HANDBOOK OF Practical Medicine BY | Dr. HERMAOT EICHHORST, m — --- PROFESSOR OF SPECIAL PATHOLOGY AND THERAPEUTICS AND DIRECTOR OF THE UNIVERSITY MEDICAL CLINIC IN ZURICH VOLUME III DISEASES OF THE NERVES, MUSCLES, AND SKIN ONE HUNDRED AND FIFTY-SEVEN WOOD ENGRAVINGS NEW YORK WILLIAM WOOD & COMPANY 1886. Copyright by WILLIAM WOOD & COMPANY. 1886. PRESS OF 8TETTINER, LAMBERT 4 CO., 189 4 1S1 CROSBY ST., NEW YORK. TABLE OF CONTENTS. DISEASES OF THE NERVES, MUSCLES, AND SKIN. SECTION V. DISEASES OF THE NERVES. PART I. PAGES Diseases of the Peripheral Nerves, ..... 1-77 A. Diseases of the Motor Nerves, ..... 1-46 a. Paralysis of the motor nerves. Akinesis, . . . 1-36 1. Facial paralysis, . . . . . 1-13 2. Motor trigeminus paralysis, .... 13-14 3. Spinal accessory paralysis, .... 14-16 4. Hypoglossal paralysis, ..... 16-18 5. Radial paralysis, ..... 18-22 6. Median paralysis, ..... 22-23 7. Ulnar paralysis, ..... 23-25 8. Musculo-cutaneous paralysis, .... 26 9. Axillary paralysis, ..... 26-27 10. Combined paralysis of the nerves of the arm, . 27 11. Peripheral paralysis of the scapula and trunk nerves, ...... 27-30 а. Paralysis of serratus magnus, . . 27-28 б. Paralysis of pectorales, ... 28 c. Paralysis of rhomboids and levator anguli scapulae, ..... 29 d. Paralysis of latissimus dorsi, . . 29 e. Paralysis of subscapularis and teres major, 30 /. Paralysis of infraspinatus and teres minor, 30 g. Paralysis of extensors of the back, . . 30 h. Paralysis of abdominal muscles, . . 30 12. Phrenic paralysis. Paralysis of the diaphragm, . 30-31 13. Peripheral paralysis of nerves of lower limb, . 31-36 a. Crural paralysis, .... 31-33 b. Obturator paralysis, . . . 33-34 c. Gluteal paralysis, .... 34 d. Sciatic paralysis, .... 34-36 b. Spasm of the motor nerves. Hyperkinesis, . . . 36-45 1. Spasm of facial nerve, .... 36-40 a. Diffuse clonic facial spasm, . . . 37-39 b. Diffuse tonic facial spasm, . . 39 c. Partial tonic and clonic facial spasm,' . 39-40 2. Spasm of the motor trigeminal branches, . 40-41 3. Spasm of hypoglossal nerve, .... 41 4. Spasm of spinal accessory nerve, . . . 41-42 5. Spasm of muscles of neck, scapula, and arm, . 42-43 IV TABLE OF CONTENTS. PAGE a. Spasm of obliquus capitis inferior, . 43 b. Spasm of splenius capitis, ... 43 c. Spasm of rhomboid, ... 43 cl. Spasm of levator anguli scapulae, . . 43 6. Spasm of respiratory muscles, . . . 43-45 a. Clonic spasm of diaphragm, . . . 43-44 b. Tonic spasm of diaphragm, . . 44-45 7. Spasm of abdominal muscles, .... 45 8. Spasm of muscles of lower limbs, ... 45 9. Cramp, ....... 45 B. Diseases of the Sensory Nerves, . . . 46-69 a. Neuralgia, ....... 46-62 1. Trigeminal neuralgia, .... 46-51 2. Cervico-occipital neuralgia, .... 51-53 3. Phrenic neuralgia, ..... 53 4. Cervico-brachial neuralgia, .... 53-55 5. Dorso-intercostal neuralgia. . . . 55-57 Appendix. Neuralgia of the breast/ Mastodynia, . 57 6. Lumbo abdominal neuralgia, . . . 57-58 7. Crural neuralgia, ..... 58 8. Obturator neuralgia, .... 58 9. Neuralgia of external cutaneous nerve, . . 58 10. Sciatica, ...... 58-61 11. Spermatic neuralgia, ..... 61-62 12. Coccygodynia, ..... 62 13. Neuralgia of the joints, .... 62 b. Anaesthesia, ....... 62-69 I. Preliminary remarks, ..... 62-68 Examination of sense of touch, ... 63 • Examination of sense of pressure, ... 64 Examination of sense of time, ... 64 Examination of sense of position, ... 64 Examination of sense of temperature, . . 65 Examination of sense of pain, ... 65 Trigeminus anaesthesia, .... 68-69 C. Diseases of the Nerves of Special Sense, .... 69 1. Diseases of the olfactory nerve, .... 69-70 a. Hyperosmia, ...... 69 b. Anosmia, ...... 70 c. Parosmia, ...... 70 2. Diseases of the gustatory nerve, .... 70-71 a. Hypergeusia, ...... 71 b. Ageusia, ...... 71 c. Parageusia, . . . . . . 71 D. Anatomically Demonstrable Diseases of the Nerves, . . 71-77 1. Neuritis, ........ 71-74 2. Multiple neuritis, ...... 74-77 PART II. Diseases of the Spinal Cord, ...... 77-176 A. Diseases of the Substance of the Cord, .... 77-147 a. Non-systemic diseases of the cord, .... 77-99 1. Spinal anaemia, ..... 77-78 2. Spinal liyperaemia, ..... 78-79 3. Spinal hemorrhage, ..... 79-81 Appendix. Capillary spinal hemorrhage, . . • 81 4. Acute myelitis, ..... 82-90 5. Chronic myelitis, . . . • . 90-91 6. Multiple cerebro-spinal sclerosis, . . . 91-98 7. Tumors of the spinal cord, .... 98 8. Syringomyelia and hydromyelia, . . . 98-99 b. System diseases of the cord, ..... 100-138 Simple system diseases of the cord, . . . 100-130 TABLE of contents. V PAGE 1. Tabes dorsalis, ...... 100-112 2. Spastic paralysis, ..... 112-114 3. Acute anterior poliomyelitis in infants, . . 114-120 4. Acute, subacute, and chronic anterior poliomye- litis in adults, ..... 120-122 5. Spinal progressive muscular atrophy, . . 122-130 Combined system diseases of the cord, . . . 130-138 1. Hereditary ataxia, ..... 130 2. Secondary degeneration of the cord, . . 130-135 a. Descending secondary degeneration, . 131-134 b. Ascending secondary degeneration, . 134 c. Combined secondary degeneration, . . 134-135 3. Amyotrophic lateral sclerosis, . . . 135-138 c. Traumatic diseases of the cord, .... 138-147 1. Unilateral lesion of the cord, . . . 133-141 2. Acute injuries of the cord, .... 141-143 3. Concussion of the cord, .... 143-144 4. Slow compression of the cord, . . . 144-147 B. Functional Diseases of the Cord, ..... 147-162 1. Spinal irritation, ...... 147-148 2. Spinal neurasthenia, . . . . . 148 3. Acute ascending spinal paralysis, .... 149-150 4. Reflex paralyses, ...... 150-151 5. Psychical spinal paralysis, ..... 151 6. Paralyses after acute diseases, .... 151 7. Toxic spinal paralyses, ...... 151-155 a. Lead paralysis, ..... 151-154 b. Arsenic paralysis, ..... 154 c. Phosphorus paralysis, .... 154 d. Carbonic acid gas and bisulphide of carbon paralysis, 154 e. Ergot paralysis, ..... 154 /. Alcoholic paralysis, ..... 155 8. Writer’s spasm, ...... 155-158 9. Tetany, ........ 158-161 10. Saltatory spasms, ...... 161-162 11. Primary spinal muscular spasms, .... 162 C. Diseases of the Spinal Meninges, ..... 162-176 1. External spinal pachymeningitis, .... 162-164 2. Internal spinal pachymeningitis, .... 164-167 a. Hypertrophic pachymeningitis, . . . 164-166 b. Hemorrhagic pachymeningitis, . . . 166-167 3. Acute spinal meningitis, ..... 167-170 4. Chronic spinal meningitis, ..... 170-172 5. Meningeal apoplexy, ...... 172-174 7. Meningeal tumors, ...... 174-176 PART III. Diseases of the Medulla Oblongata, ..... 176-190 1. Glosso-labio-laryngeal paralysis, ..... 176-185 2. Hemorrhage into the medulla oblongata, .... 185-186 3. Embolism and thrombosis of the medulla oblongata, . . 186-188 4. Acute bulbar myelitis, ....... 189 5. Tumors of the medulla oblongata, .... 188-180 6. Injuries, acute and slow compression of medulla oblongata, . 189-198 PART IV. Diseases of the Brain, ....... 190-301 Diagnostic Preliminary Remarks, ..... 190-191 a. Focal symptoms in diseases of the cortex, . . . 191-196 b. Focal symptoms in diseases of the centrum ovale, . . 196-197 c. Focal symptoms in diseases of the internal capsule, . 197-199 VI TABLE OF CONTENTS. PAGE d. Focal symptoms in diseases of the basal ganglia, . , 199 e. Focal symptoms in diseases of the crura cerebri, . . 199-201 /. Focal symptoms in diseases of the pons Varolii, . . 201-203 Appendix. Focal symptoms in diseases of the optic thalamus, external capsule, corpora quadrigemina, cere- bellum, and cerebellar peduncles, . 203 g. Focal symptoms in diseases of the base of the brain, . . 203-205 h. Aphasic symptom-complex, ..... 205-210 A. Diseases of the Substance of the Brain, .... 210-253 1. Anaemia of the brain, ..... 210-213 2. Hyperaemia of the brain, ..... 213-217 3. (Edema of the brain, ..... 217-218 4. Cerebral hemorrhage, ...... 218-229 Appendix. Capillary cerebral hemorrhage, . . 229 5. Cerebral embolism and thrombosis, .... 229-233 6. Cerebral inflammation and abscess, . . . 233-233 Appendix, a. Congenital encephalitis, . . . 238 b. Acute infantile polio-encephalitis,’ . 238-239 7. Tumors in the cranial cavity, .... 239-245 8. Animal parasites in the cranial cavity, . . . 245-246 a. Cysticercus cellulosae, .... 245 b. Echinococcus, ..... 246 9. Aneurism of the cerebral arteries, .... 246-247 10. Hydrocephalus, ...... 247-251 a. Acquired hydrocephalus, .... 248-250 b. Congenital hydrocephalus. . . . 250-251 11. Hypertrophy of the brain, ..... 251-252 12. Atrophy of the brain, ..... 252-253 B. Diseases of the Cerebral Meninges, ..... 253-262 1. Internal hemorrhagic pachymeningitis, . . . 253-256 2. Thrombosis and inflammation of the cerebral sinuses, . 256-260 3. Meningeal hemorrhages, ..... 260-262 C. Functional Diseases of the Brain, ..... 262-301 1. Epilepsy, ....... 262-270 2. Eclampsia, 270-271 3. Tetanus 271-277 4. Chorea, 277-282 5. Praehemiplegic and posthemiplegic chorea, . . 282-283 6. Athetosis, ....... 283 7. Paralysis agitans, ...... 283-288 8. Tremor, ........ 288-289 9. Vertigo, ....... 289-291 10. Catalepsy, . . . . . . .291 11. Hysteria, ....... 291-300 12. Cerebral neurasthenia, ..... 300-301 PART V. Diseases of the Sympathetic, ...... 301-311 1. Hemicrania, ........ 301-305 2. Progressive facial hemiatrophy, ..... 305-307 3. Facial hemihypertrophy, ...... 307-308 4. Irritative conditions of the cervical sympathetic, . , 308-309 5. Paralytic conditions of the cervical sympathetic, . . . 309-310 6. Symmetrical gangrene, ...... 310 7. Myxoedema, ........ 311 8. Hydrops articulorum intermittens, .... 311 SECTION VI. DISEASES OF THE MUSCLES. 1. Pseudohypertrophy of the musfcles, ..... 312-316 2. True hypertrophy of the muscles, . . . . * . 316-317 TABLE OF CONTENTS. VII PAGE 3. Myositis ossificans progressiva, ..... 317-318 4. Ischaemic muscular paralysis, ..... 318 SECTION VII. DISEASES OF THE SKIN. PART I. Inflammations of the Skin. Dermatitides, . * . . 319-847 A. Erythematous Inflammations of the Skin, . . . 319-325 1. Urticaria, ....... 319-321 2. Erythema nodosum, ..... 322-323 3. Erythema exsudativum multiforme, . . . 323-324 4. Acrodynia, ....... 324 5. Pellagra, ....... 324-325 B. Vesicle-like Inflammations of the Skin, .... 325 -331 1. Eczema, ........ 325-330 2. Miliaria, ....... 330-331 C. Vesicular Inflammation of the Skin, ..... 331-333 Pemphigus, ....... 331-333 D. Pustular Inflammations of the Skin, .... 333-340 1. Impetigo and ecthyma, ..... 333-335 2. Acne vulgaris, ....... 335-336 3. Acne mentagra, ...... 336-338 4. Acne rosacea, ....... 338-340 E. Scaly Inflammations of the Skin, ..... 340-344 1. Psoriasis, ........ 340-344 2. Pityriasis rubra, ...... 344 F. Papular inflammations of the Skin, ..... 344-347 1. Prurigo, ....... 344-346 2. Lichen scrophulosorum, ..... 346 3. Lichen ruber, ... ... 346-347 PART II. Secretory Anomalies of the Skin, ..... 348-353 A. Secretory Anomalies of the Sweat Olands, . . . 348-350 1. Hyperhidrosis, ....... 348-349 2. Anhidrosis, ....... 349 3. Parhidrosis, ....... 349-350 a. Osmhidrosis, ..... 349 b. Chromhidrosis, ...... 350 c. Urhidrosis. ...... 350 B. Secretory Anomalies of the Sebaceous Olands, . . . 350-353 1. Seborrhcea, ....... 350-352 2. Asteatosis, ....... 352 3. Parasteatosis, ...... 352-353 a. Comedo, ....... 352 b. Milium, ...... 353 PART III. Hypertrophy of the Skin, ....... 353-360 A. Hypertrophy of the Cutaneous Pigment, . . . 353-355 1. Naevus, ........ 353-354 2. Chloasma, ....... 354-355 B. Hypertrophy of the Epidermis. Keratosis, .... 355-356 Ichthyosis, . . ... . . . 355-356 C. Hypertrophy of the Hair. Hirsuties, .... 356-357 VIII TABLE OF CONTENTS. PAGE D. Hypertrophy of the Nails. Onychauxis, . . . 357 E. Hypertrophy of the Connective Tissue, .... 357-360 Sclerema adultorum, ...... 357-359 Appendix: Sclerema neonatorum, .... 359-360 PART IV. Atrophy of the Skin, ....... 360-364 A. Atrophy of the Cutaneous Pigment. Leukoderma, . . 360-361 B. Atrophic Changes in the Hairs, ..... 361-364 1. Canities, ....... 361 2. Alopecia and atrichia, ...... 362-363 3. Alopecia areata, ...... 363 4. Trichorhexis, ....... 363 C. Atrophy of the Cutis Tissue, ..... 364 Xeroderma, ........ 364 PART V. Neuroses of the Skin, ....... 364-365 Pruritus, ........ 364-365 PART VI. Parasites of the Skin, ....... 365-383 A. Animal Parasites. Dermatozoonoses, .... 365-375 1. Scabies, ........ 365-372 2. Acarus folliculorum, ..... 372 3. Pediculi 372-374 a. Pediculus capitis, ..... 372-373 h. Pediculus vestimentorum, .... 373-374 c. Pediculus pubis, ..... 374 4. Fleas 374 a. Pulex irritans, ..... 374 h. Pulex penetrans, ..... 374 5. Bedbug. Cimex lectularius, .... 374 6. Filaria medinensis, ...... 374-375 7. Cysticerci, ....... 375 B. Vegetable Parasites of the Skin. Dermatomycoses, . . 375-383 1. Pityriasis versicolor, ..... 375-377 2. Favus . 377-379 3. Herpes tonsurans, ...... 380-383 HANDBOOK OF PRACTICAL MEDICINE. SECTION V. DISEASES OF THE NERVES. PART I. DISEASES OF THE PERIPHERAL NERVES. A. DISEASES OF THE MOTOR NERVES. a. PARALYSIS (AKINESIS) OF THE MOTOR NERVES. 1. Paralysis of the Facial Nerve. (Bell’s Paralysis. Prosoplegia.) I. Etiology.—Peripheral facial paralysis is that form of disease ■whose causes are situated between the peripheral terminations of the nerve, and the point at which the trunk of the nerve enters the sub- stance of the central nervous system, at the posterior edge of the pedun- cle of the pons. The paralysis also presents a peripheral character if the central fibres of the nerve are injured before they enter the nucleus in the floor of the fourth ventricle. The peripheral course of the nerve may be divided into an intracra- nial portion, the part contained in the Fallopian canal, and the purely peripheral terminations. Exposure occupies a prominent place among the causes of peripheral facial paralysis (rheumatic form). The paralysis sometimes follows the exposure at once, sometimes in a few hours or days. The paralysis is often produced by riding in a car near an open window, look- ing out of a window when the face is warm, standing at a windy corner of a 1 2 DISEASES OF TIIE MOTOR NERVES. street, etc., and especially on that side which is exposed to the wind or cold air. Sleeping near a cold, damp wall is also sufficient to produce the paralysis In other cases traumatism is the cause of the paralysis. This disease has been observed as the result of a slap in the face, the blow of a rapier, the application of the forceps during delivery. Tumors of the pelvis, and a narrow pelvis are also said to produce facial paralysis in the new-born. Blows, stab-wounds, gunshot wounds, may paralyze the nerve. The disease also results not infrequently from eurgical operations upon the parotid gland, and it has been observed after stretching of the nerve in convulsive tic. It is sometimes the re- sult of severe injury to the skull, with subsequent fracture and hemorrhage, since an accumulation of blood in the Fallopian canal is apt to impair the func- tion of the nerve. Diseases of the parotid gland, enlargement of the submaxillary lym- phatic glands, abscesses in the region of the lower jaw, or suppuration of tubercular lymphatic glands, with subsequent formation of cica- trices, may also give rise to the paralysis, either as the result of com- pression or direct implication of the nerve in the morbid process. May described facial paralysis in leuksemia from leukaemic infiltration of the nerve. The disease is often the result of aural affections. According to Graig, the paralysis may be caused by an accumulation of wax in the ear, and may rapidly disappear when the cerumen is removed. It has also been assumed that catarrhal inflammation of the cavity of the tympanum may implicate the facial nerve. The connection between tubercular processes in the temporal bone and facial paralysis is clearer, because the destructive process is apt to extend to the trunk of the nerve. The paralysis is sometimes produced by neoplasms or hemorrhages in the Fallopian canal. In certain cases intracranial diseases are the causes of peripheral fa- cial paralysis, for example, meningitic changes, exostoses, tumors, an- eurisms of the vessels at the base of the brain, etc. The infectious diseases occasionally act as a cause (diphtheria, ery- sipelas, typhoid fever, variola, and dysentery). Several cases have also been described after herpes zoster. Peripheral facial paralysis is not in- frequently the result of syphilis. The lesion is sometimes intracranial (chronic meningitic processes, exostoses, or gummata), sometimes it con- sists of an exudative process within the Fallopian canal. French writers assert that the paralysis sometimes occurs temporarily at the beginning of the secondary stage of syphilis, particularly in females. The disease is said to have been observed in lead poisoning, and also after over-exertion of certain facial muscles. The disease is an unusually frequent one. It is observed more often in men because they are more exposed to the various causes, and is more frequent in middle life for a similar reason. Eulenburg observed a pa- tient who had had the disease twice on the right side, and three times on the left side. II. Anatomical Changes.—I have had the opportunity of making a post-mortem examination of a case of facial paralysis, following tuber- cular disease of the petrous portion of the temporal bone. The changes were identical with those observed shortly after section of a nerve in an- imals: degeneration of the medullary substance into small fragments, DISEASES OF THE MOTOR NERVES. 3 destruction of the axis cylinders, increase of the nuclei in the sheath of Schwann, increase of the interstitial connective tissue and of its nuclei (Fig. 1). Similar appearances were described by Kaase in a case of six weeks’ standing. In this case the frontal muscle showed fatty de- generation of the fibrillse, increase of the interstitial connective tissue, and an accumulation of fat within it. These changes must always be expected when the lesions which have given rise to the facial paralysis have interrupted the continuity of the nerve fibres. If the causes disappear, the anatomical changes may be repaired. The restoration of the parts may remain absent if the lesion has lasted too long or if a large part of the nerve has been entirely destroyed. Fig. 1 Degenerated nerve fibres from the facial nerve, which was paralyzed as the result of tuberculosis of the petrous portion of the temporal bone. Osmic acid preparation. Enlarged 275 times. In mild, temporary paralyses, the lesions are probably less severe. In not a few cases, they consist probably of inflammatory swelling and changes in the connective-tissue portions of the nerve, which tempora- rily compress the nerve fibres and impair conduction. As a matter of course, such conditions will be more serious if situated within the Fallo- pian canal, on account of its narrowness and unyielding character. IIT. Symptoms.—The symptoms of facial paralysis are not confined to purely motor disturbances in all cases. According to some authors, the facial nerve contains secretory fibres at its origin from the pons, so that it is not surprising that disturbances in the secretion of saliva may occur in facial paralysis. At the ganglion geniculatum, the facial nerve receives gustatory nerve fibres from the trigeminus through the agency of the petrosus superficialis major (but the gustatory fibres soon 4 DISEASES OF THE MOTOR NERVES. leave the facial nerve with the chorda tympani), and hence the symp- toms of facial paralysis may include disturbances of taste. Finally, since the facial nerve innervates the stapedius muscle through the agency of the stapedius nerve, auditory disturbances may also be pro- duced. The symptoms of facial paralysis may occur suddenly or be preceded by prodromata (pain in the ear and face, dizziness, etc.). In some cases, long-standing otorrhoea and the signs of tuberculosis of the petrous por- tion of the temporal bone prepare us for the possible onset of facial paralysis. The first symptoms are often noticed by the patient’s family or acci- dentally by himself on looking into a mirror. Sometimes the patient complains merely of imperfect closure of the lid and epiphora, although the paralysis must have been present for several days. Some patients Fig. 2. Expression of the face, during the act of laughing, in a woman suffering from peripheral paraly- sis of the left facial nerve. complain of a feeling of weight, stiffness, or coldness on one side of the face, or of a sour, salty, or metallic taste upon one-half of the tongue. The motor disturbances are the most prominent symptoms. The affected half of the face is destitute of folds, smooth, drawn towards the healthy side, and remains motionless during laughter, crying, or talking (Fig. 2). On account of paralysis of the frontal muscle, the forehead is some- what higher on the affected than on the healthy side; it is smooth, and remains so when the attempt is made to wrinkle it. On account of paralysis of the corrugator supercilii, the glabella on the affected side remains smooth when an attempt is made to wrinkle the integument in this region. The eyebrow is lower than on the healthy side. Paralysis of the orbicularis palpebrarum causes the upper lid to DISEASES OF THE MOTOR NERVES. 5 appear smaller than on the healthy side, and hence the palpebral fissure to appear larger. The eyeball is sometimes more prominent. The patient is unable to close the lid (lagophthalmus paralyticus), though the palpebral fissure becomes somewhat narrower in the attempt. Inasmuch as the eyeball is rolled upwards and inwards (more rarely upwards and outwards) by associated movements, the sclera and the lowermost segment of the iris make their appearance upon attempting to close the paralyzed lid. All these movements are usually spasmodic and irregular. The explanations of the diminution in the size of the palpebral fissure during the attempt to close the lid are unsatisfactory. Some assume an unequal paraly- sis of the various layers of the orbicularis. Henle believes that the levator pal- pebrm relaxes, contrary to the rule, during the attempt at closure, and thus ren- ders possible the phenomenon referred to. The patients are very much annoyed by constant epiphora, the result of paralysis of Horner's muscle, which changes the position of the lachrymal points in such a way that the lachrymal fluid, cannot enter them freely. After a while, the paralysis may be associated with con- junctivitis, ulceration of the cornea, or even deeper-seated diseases of the eye. Marked ectropium paralyticum of the lower lid develops not infrequently. The tip of the nose is directed towards the healthy side. The nostril on the affected side is smaller than that on the other side on account of the paralysis of the muscles which move the ala nasi. The patient often complains of a peculiar feeling of dryness in the affected side of the nose and diminished sense of smell, the result of dryness of the mucous membrane on account of the imperfect flow of tears through the lachry- mal canal, and of the diminished size of the nostril. The naso-labial fold is lessened or abolished on the paralyzed side. The angle of the mouth is depressed and drawn towards the healthy side; this is also true of the chin. The mouth is more or less open on the paralyzed side, and often permits the escape of saliva and fluids. For this reason, many patients, in drinking, throw the head backwards and towards the healthy side. Articulation is interfered with on account of the imperfect closure of the lips. This is most marked in the enunciation of the labials, the paralyzed cheek flapping to and fro in the attempt. Whistling, blowing, expectoration are also interfered with or rendered impossible, because the air escapes from the paralyzed side of the mouth. The movements of the tongue and of deglutition are undisturbed (the stylohoid and biventer mandibulse muscles are supplied by the facial nerve, but are of such minor importance that their paralysis is unnoticed). The apparent deviation of the tongue when protruded is simply the result of the drawing of the mouth towards the healthy side. Although the movements of mastication are unaffected, this function is interfered with to a certain extent by the paralysis of the buccinator muscle. Food may accumulate between the gums and the cheek, and must then be removed with the fingers or by pressure upon the cheek from the outside. Paralysis of the branches which supply the muscles of the concha is 6 DISEASES OF THE MOTOR NERVES. recognizable, on inspection, in those individuals who possess the power of moving the ear, or by electrical examination of the muscles. The sensibility of the integument is almost always intact, with the exception of the rare cases in which the cause of paralysis is situated so far peripherally that the inosculating peripheral ramifications of the trigeminus are also affected. Vaso-motor disturbances are never observed. Berger reports one case in which the hair turned gray upon the paralyzed side. Reflex and associated movements are always absent in peripheral as opposed to central facial paralysis. Auditory disturbances are observed under certain circumstances. If a peripheral facial paralysis is the result of intracranial processes or tu- bercular and inflammatory changes in the petrous portion of the tempo- ral bone, audition may be impaired or abolished, either because the acoustic nerve has also been injured or on account of the destruction of the auditory apparatus within the tympanic cavity. On the other hand, the facial paralysis in itself may be associated with increased power of hearing (hyperacusis, oxyokoia). Hitzig also mentions that some patients hear a low note upon voluntary contraction of the frontal mus- cle. These phenomena are explained by the fact that the stapedius muscle is supplied by the facial nerve. If this muscle is paralyzed, the tensor tympani assumes the upper hand and produces the hyperacusis (the modus operandi has not been satisfactorily explained). Disturbances of taste are possible, owing to the fact that the facial nerve receives gustatory fibres, at the ganglion geniculatum, through the nervus petrosus superficialis major. These fibres leave the facial nerve in the chorda tympani, so that disturbance of taste will occur only when the lesion is situated between the ganglion geniculatum and the exit of the chorda tympani. The patients complain not infrequently of subjective perverse sensations of taste (salty, metallic, etc.). In severe cases the patients lose the sense of taste entirely (ageusis). or it is distinctly diminished or perverted in the anterior two-thirds of the tongue on the paralyzed side (the posterior third is supplied by the glosso-pharvngeal nerve). In testing the sense of taste, the tongue should be protruded (the eyes being closed), and its tip and edge brushed with various salty, sweet, sour, and bitter solutions. The tongue should not be withdrawn into the mouth during the experiment. Taste may also be tested with the galvanic current. A wire electrode, terminating in a small button, should be employed (vide Vol. I., Fig. 30), The object of the examina- tion is to determine whether the first sensation of taste is produced on both sides by the same number of elements on touching the tongue with the electrode, and whether the patient is able to discern that the anode produces a more intense gustatory sensation of a more metallic, sour taste, while the action of the cathode is less intense, and the gustatory sensation more biting and salty. The indifferent electrode, i. e., the one which is not in contact with the tongue, may be placed upon any indif- ferent spot, for example, the sternum. The test is begun with one ele- ment, and the strength of the current gradually increased, if necessary. The prickling sensation produced by the current must be distinguished from gustation. The tactile sensibility of the tongue is not infrequently diminished upon the paralyzed side. DISEASES OF THE MOTOR NERVES 7 Many patients complain of diminished salivary secretion and a feel- ing of dryness in the affected half of the buccal cavity. The connection of the ganglion geniculatum with the spheno-palatine ganglion, through the agency of the nervus petrosus superflcialis major, also explains the possible occurrence of paralysis and changes in position of the uvula and soft palate. The motor fibres in question pass from the facial into the palatine nerve. On opening the mouth, the arch of the palate is found depressed on the paralyzed side, and flutters to and fro on forced respiration. The tip of the uvula almost always projects towards the healthy side, but it must be remembered that deflections of the uvula may occur in the healthy subject. The electrical reactions of the paralyzed muscles are very important with regard to diagnosis and prognosis. Facial paralysis may be divided into mild, moderately severe, and severe forms, according to the charac- ter of the electrical reactions. In the mild form, there are hardly any changes in the electrical irrita- bility to the faradic and galvanic currents, the muscles reacting (both directly and indirectly) as well as on the healthy side. In some cases, indeed, th indirect electrical irritability is increased for a few days after th( paralysis, so that a milder current suffices to produce minimal contractions of the paralyzed muscles. Paralyses which present such re- actions until the seventh day offer a very favorable diagnosis. They usually recover within two or three weeks without special treatment. The moderately severe form of facial paralysis presents the partial degeneration reaction. If electricity is applied to the nerve (indirect stimulation), a slight increase of excitability may be noticeable ior a few days after the paralysis, but towards the end of the first week the faradic and galvanic excitability diminishes more and more, as is shown by the fact that the muscular contractions on the paralyzed side are less vigor- ous than on the healthy side, although the minimal contractions often are produced by the same current on the two sides. The electrical re- actions on direct stimulation of the muscles are entirely different. They present qualitative and quantitative changes which grow more profound during the second and third weeks of the disease. Towards the end of the first week the faradic reaction gradually diminishes. The galvanic excitability also diminishes somewhat during the first wTeek, but it grows more active during the second week. The mildest current is often suf- ficient to produce muscular contractions on the paralyzed side. But these contractions are slow, prolonged, and feeble, and are apt to become tetanic, often during the entire duration of the passage of the current. At the same time the law of normal contraction changes. If a healthy muscle is stimulated with an increasing strength of current, the contrac- tions will occur in the following order: Cathodal closure contraction (CaCIC). Anodal closure contraction (AnCIC). Anodal opening contraction (AnOC). Cathodal opening contraction (CaOC). In peripheral paralysis, AnCIC follows CaCIC very rapidly at the be- ginning, soon it appears with the same strength of current, and finally AnCIC exceeds CaCIC. This is also true of CaOC which soon becomes equal to AnOC, though it rarely exceeds the latter. The moderately severe form usually recovers in four to six weeks, at the latest in eight to ten weeks. It disappears without leaving any 8 DISEASES OF THE MOTOR NERVES. sequelae (twitchings or contractures). Voluntary power often returns before the changes in the galvanic excitability have disappeared. In the severe form of the disease, complete degeneration reaction is observed. The excitability of the nerve to both currents diminishes at once or after a slight increase of excitability for one or two days. This diminution of excitability spreads from the central portions of the nerve to the periphery, and finally the electrical irritability disappears entirely. It may remain absent for weeks and months or, in incurable cases, per- manently. Direct stimulation of the muscles, on the other hand, reveals the changes which we mentioned above in our description of the moder- ately severe form. Fio. 3. Frontal muscle. Corrugator supercilii. palpebrarum.. Compressor nasi. Levator lab. sup. alaeque nasi. Superior facial branch.. Trunk of facial nerve... Retrahens and attollens auri muscles Levator lab. sup. propr. Zygomatic min. Dilator naris. Occipital muscle Zygomat. maj. Middle facial branch.. Stylohyoid muscle Digastric muscle Orbicularis oris. Inferior facial branch. Levator menti. Quadratus. Triangularis menti. Motor points of the facial nerve and the facial muscles supplied by it. In addition to an increase of galvanic excitability, the muscles also manifest increased mechanical excitability. In many cases of severe facial paralysis, a period of one to one and one-half years elapses before recovery occurs. At all events, voluntary contractions are hardly ever observed before the end of the second or third month. Recovery is not infrequently incomplete; twitchings and contractures persist in the previously paralyzed muscles. Voluntary power returns before the indirect electrical excitability, i. e., the nerve fibres have become capable of conducting the stimulus of the will be- fore they react to peripheral stimuli. In the incurable cases, the in- creased excitability to the galvanic current gradually disappears, and the muscles finally become altogether inexcitable. DISEASES OF THE MOTOR XERVES. 9 The changes of electrical excitability which we have described depend upon definite anatomical changes in the nerves and muscles. Experiments on animals prove that when a peripheral nerve is cut, the medulla and axis cylinder of the fibres in the peripheral portion undergo degeneration and become incapable of conduction. The more the degeneration of the nerve progresses, the more its electrical excitability diminishes. Anatomical changes also appear in the mus- cles supplied by the cut nerve. About the second week, the muscular fibres be- come narrower, the transverse striation less distinct, the muscle nuclei increase in number, and the interstitial connective tissue proliferates. E. Neumann showed that muscles in this condition lose the power to react to currents of short duration (faradism), but react to galvanic currents of sufficient duration in the manner known as degeneration reaction. After the degeneration of the nerve has lasted for some time, a regeneration of the fibres occurs, if the conditions are favorable. At first, the new fibres are destitute of medulla, and are unable to conduct peripheral impulses to the mus- Fig. 4. Bilateral facial paralysis. Face in profile. After Wright. cles, although they conduct the will power. The electrical excitability appears to be dependent on the presence of the medulla. In the mild form, there is probably no anatomical change in the nerve or mus- cle; in the moderately severe form the anatomical disturbances in the nerve are only temporary, but the muscular tissue presents more marked lesions. In in- curable cases the atrophy of the muscular fibres and increase of the connective tissue become so excessive that the electricai excitability is entirely lost. Motor points are those places from which a muscle can be made to react most readily to electrical stimulation. The motor points of the facial muscles are shown in Fig. 3. As a rule, peripheral facial paralysis is unilateral, and affects almost all branches of the nerve. Bilateral facial paralysis (diplegia facialis) is rare. It is sometimes 10 DISEASES OF THE MOTOR NERVES. found that, after exposure, at first one nerve is paralyzed, and after a few days the other facial nerve is also paralyzed. Or bilateral paralysis may be the result of lesions of the petrous portion of both temporal bones, or of intracranial processes. Maingauld described diplegia facialis after diphtheria. Sometimes the paralysis on one side is peripheral, on the other side it is central in its origin. Persons suffering from diplegia facialis have entirely lost the power of mimetic movements. We may hear the patients laugh or cry, but their features remain rigid and set. There is inability to close the lids, the mouth is open, the upper lip often hangs down like a snout, saliva dribbles from the mouth. Speech is indistinct and nasal. Deglutition is impaired, and many patients are compelled to push the food, with the fingers, back of the palate. Fig. 5. Facial expression in bilateral facial paralysis. Full face. After Wright. Various causes may give rise to incurability of the paralysis, viz., tubercular processes in the petrous portion of the temporal bone, opera- tions, injuries, etc. In certain cases, recovery is incomplete. The muscles remain paretic, and tvvitchings and contractures are observed. If the paralysis is permanent, the facial muscles and integument undergo atrophy. IV. Diagnosis.—The recognition of facial paralysis as such is not difficult, and, as a rule, it is also easy to differentiate the central from the peripheral form. It is characteristic of central facial paralysis that: a. The movements of the forehead and eyelid are usually unaffected, except when the disease is the result of a lesion of the pons which affects the course of the facial nerve on the peripheral side of the facial nucleus. DISEASES OF THE MOTOR NERVES. 11 b. The electrical excitability is unchanged or is even increased for a few days. c. There is usually paralysis of the limbs on the same side, except in certain cases of pons lesion, in which the limbs are paralyzed on the opposite side of the body. d. According to Strauss, the secretion of perspiration after sub- cutaneous injections of pilocarpin is unaffected on the paralyzed side in central facial paralysis, but is delayed and diminished in peripheral facial paralysis. The following anatomical details must be considered with regard to the situation of the paralysis (vide Fig. G): 1. In paralysis whose causes are outside of the stylo-mastoid foramen, the symptoms will consist simply of paralysis of the facial muscles (vide Fig. 6, 1). Fiq. 6. Schematic representation of the course of the facial nerve. fc, trunk of facial nerve; ac, trunk of acoustic nerve; pai, internal auditory foramen; Gg, geniculate ganglion; psm, nervus petrosus superfleialis major; sip, stapedius nerve; cht, chorda tympani; fst, styloid foramen; nap, post, auricular nerve; bv and sth, nerves to the digastric and stylohyoid muscles; trg, trg', trg", trg'", trunk and the three branches of the trigeminus; Gsp, sphenopalatine ganglion; ig, lingual nerve. 2. If the cause of paralysis is situated in the lower part of the Fal- lopian canal, but below the point of departure of the chorda tympani, the paralysis of the facial muscles is associated with paralysis of the muscles of the ear and the occipitalis muscle, which are supplied by the posterior auricular nerve (vide Fig. 6, 2). 3. If the lesion is situated within the canal between the origin of the stapedius and chorda tympani, nerves, we will find: paralysis of the facial muscles, the muscles of the ear and occipitalis, disturbances of taste and salivary secretion (vide Fig. 6, 3). 4. If the lesion is situated between the ganglion geniculatum and 12 DISEASES OF THE MOTOR NERVES. the origin of the stapedius nerve, the symptoms produced are: paralysis of the muscles of the face, external ear, and the occipitalis, disturb- ances of taste, salivary secretion, and audition (vide Fig. 6, 4). 5. If the lesion is situated immediately above the nervus petrosus superficialis major, or at the ganglion geniculatum itself, paralysis of the palate will be associated with the symptoms mentioned in the pre- ceding section. G. If the lesion is situated above the ganglion geniculatum and in the intracranial portion of the nerve, disturbances of taste will be absent, but paralysis of the facial muscles, occipitalis, external ear muscles, dis- turbances of hearing and salivary secretion, and palatal paralysis will remain. In this form of disease, the adjacent nerves are often paralyzed, for example, the abducens, and particularly the acoustic. V. Prognosis.—The prognosis depends in the first place upon the cause. If the latter cannot be relieved, there is no hope of recovery of the paralysis. Paralyses of the facial nerve which occur during delivery recover spontaneously in one to two weeks, and rarely interfere with nursing. As a general thing, the prognosis is more favorable in young persons. Above all, however, it depends on the condition of the electrical excita- bility (vide page 7). VI. Treatment.—Causal treatment should first be instituted. For example, syphilitic lesions must be treated with mercury and iodine. Compressing tumors and abscesses must be treated according to surgical principles. In rheumatic facial paralysis we may recommend hot baths and iodide of potassium ( 3 iij. : 1 vij., one tablespoonful t. i. d.). Local treatment must also be adopted. Not much can be expected from applications of iodine, leeches, etc. Good results are said to have been obtained from subcutaneous injections of strychnine in certain forms of paralysis, especially after diphtheria. But real benefit is obtained from electrical treatment alone. However, our hopes must not be pitched too high, since the anatomical changes in the nerve and muscles will run their course despite all treatment. It appears possible to shorten the duration of the disease only in so far as the electrical treatment of the nerves may hasten the removal of the products of inflammation, and the direct stimulation of the muscles counteracts the atrophic changes. If the paralysis is situated in the Fallopian canal or the intracranial portion of the facial nerve, the galvanic current should be passed trans- versely through the head, the anode being placed immediately in front of the mastoid process on the affected side, the cathode on the correspond- ing part on the opposite side. Each sitting should last two to five min- utes, and be repeated three to four times a week. The current should not be strong enough to produce pain or vertigo. If the paralyzed muscles react to the faradic current, this should be apnlied to each individual muscle, so that the latter undergoes several successive contractions. The indifferent pole is applied to the sternum, the other to the motor points of the muscles (vide Fig. 3). The electrode applied to the motor points should be small, thoroughly moistened, and firmly applied. Strong currents must be avoided, since they are apt to give rise to electrical contracture of the muscles and serious deformity of the face. The duration of the entire sitting should not be longer than three or five minutes. Some physicians recommend the application of the faradic current even if the paralyzed muscles have lost their faradic excitability. In such cases we prefer the galvanic current.. The indif- DISEASES OF THE MOTOR NERVES. 13 ferent pole (preferably the anode) is applied to the sternum, the cathode is drawn across the individual muscles (so-called labile application). If the faradic irritability of the muscles returns as the paralysis improves, we may use the faradic and galvanic currents alternately. In old cases of peripheral facial paralysis, Rosenthal recommended intra-buccal galvanization, i. e., the anode is placed on the mucous membrane of the cheek, the cathode externally upon each individual muscle. Landois and Mosler em- ployed the simultaneous application of the galvanic current to the nerve and the faradic current to the muscles. If contractures and spasmodic twitchings persist in the muscles after peripheral facial paralysis, we may endeavor to relieve the contracture by the application of stabile constant currents (one pole on the mastoid process, the other fixedly on the pes anserinus or the individual muscles). Stretching or massage of the contractured muscles may also be recommended. Many patients attempt to relieve themselves by intro- ducing small globes between the cheek and jaw. Myotomy and tenotomy of the shortened muscles have been occasionally resorted to, or the attempt has been made to compensate for the facial deformity by producing vig- orous faradic irritation and electrical contracture of the healthy muscles. 2. Motor Trigeminus Paralysis. (Paralysis of the Muscles of Mastication.) 1. The third branch of the trigeminus contains only motor fibres. These form a separate nerve root at the point at which the trigeminus emerges from the brain near the anterior border of the middle peduncle; this root is smaller than the sensory trigeminus root, and is usually situ- ated immediately in front of the latter. The inframaxillary branch leaves the skull through the foramen ovale to pass to the muscles of mastication—the temporal, masseter, external and internal pterygoids, mylo-hyoid, anterior belly of the digastricus, tensor tympani, and splieno- staphylinus. Peripheral paralyses in the distribution of the third branch of the trigeminus are exceedingly rare. During its extracranial course the nerve is situated so deep that it is with difficulty accessible to refrigera- tory (rheumatic) influences. Furthermore, tubercular, syphilitic, or other diseases of the sphenoid bone are so uncommon that they are only exceptional causes of paralysis. The most frequent causes of peripheral paralysis of this nerve are intracranial diseases—meningitis, syphilitic changes, tumors, and aneurisms. At the same time, the first and second branches of the nerve are often implicated, and the disease often extends to adjacent cerebral nerves—for example, the facial or abducens. 2. In the disease under consideration there is loss of power in the muscles of mastication. During this act, the projection of the temporal and masseter regions remains absent, and upon applying the fingers we miss the hard swelling which is usually felt over the contracting muscles. On account of paralysis of the pterygoids, the jaw is deflected toward the paralyzed side during each movement of mastication. The patients are unable to move the jaw voluntarily towards the healthy side. They attempt by the aid of the tongue to push the bolus of food between the jaws on the unaffected side. Changes in the position of the palate and auditory disturbances on 14 DISEASES OF THE MOTOR NERVES. account of the paralysis of the spheno-staphylinus and tensor tympani muscles are conceivable, but have not been recognized with certainty. According to Lucae, paralysis of the tensor tympani is shown by the fact that the patient hears a low murmur subjectively, but is unable to recognize low notes objectively. There are usually disturbances of sensation. These may be confined to the third branch, or affect all branches of the trigeminus (vide article on Anaesthesia of the Trigeminus). The electrical reactions of the paralyzed muscles correspond to those observed in ordinary peripheral paralysis. Little is known concerning the reaction of the paralyzed nerve, on account of its deep situation. Atrophy and contracture of the muscles may develop after paralysis of long standing. The lower jaw is then drawn strongly upwards. Fig. 7. ,M. temporalis Mi masseteiv if the paralysis is bilateral, the lower jaw drops and is immovable. This is often noticed during the final agony. 3. The treatment must be etiological and local. The former depends upon the causation, the latter consists of electrical applications. If the disease is the result of intracranial lesions, the constant current should be passed transversely through the skull. In addition, applications should be made directly to the paralyzed muscles. The motor points are shown in Fig. 7. 3. Paralysis of the Spinal Accessory Nerve. 1. The spinal accessory nerve is composed of numerous nerve roots, of which the lowermost may be followed into the spinal cord to the Motor points of the masseter and temporal muscles. DISEASES OF THE MOTOR NERVES. 15 level of the sixth and seventh cervical vertebrae, while the uppermost emerge from the medulla oblongata. After the roots have united into the trunk of the nerve, they leave the skull through the jugular foramen. The nerve then divides into an anterior, internal branch, and a pos- terior, external branch. The former joins the pneumogastric, and passes into the recurrent laryngeal, pharyngeal, and cardiac branches of the vagus. The external branch supplies motor fibres to the sternomastoid and trapezius. These muscles also receive motor fibres from the cervical plexus. According to Bernard, the external branch of the spinal ac- cessory is composed chiefly of fibres of spinal origin. The symptoms of paralysis of the nerve are most distinct when the Fig. 8. stern o-cleido-mas- toid muscle. Spinal accessory nerve. Trapezius muscle, Motor points of the sternomastoid and trapezius muscles and the spinal accessory nerve, external branch is alone affected; that of the internal branch will not be considered here. The causes of peripheral paralysis of the external branch include: cold, wounds, tumors, and abscesses in the neck, diseases of the cervical vertebrae, rarely intracranial lesions. 2. In unilateral paralysis of the sternomastoid muscle, the head is held somewhat obliquely (caput obstipum paralyticum). The face looks towards the paralyzed side; the chin is turned towards the same side, and is directed slightly upwards (unopposed action of the healthy muscle). Passive motion of the head from before backwards is possible, but the active motion is performed only with the aid of auxiliary muscles. If the paralysis has lasted a long time, the muscle undergoes in- 16 DISEASES OF THE MOTOR NERVES. creasing atrophy. The healthy sternomastoid undergoes permanent contraction, and caput obstipum spasticum gradually develops. When both muscles are paralyzed, the head is held straight, but its motion backwards and upwards is rendered very difficult, and the pro- jection of the muscle on each side of the neck remains absent. In unilateral paralysis of the trapezius, the scapula is lower on the paralyzed than on the healthy side. It is also farther removed from the spine, the upper inner angle being farther removed than the lower angle. The weight of the arm draws the upper outer angle of the scapula forwards and downwards, and this elfect is increased still more by the contraction of the levator anguli scapulae and rhomboid muscles. The supraclavicular fossa is unusually deep. The raising of the shoulder is interfered with, and also the approximation of the scapula to the spine. Elevation of the arm above the horizontal is also interfered with, because the scapula is imperfectly fixed upon the thorax. In bilateral paralysis of the trapezii, the back appears unusually broad and curved. The head is usually inclined towards the chest. In combined paralysis of the sternomastoid and trapezius, the symp- toms include all those described above. If the trunk of the nerve is paralyzed, the symptoms of paralysis of the palate and of the recurrent laryngeal nerve are superadded (vide Vol. I., page 196). Increased frequency of the pulse has been observed in bilateral paralysis of the nerve (the cardiac branches of the vagus are derived in part from the spinal accessory). The electrical reactions of the paralyzed nerve and muscles corre- spond to those described with regard to facial paralysis. 3. Treatment includes the removal of the cause, and the application of electricity. If the disease is the result of intracranial causes, the galvanic current should be passed transversely through the skull; in ad- dition, electricity should be applied to the paralyzed muscles. The motor points and the superficial course of the nerve are shown in Fig. 8. Orthopaedic measures and myotomy are indicated in old cases, asso- ciated with contracture. 4. Paralysis of the Hypoglossal Nerve. (Glossoplegia.) 1. The hypoglossal nerve emerges from the groove between the olivary body and pyramid—the prolongation of the anterior lateral fur- row of the spinal cord. After the roots have united into a trunk, the latter passes through the anterior condyloid foramen, and is distributed to the tongue muscles (hypoglossus, genioglossus, styloglossus, lingual), to the geniohyoid, omohyoid and sternohyoid, and to the sternothyroid and hyothyroid muscles. In unilateral paralysis of the hypoglossus, the tongue, when protruded, deviates to the paralyzed side, on account of the unopposed action of the normal genioglossus muscle. The paralyzed half of the tongue is more deeply furrowed, and often presents lively fibrillary contractions ; it often undergoes atrophy, after the paralysis has lasted for some time. The disturbances in the movements of the tongue are especially noticeable in mastication and talking. The formation of the bolus is imperfect, and particles of food often remain upon the paralyzed side. On account of the diminished mobility of the bolus in the mouth, many DISEASES OF THE MOTOR NERVES. 17 patients complain of diminished gustatory sensation. The tongue nor- mally separates the buccal from the pharyngeal cavity during degluti- tion. This is imperfectly effected in paralysis of the tongue, so that food and drink regurgitate into the buccal cavity during deglutition. For the same reason the patients experience difficulty in swallowing saliva, and often expectorate it. In some cases the chief symptom is difficulty in the articulation of linguals, l. s, sch, and also of Tc, g, ch, r. u, s, f. Singing (the produc- tion of high and falsetto notes) is also interfered with, because these re- quire associated movements of the tongue. In bilateral hypoglossal paralysis, the tongue is motionless in the buccal cavity, and the disturbances of speech and mastication become Fig. 9. ■D’. hypo^losgus. M sternoliyoideua. M. omohyoidens. M. Btemothyreoideus. Motor points of the hypoglossus nerve and the muscles supplied by it more marked. The saliva sometimes flows almost uninterruptedly from the mouth. The electrical reactions are the same as in other peripheral paralyses. 2. Peripheral paralysis of the hypoglossus is rare. Gendrin reported a case in which the nerve was compressed by hydatids within the condy- loid foramen. Weir Mitchell observed it after a gunshot wound. It has also been observed as the result of operations or the growth of tumors. 3. Treatment consists in the main of the application of electricity. The motor points of the muscles are shown in Fig. 9; the peripheral trunk of the nerve is found immediately above and behind the greater cornu of the hyoid bone. In addition, electricity may be applied di- 18 DISEASES OF THE MOTOR NERVES. rectly to the tongue. The most suitable electrode for this purpose is the one depicted in Vol. I., Fig. 50. In galvanization of the trunk of the nerve, the cathode is applied to the point shown in Fig. 9, the anode to the back of the neck. 5. Paralysis of the Radial Nerve. I. Etiology.—Among the peripheral paralyses of the nerves of the arm, that of the radial nerve occurs most frequently. Its long and su- perficial course makes it easily accessible to rheumatic and traumatic in- fluences. The most frequent cause is traumatism; cold (rheumatic or refrigeratory paralysis) is a rarer etiological factor. Isolated radial par- alysis is observed not infrequently in hysteria and lead poisoning, but it is not probable that this is the result of peripheral disturbances. The disease also occurs after infectious diseases (typhus fever, acute articular rheumatism). In rare cases it seems to be the result of over- exertion of the muscles supplied by the nerve. The most frequent form of peripheral radial paralysis is the so-called “ sleep ” paralysis.’ It develops in individuals who, while drunk or worn out, have fallen asleep in a position in which they pressed upon the outer surface of the arm and with it the radial nerve, especially at the bend in its course. The patients some- times fell asleep with the head resting on the arm, and the latter pressing upon the sharp edge of the bed, etc.; sometimes the arm was drawn alongside the chest, and the protracted lateral decubitus and weight of the body produced the compression; or the arm was drawn up under the head. The paralysis is more frequent on the right side, because most people are accustomed to sleep upon the right side of the body. The more profound the sleep, the greater the danger of paralysis. It rarely occurs after natural sleep at night, but usually in drunkards or in laborers who take a short nap at noon. The paralysis is usually present on awaking, in rarer cases the patients first complain of numbness and tingling in the forearm, and this is followed in a few hours by paralysis. The triceps and the cutaneous sensibility of the arm and forearm are unaffected, because the com- pression generally takes place below the point at which the nerves to these parts are given off. If the pressure has been produced upon the upper third of the dorsal surface of the forearm, the supinator longus will not be paralyzed. Crutch paralysis is the term applied to that form of the disease which results from using poorly fitting crutches. It sometimes develops within a few hours after first using the crutches, sometimes after the lapse of days and weeks. The radial nerve is generally paralyzed on the side corresponding to the disease which ne- cessitated the use of crutches. The paralysis sometimes occurs unexpectedly, sometimes it is preceded by paresthesia. The ulnar and median nerves are often also paralyzed to a less extent. The radial nerve is affected mainly or exclusively because it is situated mox-e posterially and interiorly than the other nerves of the brachial plexus and is thus especially accessible to the pressure of the crutch. Prisoner’s paralysis is the term applied by Brenner to cases in which prisoners, whose arms are tied behind them, suffer from compression and paralysis of the radial nerves. Radial paralysis also occurs frequently in Russia in infants and coachmen; in the former, on account of the custom of tying the arms firmly to the chest and then laying the children on the side; in the latter, from the habit of tying the reins tightly around the arm. Water carrier’s paralysis is produced by carrying very heavy pails of water in such a manner that the arms are placed under the handle, and the pail rests upon the anterior surface of the chest and abdomen. The handle is, therefore, very apt to compress the radial nerve. Traumatic radial paralyses also include cases which are the result of a blow, fall, incised or gunshot wounds, fracture or dislocation of the humerus. In such cases other nerves are also affected. In cases of fracture, the nerve may be di- rectly injured by fragments of bone or by excessive growth of callus. This is most apt to occur in fracture of the lower third of the humerus. II. Anatomical Changes.—We are justified in assuming the same DISEASES OF THE MOTOR SERVES. 19 conditions in the nerve and muscles that have been described in the section on facial paralysis. Bernhardt reported a case, after typhus fever, in which there was a neuritic swelling, three centimetres in length, in the course of the nerve. Above this point the nerve fibres were in- tact, below they were destroyed. The muscles innervated by the radial nerve presented a considerable proliferation of nuclei and indistinctness of the transverse striation. III. Symptoms.—Peripheral paralysis of the radial nerve may be manifested by disturbances of motion and sensation. The former are more striking and constant, the latter may be entirely absent. The following muscles are supplied by the radial nerve: triceps, supinator longus, supinator brevis, extensor digiti quinti proprius, ulnaris externus, anco- Fig. 10. Fig. 11. Distribution of the cutaneous branches of the radial and other nerves of the arms. Fig. 10.—Dorsal surface of the upper limb. 1. sc., supraclavicular nerves. 2. ax., axillary nerve. 3. cps., superior posterior cutaneous branch of the radial nerve. 4. cmd., internal cutaneous nerve. 5. cpi., pos- terior inferior cutaneous branch of the rad- ial nerve. 6. cm., greater internal cutaneous nerve. 7. cl., lateral cutaneous nerve. 8. u., ulnar nerve. 9. ra., radial nerve, 10. me., median nerve. Fig. 11.—Volar surface of the upper limb. 1. sc., supraclavicular nerves. 2. ax., axillary nerve. 3. cmd.., internal cutaneous nerve. 4. cl.. external cutaneous nerve. 5. cm,., great- er internal cutaneous nerve. 6. me., median nerve. 7. u., ulnar nerve. nseus quartus, abductor longus pollicis, extensor pollicis longus et brevis, exten- sor indicis proprius. The brachialis internus receives a branch from the radial nerve and also from the nervus perforans Gasserii. The posterior superior cutaneous branch supplies the posterior surface of the arm as far as the elbow joint, the inferior posterior cutaneous nerve supplies the extensor aspect of the forearm as far as the wrist. The terminal 20 DISEASES OF THE MOTOR NERVES. cutaneous filaments of the nerve supply the radial half of the dorsum of the hand, the entire dorsal surface of the thumb, the first and second phalanges of the index and middle fingers (vide Fig. 10 and 11). The motor disturbances are easily recognized. When the arm is held horizontally, the hand is kept in a position of volar flexion and slight pronation, the fingers are flexed, the thumb is flexed and bent under the fingers (vide Fig. 12). The patients are unable to extend the hand and fingers; the grasp is feeble. The fingers cannot be employed in deli- cate manipulations. Supination of the forearm and, if the triceps is paralyzed, extension cannot be performed. Dorsal flexion of the basal phalanges is rendered impossible on account of paralysis of the extensor digitor. communis. Dorsal flexion of the middle and last phalanges is effected by the interossei (supplied by the ulnar nerve), but these only act when the basal phalanx is extended, so that the latter must first be pas- sively extended before the other phalanges can be extended. The feebleness of the grasp is also the result of paralysis of the common extensor, since the flexors Fig. 12. can only act vigorously when the extensors also contract, and thus separate as much as possible the points of origin and insertion of the flexors. The grasp becomes stronger as soon as the hand is passively extended. For the same reason, adduction and abduction of the fingers are not performed properly until the hand and fingers are extended. Paralysis of the ext. radial, longus et brevis and the ext. ulnaris is shown by the fact that adduction and abduction of the hand are interfered with or abolished. If the arm is extended, supination of the forearm is not possible, because the supinator brevis is incapable of function. If the fore- arm is flexed, supination may be effected by the biceps. Paralysis of the triceps and anconseus is shown by the absence of resistance to passive flexion of the forearm. Paraesthesiae occur much more frequently in radial paralysis than sensory disturbances which are objectively demonstrable. The patients complain of a feeling of coldness, numbness, and formication. Since the majority of paralyses of the radial nerve originate at the point of flexion of the nerve, sensory disturbances are occasionally present only upon the dorsum of the hand. Even if the lesion is situated higher, sensory dis- Position of the fingers and hand in peripheral radial paralysis in a man aet. 25 years. DISEASES OF THE MOTOR NERVES. 21 turbances may be absent, because other nerves act vicariously for those in which conduction is interrupted. Yaso-motor disturbances, viz., diminution of temperature and livid color of the skin, are occasionally observed. Thickening of the joints of the fingers and hand, and nodular thick- enings on the extensor tendons (tenosynitis hypertrophica of Gubler) may also occur, but their mode of origin is unknown. Atrophic changes de- velop in the muscles if the paralysis lasts a long time. The electrical reactions of the nerve and muscles are the same, in general, as in peripheral facial paralysis. Tn “sleep” paralysis, the elec- trical irritability of the peripheral portion of the nerve is almost always retained, and often increased. Irritation of the central end produces no effect, so that the site of the lesion can thus be determined with accuracy. In one case Fischer noticed increased mechanical irritability of the muscles. The duration of the disease varies extremely. Crutch paralysis usu- Fig. 13. Triceps (external head). Triceps (long head). Brachialis internus. Supinator longus. Radial nerve. Supinator brevis Radialis ext. long. Ulnaris ext. Extensor digit, commun. Extensor digit, minim Radialis ext. brevis. Extensor pollie. brev. Abductor pollie. loi g. Extensor indicis Extensor pollie. long. ally recovers most rapidly. Sleep paralyses generally require four to six weeks before recovery is established. IV. Diagnosis.—The peripheral character of the paralysis is usually evident from the fact that the radial nerve alone is paralyzed. But Raynaud described a case in which a solitary tubercle in the fissure of Rolando at the origin of the second frontal convolution gave rise to isolated paralysis of the radial nerve. Apart from the rarity of such cases, the peripheral nature of the cause in this disease is usually evident from the previous history, the objective changes, and electrical exami- nation. Lead palsy of the radial is usually bilateral, the supinators are almost always unaffected, and, as a rule, other symptoms of lead poison- ing have been present. The situation of the lesion will be easily recog- nized from the number and grouping of the paralyzed muscles, the sensory disturbances, and particularly from the electrical examination of the trunk of the nerve. v V. Prognosis and Treatment.—The prognosis is usually good, and the hope of recovery should not be abandoned even if the paralysis has lasted a long time. Motor points of the radial nerve and the muscles supplied by it. 22 diseases of the motor nerves. Treatment should first be directed toward the removal of the cause. In crutch paralysis better fitting crutches should be worn; dislocations must be replaced; if the nerve is compressed by callus, the latter must be removed and the nerve freed; if a cicatrix has formed in the nerve as the result of injury, it must be excised and the ends united with sutures, etc. Local treatment consists exclusively of electrical applications. The motor points are shown in Fig. 13. Remak recommended the use of gal- vanism, the cathode upon the site of lesion, the anode upon an indiffer- ent part (the sternum), current of moderate strength. The faradic cur- rent is preferable in applications to the muscles; three to four sittings weekly, each lasting three to five minutes. 6. Paralysis of the Median Nerve. I. Etiology.—Peripheral paralysis of the median nerve is much rarer than that of the radial nerve. In the majority of cases it is trau- matic, the nerve being injured, as a rule, in the forearm (not infre- quently immediately above the wrist) by stab or incised wounds, etc. It is observed occasionally after unskilful venesection at the bend of the elbow. Injury by pieces of glass is relatively frequent. Rheumatic paralysis of this nerve is rare. The disease is observed occasionally after acute infectious diseases (variola, typhoid), and also as the result of neuritis. II. Symptoms and Diagnosis,—If the lesion is situated imme- diately above the wrist, the paralysis is confined to the muscles of the ball of the thumb (abductor, flexor, and opponens pollicis brevis); the adductor pollicis brevis escapes because it is supplied by the ulnar nerve. In addition, there is paralysis of the first and second lumbricales. If the lesion is situated higher, there is also paralysis of the larger part of the volar muscles of the forearm, viz., pronator teres, flexor carpi radialis, palmaris longus, the superficial and deep flexors (these also receive branches from the ulnar nerves), flexor longus pollicis and pronator quadratus. Paralysis of the flexor digitorum sublimis causes inability to flex the second phalanges; as the result of paralysis of the deep flexor, the termi- nal phalanx of the second, and often of the third linger cannot be flexed. The first phalanges are flexed by the interossei, which also extend the second and third phalanges (innervation from the ulnar nerve). Excessive contraction of the interossei sometimes produces hyperextension of the second and third phalanges, and a sort of subluxation. Volar flexion of the hand is impaired; it is effected by the ulnaris internus. If the forearm is extended, pronation cannot be performed; when flexed, it can be pro- nated imperfectly by the aid of the supinator longus. Paralysis of the muscles of the ball of the thumb incapacitates the thumb from all delicate manipulations. Its phalanges cannot be flexed, and the movement of opposition cannot be effected. The non-paralyzed adductor pollicis (supplied by the ulnar nerve) draws the thumb against the index finger, and the extensors flex it strongly towards the dorsum. Sensory disturbances may be entirely absent because the cutaneous branches of the ulnar and radial nerves vicariously perform the function of the median. In other cases there is loss of sensation on the radial half of the palm of the hand as far as the median line of the fourth finger, and on the dorsal surface upon the terminal phalanges of the DISEASES OF THE MOTOK NERVES. 23 thumb and second and third fingers (vide Figs. 10 and 11). The anaes- thesia is often most marked on the tip of the index finger. Trophic disturbances occur with relative frequency. The affected fingers have a peculiar smooth and shining appearance (glossy skin), and the hairs are unusually long and abundant; the nails become thickened and distorted and exfoliate; pemphigus-like vesicles and ulcerations may forjn upon the terminal phalanges. Atrophy of the muscles often develops after the paralysis has lasted a long time. Pronator teres. Fig. 14. Median nerve. Flexor digit, commun. profundus. Flexor carpi radialis. Flexor digit, sublimis. Flexor pollic. long. Median nerve. Abductor pollic. brev. Opponens pollicis. Flexor pollic. brev. Abduct, poll. brev. 1st and 2d lum- , bricales. Motor points of the median nerve and the muscles supplied by it. The electrical excitability of the nerve and muscles corresponds to that usually observed in peripheral paralysis. III. Peognosis and Tkeatment are the same as in radial par- alysis. 7. Paralysis of the Ulnar Nerve. 1. The most frequent cause of peripheral ulnar paralysis is trauma- tism: pressure of a crutch, fracture of the humerus and compressing Fig. 15. Claw-hand. Palmar surface. After Duchenne. callus, tumors, gunshot or incised wounds, etc. Compression paralysis sometimes develops after prolonged dorsal decubitus. Duchenne observed it in laborers who are compelled to press the elbow for a long time against 24 DISEASES OF THE MOTOK NERVES. a firm support. Rheumatic or neuritic paralyses, and those occurring after infectious diseases, are much rarer. 2. The symptoms are readily interpreted. In paralysis of the muscles of the ball of the little finger (abductor, flexor brevis, opponens), the movements of the little finger are almost entirely abolished. Paralysis of the interossei and third and fourth Iumbricales causes impairment or Fig. 16. Claw-hand. Dorsal surface. After Duchenne. abolition of the movements of adduction and abduction. In addition, the first phalanges cannot be flexed, and the others cannot be extended (paralysis of the interossei). As the ulnar nerve supplies the ulnar por- tion of the flexor profundus digitorum, flexion of the two or three outer fingers is impaired. Paralysis of the adductor pollicis prevents active ap- proximation of the thumb to the index finger. Flexion and adduction Fig. 17. Opponens digit. minim. 3d and 4th iumbricales. Flexor digit, minim. Abduct, min. digit. Ulnar nerve. Flexor carpi ulnaris. Ulnar nerve. Palmaris brevi6. Motor points of the ulnar nerve and the muscles supplied by it. Volar surface of the arm. of the hand toward the ulnar side cannot be performed if the ulnaris in- ternus has been paralyzed. If cutaneous branches of the ulnar nerve are affected, sensation will be impaired upon the ulnar portion of the palm of the hand as far ae the median line of the fourth finger. Upon the dorsal aspect cutaneous sensibility is affected as far as the median line of the middle finger (vide; DISEASES OF THE MOTOR NERVES. 25 Figs. 10 and 11). Sensory disturbances may be entirely absent on ac- count of the vicarious action of other nerves of the arm. Trophic disturbances, on the whole, are rare. After long duration of the disease, muscular atrophy sets in, especially in the ball of the little finger and the interosseous spaces. The hand not infrequently assumes a peculiar shape, which is known as the claw hand. On account Fig. 18. Abductor digit, minim. 1st, 2d, 3d and 4th interossei. The same. Dorsal surface of the arm. of the paralysis of the interossei and lumbricales, the extensor digitorum communis becomes excessively contracted, and the first phalanges are flexed so strongly towards the dorsum that they become slightly luxated. At the same time, the second and third phalanges are strongly flexed by the action of the flexors, so that the tips of the fingers are im- bedded in the palm of the hand (vide Figs. 15 and 16). These changes Fig. 19. Musculo-cutaneous nerve. Biceps. Braehialis interims. Motor points of the musculo-cutaneous nerve and the muscles supplied by it. are especially marked in the fourth and fifth fingers, because the first and second lumbricales (second and third fingers) are supplied by the median nerve. The electrical reactions are the same as in other peripheral paralyses. 3. The treatment is the same as that of radial paralysis. The motor points are shown in Figs. 17 and 18. 26 DISEASES OF THE MOTOR NERVES. 8. Paralysis of the Musculo- Cutaneous Nerve. Isolated peripheral paralysis of this nerve is very rare, and it gen- erally escapes even in combined paralysis of the nerves of the arm. Erb noticed isolated paralysis of the nerve after extirpation of a tumor in the supraclavicular fossa. The motor disturbances produced are paraly- sis of the biceps, coracobrachialis, and brachialis interims; but the latter muscle is also supplied by the radial nerve. The forearm can be flexed very imperfectly or not at all upon the arm. This is most marked in supination of the forearm; in pronation, the supinator longus aids in flexing the forearm. Any sensory disturbances which may be present are found upon the radial surface of the forearm (vide Figs. 10 and 11). 9. Paralysis of the Axillary Nerve. Peripheral paralysis of the axillary nerve is most frequently of trau- matic origin, but several cases of rheumatic paralysis have also been de- Fig. 20. Dorsalis scapulae nerve Axillary nerve.. Xiong thoracic nerve (serratus magnus. Ant. thoracic nerve (pectoral muscles) Phrenic nerve... Erb’s supraclavicular point. scribed. Not infrequently it follows inflammation of the shoulder joint, perhaps because the inflammation extends to the axillary nerve and gives rise to neuritis. The motor disturbances consist simply of loss of function of the del- toid muscle, so that the patient is unable to lift the arm to the hori- Brachial plexus. DISEASES OF THE MOTOR NERVES. 27 zontal. The teres minor may be affected, but no noticeable symptoms are thereby produced. After paralysis of long standing, the deltoid undergoes atrophy, a deep horizontal furrow is felt and seen beneath the acromial end of the clavicle, and the head of the humerus is excessively movable in its socket. Sensory disturbances may be found upon the external and posterior surfaces of the arm (vide Figs. 10 and 11). The motor point is shown in Fig. 20. 10. Combined Paralysis of the Nerves of the Arm. Peripheral paralysis of several nerves of the arm occurs not infre- quently, but, as a rule, that of one nerve, particularly the radial, pre- dominates. This form of disease is to be expected if the cause of paralysis is located in the brachial plexus. Seeligmueller claims that paralysis of the plexus is often associated with disturbances of the sym- pathetic, contraction of the palpebral fissure and pupil, and abnormal redness of the skin. From the previous remarks on paralysis of the individual nerves, we can readily determine what nerves are affected in each case. Traumatism is an unusually frequent cause of combined paralysis of the nerves of the arm. This includes dislocation of the head of the humerus (especially subcoracoid dislocation), fracture of the humerus or clavicle, a blow or fall on the shoulder, more rarely incised or gunshot wounds in the lower part of the neck. The disease has also been ob- served as the result of the use of crutches, and of tumors in the neck. A special form of disease is that in which the paralysis is confined to the deltoid, biceps, brachialis anticus and supinator longus, and occa- sionally involves the infraspinatus, supraspinatus, and supinator brevis. Erb showed that these muscles can be made to contract by placing one electrode of a faradic current alongside the transverse process of the sixth cervical vertebra about two to three centimetres above the clavicle, and a little behind the external border of the sterno-mastoid (vide Fig. 20). Hence the nerves supplying the muscles in question must be situated in close apposition at this locality (Erb’s supraclavicular point). This form of paralysis may be the result of rheumatic causes, tumors in the neck, injury to the shoulder, and parturition. Ducnenne applied the term parturition paralysis to those cases of combined paralysis of the nerves of the arm occurring in the new-born as the result of difficult labor. The paralysis usually follows luxation or fracture of the humerus, fracture of the clavicle or scapula, more rarely direct compression of the plexus. These accidents may happen during version, application of the forceps, application of the hook, etc. It is doubtful whether the disease may occur during natural labor if the pel- vis is narrow. The paralysis should not be mistaken for separation of the epiphysis of the humerus. Combined paralysis of the nerves of the arm may also be the result of fractures and dislocations of the lower end of the humerus or radius, the application of tight bandages, etc. 11. Peripheral Paralysis of the Nerves of the Scapula and Trunk, a. Peripheral Paralysis of the Serratus Magnus. I. Etiology.—The serratus magnus is supplied by the long thoracic nerve. On account of the long and superficial course of the nerve, the muscle is frequently paralyzed. 28 DISEASES OF THE MOTOR NERVES. Amongthe causes are rheumatic influences, and still more frequently traumatism (fall, blow, incised wounds, surgical operations, carrying heavy loads on the shoulder, etc.). In not a few cases the disease is the result of over-exertion of the muscle, for example, in sawing, mowing, etc. Seeligmueller observed paralysis of the left serratus magnus in a feeble nurse who over-exerted herself in carrying a heavy child. It some- times develops after infectious diseases, particularly typhoid fever, but also after diphtheria. The right serratus is more frequently affected. The disease is much more frequent in males than in females; it is rare under the age of fifteen years. II. Symptoms.—The symptoms consist chiefly of changes in the po- sition of the scapula, which are noticeable during repose, but are much more marked when the arm is raised. As a rule, they develop slowly, and are usually preceded by pains in the supraclavicular region and top of the shoulder (implication of cutaneous branches of the brachial plexus). After the paralysis appears, the primary neuralgia not infre- quently gives way to cutaneous anaesthesia. When the arm is dependent, the inner border of the scapula is more closely approximated to the spine than on the healthy side, and the lower angle of the bone is separated from the trunk to an unusual degree. At the same time the lower angle is nearer the spine than the superior in- ternal angle, and accordingly the superior external angle is abnormally de- pressed. This is owing to the fact that, on account of the serratus par- alysis, the trapezius, rhomboids, and levator anguli scapulae assume the upper hand, and draw the scapula towards the spine. In the same wav, the pectoralis major, biceps, and ooraco-brachialis lift the lower angle of the bone away from the trunk. The contracted rhomboids and le- vator anguli scapulae are not infrequently visible beneath the skin as more or less thick strands between the scapula and spinal column. If these muscles are also paralyzed, the change in the position of the scap- ula is lessened. Nor must it be forgotten that primary contracture of these musclefe may produce the same position of the scapula as is seen in serratus paralysis, except that, in the latter, passive movements of the scapula are readily performed. The changes become more marked when the arm is raised in ‘front. The scapula then approaches the spine still more closely, and together with the lower angle of the bone is separated very markedly from the surface of the thorax (vide Fig. 21). The patients are unable to raise the arm slowly and steadily above the horizontal, because this movement requires rotation of the scapula by the serratus magnus. Elevation of the arm to the vertical position becomes possible if the scapula is pushed forwards passively, and its edges are pressed against the thorax. Some patients are able to raise the arm to the vertical by a swinging mo- tion. The power of crossing the arm, or pushing it forwards, is also lost, since these movements are effected by the serratus. The patients are unable to offer any resistance to passive retraction of the scapula. The electrical changes are similar to those observed in other periphe- ral paralyses. The motor points are shown in Fig. 20. The nerve is also readily reached in the axilla. If the muscle undergoes atrophy af- ter paralysis of long standing, the digitations of the muscle, which are readily seen on the healthy side when the arm is raised, disappear and the lateral surface of the thorax is flattened. b. Paralysis of the Pectoralis Major and Minor.—Both muscles are DISEASES OF THE MOTOR NERVES. 29 supplied by the anterior thoracic nerves. They are very rarely paralyzed alone. Such an isolated paralysis would be shown by the impairment or abolition of abduction of the arm against the trunk, and inability to resist passive abduction of the arm. The patient is also unable to place the hand of the paralyzed side upon the opposite shoulder, if the mus- cles undergo atrophy, the infraclavicular region will be unusually flat. The motor points are shown in Fig. 20. c. Paralysis of the Rhomboids and Levator Anguli Scapulae.—These muscles are supplied by the dorsalis scapulae nerve. Isolated paralysis of the muscles will produce no special symptoms. If the trapezius is also Fig. 21 Position of the scapula in paralysis of the serratus magnus, during elevation of the arm in front. After Duchenne. paralyzed (vide page 16), the paralysis of the rhomboids is shown by the inability to approximate the scapula towards the spine, that of the leva- tor anguli scapulae by inability to move the shoulder upwards. d. Paralysis of the Latissinius Dor si.—Isolated paralysis of this muscle, which is supplied by the subscapular nerves, is rare. In this dis- ease adduction of the arm against the trunk is diminished, the raised arm can be drawn downwards with less force, and the hand can with dif- ficulty be carried towards the buttocks. Rotation of the arm internally 30 DISEASES OF THE MOTOR NERVES. is very little or not at all impaired, since the subscapular and teres major muscles act vicariously in performing this movement. e. Paralysis of the Subscapular and Teres Major (internal rotators of the arm).—These muscles are also supplied by the subscapular nerves. The predominance of the external rotators causes the arm to assume a false position, the volar surface of the hand being directed anteriorly and externally. Hence, manipulations of the hand upon the opposite half of the head and body are rendered difficult or impossible, and the patients are unable to rotate the arm internally. f. Paralysis of the Infraspinatus and Teres Minor (external rotators of the arm).—This form of paralysis is more frequent than that of the internal rotators of the arm. The infraspinatus muscle is supplied by the subscapular nerve, the teres minor by the axillary nerve. If the arm is passively rotated internally, the patients are unable to ro- tate it outwards. If there is atrophy of the infraspinatus, the infraspi- nous fossa is abnormally flattened or depressed. The internal rotators generally eive the arm a false position, the ulna looking forwards. Paraly- sis of the infraspinatus interferes with drawing, writing, and the use of the needle, since these manipulations necessitate external rotation of the arm. g. Paralysis of the Extensors of the Back.—This disease is relatively frequent after typhoid fever; it is sometimes the result of traumatic or rheumatic causes. In paralysis of the lumbar extensors, the chest of the patient, in standing, is bent over backwards, while the lumbar spine presents lor- dosis. While the patient is sitting, on the other hand, the lumbar spine presents kyphosis, which disappears during dorsal decubitus. The patient has a waddling gait. If he is sitting upon the floor, and endeavors to assume an erect position, he first makes rotary movements of the trunk, then grasps the thighs with the hands, and gradually, as it were, climbs up his own thighs. If the muscles have undergone atrophy, the loins are notably smaller. In paralysis of the dorsal extensors, the spine presents paralytic kyphosis in the erect position, scoliosis if the paralysis is unilateral. These changes disappear in dorsal decubitus. h. Paralysis of the abdominal muscles is very rare. If it is unilate- ral, the umbilicus will be drawn towards the healthy side during each expiration. In bilateral paralysis, the patients walk with the body bent over forwards; in addition, there is lordosis of the lumbar spine. Expiratory movements (coughing, sneezing, micturition, defecation, etc.) are difficult or impossible. The abdomen appears distended. The treatment of the various forms of paralysis mentioned includes the application of electricity, baths, massage, and gymnastic exercises. In hopeless cases orthopaedic apparatus may be applied. 12. Paralysis of the Phrenic Nerve. 1. Paralysis of the diaphragm appears to be produced more fre- quently by direct lesions of the muscle than by diseases of the phrenic nerve. It is not uncommon in pleurisy and peritonitis, when the in- flammatory process extends to the serous lining of the diaphragm. The trunk of the phrenic nerve is affected most frequently by tumors and abscesses in the neck. Rheumatic paralysis of the diaphragm has been observed in a number of cases. Whether the paralysis occurring in DISEASES OF THE MOTOR NERVES. 31 lead poisoning and hysteria should be regarded as peripheral is more than doubtful. Oppolzer observed spontaneous paralysis of the dia- phragm at the period of puberty. In all these cases the paralysis sometimes affects the entire muscle, sometimes it is unilateral or even more circumscribed. 2. The symptoms are easily recognized, but it must be remembered that the respiratory disturbances may be absent during quiet breathing. Upon exposing the patient, it is found that the epigastrium and the hypochondria are retracted during inspiration, and protrude during expi- ration. If the hand is introduced beneath the thorax, it is not elevated by the diaphragm during inspiration, and the lower border of the liver is found to ascend during inspiration and descend during expiration. Continued loud speaking or singing produces dyspnoea and exhaustion ; pressing movements are also rendered difficult. * The patients get out of breath in walking, or going up-stairs, and the number of respirations may be increased to fifty per minute. Bronchial and pulmonary inflam- mations are extremely dangerous in this condition, because the power of coughing is impaired, so that dangerous congestion of the lungs and suffocation are apt to develop. In one case Eulenburg noticed abolition of the reaction of the phrenic nerve to the faradic current. Electrical examination must be confined to the trunk of the nerve, which may be reached on the outer side of the sternomastoid, immediately above the omohyoid muscle (vide Fig. 20). 3. The prognosis is always grave. Treatment consists mainly of appli- cations of electricity, in addition to removal of the causes. Both currents have been employed. One pole (cathode of constant current) is placed on the trunk of the nerve, the other on an indifferent spot (sternum, etc.), or on the hypoehondrium. Contraction of the diaphragm is shown by protrusion of the epigastrium, and entrance of air into the air passages, accompanied by a movement of hiccough. Passage of the current transversely through the diaphragm is not attended with much success. 13. Peripheral Paralysis of the Nerves of the Loiver Limbs. Peripheral paralysis of the nerves of the lower limbs is rare; paralysis in this locality is usually spinal or cerebral in its origin. a. Peripheral paralysis of the crural nerve has been observed in dis- eases and tumors of the lower part of the spine, hemorrhages near the cauda equina, inflammation of the psoas muscle and pelvic cellular tis- sue, tumors of the pelvis, dislocations and fractures of the femur, in- cised or gunshot wounds, after acute infectious diseases, etc. Paralysis of the quadriceps feinoris has been observed not infrequently in connec- tion with inflammation of the knee-joint. Paralysis of the crural nerve is shown by motor disturbances of the iliopsoas, pectineus, sartorius, and quadriceps femoris. Paralysis of the iliopsoas muscle is shown by inability to flex the thigh upon the abdo- men, that of the quadriceps femoris by inability to extend the flexed thigh. These muscles are also important in walking and in passing from the sitting to the eredt position, so that these movements are seriously interfered with when the parts are paralyzed. After paralysis of long standing, the muscles undergo atrophy, some- 32 DISEASES OF THE MOTOR NERVES. times to such an extent that the anterior surface of the thigh seems to be covered merely by the integument. Sensory disturbances, when present, are found upon the anterior and inner surface of the thigh and the inner surface of the leg (vide Figs. 22 and 23). If the cause of paralysis is situated very high, other sensory nerves may also be affected. In paralysis of the external cutaneous nerve, sensation is diminished or abolished upon the outer surface of the thigh down to the region of the knee. Sensory disturbances on the scrotum, lower part of the abdomen or loins must be attributed to Fig. 22. Fig. 23. Distribution of the cutaneous nerves of the lower limbs. After Henle. Fig. 22.—Anterior surface. 1, crural nerve; 2, external cutaneous nerve; 3, ilio- inguinal nerve; 4, lumbo-inguinal nerve; 5, external spermatic nerve; 6, posterior cutan- eous nerve; 7, obturator nerve; 8, saphenus major nerve; 9, communicans peronei; 10, superficial peroneal nerve; 11, deep peroneal nerve; 12, communicans tibialis nerve. Fig. 23.—Posterior surface. 1, posterior cutaneous nerve; 2, external cutaneous nerve; 3, obturator nerve; 4, posterior median cu- taneous nerve (peroneus nerve); 5, communi- cans peronei; 6, saphenus major nerve (crural nerve); 7, coinmunicans (tibialis; 8, nervus cutaneus plantaris proprius (tibialis); 9, plan- taris medius (tibial nerve); 10, plantaris late- ralis (tibial nerve). implication of the ilio-hypogastric, ilio-inguinal, lumbo-inguinal, and external spermatic nerves. The electrical reactions present no changes from the general rules. DISEASES OF THE MOTOR NERVES. 33 The nerve trunk can only be reached for a short distance immediately beneath Poupart’s ligament, but the muscles are more readily accessible to electrical exploration and treatment (vide Fig. 24). In galvanic ap- plications, the anode hould be applied to the loins, the cathode to the exit of the nerv< immediately beneath PouparPs ligament. b. Periphera paralysis of the obturator nerve is even rarer than that of the crural nerve; sometimes both nerves are paralyzed. Iso- Fig. 24. Crural nerve. Tensor fasciae latae. Obturator nerve. Obturator nerve Pectineus nerve Quadriceps femoris(com- mon point). Crural nerve. Adductor magnus. Rectus femoris. Adductor longus Crural. Vastus ext. Vastus int. Peroneal nerve. Gastrocnemius. Tibialis anticus Extens. digit, com- mun. long Soleus. Peroneal nerve. Peroneus longus riexor halluc. long. Tibial nerve. Peroneus brevis Extenc. halluc. long... Abductor digit, min. Extens. digit, com- mun. brevis Motor points of the nerves and muscles of the lower limb on the anterior surface. Dorsal interossei. lated paralysis of the obturator nerve has been observed after difficult labor and in obturator hernia. The motor paralysis affects all the adductors, the obturator externus, gracilis, and usually the pectineus, which is also supplied by the crural. The patients are unable to move the thigh towards the median line (par- alysis of the adductors). In sitting or lying, they are unable to cross the affected leg over the healthy one, or to turn over from the back upon the belly, or vice versa. External rotation of the thigh is also inter- fered with. 34 DISEASES OF THE MOTOR NERVES. Sensory disturbances are noticed upon the inner surface of the thigh as far down as the knee (vide Fig. 23). c. Peripheral paralysis of the gluteal nerves is shown by motor dis- turbances in the gluteal muscles, the obturator interims, pyriformis, and tensor fasciae latae. There is impairment of internal and external rota- tion, and abduction of the thigh. The patient cannot pass from a bent- over forward position to an erect position of the body. Walking and ascending stairs are interfered with, because it is the function of the ilio- psoas and gluteus maximus to fix the trunk upon the thigh and main- tain equilibrium, but on account of paralysis of the gluteus the iliopsoas gains the upper hand and draws the trunk forward. When atrophy of the muscles occurs, the buttock appears thin and flattened. The motor points are shown in Figs. 24 and 25. d. Peripheral paralysis of the sciatic nerve is the most frequent form of paralysis of the nerves of the lower limbs. This is owing to the long and superficial course of the nerve. According to the location of the lesion, the paralysis affects the entire nerve or individual branches, particularly the peroneal or tibial nerves. The paralysis is sometimes confined to a few of the muscles supplied by the peroneal nerve. Diseases of the lumbar spine, hemorrhages near the cauda equina, fractures of the pelvis or sacrum, fractures and dislocations of the thigh or leg, pelvic exudations and tumors, difficult labor, wounds, blows or falls in the region of the buttocks, removal of tumors, tight-bandaging, etc., are the chief traumatic causes of sciatic paralysis. It has been ob- served in the new-born after attempts at extraction. Zenker and Roth have described compression-paralysis of the peroneal nerve in potato- diggers who maintain a crouching or kneeling position for a long time. Sciatica is sometimes followed by paralysis of the nerve. Rheumatic paralysis is observed occasionally in individuals who are required to stand in cold water. Neuritic and hysterical paralyses of the sciatic have also been described. The posterior muscles of the thigh supplied by the sciatic nerve are least frequently paralyzed, and only when the lesion is situated very high. The muscles in question are the obturator internus, gemelli, quadratus, semitendinosus. semimembranosus, long head of the biceps (the short head is supplied by the peroneal nerve). In paralysis of these muscles, rotation and adduction of the thigh are impeded, and the patient is un- able to draw the leg against the posterior surface of the thigh, or to re- sist passive extension of the leg. The gastrocnemius (supplied by the tibial nerve) is able to effect slight flexion of the leg. As a matter of course, walking is interfered with to a considerable extent. Paralysis of the peroneal nerve, if complete, affects the tibialis anti- cus, extensor hallucis longus, extensor communis longus, the peronei, extensor digitorum brevis, and extensor hallucis brevis. The disease is easily recognized. The foot assumes the varo-equinus position, and the patient is unable to flex the foot or the first phalanges of the toes to- wards the dorsal surface. During the attempt to walk, the foot hangs downward so that the toes are dragged along the floor unless the limb is unusually flexed at the hip joint. When the foot comes in con- tact with the ground, it first touches with the tips of the toes and the outer edge of the foot. In isolated paralysis of the tibialis anticus, dorsal flexion and adduc- tion of the foot are interfered with. Dorsal flexion is effected vica- riously, in part by the extensor longus digitorum (the foot is abducted at DISEASES OF THE MOTOR NERVES. 35 the same time); the extensor hallucis longus also aids the paralyzed muscle, at the same time adducting the foot. But these muscles cannot assume fully the function of the tibialis anticus, the calf-muscles acquire the predominance, and the foot is drawn into pes equinus position. In isolated paralysis of the extensor longus digitorum, dorsal flexion and adduction of the foot are impeded. The first phalanx of the four outer toes cannot be extended. The function of the paralyzed muscle is performed vicariously by the tibialis anticus and extensor hallucis longus, but eventually the flexors undergo antagonistic contraction and the foot assumes pes varo-equinus position. In isolated paralysis of the peroneu* longus, adduction of the extended foot is impossible. At the same time the arch on the inner side of the foot is destroyed because the peroneus longus normally exerts traction on the cuneiform and scaphoid bones. Pes planus paralyticus is thus pro- duced. In walking, the patient first brings the outer edge of the foot in contact with the floor; he complains of pain in the external malleolus, and is quickly tired. In isolated paralysis of the peroneus brevis, pure adduction of the foot is impossible; this movement can only be effected if attended with dorsal flexion (contraction of extensor longus), or plantar flexion (contraction of peroneus longus). Peripheral paralysis of the tibial nerve affects the following muscles: gastrocnemius, soleus, plantaris, popliteus, flexor longus digitorum, tibi- alis posticus, flexor hallucis longus, flexor brevis digitorum, abductor hal- lucis, flexor brevis hallucis, adductor hallucis, interossei, and lumbricales. If all these muscles are paralyzed, plantar flexion of the foot is almost entirely abolished (effected slightly by the peroneus longus); plantar flex- ion and adduction of the toes are impossible. Predominance of the ex- tensors gives rise to pes valgo-calcaneus. In isolated paralysis of the gastrocnemius and soleus, plantar flexion of the foot is markedly impaired; it is performed to a certain extent by the peroneus longus and flexor longus digitorum. The calf-muscles also adduct the foot, so that when they are paralyzed the abductors also gain the upper hand. Hence pes calcaneus develops with a tendency to pes valgus. Paralysis of the tibialis posticus interferes with adduction of the foot and elevation of its inner surface, i. e., it favors the production of pes valgus. Paralysis of the flexor digitorum communis longus is shown by ina- bility to flex the second and third phalanges of the four outer toes. Flex- ion of the first phalanges is performed by the interossei, which also ex- tend the second and third phalanges. In paralysis’of the flexor hallucis longus, there is loss of plantar flexion of the last phalanx of the great toe. Paralysis of the interossei may give rise to the development of club-foot, from predominance of the extensor communis and flexor digitorum longus. The electrical reactions of the paralyzed muscles are similar to those so often mentioned. More or less marked atrophy and contracture de- velop after paralyses of long standing. Sensory disturbances are observed not infrequently; their distribution is shown in Figs. 22 and 23. Trophic changes have been described, particularly in paralysis of the trunk of the sciatic nerve. They consist of coldness, cyanotic color of the integument, rapidly developing decubitus over the malleoli, heels, 36 DISEASES OF THE MOTOR NERVES. buttocks, and trochanters, increased growth of hair, thickening of the nails, pemphigoid vesicles, etc. Paraesthesise have also been observed. The diagnosis of paralysis of the sciatic nerve is not always easy; it must be based on accurate anatomical and physiological knowledge, strict analysis of the individual symptoms, and careful electrical exploration. The prognosis is not always good; it depends on the causes of the dis- ease and the results of electrical exploration. The treatment consists chiefly in the application of electricity. Fig. 25. Glutseus max. Sciatic nerve. Biceps (long head)., Adductor mag. Semitendinosus. Peroneal nerve. Biceps (short head) Semimembranosus. Tibial nerve. Peroneal nerve Gastrocnemius (exter- nal head). Tibial nerve. Gastrocnemius (inter- nal head). Soleus. Flex. dig. comm. long. Flex, halluc. long. Tibial nerve. Motor points of the sciatic and its branches, the peroneal and tibial nerves. The motor points are shown in Figs. 24 and 25. In hopeless cases, the use of orthopaedic apparatus is indicated. b. spasm (hyperkinesis) of the motor nerves. 1. Spasm in the Distribution of the Facial Nerve. {Mimic Facial Spasm. Prosospasmus.) Spasms in the facial muscles are usually clonic, more rarely tonic. They may extend over the entire distribution of the facial nerve, or affect only individual muscles. DISEASES OF THE MOTOR NERVES. 37 a. Diffuse Clonic Facial Spasm, (Tic convulsif.) I. Etiology.—The disease occurs more frequently in males than in females, and is more common in advanced years than during childhood. It is sometimes the result of direct injuries to the facial nerve, sometimes it is a reflex effect of disturbances in other nerve tracts. In certain cases, a cold has been mentioned as the immediate cause of the disease. Other patients attribute it to injury. A number of cases have been reported in which the facial nerve was compressed or irritated by enlarged glands, diseases of the petrous portion of the temporal bone, exostoses, tumors at the base of the skull, aneurism of cerebral ar- teries, etc. The reflex variety of facial spasm occurs most frequently in painful diseases in the distribution of the trigeminus (diseases of the lids and eye- ball, painful dental affections, ulcerative processes in the nasal and buccal mucous membrane, neuralgia, etc.). Mimic facial spasm also develops not infrequently in diseases of the genital apparatus, or irritation of the intestinal mucous membrane by worms. Moreover, painful pressure points are sometimes found on the spine, wrist-joints, and other parts of the body, treatment of which occasionally exerts a magical effect upon the reflex facial spasm. There is no doubt that in some cases heredity plays an etiological part. But it must be remembered that the spasm is not always inherited as such, but that there is often merely a general neuropathic taint, manifested in the ancestors by hysteria, epilepsy, or other neuroses. In some patients the nervous disposition is acquired, particularly during the course of chlorosis. Mimicry is occasionally an etiological factor. Frequent “ making faces” may finally terminate in well-marked facial spasm. In a large number of cases no cause can be discovered. II. Anatomical Changes.—Nothing is known concerning the anatomical changes in this disease. The cases examined have given almost entirely negative results. III. Symptoms. —Mimic facial spasm consists of involuntary grimaces which occur in paroxysms. The patients suddenly wrinkle the brow, wink the lids, snuffle with the nose, and distort the whole face. The contractions are usually unilateral, rarely bilateral. They sometimes occur spontaneously, sometimes after physical or mental exertion. As a rule, they last only a few seconds; occasionally there are abortive attacks, in which a quick contraction passes rapidly over one side of the face. In some cases, only a few attacks occur daily; in others, twenty, thirty, or even more, in a single hour. Remissions and exacerbations are noticed, and depend chiefly upon the mental and physical condition of the patient. The twitchings generally cease during the night, but this rule presents exceptions. Some patients can voluntarily moderate the intensity of the contractions, but the will is powerless in the majority of cases. The palatal, digastric, and stylohyoid muscles are always, the auricular muscles and platysma inyoides are usually, unaffected. The twitching may predominate in certain of the facial muscles, and this may vary in different attacks. In very violent and obstinate cases, the spasm may extend to other groups of muscles, viz., to the tongue, neck, and limbs. The secretory and gustatory fibres of the facial nerve are unaffected. 38 DISEASES OF THE MOTOR NERVES. In a number of cases, crackling, ringing, or roaring has been heard in the ear during the spasms (spasm of the stapedius?). Pressure points should always be looked for. These are points which correspond to individual sensory nerves, and are very sensitive to pressure; the latter may suddenly abolish, more rarely intensify, the spasmodic attack. They may be found along the supra-orbital or infra-orbital nerve, on the mucous membrane of the nose or mouth, transverse or spinous processes of the cervical vertebrae, sternum, or intercostal spaces, wrist- joints, etc. Tic convulsif is unattended with pain, but some patients complain of a peculiar tired feeling in the affected muscles. The electrical reactions of the nerve and muscles are unchanged. The disease lasts months and years; in many cases for life. IV. Diagnosis.—The recognition of the disease is easy, but it is often difficult to ascertain its cause. V. Prognosis.—The disease is never dangerous to life. If the cause can be removed, the prognosis is usually favorable; if not, the disease is generally incurable. VI. Treatment.—Causal treatment requires the most careful atten- tion. In some cases, the extraction of a carious tooth has effected a rapid and permanent cure. In nervous individuals, we order nervines (potassium bromide, valerian, asafoetida, zinc, etc.); in chlorotic per- sons, iron preparations. If the disease is the result of cold, resort should be had to the use of baths, diaphoresis, alcoholic frictions, leeches be- hind the ear, etc. Pressure points should also be treated. Applications of the galvanic current may be made, the cathode being placed on an indifferent spot (sternum, etc.), the anode upon the pressure point. The current should not be too strong, and the sitting not prolonged beyond five minutes. The same treatment may be employed if the tic is associated with trigeminal neuralgia. If the latter is obstinate, neurotomy or neurec- tomy of the nerve affected by neuralgia sometimes proves successful. If there are no causal indications, narcotics may be injected subcu- taneously (I£ Magendie’s solution, £ syringeful; atropine, gr. : 3 iij., \ syringeful; strychnine, gr. iss. : 3 iij., i syringeful; curare, gr. iss. : 3 iij., syringeful). As a rule, better results will be obtained from the use of electricity, although great patience is requisite. The preference is generally given to the galvanic current. The anode is placed on the trunk of the nerve immediately in front of or behind the ear, the cathode upon an indifferent spot. The anode may also be applied stabile or labile to the individual muscles. Benedikt favors frequent changes of polarity. In diseases of the ear or base of the brain, the current may be passed transversely through the mastoid processes. In some cases, Erb and Berger advise the appli- cation of a large anode (head electrode) to the parietal bone,'particularly when the disease is the result of central causes, in order to reach the cortical centre of the facial nerve. Remak recommends galvanization of the cervical sympathetic, the anode immediately behind the angle of the lower jaw to the outside of the carotid artery, the cathode on an indifferent spot. The same author also obtained good effects from descending currents, i. e., anode on the central, cathode on the peripheral portion of the nerve. Frommhold recommended faradization of the muscles with currents of gradu- ally increasing strength. Various surgical operations have been performed to relieve the dis- ease. Thus, incision of the nerve and muscles has been performed. DISEASES OF THE MOTOR NERVES. 39 Stretching of the nerve has been done with apparently good results, but Bernhardt showed that the effect is only temporary. b. Diffuse Tonic Facial Spasm. This disease is rare and is usually the result of previous facial paraly- sis; less frequently it is an independent, primary affection. The side of the face is stiff and rigid, the lines and grooves are unusually deep, the face appears drawn towards the affected side, the eyebrow is elevated; rigidity of the cheek sometimes interferes with mastication. The disease has been treated by galvanization of the contractured muscles, faradiza- tion of the healthy facial muscles, introduction of wooden globes under the cheek on the affected side. c. Partial Tonic and Clonic Facial Spasm. Contractions of individual facial muscles occur in many otherwise healthy persons as soon as they become excited. In others contractions occur during mental and physical rest, in the lips, alae nasi, corrugator supercilii, frontalis, and even the auricular muscles. Contractions of the zygomatici cause a laughing expression (risus sardonicus). Rosenthal noticed isolated contractions of the palatal muscles. Practical significance attaches to spasm of the orbicularis palpe- brarum ; this is either tonic (blepharospasm) or clonic (nictitating spasm). The causes of both varieties are almost identical. In the ma- jority of cases they result from diseases of the eye (diseases of the con- junctiva and cornea, foreign bodies, and other ocular affections attended with pain). A bright light will sometimes produce blepharospasm in otherwise healthy individuals. It may also occur in trigeminal neuralgia and diseases of the nasal, buccal, and palatal mucous membrane, and the teeth. As a matter of course, the spasm is the result in such cases of reflex processes which are conveyed from the sensory branches of the trigeminus to the facial nerve. The spasm may also be produced by irritation in other sensory tracts, for example, the uterine, intestinal nerves, etc. The causes of certain cases are unknown. In blepharospasm the lids are suddenly and spasmodically closed; in some cases there is narrowing of the palpebral fissure. The spasm is al- most always bilateral, lasts several seconds or minutes, even hours, and then ceases for a longer or shorter interval. In certain cases the spasm continues for weeks and months, so that the patient is constantly unable to see. The attacks often occur spontaneously, often as the result of bodily or mental excitement or ocular irritation. Apart from the de- formity, the patients suffer from the fact that they may be suddenly rendered blind, in a mechanical manner, while walking the streets. The vigor of the contractions is usually so great that the lids cannot be for- cibly opened. Towards the close of the seizure, its duration may some- times be shortened by forcible separation of the lids. Pressure points are sometimes found, pressure on which causes sudden cessation of the spasm. Graefe distinguishes primary and induced pres- sure points; the former are present from the beginning of the disease, the latter develop during its course. These pressure points are observed most frequently along the supra- orbital, next along the infraorbital nerve, and also on the mucous mem- brane of the nose, mouth, palatal arch, on the spine, wrist-joints, etc. 40 DISEASES OF THE MOTOR NERVES. Blepharospasm sometimes gives rise to diffuse facial spasm, and even to spasm of more remote muscles, for example, on the back of the neck. Clonic spasm of the lids (nictitating spasm) is more frequent than ble- pharospasm, and in many individuals is merely a bad habit. It consists merely of winking movements. The remarks made concerning blepharo- spasm also hold good concerning this variety. The prognosis of both affections is not always good; the disease is gen- erally very obstinate, often incurable. The treatment is the same as that of diffuse clonic facial spasm. 2. Spasmodic Conditions of the Trigeminal Motor Branches. {Spasm of the Muscles of Mastication.) 1. The changes in question affect the temporal, masseter, and ptery- goid muscles. The spasm of these muscles is sometimes tonic, some- times clonic. In the former event, the muscular contractions recur so rapidly as to produce the impression of a permanent muscular contrac- tion; in clonic spasm, the individual contractions can be distinctly dis- tinguished from one another. In the majority of cases, the spasms are the result of central changes, not often of peripheral lesions. Exposure, injury to the nerve, and tri- geminal neuralgia have been mentioned as causes. A relatively fre- quent cause are diseases of the teeth (eruption of the molar and wisdom teeth), inflammations of the periosteum of the inferior maxilla or temporo-maxillary joint. Reflex spasms occur in children suffering from worms, after peri- pheral injury, and painful cicatrices. 2. Spasm of the muscles of mastication is almost always bilateral. In tonic spasms, the contracted inasseters and temporals protrude beneath the skin, and feel as hard as a board. The patients have very little or no power of drawing the lower jaw downwards or from side to side. As a rule, the mouth cannot be possibly opened by any amount of force which can be used with safety. This condition is known as tris- mus. Speech is difficult, and the patients are sometimes unable to take even fluid food into the mouth. Such conditions may last days and even weeks. The best known form of clonic spasm of the muscles of mastication is the chattering of the teeth, which occurs when the individual feels very cold; the movements then occur from above downwards. In some cases, lateral movements are produced (grinding of the teeth). The tongue,, gums, and mucous membrane of the mouth may be thereby injured. 3. Nothing is known concerning the anatomical changes. 4. The diagnosis is almost always easy. Tonic spasm is distinguished from ankylosis of the temporo-maxillary joint by the absence of the hard contraction of the muscles; in addition, the history of the disease is different. In doubtful cases, the patient may be anaesthetized with chloroform, whereupon the muscular spasm will subside, while the ankylosis persists. 5. The prognosis depends upon the etiology. G. Treatment should first be directed towards the removal of the causes. A subcutaneous injection of morphine into the cheek seems to be the most reliable method of relieving the spasm. Chloroform may be used in very violent and obstinate cases. Electricity may also be DISEASES OF THE MOTOR NERVES. 41 employed—the galvanic current- transversely through the masseters, at first with feeble currents, then gradually increased, and as gradually diminished. Benedikt recommends frequent changes of polarity. Strong faradic currents, especially the wire brush, afford good results in some cases. In chronic cases, the attempt has been made to gradually relieve the trismus by the introduction of wooden wedges of gradually increasing size between the rows of teeth. It may be necessary to nourish the patient by means of the oesophageal sound, through the nose, or by means of nutritive enemata. 3. Spasm in the Distribution of the Hypoglossal Nerve. Spasmodic conditions in the hypoglossal tract are shown by abnormal movements of the tongue; they are rare, more frequently central than peripheral, and usually have a clonic, more rarely a tonic character. We must distinguish between masticatory and articulatory hypoglossal spasms. The latter have been called aphthongia. This consists of attacks in which the tongue is moved involuntarily in all directions. In one of my cases, the tongue had been pushed against the teeth with such force that losses of substance occurred on the surface of the tongue. As a matter of course, speech and mastication are interfered with during the attacks. They occur in anaemic, nervous, and hysterical individuals, sometimes during trigeminal neuralgia or mimic flicial spasm. The hypoglossal spasm is sometimes primary, and the facial spasm develops later. Sensory disturbances have been observed upon the mucous mem- brane of the tongue, lips, and mouth. The treatment is similar to that of facial spasm. 4. Spasm in the Distribution of the Spinal Accessory. 1. Spasm in the distribution of the spinal accessory affects the sterno- mastoid and trapezius muscles. The spasm may be tonic or clonic, uni- lateral or bilateral, and affect one or both of the muscles mentioned. Some cases are undoubtedly rheumatic, others are traumatic in their origin; they may arise from over-exertion or lifting heavy weights. It is sometimes observed after infectious diseases (typhoid, puerperal fever, etc.). Or it may be the result of diseases of the spine (tubercu- losis, tumors, fractures, etc.). Reflex influences can sometimes be demonstrated, for example, teething in childhood, helminthiasis, ute- rine diseases, etc. It is not infrequently impossible to ascertain the cause, and many cases of supposed peripheral diseases are undoubtedly central in their origin. This is true of nervous and hysterical indi- viduals in whom spasm of the spinal accessory may alternate with or be followed by epilepsy, idiocy, or insanity. Central causes are directly demonstrable in certain cases. 2, In unilateral clonic spasm of the sternomastoid, the head is turned at each muscular contraction in such a manner that the chin looks toward the healthy side, and the mastoid process and lobe of the ear on the affected side are approximated to the clavicle. The con- tracted muscle is visible under the skin as a tense strand. If clonic spasm of the trapezius is present at the same time, the head is drawn further backwards and the shoulder upwards, so that the occi- put and shoulder are sometimes brought in contact. In certain cases, the contraction is irregularly distributed in the trapezius, so that more 42 DISEASES OF THE MOTOR NERVES. or less torsion of the scapula results. The contractions of the sterno- mastoid and trapezius may alternate with one another, the vigor of one may predominate over that of the other, or both may be synchronous and equal in power. In clonic spasm of both sternomastoids and trapezii, the symptoms vary according as the spasm occurs synchronously or alternately on the two sides. In the former event, the head performs nodding movements, but in the majority of such cases, other muscles of the neck are also implicated. This form occurs almost exclusively in children from the period of dentition to that of puberty. If the contractions occur alter- nately on the two sides, the head is wagged to and fro. The spasm is sometimes unilateral at first, and later spreads to the other side. The attacks occur spontaneously, or they are produced by bodily or mental excitement. They usually cease during sleep, but many patients complain that they interfere with falling asleep. The number and duration of the attacks are subject to great variation. Many patients complain of a peculiar feeling of tension or exhaustion in the affected muscles, which may become intensified into severe pain. Pressure points are not frequent. Other groups of muscles often take part in the spasm, for example, those of the eyes, face, throat, shoulder, limbs, and in rare cases even general convulsions are produced. Romberg described oedema and paresthesia of the arms as the result of pressure on the vessels and nerves in implication of the scaleni. The disease may last weeks, months, years, even a lifetime. Tonic spasms of the sternomastoid and trapezius muscles produce permanent abnormal positions of the head (caput obstipum spasticum). The position which will be assumed by the head, according as one or both muscles are affected unilaterally or bilaterally, is evident from pre- vious considerations. The condition is sometimes congenital, or develops in early child- hood, and thus often gives rise to secondary changes in the spinal column. The spine presents a convex curve toward the healthy side, the individual vertebrae appear smaller on the diseased side, and even the growth of the face may be retarded. The tonically contracted muscles are often hypertrophied, their antagonists atrophied. 3. The Prognosis of tonic and clonic spasms of the spinal accessory nerve is not always good. As a rule, there is no chance of recovery unless the cause can be removed. Many patients have been driven to suicide by their obstinate disease. 4. Treatment must first be directed to the removal of the cause of the disease. The chief local method of treatment, apart from subcu- taneous injections of morphine, curare, atropine, or strychnine, is the ap- plication of electricity—constant stabile current, anode to the affected nerve or muscle. Busch obtained very rapid and successful results from the use of the actual cautery. Orthopedic apparatus and gym- nastic exercises may become requisite. Excision of the nerve and myotomy of the muscles are hardly justifiable. 5. Spasm of the Neck, Scapula, and Arm. These muscles are supplied by the cervical and brachial plexuses. The spasms may be tonic or clonic, unilateral or bilateral, and affect a single muscle or various groups of muscles. We will refer to only a DISEASES OF THE MOTOR NERVES. 43 few varieties. The etiology, prognosis, and treatment are the same as in spasm of the spinal accessory nerve. a. Spasm of the obliquus capitis inferior.—Contraction of this muscle simply rotates the head in a horizontal line. In unilateral clonic spasm there are constant rotatory movements towards the affected side; in bilateral spasm there is rotation in both directions (rotatory tic). In fixation of an object the patients must hold the head between the hands in order to prevent the movements. In tonic spasm the head assumes a constant abnormal position to one side. b. Spasm of the splenius capitis.—This muscle draws the head backwards; at the same time the face turns towards the contractured side, the chin is depressed and approaches the shoulder on the same side. The contracted muscle projects beneath the anterior border of the trapezius, the sternomastoid appears flaccid on the affected side, tense Fig. 26. Position of the head in spasm of the right splenius capitis muscle upon the other side. Tonic spasm of the muscle is much more frequent than the clonic form. c. Spasm of the rhomboid has hitherto been observed only in the tonic form. On contraction of this muscle, the lower angle of the scapula is elevated, its inner edge approaches the spine, and its direction changed so that it runs from below internally, upwards externally. The contracted muscle can be felt, and often seen in the interscapular space. Elevation of the arm to the vertical position meets with resistance. d. Spasm of the levator anguli scapulce produces elevation of the scapula, especially its upper inner angle, and bends the head back- wards. The contracted muscle is visible in the supraclavicular fossa. 6. Spasm of the Respiratory Muscles. a. Clonic spasm of the diaphragm is called hiccough, singultus. Upon sudden contraction of the diaphragm in this condition, the in- 44 DISEASES OF THE MOTOR NERVES. spiratory current of air enters the air passages with a loud noise, but is suddenly checked by closure of the rima glottidis. The ailment is more frequently central than peripheral in its origin, and is especially fre- quent in nurslings. In rare cases it is the result of irritation of the trunk of the phrenic nerve by mediastinal tumors, aneurisms, pericar- ditis and pleurisy. Singultus sometimes occurs in diaphragmatic pleurisy. It develops more frequently in a reflex manner, for example, in overloading of the stomach, ingestion of too hot or too cold food, dis- eases of the intestines or liver, biliary or renal calculi, uterine diseases and peritonitis. It is especially noteworthy that prostatic diseases give rise not infrequently to hiccough. Among the forms produced by central causes are included those cases which occur in diseases of the brain and meninges, in hysterical and anaemic individuals, during severe diseases, for example, after losses of blood, cholera, dysentery, cancerous cachexia, malaria. The attacks may be so severe that sixty to eighty contractions of the diaphragm occur in a minute. The patients then suffer from dyspnoea, talking and eating are interfered with, and pain is felt in the epigastrium and insertion of the diaphragm. Pressure points are sometimes noticed in remote parts. The attacks may last hours, days, weeks, even months, sometimes almost uninterruptedly, sometimes with free intervals. They usually cease at night, but interfere with falling asleep. The disease sometimes resists all methods of treatment. We should endeavor to remove the causes and divert the attention of the patient. In several of my cases, rapid recovery was produced by constantly count- ing aloud at a uniform rate of rapidity. Vigorous straining, with closed rima glottidis, passage of the oesophageal sound, or injection of cold water into the oesophagus until suffocation threatens, have also been re- commended. It is best to employ narcotics subcutaneously in the region of the diaphragm. In a colleague, get. 72 years, I obtained rapid success from the hourly administration of $ Potassium bromide, gr. viiss.; ext. belladonnae, gr. -J-. Vigorous cutaneous irritants—sinapisms or the faradic current—to the diaphragmatic region have also been tried. Re- covery has been effected in some cases by galvanic or faradic treatment of the phrenic nerve. Finally, the lower part of the thorax has been compressed and the head firmly pressed against the chest a number of times, in order to produce vigorous expiratory movements. b. Tonic spasm of the diaphragm, as the result of peripheral causes, has been observed after a severe cold or after intercostal neuralgia, mus- cular and articular rheumatism. As the result of central disturbances of innervation, it has been observed in tetanus, epilepsy, and hysteria. The disease is extremely dangerous, and will inevitably result in death unless speedily relieved. The symptoms are easily recognized. The lowermost part of the thorax appears very dilated, but takes no part in the respiratory move- ments. The lower border of the right lung, and occasionally the heart, are lower than normal. The epigastrium is very prominent, and the normal respiratory movements of the diaphragm cannot be felt on pal- pation of the hypochondria. The upper part of the chest moves vigor- ously. The patient complains of dread of suffocation, has a cyanotic appearance, a small, hurried pulse, and is hardly able to talk in a loud tone. If rapid relief is not brought, death occurs from suffocation. The treatment consists of the application of strong cutaneous irri- DISEASES OF THE MOTOR NERVES. 45 tants—hot compresses to the region of the diaphragm, mustard poultices, the faradic brush. We may give a subcutaneous injection of morphine or chloroform by inhalation; in addition, faradization or galvanization of the phrenic nerve. Appendix. Numerous other spasmodic conditions of the respiratory muscles have been described, but their combinations are so manifold that they cannot be described from a general standpoint. This group includes spasms of sneezing (ptarmus s. sternutatio convulsiva), of yawning, crying, laugh- ing, shouting. As a rule, the causes are central, as in hysteria and or- ganic diseases of the nervous system, or the result of reflex irritation. 7. Spasm of the Abdominal Muscles. Westphal reported a case of clonic spasm of the abdominal muscles, which was relieved by the actual cautery. I observed a similar case in an hysterical boy of nine years. Tonic spasms of central origin occur in meningitis, tetanus, etc. 8. Spasm in the Muscles of the Lower Limbs. Spasms rarely occur in the muscles of the lower limbs. They may be tonic or clonic, and sometimes extend to all the muscles of the lower limbs. We cannot enter into a detailed description, but, with regard to the function of the various muscles, refer the reader to the section on paralysis. 9. Cramp. 1. Cramp is a term applied to a tonic muscular spasm associated with pain. It often lasts only a few seconds, and at all events, its duration is very brief. The best known form is spasm of the calves of the legs. This is a painful, tonic contraction of the muscles, which project with sharp con- tours, and are very tender on pressure. Nevertheless, the muscles are not contracted ad maximum. After the muscles are relaxed, at the end of a few seconds or minutes, a peculiar feeling of tension and exhaustion not infrequently is left over, and the muscles remain for a long time very tender on pressure. Ecchymoses are sometimes formed during the cramp. It is especially apt to occur at night, sometimes recurs very rapidly, dis- turbs sleep, or produces such violent pain as to give rise to syncope. Cramps also develop in other muscles, but particularly in the lower limbs. Schultz claims to have found increased electrical excitability of the affected muscles. 2. Among the causes of such conditions may be mentioned: a. Over- exertion of the muscles, for example, cramps in the calves after long walks, dancing, etc.; b. Nutritive disturbances, for example, in cholera, as the result of losses of fluid (according to Erb, this also occurs in dia- betes mellitus); c. Circulatory stasis, for example, the cramps in the calves in varicose veins and pregnancy. 3. Treatment consists of rest on the back (although many persons are relieved by hyperextension of the muscles), subcutaneous injections of morphine, friction or kneading of the muscles, inunctions of alcoholic solutions. 46 DISEASES OF THE SENSORY NERVES. B. DISEASES OF THE SENSORY NERVES. a. NEURALGIAS. 1. Trigeminal Neuralgia. (Facial Neuralgia, Prosopalgia, Tic Douloureux.) I. Etiology.—Among all the forms of neuralgia, that of the trigem- inus is the most frequently observed. This is owing to its long course, the situation of many branches in narrow, bony canals, and the super- ficial position of its terminal ramifications. It is most frequent in women, and from the twentieth to fiftieth years. It is very rare in childhood, more frequent in old age. The processes of the period of involution, i. e., the fortieth year, on the average, in males, the menopause in female, favor the development of the disease. It is said to be more frequent in cold than in warm climates. According to some writers, individuals belonging to the well-to-do classes are predis- posed to the affection. With regard to Goettingen, I may state that it is very common among the laboring classes. The causes of the disease may be divided into five groups, constitu- tional, infectious, toxic, local, and reflex. Hereditary factors are active in many cases. Sometimes we observe families in which several generations have suffered from trigeminal neuralgia, sometimes there is an hereditary nervous taint, so that different members of the family suffer from hysteria, epilepsy, psychopathies, or neuralgias. In some individuals the nervous disposition is acquired as the result of excesses, mental and bodily over-exertion, worry. Trigeminal neuralgia develops not infrequently in anaemia and chlorosis, which have been produced by vital losses, such as occur after pro- tracted diarrhoea, rapidly following pregnancies, and excessive lactation. Among the infectious forms the most important are those which are the result of malaria. In such cases the supraorbital nerve is almost always affected. The neuralgic attacks generally occur daily at the same time, more rarely they pre- sent a tertian or quartan type. But we have seen many typical cases of inter- mittent supraorbital neuralgia in individuals who were entirely free from malaria. The disease may also occur in typhoid fever and recent syphilis. In the majority of cases, however, syphilitic trigeminal neuralgia is the result of exostoses, gummata, inflammation, etc., at the base of the skull or within the bony canals. Toxic trigeminal neuralgia has been observed in lead and mercurial poisoning. The disease is very often the result of direct injury to the nerve, for example, as the result of cold, injury, inflammation of the periosteum, unskilful extrac- tion of the teeth, caries and exostoses of the teeth, eruption of the wisdom teeth. Gross has called attention to obstinate neuralgia in toothless old people in whom the empty alveoli are gradually filled with bony substance, which irritates the alveolar nerves. Trigeminal neuralgia may be the result of diseases of the ear, inflammation of the frontal sinuses with retention of secretion, and straining of the eyes. The causes of the neuralgia must often be sought in the narrow bony canals through which the branches of the nerve pass. Compression and irritation of the nerve may be brought about by inflammation, thickening, and deposits in these localities, in many cases by simple distention of the blood-vessels. This danger is so much greater the narrower the bony canal, and the more numerous the blood-vessels situated within it. The causes of neuralgia are sometimes found at the base of the skull, for example, inflammations, exostoses, tumors or aneurisms which press upon the trunk of the trigeminus. Reflex trigeminal neuralgias include those which occur in uterine, ovarian, and intestinal diseases. The causal connection cannot be doubted in those cases DISEASES OF THE SENSORY NERVES. 47 in which the neuralgia disappears as soon as the primary disease is relieved.. Trigeminal neuralgia sometimes develops after injury of remote nerve tracts. II. Anatomical Changes.—Little is known concerning the anatomicaL changes in trigeminal neuralgia. Unusual redness and succulence of the affected nerve branches have been observed in some cases; in others, prolifera- tions or calcification of the neurilemma, fatty and atrophic changes in the nerve- fibres or cells of the Gasserian ganglion. In Cruveilhier’s celebrated case, nodules of carcinoma were -found in the neurilemma of the peripheral branches of the facial nerve and the inosculating trigeminal fibres. III. Symptoms.—Trigeminal neuralgia is almost always unilateral,, and, according to Canstatt, is more frequent on the right side (?). Bi- lateral neuralgia is extremely rare, and occurs only in the supraorbital nerve. It is equally rare that the neuralgia affects first one, then the other trigeminus. In a larger number of cases the disease spreads from one branch to a second or third. The ophthalmic nerve is affected most frequently, particularly the supraorbital branch. Next in order of frequency is supra maxillary neur- algia, that of the infraorbital nerve being the most frequent in this, class. The inframaxiliary branch is least frequently affected; neuralgia of the mental or alveolar branches is the most frequent. The entire nerve is rarely affected, and then only when the neuralgia is the result of intracranial causes, or of lesions affecting the trunk of the nerve. It is also rare to find all the ramifications of a single branch affected. The more the neuralgia is confined to the finer twigs, the more we are justified in assuming peripheral causes. Some branches exhibit very little tendency to neuralgia; this is particularly true of the auriculo-temporal nerve. The neuralgic attacks not infrequently develop suddenly, in other cases they are preceded by prodromata. The latter almost always con- sist of paraesthesise : a feeling of stiffness, pricking, formication in the affected parts. The neuralgia itself is characterized by attacks of pain, which some- times have a boring or burning, sometimes a lancinating character. Some patients experience a sensation as if the nerve were being drawn out slowly, or as if the bones were slowly crushed. The pain is some- times situated deeply, sometimes superficially. Some patients state that the pains radiate from the centre towards the periphery; much more rarely they pursue an opposite course. All patients agree that the pains are atrocious, and render them incapable of doing anything, so that very few are able to keep on with their occupation. The pain al- ways extends along certain tracts of the nerve. In some cases it radi- ates into more remote parts, such as the back of the neck, and the ex- tremities. The attack usually lasts only a few seconds; in abortive attacks a single, lightning-like spasm of pain is experienced. The number of attacks within an hour may be very considerable. In other cases attacks of variable duration occur at irregular intervals dur- ing the day. In intermittent neuralgia the attack recurs at a definite hour in the day, usually in the morning, or at noon, and disappears at the end of a certain time. In very rare cases it begins with a chill and ends in a sweat. In many cases no immediate cause of the individual attacks can be demonstrated. In others they occur after exposure to a draught, on slight contact with the integument of the face, upon touching certain definite points, eating hard or cold articles of food, etc. Some patients 48 DISEASES OF THE SENSORY NERVES. suffer after mental or physical excitement, if the eye is annoyed by a bright light, or the ear by shrill tones, on yawning, sneezing, laughing, often at the mere thought of an attack. In the interparoxysmal period many patients feel entirely free from pain, others are tormented by more or less violent painful sensations. Pressure points constitute a frequent, though by no means constant symptom. These are points which are situated in the affected nerve tracts, and are either the only parts which are painful on pressure or pain more than other parts. These points are sometimes present during the attack alone, sometimes during the interparoxysmal period. Pressure upon them may provoke a neuralgic paroxysm; strong pressure some- times relieves the pain, while gentle pressure increases it. Trousseau showed that pressure points are sometimes found upon the spinous processes of the second and third cervical vertebrae, or the ex- ternal protuberance of the occipital bone. Vaso motor disturbances are very often present during the attack. The affected half of the face, or a circumscribed nerve tract is very red, the arteries, especially the temporals, are unusually dilated and pulsate vig- orously, and the cutaneous veins are also dilated. The skin has a puffy, peculiar shining appearance, is unusually warm, and covered with per- spiration. The beginning of the attack is preceded by ansemia of the skin. The conjunctiva is often injected, and this may even terminate in oedema (chemosis). The lachrymal secretion is increased, the eyeball seems to protrude from its socket. The nasal mucous membrane secretes an increased amount of mucus, which is sometimes tinged with blood. In rarer cases the secretion of mucus is diminished. There is sometimes an increased secretion of saliva, and the gums may present swelling, aphthous excoriations, and hemorrhages. In rare cases the patients complain of perverse gustatory sensations or auditory disturbances. The trophic changes are closely allied to the vaso-motor disturbances. An excessive development of the panniculus adiposus sometimes forms upon the affected side, and even the bones may undergo hyperplasia. In other cases atrophic processes are observed, likewise herpes, acne, lichen, and erysipelas on the affected parts. The hairs may become rough, fractured, suddenly grow gray or fall out. In some cases we notice an alternation of pigmented with white (unpigmented) hairs, the latter hav- ing developed during the individual attacks of neuralgia. Among the rarer phenomena are ophthalmia neuroparalytica, which has been at- tributed to functional disturbances of certain trophic fibres in the tri- geminus. Glaucoma and, according to Bull, iritis and chorioiditis have also been observed after trigeminal neuralgia. The sensibility of the integument of the affected nerves is not infre- quently changed. It is generally heightened at the beginning of the disease, later it is diminished. Sensory disturbances are sometimes no- ticeable only during the attacks. involuntary contractions of the facial muscles are sometimes observed during the seizures, so that tic douloureux is complicated with tic convul- sif. In certain cases contractions occur in the muscles of the neck and limbs; in Sinklar Holden's case there were widespread tonic muscular spasms. The duration of the disease may vary from a few days to a number DISEASES OF THE SEKSOKY NEKVES. 49 of years; it sometimes lasts a lifetime. It disappears occasionally during intercurrent diseases, or alternates with neuralgia of other nerves. Eelapses are frequent, and sometimes recur after the lapse of years. Some patients suffer from profound melancholy, and may even be driven to commit suicide. Others become shy, because noisy surround- ings provoke an attack. Still others lose strength from loss of sleep or refusal to take food (because mastication gives rise to a paroxysm). IV. Diagnosis.—The diagnosis is easy, if we bear in mind the par- oxysmal character of the pain, its distribution, and the presence of pain- ful points. 1. Ophthalmic neuralgia. The pain is situated in the upper lid, the frontal re- gion as far as the vertex, the eyeball and its socket, the base of the nose and its integument as far as the tip, the anterior portion of the nasal cavity (vide Fig. 27). Fig. 27. Distribution of the trigeminus to the face. a. Supraorbital neuralgia: pain in frontal region, upper lid, and root of nose. Pressure points ; the most constant one at the supraorbital foramen or notch, less constantly on the upper lid (palpebral point), the parietal eminence (parietal point), the inner angle of the eye or cartilage of the nose; sometimes the entire nerve tract is sensitive. b. Ciliary neuralgia. Most violent pain in the eyeball; a symptom of many ocular diseases. 2. Supramaxillary neuralgia. Pain situated in lower lid, cheek, upper lip, lateral part of nose, region of malar bone, and anterior part of forehead, upper row of teeth, gums, and nasal cavity. a. Infraorbital neuralgia. Situation of pain: lower lid, cheek, upper lip, lat- eral part of nose; sometimes upper teeth, and mucous membrane of cheek; if the nervus subcutaneus malse is involved, in region of malar bone, and ante- rior part of forehead. Pressure points : most constantly at infraorbital foramen, more rarely on the upper lip (labial point), malar region (malar point), alveolar processes of upper jaw (alveolar point), rarely on the gum. 50 DISEASES OF THE SENSORY NERVES. b. Alveolar neuralgia is confined to the alveolar processes of the upper jaw. 3. Inframaxillary neuralgia. Situation of pain: region of chin and lower jaw, raucous membrane of cheek, inferior alveolar process, tongue, external ear, and forehead. a. Mental neuralgia. Pain in the chin; pressure point at the mental fora- men. b. Lingual neuralgia (glossalgia). Pain in one-half of the tongue; sometimes unilateral coating and increased thickness of the tongue. Painful point at the side of the tongue; sometimes increased salivation, and involuntary movements of the tongue. c. Inferior alveolar neuralgia. Pain in lower alveolar processes. d. Aurieulo-temporal neuralgia (very rare). Pain in external auditory canal, concha, and temple. V. Prognosis.—This depends in great part upon the etiological fac- tors. Not all cases in which no cause can be ascertained present a favorable prognosis. If heredity plays a part in the etiology, we must expect great obstinacy and frequent relapses of the disease. The longer the neuralgia has lasted, the slighter are the chances of recovery. The prognosis of intermittent neuralgia is favorable. VI. Treatment.—The causal treatment varies, of course, with the etiology. In intermittent neuralgia we may give quinine (gr. xv., two hours before the expected attack, for three days in succession); if qui- nine is not tolerated, it is replaced by Fowler’s solution (ten drops t. i. d., after meals). If the disease is the result of exposure, we should or- der diaphoretics, give salicylic acid internally (gr. v]j. every hour, until tinnitus aurium is produced), and cover the parts with wadding. Syphi- litic cases are treated with iodine and mercury, anaemic cases with iron, etc. In the symptomatic treatment of trigeminal neuralgia we regard qui- nine and arsenic as the most important internal remedies. Quinine often does not act until given in very large doses (gr. lxxv. or more). Among other internal remedies may be mentioned: Aconit. (3 Aconi- tin.,gr. f; ext. hyoscyam., gr. xv.; pulv. liq., q. s. u. ft. pil. No. 50. D. S. One to two pills morning and evening); Colchicum(B Tinct. colchici, 3 iij.; tinct. aconiti, 3 iss. M. D. S. Fifteen drops t. i. d.); Acid sali- cylic., gr. xv. every hour; potassium iodide, gr. x. t. i. d.; 3 Argent, nitrat., gr. xv., argill. albas, q. s., f. cum aq. dest. q. s. pil. No. 100. D. S. One pill t. i. d., after meals; Auro-natrium chloratum, gr. v.; ext. dul- camar., gr. 1., f. pil. No. 50. D. S. One pill t. i. d; phosphorus, zinc, mercurial and copper preparations; opium, belladonna, strychnia, chloral hydrate, butylchloral ($ Butylchloral hydrat., gr. lxxv.; glycerin., 3 v., aquae, § iv. M. D. S. One tablespoonful every five to ten min- utes), potassium bromide ( 3 i.—iij. in a single dose), tinct. gelsemii (live to twenty drops t. i. d.), amyl nitrite (five drops by inhalation until the face is reddened), etc. Among external remedies the most important is electricity, then fol- lows the subcutaneous injection of narcotics. As a rule, the galvanic current is indicated. Feeble currents should be employed; its strength may be gradually increased during the sitting; the stabile application is preferable; the anode is placed upon the affected parts, especially upon pressure points; the cathode, to the back of the neck or indifferent part. The sitting should not last longer than three to five minutes, but sometimes two to three sittings daily are advisable. Some authors recommend descending currents, i. e., the anode central, the cathode on the peripheral parts. In intra-cranial disease, the current is passed transversely through the skull. DISEASES OF THE SENSORY NERVES. 51 The faradic current may be employed with the wire-brush, but this can rarely be applied to the face, on account of the severe pain produced thereby. M. Meyer showed that it sometimes acts very well when ap- plied to the back of the neck. The remedies which may be employed subcutaneously are morphine (gr. iss. : 3 i., 1 syringeful), atropine (gr. ss. : 3 i., £ S}n-ingeful), strychnine (gr. iss. : 3 i., syringeful), chloroform, and ether. The patients themselves should not be allowed to make injections of mor- phine, since they are apt to fall into the morphine habit. It is a note- worthy fact that patients suffering from neuralgia often present a remark- able tolerance to narcotics. For example, Trousseau recommended as much as 3 iiss. of opium or 3 i. of morphine daily. Among other external methods of treatment may be mentioned : aquapunc- ture, inunctions of veratrine, belladonna, morphine, chloroform, ether, croton-oil collodion—linear cauterization along the nerves—blisters, leeches, chloroform poured on cotton and placed behind the ear, and compression of the nerves. In desperate cases, surgical operations may be resorted to, such as ligature or compression of the carotid, nerve stretching, neurotomy, and neurectomy. Compression of the carotid was successfully employed by Earle, Gerhardt, and Seifert. Nussbaum and Patruban have had good results from ligature of the artery. Nerve stretching is the mildest operation, but the most uncertain in its effects. Nor can neurotomy be regarded as a radical operation. Neurectomy offers the greatest chances of suc- cess, but relief can only be expected with certainty if the operation has been performed on the central side of the site of the neuralgia. Ex- perience has shown, however, that the neuralgia is sometimes relieved for a longer or shorter period, even if the affected part was not removed. A. Wagner collated 134 cases of excision of the nerve in trigeminal neuralgia, and found: Recovery for years 25 times (18.7$). “ “ months 18 “ (13.4$). Operation unsuccessful .... 9 “ (6.6$). Death 6 “ (4.5$). Result unknown 24 “ (18.0$). Relapses 52 “ (38.8$). 2. Cervico- Occipital Neuralgia. (Occipital Neuralgia.) I. Etiology.—Cervico-occipital neuralgia affects branches of the cervical plexus (four upper cervical nerves). The occipitalis major is most frequently affected* in rarer cases the other sensory branches, viz., occipitalis minor, auricularis magnus, subcutaneus colli inferior, and supraclavicular. Under unfavorable circumstances, accordingly, the pain may extend over the back of the neck and occiput, the posterior surface of the ear, the anterior and lateral parts of the neck, scapula, and upper part of the chest. The disease is more frequent in women, from the 20th to 50th years of life. Heredity is rarely demonstrable; the affection is often found in anaemic, hysterical, and nervous individuals. 52 DISEASES OF THE SENSORY NERVES. Exposure is mentioned as the cause of many cases; in others it is the result of injury. Compression of the nerves by swollen lymphatic glands, tumors, or dilatation of the vertebral arteries is found occasionally. In some patients, the disease is the result of affections of the vertebrae or cervical cord (tuberculosis, osteoma, gumma, periostitis of the vertebrae, meningitis, hemorrhage, etc.). In a few cases it is associated, perhaps, with catarrhal disease of the middle ear. Several cases have been observed after infectious diseases, or as a reflex symptom of intestinal affections, perhaps also of the eruption of the wisdom teeth. Inter- mittent forms dependent on malarial infection are much rarer than the corresponding forms of trigeminal neuralgia. It is sometimes radiated from trigeminal neuralgia. Obstinate cases occur with relative fre- quency in uraemia. II. Symptoms.—The symptoms of pure occipital neuralgia consist of paroxysms of pain which start in the upper part of the back of the neck, and radiate along the occiput to the vertex (vide Eig. 27). The pains are sometimes excruciating, and a dull sensation of pain and peculiar feeling of stiffness in the neck often persist during the inter-paroxys- mal period. The movements of the head are often interfered with. The duration and number of the paroxysms are subject to great varia- tions. The attacks sometimes occur spontaneously, sometimes follow excitement, vomiting, coughing, careless rotation of the head, pressure on the back of the neck, etc. Both nerves are not infrequently affected, one more markedly than the other. The pains sometimes radiate into remote nerve tracts. This occurs with relative frequency into the trigeminus (anastomosis with the frontal nerve) in the temples, more rarely into a larger part of the trigeminal distribution, or into the brachial plexus. The most constant pressure points are the occipital point (between the mastoid process and first cervical vertebra, corresponding to the exit of the occipital nerve) and the parietal point (upon the parietal emi- nence). More remote painful points may be found on the spinous pro- cesses of the cervical vertebrae. Slight contact Avith the painful points often produces neuralgic attacks. The entire course of the nerve is often tender on pressure. The affected parts are almost always hyperaesthetic at the beginning of the disease. Vaso-motor disturbances are often present, and are probably produced by sympathetic nerve fibres, since they are not infrequently associated with pupillary changes. These symptoms consist of redness of one-half the face or the ear, injection of the conjunctiva, sometimes lachrymal and nasal hypersecretion, unusual Avarmth and feeling of increased heat in the face; the pupils are generally narroAV, more rarely dilated. Some patients complain of difficulty of hearing and ringing in the ears. Trophic changes have been rarely described. Rosenthal noticed alopecia, Romberg observed small sAvellings, which developed upon the occiput during the attack and disappeared after its cessation. Rheumatic neuralgia is attended not infrequently Avith swelling of the cervical lymphatic glands. During violent seizures, tonic or clonic muscular spasms may develop in the face, limbs, or throughout the entire body. Violent vomiting during the attacks has also been described. The duration of the disease varies from a few weeks to several months or years. Incurable cases are much rarer than in trigeminal neuralgia. DISEASES OF THE SENSORY NERVES. 53 Neuralgias of the other nerves belonging to the cervical plexus are readily rec- ognized by the following symptoms: Neuralgia of the occipitalis minor gives rise to pain in the lateral part of th occiput as far as the ear; painful point behind the mastoid process at the exit o! the nerve beneath the skin (vide Fig. 27). b. Neuralgia of the auricularis magnus causes pain on the posterior aspect of the concha, above the mastoid process and over the parotid; painful point a little above the middle of the neck, between the trapezius and sternomastoid, and also upon the concha. c. Neuralgia of the subcutaneus colli inferior : pain in the lower, middle, and anterior parts of the neck; painful point, same as in neuralgia of auricularis. d. Neuralgia of the supraclavicular: pain in the acromial region, shoulder, and upper part of the chest. III. Diagnosis.—The diagnosis is easy, but it must not be forgotten that these neuralgias sometimes precede for years a latent affection of the cervical vertebrae and spinal cord. Hence these parts should be carefully examined in obstinate cases. IV. Prognosis.—This is much more favorable, as a general thing, than that of trigeminal neuralgia, but depends chiefly on the etiology. V. Treatment.—The treatment, in general, must follow the prin- ciples laid down in the consideration of trigeminal neuralgia. The chief remedies are quinine internally, morphine subcutaneously, and the galvanic (more rarely the faradic) current transversely through the upper part of the nucha. In recent cases we may employ flying blisters and warm applications. In obstinate cases surgical interference may be resorted to. 3. Phrenic Neuralgia. 1. The occurrence of neuralgia of the phrenic nerve has been reported a num- ber of times by the older authors, and more recently by French writers. 2. The disease is said to occur either as an independent affection or during the course of diseases of the pleura, pericardium, myocardium, aorta, liver, spleen, kidneys, stomach, intestines, and peritoneum. Under such circumstances it may take a prominent part in the symptomatology, and, in angina pectoris, for example, may be the cause of the overpowering pains. In addition, exposure, injury, hys- teria, and epilepsy have been mentioned as causes. 3. The chief symptom is pain, located chiefly at the base of the chest, but oc- casionally running along the entire course of the nerve. The pains increase paroxysmally, but not infrequently persist in a less degree; they may be unilateral or bilateral. The pain often radiates into remote nerve tracts—into the arms, neck, chin, nucha, but most constantly into the shoulders. Pressure points are found in the following localities : a. anterior points of in- sertion of the diaphragm, especially on the ninth rib; b. posterior points of inser- tion of the diaphragm, especially the lowermost rib; c. lateral part of the neck upon the scalenus anticus; d. on the sternum at the level of the second and third intercostal spaces; e. over the spinous processes of the second and fifth, rarely the sixth cervical vertebrae We usually find disturbances of the respiratory movements: jerky, superficial, painful inspiration, singultus, 3rawning, etc. Deglutition may also be interfered with. Great terror and a feeling of impending dissolution are sometimes present. Relapses may occur. 4. The diagnosis is difficult. The disease cannot always be distinguished from an affection of the diaphragmatic pleura or the peritoneum. 5. Treatment: Mustard poultices, leeches, cups, blisters, injections of mor- phine, electricity. 4. Cervico-Brachial Neuralgia. I. Etiology.—The brachial plexus is derived from the four lower cervical and first dorsal nerves. Neuralgias of this plexus are not rare, and occur somewhat more frequently in men than in women. 54 DISEASES OF THE SENSORY NERVES. Some eases are the result of exposure, a much larger number are due to injury. The traumatic causes include fall, blow, incised or gunshot wounds, fracture or dislocation, formation of callus, aneurism of the aorta or subclavian artery, swollen glands in the axilla, neuromata or other tumors, tuberculosis or cancer of the spine, phlebectomy, wounds, injuries to the little fingers, amputation-neu- romata. Allied to this form is that variety of neuralgia produced by over-exer- tion of the muscles, as in playing piano, sewing, etc. Brachial neuralgia sometimes follows articular alfections of the elbow, hand, or shoulder. It is sometimes radiated from trigeminal or cervico-occipital neur- algia, angina pectoris, diseases of the liver and spleen. According to Salter, it may be a reflex effect of dental irritation. Chlorosis, anaemia, hysteria, malaria, and lead poisoning appear to be the starting-point of the disease in some cases. II. Symptoms.—The disease is almost always unilateral. Bilateral neuralgia has been reported as the result of cancer of the spine and of over-exertion in gymnastic exercises. The right arm seems to be affected more frequently than the left. As a rule, a number of the cutaneous nerves are affected simultane- ously, and motor disturbances are generally present. The chief symptom is pain, which may be shooting, boring, burn- ing, etc. Pains of unusual intensity have been observed after gunshot wounds of the nerves (causalgia). The patients are often unable to localize the pains. They sometimes radiate into the neck, occiput, face, or intercostal spaces. In many places the pains are constant, but pre- sent paroxysmal exacerbations. The paroxysms are especially apt to occur at night after going to bed, or after a careless movement of the arm. Some patients experience relief from carrying the arm in a sling or supporting it with the other hand; others are relieved by extension of the limb. The painful points vary according to the affected nerve tracts; they are not constant, and sometimes entirely absent. In radial neuralgia, the pressure points are: The point of flexion of the nerve in the arm, and the dorsal surface of the forearm immediately above the wrist. In ulnar neuralgia: A point between the internal condyle and olecranon, and the anterior surface of the forearm immediately below the head of the ulna. In median neuralgia, the painful points are: The bicipital sulcus, the fold of the elbow, the radial side of the volar surface of the forearm immediately over the head of the radius. Other pressure points are: The supraclavicular and axillary fossae, lower angle of scapula, and the points of exit of the various cutaneous nerves. The more remote pressure points are the spinous processes of the four lower cervical and two or three upper dorsal vertebrae. Circulatory changes (pallor or redness of the skin) are not infre- quent. There is sometimes an abnormally profuse formation of sweat. Among the trophic changes may be mentioiied herpes zoster, urti- caria, eczema, pemphigus, increased growth of hair, changes in the nails, glossy skin, etc.; the muscles often undergo atrophy. Motor disturbances are frequent, and consist of fibrillary twitehings, a feeling of stiffness, paresis, paralysis, more rarely tonic and clonic spasms. The patients often complain of a feeling of rigidity and stiffness in the muscles, and the fingers are permanently extended like claws. DISEASES OF THE SENSORY NERVES. 55 Gross muscular power may be better retained than fine manipula- tions, such as writing, sewing, etc. Parsesthesiae (feeling of coldness, formication) are frequently men- tioned. III. Diagnosis.—The diagnosis of brachial neuralgia is easy, but the recognition of the etiology and site of the disease may be very difficult or even impossible (vide Figs. 10 and 11). IV. Prognosis.—This depends almost entirely upon the etiology. The neuralgia generally disappears if the cause is removed. V. Treatment.—The treatment follows the same general principles that have been laid down in the consideration of trigeminal neuralgia. The local measures include: carrying the arm in a sling, absolute rest, subcutaneous injections of morphine, and electricity. The galvanic cur- rent is generally employed; stabile application, anode upon the painful points or the affected nerve trunks, or a descending current along the nerves. Nerve stretching is said to have been successful in some cases. Neur- ectomy should not be performed, as a rule, because it gives rise to paralysis. 5. Dorso-intercostal Neuralgia. (Intercostal Neuralgia.) I. Etiology.—The intercostal nerves, after leaving the interverte- bral foramina, divide into a posterior (dorsal) and anterior (intercostal) branch. Neuralgia occurs most frequently in the latter, rarely in the dorsal branches alone, somewhat more frequently in both. The site of the pain is very extensive, since the dorsal branches sup- ply the integument of the back down to the crest of the ilium, the inter- costal branches supply the lateral and anterior surfaces of the chest and abdomen as far as the symphysis pubis. The first dorsal nerve also passes into the brachial plexus, and supplies the inner surface of the arm. Intercostal neuralgia is more frequent in women than in men, and from the age of twenty to fifty years. Anaemia, chlorosis, and nervous- ness possess a still greater etiological significance than in many other neuralgias. Exposure and traumatism are mentioned as frequent causes. The traumata include: a fall, blow, fracture of the ribs and unfavorable de- velopment of callus, tuberculosis of the ribs, neuromata and other tumors, pressure of aneurisms on the spine; tuberculosis, cancer, periostitis, syphilis of the vertebrae or spinal meninges, etc. Intercostal neuralgia is sometimes the result of diseases of the respir- atory organs, heart, stomach, intestines, liver, or spleen. It is associated not infrequently with pleurisy and pulmonary phthisis, and also with nervous affections of the heart; on the other hand, cardiac neuroses are apt to develop after an attack of neuralgia. Intercostal neuralgia has also been known to develop after gastralgia, or painful affections of the liver and spleen. It sometimes develops during convalescence from severe diseases, particularly typhoid fever. Malaria is a not infrequent cause. Intercostal neuralgia may also appear as one of the effects of lead 56 DISEASES OF THE SENSORY NERVES. poisoning, as a reflex symptom of uterine or ovarian disease, and as a, radiated symptom in trigeminal, occipital, and cervico-bracliial neur- algia. II. Anatomical Changes.—Very little is known in this regard. Thickening and hypersemia of the neurilemma, degeneration of the nerve fibres, and neuromata have been observed in a few cases. The disease is not infrequently a true neurosis, which does not present any anatomical changes. III. Symptoms.—Intercostal neuralgia is commonly unilateral; cases of bilateral disease are much rarer. It occurs more frequently on the left side. This is attributed to the fact that the venous blood on the left side passes in a roundabout way through the vena hemiazygos to the inferior vena cava, so that stasis and compression of adjacent structures are more likely to happen on this side. As a rule, two or three adjacent intercos- tal nerves are affected at the same time. The fifth to ninth intercostal nerves are involved most frequently. The pain may occur in paroxysms, or may persist constantly in a milder degree. It may be so violent and obstinate as to deprive the patient of sleep. The pain is described as burning, sticking, lancinat- ing, etc. It sometimes extends half-way around the thorax, sometimes is especially violent in circumscribed localities. It often radiates into the arm. If the disease is bilateral, the patients experience the sensa- tion of a constricting band around the thorax. Coughing, sneezing, deep respirations, loud talking, etc., produce paroxysms of pain or inten- sify existing pains. On this account the patients often speak in a low tone, breathe superficially, and sometimes look like asthmatic individuals. Slight pressure on the skin may intensify the pain; firm pressure not in- frequently relieves it. The patients sometimes assume a bent position, the spine usually presenting a convexity towards the healthy side. There are three principal painfhl points: one immediately adjacent to the spine, corresponding to the exit of the nerve from the interverte- bral foramina (vertebral point), the other at the middle of the nerve where the nervus perforans lateralis ramifies in the lateral part of the thorax (lateral point), and a third along the edge of the sternum (ster- nal point) or on the rectus abdominis, where the anterior perforating nerve makes its exit. Pressure points are also found not infrequently on the spinous processes of the dorsal vertebrae. Cutaneous hyperesthesia is-often found in the distribution of the affected nerve, sometimes diffusely, sometimes in circumscribed spots; anesthesia is observed more rarely, and usually in old cases. Trophic disturbances are often present, herpes zoster being the most frequent. The neuralgia may precede or follow the ‘zoster. If zoster occurs without neuralgia (generally in children), it must be assumed that only the trophic fibres are diseased, and that the sensory fibres have escaped. AVoaker noticed foul-smelling perspiration during the attacks. The course and duration of the disease depend on the causes. In a number of cases it is followed by hysteria or cardiac neuroses. IV. Diagnosis.—The recognition of the disease is easy. In rheuma- tism of the muscles of the chest, the muscles themselves are sensitive to pressure, and the pain is constant. In pleurisy, other changes in the respiratory apparatus are present. Inflammation of the ribs gives rise to a visible swelling. In making a diagnosis, Ave should not be satisfied until the etiology is established. DISEASES OF THE SENSORY NERVES 57 V. Prognosis is unfavorable only when the disease is produced by incurable lesions. VI. Treatment.—The treatment is causal and local. The latter as in other neuralgias : morphine subcutaneously, and the galvanic, more rarely the faradic, current. The current should be strong, stabile, the anode to the painful points, or a descending current along the affected nerves. In other respects the treatment is similar to that of trigeminal neuralgia. Nussbaum recently performed nerve stretching, but the re- sults Avere not permanent. Appendix. Neuralgia of the Mammary Gland (Mastodynia) is a variety of intercostal neuralgia, since the breast is supplied by the second to sixth intercostal nerves, in addition to the supraclavicular nerves. Neuralgic affections of the breast occur almost exclusively in women. It hardly ever develops before puberty, usually from the sixteenth to the thirtieth year, rarely later, Ansemia, chlorosis, hysteria, and nervousness not infrequently form the basis of the disease. In some cases it is attributed to injury, uterine affections, protracted lactation, and menstrual dis- turbances. Nodular indurations are sometimes found in the gland, and often disappear with the cessation of the neuralgia. Mastodynia is often bilateral; according to some writers it is more frequent on the left side. The patients complain of a violent burning or lancinating pain which increases paroxysmally and sometimes lasts several hours. Vomiting may occur at the height of the paroxysms. The slightest contact with the skin in- creases the pains, and their intensity is also increased, as a rule, shortly before menstruation (congestion of the breast ?). The patients often experience a sensa- tion of tension and weight in the nipple. The pain is either diffused over the en- tire gland or it is localized in certain points. It often radiates into the neck, shoulders, arms, and back. Pressure points are not constant or characteristic. The nipple is generally very sensitive to pressure, often also circumscribed parts of the gland. Painful points are also found on the spinous processes of the lower cervical and upper dorsal (especially the second and fifth) vertebrae. A secretion of milk or a colostrum-like fluid has been observed in a few cases after each paroxysm of pain. Alfter observed herpes zoster after mastodynia. The disease may last many years and drive the patient to despair. The diagnosis is usually easy. Inflammatory conditions are associated with cutaneous changes and elevated temperature : malignant growths, which may produce similar pains, present a constant growth. The prognosis is not always favorable. Treatment,—The breast should be kept elevated. Inunction with narcotic ointments. Cooper recommended: B Extract. Belladonnse, Cerat. Cetacei aa§ ss. M. D. S. Externally. Subcutaneous injections of morphine, electricity. Due attention should be paid to anaemia or other predisposing conditions. As a last resort the breast may be extirpated. 6. Lumbo-Abdominal Neuralgia. Lumbo-abdominal neuralgia affects the short nerves of the crural plexus—ilio- hypogastric, ilio-inguinal, lumbo-inguinal, and external spermatic, a. The ilio- hypogastric nerve is distributed to : the integument of the hip and upper part of the liypogastrium. 0. Ilio-inguinal nerve : integument of the mons veneris and tensor fasciae latae muscle, c. Lumbo-inguinal nerve : median part of the groin and thigh half-way down. d. External spermatic nerve: scrotum or labium majus and inner surface of the thigh. As a rule, several or all of these nerves are affected at the same time. The pain is generally felt in the integument of the loins as far as the buttocks, the hy- pogastrium, mons veneris, scrotum (or labium majus) and the inguinal region. Among the causes mentioned are: exposure, diseases of the spine and meninges, 58 DISEASES OF THE SENSORY NERVES. pelvic exudations or tumors, and flexions of the uterus. The neuralgia is more frequent on the left side. The pains possess the ordinary neuralgic character. Pressure points are found along the spine (lumbar point), in the middle of the crest of the ilium (iliac point), on the scrotum, labium, occasionally on the cervix uteri. The neuralgia may be associated with contraction of the cremaster muscle, priapism, discharge of semen, leucorrhoea, and vesical tenesmus. The treatment is the same as in other neuralgias. 7. Crural Neuralgia. 1. Crural neuralgia is a rare affection. It is observed most frequently among the laboring classes in males, in whom exposure and over-exertion are not infre- quent causes. It may also be the result of injury : compression by exudations around the spine, psoas and pelvic organs, pressure of the uterus or swollen lym- phatic glands in the pelvis and groins, aneurism of the crural artery, inguinal her- nia, luxation of the femur, stab and gunshot wounds, etc. Seeligmueller claims that sprain of the ankle joint often gives rise to neuralgia of the saphenus major nerve. Crural neuralgia sometimes follows sciatica. 2. The pains extend along the inner surface of the thigh to the knee, and fol- lowing the course of the saphenus major nerve, may pass along the inner sur- face of the leg to the great toe. The neuralgia is sometimes confined to a single cutaneous branch. The pains are increased on movement of the limb, and are often more severe at night. They occasionally radiate into more remote regions, particularly into the loins. The pressure points are: a. Crural point, below Pou- part’s ligament, corresponding to the exit of the crural nerve; 6. Anterior thigh point, at the exit of the saphenus minor through the fascia lata; c Knee point, inner surface of the knee joint; d. Plantar point, immediately in front of the ankle; e. Toe point, at the base of the big toe. Hypersesthesia is often, anaesthesia is rarely present. Some patients complain of formication, coldness, and a feeling of stiffness. Vaso-motor or trophic distur- bances are rare. 3. The treatment, apart from causal treatment, is the same as that of sciatica. 8. Obturator Neuralgia. I Obturator neuralgia possesses more of a surgical interest, because it is an im- portant sign of incarceration of herniae in the obturator foramen. Pains then develop upon the inner surface of the thigh as far as the knee, associated with numbness, formication, and usually with inability to adduct the thigh (because the motor fibres of the nerve have also been compressed). The treatment consists in reposition of the hernia. 9. Neuralgia of the External Cutaneous Nerve. The pains extend along the outer surface of the thigh as far as the knee. The disease is generally associated with crural neuralgia, and rarely exists alone. 10. Sciatica. (.Ischialgia. Malum Cotunnii.) I. Etiology.—Neuralgias of the sciatic nerve are very common. They are more frequent in men than in women, exceptional in child- hood, and develop, as a rule, between the ages of twenty and sixty years. Anaemia, chlorosis, and hysteria possess much less etiological import- ance than in neuralgias of other nerves. Exposure to cold and wet, and injury, on the other hand, are the most frequent causes of the disease. Traumata affecting the sciatic nerve include: tumors and inflammations of DISEASES OF THE SENSOEY NEEVES. 59 the meninges, with compression of the sciatic nerve; tuberculosis, cancer, gum- ma, exostoses, and periostitis of the vertebrae, curvature of the spine, pelvic in- flammations and tumors, flexions of the uterus, compression by the pregnant uterus, difficult labor and compression by the child’s head, distention of the rec- tum with faeces or foreign bodies, dislocation or fracture of the femur, exostoses on the bones of the lower limbs, sciatic hernia, fall or blow on the buttocks, con- stant sitting and riding, heavy lifting; incised or gunshot wounds; neuromata and other tumors with pressure on the nerve; aneurism of the abdominal aorta and popliteal artery, etc. Sciatica is sometimes associated with constitutional diseases, for ex- ample, gout. It sometimes precedes diabetes mellitus and locomotor ataxia, probably as the result of central causes. Certain cases are the result of infectious diseases, viz.: malaria, syphilis (without the formation of gummata), gonorrhoea, typhoid fever (particularly during convalescence). In rare instances it is the result of toxic influences, for example, in lead and mercury poisoning. Whether hemorrhoids and checked sweating of the feet give rise to sciatica has not been determined with certainty. Climatic and meteorological conditions are not devoid of influence in this disease. Some English and German writers report an unusual fre- quency of the disease in certain localities. It is known to every expe- rienced physician that cases of the disease are more frequently observed during cold seasons in which there are rapid changes of temperature. II. Anatomical Changes.—These may be entirely absent, even if the disease has lasted a long time. In other cases liyperaemia of the nerve, varicose dilatation of its blood-vessels, swelling and increase of the connective tissue, atrophy and fatty degeneration of the nerve fibres have been observed. Josset recently reported a case in which an obsti- nate sciatica was cured by puncture of the nerve sheath and evacuation of half an ounce of serum. III. Symptoms.—As a rule, sciatica is unilateral, though Ilasse main- tained that it is not so infrequently bilateral as is generally believed, but that the pain on one side may be comparatively slight, and therefore overlooked. The disease sometimes begins on one side and then passes to the other, sometimes it is bilateral from the start, particularly in dis- eases of the meninges or spine. The pain may affect the entire distribution of the nerve, or be con- fined to individual branches (generally the posterior cutaneous, occa- sionally the plantar nerve). In the former event the pain extends over the buttock, posterior surface of the thigh, the entire leg and foot, with the exception of their inner surface (vide Figs. 22 and 23). As a rule, the pains are constant, but their intensity increases in paroxysms, which may assume an intermittent character, even when pro- duced by organic lesions. They are described as burning, tearing, stick- ing, boring, etc. As a rule they run from above downwards, rarely in the opposite direction. The paroxysms often develop spontaneously, in other cases they are produced by an incautious movement of the limb, slight pressure, laughing, sneezing, etc. In one of my patients unusu- ally violent paroxysms occurred at the period of menstruation. As a rule, the paroxysms subside so much more quickly the more quiet the patient keeps. Some patients, on the other hand, are relieved while walking about, or firmly compressing the sciatic nerve. Vomiting sometimes occurs at the height of the paroxysm. Tonic or clonic twitchings are noticed occasionally, and the heel may be drawn 60 diseases of the sensory nerves. against the buttock. The pains radiate not infrequently into the sacral region or the distribution of the crural nerve. Sciatica may also be as- sociated with intercostal neuralgia. Pressure points may be entirely absent, in other cases they are incon- stant. The nerve is sometimes tender on pressure along its entire course. Among the most frequent painful points are : a, a point along the sacrum at the level of the posterior superior spine of the ilium; b, lower border of gluteus maximus at the exit of the nerve from the sciatic foramen; c, immediately be- hind the trochanter major; d, middle of the posterior surface of the thigh, cor- responding to the exit of the posterior cutaneous nerve; e, bend of the knee (tibial nerve); /, immediately below the head of the fibula (peroneal nerve); g, behind the malleoli; h, several points on dorsum of foot or the calf. The sacral plexus is sometimes found to be tender on pressure when examined per vaginam or rectum. Changes in the color of the skin and trophic disturbances are gener- ally absent. In very rare cases mention is made of abnormal redness of the skin, increased heat and diaphoresis, increased growth of hair, out- break of herpes zoster and furuncles. Sensibility may be intact, but hypersesthesia or anaesthesia has been observed in a number of instances. The patients complain not infre- quently of paraesthesiae: a feeling of coldness, pricking, burning, formi- cation, stiffness. Emaciation of the muscles with secondary paretic symptoms is not infrequent in chronic sciatica, and is often the result of disuse of the limb. But marked atrophy sometimes develops very early and rapidly, and has been attributed by Landouzy to neuritic changes in the sciatic. In one case Graves observed hypertrophy of the muscles. The patellar tendon reflex was unchanged in all of my cases. The patients often assume a peculiar position. They generally lie upon the healthy side, with the thigh drawn up and the knee bent, in order to avoid stretching the nerve. They avoid walking altogether or tread upon the floor very carefully, favoring the limb as much as possi- ble. Many patients complain of violent pain while sitting, and are com- pelled to assume a recumbent position almost constantly. Increased bodily temperature is sometimes observed at the beginning of the disease. The patients often complain of constipation, associated with increasing violence of the paroxysms of pain. Braun shoived that the urine not infrequently contains sugar. Sciatica may run its course in two to six weeks, but is more often chronic. Cases have been known to last more than thirty years. In rare cases spontaneous recovery ensues at the end of years. There is al- ways a great tendency to relapses. IV. Diagnosis.—The diagnosis is easy, inasmuch as the pains often run along the exact anatomical course of the disease. It may be mistaken for: a, coxitis, which is excluded by the charac- teristic position of the body, pain on rotation of the limb or on com- pression against the acetabulum; b, psoitis, in which a characteristic position is also noticeable; c, muscular rheumatism, the pain is irregu- larly distributed, and is produced particularly by pressure on the mus- cles; d, hysterical joint affections, in Avhich a diagnosis can often be made only after prolonged obser\’ation. V. Prognosis.—This varies according to the etiology of the disease. VI. Treatment.—Apart from causal treatment, the leg should be DISEASES OF THE SENSORY NERVES. 61 kept quiet, the food should be easily digestible, and daily evacuation from the bowels secured. The entire limb should be rubbed every morn- ing and evening with Stokes* liniment: Iji 01. terebinthin., Aq. communis aa 3 xiv. Vitelli ovi i. 01. lini 3 iss. F. linimentum. and the limb then wrapped in cotton batting; iodide of potassium ( 3 iij. : § vij., one tablespoonful t. i. d.) should be given internally. This treatment will suffice in many cases. I have seen good and permanent results in a number of cases from change of air. Electricity justly plays a prominent part in treatment, although I have seen its application followed by an aggravation of the symptoms in a number of fresh cases. The galvanic current is usually preferred: large electrodes, a strong current, anode stabile to the painful points, or a descending stabile current, or successive galvanization of small, consecutive stretches of the nerve. Benedikt introduced one pole into the rectum, and placed the other upon the sacrum. Ciniselli recom- mended the constant application of zinc and copper plates, connected by a me- tallic wire. Some authors recommend the use of the faradic current, either as the electric brush or moxa. Great benefit may be derived from baths of all kinds. Among other methods of treatment may be mentioned : a. Derivatives : cups, blisters, moxa, actual cautery, aquapuncture, subcutaneous injection of nitrate of silver, alcoholic inunctions, inunctions with veratrine or croton oil, etc. b. Narcotics: morphine or atropine subcutaneously, belladonna in ointment or endermically, chloroform and chloral hydrate by enema, etc. c. Antirheumatics : aconite, colchicum, potassium iodide, salicylic acid, etc. d. Specifics: turpen- tine, arsenic, quinine. Tinct. gelsemii, 5-20 drops t. i. d., had a very rapid effect in several of my cases. Neuber recently recommended osmic acid subcutaneously in all kinds of neuralgia. In my own hands, this remedy (gr. viij. : 3 iij., a half- syringeful subcutaneously) gave no results in a large number of cases, and many patients complained of severe, sometimes very protracted pain at the site of in- jection. Among the surgical remedies may be mentioned massage and nerve stretching. Nerve stretching has recently been performed as a blood- less operation, the limb being flexed as strongly as possible upon the ab- domen. In one case I obtained temporary good effects from this plan. 11. Spermatic Neuralgia. In spermatic neuralgia, attacks of paiu occur in the testicles and epididymides, and extend along the seminal duct to the loins. The testicles and epididymides are tender on pressure, and are sometimes swollen. The pain may be so violent that the patient is covered with cold sweat, and suffers from chattering of the teeth, attacks of syncope, convulsions, and vomiting. The left testicle is most frequently affected. The disease often develops at the period of puberty. The patients are often pale, nervous individuals, who have practised masturbation or indulged in sexual excesses. In other cases, the disease has been attributed to sexual con- tinence. Injury, exposure, and varicocele are also regarded as causes. Inter- 62 DISEASES OF THE SENSORY NERYES. mittent neuralgia, which disappears after the administration of quinine, is some- times observed. The majority of German writers believe that the disease is an affection of sym- pathetic fibres in the testicles. The treatment consists of elevation of the testicle by means of a suspensory, inunctions with belladonna ointment, subcutaneous injections of morphine, luke- warm baths, electricity, iron, quinine, arsenic, or potassium bromide. Castra- tion has been performed in obstinate cases. Appendix. A number of other neuralgic affections, which cannot easily be localized, may develop in the external genitals and perineal region. They are usually the result of cold, injury, onanism, and sexual excesses. We may briefly mention : a. Neuralgia of the penis and glans penis: attacks of pain in the penis or glans, sometimes associated with priapism, involuntary discharge of semen, and disturbances of micturition. b. Neuralgia of the scrotum (or labia majora). c. Neuralgia of the urethra. d. Ano-vesical neuralgia: spasm of the sphincters of the x’ectum and bladder, with hypersesthesia (more rarely anaesthesia) of the perineum. e. Ano-perineal neuralgia. 12. Coccygodynia. This term is applied to attacks of pain in the coccygeal region, which increase on sitting, pressure, walking, and bodily exertion. It almost always occurs in women, and is attributed to a fall, injury, delivery, more rarely to a cold. In the majority of cases, the disease is probably not a neuralgia, but the result of organic changes in the coccyx. Seeligmueller produced rapid recovery in an obstinate case by the application of the faradic current. As a rule, surgical interference is necessary : subcutaneous separation of all the tendons and muscles inserted into the coccyx, or removal of the bone itself. 13. Neuralgia of the Joints. 1. This disease occurs generally in anaemic and hysterical women, more rarely in robust individuals or in men. Exposure, injury, acute diseases, violent emo- tions, diseases of the digestive tract and genital apparatus are mentioned as causes. 2. The affection is characterized by paroxysmal pain in the joints. The hip or knee joints are generally, other joints are rarely affected ; sometimes the small joints, for example, of the fingers are affected. As a rule, only one joint is involved. The pains often extend beyond the articular region proper. During the par- oxysm, the integument over the joint may present redness, heat, and swelling, but these symptoms generally disappear when the pain subsides. The skin is often very sensitive to slight pressure, while vigorous pressure is often well tolerated. Muscular twitchings may occur during the attack, or the patient per- manently assumes an abnormal position of the limb, which is usually kept in a position of extension (in joint inflammations the limb is usually flexed). Pres- sure points are found not infrequently over the joints. If the disease lasts a long time, contracture and atrophy of the muscles may ensue. The disease may last for years. In cases of marked hysteria the prognosis is not very good. 3. The treatment must be partly moral; we must endeavor to persuade the patient to use the limb. In addition, we may order nervines, iron,'quinine, nar- cotics, sea-bathing, the faradic and galvanic current, etc. 1. Anaesthesia. 1. Preliminary Remarks.—Anaesthesia is the term applied to all morbid processes in the sensory nerve tracts which give rise to DISEASES OF THE SENSORY NERVES. 63 diminution or complete loss of sensation. This may occur in all kinds of sensory nerves (cutaneous, muscular, visceral, etc.), but we will here discuss cutaneous anaesthesia alone. The sensory cutaneous nerves convey two principal forms of sensa- tions, viz.: tactile sensibility, and general sensations. Tactile sensibility includes: a. Simple tactile sensibility, i. e., the pure sensation of contact. b. The sense of pressure. c. The sense of location. d. The sense of temperature. General sensation includes the sensation of pain and electrical sensi- bility, also the feeling of tickling, itching, and other sensory processes which are coupled with pleasure or pain. The methods of examination require skill and care, and the patient must pos- sess a certain amount of intelligence and power of observation. It is best to have the patient assume a comfortable, recumbent posture during the examina- tion, and to blindfold his eyes. He should be clearly in- formed as to the stages of the examination. To determine the simple sense of contact the skin is slowly and carefully touched with the tip of the finger, or the head of a pin, and the patient directed to say whether he experiences a tactile sensation or not. The article em- ployed should possess approximately the same temperature as the skin, since otherwise a tactile sensation may be mistaken for one of temperature. In addition, the skin is touched with smooth, rough, and woolly substances, the character.of whose surface must be described by the patient. In examination of the sense of pressure, the limb upon which the examination is made should be placed on a firm base, since otherwise the sense of pressure would be esti- mated, not by the cutaneous nerves, but by the resistance over- come by the muscles. The simplest method is that of cover- ing the integument with a disk of wood, and then placing coins upon it at regular intervals. Eulenburg devised for this purpose a barsesthesiometer, which consists of a rod movable by means of a spring, and which at the same time moves the index on a dial plate. The numbers on the dial plate indicate in grammes the amount of pressure requisite to push the index to the number in question (Fig. 28). Kaumler and Aubert found that the following were the minimum amounts of pressure which could be felt: Fig. 28. Barsesthesiometer. Forehead, Temple, Dorsum of hand, Forearm, Fingers, Chin, Abdomen, Nose, Finger Nails, 0.04-0.05 gm. 0.002 grams. 1.0 0.005-0.015 gm. Dohrn found that the smallest increments of weight which could be detected, if the original weight were one gm., were as follows : Third phalanx of the fingers, 0.499 gm. Fold of the knee Dorsum of the foot 0.5 “ Dorsum of the hand 1.156 “ Second phalanx of the finger.. 0.771 “ First “ “ “ 0.82 “ Forearm Sternum 3.0 “ Leg 1.0 “ Umbilical region 3.5 “ Palm of hand 1.018 “ Back Eulenburg found by means of his baraesthesiometer that the following differ- ences in pressure could be detected : 64 DISEASES OF THE SENSORY NERVES. Forehead, Lips, Dorsum of tongue, Cheeks, Temple, Phalanges of fingers, Forearm, Hand, Arm, ■4?-^ In examining the sense of locality, two factors must be considered, viz., the proper localization of a stimulus, and the recognition of the tactile circle. To determine the former, an irritant is applied to some part of the skin, and the patient (with closed eyes) directed to describe the situation of the point of irrita- tion. The measurement of the tactile circles is made by means of compasses or Sieveking’s aesthesiometer. The former is an ordinary pair of compasses with blunt tips, the separation of which from one another may be read off in milli- metres (vide Fig. 29). The aesthesiometer is composed of a brass rod. divided into millimetres, to one end of which is fixed a vertical arm, provided with a sharp tip, while a second one may be moved to and fro. In using the instrument (Fig. 30), both tips should be applied at the same time, and with uniform pres- sure. The peripheral boundaries of a tactile circle are found at those places at which the tips of the aesthesiometer are no longer felt single, but double. Their size depends upon the age of the individual, being less in childhood. Landois furnishes the following table of measurements in an adult, and a boy of twelve years. Fiq. 29. Fig. 30. Sieveking’s aesthesiometer. Adult. Boy. Mm. Mm. Tip of the tongue.... 1.1 1.1 Third phalanx of finger (volar). 2.3 1.7 Lips 4.5 3.9 Second phalanx of finger (volar) 4 5 Third “ “ “ (dorsum) 6.8 3.9 4.5 Tip of nose 6.8 4.5 Head of metarcarpal bones (vo- lar) 6.8 4.5 Dorsum of tongue ) q n Metarcarpus of thumb f 6.8 Great toe (plantar) .11.3 6.8 Second phalanx of finger (dorsal) 11.3 9.0 Cheek 11.3 9.0 Lids 11.3 9.0 Hard palate (middle) .. 13.5 11.3 Skin over malar bone (anteri- orly) 15.8 11.3 Metastarsus of great toe (plan- tar) 15.8 9.0 Hirst phalanx of finger (dorsal) 15.8 9.0 Head of metarcarpal bones (dorsal) 18.9 13.5 Inner surface of lips 20.3 13.5 Compasses. Adult. Boy. Mm. Mm. Skin of malar bone (pos- teriorly) 22.6 15.8 Forehead (below) .22.6 18.0 Heel (behind) .22.6 20.3 Occiput (below) .27.1 22.6 Dorsum of hand .31.6 22.6 Chin (below) .38.8 22.6 Vertex .33.8 22.6 Fold of knee .36.1 31.6 Sacrum j Gluteei i [40.6 33.8 Forearm j Leg ! t 40.6 36 1 Dorsum pedis near the toes .40.6 36.1 Sternum .45.1 33.8 Back of neck (high up). .54.1 36.1 Spine .54.1 . . Middle of neck Arm ] .67.7 1 ' ( Thigh Middle of back j 16 ( 31.6-40.6 DISEASES OF THE SENSORY NERVES. 65 * In order to determine the temperature sense of the integument, Nothnagel em- ployed round vessels of wood, with a metallic bottom, and filled with water at different temperatures. Eulenburg constructed a thermaesthesiometer. This con- sists of two thermometers, with large mercury bulbs, fastened to a stand upon which they can be moved to and fro. The simplest method of examination is to blow upon the skin, at the same time directing the patient to tell whether he no- tices the difference. Or the same part of the skin is successively touched with media at various temperatures, and the differences in sensibility noted. The abil- ity to differentiate temperatures is most marked when the temperatures employed range about that of the body. Nothnagel furnishes the following table of the minimum of difference of temperature which can be detected in different parts of the skin: Forearm Arm 0.2° C. Palm of hand.. Dorsum of foot 0.5-0.4°C. Dorsum of hand 0.3’ “ Cheek 0.4-0.2° “ Temple 0.4-0.30 “ Upper part of abdomen (middle) Thigh 0.5° “ Chest (superiorly, exter- nally) Upper part of abdomen (laterally) Calf Sternum. 0.6° “ 0.5° “ Leg (extensor side) 0.7° “ Back (laterally) 0.9° “ Back (middle) 1.2° “ To test the sense of pain, the skin may be pricked with a pin, pinched, the hairs pulled, etc. Disturbances of the sense of touch and pain do not always go hand in hand. Retention of tactile sensation and loss of the sense of pain are known as analgesia. Leyden and Munk also tested the electro-cutaneous sensibility. They employed a pair of copper compasses with an insulated handle, which was connected with the secondary coil of an induction apparatus, and noted the position of the cylinder when the patient experienced the first sensation, and also the first sensa- tion of pain. Bernhardt furnishes the following table: A. General Sensibility of the Skin to the Electrical Current. Tip of tongue 17.5 cm. Palate •. • • 16.7 “ Tip of nose 15.7 “ Lids 16.2 “ Gums 16.2 “ Dorsum of tongue 15.2 “ Vermjlion of lips 15.1 Cheeks 14.8 “ White of lips 14.5 “ Forehead 14.4 ‘‘ Acromion 13.7 “ Neck at lower jaw 12.7 cm. Arm 12.6 “ Vertex 12.5 “ Sacrum 12.35 “ Thigh 12.3 “ Dorsum of first phalanx Dorsum of foot Dorsum of second phalanx... 11.75 “ 12.0 “ Dorsum of the metacarpus. Dorsum of hand 11.6 “ Sternum Cervical spine. 13.0 “ Leg Tip of finger (volar). 11.5 “ Upper dorsal spine. Arm Buttocks Tip of finger (dorsal) 11.3 “ Volar surface of metacarpus.. 10.9 “ Tip of toes 10.6 “ Middle phalanx (volar) 10.5 Palm of hand 10.5 “ Thumb 10-5 “ First metatarsal bone (plantar) 10.2 “ Middle dorsal spine. Occiput Loins 12.8 “ 12.7 ‘ B. Electro-Cutaneous Sensibility to Pain. Lids 14.2 cm Palate 43.9 Tip of tongue 14.12 Lower part of forehead 12.6 cm. Vermilion of lips. Cheeks 12.5 “ Gums Tip of nose... ■White of lips 13.0 Occiput 12.0 Throat below the jaw 11.8 Upper dorsal spine H-7 “ 66 DISEASES OF THE SENSORY NERVES. Middle dorsal spine 11.6 cm. Cervical spine 11.5 “ Sternum 11.4 “ Dorsum of first phalanx 9.7 cm. Forearm 9.3 “ Acromion Sacrum. . 11.25 “ Dorsum of metacarpus “ “ foot 9.2 “ Loins 11.20 “ Buttocks 11.1 “ Dorsum of tongue 10.8 “ “ “ last phalanx 9.0 “ “ “ second phalanx. .. 8.7 “ Volar surface of last phalanx.. 8.4 “ Middle of thumb 8.0 “ Volar surface of second phalanx .... 7.9 “ Volar surface of metacarpus.. 7.6 “ Palm of hand 7.5 “ Tip of toes 6.5 “ Plantar surface of metatarsus 4.0 “ Vertex Leg... Thigh. 10.2 “ Arm 10.1 “ Dorsum of hand 9.9 “ Knee 9.8 “ The figures given in the preceding tables represent averages which may vary more or less under normal conditions. It is well to compare symmetrical parts of the body in making examinations, although it sometimes happens that both sides of the body are affected. Total anaesthesia is paralysis or paresis of all modes of sensation; partial anaesthesia is diminution or abolition of individual modes of sen- sation. The various forms of sensation maybe disturbed in different com- binations. Anomalous conditions of anaesthesia are sometimes observed. With regard to the sense of temperature, for example, the patients may not alone feel heat and cold less distinctly, but they may mistake heat for cold, and vice versa. Double sensations may also be felt. In tabes, for example, the prick of a pin may first produce a tactile sensation, and later a sensation of pain. Naunyn observed in tabes a double sensation of pain, the first feeble, the later one more severe, as the result of a single prick of a pin. Oases are also known in which the prick of a pin pro- duces three or four sensations (polyaesthesia). In addition, the period between the irritation and the sensation may be unusually long (delayed sensation). Cutaneous anaesthesia may be circumscribed or diffuse. It is some- times confined to the distribution of one or more nerves. In spinal affec- tions it is not infrequently distributed like paraplegia (paranaesthesia). Finally, in cerebral diseases it may be unilateral (hemiansesthesia). _ II. Etiology.—The causes of anaesthesia are situated in the peripheral terminations of the sensory nerves, in those parts of the cerebral cortex in which the peripheral stimulus is converted into sensation, or in the paths of conduction between the two. Hardly anything is known concerning diseases of the peripheral ter- minations of the cutaneous sensory nerves. It is true that Meissner found degenerative changes in the tactile corpuscles in cerebral diseases, but affections of the brain and cord are entirely excluded from the fol- lowing considerations. Hence our chief attention will be paid to dis- turbances of conduction in the peripheral nerve tracts. The sensibility of the skin depends very materially upon the normal circulation of the blood. Anaesthetic symptoms always develop in a part from which the blood has been expelled by means of an Esmarch ban- dage, or in which stasis has been produced by compression of a vein. This also occurs in circulatory disturbances as the result of morbid changes (arterial embolism, venous thrombosis, etc.). Cutaneous anaesthesia is sometimes the result ot‘ thermic influences. Thus, congelation of the skin by means of ether reduces the sensibility DISEASES OF THE SENSORY NERVES. 67 to such an extent that surgical operations may he performed in a painless manner. Increased heat may act in a similar manner. In some cases probably, circulatory changes are produced chiefly or exclusively by the action of temperature; in others, perhaps, there are direct effects on the terminations of the sensory nerves. Allied to thermal influences are the chemical noxa, which produce anaesthesia if they act upon the skin. Thus, it is well known that work- ing in lye, strong acids, or carbolic acid rapidly produces anaesthesia. It is also claimed that the action of the electrical current upon the skin influences the sensibility of the latter. Toxic anaesthesia of the skin is that form which develops after the use of narcotics, when employed subcutaneously or in the form of ointment. Thus, subcutaneous injections of morphine may diminish cutaneous sensibility by direct action upon the terminations of the sen- sory nerves. Anaesthesia has also been observed in poisoning with lead, ergotin, or carbonic oxide, but this is perhaps the result of central causes. Anaesthesia has also been observed after infectious diseases (typhoid fever, diphtheria, syphilis, etc.). In the majority of cases, however, morbid processes are found in the peripheral nerves (rheumatic and traumatic influences, inflammations of the nerves, compression by tumors, etc.) III. Symptoms.—Cutaneous anaesthesia is easily recognized if the methods of examination are carried out in intelligent patients. In a thorough examination, all qualities of sensation should be submitted to test. In addition, the anaesthetic district should be mapped out. In partial anaesthesia, the symptoms may vary from time to time, inasmuch as the individual qualities of sensation may disappear or reap- pear at different times. In some cases the patients call attention to the anaesthesia, because they notice diminished sensation on touching objects, of feel as if they were walking on felt or wool, etc. If the hands are affected, the patient is apt to drop objects as soon as the eye is turned in another direction. Some patients also complain of paraesthesia (coldness, feeling of stiff- ness or tension, prickling, formication). In the simplest cases nothing is noticed beyond the objective signs of amesthesia. In other cases, there are a number of disturbances of inner- vation, which depend upon an affection of other nerve tracts in addition to the sensory fibres. For example, the most violent neuralgic pains may be felt in the affected nerve tract despite the absolute anaesthesia (anaesthesia dolorosa). Thus, a tumor which compresses a nerve may interrupt conduction from the skin to the tumor, i. e., produce anaesthesia. At the same time the tumor may irritate the central end of the nerve in such a manner as to produce in the central organ a sensation of pain which will be referred to the peripheral distribution of the compressed nerve. Motor disturbances will be present if mixed nerves are affected, and may appear as paresis or paralysis, tonic or clonic spasms. Keflex movements are always abolished in purely peripheral anaesthe- sia, simply because the stimulus is not conveyed to the cord or brain. Vaso-motor fibres are not infrequently affected at the same time as the sensory fibres. The anaesthetic parts then present either unusual pallor, or, more frequently, unusual redness and livid discoloration of the skin; oedema and puffiness of the skin may also be noticed. This is 68 DISEASES OF THE SENSORY NERVES. usually associated with changes in the cutaneous temperature (unusual heat or cold). Anaesthesia may also he associated with trophic changes, as the result of an affection of trophic nerve fibres in the lesion. These changes include abnormal growth of hair, excessive formation and desqua- mation of epidermis, marked thickening and gloss of the fingers, inflammation of the nails, development of furuncles, herpes, pemphigus, extravasations, etc. IV. Diagnosis.—As a rule, the diagnosis of cutaneous anaesthesia is not difficult. We should always endeavor to ascertain the cause and situation of the anaesthesia. An important distinction between peri- pheral and central anaesthesia is the absence of reflex movements in the latter. In addition, the concomitant symptoms and the distribution of the cutaneous anaesthesia must be considered in the diagnosis of the site of the lesion. V. Prognosis.—This depends entirely on the etiology of the disease. VI. Treatment.—This should be first directed towards the removal of the cause. In addition, we must rely on local measures, especially alco- holic and irritating inunctions, and electricity. In employing galvan- ism, the anode is placed on an indifferent spot, the cathode is methodi- cally stroked to and fro over the anaesthetic region (labile application). The irritant effect is increased if the wire brush is connected with the cathode. In faradic applications, the electrodes should not be too moist, and should not be pressed too firmly upon the skin. The faradic brush may also be applied in a labile manner. As an illustration of anaesthesia of a special nerve, we will discuss: Ancesthesia of the Trigeminus Nerve. I. Etiology.—The disease is not very frequent; it may affect the entire distribution or individual branches alone. Among the causes mentioned are exposure and injury. In the former event, individual branches are alone affected. Injuries to the nerve may be of various kinds—stab and gunshot wounds, falls, blows, surgical operations, extraction of teeth, abscesses, compressing tumors, inflammations and other diseases of those bones of the skull and face through whose foramina branches of the nerve take their course; exostoses, tumors, etc., of the base of the skull, meningeal dis- eases, etc. II. Symptoms.—As a rule, anaesthesia of the trigeminus is unilat- eral. If the entire distribution of the nerve is involved, the motor branch will also be affected, causing paralysis of the muscles of mastica- tion on one side (vide page 13). In total trigeminal hemianaesthesia, there is loss of sensation in the face, the forehead as far as the vertex, the external, upper part of the concha, and the mucous membrane of the eye, nose, and buccal cavity. The patients suffer occasionally from paraesthesiae or from neuralgic pains. Circulatory and vaso-motor disturbances are not infrequent: redness and swelling of the integument of the face, changes in perspiration and the temperature of the skin. Attention has long been attracted by certain trophic disturbances— hemorrhages and ulcerations of the buccal mucous membrane, loosening of the teeth, herpes, still more by inflammatory changes in the eye (ophthalmia neuroparalytica). In the latter cases, we find injection and diseases of the nerves of special sense. 69 swelling of the conjunctiva, opacity and acute destruction of the cornea, followed by loss of the entire eyeball. Meissner endeavored to show experimentally that ophthalmia neuroparalytica is due to the destruction of certain trophic fibres situated in the median part of the trunk of the trigeminus. Some authors maintained that the trophic fibres do not really belong to the trigeminus. It was shown that the ocular changes do not develop unless the nerve is injured at the Gasserian ganglion or on its peripheral aspect, i. e., after sympathetic nerve fibres have joined the nerve. Numerous observers claimed, on the other hand, that the ocular affection is a traumatic keratitis, the result of the fact that, on account of the anaesthesia of the cornea, the eye is readily injured, and perhaps because, on account of inter- ference with the movements of the lids, germs find a ready entrance into the corneal tissue. There is sometimes ansesthesia of the entire conjunctiva and cornea, more rarely the sensibility of the cornea is retained. In the former event, touching the cornea produces neither increased secretion of tears nor winking, an important distinction from central anaesthesia. Wink- ing will be produced if a bright light is allowed to fall upon the retina. The application of stimuli to the nasal mucous membrane does not produce any reflex effect (sneezing); this is also true of irritation of the buccal mucous membrane. Gustatory disturbances have sometimes been observed, even though the facial nerve was intact. Hence it seems that the lingual branch of the trigeminus does not always receive all the gustatory fibres from the facial through the chorda tympani, but that the trigeminus may contain such fibres from its origin. Unilateral coating of the tongue has been described in some cases. Nothing is known concerning disturbances of salivation or audition in this disease. If the lesion is situated at the base of the skull, the adjacent cerebral nerves, particularly the facial, acoustic, glosso-pharyngeus, and the nerves of the ocular muscles, are often paralyzed. The duration and course of the disease depend entirely upon its causes. IIT. Diagnosis, Prognosis and Treatment.—The recognition of the disease is easy. The more the individual branches of the nerve are alone affected, the more peripherally is the lesion situated. In central anaesthesia the reflexes are always retained, if the lesion is situated on the central side of the trigeminal nuclei. The prognosis depends on the etiology. The treatment is the same as that of cutaneous anaesthesia in general. If the eye is affected, it must be suitably protected. Some writers claim to have obtained beneficial effects from the direct application of elec- tricity to the eye. C. DISEASES OF THE NERVES OF SPECIAL SENSE. 1. Diseases of the Olfactory Nerve. (llyperosmia, Anosmia, Parosmia.) Very little is known concerning diseases of the olfactory nerve. Many indi- viduals suffer from them for a long time until they are revealed by accident. 1. Hyperosmia or olfactory hypercesthesia is manifested by the fact that the patients smell substances which normal individuals are unable to detect, or they are so strongly affected by certain odors that they suffer in consequence from syncope, vertigo, headache, and even general convulsions. Cases have "been 70 DISEASES OF THE NERVES OF SPECIAL SENSE. known in which individuals educated the olfactory sense to such a degree that they could trace objects like dogs or birds of prey. Hyperostnia generally affects hysterical, nervous, or psychopathic individuals, and is, therefore, more often the result of central than of peripheral causes. 2. Anosmia or olfactory anaesthesia means the diminution or abolition of the sense of smell. In examinations those substances should be avoided which, like ammonia and acetic acid, irritate the nasal mucous membrane, and thus stimu- late the trigeminus. Substances possessing a pleasant and those possessing an unpleasant odor should be employed, since the individual may be anaesthetic to one class and not to the other (partial anaesthesia). According to Althaus, irrita- tion of the nasal mucous membrane with the constant current produces a smell like that of phosphorus (?). Anosmic patients sometimes complain of subjective, usually unpleasant olfac- tory sensations; this corresponds to anaesthesia dolorosa. Many patients also complain of gustatory disturbances. This is only true of those articles of diet whose flavor depends chiefly on the olfactory sense, for ex- ample, the bouquet of wines, the smell of cheese, meat, fruit, etc. This only occurs in bilateral anosmia. The disease may be congenital or acquired. Cases have been reported in which the olfactory nerve was absent. Anosmia is sometimes attributed to cold, more frequently to injury. According to Ogle, a blow on the occiput may, by contre- coup, tear the fibres passing through the ethmoidal foramina from the olfactory bulbs. It is sometimes the result of nasal affections (acute and chronic coryza, polypi). Tumors, inflammations or exostoses at the base of the skull, etc., may compress the olfactory nerve and impair its function. Anosmia is sometimes associated with aphasia and right hemiplegia in disease of the jeft island of Reil. According to Althaus, olfactory neuritis, followed by anosmia, is a not very rare disease (?). Prevost attributes the anosmia of old age to atrophic changes in the olfactory bulbs. It has been observed occasionally after continued stimulation of the olfactory nerve, or as the result of irritating nasal injections and douches. Raynaud observed intermittent anosmia; it has also been reported after acute infectious diseases. In certain cases the disturbance of olfaction is the result of disease ot the tri- geminus or facial nerve. In trigeminal anaesthesia the sensibility of the nasal mucous membrane for biting and irritating odors is impaired, and if the anaes- thesia is peripheral, sneezing or other reflexes cannot be produced by tickling the mucous membrane. Olfaction proper may also be impaired by diminution of the lachrymal secretion, so that the nasal mucous membrane becomes dry and less sensitive to smells. Anosmia may also develop in facial paralysis, because paralysis of the lower lid impedes the flow of tears into the nose, and also because the paralysis of the muscles of the ala nasi impede the entrance of air into the nostril. The prognosis is bad if the causes cannot be removed. In addition to causal treatment, the galvanic or faradic current has been applied externally to the nose or directly to the nasal mucous membrane by means of sound-shaped elec- trodes; strychnine has been recommended subcutaneously, internally, or locally to the nasal mucous membrane (strychnine, gr. iss.; ol. amygdal., 3 iij.). 3. In parosmia there are unpleasant subjective sensations of smell, or the patient perceives unpleasant odors as pleasant, and vice versa. This is observed in hysterical and insane individuals, in epileptics as the so-called aura, sometimes in anatomical lesions of the olfactory nerves or in central diseases, if the central fibres of the olfactory nerves are affected. This group includes the predilection for certain smells which are generally regarded as unpleasant, for example, Schiller’s predilection for rotten apples. 2. Diseases of the Gustatory Nerves. (Hypergeusia. A geusia. Parageusia.) It is generally held at the present time that gustation upon the anterior two- thirds of the tongue is supplied by the lingual branch of the trigeminus; upon the posterior third of the tongue, soft palate, anterior palatal arch and pharynx, by the glosso-pharyngeal. Gustatory disturbances from diseases of the glosso-pharyngeal nerve alone are Unknown. We have previously shown that diseases of the facial nerve may be DISEASES OF THE PEKIPHEBAL NEBVES. 71 associated with disturbances of taste (vide page 6). If we pass from the peripherv along the course of the gustatory fibres towards the brain, the anterior two-thirds of the tongue are found to be supplied by the lingual branch of the trigeminus The greater part of these gustatory fibres pass in the chorda tympanito the faciai nerve. They again leave the facial at the geniculate ganglion, pass through the nervus petrosus superficialis major to the trigeminus, and through the spheno- palatine ganglion to the second branch of the trigeminus (vide Fig. 6). Some authors believe that the gustatory fibres in the trigeminus are derived from the glosso-pharyngeus. The simple gustatory sensations are: sour, sweet, bitter, and salty. Sour may be tested by dilute vinegar, sweet by sugar in solution, bitter by aloes, colocynth strychnine, salty by sodium chloride, etc. Irritating and concentrated solutions should be avoided. During the examination the patient should close his eyes, and protrude the tongue, the surface of which is touched in various places with a piece of rolled-up blotting paper, dipped in the solutions previously mentioned. A little brush or a glass rod may also be used, but the drops of fluid should not be too large. The patient should not withdraw the tongue until he has indicated that he has tasted the substance. Before experimenting with another substance the mouth should be carefully rinsed with water. It should be remembered that bitter is perceived most distinctly by the root of the tongue, sweet by the tip, and sour by the edges. a. In gustatory hypercesthesia or hypergeusia the patients can taste minimum traces of a substance, or the gustatory sensations produce an unusual degree of pleasure or disgust. This is observed in hysterical and nervous individuals. b. Gustatory ancesthesia or ageusia is the diminution or abolition of the sense of taste. Only a few gustatory qualities may be abolished, or in addition to ageusia, the patient suffers from perverse subjective sensations of taste. The dis- ease may be bilateral, unilateral, or circumscribed. The conduction of the sen- sations is often delayed. Ageusia is observed when the tongue is thickly coated, the buccal mucous membrane abnormally dry, and when too hot or cold substances are ingested. This is evidently the result of implication of the terminations of the lingual and glosso-pharyngeal nerves. Ageusia also occurs in diseases of the lingual nerve, and is a frequent symptom of trigeminus anaesthesia and facial paralysis. The not infrequent association of gustatory disturbances and diseases of the middle ear is effected through the chorda tympani. Treatment consists of galvanic applications to the tongue or lingual nerve, to the petrous portion of the temporal bone, or transversely through the head. c. Parageusia appears most frequently in hysterical and insane individuals. The gustatory sensations are generally nauseous and perverse, and may give rise to special delusions in the insane. Wernich noticed a bitter taste in the mouth after a subcutaneous injection of morphine, in feeble individuals, and in himself after prolonged fasting. Parageusia is sometimes associated with ageusia. D. ANATOMICALLY DEMONSTRABLE DISEASES OF THE PERIPHERAL NERVES. 1. Inflammation of the Nerves. Neuritis. I. Anatomical Changes.—Inflammatory changes in the nerves may be located in the interstitial connective tissue (perineuritis) or in the nerve fibres (parenchymatous neuritis). The inflammation is some- times confined to a circumscribed region (circumscribed neuritis) or it spreads further and further (neuritis migrans) in a centripetal or centri- fugal direction. The process may spread continuously along the nerve, or it may overleap longer or shorter stretches of the nerve (neuritis dis- seminata). The anatomical changes in perineuritis vary according as the disease is acute or chronic. In acute perineuritis the nerve is unusually congested, its vessels dis- tended, and small extravasations of blood are noticed here and there. 72 DISEASES OF THE PEJRIPIIEKAL NEKVES. The surface of the nerve is less shining than usual, the inflamed part is swollen and very succulent, and the macroscopic transverse striation less distinct. On microscopical examination the blood-vessels in the neurilemma are found unusually full, their walls are sometimes thickened and particularly shining, and the nuclei are occasionally increased in number. Upon the outer surface of the vessels are found accumulations of round cells which are especially profuse in places. Some of these white blood-globules con- tain very fine granules of fat. In some places the blood-vessels are torn, and red blood-globules are found free in the cellular tissue. The connective-tissue parts proper of the neurilemma are swollen, and their cells increased. If the neuritis is violent, the originally interstitial changes are complicated by parenchymatous changes, evidently as the result of the circulatory disturbances. These changes are similar to those observed in the peripheral parts of a nerve after experimental section—degeneration amd disappearance of the medullary matter, followed by destruction of the axis cylinder, and marked nuclear prolifer- ation in the sheath of Schwann. This parenchymatous degeneration is generally most marked near the perineurium. If the acute neuritis recovers, the congestion disappears more and more, the extravasations are absorbed, the emigrated white blood-glob- ules undergo fatty degeneration and are absorbed, and the nerve gradu- ally assumes its normal appearance. Recovery takes place much more slowly if the interstitial process has been followed by parenchymatous; changes. Very acute perineuritis may terminate in the formation of foci of pus, and these, if sufficiently large, may entirely destroy conduc- tion in the nerve. This is most apt to occur if the perineuritis has been excited by suppuration in the vicinity of the nerve. Even gangrene has been observed under such circumstances. Acute perineuritis not infrequently becomes chronic, or the inflam- mation may be chronic from the start. We then find proliferation and increased consistence of the interstitial tissue, a grayish-red color of the nerve, sometimes a grayish-black or graphite-like appearance, due to pig- ment left over after previous hemorrhages. The increase of connective tissue, shown by the abnormally-wide interstices, is especially distinct on transverse section of hardened nerves. The individual fibres are some- times constricted to such an extent that they undergo atrophy, and the nerve may be converted finally into a solid band of fibrous tissue which is destitute of nerve fibres (sclerotic neuritis). Corpora amylacea arc found occasionally at the site of inflammation. Chronic perineuritis may develop in a single circumscribed spot, it may spread continuously over a large tract, or it may skip over certain parts. In the latter event the inflamed portions of the nerve not infrequently form nodular or spindle-shaped prominences (neuritis nodosa). These thickenings may follow one another in the shape of a rosary. The inflamed parts of the nerve not infrequently present fibrous adhesions to surrounding parts. Parenchymatous neuritis is rarer than perineuritis, and still rarer as an independent alfection. It occurs most purely if the continuity of the nerve has been interrupted in any part of its course. The peripheral portion of the nerve then presents a series of processes which are known as degeneration, and which are partly inflammatory in their origin (neu- ritis degenerativa) (vide Fig. 1). II. Etiology.—There can be no doubt that neuritis may develop as diseases of the peripheral nerves. 73 the result of a cold, but in a much larger number of cases it is the result, of injury. Among the numerous forms of traumatism we may mention incised and gun- shot wounds, falls, blows, dislocations, fractures, compression by tumors lifting heavy loads, etc. Neuritis sometimes develops in amputation stumps. In. some cases the inflammation extends from surrounding parts. This is observed in pelvic abscesses, tubercular diseases of the spine, inflamma- tion of the joints and sheaths of the tendons; after pleurisy, pneumonia, and phthisis; in progressive muscular atrophy, according to Friedreich; in cancer and sarcoma, particularly of the vertebrae. According to Leyden, many cases of reflex paralysis are the result of the extension of neuritis migrans to the spinal cord. Neuritis sometimes follows infectious diseases (typhoid and relapsing fever, erysipelas, variola, diphtheria, syphilis, leprosy). Toxic neuritis occurs most frequently in lead poisoning, but this form still requires careful investigation. It also develops in phosphorus poisoning. No causes can be demonstrated in certain cases, and some authors assume a predisposition to neuritis in certain individuals. III. Pathological Significance of the Disease.—The experi- mental investigations of Tiesler, Feinberg, and Klemm have shown that neuritis may extend to and implicate the meninges and substance of the spinal cord, or that it may pass from the nerves of one side of the body to those of the other side without affecting the cord. Similar observa- tions have been made in human beings. It has been observed repeatedly in tetanus that neuritis disseminata, starting from a peripheral wound, has extended to the spinal cord. It is also assumed that migrating neuritis forms the connecting link in reflex epilepsy, following cicatrices in which sensory nerves are imbedded. Leyden supposes—and not without reason—that certain complexes of symptoms which have been attributed hitherto to anterior poliomyelitis are really due to extensive neuritis. A wide field of investigation is here opened, especially since the results of experimental investigations have been disputed. IV. Symptoms.—Among the symptoms, the local phenomena play an important part from a diagnostic standpoint. They include increase in the consistence of the nerve, nodular thickenings, and pain on pressure. The pains are especially severe if the nerve is rolled to and fro between the fingers. The pain may be confined to certain parts of the nerve, or extend along its entire course. In some cases we notice a streaked or more diffuse, erysipelatous redness along the course of the nerve, with local diaphoresis and increased warmth. The disturbances of innervation vary according as the neuritis affects a motor, sensory, or mixed nerve. In acute neuritis of sensory nerves, tactile sensation is generally di- minished in the distribution of the nerve, while pain sensation is in- creased (hyperalgesia). If the nerve fibres are destroyed, this is followed by loss of pam-sensation (analgesia). The patients often complain of parsesthesiae, burning, pricking, formication, an abnormal feeling of heat or cold, etc. Spontaneous pains are almost always present. They are generally constant, but are increased on pressure, or they in- 74 DISEASES OF THE PERIPHERAL NERVES. crease spontaneously in paroxysms. Intermittent paroxysms, like those of neuralgia, are rarely observed. The pains often radiate into remote nerve tracts. Trophic changes are not infrequent: herpes zoster, pem- phigus, thickening and desquamation of the epidermis, glossy fingers, changes in the nails, etc. Motor irritative symptoms (twitchings, spasms, contractures) sometimes develop as reflex symptoms. Neuritis of motor nerves results in paresis, paralysis, tonic and clonic spasms, and contractures. These changes may undergo rapid resolution if they are the result of compression of the nerve fibres by inflammatory swelling; they are more permanent if the nerve fibres them- selves have taken part in the inflammation. In the latter event, trophic changes in the muscles (diminution in the size of the individual bundles of muscular fibres, unusually distinct transverse striation, and increase of the nuclei of the sarcolemma) are apt to develop very rapidly. At the outset, the electrical irritability is not infrequently increased, but if the inflammation is severe, the symptoms of degeneration re- action will develop (vide page 7). Acute neuritis of mixed nerves presents a mixture of the symptoms mentioned above. Sensation is lost at an earlier period, and to a more marked degree than motion, but it returns earlier than the latter when recovery begins. Chronic neuritis presents the same symptoms as the acute form, except that they develop more slowly and run a milder course. The disease sometimes lasts for months and years. Recovery may be complete, or permanent disturbances may be left over. V. Diagnosis.—The diagnosis of neuritis is difficult if local changes in the nerve are absent. It may be mistaken for a, neuralgia: in this the pain is intermittent, and Valleix* pressure points constitute a more prominent symptom; b, muscular rheumatism: pain is produced by direct pressure upon the muscles; c, embolism or thrombosis of the vessels of the limbs: circulatory disturbances (pulselessness, oedema, cyanosis) are noticeable, d. The differentiation between neuritis nodosa and neuroma is not always possible, even anatomically. VI. Prognosis.—A favorable prognosis can only be given in those cases in which the disease is the result of causes which can be readily removed. But the possibility of the extension of the process to the spinal cord should always be kept in mind. VII. Treatment.—Apart from causal treatment, we must rely ex- clusively on local measures : absolute rest, alcoholic inunctions, blue ointment, potassium iodide ointment, tincture of iodine, local wTarm baths, at times ice, leeches, cups, blisters, and, if the pain is very se- vere, subcutaneous injections of morphine. Electricity is one of the best remedies; stabile constant current, anode to the painful points, cathode indifferent or on a central painful point. We prefer feeble currents, others recommend strong currents. If the pain is very intense, good results may be obtained from the faradic brush or moxa. In chronic neuritis we may resort to electricity, massage, nerve stretching, various baths, and cauterization. 2. Multiple Neuritis. {Progressive neuritis. Disseminated neuritis. Polyneuritis.) I. Etiology.—Neuritis sometimes occurs as an independent affec- tion in many peripheral nerves, and may run an acute, subacute, or chronic course. Acute multiple neuritis may prove rapidly fatal. DISEASES OF THE PERIPHERAL HERVES. 75 The sudden onset, the rapid and febrile course of the disease raise the suspicion that we have to deal with an infectious process. Chronic forms of the disease also appear to be connected with infectious pro cesses. For example, Scheube and Baels regard beriberi as miasmatic m its origin, and dependent on an extensive neuritis (paneuritis). Traumatism has been mentioned as a cause of polyneuritis. The disease has also been observed after infectious diseases, such as parotitis, acute articular rheumatism, and, according to Leyden diph theria, typhoid and relapsing fever, erysipelas, syphilis, and phthisis It generally occurs between the ages of twenty-one and thirty years but Webber reported a case in a child of nine years. ' II. Symptoms.—Acute multiple neuritis is not infrequently pre- ceded by prodromata. In one of my cases, the patient suffered from periodical chills, fever, and sweat. In other cases, there is merely a feel- ing of general malaise. The manifest symptoms generally begin with pain and paresthesia. Fig. 31. Paral. of pero- neus sinister P. of peroneus sin. profund. Paral. of tibia- lis sinister . of radial sin* r ural sin. crura P. of N. ulnar et median sin. P. of axill. sin. et rad. dext. P. of uln. med et axillar. dext Total Amauros Course of the temperature and occurrence of the paralyses in acute multiple neuritis in a woman set. 66 years. The pain is described as burning, boring, lancinating, and may be very intense; it may be superficial or deep. A feeling of paresis and stiffness soon becomes noticeable in the dis- tribution of the nerve, and rapidly passes into well-marked paralysis. In my case the paralysis occurred almost as suddenly as a stroke of apoplexy. The electrical irritability of the paralyzed muscles and nerves rapidly sinks, and degeneration reaction may be noticed within a few days. If the paralysis does not soon recover, the muscles rapidly atrophy and later undergo contracture. The motor nerves are chiefly, sometimes almost exclusively affected. Sensory disturbances are not infrequently present to a very slight de- gree. Yaso-motor changes—oedema, cyanosis and diminished tempera- ture of the skin—are often noticed. Secretory and trophic cutaneous disturbances may also occur. The tendon and cutaneous reflexes in the distribution of the affected nerves are lost. 76 DISEASES OF THE PERIPHERAL NERVES. The affected nerves are not infrequently tender on pressure. The situation becomes very dangerous when the disease exhibits a ten- dency to spread. In a case under my observation, the symptoms began in the left peroneal nerve, then spread from one nerve to the other, from the legs to the arms, finally to the optic and pneumogastric nerves. Fig. 31 shows the temperature and date of the paralyses in this case. Impli- cation of the vagus (shown by acceleration and irregularity of the heart’s action, and by difficulty in breathing) is especially grave. Although the disease generally spreads from below upwards, this does not always hold good. It may cease at any time, and the paralysis may recover in part, while atrophy and and contracture of the muscles occurs in other parts. The bladder and rectum are usually unaffected. Albuminuria has been observed a number of times; icterus has been described in two cases. Fig. 32. Transverse section of the left median nerve in acute multiple neuritis. Three nerve bundles are visible, with numerous extravasations of blood, partly within them, partly in the surrounding connective tissue (per, perineurium). Also numerous extravasations in the more remote epineurium, ep. Enlarged 90 times. The symptoms of subacute and chronic multiple neuritis are similar to those of the acute form, but develop more slowly and less violently. III. Anatomical Changes.—We have little to add to the remarks made concerning neuritis in general. In acute multiple neuritis, the inflammation may be chiefly intersti- tial or chiefly parenchymatous. In my own case, the changes were mainly interstitial. The peripheral nerves were unusually red, opaque, and succulent, and the microscope showed unusual distention of the ves- sels, and very numerous extravasations of blood in the insterstitial con- nective tissue (vide Fig. 32). On more detailed examination, the vessels were found to be very tor- tuous and dilated in places, the walls were streaked, vitreous, and thick- diseases of the spinal cord. 77 oned, and contained numerous endothelial nuclei; outside of the ves- sels were accumulations of round cells, mixed with granulo-fatty cells in addition, swelling of the connective-tissue fibrillae and proliferation o the cellular elements of the interstitial tissue. Degenerated nerve fibre and lively proliferation of nuclei within the sheath of Schwann were found in the nerve bundles, particularly near the extravasations of blood. Mueller observed fatty changes and swelling of the paralyzed museles. The brain, spinal cord, and roots of the spinal nerves are intact. IV. Diagnosis.—This is not always easy. Cases which run an acute, ascending course remind us of acute ascending spinal paralysis, but the latter presents no sensory disturbances or changes in electrical irritability. Multiple neuritis may also be mistaken for poliomyelitis; here, like- wise, the presence of sensory disturbances is an important diagnostic feature. V. Prognosis.—The prognosis is always serious. In acute multiple neuritis there is danger of death when cerebral nerves, particularly the vagus, become affected. The prognosis is also serious from the fact that the paralysis often persists and cripples the patient. VI. Treatment.—In the acute form salicylic acid (four to six doses of fifteen grains every quarter-hour) should be given to combat the fever and infection. Violent pains may be relieved by narcotic inunctions (for example: chloroform, 3 iij.; liniment, volatil., § iss. M. D. S. To be used t. i. d.) or subcutaneous injections of morphine. After the acute symp- toms have subsided, the paralyzed muscles may be faradized and the nerves treated with the galvanic current (anode labile, cathode indiffer- ent). If the faradic irritability of the muscles is lost, they should be treated by labile applications of the cathode of the galvanic current. Potassium iodide may be given internally. Massage and indifferent ther- mal waters have been employed in old cases. PART II. DISEASES OF THE SPINAL CORD. A. DISEASES OF THE SUBSTANCE OF THE SPINAL CORD. a. UNSYSTEMATIC (ATYPICAL) DISEASES OF THE CORD. 1. Ancemia of the Spinal Cord. I. Etiology.—Our clinical knowledge of this disease is very scanty. Its causes may be local or general. The former include: compression, embolism, or thrombosis of the abdominal aorta, embolism or thrombosis of fine vessels in the spinal cord, and compression of the cord. The general causes include: profuse losses of blood, chlorosis, protracted suppuration, etc. Brown-Sequard attributes reflex paralysis to spasm of the arteries in the spinal cord. In 1667, Stenson produced paralysis of the muscles, sphincters, and sensation by compression of the abdominal aorta in animals (anaemia of the spinal cord). Panum produced embolism of spinal vessels by injecting substances into the blood. t II. Anatomical Changes.—The substance of the spinal cord is pale, and the gray matter is depressed below the white matter. The latter is softened, more 78 DISEASES OF THE SPINAL COED. rarely its consistence is increased. Red and yellow softening is sometimes observed as an expression of anaemic necrosis of the cord. If the anaemia is the result of compression or embolism of small vessels in the cord, the periphery of the anaemic focus will be marked by unusual congestion of the vessels and extravasations of blood. Leyden’s observations indicate that microscopical ex- amination is necessary to detect fine emboli in the cord. The meninges are also anaemic, but the venous plexuses in the peridural cellu- lar tissue are occasionally distended with blood. We must be on our guard against mistaking these appearances for cadaveric changes in the cord, particularly if no causes of anaemia are demonstrable. Hi. Symptoms.—If anaemia of a large part of the lumbar cord suddenly oc- cur, for example, as the result of embolism of the abdominal aorta, it will be followed by rapid paralysis of the lower limbs, loss of sensibility and reflex irritability, and paralysis of the bladder and rectum. At the same time the pulse in the crural arteries disappears or becomes very small, and the limbs undergo gangrene unless the collateral circulation is quickly re-established. Embolism of smaller vessels of the cord may not give rise to symptoms. To spinal anaemia as the result? of general anaemia have been attributed con- ditions of paresis, paralysis, tremor, hyperaesthesia, anaesthesia, and increased reflex excitability. Such conditions may disappear as soon as the general anaemia is relieved. IV. Diagnosis.—The diagnosis is not always easy; it depends particularly upon the demonstration of anaemia as a cause of the condition. V. Prognosis.—The prognosis is unfavorable if nutritive disturbances occur in the cord and are followed by symptoms of organic lesions. VI. Treatment.—This is chiefly causal and symptomatic. Brown-Sequard recommends dorsal decubitus with elevated head and limbs. Bags of hot sand or hot water may be applied to the back. Strychnine, opium, and amyl nitrite have been recommended. In other respects, purely symptomatic treatment. 2. Hypercemia of the Spinal Cord. I. Anatomical Changes.—The term congestion of the cord is often employed by physicians who are anxious to make fine diagnoses, but our knowledge of this condition is almost nil. On transverse section of the congested cord, the white substance has a rosy red appearance, presents numerous dots of blood, unusually large and sinuous vessels, in places true extravasations. The gray matter has a red, sometimes almost brownish-red color. The consistence of the cord may be increased or diminished. The meninges also appear congested, and the veins of the peri- dural tissue are sometimes sinuous and dilated. The spinal fluid is not infre- quently increased, sometimes cloudy, occasionally tinged with blood. Congestion and even hemorrhages of the nerve roots have been noticed in some cases. Hyperaemia of the cord may have been present during life, although the appearances have disappeared in the dead-house. The reverse also holds good, i. e., congestion of the cord may appear to be present after death, either as the result of prolonged position on the back, or cadaverous decomposition, etc. II. Etiology.—Active spinal congestion may be the result of cold, shock, in- flammation, infectious diseases, bodily exertion, onanism, excessive coitus, poisoning with carbonic oxide, strychnia, alcohol, prussic acid. It may also develop in congestive conditions of certain abdominal organs, for example, in menstrual and hemorrhoidal hemorrhages, or in the absence of customary hem- orrhages of this character. Passive spinal congestion may be the result of general disturbances in cardiac and pulmonary diseases. Or the causes of stasis may be local stasis of the portal vein, abdominal tumors, pregnant uterus. This also includes spasmodic condi- tions (epilepsy, tetanus, uraemia, agonal spasms, etc.) in which congestion and hemorrhages, particularly into the peridural tissue, often occur, and were often falsely regarded as the causes of these diseases. III. Symptoms.—The symptoms of active and passive spinal congestion are alike; the lower limbs are generally affected. Among the symptoms mentioned are: a feeling of pressure, tension, and pain in the spine on external pressure, a cinc- ture feeling around the belly, pains in the limbs, hyperaesthesia, paraesthesia, rarely anaesthesia, twitchings in some of the muscles, rarely complete paralysis, increased reflex excitability, and galvanic irritability. The bladder and rectum DISEASES OF THE SPINAL CORD. 79 are rarely paralyzed. If the upper cervical cord is affected, there may be disturb- ances of respiration and cardiac action. Cerebral congestion may also be pres- ent, and its symptoms may occupy the foreground. According to Brown-Se- quard, the symptoms increase in dorsal decubitus, decrease in abdominal decu- bitus or in the standing position. Others maintain that the symptoms increase in the erect posture. They often vary with remarkable rapidity. IV. Treatment—We may apply cups or leeches (ten to twenty) to the spine, or apply leeches to the anus or cervix uteri, ice bags to the spine, foot or hand mustard baths; internally ergotin or belladonna. The patient should assume ab- dominal or lateral decubitus, and the bowels should be thoroughly evacuated daily, 3. Hemorrhage of the Spinal Cord. {Spinal Apoplexy. Hcematomyelia.) I. Etiology.—Primary hemorrhages into the cord are rare, and Charcot and Hayem deny their occurrence. At all events secondary hemorrhages are much more frequent, especially in connection with pre- vious inflammation of the spinal cord (luematomyelitis). Among the causes of primary spinal hemorrhage are injuries, cold, bodily strain, coitus, sexual excesses in general, stasis following cardiac, pulmonary, and hepatic diseases. Previous disease of the spinal cord or the immediate vicinity also favors the development of spinal hemor- rhage. Males are affected more frequently than females. II. Anatomical Changes.—The hemorrhagic focus in the cord cannot infrequently be recognized beneath the pia mater, as soon as the dura mater has been laid open. It often shows through the pia mater as a bluish-black mass, and sometimes causes a prominence of the men- inges. The pia mater may even be ruptured, and the blood escape into the subarachnoid cavity. The upper cervical or the dorsal portions of the cord are most fre- quently affected. There is usually only one extravasation. It almost always begins in the gray matter, particularly the anterior horns, and not. infrequently occupies the entire section of the cord. In rare cases the blood extends along the length of the cord, following the longitudinal fibres in the white matter, and attains a length of more than ten cm. Iieeent hemorrhages have a blackish-red, older ones a brownish-red, rusty brown, even ochre-yellow color. In recent foci the blood is partly coagulated, and the adjacent nerve tissue is generally in a condition of red or yellow inflammatory softening. ' After a while a sort of fibrous capsule may form around the hemorrhage, and the blood is replaced by serous fluid (so-called apoplectic cysts). Smaller extravasations gener- ally terminate in a sort of connective tissue, pigmented cicatrix. Spi- nal hemorrhages may not alone be followed by meningeal hemorrhages, but occasionally by fibrous and even purulent inflammations. Among the complications and sequelae are inflammatory changes and secondary degeneration of the cord (vide the section on secondary spinal degenerations). III. Symptoms.—The disease is characterized by the sudden (apoplec- tiform) occurrence of paralytic symptoms, which vary according to the situation and extent of the hemorrhage. The symptoms generally cor- respond to those of complete section of the cord, sometimes to those of a unilateral lesion. In other cases they indicate exclusive or chief implication of the anterior, more rarely the posterior horns. As a rule, the symptoms occur suddenly without prodromata, more 80 DISEASES OF THE SPINAL CORD. rarely they are preceded for a few hours or days by morbid phenomena, which indicate congestion of the cord and meninges (pain in the back, stiffness in the spine, paraesthesiae in the limbs, etc.). Consciousness is not impaired at the onset, unless the hemorrhage is situated high up in the cervical enlargement of the cord. In some cases the symptoms of shock are manifested. In the beginning, the bodily temperature is unchanged; in the next few days there is sometimes a slight rise of temperature. High fever develops in the later course of the disease if it becomes complicated with cystitis, ammoniacal decomposition of the urine, and bed-sores. The majority of patients complain at first of more or less violent pain in the spine, corresponding to the site of hemorrhage, but the pain generally subsides in a few hours. The pain is usually associated with paralysis, as a rule paraplegia, more rarely spinal hemiplegia or monoplegia. The paralysis is often complete from the beginning, in other cases it is incomplete at first, but increases in severity during the next few hours. It affects motion and sen- sation, the bladder and rectum. The reflexes are often abolished or en- feebled, but, if the cord has been completely cut across, the reflex irri- tability below the site of lesion will be increased at the end of a few days. The reflexes will remain absent permanently if an extensive hem- orrhage has taken place into the lumbar part of the cord, or if the an- terior or posterior nerve roots are affected (in the latter event the re- flexes will be abolished merely in the distribution of the affected nerves). Destruction of the anterior horns of gray matter or the anterior roots is shown by rapid atrophy of the paralyzed muscles, and the develop- ment of the degeneration reaction. Spontaneous twitchings are some- times observed in the paralyzed muscles, probably as the result of irrita- tive conditions below the site of hemorrhage. Vaso-motor and trophic disturbances in the paralyzed limbs have also been described. Hauna- turia and albuminuria often develop in a short time. Death may follow almost instantaneously if the hemorrhage is situated so high as to involve the medulla oblongata and its respiratory centre. In hemorrhages near the cervical enlargement, the symptoms of paralysis of the diaphragm may occur (affection of the phrenic nerve) and produce fatal suffocation. The disease may also be protracted for weeks, months, and even a couple of years. In certain cases, acute decubitus or cystitis and ammoniacal decomposition of the urine may give rise to septicaemic symptoms, increasing exhaustion, and death. IV. Diagnosis.—The chief interest attaches to two factors in diag- nosis—to the sudden occurrence of the symptoms, and to the predomin- ance of paralytic phenomena. Although meningeal hemorrhage may occur with equal suddenness, irritative symptoms, viz., pain, muscular twitchings, etc., predominate in this disease. In hemorrhagic central myelitis, extensive paralysis may likewise develop in a very short time, but the spread of the process can usually be made out with distinctness. Acute anterior poliomyelitis begins with fever, the paralytic symptoms do not develop so suddenly, and sensory disturbances, paralysis of the bladder and rectum, and decubitus are absent. Cerebral hemorrhage is readily excluded by the absence of paralysis of cerebral nerves, particu- larly of the facial nerve; in addition, the paralysis is generally hemi- plegic. The recognition of the site of hemorrhage is usually easy. It may often be suspected from the location of the pains or cincture feeling. If DISEASES OF THE SPINAL CORD. 81 the lumbar cord is involved, we generally find paraplegia of the lower limbs, paralysis of the bladder and rectum, and loss of reflex irritability; priapism is sometimes noticed. In dorsal hemorrhage, the symptoms remain the same, except that reflex movements reappear or are increased, and that the abdominal muscles are paralyzed. Cervical hemorrhao-e causes paraplegia of all the limbs, and sometimes paralysis of the phrenic nrrve. Bulbar symptoms (pupillary changes, slowness or acceleration of the pulse, difficulty in deglutition, etc.) supervene if the hemorrhage is situated still higher. Y. Prognosis.—The prognosis is unfavorable, since permanent para- lyses are left over, even if the clot is absorbed. Death may occur under different circum- stances with varying rapidity. VI. Treatment.—If there are symptoms of spinal congestion, ten to twenty leeches or cups should be applied to the spine, or five to ten leeches to the anus or cervix uteri. Daily evacuations from the bowels should be secured. The patients should be kept as quiet as pos- sible, upon a Chapman bag filled with ice or a water-bag. Potassium iodide ( 3 iij. : § iij., one tablespoonful t. i. d.) should be given internally, to facilitate absorption of the extravasation. After the cessation of the acute symptoms (in six to ten weeks), the gal- vanic current may be applied (at first the anode, then the cathode) stabile to the site of the disease, for five minutes three times a week, the indifferent electrode on the sternum. The Chapman rubber-bag is extremely important in the treatment of diseases of the cord. It consists of three long rubber-bags, each of which is larger than the one above it (vide Fig. 33). The bags are filled with ice until the latter reaches to the lower end of the adjacent bag. In order to prevent inflammation of the skin, a piece of linen should always be interposed between the rubber-bag and the integument. The bag should be refilled as soon as the ice has melted. Appendix. Capillary (punctate) hemorrhages of the spinal cord usually possess no clinical significance. Para- lytic symptoms can only be expected when they are very numerous and closely aggregated. The hemor- rhages are found not infrequently on a transverse section of the cord, either exclusively or chiefly in the gray matter. They are rarely larger than a fine dot. Unlike bleeding vessels, they cannot be removed by a stream of water or by the fingers. They are situated in the lymphatic sheaths of the vessels, which are sometimes ruptured, so that the blood is free in the tissues. The hemorrhages often constitute an agonal symptom, and are also found in spasmodic diseases, in which they may be associated with meningeal hemor- rhages. They are often found in infectious and severe constitutional diseases. These hemorrhages have also been produced experimentally in animals which were placed in rarefied air; they were so numerous as to give rise to paralytic symptoms. Similar conditions have also been observed in men who worked for Fig. 33. Chapman’s Rubber Bag. natural size. 82 DISEASES OF THE SPINAL CORD. a long timein compressed air and then passed into the general atmosphere. In these cases, however, hemorrhages were not found in the spinal cord. In a case of this kind, Leyden found numerous cavities in the cord surrounded by large cells, which he regards as altered white blood-globules. He explains the appear- ances by Hoppe’s experiments, according to which, in animals placed in rarefied air, the gases partly escape from the blood and produce further serious changes. 4. Acute Inflammation of the Spinal Cord. Acute Myelitis. I. Etiology.—Acute myelitis is one of the rarer diseases. It is rela- tively frequent in middle life (fifteen to thirty years), and more frequent in men than in women. A predisposition to the disease is engendered by alcoholism, dissipa- tion, overwork, living in damp rooms, etc. Under such circumstances myelitis may be produced by very slight causes. Myelitis may be primary or secondary. The former includes rheu- matic, traumatic, and toxic forms; it may also be the result of violent mental excitement. Some claim that the disease may follow excesses in venery, onanism, cessation of menstrual and hemorrhoidal hemorrhages, but this is not beyond dispute. There can be no doubt that a cold is a not infrequent cause of myelitis; it oc- curs occasionally after a wetting, sleeping on the damp ground, etc. Traumatic myelitis is still more frequent than the rheumatic form. It is ob- served after wounds of the cord, fracture and dislocation of the vertebrae, even after violent concussion of the spine or of the entire body. Toxic myelitis is better known experimentally than clinically. It has been produced in animals by poisoning with phosphorus, arsenic, mercury, lead, car- bonic oxide, and alcohol. Secondary acute, myelitis often follows diseases of the vertebrae or meninges (tuberculosis or cancer of the vertebrae, inflammations, hemor- rhages, and tumors of the meninges). It is sometimes a sequel of neu- ritis migrans, occasionally of previous diseases of the spinal cord itself. It may also develop during or after certain acute and chronic infec- tious diseases, viz , diphtheria, pneumonia, typhoid fever, articular rheumatism, pyasmia, puerperal fever, malaria, and especially syphilis. Perhaps certain cases of myelitis are associated with pulmonary phthisis. II. Anatomical Changes.—So far as is known, the process begins with changes in the interstitial tissue (vessels and neuroglia), and these are immediately followed by an affection of the nervous tissue proper. The dorsal cord is affected most frequently, next the lumbar and cervical portions. The first changes almost always occur in the gray substance of the cord (central myelitis), to which it may be confined; in other cases it ex- tends to the white matter. Sometimes the entire transverse section of the cord is inflamed (transverse myelitis), sometimes there is only a small spot of inflammation (circumscribed myelitis), which is perhaps confined to one-half of the cord. In certain cases there are numerous foci of inflammation which may be so small as to be recognizable only under the microscope. In rare cases the inflammatory changes are confined to the periphery, and are associated with meningeal changes (perimyelitis or myelo-m eni ngitis). When acute myelitis attains certain dimensions, the color and con- DISEASES OF THE SPEXAL COED. 83 sistence of the parts are changed. Their consistence is diminished, though softening of the cord may also be non-inflammatory in character. Thus we sometimes find post-mortem softening of the cord, particularly in the dorsal portion, in bodies which have lain on the back for a long time during the summer months. Hence other changes must also be present in order to prove the inflammatory character of the softening. Upon section, the softened parts project abbve the cut surface and form a more or less soft pulp; in some cases they are entirely fluid. The nor- mal markings are indistinct or entirely obliterated. According to the duration of the inflammation, the softened parts present a different color (red, yellow, gray softening). In red inflammatory softening of the cord, the parts have a bright-red, brownish-red, or chocolate color. Numerous extravasations are often found in the surrounding parts, sometimes in the inflamed parts them- selves (hemorrhagic or apoplectiform myelitis). Gradual absorption and transformation of the blood pigment and in- creasing fatty degeneration of the constituents of the cord give rise to yellow softening. Finally the pigment disappears in great part, the fatty elements are absorbed, resulting in gray softening. Microscopical examination should be made, partly on the fresh, partly on the hardened cord. In the former method, scrapings from the knife-blade may be examined in a one-lialf-per-cent solution of sodium chloride, or in diluted glycerin. The cord may be hardened in potassium bichromate or ammonium chromate, the dura mater having first been opened and the cord cut into sections three to five cm. in length. The cord is placed in a one-per-cent solution of the harden- ing fluid for one week, and the strength of the fluid increased one per cent weekly for a month. It becomes fit for making sections after it has been eight to twelve weeks in the five-per-cent fluid. The first microscopical changes in acute myelitis appear in the blood-vessels and neuroglia. The vessels, especially the small veins, are unusually dilated, sometimes very sinuous. Their walls are peculiarly thickened and shining, occa- sionally fibrillated, and the nuclei increased in number. The lymph sheaths are unusually wide, and contain red or white blood-globules. Extravasations may also occur through these sheaths themselves, and appear upon their outer surface. At the same time, changes develop in the neuroglia; its cellular constituents increase in size and number, and their nuclei also proliferate. Some of these cells are perhaps emigrated leucocytes. The basement substance of the neuro- glia is swollen. These lesions are soon followed by changes in the nerve fibres and ganglion cells. The medullary substance of the fibres coagulates, becomes finely granular, takes carmine staining, and finally disappears entirely. At the same time the axis cylinders undergo striking changes in shape. In places they are enormously dis- tended into a spindle-shape; several of these enlargements sometimes follow one another, like a rosary. At the same time, the axis cylinder becomes homogene- ous, vacuolse form in it, and nuclear proliferation has also been described. Next it becomes granular, and later is absorbed. The ganglion cells lose their granular and fibrillated structure, and assume a swollen, homogeneous, and vitreous appearance. They often contain vacuoles. The prolongations are thickened and often separated from the cells. The nucleoli become indistinct, but sometimes proliferate; the nucleus finally becomes more and more indistinct. The cell substance becomes more granular and fatty, and is absorbed; the affected cells often contain an abnormal amount of pigment. Some of the ganglion cells do not disappear, but are converted into small round bodies without prolongations which may remain for a long time in that condition. Foerster observed calcification of the ganglion cells. An important phenomenon is the abundant development of granulo-fatty cells, which are found not alone in inflammation, but also in necrotic processes. These cells are round, composed of fine granules of fat, sometimes contain one or more drops of myelin, and generally disclose a nucleus after staining with carmine. 84 DISEASES OF TIIE SPINAL COED. In hardened preparations they are detected most readily after treatment with potash. These granulo-fatty cells are present in remarkable numbers. They are partly free in the interstices, partly in the lymphatic sheaths of the vessels. In our opinion, they play an important part in the absorption of the fatty masses which result from degeneration of the nerve fibres and ganglion cells. To render the absorption of the fat possible, wandering cells are requisite, which will become stuffed full with fat, and then make their way into the lymphatic sheaths of the vessels. In addition to the granulo-fatty cells, we also find laminated amyloid bodies, whose origin and significance are unknown. In some cases a sort of coagulated exudation is noticeable. It forms vitreous, colloid clumps which are situated partly in the lymphatic sheaths, but in great part upon the external wall of the blood-vessels, sometimes free in the interstices. The extravasated red blood-globules are gradually destroyed, their pigment is deposited in granules or crystalline form, or it is imbibed by the granulo-fatty cells or by larger drops of fat. If the inflammation is very intense, it may terminate in the forma- tion of a circumscribed deposit of pus in the cord (abscess of the spinal cord). This rare occurrence is observed most frequently when the mye- litis is traumatic in origin, and foreign bodies have remained in the cord. If the inflammatory process is protracted, it may terminate in the formation of cysts. The softened parts of the spinal cord become more and more fluid, forming at first an emulsion-like, then a milky, finally a serous fluid. At the same time the surrounding neuroglia proliferates so that a fibrous capsule forms around the fluid. The cyst is often multilocular. In some cases the originally softened spot in the cord undergoes sclerosis, and the disease then usually becomes chronic. The indurated tissue is composed chiefly of new-formed neuroglia which is rich in cells, contains few nervous elements, granulo-fatty cells, and corpora amylacea. Dujardin-Beaumetz has applied the term hyperplastic myelitis to a certain anatomical form in which the interstitial inflammatory changes are especially marked, and the inflamed parts are firm to the feel. The ascending and descending secondary degenerations will be dis- cussed in a subsequent chapter. As a rule, the meninges, particularly the pia mater, also take part in the inflammation. The pia mater is reddened, succulent, occasionally infiltrated with pus. According to Schultze, acute myelitis following syphilis is characterized by marked affection of the meninges and vascu- lar apparatus. The nerve-roots have been found reddened and swollen, and some- times present spindle-shaped enlargements; nuclear proliferation and degeneration of the nerve-fibres'may be seen under the microscope. Degenerative changes have also been observed in the peripheral nerves; increase of the nuclei, unusually distinct transverse striation, more rarely fatty degeneration in the muscles, have been described. Among other organic changes in acute myelitis may be mentioned : bed- sores; inflammation, hemorrhage, ulceration and partial desquamation of the mucous membrane of the urinary passages, particularly the bladder and pelvis of the kidney; decomposed urine in the bladder; not infrequently multiple ab- scesses in the kidneys; hemorrhages into the suprarenal capsules. III. Symptoms.—The symptoms of acute myelitis may begin sud- denly or may be preceded by prodromata for a few hours or days. The prodromata are often of a general, indefinite character: chilly sensa- DISEASES OF THE SPINAL COKD. 85 tions, elevation of temperature, anorexia, increased thirst, general mal- aise, etc. The symptomatology is sometimes like that of an acute infec- tious disease; it begins with a chill, followed by high temperature, and then the other manifest symptoms of myelitis develop rapidly and un- mistakably. In children general convulsions may occur. The suspicion of an acute spinal affection must be aroused if the symptoms described are followed by disturbances of innervation, such as formication in the limbs, a feeling of coldness, shooting pains, etc. Retention of urine, more rarely incontinence of the bladder, is occasion- ally one of the first symptoms. Local changes soon become noticeable. The patients complain of pain in a circumscribed part of the spine, corresponding to the site of disease. The pains are sometimes spontaneous, or they are provoked by movement of the spine, pressure, etc. Many patients complain of a constricting, band-like feeling which extends from the painful spot around the abdomen or thorax. Cardialgic symptoms sometimes appear at an early period. In the mean time, the disturbances of innervation have become more distinct. Irritative symptoms (pain, hypersesthesia, twitchings, and contractures of the muscles) are temporary in character, and generally present only at the beginning of the disease, while, as a rule, paralyses constitute the chief feature of the symptomatology. The pains are usually neuralgiform in character; they are sometimes localized in cer- tain parts, for example, the joints. The pains are sometimes present after the sensory and motor nerves are completely paralyzed (anaesthesia dolorosa). Paralysis of the muscles is one of the chief symptoms of acute myelitis. It may be complete or incomplete, but the paralyzed parts are always flaccid. Transverse myelitis of the lumbar cord gives rise to paraplegia of the lower limbs, in addition to paralysis of the bladder and rectum. In a similar affection of the dorsal cord, the abdominal muscles are also paralyzed, so that the patients cannot cough and strain. Under such circumstances, even a mild bronchitis may be a source of danger. In myelitis of the cervical enlargement, the arms and chest muscles are also paralyzed. Hence inspiration is interfered with to such an extent that diaphragmatic breathing becomes unusually vigorous. In cervical mye- litis, the paralysis is sometimes confined to the arms, while the legs escape. Inflammation of the upper part of the cord is shown by implica- tion of bulbar nerves: unilateral or bilateral myosis, slowness of the pulse (twenty-eight beats in a minute in one case), disturbances of deglu- tition, difficulty in articulation, etc. Redness and increased heat of the face and neck indicate paralysis of the sympathetic. Descending optic neuritis, with subsequent atrophy, has also been described. Painful attacks of palpitation of the heart are sometimes observed. The chief danger in cervical myelitis arises from paralysis of the phrenic nerve; respiration is then impeded, and death takes place from asphyxia. The nutrition of the paralyzed muscles may be unimpaired for along time, until atrophy from disuse gradually develops. But in some cases there is rapid emaciation, as the result of destruction of the large (trophic) cells in the anterior horns of the gray matter, or of implication of the nerve-roots in the morbid process. In the latter event, the degeneration reaction is produced in the paralyzed muscles. In atrophy from disease, the electrical irritability 86 DISEASES OF THE SPINAL CORD. gradually diminishes to a slight extent, and to an equal degree to both currents. At first the cutaneous sensibility is occasionally diminished or ab- olished only for certain modes of sensation; later, complete anaesthesia generally develops. In the former event, delayed conduction is some- times noticeable. Certain patients experience a sensation of vibration of the entire limb after the application of circumscribed stimuli, for example, the prick of a pin (dysassthesia). Yaso-motor disturbances are almost always noticeable. The para- lyzed limbs are reddened or livid, warmer than normal, and do not sweat. Brieger found that the paralyzed parts remained dry even after dia- phoresis was produced by injections of pilocarpine. After the disease Fig. 34. Acute decubitus in dorsal myelitis. 1, gangrenous; 2, erythematous portion. After Charcot. has lasted for some time, the paralyzed parts become* pale and cold. (Edema of the skin and swelling of the joints are not infrequent. Nor are trophic changes rare. They consist of active desquamation of the epidermis, erythema, vesicular eruptions, and especially acute decubitus. This develops most frequently over the sacrum, next over the trochanters, malleoli, and heels. The skin reddens, then vesicular elevations form, and finally the tissues undergo rapid gangrenous de- struction. This often spreads with terrible rapidity, extends through the spinal column, and invades the meninges and spinal cord. The development.of decubitus is favored by pressure on the parts, but it may also develop independently, as the sole result of trophic disturbances. It has been attributed to disease of the posterior horns and the adjacent, parts of the posterior columns of the cord. DISEASES OF THE SPINAL COED. 87 Reflex irritability is affected in various ways. If the inflammation extends through the lumbar cord, reflex action in the lower limbs is necessarily abolished. If the lesion is situated higher, the reflex irrita- bility of the lower limbs may be diminished or abolished at first as the result of the severe general disturbance of the cord, but later the reflex irritability is increased and does not disappear again until the inflamma- tion has assumed larger proportions. The cutaneous and tendon reflexes are affected in the same way. Important changes in the urine very often develop at an early period, and it has been assumed by some that these are the result of trophic changes, not of simple stagnation of urine. The urine becomes bloody, albuminous, cloudy, and ammoniacal, and the retention of urine may give rise to septicaemic and pyaemic conditions. Engelken ob- served sugar in the urine in dorsal myelitis. The bladder and rectum are paralyzed from the beginning (in lum- bar myelitis), or not until a later period of the disease. As a rule, there is at first retention of urine (paralysis of the detrusor vesicae). and incontinence occurs at a later period (paralysis of the sphincter vesicae). Or paralysis of both muscles occurs simultaneously, i. e., there is a con- stant flow of urine, although the bladder is not thoroughly emptied. A similar condition obtains with regard to the rectum—at first obstinate constipation, later involuntary evacuations. In cervical and dorsal myelitis, priapism is not infrequent; the erection is generally flaccid, but painful. Involuntary discharge of semen has also been described. The paralysis sometimes begins suddenly at night, and within a few hours or days spreads upwards or downwards, or in both directions, dis- turbances of innervation on the part of the medulla set in, the tempera- ture of the body often becomes hyperpyrexia!, and finally death occurs from the excessive rise of temperature or from suffocation. This is especially apt to occur in hemorrhagic myelitis. In other cases, the disease lasts one to three weeks; exhaustion, de- cubitus, ammoniaBmia, septicsemic and pyaemic conditions, or a compli- cating pneumonia put an end to life. In still other cases, the disease runs a subacute course, and lasts many weeks. French writers apply the term recurrent myelitis to a form which is charac- terized by relapses, the intervals sometimes lasting several months. If the disease becomes chronic, certain paralyses disappear, others remain permanent. Recovery of the paralysis is possible in those cases in which certain parts of the cord are compressed by inflammatory swelling or oedema, and this pressure is relieved. Muscular twitehings and contractures, and exaggeration of the tendon reflexes indicate sec- ondary degeneration in the cord. Complete recovery can hardly be looked for. IV. Diagnosis.—The recognition of acute myelitis is usually easy. It is distinguished from acute spinal meningitis by the fact that in the latter the irritative symptoms are more marked, the paralysis less marked. In spinal and meningeal hemorrhage, the symptoms begin more suddenly, and in the latter affection there are marked symptoms of irritation; in addition, a greater degree of recovery is possible. Ascend- ing myelitis may be mistaken for Landry’s ascending paralysis, but in the latter, the electrical excitability is unchanged, and the course of the 88 DISEASES OF THE SPINAL CORD. disease is usually more rapid. In multiple neuritis, the electrical irri- tability of the paralyzed nerves and muscles rapidly diminishes. The differentiation from hysterical paralysis is sometimes difficult, but this disease generally afEects women, and other symptoms of hysteria are usually present. We should also endeavor to ascertain the height of the morbid pro- cess. We must therefore take into consideration the painful points on the spine, the distribution of the motor paralysis, and particularly the extent of the cutaneous anaesthesia. If the latter is tested from below upwards, the boundary of the anaesthetic region will be found a little below the site of inflammation in the cord. In lumbar myelitis, the anaesthesia usually extends about to the level of the umbilicus. In mye- litis of the lower dorsal cord, the skin is anaesthetic as far as the lower end of the sternum. In myelitis of the upper part of the dorsal cord, the anaesthetic zone extends to the axilla; in cervical myelitis it involves the upper limbs. The following statements may be made concerning the extension of the inflammation over the transverse section of the cord. Motor paraly- sis indicates an affection of the lateral columns, particularly the inner- most parts and adjacent gray substance (pyramid tracts). . If the motor paralysis is followed by rapid atrophy and degeneration reaction in the paralyzed muscles and nerves, we may assume destruction of the anterior horns (poliomyelitis) or interruption to conduction in the anterior roots. The latter is more probable if marked cincture feeling and pains are noticed. Sensory disturbances indicate implication of the posterior columns, posterior horns, or posterior roots. V. Prognosis.—The prognosis is almost always unfavorable as re- gards recovery. The greater the tendency to spread transversely or along the cord, the more unfavorable is the prognosis. Decubitus, alkaline decomposition of the urine, paralysis of the phrenic, and bulbar symptoms are especially grave symptoms. VI. Treatment.—Causal treatment should be adopted if the acute myelitis is the result of syphilis. We may then order inunctions of mercurial ointment (gr. lxxv. daily) and potassium iodide internally (gr. xij. t. i. d.). Some authors recommend the internal administration of calomel. Mercury has also been recommended as an active antiphlo- gistic even in cases of non-syphilitic origin. In the majority of cases, the treatment must be purely symptomatic. The patient’s bed should be perfectly smooth, in order to avoid pressure and thus prevent bed-sores. He should lie upon the side or abdomen as much as possible, and frequently change the position of the body. In addition, the skin should be rubbed daily with alcohol in order to harden it. If the skin grows red or decubitus begins, the parts should be covered with adhesive plaster which is renewed daily. In addition, an air bag should be used. But if the bed-sore has already spread widelv, the best services are rendered by the permanent water bath (28° to 30° R.). In retention of urine, the bladder should be catheterized three times a day, care being taken to keep the catheter scrupulously clean by keep- ing it constantly in a five-per-cent solution of carbolic acid. If the urine is constantly dribbling away, a rubber urinal may be given to male patients, while females may use a bed-pan encased in rubber. In our opinion, the permanent introduction of a catheter into the bladder is DISEASES OF TIIE SPINAL COED. 89 less advisable. We should always endeavor to avoid soiling the skin with urine, since this is apt to result in decubitus. If the urine has undergone decomposition, it may be caught in ves- sels in which fifteen to seventy-five grains of naphthalin have been placed to correct the urinous odor. We have also seen good results from the internal administration of naphthalin (gr. vij. every two hours), but the remedy must be discontinued in some patients because it produces intolerable burning in the urethra, and even albuminuria. We should then order potassium chlorate, salicylic acid, etc., and wash the bladder at regular intervals (vide Vol. II., page 122). If the patients suffer from constipation, we may employ the remedies recommended in Yol. II., page 334; if incontinence of fasces occurs, a bed-pan should be used at regular intervals. The greatest care should be taken to clean the patient at once, as soon as he has soiled himself. The diet should be nutritious, but easily digestible. Tea, coffee, and alcoholics must be avoided. Local antiphlogosis is important. This is best efEected by means of Chapman’s ice-bag (vide Fig. 33), or by an ordinary ice-bag or water-bag applied to the spine. Derivati ves may also be applied in the neighborhood of the spine, the best being alcoholic or other stimulating inunctions. But we object to the employment of dry cups, leeches, blisters, tartar emetic ointment, actual cautery, since they favor the development of decubitus. Applica- tions of tincture of iodine to the spine must also be made with caution; inunctions of potassium iodide or iodoform (1:15) ointment or iodoform collodion are preferable. Among internal remedies, potassium iodide (gr. xij., t. i. d.) is the most highly esteemed, but too much should not be expected from it. In anaemic individuals, preference should be given to the preparations of iodide of iron. Patients who complain of painful twitchings in the limbs or other violent pains, require subcutaneous injections of morphine. After the acute symptoms have subsided, we may employ the ner- vines, concerning whose efficacy opinions vary greatly. We may mention nitrate of silver, auro-natrium chloratuin, strychnine, arsenic, phos- phorus. If irritative symptoms are absent, electrical treatment is much more strongly indicated at this stage of the disease.. In electrical treatment of the site of. disease, the galvanic current is alone employed: current not too strong, sittings two to three times a week, not more than five minutes at a time. If there is only one focus of disease, the anode and cathode may be used stabile alternately, with large electrodes. Stabile ascending and descending currents may be employed alternately if there are several foci of disease. Galvanization of the cervical sympathetic has also been recommended: one electrode on the sternum or last cervical vertebra, the other on the side of the neck immediately below the angle of the lower jaw . The faradic current may be applied to the pai-alyzed muscles to prevent atrophy from disuse, and also in paralysis of the bladder and rectum. After the patients begin to move their limbs, they must be warned against over-exerting themselves. They must especially avoid sexual intercourse. Patients who are unable to travel may take baths during the summer, especially chloride of sodium or thermic baths. Cold-water cures some- 90 DISEASES OF THE SPINAL OORD. times produce surprisingly good results. In ordering baths of any kind, it should be remembered that they should not be too warm (not above 28° R.), too frequent (not more than three to four times a week), or too prolonged (ten to fifteen minutes). 5. Chronic Inflammation of the Spinal Cord. Chronic Myelitis. I. Etiology. — The causes of chronic myelitis are the same as those of the acute form, except that a congenital or acquired hereditary pre- disposition is much more marked. II. Anatomical Changes.—The cord may appear normal to the naked eye, although the microscope reveals extensive changes. In many cases macroscopic changes are noticeable. As a rule, the cord is unusually firm at the affected parts. These parts are generally diminished in size, and the cord appears depressed and flattened in cir- cumscribed localities. These have a gray or grayish-yellow color, appear transparent, and sometimes shine through the pia mater. The meninges over the affected parts are often thickened, adherent and congested, and the pia mater can be removed with difficulty from the substance of the cord. In rarer cases, chronic myelitis appears as softening (myelomalacia). After absorption of the inflammatory products, cavities may develop (syringomyelia). The cavities, which are filled with serum, may attain considerable size, or in other cases they impart to the cord a sieve-like appearance (myelitis cribrosa). Chronic myelitis affects the dorsal region most frequently, next the cervical and lumbar enlargements. The same conditions hold with regard to distribution and extent of the inflammation as obtained in acute myelitis. If the gray matter is chiefly or exclusively affected, the process is known as chronic central myelitis. Hallopeau has described a peri-ependymal sclerosis, which is confined, in the main, to the connective tissue surrounding the central canal. In chronic myelo-meningitis the peripheral portion of the white substance is affected; this often follows a previous meningitis. Chronic myelitis may also be circumscribed, transverse, and multiple (disseminated, insular). The latter form must not be mistaken for sec- ondary degeneration of the cord, which may follow a chronic inflamma- tory process iii the cord. Among the microscopical changes in chronic myelitis, those in the interstitial connective tissue are the most prominent, although a strict differentiation can- not be made between interstitial and parenchymatous inflammatory processes. The neuroglia presents increase of the interstitial tissue and the cellular ele- ments. The spider cells are unusually abundant and distinct, often enlarged and contain several nuclei. In addition, there are cells of a lower grade of develop- ment, and even simple round cells. The interstitial tissue is gradually replaced by distinctly fibrillated connective tissue. The blood-vessels are thickened, their nu- clei increased, and their lymphatic sheaths unusually wide, and filled with fat, granulo-fatty cells, pigment, or in places with white, more rarely red, blood-glob- ules. The blood-vessels may be dilated in some parts, in others filled with clots. Granulo-fatty cells may be entirely absent; at all events they are much rarer than in acute myelitis. Amyloid bodies are more numerous. The medullary sheaths of the nervous elements undergo degeneration. The axis cylinders may present numerous spindle-shaped dilatations; th% inflamma- DISEASES OF THE SPINAL CORD. 91 tory foci not infrequently contain numerous sclerosed, hypertrophic axis cylin- ders, without medullary sheaths. The ganglion cells are usually smaller, very granular and pigmented, and often retracted into small round clumps. In other places they contain vacuolae. Atrophic and sclerotic changes hare been observed in the nerve roots and even in the peripheral nerves, in some cases. Degenerative- atrophy of the muscles has also been seen. Among other organic changes maybe mentioned inflammation of the- bladder, urinary passages and kidneys, pneumonic, phthisical, hypo- static changes in the lungs, decubitus, etc. Jir, Symptoms.—The symptoms begin not infrequently in an acute, febrile manner, or several acute relapses follow one another before the disease becomes chronic, while in other cases the development of the disease is slow and dragging from the start. Apart from the gradual onset of the affection, the symptoms are very similar to those of acute myelitis. It often begins with paraesthesias, crawling, coldness, burning, etc. These are often associated with neuralgiform pains which may be very violent and are sometimes confined to definite localities, for ex- ample, the joints. Many patients complain of pains in the back and a cincture feeling. Paralyses of motion and sensation gradually super- vene. The first signs of weakness generally appear first in the lower limbs, rarely in the upper limbs, somewhat more frequently in all the limbs. Spinal hemiplegia or even paralysis of a single limb may occur if the inflammatory focus in the cord is sufficiently circumscribed. The paralysis sometimes begins in the lower limbs, and then gradually ex- tends to the upper limbs and even to the bulbar nerves. Paralysis of the bladder and rectum is sometimes an early symptom, and at all events it appears sooner or later. Priapism, seminal ejaculations, and impo- tence are also observed. The same conditions obtain with regard to the reflexes, nutrition, and electrical excitability as in acute myelitis (vide page 85). In the later course of the disease we not infrequently notice tension and con- tracture of the paralyzed muscles and increase of the tendon reflexes— symptoms which are probably associated with secondary degeneration in the lateral columns of the cord. Acute pyrexial exacerbations sometimes occur and are almost always followed by an aggravation of the symptoms, especially the paralysis. Erb states that he has seen the symptoms improve after typhoid fever and scarlatina. The disease may last many years (ten to twenty); complete recovery hardly ever occurs, and some of the symptoms will persist even in the most favorable event. The disease sometimes takes an unexpected acute turn, the symptoms of acute myelitis develop, rapidly extend upwards, and prove fatal from paralysis of the bulbar nerves. Other patients die from gradual exhaustion, or bed-sores and cystitis develop, followed by pyaemic and septicaemic conditions. In some cases the clinical history changes and merges into that of multiple cerebro-spinal sclerosis. IV.—Diagnosis, Prognosis, and Treatment are the same as in acute myelitis. 6. Multiple Cerebro-spinal Sclerosis. I. Etiology.—The disease is most frequent between the fifteenth and thirty-fifth years, and is rare after the age of forty-five. According Kig 35 Spinal cord and posterior part of brain in multiple oerebro-spinal sclerosis. After Leyden. The sclerotic parts are readily recognized by their darker color, a-h, sections of the cord; a, medulla oblongata- b c cervical cord; d, e, dorsal cord; f-h, lumbar cord. DISEASES OF THE SPINAL COED. 93 to Charcot and Moric it is not very infrequent in childhood. Three con- genital cases (without autopsy) have been reported. Heredity has been demonstrated in some cases. Many writers attri- bute the disease to cold, exposure to wet, injury or mental excitement. Pregnancy is said to favor its development. In some cases it follows acute infectious diseases, such as typhoid fever, variola, cholera, scarla- tina, etc. According to some statements multiple sclerosis may be pro- duced by hysteria (?). II. Anatomical Changes.—Multiple sclerosis appears in the form of inflammatory foci which are irregularly scattered throughout the brain and cord. Their number and size vary exceedingly. Sometimes there are more than a hundred foci, in other cases very few. Their size varies from a barely visible speck to a spot five to ten centimetres in size* Some foci are so small as to be visible only under the microscope. Fig. 36. Transverse section of the cervicaJ enlargement in multiple sclerosis. Osmic acid preparation. The light parts in the spinal columns are sclerosed. Enlarged 10 times. After Bramwell. The superficial plaques are generally visible through the pia mater with a grayish yellow, pearl-gray, or bluish-gray color. They sometimes project above the surrounding parts, sometimes they are depressed. As a rule, they are harder than the normal cord, more rarely they are gela- tinous and soft. Transverse sections sometimes assume a light rosy-red color when exposed to the air. As a rule, a more or less abundant juice can be scraped from them with the blade of the knife. The plaques vary in shape, and usually are sharply defined (vide Figs. 35 and 36). Under the microscope, how- ever, they present gradual transitions into the normal tissues. The in- dividual plaques are sometimes connected with each other by a less markedly inflamed portion, but this is not the rule, as is claimed by Buchwald. Many of the patches contain yellow dots and streaks (fatty, thickened vessels). 94 DISEASES OF THE SPINAL CORD. The inflammatory foci are distributed in an entirely irregular man- ner. In the cord the white substance is preferably affected; the changes are sometimes especially marked along certain columns. Secondary de- generations are generally absent, even if the sclerotic patches are so ex- tensive as to interrupt the paths of conduction. Schulze attributes this to the fact that, on account of the long persistence of the axis cylinder, a real destruction of the conducting paths rarely occurs. The medulla oblongata and pons are very often affected; the floor of the fourth ventricle presents a certain degree of predilection. The cerebellum often escapes; if not, the sclerotic patches are al- most always found in the white matter. This is also true of the cere- brum, in which the most frequently affected parts are the walls of the lateral ventricles, corpus callosum, centrum semiovale, corpus striatum, and optic thalamus. In addition to multiple sclerosis, diffuse sclerosis of the brain has also been found. The microscopical changes in multiple cerebro-spinal sclerosis are similar to those of chronic myelitis. The characteristic feature is proliferation of the con- nective tissue, with destruction of the nervous elements. In the most recent patches, Deiter’s cells are found enlarged, and their nuclei increased; in addition, increase of the interstitial tissue. The neuroglia presents an unusual abundance of cells and nuclei, partly the result of increase of the elements previously pres- ent, partly of the emigration of white blood-globules from the vessels. Masses of found cells are found in many places on the external wall of the vessels. Finally, the interstitial tissue is converted into firm fibrillated connective tissue. At the same time, the blood-vessels are thickened, are dilated into a spindle shape in places, their nuclei are increased; the lymphatic sheaths, which are di- lated here and there, contain fat granules, granulo-fatty cells or larger accumula- tions of fat. On the external wall of the vessels we sometimes find accumula- tions of granulo-fatty cells, sometimes a larger or smaller number of fat crystals. The number of granulo-fatty cells varies, but they disappear almost entirely in older plaques. The amyloid bodies are more numerous. The medullary sheaths of the nerve fibres degenerate and disappear, the axis cylinders are dilated into a spindle shape, become firmer, and have a dull gloss. They are very resistant, and often persist in very old plaques. The ganglion cells often contain an unusual amount of yellow pigment, become granular, lose their prolongations, and are converted gradually into small round structures. The formation of vacuolae within them is also observed. Many authors believe that the lesion begins in the nervous elements proper, and that the proliferation of the neuroglia is a secondary process. Others regard the blood-vessels as the starting-point of the disease. It is not impossible that there are various modes of development. The blood-vessels have been regarded as the starting-point, particularly in those cases in which the process follows an infectious disease. The spinal meninges are sometimes unchanged. At other times they are thickened, congested, and adherent over the sclerotic patches. Gray sclerotic patches have also been found in the cerebral nerves and the spinal nerve roots. Whether they also occur in the peripheral nerves has not been positively settled. Degenerative atrophy and fatty degen- eration of the muscles have been observed at times, particularly when the anterior horns of gray matter have been affected. Leyden discov- ered sclerotic changes in the muscles. Among the changes found in other organs may be mentioned: decu- bitus, cystitis, pyelonephritis, pneumonia, phthisis, bronchitis, and some- times changes in the joints and bones. III. Symptoms.—The symptoms of multiple sclerosis present an unusually manifold character. Sometimes the cerebral, sometimes the DISEASES OF THE SPINAL COED. 95 spinal symptoms predominate. But, as a rule, certain characteristic phenomena, viz.: volitional tremor, nystagmus, scanning speech, pa- retic symptoms, and apoplectiform attacks, are always observed. At the beginning of the disease, the symptoms often have a vague character. Some patients complain of headache or vertigo, others of re- peated attacks of vomiting and gastric pain (crises gastriques), still others manifest spinal disturbances, particularly paraesthesiae and neuralgiform pains in the lower limbs. The situation becomes more serious when paralytic symptoms develop. The motor disturbances are more prominent; sensory paralysis is some- times absent during the entire course of the disease. The patients are easily tired in walking; the paresis gradually increases and extends to the trunk and upper limbs. it is especially characteristic that each volitional movement is attended by violent tremor (volitional tremor). If the patient rises from a seat the trunk totters, generally from before backwards, and vice versa; when directed to move the head this part wags to and fro. If the patient is directed to place the fingers slowly upon the head of a pin, etc., the limb undergoes incessant zigzag, shaking movements. The more the patients hand approaches the desired object the more vigorous the movements be- come. They cease, as a rule, during rest. This volitional tremor is so characteristic of multiple sclerosis that great, perhaps insurmountable obstacles will be encountered in diagnosis if the symptom is absent. Charcot attributed the volitional tremor to the change in the axis cylinder of the sclerotic patches and to its persistence, so that the impulse of the will reaches the muscles in an intermittent manner. It is more probable that this symptom is the result of an affection of certain parts of the central nervous system, perhaps the pons and more anterior portions of the brain. Nystagmus is an equally important symptom. It almost always de- velops when the patient is directed to look at an object steadily, or to follow with the eyes an object that is moved about. The eyes are then observed to twitch from one side to the othei\ Nystagmus is observed in about half the cases, but its cause is unknown. There may also be very peculiar changes in speech. The patients speak slowly, scan the different syllables in a monotonous tone, often in a very high pitch. At a later period speech often becomes indistinct if paralysis and atrophy of the muscles of the tongue, palate, and lips be- come more marked. The pronunciation of the consonants I, p, g, and t is usually first affected. Leube noticed, on laryngoscopic examination of a patient, that the closure of the vocal cords during phonation was suddenly interrupted for a short time; Lomikowski described trembling movements of the vocal cords. Apoplectiform attacks occur in many cases during the course of the disease, sometimes at its onset, sometimes at a later period. The attacks generally begin suddenly, are attended with disturbance of consciousness, but rarely with complete unconsciousness, and sometimes with epilepti- form convulsions. The bodily temperature is often markedly elevated (occasionally to 40° or 42°), and hemiplegia is often left over, but gene- rally disappears in a few days. The entire condition is very often im- paired after recovery from these attacks. In addition to the chief symp- toms already discussed, there are a number of other phenomena of spinal, bulbar, or cerebral origin. 96 DISEASES OF THE SPINAL CORD. Sensory disturbances may be entirely absent. In other cases, certain qualities of sensation may be abolished, but complete anaesthesia is rare. Paresis of the muscles is more frequent than complete paralysis. Rigidity and muscular spasms, which may develop spontaneously or only after purposive movements, are sometimes observed at a very early period. Contractures gradually develop, particularly in the muscles of the back of the neck and the adductors of the thigh, at a later period in the flexor muscles of the limbs, so that the patients become unable to walk. Pre- vious to this the gait is awkward or stiff, like that of spastic spinal paralysis. Distinct ataxia occasionally develops if the posterior columns, particularly the bandelettes externes, are affected in a marked degree. Paralysis of the bladder and rectum sometimes occurs at a very early period, but often disappears; at a later stage it remains persistent. This opens the way for the development of cystitis, pyelonephritis, ammon- semia, septicaemia, and pyaemia. The sexual function is gradually abol- ished. Vaso motor disturbances (abnormal color of the skin, changes in tem- perature and perspiration, gangrene and oedema of the skin) have been observed in some cases. Trophic changes may also occur, viz.: decubitus, herpes, bullous eruptions, abnormal growth of hair, changes in the nails, swelling of the joints, etc. Individual muscles may rapidly atrophy and lose their faradic excitability; this takes place if the ganglion cells in the anterior horns of gray matter are destroyed. Increased galvanic excitability has sometimes been demonstrated in the contractured muscles. Reflex excitability is markedly exaggerated in the majority of cases. This is true not alone of the cutaneous, but also of the tendon reflexes. Gentle tapping of the patellar tendon produces vigorous clonic contrac- tions of the muscles of the corresponding limb, sometimes also in the other limb. Rapid dorsal flexion of the foot causes trembling move- ments of the whole limb, which often cease on sudden plantar flexion of the great toe (reflex inhibition). Vigorous reflex contractions are also produced by tapping the tendons of the biceps and triceps, etc. If extensive changes occur in the medulla oblongata, symptoms de- velop which are similar to those of bulbar paralysis. The tongue under- goes atrophy and is moved with difficulty; speech becomes so indistinct as to terminate finally in a mere grunt; deglutition is impaired, closure of the epiglottis and of the naso-pharyngeal cavity is impaired, and the patients often swallow the wrong way; the lips atrophy, and can no longer be closed. Attacks of palpitation and dyspnoea occasionally set in, and may prove fatal (paralysis of the pneumogastric). Other cerebral nerves may also be paralyzed, and this may give rise to deafness, unilateral or bilateral ageusia, anosmia, ptosis, paralysis of one or all the ocular muscles (in the latter event the eyeball is immovable), unilateral or bilateral myosis, or mydriasis. Many patients complain of flashes of light before the eyes, and gradually become amblyopic. Amau- rosis is rare. Ophthalmoscopic examination reveals atrophy of the optic nerve, the papilla being abnormally white, and the retinal vessels unusually narrow. Uhlhoff found atrophy of the disc in 25# of the cases, marked optic neuritis in 16#. Eulenburg recently described a case in which optic atrophy and com- plete amaurosis preceded the first spinal symptoms for five years. Vertigo is a very frequent spinal symptom. The patients may have DISEASES OF THE SPINAL CORD. 97 the sensation either that objects are revolving around them or that they themselves are revolving. The vertigo is sometimes not of central origin, but the result of ocular paralysis and diplopia. There is often a remarkable variability of mood; the patients laugh and cry without motive. They often become apathetic and dull, and the facial expres- sion becomes apathetic. Mania, dementia, delusions of grandeur, etc., develop in some cases. The disease may last twenty or even thirty years. Kemissions and exacerbations occur not infrequently. The former may be so pro- nounced as to raise the vain hope of recovery. Charcot recognizes three stages of the disease: the first stage, until the development of contractures which compel the patient to keep con- stantly in bed; the second stage, in wThich the characteristic symptoms of the disease are present, and which often lasts many years; the third stage, a period of increasing marasmus. The disease always terminates fatally. Death is the result of increas- ing marasmus, sometimes accelerated by violent diarrhoea; of decubitus and vesical paralysis, with their sequelae; of an apoplectiform seizure; of advancing bulbar symptoms, or finally of intercurrent diseases. IY. Diagnosis.—In addition to nystagmus, disturbances of speech, vertigo, and apoplectiform attacks, volitional tremor possesses a very great diagnostic significance. The disease is not apt to be mistaken for •other affections which are associated with tremor. In paralysis agitans, the tremor persists during: repose, hardly ever affects the head, and the patients are able to control it for a time by an effort of the will. In addition, the motor symptoms are less marked, sensory disturbances and paralysis of the bladder are absent, and the disease generally begins beyond the age of forty years. In chorea, the movements present greater excursions and persist during repose; paralyses and sensory disturbances are absent. Westphal recently described two cases in which the symptoms of multiple sclerosis existed for years, but the autopsy revealed no lesion of the nervous system. There is, therefore, a neurosis whose clinical history is so like that of multiple sclerosis that it cannot be distinguished from it with certainty. Optic nerve changes would be positive evidence in favor of the diagnosis of sclerosis. On the other hand, there may be extensive multiple sclerosis without the typical clinical history of the disease. French writers have applied to this form the term sclerose en plaques fruste (atypical sclerosis). This variety sometimes presents only cerebral symptoms (vertigo, headache, apoplectiform or epileptiform attacks), although the autopsy shows ex- tensive spinal sclerosis; other cases simulate the history of ordinary myelitis, etc. The history of multiple sclerosis may also be very similar to that of locomotor ataxia. But in ataxia the patellar reflex is absent, and sen- sory symptoms predominate, while the motor power of the muscles is very little impaired. It may be very difficult to distinguish multiple sclerosis from progressive paralysis of the insane, since, apart from the fact that both affections may be combined, tremor, speech disturbances, pupillary changes and apoplectiform attacks may be observed in uncom- plicated progressive paralysis. Y. Prognosis.—The disease always terminates fatally, though life may be prolonged for a long time. 98 diseases of the spinal cord, VI. Treatment.—The treatment is the same as that of myelitis (vide page 88). 7. Tumors of the Substance of the Spinal Cord. I. Anatomical Changes.—Tumors rarely occur in the substance of the spinal cord, and can hardly ever be diagnosed with certainty during life. The most frequent form is glioma; next, pure sarcoma: myxosarcoma and fibrosarcoma have also been observed. Tubercles and gummata will be consid- ered in Vol. IY. Glioma affects mainly the enlargements of the cord, particularly the cervical enlargement. According to Virchow, it starts from the neuroglia; according to Klebs, from the nerve fibres and ganglion cells. It is sometimes unusually vas- cular (telangiectatic glioma), and is infiltrated with extravasations and blood cysts. Mixed forms of glioma are also observed. The size of the tumors varies from that of a hempseed to that of a hazelnut, or even much larger. They are usually round, but occasionally elongated, and sometimes extend along the entire cord into the medulla oblongata. They are often sharply circumscribed, occasionally surrounded by a fibrous capsule ; more rarely they pass gradually into the substance of the cord. The cord is often softened in the vicinity of the tumors, or secondary degen- eration may result, etc. II. Symptoms.—Despite their large size, tumors of the cord sometimes remain entirely latent. In other cases, the most varied symptom complexes are ob- served. In sudden hemorrhages into and rapid enlargement of a tumor, the symptoms of haematomyelia are produced. More or less acute signs of compres- sion of the cord are most apt to develop. Or the signs of transverse ascending and descending myelitis are produced. Tabetic or spastic symptoms are noticed, according as the posterior or lateral columns are involved. The symptoms of progressive muscular atrophy or the various forms of poliomyelitis have been observed, if the ganglion cells of the anterior horns were affected. The symp- toms of unilateral lesion of the cord have also been described. Or vague, inde- finable spinal symptoms make their appearance. The disease may last for many years. Death results from intercurrent diseases or increasing marasmus. III. Etiology.—Nothing is known concerning the etiology of the tumors. Trauma, cold, pregnancy, mental excitement have been mentioned as causes. IV. Diagnosis.—The diagnosis is generally impossible. As a rule, we must be satisfied with the diagnosis of a spinal affection. We may suspect a neoplasm if the symptoms have been preceded by phthisis, scrofula, or syphilis. V. Prognosis.—With the exception of gummata, the prognosis is always bad. VI. Treatment.—Gummata are treated by antisyphilitic remedies. The treatment of other forms of tumor is purely symptomatic. 8. Syringomyelia and Hydromyelia. Formation of Cavities in the Spinal Cord. 1. Cavities in the cord may be congenital or acquired. They sometimes extend the entire length of the cord, from the lower part of the fourth ventricle to the conus terminals, somtimes they are very short. On transverse section, they form narrow fissures or elongated, rounded, or irregular cavities; their size often varies in different places. A number of cavities are sometimes closely aggregated. They are generally most extensive in the cervical and dorsal por- tions of the cord, so that these parts may form a fluctuating sac, which gener- ally contains clear serous fluid. The fluid is rarely hemorrhagic or flocculent. The wall of the cavity is often composed of firm connective tissue. Under the microscope, this is found to consist of branching cells, fibrillated intercel- lular substance, a few granulo-fatty cells, and thickened blood-vessels. The latter may be very brittle, and give rise to hemorrhages. In other cases, the cavity is situated in a gray, gelatinous mass composed of intercellular substance and round cells. The inner surface of the cavity sometimes is covered with cylindrical epithelium; sometimes this is absent. The cavities are situated most frequently between the posterior columns of the cord, but often change their position at different heights. They are often independent of the central canal; in other cases they merge into it in places. DISEASES OF THE SPINAL CORD. 99 Sclerosis, especially of the columns of Goll or Burdach, acute and chronic mye- litic foci, etc., are also often present. 2. Simon suggested that a distinction should be made between syringomyelia and hydromyelia, the latter term being applied to those cavities which result from dilatation of the central canal. These dilatations, apart from congenital cavities, may be the result of inflammatory proliferation and subsequent retrac- tion of the connective tissue surrounding the central canal or of circulatory dis- turbances in the cerebellar fossa as the result of tumors. Simon and Westphal believe that softening of tumors and subsequent absorp- tion may give rise to the formation of cavities in the cord, but Leyden claims that these are apt to be mistaken for inflammatory new-formations or coagulation at the periphery of the cavities. Hemorrhages ana inflammatory softening may also lead to the formation of cavities, after absorption has taken place. Simon attributes some cases to men- ingeal adhesions. Fig. 37. Fig. 38. Two cases of syringomyelia without symptoms during life. o-6, cervical cord ; c-e, dorsal cord Natural size. Eichhorst and Naunyn observed syringomyelia develop in new-born dogs, whose spinal cord had been strongly compressed at one spot soon after birth. 3. In a number of cases, very large cavities have been found which had given rise to no symptoms during life, as is shown in two cases which came under our own observation (Figs. 37 and 38). Spinal symptoms were absent in both cases, although the cavities extended from the first cervical to the first lumbar nerves. An attempt has been made recently to construct a symptom complex for certain cases: slowly-progressing atrophy of the upper limbs, partial sensory disturb- ances, especially changes in temperature and pain sensibility, vaso-motor and trophic cnanges, absence of the tendon reflexes, rarely rigidity of the muscles and contractures; bulhar symptoms often supervene at a later period. 100 DISEASES OF THE SPINAL CORD. b. SYSTEM DISEASES OF THE SPIRAL CORD. Simple System Diseases. 1. Gray Degeneration of the Posterior Columns. Tabes dorsalis. {Sclerosis of the Posterior Columns. Progressive locomotor ataxia.) I. Etiology.—Locomotor ataxia is the most frequent disease of the spinal cord. It is much more common among men than among women, and is chiefly a disease of middle life, particularly between the age3 of 30 and 40 years. It rarely begins after the age of 50 years or during the period of childhood. Among its causes syphilis occupies a prominent part. Although our experience corroborates that of Leyden and Westphal, who maintain that Fournier and Erb have exaggerated the importance of this etiologi- cal factor, nevertheless it cannot be denied that a history of syphilis is often obtained in this disease, and that an inunction treatment produces surprising results in not a few cases. From our present knowledge it would appear that ataxia is particularly apt to follow syphilis if the symptoms of the latter were mild and were not thoroughly treated. Tabes dorsalis is one of the late sequelae of syphilis (usually five years, often ten to twenty years, after infection). Some writers maintain that syphilis merely causes a sort of weakness of the spinal cord, so that other hardly demon- strable causes may give rise to tabes. Cold is often mentioned as a cause, but it is probable that this will act as an etiological factor only if there is an abnormally slight power of resistance of the spinal cord, either congenital or acquired. Among causes of a similar character may be mentioned: over-exertion, injury, concussion of the spine, mental excitement, excessive lactation, sexual excesses, etc. The disease sometimes appears after acute infectious diseases, such as pneumonia, typhoid fever, articular rheumatism, cholera, etc. Tuczek observed the symptoms of ataxia after chronic poisoning with ergot, and Leyden makes a similar statement with regard to pellagra. Heredity plays a prominent part in certain cases. Thus, Carre ob- served the disease in the grandmother, mother, seven brothers and sisters, and nine other relatives. Westphal showed that the disease develops not infrequently during the course of progressive paralysis of the insane. II. Anatomical Changes.—In exceptional cases the spinal cord appears normal to the naked eye, although the microscope reveals ad- vanced changes. The disease is often evident from the shape, color, and consistence of the cord. The posterior surface appears flattened and narrowed, and if the pia mater has remained transparent, a gray, pearl-gray, or yel- lowish-gray tissue is seen in a position corresponding to the posterior columns. As a rule, the consistence of this part is increased, rarely di- minished. These appearances are often concealed by changes in the pia mater, which is thickened and opaque over the affected parts of the cord, contains numerous sinuous vessels, is occasionally markedly pigmented and adherent to the arachnoid and dura mater. Opacities and cal- careous plates are often found on the arachnoid and dura mater. DISEASES OF THE SPINAL COSD. 101 On transverse section of the cord, the posterior columns are found to have a pearl-gray or yellowish-gray color. These parts are often trans- parent; they are sometimes unusually firm, in other cases soft and gelatinous. The changes are generally most marked in the upper lum- bar and lower dorsal portions of the cord (vide Fig. 39). In the lower lumbar region they are often confined to the columns of Burdach, in the cervical region to the columns of Goll. Even where the changes are most marked, islets of the posterior columns often remain intact. This is especially true, as is shown in Fig. 40, of the vicinity of the posterior gray commissure and the part immediately adjacent to the posterior horns. The changes may some- times be followed to the medulla oblongata into the funiculi graciles, and gradually dis- appear. In a few cases, changes have also been found in the peripheral layers of the pons and the corpora quadrigemina. The posterior spinal roots are atrophic and gray, and present changes similar to those observed in the cord. These changes never extend beyond the intervertebral ganglia. The cauda equina contains thin, gray strands which correspond exactly to the atrophic posterior spinal roots. Gray degeneration of the cerebral nerves has been observed in a number of cases, par- ticularly in the optic nerve. It begins in the immediate vicinity of the eyeball and the peripheral layers of the trunk of the nerve, and may gradually extend along the optic tract to the geniculate bodies. Similar changes have been observed in some of the nerves of the ocular muscles, in the trigem- inus, hypoglossus and pneumogastric, even in the nuclei on the floor of the fourth ven- tricle. The brain presents no change, unless the ataxia is a complication of progressive paral- ysis of the insane. Friedreich first noticed atrophy of nerve fibres, and increase of the interstitial tissue in the peripheral nerves. Degenerative and atrophic conditions have also been observed in the nerves of the muscles. Microscopical examination of the degenerated portions of the posterior columns shows disap- pearance of the nerve fibres, and the presence either of a rather large-meshed connective tissue, which is poor in cells (vide Fig. 41) or of a more delicately fibrillated con- nective tissue (vide Fig. 42). In some parts the connective tissue is firmly fibrillated. Granulo-fatty cells are entirely absent in places, in others they are more or Fig. 39. Transverse sections of the cord in advanced degeneration of the posterior columns, o, upper cervical region; b, cervical en- largement; c, upper; d,middle; e, lower dorsal cord; /, lumbar enlargement. The sclerotic portions are light in color. Natural size. After Leyden. 102 DISEASES OF THE SPINAL COED. less numerous. The number of amyloid bodies is very considerable. The blood vessels are usually thickened, and their walls contain an unusual number of nu- clei. Their lymph sheaths may contain accumulations of fat granules and gran- Fig. 40. Transverse section of the middle dorsal l-egion. The degenerated parts are light in color. En- larged 10 times. After Leyden. ulo-fatty cells. The nerve fibres are partly destroyed, in part they consist of naked axis cylinders, the medullary sheath having undergone absorption. Opinions differ with regard to the nature of these changes. Leyden looks upon the process as a primary, non-inflammatory degeneration of the nerve Fig. 41. Fig. 42. Fig. 41.—Tissue with coarse and firm network. From the degenerated foci in the cord. Fig. 42.—With finer network. Contains thick- ened blood-vessels and persistent nerve fibres. After Leyden. fibres, with secondary implication of the connective tissue. Others regard the process as primarily inflammatory; Charcot regards the nervous tissue as the starting-point of the inflammation (chi-onic parenchymatous myelitis) and the DISEASES OF THE SPINAL CORD. 103 connective-tissue changes as secondary, others consider the process a chronic pri- mary interstitial myelitis. Some observers have associated the disease with primary changes in the blood- Fig. 43. Transverse section of the cervical enlargement in tabes, with atrophy of right anterior horn. After Charcot, av, atrophic anterior horn; be, bandelettes externes. vessels. Still other writers regard the inflammation of the pia mater and arach- noid as the primary lesion. The posterior horns of gray matter usually take part in the process. They ap- Fig. 44. Fig. 45. Gray degeneration of the bandelettes externes in beginning tabes. After Charcot. Fig. 44.—Middle cervical region. Fig. 45.—Lower dorsal region; be, bandelettes externes. pear small, their nerve fibres are diminished in size or have disappeared, the connective tissue is unusually abundant, and the ganglion cells are shrunken, often filled with an unusual amount of yellow pigment, and many of the cells are destroyed. 104 DISEASES OF THE SPINAL COED. Clarke’s columns in the dorsal cord often present a grayish discoloration to the naked eye. Under the microscope we find atrophy and disappearance of the nerve fibres and increase of the connective tissue, but the ganglion cells are usu- ally intact. The morbid process often extends from the posterior columns along the peri- phery to the lateral columns. Sometimes it extends only to the cerebellar tracts, in other cases it passes deeper into the lateral columns, occasionally it even ex- tends to the anterior columns. Finally, Charcot and Pierret found that, in rare cases, the morbid process extends to the large ganglion cells of the anterior horns. After undergoing pigment degeneration, the ganglion cells shrink and dis- appear, and the corresponding anterior horn appears atrophic (vide Fig. 43). These Fig. 46. Fig. 47. Beginning changes in lumbar cord in tabes, After Struempell. Advanced changes in lumbar cord in tabes. After Struempell. processes correspond to atrophy of muscles, and degeneration reaction during life. Very little is known concerning the post-mortem appearances in the initial stages of tabes. According to Charcot, the primary site of disease is situated in the internal root fibres (bandelettes externes) in the lateral part of the column of Burdach near the posterior horn. All the other anatomical changes are said to be secondary in character, particularly the affection of the columns of Goll, which is regarded merely as an ascending secondary degeneration. Struempell has come to the following conclusions with regard to the distribu- tion of the lesions: In the lumbar cord, the changes begin symmetrically in the middle portions Fig. 43. Fig. 49. Beginning changes in dorsal cord in tabes. After Struempell. Changes in cervical cord in tabes. After Struempell. of the posterior columns, and intact parts are left anteriorly between them and the posterior gray commissure and posteriorly between them and the outer boundary of the posterior columns (vide Fig. 46). As the disease progresses, the process extends posteriorly, but a small oval or triangular field, along the poste- rior longitudinal sulcus, is generally left intact (vide Fig. 47). The most anterior portions of the posterior columns always remain intact. In the dorsal cord, the process begins in two lateral fields from which fibres mainly radiate into the posterior horns. In addition, two median strips, which DISEASES OF THE SPINAL CORD. 105 are situated along the posterior longitudinal sulcus, are affected very early (vide Fig. 48). Later, the entire posterior column degenerates, but the posterior exter- nal portion persists unchanged for an unusual length of time. In the cervical cord, the change is first noticed in the columns of Goll, more markedly posteriorly than anteriorly. Two anterior and two posterior external fields remain intact for a long time (vide Fig. 49). It would appear, accordingly, as if the total degeneration of the posterior columns consists of the gradual affection of smaller systems of fibres which are functionally similar. In some cases, scattered sclerotic patches have also been found throughout the cord. IIT. Symptoms.—The most important and constant symptom of tabes dorsalis is inco-ordination of voluntary movements, ataxia, with unimpaired or slightly diminished muscular power. Locomotor ataxia is an exquisitely chronic disease, which may last more than thirty years. Leyden distinguishes a neuralgic, ataxic, and paraplegic stage. In the first (neuralgic) stage neuralgiform pains plav a prominent part. These may be associated with paraesthesiae, ocular paralyses, pupillary changes, optic atrophy and amaurosis, loss of the patellar tendon reflex, anaesthesiae, disturbances of the bladder and rectum, and changes in the joints. This stage varies in duration from several weeks to many years. In the second (ataxic) stage, the symptoms of ataxia become more prominent. These almost always appear first in the lower limbs, often at a later period in the arms; they rarely begin in the upper limbs. This stage may also last many years. The third (paraplegic) stage begins when the patient is no longer able to move the lower limbs, and is confined to bed. In some cases, death is the result of bed-sores, paralysis of the bladder with alkaline decomposition of the urine, ulceration and necrosis of the vesical mucous membrane or pyelonephritis. Others die of pulmonary phthisis (a frequent termination), or general marasmus, which is not infrequently accelerated by profuse diarrhoea or by obstinate vomiting as the result of so-called gastric crises, or intercurrent diseases. In several cases, Ley- den observed acute delirium with coma, and a fatal termination. We will now consider the individual symptoms somewhat more in detail. Neuralgiform pains are among the most constant and earliest symp- toms. As a rule, they are described as lightning-like, shooting, stick- ing, boring, or crushing. They are often so violent that the patients cry out aloud. They are almost always situated deeply, rarely in the integument; the latter is often hyperaesthetic in the situation of the pains. The pains sometimes appear along certain nerve tracts, some- times as hemicrania, or chiefly in the joints, or they may not follow a sharply defined anatomical course. They are often especially severe at night. Remissions and exacerbations are frequent, according to the temperature and barometer; the exacerbations are most marked in rainy, stormy weather, with a low barometer. As a rule, the pains first appear in one, then in the other lower limb, and are not infrequently regarded as sciatica. The pains usually appear in the upper limbs at a later period, and are apt to extend along the dis- tribution of the ulnar nerve. The majority of the patients also complain of girdlingj5ains(cincture feeling) around the chest or abdomen. 106 Visceral neuralgias may also develop; violent gastralgia with vomit- ing (gastric crises), violent burning in the urethra and rectum, associ- ated with dysuria and tenesmus, occasionally with dysentery-form stools, etc. In rare cases, the pains are felt along the cerebral nerves, generallv along the occipital, next the trigeminal nerves. The pains often continue during the further course of the disease. Paraesthesiae constitute a very constant symptom, and, as a rule, develop at a very early period. The patients complain of a feeling of coldness, burning, prickling, or formication. Many complain that they do not feel the floor in walking, that they have a sensation as if walking on felt, wool, or feathers, or on a bladder filled with water. The paraesthesiae usually appear first in the lower limbs, and are generally more marked in the feet and legs. At a later period, they extend to the upper limbs, and even the trunk may be affected. Ilyperaesthesia is not a very frequent symptom. It is sometimes as- sociated with the neuralgiform pains in the skin, and may rapidly change its location. Some patients do not experience pain on irritation of the skin unless the irri- tant is very severe, but the pain is then unusually violent. Leyden has applied to this phenomenon the term relative hyperaesthesia. The patients rarely complain of pain in the back. M. Meyer has called attention to the presence of pressure points on the spine, and has had good results from treating them with electricity. According to Leyden, anesthesia occurs in every case of tabes, but careful examination is sometimes requisite in order to detect it. In many cases there is partial anesthesia, in more advanced cases it may be complete. It is generally most marked in the feet and legs, but in the beginning of the disease it is sometimes confined to circumscribed parts of the integument, for example, the perineum, the lateral and posterior part of the thigh, scrotum, etc. The sensation of tickling is generally lost first, then the sensation to touch and pain, later the other modes of sensation. Delayed conduction is a not infrequent symptom. If the skin is pricked with a pin, several seconds (up to five) may elapse before the sensation is perceived by the patient. Hertzberg and Nothnagel also ob- served delayed conduction of'temperature impressions. Naunyn recently described double sensation, i. e., the patient, after a single prick of a pin, first experienced pain, and after an interval, a second, more in- tense pain. E. Remak noticed in one patient that the prick of a pin was first felt as a simple touch, and after an interval as pain. Fischer noticed polyaesthesia, i. e., one point was felt as several. In the early stages of the disease, Berger noticed that feeble cutaneous irritants were perceived, but stx-ong ones were not perceived. E. Remak calls attention to the readiness with which the sensory nerves are exhausted. If the skin is faradized, the patient, after a while, states that he no longer feels anything. The current must then be increased, but again a point arrives at which the sensation which was previously present disappears. Mendelssohn showed that the electrical reaction of the sen- sory cutaneous nerves is changed in tabes. There is often a prolonged after-sen- sation, so that rapidly following stimuli merge into one. Leyden’s investigations liave shown that the anaesthesia affects not alone the skin, but also the fasciae, tendons, and muscles. The impair- ment of muscular sense is especially important. DISEASES OF THE SPINAL COED. DISEASES OF THE SPINAL COED. 107 If the patient’s leg is slowly and carefully raised while his eyes are closed, and he is directed to raise the other leg to the same extent, gross mistakes are made. If theleg is placed in a sling, and passive movements of the thigh, leg, or foot are made, the patient is unable to tell the position of the limb. If one leg is carefully placed over the other he is unable to tell which leg is uppermost. If he is directed, while the eyes are closed, to bring the fingers of the two hands in contact, he hunts for them in the air, etc. The sense of effort, however, is retained, according to Leyden. This is tested by placing a folded handkerchief upon the extended limb, after the latter has been placed upon a support, and directing the patient, with the eyes closed, to tell differences in weights placed upon the handkerchief. Electro-muscular sen- sibility may also be unchanged, but it is sometimes diminished. The Brach-Romberg symptom is generally attributed to changes in the muscular sense. This is shown by the tottering movements of the patient in the dark, or when the eyes are closed. It is evident that in the light the eye is able, to a certain extent, to overcome the defect in the muscular sense. The tottering is especially marked when the feet are brought together. The cutaneous reflexes present no characteristic changes. They may be unchanged, diminished, increased, or delayed. When the prick of a pin on the sole of the foot gives rise to reflex contractions of the leg, the patient sometimes mistakes the perception of the muscular contractions for that of the prick itself. The condition of the patellar tendon reflex is an extremely important symptom. This is tested by directing the patient to cross one knee over the other, and by tapping the tendon above the patella quickly with the percussion hammer or the ulnar side of the hand. Or the patient allows the limb to hang loosely over the edge of the bed, and the patella tendon is then tapped. Or the physician’s hand is placed under the knee-joint of the patient, the limb is slightly elevated, and the tendon percussed. In tabetic patients, the reflex (contraction of the quadriceps and pro- pulsion of the leg) remains absent in almost every case. This is one of the earliest symptoms of ataxia. Its appearance indicates the existence of foci of degeneration in the external portions of the posterior columns in the upper lumbar region or its transition to the dorsal region. Vaso-motor, secretory, and trophic changes may remain absent during the entire course of the disease. In other cases there is a diminution in the temperature of the skin of the affected limbs corresponding to a sen- sation of coldness. Unilateral and local hyperidrosis and ptyalism have been observed. Erythema, herpes, bullous and nodular eruptions may appear, and acute decubitus with its sequelae may also develop. Pooley described unusual desquamation of the epidermis; Ballet and Until ob- served ichthyotic changes on parts of the skin which were anaesthetic, hyperaesthetic, or the site of severe pains. Strauss described cutaneous hemorrhages. Thickening, Assuring, and falling out of the nails have been reported in a few cases. Falling out of the teeth has also been reported, and according to this is always preceded by hyperaesthesia or anaesthesia at the site of the tooth. The panniculus adiposus and muscles may remain normal for a long time, and emaciation does not occur, in many cases, until the patient has been confined to bed for a long time. But rapid atrophy and de- generation reaction (usually in the upper limbs) occur if the ganglion cells of the anterior horns are destroyed. According to Charcot, an im- portant, early diagnostic sign of tabes is hemiatrophy of the tongue, gen- erally associated with ocular paralysis. 108 DISEASES OF THE SPINAL CORD. Charcot also includes among the trophic disturbances certain peculiar joint changes, which often occur very early, more rarely in the later stages of the disease. The knee-joint is more frequently affected, next the shoulder (especially on the right side), elbow, hip, and wrist. The disease is unattended with fever or pain, but with marked swelling which sometimes extends over a considerable part of the limb. The swelling, which generally consists of an accumulation of serum or sero-bloody fluid in the joint, may disappear after weeks or months without evil effects, or it terminates in erosion of the cartilages and ends of the bones; the joints then creak on motion, and spontaneous dislocations may de- velop (vide Big. 50). Suppuration and perforation of the joint are very rarely observed. Charcot has also noticed fragility of the bones, terminating in spontaneous fractures. The lower limbs are generally affected, especially the thighs. Re- covery is not infrequently attended with an abnormal development of callus. In such cases, Blanchard found disappearance of the lime salts and rarefaction of the osseous tissues in the neighborhoood of the Haversian canals, most markedly near the medullary cavity. These changes are connected with the development of the tabetic foot. In Fig. 50. Fig. 51. Fig. 50.—Eroded head of humerus in tabes dorsalis. Fig. 51.—Normal head of humerus. After Charcot. this condition the scaphoid and internal cuneiform bones project strongly on the inside, while the metatarsus falls back on the outside, so that a characteristic pro- jection forms at the first tarso-metatarsal joint. In one case Kroenig described spondylolisthesis. Among other secretory and trophic disturbances we may finally mention varicocele, swelling of the testicle, and mal perforant du pied. Motor disturbances play a prominent part in the symptomatology of tabes. Paralysis is either altogether absent or occurs only at a late stage of the disease as the simple result of prolonged disuse. Temporary hemiplegic or paraplegic paralyses are observed occasionally, and are re- garded by Leyden as exhaustion paralyses. But despite the fact that the patients generally possess sufficient power, they present the signs of motor inco-ordination or ataxia. In walking, the legs are separated widely, the heels are brought forcibly on the ground, and irregular move- ments are performed in lifting the limbs. The gait becomes uncertain and zigzag, and the patients are unable to walk in a straight line. These disturbances become especially marked on making sudden turns, walk- DISEASES OF THE SPIXAL COED. 109 ing up-stairs, etc., or on closing the eyes. The patient carefully follows every movement with his eyes. As the symptom progresses, he is no longer able to walk without assistance. Finally, the feet make such violent, irregular movements that he is confined permanently to the chair or bed. Ataxic movements sometimes occur in the upper limbs, so that the patient performs irregular, unnecessary movements in threading a needle, etc. In advanced stages he is unable to write, eat, or clothe himself, and becomes as helpless as a child. The electro- muscular irritability remains unchanged. According to Leyden, ataxia is merely the result of extensive anaesthesia (sen- sory ataxia), including not alone cutaneous anaesthesia, but particularly diminu- tion or abolition of the muscular sense. It has been contended, in opposition to this view, that ataxia may exist without disturbance of sensation, and also that anaesthesia occurs without ataxia. Friedreich explains ataxia by the paralysis of definite co-ordinating nerve tracts (motor ataxia) which convey the co-ordinating impulse from the centre in the brain through the posterior columns (or cerebellar tracts?) to the periphery. It must be remembered, however, that no nerve tracts of co-ordination have yet been discovered. Cyon believes that ataxia is the result of an interruption of reflex paths in the spinal cord. Muscular twitchings are rare and generally result from neuralgic pains; contracture of the muscles is equally rare. Disturbances of the bladder and rectum are frequent and often very early symptoms. The patients often suffer from incontinence or from inability to empty the bladder. In the later stages of the disease, com- plete paralysis of the bladder may occur and result in stasis of urine, cysti- tis, pyelitis, nephritis, pyaemia, and septicaemia. There may also be in- voluntary evacuations from the bowels, or obstinate constipation. Ocular symptoms are very often present and are extremely important in diagnosis. Paralysis of ocular muscles is shown by ptosis, strabismus, diplopia, and vertigo. The motor oculi is most frequently affected, then the abdueens. and then the trochlearis. The pupils are often no larger than the head of a pin (spinal myosis). They react very little or not at all to light, but change their dimensions during accommodation. The pupils are sometimes unequal. Amblyopia is often a very early symptom, and may terminate in complete blindness. This is sometimes observed for years prior to the first distinct signs of ataxia. The ophthalmoscope shows a very white color of the disc, the lamina cribrosa is unusually distinct, the retinal arteries narrowed. The field of vision is more and more constricted, not concentrically, but by the loss of sectors. There are also peculiar disturbances of color sense, viz., the development of insensibility to certain colors; first for red and green; yellow, and particularly blue, are retained longest. Visceral crises is the term applied to peculiar attacks which affect one or more of the viscera (stomach, larynx, pharynx, kidneys, urethra, etc.). Gastric crises are the best known among these symptoms. They consist of attacks of violent gastric pain, associated with protracted gagging and vomiting, at first of the gastric contents, later of mucus, and then bilious fluid. These attacks sometimes last only a few hours, sometimes several days. They produce great exhaustion, and even 110 DISEASES OF THE SPINAL COED. terminate fatally. Such conditions sometimes follow or are associated with unusually violent neuralgiform pains. Diarrhoea and hemor- rhages from the genitals (in women) have been observed during the attacks. James Russel noticed diminution of urine and urea, and albu- minuria. Buzzard states that gastric crises occur particularly in pa- tients who suffer from joint affections. They are sometimes an early symptom (prior to the ataxia), but recur from time to time at a later period. Lepine also describes painless gastric crises, characterized by profuse vomiting, which may be so obstinate as to endanger life. Intestinal crises consist of attacks of diarrhoea associated with pain ; they may be attended by salivation and hyperidrosis. Laryngeal and pharyngeal crises are attacks of dyspnoea and suffoca- tion and difficulty in deglutition, which may be associated with cyanosis and temporary protrusio bulbi. In renal crises there are violent attacks of pain, similar to renal colic; the secretion of urine is diminished, but it contains no blood or pus. The attacks may last a week. Pitres has observed, in women, clitoris crises, i. e., attacks of volup- tous sensations similar to those experienced during coitus. Priapistic and spermatorrhoeic crises have been observed in men. The development of the crises has been attributed in part to degene- ration of the peripheral nerves, in part to degeneration of the nuclei of the cerebral nerves. Circulatory symptoms have been described in a number of cases. The pulse is often very rapid, and attacks of palpitation, terror, and pain in the heart (crises cardiaques) are also mentioned. Eulenburg noticed very marked dicrotism of the pulse. Berger and Rosenbach noted the frequent coincidence of tabes and aortic insufficiency. Diseases of the cerebral nerves, apart from the optic and the nerves distributed to the ocular muscles, occur quite rarely. Tinnitus aurium and hardness of hearing have been described in a number of cases. Trigeminus amesthesia is sometimes observed; likewise paralysis and spasms in the distribution of the facial nerve. Disturbances of the sexual functions are observed particularly in males. At the onset of the disease there is often increased sexual desire, and the semen is discharged very quickly ; pollutions occur very often. These symptoms, however, gradually give way to impotence. The psychical functions are often affected. The majority of writers mention the cheerful disposition of the patients; but, if closely watched, this very disposition is often seen to be morbid. Well-marked insanity occurred seventeen times in eighty-nine tabetic patients (Moeli). Bern- hardt recently called attention to apoplectiform attacks, but these occur much less frequently in tabes than in multiple sclerosis. The following tables by Bernhardt (58 cases) and Erb (56 cases) show the frequency of the individual symptoms in this disease : DISEASES OF THE SPINAL CORD. 111 Bernhardt. Erb. 1. Absence of patellar tendon reflex 100.0 per cent 79.5 74.1 39.6 27.2 48.4 10.3 85.9 31.6 34.4 90.2 92.0 94.1 43.7 9.6 5.2 “ 98,0 per cent 92.5 81.0 38.7 54.0 50.0 12.4 6&.0 89.5 83.5 97.9 100.0 78.5 2. Lancinating pains 3. Paresis of bladder 4. Paralysis of ocular muscles 5. Myosis 6. Rigidity of pupils 7. Optic atrophy 8. Sensory disturbances 9. Analgesia 10. Delayed conduction of pain 12. Feeling of exhaustion 13. Ataxia 14. Sexual weakness 15. Joint affection 16. Crises gastriques .. IV. Diagnosis.—At the onset of the disease it may he mistaken for rheumatism, hemierania, sciatica, gastric catarrh, hypochondria, and hysteria. We must take into consideration the condition of the patel- lar reflex, the reflex rigidity of the pupil, temporary ocular paralyses, myosis, irregularity of the pupils, sensory disturbances, paralysis of the bladder and rectum. The earliest symptoms, and one of the most im- portant, is the absence of the patellar tendon reflex. This is occasion- ally absent in healthy individuals. It may be absent in individuals who belong to neuropathic families, in old age, and, according to Schreiber, in chronic alcoholism. With regard to the diagnostic significance of ataxia, it must be re- membered that it may occur in diseases of the cerebellum (cerebellar ataxia), and that it also appears occasionally after acute infectious dis- eases (acute ataxia). In the former event other cerebellar symptoms will be present, such as constant vomiting, occipital pain, vertigo, etc. Dejerine has recently claimed that degenerative changes in the peripheral nerves alone may produce the symptomatology of tabes dorsalis. He applies to the disease the term neurotabes peripherique. V. Prognosis.—The prognosis is always unfavorable. The hope of improvement, rarely of complete recovery, can only be entertained if the disease is the result of syphilis. VI. Treatment.—If there is a suspicion of syphilis, we should order mercurial inunctions, and give potassium iodide internally. The symp- toms may grow worse for a few weeks after the inunctions are begun, but their continued application sometimes produces remarkable results. If the patient has not had syphilis, nothing remains except to treat annoying symptoms. In general, the treatment employed in myelitis may "also be adopted in this disease. Great care should be exercised, however, in the administration of ergotin, since Tuczek has shown that chronic ergot poisoning may give rise to tabes. Moreover, sudden par- alysis has been known to develop in these patients after the use of er- gotin. A certain amount of good may be derived from the use of electricity. The galvanic current is chiefly employed; stabile or labile spinal current, 112 DISEASES OF THE SPINAL CORD. ascending or descending; or a spinal cord-sympathetic current. If spi- nal pressure points are present, they may be treated with the anode. Eumpf has recently recommended the faradic brush. If the galvanic current is employed, it should not be very strong, the sittings should not last more than ten to fifteen minutes, nor be held oftener than once a day. The electrodes should always be large in galvanization of the spinal cord. In ol der to employ the spinal cord-sympathetic current, the cathode is placed immediately below and behind the angle of the lower jaw, upon the upper cervi- cal ganglion of the sympathetic, while the anode is slowly passed, at short inter- vals, along the spine, at first on one side, then on the other. In using the faradic brush, Rumpf employed a strong current; the brush (cathode) was applied a number of times to the trunk, back, and limbs until the skin was thoroughly reddened. Duration of the sitting ten minutes, daily or every other day. The administration of morphine and narcotics in general plays an important part in the treatment of individual symptoms. 2. Spastic Spinal Paralysis. (Lateral Sclerosis of the Cord. Tabes dorsalis spasmodica.) I. Etiology.—In the majority of cases this disease is a complication of various other affections of the spinal cord. The primary form of the disease is more frequent in men than in women, and particularly from the ages of thirty to fifty years. Cold, injury, mental and bodily exhaustion, etc., are mentioned as causes. Congenital predisposition and a neuropathic taint seem to play an impor- tant part in etiology. The disease is not infrequent in childhood. The marriage of relatives and congenital syphilis seem to be causal factors. The etiology of secondary or symptomatic spastic spinal paralysis is the same as that of the primary disease (various forms of myelitis, "syph- ilitic spinal paralysis, spinal paralysis after acute diseases, hydromyelus, internal hydrocephalus, lead poisoning, multiple sclerosis). Spastic symptoms have even been observed in rare cases of locomotor ataxia. II. Anatomical Changes.—From a theoretical standpoint, Erb at- tributed primary spastic spinal paralysis to disease of the lateral col- umns of the cord. The autopsies of v. Stoffella, Morgan, Dreschfeld, and Bramwell seem to confirm this view. v. Stoffella’s case presented gray degeneration of the lateral columns, most marked in the lumbar and lower dorsal region, slightly marked in the cervical cord. The disease affected the posterior part of the lateral columns, extended internally to the posterior horns, externally to the pia mater. No microscopical examination was made. The appearances in Bramwell’s case are shown in Fig. 52; it is evident that the degeneration is confined to the pyramid tracts. Westphal questions that the symptom-complex of spastic spinal par- alysis is always the result of an affection of the lateral columns. III. Symptoms.—In uncomplicated cases the symptoms consist of paresis, later of paralysis of the muscles, with rigidity and contracture, exaggeration of the tendon reflexes, and spastic gait. "Sensation and the functions of the bladder and rectum are unaffected. The symptoms, as a rule, begin in the lower limbs, and gradually ex- DISEASES OF THE SPINAL COED. 113 tend to the trunk and upper limbs. They rarely travel in the opposite direction. Still more rarely they are confined to one limb, or to the up- per and lower limb of one side. The patients first complain of a feeling of weakness in walking; this is soon followed by stiffness of the muscles daring active and pas- sive motion. Some patients complain of twitchings in the muscles. Gradually, muscular contractures develop. These affect the extensors and adductors of the thighs, the plantar flexors of the feet, the latter giving rise to pes varo-equinus. In walking, the limbs are often held as stiffly as two sticks. The patients are hardly, or not at all, able to lift the feet from the ground in walking, and therefore move the pelvis to and fro.; the trunk is often bent over forward. At the same time the thighs pass each other with difficulty, on account of the contracture of the adductors. If the patient, in sitting down, brings the toes in con- tact with the floor, the leg will undergo trembling movements, and a Fig. 53. Anatomical changes in primary spastic spinal paralysis. After Bramwell. The degenerated parts in the crossed pyramid tracts are shaded. Upper dorsal region. Enlarged 10 times. sort of hopping movement is sometimes noticed when the patient, in walking, touches the floor with the tips of the toes (vide Figs. 53 and 54). The electrical irritability of the muscles is either unchanged or slightly diminished. The muscular contractures may become so exces- sive that the patient is confined to his bed. The flexor muscles may also undergo contracture, and similar changes may appear in the muscles of the trunk and upper limbs. In uncomplicated cases, the cutaneous sensibility is unchanged. Some patients suffer from panesthesiae or are very sensitive to cold. There are no vaso-motor and trophic disturbances. The cutaneous reflexes are unchanged or increased, but occasionally diminished. The tendon reflexes are always increased. This is best shown with regard to the patellar reflex. Foot clonus is also present, i. e., if the extended limb is raised, and dorsal flexion of the foot is sud- denly performed by the physician, the limb undergoes rapidly succeed- 114 DISEASES OF THE SPINAL CORD. ng trembling motions; these may be suddenly checked, in some cases, by plantar flexion of the great toe. Reflex muscular contractions mav also be produced by tapping other tendons (tendo Achillis, tendon of peronei, biceps of the arm and leg, triceps, supinators, extensors and flexors of the forearm, etc.). The vesical, rectal, and sexual functions are unimpaired. In the secondary forms of the disease, other symptoms, which de- pend upon the primary affection, may also be present. The disease runs an acute (within a few weeks), subacute, or chronic course (more than thirty years). IV. Diagnosis.—The disease can hardly be mistaken for any other if the cardinal symptoms are taken into consideration. V. Prognosis.—In the secondary form of the disease the prognosis Flo. 53. Fig. 54. Mode of walking in spastic spinal paralysis. After Adams. Mode of standing in spastic spinal paralysis. After Little. depends upon the primary affection; in the primary form it is relatively favorable, since recovery has been observed in a number of cases. YI. Treatment.—In primary spastic paralysis the best effects are obtained by the galvanic spinal current, as employed in tabes (vide page 112); in addition, warm baths (30° R.) and potassium iodide. The treatment of the secordary form is the same as that of the dis- ease which has given rise to it. Southam claims to have cured a case by nerve stretching. 3. Acute Spinal Atrophic Infantile Paralysis. Acute Anterior Infantile Poliomyelitis. I. Etiology.—This disease occurs chiefly in childhood, most fre- quently from the age of six months to four years. It is rare in nurs- DISEASES OF THE SPINAL CORD. 115 lings before the period of dentition, though Duchenne, Jr., observed two cases in infants of twelve days and one month respectively. The disease is also rare after the age of seven years. Boys are affected more frequently than girls. As a rule, no direct causes are demonstrable. It develops particularly during the summer ; I have also seen several cases develop at the same time in adjacent lo- calities. In fact the disease looks in many respects like an infectious disease. Whether heredity exerts an influence in this malady is not known with certainty. Several children in a family are sometimes affected; occasionally, other children in the family have died in eclampsia. It may also occur in families in which insanity or other nervous diseases have been observed in pre- vious generations. The etiological influence of dentition, cold, injury, etc., has been grossly overesti- mated. The disease develops not infre- quently during or after infectious diseases, viz., pneumonia, diphtheria, scarlatina, acute gastro-enteritis, etc. The attack often occurs during the night without any demonstrable cause. The chil- dren go to bed in perfect health and are paralyzed during sleep. It is not true that rachitic and scrofulous children are predis- posed to the disease. II. Anatomical Changes.—This dis- ease is an acute inflammation of the gray matter of the spinal cord, which is localized mainly or exclusively in the anterior horns, and there gives rise to disappearance of the large motor and trophic ganglion cells. Leyden has recently called attention to the fact that diseases which are clinically exactly like atrophic infantile paralysis may be the re- sult of other lesions, particularly of inflamma- tory processes, which are situated in the menin- ges and the white matter of the cord, and extend, secondarily, to the gray matter and its large gang- lion cells. In the following remarks we refer only to the typical form of the disease. The majority of anatomical observations were made in patients who had had the dis- ease for many years. In one case the disease had lasted only two months. In relatively recent cases the anterior horns of the cord contain one inflammatory focus, but more frequently there are several myelitic foci, generally in the lumbar or cervical enlargements. They may be uni- lateral or bilateral, microscopic in size or three to four cm. in dimensions. The foci generally have a brownish-red or grayish-red color and dimin- ished consistence. Fig. 55. Distribution of the foci of disease in the gray matter in acute spi- nal, atrophic infantile paralysis. After Roth. a, Transverse section through the conus medullaris, 13 mm. above the filum terminale; b, trans- verse section through the lumbar enlargement, 10 mm. higher; c, transverse section through the middle of the lumbar enlarge- ment, 7 mm. higher; d, trans- verse section through upper part of lumbar enlargement, 6 mm. higher; e, lumbar cord near the dorsal region, 7 mm. above d. Enlarged 2 times. 116 DISEASES OF THE SPINAL CORD. Microscopic examination of the foci shows unusual fulness of the blood-vessels, changes in their walls, and increase of the neuroglia. The vessels present aneu- rismal dilatations in places; their walls contain an unusual number of nuclei and are thickened. The lymphatic sheaths contain fat granules, granulo-fatty ceils, white blood-globules, rarely hsematoidin. Granulo-fatty cells are also found, in greater or lesser numbers, in the myelitic foci. They were entirely absent in one of Leyden’s cases, but were replaced by peculiar epithelioidal cells which the writer regarded as genetically identical with granulo-fatty cells. The neuroglia is increased in amount and in the number of cellular elements. The ganglion cells in the anterior horns are partly destroyed, some of them contain vacuolse. The nerve fibres which enter the anterior horns also undergo degeneration. Charcot regards the disease as a parenchymatous myelitis, others think the con- nective tissue forms the starting-point (interstitial myelitis). At all events, we Fig. 50. Acute spinal atrophic [infantile paralysis. Transverse section through the lumbar enlargement. The middle group of cells in the right anterior horn is atrophied and sclerosed. Enlarged 10 times. After Charcot. sometimes find foci which appear to be confined exclusively to some of the groups of ganglion cells (vide Fig. 56). In cases which have lasted for years the myelitic foci are sclerosed. At the same time the corresponding horn diminishes in size, and the white matter often increases in consistence, and undergoes atrophy (vide Fig. 57). The ganglion cells of the anterior horns have often disap- peared in places, or those which remain contain yellow pigment, are atrophied, or may present amyloid degeneration or sclerotic distention (Rosenthal). The poliomyelitic foci are sometimes converted into cystic spaces, which are traversed by a network of connective tissue. Degenerative changes develop not infrequently in the lateral columns, DISEASES OF THE SPINAL CORD. 117 occasionally even in the anterior columns. Clark’s columns were af- fected in some cases. The posterior nerve roots are unchanged; the anterior roots corre- sponding to the diseased portion of the cord undergo atrophic changes. They appear thin and gray, and the microscope shows disappearance of nerve fibres and increase of the interstitial tissue. Similar changes are also found in the peripheral nerves. The paralyzed muscles often have a strikingly pale-red color; at a later period this sometimes changes to a brownish-red. In the early stages the microscope shows diminution in the size of the fibres and in- crease of the nuclei of the sarcolemma (Leyden found a few hypertrophic fibres among the atrophic ones); in some fibres there are fissures resem- bling those of Zenker’s typhoid degeneration of the muscles. At a later period the transverse striation becomes obscured, and fat granules make their appearance. The interstitial connective tissue increases in amount Fig. 57. Acute spinal atrophic infantile paralysis. Transverse section through the cervical cord. Right anterior horn atrophic and sclerosed, the white columns diminished in size on same side. Paralysis of right arm during life. Death 50 years after the attack of paralysis. Enlarged 10 times. After Charcot. and in the number of nuclei. The adipose tissue sometimes increases to such an extent that the volume of the muscle seems to have enlarged. Upon section, such muscles look like a mass of fat, in which are seen a few pale streaks of relatively normal muscular tissue. In other cases the muscles are converted into thin, connective-tissue, tendon-like strands. In one case Dejerine found complete atrophy of the intermuscular nerves and nuclear proliferation in the sheath of Schwann. The panniculus adiposus of the paralyzed limb, as a rule, is unusually well developed; but the vessels, ligaments, fasciae, and bones undergo atrophy. The thickness of the bones, particularly of the compact sub- stance, is diminished, and they are sometimes as flexible as in osteo- malacia. In one case, Sander described slight development of the central con- volutions of the brain, but the disease was associated with idiocy. 118 DISEASES OF THE SPINAL CORD. III. Symptoms.—The symptoms consist of the sudden occurrence of completely developed, non-progressive, flaccid paralysis, with rapid atrophy of the paralyzed muscles, rapid development of degeneration reaction in the paralyzed muscles and nerves, abolition of the cutaneous and tendon reflexes, intact sensation, bladder, and rectum, and absence of trophic changes in the skin. The paralysis sometimes occurs unnoticed, sometimes it develops with febrile and cerebral symptoms. In some cases the paralysis is discovered accidentally. The patients have per- haps had some illness, and when they attempt to leave the bed, they are found to be unable to walk. Or the child is brought to the physician because it learns to walk very late, uses the hands awkwardly, etc., and the most superficial ex- amination then shows severe paralyses and deformities. In many cases it is said that the children have gone to bed well, and were found to be paralyzed on wak- ing the next morning. In other cases, epileptiform convulsions occur, either unexpectedly or after several days of general malaise, anorexia, restlessness, etc. The patients lose consciousness, become convulsed, are sometimes bathed in perspiration, and have a high fever. The spasms may last one or more hours, in rare cases recur at definite intervals, and are often looked upon as the result of teething. When the convulsions disappear, the weakness or paralysis of the mus- cles at once becomes noticeable. The fever may last several days after the spasms have ceased. It generally lasts two to three days, rarely more than a week; it ranges between 39-40° C. The paralysis affects the lower limbs much oftener than the upper ones; there is often paraplegia of the lower limbs. Occasionally the arm and leg on the same side are paralyzed, or the arm on one side, the leg on the other; in rare cases both upper limbs are paralyzed. The muscles of the trunk, back, scapulas, more rarely the neck, may also be involved. In very exceptional cases the facial muscles are attacked. In many cases the disease at first attacks all the muscles of a limb, but in the next few days or weeks the paralysis disappears in most of the muscles, but persists in others. In very rare instances the paralysis disappears entirely (temporary paralysis). Careful observation shows that the muscles are very often affected in certain definite groups. This indicates that certain parts of the cord are apt to be affected, and that, on the other hand, spinal centres for definite groups of muscles are situated in close proximity in such localities. E. Remak distinguishes two types of the disease in the upper limbs : a, the arm type, involving the deltoid, biceps, brachialis internus, and the supinators; b, the forearm type, affecting chiefly the extensors, and leaving the supinators intact. The centres for the extensors and flexors of the forearm probably are relatively remote from one another, the former in the middle of the cervical enlargement (fourth and fifth cervical nerve roots), the latter lower (eighth cervical and first dorsal nerves). In paralysis of the dis- tribution of the crural nerve, the sartorius generally escapes, while in paralysis of the quadriceps femoris the tibialis anticus is not infrequently also affected ; the latter muscle .generally escapes in spinal paralysis of the peroneal nerve. These phenomena also indicate a peculiar arrangement of the muscle centres in the cord. According to Kahler and Pick, the spinal centre of the calf muscles is situated near the fourth and fifth dorsal roots. The electrical reactions of the paralyzed muscles and nerves present very important changes, viz., those of degeneration reaction (vide page 8). The electrical changes appear within a few days after the development of the disease. DISEASES OF THE SPINAL COED. 119 The paralyzed muscles are often tender on pressure. Cutaneous hvpersesthesia is sometimes observed at the onset of the disease. The paralyzed muscles rapidly undergo very marked atrophy. This can sometimes be followed distinctly from week to week. The disappear- ance of the muscles is sometimes marked by an abundant deposit of fat. Fibrillary twitchings in the atrophic muscles have often been described. The panniculus adiposus generally becomes unusually abundant, so that it may be difficult to feel the thin bellies of the muscles. The skin is generally very cool, bluish-red and marbled in appearance, sometimes cedematous and fissured, or covered with cold perspiration. A tendency to ulceration and the development of frost-bites is mentioned by some writers. The difference of temperature between the healthy and paralyzed limbs may exceed 15° C. According to Tartiere, the paralyzed limb, during the initial febrile period, is 1-2° C. warmer than the corresponding healthy limb; later the limb gradually grows cooler. If the paralysis is extensive, the cutaneous and tendon reflexes are entirely abolished within the domain of the paralysis. The bladder and rectum are unaffected; at the most, there is incon- tinence at the beginning of the disease, rarely retention of urine and constipation. The atrophic changes extend to the bones, fasciae, tendons, etc. The pulse of the paralyzed limbs has been known to become smaller. If the disease has begun in early childhood, the paralyzed parts often remain as mere rudiments. The difference in length of the corresponding bones on the healthy and paralyzed sides may exceed twenty centimetres, but, as a rule, it is- much less. Seeligmueller has observed, in a few cases, unusual length of the bones in the paralyzed limbs. The disease terminates with the development of deformities. Several factors concur in their production. In some cases they are the result of contracture of the non-paralyzed muscles. In other cases, however, the paralyzed muscles themselves undergo contracture, and the action of gravity upon the limbs then aids in producing deformity. In the foot we generally find pes equinus or varo-equinus, rarely pes valgo-equi- nus or calcaneus. At the knee we not infrequently find genu recurvatum, i. e., the leg can be extended to a much larger angle than normally. Contracture at the hip-joint is a rarer sequel. Scoliosis, lordosis, rarely kyphosis, may result from partial paralysis of the muscles of the back. Contracture of the pectoral and latissimus dorsi sometimes impairs the mobility of the shoulder-joint. Or, on account of paralysisjof the deltoid, the shoulder-joint becomes loose, inasmuch as the weight of the arm draws it downwai’ds ; the capsule of the joint is relaxed and a deep furrow is often visible between the spine of the scapula and the head of the humerus. Contracture at the elbow-joint is rare ; it is more frequent in the hand and fingers. The onset of atrophic infantile paralysis is almost always acute; in rare cases it runs a subacute course, and the paralyses do not develop for several days. Acute exacerbations followed by fresh paralyses are some- times observed. Life is rarely, if ever, endangered. IV. Diagnosis.—The differential diagnosis must take into consid- eration : a. Progressive muscular atrophy; this hardly ever occurs in childhood, except in the hereditary form; it develops very slowly. 120 DISEASES OF THE SPINAL CORD. b. Pseudo-hypertrophy of the muscles; this develops very gradually, and muscular atrophy remains absent. c. Spastic spinal paralysis; muscular atrophy and degeneration are not produced, and the tendon reflexes are increased. d. Parturition paralyses; these are present from birth, labor has usually been difficult; sensory disturbances are generally noticeable. e. In acute central or transverse myelitis, in haematomyelia and com- pression myelitis, sensory disturbances are generally present; there are often disturbances of the bladder and rectum, trophic changes in the skin, increased cutaneous reflexes, absence of degeneration reaction. f. Multiple degenerative neuritis is generally associated with sensory disturbances. Y. Prognosis.—The prognosis is not especially favorable. As a rule, there is no danger to life, but we are unable to relieve the paralysis. VI. Treatment.—During the period of the initial fever and. spasms, we may order a warm bath (28° R.), lasting half an hour, with cold douches, and then an ice-bag to the head. After the paralysis makes its appearance, the Chapman ice-bag may be applied to the supposed site of disease in the cord. Leeches, cups, and derivatives of all kinds have also been applied. Potassium iodide may be given internally to aid absorption of the inflammatory foci; ergotin and belladonna have also been given for the same purpose. After the most acute symptoms have subsided, we may attempt to aid absorption by the use of the galvanic current (large electrodes), at first the anode (two to three minutes), then the cathode over the site of disease. The paralyzed parts are treated with the galvanic or faradic current, the latter only when the muscles respond. The electrodes should be thoroughly moistened, and strong currents should be used in order to penetrate the skin and panniculus adiposus. In a number of cases we employed, at the same time, the galvanic spinal current and peripheral faradic stimulation of the muscles. Gymnastics, massage, tenotomy, and orthopaedic instruments may be employed to prevent and relieve deformities. 4. Acute, Subacute, and Chronic Spinal Atrophic Paralysis of Adults. Acute, subacute, and chronic anterior poliomyelitis of adults. These morbid processes are in part identical with, in part very closely allied to, acute atrophic infantile paralysis. a. Acute spinal atrophic paralysis of adults corresponds entirely tc the similar disease in childhood. Men are attacked more frequently than women; it generally occurs before the age of thirty years. Among the causes adduced are cold, overexertion, and excesses in Bacclio et Yenere. It has been observed a number of times after infectious dis- eases in women, particularly after puerperal fever. A certain etiological influence is sometimes attributed to heredity, tuberculosis, and syphilis. The first symptoms are those of a general febrile affection, but con- vulsions are not produced. It may begin with a violent chill, followed by high temperature, headache, delirium, sometimes vomiting and diarrhoea, often followed by a typhoid condition. Bramwell described temporary aphasia in one case. The fever generally lasts a week, some- DISEASES OF TIIE SPINAL COED. 121 times more than two weeks. The patients often complain of pain in the back and limbs. More or less extensive flaccid paralysis makes its appearance in a few hours, occasionally in a single night, more rarely in the course of several days. This mav be confined to a single group of muscles, or an entire limb; it sometimes appears as hemiplegia, paraplegia, or crossed paraly- sis; it rarely attacks the muscles of the neck, hardly ever those of the face. In a few cases the respiratory muscles were affected, and the dis- ease then ended fatally by producing suffocation. In a few cases the paralysis gradually disappears in a few weeks or months (temporary paralysis); in others the paralysis disappears in some muscles, but persists in others. The paralyzed muscles are often sensi- tive on pressure, and rapidly undergo atrophy; degeneration reaction is also produced. As a matter of course, the growth of the bones is not interfered with, as in children, but contractures of the muscle and, to a less extent, deformities are produced. The skin of the paralyzed parts is cold, often bluish-red, and does not perspire; it is sometimes oedema- tous. Sensibility is retained, but paraesthesiae and cutaneous hyper- aesthesia are sometimes present at the outset. Reflex irritability is abolished in total paralysis of a limb, otherwise it is diminished or unchanged. The functions of the bladder and rectum remain normal, though vesical paralysis is occasionally noticed at the outset. The sexual powers are unaffected. The prognosis as regards life is generally favorable, although a fatal termination is possible. The remarks made concerning the anatomical changes, diagnosis, and treatment of this disease in children also hold good in adults. b. Subacute and chronic spinal atrophic paralysis of adults occurs at a more advanced age (thirty to fifty years), but Erb recently observed a case in a child of six years. The causes are sometimes the same as those of the acute form, sometimes no cause can be discovered. Remak showed that lead poisoning may give rise to this disease. It generally begins gradually without any severe impairment of the general condition. The patients tire easily in walking, and, finally, well- marked paralysis develops. As a rule, it begins in the lower limbs, and then extends along the trunk to the upper limbs; more rarely the para- lysis progresses in the opposite direction. It may also be confined to a few groups of muscles. It begins most frequently in the extensors of the legs; in the upper limbs, likewise, the extensors of the forearms are first affected. The paralysis gradually extends from one group of mus- cles to another. According as this occurs in the course of weeks or of months and years, the disease is called subacute or chronic. The mus- cles of the neck are not infrequently affected. The disease may even extend to the bulbar nuclei, bulbar symptoms then develop, and death occurs from suffocation, etc. The character of the paralysis (apart from its progressive quality) is the same as that of acute atrophic paralysis, i. e., the paralysis is always flaccid. It may entirely disappear in the course of weeks or months, or it disappears only in part while other mus- cles undergo rapid atrophy. This may be followed by contracture and a hard tendinous condition of the muscles. The electrical irritability is the same as in infantile paralysis; in the beginning, the mechanical irri- tability of the muscles may be increased. Improvement generally follows an opposite course to the paralysis, i. e., first in the arm, then in the legs; the muscles supplied by the pero- 122 DISEASES OF THE SPINAL CORD. neal nerve often remain paralyzed. Fibrillary contractions are often observed in the paralyzed muscles. Some patients complain of parsesthesias, but the cutaneous sensibility is objectively unchanged. Disturbances of micturition are sometimes observed at the beginning of the disease, but they disappear at a later period. The joints and sheaths of the tendons are sometimes swollen. The cutaneous and tendon reflexes are abolished if a limb is completely paralyzed, otherwise they are diminished or unchanged. In progressive cases death occurs in one to four years. Authors are agreed that the lesion consists chiefly of destruction of the ganglion cells of the anterior horns; atrophy of the cells of Clark’s columns, and of the anterior portions of the posterior horns, is also mentioned. The neuroglia may be unchanged or increased; there may also be proliferation of the nuclei in the walls of the vessels, and atrophy of the fibres passing out of the anterior horns and of the anterior nerve roots. Degenerative changes have also been observed in the columns of the cord, the peripheral nerves, and paralyzed muscles. The diagnosis is not always easy, especially in old cases. It is dis- tinguished from progressive muscular atrophy by the following features: the paralysis precedes the atrophy, it is not fascicular, but affects the muscles en masse; in progressive muscular atrophy, the reflexes are retained, the disease is slower, but less unfavorable as regards the main- tenance of life, recovery does not occur, and degeneration reaction occurs only in those parts of the muscles which are affected with special intensity. In amyotrophic lateral sclerosis, muscular rigidity and spasms, and increased tendon reflexes are noticeable. Multiple degenerative neuritis is attended with sensory disturbances. The prognosis is favorable as regards life, but less favorable as regards complete recovery. The treatment is the same as that of the acute form. 5. Progressive Spinal Muscular Atrophy. {Amyotrophia spinalis progressiva. Polyomyelitis anterior chronica disseminata.) I. Etiology.—In spinal progressive muscular atrophy, there is a progressive disappearance of voluntary muscles, beginning in the upper limbs, and first affecting only parts of the muscles (fascicular), and un- attended with paralysis, apart from the loss of power due to the dis- appearance of the muscular fibres. There are no disturbances of sensa- tion, or of the functions of the bladder and rectum. All these changes are the results of a primary chronic affection of the anterior columns of the cord, particularly of the large ganglion cells. As a rule, the disease occurs between the ages of 30 and 50 years. Cases have also been reported in which the disease began in childhood—espe- cially when it is propagated in families from one generation to another— but the belief is now growing that these cases are really due to a primary affection of the muscles. We shall, therefore, discuss them under the head of juvenile muscular atrophy, or dystrophia musculorum progressiva. Heredity is often mentioned as a cause of progressive muscular atro- phy, but this applies more particularly to the juvenile form. DISEASES OF THE SPINAL CORD. 123 The disease is often connected with overstrain of certain muscles and groups of muscles. In other cases it is attributed to injury, cold, onanism, and sexual excesses. It has been claimed that the malady occurs after infectious diseases (measles, scarlatina, small-pox, cholera, acute articular rheumatism, typhoid and puerperal fever, syphilis; according to Jackson and Clark, even after vaccination), but it has probably been mistaken for paralysis and atrophy resulting from myelitis, neuritis, or changes in the muscles themselves. This is also true of the injurious effects of lead and arsenic. Progressive muscular atrophy is more frequent in men than in women, probably because the former are more exposed to the etiological influences. II. Symptoms.—Atrophy and, in connection with it, weakness of the muscles develop very gradually. As a rule, this begins in the inter- ossei and the muscles of the thenar and hypothenar eminences, so that Fig. 58. Fig. 59. Dorsum of hand with depressed interosseous spaces in progressive muscular atrophy, in a woman set. 34 years. Right hand. Left hand. the patients first complain of stiffness in the fingers and inability to per- form delicate manipulations. These disturbances are increased by cold and diminished by warmth. According to Eulenburg, the first interosseus is one of the very first muscles affected. Atrophy of the interossei is shown by the deep grooves in the interosseous spaces (vide Figs. 58 and 59). The ball of the little finger and thumb becomes flattened, and the subjacent bones can be felt more distinctly (vide Figs. 60 and 61). In addition, the fingers assume unusual positions. The muscles first attacked in the ball of the thumb are the adductor and opponens pollicis. On account of the pre- dominance of the extensors and abductors of the thumb, the latter is brought into a position of abduction and dorsal flexion (ape-hand). Atrophy of the interossei gives rise to the development of the so-called claw-hand, as the result of the predominance of the lumbricales; the first phalanges are hyper-extended, the second and third phalanges are strongly flexed. The claw-hand also develops in other affections, for 124 DISEASES OF THE SPINAL CORD. example, in trau-matic ulnar paralysis, but in this disease the middle and ring fingers are most markedly affected (vide Figs. 62 and 63). If the lumbricales undergo atrophy the palm of the hand is flattened, but the extensor digitorum continues to extend the first phalanges. The Fig. 60. Fig. Cl. Right hand. Left hand. Palm of hand with atrophy of thenar and hypothenar eminences. The same patient, disease sometimes jumps from the muscles of the hand to the deltoid. In this muscle it is especially evident that the atrophy occurs in bundles, not en masse. At first the posterior and middle thirds are chiefly Fig. 62. Fig 63. Fig. 62.—Claw hand in progressive muscular atophy. After Duchenne. Fig. 63.—Claw hand in paralysis of the interossei as the result of injury to the ulnar nerve. affected. When the entire muscle has undergone atrophy, the shoulder looks flat and angular, and the edges of the bones appear very distinctly. As a matter of course, the movements of the arm are interfered with, and, DISEASES OF THE SPINAL COED. 125 if the scapular muscles are also attacked, the arm hangs alongside the trunk almost like an inert mass. If the ligaments of the shoulder-joint are very flaccid, subluxation of the head of the humerus may result. In other cases the disease spreads from the finger muscles to those of the forearm, especially the extensors. The supinators usually escape unless the flexors become involved. The atrophy may be so extensive that the forearm consists of hardly anything beyond skin and bones, and the interosseous space forms a deep groove (vide Figs. 64 and 65). Among the muscles of the arm the triceps is the last to be affected, so that the arm is almost always extended. Fig. 64. Fig. 65. Appearance of the hand and forearm in two cases of progressive muscular atrophy. Dorsal surface. After Duchenne. The right hand is generally the first attacked, more rarely the left hand or both at the same time. In the majority of cases, after the mus- cles of one side of the body have been attacked, the corresponding ones on the other side are involved before the morbid process extends to higher or lower groups of muscles. If the disease is regarded as spinal in its origin, it must be assumed that the process extends from one-half of the cord to the other before it spreads in a longitudinal direction. As a rule, the muscles of the scapula and trunk are not attacked until the arms have undergone considerable emaciation. According to Du- 126 DI8EASES OF THE SPINAL CORD. chenne, they are attacked in the following order: lower part of the trapezius, pectorals, latissimus dorsi, rhomboid, scapularis, extensors ami flexors of the head, deep muscles of the back, abdominal muscles, finally the neck muscles and rotators of the head. Here, also, the dis- ease often begins on one side, or is more marked on one side than on the other. If the muscles of the loins are affected, the spine is unusu- ally curved anteriorly, so that, in the vertical position, a vertical line dropped from the shoulder falls behind the sacrum (vide Fig. 66). If the abdominal muscles are atrophied, a slight bronchitis may prove dan- gerous, inasmuch as the energy of coughing is interfered with, the bron- Fig. 66. Fig. 67. Position of the body in atrophy of the lumbar muscles in progressive muscular atrophy. After Duchenne. Position of the body in paresis of the abdomi- nal muscles in progressive muscular atrophy. After Duchenne. chial secretion may accumulate, and death occur from suffocation. Fee- bleness of the abdominal muscles also causes marked projection of the spine anteriorly, but a vertical line dropped from the shoulder passes through the sacrum (vide Fig. 67). The diaphragm sometimes takes part in the atrophic process. The lower limbs are usually attacked last. The flexors of the legs are affected earliest and most markedly. Fibrillary (more properly fasicular) muscular twitchings are an al- most constant symptom of progressive muscular atrophy. They con- sist of repeated brief contractions which always affect only individual DISEASES OF THE SPINAL COED. 127 parts of a muscle, now here, now there. They are especially active on disrobing, blowing on, tapping or faradizing the muscles. They some- times appear in muscles which do not present any visible emaciation, but may be entirely concealed by a fat integument. In some cases they are so vigorous as to cause involuntary twitchings of the fingers, arm, or leg. The electrical irritability of the paralyzed muscles corresponds, in general, to the degree of atrophy. The more the muscular substance is lost, the more the electrical irritability of that muscle diminishes until it is entirely abolished. Careful examination, however, shows that par- tial, then complete degeneration reaction is manifested in parts of the muscle. If a small anode is placed in the mastoid fossa or adjacent part of the neck, and a large electrode between the scapulae, more or less vigorous movements will be produced in the arm on the side opposite to the anode. This phenomenon, to which the term diplegic contractions has been applied, is observed at times in this disease, but is by no means characteristic. If the muscles of a limb are extensively affected, the integument is often bluish-red, marbled, and feels cold; its temperature has been found markedly diminished (5° C.). Some writers have observed an increase of temperature (0.5° C.) at the beginningof the disease. The skin pre- sents a tendency to trophic changes: thickening, formation of scales, diminished growth of hair, tendency to ulcerations, herpetic and pem- phigoid eruptions, thickening of the nails, etc. An abnormally abundant production of sweat has also been observed, particularly in rapidly progressing or far advanced cases. Swelling of the joints and phalanges is sometimes described. Sensory cutaneous disturbances are almost always absent; at the most the patients complain of a feeling of coldness in the limbs. The cuta- neous and tendon reflexes disappear more and more with the extension of the disease. The functions of the bladder and rectum are unaffected. Oculo-papillary changes were often noticed. The pupils were unusu- ally narrow on one or both sides, reacted slowly to light, and lost the ability to dilate. Landouzy mentions changes in the ocular muscles in one case. Impaired sight and flattening of the cornea were also mentioned in one case. The general condition is very little affected; slight febrile movement occurs occasionally, and is explained by Friedreich as absorption fever, the result of the absorption of chemical products of the muscular de- generation. The disease advances very slowly and, as a rule, lasts many years. The patient finally loses the use of his hands and arms, is unable to move his legs, and becomes utterly helpless. The mental powers gen- erally remain intact. The condition becomes even more distressing when it is complicated with bulbar symptoms; atrophy and paralysis of the muscles of the face, tongue, pharynx, and larynx. In some cases the latter symptoms first develop, and are followed by the symptoms of progressive muscular atrophy. Death occurs from intercurrent diseases or increasing marasmus, or 128 DISEASES OF THE SPINAL COED. bulbar symptoms give rise to difficulty in deglutition, inanition, “ for- eign-body ” pneumonia, etc. III. Anatomical Changes.—According to Charcot, progressive muscular atrophy is dependent on a primary chronic destruction of the large ganglion cells in the anterior horns of the spinal cord. The French writers attribute these changes to inflammatory lesions of the ganglion cells, which give rise to pigment degeneration and atrophy, or to sclerotic atrophy and complete disappearance of the cells. Any changes which may be present in the interstitial tissue (nuclear prolifer- ation, dilatation, thickening, and fatty degeneration of the blood-vessels) are said to be merely secondary. Others maintain that the process begins in the interstitial tissue, or that both modes of origin are possible. If the lesion is well marked, the corresponding anterior horn, and even the entire half of the cord are diminished in size (vide Fig. 68). Degeneration has also been noticed in the white columns, particularly the lateral columns. Fig. 68. Transverse section of the cervical cordin progressive muscular atrophy. The right anterior horn and right half of the cord are diminished in size, the ganglion cells of the right anterior horn have disappeared with the exception of a few cells in the external pos- terior angle. Enlarged 10 times. After Charcot. The anterior nerve roots are often thin, gray, and in a condition of fatty degeneration and atrophy. Degenerative changes have also been observed in the peripheral nerves. Friedreich’s examinations concerning the muscular changes have fur- nished the following results: They begin in the intermuscular connective tissue (perimysium internum), with increase in amount and nuclear proliferation; this is followed directly by changes in the muscular sub- stance; the nuclei of the sarcolemma proliferate; there is gradual disappearance of the muscular substance proper; some fibres undergo waxy degeneration, others cloudy swelling; some fibres are split longitu- dinally, others in transverse sections; finally, some of the fibres appear split up into their elementary constituents. At the same time the mus- cle substance gradually disappears, so that, in numerous places, the sar- colemma contains nothing but nuclei. These changes often occur only DISEASES OF THE SPINAL CORD. 129 in certain parts of the muscle. The atrophic muscle appears pale, oc- casionally brownish-red (unusual amount of pigment in the fibres). Finally, it may be converted into a sort of tendinous structure (fibrous degeneration). Fatty degeneration of the muscular fibres and accumu- lation of fat in the interstitial connective tissue are rare, but are some- times so extensive as to cause increased size of the muscle. IV. Diagnosis.—The diagnosis is usually easy if we bear in mind the beginning of the disease in the ball of the thumb and little finger, and in the interossei, the absence of sensory disturbances, the develop- ment of fascicular atrophy, and then of weakness of the muscles, the fibrillary contractions, and the intact condition of the bladder and rec- tum. The disease may be mistaken for: a. Juvenile progressive muscular atrophy J this is often hereditary and generally begins in childhood; it often begins in the lower limbs. Duchenne sometimes noticed a pecular impairment of motion of the lower lip in the beginning of the disease. Moreover, the juvenile atro- phy is much slower than the spinal form, fibrillary contractions are usually absent, the atrophic muscles often increase in size from the inter- stitial proliferation of fat, and the affected muscles do not present the degeneration reaction. b. Multiple degenerative neuritis, when very extensive and slow in its course, may also resemble progressive muscular atrophy. The differ- ential points are: the occurrence of paralysis prior to the atrophy, the occurrence of pain, paraesthesiae and objective sensory disturbances of the integument; the affected muscles and nerves are often tender on pressure. c. Acute, subacute, and chronic poliomyelitis are also characterized by paralysis, muscular atrophy, degeneration reaction, absence of sen- sory disturbances; but the process does not extend in such a typical manner as in spinal progressive muscular atrophy, and, in addition, the paralysis develops first, the atrophy later. d. Muscular atrophy is sometimes secondary to other diseases of the spinal cord, and occurs whenever myelitis, tabes, multiple sclerosis, tumors, etc., affect the ganglion cells in the anterior columns of the cord. The differential diagnosis depends upon the fact that the muscu- lar atrophy is preceded by other signs of spinal disease. V. Frognosis.—The prognosis is not favorable, since we are hardly able to restore the atrophied muscles to the normal condition and to pre- vent the spread of the disease. The more extensive and rapid the atrophy the more gloomy the prognosis as regards danger to life. Bul- bar symptoms generally accelerate the fatal termination. Under other circumstances life may be prolonged for many years. VI. Treatment.—Overstrain of muscles must be avoided and, if the signs of muscular atrophy make their appearance, the injurious oc- cupation must be abandoned forthwith. The remedies recommended in myelitis (vide page 88) have been employed in this disease, but very little can be expected from them. The cautious employment of massage and rational gymnastics may be recommended. Electricity remains our chief remedy. The most suit- able mode of application is the galvanic spinal current (large elec- trodes, the anode for the first three to five minutes, then the cathode over the site of disease, or the ascending and descending spinal cur- rent). This may be followed by peripheral galvanization of the indi- 130 vidual muscles, the cathode labile to the muscles, the anode on an indif- ferent spot, or over the lumbar or cervical enlargement, according as the application is made to the lower or upper limb. Galvanization of the cervical sympathetic has also been recommended. The muscles may be treated peripherally with a not too strong faradic current. Treatment requires patience on the part of the physician as well as the patient. COMBINED SYSTEM DISEASES OF THE SPINAL CORD. 1. Hereditary Ataxia. {Friedreich’s Disease.) This disease is pre-eminently hereditary. For example, Friedreich observed nine cases in three families; Immermann and Ruetimeyer described eleven cases in two families. Unlike ordinary tabes, the female sex is more often affected. The first symptoms begin at the age of 4 to 7 years, or at the period of pu- berty. Ataxia is a prominent symptom from the beginning, while sensory dis- turbances remain absent or do not de- velop until very late ; lancinating pains are rare. The ataxia extends very rapid- ly to the upper limbs, or it affects the upper and lower limbs at the same time. Ataxia of the ocular muscles (ataxic nystagmus) and disturbances of articu- lation (ataxia of the muscles of speech) may also occur. The Brach-Romberg symptom was observed in a number of cases. The ocular symptoms (ocular paralyses, reflex rigidity of the pupils, amaurosis), so common in ordinary ataxia, are wanting. The vaso-motor and secretory symptoms observed are polyuria, salivation, and hvperidrosis. No disturbance of the bladder, no bed- sores ; the patellar reflex absent. At a later period, the muscles become para- lyzed and contractu red. In a fatal case, degeneration was found, not alone in the posterior col- umns (most markedly in the cervical cord), but also in the lateral columns and, in the cervical portion, in the anterior columns (vide Fig. G9). The treatment is the same as that of tabes dorsalis. 2. Secondary Degeneration of the Columns of the Spinal Cord. We distinguish ascending, descend- ing, and combined secondary degeneration in the spinal cord. DISEASES OF TIIE SPINAL CORD. Fig. 69. Anatomical changes in the cord in Fried- reich’s hereditary ataxia. The diseased parts are shaded, a-c, cervical cord • d, dorsal cord ; e-g, lumbar cord. After Friedreich. DISEASES OF THE SPINAL CORD. 131 a. Descending secondary degenerat ion of the columns of the spinal cord follows diseases of the brain, and occupies the domain of the pyramid tracts. Hence the changes are found in the posterior part of the lateral columns (the so-called lateral column-pyramid tract), and in the inner- most parts of the anterior columns, next to the anterior longitudi- nal fissure (vide Fig. 70, 1 pvs and 3 psb). Both fields contain nerve tracts which convey the stimulus of the will from the brain to the peri- phery. As the cerebral lesion generally affects only one side of the brain, the degeneration in the cord is also found only in one pyramid tract. But since the lateral column-pyramid tract contains fibres which decussate in Fig. TO. Schematic representation of the distribution of the principal tracts in the spinal cord. 1 pvs, anterior column-pyramid tract (undecussated) ; 2 vsr, antero-lateral column (divided into anterior fundamental column and lateral column) ; 3 psb, lateral column-pyramid tract (de- cussated) ; 4 ksb, lateral cerebellar tract; 5 aks, columns of Burdach ; G iks, columns of Goll. Enlarged 2 times, a, Level of first cervical nerve ; b, third cervical nerve ; c, sixth cervical nerve ; d, third dorsal nerve ; e, sixth dorsal nerve; /, twelfth dorsal nerve ; g, fourth lumbar nerve. the pyramids, while the pyramid-anterior column tract does not decussate, the secondary degeneration in the former will be found on the side op- posite to the cerebral lesion, in the latter on the same side. It must not be forgotten that, according to Flechsig’s researches, there are remarkably great individual differences in the proportion be- tween the decussated and non-decussated fibres of the pyramid tracts. The decussation is sometimes complete, so that no degeneration can occur in the anterior columns. On the other hand, the degeneration in the anterior column may be unusually marked, because very slight decussa- 132 DISEASES OF THE SPINAL CORD. tion has taken place in the pyramids. Pitres reports four cases in which degeneration of both lateral column-pyramid tracts followed a unilateral lesion of the brain. As a matter of course, not all diseases of the brain are followed by secondary degeneration of the cord. This only occurs when the pyramid tracts have been interrupted in any part of their course. If these tracts are followed centrally from their decussation, they will be found to pass through the pons into the middle and inferior parts of the pedunculus cerebri, then to the posterior division of the internal capsule, and thence to the motor regions of the cerebral cortex (anterior and posterior central convolutions). Diseases of other parts of the cortex or brain will not be followed by secondary degeneration of the spinal cord. If the pyramid tract is affected in the cerebrum, the secondary de- generation is noticed in the peduncle, pons, and the corresponding side of the decussation in the medulla (vide Fig. 71). The middle (more Fig. 71 Secondary degeneration of the cerebral peduncle, pons, and medulla oblongata. The shaded parts marked * are degenerated. After Charcot. rarely also the internal) portion of the peduncle appears gray, trans- parent, grayish-yellow or red, and occasionally atrophic (vide Fig. 72, a). The pons is also atrophied; but here the degenerated pyramid tract is visible only on transverse section, upon which it appears gray and reduced in size when compared with the intact side (Fig 72, &). The pyramid is also gray and diminished in size, so that the olivary body is more distinct than its mate. The changes in the spinal cord can be only followed in transverse sections, and in many cases microscopical examina- tion is necessary. If the cord is hardened in chromic acid or bichromates, the degenerated portions assume a light-yellow color, but the yellow region is often larger than the degeneration itself. The degenerated parts stain very deeply with carmine and aniline colors, on account of the abundance of connective tissue and the dearth of nerve-fibres. The shape and extent of the foci are shown in Fig. 72, e to h. The degeneration of the pyramid-anterior column tract diminishes more and more in its downward course and ceases in the upper part of the lumbar DISEASES OF THE SPINAL COED. 133 cord. The degeneration in the lateral column (on the opposite side) is most extensive in the cervical cord, where it has a triangular or wedge-shape ; in the dorsal cord it is less extensive and round. In the lumbar cord it again becomes triangular, and gradually approaches the surface of the cord until it is immediately beneath the pia mater. It terminates at the level of the third and fourth sacral nerves (Fig. 70). Fig. 72. Transverse sections of the cerebral peduncle, pons, medulla oblongata and spinal cord, in a condition of secondary degeneration (shaded portions) following a lesion in the right cerebral hemisphere ; a, peduncle ; b, pons ; c. medulla oblongata ; d, decussation of the pyramids ; e, cervical enlargement; /, dorsal cord ; g, lumbar cord ; h, conus medullaris. The first changes in descending degeneration appear in the nerve fibres them- selves. Kahler and Pick detected them on the eleventh day after an injury to the brain, and perhaps they begin even earlier. Its rapid extension, and its lestriction to definite systems of fibres, precludes the idea of a propagated inflammation, and justifies the conclusion that we have to deal with a degenerative atrophy, the re- sult of a separation of the nerve fibres from their trophic centres. The degenerated fibres undergo loss of the medullary sheath and, finally, of the 134 DISEASES OF THE SPINAL COED. axis cylinders; according to Henle, atrophy of the axis cylinders precedes disap pearance of the medullary sheaths. At a later period, the interstitial connective tissue increases secondarily in amount, granulo-fatty cells and amyloid bodies appear in it, the walls of the vessels become thickened, and their lymphatic sheaths contain fat granules and granulo-fatty cells. As a rule, the gray matter is unchanged. In rare cases, the anterior horn on the side opposite to the cerebral lesion is diminished in size, and its ganglion cells are atrophied, corresponding to atrophy of the paralyzed muscles during life. If the changes have lasted a long time, proliferation of the interstitial connec- tive tissue, and disappearance of the nerve fibres may take place in the periphe- ral nerves of the limbs which have been paralyzed as the result of the cerebral lesion, and the corresponding muscles may present diminished size, fatty degen- eration or proliferation of the nuclei of the sarcolemma, and increase of the inter- stitial connective tissue, or proliferation of fat. The contractures to which hemiplegics become subject, and the exag- geration of the tendon reflexes, are attributed to the secondary degenera- tion. The prognosis of this process is unfavorable, because restitutio ad inte- grum is impossible. The treatment is the same as that of the primary disease. b. Ascending secondary degeneration of the columns of the spinal cord occurs as the result of disease of the posterior nerve roots or spinal ganglia. Senger produced it experimentally in dogs by section of the posterior nerve roots ; in man it is observed most distinctly in disease of the cauda equina. It is con- fined to the columns of Goll and to the lateral cerebellar tracts (Fig. 73, a to *). In the columns of Goll it may be traced as far as the restiform bodies of the medulla, in the cerebellar- tracts it extends to the cerebellum. On account of the primary affection, this degenera- tion is usually bilateral. The degeneration of the columns of Goll is assumed to occur when they are separated from their trophic centres— the spinal ganglia. Some authors regard the columns of Clark as the trophic centres of the cerebellar tracts, but whether these tracts contain centripetal or centrifugal fibres is unknown. Ascending degeneration gives rise to no clinical symptoms. c. Combined secondary degeneration of the columns of the spinal cord occurs when the continuity of the cord is interrupted entirely or in part. In the former event, for example, in compression of the cord, the columns of Goll and the cerebellar tracts degenerate above the primary disease (ascending degeneration), the decussated and non-decussated pyramid tracts degenerate below the focus of disease. But the cerebellar tracts are only affected if the primary disease is situated in the dorsal or cervi- cal region, since their supposed trophic centre, the column of Clark, be- gins in the middle of the dorsal region. The secondary degeneration does not begin in the immediate vicinity of the primary disease. The latter generally presents a diffuse change of the entire section of the cord, then follows, in an upward direction, degeneration of the entire posterior columns and, finally, of the columns of Goll alone (Fig. T3, c Fig. 73. Distribution of ascending secondary de- generation a, cervical cord ; b-d, dor- sal cord. Site of compression of the cord at e; /, lumbar cord below the site of compression with secondary descending degeneration. Natural size. DISEASES OF THE SPINAL COED. 135 and d). As a matter of course, the degeneration is bilateral, unless one- half of the cord alone is diseased. Secondary degenerations sometimes follow circumscribed affections of the cord. 3. Amyotrophic Lateral Sclerosis. I. Etiology.—Charcot applied this term to a disease which is, to a certain extent, a combination of primary degeneration of the pyramid- lateral tracts and of the large ganglion cells in the anterior horns and in the nuclei of the medulla, particularly the hypoglossus, pneumogastric, spinal accessory, and facial. Cold and exposure to wet are generally mentioned as the causes of the disease. It is most frequent from the ages of twenty-five to fifty years ; women are affected more often than men. Weir Mitchell reported a case which was appar- ently due to working in lead. Seelig- mueller described four cases in brothers and sisters whose parents were cousins. In these cases the disease began in in- fancy. II. Anatomical Changes.—Accord- ing to Charcot, the disease begins in the lateral columns of the cord (pyramid tract). It is most extensive in the cer- vical cord, and gradually diminishes to- wards the lumbar region (Fig. 74). In- feriorlv, the degenerated parts gradually approach the pia mater ; superiorly, it may be traced to the lower part of the pons (as far as the pyramid tracts are collected into a bundle), and even into the foot of the peduncle. The internal capsule almost always escapes. In some cases the undecussated portion of the pyramid tract has been found to be dis- eased. According to Charcot, the disease is a primary inflammation of the nerve fibres, which gives rise secondarily to an affec- tion of the interstitial connective tissue. The microscope reveals proliferation of the interstitial tissue, destruction of nerve fibres, thickening of the ves- sels, granulo-fatty cells, and amyloid bodies. Perhaps it is more proper to regard the disease as an atrophy of the nerve fibres and ganglion cells. Through the medium of the diseased nerve fibres, the disease is said to extend secondarily to the gray matter of the anterior horns; the neur- oglia then proliferates, the ganglion cells atrophy and disappear. These changes are most marked in the cervical region, gradually diminish in a downward direction, and are generally absent in the lumbar cord. Fig. 74. Changes in amyotrophic lateral sclerosis. After Charcot, a, medulla oblongata; b, cervical cord ; c, dorsal cord ;| d, lumbar cord. The diseased parts are darkly shaded. Natural size. 136 DISEASES OF THE SPINAL CORD. Superiorly, they extend to the ganglion cells of the nuclei in the me- dulla, particularly of the hypoglossus, pneumogastric, spinal accessory, and facial. Atrophic and degenerative changes are found in the anterior spinal roots and the peripheral nerves. The corresponding muscles are atro- phic, the interstitial connective tissue is increased and often contains an unusual amount of adipose tissue, so that the muscle may appear even larger than normal. Leyden showed that the mode of development is not always as regular as in the description just given, but that the disease sometimes begins in the gray matter, and then extends to the white substance. In addition, he showed that the posterior columns are sometimes affected at the same time. Fig. 75, which, is taken from Leyden’s work, shows gray degeneration of the columns of (Joll. Weiss reported a case in which the ganglion cells of the posterior horns had un- dergone atrophy, and attributes to this lesion the decubitus which developed upon the trochanters. III. Symptoms.—The clinical history is a combination of that of Fig. 75. Changes in amyotrophic lateral sclerosis with implication of the'columnsof Goll. Cervical enlarge- ment. Diseased parts are shaded. After Leyden. Enlarged 5 times. spastic spinal paralysis and of progressive muscular atrophy and bulbar paralysis. Sensation and the bladder and rectum are unaffected. The scene generally opens with paralysis, rigidity, spasms and contractures of the muscles, then rapid emaciation. As a rule, the symptoms begin in the upper limbs and extend downwards, but atrophic changes do not occur in the lower limbs. Atrophy and paralysis follow in the dis- tribution of the hypoglossus, vagus, spinal accessory, and facial. More rarely, the symptoms begin in the lower limbs or in the distribution of the bulbar nerves. The first symptoms in the upper limbs occur with or without pro- dromata (formication and other paraesthesias). The limbs feel weak and well-marked paralysis.gradually develops, followed by stiffness, spasms and contractures. The arms are drawn against the trunk, and motion at the shoulder-joint is attended with pain; the forearms are semi-flexed and at the same time pronated, and there is generally contracture at the DISEASES OF THE SPINAL COED. 137 wrist-joint in a position of pronation, with the fingers drawn into the palm of the hand (Fig. 76). These symptoms are the result of disease of the pyramid tracts. The affection of the gray matter is shown by rapid atrophy of the mus- cles of the arms, affecting large masses at one time. Fibrillary contrac- tions are observed during the emaciation. The atrophic muscles are tender on pressure, and generally show the partial degeneration re- action. If the process extends to the trunk and lower limbs, the patients complain of stiffness in the back, and are hindered in sitting up, and moving the head ; they are compelled finally to keep to bed. The gait peculiar to spastic spinal paralysis is produced as the result of muscular rigidity and contracture, and the tendon reflexes are exaggerated. As a rule, the lower limbs do not undergo atrophy. Bulbar symptoms begin with atrophy and fibrillary contractions in Fig. 76. Position of the forearm and hand in amyotrophic lateral sclerosis. After Charcot. the tongue, and interference with articulation. Paralysis of the palate then gives rise to difficulty in deglutition, and speech becomes indistinct and nasal. The lips atrophy, the mouth is half opened, and continually discharges saliva. The expression of the face is tearful, and, while the forehead appears wrinkled, the lower half of the face is devoid of expres- sion. This condition often leads to “ foreign-body ” pneumonia or at- tacks of suffocation and death. Charcot regards the disease as absolutely fatal in one to three years, but Weir Mitchell observed recovery under the use of potassium iodide and sulphur baths. IV. Diagnosis.—The disease is distinguished from progressive mus- cular atrophy by the fact that in the latter the paralysis and atrophy go hand in hand, the atrophy is fascicular and generally begins in the in- terossei, the thenar and hypothenar eminence; muscular rigidity does not occur, and the tendon reflexes are lost. It is distinguished from hypertrophic cervical pachymeningitis by the predominance, in the latter, of irritative symptoms at the outset, the development of’severe sensory disturbances, non-extension to the bulbar 138 TRAUMATIC AFFECTIONS OF THE SPINAL CORD. nuclei, and the possibility of recovery. The treatment is similar to that of spastic spinal paralysis. C. TRAUMATIC AFFECTIONS OF THE SPINAL CORD. 1. Unilateral Lesions of the Spinal Cord. (Broivn-Sequard’s Paralysis.) I. Etiology.—Cases in which one-half the transverse section of the ■cord is rendered incapable of function present characteristic clinical symptoms, independent of the etiology of each individual case. It occurs most frequently as the result of wounds with a knife or dagger, which have injured only one-half the cord. This happens more rarely in fractures, luxations, exostoses, or neoplasms of the vertebrae. An unilateral lesion may also be produced by exudations, hemorrhages or tumors of the meninges, myelitic foci, sclerosis, hemorrhages and neoplasms of the cord. Kosenthal and Paoluzzi observed each a case following a cold. II. Symptoms.—The characteristic feature of the symptomatology of an unilateral lesion of the cord is the occurrence of motor paralysis on the same side and sensory paralysis on the opposite side. If the disease is situated high up, we will find motor paralysis of the arm and leg on the injured side, and loss of sensation on the opposite half of the body exactly to the median line and to the level of the site of disease. If the morbid process affects the dorsal cord, motion is paralyzed in one lower limb, sensation in the other lower limb. These symptoms may develop suddenly as the result of injury, often slowly as the result of other causes. They may lose in distinctness if the -spinal affection extends to the other side of the cord. Upon the side of the body corresponding to the injured side of the cord, there is complete or almost complete paralysis of all the muscles whose nerves leave the cord below the site of injury. The thoracic and abdominal muscles are affected, according to the level of the disease. At the same time, hyperaesthesia is noticeable in the paralyzed parts. As a rule, this affects all modes of sensation, more rarely the hyperaes- thesia is partial, i. e., it affects only certain qualities of sensation. The muscular sense is sometimes retained, sometimes absent. The upper border of the hyperaesthetic region is formed by a narrow anaesthetic zone (Fig. 77, b). " This is the result of the direct injury of the posterior nerve-roots. Above this is another hyperaesthetic zone which extends beyond the median line to the other side of the body (Fig. 77, c and c'). The symptoms mentioned are associated with vaso-motor disturb- ances, viz., redness and increased heat of the skin. If the injury affected the cervical cord high up, there will be unilateral symptoms of paralysis of the sympathetic on the same side: redness and increased heat of the ■side of the face and concha of the ear, contraction of the pupil, narrow- ing of the palpebral fissure, injection of the conjunctiva, increased flow of tears; hemicrania has also been noticed. Trophic disturbances are often though not constantly observed; they depend probably on implication of the nerve-roots. Acute decubitus has been observed; sometimes the paralyzed muscles manifest loss of TRAUMATIC AFFECTIONS OF THE SPINAL CORD. 139 faradic excitability. Alessandrini mentions pain in the joints on the paralyzed side, the result of extravasations of blood into the joints. After a while, the paralyzed muscles undergo atrophy from disuse, associated with diminution of electrical irritability. The cutaneous and tendon reflexes have been found increased in a number of cases. Paralysis of the bladder and rectum is frequently described. Fischer observed erection of the penis; sexual power is generally abolished. As a rule, there is complete, moie rarely partial, anaesthesia on the side of the body opposite to the site of the lesion; the muscular sense is alone retained. Motor power is almost always intact on this side, but Fig. 77. Schematic representation of the symptoms in a unilateral lesion of the left side of the dorsal cord. a. Paralysis of motion and vaso-motor nerves, hyperaesthesia ; b, anaesthetic zone (from injury to the sensory nerve roots); c, upper hypersesthetie zone ; &, the same on the uninjured side : d, anaesthesia. slight paresis is occasionally noticed. The reflexes are unchanged, and vaso-motor disturbances are absent; in rare cases the temperature of this Bide of the body is elevated. Above the region of anaesthesia is a narrow zone of hyperaesthesia, continuous with that on the opposite side of the body (Fig. 77, c'). The patients often complain of a cincture feeling, which corresponds to the level of the lesion. Pain and paraesthesiae may occur upon one or the other side of the body. If the cause permits, the symptoms are capable of recovery. In such 140 TRAUMATIC AFFECTIONS OF THE SPINAL CORD. cases, according to Brown-Sequard, the motor functions recover earlier than the sensory functions, in contradistinction to what happens after the interruption of conduction in peripheral nerves. In other cases the symptoms persist, or cystitis and decomposition of urine set in and the patients die, or finally the morbid process spreads and the symptoms of a diffuse lesion of the cord make their appearance. The symptoms of unilateral lesion of the cord are most sharply defined if the dorsal cord is affected. In affections of the cervical enlargement, the paralysis in the upper limbs is often confined to certain groups of muscles, because the nerve-tracts for the individual muscles are relatively far removed from one another in this locality. The cutaneous nerves are here given off in such a manner that the hvperaesthetic and anaes- thetic zones are not circular but irregular in shape. III. Diagnosis, Prognosis, and Treatment.—The diagnosis is Fig. 78. Fig. 79. Fig. 78.—Schematic representation of the course of the fibres in the cord. After Brown-Sequard. v, uncrossed motor fibres ; v', uncrossed vaso-motor fibres ; sni, uncrossed fibres of muscular sense ; s, decussating sensory fibres. Fig. 79.—Schematic representation of the anaesthetic zone on the side of the lesion. The (shaded) focus of disease has interrupted all the sensory fibres on the left side which have entered the cord lower down, while it interrupts only a few of the sensory fibres on the right side. After Brown-Sequard. easy, since in cerebral processes the paralysis and anaesthesia are always on "the same side, and cerebral nerves are also affected. In hysterical liemianaesthesia the special senses are also anaesthetic. The prognosis and treatment depend on the primary disease. IV. Pathnlogico-physiological Remarks. The motor nerve-fibres pass from the cerebral cortex to the internal capsule and the foot of the cerebral peduncle, thence through the pons, and, after the decussation in the medulla oblongata, pass in great part into the opposite side of the spinal cord. Here they pass along the posterior part of the lateral column (Fig. 70, 3 psb), then into the gray matter and the anterior nerve roots of the same side. Hence a unilateral lesion of the cord must produce paralysis of all the motor nerves on the same side which are situate 1 below the lesion. TRAUMATIC AFFECTIONS OF THE SPINAL CORD. 141 But it must be remembered that the decussation of the motor fibres in the medulla is not complete, a small portion remaining upon the same side of the cord. This is the pyramid-anterior column tract, which is adjacent to the ante- rior longitudinal fissure (Fig. 70, 1 pvs). This tract decussates within the spinal cord, and passes to the other side. Hence, a slight degree of motor paralysis may develop upon the side opposite to the spinal lesion. Flechsig has shown that, in some cases, the undecussated pyramid tract may be the larger, so that, in excep- tional instances, the paralysis may be situated on the side opposite to the spinal lesion. The sensory fibres must be assumed to decussate within the spinal cord, since this alone wili explain the crossed anaesthesia in unilateral lesion of the cord (vide Fig. 78). The fibres for muscular sense and the vaso-motor fibres do not decussate in the cord, since they are paralyzed on the side of the lesion. According to Brown-Sequard, the decussation of sensory fibres of the different qualities of sensation occurs at different levels in the cord; going from below up- wards the fibres for tactile sensation first decussate, then those for tickling, pain, and temperature. The hyperaesthesia on the side of the lesion is explained by some as the result of irritation of the sensory nerve fibres by the wound, by others as the result of paralysis of inhibitory mechanisms. For an explanation of the narrow anaesthetic zone on the paralyzed side, we refer to Fig. 79. 2. Acute Injuries of the Spinal Cord. I. Etiology.—As a rule, acute injuries of the spinal cord are asso- ciated with external traumata. In some cases, however, severe lesions of the spinal cord are produced bv an injury, although nothing is noticeable in the spine or soft parts. Moreover, sharp weapons may penetrate the intervertebral spaces and injure the cord without injuring the bony parts of the spine. Acute injuries of the cord are relatively frequent in fractures and dis- locations of the vertebrae. Detached fragments of the bone may enter the cord, or the dislocation narrows the spinal canal and compresses the cord. In certain cases this is preceded by disease of the vertebrae, most frequently tuberculosis. In such an affection of the atlas and axis, a sudden movement of the head may dislocate the odontoid process and compress the cord. Or the carious vertebrae sink in and produce such marked flexion and narrowing of the spinal canal as to injure the cord. Charcot observed rupture of the cord in the new-born as the result of excessive traction during delivery. II. Anatomical Changes.—If death occurs soon after a simple in- cised or stab wound, we will find a gaping wound in the cord which is generally filled with blood clots. The substance of the cord soon under- goes swelling and softening at the cut ends, and the microscope shows fatty degeneration of the tissue elements. This terminates in the forma- tion of a connective tissue which is rich in cells, which continues to proliferate and thus restores the continuity of the cord by a sort of cicatricial tissue. Whether the regeneration of nerve fibres occurs in man is unknown, though clinical experience favors the belief in such an occurrence. The wound in the cord sometimes contains a part of the weapon, and under such circumstances an abscess is apt to develop. If the patient survives the injury for a long time, ascending and descending secondary degeneration will develop. In other cases, the cord undergoes contusion, hemorrhagic disintegra- tion, or rupture. Fatty degeneration, softening, and secondary degener- 142 TRAUMATIC AFFECTIONS OF THE SPINAL CORD. ations follow. Tlie meninges may take part in the changes, or remain entirely intact. III. Symptoms.—As a rule, there is paraplegia of motion and sensa- tion, paralysis of the bladder and rectum, and changes of reflex excita- bility. Vaso-motor symptoms (changes in the color and temperature of the skin, and in the formation of perspiration) have not infrequently been described. Priapism is a frequent symptom; the penis is generally semi-erect or flaccid. This is observed most commonly in injury of the cervical or dorsal cord; it is absent if the lesion is situated below the third lumbar vertebra. All these symptoms occur very soon after the injury. In injury of the cord above the cervical enlargement, death may occur very rapidly. If life is spared, all the limbs are paralyzed as re- gards motion and sensation; reflex irritability is sometimes diminished or abolished immediately after the injury, but is increased after the cord has, to a certain extent, recovered its tone. Retention of urine and fasces is often observed at the start, but this disappears after a time, and may be followed by paralysis of the bladder and rectum (cystitis, ammo- niasmia, decubitus). Paralysis of the abdominal and thoracic muscles interferes with respiration; if the diaphragm is paralyzed, death from suffocation will probably result in a short time. Implication of the medulla oblongata will be shown by difficulty in deglutition, vomiting, slowness of the pulse, pupillary changes. Abnormally high temperature of the body has iieen observed in several cases. According to the experi- ments of Naunyn and Quincke, there are certain cerebro-spinal fibres which inhibit the production of animal heat. Injury to the cervical enlargement is also followed by motor and sen- sory paraplegia of all the limbs. The reflexes, the bladder, and rectum pre- sent the same changes as have been described above. Respiration is im- peded on account of paralysis of the thoracic and abdominal muscles. The cerebral nerves are unaffected, at the most there are pupillary changes (cilio-spinal centre in the cervical cord). In injury to the dorsal cord, the motor, sensory, and vaso-motor dis- turbances are confined to the lower limbs; bladder and rectum as de- scribed above. The situation of the injury can be determined by accu- rately localizing the upper boundary of anaesthesia. The anaesthetic region is sometimes bounded by an apparently hyperaesthetic zone. In Nieden’s case of injury of the cord at the level of the first dorsal verte- bra, the temperature in the rectum, on the day of admission to the hos- pital, was only 35.1° C., on the following day (day of death) only 27.5° C. In injury to the lumbar cord, there is paraplegia of the lower limbs, permanent paralysis of the bladder and rectum, and abolition of reflex irritability. The paralyzed muscles often present rapid atrophy and loss of faradic excitability. The disease may last for weeks, months, or years. But, as a rule, death soon occurs as a direct result of the spinal lesion. It often fol- lows at a later period as the result of increasing marasmus, paralysis of the bladder, and decubitus. Recovery is rarely observed, and only after partial or comparatively slight injuries. IV. Diagnosis, Prognosis, and Treatment.—The diagnosis is easy, when motor and sensory paraplegia follows an injury to the spinal column or its vicinity. The prognosis is almost always unfavorable, and recovery can hardly ever be expected. The treatment depends upon the causal conditions. Opinions are TRAUMATIC AFFECTIONS OF THE SPINAL CORD. 143 divided with regard to the advisability of trephining. In other respects the treatment is purely symptomatic : absorbents (iodine, mercury), care- ful attention to the bladder and rectum, prevention of bed sores, con- stant current. 3. Concussion of the Spinal Cord. (Railway Paralysis.) I. Etiology.—Concussion of the spinal cord is the term applied to those diseases of the cord which are the result of violent mechanical in- jury of the entire body, or chiefly of the spinal column, without injury to the vertebrae or meninges. This may occur after a fall or blow upon the spine or buttocks, feet, or arms. Special attention has been paid recently to concussion after railway accidents (railway spine), in which the severity of the symptoms is often entirely disproportionate to the antecedent lesion. Rigler suggests that this is owing to the fact that fright aids materially in producing the spinal symptoms. Locomotive engineers and brakemen sometimes suffer from spinal symptoms, al- though they have suffered no gross concussion as in railway accidents. II. Anatomical Changes.—Anatomical changes may be wanting, although death occurs shortly after the accident. This was observed by Leyden, in a case which proved fatal in five days, and by Fischer in a case which ended fatally in two days. We must then assume purely molecular changes in the substance of the cord. In other cases hemorrhages are found in the cord and its meninges. If they are numerous and extensive, they may be followed by inflamma- tion and softening processes in the cord. In still other cases, the symptoms of chronic meningitis, myelitis, or myelo-meningitis gradually develop. In a case of this kind, in which death occurred three years after a railway accident, Leyden found a cheesy, tubercular inflammation in the peridural cellular tissue, and acute myelitis in the cervical enlargement, with ascending and descend- ing secondary degeneration. The inflammation had also passed through the intervertebral foramina, into the left brachial plexus. The development of tumors, especially gliomata, is also mentioned as. a sequel of spinal concussion. III. Symptoms.—The symptoms are extremely variable. In one series of cases the accident is immediately followed by the signs of shock (small pulse, accelerated breathing, cool and cyanotic skin, paralyses, involuntary evacuations, etc.) which terminates fatally in a few hours or days. In other cases, the symptoms of collapse are less marked and gradu- ally disappear, the paralyses gradually improve, and complete recovery occurs at the end of day3 or weeks. In a third group of cases, recovery may be delayed for years, but finally becomes complete. Of great practical importance are those cases in which no morbid phenomena are observed immediately after the accident, and the symp- toms of a chronic affection of the cord or meninges do not develop until after the lapse of weeks, even of months. Sometimes meningeal, i. e., irritative symptoms predominate, some- times spinal symptoms, i. e., paralyses. In some cases the symptoms resemble those of multiple spinal sclerosis (Westphal), sometimes those 144 traumatic affections of the spinal cord. of spastic spinal paralysis, etc. Such cases, as a rule, terminate in death. If the brain has also suffered concussion, the symptoms of the latter generally obscure the spinal phenomena. In other patients, cerebral symptoms (mania, progressive paralysis of the insane, etc.) develop at a late period. In four cases of railway spine, Wharton Jones observed amblyopia as the re' suit of atrophy of the optic nerve. IV. Diagnosis.—The diagnosis is easy if there is an undoubted relation between the spinal symptoms and a previous concussion of the body or spinal column. In guarding against simulation after railway acci- dents, Schulz recommends attention to the tendon reflexes which, he claims, are always changed, sometimes exaggerated, sometimes dimin- ished. V. Prognosis.—The prognosis is always serious. The symptoms sometimes grow unexpectedly worse, or they do not appear until a long time after the accident. The prognosis is especially grave when we are justified in assuming serious changes in the substance of the cord. VI. Treatment.—If the symptoms of shock predominate, we should order stimulant measures: friction of the skin, coffee, brandy, camphor, musk, ammonia, etc. If the disease runs a chronic course, we may order absorbents, par- ticularly potassium iodide, iodine and iron baths, and electricity. In other respects, purely symptomatic treatment. 4. Slow Compression of the Spinal Cord. (Compression Myelitis.) I. Etiology.—The causes of compression sometimes enter the spinal canal through the intervertebral foramina; they start from diseases of the vertebrae themselves, from changes in the peridural cellular tissue and meninges, or from diseases of the spinal cord itself. Among lesions of the first class may be mentioned aneurisms of the abdominal aorta, which have eroded the vertebrae, abdominal echino- cocci, neoplasms and inflammations which have extended through the intervertebral foramina into the spinal canal. Among the diseases of the vertebrae, tuberculosis occupies a promi- nent part. Of rarer occurrence is vertebral cancer, which is gen- erally secondary, more rarely primary. In certain cases, the compres- sion of the cord is the result of syphilitic changes in the bones, osteomata, exostoses, luxation or arthritic changes in the vertebras, etc. The compression is sometimes the result of thickening of the odontoid process. Diseases of the meninges and peridural tissue, which may give rise to compression, include inflammatory changes, neoplasms, and parasites. In some cases, the primary affection is situated in the vertebra?, but is followed by changes in the meninges, which exercise pressure on the cord. Compression of the cord is rarely the result of the diseases of the cord itself. This has been observed in tumors of the cord (glioma, sar- coma, carcinoma, tubercle, gumma) and in cystic dilatation of the cen- tral canal. TRAUMATIC AFFECTIONS OF THE SPINAL CORD. 145 The changes described above may not alone give rise to compression of the cord, but also to inflammatory processes in the meninges, nerve roots, and the cord itself. II. Anatomical Changes.—So far as regards the mechanical results of compression, the cord will be found flattened and thinned at the site of compression. These appearances are sometimes unilateral, sometimes they extend around the entire circumference of the cord. The parts immediately above and below the site of compression are some- times dilated into a spindle shape (vide Figs. 80 and 81). These mechanical effects are not the chief factors in the clinical symptoms, but the latter are the result of the inflammatory changes which often affect the nerve roots, meninges, or the cord itself. in the majority of cases, the cord is, indeed, thin and flattened, but at the same time it is soft, diffluent, sometimes very pale and trans- parent, sometimes injected, i. e., it presents the appearances of trans- verse myelitis. If the changes have existed for some time, the affected Fig. 80. Fio. 81. Anterior surface of cord. Posterior surface. The dura mater opened and turned back. Annular compression and narrowing of the cord (at k) as the result of cancer of the vertebrae in a woman aet. 34 years. Natural size. Complete interruption to conduction during life. part of the cord not infrequently becomes very firm and sclerotic, and ascending and descending secondary degeneration develops. The lesions are chiefly of an interstitial character; the cellular elements of the neuroglia increase in number and size, and the nuclei also increase in number; the basement substance becomes more abundant. The blood-vessels present thickening of their walls, increase of the nuclei, and fatty degeneration. The medullary sheath of the nerve fibres undergoes granular disintegration and gradu- ally disappears; the axis cylinders are swollen, and contain vacuolae; later they are destroyed. Distention, increase of the nuclei and pigment, vacuolae, and atrophic changes have been observed in the ganglion cells. The nerve roots and intervertebral ganglia also present inflammatory and atrophic changes, the former constituting the initial, the latter the terminal stage. The meninges at the site of compression are either markedly con- gested or unusually pale. They are often thickened, opaque, and adherent to one another. These changes may play a prominent part in the history of compression-myelitis. This is particularly true of the 146 TRAUMATIC AFFECTIONS OF THE SPINAL CORD. majority of cases following vertebral caries, since compression of the cord is rarely the result of flexion of the spinal canal, but rather of inflammation and thickening of the outer surface of the dura mater (external pachymeningitis). In rare cases of vertebral caries, pus enters the peridural space and compresses the spinal cord. HI. Symptoms.—Compression-myelitis may be divided into the pro- dromal, irritative, and paralytic stages. The symptoms of the prodro- mal stage depend upon the causes of the disease in each individual case. The irritative stage is characterized by symptoms which indicate irrita- tion of the meninges, nerve roots, and cord. The symptoms of the paralytic stage depend upon compression and inflammation of the spinal cord. These stages are not always sharply defined. When the compression is the result of intra-medullary diseases, the symptoms generally begin with paralytic phenomena. We cannot enter into a detailed description of the prodromal phenomena; the chief ones are pain and tenderness in certain parts of the spine, pain during movement, and curvatures of the spine. Inflammatory irritation, particularly in the nerve-roots, is shown by neuralgiform pains. These radiate into the limbs, or pass around the trunk (cincture feeling) ; they are sometimes localized in definite parts, and may be especially severe at night. They are sometimes increased on movement and concussion of the spine. Iiypersesthesia and parsesthesiae are often noticed in the distribution of the affected nerves. Charcot has also observed dysaesthesia (vide page 86). Trophic disturbances (herpes zoster, bullous eruptions, acute decubitus, joint changes, etc.) have been observed not infrequently. The patients sometimes complain of twitchings and contractures in the muscles. Paralysis slowly develops and gradually occupies the foreground. It occasionally develops very rapidly, almost in an apoplectiform manner. In compression of the cervical cord, it sometimes happens that the arms alone are paralyzed. Previous hyperaesthesia gradually gives way to increasing anaesthesia, although complete anaesthesia is rare. In many cases, sensation is very little affected, despite the severe motor symptoms. Delayed conduction is sometimes noticeable. In addition to anaesthesia, the patient may suffer from the most violent pains (anaesthesia dolorosa), particularly in cancer of the vertebrae. If these symptoms are the result of compression of individual nerve-roots, they will be confined to circumscribed areas, and associated with loss of reflex excitability in the affected nerve-tracts. The affected muscles then undergo rapid atrophy, and degeneration reaction develops. But if the symptoms result from compression of the spinal cord itself, the motor and sensory disturbances almost always as- sume a paraplegic character, and the cutaneous and tendon reflexes are considerably increased. The signs of spinal hemiplegia occur in very rare cases as the result of unilateral compression of the cord. Reflex excitability is abolished if the lumbar cord is compressed, or if extensive changes in the gray matter have extended from a focus situated higher up. The paralyzed limbs sometimes present vaso-motor symptoms : discoloration of the skin, elevation of temperature, and abnormalities in the production of perspiration. Kahler and Pick described a case in which the motor irritation began with ataxic symptoms. Disturbances 147 FUNCTIONAL DISEASES OF THE SPINAL COED. of the bladder and rectum occur from the start in diseases of the lumbar cord. Under other conditions, they may remain long unaffected. Complete or almost complete recovery may take place, even if the para- lysis is very marked. Improvement often occurs with surprising rapidity. I know of a case of complete paraplegia of three or four years* duration, following vertebral caries, in which, at the end of that time, improve- ment occurred with such rapidity that the patient was able, at the end of two weeks from the first signs of recovery, to walk unaided to the dining- room. In such cases, we may not assume acute regeneration of com- pressed and destroyed nerve elements. It must be assumed that the few intact nerve fibres at the site of compression suffice, when the compres- sion ceases, to conduct impressions. Some cases present repeated exacerbations and remissions. In others, the disease progresses uninterruptedly. Increasing marasmus, decubi- tus, cystitis, and ammoniaemia, more rarely sudden bulbar paralyses, cause the fatal termination. Secondary degeneration is shown by the fact that the previously flaccid paralyzed muscles become stiff, and twitchings and contractures make their appearance. In the lower limbs, the extensors are at first chiefly affected, but later the flexors becomes involved to a more marked extent—the thighs are strongly flexed and drawn upwards, and the legs are flexed so that the heels come in contact with the thighs. Secondary degenerations may also give rise to recurrent paralyses, i. e., paralysis of the upper limbs becomes associated with paralysis of the lower limbs, which resulted from a morbid process in the lumbar or dorsal cord. This must be explained on the assumption that the secondary degenera- tion has interrupted the paths of conduction to the upper limbs. IV. Diagnosis.—While the diagnosis of compression of the cord is usually easy, that of the cause of each individual case may be difficult. This is especially true if no atyiormality can be discovered in the spinal column, and if the previous history furnishes no clue. V. Prognosis.—This depends upon the etiology, and, as a matter of course, it is unfavorable when the cause cannot be removed. Other- wise, improvement and even complete recovery are not infrequent, par- ticularly in vertebral caries. VI. Treatment.—This must first be directed towards the removal of the cause. In other respects, the treatment is similar to that of acute and chronic myelitis (see page 88). B.—FUNCTIONAL DISEASES OF THE SPINAL CORD, OR SPINAL NEUROSES. 1. Spinal Irritation. 1. The term spinal irritation is applied to a symptom-complex characterized by pain in the spine, associated with neuralgiform pains in the skin or viscera, vaso- motor and secretory disturbances, motor weakness, functional cerebral changes, etc., and not dependent on an anatomical lesion of the cord. The condition has been attributed to spinal anaemia or hyperaemia, meningitic irritation, or changes in the sympathetic. Some writers deny the very existence of spinal irritation. 2. This condition is observed most frequently in women, and is often associated with hysteria, chlorosis, and anaemia. Bodily and mental strain, exhausting dis- eases, excesses in venery, abuse of alcohol or opiuni, and heredity have been men- tioned as causes. It occurs generally from the age of 15 to 30 years. 148 FUNCTIONAL DISEASES OF THE SPINAL COED. 3. The most constant symptom is pain in the spinal column. It most frequently affects the dorsal spine, but is also observed in other parts. It occurs spon- taneously, but becomes especially severe on pressure upon the spinous processes, and may be so violent as to give rise to syncope or epileptiform seizures. It also becomes evident on passing over the spine a sponge dipped in hot water, or the cathode of the galvanic current. The adjacent integument of the spine is not infrequently very hypersesthetic. Hammond also describes a deeper pain which is produced by percussion of the spine. In addition, there are eccentric symptoms of irritation which vary according to the affected portion of the cord. In changes in the cervical cord, we notice headache, vertigo, visual disturbances, tinnitus aurium, hypersesthesia of the face, depression, insomnia; in other cases, somnolence, neuralgiform pains in the face, neck, upper limbs; nausea and vomiting. The eccentric dorsal symptoms of irritation include palpitation, asthmatic attacks, nervous cough, intercostal neuralgia, gastralgia, vomiting, singultus, etc. Lumbar irritation is charac- terized by pains in the back, lower limbs, bladder, rectum, uterus and ovaries, strangury, polyuria, etc. Paraesthesise, muscular pareses, spasms, and vaso-motor changes are not un- common. The disease may last months and years, but hardly ever leads to more serious affections. 4. The diagnosis is usually easy after prolonged observation. 5. The treatment consists of bodily and mental rest, nutritious and abundant food, the administration of quinine, iron, cod-liver oil, cold-water treatment, a trip to the country, and the use of the galvanic spinal current (descending, not too strong or prolonged, anode or cathode to unusually painful vertebras). The faradic brush to the spine, or galvanization transversely through the skull, has also proved useful. Strychnine, potassium bromide, zinc, arsenic, phosphorus, and opium have also been recommended. 2. Functional Weakness of the Spinal Cord. Spinal Neurasthenia. 1. The etiology of spinal neurasthenia is the same as that of spinal irritation, but the two conditions are not identical. Spinal neurasthenia is especially fre- quent in men, particularly among the higher classes. 2. The symptoms consist of abnormal functional irritability and weakness of the spinal cord. It is often associated with cerebral neurasthenia. It is dis- tinguished from spinal irritation mainly by the fact that the motor disturbances predominate, while sensory symptoms may be entirely absent. The patients are easily tired on walking or standing. They often experience that feeling of muscular exhaustion which is felt by healthy individuals only after unusual exertion. This is often felt immediately after waking. The gait is stiff, trembling, and uncertain. Similar symptoms may develop in the upper limbs (while writing, etc.). Sleep is restless and disturbed by dreams. The patients become depressed, irritable, and shy. Many complain of vertigo, a feeling of pressure in the head, ringing in the ears; in company, they suffer fx-om a feeling of terror and palpita- tion ;. in theati’e, they have a dread of fire, etc. Sexual excitement is often noticeable, but its gratification is attended not in- frequently with premature ejaculation of semen, and may be followed by syncope (in one of my cases by palpitation and epileptiform seizures). Anorexia, eructations, flatulence, and constipation are observed not infre- quently. Some patients complain of paraesthesise, vaso-motor disturbances (coldness of the hands and feet), hyperaesthesia of the back. The disease is capable of recovery, often not until after the lapse of months and even years. 3. The treatment is similar to that of spinal irritation. Erb prefers the ascending galvanic spinal currents. Good effects have been obtained from general faradization : the patient is placed in a bath-tub filled with lukewarm water, in which is put the cathode of the secondary current, or the feet are placed upon a large cathode, while a large anode is gradually passed over the different parts of the body from above downwards. Or the physician takes the anode in one moistened) hand, while the patient’s body is stroked with the other (also mois- tened) hand. Duration of each sitting ten minutes, every two to three days. FUNCTIONAL DISEASES OF THE SPINAL COED. 149 3. Acute Ascending Spinal Paralysis. (Kussmaul-Landry’s Paralysis.) I. Etiology.—The symptoms of this disease consist of progressive paralysis from below upwards, with retention of electrical irritability in the paralyzed muscles, absence of atrophy, of sensory and trophic dis- turbances, of paralysis of bladder and rectum, and of anatomical changes in the nervous system. The disease is rare, but is much more common in men than in women, and, as a rule, appears between the ages of twenty and forty years. The causes are often unknown. It has been attributed to cold, sup- pression of menstruation, and mental excitement. Bablon observed it after coitus in the standing position. Ic is relatively frequent after acute infectious diseases, and has also been attributed to syphilis. II. Symptoms.—The paralysis develops unexpectedly, or is preceded by prodromata. The latter consist of chilliness, slight fever, pain in the back and limbs, formication, and other paraesthesiae. The motor paralytic symptoms do not always follow a strictly ascend- ing course. They begin in one or both feet, then affect the legs, thighs, loins, abdomen, chest, hands, forearms, and arms, then the neck, and finally the bulbar nerves. Westphal described a case in which bulbar paralyses were alone observed. In rare cases the paralysis pursues a descending course. The motor paralysis begins, as a rule, with paresis which gradually deepens into complete paralysis; the limbs remain flaccid. The patients first experience a tired feeling in the legs, and are soon compelled to take to bed. If the dorsal muscles are affected, they are unable to sit up, and paralysis of the abdominal muscles interferes with defecation, coughing, sneezing, i. e., with all expiratory processes. Paralysis of the intercostal muscles impedes inspiration. Gradually the movements of the hands, forearms, and arms are impaired, then the movements of the head are interfered with. Phrenic paralysis will pro- duce the most marked dyspnoea. Then bulbar symptoms gradually make their appearance. Speech becomes difficult on account of paralysis of the hypoglossus. Paralysis of the palate and oesophagus makes the speech nasal, and produces diffi- culty in deglutition. The pulse becomes very much accelerated, and attacks of suffocation occur which terminate fatally. As a rule, the cerebral nerves remain unaffected. The paralyzed muscles retain their electrical irritability to the last, and do not undergo atrophy. Cutaneous sensibility is very little, if at all, affected. Anaesthesia and hyperaesthesia have been observed in a few cases. Delayed conduc- tion of the sensations of pain and temperature has also been reported. Diminution of muscular sense has also been noticed. Decubitus and other trophic disturbances do not occur. The cutaneous and tendon reflexes are unchanged at first, but gradu- ally they are diminished and finally abolished. The bladder and rectum are not paralyzed, although temporary re- tention of urine sometimes occurs at the outset. The general condition may be unchanged. Febrile movement may 150 FUNCTIONAL DISEASES OF THE SPINAL COED. or may not be present. Enlargement of the spleen and albuminuria have been observed in some cases. The disease runs an acute, progressive course. Death occurs gener- ally in the middle of the second week of the disease, sometimes in two or three days, at others in two or three weeks. In rare cases recovery ensues even after bulbar symptoms have devel- oped. Several months often elapse before the status quo ante is restored. Remissions and exacerbations, with a finally fatal termination, have also been observed. III. Anatomical Changes.—The nervous system presents no anatomical changes in cases of this disease. But enlargement of the spleen and swelling of the intestinal lymph follicles and mesenteric glands have been observed in a number of cases, and tins lends a certain degree of plausibility to Westphal’s suggestion that the disease is the result of some unknown infection. IV. Diagnosis.—The disease is distinguished from ascending mye- litis by the absence of fever, sensory disturbances, paralysis of the bladder and rectum, decubitus, and changes in electrical excitability. Acute anterior poliomyelitis does not possess a progressive character, and results in rapid muscular atrophy and loss of electrical excitability. In acute multiple neuritis, sensory disturbances predominate, and the elec- trical irritability of the affected nerves and muscles rapidly diminishes. V. Prognosis.—The prognosis is always grave, although recovery is not impossible. The more acute the course, and the more prominent the bulbar symptoms, the earlier will the fatal termination occur. VI. Treatment.—If the disease has been preceded by syphilis, anti- syphilitic remedies must be administered. Other measures recommended are: a. Externally—actual cautery, cups, leeches, ice-bag, derivatives to the spine, cold compresses, b. In- ternally—potassium iodide, ergotine, atropine, etc. The galvanic spinal current may also be employed. 4. Reflex Paralysis. 1. This term is based on the theory that diseases of the peripheral organs may impair the function of the spinal cord to such an extent as to give rise to spinal paralyses, which almost always appear as paraplegia. The disease is most fre- quent as the result of affections of the genito-urinary apparatus and intestinal tract; it has also been observed after injury, inflammations of joints, and cold. Among the diseases of the urinary apparatus, we may mention cystitis, reten- tion of urine, nephritis, and calculi. The morbid changes in the genital tract include gonorrhoea, stricture, phimoses, hypertrophy of the prostate, hydrocele, flexions and ulcerations of the uterus. Reflex paralysis is also said to follow dysentery, more rarely simple diarrhoea, improper administration of cathartics, constipation, colic, worms. Paralyses of a spinal character have been observed after gunshot wounds which did not directly involve the paralyzed limbs. They have also been reported as the result of ulcers of the skin and of a cold. 2. Brown-Sequard believes that the paralysis is the result of spinal anaemia due to reflex spasm of the vessels, but it is hardly conceivable that such a spasm may last for years. Jaccoud believes that the peripheral irritation directly inhibits and thus exhausts the functions of the spinal cord. In recent times, however, the view is gaining ground that the majority of the cases are the result of anatomical lesions. As a rule, we have to deal with inflammations which extend from the primarily diseased organ along the peripheral nerves or blood-vessels to the con- tents of the spinal canal, so that the affection is really the result of ascending or de- scending degenerative neuritis, meningitic changes, or myelitic processes. But the FUNCTIONAL DISEASES OF TIIE SPINAL COED. 151 possibility of reflex paralysis in the strict sense must be granted, particularly when the paralysis disappears almost immediately after its cause is removed, 3. The symptomatology varies according as the disease is the result of neuritis, meningitis, or myelitis. The prognosis depends upon the etiology, and this is also true of treatment. 6. Psychical Spinal Paralysis. {Fright Paralysis.) Paraplegia is sometimes produced by profound emotions. Kohts and Leyden have referred recently to the great influence of fright in the development, not alone of functional, but also of organic diseases of the spinal cord. Their observa- tion is based on the abundant material furnished during the bombardment of Strass- burg. Russel Reynolds and Riegel have called attention to the fact that para- plegia may result from the influence of the imagination, particularly in feeble, exhausted individuals. Sometimes there is complete paralysis, in other cases merely paresis; the bladder and rectum are generally intact. Paraesthesiae and anaesthesia are not infrequent. The treatment is chiefly moral. Iron, quinine, strychnine, electricity, cold frictions, etc., may become necessary. 6. Paralyses after Acute Diseases. {Infection Paralyses.) 1. These cases are observed most frequently after acute infectious diseases, particularly after certain epidemics. As a rule, the paralysis develops during convalescence, but it has also been observed at the outset. The best-known form is that which occurs after diphtheria of the pharynx, other mucous membranes, and skin. It generally occurs in the second or third weeks after recovery, sometimes in the sixth and eighth weeks. It has also been observed after catarrhal angina, and even after herpes pharyngis. Paralyses sometimes occur after typhoid diseases, particularly after typhoid fever; also after dysentery and cholera. Cases have also been reported after the acute exanthemata (variola, scarlatina, measles, erysipelas, herpes zoster), after erythema nodosum, urticaria febrilis, purpura, puerperal fever; also after pneu- monia, whooping-cough, articular rheumatism, pleurisy, malaria. 2. In one series of cases the paralysis is confined to a single nerve, and occa- sionally even to smaller groups of muscles. In other cases an entire limb is para- lyzed, and paraplegic conditions may develop, usually without implication of the bladder and rectum. Or we find the symptoms of acute ataxia, multiple sclerosis, progressive muscular atrophy, spinal atrophic paralysis, acute ascending paralysis, etc. Cerebral hemiplegia with or without aphasia, or the latter affection alone, may develop. It evident that all these conditions cannot be produced by the same anatomical lesions. The lesions which have been observed are: degenerative neuritis, diffuse mye- litis, or disseminated myelitic processes (found after variola by Westphal), multi- ple sclerosis (also observed after variola), meningitic changes extending to the anterior nerve-roots (in diphtheria), cerebral embolism or thrombosis, etc. It is now assumed that the majority of cases of paralysis after acute infectious diseases are the result of anatomical lesions, but in rarer cases functional affec- tions of the spinal cord are observed—for example, acute ascending paralysis which presents no anatomical basis. In some instances of unusually rapid disap- pearance of the paralysis, we must assume conditions of exhaustion of the spinal cord (asthenic paralysis). The intermittent paralysis of malaria must also be re- garded as a functional affection. It is characterized by the development of a usually progressive paralysis, with or without anaesthesia, and paralysis of the bladder, which disappears at the end of a few hours after a sweat. The attacks recur at stated intervals, and are cured by anti-malarial remedies. 7. Toxic Spinal Paralyses. More or less severe paralysis may be produced by poisoning with lead, arsenic, phosphorus, mercury, carbonic oxide, alcohol, tobacco, camphor, 152 FUNCTIONAL DISEASES OF THE SPINAL CORD. copaiba, ergot, absinthe, opium, belladonna, strychnine, etc. The par- alyses may be confined to individual groups of muscles, may extend to larger nerve-tracts or to entire limbs, or may be of a hemiplegic or para- plegic character; they may be associated with anaesthesia or hyperaesthe- sia, or sensation may be unaffected. We will here discuss a few of the most frequent forms of toxic paralysis. a. Lead Paralysis. 1. Lead paralysis is one of the later symptoms of lead poisoning, and is usually preceded by the formation of a blue line on the gums, more or less frequent colic, and lead arthralgia. Tanquerel des Planches reports one case in which the lead paralysis was produced a week after the patient began working in lead. Usually a number of years elapse before the paralysis is produced. Excessive use of alcohol and strain of certain groups of muscles are said to favor the development of lead paralysis. It is unnecessary to enter here into the various ways in which the system may be poisoned with lead. 2. As a rule, the paralytic symptoms develop very gradually, but more rarely they begin suddenly. Sometimes they follow immediately upon an attack of lead colic. In the majority of cases, the paralysis is confined to the upper limbs, often only to those muscles which are supplied by the radial nerve. The muscles of the lower limbs are rarely, those of the back still more rarely, affected. Duchenne also observed lead paralysis of the intercostal mus- cles and diaphragm. The paralysis generally begins in the right arm (in left-handed per- sons, in the left arm), but the corresponding muscles of the other arm soon become affected. The extensor digitorum communis is first affected, and there is difficulty in ex- tension of the first phalanges of the second and third fingers. Then the extensor digit, quint, propr. and extensor indie, propr. become affected; this is followed by paralysis of the extensor carpi rad. et ulnar., next of the extensor pollic. long, et brev.; the abductor pollic long, resists for a long time, and is finally affected with the muscles of the ball of the thumb. The interossei. particularly the first, also become involved. It is characteristic that the supinator longus et brevis remain intact, unless the biceps and brachialis internus becomo involved. Paralysis of the latter group is generally preceded by paralysis of the deltoid. The triceps is affected very late or not at all. In the lower limbs the peronei are first affected, then the extensors of the leg, but the tibialis anticus remains intact. Degeneration reaction develops in the paralyzed muscles. The direct and indirect faradic irritability of the muscles is gradually abolished, but the paralysis is sometimes more extensive than the disturbances of faradic excitability. If the paralyzed muscles have not lost their faradic irritability, their function is often restored after a few electrical sittings. Direct galvanic stimulation of the muscles shows increased excitability, slow contractions, and predominance of AnCIC. The increased galvanic excitability soon disappears, but AnCIC remains predominant. Par- tial degeneration reaction is observed in muscles which are not very markedly affected. If the degeneration reaction is complete, the muscles will not recover, if at all, until the end of three to four months. The muscles often recover voluntary power, although they are still FUNCTIONAL DISEASES OF THE SPINAL CORD. 153 inexcitable to the faradic current. Diplegic contractions have been ob- served in a number of cases (vide page 127). During the continuance of the degeneration reaction, the mechanical excitability of the muscles is increased, and they sometimes present fibrillary contractions. The paralysis is followed by atrophy of the mus- cles, so that the interosseous spaces appear hollowed out. A deep groove is seen on the dorsal surface of the forearm, the shoulder is flattened, etc. Symptoms similar to those of progressive muscular atrophy have been observed in some cases of lead poisoning. The cutaneous and tendon reflexes are abolished in the regions in which the muscles have lost their electrical excitability. Trophic disturbances are sometimes noticed : enlargement of the sheaths of the tendons (tenosynitis hypertrophica), enlargement of the phalanges, etc. The disease runs a chronic course. Eelapses sometimes occur, although the patient was not exposed anew to the influence of lead. 3. The anatomical changes in the muscles consist of narrowing of the fibres, increase of the nuclei of the sarcolemma, gradual disappear- ance of the muscle substance, proliferation of the interstitial tissue, and sometimes of the adipose tissue. Some authors regard the muscular changes as primary, the changes in the nervous system as secondary, i. e., as propagated from the muscles. Others maintain that changes in the peripheral nerves are primary (degenerative atrophy). In one case Westphal noticed changes in the radial nerve which he attributed to regenerative processes (finest nerve fibres surrounded, in bundles, by a common sheath). The clinical symptoms point distinctly to an affection of the spinal cord. They are so like those of subacute and chronic atrophic spinal paralysis that it has been assumed that the lead poisoning first gives rise to a functional disease of the large ganglion cells of the anterior horns of the spinal cord, and this in turn to secondary changes in the periphe- ral nerves and muscles. 4. The diagnosis is usually easy, not alone from the etiology, but also from the characteristic distribution of the paralysis (radial nerve with intact supinators). In peripheral radial paralysis, the supinators are af- fected, as a rule, sensory disturbances are present, and peripheral causes are demonstrable. The differential diagnosis from spinal atrophic para- lysis may be difficult in the absence of a previous history and of other symptoms of lead poisoning. 5. The prognosis is not favorable, as a rule, because the patients generally suffer from relapses unless they give up their occupation. Eelapses may also occur without the intervention of renewed poisoning. In individual cases, the prognosis depends chiefly on the extent of the paralysis and the electrical irritability of the paralyzed muscles. Cases which approach generalized lead paralysis offer a more serious prognosis. In muscles which have lost their faradic excitability, re- covery cannot be expected before the end of three or four months, if at all. 6. Prophylaxis is an important feature in treatment, and chiefly involves the proper construction of factories. After the paralysis has developed, potassium iodide (gr. xij. t. i. d.) may be given internally. Annuschat has recently shown that this facilitates the excretion of lead from the body. In addition, warm baths, particularly sulphur baths (30° E., fifteen to thirty minutes’ duration). We may also apply the 154 FUNCTIONAL DISEASES OF THE SPINAL COED. galvanic spinal current (large electrodes, vigorous current, at first the anode for two to three minutes, then the cathode to the cervical en- largement). Also the galvanic current labile, the anode being placed in the cervical enlargement, the cathode stroked methodically over the individual muscles. The faradic current may be employed if the mus- cles retain their faradic excitability. Galvanization of the sympathetic has also been recommended. b. Arsenic Paralysis. 1. Arsenic paralysis is more often the result of acute than of chronic poison- ing, and may develop in a few days. It is distinguished from lead paralysis by affecting chiefly the lower limbs, by the more rapid atrophy of the paralyzed muscles, and the prominence of sensory disturbances. 2. As a rule, there is paraplegia of the lower limbs, more rarely of all the limbs or the upper limbs alone. The paralysis and atrophy of the muscles are often preceded by violent pains; and numbness, formication, and analgesia are noticed not infrequently. The electrical irritability, the cutaneous and tendon reflexes present the same changes as in lead paralysis. In one case, Seeligmueller observed marked tabetic symptoms. 3. In pieces of the muscle, which had been removed from the patient by har- pooning, Da Costa noticed narrowness of the muscular fibres, increase of the nuclei of the sarcolemma, in other parts waxy degeneration, slight fatty degen- eration, increase of the interstitial connective tissue, and accumulation of fat in it. Nevertheless, Da Costa assumes a spinal origin of the paralysis. In their experimental investigations, Mierzejewski and Popof observed poliomyelitis, but the process often extended into the white matter. 4. The treatment is the same as in lead paralysis. c. Phosphorus Poisoning. Acute and chronic phosphorus poisoning may also give rise to paralyses, in the form of partial paralysis, monoplegia, and paraplegia. Pains, paraesthesiae, and objective sensory disturbances have also been observed in the paralyzed parts. The situation of the lesion is not known with certainty. Degeneration of the peripheral nerves has been observed, and likewise changes in the spinal cord. Danillo and Vulpian have recently made experiments on dogs. In acute poisoning, they found hyperaemia and an accumulation of pigment in the vessels of the anterior horns, and swelling and the development of vacuolae in the ganglion cells themselves; in chronic poisoning, the white matter also took part in the process. d. Carbonic Oxide Cas and Bisulphide of Carbon Paralysis. Paralyses have been described after a number of cases of carbonic oxide poisoning. These paralyses may be peripheral, spinal or cerebral in origin, and are probably the result of hemorrhages with secondary inflammatory and degenera- tive changes. These remarks hold good concerning paralysis after poisoning with bisulphide of carbon, to which workmen in India-rubber factories are especially liable. e. Paralysis after Ergot Poisoning. Ergotism. (Raphania. Morbus Cerealis.) Paralyses after ergot poisoning are almost always spinal in character. In three cases (in one family) under my observation, marked atrophy and contrac- tures of the muscles had developed. Little is known concerning the site of the disease. Tuczek recently described very marked changes in the posterior columns; the knee jerk was absent in these cases during life, and the Brach- Romberg symptom and ataxia had also been observed in some cases. Treatment according to general principles. Pellagra and ergotism are probably identical. FUNCTIONAL DISEASES OF THE SPINAL COED. 155 /. Alcohol Paralysis. Spinal paralytic symptoms may develop in acute, more frequently in chronic, alcoholism. It is well known that some individuals, when intoxicated, keep a clear head, while the feet become ‘‘groggy.” Certain alcoholic drinks have a special power of affecting the legs. Paraplegia, ataxia, and cutaneous hyperaesthesia have been observed in chronic alcoholism. The latter are perhaps associated with meningitic changes. The condition of the tendon reflexes is indicated on page 111. The symptoma- tology may be very similar to that of tabes (pseudo-tabes). The treatment con- sists in gradually weaning the patients from their bad habits. 8. Writer’s Spasm. Mogigraphia. (Graphospasm. Cheirospasm.) I. Etiology.—Writer’s spasm is most frequent from the twentieth to fortieth years; it never occurs in childhood, and is rare in old age. The disease almost always attacks men. The causes are variable. In some patients there is a congenital nervous disposition, inasmuch as epilepsy, hysteria, and other neuroses are observed among the relatives, and perhaps the patient himself was nervous since youth. In other cases acquired nervousness constitutes the predisposition to writer’s spasm, for example, in masturbators and those who indulge in excesses in Baccho et Venere. Strong mental excitement may produce or intensify the disease. Some patients attribute their complaints to cold or injury, for ex- ample, a wound of the finger, running a needle into it, wearing tight gloves, etc. • In rare cases an inflammation of some of the nerves of the brachial plexus has acted as the cause of the disease. Runge describes a case which resulted from periostitis of the arm. The most frequent cause, however, is strain or a bad position of the hand in writing. It is stated not infrequently by the patients that the first symptoms appeared while making the balance sheet at the end of the year. The disease has also been attributed to the use of steel pens, but this cannot be the sole cause since it was observed before their introduction. II. Symptoms.—As a rule, the symptoms develop very gradually. There are sometimes certain prodomata, such as a feeling of pressure in the head, depression, excitement, poor sleep, nervous dyspepsia, etc. The manifest symptoms begin as more or less impediment to the act of writing, but after a time (sometimes not until the lapse of months and years) writing becomes impossible. The first muscles affected are those employed in writing, viz., the interossei and lumbricales, the muscles of the ball of the thumb, and the extensors and flexors of the forearm. The spasm may also extend to the muscles of the arm, shoulder, and even the neck. Sometimes only a few, in other cases many groups of muscles are affected. Benedikt distinguishes spastic, tremulous, and paralytic writer’s spasm. The spastic form is the most frequent, the paralytic variety the rarest. One form is sometimes complicated by another. 156 FUNCTIONAL DISEASES OF THE SPINAL CORD. Spastic writer’s spasm consists of tonic, more rarely clonic muscular spasms, which impair or prevent the sure manipulation of the pen. In some cases there is flexion spasm of the thumb, so that, on attempting to write, the thumb is drawn spasmodically into the palm of the hand. In other cases there is spasmodic flexion or extension of the index finger. If the extensors of the thumb and index finger are affected at the same time, the pen will drop from the hand. The spasm sometimes affects the extensors or the abductor and opponens digiti minimi, and is associated with such distressing pain that it becomes impossible to continue writing. Spasm of the flexors of the wrist joint is not infrequent. If it occurs in the flexor and extensor carpi ulnaris, the hand is drawn forcibly across the paper. Various other combinations of spasm may also be observed. Tremulous writer’s spasm is characterized by trembling movements which occur only during writing. Paralytic writer’s spasm is really writer’s paralysis. It is shown by a feeling of increasing exhaustion and tension which develops during the act of writing, and becomes so severe that the hand is held quiet on the paper. The disturbances of co-ordination in question sometimes occur at each attempt to write, in other cases only after prolonged writing. Mental excitement exercises a marked influence upon the disease. The gross power of the muscles affected bv spasm is in no wise im- paired. Many patients can also perform, without difficulty, other deli- cate manipulations, such as threading a needle, sewing, playing piano, etc. In addition to writer’s spasm, the patient may also suffer from spasm of other groups of muscles; viz., strabismus, stuttering, pharyngeal spasm, spasm in the muscles of the back of the neck, also tremor and paresis of the legs. The affected muscles are sometimes tender on pressure. Complaint is made not infrequently of paraesthesiae: a feeling of cold- ness, burning, formication, etc. Some authors have noticed vaso-motor disturbances (pallor of the fingers and a feeling as if they were dead) at the beginning of the spasm. The patients sometimes complain of neur- algiform pains, most frequently in the distribution of the ulnar nerve, next in that of the median nerve. The nerves of the arm are occasion- ally tender on pressure, and neuritic swellings have sometimes been ob- served upon them. Painful pressure points are sometimes found on certain parts of the bones of the arm or on some of the cervical spinal processes. The electrical irritability of the affected muscles is generally un- changed; it is sometimes slightly diminished, more rarely increased. Gowers describes abolition of electro-muscular and electro-cutaneous sensibility. Eulenburg has observed qualitative changes in the electrical irritability of the nerves supplying the affected muscles (predominance of AnCIO and early appearance of A11OC, and CaOC). The disease continues to grow worse unless the patients are able to give up writing for a long time. The more the disease progesses, the more the written characters are changed. The writing often looks as if written by a beginner, or while riding over a rough road, and finally legible characters can no longer be made. Many patients help themselves at first by using thick penholders or quills, by writing with the arm elevated or with changed position of the FUNCTIONAL DISEASES OF THE SPINAL CORD. 157 wrist-joint and fingers. Others learn to write with the left hand. But, unfortunately, the same symptoms develop not infrequently in the left arm, or writing with the left hand causes very annoying spasmodic con- ditions in the right arm. III. Pathogenesis.—The disease is probably the result of purely functional dis- turbances, These are evidently situated in the spinal cord, because the act of writing requires the delicate co-ordination of adjacent groups of muscles, and tiie co-ordinating centres of these muscles are situated in the cervical enlarge- ment of the cord. Abnormal irritability, ready exhaustion, and irregular stimu- lation of these centres suffice to explain the symptoms of writer’s spasm. In some cases, however, the primary disturbance is situated in the brain, as is shown by the feeling of pressure in the head, vertigo, mental depression, etc. In other cases the starting-point is at the periphery (neuritis, periostitis, etc.). IV. Diagnosis.—The diagnosis is easily made. We must always endeavor to determine the variety of the disease, and for this purpose must carefully study the disturbances during the act of writing. We should also search carefully for pressure points. V. Prognosis.—The prognosis is not very favorable. Recovery is rare unless the patient abstains permanently from writing. VI. Treatment.—Writing must be strictly prohibited for many months. If hereditary factors or an acquired nervous disposition enter into the etiology, we should prescribe potassium bromide, iron, quinine, cold-water cures, a stay in the country, and careful massage of the muscles. Injurious habits must be given up, and peripheral lesions (injury, periostitis, neuritis) treated in the ordinary way. If pressure points are present on the spinal column, the anode of the galvanic cur- rent should be applied to them (cathode to the sternum, daily sitting for five minutes, current not too strong). Treatment with the galvanic current likewise offers the best hopes of success under other circumstances. If cerebral symptoms are prominent, feeble currents should be passed transversely and obliquely through the skull. A spinal current may also be applied to the cervical cord. Peri- pheral galvanization may be applied to the affected muscles and nerves— the labile current in the tremulous and paralytic varieties, the stabile current in the tonic form (according to Eulenburg the anode is prefer- able). Galvanization of the cervical sympathetic has also been recom- mended. M. Meyer obtained good results from faradization of the indi- vidual muscles, but this must be avoided in the spastic variety. Erb applied permanently a simple galvanic element (copper and zinc plates connected by a wire and placed over a nerve trunk of the arm upon a moist piece of linen). The treatment must be continued for a long time in all cases. Good results have been obtained recently from massage of the affected muscles and gymnastics, but it is advisable to have the treatment carried out by a skilled specialist. Numerous other measures have been employed in this disease: a, alcoholic and narcotic inunctions, douches, blisters, cups, derivatives of all kinds, ice-bag, ether irrigation of the spine; b, narcotics and nervines; c, mechanical apparatus (thick, cork penholders, rings to fasten the penholders, bandages to the wrist- joint); d, nerve stretching. Appendix.—Similar disturbances may occur in other fine manipulations which necessitate the co-ordinated action of groups of muscles. The gross power of the muscles is unchanged, but their power of co-ordinated action is lost (co-or- dinating professional neuroses). 158 FUNCTIONAL DISEASES OF THE SPINAL COED. Most closely allied to writer’s spasm is telegrapher’s spasm. Pianist’s spasm occurs particularly in young ladies, and usually in the right hand. Violinist’s spasm may affect either hand. Tailor’s and shoemaker’s spasm is manifested in the muscles of the hand and arm, and renders impossible the use of the scissors, needle, etc. Similar conditions are observed in smiths, masons, sawyers, weavers, watchmakers, printers, etc., and also in the lower limbs, in turners, sewing machine operators, dancers, etc. Spasm of the larynx has been described in players on the clarionet. 9. Tetany. I. Etiology.—Tetany manifests itself by the occurrence of tonic muscular spasms, which come and go in paroxysms, affect certain groups of muscles, and are associated with increased electrical and mechanical excitability of the corresponding motor nerves. The disease occurs most frequently at a youthful age. It is not in- frequent in teething children, later it occurs particularly at the period of puberty (thirteenth to thirtieth years). It is rare in later life. Rachitic, pale, and feeble individuals exhibit a predisposition to the disease. Some authors attribute a certain degree of influence to heredity. Murdoch observed tetany in several brothers and sisters, and Bouchut states that it is particularly frequent in children whose parents are ner- vous and suffer from neuroses. Among the not infrequent direct causes are colds, particularly from sleeping in damp rooms, camping out, etc. The influence of rheumatic causes also appears to be shown by the fact that tetany is often associated with swelling of the joints, and that it is especially frequent in the cool months. It often appears to be the reflex effect of peripheral irritation (teeth- ing, worms, overloading of the stomach and intestines, suppression of the menses, pregnancy, lactation, operation for goitre). Tetany sometimes follows acute infectious diseases or exhausting dis- eases. These conditions probably produce, in many cases, merely a pre- disposition, and other influences are necessary to produce the disease itself. It is sometimes the result of violent excitement. A number of cases have been reported in which tetany occured as an epidemic in schools and similar institutions. II. Symptoms.—The attacks of spasm are almost always preceded by certain prodromata: dragging and tearing pains in the limbs, a feeling of coldness, formication, etc. The prodromata may last for days and weeks. In rare cases cerebral symptoms occur: vertigo, ringing in the ears, a feeling of confusion. The tonic muscular spasms sometimes follow the prodromata sponta- neously, and in certain patients are apt to occur at night, or they appear after bodily strain or mental excitement. In typical cases they are confined to the flexors of the fingers and wrists; they are almost always bilateral, exceptionally unilateral. They often extend to the flexors of the forearm and the adductors of the arm. In exceptional cases the spasm affects the extensors of the fingers and wrist, or both the flexors and extensors. The muscles of the lower limbs are sometimes affected, sometimes only the plantar flexors of the toes, or the calf muscles, occasionally even the extensors and adductors of the thigh. FUNCTIONAL DISEASES OF THE SPINAL COED. 159 The spasm extends more rarely to the muscles of the back, abdomen, and chest, to the muscles of the pelvis and diaphragm. Indeed, the spasm finally may become general, and affect the muscles of the face, larynx, pharynx, tongue, oesophagus, and detrusor of the bladder. In typical cases, the position of the affected fingers and hands is so characteristic that it almost suffices to warrant a diagnosis. Trousseau compares it to the position assumed by the obstetrician when he attempts to introduce the hand into the vagina. The thumb is strongly adducted and bent into the palm of the hand; the other fingers, particularly the fourth and fifth, are strongly flexed in the metacarpophalangeal joint, and extended in the phalangeal joints; the palm of the hand is deeply hollowed, and the entire hand is strongly flexed towards the ulnar side, if the flexors of the forearm are affected, the forearm appears semi-flexed; in spasm of the adductors of the arm, the arms may be so strongly drawn against the thorax that the flexed forearms cross each other over the epigastrium. In spasm of the flexors of the toes, the great toe is drawn under the adjacent toes; spasm of the calf muscles is shown by pes equinus, pes varo-equinus, more rarely by pes valgo-equinus. In the knee-joints, the lower limbs are usually extended, and the thighs are adducted against one another. In tonic spasm of the muscles of the back, the spinal column appears strongly curved anteriorly. Spasm of the thoracic muscles and diaphragm may give rise to threatening symptoms of suffocation. Spasm of the muscles of the neck and throat causes cyanosis of the face and protrusion of the eyeballs as the result of venous stasis. The contours of the muscles often stand out sharply beneath the skin. Fibrillary contractions are sometimes visible during the spasm. The muscles are firm, and more or less tender on pressure. The contractures can usually be overcome after a certain degree of effort, but the limb returns to its former position as soon as it is released. The spasmodic attacks vary in duration from a minute to one or more hours, and even three days. The contractures persist, though less vigorously, during sleep. The number of attacks also varies greatly. Sometimes single attacks occur at intervals of days, weeks, and months, and occasionally the dis- ease terminates with one paroxysm. In other cases, numerous seizures recur in the course of a single day. During the attack, the majority of patients suffer from annoying sensations: a feeling of coldness, prickling, formication, etc. Some complain of a painful feeling of tension in the contracted muscles, others of neuralgiform pains, which may be confined to certain nerve tracts; central symptoms may also be noticed (vertigo, pressure in the head, ringing in the ears, etc.). Great diagnostic significance attaches to three other symptoms, viz., Trousseau’s phenomenon, the increase of the electrical and of the mechanical irritability of the motor nerves. Trousseau’s phenomenon is the ability to produce a seizure of tetany by pressure upon the nerve trunks or arteries of the arm. The attack occurs after the pressure has been exercised one to two minutes, and disappears when the pressure is discontinued. In some cases, pressure on the artery alone produces an attack, while compression of the nerve is useless. This symptom is very rarely absent, and so long as it can be produced, we must be prepared for the recurrence of spontaneous attacks of tetany. A few cages have been reported in which pressure on other parts of the body also produced attacks, for example, compression of the cervical sympathetic and 160 FUNCTIONAL DISEASES OF THE SPINAL COED. carotid, pressure and faradic irritation of painful points on the spine, or pressure on the muscles of the wrist joint and on the radial artery. Czerny observed a i attack follow elevation of the arm. The symptom is produced with more diffi- culty in the lower limbs by pressure on the crural artery or sciatic nerve. The electrical irritability of the motor nerves is increased. A faradic current of very slight strength, when applied to the nerve, suffices to produce muscular contractions. On the application of the galvanic current (to the nerve) CaCIC and AnOC occur very early, CaCITe and AnCITe soon follow, and it is a peculiar fact that AnOTe is produced without difficulty. Chvostek claims to have observed CaOTe in two cases. These remarks hold good concerning the nerves alone, not concerning the muscles supplied by them. The facial nerve, as a rule, remains unaffected. So long as these electrical changes persist, the attacks of tetany may relapse. The mechanical irritability of the motor nerves is increased pari passu with the electrical irritability, so that gentle tapping on the nerve will produce con- tractions in the corresponding muscles. As a rule, the facial nerve is not affected. The appearance of the parts affected with tetany is often unaltered, in some cases swelling of the joints with redness and oedema has been observed. The cutaneous sensibility is generally changed, but sometimes very slightly. Manouvriez observed partial anaesthesia even in the intervals between the attacks. Ilasse states that the more marked the anaesthesia the more severe the attacks of spasm will be. He also observed abolition of the muscu- lar sense, so that the patients could only hold objects by the aid of the sense of sight. Painful pressure points on the spine are reported in a number of cases. The general condition is often unaffected. Some patients complain of dyspepsia and drowsiness, or, on the other hand, of excitement. The height of the attack is sometimes accompanied by profuse perspiration or fever, or both. As a rule, the disease terminates in recovery, though slight contrac- tures and pareses may persist for a long time. Kussmaul observed retinitis as a sequel. In children, the height of the disease may be attended with fatal eclampsia. Death may also result from increasing exhaustion and persistent diarrhoea. III. Anatomical Changes and Pathogenesis.—Nothing is known concern- ing the anatomical changes in tetany. Hemorrhages into the spinal meninges, increase and sanguinolent color of the spinal fluid, softening and sclerosis of the cord, minute hemorrhages into the cord, and thickening of the vessels, have been observed in a number of cases; but these are either accidental complications, or the secondary effects of the tetany. It is now generally conceded that the disease is neuropathic in its origin, but it is questionable whether the starting-point is in the nerves, spinal cord, brain, or sympathetic. The cerebral theory is opposed by the fact that, in the majority of cases, cerebral symptoms are absent, and the cerebral nerves are usually un- affected. The increased electrical and mechanical excitability of the motor nerves seems to point to its peripheral origin, but this may also be a secondary effect of spinal changes. If we take into consideration that the disease is often produced in a reflex manner (necessarily through the medium of the spinal cord), and that pressure points are found on the spine, it seems plausible to assume a spinal origin of the disease, and to explain it by increased irritability of the ganglion cells of the anterior horns, upon which depend the secondary changes in the peripheral nerves. N. Weiss thinks that the sympathetic is the starting-point of the disease, and that its irritation gives rise to the circulatory changes in the oord. IV. Diagnosis.—The diagnosis is easy if we bear in mind the cardi- FUNCTIONAL DISEASES OF THE SPINAL CORD. 161 nal symptoms: intermittent tonic spasms in certain groups of muscles, Trousseau’s phenomenon, and increased electrical and mechanical ex- citability of the nerves. The disease is distinguished from tetanus by the fact that the latter first mani- fests itself by trismus. In hysterical spasms and the co-ordinating professional neuroses, the mechanical and electrical irritability of the nerves is not increased. Some cases of spasmodic ergotism possess very great similarity to tetany, but are distinguished from the latter by the etiology. Y. Prognosis.—The disease almost always terminates in recovery, although months may elapse before it disappears entirely. The patient cannot be regarded as completely cured until Trousseau’s phenomenon and the increased excitability of the motor nerves have disappeared. Trousseau recognized three degrees of severity of the disease: in the mildest, it is confined to the muscles of the limbs and general symptoms are absent; in the second grade, the muscles of the trunk are affected, the attacks are more frequent and violent; in the third, there are dis- turbances of the general condition. YI. Treatment.—Our attention must first be directed to the re- moval of the cause. In rheumatic cases, we order potassium iodide, sali- cylic acid, and sweat baths; in suppressio mensium, warm foot baths and leeches to the cervix uteri, etc. Narcotics and nervines have been recommended against the disease itself, but no single remedy is especially efficacious. We may mention: potassium bromide, chloral hydrate, opium, belladonna, curare, chloroform, ether, valerian, arsenic, etc. The remedies may be admin- istered in various ways. Cups, blisters, ice-bags to the spine, lukewarm baths, cold-water cures, etc., have also been recommended. Good results have been obtained from the use of electricity, but no single method of application seems to be especially useful. If there are painful spinal points, the anode of a constant galvanic current (not too strong) may be applied to them, the cathode to the sternum; each sitting two to four minutes, every other day. The anode may also be applied to the cervical or the lumbar enlargement. Or the peripheral nerves are galvanized labile with the anode, which is slowly stroked towards the nerve plexus. Anodal applications may also prove effective during the spasmodic seizures. If the fara- dic current is employed at all, it should be applied as a feeble current to the spine and nerve trunks. 10. Saltatory Spasms. Seven cases 6f this disease have been reported. It occurred particularly in nervous and hysterical individuals with a neuropathic hereditary taint. Upon bringing the foot to the ground, and in standing and walking, clonic mus- cular contractions occur of such a vigorous character that the entire body under- goes a hopping, dancing movement. The spasms were confined to the lower limbs, or they also involved the upper limbs and the muscles of the trunk and back of the neck. They were accompanied by drawing pains, and in two cases occurred in paroxysms and were accompanied by a sort of aura. No paralysis, anaesthesia, or other severe spinal symptoms. Some patients complained of spinal tenderness, and Guttmann could produce attacks by pressure on the spine. There is evidently increased reflex excitability of the ganglion cells of the anterior horns in this affection. Frey attributes it to a definitely localized myelitis; Erb is inclined to regard some of the cases as spastic spinal paralysis. Spontaneous 162 DISEASES OF THE SPINAL MENINGES. improvement occurred in some cases, while others were incurable. Warm baths, ice and wet cups to the spine, narcotics, nervines, and electricity have been em- ployed in treatment. 11. Primary Spinal Muscular Spasms. {Thomsen’s Disease.) I. ETIOLOGY.—In this disease, tonic spasm of the muscles occurs during volun- tary movements, and either delay or entirely abolish the execution of the intended movement. The disease is also known as myotonia congenita, tonic spasms in voluntarily moved muscles, and hypertrophic spastic spinal paralysis. Heredity plays a very important part in the etiology. In Thomsen’s family the disease occurred in five generations. Schoenfeld observed the development of the disease as the result of fright. Other causes are unknown. II. Symptoms.—The symptoms are confined chiefly to the voluntary muscles, but Seeligmueller observed in one case formication and a feeling of coldness in the limbs, in another case absence of the tendon reflexes. The bladder and rec- tum were always unaffected. The muscles of the lower limbs were most affected, next those of the upper limbs. In some cases the muscles of the tongue, face and eyes, and of mastica- tion were also involved. In this disease, voluntary movements cannot be carried out immediately be- cause tonic spasm develops in the muscles which arc to be moved. If the patients wish to rise and walk, they feel a disagreeable feeling of tension; some time elapses before the resistance is overcome. The spasms may be so violent that the patients fall and roll involuntarily about the floor. If they have grasped an ob- ject with the fingers, they are unable to let it drop at once. Affection of the tongue is shown by hesitating speech and awkwardness in mastication. Resistance is also experienced during passive movements. The muscles are often unusually large, generally feel very firm, and, on mechanical and faradic irritation, form thick ridges which persist for a long time. The faradic and galvanic excitability is unchanged. Fibrillary contractions are sometimes observed in the muscles. Continued movement and warmth diminish the spasms, mental excitement and cold intensify them. The first symptoms are often noticeable in the cradle. During childhood the patients attract attention by their awkward manner; in rare cases the symptoms do not begin until the twentieth year or later. The disease continues for life, but remissions and exacerbations have been described. III. Anatomical Changes.—In one case, examination of a piece of excised muscle showed nothing beyond somewhat unusual width of the fibrillse. The disease is generally regarded as spinal in its origin, but nothing further is known of its nature. IV. Diagnosis.—The diagnosis is easy. It is distinguished from muscular hypertrophy by the absence of changes of electrical excitability and the presence of spasms. V. Treatment is of no avail. Some relief is said to have been obtained by gymnastic exercises. Trial should be made of baths and electricity. C. DISEASES OF THE SPINAL MENINGES. 1. Inflammation of the External Surface of the Dura Mater. External Spinal Pachymeningitis. (Peripachymeningitis. Perimeningitis Spinalis.) I. Anatomical Changes.—The inflammatory process in question is situated on the outer surface of the dura mater in the loose, fatty connective tissue which separates the dura mater from the inner surface of the spinal canal. In the majority of cases the inflammation is circumscribed, hardly occupying more DISEASAS OF THE SPINAL MENINGES. 163 than the height of one to three vertebrae; more extensive inflammations are rare. In some cases there are several separate foci of inflammation. The inflammation is most marked on the posterior surface, chiefly because the connective tissue is most abundant in that locality, perhaps in part on account of the influence of the force of gravity. It rarely extends beyond the cervical region, because the extradural cellular tissue gradually diminishes in the upper part of the cord. In a series of cases the inflammatory products constitute a thickening and cellular inflammation on the outer surface of the dura mater and in the peridural cellular tissue. This may be associated with more or less swelling and redness at Fig. 82. External spinal pachymeningitis at the level of the fifth to seventh dorsal vertebrae. Natural size. Spinal cord seen from behind. Dura mater (DM) drawn to one side, on its outer surface a cheesy mass on the left side. Symptoms of compression of the cord (K) during life. Starting- point of the lesion in a right-sided cheesy pleurisy, which extended through the intervertebral foramina to the spinal canal. the site of disease. In other cases the outer surface of the dura mater is covered with a thick, callus-like membrane, which is almost fibrinous in appearance. Well-marked abscesses are found in some cases. Dry, cheesy, tuberculous masses of considerable size may also be produced (vide Fig. 82). In chronic cases fibrous thickenings and adhesions to the outer surface of the dura mater are found. The inflammation extends not infrequently to the inner surface of the dura 164 DISEASES OF THE SPINAL MENINGES. mater, giving rise to swelling, redness, infiltration, abscess, or cheesy tubercu- lous processes. Even the arachnoid and pia mater may take part in the inflam- mation. In a series of cases the process results in simple compression of the cord and nerve roots, in others it gives rise to compression myelitis (vide page 145). II. Etiology.—External spinal pachymeningitis is almost always a secondary condition, indeed it is questionable whether it is ever primary. The primary morbid process is generally situated near the spine, whence the inflammation extends through the intervertebral foramina to the peridural space. It has been observed utter tuberculosis or inflammation of the vertebrae, pleuritis, peri- pleuritis, syphilitic ulcers of the pharynx, suppuration of the cellular tissue of the neck, psoas abscess, and deep spreading decubitus It may also be produced by other conditions, particularly suppurations in the thorax, peritoneum and pelvis, and in migrating neuritis. Syphilis must also be mentioned as a cause. III. Symptoms.—The symptoms are very similar to those of spinal meningitis. Most patients complain of stiffness in the back, which is especially noticeable while sitting or standing, or on rotating the spine. The spine is tender on pressure over parts corresponding to the inflammation. A blow on the head or shoulders, the passage of a sponge dipped in hot water, or the slow labile application of the cathode of a galvanic current causes pain ex- clusively or chiefly in these localities. Visible or palpable changes in the spine (swelling, redness, fluctuating tumors, etc.) are noticeable if the affection is secondary to disease of the spinal column. The patients often complain of a cincture feeling around the trunk, corre- sponding to the approximate site of disease. Violent pains—usually in paroxysms—are experienced, either along the spine or radiating into the extremities. Hypersesthesia, hyperalgesia, and paraesthesiae are often observed. In addition, there may be tonic or clonic twitchings and con- tractures in the muscles of the extremities. Paralysis and anaesthesia may be looked for, if pressure on the nerve roots has interfered with conduction. The reflex irritability is then destroyed, and the paralyzed muscles undergo atrophy. The electrical irritability of the paralyzed muscles is the same as in peripheral paralysis (vide page 7). If the cord is compressed, motor and sensory paraplegia will develop below the site of compression, with parassthesia, increased reflex excitability, vesical disturbances (at first retention, later incontinence), perhaps incontinence of faeces and decubitus (vide page 146). The disease generally runs a subacute or chronic course. Fever is occasionally noticeable, often as the result of the primary dis- ease itself. IV. Diagnosis.—The diagnosis is not easy. The chief points to be considered are the etiology and the irritative symptoms mentioned above. It is distinguished from spinal meningitis by the absence of rigidity of the neck, since the cervical region is almost always unaffected. V. Prognosis.—The prognosis is always grave. The majority of cases termi- nate fatally, but Leyden has shown that recovery is possible. VI. Treatment.—Treatment must first be directed towards the removal of the causes. In other respects it is the same as that of spinal meningitis (vide page 170). 2. Inflammation of the Inner Surface of the Spinal Dura Mater. Internal Spinal Pachymeningitis. Internal spinal pachymeningitis generally runs a chronic course, and occurs as the hypertrophic or hemorrhagic varieties. a. Hypertrophic internal spinal pachymeningitis consists of inflammatory proliferations and fibrous thickenings on the inner surface of the dura mater. In the majority of cases similar changes have developed upon the arachnoid and pia mater, so that the spinal cord is constricted by a ring of connective tissue which sometimes attains a thickness of one cm., often presents concentric lamellae, and contains numerous interstitial spaces (vide Fig. 83). The proliferation is generally most marked posteriorly, where there are usually extradural adhesions to the pos- terior ligament. The changes are generally circumscribed, the lower half of the cervical enlargement being most frequently affected (pachymeningitis cervicalis hypertrophica). . The dangers of the disease consist in the constriction of the nerve roots and DISEASES OF THE SPINAL MENINGES. 165 spinal cord. The symptoms of compression of the cord are gradually followed by those of compression-myelitis. The gray matter will be affected with special severity, and it is perforated by new-formed canals (vide Fig. 83). The latter are found chiefly in the gray commissure, are lined with a membrane, and contain serous fluid. Fig. 83. Transverse section through the middle of the cervical enlargement in hypertrophic, internal spinal pachymeningitis. After Charcot. A, thickened dura ; C, new-formed cavities in the gray matter ; B, nerve roots. The disease is rare. It has been attributed to colds, and living in damp places. Symptoms will not be produced unless the nerve roots are compressed and later paralyzed, or the cord itself undergoes compression. Charcot distinguishes a stage of irritation (lasting two to three months), and a stage of paralysis and atrophy. Fig. 84. Most frequent position of the hand in hypertrophic cervical pachymeningitis. After Charcot. In the stage of irritation, the patients complain of pains in the upper part of the spine, the occiput, between the shoulderi, and in the arms (particularly in the large joints). Pressure on the spine does not give rise to pain. The majority of the patients complain of stiffness in the back of the neck, and a feeling of con- striction in the upper part of the chest. The pains appear in paroxysms or in- 166 DISEASES OF THE SPINAL MENINGES. crease periodically in intensity. Hyperaesthesia, and occasionally paraesthesiae, are noticeable in the upper limbs. Vesicular eruptions, marked desquamation and roughness of the epidermis may also make their appearance. The muscles not infrequently present tonic or clonic contractions, rigidity, and contractures. These symptoms are evidently the result of irritation of the nerve roots which pass through the hyperplastic portions of the dura mater. The second stage is characterized by paralysis of muscles in the upper limbs, fibrillary contractions and atrophy of the paralyzed muscles, changes in electrical irritability (such as occur in peripheral paralysis), and anaesthesia. As a rule, the ulnar and median nerves are paralyzed, the intact extensors of the forearm acquire the predominance and produce permanent dorsal flexion of the hand, while the fingers are flexed at the second and third joints (vide Fig. 84). If the morbid process is situated very high, the radial nerve will be paralyzed, and the hand will permanently assume a flexed position (vide Fig. 85). All these symp- toms are the result of compression and complete interruption to conduction in the spinal roots. If the spinal cord itself becomes compressed, paretic and paralytic symptoms will develop in the lower limbs. The muscles undergo atrophy merely as the re- sult of disuse, and their electrical irritability is unchanged. We will find in- creased reflex excitability, diminished sensibility, disturbances of the bladder, decubitus, etc. Fig. 85. Position of the hand in radial paralysis, as the result of hypertrophic cervical pachymeningitis. After Ross. The disease often lasts for many years, but recovery is possible. The compli- cation with pulmonary phthisis is relatively frequent. The diagnosis is not very difficult. The second stage may be mistaken for progressive muscular atrophy, but the latter is not preceded by an irritative stage, begins generally in the interossei, the thenar and hypothenar eminences, and sometimes extends to the nerve-nuclei in the medulla, and gives rise to bulbar paralysis; hypertrophic pachymeningitis hardly ever extends to the medulla oblongata, and although it causes paralysis of the lower limbs, the muscles do not undergo rapid atrophy or changes in electrical excitability. In amyotrophic lateral sclerosis there is no stage of irritation, sensory disturb- ances are absent, the disease runs a more rapid course, affects the upper and lower limbs in a uniform manner, and almost always proves fatal by extension to the medulla oblongata. The differential diagnosis must also be made from tuberculosis of the spine, tumors of the spine and meninges, and external spinal pachymeningitis; the chief points to be considered are pain and deformity in the spine, tuberculosis of the lymphatic glands and lungs, and tumors in other organs. The treatment is similar to that of spinal meningitis. b. Hemorrhagic internal pachymeningitis corresponds exactly to haematoma of the cerebral dura mater. The inner surface of the dura mater is covered with more or less extensive, extremely vascular membranes. These may often be separated into several layers, between which is situated partly fluid, partly clotted blood. Under the microscope we find haematoidin crystals and red blood- DISEASES OF THE SPINAL MENINGES. 167 globules in various stages of destruction. The extravasations may be so large as to compress the nerve-roots and spinal cord. The pia mater sometimes takes part in the hemorrhage, and the spinal fluid is tinged with blood. In some cases the change extends along the entire length of the cord, in others it is confined to small, scattered foci. Similar changes are generally found on the cerebral dura mater, because both conditions are the results of the same causes. They are observed in the insane and in drunkards; Leyden reports one case after injury. In many cases the disease remains latent, in others it produces the symptoms of irritation or paralysis of the nerve-roots or spinal cord. These symptoms may be attributed to hemorrhagic pachymeningitis if the etiological factors are present. Sudden signs of meningeal hemorrhage may develop if vessels in the new mem- branes rupture and produce an extensive hemorrhage. The treatment is similar to that of spinal meningitis. 3. Acute Spinal Meningitis. I. Etiology.—Inflammations of the arachnoid (arachnitis) and pia mater (piitis) are almost always associated with one another, and are known as spinal meningitis or leptomeningitis. They are sometimes confined to the cord or to parts of it, sometimes they extend to the cere- bral meninges or vice versa (cerebro-spinal meningitis). We will here discuss spinal meningitis alone. Colds (sleeping on the damp ground, working in water, etc.) and injuries are mentioned not infrequently as causes. Spinal meningitis is sometimes the result of simple concussion or lifting heavy weights, in other cases it is produced by fracture or dislocation of the vertebrae, stab or gunshot wounds, etc. Secondary inflammations are more frequent. In case a pulmonary cavity perforated the spinal canal and set up spinal meningi- tis. It may also be the result of any of the etiological factors which give rise to external spinal pachymeningitis (vide page 164). Spinal meningitis occurs occasionally in connection with infectious diseases: pneumonia, typhoid fever, cholera, dysentery, etc. Hasse ob- served several cases after articular and muscular rheumatism. It is more frequent in the male sex, particularly in childhood and middle age. II. Anatomical Changes.—These are divided into the stage of hyperaemia and beginning exudation, that of the completed exudation, and that of resolution. In exceptional cases death occurs in the first stage. The pia mater and arachnoid tissue are unusually red, swollen, and succulent. The redness is diffuse and uniform, or depends upon unusually distended, finer blood-vessels. Here and there are more or less numerous and ex- tensive extravasations. The larger vessels are sinuous and distended to the point of bursting. The surface of the pia mater and arachnoid tissues looks loosened and velvety. The spinal fluid is cloudy and con- tains flocculi. The second stage begins with the deposit of purulent or fibro-purulent flakes. These continue to increase, and finally cover the surface of the pia mater, the arachnoid tissue, and even the inner surface of the dura mater with purulent or fibrinous deposits, which are often dotted with blood. These changes are circumscribed or diffuse, according to the etiological factors. They are most marked on the posterior surface (in- fluence of the force of gravity), and diminish towards the medulla, ob- 168 DISEASES OF THE SPINAL MENINGES. longata. Even if cerebral meningitis is also present, the medulla often escapes entirely, or almost entirely. In the third stage, the purulent masses are gradually absorbed, but thickenings and abnormal adhesions of the meninges usually remain as permanent residua. As a rule, the inflammation is not confined to the pia mater and arach- noid tissue, but attacks important adjacent structures. Unimportant features are the inflammatory processes which are often seen on the inner and outer surface of the dura mater, and the hemorrhages in the peridural cellular tissue. Much more important are the changes in the nerve roots and spinal cord. The microscope shows hyperaemia of the nerve roots, infiltration of the interstitial tissue with round cells, and degeneration of the nerve fibres. It is not astonishing that the spinal cord should take part in the in- flammation, since the pia mater sends innumerable prolongations into the interior of the cord. In many cases, the cord, on transverse section, appears diffluent, cedematous, and injected in places, in other parts ex- tremely pale. In not a few cases, changes are only observed upon microscopic examination of sections of the hardened cord. They are sometimes very slight, and are partly parenchymatous, partly interstitial in character. In places, the axis cylinders are found swollen and un- usually large; in addition, the medullary sheaths may be degenerated, the neuroglia increased in places, and its nuclei proliferated. The pro- longations of the pia mater into the cord present distention of the vessels, emigration of white blood-globules, and increase of the cellular elements. In the gray matter the secondary changes are less marked than in the white matter, but the ganglion cells are not infrequently swollen. Atrophy and degeneration of the cord, particularly in the posterior columns, have also been observed. III. Symptoms.—The manifest symptoms are not infrequently pre- ceded by prodromata, such as anorexia, chilly sensations, general mal- aise, etc. The scene is sometimes opened by a single severe chill, followed by fever, of no particular type, which may attain a considerable height (40° C.). The symptoms attributable to the meningitis itself are relatively slight. As the pia mater is very rich in nerves, we may attribute to in- flammation of this membrane the pains and stiffness in the spinal column, which increase on movement. But, as a rule, these pains are not increased by pressure on the spine, the passage of the cathode of a gal- vanic current, etc. All other symptoms are the results of irritation or paralysis of the spinal nerves, or implication of the spinal cord itself. Almost all patients complain of radiating pains in the limbs, chest, or trunk, as the result of irritation of the posterior nerve roots. The same cause gives rise to the cincture feeling around the thorax or abdomen. There is hyperaesthesia and hyperalgesia of the skin, so that very severe pains are produced on gently touching or pricking the integument. Muscular sensibility is also increased very greatly; the patients cry out aloud when the muscles are carefully pressed between the fingers. Muscular twitchings are frequent. They are sometimes reflex, as the result of previous pain, sometimes the result of pressure on the mus- cles, or volitional movement, or they may be apparently spontaneous. diseases OF THE SPINAL MENINGES. 169 Stiffness of the muscles or contractures are observed not infrequently, the latter involving chiefly the extensors. If the process extends to the cervical cord, the muscles of the back of the neck undergo tonic contracture (rigidity of the neck). The head is drawn more or less backwards, and the occiput is bored deep into the pillow. Active and passive movements of the head anteriorly, and some- times rotatory movements, are impeded or entirely prevented. The entire body can often be lifted by the occiput like a rigid piece of wood. Contracture of the muscles of the back is shown by the unusual an- terior convexity of the spine, so that the trunk touches the bed only at the occiput and sacrum. Contracture of the chest muscles interferes with inspiration; con- tracture of the abdominal muscles produces retraction of the abdomen. Retention of urine and faeces is a common symptom, and is attributed to spasm of the vesical and rectal sphincters. The urine is generally scanty, dark in color, and contains a sediment. Not infrequently there are changes in the pupils (contraction or in- equality) as the result of disturbed innervation of the cilio-spinal centre. Other symptoms, such as acceleration of the pulse and respiration, etc., depend upon the fever, rather than upon the meningitis. The symptoms described must be regarded as irritative phenomena, and form the first stage of the disease. Recovery may occur, or the dis- ease may progress to the second or paralytic stage. The transition is not sharply defined, and irritative and paralytic symptoms are often present, at the same time. Paralytic symptoms must be looked for when the nerve roots are changed to such an extent as to render conduction im- possible. Anaesthesia and analgesia take the place of hyperaesthesia and hyperalgesia. The muscles become paretic, then paralyzed, and show the signs of degeneration reaction. They undergo degenerative atrophy after the disease has lasted for some time. Reflex irritability is abol- ished. The function of the bladder is disturbed—at first retention, later incontinence. The urine is often unusually watery, pale, and abundant; it sometimes contains sugar. These symptoms may also disappear. Indeed, recovery may occur in a comparatively short time, if the paralysis is the result of pressure, rather than of parenchymatous changes in the nerves. In many cases, per- manent paralysis and atrophy of certain muscles are left over, or the signs of a chronic spinal affection make their appearance. Great dangers may arise if the inflammatory process extends upwards and attacks the medulla oblongata. This is shown by difficulty in speech and deglutition, frequent vomiting, irregular respirations, which some- times assume the Cheyne-Stokes type; the pulse, at first slow, becomes so rapid that it can no longer be counted, and the temperature often becomes hyperpyrexial. Death may result from suffocation, paralysis of the heart, or excessive rise of temperature. The disease sometimes lasts only a few days, occasionally weeks and months; sequelae may persist for life. IV. Diagnosis.—The diagnosis is usually easy. It is distinguished from rheumatism of the muscles of the back by the facts that, in the lat- ter affection, severe and febrile constitutional symptoms are gener- ally absent, that the muscles are tender on pressure, and that there are no muscular twitchings, sensory disturbances in remote parts or ves- ical symptoms. Meningitis with extensive, long-continued muscular twitchings may simulate tetanus, but the latter presents no sensory 170 DISEASES OF TIIE SPINAL MENINGES. changes and bladder symptoms, the muscles of mastication generally take part in the tonic contractions, and the contractions are increased by peripheral irritations. Finally, acute meningitis may be mistaken for acute myelitis. In myelitis the irritative symptoms are less promi- nent, while paralysis generally develops early. In myelitis the pains in the back are less and hypersesthesia is generally absent, while anaesthe- sia develops very early; vesical paralysis and ammoniacal decomposition of the urine are soon produced; fever is slight or absent; trophic cuta- neous changes are more frequent than in meningitis. V. Prognosis.—The prognosis is always grave. The more promi- nent the paralytic symptoms the more dangerous is the situation. If symptoms of implication of the medulla oblongata or brain make their appearance, recovery is exceptional. It must also be remembered that permanent paralyses and atrophies are left over not infrequently, or that the signs of a chronic spinal affection finally develop. YI. Treatment.—This is similar to that of acute myelitis (vide page 88). 4. Chronic Spinal Meningitis. I. Etiology.—Chronic spinal meningitis or leptomeningitis either develops as such from the start, or it forms the terminal stage of an acute attack. The latter is apt to occur if there are repeated exacerbations of the inflammation in rapid succession, or if injurious influences exercise their effect during the stage of convalescence. The etiology is, in part, the same as that of acute meningitis, but certain etiological peculiarities must be taken into consideration. Thus, there can be no doubt that certain cases are produced by alcoholic ex- cesses. Chronic meningitis also occurs in syphilis and leprosy. Ac- cording to Koehler, chronic diseases of the lungs, heart, or liver predis- pose to the disease by producing circulatory stasis. Finally, it often, indeed almost constantly, accompanies many chronic diseases of the cord; for example, tabes dorsalis, multiple sclerosis, etc. Most authors regard the meningitis, under such circumstances, as a sequel and complication of the chronic spinal affection, while others consider the meningitis pri- mary, the spinal disease secondary. fl. Anatomical Changes.—The lesions rarely extend over the entire length of the cord, but are generally confined to more or less ex- tensive, often multiple foci. The lower portions are most frequently, the upper cervical region rarely, affected. The changes are usually more marked on the posterior surface. Chronic meningitis is characterized by thickening and fibrous opaci- ties of the pia mater and arachnoid. The new-formed connective tissue may attain a thickness of several millimetres, and feel as hard as carti- lage. Calcification and ossification also occur, particularly in the arach- noid tissue. In many cases the inflamed parts are unusually filled with blood, particularly in the veins and capillaries. There may also be an abnormal production of pigment, resulting in brownisli-red or black patches (secon- dary to previous hemorrhages). It must be remembered that pigmenta- tion of the meninges, particularly in the cervical region, occurs in healthy individuals in old age. There are numerous, sometimes very extensive adhesions to the dura mater. The spinal fluid is often excessive in amount, and is not infre- DISEASES OF THE SPINAL MENINGES. 171 quently cloudy and mixed with flocculi. In rare cases it assumes a more purulent character. On making a transverse section of the cord, it is sometimes seen that the prolongations of the pia mater into the substance of the spinal cord are unusually broad. The pia mater becomes so adherent to the cord that it cannot be detached from the latter without producing losses of substance. The dura mater presents thickening, calcification, and adhesions, and its inner surface is often nodular and granular. The microscope reveals connective-tissue proliferations which contain chalky concretions. The nerve roots are often flat and atrophic, the result of compression by the connective-tissue new-formations. Internally they present in- flammatory processes, and the microscope not infrequently shows degen- erative changes in the nerve fibres. The spinal cord may contain macroscopic or microscopic foci of dis- ease—annular sclerosis, ascending and descending secondary degenera- tion, destruction of nerve fibres, interstitial proliferation of connective tissue in spots, etc. III. Symptoms.—The symptoms are similar in many respects to those of acute meningitis, but they are less violent, more often present remis- sions and exacerbations, and are unattended with fever, unless accompa- nied by some febrile complication. We will merely point out that the symptoms are irritative or paralytic, or a combination of the two. There are frequent complaints of pain and stiffness in the spine, and of rigidity of the back of the neck, if the disease is situated sufficiently high. The pains increase on motion, but not on pressure upon the spine. Complaint is often made of a cincture feeling and radiating pains in the limbs. Hyperaesthesia and paraesthesiae are often noticed in the beginning, and are followed at a later period by anaesthesia, which is usually incomplete. G. Fischer observed polyaesthesia in a number of Gases. Tonic or clonic muscular twitchings or contractures occur very commonly, and micturition and defecation are often delayed. If the compression of the nerve roots increases or their nerve fibres degenerate, paralytic symptoms will become prominent. They appear more fre- quently as paresis than paralysis, and often increase in dorsal decubitus, in other cases during the erect position. They are followed by degener- ative atrophy of the paralyzed muscles, degeneration reaction, and aboli- tion of reflex irritability. Paralysis of the bladder and rectum, and decubitus will ensue if the lower spinal nerves or the cord itself are impli- cated. The disease sometimes lasts for years. It may terminate in recovery, or permanent paralyses and atrophy remain, or acute fatal exacerbations develop, or the process extends to the medulla oblongata, or death is the result of decubitus, or of cystitis and ammoniacal decomposition of urine. Chvostek claims that the calcareous plates mentioned above (but whose inflammatory origin is not always certain) may be the source of very obstinate pains. IV. Diagnosis.—The diagnosis is sometimes very difficult, and if it is associated with an affection of the cord itself, it will be almost im- possible to differentiate the symptoms of both diseases. In general, the principles laid down in the differential diagnosis of myelitis hold good here. The onset of the malady may be mistaken for tabes, but the lat- ter presents no paralytic symptoms, pupillary changes are generally no- ticed, the anaesthesia is more marked, the patellar reflex disappears early, 172 DISEASES OF THE SPINAL MENINGES. the radiating pains are more violent, and ataxic symptoms soon appear. Spinal irritation, for which the disease may also be mistaken, affects anaemic, hysterical, nervous individuals, paralytic symptoms are absent, the spine is tender on pressure, and there is a great disproportion be- tween the subjective complaints and objective changes. V. Prognosis.—The prognosis depends on the same factors as that of acute spinal meningitis, and this is also true of treatment. 5. Meningeal Apoplexy. (Hcematorrhachis.) I. Anatomical Changes.—Meningeal hemorrhages occur most fre- quently into the loose peridural cellular tissue which separates the dura, mater from the bony spinal canal. They fill the epidural space (Fig.. Fig. 86. Transverse section through the vertebral column and spinal cord (schematic). ip, internal periosteum of the vertebrae; dm, dura mater ; ad, arachnoid ; hw, posterior nerve root; Id, ligamentum denticulatum ; vw, anterior nerve root; 1 epr, epidural space ; 2 sdr, subdural space; 3 sar, subarachnoid space. 86, 1 epr), and are known as epidural apoplexy, A second site is the subdural space (Fig. 8G, 2 sdr), between the dura and arachnoid (subdu- ral or arachnoidal apoplexy). Finally, hemorrhages may occur in the meshed tissue between the arachnoid and pia mater, the ■subarachnoid space (Fig. 86, 3 sar), and are known as subarachnoid apoplexy. In epidural apoplexy, the hemorrhage rarely extends along the entire cord, but only over a few vertebrse, or occurs in several scattered foci. The hemorrhage is sometimes confined to the posterior surface, or also extends to the sides; it rarely involves the entire circumference of the cord. The blood generally forms dark-red, loose clots, which may be so extensive as to push the dura inwards and compress the cord. The dura itself, or its outer surface, may present bloody suffusions, and ex- travasions are also observed in the nerve roots. The vessels of the dura mater are often congested. Secondary changes are slight or entirely ab- sent. The clinical symptoms indicate that these lesions are capable of re- DISEASES OF THE SPINAL MENINGES. 173 covery. The blood-clots are probably absorbed as in other organs, and deposits of pigment and adhesions are generally left over. In especially unfavorable cases there may be irreparable atrophy of some of the nerve roots and grave changes in the substance of the spinal cord. The changes in subdural apoplexy are the same as in internal hemor- rhagic pachymeningitis (vide page 166). In subarachnoid apoplexy, the amount of blood may be very consider- able. It is sometimes derived from hemorrhages within the skull, and may extend along the entire length of the cord. The spinal cord and nerve roots are not infrequently compressed. II. Etiology.—Meningeal apoplexy is one of the rarer diseases, and is more common in men than in women. In some cases no cause can be discovered. Not infrequently it is attributed to injury (incised and gun- shot wounds, fall, blow or violent concussion of the spine, lifting heavy loads, instrumental extraction of the new-born). In some cases the hemorrhage is associated with diseases of adjacent organs (tuberculosis or cancer of the spine, rupture of aortic aneurism into the spinal canal, acute inflammations of the cord and its menin- ges). It is sometimes the result of excessive active or passive congestion of the meninges. This occurs in suppressio mensium, or suppressed hem- orrhoidal hemorrhages, in cardiac hypertrophy, violent excitement; in those who have died of tetanus, eclampsia, epilepsy, chorea, hydropho- bia or asphyxia; in toxic spasms; in chronic diseases of the heart, lungs and liver. Meningeal hemorrhages sometimes occur in infectious diseases, as the result of so-called blood dissolution or the hemorrhagic diathesis. Finally, they may be derived from a cerebral hemorrhage which has flown into the spinal canal, or from rupture of the vertebral or spinal artery. It is not known whether the hemorrhage is ever the result of pri- mary affections of the vessels. III. Symptoms.—The symptoms are characterizd by their sudden onset and apyrexial course. Prodromata are rare and result from conges- tion of the cerebral and spinal meninges (slight pains in the back, a feel- ing of heaviness, etc.). Slight febrile movement sometimes occurs on the second or third day as the result of reactive inflammation. Consciousness almost always remains intact, unless the hemorrhage is situated very high, or is very large in amount. The patients suddenly complain of pain in a certain part of the spine. The pains often extend along the entire spine, shoot into the arms, chest, abdomen, or legs, according to the site of the hemorrhage, and give rise to a cincture feeling around the chest or belly. The spine is not tender, but there is a feeling of stiffness, and even rigidity of the back of the neck if the hemorrhage is situated high up. These symptoms result in part from irritation of the meninges, in part from irritation of the nerve roots. Irritative and paralytic symptoms may be closely connected in the further course of the disease. The former include hyperaesthesia of the skin, paraesthesia, tonic and clonic muscular twitchings and contrac- tures; the latter include partial, rarely complete, anaesthesia and motor paralysis. The paralyses are often slight at first, but increase at the end of a few hours. In other cases, the paralysis improves very rapidly. Atrophy of the muscles, degeneration reaction, and abolition of reflex 174 DISEASES OF THE SPINAL MENINGES. excitability may be expected if the nerve roots are compressed for a long time. If the substance of the spinal cord is affected, paralysis of the bladder and rectum, cystitis, and decubitus may develop. As a rule, the disease lasts from two to eight weeks, but in not a few cases the duration is much longer. Death sometimes occurs, with symp- toms of shock, very soon after the beginning of the hemorrhage. In other cases, the hemorrhage is situated so high that death results from disturbances of innervation in the medulla oblongata. The disease is sometimes complicated with meningitis, and the extension of the latter to the medulla oblongata causes the fatal termination. Recovery is often incomplete, and permanent paralysis and atrophy of groups of muscles are left over. IY. Diagnosis.—The diagnosis is generally easy; special import- ance must be attached to the apoplectiform beginning of the symptoms, and their apyrexial course. In acute spinal meningitis, there is febrile movement, the irritative symptoms are more intense, and the symptoms develop more gradually. In acute myelitis and in hemorrhage into the cord, the pains are slight or absent, paralytic symptoms predominate, and there is a rapid development of trophic disturbances, decubitus, paralysis of the bladder, and decomposition of the urine. In concussion of the spine, also, the irritative symptoms are less marked, paralytic symptoms are prominent from the beginning. The localization of the hemorrhage is not difficult. If the lumbar cord is affected, the symptoms refer chiefly to the lower limbs, bladder, and perineal region, and priapism is occasionally observed; hemorrhages into the dorsal region are attended by a cincture feeling around the ab- domen or thorax; cervical hemorrhages are attended by irritative and paralytic symptoms in the upper limbs; hemorrhages in still higher regions are followed by bulbar symptoms. In addition, the localization of the pain in the spine must be taken into consideration. Whether the hemorrhage is epidural, subdural, or subarachnoidal depends par- ticularly on the etiology. Y. Prognosis.—A relatively large number of cases terminate in com- plete, or almost complete, recovery. The situation is so much more serious the nearer the hemorrhage is to the medulla oblongata, the larger it is, and the more the nerve roots and cord are compressed. YI. Treatment.—This is similar to that of hemorrhages into the substance of the spinal cord (vide page 81). 6. Tumors of the Spinal Meninges. I. Anatomical Changes.—These tumors may be epidural, subdural, or sub- arachnoidal, but clinically their symptoms depend merely on irritation of the meninges and of the substance of the cord or paralysis of these parts by exces- sive compression. Tumors which measure more than ten centimetres in length or four to five centimetres in thickness are exceedingly rare. Further growth is only possible by proliferation through the intervertebral foramina and continued growth outside of the spinal canal, or by implication of the bodies of the verte- brae in the neoplastic process. Meningeal tumors start most frequently from the dura mater, and are situ- ated either upon its outer surface or project from its inner surface into the subdural space; they start less frequently from the pia mater or arachnoid tissue. The meninges in the vicinity are often inflamed. The growths are generally round or oval in shape, and often bore a hole into the substance of the cord (vide Figs. 87 and 88). They are almost always single, rarely multiple. In some cases, tumors are found only on the spinal meninges, in others they are also present in the cranial cavity, the spine, adjacent organs, or remote parts of the body. DISEASES OF THE SPINAL MENINGES. 175 Fibroma, lipoma, myxoma, sarcoma, psammoma, melanoma, neuroma, tubercle, gumma, enchondroma, osteoma, and carcinoma are the varieties of meningeal tumors which have been described. Cancer of the meninges is rarely primary, but usually extends from adjacent parts or spreads by metastasis. Closely allied to neoplasms are the animal para- sites, viz., echinococci and cysticercus cellulosae (in one case reported by Westphal). Circumscribed foci of inflammation and hemorrhage of the meninges are co- ordinate with tumors from a clinical standpoint. After the neoplasms have attained a certain size, they compress the nerve roots and spinal cord. At first the nerve roots are swollen, succulent, and reddened; later they become gray and atrophic. Compression of the cord rarely gives rise to simple circular atrophy, but, as a general thing, to compression myelitis which is especially apt to progress below the site of compression, and not infrequently gives rise to secondary degeneration. In rare cases, there is purulent liquefaction of the lower portion of the cord. II. Etiology.—Meningeal tumors occur most frequently in males in middle life. Their causes are generally unknown. They are sometimes attributed to injury and cold. According to some authors, the tumors are apt to develop or increase rapidly during pregnancy and the puerperal condition. Leyden con* Fig. 87. Fig. 88. Anterior view. Tumor growing from the spinal dura mater. After Charcot. Compression of the cord visible after removal of the tumor. siders mental excitement, especially fright, as a possible cause. Tumors are hereditary in some families. III. Symptoms.—As a rule, symptoms do not appear until the nerve roots or spinal cord are affected. They are sometimes preceded for years by peculiar painful sensations in certain parts of the spine, which may increase on making certain movements, and are probably the result of local irritation by the tumor. Some portions of the spine may be tender on pressure. The irritative symptoms increase in severity when the tumor begins to grow. The patients complain of a cincture feeling, and suffer from radiating pains in the limbs, cutaneous hypersesthesia and paraesthesiae; tonic and clonic muscular twitchings and contractures make their appearance. The stage of irritation passes more or less suddenly into that of paralysis, characterized by anaesthesia, and paresis or paralysis of the muscles. If these symptoms depend on compression and subsequent degeneration of the nerve roots, atrophy of the muscles, degeneration reaction, and loss of reflex excita- bility will soon make their appearance. In other cases, the paralytic symptoms indicate implication of the cord. If the tumor starts from the anterior surface of the meninges, muscular paralysis will occur very early; if it starts from the posterior surface, sensory disturbances will be more prominent. 176 DISEASES OF THE MEDULLA OBLONGATA. In some cases, the compression-is confined to one-half of the cord, and the symptoms of a unilateral lesion are produced, i. e., paralysis and hypersesthesia on the side of the compi’ession, anaesthesia on the other side (vide page 138). If the tumor simply interrupts conduction in a transverse section of the cord, paraplegia, anaesthesia, paralysis of the bladder and rectum, increase of the tendon reflexes and of reflex excitability are noticeable. If simple compression is followed by compression myelitis which extends deep into the lumbar cord, reflex irritability becomes lost, the paralyzed muscles atrophy, and lose their electrical excitability. Descending degeneration of the pyramid tracts may be suspected if muscular contracture and twitchings set in and the tendon reflexes are markedly increased. As a matter of course, the clinical nistory may vary from time to time. As a rule, the disease progresses uninterruptedly to an unfavorable termina- tion. Recovery is only possible in the case of inflammatory and syphilitic pro- ducts. The disease may last months or years. Death is sometimes the result of marasmus, or is brought about by the primary tumor in other organs. In some cases, it results from decubitus or cystitis and ammoniacal decomposition of the urine. Acute meningitis sometimes develops and proves fatal. If the tumors are situated very nigh, oulbar symptoms may be produced and terminate in death. IV. Diagnosis.—No single symptom is positive evidence of a meningeal tumor. The same symptoms also occur in other conditions. We infer that they are produced by tumors when the presence of new growths may be demon- strated in other organs or in the vicinity of the spinal column, or when the patient is scrofulous, phthisical, or syphilitic. If these diagnostic aids are wanting, we must suspect a meningeal tumor if there are symptoms of increasing compres- sion of the cord, which start in a circumscribed region. The diagnosis of the level of the tumor is usually easy. Sometimes it is evi- dent from visible changes in the spine; in other cases the patients feel pain in this spot, or the spine is tender over certain parts. In addition, we are aided by the situation of the cincture feeling, and the distribution of the eccentric pains, sensory disturbances, and paralyses. In tumors of the cauda equina, the patients complain of the most violent pains in the sacral region, anaesthesia develops, with paralysis and atrophy of the muscles, abolition of electrical and reflex excitability, and the bladder and rectum are often paralyzed. True spinal symptoms (motor and sensory para- plegia) are absent, and the symptoms occur only in the distribution of certain peripheral nerves. V. Prognosis.—Recovery is possible in those tumors alone which are the result of syphilis. VI. Treatment.—The treatment is similar to that of intramedullary tumors. PART III. DISEASES OF THE MEDULLA OBLONGATA. 1. Progressive Bulbar Paralysis. Glosso-labio-laryngeal Paralysis. I. Etiology.—Progressive bulbar paralysis depends on disappear- ance of the large ganglion cells of the nerve nuclei situated in the floor of the fourth ventricle. These cells correspond in function and anato- mical arrangement to the large ganglion cells in the anterior horns of the spinal cord. The disease is not very frequent, nor is it exceedingly rare. It is more common in men than in women, and from the age of forty to sixty years; it is also somewhat more frequent among the better classes. Colds and injuries of all kinds are often mentioned as direct causes. Stein described a case as the result of strain from protracted blowing of wind instruments. It has also been attributed to mental excitement. DISEASES OF THE MEDULLA OBLONGATA. 177 The influence of heredity has not been proven with certainty. Syphilis is mentioned as a cause in a number of cases. The first symptoms sometimes develop during convalescence from infectious diseases. Progressive bulbar paralysis may be primary or secondary. The former variety develops independently, not infrequently extends sec- ondarily to the spinal cord, and gives rise to the symptoms of spinal progressive muscular atrophy. The secondary form follows progressive muscular atrophy or amyotrophic lateral sclerosis. II. Symptoms.—As a rule, the disease begins gradually, and its further progress is also slow but uninterrupted. In very rare cases, it has a sort of apoplectiform beginning, as in KussmauFs patient, who suddenly noticed difficulty in speech while preaching. The prodromata generally consist uration of the disease, several weeks or months; fatal termination not infre- quent. It is probably the result of poisoning with spoiled grain. 5. Pellagra. I. Etiology.—The disease is endemic in certain parts of Spain, France, Rou- mania, but particularly in Northern Italy. In Lombardy, for example, more than thirty per cent of the population have been attacked. In 1879, nearly 98,000 in- dividuals were attacked in Italy, nearly 41,000 in Lombardy alone. The disease also occurs sporadically in other localities. Among the Italians the disease occurs only among the rural population, and almost always among those who use maize as an article of diet. Some attribute the disease to the non-nitrogenous character of maize, but it must be remembered that pellagra is sometimes absent in certain districts, despite the almost exclusive use of maize as an article of food. Others state that in the affected districts, the maize employed is unripe and mouldy. Attention has been called to the fact that the disease does not prevail in those countries in which maize is used only when dried. Opinions also differ as to whether the disease is produced by certain fungi, or by noxious chemical substances. According to these views, the disease belongs to the same category as those produced by the ingestion of spoiled cereals. But it is said that pellagra may de- velop in those who never come in contact with maize, so that it is looked upon by some as the result of poor nourishment and bad surroundings. It is also claimed i that the disease is hereditary. inflammations of the skin. 325 II. Symptoms.—The chief symptoms are cutaneous changes, disturbances of digestion, and nervous disturbances. The disease is generally chronic and may last ten to fifteen years. The first symptoms begin in April to June, and subside in autumn, to reap- pear more severely in the following year. On those parts which are exposed to the sun, erythematous patches develop- these desquamate at a later period, and leave behind a dark olive discoloration. The skin becomes fissured and covered with ulcers, crusts, and nodes. The mucous- membrane of the mouth and the nails become diseased. The patients suffer from fever and diarrhoea, complain of formication in the hands, muscular tre- mor, paralysis. Ptosis, hemeralopia, and diplopia make their appearance. The patients are profoundly depressed and insanity may develop, Death occurs finally from increasing exhaustion. III. Anatomical Changes.—These are practically unknown. IV. Treatment.—Recovery can be looked for only at the onset of the dis- ease. We should order good food, arsenite of potash and acetate of potash. Good results are also said to have been obtained from sulphur waters and baths. 1. Vesicle-like Inflammations of the Skin. Dermatitides Vesiculosa:. 1. Eczema. I. Etiology.—The causes of eczema may be local or general. The local causes may be mechanical, thermal, or chemical. The mechanical causes include obstinate scratching and rubbing the skin (In itching skin eruptions, such as prurigo, puritus, or urticaria, in scabies, wearing a rough hat, stiff collar, suspenders, etc.); constant friction of two opposed sur- faces of the skin; finally, the eczema of the lower limbs produced by varicose veins. Eczema caloricum often develops in the summer upon those parts of the in- tegument which are exposed to the sun. The group of chemical causes is very large. Thus, cutaneous applications of turpentine, croton oil, mustard, tartar emetic, mercurial and iodine preparations may give rise to eczema. In certain individuals eczema is produced even by the application of bland ointments. It is also observed in those who work in irritat- ing substances (washerwomen, bakers, book-binders, mirror-polishers, etc.). It also occurs from wearing underclothing colored in poisonous dyes, particlurly ar- senical aniline colors. Among the eczemas of chemical origin must be included those produced by constant contact with perspiration, as in the axilla, inguinal folds, etc. It may develop on the lobe of the ear, as the result of discharge from the ear, on the eyelids, as the result of profuse lachrymation in conjunctivitis, on the upper lip after coryza, on the genitals after leucorrhoea. It is not infrequent upon the nates of infants who suffer from diarrhoea, and in whom the buttocks are for a longtime in contact with the diarrhceal stools. Symptomatic eczemas include those which are the result of internal diseases. There is danger, however, of mistaking an accidental compli- cation as an etiological factor. Thus, the closeness of the relation be- tween rickets or scrofula and eczema has been overestimated. It is known that patients suffering from Bright's disease and diabetes often suffer from obstinate eczema, and gastro-enteritic diseases and uterine affections often present the same complication. In some women, eczema occurs with a certain regularity at the menstrual period, in others it de- velops during each pregnancy. Violent mental excitement is occasion- ally mentioned as a cause. Eczema is somewhat more frequent in the male sex. Age possesses little influence, except that the disease is rare before the age of six months. The influence of heredity is not proven, nor does the disease possess contagious properties. Some individuals manifest a predisposition to eczema. It develops 326 INFLAMMATIONS OF THE SKIN. in them after very trifling causes, and local causes produce it in a reflex mariner in parts not directly attacked. IT. Symptoms and Diagnosis.—The outbreak of eczema is pre- ceded not infrequently by prodromata, particularly if the eruption is not the result of local causes. The patients feel chilly and weak, look pale and exhausted, and have slight fever. These symptoms generally sub- side with the outbreak of the eruption, but reappear at each relapse or exacerbation. Eczema results in the production of an itching eruption, which is more often chronic than acute. It may appear in the form of closely aggregated, irregularly distributed, pale-red or dark-red papules (eczema papulosum), of smail vesicles (eczema vesiculosum), or of pustules (eczema pustulosum). The skin may be red and moist (eczema rubrum et madidans); or the vesicles rupture, and their contents dry into thin, honey-yellow, rubber-like crusts (eczema crustosum); or the pustules are converted into thick, grayish-green or brownish-red crusts (eczema impetiginosum); or, finally, the integument is red, but does not weep, and is covered with thin, numerous scales (eczema squamosum). All these forms are different stages of the same fundamental process. This is shown by the simple experiment of applying an irritant, such as croton oil, to the skin. Mild action of the oil produces erythema, at first hypersemic, then exuda- tive ; stronger action results in eczema papulosum. If the irritant acts still more vigorously, serous, later purulent vesicles develop on the papules (eczema vesicu- losum and pustulosum); when their contents dry, eczema crustosum and im- petiginosum result. If the crusts fall off, a reddened, weeping cutis often appears (eczema rubrum et madidans). As the process heals, the weeping ceases, and fine scales form (eczema squamosum). If the irritant action is slight, eczema papulosum alone is produced. If the irritation is very intense, the preceding stages may be skipped, and eczema vesiculosum or pustulosum forms at once. The various stages of development are sometimes found side by side in the same individual. Eczema may be partial or general (rare), acute (duration, two to eight weeks), or chronic. Eczema of the scalp (eczema capillitii) appears commonly in the form of impetiginous or squamous eczema. In the former we find thick, gray- ish-green or dirty-brown crusts, intimately adherent to the hairs. They are mixed with sebaceous secretion, and may diffuse a sour, rancid smeli. If not kept clean, the scalp is apt to harbor lice, and, on the other hand, lice may give rise to impetiginous eczema. In such cases, the occiput and parietal regions often present prominences which, upon removal of the crusts, discharge green, creamy pus. The presence of pediculi is also shown by the nits on the hairs. In filthy individuals, the hairs may be matted together into an inextricable mass, containing crusts, innumerable lice and nits, and give rise to a pestilential stench (plica polouica). Impetiginous eczema may be circumscribed or involve the entire scalp, and may also extend to the forehead, ear, and neck. The ad- jacent lymphatic glands are very often swollen. In infants, impetiginous eczema of the scalp may be secondary to seborrhcea, the secretion decomposing and irritating the scalp. If the crusts are removed, the corium appears reddened and weep- ing. When recovery takes place, the weeping ceases, and the reddened surface becomes covered with fine, white scales (eczema squamosum). In some cases, eczema squamosum develops as such. It is an annoying INFLAMMATIONS OF THE SKIN. 327 and often obstinate affection, the scalp being always covered with more or less numerous white scales. Eczema of the scalp is distinguished from seborrhcea by the fact that, in the latter, after removal of the crust the surface is not red or weeping, the glands are not swollen, and the disease does not extend beyond the scalp. It is dis- tinguished from favus by the absence of spores in the crusts, and of the sulphur- yellow color, plate-like shape and peculiar smell of the favus crusts. Psoriasis of the scalp is associated with characteristic patches of psoriasis in other parts of the body. Eczema faciei may extend over the entire face or be confined to cer- tain parts. Diffuse eczema is not infrequent in infants beyond the age of five months. It generally appears as eczema crustosum or eczema rubrum et madidans. In the former, the face is covered with light-yellow crusts, which are often so closely aggregated as to form a sort of mask; in the latter, the face is red, moist, and sticky. The fluid is alkaline and very poor in cellular constituents. Eczema crustosum is often found in some parts of the face; eczema rubrum et madidans, in other parts which are on the way to recovery. Eczema of the ear is apt to attack the posterior surface of the concha; it appears generally as eczema crustosum or impetiginosum. The concha is often very much swollen, and the swelling of the external auditory canal may interfere with audition. Eczema is often compli- cated with otorrhcea, or the former creeps along the external auditory canal. In some cases, the otorrhcea is primary, and gives rise to eczema. The latter often leaves behind deep and painful rhagades, which are sometimes covered with a gray, lardaceous coating, and emit afoul odor. Eczema nasi affects the nostrils or the nasal mucous membrane. The nostrils are sometimes occluded by crusts, so that the patients are forced to breathe through the mouth. Snoring, stenotic sounds are produced on attempting to breathe through the nose. This condition is not de- void of danger in the new-born and nurslings, and may give rise to venous stasis, cyanosis, and pulmonary congestion. In not a few cases, moreover, the disease is the starting-point of facial erysipelas. If the eczema attacks the outer integument of the nose, very painful fissures may form in the naso-labial folds. Eczema labiorum often gives rise to considerable swelling and de- formity of the lips; they are thickly covered with brown or bloody crusts, and contain numerous painful, bleeding rhagades. Eczema superciliorum and eczema palpebrarum produce great de- formity. In the latter, the free border of the lid is not infrequently affected, and there may be secondary blepharitis. Eczema barbce (usually pustular or impetiginous) is still more annoy- ing. Unlike sycosis, it very often extends beyond the beard. The two diseases are apt to be mistaken if the eczema extends to the hair folli- cles, and allows the hair to be readily removed with the tweezers. Eczema nuchce usually extends from the scalp. It often occurs inde- pendently in fat babies, in whom it develops between the horizontal folds of skin as the result of friction. If cleanliness is not enforced, these parts may undergo gangrene and ulceration, and, in rare cases, death has occurred in collapse or eclampsia. Eczema rnammce is more frequent in women than in men. In stout women, eczema intertrigo develops not infrequently under the folds of the breast. In nursing women, eczema often occurs around the nipple, 328 INFLAMMATIONS OF THE SKIN. and is frequently associated with very painful rhagades. Very severe eczema may extend to the mammary gland, and give rise to mastitis. Eczema umbilici is observed particularly in obese individuals, and is extremely obstinate. Eczema of the genitals occurs in both sexes. In males, it attacks the scrotum and dorsum penis, while the glans and inner surface of the pre- puce escape. The scrotum is affected particularly in those parts which are in contact with the thighs. The disease may be associated with marked inflammatory oedema, so that the scrotum and penis are swollen and misshapen. After it has lasted a long time, the skin may undergo thickening and deform the genitals. The inflammation often extends to adjacent parts of the integument. In women, the labia majora and mons veneris are most frequently affected, but the eczema sometimes extends to the labia minora and even to the vagina, giving rise to pruritus and secondary leucorrhcea. In other cases, leucorrhcea causes secondary eczema of the external genitals. Eczema ani is annoying from the intolerable itching, and may give rise to painful rhagades, muco-purulent inflammation of the rectum, or prolapsus ani. Eczema extremitatum is found not infrequently upon symmetrical parts of the limbs. In eczema of the folds of the elbow or the popliteal spaces, rhagades often form and interfere with the movements of the upper or lower limbs. The disturbances become still greater if the extensor and flexor surfaces are affected at the same time. Eczema interdigitale is extremely annoying, and, if pustular in char- acter, may be mistaken for scabies. Eczema digitorum sometimes affects only certain parts of the fingers; if the tips are attacked, the patients generally complain of formication in the fingers. The nails are sometimes involved, and may be exfoliated. Eczema voice manum often produces epidermoidal thickenings and deep-red, bleeding, or weeping rhagades. It may be mistaken for psoriasis, but in this affection patches of psoriasis are present in other parts. Eczema vesiculosum and pustulosum are also found here, but, as a rule, the thick epidermis interferes with the production of fully developed vesicles. Eczema antibrachiorum appears not infrequently as a papular or vesicular variety. In the former, the skin is red, hot, and covered with numerous flat or pointed elevations; in the latter, it presents vesicles filled with fluid. Both forms occur not infrequently in harvest time as eczema caloricum. I have also observed them as the result of contact with rhus toxicodendron. In Eczema anticrurium, the reddened skin feels sticky, and is cov- ered with very fine, clear drops. The fluid stains the underclothing yellow, and stiffens it. In the process of recovery, there is often a transition to squamous eczema. Eczema universale is rare. In many cases, the term may not be used literally, since some parts of the skin are intact. In the majority of cases, eczemas disappear without leaving sequelae. If very persistent, they may reduce the patient on account of the loss of appetite, and the disturbance of sleep caused by pruritus. Chronic ec- zema is sometimes followed by albuminuria; but, on the other hand,, nephritis may also give rise to eczema. III. Anatomical Changes.—The same anatomical changes ara INFLAMMATIONS OF THE SKIN. 329 found as in the formation of papules, vesicles, and pustules in other eruptions. In papular eczema are found: dilatation of the vessels in the upper layers of the cutis, serous exudation, emigration of white blood-globules, and swelling of the cells of the rete Malpighii. In vesicular eczema, the epidermis is separated in places from the rete Malpighii by the inter- position of serous fluid. The vesicles are not infrequently multilocular, the septa being composed of flattened cells of the rete Malpighii, which have been pressed together. If numerous round cells enter the serous contents, pustular eczema develops. The pus-corpuscles are derived in part from the vessels of the cutis, in part from the cells of the rete Mal- pighii. A complete restitutio ad integrum may take place, but, in chronic cases, the cutis is unusually rich in cells, thickened, the blood- vessels and lymphatics are dilated, the sebaceous glands and hair follicles have partly disappeared, the sweat glands degenerated. Occasionally there is infiltration of the subcutaneous cellular tissue with round cells,, and unusual pigmentation of the deeper layers of the rete Malpighii. IV. Prognosis.—The prognosis, as regards complete and permanent recovery, is only unfavorable if the disease is the result of incurable con- stitutional causes. V. Treatment.—The treatment depends mainly on the etiology. If the disease is the result of local injuries alone, local remedies alone are indicated. In papular eczema, characterized by redness and heat of the skin, we may apply cool compresses of liq. alumin. acet. (1$), aqua plumbi or aqua plumbi Goulardi and water aa. To relieve violent itching, dust the parts at night with carbol-vaselin (1 : 15). If the pruritus is not severe, apply some dusting powder twice a day, for example, $ Flor. zinci, Sem. lycopod., aa 3 i-; Amyli, 3 iv. M. D. S. As a general thing, vesicular and pustular eczema require treatment with bland oils or ointments, for example, the application of ol. olivae, ol.amygdal., or unguent, simplex, etc. In eczema crustosum or impetiginosum, the crusts must first be removed. This may be done by frequent application of the above-men- tioned oils for two hours, or the application to the skin of a piece of flannel dipped in oil. After the crusts are removed, the eczema is thus converted artificially into an eczema rubrum et madidans, and may be treated as such. In our opinion, the best ointment hitherto recommended in this disease is ung. diachylon Hebrae; if the itching is violent, it may be mixed with carbolic acid (1 : 50), if there is profuse weeping, with tannic acid (3 : 50). The ointment is smeared on pieces of old linen, and carefully applied with a flannel bandage. Unna impregnates mull with the oint- ment, and applies this directly as a bandage. The number of ointments recommended in eczema is legion. Niemeyer extols white precipitate ointment as an almost sovereign remedy, and also obtained good results from corrosive sublimate (1 : 300). Lead and zinc ointments, oint- ments of nitrate of silver, subnitrate of bismuth, etc., are also recommended. In squamous eczema, the skin should be anointed several times a day and strewn with the previously mentioned dusting powder. In very obstinate cases, tar preparations may be employed. 01. rusci or ol. fagi et ol. oliv. aa may be applied once a da}T, so long as the scales are freely desquamated. Then the applications may be made at longer intervals, 330 INFLAMMATION'S OF THE SKIN. but must be continued until the formation of scales ceases. In marked infiltration and thickening of the skin, good results are obtained from .soap inunctions or applications of caustic potash (1 : 2 of water). The latter is applied once a week, and followed immediately by cold compresses to relieve the pain. Indifferent baths and cold-water cures are useful in some cases. If rhagades have formed behind the ear, salicylated cotton smeared with ointments may be applied. In eczema of the nose, tampons smeared with ointments should be introduced several times a day. In eczema of the scrotum, a suspensory bandage must be worn. In eczema of the rectum, suppositories containing oxide of zinc or tannic acid may be introduced. The internal remedies include iron, iodine, and arsenic, according to the constitutional condition of the patient. 2. Miliaria. Miliaria forms small, scattered vesicles which are transparent and clear (miliaria crystallina), or are surrounded by a red zone (miliaria rubra), or present a cloudy, almost purulent appearance (miliaria alba). They occur exclusively or chiefly on parts which are covered by clothing, nnd are almost always the result of increased production of sweat (sudamina). The eruption appears in healthy individuals after profuse sweating in hot weather, or is produced artificially by sweat cures arid cataplasms. It often develops during the crisis of acute febrile diseases. It is fre- quent in acute articular rheumatism, in the stage of recovery from typhoid fever, in phthisis, miliary tuberculosis, pyaemia, puerperal fever, measles, scarlatina, small-pox, the cold sweats of cholera, and even in agonal sweating. A very trifling increase of cutaneous perspiration will produce sudamina in some individuals. On account of the varying irritability of the skin, miliaria crystallina persists as such, while in others, it is rapidly converted into the two other forms. Sometimes, indeed, miliaria crystallina remains almost entirely absent. Miliaria crystallina forms clear vesicles, varying from the size of a millet seed to that of a pin’s head; in rare cases a few attain the dimen- sions of a pea. When punctured, they discharge a clear fluid of a neu- tral or feebly alkaline reaction. The smallest vesicles are often better felt than seen. Sometimes there are thousands of vesicles on the skin, in other cases only a few. They sometimes disappear very rapidly. The fluid evaporates, the epidermis sinks in, forming small white ele- vations, or the vesicles rupture and the superficial layers of the epi- dermis are cast off. The eruption gives rise to no notable symptoms, at the most to slight pricking and itching. In some cases new outbreaks continue to form, so that the eruption lasts several days or Aveeks. In not a few cases it passes into Miliaria rubra.—The contents of the vesicles become cloudy and a red zone forms around the periphery, as the result of decomposition of the vesicular contents and irritation of the deeper layers of the skin. If the cloudiness increases and the red zone disappears, miliaria alba is the result. Both forms heal by desiccation of the contents of the ves- INFLAMMATIONS of the skin. 331 icles and desquamation of the superficial epidermis. Treatment is un- necessary. Haight’s examinations show that the vesicles are situated above the excretory ducts of the sweat glands, and consist of elevation of the stra- tum corneum. They are the result of occlusion or insufficient calibre of the excretory ducts in question. c. Vesicular Inflammation of the Skin. Dermatitis Bullosa. Pemphigus. (Pompholix.) I. Symptoms.—The chief symptom of pemphigus is the occurrence of vesicles upon the skin, varying from the size of a pea to that of the palm of the hand or even more. The contents of the vesicle are, at first, of a wine-yellow color, transparent, serous, and of neutral reaction; later they become alkaline, cloudy, and pus like. The vesicles either rupture spontaneously, laying bare the red weeping corium, which is gradually covered with epidermis, and leaves behind a red, later brown patch; or their contents dry into thin yellow, brown or blackened crusts which fall off. Closely aggregated vesicles are known as pemphigus confertus, isolated ones as pemphigus disseminatus. In very rare cases only a single vesicle forms (pem- phigus solitarius). If the vesicles are arranged in rows, the term pemphigus gyratus is applied; if young vesicles form around an older one, pemphigus circinatus. Vesicles whose contents have a bloody color are called pemphigus hemorrhagicus. Vesicles have also been observed upon the mucous membrane of the lips, cheek, pharynx, nose, epiglottis, bronchi, vagina, gastro-intestinal tract, and conjunctiva. The development of vesicles upon the epiglottis may lead to fatal oedema of the glottis, and it is also claimed that pem- phigus of the gastro-intestinal mucous membrane may be followed by perforation. Three varieties of pemphigus have been distinguished, viz.: pemphi- gus acutus, chronicus, and foliaceus. a. As a rule, acute pemphigus does not last more than a month. It is more frequent in children than in adults; and may be epidemic in maternity hospitals. As a rule, the first vesicles appear, in the new- born, from the fourth to the ninth days. A number of cases of direct contagion have been observed. It has also been found that when a large number of cases occurred in a town, the children had been cared for by a certain midwife. Inoculations with the contents of the vesicles, how- ever, almost always are followed bv negative results. Cases have been observed in which the disease ran a febrile course and terminated fatally, generally as the result of complication with pneumonia or gastro-enter- itis. Acute pemphigus may also occur in adults, but rarely runs an apyrex- ial course. The eruption is often preceded for one to three days by pro- droinata, viz., general malaise, anorexia, disturbed digestion, chill and fever. The temperature increases with the appearance of the eruption, and may recur at each new outbreak. We often notice erythematous and urticaria-like places, upon which the vesicles form. The vesicle is often surrounded by a red zone, gradually increases in size and becomes 332 INFLAMMATIONS OF THE SKIN. tense, causes a disagreeable sensation of tension. It finally bursts or dries, while new ones form in other parts. Vesicles in the mouth produce pain and fcetor ex ore; the buccal mu- cous membrane appears macerated in places. In pemphigus of the bron- chi, membranous structures are sometimes expectorated (vide Vol. I., page 223). Cardiac murmurs, enlargement of the spleen, occasionally albuminu- ria and haematuria have been observed as complications. b. Chronic pemphigus lasts months and even years. In some cases the eruption continues uninterruptedly, in others there are periods of health followed bv relapses. The disease may be entirely apyrexial, or there are temporary elevations of temperature. The patients may grad- ually grow very feeble, Bright’s disease and waxy degeneration of the large abdominal glands may develop, and finally the patients may die from general marasmus. Stokes reported one case of exfoliation of all the nails following pemphigus of the fingers, and another case in which the vesicles appeared upon the scalp. A fatal termination is almost in- evitable if the disease is converted into: c. Pemphigus foliaceus. This form may also develop as such from the start, and Behrend described an epidemic of this kind in the new- born. In pemphigus foliaceus, as a rule, the vesicles are small and flaccid, so that the epidermis upon them appears wrinkled. When the vesicle bursts, new skin does not form, so that new vesicles continually recur, and the corium is laid bare more or less extensively. Hebra also ob- served a necrotic (diphtheritic) deposit upon the exposed corium. The disease almost always terminates fatally with the symptoms of increasing exhaustion. II. Anatomical Changes.—Recent vesicles are multilocular, the septa consisting of agglomerated scales of epidermis; older vesicles are unilocular. Upon the inner surface of the raised epidermis, there are often small appendages which correspond to follicles. The cells of the rete Malpighii are often broken up into granular masses, and the pa- pillae infiltrated with round cells. In one case o£ pemphigus foliaceus J. Neumann observed dilatation of the sweat glands. On perforation of the vesicles, the fluid almost always discharges readily, but Kuester reported a case in which some of the vesicles con- tained a gelatinus mass which was not discharged. The fluid contains changed white and red blood-globules, the remains of epithelium cells, granular detritus, and schizomycetes. In our opinion, however, the presence of the latter does not justify a conclusion as to the parasitic na- ture of the disease. The chemical constitution of the fluid does not differ essentially from that of vesicles produced by a burn or a fly blister. Urinary analyses also give negative results. III. Etiology.—The disease is more frequent in children than in adults, and in men than in women. Heredity has been occasionally no- ticed. It has been observed during pregnancy or the puerperal condition. Some cases are contagious in their origin. They may occur in infec- tious diseases, viz., pyaemia, puerperal fever, ulcerative endocarditis, inflammations of the skin. 333 scarlatina, measles, small-pox, intermittent fever, and syphilis. Syphi- litic pemphigus occurs almost always in children. It appears mainly, sometimes almost on the soles of the feet and palms of the hand. The eruption is sometimes present at birth or in still-born babes. Toxic pemphigus sometimes follows the administration of potassium iodide or bromide, and salicylic acid. IV. Diagnosis.—The diagnosis is generally easy. It may be mis- taken for malingering (action of blisters), burns, eczema, herpes iris, im- petigo, urticaria bullosa, and erythema bullosum. Baerensprung detected intentional fraud by finding, with the microscope, bits of the wings of the Spanish fly upon the vesicles. The vesicles of burns are recognized by the previous history. Eczema produces smaller vesicles, and the general condition is unaffected. The differential diagnosis from herpes iris is extremely difficult at first, but is decided by the subsequent history. In urticaria bullosa the itching is intolerable and wheals are also present. In erythema bullosum we also find characteristic firm nodes which are not covered with vesicles. V. Prognosis.—This depends upon the nature and etiology of the disease. In pemiphigus foliaceus recovery is rare, in the acute form it is the rule. In chronic pemphigus the prognosis becomes serious if ex- haustion and albuminuria make their appearance. VI. Treatment.—Prophylaxis is important in some cases, particu- larly in pemphigus neonatorum (isolation of affected infants, avoidance of too hot baths, etc.). Little can be expected from the administration of internal remedies. Iron, quinine, arsenic, iodine, acids, etc., have been tried. If the patients complain of pain in the vesicles, the latter should be punctured and powdered with : IjlFlor. zinci, Semin, lycopod aa 3 i. Amyli 3 v. M. D. S. To be used as a dusting powder; or the vesicles are covered with linen which has been smeared with carbolized oil, carbol-vaseline, etc. In addition, we may give a daily lukewarm bath It.) containing 1 x.-xvi. of soda, or a corrosive sublimate bath ( 31.—iij.) every other day. In pemphigus foliaceus permanent baths may be recommended. In other respects symptomatic treatment. d. Pustular Inflammations of the Skin. Dermatitides Pustulos^e. 1. Impetigo and Ecthyma. I. Symptoms and Etiology.—The terms impetigo and ecthyma are applied to eruptions consisting of scattered pustules; secondary crusts are still more frequent than the pustules. The term impetigo was formerly applied to pustules which do not exceed the Bize of a pea, ecthyma to larger ones, but there are such numerous transitions between the two that the distinction lias been abandoned. Hebra showed that in the large majority of cases, impetigo and ecthyma are symptoms of underlying processes. 334 inflammations of the skin. Their causes may bo local (idiopathic) or general (symptomatic). The local causes, like those of eczema, are mechanical, thermal, or chemical (vide page 325). Among the general causes are pyaemic processes, syphilis, glanders, and post-mortem wounds; also protracted, exhausting diseases, particu- larly typhoid fever. Impetigo sometimes occurs in healthy persons without any demon- strable cause, lasts one to two weeks, is accompanid by fever, and then disappears entirely. The disease here develops idiopathically. This is also true of the contagious impetigo of Tilbury Fox, and the herpeti- form impetigo of Hebra. In contagious impetigo, pustules first appear upon the face, then upon the scalp, neck, trunk, and limbs, in a few cases upon the buccal mucous membrane and tonsils. The pustules dry up and form crusts, and the latter fall off without leaving a cicatrix. The eruption is sometimes preceded by febrile prodromata, and the fever lasts several days after the outbreak of the eruption. As a rule, it recovers spontaneously by the end of the second week, often earlier, sometimes not until the sixth week. Unna observed several relapses. A number of epidemics have been observed and several undoubted cases of infection. Several writers performed successful inoculations with the contents of the pustules, even upon the affected individual. The contents of the pustules contain pus-corpuscles, epithelium cells and granular detritus. Micrococci have also been found. Kaposi observed higher fungi with fructification organs, and regards the disease as parasitic. Other writers could not confirm these results. Impetigo herpetiformis was first observed by Hebra in five cases in pregnant women or soon after delivery. Recovery occurred only in one case. The following was the clinical history: The eruption began on the inner surface of the thighs, and then ex- tended to the anterior surface of the abdomen; the face and limbs, even the tongue, were sometimes attacked. Groups or circles of pustules first appeared and dried into crusts; these were followed by new crops in the vicinity. Upon removal of the crusts a reddened, weeping, but never ulcerated surface was exposed; it was sometimes covered with a smeary, grayish-white deposit, which occasionally emitted a disagreeable odor. Proliferations were sometimes observed upon the affected integument. The eruption and also subsequent relapses were preceded by chills and elevation of temperature. Bloody diarrhoea was observed occasion- ally. Death occurred from increasing exhaustion. II. Diagnosis.—The diagnosis is easy. It is important to distin- guish between ordinary and syphilitic impetigo. In the latter, other signs of syphilis are generally present, and, on removing the crusts, we find a deep, crater-like loss of substance covered with a grayish-yellow mass; in ordinary impetigo, the loss of substance is confined to the epidermis. Contagious impetigo is distinguished from impetiginous eczema by the absence of itching. III. Prognosis.—This depends upon the etiology. In contagious impetigo, it is very good; in the herpetiform variety, it is almost always fatal. IY. Treatment.—The treatment must first be directed against the INFLAMMATIONS OF THE SKIN. 335 primary disease. In addition, the crusts should be thoroughly oiled, and, after their removal, the affected parts treated with bland oint- ments. 2. Acne Vulgaris. (Varus.) Acne vulgaris is an inflammation of the sebaceous glands, and in places of the hair follicles, which gives rise to the formation of red papules, nodes, and pustules. It is divided into five classes, viz., acne dissemi- nata, frontalis, cachecticorum, syphilitica, and artificialis. a. Acne disseminata is a very wide-spread affection. It is very rare in childhood, but almost always begins at puberty and often lasts for years. The eruption is most profuse and constant on the forehead, chest, and back, rarer on the arms and thighs; the soles of the feet and palms of the hand always escape (absence of sebaceous glands). Arlt observed acne of the conjunctiva. Seborrhcea and the formation of comedos are generally observed at the same time. Indeed, the latter gives rise in many places to acne, because the stasis produced by the comedo results in inflammatory irri- tation. In the mildest form we find little red papules, in the middle of which is a black comedo (acne punctata), in other places a pustule has formed upon the nodules (acne pustulosa). The inflammation extends not infrequently to the adjacent cutis, and forms red, very painful nodes, from the size of a pea to that of a bean (acue indurata); in many cases, pus does not escape until the scalpel is introduced very deeply. The papules, nodes, pustules, and comedos may be so numerous as to cause great deformity. Exacerbations and remissions are noticeable. The nature of the etiological relation between puberty and acne is entirely unknown. On microscopical examination, the excretory portion of the sebaceous follicle is found occluded by thickened sebum, the gland itself is dilated and filled with fat granules, cellular detritus, and pus-corpuscles. The adjacent cutis is congested, and more or less infiltrated with round cells. If lateral pressure is exercised upon the acne, the plug of sebum with its black head first appears, and is followed by milky or purulent, pasty or more fluid contents. b. Acne frontalis is distinguished from acne disseminata, as regards its mode of development, by the fact that it is not preceded by the forma- tion of comedos. It occurs exclusively on the forehead, particularly near the hair. The papules or pustules are flat, and often carry a small, central crust. This is deeper than the periphery of the nodule, so that the latter forms a sort of wall. When the crust drops off, a slightly de- pressed cicatrix remains. c. Acne cachecticorum develops after long protracted and exhausting diseases; it is associated not infrequently with pityriasis tabescentium and lichen scrophulosorum. It is probably produced by hyperplasia of the epithelium of the sebaceous follicles, as the result of cachexia with subsequent inflammatory irritation. cl. Acne syphilitica (vide article on Syphilis, Vol. IV.). e. Acne artificialis. The best known form is tar acne, produced by local .applications or by inhalations of tar vapor. If the skin is coated with tar, black specks (particles of tar) are observed in the sebaceous 336 INFLAMMATIONS OF TIIE SKIN. follicles, and later the acne changes appear. If tar is inhaled, it is probably deposited in part in the sebaceous follicles, and there produces inflammation. Tar acne is also produced in those who work in tar pro- ducts (creasote, benzin, petroleum, etc.). Acne also develops from the use of iodine and bromine preparations and chrysarobin ointment. The diagnosis of all the varieties of acne is easy, the prognosis is un- favorable so far as regards thorough and permanent cure. In acne cachecticorum, reliance must be placed on cod-liver oil, tonics, and nutritious food; local treatment is hardly necessary. In acne disseminata, we should first attempt to prevent the formation of comedos. If there is an abundant formation of papules or nodes, mer- curial ointment should besmeared on leather and applied at night to the affected parts. The next morning the skin is carefully washed with the following: I£ Saponis virid., 3 iij., Spiritus vini, | iv.; filtra et adde 01. lavandul., 01. bergamotae, aa gtt. v. M. D. S. To be used externally. Large, painful nodes should be poulticed, and then incised. If there is a profuse formation of pustules, these should be punctured, and their contents discharged; the skin may then be covered with Hebra’s diachylon plaster. We may briefly mention the following other plans of treatment: a. Applica- tions of corrosive sublimate (gr. | to is®!. : § iiiss.); b. application of tinct. iodin., tinct. benzoes, or tinct. cantharid.; c. treatment with sulphur or glycerin soaps; d. (Zeissl’s sulphur paste) Lac. sulph., Kali, carbon., Glycerin., Spirit, vin. dilut., aa. M. D. S. Smeared on leather, and applied every night, removed with soap in the morning, etc. All these remedies seek to produce active desquamation of the superficial layers of epidermis, and thus to keep the excretory ducts of the glands free. 3. Acne Mentagra. (Sycosis.) I. Etiology.—The term sycosis is applied to a chronic inflammatory process in the hair follicles, which gives rise to the formation of papules, nodes, diffuse infiltrations of the skin, pustules, and crusts. Two forms are distinguished, the parasitic (produced by tricophyton tonsurans), and the non-parasitic. The disease is observed almost exclusively in bearded men. A dense growth and very thick hairs in the beard predispose to sycosis. The causes of non-parasitic sycosis are unknown. Among those which have been assumed are shaving with a dull razor, uncleauliness, irritation by snuff, highly spiced food. In some cases, it follows eczema. Chronic coryza may also give rise to sycosis if the secretion constantly flows upon the upper lip, and irritates the follicles. Hebra believes that in sycosis a new hair grows in an old hair follicle before the previous one has fallen out, and thus produces mechanical irritation and inflammation of the hair follicle. Werthheim assumes that the beard hairs are too thick, so that the follicle does not afford sufficient room for the transverse section of the hair. Parasitic sycosis is produced by direct infection writh herpes tonsu- rans, either from animals (cow, horse, dog) or from man to man. The disease affects the head most frequently, and has therefore been called folliculitis barbae. More rarely it attacks the eyebrows or lids, still less frequently the hair of the axilla, mons veneris, the vibrissas of INFLAMMATIONS OF THE SKIN. 337 the nose, or the scalp. In the latter locality, the disease is almost always secondary to eczema. If. Symptoms.—The development of the eruption is generally pre- ceded by a feeling of tension and pricking in the affected parts. Then there appear red papules and nodes, whose centre is perforated by a hair. Adjacent nodes come in contact, and form diffuse nodular elevations; not infrequently there are extensive infiltrations of the skin. Pustules appear in places upon the nodes, and either rupture spontaneously or dry into yellow or gravish-yellow crusts, which are likewise perforated by a hair. In those localities in which a hair is situated in the pustule, Fig. 135. Hair containing fungi from a node of parasitic sycosis. Half of the hair alone is drawn. After Kaposi. the former is readily removed on making traction. The root portion appears thickened, and the root sheaths infiltrated with pus; the hair is often bent at an angle immediately above the bulb. In parasitic sycosis, the hair is peculiarly dry, fibrillated, and discolored. After removal of the hair, a little drop of creamy pus often escapes. If the crusts are softened and removed, we often find reddened but dry surfaces, which are sometimes elevated like condylomata, present the appearance of proud flesh, or are perforated like a sieve, the indi- vidual openings containing pus. After the process has lasted for some time, certain parts of the skin may be entirely destitute of hair. This condition persists, inasmuch as the hair follicles have been obliterated by 338 inflammations of the skin. the inflammation. The submaxillary lymphatic glands become swollen if the cutaneous changes are extensive. In non-parasitic sycosis, the changes described are confined strictly to the beard; in the parasitic form, they are apt to extend to adjacent parts of the face or neck. The changes characteristic of herpes tonsu- rans make their appearance in sharply defined circles, which are covered with little vesicles or scales. Non-parasitic sycosis may last a very long time, sometimes even more than thirty years. Parasitic sycosis generally runs a rapid course. III. Diagnosis.—The diagnosis is easy. Sycosis is distinguished from eczema by the fact that in the latter the affected skin is moist and itching, and that it is not confined to the hairy parts. The microscope readily distinguishes parasitic from non-parasitic sycosis; in the former, the hairs contain threads and spores of tricophyton tonsurans (vide Fig. 135). The fungus is formed earliest between the hair and inner root sheath, then it spreads into the root sheaths, finally into the substance of the hair. The hairs become transparent if treated for fifteen to twenty minutes with potash (1 : 3). Among four hundred examinations, Michelson and Schueppel found the fungus only in one hair out of twenty. IV. Prognosis.—The prognosis is good. The disease may recover spontaneously, and is amenable to treatment, but it exhibits a tendency to relapse, V. Treatment.—In non-parasitic sycosis, the beard should be closely clipped if the disease is extensive. The beard should be shaved daily, even long after the disease has recovered, in order to prevent a relapse. Crusts are removed by fatty inunctions (two hours), pustules are opened, and the hairs contained therein are removed daily with a pair of tweezers. Only one hair should be grasped at a time and trac- tion made in the direction of the hair. The entire diseased district should not be treated in the first few sittings, since this may give rise to peculiar conditions of excitement, and even to syncope. Epilation must be continued until the formation of nodes and pustules has ceased. Behrend has recently employed the sacrificator with success. The re- maining infiltration may be treated with Hebra’s diachylon plaster or mercurial ointment; if the infiltration is very thick, with Zeissl’s sul- phur paste. Parasitic sycosis may be treated with applications of turpentine, corrosive sublimate, nitrate of silver, acetic acid, or powdered sulphur. Appendix. Hebra applied the term sycosis framboesiformis to an affection located at the border of the neck and hair, and which gives rise at first to the development of nodes, each of which is perforated by a hair. Later, the coalescence of the nodes causes a raspberry-like infiltration of the hairs, and which, in many cases, cannot be removed except by cauterization or excision. The disease is chronic; it is per- haps the result of mechanical causes (friction of the collar.' 4. Acne Rosacea. I. Symptoms and Anatomical Changes.—The disease occurs exclusively upon non-hairy portions of the face, generally the nose, next the cheeks, chin, or glabella. It may also extend continuously over INFLAMMATIONS OF THE SKIN, 339 large portions of the face, sometimes to the border of the hair, and even to the back of the neck. In the mildest grades, there is unusual redness of the skin, partly diffuse, partly in the form of unusually dilated and sinuous cutaneous vessels. It usually increases after eating or excitement. It is often as- sociated with seborrhcea. As the disease grows more severe, soft, painless, red nodules, varying from the size of a lentil to that of a pea, appear upon the reddened skin. In addition, there is often an abundant development of comedos and acne vulgaris. Pustules are rarely observed. The process is the result of marked dilatation and in part of new- formation of vessels of the cutis, dilatation of the sebaceous glands, with stagnation of their secretion, and the formation of a gelatinous connec- tive tissue in the cutis. Spontaneous recovery is possible, even in this stage, by absorption of the newly formed connective tissue. In the majority of cases, however, the process continues to advance. Large nodes then develop, generally situated on a broad base, more rarely pedunculated. If the disease attacks the nose, great deformity is produced; the organ some- times attains the size of two fists, and looks like a large rough potato, etc. (rhinophyma). II. Etiology.—In many cases, the disease is the result of alcoholic excesses. The greatest danger is run by wine drinkers, next by brandy drinkers, finally by beer drinkers. Those wines which are rich in ethereal oils and acid are the most injurious in their effects. In whiskey drinkers, the nose is usually smooth and bluish-red; in wine bibbers it is generally covered with red protuberances; in beer drinkers,with cyanotic tubercles. Acne rosacea is sometimes found in individuals who suffer from diseases of the digestive tract (stomach, intes- tines, liver). In women, it is almost always the result of diseases of the sexual apparatus: amenorrhoea, uterine diseases. It is most frequent in females at the beginning of puberty or the menopause; in males, ft develops beyond the age of 35 years. In some women, the first signs appear during pregnancy or childbed. It has been often observed after protracted cold-water cures. Finally, the disease may follow local injuries (frequent exposure to rough winds or to fire). III. Diagnosis.—The diagnosis of the disease is easy. It may pos- sibly be mistaken for frost-bites, lupus, carcinoma, syphilis, and rhino- scleroma. In frost-bites, the skin is bluish-red, and the cutaneous veins are not dilated. Lupus erythematosus is characterized by profuse formation of scales and the development of cicatrices. In lupus vulgaris, there are brownish-red nodules, which are apt to break down and cicatrize. Carcinoma, as a rule, soon ulcerates. This is also true of syphilis; in addition, other evidences of syphilis are noticeable. IY. Prognosis.—The disease is often very obstinate. The de- Fig. 136. Lancet-shaped needle fo scarification- 340 INFLAMMATIONS OF THE SKIN. formity is often so great that the patients are a laughing-stock in the community. V. Treatment.—We must first endeavor to remove the cause of the disease, and this in itself is sometimes sufficient to effect a cure. In ad- dition, local treatment must be adopted. In the mildest form (simple redness), we recommend that the skin be brushed every night with collodion or sublimate collodion (gr. f : | i.). We have also obtained good results from an ointment of tannin and ergotin (ung. diach. Ilebrae, 3 v., acid, tannic., ergotin., aa 3 ss. M. D. S. To be smeared on linen, and applied every night). The second grade of the disease may be treated with mercurial oint- ment and, if there is marked vascularization, by scarification with a lancet-shaped needle (Fig. 136). ZeissePs sulphur paste, iodine and sulphur preparations may be employed to relieve marked infiltrations. Cases of the third grade must be treated by surgical interference, i. e., removal of the new-formations. e. Scale-forming Inflammations of the Skin. Dermatitides Squamosa. 1. Psoriasis. I. Symptoms.—Psoriasis is a chronic skin disease which leads to the production of abundant scales possessing a gloss like that of mother-of- pearl. If these are removed with the nail, a reddened, easily bleeding base makes its appearance. The individual efflorescences begin as a reddened, slightly elevated patch, which is covered, at the end of a few days, with an increasing number of scales, and, at the same time, increases in size. The smallest efflorescences form little dots which shine like asbestos (psoriasis punc- tata); when they attain the size of a lentil, the skin looks as if sprinkled with mortar (psoriasis guttata). In some places, the scales disappear in the centre of the patch, but extend further at the periphery (psoriasis orbicularis). Adjacent patches not infrequently coalesce and produce complicated figures (psoriasis gyrata). If the scales extend continuously over a large area, it is known as psoriasis diffusa. The term psoriasis nigra is employed when the scales have a brownish or blackish appear- ance (particularly in old cases). The eruption first appears on the extensor side of the elbows and knees, and these parts are rarely unaffected in extensive psoriasis. As a rule, the scalp is next affected, thick hillocks of scales being formed and matting the hairs together. At the border of the hair, the patches often extend to the adjacent integument of the face and neck. The concha and external auditory canal are very often affected, but there are many cases in which the eruption extends over the entire body. The mucous membranes are always intact. The volar surfaces of the hands and feet are rarely affected, in contradistinction to psoriasis syphilitica. Psoriasis sometimes develops on the nails; white patches first appear, then the nail thickens, becomes lamellated, and crumbles to pieces. In some patients, a few patches persist, perhaps for life; in others, there may be very little unchanged integument. Remissions and exacer- bations occur very often. The eruption sometimes disappears sponta- neously, and remains absent for months and years. As a rule, the cause of the relapse cannot be ascertained. INFLAMMATIONS OF THE SKIN. 341 Very violent exacerbations may be associated with slight fever, pain in the 'joints, and neuralgic symptoms. The patients often suffer no subjective disturbances, but at first some complain of itching. If the psoriasis is very marked at the large joints, very painful rhagades develop not infrequently, and render motion distressing. In inveterate psoriasis of the face, we also find painful fissures, occasionally also ectropium. As a rule, individuals suffering from extensive psoriasis do not perspire much. Cutaneous sensibility is sometimes diminished, and albuminuria has also been observed. If the disease is very obstinate and extensive, the patient may suffer from anorexia, with increasing feebleness and exhausting diarrhoea, and these symptoms occasionally terminate fatally. If spontaneous recovery ensues, the scales fall off, the skin is at first red and infiltrated, but gradually grows pale and returns to the normal. In some cases, pigmented spots persist upon the legs. Fio. 137. Spores from the psoriasis membrane. After Lang. Etiology.—Little is known concerning the causes of the disease. Heredity exercises an important influence; the inheritance is sometimes direct from the parents, sometimes from the grandparents or collateral branches of the family. The predisposition to psoriasis alone is inher- ited, and the development of the disease requires the interposition of certain external irritants. The latter include traumatism. Hence the early appearance of psori- asis on the elbows or knees, because these parts are particularly subject to friction. J. Neumann showed that the disease not infrequently fol- lows eczema intertrigo, the latter being secondary to traumatism. All other statements with regard to the etiology of psoriasis are either improbable or unproven. Next to eczema, psoriasis is the most frequent of skin diseases. As a rule, it does not begin before the sixth year, nor after the fortieth year* It seems to be somewhat more frequent in men than in women. 342 INFLAMMATIONS OF THE SKIN. According to a few statements which have been made, psoriasis is con- tagious. Lang recently found a fungus (epidermidophyton) in this disease, so that h classes it among the dermatomycoses. Very few writers have succeeded in veri fying Lang’s statements. The following is a brief description of his method and results. If the scales upon a patch of psoriasis are carefully removed, a thin, transpar- ent, little membrane is brought into view. This is quickly removed with a pait Fig. 138. Fungus threads from the psoriasis membrane. After Lang. of forceps, and placed in a five-per-cent solution of potash. After the scales have swollen and become transparent (at the end of a few minutes), we will find be- tween them, round, oval, and elongated spores, 0.006 to 0.008 mm. broad and twice as long (vide Fig. 137). If the membrane is placed in a solution of potash which has been mixed with equal parts of glycerin and water, the spores will de- velop, at the end of two or three hours, into long, rarely branched threads, whose free end is either rounded or swollen (vide Fig. 138). III. Anatomical Changes.—Since some of the lesions disappear after death, sections must be taken from the living subject. In the cutis are observed elongation and increased breadth of the pa- INFLAMMATIONS OF THE SKIN. 343 pillse, dilatation and sinuosity of the vessels, profuse emigration of white blood-globules, and accumulation of the latter, particularly upon the outer wall of the vessels. J. Neumann also found the sweat glands filled with round cells. In the rete Malpighii the lowermost palisade-like epi- thelium cells, which are arranged normally in one row, now occupy several rows; the higher epithelium cells have lost their processes, and also present nuclear proliferation and fission. IV. Diagnosis.—The disease possibly may be mistaken for eczema squamosum, seborrhcea capillitii, pityriasis rubra, pemphigus foliaceus, lichen ruber, lupus erythematosus, lupus exfoliativus, rupia, psoriasis syphilitica, favus, and herpes tonsurans. Eczema squamosum presents marked pruritus, often weeps, and is preceded by the formation of vesicles. Seborrhcea capillitii occurs particularly in the new-born, never extends beyond the border of the hair, and, upon removal of the crusts, a red, bleeding surface is not exposed. Pityriasis rubra is distinguished from psoriasis by its course ; it leads to ma- rasmus and serious general disturbances. This is also true of pemphigus folia- ceus, in which, moreover, vesicles are formed. In lichen ruber, the efflorescences are smaller, covered with fewer scales, and, as a rule, are arranged in contiguous groups. Lupus erythematosus develops chiefly on the nose and cheeks; on removal of the scales, their lower surface is found to present prolongations which project into the sebaceous follicles; after recovery from lupus, cicatrices and pigmentations are left over. Lupus exfoliativus produces fewer scales, ancL'on their removal the surface is found reddened, but not bleeding. After removal of a rupia crust, a deep, crater-shaped ulcer appears, with a lardaceous base. Psoriasis syphilitica is attended with a slighter formation of scales, which ad- here more firmly, the base is brownish-red; it is localized on the palms of the hands and soles of the feet, and other evidences of syphilis are present. Favus and herpes tonsurans are recognized with the aid of the microscope by the presence of the characteristic fungi. Y. Prognosis.—The prognosis is almost always good as regards life, but is unfavorable as regards complete recovery, since it is impossible to prevent relapses. YI. Treatment.—Internal treatment should be combined with ex- ternal treatment. We have succeeded in almost every case with the following simple plan. The patient receives: I> Aq. amygdal. amar., Liq. potass, arsenit aa 3 ss. M. D. S. Five drops t. i. d. after meals; the dose is increased by one drop every third day. In addition, the patient should take a daily bath at 30° K. (lasting two hours), in which 3 iij.-vi. of potassium sulphate are dissolved. Im- mediately after the bath, the following ointment is rubbed into the patches with a brush, until the scales are removed as thoroughly as pos- sible. 1)1. Sapo. virid., Picis liquidae, Lact. sulphur., Spirit, vini dilut aa 3 i. M. D. vS. To be used externally. 344 inflammations of the skin. We will mention a few other remedies which have been employed in this dis- ease. a, Internal remedies. Iodine and mercurial preparations, carbolic acid, salicylic acid, tar preparations, copaiba, carbonate of ammonia, phosphorus, etc.; also exclusive meat diet, b, External remedies. Subcutaneous injections of arsenical preparations, douches, hydropathic packs, permanent baths, cures n Aix, Kreuznach, Pfaffers, etc., preparations of tar, iodine, and sulphur, cauteri- zation with acetic acid or corrosive sublimate, chrysarobiu ( 3 i j, ; vaseliu 3 x.), pyrogallic acid ( 3 i. : x.), thymol, iodoform. 2. Pityriasis Rubra. I. Symptoms.—This is a very rare disease. The skin reddens and desqua- mates without any previous effloresence. Later the skin grows thinner, is tense, and appears to have become too small for the body. The face assumes a stiff, mask-like expression, the limbs are in a forced position, midway between flexion and extension. Rhagades form here and there. Alopecia often develops at a later period. The disease sometimes Rtarts from a certain part, sometimes it is diffuse from the beginning;at all events, it tends to spread over the entire body. The disease is almost always chronic, and may last several years. Gangrene of certain parts has been observed. At the same time marasmus sets in, and terminates fatally. II. Diagnosis.—It is distinguished from squamous eczema by the absence of moisture of the skin and of marked itching. In lichen ruber, the formation of scales i3 attended with the development of nodules; lupus erythematosus occurs chiefly in the face. III. Anatomical Changes.—Hebra found, at the onset, profuse infiltration of the upper layers of the cutis with round cells, later atrophy of the epidermis and papillary body, atrophy of the sweat glands and sebaceous glands, and sclerosis of the cutis tissue. Phthisical changes have been observed in the lungs and intestines. IV. Etiology.—The causes and nature of the disease are unknown. V. PROGNOSIS.—The prognosis was formerly regarded as absolutely fatal, but some cases of recovery have been recently reported. VI. Treatment.—Internal administration of ai’senic or carbolic acid, exter- nally baths and fatty inunctions. f. Papular Inflammations of tiie Skin. Dermatitides Papulos-e. 1. Prurigo. I. Symptoms.—Prurigo is characterized by the appearance of scat- tered papules, from the size of a pin's head to that of a hempseed, which either possess the normal color of the skin, or are pale red. On punc- ture, they discharge a clear serous fluid. The disease is chronic, and is attended with intolerable itching. The first symptoms often appear in childhood, generally towards the end of the first year, and may then last for the remainder of life. They often appear as an obstinate, relapsing urticaria. The characteristic prurigo papules gradually develop under the epidermis, so that they are better felt than seen. Later the papules project more and more above the level of the skin. They appear first and most abundantly upon the legs, then upon the thighs, forearms, arms, and trunk. A few also appear upon the face. Upon the scalp we only find vigorous branny desquamation of the skin, and dryness and falling out of the hairs. The popliteal space, elbows, axillae, palms of the hands, soles of the feet, and genitalia always escape. The intolerable itching is most severe at night, especially when the patients are warm in bed. Secondary efflorescences develop as the re- sult of the mechanical irritation by scratching. The apex of the inflammations of the skin. 345 scratched papule acquires a bloody crust, or is converted into a pustule. Pustules, eczema, and urticaria also develop in places which are free from prurigo papules. The lymphatic glands become swollen, particu- larly in the groins, where they may form masses as large as a pigeon's egg. These are somewhat characteristic of the disease, and are known as prurigo buboes. The glands rarely suppurate. After the disease has lasted a long time, the skin assumes a brown color (melasma), and feels infiltrated and thickened. The furrows of the skin are not infrequently unusually deep. The skin is generally dry, produces but little perspira- tion, and is often covered with scales. Warty elevations are sometimes found upon the legs, and the muscular system may undergo considera- ble emaciation. The general condition may suffer from disturbed sleep. Eemissions and exacerbations are frequent. The symptoms increase during the winter, and may disappear almost entirely during the sum- mer. II. Etiology.—The causes of the disease are unknown. Heredity seems to exert an influence in some cases, but since prurigo does not de- velop before the end of the first year, we must assume that merely the predisposition of the skin to prurigo is developed. It has been attributed to highly spiced diet, scrofula, rickets and phthisis (?). It is more fre- quent in males than in females, and also among the children of the poorer classes. III. Anatomical Changes.—Hebra attached chief importance to the collection of a fluid substance between the cells of the rete Malpig- hii, which served to nourish the cells, but was secreted in excessive amounts. J. Neumann noticed cell proliferation in the papillae, and swelling of these bodies by inflammatory, purely serous exudation. Derby states that each papule is perforated by a hair. He also de- scribed hypertrophy of the arrector pili, increased development of the external root sheath and bulbous involutions of the hair follicles. These changes are of minor importance. Gay noticed dilatation of the lymph spaces in the cutis. The following changes have also been described: Proliferation of the cells of the rete Malpighii, proliferating processes in the sweat glands, in old cases atrophy of the sebaceous and sweat glands, and abnormal deposit of pigment in the layers of the cutis. Schwimmer claims that prurigo is a trophoneurosis. In our opinion, however, the pruritus is secondary to the development of the prurigo papules. IV. Diagnosis.—The diagnosis is easy, if we bear in mind the char- acteristic shape and distribution of the efflorescences. We must be careful to avoid regarding secondary cutaneous changes as the primary lesion. V. Prognosis.—The disease is capable of recovery if treated early. Permanent recovery is not infrequent in children. But if the disease has lasted more than four years, complete recovery will hardly ever be obtained. Vr. Treatment.—Much cannot be expected from the use of inter- nal remedies. Arsenic and carbolic acid have been particularly recom- mended. The general condition should also be treated. The following is the simplest and most certain plan of local treat- ment: Every night the patient is rubbed with green soap; in the morn- ing he takes a bath (for two hours) at 30° It., § iij.-vi. of potassium sulphate being added to each bath. Then the entire skin is anointed 346 inflammations of the skin. with carbol-vaseline (3 : 50). This plan must be continued for a long time, even after the papuler have disappeared. Good effects have been obtained from subcutaneous injections of pilocarpine or carbolic acid. The treatment recommended for psoriasis is also much in vogue for prurigo. 2. Lichen Scrophulosornm. I. Symptoms.—In this disease are found papules about the size of a pin’s head, of a pale red, livid red or brown-red color, with a little scale upon the apices. If the latter is removed with the nail, the mouth of a hair follicle appears, the vicinity of which is slightly raised like a wall. These papules are generally arranged in round groups, rarely in circular lines. They itch slightly or not at all, and disappear spontaneously after branny desquamation. The disease is chronic, and often lasts for years. The first efflorescences appear upon the back, chest, and abdomen, later upon the limbs, particularly the flexor surfaces; finally, the face and scalp may be affected. In advanced cases, large areas maybe in- volved. Acne and eczema may also be present, the latter particularly on the genitalia. II. Etiology.—The disease is most common in children, especially in boys. It is rare beyond the age of 20 years. The patients generally present the evidences of scrofula. The skin is often very pale, and is peculiarly fatty to the feel. In exceptional cases, phthisical changes are noticed. III. Anatomical Changes.—Kaposi found infiltration of the cutis with round cells in the immediate vicinity-of the hair follicle and its se- baceous glands, and in the papillae immediately adjacent to the follicle, round cells in the follicles themselves, and accumulation of epidermis cells in the mouth of the hair follicle. IY. Diagnosis.—The diagnosis is easy. In squamous eczema, there is severe itching, and many papules are converted into vesicles and pus- tules. Lichen syphiliticus affects chiefly the flexor surfaces of the limbs, and the papules are often as large as a pea. Y. Prognosis.—The prognosis is good, since there is no danger to life and the disease is not incurable. VI. Treatment.—This consists of the internal and external adminis- tration of cod-liver oil. one tablespoonful internally morning and even- ing, inunctions externally t. i. d., and the parts then covered with flan- nel. 3. Lichen Ruber. I. Symptoms.—This extremely rare disease appears as scattered pap- ules, as large as a pin’s head, of a pale red or brownish-red color; they are sometimes pointed and covered with thin scales, sometimes flat, and appear umbilicated. Both forms are very often combined. The first papules appear on the chest, abdomen, genitalia, or flexor surfaces of the limbs. New ones gradually appear and finally they are so closely aggregated as to come in contact. In the course of years, al- most the entire integument may be attacked. The scalp, axillae, and mons veneris are generally unaffected, the hairs of other parts fall out. Peripheral circles of papules sometimes sprout up around central INFLAMMATIONS of the skin. 347 ones, or the latter disappear, leaving behind pigmentation and cicatri- cial changes, while the process extends at the periphery. in old cases, the palms of the hands and soles of the feet are covered with thickened, fissured epidermis, the nails are also thickened, brittle, brownish, or thinned. The papules have also been observed on the mu- cous membrane of the mouth. The red, scaly skin is often diffusely in- filtrated, and painful, bleeding rhagades are formed; the limbs are kept semi-flexed, and movement is painful. If the process is left to itself, increasing marasmus sets in, and finally death. In some cases sleep is disturbed by pruritus, and this accelerates the collapse. II. Etiology.—The disease is more frequent in men. It develops mainly between the ages of ten and forty years, rarely earlier, though Kaposi reports a case in a child of eight months. It causes are un- known. III. Anatomical Changes.—Examination of the skin shows noth- ing which has not also been observed in other chronic skin diseases. We may mention infiltration of the papillae with round cells ; obliteration, sometimes dilatation of blood-vessels in the papillae ; occasionally colloid degeneration of the walls of the vessels, in umbilicated papules, the papillae corresponding to the umbilication are atrophied; the external root sheath of the hair follicles is unusually well developed; hypertrophy of the arrectores pili; fibrillation of the lower end of the hairs; increase of the cells in the rete Malpighii and epidermis. IV. Diagnosis.—The diagnosis is generally easy. The disease is distinguished from papular and squamous eczema by the fact that vesi- cles and pustules have generally been present in the latter affections. Psoriasis forms thicker scales, and the patches increase peripherally, while lichen papules always retain the same size. Lichen ruber is dis- tinguished from lichen scrophulosorum by the absence of a tubercular etiology, and by the different distribution of the eruption. V. Prognosis, Treatment.—The prognosis is good, since Hebra found that successful results are obtained by the internal or subcuta- neous administration of arsenic In marantic individuals, good diet and iron preparations are important. If there is violent itching, the skin should be anointed night and morning with carbol-vaseline (3 : 30). In- stead of arsenic, Unna recently recommended the following ointment: Unguent, zinc, benzoat., 3 x., Acid, carbolic., 3 iij., Hydrarg. bichlo- rid., gr. iv. M. D. S. To be rubbed into the skin morning and evening. The patient then remains between woollen blankets. 348 SECRETORY ANOMALIES OF THE SKIN. PART II. SECRETORY ANOMALIES OF THE SKIN. A. Secretory Anomalies of the Sweat Glands. I. Increased Secretion of Sweat. Hyperhidrosis. (.Epliidrosis.) Unusually profuse production of sweat may affect the entire integu- ment (hyperhidrosis universalis) or be confined to certain regions (hy- perhidrosis localis). Hyperhidrosis universalis is often observed in well-nourished, obese individuals who perspire profusely on slight exertion. This perspiration is most abundant in inclosed portions of the body (axillae, anal groove, etc.). The excessive perspiration often produces further cuta- neous changes. At first sudamina develop (vide page 330). In other cases, the skin appears macerated and slightly reddened, especially where two surfaces rub against one another (chafing, intertrigo). In epileptics, profuse diaphoresis has sometimes been observed, either in the place of the epileptic attacks, or shortly preceding them. We will not consider the diaphoresis observed during the course of internal diseases, since this is a symptom of the diseases in question. Hyperhidrosis localis may be unilateral or circumscribed still more narrowly. Unilateral hyperhidrosis has been observed in the course of various nervous diseases (idiocy, Basedow’s disease, asthma). Pikroffsky re- ports a case in which the ingestion of food always produced sweating on the right side of the body. In Kaposi’s case, it occurred upon the face on one side, and the trunk and limbs on the opposite side. In some cases, unilateral sweating is confined to the face. This has been observed in general paralysis of the insane, in phthisis with large cavities (the sweating side corresponded to the side of the cavity). In Donder’s case, it always occurred during mastication. In one case, Riehl found that the superior ganglion of the cervical sympathetic on the affected side was swollen and reddened, infiltrated with round cells, the vessels distended, the ganglion cells and nerve fibres atrophied, and containing a punctate hemorrhage. Hyperhidrosis localis is sometimes very circumscribed. In one case, diaphoresis occurred, at certain hours of the day, upon the dorsal surface of the right hand and forearm. This was relieved by quinine. Excessive sweating in the axillae not infrequently stains the clothing of a yellowish-red color; in addition it produces a disagreeable odor of sweat. It may be followed by intertrigo and eczematous changes. The parts should be washed morning and evening with: R Acid, tannic gr. vi. Spirit, vin. dilut 3 iij. and then dusted with: SECRETORY ANOMALIES OF THE SKIN. 349 3 Acid, salicylic., Flor. zinci aa 3 v. Talci praeparat 3 x. M. D. S. Dusting powder. In hyperhidrosis of the palms of the hands, the parts are moist, often clammy and cyanotic. The patients leave moist traces upon everything they touch. If the hyperhidrosis is persistent, the epidermis, in places, is raised in vesicles, or it has a dull white color, and scales in more or less extensive shreds. This is observed relatively often in chlorotic females who suffer from menstrual disturbances. It often ceases spon- taneously, but relapses may occur. Hyperhidrosis of the feet is still more annoying to the patient. Marked maceration and shedding of the epidermis produce violent pain and may render walking impossible. The disagreeable odor (bromhidrosis) is so pronounced that we can gen- erally recognize the disease by the sense of smell. Hebra showed that the bad odor results from the decomposition of the sweat which has been absorbed by the stockings. In slight grades, daily foot baths, frequent change of stockings, and the dairty application of the above-mentioned dusting powder, especially between the toes and stocking, will suffice. In advanced cases, we may order unguent, diachylon Hebrae, which is smeared thickly on a piece of linen in which the foot is placed. Small pieces are inserted between the toes. The ointment is renewed every twelve hours. In six to twelve days the macerated epidermis is cast off, and replaced by healthy epider- mis. The dusting powder should then be continued for a little while, 2. Diminished Secretion of Sweat. Anhidrosis (Hypliidrosis). Anhidrosis almost always occurs as a symptom of other diseases, such as diabetes mellitus, diabetes insipidus, chronic interstitial nephritis, cancer, cachexia in general. Partial anhidrosis may also be secondary to other skin diseases, over the site of disease (eczema, prurigo, psoriasis, lichen, ichthyosis). Finally, it may be the result of nervous influences. According to Strauss, it occurs on the paralyzed side in peripheral facial paralysis, but not in central paralysis. In paralyzed parts of the body, hyperhidrosis is sometimes noticed, sometimes anhidrosis, according to the occurrence of paralysis or irritation of the several nerve fibres which run along the peripheral nerves. 3. Changes in the Quality of the Sweat. Parhidrosis (Osmhidrosis, s. Bromhidrosis, Chromhidrosis, Hcemathidrosis, Urhulrosis). Changes in the quality of the sweat may affect its odor, color, or chemical constitution. a. An unusual odor of the sweat is known as osmhidrosis or brom- hidrosis. In some cases, a bad odor is observed immediately after the secretion of the sweat; in others, it is the result of decomposition of the secretion. Frigerio recently reported two cases in which the sweat of idiots smelled like musk. Szokalski healed a nervous lady with hydro- pathic packs, and for two weeks the perspiration had the odor of violets. An urinous odor of the sweat may be detected in uraemic cases. 350 SECRETORY ANOMALIES OF TIIE SKIN. b. Abnormal color of the perspiration is known as chromhidrosis. Yellow, blue, green, black, and bloody sweat has been observed. In jaundice the underclothing is not infrequently stained yellow by the perspiration. A number of cases of blue perspiration (cvanhidrosis) have been re- ported. In I860 Foote collected thirty-eight cases. It generally occurred in women, who were often anaemic and suffered from uterine diseases. The abnormal production of sweat was localized, most frequently on the lower lids, most rarely on the back of the hand, never upon the posterior surface of the body. Ipavic found shapeless masses of pigment in the secretion. The blue pigment has been found in a number of cases to be allied to indican. In Bergmann’s case the blue color was produced by fungi. Bloody sweat (hEemathidrosis) does not belong properly in this cate- gory. It is the result of unusual fragility of the finer cutaneous vessels, the blood being extravasated into the immediate vicinity of the sudori- parous glands or into their lumen. This condition is often simulated. c. Among the anomalies in the chemical constitution of the sweat urhidrosis may be briefly mentioned. In this condition urea is excreted upon the integument in the form of white scales. This has ob- served in suppression of urine in cholera or nephritis, and is often asso- ciated with uraemia (vide Yol. II., page 261). B. Anomalies in the Secretion of the Sebaceous Glands. 1. Increased Sebaceous Secretion. Seborrhcea. Two forms of this condition are distinguished, viz., seborrhoea oleosa and seborrhoea sicca. In the former, masses of fat are deposited on the surface of the skin, and either impart to it an unusually fatty gloss, or remain as thick, fatty scales and crusts. In seborrhoea sicca, there is excessive desquamation of thin scales and epidermis, mixed with drops of fat. Both forms may occur in the same individual. The dis- ease may be general or local. a. Seborrhoea of the scalp is most frequent during the first year of life. The scalp is covered more or less extensively with fatty scales or with yellowish-gray, greenish-gray, or blackish crusts, which may attain a thickness of several millimetres. The dark color is the result of ad- mixture with dirt. These deposits never extend beyond the scalp. They often have a rancid odor, are peculiarly fatty to the feel, and are composed of drops of fat mixed with epidermis cells. If carefully removed, the underlying skin is found to be pale and unchanged. If the masses of sebum decompose and become irritating, the underlying skin reddens or it becomes eczematous and moist. The hairs are apt to come out while removing the masses of sebum. If the condition is left untreated, the profuse secretion of sebum ceases in the second or third year, the accumulated masses of fat become dryer and more brittle, and are cast off by the growing hairs. But the condition should be relieved as quickly as possible. If the deposits are thin, the affected parts should be rubbed vigorously every morning and evening with ol. olivas, ol. amygdal., or other fats, and the scalp then washed thoroughly with green soap. If there is a thick accumula- tion of fatty masses, they should be rubbed with oil every two hours, and a flannel cap placed on the head; when the crusts have been re- SECEETOEY ANOMALIES OF THE SKIN. 351 moved, at the end of twelve to twenty-four hours, the parts should again be washed with soap. To prevent a relapse, the washing and inunc tions should be continued morning and evening for some time. in adults, the disease is rarely so severe as in infants. It occurs: much more frequently as seborrhcea sicca. There is profuse desquama- tion of white, fat-containing epidermis scales, which make the hair appear unclean, and often covers the coat collar. This condition is known as pityriasis capillitii. it often gives rise to defluvium capillo- rum, and finally to alopecia. After recovery from the disease, the hairs are generally restored. In some cases, no cause can be ascertained; in others, the condition is preceded by. inflammatory diseases of the skin (eczema, small-pox); in still others by constitutional diseases (chlorosis, syphilis). The treatment includes general and local measures. Iron, iodine, and mercury must be employed according to the causal indication. At night, the scalp should be rubbed with alcohol, in the morning with oil. b. Seborrhcea of the face is most marked on the forehead, temples, nose, and chin. The parts have an unusually fatty gloss, the skin feels fatty; in rare cases, the fat collects in scales and crusts. The mouths of the sebaceous glands are unusually wide, and contain a more or less pro- jecting mass of fat. Dust is apt to settle upon them, giving the patients a speckled, dirty appearance. In seborrhoea of the nose, the cutaneous vessels situated between the openings of the sebaceous ducts are injected and sinuous. The condi- tion is not infrequently present only at the period of puberty, and is especially severe in brunettes. Treatment is similar to that of seborrhoea of the scalp. c. Seborrhcea of the genitals i3 especially apt to develop in males who suffer from phimosis. The smegma collects at first in the coronary sul- cus, but may finally encrust the entire glans. In hot weather or after exercise, the secretion is apt to decompose, produces balanitis and balano-posthitis, and may finally give rise to excoriations and con- clylomata. The patients often suffer from herpes progenitalis, and, in children, the violent itching may result in onanism. If the smegma stagnates for a long time, preputial calculi may form. The treatment consists of relief of the phimosis by gradual disten- tion or operation, removal of the smegma by oily inunctions, and pre- vention of its reaccumulation by careful washing with soap, and intro- duction of charpie smeared with zinc ointment or with tannin and glycerin into the preputial sac. Seborrhcea genitalium is also observed in females, especially in little girls. The sebum accumulates in the vicinity of the clitoris and be- tween the labia majora and minora. cl. General seborrhcea occurs in adults as the result of chronic wasting diseases.. The entire integument is covered with fine, fat-con- taining scales. This condition is termed pityriasis. The patients should be nourished as generously as possible, and should take lukewarm baths followed by fatty inunctions. In the new-born, the production of sebum, which forms the vernix caseosa, sometimes continues for a few days. The little ones look as if covered by a thin, shiny membrane, which contains numerous fissures (ichthyosis sebacea). This may be associated with refusal to take nourishment, and unusually low bodily temperature, so that the children cjje in collapse. If they refuse to nurse, they should be fed with the 352 SECRETORY ANOMALIES OF THE SKIN. spoon, warming flasks applied to the body, a protracted warm bath (34° R.) given three or four times a day, and the entire integument rubbed with oil. 2. Diminution of the Sebaceous Secretion. Asteatosis. (Oligosteatosis.) Diminution of the sebaceous secretion may be congenital or acquired. The skin is unusually dry, has a tendency to form painful and often bleeding rhagades, desquamates more or less actively, and has a rough appearance. * This condition may be congenital, either alone or in combination with congenital diseases of the skin, for example, prurigo and ichthyosis. The acquired form may also be associated with certain skin diseases, such as psoriasis, lichen ruber, etc. It may be confined to the back of the hands and forearms in individuals who wash themselves frequently, especially if the water contains a good deal of lime or irritating soap. This is noticed particularly in the winter. The treatment consists of inunctions of vaseline or cold cream. Glycerin, which is such a favorite remedy among the laity, not infrequently aggravates the disease by ex- tracting water from the tissues. The patients should wash less fre- quently and only in lukewarm water, and should wear gloves in winter. 3. Anomalies in the Excretion of Sebum. Par asteatosis. a. Comedo. I. Symptoms.—Comedos are little black specks which correspond to the excretory ducts of the sebaceous glands, and in places are slightly elevated above the level of the skin. On pressure, the black speck is extruded, and is often followed by a yellow, spiral, thread-like structure. The latter consists of sebum, and, under the microscope, is found to be composed of fat and fatty epidermis cells, occasionally of cholestearin crystals. In many cases we also find downy hairs and acarus follicu- lorum. Comedos develop most abundantly in those parts which are rich in sebaceous glands (forehead, nose, lips, chest, and back). They may occur alone, or are associated with seborrhcea. They are sometimes so numerous that the skin presents a black-speckled appearance, or in places they are so closely aggregated as to form wart-like prominences. They may‘also give rise to inflammation of the sebaceous follicles (acne). Kuestner calls attention to the constant presence of comedos on the tip of the nose in the new-born. II. Etiology.—The causes of the retention of the sebum cannot always be ascertained. In some cases it is the result of mechanical occlusion of the excretory duct, as is observed in workers in tar or petro- leum, or in individuals who, despite the fact that their integument is fatty, rarely wash the face with soap. In others, it is the result of the production of unusually stiff sebum. Comedos often develop in anaemic and exhausted individuals, very often at the period of puberty. III. Treatment.—The treatment consists of mechanical removal of the comedo by means of a watch key, etc. To increase the tonus of the dilated follicles, we may apply irritating washes, for example, Hebra’s HYPERTROPHY OF THE SKIN. 353 green soap (vide page 336). This should be done at night. General treatment must be adopted in chlorotic, scrofulous, or anaemic indi- viduals. b. Milium. 1. Milium forms light-yellow or grayish-white papules, varying from the size of a millet seed to that of a pin’s head, and which often are slightly elevated above the surface of the skin. Upon slitting the epi- dermis and exercising pressure, a grayish-white papule appears. Under the microscope this is found to be composed of lamellae of epidermis cells and a fat-containing nucleus. This is the result of obliteration of the excretory duct of a sebaceous gland, so that an accumulation of epider- mis cells takes place in a lobule, or in the entire gland, and dilates it. The epidermis passes over the papule, so that the former must be de- stroyed before the contents of the latter are laid bare. Milium is distin- guished from comedos by the fact that the latter occupy the excretory duct of the sebaceous glands. Calcification of milium has been observed in some cases. Wagner reported a case of colloid milium, i. e., the papules were the result of colloid degeneration of the epidermis cells. The disease is most frequent upon the integument of the eyelids and adjacent parts of the cheeks and forehead, next upon the lips, the penis, and inner surface of the labia minora. They are sometimes so numerous upon the corona of the glans penis as to form a wreath. 2. The disease is often noticed at the periphery of cutaneous cica- trices, for example, those produced by burns, syphilis, or lupus. It is also frequent in parts which have been the site of previous skin diseases, for example, pemphigus. In some cases it seems to be the result of a primary anomaly of secretion, inasmuch as epidermis cells are deposited in abundance within the lobules of the gland, but do not undergo fatty degeneration and remain within the lobule. Kuestner observed an abundant development of milium in children born prematurely. If they are very numerous in the face, the epidermis should be nicked with a fine bistoury, and the contents removed by pressure. PART III. HYPERTROPHY OF THE SKIN. A. Hypertrophy of the Cutaneous Pighent. 1. Ncevus. Naevi are congenital accumulations of pigment in the skin. They form brownish or brownish-black, flat, and smooth patches (naevi spili), or they are uneven and warty (naevi verrucosi), or pedunculated (naevi mollusciformes), or covered with bristling, thick dark hairs (naevi pilosi). The size and number of the naevi are extremely variable. They are sometimes so numerous that the skin assumes a speckled appearance. They are situated not infrequently along the course of certain nerves, and, like herpes zoster, only upon one side of the body (nerve naevi). 354 HYPERTROPHY OF THE SKIN. The formation of the pigment has been regarded, accordingly, as the result of trophic disturbances, and this view seems to be favored by the fact that other unmistakable nervous symptoms are sometimes notice- able. Ngevi generally present a tendency to further growth. In later years they are occasionally the site of development of sarcoma or cancer, and may be the source of secondary infection of other organs. Anatom- ical examinations have shown that there is not alone an accumulation of pigment in the lowermost cell layer of the rete Malpighii, but that there is sometimes an abnormal development of pigment in the cutis and its obliterated vessels. The question of removal by operation comes up only with regard to smaller naevi. 2. Chloasma. Chloasma is the term applied to an acquired development of pigment in the skin, and is either a primary (idiopathic) or symptomatic skin disease. Idiopathic chloasma includes freckles (ephelides, lentigines). These form light-brown patches which may attain the size of a lentil, and are especially numerous in the face (nose and adjacent parts of the cheeks). But since they are also found on parts which are constantly covered with clothing, for example, the flexor surfaces of the arms and the genitalia, it is evident that the action of the rays of the sun is not their sole cause. Individuals with a delicate complexion are especially apt to be affected with freckles. They are most marked in the spring and summer, and grow pale or even disappear in winter. They are rare before the age of six years or beyond the fortieth year. They may be removed temporarily by remedies which produce an abundant desquamation of epidermis: soap inunctions, tincture of iodine, corrosive sublimate (gr. viij. : §ij.). In many individuals, they disappear spontaneously at the completion of puberty. The term traumatic chloasma is applied to those pigmentations which follow mechanical irritation of the skin. It is often observed in places upon which pressure has been exercised for a long time by bandages, etc., also after violent and repeated scratching (prurigo, eczema, scabies, pediculi). As the effect of clothes lice, tramps sometimes acquire such a dark color of the skin as to look like mulattoes (melasmas, melano- derma, nigrities). Chloasma caloricum is the term applied to the dark color of the skin produced in many individuals (often within a few hours) by expo- sure to the sun and air. Toxic chloasma may be produced by the application of irritating sub- stances to the skm. The application of a mustard plaster or fly blister very often leaves a brown discoloration of the integument. Among the symptomatic forms of the affection, chloasma uterinum deserves special mention. It forms brownish-yellow patches which, un- like the somewhat similar patches of pityriasis versicolor, are not shin- ing, do not desquamate, and do not contain the fungus (mikrosporon furfur) peculiar to pityriasis. It is observed in women who menstruate irregularly, or suffer from diseases of the uterus and ovaries. In many women it occurs during pregnancy (chloasma gravidarum). It generally disappears at the menopause. The forehead, cheeks, lips, and chin are its most frequent sites. Chloasma cachecticorum is observed, not infrequently, in marantic HYPERTROPHY OF THE SKIN. 355 individuals (malarial cachexia, marasmus of syphilis, cancer, pulmonary phthisis). Pigmentations are not infrequently left over in places which have been the site of chronic skin diseases. B. Hypertrophy of the Epidermis. Keratosis. Cutaneous changes which depend chiefly on hypertrophic conditions of the stratum corneum are known as keratoses. They may either exist alone or be associated with hypertrophy of the papillary body. Among the keratoses which are confined to the stratum corneum, are a series of cutaneous changes which are so frequent that they merely require bare mention. These include callosities (tyloma), which are gen- erally the result of frequently recurring pressure; corns, which are one variety of cutaneous callosity, and horns (cornua cuta-nea). The keratoses, in which the papillary body is affected, include warts, condyloma acuminatum, and ichthyosis. The latter alone possesses medi- cal interest. Ichthyosis. I. Symptoms axd Diagnosis.—Ichthyosis is a chronic, usually con- genital disease, in which more or less thick deposits of epidermis form upon the skin. In the mildest grades, the skin is covered by irregularly formed plates of epidermis, which are bounded by deep furrows. At the same time, the skin feels peculiarly rough and dry, and presents a great tendency to desquamation of the most superficial epidermis layers (ichthyosis sim- plex). If the central portions of the individual fields of epidermis are depressed, while the edges are slightly elevated, it is known as ichthyosis scutelata. In some cases the scales, particularly at the periphery, have a mother-of-pearl gloss. In many cases, they assume a greenish or greenish-gray color. The highest grade of development of the disease is reached in ichthyosis cornea and ichthyosis hystria. In the former, the scales of epidermis are as hard as horn, thick, curved; in the latter, they form prickle-like prolongations and prominences. As a matter of course, such changes produce great deformity, particularly since the nodules are not infrequently almost black. Various forms of ichthyosis are sometimes observed in the same in- dividual. The condition may be general or circumscribed; the latter form is less frequent. The first changes generally appear at the end of the first year of life, often not until much later. Cases of congenital ichthyosis have been reported, but good authorities maintain that these cases were really in- stances of seborrhcea. Hereditary influences are not-exerted at once, but some time after birth. The extensor surfaces of the elbows and knees are first affected, later the changes spread more and more, but the flexor surfaces of the joints, axillae, genitals, palms of the hands, and soles of the feet almost always remain intact. In the face and scalp, as a rule, we find merely active desquamation; the hair of the scalp is unusually dry and has a tendency to fall out. The affected parts rarely perspire. Many pa- tients complain of annoying pruritus. Deep, painful rhagades some- times develop, but they rarely penetrate into the cutis. The thick, tense 356 hypertrophy of the skin. epidermis may interfere with the free movement of the joints, so that they are kept almost constantly in a semi-flexed position. In marked ichthyosis of the face, impaired mobility of the lids and ectropium have been observed. Ichthyosis is sometimes associated with other skin diseases (eczema, lupus, measles, small-pox). Mapother has observed cardiac hypertrophy, which he attributes to disturbance of the cutaneous circulation. Increase and diminution of diuresis have been observed in this disease. In one case, W. Boeck de- scribed the development of a cataract and retinitis pigmentosa, with atrophy of the optic nerve. II. Etiology.—Little is known concerning the causes of the disease. In some families it is hereditary, and Nayler was able to trace it back for six generations. Sometimes only one child is attacked; in other cases, the male or the female children. The disease may also skip a generation. According to Gaskoni, ichthyosis often appears in families which suffer from eczema, asthma, phthisis, and gout. It is sometimes acquired, particularly in parts of the body which have been the site of chronic skin diseases. Ichthyosis runs a chronic course, and generally lasts for life. Spon- taneous recovery is exceptional. Exacerbations and remissions are ob- served not infrequently. III. Anatomical Changes.—The anatomical changes affect not alone the epidermis, but also the cutis and subcutaneous cellular tissue. The panniculus adiposus is considerably atrophied, and sometimes dis- appears almost entirely. In the cutis, we find hypertrophy of the pa- pillae, often to a very marked extent. Their vessels are unusually wide, sometimes thickened. The epidermis shows considerable increase of the cornified cell-layers, while the juicy cells of the rete Malpighii are sometimes reduced to a single layer. There is sometimes increase of the nuclei in the epithelium cells of the mucous layer. Some writers mention very distinct development of the prickle layer and an excessive amount of the intercellular substance. Brown and black pigment granules are found within and without the epidermis cells. J. Neu- mann observed atrophy of the sebaceous and sweat-glands. IY. Prognosis.—The prognosis is unfavorable, since the disease can only be relieved temporarily. However, there is no danger to life. V. Treatment.—Active desquamation of the epidermis should be stimulated by inunctions of green soap at night, and a warm bath (30° R.), containing $ viij.-xvi. of soda, every day. This object may also be secured by protracted baths, wearing rubber garments, in- unctions of cod-liver oil or resorcin ointment (3-20 per cent), etc. In- ternal treatment is useless. 0. Hypertrophy of the Hairs. Hirsuties. (Hypertrichosis. Polytrichia. Trichauxis.) In this condition, the hairs develop in abnormal numbers or in ab- normal parts of the body. The condition may be congenital or acquired. The following are the principal forms: HYPERTROPHY OF THE SKIN. 357 a. Children are sometimes born with very long and abundant hair on the scalp, but this almost always drops off after a certain length of time. b. In some cases, the entire body, including the face, is thickly cov- ered with hair. This form is generally hereditary. The development of the teeth in such individuals is usually defective. c. Thick hairs develop not infrequently upon naevi. d. A beard sometimes appears in women, especially in those who are sterile or suffer from menstrual anomalies. e. An abnormal formation of hair sometimes takes place on wounds and inflammations of the skin; also upon paralyzed limbs. /. Some individuals present an unusual development of the hair of the beard and scalp, so that the hairs may flow to the ground. If the abnormal growth is scanty, the hairs may be removed with tweezers, but permanent recovery is only effected by destruction of the hair-follicle. This may be done with caustic pastes and the galvano- cautery. D. IIypeetrophy of the Nails. Onychauxis. The changes produced by hypertrophy of the nail substance belong to the domain of surgery. The nail may increase in thickness, or it becomes unusually long and broad, or both conditions are combined. It is sometimes bent like a horn or claw (onychogryphosis), or is raised from the nail-bed, or gives rise to inflammation of the nail-furrow (paronychia). Hypertrophic nails are usually rough, brittle, uneven, and discolored. This condition may result from local injuries (pressure), or other chronic skin diseases (psoriasis, prurigo, lichen, ichthyosis, etc.) or con- stitutional diseases (chlorosis, syphilis, pulmonary phthisis). E. Tissue Hypertrophy. Sclerema of Adults. {Scleroma. Sclerodermia.) I. Symptoms.—Sclerema appears generally as a chronic change in the skin, which gives rise to a peculiar condensation, hardening, and re- traction of the affected parts. The changes sometimes occur in patches (partial) or they may be dif- fuse. They are found most frequently in the upper half of the body. They may develop imperceptibly so that, at the most, the patient’s at- tention is attracted by a feeling of unusual tension and slight itching, rarely by rheumatoid pains, or they are noticed accidentally; at first the skin is sometimes cedematous, or there may have been preceding erysipe- latous changes. In the beginning, the skin is slightly elevated and contains a doughy infiltration. A striking condensation soon sets in and no longer permits the skin to be raised into folds. This increases more and more, and the skin becomes immovably adherent to the underlying tissues, the perios- teum, sheaths of the tendons, or fasciae of the muscles. The skin may look normal, or it is unusually pale and alabaster colored, or rosy-red to brownish-red. It sometimes contains more or less numerous and large 358 HYPERTROPHY OF THE SKIN. patches of pigment, in other cases certain regions contain an unusually small amount of pigment. The periphery of the sclerotic patches is sometimes very much congested, particularly when the process is ad- vancing peripherally. The longer the disease lasts and the more it advances the more marked become the symptoms in the parts first attacked. The origi- nally elevated portions of the skin become more and more depressed, and form, in a measure, firm, band-like stripes which compress the underly- ing structures. Thus, the chest is sometimes found divided into two parts, or compression of veins produces oedema, etc. The skin may also grow as thin as paper, very red, desquamating, and exquisitely atrophic. The cutaneous functions may remain entirely intact. The produc- tion of sebum and perspiration is usually unchanged. Cutaneous sensi- bility is generally retained, exceptionally it is blunted. The tempera- ture of the skin may be increased, diminished, or normal. Other exanthemata (acne, herpes zoster, variola) develop not infrequently upon the sclerotic parts. Ulceration and gangrene of the skin have also been observed. As a matter of course, the firm sclerotic skin, acting like a narrow, unyielding cuirass, will produce various functional disturbances and pressure effects. In diffuse facial sclerema, the face becomes rigid, desti- tute of folds, incapable of expression, and the patient lives, in a mea- sure, behind a mask. Impaired mobility and ectropium of the lids set in, painful rhagadesform at the mouth, which grows smaller and smaller. Paulicki described a case in which he was compelled to remove several teeth from the upper jaw in order to render possible the introduction of food. The condition grows still more distressing if the mobility of the arms has been almost abolished as the result of sclerotic changes around the elbows, hands, and fingers. Diffuse sclerema in the neck interferes with the movements of the head. Sclerema around the joints of the limbs gives rise to stiffness of the joints, painful rhagades, and changes in position. ' In extensive sclerema of the integument of the thorax the patients complain of a feeling of constriction and anxiety. Sclerema of the penis may render erection impossible. Similar changes are sometimes observed upon the mucous membranes (tongue, fauces, larynx, vagiua). As a rule, the disease is chronic, more rarely it runs an acute course. In the acute cases, the cutaneous changes are generally preceded by oedema of the skin. The sclerotic parts often become soft, while others are being diseased. Death occurs generally with the signs of increasing marasmus. Rossbach described a combination of sclerema and Addi- son’s disease. II. Anatomical Changes.—The anatomical changes appear princi- pally in the cutis and subcutaneous cellular tissue. The epidermis is almost entirely unchanged, with the exception of circumscribed prolife- rations of the rete Malpighii and accumulations of pigment. The cutis shows proliferation and condensation of the connective-tissue elements and elastic fibres. The vessels are narrowed in places. Upon their outer wall, and also in other parts, are observed nest-like accumulations of round cells. There is also an increase of connective tissue in the subcu- taneous cellular tissue, while the adipose tissue proper disappears more and more. Accumulations of round cells are also found in this locality. HYPERTROPHY OF THE SKIN. 359 All other cutaneous changes appear to be secondary; they include ac- cumulation of pigment in the cutis, dilatation of the excretory ducts of the sweat glands, hypertrophy of the smooth muscular fibres, etc. The following lesions have been found in other organs: tubercular changes in the lungs and other viscera, cirrhosis of the liver and kid- neys, cardiac hypertrophy, obliteration of the thoracic duct. III. Etiology.—Little is known concerning the causes of the dis- ease. Among those mentioned are erysipelas, injury, mental excite- ment, and cold. The disease is much more frequent in women than in men. It is exceptional in childhood, and generally develops beyond the age of twenty-five years. Cruse observed one case in which the disease developed a few days after birth. We know as little concerning the nature of the disease as we do concerning its causes. Some authors regard it as an inflammation, others as a disease of the lymphatics ; the majority of writers regard it as a trophoneurosis. Eulenburg recently called attention to the inti- mate relations between scleroderma and facial hemiatrophy. IY. Prognosis.—The prognosis is not very favorable, although a few cases of recovery have been reported. The disease generally advances uninterruptedly, and proves fatal by exhaustion at the end of months or years. V. Treatment.—The best results are obtained by massage, oily inunctions, and the application of emplast. mercuriale. Buelau recently cured a case with sodium salicylate ( 3 i. daily), which he administered for months. Good effects have been obtained from galvanization of the sympathetic and of the affected parts of the skin. Appendix. Sclerema Neonatorum. I. Etiology.—The disease is similar to scleroderma in certain exter- nal appearances, but, anatomically and etiologically, it is entirely different. It generally attacks children during the first few months of life; in rare cases, it begins in the second, or even in the third year ; in a few instances it was congenital. It occurs most frequently in the winter, in the children of the poorer classes. The children were not infrequently born prematurely, or were asphyxiated at birth, and suffered from atelectasis, bronchitis, broncho-pneumonia, gastro-enteritis, or congenital valvular disease. II. Symptoms.—The first changes appear upon the integument of the calves; then it extends to the feet, thighs, abdomen, chest, face, and upper extremities. The skin is at first cedematous and slightly reddened; then it becomes peculiarly rigid, cannot be raised in folds, and is very cold. It is peculiarly smooth, and either slightly reddened or assumes a waxy pallor. Cutaneous sensibility is diminished or abolished. The more the cutaneous changes extend the more the movements of the child are interfered with. If the face is attacked, it acquires a rigid, unchangeable expression, like that of an old man. The mouth can hardly be opened, and infants are unable to nurse. The integument is as cold as that of a frozen corpse. The bodily tempe- rature is constantly lowered (22° C.). The pulse becomes slow and feeble. The second heart sound is hardly audible. The children are generally apathetic, occasionally they moan feebly. 360 atrophy of the skin. Cyanosis and jaundice are observed not infrequently as the result of changes in other organs. Death generally occurs after increasing collapse and progressive diminution of temperature. More rarely the hardened portions of skin soften and recovery ensues, after gradual elevation of the bodily tempe- rature. Improvement is sometimes only temporary. Death may occur in a few hours ; the disease rarely lasts longer than two weeks. III. Anatomical Changes.—The anatomical changes consist mainly of rigidity of the subcutaneous cellular tissue. Demme found fatty degeneration of the heart muscle; Parrot noticed ecchymoses in the mucous membrane of the bladder. Langer has shown that, in the new- born, the fat contains larger amounts of the solid fatty acids (palmitin and stearin acids) than in adults, and is therefore more solid, and melts at a higher temperature. Hence a slight diminution of the bodily temperature will make it firm and rigid. Such a depression of tempe- rature may occur very readily from disturbances in the cutaneous circu- lation, which are apt to develop in the diseases mentioned under the head of Etiology. IV. Prognosis and Treatment.—The prognosis is almost always fatal. Repeated warm baths (half-hour) at 37° C. should be ordered. After the bath, the child is placed in a warm bed, and warming flasks applied to the body. Artificial feeding must be resorted to. Camphor may be injected subcutaneously. Careful massage and faradization of the muscles have also been employed. PART IV. ATROPHY OF THE SKIN, A. Atrophy of tiie Cutaneous Pigment. Leukoderma. {Leukopathia. Achromatia.) A deficiency of cutaneous pigment is shown by the unusually white color of the skin, either in patches or diffusely. "Congenital conditions are known as albinism, acquired conditions as vitiligo. All forms of pigment atrophy are more frequent in negroes. a. General .albinism is shown by the brilliant white color of the skin. The hairs are yellowish-white, and have a silky gloss. The iris and choroid are poor in pigment, and present a red reflex in direct sun- light. Heredity is observed in some cases. b. Partial albinism consists of the formation of patches of light skin. They are most frequent upon the genitalia, scalp, chest, back of the hands and fingers, and are not infrequently situated on symmetrical parts. The hair on the affected parts is also poor in pigment, and has a gray or white color. The patches generally remain stationary, but sometimes they increase gradually in size. c. Vitiligo occurs, in the majority of cases, as an idiopathic change in the integument. Violent excitement, exhausting diseases (typhoid fever), and injury are sometimes mentioned as causes. The symptoms often appear quite suddenly. Naecke states, with regard to" his own ATROPHY OF THE SKIN. 361 case, that he noticed the first changes during a railway trip. As a rule, the disease develops in adults, but cases have been reported at the age of twenty-one days, five and eighteen years respectively. This condition is easily recognized. The skin contains light white patches with very darkly pigmented borders. In one of my cases, a small, dark pigmented spot was found near the middle of each white patch. The patches gradually increase in size, coalesce, and finally occupy the greater part of the body. At certain times the patches may increase rapidly in size and number ; then, again, they may remain stationary for a long time. They often follow the distribution of the cutaneous nerves. The functions of the skin are unchanged. Vitiligo occurs symptomatically in those parts of the skin which have been subjected to injury and ulceration (white color of cutaneous cica- trices). It develops not infrequently in localities which have been sub- ject to protracted pressure by bandages, etc. It may follow various cutaneous eruptions. These conditions are characterized anatomically by deficiency of pig- ment in the lowermost layers of the rete cells. Treatment is powerless. B. Atrophic Changes in the Hairs. 1. Canities. (Poliosis.) Gray hair may be congenital or acquired. It is congenital in albin- ism; in diffuse albinism it affects all the hairs on the body, in partial albinism only those places which are destitute of pigment. In some individuals, small patches of gray hair appear congenitally, indepen- dently of albinism. Senile canities is one of the physiological forms of this condition. It begins, as a rule, in the temples, and then extends to the hair of the scalp and beard. In some families it appears very early. The process is the result of an insufficient supply of pigment by the hair papilla, so that the cortical layers of the hair become poor in pigment. The gray color begins at the hair bulb. At first, the disturbances in the formation of pigment are occasionally temporary, so that the hairs present alternate gray and dark portions. If the hair grows gray independently of age, the condition is known as premature canities. This is observed after typhoid fever, syphilis, erysipelas, etc., if the hairs have fallen out and then grown again. They not infrequently become gray and scanty. The hairs may also grow gray after skin eruptions and cicatrices, and in vitiligo. It is well known that premature grayness may be the result of loose habits and violent emotions. It may also be the result of nerv- ous influences. Thus the hairs sometimes grow gray in hemicrania and neuralgia in the affected nerve tracts. Berger observed it in facial paralysis. The hairs may grow suddenly gray in consequence of violent emo- tions. In one of these cases, Landois and Lohmer observed air-bubbles in the gray hairs, but Kaposi claims that they may also be present in hairs which are not gray. 362 ATROPHY OF THE SKIN. 2. Alopecia and Atrichia. 1. Complete absence of hair may be congenital or acquired. Con- genital atrichia is often associated with absence of the teeth; sometimes the hairs developed at the age of two or three years. Acquired atrichia occurs occasionally after violent emotions. Todd described a case in which a man who was struck by lightning lost all his hair and nails; in another patient the loss of hair followed concussion of the brain. Crisp observed atrichia after malaria, which was associated with anaesthesia of the left side. It is evident, therefore, that this condition is influenced by nervous disturbances. In some cases, however, no cause can be dis- covered. This happened in two of my own cases. The falling out of the hair (defluvium capillorum) generally begins on the scalp, then ex- tends to the beard, eyebrows, eyelids, axillae, and mons veneris, so that the patients are entirely destitute of liair. This sometimes takes place within a few weeks. 2. Falling out of the hair is a physiological process in old age (alope- cia senilis). It is generally preceded by canities. The senile defluvium either begins on the forehead and temples, and gradually extends to the vertex, or the first bald spots appear at the vertex. The bald spots are glossy and often covered with yellow or dirty gray scales of accumulated sebum. Senile defluvium is observed occasionally in the beard, but this is exceptional. The process must be attributed to senile changes in the skin. Koelliker lays stress on obliteration of the vessels in the hair papillae. 3. Falling out of the hairs in earlier years is known as premature alopecia. In some families it is the result of an inherited predisposition; in other cases, of nervous influences (mental strain, worry, grief, liemi- crania, dissipation). Alopecia sometimes follows infectious and constitutional diseases (typhoid fever, febrile infectious diseases in general, pulmonary phthisis, cancer, and marantic conditions). Many women suffer from very marked alopecia after childbed. If the condition is only temporary, a new growth of hair makes its appearance after a while, and is occasionally even more abundant than the preceding growth. Alopecia is sometimes the result of local changes in the scalp. It is associated not infrequently with seborrhoea of the scalp, also with erysip- elas, eczema, prurigo, lupus, psoriasis, lichen, favus, herpes tonsurans, and with variola, sycosis, and syphilides of the scalp. It is incurable if these diseases have given rise to destruction of the hair papillae and follicles. 4. The various forms of alopecia must be treated in almost the same way. At first, the causal conditions must be taken into consideration. Locally we should apply irritating alcoholic lotions, followed bv inunc- tions with oils, for example : IJ Spirit, vin. dilut § iij. Acid, carbolic 3 ss. M. D. S. To be rubbed in morning and evening. B 01. macidis 3 iij. 01. oliv 3 x. M. D. S. To be used as hair oil; or, ATROPHY OF THE SKIN. 363 5 Acid, carbolic 3 ss. Sodii salieylat 3 iss. Vaselin 3 x. M. D. S. To be used as pomade. 3. Alopecia areata s. Celsi. 1. The changes in alopecia areata consist of the complete loss of hair in sharply defined, round spots, which look as if shaved with a razor. The spots gradually increase in extent. If a number of spots are present, adjacent ones often coalesce and produce irregularly-shaped patches. In very advanced cases, there may be almost complete loss of the hair on the head, and the beard may be similarly affected. The cutaneous sensibility of the bare spots is sometimes diminished. The hairs which are situated at the boundaries of the bald spotsare often unusually loose. In some cases the disease is hereditary or it ap- pears in several members of the same family. It lasts for months and years. There is often a sudden remission in the symptoms, followed by the growth of downy hairs, later of normal hairs. 2. The majority of writers attribute the disease to trophoneurotic disturbances. In our opinion some of the cases, at least, are parasitic in their origin. The distribution of the spots, their shape and growth, favor the latter view more than the former. The treatment is the same as that of alopecia. 4. Trichorhexis. 1. The ends of the hairs not infrequently split up. This occurs par- ticularly in long hairs, most frequently in the long hairs of the head in women, more rarely in the long hairs of the male beard. It is probably a nutritive disturbance, perhaps the result of the excessive growth of the hair. The treatment consists in cutting the hair. 2. Trichorhexis nodosa occurs almost exclusively in the hairs of the beard, rarely in those of the eyebrows. In places the hairs form nodular distentions, which are sometimes so numerous as to present a rosary-like appearance. The hairs are situated firmly in their follicles, but readily break spontaneously or upon traction on the individual nodes. In places, they run into spherical prominences and present a gnawed ap- pearance. Under the microscope it is found that the changes begin with a slight spindle-shaped dilatation of the hair. Next the cortical layers in this locality split up, while the medullary parts are often filled with large drops of fat, and press outwards more and more. But in many places the medullary cells are entirely absent. Finally, the cortical fibres of the upper and lower portions of the hair look like two brushes which are pushed into one another. The causes of the disease are unknown. Wolf berg believes that many cases are mechanical in their origin, and result from very strong friction of the hairs in drying them after washing. I recently cured two cases bv advising the parties to discontinue rubbing the head after washing. Whether all cases of trichorhexis are due to this cause, is not settled. 364 neuroses of the skin. 0. Atrophy of the Cutis Tissue. Xeroderma. Kaposi distinguished two forms of this disease, one running its course with, the other without the formation of pigment in the skin. The skin appears peculiarly tense, thin, and shiny, or is covered with small scales ; its sensibility is retained, but it cannot be lifted readily into folds. The movements of the limbs are impeded, and the latter are kept semi-flexed; ectropium and narrowing of the nostrils and mouth become noticeable. In those forms which are associated with the formation of pigment, cancer and sarcoma of the skin developed in a number of cases. The prognosis is unfavorable. PART V. NEUROSES OF THE SKIN. Itching of the Skin. Cutaneous Pruritus. I. Etiology.—Cutaneous itching is an annoying symptom in many skin diseases, but we refer now only to that form which is independent of anatomical changes in the skin, and constitutes an independent func- tional disturbance of the cutaneous sensory nerves. It is observed not infrequently in old age, perhaps as the result of senile processes of invo- lution in the skin. In other cases it is the result of general diseases and local affections of internal organs, such as diabetes mellitus, Bright's dis- ease, jaundice, cancer, diseases of the liver, stomach, uterus, and ovaries. Pruritus is sometimes noticed at a very early stage of cancer. Some women complain of intolerable itching during pregnancy, and, according to Head, this symptom gives rise not infrequently to premature labor if it appears in the second half of pregnancy. Duhring applied the term pruritus hiemalis to those cases which occur in certain individuals on cold autumn and winter days. Pruritus has also been observed after violent excitement. II. Symptoms.—The itching is sometimes felt constantly, sometimes it occurs in paroxysms. In the latter event, it appears particularly at night, or when the patient is very warmly clad. Mental emotion and the dread of an attack may also provoke a seizure. The patients often fall asleep quietly, but are roused during the night by the itching. In many the itching is so violent that they are compelled to avoid society, since they are unable to resist the desire to scratch. The patients are often pale, emaciated, and excited; they may even be driven to insanity and suicide. The scratching leaves traces behind, in the shape of wheals, nodules, eczema, pustules, and excoriations. It is often difficult to decide whether the eruption or the pruritus is primary. III. Prognosis.—The prognosis is favorable only when the causes can be removed. It is unfavorable in the pruritus of old age, Bright’s disease, etc. IV. Treatment.—The etiological indications must first be met. In addition, the skin should be anointed morning and evening with car- bol-vaseline (3 :50), and the following prescription ordered: R Potass. PARASITES OF TIIE SKIN. 365 bromid., 3 iij.; Ext. belladonnae, gr. ivss.; Acid, carbolic., gr. xv.; Pulv. et succ. liq., q. s. ut ft. pil. No. 50. D. S. Two pills to be taken four times a day. A large number of other remedies have been employed in this disease. We may mention the following; Veratrine, chloral hydrate, morphine, etc., douches or baths with soda, corrosive sublimate, etc., applications of ether, alcohol, chloroform. PART VI. PARASITES OF THE SKIN. DERMATOSES PARASITARIA1. A. Animal Parasites. Dermatozoonoses. 1. Itch. Scabies. I. Etiology and Anatomical Changes.—The term itch is ap- plied to an artificial eczema which is partly produced by the direct irrita- tion of the acarus scabiei (sarcoptes hominis), partly by the scratching superinduced by the intolerable pruritus occasioned by the parasite. The acarus scabiei belongs to the family of acarinae and to the class arachnidae. Each patient harbors many more female than male mites. The female is larger than the male (the former is 0.27 to 0.45 mm. long, 0.2 to 0.35 mm. broad; the latter is 0.23 to 0.25 mm. long, 0.16 to 0.20 mm. broad), and, to the naked eye, appears as an irregularly round, gray, slightly transparent little nodule, which is barely visible. Under the microscope, it is found to be shaped somewhat like a crab, and pendulum-like movements of its eight feet and head are often ob- served. It becomes more transparent without undergoing any other changes, if a solution of potash (1 : 3) is added to the preparation. The head is situated at the anterior extremity upon the dorsal sur- face (Fig. 139). It possesses two pairs of mandibles with three segments, and, to the outside of these, two three-jointed palpi provided with bristles. The lateral surfaces of the body present numerous constrictions, and from them project two anterior and two posterior pairs of feet. The anterior pairs have five segments , and at their free end carry a pedun- culated sucking disk (ambulacra); the posterior pair possesses only three segments, and terminate in long bristles. Upon the broad dorsal surface are found numerous furrows and a number of rows of spines, the middle ones being convex anteriorly, the posterior ones convex posteriorly. In addition, there is a row of more or less pointed and long thorns. At the posterior end of the body, they are arranged in four rows, fourteen in number. Upon the ventral surface of the female, the head can readily be traced from the oesophagus. Near the posterior extremity is a fissure which leads to the vagina; more or less developed ova are often visibile in the belly (Fig. 140). At the posterior extremity is found the anal opening, with long bristles on each side. No respiratory organs can be discovered, and the animals can live for a long time when de- prived of air. The female acarus is said to live twenty to sixty days. The male acarus is smaller than the female, and the posterior pair of feet possesses a pedunculated disk, while the third carries a long bristle, as in the female. There are a smaller number of thorns and spines on 366 PARASITES OF THE SKIN. the dorsal surface. Upon the ventral surface is seen the fork-shaped penis, situated in a horseshoe like sheath of chitin (Fig. 141). Probably a single act of sexual intercourse suffices for the production of a large number of viable ova. The latter are said to number about fifty, one or two ova being deposited on a single day. According to Gudden, the male dies six to eight days after intercourse. When a female acarus is impregnated, it bores a passage (acarus burrow) through the stratum corneum into the rete Malpighii. This process can be traced by placing a living acarus on the skin. It bores Fig. 139. Female sexually mature acarus, seen from dorsal surface. Enlarged 300 times. After Kaposi. its way to the deeper layers of the epidermis by aid of the mandibles. The burrow is generally curved or S-shaped; it often contains dirt or coloring matters so that it appears as a punctate, black streak. The animal is situated at the end of the burrow, and not infrequently can be recognized as a light spot with the naked eye, and can often be removed by the introduction of a needle. The length of the burrow is generally 0.5 to 1.0 cm., sometimes as many as 5 cm. The mite may bore a dis- tance of 0.5 mm. in a day. Under the microscope, it is found that the burrow begins at the PARASITES OF THE SKIS. 367 surface of the epidermis with a slight, funnel-shaped dilatation, and also ends in a slight enlargement. The female is always found at the blind extremity of the burrow. As it makes its way into the skin, it leaves ova in its track, the older ones being at the entrance, the young- est ones immediately behind the mother. The number of ova may amount to fifty, but on the average only ten to twenty are present. Mingled with the ova are black granules of faeces. The mite dies after having deposited a sufficient number of ova. The acarus bores deeper and deeper into the skin, because it finds nourishment only in the juicy cells of the rete Malpighii, while the irri- Fio. 140. Female sexually mature acarus, seen from the ventral surface. Enlarged 300 times. After Kaposi. tation which it exercises produces cornification of the surrounding epi- dermis cells, so that it is compelled constantly to seek new layers of epithelium. The irritation is also shown by inflammatory changes in the cutis below the burrow, so that papules, vesicles, and pustules form, and elevate individual portions of the canal. The female acari alone are found in the burrow, the males are gener- ally found in its vicinity in superficial furrows of the epidermis. The ova are oval in shape, 0.16 mm. long and 0.11 mm. broad. The youngest present numerous fission processes, while the older ones contain the rudiments of the head and feet. In six to twelve days the ovum de- velops into a larva. 368 PAKASITES OF THE SKIN. The larva (vide Figs. 143 and 144) breaks through the shell of the ovum, and makes its way through the burrow to the surface of the epi- dermis. According to some writers, it makes its way to the surface through air holes in the burrow. On the average, they attain a length of 0.15 mm. and a breadth of 0.10 mm. Several free larvae are often found in the burrow. After they have reached the surface of the epi- dermis, they burrow a superficial nest in which they develop further. The larvae have only six legs, and present no sexual differences. They moult three times, according to some writers, four times. After the first moult the animal possesses eight legs, after the third moult it is sexually mature. According to Gudden, the first moult takes place from the fourteenth to seventeenth days, and each moult lasts five days. The disease is always the result of the direct conveyance of the larvae, Fig. 141. Male acarus seen from the ventral surface. Enlarged 300 times. After Kaposi. bnt this requires prolonged and intimate contact with patients suffering from itch. It occurs most frequently from sleeping in the same bed, and is rarely the result of contact with the hands. If nurses and moth- ers suffer from itch, the nursling is often infected, because the breast is a favorite site of the mites. It has been erroneously held that the dis- ease cannot be conveyed in the underclothing. Scabies can be conveyed not alone from man to man, but also from animals to man. The parasite has been found in the dog, cat, horse, cow, sheep, rabbit, fox, elephant, etc. Certain trades (shoemakers, smiths, bakers, tanners) present a pre- disposition to the disease, while others, especially cigarmakers, are gen- erally not attacked. The disease is generally more frequent in the winter, and is more common among men than among women. PARASITES OF THE SKIN. 369 II. Symptoms.—The favorite habitats of the itch-mite are those places in which the horny layer of the epidermis is thin, and the cells of the rete Malpighii are juicy. Such places are: the skin between the fin- gers, the flexor surfaces of the wrist and phalangeal joints, the palm of Fig. 142. Acarus burrow, cut from the integument of the loins. Slightly enlarged. After Kaposi. the hand in children and individuals with a delicate integument, the extensor surface of the elbow, the anterior axillary fold, the nipple and umbilicus (particularly in women), the genitalia, the region of the tro- chanters, buttocks, knee, and inner border of the foot. The parasite is 370 PARASITES OF THE SKIN. particularly abundant upon the buttocks in individuals who work in a sitting position, for example, shoemakers. The acarus is also apt to be found in parts which are subjected to prolonged pressure by bandages, etc. Ilebra observed itch burrows upon the mucous membrane of the urethra. The face is generally unaffected, except in nurslings who ac- quire the disease from the mother or nurse. The cutaneous changes produced by the parasites and by scratching are not always identical locally. The itching produced by the acarus is always radiated to parts which remain free from the parasite, and such parts are also scratched by the patients. The scratch efflorescences are found chiefly in parts which are easily reached by the patient’s hand (anterior part of chest and abdomen, inner surface of thighs and knees). Fig. 143. Fig. i44. Larva with six legs, seen from the ventral surface. Larva during second moult. After Kaposi. The efflorescences of scabies are composed of papules, vesicles, pus- tules, crusts, and excoriations. The term scabies norwegica is applied to very severe and inveterate cases, in which thick crusts form, particularly upon the face and scalp. The finger nails are also affected, being discolored, fissured, and thick- ened. After being treated with potash, the nails are found to contain innumerable ova, larvae, and nests of acari (vide Fig. 145). The sole complication is the enlargement of the lymphatic glands in the vicinity of extensive eczema. Suppuration of the buboes has been observed after extensive changes on the penis. The patients generally complain of nothing beyond intolerable itch- ing, particularly at night. This ceases during the course of febrile dis- eases, because the mature acari are killed by the increased bodily tern- PARASITES OF THE SKIN. 371 perature. When the temperature returns to the normal, the ova deposited in the burrows mature, and the symptoms then return. III. Diagnosis.—As a rule, the diagnosis is easy, but is only posi- tive after the finding of the mites, ova, or larvaB. The burrows, which should be looked for between the fingers and upon the penis, are also characteristic, but they may be subjected to such severe scratching that it is hardly possible to find either them or the parasite. Even in such cases the diagnosis is usually easy, if we bear in mind the distribution of the efflorescences. IV. Prognosis.—The prognosis is good, since we are able to kill the parasites, and thus remove the cause of the cutaneous lesions. V. Treatment.—In order to kill the parasites, the following should be rubbed into the skin morning and evening for two successive days: B Balsam. Peruvian., Styracis liquid aa 3 i. M. D. S. To be rubbed in morning and evening, and after the sec- Fig. 145. Crusts from scabies norwegica. ond day a warm bath should be taken daily for three days and the parts washed with soap. In addition, the underclothing and bedding should be changed and boiled, the remainder of the clothing exposed to hot va- por in order to kill any parasites which may be present in these articles. To relieve the eczema produced by the mites, we recommend oily inunctions, bland ointments, or the ordinary remedies in eczema. We may mention some of the other remedies which have been employed in this disease: Carbolic acid, naphthol, naphtholin, ol. bergamottae, sulphur, mer- cury, tar, etc. The following ointments maybe mentioned: Calcis 3vij. Sulphur, citrin 3 xiij. Coque cum. Aq. § xvi. Ad remanent 3 x. D. S. To be rubbed in. 5 Flor. sulphur., 01. cadini aa 3 v. Sapon. virid., Axung. porci .aa 3 x. M. D. S. To be rubbed in. 372 PARASITES OF TIIE SKIN. IJ Styrac. liquid,, Flor. sulphur., Cretee albae aa, 3 iij. Sapon. virid., Axung. porci aa3vi. M. D. S. To be used externally. If the ointments irritate the skin too strongly, they may give rise to albumi- nuria, but this is a rare event. 2. Acarus Folliculorum. (Demodex folliculorum. Mcicrogaster platypus.) In many individuals this parasite is found in the sebaceous and hair follicles, but does not give rise to any other cutaneous changes. It is found with special frequency on the bald head of old people, next upon the forehead, cheeks, nose, upper lip, and external auditory canal. It may be obtained by expressing the con- tents of the follicles, and then placing the latter, with a drop of oil, upon the object glass. As many as twenty have been found in a single follicle. The anatomical (vide Fig. 146) characteristics are: An elongated, cylindrical, worm-shaped animal, 0.08-0.12 mm. long, 0.02 mm. broad; at the anterior end are two man- dibles and two lateral palpi; on the thoracic portion, four pairs of feet; the abdomen is four times as long as the anterior portion. Smaller, six-legged mites have also been described. When conveyed to animals, it is said that severe cutane- ous lesions are produced. 3. Lice. Pediculi. There are three varieties of lice, viz.: Pediculus capitis, pediculus vestimentorum, and pediculus pubis. a. Pediculus capitis (head louse) is found only on the scalp. It is about two mm. long, and has six feet provided with hooks. The females are always more numerous than the males. In fertilization, the female sits upon the male. The former lays about fifty ova, or nits. These adhere to the hairs by means of a sheath of chitin which surrounds the hairs (Fig. 148, a). The oldest ova are those situated next to the scalp. At the end of three to eight days the young escape from the ova, and are fully developed in eighteen to twenty days. Within six weeks, the fe- male may bear six thousand young. An artificial eczema is produced upon the scalp, inasmuch as the lice give rise to pruritus, and the consequent itching mechanically irri- tates the scalp. In combing, the painful spots are spared, so that the lice find favorable conditions for development within the sticky hairs and upon the bleeding skin, which is covered with pustules or crusts. Finally, the hairs form a densely matted mass, containing pus, crusts, and blood, and which often has a nauseous and quite characteristic smell. The ec- zema often extends to the adjacent skin, the neighboring lymphatic glands become swollen, the patients are sleepless on account of the in- Fig. 146. Acarus folli- culorum. Enlarged. PARASITES OF THE SKIK. 373 tolerable itching, lose their appetite, and run down in health. The back of the head is particularly apt to be affected. In making a diagnosis, our attention should be directed to the pres- ence of nits; the nearer they are to the tips of the hairs the older is the disease. Treatment consists of the application to the hair of ung. hydrarg. cinereum, or of the following: B 01. petri italici § iiss. 01. olivae f i. Balsam. Peruvian 3 ij. M. D. S. Externally. Fig. 147. Fig. 148. Fig. 150. Male head louse. En- larged. Fig. 149. Female clothes louse. Enlarged. Hair with chitin sheaths and nits. Enlarged. Crab louse. Enlarged In this manner the lice and nits are killed; they must then be re- moved by disentangling and combing the hair. The chitin sheaths ad- here very firmly to the hair, and are removed more readily by washing with vinegar. b. Pediculus vestimentorum (clothes louse) is the largest variety of louse in man, and attains a length of three to five millimetres (Fig. 149). Its habitat are the folds of clothes, particularly of the shirt. It is found chiefly on the neck and between the shoulder blades, on the sacrum, nates, external surface of the thigh, and immediately above the wrist* 374 PARASITES OF THE SKIN. joint. It deposits its ova in a rosary-like arrangement within the folds of the skin, and rarely leaves its habitat except to seek nourishment on the skin. It is, therefore, rarely found on the skin, but must be sought for in the folds of the underclothing. Its sting produces pruritus and wheals. Individuals who have suffered from body lice for a long time present open wounds, crusts, pustules, excoriations, even furuncles and extensive ulcers. When the efflorescences recover, they are followed at first by white cicatrices, but later they give rise to a deep-brown, even blackish diffuse pigmentation of the skin. The treatment consists in placing the clothes in a vessel heated to 60-65° R., and thus killing the parasites. The eruption is treated in the ordinary way. c. Pediculus pubis (crab louse) is only one millimetre in length (Fig. 150), and is found most frequently in the hair on the genitalia. It may also occur in the hairs of the axillae, limbs, chest, beard, and eyebrows, but not upon the scalp. It is acquired most frequently during coitus, and gives rise to itching and eczema. Treatment similar to that of pediculus capitis. 4. Fleas. Pulices. a. The common flea, pulex irritans, has its habitat in the folds of the underclothing. Its sting produces a minute extravasation of blood, which is surrounded by a hyperaemic zone, which grows pale on pressure. The latter also disappears spontaneously with great rapidity, while the petechia lasts for days. Dirty individuals are often covered with flea bites, and if they are dull and suffer from high fever, difficulty in diag- nosis may arise if typhoid fever is prevalent. Chief importance must be attached to the distribution of the petechiae, and to the presence of roseola around some of them. In individuals with a delicate skin, fleas give rise to wheals. b. Sand flea (pulex penetrans) is found in America, most frequently on sandy beaches. The female bores into the skin, gorges itself with blood, and in two to five days produces inflammatory changes in the skin, which may terminate in ulceration, gangrene, and even erysipelas, lymphangioitis, and tetanus. 5. Bed Bug. Cimex lectularius. The sting of the bed-bug produces wlieals, not infrequently a reflex eruption of urticaria, which is attended with annoying pruritus. As a result of the scratching, the wheals are often excoriated and covered with crusts. The diagnosis is not always easy. 6. Guinea Worm. Filaria Medinensis. This worm is found chiefly on the west coast of Africa. It may at- tain a length of one metre. " Its habitat is the subcutaneous cellular tissue which it probably reaches from within, inasmuch as it is swallowed in the drinking-water and carried by the blood-vessels to the periphery of the body. It gives rise to abscesses of the skin, ulcerations, furuncles, and gangrene, produces fever, and even convulsions. If it projects PAEASITES of the skin. 375 from an open wound, it should be wound around a little stick, and gradually withdrawn in the course of a few hours. 7. Cysticerci of the Shin. Cysticercus cellulosce sabcutaneus. Cysticerci of the skin generally form round or slightly flattened tumors, which are usually as large as a hazelnut. They are painless on pres- sure, have a peculiar, firm, cartilaginous resist- ance, and are movable to a certain extent. They are most apt to be mistaken for swollen lym- phatic glands, and a positive diagnosis can only he made by extirpation. We then find a dull white vesicle which, when cut open, discharges a clear fluid, and, upon its inner surface, con- tains the head which is recognizable externally by a thickening and slight depression of the vesicle. The head often moves vigorously under the microscope (vide Vol. II., Fig. 29). Hundreds of cysticerci are often found in one individual, in other cases only a few. They may gradually grow smaller and disappear, while new parasites sprout up in other localities. Cysticerci are often found in other organs, viz., the brain, eye, and other viscera. In rare cases, the patients also harbor tape- worms. Self-infection is conceivable only in the event that proglottides passed from the intes- tines into the stomach, and were there dissolved by the gastric juice. The treatment consists of extirpation of the tumors, if they are not too numerous. Fig. 151. B. Vegetable Parasites of the Dermatohycoses. 1. Pityriasis versicolor. I. Symptoms and Etiology.—Microsporon furfur, the fungus of pityriasis versicolor, proli- ferates in horny layers of the epidermis, and, according to Gudden, also penetrates the epider- moidal portions of the hair follicles. The skin is covered with orange-yellow, brownish-yellow, or dark-brown patches which are slightly elevated above the adjacent skin, and glisten slightly or not at all; in old cases, they are scaly and fissured. They can be readily removed by scratching with the finger-nail. This lays bare the reddened cutis which bleeds from numerous small openings. If the epidermis scales are placed on an object glass, and a drop of Female Guinea Worm. Natural size. 376 PARASITES OF THE SKIN. potash (1: 3) added, the fungi become clearly visible at the end of ten to fifteen minutes, after the epidermis cells have swollen and become transparent. They form round heaps of spherical conidia, with a dia- meter of 0.005-0.007 mm. They contain not infrequently a nucleus-like structure or granular protoplasm (vide Fig. 152). Mycelium threads are also present. The older ones contain transverse partitions and one or more nuclei in the individual subdivisions. In some places, the round conidia sprout into mycelium threads; in others, conidia sprout from the latter. The patches of pityriasis versicolor are almost always found on cov- ered portions of the body. They generally appear first on the chest, then extend gradually to the neck, abdomen, and back. They are sometimes found in the axillae, on the mons veneris, in the inguinal folds, and on the inner surface of the thighs. In exceptional cases, they are present in the face, never on the hands and feet. Large portions of the integument are often changed in the manner described, as a result of the coalescence of smaller patches. The centre Fm. 152. Microsporon furfur, a. Mycelium threads ; 0. Conidia ; c. Epithelium cells. of the patches sometimes clears up, which the change continues to ex- tend at the periphery. Subjective symptoms are entirely absent, or there is slight itching, especially while perspiring. The disease does not occur during childhood or old age. Exacerba- tions and remissions are noticeable, and sometimes the disease disappears temporarily. Koebner succeeded in inoculating the fungus upon his own integument and upon that of rabbits; but infection from man to man is rarely observed in practice. II. Diagnosis.—The ready desquamation of the pigment patches distinguishes this from most other pigment changes of the skin, and, in addition, the fungus is readily found with the microscope. III. Treatment.—This consists chiefly of cleanliness. The skin should be rubbed, for several successive evenings, with sapo viridis or with: IJ, Sapon. virid., Lact. sulphur., Picis liquid., Spts. vin. dilut aa 3 i. M. D. S. To be rubbed in at night, PAKASITES OF THE SKIN. 377 and in the morning it should be carefully washed with a woollen cloth. No spot should be overlooked, since it will serve as a fresh starting- point for the disease. 2. Favus. (Tinea favosa. Porrigo favosa. Dermatomycosis achorina.) I. Symptoms and Anatomical Changes.—The fungus of favus (Acharion s. Oidium Schoenleinii) is found almost always on the scalp. When present on other parts, it starts, as on the scalp, from the hair-fol- licles. It rarely affects the nails (onychomycosis favosa). The disease appears at first as yellow points (as large as a pin’s head) beneath the epidermis; they are perforated by a hair. The spots gradually increase to the size of a pea, bean, or ten-cent piece. At the same time, a central umbilication appears, while the periphery becomes elevated, and the so-called favus cup is thus shaped like a plate. Fig. 153. Achorion Schoenleinii from the lower layers of the favus cup. After Kaposi. When the favus cups are separate, the disease is known as favus dispersus; when they coalesce, as favus confertus. In old cases, the entire scalp may be attacked. The deposits on the skin not infrequently lose their original sulphur color, and become whitish-yellow, light gray, or dirty gray. If the favus crusts are removed, they may be ground between the fingers, and emit a peculiar mouldy, musty odor. If particles are treated with water or potash, and examined under the microscope, they are found to consist, apart from a few epidermis cells, fat drops, granular detritus, and schizomycetes, of numerous gonidia and mycelium threads of Achorion Schoenleinii (Fig. 153). The gonidia predominate in the lower layers of the crusts; the mycelium threads, in the upper layers. The gonidia are round, band-shaped, or cask-shaped, and are found singly or in groups or rows, while the mycelium threads are segmented, and in places branched. Achorion Schoenleinii belongs to the mould fungi (hyphomycetes). It can be conveyed to other individuals. The old view that it is identical with the fungua of pityriasis versicolor and herpes has been abandoned. 378 FAEASITES OF THE SKIN. The increasing development of the favus crusts is attended with im- portant changes in the hairs and epidermis. At first the fungus devel- ops only in the funnel-shaped space situated at the opening of the hair- follicle, so that it is surrounded like a ring by epidermis. But it soon spreads deeper into the follicle, and gives rise to nutritive disturbances Fig. 154. Hair and root sheaths, in favus, infiltrated with conidia and mycelia. in the hair, partly as the result of pressure, partly by destruction of the hair-papilla. The fungus passes between the external and internal root- sheaths of the hair, later it perforates the upper cuticle of the hair, and enters the cortical layers. The mycelia predominate in this region (vide Fig. 154). The hairs appear dry, destitute of gloss, break readily, can be readily removed on slight traction, or fall out spontaneously. If PARASITES OF THE SKIN. 379 the papilla has been destroyed, regeneration of the hair is impossible, and the part remains permanently bald. If a crust is removed in the earlier stages, the cutis is often found to be red and slightly moist. Later it is covered with young epidermis, so that the removal of the crust shows a delicate, glistening epidermis, which looks almost like a cicatrix. Atrophy of the sebaceous glands, cystoid formations in them, in rare cases cutaneous ulcerations have also been observed. The development of favus is associated with itching. Eczema of the scalp and swelling of the adjacent lymphatic glands are sometimes ob- served as complications. In a few cases herpes tonsurans and favus have been noticed in the same individual. In filthy persons, favus may last thirty years or more, the masses of the fungus accumulating above each other in thick crusts. If favus develops on other parts of the body, the crusts generally fall off at an earlier period and spontaneous recovery occurs, except in rare cases. In favus of the nails (onychomycosis favosa), the nails are thickened, fissured, brittle, and destitute of gloss, are exfoliated in parts, and on the addition of potash are found to contain Achorion Schoenleinii. The infection probably is the result of scratching the scalp which is covered with favus. II. Etiology.—The disease is either conveyed from animals, or from man to man. It is often found in mice, but the fungus is generally con- veyed to man by the cat, the latter being infected by mice or rats. Favus has also been observed in dogs, rabbits, chickens, cows. The greater the degree of uncleanliness the greater is the danger of infection of one individual by another. The disease is most frequent in children or young people, and also in the male sex. III. Diagnosis.—The diagnosis is rendered extremely easy by the aid of the microscope, so that a mistake is hardly possible. IV. Prognosis.—The prognosis is good, except that the hair will not be restored in parts which have become bald, if the hair follicles have been destroyed. Y. Treatment.—In favus of the scalp, the crusts should be oiled for two hours, and then covered with a piece of flannel dipped in oil, until the crusts can be entirely removed. The scalp is then carefully washed morning and evening with green soap. After each wash, all unhealthy looking hairs should be removed with the fingers or a pair of tweezers, together with all the hairs in the immediate vicinity of the former crusts (in order to prevent reinfection from the fungus which has been left in the follicles). The parts are then rubbed with corrosive sublimate and alcohol (gr. iij. : f iiiss.). This procedure should be continued four to twelve weeks, and the patients should be kept under observation for weeks afterwards, in order that the treatment may again be instituted if a relapse occurs. Other parasiticides have also been recommended, such as carbolic and salicylic acids, sulphur, tar, creasote, benzin, Peruvian balsam, styrax, turpentine, etc. In favus of the nails, the affected parts should be excised and painted with corrosive sublimate collodion (1 : 20). 380 PARASITES OF THE SKIN. 3. Herpes tonsurans. {Tinea tondens. Tricliomyces s. Dermatomycosis tonsurans.) I. Anatomical Changes.—The fungus of herpes tonsurans (tri- cophyton tonsurans) is found not alone on the scalp, but also upon parts which are covered with downy hairs. In the beard, it gives rise to syco- sis parasitaria (page 336), and in parts of the skin which are constantly protected and kept moist, it gives rise to eczema marginatum. It also develops occasionally in the substance of the nails (onychomycosis ton- surans). Upon the scalp and on most other parts of the skin, the changes pro- duced bv the fungus appear in three forms, herpes tonsurans vesiculo- sus, maculosus, and squamosus. The latter is a later stage of the other two. Fig. 155. Epidermis scale in herpes tonsurans squamosus, containing more mycelia than conidia. After Kaposi. Herpes tonsurans vesiculosus is attended at first by the development of small, clear, cloudy, or even purulent vesicles, which are generally not larger than a pin's head. These soon dry into thin scales, at the peri- phery of which new vesicles appear in a circle, and this may continue until a surface larger than the palm of the hand is affected. While ves- icles are still distinct in the peripheral zones, the central portions show the changes of herpes tonsurans squamosus ; indeed, the centre itself may have entirely recovered. Adjacent circles may come in contact and form chain-like figures. In old and neglected cases, the larger pirt of the surface of the body may be affected. In herpes tonsurans maculosus we notice, at first, small pale-red or brownish-red patches, which are slightly elevated above the healthy skin. While the patch pales and becomes covered with thin scales, a new red zone appears at the periphery, and this process is repeated as in the ve- sicular form. The fungus must be looked for in the peripheral zones. In herpes PARASITES OF THE SKIN. 381 squamosus, they are contained in the scales; in herpes vesiculosus, in the epidermal covering of the vesicles, but repeated examination is often necessary in order to discover them. In order to make the microscopi- cal preparation transparent, a solution of potash (1 :3) should be added. Like the fungus of favus, that of herpes tonsurans appears in the form of round, oval, cask-shaped, homogeneous, granular, or nucleated gonidia and thread-shaped mycelia (Fig. 155), but the latter are more abundant than in the favus fungus. They are often branched, and filled with granular protoplasm, vacuoles, or nuclei. The fungus is situated between the cells of the stratum corneum and the upper cells of therete Malpighii. Flo. 156. Hair in herpes tonsurans. After Kaposi. Herpes tonsurans of the scalp occurs most frequently in the squa- mous form. The circles often extend to the integument of the forehead or nape of the neck. Within the circles the hairs break very readily, so that spots which are almost bald are found upon the scalp. The hairs are readily removed by traction, and, under the microscope, it is found that the fungus has penetrated between the root sheaths of the hair follicle, and also into the cortical substance of the hair (vide Fig. 156). Asa rule, the papilla is not destroyed, so that the hair is restored, after re- moval of the fungus. Onychomycosis tonsurans causes opacity, thickening, Assuring of the nail which may finally be exfoliated. It affects only the finger nails, probably as the result of self-infection in scratching herpetic patches. The herpes on the skin is sometimes recovered, although onychomy- 382 PAKASITES OF THE SKIN. cosis continues. The fungus elements are distinctly visible, under the microscope, in nail scrapings which have been cleared up by the addi- tion of potash (vide Fig. 157). Sycosis parasitaria has been discussed on page 336. Huebner has shown that the eczema marginatum of Ilebra is nothing more than herpes tonsurans. It is observed most frequently on the inner surface of the thigh and scrotum, and may extend to the pubes and perineum. It occurs more rarely in the axillae, the folds under the breast, umbilicus, or other parts. It forms hyperaemic patches, which are covered with vesicles, pustules, scales, and crusts, and have a zigzag, sharp border. The microscope reveals fungi in the scales, but, according to Ilebra, they never penetrate into the hair follicles. The peculiar appearance of eczema marginatum is probably owing to the fact that the diseased Fig. 157. Onychomycosis tricophytina. Potash preparation. After Kaposi. parts, on account of their protected position, are constantly bathed in a warm, moist atmosphere, or that herpes tonsurans complicates a pre- existing eczema. The disease may last for years, but spontaneous recovery sometimes takes place. The subjective symptoms consist merely of itching, and even this is not constant. II. Etiology.—Inoculation proves that the disease is produced by the fungus. Infection from man to man is more frequent than in favus, and the disease occurs endemically in families, schools, and barracks. It is sometimes conveyed from barber shops through the medium of unclean shaving utensils. In other cases, it is contracted from animals (dog, cat, horse, cow, rabbit). The disease has also been observed in individuals who live in damp apartments, constantly use damp under- clothing or bedding, or warm poultices. It is observed most frequently parasites of the skin. 383 in the spring and autumn, and in damp weather, and chiefly attack children and young people. III. Diagnosis, Prognosis, Treatment.—The diagnosis is ren- dered positive by the discovery of the fungus. The prognosis i3 good, the treatment similar to that of favus, but recovery is effected more rapidly. INDEX. Abdominal muscles, paralysis of, 30 spasm of, 45 reflex of, 222 Abscess of the brain, 233 spinal cord, 84 Absentia epileptica, 266 Acarus folliculorum, 372 scabiei, 365 Achorion Schoenleinii, 377 Achromatia, 360 Acne artificialis, 335 cachecticorum, 335 disseminata, 335 frontalis, 335 mentagra, 336 punctata, 335 pustulosa, 335 rosacea, 338 vulgaris, 335 Acrodynia, 324 iEsthesiometer, 64 Ageusis, 71 Agraphia, 209 Albinism, 360 Alcohol paralysis, 155 Alexia, 209 Alopecia, 362 areata, 363 Celsi, 363 Amimia, 210 Amyotrophic lateral sclerosis, 135 Amyotrophy, spinal progressive, 122 Anaemia of the brain, 210 spinal cord, 77 Anaesthesia, 62 dolorosa, 67, 85 gustatory, 71 olfactory, 70 trigeminal, 68 Anarthria, 177 Aneurism of cerebral arteries, 246 miliary, of cerebral arteries, 220 Anhidrosis, 349 Anosmia, 70 Anuria, hysterical, 298 Ape-hand, 23 Aphasia, 205 amnesic, 207 ataxic, 205 motor, 205 25 Aphasia, sensory, 206 total, 206 Apoplexy, cerebral, 218 of the cerebral meninges, 260 of the medulla oblongata, 185 of the spinal meninges, 172 spinal, 79 Apraxia, 209 Arm centre, cortical, 192 Arsenic paralysis, 154 Articular changes in tabes dorsalis, 108 Articular neuralgia, 62 Ascending spinal paralysis, 149 degeneration of spinal cord, 134 Asemia, 205 Associated movements, 225 Asteatosis, 352 Asymbolia, 205 Ataxia, 100 hereditary, 130 Athetosis, 283 Atrophic infantile paralysis, 114 Atrichia, 362 Atrophia musculorum lipomatosa, 312 Atrophy of the brain, 252 of face, unilateral, 305 of skin, 360 Auditory disturbances in facial paraly- sis, 6 Aura, epileptic, 264 Axillary paralysis, 26 Base of brain, focal symptoms in dis- eases of, 204 Barsesthesiometer, 63 Bell’s palsy, 1 Beriberi, 75 Blepharospasm, 39 Borborygmus, hysterical, 297 Brachial neuralgia, 53 Brach-Romberg symptom, 107 Brain, diseases of, 190 abscess, 233 anaemia, 210 atrophy, 252 cancer, 240 cysts, 239 apoplectic, 219t embolism, 229 encephalitis, 233 386 INDEX. Brain, encephalitis, congenital, 238 glioma, 239 hemorrhage, 218 punctate, 229 hypersemia, 213 hypertrophy, 251 neuroses, 262 oedema, 217 parasites, 245 thrombosis, 229 tumors, 239 Bromine acne, 336 Bromhidrosis, 349 Brown-Sequard’s paralysis, 138 Bulbar myelitis, 188 nuclei, paralysis of, 176 Bulbar paralysis, apoplectiform, 186 chronic, 176 Bulimia, hysterical, 299 Cachexie pachydermique, 311 Callositas, 355 Canities, 361 Capsule, external, 203 internal, 197 Capillary hemorrhages in brain, 229 in spinal cord, 81 Caput obstipum, paralytic, 15 spastic, 42 Catalepsy, 291 Carbon bisulphide paralysis, 154 Carbonic oxide gas paralysis, 154 Causalgia, 54 Central convolutions, focal symptoms in diseases of, 192 Centrum ovale, focal symptoms in dis- eases of, 196 Cerebellar peduncles, focal symptoms in diseases of, 203 Cerebellum, focal symptoms in diseases of, 203 Cerebral arteries, aneurism of, 246 Cerebral cortex, focal symptoms in dis- eases of, 191 Cerebral hemorrhage, 218 Cerebral meninges, diseases, 253 hemorrhage, 260 inflammation, 253 Cerebral nerves, exit of, 205 vessels, diseases of, 229 aneurism, 246 distribution, 208 embolism, 229 syphilis, 230 thrombosis, 229 sinus, inflammation of, 256 symptoms, diffuse, 190 . focal, 190 Cerebro-spinal sclerosis, 91 Cervico-brachial neuralgia, 53 occipital neuralgia, 51 Chapman’s rubber bag, 81 Cheirospasm, 155 Chloasma, 353 Choked disk, 243 Cholesteatoma of brain, 239 Chorea, 277 congenital, 277 gravidarum, 278 post-hemiplegic, 282 prsehemiplegic, 282 Chromhidrosis, 349 Cimex lectularius, 374 Cincture feeling, 85 Clavus hystericus, 295 Claw hand, 24, 123 Claus trum, 203 Clothes lice, 373 Cnidosis, 319 Coccygodynia, 62 Comedo, 352 Compression-myelitis, 144 Concussion, spinal, 143 Conditions, epileptoid, 267 Conduction, delayed, 106 paths ot', in spinal cord, 131 Contractions, diplegic, 127 Contracture, hysterical, 293 secondary, 131 Copiopia, hysterical, 296 Corpora quadrigemina, focal symptoms in diseases of, 203 Corpus striatum, focal symptoms in diseases of, 199 Cortical centres, motor epilepsy, 191 Cramp, 45 Crura cerebelli, focal symptoms in dis- eases of, 203 Crura cerebri, focal symptoms in dis- eases of, 199 Crural nerve, neuralgia of, 58 paralysis, 31 Crutch paralysis, 18 Crises, gastric, 95 intestinal, 106 Cyanhidrosis, 350 Cysticercus of brain, 245 skin, 375 Cysts, apoplectic, 219 Decubitus, acute, 86 Defluviutn capillorum, 362 Degeneration of lateral columns, 131 of posterior columns, 110 reaction, 7 secondary of cord, 130 Demodex folliculorum, 372 Dermatitis, 319 Dermatomycoses, 375 Dermatoses parasitariae, 365 Dermatozoonoses, 365 Dermoid cyst of brain, 239 Descending degeneration of spinal cord, 131 Diaphragm, neuralgia, 53 paralysis, 29 spasm, 44 Diplegia facialis, 9 Double sensation, 66, 106 Duchenne’s disease, 312 Dura mater, cerebral, diseases of, 253 spinal, diseases of, 162 INDEX. 387 Dysesthesia, 86 Dystrophia musculorum progressiva, 312 Echinococcus of brain, 245 spinal meninges, 175 Eclampsia, 270 Ecthyma, 333 Ectropium, paralytic, 5 Eczema, 325 caloricum, 325 capillitii, 326 faciei, 327 marginatum, 380 Embolism of cerebral arteries, 229 of medulla oblongata, 186 Emprosthotonus, 247 Encephalitis, 233 Encephalomalacia, 229 Encephalorrhagia, 218 Enchondroma of brain, 239 spinal meninges, 175 Enteralgia, hysterical, 297 Ephelides, 353 Ephidrosis, 348 Epidermidophytes, 342 Epilepsy, 262 hystero-, 294 Jacksonian, 194 Epileptoid conditions, 267 Epiphora, 5 Erb’s supraclavicular point, 27 Ergotism, 154 4 Erythema, epidemic, 324 exudative, 323 hyperaemic, 319 nodosum, 322 Etat crible, 215 Facial hemiatrophy, 305 hypertrophy, 307 neuralgia, 46 paralysis, 1 spasm, 36 Fatty emboli of brain, 230 Favus, 377 Fibrillary twitchings, 126 Fibroma of brain, 239 medulla oblongata, 188 spinal meninges, 175 Filaria medinensis, 374 Flexibility of muscles, waxy, 291 Folie musculaire, 281 Friedreich’s disease, 130 Fright paralysis, 151 Gastric crises in ataxia, 109 Gangrene, symmetrica], 310 Globus hystericus, 297 Glossalgia, 50 Glossoplegia, 16 Gluteal paralysis, 34 Glosso-labio-laryngeal paralysis, 176 Graphospasm, 155 Guinea worm, 374 Gustatory nerves, diseases of, 70 Gustatory nerves, diseases of, ageusia, 71 hypergeusia, 71 parageusia, 71 Hair, diseases of, 381 Haemathidrosis, 350, 172 Hsematoma of dura mater, 254 Haematomyelia, 79 Hsematomyelitis, 79 Haematorrhacbis, 172 Haemoptysis, hysterical, 298 Head tetanus, 276 Hemorrhage of brain, 218 medulla oblongata, 185 spinal meninges, 172 spinal cord, 79 Hemianaesthesia, 199 Hemianopsia, 195 Hemiatrophy, facial progressive, 305 Hemichorea, 281 Hemicrania, 301 Hemihypertrophy, facial, 307 Hemiopia, 195 Hemiplegia, alternate, 201 cerebral, 222 hysterical, 293 spinal, 139 Hereditary ataxia, 130 Herpes iris, 323 tonsurans, 380 Heterotopia, 239 Hiccough, 43 Hirsuties, 356 Hydrocephaloid, 211 Hydrocephalus, 247 acquired, 248 acute, 248 congenital, 250 external, 249 intermeningeal, 247 Hydromyelia, 98 Hydrophobia, hysterical, 297 Hydrops articulorum intermittens, 311 Hyperacusis, 6 Hyperaemia of brain, 213 spinal cord, 78 Hyperaesthesia, gustatory, 69 olfactory, 70 Hypergeusia, 70 Hyperhidrosis. 348 Hyperosmia, 69 Hypertrichosis, 356 Hypertrophy of brain, 251 face, unilateral, 307 hair, 356 nails', 357 skin, 353 Hyphidrosis, 349 Hypoglossal paralysis, 16 spasm, 41 Hysteria, 291 Hystero-epilepsy, 294 Ichthyosis, 355 Impetigo, 333 388 INDEX. Infantile paralysis, 114 acute atrophic, 114 cerebral, 238 spinal, 114 Infectious paralysis, 151 Intercostal neuralgia, 55 Intestinal crises in ataxia, 110 Ischialgia, 58 Itch, 365 Itching, cutaneous, 364 Jacksonian epilepsy, 194 Joint changes in ataxia, 108 neuralgia of, 62 Keratosis, 355 Kussmaul-Landry paralysis, 149 Lagophthalmus, paralytic, 5 Laryngeal crises, in ataxia, 110 Lateral sclerosis, 112 Latissimus dorsi, paralysis of, 29 Lingual spasm, 41 paralysis, 16 Lead paralysis, 151 Lenticular nucleus, focal symptoms in diseases of, 199 Lentigines, 353 Levator anguli scapulae, paralysis of, 29 Leptomeningitis, 167 Leukoderma, 360 Leukomyelitis, chronic posterior, 100 Leukopatliia, 360 Lice, 372 Lichen ruber, 346 scrophulosorum, 346 Lipomatosis musculorum progressiva, 312 Locomotor ataxia, 100 Lumbo-abdominal neuralgia, 57 Macrogaster platypus, 372 Malum Cotunnii, 58 Mastodynia, 59 Median paralysis, 22 Medulla oblongata, diseases, 176 compression, 189 embolism, 186 hemorrhage, 185 inflammation, 188 injuries, 189 thrombosis, 186 tumors, 188 Melasma, 354 Meniere’s disease, 290 Meningeal apoplexy, 172, 260 Meninges, anatomy of, 260 Meningitis, spinal, 167 Mentagra, 336 Microsporon furfur, 376 Migraine, 301 Miliaria, 330 Miliary aneurisms of cerebral arteries, 220 Milium, 353 Mogigraphia, 155 Multiple sclerosis, 91 Muscles, diseases of, 312 ischaemic paralysis, 318 pseudo-hypertrophy, 312 of mastication, spasm of, 40 progressive ossification, 317 Muscular atrophy, hereditary, 312 juvenile, 312 spinal, 122 Muscular hypertrophy, false, 312 true, 316 Muscular spasms, primary spinal, 162 Muscular twitchings, fibrillary, 126 Musculo-cutaneous nerve, paralysis of, 26 Myelitis, acute, 82 apoplectiform, 83 chronic, 90 disseminated, 91 hemorrhagic, 83 Myelo-malacia, 83 Myelo-meningitis, chronic, 90 Myxoedema, 311 Myositis ossificans progressiva, 317 Naevus, 353 Nerves, diseases. 1 inflammation, 71 Nerves of arms, combined paralysis of, 27 Neuralgia, 46 alveolar, 50 ano-vesical, 62 cervico-brachial, 53 cervico-occipital, 51 ciliary, 49 crural, 58 facial, 46 inferior alveolar, 50 inframaxillary, 50 infraorbital, 49 intercostal, 55 lingual, 50 lumbo-abdominal, 57 mental, 50 mammary, 57 obturator, 58 of joints, 62 ophthalmic, 49 phrenic, 53 sciatic, 58 spermatic, 61 supraorbital, 49 supratnaxillary, 49 trigeminal, 46 Nettle rash, 319 Neurasthenia, cerebral, 300 spinal, 148 Neuritis, 71 multiple, 74 nodose, 72 Neuroses of the brain, 262 joints, 62 skin, 364 spinal cord, 147 INDEX. 389 Nictitating spasm, 40 Nucleus lenticularis, focal symptoms in diseases of, 199 Nystagmus, 95 Obturator neuralgia, 58 paralysis, 33 Occipital lobe, focal symptoms in dis- eases of, 195 Occipital neuralgia, 51 CEdema of brain, 217 Olfactory nerve, diseases, 69 anosmia, 70 hyperosmia, 69 parosmia, 70 Oligosteatosis, 352 Oliguria, hysterical, 298 Onychauxis, 357 Onychogryphosis, 357 Onychomycosis favosa, 377 tonsurans, 380 Ophthalmia, neuro-paralytic, 69 Ophthalmic neuralgia, 49 Opisthotonus, 274 Osmhidrosis, 349 Ovarialgia, 295 Ovum hystericum, 295 Oxyokoia, 6 Pachymeningitis, cerebral, 253 external spinal, 162 internal spinal, 164 Papillitis, 243 Parageusia, 71 Paralysis, acute ascending, 149 agitans, 283 arsenic, 154 after acute diseases, 151 alcohol, 155 bisulphide of carbon, 154 carbonic oxide, 154 facial, 1 fright, 151 glosso-labio-laryngeal, 176 infectious, 151 lead, 152 motor trigeminus, 13 phosphorus, 154 psychical spinal, 151 railway, 143 reflex, 150 spastic, 112 toxic spinal, 151 Paraplegia, urinary, 150 Parasteatosis, 352 Parhidrosis, 349 Parietal lobes, focal symptoms in dis- eases of, 194 Parkinson’s disease, 283 Parosmia, 70 Patellar tendon reflex, 107 Pectoral muscles, paralyis of, 28 Pediculus capitis, 372 pubis, 374 vestimentorum, 373 Pedunculi cerebri, focal symptoms in diseases of, 199 Pellagra, 324 Pemphigus, 331 Perimeningitis spinalis, 162 Perineuritis, 72 Peripachymeningitis spinalis externa, 152 Peroneal paralysis, 34 Pharyngeal crises in ataxia, 110 Phlebitis of cerebral sinuses, 257 Phosphorus paralysis, 154 Phrenic nerve, neuralgia, 53 paralysis, 30 Piano-player’s spasm, 158 Pica hysterica, 295 Pigment atrophy of skin, 380 emboli of brain, 230 Pityriasis rubra, 344 versicolor, 375 Pleurostliotonus, 274 Plica polonica, 326 Polioencephalitis, acute, 238 Poliomyelitis, acute infantile, 114 chronic, 122 of adults, 120 Poliosis, 361 PolyEesthesia, 66 Polyneuritis, 74 Polytrichia, 356 Pompholix, 331 Pons, focal symptoms in diseases of, 201 Post-hemiplegic chorea, 282 Praehemiplegic chorea, 282 Praeputial calculi, 351 Pressure points, hysterical, 295 Valleix’, 48 Progressive muscular atrophy, 122 Prosopalgia, 46 Prosoplegia, 1 Prosopodysmorphia, 305 Prosospasmus, 36 Prurigo, 344 Pruritus, 364 Psoriasis, 340 Pulex irritans, 374 penetrans, 374 Pupils, reflex rigidity of, 109 Radial paralysis, 18 Railway paralysis, 143 Raphania, 154 Reflex epilepsy, 263 hysteria, 292 paralysis, 150 vertigo, 290 Rhinophyma, 339 Rhomboids, paralysis of, 29 Risus sardonicus, 273 Saltatory spasms, 161 Sand flea, 374 Sarcoptes hominis, 365 Scabies, 365 Sciatica, 58 390 INDEX. Sclerema adultorum, 357 neonatorum, 359 Scleroderma, 357 Scleroma, 357 Sclerosis, multiple, 91 of lateral columns, 112 of posterior columns, 100 periependymal, 90 Sebaceous secretion, anomalies of, 350 Seborrhoea, 350 Serratus magnus, paralysis of, 27 Singultus, 43 Sinuses, cerebral, inflammation of, 257 thrombosis of, 257 Skin, diseases of, 319 atrophy, 360 hypertrophy, 353 inflammations, 319 erythematous, 319 papular, 344 pustular, 333 scaly, 340 vesicle-like, 325 vesicular, 331 neuroses, 364 parasites, animal, 365 vegetable, 375 secretory anomalies, 348 Sleep paralysis, 18 Spasmus nictitans, 40 Spastic gait, 114 spinal paralysis, 112 Speech centres, cortical, 208 Spermatic neuralgia, 61 Spinal accessory, paralysis of, 14 Spinal cord, diseases of, 77 abscess, 84 acute inflammation of anterior horns, 114 acute injuries, 141 anaemia, 77 combined system diseases of, 130 compression, 144 concussion, 143 formation of cavities in, 98 functional weakness, 148 hemorrhage, 79 hyperaemia, 78 inflammation, acute, 82 chronic, 90 irritation, 147 lateral sclerosis, 112 multiple sclerosis, 91 punctate hemorrhages, 81 sclerosis of posterior columns, 100 secondary degeneration, 130 tumors, 98 unilateral lesions, 138 Spinal meninges, diseases of, 162 hemorrhage, 172 Status eclampticus, 270 epilepticus, 266 hystero-epilepticus, 294 St. Vitus’ dance, 277 Sudamina, 330 Supraclavicular point. 27 Supraorbital neuralgia, 49 Sycosis, 336 Sympathetic, irritative conditions of, 308 paralytic conditions of, 309 Syncope, 212 Syringomyelia, 98 Tabes dorsalis, 100 spasmodica, 112 Tactile sensation, examination of, 64 Tar acne, 335 Tegmentum, 201 Telegrapher’s spasm, 158 Tendon reflexes, 107 Tenosinitis hypertrophica, 21 Tetany, 158 Tetanus, 271 Thalamus opticus, focal symptoms in diseases of, 199 Thermaesthesiometer, 65 Thrombosis of cerebral sinuses, 256 vessels, 229 Thomsen’s disease, 162 Tibial paralysis, 34 Tic convulsif, 37 douloureux, 46 rotatoire, 43 Tinea favosa, 377 tondens, 380 Toxic spinal paralyses, 151 Tremor, 288 Trichauxis, 356 Trichomycosis, 380 Tricophyton tonsurans, 380 Trichorhexis, 363 Trigeminal anaesthesia, 68 neuralgia, 46 paralysis, 13 spasm, 40 Trismus, 273 Trophoneurosis facialis, 305 Trousseau’s phenomenon, 159 Tumors of brain, 238 medulla oblongata, 188 spinal cord, 98 spinal meninges, 174 Ulnar paralysis, 23 Urine, spastic, 298 Urticaria, 319 Vaginismus, 298 Valleix’ pressure points, 48 Varus, 335 Vertigo, 289 a stomacho laeso, 290 cardiac, 290 epileptic, 267 senile, 289 Vitiligo, 360 Waxy flexibility of muscles, 291 Word blindness, 209 deafness, 206 Writer’s spasm, 155 Xeroderma, 364 Zone, epileptogenic, 268