In such cases they are often hard, and the distribution of the affection is the same as that of the double change in typical cases. Such cases illustrate the relation of this form to the simple atrophy described in the next section. The disease with which confusion is most common is the so-called "congenital spastic paraplegia" (p. 495). Both diseases affect children ; in both there are weakness of the legs and contraction of the calf muscles, and in both the muscles are frequently large. The chief distinctions have been already mentioned. The most important are the preservation and excess of the knee-jerk in spastic paraplegia, the tendency to spasm of the legs—the facts that the contracture is active and can be overcome, that the patient does not rise from the ground * 'Pseudo-hypertrophic Muscular Paralysis,' London, 1879. 582 SPINAL CO WD. in the way peculiar to pseudo-hypertrophic paralysis,—and the oppo- site tendency of the two diseases. Congenital dislocation of both hips sometimes presents a superficial resemblance. Spinal muscular atrophy is only likely to be confused witb the simple atrophy. Between the two forms of idiopathic atrophy the distinction is scarcely one of diagnosis proper ; it is rather a question of the category in which a case should be placed. The most important distinction is the freedom of the calf muscles from enlargement in the atrophic form. The face is not affected in pseudo-hypertrophy as it often is in idiopathic atrophy, except only in some intermediate instances. If more than one member of a family is affected, some of the sufferers will usually present characteristic symptoms of the special form, for it is remarkable with what constancy the two types generally remain distinct (see p. 567). Prognosis.—In the case of any child with pseudo-hypertrophic paralysis, the prognosis is most grave. It is almost certain that each year will bring increasing disability, and that the patient will not reach adult life. It is only when the disease develops late, and the symptoms do not become considerable until after twenty years of age, that there is a possibility that the disease may not attain its ultimate degree, but even in such cases this hope is seldom realised. In any case, and at any age, it is unlikely that the patient will live more than seven years after the power of standing is lost. But even in this con- dition arrest seems to take place in the progress of the disease. One patient is known to the writer who presents a typical picture of the pseudo-hypertrophic type, who is now over forty, and has never been able to run. He has remained stationary certainly during the last eight years, probably longer. Treatment.—As a congenital developmental malady, pseudo-hyper- trophic paralysis is one of those diseases in which medicine is neces- sarily powerless to cope with the essential elements of the process. As may be therefore expected, no drug has been found to exert an influence on the course of the affection, although such nervine tonics as phosphorus and arsenic have been thought sometimes to retard for a time the progress of the weakness. The stimulation of the muscles by electricity has been employed and advocated, but, however sedulously employed, no distinct result follows the use of either faradism or voltaism. It must be remembered, moreover, that electricity is a very feeble agent in stimulating the growth of muscular fibres, compared with the physiological stimulus of voluntary effort. Muscular exercise may reasonably be looked to in order to make up, in some degree, what is lacking in this disease, and does seem to have some influence in retarding the failure of power. It may perhaps induce further growth, or greater power in the muscular fibres that have not yet suffered, or actually supplement the defective trophic energy. When muscular exercise is stopped, there is certainly a quicker failure of strength. Hence it is desirable that the patient should carry out SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 583 carefully planned gymnastic exercises, so arranged as to call into action the muscles that most need help. These, thoroughly per- severed in, have seemed, more than any other means, to retard the disease. Although they have not in any case arrested it, the trouble that is necessary to arrange the method is certainly well spent. Rubbing and massage improve the circulation, and help, especiallv when combined with passive movements, to lessen the tendency to muscular contraction and consequent deformities. The influence of muscular exercise renders it very important to maintain locomotion as long as possible. The ability to stand and walk is generally lost, through the contraction of the calf muscles, some time before the muscular weakness would take the patient off his feet. In such cases tenotomy may restore the power of walking for some years, and when the contracture returns, its removal has, a second time, enabled walking to be resumed. The operation is thus distinctly beneficial, and should be performed as soon as the actual need for it arises, and division of the tendon is far better than any imperfect substitute. During the later stages of the disease great care is required to preserve the patient from catarrh, which helps to excite the pulmonary mischief that so often ends hfe. Similar care is also needed during any intercurrent malady which the patient may contract. Simple Idiopathic Muscular Atrophy.* The cases in which there is no muscular enlargement, in which wasting is manifest from the first in the size of the muscles, are much more rare than the pseudo-hypertrophic disease. They belong to several types, more or less distinct, of which the most common is that to which Erb has given the name of "juvenile," and of which most instances are probably the pseudo-hypertrophic disease without mus- cular enlargement; others are more special, since the lower hmb muscles have suffered but little. A more striking variety is that which is characterised by the affection of the muscles of the face in addition to those of the shoulder girdles—the " facio-scapulo-humeral type " of * The most important writings on the subject (besides those specially quoted) are those of Duchenne in 'Electrisation localise' (p. 60of Poore's translation, published by the New Sydenham Society); B;irsickow, 'Inaug. Dissert.,' Halle, 1872; Leyden, ' Klin. d. Ruckenm. Krauk.,' Bd. ii, p. 525; Mobius, " Hered. Nervenk.," Volkmann's 'Klin. Vortrage,' No. 171; Lnndouzy and Dejerine, 'Revue de Med.,' 1885, pp. 81 and 251; Marie and Guiiion (a series of cases observed at the Salpetriere), ib., 1885; Sachs, 'New York Med. Journ.,' Dec. 15th, 1888; Hitzig,'Berlin, klin. Wochen- schr.,' 1888; Singer, 'Zeitsch. f. Heilk.,' Bd. viii. Especially valuable are the papers by Erb, 'Dent. Archiv f. klin. Med.,' Bd. xxxiv, 1884, and 'Neurol. Centralbl.,' July 1st, 1886, with numerous later writings. Bibliographical references, &c, will be found also in Tooth's ' Thesis on the Peroneal Type/ and in my Lecture on Pseudo-hypertrophic Paralysis (1879), and in Sachs' article (loc. cit.). 584 SPINAL CO WD. Landouzy and Dejerine. In a third variety the affection begins in the legs, and is peculiarly slow in course. Some other types may ultimately be differentiated, but it is important to recognise the fact that even those that we can now distinguish, as the most pronounced in their features, do not keep entirely distinct. They are connected, Pia. 168.—Simple idiopathic muscular atrophy. From photographs kindly lent by Dr. J. H. Crocker. Particulars of these cases and many similar are given in an excellent thesis on this disease by Dr. Crocker. by intermediate forms, not only with each other, but even with the pseudo-hypertrophic disease, as already mentioned.* But these are unusual; as a rule the two latter types remain distinct in the families in which they occur, and this is the justification for their separate description. In those families in which simple muscular atrophy occurs, however numerous the cases, however different the distribu- tion of the disease, and however various the ages at which it begins, cases rarely present the distinctive characters of pseudo-hypertrophic paralysis. There is less constant separation between the simple " juvenile " and the facial forms. Although they often keep distinct, the affec- tion of the face has been absent in a few cases in a family in which it * E.g. case described and collected by Marie and Guinon (loc. cit.), connecting the pseudo-hypertrophic form with both the juvenile and the facial. SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 585 was the first part to be affected in most sufferers. Thus a man with simple atrophy, beginning at fourteen in the shoulder and thigh muscles, whose face was unaffected, had a d.ughter who began to suffer at eleven, and in whom the face, scapular, and arm muscles were involved.* The peculiar " peroneal type " is not included in this outline, and the statements here made do not apply to it. Causks.—We are able to trace no cause beyond the congenital tendency, already considered, shown by the occurrence of many cases in the same family, and in more than one generation. In one remark- able series recorded by Barsickow, twenty-four cases were distributed through five generations, and the disease was also traced through five generations in a group described by Landouzy and Dejerine It is very rare for the disease to be confined to one generation, far more rare than for pseudo-hypertrophic paralysis to be so confined. But, as in the case of most congenital hereditary diseases, cases that are apparently isolated are occasionally met with, fcuch isolated cases are rare—more so, probably, than in the pseudo-hypertrophic form; al- though wider observation may show that they are more frequent than we now suspect. In the families of the patients shown in Figs. 169-172 no example of analogous disease could be heard of. Both sexes suffer; in a few families, females chiefly; in others, males ; in most, both have been affec:ed. The age at which the disease first manifests itself is extremely variable. It may begin as early as twof or three,X and as late as sixty years. But the onset is seldom during childhood; in the majority of cases the disease shows itself between fifteen and thirty-five; that is, during the later period of growth and the early period of adult life. Even in the same family, the variations may be extreme; in that described by Barsickow tbe date of the onset of seventeen cases was known, and was as follows :— in one at 12; in four between 15 and 20; in seven between 20 and 30; in three between 30 and 40 ; in two after 40. A woman aged fifty-two began to suffer at 30, but her son at 3 years of age.§ Sex has no influence on the date of onset, nor, as a rule, can any relation be traced between the date and the place at which the wasting begins. When the wasting begins in the face, the disease more frequently commences in childhood than when the first symptoms are in the limbs, but in some instances the atrophy has commenced in the face late in life, and this in the same family in which other sufferers have been young. Thus in the sexual proclivity, and in the date of onset, there is a marked difference between this form and pseudo-hypertrophy, the latter showing a stronger tendency to affect males, and to manifest itself in childhood. The "juvenile" form, as a rule, presents less difference. * Troisier and Guinon, 'Rev. de Med.,' 1889, p. 48. See also Singer, 'Zeit. r' Heilk.,' viii, p. 229. t Kreske, ' Munch, med. Wochenschr.,' 1886. J Landouzy and Dejerine, loc. cit. § Ibid. 586 SPINAL CORD. As a rule, no direct exciting cause can be traced. In a few instances the onset has succeeded some other morbid process, such as chlorosis, acute disease, or rheumatic affections due to exposure to cold; and the depression of general health resulting from these may have determined the time of onset, but is not likely to have done more. In other in- dividuals of the same families the disease has developed without the aid of any exciting influence. Symptoms.—The onset is always gradual. Weakness and wasting come on together, and are noticed simultaneously, unless the com- mencing atrophy is concealed by subcutaneous fat. The atrophy generally begins in the upper arm and shoulder muscles, having, in the most common " juvenile" form, a similar distribution in these parts to that of pseudo-hypertrophic paralysis. In the facial form, however, this part usually suffers first, as in the lad figured on p. 589. In rare cases the wasting not only begins in the legs, but remains limited or almost limited to them. In the part first affected the dis- ease slowly increases, and thence it usually spreads. The onset may be symmetrical on the two sides, or one side may suffer some time before the other. Of the arm muscles, the weakness and wasting are noticed first in the biceps and triceps, and with these the supinator longus often suffers. But examination generally shows that the lower part of the pectoralis and latissimus dorsi are greatly wasted, a loss of which the patient may be little aware, on account of the relative unimportance of these muscles. Sometimes the upper part of the pectoralis, and even the pectoralis minor, are also affected. The tendency to atrophy of the lower part of the pectoralis and latissimus is a character which, as already stated, is common to this disease and pseudo-hypertrophic paralysis, but not invariable in either. The deltoids are rarely in- volved ; in many cases they are normal; sometimes they have been thought to be unduly large ; in a few instances they have been wasted. The serratus magnus is often affected (Fig. 172), but may escape, even in a severe case. The supraspinatus and infraspinatus may also suffer, but are often normal, or even enlarged; the trapezius and rhomboids have been affected in many cases; sometimes much atro- phied, especially in the " juvenile" form. The forearm muscles generally escape, with the exception of the supinator longus. Occasionally there has been some weakness of the long extensors or flexors of the fingers, with or without slight visible wasting. In the case mentioned on the next page the extensors of the phalanges of the thumb were involved on the left, and the radial extensor of the wrist on the right side. Rarely the forearm muscles have been much atrophied. In several instances there has been some atrophy of the small muscles of the hands, the thenar and interosseal muscles, or the interossei only, as in the case of Landouzy and Dejerine ; but in the majority the integrity of these muscles is a marked feature of the disease and a contrast to the spinal form. SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 587 The affection of the face is peculiar. There is commonly a failure of the zygomatic muscles, and, in consequence, a loss of the naso-labial furrow, and a curious alteration in the smile; instead of the angles of the mouth being drawn outwards and upwards, they are moved upwards by the elevators of the upper lip and angle of the mouth. The orbicularis oris is also affected, and, in consequence, the lips arehabitually separated, the lower lip projects, the patient cannot "pout" or whistle, and the articulation of labials is imperfect. The face has a dull expression, and the aspect is very peculiar; it has been termed, by Landouzy and Dejerine, the " myopathic face." In one case, observed by them, the face was unequally involved on the two sides. Rarely (as in Fig. 171) the frontales have been involved, and the orbicularis palpebrarum has been weak, and the eyes cannot be completely closed. Weakness of the eyelids was supp^seil to be the cause of distinct exophthalmos present in one woman.* In the case described by Kreske, inability to close the eves was noted at three, and at ten the paralysis of the face was absolute. Wasting of the muscles may be indistinct, because the contour of the face is only to a slight degree influenced by the substance of the muscles The projecting lower lip may, indeed, appear to be thicker than normal. In many cases the buccinators have been affected, in some instances they have been normal, and then have drawn out the angles of the mouth in smiling. The tongue has been always un- affected, and so also have the pharynx, larynx, muscles of mastication, and the eyeball muscles f The muscles of the spine have sometimes been normal, sometimes they have been considerably atrophied.X The intercostals are often * Landouzy and Dejerine. t In a singular case under my care some years ago, an affection of the facial muscles, similar to that of idiopathic muscular atrophy, was associated with paralysis of ocular muscles. The patient was a girl t wenty-seven years ot age ; there were no indications of syphilis, nor could any history of muscular atrophy in the family be ascertained. The ocular palsy commenced gradually at twenty-four, and increased until the movements of both eyes upwards, of the left eye inwards, and the right out- wards, were lost, and all other movements were weak< ued. The eyelids drooped slight ly ; the internal ocular muscles were normal. The affection of the face followed that of the eyes ; the zygomatic muscles were powerless, so that the smile consisted only in elevation of the upper lip; the orbicularis was weak. The palate, pharynx, and larynx were normal. The aims became feeble, and the flexors of the hips almost powerless. There was no visible change in the nutrition or electrical irrita- bility of the muscles; the knee-jerk was normal. If the case was central, as it appeared to be, the peculiar affection of the lips and zygomatics is not confined to idiopathic muscular atrophy. If the disease was muscular, the eyeball muscles do not invariably escape. With this case may be noted one recorded by Oppenheim ('Charite Annalen,' xiii) as the "juvenile" form, with derangement of the lateral movement of the eyes, nystagmus, and some laryngeal palsy. The shoulder and thi"-h muscles suffered chiefly, but below the knee, the peronei—a noteworthy aberration from the type. t Atrophy began in the back muscles at forty-four in a case recorded by Musso 588 SPINAL CORD. affected in the later stages, but rarely in extreme degree. The diaphragm also sometimes suffers. The abdominal muscles have been involved in only a few instances. In the legs the muscles most commonly affected are the flexors of the hip, the extensors of the knee, and less frequently the glutei. The muscles below the knee have escaped in many cases: when they have suffered, the atrophy has often been general. When the peroneal and anterior tibial muscle - have been specially affected, as in the case shown in Fig. 172, the case has generally ben of the peculiar "peroneal" type to be presently mentioned, although it is possible that some instances of the kind are on the borders of the group now under con- sideration. The electric irritability of the affected muscles is usually lessened in proportion to the wasting, and equally to both currents. Indeed, the diminution seems sometimes out of proportion to the wasting, and great when the atrophy is slight. There is no trace of degenerative reaction, and there is not even the longer persistence of voltaic than of faradic irritability which occurs in the more chronic cases of spinal atrophy. Fibrillation is almost always absent, but not quite in- variably ; hence its absence cannot be made distinctive, still less its presence. Myotatic irritability is lessened or lost; it is never increased. Some shortening of muscles has been occasionally noted, frequently in the calf muscles, rarely in the biceps. All other functions of the nervous system are unaffected. Sensi- bility is normal. In a few cases transient rheumatoid pains have accompanied a rapid development of the disease in the arms, but in the vast majority of cases the disease is painless. The sphincters are unaffected, and there is no tendency to trophic or vaso-motor dis- turbance. As the muscular atrophy progresses, the form of the affected parts becomes changed just as in spinal atrophy. Deformities may also occur, chiefly from the shortening of less affected muscles, but these rarely reach the considerable degree common in other forms of muscular wasting. Lordosis occurs in the upright posture, and is probably due to the same mechanism as in pseudo-hypertrophic paralysis, ceasing, as in that disease, when the patient sits (compare Figs. 169 and 172). When the muscles of the lower leg are involved talipes may develop. The course and duration of the disease are exceedingly variable. The atrophy may remain limited to the part in which it begins. The face alone has been affected in some members of a family, although in other members the limbs subsequently suffered. In cases in which the wasting spreads, years may intervene before the extension takes place. In one case, for instance, the right arm became affected at (tribution of the atrophy and projec- tion of the scapula? are seen in Fiir. 172.* * The patient was a lad sixteen years of age. The following is an abstract of the notes of his case. In his family no history of any similar affection can be ascertained. There is conclusive evidence that he had a hard chancre at the age of three, followed by secondary symptoms. The muscular wasting began gradually during childhood; even when very young there was little movement in the face, and that ceased at the age of six or seven. Walking became difficult about three years ago. The face is almost mo ionless: an effort to smile causes only a just perceptible movement of the left cheek, the amount of which is fairly indicated by the difference between Figs. 170 and 171. It is accompanied by a distinct movement of the ears. The lips are full and can be brought together, but not shortened. The eyelids cannot be made to meet, even with a strong effort, being then £ inch apart. Forehead absolutely motionless. Eyeballs prominent, movements normal. Masseters, tongue, pharynx, and larynx unaffected. In the neck the sterno-mastoids are very small and feeble, the omo-hyoids large and strong. The following muscles seem quite gone— 590 SPINAL CORD. begins in childhood its progress is sometimes very slow. Thus in one case the affection of the face was first noticed at five, at twelve the arms began to suffer, and a few years later the flexors of the hip became weak, but the patient was still able to walk at the age of forty. The disease may increase until deve- lopment is over and then remain stationary, as in a case in which, at forty-four, there had been no change since the age of twenty. The patient's daughter was more severely affected.* On the other hand, the progress of the disease may be more rapid and uni- form, and the atrophy may reach its widest distribution in eight or ten years. In most cases, even of severe type, the wasting do s not become universal, but remains limited to the muscles mentioned above, but occasionally hardly any muscles of the body may escape. The duration of the disease varies from ten to fifty years. Death has never occurred as the direct result of the malady. In the cases of most severe degree and rapid course the patient has usually died from phthisis, pro- bably related to the deficient breathing power, just as in the sufferers from pseudo-hypertro- phic paralysis. In most cases, however, death has been due to other maladies, and has not been in any degree the consequence of the muscular disease. Pathological Anatomy.—In general, the condition of the mus- cular fibres resembles that met with in pseudo-hypertrophic para- lysis, the increase of interstitial tissue being wanting except in those trapezius (except, perhaps, a little of the middle part of the right), rhomboids, deltoid, pectorales, latissimus dorsi, serrati, bice|s, brachialis, triceps, supinator longus. The lev. ang. scapulae, supra- and infra-spinatus are unaffected; the latter is large, but probably only hypertrophied from over-use. The supinator longus is feeble on the left, powerless on the right side. The extensors of the phalanges of the thumb are lost on the left side, and the extensor carpi radialis on the right All the other forearm and hand muscles appear to be unaff cted. The erectors of the spine are small and feeble; intercostals strong, diaphragm powerless, abdominal muscles weak. In the legs the glutei and flexors of the knees seem normal, the flexors of the h,ps weak, extensors of the knees small and feeble, muscles of the lower le- ather small and feeble, but only the peronei are powerless, right-angled contracture of ankle-joint with tendency to varus. Knee-jerk absent. Circumference (in inches) of upper arms (middle), R. Stf. L. 5J; of forearm (maximum), each 8; of th.ghs (m.n,in.»2 inches above patella), R. 10*, L. 9*, calves (maximum), R. 10T L. 11. Electric irritability much lowered in all affected muscles to each current; in most no contraction can be obtained. Sensation, the sphincters, and the visceral functions are unaffected. * Landouzy and Dejerine, loc cit. SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 591 cases that really belong to this form, but in which the characteristic enlargement is absent, because no fat-cells are developed in the tissue. A multiplication of nuclei is, however, sometimes seen. The chief change is sometimes a simple narrowing of the fibres, "^ith an ultimate disappearance of the transverse striation. Degenerative changes are frequently met with, indistinct striation or granular, fatty, or " waxy " transformation being seen here and there, alike in narrowed or enlarged fibres, and in those that retain their normal calibre; occa- sionally fibres present longitudinal striation, Assuring, or vacuolation ; but in other cases, or in some muscles (especially in the " juvenile " form), a remarkable increase has been found in the size of fibres in excised fragments,* even of muscles that are below the normal size. It seems to show definite pathological enlargement. The statements made regarding the spinal cord in the pseudo- hypertrophic form are strictly applicable also to this variety. It is normal as a rule, to which exceptions are so rare that they can have no relation to the malady, save that of secondary indirect consequences. The nerves also are normal, if the cases are eliminated in which the symptoms indicate the peroneal form. Thus the facts ascertained regarding this type do not suggest any special addition to the general conclusions intimated in the introduc- tory paragraphs. The affection appears to be the result of a primary developmental tendency, involving the muscular tissue only, and cannot be regarded as a secondary result of the interstitial changes, except in a trifling, occasional, and unimportant degree. Still less is it a consequence of changes in the spinal cord. If it is in any measure the result of failure in the nutrition of the terminal structures of the nerve-fibres (by which the nervous and muscular tissues are connected, and which is perhaps to be regarded as intermediate between the two), the fact has yet to be demonstrated, and its significance ascertained. Diagnosis.—The two most important diagnostic indications are the affection of more than one member of the same family, and the onset of the disease before adult life is reached. The former is practically conclusive ; and the latter should always suggest the probable idiopathic nature of the case. In isolated cases the diagnostic difficulty is much greater, and no indication is actually conclusive, except, perhaps, the affection of the face. Commencement during childhood is also of great weight. It is most unlikely that progressive muscular atrophy, beginning under ten, is of spinal origin, but I have known such atrophy, certainly spinal, to commence at the age of fourteen.f The peculiar affection of the zygomatic muscles is very characteristic, but we cannot vet sav that it is pathognomonic (see note on p. 587), and the affection of the lips must be carefully distinguished from that due to the bulbar palsy so commonly associated with spinal atrophy. Of * See especially Schulze, ' Ueber den mit Hypertrophic verbundenen Muskel- schwund,' Wiesbaden, 1886, and Hitzig, loc. cit. t See, however, p. 597. 592 SPINAL CORD. the distribution of the wasting, that of the latissimus and lower half of the pectoralis, and the escape of the hand muscles are the most im- portant characteristics, although they are not by themselves con- clusive, since they are sometimes met with in spinal atrophy. But the most important distinctions between spinal and idiopathic atrophy, whenever they are available, depend upon the symptoms of a lesion of the cord, or of the bulbar nuclei. Especially significant is the excess of the knee-jerk which results from lateral sclerosi.s, a conclusive indication of spinal disease, rendering the spinal origin of the atrophy all but certain. The distinction from the pseudo-hyper- trophic form has been already considered; that from the peroneal type will be presently mentioned. Prognosis.—The extreme variations in the course of the disease render the prognosis in any individual case both uncertain and difficult to formulate. Speaking generally, chronicity favours arrest, and the later the symptoms appear the slower will be their progress. The prognosis is distinctly less grave in the simple atrophy than in the "juvenile " atrophic variety of the pseudo-hypertrophic disease, and in a considerable number of cases, perhaps one half, the malady has not appeared to shorten life. Even in cases that begin during youth it is therefore possible that the patient may reach old age. It seems also to be better in the cases that do not involve the facial muscles. Treatment.—It is not yet clear that idiopathic muscular atrophy can be influenced by treatment in any considerable degree. Most published records of cases are almost silent on the subject, and the disease is so rare that few individuals have an opportunity of forming an opinion. It might be assumed that the essential cause of the disease, a congenital tendency, withdraws it from the range of thera- peutics, but the course of the malady is very different from that of some other diseases which own a similar cause. The extreme variations in the date of onset, the fact that the disease may not be manifested until late in life, and the long period that may intervene between its onset and extension, all suggest that other influences co-operate with the congenital tendency in determining the development of the malady. It is quite possible, therefore, that the first inference from the history of the disease may not be altogether correct, although it must be admitted that we have not as yet any evidence that the disease is susceptible of influence from drugs. Electrical treatment and mass- age have been thought to do good and even to produce arrest (Erb), but the variable tendency of the malady renders the evidence of arrest insufficient. If voluntary exercise is practicable, this is a far more efficient stimulus to muscular growth than any electrical application, and it is probable that such exercise, carefully persevered in, may do something to prevent the occurrence of the malady in those pre- disposed to it, and even to retard its progress in those who are already attacked. In this connection it is noteworthy that very few of the sufferers have been engaged in occupations that involve active PERONEAL TYPE OF AMYOTROPHY. 593 muscular exertion. Over-exertion should, however, be carefully avoided. The general health should be attended to, and any defect removed as speedily as possible, both in those who suffer and in those who are related to sufferers, since, as we have seen, depressing influences may apparently excite the development of the disease, and it is therefore reasonable to suppose that they may accelerate its course, and lessen any tendency there may be for the morbid process to become stationary. The Peroneal Type of Family Amyotrophy. (Neuritic Muscular Atrophy.) The name " peroneal type " has become current as the most con- venient designation for the variety of muscular atrophy, occurring in early life, to which it was applied by Dr. Howard Tooth in a Thesis published in 1886.* This was the means of calling general attention to the form, of which, however, an account had been published shortly before by Charcot and Marie,f and many cases had been pre- viously described, in most instances without recognition of their special character. J The cases of this form present certain resemblances to the idiopathic atrophies just described—resemblances sufficiently important to have led to the description of these cases in association with the primary myopathies, embracing, as they do, the age of the sufferers, the occurrence of the disease in members of the same familv, its gradual onset, and its very slow but progressive course. Yet this position must be regarded as provisional only, and probably erroneous. The distribution of the wasting involves a constant difference from the idiopathic muscular affections, and some of the cases, otherwise inseparable from the rest, present features that indicate neuritis. Tlu- condition may have, as an antecedent, an acute specific disease—a circum- stance that has the same significance. The facts ascertained con- cerning this form must, therefore, be carefully excluded from our generalisation regarding idiopathic atrophy. In this disease, males suffer about twice as frequently as females. It generally begins in the second half of childhood, and very seldom after twenty, although cases have been described beginning as late as forty. It is occasionally hereditary, and still more frequently collaterals suffer, several brothers and sisters being affected. The wasting is first apparent in the extensor longus hallucis, or extensor communis digitorum, or in the peronei muscles. According to Tooth it very often begins in the latter, and occasionally m the gastrocnemius, but it is probable that it occurs simultaneously or even earlier in the * 'The Peroneal Type of Progressive Muscular Atrophy,' London, Lewis, 1886. t 'Kevue de Med.,' 1886, p. 97. + By Friedreich, Eichhorst, Oppenheimer, Ormerod, and others. A table of thirty collected cases (some doubtful) is given by Tooth. VOL. I. 38 594 SPINAL CORD small muscles of the foot, where it readily escapes observation. Such early atrophy in the feet has, indeed, been actually found in some cases that came under observation at an early stage.* The calf muscles suffer subsequently, and still later those of the thigh, especially the vastus internus. The unequal affection of the muscles of the leg causes the early development of club-foot, which, especially in children, becomes a characteristic symptom.f The arms are only invaded, in most cases, some years after the legs, so slow is the course of the disease. The intrinsic muscles of the hands (thenar, hypothenar, and interosseal muscles) are first attacked, and subsequently those of the forearm: sometimes the extensors and sometimes the flexors suffer first and most; while the supinator longus remains normal, and so do the muscles of the shoulder, neck, and back. The affection, however, does not necessarily commence in the lower limbs, and the face may be affected (Hoffmann). The atrophy is often symmetrical, but occa- sionally the muscles on one side waste first and most. The claw-like deformity of the fingers may result from the affection of the intrinsic muscles of the hand. This is so rare in early life from any other cause that its significance is considerable, and almost distinctive when combined with the deformity of the feet just mentioned. The case shown in Pig. 173 was probably an example of this type. J Fig. 173.—Advanced muscular atrophy, probably of the "peroneal type." (Drawn by Dr. Spencer, from a photograph.) The affected muscles (especially in the hand) occasionally present slight fibrillation. Their electric irritability is diminished sooner, and * Hoffmann, 'Arch. f. Psych.,' xx, p. 660; Joffroy, ' Gaz. Hebd.,' 1886, No. 18. t See Sachs, * Brain,' Winter part, 1889. I It was given in the first edition as an example of simple atrophy. The patient was a man aged twenty-seven at the time of his death (in University College Hospital). No history of any analogous case in his family could be ascertained. The affection began at the age of fourteen, when his feet began to turn in so that he walked on the outer side of the foot, and soon he noticed gradual wasting of the legs, which slowly progressed, and about the age of twenty-four the arms also began to suffer. When first seen, a few months before his death, the muscular atrophy was universal, and the subcutaneous fat had also disappeared. Even the hands were greatly wasted; there was a hollow in the position of the thenar eminence, just as in progressive muscular atrophy, and the interosseal muscles were also greatly wasted. There was slight fibrillation. The intercostals were paralysed. The wasting of the legs was extren.e; the maximum circumference of the calf was PERONEAL TYPE OF AMYOTROPHY. 595 in greater degree, than in the ordinary idiopathic atrophy.while a still greater difference is presented by the fact that faradic irritabihty may early become extinct, and that there may be a distinct reaction of degeneration. In connection with this should be noted the important fact that cutaneous sensibility, though often nonnal, is sometimes impaired or lost, especially over the region in which the atrophy is greatest, or upon the soles of the feet. Pains occur in some cases, and so also do spontaneous spasmodic contractions, especially in the muscles of the thigh. The muscle-reflex action is lessened or lost in the affected regions, but there may be extensive atrophy below the knees, without loss of the knee-jerk, if the thigh muscles are pre- served. Cutaneous reflex action presents considerable variations, and is preserved more often than would be expected. Yaso-motor dis- turbance sometimes occurs (Sachs). The nature of these cases has still to be demonstrated. Their very slow course, the time of life at which they begin, and the affection of several members of the same family, are features analogous to the idiopathic atrophy ; but a marked contrast to this is presented by the tendency of the malady to succeed an acute specific disease, measles, and this also may appear as a family tendency. This feature re- sembles the causation of multiple neuritis, and the electrical reaction of degeneration is conclusive proof of preponderant changes in the motor nerves, while anaesthesia demonstrates that, in some cases, the sensory fibres are also affected. In such cases a peripheral neuritis, motor or total, of extremely chronic course and pecuhar origin, must be recognised as the only possible lesion, and it was actually found, in one case by Priedreich, and in another by Gombault. Dubreiulh* also, in a case which he examined, found that there were inflammatory changes in the nerves, the spinal cord being normal. If this is the cause of the symptoms in some instances, the question arises whether it is not the lesion in all the cases of this peroneal type. Such a lesion is conceivable; the degenerative form of neuritis presents every degree of chronicity, and may be limited to the motor fibres and to certain muscles. This pathology was advocated as the probable one by Tooth, who pointed out that it would also enable us to understand the occurrence of. fibrillation, which is extremely rare in the idiopathic atrophies. It is, indeed, asserted by Hoffmann that not only are the peripheral nerve-fibres the seat of a primary degene- ration, but that this change ascends the nerves to the anterior and posterior roots, and involves, in a secondary manner, the elements of only seven inches; the feet were everted, the sole hollowed, and the toes flexed. The patient died from diarrhoea. The muscles were found to be small and pale. The chief microscopical change was intense granular and fatty degeneration of the fibres. A very few normal fibres were seen in some muscles. There was no increase of interstitial tissue. Microscopical examination revealed no morbid changes in the spinal cord. The nerves, unfortunately, were not examined. * ' Rev. de Med./ 1890; 'Neur. Cent.,' 1891. 596 SPINAL CORD. the spinal cord, especially the fibres of the posterior median columns (which continue the path from the muscles) and the motor cells of the anterior cornua. But we do not know how far the premature failure of nutrition is a secondary process, transmitted from below, or how far it is the result of a defect in vital energy, shared by the central as well as the peripheral nerve-elements. The intimate relation between the motor nerves and the muscular fibres should also be kept in view in this connection. There may be a morbid tendency in the nerves similar to that of the muscles. including a liability to early slow degeneration, analogous to that which the muscles present, and equally prone to occur in several members of a family. 3ut it is desirable that the neuritic nature of the affection shouia De placed on a broader basis of ascertained fact before it is, j-ilowed expression in the name given to the disease. It should also be remembered as possible that the atrophy may be idiopathic in some cases, while in others it may be secondary to such a neuritis as above mentioned. There is nothing difficult, or even anomalous, in the conception of a congenital tendency to premature failure of nutrition in the peripheral nerve-fibres, like that which, in the posterior column and other fibres, seems to underlie " hereditary ataxy," or which, on the other hand, in the muscles is the apparent cause of idiopathic atrophy. Further, if the lesion is really neuritic, we can understand that an acute specific disease like measles should occa- sionally be its excitant, although its occurrence in families shows that a congenital tendency must be called into activity by the virus, and the cases must be distinguished from those in which a pure neuritis is in- duced by the influence of the poison of the specific disease. An acute specific disease, the virus of which is known to be capable of inducing the degeneration of " parenchymatous " neuritis, may readily excite this state in each of several members of the same family if a congenital tendency to it exists in them. It may readily evoke that which it could, even alone, produce. According to this theory, a tendency to nerve degeneration, acting alone, may lead to the early failure of nutrition of the nerves, while the wasting of the muscular fibres may be either a consequence or a concomitant, in part or altogether. Thus the muscles may atrophy because the nerves have degenerated, or because they also have a tendency to atrophy, or from both causes combined. Nerve and muscle may alike share the congenital imper- fection in some cases, while in others its primary incidence is on the nerves alone, the muscles suffering in consequence of the changes in the nerves. The congenital association may sometimes be even more extensive, and a tendency to the early failure of structures in the central nervous system may be conjoined, giving rise to cases of com- plex aspect and character. It is especially important to note, in this connection, the occurrence of cases that occupy an intermediate position, and combine the characters of this and the myopathic types. Such combined cases are MUSCULAR ATROPHY. 597 usually partial only, but such partial cases, when combined, ultimately cover the whole intermediate ground. For instance, the condition of the legs in the " peroneal type " has co-existed with that of the arms in the "juvenile form" in several recorded cases.* Thus the possibility must be recognised that the cases of this type vary, even more than their characters suggest, in the degree in which the morbid tendency acts upon nerve or muscle, or both, as well as the degree in which its activity is spontaneous or induced. Hence the cases may here be only partly out of place—some, perhaps, not at all; and their position, as forms of " neuritis," might be equally open to exception. The progressive character of the cases of this type is commonlv pro- nounced ; and, even if slow, it renders the prognosis gloomy, and the scope for treatment small. So far as anything can be done, it is by the measures already mentioned in the account of the treatment of the maladies to which the cases approximate, the primary diseases of the nerves on the one hand, and of the muscles on the other. Family Form of Muscular Atrophy in Children with Spinal Lesion. The above seems to be the most suitable title for a series of cases described in recent years by Werdnig f and Hoffmann X in Germany, and Bruce and John Thomson § in this country. The condition is marked by the occurrence of similar atrophy in more than one member of the family, although in Bruce and Thomson's case the condition was an isolated one. It is characterised by the onset of weakness, especially in the hip and back muscles, about the age of from seven to twelve months, in children previously healthy. The weakness gradually impairs and finally abolishes the power of walking, and similar weakness usually attacks the upper limbs as well as the legs, and even the small muscles of the hand may be affected. The condition is one of marked atrophy without sensory impairment, although in one case there was a curious insensibility to the pains of faradic stimulation of the affected muscles. In many of the muscles the reaction of degeneration may be present, and occasionally bulbar symptoms are superadded. The condition culminates in one of extreme helplessness, with marked wasting of muscles without any fibrillary twitching, although death did not take place in some cases until the age of six was attained. No hypertrophy has been noted in any case. * E.g. by Hoffmann, 'Berlin, klin. Wochenschr.,' 1887, No. 22; and Eisenlohr, 'Neur. Centralbl.,' 1889, p. 565. f 'Arch. f. Psych,' 1891 and 1894. X ' Deutsch. Ztsch. fur Nervenheilk.,' 1893 and 1397. § 'Edin. Hosp. Reports,' 1893. 598 SPINAL CORD. The conditions found after death were marked atrophy of muscular fibres, although occasionally some fibres were hypertrophied. Atrophy also of nerves and anterior roots was found, and wasting of the cells in the anterior horns. The latter was distinct, and this, with the absence of any hypertrophy at any time (although one child had been noted as very fat which afterwards became much wasted), marks off the cases distinctly from those of pure muscular dystrophy. The type possibly, like the peroneal, forms a connecting link between cases of spinal pro- gressive muscular atrophy and those of true myopathy without any spinal lesion. The presence of definite changes in the cells of the anterior horn and the anterior nerve-roots connects the cases with the former, while a connection with the latter is formed by the simple wasting with occasional hypertrophy of isolated muscular fibres, and by the occurrence of the disease in more than one member of a family. Diagnosis.—The age at which the disease occurs, the absence of fibrillary twitching, and the early suppression of the reflexes, as well as the frequent occurrence of more than one case in the same family, will sufficiently distinguish these cases from ordinary progressive muscular atrophy. On the other hand, the absence of any hyper- trophy, the affection of the small muscles of the hand, and the occasional presence of bulbar symptoms will mark them off from cases of true muscular dystrophy. In every case which comes under notice hypertrophy in some muscles, especially the infraspinati, should be carefully looked for, as it may turn out that the cases are more closely connected with myopathic cases than is as yet apparent from the evidence. Prognosis.—This seems to be extremely bad; the cases go on from bad to worse, the weakness becomes greater, the atrophy more pro- nounced, until death occurs. But, as has been stated above, this has not unfrequently been delayed as late as the sixth year. Treatment.—The nature of such cases, indicating as they do an inherited tendency to early death in the muscular fibres and their correlated nervous structures, precludes the hope of successful treat- ment. The administration of strychnia hypodermically is indicated, although the age of the patient renders extreme care necessary in the choice of doses. It is also possible that galvanism, combined with massage and passive exercise, might have a beneficial effect. And, of course, care must be taken to ensure wholesome and judicious feedino- and satisfactory hygienic conditions. Periodic Family Paralysis. Under this name Goldflam * has described a condition of which examples had been previously published by Westphal, Cousot, and Schachnowitsch. It is characterised by recurrent paralysis commencing * Berlin Congress, 1890; 'Neur. Cent.,' 1890, p. 638. MUSCULAR HYPERTROPHY. 599 usually in tho legs, involving also the arms, and passing off in the reverse order after a period varying from twenty-four hours to three days. During the attack of paralysis the patient is sleepy, but there is no impairment of consciousness, sensibility is retained, and the paralysis is flaccid, with diminished knee-jerks and loss of plantar reflexes. Speech and swallowing are not interfered with. In Gold- flam's case there was great diminution of faradic irritability in the upper limbs, and complete loss in the lower limbs. After the attack had passed off the nerves in both arms and legs reacted normally. Eleven members of the family suffered from similar attacks of paralysis. They began between fifteen and twenty, and increased in number as age advanced, although the individual attacks did not last so long. In the patient whose case is particularly described there were only two attacks in the first year, but after three years they occurred every fortnight. The condition as regards etiology is obscure. Goldflam's opinion is that it is the result.of auto-intoxication—a view which is favoured by the fact that in his patient obstinate constipation persisted during each attack of paralysis. Apparently the disease does not in any way tend to shorten hfe, but treatment is of little if any effect. Muscular Hypertrophy. The occurrence of a true hypertrophy of muscles, as a condition of disease, is exceedingly rare. In most cases in which the muscles are enlarged, the increase in size is due to a growth of interstitial tissue, fatty or fibrous, such as has been described in the chapter on pseudo- hypertrophic paralysis. We have seen that muscular fibres larger than normal have been described in that disease, and also in some cases of simple atrophy. When this increase in size has been met with only in excised fragments, it is possible that the condition may have been due to a vital contraction excited by the process of excision, and such evidence of hypertrophy is certainly inadequate ;* only when * Since the above was written, the doubt there expressed has been confirmed by an observation made for me by Dr. H. R. Spencer. A fragment of the gastrocnemius of an amputated leg was excised immediately after the amputation, and the fibres were coin pared with those of the muscle twenty-one hours later. In order to ascertain more definitely whether a vital contraction persisted as an apparent increase in size, a part of the excised fragment was separated and faradised. The average size of the fibres in the muscle was T|o inch, in the fragment excised 1 inch, in the fragment faradised T-iT inch. Since the division of the nerve durin"- the amputation may have caused some contraction, it is possible that the difference in size produced by excision may be even greater than these figures represent. [I leave the above note unchanged because, since it appeared io the first edition, the observation and doubt have been fuily confirmed by various observers, e.g. by Oppenheim and Siemerliug, 'Med. Centralbl.,'1889, No. 39.] It is inte- resting, however, to note that enlarged muscular fibres have been found in the atrophied muscles in infantile paralysis. 600 SPINAL CORD. it is found after death can its occurrence be regarded as beyond ques- tion. Nevertheless true hypertrophy of fibres is a change that may be expected to be occasionally met with in cases that are due to a con- genital tendency, and its presence, even in muscles that are the seat of atrophy, need, therefore, excite no surprise. It was met with by Bruck in a remarkable case of general muscular enlargement in an idiotic child, in whom it apparently developed after birth. The affec- tion first showed itself in the tongue, but the muscles presented spasmodic contractions, and the case, like most of the kind, was evidently anomalous in its features. Muscular hypertrophy has been found in the singular malady described in the next section (Thomsen's disease). It has also been met with, in very rare instances, as a wide-spread or partial condition, usually associated, strange to say, with either diminished power or with a morbid readiness of fatigue.* The muscles most frequently affected have been those of the shoulder and upper arm, or of the thigh and calf, on one side or on both. It has also been observed in the glutei, spinal muscles, and trapezii. The causes are obscure, but it has been ascribed to over-exertion. The diameter of the fibres has been increased to double the normal, a maximum of -g^ inch having been met with (Eulenberg), whereas the normal maximum may be taken as -^^ inch. An increase of the nuclei has been observed, without any overgrowth of the interstitial tissue. The condition is manifested by an increase in the size of the muscles, which are also firm. The circumference of the limb is greater than normal, and when the change is unilateral the difference between the limbs of the two sides may be very striking. The maximum circumfer- ence of the calf has been as much as seventeen inches. The muscles are soon exhausted, and have been weak in some cases, while in others there has been abnormal strength for brief exertion. The electrical, mechanical, and myotatic irritability of the muscles has usually been found unaltered. The disease may be suspected if a marked increase in size in an adult is accompanied by impaired power of sustained exertion, if the muscles are firm, and the patient does not manifest other indications of pseudo- hypertrophic paralysis. The diagnosis can, however, only be made with certainty by the microscopical examination of an excised fragment, and even then subject to the reservation mentioned on the previous page. The meagre facts regarding the course of the disease suggest that it usually persists without getting either better or worse. Treat- ment appears to have but little influence upon it. A singular case has been reported by Eulenberg,f which differs in * Auerbaeh, ' Virchow's Archiv,5 Bd. liii, pp. 234 aud 397; Berger, * Deut. Archiv f. klin. Med.,5 Bd. ix, 1872, p. 363 ; Friedreich, ' Ueber Prog. Muskelatrophie,&c.,' 1873; Eulenberg, ' Real-Kncyc lopadie,5 Bd. ix, p. 354. A very similar case is described by Pal, * Wieii. kliu. Wochenschr.,5 1889, No. 10. t ' Deutseh. med. Wochens'hrift,' 1885, No. 12. THOMSEN's DISEASE. 601 many particulars from the form of disease above described, and illustrates the complex relations of enlargement of the muscular fibres and its connection with degenerative processes. A man aged thirty- six presented an enormous enlargement of the muscles of the left leg, which were soft and flabby and weak, with lowered irritabihty. The condition had slowly developed after a fall on the back at ten, which caused imperfect paraplegia, motor and sensory. A year later, during pleurisy, he had thrombosis of the left femoral vein. In an excised fragment of the gastrocnemius the muscular fibres were large, the maximum being Ti^ of an inch; they presented fatty and vitreous degeneration, and fat was seen between the fasciculi. The muscles of the other leg were somewhat wasted, but the fibres were also enlarged and degenerated. It would appear as though the condition had resulted from a traumatic lesion of the spinal cord, and had been intensified in the left leg by the influence of the thrombosis and resulting vascular disturbance. THOMSEN'S DISEASE; MYOTONIA CONGENITA. The malady thus designated may be considered here, notwith- standing the obscurity of its nature, because it agrees with the diseases last described, in that the symptoms are muscular, and that the disease seems often congenital and occurs in families. It has been named after the physician whose description gained for it general notice, and who is himself its subject, but it had been previouslv described by Leyden, and hinted at, long ago, by Sir Charles Bell.* It is not always congenital, and " Transient Myotone " would be a more exact name. The disease is characterised by a peculiar rigidity of the muscles, which comes on when they are first put in action after a period of rest. The rigidity is transient, and when it has passed off, it does not return * Bell's ' Nervous System,5 Case 184, p. 436. The objections to cognoininal nomenclature of disease are certainly reduced to a minimum when the first describer of a rare disease is also its subject. The most important papers on the disease are those of Leyden, ' Klinik der Ruckenmarkskr.,'1874, Bd. i,p. 128; Thom>en, 'Arch. f. Psychiatric,' Bd. vi, 1876, p. 702, also ' Centralbl. f. Nervenkr.,' 1885, p. 193; Bernhardt, 'Virchow's Archiv,' Bd. lxxv, 1879, p. 516, and 'Centralblatt f. Nervenkr./ 1885, p. 122; Ballet and Marie, 'Arch, de Neur.,' 1883, No. 13; Mobius, ' Schmidt's Jahrb.,' Rd. exeviii, 1883; Ringer and Sainsbury, ' Lancet,' 1884, pp. 767, 816, and 8fi0; Erb, ' Die Thomsen'sche Krankheit,' Leipzig, 1886, also 'Deut. Archiv f. klin. .Med ,' 1890, xlv, p. 529; Seifert, ib., xlvii; M;trie, in ' Encycl. des Se. Med.,' 1886; Hale White, ' Brain,' April, 1886, and ' Gin's Hosp. Rep.,5 vol. xlvi (a very valuable paper, with bibliography); Jacobv, Journ. of Neur. and Ment. Dis.,' 1.^87, xiv, p. 23; Jolly, * Siidwest. Neurol.,* Baden, June, 1890; Buzzard, ' Lancet,' 1887. 602 SPINAL CORD. as long as exertion is continued. The malady is often hereditary, and usually affects several members of the same family. In that of Thomsen, cases can be traced through five generations. It appears to be more common in Scandinavia and Germany than in France or England, but it is a rare disease; * and although a considerable number of clinical cases have now been recorded, there has been no post-mortem examination. There is little to attract attention in the slighter forms, and the rarity of these may ultimately be found to be less than at present appears. Both sexes suffer. In most cases the symptoms have been first noted in childhood, between four and ten years of age, sometimes even in the cradle. They increase during the period of muscular development, and then remain stationary. A few patients have seemed free until about the period of puberty, but even in such in- stances it is probable that the tendency was congenital in origin, since the cases occurred in families, other members of which suffered earlier. But in a few cases symptoms apparently identical with those of the congenital disease have come on in early manhood after some exciting cause—in one case a lightning stroke, in another a sudden alarm.f Severe and prolonged exertion during two years preceded the onset of very characteristic symptoms in a man of twenty-five, without heredity.]; In such cases the disease has been apparently acquired. The characteristic symptom is tonic spasm of the muscles when they are put in action after a period of rest. As soon as the patient attempts to move, the muscles become rigid. The rigidity may make movement impossible while it lasts, or may merely lessen the possible range of movement. After a few minutes, or less, the spasm passes away, to be renewed, but in slighter degree, by a fresh attempt. If the movements are continued, the spasm soon becomes trifling, and does not return until after a period of rest. The longer the rest, the more troublesome is the spasm. The subject can walk for hours without fatigue when it has passed off. The rigidity is sometimes lessened by alcohol and increased by attention and by fear of it; the more the sufferer tries to overcome the stiffness, the less is he able to do so. It is also worse in cold and damp weather. In a severe case, a slight impulse will make the person fall, and it may then be impossible for him for some minutes to rise from the ground. The arms are usually less affected than the legs, but in some cases the rigidity fixes the fingers for a short time on an attempt to use the hand. The muscles of the face are usually free ; mastication mav, however, be interfered with by the spasm in the muscles of the jaw". Rarely, the : * In England cases have been observed by Buzzard, Herschell, Hale White, Bcnham, Chapman, and others. t Engel, < Phil. Med. Times,' 1883, p. 412; Schonfeld, < Berlin, med. Wochenschr.,' 1883, No. 27. X Mover, 'Med. News,' 1890. thomsen's disease. 603 tongue or farvs has been affected; still more rarely the muscles of the eyeball, interfering with its movement and retarding the descent of the upper lid.* Most voluntary muscles, indeed, seem liable to suffer, even the muscles of the larynx and pharynx ; those concerned in the processes of respiration, defecation, micturition, and coitus have also been involved. Sometimes the spasm is greater on one side of the body than 01 the other. The mueMes are always well nourished ; they are often, indeed, above the norma' size, and possess more than normal strength, but they are sometimes less strong than is normal, even when large. Thorn sen believes that the more the muscles are employed the less severe is the spasm, and that a life of active exertion produces some per- manent amelioration in the disease. The malady is, however, a source of some disability, and of considerable annoyance ; in the words of Thomsen, " it casts a shadow over the lives of the sufferers," and may have caused the mental irritability and hypochondriacal tendency that have been conspicuous in some cases. Careful investigations of the muscular phenomena have been made by several observers, and that by Erb is especially instructive. In his case a single brief effort caused tonic contraction which lasted for twenty-five seconds. Momentary electrical stimulation of the nerves caused only a momentary contraction of the muscles, but continued stimulation always causes a prolonged contraction, the "myotonic reaction" of Erb. In certain muscles, moreover, an uninterrupted current caused peculiar wave-like contractions, about one per second, passing from the negative to the positive pole.f Any strong stimu- lation of the muscle itself caused a prolonged after-contraction.J The irritability of the nerves is generally normal in degree ; that of the muscles is normal or increased to voltaism. In some cases the anodal closure contraction has occurred with undue readiness, and the "latent interval" after stimulation has been found unchanged (Hale White) or increased.§ The muscles are remarkably sensitive to mechanical stimulation, and firm pressure may cause a tonic contrac- tion lasting from twelve to twenty seconds. In all undoubted cases of this disease sensibility has been intact, and the superficial reflexes have been unaltered. Myotatic irritability is normal or increased. Once developed, the condition seems to persist, with little change, through life, but in one case, a female (in whose family were other casesj, considerable improvement is said to have followed marriage.|| * Raymond, ' Gaz. Med. de Paris,' June, 1891. f Although Erb, SeitVrt, and others have noted this, some observers (as Hale White) have failed to ohtain the phenomenon. + Jolly has found that repeahd stimulations by either current, without too long in interval between the successive stimulations, tend to render the afier-contraction less and less evident, until it ceases to occur ('Neur. Centralbl.,' 1890, p. 438). § -025 or -03 sec. instead of -01 (Bluminau, 'Neur. Cent.,5 1888, p. 679). || Herschell, ' Lancet,' l'eh. 1, 1890. 604 SPINAL CORD. In some instances the symptoms are slight, and remain so, even when they begin in early life and occur in the same families as severe cases. Such cases, when isolated, may readily be overlooked. Pathology.—An examination of the central nervous system has yet to be made, but it is unlikely to jield results of novelty or im- portance. The state of the muscular fibres has been ascertained from excised fragments—a method which, however, involves the fallacy, already mentioned (p. 599, note), of possibly stimulating the fibres to contraction. At the same time the evidence of hypertrophy appears conclusive. Where the minimum width was the same as in health, the maximum diameter was double the normal (Erb). In other cases the maximum or even average diameter in fragments excised under chloro- form was double that observed after death in unaffected persons; and that the size was pathological was rendered probable by the aspect of the fibres, which presented indistinct striation, fewer " sarcous elements," irregular, non-parallel edges, and sometimes vacuolation. An increase of the nuclei and of the interstitial connective tissue has been found.* The manifestation of the disease is in a disorder of the functions of the muscles, and most writers on the subject have followed Leyden in regarding the malady as essentially muscular in nature, as consisting in an altered functional condition of the muscular tissue. This opinion is strongly supported by the frequent alteration in electrical excitability (which can hardly be otherwise interpreted than as an indication of a change in the mode of action of the contractile muscular protoplasm), by the structural changes, and also by the interesting experiments of Einger and Sainsbury, who found that certain salts, such as sodium phosphate, are capable of causing in the fro©- tonic spasm bearing considerable resemblance to that of Thomsen's dis- ease, and that such spasm persists not only after the nerve has been divided, but after the intra-muscular nerve-endings have been paralysed by curara. This does not prove that Thomsen's disease is muscular in origin ; it is a proof that a similar state may be due to the mus- cular tissue, but no proof that this is the sole element in Thomsen's disease. We must remember that the malady has apparently resulted, in rare cases, from influences acting on the nervous system in adult life, and also that, in the congenital cases, the spasm only develops, as a rule, after some years of normal action. It may thus be an acquired disease, and the case related at the end of this chapter shows that similar spasm may be due to a primary affection of the cord. The spasm is a transient consequence of rest. But "rest" is not inactivity, either in the nerve-cells or muscles. Muscular " tone " and adaptation to posture mean an unceasing flow of nerve-force from the cells, an overflow perhaps, due to the perpetual elaboration of energy which keeps the cells ready for instant response to the * Erb, Seifert, and also Nearonow, ' St. Petersburg psych. Gesellsch.,' 1889 • see 'Neur. Cent.,5 1889, p. 239. Hale White found no increase in the nuclei. THOMSEN'S DISEASE. 605 voluntary stimulus. The tonic activity then ceases, or at least does not interfere with the different action excited by the will. But the phenomena of Thomsen's disease suggest that the cells respond abnormally to the voluntary stimulus, that this causes at first an increased tonic activity, slowly ceasing as their energy is lessened by action. Wide as is the difference between the muscular and nervous tissues, we must remember that they have some conditions in common. The dependence of the nutrition of the muscles on that of the motor nerve-fibres and cells is a very remarkable fact, and so also is the in- fluence of the functional activity of the cells and fibres in causing a similar condition in the muscular tissue. To say that the two struc- tures are connected is hardly an explanation of the fact. Whatever is the nature of the relation between them, it is at least conceivable that an abnormal functional state, congenital in origin, may be common to the two, and that the peculiar over-action in the muscles may be accompanied by a similar over-action in the ganglion-cells of the spinal cord, and even in the pyramidal cells of the cerebral cortex. It is even conceivable that the condition of the nerve-cells may be the primary change, and that of the muscles may be secondary, although when produced it is in some degree independent, and may be excited independently by local stimulation. Such a theory enables us to understand the two facts above mentioned—the influence of emotion and the acquisition of the disease, each of which seems to be incon- sistent with a purely muscular pathology. Treatment.—No treatment, properly so called, appears to exert any influence on the disease. The congenital malady persists through life; in the cases in which a similar condition has apparently been acquired, it has also been persistent. The only influence that has appeared to Thomsen to ameliorate the condition is a life of active muscular exertion. But it is possible that the influence of thera- peutics is not yet exhausted. Congenital Paramyotone.—Under this name Eulenberg has de- scribed * a strange family affection, allied to Thomsen's disease in its o-eneral character, although differing very much in its special features, and equally obscure in nature. The malady was widely spread in the affected family, and could be traced through six generations, but appears now to be dying out. Its congenital character was shown not only by its multiplicity, but also by the fact that in some individuals it was manifested immediately after birth. The symptom was tonic spasm, lasting from a quarter of an hour to several hours, excited cnieflv by cold, although often by merely slight cold. The rigidity was followed for a time by weakness. The facial muscles were very prone to become thus rigid, especially the orbiculares palpebrarum and oris; and while the contraction lasted the patient was often unable to speak or to open the eyes. The rigidity was slighter in the legs than in the * ' Neurologisches Centralblatt/ 1886, p. 265. 606 SPINAL CORD. arms, but the subsequent weakness was equally marked. Warmth removed the spasm. There was no persistent loss of power, and no increase of mechanical irritability. The electrical excitability of the nerves was normal; that of the muscles was lowered to each current, and there was an abnormal tendency to tetanic contraction during the passage of the current. Eulenberg speculates that the symptoms may be due to reflex vaso-motor spasm in the muscles, because the diminution of the blood-supply to muscles renders them weak; but it is clearly equally possible that the two certain phenomena, the sensory impression and the muscular contraction, may be directly connected. Ataxic paramyotone seems the best provisional designation for an icquired condition of which one case has come under my notice. Persistent tonic spasm, like the transient spasm of Thomsen's disease, was associated with distinct ataxy, and also with weakness and some anaesthesia. The symptoms commenced gradually in the legs, in a healthy man aged 40, without neurotic heredity; it invaded the arms six months later, and increased more rapidly in the arms than in the legs. At 411 his state was this : a well-built man, with well-developed muscles, unduly firm in all parts except the neck and head. The firmness was due to tonic spasm, which never ceased. It was present on waking in the morning, and through the day interfered with all movements, making them slow and stiff. He rose from a seat slowly and with difficulty; when standing there was slight unsteadi- ness, increased by closing the eyes, and a slight impulse or stumble in walking would cause a fall, chiefly because the spasm prevented the needed quickness of movement to save him. Prolonged exertion had no influence on the tonic spasm, which opposed passive as much as active movement. Power in arms and legs was lessened, but not considerably. The grasp = 50 and 55 ko. The extensors of the fingers were weaker than the flexors, but could act perfectly although involuntary flexion followed the slow extension. The electrical irritability of the muscles seemed to be normal. Inco-ordination was especially marked in the hands ; with eyes shut, buttoning his coat was almost impossible; the attempt was made with thumb and fore- finger, the others being flexed, and he could touch his nose only after many wandering failures. On the palms, from the wrist to the tips of the fingers, sensibility was lost to touch, slightly delayed to pain, little changed to temperature. Slight tactile loss extended to the back of the last phalanges; on the back of the hands it was normal. A similar but slighter loss existed on the soles: he often felt as if walking on a rounded surface. The size and weight of objects placed in the extended hand could not be recognised. No trace of the knee-jerk or other evidence of myotatic irritability could be elicited, but the spasm was enough to explain the failure, and its real condition is uncertain. Mind, special senses, and cranial nerves were unaffected. TUMOURS. 607 Unfortunately the course of the affection could not be observed. Its symptoms must have been due to disease of the spinal cord, and they are instructive as showing that muscular spasm, like that of Thomsen's disease, may be thus produced. The time may not have been sufficient for the production of changes in the irritability of the muscles, but we must also remember that differences in the influence on the muscles may be connected with the defective power. TUMOURS OF THE SPINAL CORD. Morbid growths within the spinal canal may spring from the mem- branes, or may grow in the substance of the cord itself. The differ- ence in seat entails some difference in symptoms, but it is nevertheless convenient to consider the two classes together, because they have many symptoms in common, and it is often impossible to carry the diagnosis farther than the existence of an intra-spinal tumour. Etiology.—The general causes of these growths correspond, for the most part, to those concerned in their production in other situations, and present few peculiarities that merit special mention. Fatty growth outside the dura mater occurs early in life ; malignant tumours develop late. Of tumours within the dural sheath, myxomata are chiefly met with in middle life, tubercular growths occur occasionally in childhood, but generally between fifteen and thirty-five (Herter *) ; lipomata are congenital. Males are a little more prone to suffer than females, f Of the diathetic conditions which give rise to tumours elsewhere, only two, syphilis and tubercle, are effective in causing growths which commence within the spinal canal. Parasitic tumours occur, due to the same influences which produce them in other situations A few rare growths appear to be congenital in origin, due to the abnormal development of germinal tissue, while the more common gliomata within the cord arise from embryonal tissue, which has suffered an arrest of its normal development. Of the causes of other forms of tumour we know practically nothing. Injuries, such as a blow on the spine, have been supposed to be occasional causes, and their influence in rare instances has seemed possible, but the evidence is not so strong as it is in the case of tumours in some other situations. In many * Herter, ' Journ. of Mental Dis.,' 1890, has analysed twenty-six cases. f A collection of facts relating to these points, by Mr. Victor Horsley, will be found in the paper written by him and myself on the case of successful removal of a tumour from the spinal cord, ' Med.-Chir. Trans.,' 1889; but the numerical basis is far too meagre to supply more than statistical suggestions. It will be necessary to wait for a considerable time before adequate data are obtained. A very important paper by Allen Starr (* Am. Journ. of Med. Sei.,' 1895. June), deals with an addi- tional series of cases. 608 SPINAL CORD. cases the first symptoms have immediately followed some exposure to cold and wet, and it seems probable that their influence may have excited secondary processes in the nerve-elements which were already deranged by the growth, and may thus have frequently evoked the first sym- ptoms of the tumour, but it can have had no share in the production of the growth itself. Traumatic haemorrhages may, however, result in cystic formations, which have been mistaken for new growths. Pathological Anatomy.—The growths within the spinal canal may develop outside the dura mater, inside the dura mater, or within the substance of the cord. The extra-dural tumours may spring from the membrane or from the tissue between the membrane and the bone, or may grow into the canal from the outside, through the intervertebral foramina. Subdural tumours may proceed from the inner surface of this membrane, from the arachnoid, or from the pia mater (Fig. 170). Tin- growths in the cord may spring from the pia mater, or may develop in the substance of the cord. They sometimes proceed from the peculiar tissue which surrounds the central canal. The forms of extra-dural tumours are lipoma, from an overgrowth of the fat which normally exists between the membranes and the bone; and parasitic tumours, chiefly echinococci; but all are rare.* Growths also occur that spring from the bones or intervertebral tissue—enchon- droma, sarcoma, and cancerous tumours, which have been already considered. Far more frequent are collections of inflammatory pro- ducts from bone disease, but these do not come into the category of morbid growths. FiG. 174.—Myolipoma of the spinal cord. A, transverse section of the tumour and of the conus medullaris of the spinal cord, to which the growth was attached, and of which the grey matter is represented by the dotted shading CM. », sections of nerve-roots, partly enclosed in the tumour; m, bundles of muscular fibres. B, part of the tumour more highly magnified, showing the fat- cells, of which it was chiefly composed; p.m., pia mater of the cord, of which I.e. is part of the lateral column. C, part of the tumour, still more magnified, showing striated muscular fibres, fibrous tissue, and fat-cells (see also Fig. 167, p. 580). The tumour had caused no symptoms. * An adeno-sarcoma has also been met with (Hodenpyl, 'Am. Journ. Med. Sc..' 1888). TUMOURS. 609 The tumours which begin within the dura-matral sheath are chiefly syphilomata, sarcomata, and myxomata, sometimes containing cysts or " brain-sand." Tubercular and parasitic tumours are rare, but both echiuococci and cysticerci have been met with, developing in the meshes of the arachnoid. Fatty tumours have been found in a few instances, and may contain muscular fibres. They are congenital and sometimes associated with spina bifida (q. v.). Fig. 174 represents such a tumour, a myolipoma consisting of fatty tissue and striated muscular fibres, which had grown from the pia mater or meshes of the arachnoid, and was found in a case of tabes.* Neuromata occur on the nerve-roots, and may compress the cord.f The growths within the substance of the cord itself are more diverse in character. Syphiloma and glioma are the most common ; sarcomata, myxomata, and tubercular tumours also occur, containing the characteristic bacilli, and always associated with tubercle else- where. HycYtids are occasionally met with.J Some growths have a compound character, and have been termed myxo-sarcoma, glio- sarcoma, and fibro-sarcoma. Sarcomata and gliomata are sometimes very vascular, and have been termed " angio-sarcoma " and " angio- glioma." It is far more common for the tumour to spring from the pia mater or from the peri-ependymal tissue around the canal than for it to begin among the nerve-structures, but tubercular growths, usually begin in the substance of the cord and usually on one side. Extra-dural growths are always single ; those within the dura mater are often single, but sometimes two or three co-exist; or the growth may be diffuse, as in a sarcoma of the pia mater, which extended as high as the sixth pair of cerebral nerves, and as low as the cauda equina. § Neuromata or sarcomata on the nerve-roots are often multiple, and sometimes are very numerous. Neuro-fibromata on almost all the nerves of the body have been observed to coincide with a similar extra-dural growth compressing the spinal cord. Tumours within the spinal cord are also usually single, even those of tubercular nature, but occasionally more than one growth is found. The size attained by growths outside the cord is necessarily moderate, in consequence of the limitation of the space in which they grow. They vary from the size of a pea to a width of one and a length of two inches, which is rarely exceeded, and chiefly by extra-dural tumours. Those that develop from the pia mater are usually smaller * See 'Path. Soc. Trans.,' vol. xxvii, 19. Another rare case is one of lymph- angioma of the pia mater (Traube, 'Neur. Cent.,' 1887). + Myxo-fibromata may also form on the nerve-roots, and even extend on to the cord. See Bruce and Mott,' Brain,' July, 1887. X Ransom and Anderson, ' Brit. Med. Journ./ 1892 (found only after death though operated on), and a case under my care in which the hydatids were found and removed by Mr. Horsley during life. In other cases they have been met with post mortem. § Pasteur, ' Brit. Med. Journ./ July, 1887. vol. I. 39 610 SPINAL CORD. than those that spring from the dura mater. Multiple tumours of the nerve-roots are generally small. Adhesions often form between the growth and the membrane from which it does not arise. The tumour compresses the nerve-roots and the spinal cord (Figs. 175, 178). The compression produced by tumours within the dura mater is always greater than that by tumours outside this membrane. The amount of pressure is proportioned to the size of the tumour and its consistence. A soft growth outside the sheath may attain a con- siderable size, and even extend through the intervertebral foramina, without exerting much pressure on the cord itself. Even such exten- sion to the outside seldom causes a swelling that can be felt. Probably the Bontgen rays would yield useful information. At the compressed part the cord is narrowed and softened, usually indented or flattened, because the pressure is either from one side, from the front, or from the back. Barely the degree of pressure is so great that the cord is reduced to the size of a crow-quill, and it has even been apparently interrupted at the spot, the upper and lower portions being conical, and their pointed extremities connected only by membranous tissue. The softening of the cord depends on inflammation, the " pressure- myelitis " considered in a preceding chapter (p. 390), and it presents the tissue changes that have been there described. Secondary inflam- mation may extend down the cord below the growth, or for a short distance above it, often unequally in the different elements—sometimes in the grey matter into the lumbar enlargement, and even on one side only (Francotte, see p. 617, fu-dnote). The usual secondary degenera- tions are commonly conspicuous. The growths that involve the cauda equina often attain a larger size than those that occur higher up, because this part of the vertebral canal is large, and the nerve-roots occupy but a small part of it. Most tumours in this situation are sarcomata or fibro-sarcomata, but it is a not uncommon seat of syphilitic growths. They usually spring from the tissue of the arachnoid, and often surround and include the nerves (Fig. 179), the amount of damage to which is very variable. Multiple tumours outside the cord are sometimes verv numerous. They are usually sarcomata, and spring from the membranes and sheaths of the nerve-roots. They are various in size, ranging from that of a hazel-nut to that of a pin's head, and many very small growths a,re often scattered among the nerves of the cauda equina. In some cases of this character similar growths have existed in the cerebral membranes. The tumours within the spinal cord are usually small, seldom ex- ceeding half an inch in diameter, and usually less, even when they give rise to considerable impairment of function. But their vertical extent often exceeds their transverse diameter, and sometimes they grow through a considerable extent of the spinal cord. Gliomata, and especially the gliomatous growths that spring from the central region, and arise from embryonal neuroglial tissue (persistent by arrest of TUMOURS. 611 Fio. 175. Fig. 176. Fig. 177. Fig. 175.—Tumour growing from the inner surface of the dura mater, and com- pressing the spinal cord in the mid-dorsal region. The tumour, 3 cm. long, was a sarcoma in which the cells were arranged in concentric groups, the centres of which had undergone calcification. The spinal cord was softened and dark in tint at the compressed part.* (After Lancereaux.) Fig. 176.—Sarcoma growing between the arachnoid and pia mater in the mid- dorsal region of the cord. The tumour had sprung from the meshes of the arach- i:od, and was only slightly adherent to the pia mater. The spinal cord was compressed and softened. In the figure the dura-matral sheath has been laid open, except at the top, and the arachnoid has been opened over the lower half of the tumour, which, 5 cm. long, lies on the posterior and (right) lateral aspect of the cord.f (After Lancereaux.) Fig. 177.—A tumour (T) growing from the dura mater, and compressing the right .side of the spinal cord at the origin of the 4th, 5th, and 6th cervical nerves. The tumour was a spindle-celled sarcoma springing from the arachnoid. J (After Leyden.) * The patient was a woman seventy-one years of age, paraplegic, with strong flexor contracture of the legs, loss of power over the sphincters, and considerable impair- ment, but not absolute loss, of sensibility. Tjlie symptoms came on gradually six years before death. (Lancereaux, 'Atlas d'Anat. Path./ p. 444.) t The patient was a woman twenty-eight years of age. The first symptom was pain, radiating over the upper part of the abdomen on the right side, and after- wards extending to the leg and to the left side. After a few months, weakness of the legs gradually came on, and became absolute, with loss of sensation and of power over the sphincters. Extensive bed'iies were the immediate cause of death, which occurred eighteen months after the on?et. (Lancereaux, 'Atlas/ p. 447.) X The patient was a man aged thirty-five. At twenty-eight pain commenced in 612 SPINAL CORD. Fig. 17S. Fig. 170. Fig. 180. Fig. 178.—Tumour of dura mater opposite the upper part of the lumbar enlarge- ment, compressing nerve-roots and spinal cord. (From a preparation in University College Museum. Drawn by Dr. H. R. Spencer.) Fig. 179.—Tumour of the cauda equina surrounding and enclosing many of the nerve-roots. The cord itself was unaffected. The structure of the tumour was that of a fihro-sarcoma.* Fig. 180.—Neuromata of the cauda equina. (After Lancereaux.) The growths had apparently given rise to no symptoms. the right forearm, and continued, intermitting, for some years, until at thirty-four it extended through the whole arm to the neck beside the spine, where it was increased by movement. Similar pain afterwards came on in the left arm. Then followed weakness in the right arm, slight spasm in the right leg, and tinglino- in the left. The arm became almost powerless and wasted, the right leg weak, and flexion of the neck caused severe local pain. These symptoms continued and increased, and pain in the left leg came on. The cervical spine became tender, and movement of the head to the right was limited. Then both legs became weak, and sensibility was lost as high as the nipples. The paraplegia became absolute, bed- sores formed, and the patient died seven years after the onset of the symptoms. Softening of the spinal cord extended down into the dorsal region. (Leyden, 'Klin. der Riickenmarkskr./ Bd. i, p. 450.) * The patient was a man aged twenty-eight, whose symptoms commenced nine months before death, and consisted in severe pains in the legs and progressive weak- ness, the power of standing being lost about four months after the onset. A little power in the flexors of the hips and the extensors of the knees persisted almost to the last, but the knee-jerk was lost. All the muscles of the legs wasted, those below the knee extremely, and even when the patient was first seen electrical irritability was greatly lowered to both currents^without any reaction of degeneration. Tactile sensibility was impaired in each foot and lower leg, more in the right than in the left, and chiefly in the region supplied from the sacral plexus. Sensibility to pain was not affected. The bladder was affected early, and symptoms of pvelo-nephritis already existed. The kidney disease was the immediate cause of death, which was preceded by several convulsions, apparently ursemic. A microscopical examination showed considerable damage to many nerve-roots involved in the tumour, while others had escaped. The muscles presented intense granular degeueration with some longitudinal striation, and increase of the interstitial nuclei. TUMOURS. 613 development, and often associated with syringomyelia), are those which have most frequently a considerable vertical extent. Such a glioma has been known to reach from the medulla oblongata to the lumbar region, and often extends up from the cervical region to the base of the brain. The cord is enlarged at the seat of a tumour, and the precise character of the enlargement depends on the position of the growth. In an infiltrating glioma of the upper part of the cord the increase in size has been so great that the wall of the foramen magnum caused a constriction around the swollen cord. Often the abnormal colour of the tumour is perceptible on the surface. The consist- ence of the cord may be lessened in soft growths, but the tumour is commonly firmer than the normal cord, and the differ- ence is frequently increased by softening in the vicinity of the growth. If the tumour reaches the surface the pia mater and arachnoid may be thickened at the spot, and they may even be adherent to the dura mater, but there is rarely any extension of the meningitis to other parts. On section the growth is usually very distinct, since its aspect contrasts with that of the nerve-substance. Only glioma and myxoma resemble the normal grey substance in appearance, but the new tissue is usually distinct in position. These tumours in some cases blend with the substance of the cord, but in other instances they are bounded by an area of softening which often iso- lates even invading growths. Some tumours are sharply limited. It may be difficult to say in what structure the tumour began, but this may sometimes be ascertained by an examination of the upper and lower parts, where the growth is commonly limited to that part of the cord in which it first originated. Thus in Fig. 181, B, the tumour occupies a very large area, although Fig. 181.—Tumour of spinal cord, springing from the tissue around the central canal. A, upper part of the tumour in the middle of the cervical region ; the growth is here within the posterior commissure. B, section through the largest part of the tumour, which occupies the whole central region of the cord. The vertical extent was 2 cm. It was a sarcoma composed chiefly of spindle-cells arranged in fasciculi and in concentric layers. The patient was suffering also from a cerebral tumour causing hemiplegia, and the spinal growth, which apparently developed rapidly during the final period of palsy and prostra- tion, was not suspected during life. 614 SPINAL CORD. the nearly equal extent on each side suggests its central origin, and this is clearly seen in the section through the upper part of the growth, in which the posterior commissure can be traced in front and behind the small area of growth, pointing to the periependy- mal tissue as its source. Syphilitic tumours commonly originate from the pia mater, as they do also in the brain, and the mem- brane in their vicinity is often thickened. They both invade and compress the nerve-tissue. An instance of such a gumma of the cord is shown in Fig. 182. It probably commenced at the furrow opposite FiG. 182.—Syphiloma in the spinal cord, occupying the position of the posterior cornu and adjacent parts of the posterior and lateral columns, in the lower cervical region. The tumour presented the usual combination of grey translucent, and yellow cheesy areas. A second similar, but much smaller tumour existed higher up. The symptoms were complicated by hemiplegia, &c, of cerebral origin, due to a gumma in the brain. Para- lysis with rigid flexor contracture of the left arm and leg were apparently due to the growth. The disease was certainly syphilitic, but it is note- worthy that it had developed during continuous treatment by full doses of iodide, which had entirely removed earlier symptoms, but to which the system had apparently become accustomed. the head of the posterior cornu, which it has destroyed, and the pres- sure which it exerted is evident from the displacement of the posterior median septum. In all forms of tumour the central canal is often obliterated by the pressure, and may be slightly dilated higher up; this dilatation is especially common from growths that begin in the peri-ependymal tissue. The considerable enlargement of the canal, termed " syringomyelia," is generally associated with a peculiar growth in this position, probably congenital in origin; the condition is described in another chapter. In other forms of tumour, cysts occasionally develop, and haemorrhage may occur into such cvsts. or into the softened tissue in the vicinity of the tumour, or even in the TUMOURS. 615 substance of a soft growth itself, especially when this is a glioma. From theregion of the growth, secondary degenerations can frequently be traced upwards and downwards, but these are often shghter than the apparent damage would suggest, sometimes by reason of the remarkable tolerance of the nerve-fibres to pressure if this is slowly developed, sometimes because a rapidly growing tumour has not given time for them to become conspicuous. As regards vertical position, growths may occur in any part, but are said to be most frequent beneath the lower cervical spines, and in the upper and lower dorsal regions, because (it is conjectured) there is least room at these places, although why the result should follow from the cause is not clear. Symptoms.—The symptoms produced by tumours within the spinal canal, whether these are within the cord or outside it, resemble in their general characters those which we have already considered as resulting from growth and caries in the bones of the vertebral column. The resemblance is most close in the case of extra-dural growths, and least so in that of tumours within the substance of the cord. The chief differences are the relative preponderance of symptoms of early irritation of the cord itself when the growth is within it, and the frequent indications of a transverse extension of the damage from one side of the cord to the other. In the majority of cases pain is prominent through the whole course of the disease. It is usually the earhest effect, severe both before and after the development of other symptoms. The pain may be intense along the course of the nerves which arise at the level of the tumour, and also in the parts supplied by nerves below that level, e. g. in the legs, but it is not felt above the growth. It may be a sharp acute pain, but has often a "burning" character, and is sometimes " stabbing" or "rending." Dull aching pain may be felt between the attacks of severe pain, or before them, and may then give rise to the most frequent of all diagnostic errors—mistaking grave organic disease for simple rheumatism, on account of the similarity in the character of the pains. The intensity of the severe pain is usually very great, and it has more than once led the unhappy sufferer to attempt suicide. The pains are often felt on one side first, in one arm, in one side of the trunk at a given level, or in one leg, and a considerable time may elapse before they extend to the other side. Occasionally the pain is bilateral from the first. Dr. Starr has drawn attention to the rarity of tenderness of the nerves in the line of the pain.* It is o-enerally greatest when the tumour compresses the cord from behind forwards, or vice versa (Horsley) ; this is open to more than one explanation. Pain is sometimes increased by movement, but rarely in the intense degree common in tumours of the bone. When the growth is in the lower lumbar region, the pain is often first referred to the soles, and seems to ascend. The sensory loss, due to subse- * Allen Starr, 'Amer. Journ. .Med. Si-.,' 1895. 616 SPINAL CORD. quent nerve destruction, follows a similar course. Pain is sometimes felt in the spine, frequently when the growth begins in the dura mater, rarely when it is within the substance of the cord. Tenderness of the spine often exists in the former cases, but is on the whole not common. Other subjective sensations may occur with the pain or in the intervals—" numbness," tingling, formication, &c, and they give significance to the pains as an indication of organic damage to the nerve-structures. The root-pains in the trunk are often accom- panied by a sense of constriction, which may be very distressing. Hyperaesthesia of the skin frequently accompanies pain felt at the level of the tumour, less commonly that in the parts below. Yery rarely pain is absent; chiefly in extra-dural lipoma, probably from the nature of the growth. Muscular spasm is another common symptom, most pronounced when the tumour springs from the membranes. There may be some rigidity of the back opposite the seat of the growth, usually associated with local pain. It is most marked when the disease is at the more mobile parts of the spine, especially when it is in the cervical region. In such cases the rigidity may be painful, and the pain may be increased by movement. Severe spasm in the abdominal muscles is often associated with severe girdle-pain. Contractures may develop in the limbs, both in those supplied by the nerves which arise at the level of the tumour, and are directly irritated by it, and also, although less commonly, in the parts supplied from the spinal cord below the level of the growth. Thus the tumour in one half of the cord in the cervical region (shown in Fig. 182) caused persistent flexor contracture in the arm and leg on the side of the growth, and in the early stage of dorsal tumours one leg only may be rigid, or more so than the other. The seat of rigidity thus needs to be specially noted, as well as its character, if we are to obtain from it diagnostic guidance, because it may be due to the irritation either of the nerve-roots or of the conducting tracts. Both forms sometimes occur before loss of power, but pain generally precedes them. Paralysis, of gradual onset, is almost invariably one of the sym- ptoms. Paraplegia is the most common form, but all four limbs may be paralysed by a growth in the cervical region. Yery commonly one leg becomes weakened before the other, and occasionally one arm and leg suffer before those of the other side. Tumours which are situated in the middle line or in the centre of the cord, however, usuallv affect both sides at the same time, and the effects of a congenital growth may thus accompany and complicate those of an associated syringomyelia (q. v.). 'Ihe proximal parts of the limbs seem, as a rule, to be first allected, although exceptions are occasionally met with. The palsy, gradual in onset, is usually also slow in its extension, the rate of its increase depending on the rate at which the tumour grows and compresses the spinal cord. This is the characteristic course of TUMOURS. 617 the paralysis produced by a tumour. But in a large number of cases the loss of power comes on in a subacute, or even an acute manner, in consequence of the myelitis excited by the compression, which in such cases may run a course of independent rapidity. When the inflam- mation is thus in excess of its cause, the palsy may lessen as damage from the inflammation subsides to the degree of the damage from pressure. The symptoms that depend on compression slowly but surely increase as the tumour grows, and usually attain a high degree of intensity; the loss of power in the legs, for instance, becoming abso- lute and remaining so. Loss of sensation may come on with the loss of motor power; more often after this has become considerable. It may be slight or partial at first, occasionally for a long time, but tends to become complete as the damage to the cord increases, and it often ascends the legs. It corresponds in distribution to the motor palsy when the disease is below the middle of the dorsal region ; but if situated higher, and on one side, the sensory loss is often greater on the side opposite to the motor paralysis. Tumours of the cord furnish a con- siderable proportion of the cases in which the crossed symptoms of a unilateral lesion are well marked (see p. 272). In addition to the loss of sensation which results from the damage to tlie cord itself, areas of ansesthesia may exist in the region supplied by the nerves which are damaged by the growth, and in which the severe radiating pains are felt. If there is crossed sensory and motor palsy, these root symptoms exist, chiefly on the side opposite to the anaesthesia in the limbs. Inco-ordination of movement is not a common symptom of spinal tumours, but has been occasionally met with in cases of growth invading the posterior columns, and also as a result of multiple tumours of the nerve-roots (see p. 478;. Loss of power usually co-exists and quickly becomes predominant when the growth is in the cord. The condition of reflex action depends on the position of the tumour. In the lumbar enlargement or the cauda equina a growth abolishes reflex action in the legs, and in any position the trunk- reflexes are lost at the level of the lesion. But when the disease is situated higher up, reflex action is increased, and the excess of culaneous reflex action is a very marked and earlv symptom of the disease; it is lessened and lost only when the lower part of the cord is damaged by secondary myelitis (superadded to descending degenera- tion and distinct from it). The myotatic irritability presents also the increase that invariably results from damage to the pyramidal tracts, and the usual tonic spasm also gradually develops and often readies a high decree. Its loss, with muscular relaxation, sometimes met with under these conditions, depends on a descending myelitis, sometimes slight and partial.* Muscular contracture is superadded more * As was found to be the case by Francotte ('Fibrome de la Dure-mere spinale,' Lie^e, 1SS8) in a case of tumour compressing the upper dorsal region. Slight 618 SPINAL CORD. frequently in tumours than in many other diseases, and rigid spasm in the flexors of the knee and hip may keep the heels in contact with the nates. Wasting of the muscles is for the most part confined to the regions supplied by the damaged nerve-roots. In tumours of the lumbar enlargement and cauda equina the atroph-y of the muscles of the legs is a very conspicuous symptom. Considerable muscular wasting in the legs may result from an irritable growth in the cord above the lumbar enlargement, even in the cervical region, (but such atrophy does not reach the extreme degree produced by growths in the lumbar enlargement or cauda equina,) and this condition is further dis- tinguished by the preservation of the muscle-reflex actions (knee- jerk, &c ), and often by their excess (foot-clonus). Yaso-inotor dis- turbance sometimes occurs in the early stage of the disease, chiefly in the distribution of irritated roots, where flushing of the skin has been noted, and the so-called " meningitic streak " (" tache spinale ") may often be produced. Occasionally vaso-motor oedema is a con- spicuous early symptom. In the later stages bedsores are very common and often severe. Dilatation or contraction of the pupil is common when a tumour is situated in the lower cervical region. Loss of control over the sphincters usually accompanies motor palsy in the legs; their state corresponds with that of reflex action (p. 267). The course of the symptoms is variable, and depends on the rapidity of growth of the tumour, and on the share which secondary myehtis takes in the production of the symptoms. As a rule the root symptoms occur first, and in growths outside the cord they may exist alone for months and even, in the case of a slowly growing tumour, for years before the symptoms of damage to the cord itself are added. On the other hand, they may be entirely absent in growths which commence within the cord itself. In some cases the symptoms are steadily progressive from first to last. In others the progress is intermittent; periods of increase in the symptoms alternate with stationary periods. Their course is variable, even in cases in which the seat of the tumour and its nature are the same, because they depend on the secondary changes in the nerve-elements, and the course of these (such as the myelitis induced by pressure) is subject to variations, the cause of which is often indistinct. Thus the chronic course of the symptoms is often varied by periods of rapid and even sudden increase, espe- cially in the case of growths that involve the spinal cord itself; and symptoms that have thus developed with rapidity are apt (as already mentioned) to subside, if not completely, at least in considerable degree. Hence a rapid increase of the cord symptoms may be followed by positive improvement for a time, but scarcely ever by an descending inflammation of the right anterior cornu coincided with flaccid palsy of the right leg. It should have been mentioned that the connection of a similar loss of myotatic irritabil ty with descending inflammation in dorsal myelitis (referred to at pp. 2(5-1, 271 and 300) has been proved in two other cases by Francotte (loc. cit., p. 9). TUMOURS. 619 actual disappearance of the manifestations of the disease. The most important element in the course of the disease is the tendency to a lateral extension of the symptoms, the expression of the transverse extension of the damage, as the several structures of the cord, at the same level, successively suffer. Although there is sometimes an exten- sion downwards of the interference with the central functions of the cord, when secondary myelitis descends to the lumbar enlargement, there is scarcely ever an extension upwards above the level of the initial interference with function. A very small, slowly growing tumour, even within the cord, sometimes causes no symptoms. The chief differences between the symptoms of tumours of the cord and membranes, besides those mentioned on p. 615, are that, in the latter, the root symptoms are more often severe, and that the cord symptoms occur later, and are at first more limited in extent. Spinal pain, tenderness, and rigidity are more common. In cord tumours the radiating pains, due to irritation of the nerve-roots, are more often trifling or absent, unless the growth begins in the neighbourhood of the posterior horn ; then they may be pronounced. The cord symptoms are often bilateral from the first, and in central tumours they may develop equally on the two sides. If they are unilateral at the onset they extend to the other side sooner than in the case of meningeal growths. In the case of tubercular growths the symptoms of irrita- tion are usually subordinate to those of impaired conduction, and. pain is felt chiefly in the legs (Herter). Extensive muscular atrophy is more common in tumours of the cord than in those of the membranes (except in the case of tumours of the cauda equina), because central tumours may damage the grey matter through a considerable vertical extent, and are most common in the enlargements, and also because mvelitis spreads in the grey matter- far more frequently when the exciting growth is in the cord itself, than when it is in the mem- branes. In tumours of the cervical region, the interference with movement of the neck, from the rigidity of the muscles, is often well marked, especially when the tumour is in the membranes. The pains due to irritation of the nerves are felt in the arms, and are often associated with muscular atrophy. The excess of reflex action in the legs is very great, and if the influence of the tumour is chiefly on one side, hemiplegic weakness, with crossed anaesthesia, is present. Growths in the dorsal region of the cord usually cause severe radiating pains in the trunk, often accompanied by an intensely painful sense of constriction, by hyperaesthesia, and sometimes by anaesthesia. The simple, merely sloping course of the dorsal nerves reveals the pre- cise position of the disease more clearly than do the symptoms in the arms when the tumour is in the cervical region. The interference with the trunk-reflexes often corroborates the indications afforded by the subjective symptoms. Spinal tenderness may be also present, but rigidity of the spinal muscles is not common. Keflex action in the 620 SPINAL CORD. legs presents the same excess that results from tumours in the cervical region, but sometimes, especially when the growth is near the lumbar enlargement, or the pressure myelitis has been acute, the descending myehtis, as we have seen, may abolish the reflex action and remove spasm, if this previously existed. The symptoms produced by tumours which involve the lumbar enlargement vary considerably according to the precise position of the growth. The characteristic pains are felt in the legs, and the muscles supplied from the part invaded or compressed undergo atrophy, and present loss of reflex action and of myotatic irritabihty; but the anaesthesia is often limited in area. A growth in the upper part of the enlargement may cause wasting only in the flexors of the hip and extensors of the knee, with loss of the knee-jerk and anaes- thesia in the front of the thigh, while the muscles below the knee present simple palsy with myotatic excess. Thus a man, who had had syphilis, complained of pain in the left groin and thigh, and presented wasting of the extensors of the knee, with anaesthesia in the front of the thigh; there was loss of the left knee-jerk, and a foot-clonus on each side. He recovered partially, but there was doubtless a small syphiloma at the upper part of the lumbar enlargement on the left side, interrupting the reflex arc, damaging the left motor and sensory roots, and compressing both pyramidal tracts. A growth in the membranes adjacent to the middle or lower part of the lumbar enlargement usually causes symptoms of wide distribution, affecting the whole of both legs, and the early symptoms of irritation often involve the distribution of the upper lumbar nerves. But a growth at the same level within the cord may affect chiefly the muscles of the lower leg, and cause anaesthesia in the region supplied from the sacral plexus, There may also be palsy and wasting of all the muscles of both legs, rom extensive secondary myelitis, but even then the sensory loss is usually limited. In lumbar tumours there is early palsy of the bladder and sphincters. Examination of the sphincter ani shows absolute paralysis, and not the pure reflex action present when the disease, arresting voluntary influences, is higher up the cord. The tendency to bedsores is commonly strong in tumours of this part. Growths situated in the cauda equina, which are below, and do not affect, the cord itself, produce symptoms very similar to those due to tumours of the lumbar enlargement, but the symptoms are bilateral from the first in the majority of cases. Barely one leg is affected alone at the outset. The symptoms usually begin in the lowest parts of the legs, which are throughout involved in greater degree than the upper parts, and the flexors of the hip may escape altogether. Muscular contraction is much less common than in tumours situated higher up. The anaesthesia is chiefly in the region supplied by the sacral plexus; the pains, usually very severe, are first felt in the same region, and there may be severe pain on each side of the sacrum radiating to the region of the sciatic nerves. The muscles below the TUMOURS. 621 knee rapidly waste, and often (out not always) present the degenera- tive reaction. Tliese symptoms were well marked and characteristic in the case figured and described at p. 612 (Fig. 179), and the condi- tion of the muscles suggests that the absence of any voltaic irritability in the muscular fibres was due to their early and intense fatty degene- ration. In many cases the symptoms are irregular in distribution, the nerves are included in the growth, and are often damaged unequally, sometimes less than might be expected from the size of the tumour, which may be considerable before its expansion is arrested by contact with the bony walls of the canal. Hence the loss of sensation may be partial, and reflex action may not be completely abolished. In the case above mentioned, for instance, a prick on the sole caused a reflex contraction of the muscles in the upper parts of the legs, but of these alone. In many cases, however, the loss of sensation has been abso- lute, and reflex action also has been entirely lost. The tendency to trophic changes is great, and an affection of the sphincters is almost invariable. Cystitis and its consequences readily occur, and may reach a high degree, ih consequence of residual accumulation, when the patient is conscious only of slight difficulty of micturition. Multiple tumours (met with especially in cases of tubercle and gliomatosis) may give rise to very complex symptoms. If there are only two tumours, they may be indicated by the successive develop- ment of focal symptoms, similar in character but different in seat. In some cases in which there are many growths, only one or two of the largest have caused symptoms, and the smaller tumours have run a latent course. In other cases in which many tumours have caused slight symptoms, these have simulated closely a system-disease of the cord. Thus, in the remarkable case recorded by Hughes Bennett, multiple growths on the posterior nerve-roots produced the characteristic manifestations of locomotor ataxy.* When cerebral tumours have co-existed with multiple spinal growths, the symptoms of the latter have usually been lost in those of the intra-cranial disease which has often preceded the spinal lesion. The duration of the symptoms of tumours of the cord and mem- branes, those of syphilitic nature being excluded, varies from three months to five, or even ten years. Equally variable, but shorter, is the time that elapses before the symptoms reach their full develop- ment, which depends partly on the secondary inflammation, partly on the rate of growth of the tumour. From the former cause, the time may be only a few days, when the myelitis is acute; from the latter it may be as short as three or four weeks, in tumours of tubercular or syphilitic nature. In the majority of cases death ensues at the end of from one to three years from the commencement of the symptoms, but these last longer when the growth is outside the dura mater than when inside the sheath. The immediate cause of death is usually the direct or indirect effect of the tumour; but in syphilis death is sonie- * ' Clin. Trans.,' 1885. 622 SPINAL CORD. times due to disease elsewhere, and in tubercle, frequently to general pulmonary tuberculosis (which usually precedes the spinal growth), or sometimes to meningitis. Diagnosis.—The evidence of a growth consists in the symptoms of a focal lesion of slow development, and especiallv in the presence of signs of compression and irritation (pain and rigidity), while the sig- nificance of these is increased by indications that the disease began at the surface of the cord, and sometimes by the history of a cause, as syphilis. Although no symptom is actually pathognomonic, yet the combination of the symptoms, and their course, are in most cases sufficiently characteristic. Those of greatest diagnostic importance are, first, the pain that is felt in the parts at the level of the tumour, or below it, and sometimes in the spine; secondly, the progressive paralysis, motor and sensory. Of less but still considerable importance are the rigidity of the muscles of the spine, the muscular contractions in the limbs, and the early and marked excess of reflex action when the cord itself is involved. In the course of the disease the most important features are the steady progress of the symptoms, and especially their commencement on one side and extension to the other. Of causal indications that occasionally assist the diagnosis, the most important are a history of constitutional syphilis, the presence of tubercular disease elsewhere, and, in rare instances, the existence in other parts of such multiple growths as are known to occur also within the spinal canal, especially multiple sarcomata and neuromata. The diagnosis of multiple growths depends on the recognition of the successive development of the characteristic symptoms in more than one focus. It is rare for more than two of many tumours to cause definite symptoms. The greatest absolute difficulty in the diagnosis of a spinal tumour is presented by the cases sometimes met with, in which an intra-cranial tumour precedes the growth within the vertebral column, and the symptoms of the latter are overlooked in the presence of the severe manifestations of the former. In most cases, however, the additional symptoms, which usually exist, may be detected by careful observation, aaid their significance recognised. Growths involving the cauda equina cause symptoms like those of tumours in the lumbar enlargement, save that the effects are from the first bilateral in even more pronounced degree, and the evidence of inter- ference with the nerves (loss of reflex action, nerve pain, &c.) is even more conspicuous. The differential diagnosis involves the distinction from diseases of the vertebral bones, of the membranes, and of the cord itself. Caries of the spine has many symptoms in common with tumour, but the root pains are rarely very severe, and the effects of compression of the cord are usually bilateral, either from the first or very soon after their commencement; the paralysis seldom reaches a considerable degree in one leg before the other suffers. The signs of bone disease are rarely long absent, and repeated examination usually reveals tenderness and TUMOURS. 623 irregularity of the vertebral spines. From growths in the bones of the spinal column the diagnosis may at first be impossible. But the pain of tumour is rarely increased by movement to the same intense degree as when the growth commences in the bone, unless the tumour is in the cervical region of the cord, and then the greater accessibility of the vertebral column renders the exclusion of bone growths comparatively easy by local examination. In the dorsal region a growth in the bone may long escape detection, but even here the influence of movement on the pain is often extreme, far greater than in the case of tumours within the canal. The effect of the movement of the vertebrae on the nerve-roots, when compressed as they pass through the foramina, is far greater than when they are compressed within the canal. Sooner or later a local enlargement may present itself ex- ternally, and show the nature of the case. " Hypertrophic pachymeningitis," affecting the cervical region, is the only meningeal disease which closely simulates the symptoms of tumour, but its effects are usually from the first bilateral, and they have a considerable vertical extent. Hence it is only with central tumours, which grow through several inches or more of the cord, that the disease is likely to be confounded. In each malady there may be muscular atrophy in the arms, and paralysis, without wasting, in the Lgs But in central tumours the pains in the arms are usually much slighter than in the thickening of the membrane, and there is rarely the early and limited impairment of all forms of sensation which results from the damage to the nerve-roots in the latter disease. This is also true of syringomyelia, in which tactile sensibility usually persists, al- though untypical cases may present much difficulty The diagnosis is considered more fully in the account of that disease. The affection of the cord itself which most closely simulates the symptoms of tumour is a very chronic transverse myelitis. In such a case as that shown in Fig. 108, p. 383, the diagnosis may be a matter of extreme difficulty. The radiating pains in this case were severe and local, and the limitations of the symptoms, for a long time, to one side, with crossed sensory and motor palsy, presented an almost perfect analogy to the effects of a growth. But it is very rare for severe and acute radiating pains to result from focal myelitis, although a painful sense of constriction is common; moreover, in tumour, one half of the cord seldom suffers severely without the functions of the other half also being very soon impaired in some degree. The limitation of chronic myelitis to a single focus is also very unusual; a consider- able vertical extent of the cord is usually involved in varying degree. Hence the practical difficulty in diagnosis is not so great as, at first sicht, might appear. Acute or subacute myelitis can only be con- founded with a growth in cases in which inflammation results from pressure, and develops with independent energy and rapidity. In such cases the occurrence of myelitis must be recognised, and the diagnostic problem is the detection of the preceding symptoms of the 624 SPINAL CORD. growth that excites the inflammation. This is usually easy; the severe pains, and commonly also the slighter symptoms of paralysis, which existed before the rapid increase in the loss of power, are suffi- cient proof of a chronic morbid process, to which the inflammation is secondary. The early pains are often thought to be neuralgic, but their con- stancy and continuance should suggest organic irritation; their seat, moreover, is rarely that in which neuralgia is common. The pain produced by tumours of the cauda equina is often felt first in the sciatic area, and thought to be sciatica; but it is commonly from the first bilateral, whilst sciatica is almost invariably one-sided, and bilateral sciatic pain should always suggest irritation where the sen- sory fibres from both sides are near together, and can be irritated by a single cause, i. e. it should suggest disease within the vertebral canal. In all cases, however dubious the early pains may be, other symptoms soon become added, and prove that there is more than a simple neu- ralgia. But the effect of the organic disease on other parts of the nervous system may evoke any functional derangement to which the patient is predisposed, and it is most important not to permit the diagnosis to be thereby misled, or the gravity of organic symptoms to be under-estimated.* If the existence of a tumour is clear, two questions remain —its seat and nature. The interference with the elements of the cord shows its lateral seat, but this is of small practical importance compared with the evidence of its vertical position, in any case in which an operation is contemplated. The latter is indicated by the level of the transverse symptoms, especially the upper level of the sensory or motor loss, or sensory irritation; but it is of special importance to note that the growth is often above this, and never, or almost never, lower. It may be even a distance of three or four vertebrae above the pair of nerves corresponding to the highest level of the anaesthesia or pain. This discrepancy is especially noticeable when the growth is in the cord; it is least when the tumour is extradural; and if this is so situated as to affect a nerve on one side, there is often a strict correspondence between the symptoms and the situation of the lesion. It is explained by the upward course of many posterior root- fibres. The nature of the tumour is also of great practical importance in * Thus the patient from whom the tumour was removed (see p. 627) had once had some convulsive attacks, and the intense pain due to the growth having caused slight meutal symptoms, I was asked to see him to decide the question of the hysterical nature of the affection. The fact is peculiarly instructive from a diagnostic point of view. Not less so is a case of central glioma in a girl (sent to me by Mr. P. B. Mason, of Burton-on-Trent), in which a central growth in the cervical region extended up into the medulla, and caused at last universal palsy. The first symptoms immediately followed severe mental disturbance; to this they were naturally ascribed, and thought to be functional. A similar sequeucc is met with in cerebral tumours (q. v.). TUMOURS. 625 many cases. If the patient has had constitutional syphilis the syphilitic nature of the growth is highly probable, and the probability is further raised in degree if the growth developed rapidly, so that the symptoms attained a considerable intensity in less than three months from their onset. The co-existence of a cerebral lesion also increases the likelihood of the syphilitic nature of the growth. Either of the last two considerations suggests the same conclusion in any case in which syphilis, although not proved, is possible; but it must be remembered that cerebral and spinal tumours, of other than syphilitic nature, may co-exist. In the same way, tubercular and scrofulous processes suggest the tubercular nature of a tumour. Most cases of tubercular growths have occurred in adults, the subjects of phthisis. The diagnosis is made more probable by rapidity of course, by the speedy extension of the symptoms to the second side, by the slightness of evidence of irritation, and, in some cases, by periods of arrest of the progress of symptoms that were slow in their development. Such arrest indicates an arrest of the growth of the tumour, which we cannot infer from the subsidence of symptoms that developed rapidly, and may have been due to secondary inflammation. When a rapid onset is due to this cause, irritation symptoms are usually pro- nounced.* Tumours elsewhere always constitute strong evidence of the nature of one in the cord, but such an indication is rarely avail- able, since the spinal canal is rarely the seat of secondary growths. Hydatids can only be diagnosed if others are present where their nature can be recognised; this has hardly ever been the case in the rare instances in which such tumours have existed within the spinal cord. Multiple tumours are probably either tubercle, sarcoma or neuroma. In the absence of these indications a meningeal tumour is probably a sarcoma, perhaps fibrous or myxomatous, and one within the cord is probably a glioma or tubercular, because these are the most frequent growths in those situations. A diagnosis founded on mere frequency of occurrence has necessarily only a low degree of probability, and must be sometimes wrong; but it may be highly probable that the oTowth is one of two or three kinds, and this may be of considerable practical value. To the surgeon the point is of great importance. Pbognosis.—Unless the tumour is syphilitic, or can be removed, the prognosis is necessarily most grave. Of all syphilitic lesions, 0-rowths are those that are most amenable to treatment, and the effects of which most certainly pass away if they have not reached an extreme degree or lasted too long a time. If, however, the damage has been allowed to remain unchecked for several months, recovery * Thus numbness in the left leg, with increased sensitiveness to pain in the thigh, was quickly followed by complete paraplegia; the hyperasthesia became restricted to the region supplied by the first lumbar nerves. Death occurred two months after the onset of the symptoms, and a tubercular tumour was found in the upper part of the lumbar enlargement, occupying almost the whole thickness of the cord (Ludeck,' Jabrb. d. Hamburg. Staatskr.,' 1896). 626 SPINAL CORD. may be imperfect. Tumours of most other kinds steadily increase, and the resulting damage is on the whole steadily progressive, although its course may be varied by stages of rapid (myelitic) increase in the symptoms, followed by stationary periods and even by transient improvement. In the case of growths outside the cord the prognosis has been rendered much less gloomy by the progress of surgery. Treatment.—If the growth is syphilitic, appropriate treatment should be energetic and prompt, so as to effect some diminution of the pressure as quickly as possible, since the longer this continues the more considerable are the degenerative changes, and the longer these will endure. Even the influence of a few days before treatment becomes effective may make a difference of weeks in the duration of symptoms, and lessen the degree of ultimate recovery. Whenever the symptoms suggest a tumour, and syphilis is possible, it is most important that suitable treatment should be employed; it can do no harm if the tumour is not syphilitic, and may save the patient's life and strength if it is. Syphilis can only be excluded when there has been no possibility of infection. In many cases of late syphilitic lesions there is no history of secondary syphilis, and in others there is no history of a primary sore. Hence it is a priori certain that in some cases of late lesions a history of both primary sore and secondary symptoms will be absent, and, as a matter of fact, such cases are met with not unfrequently. Of course these cases cannot be counted as syphilitic in any scientific investigation into the influence of this disorder, but in treatment we have often to allow weight to considera- tions which are insufficient to influence scientific investigation, and treatment determined by the mere possibility of syphilis is often justified by its results. Tubercular tumours are also amenable to treatment to some extent, but they are too rare to be of much practical importance. In most other cases we can do little more than treat symptoms, relieving pain by sedatives, watching the state of the bladder, preventing the occurrence of cystitis, and guarding the patient from bedsores. We must remember that sedatives will probably be needed for a long time, and they must therefore be used as sparingly as possible, lest custom and tolerance deprive them of their power. Cocaine may be used in many cases as an aid in economising the influence of morphia. But many tumours within the spinal canal may be removed, at any rate if they are outside the substance of the cord. The anticipation that such growths would be found removable was expressed in the first edition of this book (1886), in words that may be quoted because they were soon afterwards realised :—" Modern methods render the opening of the spinal canal far less formidable than it formerly was, and the removal of a tumour from the membranes of the cord would involve less immediate danger of serious consequences than the removal of a tumour from the brain." TUMOURS. 627 On the other hand, growths within the spinal cord are in a very different position with regard to surgical procedure, since the removal of such a tumour could hardly fail to cause a traumatic inflammation that would damage and perhaps destroy all the elements of the cord at the spot, and would probably be permanent in its effects, especially when these structures have already suffered from pressure. At the same time the early removal of a small growth might possibly be followed by the regeneration of conducting fibres that are on the other side of the organ, and the return of their function, lost only through the effects of pressure. In a man with complete paraplegia, motor and sensory, of slow development, accompanied by attacks of agonising spasm, a diagnosis of tumour led me to advise the removal of the growth. This was done by Mr. Horsley, and the result has been the permanent recovery of the patient. Although the intense spastic paraplegia showed that there must have been complete degeneration of the pyramidal fibres, every indication of this has passed away. The tumour was a myxofibroma, about the size of a split almond, which had so compressed the cord in the npper dorsal region as to reduce its thickness to about one half. It was within the dural sheath, and adherent to the cord.* It is certain that many growths might be removed without difficulty, and with a secure result, although not many instances have been since recorded. In connection with an operation, a question sometimes arises that is of very great importance, and often of equal difficulty. The sym- ptoms are consistent with the syphilitic nature of the growth ; and this cause and nature cannot be excluded, except by the disproof afforded by the inutility of treatment. But it is essential that this disproof should be afforded before an operation is decided on; and the question arises,how long should be allowed for this process of practical exclusion, __now long should treatment be continued without result to justify the last resort ? It needs to be longer when the symptoms are of con- siderable duration than when they are recent, since secondary changes of lono- duration cannot be quickly removed. Time is needed in every instance to permit a trustworthy conclusion, but a month is pro- bably always enough to enable a result to be reached that will justify either further delay on the one hand, or immediate procedure on the other. Finally, one injunction given by Mr. Horsley may be emphatically endorsed. If it is clear that the growth is not syphilitic, and that no o-ood can be done by other treatment, delay in an operation can only cause harm—can only result in a less favourable state for the proceed- * The details of the operation are full of instruction in reference to similar procedures, and are given in the account of the case in the 'Med.-Chir. Trans.,' vol. Ixxi, 1888. The surgical aspect of the subject is too large to be entered on here. 628 SPINAL CORD. ing, less chance of recovery, less degree of recovery, longer and greater suffering, and should on every ground be avoided. CAVITIES AND FISSUEES IN THE SPINAL CORD (syringomyelia, hydromyelia, hydrorrhachis interna).* Cavities in the spinal cord, distended with liquid, are met with at all ages, and those which present certain features, and often cause certain symptoms, are now known by the above terms. The following figures illustrate the most important facts regarding this morbid state, and its somewhat complex conditions will be best understood by con- sidering the appearances presented in these, and their significance, as described in the explanations. The term " Syringomyelia " is applied to all cavities in the cord with well-defined limits; but the majority of these (with the exception of such as exist in tumours of manifestly different nature), whatever their condition or form, or the changes they have undergone, are sur- rounded by a layer of embryonal neuroglial tissue, and outside this the white substance of the cord is deficient in amount. Wherever met with, or whatever the secondary changes the tissue presents, this fact of environment stamps the cavity or cavities (for there may be two) as congenital, because this abnormal material is due to a per- sistence of the embryonal tissue from which the cord is developed. The cavities are thus due partly to defective closure of the tube which is first formed (residual portions of which become distended by accumulation of liquid), and partly to the breaking down of this per- sistent embryonal tissue or to tissue formed from it by a process of growth. Moreover the cord sometimes suffers serious damage from pressure, owing to the distension of the cavity by the liquid which accumulates within it, or by growth of the adjacent tissue. The con- dition is not rare, but is often overlooked, especially in its slighter forms, and is readily misinterpreted when it is associated with acquired disease—as in the condition illustrated in Big. 109, p. 385, which is very instructive in this connection. The term " Hydromyelia" has been applied to the simpler f orms,f in which the cavity is merely the • During the last few years many cases of this disorder, in which the condition was verified by post-mortem examination, have been published in this countrv as well as in France, Germany, and America. Several monographs have also appeared, the most noteworthy being those of Hoffmann ('Deutsch. Ztsch. f. Nervenhiillc.' 1892) and Schlesinger (" Die Syringomyelic," ' Leipzig and Wien, Franz Deuticke ' 1895). To these the reader is referred for more detailed information on this interesting disease. t See Leyden, * Virchow'i Archiv.' Bd. lxviii, p. 1. Hoffmann (loc. cit.) divide- SYRINGOMYELIA. 629 dilated central canal; but as there is no real difference between this and other varieties, the designation, being unnecessary and even mis- leading, is falling into disuse. To understand the origin of these conditions it is necessary to remember the mode of development of the spinal cord. The sides of the primitive furrow of the embryo coalesce, so as to form a canal of relatively large size, the walls of which are thinner in front and behind than at the sides, and consist of elongated cells, some of which are arranged regularly at the inner surface of the cavity, like an epithelium. The anterior wall first becomes thickened, to form the white commissure and the front part of the grey, while an abundant growth of cells occurs at the sides of the tube, and extends forwards (i.e. downwards in the position of the embryo), thus forming the lateral and anterior columns ; between these two projections is the depression of the anterior fissure. Next occurs a growth backwards of the now thick sides, which forms the posterior parts of the lateral columns and the adjacent part of the posterior columns, and with this the posterior roots are connected; this forms the " root- zone " of the posterior columns. The posterior median columns are formed later. The central canal extends backwards between these two rudimentary postero-external columns, being closed behind only by a thin layer of cells. As the posterior columns increase in thick- ness the posterior part of the canal becomes narrowed, and its walls unite near its anterior extremity so as to form the posterior grey commissure, and divide the canal into two parts. Of these the ante- rior becomes the permanent canal, while the posterior is reduced to a narrow fissure between the posterior columns. Ultimately this poste- rior narrow part becomes closed by a growth of cells which occurs from behind forwards, as the median parts of the posterior columns develop. All these parts consist first of embryonal cells, which afterwards undergo a transformation into the nerve-elements proper, and the order of transformation is the same as that in which the parts were formed, the posterior median columns latest. The cells of the grey matter are formed before the fibres of the white columns. Some of the embryonal elements undergo a different and slighter change. They may almost be said to , persist, constituting the neuroglia, and the gelatinous grey substance continuous with it around the cord, and also massed at the posterior root fissure and around the central canal. The central canal ultimately hes in the anterior part or middle of the grey commissure. It may persist through life as a cavity, cir- cular in section, or as a slit, antero-posterior or transverse, and is lined with epithelium (Fig. 183). Around the canal there are the cases as follows:—I. Hydromyelus, which runs a latent course without recog- nisable symptoms. II a. Primary (central) gliosis, with or without hydromyelus: (1) without cavity formation; (2) with splits and cavity formation. II J. Central glioinatosis, with or without cavity formation. 630 SPINAL CORD. usually many nuclear elements, especially on each side of it, and these frequently fill up the lumen of the canal, so that its position is indicated only by an oval mass of small cellular elements (Fig. 183, d). The obliteration of the canal often occurs quite early in life, and is no evidence of any morbid process. The canal may be found obliterated in one part of the cord, and patent in another (c, d, Fig. 183). The simple closure of the canal by nuclei does not usually cause any disten- sion of the part which is above the closed portion, or, at any rate, not more than a very slight increase in size, so trifling that its signifi- cance is open to question. ■-;-:.:: Syringomyelia occurs chiefly in the y --,-- tJ^^p^v . cervical and upper dorsal regions of the "-y' -'. cord. The cavity is often closed below j-?r- •■"--^&y a \>j gliomatous tissue, and the excess of this may extend up into the medulla and even pons. Occasionally the cavity exists ^]f._ , , „ */. through the whole length of the cord, "jZiy."' and may extend into the medulla oblon- >yv/ gata, and then affect the aqueduct of Sylvius and the tissue around it. - yy^y^i:. In the simple condition found in young y ' children, or in adults when no secon- ^y0yi>Myy:' dary changes have occurred, the morbid change presents the two features already mentioned—a quantity of tissue of trans- __„,-..*;... .....;;_;•;'■ -.:.\ lucent aspect, which, from its structure, '-iC.-.:."',':-' ..v-'" - is clearly persistent embryonal tissue in '•^--i^^'''^' y^". -•' -. which nerve-elements have not deve- \'/- loped, and a cavity due to imperfect con- u traction of the canal. The change is FlLl?co^:tLt™lJ ^™y* «o»ft»d to the posterior UK of a transverse slit in A, a vertical the cord, and usually to the posterior slit in C (from the conusmedul- columns, which, as we have seen, are lans), while in B it is circular. „ , , In each it is lined by columnar formed last. It may, however, be pre- epithelium and surrounded by sent in one or both posterior horns, in cellular elements, rounded, or which cavitieg alsQ b formed. The angular from compression, . J -tiiC mingled with granules. In 1), persistent embryonal tissue may be evi- which is from the same spinal dently increased by a process of various cord as C, the position of the -. „ .Tin canal is occupied by a mass of degrees of growth, and the cavity enlarged nuclear tissue. by distension. Further, when the persis- tent tissue is considerable in quantity it may break down, and thus give rise to a new cavity, or enlarge that which has developed from the primitive canal. Thus the cavity may be distinct from the canal, and in some cases the abnormal tissue around it is very small in amount, and reduced even to a mere wall. It may also be separate, because it is the hinder part of the embryonal canal, cut off by coalescence of the walls. SYRINGOMYELIA. 631 These conditions are shown very well in the adjoining figures, after Leyden (Figs. 184, 185). In the first, at a, the cavity presents nearly the shape which it has at one period of development, before the formation of the posterior columns is completed, and without Fig-. 184.—Syringomyelia, from a child two years old, with encephalocele and absence of cerebellum. (After Leyden.) In A, cervical region, the central canal is large, lined with epithelium, and from it a medial fissure extends backwards nearly to the periphery of the c>rd, limited by a layer of homogeneous tissue, more abundant at the posterior limit. In H, lower down, the fissure is enlarged to a cavity of considerable size, while in C it is still larger, and the posterior columns are reduced to a narrow zone between the layer of tissue which bounds the cavity and the grey substance. the separation into two parts produced by the formation of the pos- terior commissure. It is bounded by a narrow layer of embryonal tissue, which widens out behind, having nearly the shape of the pos- terior median columns, which are, as we have seen, the last to be formed. In b and c the cavity is much larger, and the posterior columns are smaller, either by an earlier arrest of development or by greater distension, or, most probably, by the influence of both these agencies. The cavity extends up to the posterior surface of the cord, and is closed in there only by a narrow layer of cellular structure. In Fig. 185 we have somewhat more complex conditions. The cavity in the first section closely resembles in appearance that in a of the last figure, but differs in the important fact that the posterior com- missure has apparently been formed and the central canal developed in the normal manner, although it has become obliterated by nuclei. This is clear if the commissure is compared in the several figures. The cavity, therefore, does not, as in Fig. 184, represent the whole of the primitive canal, but only the posterior portion after its division. The adjacent tissue is much more abundant than in the other case. The projection into the posterior extremity of the cavity indicates a process of active growth, which is also shown by the irregularity of the cavity in b, the large amount of tissue, and the wide separation of the posterior horns. In c, from the lower part of the cord, the embryonal tissue occupies two oval areas in the posterior column (by mistake, clear in the figure), while the cavity is closed or nearly so. (Lower down, a cavity existed in the centre of each of these areas, apparently due to breaking down of the tissue.) In d, again, the embryonal tissue occupies only the middle line, as a wedge-shaped area, due to the defective formation of the medial part of the posterior columns. It has been mentioned that the neuroglia may be regarded as a persistent, slightly modified embryonal tissue, and these exuberant 632 SPINAL CORD. m iv ^/jyyA ■■-yi'py^r' ■\»Ml:."iii ¥fy ,M<$xr masses of tissue bear considerable resemblance in structure to gliomata, so that the condition has been called " ghomatosis." In each of these cases the brain participated in the defect of development; there was internal hydro- cephalus, and the cerebellum was absent. The cavities in the adult cord present many varieties. The most common form resembles in its essential features the con- genital disease Avhich we have just con- sidered. Between the two there are also differences, but the resemblance is suffi- ciently close, and the origin of the differ- ences is sufficiently clear, to make it prac- tically certain, as already mentioned, that the two forms are really the same, and that the form met with in adults is the congenital condition, persisting until later life. Of the characters which this form has in common with the congenital disease, the most important are the position of the cavi- ties and the presence of tissue in their vicinity of embryonal or gliomatous nature. The differences depend on an apparent increase of this tissue by a process oi growth, on the greater damage to the other parts of the cord by the distension of the cavity, and on the extent to which the for mation of new cavities or enlargement of Fn*. 185. — Syi n,ri myclia, old ones takes place by a process of disin- from a child aged two and a tegration of the newly formed or persistent halt years, with internal by- . J r drocephalus and absence of tissue. The damage to the cord produced cerebellum. (After Leyden, by distension of the cavity involves most ' Virchow's Arch./ Bd. ,-, -, , . ,. _, Ixviii.) A, B, cervical re- the nearer ano- less resisting parts. The gion; gelatinous (embryo- grey substance, therefore, suffers in greatest oal) tissue in the posterior de the wWte columns to an ext t columns eucloses a medial , . cavity, lined in places with that depends in part on the precise posi- cylindrical epithelium, and tion of the cavities, as presently to be de- believed (probably wrongly) -i j rru i . i i • y scribed, the latter also present, in many cases, the complicating changes of second- ary degeneration, ascending or descending to be the central canal. C, lower dorsal; in each poste- rior column is a mass of similar gelatinous substance (which, by a mistake, is as shown in Fig. 186, due to the com- shown in C as an open cavity). In D, lumbar region, this tissue occupies only the posiiion of the pos- terior me lian columns. pression of certain tracts at some specially affected spot. As the simplest condition, we maj have a dilatation of the central canal surrounded by gliomatous tissue disposed as in congeuital cases. This tissue is often more abundant, and forms a more distinct SYRINGOMYELIA. 633 mass, lower down the cord, below the cavity. A good example of this condition in slight degree is presented by the cord, the seat of chronic £ myelitis, represented at Fig. ' 109, p. 385. In the cervical region (a) there is a large central canal, bounded by a thick layer of gliomatous tissue. In the inner part of this tissue, limiting the cavity, is a sinuous membrane, fibrous in structure. The origin of this membrane is not easy to explain, but it is often found in cavities of this character, and is evidence of the similar nature of those that differ much in other respects. In the lumbar region (b) the tissue, which bounds the cavity in the other section, forms a large round mass in the posi- tion of the canal, obliterating it. When a central cavity ap- pears not to be the (-anal itself, but to be situated behind, it is then apparently often due to a persistence of the fore-part of the posterior portion of the canal, after the posterior com- ^r FiG. 186.—Syringomyelia, from a case of tumours of the pons and cauda equina, with some diffuse sclerosis in the dorsal region of the cord. A, B, and C are sections of the cervical enlargement. The large cavity in A is perhaps the dilated canal, since it is lined in front with epithelium, but in front of it, in the posterior commissure, is a group of nuclei like an obliterated canal. The zone of tissue around the cyst is composed of interlacing fibres and nuclei, and processes extend from it into the posterior columns both in front and behind. In B the cavity is smaller and the wall thicker, while in C the tissue about it forms a considerable mass, and a second small cavity has formed in the middle line, apparently by the breaking down of the tissue. In the dorsal region (D) there was merely an unusually large accumulation of nuclei iu the position of the canal, which, in the lumbar region, had the normal aspect (E). The cord presents degeneration of the right pyramidal tract (descending from the tumour in the pons), and of the post. med. cols, and ant. lat. ascending tract, pro- bably ascending from the sclerosis. 634 SPINAL CORD. missure has been formed. In Fig. 186, for instance, we have a central cavity, but in the commissure in front of this is a mass of nuclei having the usual aspect of an obliterated canal.* The cavity is surrounded by a zone of tissue, which in a and b sends off a fringe of processes, especially backwards. This tissue is increased in the lower part of the cervical region (c). In b a small cavity is formed between the tissue and the grey matter by breaking down, and in c another exists in the middle line behind the growth, probably due to deficient closure of the original fissure, and increased by a destructive process. Still lower, the commissure resumes its normal appearance, but the collection of nuclei in the position of the canal is unusually large (d). In the lumbar region the canal is patent (e). The degeneration of the posterior median column and of the lateral columns is secondary. We have seen that in the congenital cases we must recognise a process of growth of the persistent embryonal tissue to account for some of the conditions met with, and a like process is suggested by the central mass in Fig. 109, b. Hence it is not surprising that in many cases the growth should attain the dimensions, and assume the characters, of a positive tumour. In most cases the tumour has been central in position, and has had the structure of a glioma. It has occupied a large part of the area of the cord at a certain level.f In the chapter on the tumours of the cord it has been pointed out that sarcomata also may grow from the tissue around the central canal, as in the case shown in Fig. 181. Hence it is not surprising that the condition of syringomyelia, even if this is congenital in origin, should be frequently associated with definite tumours. The growths have often been multiple, apparently the result of a wide-spread tendency, and perhaps connected with a wide-spread persistence of embryonal tissue, of which remarkable instances are sometimes met with. In the case shown in Fig. 186 there was a tumour of the pons and also one of the cauda equina. The nature of the growths is uncertain, but they were probably either sarcoma or glioma. The same tendency to morbid growths is illustrated also by Fig. 187, which is similar in many respects to that just considered. In this case also there was a tumour of the pons and one of the cauda equina, and there was also a central growth in the dorsal region, occupying the greater part of the area of * This is the probable interpretation. At the same time it is possible that the nuclei have not this significance, and that it is really the central canal. It is often more difficult than might be imagined to say whether a cavity does or does not represent the central canal. The presence or absence of an epithelial lining has generally been taken as a criterion, but it is doubtful whether this has any signifi- cance. Around the whole of the original cavity the inner layer of cells is arranged as an epithelium, and if any part of it persists it is probable that epithelium will persist also. Moreover the epithelium often disappears from the wall of the dilated central canal itself; always where it is enlarged by breaking down of tissue. t As in an interesting case described and figured by Riesinger, ' Virchow's Archiv,' Bd. xcviii. SYRINGOMYELIA. 635 the cord, to which the ascending degenerations were secondary. In a there is a large central cavity which is probably not the central canal, since, as in the last figure, _ the position of this is marked by the oval group of nuclei in the anterior part of the grey commissure. The zone of tissue which bounds it is narrow, but a few processes are given off behind. In b, first dorsal, this tissue forms a compact mass, and the pro- cesses are numerous and very similar to those in the last figure. In c the commissure is reduced almost to normal conditions. In this cord we have also an instance of the fact that cavities may occur in other parts, very similar in their general characters to those that occur in the central region. In b a large cavity occupies the intermediate grey matter and posterior cornu on the right side, with some morbid tissue bounding it on the medial side. In c the cavity is smaller Fig. 187.— Syringomyelia, from a case in whhh there were tumours in the dorsal region of the cord, the can la equina, and the pons Varolii. A, mid-cervical region. A large oval cavity lies behind the grey commissure, surrounded by a narrow wall, chief!v composed of fine fibres, but with a wavy membrane on the inner surface. In front of the posterior commissure, an oval group of nuclei has the aspect of an obliterated central canal. A few short processes extend from the wall of the cavity into the posterior columns. There is secondary ascending defeneration of the post. med. cols., right direct pyramidal tract, and ascending antero-lateral tract in all the sections. B, first dorsal. Behind the posterior commissure is a growth consisting of small cells,round and fusiform, the latter with round nuclei. It contains many vessels with thickened walls. A fringe of fine processes extends from it into the posterior columns. An irregular cavity occupies, on the ri«;ht side, the posterior half of the grey matter, which is reduced to a narrow layer around the cyst. This is lined by a delicate nucleated membrane, outside which is a thicker membrane, lying in folds, the section of which is thus sinuous. Out- side this again is a small-celled growth similar to that behind the commissure. In C a little lower, this cavity is smaller, the sinuosities of the wall greater, and the growth outside it more abundant. (Still lower the area was entirely occupied by the growth.) In the posterior commissure there is only a quantity of loose nucleated tissue in the situation of the growth.* * For the opportunity of drawing these sections I am indebted to Dr. Drecbfeld. A full account of the case has been published by Dr. Harris in 'Brain,' Jan., 1886. The largs growths were sarcomata. 036 SPINAL CORD. and the tissue around it is more abundant, but easily distinguish- able from the grey substance, while a little lower down the cavity disappeared and the tissue formed a compact rounded mass. The cavity is lined by a delicate layer of cellular mem- brane; outside this is a fibrous membrane, lying in folds which appear as sinuosities in the section. The existence of this membrane shows that the cavity is not simply formed by the breaking down of the tissue. The tissue is quite similar in structure to that which is behind the commissure in b.* The posterior cornu is not an uncommon seat of cavities, which may extend through the whole length of the horn. An example of this is shown in Fig. 188. Haemorrhage had occurred into the cervical region of the cord (a), which was enlarged and distended with blood, so that the precise character of the cavity in this region was indis- tinguishable; the blood also filled the cavity through the * In connection with the tumour of the cauda equina in these two cases, it may be mentioned that the same coincidence has been observed in other instances. There was a tumour in that situation, for iustance, in the case de- scribed by Riesinger, who rightly re- garding the condition as congenital in origin, suggests that the tumour may be connected with the fact that the embryonal cord occupied the entire length of the canal. Fin. 188.—Sections of a spinal cord in which a cavity existed throughout its length. Haemorrhage in the cervical region was the immediate cause of death. The extra- vasation had there distended the cord (A), and had burst into the cavity, which was filled with blood. A smaller cavity existed in the right cornu, in the upper dorsal region (B). In most parts the inner surface was sliehtlv irregular, as if pro- duced by breaking down of the tissue, but near the position of the central canal a sinuous membrane existed in places, without, however, any epithelial covering. SYRINGOMYELIA. 637 entire length of the cord. In the upper dorsal region (b) there are two cavities, one in each posterior cornu, but that on the right ceased a little lower down, while the other extended to the lumbar region, as shown in the figure, reaching almost to the surface of the cord. The upper and inner extremity of this cavity is in the position of the central canal, no other trace of which exists. There is some abnormal tissue in the neighbourhood of the commissure, and also in c, where irregular tracts pass transversely from the median septum into the fore-part of the posterior columns. The presence of this tissue, and the relation to the central canal, suggest a congenital origin. During the reduction in size of the canal, in the development of the cord, the cavity presents at one period short lateral processes, and we can therefore understand how a still earlier arrest of develop- ment may lead to the persistence of a lateral process on one side or both, surrounded by residual embryonal tissue, and that the cavity should afterwards extend in this tissue or in the grey matter by a process of growth and disintegration, such as probably had occurred in Fig. 188, r>. A comparison of d and e suggests that the two cavities were united in the middle line in the upper part of the cord, where the haemorrhage took place. In the conditions we have hitherto considered, definite limited regions of the cord have been involved through a considerable vertical extent. The changes are sometimes, however, much more diffuse in their dis- tribution, as is shown by tire remarkable lesions represented in Fig. 189. In this cord, which is that of an adult, we have a combination of the same two conditions of abnormal tissue and cavities. Scattered through the nerve-substance are tracts of a peculiar tissue, represented by the darker shading of the figure, and in many regions thus affected there are cavities, for the most part fissure-like, as if the cord had been split here and there. At first sight the appearance suggests an active and recent morbid process; nevertheless I think that the congenital origin of the condition is beyond doubt. It will be observed that the morbid changes, as in the otl er forms of syringomyelia, are chiefly in the posterior half of the cord; small areas of disease in the anterior columns, in the sections e and f, are the only exceptions. The minute structure of the abnormal tissue was exactly like that of the normal o-elatinous layer beneath the pia mater. Besides the conspicuous areas hgured, it could be traced here and there, in small tracts, through the whole of the posterior columns and the hinder parts of the lateral columns, and also in the posterior horns, in the grey matter of which it could be readily distinguished. The relation of the cavities to this substance is distinct; where they extend beyond it, this is apparently the result of the distension of the cavities and an actual Assuring of the cord, along the lines of connective tissue, by the pressure of the contained liquid. The medial cavity in c is doubtless due to defective closure of the original fissure between the posterior columns. In the lumbar region the nerve-fibres are absent from the front of the posterior 638 SPINAL CORD. columns, where a coarse network of this residual tissue encloses empty spaces. The damage to the grey matter may entail alterations in the related nerves, and even, in cases of long duration, in those connected with the posterior roots. In the peripheral nerve-fibres of the skin and muscles, changes of the ordinary chronic degenerative character were found by Dejerine in cases in which sensation was altered or the muscles wasted. Thus these various forms of syringomyelia, in spite of their varia- tions in seat and form and general aspect, when closely studied, seem all to be connected with gliomatous tissue ; and that the morbid state takes its origin in abnormal conditions during the development of the cord is practically certain from their seat and features. This lesson is clearly taught by the facts shown by the cases here illustrated. It is probable, therefore, that this conclusion is also true of cavities of similar character and position in which no gliomatous tissue can be recognised; and most of the hypotheses regarding the origin of such cavities from processes of simple myelitis and the like have no suffi- cient foundation. But we are still ignorant of the mechanism by which the defect in the process of development is brought about. It has been extensively ascribed to an inflammation of the embryonal neuroglia at an early stage of development, but of this there is no real evidence. It is, moreover, no explanation to assume a primary intra-uterine hyperplasia of the embryonal tissue. It is, indeed, possible that more than one morbid process during the early stage of development may cause the condition, and that closure of the canal below may have consequences during development which it has not at a later period. But it is important to recognise the fact that there is a gradation between the chief varieties, and that some are associated with developmental defects in the brain, to which they can only be related as the common expression of a defect in the develop- mental tendency of the germinal tissue ; and what must be true of Borne forms is probably true of most. This may seem only to push the difficulty into the region of the inexplicable, but it is only placing the origin of the malady where we are compelled to refer the causa- tion of so many congenital diseases, which, after all, bear but a small proportion to the physiological characteristics that spring from the same source. From these considerations it is probable that cases of syringomyelia are divisible into two classes: (1) those in which there is a congenital anomaly which may afterwards take on a process of overgrowth as distinguished from development, characterised clinically by very gradual onset of symptoms lasting, it may be, throughout several years ; (2) those in which there is actual central new growth, frequently with cavity formation ; and it may be associated with new growths elsewhere — glioma, sarcoma, syphiloma, — in which the course is a much more rapidly fatal one. The symptoms of the disease have followed some illness, mental SYRINGOMYELIA. 639 shock or anxiety, and traumatic influ- ences, but it is probable that in no case have these done more than excite the manifestations of pre-existing dis- ease, or induce local changes in the morbid state. The possible influence of injury has certainly been over- estimated, since in some of the cases in which it seemed effective the malady was unquestionably congenital, and the traumatic influence only terminated its latent stage.* Symptoms.—The manifestations of syringomyelia depend on the secon- dary processes of distension and growth, and the damage thus produced to the functional elements of the cord.f * Among the chief papers in wThich the sub- ject will be found discussed are those of Schultze (see below); Hellich, 'Arch. Koheme d. Med.,' 1890, iii, No. 4; Krouthal, 'Neur. Centialb.,' 1888, p. 333 j Oppenheim, 'Charite Annalen,' 1886, p. 409; Hoffmann and Schlesinger, loc. cit. t They have been fully described by Schultze, 'Zeitschrift f. klin. Med.,' 1888, p. 525; and 'Verb. Cong. Inn. Med.,' 188 J; and by Allen Starr,' Am. Journ. Med. Science,' 1888, vol. xcv. b'iG. 189.—Cavities in the spinal cord. A, mid- cervical, presenting merely some increase of connective tissue in the left lateral column. In B there are several cavities having the aspect of distended fissures, the largest in the middle line of the posterior columns and the right posterior cornu ; smaller ones in the lateral columns. Adjacent to each is a quan- tity of dense tissue, which had a peculiar and unilorm structure. It consisted of a very fine network of fibres with minute nuele.tr bodies in the interstices. No larger cells were observed. Throughout the posterior and lateral columns this tissue could be seen, here and there, thickening the neuroglia, where no conspicuous masses were formed. It could also be traced in the posterior cornu, and was readily distinguished from tho spongy sub- stance by its slighter staining. Tiie distri- ( bution of this tissue is shown in the other •! sections by the darker shading. In C the V fissure in the middle line is narrow. In E and P the anterior part of the posterior columns contained a coarse network ot this tissue, and no nerve-fibres. The central canal was obliterated, but the group of nuclei that traced throughout the cord. y^^yy 3*, ■^ • VI vjy> o ■wm marked its position could be 640 SPINAL CORD. Hence the state is sometimes discovered after death, when it has given rise to no symptoms, and its existence has not been suspected during life. In young children, indeed, it appears never to cause any definite symptoms, while the disturbance of function is variable in occurrence and degree—much more so than in character. The central position of the disease entails considerable uniformity in the distri- bution of its local consequences, and hence also in the derangement of function that results from simple increase in the lesion either by dis- tension or growth. Hence the symptoms are often such that they have considerable diagnostic importance, although in a minority of cases they are less uniform in character, probably because the disease is unsymmetrical, or irregular in position or extension, whether the symptoms are due to the distension of a cavity, or to this combined with adjacent growth of tissue. It then often causes symptoms indis- tinguishable from those of a tumour of neoplastic, nature. Moreover the precise level at which the chief morbid process takes place leads to a corresponding variation in the position, and therefore in the general aspect, of the symptoms it produces. The fact that the lesion is almost always greater at the cervical region causes the arms to be the most common seat of its manifestations, while the occasional inva- sion of the fourth ventricle by the associated growth, and the occur- rence of coincident secondary changes in this part, explain the involve- ment of some of the cranial nerves that has been met with in a few instances. The symptoms are usually of slow development, increasing gradually in the course of years. Their main features are twofold, of which one is clearly and certainly intelligible, while the explanation of the other is a matter of hypothesis, although also not difficult to under- stand, at least in part, if the opinions expressed in the chapter on the functions of the cord are correct. The two leading features are loss of sensibility, chiefly to pain and temperature, and muscular atrophy, resembling in characters that met with in the " progressive " spinal form. Of the two, the sensory loss is the earlier and more constant. The muscular atrophy is a necessary consequence of the damage to the anterior cornua from the compression they endure, when and where the central cavity or adjacent growth attains such a size as to damage them seriously, and they may be reduced to a mere zone between the cavity and the outer ring of white substance. The de- struction of the motor nerve-cells involves the degeneration of the nerves and the wasting of the muscles. The loss of sensation is intelligible if the path of painful impressions is by the posterior commissure.* The enlargement of the central canal and disease in its vicinity can hardly fail to damage early and much the fibres that cross at the level of the chief lesion, and constitute the path from posterior roots not very far below. The course of thermal sensations * See p. 224 as to a tract in the grey commissure described by Ciaelinski CNpo, Cent.,'1896). B ^ SYRINGOMYELIA. 641 is still quite unknown; the only fact we have—the frequency with which such sensibility and that to pain are involved together—points to contiguity of path, and prevents surprise at the special affection of this form of sensibility in syringomyelia. Tactile sensations are lost only in rare cases; our ignorance of their path prevents us from ex- plaining the fact, but we know, from other facts of disease, that it is distinct from that for pain. Moreover, the occasional localisation of the morbid process in the posterior columns, and even cornua, may explain the involvement of all forms of sensibility, and also its occa- sional restriction in area, since it may be due to direct interference with the posterior root-fibres after they have entered the cord. In many cases the affection of sensation of pain and temperature is equal; in others the latter is lost to a greater degree and extent than the former. Its loss is often the earliest symptom, as the scars of burns may show. The loss to heat and cold may not correspond. Thermal or painful hyperaesthesia has preceded the loss, as with other forms of sensation when destroyed by processes that slowly damage the fibres, and irritate before they interrupt. Perversion of sensation has been noted, heat being felt as cold, and vice versa. Spontaneous sensations are common, doubtless from the irritation of the fibres in the early stage, or of their upper portions when they are inter- rupted—feelings of heat or cold, and in some cases pains, various in character, sometimes paroxysmal like neuralgia, or sharp and brief like those of tabes, and occasionally referred to the joints, or felt chiefly in some part adjacent to the seat of the other symptoms. Pain in the spine may be complained of, and is, perhaps, a direct effect of the disease. Cramps also and shooting pains sometimes occur. Often the malady causes no suffering. The loss of sensation is usually sharply limited, and the arms or upper half of the trunk are its common seat. It is usually found in the same part as the mus- cular wasting, but is more extensive, especially below the seat of atrophy. Thus, when the muscles of the shoulders and upper arms only are wasted, the sensory loss may be in the forearms and hands. This we should expect from the fact that the crossing of the sensory path is some distance above its entrance into the cord, while the motor roots arise from nerve-cells mostly near their level of exit. Exceptions may be due to the affection of the root-fibres, as explained above. Further, the fact that the distension and damage always extend through a considerable vertical area of the cord makes the relation of the two sets of symptoms more extensive and less regular than if the disease were limited to a small region. The " muscular sense " is said to have been generally normal when tested. Occasionally there has been unsteadiness on standing with the eyes closed. The motor symptoms usually come on after the sensory loss, long after in slight cases, and consist in muscular weakness and wasting in the upper limbs; while, if the legs suffer, it is generally from simple VOL. 1. 41 642 SPINAL CORD. spastic paralysis, such as would result from, and is no doubt due to, compression of the pyramidal tracts by the disease in the upper part of the cord. It is rarely complete. The unsteadiness of move- ment above mentioned we may connect with the tendency of the lesion to involve the posterior columns, and so probably to inter- fere with the path from the muscles to the cerebellum. Rarely there is atrophy of the legs similar to that of the arms, and in such cases the disease extends into the lumbar enlargement. Reflex action in the legs varies according to their state ; it may be normal or increased : the knee jerks are often augmented, with rectus- and foot-clonus, or, in the cases last mentioned, myotatic irritability may be lost—very rarely on one side only. A curious tremor of the limbs has been noted in some cases. The muscular atrophy in the arms begins in and chiefly affects certain parts, according to the position of the greatest damage to the grey matter of the cord. It may be in the hand and region of the ulnar nerve, or in the muscles supplied by the musculo-spiral and radial nerves, or in the shoulder and upper arm muscles.* It is a slow wasting, with gradual lowering of the electrical irritability, as in progressive muscular atrophy, although, as in that disease, some groups of muscles may present indications of the reaction of degene- ration in the early stage of their affection. Fibrillation is common. As the wasting and weakness increase in the part first affected, they spread to others, to the rest of the limb, and to the adjacent parts of the trunk. Weakness of the trunk muscles often leads to lateral curvature of the spine; and the convexity, owing to posture, is usually to the left. The occurrence of similar symptoms in the legs is ex- tremely rare. Both sides usually suffer together; a unilateral affec- tion has indeed been observed, but is altogether exceptional. The sphincters may escape or be involved. Trophic, disturbances in the extremities affected with sensory loss are not uncommon. The skin may become thin and glossy, or thick and horny. Acute changes may occur—eczema, herpes, or bullae ; whitlows; deep, obstinate ulceration, and even gangrene. More frequent, however, is simple vaso-motor disturbance, coldness and lividity of the extremities, or redness with swelling and heat, and sometimes a tough oedema, which may be local like a tumour, and afterwards pass away. The nails share the trophic changes in the hands, becoming grooved, fissured, and cracked; they mav even drop off. The secretion of sweat is lessened in the part, as was well marked in one unilateral case,f or it may be increased. The action of pilo- * Blocq thinks that spastic paraplegia is chiefly met with in the cases in which the atrophy begins in the region of the ulnar nerve, and tabetic symptoms in the legs when it begins in the radial area ; but the data for the generalisation need to be more extensive. t Allen Starr, 'Am. Journ. Med. Sc.,' May, 18S8; Rumpf, ' Neur. Cent.,' 18F9 p. 257. SYRINGOMYELIA. 643 carpine has been found to be delayed, although ultimately increased (Grasset). The bones may become thickened or brittle, and joint changes (Charcot's joint), like those of tabes, sometimes occur.* It is not common for the symptoms to extend into the region of the cranial nerves, although in occasional cases various disturbances of function have occurred, presumably due to the extension of the changes into the medulla and pons, and chiefly met with when there is upward extension of the associated growth, already mentioned. Thus there have been paralysis of one vocal cord, or of both, of the tongue, the palate, and of the face, difficulty in swallowing, disorder of respiration and of the heart's action. Taste and smell may be affected, and there may be sensory impairment in the face. Certain disorders may occur in the eyes, probably due to disease of the path of the sympa- thetic in the cord, or to that of the fourth ventricle. Thus the pupils are often unequal, the smaller being on the side of the more severe cord symptoms, on which the fibres for the radiating muscle of the iris are likely to be damaged. Narrowing of the palpebral fissure and slight ptosis have been also noted. Nystagmus is not rare.f The course of syringomyeha is, as a rule, slow, and measured by years, although an apparent exception is presented by the cases in which it is associated with spreading overgrowth of the adjacent gliomatous tissue, or in which acute destructive processes occur in this and spread to its vicinity.' In such cases a considerable development of the disease may be attained before symptoms are produced, and these may rapidly reach a considerable degree, and cause death in a few months or even less. ' In most cases death is the result of exhaustion, of the impairment of the functions of the medulla, or, more com- monly, of some complication—bedsores, cystitis, and the like. Diagnosis.—The resemblance of the disease to more common maladies led to its confusion with them during life, until the careful observations of the last few years have established features by which its existence can often be at least surmised, 'the most im- portant characteristic is the combination of muscular atrophy with still earlier sensory loss, involving temperature and pain far more than tactile sensibility. But the occasional implication of all forms of sensation must be kept in mind, and also the fact that in slight and slow or anomalous cases the sensory symptoms may long predomi- nate, and for a time exist alone. The position of these symptoms (in the arms), and their frequent combination with spastic palsy in the legs, is a further characteristic—not, however, unequivocal. Cervical pachymeningitis causes symptoms which, in general * Nissin, 'Arch. f. klin. Chir.,' Bd. xlv; 'Neur. Centralb.,' 1893, p. 100; Sokoloff, ' Deutsch. Ztschr. f. Chir.,' Bd. xxxiv; * Neur. Centralb.,' 1893, p. 101; Galloway, ' Lancet,' 1891, vol. i. f Contraction of the fields of vision, especially for colours, has bf en observed but s not easy to explain (Dejerine and Turland). 644 SPINAL CORD. character and in distribution, alike in the arms and the legs, very closely resemble those of syringomyelia ; but the affection runs a more rapid course, the anaesthesia involves all forms of sensibility, and has not a greater but a less extent than the muscular wasting; the two correspond more closely in their seat; pain is a far more prominent symptom, and the reaction of degeneration is common in the wasting muscles. Tumours of the spinal cord only cause symptoms of like character, and especially of similar symmetry, when they are central in situation, and the diagnosis may then be very difficult and even impossible. But the resemblance is often more than superficial, for such growths generally arise from residual gliomatous tissue, and are such as are frequently associated with syringomyelia. It is chiefly from the more rapid development of symptoms, and their more speedy extension, that such a growth can be suspected; and only the presence of slighter chronic preceding symptoms of the character above described would justify the expecta- tion that a cavity is associated with the growth. Progressive muscular atrophy is sufficiently distinguished by the absence of impairment of sensation, and in peripheral neuritis the pains, mode of onset, and degenerative reaction in the muscles should preclude any danger of mistake. In " Morvan's disease," to be pre- sently described, the symptoms may bear a close resemblance to those of syringomyelia, and it is probable that they are due to a similar condition of the spinal cord, so that it is to be recognised merely as a variety of syringomyelia. As a rule, however, the early loss of tactile sensibihty, and the greater prominence of trophic disturbance in the tissues, especially the painless whitlows, enable the diagnosis to be made. There is only one acute affection of the cord that enters into the diagnostic problem, and that is spinal haemorrhage. It has been mentioned in the account of this condition that the hamiorrhao-e is sometimes into a pre-existing cavity—as in the case shown in Fig. 188. The presence of a cavity into which the blood has been effused may be suspected if the haemorrhage has been preceded by any symptoms suggestive of syringomyelia, inquiry for which should always be made; or if a rapid extension occurs through a consider- able vertical extent of the cord, distinctly abolishing its central functions. The malady, however, varies much in seat and characters, as is evident from even a cursory glance at the illustrations given above; the symptoms, of necessity, vary with the lesion. The diagnosis may be difficult and even impossible in such cases, especially in the early stages and slighter forms, when irritation and pain predominate, and even neuralgia may be simulated. It may be necessary to wait for time to show the course of the symptoms. Their progressive increase in spite of variations, should always be taken into account; it fre- quently is the first feature that suggests the nature of such a 'disease, contrasting, as it does, with the tendency of inflammatory affections ANALGIC PANARITIUM. 645 to arrest and improvement. A peculiar difficulty is presented by the cases, not few, in which the first symptoms follow some influence— an illness, a blow, or even mental disturbance—that seems to be their cause, and suggests disease of very different nature. Often then, also, it is only by waiting and watching that a right opinion can be formed. When bulbar symptoms come on rapidly, the nature of the case can only be inferred from previous spinal symptoms. The Prognosis and Treatment of syringomyelia are subjects on which, unfortunately, its nature permits httle to be said. If its existence can be recognised the malady is generally advanced, and its observed rate of progress is the only ground on which a forecast can be based. When the central functions of the cord are considerably impaired, and the symptoms are steadily increasing, it is rare for life to be prolonged for more than one or two years, and the subacute onset of considerable paralysis may herald a course that leads to death in a few months. On the other hand, a stationary condition may last for many years. Treatment can do nothing for the morbid state, nor is it likely that the progress of spinal surgery can afford the means of relief.* The severity of some of the individual symptoms may, however, be lessened by appropriate measures; especially trophic changes may be diminished by care and early treatment, bedsores may be prevented, cystitis guarded against, and if any acute para- lysis occurs, the possibihty of some recovery may suggest the main- tenance of the irritability of the muscles by electricity, which cannot be expected to influence the slower atrophy. Pain may need the customary sedatives ; but early pain, especially with the hyperaesthesia that depends on the intensification of the nerve-impulses at the irritated part, may be much lessened by the administration of cocaine, used as in tabes. Sudden pain in the spine may indicate commencing haemorrhage, and should lead to the adoption of the posture and other measures appropriate to that grave affection. Analgic Panaritium; Morvan's Disease. By the term Morvan's Disease is generally known an affection that was called Panaritium Analgicum, or " Painless Whitlows," by the physician of Brittany, Morvan, who, in 1883, first described it.f Observations on it are still few,J but, judging from two fatal cases,§ it * In one case under my care the spinal canal was opened and the cavity drained, but without improvement. f 'Gaz. Hebd.,' 1883, Nos. 35-44. t The chief writings are those of Louazel, ' La Maladie de Morvan, Paris, 1890; Joffroy and Achard, 'Arch, de Med. exp.,' 1890; Charcot, 'Prog. Med.,' 1890, Jfos. 11 and 12; Hackel, 'Munch, med. Wochenschr.,' 18S9. 8 Gombault, quoted by Charcot; Joffroy and Achard, 'Arch, de Med. exp.,' 1891. 646 SPINAL CORD. appears to consist in a combination of a condition of syringomyelia, or of the associated gliomatosis, with a peripheral neuritis in the extre- mities. The symptoms make the constancy of the neuritis probable ; we must wait to learn how far the morbid state of the cord is constant, and whether the changes in the nerves take origin in developmental conditions. It is quite possible that they may share the condition of arrested development, entailing a liability to later morbid changes, especially in view of the analogous conditions observed in the case mentioned on p. 529.* At the same time it is possible that the symptoms of this affection may be due to local neuritis of varied nature, and we must be cautious in inferring from them that the pathological state is the same in origin in all cases. In some instances the malady has been apparently set up by an injury. The affection has been met with in both sexes, but more frequently in males, and has generally commenced during the first half of adult life, between twenty and forty. When local injury has preceded the symptoms it has sometimes been at a considerable interval (Hackel), and it has been unilateral whenthe latter have been bilateral, so that its relation to them is uncertain. The characteristic symptoms are in the upper extremities; only in rare cases do the feet suffer at a late period. Neuralgic pains may occur first, but the definite symptoms consist of weakness and muscular wasting in the hands and forearms, loss of all forms of sensation, and especially a peculiar trophic change—whitlows on the fingers, with recurring deep ulcerations in various parts of the digits; those near the extremity of the fingers may only heal with the loss of some of the terminal phalanges. The loss of sensibility involves all forms, and usually precedes the occurrence of the whitlows, so that these are painless, a peculiarity which constitutes the most salient feature of the disease, and suggested, in the first instance, its special character. Occasionally the trophic disturbance precedes the anaesthesia, and the whitlows and ulcers are then painful. The latter are deep, and often resemble the perforating ulcers of tabes; cracks in the skin accompany them, and the nails shrivel and split. Yaso-motor derangements, lividity and pallor, often precede and accompany the disturbance of nutrition. The progress of the affection is very slow, and extends over many years; one hand is usually affected some time before the other. The electrical irritability of the nerves of the part has been found normal in the early stage, and slowly vanishing as the malady pro- gressed. Although the trophic changes are limited, as a rule, to the hands, and the muscular wasting does not extend above the forearms, the loss of sensation is occasionally more extensive, involvinc the whole arms, parts of the trunk, and even the face. An affection of * In a case recorded by Jolly (' Charite Ann.,' xvi, 1891) there was also a con- genital anomaly of the fingers, a web of skin between the third and fourth fingers of each hand. SPINA BIFIDA. 647 the shoulder-joint has been observed.* The feet are occasionally, though rarely, the seat of anaesthetic ulceration ; the legs have also been found weak, with excessive knee-jerk and foot-clonus (Hiickel). In the autopsy that was made by G-ombault neuritis was found in both arms, and also a diffuse overgrowth of connective tissue in the posterior part of the grey matter of the cord and the posterior columns. This growth involved also the coats of the vessels, which were in places so thickened as to obliterate their cavity. Neuritis has also been invariably found in the extremities of the fingers when these have dropped off. The features of the malady are so peculiar that, if they are known, the nature of a case cannot well be mistaken. Anaesthetic leprosy presents the closest resemblance, but in this the peculiar ulcerations are absent, and pigmentary alterations occur in the skin ; while in Raynaud's disease there is not the peculiar loss of sensibility, nor an equal tendency to whitlows, and vaso-motor disturbance is a more conspicuous feature. In the peculiar malady known as " sclero- dactyla " (a form of scleroderma that affects the fingers and face) there is no loss of sensibility or tendency to destruction of the finger ends. Simple syringomyelia is distinguished by the common absence of the whitlows, by the subordination, in time and degree, of the trophic changes to the other symptoms, and by the common preserva- tion of tactile sensibility. But the distinction is probably not an absolute one. In Morvan's disease there is peripheral neuritis as well as syringomyelia, and to this- is due its special features, and especially the early and intense trophic disturbance.f Spina Bifida. Spina Bifida, or split spine, depends on a defect in the closure of the vertebral arches, which usually leads to the protrusion of the membranes as a sac, forming an external tumour, into which the lower part of the spinal cord often extends, normal or variously altered in conformation, sometimes even reduced to a neural hning of part of the wall. Barely there is no external prominence—a form known as " spina bifida occulta." J The condition is most common in the lumbar reo-ion of the spine; sometimes is present at more than one place, very rarely in the whole length of the vertebral column. It is met with in about one child out of every thousand born (Chaussier). The * Morvan,«Gaz. Hebd.,5 18S7, No. 34. t The absence of any fundamental difference between this malady and syringo- myelia has been pointed out by Bernhardt (' Verh. Vert-ins inn. Med.,' Berlin, January 19th, 1891) and Jolly (loc. cit.). But the additional element of neuritis must not be ignored. t The best accounts of spina bifida are in the 'Report of the Committee of the Clinical Society" ('Transactions,' 1885), and Bland Suttou's "Lectures on Evolution in Pathology" ('Lancet,' February 25th, LSSS). 648 SPINAL CORD. disease is one of chiefly surgical interest, and therefore only an outline of the more important facts is here given. The spinal cord, whether normal or not, generally reaches lower than usual in the vertebral canal, as it does at the early period of development, when the morbid state is produced,—becoming adherent at its lower extremity and remaining so. In many cases the central canal of the cord is enlarged above, and the lower part of the cord may also be similarly distended. The precise condition presents many variations, which can be, in part at least, understood by what is known of the process of development, a subject that has been very ably discussed by Bland Sutton. The essential element in spina bifida, the defect in the vertebral arches, depends on a deficiency in that ingrowth of the mesoblast from each side which should enclose the embryonal spinal cord, and form bone, after the superficial epiblastic layers have united to form the epidermis. A similar ingrowth of mesoblast forms the corium, muscle, A.c This apparently takes place in excess in spina bifida occulta, and leads to a curious condition, usually present—an excessive growth of hair over and about the affected part, which is generally the lumbo-sacral region. On the other hand, in many cases in which there is a tumour, this superficial mesoblastic ingrowth seems to be deficient, as well as that for the vertebral arches, so that at the upper part of the tumour there is an area in which there is no proper skin, but a peculiar shiny membrane destitute of hair. It is probably this superficial mesoblastic deficiency that permits the protrusion, and formation of an external tumour. In spina bifida occulta the defect in the arches can be felt on palpation, either in the lumbar or sacral region, and the spinal cord extends lower than normal, as in the ordinary form. The latter, in which there is an external tumour, presents three chief varieties, FlO. 190.—Spina bifida: sections of a spinal cord, from a case the symptoms and history of which I was unable to ascertain. In A, cervical region, the only abnor- mality is a large cruciform central canal and an unusually thick grey commissure. This continues through the dorsal region, at the lowest part of which there is a great change. In B, the canal is larger, and the necks of the posterior horns (and posterior vesicular columns) are united by much commissural tissue; in this, many vertical fibres could Vie seen, and others running from before backwards in the middle line. In C, an extension of the canal backwards has taken place, and it is bounded by a sinuous membrane; the outer part of the grey substance is atro- phied. In D, the cavity has extended into each posterior horn, almost up to the surface of the cord, in part by a breaking down of tissue, because the membrane limiting the enlarged canal remains undestioyed. In E, still at the junction of the dor-al and lumbar region*, the cavity has receded irom the left horn. In F, the division of the cord has taken place, not in the direction of the cavity in the horu (which is filled up), but in the middle line, at or close to the median septum. In G, a wider separation of the posterior columns has taken place, and a cavity has formed on the right side, which extends into the horn, and almost cuts off the posterior column. In H, the cord is spread out and formed part of the wall of the sac. The posterior nerve-roots (p r) mark the position at which the posterior horn comes to the surface. The grey matter is in many parts atrophied and translucent, and, in H, contains many large ve.-sels. The septal lobulation on the surface of the cord is greater than normal. SPINA BIFIDA. Fig. 190. 649 ' '"*-' ■- y y% -— wy:y y y?wm:^:.:- Y "0J;'-."X -~.^y , V' ~^~ 650 SPINAL CORD. according as the sac contains only the spinal membranes (meningocele), the spinal cord as well as the membranes (meningomyelocele), or the latter distended by enlargement of the central cavity (syringo- myelocele). These are the chief classes; they do not, indeed, exhaust the rarer forms, but to take full cognizance of these would entail a very complex list of varieties.* Of the several forms, that without an external tumour has been least frequently met with, although it is probable that a knowledge of the significance of the growth of hair in the lumbar region would lead to the detection of this state in many cases in which it is now undiscovered. Putting this form aside, simple meningocele and syringomyelocele are both rare; the common form is meningo- myelocele, in which the cord, altered or intact, extends within the sac. The Clinical Society's Committee found that this was the condition in 62 per cent, of the cases in which there was an external tumour. The lower part of the spinal cord is generally adherent to the posterior wall of the sac, where its traction often causes a depression on the surface, always at the membranous area, which, as already mentioned, is generally to be observed in the upper portion. The cord may again become free, and extend downwards in the cavity, or it may be flattened, expanded, and lost in the wall, of which its tissue really forms an inner layer. In this layer there is no distinction of grey and white substance. In either case the lower nerves arise in the wall, and pass, first in this, and then forwards, across the cavity, to their fora- mina of exit. The arachnoid always extends into the sac, and the fluid is that contained within the subarachnoid space; sometimes there is an external opening from which the fluid flows. As a rule, the central canal of the cord is not continuous with the sac; and it may be closed, even in the condition of syringomyelocele, in which the canal is dilated. In other cases the canal opens into the cavity, sometimes by only a small aperture, even when the lower part of the cord expands into the wall, and the nerves course along the wall in a layer continuous with the arachnoid and superficial to the membrane that represents the cord-tissue from which they arise. As stated, ordinary syringomyelia may exist in the upper part of the cord. The extension of the cord in the wall of the sac probably indicates a developmental defect similar to that of the bony canal; in the lumbar region the primitive canal has failed to close, so that the cord is open posteriorly, and the two posterior columns may even be far apart, or the cord may even be applied, in the form of a thick or thin lamina, to the wall of the sac. An instructive although rare example of the involvement of the cord in the developmental effect is shown in Fig. 190, which illus- trates also the manner in which the latter may involve in some degree the whole cord. In the cervical region the grey commissure is unusually large, and the canal is cruciform, a shape which it presents • Several other varieties are enumerated by Bland Sutton (loc. cit.). SPINA BIFIDA. 651 at one period of development, and which is here persistent. This condition obtains throughout the dorsal region until, in the lower part, the tissue behind the commissure is so abundant as to unite the necks of the posterior horns Below this the canal enlarges into a condition of syringomyelia, surrounded by the abnormal tissue which, as we have seen, is commonly associated with such enlargement; the canal is limited, moreover, by the sinuous membrane that is so often met with (see p. 633). The cavity extends also into the posterior horns, clearly by a process of disintegration, since in d the membrane lining the enlarged canal persists, and marks the limit of the canal and the extent of the simple disintegration. The progressive separation of the posterior columns is shown in f, q, and h. In the lowest part of the cord, the development of the posterior columns has been appa- rently hindered, as will be observed if g be compared with f. In the former there are also some fissures in the grey substance, formed apparently by disintegration. The grey substance of the cord is con- spicuously wasted in the lumbar region, thin and translucent. In rare cases there has been no proper development of the cord. It was represented by a mere nerve-like string in a child, who also had hydrocephalus, but lived five weeks. Another child of the same parents had a similar condition.* Symptoms.—If the cord is intact, symptoms may be absent. In the cases in which there is an external opening, and a constant escape of cerebro-spinal fluid, the child usually dies in a few weeks. In other cases the defective development of the lower part of the cord, or its distension in syringomyelocele, is manifested by an absence of function, amounting to complete paraplegia in severe cases, which also seldom live. Some cases, however, survive, with paralysis and wasting of the legs, and often absence of power over the sphincters. In slighter forms the paralysis and wasting have been partial, either existing from the first, or supervening at some later period, probably from the occurrence of damage to the nerve-roots or cord-tissue by in- creased tension, or by inflammation; of the latter abundant traces may be found after death, and various external influences may readily set it up. Some children, whose legs have appeared natural, have never been able to stand; possibly the defect in the posterior columns has o-iven rise to a sort of congenital tabes. Even in the slighter forms, including spina bifida occulta, paralysis and atrophy have come on after some years, and even after adult life has been reached. Indeed, in the unsuspected forms without a tumour, there may be special danger of injury to the unprotected structures, and damage to the nerve-roots. The muscular paralysis and atrophy have been usually below the knees, and the muscles least prone to suffer are the tibiales antici. Hence talipes varus tends to occur. These muscles may alone persist, probably from the higher position of origin of their nerves (Eemak). Another peculiarity of these cases is the tendency * S. Wolfe, ' Phil. Rep.,' June 2nd, 1888. 652 SPINAL CORD. to perforating ulcer in the feet, which has several times necessitated amputation. Chronic changes in the tarsal and metatarsal bones have also been met with, somewhat like those of tabetic arthro- pathy.* The ulcers suggest neuritis, which was found in one case; and, in this and others, the arteries have presented thickening of the muscular coat, even leading to their closure. These symptoms may be greater on, or confined to, one side, and on this the knee-jerk has been lessened.f These points of resemblance to tabes may also be due to the greater degree of exposure to damage of the posterior roots, as well as to neuritis, perhaps descending. The treatment of spina bifida is purely surgical. That of the con- sequences just described is the same as for similar states in other diseases. TRAUMATIC LESIONS OF THE SPINAL CORD. Injuries to the cord fall within the province of the surgeon, but some account of them is needed because the subjects often afterwards come under medical observation, and because the cases present every gradation to the maladies that have been described in the preceding pages. Causes.—In fractures and dislocations of the spine, the cord gene- rally suffers compression or laceration, as already described in the chapter on injuries of the vertebral column. The cord may also be directly wounded by stabs and gunshot injuries, in which it may be divided completely or partially. Such injuries furnish a considerable proportion of the cases of unilateral lesion of the cord. In gunshot wounds the cord more often suffers from displaced fragments of bone than from the ball itself. Far more common than direct injury is damage to the cord by con- cussion of the spine, either local or general. G-unshot wounds occa- sionally furnish examples of local concussion ; a bullet may strike the spinal column and. lodge in its vicinity, with the effect of causing immediate paraplegia, as complete as if the cord were divided, and yet it may be found that the spinal column has not been injured, and the cord is merely softened at the spot. Other causes of concussion are the fall of heavy bodies on the back, such as a beam of timber or a * In one case Sutton found the compact tissue very scanty, and the bones filled with semi-fluid fat; a deep ulcer reached a carious spot. t Details of cases by Fischer, v. Recklinghausen, Brunna, and others, are quoted by Bland Sutton (loc. cit.). See also Delafosse, ' These de Paris,' 1874; Remak, ' Berlin, kl. Wocbenschrift,' 1885. TRAUMATIC LESIONS. 653 sack of corn, a blow on the back from some blunt weapon, a fall upon the back, either on a flat surface or on some projecting object. Less frequently the cord suffers from a general concussion of the body, in which the spinal column is not specially involved. The cervical region is occasionally damaged in falls on the head. Railway accidents are frequent causes of concussion of the spinal cord; the back may be struck with violence when the body is thrown from one side of the carriage to the other. Another common cause is a fall from a horse upon the back, or a fall downstairs, in which the spinal column is bumped against the edges of the steps. A violent bending of the spine may also injure the cord directly, especially in the more mobile cervical portion, where the region of the fourth and fifth vertebrae is especially apt thus to suffer (Thorburn).* The jar of the spine caused by a jump from a height may even be effective. Occa- sionally effects very similar to those which are produced by a blow on the spine are caused by a sudden contraction of the spinal muscles in some violent effort, a " rick of the back," as it is popularly termed. It is possible that, in such cases, the primary damage is sometimes to the vertebral ligaments and articulations, and that the cord suffers secondarily. The symptoms may only come on a few hours after the injury in such cases, as if effused blood compressed the cord, or the tension upon it and slight damage set up a graver inflammation. Thus a soldier, in a drunken quarrel, was extended by four comrades, two pulling on his feet and two on his arms, while a fifth sat on his back. No immediate effect followed, but the next morning there was complete paralysis of both arms and legs, which very slowly passed away. Pathology.—The anatomical lesions in cases in which the vertebral column is not injured vary much in different cases. Haemorrhage is often found, sometimes outside the dura mater, sometimes on the inner surface of the membrane, in the pia mater, in the substance of the cord itself, very rarely into the central canal, f Occasionally the substance of the cord has been found lacerated when the vertebral column has not been injured. In many cases there is local softening, commonly yellow in tint, sometimes mingled with red, often involving the whole thickness of the cord, and occasionally extending, as central softening, through a considerable vertical extent. Under the micro- scope the usual products of inflammation are seen, sometimes with hsematoidin crystals. Such softening may occur rapidly in severe local concussion, and be found complete a few weeks, or even a few days, after the injury.^ On the other hand, in some cases of complete * • Brain,' January, 1887. t As in a case reported by Chucan and Wickham, ' Prog. Med.,' 1887. Probably it is only when the canal is previously dilated that this occurs, as it may, without serious injury to the nerve-tissue. X Edmunds, ' Brain,' vol. vii, p. 103; Obersteiner, ' Wien. med. Jahrb.,' Bd. iii, 1879 j Lochner,' Bayer. Aerztlich. Int.-Bl./1857, No. 42; Fromiiller,« Memorabilien.' 654 SPINAL CORD. paralysis, no lesion of the cord has been found, either with the naked eye or the microscope, a few days after the injury.* In other instances, in which the cord is examined some weeks 01 months after the accident, the signs of chronic myelitis are found, in scattered foci or more diffuse tracts, in the white columns or grey substance. The nerve- fibres are wasted, and the connective-tissue elements are increased in quantity, and in the early stages there may be aleucocytal infiltration about the vessels, dilatation of the capillaries, and minute extravasa- tions, although none may have been visible to the naked eye. In the anterior cornua the motor nerve-cells may be damaged, sometimes swollen and vacuolated, or shrunken, and the anterior root-fibres may be degenerated. The grey matter is especially apt to suffer when the enlargements are injured; in the dorsal region the change may be confined to the white columns. Ill-defined cavities may exist in old cases, where the nerve-elements have perished. The usual ascending and descending degenerations may be found above and below the most damaged parts. Occasionally there are indications of meningitis, diffuse or disseminated, and sometimes confined to the dura mater. Svmptoms.—The effects, immediate and remote, of injuries of the spinal cord extend over almost the whole range of symptoms of cord disease, and their variations in character and course are almost infinite. It is therefore neither practicable nor necessary to do more, in this place, than to describe their general characters. According to the difference in course, we may divide them into three classes. (1) Those in which the injury causes immediate and severe paralysis, due to instant damage to the spinal cord, the consequence of its laceration, compression, or concussion. (2) Those in which there are at first either no symptoms or only trifling disturbance of function, but in which grave symptoms come on a few days or weeks after the injury. (3) Those in which there are no early symptoms, or only slight and transient disturbance, but at the end of one or several months symptoms gradually come on, often such as indicate disease of some definite system or structure of the cord, degenerative in nature. (1) The first class, in which the injury causes instant and considerable disturbance of function, includes the cases in which the cord is directly injured, and also some in which there is no visible sign of damage if the patient dies within a few days. In the former class there is often a manifest lesion of the spine, and the cases are, at least at first, purely surgical in their practical relations. In the latter the mechanical influence has apparently abohshed the function of the nerve-elements. If such patients live longer, either quick recovery 1870, No. 12. In the last, described further on, softening was found thirty-two hours after the injury. * Fischer, 'Deut. Zeitschr. f. Chirurg.,' 1883, Bd. xix. TRAUMATIC LESIONS. 655 ensues, or local softening from disintegration of the fibres that are most damaged. It is an interesting fact that concussion may thus derange function. The absolute integrity of structure on early micro- scopical examination shows that the result is not due to any minute vascular lesion. The effect has been compared by Reynolds, not inaptly, to the demagnetisation of iron by a blow. Doubtless the influence is exerted on the molecular nutrition of the nerve-elements, and the possibility of recovery, or the subsequent structural dis- integration, depends upon the degree of nutritional damage.* The symptoms, in these cases of severe and immediate effect, are generally those of complete impairment of function. When the injury is direct and partial, such as a hemisection by an incised wound, or a partial bruise of the cord by a spiculum of bone being driven against it (as in the case mentioned at p. 236), the effect may be a partial (e. g. one-sided) derangement of function; but in most other cases there is abolition of all the conducting functions at the level of the injury. There is complete paraplegia, motor and sensory, with loss of power over the sphincters. The symptoms are thus those of a total transverse lesion at the affected level (see p. 269). When the cervical region is injured, the arms are necessarily affected according to its seat. Such cases often illustrate very clearly the relation of arm-function to the cord.f The fibres for the sympathetic are often implicated, especially those for the iris, causing inequality of the pupils. Reflex action below, abolished at first by shock, usually soon returns and becomes excessive, but remains absent if the lumbar enlargement is damaged, or is invaded by haemorrhage; it may be again lost by the downward extension of secondary inflammation, which is equally effective when partial (in the posterior columns or grey matter) as when total, and is more difficult to detect in the former case. J Loss of consciousness is occasionally produced by an injury which does not directly involve the head, as in the case mentioned on p. 656 ; vomiting is very common at the outset. The cases of direct injury often run a severe and rapid course ; and when the secondary inflam- mation spreads downwards, or the lower part of the cord is injured (as * These conclusions have been recently formulated more definitely, but without essential extension, by Schmaus, partly Iroin experiments on rabbits ('Munch, med. Wocbensch.,' 1890). t See especially Thorburn, 'Brain,' January, 1887. t This is the explanation of most cases of injury above the lumbar enlargement, with permanent loss of myotatic irritability, or of all reflex action, as in those described by Bovvlby ('Lancet,' 1890, i, 1071). Such descending inflammation must not be confused with the descending degeneration in the pyramidal tracts which entails myotatic excess. The very rare exceptions mentioned on p. 264, in which such loss exists with no lesion to explain it, may be associated with the fact that myotatic irritability is sometimes lost in cases of cerebellar tumour. But the fact that superficial reflex action in the legs is never lost unless the lower part of the cord is diseased, is one of the most certain in pathology. Proof of such descending inflammation is given in the chapter on tumours (p. 617, note). 656 SPINAL CORD. is frequently the case), the tendency to trophic changes in the skin, and to the occurrence of cystitis and pyelo-nephritis, is very great. (Edema of vaso-motor origin, and effusion into joints, may be pre- sent in the early stage. If the cord has been directly injured in its whole thickness, survival beyond a fortnight is rare. "When it is damaged indirectly, with secondary softening—in what may be termed concussion myelitis—death occurs less rapidly, but many patients die at the end of four or six weeks, while in those who survive the first two months slow recovery often occurs. Even in such cases death sometimes occurs very quickly, but it is possible that there is then a laceration of the cord. A man, whose case has been recorded by From till er, was struck on the back, at the level of the third dorsal, by a heavy beam, and had loss of motion and sensation up to the level of the nipples. The palsy of the muscles of respiration increased, and he died from asphyxia at the end of thirty-two hours. At the spot struck the cord was reduced to a pulp for 3| cm., without any heemorrbage. The following case illustrates the occasional loss of consciousness when there is no evidence of any cerebral lesion. A heavy weight fell upon a man's back; he was unconscious for two days, and at the end of that time the legs were completely paralysed, and continued co for three months, with retention of urine. Then improvement com- menced, in the left leg before the right, and in the latter some spasm developed. At the end of six months he could walk across the room on crutches. Improvement continued, but at the end of two years his condition became stationary, and when I saw him, six years after the accident, he could only walk half a mile; the right leg was still weak in all parts, and a foot-clonus was present in each leg, greater in the right than in the left. In cases in which the lowest part of the back receives the force of the blow, as when a severe fall ends in the sitting posture, and the sacral region is struck, the nerves of the cauda equina seem often to be specially damaged, and the posterior roots in greater degree than the anterior. The effect is to cause loss of sensibility in the legs, varying in extent and seat according to the part injured, in some instances specially great about the anus, in others extending over almost the whole of the legs, in others again it is chiefly in the sciatic area; all forms of sensation are usually involved. It is generally accompanied by some muscular paralysis and rapid atrophy, with the reaction of degeneration, especially in the muscles below the knees. Barely no muscular paralysis exists; but there is loss of power over the sphincters in most cases. Beflex action is lost, and trophic changes are readily produced, both on the feet and over the sacrum. The sensory loss is often permanent, the injury to the nerve-roots being apparently too severe to permit recovery. As the case just mentioned shows, when the earlier effects of the injury are survived and improve- ment sets in, it is remarkable how long this may continue, and how TRAUMATIC LESIONS. 657 considerable a degree of recovery may be ultimately attained, it may be in the course of three or four years. (2) In cases of the second class initial symptoms are absent or slight. After the accident the sufferer may not imagine himself injured, and may be able to walk some distance without inconvenience. In other instances there is tingling in the legs, or in all the limbs, immediately after the concussion, sometimes with some weakness of the hmbs, more often with a feeling of stiffness. In the course of a few days graver symptoms come on, usually attended with spinal pain and tenderness, sometimes with some stiffness of the back, and often with pyrexia. Tingling in the limbs increases or develops, and is accom- panied by weakness, which often goes on to complete paralysis in the course of one to four weeks. The symptoms vary in their character and distribution, according to the position of the morbid process and its extent. In some cases, in which the dorsal region is most affected, the symptoms are those of simple paraplegia, usually with spasm, and sometimes with early contraction of the muscles. In other cases, in which the grey matter of the enlargements suffers, there is scattered muscular atrophy in the limbs, often with indications of the degene- rative reaction. Tremor in the limbs is conspicuous in some instances. A girdle-pain in the trunk, or sense of constriction in the limbs, is very common. The sphincters generally suffer, and the tendency to trophic changes is usually strong. The character and course of the symptoms is that of a subacute myelitis, and the meagre facts of morbid anatomy leave little doubt that this is the common lesion. Thus a lady was severely shaken in a railway collision. She seemed immediately after the accident to have suffered no injury, but in a few days paraplegia developed, and from its consequences she died six weeks after the accident. Throughout the dorsal region of the cord I found indications of subacute myehtis, chiefly in the white columns, varying in its extent in different regions, but most distinct in the pyramidal tracts.* Complete motor and sensory palsy, up to the level of the umbilicus, developed in the course of a week, after a fall downstairs in which the back struck successive steps. Yet the patient was able to walk immediately afterwards. The symptoms in these cases are sometimes unilateral. A man, driving under a low archway, leaned back to save his head, and his spine was pressed suddenly against the sharp edge of the seat-back. He felt but little immediate effect, but in the course of two or three days complete motor palsy of the left leg came on, accompanied by hyperaes- thesia, but without any loss of sensation either in that leg or in the other. Power slowly returned at the end of three months, and was in time perfect. In some cases of this kind the symptoms are due * In the face of such a case as this, it is superfluous to discuss the question raised by some writers whether or not the cord can suffer concussion. Moreover it is certain that such an effect as was extreme in this case, may and must often occur in slighter degree. VOL. I. 42 658 SPINAL CORD. not to direct damage to the cord, but to its compression by inflam- matory products outside it, the result of injury to the vertebral column. A clergyman was thrown from his horse, and there was immediately sufficient weakness of the legs to prevent him from walking; this subsequently increased, so that at the end of a fort- night the right leg was completely paralysed, while the left retained considerable power. There was a girdle-pain at the level of the umbilicus, and a bedsore formed, but he slowly improved, and regained the power of standing at the end of eight months. Such symptoms may come on weeks after the concussion, especially when the effects of this are so slight as to be disregarded, and the patient leads his usual life. When the damage involves the grey matter, the extent of the muscular wasting varies greatly. It seldom affects both arms and legs, but it is usually irregular in distribution, sometimes wide-spread, sometimes limited. Thus a young man fell from a horse and pitched on the head. He was stunned, and on recovering consciousness about two hours later felt " pins and needles " in both hands and pain in the back, followed by swelling of the neck and difficulty in moving it. The tingling ceased, but was followed by a sense of oppression about the shoulders, and persistent pain in the cervical region of the spme. When I saw him, two months later, there was some weakness of the right arm and wasting of the two outer interossei, and of that part of the long extensor which acts on the two outer fingers, with loss of faradic and preservation of voltaic irritability. Sensory symptoms are prominent in some cases of this class. Besides the pain in the spine, to be presently mentioned, pains are often felt in the legs, various in character; still more frequent are spontaneous sensations of tingling, " pins and needles," and the feelings of defective sensibility described as "numbness." Various forms of hyperaesthesia are also common, with or witiiout such subjec- tive sensations. This may exist in any part, in the soles, feet, thighs, or not infrequently about the genitals. In the latter region, and about the anus, a sense of coldness is often complained of. In these regions there may be a distinct defect of sensibility, but this is slighter and less frequent than in the cases of the first class. Some degree of anesthesia to touch may be associated with increased sensitiveness to stronger impressions. These sensory disorders may exist alone or be accompanied by motor weakness. Slight unsteadiness or definite inco-ordination is present in some cases, usually resembling that met with in ataxic paraplegia. In cases which survive the acute stage there is usually slow improve- ment, which is often ultimately very great. In many cases recovery is incomplete, but improvement goes on for years, as it does in the cases of considerable damage to the cord already mentioned ; the ultimate degree attained is commonly much greater than in cases of corresponding character and severity due to other causes than injury. TRAUMATIC LESIONS. 659 Some permanent symptoms are left, chiefly when the initial deiange- ment of function has been severe, and has lasted for some time. (8) In the cases of the third class, chronic symptoms slowly follow an injury at an interval usually of some months, and the cases have the aspect less of a traumatic lesion of the cord than of a primary cord disease, the relation of which to the injury is rather an inference from the sequence, coupled with the absence of other causes, than an obtrusive fact, as in the cases of the first and second classes. The sym- ptoms are usually those of a definite system disease of the cord, less frequently those of a disseminated chronic myelitis of irregular distri- bution, still more rarely those of chronic focal myelitis. Primary spastic paraplegia, ataxic paraplegia, insular sclerosis, locomotor ataxy, and progressive muscular atrophy are the diseases which most frequently thus result. The fact that an injury is occasionally the cause of these maladies has been already mentioned in the account of their etiology, and the symptoms of such cases so far resemble those that are due to other causes that it is not necessary here to add anything to their his- tory as already given.* We must assume that the shock to the nerve- elements causes a slow perversion of nutrition, which is only mani- fested by disturbance of function when it has gradually attained a certain degree. Occasionally other causes co-operate, capable of producing degeneration. Previous syphilis, or neurotic inheritance, can sometimes be traced, and it is a reasonable assumption that the predisposition thus arising may assist in rendering the traumatic influence efficient, or in augmenting its effects. Intermediate cases connect this class with the last, cases in which we must assume, from indications of chronic inflammation, that definite injury was produced at one or more spots. An instance of this, and also of focal myelitis, was presented by a man with permanent spastic paraplegia and an intense girdle-pain at the level of the umbilicus. These symptoms commenced three months after a jump from a table, and slight unsteadiness, with pains in the legs, connected the jump and the paralysis. The several consequences of injury, which we have considered as oc- curring in separate form, are not only connected by intermediate cases, but are also sometimes distinctly combined. Thus an actual and immediate lesion of the cord may be associated with an early and severe increase in the symptoms from the development of subacute mvelitis in other parts. The traumatic inflammation, at the spot damaged, often attains an intense degree, and runs a severe course, in consequence of the influence which may give rise to such inflammation, apart from a positive lesion; and, in both cases, the damage to the cord may be perpetuated by a degenerative tendency It is very common, for instance, for an injury to the cord, in those who have had * A case may, however, be mentioned in which typical tabes followed slowly a fall on the back, recorded by Barbour ('Journ. of Nervous and Mental Diseases,' March, 1891, Case IV). 660 SPINAL CORD. syphilis, to cause acute symptoms which subside, but not perfectly; and the residual disturbance of function may persist, and even increase in the course of years, in consequence of the influence of the previous syphilis in rendering the nerve-elements prone to degenerate. Again, it has been pointed out that the gouty diathesis is an unquestionable cause of myelitis, and often of the grave relapsing and spreading dis- seminated variety. A concussion of the cord, which causes only slight symptoms, may excite the occurrence of this form of myelitis in persons thus predisposed; the symptoms of the later inflammation may come on months after the injury (the effects of which ha/e generally not quite passed away), and are sometimes excited by some over-exertion, or slight fresh concussion which would have had no effect on a healthy individual. I have known the symptoms of insular sclerosis, cerebral and spinal, to quickly follow traumatic paraplegia. One other symptom remains to be considered, which is common to all forms of traumatic lesion of the cord, and is often severe and per- sistent when other symptoms are slight—spinal pain. It may con- tinue for years after other symptoms have ceased, and probably depends on a neuralgic state of the nerves of the membranes or of those of the vertebral column; often, probably, the pain depends on the nerves of the joints and ligaments of the spine. It is essentially a traumatic spinal neuralgia. The pain may be felt at one or more spots; when severe, it often extends through a considerable length of the spine, and sometimes passes up to the occiput. It is occasional] v rcferred to the sacrum, and may there have the character of a sense of weight or more vague discomfort. The pain is associated with tenderness of the spine, usually deep-seated, chiefly developed at the injured part, but sometimes present also at other spots. It may gradually assume the features of a true neuralgia, may occur in paroxysms, and be induced by mental and other influences which do not act directly on the spine, as well as by exertion, posture, and other agencies that may immediately influence the affected structures. This condition is often called " spinal irritation." The cause of traumatic lesions of the cord often acts also on the brain. A cerebral lesion may occur from the violence which affecis the cord; the cerebral symptoms then co-exist with those of the spinal lesion, and may mask the latter during the early stage. More common, however, is functional disturbance of the brain, the result, partly, perhaps, of the physical concussion, but chiefly of the mental shock which a serious accident necessarily causes. The resulting condition is favorable to the development and persistence of subjective sensory symptoms. Attention, maintained by concern, has a powerful in- tensifying influence on all forms of nerve-pain, and certainly aids in keeping up the pain in the back, and even the tenderness which follows injuries to the spine. So marked is the influence of " nervous- ness " on the subjective symptoms, that it has been even maintained that in a large number of cases of concussion of the spine the TRAUMATIC LESIONS. 661 symptoms are of hysterical origin.* Well-marked symptoms of hysteria are sometimes manifested by these patients. But, on the other hand, it is necessary to avoid the danger of over-estimating the effect of mental influence, and of regarding, as entirely due to this, symptoms which are real, and are merely intensified by attention. The danger is especially great in cases of railway injuries, concerning which an unbiassed judgment is not easy to secure, and in which, when objective symptoms are absent, it is easy to minimise suffering, and attribute too much to the mental condition. The sinister influence of litigation on the intellect may be traced very widely.f I believe that it is rare for symptoms to be purely mental. It is often asserted by those employed for railway companies that subjective symptoms quickly subside when the sufferer's " claims " are settled, but it should be remembered that mental anxiety is a potent cause of diseases of the nervous system, and must be strongly opposed to recovery from genuine disorders. The occurrence of improvement when suspense is at an end is thus no proof in itself of the nature of the case, and its significance has been unquestionably over-estimated ; moreover, in a great many individuals whom I have had an opportunity of observing long after they had received their "damages" (as the expression curiously runs) this subsidence had not occurred, and even the " sove- reign balm " of substantial compensation has appeared to do very little for the relief of the sufferer. These opinions have been formed from a study of cases other than those that involve litigation, in which no elements existed to bias the judgment, and from a comparison of these with many " railway " cases observed apart from forensic proceedings. Those who desire to learn what can be said on the subject of " railway spines," as they have come to be termed, when viewed from the opposite sides, will find abundant material for consideration in the writings of Erichsen (' On Concussion of the Spine,' London, 1875) and Clevenger (' Spinal Concussion, or Erichsen's Disease,' Philadelphia, 1889) on the one side, and of Page (' Injuries of the Spine and Spinal Cord,' London, 2nd ed., 1885) on the other. Scattered papers by J. J. Putnam, Walton, Spitzka, Buzzard, and others, more or less instructive, will be found epitomised in Clevenger's work, where indeed is collected the pith of almost all that has been written on the subject. Diagnosis.—The chief points in the diagnosis of traumatic lesions of the cord have been already incidentally considered. Immediate symptoms may be due to laceration, haemorrhage, or to simple con- cussion, and the diagnosis between these is not always possible at first. If there are immediate symptoms of a partial lesion, these * J. J. Putnam, ' Boston Med. and Surgical Journal,' 1883, Sept. 6th. f Not many years ago it was customary for the " experts " who gave evidence on behalf of railway companies to deny that the spinal cord could be injured if the legs were unwasted. Although the opinion dare not now be expressed, its significance is not without analogies at the present day. 662 SPINAL CORD. indicate direct injury, while the rapid subsidence of the distuibance of function renders simple concussion probable, and excludes any considerable direct injury. The later development of paralysis in- dicates myelitis, unless there is evidence of considerable irritation of the nerve-roots at a certain level, which suggests inflammation outside the cord, and perhaps even outside the dura mater. The greatest diagnostic difficulty is presented by the cases just mentioned, in which the symptoms are subjective, and anxious attention has been long given to the local discomfort. The chief elements in the diagnosis of these cases have been, however, already indicated. It is important to search for, and to give due weight to, any symptoms beyond the simple spinal pain. Slight " tingling" or "creeping" sensations may be of cerebral and " functional" origin, but apersistent sensation of " pins and needles" rarely is of that nature. A definite sense of constriction is also strongly suggestive of organic disease, and so is a well-marked difference in the power of the muscles on the two sides. The latter is of least significance if the excess is slight, general, and on the right side—of much greater significance if the diminution is partial, and affects only certain groups of muscles, such as the flexors of the hip and knee, or the peronei. Any impairment of power over the bladder or rectum is of great diagnostic importance; loss of sexual power, on the other hand, is of little value, since this function is readily depressed by mental anxiety and preoccupation. A slight change in reflex action is most significant when it is partial. A foot- clonus or rectus-clonus is strong presumptive evidence of organic mischief. A slight excess of the knee-jerk is of little value ; although it probably always indicates some changes in the nutrition of the spinal cord, it does not indicate structural disease. In all cases it should be remembered that the absence of any common symptom is of far slighter significance, as evidence of integrity of the cord, than is the presence of that symptom as evidence of disease. It may seem superfluous to insist on a consideration so elementary, but it is still possible, as experience proves, for a medical witness to assert in a court of law that a claimant's spinal cord cannot have been injured because some symptom is absent, the presence of which would be important. Prognosis.—Immediately after an accident a cautious prognosis should be given, even if the symptoms are sliglit, on account of the possibility that grave disturbance may develop in the course of a few days. In developed cases the prognosis must in general be o-uided by the same considerations as those which determine our estimation of the probable course of symptoms of similar character and severitv due to spontaneous myelitis. To this there are, however, two general exceptions. First, the danger of death, if any exists, is greater in traumatic cases than in others, as long as the symptoms are increasing. Secondly, if there is no danger to life, or such danger has passed, the prospect of improvement is distinctly greater than in a case of similar TRAUMATIC LESIONS. 663 features but of non-traumatic origin. If the symptoms are slight or moderate in degree approximate recovery may be anticipated, although slight symptoms often endure for a very long time. Indeed, in many cases recovery, although approximate, is not perfect. The patient is never quite as strong, never becomes quite as capable of exertion, as before the injury. A cautious prognosis should also be given whenever there is the late and gradual onset or increase of symptoms that suggests a degenerative process. Such degeneration presents far less tendency to arrest or subsidence than do the earlier lesions. As a rule the sooner symptoms occur the better is the prospect of ultimate improvement or recovery, provided they are not so severe as to be incompatible with life. Tbeatment.—The early treatment of these cases, and much of the later treatment of those in which the spinal column is injured, is purely surgical. The points of medical character alone need special mention, and many of these have been anticipated in the preceding pages. In all cases in which spinal symptoms are present im- mediately after an injury, however slight those symptoms may be, absolute rest should be insisted on for some days or weeks, according to the severity of the early symptoms. I his is necessary on account of the secondary inflammation, which, as we have seen, so often occurs. The treatment of developed symptoms must be conducted on the same general principles as in cases of myelitis; the details need not be here repeated. If there is muscular wasting, it is important that the nutrition of the muscles should be maintained by electrical stimula- tion, since a very considerable amount of ultimate recovery may be anticipated, and it is important to keep the muscular tissue as far as possible in a condition to respond to the nerve-power when this returns. If there is reason to believe that there is inflammation of the membranes, or inflammatory effusion outside the cord, com- pressing it, mercury may be given, but this condition is probably much more rare than might be anticipated. The influence of mercury on inflammation of the substance of the cord is doubtful. The chief element in treatment is patiently to permit time to do its work, and the tissues to slowly regain such integrity of structure and function as is possible; meanwhile preserving the patient from all influences likely to interfere with the process or to setup other mischief, such as cystitis or bedsores, which would entail fresh danger. There is, however, one therapeutic measure that is of unquestionable value in the treatment of the later stages, especially of the cases in which the recurring symptoms suggest a relapsing myelitis as the sequel of injurv ; and that is the repeated application of a mild " actual cautery" on each side of the spine opposite the affected region. Several applications should be made, with or without an anaesthetic. It is not desirable to lessen the pain by cocaine, because this is likely to interfere with the influence of the proceeding, the beneficial cliaracter 6G4 SPINAL CORD. of which is undoubted.* The degenerative sequelae of injuries to the cord need the same treatment as the similar degenerations that occur apart from traumatic influences. Whenever there is evidence of dis- placement of the bones, or reason to suspect that the cord is compressed by fractured fragments, or even by products of secondary inflammation outside it, the propriety of trephining the spine needs to be considered. The problem is chiefly surgical, but the fact that it will probably not be necessary to open the dura mater increases the desirability of giving the patient this chance of relief. If needed, the sooner the measure is adopted, when improvement has ceased, the better. The treatment of the neuralgic condition of spinal pain and tender- ness, which so often succeeds injury, is frequently difficult. Counter- irritation is often useful, either by the actual cautery, blisters, iodine, or repeated sinapisms. Of sedatives, Indian hemp is most effective, next to morphia, which should be used as seldom as possible. Hypo- dermic injections of cocaine may be tried. When all active mischief is over, and the pain has become purely neuralgic, it is often neces- sary to encourage the patient to neglect it in some degree, and to exert himself in spite of it, while avoiding whatever increases it in considerable degree and for a considerable time. At the same time extreme care should be observed by all persons who possess the constitutional states above mentioned, predisposing them to myelitis, &c. This is especially necessary when any symptoms persist, and often difficult to secure, except by uncompromising insistence, in those who have been accustomed to a life of active exertion. FUNCTIONAL AND NUTRITIONAL DISEASES. Functional Diseases. "Very little is known, though much is heard, of functional diseases of the spinal cord. It is, indeed, open to doubt whether there are any morbid states which can accurately be thus designated; as was pointed out in the Introduction, most morbid states thus described are either due to disturbance of cerebral functions, or are the result of changes in the nutrition of the elements of the cord. The deranged function may be an expression of altered nutrition, as it is of altered structure, but such cases can only be termed " functional " by a loose misuse of words. We have an example of the transference of our conceptions of functional derangements from the brain to the cord, in the fact that hysterical paraplegia is often regarded as a functional affection of the cord because the symptoms have the same distribution as those of organic diseases of the cord; but a little consideration * For first directing my attention to the fact, and the evidence supporting it in these cases, I am iudebted to Dr. John Anderson. FUNCTIONAL DISEASES. 665 will show that, in a case of purely hysterical paraplegia, the morbid functional condition is cerebral; the brain-centres which act on the legs are at fault, but the condition of the functions of the cord itself may be absolutely normal. The spinal motor centres are in a state of inactivity because the related cerebral centres are inactive, but this is no more a diseased condition of the cord than is its corresponding functional state during physiological rest. Hysterica1 paraplegia will be described, with other palsies of like origin, in the chapter on hysteria—a malady for which the term " functional " is often employed in various ways, as a convenient euphemism. At the same time, it must be remembered that there is no sharp line of demarcation between functional derangement and nutritional changes. As already mentioned, no functional state can exist without leaving behind it some corresponding change in the finer molecular nutrition of the structures; and if functional derangement of lower structures results from that of higher cerebral centres, and is maintained for long, the change in nutrition that results may be considerable, and may be so definite as to persist even after its cause has ceased to act. Moreover the general enfeeblement of defective nutrition of the nerve-elements is a potent cause of this functional disturbance, and at once facilitates and augments such effects. The process may be observed in many cases not only of hysteria, but also of other derangements of the cerebral functions, and it is seen also in lower centres as an effect of pain. Isolated disturbance of functional centres in the cord does, however, sometimes occur. It is seen in the conditions of inhibition which are designated " reflex paralysis." Such palsies were once thought to be common and persistent, but it has been proved that many, and it is probable that all, cases of considerable and prolonged palsy, formerly thought to be of reflex origin, are due to organic disease, either primary in the cord or secondary to an ascending inflammation of nerves. But transient paralysis sometimes occurs, which cannot be otherwise explained than as an inhibition of a spinal centre, due to peripheral irritation. Such, for instance, is the curious inability to pass urine which sometimes follows an operation on the anus,—the division of a fistula, for instance, or the removal of haemorrhoids. The inability may continue absolute for several days. Transient weakness of one arm is said sometimes to follow an operation for empyema (Lepine), but the fact that the weakness may be attended by choreoid movements in both arm and leg of one side (Weil) makes it probable that the influence is exerted on a ceiebral rather than on a spinal centre.* Considerable paraplegia was thought to be sometimes a reflex effect of disease of the bladder, or of a calculus or other organic disease in the kidney, but it is probable that such cases are always of organic nature. Ascending neuritis, reaching the cord, * Paralysis and wasting of serrati magni and infra-spiuati muscles have, bow- ever, followed double empyema (Cayley,' Clin. Soc. Trans.,' 1898, vol. xxxi). 666 SPINAL CORD. has also been proved to be the cause of lasting symptoms in many cases supposed to be of reflex origin. In one important class of cases in which functional disturbance of the cord is purely secondary to a morbid state of the brain, organic or not, as has been already men- tioned, the expression in the limbs of all deranged functions of the brain is through the spinal cord; but such disturbance of the cord is purely secondary, and ceases when the cerebral centres resume their normal state; or, if it is continued longer, this is merely for a brief space of time, until the disturbed structures can regain their normal state. Thus, in idiopathic epilepsy, the convulsion is produced through the agency of the spinal structures, and their over-action may leave them so exhausted that the reflex functions are for a short time abolished. But such conditions cannot be regarded as coming into the category of functional disease of the cord. The nearest approach to such disease is presented by certain forms of spasmodic disorder, such as transient fixed spasm, catalepsy, and certain forms of tonic spasm, which depend proximately on spinal centres; and by some varieties of neuralgic and other painful affec- tions or dysaesthesiae, in which the sensory elements of the cord are deranged in action. But we can seldom feel sure that the symptoms in the former class are dependent on a primary derangement of the cord; more often they are clearly secondary to disturbance of cerebral centres, which may indeed co-exist, and the cases are better described among the general functional affections of the nervous system ; while those of the second class have features and alliances which make it more convenient to describe them among the forms of neuralgia. In another series of cases, derangement of the motor functions of the spinal cord is secondary to pain, generally that which has such a seat that it is increased by movement; sometimes pain that is not related to movement, but is so intense as to act, by mere severity, on related structures. It may be in the spine itself, in the trunk, or in the limbs. Over-action of the motor centres and spasm may be the result, or the centres may be inhibited, causing a pseudo-paralysis, which may be real, but often blends with a voluntary indisposition to move the parts, lest pain be produced. Spasm is generally brief, and the reflex result of some sudden pain, as is often seen in the case of the " lightning pains " of tabes. When more prolonged contracture results, as in cases m which hysterical contracture follows some painful affection of a limb, the co-operation of cerebral centres cannot be excluded. The inhibitory influence is strikingly seen in the immobility of one half of the thorax in pleurodynia; and in brachial neuritis the effect may render it impossible to say whether or not there is real motor weakness. Some forms of spasm may perhaps be due to primary disorder of the spinal centres, such as the peculiar cramp in the hands, coming on during sleep, that is described in Vol. II as " nocturnal tetany," and the startings of the limbs on going to sleep ; but, for the most part, these spasmodic affections are either FUNCTIONAL DISEASES. 667 secondary to morbid states of the cerebral motor centres, or form part of diseases of wider range in connection with which they are described. Other cases which may be regarded as functional are those in which symptoms, commonly subjective in character, result from some morbid blood-state. The conditions which most frequently have this effect are gout and diabetes. Occasionally there is defi- nite failure of power, lasting for a few days or weeks, without objective symptoms, and passing away. But the most common symptoms from this cause are sensory and subjective,—feelings of tingling and formication in the legs, dull aching, and sometimes actual pain; this is usually transient, but occasionally continues for some days or weeks, various in position, but in gouty cases often felt in the heels. Such symptoms due to morbid blood-states occur chiefly during the second half of life. Those of gouty origin, like other symptoms of the same class, are especially common in persons who inherit a tendency to gout, but have not suffered from attacks of definite arthritis. In the diagnosis of functional disorders the first element is the ex- clusion of any sign of positive disease, and the second is the discovery of some morbid state capable of giving rise to the functional derange- ment, or of associated symptoms unequivocally functional in character. The first of tliese is that of primary and paramount importance, which, alike in practice and reasoning, should precede the others. The various points involved in the diagnosis of hysterical affections are described in the chapter on that disease in Vol. II; one only need be mentioned here—the importance which attaches to the state of myotatic irritability in the legs, and the great difficulty in ascertaining it presented by many of these cases. Permanent excess shows that there is more than functional derangement; although it does not exclude the latter, it indicates changes in nutrition, and will be re- turned to presently. The cases in which the knee-jerk is apparently absent present a special difficulty. It is never really absent in func- tional disorder (except when the centres are exhausted by violent convulsion), any more than it is in health. Failure to obtain it is due to the inability of the patient to relax the muscles, which may render attempt after attempt futile, until, in some fortunate moment, relaxation is secured and a characteristic jerk is obtained. The expedients that facilitate the attempt have been already mentioned (p. 21), and the subject has been sufficiently discussed in the account of the diagnosis of tabes. The treatment of functional disorders is that of the morbid states to which they are due, or of which they form part, and does not need special description. That of the symptoms due to toxic influences is necessarily the removal of the condition which causes them, but they may be to some extent relieved by sedatives, of which bromide of potassium, cocaine, Indian hemp, cimicifuga, and small (7 or 10 gr.) doses of chloralamide are th^ most effective. 668 SPINAL CORD. NUTKITIONAL DISEASES. Among the cases often classed as functional diseases of the spinal cord are some in which objective symptoms of deranged function, slight in degree but definite in character, persist for months, years, or for life. They commence chiefly in those in the early and middle period of adult life, and are more common in women than in men. Such symptoms are inability to walk more than a short distance without fatigue, impaired nutrition of the legs, slight increase of myotatic irritability, often associated with pain in the back, aching in the legs (sometimes amounting to actual pain), and various spontaneous sensa- tions of tingling, " pins and needles," formication, and the like. There is often aching in the legs at night, especially when the patient lies on the back, and hence probably due to passive accumulation of blood in the spinal Aressels. Such symptoms occur especially in those of neurotic disposition, who often present other signs of the nervous weakness that it is now fashionable to term "neurasthenia." In many cases, if the history of such symptoms is traced, they will be found to date from some definite exciting cause, from an attack of acute illness, such as typhoid fever or acute rheumatism, from pregnancy, a fall, over- exertion, and the like, or to have come on during a period of general or nerve weakness, anaemia, anxiety, &c. Enfeeblement of the nervous system often results, and the impaired nutrition of the cord may be only part of a similar general state. A slight increase in mvotatic irritability is exceedingly common, enough to permit the knee-jerk to be obtained by tapping the depressed patella ; but there is rarely a distinct clonus, at most only two or three jerks, quickly ceasing. We cannot conceive that symptoms so persistent can depend on any mere functional derangement; it is probable that they depend upon changes in the finer nutrition of the nerve-elements, too slight to be detected by the microscope, but causing a corresponding and persistent alteration of function. We have seen that the termination of the upper segment of the motor path is probably that structure of the cord which has least nutritional stability, and is therefore most susceptible of nutritional derangement. Its degeueration is the apparent cause of persistent excess of myotatic irritability, and hence we can understand the frequency with which there is such an excess in these cases. There are probably gradations between such conditions and actual structural disease in which minute examination reveals visible alteration; and there are certainly gradations between the symptoms above described, and those in which the derangement of function is so considerable and special that the case must be reo-arded as one in which actual disease exists, of one or other of the types described in the preceding pages. We have already had occasion to consider these nutritional changes as probably underlying the con- dition of arthritic muscular atrophy, and we have seen that the altera- NUTRITIONAL DISEASES. 669 tions in spinal nutrition in that disease are apparently the result of the impressions on the peripheral nerves. In women such a con- dition is often associated with uterine or ovarian pain, and with sacral pain apparently of uterine origin. It is possible that the condition we have been considering is sometimes secondary to such uterine pain, which acts in a manner somewhat analogous to that in which joint inflammation acts, and that this is the explanation of many of the cases in which a reflex disturbance of the functions of the cord has been supposed to be of uterine origin. The condition is also often associated with spinal pain and tenderness, which may have a similar influence. In the diagnosis of these nutritional affections of the spinal cord it is important to remember that they may be closely simulated by analogous changes in the peripheral nerves, constituting the slighter degrees and forms of polyneuritis. The chief points in the distinction have been described in the account of that disease. It is in the parenchymatous forms, and especially in the sensory varieties, that the danger of confusion is apt to arise. Symmetry in the distribution of the subjective sensations, or positive anaesthesia, and their localisation in the extremities, are the most important features of neuritic change. Connected with this distinction is another, of not less importance. Nutritional changes, equally with the simpler functional derangement, may be the result and expression of the action of some toxic blood- state, and all that has been said in connection with mere alteration in function applies also to the class now under consideration. Toxic influences cannot, indeed, act for long without leading to changes in nutrition, which may speedily attain a degree that amounts to visible structural disease. A search for such an agency should never be neglected in any case in which the symptoms have not followed an adequate cause, and do not form part of a general state of the same nature. But it must be remembered that the peripheral nerves are, as a rule, more susceptible to toxic influences than is the spinal cord, and this fact gives additional weight to any indications that it is from these that the symptoms proceed. Lastly, symptoms suggestive of mere changes in the finer nutrition of the nerve-elements are fre- quently the earliest indications of organic disease of one or another of the types already described, and in all recent and progressive cases their general character and aspect must be carefully considered, and compared with the known features of the various organic diseases. The cases with such slight but persistent symptoms as have been just described vary much in their features, and may present all sorts of slight symptoms, in the utmost diversity of degree and combina- tion. To consider them in detail would be to describe an indefinite series of individual cases, no two of whfch are identical. The precise degree and manner in which the ne/ve-elements suffer may, it is evident, be almost infinitely various. Their corresponding manifesta- 670 SPINAL CORD. tions present features, combinations, and gradations that entirely baffle an attempt to designate them, or even to perceive definite types about which they can be grouped. These are some of the cases of disease which exemplify the failure of types in practical work, the error involved in the attempt to give names, and the paramount importance, in the process of diagnosis, of considering what morbid condition the symptoms indicate, and of dealing with each case as a new problem, sui generis, whether or not it is ultimately found to be one of a familiar series. This method, moreover, conducts the practitioner at once to the morbid processes that need treatment, and should determine the character of his efforts to alter that which is at fault. It is unfortunately not common for the indications of nutritional disturbance of the cord, when they have been long established, to pass away altogether, although some degree of improvement can often be secured; and in many cases, especially in those of brief duration, approximate restoration to a normal state may take place. The treatment necessarily varies according to the precise con- dition that exists, and the causes on which it depends. The removal of these as far as possible, and of any influence likely to depress the nervous system, must be the first consideration. It should be remem- bered that no part of the nervous system is unaffected by mental depression, and that impairment of the general health may render im- possible recovery from local disease. From these general principles the details of the treatment of individual cases, too various to be here described, may readily be deduced. Therapeutic measures that are thus reasoned out and determined on by the indications of the special case are far more likely to be successful than those that are simply taken from a description of treatment. The only points that need special mention are, first, the importance of securing mental tranquillity by producing the conviction, when possible, that no grave disease exists or is impending, and with it the disregard of those slighter sensations of discomfort that become more aggressive and disabling the more they are noticed. At the same time it is important that the patient should avoid all over-exertion, all risk of falls or chills, and should be espe- cially careful in regard to sexual intercourse, which often has a peculiar effect in augmenting the symptoms ; and in the unmarried, perfect continence should be enjoined. Often, indeed, in the case of men, the mental preoccupation causes an apparent failure of sexual desire, which itself is a source of concern—generally groundless. Beassurance on this point frequently helps to secure the desired mental state. Equally important is it to disabuse the sufferer's mind of the idea that seminal loss is weakening—an error widely prevalent; the truth being that any depressing influence comes only from the associated nervous action. But it is important to lessen undue frequency of nocturnal emissions, and for this nothing is so effective as Milton's remedy, large doses of the APPENDIX. 671 tinct. ferri perchlor. (ill xx or xxx) three times a day, couoled with the avoidance of lying on the back. The relief of disabling pain, by the measures described in the chapter on neuralgia, and by the treatment of any local morbid state, is indispensable. Best from work, the improvement of the general health, and the administration of nervine tonics, such as arsenic, phosphorus, quinine, strychnia, and the like, are the chief other points in treatment. A course of massage, or of gentle faradisation of the muscles, is also often useful. APPENDIX.* THE MUSCLE-SPINDLE. In 1802 Kolliker first described the muscle-spindle, and in the following year Kiihne added considerably to the description given by Kolliker. Both these investigators considered that the muscle-spindle was a stage in the development of muscle and nerve, and although in the following years a considerable number of investigators on the subject published their researches, it was not till 1888 that Kerschner aro-ued the sensory nature of the muscle-spindle. In 1893 Buffini described an annulo-spiral nerve termination within the spindle, but it remained for Sherrington in 1894 to prove by experiment that the nerve supplving the spindle passed up in the posterior root and definitelv to settle the sensory nature of the muscle-spindle. Distribution.—Muscle-spindles have been found in nearly all skeletal muscles of the body, excepting the eye muscles and the diauhragm. They are abundant in the small muscles of the hand and in the arm muscles, and are more numerous in the belly of the muscle than near the tendon. In relation to this statement it is well to recognise that the musculo-tendon organs are found to be numerous in the region of the tendon. The muscle-spindle is present at all ages from the fourth month of foetal life onwards. Size.—The size of the muscle-spindle varies considerablv, not only in the same muscle but also with regard to the length of the muscle, and the age of the subject, being longer in the adult than in the child, * The following account of the muscle-spindle has been kindly written by Dr. P. E. 1'atten, whose able and industrious researches on the subject render this expres- sion of his views most valuable. 672 APPENDIX. and in the larger muscles. Its average length is from 2 to 4 mm. (tV *° xg- of an inch), but it may measure as much as 12 mm. (^ inch). The average breadth at the equatorial region is from 15 to '4 mm. No reliable estimate of the number of muscle-spindles within the muscles has yet been made, but seventy-nine have been found in one biceps. Varieties in the muscle-spindle exist. Thus, they are not always single, but may be compound, by the junction of two or more, so 1 hat the pole of one spindle enters into the equatorial region of another. Again, it is not uncommon to find spindles joined at their poles; as many as three have been found in a row. Buffini distinguishes three classes of spindles according to the complexity of their nerve termina- tions. The muscle-spindle lies parallel to the muscle-fibre of the muscles in which it exists, and not unfrequently parallel to a nerve. It may he wholly in muscle tissue, or partly in muscle tissue and partly in the connective tissue round the muscle bundles, or wholly in the connec- tive tissue. Description.—The nomenclature adopted in the following description is that suggested by Sherrington, and the diagrams given will show the parts alluded to. The muscle-spindle is of the shape which its name implies. It is formed by a capsule enclosing two or more fine Fia. 191. Muscle Spindis Pole: ci"«»wsn Equatorial, Region |Mr«AM..CULA4 Pole (aramo Cap*ui£ op Spindle f NOT HOTOH.1 k. RUFriNl J muscle-fibres. The capsule resembles the Henle sheath of a nerve, and at the equatorial region of the spindle consists of eight or more laminae, while at the poles it diminishes to a single lamina, and is lost on the sheath of the muscle-fibre. The muscle-fibres which enter the spindle are of smaller size than ihe normal fibres composing the muscle, the intra-fusal fibres measuring about -02 mm., while the extra-fusal fibres measure about •06 mm As a rule, two or three of these fine fibres enter the pole of a spindle; as they pass towards the equatorial region thev undergo division, so that at this region of the spindle there may be eight or ten APPENDIX. 673 fine fibres, some of them measuring only *008 mm. At a certain point in the equatorial region some of the muscle-fibres lose their trans- verse striation and nuclei appear in the substance of the muscle fibre. These nuclei gradually increase in number till they completely fill the fibre, then after a short distance they become less numerous, and the muscle-fibre again resumes its striation. At the equatorial region the muscle-fibres do not fill the whole spindle, but lie to one side. As they pass to the distal end of the spindle they become joined again and pass out of the spindle as two or three fibres. It will be seen from the. above description that a transverse section of the spindle may at a given point in the equatorial region seem to contain no FiG. 192.—Normal spindle of child in transverse section. Magnified 250 diameters. 1. Section near the pole. The areas marked with vertical lines are muscle-fibres in transverse section. 2. Nerve entering into spindle. Many of the dark bodies in contact with the muscle-ribres are nerve-fibres. 3. Nearer the equatorial region the sheath has acquired considerable thickness. 4. At the equatorial region the muscle-fibres have undergone consider. able modification, and are no longer recognisable as such. 5. The spindle near the opposite pole; the muscle-fibres have resumed their natural appearance. 6. At the distal pole of the spindle. vol. i. 43 674 APPENDIX. muscle-fibres, the structures of such having been so profoundly modified (Fig. 192, 4). Nerve-supply.—The nerve-supply of the spindle is always large—as a rule at least two nerves pass to it, one at the equatorial region and another at the distal or proximal end. It is, however, by no means uncommon to find spindles with four or five nerves. The nerve passing to the equatorial region always contains a nerve-fibre of large size measuring about "008 mm. This nerve on entering the spindle loses first its Henle sheath, which fuses with the sheath of the spindle, and next, after entering its medullary sheath, it then divides into two and forms the annulo-spiral nerve termination of Buffini, winding round the muscle-fibres at the point where the nuclei are situated in the muscle-fibre. From the nerve that enters the equatorial region other fibres pass towards the poles of the spindle and lie between its muscle- fibres ; the mode of termination of these fibres is uncertain in man, but probably corresponds to the secondary ending described by Buffini. The nerves which enter the poles of the spindle are nearly always composed of fine nerve-fibres having a diameter of -004 mm.; they likewise pass between the muscle-fibres of the spindle and pass towards the equatorial region. The question whether the muscle-spindle contains a motor nerve termination is one that has not yet been determined, for the third form of nerve ending described by Buffini and named the " plate ending" is said by him not to be motor. Owing to the number of nerve-fibres within the spindle there is a plexiform arrangement of nerves between the muscle-fibres and the sheath of the spindle, but so far as can be ascertained they do not intercommunicate to form a true plexus. These nerves are myelinated. Blood-vessels.— The muscle-spindle is supplied by arteries and veins, which most frequently enter the spindle near its equatorial region. Under certain pathological conditions the muscle-spindle, owing to its apparent immunity from change, stands out in striking contrast to the surrounding muscle tissue. In all wasting diseases, and especially in phthisis, the muscle-spindle forms a very marked feature in sections of the muscle, but no change has been demonstrated in the structure of the spindle. It is for the same reason more striking in the muscles of a child than those of an adult. In infantile paralysis, although all the surrounding muscle tissue may have been atrophied or have undergone fatty degeneration, yet the muscle-spindle is normally preserved and supplied by a perfectly normal nerve. Similarly in progressive muscular atrophy exactly the same condi- tion can be demonstrated, although in tliese cases the atrophy of the surrounding muscle may not be so extensive. In the myopathies the muscle-spindle forms a very striking appear- ance, as is shown by the description given of them in published cases of this disease. They remain, however, perfectly normal both with APPENDIX. 675 regard to their nerve-supply and the character of their muscle- fibres. In peripheral neuritis certain changes have been described within the muscle-spindle both as regards the muscle-fibres and also as regards the nerves; in other cases, however, they have been shown to be perfectly normal. In tabes dorsalis, although the external form of the spindle and the nerves passing to it have been found to be normal, certain changes have been described in the intra-fusal muscle-fibres. The evidence, however, on this point is insufficient at the present time to justify us in regarding the changes described as constant in this disease. References.—Sherrington, 'Journal of Physiology,' vol. xvii, p. 237, 1895; Rtjffini, 'Journal of Physiology,' vol. xxiii, p. 190, 1898; Batten, 'Brain,' vol. xx, p. 138, 1897. INDEX. Abdominal reflex, 20 Abductor minimi digiti, 52 — pollicis, 44, 52 Abscess of spinal cord, 377 Accessory haematomyelia, 458 Action, antergic, 10 — reflex, 19 — synergic, of muscles, 10 Acute anterior polio-myelitis, 396 — ascending paralysis, 371, 427 — atrophic paralysis, 396 — myelitis, 344 Adductor brevis, 47 — longus, 47 — magnus, 47 — pollicis, 52 Adductors of thigh, 47, 232 iEsthesiometer, 14 Afferent tract crossed, 223 Albinism and pseudo-hypertrophic para- lysis, 569 Alcoholic ataxia, 153, 159 (see Pseudo- tabes) — meningitis, chronic, 324 — neuritis, 150 — pseudo-tabes, 159, 173,175, 372, 481 Alcoholism iu myelitis, 347, 380 Alimentary canal, nerve-centres for, 247 Allocheiria, 14, 453 — in tabes, 4 33 Amyloid bodies, 348, 527 Amyotrophic lateral sclerosis, 531 (see Progressive muscular atrophy) Ansemia of spinal cord, 339, 340, 513 Anaisthesia, 13 _ dolorosa, 260, 393 Analgesia, 15 Analgic panaritium, 645 Anastomotic artery, 227 Anatomical diagnosis in cord disease, 253 Anatomy of spinal cord, 200 Aneurism, erosion of vertebrae by, 305 Angioglioma, 609 Angiosarcoma, 609 Angular curvature, 287, 290, 291 Ankle-clonus, 22 Annular myelitis, chronic, 382 — sclerosis, 382 Anode, 73 Vntergic contraction, 10 Anterior central artery, 227 — column, 201 — cornua, anatomy of, 204 — crural nerve, diseases of, 115 --------neuritis of, 134 — ground-fibres, 223 — lateral arteries, 227 — median arteries, 226 — — fissure, 201 — polio-myelitis, 395 — pyramidal tracts, 207, 209 — radicular arteries, 227 — root-fibres, 207, 224 — spinal artery, 226 -----vein, 227 Antero-lateral column, 201 — tract, ascending, 201, 208, 222, 470 -----degeneration in tabes, 470 -----descending, 215, 223 Arachnitis, 309 Argyll Robertson pupil, 455 Arm, combined palsies of nerves of, 110 — diseases of nerves of, 110 — motor points, 38, 39 — muscles, 34 Arteries of spinal cord, 226—228 Arthritic muscular atrophy, 559 Arthritis, vertebral, 307 Articulations of spine, diseases of, 307 Ascending neuritis, 82, 85 — paralysis, acute, 371, 427 Ataxic paraplegia, 503—511 678 INDEX. Ataxy, 258 — cerebellar hereditary, 524 — hereditary (Friedreich), 519 — in multiple neuritis, 153, 159 (see Pseudo-tabes) — in tabes, 449 — of movement, 10 Athetosis, double, 496 Atrophic spinal paralysis, acute, 396 -----— subacute and chronic, 424 Atrophy, atonic muscular, 540 — idiopathic muscular, 564 — muscular, from over-use, 563 — — family form of, with spinal lesion, 597 — — peroneal form, 593 — of auditory nerve, 457 — of optic nerve, 457, 503 — progressive muscular, 531 — pseudo-hypertrophic, 564, 567 Axis-cylinder, compound character of, 55, 62 — process, 55 Axites, 56 Axon, 55, 204 B Bedsores, changes in nerves near, 68, 83 Bending of spine, violent, 586, 591 Beri-beri, 186 Biceps cruris, 47 — muscle, 39 Bladder, centre for, 245 (see Sphincters) — condition of, in pseudo-hypertrophic paralysis, 575 — ulceration of, in myelitis, 362 Blood-supply of cord, 226 Bones in infantile palsy, 404 — in syringomyelia, 643 — nutrition of, 245 Brachial neuritis, 119 — plexus, diseases of, 98 Brachialis anticus muscle, 38 Bronchial crises, 482 Brown-Sequard, experiments on sensation, 234 Burdach's column, 200,219 c Caisson disease, 433 Calf muscles, centres for, 232 Callus, effects of, on nerves, 101 Qaput cornu posterioris, 206, 225 Carcinoma of cord, 608 Caries of spine and tumour, 303 -----disease of cord in, 286 -----syphilitic, 305 Cauda equina, tumour of, 216, 610 --------and syringomyelia, 636 Cautery, actual, in traumatic lesions, 664 Cavities in cord, 629 Cell-body, structure of, 59 Cells of anterior horn, 204 — unipolar, 57 Cellulifugal dendrites, 58 Cellulipetal dendrites, 58 Central canal, 224 Cerebellar ataxy, hereditary, 524 — tract, direct or dorsal, 207, 209, 220 -----ventral, 208,222 (see Antero-lateral ascending) — tumour and tabes, 483 Cerebro-spinal motor segment, 213 Cervical enlargement, localisation in, 231 — muscles, centres for, 231 — vertebrae, fracture of, 283 Charcot's joint disease, 266, 459, 643, 652 Cheyue-Stokes breathing, 318 Chronic atrophic paralysis, 531 — meningitis, 322 — myelitis, 378 — polio-myelitis, 424 — spinal muscular atrophy, 531 Circulation in cord, 226 Circumflex nerve, disease of, 103 Clarke's column, 206, 221 -----in tabes, 471 Clasp-knife rigidity, 265, 493 Classification of nervous diseases, 1, 2 | Claw-like hand, 43, 109, 539 Clonus, foot, 11, 12, 22 — spurious, 501 Coarse disease, 1 Cold, exposure to, in cord disease, 277 Collaterals, 55 Column, antero-lateral ascending, 201 208, 222, 470 -----descending, 215, 223 — of Burdach, 200, 219 — of Clarke, 206, 221 — of Goll, 200 — of Gowers, 201, 208, 222, 470 (see Antero-lateral ascending) — of Turck, 210 — posterior, 215 INE Column, posterior vesicular, 206 — postero-external, 200, 219 — postero-median, 200, 207 Combination of symptoms in cord disease, 269 Comma-shaped degeneration, 216, 219 Commissural artery, 226 Commissures of cord, 201, 223, 224 Compression, effects of, on nerves, 80 — myelitis, 276 — of cord, 390 Concussion myelitis, 652 Conduction in cord, 228, 233 Congenital paramyotone, 605 — spastic paraplegia, 495 — tabes and spina bifida, 651 Congestion, 2 Contraction, fibrillary, 8, 257, 539 — idio-muscular, 8 — in pseudo-hypertrophic paralysis, 574 — myotatic, 26 Contracture, 12, 256 — after facial palsy, 77 Contra-lateral muscles, 34 Convulsions in cord disease, 269 Co-ordiu:ition of movement, 11, 242 Cord, 274 — abscess of, 377 — affection, symptoms of, 253 — anatomy, 199 — blood-supply of, 226 — cavities and fissures in, G29 — degenerations of, 412 — diseases of, 199 — embolism of, 377 — functions, 228 — grey substance of, 203 — in peripheral neuritis, 1C8, 176 — inflammation of, 343 — membranes of, 199 — softening of, 275, 276 — tumours of, 607 Cornu-commissural tract, 220 Corpora amylacea, 348, 527 Cramp, 17 Cremasteric reflex, 20, 232 Crises in tabes, 462 Crossed afferent tract, 223 — pyramidal tracts, 209 — sensation, 272 Cross-legged progression, 496 Crureus muscle, 47 x. 679 Crutch palsy, 105 Cuneate nucleus, 219 Curvature, angular, 287, 290, 291 — of spine, lateral, 307 — in Friedreich's disease, 523 — in idiopathic muscular atrophy, 588 — in infantile paralysis, 408 — in pseudo-hypertrophic paralysis, 575 — in progressive muscular atrophy, 538 — in syringomyelia, 642 — lateral, 307 Cutaneous reflexes, 20 — sensibility, representation of, in cord, 238 Cysticerci of cord, 609 Cysts in cord tumours, 614 D Deafness in tabes, 457 Decussation of sensory fibres in cord, 234, 235 Deep reflexes, 19, 20, 238 Deformities from infantile palsy, 405 Degeneration, 4 — bilateral, in cord, 211 — comma-shaped, of cord, 216, 219 — fatty, of muscle, 546 — granular, 546 — in cord, 217 — in myelitis, 355 — irritative character of, 68 — reaction of, in muscle, 31, 32 -----in sensory nerves, 405 — retrograde, 215 (foot-note) — secondary, of nerves, 65 — Wallerian, 65 Degenerations of cord, 274 -----ascending, 208, 215 -----descending, 208, 210 — vitreous, of muscle, 70, 546 Degenerative neuritis, 32 — reaction, 32 Deiter's cells, 201, 351 Delay of sensation in tabes, 452 Deltoid muscle and centre, 36, 231 Dendrite, 55 — cellulipetal, 58 Dendron, 55 Descending antero-lateral tract, 215 — degenerations, 208, 210, 223 Deuteropathic progressive muscular atrophy, 532 630 INDEX. Development of cord, 629 Diabetes, sclerosis in, 513 Diagnosis, pathological, 274 Diaphragm, action of, 33 — centre for, 231 — inflammation of, 97 — paralysis of, 33, 99, 537 Diffuse myelitis, 341 Diphtheria and cord disease, 278 Diphtheritic neuritis and tabes, 483 Direct cerebellar tract, 207, 209, 220 — pyramidal tract, 207, 209 Disease, nature of, 278 — nutritional, 2, 664, 668 — organic, 2 — scat of indications of, 278 — structural, 2 Dislocation of spine, 281 Disseminated myelitis, 351, 353, 365, 370 — neuritis, 84 — sclerosis, 275 Diver's paralysis, 453 Dorsal reflex, 20 — vertebras, fracture of, 286 Duchenne's disease, 445 Dura mater, hsematoma of, 323, 327 -----tumours of, 308, 607 Dynamometer, 9 Dysaesthesia, 15 Dyslexia, 341 Dystrophies, muscular, 563 Dystrophy, muscular, 563 K Ecbinococci, 543 Elbow extensors, centre for, 231 — flexors, centre for, 231 Electrical irritability, 29—31 -----in functional disease, 32 — reaction, changes in, 75 -----in progressive muscular atrophy, 539 — treatment in infantile paralysis, 422 Elephantiasis neuromatodes, 93 Embolism of cord, 377 Embryonal tissue and syringomyelia, 629, 632 -----and tumours, 613, 634 -----in nerves in Friedreich's disease, 529 — — persistence of, 62y Emphysema, subcutaneous, in myelitis, 362 Empyema, paralysis from, 665 Encephalomyelitis, disseminated, 344, 365 Enchondroma of cord, 608 Endemic neuritis, 185 Epidemic meningitis, cerebro-spinal, 322 -----partial, 320 Epigastric reflex, 20 Erb's paralysis, 112, 407, 565 Erosion of spine by aneurism, 305 Essential paralysis of children, 395 (see Infantile paralysis) Excentric pain, 260 Excitation, 61 Exophthalmos in pseudo - hypertrophic paralysis, 587 Exostoses, vertebral, 304 Exposure in cord disease, 277 Extensor quadriceps, 47 Extensors, nerve-centres for, 232 — of ankle, 50, 52 — of elbow, 231 — of fingers, 40, 232 — of foot, 51 — of knee, 47, 232 — of thumb, 42—44 — of toes, 50, 52 — of wrist, 40, 231 External meningitis, 309 — ophthalmoplegia, 457 — popliteal nerve, disease of, 117 Extra-dural tumours of cord, 607 Extra-meningeal haemorrhage, 320 Eye symptoms in tabes, 457 Eyeballs, trophic changes in, 28 F Pace in idiopathic muscular atrophy, 587 — in neuritis, 161 — in progressive muscular atrophy, 538 facial nerves in leprous neuritis, 193 — type of muscular atrophy, 565, 587 False neuroma, 90 Faradism, 29, 75 — in infantile palsy, 422 Fasciculi of nerve-fibres, 63 Fatty degeneration of muscle, 546 Fibres, grey, 63 — non-medullated, 63 - regeneration of, in cord, 356 IND. Fibrillation of muscle, 8, 257, 539 Fibrils, cellulifugal, 58 — primitive, 55, 56, 62 Fibromata in nerves, 90 Fifth nerve, degeneration of, in tabes, 451, 453, 474 Fingers, extensors of, 40, 232 — flexors of, 41, 232 Fissures in cord, 629 Flat-foot, 50 Flexibilitas cerei, 27 Flexors, nerve-centre for, 232 — of elbow, 231 — of fingers, 41, 232 — of foot, 52 — of knee, 232 — of wrist, 40, 232 — long, of fingers, 52 — short, of fingers, 52 — long, of thumb, 44 — short, of thumb, 44 -----of little toe, 52 Foot muscles, 48, 232 -----nerve-centres for, 232 — phenomenon, 22 Foot-clonus, 12, 22 — nerve-centres for, 232 Forearm, muscles moving the, 37 Fracture of spine, 282 Fractures, spontaneous, of boue, 459 Friedreich's disease, 519 Functional disease, 1, 276, 664 Functions, mutual relations of, 249 — of cord, 228 G Gait in Friedreich's ataxy, 520 — in pseudo-hypertrophy, 569, 735 — in spastic paraplegia, 494 — in tabes, 449 G;inglion-cells, 203, 204 Gastric crises, 462 Gastrocnemius, 48 Gelatinous grey substance, 203 Gemelli muscles, 46 General causation of cord disease, 277 — paralysis and ataxic paraplegia, 507 -----and tabes, 446, 466, 482 Girdle-pain, 261, 360,657 Glia-cells, 201 GHoma in nerves, 91 — of cord, 610 EX. 6S1 Gliomata in relation to nervous system, 4 Gliomatosis, 4, 632 Glossy skin, 28, 86 Gluteal muscles, 45, 232 — reflex, 20 Gluteus maximus, 45, 232 — medius, 45, 232 — minimus, 46, 232 Glycosuria in tabes, 467 Golgi's method, effect of, on conceptions of nervous system, 53 GolPs column, 200 Gonorrhoea and myelitis, 278, 347 — and neuritis, 147 Gout and cord disease, 380, 660 — aud myelitis, 380 — and neuritis, 137 Gowers' tract, 201, 208, 222, 470 (see Antero-lateral ascending) Gracilis muscle, 47 Granular degeneration of muscles, 546 Grey commissure, 201, 224 — substance, 203 -----of Rolando, 206 Ground-fibres, 223 Growths in spinal column, 299 -----cord, 299, 607 Gunshot wounds of spine, 652 H Haematoma of dura mater, 323, 327 Haematomyelia, 437 Haematorrhachis, 334 Haemorrhage into cavities of cord, 438 644 — into central canal, 653 — into cord, 320, 437 — into spinal membranes, 320, 334 ----------and meningitis, 320 Haemorrhagic myelitis, 348, 359, 366 Hand in idiopathic muscular atrophy, 5S6 — in progressive muscular atrophy, 539 — in pseudo-hypertrophic paralysis, 571 — muscles moving the, 40 -----nerve-centres for, 232 Heart action in cervical cord disease, 267 -----in tabes, 267 — disease in tabes, 466 Hemiatrophy of tongue, 409 Hemiparaplegia, 254, 272 Hemiplegia, spinal, 272 Henle's sheath, 63 682 INDEX. Hereditary ataxy, 519 — cerebellar ataxy, 524 Herpes zoster in carl s, 290 Herpetic neuritis, 196 Hip-joint, muscles moving the, 45 — nerve-centres for, 232 Horn, lateral, 203, 205 Humerus, dislocation of, and paralysis, 111 — fracture of, and paralysis, 111 Hutchinson's mask, 453 Hyaloplasm, 56, 60 Hydatid disease of cord, 6C9 -----of spine, 306 Hydromyelia, 628 Hydrorrhachis interna, G-S Hypersemia of cord, 359, ;*42 Hyperesthesia, 15, 259 — in cord disease, 259 Hyperalgesia, 15, 259 — in cord disease, 259 Hyperpyrexia in cord disease, 268 Hypertrophic pachymeningitis, 326, 623 Hypertrophy, muscular, 599 Hypotonic musculaire, 256 -----in tabes, 461 Hysteria and myelitis, 372 Hysterical paraplegia, 665 I Idio-muscular contraction, 8 Idiopathic muscular atrophy, 583 — neuritis, 146 Iliacus muscle, 46, 232 Impulses, nervous, origin of, 58 Incisions of Schmidt, 63 Incontinence of urine, 246, 361 -----overflow, 246, 361 -----reflex, 246, 361 Inco-ordination, mechanism of, 477 — of movement, 10, 257 Indentations of Lautermann, 63 Infantile paralysis, 396 — — regression in, 408 Infection in cord diseases, 277 Inflammation of cord. 343 — of membranes, 322 — of nerves, 82 — parenchymatous, 4 jnfra-spinatus muscle, 37 -----in pseudo-hypertrophic palsy, 570 Injury in cord disease, 277 — to nerves, 80 Intercostals in progressive muscular atrophy, 537 Intermediate grey substance, 203 — group of cells, 205 — process, 205 — septal artery, 227 — septum of cord, 215 Intermedio-lateial tract, 205 Internal meningitis, 313 -----chronic, 322 — popliteal nerve, 117 Internode, 62 Interossei of foot, 51, 52 — of hand, 41 Interstitial neuritis, 82, 83, 85 Intra-ineningeal haemorrhage, 320 Intra-spinal tumours, 607 Irritability, electrical, of nerve and muscle, 29,71 — of muscle, reflex, 26 Irritation, spinal, 660 Irritative character of secondary degenera- tion, 68 — degeneration of pyramidal fibres, 266 J Jaw-jerk, 495 Jendrassik's method, 21 Joints in infantile palsy, 405 — in tabes, 459 — nutrition of, 245 Juvenile muscular atrophy, 565 K Kak-k6, 186 Kathode, 73 Kidney disease in ataxic paraplegia, 456 -----in tabes, 416 Kinetoplasm, 60 Klumpke's paralysis, 113 Knee, extensors of, 47, 232 — flexors of, 47, 232 — muscles moving the knee, 47 Knee-jerk, 20, 21, 24 — centre for, 239, 252 — in diphtheria, 477 (footnote), 481 — in Friedreich's disease, 521 — in idiopathic muscular atrophy, 588 — in leprous neuritis, 198 — in pseudo-hypertrophic palsy, 575 — in tabes, 448 — latent period of, 25 INDEX. 683 Knee-jerk, loss of, 264. 272, 448, 617 — return of, in tabes, 455 (footnote), 464 Kolliker, 53 L Laceration of cord, 652, 654 Lameness, intermittent, 341 Landry's paralysis, 371, 427 — — and neuritis, 427 Laryngeal crises, 462 — nerves, affections of, in neuritis, 161 — — — in tabes, 462 Latent period, 24 Lateral arteries of cord, 227 — column of cord, 201 — curvature, symptoms of, 307 (see Lor- dosis) — horn, 205 — limiting layer, 207, 210, 221 — sclerosis, primary, 489 — tracts, 207, 209, 492 Lathyrism, 37 Latissimus dorsi in pseudo-hypertrophy, 580 Lautermann, indentations of, 63 Lead palsy, distribution in, 161 Leg, centre for, 232 — disease of nerves of, 114 —- motor points of, 46, 48, 49 — muscles of, 4 5 Leprosy, anaesthetic, 192, 191 — — mutilations in, 195 Leprous neuritis, 192 Leptomeningitis, 309 — chronic, 323 Leucocythaemia, nerves in, 85 Levator anguli scapulae, 35 Lightning pains, 448, 451 Limb, lower, nerves of, 14 — — paralysis of, 114 — upper, nerves «f, 98 — — paralysis of, 100 Lipoma of cord, 608 Lipomatous muscular atrophy, 567 Lissauer's tract, 221, 225, 226, 469 Live flesh,9 Localisation of function in cord, 230 Locomotor ataxy (see Tabes), 444 Lordosis in Friedreich's disease, 523 — in idiopathic muscular atrophy, 588 — in progressive muscular atrophy, 538 Lordosis in pseudo-hypertrophic muscular atrophy, 575 Lower limbs, muscles of, 45 Lukewarmness, 16 Lumbar enlargement, localisation in, 232 — plexus, diseases of, 115 — region, tumours of, 620 Lumbricales of foot, 52 — of hand, 41 M Main-en-griffe, 43, 109, 539 Median nerve, disease of, 107 Medullary sheath, 62 Membranes of cord, diseases of, 199, 308 -•---tumours of, 607, 609, 615, 619 Meningeal haemorrhage and meningitis, 320 Meningitic streak, 318, 618 Meningitis and haematomyelia, 320 — and primary lateral sclerosis, 323 — and rheumatism, 320 — and tetanus, 320 — spinal, 309 -----external, 309 — — internal, 313 — — — acute, 313 -------chronic, 322 Meningocele, 650 Meningo-myelitis, 313, 384 Meuingo-myelocele, 650 Menstruation and myelitis, 346 Mental distress in cord disease, 277 Metameres, lb9 Micturition, mechanism of, 247 Middle form of reaction, 32, 393 Mixed reaction, 32, 393 Morphia in neuritis, 89 j Morvan's disease, 645 -----and Raynaud's disease, 647 — — neuritis in, 647 — <— sensibility in, 646 Motor conduction in cord, 228 — over-action, 255 — path, 213, 228 — points for arm, 38, 39 -----for leg, 46, 48, 49 — segments, disease of, 254 -----upper and lower, 213, 254 — symptoms, 8 — — in cord disease, 254 -----in tabes, 449 684 INDEX. Movement, co-ordination of, 10, 242 — direction of, 11 — inco-ordination of, 10, 257 — spontaneous, 11, 450 Movements, representation of, in cord, 230 Multiple neuritis, 138 — neuroma, 92, 609 — tumours of cord, 621 -----of nerve-roots, 621 -------and tabes, 621 Muscle spindles, 16, 671 Muscle-reflex action, 20 — centres, 240 Muscles, action and paralysis of, 33 — antergic, action of, 10 — changes in, 29 — — in neuritis, 168 — — secondary to nerve lesion, 70 — contra-lateral, 34 — fatty degeneration of, 546 — in peripheral neuritis, 70,168 — nutrition of, 244 — nutritive changes in, 70 — peripheral guidance of, 11 — reflex action, 20 — sensory nerves of, 17, 26 — synergic action of, 10 — vitreous, 70, 546 Muscular anaesthesia in tabes, 454 — atrophy, arthritic, 559 — — chronic spinal, 531 — — facial type, 565, 587 -----family form in children with spinal lesion, 597 — — from over-use, 563 — — idiopathic, 583 -----in lead, 161, 534 -----in tabes, 466 — — Landouzy-Dejerine type, 565 — — peroneal type, 534, 593 — contraction, paradoxical, 27 — dystrophies, 563 — exertion, excessive, and cord disease 278 — hypertrophy, 578, 599 — sense, 16, 18, 237, 259 ■— sensibility, 16 -----test for, 18 Musculo-cutaneous nerve, 104 Musculo-spiral, 104 Myelin, 62, 63 Myelitis, acute, 344 Myelitis and alcoholism, 347 — and cold, 345 — and fevers, 346 — and gonorrhoea, 347 — and gout, 380, 660 — and hysterical paralysis, 372 — and injury, 345 — and Landry's paralysis, 371 — and meningitis, 320, 372 — and menstruation, 345 — and multiple neuritis, 372 — and muscular action, 345 — and organisms, 346, 347 — and peripheral irritation, 347 — and smallpox, 347 — and syphilis, 347, 380, 384 — and toxic blood-states, 346, 368 — central, 355, 366, 370 — chronic, 378 -----annular, 382 — compression, 276, 353, 391 — diffuse, 344 — disseminated, 351, 353, 365, 370, 378 — focal, 365 — girdle-pain in, 360 — haemorrhagic, 348, 359, 366 — parenchymatous, 366 — reflexes in, 360 — sclerotic, 863 — sphincters in, 361 — transverse, 365, 378 — trophic changes in, 362 Myolipoma of cord, 580, 608 M \ opathic atrophy, 563 -----face, 565, 587 Myopathies, Erb's juvenile, 564 — idiopathic, 583 — Landouzy-Dejerine, 565 Myosis, spinal, 266, 455 Myositis, 168, 185 Myotatic contractions, 26, 238 — irritability, 19, 238 -----in arthritic atrophy, 560 Myotonia congenita, 601 Myxo-fibroma, 91 Myxoma in nerves, 90, 91 Myxomata of cord, 609, 613 N Nails in syringomyelia, 642 Nansen's researches, 53 IND EX. 685 NecTt, injuries of, and paralysis, 111 Nephralgic crises, 462 Nerve, anterior crural, 115 — cells, functions of, 58 — — relation of, to nerves, 57 — circumflex, 103 — endings, changes in, 69 — energy, 65 — fibres, functions of, 64 -----sizes of, 207 — force, generation of, 57 — impulse, nature of, 61 — inflammation, 82 — injury and degeneration, 71, 80 — lesions, 78, 79 — median, 107 — musculo-cutaneous, 104 — musculo-spiral, 104 — obturator, 116 — phrenic, 96 — plantar, 117 — posterior thoracic, 101 — popliteal, 117 — sciatic, 116 — superior gluteal, 116 — supra-scapular, 102 — ulnar, 108 Nerve-roots, cervical, 99 — dorsal, 99 — lumbar, 114 Nerve-stretching in tabes, 4S9 Nerves, bulbous, 93 — 95 — compression of, 80 — diseases of, 62 — growths in, SO — inflammation of, 82 — irritation of, in caries, 288 — lesions of, 65 — of arm, combined palsies of, 110 — of lower limb, 114 — of upper limb, 98 — physiology of, 63 — regeneration of, 6(>, 69 — sclerosis of, 84 — secondary degeneration of, 65, 66 — special, diseases of, 96 Nervi nervorum, 63 Nervous system, diseases primary secondary, 3 — — function, 7 — — general constitution of, 53 Nervousness, 660 Neuralgia, intercostal and spinal growths, 302 Neurasthenia, 668 Neurilemma, 62 Neuritic muscular atrophy, 534, 593, 597 (see Peroneal form). Neuritis, 82 — adventitial, 83 — after acute diseases, 147 — — injuries, 80 — alcoholic, 150 — and atrophic paralysis, 426 — and endarteritis, 152 — and gout, 137, 147 — and hysteria, 176 — and inflammation, 4 — and myelitis, 372 — and pachymeningitis, 174 — and poliomyelitis, 174 — and tabes, 169, 481 — ataxic form, 158 — atheromatous, 151 — brachial, 119 — cancerous, 82 — chronic, 85 — classification of, 144 — crural, 133 — degenerative, 144 — diabetic, 144, 150 — diffuse, 84 — disseminated, 84 — endemic, 185 — face in, 156 — focal or disseminated, 84 — gonorrhoea!, 147 — herpetic, 196 — idiopathic, 146, 151 — inco-ordination in, 158 — in infantile paralysis, 400, 414 — in leprosy, 192 — in leucocythaemia, 85 — in Morvan's disease, 647 — in peroneal atrophy, 595 — isolated, in acute disease, 83 — lipomatous, 85 — malarial, 185 — memory in, 152 id — migrans, 67, 82, 85 — motor form, 153 — multiple, 82, 13S — —■ complications. 163 -----course, 161 686 Neuritis, multiple, diagnosis, 172 -----pathological anatomy, 164 — — pathology, 169 -----• prognosis, 178 — — symptoms, 152 — — treatment, 181 — near bedsores, 68,83 — nystagmus in, 157 — ocular movements in, 156 — optic, in ataxic paraplegia, 506 — — in chlorosis, 341 — — in cord disease, 269 — — in multiple neuritis, 163 -----in myelitis, 362 — organismal, 146 — pain in, 154 — parenchymatous, 82, 84 — peripheral, 138 (see Multiple). — proliferative, 85 — psychical symptoms in, 152 — radicular, 119, 303 — rheumatic, 82,146, 149 — senile, 146 — sensory form, 153 — septicaemic, 146, 148 — spinal cord affection in, 168, 176 — syphilitic, 85,146 — tongue in, 156 — toxaemic, 144 — toxic, 144 — treatment, 88 — tremor in, 155 — trophic changes in, 160, 172 — tubercular, 147 — varieties of, 82, 144 — vocal cords in, 156 Neuro-fibroma, 93 Neuroglia, development of, 629 — structure of, 57, 201 Neurokeratin, 62, 202 Neuroma, 90 — amputation, 93, 95 — amyelinic, 90 — false, 90 — multiple, 92, 609 — myelinic, 90 — of nerve-roots, 544 — plexiform, 91, 93, 94, 96 Neuromatodes elephantiasis, 93 Neuromyositis, 134 Neuron, 55 — cerebro-spinal, 213 INDEX. Neuron, spino-muscular, 213 Neuropathic disposition in cord disease, 277 Neuropilema, 54 Neurotabes, 175, 448 (see Pseudo-tabes) Nodes of Ranvier, 62 Nuclei, internodal, 63 Nucleus cuneatus. 219 — function of, 59 — gracilis, 216, 219 — post-pyramidal, 219 Nutrition, changes in, 127, 277 — influence on, of cord, 244 Nutritional disease, 1 -----of cord, 2, 664, 668 Nutritive changes in muscles, 70 -----in skin, 28 Nystagmus in ataxic paraplegia, 506 — in Friedreich's disease, 521 — in multiple neuritis, 157 — in progressive muscular atrophy, 542 — in spastic paraplegia, 495 — in syringomyelia, 643 0 Obstetrical paralysis, 113 Obturator internus, 46 — nerve paralysis, 116 Ocular symptoms in tabes, 45" (Edema, vaso-motor, 618 Operation for tumour, 626 Ophthalmoplegia, 457 Opponens pollicis, 44 Optic atrophy, 457 -----in ataxic paraplegia, 506 -----in family spastic paralysis, 503 Optic neuritis in chlorosis, 341 -----in multiple neuritis, 163 -----in myelitis, 362 Organic disease of cord, 1 Organismal neuritis, 146 Organisms in beri-beri, 186 — in myelitis, 346, 347 Oval field of Flechsig, 218 Overflow incontinence, 246, 361 Over-use, muscular atrophy from, 563 P Pachymeningitis, 174, 309, 556 — and progressive muscular atrophy, 556 — cervical hypertrophic, 326, 623 — cervical, and syringomyelia, 644 INDEX. 687 Pachymeningitis, chronic, 322 — external, 309 — internal haemorrhagic, 309 Pain, conduction of, in cord, 236 — in cord diseases, 260, 393 ------tumours, 393, 615 — sensibility to, 15, 236 -----in syringomyelia, 641 Pains, excentric radiating, 260 Palmar fascia, contraction of, 41 1'alsy, Erb's type of, 112, 565 — infantile, 396 Paradoxical muscular contraction, 27 Paraesthesia, 15 Paralysis and paresis, 9 — acute ascending, 371, 427 — agitans, tremor in, 12 — atrophic spinal, 395, 424 — essential, of children, 396 — from lessened pressure, 453 — infantile, 396 -----electricity in, 421 — — neuritis in, 400, 414 — of muscles, 33 — periodic, 598 — pseudo-hypertrophic, 564, 567 Paramyotone, ataxic, 606 — congenital, 605 Paraplegia, 253 — ataxic, 503 — — and meningitis, 331 — chlorotic, 341 — congenital spastic, 495 — dolorosa, 261, 301 — hereditary spastic, 503 — primary spastic, 489 ---------and ataxic, 499 ---------family form, 503 —------infantile form, 495 — simple senile, 530 Parasitic tumours of cord, 608, 609 Parenchymatous inflammation, 4, 274 — myelitis, 366 — neuritis, 82, 84 Paresis, 9 Pathological diagnosis of cord disease, 274 Pathology and etiology of cord disease, 274 Pectineus muscle, 47 Pectoralis major, 37 Pellagra, 511 Pelvic outflow, 218 perimeningitis, 309 Perineuritis, 82, 83 Perineurium, 63 Periodic paralysis, 598 Peripachymeningitis, 309 Peripheral arteries of cord, 227 — nerves in tabes, 473, 480 — neuritis, 138 (see Neuritis). Peroneal nerve, paralysis of, 117 — type of atrophy, 534, 593 — — combined with idiopathic, 597 Peroneus longus muscle, 50, 232 — brevis muscle, 52 Phrenic nerve, diseases of, 33, 96, 97 Phthisis and peripheral neuritis, 1C9 Plantar nerves, diseases of, 117 -----reflex, 20 Tlexiform neuroma, 91, 93, 94, 96 Plexus, lumbar, 114, 115 — sacral, 114, 116 Polio-myelitis, 396 — chronic and subacute, 313, 386, 424 Polyaesthesia, 14, 453 Polymyositis, acute, 185 Polyneuritis, 82, 138, 173 — septicaemic, 146, 148 — tubercular, 147 Popliteal nerves, diseases of, 117 Popliteus muscle, 48 Post-pyramidal nucleus, 219 Posterior central artery, 227 — column, function of, 215 — cornual artery, 227 — ground fibres, 207 — intermediate septum, 200 — lateral arteries, 227 — medial artery, 227 — median column, 200 — — septum, 200 — nerve-roots in tabes, 472 — pyramid of medulla, 219 — radicular artery, 227 — root fibres, 207, 225 -----zone, 200 — spinal vein, 227 — thoracic nerve, 101 — vesicular tract in tabes, 206, 471 Postero-external column, 200, 215, 219 Postero-median column, 200, 207, 215 Posture, adaptation to, 241 — loss of sense of, 18, 237, 259, 454 Pott's disease, 286 Power, measurement of, 9 688 INDEX. Pressure myelitis, 276, 353, 391 — sense of, 14 Priapism, 263 Primary hsematomyelia, 437 — lateral sclerosis, 489 — — and general paralysis, 497 — — and hysteria, 501 —-----infantile, 495 — spastic paraplegia, 489 — — — family form, 503 --------infantile, 495 Primitive canal of cord, 629 — fibrils, 55, 56, 62 — sheath, 62 Progressive muscular atrophy, 531 --------and pachymeningitis, 556 --------and syringomyelia, 556 -----— and tabes, 466 Pronators, 40 — nerve centres for, 232 Protopathic progressive muscular atrophy. 532 Protoplasmic processes, 56 Pseudo-hypertrophic paralysis, 564, 567 -----mode of rising in, 572 -----varieties of, 576 — tabes, 159, 173, 175, 372, 481 Psoas muscle, 46, 232 Ptosis in tabes, 456 Pulse in tabes, 462 Pupil in cord disease, 266 — in myelitis, 362 Pyramidal fibres, 207, 209, 210, 255 -----mode of ending in cord, 212 — tracts in progressive muscular atrophy, 550 Pyrexia in cord disease, 268 Pyriformis muscle, 46 Q Quadratus femoris muscle, 46 Quadriceps, 47 — centre for, 232 Qualitative changes in irritability, 73 Quantitative changes in irritability, 73 R Eachialgia, 260 Radiating pains, 260 Radicular neuritis, 119, 303 Railway spine, 661 Ramon y Cajal, 53 Ranvier, nodes of, 62 Reaction, normal, 73 — of degeneration, 31, 32, 71 -----in infantile palsy, 403 -----mixed form, 32, 393 Rectal crises, 462 Rectum, centre for, 245 Rectus femoris, 47 Redecussation in cord, 211 lied softening of cord, 348 Reflex action, 19, 238, 240, 262, 263 -----cutaneous, 19 -----in nerve injury, 79 -----muscular, 20 -----two kinds of, in cord, 238 — arc, 19, 239 — centre, 19, 239 — paralysis, 665 — spasm, 264 Reflexes, deep, 20 — superficial, 19 -----latent period of, 24 Regeneration of fibres in cord, 356 — of nerves, 69 Regressive period in infantile palsy, 408 Reinforcement, 21 Representation of movements in cord, 230 Resistance in nerve phenomena, 54 Resisting power, deficiency in, 6 Reticular formation, lateral, 202 -----posterior, 203 Rheumatic neuritis, 82,137, 145 Rheumatism of dorsal muscles, 320 Rhomboids, 35 Rigidity, clasp-knife, 265, 493 — in cord diseases, 256 — in progressive muscular atrophy, 541 Rolando, grey substance of, 206 Romberg's symptom, 449 Root pains, 260 — symptoms in compression, 393 — zone, 200 Root-fibres, cause of, 224 Roots, anterior, 224 — distribution of, 225 — posterior, 225 S Sacral plexus, diseases of, 114, HQ ! Sartorius muscle, 232 | Scapular muscles, 34. 231 INDEX. Schmidt, incision of, 63 S-hultze, Max, observation of, 55 Schwann, white substance of, 62 — sheath of, 62 Sciatica, 123 Sciatic nerve, disease of, 116 Sclerodactyla, 647 Sclerosis, amyotrophic lateral, 531 — annular, 382 — combined lateral and posterior, 503 — focal, 386 — from anaemia, &c, 513 — from pellagra, 511 — from toxic blood-states, 511 — in chronic muscular atrophy, 550 — insular, 4, 275 — lateral, and meningitis, 323, 489 — secondary,4 Sclerotic myelitis, 386 Secondary degeneration of cord, 208, 210, 215 -----ascending, 208, 215 -----descending, 208, 210 -----of nerves, 65 — tabes, 418 Semimembranosus, 47 Semitendinosus, 47 Sensation, localisation of, 13 — path of, 233 — rhythmical recurrence, 453 Sensations, spontaneous, 261 Sense, muscular, 16 — of pain, 15 — tactile, 13 — temperature, 15 Sensibility, modes of testing, 13 — modifications of, 14 — muscular, 237 — recurrent, 78 — tactile, 13, 236, 238 — to electricity, 15 — to pain, 15, 236 — to temperature, 15, 237 Sensitiveness, increased, 259 Sensory conduction in cord, 233 — symptoms, 13, 78, 258 — — in nerve lesions, 78 -----in tabes, 450 Septicaemia in cord diseases, 277 Septicaemic polyneuritis, 145 Septomarginal tract, 218, 220 Septum, posterior intermediate, 200, 215 VOL. 1. Septum, posterior median, 200 Serratus magnus, 35, 102, 231 -----nerve to, 101 Sexual functions, centre for, 248 — power in nutritional disease, 670 -----in tabes, 454 in traumatic lesions, 662 Sheath, primitive, 62 Shoulder dislocation, palsy of nerves in, 111 — fracture, 111 — muscles moving the, 34 Skin, glossy, 28 — nutrition of, 28, 245, 266 — representation in cord, 250, 251 Sleep palsies, 101 Softening of cord, 348 -----red, 348 -----white, 348 -----yellow, 348 Soleus muscle, 48 Spasm, 11 — clonic, 11, 256 — in cord disease, 255 — in meningitis, 317 — in progressive muscular atrophy, 541 — reflex, 264 — tetanic, 13 — tonic, 11, 255 Spastic paralysis, family form, 503 — paraplegia, congenital, 495 -----in caries, 291 -----primary, 489 Special senses, nature of, 61 Sphincter ani, centre lor, 245 Sphincters in neuritis, 161 — in tabes, 448, 458 — paralysis of, 245—247, 267 Spider-cells, 201, 351 Spina bifida, 647 — — arthropathy in, 652 -----deformities in, 652 -----occulta, 647 — — trophic changes in, 652 Spinal column, growths in, 299 — cord, abscess of, 377 -----anaemia of, 339, 513 — — anatomy of, 200 -----blood-supply of, 226 — — compression of, 390 -----degeneration of, 442 -----diseases of, 199, 339 — — embolism, 377 44 690 INDEX. Spinal cord, functions of, 228 — — haemorrhage into, 437 -----hyperaemia of, 342 -----inflammation of, 342 (see Myelitis) — — softening of, 275, 348 — — structure of, 200 — — symptoms of disease of, 253 — curvature in idiopathic atrophy, 588 -----in infantile palsy, 408 — — in progressive muscular atrophy, 538 -----in pseudo-hypertrophy, 575 — epilepsy, 265 — hemiplegia, 272 — irritation, 295, 660 — membranes, 199 — meningeal haemorrhage, 320 — meningitis, 309 — muscular atrophy, 531 — paralysis, acute atrophic, 396 — — subacute, chronic, 424 Spindles, muscle, 16, 671 Spine, caries of, 286 — concussion of, 652 — diseases of, 281 — — of articulations of, 307 — dislocation of, 281 — fracture, 282 — gunshot wounds of, 652 — injuries of, 281 — syphilitic diseases of, 305 — tumours of, 299 Spino-muscular motor segment, 213 Soongioplasm, 56, 60 Spongy grey substance, 203 — zone, 207 Spontaneous movements, 11 -----in tabes, 450 — sensations, 261 Sterno-mastoid, 34 Stretching nerves in tabes, 489 Structural diseases, 2, 277 Strychnia in muscular atrophy, 557 Subscapulars, 37 Supinator brevis, 40 — longus, 39 Supinators, 231 — in idiopathic atrophy, 586 Supra-scapular nerve, 102 Supra-spinatus, 37 Suspension in tabes, 489 Symptoms, combination of, 269 Symptoms in cord disease, 253 — mental, 8 — mode of investigation, 7 — motor, 8, 254 — sensory, 13, 78, 258 Synergic contraction, 10 Syphilis and spinal degenerations, 278, 347, 380, 384 — and injury to cord, 659 — and tabes, 446 — in Landry's paralysis, 432 — in progressive muscular atrophy, 534 Syphilitic caries, 305 — diseases of cord, 278 — meningitis, 330 — neuritis, 146 Syphilomata of cord, 614 Syringomyelia, 628 — and cervical pachymeningitis, 614 — and haemorrhage, 644 — and injuries, 639 — and leprous neuritis, 196, 647 — and meningitis, 331 — and myelitis, 384 — and progressive muscular atrophy, 556, 644 — and tumours, 610, 613, 631, 644 — Charcot's joint in, 643 — motor symptoms in, 642 — muscular atrophy in, 642 — operation in, 645 — pain sense in, 234, 260, 640 — sweating in, 643 — temperature sense in, 23 4, 260, 640 Syringo-myelocele, 650 S\ stem diseases, 253, 254, 274, 442 T Tabes dorsalis, 444 -----and alcoholism, 448 -----and ataxic paraplegia, 466 -----and cerebellar tumour, 483 — — and concussion, 447 -----and diphtheritic paralysis, 483 — — and disease of posterior roots, 478 (foot-note) — — and general paralysis, 446 -----and myelitis, 448 -----and neuritis, 481 — — and soft sores, 447 -----and syphilis, 466, 482 INDEX. 691 Tabes dorsalis and tumours of nerve-roots, 478 -----Charcot's joint in, 459 — — congenital, 651 — —■ crises, 461, 462 — — deafness in, 457 — — electricity in, 488 — — eye symptoms in, 445 — — heart disease in, 466 — — lightning pains in, 448 -----Lissauer's tract in, 469 -----motor symptoms in, 449 -----ocular symptoms in, 445 — — optic atrophy in, 457 -----pathological anatomy of, 467 -----pathology of, 474 — — reflex action in, 454 -----— symptoms in, 474 — — secondary, 448 — — sensory symptoms in, 450 — — sexual power in, 454 -----sphincters in, 448, 458 — — suspension in, 489 -----trophic and vaso-motor symptoms in, 459 — — visceral symptoms in, 461 Tabetic foot, 461 — multiple neuritis, 448, 481 — neuralgia, 481 — ptosis, 456 Tache spinale, 318, 618 Tactile sensibility, 236 Talipes calcaneus, 50 — in infantile palsy, 406 — in pseudo-hypertrophy, 574 — valgus, 51 — varus, 51 Temperature sense in syringomyelia, 234, 260 -----path of, 15, 237, 640 Tendon-reflex, so-called 19—21, 26 Tensor vaginae femoris, 46 Teres major, 37 — minor, 37 Tetanus and meningitis, 320 — neonatorum, 334 Tetany, nocturnal, 666 Thenar muscles, 44, 45 _____centre for, 232 Thigh, adductors of, 47 — motor points, 46, 49 — rotators, 46 Thomsen's disease, 601 — — and pseudo-hypertrophy, 576 Thoracic muscles, 33 Thrilling sensations, 15 Thrombosis in cord vessels, 276 Thumb muscles, 42 Tibialis anticus, 50, 232 — posticus, 52 Tic and tabes, 451 Tingling sensations, 15, 81 Toes, muscles moving, 52 Tone, muscular, 8, 12, 26 Tonic atrophy of muscles, 541, 553 — spasm,11 Torticollis, muscles affected in, 34 'Touch, sensibility to, 13 Toxic influences in Landry's paralysis, 432 — — in nervous disease, 5, 277 — — in tabes, 5 Tract, antero-lateral ascending, 208 ----- descending, 215 — comma-shaped, 216, 219 — cornu-commissural, 220 — direct cerebellar, 207, 209, 220 — Gowers', 201, 208, 222, 470 — intermedio-lateral, 205 — Lissauer's, 221, 225, 226 — septo-marginal, 218, 220 Tracts, pyramidal, 207, 209, 210, 255 Transverse lesions of cord, 264, 269, 271 -----knee-jerk in, 264 — myelitis, 365, 378 Trapezius, 34 Traumatic lesions of cord, 652 — spinal neuralgia, 660 Tremor, 257 — contractions in, 12 Triceps, 37 — paralysis of, 231 Trophic changes in myelitis, 362 — — iu tabes, 459 — disorders, 28 -----in concussion, 655 — disturbance in cord disease, 265 — nerves, 27, 28, 79 Tubercula dolorosa, 92, 95 Tubercular meningitis, 317 — polyneuritis, 147 — tumours of cord, 699, 619 Tumours of cord, 299, 607 -----and hysteria, 624 -----and membranes, 619, 622 692 INDEX. Tumours of cord, surgical treatment of, 626 — of spine, 299 -----and caries, 303 U Ulcer, perforating, 459; in spina bid 652 Ulnar nerve, disease of, 108 Ultimum moriens, 536 Unilateral lesions of cord, 235. 272 -----sensibility in, 235, 272 Unipolar cell, 57 Upper arm type of palsy, 407 — limb muscles, 34; nerves, 98 Urethral crises, 462 Uterine disease and cord disease, 669 — functions, centres for, 248 V Vacuolation of cells, 351 Vagus in peripheral neuritis, 179 Vascular thickening in tabes, 471 Vaso-motor centres, 248, 265, 266 — disorders, 79 -----in tabes, 459 Vasti muscles, 47 Veins of cord, 226 Vertebrae, erosion of, 305 Vertebral arthritis, 307 — column, diseases of, 281 -----aneurism, erosion by, 305 -----growths, 299 Vertebral column, hydatids of, 306 -----syphilitic disease of, 305 -----fracture of, 282 — exostoses, 304 Vesical crises, 4( 2 — control, 245 > Vessels of cord, 226 Visceral disturbance, 245, 267 — pains in tabes, 452, 461 — symptoms in tabes, 461 Vitreous degeneration, 70, 546 Vocal cords in tabes, 463 Voltaism in diagnosis, 30 W Waldeyer, 53 Wallerian degeneration, 65 Wasting palsy, 531 Westphal's symptom, 407 White commissure of cord, 201, 223, 224 — softening, 348 — substance, 207 Whitlows, painless, 645 Wrist muscles, 40 -----centre for, 231, 232 Y Yellow softening, 348 Z Zone, spongy, 207 Zygomatic muscles in idiopathic atrophy, 587 CATALOGUE No. 1. READ "SPECIAL NOTE" BELOW. NOVEMBER, 1899. CATALOGUE Medical, Dental, Pharmaceutical, and Scientific Publications, WITH A SUBJECT INDEX, OF ALL BOOKS PUBLISHED BY P. BLAKISTON'S SON & CO. (Established 1843), PUBLISHERS, IMPORTERS, AND BOOKSELLERS, 1012 WALNUT ST., PHILADELPHIA. SPECIAL NOTE. The prices as given in this catalogue are absolutely net, no discount will be allowed retail purchasers under any consideration. This rule has been established in order that everyone will be treated alike, a general reduction in former prices having been made to meet previous retail discounts. Upon receipt of the advertised price any book will be forwarded by mail or express, all charges prepaid. ________________ We keep a large stock of Miscellaneous Books relating to Medicine and Allied Sciences, published in this country and abroad. Inquiries in regard to prices, date of edition, etc., will receive prompt attention. The following Catalogues sent free upon application:— CATALOGUE No. 1.—A complete list of the titles of all our publications on Medicine, Dentistry, Pharmacy, and Allied Sciences, with Classified Index. CATALOGUE No. 3.—Pharmaceutical Books. CATALOGUE No. 4.— Books on Chemistry and Technology. CATALOGUE No. 5.—Books for Nurses and Lay Readers. CATALOGUE No. 6.—Books on Dentistry and Books used by Dental Students. CATALOGUE No. 7.—Books on Hygiene and Sanitary Science ; Including Water and Milk Analysis, Microscopy, Physical Education, Hospitals, etc. CATALOGUE No. 8.—List of about 300 Standard Books classified by Subjects. SPECIAL CIRCULARS.__Morris' Anatomy; Gould's Medical Dictionaries ; Moullin's Surgery ; Books on the Eye ; The ? Quiz Compends? Series, Visiting Lists, etc. We can also furnish sample pages of many of our publications. 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Revised by Reynold W. Wilcox, m.a., m.d., ll.d., Professor of Clin- ical Medicine and Therapeutics at the New York Post-Graduate Medical School and Hospital; Visiting Physician St. Mark's Hospital; Assistant Visiting Physi- cian Bellevue Hospital. Fourth Edition, thoroughly Revised. i2mo. 704 pages. Cloth, $3.00; Leather, $3.50 WILLIAMS. Manual of Bacteriology. By Herbert U. Williams, m.d., Pro- fessor of Pathology and Bacteriology, Medical Department University of Buffalo. With 78 Illustrations. i2mo. Cloth, $1.50 WILSON. Handbook of Hygiene and Sanitary Science. By George Wilson, m.a., m.d., f.r.s.e., Medical Officer of Health for Mid-Warwickshire, England. With Illustrations. Eighth Edition. i2mo. Cloth, $3.00 WILSON. The Summer and its Diseases. By James C. Wilson, m.d., Prof, of the Practice of Med. and Clinical Medicine, Jefferson Med. Coll., Phila. Cloth, .40 WILSON. System of Human Anatomy. 1 ith Revised Edition. Edited by Henry Edward Clark, m.d., m.r.c.s. 492 Illustrations, 26 Colored Plates, and a Glossary of Terms. Thick i2mo. " Cloth, $5.00 WINCKEL. Text-Book of Obstetrics ; Including the Pathology and Therapeutics of the Puerperal State. By Dr. F. Winckel, Professor of Gynecology and Director of the Royal University Clinic for Women in Munich. Authorized Translation by J. Clifton Edgar, a.m., m.d., Adjunct Professor to the Chair of Obstetrics, Medical Department, University City of New York. With nearly 200 Handsome Illustrations, the majority of which are original with this work. Octavo. Cloth, $5.00; Leather, $6.00 WINDLE. Surface Anatomy and Landmarks. By B. C. A. Windle, d.sc.m.d., Professor of Anatomy in Mason College, Birmingham, etc. Second Edition, Revised by T. Manners Smith, m.r.c.s., with Colored and other Illustrations. i2mo. Cloth, $1.00 WOAKES. Deafness, Giddiness, and Noises in the Head. By Edward Woakes, m.d., Senior Aural Surgeon, London Hospital; assisted by Claud Woakes, M.R.C.S., Assistant Surgeon to the London Throat Hospital. Fourth Edition. ' Illustrated. i2mo. Cloth, $2.00 WOOD. Brain Work and Overwork. By Prof. H. C. Wood, Clinical Professor of Nervous Diseases, University of Pennsylvania. i2mo. Cloth, .40 WOODY. Essentials of Chemistry and Urinalysis. By Sam E. Woody, a.m., m D., Professor of Chemistry and Public Hygiene, and Clinical Lecturer on Diseases of Children, in the Kentucky School of Medicine. Fourth Edition. Illustrated. i2mo. In Press. From the Southern Clinic. " We know of no series of books issued by any house that so fully meets our approval as these ? Quiz-Compends ?. They are well arranged, full, and concise, and are really the best line of text- books that could be found for either student or practitioner." BLAKISTON'S ?QUIZ=COMPENDS? The Best Series of Manuals for the Use of Students. Price of each, Cloth, .80. Interleaved for taking Notes, $1.25. S^° These Compends are based on the most popular text-books and the lectures of promi- nent professors, and are kept constantly revised, so that they may thoroughly represent the present state of the subjects upon which they treat. The authors have had large experience as Quiz-Masters and attaches of colleges, and are well acquainted with the wants of students. They are arranged in the most approved form, thorough and concise, containing over 600 fine illustra- tions, inserted wherever they could be used to advantage. Can be used by students of any college, and contain information nowhere else collected in such a condensed, practical shape. ILLUSTRATED CIRCULAR FREE. No. 1. HUMAN ANATOMY. Sixth Revised and Enlarged Edition. Including Vis- ceral Anatomy. Can be used with either Morris's or Gray's Anatomy. 117 Illustrations and 16 Lithographic Plates of Nerves and Arteries, with Explanatory Tables, etc. By Samuel O. L. Potter, m.d., Professor of the Practice of Medicine, College of Physicians and Surgeons, San Francisco; late A. A. Surgeon, U. S. Army. No. 2. PRACTICE OF MEDICINE. Part I. Sixth Edition, Revised, Enlarged, and Improved. By Dan'l E. Hughes, m.d., Physician-in-Chief, Philadelphia Hospital, late Demonstrator of Clinical Medicine, Jefferson Medical College, Philadelphia. No. 3. PRACTICE OF MEDICINE. Part II. Sixth Edition, Revised, Enlarged, and Improved. Same author as No. 2. No. 4. PHYSIOLOGY. Ninth Edition, with new Illustrations and a table of Physio- logical Constants. Enlarged and Revised. By A. P. Brubaker, m.d., Professor of Physiology and General Pathology in the Pennsylvania College of Dental Surgery; Demon- strator of Physiology, Jefferson Medical College, Philadelphia. No. 5. OBSTETRICS. Sixth Edition. By Henry G. Landis, m.d. Revised and Edited by Wm. H. Wells, m.d., Instructor of Obstetrics, Jefferson Medical College, Philadelphia. Enlarged. 3 Plates and 47 other Illustrations. No. 6. MATERIA MEDICA, THERAPEUTICS, AND PRESCRIPTION WRITING. Sixth Revised Edition (U. S. P. 1890). By Samuel O. L. Potter, m.d., Professor of the Practice of Medicine, College of Physicians and Surgeons, San Francisco! No. 7. GYNECOLOGY. Second Edition. By Wm. H. Wells, m.d., Instructor of Ob- stetrics, Jefferson Medical College, Philadelphia. 140 Illustrations. No. 8. DISEASES OF THE EYE AND REFRACTION. Second Edition. Includ- ing Treatment and Surgery and a Section on Local Therapeutics. By George M. Gould M.D.,and W. L. Pyle, m.d. With Formulae, Glossary, several useful Tables, and 100 Illustrations, several of which are colored. No. 9. SURGERY, Minor Surgery, and Bandaging. Fifth Edition, Enlarged and Im- proved. By Orville Horwitz, b.s., m.d., Clinical Professor of Genito-Urinary Surgery - and Venereal Diseases in Jefferson Medical College; Surgeon to Philadelphia Hospital etc With 98 Formulae and 167 Illustrations. ' No. 10. MEDICAL CHEMISTRY. Fourth Edition. Including Urinalysis Animal Chemistry, Chemistry of Milk, Blood, Tissues, the Secretions, etc. By Henry Leffmann m.d., Professor of Chemistry in Pennsylvania College of Dental Surgery and in the Woman's Medical College, Philadelphia. No. 11. PHARMACY. Fifth Edition. Based upon Prof. Remington's Text-Book of Phar pv7'h 1 I Fr n STE™T' M-D- pth-g" late Qui^-Master in Pharmacy and Chemistry, Philadelphia College of Pharmacy; Lecturer at Jefferson Medical College No 12. VETERINARY ANATOMY AND PHYSIOLOGY. Illustrated Bv Wm. R. Ballou, m.d., Professor of Equine Anatomy at New York College of Veterinary Surgeons; Physician to Bellevue Dispensary, etc. With 29 graphic Illustrations &Ty No. 13. DENTAL PATHOLOGY AND DENTAL MEDICINE Third FHV Illustrated. Containing all the most noteworthy points of interest to the Dental Studen and a Section on Emergencies. By Geo. W. Warren n n <; n,i»fnfrr • To Tr ?. vania College of Dental Surgery, Philadelphta ' ' Chief of Chnical Staff, Pennsyl- No. 14. DISEASES OF CHILDREN. Colored Plate Bv Map™ t> u Professor of Diseases of Onldren, Chicago Medic^aSS' llclTSiL^Z^' No. 15. GENERAL PATHOLOGY AND MORBID ANATOMV „ th f tions By H. Newberry Hall, ph.g., m.d., Pr^oSor of P^thUgy^Id Me^ca iChem" istry, Chicago Post-Graduate Medical School. Second Edition ivieaicai cnem- N°'pIhUadeI?Il,SEp?Er °F Tn,E SKIN- ^ >Y F- Schamberg, m.d., Instructor at Philadelphia Polyclinic. 99 Illustrations. Price, each, strongly hound in cloth, .80. Interleaved for taking Notes, $1.25. Published Annually for 49 Years. The Physicians Visiting List. (LINDSAY & BLAKISTON'S.) Issued in November of each Year. In order to improve and simplify this Visiting List we have done away with the two styles hitherto known as the " 25 and 50 Patients plain." We have allowed more space for writing the names, and added to the special memoranda page a column for the "Amount" of the weekly visits and a column for the "Ledger Page." To do this with- out increasing the bulk or the price, we have condensed the reading matter in the front of the book and rearranged and simplified the memoranda pages, etc., at the back. The Lists for 75 Patients and 100 Patients will also have special memoranda page as above, and hereafter will come in two volumes only, dated January to June, and July to December. While this makes a book better suited to the pocket, the chief advantage is that it does away with the risk of losing the accounts of a whole year should the book be mislaid. The changes and improvements made in 1896 met with such general favor that the sale increased at once more than ten per cent, over the previous year. CONTENTS. PRELIMINARY MATTER.—Calendar, 1900-1901—Table of Signs, to be used in keeping records— The Metric or French Decimal System of Weights and Measures—Table for Converting Apothecaries' Weights and Measures into Grams—Dose Table, giving the doses of official and unofficial drugs in both the English and Metric Systems—Asphyxia and Apnea—Complete Table for Calculating the Period of Utero-Gestation—Comparison of Thermometers. VISITING LIST.—Ruled and dated pages for 25,50,75, and 100 patients per day or week, with blank page opposite each on which is an amount column, column for ledger page, and space for special memoranda. SPECIAL RECORDS for Obstetric Engagements, Deaths, Births, etc., with special pages for Addresses of Patients, Nurses, etc., Accounts Due, Cash Account, and General Memoranda. SIZES AND PRICES. REGULAR EDITION, as Described Above. BOUND IN STRONG LEATHER COVERS, WITH POCKET AND PENCIL. For 2<; Patients weekly, with Special Memoranda Page....................$1 00 50 " " " " " ..................* 25 if Tanuary to Tune 1 „ „ Pn « « « " " 2 Vols. Kti.t->i > ..... . 2 OO 5° \ July to December J 75 « •.......•«*■ {{*£&££,}......*°° .co « - •.....-°MS»£imU......22S PERPETUAL EDITION, without Dates. No 1. Containing space for over 1300 names, with blank page opposite each Visiting List page. Bound in Red Leather cover, with Pocket and Pencil,................$1 25 No. 2.'Same as No. I. Containing space for 2600 names, with blank page opposite........150 MONTHLY EDITION, without Dates. No 1. Bound, Seal leather, without Flap or Pencil, gilt edges,................ 75 No'. 2. Bound, Seal leather, with Tucks, Pencil, etc., gilt edges,................I 00 flg^-All these prices are net. No discount can be allowed retail purchasers. Circular and sample pages upon application. MORRIS' Text=Book of Anatomy SECOND EDITION Thoroughly Revised and Greatly Improved 790 Illustrations, of which many are in Colors Royal Octavo. Cloth, $6.00; Sheep, $r.00; Half Russia, $8.00 Two Reviews Recently Published by Two Leading Medical Journals From From The Medical Record, New York. The Philadelphia Medical Journal. " The reproach that the English lan- guage can boast of no treatise on anatomy deserving to be ranked with the masterly works of Henle, Luschka, Hyrtl, and others, is fast losing its force. During the past few years several works of great merit have appeared, and among these Morris's " Anatomy " seems destined to take the first place in disputing the palm in anatomical fields with the German classics. The nomenclature, arrange- ment, and entire general character re- semble strongly those of the above-men- tioned handbooks, while in the beauty and profuseness of its illustrations it sur- passes them. This edition otters but few changes ; a chapter on the skin has been added, and a useful list of vestigial and abnormal structures has been compiled. Sections especially worthy of praise are those on surgical and topographical anat- omy, and the chapter on the nervous system is presented with great clearness and fullness. The ever-growing popu- larity of the book with teachers and students is an index of its value, and it may safely be recommended to all inter- ested." " Of all the text-books of moderate size on human anatomy in the English lan- guage, Morris is undoubtedly the most up-to-date and accurate. The changes from the first edition are not marked ; perhaps the most noticeable feature is that there are twenty less cuts than in the first edition. Those which have been omitted, however, will not be greatly missed. The saving of space by the omission of a discussion of histology is a decided advantage, giving room for much matter of importance in these days when every student is obliged to own a special treatise on histology. To enumerate the numerous differences which are notice- able in the descriptions given by this book from those in many of the older anatomies would require too much space. The changes, however, almost without excep- tion, tend toward an improved nomen- clature and greater accuracy. This is particularly noticeable in the parts de- voted to descriptions of the abdominal viscera and the joints-----For the stu- dent, the surgeon, or for the general prac- titioner who desires to review his anatomy Morns is decidedly the book to buy " VThe illustrations in number, correctness, and excellence of execution are equaled by no similar treatise, about $1000 having been expended on new and improved blocks for this edition alone. Handsome circular free i